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Paul Craig Roberts
The show trial of a somewhat arbitrarily selected group of 21 surviving Nazis at Nuremberg during 1945-46 was US Supreme Court Justice Robert Jackson’s show. Jackson was the chief prosecutor. As a long-time admirer of Jackson, I always assumed that he did a good job.
My admiration for Jackson stems from his defense of law as a shield of the people rather than a weapon in the hands of government, and from his defense of the legal principle known as mens rea, that is, that crime requires intent. I often cite Jackson for his defense of these legal principles that are the very foundation of liberty. Indeed, I cited Jackson in my recent July 31 column. His defense of law as a check on government power plays a central role in the book that I wrote with Lawrence Stratton, The Tyranny of Good Intentions.
In 1940 Jackson was US Attorney General. He addressed federal prosecutors and warned them against “picking the man and then putting investigators to work, to pin some offense on him. It is in this realm—in which the prosecutor picks some person whom he dislikes or desires to embarrass, or selects some group of unpopular persons and then looks for an offense—that the greatest danger of abuse of prosecuting power lies. It is here that law enforcement becomes personal, and the real crime becomes that of being unpopular with the predominant or governing group, being attached to the wrong political views or being personally obnoxious to, or in the way of, the prosecutor himself.”
Later as a Supreme Court justice Jackson overturned a lower court conviction of a person who had no idea, or any reason to believe, that he had committed a crime.
Having just finished reading David Irving’s book Nuremberg (1996), I am devastated to learn that in his pursuit of another principle, at Nuremberg Jackson violated all of the legal principles for which I have so long admired him. To be clear, at Nuremberg Jackson was in pursuit of Nazis, but their conviction was the means to his end—the establishment of the international legal principle that the initiation of war, the commitment of military aggression, was a crime.
The main problem with the trials is that WW II was started by the British with their declaration of war against Germany, not by Germany.
Another problem was that at Nuremberg people were tried on the basis of ex post facto law—law that did not exist at the time of their actions for which they were convicted.
Moreover, the sentence—death by hanging—was decided prior to the trial and prior to the selection of defendants.
Moreover, the defendants were chosen and then a case was made against them.
Exculpatory evidence was withheld. Charges on which defendants were convicted turned out to be untrue.
The trials were so loaded in favor of the prosecution that defense was pro forma.
The defendants were abused and some were tortured.
The defendants were encouraged to give false witness against one another, which for the most part the defendants refused to do, with Albert Speer being the willing one. His reward was a prison sentence rather than death.
The defendants’ wives and children were arrested and imprisoned. To Jackson’s credit, this infuriated him.
President Franklin D. Roosevelt, General Eisenhower, and Winston Churchill thought that surviving Nazis should be shot without trial. Roosevelt laughed about liquidating 50,000 German military officers. Eisenhower told Lord Halifax that Nazi leaders should be shot while trying to escape, the common euphemism for murder. Russians spoke of castrating German men and breeding German women to annihilate the German race. US Treasury Secretary Henry Morgenthau wanted to reduce Germany to an agrarian society and send able-bodied Germans to Africa as slaves to work on “some big TVA project.”
Robert Jackson saw in these intentions not only rank criminality among the allied leadership but also a missed opportunity to create the legal principle that would criminalize war, thus removing the disaster of war from future history. Jackson’s end was admirable, but the means required bypassing Anglo-American legal principles.
Jackson got his chance, perhaps because Joseph Stalin vetoed execution without trial. First a show trial, Stalin said, to demonstrate their guilt so that we do not make martyrs out of Nazis.
Whom to select for the list of 21-22 persons to be charged? Well, whom did the allies have in custody? Not all those they desired. They had Reichsmarschall Herman Göring who headed the air force. Whatever the valid charges against Göring, they were not considered to be mitigated by the fact that under Göring the German air force was mainly used against enemy formations on the battleground and not, like the US and British air forces in saturation terror bombing of civilian cities, such as Dresden, Tokyo, Hiroshima, and Nagasaki, or by the fact that in Hitler’s final days Hitler removed Göring from all his positions, expelled him from the party, and ordered his arrest.
The Nuremberg trials are paradoxical in that the law Jackson intended to establish applied to every country, not to Germany alone. The ex post facto law under which Germans were sentenced to death and to prison also criminalized the terror bombing of German and Japanese cities by the British and US air forces. Yet, the law was only applied to the Germans in the dock. In his book, Apocalypse 1945: The Destruction of Dresden (1995), Irving quotes US General George C. McDonald’s dissent from the directive to bomb civilian cities such as Dresden. Gen. McDonald characterized the directive as the “extermination of populations and the razing of cities,” war crimes under the Nuremberg standard.
They had foreign minister Ribbentrop. They had field marshals Keitel and Jodl and the grand-admirals Raeder and Dönitz. They had a German banker, who was saved from sentencing by the intervention of the Bank of England. They had a journalist. They had Rudolf Hess who had been in a British prison since 1941 when he went to Britain on a peace mission to end the war. They wanted an industrialist, but Krupp was too old and ill. He was devoid of the persona of a foreboding evil. You can read the list in Irving’s book.
Göring knew from the beginning that the trial was a hoax and that his death sentence had already been decided. He had the means (a poison capsule) throughout his imprisonment to commit suicide, thus depriving his captors of their planned humiliation of him. Instead, he held the Germans together, and they stood their ground. Possessed of a high IQ, time and again he made fools of his captors. He made such a fool of Robert Jackson during his trial that the entire court burst out in laughter. Jackson never lived down being bested in the courtroom by Göring.
And Göring wasn’t through with making his captors look foolish and incompetent. He, the field marshalls and grand admiral requested that they be given a military execution by firing squad, but the pettiness of the Tribunal wanted them hung like dogs. Göring told his captors that he would allow them to shoot him, but not hang him, and a few minutes before he was to be marched to the gallows before the assembled press and cameras he took the poison capsule, throwing the execution propaganda show into chaos. To this injury he added insult leaving the prison commandant, US Col. Andrus a note telling him that he had had 3 capsules. One he had left for the Americans to find, thus causing them to think his means of escaping them had been removed. One he had taken minutes prior to his show execution, and he described where to find the third. He had easily defeated the continuous and thorough inspections inflicted upon him from fear that he would commit suicide and escape their intended propaganda use of his execution.
There was a time in Anglo-American law when the improprieties of the Nuremberg trials would have resulted in the cases being thrown out of court and the defendants freed. Even under the ex post facto law and extra-judicial, extra-legal terms under which the defendants were tried, at least two of the condemned deserved to be cleared.
It is not clear why Admiral Donitz was sentenced to 10 years in prison. The chief American judge of the Tribunal, Francis Biddle, said: “It is, in my opinion, offensive to our concept of justice to punish a man for doing exactly what one has done himself.” “The Germans,” Biddle said, “fought a much cleaner war at sea than we did.“
Jodl, who countermanded many Nazi orders, was sentenced to death. The injustice of the sentence was made clear by a German court in 1953 which cleared Jodl of all Nuremberg charges and rehabilitated him posthumously.
The French justice at the Nuremberg Tribunal said at the time that Jodl’s conviction was without merit and was a miscarriage of justice.
The entire Nuremberg proceeding stinks to high heaven. Defendants were charged with aggression for the German invasion of Norway. The fact was kept out of the trial that the British were about to invade Norway themselves and that the Germans, being more efficient, learned of it and managed to invade first.
Defendants were accused of using slave labor, paradoxical in view of the Soviets own practice. Moreover, while the trials were in process the Soviets were apparently gathering up able-bodied Germans to serve as slave labor to rebuild their war-torn economy.
Defendants were accused of mass executions despite the fact that the Russians, who were part of the prosecution and judgment of the defendants, had executed 15,000 or 20,000 Polish officers and buried them in a mass grave. Indeed, the Russians insisted on blaming the Germans on trial for the Katyn Forest Massacre.
Defendants were accused of aggression against Poland, and Ribbentrop was not permitted to mention in his defense the Molotov-Ribbentrop Pact that divided Poland between Germany and the Soviet Union, without which Germany could not have attacked Poland. The fact that the Soviets, who were sitting at Nuremberg in judgment on the Germans, had themselves invaded Poland was kept out of the proceedings.
It goes on from here endlessly. The Nuremberg Trials stand as the worst injustice in Western judicial history. It served to cover up the war crimes of the allies and to magnify out of all proportion those of Germany.
Original Article: https://paulcraigroberts.org/tyranny-at-nuremberg-2/
Telegram | Forbidden Truth
For 45 years, the world called her a living saint.
Mother Teresa. Nobel Peace Prize. Blessed by three Popes. Worshipped by billions.
She was running the largest child trafficking pipeline in history.
And the Vatican knew.
THE CALCUTTA OPERATION
Between 1962 and 1997, Teresa's Missionaries of Charity processed over 3 million orphans through 517 homes in 100+ countries.
Exposed records show:
She didn't save those children. She sold them.
THE CONNECTIONS THEY HID
THE VATICAN VAULT
In 2017, Indian police raided a Missionaries of Charity home in Ranchi.
They found nuns selling babies for $1,800 each.
The Vatican's response? Silence.
Pope Francis fast-tracked Teresa's sainthood in 2016 — one year BEFORE the raid. They canonized her to make her untouchable.
The Vatican Bank processed $8 billion in anonymous donations through Teresa's network between 1970 and 1997. No receipts. No records. No questions.
Where did the money go?
Where did the children go?
Same answer. Same network. Same people.
THE EPSTEIN CONNECTION
Haiti → Dominican Republic → Virgin Islands.
This was Epstein's route. But it was Teresa's route 30 years earlier.
The orphanages she built became the supply chain for what came after.
Brunel used her agencies. Maxwell used her contacts. Epstein used her infrastructure.
She built the machine. They just turned it on.
The Nobel Prize. The sainthood. The hospitals named after her.
All of it — a cover for the greatest child trafficking operation ever constructed.
3 million orphans. Zero accountability. One "saint."
The truth doesn't care about your feelings.
Original Article: https://t.me/c/3233625802/176
Related:
TheAwakeNation.com
New bombshell [2020] intel reveals that Dr. Anthony Fauci is the son of the late Mother Teresa, who was a child trafficker for Jeffrey Epstein!
WELCOME TO THE FALL OF THE FALSE IDOLS: We all know the name Mother Teresa. She won a Nobel Peace Prize for her so-called humanitarian work and founded the Missionaries of Charity.
When She was on her world tour she gathered millions (rumored to be billions) of dollars from the rich, because they foolishly believed that she would be able to help the poor and suffering in India. Many people would believe that India was and currently is eternally grateful to her. How wrong they are! But what did she really do with all that money? It surely wasn’t used to improve the conditions of the suffering. Mother Teresa was not a living saint and in fact was somewhat morally corrupt — with a lot of evidence.
Mother Teresa’s money was mostly spent on funding Pedophilia and child rape, and not on the poor. She built a hundred facilities all over the world with her name and organization ‘Missionaries of Charity’ on each one. Most of them were nunneries and Papist-run children’s homes. where millions of children were abused, beaten and sodomised on a daily basis.
Many of these children were brainwashed and conditioned into cult-like-thinking, to make them act like her, thus sprang her “cult of suffering.” Ever wondered why the Catholic Church rushed to canonize Mother Teresa after her death? Turns out she was a child trafficker, selling babies & funneling between $50-100 million/year to the Vatican. Mother Teresa’s connections include Baby Doc Duvalier, the Haitian dictator, Saving’s and Loan criminal Charles Keating, and Robert Maxwell, the father of Jeffrey Epstein’s child sex trafficking partner, Ghislaine Maxwell. And here’s the kicker! Mother Teresa opened the D.C. based Home for Infant Children with none other than Hillary Clinton. This orphanage of sorts was quietly closed in 2012.
Original Article: https://theawakenation.com/satanism/child-trafficker-mother-teresa-was-anthony-faucis-mother/
These pages contain videos that focus on the truth.
Pilots State The Earth Is Flat They don't adjust for the curve because it does not exist. Planes fly over a flat earth. Pilots are aware of correct flight routes based upon a flat earth map. They know the truth.
~ Source: https://t.me/Truth11com/60330
~ Source: https://t.me/PsyOpsMemes/48347
The truth is told very well with images. A picture says a thousand words, and memes a few more. These pages have lots of images and memes that focus on the truth. Click image to enlarge + use arrows to navigate.
AmericanThinker.com
William Grice
A Study in Disarmament
“Have you any arms?”
“I have my old service revolver and a few cartridges.”
“You had better clean it and load it. He will be a desperate man, and though I shall take him unawares, it is as well to be ready for anything.”
I went to my bedroom and followed his advice. When I returned with the pistol, the table had been cleared, and Holmes was engaged in his favourite occupation of scraping upon his violin. — Arthur Conan Doyle, A Study in Scarlet (1887)
It is difficult to imagine a scene more alien to the modern British nanny state.
Not because Arthur Conan Doyle’s London was safer than ours, but because Watson’s possession of a service revolver is treated as entirely unremarkable.
Sherlock Holmes asks whether he has arms. Watson replies that he does. Faced with a desperate and potentially dangerous man, he is told to clean the revolver, load it, and bring it with him.
Since the Dunblane Massacre in 1996, however, the UK Parliament has passed extraordinarily restrictive Firearms Acts that effectively banned private handgun ownership across Great Britain.
Speaking on The Joe Rogan Experience, Restore Britain leader Rupert Lowe MP argued, “they don’t want the public to have guns... we now have a society that needs radical change and we need to release the individual.”
Cue much shock and horror from the chattering classes and mainstream media.
Yet, aside from joining the Armed Forces or police, ordinary Britons are completely disarmed, and public weapons training is all but strangled by government mandate.
Granted, a privileged few are allowed weapons: landed gentry boasting Shotgun Certificates, gamekeepers begging police for Firearm Certificates, and some target shooters at clubs.
But past the wall of red tape lies a clear rejection of liberty. The UK’s laws treat the ideal that a free citizen has the right to arm himself and his family against danger as completely illegitimate.
Laughably, enthusiasm for armed policing has collapsed within the force itself: a direct result of putting a police marksman on trial for murder after he stopped a black gang member, Chris Kaba, who was using an SUV as a weapon against police. Color me shocked.
For context, it was a getaway car tied to escalating violence: masked men fired a shotgun outside a primary school the night before and, earlier, Kaba had shot a man in both legs at a nightclub.
A good thing Sherlock wasn’t on the case, then, for if A Study in Scarlet were set in modern Britain, Holmes’s famous line wouldn't be “You had better clean it and load it,” but “You had better hide it, Watson, or the Armed Crime Unit will be raiding 221B before we even catch the cab”!
Firearms, Foreigners, and the Channel Fantasy
As a boy I fired a 20-gauge double-barrelled shotgun in Devonshire, and I’ve had plenty of trigger time on the British Army Reserve’s SA80 L85A2/A3, and it’s a bloody fun rifle. Low recoil, built like a brick, and easy enough to strip, clean, and zero, these rifles all happily take a beating and still perform well during Annual Combat Marksmanship Tests.
I’ve played with the semi-automatic L98A2 variant, too, though Heckler & Koch only ironed out the mechanical gremlins in the big boy’s version, I believe.
Escaping the UK’s suffocating gun laws, in any case, I’ve also managed to have a blast with the Glock 17 and a CZ 452-2E ZKM, bolt-action rimfire rifle out in Chiang Mai, northern Thailand.
However, from 5.56mm NATO to 9mm rounds, even down to humble .22 rimfire, the authorities in London regard such pursuits with disdain when undertaken by white Britons.
The irony is deafening. Europe is being flooded daily with military-aged male illegals from the Middle East, Africa, and parts of South Asia, while Anglo-Saxons have no Second Amendment rights.
Men who revel in sexual violence towards non-Muslim women, as exemplified by Pakistani rape gangs, or carry out deadly terror attacks across Europe in defence of their “holy” Qur’an.
Moreover, until recently, such men, if granted protection, could even bring pre-existing spouses and children to the countrywithout meeting the salary requirements or paying any visa fees. They never even applied for an entry visa but are still provided free room and board in hotels.
British citizens who marry foreign nationals, by contrast, must generally meet that £29,000 minimum income requirement and pay substantial visa fees. Naturally.
Genuine refugees, whether Afghan schoolgirls, Christian Karenni in Burma, or South African Boer families fleeing persecution, are completely crowded out by this predatory invasion.
Perhaps it’s no surprise the UK Government doesn’t want an armed populace then.
After all, community militias equipped with SA80s could deliver effective section fire up to 400 metres from recreational speedboats and defend the Channel, leaving politicians red-faced.
Deliberate fire at 10 rounds per minute would easily suppress and halt enemy people smugglers.
Then again, under such a fantasy scenario, rules of engagement would likely compel Border Force, Port and Maritime Regiments, and the Royal Navy to prevent such community action.
After all, nothing offends the modern British state quite like self-defense, especially pre-emptive; when human rights lawyers like Lord Hermer rule the roost, self-preservation becomes the real crime.
American Freedom
In America, the Founding Fathers understood what London’s political class forever refuses to admit: a disarmed populace is not a peaceful society, but a conquered one. A dying democracy.
The Second Amendment isn’t really about clay pigeons; it is the ultimate check on state overreach and a declaration of individual liberty. Here in the UK, we have lost that freedom.
It doesn’t matter whether you are a policeman, teacher, clergyman, doctor, or serve in His Majesty’s Armed Forces. Law-abiding citizens in the UK face strict restrictions on weapons.
Meanwhile, foreign criminals in South London and Islamists still acquire illegal firearms.
Full Second Amendment rights might go too far for Britain, in my opinion, but granting them to emotionally mature, active community members would be a net positive.
Considering our demographic changes and the nature of recent attacks, this should certainly extend to all native-born women.
One need only consider the case of the Sudanese migrant, Hadi Alodid, to understand why; the sub-human attempted to behead a man with a kitchen knife in Belfast and gouged out his eyes.
This is one of countless horrors, and by disarming Anglo-Saxons (while abandoning border control), London is forfeiting its legitimacy, little by little. The people have had enough.
Some Americans don’t know how precious their Bill of Rights really is.
The right to keep and bear arms.
Image: Source
Original Article: https://www.americanthinker.com/articles/2026/08/the-british-nanny-state-no-guns-allowed/
LewRockwell.com
John & Nisha Whitehead | The Rutherford Institute | Rutherford.org
“Behind the ostensible government sits enthroned an invisible government, owing no allegiance and acknowledging no responsibility to the people.“—Theodore Roosevelt
What began publicly as Donald Trump’s lavish, taxpayer-funded vision of a gilded White House ballroom is now being justified by the administration—in and out of court—as a matter of national security.
To President Trump, it seems, a ballroom by any other name is a bunker.
And what a bunker it is.
Court documents indicate the massive subterranean military complex being constructed five stories beneath the White House grounds will include bomb shelters, a hospital, “top secret military structures and equipment, military-grade venting, a single integrated air conditioning and heating system, sniper nests and a drone port on top.”
Stephen Miller, Trump’s White House Deputy Chief of Staff, has explicitly invoked “continuity-of-government interests“ in defending the ballroom/bunker project, arguing that the reinforced underground military installation is necessary to ensure uninterrupted presidential command during an attack or global crisis.
The White House, however, already has a bunker built for precisely this purpose.
According to former officials, a nuclear-hardened facility buried more than 60 feet underground was secretly completed during the Obama administration. It can reportedly shelter dozens of officials for weeks and provide the president and senior officials with a secure command center during an extreme national-security crisis.
Which raises an obvious question: if the White House already has a nuclear-hardened Continuity of Government bunker, why does it need another one?
What threat justifies a new five-story military complex beneath the People’s House—one large enough to include bomb shelters, a hospital, military infrastructure, sniper positions and drone facilities? And if this is really about national security, why has so much of the project been wrapped around a ballroom that the administration initially presented as something quite different?
It is telling that they are building it at breakneck speed.
According to court filings, hundreds of workers have been laboring around the clock, 20 hours a day, seven days a week, to push the project forward as quickly as possible.
The message seems clear: get far enough along, fast enough, and it becomes that much harder for Congress, the courts or some future administration to undo what has already been built.
There is a lesson in that, and it speaks to much more than a ballroom or a bunker.
That is how the architecture of authoritarian government becomes permanent: Build the surveillance system. Build the detention centers. Expand the raids. Normalize executive rule by decree. Weaken the courts. Sideline Congress. Militarize the machinery of enforcement. Then hand it all to the next administration.
The faces change. The powers remain.
So much of what Trump is using today was inherited from presidents before him. So much of what he is building now will remain available to presidents after him.
That is the deeper problem with the Bunker State.
It is not merely about where government officials go when disaster strikes.
It is about the mindset of a government that increasingly treats preservation of its own power as the highest form of national security.
There is a grim irony in watching Washington spend enormous sums fortifying itself against catastrophe while government itself lurches from crisis to crisis and foreign conflict to economic disruption. Again and again, the pattern is the same: create or exploit the crisis, invoke extraordinary powers to manage it, insulate those in power from the consequences, and leave the public to absorb the cost.
That is the bunker mentality in practice.
And Continuity of Government gives it a blueprint to follow.
Continuity of Government planning, or COG, was devised during the Cold War to ensure that the federal government could survive a Soviet nuclear attack. If Washington were destroyed, surviving officials would disperse to secure locations, maintain command and eventually reconstitute constitutional government.
The goal, at least in theory, was survival long enough to restore constitutional order.
But 9/11 changed the equation.
Nearly twenty-five years later, we are still living with the consequences.
The terrorist attacks of September 11, 2001, did more than kill nearly 3,000 people. They gave Washington the crisis it needed to dramatically expand emergency powers, surveillance and the national-security state.
COG was part of that transformation.
What had been designed for doomsday became part of everyday government. The bunkers at Raven Rock and Mount Weather were part of the plan to keep Washington functioning even if Washington itself could no longer function.
The government has spent billions making certain that it can survive almost anything. But survival of the government is not the same as preservation of the republic.
Presidents, agencies, military commands, intelligence operations and critical records can all be relocated so that the machinery of government can keep functioning underground.
But what about the Constitution?
That is the question all of this elaborate government survival planning never answers satisfactorily. Who guarantees that Congress remains meaningful, the courts independent, elections intact, emergency powers temporary and the rights of the people protected?
Those questions matter because COG is no longer merely about bunkers.
It is part of a much larger emergency state—a government that has learned to govern through crisis, fear and claims of necessity.
After 9/11 came the Patriot Act, warrantless surveillance, secret courts, watchlists, military detention and a vastly expanded national-security state. COVID showed how quickly emergency orders could intrude on movement, assembly, commerce and ordinary constitutional processes in the name of public safety.
Wars have expanded executive power. Border emergencies have expanded executive power. Civil unrest has expanded executive power. Public-health emergencies have expanded executive power.
The emergencies change. The response does not: government claims extraordinary powers, and the extraordinary gradually becomes ordinary.
This is the real danger of a government accustomed to governing by emergency: the trigger does not have to be Armageddon. It can be terrorism, a cyberattack, a pandemic, civil disorder or some broadly defined threat to national security. It merely has to be a crisis serious enough for those in power to declare that ordinary rules can no longer apply.
The most dangerous words in government are often some variation of: this is an emergency.
That is when temporary measures become precedents, precedents become policies, and policies become permanent powers.
This is how the police state grows—incrementally, across administrations and parties.
Every president inherits the emergency powers, secret directives, surveillance machinery, militarized forces and weaponry assembled by his predecessors. Every president adds something to the arsenal. And every president leaves the next occupant of the White House more powerful than the one before.
Trump inherited Obama’s powers. Obama inherited Bush’s. Bush inherited those accumulated before him. And whoever follows Trump will inherit everything Trump leaves behind.
That is the lesson of the modern police state: presidents are temporary. The powers they leave behind are not.
Trump did not invent the Bunker State. He inherited it—and he is expanding it while further erasing the lines between presidential power, personal power and the national interest.
The government beneath Trump was built over decades, with the complicity of presidents, Congresses and courts that repeatedly allowed extraordinary powers to become permanent.
And behind it all sits another government—a shadow government—that elections rarely disturb.
More than a decade ago, we warned that America effectively had two shadow governments: Continuity of Government, the emergency government waiting in the wings for catastrophe, and the Deep State, the permanent government that carries on regardless of who occupies the White House.
Today, it’s hard to tell them apart.
One operates in the background. The other waits for the so-called emergency. But both run on the same machinery.
The Deep State supplies the permanent personnel and institutions. The surveillance state supplies the intelligence. The militarized police state supplies the enforcement. The presidency supplies the command authority. Continuity of Government supplies the emergency architecture. And the bunker supplies the headquarters.
Under ordinary circumstances, these systems may appear to operate separately.
Under emergency conditions, they can become one.
That is how the permanent state becomes the emergency state. And that is when Continuity of Government becomes Continuity of Tyranny.
The issue is not whether government officials have somewhere safe to go during an attack. The issue is what kind of government emerges afterwards.
A constitutional republic depends on divided power, public accountability and limits that cannot disappear whenever a president invokes emergency.
A bunker government is built on a very different logic. Command must continue. Government must survive. Constitutional restraints become negotiable.
That is the bunker mindset.
And increasingly, we do not need an actual bunker to see it at work.
We see it whenever presidents bypass Congress in the name of necessity, whenever surveillance expands in the name of security, and whenever courts are treated as obstacles rather than constitutional checks.
The bunker mentality begins long before anyone goes underground. It begins the moment government decides its own power matters more than constitutional restraint.
That is why the central question is not simply whether the federal government will survive the next catastrophe.
It almost certainly will.
The government has spent decades and untold billions making certain of that.
The more important question is whether constitutional government survives with it.
Will Congress retain meaningful authority? Will the courts continue functioning independently? Will elections remain meaningful? Will habeas corpus remain intact?
Or will the next emergency merely provide the justification for suspending restraints that have already been weakened in practice?
These are not questions for some distant doomsday.
They are questions for right now.
A government that already possesses mass surveillance, militarized police, detention powers, biometric tracking, drones and facial recognition does not need to invent the machinery of authoritarian control during an emergency.
It already has it.
All an emergency does is change the rules governing how freely that machinery can be used.
That is why the government’s obsession with Continuity of Government should concern anyone who cares about continuity of constitutional government.
A bunker can preserve a president—it cannot preserve a republic. A military command center can ensure continuity of power—it cannot ensure continuity of liberty.
Stanley Kubrick depicted the grotesque logic behind government survival in Dr. Strangelove more than 60 years ago.
As political and military leaders push the world toward nuclear annihilation, Dr. Strangelove proposes retreating into a government bunker, where officials, military leaders and other carefully selected survivors can wait out the radioactive fallout and eventually emerge to rebuild civilization in their own image. The people being saved, naturally, include many of the same people who helped create the catastrophe.
Kubrick’s black comedy bears an unnerving resemblance to current events.
The unsettling question is the same: when catastrophe comes, will the government preserve constitutional government—or merely preserve itself?
A constitutional government is defined by the limits placed on those who govern.
Serious government requires presidents who respect the limits of office, a Congress that exercises its authority, courts willing to restrain power, military force subordinate to constitutional authority, and citizens who understand that liberty depends on keeping power restrained.
The Founders understood this better than most.
They did not design the Constitution on the assumption that those who govern would always be wise, honorable or restrained. They assumed the opposite. They understood that power attracts ambition, that ambition seeks more power, and that government must therefore be divided, checked and bound down by law.
Thomas Jefferson put it bluntly: “In questions of power, let no more be heard of confidence in man, but bind him down from mischief by the chains of the Constitution.”
Those chains are already being weakened.
Presidents declare emergencies. Presidents wage wars without meaningful congressional restraint. Presidents deploy military forces. Presidents conduct surveillance. Presidents issue decrees carrying the force of law. Presidents inherit extraordinary powers from their predecessors and add still more for whoever comes next.
Meanwhile, as we make clear in Battlefield America: The War on the American People and its fictional counterpart The Erik Blair Diaries, the unelected machinery of government carries on.
This is what happens when a constitutional republic adopts a bunker mindset: government survival becomes the priority, and constitutional survival becomes an afterthought.
That is backwards.
The government exists to preserve liberty. Liberty does not exist to preserve the government.
If constitutional government cannot survive above ground, in ordinary times, when the courts are open, Congress is sitting and elections are still being held, there is little reason to believe it will somehow be resurrected underground in the wake of a national catastrophe.
What deserves continuity is not merely the federal bureaucracy.
What deserves continuity is the Constitution. The separation of powers. The rule of law. Representative government. Due process. Habeas corpus. The rights of the people.
That is what must survive.
And if we cannot preserve those things now—before the sirens sound, before the government retreats underground, before some president invokes the next great emergency—then no bunker, however deep, however secure and however lavishly equipped, will save the republic.
Because the Constitution cannot survive in a bunker underground if we have already allowed it to die above ground.
Original Article: https://www.lewrockwell.com/2026/08/no_author/the-bunker-state-the-government-will-survive-but-will-the-constitution/
The overlooked evidence on DMSO’s effects on circulation, blood clots, stroke, brain injury, heart disease, and common peripheral vascular disorders—and its potential to transform medicine.
A Midwestern Doctor | substack.com/@amidwesterndoctor
•DMSO is an “umbrella remedy” whose combination of therapeutic properties makes it uniquely suited to treat “incurable” conditions. This article will focus on the extensive evidence DMSO safely eliminates clots, protects the blood vessels, and restores circulation, as impaired blood flow is one of the most common causes of disease but challenging to manage with conventional options.
•DMSO revolutionizes the treatment of strokes, as it not only eliminates the stroke, but also can be started hours earlier than normal treatments and is able to heal the injured tissue that would otherwise be lost. Extensive evidence, and now reader reports show that were it to be widely adopted, millions could be spared from the disability or death they cause each year.
•DMSO is also uniquely suited to treating brain bleeds, traumatic brain injuries, and concussions, as it relieves pressure on the brain while restoring vital circulation and reviving dying brain cells. Extensive evidence and reader reports again show its utility here.
•Because the heart, like the brain, is exquisitely sensitive to its blood supply being cut off, many of DMSO’s properties have also been repeatedly shown to have immense value in heart attacks alongside many other severe heart conditions.
•DMSO has been extensively used for peripheral circulatory disorders, with hundreds of readers, mirroring the existing evidence, reporting it eliminating varicose veins present for decades, dissolving clots and DVTs, restoring color and sensation to blue, purple, or black ischemic limbs, healing venous, diabetic, and pressure ulcers, and resolving Raynaud’s, frostbite, and hemorrhoids, frequently within days.
•This article summarizes the extensive data demonstrating DMSO’s efficacy for circulatory and vascular conditions (approximately 1500 studies and 160 pertinent reader testimonials) and provides practical guidance on DMSO protocols and complementary approaches for the neurological and vascular conditions discussed throughout this series.
Decades ago, I learned that DMSO was an excellent therapy for strokes and then subsequently had numerous experiences where someone I told to take DMSO had their full stroke resolve on the way to the hospital (sparing them from a life of expected disability), after which I started also using DMSO for successful post-stroke recoveries. When you consider both how debilitating strokes typically are and that, for decades, there has been only piecemeal progress on reducing the suffering they cause, it’s hard to put into words how upsetting this has been for me.
So, once I realized I’d stumbled upon being the custodian of a widely read publication, one of my first major projects was to write “The Evidence DMSO Could Save Millions From Brain and Spinal Injury,” which struck the same chord in many readers that it had in me, and was seen by millions (many of whom subsequently shared DMSO saved them from a stroke).
In the process of researching that article and the reader requested ones which followed (on the myriad of other transformational uses for DMSO), I gradually realized that a massive volume of buried DMSO literature existed, and felt that due to the support I’d received from readership here, I had the obligation to make that lost knowledge (and the thousands of reader DMSO testimonials—currently 7,500) widely available.
Note: some of the most dramatic neurological recoveries readers shared (which can be viewed in filmed interviews) include from terminal ALS, terminal bulbar ALS, advanced CJD (the 100% fatal prion disease), sight that had been lost for nearly 75 years, and the same spinal cord injury that left Christopher Reeve on a vent for life.
The fastest way I could see to actually do that was to search the key English and foreign databases for each term for DMSO (rather than every possible keyword combination), then filter out the medically relevant studies and compile them and condense them into articles.
Given how much was there, I was initially unsure if this was possible, but over six grueling months (where I was forced to cut back on everything else and hence published less here), I learned a lot, and with the tools that have never before been available, eventually collected 15,000 summarized studies.
Note: in the process of doing the same for the medical ozone literature base, I recently discovered there is one large DMSO database I missed that will need to be done in the near future.
Once they were compiled, I polled the supporters here on which topics had the most interest, and the overwhelming answer was neurology. On one hand I supported starting there, as most of the therapeutic mechanisms which underlie how DMSO works are interwoven with neurology (and I believe laying out the mechanistic basis for how DMSO works is critical for the therapy’s adoption), but I was also hesitant as this was single most challenging part of the topic to synthesize (due to the ultimately 4,500 studies which would need to be incorporated).
Nonetheless, starting at the end of April, I was able to begin publishing them, and this article, at last, marks the final part of that series. The previous ones, which provided the mechanistic basis for much of what is discussed in this article are as follows:
This article covers how circulatory impairments underlie many neuropsychiatric disorders and how DMSO:
•Biophysically eliminates microclots along with preventing immune cells from obstructing capillaries, facilitating lymphatic and venous drainage.
•Counteracts a broad range of inflammation and free radicals
•Shields cells from diverse lethal stressors and excitotoxins
•Protects ATP production, restarts dormant cells, and restores parasympathetic (vagal) tone (e.g., through acetylcholinesterase inhibition)
•Effectively delivers a variety of therapeutic agents to the central nervous system.
This article also extensively covers:
•How DMSO facilitates neuronal regeneration by stabilizing microtubules and differentiating stem cells into replacement neurons.
•How DMSO’s other established therapeutic mechanisms (e.g., muscle relaxation, tissue regeneration, and interruption of pain transmission) reduce or eliminate spinal pain.
This article also extensively covers how:
•DMSO’s biophysical effects on water temporarily shift the phase of cell membranes and the cytoskeleton, creating a reversible cellular reset that restores normal structure and function (along with uniquely enabling DMSO to transport substances across biological barriers without damaging them).
•DMSO selectively blocks the small nerve fibers that transmit chronic pain
•DMSO supports peripheral nerve regeneration (e.g., with membrane resealing)
•Through neuronal resets, DMSO can eliminate the source of chronic pain and autonomic dysfunction.
In this article, I will cover one of DMSO most extensively studied mechanisms: how it works through several well-established anticoagulation pathways to reduce clotting, dilate vessels, protect blood vessels and improve circulation (which works synergistically with its biophysical ability to eliminate micro-clotting discussed in the first part of this series).
Note: if the information in the next section is too dense, you can skip ahead to the “Current Stroke Management” section.
Platelets, the tiny cell fragments that clump together to initiate clotting, are one of the most common targets of blood-thinning medicines (e.g., aspirin) and likewise one of the most thoroughly studied targets of DMSO. Collectively, this evidence shows DMSO independently inhibits platelet aggregation, adhesion, and activation, and most importantly, does so through several converging mechanisms at once.
For example, one study examining the full panel of platelet agonists (the natural triggers that switch platelets on) found DMSO inhibited human platelet aggregation induced by ADP, adrenaline, arachidonic acid, collagen, and PAF, with the strongest effect against ADP. Multiple independent groups, in turn, have reproduced these results.1,2,3
Likewise, across studies, DMSO has been found to inhibit platelet aggregation (clumping) triggered by ADP, epinephrine (adrenaline), arachidonic acid, collagen, thrombin, and platelet-activating factor, in a concentration-dependent manner, with ADP-induced aggregation typically the most sensitive to DMSO.1,2,3 At the level of activation markers, DMSO-containing systems suppress the surface proteins that report a platelet has “switched on”—P-selectin (CD62P), PAC-1, GPIIb/IIIa, CD63, and platelet factor 4 (PF4)—and reduce the release of ATP and dense-granule contents.1 DMSO also directly binds platelet factor 4, disrupting its aggregation at the molecular level.
Note: these effects are concentration and time dependent. At the low-to-moderate concentrations relevant to therapeutic use, the antiplatelet effect reverses once DMSO is washed out—consistent with DMSO's rapid diffusion out of cells, which is why platelets cryopreserved in DMSO lose adhesion and aggregation during cold storage yet regain functionality once thawed and infused.1,2 At the higher concentrations or longer exposures reached only outside normal use, the inhibition can persist even after removal,1 reflecting a more durable structural change. However at the higher doses, such as the concentrations reached after a DMSO-cryopreserved cell infusion (0.2–0.6%), DMSO still measurably inhibits ADP, thrombin, and TRAP-induced platelet aggregation,1,2 frequently causes transient circulating coagulation inhibitors and prolonged clotting times1,2 and at high topical doses can modestly lower the circulating platelet count.1
•DMSO selectively inhibits cyclooxygenase-1 (COX-1) and thromboxane A₂ synthase,1,2 (e.g., 0.5% DMSO reduced total COX activity by 36%1) cutting production of thromboxane A₂ (the potent signal platelets use to recruit one another). Adding the synthetic thromboxane analogue U46619 restored platelet aggregation despite DMSO’s presence,1 confirming that DMSO’s suppression of aggregation runs through the thromboxane pathway.
•DMSO raises intracellular cAMP and cGMP (the secondary messengers that hold platelets in the resting state) providing a thromboxane-independent brake on platelet activation.
•Because DMSO restructures the water in and around the cell membrane (detailed here), it alters membrane fluidity directly, desensitizing platelets to their agonists independent of COX-1—an effect visible under the microscope as a marked reduction in the filopodia platelets extend when activating.1 This biophysical membrane action also likely explains DMSO’s suppression of shear-induced platelet activation,1 where DMSO cut platelet adhesion under flow to roughly a fifth of control,1 and connects to the same phase-transition effects DMSO exerts on the platelet membrane’s phospholipids.1 A separate study of platelets forced through the non-physiological shear stresses generated by mechanical heart-assist devices found the same protection, and in a revealing pattern that mirrors the concentration-dependent membrane stages described earlier: low concentrations of DMSO sharply reduced shear-induced activation, while the effect reversed at higher concentrations as DMSO began permeabilizing the membrane—and DMSO-treated platelets, though shielded from mechanical activation, still responded normally to chemical agonists, confirming it desensitizes platelets to physical force rather than simply disabling them.1 Notably, in that same body of work the conventional antiplatelet drugs, designed to block platelets through specific chemical pathways, were overwhelmed by these device-level physical forces, whereas DMSO, acting on the membrane itself, was not.1 At higher concentrations this progresses to increased membrane permeability, at which point DMSO releases the platelet’s internal contents through a mechanism distinct from thrombin’s.1
•DMSO reversibly inhibits platelet serotonin uptake, thereby (reversibly) reducing the amount of serotonin stored in (and later released from) dense granules that is available to amplify platelet aggregation.1
•Since hydroxyl radicals trigger platelet serotonin release and aggregation, DMSO’s extensively documented scavenging of these radicals1 blocks radical-mediated platelet activation1 and thrombus (clot) formation.1 In living microvessels, this was directly visualized: intraperitoneal DMSO more than doubled the time to platelet aggregation in injured mouse brain pial arterioles (117 vs. 57 seconds), and in the same vessels prevented the reactive arteriolar dilation that normally accompanies the injury (holding their diameter near baseline versus a 22% widening in controls).1 As such, DMSO’s radical-scavenging action, in addition to reducing inflammation, also produces both an antiplatelet and a vasomotor effect simultaneously.
Note: as each of these effects is concentration dependent, not every study finds an effect on every pathway (e.g., one group reported DMSO did not inhibit thromboxane production in platelets and did not protect rabbits from arachidonic-acid–induced pulmonary thrombosis1,2).
These effects, in turn have been demonstrated their utility in a variety of living systems:
•In a dog model of critical coronary stenosis (where platelets aggregating at a narrowed artery routinely cause cyclic drops in coronary blood flow) intravenous DMSO dose-dependently reduced (by up to 85%) those flow reductions without altering blood pressure, heart rate, or cardiac output, isolating the effect to platelet aggregation itself.1
•In a rat carotid-injury model, IV DMSO (2 g/kg) virtually abolished thrombus formation despite clear endothelial damage, with electron microscopy showing only spherical, non-activated platelets where clots should have been.1,2
Note: because the clotting was prevented at a site of genuine vessel injury, these results1 are applicable to settings like microvascular and reattachment surgery, where a damaged vessel must stay patent long enough to heal.
Finally, DMSO’s effects on platelets (inhibition of aggregation and suppression of activation markers such as P-selectin, PAC-1, GPIIb/IIIa, and PF4) have also been observed when DMSO has been combined with a variety of natural compounds (which for reader ease I mark with ⬖) such as xanthohumol,⬖ wine polyphenols,⬖ Ginkgolide B,⬖ and vitexicarpin.⬖
One of the more unusual reports came from a Russian practitioner combining DMSO with aspirin in "structured water," across a range from conventional doses down to ultra-low dilutions. Using nocturnal leg cramps in the elderly as a readout, he reported that conventional doses reliably prevented recurrence — cramps returned on withdrawal and stopped again on resumption — with the effect persisting even as aspirin was diluted roughly a thousandfold, becoming borderline around the nanogram range (~10⁻⁹) and disappearing by ~10⁻¹². He also described rapid relief in acute vascular events such as heart attack and stroke.1
DMSO also acts directly on the coagulation cascade itself, and does so at nearly every level (the initiating trigger, the central enzyme thrombin, and the fibrinolytic system that dissolves clots once they form) giving DMSO a breadth of anticlotting activity that few single agents possess:
•Tissue factor (TF) is the key protein that ignites the entire clotting cascade (and is a critical link between inflammation and thrombosis). DMSO, in turn, suppresses TF expression and activity by inhibiting JNK and p38 MAP kinase signaling and prevents arterial thrombus formation in living animals, without detectable toxicity.1,2 Because it simultaneously reduces the smooth-muscle overgrowth that causes stents to re-occlude, DMSO has been repeatedly proposed as a drug-eluting stent coating due to it being a rare agent that both lowers clotting risk and restenosis risk (unlike conventional stent drugs like sirolimus and paclitaxel, which reduce restenosis but increase TF expression and thrombosis risk).1,2,3
•DMSO also acts on the coagulation enzymes themselves. It directly alters thrombin, the central clotting enzyme, changing its catalytic behavior through a conformational shift and—notably—reducing heparin’s ability to inhibit it.1 In the invertebrate clotting systems used as sensitive models of the cascade, DMSO reversibly blocked the activation step that switches on the dormant clotting zymogen (enzyme precursor), without inhibiting the already-active enzyme, in both the Limulus and Carcinoscorpius systems (highly sensitive clotting cascades)1,2—indicating DMSO acts on the trigger that starts the clotting cascade.
DMSO hence not only prevents clots from forming but, when applied topically, actively dissolves already-established venous thrombi while inhibiting arterial platelet thrombus formation. Finally, in a rat carotid-artery injury model intravenous DMSO eliminated thrombus formation at both crush and incision sites despite clear endothelial damage. Electron microscopy showed only minimal platelet-fibrin deposits and, spherical, non-activated platelets where clots should have formed (with DMSO’s antithrombotic effect statistically superior to the barbiturates and methylprednisolone tested alongside it).
Its ability to eliminate clots already present appears to be due to it augmenting the body’s natural clot removal pathways as DMSO activates streptokinase-initiated fibrinolysis across a wide concentration range (1.5–50%), stimulates production of tissue plasminogen activator (tPA), the body’s principal clot-dissolving enzyme and reduces plasminogen activator inhibitor-1 (PAI-1), the main physiological brake on that process.
This is cited so consistently that “fibrinolytic activity” appears as a standard listed property of DMSO throughout the clinical literature,1,2,3,4 or as described by a Russian review: intravenous DMSO lengthens clotting time, suppresses platelet aggregation (initial clot formation), normalizes fibrin formation (clot solidification), and being fibrinolytic, normalizes fibrinolysis.1
All of this touches on a key contrast I’ve noticed between pharmaceutical drugs and effective natural therapies. Pharmaceuticals tend to target a single pathway (or a few) as forcefully as possible, which produces both their immediately evident effects and, frequently, significant side effects. Time-tested natural agents instead often nudge many pathways at once toward a converging end, making them less immediately potent (their effect being distributed rather than concentrated) but also much better tolerated and often longer-lasting, since the body doesn’t develop the reflexive tolerance it mounts against a pathway being aggressively shifted in one direction.
Note: as with many of DMSO’s effects, its fibrinolytic action normalizes rather than simply pushing one direction—in cancer cells it suppressed urokinase-type plasminogen activator (uPA—which facilitates metastasis), the reverse of its tPA-stimulating effect in normal cells, consistent with DMSO restoring dysregulated systems toward baseline.
Clinically, this translates to DMSO improving coagulation across a broad range of situations. For example, in 42 patients with rheumatic diseases (including scleroderma and Raynaud’s), blinded thromboelastography showed DMSO normalized both fibrin formation, with accompanying improvement in microcirculation. Likewise, DMSO added to sepsis, endotoxemia, and disseminated-intravascular-coagulation models and paired with a long and chemically unrelated list of agents, has repeatedly reduced elevated fibrinogen and corrected the underlying coagulopathy.1,2,3,4,5 Similarly, DMSO appears in numerous topical thrombosis and thrombophlebitis formulations where it both facilitates the delivery of and synergistically enhances the effects of the other anti-thrombotic agents present.1
Note: DMSO’s broad range of effects also allows it to treat challenging clotting situations. For example, when the immune system breaks down myelin, the exposed phospholipids in the debris can trigger clotting that starves nerves of blood (a proposed secondary driver of multiple sclerosis) and while conventional anticoagulants don’t touch this pathway, a Russian study found DMSO inhibited myelin-triggered clotting dose-dependently.
In medicine a balance often has to be struck between a therapeutic effect and the toxicity it entails, and getting it right can be quite challenging, such as in ensuring chemotherapy kills enough cancer cells without killing too many normal ones. Blood thinning poses another version of this problem: coagulation can predispose someone to severe complications (e.g., embolic strokes), but too little of it is also dangerous, since a minor injury can then produce a large hematoma and a blow to the head a lethal brain bleed.
For this reason, medicine typically reserves anticoagulants for those already at risk of clotting complications, as in atrial fibrillation, where the irregular rhythm lets clots form in the heart that can then travel to the brain and cause a stroke. It then tightly controls the degree of anticoagulation, doing enough to prevent the major event without raising bleeding risk any more than necessary. However, this is still far from perfect. Many individuals experience significant complications from anticoagulants each year, partly from incorrect dosing or monitoring, and partly because a perfect balance between preventing thrombosis and avoiding bleeding simply cannot always be achieved in the individual patient. All of this hence raises a few questions regarding DMSO.
First, can natural “anticoagulants” with a broader spectrum of action be used in lieu of the more potentially dangerous anticoagulants? Ultimately this is a difficult question to answer, as understandably, no clinician I know has taken the risk to attempt this in high risk situations (e.g., atrial fibrillation) and see if it suffices to stop the clotting (whereas gargantuan sums of data were needed to accurately assess the merit of pharmaceutical anticoagulants). However, in lower risk situations (e.g., preventing a heart attack over the next twenty years, or improving chronic illness symptoms resulting from excessive blood clotting), I have seen the natural alternatives perform extremely well without significant risk. Likewise, in acute situations (e.g., a heart attack or stroke), I have seen numerous cases where they (e.g., DMSO or a zeta potential restoration) resolved the incident prior to conventional options arriving. A few readers, in turn, have shared stories like quitting a problematic lifelong Eliquis prescription, noting DMSO not only prevented clots from forming but also dissolved existing ones and that “I’d be dead if DMSO didn’t work.”1 I, however, do not think this is wise, as the data simply does not exist to determine if this is appropriate to do, and as such, I instead favor the natural anti-clotting approaches in cases where it seems likely someone would benefit from blood thinning but their inherent risk of a severe clotting complication is too low to justify conventional anticoagulation.
Note: while safer than conventional anticoagulants, many of the natural anticoagulants are still not completely safe (e.g., since mass consumption of generic nattokinase⬖ came into vogue to counteract the spike protein, I have periodically come across cases of them causing a problematic bleed both within my social circle and from readers here).
Second, since DMSO potentiates the actions of pharmaceutical medications, is it safe to take with other anticoagulants? Presently, there is simply not enough data to answer this, but from everything I’ve been able to find, I lean to “yes,” with three major caveats: DMSO cannot be taken within at least two hours of the anticoagulant, coagulation must be carefully monitored to ensure excessive anticoagulation is not occurring (which should happen anyways) and IV DMSO should never be mixed with an anticoagulant in the same infusion. The limited datapoints I have to go off for this assessment are that:
•The German DMSO community, which has the most experience combining DMSO with conventional anticoagulants, considers this acceptable, citing patient reports, existing data that DMSO does not competitively inhibit clotting factors or irreversibly block platelet prostaglandins the way pharmaceutical anticoagulants do, and that in practice no meaningful changes in Quick-Wert (PT activity %) or INR values appear in patients on anticoagulants who use DMSO—although they did note DMSO can reduce the dose of aspirin (which targets platelets rather than the coagulation cascade), with multiple users “switching to 50 mg every other day and their coagulation values still being ‘as desired.’” That said, they still advise starting DMSO slowly, routinely checking coagulation values, and spacing it out from anticoagulants taken during the day.
Note: in the previously mentioned Russian study (where very limited information was provided), DMSO was reported to work synergistically with aspirin and no toxicity was mentioned from this combination.1
•DMSO–heparin combinations have a long track record of safety in topical and oral formulations. DMSO enhances heparin’s anticoagulant action and, through its membrane-transport properties, can even render heparin orally absorbable when the two are formulated together (rather than via the injection typically required for heparin). Likewise, the commercial gel Dolobene (Долобене), which combined DMSO with heparin has been widely used for decades without issues (as has Phlebolan spray, although only certain Phlebolan formulations contained heparin).
Note: Jim McCann (the inventor who brought the DMSO hematoxylin cancer therapy to Ecuador) emphasized that he had seen serious bleeding issues when IV DMSO was combined with IV heparin.
•Due to the size of the readership of this newsletter, I've had a unique window for identifying rare complications of DMSO, so over the last two years, I've kept a careful eye out for bleeding incidents linked to DMSO, of which a few reported nosebleeds after DMSO, a reader who'd used topical DMSO and then had a shoulder surgery cancelled because their PTT was 71,1 a friend on Eliquis whose small finger cut bled for two hours,1 and a reader I reached out to after learning they developed a GI bleed, which we concluded may have been linked to them taking a high oral DMSO dose concurrently with a high dose of nattokinase⬖ twice a day.
Note: conversely, many readers have also reported bleeding wounds healing with DMSO.
•The existing literature indicates at low doses (which is what can realistically be reached in the body from most uses), DMSO does not meaningfully affect standard clotting parameters at all (e.g. 1.1% did not affect clotting in a zebrafish model1 and 0.1% had no effect on human plasma PTT1). Conversely, at higher IV doses, according to one Russian review, DMSO (10–20%) lengthens clotting and bleeding time, decreases platelet aggregation and increases fibrinolysis,1 while at even higher IV doses, promotes coagulation (e.g., ≥20% precipitates fibrin and consumes fibrinogen1 and ≥50% in monkeys caused instant hemolysis and fibrinogen precipitation alongside transiently shortening PTT1).
Note: due its safety, much higher doses of DMSO are routinely tested than most other agents, and as a result, toxicity often only shows up at DMSO concentrations orders of magnitude higher than most drugs. In tandem, because of how rapidly DMSO spreads through the body and dilutes, unless high IV doses are used or concentrated DMSO in ingested, it is quite difficult to reach DMSO’s toxic concentrations.
•Within the IV stem cell literature, complications are periodically reported from high dose DMSO infusions given to frail cancer patients, in the studies which looked at this, a small, transient increase in blood clotting was typically observed.1,2 Conversely, one case report exists of two elderly patients receiving IV DMSO then developing shortened prothrombin and partial-thromboplastin times (where the clinicians concluded this was likely due to quinine, indomethacin, or a phenothiazine being taken concurrently as they had not seen anything similar in comparable patients receiving IV DMSO).1 Additionally, from extensive review I was able to find three other cases exist where DMSO was linked to a problematic bleed,1,2,3 which given their rarity, makes it difficult to determine if DMSO or another variable was the causative factor.
Note: while DMSO in general helps CNS (e.g., brain) conditions, IV DMSO produces the most dramatic improvements. I initially thought this was likely due to more DMSO being able to reach the CNS, but now suspect it might be due to direct anticoagulation occurring alongside DMSO’s other effects.
•At lethal or near-lethal doses (far above ordinary use), especially concentrated IV DMSO, animal studies often show hemolysis plus pulmonary or GI hemorrhage.1 Much of the hemolysis and some fluid-shift injury is osmotic and can be produced by other strongly hypertonic infusions at similar osmolar loads. DMSO’s high LD50 (toxic doses) is why those concentrations are reachable at all, as typically a different toxicity of a drug would make it lethal far below the levels needed for osmotic damage to occur.
In short, excessive bleeding on DMSO appears to be rare and when it does occur, typically mild. Nonetheless, if anticoagulants are being taken, care must be taken to ensure coagulation parameters are routinely monitored and DMSO is not directly combined with any of them.
Note: the consistent finding across decades of animal safety studies is that diluted DMSO is remarkably well-tolerated, and that its one dose-dependent liability on the blood is transient hemolysis at high intravenous concentrations. Rhesus monkeys given intravenous DMSO at 3 g/kg (as a 40% solution) daily for nine consecutive days showed no significant or lasting changes in blood chemistry, hematology, urine, or ocular, neurological, and cardiovascular parameters over four months of follow-up. Cats given intravenous DMSO every other day across ten doses maintained normal hematology and biochemistry throughout, with no cumulative or delayed adverse effects, and a DMSO-containing mixture fed chronically at up to five times the therapeutic dose produced no adverse changes (if anything, hematologic parameters improved). The primary issue repeatedly seen is that highly concentrated intravenous DMSO has been associated in older toxicity reports with local vascular irritation and transient hemolysis (e.g., 10% intravenous DMSO given to horses produced a transient dip in red-cell and hemoglobin counts that recovered within 24–48 hours).
Prostaglandins and thromboxane are the short-lived signaling molecules the body makes from arachidonic acid (via the cyclooxygenase, or COX, enzymes) to control clotting, vascular tone, and inflammation. The system has two opposing sides, thromboxane A₂ (TXA₂), which drives platelet aggregation and vasoconstriction and prostacyclin (PGI₂) and PGE₁, which do the reverse, dispersing platelets and dilating vessels. As such, the balance of these heavily influences whether blood clots and vessels constrict, or blood flows and vessels open.
DMSO is often described as a prostaglandin inhibitor (an aspirin-like agent that blocks COX) as for platelets, DMSO selectively inhibits COX-1 and thromboxane A₂ synthase,1,2 cutting TXA₂ production and in cholesterol-fed rabbits, DMSO lowered arterial atherosclerosis, an effect attributed to its reduction in platelet thromboxane B₂ (a stable marker of TXA₂) while prostacyclin was untouched.1 So, since DMSO raises PGE₁ and cAMP while decreasing thromboxane and fibrinogen,1 it shifts the balance towards reducing clotting and dilating vessels.
Note: the fuller picture is more complex than “DMSO blocks COX,” as data shows DMSO is not uniformly a prostaglandin-synthesis inhibitor. In one study it increased arachidonic-acid oxidation rather than inhibiting it, didn’t suppress thromboxane, and led its authors to propose it acts as a reducing cofactor rather than a blocker.1 Another found DMSO had no effect on thromboxane yet stimulated PGE₂ and concluded DMSO’s anti-inflammatory action doesn’t run through an arachidonic-acid metabolism at all.1 On skin, DMSO releases prostaglandins and arachidonic acid into the tissue1 (much as histamine does), while in cultured aortic endothelial cells it actually inhibited prostacyclin.1 All of this argues that DMSO doesn’t switch the eicosanoid system off but rather rebalances it, with the net effect in platelets and vessels tilting toward the antithrombotic, vasodilatory side (consistent with DMSO’s broader tendency to normalize dysregulated systems rather than force them one way). Likewise, as we’ve seen before, the effect is also context-dependent, as in some models DMSO adds nothing, and did not improve sevoflurane’s cardioprotection when tested on its own.
Finally, DMSO has also been used to therapeutically deliver beneficial prostaglandins. In one report, topical PGD2 combined with DMSO was used to save digits (fingers or toes) that would otherwise be lost from acute inoperable thrombosis,1 and has been used to deliver agents that act upon this system (e.g., tetrahydroxystilbene⬖1 and curcumin⬖1 to relax the superior mesenteric arteries and arterioles).
Two closely related molecules cyclic AMP (cAMP) and cyclic GMP (cGMP), once elevated, in platelets, reduce their aggregation and in vascular smooth muscle trigger vessel relaxation and widening.
DMSO raises cAMP through both increasing its production and by slowing its breakdown. On one hand, DMSO directly stimulates adenylate cyclase,1,2,3 the enzyme that synthesizes cAMP; in heart tissue this stimulation was maximal at around 10% DMSO, comparable in magnitude to the beta-agonist isoproterenol and additive with it—yet DMSO’s effect was unaffected by α- or β-adrenergic blockade, meaning it works independently of the adrenergic receptors those drugs act on.1 DMSO also was found to inhibit cyclic AMP phosphodiesterase1 (the enzyme that degrades cAMP), which would further raise cAMP levels.
As such, in platelets DMSO significantly raises both cAMP and cGMP (through a channel entirely separate from its COX-1 inhibition), further supporting its antiplatelet effects.1 In blood vessels, DMSO likewise raises cGMP and relaxes the vessel wall through a nitric-oxide/cGMP-dependent pathway.1
Note: like DMSO’s other effects, this one is concentration-dependent and not universal—at lower concentrations or in certain tissues DMSO showed no measurable effect on the cyclase system.1,2,3
Blood flow is controlled by smooth muscle surrounding the lining (endothelium) of the blood vessels, which tightens to restrict flow. As such, DMSO’s ability to relax that muscle provides another key way for it to restore tissue circulation. DMSO’s circulatory-promoting properties turn up across nearly every vascular bed studied (e.g., aorta, coronary, pulmonary, mesenteric, renal, cerebral, umbilical, and saphenous) both relaxing vessels by itself and serving as the medium through which other vasodilators are delivered without impeding their effect.1,2,3,4
In the aorta, DMSO produced a concentration-dependent relaxation of contracted aortic rings through an endothelium-dependent pathway (via nitric oxide and cGMP), and an endothelium-independent one that inhibits calcium channels in the smooth muscle and reduces the muscle’s sensitivity to calcium (partly via Rho-kinase).1,2 Likewise, in another study, DMSO relaxed aortic rings by 42-99% and renal arteries by 80% (in part through voltage-gated potassium channels),1 in another DMSO relaxed mesenteric artery preparations, and in drug references, vasodilation is one of dimexide’s (DMSO) recognized pharmacological properties.1Note: since one of DMSO’s relaxing effects acts directly on smooth muscle, it likely can work on damaged vessels where the endothelium is no longer responsive to stimuli.
Additionally, part of DMSO’s local vasodilation is histamine-mediated—the same mechanism behind the warmth and flushing people often feel where DMSO is applied. Importantly, this is a controlled dilation rather than tissue injury, as when DMSO was injected into a limb, it markedly increased lymph flow while the protein content of that lymph fell (the opposite of what happens with a burn or a caustic agent, where protein rises) and tissue examination showed only vasodilation and occasional edema, but no cell necrosis (death).1 DMSO hence opens vessels and shifts fluid without damaging the tissue.
Note: combined with hydrogen peroxide as an oxygen source, topical DMSO raised skin-flap survival to 92% versus 71% in controls, an effect the authors attributed partly to DMSO’s vasodilatory, histamine-like action.1
The classic way a blood vessel dilates is that the endothelium produces nitric oxide, which diffuses into the surrounding smooth muscle and triggers relaxation there through cGMP. For this reason, many integrative cardiovascular health approaches focus on supporting endothelial nitric oxide production.
Much of DMSO’s own vasorelaxation runs through the nitric oxide/cGMP pathway as in isolated aorta, DMSO’s relaxation is blunted by removing the endothelium or by blocking nitric oxide synthase with L-NAME, while conversely, DMSO raises tissue cGMP the downstream marker of nitric oxide signaling1 and at 10% redistributed intracellular nitric oxide into mobile membrane vesicles.1
Furthermore, since DMSO effectively scavenges reactive oxygen species (which cripple the endothelium’s ability to make and use nitric oxide), DMSO is able to preserve the ability of blood vessels to dilate (e.g., protected against cigarette-smoke-induced impairment of nitric oxide production and vasodilation in rabbit aortas and human endothelial cells)1 and, from the opposite direction, DMSO's radical scavenging restored an endothelium-dependent, nitric-oxide–mediated relaxation that iron had blocked in aortic rings.1
Simultaneously, DMSO can counteract nitric oxide when it’s excessive, both by scavenging it directly (DMSO scavenges radicals including nitric oxide), as when IV DMSO in horses modestly raised systolic blood pressure,1 and by throttling its production, as when 2.5–3.5% DMSO (but not 1%) cut endothelial nitric oxide output1—an effect reversed by adding extra arginine (a common supplement used to enhance nitric oxide production).
Collectively, this suggests that DMSO normalizes nitric oxide function, both by preserving it when it would otherwise be impaired, but also by counteracting it if it becomes excessive and harmful (as at low doses, DMSO typically does not affect nitric oxide).
Finally, DMSO has also been used to deliver agents which preserved or restored nitric oxide mediated relaxation such as resveratrol,⬖1,2 hesperidin,⬖ (reducing hyperhomocysteinemia-induced cognitive deficits),1 thymoquinone,⬖1 red-clover isoflavones,⬖1 genistein, ⬖1,2,3,4 (e.g, for fructose-fed hypertension1) methylated quercetin flavonoids and phenylbutanoids,⬖1 Bacopa monnieri flavonoids and saponins,⬖1 tetrahydroxystilbene glucoside,⬖1 astragaloside IV,⬖1 cinnamaldehyde,⬖1 Jasminum sambac extract,⬖1 ursolic acid,⬖1 Acer okamotoanum sap,⬖1 phloridzin,⬖1 adenosine,⬖1 a Periplaneta americana metabolite,⬖1 a polyphenol nutraceutical,⬖1 the soluble guanylate-cyclase activator cinaciguat,1 the PPAR-γ agonist rosiglitazone,1 17β-estradiol,1,2 a STAT3 inhibitor,1 a selective adenosine kinase inhibitor,1 a PPAR-α agonist,1 and an angiotensin peptide analog.1
A large body of literature shows DMSO’s free-radical scavenging (discussed below) protects a wide range of blood vessels from the constriction and endothelial dysfunction caused by oxidative stress, hence keeping vessels from closing down:
Lastly, DMSO also shielded endothelial cells from the injury driven by infection and its toxins, including bacterial endotoxins1 and Pseudomonas aeruginosa1 products.
Note: DMSO’s direct vasorelaxation is concentration-dependent so at the higher concentrations DMSO reaches its own clear relaxing effect, but at the low concentrations used in many solvent experiments, it frequently shows no measurable effect on vascular tone.1,2,3
Free radicals are atoms or molecules that contain one or more unpaired electrons, which makes them highly reactive and potentially damaging to tissues such as fats, proteins, and DNA. DMSO’s most well-recognized property is its ability to scavenge (neutralize) free radicals—particularly the hydroxyl radical, one of the most damaging reactive species, of which DMSO is among the best-known scavengers (there are 135,000 results on Google Scholar for “DMSO radical scavenger”). Its reaction with the hydroxyl radical, in fact, is so reliable that DMSO is used as a standard molecular probe for detecting and quantifying hydroxyl radicals in biological systems as the hydroxyl converts DMSO into a stable, easily measured marker.1,2
Note: two of the most commonly observed (and studied) scavenging effects of DMSO are its reduction of free-radical-induced lipid peroxidation and its preservation of the body’s own antioxidant enzymes.1 Additionally, DMSO’s radical scavenging is dose dependent,1 can directly suppress hydroxyl-radical production in solution,1 and delivers vascular protection other approaches cannot—in a cobra-venom model of complement-driven vascular injury, it prevented the microvascular damage (capillary congestion and leukocyte plugging) that cyclooxygenase inhibitors, an iron chelator, and a thromboxane synthetase inhibitor all failed to touch.1
Since the thin lining of the blood vessels (the endothelium) is highly vulnerable to oxidative damage, DMSO’s ability to scavenge radicals has shown a variety of key therapeutic effects including:
•Preventing endothelial dysfunction and preserving vessel dilation.1
•Protecting aortic endothelial cells from radical-triggered programmed death.1•Blocking the reactive-oxygen signaling that switches on the adhesion molecules (ICAM-1, VCAM-1, E-selectin) endothelial cells use to catch and recruit inflammatory white cells (detailed here) largely by inhibiting the master inflammatory switch NF-κB—thereby preventing those white cells from sticking to the vessel wall, plugging the smallest vessels and causing the microstrokes which underlie many illnesses (e.g., vaccine injuries).
•Blocking the radical-driven stiffening of endothelial cells that would otherwise impair blood flow.1
As such, many studies have shown DMSO protects the endothelium from oxidative stress and free radical injury.1,2,3,4,5,6,7,8,9,10, 11,12,13,14,15,16,17,18,19,20, 21,22,23,24,25,26,27,28,29,30, 31,32,33,34,35,36,37,38,39,40, 41,42,43,44,45,46,47,48,49,50, 51,52,53,54,55,56,57,58,59,60, 61,62,63,64,65,66,67,68,69,70, 71,72,73,74,75,76,77,78,79,80, 81,82,83,84,85,86,87,88,89,90, 91,92,93,94,95,96,97,98
In addition to neutralizing the free radicals that constrict vessels and injure the vessel wall, DMSO protects against a second wave of radical damage: when a vessel’s blood flow is cut off and then restored, the oxygen-starved (ischemic) tissue converts the returning oxygen into a burst of radicals, creating a “reperfusion injury” that often exceeds the damage from the initial blood loss. As such, in virtually every part of the body (particularly the central nervous system), DMSO has been repeatedly shown to protect organs and tissue from oxidative stress and otherwise devastating reperfusion injuries.1,2,3
For example, DMSO:
•Significantly reduced the microcirculatory vascular leakage caused by a radical-generating system in hamster cheek pouches.1
•Reduced vascular permeability and edema in thermally burned skin.1
•Protected dermal microvessels from burn injury.1•Reduced vascular permeability, edema, and tissue injury in gut and mesenteric ischemia-reperfusion, performing comparably to the antioxidant enzymes superoxide dismutase and catalase.1,2,3,4,5,6,7,8
•Reduced damage in hemorrhagic shock and ischemic gastric injury.1,2,3,4,5,6,7,8,9,10•Protected the lung and pulmonary vasculature from radical injury.1,2
•Prevented the secondary lung injury that radicals inflict on distant organs after a period of hind-limb ischemia.1•Reduced endotoxin- and shock-driven organ injury.1
•Improved skin-flap and free-tissue survival by blunting reperfusion radical injury.1,2
•Protected the liver during cold-ischemic preservation.1,2
•Used to counteract the reperfusion radical injury implicated in equine laminitis.1,2,3,4
Note: in many cases, these protective effects are dose-dependent (e.g., in a rat limb ischemia-reperfusion the dose used only gave partial protection,1 while in a lung toxin model, a fairly high dose was needed to provide protection1).
The innermost surface of the endothelium is coated with the glycocalyx, a fragile, sugar-rich gel layer that regulates permeability, shields the cells from shear, and keeps clotting and inflammation in check. In shock, sepsis, and reperfusion, this layer is stripped away (”shed”), and its loss is now recognized as an early, pivotal event in vascular collapse.
Note: sulfates are one of the most effective biological molecules for restoring (vital) zeta potential. The glycocalyx is structured so that abundant sulfates on it form a (continually regenerating) liquid crystalline gel around the glycocalyx which repels other substances from entering the endothelium and independently drives blood circulation (all of which is detailed here)—making the glycocalyx one of the most critical components of cardiovascular health.
Many studies, in turn, show DMSO protects the glycocalyx along with the underlying endothelium:
•In a mouse model of LPS-induced acute respiratory distress, systemic DMSO preserved the pulmonary endothelial glycocalyx (staining intensity roughly four times that of untreated injury), cut protein leak into the airspaces, and reduced inflammatory cell counts; in human endothelial cells it prevented glycocalyx shedding by blocking the enzyme (a matrix metalloproteinase) that cleaves it from the cell surface.1
•In a rat hemorrhage-resuscitation model, DMSO reduced glycocalyx shedding and the accompanying coagulopathy.1
•At the level of the underlying matrix, DMSO restored the normal structure of heparan-sulfate proteoglycan in endotoxin-exposed endothelial cells,1 and prevented endotoxin-induced lung protein leak while preserving the endothelium’s ability to relax.1
•DMSO also inhibited apoptosis in nutrient-deprived human endothelial cells by promoting DNA replication and survival,1 and protected them under oxidative stress by raising heme oxygenase-1 and reducing apoptosis through several cytoprotective pathways.1
•In the equine ascending colon, DMSO protected against the capillary permeability changes caused by ischemia-reperfusion injury.1
Note: DMSO has also been used in combination with a variety of agents to promote endothelial growth and repair (e.g., in studies of endothelial proliferation, migration, tube formation, differentiation, and progenitor-cell-driven revascularization). Agents combined with DMSO to create these effects on the endothelium include: curcumin, ⬖1 resveratrol,⬖1 luteolin,⬖1 kaempferol,⬖1 diosgenin,⬖1 icariin,⬖1 arnebin-1,⬖1 celastrol,⬖1 dihydroartemisinin,⬖1 alkannin,⬖1 sulforaphane,⬖1 ginsenoside Rg3,⬖1 Illicium henryi extract,⬖1 dracorhodin,⬖1 onychin,⬖1 Echinacea extract,⬖1 13-cis retinoic acid,1 fluvastatin,1 simvastatin,1 atorvastatin,1 dihydrotestosterone,1 recombinant proteoglycan-4,1 sirolimus1 rapamycin,1 a demethylating agent,1 a Kir2.1 blocker,1 or a JAK2 inhibitor.1
Roughly 3.1% of adult Americans have experienced a stroke (a figure I expect to rise from the COVID-19 vaccines). Each year, this translates to about 800,000 people in the United States having a stroke, and in 2022, 165,393 died (making it the fifth most frequent cause of death in the United States), with between 20-40% of survivors experiencing long term disability from the stroke.
Because of the harm strokes pose to society, and the rate at which brain tissue deteriorates once its blood supply is lost, the medical system emphasizes doing everything that can be done to treat strokes as soon as possible. Unfortunately, there is a fundamental limitation to how strokes are addressed which makes it impossible to ever eliminate the immense toll strokes place upon society.
This is because three types of strokes exist, ischemic strokes (which are typically caused by a blood clot obstructing the artery), a brain hemorrhage (where bleeding is both directly toxic to sensitive brain tissue and creates large blood pockets that compress and damage the brain), and transient ischemic attacks (TIAs)—which are not classically considered strokes.
Note: TIAs occur when someone shows clinical signs of a stroke that resolves on its own (and typically does not have stroke imaging findings). I believe TIAs often represent microstrokes occurring (as the microclots are too small to be seen with conventional brain imaging and typically resolve on their own)—a subject I went into much more detail here as these visually detectable microstrokes frequently underlies vaccine injuries and many other chronic illnesses.
The essential challenge with managing strokes is that it’s nearly impossible to reliably differentiate an ischemic stroke from a hemorrhagic stroke without imaging (we’ve tried for a longtime, and while there are a few diagnostic signs that suggest one or the other, they are not reliable enough for the degree of certainty required). This matters because opposite approaches are taken to ischemic strokes and hemorrhagic strokes—with ischemic strokes a powerful clot busting medicine (tPA) is used to restore circulation, whereas with hemorrhagic strokes (13% of strokes in the developed world), a variety of steps are taken to reduce further bleeding in the brain (which can include brain surgery).
As such, when a stroke occurs, while it is urgent to treat it as soon as possible (as “time is brain”), the standard approach (tPA) cannot be used until a CT scan has ruled out a hemorrhagic stroke (as giving tPA for a hemorrhagic stroke is devastating or lethal). Because of this, definitive stroke treatment cannot begin until it has been recognized, an ambulance gets them to an ER, a CT scan has been completed, a diagnosis is made, and that diagnosis reaches the treating physician—all of which, despite the best efforts by the medical system to expedite the process, often takes hours.
Worse still, the statistics on tPA (approved in 1996 and still the only FDA approved treatment for ischemic strokes) aren’t actually that good. Presently, tPA is only approved to be given within 3 hours of a stroke starting (as its likelihood of benefitting a patient decreases with time), and in practice, it is often given up to 4.5 hours after symptoms start (since some degree of benefit still exists).
When that window is met (which only happens about 25% of the time and ultimately results in roughly 1.8%-8.5% of ischemic stroke patients receiving tPA), the existing data shows that only 13% percent of patients who receive tPA significantly benefit from it (39% return to normal, compared to 26% who would return to normal without treatment), with an additional 19% of tPA users experiencing some degree of improvement (but not a full recovery) from it.
Worse still, tPA can cause significant bleeding, which is sometimes minor (e.g., gum bleeding), but also carries a 6.4% risk of a symptomatic brain bleed, and a 1.6% risk of a serious systemic hemorrhage (along with other issues such as a 1.3% to 5.1% risk of angioedema and tPA frequently causing reperfusion injuries). In turn, many risk factors exist for the increased bleeding (e.g., a few common risk factors can lead to a 33% chance of tPA causing a fatal bleed), and there have been many lawsuits for either giving or not giving tPA to a stroke patient. Additionally, tPA is a poor choice for larger obstructions (e.g., one within the internal carotid artery), which instead must be physically removed. In short—many ICU doctors I know are quite hesitant to use tPA as they have seen cases where it dramatically improved patients, many where it did not do anything, and quite a few disasters (especially in the early days of the therapy where it was used for heart attacks and then often caused the patient to have a fatal or debilitating brain bleed).
Note: the best data exists for tPA being injected directly into the obstructed artery with interventional radiology. Unfortunately, while many premier institutions offer this, it is a specialized procedure that is not available at most hospitals.
Finally, there is essentially no therapy for recovery from stroke—which in short explains why stroke is the second leading cause of death and the third leading cause of disability worldwide.
As the previous section shows, there are insurmountable limitations to how strokes can be managed. DMSO, however, completely changes this equation as:
•It effectively treats ischemic strokes.
•It partially treats hemorrhagic strokes.
•It carries no known risk of worsening a hemorrhagic stroke.
•It can be easily administered at home or on an ambulance.
•In addition to addressing the circulatory issues, independently protects brain tissue from stroke damage.
•Prevents the reperfusion injuries which follow strokes.
•Can heal damaged brain tissue after a stroke.
As such, DMSO makes it possible to eliminate the multi-hour delay typically required for stroke treatment, often is a safer can be a more effective stroke treatment option than the conventional alternatives, and provides one of the only existing options to heal the permanent disability that follows a stroke.
This is why researchers like Jack de la Torre MD devoted their entire careers to producing a robust body of evidence DMSO could treat strokes, as they knew it was unlikely any other agent would ever be able to solve the ischemic-hemorrhagic stroke dilemma.
Note: many readers have reported to me successfully treating strokes at home or on the way to the ER with DMSO and hence, due to increasing skepticism towards hospital care,1 have advocated for home DMSO in lieu of going to the hospital. This is extremely unwise, as if a significant hemorrhagic stroke is occurring, DMSO cannot work as the primary treatment. Rather, the correct course is to use DMSO on the way to the hospital, and then if the whole thing is written off as a TIA (which many people have shared happened to them after they used DMSO, it resolved the stroke midway to the ER, and ER could then not decide if a stroke had happened), simply be grateful you had the optimal outcome when things could have easily been much worse. In short, the existing management we have for strokes is correct, and DMSO should be viewed as way to improve the results it yields rather than a replacement for it.
Many stories like these two Archie Scott reported1 exist throughout the DMSO literature:
A Los Angeles school teacher had a major stroke shortly after the start of the Christmas break. She was unconscious on her living room floor. DMSO treatment was started immediately after the stroke. The DMSO was first applied topically to her head within minutes of the stroke. Less than one hour after the stroke she was given DMSO by intramuscular injection. This patient was never taken to the hospital for this stroke. A prominent surgeon who was a family friend told the husband of this patient that it was important to keep her out of the hospital. The surgeon said that even though the treatment was completely legal, it would be difficult to get approval to give the DMSO especially by injection at his hospital.
This patient made a dramatic recovery. She regained consciousness later in the day in which she had her stroke. Treatment continued for the next week. Each day she received two topical applications of DMSO, one intramuscular injection of DMSO, and two doses of one teaspoonful of DMSO in juice. Her condition improved each day. When school resumed after the first of January, this teacher was back in the school teaching the students as if nothing had happened during the Christmas vacation. She continued teaching until she retired, healthy and with no disability.
A lady was in a coma in a convalescent hospital and had been in the coma since her stroke three months ago. She was given little chance of recovery and was expected to remain in a vegetative state until her death.
When I first observed this lady, there was no response to any type of stimulus. She was alive, but appeared lifeless. It was decided that her treatment should be topical DMSO daily….One month after the start of treatment, there were positive signs in the lady. Her brain was starting to respond to the DMSO. The treatment continued, and four months after treatment started this lady was able to return to her home [where treatment continued].
Three years after the start of DMSO treatment this writer returned to visit this patient. At this time the lady was living a normal life, not the life of a stroke victim. She was able to look after the house and walked normally.
The only lingering effect of the stroke was a slight speech defect. At this time she said that her memory was better than that of her husband who had not had a stroke and who was considered to be completely normal.
Note: there are also many reported cases of individuals who took DMSO for musculoskeletal or pain disorders (by far the most common use of DMSO) who then experienced a permanent improvement of stroke symptoms.
Extensive data, in turn, corroborates these remarkable stories.
Due to the ethical issues with creating and then treating strokes in humans, most of the research in this field has been conducted in animals (which I hold many strong ethical objections to). As such, the only human study has been conducted in ischemic strokes was a 2002 trial, where IV DMSO given with fructose diphosphate twice daily to 11 patients (mean age 65) with acute or subacute ischemic stroke was well tolerated and, when started within 12 hours of stroke onset, left 63% “improved” or “markedly improved” versus 20% of those on standard care at three months, and the benefit held even when treatment began well after the stroke.
Note: animal studies further corroborate DMSO-FDP value. In rabbits whose brains were driven to flatlined (isoelectric) EEGs by combined hypoxemia, hypotension, and carotid occlusion, DMSO-FDP given after five minutes of electrical silence restored brain activity far faster and let all animals survive with minimal damage, versus only 22% survival (severely disabled) on saline, and in mice given head impacts (another area DMSO helps), DMSO-FDP was the most protective and DMSO alone the second, while FDP and the rest gave no benefit, confirming DMSO was therapeutic. Finally, when DMSO-FDP was given to rats with poor chronic blood flow to the brain (due to carotid obstruction), there was a 54% improvement in visuo-spatial memory1,2 (which is corroborated by dementia patients who’ve improved from DMSO).
•A Russian patent treated perinatal hypoxic encephalopathy in newborns by daily electrophoresis of vitamin E⬖ in DMSO. In three term infants 6–7 sessions produced disappearance of limb tremor (chin tremor remaining only with crying), normalization of muscle tone, return of tendon and support/automatic-walking reflexes, loss of the spontaneous Moro reflex, and restoration of the Babkin reflex, with faster clinical recovery than intramuscular vitamin E⬖ plus standard care.
•One physician reported knowing of a patient of Stanley Jacob’s whose stroke was successfully treated with DMSO.1Note: I have corroborated through multiple sources that Stanley Jacob successfully treated numerous strokes with DMSO, but I have not been able quantify how many in total were treated or what the success rate was.
Additionally, numerous reviews support DMSO’s use in humans with strokes. These include:
•A 2009 pharmacology review by Jack de la Torre and Stanley Jacob of DMSO in cardiac and CNS damage (arguably the most detailed one in print) showed intravenous DMSO elevated cerebral blood flow, limited infarct volume after middle-cerebral-artery occlusion, preserved the vulnerable CA1 and dentate neurons and facilitated recovery from acute or chronic cerebral ischemia.1
Note: de la Torre was publishing papers on DMSO treating strokes fifty years ago1 and likewise, a 1982 paper1 acknowledged DMSO was being used to treat strokes.
•A 1992 Chinese review that concluded DMSO protects ischemic brain tissue and blocks the secondary pathological processes that follow cerebral ischemia, outperforming mannitol, dexamethasone, and barbiturates as a neuroprotectant.1
•A 2010 Chinese review of DMSO’s effects on the heart and central nervous system (which noted authors had identified over 10,000 articles on the biological effects of DMSO).1
•A 2012 Chinese review classified DMSO as a classic antioxidant with therapeutic effects on ischemia reperfusion injury across many organs (and noted it had already been used clinically abroad for cerebral reperfusion injury).1
•In a 2018 Ukrainian physical-rehabilitation review where DMSO appears as an iontophoresis solvent in post-stroke and disability rehabilitation protocols.1
•A 2022 Russian review from Osh State University argued that drug electrophoresis (driving charged medication ions through the skin with direct current) is among the most valuable physiotherapy methods for cerebrovascular disease (stroke and TIA) and peripheral-nerve disorders. Within it, DMSO is used as a carrier that lets otherwise water-insoluble drugs dissociate and be pushed through the skin. In acute stroke in the early recovery period, this was applied to the eyelids and back of the neck with heparin added for ischemic stroke and iodine substituted for hemorrhagic stroke.1
DMSO has repeatedly been shown to reduce the core injury of an ischemic stroke:
•A rhesus monkey study blocked the MCA for 4 hours, gave DMSO, dexamethasone, or nothing, and then opened the MCA after it had been blocked for 17 hours. DMSO gave significant protection from the severe neurological deficits and loss of arterial blood flow the other two groups developed.
•A squirrel monkey study blocked the left MCA for 4 hours, after which the animals were given a variety of different treatments (e.g., saline, hemodilution, or hyperbaric oxygen at 2 atmospheres). Seven days after treatment, 8 of 10 DMSO treated monkeys were alive (with 2 having mild contralateral muscle weakness), while 75% of those receiving hyperbaric oxygen survived, and just 34% of those receiving hemodilution survived (with the last two groups also having more significant neurological deficits). Finally, combining either of these treatments with DMSO produced slightly worse results than just DMSO alone.
•In experimental canine middle cerebral artery embolectomy, DMSO (or low-dose methylprednisolone) extended the grace period to 6 hours following embolization and protected the cerebral tissue from the injury of ischemia and post-ischemic reperfusion (with no infarcted tissue in DMSO treated animals and a 1.45 cm3 area of infarction in untreated ones).1,2,3,4
•In a canine model of severe cerebral ischemia (where blood flow was cut by 90% for an hour), DMSO given alone as pretreatment allowed EEG activity to re-emerge after recirculation where untreated animals showed none. In a second canine study, in brains subjected to 14 minutes of complete ischemia and then reperfused for an hour, DMSO added to the reperfusion blood lowered a marker of lipid peroxidation (TBAR) back to control levels, restored roughly three quarters of the lost energy stores (ATP and creatine phosphate), cut lactate accumulation by 60%, and produced a marked return of EEG and auditory evoked potentials that untreated brains entirely lacked. Adding a platelet-activating factor antagonist on top of the DMSO further improved mitochondrial energy markers, though the reduction in lipid peroxidation was attributable to DMSO alone.
Note: the first study also found vitamin E⬖ restored brain function, mirroring forgotten Russian research on how to counteract the biological consequences of chronic stress on the brain with DMSO and vitamin E.⬖
•In a canine model of pressure-induced focal ischemia worsened by ethanol exposure (done to model head trauma from a drunk driving car accident), DMSO significantly reduced brain lesion volumes under both normotensive and hypotensive conditions and scavenged the hydroxyl radicals generated from ethanol metabolism.
•When seven different therapies were compared head-to-head in a canine model of severe pressure-induced focal ischemia, intravenous DMSO produced the best neurobehavioral recovery scores and the smallest lesion volumes, with reduced edema, necrosis, and cavitation.
•In a rat transient focal ischemia model done with 90-minute middle cerebral artery occlusion followed by reperfusion (as the MCA is one of the most commonly sites of consequential strokes and hence often blocked to simulate strokes), DMSO given 30 minutes before ischemia dose-dependently reduced cortical and striatal infarct volumes (how much brain tissue was damaged), and at the higher dose also significantly improved neurological motor function (while a low dose produced no benefit).
•In rats, DMSO given 30 minutes prior to MCA occlusion significantly reduced the amount of permanently damaged brain tissue1,2,3 In another, DMSO immediately after occluded MCA blood flow was restored reduced rat infarct size and blood-brain-barrier damage (as measured by MRI), with enhanced protection and reduced MMP-2/MMP-9 activity (enzymes that breakdown the blood–brain barrier) when combined with DPI. Additionally, oral DMSO with vitamins C⬖ and E⬖, given 12 hours after rat MCA occlusion, significantly reduced oxidative stress.
•In rats, DMSO one hour before or after MCA and carotid occlusion significantly reduced rat brain edema and infarct volume. In rats with focal cerebral ischemia DMSO reduced brain water content and lipid peroxidation, preserved Na⁺-K⁺-ATPase and superoxide dismutase activity relative to saline controls, and markedly improved brain edema and ischemic tissue damage.
•In rats subjected to four vessel occlusion (which cuts off almost all blood flow to the brain) DMSO partially reduced mitochondrial malondialdehyde and free fatty-acid accumulation after reperfusion.
•In neonatal (7 day old) rats with hypoxia-ischemia brain damage, DMSO injected into the brain reduced infarct volume and brain injury (particularly within the cortex) along with inhibiting the breakdown of MAP2 and fodrin, suggesting neuroprotection via calpain inhibition.
•In gerbils subjected to carotid ischemia-reperfusion, DMSO, significantly reduced delayed neuronal death and lowered markers of hydroxyl radical activity that accumulates after reperfusion.1 In another study, intraperitoneal 10% DMSO before ischemia cut gerbil mortality from 60% to as low as 14%, reduced the proportion of ischemic hippocampal neurons (from 71% to 46% at the higher dose), and blunted neurological signs.1,2
•In a thrombotic (clot) stroke mouse model, daily DMSO (given for five days after the infarction) prevented the shrinkage and nuclear condensation of injured neurons and, most strikingly, sharply reduced the excessive astrocytic scarring response (gliosis) in the damaged cortex and hippocampus, restoring the astrocytes toward their normal morphology.1,2
•In decapitated mice (with blood flow hence being cut off to the brain), DMSO prolonged the time the animal continued to gasp for breath and produced a dose-dependent relaxation of pre-contracted vascular smooth muscle, pointing to a vasodilatory contribution to its anti-ischemic effect.1 An earlier report found DMSO was protective experimental hypoxic respiratory depression.1
•In a rat model of deep hypothermic circulatory arrest, the DMSO solvent-control group “unexpectedly” showed some of the same organ-protective effects as the active drug (ebselen) it was carrying.
Note: many of these results argue that giving IV DMSO beforehand could reduce the complications of many challenging surgeries (e.g., a coronary bypass). Unfortunately, much in the same way ultraviolet blood irradiation dramatically reduces bad surgical outcomes, neither has been adopted for this purpose.
Beyond reducing the core infarct, DMSO also protects the penumbra. Frequently in strokes, an area will form where blood has been impaired, but brain tissue has not yet died (known as the penumbra and the key target of most stroke management). In a rat stroke study where DMSO was administered an hour after brain blood flow had been permanently cut off, MRI imaging showed that DMSO stopped the region of dying brain tissue from continuing to expand, hence allowing a penumbra (rather than additional dead tissue) to form around the stroke site (particularly within the cortex).
Note: beyond the classic penumbra, groups of cells can also enter a shocked state where their normal functions cease (and they eventually die). As discussed here, this “penumbra” also responds to DMSO (which is one reason tissue often comes back to life following DMSO treatment and why the sooner DMSO is used after a brain or spinal injury, the better the results typically are).
•In guinea-pig hippocampal slices, 0.4% DMSO alone more than doubled the latency to irreversible ischemic depolarization (from 2.9 to 7.1 minutes) under combined oxygen-glucose deprivation while also reducing its amplitude, an effect further augmented when DMSO was combined with nimodipine.
•In rat hippocampal slices, 10 mM DMSO completely prevented the hypoxia-induced drop in serotonin (5-HT) release and directly increased spontaneous release under normoxia (indicating a direct stimulatory action on serotonergic neurons).
Finally, DMSO also potentiated hypoxic preconditioning on its own: given intraperitoneally or directly into the hippocampus, it increased rats’ resistance to severe hypoxia by roughly 79% and 111% respectively over controls (via α7-nicotinic receptors).
Note: a veterinary text1 (along many with other parts of the veterinary literature1) also highlighted DMSO’s edema-reducing, diuretic, and anti-inflammatory effects in cerebral ischemia. Likewise, in veterinary neurology, DMSO was used therapeutically or as a carrier in temporohyoid osteoarthropathy with acute neurological signs1, post-anesthetic air embolism with neurologic sequelae in a horse1, critically ill neonatal foals1, a filly’s watershed cerebral infarction1, and a 2-day-old filly with hypoxic-ischemic encephalopathy given IV DMSO.1
In addition to the extensive research showing that DMSO restores blood circulation and prevents reperfusion injuries in those (previously ischemic) tissues, numerous studies have shown DMSO mechanistically protects the brain from strokes:
•In anesthetized cats, DMSO significantly enhanced brain oxygenation (particularly in the caudate nucleus).
•DMSO was shown to preserve the neurological function of hippocampal brain tissue samples once their oxygen or glucose were withdrawn (with similar results seen in this study).
•When infused directly into the rat brain, DMSO alone reduced ischemia-induced (blood loss induced) extracellular glutamate (the excitotoxin that drives much of the neuronal death in a stroke) by 51% and modestly preserved the vulnerable hippocampal CA1 neurons relative to controls.
•DMSO down-regulated aquaporin-4 expression (a key driver of the brain swelling that follows an occlusion) after MCA occlusion in the rat.
•DMSO was found to protect the integrity of the blood-brain barrier integrity after MCA occlusion.
•Diazoxide and DMSO prevented the learning dysfunction and brain damage that follow carotid artery occlusion (with DMSO alone restoring) Morris-water-maze learning and preventing COX-2-positive neuron loss in the dentate gyrus.
Corroborating DMSO’s benefits for strokes, numerous readers here shared the following with me:
•A medicinal chemist with a background in neuroscience, recognized his own stroke the moment it began: “Right after waking up I went to the toilet and noticed that I had lost control of my palm. I walked to bed and I froze, unable to lay down.” He had his wife get him diluted DMSO, drank most of it over the next hour, and went to the hospital—by which point he had lost speech (Polish entirely, English partially), leaving him, a Pole, to communicate in English in a Polish hospital. “I credit DMSO for not losing movement ability,” he wrote. His speech recovered well enough that he returned to full-time work as a scientist six weeks later, and he now drinks a small maintenance dose daily.1
•One week after her husband’s stroke, which had left him with severe pain, vertigo, exhaustion, and partial paralysis of the left side of his face, arm, and leg, a reader discovered this series. She then applied undiluted DMSO to his face, neck, and shoulder two to three times a day; the pain, she reported, “went away almost instantly every time.” Within about two weeks he began walking short distances without a cane. “Only 3 months after the stroke he walked with me unassisted to a friend’s house carrying a guitar, and was able to play the guitar and sing flawlessly while standing with one foot on a chair. My jaw was on the floor... ‘You’re all witnessing a freakin’ miracle right now. This man had a stroke three months ago, and now he’s playing his guitar like nothing happened!’”1
Thanks for saving my life. I had a stroke recently, and because of your article on dmso and strokes, was given some by my partner. Three minutes later I was OK again. I continue to read your articles daily.1
I have been in health chats where twice now, folks were in the chat and were having a stroke, they both had DMSO on hand & took 1 oz it both were stopped within 10-15 min and reversed any damage.1
I just recently had a stroke but used DMSO immediately ( I had my wife apply it in the hospital within hours of my stroke) and I’m about 95% back to normal and hoping to be 100% soon.1
•A wife whose husband had atrial fibrillation and two microclot strokes in 2024 treated a recurrence herself the following year: when both his legs went numb with pins and needles, she applied DMSO and “Within two hours he was 70% better,” and after a second identical treatment “everything was cleared up and did not return” (months later she used the same protocol over his chest for a suspected pulmonary embolism, with the same result).
•Another wife, reported DMSO “Made a world of difference” for her husband’s entire-left-side deficit,1 another reported their husband’s two mini-strokes cleared within a few hours,1 another reported that when her husband woke up unable to speak and with numbness in his cheeks, she began DMSO, and there was “a huge improvement from a week ago” as he was speaking in complete sentences most times.1
•A reader who saved her mother from a third stroke shared “It was miraculous!”1; another reported it saving a family member from a stroke.1 Likewise, a reader whose father began showing stroke symptoms wrote: “Thankfully I had some 99.9% DMSO on hand. The improvement was remarkable….“The Lord might have just used you to save my dad’s life.”1
Interestingly, many readers have reported stories matching my own experience of giving someone DMSO and then having the ER be confused because they could not find any signs of stroke:
•After a reader woke at 4:30 a.m. and found his left side would not respond when he tried to walk stated he immediately knew to use his DMSO and over the next 4 hours “My walking returned to normal but my reach and grab with my left arm/hand would not allow me to pick green beans in my garden.” He hence called 911, walked down his own hill to greet the firemen, and talked the EMTs out of taking him; the next morning his clinic’s nurses sent him to the hospital by ambulance, where monitoring, a CT scan, and echocardiograms found “no evidence of stroke,” and his remaining left-hand impairment recovered over two weeks with self-directed therapy. His conclusion: “In every interaction with medical personnel I strongly recommended that DMSO should be the first/immediate action when stroke symptoms are detected. Waiting for an ambulance or an emergency room visit to respond is a tragic waste of time.”1
•A 76-year-old man in excellent health had a nearly identical experience 36 hours after giving a double-red blood donation: he woke at 4 a.m. with trouble walking and gripping on his left side, and applied DMSO based on what he had read here. Hospital testing “has not found/confirmed stroke,” and he reported rehabbing himself until symptoms had “disappeared 97%.”1
•Another reader who was already familiar with DMSO and kept it on hand took it during an apparent stroke: “The ER doc came in to tell me that I had not stroked, despite speech impairment and other signs. I told him I took DMSO.”1
•The reports extend well beyond the acute window into recovery from established strokes. One reader’s husband, who had suffered eight strokes, takes DMSO three times a week; two years after his last stroke, in her words, “recovery great, he has some aphasia but still thinking great speaking to others although he’s an introvert and has lost some confidence in himself he is still living life to its fullest playing with grandkids gardening home renovations and going to the gym and doing a full work out which includes 30 chin ups!”1 A caregiver eight weeks into treating a stroke patient (who noted the changes “began almost immediately, after the very first treatment”) observed a cascade of gains: stronger voice and markedly improved speech, dramatically improved swallowing (he could again eat normal-sized meals, and even swallow while the TV was on, previously a choking hazard), self-feeding with the affected hand; improved energy, strength, and balance; and, “the most recent and undeniable change,” the return of his sense of taste. On one lucid day he zipped up his own jacket—notable, she wrote, “because the fine motor skills in his right hand were quite impaired by the stroke” and “even he commented at the time that it was remarkable.”1 Another reader watching his mother’s recovery described her damaged right side visibly “waking up”, regaining feeling and strength until one day she exclaimed, “Hey look, I’m sanding with my right hand!”1
•Others report gains across the full range of stroke severity. One reader had a large stroke that “affected every joint on my right side” and used DMSO with CBD: “One year later? Only my knee and two fingers (pinky and ring) are still ‘lazy’ but each month I notice an improvement... I couldn’t write but I can now. I’ve learned to type with 8 fingers but the other two are still improving.”1
•Another reader began giving her 72-year-old husband DMSO six weeks after his stroke; over two and a half weeks “he improved and slowly regained more function so that he could swim again,” and a later course brought further gains. She noted the oral route seemed to act faster, though its garlic-like odor kept him homebound—so he switched to applying DMSO nightly to his temples, forehead, and neck, on which he continued to slowly improve.1
•A 65-year-old who’d had a series of small strokes reported that after starting DMSO the improvement in mental acuity was “amazing” alongside whole-body pain relief;1 a physician who ran an IV chelation and ozone clinic recalled an “amazing recovery” in a stroke patient given IV DMSO;1 and caregivers successfully treating loved ones after strokes (e.g. “a very bad stroke1”) or an ischemic stroke and reporting steady, believable progress.1,2,3
•A grandfather who nebulized DMSO for decades survived multiple strokes and “amazed doctors by how quickly he recovered,” living to 94.1 Another reader stated flatly that DMSO saved him from a stroke a decade ago.1
Finally, many readers describe using oral DMSO as ongoing stroke prevention. One was having strokes two or three times a week until he started DMSO (originally bought for sciatic nerve pain): “the strokes stopped happening... once it is in the blood stream it works everywhere.”1 Another also reported DMSO stopped their strokes,1 Likewise, a diabetic who’d had two strokes from clotting that monitoring his own blood under a microscope, found daily oral DMSO kept his red cells out of rouleaux formation and “the clots at bay.”1
Note: these readers were almost certainly suffering from what would be diagnosed as “TIAs” and the fact that both DMSO prevented their recurrence and that one reader could link this to DMSO eliminating blood sludging argues for my theory many TIAs are actually microstrokes triggered by things like zeta potential disruption.
In short, I hope all of this (and what is to come) makes it clear why I feel so strongly about DMSO becoming a standard therapy for strokes. Nonetheless, as discussed earlier, it is absolutely critical you do not avoid emergency care just because DMSO is available and rather treat it as complementary therapy as you wait for conventional care.
Since DMSO is both a non-toxic solvent and able to deliver a variety of agents (e.g., through the skin), that rare combination results in it being used as a “vehicle control” in many studies. In these studies, DMSO is typically assumed to be inert (and hence not independently tested for an effect), but in some cases is tested, where it often yields a therapeutic effect (which I’ve noticed authors often do not disclose). As a wide number of agents combined with DMSO all yield therapeutic effects similar to those seen with DMSO, this suggests that DMSO plays a direct role in the effects observed, particularly since DMSO frequently potentiates the agents it is combined with. This dynamic I believe likely accounts for why many agents that succeed in preclinical studies (where DMSO is also used) fail in clinical studies where DMSO is not also used.
Note: replication failure is one of the largest problems in science.
As such, I include these combinations here (most of which were used for focal brain ischemia) both to highlight the shared effects seen across many agents (that potentially are due to DMSO) and to provide insights to readers looking for additional treatment strategies. To make these section easier to skim, all natural agents are marked with a ⬖.
Polyphenols & flavonoids — curcumin⬖ (reduced infarct size and cell death)1,2,3,4,5,6,7,8,9,10,11,12,13,14; resveratrol⬖ (reduced infarct size and preserved neurons, including in elderly and recurrent-stroke rats)1,2,3,4,5,6,7,8,9,10,11; baicalein⬖ (reduced infarct size and cell death)1,2; chrysophanol⬖ (reduced infarct size and cell death as a pre-treatment)1,2; quercetin⬖ (reduced infarct size)1,2; chrysin⬖ (improved movement and memory and reduced oxidative stress)1,2; nordihydroguaiaretic acid⬖ (reduced neurological deficits and infarct size)1; apigenin⬖ (reduced inflammation)1; mangiferin⬖ (reduced neurological deficits when given before ischemia)1; shikonin⬖ (reduced infarct size and oxidative stress)1; trifluoro-icaritin (reduced neurological deficits and infarct size)1.
Alkaloids & related plant compounds — berberine⬖ (reduced infarct size and cell death)1,2,3,4; evodiamine⬖ (reduced infarct size)1,2,3; rutaecarpine⬖ (improved movement and raised neurotrophic factors)1,2,3; cynandione A⬖1; vinpocetine⬖ (reduced infarct size and inflammation)1; sinomenine⬖ (reduced inflammation)1; piperine⬖ (reduced injury)1; carvacrol⬖ (reduced injury)1.
Terpenoids, saponins & quinones — astragaloside IV⬖ (protected neurons and reduced cell death)1,2,3,4,5; celastrol⬖ (reduced neurological deficits and infarct size)1,2; the cembranoid 4R⬖ (reduced infarct size and cell death)1; ginsenoside Rb1⬖ (reduced neuronal death)1; bilobalide⬖ (reduced neurological deficits and infarct size)1; tanshinone IIA⬖ (reduced infarct size when given after stroke)1; sulforaphane⬖ (reduced infarct size and inflammation)1; triptolide⬖ (reduced infarct size, swelling, and neurological deficits)1; picroside⬖ (protected mitochondria and reduced cell death)1; ursolic acid⬖ (reduced infarct size and improved neurological scores)1; Z-guggulsterone⬖ with boswellic acid⬖ (improved neurological function and promoted new blood-vessel growth)1; salvinorin A⬖ (reduced inflammation and swelling and protected the blood-brain barrier)1,2,3,4; herkinorin (reduced brain swelling and improved neurological function)1,2.
Whole-herb & multi-herb extracts — kava extract⬖ (reduced cell injury and inflammation)1; Gastrodia elata extract⬖ (reduced infarction by shifting immune cells toward healing)1; Ptychopetalum olacoides extract⬖ (protected brain tissue from oxygen deprivation)1; Angelica sinensis extract⬖ (improved neuronal survival and regrowth)1; Ginkgo biloba extract⬖ (prolonged survival and reduced injury)1,2; Viola spathulata extract⬖ (reduced infarct size)1; Zhenbao Pill⬖ (reduced inflammation and cell death)1; Qing-Nao-Tong-Luo Recipe⬖ (reduced infarct size and improved neurological function)1; Tongxinluo⬖ (protected the blood-brain barrier and circulation)1; Shenmai injection⬖ (reduced deficits and infarct size)1.
Other natural compounds — stilbazulenyl nitrone⬖ (was highly neuroprotective as an antioxidant)1; docosahexaenoic acid⬖ (protected brain cells from oxygen deprivation)1.
Kinase & MAPK-pathway inhibitors — an ERK inhibitor (improved survival and protected mitochondria after cardiac arrest, and reduced infarct size)1,2,3,4,5,6; a PI3K inhibitor (reduced injury in diabetic brain injury)1; a p38 MAPK inhibitor (reduced cell death and swelling and improved neurological function)1,2,3,4,5,6,7,8; a JNK inhibitor (protected neurons and improved survival)1,2,3; rapamycin (reduced infarct size)1,2,3,4; Mdivi-1 (reduced oxidative stress and cell death)1,2; a STAT3 inhibitor (reduced injury)1; anisomycin (improved neuronal survival)1; a PTEN inhibitor (promoted neuronal repair)1; HIF prolyl-hydroxylase inhibitors (induced protective autophagy)1; bosutinib (reduced infarct size and inflammation)1; a TAK1 inhibitor (improved neurological scores and reduced infarct size)1; 5’-deoxy-5-iodotubercidin (reduced infarct size by up to 57%)1; 2-Cl-MGV-1 (promoted new blood-vessel growth)1.
Cell-death & protease inhibitors — caspase inhibitors (reduced infarct size and cell death)1,2,3,4,5; cathepsin inhibitors (reduced infarct size and cell death)1,2,3,4; a Notch/γ-secretase inhibitor (drove stem cells toward neurons and aided post-stroke regrowth)1,2; necrostatin-1 (reduced necroptosis and improved myelination and memory)1,2,3; cyclosporin A (protected neurons)1; a calpain inhibitor (reduced cell death and injury)1,2; a PARP inhibitor (reduced infarct size)1; thalidomide (reduced infarct size and cell death)1.
HDAC & epigenetic inhibitors — an HDAC inhibitor (trichostatin A) (reduced infarct size and inflammation)1,2,3; an HDAC inhibitor (SAHA) (reduced infarct size by up to 57%)1,2; an HDAC inhibitor (MS-275) (reduced infarct size)1; an HDAC inhibitor (TSA) (reduced infarct size and inflammation)1; an EZH2 inhibitor (improved coordination and reduced injury)1.
Nuclear-receptor & metabolic modulators — pioglitazone (reduced neurological deficit, swelling, and inflammation)1,2,3,4; all-trans retinoic acid (reduced infarct size as a post-treatment)1,2,3; a PPARγ inhibitor1,2; LXR agonists (reduced infarct size)1; rosiglitazone (reduced infarct size, and in DMSO cut it by roughly half where DMSO alone was inert)1; a thyronamine analog (induced protective hypothermia)1; a PPARα agonist (bezafibrate)1; an SGLT2 inhibitor (empagliflozin) (reduced microvascular injury)1; an Nrf2 activator1; an ALDH2 activator1.
Receptor ligands & ion-channel modulators — an adenosine A1 agonist (improved outcomes and reduced injury)1,2,3,4; an α7-nicotinic modulator (reduced damage after stroke)1; dexmedetomidine (reduced mitochondrial fission and cell death)1,2,3; octanol, a gap-junction blocker (reduced infarct size after longer ischemia (worsening it after brief ischemia))1,2,3; a TRPC1 blocker (reduced calcium overload and cell death)1,2; nimodipine (improved neuronal survival)1; bumetanide (reduced swelling)1,2; an LPA2 agonist (improved survival)1; a GABAA α5 inverse agonist (promoted motor recovery)1; a nucleoside-transporter inhibitor (reduced infarct size)1.
Cannabinoid-system modulators — a CB1 agonist (acted through mitochondrial CB1 receptors)1,2; a CB2 agonist (reduced injury)1,2.
Hormones, steroids & vitamins — estrogen (reduced infarct size and cell death)1,2,3,4,5,6,7,8,9; progesterone (reduced infarct size and improved recovery, less so in aged animals)1,2,3,4,5,6,7,8,9; tamoxifen (reduced injury)1; vitamin D3⬖ (reduced infarct size and increased blood flow)1; vitamin K2⬖ (reduced swelling, cell death, and inflammation)1; erythropoietin (reduced injury, including intranasal delivery)1,2; leukemia inhibitory factor (protected neurons)1.
Repurposed clinical drugs — 4-methylcyclopentadecanone (reduced infarct size and inflammation)1; a norcantharidin MMP-9 inhibitor (improved scores and protected the blood-brain barrier)1; modafinil (reduced infarct size and swelling)1; cilostazol (protected brain blood vessels)1,2.
Other synthetic / pharmacological agents — an nNOS inhibitor (reduced infarction by 70-92%)1; an azulenyl nitrone (STAZN) (was neuroprotective)1; Z-11 (reduced neurological deficits and infarct size)1; a 12/15-LOX inhibitor (reduced infarct size and inflammation)1; electroacupuncture with microRNA delivery (reduced deficits and promoted stem-cell regrowth).1,2,3,4
The combination data also extend beyond focal ischemic stroke to the following models:
Neonatal & perinatal hypoxic-ischemic models — hesperidin⬖ (reduced oxidative stress and improved survival)1; baicalin⬖ (cut neonatal infarct size roughly in half)1; notoginsenoside R1⬖ (improved survival)1; melatonin⬖ (reduced infarct size and improved brain metabolism)1,2,3; a JNK inhibitor (reduced neonatal cell death)1,2; dantrolene (reduced cell death and injury)1; an adenosine A2A antagonist (reduced brain damage and cell death)1,2,3; 2-methoxyestradiol (reduced swelling and cell death)1; indomethacin (reduced infarct size and protected the blood-brain barrier)1; miconazole (improved myelination in white-matter damage)1; G-CSF (reduced neonatal cell death)1; H2S donors (reduced injury and promoted remyelination)1,2.
Cardiac-arrest & global-ischemia models — ellagic acid⬖ (improved kidney function after global ischemia)1; Gynostemma pentaphyllum⬖ (improved outcomes after cardiac arrest)1; necrosulfonamide (improved recovery by blocking programmed cell death)1; a TLR4 inhibitor (reduced neuron loss after cardiac arrest)1; oxcarbazepine (protected neurons after cardiac arrest)1; WIN 55,212-2 (reduced infarct size and induced protective hypothermia that prolonged survival)1,2,3,4,5; salubrinal (improved outcomes and preserved mitochondria after cardiac arrest)1,2; glibenclamide (raised 7-day survival after cardiac arrest)1; genistein⬖ (increased neuron survival after cardiac arrest)1,2; paclitaxel (protected neurons after cardiac arrest)1,2.
Beyond protecting brain tissue once a stroke is underway, as highlighted previously in the endothelial data, DMSO also acts directly on the cerebral vessels themselves, changing their tone, their reactivity to constrictors and dilators, and the blood flow they carry.
Like many other properties of DMSO, its effect on cerebral vessel caliber (width) depends heavily on dose. In a cat study examining pial (brain) arterioles both in vitro and in vivo, DMSO concentrations from 0.0001% to 0.5% produced no significant change in arteriolar caliber, while 1% DMSO dilated them by 19%—and on isolated cerebral arteries, high-concentration DMSO reversed constriction induced by PGF₂α (85% reversal), serotonin (60%), and potassium (13%).1 That study also found that intravenous 10% DMSO (1 g/kg) produced rapid, measurable brain shrinkage within 10–15 minutes, consistent with DMSO’s edema reducing properties.1
Conversely, some of DMSO’s effects on cerebral vessels actually work by blocking dilation, and this too traces back to its radical scavenging. This is because hydroxyl radicals themselves dilate cerebral microvessels, so when acetaldehyde and xanthine oxidase were used to dilate mouse pial arterioles, free-radical scavengers including DMSO stopped that dilation.1 Likewise, DMSO inhibited the pial arteriole dilation produced by a radical-generating xanthine oxidase acetaldehyde system while leaving carbon dioxide induced dilation untouched.1 This selectivity (blocking only the radical-driven dilation) hence indicated DMSO was scavenging radicals rather than acting as a general vasomotor agent.1 Likewise, in canine basilar arteries, DMSO reduced the Fe²⁺-mediated inhibition of endothelium-dependent relaxation by scavenging hydroxyl radicals.1 DMSO hence does not push vascular tone in a fixed direction like a typical pharmaceutical, rather normalizes vascular function by removing the radical signal, so it dilates a vessel radicals were constricting and blocks a dilation radicals were driving.
DMSO also independently blocks ATP-sensitive potassium (KATP) channel mediated cerebral vasodilation, and it does so at very low concentrations (within the range routinely used just to dissolve a test compound). In anesthetized rats, DMSO dose-dependently inhibited pinacidil-induced dilation of pial arterioles at 0.01-0.2%, with significant inhibition at the very bottom of that range.1 Notably, DMSO alone did not change the baseline vessel diameter, and the effect reversed within 15 minutes of washing the DMSO out.1 A companion report found the same for very low dilutions of both ethanol and DMSO,1 and in cats, DMSO inhibited the cerebral arteriolar dilation produced by hydrogen peroxide and KATP openers at under 1 mmol/L (which those authors attributed to potassium-channel blockade rather than radical scavenging).1
That said, when perfusion is measured across the whole brain rather than in isolated vessels, DMSO consistently raises cerebral blood flow (e.g, this was a key focus of forgotten Russian research on reversing the effects of chronic stress). In a 1986 rabbit brain-edema study, a 20% DMSO bolus raised cerebral blood flow by roughly 75-77% in both hemispheres almost immediately, with flow still elevated an hour later.1 Pretreating with indomethacin did not prevent this rise, which indicated the increase was not prostaglandin-mediated, and the intracranial pressure still fell despite the higher flow (as DMSO rapidly pulls water out of the brain).1 Low-dose intravenous DMSO did much the same in a canine model of myocardial ischemia, raising both cardiac output and cerebral blood flow while lowering vascular resistance, with no adverse change in heart rate or blood pressure.1 Likewise, when given an hour after an experimental brain hemorrhage, DMSO held brain oxygen and glucose consumption near baseline, curbed the excess lactate, stabilized or increased blood flow (partly by raising blood osmolarity), completely prevented the surge in lipid peroxidation, and eliminated the early mortality seen in the untreated animals (0% versus 25%).1
Note: DMSO’s effect on central cardiovascular control has been found to be transient and local rather than systemic. Injected directly into the brainstem cardiovascular center (the NTS), 40% DMSO produced only a brief 1-2 minute drop in blood pressure and heart rate before returning to baseline, with no lasting change (consistent with DMSO’s rapid diffusion out of tissue).
Agents dissolved in DMSO have also been shown to dilate the cerebral vessels such as an activator of ATP-sensitive potassium channels,1 various PDE5 inhibitors,1 apigenin,⬖1 (which relaxed the basilar artery), tetrahydroxystilbene glucoside,⬖1 (which in rats relaxed the mesenteric artery while protecting carotid flow),1 a gamma-secretase inhibitor (that reduced the vasospasm following a subarachnoid hemorrhage).1
Finally, these cerebral-perfusion effects are often used as a rationale for clinical applications. For example, in a horse that developed seizures and blindness after surgery, intravenous DMSO was given specifically for its radical scavenging and thromboxane inhibition to maintain the brain’s blood supply, after which the seizures stopped by day 3 and the vision partially returned over the following months.1 Likewise, the Russian clinical literature describes dimexide (DMSO) as relieving brain-tissue swelling, improving cerebral blood flow, and normalizing cerebral hemodynamics.1 One unusual Russian diagnostic protocol even applied a DMSO, nicotinic acid,⬖ and novocaine compress to the forehead to test whether increasing forehead blood flow improved a patient’s vision, using that result to predict who would benefit from surgery on the branches of the carotid artery.1
Hemorrhagic strokes are among the most difficult conditions in all of medicine to treat, and despite decades of work, there has been remarkably little progress in neurocritical care—particularly in preventing the long-term paralysis and disability that so often follow a brain bleed. This is because a hemorrhage sets off a cascade of injuries that conventional medicine has no single agent to address, whereas DMSO, remarkably, addresses each of them at once.
When blood escapes into the brain, three things happen more or less simultaneously. First, the swelling and accumulating blood raise the pressure inside the rigid skull (the intracranial pressure, or ICP), and brain tissue is exquisitely sensitive to being compressed—yet there is no good agent for lowering ICP (the most commonly used drug, mannitol, can produce a “rebound” in which pressure climbs higher than where it started). Second, the blood-brain barrier begins to break down, allowing still more fluid into the brain. Third, as the spilled blood cells die, the iron they release generates free radicals that destroy surrounding brain cells,1 while inflammatory processes triggered by the blood injure tissue further and drive additional cell death.
Remarkably, DMSO addresses each of these.1 It rapidly lowers ICP without the risk of rebound,1 and unlike most ICP-lowering agents it does not do so by cutting blood flow to the brain—instead it increases cerebral perfusion without raising blood pressure or heart rate,1 which matters because brain cells die within minutes of losing their blood supply. That improved flow is also what clears the leaked blood, and DMSO is excellent at reducing the accompanying brain edema.1
Note: I suspect rebound ICP is the brain’s attempt to restore its own blood supply; because DMSO already guarantees that supply, there is nothing to rebound from. Consistent with an osmotic rather than a direct vascular mechanism, one study in anesthetized cats found IV DMSO never constricted the cerebral arteries across an enormous concentration range, and only relaxed already-contracted vessels—while still shrinking the brain by pulling out excess fluid.
Beyond pressure and perfusion, DMSO lowers the inflammatory cytokines (IL-1α, IL-1β, IL-6) tied to stroke and tissue injury1,2 and calms overactive immune signaling.1,2 It also directly counters the damage from blood breakdown products: its free-radical scavenging limits platelet aggregation at injured microvessels and prevents blood from flooding the injury site (reducing secondary ischemic injury).1 At just 0.5% DMSO protected basilar-artery smooth muscle from oxyhemoglobin-induced contraction membrane blebbing, and cell death by scavenging hydroxyl radicals1 and it reversed iron-mediated damage to vessel relaxation in canine basilar arteries.1 DMSO likewise prevented bilirubin toxicity in myelinated axons, protecting nerve fibers from another toxic product of degrading blood.1
In short, no comparable agent exists for lowering ICP—one of the greatest unsolved challenges in neurocritical care—and many drugs that succeeded in animals have failed in human trials.1 Beyond removing edema, limited human work also suggests DMSO can somehow reduce the ongoing spilling of blood into the brain, through a mechanism that has not yet been definitively worked out.
Note: DMSO additionally lowers JAK2/STAT signaling,1 suppresses neurotoxic NMDA/AMPA ion currents,1 prevents iron-induced lipid peroxidation and focal edema,1 and partially inhibits PARP-1.1
The potential of DMSO here was recognized decades ago by Jack de la Torre, who when watching a near-dead experimental animal revive with DMSO recounted:
It was, as if the hand of God had somehow touched the animal’s forehead. “I don’t believe it,” I stammered. But it was true. I felt a tingling in my spine because this reawakening of a virtually dead animal had all the markings of a medical breakthrough.
Note: de la Torre’s observations were based partly on his repeated finding that animals with flatlined EEGs—which normally precede brain death—had their EEGs return within about ten minutes of receiving DMSO. As so often in this story, the discovery was never developed and was instead quietly laid to rest in the coffers of forgotten medicine.1
In experimental brain hemorrhages, DMSO given an hour after the bleed prevented the collapse of the brain’s antioxidant defenses and cut mortality to zero (vs. 25% in controls by three hours). In rats, it held lipid-peroxidation products at normal levels rather than letting them climb; in cats, it kept oxygen and glucose metabolism near baseline and blunted the flood of lactate an injured brain pours into the bloodstream. The authors doubted the improved flow was vasodilation as DMSO only widens vessels at 1%+ concentrations, well above those reached at 0.3 g/kg and attributed it instead to the compound’s antiedematous action: by raising blood osmolarity (335→352 mosm/L), DMSO drew fluid out of the swelling brain, an effect they compared to glycerol’s; the accompanying drop in brain lactate, they suggested, aided the same anti-edema process..1,2
The protection reaches the molecular level too: in hemorrhagic shock, another state where the brain loses its blood supply, DMSO quieted the inflammatory driver NF-kappaB while boosting the survival protein HSP70.
Note: much of this foundational Russian work on DMSO in acute intracerebral hemorrhage is collected in a dedicated chapter (by M.B. Plotnikov) of a Russian monograph on DMSO in clinical practice.1 Interestingly, much of Plotnikov’s later work (I just came across and need to read in detail) revolved around the hypothesis that increased blood viscosity (which included oxidized red blood cells clumping together, and after ischemia–reperfusion injuries occurred were further oxidized) was not only a marker but an amplifier of many diseases, particularly high blood pressure, chronic cerebrovascular disease, brain ischemia, and ischemic heart disease, and to a lesser extent venous insufficiency, diabetes, radiation injury, and shock—dovetailing with my understanding of the subject. As he worked in a Soviet/Russian cerebral-pharmacology and viscometry tradition he appears not to have engaged with the Western blood-sludging or zeta-potential or microstroke research, and hence arrived at a variety of different disease and treatment insights than what I’ve come across.
•In a study of 11 patients with dangerously high ICP and Glasgow Coma Scores of 4–6 following brain trauma, encephalitis or subarachnoid hemorrhage (patients on the verge of death for whom standard therapy had failed), IV DMSO (1 g/kg) promptly lowered ICP (mean drop ~23 mm Hg at 30 min) and produced a brisk diuresis. Three patients survived with good functional recoveries; the others died despite ICP control. Unlike barbiturates, which lower systemic arterial pressure and force patients into a coma, DMSO did neither—so cerebral perfusion pressure rose as ICP fell and patients remained clinically examinable.
•A second paper reported on nine patients who suffered partial or total paralysis after surgical repair of a ruptured aneurysm and had remarkable responses to DMSO:
In de la Torre’s own book,1 IV DMSO for ruptured aneurysms in humans is likewise reported to reverse progressive hemiplegia, relieve vasospasm and the resulting low cerebral blood flow, and improve motor deficits.
That DMSO limits bleeding is not unique to the brain—it has been observed in other organs, indicating this is a general property of DMSO. In a pig model of myocardial ischemia-reperfusion, intracoronary DMSO essentially eliminated intramyocardial hemorrhage (0 of 8 DMSO animals vs. 7 of 7 controls by cardiac MRI, and 1 of 10 vs. 8 of 8 by pathology) and reduced microvascular obstruction by 45%, with no hemodynamic or arrhythmic side effects.1 A Russian literature review likewise lists hemorrhages among the conditions DMSO (with antibiotics) is applied to directly, alongside bruises, sprains, and edema.1 Finally, in children with hemophilia, topical DMSO has been used as part of physiotherapy protocols for acute joint bleeding (hemarthrosis)—applied for 2–4 days to relieve pain, prevent intra-articular clotting, and reduce the progression toward joint damage.1,2
As before, many agents have been combined with DMSO here and demonstrated efficiacy for intracerebral and subarachnoid hemorrhages, many of which targeting the same injury cascades DMSO itself acts on (e.g, oxidative stress, inflammation, blood-brain barrier breakdown, edema, vasospasm, and neuronal death).
Natural agents — curcumin⬖ (reduced brain-cell death and mortality, protected the blood-brain barrier and reduced swelling, and outperformed nimodipine against vasospasm)1,2,3; resveratrol⬖ (improved neurological outcomes and reduced cell death, swelling, and inflammation)1,2,3; 6-gingerol⬖ (improved neurological function and reduced swelling, cell death, and inflammatory cytokines)1; quercetin⬖ (reduced oxidative stress, cell death, swelling, and vasospasm)1; allicin⬖ (improved neurological outcomes and protected the blood-brain barrier)1; honokiol⬖ (reduced cell death and improved cognition)1; genistein⬖ (reduced inflammation and improved neurological outcomes)1,2,3; sulforaphane⬖ (improved outcomes)1,2; EGCG⬖ (green-tea polyphenol; reduced oxidative injury and cell death)1; naringenin⬖ (improved neurological outcomes and reduced inflammation)1; piperine⬖ (relieved vasospasm)1; triptolide⬖ (reduced cell death and inflammation)1; salvinorin A⬖ (relieved vasospasm)1,2; schisandrin A⬖ (reduced pyroptosis, an inflammatory form of cell death) 1; astragaloside (A and IV)⬖ (improved neurological outcomes and reduced vasospasm)1,2; anethole trithione (a hydrogen-sulfide donor; reduced inflammation) 1; omega-3 polyunsaturated fatty acids⬖ (improved outcomes and increased protective autophagy)1.
A parallel set of targeted pathway inhibitors and drugs dissolved in DMSO also hemorrhagic reduced brain injury:
Cell-death pathway inhibitors — necroptosis inhibitor1,2,3,4,5; caspase-1 inhibitor1; caspase-3 inhibitor1,2,3; ferroptosis inhibitor1,2; necrosulfonamide1; caspase inhibitor1.
Kinase, signaling & channel inhibitors — ERK inhibitor1,2,3; p38 MAPK inhibitor1,2,3; JNK inhibitor1; HIF-1α inhibitor1,2,3,4; LRRK2 inhibitor1,2; STING inhibitor1; PTEN inhibitor 1; PTP1B inhibitor1; HDAC inhibitor1; Drp1 inhibitor1; IRE1α inhibitor1; AP-1 inhibitor 1; TRPC channel blocker1; FAK inhibitor1,2; aquaporin-regulating ERK inhibitor1; valproate and related HDAC inhibitors (improved survival in hemorrhagic-shock and TBI models)1.
Iron, heme & inflammatory-pathway agents — TLR4 blocker1,2; heme oxygenase-1 inhibitor1,2; iron chelator1; mTOR inhibitor1,2; tin-mesoporphyrin, a heme oxygenase inhibitor1.
Receptor ligands, growth factors & neuropeptides — TSPO ligand1,2; FGF-21; mitoNEET ligand1; ghrelin1; IGF-11; orexin-A1; apelin-131; sufentanil1; siponimod1; recombinant neurotrophin-41.
Other drugs & compounds — mGluR1 antagonist1; cyclosporine A1,2; 2-methoxyestradiol1; dabigatran1; glibenclamide1; tamoxifen1; praeruptorin E1; didymin1; H₂S donor AP391; chelerythrine1; Nur77 modulator1; rosuvastatin and simvastatin (reduced tPA-related hemorrhage and infarct)1
Note: an emodin⬖ study in acute pancreatitis (DMSO alone as a solvent) reduced tissue hemorrhage scores as one marker.
I have argued the reason many transformative medical therapies do not enter medical practice despite widespread public demand for them is because we exist within a “pay to play” system, where access to the mainstream medical marketplace can only be earned if massive amounts of money are spent to secure an FDA approval—which is problematic as approval is largely dependent upon the money spent, not the quality of the therapy (which is essentially why the medical medical marketplace is crowded with mediocre and harmful therapies).
A key piece of evidence for my contention is that while many of the transformative (but off-patent) therapies I have come across are effectively barred from mainstream care, once the therapy is repackaged into something far more expensive and proprietary, it is often a widely embraced therapy (e.g., while used globally with immense data behind it, ultraviolet blood irradiation is not permitted in American medicine, but UVBI combined with a photosensitizer—extracorporeal photopheresis—is a widely used and extremely expensive therapy here and likewise many proprietary DMSO containing drugs have been approved by the FDA).
So, while “unsafe” DMSO is not used for strokes despite fifty years of pleas and research—it simultaneously is. Specifically, a common way many blood vessel issues are addressed is by threading a catheter into an easy-to-reach artery (for example the groin or the wrist) and then guiding it through the vessels to the site of the problem and doing something there, such as placing a stent, so you do not have to open the body surgically to get to that spot.
One common reason this is done is to cut off blood flow in a vessel, for example a bleeding artery. One popular way to do that uses DMSO to dissolve a polymer that is not soluble in blood, thereby allowing it to stay liquid in the catheter, so it can be pushed to the target. However, once it is injected into the bloodstream, the DMSO diffuses away and the polymer precipitates into a cast that plugs the vessel and stops flow. As such, tens of thousands of published papers exist on this DMSO combination1,2,3 (with numerous readers sharing they recognized DMSO because it was in one of those agents).
Note: while generally safe1 (with an experienced operator), since very high concentrations of DMSO are used to dissolve the polymers, they have to injected slowly so the vessels and brain tissue are not injured by a highly concentrated burst of DMSO (whereas in contrast much lower DMSO concentrations are typically used in DMSO IVs). Additionally, since the polymer plugs can travel from the target site, side effects periodically happen (and comprise a significant portion of the small number of side effects which have been reported for DMSO—as all agents used at the time of an adverse event are typically reported).
My most impressive experience with DMSO has been post a hemorrhagic stroke my Father had due to anticoagulant use for atrial fibrillation. Free iron from hemorrhage, especially in the brain, is quite possibly the most inflammatory event that can happen and responds to DMSO.
After IV DMSO he was totally mentally restored in 4 hours, sitting up in bed asking what his Dr said about his condition and was discharged in 36 hours with NO complications!! — From a physician reader
Several readers have described applying DMSO in the immediate aftermath of an aneurysm or brain bleed. The most detailed came from a reader whose 84-year-old mother suffered a grade 3 brain aneurysm and subarachnoid hemorrhage: about 90 minutes after the event, as paramedics loaded her into the ambulance, the reader applied topical DMSO, with a smaller application in the ER hours later and small amounts perhaps six times over the next two weeks in the ICU. She went on to make a nearly complete—possibly complete—neurological recovery, with her remaining issues (weakness, UTIs) plausibly attributable to six weeks of bed rest. The reader described her recovering in sudden increments, as if her brain were “re-indexing” visual and motor skills and finding neural pathways that had been misplaced after the aneurysm.1 In a follow-up roughly a year later, the same reader reported that despite a subsequent fall and subdural hematoma (during which DMSO was only applied several days late), his mother remained in assisted living with most of her cognitive function and mobility intact—an outcome he understood to be exceptional for someone her age.1
Another reader described her own nonaneurysmal brain hemorrhage following an ice bath, three weeks after first buying DMSO on the strength of these articles. Her partner applied DMSO immediately; she went to the hospital, then resumed topical DMSO at home. At a follow-up scan, the neurosurgeon reportedly expressed surprise both that she had not developed cerebritis after the hemorrhage and that she had improved so markedly in such a short time.1
A reader whose 93-year-old grandmother had suffered several brain injuries over eighteen months—including a stroke and two brain bleeds caused by a fall with a blow to the head—reported that treating her with DMSO “made her recovery much faster.”1 Another reader survived a brain hemorrhage three weeks after buying DMSO on the strength of these articles; after the hospital misdiagnosed her, she applied it topically and then took it orally twice a day, and came through with “no inflammation and very little residual issues.” In her words, “without [@MidwesternDoc] I don’t think I would be alive today.”1
A reader who purchased DMSO for her mother-in-law—who had suffered a brain aneurysm seven years earlier—noted improvements across a range of unrelated issues (plantar fasciitis, knee-replacement swelling, varicose veins, arthritic hands) and was watching to see whether cognition and brain fog would improve over time. In the same report, the reader’s husband, who suffered near-constant neck and head pain and worsening migraines, applied DMSO once and reported his headache and neck pain were “GONE.”1
DMSO’s ability to relieve the pressure a mass places on neural tissue was also illustrated in a non-hemorrhage case. A clinician reader who shared he’d seen several glioblastomas resolve with mebendazole described one patient left virtually blind in one eye because the tumor had compressed the optic nerve; even after eight months of treatment fully eliminated the tumor, the blindness remained. After being shown DMSO eye drops, the patient used them once—and by the next morning his wife reported his vision had returned to normal.1 Though the tumor was gone, the compressive injury to the nerve had persisted until DMSO addressed it, mirroring the way DMSO relieves the pressure and secondary injury that follow a brain bleed.
Likewise, another reader’s partner (aged 75) was diagnosed with an inoperable 8 cm glioblastoma causing a slow brain bleed, losing the ability to speak and developing right-side paralysis, with a prognosis of three weeks to live. After copious topical DMSO, motor function began returning within 24 hours; over the following weeks the partner regained the ability to feed himself, communicate using Google Translate, and perform basic activities, and by week four could walk with a walker. A new CT scan at day 55 showed no brain bleed and reduced tumor metrics.1
Collectively, these reports mirror what was reported within DMSO literature and again suggest (provided another anticoagulant is not being taken), DMSO does not expose individuals with an active brain bleed to a serious risk. That said, the far smaller number of hemorrhagic testimonials makes me less confident in this assessment (e.g., if someone had used DMSO for a hemorrhagic stroke and died I would not have heard from them and within a sample that small that possibility can’t be excluded). However, given that hemorrhagic strokes are much rarer than ischemic strokes (13% vs. 87%), even if every case where a reader had used DMSO for either type of stroke was reported to me, I would still expect to receive far less hemorrhagic stroke reports. Notably, the ratio between all the ischemic and hemorrhagic stroke reports I’ve received here is fairly close to their expected distribution within the population, again suggesting there is not a significant (hidden) pool of readers with bad DMSO hemorrhagic stroke experiences.
While ischemic strokes are difficult to treat, hemorrhagic strokes and severe traumatic brain injuries are often more challenging still, and after decades, progress in neurologic intensive care has been limited, particularly in preventing the long-term paralysis and disability that follow a serious head injury.1 The core problem is that the initial impact is only the beginning, as in the hours and days that follow, a secondary injury unfolds, as swelling raises the pressure inside the rigid skull, circulation to the injured tissue falls, free radicals are generated in large quantities, and cells that survived the initial trauma begin to die.
This secondary cascade, together with the impact itself, determines whether a patient lives, and whether they recover. DMSO addresses that cascade at almost every point at once. It rapidly draws off the excess fluid driving intracranial pressure, restores circulation to the compromised tissue, scavenges the free radicals generated by the injury, and directly protects neurons from dying. Because a traumatic brain injury requires all of these problems to be solved simultaneously (something conventional care attempts with a different intervention for each, with the therapies often having conflicting effects and hence requires careful balancing between them), an agent that does all of the needed actions together is uniquely suited to the task. What follows is the extensive and largely forgotten evidence that DMSO does here.
Note: conflicting evidence exists supporting the use of progesterone, hypothermia, and hyperbaric oxygen therapy for traumatic brain injuries, but none of these approaches are in widespread use. Strong evidence also supports the use of methylene blue but it also is rarely used. Finally, certain trials (e.g., with progesterone or with an adenosine kinase inhibitor) find those therapies work even better if combined with DMSO.
The most striking human evidence concerns DMSO’s ability to rapidly lower the dangerously high intracranial pressure (ICP) that follows severe head injury, an effect that repeatedly translated into improved survival and neurological recovery.
Note: typically agents that lower ICP also lower (necessary) cerebral perfusion. As DMSO instead protects both, it is hence uniquely suited for these situations (e.g., while pentobarbitone and DMSO lowered ICP comparably (a 66% versus 45% drop)—pentobarbitone dropped systolic pressure by an average of 20 torr while DMSO caused no such drop, preserving cerebral perfusion1).
A pivotal study on this followed ten patients with closed head trauma and severely elevated ICP (40 to 127 mmHg, against a normal 5 to 13 mmHg) who received IV DMSO. In most cases ICP began dropping within 30 minutes, falling on average 28 mmHg after 24 hours and 58 mmHg after six days, with the reduction in brain swelling confirmed by CT scans. At a six-day neurological assessment, six patients had mild or no impairment and two had moderate impairment (two eventually died of their injuries), and by three months seven had minimal to no impairment. No adverse effects from DMSO were observed.1,2,3 This study, in turn, built on an earlier report of ten patients with severe closed head injuries, where DMSO rapidly reduced ICP and increased cerebral perfusion without lowering systemic blood pressure, and again improved the neurological course and outcome.1
These results were replicated across other studies. In a prospective study of 10 patients with severe closed head injury, marked brain swelling, and Glasgow Coma Scale (GCS) scores of 6 or below, IV DMSO (given whenever ICP reached 25 mmHg) dropped ICP markedly within 10 minutes (mean maximum reduction of 23.5 mmHg), raised cerebral perfusion pressure as ICP fell, and produced no rebound; seven of ten survived, six without gross deficits.1 In 12 patients with traumatic brain injury and elevated ICP, IV DMSO (given on average twice) rapidly reduced ICP in 21 of 23 treatment sessions, with the non-responding sessions also failing to respond to mannitol or furosemide, and no effect on blood pressure or other side effects.1,2 Likewise, a trial of 35 patients with severe head injury undergoing emergency cranial surgery found IV DMSO controlled ICP in 75% of cases (versus 53% with standard therapy), and controlled it in half of the patients who had already failed conventional treatment.1
The speed of the effect impressed even DMSO’s contemporaries. At a 1980 Congressional hearing on DMSO,1 Dr. Stanley Jacob discussed Oregon data (published in 19831) on 11 patients with intracranial hypertension from mixed causes, 5–6 of whom were already unresponsive to barbiturates and mannitol (3 of the barbiturate nonresponders after head trauma). IV DMSO dropped ICP to the normal range within 3–5 minutes in all 11 and was repeated as needed to keep ICP below 20 mmHg with three patients expected to die recovered well. A further five patients started on DMSO earlier did markedly better than those given it only after other measures had failed.
Finally, a report discussed by Dr. de la Torre1 (which I could not locate) detailed five patients with closed head injuries and high ICP that rapidly fell with IV DMSO. A 1.5 year old with a GCS of 7 and ICP of 30 mmHg fully recovered over 3 weeks, and a 7 year old admitted with a GCS of 5 and ICP of 25 mmHg fully recovered after 8 weeks; the three others (aged 17 to 52 with GCS scores of 3 to 5, two with ICPs above 50 mmHg) initially responded but did not survive.
Note: an early and candid 1982 report by UC San Diego researchers captured both the promise and the practical problem with DMSO in this era. The authors found the drug “often initially successful in controlling ICP” and “occasionally effective when barbiturates have failed” (and noted the ICP drop was too rapid to be a simple diuretic effect, implying a distinct mechanism), but struggled with its administration, as concentrated DMSO could dissolve standard IV tubing and the large fluid volumes then used were poorly suited to a head-injured patient (making prolonged control of ICP challenging to calibrate). These were solvable problems as refined protocols were developed (e.g., later work used lower concentrations and different IV materials to avoid them), but at the time they blunted enthusiasm for a therapy that was otherwise working.1,2,3 Likewise, a 1981 NIOSH report documented that staff at San Francisco General Hospital developed headaches and nausea (likely due to concentrated dimethyl sulfide) while working in rooms with patients receiving high-dose IV DMSO for an experimental cerebral-edema protocol, and that the problem resolved once room ventilation was improved1—something which has required clinics offering IV DMSO to often have a “DMSO only day” and that could likely also be addressed with appropriate air filters.
DMSO’s use for traumatic high ICP is also recognized in veterinary medicine, where its edema and pressure-lowering effects have long been utilized in large animals. A 1991 veterinary review of IV DMSO for traumatic brain injury in horses describes its use to reduce cerebral edema, intracranial pressure, and anoxia (with a regimen used at Oregon State University given slowly, generally twice daily), noting that DMSO increases localized circulation and cortical vasodilation, reduces platelet aggregation and fibrin thrombus formation in small injured vessels, protects endothelium, and reduces elevated ICP.1 Likewise, in equine clinical guidance, IV DMSO is indicated for acute head trauma resulting in high intracranial pressure and cerebral edema,1 and in parallel, a broader review of DMSO in equine medicine covers its application to central nervous system trauma among other indications.1 Similarly, in one case report, a 10-month-old filly presenting in coma after severe skull-brain trauma, IV DMSO was given as part of aggressive supportive therapy,1 and an early proprietary DMSO formulation was evaluated in craniotomized (skull opened) dogs for its effects on cerebral edema and inflammation.1 In another, a 2-day-old Quarter Horse filly with perinatal asphyxia and hypoxic-ischemic encephalopathy, given DMSO as part of supportive care, recovered fully by discharge,1 and a goat with polioencephalomalacia treated with IV DMSO alongside corticosteroids and mannitol showed progressive neurologic improvement with MRI-confirmed resolution of the lesion.1
A separate line of human research, largely published in the Ukrainian and Russian literature, approached DMSO from the angle of its free-radical scavenging rather than its pressure-lowering effect, and provides some of the strongest controlled human TBI data in this section.
The most substantial came from a 2003 dissertation at the Romodanov Neurosurgery Institute in Kyiv, which combined rat experiments with a controlled trial in 135 severe TBI patients. It established that lipid peroxidation, a key driver of secondary brain damage, activates within 3 hours of injury, peaks around days 3 to 7, tracks with injury severity, and persists for at least a year. In a controlled arm of 75 of those severe TBI patients, adding intravenous DMSO (first dose 3 to 5 hours after trauma and a second the following day) to standard therapy reduced lipid peroxidation markers by 22% by day 8 (versus a 15% rise in controls), raised the peroxide resistance of red cells by 71% (versus 13% in controls), and accelerated the regression of major neurological syndromes, with significant improvement in general cerebral (66.6%), meningeal (95.8%), asthenic (46.1%), and vegetative (95.6%) symptoms compared to standard therapy alone.1 The parallel rat work found that the same intraperitoneal DMSO regimen significantly reduced lipid peroxidation products in brain and blood (TBARS by 8 to 34%, Schiff bases by 27 to 68%) and raised red-cell resistance to peroxide-induced hemolysis by 11 to 51%, with the antioxidant effect sustained out to 21 days.
Note: these results have many intriguing correlations to Plotnikov’s previously mentioned research and the Russian chronic stress discussed in the first part of the series all of which suggests DMSO can counteract primary causes of acute and chronic neurodegeneration.
Likewise, this antioxidant framing recurs throughout the Russian-language reviews, where DMSO is classified as a synthetic radical scavenger noted for trapping the highly damaging hydroxyl radical and for providing a “high and stable” antioxidant effect in severe craniocerebral trauma, raising the body’s antioxidant status and preventing secondary brain damage.1
The human findings above have been reproduced and mechanistically dissected across a wide range of animal brain injury models.
•Compression and pressure injuries: Because any brain bleed or concussive impact risks putting pressure on part of the brain (for instance from an expanding clot), the models that mimic this are especially relevant. The most dramatic was a study in which an expanding balloon was placed in the brains of 40 rhesus monkeys to simulate a hematoma. All 10 saline-treated monkeys died, versus 10 of 15 surviving with urea (66.7%) and 14 of 15 with DMSO (93.3%), and among survivors neurological deficits occurred in 4 of 10 urea-treated animals versus only 1 of 14 given DMSO.1,2 This study, in turn, was preceded by an earlier study of 30 monkeys with similar results.1Note: urea was previously regularly used as a diuretic,1 and while it is now mostly (but not completely1) forgotten. We have found one oral urea formulation to be very helpful for certain types of edema and swelling.
Pressure injuries in dogs told the same story. In dogs with reduced blood pressure, pressure was applied directly to the brain for an hour, cutting off cerebral blood flow and producing necrosis, cavitation, edema, and deficits on the opposite side of the body. Against a panel of agents (barbiturates, mannitol, dextran, methylprednisolone), DMSO was the most effective: compared to no treatment, it improved neurobehavioral scores by 220%, reduced lesion volume by 93%, and prevented death in 5 of 6 dogs. Since blood alcohol worsens the damage from a traumatic brain injury (as occurs in drunk driving), the experiment was repeated with high blood alcohol, where DMSO still reduced brain tissue damage by 60%.1,2,3 In a related model, pressure-induced ischemia applied to the somatosensory cortex killed every untreated dog within days, whereas with IV DMSO five of six survived with no neurological or behavioral changes and preserved evoked potentials. A further comparison of seven therapies likewise found DMSO the most effective against pressure-induced focal ischemia. Likewise in rats with diffuse axonal brain injury, DMSO significantly reduced c-fos and c-jun gene expression in neurons across the cortex, white matter, brain stem, thalamus, and cerebellum, with the most pronounced reduction 2 hours post-injury compared to controls1—which is noteworthy as these genes drive inflammation and neuronal cell death in the window immediately after traumatic brain injury.
Note: one of the more intriguing findings across these compression studies was that neurological function was frequently preserved even when injury was still present in the brain tissue itself, suggesting DMSO protects function above and beyond what its effect on visible damage would predict.
•Edema models: A large body of rabbit work established DMSO’s anti-edema effect. A rabbit study that created lethal brain edema by freezing part of the brain found DMSO significantly reduced ICP and edema within 5 minutes while raising cerebral perfusion and leaving central venous pressure unchanged.1 This was reproduced repeatedly, including a follow-up with similar results,1 one using slow infusion rather than a bolus,1 another one that also found a 20% solution reduced ICP more reliably than 30% or 40% (at 1.0 to 2.0 g/kg),1 two others showing a synergistic effect with a barbiturate (where DMSO enhanced the ICP reduction while counteracting the barbiturate’s reduction of brain blood flow),1,2 one indicating the effect was mediated through sodium mobilization,1 and a final set showing indomethacin partly blocked DMSO’s ICP reduction, implicating prostaglandins.1,2,3
Note: highlighting DMSO’s normalizing properties, while DMSO lowers pathologically elevated ICP, in anesthetized rabbits with normal pressures, intravenous DMSO produced a prompt, significant rise in cerebrospinal fluid pressure (up to 66 mm H₂O, lasting under a minute)—and, unlike norepinephrine or epinephrine, it did so with no change in systemic blood pressure, respiration, or anything else, pointing to a local cerebral vascular or blood-CSF barrier effect.1
A Chinese study likewise used DMSO for acute cerebral edema.1 The effect held in other edema models too: in rabbits with brain edema induced by injecting pertussis vaccine into the carotid artery, IV DMSO effectively reduced ICP and edema,1 and in rats with edema induced by injecting iron (FeCl₂) into the brain, intraperitoneal DMSO reduced edema by 23% initially and left treated rats with far less edema at 24 hours.1 Similarly in cats exposed to standardized cortical freeze injury, DMSO reduced Evans blue extravasation—a marker of blood-brain-barrier disruption and vasogenic edema—acting as a hydroxyl-radical scavenger and grouped with deferoxamine as effective.1 Finally in a rat frozen-brain-injury model, DMSO (0.4 g/kg*) significantly reduced brain water content and neuronal apoptosis, outperforming tetramethylpyrazine at relieving the edema.1
Note: the older pertussis vaccine (which was notorious for causing severe brain injuries) contained a toxin that disrupted the blood-brain barrier and created brain inflammation. In that study, injecting it into the artery feeding the brain was used as a reliable way to induce brain damage.
•Missile and penetrating injuries: To simulate DMSO’s protective effects against gunshot wounds, missile injuries (frequently with BB pellets) were created in monkeys. Compared to mannitol, DMSO produced significantly better cerebral perfusion and oxidative metabolism along with an 86% survival rate (versus 75% for mannitol and 55% untreated).1 These results were replicated in a more detailed follow-up1 and by two other groups.1,2 A direct comparison to mannitol in rhesus monkeys with a standardized occipitofrontal missile injury confirmed DMSO better preserved cerebral blood flow, perfusion pressure, and oxidative metabolism than mannitol,1 and a further monkey study comparing 50% DMSO to mannitol for experimental brain gunshot wounds tested repeat dosing whenever ICP exceeded 20 mmHg.1
•Impact and weight-drop models: Numerous studies simulate closed head trauma by dropping weights on the heads of animals, and DMSO consistently protected against the resulting damage. In injured rats it reduced neuronal apoptosis, increased anti-apoptotic Bcl-2 expression across 6 to 168 hours post-injury,1 and raised Survivin and NF-κB expression in injured tissue, all reducing cell death.1 Functionally, DMSO improved cognitive and locomotor performance (such as solving mazes) while reducing anxiety, oxidative stress, inflammation, necrosis, and axonal damage,1 and separately reduced memory deficits by 62% a week after injury.1 A particularly rigorous study found that DMSO significantly reduced secondary neuronal degeneration in the hippocampus, with a magnitude of neuroprotection statistically indistinguishable from curcumin⬖ or alpha-tocopherol⬖ tested alongside it, leading the authors to conclude DMSO itself acted as a neuroprotective agent.1 In mice, DMSO combined synergistically with fructose 1,6-diphosphate (FDP) to protect motor function, survival, and cortical and hippocampal neurons from these injuries.1
Note: in animal experiments simulating severe brain injury, DMSO has also been shown to strengthen respiration (which otherwise becomes shallow and may stop), and in both humans and animals it often significantly increases urination through its diuretic action.
•Free-radical scavenging: DMSO also attenuated free-radical-mediated neurotoxicity in traumatized rat hippocampal neuron cultures, reducing apoptosis in uninjured neighboring cells by scavenging reactive oxygen species,1 providing a cellular-level mechanism to for its protective effects here.
Jacob and de la Torre’s capstone review of this literature,1 summarized the whole picture: low-dose intravenous DMSO restores cardiac output and cerebral blood flow, inhibits tissue-factor expression, scavenges free radicals, suppresses platelet aggregation, and in CNS models and patients rapidly lowers intracranial pressure without rebound, reduces edema, raises cerebral perfusion pressure, limits infarct volume, and preserves vulnerable hippocampal neurons.
To put all of this into context:
A January 11, 1981, news report in the Ocala Star Banner [page 6] carried the headline “DOCTOR CLAIMS DMSO SAVED 11.” The story read:
SAN DIEGO (AP) - A doctor at the University of San Diego [UCSD] credits the controversial drug DMSO with saving the lives of 11 people who suffered severe head injuries.
Dr. Perry E. Camp, a UCSD Medical School neurosurgeon, said Friday that dimethyl sulfoxide was effective for 11 of 30 people judged near death and for which other lifesaving methods have proved useless.
“To take patients like that and have even one out of 10 survive is phenomenal,” Camp said. “The fact that we have any survivorship at all . . . doesn’t sound like much, but it is extremely encouraging,” Camp said.
Note: many of the same principles discussed above hold true for concussions, and the pioneers of DMSO felt DMSO was an essential treatment for athletes after they experienced one, particularly since concussions can predispose the athlete to long-term cognitive issues (e.g., both boxers and professional football players have a threefold risk of dementia).
Like many other neurological conditions, a variety of agents dissolved in DMSO have shown promise in treating traumatic brain injuries, and convergent effects seen suggest some of the effects arise from DMSO rather than the active agent.
For example, in a controlled cortical impact study using DMSO as the vehicle for glibenclamide, the authors reported “unexpected independent beneficial effects” of DMSO itself, particularly in female mice, in which DMSO alone significantly downregulated the neurodegeneration markers TDP43 and TAU and helped restore cerebral blood flow by 21 days post-injury, comparable to the drug it was merely supposed to be dissolving. The authors flagged these as novel, previously unrecognized protective effects.
Note: this response illustrates why the protective effects of DMSO are rarely recognized in combination studies as the authors frequently can’t even conceive they could be present to begin with (despite a vast body of evidence already showing it).
The TBI combinations were as follows:
Natural agents — curcumin⬖ (reduced inflammation, oxidative stress, and seizure susceptibility)1,2,3; tetrahydrocurcumin⬖ (curcumin’s more absorbable form; enhanced autophagy and restored antioxidant enzymes)1; resveratrol⬖ (reduced cell death and modulated autophagy)1,2,3,4; quercetin⬖ (reduced swelling and cell death)1; sulforaphane⬖ (reduced swelling, contusion size, and oxidative stress)1; alpha-lipoic acid⬖ (improved neurological scores and reduced cell death)1; honokiol⬖ (from magnolia bark; protected the blood-brain barrier and reduced oxidative stress)1; vitamin K₂⬖ (reduced inflammation)1; docosahexaenoic acid (DHA)⬖ (the omega-3 fatty acid; improved autophagy and reduced inflammation)1,2,3,4; erianin and the mangrove-fungus derivative C53N (from Dendrobium; reduced inflammation, oxidative stress, and cell death (isolated research compounds rather than accessible remedies))1,2; Morin⬖ with MK-801 (lowered dementia and inflammatory markers after repetitive TBI)1; Auraptene⬖ (reduced oxidative stress and inflammation)1.
Note: the hormones progesterone and 17β-estradiol were also repeatedly delivered in DMSO and found protective after TBI, reducing swelling, oxidative stress, and inflammation while improving neurological outcomes. 1,2,3 Notably, in one progesterone study the DMSO-only arm itself showed the same pattern of benefit1 (reduced swelling and cell death and improved neurological scores over time), an ambiguity in the source data that again points to how independent DMSO effects get folded into the “vehicle” group.
A far larger set of studies used DMSO to deliver targeted pathway inhibitors and other synthetic compounds. Across these, the agents below repeatedly reduced brain swelling, cell death, oxidative stress, and neurological deficits, with the DMSO-only arm often following the same protective direction.
Oxidative-stress & Nrf2 agents — Nrf2 activators apocynin1,2; and tert-butylhydroquinone1.
HDAC & epigenetic inhibitors — HDAC inhibitors1,2,3.
Cell-death & protease inhibitors — necroptosis inhibitors1,2; a cathepsin, a calpain inhibitor1 and a selective PAR-1 inhibitor (improved depression-associated behaviors, social interaction and hippocampal-associated cognitive impairment).1
Autophagy & mTOR modulators — autophagy modulators1,2,3; an Epac2 inhibitor1; an mTOR inhibitor (rapamycin)1.
Receptor ligands & agonists — an S1P1 agonist and a bile-acid-receptor agonist1,2; a translocator-protein ligand1; a histamine-receptor ligand1.
Other pathway & enzyme modulators — a matrix metalloproteinase inhibitor1,2; a PTEN inhibitor1; an adenosine kinase inhibitor1; mitochondrial uncouplers1; a spinogenic agent1; a CRMP2-derived peptide1; cypin activators1; an anti-inflammatory (ATB-346)1; salubrinal (improved motor and cognitive function and reduced lesion size)1; an ADAM inhibitor (reduced lesion size and axonal injury)1.
Edema model combinations — curcumin⬖ (reduced brain swelling and inflammation)1; quercetin⬖ (reduced oxidative stress, brain swelling, cell death, and vasospasm)1; kadsura pepper stem extract⬖ (reduced hematoma size)1; a JAK2 inhibitor with dexmedetomidine (reduced brain swelling and cell death)1; a KMO inhibitor1.
Within the DMSO literature, there are periodic cases of dramatic concussion recoveries following DMSO. For example, one author shared the case of a woman who had received a severe concussion from falling off a horse, after which she had trouble walking, would suddenly neurologically decompensate (e.g., dropping things), and had memory issues alongside foggy headaches. Thirteen years later, she received an injection of DMSO, immediately had a large improvement, and further improved with subsequent injections.
Readers recovering from traumatic brain injuries, concussions, and related head trauma have reported similar benefits from DMSO.
The most mechanistically intriguing report came from a reader who is post-traumatic brain injury since 2017 and lives with cervical instability and a CSF leak that leaves her with recurring concussion-like symptoms. Even at a low dose she could tolerate, she found DMSO noticeably lowered her intracranial pressure, along with reducing daytime fluid retention, improving her distance vision and bowel function, and lessening food reactivity. She noted this could be particularly helpful for others with raised intracranial pressure, since, as in her case, elevated ICP can itself produce CSF leaks.1
Other readers reported briefer successes: one for sciatica and brain trauma1 (”It works!”), and another for finger joints and a head injury.1
Several readers have described using DMSO specifically for concussion. One with a concussion said it was “saving me and helping me to continue working,”1 another used it for post-concussion and whiplash injury,1 and another, recovering from fifteen concussions and a broken back after a 1992 Grand Canyon fall found success with castor oil⬖ and DMSO.1
Another reader described slipping on a wet floor and landing on her cheekbone with nothing but her glasses to break the fall—”I could feel my brain slam inside my head.” Within 30 minutes her cheek and eye had puffed up severely; she ingested DMSO and lathered it on her face, continuing for three days. By day five the bruising was already in its final yellowing stage. “I think had I not had DMSO in my house, I would be suffering from symptoms of concussion now,” she wrote, adding that she now keeps a bottle in her handbag at all times.1
The most detailed concussion account came from a reader who said DMSO “gave me my life back” after a shoulder injury with a concussion of the upper back left everything from his neck to his left hand inflamed and painful, and left him feeling systemically ill for months. Standard anti-inflammatories were useless. Starting a topical DMSO once nightly, he felt “not sick for the first time in months” within about three weeks. He described the pain first being suppressed, then localizing to its true source (his neck rather than the shoulder), then resolving, alongside a range of incidental benefits (a chronic wrist problem, thumb inflammation, eye floaters, a fading scar, and body odor all improved). He also found an on-off strategy worked best, applying for several days then pausing, observing that each time he stopped, the pain would briefly spike and then settle to a new low, as though removing DMSO let the body “better see where the problems really are.”1
One reader even tried it for a rare eye condition tied to an old concussion. He has superior oblique myokymia, a “twitch behind the eye” that makes his vision jump and occasionally double (alarmingly, sometimes while driving at speed), which had been attributed to a concussive injury from a serious car accident in which an airbag knocked him out. After a neuro-ophthalmologist offered only anti-convulsant drugs with “awful” side effects, he tried a 10% DMSO solution in distilled water as an eye drop, which temporarily “hit the off switch.” It didn’t cure the condition, but gave him, in his words, an actual tool in the toolbox.1
Note: concussions are notoriously difficult to manage (e.g., I have only found one approach that seems to work consistently for them), so the possibility a simple and widely accessible option exists is immensely encouraging as it would benefit many. However, while the evidence strongly argues for DMSO’s use in severe traumatic brain injuries, there is much less data for typical concussions, and it is quite likely the results for DMSO on those injuries were will be highly variable with not everyone experiencing a noticeable benefit from DMSO.
Because the heart, like the brain, is exquisitely sensitive to oxygen deprivation and to the flood of free radicals that accompanies the restoration of blood flow, DMSO’s protective and circulation-promoting effects have shown promise for many heart conditions (e.g., physiologic concentrations of DMSO enhanced respiratory control ratio and viability of heart cardiomyoblasts1).
For example, DMSO’s scavenging ability has been shown to protect the heart from many stressors. These includes protecting heart-muscle contractility from iron-induced oxidative injury,1 completely blocking radical-mediated damage to the calcium-handling machinery of cardiac cells,1 preserving the sodium-potassium pump during ischemia-reperfusion,1 protected the cultured chick embryo cardiac myocytes from injury caused by hydrogen peroxide,1 and preventing lipid peroxidation of heart-cell membranes under bacterial-toxin stress.1
As DMSO’s therapeutic properties in strokes directly translate to heart attacks, many studies have explored it here:
•When the heart’s blood supply is impaired, its ability to pump is as well (which is part of why heart attacks are a downhill spiral, as the heart loses the ability to give itself the blood it needs). When heart attacks were modeled (e.g., by ligating the coronary artery to impair the heart’s blood supply), DMSO was able to counteract this. For example, in a dog heart attack study, an IV bolus of DMSO raised cardiac output to 1.65 L/min by the third hour versus 1.15 L/min in untreated controls, alongside lowering systemic vascular resistance and increasing cerebral blood flow.1 Likewise, in another dog study, intravenous DMSO (2 g/kg as a 50% solution*) transiently raised cardiac index from 4.56 to 6.91 L/min/m² and stroke index from 36 to 45 ml/beat/m² while dropping systemic vascular resistance.1
•In addition to preserving the heart’s vital function, many studies have shown DMSO prevents damage to the heart itself. In isolated rat hearts subjected to global ischemia-reperfusion, three days of intraperitoneal DMSO pretreatment (550 mg/kg*) cut infarct size from 50.0% to 21.2% and improved post-ischemic left-ventricular function.1 In rats where the coronary supply was cut for 30 minutes and then reperfused for 120 minutes, DMSO preserved coronary blood flow and reduced both the resulting necrosis (tissue death) by 57.6% and the ensuing left-ventricular dysfunction (an effect that was greater when DMSO was given for several days beforehand rather than immediately prior to occlusion).1 In another rat study, DMSO reduced the damaged portion of the heart by 76.18%,1 and in another it prevented contracture bands from forming in ischemic heart tissue (a common long-term complication of heart attacks).1
•Similarly, in pigs, DMSO significantly reduced intramyocardial hemorrhages and gross pathological changes,1 and in another study improved overall heart attack outcomes.1 In rabbits, giving hydrogen peroxide (H₂O₂) concurrently with DMSO immediately after occlusion reduced the damage still further, presumably by supplying oxygen to the starved tissue.1 Consistent with this, in models of heart attack DMSO reduced the oxidative markers and preserved the antioxidant enzymes that track myocardial injury.1,2
Furthermore, a large part of the damage in a heart attack comes not from the loss of blood flow itself but from its restoration, and DMSO addresses this reperfusion injury directly. In perfused rat hearts, 10% DMSO attenuated the oxygen paradox, reducing reoxygenation creatine-kinase release from 25.3 to 7.2 IU/g and cutting calcium-paradox enzyme release from 134.1 to 54.9 IU/g,1 and it likewise protected against the reperfusion injury caused by calcium-containing solutions.1 In isolated cardiac muscle it preserved contractility during hypoxia,1 an effect echoed in rabbit studies of preserved contractile strength1 and maintained cardiac output and brain perfusion in dogs.1
This same protection extends to hearts held for surgery or storage: in isolated rat hearts, 0.5% DMSO reduced post-storage contractile dysfunction during hypothermic ischemic storage,1 and when added to cardioplegic solutions (used to stop the heart during surgery) at 0.55%, fully preserved mitochondrial respiration after two hours of global ischemia.1 Combined with cardioplegia and alpha-tocopherol,⬖ DMSO likewise improved rat-heart function through ischemia.1,2 Beyond ischemia, it protected against endotoxin-induced myocardial injury,1 improved survival in endotoxemic rats,1 and shielded the heart from intravenous potassium (given at the dose used in lethal injections).1 Most notably, with a cardiac enzyme that normally breaks down ATP (extracted from cow hearts) once mixed with DMSO, it instead synthesized ATP, suggesting DMSO can create a cellular environment that favors energy generation—particularly when the conditions cells normally rely on for it are absent (e.g., during a heart attack).1
Reviews have accordingly proposed DMSO as an antioxidant therapy for myocardial ischemia reperfusion injury1 and summarized its cardiac and CNS pharmacology,1 and reviews of renal and organ protection in aortic surgery note that low-dose IV DMSO restored cardiac output after coronary ligation in dogs while scavenging free radicals, blocking Na⁺/Ca²⁺ influx, and suppressing platelet aggregation.1
Note: as DMSO’s effects are dose and administration dependent, some studies found weaker results. For example, where DMSO served only as the solvent control, it sometimes protected on its own: in a rat deep-hypothermic-circulatory-arrest model testing ebselen, the DMSO solvent-control group itself showed partial protection on several markers, limiting attribution of the benefit to the drug.1 Likewise, in a canine model of coronary occlusion and reperfusion, intravenous DMSO reduced infarct size but not to a statistically significant degree (43.7% vs. 53.4% in controls),1 in two others the benefit was small1,2 and in another heart attack study I located, DMSO provided no benefit (which was likely due to 50% DMSO being directly infused).1 All of this indicates that while helpful, it is not guaranteed DMSO will be able to help every heart attack.
Lastly according to one of the main DMSO authors,1 DMSO was used to treat angina pectoris, heart attacks and prevent heart attacks by physicians in Chile (likely at the dose of 2g/kg). However, despite my best efforts, I could not locate the published paper he referred to with the limited information provided, so it’s likely impossible to corroborate this claim.
Many agents delivered in DMSO reduced infarct size, apoptosis, or oxidative injury in myocardial ischemia-reperfusion and cardiac-arrest models.
Polyphenols & flavonoids — curcumin⬖ (reduced inflammatory cytokines and oxidative stress) 1,2,3,4,5; resveratrol⬖ (reduced oxidative stress and inflammatory cytokines) 1,2,3,4; quercetin⬖ (shrank the infarct) 1; lycopene⬖ (reduced heart-cell death) 1; propolis⬖ (improved heart function) 1; dihydromyricetin⬖ (reduced inflammatory cytokines and cell death) 1; eriocitrin⬖ (improved cell survival and oxidative stress) 1; danshensu⬖ (reduced oxidative stress and cell death); Licochalcone A⬖; curcumin⬖; quercetin (with Ala-Gln)⬖; eriocitrin⬖; tanshinone IIA (PLGA nanoparticles)⬖ (protected against oxidative damage); genistein⬖ (reduced oxidative stress); flavonols⬖ (preserved the heart’s pumping strength); mangiferin⬖ (antioxidant protection against a chemically induced heart attack) 1.
Alkaloids & terpenes — carvacrol⬖ (reduced infarct size and cell death, and reduced mitochondrial fission)1,2,3; higenamine⬖ (reduced infarct size and improved heart function) 1; notopterol⬖ (improved heart function and reduced scarring)1.
Saponins, terpenoids & other botanicals — ginsenoside Rh2⬖ (reduced inflammatory cytokines) 1; ginsenoside 20(S)-Rh2⬖ (improved heart function)1; ginsenoside Rd⬖ (cut infarct size from 36% to 21%, and shifted immune cells toward healing)1,2; magnolol⬖ (reduced infarct size)1; honokiol⬖ (reduced infarct size) 1; asiatic acid⬖ (reduced cell death and oxidative stress)1; curculigoside⬖ (improved cell survival and reduced infarct size)1,2; tanshinone IIA⬖ (reduced cell death and inflammation)1,2; astragaloside IV⬖ (promoted new blood-vessel growth)1,2; triptolide⬖ (reduced inflammation and scarring)1.
Anesthetic (pre-/postconditioning) agents — propofol (reduced cell death)1,2; sufentanil1; sevoflurane (reduced infarct size 36% vs 56%)1,2; desflurane (reduced infarct size 48% to 19%) 1; isoflurane1.
Mitochondrial & metabolic-pathway agents — hydrogen sulfide donors (repeatedly reduced infarct size, including in diabetic hearts)1,2,3,4,5; rapamycin (protected diabetic and normal hearts, cutting infarct size from 36% to 13%)1,2,3,4; Mdivi-1 (reduced infarct size and cell death, including in diabetic and pre-diabetic hearts)1,2; MOTS-c (reduced infarct size)1; diazoxide (reduced oxidative stress and preserved mitochondria)1,2; carbon monoxide-releasing molecules (reduced injury)1,2,3.
Repurposed clinical drugs & metabolic agents — dapagliflozin (reduced inflammatory infiltration)1; canagliflozin (improved heart function)1; lovastatin1; simvastatin (reduced infarct size 39%)1; atorvastatin (reduced infarct size)1; roxadustat (reduced infarct size and cell death)1; ciglitazone (reduced infarct size and inflammation)1; tert-butylhydroquinone (tBHQ)⬖ (reduced oxidative stress); compound C⬖; γ-secretase inhibitor⬖ (reduced oxidative stress); nifedipine and diltiazem⬖ (reduced inflammation and oxidative stress); pioglitazone⬖; NS398 / Ca-channel blockers⬖; sorafenib (toxicity model)⬖; probucol⬖ (reduced ferroptosis, a form of iron-driven cell death); allopurinol⬖; DMOG (HIF-1α activator)⬖; pioglitazone (PA/high-glucose)⬖; agent (equal-volume ip DMSO vehicle)⬖; netrin-1⬖ (reduced oxidative stress and cell death); ferrostatin-1 (reduced ferroptosis)1; 3-iodothyronamine (reduced infarct size)1.
Hormones — 17β-estradiol (reduced microvascular damage)1,2,3.
Cell-death & protease/lipoxygenase inhibitors — ilomastat (reduced infarct size)1; MI-2 (restored the cell’s ferroptosis defenses)1; necrosulfonamide (improved recovery after cardiac arrest by blocking programmed cell death)1; ML355 (improved heart function in pigs and monkeys)1; zVAD-FMK (reduced injury) 1.
Receptor, kinase & other targeted agents — MMI-0100 (cut the loss of heart function by half and halved scarring)1; MHBFC (reduced infarct size and inflammatory cytokines)1; ginkgetin (reduced infarct size and inflammation)1; IB-MECA (reduced infarct size by about 40% in dogs)1; 9-phenanthrol (reduced infarct size from 38% to 9%)1; LGK-974 (improved heart function 62% vs 41%)1; ticagrelor (reduced inflammation)1; MG132 1; L41 (reduced infarct size and spurred heart-muscle regrowth)1; SEW2871 (shifted immune cells toward healing)1; left-ventricular unloading1; HU-210 (reduced infarct size).1
While CPR can produce miracles, the reality is that it typically doesn’t (e.g., 10.5% of people with heart attacks resuscitated out of the hospital by EMS survive1 and 22-24% of those resuscitated in the hospital survive1). Because of this, I’ve put quite a bit of thought over the years into how this can be improved, and in parallel, we’ve collectively had quite a few cases where something we expected to work (e.g., a natural agent which improves circulation or eliminates clotting) did, including a few cases with DMSO. Given DMSO’s properties described above, I’ve hence repeatedly wondered if injecting DMSO during a cardiac code (CPR protocol) could have saved the person—but due to how unorthodox this was, this was understandably impossible to test. Likewise, while I know of cases where DMSO has been used to treat a heart attack, the reality of the situations around heart attack make giving it quite difficult, so I have much less experience with this than DMSO for strokes. As such, while I suspect it would be lifesaving, that is nothing more than a guess without adequate clinical experience to begin corroborating it and hence not something I can stand behind.
For that reason, I did not previously broach this, but nonetheless a few reader tried it anyways and reported success in stopping heart attacks,1,2,3,4,5,6,7 along with two who stated it healed complications of COVID vaccine induced heart attacks.1,2
Of these, the most interesting one that came from a woman who described her husband getting through what she characterized as a heart attack with a blockage and ischemia, using DMSO and aspirin at the onset and then frequent DMSO over the following days, and coming through it with no measurable heart damage and feeling nearly normal a week later.1 Notably, she independently described the same three-stage structure this section lays out: an initial circulatory phase, in which she believed the DMSO and aspirin opened the blockage in the first minutes; then the oxidative-stress phase of the first few days, in which frequent DMSO was aimed at preserving the heart tissue that reperfusion would otherwise damage; and finally the fibrosis phase from roughly days three to seven, each of which she noted, called for a different approach.1
Note: one reader also reported DMSO helping angina,1,2 and another concerning chest pain.1
DMSO also limits the death and scarring of heart muscle. In rats given isoproterenol (a standard chemical model of infarct-like injury), DMSO reduced fiber necrosis, prevented ventricular aneurysm formation and cardiac rupture, and left a smaller residual area of fibrosis,1 an effect confirmed in a second isoproterenol study,1 in further work showing reduced oxidative stress after isoprenaline,1 and in dedicated work on DMSO and experimental myocardial necrosis.1 Finally, DMSO reduced the several-fold rise in creatine kinase, LDH, and α-hydroxybutyrate dehydrogenase and reduced histologic damage after isoprenaline.1
In a D-galactose accelerated-aging model, subcutaneous 4% DMSO lowered TGF-β1, normalized cardiomyocyte diameter, and reduced fibrotic area to near-control levels, an anti-fibrotic effect the authors attributed to DMSO itself.1 In a series of studies on copper deficiency (which drives cardiac hypertrophy), chronically administered DMSO inhibited the hypertrophy, anemia, and heart-copper depletion via hydroxyl-radical scavenging, attenuated the rise in heart weight and water content, and preserved mitochondrial and myofibrillar ultrastructure.1,2,3 Consistent with a radical-mediated mechanism, DMSO also reversed the copper-induced impairment of force generation, calcium handling, and myosin-ATPase activity in cardiac muscle1,2
Note: DMSO also protected older rat hearts from the stress caused by prolonged immobility and from dietary copper deficiencies.1,2,3,4,5
In the fibrosis and remodeling literature, the same anti-fibrotic or anti-hypertrophic effects was seen with many agents delivered in DMSO.
•Natural agents — curcumin⬖ (raised antioxidant defenses and reduced heart-muscle damage); curcumin⬖ (protected against heart-muscle damage); genistein⬖ (reduced hypertrophy, oxidative stress, and inflammation); atractylenolide III⬖ (reduced post-heart-attack scarring); gCTRP9⬖ (protected injured heart cells); RGS6 with DPI⬖ (reduced remodeling); CRIF1 with NAC⬖ (protected injured heart cells); Maresin 1⬖ (protected heart cells); andrographolide⬖ (reduced hypertrophy and scarring); baicalein⬖ (reduced heart-muscle damage, scarring, and inflammation); β-carotene⬖ (reduced inflammation and scarring); resveratrol⬖ (reduced fibroblast overgrowth); tanshinone IIA⬖ (reduced hypertrophy); asiaticoside⬖ (reduced hypertrophy); salvianolic acid B⬖ (improved heart function); anacardic acid⬖ (blocked hypertrophy); colchicine⬖ (reduced fibrosis); nimbolide⬖ (reduced fibrosis in diabetic hearts); Buyang Huanwu Decoction⬖ (reduced post-heart-attack cell death).
•Pharmaceutical & synthetic agents — valsartan (reversed chemotherapy-induced remodeling)1; a JNK inhibitor (reduced fibrosis)1; a LOXL2 inhibitor (reduced fibrosis and hypertrophy)1; an EZH2 inhibitor (reduced fibrotic proteins)1; a GCN5 inhibitor (reduced hypertrophy and fibrosis)1; salubrinal (improved function in heart failure)1; rapamycin (improved pressure-overload hypertrophy)1; a Pannexin1 inhibitor (reduced hypertrophy and fibroblast activation)1; an H2S donor (reduced remodeling and blood pressure)1; dasatinib (reduced fat buildup and fibrosis in diabetic hearts)1.
In 42 severely ill patients with septic complications of post-resuscitation disease, intravenous DMSO was an effective therapy, including in cases where the sepsis arose from antibiotic-resistant bacteria.1
Additionally, DMSO has been used with a wide variety of agents to protect chemically injured, septic, and metabolically stressed hearts where it frequently reduced cardiac enzymes, oxidative stress, inflammation, and apoptosis:
•Chemotherapy cardiotoxicity — Cissus verticillata⬖; Irvingia gabonensis extracts⬖ (reduced heart-injury markers); ursolic acid⬖1,2 (improved heart function and reduced cell death); silibinin⬖ (promoted protective autophagy); necrosulfonamide (restored antioxidant enzymes)1; necrostatin-1 (reduced heart-injury markers and inflammation)1; a PARP inhibitor (reversed apoptosis and remodeling)1; azilsartan (reduced oxidative stress and cell death)1,2; selenium⬖ (reduced inflammation and cell death); avenanthramide-C⬖ (reduced oxidative stress and inflammation); rutin⬖ (raised antioxidant defenses and reduced inflammation).
•Sepsis-induced cardiac injury — Trimetazidine⬖ (protected against sepsis heart injury); D3T⬖ (raised antioxidant defenses); a pancreatitis-ascitic-fluid injury model (DMSO solvent control); paeoniflorin⬖ (reduced vascular leakage and inflammation); astragaloside IV⬖ (reduced oxidative stress and inflammation); astaxanthin⬖ (reduced injury signaling); curcumin⬖ (reduced heart-injury markers); luteolin⬖ (enhanced protective autophagy); sulforaphane⬖ (reduced inflammation); xanthohumol⬖ (reduced inflammation and cell death); octreotide (reduced inflammation and raised antioxidant defenses)1; simvastatin (reduced heart-injury markers and inflammation)1.
•Diabetic cardiomyopathy — GLP-1 drugs⬖ (reduced oxidative stress in heart blood vessels); tadalafil (protected mitochondria)1; rapamycin (reduced oxidative stress)1,2; ferrostatin-1 (reversed ferroptosis, a form of iron-driven cell death)1; honokiol⬖ (reduced high-glucose fibrosis); resveratrol⬖ (reduced inflammation); EGCG⬖ (restored cell-to-cell coupling).
In pulmonary hypertension and pulmonary embolism, where the right heart is strained by elevated pressures, DMSO delivered agents benefited right-ventricular function and pulmonary vascular remodeling:
•Myocarditis — A proteasome inhibitor (reduced inflammation and apoptosis);1 an α7-nicotinic agonist,1,2 (reduced inflammation and cell death); carbon monoxide-releasing molecules (reduced mortality and heart injury);1 a 3C protease inhibitor (antiviral protection);1 an androgen-receptor inhibitor (reduced inflammation and enhanced autophagy);1 a tyrphostin (reduced inflammation).1
•Arrhythmias — A calpain inhibitor (reduced atrial-fibrillation incidence); mexiletine (shortened repolarization in long-QT models); fisetin⬖ (reduced atrial inflammation and fibrosis after heart attack); valsartan or an ERK inhibitor (reduced atrial fibrosis and remodeling).
•Pulmonary Hypertension (which also damages the heart)—Curcumin⬖1,2 (reduced platelet activation and heart-injury markers); resveratrol⬖ (reduced inflammation and heart strain); isoliquiritigenin⬖ (reduced right-heart pressure and oxidative stress); icariin⬖ (reduced inflammation); a fission inhibitor with 17β-estradiol (reduced right-heart enlargement and shifted immune cells toward healing); a TRAF6 inhibitor (improved right-heart function); a Pannexin-1 inhibitor (improved pulmonary artery flow).
Several of DMSO’s standalone cardiac actions cut across all of the above. DMSO is a direct vasomotor agent, producing endothelium-independent relaxation of coronary and pulmonary arteries1. As a hydroxyl-radical scavenger it also attenuated tempol-induced falls in blood pressure, heart rate, and sympathetic nerve activity1. As discussed earlier, DMSO also protects coronary endothelium-dependent relaxation against oxidative injury, inhibits platelet aggregation, and suppresses tissue-factor expression and arterial thrombus formation—vascular protections equally relevant to the heart. A DMSO–aspirin preparation was likewise reported to reduce erythrocyte aggregation, normalize fibrin formation, lower peripheral vascular resistance, and improve microcirculation1. In the vehicle-delivered atherosclerosis and vascular-injury literature the same effects recur, with cinnamaldehyde⬖1 cutting serum lipids and raising heart antioxidant enzymes in atherosclerotic rats, hesperetin⬖1 limiting diesel-exhaust cardiovascular oxidative damage, and kolaviron⬖1 attenuating angiotensin-II/LPS-driven vascular smooth-muscle proliferation.
On the muscle itself it exerts direct, concentration-dependent effects on contractility, rate, and electrophysiology1,2,3: at low doses positive inotropy1—a moderate increase at 3% becoming marked at 6%1—while potentiating the inotropic response to isoprenaline1; still higher concentrations reversibly depress contractility1 or produce a mild hyperpolarization that prolongs the action potential1. These effects are independent of beta-adrenergic receptors1 and typically do not alter cardiac rhythm1, though the rate response is dose-dependent: 1–3% DMSO slightly raised heart rate while 6–10% markedly slowed it, an effect reversed by atropine1 and thus mediated through cholinesterase inhibition.
Note: DMSO and colchicine were found to increase myocardial work output.1
DMSO increased cardiac output during hypoxia1 and, given IV to dogs, raised cardiac output, stroke volume, and central venous pressure1. DMSO further protects cardiac t-tubules from stress-induced sealing1. On the parasympathetic side it inhibits cardiac acetylcholinesterase, lowering the vagal threshold and potentiating acetylcholine’s slowing of the heart rate.1
As discussed earlier, DMSO’s radical scavenging protects cardiac calcium handling, the sodium-potassium pump, and heart-muscle contractility against iron- and peroxide-driven injury making antioxidant protection equally relevant here. Beyond those, in cell-free and isolated-heart systems DMSO acts as a direct radical scavenger on its own: it neutralized electrolytically generated oxygen radicals in an enzyme-free buffer1, protected rabbit hearts against radical-driven rises in coronary and end-diastolic pressure and albumin leakage1, raised coronary release of protective uric acid in guinea-pig hearts1, and served as the reactive-oxygen scavenger confirming the antioxidant basis of protection against ischemia-reperfusion injury1. It also limits stress-induced lipid peroxidation in the myocardium1 (most pronounced in aged hearts), and in H9c2 cardiomyocytes it upregulates heme oxygenase-1 via p38 MAPK and Nrf2 to protect against hydrogen-peroxide injury1.
DMSO has long been used to turn cancer cells back into normal cells and to steer stem cells into the cell types the body needs — a way to replace and repair damaged tissue, including the nervous system. A large body of work shows the same thing for the heart: DMSO alone reliably drives stem cells to become cardiomyocytes.
When stem cells are exposed to DMSO alone they are most often reported to become heart tissue, which points to a real role for DMSO in cardiac stem-cell protocols.
A very large literature has since used DMSO as a cardiomyocyte-differentiation inducer across many starting cell types, with the same result recurring: exposure to DMSO (typically 0.5 to 1 percent) drove the cells to switch on cardiac genes and structural muscle proteins and, in most reports, to form spontaneously beating cardiomyocytes.
By far the most studied model is the P19 (and P19CL6) embryonal carcinoma line, in which DMSO alone reliably produced beating cardiomyocytes and became the standard system for dissecting how it works.t1,2,3,4,5,6,7,8,9,10, 11,12,13,14,15,16,17,18,19,20, 21,22,23,24,25,26,27,28,29,30, 31,32,33,34,35,36,37,38,39,40, 41,42,43,44,45,46,47,48,49,50, 51,52,53,54,55,56,57,58,59,60, 61,62,63,64,65,66,67,68,69,70, 71,72,73,74,75,76,77,78,79,80, 81.
The effect shows up across source cell type after source cell type. DMSO alone has turned bone-marrow mesenchymal stem cells,2 into myocardial cells, adipose-derived stem cells into cardiomyoblast-like cells, and fetal liver stem cells into cardiomyocyte-like cells. It has also driven fetal cardiomyocytes to proliferate and boosted the direct reprogramming of fibroblasts into cardiomyocytes roughly five-fold.
The same DMSO-driven differentiation has been reported across species and stem-cell source: in goat embryonic stem cells, mouse embryonic stem cells1,2,3,4,5, human embryonic stem cells1,2,3,4,5, human bone-marrow stem cells, cardiac progenitor cells, and mouse embryonic fibroblasts.
Lastly, the same differentiation was also achieved when DMSO was combined with many other agents including 5-azacytidine, a cocktail of growth factors including BMP and FGF, retinoic acid with 5-azacytidine, oxytocin (which worked synergistically with DMSO) and many others.1,2
Note: the effect is again concentration-dependent. At high concentration the picture reverses: a brief exposure to 10 percent DMSO disrupted muscle fibers and suppressed proliferation in cultured heart and cardiac endothelial cells,1,2
DMSO endothelial protective effects also allow it to prevent atherosclerosis itself. In rabbits fed a cholesterol-overloaded diet, oral DMSO reduced the resulting atherosclerosis by 30—40% and halved the cholesterol accumulating in the tissue.1 Beyond limiting the damage, it also supported the vasculature’s ability to rebuild itself, as DMSO promoted the differentiation of human embryonic stem cells into endothelial, cardiac, and blood-cell precursors—the early cells the body draws upon to build new vessels and blood.1
Finally, a series of studies in the cells lining human umbilical veins (a standard laboratory stand-in for the vessel wall) point to a protective and anti-inflammatory action there. Pretreatment with 2.5% DMSO reduced the neutrophil adhesion TNF-α normally triggers, which is one of the first steps of vascular inflammation and the initiating event in atherosclerosis.1 In nutrient-starved cells it blocked programmed cell death by promoting DNA replication and enhancing survival,1 and under oxidative stress it raised heme oxygenase-1 and reduced apoptosis through several anti-inflammatory and cytoprotective pathways.1
As DMSO is a mild vasodilator which simultaneously increases parasympathetic tone and scavenges the radicals that stiffen and constrict vessels, there is a mechanistic basis for it reducing blood pressure. However, the direct evidence is quite limited and most of what exists is indirect.
For example, DMSO is used as a transdermal penetration enhancer for conventional antihypertensives such as diltiazem and labetalol, where it improves both how much of the drug crosses the skin and how far the pressure falls in hypertensive animals.1,2 More importantly, it protects the vessels hypertension damages rather than merely the number on the cuff, as in rats made hypertensive with angiotensin II, DMSO reduced vascular hyperpermeability, smooth-muscle necrosis, and fibrin deposition in the small arteries by scavenging free radicals1—guarding the vessel wall even in cases where it did not move the pressure at all.
Note: as I’ve shown throughout the series, the primary value of DMSO for cardiovascular disease is its ability to protect the tissue rather than meet a numerical blood pressure threshold (which is often not even healthy).
DMSO is not, however, a blood pressure drug in the way an ACE inhibitor is, and as with every other system, its effect is concentration dependent. At the low solvent-level doses used in most research it is close to neutral, as DMSO-alone control groups repeatedly show no meaningful change in mean arterial pressure.1,2 Any lowering emerges only at the higher therapeutic concentrations where the vasodilation becomes pronounced, and at the far end of the range the direction reverses entirely—the same counter-current already seen when DMSO scavenged enough nitric oxide to nudge blood pressure up in horses. The clearest illustration of this is what happens when stem cell grafts cryopreserved in concentrated (10%) DMSO are infused rapidly, which produces a transient rise in blood pressure proportional to the DMSO dose1—the same high-concentration ceiling described in the safety section above. In short, DMSO is a mild and dose-dependent vasodilator whose most consistent contribution in hypertension is protecting the blood vessels rather than driving down the number on the cuff.
Readers, in turn, have described exactly what the mechanism predicts, and frequently stumbled upon it by accident. One woman had been applying DMSO to her husband’s belly at night for a pulled muscle when a checkup found his blood pressure had normalized; months of magnesium and potassium had only brought him to 150/90, but he now read 125/80.1
The pattern which recurs the most however is a rapid drop following a single oral dose. A 73-year-old found half a teaspoon in water took him from a usual 148/90 to 109/70 within thirty minutes, which he described as “way better than the meds I used to take.”1 Another, who had been pushed up to 40 mg of lisinopril and was applying DMSO over his carotids, watched a pre-DMSO 159/95 fall to 106/75 on the first reading afterwards.1 Others reported oral DMSO doing “more for my general inflammation and BP than aspirin or these days BP meds,”1 blood pressure finally dropping after years of unsuccessful diet, exercise, and weight changes,1 and a more modest shift from 160/90 to 150/80 which arrived alongside easier urination and sharper vision.1
Consistent with this being vasodilation rather than something else, a few readers instead noticed it as mild low-pressure symptoms when they used DMSO aggressively, one describing feeling “rather unsteady” with unusually flat and invisible hand veins during heavy use1 (which the German DMSO community believes accounts for why some people get temporary headaches from significant DMSO use). In others it was simply folded into a much broader recovery, such as the reader treating a vaccine injury with oral DMSO who listed normalized blood pressure among a long list of improvements,1 and another who found his blood pressure and cholesterol returned to normal once DMSO allowed him to discontinue Humira.1
Given all of this, I would expect DMSO to help certain kinds of blood pressure but not others (as many different things can cause the elevation). That said, blood pressure is not always a thing you want to treat (sometimes it being elevated is helpful)—although in the cases where it’s helpful to be elevated (to maintain perfusion through aging arteries), DMSO would likely at least somewhat bridge the gap due to its ability to promote circulation.
Note: because a few of these drops were both large and rapid, anyone already on blood pressure medication should monitor their pressure when starting DMSO rather than assume the two simply stack, as the reader above who was on 40 mg of lisinopril illustrates how quickly the combination can move things.
In addition to protecting tissues from death, DMSO is remarkably effective at removing excess fluid from outside the bloodstream, increasing circulation, and clearing circulatory obstructions such as clots, along with many other conditions which result from impaired circulation (and microcirculation).
Note: numerous observations of the years have led me to believe blood congestion is a primary cause of many ailments including varicose veins and hemorrhoids.
The pioneering DMSO researchers documented this early. Stanley Jacob found1 that half of Raynaud’s patients had their symptoms eliminated and that thrombophlebitis responded excellently, while two investigators using plethysmography demonstrated objective improvement1 in peripheral-artery insufficiency in a large number of patients given topical DMSO. DMSO was also shown to relieve diabetic circulatory problems including peripheral neuropathy1 and diabetic ulcers, where one study1 of hundreds of patients reported over a 94% success rate — and to help prevent future amputations (data which has since been extensively corroborated).
The early clinical series were substantial. A study of 67 patients with varicose ulcers1 (39 women, 28 men) found a remarkable response even in chronic ulcers that had been present for years and had failed other treatments. Likewise a larger early1 study found:
DMSO’s vasodilatory action has long been invoked for frostbite, diabetic ulcers, and varicose ulcers1, and over a hundred studies have since corroborated these results.
Venous disease and varicose veins. The most consistent modern use is topical, much of it centered on Dolobene — a gel of DMSO, heparin, and dexpanthenol in which DMSO both carries the heparin through the skin and adds its own analgesic and anti-inflammatory action. Dolobene has been evaluated across the venous disorders1, used specifically for varicose vein disease1, and ranked by vascular surgeons and pharmacists among the priority topical agents for varicose veins1.2,3,4,5 An early double-blind study of 55 patients1 tested topical DMSO for chronic venous insufficiency, and a 1975 New York Academy of Sciences report1 documented its use across venous stasis, dermatosclerosis, and lymphedema. It recurs throughout the topical treatment of chronic venous insufficiency and post-thrombophlebitic disease1 and appears in the formulation literature for antivaricose gels1 and horse-chestnut/aescin preparations1 as the penetration enhancer of choice.1 This indicates DMSO may also play a wall-strengthening role (e.g., in a mouse model of venous hypertension1 that reproduces varicose remodeling, agents delivered transdermally in DMSO prevented the pathological changes in vein structure and smooth muscle that drive the disease).
Thrombophlebitis, superficial venous thrombosis and hematomas. DMSO-based gels are commonly used here. A randomized, double-blind trial of a Phlebolan spray1 and related studies1,2,3 support topical DMSO-heparin (and the topical DMSO heparin gel Dolobene) for superficial thrombophlebitis.1 Likewise Dolobene recurs as a standard thrombophlebitis and thrombosis therapy throughout the literature, including for combined deep and saphenous-vein thrombosis.1,2,3 DMSO (alone) gels have also been used to treat acute thrombophlebitis1, superficial-vein thrombosis1, and chemotherapy-induced phlebitis.1,2,3 Electrophoretic DMSO has also resolved intramuscular-injection hematomas in hemophilic children, clearing the bruising well enough to let their therapy continue.1
Venous, trophic, and diabetic ulcers. DMSO’s ulcer record (e.g., the greater than 94% success rate and the 67-patient varicose-ulcer series above) are highlighted in many papers discussing the use of large DMSO containing wound-dressing for venous trophic ulcers and lipodermatosclerosis1, chronic trophic leg ulcers1, post-thrombophlebitic trophic ulcers1, venous ulcers and chronic venous insufficiency (in one study a DMSO powder healed 95% of patients at 3 months versus 70% on placebo),1,2 and trophic ulcers of atherosclerotic origin (with a DMSO powder)1. In 58 patients with chronic purulent wounds from vascular disease or diabetic angiopathy, negative-pressure instillation of 20% DMSO produced faster cleansing, near-complete granulation in 76% by the first dressing change, and healing 1.5–3× faster than standard care.1,2 The diabetic-foot thread is distinct: in 80 diabetic patients with lower-extremity ulcers, DMSO dressings combined with an oxygen-carrying perfluorocarbon cut mean healing time to 17 days versus 47 for standard care, with faster bacterial clearance and a better microcirculatory index by day 22.1 DMSO is also used as an antiseptic and penetration enhancer in diabetic-foot and gangrenous-wound protocols1, in diabetic wound management with documented perfusion improvement1, for necrobiosis lipoidica and other diabetic skin conditions1, and as the vehicle in experimental diabetic-wound and angiogenesis models.1
Scleroderma and Raynaud’s. In addition to the 50% Raynaud’s symptom-elimination figure from the original DMSO literature, DMSO is a standard component of scleroderma care specifically for its microcirculatory action. DMSO with nicotinic acid⬖ has been used to treat systemic scleroderma,1 and topical DMSO (often paired with heparin) is mentioned as a treatment throughout the scleroderma treatment literature1, including pediatric localized scleroderma1, explicitly to improve microcirculation and soften dermatosclerosis.1,2,3,4,5,6,7,8 (where in one study, blood flow was increased 20% by DMSO and 500% by DMSO with nicotinic acid⬖1). It also appears in systemic lupus with acrocyanosis and Raynaud-type lesions1, in vasculitis1 with cutaneous circulatory involvement, and as the vehicle for vasoactive agents in scleroderma1.2Note: many more scleroderma studies are discussed here.
Tissue perfusion, flap and graft survival. The most objective experimental evidence that DMSO raises tissue blood flow comes from surgical flap models, where perfusion decides whether ischemic tissue lives. In 48 rats with abdominal island flaps1, systemic DMSO significantly increased perfusion (by laser Doppler and perfusion fluorometry) and improved flap survival. In ischemic dorsal skin flaps1, 5% DMSO reduced distal necrosis and produced greater neovascularization and earlier repair. The benefit recurs across independent models such as pedicle-flap necrosis1,2,3,4 composite and vascular allografts1, or nipple-areolar and penile tissue salvage1.2 The same perfusion gain runs through a large wound-healing literature, where DMSO (alone or as carrier) increases skin blood flow1, normalizes capillary permeability and microcirculation1, improves isolated-organ perfusion1, and accelerates granulation and revascularization in trophic ulcers, burns, and other wounds.1,2,3Note: many additional DMSO skin flap studies can be read here.
Surgery. In addition to protecting skin flaps (a common challenge in plastic surgery), DMSO also addresses many other challenges. In breast reconstruction, applying topical 60% DMSO before each tissue-expansion session cut expansion time by roughly a third, allowed greater volume per session, and reduced pain1, across two clinical series.1 Topical DMSO salvaged (saved) an ischemic nipple-areola complex1 after reduction mammoplasty by restoring perfusion, and as a trauma wound dressing used in nearly ten thousand cases it dilated capillaries and improved microcirculation1. Finally, in 154 patients undergoing surgery to restore blood flow to an acutely ischemic leg, intravenous DMSO added before reperfusion reduced markers of reperfusion injury1 ( lower peak lactate, faster normalization, fewer cases of kidney and cardiopulmonary dysfunction) though amputation and mortality were unchanged.
Hemorrhoids and frostbite. DMSO is used in topical mixtures for acute thrombosed hemorrhoids1 and hemorrhoidal thrombosis1, in a placebo-controlled trial of an MSM⬖-containing gel1 (MSM being DMSO’s oxidized metabolite), and in anorectal wound healing after hemorrhoid surgery1.2,3 For frostbite, a peripheral cold-ischemic injury, DMSO appears in the treatment guidelines for local cold trauma1, in military cold-injury research1, and as a carrier delivering heparin into cold-injured tissue1.2,3,4,5Note: Stanley Jacob (the pioneer of DMSO) treated hemorrhoids with DMSO,1 other DMSO authors have advocated for using DMSO to treat them, and Merck (in their early clinical trials) reported that it improved recovery after their surgical removal.1
Arterial and ischemic limb disease. The arterial side is thinner than the venous but present: DMSO has been used adjunctively for arterial disease of the extremities1, for chronic purulent wounds from advanced peripheral arterial occlusive disease1, with hyaluronidase for ischemic limb edema1, and for vaso-occlusive hand-foot crises1 where Dolobene relieved pain and edema. It also improved facial arterial blood flow after surgery1.
Veterinary peripheral circulation. In veterinary medicine, where DMSO is a mainstream drug, it is used for equine laminitis to improve digital perfusion1, distal-limb edema1, and aorto-iliac thrombosis1, in regional limb perfusion1 and tendinitis1, for bovine hoof and teat lesions1, and as anti-endotoxemic support in colic and peritonitis1 where circulatory collapse is the threat.1,2
DMSO also completely abolished toxin-induced constriction of lymphatic microvessels1, protecting lymphatic as well as blood-vessel tone.
Many agents have also been combined with DMSO to topically treat the same conditions DMSO alone also treats.
Many agents combined with DMSO, like DMSO alone, speed cleansing, granulation, and closure of venous, trophic, diabetic, and traumatic wounds:
•Antiseptics & antibiotics (topical wound care) — furacillin + sensitivity-selected antibiotics (25% DMSO cleared monoflora by day 5–6 and healed varicose/post-thrombophlebitic ulcers in 16 days, 2.2x faster with phototherapy)1; chlorhexidine (multimodal venous trophic-ulcer regimen; remission in 80–95% of 152 cases)1; bactosin + sulbactam (DMSO antiseptic irrigation of contaminated vascular-trauma wounds; fewer thromboses, infections, amputations),1 photoditazine plus photodynamic therapy (gunshot wound treatment aiding cleansing and microcirculation)1,2.
•Anesthetics & anti-inflammatories (compounded dressings/ointments) — Anikol, a patented anilocaine ointment (~190-min surface anesthesia; infected wounds closed in 7 days, frostbite healed in 8)1; splenic preparation splenodimexide (anorectal wounds; complications cut >1.5x, faster granulation)1
•Free-radical scavengers & flavonoids (ulcer healing) — Quercetin⬖ (10% DMSO vehicle showed no independent effect while quercetin-in-DMSO drove angiogenesis and closure in diabetic wounds)1; loureirin A⬖ (promoted vascularization and wound healing via miR-339-5p/Wnt).1
DMSO is frequently combined with other anti-clotting agents:
•Natural compounds — curcumin⬖ (dose-dependently reduced platelet aggregation, CD63, GMP-140 in pulmonary embolism)1; berberine⬖ (prolonged mesenteric-artery occlusion time; reduced venous thrombosis and NET formation in colitis)1; senkyunolide I (reduced platelet activation and NET formation in sepsis).1
•Anticoagulants & other pharmaceuticals — rivaroxaban (suppressed leukocyte adhesion and microthrombus formation in diabetic microvasculature)1; aspirin (DMSO + aspirin stopped nocturnal leg cramps within a day)1. Nadroparin (15% DMSO carried this LMWH into tissue to prevent Nicolau syndrome skin necrosis after sclerotherapy)1; hydrocortisone (90% DMSO potentiated hydrocortisone ~10-fold and, alone, prolonged arteriolar flow-stop time and sped flow restoration after venous thrombosis)1; Procaine + heparin (corrected vascular tone and arterial-bed filling in chronic interstitial parotitis).1
•Signaling-pathway inhibitors (thrombosis mechanism) — PI3K inhibitor wortmannin (malnutrition-driven venous thrombosis)1; suberoylanilide hydroxamic acid(improved survival and clot quality in sepsis coagulopathy)1; Tubastatin A (HDAC6) (reduced renal microcirculatory thrombin and NET formation in sepsis).1
•Polyphenols & natural vasorelaxants — resveratrol⬖ (near-complete relaxation of human intrapulmonary arteries, partly NO-dependent)1; garlic diallyl trisulfide⬖ (endothelium-independent relaxation of intrarenal arteries, Emax >91%)1; tetrahydroxystilbene glucoside⬖ (mesenteric relaxation via COX-2/TXA2 and K+/Ca2+ channels)1; cannabidiol (potent inhibition of small-resistance-artery contraction, stronger in smaller vessels)1; resveratrol ⬖ + CAPE⬖ silibinin⬖ (concentration-dependent relaxation of human umbilical artery).1
Polyphenols & flavonoids — resveratrol⬖ (raised hypoxic endothelial viability and SIRT1/PGC-1α; lowered inflammatory IL-6, ICAM-1, ROS)1; resveratrol⬖ plus atorvastatin (synergistically enhanced bone marrow stem cell endothelial differentiation and stent re-endothelialization beyond either alone)1; kaempferol⬖ (protected islet microvessel endothelium from fatty-acid injury)1; astragaloside IV⬖ (improved aortic-endothelial viability, migration, tube formation under hypoxia).1
Endothelial-barrier disruption — ulinastatin (blocked endothelial hyperpermeability via p38)1; HSPA12B pathway inhibitors (preserved endothelial barrier function),1 thymoquinone⬖ (sepsis) (improved mesenteric-artery blood flow and aortic function,)1. resveratrol⬖ (cut sepsis leukocyte/platelet adhesion, improved survival),1 genipin⬖ (reduced LPS-induced vascular hyperpermeability via SIRT1).1
Neointimal Vascular Remodeling after Artery Injury — celastrol⬖ (restored contractile VSMC markers)1; ursolic acid⬖ (also reduced NF-κB/PCNA)1; YM2016361; a Pol I inhibitor;1 enalaprilat (DMSO alone demonstrated a modest reduction in remodeling).1
Since DMSO is easy to utilize for peripheral circulatory conditions, many readers have attempted it, and their testimonials mirror the successes for these conditions seen in the trials.
Varicose and spider veins. This is the single most common circulatory use readers describe, and the reports are strikingly consistent: repeated topical application (typically 70-100% DMSO,* often in aloe⬖ or castor oil,⬖ once or twice daily) shrinks, softens, fades, and in many cases eliminates the veins, frequently after they had been present for decades. One reader sprayed 100%* DMSO on varicose veins nightly and reported that “in 13 months they are entirely gone,”1 another in New Zealand treated badly “varicosed” saphenous veins roughly half a dozen times over a week and found the change (documented in before-and-after photos) durable: “I am fairly sure that the applications are not maintaining the varicose vein recovery-they are fixed.”1 A third watched veins that “stuck out about 1/2 inch” recede to “about 1/8 of an inch,”1 and one posted a 24-hour before-and-after showing a large varicosity essentially gone.1 Many more described veins that “just disappeared” along with the aching and end-of-day leg pain,1 that faded or shrank steadily with continued use1,2,3,4,5,6,7 that became “much smaller, softer” with the previous sensation of “thickness” gone1 or that improved only on the treated leg while the untreated leg served as an inadvertent control.1 A woman treating her elderly relative’s chronic venous insufficiency tracked it week by week—roughly 20% improvement in the first week, 50% by the second, 75% by the third.1 Several noted the veins returned when treatment stopped1 and a minority saw little or no effect,1,2 but the dominant pattern was steady improvement of veins that conventional medicine treats only by stripping or ablation.1,2,3,4,5,6These are some of the many pictures I’ve received:
Blood clots and DVT. Readers reported both topical and oral DMSO dissolving existing clots and preventing new ones, often as a deliberate replacement for prescribed anticoagulants. One who had been told to take Eliquis for life stopped it and switched entirely to oral DMSO to dissolve clots in the legs and lungs: “I’d be dead if DMSO didn’t work.”1 Another treated a bad DVT running from above the knee to the ankle with topical DMSO (plus lumbrokinase⬖ and serrapeptase⬖) and “dissolved the clot in 2.5 months,” declining the year of Eliquis doctors advised.1 A mother whose son had hip-bone necrosis from a clot lodged in a small twisted vein reported that after starting DMSO “within 3 days he was able to walk without pain,” and that the hip healed without the scheduled surgery.1 One reader whose arm had visible hardened clots from an IV reaction for months found “the clots were gone within three days” of applying DMSO gel,1 and another watched a large hard lump on a calf vein resolve until “it is gone now and the area soft.”1 Another described using DMSO to resolve a clot in an 89-year-old’s leg.1
Raynaud’s and cold extremities. For Raynaud’s, the reported effect is often nearly immediate. One reader who came in from shoveling snow put DMSO on the fingertips and was “instantly warm”;1 another applied it to the toes and it “changed the color of my toes back to normal.”1 A regular user reported applying it two or three times daily to her hands with “great success, no longer needing to wear fingerless gloves around the house...It has been life changing,”1 while another with cold hands happened to track the effect on a pulse oximeter and watched readings climb after each application.1 Others described relief of the spasms, discoloration, and stiffness,1,2,3 marked overall improvement in circulation alongside the Raynaud’s,1 and one reported that five consecutive days of DMSO “cured Chilblains and Raynaud’s for the entire winter season.”1 Several with autoimmune-associated Raynaud’s (lupus, scleroderma, rheumatoid disease) folded it into broader regimens with reported relief.1,2,3
Ischemic and discolored limbs. Many reported normal color and warmth to feet and legs that had gone blue, purple, or black from poor perfusion. A daughter treating her 85-year-old mother’s severe foot neuropathy (toes and ankles “a blackish blue color,” numb, with nightly cramping) described the results after three weeks as “amazing” “the normal color has returned to her feet and legs...she now has feeling back in both of her heels.”1 Another reader rubbing DMSO cream on the feet nightly found that “on the fourth morning I looked down at my feet and all the purple mottling was completely gone.”1 One person watched an elderly mother’s “blue-black toes...from frostbite” return “to a healthy pink—permanently” after a single application of DMSO with magnesium.1 An 84-year-old with a decades-old radiation wound near the bone that had never fully healed reported that once she applied DMSO gel, “the skin color has returned to normal and circulation is now almost normal, my foot does not swell from lack of circulation.”1 Many others described impaired circulation, cold feet, leg swelling, and perfusion-related pain improving with topical or oral use1,2,3,4,5,6 including a post-COVID reader whose cyanotic, “bluish purple” legs looked “a normal healthy colour...for the first time in 3 years.”1
Frostbite and cold injury. Frostbite is a peripheral cold-ischemic injury, and readers reported DMSO restoring warmth and color to affected tissue, often within hours, particularly when applied promptly. One who “burned” a hand with liquid refrigerant until “half of my hand went numb and changed color” applied DMSO and reported the hand “back to normal” two days later, with only a little surface skin peeling.1 A second described the same refrigerant injury (a hand “numb for 24 hours and changing color”) returning to normal in three days, adding that “immediate or even preemptive application is essential.”1 Another reported that on a “almost frost bite,” DMSO “restored warm asap.”1 These mirror the documented reports of frostbitten and blue-black toes regaining healthy color after DMSO.
Venous, diabetic, and pressure ulcers. DMSO’s reported effect on chronic wounds and ulcers is among the most consistent in this collection. A reader watched an elderly friend’s leg “a six inch diameter festering mess” that a year of medical treatment had failed to close, with surgeons wanting to cut “turn into clean skin” over a month of DMSO.1 A 12-year user reported that DMSO “saved a 75-year-old woman’s leg” doctors wanted to amputate: “she walks now despite being bedridden before.”1 Wives caring for diabetic husbands with chronic venous ulcers—one after a year of wound-care visits and twice-weekly home nursing—described the ulcers improving significantly within two weeks of switching to DMSO gel1 and not recurring afterward.1 A diabetic reader healed three foot ulcers with DMSO gel and pursued IV infusions to improve leg blood flow,1 and a man given DMSO cream by an acquaintance saw “a 2 inch ulcer” on his arm heal over “in a couple of weeks.”1 The same pattern appears with pressure sores: a family applied 80% DMSO to a bedbound 101-year-old’s bedsores and reported her skin “became normal in just a matter of days,”1 and a caregiver treating early Alzheimer’s incidentally cleared his wife’s “horrid bed sores,” leaving her “with no sores or irritated pink skin.”1 Others reported healing of diabetic leg ulcers, lupus-related skin ulcers, and assorted chronic sores, often in combination with iodine, silver, or chlorine dioxide.1,2,3,4,5,6
Hemorrhoids. Because a hemorrhoid is essentially a swollen, clotted vein, readers repeatedly found it responded to DMSO the way varicosities did—often within days (to the great surprise of skeptical readers).1 One applied “two drops of DMSO on a hemorrhoid I had for years” and reported that “after a single dose, it shrank to the size of a grain of sand.”1 Another reported that two friends “had their hemorrhoids vanish after a single subcutaneous thigh injection of .5ml of DMSO,” including one who had had them for 15 years.1 A reader whose doctor had diagnosed a hemorrhoid and written a prescription instead applied DMSO to the bulge and reported it “gone” after three days,1 and another who makes DMSO-cocoa butter suppositories reported they “heal and relieve hemorrhoids immediately...Prep H is useless.”1 Many more described hemorrhoids shrinking, clot release accelerating, and pain and itching resolving with topical gels, suppositories, or oral use, frequently after over-the-counter suppositories had failed.1,2,3,4,5,6,7,8,9,10,11
Lastly, readers describe a number of adjacent circulatory and lymphatic uses that don’t fit neatly under a single heading. DMSO was credited with improving lymphedema and restoring sensation in a diabetic reader’s legs and feet (from roughly 20% to 85% feeling),1 softening the “cord” of post-surgical axillary web syndrome until it “feels like a thin cotton string,”1 and relieving lymphatic congestion in the neck and shoulders.1 Two readers with pigmented purpuric dermatosis (capillaritis) reported the discoloration fading—one by “at least 50%” after months of oral DMSO following chemotherapy-induced capillaritis on both shins,1 another finding that DMSO “drains blood from purpura in my older skin within 3-4 days.”1 A reader with peripheral arterial disease found DMSO cream slightly eased claudication pain enough to resume treadmill walking,1 and a post-COVID reader reported it changing “the micro clotting and total arterial blockage” of a popliteal artery.1
When I began this series nearly two years ago, I stated at the start the evidence showed DMSO could save millions from neurological disability or death. Now that I have been able to present that evidence, it should be clear there is something real here, and a lot of the suffering that happens doesn’t need to. I cannot begin to describe how much I wish DMSO could become the standard of care for strokes, and it is for that reason that I have tried so hard with pieces like this to effectively make the case for that to happen.
At the same time however, another one of DMSO’s unique characteristics is that even if the medical system wants to maintain its narrow paradigm of how medicine must be practiced, DMSO can still be used by anyone who has taught themselves how to do so. This is critical, both because it means an option exists now that can be taken to avoid these devastating outcomes, but also because the one type of pressure medicine does respond to is external economic ones (e.g., individuals shifting enough of their medical spending to a superior alternative that medicine is motivated to provide a service that is good enough to recapture those customers). So, since DMSO can address so many both common and rare “incurable” ailments, it not only provides an immediate and tangible benefit to those who use it, but also, through doing so, provides the critical grass roots pressure for it to shift the entire medical system.
As such, in the remainder of this article, I will provide:
[Article continues behind The Midwestern Doctors paywall you can go to the Original Article: location and claim a free post to read the rest or sign up with the midwestern doctor on substack.]
Original Article: https://www.midwesterndoctor.com/p/dmso-heals-blood-vessels-and-could
These pages contain videos that focus on the truth. This page is focused on the Nepal flash flood mud slide. Notice the masonic signalling number 33 used in news reports. 33 Indians, 33 UK Nationals, 33 Missing Americans, Tourists from 33 countries...
Nepal Flash Flood Mud Slides Scripted? 33 Masonic Number Used Repeatedly
These pages contain videos that focus on the truth.
Add Lake America Onto This List
Reporter Asks Why Our Military Serves Israel First
"I witnessed the rituals they perform, drinking human blood, and if they had noticed me, they would have killed me." A few days after this statement, Princess Diana died in a strange and mysterious traffic accident. ~ Source: https://t.me/c/3233625802/173
~ Source: https://t.me/HBMW88/29492
The truth is told very well with images. A picture says a thousand words, and memes a few more. These pages have lots of images and memes that focus on the truth. Click image to enlarge + use arrows to navigate.
These pages contain videos that focus on the truth.
Trump Re-Names Lake Ontario, Lake America ~ Source: https://t.me/OrwellianDystopia/99905
~ Source: https://t.me/NoQuarterCorner/7437d
THE RECKONING BEGINS: Vaccine-Injured Canadians TAKE PARLIAMENT HILL For The ALLISON INQUIRY ~ Source: https://pressfortruth.ca/the-reckoning-begins-vaccine-injured-canadians-take-parliament-hill-for-the-allison-inquiry/
~ Source: https://t.me/OffTheGridOfficial/10891
The late ‘Illuminati’ Hollywood puppet, Dolly Parton, accompanied by Jenifer Aniston and Sandra Bullock — toasting the demon Azazel. ~ Source: https://t.me/c/3233625802/166
The truth is told very well with images. A picture says a thousand words, and memes a few more. These pages have lots of images and memes that focus on the truth. Click image to enlarge + use arrows to navigate.
Dylan Eleven | Truth11.com
With millions dead and injured from the Covid bioweapon 'vaccines'; Instead of banning them, the FDA approves more deadly injections. This shows a clear signal that they are still engaged in the genocide program. At what point will these people be stopped and held accountable?
Nicolas Hulscher, MPH | Focal Points | Courageous Discourse
FDA Approves New Pfizer and Moderna XFG mRNA COVID Shots Based on Data From Just 8–10 Mice.
The new formulations were approved before their human safety and immunogenicity studies even began.
The FDA has approved Pfizer and Moderna’s new 2026–2027 XFG-adapted mRNA COVID-19 vaccines even though the XFG-specific evidence publicly presented to regulators was preclinical animal data involving just 8–10 mice per group.
The reach of these dangerous approvals is sweeping: Pfizer can now be given to every American age 65 and older and to “high-risk” individuals as young as 5, while Moderna extends all the way down to “high-risk” infants just 6 months old.
The human safety and immunogenicity studies of the new formulations had not even begun when FDA granted approval.
Pfizer’s new COMIRNATY formulation was approved on August 27, 2026, while its prospective human study of the 2026–2027 formula is scheduled to begin August 31—four days later.
Moderna’s new SPIKEVAX formulation was also approved on August 27, but its Phase 3b/4 human study of the 2026–2027 SPIKEVAX and MNEXSPIKE formulations is not scheduled to begin until November 16—nearly three months after approval.
FDA’s own 2026 vaccine-selection materials distinguish between human data from earlier/current COVID vaccines and animal immunogenicity data for the new candidate vaccines.
Pfizer’s FDA presentation shows the XFG candidate was tested in 10 mice per group.
Moderna’s FDA presentation shows its key XFG experiment used 8 mice per group.
The approval letters reveal another troubling development: FDA also released both manufacturers from previously required placebo-controlled postmarketing studies, citing operational and feasibility problems. Pfizer’s abandoned study would have investigated circulating spike antigen and post-vaccination symptoms, while Moderna’s would have evaluated safety of variant-containing formulations.
Rather than requiring new human data before approval, FDA relied in part on human safety and immunogenicity data from previous COVID-19 vaccine formulations and extrapolated that evidence to the newly updated XFG products, while the XFG-specific evidence itself remained preclinical.
This reliance on older-formulation data is especially concerning given the millions of deaths, injuries, and disabilities, along with demonstrated cardiotoxicity, neurotoxicity, carcinogenicity, body-wide biodistribution, and years-long persistence.
This is extremely worrisome and needs to be reversed immediately.
Source: https://www.thefocalpoints.com/p/breaking-fda-approves-new-pfizer
Original Article: Truth Warrior Suggested
Exposing The Darkness by Lioness of Judah Ministry | lionessofjudah.substack.com
Greg Hunter | USAWatchdog.com
Dr. Joe Sansone is a Florida psychotherapist and has been one of the only people to sue to take the CV19 bioweapon vax off the market in his state.
He lost his case despite the fact the CV19 injections have been proven to cause heart disease, autoimmune problems, blood clotting and so-called “turbo-cancers” that are still popping up everywhere. The latest data from the Bureau of Labor Statistics (BLS) shows “US Disabilities Hit an All-Time High of 37 Million In July: UP 23% Since Feb 2021.”
Since early 2021, CV19 bioweapon injections caused an additional 7 million people to be permanently disabled, and millions have been killed globally. No matter how high the death and injury numbers get, Sansone still contends the “World is Ignoring Disaster of CV19 Bioweapon Vax.” How can this be? Dr. Sansone lays out his case in a new book showing a world run by“Psychopathic Authoritarianism.” This is not a fluke or an accident. Dr. Sansone says, “On a systemic level, I call it “Psychopathic Authoritarianism,” and we are seeing that across the country. With the CV19 shots, the bottom line is these mRNA injections are biological and technological weapons of mass destruction.
The people that deployed this know this. In my case in Florida, the late Dr. Francis Boyle, who gave an affidavit for my case (Boyle wrote the 1989 Bio-Weapons Act), publicly stated the Covid injections were, in fact, offensive biowarfare weapons based on the law he wrote. . .. What we are seeing is true unadulterated evil. That is really what my book is all about. In order to defeat these people, you need to know who you are fighting against. These are not normal people who are running the world right now.”
Dr. Sansone says, “The bottom line is most people that we know will have a shortened life span from these injections. Now, I am not saying they are going to die tomorrow, but if you give me a chronic disease or illness . . . I am not going to live as long as I would without it. If that is not going to wake people up, I don’t know what will. “Psychopathic Authoritarianism” is a systemic level disease of the society as a whole.”
Singer Dolly Parton just passed away, reportedly after a “brief cancer battle.” Parton funded research for the CV19 vax. She got a shot on camera and adapted one of her songs to sing to encourage people to get their CV19 vax. She changed the name in her hit song “Jolene” to “Vaccine.” While she was doing this in 2021, CV19 vax deaths and injuries were already piling up and being covered up by the CDC and FDA.
Parton had what appears to be some sort of turbo cancer that is common after taking the CV19 vax. Was Parton killed by the CV19 injections? We will probably never know. Dr. Sansone says, “Honestly, Dolly Parton was exploited. I think she died due to the CV19 shots. I don’t know that for a fact, but that seems reasonable to assume. I seriously doubt that Dolly Parton would have wanted to injure anybody.
The idea putting these celebrities out there promoting these injections is totally unethical. . .. You have to understand, these people are sadistic. They get off in causing pain in others and humiliating other people. They have fun doing this. They are getting off on giving people chronic diseases and illnesses. Exploiting Dolly Parton and giving her poison while she is promoting poison . . . that’s sadistic. That is evil behavior. I think it is all done on purpose.”
There is more in the 31-miniute interview.
Join Greg Hunter of USAWatchdog as he goes one-on-one with Dr. Joe Sansone, as he highlights his new book called“Psychopathic Authoritarianism,” and talks about the systemic evil in our world, and what you need to know about it for 8.26.26.
Source: https://usawatchdog.com/cv19-bioweapon-vax-is-psychopathic-authoritarianism-dr-joe-sansone/
Image: Source [Edited]
Original Article: https://lionessofjudah.substack.com/p/dr-joe-sansone-cv19-bioweapon-vax
Related:
TapNewsWire.com | Pete Fairhurst
Lionel Mandrake | Worldlyturnings | 1yfgk.substack.com
(Dollyland Media) Singer Dolly Parton just passed away, reportedly after a“brief (turbo) cancer battle.”
Dolly Parton didn’t just jab in public. She helped funded mRNA research at Vanderbilt University to help create the CV19 Vax that has killed and maimed millions.
Did they really need her money? Of course not. What they needed was someone to get on camera who had millions of fans who that would do anything she said. They are devious Satanic bastards that play on our souls though our pride.
They succeeded and Dolly paid the ultimate price.
They got her to get the shot she helped produce on camera. They even got her to adapt one of her songs to encourage people to get their CV19 Vax. She changed the name in her hit song “Jolene” to “Vaccine.”
While she was doing this in 2021, CV19 Vax deaths and injuries were already piling up and being covered up by the CDC and FDA. She should have known, but her myopic world was already thinned out in 2021 to declare any negative information about the Vax “misinformation”.
But, Truth is like a Lion and there was enough data out there to tell anybody with a brain that something was amiss. Over the years since she convinced many people to Jab, the massively strong evidence against the Jab surfaced against the tide. That evidence apparently never reached her eyes and ears.
I have no hatred for anyone, let alone someone like Parton who did a lot of great things to help people over her lifetime. On balance, that doesn’t tip the scales for me. So, how can we lionize Dolly Parton when she likely passed on the fate she suffered through at the end to so many of her adoring fans that followed her ignorant lead? My left wing local R&R radio station has been playing her music ALL DAY.
Nice lady. Good heart, good motives and jugs. But, no brain.
As she was dying from what we now call Vax induced “turbo cancer”, she made a statement to her nephew. Nowhere in her last, dying words was there any sense of humility about how she might have been wrong about the Jab and especially her financing of the project. No regrets at all? Were you really that brainwashed?
This makes her not just an innocent victim but an active player, even indirectly. In my view, that is hard to forgive, except by Him.
After the last 5 years, I have discovered how painfully hard it is for people to admit to either taking the Jab to begin with or (worse) inducing others to do so as opinion leaders in media, government, medical and education professions.
Vaccine, Vaccine sung to Jolene, Jolene and based on the hit Two Doors Down:
Two more jabs, were laughing and drinkin’ and having a party
And, two jabs more, and we’ll soon be not around.
Actual lyrics here….no conspiracy.
Dolly Parton’s ego and pride to “help the world” may have caused her fall. There are so many out there like Dolly, aren’t there?
And, as a Christian, she should have known about Satan’s trap.
May she rest in peace.
Sic Semper Tyrannis
Source: https://www.theburningplatform.com/2026/08/26/dollyland/#more-425318
Original Article: https://tapnewswire.com/2026/08/27/dollyland/
Part 1 of 2: How governments turn everyday metadata into surveillance kill chains.
Etienne de la Boetie | substack.com/@artofliberty
Sterlin Lujan | Advocates for Self-Government | theadvocates.org
In 2014, former NSA and CIA director Michael Hayden uttered these words with a straight face. He was not being apologetic but rather bragging about his agency’s capabilities. His comment admits a difficult truth about why governments upgrade their surveillance apparatus. They seek to spy on their population, but the ability to kill “enemies of the state” is the ultimate expression of all surveillance.
Most people do not understand how metadata—“data about data”—is used in government “kill chains,” nor do most realize how much that capability is growing. Though such technology is putatively for foreign threats, these kill chains can eventually be turned against any domestic population.
With this threat escalating, we need solutions that invalidate it, which the crypto and cypherpunk communities are already deploying. But before looking at them, we must understand how the US government and military exploit metadata analysis not only to spy but also to develop these kill chains for targeted assassination. Then, we can determine what countermeasures we can muster to defend ourselves and secure a better future with a new kind of “oblivious” institution.
First, what exactly is a kill chain?
It is the series of steps a government agency takes in the process of surveilling a person or persons and then green-lighting their assassination via drone bombing. The targeting framework used by US military and special operations units to hit targets is called F3EAD: Find, Fix, Finish, Exploit, Analyze, and Disseminate. The Finish phase is the visible attack that people can see and scrutinize. The Find and Fix phases focus on identifying and locating the target. They rely on preexisting surveillance technologies deployed by the CIA and the NSA, much of the same architecture that has also been used on US citizens.
Snowden revealed this program in 2013. He disclosed the existence of XKeyscore, an NSA system that lets analysts search collections drawn from a variety of sources: emails, chats, browsing histories, and all associated metadata. The who, when, where, and duration are all indexed and retrievable, even if the content remains private. Governments no longer require content for ongoing surveillance. What they prize is metadata. The message’s content is irrelevant by comparison.
What they get from accumulating this metadata is unparalleled pattern recognition. They use these newfound patterns to determine their targets’ relationships, daily habits, and documented connections. It provides a level of granularity that content alone cannot achieve.
Location data compounds this knowledge and makes the graphing process relatively straightforward. Cellphone towers generate records. Military intelligence agencies use Stingray-class devices to geolocate phones. Together, these technologies reveal the “pattern of life.” This is the surveillance piece of the kill chain logic. It allows intelligence agencies to track their targets for months, sometimes years, before pressing the red button.
The US military and intelligence community maintain two types of strike decisions: the personality strike and the signature strike.
The personality strike is precise. It relies on more than metadata. The individual is confirmed through multiple sources, including live human intelligence. A team assembles a dossier, pinpoints the individual, and authorizes a strike.
We have a documented example of how this “kill chain” operates from find to finish.
In 2020, a US-led drone strike killed Qasem Soleimani, commander of the IRGC’s Quds Force. The operation combined human intelligence with pattern-of-life analysis. That analysis was built over years. US and allied agencies had mapped his movements through signals intelligence for well over a decade. In the end, JSOC liaisons worked with Israeli counterparts to track his cellphone patterns. The Israelis held his numbers and handed them to US agencies, who traced his active handset to Baghdad even though he had switched phones three times in the six hours before boarding.
Long story short, the CIA knew Soleimani would be there. They wanted to confirm his whereabouts through human assets on the ground. Informants at the airport in Damascus tipped off the CIA when his plane took off, and American assets at Baghdad’s airport confirmed its arrival. After he left via his convoy, an MQ-9 Reaper drone circling in the sky above launched Hellfire missiles, killing him, Abu Mahdi al-Muhandis, deputy commander of Iraq’s Popular Mobilization Forces, and five others.
The other type of strike is more alarming. It is called a signature strike, and it relies solely on metadata and pattern-of-life behavior. The operators select individuals to target based on their behaviors and activities. It is a speculation-based hit; in reality, it is just targeting phones and information. The analysts do not know if it’s the actual target. There is no eyewitness to verify that the signature matches a specific person. When a pattern crosses a threshold, the team’s ranking officer authorizes the hit. The aggregate pattern must match a predefined lethal signature. This is called probabilistic killing. It is derived from unsubstantiated surveillance patterns.
All of this information was once top secret but was eventually leaked.
The practice was confirmed in the “Drone Papers,” leaked by Daniel Hale and published by The Intercept in 2015. The papers show that during five months of Operation Haymaker in northeastern Afghanistan, roughly 90% of the people killed were not the intended targets. Across the broader campaign, more than 200 people were killed. Only 35 of them were the intended targets. These individuals are classified as EKIA, “enemy killed in action,” even though they were never confirmed as combatants. It is a way for the US military to make its errors appear palatable to the media. More on this shortly.
These capabilities have been expanded in recent years by tech companies like Anduril Industries, but especially by Palantir. Think of Palantir as the epitome of surveillance weapon technology. Its Gotham software is embedded in tech operated by the CIA, the Department of Defense, ICE, and various domestic police departments. Palantir was co-founded and funded in 2003 by Peter Thiel. The CIA, via In-Q-Tel, also invested early.
Palantir’s goal as a software company is to expertly combine intelligence inputs. It integrates satellite imagery, financial transaction data, biometric data, and social network mapping, aggregates it all, and produces a detailed social graph: an offering we can call surveillance-as-a-service. This kind of analysis enables Palantir to piece together a person’s relationship network based on interaction activity. Any seemingly innocuous piece of info is metadata that can be gobbled up for social graphing. Palantir is now thoroughly embedded in the targeting and data-collection regimes of various government agencies.
The Pentagon released its targeting program, Project Maven, in 2017. They intended it to be their computer vision and drone-footage processing program. It was eventually transformed into an AI-targeting platform. At the outset of that program, the Pentagon hired Google to oversee it, but they left in 2018. Google employees took issue with the idea of supporting an autonomous weapons platform. Approximately 4,000 employees signed a petition to reject it. Seeing the opportunity, Palantir signed a contract to take over.
In 2025, Palantir CEO Alex Karp and Nicholas Zamiska published The Technological Republic: Hard Power, Soft Belief, and the Future of the West. The book is a “sweeping indictment of the West’s culture of complacency, arguing that timid leadership, intellectual fragility, and an unambitious view of technology’s potential in Silicon Valley have made the U.S. vulnerable in an era of mounting global threats.” Instead of working to solve national problems, Karp and Zamiska complain, Silicon Valley has chosen to focus on consumer-facing applications.
Their argument, in part, is that tech entrepreneurs and developers are obligated to the state: “Silicon Valley owes a moral debt to the country that made its rise possible.” Its engineering professionals and elite carry “an affirmative obligation to participate in the defense of the nation,” saying that soft power is finished, that free and democratic societies need to prevail with hard power, and that “hard power in this century will be built on software.” By advancing this thesis, of course, they are also defending their own company and its objectives.
Is software-enhanced weaponry a critical piece of future hard power? Is it a question of whether the tools will be built or merely who will build them?
Some argue the US’s foes will not debate the morality of producing surveillance or weapons platforms. They will just do it. Thus, the argument for such programs is a zero-sum arms race: if the US does not build automated targeting and precision weaponry, a bad person or persons will.
Is this a self-defeating argument, however? Karp appears ready to gaze into the abyss so long that it gazes right back, which is exactly what has happened with him and the US surveillance industrial complex. Is there any such thing as a “good guy” who will do the right things with weapons, AI, or weapons platforms? Effectively, whenever an individual or group has catastrophe weapons or large caches of arms at their disposal, there is always a concern that they will use them for ill or harm. And currently, judging by the state of the current system, its AI arsenal and machinery seem ready-made for misuse.
The most troubling problem with all autonomous warfare tech is that by relying on probabilistic killing and aggregated pattern analysis, one must accept potentially random outcomes. The military and government can only hope they hit the intended target.
However, the truth may be even more ominous. The Drone Papers tell a story of purposeful design behind this inadvertent killing. The way the system is constructed, whoever gets killed is of no consequence as long as a designated target is assassinated occasionally.
For example, the US military and its allies have hit many civilian locations, seemingly without remorse or consequence. These include: the MSF hospital in Kunduz, Afghanistan, obliterated by an AC-130 gunship in 2015; the Dahyan school bus in Yemen, hit in 2018 by a Saudi-led coalition airstrike using a US-supplied bomb; the Al-Shifa pharmaceutical factory in Sudan, leveled by US cruise missiles in 1998; and the Shajareh Tayyebeh elementary school in Minab, southern Iran, hit on February 28, 2026, in a strike that killed at least 165 children, teachers, and parents.
The government might have investigated itself for these strikes, but it typically finds no wrongdoing. The government gives itself allowances for noncombatant casualties, and they usually simply count accidental deaths as a bureaucratic statistic. In this vein, a system that consistently produces a specific outcome appears specifically designed to do so. In other words, the system appears designed to kill innocent bystanders, or at least has a tolerance for a certain amount calculated into it.
The signature strike logic does not only apply to assassinations in foreign lands; it can be deployed domestically against its own residents and citizens. The signature strike logic makes it far easier to dehumanize targets as mere patterns and bits of data. Local police and ICE agents are already using this technology’s surveillance capabilities for predictive policing.
In many ways, what is happening reads like Philip K. Dick’s Minority Report. There is a framework in place that predicts who will commit a crime and judges those people without due process, much less a trial by their peers. Given the frequency with which fiction becomes reality, is it so hard to imagine that individuals may soon have their own “minority report,” for which the government claims its only viable course of action is targeted assassination?
The very existence of this technology is a serious cause for concern. It has already been abused, and it will undoubtedly continue to be. Our purpose here is not fearmongering, however. Rather, by understanding what is happening, we can better address it.
The kill chain architecture has a major dependency: metadata aggregation. If large numbers of people remove their metadata signals, pattern-of-life analysis becomes harder to generate. The surveillance machinery, specifically the “find” phase of F3EAD, is thus rendered significantly more difficult.
Whether that would cause the government to rethink its controversial surveillance programs is an open question. Either way, there are techniques and technologies that anyone can use to enhance their privacy or reduce their metadata footprint. And those will be the subject of Part 2.
Source: https://www.theadvocates.org/the-metadata-kill-chain-from-surveillance-to-drone-strike/
Image: Source [Edited]
Original Article: https://dailynewsfromaolf.substack.com/p/your-phone-data-can-become-part-of
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...instead of delivering on his campaign promises, instead of working on accountability, reform, justice for the covid scamdemic crime victims, or anything even remotely related, Bobby keeps showering bioweapons manufacturers with money .., approving new mRNA poison shots, not removing the PREP Act liability shield for the crime cartel..
Sasha Latypova | Due Diligence and Art| sashalatypova.substack.com
Who Owns Bobby Part 1 is here. [on Truth11.com here] In it I addressed the major donors to Kennedy’s MAHA Alliance campaign (~$8M). Just to close the loop on the political campaign financing, the Federal Election Commission’s Kennedy campaign filings show the total campaign raised about $67.3M during the 2023–2024 cycle. Nicole Shanahan contributed $20M, and the rest of the financing came from ~180K individual small donations. One might say, surely, Nicole owns Bobby now, right? Not so. Let’s not confuse Political Charity with Political Enterprise. Nicole’s wealth is the former: she has a lot of money, true, but it’s all from the divorce settlement with Sergey Brin. There is no coalition of corporations that will profit from government connections and military-intelligence contracts, and therefore, nothing to build a lasting “public-private” empire or a winnable political campaign upon. In US politics, it’s not the candidate who is running for office. It is the corporate-intelligence-military alliance which invests in their political puppet candidate and expects returns when they are placed in power.
As Catherine Austin Fitts stated - it’s not the cash per se that funds the political campaigns, it’s the capital gains that do so. For a political run to be winnable, the funding must come from ideally several major industries that will profit from government handouts, favorable regulations, military and “science” grants and contracts - i.e. the financial “returns” on “investment” that the corporations made backing a politician that will deliver for them. At the same time, major intelligence agency alliances will ensure similar profiteering scheme for the intelligence contractors running a variety of money laundering, regime changes, weapons, drugs and human trafficking schemes globally. These elements of corporate-deep state -military marriage were absent from Kennedy 2024 run, thus, his campaign was a-priory unwinnable. The play was simple - take Nicole’s money and deliver the energized health freedom base to Trump. It worked.
Nicole herself seems too idealistic to attempt such an enterprise. She was relieved of her charitable $20M and unlikely to have another $20M stuck between the sofa cushions for the next season. Thus, she was a useful stepping stone but was immediately dumped by the roadside (and literally bleeding from a 20+ week miscarriage, likely from the mRNA shot) once Kennedy officially negotiated a deal with Trump. IMO, that deal had been pre-negotiated way earlier than that.
While this post centers around RFK Jr’s daughter-in-law and Kennedy 2024 campaign manger: Amaryllis Fox Kennedy, who is married to RFK Jr’s oldest son RFK III, I would like to point out that it is not because Amaryllis is a CIA agent. That’s just her pedigree. A much more important aspect to answering the question “Who Owns Bobby?” is Amaryllis’s stepfather, Stephen Rales, as discussed below. I am including a few links from the Internet Archive, as it seems that the data about Amaryllis and her family has been substantially scrubbed from the internet. Many of these source articles were assembled for me by a reader, and I thank them for this contribution.
Amaryllis is a “former” CIA agent and spy. She joined the CIA at age 22 (but IMO was in the “CIA youth” grooming program since her teens) and served between 2002 and 2010, working on counterterrorism. The official narrative claims she departed the CIA in 2010, however, there is no such thing as “ex-CIA”.
In 2014 Amaryllis was introduced to RFK Jr’s oldest son via a mutual friend at the Burning Man - a very popular annual party in Nevada desert, attended by financial, tech and government elites, and swarming with intelligence assets. Prostitution is legal in Nevada, and practically everything else is legal in the Nevada desert. The festival is awash with drugs and sex and overtly Satanic themes. Here is a good article about it by Nicole Shanahan, who, likewise, met her billionaire ex-husband Sergei Brin at the Burning Man. It will give you an idea on the circumstances under which “former” CIA hotties mate with high value targets like RFK III. Amaryllis is older than the 3rd, and has been around many blocks. She had been previously married (twice, according to some sources). I cannot find the information about the 1st marriage, but her second one was to Dean Fox, from whom she has a daughter, Zoë Victoria, born in 2009, and whose name she retained after marrying for the 3rd time to the 3rd. No public information about Dean Fox is available. It is known that he met Amaryllis Fox while both were serving undercover for the CIA in Shanghai. The dates of marriage or divorce are not available.
Amaryllis and RFK III got married in 2018 and have 2 kids. I am not implying in any way that the relationship is not genuine. All people can fall in love.
Amaryllis’s bio (and here) is quite breathtaking:
While many of her contemporaries were worrying about prom and spring break, Fox was volunteering in a Mai Laa refugee camp on the border of Thailand and Burma. As she recalled in a Paper Mag interview (note, link has been scrubbed), though she was only 17, she knew one thing for certain when she arrived at the airport to go home: she didn’t want to.
Instead, she spent two more years there working in health clinics and helping to raise funds for them. She also entered the journalism arena, recording a rare interview with Aung San Suu Kyi for the BBC, which would land her in a Burmese prison for a short time (!!!)
Here is Amaryllis herself retelling that horror imprisonment (mmm, more like a brief detention at the airport as far as I can tell) to the authors of “Freakonomics” books. I read both the Freakonomics and the SuperFreakonomics, and they are very interesting works.
However, holy shirt! Conducting an interview with a globo-deep state puppet Aung San Suu Kyi (CIA asset, anyone?) for a globo-deep state propaganda outlet (BBC) and earning street cred in a Burmese prison at age 17? Or maybe 19? (Depending on who is retelling the story). Check! I am wondering why BBC had a shortage of credentialed journalists that day to assign such a high profile the interview to a random teenager… but ok. Here is an on-point and a very entertaining discussion about Amarylis obviously being a Young Pioneer groomed by the CIA/British intelligence, starting at the tender age of around 8 yo (at 17 min):
I recommend listening to the entire podcast. Amaryllis is a liar and quite a mediocre, lazy one at that. That’s true to character - “woke AF” Marxists tend to be lazy-mediocre types after all.
As to the high profile Burmese interviewee, Aung San Suu Kyi, whom possibly underage Amaryllis was interviewing for BBC and then smuggling the film out in her um…[redacted]… because reasons - the notorious Aung San Suu Kyi drew criticism from several countries, organizations and figures over Myanmar's inaction in response to the Rohingya genocide in Rakhine State and refusal to acknowledge that the Tatmadaw (armed forces) had committed massacres.[13][14][15][16] Under her leadership, Myanmar also drew criticism for prosecutions of journalists.[17] In 2019, Aung San Suu Kyi appeared in the International Court of Justice where she defended the Myanmar military against allegations of genocide against the Rohingya people.[18]
Given that she was awarded the Nobel Peace Prize, we can safely assume the genocide accusations were very valid.
After being imprisoned (again!) following Myanmar's military coup in February 2021, Aung San Suu Kyi was serving a lengthy prison sentence at an undisclosed location in Naypyidaw. In April 2026, Myanmar's military government announced that it had reduced her sentence as part of a broader amnesty and transferred her from prison to house arrest (or a designated residence). Again.
Back to Amaryllis’s incredible adventures. By 2002 she returned home from hot climates: she went to Oxford for an undergraduate degree, and then returned to the US to attend a master’s program at Georgetown:
While at Georgetown she developed a remarkable algorithm for predicting terrorist activity and was asked by the university’s CIA Officer in Residence Dallas Jones to share it with Langley.
Per Fox’s bio for Big Think, she “began work as a political and terrorism analyst for SE Asia, commuting between Langley and Georgetown to finish her degree with honors.”
Gosh! Straight out of many Hollywood scripts: youth, beauty AND brains of a white-hat terrorist-hunting hacker… when did she gain that technology expertise? The algorithm itself is a no-brainer though: the CIA does not need any special algorithms to predict their own operations. They just needed to give extra oomph to Amaryllis’s bio by advertising this amazing “code” that she allegedly made.
Speaking of super-freaking coincidences. Another story about terrorism-predicting computer code appears in the book SuperFreakonomics (see above link to Amaryllis’s talk on the authors’ podcast). It describes an experimental project by a British bank fraud investigator, Ian Horsley (identified by name in Freakonomics blog posts), working with economist Steven Levitt to explore whether retail banking data could identify “potential terrorists”. Translation: install mass warrantless surveillance of the citizen’s financial transactions under pretenses of “fighting terror”.
The project began after the 2005 London bombings (7/7). But of course, right around installation of the Patriot Act, the PREP Act, and related pillars of the global totalitarian regime, we have a London focused problem-reaction-solution incident. Let’s see who the main perpetrators were:
Mohammad Sidique Khan, aged 30. The ringleader of the four bombers, he also lived in Beeston, Leeds, with his wife and young child. He worked as a learning mentor at a primary school. Khan was the second to detonate a bomb, on the number 216 train, killing seven people, including himself.
Readers, the compounding of coincidences overwhelms me! Perhaps, the public awareness of the terrorists ringleader’s name, as well as the train number are the deciding factors that got the Mayor of London Sadiq Khan elected to his office in 2016? Isn’t that how the democratic democracy works?
In re the banking surveillance algorithm, Ian Horsley proposed using the same statistical techniques banks use to detect fraud, but instead of identifying fraudulent customers, the algorithm would identify individuals whose “banking behavior resembled that of known terrorists”. The proposed process was:
The SuperFreakonomics book deliberately disclosed only a few surveillance variables. According to the Freakonomics material, some characteristics associated with known suspects included:
Another personal note: my husband discovered a clever Muslim technology - hijab magnets - on Amazon. He uses them to secure the mountain biking elbow guards so they don’t slide down on rough descends… Combined with my anti-Pandemic-Crime career and name, we must be on soooo many terrorist watch lists, I can only imagine! My children got me a this sticker:
I think it is very clear what these super-amazing code algorithms are - nothing other than age-old profiling tactics. The only thing that’s different post 2005 is the technocratic totalitarians in power have justified what used to be illegal warrantless surveillance and racial profiling under the slogans of “the war on terror”. The CIA and their international collaborators provided the acts of terrorism required for the illegal laws, including the Patriot Act, the PREP Act similar legislation to be passed in the UK.
Ok, enough digressions, back to Amaryllis.
Amaryllis became the campaign manager for RFK Jr’s 2024 presidential campaign after Denis Kucinich was pushed out by the same donor class who demanded Kennedy run as an independent. Kennedy simply replaced Kucinich with his own British spook of a daughter-in-law who had zero political experience. Consequently, RFK Jr negotiated Amaryllis position for CIA deputy director in the Trump administration. In 2024 Amaryllis was installed by Trump as Deputy Director of National Intelligence for Policy and Capabilities and Associate Director for Intelligence and International Affairs at the Office of Management and Budget. She is also a member of Trump’s Intelligence Advisory Board. That’s quite a lot of CIA titles for someone claimed to be “ex-CIA”!
Amaryllis resigned in 2026, together with Tulsi Gabbard. Amaryllis became a partner at Ballard Partners, where she will co-Chair the firm’s Emerging Technology and AI Practice Group. According to published news articles, Ballard Partners are overjoyed to have her on board (who wouldn’t be?):
“We are thrilled to welcome Amaryllis to Ballard Partners and to our Emerging Technology and AI Practice Group,” said firm founder and President Brian Ballard.
“She has operated at the very highest levels of the intelligence community and the federal budget process, and few people in the country understand as well as she does how government funds, oversees, and adopts advanced technology. As artificial intelligence transforms every industry and every corner of government, her judgment and experience will be invaluable to our clients.”
The firm represents dozens of companies in all major sectors, as well as numerous local governments and academic institutions. Client list includes Palantir, Meta, Bayer pharma, Blackstone, NYSE, LA28 Olympic Games, MLB, NBA, NY Yankees, NFL, PGA Tour, Amazon, Anthropic and many more!
Danaher Corp will likely be a juicy addition to the client list, and that might be the real reason behind Brian Ballard’s excitement over his new partner. Now, we are getting to the real answer on who owns Bobby. Let’s look into the business of mRNA bioweapons.
Amaryllis’s parents are part of several prestigious clubs: the Billionaires, the Looters and the Bioweapons. Amaryllis’s father is the American economist Hodson Thornber, who was heavily involved in the plunder of the USSR post its collapse. Thornber has been part of the highest levels of British finance and intelligence operations over the last forty years. He helped loot energy and transportation logistics in the U.S. and Great Britain in the 1980s on behalf of global finance, and then went to work for Renaissance Capital of London and Moscow in privatization looting operations in the former Soviet states of Russia, Kazakhstan, and Ukraine in the 1990s. Renaissance partnered repeatedly with George Soros in these schemes. Here is his bio including ties to Russia, Ukraine, etc.
Amaryllis’s mother is a “British actress” Lalage Damerell. Note that numerous sources refer to her as a “British actress”, as if she is well-known, but there is no information about her alleged acting career, and no major film or theater credits. Also note that in at least some of Amaryllis’s own interviews, she refers to intelligence agency jobs as “method acting”. In 2012, after divorcing Thornber, Lalage married billionaire Steven Rales (who became Amaryllis’s step-father, and RFK Jr’s in-law).
Rales is the co-founder and chairman of Danaher Corporation, a global scientific and biomanufacturing/biotech behemoth, with approximately $25B annual revenues, generating $3.6B net profit, but a lot more in free cash flow. In 2020 Danaher was contracted by the FDA to produce Covid tests.
“On Monday, March 2, 2020, Dr. Stephen Hahn the FDA’s commissioner, said that the agency had taken actions to allow private labs and companies to begin making their own coronavirus tests in order to greatly expand the U.S. capacity to test for the virus. Hahn went on to note, “There will be—the estimates we’re getting from industry right now, by the end of this week, close to a million tests will be able to be performed.” The following morning, a spokeswoman for the U.S. Department of Health and Human Services noted that Dr. Hahn was referring to tests being produced by an outside manufacturer, Integrated DNA Technologies. IDT is a division of Danaher which was acquired in early 2019.
Danaher’s main business lines are in the biotechnology sector. This segment supplies equipment, consumables, and software used to develop and manufacture biologic drugs such as monoclonal antibodies, vaccines, gene therapies, and cell therapies. Major brands include Cytiva and Pall Corporation. Danaher products include bioreactors, cell culture media, chromatography systems, filtration systems, single-use manufacturing equipment [note: this is favored by mRNA and other injectable bioweapons manufacturers, due to un-auditable manufacturing - the production line is assembled with bags full of unidentifiable junk and literally disappears after the product is made], process development instruments and manufacturing software. In other words, Danaher is the proverbial ‘buckets & shovels’ supplier to the Gold Rush, i.e. the party who is the most likely to profit off the futile, deadly and guaranteed to fail casino of the “genetic editing revolution” that so far cranked out a ton of poison but not much else… However, the contractors who build a chain of guaranteed-to-fail casinos, provide construction materials, furniture and gaming equipment are guaranteed to succeed no matter what ultimately happens with the casino.
Danaher was in 2020, and remains to date a major supplier of biomanufacturing equipment, including disappearing manufacturing lines (single use) for Pfizer and Moderna mRNA vaccines. Clearly, the future of mRNA poison is tightly linked to Kennedy clan now, and at a minimum, will ensure wealth and happiness of RFK Jr’s grandchildren, children of RFK III. In addition to superior wealth, these lucky kids are also highly likely to be unvaccinated, while the government will be forcing yours to be poisoned with bioweapons at gun point. Rales is a long term political donor to the Democrats, RFK Jr is a life-long Democrat, and so is Trump. Both are committed to looting, AI surveillance and centralizing the government power while squeezing the mom and pop harder. Is the mRNA bioweapon wealth likely to be a major source of finance of RFK Jr’s anticipated presidential run in 2028?
Danaher Corporation established a near monopoly position in biomanufacturing equipment space today. Starting around 2016, Danaher has been strategically acquiring companies (33+ companies) that ended up reaping gigantic profits for them during the covid scamdemic. Did they have a crystal ball, I wonder? Maybe Amaryllis produced another cracking prediction algorithm?
September 2016: Danaher acquired CEPHEID for ~$4B. Cepheid Covid Response (Archive, April 2020)
March 2018: Danaher acquired INTEGRATED DNA TECHNOLOGIES (IDT) for ~ $1.9B.
NYT Article (Archive, March 2020) mentions IDT as a contractor.
IDT’s COVID-19 Response (Fact Sheet - June 2020).
SARS-CoV-2 probes and other COVID-19 research reagents (Archive, June 2020).
June 2021: DANAHER acquired ALDEVRON for ~ $9.6B
Aldevron Covid Response (Archive November 2020).
DANAHER’s profits (Fortune 500)
Archive, Jun 2020 Excerpt: “... the company has benefitted from strong sales of its COVID-19 diagnostic tests.”
DANAHER as recipient of gov contracts
In addition to being a biomanufacturing mogul, Rales is also a major Hollywood investor, having financed several Wes Anderson films (which I enjoy very much).
Prior to the scamdemic Rales’ net worth was $3B and after the scamdemic it grew to approximately $9B (!) That’s a lot of dry powder for financial campaign contributions, and what a great in-law to have for a political royalty clan! Quite a catch.
Is anyone surprised that instead of delivering on his campaign promises, instead of working on accountability, reform, justice for the covid scamdemic crime victims, or anything even remotely related, Bobby keeps showering bioweapons manufacturers with money (that ultimately flows into Stephen Rales pockets), approving new mRNA poison shots, not removing the PREP Act liability shield for the crime cartel, and, in spare time, running a cooking show with celebrity chefs?
Original Article: https://sashalatypova.substack.com/p/who-owns-bobby-part-3-cia-danaher
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Darth Vader Defends Flock Camera Use
Canada | Two Tier Policing
Two MASSIVE COVID shot studies involving 8.7 MILLION people confirm Fauci and Gates injected the world with CANCER:
— Nicolas Hulscher, MPH (@NicHulscher) August 21, 2026
BREAST CANCER: +54%
PROSTATE CANCER: +69%
LUNG CANCER: +53%
BLADDER CANCER: +62%
COLON CANCER: +35%
STOMACH CANCER: +34%
THYROID CANCER: +35% https://t.co/erVexj5Am8 pic.twitter.com/2UUJ4OUTpd
We have published this before on Truth11.com | Worth seeing again
Lake Pleasant, Indiana ~ Source: https://www.facebook.com/reel/1632869088263146
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