What's Wrong With Jordan Peterson's Health?

Mikhaila reached out to me and this is our discussion.

Jordan Peterson’s health has been suffering tremendously.

Mikhaila, his daughter, saw that what was ailing him was affecting so many systems of his body that it had to all be connected and began to wonder if it was a form of mitochondrial dysfunction.

In trying to research whether mitochondrial dysfunction could be driven by the turning points in his health problems like SSRI withdrawal, benzodiazepine withdrawal, and toxic mold, she found my work and reached out to me.

This is the conversation that we had:

My hypothesis is as follows.

Mikhaila shares half of Jordan’s genes and has been more detailed about her own health journey going back to childhood, so we start with her.

She had juvenile arthritis symptoms starting at 2 and a diagnosis at 7. She went on Enbrel, a “biologic” (a pseudoscientific regulatory term) that opposes the action of the inflammatory mediator tumor necrosis alpha (TNF-alpha); and on methotrexate, which inhibits folate and adenosine metabolism. Methotrexate raises adenosine, which inhibits T cell proliferation. Its inhibition of folate metabolism is thought to be more relevant to cancer but its adenosine-mediated inhibition of T cell proliferation is thought to be more relevant to autoimmune arthritis.

The next year, at age 8, she was diagnosed with depression and put on SSRIs.

My hypothesis is that she has an underlying block in mitochondrial metabolism leading to CoA sequestration, which occurs when CoA-requiring pathways fail to complete properly. This leads to secretion of TNF-alpha as part of a cellular stress response. TNF-alpha serves to increase carnitine transport into the cell. The carnitine then trades places with CoA, detoxifying the metabolic intermediates and carrying them out into the urine, allowing CoA metabolism to continue.

Blocking the TNF-alpha is a double-edged sword. On the one hand, the elevated TNF-alpha will interact with genetic predispositions to certain types of immune dysfunction and with suboptimal joint mechanics to produce an autoimmune disease. Blocking the TNF offers relief from the autoimmunity, but then in doing so makes the cells that were releasing it as a stress signal unable to mitigate their CoA sequestration. This may lead to a plethora of side effects, and for Mikhaila this was depression.

I do not discount that inhibition of folate metabolism by methotrexate could have messed with her methylation system, but Mikhaila remains very intolerant of methylfolate and thrives on a low-folate all-meat diet, and I do not think any of her health problems are explained merely by a methylation deficit.

Her first major advance was going on an elimination diet that eventually morphed into the red meat carnivore “Lion Diet.”

T cells are fueled by glucose and glutamine during active inflammation, and when they transition to resolving inflammation a major drop in glucose and glutamine is a central hallmark of the metabolic shift.

The zero-carb nature of the Lion Diet helps resolve T cell inflammation and displaces the need for methotrexate.

The large amount of red meat provides carnitine, which addresses CoA sequestration from the point of carnitine supply, relieving the need of cells to secrete TNF-alpha to signal carnitine demand. The carnitine in the red meat thereby helps relieve the need for the Enbrel.

Since her elimination diet gave her the first relief of depression she had experienced, it led her to go off the SSRIs.

Going off SSRIs produced 2.5 years of new-onset neurological dysfunction, which I contend was new-onset mitochondrial dysfunction. This may have interacted or blended with the mitochondrial dysfunction that initially led to the arthritis, or it may have just been a completely new acquired mitochondrial disorder thrown on top of the existing problems.

Throughout this story, various exposures to toxic mold occurred that made her problems worse, including one in 2022 that gave her a whole new list of problems that only moving away from the mold was able to solve. Mold toxins are mitochondrial toxins, so exposure to them would cause a third layer of mitochondrial dysfunction.

Jordan had been on SSRIs for over twelve years, but when he saw Mikhaila cure her depression with the early precursor to the Lion Diet, he followed her approach. Having gotten rid of his own depression, he too went off SSRIs around the same time as she did. This led to akathisia, a catastrophically debilitating movement disorder. I contend that this is SSRI withdrawal-induced new-onset mitochondrial dysfunction.

He then had a terrible reaction to apple cider that had sodium metabisulfite as a preservative. This led him to be unable to sleep for two or three weeks. He became green and hunched over, and couldn’t walk.

For this he was placed on clonazepam, a benzodiazepine.

Sulfite has to be converted to sulfate, which requires the mineral molybdenum and the transfer of electrons from the sulfite to the mitochondrial respiratory chain.

Mitochondrial dysfunction will prevent sulfite clearance.

Zero-carb diets will increase endogenous sulfur production and diets that lack liver and legumes are low in molybdenum.

The mitochondrial dysfunction induced by the SSRI withdrawal would inhibit sulfur clearance and the diet that helped Jordan and Mikhaila cure their depression would keep the sulfur-detoxification system maximally occupied.

If sulfite is not quickly metabolized to sulfate, it converts to S-sulfocysteine, which is a neurotransmitter that activates glutamate receptors.

Sulfite itself is mitochondrially toxic, so if it crosses a critical threshold it can elicit a storm of excess sulfur catabolism and impaired sulfur clearance that keeps S-sulfocysteine levels high. That vicious cycle could explain why the sleep loss lasted 2-3 weeks.

Clonazepam directly opposes S-sulfocysteine in that it binds to GABA receptors making GABA more powerfully activate them, which counteracts the S-sulfocyteine’s activation of glutamate receptors.

Peterson stayed on clonazepam for three years and then tried going off of it, but this caused an even worse case of akathisia than he experienced from SSRI withdrawal. It lasted three years, and it made him suicidal.

Clonazepam can alter calcium signaling in mitochondria in opposite ways depending on the preexisting state of the mitochondrial function. Possible effects of withdrawal include a catastrophic energetic supply/demand imbalance and precipitation of calcium causing damaging deposits that jam up the mitochondrial infrastructure. It is very possible that the clonazepam was causing progressive mitochondrial dysfunction the entire time he was on it and that it only became apparent once the GABA breaks on energy demand were removed by withdrawal.

He briefly restarted an SSRI during this time but it didn’t help and it made him so fatigued he needed four extra hours of sleep per day.

Ultimately, the final version of the all-meat Lion Diet helped Jordan recover from akathisia.

More recently, however, his parents died and he had been cleaning out their moldy basement preparing for a big move, and this led to an attack of pneumonia and sepsis and a return of his akathisia.

The mitochondrial toxins in the mold thus became his third acquired mitochondrial disorder, the first two from withdrawal from SSRIs and benzodiazepines.

Jordan and Mikhaila share a lot in their health history but her mom has none of these problems and has never been on SSRIs. Thus, it is very likely there are genetic predispositions to these problems that Jordan and Mikhaila share.

The Lion Diet is overall extremely helpful but could probably benefit from specific strategies around managing sulfur metabolism.

I will do what I can to help them, starting with looking at their mitochondrial function. I think more specific data will provide insights that they can use to convert the vicicous mitochondrial cycles to virtuous mitochondrial cycles and I hope and pray for Jordan’s robust and lasting recovery.