What causes autism?
- Thomas P Seager, PhD
- 14 hours ago
- 23 min read
Autism is a mitochondrial disorder with an immunological trigger
Summary
The current consensus is that the origins of autism are complex and multi-factorial. However, there is a simpler explanation that encompasses all other theories. That is, autism originates in mitochondrial impairment.
Mitochondrial abnormalities, either prenatally, during pregnancy, or in the earliest years of life when brain development is most critical, multiple risk factors for a later autism diagnosis by several times.
Therapies targeting mitochondrial function, such as nutritional supplements that support metabolism, have successfully treated autism by reducing the severity of symptoms.
Cold plunge therapy remains an untested intervention, although warm water hydrotherapy has shown positive results and case studies in children diagnosed with autism spectrum disorder (ASD) suggest the mitochondrial benefits of cold plunge might have positive effects for treating autism.
The Phone Call That Changed My Science
It was May 8th, 2020 when I was sitting in my car alone in the parking lot outside a barber shop that had just been allowed to reopen during the COVID lockdowns. I was staring into the rearview mirror, admiring my new haircut -- the first I'd had in months -- when my phone rang.
A producer of The HighWire show was on the phone. He had read a viral article, to which I contributed, called The Curve Is Already Flat (Kay 2020) criticizing the lockdowns. The article presented data from the CDC demonstrating that COVID-19 was in community spread as early as Nov 2019. It was censored on social media, and the producer wanted me to appear on The HighWire to be interviewed by Del Bigtree so more people could hear the message.
I told him, "I will talk about lockdowns. I will talk about theCDC data. I will talk about disaster response and human resilience, but I will not talk about vaccines."
He said, "That's OK. You can talk about whatever you want."
At that time, there were hardly any tenured University faculty willing to go on record in opposition to the lockdowns, and he later told me that my appearance might help other scientists come forward with their views, despite threats of censorship and retribution at their home institutions.
He was right, but in that moment, my concern was that appearing with Bigtree would somehow discredit me as some kind of anti-vaxx nutjob.
So I asked him, "What is it with you and vaccines, anyway? Why are you so committed to being anti-vaxx?"
He then told me a story that changed my understanding of science, my career as a researcher, my views on vaccines, and my life.
He said, "I have two medically-documented, vaccine-injured, autistic sons. Both of them regressed into autism immediately after their vaccine injuries.
"They were both normal, engaging, outgoing boys until they were injured by vaccines."
"There has never been a real study as to whether vaccines cause autism," he told me. "And, in a way, it doesn't matter... no scientist, no clinical or epidemiological trial, no peer-reviewed journal article can deny my experience as a parent."
So I did The HighWire show.
There's no record of my appearance, as far as I know, because Bigtree and The HighWire were scrubbed from the internet a few months after my appearance. Nevertheless, when I reflect on how naive I was about censorship and the extent of persecution that was in store for those scientists that were critical of official policies, I know I would cringe if I were to rewatch myself. Since then, my views on vaccines, on COVID, and on science have changed.
I no longer treasure the randomized, double-blind, placebo-controlled, clinical trial. As I wrote in my Uncommon Cold (Seager 2024) book:
Nothing matters more than your N=1 personal experience. - Seager (2024).
What I could not have known then was that many of the faculty, like Jay Bhattacharya, MD/PhD, who were once vilified, censored, persecuted, and pilloried by government officials and the mainstream media would later be vindicated and appointed to lead the institutions that were once used against them. Moreover, one of the most important goals in their new official capacities is to investigate the very question that The HighWire prompted me to confront more than five years ago.
What causes autism?
Increasing rates of autism diagnosis
Rates of autism spectrum disorder (ASD) diagnosis have increased exponentially in the last decade. For example, children aged zero to four years old were almost five times as likely to be diagnosed with ASD in 2022 than 2011 (Grosevenor et al. 2024). However, expanded screening and changes in diagnostic criteria contribute the increase (Lundström et al. 2022). While the temptation in epidemiology is to seek correlations between the diagnostic timelines and hypothetical causes, such as changes in vaccine status, or 5G wireless exposures, or microplastics, or mold, or any other hypothetical underlying cause of autism, these correlations are specious distractions that cloud investigation into the root causes.
The most informative cases with regard to etiology are those that are most severe. Sometimes referred to as profound autism, these are cases that are non-verbal, exhibit stereotypical behaviors such as stimming (soothing self-stimulation) and self-injury, experience difficulties in sensory-processing, and sometimes suffer from seizures. In these cases, diagnostic signals are strongest, and rates of false positive diagnosis low. However, timeline data on this subpopulation is unreliable, partly because changes in the way autism is now coded by clinicians makes it difficult to make intertemporal comparisons (e.g., Russell et al. 2022), and partly because what was once coded as some other intellectual or developmental disorder is now being coded as autism (e.g., Cardinal et al. 2021).
That means the epidemiological data regarding autism is useless for uncovering its origins. Most of the work in autism etiology suffers from a serious shortcoming. It lacks a mechanistic understanding of modes of action. That is, epidemiological correlations and associations over time do nothing to improve our understanding of brain development, neurodevelopmental regression, or the onset of ASD. As a consequence, most clinicians and scientists will say things like "The etiology of autism is complex, multifactorial, and difficult to decode. More research is needed."
The problem is that more of the same type of research that has failed to clarify answers to the most basic questions will only add to the confusion. It's no wonder that the public grasps for oversimplified explanations like "Vaccines cause autism," and who could blame them?
What I Didn't Know About Type 1 Diabetes
In 2001 I had just completed my doctoral dissertation when my son was diagnosed with Type 1 diabetes. It was December, and he had a fever for a few days, like lots of kids do, but he didn't get better.
He got worse.
Finally, my wife called his pediatrician, who was also our next-door neighbor. She described our son's symptoms and at first the doctor didn't seem too concerned.
"It's probably just the flu," he said. "There's been something going around, and I've been getting a lot of calls about sick kids,"
But then my wife said, "Plus, he's peeing the bed. A lot," and that gave the doctor pause.
"Meet me in the emergency room right away," he said. "Your son has diabetes and your life is going to change."
The hospital was across the street from our house. I carried my son into the emergency room. I don't really remember what happened next. Someone must have taken him from my arms and admitted him to the Pediatric Intensive Care Unit.
They put him on an insulin drip. I sat next to him all night, practicing my injection technique with an insulin syringe and an orange so that when he was discharged, I would know how to administer the insulin shots that would allow his body to process carbohydrates.
Compared to a diagnosis of autism with neurodevelopmental regression, Type 1 diabetes seems easy. As long as I could monitor my son's blood glucose levels and calibrate his insulin injections for his diet and exercise, his prognosis would be excellent. Nothing else would really be required.
But that knowledge did little to relieve my grief and shame. I couldn't believe I didn't know what was happening with him, and I couldn't understand what might have caused it.
It wasn't until years later, when I was sitting in a dentist's office thumbing through the pages of an old Reader's Digest, that I read about the new results of a longitudinal study out of Finland that revealed the cause of diabetes. By tracking Vitamin D levels in pregnant women and their newborn children, Finnish researchers discovered that a deficiency of Vitamin D during the first year of infancy, when the immune system is undergoing its most critical developmental stage, predicts risk of later onset of Type 1 diabetes (Hyppönen et al. 2001).
My son was born in late October, in northern New York. Although my wife and I paid close attention to her diet to ensure sufficient protein intake while she was pregnant, we hadn't given a thought to her Vitamin D status, or his. In retrospect, it makes sense to me that there's no way he would have gotten enough sunshine during the first few months of his life, given our latitude and the season in which he was born. It would be no surprise to have learned he was Vitamin D deficient, but back when he was an infant I didn't know to check.
I wrote about the relationship between Vitamin D status in the first year of life and later onset of autoimmune disorders in my article Reordering Autoimmune Disorders. What I discovered is that all autoimmune disorders, including Type 1 diabetes, rheumatoid arthritis, multiple sclerosis, and Parkinson's, originate in deficiencies of Vitamin D during that critical stage of immune system development that takes place after birth.
The reason this remains hidden from medical researchers is that the onset of the autoimmune disease is disconnected from its origins by several decades. The Finnish study that revealed the cause of Type 1 diabetes began in the 1960's and wasn't published until 2021. That is, Vitamin D levels at the time of disease onset might be normal, but the critical determining factor is the level of Vitamin D during development of the immune system. Without Vitamin D during this critical stage, the immune system will not follow a typical developmental trajectory. Instead, it will be predisposed for onset of autoimmune disorder when activated by an immunological event, as in the case of my son's fever. None of this could have been made clear without the patient, fastidious, longitudinal work done over nearly half a century by the Finnish researchers. Even if we started new studies on other autoimmune disorders, the research required might not be available for at least another ten years. It is only after the fact that the conclusion seems obvious.
Mitochondrial dysfunction in autism
While Type 1 diabetes is an immunological disorder, autism is neurological. That is, diabetes results from atypical development of the immune system, while autism results from atypical development of the brain. Coincidentally, the immune system and the brain are in their most rapid stages of development at the same time, namely late-stage pregnancy and the first several years of life. It is likely that Vitamin D plays a role neurological development (Botelho et al. 2024), but its role in immunological development is much stronger. The critical factor in neurological development is mitochondrial function.
Just like immunological development relies on Vitamin D, neurological development relies on mitochondrial function.
There is a close association between autism spectrum disorder (ASD) and mitochondrial impairment. For example, fifteen years ago, a study of young autistic children in California discovered that up to 80% had blood markers indicating some degree of mitochondrial injury and/or metabolic disorder (Giulivi et al. 2010, Frye & Rossignol 2011). Since then, disrupted mitochondrial function in ASD patients has been revealed in several clinical trials and corroborated in animal models (Khaliulin et al. 2025).
Mitochondrial impairment during pregnancy is one of the strongest predictive factors of autism risk later in life. Every condition associated with gestational metabolic disorder, including pre-eclampsia, gestational diabetes, and placental insufficiency, more than doubles the risk of ASD later in the child's life. Moreover, use of valproate (an anti-epileptic drug sometimes used to treat migraine headaches) during pregnancy more than quadruples the odds of autism (Hoirisch-Clapauch & Nardi 2019) by disrupting mitochondrial energetics (Salsaa et al. 2020). Even prenatal environmental exposures that impinge upon mitochondrial function are implicated in increased risk of ASD (Frye et al 2021).
At least since 1998, some scientists have hypothesized that autism is a mitochondrial disease (Lombard 1998). Such speculation makes sense, given the intense metabolic requirements of the brain and the fact that neurons are among the cells most densely packed with mitochondria. Any disruption in healthy mitochondrial function is sure to impact brain function. Many competing theories on the causes of autism, including mold toxicity, non-native electromagnetic frequency exposure, or heavy metal poisoning can be collected under the mitochondrial theory once researchers recognize that each of these environmental stressors acts through the mitochondria.
Certain metabolic profiles are so closely associated with ASD in young children that blood panels may be used as diagnostic aids (e.g., Barone et al. 2018). However, I think there are two reasons why the etiology of autism is still so poorly understood:
Autism can emerge without evidence of acute mitochondrial impairment at the time of onset, because the critical mitochondrial insufficiency may have been present earlier in life during phases of intense neurological developmental,
Mitochondria dysfunction only primes the brain for autism by steering it towards atypical developmental trajectories. Clinical presentation of stereotypical autistic behaviors might not be revealed without some immunological activation (e.g., fever, illness, or vaccine) that initiates autism. Thus, an association between the immunological event and onset of autism can mask the root cause.
Both of these points of confusion can be resolved by a new theory of the origins of autism that I will present here.
Immunoactivition initiates neurodevelopmental regression
One of the tragic hallmarks of new diagnoses of autism is the sudden onset of neurodevelopmental regression (NDR) -- i.e., loss of developmental milestones that had previously been obtained, such as speech -- following an immunological activation. For example, vaccines activate the immune system and can cause neuroinflammation that modifies neurological operations. Additionally, the aluminum and mercury in vaccines are toxic to mitochondria and may present increased neurological risks (de Oliveira 2022). However, vaccines are not the only immunological event that can initiate onset of autism. When mitochondrial abnormalities are present, a fever can be sufficient to initiate NDR, even in the absence of a recent vaccination (Shoffner et al 2010).
In the absence of acute immunological activation, such as vaccination or infection, the onset of autism with NDR may be particularly enigmatic. In such cases, acute environmental insult to mitochondria may be the initiating event. For example, Frye et al. (2022) found a relationship between environmental exposure to air pollution measured as concentrations of PM2.5 (suspended particles measuring less than 2.5 microns in diameter) an onset of NDR. It is already well-established that PM2.5 exposures adversely impact mitochondria. One possibility is that multiple environmental insults increase accumulated mitochondrial stress, such that any additional acute exposure overwhelms mitochondria that are already chronically impaired, resulting in an inflammatory response that initiates the onset of NDR.
Mitochondrial therapies treat ASD
One of the strongest lines of evidence supporting the mitochondrial theory of autism is the fact that therapies targeting mitochondria are effective for treating autism in children (Frye 2020, Nabi et al. 2023). There may be two reasons for it:
Autism is diagnosed on the basis of behaviors, and most therapies enlist cognitive resources to modify those behaviors. That is, autism is currently treated by teaching children cognitive behavioral coping strategies. Unfortunately, learning is an energetically intensive activity that relies on mitochondria to power neural development. When mitochondrial function is impaired, learning is impaired. Thus, mitochondrial support might improve the efficacy of typical behavioral therapies. And,
Mitochondria are essential to the physiological development of new neural pathways. That is, the atypical brain development patterns characteristic of autism cannot be remodeled without relying on mitochondria. Only healthy mitochondria can power high functioning redevelopment patterns, thus mitochondrial interventions may direct neuroplasticity towards improved neural function.
L-Carnitine
Fat metabolism plays a critical role in brain development. While most people think of dietary fat as primarily an energy source for the body, what they don't realize is that fats provide the structural scaffolding of cell membranes, nerve tissue, and the brain. More than 60% of the brain is composed of fat molecules, and L-Carnitine is essential to the mobilization and metabolism of those fats. Where L-Carnitine is insufficient, fat utilization suffers and altered fatty acid metabolism is involved in the pathogenesis of autism.
Supplementation of carnitine to alleviate behavioral and cognitive symptoms in ASD patients due to the deficit is absolutely necessary as a potential treatment method. - Kępka et al. 2021
When a team of researchers administered L-carnitine supplements to a group of nineteen autistic children between 3-10 years old, they observed significant improvements in diagnostic evaluation criteria, compared with controls. Scores on the Childhood Autism Rating Scale (CARS), the Autism Treatment Evaluation Checklist (ATEC), and hand muscle strength, all improved after three months. Although all subjects in the experimental group were given the same dose per body weight, increased blood serum levels of carnitine were associated with greater improvement on these measures of autism severity, suggesting a dose-response relationship that might aid in the design of individual L-carnitine therapy protocols (Geier et al. 2011).
CoQ-10
Ubiquinone, better known as coenzyme Q-10 (CoQ-10) is a fat molecule that facilitates electron transport in the mitochondria. Therefore, Co-Q10 is essential for mitochondrial respiration. Deficiencies in Co-Q10 are associated with mitochondrial dysfunction, and correction of these deficiencies by supplementation has been employed as a treatment for several neurological disorders including Alzheimer's, Parkinson's, multiple sclerosis, epilepsy, and autism (Pradhan et al. 2021). When a supplement including Co-Q10 and other nutrients targeting mitochondrial support was administered to sixteen autistic children for twelve weeks in a double-blind, randomized cross-over trial, significant improvements were observed in both mitochondrial function and parent-rated scales of autism severity (Hill et al. 2025).
Magnesium
I've written extensively about the benefits and importance of magnesium supplementation for mitochondrial health. In particular, my article Magnesium for Mental Health pointed out that magnesium supplements are at least as effective as anti-depressant medications in the treatment of mood disorders like major depression. It is already well known that magnesium supports mitochondrial function and brain metabolism. Thus, it may come as no surprise that a recent study found that autistic children have considerably lower blood serum magnesium concentrations, compared to neurotypical children, indicating an association between possible magnesium deficiency and clinical presentation of autism (Almalki et al. 2025). Treating twenty-seven children aged 9-12 years with a nutritional supplement containing magnesium and vitamin B6 resulted in a significant improvement in symptoms of autism when compared to a placebo control group (Khan et al. 2021).
Folate
In his book The Folate Fix (Frye 2025), Richard E Frye MD/PhD explains the role of folate metabolism on mitochondrial function, and the success of folate therapies for treating ASD. Because cerebral folate deficiencies (CFD) have been linked to ASD, administration of leucovorin, a prescription form of folate used to treat adverse side effects of some chemotherapy drugs in cancer patients, has successfully improved symptoms of autism in some child patients -- particularly those with disrupted folate receptors or metabolism.
Gastrointestinal (GI) microbiome therapies
Several studies have reported success in treating autism by altering the gut microbiome (Karhu et al. 2020) -- e.g., through fecal transplants or nutritional interventions. While improvements in severity of autism symptoms after modification of the gut microbiome have been reported in the scientific literature, I think speculation about the relationship between gut microbiome and the immune system are misplaced (e.g., Krajmalnik-Brown et al. 2015). What gets overlooked too often is the relationship between gut microbiome and mitochondria.
Perhaps it should be no surprise that the gut microbiome works in concert with mitochondria to govern metabolism. However, the interplay between the two has only recently revealed that mitochondrial function is modified by the distribution of free fatty acids produced in the gut. For example, propionic acids are short-chain FFA produced in a healthy human colon via fermentation of dietary fiber by gut microbiota. Artificial propionic acids are used as bacticides and fungicides to preserve grains. Medicinally, propionic acids represent the largest class of non-steroidal anti-inflammatory drugs (NSAID), including ibuprofen and naproxen, typically administered for pain relief and also known to increase risk of gastrointestinal lesions (Elliott et al. 1988). In modest concentrations, propionic acid helps modulate insulin sensitivity, may guard against obesity, and has beneficial anti-inflammatory properties (Chen et al. 2025). However, at larger concentrations propionic acid is a neurotoxin used to induce autism in animal models by disrupting glutathione metabolism and interfering with energy conversion in the brain (El-Ansary et al. 2012).
Butyrate is another FFA produced via fermentation by gut microbes. Unlike propionic acid, butyrate enhances mitochondrial function and likely has neuroprotective (rather than neurotoxic) properties. In cell lines drawn from boys with autism, butyrate improved markers of mitochondrial respiration (Rose et al. 2018). In mice, maternal treatment with sodium butyrate reduced autism-like traits in offspring (Christiano et al. 2020).
Typically, the healthiest individuals have the most diverse gut microbiomes, contributing to high metabolic flexibility and freedom from chronic illness (Zachos et al. 2024). By contrast, autistic individuals typically have low gut biodiversity and suffer from gastrointestinal (GI) disturbances. In children diagnosed with ASD, butyrate-producing microbiota are typically deficient (Liu et al. 2019), while propionic acid-producing microbiota are typically in excess (He et al. 2023). Because alterations in gut microbiome modify blood serum free fatty acid profiles (e.g., Rodríguez-Carrio et al. 2017), the success of therapies for autism that target the gut microbiome may be attributable to changes in FFA that favor butyrate versus propionic acids, thus promoting mitochondrial function.
Additional therapies targeting mitochondria
One of the best known advocates for mitochondrial/metabolic approaches to treating mental health is Dr. Chris Palmer, a practicing psychiatrist on the faculty at Harvard and author of the popular book Brain Energy (Palmer 2022). In his book, he describes the success he's observed treating serious mental health disorders like schizophrenia with a ketogenic diet.
Ketones are an intermediary product of fat metabolism. That is, when carbohydrate intake is low, the body will switch to burning fat, while maintaining adequate blood glucose levels through a process called gluconeogenesis that forms glucose from non-carbohydrate precursors (including amino acids). During fat metabolism, ketones are formed in liver mitochondria. Those ketones then travel throughout the bloodstream and can be used by mitochondria elsewhere in the body to form the ATP necessary to power all energetic processes including cognition, exercise, growth, and wound repair.
Recently, Palmer has turned his attention to the mitochondrial origins of autism. Presumably, he's curious about the potential of a ketogenic diet to improve brain function in ASD the same way that it treats other neurological disorders. His intuitions are likely well placed.
According to Brigham Young University cell biologist Benjamin Bikman, PhD, whenever ketones are present in the bloodstream, they will cross the blood-brain barrier and be preferentially metabolized in the brain. The brain cannot metabolize fats directly. It can only metabolize glucose or ketones, and Bikman says that the brain runs better on ketones. That description is consistent with Palmer pointing out that for at least a hundred years, medical doctors have understood that ketosis prevents seizures in epileptics -- suggesting that ketones have neuroprotective features and benefit brain metabolism.
A state of ketosis is also understood to benefit mitochondrial function more generally. Carbohydrate metabolism produced reactive oxygen species (ROS) in the mitochondria that result from stray electrons that fail to proceed to synthesis of ATP. These ROS are typically neutralized by melatonin and other anti-oxidants present in the mitochondria before they can do much damage. Moreover, their presence signals the body to undergo mechanisms to upgrade mitochondrial quality, including mitophagy (elimination of damaged mitochondria) and mitobiogenesis, which is production of new mitochondria. Thus, in limited quantities ROS represent a hormetic stressor that benefit mitochondrial function. However, when carbohydrate intake is too great, especially without a recovery period of fasting or ketosis, or melatonin levels are inadequate due to poor light hygiene or sleep disruptions, the excess ROS can damage mitochondrial DNA and result in chronic impairment of mitochondrial function. Thus, periods of ketosis are therapeutic in the sense that they permit mitochondrial recovery, increase metabolic flexibility, improve insulin sensitivity, and boost metabolism.
Ketosis as therapy for ASD
The potential for a ketogenic diet to treat autism has not been investigated until recently. There are no guidelines for clinicians seeking to prescribe ketosis for their patients seeking non-medical, non-behavioral therapies for ASD. This fact may discourage parents and other care providers from experimenting with a ketogenic diet, given that feeding disorders are common among children diagnosed with ASD, and compliance is a barrier to maintaining a ketogenic diet. For example, a child with sensory processing issues may exhibit narrow food preferences, like chicken nuggets and macaroni and cheese, that are incompatible with maintaining ketosis. Nevertheless, a number of clinical trials suggest that a ketogenic diet can reduce the severity of autism measures like CARS (Öztürk et al. 2025).
Cold Plunge Therapy for ASD
In the earliest days of Morozko, in 2019-2020 when we were building ice baths in the backyard, one of our first employees was an Arizona State University student with a background in sheet metal work. He was clever, creative, and dedicated to the task of building better ice baths. However, his employment was complicated both by his studies and his obligations as the parent of a young, non-verbal autistic child.
Some days, the only way for him to balance his competing responsibilities was to bring his child to work in the backyard. Fortunately, this yard had a swimming pool, like a lot of homes in Phoenix, and his son could spend hours happily swimming and splashing in the water, wearing his life jacket and playing with his pool toys. What impressed me about that was that the child didn't care how cold the water was.
Phoenix never gets below freezing, but during the winter the typical unheated swimming pool water can get down into the 50's Fahrenheit, which is enough to initiate the gasp reflex in most people. It's also cold enough to induce shivering in a small boy after a couple of hours of splashing around swimming and playing in the cold water. But the cold temperatures didn't bother this child. He would only reluctantly come out of the pool to eat, rest, or go home at the end of a shift.
It was several weeks after bringing his son to work at Morozko that I got a text message from our employee announcing that he had witnessed his son's first word. At the time, I thought that was a wonderful coincidence. It had never occurred to me that the cold swim sessions might confer neurological or metabolic benefits, but I'm beginning to consider that now.
I've heard from other parents that their autistic children love the water. In fact, hydrotherapy has been proven effective for reducing severity of symptoms in children diagnosed with ASD (e.g., Kalra et al. 2025). However, I've never seen a study of the effects of cold plunge therapy and autism. Hydrotherapy trials typically employ water temperatures close to thermoneutrality -- i.e., 90F (32C, e.g., Mills et al. 2020). These studies usually attribute benefits to the increased physical activity, positive social interactions, and the the soothing effects of hydrostatic pressure.
It is also possible that cold plunge therapy confers the additional benefit of mitochondrial biogenesis, stimulation of endogenous ketones, activation of brown fat, and increased secretion of neuroprotective factors like RMB-3 (a cold shock protein), Fibroblast Growth Factor (FGF-21), and Brain Derived Neuroprotective Factor (BDNF). I've written about the brain benefits of ice baths in several articles that are catalogued here https://www.morozkoforge.com/ice-bath-science/categories/ice-bath-brain. In summary, ice baths have been used to reverse cognitive decline, recover from traumatic brain injury (TBI), improve memory, and resolve major depression.
Given the proven therapeutic effects of ice baths that I wrote about in Ice Baths for Mitochondrial Therapy, it seems reasonable to ask:
Could cold plunge also treat autism by stimulating mitobiogenesis and correcting metabolic dysfunction?
In a subsequent article, I will introduce you to the Mother of an autistic child who swears that cold plunge therapy changed her son's life.
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About the Author
Thomas P Seager, PhD is an Associate Professor in the School of Sustainable Engineering at Arizona State University. Seager co-founded the Morozko Forge ice bath company and is an expert in the use of ice baths for building metabolic and psychological resilience.
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