How to treat autism via metabolism

Therapies that target mitochondria improve outcomes in ASD patients

Autism diagnosis in triplets

Nicole Rincon is the Mother of triplets, two of whom experienced neurological regression at the age of two and were diagnosed with autism spectrum disorder (ASD). Although they had been vaccinated, their diagnosis wasn’t an immediate response to a vaccine injury—like so many other children we hear about. Instead, their regression was more gradual. The first warning signs appeared at about eighteen months, with severe regression unfolding over the course of week at about two years old.

The pediatricians told Rincon there was nothing that could be done to improve her children’s neurological capacities and that they would likely depend on her care for the rest of their lives.

She wasn’t ready to accept that.

As a physician’s assistant (PA), Rincon was trained to read the medical literature, and what she found there contradicted her pediatricians advice. She discovered that therapies targeting metabolism could improve treatment outcomes in children with ASD.

Metabolism has two components

It should be clear that metabolism begins with the gut microbiome. Although saliva and stomach acid help to break food down into digestible parts, it is the microbioate in the gut that convert those parts into glucose and free fatty acids —i.e, the forms that can be absorbed into the bloodstream and converted to ATP (or heat) by the mitochondria. So there are two essential components to metabolism: 1) the gut microbiome, and 2) the mitochondria.

Ironically, neither of these components is driven by the DNA in your nucleus. As I wrote in The Genetic Self: Debunking DNA, 99% of the DNA on which your body depends doesn’t even belong to you, at least not in the sense that was derived from the sexual reproduction of your parents and housed in your cell nucleus. It is the DNA of the microbiota in your gut microbiome that govern digestion, and the mDNA in your mitochondria that govern conversion of metabolic substrates that result from digestion into the chemical energy that drives almost all processes within the body, including growth, injury repair, exercise, brain development, and even thought.

It’s probably no surprise that children diagnosed with ASD typically exhibit gut disturbances (Settani et al. 2021). That impacts the brain in three ways: 1) through the vagal nerves, which connect the brain and gut, 2) through production of neurotransmitters like serotonin, norepinephrine, that modulate brain function, and 3) production of short-chain fatty acids (FA) that fuel mitochondria.

Because mitochondria are metabnolically downstream of the gut, they can be adversely impacted by gut dysbiosis. For example, the distribution of FA is critical to mitochondrial function. The vast majority of those FA are either acetate, propionate, or butyrate. In children with ASD, levels of acetate and butyrate are typically low, and propionate elevated (Lui et al. 2019). That’s problematic, because in excess propionate is a neurotoxin. In fact, injections of propionate have been used to induce autism in laboratory animals. Thus, in when the gut microbiome is disturbed, the modified distribution of FA can inhibit healthy mitochondrial function.

During intense periods of neurological development—i.e., pregnancy and the first three years of life in particular—the mitochondria both provide the chemical energy necessary to power brain growth, and also steer the trajectory of that growth. That is, mitochondria guide the bursts of neuron development in the growing brain of the fetus and young children, and they dictate the pruning of neural connections to ensure neurotypical brain function.

As I wrote in What Causes Autism?, mitochondrial impairment can result in atypical neurological development in two ways: 1) underpowered neuron growth, and 2) improper pruning of neural connections. That’s why there is such a strong association between risk of autism in children under ten years old and mitochondrial dysfunction. So the gut microbiome and mitochondria work together, and the brain relies on them both. Healthy mitochondria, in particular, are essential to neurotypical brain development.

Metabolic therapies treat autism

Rincon’s reading motivated her to start her sons on an omega-3 supplement. She realized that healthy brain development relies on omega-3 fatty acids like DHA (docosahexaenoic acid, Cunnane & Stewart 2010). Moreover, omega-3’s promote healthy mitochondrial membranes.

This point about membranes deserves further explanation. All cell and organelle membranes are made up of phospholipids. The core building blocks of these phopholipids are fat molecules. That is, fats aren’t just used by the body for energy. They become incorporated into the tissues of the body in the form of these phospholipids.

When omega-3’s are abundant in the diet, they become the material basis for the phospholipid membranes—including the outer and inner mitochondrial membranes—and transport processes across these membranes built with omega-3 fats works well. However, when omega-3’s (like those found in seafood) are scarce, and omega-6 fats are abundant (like those found in soybean oil, cottonseed oil, corn oil, and all seed oils), then the phospholipid membranes must be built with these omega-6’s and their performance suffers.

Replacing the phospholipids constructed with omega-6 fats with new membranes constructed with omega-3 is typically a slow process that can require years. However, it took the Rincon children only a week to exhibit improvements in behavior after adding the omega-3 supplement. That suggests the omega-3 supplements were supporting neural development more directly.

Get rid of glyphosate

Next, Rincon switched her whole family to all organic foods. Urine testing revealed that her children had elevated levels of glyphosate in their bodies. Remember that glyphosate is the herbicide produced by Monsanto (later purchased by Bayer) to improve yields of Roundup Ready genetically modified corn and soybean crops. It has become ubiquitous in American agriculture, contaminating every food crop by traveling far beyond the borders of the fields on which it has been sprayed. Although it is considered non-toxic to humans—i.e., it only kills non-GMO plants—tests in laboratory animals have demonstrated that glyphosate is devastating to the gut microbiome (e.g., Lehman et al. 2023). Moreover, glyphosate alters intestinal permeability, mucus secretion, and interferes with lipid metabolism (da Cunha Ignácio et al. 2024).

In the case of her children, the elevated glyphosate levels in their urine might have helped explain the diarrhea that accompanied their neurological regression. While organic foods are not free of glyphosate entirely, by switching to all-organic Rincon was able to reduce their urine glyphosate levels by 94% (Shaw 2017). Their digestion and their ASD symptoms improved further.

Encouraged, Rincon went deeper into mitochondrial therapy.

Target mitochondria to recover neurological function

Nutritional Supplements that Support Mitochondria

Dietary interventions typically support mitochondrial function by providing the nutrients necessary to catalyze oxidative respiration inside the mitochondria. For example, in additiona to the omega-3’s, Rincon started her children on magnesium supplements, because magnesium is involved in hundreds of metabolic reactions and essential to the action of ATP. She added other supplements that either support, stimulate, or protect mitochondria so that her young children might leverage the neuroplasticity they still had to reorient the trajectory of their brain development. There are several supplements that are inexpensive, easy to tolerate without adverse effects, and simple to dose.

Here’s a partial list:

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).

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).

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.

Dihydrogen-pyrroloquinoline quinone (PQQ)

Oxidative respiration to produce ATP relies on a myriad of complex electron carriers that convert metabolic substrates like free fatty acids, glucose, and ketones, to carbon dioxide and water. Perhaps none of them is more effective and durable than PQQ. Animals that are fed diets deficient in PQQ typically develop abnormalities characteristic of mitochondrial dysfunction. In 2010, that observation motivated a group of scientists at University of California Davis to investigate the role of PQQ supplementation in mitochondrial function. They discovered that administering PQQ to mice does more than support mitochondrial function. PQQ stimulates mitobiogenesis (Chowanadisai et al. 2010).

Since that discovery, several clinical trials have applied PQQ supplementation to treat cognitive disorders associated with mitochondrial dysfunction, including Alzheimer's and Parkinson's (Xie et al. 2025). One recent review reported "treatment with PQQ may improve neuronal resilience and cell viability, ultimately delaying the progression of neurodegeneration" (Canovai & Williams 2025).

Because PQQ is not manufactured by the human body, but plays an indispensable role in mitochondrial and neural function, some medical scientists suggest that it should be recognized as a vitamin. As such, the FDA would be called upon to establish a recommended daily allowance (RDA) that could be published on food labels. As far as I can tell, there is little policy support for this suggestion. Nonetheless, the best food source of PQQ is dark chocolate, which contains 20-30 times the PQQ found in next-best sources like kiwi fruit, papaya, green tea, and parsley. This may help account for recent studies that show drinking cocoa and eating dark chocolate improves circulation and cardiovascular health.

There has never been a study investigating use of PQQ to treat autism. However, the fact that human breast milk is rich in PQQ suggests to me that it is an essential micronutrient for healthy neurological development. The fact that prenatal PQQ deficiency of PQQ results in reduced mitochondrial content emphasizes the importance for pregnant and nursing women to obtain sufficient PQQ from their diet (Jonscher et al. 2021). For older children who are eating solid foods, supplementing with PQQ or serving dark chocolate could help treat autism, support neurological development, improve mitochondrial function, without risk of adverse side effects.

Mitochondrial Stimulation

When the mitochondria have the nutritional resources they need, they can be stimulated to a higher level of function by exogenous factors. There are priarily three types of stimulants:

• foods, like hot chili peppers, and supplements like berberine,

• light, especially infrared light, and

• cold exposure.

The foods and supplements have little effect, compared to red light and cold, so I’ll focus on these last two.

Red light therapy for autism

Red light is at the extreme long end of the visible spectrum, while infrared light is invisible to the human eye. Together, they span wavelengths greater than 600nm and less than about 1300nm (~λ = 600–1300 nm). The most abundant source of infrared light is the sun. It is always present in direct sunlight, at all times of day, and dominates the solar spectrum during dawn and sunset, when the blue and ultraviolet wavelengths are filtered out by the atmosphere. However, it often surprises people to learn that near infrared (NIR) light is abundant in shady forests. Together with green, invisiable NIR wavelengths between 700-800nm dominate the spectrum beneath the forest canopy.

Infrared light will penetrate several centimeters into the skin to reach the mitochondria in subcutaneous fat, muscles, and other cells. Certain wavelengths can even reach the brain. Mitochondria are sensitive to infrared wavelengths. They absorb the light energy, which stimulates ATP production.

The use of light therapy on the brain is called transcranial photobiomodulation and it “has been reported to improve a range of behavioural measures, including social awareness, communication and motivation, and a reduction in restricted and repetitive behaviours” applied regularly for several weeks (Hamilton et al. 2022). The benefits can be long-lasting—up to twelve months.

Cold plunge therapy

Cold exposure is known to be a powerful stimulant for mitophagy and mitobiogenesis. In combination, these two processes improve the overall health and function of mitochondria by eliminating the damaged and replacing them with new. In one study of mice, researchers found that the extended cold exposure resulted "both degradation of mature mitochondria by mitophagy and synthesis of new mitochondria that led to a net increase in the total amount of mitochondria" (Yau et al. 2021). In this case, the increased mitochondrial content is likely in response to the demand for thermogenesis—i.e., the production of heat from glucose and fats to keep the body warm.

Despite the beneficial effects of cold on metabolism and mitochondria, there are no clinical trials investigating whether cold plunge therapy is effective for treating autism. Nonetheless, I’ve heard from several parents who tell me 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) and the parents I’ve spoken with agree. What’s remarkable about their stories is that their ASD children don’t seem to care whether the water is warm or cold. In several cases, parents have reported to me that their children would be playing in the water, shivering and teeth chattering, and yet still resist instructions to come out and dry off. Based upon anecdotes reported to me from parents who notice improvements in their children’s stereotypical behaviors after cold water swimming, I suspect that the mitochondrial stimulation provided by the cold is likely benefiting brain function.

Mitochondrial protection

Cold plunge for the brain

It is also possible that cold plunge therapy confers the additional benefit of 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.

Maintain good light hygiene & sleep patterns

One of the most important mitochondrial protection agents is melatonin. Known as the ancient anti-oxidant, melatonin donates electrons to the reactive oxygen species (ROS) that are the byproduct of oxidative respiration. That is, when electrons are moving down the mitochondrial transport chain to convert glucose and other metabolic substrates to ATP (or heat), inevitably some aberrant electrons get taken from, or wind up in, the wrong molecules. The result are highly reactive ROS.

A little bit of ROS can be a good thing, because it serves to signal mitobiogenesis. However, when mitochondria are overwhelmed (e.g., by a blood glucose spike) the excess ROS must be neutralized by melatonin or other anti-oxidants. If melatonin stores in the mitochondria are depleted by a lack of sleep, or lack of darkness at night, then those ROS will attack mDNA, damaging the mitochondria and resulting in poor function.

Melatonin is produced during sleep, and works best when days are bright and nights are dark. Therefore, good sleep and good light hygiene (e.g., no blue light at night) is essential for protecting mitochondria.

Ketosis

Chronic consumption of excess carbohydrates, without periods of ketosis or intermittent fasting, can be very damaging to mitochondria. Carbohydrates are converted to glucose in the gut. Simple carbohydrates like sugar and refined starches are converted most quickly. When that glucose enters the bloodstream, it typically causes a blood glucose spike that requires the pancrease to produce more insulin to help shuttle the glucose across cell membranes, out of the blood and into the cells where it can reach the mitochondria for procesing. During blood glucose spikes, the mitochondria are called upon to work fast and hard. The result will be excess ROS that damage mDNA.

As long as the mitochondria have a recovery period during which carbohydrate intake is low, they will suffer no permanent damage from the temporary blood glucose spike. That recovery period could be fasting, or it could be switching from carbs to a high-fat diet that switches the metabolism from carbohydrate burning to fat burning — a phenomenon known as metabolic flexibility. However, when consumption of excess carbohydrates is constant and chronic, the mitochondria will never recover. Instead, the degenerate further.

To protect damaged mitochondria from further insult, the body develops something called insulin resistance — which is when the cell membranes become less sensitive to the action of insulin, resisting the passage of glucose from the bloodstream into the cell. The result is that blood glucose spikes become higher and last longer. Eventually, Type 2 diabetes will result.

Insulin resistance is at the origins of every leading cause of death from chronic illness in the United States. It leads to metabolic dysfunction, Alzheimer’s, is associated with obesity and sleep apnea, and causes heart disease. Moreover, insulin resistance is characteristic of mental health disorders, including schizophrenia and epilepsy. I even knew one woman who suffered from anorexia, and yet was diagnosed with Type 2 diabetes because her scant diet consisted of little more than Coca-cola and aspirin. In other words, she was on an all-carbohydrate diet, despite eating fewer than 800 calories on most days.

A ketogenic diet has been proven effective for treating all of these mental health disorders, including epilepsy, schizophrenia, and anorexia. In general, the brain prefers to metabolize ketones whenever they are present in the bloodstream, oevr glucose. Perhaps that’s because ketones help protect the brain by allowing mitochondrial recovery. For example, when researchers in Hawaii administered three months of a gluten-free ketogenic diet to fifteen ASD-diagnosed children between the ages of two and seventeen, they observed improvements in the core behavioral features of autism. After six months, two-thirds of the particpants exhibited improvement in diagnostic scores.

Avoiding environmental toxins

The last prudent course of action to protect mitochondria is to avoid exposure to toxins that damage or disrupt metabolism. These include adjuvants in vaccines, such as aluminum salts and mercury, which are have no metabolic role in the body. Other toxic agents, including microplastics, mold and fungus, and even non-native electromagnetic frequencies (e.g., 5G wireless) can disrupt mitochondrial function.

Total load and threshold

Mitochondrial insults are likely additive. That is, a lack of sleep combined with exposure to mercury is worse than either one alone. Because the mitochondria are the source of physiological resilience, a small number of exposures or injuries are insufficient for symptoms of mitochondrial dysfunction to emerge. However, it is likely that each loading pushes mitochondria closer to a threshold below which ordinary brain functions will be lost. This threshold effect could explain why the brain might appear to be working normally for months or years, as the child meets neurological developmental targets, until a fever or some other immunological event further impairs brain function, a physiological threshold is crossed, and neurological capacities are lost.

When the child is young and the brain retains neuroplasticity, therapies that target metabolism — i.e., gut microbiome & mitochondria — can help the energy systems of the brain recover, and reorient the trajectory of neurodevelopment along more typical pathways.

If only the parents, who are of course the primary caregivers of young children diagnosed with ASD, are aware and able to act.

References

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