This guide is written for parents who are considering photobiomodulation as an adjunctive therapy to treat underlying symptoms of autism. It draws on the one randomized controlled trial in pediatric autism, on the broader photobiomodulation literature in traumatic brain injury and dementia, on the underlying mechanisms established across dozens of preclinical and human studies, and on clinical observations from practitioners applying this therapy. Some of the specific site-and-outcome pairings described here are clinical anecdotes supported by mechanistic reasoning rather than by dedicated trials. Photobiomodulation is exploratory and promising, with a favorable risk profile. This guide is not medical advice. Device use should be discussed with the child’s clinician.

Why This Approach Makes Sense to Consider

Photobiomodulation is emerging as a therapeutic modality for individuals with autism. It is relatively safe and easy to administer. Other treatment options involve changing diet or taking vitamins or other medications, which can be challenging for an individual who is a picky eater and also presents with significant hypersensitivity to their environment. Psychiatric medications in particular carry meaningful metabolic and physiological costs, discussed in detail in the Working Against the Child article (johnferreraphd.substack.com). This makes PBM a viable option that can be used as a complement to other therapies by improving cerebral blood flow and mitochondrial functioning.

Autism symptoms operate through physiological mechanisms that involve mitochondrial dysfunction, chronic inflammation, autonomic imbalance, and/or cortical network disruption. Photobiomodulation affects those mechanisms directly. It increases mitochondrial ATP production through the photodissociation of nitric oxide from cytochrome c oxidase, increases regional cerebral blood flow, reduces local inflammation, shifts microglial activity toward an anti-inflammatory state, and modulates cortical excitability and network connectivity. It has also been demonstrated to support the body’s detoxification pathways, as described in the next section.

These effects have been demonstrated in controlled human trials across multiple conditions. When applied to the prefrontal cortex, photobiomodulation improves attention, executive function, and emotional regulation in healthy adults (Barrett and Gonzalez-Lima, 2013) and in adults with chronic traumatic brain injury (Naeser et al., 2014). When combined with intranasal application, it improves cognition, sleep, and behavioral regulation in dementia (Saltmarche et al., 2017). When applied to selected brain areas in young children with autism, it produced statistically significant reductions in autism severity ratings and in irritability, hyperactivity, and stereotypic behavior in the one randomized controlled trial published to date (Fradkin et al., 2024).

Supporting the Body’s Detoxification Pathways

Beyond the direct effects on brain function, an emerging biomedical hypothesis holds that photobiomodulation supports the body’s ability to mobilize and excrete accumulated environmental toxins, particularly heavy metals such as aluminum, mercury, and lead that have been implicated in neurodevelopmental disorders. The mechanistic argument runs through the Nrf2 antioxidant response pathway. Photobiomodulation produces a transient burst of reactive oxygen species that activates Nrf2, the master transcriptional regulator of the antioxidant response, which in turn upregulates the transcription of glutamate-cysteine ligase, the rate-limiting enzyme in glutathione synthesis, along with glutathione S-transferases and other detoxification enzymes. Glutathione is the body’s principal intracellular chelator of heavy metals, forming conjugates that are actively transported out of cells through the MRP transporter system and eventually excreted through bile and urine. This pathway operates through documented biochemistry, and it is one of the primary mechanisms by which the body normally handles heavy metal exposure.

In a recent case report, Zaharakis and Bogner (2026) documented alterations in urinary metal excretion in a five-year-old boy with autism spectrum disorder and elevated baseline urinary aluminum, following the initiation of pulsed 660 nm photobiomodulation. Serial urine specimens analyzed by ICP-MS/MS (i.e., Inductively Coupled Plasma Tandem Mass Spectrometry) showed a temporal increase in urinary aluminum from baseline values of approximately 10 micrograms per gram of creatinine to a peak of 98 micrograms per gram after several days of treatment. This is a single-case observation rather than a controlled trial, but it represents the first published biomarker evidence in a pediatric autism population consistent with this detoxification mechanism. The 660 nm wavelength used in the Zaharakis/Bogner case is often paired with transcranial near-infrared (typically 810 to 1064 nanometers) for combined detoxification and deeper cortical effects. 660nm red and 810 to 1064nm infrared act through similar cellular mechanisms but have different tissue penetration profiles, with red light better suited to intranasal and surface applications and near-infrared better suited to reaching cortical structures through the skull.

Safety

Photobiomodulation has a favorable short-term safety profile. Fradkin (2024) reported no serious adverse events. Mild transient events during the first three weeks included overexcitement, headache, and irritability. These are consistent with a real neuromodulatory effect and typically resolve on their own.

On seizure risk specifically, the preclinical evidence indicates that transcranial photobiomodulation is anticonvulsant rather than proconvulsant. Multiple animal models of epilepsy show that PBM reduces seizure frequency, reduces epileptiform discharges, and protects the GABAergic interneurons that normally suppress seizure activity. Tsai (2022) demonstrated this with 808 nm PBM in peripubertal rats. A 2024 kainic acid model showed significant reductions in interictal epileptiform discharges with both 808 nm and 940 nm. A clinical trial of PBM for drug-resistant epilepsy is currently recruiting at Beth Israel Deaconess Medical Center. The mechanisms photobiomodulation engages are protective against seizures, not permissive of them.

Standard clinical caution applies. If your child has a history of seizures or diagnosed epilepsy, discuss any new therapy with the treating neurologist before starting. This is true of any intervention. If new seizure activity, persistent headache lasting more than two or three weeks, sleep disruption, or regression in previously acquired skills develops after starting photobiomodulation, stop treatment and consult the prescribing clinician.

Practical Guidance for Using This Therapy

Work with a provider who can specify the device parameters they are using. Photobiomodulation has a biphasic dose response, meaning too little produces no effect and too much can produce the opposite of the intended effect.

Decide in advance what outcomes you are watching for and how you will measure them. For sleep, use actigraphy (i.e. a wearable motion sensor) or a structured sleep diary. For behavior, use a standardized rating scale such as the Aberrant Behavior Checklist at baseline and every four weeks. For motor coordination, record videos of specific tasks at baseline that you can compare to later footage. Parent global impression alone is subject to the same expectancy effects that affect any home therapy, and objective outcomes protect you against both underestimating and overestimating what is happening.

Set a stopping point. If four to six weeks of consistent use has produced no measurable change on the outcomes you selected, reassess with your provider. Not every intervention works for every child, and continuing something that is not helping displaces attention from something that might.

Keep photobiomodulation in perspective as one tool in a broader plan. The children in the Fradkin trial who improved were also receiving behavioral therapies, speech therapy, and occupational therapy. Photobiomodulation was added to that foundation. It is not a substitute for the active therapies with their own evidence base, and it works better when paired with them.

Consider the biomedical foundation the child is on. Photobiomodulation targets mitochondrial function, inflammation, and autonomic balance. If nutritional cofactors for mitochondrial function are depleted, if underlying inflammation drivers are not being addressed, or if the gut is contributing to systemic inflammation without being treated, the light therapy is fighting against those headwinds. Families using photobiomodulation as part of a broader biomedical framework, including nutritional support, dietary interventions, and gut treatment where indicated, typically see more benefit than families using it in isolation.

Target Sites and Potential Benefits

The sections below walk through each target site: what it reaches, what it does, and what the evidence shows. The diagram on the following page shows all six sites for reference.

Figure 1. The six photobiomodulation target sites.

1. The Nose (Intranasal Application)

What it targets

The intranasal approach delivers light through the nostril to reach the highly vascularized nasal cavity, the olfactory nerve pathway, and blood circulating close to the surface. Light entering here bypasses the skull barrier and reaches limbic structures connected to the brain’s emotional regulation and sleep centers. Because the tissue between the nostril and the base of the brain is thin, this route delivers light more efficiently than transcranial application for reaching midline structures.

Reported benefits

Improved sleep onset. Deeper sleep. Calming effects when the child is dysregulated, often within minutes of a session. Mood stabilization over time. Reduced anxiety.

What the research shows

Saltmarche et al. (2017) demonstrated significant cognitive improvement in dementia patients who received combined transcranial and intranasal photobiomodulation, along with improvements in sleep quality, reduction of angry outbursts, and improved behavioral regulation. The intranasal delivery mechanism has been characterized across the broader photobiomodulation literature and works the same way regardless of the underlying condition, with studies now spanning dementia, mild cognitive impairment, traumatic brain injury, Parkinson’s disease, and healthy adults.

2. The Forehead (Prefrontal Cortex)

What it targets

The prefrontal cortex sits behind the forehead at a depth readily reachable by near-infrared light. This is the region most involved in executive function, emotional regulation, attention, and top-down control of reactive behavior. It is the most common and best-studied transcranial photobiomodulation target.

Reported benefits

Reduced frequency and intensity of meltdowns and emotional outbursts. Improved attention span. Better frustration tolerance. More consistent eye contact. Increased flexibility with routine changes.

What the research shows

This is the strongest evidence base for photobiomodulation at any brain target. Fradkin (2024) targeted prefrontal areas in the pediatric autism protocol and reported significant reductions in Aberrant Behavior Checklist Irritability and Hyperactivity subscales. Barrett and Gonzalez-Lima (2013) showed in a placebo-controlled study of healthy adults that transcranial infrared laser stimulation of the prefrontal cortex significantly improved sustained attention, working memory, and affective state. Naeser et al. (2014) documented significant cognitive improvement including executive function and verbal learning in adults with chronic traumatic brain injury after LED treatment targeting prefrontal and other cortical areas. The underlying mechanisms of improved mitochondrial function, increased ATP production, and increased cerebral blood flow in the prefrontal cortex are documented in Hamblin (2018).

Three converging lines of evidence across autism, healthy adults, and traumatic brain injury all target the same anatomical region and show improvements in the same functional domains. This is the site where a family is most likely to see meaningful change.

3. The Temples (Temporal Lobes)

What it targets

The temporal lobes sit under the temples and are involved in auditory processing, language comprehension, and sensory integration. They are also key nodes in the Default Mode Network, a system of interconnected brain regions whose disrupted functioning is a shared feature of autism, traumatic brain injury, and multiple other conditions. Applying light here targets both language and sensory processing directly and network-level regulation more broadly.

Reported benefits

Reduced sensory overload in loud or busy environments. Improved receptive language and following of instructions. Better auditory filtering. Reduced repetitive behaviors and stimming.

What the research shows

Fradkin (2024) included temporal targets in the pediatric autism protocol and reported significant reductions in stereotypic behaviors. Naeser et al. (2014) documented cognitive improvements in traumatic brain injury patients after LED application to cortical nodes of the Default Mode Network, including temporal areas. Since Default Mode Network dysfunction is present in both conditions, the mechanism of improvement transfers directly across them.

4. The Neck (Vagus Nerve and Carotid Arteries)

What it targets

The cervical vagus nerve lies close to the surface at the sides of the neck, at the level of the first and second cervical vertebrae along the front border of the sternocleidomastoid muscle. The carotid arteries run in this region as well, supplying blood to the brain. The vagus nerve is central to parasympathetic regulation, which controls the calming and digestive functions of the nervous system. Its stimulation produces documented effects on heart rate variability, anxiety, and gastrointestinal function.

Reported benefits

Lower baseline anxiety. Easier transitions between activities. Better tolerance of unexpected changes. Improvement in digestion and constipation through parasympathetic activation. Better stress recovery.

What the research shows

The vagus nerve as a target for anxiety and autonomic modulation has substantial evidence from transcutaneous vagal nerve stimulation studies across anxiety disorders, depression, PTSD, and functional gastrointestinal conditions. Photobiomodulation applied at this anatomical target engages the same nerve fibers and the same downstream pathways. The mechanism (increased mitochondrial function and blood flow at a site anatomically continuous with vagal fibers) is documented in Hamblin (2018) and produces effects consistent with what practitioners report.

5. The Abdomen (Gut and Enteric Nervous System)

What it targets

The abdomen contains the enteric nervous system, sometimes called the second brain, along with a large population of immune cells and the gut microbiome. Gastrointestinal symptoms, gut inflammation, and constipation are extremely common in children with severe autism and are often driving components of behavioral dysregulation. Applying light here reduces local inflammation, influences the gut-brain axis, and reduces the systemic inflammatory burden affecting brain function. The depth of penetration depends on body composition. In leaner children, light reaches deeper abdominal tissue, while in children with more subcutaneous fat the effect concentrates in more superficial anterior tissue. The anti-inflammatory effect applies wherever the light reaches, so meaningful benefit is available across body types even if the depth of reach differs.

Reported benefits

Reduced bloating and abdominal discomfort. Improvement in constipation. More regular bowel movements. Secondary improvements in behavior, focus, and mood attributed to reduced systemic inflammation. Reduction in what parents often describe as brain fog.

What the research shows

Photobiomodulation has well-documented local anti-inflammatory effects, reducing TNF-alpha, IL-1beta, and IL-6, and shifting immune cells toward an anti-inflammatory state. These effects are described across dozens of studies reviewed in Hamblin (2018). The anti-inflammatory mechanism applies to intestinal tissue that receives adequate light energy. Practitioners applying PBM to the abdomen report improvements in gastrointestinal symptoms consistent with this mechanism.

6. The Base of the Skull (Brainstem and Cerebellum)

What it targets

The base of the skull, where the head meets the neck, has thinner tissue coverage than most other cranial regions, making it more accessible to light than deeper structures approached through thicker bone. Practitioners apply light here to influence the brainstem, which regulates arousal and basic autonomic function, and the cerebellum, which coordinates motor function and participates in cognitive and sensory processing. The target is the suboccipital area at the base of the skull, which typically has thin or no hair coverage. Application should focus on skin contact or close proximity to skin at this suboccipital region. If hair is present at the treatment site, parting the hair for direct or close-to-skin application improves light delivery, though near-infrared penetrates thin hair reasonably well.

Reported benefits

Improved balance and coordination. Reduction in repetitive motor behaviors. Better handwriting. Improved regulation of arousal states, including calming for hyperaroused children and activation for underaroused ones.

What the research shows

Photobiomodulation’s core mechanisms of improved mitochondrial function, increased blood flow, and reduced neuroinflammation apply to brainstem and cerebellar tissue in the same way they apply to cortical tissue. Cerebellar dysfunction has been implicated in autism, and improvements in motor coordination follow from the same mechanisms that drive cortical improvements. This site has less dedicated PBM research than prefrontal or temporal targets, and the specific target-outcome connections rest more heavily on clinical observation and mechanistic reasoning than on trial data.

Suggested Session Protocol (Fradkin-style Ongoing Approach)

The published trials use different session structures depending on the device and target. The Fradkin (2024) autism trial used a whole-cortex headband for three to six minutes per session, twice per week for eight weeks. Naeser’s (2014) traumatic brain injury protocol applied a handheld LED cluster to eleven scalp locations for approximately ten minutes each, three times per week for six weeks. Saltmarche’s (2017) dementia protocol combined transcranial and intranasal application for a total session of twenty-five minutes, three times per week initially. For a multi-site protocol using a handheld device across the six sites described in this guide, the following synthesis of these parameters provides a reasonable starting point.

Session Structure

A single pass through the six sites in sequence, allocating time to each based on the depth of the target and the strength of the mechanism at that location, produces a total session length consistent with the published protocols. Apply light to the nose for two to three minutes, to the forehead over the prefrontal cortex for three to five minutes, to each temple for two to three minutes (four to six minutes total for bilateral application), to each side of the neck at the vagal region for one to two minutes (two to four minutes total), to the abdomen for three to five minutes, and to the base of the skull for two to three minutes. Total session time ranges from sixteen to twenty-six minutes.

Figure 2. Session protocol sequence and timing.

Frequency and Course Duration

Administer two to three sessions per week for a minimum of eight weeks before formal reassessment. This matches the frequency used across the Fradkin, Naeser, and Saltmarche protocols, and gives the mechanisms (mitochondrial upregulation, cerebral blood flow changes, anti-inflammatory shifts) time to produce cumulative measurable effects. Some families continue at the same frequency indefinitely if the child is responding; others reduce to one to two sessions per week as maintenance after an initial eight to twelve week course.

Ramp-Up During the First Weeks

The Fradkin protocol ramped session duration up over the first several weeks rather than starting at full dose. For the first one to two weeks, apply approximately one to two minutes per site (total session eight to twelve minutes), twice per week. This allows the family to assess tolerance and identify any early adverse responses, which are most likely to occur in the first three weeks and typically include transient overexcitement, headache, or irritability. From week three onward, increase to the full protocol times listed above.

What the Child Can Do During Sessions

The child does not need to sit quietly or focus during the session for the therapy to work. Photobiomodulation acts at the tissue level, on cytochrome c oxidase and downstream mitochondrial and cellular processes, and these effects do not depend on the child’s cognitive state or attention. Light applied to prefrontal cortex produces the same photoactivation of cytochrome c oxidase whether the child is watching a preferred show, playing on a tablet, or sitting still. For a child with a severe presentation, allowing a preferred screen, sensory activity, or favorite toy during the session is often the difference between a successful session and a struggle, and there is no physiological reason to withhold this. Two soft preferences worth considering: calmer content during the neck (vagal) portion of the session, since the goal at that site is parasympathetic activation (a net calming effect), and highly stimulating content can work against this. When working on these vagal sites specifically, a five to ten minute quiet period after the session before returning to screens or other stimulation is recommended, which gives the nervous system time to integrate the shift in state. Neither preference is required, but both may enhance the observable benefit.

Reassessment

If no measurable change on the outcomes selected at the start (sleep quality, behavioral ratings, motor tasks, or other pre-specified metrics) has occurred by week six to eight of consistent use, reassess with the provider before continuing. Not every person responds to photobiomodulation, and continued application at the same protocol without response is unlikely to be productive. Consider whether the parameters should change, whether a different site combination should be tried, whether it is time to introduce or adjust a dietary or supplement intervention that could work alongside the photobiomodulation, or whether the therapy is not the right fit for this child.

Alternative Protocol (Bogner Short-Course Approach)

A distinctly different protocol emerges from the Bogner case report on urinary aluminum excretion. Rather than an ongoing weekly schedule over months, the Bogner approach uses a short intensive course designed to support a specific biochemical outcome. The parameters as reported in the published case are three sessions per day, fifteen minutes each, for six consecutive days, totaling eighteen sessions. Light was applied circumferentially around the cranium including the frontal, bilateral temporal and parietal, and occipital regions, with continuous motion and no more than sixty seconds at any single point. The device used was the DCL-6R multi-diode red laser at 660 nanometers with dynamic frequency cycling at 9, 33, and 60 Hz.

Figure 3. Bogner protocol.

This protocol is not directly comparable to the Fradkin-style ongoing approach described above and should not be understood as a replacement for it. It was designed for a specific short-course biomarker outcome (urinary aluminum excretion) in a case report of a single child. The evidence base for what it accomplishes clinically over longer periods is not established. Families interested in this approach should discuss it with a provider familiar with the Bogner methodology, since the intensive daily frequency and the specific device parameters differ enough from the standard therapeutic protocols that they represent a distinct clinical strategy rather than a simple variation.

Some families and providers layer a short-course intensive protocol like the Bogner approach into a broader ongoing protocol, using the intensive block during a specific detoxification-focused window and returning to the two-to-three-sessions-per-week structure for maintenance. This layered approach is not tested in controlled research but reflects how clinicians integrating multiple frameworks are actually using the therapy in practice.

A Note on Device Parameters

Device outputs across consumer photobiomodulation devices vary widely. A less powerful device may require longer exposure per site to deliver comparable energy to the tissue, while a more powerful device (particularly Class IV lasers) may need shorter exposure to avoid overdosing at the upper end of the biphasic dose response. The child’s provider should confirm the device output before applying this or any other protocol. More research is needed to establish device-specific protocols with confidence, and the times above should be considered a reasonable starting framework rather than fixed rules.

To maximize how much of the applied light actually reaches the target tissue at any site with hair coverage, part the hair to allow direct or near-direct application to the scalp. Hair absorbs and scatters red and near-infrared light, and the attenuation is greatest with dense or dark hair. Make sure the hair is dry before applying the device, as water in wet hair further absorbs the therapeutic wavelengths.

Summary

Photobiomodulation applied to different areas of the head and body targets different physiological systems that operate through the same underlying mechanisms regardless of the diagnosis of the person receiving treatment. The forehead and temples have the strongest evidence base, with converging support from pediatric autism, healthy adult, and traumatic brain injury studies. The nose has direct evidence from dementia work with reported effects that match what families describe in autism. The neck engages a well-characterized parasympathetic target with strong evidence from electrical stimulation studies of the same anatomy. The abdomen applies well-established anti-inflammatory mechanisms to gastrointestinal tissue. The base of the skull is where clinical observation and mechanistic reasoning carry more weight than dedicated trial data. Across sites, an emerging body of evidence suggests photobiomodulation may also support the body’s detoxification pathways through the Nrf2 antioxidant response and glutathione-mediated metal clearance, with the Bogner case report providing preliminary biomarker evidence in a pediatric autism population.

For families facing a severe presentation and weighing the alternatives, photobiomodulation is a low-risk exploratory therapy with a real mechanism, some direct evidence, and substantial supporting evidence from adjacent conditions. It can be tried alongside behavioral therapies, biomedical support, and standard medical care, and the results can be tracked objectively.

References

Barrett, D. W., & Gonzalez-Lima, F. (2013). Transcranial infrared laser stimulation produces beneficial cognitive and emotional effects in humans. Neuroscience, 230, 13-23.

Fradkin, Y., De Taboada, L., Naeser, M., Saltmarche, A., Snyder, W., & Steingold, E. (2024). Transcranial photobiomodulation in children aged 2-6 years: a randomized sham-controlled clinical trial assessing safety, efficacy, and impact on autism spectrum disorder symptoms and brain electrophysiology. Frontiers in Neurology, 15, 1221193.

Hamblin, M. R. (2018). Mechanisms and mitochondrial redox signaling in photobiomodulation. Photochemistry and Photobiology, 94(2), 199-212.

Naeser, M. A., Zafonte, R., Krengel, M. H., Martin, P. I., Frazier, J., Hamblin, M. R., Knight, J. A., Meehan, W. P., & Baker, E. H. (2014). Significant improvements in cognitive performance post-transcranial, red/near-infrared light-emitting diode treatments in chronic, mild traumatic brain injury: open-protocol study. Journal of Neurotrauma, 31(11), 1008-1017.

Saltmarche, A. E., Naeser, M. A., Ho, K. F., Hamblin, M. R., & Lim, L. (2017). Significant Improvement in Cognition in Mild to Moderately Severe Dementia Cases Treated with Transcranial Plus Intranasal Photobiomodulation: Case Series Report. Photomedicine and Laser Surgery, 35(8), 432-441.

Zaharakis, A., & Bogner, C. (2026). Alterations in urinary metals following pulsed 660 nm photobiomodulation in a pediatric patient with autism spectrum disorder: a case report. Frontiers in Pediatrics, 14, 1819736.

If your child has been prescribed Risperdal, the brand name for risperidone, for meltdowns, aggression, or agitation, you are probably dealing with intense, disruptive behavior at home. The medication is meant to calm it, and often it does, at least at first. But many parents notice something else within a few months: the weight climbs, the appetite becomes bottomless, and the child begins to crave and demand carbohydrates and sweets in a way that feels almost compulsive. Families are frequently told this is just a side effect to manage, or worse, treated as though the child simply needs more discipline around food. The improvement in behavior is real and noticeable while the medication is on board, but over time the behaviors can intensify, and the answer offered is often a higher dose or another medication added on top.

That pattern is easier to see clearly through analogy. Think of industrial agriculture. A pesticide is applied to kill the weeds, and it works for a while, but the weeds adapt and grow resistant. The response is a stronger pesticide, or a second one layered on top, and then a third. After years of this repeated cycle what you are left with is soil stripped of its nutrients and crops loaded with the very chemicals that were supposed to help. Conventional psychiatric care often follows the same logic: suppress the symptom, and when it breaks through, suppress it harder. The biomedical approach works more like regenerative agriculture. Rather than attacking the weeds with ever-stronger chemicals, it nourishes the soil itself, using natural methods to restore balance. When the soil is healthy, the weeds lose their foothold, not because something killed them, but because the conditions that let them thrive are no longer there.

Over time, most psychiatric medications mask the problem without ever fixing it. In an earlier piece, The Diagnosis Was Supposed to Be for Life, I wrote about how the metabolic state of the brain is not a bystander in psychiatric and behavioral symptoms. A diet built on sugar and refined starch drives the trouble: blood sugar swings up and crashes down, cells grow resistant to insulin, and the cravings for sugar only intensify. This whole cycle is woven into mood instability, irritability, and dysregulation. That is the uncomfortable heart of this article: many of the medications prescribed for these very problems can deepen the metabolic dysfunction that helps fuel them. They can end up working against the child.

Risperdal is the clearest example of this, but it is far from the only one. Before we look at the medications one by one, though, it is worth being clear about what we should be aiming at in the first place.

The goal is a well child, not just a quiet one

No parent wants a child who is simply quieter. They want a child who is well. If a child is in genuine crisis, in real distress or real danger to themselves or others, there is nothing wrong with reaching for a medication to get through it. Sometimes it is the humane and necessary thing to do. But using a drug to weather a crisis does not mean a child has to stay on it for years. Too often the short-term rescue quietly becomes the long-term plan, and no one ever goes back to revisit it. Instead, the prescriber often piles on additional medications in an attempt to manage the behavior.

Back to the farming analogy. A medication like Risperdal is a way of cutting the weeds down at the surface. It clears them for a while, and the yard looks cleaner. But if the soil underneath stays depleted and out of balance, the weeds grow back, often with a vengeance, and you find yourself cutting them again and again. The alternative is to fix the soil. Tend the foundation, feed what is depleted, and the weeds lose their grip on their own.

That is why, if your child is on one of these medications, the foundational work becomes more important than ever, not less. Hold to the dietary principles, make the changes, add the supplements that genuinely help, do as much testing as you reasonably can, and work with the prescriber toward the goal of getting your child off the medication when it is safe to do so. The drug can buy time. It is the foundation that makes the time count.

First, a necessary warning: never stop or reduce these medications on your own

Because everything above points toward eventually reducing medication, this warning has to come first. Do not stop any of these medications, and do not lower a dose, abruptly or without your prescribing physician. This is especially true of the antipsychotics like Risperdal and Abilify, which have to be tapered slowly and under supervision. Stopping suddenly can cause withdrawal effects that include nausea and trouble sleeping, abnormal involuntary movements called withdrawal dyskinesia, and a rebound of irritability and agitation that can be worse than what you started with. That rebound matters enormously to understand, because a child who falls apart after a rushed or unsupervised taper looks like proof the drug was necessary, when in reality you may be seeing withdrawal rather than the return of the original problem.

The same principle that runs through all biomedical work applies here: slow and steady is the only pace that works. The goal is to build a stronger foundation underneath your child, put real supports in place, and then, if it makes sense, work with the prescriber to reduce a medication carefully and gradually.

Two ways a medication can push a child toward sugar

With that in mind, here is a plain guide to the common medications children are given for behavior, mood, and attention, and where each one sits on two things that matter enormously for a child: how it affects the body’s sensitivity to insulin, and how it affects appetite and craving.

Before any single drug, it helps to separate two different effects. The first is insulin resistance. When a medication makes muscle, liver, and fat less responsive to insulin, the body compensates by releasing more of it. Higher insulin drives sugar into storage, sometimes overshooting into a reactive low, and those swings are felt as hunger and craving, almost always for the fastest fuel available: sugar and starch. Here the craving is downstream of a metabolic problem the drug created.

The second is a direct drive to eat. Several of these medications act on the brain’s own hunger machinery to increase appetite, and specifically to increase carbohydrate seeking. This craving is not downstream of anything. It is the drug pressing the hunger button directly.

The medications that cause the most trouble are the ones that do both at once, and those come first.

Antipsychotics: risperidone (Risperdal) and aripiprazole (Abilify)

These are the drugs most often given to children for irritability, aggression, and agitation, particularly in autism, and they are the hardest case because they hit both levers at the same time.

Risperdal and Abilify impair insulin sensitivity directly. In a 2018 randomized trial published in JAMA Psychiatry, children who had never taken an antipsychotic before were followed after starting one. In just twelve weeks, using precise laboratory measurement rather than weight alone, their insulin sensitivity dropped and their body fat rose. Notably, this class can worsen insulin handling even without weight gain.

And they also drive appetite centrally. Risperidone reduces signaling at a receptor called the melanocortin-4 receptor, one of the brain’s main satiety brakes, the system that tells a child they are full. Blunt that brake and hunger climbs, with a particular pull toward carbohydrates. Abilify is often described as the more metabolically gentle of the two, and on average it is, but gentler is not the same as gentle, and it still carries a real metabolic cost in many children.

What this boils down to is that carbohydrate craving associated with psychiatric meds is driven by their pharmacology. The medication is pressing the hunger button directly, and then, through insulin resistance, setting up the blood-sugar swings that make the craving worse.

Stimulants: methylphenidate (Ritalin, Concerta) and lisdexamfetamine (Vyvanse)

The stimulants, the most commonly prescribed medications for childhood ADHD, which are also very commonly prescribed for improving attention and focus in autism, work differently than Risperdal and Abilify. Their main effect is appetite suppression. They reduce how much a child eats, including fat and carbohydrate, and there is no strong signal that they meaningfully harm insulin sensitivity over time. The visible effect in children is reduced appetite and, at times, slowed growth that a doctor should be watching.

The catch is the rebound, and it is one many parents notice before any clinician mentions it. Appetite suppression tracks the drug’s active window, and when the medication wears off, hunger does not simply return to normal. It often comes back with a vengeance: a small breakfast, a barely touched lunch during the medication’s peak, and then intense, sometimes voracious hunger in the late afternoon and evening, reaching for exactly the fast carbohydrate we are trying to limit, at the end of the day when everyone’s resolve is already spent. The stimulant does not erase the sugar problem so much as compress it into the evening.

This matters most in a very common situation: a child on both a stimulant and an antipsychotic like Risperdal. The two do not cancel out. Through the school day the stimulant suppresses appetite, and in the evening the stimulant’s rebound hunger and the antipsychotic’s unopposed drive toward carbohydrate arrive together, which is why the hours after dinner can become the hardest part of the day.

Alpha-2 agonists: clonidine (Kapvay, Catapres) and guanfacine (Intuniv, Tenex)

These blood-pressure-derived medicines are used widely in children for ADHD, for tics, and to help an agitated child settle and sleep. They are often paired with a stimulant, precisely to calm the activation the stimulant can cause in a child who then struggles to settle down or fall asleep. They are interesting because they can disturb the body’s handling of sugar without driving appetite. Clonidine, acting on the insulin-releasing cells of the pancreas, can blunt insulin release and nudge blood sugar upward, but it does this without the hunger drive of the antipsychotics. The net effect is mildly unfavorable for blood sugar management, but through a completely different and far less aggressive mechanism than the antipsychotics, and without the appetite and craving problem that makes those drugs so difficult to live with.

Worth knowing, and easy to get wrong: clonidine and guanfacine do not behave the same way here. The more selective agent, guanfacine, looks roughly neutral on the body’s handling of sugar rather than harmful. One older year-long study in diabetic patients even found it improved glucose tolerance, though the longest follow-up available, spanning several years, found no change either way. Among the medications on this list, guanfacine in particular is one of the gentler options on both blood sugar and appetite, which is worth keeping in mind if a metabolic concern is already in the picture.

Atomoxetine (Strattera)

The non-stimulant option for ADHD is roughly neutral on both counts. Atomoxetine tends to produce mild appetite suppression and modest weight loss rather than gain, with some early slowing of growth in children that usually recovers, and it carries no meaningful insulin-resistance signal. On the two variables that concern us here, it is one of the quieter medicines.

SSRIs: fluoxetine (Prozac), sertraline (Zoloft), escitalopram (Lexapro)

Children are prescribed these for anxiety, depression, and OCD, and as a group they are often treated as interchangeable. On metabolism they are not. Fluoxetine (Prozac) tends toward slight weight loss early on, though that effect fades over time, and sertraline (Zoloft) and escitalopram (Lexapro) are close to weight-neutral for most children. For the majority of kids, an SSRI is not the main obstacle to a steadier diet, though which one is chosen still matters.

The exception is paroxetine (Paxil). It is rarely used in children today, for reasons that go beyond metabolism, but it is worth naming because it is the clear metabolic outlier of the class. Paroxetine is the strongest histamine blocker among the SSRIs, and that histamine blockade drives appetite and carbohydrate craving while slightly lowering the metabolic rate. On this one axis it behaves less like its own drug class and more like an older tricyclic, which is the next group.

Tricyclics: doxepin and its relatives

Tricyclic antidepressants are used far less often in children than they once were, but they still appear, sometimes for bedwetting, for sleep, for migraine and pain, and occasionally for mood. They are among the most potent histamine blockers in all of psychiatry, and histamine blockade is a strong predictor of medication-driven weight gain and carbohydrate craving. For appetite, the effect is robust: these drugs make children want to eat, and they bias that wanting toward sweets and starch.

Their effect on insulin is more complicated and depends on dose and duration, so the fair summary for a parent is this: with the tricyclics, the reliable obstacle to steadying a child’s diet is the craving, driven by histamine blockade, more than a wholesale collapse in insulin sensitivity.

A path off the medication

If your child has been prescribed Risperdal, or any of these medications, and you do not want it to be a permanent arrangement, there is a way forward, and it does not begin at the pharmacy. It begins with the foundation. Search out hidden sources of physical discomfort that a child may not have the words to describe, and start making slow and steady modifications to diet and environment. If the budget allows, work with a functional medicine practitioner to rule out gut microbial imbalances like yeast overgrowth, which can quietly fuel the very carbohydrate and sugar cravings these medications are already driving. Make these changes for the whole family, not just the child, because everyone in the house stands to benefit, and a child is far more likely to accept a new way of eating when it is simply how the household works rather than a rule aimed at them.

Go slow and steady. Give each change a few weeks before you judge it, expect progress in small increments rather than dramatic turnarounds, and remember that small gains are real gains. A child sleeping longer, a constipation pattern that begins to resolve, a meltdown that does not escalate the way it used to, these are meaningful biological signals, not coincidences. Notice them, write them down, and let them guide the next conversation with the prescriber about whether the medication still needs to be where it is.

Many of these foundational principles are the subject of an earlier piece, Biomedical Approach on a Budget, which lays out where to start regardless of what a family can spend. In a follow-up to this article, I will take up the other half of the question directly: the specific options, dietary, nutritional, and behavioral, that can actually help with agitation itself, so that the medication has less work to do and, when applied proactively, may not be needed at all.

These medications may be part of your child’s story right now. They do not have to be the whole story, and they do not have to work against the very child they were meant to help.

Contents

The Leucovorin Clinical Trials

Why a Clinical Trial Can Only Ask One Question at a Time

Why Biomedical Trials Are So Hard in the First Place

Why Real Life Never Looks Like the Study

Acting Responsibly When You Cannot Wait

Back to Cofactors: Where Practice Goes Beyond the Trials

How Genetic Testing Can Inform the Cofactor Question

How Nutrient Testing Can Help

The Honest Bottom Line

References

The Leucovorin Clinical Trials

The clinical trials that built the evidence for leucovorin in autism, including Dr. Richard Frye’s 2018 language trial¹ and the placebo-controlled studies that followed, share a striking feature. Leucovorin was given essentially by itself, tested against a placebo, with nothing else added. No methyl-B12 alongside it. No magnesium. No carefully assembled stack of supporting nutrients. Just the drug, or a placebo, and a way to measure what happened.

This can look strange, even like an oversight, because in actual clinical practice leucovorin is very often not used alone. Experienced clinicians, Dr. Frye among them, frequently pair it with cofactors like methyl-B12 and pay close attention to a child’s broader nutritional status. So why would the studies leave out the very things practitioners consider important?

Why a Clinical Trial Can Only Ask One Question at a Time

To prove that a treatment works, a study has to isolate it. If researchers had given leucovorin together with B12, magnesium, and three other supplements, and the children improved, the result would have been uninterpretable. Was it the leucovorin? The B12? The combination? Some single ingredient doing all the work while the others did nothing? There would be no way to know. The only way to show that leucovorin itself has an effect is to make it the one thing that differs between the treatment group and the placebo group. Everything else has to be held still. When the leucovorin group improved and the placebo group did not, the clean design is what allows us to say the drug was responsible.

The trial answers a narrow question: does leucovorin, on its own, beat placebo? It does not answer the question a parent and clinician actually face in the room: how do we get the best, most tolerable response in this particular child? Those are different questions, and the second one is messier, more individual, and largely outside what a clean trial can capture.

Why Biomedical Trials Are So Hard in the First Place

The single-variable problem is only the beginning of the difficulty. Autism is not one condition with one cause; it is an enormously heterogeneous label covering children whose underlying biology varies tremendously. A treatment that produces dramatic gains in one subgroup, say, children with folate receptor antibodies, may do little in another. When you average across a mixed population, a real benefit concentrated in a subset can be diluted until it looks small or vanishes altogether. This is one reason trials in autism so often produce modest or conflicting results: the populations are not uniform, and the thing that helps one child is not the thing another child needs.

Children differ in their nutrient status, their genetics, their gut function, their diet, their other diagnoses, their medications, and their capacity to tolerate a given intervention. A protocol that is right for one child is wrong for the next. Trials, by design, look for the average effect across a group, which is enormously useful for establishing whether something works at all, but which cannot tell you what the child in front of you specifically requires. The average is not the individual.

And these studies are expensive, slow, and difficult to run. They take years to design, fund, enroll, and complete. Many promising questions will never be studied in a rigorous trial at all, not because they lack merit, but because no one will pay for it, the population is too hard to recruit, or the intervention cannot be patented and therefore attracts no commercial sponsor. If families waited for a definitive trial on every combination and sequence that might help their child, most would wait forever, because those trials are never going to be run.

Why Real Life Never Looks Like the Study

Here is the deeper mismatch. A trial changes one thing on purpose. Real life changes many things at once, and usually should.

A family who decides to address their child’s health rarely does one isolated thing. They start a supplement and also clean up the diet. They remove dairy and add a therapy and improve sleep and reduce a source of stress in the home, all in the same season. This is not sloppiness. It is what caring for a child actually looks like, and often it is the right thing to do. Waiting to fix a diet or add a supplement until a study has proven that this specific diet or supplement works in isolation would mean leaving a fixable problem in place for years. Children would become adolescents and then adults while waiting for the trial. Parents cannot, and should not, freeze their child’s life into a controlled experiment.

So families are placed in a genuinely difficult position. The evidence they can point to is built on narrow, single-variable studies, while the life they are living is broad and multi-factorial. They cannot wait for the perfect trial, because for most of the questions that matter to them, the perfect trial does not exist and never will. They have to act under uncertainty, using the best available reasoning, on a timeline set by their child’s development rather than by the pace of research.

Acting Responsibly When You Cannot Wait

Acting under uncertainty is reasonable, but it carries a responsibility to act carefully, because the same conditions that make waiting impractical, a heterogeneous condition, high hopes, and few definitive answers, also make it easy to be misled by coincidence, wishful thinking, or a change that would have happened anyway. The difference between responsible and reckless real-world experimentation is not whether you wait for a trial. It is whether you experiment with discipline.

Change one thing at a time when you are trying to learn from it. This is the single most valuable habit, and it is the home version of the trial’s own logic. If you start leucovorin, a new supplement, a dietary change, and a therapy all in the same week and your child improves or worsens, you will have no idea which one did it, and you may abandon something helpful or keep something harmful. When the goal is to read a specific intervention’s effect, introduce it on its own and give it time before adding the next thing.

Know the difference between the changes you are testing and the changes you are just making. Some things, cleaning up the diet, improving sleep, removing an environmental irritant, are broadly good and worth doing regardless, and you do not need to isolate them the way you would a drug trial. The discipline of one variable at a time matters most for the specific, uncertain interventions whose effect you are actually trying to judge. So it is best to keep diet and supplements stable when trialing leucovorin.

Decide in advance what you are watching for. Before starting something, write down what you expect to change and how you will know. Vague impressions are easily colored by hope, so it helps to name specific, observable targets and track them over time. Depending on the child, those might include language gains such as beginning to speak, using words or sentences more readily, or improvements in the give-and-take of conversation and other pragmatic speech; motor and self-care goals such as progress with toileting or other daily-living tasks; quality and duration of sleep; and the frequency and intensity of meltdowns or aggressive episodes. A baseline video, a simple daily or weekly log, and a short list of the two or three changes that would matter most to your family are what let you tell a real effect from wishful thinking, which is the very thing the placebo group exists to control for in a trial.

Be willing to stop. The willingness to conclude that something is not working, or is causing harm, and to discontinue it, is what separates a thoughtful trial-of-one from an ever-growing pile of interventions nobody is willing to question. Adding is easy. Subtracting is where good judgment shows. This is especially important when increasing the leucovorin dosage. If any adverse effects arise, go back down to the last dose that was tolerated without incident.

Work with someone who can see the whole picture. A knowledgeable clinician helps hold the line between reasonable individualized care and a runaway protocol, and can catch interactions and risks a parent reasonably would not see.

Back to Cofactors: Where Practice Goes Beyond the Trials

In clinical practice, Dr. Frye and other experienced clinicians frequently do not use leucovorin in isolation. They commonly pair it with cofactors, most often methyl-B12, and attend to the broader nutritional picture. This is not a contradiction of the research; it reflects the difference between proving a drug works and optimizing how it works in an individual. The rationale is biochemical: folate does not operate alone. It works in concert with B12 and other nutrients in the methylation and one-carbon pathways, so increasing folate with leucovorin increases demand on its partners. If one of those partners is in short supply, the pathway can bottleneck, which is one proposed reason a child may respond partially, stall, or become activated. Adding the rate-limiting cofactor is meant to let the folate the leucovorin provides actually be used.

Because both leucovorin and methyl-B12 can produce activation or behavioral changes when started, introducing them one at a time makes the response far easier to interpret. A reasonable and frequently used approach is to begin with methyl-B12 alone and hold it there for a period, often around two weeks, before adding leucovorin. This does two things. It establishes tolerability, so that if the child becomes hyperactive, irritable, or sleeps poorly, it is clear the B12 was responsible and the dose can be adjusted before another variable enters the picture. And it primes the cofactor side of the pathway, so that when leucovorin is added, the B12 needed to use that folate is already on board rather than being outpaced. The pairing of methylcobalamin and folinic acid has itself been studied directly.³ If methyl-B12 is well tolerated over that window, leucovorin is then introduced on top of it and titrated slowly in the usual way. This is simply the one variable at a time discipline applied to the pairing: two weeks is a common minimum, though the exact interval is a clinical judgment, and some families hold longer if they are still reading the B12 response. It is worth being clear that the trials did not establish that this sequence outperforms starting both together; the staggered start is a matter of clinical practice and interpretability, not a proven protocol.

On methyl-B12 dosing, most families use an oral or sublingual form for practical reasons, since it avoids injections. Common daily doses fall in the range of roughly 500 to 1,000 mcg, with smaller children often started around 500 mcg and older children at 1,000 mcg. An autism-specific study using a methylcobalamin syrup, for example, used 500 mcg daily, and standard pediatric sublingual protocols commonly use 500 mcg for younger children and 1,000 mcg for those around eight and older. The injectable form has the strongest trial evidence and the most established dosing,² but the oral and sublingual routes are more practical for daily use. Because B12 is water-soluble and excess is largely excreted, these doses carry a wide margin of safety, though more is not necessarily better, and the sublingual route is generally favored over swallowed tablets because it is absorbed directly and does not depend on gut absorption.⁵ Methylcobalamin is the active, methylated form most commonly chosen, though some families and clinicians prefer hydroxocobalamin when methyl sensitivity is a concern. As with everything else here, the specific form, dose, and schedule are best sorted by working with an experienced clinician. Some families opt instead for B12 injections, usually the subcutaneous methylcobalamin route used in the research, which bypass digestion entirely and deliver a consistent, fully absorbed dose. Injections require a prescription and a clinician’s instruction, and some children tolerate them well while others find the routine difficult, so the choice between an injection and an oral or sublingual form is a practical one that families and their clinician weigh together.

The practical consequence is that the research gives you a validated tool, while the surrounding cofactor strategy is a layer of clinical judgment built on top of it. That layer is less certain, more individualized, and legitimately where reasonable clinicians differ, which is precisely why families encounter so many different opinions about what to add and when.

How Genetic Testing Can Inform the Cofactor Question

Genetic testing does not tell you whether to use leucovorin, that decision rests on the folate receptor antibody test and the clinical picture, but it can help explain and anticipate how a child handles the folate and methylation pathways, which is useful for the cofactor layer.

MTHFR genotyping is the most familiar example. The common C677T and A1298C variants reduce the efficiency of the enzyme that converts folate into its active methyl form. A child who is compound heterozygous or homozygous may process folate less efficiently, which is part of the rationale some clinicians use for favoring already-reduced forms of folate and for paying closer attention to B12 status. It is worth stating plainly that MTHFR status is widely over-interpreted; it is common in the general population, it is not a diagnosis, and it does not by itself dictate treatment. It is one input, not a verdict.

It is also worth correcting a common oversimplification, that MTHFR simply means “take methylfolate and B12.” The genotype points to a few other cofactors just as legitimately. The most overlooked is riboflavin (vitamin B2). The MTHFR enzyme requires the active form of riboflavin (FAD) to function, and the common C677T variant produces an enzyme that holds onto that cofactor less tightly, which is part of why it works less efficiently. There is real evidence that riboflavin status influences the effect of the C677T variant on homocysteine, with the clearest benefit in people who carry two copies (677TT).⁴ Riboflavin is inexpensive and safe, and it is frequently missed in the rush toward methylfolate. Two pathway partners also belong in the picture: vitamin B6 (in its active P5P form) supports the separate route that clears homocysteine down the transsulfuration branch, and choline and betaine (TMG) feed an alternative, folate-independent way of recycling homocysteine that can partly compensate when the folate route is impaired. None of this replaces B12; it simply means that when MTHFR is flagged, riboflavin, B6, and choline are reasonable parts of the conversation rather than methylfolate alone.

Where possible, the most reliable way to supply these B vitamins is not another capsule but nutrient-dense food, which delivers them in balanced, modest amounts alongside the other cofactors the body uses to put them to work. This sidesteps much of the overstimulation that comes from stacking isolated, high-dose supplements, and it happens to cover the exact nutrients the MTHFR conversation raises. Riboflavin (B2) is concentrated in liver and other organ meats, eggs, and dairy, and in fish and lean meats. Vitamin B6 is abundant in fish, poultry, and organ meats, with useful amounts in potatoes and other starchy vegetables. Choline is found above all in egg yolks and liver, which are the two standout sources, along with meat and fish. Folate, in its natural food form rather than synthetic folic acid, is richest in leafy greens, legumes, and again liver. And B12 is essentially exclusive to animal foods: shellfish such as clams and oysters are the densest sources, followed by fish, red meat, eggs, and dairy. A striking pattern emerges from that list: liver and other organ meats appear again and again, because they are among the most nutrient-dense foods in existence and happen to be rich in nearly the entire B-complex at once.

That nutrient density is exactly why organ meats were prized in traditional diets, and why they are worth returning to, but they are a hard sell at most modern dinner tables. For families who want that nutrient density without cooking liver directly, a good desiccated organ meat supplement, typically freeze-dried grassfed beef liver in capsule form, is one of my preferred ways to bridge the gap. It delivers riboflavin, B6, B12, choline, and natural folate together in their whole-food matrix, without the taste or preparation, and it tends to be far gentler and better balanced than a synthetic high-dose B-complex. It is worth remembering that the folate in liver is natural food folate, not the synthetic folic acid this discussion cautions against, so it supports the child’s overall B-vitamin status without the receptor-blocking concern that fortified foods raise.

In addition to MTHFR, COMT genotyping is increasingly asked about. The COMT enzyme helps break down dopamine and other catecholamines, and it uses a methyl group to do so. The theory is that a child with the slower (“met/met”) variant, who clears these signaling molecules more slowly, may be more sensitive to methyl donors and more prone to activation, irritability, anxiety, or sleep disruption when given methyl-B12 or methylfolate. In practice, COMT status does not usually change whether a child is treated; at most it raises a flag to start low, go slow, and watch for overstimulation, which is prudent for every child regardless of genotype. The evidence that the genotype reliably predicts who reacts is modest, so it is best treated as a hint, not a rule.

One important and often-missed distinction sits underneath the COMT conversation: leucovorin (folinic acid) is not itself a methyl donor in the way that methylfolate (5-MTHF) is. Folinic acid enters the folate cycle a step upstream and does not carry the methyl group directly, which is part of why some children who react badly to methylfolate tolerate folinic acid more smoothly. A family worried about methyl sensitivity should know that the specific form of folate matters, and that a reaction to one is not automatically predicted by the other.

Taken together, genetic markers like MTHFR and COMT are best understood as a map of the terrain rather than a set of instructions. It is worth being clear on a common point of confusion: cofactor support is not reserved for children who carry these variants. The reason is that the core rationale is biochemical and applies broadly. Folate and B12 work together in the same pathway, so increasing folate raises demand on B12 in any child, which is why methyl-B12 is so commonly paired with leucovorin regardless of genotype. What the genetic markers add is refinement rather than permission. A relevant MTHFR result might lead a clinician to pay closer attention to riboflavin or to favor an already-reduced form of folate; a slow-COMT result might argue for starting lower and titrating more cautiously with methyl donors. But these are adjustments to how a child is supported, not a gate that decides whether support is warranted. A child with unremarkable genetics may still benefit from a cofactor, and a child with a concerning-looking variant who is thriving may need nothing added. As with everything else here, the genotype helps a clinician anticipate where a particular child might bottleneck or overshoot, but it is supporting information layered onto the clinical response, not a substitute for it.

How Nutrient Testing Can Help

If genetic testing describes how a child is built to process these pathways, nutrient testing describes where the child actually stands right now, and it is arguably the more practically useful of the two for the cofactor question. The central principle is one that experienced families learn, sometimes the hard way: supplementing with a high dose of a single nutrient can unmask or even worsen a deficiency in another, because these nutrients compete, depend on one another, and share pathways. Increasing folate while another nutrient is quietly deficient is a common reason a promising start stalls.

This is the rationale for characterizing the broader nutrient picture before and during treatment rather than adding single nutrients blindly. Depending on the child, relevant testing may include B12 and its functional markers (methylmalonic acid and homocysteine), folate status, and a wider panel of vitamins, minerals, and other nutrients. Nutrients that repeatedly matter in this population include B12, magnesium, zinc, iron and ferritin, and copper, several of which interact directly with folate and with one another. Identifying and correcting a limiting deficiency can be what allows the leucovorin to work as intended, and it can prevent the frustrating pattern of chasing one nutrient while inadvertently creating a shortfall elsewhere.

A practical question is how to get this testing covered. The encouraging news is that the individual tests that matter most here are standard, widely available labs, not exotic ones. B12, folate, methylmalonic acid, homocysteine, vitamin D, ferritin and iron studies, zinc, and copper are all ordinary blood tests with established billing codes, and insurance generally covers them when a physician orders them and ties them to a relevant diagnosis or symptom rather than to routine screening. The key is that coverage follows medical necessity: a test ordered because a child has a documented symptom, a known deficiency, or a condition that raises the concern is far more likely to be paid than the same test ordered as part of a general wellness panel.

In practice, getting these tests covered by insurance means a few things for families. Ask that tests be ordered individually or as a small, targeted group aimed at a specific concern, because that is how they are covered. It is worth knowing the important exception: broad “micronutrient” or intracellular panels that bundle dozens of vitamins, minerals, and metabolic markers into one test are typically classified as not medically necessary and are usually not covered, so those often come with an out-of-pocket cost. A focused set of standard tests ordered for a documented reason will usually be covered and will answer many important questions. When in doubt, your clinician’s office or the lab can tell you in advance which codes are covered under your plan.

The Honest Bottom Line

Rigorous trials and real-world care are not enemies, but they are not the same thing, and it helps enormously to understand what each can and cannot do. A clean study can tell you that a treatment genuinely works, which is precious and hard-won information. What it cannot tell you is exactly how to weave that treatment into the complicated, individual, time-sensitive life of one particular child. That translation is the work of clinical judgment, done in partnership with families who cannot put their child’s development on hold while the research world slowly catches up.

The goal, then, is not to choose between evidence and action. It is to act on the best evidence available while applying the same discipline a good trial would use: changing one thing at a time, watching with clear eyes, setting defined expectations, and having the humility to stop when something is not working. Done that way, care stays anchored to the child in front of you rather than to the averages in a study, which is exactly where it belongs.

References

1. Frye RE, Slattery J, Delhey L, et al. Folinic acid improves verbal communication in children with autism and language impairment: a randomized double-blind placebo-controlled trial. Molecular Psychiatry. 2018;23(2):247-256.

2. Hendren RL, James SJ, Widjaja F, et al. Randomized, placebo-controlled trial of methyl B12 for children with autism. Journal of Child and Adolescent Psychopharmacology. 2016;26(9):774-783.

3. James SJ, Melnyk S, Fuchs G, et al. Efficacy of methylcobalamin and folinic acid treatment on glutathione redox status in children with autism. American Journal of Clinical Nutrition. 2009;89(1):425-430.

4. McNulty H, Dowey LRC, Strain JJ, et al. Riboflavin lowers homocysteine in individuals homozygous for the MTHFR 677C-to-T polymorphism. Circulation. 2006;113(1):74-80.

5. Rossignol DA, Frye RE. The effectiveness of cobalamin (B12) treatment for autism spectrum disorder: a systematic review and meta-analysis. Journal of Personalized Medicine. 2021;11(8):784.

Contents

Introduction

Start With Testing, More than just the FRAT

Dosing: Reaching an Active Dose, Slowly

Adverse Reactions

Cofactors, Additional Supplementation

A Note on Folic Acid

Dairy and the Casein-Free Question

Conclusion

Introduction

Among parents of children with autism, few interventions have generated as much excitement in recent years as leucovorin calcium, commonly known as folinic acid. There is a growing research literature on the treatment, but what has driven that interest are striking and recurring observations: children who had been minimally verbal or nonverbal starting to talk.

Alongside these language gains, parents describe a broader set of changes: steadier eye contact, less toe-walking, more initiation of play with peers, improved attention, and fewer repetitive behaviors. Families talk about children becoming more socially outgoing, transitioning into mainstream classrooms, and taking up hobbies once thought out of reach, from music lessons and swimming to Special Olympics. Running through these accounts is a renewed sense of optimism about independence and possibility, a feeling among parents that meaningful progress is within reach for the first time.

In interviews with the New York Post tied to Dr. Richard Frye’s research, families have described exactly this:

One family recounted that their nonverbal three-year-old spoke his first words just days after starting the drug. Another described a son moving from one or two words to full sentences over roughly six months, and later telling his mother that he had understood the world around him for years but had not been able to get the words out. A third family said their son regained full sentences within about two weeks after a speech disorder had stripped away his earlier vocabulary, went on to skip a grade, and one day told his father he loved him without the echo-like speech pattern he had had before, a moment the father described as bringing him to tears.

What makes these accounts compelling is not any single story but how many of them there are, and how consistently they echo one another. And it makes sense because there is a biological rationale and hard science that backs these claims.

The explanation for why folinic acid might produce these changes centers on folate receptor autoantibodies, which can block the transport of folate into the brain and may contribute to a subset of autism and neurodevelopmental cases. In this model, folinic acid works by bypassing that blocked pathway and restoring folate availability to the central nervous system. The idea is intuitive: if a specific, identifiable roadblock is keeping folate out of the brain, then a form of folate that can get around it might allow development to move forward in ways that had previously stalled. The best way to tell whether leucovorin or folinic acid is likely to help is to begin with a proper workup.

Start With Testing, More than just the FRAT

Leucovorin (folinic acid) is not a universal fix, and it does not help every child who tries it. Response tends to cluster in specific subgroups, particularly children who test positive for folate receptor antibodies, so the most reliable starting point is a proper workup rather than an open-ended trial. A reasonable baseline panel includes a folate receptor antibody test, MTHFR genotyping, methylmalonic acid, homocysteine, and red-cell folate, since together they help distinguish a transport problem from a conversion problem from a B12 problem. For a fuller walkthrough of how that testing sequence is meant to guide the decision, see this article: Leucovorin: From Guesswork to Workup.

Dosing: Reaching an Active Dose, Slowly

Many families report some degree of trial and error even after a complete workup, since individual response, tolerance, and the right dose still have to be worked out in practice. Reaching the right dose is a process, and how you start is as important as where you end up.

Getting to an active, effective dose matters, since a dose that is too low can look like leucovorin does not work when the real issue is under-dosing. At the same time, jumping to a full or high dose right away is one of the more common reasons families report a rough start, so a gradual titration over several weeks, watching for both benefit and side effects along the way, tends to go better than an abrupt increase.

Dose and duration work together, which is why a fair trial takes time. The clinical trials ran twelve to twenty-four weeks, and clinicians often note that fuller effects can take one to two years of sustained use, so an adequate trial is measured in months, with roughly twelve weeks at an effective dose before drawing conclusions. Under-dosing and stopping too soon both tend to masquerade as a treatment that simply did not work.

The published research offers a clear reference point. The randomized trials and Dr. Frye’s case series generally used a target of 2 mg per kilogram of body weight per day, up to a maximum of 50 mg per day, given in two divided doses, with meta-analyses describing an effective range of roughly 0.5 to 2 mg per kilogram per day. In practical terms, a parent can estimate the target by converting the child’s weight to kilograms (pounds divided by 2.2) and multiplying by 2, then capping the result at 50 mg. A 30-pound toddler, for example, weighs about 13.6 kg and would target roughly 27 mg per day. A 50-pound child weighs about 22.7 kg and targets close to 45 mg per day. A 100-pound child weighs about 45 kg, which at 2 mg per kilogram would calculate to about 90 mg per day, so that child reaches the 50 mg daily ceiling used in the studies rather than the full weight-based figure.

Those figures are the destination, not the starting line. In the trials, children were generally started at the full target dose, but that abrupt start is precisely the pattern many families in the parent community have learned to avoid, since jumping straight to target is one of the more common reasons for a rough beginning. A gentler approach that has become common in practice is to begin well below target, often at a single 5 mg dose in the morning, or even 2.5 mg for a small or reaction-prone child, and to hold that level for one to two weeks while watching for both benefit and the adverse reactions described below. If it is well tolerated, the dose is increased gradually, adding the second daily dose and climbing toward the 2 mg per kilogram target over several weeks rather than days. Since leucovorin can be activating and interfere with sleep, the larger dose, or the single daily dose, is typically taken in the morning.

Starting with OTC Forms of Folinic Acid

A common question is how over-the-counter folinic acid compares. Here the details matter, because products vary widely. Many OTC folinic acid supplements are dosed in micrograms, a thousandfold smaller unit than the milligrams used for prescription leucovorin. Researched Elements folinic acid powder, for instance, provides 5 mg (5,000 mcg) per scoop. A 50-pound child targets roughly 45 mg per day, which would take about nine scoops daily, split into two doses. A child of about 55 pounds or more reaches the 50 mg daily maximum, or ten scoops a day.

The meaningful differences with these higher-dose products are therefore not potency but regulation and precision: prescription leucovorin is FDA-regulated for quality and comes in defined tablet strengths, whereas an OTC powder relies on the family measuring the dose accurately and trusting the manufacturer’s quality control. For a child who calculates to a 50 mg daily target, reaching that dose with a 5 mg-per-scoop powder also means measuring and administering a considerably larger daily volume than swallowing tablets. None of this makes the OTC route inherently unworkable, but the unit on the label, mcg versus mg, deserves close attention, since confusing the two is an easy and consequential mistake.

Adverse Reactions

The reason to move slowly is that the body tends to push back when a dose rises too quickly, and that pushback shows up in a fairly consistent set of adverse reactions. The most frequently reported include:

• Increased hyperactivity or overstimulation

• Irritability, agitation, or aggression

• Sleep disruption

• Gastrointestinal upset

• Vocal tics or head-shaking, less common but reported

The most useful way to understand these reactions is that they are usually dose-related rather than a sign that the child cannot take leucovorin at all. In many cases they trace back to adding too much, too fast, and they tend to appear or intensify shortly after a dose is started or increased. This pattern is itself informative: a reaction that shows up within days of a step up in dose, and that is proportional to that increase, is behaving like a dose effect rather than an intolerance.

Whether these reactions fade with patience depends on which kind a family is dealing with, and the distinction matters. Mild, early effects such as a few days of increased activity, some irritability, or looser stools often settle on their own as the child adjusts to a new dose, provided the dose is not pushed higher in the meantime. Holding steady at the current level for a week or two, rather than continuing to climb, gives the body a chance to accommodate, and many families find that a reaction present in the first several days is gone by the end of the second week. This is one of the practical arguments for slow titration: it keeps any given increase small enough that the adjustment period stays manageable.

A more pronounced or persistent reaction is a different signal. Marked aggression, significant sleep loss, a clear behavioral regression, or new tics that do not ease within a week or two are generally read as a sign that the dose has climbed past what the child currently tolerates, not as something to push through. The usual response is not to stop outright but to step back down to the last dose the child handled well, hold there, and let things settle before considering a slower climb from that point. In other words, patience helps with the small stuff, while the larger reactions call for reducing the dose rather than waiting them out.

Cofactors, Folic Acid, and Dairy

Several factors outside the dose itself also shape tolerability and response, and each is taken up in the sections that follow. The presence or absence of supporting cofactors, most commonly methyl-B12, often makes a meaningful difference in how smoothly leucovorin is tolerated. Continued exposure to synthetic folic acid can work against the treatment and is worth reducing. And for some children, dairy plays a role as well, since certain proteins in cow’s milk may sustain the very antibodies leucovorin is meant to work around. Each of these deserves a closer look, starting with the cofactors, which can matter nearly as much as the leucovorin itself.

Cofactors, Additional Supplementation

In principle, the best way to decide which cofactor a child actually needs is testing, particularly MTHFR genotyping paired with functional markers like methylmalonic acid and homocysteine, which gives a more grounded answer than guessing. In practice, though, many families are working without that full picture and rely on a shorter list of cofactors that other parents and clinicians have found helpful:

• Methyl-B12 or hydroxocobalamin, by injection or sublingual

• Magnesium

• Phosphatidylserine

• Other B-vitamins

Of these, methyl-B12 is the one that comes up most consistently, and there is a logic to it. Folate and B12 work together in the same methylation pathway, so pushing folate with leucovorin while B12 is relatively low can leave the pathway unbalanced, which is one proposed reason some children become more activated or irritable when they start. Adding B12 is often described as smoothing out that response. Many families introduce it at or near the start of the leucovorin trial for this reason, whether as a sublingual form or, in some protocols, as injections, with the specific form and dose worked out with the prescribing clinician.

Magnesium is generally the first of the calming additions to try. It is an essential mineral that many children are short on to begin with, so supplementing it can correct a real deficiency rather than simply layering on another compound, and it is inexpensive, familiar, and well tolerated. Its main side effect at higher doses, looser stools, is both self-limiting and often welcome in children prone to constipation, which is common in this population, so a single change can sometimes ease activation, support sleep, and help with bowel regularity at once. Because it addresses the same early complaints that lead families to consider other calming options, chiefly overstimulation and disrupted sleep, but with a simpler profile and a longer track record, the usual sequence is to add magnesium before reaching for anything further. The form matters here: magnesium glycinate is typically preferred when the goal is calming and sleep, since it is well absorbed and gentle on the stomach, whereas citrate and oxide are more laxative and oxide in particular is poorly absorbed. It is usually given later in the day or toward evening, where its calming quality supports the wind-down toward sleep.

Phosphatidylserine occupies a different place on this list. It is a phospholipid, a fatty compound concentrated in cell membranes and especially abundant in the brain, where it plays a role in how neurons signal to one another. As a supplement it has a longstanding reputation for supporting attention and for taking the edge off stress reactivity, and it has been studied on its own for attention and hyperactivity in children, with modest and not fully settled results. In the context of leucovorin, families and clinicians tend to reach for it not because it acts on the folate pathway, which it does not, but for that calming, regulating quality. When leucovorin produces activation, irritability, or overstimulation in the early weeks, phosphatidylserine is sometimes added to smooth that reactivity, and like magnesium it is often given later in the day. It is best thought of as a supportive, symptom-smoothing addition rather than a core cofactor: unlike methyl-B12, it is not correcting anything specific to the folate machinery, and unlike magnesium it is neither inexpensive nor addressing a common underlying deficiency. For that reason it usually comes later in the sequence, tried only if optimizing dose timing, magnesium, and B12 has not settled things enough, and added on its own so its effect can be read clearly.

The other B-vitamins on this list deserve a slightly different emphasis, because they are often better obtained from food than from another bottle. Where supplemental B-vitamins are easy to overdo, whole foods deliver them in balanced, modest amounts alongside the cofactors the body uses to put them to work, which sidesteps much of the overstimulation that comes from stacking isolated, high-dose supplements. Animal foods are the richest and most bioavailable sources: seafood, particularly shellfish like clams and oysters and cold-water fish like salmon and sardines, supplies B12 and several others in abundance, while red meat is a strong source of B12, B6, niacin, and riboflavin in a form the body absorbs readily. For families who want that nutrient density without cooking organ meats directly, which are the single richest source of the B-complex but a hard sell at most dinner tables, a good desiccated organ meat supplement, typically freeze-dried grassfed beef liver in capsule form, is one of my preferred ways to bridge the gap. It offers much of what a serving of liver would, delivering B12, riboflavin, B6, and folate in their natural food matrix without the taste or preparation, and it tends to be far gentler and better balanced than a synthetic high-dose B-complex. Worth noting, too, is that the folate in liver is natural food folate, not the synthetic folic acid discussed later in this guide, so it supports the child’s overall B-vitamin status without the receptor-blocking concern that fortified foods raise.

A few practical principles tie these together and tend to make cofactor use more productive and less confusing. The first is to change one variable at a time. When leucovorin, a B12 form, magnesium, and a B-complex are all begun in the same week, a good or bad response cannot be traced to any one of them, and a genuinely helpful addition can be abandoned because it happened to coincide with an unrelated rough patch. Introducing one item, holding it long enough to read the response, and only then considering the next keeps the picture interpretable.

The second is that timing can be used deliberately. Calming additions such as magnesium are generally kept to the later part of the day, while the main leucovorin dose and any more activating supplements are given in the morning. Small adjustments of this kind often do more for day-to-day tolerability than adding yet another product.

The third, and the caution that comes up most often, is restraint. Stacking too many methyl-donor or B-vitamin supplements at once tends to cause more problems than it solves, producing exactly the overstimulation families are trying to avoid and making it impossible to tell what is helping. The more effective pattern is a short, deliberate list rather than a long one: leucovorin, usually methyl-B12, and perhaps magnesium for sleep and calming, with anything further added only for a specific reason and always one at a time. As with the leucovorin itself, the forms, doses, and combinations are best chosen with the prescribing physician rather than assembled independently, since interactions and individual needs vary considerably from child to child.

A Note on Folic Acid

Just as important as what a family adds is what they may need to remove. Folic acid is not the same molecule as folinic acid (leucovorin), and the two are generally not interchangeable in this context. Folinic acid is a reduced, active form of the vitamin that the body can use directly, whereas folic acid is the synthetic form added to fortified foods and most supplements. The distinction matters because synthetic folic acid competes for the same folate receptor that is already compromised in children with folate receptor antibodies. Rather than helping, it can occupy that transport machinery without effectively delivering usable folate to the brain, effectively working against the leucovorin a family is carefully dosing.

For that reason, families managing folate receptor antibody issues are often advised to reduce or eliminate synthetic folic acid rather than simply adding leucovorin on top of it. This is also why the natural folate found in whole foods, the kind concentrated in leafy greens, is treated differently from the synthetic version: the concern is specifically with fortification, not with folate itself.

In practical terms, avoiding folic acid is mostly a matter of steering away from processed and enriched grain products, since that is where the synthetic form is concentrated. A diet built around whole, unprocessed foods sidesteps most of it by default. When packaged foods are part of the picture, the single most useful habit is reading the ingredients list and watching for the word “enriched,” as in “enriched wheat flour,” which is the standard signal that synthetic vitamins including folic acid have been added. The usual sources to check are conventional bread, pasta, breakfast cereal, white rice, cornmeal and grits, and many snack and granola bars.

A few shortcuts make this easier at the store. Certified organic and gluten-free products are generally exempt from mandatory fortification, so an organic flour, an organic or gluten-free bread, or brown rice in place of enriched white rice will usually skip the folic acid its conventional counterpart carries. Traditionally fermented sourdough made from unfortified flour is another good option, and it often improves the availability of the natural folate already present in the grain. None of these categories is an absolute guarantee, since a manufacturer can choose to add folic acid voluntarily, so the label remains the final word: if “folic acid” or “enriched” flour appears in the ingredients, the product carries it, and if neither does, it generally does not. Over time, most families find that a handful of reliable brands and staples become the default, and the label-checking becomes quick rather than a chore.

Dairy and the Casein-Free Question

A related question many parents ask is whether leucovorin works better alongside a dairy-free, or more specifically casein-free, diet. The rationale traces back to Dr. Richard Frye’s research on folate receptor autoantibodies, which has pointed to bovine milk proteins as a possible trigger or amplifier of these antibodies in some children; his work has generally recommended that families with confirmed folate receptor antibody positivity consider reducing or removing dairy alongside starting leucovorin, since continued exposure may blunt the medication’s effectiveness. Parent communities echo this idea, with some describing a strict casein-free diet as something they were told mattered for the treatment to work as intended, though these accounts are anecdotal rather than controlled clinical evidence.

For families weighing the question, a structured dairy-free trial is often the most informative way to answer it, since the effect of removing dairy is difficult to predict and easy to test. A reasonable approach is to remove all sources of dairy and casein completely, not merely reduce them, for a defined window of about three to four weeks, and then to watch for changes not only in the areas leucovorin targets but across the board. The reason to commit fully rather than cut back partway is that casein is the specific protein of interest, and lingering exposure from small amounts can muddy the result, leaving a family unsure whether they gave the trial a fair test. A trial like this is low-risk, reversible, and diagnostic in a way that reasoning alone is not: if a few weeks off dairy bring no change, the family has an answer and can reintroduce it, and if they do notice gains, they have learned something a lab test could not have told them as directly. This kind of trial is especially worth considering when digestive issues are already in the picture, since dairy is a common driver of constipation, diarrhea, reflux, and the congestion and discomfort that often accompany them, or when there is a family history of dairy sensitivity or intolerance, both of which raise the odds that removal will help. In many children the benefits extend well beyond the folate question, showing up as calmer digestion, clearer skin, less mucus and congestion, and steadier mood and sleep, which is part of why so many families find the trial worthwhile regardless of antibody status.

Not every family goes this route, however, and some choose to keep dairy in their child’s diet, whether because their child does not have confirmed folate receptor antibodies, because dairy removal did not produce noticeable changes for them, or simply because of the practical and nutritional tradeoffs of adding another restriction to an already complex diet. This last consideration carries real weight for selective eaters, a common situation in this population, where milk, cheese, and yogurt may be among the few reliably accepted foods and can account for a meaningful share of a child’s daily calories and protein. Removing dairy from an already narrow diet without a plan to replace those calories can do more harm than good, so for these children the question is not only whether to remove dairy but whether acceptable substitutes are in place first. As with other aspects of this treatment, families are encouraged to discuss the dairy question with their prescribing physician, and ideally a dietitian or feeding specialist when eating is already restricted, rather than changing their child’s diet unilaterally, and to plan for adequate calories, calcium, vitamin D, and protein from other sources if dairy is removed for any length of time.

Conclusion

Leucovorin sits in an unusual place among interventions for autism: a decades-old, inexpensive, and generally well-tolerated medication with a plausible biological mechanism and a body of research behind it, yet one whose most dramatic effects still arrive as individual stories rather than guarantees. That combination is precisely why it deserves a measured approach. The families who tend to do best are not the ones who start fastest or highest, but the ones who test first, titrate slowly, attend to cofactors and folic acid exposure, and track their child’s response with clear eyes.

Beyond the biochemistry, families often find that simply obtaining and maintaining a steady supply of leucovorin brings its own practical hurdles, and it helps to expect them. Coverage varies quite a bit, especially for off-label use, and many families report needing prior authorization or running into shortages during periods of high demand. Compounding pharmacies come up often for a specific reason: they can prepare liquid, dissolvable, or flavored versions in custom doses that are not available commercially, which is a practical solution for younger children or anyone who cannot swallow a capsule or tablet. One thing worth watching once a child is doing well is consistency. Because tolerability and response can shift when the manufacturer or brand changes, it is worth keeping track of which version a child is taking and treating an unexpected change in effect, after a refill or a pharmacy switch, as a possible clue rather than a mystery. Where possible, staying with the same source that has been working spares a family a good deal of avoidable guesswork.

None of this should be undertaken alone. Leucovorin is a prescription medication, and the decisions surrounding it, from the initial workup to dosing, cofactors, and diet, are best made in partnership with a knowledgeable physician who can weigh them against a particular child’s history. Approached that way, with patience and good information, a trial of leucovorin becomes something a family can navigate deliberately rather than hopefully, giving the child the fairest possible chance at the gains these accounts describe.

Consider a list: bipolar disorder, schizophrenia, anxiety, depression. Then another: fatty liver disease, type 2 diabetes, obesity, PCOS, dementia, and autoimmune conditions ranging from multiple sclerosis to psoriasis and eczema. We treat these as separate problems belonging to separate specialists. A growing body of research suggests they may share more of a root than we thought, and that the same intervention can reach many of them.

A recovery no one expected, and the movement it started

For five years, the Baszucki family lived inside a crisis that would not resolve. Their son Matt, diagnosed with bipolar disorder at nineteen, cycled through manic highs and depressive lows that pulled him out of school, out of the activities he loved, and in and out of hospitals. Over that span he was prescribed roughly twenty-nine different medications and saw dozens of providers. Nothing held. The family had begun to accept that this might simply be the shape of his life.

What finally changed things was not another drug. With the guidance of Harvard psychiatrist Chris Palmer and a dietitian, Matt began a therapeutic ketogenic diet, the same high-fat, very-low-carbohydrate approach used for nearly a century to treat epilepsy. Over the following months his symptoms lifted, and three years later he described himself as completely well, living a full life his family had feared was gone. His recovery became the seed of a movement: his parents founded Baszucki Group and Metabolic Mind to fund research into what is now called metabolic psychiatry, and to bring metabolic approaches into mainstream mental health care.

Matt himself has become one of the movement’s most visible voices. He co-hosts a podcast with researcher Iain Campbell bringing together patients and clinicians using ketogenic therapy for bipolar disorder, and speaks publicly about what he went through. Matt’s story is powerful, but a single recovery, however dramatic, is not proof the same approach would work for others. What makes his case worth telling is that it arrived alongside a growing body of research suggesting that his experience was not a fluke, and that the mechanism behind it may reach far beyond bipolar disorder.

The science catching up to the story

In 2024, Stanford psychiatrist Shebani Sethi published the first United States clinical trial in nearly sixty years to test a ketogenic diet for serious mental illness. Her team followed twenty-one adults with bipolar disorder or schizophrenia, all of whom were taking antipsychotic medication and all of whom also had a metabolic abnormality such as insulin resistance, weight gain, or impaired glucose tolerance. After four months on the diet, the results were striking. Roughly seventy-nine percent showed a clinically meaningful improvement in psychiatric symptoms, and three-quarters of participants were in recovery or a recovered state by the end. Among those who entered with metabolic syndrome, everyone who adhered to the diet saw it fully resolve. Participants reported better sleep, more energy, and improved quality of life, and greater adherence was associated with greater benefit.

Sethi, who coined the term metabolic psychiatry, frames the underlying idea as an energy problem. The brain is an enormous consumer of fuel, and when its ability to use glucose is impaired, as it appears to be in many psychiatric and neurological conditions, the diet offers ketones as an alternative fuel that a struggling brain can more readily use. This was a small, single-arm pilot, not a definitive trial, and Sethi herself is careful to describe ketogenic therapy as a promising adjunctive treatment whose main purpose here was to justify larger, more rigorous studies, several of which are now underway. But as a signal, it was remarkable: a dietary change producing psychiatric improvement in exactly the population where medications so often fall short.

Not only for the most severe conditions

If the story stopped at bipolar disorder and schizophrenia, it would already be significant. What has drawn wider attention is the growing number of accounts, and a smaller but expanding research base, suggesting that metabolic and ketogenic approaches can also help with the far more common problems of depression and anxiety.

Psychiatrists and writers working in this space, among them Palmer, whose book Brain Energy laid out a unifying metabolic theory of mental illness, and Georgia Ede, a psychiatrist focused on nutritional and ketogenic approaches to mental health, have described patients who spent years on antidepressants with partial or no relief, only to find their symptoms ease substantially after changing how they eat.

The proposed reason is the same as in the severe cases, and it is worth stating plainly because it reframes how we think about mood disorders. If depression and anxiety are, in at least some people, downstream expressions of impaired brain energy metabolism, inflammation, or blood-sugar dysregulation, then it becomes less surprising that stabilizing metabolism through diet could stabilize mood. This does not mean that every case of depression is metabolic, or that diet replaces therapy and medication for everyone. It means that for a subset of people, an entirely different lever may be available.

A personal anecdote: I was not trying to treat either one, but diet fixed both

I came to this subject through my own experience, on a far smaller scale. In my late twenties, after years of psoriasis that I had been handed creams for and told to manage, what finally resolved it was not a medication but a change in what I ate. I removed gluten and most processed sugar. The psoriasis cleared. The extra weight I had carried since childhood came off. And a low-grade anxiety and depression that had shadowed me since my adolescence lifted as well. I had trialed several SSRIs through my twenties without much benefit, and had come to think of the mood as simply my temperament rather than a condition. I had not set out to treat any of it. That these turned out to be connected was not something my training had prepared me to expect. My story proves nothing on its own, and I offer it in the same spirit as Matt’s: not as evidence, but as the kind of observation that ought to prompt a question.

Keto is not always necessary; Low Carb is often enough

It is important to resist the temptation to turn this into a single prescription. A strict ketogenic diet is a serious therapeutic intervention, best undertaken with medical and dietetic supervision, especially for anyone on psychiatric medication, since improving metabolic health can change medication requirements. It is not the only path, and it is not necessary for everyone. My own case is a small illustration of the point: what I did was not ketogenic at all.

The specifics vary as much as the intensity does. For one person what matters most is removing sugar and refined carbohydrate. For another it is a particular trigger food driving inflammation, dairy or gluten or something else entirely. For another it is cutting ultra-processed food, or changing when they eat rather than what. Two people can arrive at quite different diets and still be doing the same underlying work: lowering the metabolic and inflammatory load their body cannot handle. For many people, the benefits attributed to keto come from the more general improvements a ketogenic diet happens to deliver along the way, steadier blood sugar, less refined carbohydrate, fewer ultra-processed foods, and more stable energy.

The reality is that ketogenic therapy sits at one end of a spectrum, not at the center of it. For the most severe presentations, and for epilepsy, where the evidence runs deepest and the mechanism is best understood, nutritional ketosis is likely necessary. The therapeutic effect there appears to depend on sustained ketone production itself, not on carbohydrate reduction alone. For many others, a whole-food, lower-carbohydrate pattern that never reaches ketosis is enough.

In 2009 I cut bread, pasta, and sugar. I did not think of it as low carb, and the phrase was not yet in wide use, but that is what it was, and lowering my carbohydrate load, and with it my insulin levels, was likely doing much of the work. I eat a strict low-carbohydrate diet now, and I have never needed ketosis to hold what I gained. But on the occasions when I do reach it, usually through extended fasting rather than by design, I notice that my mind feels like it works better, clearer and steadier than its baseline. Sufficient and optimal may not be the same thing. The level of intervention that resolves a problem is not necessarily the level that produces the best version of how you think, and that too is part of what the spectrum means. The principle beneath all of it, that what we eat shapes how the brain functions, applies broadly even when a formal ketogenic diet does not.

A metabolic thread running through many diseases

Perhaps the most compelling part of this emerging picture is that mental health may be one expression of something larger. The same metabolic dysfunction implicated in mood and psychotic disorders, centered on insulin resistance, impaired energy production, and inflammation, sits at the root of a striking range of common chronic diseases. Seen this way, a diet that restores metabolic function is not treating many unrelated conditions by coincidence; it is addressing a shared underlying problem that surfaces differently in different organs.

Some of these connections are well established. For type 2 diabetes and obesity, multiple randomized controlled trials and meta-analyses show that carbohydrate restriction and ketogenic diets improve blood sugar, hemoglobin A1c, triglycerides, and insulin sensitivity, often enough to reduce or eliminate medication. Non-alcoholic fatty liver disease, which is tightly linked to insulin resistance, also responds well, with studies showing substantial reductions in liver fat. Polycystic ovary syndrome (PCOS), a condition driven in large part by insulin resistance, frequently improves on lower-carbohydrate approaches, with benefits to weight, hormonal balance, and menstrual regularity.

Inflammatory and autoimmune skin conditions occupy a middle position. Psoriasis is strongly comorbid with metabolic syndrome and insulin resistance, which gives a coherent rationale for why addressing metabolic dysfunction might reach the skin, and smaller studies and case reports describe improvement on carbohydrate-restricted and anti-inflammatory dietary patterns. Eczema rests more on mechanism and individual report than on trials. In both cases the signal is real enough to be worth pursuing and too preliminary to be promised.

Further along the frontier sit multiple sclerosis and Alzheimer’s disease and other dementias, where small clinical trials and a strong mechanistic rationale, the brain’s shift to ketone fuel when glucose metabolism falters, have shown improvements in quality of life and some cognitive and functional measures, though larger trials are still needed before firm conclusions can be drawn.

Dietary trials will not be funded by industry

A word about that evidence, and about why there is not more of it. Clinical trials are expensive, and most are paid for by companies with something to sell. A dietary pattern cannot be patented, and if it works it reduces demand for the products we see advertised on television. That asymmetry shapes which questions get asked and which never do. It is a large part of why the ketogenic diet, standard care for epilepsy a century ago, was displaced once anticonvulsants arrived, and why metabolic psychiatry had to be seeded by one family’s philanthropy rather than by industry. Where the evidence here is thin, the thinness often reflects an absence of funding rather than an absence of effect.

What ties the list together is not a claim that a ketogenic diet cures everything. It is the recognition that insulin resistance and impaired cellular energy are common soil, and that many of the chronic diseases straining modern medicine, metabolic, psychiatric, and neurological alike, may share more of a root than our specialty-divided system tends to acknowledge. The question is not whether the evidence is complete. It is whether we have been funding the right questions.

This article is for general educational purposes and does not constitute medical advice. Ketogenic and other therapeutic diets can affect medication needs and should be undertaken with appropriate medical and dietetic supervision, particularly for anyone managing a psychiatric or chronic medical condition.

Resources

Metabolic Psychiatry and Mental Health

Metabolic Mind –

https://www.metabolicmind.org/

The Baszucki family’s nonprofit and the best single hub for this topic. Patient stories, clinician interviews, podcasts, plain-language explainers.

Baszucki Group –

https://baszuckigroup.com/

The philanthropy funding the research. Their Foundational Trials page summarizes the key studies.

Chris Palmer, MD –

https://www.chrispalmermd.com/

Harvard psychiatrist, originator of the brain energy theory. Articles, research, clinical work.

Brain Energy –

https://brainenergy.com/

Companion site to Dr. Palmer’s book.

Georgia Ede, MD –

https://www.diagnosisdiet.com/

Psychiatrist focused on nutritional and ketogenic approaches; author of Change Your Diet, Change Your Mind.

Practitioner Organizations and Directories

Society of Metabolic Health Practitioners (SMHP) –

https://thesmhp.org/

Clinical guidelines, the Metabolic Health Practitioner accreditation pathway, and the largest practitioner directory in this space, with more than 1,400 entries.

Low Carb USA –

https://www.lowcarbusa.org/

CME conferences, an educational video library, and a searchable research database. Founded by Doug Reynolds, who also founded SMHP.

Medical Academy of Pediatric Special Needs (MAPS) –

https://www.medmaps.org/

Training and fellowship for practitioners treating autism and related complex pediatric conditions. Clinician directory at https://www.medmaps.org/clinician-directory

Metabolic Multiplier –

https://metabolicmultiplier.org/

Volunteer-run advocacy group curating metabolic health resources; partners with SMHP.

Ketogenic Therapy (Medical and Neurological)

The Charlie Foundation for Ketogenic Therapies –

https://charliefoundation.org/

The long-standing organization for medical ketogenic therapy, originally developed for epilepsy.

Matthew’s Friends –

https://www.matthewsfriends.org/

UK-based counterpart to the Charlie Foundation.

Clinical Practices and Education

Ovadia Heart Health, Stay Off My Operating Table –

https://ovadiahearthealth.com/

Dr. Philip Ovadia, cardiac surgeon who lost more than 100 pounds and reversed his own prediabetes. Virtual clinic, book, and podcast.

Toward Health (Dr. Tro Kalayjian) –

https://toward.health/

Formerly Dr. Tro’s Medical Weight Loss. Board certified in internal and obesity medicine, lost 150 pounds, SMHP founding board member. Nationwide telehealth focused on type 2 diabetes remission, obesity, and food addiction.

Conferences

Metabolic Health Summit –

https://metabolichealthsummit.com/

Annual conference where much of this work is presented; Matt Baszucki shared his findings there in 2024.

Most parents hear about Leucovorin (i.e. folinic acid) the same way: not from a clinician, but from someone whose child seemed to change on it. A parent hears that another child, nonspeaking for years, began producing words after starting a prescription B vitamin called leucovorin. They read the testimonials. They ask their pediatrician. The pediatrician declines to order the specialized antibody test that is supposed to identify which children might respond, and declines to prescribe the drug off-label. So the parent does the only thing left available to them: they buy over-the-counter folinic acid, the supplement form of the same molecule, and they run their own trial at the kitchen table.

This is not a fringe scenario. It is, increasingly, the default one. And it is worth being honest about why it happens and what it costs, because the answer points to a specific, accessible piece of information that too few of these families are using: their child’s MTHFR status.

First, where we are with leucovorin

In September 2025, the FDA announced it was initiating approval of leucovorin, accompanied by a high-profile White House event that framed the drug as a treatment for autistic symptoms. Prescriptions surged. A national analysis later published in JAMA Network Open in May 2026 found that leucovorin prescribing for children with autism rose more than two thousand percent over prior years, climbing from a stable baseline through the latter half of 2025 in step with the media and federal attention. The drug grew scarce, creating shortages for the small number of children who had been taking it under careful supervision for years. Then the foundation shifted. In January 2026, the single largest randomized controlled trial supporting leucovorin in autism, a study of seventy-seven children, was retracted by the European Journal of Pediatrics after a reanalysis revealed statistical errors and a failure to replicate its own results. And in March 2026, the FDA’s final action turned out to be far narrower than the earlier announcement implied: the agency declined to endorse leucovorin for autism at all, approving it only for cerebral folate deficiency in patients with a confirmed FOLR1 genetic variant, a condition so rare that fewer than fifty cases have ever been identified worldwide.

This narrowing did not happen in isolation. It arrived during a broader reversal of the health-policy wave that had risen through 2025 under the banner of Making America Healthy Again. Several of that movement’s signature health initiatives stalled or collapsed within the same few months. In March 2026, a federal court in American Academy of Pediatrics v. Kennedy stayed the reconstituted federal vaccine committee’s revised childhood immunization schedule, along with the committee’s new appointments and its votes, after that committee had moved to make the hepatitis B birth dose optional rather than universal. A parallel effort to end federal recommendation of community water fluoridation, launched in April 2025 and handed to an accelerated EPA review, remained unresolved and mired in the assessment process rather than enacted. And in June 2026, in Monsanto v. Durnell, the Supreme Court ruled seven to two that federal pesticide law preempts state failure-to-warn claims over the weedkiller glyphosate, a decision widely read as a defeat for the same movement, since it shielded a pesticide manufacturer from the kind of accountability the movement had championed. The pendulum that had swung hard in one direction reached its height and swung back, and leucovorin, despite its independent scientific merits, was caught in the reversal.

The research in support of Leucovorin for Autism

Three separate randomized, double-blind, placebo-controlled trials, conducted by different research groups in different countries, have reported positive effects of folinic acid in autism, with the clearest benefit in children who test positive for folate receptor autoantibodies. Frye and colleagues, in the United States, found significantly greater improvement in verbal communication on folinic acid than on placebo, particularly in children positive for folate receptor autoantibodies. The EFFET trial in France, using an oral formulation, reported significant improvement in Autism Diagnostic Observation Schedule scores in the folinic acid group. And an Iranian trial by Batebi and colleagues, in which folinic acid was added as an adjunct to risperidone, found significantly greater improvement in inappropriate speech, stereotypic behavior, and hyperactivity than risperidone alone. The three trials differ in design, and one tested folinic acid as an add-on rather than on its own, but three independent, convergent, placebo-controlled results is not a trivial signal, and it is the part of this literature that carries real weight.

What the decision looks like with all the information

So imagine, for a moment, the opposite of the kitchen-table trial: a child whose family can obtain every relevant test before anything is started. This is the ideal case, and it is worth laying out clearly, because it shows what the improvised version is missing. With the full picture in hand, the choice between folate and methyl-B12, and between one form of folate and another, is not a guess. It follows a logic. The tree below traces that logic from the top.

The tree separates two questions that are often run together. The Folate Receptor Antibody Test (FRAT) answers a transport question: whether folate can cross into the brain, or whether autoantibodies are blocking the folate receptor and producing cerebral folate deficiency. MTHFR genotype answers a conversion question: whether the body can turn folate into its active, methylated form. The two are independent, and a child may have either problem, both, or neither. Before either is acted on, a functional B12 gate comes first, because if methylmalonic acid (MMA) is elevated, folate becomes trapped as 5-methylfolate and cannot cycle until B12 is repleted; in that case methyl-B12 is addressed first. When B12 is adequate, the FRAT result branches the decision. A positive FRAT supports getting folate into the brain, with the form chosen by MTHFR status: folinic acid when conversion is intact, since it bypasses the blocked receptor through the reduced folate carrier, or pre-converted methylfolate when MTHFR is significantly impaired. A negative FRAT offers little rationale for a folate push into the brain, so the functional markers decide instead, pointing toward methyl-B12 for a B12 problem or methylfolate for a conversion problem. Throughout, MTHFR is a complement to the FRAT rather than a substitute, and genotype indicates risk rather than proven dysfunction, so it should always be paired with functional markers.

To interpret a FRAT result in context, it should be ordered alongside a small panel that captures both the folate and B12 sides of the methylation cycle. This includes MTHFR genotyping (C677T and A1298C) for conversion capacity; methylmalonic acid (MMA) as the specific functional marker of B12 sufficiency at the cellular level; homocysteine, which reflects the combined status of folate, B12, and B6 and flags a methylation bottleneck; and red-cell (RBC) folate rather than serum folate, since RBC folate reflects tissue stores over the preceding months rather than recent intake. For B12 itself, serum B12 alone is a weak marker; where available, active B12 (holotranscobalamin) is the better test, but the more practical approach is to pair serum B12 with MMA, since an elevated MMA reveals a functional deficiency that a normal serum level would miss.

A closing note, and a call for change

There is an inconsistency at the heart of how these children are treated, and it deserves to be named plainly. The same clinical culture that will prescribe a stimulant, an SSRI, or an antipsychotic to an autistic child, each of them with no test to predict who will respond, will often refuse to so much as order a folate receptor antibody test. And the medications prescribed without hesitation are not benign. Risperidone and aripiprazole, the two agents approved for irritability in autism, carry well-documented long-term metabolic side effects: weight gain, increased appetite, elevated blood lipids, insulin resistance and a raised risk of type 2 diabetes, and increased prolactin. Because these drugs are often continued for years, those risks accumulate over a child’s development. This is difficult to square with the reluctance around folinic acid, which rests on three independent, convergent, placebo-controlled trials, carries a comparatively benign safety profile, and, almost uniquely in this field, comes paired with a biomarker that can identify in advance the children most likely to benefit. The medications prescribed freely offer no such test; they are trial and error by design, with metabolic consequences that outlast the trial. To decline the one intervention that could be made rational, while reaching readily for those that cannot, is not caution. It is habit mistaken for rigor.

The change this calls for is modest and concrete. Order the test proactively for children with Autism. Make the folate receptor antibody assay accessible through ordinary channels, cover it as the stratifying tool it is, and let the result, rather than a physician’s comfort or discomfort with an unfamiliar model, determine who is offered a trial. A positive result identifies a child with a mechanistic rationale and a favorable risk profile; a negative result spares a family a blind experiment. Either way the family learns something true. What they are given now, in the absence of the test, is the obligation to guess, and then blame for guessing. A system willing to prescribe freely, and to accept years of metabolic risk when it does, should be at least as willing to test carefully.

References

Randomized, double-blind, placebo-controlled trials

Frye RE, Slattery J, Delhey L, et al. Folinic acid improves verbal communication in children with autism and language impairment: a randomized double-blind placebo-controlled trial. Mol Psychiatry. 2018;23(2):247-256. doi:10.1038/mp.2016.168. PMD: 27752075; PMCID: PMC5794882.

Renard E, Leheup B, Guéant-Rodriguez RM, Oussalah A, Quadros EV, Guéant JL. Folinic acid improves the score of Autism in the EFFET placebo-controlled randomized trial. Biochimie. 2020;173:57-61. doi:10.1016/j.biochi.2020.04.019. PMID: 32387472.

Batebi N, Sanjari Moghaddam H, Hasanzadeh A, Fakour Y, Mohammadi MR, Akhondzadeh S. Folinic acid as adjunctive therapy in treatment of inappropriate speech in children with autism: a double-blind and placebo-controlled randomized trial. Child Psychiatry Hum Dev. 2021;52(5):928-938. doi:10.1007/s10578-020-01072-8. PMID: 33029705.

Retracted trial (cited for completeness)

Panda PK, Sharawat IK, Saha S, Gupta D, Palayullakandi A, Meena K. Efficacy of oral folinic acid supplementation in children with autism spectrum disorder: a randomized double-blind, placebo-controlled trial. Eur J Pediatr. 2024;183(11):4827-4835. doi:10.1007/s00431-024-05762-6. Retraction published Eur J Pediatr. 2026;185:109. doi:10.1007/s00431-026-06769-x.

Open-label and uncontrolled studies

Frye RE, Sequeira JM, Quadros EV, James SJ, Rossignol DA. Cerebral folate receptor autoantibodies in autism spectrum disorder. Mol Psychiatry. 2013;18(3):369-381. doi:10.1038/mp.2011.175.

Frye RE, Rossignol DA. Treatment of folate metabolism abnormalities in autism spectrum disorder. Semin Pediatr Neurol. 2020;35:100835. doi:10.1016/j.spen.2020.100835.

Systematic review and meta-analysis

Rossignol DA, Frye RE. Cerebral folate deficiency, folate receptor alpha autoantibodies and leucovorin (folinic acid) treatment in autism spectrum disorders: a systematic review and meta-analysis. J Pers Med. 2021;11(11):1141. doi:10.3390/jpm11111141. Erratum in: J Pers Med. 2022;12(5):721. PMID: 34834493; PMCID: PMC8622150.

Biomarker and mechanistic references

Frye RE, Delhey L, Slattery J, et al. Blocking and binding folate receptor alpha autoantibodies identify novel autism spectrum disorder subgroups. Front Neurosci. 2016;10:80. doi:10.3389/fnins.2016.00080.

Ramaekers VT, Sequeira JM, Blau N, Quadros EV. A milk-free diet downregulates folate receptor autoimmunity in cerebral folate deficiency syndrome. Dev Med Child Neurol. 2008;50(5):346-352.

In the realm of spiritual growth, we often hear the phrase “be grateful for what you have.” It is a common mantra, one that encourages us to appreciate our blessings and find joy in the present moment. But what if we took this idea even further? What if we learned to be grateful not just for our blessings, but for our burdens: the challenges, the struggles, the heartaches that shape us into who we are? This is the essence of radical gratitude: a profound shift in perspective that transforms our understanding of hardship from something to be endured into something to be embraced. It is the cornerstone of many spiritual traditions, a practice that invites us to view our difficulties as gifts that illuminate our path.

The Alchemy of Radical Gratitude

Radical gratitude is not merely a practice; it is an alchemical process. Just as alchemists sought to transform base metals into gold, we can learn to transmute our struggles into sources of strength and wisdom. This transformation occurs when we begin to see our burdens not as obstacles, but as opportunities for growth that ultimately shape who we are.

Viewing Burdens as Gifts

Every challenge we face carries within it a lesson, a gift waiting to be unwrapped. When we embrace our burdens, we open ourselves to the possibility of transformation. This does not mean that we deny our pain or pretend that everything is fine. Rather, it means that we acknowledge our experiences fully and choose to find meaning in them.

The hardest chapter of my life so far was watching my father live through his own worst-case scenario. In 2007 he was diagnosed with a glioblastoma and given six months to live. He survived, against every expectation, and lived until 2024. In the end it was not the cancer that took the heaviest toll. A round of seizures, presumably caused by the brain damage from his many surgeries, left him in a wheelchair, unable to speak, and barely able to move, yet cognitively intact and fully aware of everything he had lost. He was a prisoner in his own body. In January of 2020 he moved into a nursing home, and then Covid arrived. He was alone, and we could not even visit. He had gone from what I once thought was the worst case to something far worse, and I believed I could not be there for him when he needed me most.

Watching this was heartbreaking, but it also cracked me open and let the light in. It forced me to confront my own fears, my own limitations, and, ultimately, my own capacity for love. That journey taught me lasting lessons about love, vulnerability, and the fragility of life. It gave me the strength to show up consistently for him at the end of his life when he needed me the most.

The Spiritual Tradition of Radical Gratitude

Radical gratitude invites us to drop judgment, anger, and resentment – the very emotions that can weigh us down and prevent us from experiencing the full richness of life. When we practice radical gratitude, we are not merely being polite or showing appreciation; we are engaging in a transformative act that shifts our energy and aligns us with our highest selves.

In Buddhism, for example, gratitude is seen as a powerful antidote to suffering. The practice of metta (loving-kindness) begins with cultivating gratitude for oneself and extends outward to all beings. This practice teaches us that gratitude is not just a response to what we receive; it is a fundamental attitude that shapes our perception of the world.

Among the Stoics, gratitude took the form of amor fati, a love of one’s fate. Marcus Aurelius trained himself each morning to meet whatever the day delivered, welcome or unwelcome, with acceptance rather than resistance. This practice teaches us that gratitude is not contingent on good fortune; it is a discipline we bring to every circumstance, including the ones we would never have chosen.

The Core Ideas of Radical Gratitude

1. Embrace Your Burdens: Let your gratitude reach past the good and the easy to include the painful chapters that shaped you. Recognize that your struggles are not just obstacles; they are teachers. Each hardship carries a lesson, and often a strength you did not know you had. Being thankful even for what wounded you is what makes this gratitude radical.

2. Drop Judgment and Resentment: Let go of the need to blame or criticize yourself or others. Stop demanding that people be who you want them to be, and accept them as they are. Embrace self-love and forgiveness as a path to liberation.

3. Transform Your Perspective: Shift from seeing life as something happening to you to seeing it as a journey you help create. You are not a victim of circumstance, but a co-author of who you are becoming, who you are.

Releasing Judgment Is Not Passivity

In the journey of radical gratitude, we often encounter the practice of releasing judgment. It is a noble discipline, one that invites us to see beyond the surface and recognize the deeper forces beneath our actions. It teaches that even harm arises not from malice, but from misalignment, ignorance, or a distortion of the self.

But let us be clear: releasing judgment does not mean allowing harm to continue unopposed. It is not about standing by while suffering unfolds. Non-judgment is not passivity; it is a conscious choice to respond from a place of wholeness rather than reactivity. In practice, this takes three forms.

First, we seek to understand what drives the person causing harm. When we release judgment, we look honestly at the forces at play. This does not excuse harmful behavior; it allows us to see it as a product of misalignment rather than the whole of who someone is.

Second, we hold our own boundaries. Non-judgment lets us set limits without resentment. It means saying, “this is not acceptable,” while still recognizing that the person causing harm is acting from their own misalignment. We can love someone and still decline to hand them the keys to our peace, keeping a misaligned person at the distance their behavior requires without closing our heart to them.

Third, we respond to harm in order to restore what has been broken. True non-judgment is proactive. It calls us to act not out of retribution, but to restore wholeness where it has been lost, whether by intervening, speaking the truth, or creating alternatives that align with our highest selves.

Conclusion: The Gift of Radical Gratitude in the Face of Harm

Radical gratitude is not a passive acceptance of suffering; it is a transformative practice that invites us to see our challenges as profound gifts. For those who work closely with vulnerable individuals, including families affected by severe autism, this principle becomes essential. It reminds us that when systemic harm is real and ongoing, perpetuated through negligence and indifference, we are not merely reacting to injustice; we are restoring wholeness where it has been lost.

This is radical gratitude embodied: not by ignoring the wounds, but by transforming them into a teaching, a pathway, and a call to action. Our burdens are not just weights to bear; they are the very tools that shape us into who we are meant to be. As we navigate these complexities, let us remember that the wound is where the light enters us. Embrace your wounds for they are the cracks through which your light can shine, illuminating the path for others and inspiring a collective return to coherence.

Why standard testing falls short

Evaluating children who are nonspeaking, and who often also have autism and intellectual impairment, is uniquely challenging. Most assessments are designed for speaking individuals, so there are few language-free options available. And yet, this population varies enormously in cognitive and adaptive functioning, which makes assessment all the more necessary.

A defining trait of autism, in both verbal and nonverbal children, is how readily they become overwhelmed by environmental stressors. This can mean a loud room, strong emotions in others, or being asked to do something they are not ready for or are unable to complete. Such demands can trigger a meltdown or, at minimum, erode their ability to focus. The testing situation compounds this: a child who thrives on routine is pulled from school, brought to a new place, introduced to a new “doctor,” and asked to perform novel tasks. All of it reduces their capacity to manage stress and cooperate.

In response, after years of trial and error, I developed a protocol that sequences tasks deliberately to encourage participation, using subtests from standardized measures that can be expanded upon for higher-functioning children.

Before the child arrives

Evaluations usually begin with a phone call. Beyond age, grade, and school, two questions reveal a great deal: Are they speaking? and Are they learning academic material? Do they color, draw or write? Reviewing prior reports helps too: a child who was untestable, or who scored Extremely Low across the board, is a good candidate for this protocol.

Parents stay in the room

In a typical evaluation, parents wait outside. Here, they stay. Some children will not cooperate at all without a parent present, and removing the parent can trigger escape behaviors, running, disrupting the room, turning off lights, that make testing impossible. Parent presence also serves several purposes:

● It guides pacing. Parents can tell you whether a child actually knows something, so you know when to test limits and when to move on. Often a parent’s “C’mon, show the doctor what you know” is what gets a child to engage.

● It builds the alliance. Children are aware of the room’s emotional tone. Most children on the spectrum are highly sensitive to the emotions in the room surrounding them. A relaxed, productive conversation with a parent signals to the child that the examiner is an ally.

● It builds parents’ confidence in the results. Parents see their child’s real challenges firsthand, which matters especially when they are unaware of, or in denial about, the extent of impairment. They also watch the examiner structure the environment to prompt the child to respond, offering multiple attempts to answer and multiple demonstrations of each task, so they can see that a low score reflects the child’s performance rather than a lack of effort to elicit it.

The protocol, step by step

The Animal Sticker. We open with a non-standardized warm-up: sticker sheets of animals with interchangeable facial features. The child picks an animal and places one feature, usually the eyes, then writes their name on top if able. Both steps yield fine-motor information: whether the child can peel the sticker off the sheet and position it independently, and whether they can form the letters of their own name. It’s a non-threatening entry point that also surfaces frustration tolerance (do they ask for help, or fling the sheet away?) and attention. A child who cannot focus on the sticker at all, often one with severe functional limitations, is frequently unable to engage with anything that follows.

Vocabulary Knowledge. Rather than opening with the first task of the WISC-V or WPPSI-IV, which is Block Design, the first standardized task assesses vocabulary knowledge, either confrontation naming (Picture Naming/EVT) or receptive (Receptive Vocabulary/PPVT). I prefer to start with naming, since a single image on the page reduces visual load. Counterintuitively, many “nonspeaking” children who can speak single words score higher on naming than on the fully nonverbal pointing task, which overwhelms them with four images at once.

Math Problem Solving (WIAT-4). Beginning at the second item, identifying a circle, this assesses number sense, shapes, and counting. A child wandering the room will often sit down the moment the shapes appear on the screen. As the items progress, we learn that many can count with one-to-one correspondence but cannot handle the language of comparison: which is more, less, longer, or the same. They can count the number of ducks in a pond, but if asked how many would be left if 2 ducks fly away, they are unable to answer.

Word Reading (WIAT-4). Starting at alphabet items, many nonspeaking children recognize letters and words and can vocalize them. When speech is absent, a recognition format works as a screening tool. Where the child cannot engage, academic knowledge is documented through parent and teacher interviews and prior records.

Writing tasks. If the child wrote their name, showed interest in numbers, or likes to color, we proceed to Design Copy (NEPSY for ages up to 16, Beery VMI beyond), Numerical Operations (starting at 1+1), and Spelling. Non-phonetic spelling can signal a comorbid reading disability. Some nonspeaking children show a hyperlexic profile: strong decoding and spelling with weak comprehension.

The Day 1 sequence at a glance

Tasks are administered in the order below, with a brief Animal Sticker reset between each. All tasks begin at the basal item to build confidence before difficulty increases.

The interviews: autism, sensory, adaptive

Much of what follows comes from structured interviews with parents or caregivers, which are usually conducted after the child’s direct testing is complete. When a child has difficulty engaging consistently, though, the two don’t have to be kept separate: the examiner can alternate between blocks of direct testing and blocks of parent interview, using the interview segments as natural breaks that let the child settle before returning to task.

The CARS (or another autism measure) documents a presentation that isn’t always obvious in a child who is both nonspeaking and intellectually impaired. Key areas: socialization, language, transitions, emotional reactivity, sensory function, interests, and body use.

Sensory questions matter enormously. Many children cover their ears at loud sounds yet blast their own videos, seeking and avoiding at once. Reaction to pain is critical: a high pain tolerance, more common in autism, can let sprains, fractures, or tooth infections go undetected until they worsen. Food is another axis, picky eating that can rise to ARFID, sometimes with oral-motor difficulty chewing. Body-use questions capture stimming: flapping (often when happy), rocking (often when anxious), and finger movements.

Adaptive functioning, ideally via the Vineland-3, is essential, particularly for children who cannot be directly tested. It documents independence in toileting, dressing, and bathing; safety around traffic, cars, hot or sharp objects; elopement risk; and it’s required, alongside an IQ score, for SSI and OPWDD eligibility. A genuine strength in motor or adaptive skills, a child who skis, swims, or surfs well, often flags a higher-functioning profile.

Two days, not one

The first session usually ends when the child runs out of steam, with any remaining time given over to parent interviews. If the child seems capable of more, a second session helps, since many perform markedly better once the setting and examiner are familiar. Day two targets a measure of intellectual functioning (WPPSI, WISC, RIAS, or a fully nonverbal measure like the C-TONI), followed by any remaining WIAT or other academic subtests, and then the Vineland.

Common diagnostic picture

Nonspeaking children often meet criteria for Autism, Level 3, with accompanying language and intellectual impairment. The DSM-5 severity levels are worth distinguishing here: Level 1 describes a child who is autistic but has intact pragmatic language and little need for special supports; Level 2 describes a child with language comprehension deficits or processing difficulties who nonetheless retains the ability to use language for pragmatic exchange; and Level 3 describes a child whose ability to use language functionally is impaired. It’s also worth being precise about terms: intellectual impairment does not necessarily mean intellectual disability. It indicates impairments in cognitive functioning that produce a presentation functionally equivalent to an intellectual disability, without on its own establishing the formal diagnosis. Additional presentations worth screening for include Developmental Coordination Disorder, Speech-Sound Disorder, and ARFID.

A note to colleagues

If you have questions about implementing this protocol, about evaluating nonspeaking children more broadly, or about writing up the report, I would be glad to hear from you. Fellow clinicians are welcome to reach out to me at johnferreraphd@pm.me. I am always happy to schedule a time to compare notes with others working with this population or to provide guidance to clinicians who want to start. This population is increasing in number, and they need our help.

Genes Are Not Destiny. They’re Potential.

There is an old saying that genes load the gun and environment pulls the trigger. This analogy is most evident in the context of preventing disease and optimizing health and wellness. A loaded gun does nothing on its own. The trigger is where the event happens, and the trigger is the part we can reach. How our genes actually behave is remarkably responsive to how we live.

This is the piece that changes everything. The same genetic blueprint can play out in very different ways depending on the signals it receives, and many of those signals are ones we can actually change.

Gene expression is greatly affected by behavior. Diet and lifestyle are among the most powerful tools we have to shift the trajectory itself. And recognizing that is where the work of restoring and optimizing wellness truly begins.

Your DNA is not a set of rigid commands that are automatically followed. It is more like an enormous library of blueprints. Most of those blueprints sit on the shelves, unread. What determines which ones get taken down, copied, and turned into proteins is a sophisticated regulatory system called epigenetics: the biological switches that turn genes on or off without altering the underlying DNA sequence.

These switches respond to signals from the environment: nutrients, toxins, stress hormones, inflammation, gut microbes, sleep quality, exercise, and even social connection.

The Evidence Is All Around Us

Consider just a few of the many conditions that have exploded in recent decades, Obesity, Autism and Neurodevelopmental Conditions, and Cancer.

Obesity

The human gene pool hasn’t changed meaningfully in 40 years, yet obesity rates have tripled. Clearly, our genes are responding to a radically altered food environment: ultra-processed foods, seed oils, constant snacking, and metabolic disruptors.

Autism and Neurodevelopmental Conditions

Autism prevalence has risen more than tenfold since 1986 (by conservative estimates). While genetic variants exist, they cannot explain a curve this steep. The gene pool does not shift that fast. Environments do. Early-life nutrition, chemical exposures, inflammation, and microbiome disruption are all plausible drivers acting on susceptible genetics.

Cancer

While certain inherited mutations raise risk, the vast majority of genetic damage that actually drives cancer is acquired during life, from smoking, UV radiation, chronic inflammation, processed foods, and environmental toxins. These factors silence protective genes and activate harmful ones.

In each case, genetics set the stage, but the environment directs the performance.

Reframing the Problem Opens the Door to Restoring Health

This distinction is not theoretical. It is profoundly practical.

If gene expression is heavily influenced by modifiable environmental factors, then we have genuine leverage. Unlike your DNA sequence, which is fixed, your epigenome is dynamic and responsive throughout life. This is the scientific foundation for integrative and root-cause approaches:

• Optimizing nutrition and removing ultra-processed foods

• Reducing toxic burden (pesticides, plastics, heavy metals)

• Healing the gut and microbiome

• Lowering chronic inflammation

• Improving sleep, stress resilience, and nutrient status

This perspective doesn’t replace conventional medicine. It complements it. It turns a diagnosis from a dead-end verdict into a starting point for personalized, proactive care.

The genes may be loaded, but the trigger is still within reach.

Understanding which environmental and biological factors are shaping the current expression of those genes, and which of them you can actually change, opens doors that pure genetic fatalism closes. That is where real clinical work begins.

From Principle to Practice: What This Looks Like in a Real Child

This is not an abstract argument. With the Biomedical approach, the difference between fatalism and leverage shows up in concrete, testable ways. Over and over, we see the same pattern: a gene variant or a vulnerable pathway that only becomes a clinical problem under specific conditions. Change the conditions, and the picture changes. What follows are several of the most common and most actionable examples, the places where a loaded gun is sitting with someone’s finger on the trigger, and where that finger can be moved.

Methylation and the MTHFR Variant: A Genetic Bottleneck You Can Work Around

Roughly half the population carries a variant in a gene called MTHFR. This gene builds an enzyme that converts the folate you eat into its active, usable form. Certain variants slow that enzyme down, in some cases to about a third of its normal efficiency. That is the loaded gun, and the child is born with it.

But a slower enzyme is only a problem in context. Given enough of the right raw materials, the pathway often runs fine. The trigger here is nutritional: low dietary folate, high oxidative stress, or reliance on synthetic folic acid that this child’s body struggles to convert. The lever is straightforward. Supplying folate in its already-active methylated form, alongside the B vitamins that support the same pathway (B12, B6, riboflavin), can bypass the bottleneck entirely. This matters far beyond folate, because methylation is the very chemistry the body uses to switch genes on and off. It is, quite literally, where genetics and environment meet.

Cerebral Folate Deficiency and the FRAT: When the Problem Is Delivery, Not Supply

This is one of the clearest examples of why standard bloodwork can miss the real story. The brain does not pull folate out of the bloodstream passively. It relies on a specific transporter, the folate receptor, to actively carry folate across the barrier that protects the brain. In some children, the immune system produces antibodies that block this receptor. The result is a brain starved of folate even when blood folate looks completely normal.

The Folate Receptor Antibody Test (FRAT) identifies these antibodies directly. It is one of the few tests that can explain a child whose standard labs are unremarkable but whose presentation is not. The implications for B vitamin metabolism are significant, because folate is essential for neurotransmitter synthesis and for the methylation chemistry described above. The lever is notable here too. Leucovorin (folinic acid) can enter the brain through a different doorway, sidestepping the blocked receptor entirely, and it is generally insurance-covered once the antibody finding establishes the rationale. The FRAT itself is typically out of pocket, but it can reframe a child’s entire workup. There is also emerging interest in dietary contributors, since proteins in cow’s milk closely resemble the human folate receptor and may help drive these antibodies in susceptible children, which is part of why a dairy trial is often considered alongside treatment.

Gut Dysbiosis and Candida: Inflammation You Can Starve

The gut is not a sealed tube that simply processes food. It houses a vast microbial community that talks to the immune system and the brain constantly. When that community is thrown off balance, often by repeated antibiotics and/or a diet heavy in sugar and refined carbohydrate, opportunistic organisms like candida can overgrow.

This is not a benign cosmetic issue. These organisms produce metabolites that the body has to deal with, and some of them appear on functional testing such as the organic acids test. Certain bacterial byproducts can even interfere with the enzymes that regulate dopamine and norepinephrine, the very neurotransmitters tied to attention and regulation. The overgrowth also keeps the immune system in a low-grade inflammatory state, and chronic inflammation is one of the most powerful environmental signals influencing gene expression in the developing brain.

What makes this such a hopeful example is how modifiable it is. These organisms feed on sugar and refined starch. Changing the diet, restoring fiber and microbial diversity, and using targeted antimicrobial support where appropriate can shift the balance, lower the inflammatory burden, and in many children meaningfully change behavior and clarity. You are not overriding the child’s biology. You are removing the fuel.

Vitamin D: An Environmental Signal That Speaks Directly to Your Genes

If you wanted to design the perfect illustration of environment pulling genetic triggers, you could hardly do better than vitamin D. Despite its name, active vitamin D behaves less like a simple nutrient and more like a hormone. It binds to a receptor that sits on your DNA and directly regulates the activity of hundreds of genes, including many that govern immune function and inflammation.

Deficiency is now extraordinarily common, a product of indoor lifestyles, sunscreen, and geography. The loaded gun is each child’s individual sensitivity. The trigger is a modern environment that leaves many children chronically low. The lever is simple, measurable, and inexpensive: test the level, and restore it. Few interventions offer this much genetic influence for this little effort.

Iron and the Dopamine Connection: When “Not Anemic” Isn’t the Same as “Enough”

Iron is required to build dopamine. It is a necessary cofactor for the rate-limiting enzyme in dopamine production, which means a child can have low iron stores driving inattention, restlessness, and disrupted sleep long before they ever look anemic on a routine test. The standard blood count can be perfectly normal while the brain’s iron supply runs short.

The relevant number is ferritin, the body’s iron storage marker, and many children with attention and sleep complaints sit at the low end. This is the loaded gun of an individually high need meeting the trigger of an inadequate supply. Restoring iron through diet and, when indicated, supplementation can support the exact chemistry the child is struggling with.

Omega-3 Fatty Acids: Rebalancing an Inflammatory Modern Diet

The brain is built largely from fat, and one fat in particular, DHA, is a core structural component of every neuron’s membrane. The modern diet has quietly inverted the ratio of fats we evolved with, flooding us with omega-6 from industrial seed oils while leaving us short on the omega-3s that calm inflammation and support neuronal signaling. That shift nudges the whole system toward a pro-inflammatory baseline, which, as a recurring theme here, is one of the loudest environmental signals reaching a child’s genes. Increasing omega-3 intake and reducing seed oils is a foundational, low-risk adjustment that addresses this at its source.

From Reframing to Real Change: The Power of Diet and Lifestyle

Cognitive reframing, the recognition that diet and lifestyle can profoundly influence genetic expression, is not just a shift in perspective; it is the first step in successfully applying the biomedical and functional medicine approaches.

When we understand that our genes are not fixed destinies but rather potentials waiting to be activated or silenced by our environment, we unlock the power to reclaim our health. This is not about denying genetics; it’s about embracing the full picture, where genetics and environment work in tandem.

The evidence is clear: the explosion of conditions like obesity, autism, and cancer in recent decades cannot be explained by genetics alone. The environment, our diets, our exposures, our lifestyles, plays a crucial role in determining which genes are expressed and how they affect our health.

By prioritizing diet and lifestyle, we move from passive acceptance of genetic fate to proactive engagement with our biology. This is the essence of the biomedical and functional medicine approaches: addressing the root causes of disease, not just the symptoms. These interventions do not erase genetics; they work with them. They help us determine which genes stay silent and which ones come to life, allowing us to shape our health outcomes in meaningful ways.

Your biology is listening to your environment every single day. The empowering truth is that you can speak back.

I have evaluated children across the autism spectrum in New York City since 2010, and the change I have seen is not subtle. It is also not mainly at the mild end. Year after year, more of the children referred to me are profoundly affected: nonspeaking or minimally verbal, requiring constant support, unable to complete standardized testing without significant accommodation. These are Level 3 presentations, the most severely disabled end of the spectrum, and there are far more of them than there were fifteen years ago.

The standard explanation for rising autism numbers is that we have widened the definition and are simply catching milder cases that were always there. Whatever truth that holds for the mild end, it does not explain what I am seeing. The increase in my practice is driven by children at the severe end of the spectrum, those with significant cognitive and communication impairment, and their numbers have grown markedly over the past decade.

The scale of the increase is visible in the state’s own numbers. Across New York City, the count of students classified with autism has more than tripled in a little over a decade, from about 12,000 in 2011-12 to more than 40,000 today. The climb has been steady and it has accelerated.

New York City students classified with autism, 2011-12 to 2024-25. Source: New York State education data.

You do not have to take my word for what this means on the ground, because the systems built for the most significantly disabled are visibly straining to keep up. In my own field I have watched a wave of new private schools open to serve severely affected autistic children, existing programs expand, and established schools add satellite locations to meet demand that did not exist a decade ago. Private and nonpublic school enrollment is not tracked in any public dataset, so that expansion cannot be counted directly. But the public system can be. District 75, the New York City public district that serves students with the most significant disabilities, has been expanding its enrollment and opening new sites across the city. These are not programs for mild cases. They exist for children who need the most support, and they are growing.

District 75 special-class enrollment. Recent years are reported by the DOE; the two earliest bars are estimated from stated growth rates.

The same is true in the system that supports people for a lifetime. New York’s Office for People With Developmental Disabilities serves those whose disabilities are severe enough to require lifelong support, precisely the population a broadened diagnosis does not add. New York’s own Autism Cost Study reports that within OPWDD, people with an autism diagnosis are the fastest growing population in both raw numbers and percentages, even as they remain a minority of those served. The count bears that out: from the study’s figures and OPWDD’s subsequent reports, the number of people served with autism rose from about 20,800 in 2015 to more than 39,000 in 2024, nearly doubling. Autism is not the largest category in the system, but by my calculation from OPWDD’s published figures it accounts for roughly nine in ten of the system’s net growth in recent years. It is the diagnosis driving the increase.

People served by OPWDD with autism as a primary diagnosis, statewide. OPWDD serves people with substantial, lifelong impairment.

Put the pieces together and the picture is hard to miss. The number of severely disabled children is climbing, and autism is the force behind the climb. In my office, in the schools built for the most affected students, and in the system that supports the most impaired adults, the same trend appears. This is not a wider net catching milder cases. It is more children who are seriously, visibly, and permanently disabled, and increasingly those children have autism.

To tell the families of these children that nothing has really changed, that we are only counting better, is a form of gaslighting. It asks these families to distrust their own eyes, and it looks past the children with the greatest needs and the least ability to speak for themselves. The complacency also has a price. If the rise is presumed to be an illusion of definitions, then there is nothing to explain, nothing to investigate, and no reason to look for a cause. The more honest and more useful posture is to accept that the number of severely disabled children is rising, that autism is driving it, and to ask, without foreclosing any serious line of inquiry, “why?”.

Source: New York State Autism Cost Study Report (2022), prepared pursuant to Chapter 210 of the Laws of 2018, New York State Office for People With Developmental Disabilities. OPWDD enrollment figures for 2024 are drawn from OPWDD By The Numbers (2024 data). District 75 and citywide classification figures are from New York City Department of Education and New York State Education Department special education data.

A Generation Unmasked: Language Disorder, Dyslexia, and the Long Shadow of COVID

Children learn to talk by watching faces. This is not a metaphor. Early language acquisition is a multimodal process: infants and toddlers are reading lips, tracking jaw movements, mapping the visual shape of sounds to the auditory experience of hearing them. Before children understand words, they are learning the phonetic architecture of their language in part through watching the mouths of the people who speak it to them. This face-to-face channel of language learning is one of the most robust and least appreciated contributors to how children build phonological awareness, the foundational skill that later makes reading possible.

For children who spent their most critical language-learning years behind a wall of masked faces, that channel was disrupted. The cohort of children born between roughly 2017 and 2022 arrived at their peak years of receptive and expressive language development during a period when the adults around them (parents, caregivers, daycare teachers, pediatricians) were wearing masks.

What we are beginning to see in clinical settings now, as these children reach school age, is a coherent pattern of disruption across several related domains. Speech articulation disorders are among the most visible presentations: children with irregular pronunciation patterns, difficulty producing certain sounds correctly, and speech that sounds effortful or unusual in ways that stand out to parents and teachers alike. This matters beyond communication. Articulation disorders reflect underlying problems with phonological representation, and a child who cannot reliably produce the sounds of their language almost certainly does not have clean internal representations of those sounds either. Degraded phonological representations are precisely what drive dyslexia. A child who struggles to pronounce words correctly is a child at high risk for struggling to decode them in print. The articulation difficulty and the reading difficulty are not separate problems; they are two expressions of the same underlying phonological processing weakness.

Why visual input matters so much

The role of mouth and lip movement in early language learning is well established in the developmental literature. Infants as young as two to three months begin preferentially attending to mouth movements during speech, and by the time children are toddlers, visual phonological input is actively contributing to how they distinguish and internalize the sounds of their language. This is not a minor or secondary channel. Research on the McGurk effect demonstrates that what we see when someone speaks directly influences what we hear: visual and auditory phonological information are integrated in processing, not received separately. Remove the visual half of that pairing during the years when the phonological system is being built, and the construction of that system is at risk.

Masks removed precisely that input. The lower half of the face, where the mouth and jaw movements that carry phonological information are visible, was fully occluded in most settings throughout the pandemic. Clear masks were advocated for by speech-language pathologists for exactly this reason, but they were not widely adopted. For the majority of children in the majority of settings, the visual phonological channel went dark during the years it was most needed.

Implications Moving Forward

These clinical presentations do not always prompt the right referrals, and that is the central problem this cohort faces. A child flagged for articulation may receive speech therapy targeting pronunciation without anyone connecting that presentation to downstream reading risk. A child who reads some words by sight may not be identified as struggling with phonological decoding until the curriculum shifts and sight-word strategies stop being sufficient. In both cases, something important is being missed: not the symptom, but the pattern behind it.

What this generation of children needs is a clinical response that matches the coherence of the problem. Speech articulation difficulties and reading disabilities in this cohort are not independent findings requiring independent, unconnected interventions. They are expressions of the same phonological processing vulnerability, and they call for a coordinated response. Targeted speech therapy addressing phonological awareness and sound production, delivered alongside multisensory reading instruction of the kind that structured literacy programs provide, reflects that understanding. One works at the level of sound representation and articulation. The other builds the bridge from sound to print. Neither is sufficient without the other in children who present with both.

Awareness is the first requirement. Parents, pediatricians, and educators who recognize articulation difficulties in children from this cohort should understand that what they are seeing may be the leading edge of a reading disorder that has not yet fully emerged. Early referral for a comprehensive evaluation, one that assesses phonological processing, speech production, and early literacy skills together rather than separately, gives clinicians the information needed to intervene before the reading gap becomes entrenched. The window for high-yield intervention remains open for many of these children. Acting on what the speech presentation is telling us, rather than treating it in isolation, is how we keep it open.

One of the most reliable early signs of autism is a love of structured, symbolic information. Letters on refrigerator magnets. Numbers on license plates. The alphabet in Spanish, then Japanese, then Arabic, just because it’s interesting. This pattern, called hyperlexia, reflects a genuine cognitive strength: an intense, often precocious orientation toward written and symbolic material. It can be one of the first things parents notice, and it tends to reassure them that reading will be the least of their worries.

That reassurance is usually warranted. But not always.

A meaningful subset of autistic children carry a co-occurring diagnosis of dyslexia, and the combination can be clinically deceptive. These children share much of the hyperlexic profile: the fascination with letters, the eagerness to engage with academic content, the early interest in learning what written symbols mean. What they don’t share is the ease of converting that interest into fluent reading. Despite the curiosity, despite the exposure, despite genuinely trying, decoding remains a struggle. Phonics don’t stick the way they should. Words that were read correctly last week are unrecognizable today. Reading aloud remains labored even with repeated exposure to the material.

What this looks like in practice

Parents of these children often describe a confusing picture. Their child knows what letters are, can identify them on sight, and may have strong general knowledge, but stumbles over simple words, resists reading tasks, or takes far longer than expected to progress through early phonics curricula. These children are often already receiving autism-related services (speech-language therapy, occupational therapy, behavioral support), and the presence of those services can create the impression that the child’s needs are being addressed. What they are not receiving is the one thing that would actually close the reading gap: individualized, multisensory reading instruction targeting phonological decoding. The autism support addresses the autism profile. It does not teach the sound-symbol code. Without a dyslexia diagnosis to name the problem precisely, that specific instruction is rarely initiated, and the reading difficulty continues to accumulate behind a backdrop of otherwise adequate support.

Dyslexia is a phonological processing problem, a difficulty breaking spoken and written language into its component sounds and mapping those sounds reliably to printed letters. No amount of additional reading practice resolves that deficit on its own. What resolves it is explicit, systematic, structured instruction in the phonological code: the kind of teaching that Orton-Gillingham, Wilson, Lindamood-Bell, and similar structured literacy approaches provide.

Why the hyperlexia can mask the problem

The risk in this population is that the academic interest obscures the academic struggle. Parents and teachers see a child engaged with letters and assume the reading is coming. The child’s love of symbolic material gets interpreted as evidence of reading readiness, and technically, it may be. What it doesn’t guarantee is reading fluency.

By the time the gap becomes undeniable, usually around second or third grade when reading demands shift from decoding to comprehension and the curriculum begins to assume fluent reading as a baseline, months or years of remediable deficit have accumulated. The window for early intervention, when the brain is most plastic and responsive to phonological instruction, has narrowed.

Why the diagnosis matters

Identifying dyslexia in autistic children opens access to intervention that is categorically different from general reading support. Structured literacy instruction is not simply more reading practice. It is explicit phoneme awareness training, systematic phonics instruction, and repeated practice with decoding and encoding under guidance. It requires trained specialists, and in many states, it is specifically mandated for children with a documented dyslexia diagnosis.

The diagnosis also matters for school eligibility. A child who is autistic and performing below grade level in reading may receive accommodations (extended time, text-to-speech) without anyone identifying the underlying dyslexia or providing the intervention that could actually close the gap. Accommodations help a child manage a deficit. Structured literacy addresses the deficit itself. Both matter, but one requires the correct diagnostic language to unlock.

Getting the right evaluation

When a child presents with autism, strong academic interest in symbolic material, and a persistent struggle to decode, a formal diagnostic evaluation is the necessary next step. That evaluation needs to come from a licensed psychologist or neuropsychologist. In New York State, a formal dyslexia diagnosis can only be rendered by a licensed psychologist or neuropsychologist. School psychologists, operating under educational rather than clinical frameworks, identify Specific Learning Disabilities in reading but do not issue a formal dyslexia diagnosis. The same distinction applies nationally: schools evaluate and determine educational eligibility, but the clinical diagnosis requires a private evaluation.

For families in New York with commercial health insurance, the Dyslexia Diagnosis Access Act, effective January 1, 2025, now requires insurers to cover neuropsychological testing for dyslexia, with coverage capped at $6,000 per evaluation. New York is the first state in the nation to mandate this coverage, and no comparable law currently exists elsewhere. This removes a significant barrier that previously left families absorbing costs of $5,000 to $10,000 out of pocket. Families covered by Medicaid are not yet included under this law, though legislation to extend comparable Medicaid coverage has been introduced in the current legislative session and has not yet passed.

A Parent’s Introduction to the Biomedical Approach

A Budget-Friendly Starting Point for Families

This guide is built around a single, important truth: the biggest gains usually come from the basics. Sleep, food quality, gut support, and a cleaner home environment are the foundation — and they are available to every family, regardless of budget. You do not need to spend a lot of money to begin doing meaningful biomedical work for your child.

When I first began learning this approach, I struggled with how to explain it to families without it feeling overwhelming — because, honestly, it was still feeling overwhelming to me. Then one day a 19-year-old father walked into my office. He was from Far Rockaway, Queens — not a place associated with access to integrative medicine or specialty wellness resources. He hadn’t seen a functional medicine doctor or read a clinical textbook. What he had done was find a Facebook group called Health and Hope for Autism, start reading, and begin quietly changing what his child was eating and what was in their home. And it was working. He wasn’t waiting for permission or for the perfect plan. He just started with what he could do.

I think about him often when I sit across from families who feel like this approach is out of reach. If a teenage father from Far Rockaway, armed with nothing but a Facebook group and the willingness to try, could make meaningful changes — this is accessible to anyone who sees the importance of it.

Four Principles That Run Through This Entire Guide

• Selective eaters benefit enormously from a non-pressure, repeated-exposure approach to food. This strategy is free at every income level.

• Sleep is the single highest-leverage variable. Any plan that does not include attention to sleep is incomplete.

• Slow and steady is the only pace that works. Biomedical change is not a switch that gets flipped — it is a gradual recalibration of the body’s systems, and it asks for patience. Small gains are real gains: a child sleeping thirty minutes longer, a constipation pattern that begins to resolve, a meltdown that doesn’t escalate the way it used to. These are meaningful biological signals, not coincidences. Notice them, record them, and let them motivate the next step. Managing expectations is not pessimism — it is the thing that keeps families in the process long enough for the process to work.

• These changes belong to the whole family. The dietary and environmental shifts described in this guide are not a special protocol for one child — they are simply how human beings are meant to live. We are in the middle of a crisis of metabolic disease: rising rates of obesity, diabetes, autoimmunity, and inflammatory illness that are not inevitable but are, in large part, the result of the same dietary patterns and chemical exposures this guide asks you to reduce. When you remove artificial dyes from your kitchen, you remove them for everyone. When you clean the air in your home, everyone breathes it. When you build a calmer bedtime routine, the whole household benefits. What begins as something you do for your child has a way of becoming something that transforms the health of your entire family.

What’s in This Guide

1. What Tests Can Be Ordered Through Insurance

2. Budget-Friendly Diet Changes

3. Budget-Friendly Home Environment Changes

4. Affordable Supplements Worth Considering

5. Foundation Reality Check

Section 1: What Tests Can Be Ordered Through Insurance

Most families are unaware that a thoughtful primary care provider can order a substantial biomedical workup at little to no out-of-pocket cost. The key is knowing what to ask for and having a clinical reason to support it — which, for most children seen in a neuropsychological context, exists.

Ask your pediatrician or developmental pediatrician to order the following:

Covered by Medicaid and most commercial insurance when there is a clinical justification.

• Complete Blood Count (CBC) — evaluates red and white blood cell health, flags anemia and immune irregularities

• Comprehensive Metabolic Panel (CMP) — assesses kidney and liver function, blood sugar, and electrolytes

• Vitamin D (25-OH) — deficiency is extremely common and directly affects immune function, mood, and behavior

• Ferritin (iron storage) — low ferritin is one of the most overlooked drivers of sleep disruption, attention difficulties, and fatigue in children; a standard iron level alone is often insufficient and ferritin must be specifically requested

• Vitamin B12 and Folate — relevant to neurological function and methylation; important in children with dietary restriction or GI concerns

• Lead level — standard in pediatrics, but worth confirming has been done and reviewed

• Thyroid panel (TSH, free T4) — often overlooked in pediatric neuropsychological workups; low thyroid function can mimic or worsen ADHD, anxiety, and sluggishness

• Full iron panel (serum iron, TIBC, transferrin saturation) — request this specifically in addition to ferritin

Through referrals from your primary care provider (typically covered):

• Pediatric allergist or immunologist — for evaluation of eczema, asthma, recurrent infections, and allergic sensitization; skin testing and RAST panels are generally covered

• Pediatric gastroenterologist — warranted in children with chronic constipation, loose stools, abdominal pain, bloating, or selective eating patterns rooted in GI discomfort

• Pediatric endocrinologist — if thyroid labs are borderline or if growth and metabolic concerns are present

A note on advocacy: Pediatricians do not always spontaneously order this full panel. It is appropriate — and often necessary — for parents to ask specifically for each test by name and to note the clinical reasons. Most providers will comply when asked directly. Below are examples of how to frame these requests based on what you are seeing at home:

If your child struggles with behavioral dysregulation — meltdowns, emotional volatility, impulsivity, difficulty settling, or rages that seem out of proportion — you might say: “He has significant mood and behavioral dysregulation and I’d like to rule out low ferritin, since it affects dopamine regulation and sleep. I’d also like thyroid labs, because low thyroid function can look a lot like ADHD and anxiety in kids.” Vitamin D, B12, and folate are also worth requesting, as deficiencies in all three have direct effects on neurological function and emotional regulation.

If your child has ongoing digestive issues — chronic constipation, loose stools, bloating, reflux, abdominal pain, or a diet so restricted it raises concern about nutritional gaps — you might say: “She has chronic constipation and a very limited diet, and I’d like a comprehensive metabolic panel and iron panel to check for deficiencies that might be driving some of this. I’d also like a referral to pediatric GI.” A CMP can flag liver and kidney markers that sometimes shift with gut dysfunction, and ferritin in particular is often low in children with poor absorption or restricted intake.

If your child gets sick frequently or seems to have a weak immune system — repeated ear infections, frequent colds, slow recovery, persistent eczema, asthma, or recurrent respiratory illness — you might say: “He’s had four ear infections this year and gets sick more than other kids his age. I’d like a CBC to look at his white cell counts and immune markers, and a vitamin D level, since low D is one of the most common and correctable drivers of immune vulnerability. I’d also like a referral to a pediatric allergist or immunologist.”

You do not need to present as an expert. You are simply telling your child’s doctor what you are observing and asking for the tests that are clinically indicated. Write it down before the appointment if that helps — and if a request is declined, ask what clinical threshold would need to be met for the test to be ordered.

One Test Worth Knowing About: The FRAT (Folate Receptor Antibody Test)

The FRAT is not currently covered by insurance, but it identifies something that standard folate testing cannot: autoantibodies that block folate from being transported into the brain. A normal serum folate level on standard labs does not rule this out — the two tests are measuring entirely different things.

Research shows that a significant subset of children with autism and PANS/PANDAS carry these antibodies, and some show meaningful improvements in language, attention, and behavior when treated with high-dose folinic acid (Leucovorin). Crucially, if a child tests positive and a prescribing physician recommends Leucovorin, that treatment is a covered prescription medication. The diagnostic test is out-of-pocket; the treatment is not.

Cost and access: The FRAT is available through Iliad Neurosciences / Religen Diagnostics and typically runs a few hundred dollars out-of-pocket. It requires a small blood sample and can be ordered by a licensed physician or accessed through telehealth providers who specialize in this testing. It belongs in the “when you have some budget” tier of the workup — meaningful, but not the first step for a family operating on a tight budget.

Section 2: Budget-Friendly Diet Changes

You do not need to go entirely organic or overhaul your kitchen overnight. The changes below are high-impact, low-cost, and achievable on a tight budget, including with SNAP and WIC.

Remove first — these cost nothing:

• Eliminate artificial dyes — Red 40, Yellow 5, and Yellow 6 are found in cereals, fruit snacks, sports drinks, flavored yogurts, and candy. Research links these to behavioral reactivity in sensitive children. Reading labels costs nothing.

• Reduce added sugar and high-fructose corn syrup — this means replacing sweetened drinks with water and choosing plain versions of foods (plain oats vs. flavored packets, plain yogurt vs. flavored).

• Remove artificially flavored foods — artificial flavorings in processed snacks can be a low-grade irritant for children with sensory sensitivities. Common examples include artificially flavored chips and crackers (ranch, nacho cheese, sour cream and onion), fruit-flavored snack pouches and gummies, flavored popcorn, sweetened cereals with artificial fruit or chocolate flavoring, and flavored rice cakes. When reading labels, look for “artificial flavor” or “natural and artificial flavors” in the ingredient list as the trigger to avoid.

Budget-friendly staples to build around:

• Eggs — among the most affordable, nutrient-dense proteins available; provide choline, B12, and fat-soluble vitamins

• Frozen wild-caught fish — more affordable than fresh; look for sales on salmon, cod, or tilapia

• Beans and lentils — affordable protein and fiber; supportive of gut microbiome health when well tolerated. Introduce slowly and one variety at a time, as some children with sensitive guts do not tolerate legumes well initially — start with small amounts and watch for bloating, gas, or changes in stool before making them a regular staple

• Frozen vegetables — nutritionally equivalent to fresh and significantly less expensive; stock broccoli, spinach, peas, and mixed vegetables

• Oats — plain rolled oats are inexpensive, filling, and GI-supportive; avoid the flavored packets with added dyes and sugar

• Bananas — one of the most affordable fruits; good source of potassium, B6, and prebiotic fiber

• Grass-fed ground beef when on sale — better fatty acid profile than conventional; often available at warehouse stores

• Conventional ground beef — a reliable, affordable protein source; lower in omega-3s than grass-fed but still provides iron, zinc, B12, and creatine; widely available and budget-friendly year-round

• Canned sardines — inexpensive, rich in omega-3 fatty acids and vitamin D, and one of the lowest-mercury fish available

Practical approaches for selective eaters:

• Introduce new foods alongside preferred foods without pressure. A new vegetable placed on the plate without comment — night after night — is how exposure begins.

• Food chaining (linking a new food to a preferred one through small steps in flavor or texture) is a strategy feeding therapists charge for; it can be implemented at home for free.

Section 3: Budget-Friendly Home Environment Changes

The home environment is one of the most modifiable factors in a child’s neurological and immune health — and many of the highest-leverage changes cost little or nothing.

Free changes to make now:

• Open windows when weather permits — ventilation reduces indoor air pollutants and VOC accumulation, which is especially relevant in newer or recently renovated homes

• Remove fragranced products — plug-in air fresheners, scented candles, and heavily fragranced laundry products are a significant source of indoor chemical exposure; these worsen eczema, asthma, and respiratory irritation. Unscented alternatives are typically the same price or cheaper.

• Consistent bedtime routine — a predictable, calming wind-down sequence (bath, dim lights, quiet activity, sleep) is the most powerful sleep intervention available and costs nothing

• Screen-free period before bed — blue light from screens suppresses melatonin and delays sleep onset; a 30–60 minute screen-free wind-down is a free, high-yield change

• Daily outdoor time and morning sunlight — morning light exposure on the face is the most reliable way to anchor the circadian rhythm and improve nighttime melatonin production; aim for 15–30 minutes outdoors in the morning when possible

Low-cost additions (under $30):

• Epsom salt baths 2–3 times per week — magnesium sulfate is absorbed transdermally; calming to the nervous system, supportive of sleep, and helpful for constipation. A large bag of Epsom salt typically costs $6–10.

• Switch to fragrance-free laundry detergent — brands like All Free & Clear or store-brand equivalents are widely available and often no more expensive than scented alternatives

• Fragrance-free personal care products — this includes shampoo, soap, and lotions; particularly important for children with eczema

One-time investments when budget allows:

• Basic HEPA air filter for the child’s bedroom — reduces allergens, dust mites, mold spores, and particulates; entry-level models start around $40–60 and are meaningful for children with eczema or respiratory reactivity

Section 4: Affordable Supplements Worth Considering

These are not a replacement for food and lifestyle changes, but they address common deficiencies in children with neurodevelopmental profiles. Most are under $20 and available without a prescription.

• Children’s multivitamin — choose one without dyes or artificial flavors (Nordic Naturals, SmartyPants, or store-brand options)

• Vitamin D3 drops — especially important in children with limited sun exposure or dark skin tone, and in northern states

• Magnesium glycinate — often the most bioavailable form; supports sleep quality, reduces anxiety, and helps with constipation

• Cod liver oil or basic fish oil — provides omega-3 fatty acids (EPA and DHA) supportive of brain inflammation regulation and attention

Always discuss supplements with your child’s pediatrician before starting, particularly if your child takes any medications.

Section 5: Foundation Reality Check

Before pursuing any additional testing, specialty consultation, or advanced intervention — confirm that these fundamentals are actually in place:

✓ Artificial dyes and added sugars are minimized

✓ A consistent, calming bedtime routine is in place

✓ Your child is getting at least some daily outdoor time

✓ Fragranced products have been reduced or removed

✓ Your pediatrician has ordered the basic labs listed above

If these foundations are not yet in place, they are the highest-value next step — more than any specialty lab or expensive supplement.

The Restoring Balance Autism Recovery documentary tells the stories of several families who used a functional medicine approach to successfully treat the symptoms of Autism Spectrum Disorder.

The stories: The film contains interviews and video footage of individuals with Autism at various stages in their lives, before and after experiencing significant improvements. The families tell stories of how they learned about the Autism diagnosis and how they found the functional medicine approach. The families work with functional medicine doctors who help guide and individualize the treatment based on the results of various tests and the success of various interventions. The specific protocols that were followed by each family are not detailed, however all the families make significant dietary changes and also use some supplements. All the families adopt a diet that avoids processed foods, pesticides and focuses on eating high-quality, nutrient dense foods.

The theory: The film purports that the cause for the rapidly increasing rate of Autism is environmental in nature. The rationale behind this claim is the fact that Autism has been increasing at a rapid pace during the last several decades, which decreases the likelihood of a genetic etiology. Instead, it is likely that something in the environment has changed to contribute to this rise. The film goes on to present a theory of what specific environmental change or changes have contributed to the increase.

What in the environment has changed? The increased consumption of highly processed foods, the rapid increase in environmental toxins including pesticides, heavy metals, microplastics and mold or mycotoxins, as well as changing birthing practices and overuse of antibiotics that lead to sub-optimal microbial diversity in newborns. Individuals are being born with sub-optimal microbiomes during a time when the quantity and variety of environmental toxins are increasing at rapid rates.

Why do these changes lead to autism in some but not all individuals? The film purports that individuals with Autism have an excess build-up of fluids and toxins in neural tissue with reduced capacity for excretion of these toxins. This eventually leads to a sequelae of downstream effects including excess neuroinflammation. Moreover, and perhaps related to their reduced capacity to excrete toxins, individuals with Autism have sub-optimal diversity in their gut microbiomes which further impairs the body’s ability to process environmental toxins. Sub-optimal gut microbiome also leads to increased intestinal permeability and associated disruptions in nutrient absorption and immune functioning.

What about food allergies or intolerances? In addition to exposure to environmental toxins, the film notes that individuals with Autism often have food allergies or intolerances to many common foods, especially gluten and dairy (i.e. casein). Continued exposure to the food in question leads to increased inflammation as well as disruptions in intestinal permeability that lead to further complications. Most or all of the families in the film adopt a strict gluten-free, casein-free (i.e. GCFC) diet as part of their treatment plan. Depending on the specific allergy profile of the child, other foods were also avoided or limited. Depending on the toxic load, which can be heavy metals, mold or others in addition to pesticides, other supplements or medications are also prescribed.

Are the claims real? The clinical improvements that are demonstrated in the film are dramatic and undeniable. Autism is not necessarily ‘cured’, but the individuals in the documentary made significant and remarkable improvements and some in the film no longer meet diagnostic criteria for autism. Based on the anecdotes and supporting video evidence, there is no reason to doubt that the improvements in the film are real. Moreover, many instances in the peer-reviewed clinical literature support the veracity of the claims made regarding the potent clinical benefits of a functional medicine approach.

Is the functional medicine approach used for other conditions? Yes. Functional medicine approaches with empirical support in peer-reviewed research journals exist for a multitude of conditions including but not limited to Alzheimer’s Disease (ReCode protocol created by Dale Bredesen MD), Multiple Sclerosis (Wahl’s protocol created by Terry Wahls MD), Age-related macular degeneration (Chris Knobbe MD’s ancestral diet) and Type 2 Diabetes (Jason Fung MD’s Diabetes Code, and many others). The specifics of each approach varies, however the foundation of each approach is eating a diet that consists of whole foods that are minimally processed and an avoidance of refined sugar and pesticides. There is also a focus on consuming nutrient-dense foods and high-quality fats while avoiding unstable cooking oils and fats (i.e. polyunsaturated fats or PUFAs) that are prone to degradation and associated with a host of negative health sequelae. All the approaches mentioned have reversed the progression of the ‘irreversible’ disease process for which they were created, whether it is Alzheimer’s/Dementia, Multiple Sclerosis, Age-related macular degeneration, or Type 2 diabetes.

Are these solutions available to everyone? Yes and no. The solution proposed in the Restoring Balance Autism Recovery documentary is real but does not come easy. The families in the documentary required a great deal of discipline, motivation, and resolve to implement the proposed strategies. Yes there is also the monetary expense of paying for diagnostic tests and some dietary supplements, but the real difficulty in my opinion is the fact that implementing the approach requires one to carefully source and cook some or all of their own food. The good news is that the foods promoted are nutritious and can be prepared to personal taste, so improving the quality of your diet and health can taste good.

Finding a functional medicine doctor Another challenge to implementing a functional medicine approach is that it can be challenging to find a functional medicine provider to work with. There are many providers who are medical doctors, however there are also many naturopathic doctors, nutritionists, and other alternative medicine providers who are helping people apply functional medicine approaches. In addition to the approached mentioned previously (i.e. ReCode for Alzheimer’s, Wahls protocol for MS, etc.), provider directories exist at the Institute for Functional Medicine and the Chris Kresser Institute. For providers who specialize with children, there is a list of providers on the Restoring Balance, Autism Recovery website.

Read an extended discussion and opinion here:

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The “Restoring Balance, Autism Recovery” documentary (1) highlights the potential for the functional medicine approach to treat symptoms of Autism. When considered in isolation, many may find the claims made in the Restoring Balance documentary to be too hard to believe, or write them off as cherry-picked examples of success stories. When the documentary is considered within the greater context of the success of the functional medicine approach in other areas, then the claims made in the film make much more sense. Yes, they are cherry-picked examples of success stories, but that does not mean the claims are not real. The fact that there are similarly remarkable improvements documented with other ‘irreversible’ diseases using a functional medicine approach, lends to the credibility and potential reproducibility of the approach.

What is the functional medicine approach?

The functional medicine approach aims to address the underlying cause of an ailment or disease. The main ways in which this is accomplished is by improving the health of the microbiome, correcting nutritional deficiencies, identifying and eliminating harmful toxins from environmental exposure, and optimizing diet, not in that particular order.

Several functional medicine approaches with empirical evidence of their dramatic improvements have been documented. One such program is the ReCode protocol for Alzheimer’s and other forms of dementia that was developed by Dale Bredesen MD (2); another is the Wahls protocol for Multiple Sclerosis that was developed by Terry Wahls MD (3). Remarkably, both dementia and Multiple Sclerosis are known to be progressive and irreversible. The ReCode and Wahls protocol have both resulted in the cessation and even the reversal of the disease process in affected individuals. Other examples include the Ancestral Diet plan advanced by Chris Knobbe MD (4) that reverses another progressive and degenerative condition, Age-related macular degeneration, and the Diabetes code advanced by Jason Fung MD (5) that reverses Type 2 diabetes.

All these approaches, including the one outlined in the Restoring Balance Autism documentary, have in common their use of the functional medicine approach to create a personalized treatment plan for each patient. Other conditions for which the functional medicine approach is well established include most autoimmune disorders. Positive research is also accumulating in support of the approach in treating anxiety disorders, depression and even bipolar/schizophrenia that has spurred the creation of the field of Metabolic Psychiatry. Metabolic Psychiatry focuses on dietary changes and optimizing metabolic health as a treatment for mental disorders.

Functional Medicine Responds to the changing landscape of disease

The fact that Autism rates are rising shouldn’t be surprising since it is occurring during a time when we are seeing a meteoric increase in many different diseases including dementia (rates have more than doubled since 2000, from  30.5 deaths per 100,000 in 2000 to 66.7 in 2017 (6)), diabetes (type 1 and type 2), obesity, and autoimmune disorders like thyroid dysfunction. Since these diseases were either rare or non-existent prior to the modern age, they are often referred to as ‘diseases of civilization’ (7). Other diseases of civilization include coronary heart disease, age-related macular degeneration and many cancers. America is leading the world in these diseases, but the rest of the world is right behind us. Diseases of civilization have been shown to develop whenever a group of people begin to eat a diet consisting of processed foods. One of the many examples of this is the rising levels of obesity, diabetes and coronary heart disease and other diseases of civilization in places like Japan and China (8,9).

Diseases of Civilization are present wherever modern, processed foods are consumed

Most industrially-produced modern foods are highly processed by their manufacturers in order to improve profitability and palatability. The four main categories of ‘processed’ foods first sprung into use in the early 20th century, and include: refined flours or grains, refined and processed sugars, vegetable or seed oils, and trans fats. Each of these types of processing leads to a host of negative downstream health consequences. Many scientists and medical doctors noticed the changing nature of human disease profiles and made the connection to processed food early on. Weston Price, a dentist who practiced in Cleveland during the first half of the 20th century, hypothesized that modern processed food was to blame (10). In order to test his hypothesis, Price travelled around the world in search of people who had not yet adopted a Western diet. In his seminal work, Nutrition and Physical Degeneration, Weston Price found that people who didn’t eat processed foods had perfect teeth and different facial structure, better resistance to illness and better physiques as compared to people who began eating processed foods. He concluded that modern, processed foods were the cause of the “physical degeneration” that he observed in modern society. Price went on to analyze the nutritional components of the diets he studied and published them in Nutrition and Physical Degeneration, with his work and findings summarized on the Weston Price Foundation website (11).

What Price observed is still present today. There still remain groups of people who have not adopted a Western diet of processed foods, and who do not suffer from so-called ‘diseases of civilization’. There are several groups of people who have not adopted the Western Diet including Hunter-gatherers and other populations. Notably the Hadza and Maasai are nomadic tribes in central Africa who have become the subject of scientific studies because of their remarkable health that is linked to their ancestral diet. They do not suffer from heart disease, cancer or autoimmune disorders. Other remote populations who have been studied and found to exhibit the absence of diseases of civilization include the Tsimane (Bolivia), Tukisenta (New Guinea) and the Kitavans (Papua New Guinea) (12–15).

Another major environmental factor: Pesticide Use

Diseases of civilizations began to propagate long before pesticides were introduced. Nonetheless, their progression has been greatly accelerated by the use of pesticides (16). Pesticides are toxic chemicals that are designed to kill weeds and other pests. Pesticides contain heavy metals and are also toxic to humans, however, regulatory agencies have designated an arbitrary level of pesticide exposure that is deemed ‘safe’ for humans. Like the way that bacteria grow resistant to an antibiotic, weeds and other pests become resistant to pesticides. The result is that industrial farming began using different pesticides and in larger quantities. Glyphosate was introduced in the 70s and has gained a lot of recent attention because of its links to cancer and other diseases.  The amount of glyphosate being used has increased at an exponential rate since the 70’s, the time-frame of which is closely correlated to the steep rise in Autism and other disorders, like autoimmune disorders, dementia, and others. Not only does glyphosate pose a risk because of its direct toxicity, but the crops that are sprayed with it also have significant reductions in nutritional content as compared to those that are grown in healthy soil. The resulting food is missing key vitamins and minerals, in addition to being contaminated with toxic pesticide residue.

Changes in the environment and behavior lead to disruptions in the integrity of the microbiome

The microbiome is passed on from mother to child. Several factors lead to a sub-optimal microbiome at birth, the first beginning with the microbiome of the mother. If the mother has an unbalanced microbiome because of an illness, poor diet or poor metabolic health, this is the microbiome that is passed onto the child. Other factors that can reduce microbial diversity in the microbiome include cesarean delivery and breast feeding (17,18). Babies who are born via cesarean delivery miss out on maternal bacteria from the birth canal, while babies who are breast fed have been demonstrated to have superior microbiomes than their formula-fed counterparts. Moreover, baby formulas are jam-packed with a long list of ingredients that include many of the same processed ingredients that populate other unhealthy foods (like highly processed seed oils), and babies are often treated with antibiotics that serve to indiscriminately affect good and bad bacteria. The result is that so many individuals are beginning their lives with sub-optimal microbiomes. This means that they are less equipped to deal with environmental stressors like toxins, they have reduced immune capacity, and they have a reduced capacity to extract nutrition from food. At the same time, the number and quantity of environmental toxins has increased and the vitamin/mineral content in food is significantly reduced because of factors including pesticide use and agricultural practices that lead to unhealthy soil.

All these changes are likely responsible for the increase in Autism and all the other diseases of civilization.

Functional Medicine Approach: Health across the lifespan

The Restoring Balance, Autism Recovery film purports that since the increase in the prevalence of Autism is occurring at such a rapid pace, the cause is environmental in nature. Our genes themselves have not changed, but our environment and our behavior have changed. The increasing prevalence of all these disorders, therefore, is due to epigenetics, or the interaction with our genes and the environment. 

Interestingly, many of the same factors that are leading to Autism are also likely leading to the rise in other disorders of civilization. 

Therefore, successful avoidance of these environmental factors along with increased focus on improving metabolic health in parents and their children can likely prevent and maybe even reverse autism and other diseases of civilization from occurring. Implementing the dietary and behavioral changes that are recommended by a functional medicine approach can be challenging, but the benefits are remarkable and undeniable. In the process of restoring balance in autism, it is possible to optimize health span for the entire family.

1.        Restoring Balance Documentary | Autism Recovery Community. (2021).

2.        Bredesen, D. The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline. (Penguin Publishing Group, 2020).

3.        Dr. Terry Wahls, MD & Author. Dr. Terry Wahls | MS Recovery & Wahls Protocol [Official]. (2022).

4.        Knobbe, C. Ancestral Dietary Strategy to Prevent and Treat Macular Degeneration: Large Print Black & White Paperback Edition. (Cure AMD Foundation, 2019).

5.        Fung, J. & Teicholz, N. The Diabetes Code: Prevent and Reverse Type 2 Diabetes Naturally (The Wellness Code Book Two) (The Code Series, 2). (Greystone Books, 2018).

6.        Kramarow, E. & Tejada-Vera, B. DEMENTIA MORTALITY IN THE UNITED STATES, 1999–2016. Innov. Aging 2, 244 (2018).

7.        Carrera-Bastos, P., Fontes, O’Keefe, Lindeberg & Cordain. The western diet and lifestyle and diseases of civilization. Res. Reports Clin. Cardiol. 15 (2011) doi:10.2147/rrcc.s16919.

8.        Pan, X.-F., Wang, L. & Pan, A. Epidemiology and determinants of obesity in China. Lancet Diabetes & Endocrinol. 9, 373–392 (2021).

9.        NISHIKAWA, H., FUKUNISHI, S., ASAI, A., NISHIGUCHI, S. & HIGUCHI, K. Obesity and Liver Cancer in Japan: A Comprehensive Review. Anticancer Res. 41, 2227–2237 (2021).

10.      Price, W. & Price-Pottenger Nutrition Foundation. Nutrition and Physical Degeneration. (Price-Pottenger Nutrition Foundation).

11.      Weston Price Foundation Website Article, https://www.westonaprice.org/health-topics/nutrition-greats/weston-a-price-dds/

12.      Vasunilashorn, S. et al. Blood lipids, infection, and inflammatory markers in the Tsimane of Bolivia. Am. J. Hum. Biol. 22, 731–740 (2010).

13.      Sinnett, P. F. & Whyte, H. M. Epidemiological studies in a total highland population, Tukisenta, New Guinea. J. Chronic Dis. 26, 265–290 (1973).

14.      LINDEBERG, S., NILSSON-EHLE, P., TERÉNT, A., VESSBY, B. & SCHERSTÉN, B. Cardiovascular risk factors in a Melanesian population apparently free from stroke and ischaemic heart disease: the Kitava study. J. Intern. Med. 236, 331–340 (1994).

15.      Pontzer, H., Wood, B. M. & Raichlen, D. A. Hunter-gatherers as models in public health. Obes. Rev. 19, 24–35 (2018).

16.      Seneff, S. Toxic Legacy: How the Weedkiller Glyphosate Is Destroying Our Health and the Environment. (Chelsea Green Publishing, 2021).

17.      Dunn, A. B., Jordan, S., Baker, B. J. & Carlson, N. S. The Maternal Infant Microbiome. MCN Am. J. Matern. Nurs. 42, 318–325 (2017).

18.      Mueller, N. T., Bakacs, E., Combellick, J., Grigoryan, Z. & Dominguez-Bello, M. G. The infant microbiome development: mom matters. Trends Mol. Med. 21, 109–117 (2015).

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