This essay concerns what ADHD is, not what its treatment does. The treatment case is developed in The Arithmetic Pill, published earlier in this series. What follows here takes the symptom cluster medicine labels ADHD as its subject. Establishment terminology (ADHD, neurodevelopmental disorder, mental illness) appears in attribution and quotation, describing the diagnostic apparatus and its outputs. The analytical voice operates in a different register, treating the behaviors the diagnosis captures as intelligent responses to identifiable environmental causes rather than as expressions of an intrinsic disorder in the child. The essay includes a first-person account of our family's own encounter with the ADHD referral pipeline twenty years ago. That account appears in one section and is signaled by the section title; the essay returns to analytical voice thereafter.
What the Fever Knows
Parents of children diagnosed with ADHD report the same thing across households, across countries, across income brackets. When their child spikes a fever, the child becomes calm. She sits still. She listens. She holds a conversation. She reads. She falls asleep in her mother’s lap. As the fever passes, the behaviors return.
The observation is not rare. In autism, a related neurological condition that shares this neural pathway, Curran and colleagues at Johns Hopkins and the Kennedy Krieger Institute conducted a prospective study of 30 affected children during and after febrile episodes.² The results, published in Pediatrics in 2007, showed that 83 percent of the children improved on at least one autism-related behavior measure during fever, and 73 percent improved on at least two. The ADHD version of the finding has been reported by parents and clinicians for as long as Ritalin has been prescribed, and appears in Mehler and Purpura’s 2009 paper on the locus coeruleus.¹ Any parent of an ADHD-diagnosed child can watch it happen the next time the child gets sick. It occurs in her own household, without any intervention beyond the natural course of a childhood illness.
The observation rules out several of the explanations medicine has offered. The child has not become a different child during the fever. Nothing about her classroom, her diet, or her screen time is different. The teacher who reported her as inattentive on Tuesday would report her as attentive on Thursday. What has changed is her physiology. The fever has done something the medication is supposed to do and could not do the day before.
The observation is also unusually specific in its scope. It does not appear to matter what is causing the fever. Parents report the same effect from what medicine attributes to influenza, from teething, from stomach illness, from ear infections, from unexplained childhood fevers of the kind that pass in a day. The variable that produces the change in behavior is the fever itself, not the underlying illness the medical system has assigned to it. The ADHD symptom cluster is generated by a physiological state that fever specifically counteracts.
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What Happened at Our School
Twenty years ago, my wife and I were called into a meeting at our daughter’s primary school in Sydney. She was six or seven at the time, in her first year or two of formal schooling. The teachers had prepared a careful set of observations. She was very energetic. She fidgeted through lessons. She struggled to focus on what she was asked to focus on. She could be aggressive with other children. The teachers had brought these observations together with training and experience, and they were doing what their training told them to do. They wanted to refer her to a psychologist.
We knew enough to know where that pathway ended. The psychologist would evaluate her against a checklist of behaviors. She would meet enough of them to justify a diagnosis. The diagnosis would authorize a prescription. In Australia in the early 2000s, the prescription would most likely have been Ritalin. She would begin the drug at six or seven and would remain on it, in the standard progression, through her school years. What she would be like at fifteen, at twenty, at thirty, on a decade or more of daily methylphenidate, was not something the school could tell us and was not something we were prepared to find out.
We took the referral and did not act on it. What we did instead was speak with a naturopath we knew, who suggested that gluten was worth investigating. She recommended the GAPS diet, an elimination approach that removes grains, sugars, and processed foods and rebuilds the gut with bone broths, fermented foods, and traditional fats. It changed how our household cooked and ate. For a six-year-old and her parents, it was a serious commitment.
Within weeks, the behaviors the teachers had catalogued as ADHD fell away. The resolution was not partial and it was not gradual. Our daughter sat through lessons. She focused. The aggression toward other children ended. The teachers noticed. They said so. Nobody at the school suggested she had a milder case than they had originally thought or that the referral had been premature. What they saw was that a child they had described in terms that mapped onto an ADHD diagnosis was no longer describable in those terms, and the change had happened without a doctor and without a pill.
The naturopath had not tested her for anything. There was no gluten intolerance diagnosis, no celiac panel, no biochemical evidence produced before the dietary change. What she offered was an inference: children with those symptoms, in her clinical experience, often responded to gluten removal. The inference turned out to be correct in our case. Whether it would have been correct for every other child in the classroom the teachers might have referred that year is a different question. But it was correct for our child, and it would not have been asked at all in the pathway the school had proposed.
What the Fever Explains
The fever observation is the natural experiment that identifies where in the brain the ADHD symptom cluster is generated and what is doing the generating.
Forrest Maready, in Crooked, traces the evidence to the locus coeruleus, a small nucleus in the brain stem that produces norepinephrine. Norepinephrine is the neurotransmitter that governs the fight-or-flight response. When the locus coeruleus fires, the body prepares for threat: increased heart rate, heightened vigilance, muscle tension, redirected blood flow away from digestion and toward skeletal muscle, and behaviorally, the inability to sit still.³
Under conditions of injury to the locus coeruleus, the nucleus becomes hypersensitive. Trivial environmental stimuli that would not register in an undamaged brain are read as threats, and norepinephrine is released constantly. The child so affected cannot sit still, cannot concentrate on non-urgent tasks, cannot regulate emotional responses, and often suffers digestive problems because sympathetic activation diverts energy away from digestion. This is the ADHD symptom cluster as it presents in most diagnosed children.
The fever observation is explained by this mechanism directly. Generating a fever consumes enormous quantities of norepinephrine. Raising core body temperature by several degrees is metabolically expensive, and the locus coeruleus modulates the process.¹ ⁴ During the fever, the norepinephrine surplus that keeps the child in permanent fight-or-flight is drawn down. Her locus coeruleus, briefly, operates at normal levels. She becomes calm because her nervous system, briefly, is operating as it was built to operate. When the fever passes, the drawdown ends. The norepinephrine surplus returns. She is fidgety again.
What damages the locus coeruleus? Injected heavy metals. Aluminum and mercury accumulate near cranial nerve nuclei, and both are established neurotoxins. Christopher Shaw and Lucija Tomljenovic, publishing in Lupus in 2012, documented that aluminum adjuvants are neurotoxic, that the infant brain is more permeable to them than the adult brain, and that infant kidneys are less able to eliminate them.⁵ The aluminum in a single hepatitis B injection given at birth exceeds by orders of magnitude the amount the FDA considers safe for intravenous exposure in an adult. The cumulative aluminum an American infant receives from the CDC schedule through eighteen months is many times greater than what any individual vaccine’s safety trial studied.
The mechanism by which injected aluminum reaches the brain has been documented in the macrophagic myofasciitis literature, most extensively by Romain Gherardi and colleagues at the Paris-Est Créteil University medical school. Aluminum adjuvants are engulfed at the injection site by macrophages, the phagocytic cells whose job is to isolate and process foreign material. The macrophages do not break the aluminum down. They carry it, still intact, through the lymphatic system and into the bloodstream, and from there into tissues throughout the body, including the brain. The particles persist for years. Gherardi’s team documented aluminum-loaded macrophages in muscle tissue a decade or more after vaccination. The route by which those macrophages deposit their contents in the brain runs through the venous drainage of the head and neck, which passes anatomically close to several cranial nerve nuclei, the locus coeruleus among them. The chronic low-grade inflammation and metallic irritation that follows renders a small nucleus in the brain stem hypersensitive to input it would otherwise ignore. That hypersensitivity is the ADHD symptom cluster.
Mercury enters through thimerosal, a preservative still used in some influenza vaccines and in the Rho(D) immune globulin administered to Rh-negative mothers during pregnancy. Four peer-reviewed studies compiled in Neil Miller’s Review of Critical Vaccine Studies establish the epidemiological link between thimerosal exposure and the ADHD diagnosis. Geier and Geier, in Medical Science Monitor in 2005, analyzed the CDC’s own VAERS and Vaccine Safety Datalink and found significantly increased risks of the ADD/ADHD diagnosis among children who received thimerosal-containing DTaP.⁶ Young, Geier, and colleagues, in the Journal of the Neurological Sciences in 2008, analyzed 278,624 children in the VSD and found “consistent significantly increased rate ratios” for attention deficit disorder with mercury exposure from thimerosal-containing vaccines.⁷ Geier, Mumper, and colleagues, in Neuro Endocrinology Letters in 2008, established the maternal Rho(D) pathway.⁸ Geier, King, and colleagues, in Clinica Chimica Acta in 2015, reviewed 180 studies pointing in the same direction.⁹
The epidemiological picture beyond thimerosal is equally consistent. Gallagher and Goodman, in Toxicological and Environmental Chemistry in 2008, found that boys receiving the full hepatitis B triple series were approximately nine times more likely to be enrolled in early intervention or special education services than unvaccinated boys, controlling for confounders.¹⁰ Anthony Mawson and colleagues, in the Journal of Translational Science in 2017, published a pilot study comparing vaccinated and unvaccinated children aged six to twelve. Vaccinated children showed increased rates of neurodevelopmental disorders, allergies, otitis media, and pneumonia. A companion study on premature infants found that vaccinated preemies had a fourteen-fold higher likelihood of a neurodevelopmental disorder diagnosis than unvaccinated preemies.¹¹
The government-funded prospective study that would settle the question has never been conducted. Forty years into what any honest observer would call an epidemic, no government-funded study has ever compared ADHD rates in vaccinated versus unvaccinated children. Nor has such a study been conducted for autism, asthma, allergies, or any other outcome in the cluster of chronic pediatric conditions that rose in lockstep with the CDC schedule expansion following the 1986 vaccine injury liability shield.¹² The absence is a choice. Institutions that have the resources, the mandate, and the data infrastructure to conduct the study have chosen not to for four decades.
Daniel Neides, then medical director of the Cleveland Clinic Wellness Institute, put the position of clinicians who have looked in the Cleveland Plain Dealer in January 2017: “Some of the vaccines have helped reduce the incidence of childhood communicable diseases, like meningitis and pneumonia. That is great news. But not at the expense of neurologic diseases like autism and ADHD increasing at alarming rates.”¹³ Neides was disciplined by his employer within days.
The vaccination pathway does not explain every ADHD diagnosis. Our daughter’s symptoms resolved with gluten removal, which suggests either that her locus coeruleus was not damaged in a way dietary change could reverse or that a distinct mechanism was operating in her case. J.B. Handley, in How to End the Autism Epidemic, captures the wider pattern with what he calls the tornado argument: a tornado that uproots some trees can also move a house if the circumstances are right.¹⁴ The same class of insult (injected heavy metal reaching the developing brain in doses no safety study cleared) produces the severe outcome (autism, severe developmental disability) in some children, and the milder outcomes (the ADHD symptom cluster, allergies, mood dysregulation) in others. The four childhood conditions that Kenneth Bock catalogued in Healing the New Childhood Epidemics as rising together starting in the early 1990s (allergies, autism, ADHD, asthma) rose first in precisely the countries whose vaccination schedules expanded first.¹⁵ They cluster within individual children. They are, on the evidence available, expressions of one shared injury.
Other Environmental Pathways
The aluminum-locus coeruleus pathway is the most heavily documented environmental cause of the ADHD symptom cluster. It is not the only one. Several other exposures produce the same or similar behaviors, and each represents a diagnostic pathway current clinical practice does not investigate.
Dietary sensitivity is the pathway our daughter’s case involves. The most-studied mechanism by which gluten produces ADHD-type symptoms runs through the zonulin pathway that Alessio Fasano’s laboratory at Massachusetts General Hospital has documented across two decades of work.¹⁶ Gliadin peptides from wheat gluten trigger the release of zonulin, which loosens the tight junctions between the cells of the intestinal lining. The now-permeable gut allows peptides, undigested food fragments, and bacterial byproducts to enter the bloodstream. Some of these peptides, including gliadin fragments themselves, bind to opioid receptors in the brain, producing effects that clinicians observing children on gluten-free elimination trials describe as a withdrawal phase followed by behavioral improvement. Fasano’s work established that this pathway operates in individuals who do not have celiac disease. The condition Fasano calls non-celiac gluten sensitivity is common, unrecognized in standard ADHD workup, and its resolution follows the same pattern our family observed.
Fluoride, added to roughly 60 percent of American public water systems, has been documented as a developmental neurotoxin in the 2012 Harvard meta-analysis by Choi, Grandjean, and colleagues, published in Environmental Health Perspectives. The analysis reviewed 27 studies and found that children in high-fluoride areas showed measurably lower IQ scores than children in low-fluoride areas.¹⁷ Glyphosate, the world’s most heavily used herbicide, appears as residue on the wheat, oats, and corn that form the base of most American children’s diets, and disrupts the gut microbial ecology through which neurotransmitter precursors are generated.
Screen exposure from infancy is now the standard American childhood. The effects on sleep architecture, attention, and emotional regulation are documented, though the mechanisms are still being characterized. Sleep deprivation, chaotic home environments, and unresolved emotional stress each independently produce the fidgeting, distractibility, and impulsivity the ADHD checklist captures. The industrial food supply is depleted in the mineral-rich whole foods that support the developing nervous system, and the industrial seed oils that have replaced traditional fats disrupt the mitochondrial function that concentration and sustained attention depend on.
What the child is eating, what she is breathing, what she is drinking, what she is watching, what she is sleeping in, what she is emotionally metabolizing, and what she has been injected with are outside the diagnostic frame. What is inside the frame is a checklist of behaviors, filled out by a teacher, in a classroom the diagnostic apparatus does not evaluate.
The Diagnosis and Its Manufacture
The diagnosis now called ADHD has been renamed four times in the last seventy years. Each rename followed the failure of the previous biological claim.
It began as brain disease. When no brain disease could be found, it became minimal brain disease. When no minimal brain disease could be demonstrated, it became minimal brain dysfunction. When no dysfunction could be identified either, the 1980 DSM-III renamed it Attention Deficit Disorder, dropping the biological claim entirely and defining the condition as a cluster of behaviors. In 1987 the DSM-III-R added hyperactivity to the name, and there it has remained.
The category has never been abandoned. The physical basis has never been demonstrated. The renaming has been the whole activity, and what has stayed constant across the sequence is the drug. Amphetamines were in use for children’s behavioral problems by the late 1930s, and Ritalin (methylphenidate) was marketed by Ciba in the 1950s. Both drugs preceded the concept of minimal brain damage that appeared in the psychiatric literature in the 1960s. The pill preceded the diagnosis. The category was assembled around the pill.
That the diagnosis has no biological basis is the profession’s own admission. Gerald Golden, a pediatric neurologist, wrote in Seminars in Neurology in 1991 that “attempts to define a biological basis for ADHD have been consistently unsuccessful. The neuroanatomy of the brain, as demonstrated by imaging studies, is normal. No neuropathologic substrate has been demonstrated.”¹⁸ Seven years later, an NIH Consensus Development Conference issued a formal statement acknowledging that “our knowledge about the cause or causes of ADHD remains largely speculative.”¹⁹ Thomas Insel, director of the National Institute of Mental Health from 2002 to 2015, stated publicly in 2013 that DSM diagnoses lacked biological validity, after thirteen years and roughly twenty billion dollars of research funding had produced no improvement in outcomes for the conditions they named.²⁰
What the diagnosis captures instead is a checklist of behaviors. Nine criteria in the inattentive category (fails to give close attention to details, has difficulty sustaining attention, does not seem to listen, does not follow through, has difficulty organizing, avoids sustained mental effort, loses things, is easily distracted, is forgetful) and nine in the hyperactive-impulsive category. Six symptoms in either category for children, or five for adults, present in multiple settings and causing impairment, qualifies. Peter Breggin, whose Toxic Psychiatry and Psychiatric Drug Withdrawal document the psychiatric drug industry across four decades, has stated the critique cleanly: “The three categories of ADHD behavior, hyperactivity, impulsivity, and inattention, have multiple unrelated causes from an undisciplined upbringing or a boring classroom to distress over conflicts in the school or home. It can also be caused by bullying or emotional, physical, and sexual abuse. Similar behaviors can be produced by underlying physical disorders, such as head injury or diabetes. Insomnia with fatigue will produce similar behaviors.”²¹
The list Breggin gives is not speculative. Each item is documented in the pediatric literature as a cause of restlessness, impulsivity, or inattention. What the ADHD diagnosis does is take a set of behaviors that arise from any of several possible sources (dietary sensitivity, sleep deprivation, chaotic home, boring classroom, poor teaching, developmental mismatch, or the neurological consequences of the vaccination schedule) and collapse them into a single “disorder” whose location is inside the child’s brain. The classroom is not evaluated. The home is not evaluated. The diet is not evaluated. The vaccination history is not evaluated. What is evaluated is the child.
Two findings from the mainstream literature illustrate how far the diagnosis is from tracking a discrete neurological entity. Richard Morrow and colleagues, publishing in the Canadian Medical Association Journal in 2012, examined nearly a million children in British Columbia and found that boys born in December, the youngest children in their classroom cohort under the school entry cutoff, were 30 percent more likely to be diagnosed with ADHD and 41 percent more likely to be treated with medication than boys born in January.²² The children were biologically almost identical. What differed was their age relative to the classmates they were compared against. The rating scale was measuring developmental normality and calling relative youth a disorder.
Helle Wallach-Kildemoes and colleagues, in a 2015 Danish study, documented that ADHD medication prescribing correlated strongly with markers of social disadvantage: single-parent households, low parental income, low parental education.²³ If the diagnosis were tracking a discrete neurological entity, no such correlation would exist. The correlation exists because the diagnosis tracks the behaviors of children whose home environments are unstable, whose parents are stretched thin, and whose classroom conduct reflects the strain.
The diagnostic apparatus did not build itself. Paul Wender, at the National Institute of Mental Health in the late 1960s and early 1970s, published Minimal Brain Dysfunction in Children in 1971 and The Hyperactive Child in 1973, framing childhood restlessness as a biological disease requiring pharmaceutical treatment and declaring five million American children affected.²⁴ CHADD, Children and Adults with Attention Deficit Hyperactivity Disorder, was founded in 1987 as an ostensibly grassroots parent-advocacy organization and received substantial funding from Ciba-Geigy, the manufacturer of Ritalin.²⁵ CHADD’s lobbying secured ADHD’s inclusion in the federal Individuals with Disabilities Education Act in 1991, which tied federal funding to identification and gave schools an active interest in producing diagnoses.²⁶ Joseph Biederman, the Harvard psychiatrist most associated with expanding both pediatric ADHD and pediatric bipolar diagnoses, was revealed by a 2008 New York Times investigation to have earned at least $1.6 million from pharmaceutical companies between 2000 and 2007, income he had not disclosed to his employer.²⁷ The DSM committees that codify and expand the diagnostic criteria are populated with psychiatrists whose research is funded by the same manufacturers whose drugs are prescribed against the criteria they help write.
What this infrastructure has produced is a diagnostic and pharmaceutical phenomenon concentrated overwhelmingly in one country. The CDC’s National Health Interview Survey found that during 2020 to 2022, 11.3 percent of American children aged five to seventeen had ever received an ADHD diagnosis, a figure that has risen persistently across two decades of data collection.³⁷ A 2026 study published in Health Affairs Scholar documented that the United States, which contains roughly 27 percent of the population of the 36 OECD countries studied, consumes 67.6 percent of the OECD’s prescription stimulants. Per 1,000 population per day, U.S. stimulant consumption runs at 569 percent of the mean of comparison countries.³⁸ A hypothetical biological disorder afflicting one in nine of a country’s children would be observable in comparable proportions in other developed countries. What is observable instead is an American epidemic with modest parallels in Australia, the UK, and Canada (each of which shares elements of American pharmaceutical marketing regulation, school system structure, and insurance model), and a fraction of the American rate everywhere else. The condition tracks the market that produces it.
The Drug the Diagnosis Delivers
The full case against stimulant treatment of children is developed in The Arithmetic Pill, published earlier in this series.²⁸ What is essential to the present essay is the identity of the drug the diagnosis exists to deliver.
Ritalin, methylphenidate, is structurally and pharmacologically an amphetamine. This is not an interpretation. Goodman and Gilman’s Pharmacological Basis of Therapeutics, the standard American pharmacology reference, describes methylphenidate’s properties as “essentially the same as those of the amphetamines.”²⁹ The Drug Enforcement Administration classifies methylphenidate, along with amphetamine (Adderall) and lisdexamfetamine (Vyvanse), as Schedule II controlled substances, in the same DEA category as cocaine, fentanyl, and oxycodone, on the basis of their abuse potential.
The DSM-III-R, in its 1987 entry on Amphetamine and Amphetamine-Like Substance Abuse and Dependence, described the pattern of Ritalin abuse in language that maps onto the pattern of prescribed use: chronic daily use at low or high doses, throughout the day or restricted to working hours, with a tendency toward general dose increase over time. The manual added, in the same section, that “controlled studies have shown that experienced users are unable to distinguish amphetamine from cocaine.”³⁰
The best-funded long-term study of stimulant treatment for ADHD, the NIMH Multimodal Treatment of ADHD Study, followed medicated children for three, six, eight, and sixteen years, and reported no long-term benefit from medication on any measure. Children who had been medicated consistently were shorter, had higher rates of delinquency, and showed no improvement in academic or functional outcomes compared to unmedicated children.³¹ This is the treatment case The Arithmetic Pill develops in full.
Peter Breggin’s brain-disabling principle, articulated across four decades of clinical practice, states that psychiatric drugs work by partially disabling the brain and mind.³² No such drug corrects a biochemical imbalance or any other real or presumed defect. What the drug produces is a disability that the evaluator values: in the ADHD case, a stimulant-induced suppression of behavior that the teacher, the parent, or the child himself prefers to the state that preceded it. The word for this is management. The cost is documented on the labels themselves.
The costs are specific and quantified. The methylphenidate labels report, from a 36-month naturalistic follow-up, that children medicated for seven days per week throughout the year averaged 2 centimeters less growth in height and 2.7 kilograms less growth in weight over three years, without evidence of growth rebound during the period studied. Every label in the class carries a boxed warning that sudden death has been reported in patients with structural cardiac abnormalities treated with these drugs at recommended doses. Every label documents that psychotic or manic symptoms occur in approximately 0.1 percent of treated patients versus 0 percent of placebo, in patients with no prior history, at recommended doses, in short-term trials. These are findings from the pooled analysis of the manufacturers’ own trials, disclosed on the FDA-approved labels.
The FDA-approved prescribing information for the four ADHD stimulants most commonly prescribed to American children and adults (Ritalin, Concerta, Adderall XR, and Vyvanse) is available as a freely downloadable document accompanying this essay.³³ ³⁴ ³⁵ ³⁶ It documents, in the manufacturers’ own words, that every one of these drugs is a Schedule II controlled substance, every one carries a boxed warning on abuse and addiction potential, every one produces a withdrawal syndrome that includes dysphoric mood, depression, fatigue, and psychomotor disturbance, every one causes psychotic or manic symptoms in a subset of treated patients at recommended doses, and every one admits, in Section 12.1 of its label, that “the mode of therapeutic action in ADHD is not known.” The reader on one of these drugs, considering one, or with a family member on one, should read the labels for her own drug directly.
The Mother
Somewhere in America or Britain or Australia today, a teacher is preparing a set of observations about a six-year-old girl. She is very energetic. She fidgets through lessons. She struggles to focus. The teacher has training and experience. She will bring the observations together in a meeting with the girl’s parents. She will recommend a referral. The mother, if she has read this essay, will know what to ask. She will ask what is happening in the classroom that a fidgety child would react to. She will ask what the girl is eating for breakfast. She will ask what the girl’s sleep pattern looks like. She will ask what her vaccination schedule was in the first two years of life. She will not accept that a checklist of behaviors is a disease, and she will not accept that a Schedule II amphetamine is the treatment for whatever the checklist has captured. Her daughter’s next fifteen years will be different from what the pathway proposed.
How to Explain It to a Six-Year-Old
A little girl cannot sit still. She runs around the classroom. She cannot pay attention when the teacher is talking. She gets angry with the other children. Her mother is worried.
One day the little girl gets sick. She has a fever. Her body is hot. She lies on the couch with her head in her mother’s lap and listens to a story. She is calm. She sits still. She listens all the way to the end of the story. Her mother has not seen her like this in a long time.
The fever passes. The little girl runs around the room again. She cannot pay attention. She gets angry with her sister.
A doctor comes to visit. The mother tells him what happened. She tells him about the day of the fever. She asks him what he thinks.
The doctor does not want to talk about the fever. He wants to give the little girl a pill that will make her sit still all the time.
The mother does not take the pill. She wants to know what the fever knew.
New Biology Clinic
For those of you looking for practitioners who actually understand terrain medicine and the principles we explore here, I want to share something valuable. Dr. Tom Cowan—whose books and podcasts have shaped much of my own thinking about health—has created the New Biology Clinic, a virtual practice staffed by wellness specialists who operate from the same foundational understanding. This isn’t about symptom suppression or the conventional model. It’s about personalized guidance rooted in how living systems actually work. The clinic offers individual and family memberships that include not just private consults, but group sessions covering movement, nutrition, breathwork, biofield tuning, and more. Everything is virtual, making it accessible wherever you are. If you’ve been searching for practitioners who won’t look at you blankly when you mention structured water or the importance of the extracellular matrix, this is worth exploring. Use discount code “Unbekoming” to get $100 off the member activation fee. You can learn more and sign up at newbiologyclinic.com
In Print
The Unbekoming library is available in paperback, printed to order through Lulu and shipped worldwide. The shelf begins with the paradigm question underneath everything else — No Virus, the isolation problem, the collapse of virology’s foundational claims, and a disease-by-disease reappraisal — and moves through the suppressed compounds mainstream medicine set aside: The DMSO Book, Chlorine Dioxide: The Forbidden Remedy, The Iodine Book, and The Hydrogen Peroxide Book. Two more recover what’s still on the kitchen shelf: Baking Soda and The Castor Oil Book. Two more recover the minerals modern soil, water, and processing quietly stripped from the diet: The Magnesium Handbook and The Boron Book. Sitting alongside these is No Contagion, co-authored with Jamie Andrews — the case against germ theory itself, catalogued through 258 failed contagion experiments.
The critique books cover what medicine, dentistry, psychiatry, and veterinary practice have become. The Unvaccinated treats the completely unvaccinated as a comparison group across twenty chapters and five appendices. Medicalized Motherhood follows a woman through 123 documented interventions from teenage pill to postpartum discharge. Drilling for Profit treats cavities, gum disease, and crooked teeth as the dietary problem they are. What Your Vet Can’t Tell You applies the same critique to pets. Escape from Psychiatry documents the fabrication of the DSM and the specific damage of every major psychiatric drug class. The Vitamin K Injection covers what happens in the first hours of a newborn’s life.
The full shelf is at lulu.com/spotlight/unbekoming. A physical book reaches the person a Substack post never will — the skeptical relative, the friend who won’t click a link but might open a book, the visitor whose eye lands on a coffee table. Buy one to keep, and one to give away.
References
Mehler, M. F. & Purpura, D. P. (2009). “Autism, fever, epigenetics and the locus coeruleus.” Brain Research Reviews, 59(2), 388–392.
Curran, L. K., Newschaffer, C. J., Lee, L. C., Crawford, S. O., Johnston, M. V. & Zimmerman, A. W. (2007). “Behaviors associated with fever in children with autism spectrum disorders.” Pediatrics, 120(6), e1386–e1392.
Maready, F. (2018). Crooked: Man-Made Disease Explained. Feels Like Fire.
Almeida, M. C., Steiner, A. A., Coimbra, N. C. & Branco, L. G. S. (2004). “Thermoeffector neuronal pathways in fever: a study in rats showing a new role of the locus coeruleus.” Journal of Physiology, 558(Pt 1), 283–294. doi:10.1113/jphysiol.2004.066654.
Tomljenovic, L. & Shaw, C. A. (2012). “Mechanisms of aluminum adjuvant toxicity and autoimmunity in pediatric populations.” Lupus, 21(2), 223–230. Related work on macrophage transport of aluminum adjuvants: Gherardi, R. K., Eidi, H., Crépeaux, G., Authier, F. J. & Cadusseau, J. (2015). “Biopersistence and brain translocation of aluminum adjuvants of vaccines.” Frontiers in Neurology, 6, 4. Gherardi, R. K. & Authier, F. J. (2012). “Macrophagic myofasciitis: characterization and pathophysiology.” Lupus, 21(2), 184–189.
Geier, D. A. & Geier, M. R. (2005). “A two-phased population epidemiological study of the safety of thimerosal-containing vaccines: a follow-up analysis.” Medical Science Monitor, 11(4), CR160–70.
Young, H. A., Geier, D. A. & Geier, M. R. (2008). “Thimerosal exposure in infants and neurodevelopmental disorders: an assessment of computerized medical records in the Vaccine Safety Datalink.” Journal of the Neurological Sciences, 271(1–2), 110–118.
Geier, D. A., Mumper, E., Gladfelter, B., Coleman, L. & Geier, M. R. (2008). “Neurodevelopmental disorders, maternal Rh-negativity, and Rho(D) immune globulins: a multi-center assessment.” Neuro Endocrinology Letters, 29(2), 272–280.
Geier, D. A., King, P. G., Sykes, L. K., Homme, K. G. & Geier, M. R. (2015). “Thimerosal: clinical, epidemiologic and biochemical studies.” Clinica Chimica Acta, 444, 212–220.
Gallagher, C. M. & Goodman, M. S. (2008). “Hepatitis B Triple Series Vaccine and Developmental Disability in US Children Aged 1–9 Years.” Toxicological and Environmental Chemistry.
Mawson, A. R., Ray, B. D., Bhuiyan, A. R. & Jacob, B. (2017). “Pilot Comparative Study on the Health of Vaccinated and Unvaccinated 6- to 12-Year-Old U.S. Children.” Journal of Translational Science. Companion preterm study, same authors and journal.
National Childhood Vaccine Injury Act of 1986, Public Law 99-660, 42 U.S.C. § 300aa-1 et seq.
Neides, D. (2017). “Make 2017 the year to avoid toxins (good luck) and master your domain.” Cleveland Plain Dealer, January.
Handley, J. B. (2018). How to End the Autism Epidemic. Chelsea Green Publishing.
Bock, K. (2007). Healing the New Childhood Epidemics: Autism, ADHD, Asthma and Allergies. Random House.
Fasano, A. (2011). “Zonulin and its regulation of intestinal barrier function: the biological door to inflammation, autoimmunity, and cancer.” Physiological Reviews, 91(1), 151–175. See also Fasano, A. (2006). “Gliadin, zonulin and gut permeability: effects on celiac and non-celiac intestinal mucosa and intestinal cell lines.” Scandinavian Journal of Gastroenterology, 41(4), 408–419. Hollon, J., Puppa, E. L., Greenwald, B., Goldberg, E., Guerrerio, A. & Fasano, A. (2015). “Effect of gliadin on permeability of intestinal biopsy explants from celiac disease patients and patients with non-celiac gluten sensitivity.” Nutrients, 7(3), 1565–1576.
Choi, A. L., Sun, G., Zhang, Y. & Grandjean, P. (2012). “Developmental fluoride neurotoxicity: a systematic review and meta-analysis.” Environmental Health Perspectives, 120(10), 1362–1368.
Golden, G. S. (1991). “Role of attention deficit hyperactivity disorder in learning disabilities.” Seminars in Neurology, 11, 35–41.
NIH Consensus Development Conference Statement (1998). “Diagnosis and Treatment of Attention Deficit Hyperactivity Disorder.” November 16–18. Published in Journal of the American Academy of Child and Adolescent Psychiatry, 39, 182–193.
Insel, T. (2013). “Transforming Diagnosis.” National Institute of Mental Health Director’s Blog, April 29. See also Belluck, P. & Carey, B. (2013). “Psychiatry’s Guide Is Out of Touch With Science, Experts Say.” New York Times, May 6.
Breggin, P. R. (2013). Psychiatric Drug Withdrawal: A Guide for Prescribers, Therapists, Patients and Their Families. Springer Publishing Company.
Morrow, R. L., Garland, E. J., Wright, J. M., Maclure, M., Taylor, S. & Dormuth, C. R. (2012). “Influence of relative age on diagnosis and treatment of attention-deficit/hyperactivity disorder in children.” Canadian Medical Association Journal, 184, 755–762.
Wallach-Kildemoes, H., Skovgaard, A. M., Thielen, K., Pottegård, A. & Mortensen, L. H. (2015). “Social adversity and regional differences in prescribing of ADHD medication for school-age children.” Journal of Developmental and Behavioral Pediatrics, 36, 330–341.
Wender, P. H. (1971). Minimal Brain Dysfunction in Children. Wiley. Wender, P. H. (1973). The Hyperactive Child: A Handbook for Parents. Crown.
Whitaker, R. (2010/2015). Anatomy of an Epidemic: Magic Bullets, Psychiatric Drugs, and the Astonishing Rise of Mental Illness in America (2nd ed.). Broadway Paperbacks.
Individuals with Disabilities Education Act, 20 U.S.C. § 1400 (1991 amendments).
Harris, G. & Carey, B. (2008). “Researchers fail to reveal full drug pay.” New York Times, June 8.
Unbekoming. “The Arithmetic Pill: ADHD, ADD, and the Evidence.” Lies are Unbekoming Substack.
Goodman, L. S. & Gilman, A. (1985). The Pharmacological Basis of Therapeutics (7th ed.). Macmillan, p. 586.
American Psychiatric Association (1987). Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised (DSM-III-R). Entries for Amphetamine and Amphetamine-Like Substance Abuse and Dependence.
Jensen, P. S., Arnold, L. E., Swanson, J. M., et al. (2007). “3-year follow-up of the NIMH MTA study.” Journal of the American Academy of Child and Adolescent Psychiatry, 46, 989–1002. Molina, B. S., Hinshaw, S. P., Swanson, J. M., et al. (2009). “The MTA at 8 years.” Journal of the American Academy of Child and Adolescent Psychiatry, 48, 484–500. Swanson, J. M., Arnold, L. E., Molina, B. S. G., et al. (2017). “Young adult outcomes in the follow-up of the multimodal treatment study of attention-deficit/hyperactivity disorder.” Journal of Child Psychology and Psychiatry, 58, 663–678.
Breggin, P. R. (2015). “Rational Principles of Psychopharmacology for Therapists, Healthcare Providers and Clients.” Journal of Contemporary Psychotherapy, 46, 1–13.
Methylphenidate hydrochloride (Ritalin), NDA 010187. FDA-approved prescribing information, revised February 2025. FDA.gov/drugsatfda.
Methylphenidate HCl extended-release (Concerta), NDA 021121. FDA-approved prescribing information, revised September 2025. FDA.gov/drugsatfda.
Mixed amphetamine salts extended-release (Adderall XR), NDA 021303. FDA-approved prescribing information, revised April 2026. FDA.gov/drugsatfda.
Lisdexamfetamine dimesylate (Vyvanse), NDA 208510. FDA-approved prescribing information, revised April 2026. FDA.gov/drugsatfda.
Reuben, C. & Elgaddal, N. (2024). “Attention-Deficit/Hyperactivity Disorder in Children Ages 5–17 Years: United States, 2020–2022.” NCHS Data Brief No. 499, Centers for Disease Control and Prevention, National Center for Health Statistics.
Horowitz, L. M., et al. (2026). “Prescription stimulant consumption in the United States compared with 35 other countries.” Health Affairs Scholar, 4(6), qxag133. Analysis based on International Narcotics Control Board 2024 data.
The medical-industrial complex has managed to pathologize everything for profit. Thank you for the enlightening work you do.
The same thing happened to me in the school system. in 1961. The school advised me to take my four year old son to a doctor, because he was not sitting still in kindergarten.
I learned 65 years ago, that the doctor's food advice created hyperactivity in my child...and then he prescribed tranquilizers. It was a miracle! Right at this time, a friend handed me some books...and the first thing I read SUGAR CREATED HYPERACTIVITY. Then the second thing I read: TRANQUILIZERS STUNT the DEVELOPING ORGANS of CHILDREN. I immediately connected the dots...and took my son off the tranquilizers...and started learning about nutrition. I removed sugar, flour, additives and preservatives. My son settled down and wound up graduating high school with honors.