Pig Kidney Removed From Alabama Woman After Organ Rejection
Surgeons removed a genetically engineered pig's kidney from an Alabama woman after she experienced acute organ rejection, NYU Langone Health officials said on Friday.
Towana Looney, 53, lived with the kidney for 130 days, which is longer than anyone else has tolerated an organ from a genetically modified animal. She has resumed dialysis, hospital officials said.
Dr. Robert Montgomery, Ms. Looney's surgeon and the director of the NYU Langone Transplant Institute, said that the so-called explant was not a setback for the field of xenotransplantation — the effort to use organs from animals to replace those that have failed in humans.
'This is the longest one of these organs has lasted,' he said in an interview, adding that Ms. Looney had other medical conditions that might have complicated her prognosis.
'All this takes time,' he said. 'This game is going to be won by incremental improvements, singles and doubles, not trying to swing for the fences and get a home run.'
Further treatment of Ms. Looney might have salvaged the organ, but she and her medical team decided against it, Dr. Montgomery said.
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Opinion: Unraveling Autism's Surge
Autism diagnoses are surging, touching countless families, yet the reasons remain elusive, fueling debate and confusion. The Times' recent exploration of autism's rise attributes the increase mainly to broader diagnostic criteria, heightened awareness, and social influences like online communities, while firmly rejecting vaccines as one potential cause. However, it downplays the role of institutional incentives (research funding, special education staffing, therapy services, and pharmaceutical interests). Conversely, the pseudonymous 'A Midwestern Doctor' on Substack dives into vaccine-related hypotheses that the Times avoids. Neither fully delivers the impartial, rigorous analysis that I believe is needed to untangle autism's complex web. Winston Churchill once famously described the Soviet Union as 'a riddle wrapped in a mystery inside an enigma.' Ironically, this phrase was repurposed in Oliver Stone's JFK as a symbol not of clarity but of obfuscation. Like the Soviet Union or the JFK assassination, autism's enigma may defy complete resolution, but without rigorous, transparent scrutiny, it will remain shrouded in mystery; conversely, a clear lens on the knowns, unknowns, and disputes is our only hope for clarity. Autism spectrum disorder (ASD – of which severe Autism is an overlapping subset of symptoms) is a group of developmental conditions that begin in early childhood, affecting how children communicate, interact socially, and behave. Autism looks very different from case to case. Most of the population-level risk comes from over 100 inherited gene differences, each with a small impact. Many of these gene changes affect gene regulation and synaptic function—key processes in brain development. Autism likely involves mechanisms, changes in how genes are expressed without altering the DNA sequence itself. Think of the genome as a musical score: the notes don't change, but depending on who's conducting, it can sound like classical or rock. Similarly, a person may carry genetic risk but only develop autism if specific environmental cues 'activate' the genes into certain patterns, much like in schizophrenia. Research shows that the brains of people with autism often have unique features, though these can vary widely from person to person. Commonly, children with autism experience faster brain growth in early life, especially in areas like the frontal lobe (involved in planning and social behavior) and the amygdala (linked to emotions as a 'danger detector'). This overgrowth, noted between 1–14 months, can make it harder for different brain regions to 'talk' to each other effectively, leading to challenges in processing information or emotions. Instead of a city that developed organically, it's more like a centrally planned boomtown (E.g. China's ghost cities)—roads laid down too fast, towers built in haste, and entire sectors left misaligned and underused. Another shared trait is an imbalance in brain chemicals, like glutamate and GABA, which act like the brain's gas and brake pedals. In autism, there's often too much 'gas' (excitation) and not enough 'brake' (calming), which can explain sensory sensitivities or trouble focusing. Genes also play a big role—specific ones affect how brain cells connect; however, not everyone with autism has the same brain differences. Some have more pronounced changes in the cerebellum (affecting movement and coordination), linked to reduced Purkinje cells, while others show unique patterns via inflammation's elevated cytokines. As a 'spectrum', autism's underlying brain differences and their expression(s) are disparate and individualized. The rise in autism diagnoses — approximately 1 in 36 children (!!) in the U.S. according to the CDC's 2023 data… …is staggering and demands scrutiny. Yet autism is not a singular, congenital condition like rubella syndrome — where first-trimester rubella-virus exposure causes a specific set of neurologic issues in a one-to-one identity function. Instead, 'autism' has broadened into a sprawling diagnostic umbrella, encompassing a spanning 'classic autism' (a.k.a 'Kanner's Syndrome'), Asperger's, childhood disintegrative disorder, and 'Pervasive Developmental Disorder Not Otherwise Specified' (PDD-NOS). These diagnostic labels don't point to a single cause—only broad categories. Are we seeing an epidemic of biology, or semantics? As the term 'mental retardation' gave way to 'intellectual disability,' some cases were reclassified under autism's expanding umbrella. Autism once overlapped heavily with ID; now it captures a far more diverse patchwork of traits, many without cognitive impairment. Genetics play a significant role in autism, but not as dominantly as once thought. One early twin study (1977) showed identical twins (same DNA) were seven times more likely to share an autism diagnosis than fraternal twins. Yet, even identical twins don't always align—in up to half of cases, one has autism and the other does not, suggesting genes are influential but not the sole factor. Hallmayer's 2011 California twin study, though often cited, involved 192 twin pairs but with only a 17% participation rate (of those asked)—raising concerns about selection bias. Its strength lies in a careful parsing of genetic versus environmental causation using (unlike prior studies' Falconer's formula) the ACE model of Additive Genetic, Common Environment, Unique Environment factors. By contrast, a 2017 Swedish study analyzed millions of sibling and twin records, estimating heritability between 83% and 87%, with tighter statistical confidence but less fine-grained control. These studies illustrate a trade-off: precision in small samples versus power in large datasets. Together, they define the outer limits within which autism's genetic component resides — shaped by method, scale, and erstwhile definitons. The table below shows twin and family studies' presumed genetic component's falling between Steffenburg's 91% and Hallmayer's 38%. Autism Twin Study Concordance (and other Familial Pairing) Table: Note: ACE estimates are direct for Hallmayer and Sandin; the others are post hoc approximations. Falconer's formula (h² ≈ 2 × [rMZ − rDZ]) estimates heritability; interpret early studies cautiously due to small samples and diagnostic variability. Smartphone browsers may not visually capture the entire table. (including links to the studies). In a hybrid model, both wide in scope and fine in partitioning — Gaugler et al. (using the Population-Based Autism Genetics and Environment Study 'PAGES') estimated 52% of autism risk's from genetic variants. Gaugler leveraged SNP-genotyping and diverse family relationships, aiming to break down genetic risk into its components, finding influence roughly split between 'genes you inherit' (A) … and…' complex gene interactions' (D), 'new gene changes' (N), 'family environment' (C), and 'unique life experiences' (E). Havdahl conversely arrived at a genetic preponderance, based on Bai's 2019 synthesis of large-scale genomic and familial studies. Hallmayer's study reported a relatively low heritability estimate (~38%) but with a wide (lack of) confidence interval—reflecting the limitations of its small, selective sample. In contrast, Gaugler's SNP-based and case-control design yields a higher but more statistically stable estimate. This boxplot, drawn from Gaugler's Swedish cohort data, shows a clear rise in autism prevalence across birth cohorts from 1980 to 1999. It's consistent with diagnostic broadening, increased awareness, or real environmental shifts. As definitions change and milder cases are included, heritability estimates may appear lower—not because genes matter less, but because the diagnostic category itself has expanded. Here's a rough mapping, somewhat consistent temporally. The Solomonic (un)happy medium indicates more than half of autism risk is genetically set by the time of birth; however, that assessment comes with caveats. Please observe this side-by-side: NB: No diagnosis appears in either graph's lower right half because even purely environmental factors (e.g. a house fire) would likely impact both DZ twins, keeping such data points above the diagonal. Autism occupies a mixed-influence zone: genetically weighted, yet with implicit environmental triggers; not unlike schizophrenia, bipolar disorder, and Tourette's. One plausible explanation for the rise in autism diagnoses is the broadening of diagnostic criteria and increased awareness, but this shift also reflects a profound historical transformation in the concept itself. In 1911, Eugen Bleuler coined 'autism' to describe excessive fantasy and hallucinations in severe schizophrenia, a meaning that persisted through the 1950s. By the 1970s, British child psychiatrists redefined 'autism' as a lack of symbolic life— a 180° shift that coincided with the closure of institutions for the 'mentally retarded' in the 1960s, releasing children into new diagnostic frameworks — a movement catalyzed by John F. Kennedy's 1961 President's Panel on Mental Retardation, influenced by his sister Rosemary's institutionalization and the family's complex feelings — an irony, as RFK Jr. now hunts the autism epidemic's 'killer'. The Diagnostic and Statistical Manual of Mental Disorders (DSM-III) in 1980 formalized autism as a developmental disorder, shifting it from a rare condition to a spectrum encompassing a wide range of behaviors. This change, coupled with parental advocacy, drove earlier screening — often at 18–24 months — and more inclusive diagnoses. By DSM-4 (1994), Asperger's syndrome and PDD-NOS were included, capturing individuals with average or above-average intellect. DSM-5 (2013) dropped Asperger's as a named diagnosis. Importantly, DSM-5 also removed the prior exclusion that had prevented an individual from being diagnosed with both ASD and ADHD, conditions once considered mutually exclusive. This overlap expanded the diagnostic net, potentially reclassifying children with co-occurring traits. Additionally, individuals previously deemed 'retarded' (sic) were subsumed under the ('severe' end of the) autism spectrum, inflating prevalence without a true increase in abnormality cases. Sociologist Gil Eyal in The Autism Matrix views these diagnostic shifts as ultimately beneficial. Earlier diagnosis means earlier access to services: speech therapy, behavioral interventions, educational support; ideally helping those children develop better communication, social skills, and independence than previously. The decline of U.S. mental institutions may have played an indirect role in the rise of autism diagnoses—not by causing autism, but by reshaping how society categorized and responded to developmental differences once kept out of public view. Conditions previously confined to large custodial settings became newly visible, newly labeled, and (in the case of schizophrenia) medicated: Hello, Thorazine! (1953). From 1955 to 2005, residents in public mental hospitals dropped from over 500,000 to under 100,000. This shift, more abrupt for those with serious mental illness, reflected changing legal standards, new pharmaceuticals, and an optimistic vision of 'community integration.' For individuals with intellectual or developmental disabilities, the transition was slower and more deliberate—often focused on preventing new institutionalizations rather than discharging existing residents. But in both cases, the cultural shift was profound: from seclusion to exposure. Before the 1960s, terms like 'feebleminded,' 'retarded,' or even 'idiot savant' might have earned what we now call 'autistic' – while 'idiot' itself was both replaced by 'retarded', and then transformed into a mild insult. And of course, 'retarded' is now a pejorative as well, replaced by 'ID', intellectual disability. Not everyone (back then) was a Gary Cooper with Albert Einstein's mind and HL Mencken's wit. As institutional care waned, these individuals entered broader diagnostic frameworks, potentially inflating autism's labeling prevalence – separate from any independent potential increase in cases, per se. This 1915 illustration starkly illustrates how intellectual and developmental differences were once categorized with terms now considered deeply offensive—'idiot,' 'imbecile,' 'moron'—yet these labels existed because same or similar variations in cognitive and adaptive functioning were present, just framed in a harsher, cruder way. None of this implies that institutionalization was desirable—many facilities were underfunded, degrading, or worse. But it does suggest that part of autism's modern profile arose not from new biology, but from new visibility. In the early 1990s, autism was more tightly linked to mental retardation, now called 'intellectual disability'. In 1992, 72% of autism cases (3,210 out of 4,446) were associated with intellectual disability (ID). By 2005, that share had dropped to just 37% (10,410 out of 28,046). As this graph (adapted from King and Bearman's 2009 study) shows, … … autism without ID increased more than 13-fold—from 1,236 to 17,636 cases—while autism with ID rose just over threefold. From 1992 to 2005, the U.S. population grew just over 10%, yet intellectual disability (ID) diagnoses rose by 54%, and autism with ID nearly tripled. That spike in autism's most severe form points to more than shifting definitions—it may reflect real changes in early neurodevelopment. Still, confounding factors—like rising immigration, language barriers, and struggling school systems—could distort these figures. Before drawing conclusions, we need better data, sharper metrics, and more objective classification. Swedish researchers tracked autism severity in 13-year-olds, finding that as diagnoses rose, the average symptom score steadily declined, suggesting institutional pressure to have 'autism' capture milder cases. (chart clarified by @cremieuxrecueil). Sweden's autism is classified within an 'ESSENCE' -framework ('Early Symptomatic Syndromes Eliciting Neurodevelopmental Clinical Examinations'); wherein ADHD, tics, movement disorders, and epilepsy also rise in prevalence. A cynic might analogize autism diagnoses' rise to the more recent surge in gender dysphoria. Such expansions fuel jobs in special education. Autism diagnosis rates have clearly increased over the past decade, principally in the younger age groups. The 'psychiatric and mental health industrialization complex,' particularly within schools, amplifies this trend. Financial incentives for special education, therapies, and clinical services create perverse pressures for over-diagnosis, as funding and resources often hinge on an autism label. Additionally, families often gain from an ASD diagnosis, accessing benefits unavailable otherwise. The Social Security Administration reports a 154% increase in SSI recipients with ASD from 2004 to 2014 (to 28% of mental disorder cases), providing up to $943 monthly in 2024. With 19% of Americans now identifying as 'neurodivergent'—a broad category that includes ADHD, autism, dyslexia, and other cognitive differences—and with reports suggesting a majority of Britons may be doing the same, the expanding definition implies a widening diagnostic net. These map-comparisons show how autism rates grew across U.S. states from 2003 to 2011 (darker blue means more kids were diagnosed, jumping from as low as 0.1% to over 2% in some places). Many states had policies that gave schools extra money for finding kids with autism (again, darker blue); e.g., the Northeast's, the Rust Belt's and Virginia's 'rewarded' autism-rates climbed. Michigan's diagnoses (when rewarded) spiked to 1.5% by 2007; but, unrewarded, the rates dropped (NB: acknowledging, this is not a simple one-to-one explanation – as (e.g.) Minnesota's autism rates increased without reward-incentive). This kind of geographic disparity suggests we're not just mapping a condition—we're mapping responses to incentives. Take a look at (unrelated, but analagous) methadone distribution by state: supposedly the same disease (sic) of narcotic addiction for some reason 'requires' ten times more methadone in Rhode Island than in Texas or Missouri. Wisconsin uses four times the dose of neighboring Iowa. Now, autism includes Elon Musk. Have we simply disease-ified eccentricity and (occasionally) genius? The study, 'Diagnostic change and the increased prevalence of autism' documents this expansion. California's caseload has ballooned; moreover, far beyond what diagnostic trends alone would predict. Jill Escher, head of the National Council on Severe Autism, insists the exponential increase: California's caseload's jumping from a few hundred in the 1980s to over 200,000 today (even excluding 'high-functioning' cases)—reflects a real crisis, not just better detection. Moreover, Escher's Getting Real About Autism's Exponential Explosion shows… …California's autism caseload has nearly quadrupled since 2011: outpacing the national diagnosis rate for school-age children, which 'only' doubled. The excess suggests bureaucratic inflation and system-driven incentives (or something 'in the air' in California)– not just rising prevalence. Britain's Autism Research Centre director, Simon Baron-Cohen notes, ''What we call autism has itself changed to become a broader category (and with) the growth in private clinicians' offering diagnosis — it has become an industry.' 'Everyone talks about the weather, but nobody does anything about it,' wrote Charles Dudley Warner in 1897. Some realities (e.g., the weather) do not yield to our words, hopes, or policy interventions—no matter how loudly or persistently we speak around them. Severe autism is one of them. Despite decades of advocacy, legislation, and funding, the outcomes for the most profoundly affected remain largely unchanged. The National Council on Severe Autism's Jill Escher (in our conversation) put it bluntly: for many severely autistic students, special education is 'little more than glorified babysitting,' teaching daily living skills, not academics. The Individuals with Disabilities Education Act (IDEA) programs cost schools a fortune: specialized staff, autism-specific classrooms; yet Escher calls the system 'completely irrational,' a 'jerry-rigged' relic from a pre-autism-epidemic era. Cui bono? Schools get funding; teachers' unions lock in jobs; parents receive stipends; service providers cash in — but many severely autistic individuals remain dependent; moreover with the worry of 'falling off a cliff' into underfunded Medicaid care at age 21 – and/or with the (inevitable) demise of their caretaking parents. To be clear, without doubting the dedication of families or educators, one can acknowledge that 'full inclusion' backfires. Severely autistic children disrupt classrooms. My own son's middle school class, in the mid-2000s, was regularly derailed by persistent, involuntary, loud outbursts of vocal 'stimming' of a severely autistic teen despite his omnipresent aide. Might group homes be a more humane, realistic answer for such cases? Escher praises California's relatively strong system, which offers tailored care and vocational programming—serving needs without disrupting others. This isn't abandonment; it's honesty. Just as 60-year-olds don't train for the NBA, we shouldn't pretend that the most severe autism fits the academic model. Margaret Thatcher's warning still applies: eventually, you run out of other people's money. We risk Cloward–Piven -style overload: collapsing systems with unsustainable burdens, unless we build something rational now. Not every student in special education is autistic, but nearly every autistic student—especially those with severe cases—is in special ed. Today, about 15% of U.S. public school students receive special education services. That's doubled from 8% in the late 1970s, and the numbers keep growing. Of those in special ed, roughly 12% have autism. The staff structure at my local middle school today is worlds apart from my own public school experience in 1960s New York City. Back then, one teacher handled 30 students, with five or six such classes per grade, grouped by achievement level. The entire school ran with just a principal, assistant principal, secretary, nurse, and two janitors. My local middle school currently has only ~35% staff as core teachers, while ~65% are ancillary. These programs are expensive. In 2020, school districts spent nearly $39 billion on special education services—averaging over $13,000 per student (on top of the baseline ~$19,000 per student). If every state spent like the highest-spending ones, total special ed costs would reach $180 billion a year. This added burden isn't trivial, leaving the other 85% to share increasingly strained resources: overcrowded classrooms; fewer offerings in gifted, vocational, and core subjects. We cannot serve anyone well by exhausting the system. Autism has long shown a stark male predominance: roughly 3 or 4 boys diagnosed for every girl. ADHD follows a similar trend, with boys diagnosed at a 2.5 to 1 ratio. These disparities were noted as early as Leo Kanner's 1943 paper, well before today's educational culture took hold. The biological sex differences remain; but the extent to which they are ( potentially mis-) interpreted and acted upon has shifted. Christina Hoff Sommers' The War Against Boys argues that modern schools, increasingly feminized and focused on chat, collegiality, and conformity, may mismatch boys' neurodevelopmental traits — often more intense, trial-and-error, and less socially oriented — leading to over-diagnosis of conditions like autism and ADHD when boys' behaviors deviate from these expectations. Boys exhibit greater variance in IQ and behavioral traits, producing more outliers — geniuses, risk-takers, as well as those with neurodevelopmental challenges — while girls cluster closer to the mean, potentially making boys' differences more noticeable and pathologized in structured settings. The 'boy-averse' decline of recess and advent of zero-tolerance policies in schools exacerbates this mismatch. This persistent male predominance has sparked a counter-movement, especially among feminist scholars, who argue that autism in girls is under-recognized. They propose that girls 'camouflage' their symptoms—adeptly mimicking social cues to blend in—though this leads to a curious contradiction: if autism impairs social reciprocity, how can one convincingly fake it? As the old joke goes, 'sincerity—once you can fake that, you've got it made.' Mind you, some of these same scholars in peddling 'sex contextualism' essentially dispute binary sex, undercutting their argument(s). Male and female brains diverge from birth, a pattern seen across the animal kingdom — male mosquitoes prioritize mate-seeking, females blood-feeding — reflecting distinct evolutionary prerogatives. Simon Baron-Cohen's 'extreme male brain theory' suggests autism reflects an extreme male-typical profile, where 'systemizing outstrips empathizing'. Yet it's important to recognize that autism is not strictly deficit-based. It's also associated with positive traits such as pattern recognition and attention to detail. Moreover, long-term outcomes vary widely, with some autistic individuals' achieving independence, relationships, employment, and relative happiness. Autism spectrum disorder (ASD) is highly prevalent in high-income countries, but in sub-Saharan Africa, with nearly 1 billion people, it's rarely diagnosed… 'A review of the global prevalence of autism did not identify any data from sub-Saharan Africa, even though this region has a population of nearly 1 billion, 40% of whom are children younger than 14 years.' … and rarely discussed. Google-searches for 'autism' in Kenya, Congo, Zimbabwe are near zero and static these last few measurable decades. Limited psychiatric infrastructure and a focus on urgent issues like HIV, malaria, and food insecurity overshadow ASD. Autism is a 'first-world problem,' amplified by wealthier nations' resources, omphaloskeptic tendencies, and broad diagnostic criteria. Africa's ASD absence may be underdiagnosis rather than lower incidence. Anthropologist Richard Grinker, who has studied autism cross-culturally, argues that autism exists everywhere—but is recognized only where diagnostic tools, institutional priorities, and cultural interpretations align. Over 90% of studies come from Europe, the Americas, and the Western Pacific. Entire regions like Africa and the Eastern Mediterranean are effectively data voids, despite the (presumed) global nature of the disorder. China, with over 1.4 billion people, remains strikingly absent from global autism discourse, with a self-proclaimed rate of only one-third ours. The condition is labeled 自闭症 ('self-enclosure disorder') or 孤独症 ('lonely disorder'), but these are not seen as quirks or mere differences—they imply dysfunction, weakness, and detachment from societal duty. Diagnosed children are sometimes called 来自星星的孩子—'children from the stars'—but this poetic phrase belies the harsh stigma families face. Chinese society sees autism as a mark of shame or failure; to be downplayed, not spotlighted. Comparing same-wealth/ same-health societies could reveal if cultural or economic factors drive these trends. Cross-cultural-, cross-national- will be more difficult, given the absence of baseline data, terms, and agreements of importance. Several societal and biological factors may contribute to autism rates, either directly or indirectly. The trend toward older parental age is significant. Advanced paternal and maternal age is associated with increased risks of genetic mutations and conditions like gestational diabetes, which may elevate autism risk. Older sperm and eggs accumulate DNA damage, potentially affecting neurodevelopment. Studies suggest a 10% increased autism risk per decade of parental age. Smaller family sizes and fewer siblings may also play a role. Children with fewer siblings experience reduced socialization opportunities, potentially exacerbating autistic traits. Bruno Bettelheim's 'lonely child' hypothesis suggested that social withdrawal stemmed from emotional deprivation: cold 'refrigerator parents' implies social difficulties. His theory aligns with this study: 'Having Siblings is Associated with Better Social Functioning in Autism Spectrum Disorder'. Modern parenting, with its intensified focus on (fewer) children fosters scrutiny for any potential developmental delays. Additionally, the increase in divorce rates over the past decades has led to more single-parent households, which can impact (and stress) early childhood development. Environmental factors like fluoride, aluminum, glyphosate, and Wi-Fi have been proposed as contributors, but evidence is sparse and often anecdotal. Fluoride in water has been present throughout the decades (1950s-1980s) when autism rates remained low; if it were a smoking gun, the surge in diagnoses wouldn't have waited until the 1990s– although fluoride exposure exceeding 2x the upper limit may correlate with minor IQ reductions. Glyphosate, a herbicide, and Wi-Fi radiation lack robust data's tying them to ASD. Thimerosal, an organomercury preservative, was largely removed from childhood vaccines by the early 2000s—thus largely cleared as a suspect in autism's rise. By contrast, the current adjuvant, aluminum (as insoluble phosphate-, or hydroxide-salts), plays a different biological role: not as preservative but as immune stimulant — designed to provoke local inflammation and enhance antigen presentation by the immune system. It is present in small amounts and typically cleared from the body quickly, but animal studies raise concerns: one found it can cause chronic inflammation at the injection site and gradually migrate to the brain, while another showed it can persist in the brain for months, potentially leading to inflammation. Lyons-Weiler (2018) suggests that autism may involve impaired cellular detoxification, with aluminum and other toxins' exacerbating genetic predispositions through immune activation and gene-environment interactions. His chart compares aluminum exposure from vaccines over a child's first 800 days under different plans. A 2022 study also linked aluminum in vaccines to asthma in some kids, calling for more research. While the CDC finds no clear adjuvant/autism link, Lyons-Weiler's work pushes for studying how aluminum and other toxins might affect kids differently based on their genes. The pineal gland, sometimes implicated in autism theories via melatonin dysregulation, shows no direct causal connection. Higher-dose ultrasound during pregnancy has been studied for potential neurodevelopmental effects, with no clear link to autism. Ultrasound remains a standard prenatal tool due to its safety at recommended levels. Prenatal acetaminophen -use is not associated with autism risk. Escher, research philanthropist, advocates for exploring non-genetic inheritance, where pre-conception environmental exposures like anesthetics or Depakote may cause epigenetic changes in parental germ cells, leading to transcriptional errors in offspring. Vaccines, particularly the measles-mumps-rubella (MMR) vaccine, have fueled autism speculation since Andrew Wakefield's 1998 Lancet study and 1999 follow-up, retracted in 2010 for ethical and methodological flaws. In a recent interview, Wakefield states he had disclosed external funding to his university. Conversely, pharmaceutical-funded studies may escape similar scrutiny. Dr. Wakefield warned that the original 1960s' MMR safety studies were 'conducted (without adequate informed consent) on vulnerable populations, such as children in mental institutions', a claim not unfounded. In 1969, (VACCINES' author) Dr. Stanley Plotkin published a rubella vaccine trial explicitly involving mentally retarded and orphaned children as test subjects. Yet when deposed in 2018, Plotkin, with full recall of his 1959 Congo fieldwork's town-names, couldn't remember testing on the mentally handicapped; while later conceding 'that's what I did'. His selective non-memory is striking. The eternal claim that vaccines were 'thoroughly studied' must be judged against these vanishingly small and ethically murky early trials. Separately, a million Congolese received vaccines, but autism is essentially never identified in such a setting. Wakefield, rather than asserting MMR definitively caused autism, proposed separating measles, mumps, and rubella vaccines for individual testing to isolate potential risks– — a reasonable scientific hypothesis stifled by his vilification (arguably, disproportionate). Measles has a well-documented history of (rare) neurologic complications, including acute encephalitis. Rubella, although known for congenital neurologic effects, has not been similarly implicated in postnatal issues. Two major Danish cohort studies — one in 2002 and a follow-up in 2019 — each enrolling the entire Danish child population found no link between MMR vaccination and autism. Nonetheless, public distrust persists, amplified by the 1986 National Childhood Vaccine Injury Act (NCVIA) — which initially shielded manufacturers from liability and subsequently forged an expansion of the childhood vaccine schedule (from targeting 7 diseases with 8–10 doses in 1986 to 16 diseases with approximately 47–55 doses by age 18 in 2025) Once a vaccine's on the CDC's list, it's a free pass — no marketing needed, just profit, raising suspicions about untested risks. That cozy setup makes sensible suspecting Big Pharma's erring on the side of profit (vs. public safety), e.g. with hepatitis B shots for babies who are decades removed from the skills or interest for that illness' modes of transmission (sexual, IV). Big Public Health follows along for the (regulatory capture) ride (as seen when the CDC's ACIP rapidly endorsed Merck's Gardasil HPV vaccine in 2006 despite up to 64% of members' having potential conflicts of interest). Why rush MMR at 12–15 months—when neurogenesis, synaptogenesis, and myelination are still underway, and the brain (theoretically) more susceptible to immune stress? If the highest measles risk lies in infancy—and if maternal antibodies cover (most of) that period, what's really lost by waiting until age 3 or 4, aside from pediatric calendar convenience? With autism far more common in boys, and rubella primarily a concern for pregnancy, a delayed or sex-differentiated schedule seems not just reasonable—but overdue. Autism likely starts in the womb, tied to embryologic neurodevelopment, as shown in developmental timelines where neurogenesis and gliogenesis peak prenatally, so pinning it on vaccines given after birth assumes a sudden postnatal shift. Some argue vaccines, particularly MMR's measles component and aluminum, may trigger brain inflammation during critical windows like synaptogenesis (0–5 years) and myelination (up to 20 years), potentially raising autism-risk via cytokines, autoantibodies, and/or brain enlargement in those prone to immune overactivation. The vaccine-autism debate centers on 'regression'—toddlers' suddenly losing language, eye contact, or motor skills, often after a fever, illness, or immunization. Are there solid cases of kids' thriving, then crashing into autism at 6 months or 2 years after a shot? Two studies in 2018 gave different assessments. One claimed 'about 22% of ASD kids experience '', typically at 21 months, with autism (but not with milder PDD-NOS or Asperger's); whereas Ozonoff (2018) followed high-risk infants and found declining social engagement in ~3/4 of children who developed autism. The notion that autism is entirely predetermined by prenatal neurodevelopment overlooks postnatal brain plasticity, particularly during critical periods like toddlerhood. Schizophrenia, which often emerges in late adolescence, illustrates how dysregulated synaptic pruning — a process refining neural connections — can alter brain function, potentially triggered by environmental factors like infections or toxins. One striking clue: 3–5% of children experience febrile seizures, and a Swedish study found that 40% of such cases preceded an autism diagnosis. This points to a broader mechanism of cytokine-driven neuroinflammation, where immune overactivation damages the developing brain. 'Regression' challenges the idea that autism is always present from birth. If true, early detection might change a child's trajectory. Brownstone Institute's Jeffrey Tucker wonders if 'declining trajectories… may be more the rule than the exception,' and urges that even vaccines, long taboo as a suspect, be put 'on the table' for rigorous investigation. Mr. Tucker has had longitudinal observation of childhood autism (his nephew Joel's; recounted in Like a Crown: Adventures in Autism). As HHS Secretary, Robert F. Kennedy Jr. urged that all hypotheses—however inconvenient—be tested rigorously. That remains the clearest path through the fog surrounding autism's true origins. Whether or not vaccines contribute to autism, one thing is clear: we may be overusing them. The 1986 National Childhood Vaccine Injury Act (NCVIA) shielded manufacturers from liability, treating universal vaccination as a societal good; ostensibly to avoid a 'tragedy of the commons': depriving the many because of the civilly litigated side effects of a few. But removing accountability while mandating use created a dangerous asymmetry: liability-free, government-endorsed, and increasingly profitable. In the 1960s, parents held chickenpox and measles parties to build natural immunity. Today, we vaccinate for diseases that have largely vanished—like polio and rubella—raising the question: are we vaccinating out of necessity or inertia? The low autism rates reported among Amish and Orthodox Jewish communities may stem from their vaccine avoidance, although Autism Matrix' Gil Eyal asserts that there are 'plenty of autism cases among Orthodox Jews in more integrated communities' (a point that is not necessarily dispositive, if 'integrated' coincides with vaccine compliance); however when studied, autism appears far less frequently among Ultra-Orthodox Jews (and Israeli Arabs); half and one third (respectively) the general Israeli population's rate. Explanations vary: cultural filters; less psychiatric contact; younger parental age; adherence to traditional, less cognitively complex tasks; avoidance of modern influences— and of course, fewer vaccine-exposures. Vaccine skepticism is often met with fierce condemnation. Andrew Wakefield's exile and the COVID-era silencing of dissent show how quickly the label 'anti-vaxxer' is weaponized. Yet the COVID-19 vaccine push for children—despite their minimal risk from the virus—exposed a troubling indifference to real harms like myocarditis. I've given thousands of vaccines as a physician and taken many myself. But not every shot fits every person. A yellow fever vaccine makes sense in West Africa, not Nebraska. Context matters. Tailoring vaccines to individual risk isn't 'anti-vaccine' any more than abjuring a ski parka at the beach is 'anti-clothing.' Understanding autism's rise requires broader comparisons—between vaccine-heavy societies and those with lighter or delayed immunization schedules, especially within similarly developed nations. Cultural norms, diagnostic thresholds, and environmental exposures all interact. Without this wider lens, we risk mistaking institutional trends for biological truths. If we had a time machine to 1950s New York, we'd find no concept of ADHD and a much narrower definition of autism (of course, labeled differently); often confined to psychiatric institutions. Society then, for all its faults, was in many ways more orderly: lower rates of street crime, drug use, and public disorder. Deinstitutionalization's 'humane' ideal traded structured care for societal chaos: freeing people from asylums while believing community integration would fill the gap. The 'magic air' of the streets failed to heal deep mental health issues. Homelessness has experienced a ~1500% increase, coincident with the autism epidemic. Similar 'good intentions' (via 1960s' reform-minded Rockefeller University) sowed narcotic abuse as Methadone Maintenance Ignited America's Opioid Crisis, with a similar rise: late 20th-, early 21st- century. Four seemingly unrelated trends –opioid addiction; autism diagnosis; homelessness; and children of divorce — have each dramatically risen in the wake of deinstitutionalization, the collapse of stigma, and the move toward visibility over concealment. Correlation is not causation—but when four trendlines rise in lockstep, we ought to ask why. This isn't to say autism's rise has a single cause—or that it can be traced neatly to deinstitutionalization, diagnostic expansion, or any one trend. Other forces may be at play: epigenetic stresses passed quietly through generations; the fragmentation of family life; the atomized isolation of childhood; rising exposure to psychoactive substances; environmental or medical factors: anesthesia, vaccine adjuvants, synthetic foods, endocrine disruptors, advanced age of conception. The shift from structure to permissiveness, from 'no' to 'why not?,' has had a thousand ripple effects, many of them invisible until they spike upward in data. Charlie Chaplin noted that, 'Life is a tragedy in close-up and a comedy in long-shot.' Perhaps the opposite applies here: up close, these shifts felt like progress—modernization, liberation, inclusion. But stepping back, the pattern may reveal something darker. And only with that distance can we start to ask whether we need to rebuild guardrails, reinvest in structure, or rethink what we've normalized. Are we over-labeling traits that once went unnoticed? In football, an 'ADHD' kid might shine on defense, while a 'mildly autistic' lineman excels through preparation, showing context shapes strengths. Different contexts highlight different strengths, not deficits—and that extends beyond the field. Today, nearly 40% of young people identify as sexually divergent, and almost 20% claim neurodivergence, suggesting a shift from biology to social identity as diagnostic labels proliferate. The line between genuine disorder and mere difference blurs, especially when the language of activism and resistance reframes personal traits as identity markers. Yet, as the football players demonstrate, cohesion and teamwork come from learning the same playbook, even if offense and defense see the game from opposite angles. In a world where distinctions multiply and identities fragment, we risk losing sight of shared goals—risking not only our unity but our continuity, as social trends pull us further from our genetic roots and toward abstracted, self-imposed divisions. This tension plays out vividly in autism's schisms. Eyal revealed 'high-functioning' self-advocates reject stigma and dependence; while severely autistics' parents face lifelong challenges. RFK Jr.'s claim that some autistic individuals may never work sparked backlash from the former but resonated with the latter: People with profound autism 'will require lifetime, round-the-clock care,' said Profound Autism Alliance's Judith Ursitti. Eyal urges unity, highlighting how self-advocates have reshaped our understanding of even severe autism. First, by showing that behind outward symptoms there may be an active mind seeking connection, they've helped normalize the idea that communication can take many forms. Second, their influence has encouraged shifts in practice—toward adapting communication methods to the individual, through tools like picture exchange systems or adapted iPads, rather than forcing conventional norms. Cohesion, like a football team's, demands a shared playbook. The offensive lineman and defensive back, though worlds apart in style, win by aligning on the same goal. Autism's spectrum—geniuses to those needing lifelong care—needs similar alignment, lest we disease-ify differences or ignore genuine need. Autism — unlike purely genetic conditions like Rett syndrome, or purely congenital ones like rubella syndrome — almost certainly lacks a singular cause. Its 'spectrum' practically guarantees a patchwork of origins: genetic, congenital, epigenetic (via toxins, infections, vaccines, medical interventions), and societal. Teasing apart these threads demands sharper classification of clinical signs. Rubella syndrome proves that a virus can disrupt neurologic development in utero; thus, dismissing vaccines as possible postnatal contributors is not far-fetched — only later-stage. Inspired by Wakefield's perspective, we should explore delaying vaccines like MMR, typically given at 12–15 months, to reduce potential immune challenges during early neurodevelopment, or adjusting schedules based on sex—e.g., prioritizing rubella vaccination for girls due to its pregnancy risks, while delaying it for boys given autism's male predominance. Yet most of autism's dramatic rise seems fueled not by biology alone, but by diagnostic bloat, societal change, and profit-driven incentives. Special education, clinical services, and even pharmaceutical interests thrive on expanded labels. Vaccines, to date, lack proven causality — but the vitriolic and vengeful expulsion of Dr. Andrew Wakefield should serve as warning. Skeptics of rigid pro-vaccine orthodoxy during COVID-19 were likewise demonized, only to see many concerns later grudgingly validated. Was the ferocity against Wakefield evidence of scientific certainty — or fear that his questions hit too close to home? Regression into autism, once dismissed as rare or anecdotal, deserves serious scrutiny. Schizophrenia research acknowledges environmental contributors; autism, too, may involve postnatal immune injuries — whether from infection, febrile seizures, or even vaccination-triggered cascades (cytokine neuroinflammation; post-vaccine encephalitis?). The old image of autism meant institutionalization. Today, by contrast, diagnosis often sweeps in average or superior IQs, think: Anthony Hopkins, Tim Burton, Elon Musk and Dan Aykroyd — raising the question: are we pathologizing giftedness? The Amish and Orthodox Jews show strikingly lower rates, hinting that both culture and vaccination patterns might matter, though our very observation risks distorting their realities. Meanwhile, our attention-fractured world — taxing work, working taxes, drugs, video games, speed-dating — pathologizes traits once crucial for survival: focus, perseverance, loyalty to a small tribe. In a saner, older world, such traits found natural outlets; today, they're flagged for 'intervention.' First World versus Third World: Would they trade HIV or malaria for our dizzying array of mental health labels? Respectively, yes — and no (perhaps); but our challenges, though subtler, are real. We must push for transparent, hypothesis-driven research — cross-temporal and cross-cultural — to ensure we don't over-label while meeting real needs, much like a detective's unraveling a complex case, to uncover the full truth behind autism's rise. The New York Times closed its review quoting psychologist Catherine Lord: 'Whatever it is, it's not vaccines'. This logic echoes a personal anecdote: before traveling to Italy, I mentioned gas cost '$8 a gallon,' only to be corrected — by someone who didn't know the real price. When I asked, 'If you don't know what it is, how can you know what it isn't?' The answer came: 'It can't be $8/gal., because they don't use gallons or dollars.' Technically true, yet completely missing the larger point. As Arthur Conan Doyle's Sherlock Holmes famously advised: 'When you have eliminated the impossible, whatever remains, however improbable, must be the truth.' Autism's spectrum — multifocal, multicausal — demands we explore every possibility, not dismiss avenues out of convenience, cowardice, or commerce. Dr. Randall Bock graduated from Yale University with a BS in chemistry and physics; University of Rochester, with an MD. He has also investigated the mysterious 'quiet' subsequent to 2016 Brazil's Zika-Microcephaly pandemic and panic, ultimately writing 'Overturning Zika.' Follow Dr. Bock on X; YouTube; Brownstone; Instagram; Substack; America Out Loud PULSE radio (including his episode discussing this article)
Yahoo
20 hours ago
- Yahoo
Most Women Ignore This Symptom As A Subtle Sign Of A Heart Attack, But It Could Be A Matter Of Life And Death
In a recent segment on the 'Today' show, Chantrise Holliman, a mother, wife and heart health educator based in Georgia, shared the story of her heart attack and what seemed like the fairly benign symptoms that accompanied it. Holliman experienced nausea, vomiting and mild chest pressure. The first two symptoms ― which aren't commonly associated with heart attacks ― led her to believe the sensations had more to do with her dinner the night before than a serious medical concern. Like Holliman, many people don't know that stomach symptoms can, indeed, be signs of a heart attack. While not the most common warning sign (chest pain is most reported), nausea is also not uncommon during a cardiac event, according to Dr. Sean Heffron, a cardiologist at NYU Langone Health. It 'tends to depend somewhat on which blood vessel in the heart is affected,' Heffron explained. Additionally, nausea is more commonly seen in women, Heffron said, as is vomiting. Other heart attack signs in women include jaw pain, neck pain, a dull feeling of chest discomfort, upper abdomen pain, back pain and excessive tiredness, according to the Centers for Disease Control and Prevention. 'It's so important to hear stories like this, because many women think it has to be like, 'I'm clutching my chest and falling to the ground like you see in the movies,' and it can be much more subtle,' Dr. Tara Narula, a cardiologist and NBC News medical contributor, told 'Today.' Heart attacks can look very different in women than in men, which means that sufferers and doctors alike sometimes dismiss them. But it's important to recognize the signs, especially since heart disease 'is the leading cause of death for women in this country,' Narula told 'Today.' 'One woman every 80 seconds dies of cardiovascular disease.' How to tell if your nausea is part of a heart attack Related: I Was Devastated When The Love Of My Life Died. Then I Started Seeing Signs I Couldn't Explain. Related: "I Can't Wait For This To Go Out Of Style": People Are Sharing Popular Modern Trends That Are Actually Pretty Toxic 'As far as we know, it's rare that [nausea is] the only symptom of a heart attack,' Heffron explained. In Holliman's case, for example, she also said she noticed pressure in her chest. 'And, certainly, a heart attack is far from the most common cause of nausea,' Heffron said. Food poisoning, stomach flu and motion sickness are much more common culprits. So, you don't have to panic the next time you feel nauseated. But if you notice additional heart attack symptoms along with nausea or vomiting — like chest pain, sweating, heart palpitations or dizziness — it could be cause for concern. This is doubly true for someone with risk factors of heart disease like high blood pressure, high cholesterol or diabetes, Heffron said. In the absence of those additional symptoms, nausea probably isn't a cause for extreme concern. 'On occasion, nausea's the only symptom, but I think that's somewhat of an exception,' Heffron said. 'It's not so common.' How to take care of your heart health It's easy to dismiss symptoms that you don't think are indicative of a heart attack, but it's important to understand the signs of a cardiac event and how they manifest for women. Beyond that, you should know what you can do to best take care of your heart. Heffron said you can use the American Heart Association's Life's Essential 8 checklist as a resource to maintain or improve your cardiovascular health. Best practices include eating a diet full of whole foods, fruit, vegetables and lean proteins; getting enough exercise; managing factors like your cholesterol, blood pressure and blood sugar; getting sufficient sleep; and refraining from smoking. All of these behaviors can help keep your heart healthy. 'Obtaining optimal cardiovascular health really includes focusing on these eight metrics,' Heffron noted. If you do feel unwell, you shouldn't discount your symptoms, no matter how small they seem. 'I don't want to overblow it and... freak people out [by saying] all nausea's a heart attack. By all means, it's not,' Heffron said. 'But by no means is chest pain the only symptom of a heart attack.' Other, less obvious signs could be your strongest symptoms, and it's critical you get checked out if you're at all suspicious. 'If you feel unwell and are concerned about what's going on, and in particular, if you have cardiovascular risk factors... then those should be reasons to be seen by a doctor,' Heffron said. 'Don't hesitate if there's any concern.'This article originally appeared on HuffPost. Also in Goodful: Medical Professionals Are Sharing "Mundane" Things That Actually Make So Many People Sick Also in Goodful: People Are Sharing Their Biggest "How Doesn't Everyone Know This?" Facts, And I'm Honestly Embarrassed I Never Realized Some Of These Also in Goodful: "It's Nice To Feel Wanted": Guys Are Sharing The Small Gestures Women Do That Make Them Weak At The Knees
Buzz Feed
21 hours ago
- Buzz Feed
Subtle Sign Of Heart Attack Ignored By Many People
In a recent segment on the 'Today' show, Chantrise Holliman, a mother, wife and heart health educator based in Georgia, shared the story of her heart attack and what seemed like the fairly benign symptoms that accompanied it. Holliman experienced nausea, vomiting and mild chest pressure. The first two symptoms ― which aren't commonly associated with heart attacks ― led her to believe the sensations had more to do with her dinner the night before than a serious medical concern. Like Holliman, many people don't know that stomach symptoms can, indeed, be signs of a heart attack. While not the most common warning sign (chest pain is most reported), nausea is also not uncommon during a cardiac event, according to Dr. Sean Heffron, a cardiologist at NYU Langone Health. It 'tends to depend somewhat on which blood vessel in the heart is affected,' Heffron explained. Additionally, nausea is more commonly seen in women, Heffron said, as is vomiting. Other heart attack signs in women include jaw pain, neck pain, a dull feeling of chest discomfort, upper abdomen pain, back pain and excessive tiredness, according to the Centers for Disease Control and Prevention. 'It's so important to hear stories like this, because many women think it has to be like, 'I'm clutching my chest and falling to the ground like you see in the movies,' and it can be much more subtle,' Dr. Tara Narula, a cardiologist and NBC News medical contributor, told 'Today.' Heart attacks can look very different in women than in men, which means that sufferers and doctors alike sometimes dismiss them. But it's important to recognize the signs, especially since heart disease 'is the leading cause of death for women in this country,' Narula told 'Today.' 'One woman every 80 seconds dies of cardiovascular disease.' 'As far as we know, it's rare that [nausea is] the only symptom of a heart attack,' Heffron explained. In Holliman's case, for example, she also said she noticed pressure in her chest. 'And, certainly, a heart attack is far from the most common cause of nausea,' Heffron said. Food poisoning, stomach flu and motion sickness are much more common culprits. So, you don't have to panic the next time you feel nauseated. But if you notice additional heart attack symptoms along with nausea or vomiting — like chest pain, sweating, heart palpitations or dizziness — it could be cause for concern. This is doubly true for someone with risk factors of heart disease like high blood pressure, high cholesterol or diabetes, Heffron said. In the absence of those additional symptoms, nausea probably isn't a cause for extreme concern. 'On occasion, nausea's the only symptom, but I think that's somewhat of an exception,' Heffron said. 'It's not so common.' It's easy to dismiss symptoms that you don't think are indicative of a heart attack, but it's important to understand the signs of a cardiac event and how they manifest for women. Beyond that, you should know what you can do to best take care of your heart. Heffron said you can use the American Heart Association's Life's Essential 8 checklist as a resource to maintain or improve your cardiovascular health. Best practices include eating a diet full of whole foods, fruit, vegetables and lean proteins; getting enough exercise; managing factors like your cholesterol, blood pressure and blood sugar; getting sufficient sleep; and refraining from smoking. All of these behaviors can help keep your heart healthy. 'Obtaining optimal cardiovascular health really includes focusing on these eight metrics,' Heffron noted. If you do feel unwell, you shouldn't discount your symptoms, no matter how small they seem. 'I don't want to overblow it and... freak people out [by saying] all nausea's a heart attack. By all means, it's not,' Heffron said. 'But by no means is chest pain the only symptom of a heart attack.' Other, less obvious signs could be your strongest symptoms, and it's critical you get checked out if you're at all suspicious. 'If you feel unwell and are concerned about what's going on, and in particular, if you have cardiovascular risk factors... then those should be reasons to be seen by a doctor,' Heffron said. 'Don't hesitate if there's any concern.' HuffPost.
