4 Overstated
Dr. Suzanne Goh's work identified autism spectrum disorder as involving a mitochondrial energy deficit and demonstrated clinical improvements using mitochondrial therapies.
"Suzanne Goh from Harvard, Oxford-trained physician, pediatric neurologist, has done a lot of work on autism and also found it to be a mitochondrial energy deficit and treated those kids with mitochondrial therapies and they work." (said at 0:36:24)
Research led by Dr. Suzanne Goh investigated mitochondrial dysfunction in autism spectrum disorder (ASD) using in vivo magnetic resonance spectroscopic imaging (MRSI). In a 2014 study, Goh and colleagues found elevated brain lactate doublets in 13% of individuals with ASD compared to 1% of controls, concluding that mitochondrial dysfunction represents a potential neurobiological subtype of ASD rather than a universal feature or general cause of autism. Furthermore, while pilot studies have explored metabolic and purinergic interventions (such as a 10-patient pilot trial of suramin), large-scale clinical trials establishing that mitochondrial therapies are broadly effective treatments for autism have not been demonstrated.
- context: Mitochondrial dysfunction as a neurobiological subtype of autism spectrum disorder: eviden… (JAMA psychiatry 2014) · cited 167x in the literature
"Lactate doublets were present at a significantly higher rate in participants with ASD (13%) than controls (1%) (P = .001)... In vivo brain findings provide evidence for a possible neurobiological subtype of mitochondrial dysfunction in ASD." (abstract, results and conclusions)
pubmedfull study (doi) - partial: Low-dose suramin in autism spectrum disorder: a small, phase I/II, randomized clinical tri… (Annals of clinical and translational neurology 2017) · cited 112x in the literature
"Ten male subjects with ASD, ages 5-14 years, were matched by age, IQ, and autism severity into five pairs, then randomized to receive a single, intravenous infusion of suramin (20 mg/kg) or saline... The safety and activity of low-dose suramin showed promise as a novel approach to treatment of ASD in this small study." (abstract, methods and conclusions)
pubmedfull study (doi)
Insulin resistance in early life predicts the future onset of psychiatric disorders and is associated with more severe disease progression in large cohort datasets.
"In large uh like big data studies, we can see that insulin resistance in early life is a marker that predicts future onset of psychiatric conditions. And it also means that people have more severe progression of psychiatric conditions." (said at 0:56:35)
Large prospective birth cohort studies (such as the Avon Longitudinal Study of Parents and Children, ALSPAC) demonstrate that broad immuno-metabolic dysfunction in childhood and genetic liability for type 2 diabetes correlate with later psychotic experiences and atypical depressive symptoms. Furthermore, cross-sectional associations between insulin resistance and depression are observed in early adulthood. However, the claim that insulin resistance in early life independently predicts the future onset and more severe progression of psychiatric disorders overstates the longitudinal evidence: specific analyses isolating childhood insulin resistance from overall adiposity and inflammation often find modest or non-significant independent longitudinal associations with subsequent depression and psychotic symptoms.
Approximately 40% of children in the United States are overweight.
"I mean, 40% of kids are overweight. Almost every single one of those has some metabolic dysfunction." (said at 0:57:16)
The statement bundles two claims and overstates both the definition and the universality of metabolic dysfunction:
1. Overweight prevalence: Nationally representative NHANES data show that approximately 36% to 42% of US youth have excess weight (BMI ≥ 85th percentile), combining those classified as overweight (around 16–17%) and those classified as obese (around 20–22%). Describing 40% as 'overweight' is approximately correct only if combining overweight and obesity into a single category of excess body weight.
2. Metabolic dysfunction: The claim that 'almost every single one of those has some metabolic dysfunction' is overstated. Population studies in youth with obesity show that while cardiometabolic risk factors are significantly elevated compared to normal-weight peers, individual metabolic disturbances (such as low HDL in ~60%, elevated blood pressure in ~16%, or prediabetes/diabetes in ~9%) do not affect nearly all children with excess weight, and a substantial proportion have preclinical obesity without manifest metabolic or clinical impairments.
A mass spectrometry blood test developed by Quest measuring the ratio of C-peptide to insulin is as specific and predictive of insulin resistance as the euglycemic clamp test.
"Now there's a test that you should know about which has just been developed through Quest that uses mass spectrometry, which is a kind of a more sophisticated way of measuring blood analytes, that measures C-peptide, which is a precursor for insulin, and insulin, and gives you a ratio. And it's as specific and predictive of insulin resistance as the more very invasive test that you do for research called the euglycemic clamp test." (said at 0:57:36)
Quest Diagnostics developed a high-throughput liquid chromatography-tandem mass spectrometry (LC-MS/MS) assay to simultaneously measure intact fasting insulin and C-peptide (and calculate an insulin resistance probability score). However, asserting that this fasting blood ratio is as specific and predictive of insulin resistance as the hyperinsulinemic-euglycemic clamp test overstates its clinical capability. The euglycemic clamp directly measures in vivo whole-body glucose disposal under steady-state hyperinsulinemia and remains the metabolic gold standard; surrogate fasting peptide markers correlate with clamp-derived indices but do not match its definitive diagnostic accuracy. Additionally, C-peptide is not a 'precursor for insulin'—both are equimolar cleavage products of the actual precursor, proinsulin.
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