FoundMyFitness · 2016-03-14 · Rhonda Patrick (host), Peter Attia
Peter Attia, M.D. on Macronutrient Thresholds for Longevity and Performance, Cancer and More
43 claims checked against research: 4 contradicted 3 overstated 6 needing context 29 supported 1 unverified
4 Contradicted by research
As insulin levels decrease, levels of IGF-binding protein 3 (IGFBP-3) increase.
"However, as it sounds like you agree, it's pretty clear that as insulin levels go down, IGFBP-3 goes up." (said at 0:10:10)
The speaker appears to have confused IGFBP-3 with IGFBP-1 (or IGFBP-2). In human physiology, IGFBP-1 is acutely suppressed by insulin, meaning as insulin levels decrease (e.g., during fasting), IGFBP-1 levels increase. In contrast, IGFBP-3—the major circulating binding protein for IGF-1—is primarily regulated by growth hormone and is not inversely regulated by insulin in this manner. Experimental studies in humans using glucose and insulin clamps demonstrate that acute changes in insulin levels do not increase IGFBP-3 levels, whereas IGFBP-1 changes dynamically and inversely with insulin.
The gastrointestinal tract contains more immune cells than any other organ in the human body.
"I mean, you've got more immune cells in your gut than you do in any other organ in your body, and the interaction between your gut bacteria and your gut are also regulating the types of immune cells that you're making" (said at 0:20:41)
Although it is a widespread textbook and popular claim that the gut houses the majority of the body's immune cells, comprehensive cellular quantification contradicts this. A comprehensive census of immune cells across human tissues (Sender et al., 2023) established that the bone marrow (housing the vast majority of neutrophils) and secondary lymphoid tissues like lymph nodes and spleen (housing the majority of lymphocytes) contain substantially more immune cells by both number and cellular mass than the gastrointestinal tract, which accounts for only a small percentage of total human immune cells.
Over the past 50 years, the incidence or prevalence of Alzheimer's disease has increased by approximately 2.5% per year, while longevity has increased by about 0.6% per year.
"we know that in the last 50 years, the prevalence of Alzheimer's disease has gone up about 2.5%, whereas the increase in our per year, by the way—I'm sorry, that's per year—whereas we know that our longevity has increased at about 0.6% per year over that same period of time." (said at 0:42:03)
The claim that the prevalence or incidence rate of Alzheimer's disease has increased by approximately 2.5% per year over the past several decades is contradicted by epidemiological research. Longitudinal cohort studies across North America and Europe show that age-specific dementia and Alzheimer's disease incidence rates have actually declined by approximately 13% per decade (or about 1% to 2% per year) over recent decades. While the absolute total number of people living with Alzheimer's has grown due to overall population aging and population growth, the underlying age-adjusted risk per person has decreased or remained stable, rather than increasing at 2.5% per year.
- contradicts: Incidence of Dementia over Three Decades in the Framingham Heart Study. (The New England journal of medicine 2016) · cited 1055x in the literature
"Relative to the incidence during the first epoch, the incidence declined by 22%, 38%, and 44% during the second, third, and fourth epochs, respectively." (abstract, results, passage verified)
pubmedfull study (doi) - contradicts: Twenty-seven-year time trends in dementia incidence in Europe and the United States: The A… (Neurology 2020) · cited 494x in the literature
"The incidence rate of dementia declined by 13% per calendar decade (95% confidence interval [CI], 7%-19%), consistently across studies, and somewhat more pronouncedly in men than in women (24% [95% CI 14%-32%] vs 8% [0%-15%])." (abstract, results, passage verified)
pubmedfull study (doi)
In animal models, simultaneous injection of glucose and insulin transiently overcomes cognitive deficits, and administration of exogenous beta-hydroxybutyrate can overcome the deficit and reverse symptoms.
"And and I think in animal models there's some very convincing data that you can, you know—I mean, you've seen this stuff, I'm sure, more than I have, right? Simultaneous injection of glucose and insulin can transiently overcome deficit; administration of exogenous BHB can overcome the deficit by bypassing and going straight straight through alpha-hydroxybutyrate into the Krebs cycle, so where you can reverse the signs and symptoms." (said at 0:44:40)
The speaker's statement misidentifies the metabolic pathway of beta-hydroxybutyrate (β-HB). Beta-hydroxybutyrate is oxidized to acetoacetate and subsequently converted to acetyl-CoA, which enters the tricarboxylic acid (Krebs) cycle. Alpha-hydroxybutyrate is a distinct metabolite involved in amino acid catabolism and glutathione synthesis; it is not an intermediate in ketone body metabolism or Krebs cycle entry. Additionally, no published record matching simultaneous injection of glucose and insulin transiently reversing cognitive deficits in animal models was located.
Unverified means no publication matching the claim was located; it does not prove the claim false. Spotted an error? See the corrections policy - disputes from the people quoted are prioritized.