FoundMyFitness · 2019-06-10 · Rhonda Patrick (host), Elissa Epel

Dr. Elissa Epel on Telomeres and the Role of Stress Biology in Cellular Aging

46 claims checked against research: 2 contradicted 3 overstated 3 needing context 35 supported 1 corroborated online 2 unverified

Contradicted by research

0:29:06 Elissa Epelcontradictedlow

Studies by Eli Puterman show that exercise reduces ruminative thought processes.

"Your n of 1 has also been shown up in, you know, studies of exercise and studies by Eli Puterman showing that exercise actually does reduce ruminative processes." (said at 0:29:06)

The speaker mischaracterizes the findings of research led by Eli Puterman. In the primary published study on this topic by Puterman and colleagues (2011), physical activity was examined as a moderator of the physiological stress response, not as an intervention that reduced rumination itself. The study found that being physically active buffered the body against the adverse effects of stressor-induced rumination on cortisol reactivity and recovery (i.e., active individuals did not show the elevated and prolonged cortisol output seen in sedentary individuals who ruminated), but it did not show that exercise reduced ruminative thought processes.

contradicts: Physical activity moderates effects of stressor-induced rumination on cortisol reactivity. (Psychosomatic medicine 2011) · cited 104x in the literature
"Findings indicate that physical activity moderated the initial rate (B = -0.10, standard error = 0.04, p < .05) and curvature (B = -0.03, standard error = 0.01, p = .06) of the relationship between rumination and log-transformed cortisol trajectory... In sum, individuals who maintain a physically active life-style may be protected against the effects of rumination on HPA axis reactivity to and recovery from acute stress." (abstract, results, passage verified)
pubmed full study (doi)

0:38:30 Rhonda Patrick (host)contradictedvery low

Obese male mice sire female offspring that develop type 1 diabetes or autoimmune conditions.

"And there's 20, 100 studies showing male mice that are obese have female offspring that get type 1 diabetes because they get like some autoimmune thing." (said at 0:38:30)

Rodent models of paternal obesity do not demonstrate the development of type 1 diabetes or autoimmune conditions in female offspring. Instead, seminal studies show that paternal high-fat diet and obesity epigenetically transmit metabolic impairments and beta-cell dysfunction leading to impaired glucose tolerance and insulin secretion defects (phenotypes modeling type 2 diabetes pathophysiology), rather than an autoimmune etiology.

contradicts: Chronic high-fat diet in fathers programs β-cell dysfunction in female rat offspring. (Nature 2010) · cited 1339x in the literature
"Here we show that paternal high-fat-diet (HFD) exposure programs β-cell 'dysfunction' in rat F(1) female offspring... Relative to controls, their female offspring had an early onset of impaired insulin secretion and glucose tolerance that worsened with time, and normal adiposity." (abstract, results)
pubmed full study (doi)
contradicts: The anti-inflammatory agent 5-ASA reduces the level of specific tsRNAs in sperm cells of h… (Journal of diabetes and its complications 2023) · cited 8x in the literature
"Paternal obesity is an independent risk factor for developing obesity and type 2 diabetes in the following generation, and growing evidence suggests epigenetic inheritance as a mechanism for this predisposition." (abstract, introduction, passage verified)
pubmed full study (doi)

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.