HoldsUp

FoundMyFitness · 2018-07-09 · Rhonda Patrick (host), Valter Longo

How diet and lifestyle regulate longevity with Dr. Valter Longo and Dr. Rhonda Patrick

28 claims checked against research: 1 contradicted 2 needing context 21 supported 4 unverified

1

Contradicted by research

0:46:42Valter Longocontradictedhigh

Complete digestion and absorption of ingested food calories takes approximately 30 hours from the time food is eaten.

"I mean, all the digestion takes, you know, 30 hours to complete the food digestion, right? And in the from the time you eat to the time that all the calories have been taken up, it takes probably over a day." (said at 0:46:42)

The speaker confuses total whole-gut transit time with the time required for caloric digestion and absorption. The vast majority of macronutrient digestion and caloric absorption occurs in the stomach and small intestine, taking roughly 4 to 8 hours in healthy individuals (gastric emptying typically takes 2–5 hours and small bowel transit takes 2–6 hours). The remaining time (10 to 60+ hours) occurs in the large intestine/colon, which primarily absorbs water and electrolytes and forms stool, not digesting or absorbing dietary calories.

2

Needs context

0:43:07Valter Longoneeds contextmoderate

The fasting-mimicking diet selectively reduces abdominal fat while sparing subcutaneous fat and preserving or increasing relative lean body mass following refeeding in humans and mice.

"and of course you lose abdominal fat because after a few days this becomes your reservoir. I mean, every—although all the—it doesn't touch subcutaneous fat for some reason, it only goes to the main depot that have this effect. So that's great news, but the muscle is also decreased. But then when you refeed, the muscle is rebuilt... and this, no effect on subcutaneous fat and no or very little effect on even absolute lean body mass. In fact, the relative lean body mass goes up." (said at 0:43:07)

Randomized trial data on periodic cycles of the fasting-mimicking diet (FMD) in humans (such as the 100-subject trial by Wei et al., 2017) show that 3 monthly cycles of FMD reduce trunk and total body fat while largely preserving absolute lean mass and increasing relative lean body mass after normal refeeding. However, stating that FMD has 'no effect on subcutaneous fat' or 'doesn't touch subcutaneous fat' is an exaggeration; while visceral/trunk fat is preferentially mobilized, overall body fat decreases as well.

0:39:57Valter Longoneeds contextmoderate

Studies on yo-yo dieting and prolonged starvation periods show that they lower metabolic rate, which can lead to subsequent weight gain.

"there's famous papers that have shown what they call the yo-yo diets, right? They have shown that this can actually lower your metabolism if you have this prolonged starvation period. It can lower your metabolism, and then you tend to gain weight." (said at 0:39:57)

Prolonged severe caloric restriction or starvation induces adaptive thermogenesis—an acute reduction in resting energy expenditure beyond what is explained by loss of body mass. However, the speaker's claim that 'yo-yo dieting' (weight cycling) permanently depresses metabolic rate and drives subsequent weight gain is not supported by systematic evidence. Systematic reviews examining weight cycling find that the vast majority of studies show no adverse or permanent reduction in resting metabolic rate from repeated cycles of weight loss and regain. Furthermore, systematic reviews indicate that adaptive thermogenesis tends to attenuate during weight-stable maintenance.

21

Supported by research

0:03:40Valter Longosupportedvery low

Caloric restriction in monkeys completely wipes out diabetes and reduces cardiovascular disease and cancer incidence by 50%.

"I mean, in monkeys, we know that it can wipe out diabetes completely, and can reduce cardiovascular disease and cancer by 50%." (said at 0:03:40)

The claim accurately reflects findings from the landmark longitudinal study of caloric restriction in rhesus macaques at the Wisconsin National Primate Research Center (Colman et al., 2009). In that 20-year adult-onset study, animals on a 30% calorically restricted diet developed no cases of diabetes compared to control animals, and experienced an approximate 50% reduction in the incidence of cardiovascular disease and cancer. Subsequent collaborative analyses with the National Institute on Aging primate cohort confirmed that caloric restriction significantly decreases age-related morbidity and metabolic disease in rhesus monkeys, though because this evidence comes exclusively from non-human primates, certainty regarding direct translation to human clinical outcomes is very low.

0:05:44Valter Longosupportedmoderate

The University of Wisconsin monkey caloric restriction study extended mean lifespan, whereas the National Institute on Aging (NIA) monkey study did not.

"So I think it would have been difficult to get maximal lifespan, but the mean lifespan was extended in Wisconsin. It was not extended at the NIA." (said at 0:05:44)

The speaker accurately summarizes the survival findings from two major long-term caloric restriction (CR) trials in rhesus monkeys conducted at the University of Wisconsin-Madison (WNPRC) and the National Institute on Aging (NIA). In the University of Wisconsin study, CR significantly reduced overall mortality and extended lifespan/survival (Colman et al., 2009). In contrast, the NIA study found that CR initiated in young or older rhesus monkeys did not improve survival outcomes or extend lifespan compared to controls (Mattison et al., 2012). A subsequent collaborative analysis confirmed these distinct survival outcomes between the two study sites and identified differences in control diet composition, feeding regimens, and age at implementation as major contributing factors (Mattison et al., 2017).

0:08:00Valter Longosupportedmoderate

In human caloric restriction studies by Fontana and colleagues, calorie restriction alone did not reduce IGF-1 levels until dietary protein was also restricted.

"So, for example, there are human studies where they show that because the people that are restricted were eating a high vegetable protein diet, the IGF-1 was not affected... they actually did the second study, Fontana and colleagues, in the follow-up in which they restricted the proteins and then the IGF-1" (said at 0:08:00)

A 2008 study by Luigi Fontana and colleagues in Aging Cell demonstrated that long-term severe calorie restriction (CR) in humans did not lower total serum IGF-1 or the IGF-1:IGFBP-3 ratio compared to control diets, largely because the CR practitioners consumed relatively high protein levels (~1.67 g/kg/day). When a subset of these CR volunteers temporarily lowered their protein intake to ~0.95 g/kg/day for 3 weeks, serum IGF-1 significantly decreased from 194 ng/mL to 152 ng/mL. Subsequent trials, including the 2-year CALERIE study, confirmed that CR alone without protein restriction does not lower circulating IGF-1 concentrations in humans.

0:10:55Valter Longosupportedvery low

Mice with growth hormone receptor deficiency or growth hormone deficiency live approximately 40% longer than control mice.

"And what we knew from mice, from the work of John Kopchick and Andrzej Bartke, that mice that have either growth hormone receptor or growth hormone deficiency live longer, about 40% longer." (said at 0:10:55)

Extensive animal research conducted by Andrzej Bartke, John Kopchick, and colleagues demonstrates that mice with deficient growth hormone (GH) signaling—including GH receptor knockout (GHR-KO) mice and GH-deficient dwarf models (such as Ames dwarf mice)—exhibit significant increases in median and maximal lifespan, typically ranging from 40% to over 50% longer than wild-type control mice, alongside delayed onset of age-related pathology. Because this evidence comes exclusively from laboratory rodent models, the GRADE certainty for translation to humans is graded as very low.

0:11:48Valter Longosupportedmoderate

Individuals in Ecuador with growth hormone receptor deficiency (Laron syndrome) are protected from cancer, diabetes, and age-dependent cognitive decline.

"and in our work in humans where we've been following these people with the growth hormone receptor deficiency down in Ecuador—they have a syndrome called Laron syndrome—so they're very much the equivalent to the mice, and they don't have a very long lifespan. They may live a few years more than their relatives that don't have homozygous growth hormone receptor deficiency, but they're protected from cancer, they're protected from diabetes, and recent papers show that they seem to be protected from age-dependent cognitive decline." (said at 0:11:48)

Longitudinal and cross-sectional studies of the Ecuadorian cohort with growth hormone receptor deficiency (GHRD / Laron syndrome) confirm that these individuals have a near-total absence of diabetes and a marked reduction in cancer incidence compared to unaffected relatives. Furthermore, neuroimaging and cognitive evaluations of this cohort demonstrated preserved memory performance and brain structure/function resembling that of younger adults, suggesting protection against age-dependent cognitive decline.

0:13:14Valter Longosupportedmoderate

Circulating IGF-1 levels in individuals with Laron syndrome are approximately 10% of normal circulating IGF-1 levels.

"Yeah, we measured the IGF-1. It's very low. It's like 10% of the normal circulating IGF-1." (said at 0:13:14)

Individuals with Laron syndrome (growth hormone receptor deficiency/growth hormone insensitivity) have severe primary IGF-1 deficiency. Published biochemical evaluations in cohorts with Laron syndrome show extremely low circulating levels of insulin-like growth factor-1 (IGF-1), typically reduced to approximately 10% (or less) of normal control levels, accompanied by normal to elevated growth hormone levels and low or undetectable growth hormone-binding protein.

0:13:27Valter Longosupportedvery low

Human epithelial cells exposed to serum from individuals with Laron syndrome exhibit downregulation of TOR and Ras gene expression compared to cells exposed to control serum.

"we took the serum and we took human epithelial cells, and we exposed the human epithelial cells either to control serum or to the serum of the Larons, and then we looked at gene expression. And that showed that not only TOR was downregulated, so was Ras, at least gene expression-wise" (said at 0:13:27)

A landmark study by Guevara-Aguirre et al. (2011) investigated Ecuadorian individuals with growth hormone receptor deficiency (GHRD, or Laron syndrome). As part of the study's in vitro experiments, human mammary epithelial cells were cultured in medium supplemented with serum from GHRD individuals versus control relatives. The authors found that exposure to GHRD serum led to reduced gene expression of pro-aging and growth-signaling mediators, specifically TOR (target of rapamycin), RAS, and PKA, alongside upregulation of SOD2.

0:17:05Valter Longosupportedvery low

In mammalian cells, glucose levels directly activate Protein Kinase A (PKA).

"Actually, we've shown that as we have shown for yeast, we've now shown in mammalian cells that glucose levels activate PKA." (said at 0:17:05)

Preclinical studies from Valter Longo's laboratory demonstrated that glucose levels regulate protein kinase A (PKA) signaling in mammalian cell models and mice, mirroring the glucose-PKA nutrient sensing pathway previously characterized in yeast. Specifically, experimental work in mammalian cardiomyocytes and cancer stem cells showed that glucose availability stimulates PKA activity, whereas glucose restriction or fasting-mimicking conditions reduce PKA activation. Because these findings are derived from cell culture and rodent experiments, the clinical certainty remains very low.

0:27:00Valter Longosupportedmoderate

In clinical trials testing fasting-mimicking diets alongside cancer treatment, subject compliance was approximately 40% due in part to chemotherapy-induced food aversion.

"So we already—a couple hundred patients have already been involved in these multiple randomized clinical trials, and the good news is that there is no problems... So we had about a 40% thus far compliance" (said at 0:27:00)

Clinical trials evaluating cyclic fasting-mimicking diets (FMD) alongside chemotherapy in cancer patients (such as the multicentre randomized phase 2 DIRECT trial in breast cancer) have documented overall compliance rates of approximately 33% to 40% across all planned cycles. The decline in adherence across repeated treatment cycles is commonly driven by chemotherapy-associated side effects, including nausea, taste alterations, and food aversion toward the FMD components.

0:09:48Valter Longosupportedhigh

Dietary proteins and specific amino acids such as methionine and cysteine regulate circulating IGF-1 levels in mammals.

"proteins, and particularly certain amino acids—methionine, cysteine, etc.—they regulate IGF-1 levels." (said at 0:09:48)

Extensive animal research and human dietary intervention trials confirm that dietary protein intake and specific sulfur amino acids (methionine and cysteine) regulate circulating insulin-like growth factor-1 (IGF-1) levels. In both rodent models and controlled human feeding studies, dietary restriction of methionine and total sulfur amino acids (methionine and cysteine) leads to significant reductions in circulating IGF-1 concentrations along with other metabolic and endocrine shifts.

0:21:55Valter Longosupportedlow

Certain types of cancer cells can utilize ketone bodies and accelerate their growth in response to them.

"some cancers actually love to use both ketone bodies and sugar... so you can actually accelerate cancer growth with ketone bodies, but you can also hurt cancer cells with ketone bodies." (said at 0:21:55)

Preclinical studies demonstrate that while some cancers are inhibited by glucose restriction and ketogenic conditions, certain tumor types can metabolize ketone bodies (such as beta-hydroxybutyrate and acetoacetate) via ketolytic pathways to fuel cell proliferation and tumor progression. For example, in pancreatic ductal adenocarcinoma models, beta-hydroxybutyrate functions as a metabolic fuel that promotes tumor growth and metastasis. Similarly, in hepatocellular carcinoma models, activation of the rate-limiting ketolytic enzyme OXCT1 enhances ketolysis and accelerates tumor growth in mice. Because these findings derive primarily from in vitro and animal models, the certainty is low.

0:31:40Valter Longosupportedmoderate

Chronic calorie restriction continuously drives blood pressure, cholesterol, and triglycerides down, even in individuals who start with low baseline levels, as observed in Biosphere 2 and confirmed by Luigi Fontana.

"So, calorie restriction, chronic, keep driving your markers down, right? So even if you started—I mean, if you look at Biosphere 2, and these were then confirmed by Fontana and others, if you look at Biosphere 2, even people that had at the beginning a low blood pressure, they kept dropping, and by the end of it they had pressure like 85 over 55, right? And same thing for cholesterol, same thing for triglycerides. Almost everything is really dropped to very low levels." (said at 0:31:40)

Published data from the Biosphere 2 experiment and subsequent research by Luigi Fontana and colleagues confirm that chronic calorie restriction leads to marked decreases in blood pressure, cholesterol, and triglycerides, even in non-obese individuals. In the 2-year Biosphere 2 study (n=8), mean blood pressure decreased from a baseline of 109/74 mmHg to 89/58 mmHg within 6 months, along with significant reductions in total cholesterol and triglycerides. Similarly, Fontana et al. demonstrated that long-term calorie restriction (averaging 6 years) maintained markedly lower systolic and diastolic blood pressure, total cholesterol, and triglyceride levels compared to matched controls.

0:32:10Valter Longosupportedmoderate

In clinical trials, the fasting-mimicking diet does not further lower fasting glucose in individuals with normal baseline glucose around 75 mg/dL, but normalizes fasting glucose in individuals with levels over 106 mg/dL.

"Fasting glucose—the fasting-mimicking diet says it seems when if you have a blood glucose of 75, nothing changes, it doesn't drop it even more. If you had a fasting glucose over 106, almost in every case it brings you back to normal." (said at 0:32:10)

A randomized controlled trial evaluating cycles of a 5-day fasting-mimicking diet (FMD) demonstrated differential effects based on baseline metabolic risk. In a post hoc analysis, risk factors including fasting glucose were selectively and more beneficially reduced in participants with elevated baseline risk factors, whereas participants with healthy baseline levels experienced minimal change, maintaining normal glucose levels without excessive reduction.

0:33:14Valter Longosupportedmoderate

Three cycles of the fasting-mimicking diet significantly reduced cholesterol, triglycerides, IGF-1, systolic and diastolic blood pressure, and CRP in participants who had elevated baseline levels, with IGF-1 dropping by roughly 60 points in those with the highest baseline levels.

"But in people who had elevated cholesterol, it decreased cholesterol. The people that had elevated triglyceride, it decreased triglycerides. People that had elevated IGF-1, probably for even a high-protein diet, it dropped IGF-1, and the highest people dropped dramatically, you know, came down about 60 points. And people that had high fasting glucose came down. People had blood pressure that was elevated, both systolic and diastolic had major effects. The people who had CRP, systemic inflammation, in almost every case they moved back to the the normal range." (said at 0:33:14)

A randomized controlled trial evaluated 100 participants completing three monthly 5-day cycles of a fasting-mimicking diet (FMD) versus an unrestricted control diet followed by crossover. The primary analysis demonstrated significant reductions in body weight, blood pressure, and IGF-1. A post hoc stratified analysis of participants with elevated baseline risk factors confirmed that participants with elevated baseline levels experienced significantly greater reductions in total and LDL cholesterol, triglycerides, fasting glucose, systolic and diastolic blood pressure, IGF-1, and C-reactive protein (CRP), with IGF-1 falling most substantially among those in the highest baseline tier.

0:35:35Valter Longosupportedmoderate

Approximately 60% of the biomarker changes achieved after three cycles of the fasting-mimicking diet remained statistically significant three months post-intervention.

"I mean, they were about 60% of the effects were still there. So you could tell that they were smaller, but 60% of the changes were still significant." (said at 0:35:35)

In a randomized trial evaluating 100 healthy participants undergoing three monthly 5-day cycles of a fasting-mimicking diet (FMD; PMID: 28202779), post-intervention follow-up after participants returned to their normal diet showed that approximately 60% of the significant metabolic and risk-factor reductions (such as body weight, trunk fat, blood pressure, and IGF-1) persisted.

0:41:41Valter Longosupportedvery low

Mice placed on cycles of the fasting-mimicking diet eat the same total monthly caloric intake as controls due to compensatory refeeding, but still experience significant weight loss and fat burning.

"we've shown that per month, if you take mice and you put them on fasting-mimicking diet, they, you know, of course have less calories during the five-day—the four days in the case of mice—and but then their metabolism seems to be speeded up to the point that per month they eat the same calories, so they overeat everything they undereat during the the the five—the four days, right? So they eat exactly the same, but they lose a lot of weight." (said at 0:41:41)

In animal studies evaluating periodic fasting-mimicking diet (FMD) regimens (such as Brandhorst et al., 2015), mice underwent 4 days of FMD cycles followed by ad libitum refeeding. During the refeeding periods, the mice exhibited compensatory hyperphagia, resulting in equivalent total monthly caloric intake compared to ad libitum-fed controls, while still displaying significant reductions in body weight, visceral fat, and age-related biomarkers. Because the claim describes findings specifically demonstrated in rodent models, the overall certainty is rated very low.

0:45:07Valter Longosupportedmoderate

In mice and humans undergoing fasting or fasting-mimicking diets, organs and white blood cell levels temporarily shrink or reduce during fasting cycles and return to normal levels upon refeeding through stem cell activation.

"so the organs will be smaller and, you know, at the end of the the days of fasting-mimicking diet, and then you refeed it and of course they go back to the normal level, right? So there is really there is this shrinking and re-expanding effect. Now, we don't know how much of it is cells becoming smaller versus cells being killed, but clearly there is killing of cells... And we've started to show that in a multiple sclerosis mouse model, and and also the human study, there was evidence that the white blood cell level temporarily was reduced during the at the end of the fasting cycles and then went back to normal. So yeah, so we suspect that there are these this fasting-dependent depletion of both intracellular components, in autophagy, and cellular components. And then, you know, we've shown the stem cells to be activated and and the stem cell turn on in the refeeding part." (said at 0:45:07)

Preclinical and clinical studies by Longo and colleagues demonstrate that cycles of prolonged fasting or fasting-mimicking diets (FMD) induce a transient reduction in organ size and circulating white blood cell levels, followed by stem cell- and progenitor cell-mediated regeneration upon refeeding. In mice, 4 days of FMD decreased the weight and size of multiple organs, which re-expanded upon refeeding accompanied by elevated stem/progenitor cell numbers. Similarly, prolonged fasting and FMD were shown in mouse models and pilot human trials (including multiple sclerosis cohorts) to deplete white blood cells and auto-reactive immune cells via apoptosis, subsequently triggering hematopoietic stem cell self-renewal and lineage regeneration driven by down-regulation of IGF-1 and PKA signaling.

0:51:21Valter Longosupportedvery low

In a multiple sclerosis mouse model, fasting-mimicking diet cycles kill autoimmune immune cells, activate stem cells, and stimulate oligodendrocyte progenitor cells to replace damaged cells.

"Because, for example, in multiple sclerosis, you see on one side it kills the immune cells, it then turns on the stem cells, then turns on the oligodendrocyte progenitor, replaces—I mean, it's very sophisticated." (said at 0:51:21)

In a 2016 preclinical study in mouse models of multiple sclerosis (experimental autoimmune encephalomyelitis and cuprizone-induced demyelination), periodic cycles of a fasting-mimicking diet (FMD) reduced levels of pro-inflammatory immune cells (TH1, TH17, and antigen-presenting cells) through apoptosis/depletion, increased regulatory T cells, and promoted oligodendrocyte precursor cell regeneration and remyelination. Because these mechanistic findings derive from animal models, the overall certainty is rated very low.

0:57:56Valter Longosupportedhigh

Morgan Levine at Yale has identified a set of clinical biomarkers derived from large population datasets that is predictive of biological age.

"And, yeah, then Morgan Levine, she's now at Yale, she has a—she and others have a set of markers that are taken from large population, and they seem to be predictive of biological age." (said at 0:57:56)

Morgan Levine and colleagues developed 'Phenotypic Age' (PhenoAge) and its epigenetic counterpart (DNAm PhenoAge) using large population datasets, specifically the National Health and Nutrition Examination Survey (NHANES). The metric combines chronological age with a panel of nine multi-system clinical chemistry biomarkers (including albumin, creatinine, glucose, C-reactive protein, lymphocyte percent, mean cell volume, red cell distribution width, alkaline phosphatase, and white blood cell count) to quantify biological/phenotypic age, robustly predicting all-cause mortality, disease risk, and physiological functioning.

  • supports: An epigenetic biomarker of aging for lifespan and healthspan. (Aging 2018) · cited 3751x in the literature
    "While the first generation of epigenetic biomarkers of aging were developed using chronological age as a surrogate for biological age, we hypothesized that incorporation of composite clinical measures of phenotypic age that capture differences in lifespan and healthspan may identify novel CpGs and facilitate the development of a more powerful epigenetic biomarker of aging. Using an innovative two-step process, we develop a new epigenetic biomarker of aging, DNAm PhenoAge, that strongly outperforms previous measures in regards to predictions for a variety of aging outcomes, including all-cause mortality, cancers, healthspan, physical functioning, and Alzheimer's disease." (abstract, passage verified)
    pubmedfull study (doi)
  • supports: A new aging measure captures morbidity and mortality risk across diverse subpopulations fr… (PLoS medicine 2018) · cited 740x in the literature
    "Phenotypic Age was calculated based on a linear combination of chronological age and 9 multi-system clinical chemistry biomarkers in accordance with our previously established method. We also estimated Phenotypic Age Acceleration (PhenoAgeAccel), which represents Phenotypic Age after accounting for chronological age (i.e., whether a person appears older [positive value] or younger [negative value] than expected, physiologically)." (abstract, results, passage verified)
    pubmedfull study (doi)
0:53:23Valter Longosupportedhigh

Multiple clinical trials evaluating IGF-1 pathway inhibitors as cancer therapies failed.

"for example, the—the clinical trial, the multiple clinical trials that were done on IGF-1 in cancer. They failed, right?" (said at 0:53:23)

Extensive clinical trial programs evaluated IGF-1 pathway inhibitors—including anti-IGF-1R monoclonal antibodies (such as figitumumab, dalotuzumab, and cixutumumab) and IGF-1R tyrosine kinase inhibitors—across a broad range of adult malignancies (including non-small cell lung cancer, breast cancer, colorectal cancer, and pancreatic cancer). Despite promising preclinical evidence, large randomized clinical trials consistently failed to show therapeutic benefit or improved survival over standard therapy in unselected patient populations, leading to the discontinuation of most clinical development programs in this class.

0:54:23Valter Longosupportedvery low

Stem cell activation and self-renewal during fasting is low IGF-1 dependent, whereas stem cell proliferation and differentiation during refeeding are driven by high IGF-1 and insulin levels.

"the turning on of stem cells, which is also low IGF-1 dependent. So—oh, it's low? I thought it was higher. GUEST1: Right, the turning on the stem cell, not turning on the proliferation of them. It's high IGF-1—yeah. No, but the—the turning on, all right, so now is the signal, right, to self-renew, you know? Yeah. So now you have a population of—a small population of stem cells that are just active and standing by. Then probably when IGF-1 goes back up, now they are the ones that are pushed by IGF-1 to proliferate, to differentiate" (said at 0:54:23)

Preclinical studies in mice demonstrate that prolonged fasting lowers circulating IGF-1 levels and downregulates PKA signaling, which triggers self-renewal and lineage-balanced priming in long-term hematopoietic stem cells. Subsequent refeeding and restoration of growth factors (including IGF-1) promote the proliferation, differentiation, and multi-system tissue regeneration of these primed progenitor pools. Because the direct causal demonstration of this dual-phase mechanism is derived from murine and in vitro models, the certainty of evidence for this specific cellular pathway in humans is very low.

4

No source found (not proven false)

0:11:20Valter Longounverifiedvery low

Approximately 50% of growth hormone receptor deficient mice reach the end of life without obvious pathological lesions, compared to less than 10% in control mice.

"and yet about half of the mice get to the end of life without any obvious pathological lesion, so they don't develop diseases. In the controls, this is less than 10%." (said at 0:11:20)

No published record matching the specific claim that approximately 50% of growth hormone receptor-deficient (GHRKO) mice reach the end of life without obvious pathological lesions compared to less than 10% in control mice was located; this does not prove the claim false.

0:36:44Valter Longounverifiedvery low

Over 25,000 people have completed the ProLon fasting-mimicking diet with very few severe side effects reported, and no evidence that the diet caused those severe side effects.

"there's over 25,000 people that have done the fasting-mimicking diet, the ProLon, the same diet that was tested clinically, with very, very few severe side effect reports, right? And even the ones that had severe side effects, you know, they fully recovered, and there was no evidence that it was the diet that that caused them" (said at 0:36:44)

No published record matching the post-market safety data or registry of over 25,000 individuals completing the ProLon fasting-mimicking diet was located; this does not prove the claim false. While published clinical trials have evaluated the fasting-mimicking diet in smaller human cohorts (typically dozens to hundreds of participants) and reported mostly mild-to-moderate adverse events such as fatigue, weakness, and headaches, the specific figure of over 25,000 users and their post-market adverse event reporting appears to derive from unpublished commercial customer data.

1:03:37Valter Longounverifiedvery low

The biological process of autophagy originated evolutionarily in bacteria.

"I mean, of course starting with bacteria, but the process of autophagy started back then in bacteria." (said at 1:03:37)

No published record matching the claim that autophagy originated evolutionarily in bacteria was located; this does not prove the claim false.

1:04:30Rhonda Patrick (host)unverifiedvery low

Clinical studies on the fasting-mimicking diet showed a trend toward increasing mesenchymal stem cells.

"at least in the clinical studies with the fasting-mimicking diet, I think you were trying to look whether or not there was some stem cell activation, and there was sort of a trend. You had seen mesenchymal stem cells, a trend, you know, increasing them." (said at 1:04:30)

No published record matching the claim that clinical studies on the fasting-mimicking diet showed a trend toward increasing mesenchymal stem cells was located; this does not prove the claim false.

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.