HoldsUp

FoundMyFitness · 2022-03-09 · Rhonda Patrick (host), Peter Diamandis, Tony Robbins

Peter Diamandis and Tony Robbins on strategies that promote longevity now – and in the near future

52 research-tied claims examined: 3 contradicted 7 overstated 12 context 18 supported 12 unverified

18

Supported by research

0:13:10Peter Diamandissupportedlow

Using a sauna four to seven times per week significantly reduces the risk of heart attack, stroke, and lowers blood pressure.

"I had no idea the research that showed four to seven times a week could change completely the profile of you having a heart attack or a stroke, the changing of blood pressure." (said at 0:13:10)

The claim is supported by longitudinal cohort data from the Kuopio Ischemic Heart Disease Risk Factor Study (KIHD) in Finland. These prospective observational studies demonstrated that individuals using a sauna 4 to 7 times per week had a significantly lower risk of cardiovascular mortality, sudden cardiac death, stroke, and incident hypertension compared to those who used a sauna once per week. Specifically: 1. **Heart attack / Cardiovascular mortality:** Men who used the sauna 4 to 7 times per week had an adjusted hazard ratio (HR) of 0.37 (95% CI, 0.18–0.75) for sudden cardiac death and 0.23–0.30 for overall cardiovascular disease mortality compared to those taking 1 session per week. 2. **Stroke:** Men and women participating in 4 to 7 sauna sessions per week had an adjusted HR for incident stroke of 0.38 (95% CI, 0.18–0.81). 3. **Blood pressure / Hypertension:** Frequent sauna bathing (4–7 times per week) was associated with a 47% lower risk of incident hypertension (adjusted HR 0.53, 95% CI, 0.28–0.98). Because these data stem from observational cohort studies rather than randomized controlled trials, certainty is graded as low due to potential residual confounding (e.g., self-selection bias, general health status, lifestyle factors). Nevertheless, the statistical findings directly mirror the speaker's claim.

0:17:50Peter Diamandissupportedhigh

In a Veterans Administration trial of arthroscopic knee surgeries with sham controls, patients receiving sham surgery experienced equal pain relief and mobility after one year compared to those receiving real surgery.

"For knee surgeries, they decided to do a third of the surgeries as sham surgeries, placebo surgeries. They just put a mark, sewed the person up, but did nothing to the knee. A year later, the patients that had no treatment but thought they had had no pain, talked about how mobile they were compared to the ones that were—they don't even fund it anymore." (said at 0:17:50)

A landmark randomized, double-blind, placebo-controlled trial conducted at the Houston Veterans Affairs Medical Center evaluated 180 patients with knee osteoarthritis assigned to arthroscopic debridement, arthroscopic lavage, or sham surgery (skin incisions and simulated surgery without arthroscope insertion). At one and two years of follow-up, patients in the sham surgery group experienced equivalent improvements in pain and functional mobility compared to patients who received active arthroscopic debridement or lavage, with no statistically significant differences across any assessed time points.

  • supports: A controlled trial of arthroscopic surgery for osteoarthritis of the knee. (The New England journal of medicine 2002) · cited 2158x in the literature
    "At no point did either of the intervention groups report less pain or better function than the placebo group. For example, mean (+/-SD) scores on the Knee-Specific Pain Scale (range, 0 to 100, with higher scores indicating more severe pain) were similar in the placebo, lavage, and débridement groups: 48.9+/-21.9, 54.8+/-19.8, and 51.7+/-22.4, respectively, at one year (P=0.14 for the comparison between placebo and lavage; P=0.51 for the comparison between placebo and débridement) and 51.6+/-23.7, 53.7+/-23.7, and 51.4+/-23.2, respectively, at two years (P=0.64 and P=0.96, respectively)." (abstract, results, passage verified)
    pubmedfull study (doi)
0:22:26Tony Robbinssupportedhigh

The GRAIL Galleri liquid biopsy test can identify circulating cell-free DNA signals for 50 different types of cancer from a routine blood draw.

"Besides the full-body MRI, which is looking for cancers, we do a GRAIL, you know, liquid biopsy, which can find 50 different cancers in your bloodstream. It turns out as cancer cells are growing and dividing very rapidly, some of the cells rupture and you get free-floating DNA in the bloodstream. Well, GRAIL, which is now part of Illumina, started by Jeff Huber—we can we can tell his story—um, they were able to determine and find from a blood draw any number of 50 different cancer DNA sequences and and tell you you've got cancer someplace in your body." (said at 0:22:26)

The GRAIL Galleri multi-cancer early detection (MCED) test analyzes targeted methylation patterns of circulating cell-free DNA (cfDNA) in peripheral blood. In the clinical validation substudy of the Circulating Cell-free Genome Atlas (CCGA) study (NCT02889978; n = 4,077), the test demonstrated high specificity (99.5%) and detected cancer signals across more than 50 different cancer types, while accurately predicting the tissue/organ of origin in 88.7% of true positive cases.

0:29:42Peter Diamandissupportedvery low

Sirtuin enzymes are responsible for controlling the epigenome and facilitating DNA repair, but become diverted from epigenetic maintenance as cumulative DNA damage increases with age.

"Now, it turns out that the control of your epigenome, in part, is handled by seven sirtuin genes and seven sirtuin enzymes, and those sirtuins have two primary functions in life. Number one, they control your epigenome. They control which of your genes are on and which of your genes are off. The other thing it does, which is massively significant for your life, is they facilitate DNA repair. And so as we're getting older and we're exposed to radiation—you know, flying in airplanes, or smoke, or, you know, chemicals in the environment—and we start getting accumulating more and more DNA damage, your sirtuins are spending more and more time repairing your DNA instead of controlling which genes are on and which genes are off." (said at 0:29:42)

The speaker accurately describes the relocalization of chromatin modifiers (RCM) hypothesis of aging, specifically demonstrated with mammalian sirtuins. Mammals possess seven sirtuins (SIRT1–SIRT7) that regulate histone modifications, epigenetic gene silencing, and genomic maintenance. Research in cell and mouse models demonstrates that sirtuins such as SIRT1 normally repress gene expression across the genome, but dissociate from their baseline loci and relocalize to DNA double-strand breaks to facilitate repair. Over time, recurring and cumulative DNA damage diverts these chromatin-modifying enzymes away from their baseline epigenetic regulatory functions, leading to transcriptional changes and loss of epigenetic maintenance characteristic of aging. Because these mechanistic data are derived from preclinical cellular and animal models, the GRADE certainty is very low.

  • supports: SIRT1 redistribution on chromatin promotes genomic stability but alters gene expression du… (Cell 2008) · cited 848x in the literature
    "Using embryonic stem cells, we show that mammalian Sir2, SIRT1, represses repetitive DNA and a functionally diverse set of genes across the mouse genome. In response to DNA damage, SIRT1 dissociates from these loci and relocalizes to DNA breaks to promote repair, resulting in transcriptional changes that parallel those in the aging mouse brain. Increased SIRT1 expression promotes survival in a mouse model of genomic instability and suppresses age-dependent transcriptional changes. Thus, DNA damage-induced redistribution of SIRT1 and other chromatin-modifying proteins may be a conserved mechanism of aging in eukaryotes." (abstract, results, passage verified)
    pubmedfull study (doi)
0:25:46Tony Robbinssupportedmoderate

Cleerly's AI-enabled coronary computed tomography angiography (CCTA) analysis can predict heart attacks up to five years in advance by quantifying soft coronary plaque.

"So he explained to me how it opens up the arteries and how you get this score, and they can predict a heart attack five years in advance and show you what to do." (said at 0:25:46)

AI-guided quantitative coronary computed tomography angiography (AI-QCT, including platforms like Cleerly) quantifies coronary plaque burden and composition, specifically noncalcified (soft) plaque and luminal stenosis. Multicenter prospective observational data, such as the CONFIRM2 registry (median 4.3 years follow-up), demonstrate that AI-derived noncalcified plaque volume and stenosis severity independently predict major adverse cardiovascular events and myocardial infarction over an approximate 5-year horizon, significantly improving risk discrimination over traditional cardiovascular risk scores and guiding targeted medical therapy.

0:34:48Tony Robbinssupportedlow

SARS-CoV-2 enters the mitochondria and depletes cellular energy, driving long-term fatigue.

"because I'm sure you know with COVID, it goes into your mitochondria and basically steals some of the energy, that's part of the problem with fatigue" (said at 0:34:48)

Research demonstrates that SARS-CoV-2 viral components (such as the envelope E protein) localize to host cell mitochondria, disrupting mitochondrial membrane potential, electron transport chain activity, and metabolic homeostasis. Clinical studies in patients with post-acute COVID-19 and Long COVID show impaired mitochondrial oxidative phosphorylation, decreased ATP generation, and mitochondrial dysfunction, which are key contributing factors to post-COVID fatigue.

0:38:20Rhonda Patrick (host)supportedvery low

Pulsing the Yamanaka factors throughout the life of accelerated-aging mice resets cellular epigenetic programming without loss of cell identity and reverses aging phenotypes.

"what, you know, Juan Carlos Belmonte's lab and there's some others that have done this in vitro, but he was really the first to show this in an animal, it's called interrupted cellular reprogramming, where um you don't you don't want to make an adult cell lose its identity. You want it to just, you know, basically wipe wipe the program free, but uh but still be the same cell. So you want it to become, you know, younger, so so to speak. So um he showed this proof-of-principle study that adding these Yamanaka factors, but pulsing them throughout uh the life of these animals that are having an acceleration accelerated aging phenotype, he could essentially reverse aging." (said at 0:38:20)

A 2016 study from Juan Carlos Izpisua Belmonte's laboratory (Ocampo et al., Cell) demonstrated that partial cellular reprogramming via short-term, cyclic expression of the Yamanaka factors (Oct4, Sox2, Klf4, and c-Myc; OSKM) in a mouse model of premature aging (progeria) ameliorated cellular and physiological hallmarks of aging, remodeled epigenetic marks, and extended lifespan without inducing pluripotency or loss of somatic cell identity in vivo. Because this proof-of-principle evidence is derived entirely from preclinical animal models and in vitro systems, the GRADE certainty for human application is very low.

0:39:46Peter Diamandissupportedvery low

David Sinclair's lab restored vision in aged mice with glaucoma using three of the four Yamanaka factors excluding the oncogenic one, published on the cover of Nature in December 2020.

"It was the cover of Nature in December of 2020. It was like, you know, just landmark work where instead of using all four Yamanaka factors, David took in a mouse that had aged out, had become blind with glaucoma and lost its sight, and he gave it three of the four Yamanaka factors without retaining not one of them that causes that causes cancer. Um, and lo and behold, the visual system of the of the mice uh became young again to the point where they regained their vision." (said at 0:39:46)

In December 2020, David Sinclair's laboratory published a study on the cover of Nature demonstrating that viral delivery of three Yamanaka transcription factors (Oct4, Sox2, and Klf4, omitting the oncogene c-Myc) into retinal ganglion cells restored youthful DNA methylation patterns and transcriptomes, promoted axon regeneration, and reversed vision loss in both aged mice and a mouse model of glaucoma. Because this research was conducted exclusively in rodent models, the clinical evidence certainty is very low.

0:54:27Rhonda Patrick (host)supportedmoderate

A 2019 PNAS study found a direct positive association between higher levels of optimism and longer lifespan in both men and women.

"there was a PNAS study published back in 2019 that found a direct association between happiness and longevity. And people that had the higher levels, highest levels of happiness lived the longest. They were more likely—and this was true for both men and women—they were more likely—... Optimists, yes. Yeah, that was this was the study, optimists" (said at 0:54:27)

A 2019 study published in the Proceedings of the National Academy of Sciences (PNAS) analyzed data from two large prospective cohorts—women from the Nurses' Health Study and men from the Veterans Affairs Normative Aging Study—and found a dose-dependent positive association between baseline optimism levels and longer lifespan in both sexes. Participants in the highest versus lowest optimism quartiles had significantly longer lifespans (including an estimated 14.9% longer lifespan in women, with similar findings in men) and 1.5- to 1.7-fold greater odds of reaching exceptional longevity (survival to age 85 or older), even after adjusting for demographic factors, health conditions, and health behaviors.

1:01:20Peter Diamandissupportedvery low

CRISPR gene editing of the PCSK9 gene in the liver of monkeys achieved a 60% reduction in LDL cholesterol levels.

"We just saw uh CRISPR being used to edit the PCSK9 enzyme in in the liver. It's being done in monkeys, hasn't gone to men to humans yet, but it's has the demonstrated ability to reduce your LDL levels by 60%" (said at 1:01:20)

A 2021 preclinical study published in Nature demonstrated that in vivo CRISPR base editing delivered via lipid nanoparticles to target the PCSK9 gene in the liver of cynomolgus monkeys achieved near-complete knockdown of hepatic PCSK9, resulting in an approximate 90% reduction in blood PCSK9 levels and an approximate 60% reduction in LDL cholesterol levels that remained stable for at least 8 months. Because the evidence is derived from a non-human primate animal model, the certainty of evidence is graded as very low.

0:40:00Peter Diamandissupportedvery low

Partial cellular reprogramming using three Yamanaka factors has been successfully replicated in the cardiac system of mice.

"And it's since been repeated in the cardiac system of mice." (said at 0:40:00)

Animal research confirms that partial cellular reprogramming using the three Yamanaka factors (OSK: OCT4, SOX2, and KLF4, omitting the oncogene c-Myc) has been demonstrated in the cardiac system of mice. Preclinical studies show that transient OSK expression promotes cardiomyocyte dedifferentiation, overcomes cytokinesis barriers in proliferating cardiomyocytes in vivo, and enhances cardiac repair following myocardial infarction. Because evidence is limited to animal and in vitro models, the certainty of evidence for broader physiological or clinical application remains very low.

1:01:05Peter Diamandissupportedmoderate

CRISPR gene editing is being evaluated in clinical trials as a potential cure for HIV infection.

"We're seeing CRISPR now being used in a trial to cure someone who's got HIV, who's got an HIV infection, who's got AIDS." (said at 1:01:05)

The claim that CRISPR gene editing is being evaluated in clinical trials as a potential therapeutic or cure for HIV infection is supported. Clinical trials have investigated CRISPR-based therapies, such as Excision BioTherapeutics' EBT-101, which uses CRISPR-Cas9 to target and excise latent HIV-1 proviral DNA in patients. Early clinical trial findings confirmed the safety of the intervention, though it did not successfully prevent viral rebound following antiretroviral therapy interruption.

1:02:50Peter Diamandissupportedvery low

Deepak Srivastava used gene therapy to convert cardiac fibroblasts into myocytes after heart attack damage.

"And what Dr. Srivastava has done is use gene therapy—and I call it sort of cellular alchemy—to go and convert those fibroblasts into myocytes." (said at 1:02:50)

Deepak Srivastava and colleagues pioneered direct cardiac reprogramming, demonstrating that viral gene delivery of a defined cocktail of transcription factors (such as GATA4, MEF2C, and TBX5) can directly convert resident non-myocytes (cardiac fibroblasts) into functional cardiomyocyte-like cells in vitro and in vivo in rodent models of myocardial infarction, reducing scar size and improving cardiac function. Because this research is preclinical (in vitro and animal models), clinical translation in humans remains investigational.

1:05:55Peter Diamandissupportedvery low

Amy Wagers' laboratory found that GDF11 declines with age and that administering GDF11 to older mice replicates the rejuvenating benefits of young blood.

"what Amy found in her lab was a certain factor called GDF11 that is uh goes down as you age, and it appears that maybe there are factors that pull uh GDF11 out of circulation, maybe they're antibodies, maybe they're other factors. And if you give GDF11 to older mice, it seems to have all the benefits that this uh this uh blood exchange has, this young blood has." (said at 1:05:55)

The speaker accurately summarizes published findings from Amy Wagers' laboratory and collaborators. In a series of animal studies, the researchers reported that circulating levels of growth differentiation factor 11 (GDF11) decline with age in mice, and that systemic supplementation of GDF11 in aged mice reversed age-related cardiac hypertrophy, enhanced muscle stem cell function and endurance capacity, and restored neurogenesis and vascular remodeling in the brain, mirroring the restorative effects seen in heterochronic parabiosis (young-blood exchange). Because these findings are derived from preclinical animal models, the certainty is rated very low.

1:08:30Peter Diamandissupportedmoderate

Anthony Atala has engineered organs including the bladder, urethra, and esophagus, as well as full-thickness skin for transplantation using stem cells.

"Dr. Anthony Atala, who's brilliant researcher at Wake Forest, uh, for over a decade has been using stem cells and basically differentiating those and building organs. Now, they're simple organs: it's like the bladder, um it's like a urethra, it's like an esophagus. They're mostly tubular or or containment, they're not complex organs, but he's been able to do this as well as uh basically creating skin uh that can be, you know, sort of created full dermis thickness and then used for transplantation." (said at 1:08:30)

Published clinical and preclinical studies confirm that Anthony Atala and his team at the Wake Forest Institute for Regenerative Medicine have engineered tubular and hollow organ structures, including bladders, urethras, and multi-layered/full-thickness skin constructs for transplantation. In landmark clinical studies published in The Lancet, Atala and colleagues demonstrated successful surgical reconstruction using autologous cell-seeded scaffolds for pediatric bladders (PMID 16631879) and urethras (PMID 21388673). Additionally, his group has developed multi-cellular bioprinted full-thickness skin constructs that integrate and promote healing upon transplantation in animal wound models (PMID 37792956, PMID 30755653). While the pioneering human bladder and urethra implants primarily utilized autologous biopsied and expanded tissue cells (urothelial and muscle lineages) rather than pluripotent stem cells, his broader regenerative medicine program extensively develops both stem cell- and primary progenitor-derived tissue engineering.

1:11:50Peter Diamandissupportedvery low

A genetically modified pig heart was recently transplanted into the first human recipient.

"she set on this mission probably about six, seven years ago, and uh just recently demonstrated transplanting a modified pig heart into the first human recipient." (said at 1:11:50)

A published case report from 2022 documents the first transplantation of a genetically modified porcine heart into a live human patient. A 57-year-old man with end-stage heart failure received a donor heart from a pig with 10 genetic edits (including knockouts of porcine carbohydrate antigens and insertion of human transgenes to prevent hyperacute rejection). The xenograft functioned for several weeks before developing sudden failure, and life support was withdrawn on day 60 post-transplant. As evidence from a single case report, the certainty is graded as very low.

1:05:39Peter Diamandissupportedvery low

In heterochronic parabiosis experiments connecting the circulatory systems of a young mouse and an old mouse, the old mouse becomes rejuvenated while the young mouse exhibits accelerated aging.

"If you take the circulatory system of a young mouse and an old mouse, you put them together, the old mouse gets younger and the young mouse gets older." (said at 1:05:39)

Heterochronic parabiosis experiments in mice—where the blood circulations of a young mouse and an old mouse are surgically joined—consistently demonstrate a bi-directional effect. Exposure to young circulation rejuvenates the old mouse, improving stem cell function, reducing epigenetic age, restoring tissue repair, and extending lifespan. Conversely, exposure to old circulation induces pro-geronic effects in the young mouse, including elevated cellular senescence, increased markers of the senescence-associated secretory phenotype (SASP), and accelerated vascular aging. Because these findings are derived entirely from laboratory mouse models, the certainty grade for application to humans is very low.

1:25:05Peter Diamandissupportedhigh

Vaxxinity has developed an alpha-synuclein targeting vaccine for Parkinson's disease that has completed Phase 1 and entered Phase 2 clinical trials.

"It's alpha-synuclein, it's exactly what we're targeting. And so we're entering Phase 2 uh in in that. Alzheimer's is entering Phase 3, Parkinson's is entering Phase 2. Uh it's backed by the Michael J. Fox Foundation as well." (said at 1:25:05)

Vaxxinity (formerly United Neuroscience) developed UB-312, an active immunotherapeutic / synthetic peptide vaccine targeting pathological oligomeric and fibrillar alpha-synuclein for Parkinson's disease. Clinical trials have confirmed that UB-312 successfully completed its Phase 1 clinical trial evaluating safety, tolerability, immunogenicity, and biomarker target engagement in healthy volunteers and patients with Parkinson's disease (NCT04075318). Furthermore, the Michael J. Fox Foundation provided funding/grant support to analyze clinical biomarker samples (alpha-synuclein seed amplification assays) from the UB-312 Phase 1 study, and UB-312 has advanced towards Phase 2 development.

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.