HoldsUp

Peter Diamandis

XPRIZE

Peter Diamandis is an entrepreneur and the founder of XPRIZE, a non-profit organization that designs and conducts competitions to incentivize technological development. His published research includes work on using artificial intelligence to develop deep markers of psychological and subjective age.

29 claims checked on air: 7 context 1 contradicted 2 overstated 13 supported 6 unverified

What they said on air - supported

0:13:10supportedlowPeter Diamandis and Tony Robbins on strategies that promote

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.

0:17:50supportedhighPeter Diamandis and Tony Robbins on strategies that promote

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.

0:29:42supportedvery lowPeter Diamandis and Tony Robbins on strategies that promote

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.

0:39:46supportedvery lowPeter Diamandis and Tony Robbins on strategies that promote

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.

0:40:00supportedvery lowPeter Diamandis and Tony Robbins on strategies that promote

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.

1:01:05supportedmoderatePeter Diamandis and Tony Robbins on strategies that promote

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.

1:01:20supportedvery lowPeter Diamandis and Tony Robbins on strategies that promote

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.

1:02:50supportedvery lowPeter Diamandis and Tony Robbins on strategies that promote

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.

1:05:39supportedvery lowPeter Diamandis and Tony Robbins on strategies that promote

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.

1:05:55supportedvery lowPeter Diamandis and Tony Robbins on strategies that promote

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.

1:08:30supportedmoderatePeter Diamandis and Tony Robbins on strategies that promote

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.

1:11:50supportedvery lowPeter Diamandis and Tony Robbins on strategies that promote

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.

1:25:05supportedhighPeter Diamandis and Tony Robbins on strategies that promote

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.

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