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

0:09:06contradictedmoderatePeter Diamandis and Tony Robbins on strategies that promote

Placental stem cells have not been thymized and do not provoke an immune reaction when administered to any recipient.

"Another thing is that the cells from the placenta haven't developed—they haven't been thymized yet. They haven't developed an "us versus them" characteristic, so you can give placental cells to anybody, because the placenta doesn't generate an immune reaction against cells and your cells don't generate an immune reaction against placental cells." (said at 0:09:06)

The claim is contradicted on multiple biological and immunological grounds. First, 'thymization' (thymic education and selection) is a process specific to T lymphocytes, not stem cells or stromal cells. Second, while placental-derived stem cells and mesenchymal stromal cells (MSCs) possess immunomodulatory and hypoimmunogenic properties (such as lower baseline HLA expression), they are immune-evasive rather than completely immune-privileged. Published evidence demonstrates that allogeneic placental and mesenchymal cells can elicit host alloimmune responses, induce donor-specific anti-HLA antibodies, and undergo immune clearance/rejection upon administration to immunocompetent recipients.

0:12:45unverifiedvery lowPeter Diamandis and Tony Robbins on strategies that promote

Keeping bedroom temperature at approximately 65 degrees Fahrenheit allows individuals to reach deeper sleep stages.

"I keep the temperature about 65 degrees, which allows you to go deeper." (said at 0:12:45)

No published record matching the claim that keeping bedroom temperature at approximately 65 degrees Fahrenheit allows individuals to reach deeper sleep stages was located; this does not prove the claim false.

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.

0:17:08unverifiedvery lowPeter Diamandis and Tony Robbins on strategies that promote

During World War II, a doctor administered saline believing it was morphine to wounded soldiers running out of morphine, and 90% of them experienced pain relief without going into shock.

"It was actually a nurse that changed the world: she handed him saline solution and said, "Oh, we got some more morphine." Since he believed it, he told these patients with total certainty, "You'll be out of pain in the next minute or two, and you're going to be fine." Well, none of them went into shock, 90% of them were out of pain with no drugs." (said at 0:17:08)

No published record matching the claim that 90% of wounded World War II soldiers experienced pain relief and avoided shock after receiving saline substituted for morphine was located; this does not prove the claim false. Published clinical literature on placebo response under high stress (such as Henry Beecher's work following WWII) documented that placebos are effective in severe pathological pain, but reported response rates of approximately 30–35%, rather than 90%.

0:17:46unverifiedvery lowPeter Diamandis and Tony Robbins on strategies that promote

The strength of a placebo response increases with the size and invasiveness of the intervention, with larger pills producing stronger effects than smaller pills, and sham injections producing stronger effects than pills.

"Now, first of all, the size of the placebo, the size of our intervention changes everything: a little pill, certain reaction; a big pill, more; an injection, even more." (said at 0:17:46)

No published record matching the claim that the magnitude of a placebo response increases with intervention size or invasiveness (such as larger pills producing greater effects than smaller pills, or sham injections producing stronger effects than oral placebos) was located; this does not prove the claim false.

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.

0:18:15unverifiedvery lowPeter Diamandis and Tony Robbins on strategies that promote

Harvard studies showed that subjects given a barbiturate but told it was a large red amphetamine pill exhibited bodily stimulation rather than sedation.

"I'm sure you know Harvard's done studies where they take someone and give them a real drug, not a placebo, a barbiturate that's going to knock you on the ground to slow you down, and they go, "Big giant red pill, this is amphetamine. You're going to be prepared what's going to do for you." To a man or a woman, their bodies speed up." (said at 0:18:15)

No published record matching the claim that Harvard studies administered a barbiturate disguised as an amphetamine and found that every subject's physiological response reversed to stimulation was located; this does not prove the claim false.

0:24:31needs contextmoderatePeter Diamandis and Tony Robbins on strategies that promote

A National Cancer Institute study on 100,000 people found that stage 3 or 4 cancer diagnosis carries an 80% mortality rate, whereas stage 1 or 2 diagnosis carries an 80% to 99.9% survival rate.

"So, you know, the National Cancer Society did a study on 100,000 people, and they found that if you get something at stage 3 or stage 4, you have an 80% chance of dying—I like, look at it, 20% chance of living, or what to do. But their point is well made: it's really hard to turn around. If you get at stage 1 or 2, you have an 80 to 99.9% chance of survival." (said at 0:24:31)

The speaker conflates organizational names ('National Cancer Society', combining the American Cancer Society and the National Cancer Institute) and describes broad registry benchmarks as a single '100,000-person study.' Across large population-based registries such as the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) program and American Cancer Society annual reports, aggregate 5-year relative survival varies widely by cancer type. For many common cancers (such as breast, prostate, melanoma, and colorectal cancer), early-stage (localized, Stage I–II) detection is associated with 5-year relative survival rates between 80% and >99%, whereas advanced metastatic disease (distant, Stage IV) frequently exhibits 5-year relative survival of approximately 15% to 35% (corresponding to an ~65% to 85% mortality rate). However, survival differs dramatically by specific histology, organ of origin, and molecular subtypes rather than following a uniform cross-cancer rule.

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.

0:30:36needs contextmoderatePeter Diamandis and Tony Robbins on strategies that promote

Cellular NAD levels decline substantially after age 40 and into the 50s, reducing the activity of sirtuin enzymes.

"NAD is sort of a fuel in the cell that powers these sirtuins. And we can talk more in detail here, but the NAD in your in your mitochondria inside your cells, you know, is pretty good in your in your teens, 20s, and 30s, but then in your 40s into your 50s, it falls off rapidly. So just when you need more active sirtuins as the DNA damage is increasing, the fuel supply for the sirtuins starts plummeting, and then all of a sudden you're not able to, you know, control your epigenome and we get aging." (said at 0:30:36)

Nicotinamide adenine dinucleotide (NAD+) is an essential co-substrate for sirtuin enzymes (NAD+-dependent deacetylases) and poly(ADP-ribose) polymerases (PARPs). Human tissue studies demonstrate that cellular NAD+ levels and SIRT1 activity decline progressively with age, inversely correlating with accumulated DNA damage and PARP activation. However, characterizing this as a sudden 'plummet' or rapid drop-off specifically localized to one's 40s and 50s oversimplifies what human cross-sectional data show as a continuous, gradual decline across adulthood.

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.

0:45:35needs contexthighPeter Diamandis and Tony Robbins on strategies that promote

Average human life expectancy was under 40 years a century ago and is currently in the upper 70s.

"So a hundred years ago, the average lifespan was, you know, under 40. Today it's in the upper 70s" (said at 0:45:35)

The speaker's general characterization captures historical demographic trends, but combines global historical estimates with developed-world modern figures and refers to 'lifespan' rather than life expectancy at birth. A century ago (early 20th century), global life expectancy at birth was estimated to be under 35–40 years, heavily driven down by high infant and childhood mortality rather than a maximum biological lifespan ceiling of 40. Today, global average life expectancy at birth has reached approximately 73.5 years (low-to-mid 70s), while life expectancies in the upper 70s and 80s specifically characterize developed and high-income nations.

0:45:40unverifiedlowPeter Diamandis and Tony Robbins on strategies that promote

On average, scientific and medical progress currently extends human life expectancy by approximately one quarter of a year for every year lived.

"But on the average, every year that you live, science extends your life by about a quarter of a year. So for every four years, you're adding an additional year." (said at 0:45:40)

No published record matching the claim that science extends life expectancy by a quarter of a year for every year lived was located; this does not prove the claim false.

0:48:33overstatedmoderatePeter Diamandis and Tony Robbins on strategies that promote

Bowhead whales can live up to 200 years and Greenland sharks can live over 500 years.

"you know, the bowhead whale lives 200 years old, you know, the Greenland shark can live 500-plus years old." (said at 0:48:33)

The speaker bundles two longevity claims. The claim that bowhead whales can live approximately 200 years is supported; genomic and biochemical studies establish that bowhead whales (Balaena mysticetus) have an estimated maximum lifespan exceeding 200 years, making them the longest-lived mammal. However, the claim that Greenland sharks live '500-plus years' is overstated. Landmark radiocarbon dating of Greenland shark (Somniosus microcephalus) eye lenses estimated the lifespan of the largest individual at 392 ± 120 years (a 95.4% probability range of roughly 272 to 512 years). While 512 years represents the extreme upper statistical bound of the confidence interval, the mean estimate is approximately 390 years, not a definitive 500+ years.

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.

1:01:45overstatedmoderatePeter Diamandis and Tony Robbins on strategies that promote

CRISPR gene editing injected into the back of the eye has been used to treat a specific form of congenital blindness.

"We've seen CRISPR uh being used with an injection in the back of the eye uh to cure a specific form of congenital blindness." (said at 1:01:45)

In vivo CRISPR-Cas9 gene editing has indeed been delivered via subretinal injection (into the back of the eye) in clinical trials to treat a specific form of congenital blindness: CEP290-associated inherited retinal degeneration (Leber congenital amaurosis type 10). In the phase 1-2 BRILLIANCE trial (n=14), subretinal injection of EDIT-101 led to meaningful improvements in visual acuity, photoreceptor sensitivity, or mobility in 64% of participants without serious treatment-related adverse events. However, describing the therapy as having been used to 'cure' congenital blindness overstates the outcome: treatment resulted in partial improvements in visual function in a subset of patients rather than a complete restoration or cure of blindness.

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.

1:14:03unverifiedvery lowPeter Diamandis and Tony Robbins on strategies that promote

Dean Kamen's team has manufactured a bone-ligament-bone construct derived from pluripotent stem cells for knee or ankle replacement.

"what Dean has done already is actually go from these pluripotent stem cells to a bone-ligament-bone construct, it can be used for knee or ankle replacement." (said at 1:14:03)

No published record matching the claim that Dean Kamen's team has manufactured a pluripotent stem cell-derived bone-ligament-bone construct for knee or ankle replacement was located; this does not prove the claim false.

1:15:20needs contextlowPeter Diamandis and Tony Robbins on strategies that promote

A study from the London School of Business, Harvard, and Oxford found that adding one year of healthy lifespan globally is worth $38 trillion to the global economy.

"there was uh about six months ago a study done out of London School of Business, Harvard, and Oxford that said adding just one year of healthy lifespan to every human on the planet is worth $38 trillion to the global economy." (said at 1:15:20)

A 2021 study published in Nature Aging by researchers from London Business School, the University of Oxford, and Harvard Medical School (Scott, Ellison, and Sinclair) estimated that slowing aging to increase life expectancy by 1 year is worth $38 trillion. However, this economic valuation—calculated using a Value of Statistical Life (VSL) framework—applied specifically to the United States population, rather than the entire global population or global gross domestic product.

1:16:25needs contexthighPeter Diamandis and Tony Robbins on strategies that promote

50 years ago the global fertility rate was approximately 5.4 children per family, compared to about 2.4 globally today.

"Back 50 years ago, the average number of children per family was like 5.4 children per family. Today globally it's at about 2.4." (said at 1:16:25)

The speaker accurately describes the dramatic global demographic transition over recent decades, though with minor imprecisions in terminology and historical figures. Demographers measure this using the total fertility rate (TFR), defined as the average number of livebirths per woman across reproductive years, rather than "per family." Comprehensive demographic assessments (such as the Global Burden of Disease studies) show that global TFR was approximately 4.7 to 5.0 in the mid-20th century (and around 4.5–4.8 fifty years ago in the early 1970s) and has declined to approximately 2.3–2.4 in recent years (2.4 in 2017 and 2.31 in 2019).

1:21:45needs contexthighPeter Diamandis and Tony Robbins on strategies that promote

The monoclonal antibody Repatha (evolocumab) blocks the PCSK9 protein in the liver and reduces LDL cholesterol levels by half.

"I take a monoclonal antibody called Repatha, that this antibody is manufactured in a vat in New York. And um I get an injector, and every two weeks I inject about 5 mL of this of this these antibodies into my into my my leg, and those antibodies go to my liver and they block a protein called PCSK9, which is the protein that produces LDL, the bad type of cholesterol in your bloodstream. And this Repatha reduces my cholesterol, my LDL levels by a half" (said at 1:21:45)

Evolocumab (Repatha) is a human monoclonal antibody that binds to and inhibits proprotein convertase subtilisin/kexin type 9 (PCSK9), leading to an approximate 50% to 60% reduction in low-density lipoprotein (LDL) cholesterol. In the landmark phase 3 FOURIER trial involving 27,564 patients, evolocumab produced a 59% mean reduction in LDL cholesterol compared to placebo (PMID: 28304224). However, the speaker's description of the mechanism requires qualification: PCSK9 does not produce LDL cholesterol; rather, it binds to low-density lipoprotein receptors (LDLR) on hepatocytes and promotes their lysosomal degradation, reducing the liver's capacity to clear circulating LDL. Inhibiting PCSK9 prevents receptor breakdown, increasing hepatic clearance of LDL from the bloodstream. Additionally, standard biweekly dosing is 140 mg in 1.0 mL (rather than 5 mL).

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.

1:26:23needs contextmoderatePeter Diamandis and Tony Robbins on strategies that promote

Moderna designed its COVID-19 mRNA vaccine within 24 hours of receiving the SARS-CoV-2 genetic sequence from Wuhan.

"the sequence gets emailed over from Wuhan to our labs. I know from talking to Stéphane, there was a a vaccine designed within 24 hours." (said at 1:26:23)

Following the identification of the outbreak in Wuhan and the public release of the SARS-CoV-2 genomic sequence on January 11, 2020, researchers at the National Institute of Allergy and Infectious Diseases (NIAID) Vaccine Research Center and Moderna finalized the sequence design for the mRNA-1273 vaccine within approximately 48 hours (by January 13, 2020). The claim accurately reflects the rapid, sequence-directed design process of the vaccine, though the design timeline was completed over approximately two days rather than strictly within 24 hours.

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