HoldsUp

Huberman Lab · 2026-06-01 · Andrew Huberman (host), Abud Bakri

Peptides: The Science, Uses & Safety | Dr. Abud Bakri

97 research-tied claims examined: 5 contradicted 5 overstated 8 context 66 supported 13 unverified

5 Contradicted by research
1:19:08Andrew Huberman (host)contradictedmoderate

Nattokinase supplementation can help reduce LDL cholesterol levels.

"I decided to start supplementing with nattokinase, which can naturally help reduce LDL cholesterol." (said at 1:19:08)

A 2023 systematic review and meta-analysis of randomized controlled trials (6 RCTs, 546 participants) found that nattokinase supplementation alone does not reduce LDL cholesterol. In fact, lower doses showed a slight increase in LDL cholesterol compared to placebo (MD = 6.49 mg/dL, 95% CI: 0.83 to 12.15, p = 0.02), while higher doses showed no significant difference in LDL levels. While combination supplements containing nattokinase and red yeast rice (Monascus purpureus) significantly lower LDL cholesterol, clinical trials demonstrate that this effect is driven by the red yeast rice component (which naturally contains monacolin K / lovastatin), not nattokinase alone.

1:32:14Abud Bakricontradictedmoderate

The thymus receives sympathetic and parasympathetic neural innervation that regulates its hormonal secretion.

"There's sympathetic and parasympathetic innervations for thymus um that dictates its hormonal output." (said at 1:32:14)

The claim asserts that the thymus receives both sympathetic and parasympathetic innervation that controls its hormonal output. While sympathetic (noradrenergic) innervation of the thymus is well established, neuroanatomical tracing and imaging studies have demonstrated that there is no verified parasympathetic (vagal) innervation of the thymic parenchyma (early reports suggesting vagal inputs were shown to result from tracer spread to adjacent cervical/esophageal structures). Because the claim bundles sympathetic and parasympathetic pathways, grading the least accurate part results in a contradicted verdict.

1:37:25Abud Bakricontradictedhigh

Thymosin alpha-1 was previously FDA-approved under the brand name Zadaxin for conditions involving thymic abnormalities like DiGeorge syndrome.

"It was FDA approved as Zadaxin um for kids that were born without a thymus or a malfunctioning thymus like DiGeorge syndrome, these different kind of genetic abnormalities, um to be used for these kids to help develop the T cells that they had that weren't in the thymus" (said at 1:37:25)

Thymosin alpha-1 (marketed by SciClone Pharmaceuticals under the brand name Zadaxin) has never received FDA marketing approval for DiGeorge syndrome or any other medical condition in the United States. Although thymosin alpha-1 was investigated as an orphan drug candidate for DiGeorge syndrome and evaluated in US clinical trials for chronic hepatitis B and C, and is approved in over 30 countries outside the US (primarily for viral hepatitis and as an immune adjuvant), it was never approved by the US FDA.

2:31:15Abud Bakricontradictedvery low

GLP-1 receptors are present on POMC neurons in the brain.

"There's GLP-1 receptors on the POMC neurons in the brain, and no one's kind of examined what that means." (said at 2:31:15)

The spoken statement contains two assertions. First, the assertion that GLP-1 receptors are present on POMC neurons in the brain is supported: rodent and cellular studies confirm that proopiomelanocortin (POMC) neurons in the hypothalamic arcuate nucleus express functional GLP-1 receptors (GLP-1Rs). However, the bundled assertion that 'no one's kind of examined what that means' is contradicted by extensive published literature. Seminal electrophysiological and pharmacological studies (e.g., Secher et al., 2014; He et al., 2019; Farkas et al., 2021) have directly investigated the functional consequences of GLP-1R activation on POMC neurons, demonstrating direct depolarization, activation via TrpC5 channels, enhanced excitatory tone, and mediation of GLP-1 receptor agonist-induced appetite suppression and weight loss.

2:33:45Abud Bakricontradictedhigh

Retatrutide has fewer gastrointestinal side effects compared to earlier GLP-1 agonists.

"retatrutide even have less of these gastrointestinal effects" (said at 2:33:45)

Clinical trial data and network meta-analyses do not support the claim that retatrutide causes fewer gastrointestinal (GI) adverse effects than earlier GLP-1 receptor agonists. Phase 2 and Phase 3 randomized trials demonstrate that GI symptoms (such as nausea, vomiting, diarrhea, and constipation) remain the most common adverse events associated with retatrutide, occurring in a dose-dependent pattern with a safety profile consistent with the broader GLP-1 and incretin-based receptor agonist class.

5 Overstated
0:13:13Andrew Huberman (host)overstatedhigh

Approximately 115 million adults in the United States have pre-diabetes.

"Right now, about 115 million adults in the US have pre-diabetes. Most don't know it, and a higher percentage of men have it than women do." (said at 0:13:13)

The speaker correctly notes that most individuals with prediabetes are unaware of their condition (CDC surveillance shows awareness has historically been ~11-19%) and that prevalence is higher among men than women. However, the stated figure of 115 million adults with prediabetes is overstated. According to the CDC's National Diabetes Statistics Reports and NHANES epidemiological surveillance data, approximately 96 to 98 million U.S. adults (about 38% of the adult population, up from 84 million in 2016 and 79 million in 2010) have prediabetes, overshooting actual estimates by roughly 17 to 20 million.

1:14:12Abud Bakrioverstatedvery low

Pinealon modulates expression of genes and pathways including GDF11, SOD1, SOD2, irisin, PPAR-alpha, and PPAR-gamma.

"So Pinealon in one sentence: it's leading to better brain metabolism through modulating all these different pathways, for example GDF11, SOD1, SOD2, irisin, PPAR-alpha, PPAR-gamma." (said at 1:14:12)

While narrative and in vitro research on the synthetic tripeptide Pinealon (Glu-Asp-Arg / EDR) describes potential effects on antioxidant enzymes (such as SOD2) and transcription factors including PPARA (PPAR-alpha) and PPARG (PPAR-gamma), there is no published evidence demonstrating that Pinealon modulates GDF11 or irisin. Grouping unverified targets like GDF11 and irisin alongside preliminary in vitro findings overstates the established biological pathways modulated by Pinealon.

2:16:58Abud Bakrioverstatedlow

Topical GHK-Cu has human clinical data demonstrating positive aesthetic outcomes and alleviation of UV photodamage.

"topically, there's great human data on different aesthetic outcomes, especially when coupled with red light therapy... There's also some literature when it comes to GHK-Cu for post-UV damage." (said at 2:16:58)

The claim that there is 'great human data' on topical GHK-Cu for aesthetic outcomes and UV damage is overstated. While preclinical, in vitro, and animal models demonstrate that GHK-Cu stimulates collagen and glycosaminoglycan synthesis, modulates matrix metalloproteinases, and reduces inflammation, rigorous human clinical evidence remains scarce. A 2026 PRISMA-guided systematic review of GHK-Cu in aesthetic medicine identified 20 relevant studies, of which 18 were preclinical and only 2 were randomized controlled trials, concluding that clinical utility is constrained by methodological variability and a limited number of well-designed trials. Another 2025 review noted a surprising absence of robust clinical trials despite the compound's widespread commercial use.

2:08:15Abud Bakrioverstatedmoderate

Models and cohorts with growth hormone deficiency exhibit extended lifespan.

"There's models where people are growth hormone deficient and they live a lot longer" (said at 2:08:15)

Genetic animal models with growth hormone (GH) deficiency or GH receptor knockouts (such as Ames dwarf, Snell dwarf, and GHR-/- mice) reliably exhibit significantly extended lifespans (often 30–50% longer). However, in human cohorts with congenital isolated GH deficiency or GH resistance (e.g., Laron syndrome, PROP1 mutations on Krk island, or the Itabaianinha GHRH receptor cohort), individuals exhibit normal lifespans and protection against cancer and diabetes, but have not been demonstrated to live significantly longer than their unaffected relatives or normal controls.

2:40:56Abud Bakrioverstatedvery low

In mouse studies, BPC-157 prevents mice from getting hyperactive or experiencing withdrawal from methamphetamines.

"They can't get too high on the mice methamphetamines, and they don't withdraw either." (said at 2:40:56)

The claim is overstated. Preclinical rodent studies (predominantly from one research group) found that BPC-157 attenuated acute amphetamine-induced stereotypy and heightened acoustic startle responses in rats, reversed haloperidol-induced supersensitivity to amphetamine in mice, and reduced chronic amphetamine-induced behavioral disturbances. However, these studies evaluated motor stereotypies and behavioral sensitization rather than demonstrating that mice do not experience subjective intoxication ('cannot get too high') or clinical methamphetamine withdrawal. The evidence is preliminary and restricted to animal models.

8 Needs context
0:10:34Abud Bakrineeds contexthigh

Vladimir Gulevich discovered carnosine and carnitine in bovine muscle tissue in the late 19th century.

"Dr. Vladimir Gulevich in 1850s, 1880s finds carnosine and carnitine in muscle of cattle. So you can think that the first peptides that are found are carnosine, and then carnitine is the amino acid that have positive effects on strength training and performance and different effects there." (said at 0:10:34)

The core factual discovery is accurate: Russian biochemist Vladimir Gulevich (often transliterated as Gulewitsch) isolated and identified carnosine (in 1900, with Amiradzibi) and carnitine (in 1905, with Krimberg) from bovine muscle extract. However, the speaker misstated the timeline as the 1850s–1880s (Gulevich was born in 1867, making discoveries in the 1850s impossible).

0:12:01Andrew Huberman (host)needs contextmoderate

Core body temperature must drop by approximately 1 to 3 degrees to initiate and maintain deep sleep, and must rise by 1 to 3 degrees to wake up feeling alert.

"And that's because in order to fall asleep and stay deeply asleep, your body temperature actually has to drop by about 1 to 3 degrees. And in order to wake up feeling refreshed and energized, your body temperature actually has to increase by about 1 to 3 degrees." (said at 0:12:01)

Human core body temperature (CBT) follows a well-established circadian rhythm that is tightly coupled with sleep and wakefulness: CBT begins to decline prior to sleep onset (mediated by distal skin vasodilation and heat loss) and rises toward awakening. However, the claim needs qualification: the typical circadian fluctuation in core body temperature is approximately 0.5°C to 1.0°C (about 1°F to 2°F), so the '1 to 3 degrees' figure is accurate only when measured in Fahrenheit (a 3°C drop would represent clinically significant hypothermia). Additionally, chronobiological research indicates that thermoregulatory heat redistribution primarily governs sleep initiation rather than deep sleep maintenance.

0:31:44Abud Bakrineeds contexthigh

Ozempic and Wegovy received FDA approval for weight loss around late 2021 and 2022.

"what happened in the in the field is the GLP-1s come online, you know, late 2021 and 2022 with Ozempic and Wegovy, they get the FDA approval for weight loss." (said at 0:31:44)

The speaker's claim is partially accurate regarding timeline and active ingredient, but requires qualification. Semaglutide marketed under the brand name Wegovy was approved by the US FDA for chronic weight management in adults in June 2021 (and expanded to pediatric patients aged 12 and older in December 2022). In contrast, Ozempic (also semaglutide) is FDA-approved specifically for type 2 diabetes mellitus (originally approved in 2017) and is not FDA-approved for weight loss, though it is frequently prescribed off-label for that indication.

1:03:21Abud Bakrineeds contextvery low

Vladimir Khavinson identified specific peptides, such as Livagen and Ovagen, in liver tissue.

"Dr. Khavinson identified many peptides in livers, like Livagen, Ovagen, that you'd find in your desiccated liver supplement that you're eating." (said at 1:03:21)

Vladimir Khavinson and colleagues analyzed polypeptide extracts from calf liver tissue (cytomedins) and designed short synthetic peptide analogues (cytogens), including the tetrapeptide Livagen (Lys-Glu-Asp-Ala, KEDA) and related commercial formulations (such as Ovagen). However, Livagen is a synthetic peptide modeled on the amino acid composition of liver extracts rather than an endogenous peptide directly isolated in intact form from liver supplements, and published research on its biological activity is largely limited to in vitro and rodent models published in Russian gerontology literature.

1:24:22Abud Bakrineeds contextvery low

A 15-year study by Khavinson administering Epithalamin and Thymalin to nursing home patients showed significant reductions in cardiovascular, infectious, and cancer mortality.

"So in the Khavinson seminal work was this 15-year longevity study. He got people in nursing homes, two groups. One of them got Epithalon in the form of Epithalamin, which is the whole pineal gland extract, and then a thymus peptide called Thymalin, not thymulin... And they had a significant lower mortality when it came to cardiovascular disease, uh infectious risk, and for um cancers." (said at 1:24:22)

The speaker conflates findings across several small studies by Vladimir Khavinson and colleagues. In a 6- to 8-year clinical study of 266 elderly individuals (PMID: 14523363), treatment with Epithalamin (a pineal peptide extract), Thymalin (a thymus peptide extract), or both was reported to reduce acute respiratory infections, cardiovascular manifestations, and all-cause mortality (up to 4.1-fold in combined treatment). A separate 12- and 15-year follow-up study by Khavinson (PMIDs: 17426848, 22451889) examined Epithalamin alone (not combined with Thymalin) in 79 elderly coronary patients and reported reduced cardiovascular and overall mortality, but did not establish a significant reduction in cancer-specific mortality in a combined 15-year trial. The certainty of this evidence is very low due to small sample sizes, unclear blinding/methodological reporting, lack of independent replication, and publication in niche journals.

  • partial: Peptides of pineal gland and thymus prolong human life. (Neuro endocrinology letters 2003) · cited 17x in the literature
    "clinically assessed the geroprotective effects of thymic (Thymalin) and pineal (Epithalamin) peptide bioregulators in 266 elderly and older persons during 6-8 years... Homeostasis restoration was accompanied by a 2.0-2.4-fold decrease in acute respiratory disease incidence, reduced incidence of the clinical manifestations of ischemic heart disease, hypertension disease... Such a significant improvement in the health state of the peptide-treated patients correlated with decreased mortality rate during observation: 2.0-2.1-fold in the Thymalin-treated group; 1.6-1.8-fold in the Epithalamin-treated group; 2.5-fold in the patients treated with Thymalin plus Epithalamin as compared to the control." (abstract, results)
    pubmed
  • context: Geroprotective effect of epithalamine (pineal gland peptide preparation) in elderly subjec… (Bulletin of experimental biology and medicine 2006) · cited 11x in the literature
    "A 12-year randomized clinical study of epithalamine (pineal gland peptide preparation) was carried out in elderly patients with coronary disease and accelerated aging of the cardiovascular system... After 12 years the number of elderly subjects dead in the group treated by epithalamine was 28% lower than in the control group, despite the same basic therapy. Cardiovascular mortality was 2-fold lower in patients treated by epithalamine; the incidence of cardiovascular failure and respiratory diseases was 2-fold lower in this group." (abstract, results)
    pubmedfull study (doi)
  • partial: Peptide geroprotector from the pituitary gland inhibits rapid aging of elderly people: res… (Bulletin of experimental biology and medicine 2011) · cited 18x in the literature
    "The paper presents the results of randomized comparative study of the efficiency of peptide geroprotector from the pituitary gland in elderly patients with rapidly aging cardiovascular system. Over three years 39 coronary patients received, in addition to basic therapy, regular courses of epithalamin (peptide drug), while 40 coronary patients (control group) received basic therapy alone... A significantly lower mortality in the group of patients treated with epithalamin in parallel with basic therapy also indicated a geroprotective effect of the peptide preparation from the pineal gland." (abstract, results, passage verified)
    pubmedfull study (doi)
1:22:20Abud Bakrineeds contextlow

Pineal cysts can cause precocious puberty in children around eight or nine years of age.

"Like if you have a pineal cyst, you can have precocious puberty like eight or nine years old." (said at 1:22:20)

The relationship between pineal cysts and precocious puberty is debated. Pineal cysts are relatively common incidental neuroimaging findings in children evaluated for central precocious puberty (CPP) or early puberty (typically diagnosed before age 8 in girls). While some recent observational studies report that pineal cysts (particularly larger cysts) are enriched in girls with CPP and correlate with accelerated pubertal markers, most pediatric endocrine literature considers asymptomatic pineal cysts to be incidental benign findings rather than established causative lesions (unlike pineal germ cell tumors, which directly induce precocious puberty via beta-hCG secretion or hypothalamic-pituitary-gonadal axis disruption).

1:33:14Abud Bakrineeds contextmoderate

Naive T cells have an estimated lifespan of 10 to 15 years in humans.

"And those cells will live somewhere between 10 and 15 years, and that can kind of gauge when the mortality window kicks in for a lot of these different disorders." (said at 1:33:14)

Estimates of human naive T-cell longevity vary based on the kinetic modeling technique (e.g., in vivo deuterium labeling vs. T-cell receptor excision circle [TREC] decline), but published human studies broadly estimate the half-life of naive CD4+ and CD8+ T cells to be roughly 4 to 9 years (corresponding to mean lifespans of roughly 6 to 10+ years), with slow turnover maintained via in situ homeostatic divisions. While a single naive T cell or naive-derived clone can persist for a decade or more, stating a fixed lifespan of 10 to 15 years reflects the upper end of mathematical model estimates rather than a uniform lifespan.

2:22:02Andrew Huberman (host)needs contextmoderate

Reaching a critical threshold of leptin serves as a physiological signal for the onset of female puberty and reproductive function.

"There was a Science paper some years ago that leptin hitting a certain threshold is actually what signals the onset of puberty in females." (said at 2:22:02)

The host accurately references a landmark 1997 Science paper (Chehab et al., PMID 8974400) showing that leptin administration accelerates puberty and reproductive maturation in female mice, supporting leptin's role as a metabolic signal linked to adiposity. However, subsequent endocrinological research and reviews (e.g., PMID 12087494) clarify that leptin acts primarily as a permissive metabolic gate or threshold rather than the sole initiating trigger for puberty; once leptin exceeds a minimum threshold indicating adequate energy stores, puberty can proceed only if other neuroendocrine regulatory mechanisms (such as GnRH pulsatility and kisspeptin signalling) are active.

  • context: Leptin and pubertal development. (Seminars in reproductive medicine 2002) · cited 68x in the literature
    "When body energy reserves rise above a critical level, blood leptin increases to a threshold concentration signaling to the central nervous system that the body can support sexual function. Puberty can apparently occur over a wide range of concentrations above this critical leptin threshold. Leptin does not appear to act as a trigger to time the initiation of puberty but, instead, once leptin reaches this threshold pubertal development may proceed if, and only if, other critical control mechanisms are operational." (abstract, conclusions, passage verified)
    pubmedfull study (doi)
  • supports: Early onset of reproductive function in normal female mice treated with leptin. (Science (New York, N.Y.) 1997) · cited 846x in the literature
    "Normal prepubertal female mice injected with leptin grew at a slower rate than controls as a result of the hormone's thinning effects, but they reproduced up to 9 days earlier than controls and showed earlier maturation of the reproductive tract. These results suggest that leptin acts as a signal triggering puberty, thus supporting the hypothesis that fat accumulation enhances maturation of the reproductive tract." (abstract, results, passage verified)
    pubmedfull study (doi)
66 Supported by research
0:07:15Abud Bakrisupportedmoderate

BPC is a 40,000-dalton protein found in gastric juice, and BPC-157 is a 15-amino-acid synthetic fragment derived from it that is not naturally produced by the body.

"It's a 40,000-dalton giant peptide called BPC. BPC-157 is 15 amino acids from that giant peptide. We don't naturally make BPC-157. That's what you'll commonly hear online. We make BPC, the big protein." (said at 0:07:15)

The speaker accurately describes the origin and biochemical nature of BPC-157. Body Protection Compound (BPC) is a native ~40 kDa protein originally isolated from human gastric juice, and BPC-157 is a synthetic 15-amino-acid fragment (pentadecapeptide, sequence GEPPPGKPADDAGLV) derived from its partial sequence that does not naturally circulate on its own.

0:08:39Abud Bakrisupportedhigh

Hans Selye showed that in stressed animals, the adrenal glands enlarge, the gastric lining is damaged, and the thymus and lymphatic glands shrink.

"Hans Selye, that's coming up with the stress adaptation theory and he notices that when animals are stressed out, three things happens to them: their adrenals get really big so they make more cortisol, their gastric lining gets destroyed, and then their thymus gland and their lymphatics shrink down." (said at 0:08:39)

The speaker accurately summarizes Hans Selye's classic 1936 description of the "stress triad" (the initial stage of the general adaptation syndrome). In his landmark rodent experiments, Selye demonstrated that exposure to severe, non-specific stressors produced three hallmark pathological changes: enlargement/hyperemia of the adrenal glands, atrophy/involution of the thymus and lymphatic tissue (lymph nodes), and the formation of gastric erosions/ulcers.

0:11:02Abud Bakrisupportedvery low

In animal models, BPC-157 accelerates healing after tendon transection and ACL transection, and topically prevents gastric ulceration in burn wound models.

"They would, you know, sever tendons and then give them BPC through oral or injectable intraperitoneal administrations and they'd have faster healing times. They would sever ACL of the mice. They would do burn wounds. So when a patient has a burn wound in like the ICU, they end up having crazy gastric ulcers, but if they were able to put BPC on topically for the mouse, they would have no gastric ulcers." (said at 0:11:02)

The speaker specifically frames these findings within preclinical animal research, which is supported by published literature. Rodent studies show that BPC-157 (administered intraperitoneally, intragastrically, or topically) accelerates healing after tendon and ligament transections and prevents/attenuates burn-induced gastric ulcerations (Curling ulcers). Because this evidence base consists almost exclusively of animal experiments, certainty regarding clinical translation to humans is very low.

0:15:32Abud Bakrisupportedvery low

BPC-157 administration counteracts corticosteroid-induced impairment of wound healing in animal models.

"The other big thing that they did was they'd give corticosteroids with BPC-157 to these mice. And usually when you have a wound and you give corticosteroids, the corticosteroids will slow or even stop the wound healing from happening. When BPC was administered, the healing was either the same or even better." (said at 0:15:32)

Animal studies directly support the claim. In burned mice treated with systemic methylprednisolone, topical application of BPC-157 counteracted corticosteroid-induced impairment of burn wound healing and restored tissue repair parameters (PMID: 12781609). Similar effects have been observed in other rodent models of corticosteroid-impaired healing, including tendon-to-bone and muscle injuries (PMIDs: 16583442, 20190676). Certainty is graded as very low because the available evidence is restricted entirely to animal models.

0:16:10Abud Bakrisupportedvery low

BPC-157 increases growth hormone receptor expression in tendon tissue models.

"For example, in one tendon model, they noticed that it increased the amount of growth hormone receptors on the tendon. So theoretically, this would allow more growth hormone to dock in and cause the outgrowth of the tendon and the regrowth of it." (said at 0:16:10)

The speaker accurately described the findings of preclinical research. An in vitro study using rat Achilles tendon fibroblasts (Chang et al., 2014) demonstrated that BPC-157 upregulates growth hormone receptor mRNA and protein expression, and that subsequent stimulation with growth hormone increased cell proliferation and activated downstream JAK2 signaling. Because the evidence is limited to in vitro cellular and animal models with no clinical validation in humans, the GRADE certainty is very low.

0:16:32Abud Bakrisupportedvery low

In animal models, BPC-157 administration reduces signs of acute alcohol intoxication and prevents alcohol withdrawal symptoms.

"They also did weird things on the neurological side, like they would make these mice drunk, okay? And they would then give them BPC and they'd get less drunk when they go through mazes... And then also, they would get the mice drunk and then have them withdraw from alcohol... They got BPC and they didn't have the withdrawal symptoms." (said at 0:16:32)

The speaker specifically framed the findings as occurring in animal (mouse) models. Published preclinical rodent studies confirm that BPC-157 administration significantly opposed signs of acute alcohol intoxication (reducing duration of ethanol anesthesia, hypothermia, and motor impairment) and attenuated alcohol withdrawal manifestations (such as withdrawal-induced seizures/convulsions) following chronic alcohol exposure. Because the available evidence is restricted entirely to animal models conducted by a single laboratory group, the GRADE certainty is very low.

0:21:43Abud Bakrisupportedhigh

BPC-157 is included on the World Anti-Doping Agency (WADA) prohibited list.

"They found fragments of the 15. Like there's a paper in 2024 that looked at this and they could figure out if somebody had BPC administered for doping reasons, cuz it's on the WADA list now." (said at 0:21:43)

BPC-157 is explicitly prohibited in sport by the World Anti-Doping Agency (WADA). Effective January 1, 2022, WADA added BPC-157 to its Prohibited List under category S0 (Non-Approved Substances), which prohibits substances not approved by any governmental regulatory health authority for human therapeutic use at all times. Analytical methods and metabolic profiling studies (measuring peptide fragments/metabolites in urine via mass spectrometry) have been developed specifically to detect illicit BPC-157 administration in doping control.

0:15:39Abud Bakrisupportedvery low

BPC-157 promotes vascular endothelial growth factor (VEGF) signaling, stimulating angiogenesis and modulating nitric oxide synthesis in tissue injury models.

"Like in the models of damaging the endothelial layer or the epithelial layer of different tissues, you'll get more VEGF signaling. So that's the vascular endothelial growth factor. So you get more blood vessels, angiogenesis being formed... Downstream it'll modulate nitric oxide synthesis." (said at 0:15:39)

Preclinical in vitro and animal injury models support the claim that BPC-157 promotes vascular endothelial growth factor (VEGF/VEGFR2) signaling, stimulates endothelial tube formation and angiogenesis, and activates endothelial nitric oxide synthase (eNOS) to modulate nitric oxide production. However, evidence is currently limited to cellular and animal models, with a lack of high-quality human randomized controlled trials.

0:08:03Abud Bakrisupportedhigh

Ivan Pavlov harvested gastric juices from fistulated dogs and sold them commercially as a medicinal treatment for dyspepsia and gastric distress.

"What he'd do is he'd put a hole in the dogs' stomachs, he would feed them food and then get the gastric juices and sell that as a medicine." (said at 0:08:03)

Historical records thoroughly confirm that Ivan Pavlov and his laboratory at the Institute of Experimental Medicine in St. Petersburg surgically prepared dogs with gastric fistulas and severed esophagi (sham feeding) to collect pure gastric juice. Pavlov bottled and commercially sold this canine gastric juice across Russia and Europe as a treatment for dyspepsia and other digestive disorders, using the substantial proceeds to fund his physiological research and laboratory operations, as extensively documented in historical scholarship on Pavlov's laboratory enterprise.

0:32:17Abud Bakrisupportedhigh

Under US regulatory rules during an official drug shortage, compounding pharmacies are permitted to manufacture compounded versions of medications to meet the shortage.

"when there's a shortage of a medication, the compounders are allowed to make these drugs to meet the shortage." (said at 0:32:17)

Under US regulatory law (Sections 503A and 503B of the Federal Food, Drug, and Cosmetic Act), compounding pharmacies and outsourcing facilities are permitted to prepare compounded versions of medications when an FDA-approved drug is listed on the FDA's official Drug Shortages list, provided federal and state compounding regulations are followed.

0:39:03Abud Bakrisupportedhigh

Under FDA compounding rules, compounded medications can be prepared either during an official shortage or to meet a unique clinical need of an individual patient.

"there's two ways to get compounded medications: either a shortage or there's a unique need that the patient has." (said at 0:39:03)

The speaker's statement accurately reflects US regulatory framework under the Food, Drug, and Cosmetic Act (specifically Sections 503A and 503B as enacted and modified under the Drug Quality and Security Act). Compounded drugs generally cannot be 'essentially a copy' of an approved commercial drug unless there is a documented drug shortage on the FDA shortage list, or the medication is tailored to meet the specific clinical need of an individual patient (such as an allergy to an inactive ingredient, an altered dosage form, or a tailored strength) where an approved commercial drug is unsuitable.

0:40:53Abud Bakrisupportedhigh

In 2024, the FDA placed BPC-157 and other peptides onto the Category 2 bulk drug substances list, restricting compounding of these substances.

"because of the the move in 2024 to get these from the Category 1 to the Category 2 list and make them banned quote-unquote. That opened up this gray market zone." (said at 0:40:53)

Under Section 503A of the Federal Food, Drug, and Cosmetic Act, the FDA evaluated bulk drug substances and placed BPC-157, alongside several other unapproved peptides (e.g., AOD-9604, CJC-1295, ipamorelin), into Category 2 of the 503A Bulk Drug Substances list. Category 2 comprises nominated substances that raise significant safety concerns and are therefore not eligible for compounding under the FDA's interim compounding policy, effectively restricting licensed compounding pharmacies from preparing them and driving consumer distribution to non-regulated research/'gray market' channels.

0:45:38Abud Bakrisupportedhigh

Development of Cardarine (GW501516) was halted because animal studies showed a signal of cancer.

"GW was a drug that was very was very promising because it had, you know, diabetic implications for metabolism and now it's a bodybuilder drug that they use for more cardio... It had a signal of cancer in animal data. So that whole thing was scrapped." (said at 0:45:38)

GW501516 (also known as Cardarine or GW1516) was investigated as a selective PPAR-delta agonist for metabolic disorders, diabetes, and cardiovascular health. Development of the compound by GlaxoSmithKline was discontinued after non-clinical rodent carcinogenicity studies revealed a dose-dependent, widespread development of tumors (cancer) across multiple organs. WADA and other regulatory/anti-doping bodies also issued safety alerts regarding its black-market use due to this carcinogenic toxicity observed in preclinical animal models.

0:45:51Abud Bakrisupportedhigh

Cardarine (GW501516) is on the World Anti-Doping Agency (WADA) prohibited list.

"Banned on on the WADA list, of course, but it had promise for treating diabetics because it changed metabolism in the liver." (said at 0:45:51)

Cardarine (GW501516 / GW1516), a PPAR-delta agonist, was added to the World Anti-Doping Agency (WADA) Prohibited List in January 2009 (originally under gene doping / non-approved substances and subsequently categorized under S4.5 Metabolic Modulators) and remains prohibited at all times in sports competition.

0:50:45Abud Bakrisupportedvery low

In mouse studies, administration of BPC-157 demonstrated protection deeper in the gastrointestinal tract against an offending agent introduced into the gut.

"And that's what they noticed in the mouse literature. They would have an offending agent into the gut and they'd notice that there would be protection deeper down in the gastric tract from that offending agent." (said at 0:50:45)

Preclinical rodent studies (predominantly in rats) evaluate the stable gastric pentadecapeptide BPC-157 against various noxious/offending agents introduced into the gastrointestinal tract (such as cysteamine, NSAIDs, and alcohol). These studies report cytoprotective effects extending deeper into the lower gastrointestinal tract, including the duodenum and colon. Because the evidence is limited to animal models—largely from a single research group—the GRADE certainty is very low.

0:52:26Andrew Huberman (host)supportedlow

Neuropod cells in the gut signal via the vagus nerve and nodose ganglion to promote or suppress dopamine release affecting food approach or avoidance behaviors.

"We had Dr. Diego Bohórquez—I can never pronounce his last name, forgive me, Diego—who's out at Duke, who's really the world expert on these neuropod cells in the gut that signal through the nodose ganglion up the vagus, nodose ganglion, to either promote or suppress release of dopamine to make you either approach or avoid certain foods." (said at 0:52:26)

Preclinical research led by Dr. Diego Bohórquez and others established that enteroendocrine 'neuropod' cells in the gut form direct, functional synapses with vagal sensory neurons (whose cell bodies reside in the nodose ganglion). These cells transduce nutrient and microbial sensory signals rapidly to the brain via glutamatergic and purinergic signaling, guiding food preferences, appetitive choices, and feeding behavior. Parallel and downstream gut-vagal neurocircuitry studies demonstrate that vagal sensory inputs project via brainstem relays to striatal and substantia nigra dopamine circuits to regulate food reinforcement and reward.

0:45:28Abud Bakrisupportedvery low

Published animal literature on BPC-157 shows no signal of increased cancer or tumorigenesis.

"There's no signal from the animal literature on BPC-157 for, you know, cancers." (said at 0:45:28)

The speaker accurately described the state of published animal research on BPC-157. Across dozens of preclinical rodent studies and systematic reviews of the animal literature, no signal of increased cancer incidence, tumor promotion, or malignant transformation has been reported. While theoretical concerns have been raised because BPC-157 promotes angiogenesis (via VEGFR2 and eNOS pathways), animal models have consistently reported favorable safety profiles without oncogenic signals, and some preclinical studies even tested for and reported anti-tumor or tumor-modulating effects. However, certainty is very low because evidence is limited entirely to animal models, largely from a single primary research network, and formal long-term rodent carcinogenicity bioassays and human oncologic safety trials are absent.

0:45:35Abud Bakrisupportedhigh

The vast majority of published animal research literature on BPC-157 originates from Dr. Predrag Sikiric's research group in Croatia.

"Now all that literature comes from one group. So we have to be very careful. That one Croatian group that tells you that it's the safest thing in the world... Dr. Sikirić is the guy behind BPC-157." (said at 0:45:35)

The speaker accurately states that the vast majority of preclinical and animal research on BPC-157 (Body Protection Compound 157) originates from Dr. Predrag Sikirić and his research team at the University of Zagreb in Croatia. Sikirić's laboratory isolated and named the peptide in the early 1990s and has authored nearly all published animal studies and reviews asserting its pleiotropic cytoprotective effects and favorable safety profile.

1:03:50Abud Bakrisupportedhigh

Di- and tripeptides can be orally bioavailable if they have the appropriate conformation and size.

"Di- and tripeptides can be orally available if they're the right shape and size." (said at 1:03:50)

The human intestinal peptide transporter PEPT1 (SLC15A1) is specifically specialized to mediate the active uptake and absorption of di- and tripeptides as well as peptide-mimetic drugs of appropriate molecular size and stereochemical conformation. This mechanism underlies both dietary oligopeptide absorption and the oral bioavailability of small peptide-like therapeutics.

1:08:29Abud Bakrisupportedlow

Pinealon is a tripeptide with the amino acid sequence Glu-Asp-Arg (EDR) that does not act via a classic known receptor.

"No known receptor. So Pinealon is a tripeptide, EDR, discovered by the aforementioned Dr. Vladimir Khavinson." (said at 1:08:29)

Pinealon is a synthetic tripeptide composed of the amino acid sequence Glu-Asp-Arg (EDR), developed by Vladimir Khavinson and colleagues. Mechanistic studies show that it penetrates cell membranes and the nucleus directly to interact with DNA, histones, and transcription regulatory pathways rather than signaling through a classical cell-surface receptor. Evidence is derived from in vitro, molecular modeling, and animal research.

1:11:08Andrew Huberman (host)supportedmoderate

Epithalon is derived from pineal gland extract, whereas Pinealon is derived from cortex extract (Cortexin).

"Epithalon is from the pineal gland. Pinealon comes from a ground-up brain extract called Cortexin." (said at 1:11:08)

The host accurately describes the origins of these peptide bioregulators. Epithalon (also known as Epitalon or peptide AEDG) is a synthetic tetrapeptide designed based on the amino acid composition of Epithalamin, a peptide extract from the bovine pineal gland (epiphysis), and was later identified directly within the pineal polypeptide complex. Pinealon (peptide EDR) is a synthetic short peptide modeled after Cortexin, a polypeptide extract derived from bovine cerebral cortex tissue.

1:11:17Abud Bakrisupportedlow

Epithalamin administration upregulates melatonin synthesis enzymes and restores melatonin production in aged monkeys and humans.

"So Khavinson identifies—he makes a drug in Russia. It's called Epithalamin, which is the pineal gland extract, and had great effect on circadian rhythmicity. And it's rich with melatonin, basically giving people melatonin, but also you upregulate the enzyme that creates melatonin from serotonin to N-acetylserotonin to melatonin. So like when he gave it to young monkeys, the monkeys had no effect, but he gave it to aged monkeys that have decreased melatonin—and you know from puberty onwards your melatonin levels dramatically decrease—he was able to restore melatonin production in these aged animals and eventually replicated it on humans." (said at 1:11:17)

The speaker accurately describes the published findings of Vladimir Khavinson and colleagues. In female rhesus monkeys (Macaca mulatta), administration of Epithalamin or its synthetic analogue Epitalon had no effect on young monkeys but significantly increased nocturnal melatonin levels in aged monkeys. Subsequent human trials by the same group showed that Epithalamin restored nighttime plasma melatonin concentrations in elderly individuals who had diminished baseline pineal activity. GRADE certainty is low because these findings originate almost exclusively from a single research group in specialized journals with limited independent replication.

1:25:17Abud Bakrisupportedhigh

Epitalon is a tetrapeptide with the amino acid sequence Ala-Glu-Asp-Gly (AEDG).

"Epitalon is also AEDG, that's the amino acid, four amino acid." (said at 1:25:17)

Epitalon (also spelled Epithalon) is definitively established as a synthetic tetrapeptide consisting of four amino acids with the sequence Ala-Glu-Asp-Gly (AEDG).

1:29:26Abud Bakrisupportedhigh

Between the 1910s and 1940s, infants routinely underwent thymus irradiation to prevent sudden infant death syndrome (status thymicolymphaticus), causing thousands of subsequent cancer deaths.

"For example, like in the 1910s to 1940s, we irradiated the thymuses of young kids to prevent SIDS. This was considered gold-standard medicine... They thought that the thymus was too big and was sitting on the heart and that might be the cause. So tons of these kids, you know, I think at least 10,000 died from cancers." (said at 1:29:26)

Historical and epidemiological records confirm that from the early 1900s through the 1940s/1950s, infants and young children routinely received therapeutic X-ray irradiation of the thymus gland. The medical rationale was the misdiagnosed concept of 'status thymicolymphaticus' or 'enlarged thymus', which was believed to cause respiratory distress or sudden infant death. Subsequent long-term cohort studies (such as the Rochester thymus cohort and major pooled analyses) established that this practice caused substantial excess risks of thyroid cancer, benign thyroid neoplasms, breast cancer, leukemia, and other malignancies later in life.

1:30:37Abud Bakrisupportedmoderate

The human thymus grows from birth until puberty under the influence of hormones like melatonin, growth hormone, and DHEA, and undergoes involution after puberty.

"So the thymus is grown under the influence of a lot of these youthful hormones: melatonin, growth hormone, um DHEA, um and then is shrunk at the moment you hit puberty. So from the day of birth until puberty, you grow this massive thymus." (said at 1:30:37)

The speaker's description aligns with standard immunological and endocrinological understanding. The thymus reaches its maximum absolute mass around puberty, after which it undergoes progressive age-associated involution (characterized by adipose replacement and decreased thymopoiesis), largely triggered and accelerated by the surge in sex steroids at puberty. Growth hormone (GH) and the GH/IGF-1 axis exert trophic and regenerative effects on thymic tissue and thymopoiesis.

1:10:16Abud Bakrisupportedlow

Vladimir Khavinson isolated and sequenced specific regulatory peptides from thymus extracts, including Vilon, Thymogen, and Crystagen.

"So then he sequences from the pineal gland Epithalon, and from the thymus gland a couple different peptides—Vilon, Thymogen, Crystagen—that you'll be hearing about in the next few years, that on their own do a lot of the effects that the whole extract would do." (said at 1:10:16)

Vladimir Khavinson and his research group developed and characterized several synthetic peptide bioregulators derived from or modeled after organ extracts, including thymus-derived peptides such as Thymogen (Glu-Trp), Vilon (Lys-Glu), and Crystagen (Pro-Glu-Asp), as well as the pineal peptide Epithalon (Ala-Glu-Asp-Gly). Published research by Khavinson's team describes these short peptides mimicking specific immunomodulatory actions of crude extracts (such as Timalin). However, evidence evaluating these peptides originates almost entirely from a single research network with limited independent replication, warranting a low certainty rating for their broader clinical claims.

1:31:11Abud Bakrisupportedmoderate

Data published in the New England Journal of Medicine shows that removing residual thymus tissue during adult cardiothoracic surgery leads to an increased mortality signal within five years post-surgery.

"good data from New England Journal of Medicine that removing the thymus tissue, residue tissue leads to a mortality signal within the first five years after those surgeries." (said at 1:31:11)

A 2023 cohort study published in the New England Journal of Medicine (Kooshesh et al.) evaluated adult patients undergoing thymectomy compared to demographically matched controls undergoing cardiothoracic surgery without thymectomy. At 5 years post-surgery, all-cause mortality was significantly higher in the thymectomy group than in the control group (8.1% vs. 2.8%; relative risk, 2.9; 95% CI, 1.7 to 4.8), supporting the speaker's statement.

1:31:31Abud Bakrisupportedmoderate

Removing the thymus in adults is associated with increased incidence of cancer and autoimmune diseases.

"They'll have like either higher rates of cancers or, you know, higher rates of autoimmune diseases if they have their thymuses removed." (said at 1:31:31)

A landmark 2023 retrospective cohort study published in The New England Journal of Medicine (PMID: 37530823) evaluated 1,146 adult patients who underwent thymectomy matched to controls undergoing similar cardiothoracic surgery. At 5 years postoperatively, the thymectomy group showed a significantly increased risk of developing cancer (7.4% vs. 3.7%; relative risk 2.0, 95% CI: 1.3 to 3.2) and an increased risk of autoimmune disease among patients without preoperative infection, cancer, or autoimmunity (12.3% vs. 7.9%; relative risk 1.5, 95% CI: 1.02 to 2.2). Thymectomy was also associated with reduced T-cell production (signal joint T-cell receptor excision circles) and elevated proinflammatory cytokines.

  • supports: Health Consequences of Thymus Removal in Adults. (The New England journal of medicine 2023) · cited 184x in the literature
    "At 5 years after surgery, all-cause mortality was higher in the thymectomy group than in the control group (8.1% vs. 2.8%; relative risk, 2.9; 95% confidence interval [CI], 1.7 to 4.8), as was the risk of cancer (7.4% vs. 3.7%; relative risk, 2.0; 95% CI, 1.3 to 3.2). Although the risk of autoimmune disease did not differ substantially between the groups in the overall primary cohort (relative risk, 1.1; 95% CI, 0.8 to 1.4), a difference was found when patients with preoperative infection, cancer, or autoimmune disease were excluded from the analysis (12.3% vs. 7.9%; relative risk, 1.5; 95% CI, 1.02 to 2.2)." (abstract, results, passage verified)
    pubmedfull study (doi)
1:32:56Abud Bakrisupportedmoderate

Around age 15, the human body produces approximately 10 to the 8th naive T cells per day.

"So when you're, you know, 15, you're making uh 10 to the eighth magnitude of these cells every single day, they're called naive T cells." (said at 1:32:56)

Mathematical modeling and quantitative kinetics studies of human T-cell dynamics (combining Ki67 proliferation data, TCR excision circle [TREC] dynamics, and stable-isotope labeling) indicate that the human body generates on the order of 10^8 (hundreds of millions) naive T cells per day during adolescence and young adulthood through thymic export and homeostatic proliferation, declining gradually thereafter.

1:33:48Abud Bakrisupportedmoderate

Thymic involution starting at puberty is primarily driven by androgens, estrogens, progestins, and corticosteroids.

"So from the moment puberty starts till you die, your thymus is slowly shrinking. That really happens in your 20s and 30s, the majority of that under the the pressure of androgens, estrogens, progestins, and corticosteroids." (said at 1:33:48)

The speaker accurately describes the relationship between puberty, steroid hormones, and thymic involution. Age-related thymic atrophy accelerates noticeably during puberty, a process heavily influenced by the rise of gonadal sex steroids (androgens, estrogens, progestins) and adrenal corticosteroids (glucocorticoids). These steroid hormones induce thymocyte apoptosis and suppress thymic epithelial function; conversely, surgical or medical sex-steroid ablation (e.g., via LHRH antagonists) consistently demonstrates temporary thymic regrowth and renewed thymopoiesis. While thymic aging also involves intrinsic microenvironmental and stromal alterations (such as FOXN1 downregulation), steroid hormone signaling is established as a primary endocrine driver of post-pubertal involution.

1:35:01Abud Bakrisupportedmoderate

Castration reverses or reduces thymic involution.

"So like castration will undo some of the thymic involution." (said at 1:35:01)

The speaker's statement that castration reverses or reduces thymic involution is well supported by experimental and preclinical literature. Surgical or chemical castration (androgen deprivation) induces thymic regeneration, restoring thymic mass, cellularity, early T lineage progenitors, and thymocyte development in aged or atrophied animal models.

1:35:18Abud Bakrisupportedvery low

During pregnancy the thymus involutes, and it regrows during lactation under the influence of growth hormone and prolactin.

"They they involute and then will regrow during the breastfeeding period under the influences of growth hormone and prolactin." (said at 1:35:18)

Animal and mechanistic studies confirm that the thymus undergoes transient acute involution during pregnancy (driven by elevated sex steroids) and subsequently regenerates/recovers cellularity and function during the postpartum and lactation period. This recovery is positively regulated by neuroendocrine hormones, notably prolactin and growth hormone, which act directly on thymic epithelial cells and thymocytes.

1:35:27Abud Bakrisupportedvery low

Hibernating animals undergo marked thymic shrinkage during hibernation followed by regrowth during the feeding period.

"So hibernating animals will have a dramatic shrinkage of the thymus during hibernation and then a regrowth um during the feeding window." (said at 1:35:27)

Comparative biology and morphological studies in hibernating mammals demonstrate seasonal cyclic involution and neogenesis of the thymus gland. During autumn and winter hibernation, the thymus undergoes profound involution (characterized by tissue replacement with brown adipose tissue), followed by marked thymic regeneration/neogenesis and lymphocyte infiltration during the spring and summer active feeding period.

  • supports: [The annual involution and regeneration of the thymus in hibernating animals and perspecti… (Tsitologiia 2003) · cited 5x in the literature
    "Data on a unique phenomenon of annual involution and neogenesis of thymus gland in hibernating animals are reviewed. In accordance with morphological findings, the annual thymus involution in hibernating animals is close to the age-dependent thymus involution occurring in all mammals once in a lifetime... During hibernation, the thymus tissue is substituted by the brown fat tissue. In the spring, thymus gland neogenesis stats with intensive growth of epithelial tissue followed by lymphocyte infiltration and exhaustion of brown tissue." (abstract, passage verified)
    pubmed
1:35:44Abud Bakrisupportedvery low

In the TRIIM trial, administering growth hormone, metformin, and DHEA for 12 months increased thymic size on imaging, increased CD4 and CD8 T cells, improved their ratio, and improved T-cell exhaustion markers like PD-1.

"There's an interesting study, TRIIM trial from Dr. Greg Fahy. He's doing a study where he's giving a cocktail of growth hormone, metformin, and DHEA. Uh gave that for 12 months and had the thymic size increase on imaging. The amount of CD4 or CD8 T cells increased and the ratio of which improved. Uh and then some of the markers that would show like immune cell exhaustion, like PD-1 and all these different aspects of T-cell dynamics also improved." (said at 1:35:44)

The speaker accurately describes the published findings of the TRIIM (Thymus Regeneration, Immunorestoration, and Insulin Mitigation) pilot trial conducted by Dr. Gregory Fahy and colleagues (published in Aging Cell, 2019). In the trial, 9 healthy men (aged 51–65) received a combination of recombinant human growth hormone (rhGH), DHEA, and metformin for 12 months. The study reported MRI evidence of thymic fat replacement with functional thymic tissue (thymic regeneration), an increase in naive CD4 and CD8 T cells, improved naive-to-memory T-cell ratios, a decrease in CD8+ T-cell exhaustion markers (including PD-1 expression), and a reversal of epigenetic clock age by approximately 1.5 to 2.5 years. Because TRIIM was a small (n=9), open-label, single-arm pilot study lacking a randomized control group, the GRADE certainty for the therapeutic efficacy of this regimen is very low.

1:37:48Abud Bakrisupportedhigh

In several countries outside the US, thymosin alpha-1 is approved as an adjuvant treatment for hepatitis B, hepatitis C, and specific cancers.

"in other countries it's approved for adjuvant therapy for like hepatitis B, hepatitis C, and in different cancers." (said at 1:37:48)

The speaker's statement is accurate. Thymosin alpha-1 (synthetic form known as thymalfasin or Zadaxin) is approved in more than 30-35 countries outside the United States for indications including chronic hepatitis B virus (HBV), hepatitis C virus (HCV), and as an adjuvant/immune stimulant, including adjuvant use in chemotherapy for various cancers (such as in the Philippines and China).

1:38:08Abud Bakrisupportedhigh

Thymosin beta-4 is a 43-amino-acid peptide that modulates the cellular actin cytoskeleton and upregulates cell motility.

"Thymosin beta-4 seems to be uh this 43-amino acid peptide that helps in the actin cytoskeleton of cells. So if you think about it, immune cells have to move a lot. So they have to reorganize their actin cytoskeleton quite quickly. So it seems to upregulate that movement" (said at 1:38:08)

The speaker's statement is an accurate description of fundamental cell biology. Thymosin beta-4 (Tβ4) is well-characterized as a 43-amino-acid peptide that binds monomeric G-actin, regulates actin cytoskeleton dynamics/reorganization, and promotes cell migration and motility across various cell types.

1:42:27Abud Bakrisupportedmoderate

A recent landmark paper showed that NAD levels do not decrease in the blood over time.

"Although the paper last week says that it doesn't drop in blood, the landmark paper." (said at 1:42:27)

A landmark study published in Nature Metabolism (van de Weijer et al.) evaluated whole-blood NAD+ concentrations across seven independent human cohorts using validated ultra-high-performance liquid chromatography-mass spectrometry. The authors found that human whole-blood NAD+ levels remain stable across chronological age and do not decline with age or lifestyle interventions, directly supporting the speaker's claim.

1:46:18Abud Bakrisupportedhigh

Thymulin is a zinc-dependent nine-amino-acid peptide secreted by the thymus whose levels decline with age.

"Thymulin is a nine-amino-acid peptide that is the marker of thymus function. It also has very interesting neurological effects, which I think you'll find interesting, because it modulates what we're calling the thymus-pituitary-adrenal axis, thymus-pituitary-gonadal axis. Thymulin is this peptide that's secreted by the thymus, dramatically decreases with age, and is zinc-dependent." (said at 1:46:18)

The speaker accurately describes the biochemical and physiological properties of thymulin. Thymulin is an established zinc-dependent nonapeptide (nine-amino-acid peptide) exclusively synthesized and secreted by thymic epithelial cells. Its biological activity depends directly on binding zinc (1:1 stoichiometric complex), and circulating active levels decline markedly with age in parallel with thymic involution.

1:46:55Abud Bakrisupportedvery low

In hypophysectomized animal models, administering thymulin alongside hCG produces greater testosterone output than hCG alone.

"So they would get more testosterone produced when they got hCG with thymulin versus hCG alone." (said at 1:46:55)

Animal research in rat models directly supports this claim. Wise et al. (1998) examined testicular steroidogenesis in 5-week-old hypophysectomized rats and found that thymulin injection alone had no effect, but in hCG-primed hypophysectomized rats, administering thymulin led to significant increases in testosterone concentrations. Because the evidence is derived exclusively from preclinical rodent experiments, the GRADE certainty is very low.

1:49:09Abud Bakrisupportedmoderate

Thymulin levels decline as the first sign of zinc depletion, prior to drops in red blood cell zinc or serum zinc.

"The first sign of zinc depletion before RBC zinc or serum zinc decrease is your thymulin levels tank." (said at 1:49:09)

Published experimental human zinc depletion studies by Prasad and colleagues demonstrated that serum thymulin (a zinc-dependent thymic nonapeptide hormone) activity declines rapidly during mild zinc restriction (within 8 to 12 weeks), well before detectable reductions occur in lymphocyte zinc (20 weeks) or plasma/serum zinc concentrations (24 weeks).

1:51:45Abud Bakrisupportedhigh

GHK-Cu is a tripeptide made of glycine, histidine, and lysine complexed with copper, naturally present in type 1 collagen fibers.

"GHK-Cu is a tripeptide with a copper ion in the middle. It's glycine, histidine, and lysine. It's actually found in type 1 collagen fibers." (said at 1:51:45)

The speaker accurately describes the chemical composition and physiological occurrence of GHK-Cu. GHK is a tripeptide consisting of glycyl-L-histidyl-L-lysine that complexes with copper(II) ions, and the GHK amino acid sequence triplet occurs naturally within the alpha 2(I) chain of type 1 collagen.

1:52:12Abud Bakrisupportedlow

Serum levels of GHK-Cu drop from approximately 200 ng/mL in youth down to around 60 ng/mL by age 65.

"It's found to be very high in youth in serum levels. So you'll find this in the blood of anyone that we test, up to like 200, I think nanograms, whatever the unit was, and then gets down to like in the levels of the 60s by the age of 65." (said at 1:52:12)

Published literature on the tripeptide GHK (glycyl-L-histidyl-L-lysine) and its copper complex GHK-Cu describes human plasma levels declining from approximately 200 ng/mL in young adults (around age 20) to about 60–80 ng/mL by age 60–65. However, these specific concentrations originate from early narrative reports and small laboratory measurements by Pickart and colleagues rather than large, standardized modern cohort assays, leading to low certainty.

1:55:02Abud Bakrisupportedmoderate

Acute infections induce temporary thymic atrophy, followed by thymic regeneration during recovery.

"There's thymic atrophy that happens after every infection. The thymus kind of shrinks down, and then the idea is that you recover, you convalesce." (said at 1:55:02)

Published immunological evidence confirms that acute infections and inflammatory insults cause transient thymic atrophy (involution), which is subsequently followed by endogenous thymic repair and regeneration during convalescence to restore immune competence and T-cell production.

2:00:26Abud Bakrisupportedlow

A low lymphocyte-to-monocyte ratio on a standard complete blood count is associated with worse clinical outcomes across cardiovascular disease, cancer, and diabetes.

"If you type in any disorder—cardiovascular disease, cancer, diabetes—and put lymphocyte to monocyte ratio, there's a study that will talk about how low lymphocyte to monocyte ratio is associated with poor outcomes when it comes to that disease state." (said at 2:00:26)

Extensive observational literature and systematic reviews confirm that a lower lymphocyte-to-monocyte ratio (LMR)—or equivalently, a higher monocyte-to-lymphocyte ratio (MLR)—derived from a routine complete blood count is associated with worse clinical outcomes, including higher mortality and adverse events, across various cancers, cardiovascular diseases, and complications of diabetes. Because the underlying evidence base consists primarily of retrospective and prospective observational cohort studies, the GRADE certainty is rated as low.

2:00:47Abud Bakrisupportedmoderate

Cancer hazard risk begins to increase around an absolute lymphocyte count below 1,000 cells/µL, while a normal youthful range is 1,500 to 3,000 cells/µL.

"around 1,000 total lymphocytes is where the hazard of different cancer sites starts to increase. A young healthy person will be between 1,500 and 3,000 total lymphocytes." (said at 2:00:47)

Large prospective cohort data (such as the Copenhagen General Population Study of 108,135 participants) confirm that lymphopenia (defined clinically as lymphocyte count < 1.0–1.1 × 10^9/L or < 1,000–1,100 cells/µL) is significantly associated with an increased hazard of nonhematologic cancer death (multivariable HR 1.67) and hematologic cancer death (HR 2.79), as well as overall mortality. Standard clinical reference intervals for absolute lymphocyte count in healthy individuals typically span approximately 1.0–3.0 × 10^9/L (1,000 to 3,000 cells/µL, frequently 1,500–3,000 cells/µL in younger adults).

1:38:57Abud Bakrisupportedhigh

Allan Goldstein's laboratory isolated thymosin fraction 5 and identified thymosin alpha-1 and thymosin beta-4 from thymic tissue.

"Both thymosin alpha-1 and thymosin beta-4 come out of the Goldstein lab. That's the very famous lab that studied the thymus in the '70s, '80s, and '90s." (said at 1:38:57)

The statement accurately reflects biomedical and historical literature regarding the isolation and identification of thymosin peptides. Allan L. Goldstein and colleagues pioneered the purification of thymic extracts (thymosin fraction 5) and subsequently isolated and characterized individual active peptide components, including thymosin alpha-1 (Tα1) and thymosin beta-4 (Tβ4), during their extensive thymus research across the 1970s, 1980s, and 1990s.

1:41:08Abud Bakrisupportedhigh

Thymosin beta-4 is utilized as a doping agent in horse racing.

"Thymosin beta-4 is a very common doping agent... for the horses." (said at 1:41:08)

Thymosin beta-4 (TB4) and its synthetic derivatives (such as TB-500 / N-acetylated LKKTETQ) are well-documented illicit performance-enhancing and regenerative agents in equine sports. They are banned by the International Federation of Horseracing Authorities (IFHA), the International Federation for Equestrian Sports (FEI), and the World Anti-Doping Agency (WADA), and anti-doping laboratories have developed specialized assays to detect their misuse in racehorses.

1:51:48Abud Bakrisupportedhigh

Dr. Loren Pickart discovered the tripeptide GHK-Cu in the 1970s.

"there's an American researcher, Loren Pickart, Dr. Loren Pickart, who's passed now. He discovers GHK-Cu in the collagen tissue... He discovers it in maybe the mid-'70s." (said at 1:51:48)

The discovery of the tripeptide glycyl-L-histidyl-L-lysine (GHK / GHK-Cu) is attributed to Dr. Loren Pickart and colleagues in 1973, when it was isolated from human plasma as a growth-modulating factor. While the speaker informally refers to discovery in 'collagen tissue' in the 'mid-'70s', the core factual claim that Dr. Loren Pickart discovered the GHK/GHK-Cu peptide in the 1970s is well-documented and historically accurate.

1:53:28Abud Bakrisupportedlow

Studies by Loren Pickart comparing topical GHK-Cu to retinol and vitamin C creams demonstrated positive effects on skin remodeling.

"The Pickarts compared it to retinol and vitamin C creams and all these things with positive effects, and people anecdotally talk about their crow's feet going away and topically it does good for them." (said at 1:53:28)

Loren Pickart's publications and reviews on the human tripeptide GHK-Cu describe its positive effects on skin remodeling and repair, including reviews of comparative cosmetic evaluations against standard topical agents like vitamin C and retinol/retinoids for collagen stimulation, skin elasticity, and wrinkle reduction. However, the evidence base consists primarily of narrative reviews, in vitro/animal assays, and small cosmetic clinical evaluations, many of which were authored or summarized by Pickart.

2:06:05Abud Bakrisupportedhigh

Growth hormone is released in a circadian fashion predominantly in the first 90 minutes of slow-wave sleep.

"Growth hormone is a very circadian hormone that gets released in the first, you know, 90 minutes of slow-wave sleep." (said at 2:06:05)

Extensive human polysomnographic and endocrine studies demonstrate that growth hormone (GH) secretion is tightly linked to sleep architecture, with the primary and largest 24-hour secretory pulse occurring shortly after sleep onset during the first cycle of deep slow-wave sleep (SWS). In young healthy adults, approximately 70% of nocturnal GH pulses coincide with slow-wave sleep.

2:07:15Abud Bakrisupportedlow

Growth hormone stimulates the regrowth and regeneration of an aged, involuted thymus gland based on research by Dr. Fahy.

"We also know growth hormone is thymoregenerative because it stimulates the regrowth of an aged, involuted thymus gland based on Dr. Fahy's work." (said at 2:07:15)

The claim accurately describes the published findings of Dr. Gregory Fahy and colleagues. In 2003, Fahy published a case report demonstrating partial reversal of thymic involution and enlargement of functional thymic mass following recombinant human growth hormone (rhGH) and DHEA administration. In 2019, Fahy et al. published results from the TRIIM (Thymus Regeneration, Immunorestoration, and Insulin Mitigation) trial (n=9 healthy men), which utilized a regimen centered on rhGH (along with DHEA and metformin) to stimulate thymic regeneration, accompanied by improvements in epigenetic age markers and immune parameters. The overall certainty is low due to small sample sizes and uncontrolled, single-arm designs.

2:08:23Andrew Huberman (host)supportedmoderate

Larger dog breeds that produce higher levels of IGF-1 downstream of growth hormone have shorter lifespans than smaller dog breeds.

"And in species like dogs where there's tremendous variation in the amount of IGF-1 that's made between, say, a Chihuahua and a Great Dane, the breed that makes more IGF-1 downstream of growth hormone, of course, lives a lot shorter lives than smaller versions of the same species." (said at 2:08:23)

Comparative canine biology and aging research confirm that larger dog breeds exhibit higher circulating levels of insulin-like growth factor 1 (IGF-1) and significantly shorter lifespans compared to small dog breeds. Observational studies assessing serum IGF-1 across diverse purebred and mixed-breed dogs show an overall positive correlation between body weight and IGF-1 levels, in line with the well-established inverse relationship between breed size and lifespan in domestic dogs.

2:10:31Abud Bakrisupportedhigh

Growth hormone promotes the conversion of T4 to T3.

"growth hormone favors the conversion of T4 to T3, so it changes the thyroid dynamics." (said at 2:10:31)

Human clinical trials and mechanistic studies consistently demonstrate that growth hormone (GH) administration stimulates the peripheral conversion of thyroxine (T4) to active triiodothyronine (T3), resulting in decreased circulating free T4 / reverse T3 and increased circulating free T3 levels.

2:12:20Abud Bakrisupportedhigh

Growth hormone and growth hormone secretagogues reduce insulin sensitivity and can elevate HbA1c levels.

"growth hormone and secretagogues have a negative effect on insulin sensitivity, right? So people's A1Cs will usually jump." (said at 2:12:20)

Exogenous growth hormone (GH) and GH secretagogues (such as MK-677/ibutamoren) exert counter-regulatory, anti-insulin actions. Randomized controlled trials and clinical reviews consistently demonstrate that administration of GH or GH secretagogues reduces peripheral insulin sensitivity, impairs glucose tolerance, and increases circulating blood glucose and glycemic markers.

2:23:25Abud Bakrisupportedhigh

Modern GLP-1 receptor agonist medications, including retatrutide, can produce 10% to 30% body weight loss in patients.

"Now with the GLP-1s, we're getting 10, 20, even 30% of body weight being shaved off of people, especially with the new retatrutide data." (said at 2:23:25)

Randomized clinical trials confirm that modern GLP-1 receptor agonists and multi-incretin agonists (such as dual GIP/GLP-1 agonist tirzepatide and triple GIP/GLP-1/glucagon agonist retatrutide) produce mean weight reductions spanning roughly 10% to over 24%, with substantial proportions of patients achieving 20% to 30% or more body weight loss. In a phase 2 trial of retatrutide in adults with obesity, the mean weight loss at 48 weeks reached 24.2% at the 12 mg dose, with 83% achieving at least 15% weight loss. Similarly, in the SURMOUNT-1 trial of tirzepatide, mean weight loss was up to 20.9% at week 72, with 57% of participants in the 15-mg group achieving a reduction of 20% or more.

2:24:44Abud Bakrisupportedhigh

Natural GLP-1-like compound exendin-4 was discovered in the saliva of the Gila monster.

"this is another animal-derived compound, right? It's found in the saliva of the Gila monsters." (said at 2:24:44)

The claim is fully supported. Exendin-4 is a naturally occurring 39-amino-acid peptide originally isolated from the venom/salivary secretions of the Gila monster (*Heloderma suspectum*). It acts as a glucagon-like peptide-1 (GLP-1) receptor agonist and served as the basis for the synthetic GLP-1 receptor agonist drug exenatide (Byetta).

2:29:56Abud Bakrisupportedmoderate

Published literature shows that GLP-1 receptor agonists reduce alcohol cravings.

"And we know the literature shows that people now are having less alcohol cravings from this." (said at 2:29:56)

Published clinical literature, including randomized controlled trials and systematic reviews/meta-analyses, shows that GLP-1 receptor agonists (specifically semaglutide) significantly reduce alcohol cravings and consumption in individuals with alcohol use disorder or hazardous drinking patterns.

2:15:10Andrew Huberman (host)supportedhigh

Retatrutide is a multi-agonist targeting GLP-1, GIP, and glucagon receptor pathways.

"retatrutide is hitting things other than the GLP pathway. It's also GIP and glucagon pathway" (said at 2:15:10)

Retatrutide (LY3437943) is an engineered single-peptide triple receptor agonist designed to activate the glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and glucagon receptors, as confirmed in pharmacological characterizations and randomized clinical trials.

2:14:28Abud Bakrisupportedhigh

MK-677 (ibutamoren) is a non-peptide growth hormone secretagogue and ghrelin receptor agonist.

"MK is not a peptide; it's a non-peptide GHRP." (said at 2:14:28)

MK-677 (also known as ibutamoren or MK-0677) is an orally active, non-peptide growth hormone secretagogue that acts as an agonist at the growth hormone secretagogue receptor (GHSR / ghrelin receptor).

2:32:56Abud Bakrisupportedhigh

The standard starting dose of Ozempic (semaglutide) is 0.25 mg, escalating to 0.5 mg.

"You start at 0.25 and escalate to 0.5." (said at 2:32:56)

The standard label-recommended initiation and dose-escalation schedule for subcutaneous semaglutide (Ozempic) begins at 0.25 mg once weekly for 4 weeks (to minimize gastrointestinal side effects) before escalating to 0.5 mg once weekly. This titration schedule is standard across clinical trial protocols and regulatory prescribing information.

2:33:16Abud Bakrisupportedhigh

In non-diabetics, blood sugar levels do not drop very low when taking GLP-1 receptor agonists.

"The blood sugar effect for non-diabetics don't get that low" (said at 2:33:16)

The claim is supported. GLP-1 receptor agonists stimulate insulin secretion and inhibit glucagon release in a glucose-dependent manner; as blood glucose levels decrease toward normal physiological levels, their insulinotropic effect ceases, intrinsically limiting the risk of severe hypoglycemia in non-diabetic individuals receiving them for weight management.

2:35:46Andrew Huberman (host)supportedhigh

Human chorionic gonadotropin (hCG) is commonly prescribed to restore fertility in men and is mostly given during IVF cycles in women.

"So hCG, human chorionic gonadotropin, this is commonly prescribed for trying to restore fertility to men, but it's mostly being given in IVF cycles to women." (said at 2:35:46)

Human chorionic gonadotropin (hCG) is an established therapeutic agent in reproductive medicine for both men and women. In men, hCG acts as a luteinizing hormone (LH) analog to stimulate Leydig cells, boost intratesticular testosterone, and induce or restore spermatogenesis in cases of hypogonadotropic hypogonadism or steroid-induced infertility. In women, hCG is extensively used in assisted reproductive technology (ART) and in vitro fertilization (IVF) cycles as a 'trigger' for final oocyte maturation prior to retrieval.

2:36:30Abud Bakrisupportedhigh

Orforglipron is a non-peptide GLP-1 receptor agonist.

"orforglipron, which is not a peptide, but still GLP-1 agonist" (said at 2:36:30)

Orforglipron is a small-molecule, non-peptide glucagon-like peptide-1 (GLP-1) receptor agonist developed as an oral once-daily therapy for type 2 diabetes and obesity.

2:39:35Abud Bakrisupportedhigh

There are no published animal or human studies or case reports on the effects of BPC-157 in endometriosis or fibroids.

"No literature exists on either animal or human data that relates to those peptides... there's no case reports or studies that would suggest positive or negative." (said at 2:39:35)

A systematic search of biomedical literature databases (PubMed and Europe PMC) for BPC-157 (and its synonyms) combined with terms for endometriosis, uterine fibroids, leiomyoma, or myoma returns zero results. Recent comprehensive reviews of BPC-157 confirm that preclinical research has been confined largely to musculoskeletal, gastrointestinal, and ischemia-reperfusion models, and that human clinical evidence is limited to a few small pilot studies in unrelated indications (e.g., knee pain, interstitial cystitis). Thus, the speaker's assertion that no animal or human studies or case reports exist regarding BPC-157 in endometriosis or fibroids is accurate.

2:40:36Abud Bakrisupportedhigh

Russian studies have evaluated Cortexin and Cerebrolysin for traumatic brain injury (TBI).

"Yeah, there were studies in Russia on TBI when it comes to Cortexin and Cerebrolysin" (said at 2:40:36)

Numerous clinical studies published in Russian medical journals (such as Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova) have evaluated the efficacy and neurotrophic effects of both Cortexin and Cerebrolysin in patients recovering from acute and long-term traumatic brain injury.

2:40:52Abud Bakrisupportedvery low

In mouse data, BPC-157 attenuates alcohol intoxication and alcohol withdrawal.

"The mice can't get too drunk, and they can't withdraw from alcohol." (said at 2:40:52)

Published rodent studies specifically demonstrate that BPC-157 attenuates both acute alcohol intoxication (reducing ethanol-induced anesthesia, hypothermia, and mortality) and withdrawal symptoms (reducing withdrawal seizures) in mice. However, this evidence is entirely preclinical and limited to animal models from a single research group, yielding very low certainty for human clinical application.

13 No source found (not proven false)
0:05:20Abud Bakriunverifiedvery low

Russian bioregulator peptides act as epigenetic modifiers that bind to DNA grooves, and Pinealon shuttles heat shock proteins with androgen receptors.

"The Russian peptides are all epigenetic modifiers that they bind to the groove of the DNA in certain spots that either open up or close the chromatin to certain areas of genetic expression... So like pinealon that we've talked about shuttles heat shock proteins with androgen receptors." (said at 0:05:20)

The claim bundles two distinct assertions. First, preclinical and in vitro literature (primarily from Russian researchers such as Khavinson and colleagues) suggests that synthetic ultrashort 'bioregulator' peptides (including Pinealon/EDR, Epitalon/AEDG, etc.) can penetrate cell nuclei, interact directly with DNA sequences/grooves, and modulate gene expression and epigenetic marks. Second, the assertion that 'Pinealon shuttles heat shock proteins with androgen receptors' has no published scientific record or validation in the biomedical literature. While heat shock proteins (such as HSP90 and HSP70) are known endogenous chaperones that interact with the androgen receptor in human physiology, no published studies demonstrate that Pinealon acts as a shuttle for heat shock proteins and androgen receptors.

0:20:05Abud Bakriunverifiedvery low

A Croatian clinical trial evaluated rectal enemas of BPC-157 at doses up to 80 milligrams in patients with ulcerative colitis, finding no adverse events in phase 1 and absence of systemic drug levels in the blood.

"There was two very small phase 1 and phase 2 trials on rectal BPC enemas in the early 2000s from that same Croatian group... And they used enemas of BPC up to like 80 milligrams, which is much more than people would take... The phase 1 trial showed no adverse effects. And they didn't even have BPC in the systemic system too." (said at 0:20:05)

While review articles by the Croatian research group (Sikiric et al.) reference phase 1 and phase 2 clinical trials of BPC-157 (PL 14736) in inflammatory bowel disease and report an absence of side effects, full primary peer-reviewed clinical trial reports documenting rectal enema administration of doses up to 80 mg, complete phase 1 safety outcomes, and pharmacokinetic data demonstrating absence of systemic blood levels have not been published in indexed medical literature.

0:47:51Abud Bakriunverifiedvery low

In a melanoma cell line model, BPC-157 decreases VEGF expression.

"Now BPC-157 is not a uniform angiogenesis upregulator. In some models it decreases VEGF in a melanoma model, a cell line." (said at 0:47:51)

No published in vitro or in vivo studies were identified examining the effect of BPC-157 on VEGF expression in a melanoma cell line model. While reviews discussing BPC-157 describe its context-dependent modulation of angiogenesis and nitric oxide signaling across various tissue repair models, specific experimental evidence demonstrating downregulation of VEGF by BPC-157 in melanoma cells remains unlocated in the published peer-reviewed literature.

1:14:46Abud Bakriunverifiedvery low

In a study by Khavinson, athletes given Pinealon were able to maintain performance following maximal exhaustion during training compared to placebo.

"So he studied this compound on athletes and he would have them do their training session, go to exhaustion, and then do a test afterwards. And there's two groups: Pinealon and the placebo. The Pinealon group could keep their performance up despite being maximally exhausted from their training." (said at 1:14:46)

No published clinical trial or study in the indexed medical literature was identified where Vladimir Khavinson (or colleagues) administered Pinealon (the tripeptide Glu-Asp-Arg / EDR) to athletes in a placebo-controlled trial evaluating performance maintenance after maximal exhaustion. While Khavinson and colleagues have published extensively on Pinealon's neuroprotective, antioxidant, and geroprotective effects in cell cultures, animal models, and elderly human cohorts, the specific athlete exhaustion trial described by the speaker could not be verified in peer-reviewed scientific databases.

1:17:10Abud Bakriunverifiedvery low

Pinealon can cause a reduction in blood glucose and HbA1c via activation of PPAR-alpha and PPAR-gamma.

"Some will have a little drop in blood sugar because it activates PPAR-alpha, PPAR-gamma. So it'll have positive metabolic effects. So that's something to keep an eye out. And in some people even had their A1Cs drop." (said at 1:17:10)

No published studies in PubMed or Europe PMC were found demonstrating that Pinealon (the synthetic tripeptide Glu-Asp-Arg / EDR) activates PPAR-alpha or PPAR-gamma, reduces blood glucose, or lowers HbA1c in humans or animal models. While Pinealon has been investigated in limited preclinical and Russian literature primarily for neuroprotective, antioxidant, and geroprotective effects, the claimed mechanism involving PPAR activation and glycemic endpoints is unverified in the biomedical literature.

1:27:56Abud Bakriunverifiedvery low

Five days of total darkness significantly increases retinal melanopsin levels in animal models.

"Because we know that in animal studies, five days of pure darkness dramatically increases the amount of melanopsin in the retina." (said at 1:27:56)

A targeted literature search did not identify animal studies demonstrating that five days of total/pure darkness dramatically increases retinal melanopsin levels or expression. While light deprivation and exposure to specific wavelengths (such as blue light) are known to modulate melanopsin (Opn4) mRNA and protein immunoreactivity in rodents (e.g., blue light exposure reduces melanopsin expression, while photoperiods alter daily transcript profiles), no published record matching the specific claim of a dramatic increase following five days of pure darkness was located. This does not prove the claim false, but it remains unverified in the published literature.

1:22:55Abud Bakriunverifiedvery low

In Khavinson's research, Epitalon administration increased the expression of clock genes in peripheral lymphocytes and increased morning cortisol levels.

"So in Khavinson's work, he's found that it will increase the expression of the different clock genes. So in like, you know, lymphocytes that he'll measure in peripheral tissues, he'll notice that the clock genes actually change. So in a more rhythmic pattern, he'll notice that morning cortisol is higher." (said at 1:22:55)

A search of Vladimir Khavinson's published literature found no studies demonstrating that Epitalon (or Epithalon/Epithalamin) increases the expression of clock genes in human or animal peripheral lymphocytes. Khavinson's group did publish research in senescent female rhesus monkeys (Macaca mulatta) showing that Epitalon stimulated evening melatonin production and helped normalize the circadian rhythm of cortisol secretion (PMID 11524632), but the specific claim regarding clock gene expression in peripheral lymphocytes is not documented in the peer-reviewed indexed literature.

1:33:39Abud Bakriunverifiedvery low

A Nature study using MRI found that individuals with higher thymic scores had reduced mortality from cardiovascular disease and cancer.

"There's a Nature paper uh 2026 just came out that looked at cardiovascular disease and cancer mortality and all these different metrics, that they did MRIs of people, and and the people that had the higher thymic scores had less mortality across every single one of these conditions." (said at 1:33:39)

A targeted search of PubMed and Europe PMC found no published study in Nature (or other peer-reviewed journals) evaluating MRI-derived thymic scores in relation to cardiovascular disease, cancer mortality, or all-cause mortality. While prominent observational studies (such as a 2023 NEJM study by Kooshesh et al.) have linked surgical removal of the thymus (thymectomy) to increased risks of cancer, autoimmune disease, and all-cause mortality, no specific Nature study establishing an MRI-based 'thymic score' predictive of reduced mortality across these specific conditions was identified.

1:44:11Abud Bakriunverifiedvery low

Pinealon is sold over the counter in pharmacies as a dietary supplement in countries such as Russia, Kazakhstan, and Ukraine.

"And pinealon is a supplement you can find in Kazakhstan and Russia and Ukraine, wherever, all these different countries, over the counter in pharmacies." (said at 1:44:11)

Biomedical literature indexed in PubMed confirms that Pinealon (the synthetic tripeptide Glu-Asp-Arg, or EDR) is a peptide bioregulator ('cytogen') developed and investigated in Russia for neuroprotective and geroprotective uses in occupational and clinical cohorts. However, the specific commercial and regulatory claim that Pinealon is sold over the counter in pharmacies as a dietary supplement across Russia, Kazakhstan, and Ukraine cannot be verified through standard biomedical research databases, as peer-reviewed publications do not track pharmacy retail and regulatory classifications in these countries. This lack of indexing does not mean the claim is false.

1:52:56Abud Bakriunverifiedvery low

In animal studies, injecting GHK-Cu at a site distant from a surgical incision accelerates skin wound healing.

"So similar to the BPC, they would, you know, cut rats open, inject GHK copper in a different site, and they'd get faster wound repair of the skin tissue from injecting this." (said at 1:52:56)

While animal research has evaluated GHK-Cu for tissue repair (for example, local injection into subcutaneous wound chambers in rats or topical preparations), no published studies were located demonstrating that injecting GHK-Cu at a site distant from a surgical incision accelerates skin wound healing. Most in vivo wound healing models evaluate direct local application or wound chamber administration rather than distant-site systemic delivery.

2:13:10Abud Bakriunverifiedvery low

Tesamorelin combined with ipamorelin can increase IGF-1 levels into the 380s or 390s ng/mL.

"Tesamorelin, especially when combined with ipamorelin... Those two together can create a giant growth hormone response where your IGF-1 is in the 380s, 390s. Um, so that's quite high, like puberty levels of IGF-1" (said at 2:13:10)

No published clinical studies have evaluated the combination of tesamorelin and ipamorelin or demonstrated that this specific combination elevates IGF-1 levels to 380-390 ng/mL. Narrative reviews on performance-enhancing and off-label peptides note that while GHRH analogues (such as tesamorelin) and GH secretagogues (such as ipamorelin) are frequently combined in gray-market or self-administration protocols to stimulate the GH-IGF-1 axis, clinical trial data for such stacking practices and their resulting IGF-1 levels are lacking.

  • context: Safety and Efficacy of Approved and Unapproved Peptide Therapies for Musculoskeletal Injur… (Sports medicine (Auckland, N.Z.) 2026)
    "While numerous peptide drugs have undergone a rigorous approval process that evaluates both safety and efficacy, a parallel "gray market" of unapproved compounds has emerged, operating largely outside of regulatory oversight. Our objective is to present the pharmacological mechanisms, safety profiles, and regulatory status of prominent approved and unapproved peptides marketed direct to patients, including AOD-9604 (anti-obesity drug 9604), BPC-157 (body protection compound 157), CJC-1295, FS-344 (follistatin-344), GHK-Cu (glycyl-L-histidyl-L-lysine copper), ipamorelin, MOTS-C (mitochondrial ORF of the 12S rRNA type-c), sermorelin, SS-31 (elamipretide), tesamorelin (Egrifta), Tβ4 (thymosin beta-4), and TB-500 (thymosin beta-4 fragment)." (abstract, results, passage verified)
    pubmedfull study (doi)
  • context: The emerging landscape of performance-enhancing peptides modulating GH-IGF1 axis: bridging… (Frontiers in endocrinology 2026)
    "The agents most commonly encountered in clinical practice and online self-administration protocols include growth hormone-releasing hormone (GHRH) analogues (e.g., sermorelin, tesamorelin, CJC-1295 with Drug Affinity Complex [DAC], CJC-1295 without DAC), growth hormone secretagogues (GHS; e.g., growth hormone-releasing peptide-2 (GHRP-2), growth hormone-releasing peptide-6 (GHRP-6), hexarelin, ipamorelin)... Given the absence of regulatory approval for physique- or performance-related indications and the uncertainty surrounding product composition, dose, and stacking practices in unregulated supply chains, clinicians increasingly require a pragmatic framework to interpret symptoms and laboratory abnormalities in patients using these compounds." (abstract, results, passage verified)
    pubmedfull study (doi)
2:35:00Abud Bakriunverifiedlow

Retatrutide contains 39 amino acids.

"retatrutide has 39 amino acids." (said at 2:35:00)

While retatrutide (LY3437943) is biochemically characterized as a 39-amino-acid peptide triple agonist at the GIP, GLP-1, and glucagon receptors, the specific peptide length of 39 amino acids was not explicitly stated in the abstracts of the retrieved records, although retatrutide was confirmed to be a synthetic peptide agonist.

2:35:03Abud Bakriunverifiedvery low

To be classified as a biologic under regulatory standards, a molecule must contain more than 40 amino acids.

"To be a biologic, you have to be above 40 amino acids." (said at 2:35:03)

No retrieved publication abstract contained the specific regulatory text regarding the amino acid threshold. Under United States Food and Drug Administration (FDA) regulations following the Biologics Price Competition and Innovation Act (BPCI Act) and subsequent FDA rulemakings (21 CFR Part 600), the 40 amino acid threshold is used specifically to distinguish 'peptides' (40 or fewer amino acids, typically regulated as small-molecule drugs under the FD&C Act) from 'proteins' (greater than 40 amino acids, regulated as biological products under the Public Health Service Act). However, biologics also encompass many non-protein entities (such as vaccines, blood components, and gene/cell therapies), making the claim that a molecule 'must contain more than 40 amino acids' to be a biologic an imprecise description of the broader category.

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.