Dr. Tyna Moore · 2025-10-31 · Tyna Moore (host), Kyal Van Der Leest
Peptides to Support Your GLP1 Health And Weight Loss Journey | Kyal Van Der Leest of LVLUP EP. 236
43 research-tied claims examined: 4 contradicted 7 overstated 2 context 30 supported
7 Overstated
Small intestinal bacterial overgrowth (SIBO) drives insulin resistance and obesity.
"SIBO will drive, it's not a direct cause, but it will drive insulin resistance and obesity. I think it is one of the root causes of insulin resistance and obesity, especially in this country, in the US." (said at 0:17:54)
While clinical literature documents an observational association between small intestinal bacterial overgrowth (SIBO), pediatric/adult obesity, and related metabolic conditions (such as metabolic dysfunction-associated steatotic liver disease and insulin resistance), claiming that SIBO 'drives' obesity and insulin resistance as a 'root cause' overstates the scientific evidence. Systematic reviews and mechanistic evaluations emphasize that current evidence is predominantly correlational and cross-sectional; causality has not been demonstrated, and obesity or altered GI motility may just as likely predispose individuals to SIBO.
- partial: The role of small intestinal bacterial overgrowth in obesity and its related diseases. (Biochemical pharmacology 2023) · cited 19x in the literature
"Small intestinal bacterial overgrowth (SIBO), a type of intestinal microbial dysbiosis, has been gradually revealed to be associated with obesity and its related diseases... However, the causal relationship between SIBO and obesity and the specific mechanisms have not been well elucidated." (abstract, results)
pubmedfull study (doi) - context: Small Intestinal Bacterial Overgrowth and Pediatric Obesity-A Systematic Review. (Nutrients 2025) · cited 4x in the literature
"The data show that SIBO is frequently observed in obese pediatric populations and is associated with gut dysbiosis, impaired nutrient absorption, and reduced production of short-chain fatty acids. These changes contribute to increased intestinal permeability, endotoxemia, and chronic low-grade inflammation." (abstract, results, passage verified)
pubmedfull study (doi)
Dihydroberberine is approximately 40 times more bioavailable/absorbable than standard berberine.
"But dihydroberberine is about 40 times more absorbable than regular berberine. So that's going to work better for, you know, systemic glucose control" (said at 0:52:46)
The claim that dihydroberberine (DHB) is approximately 40 times more bioavailable/absorbable than standard berberine (BBR) is overstated. Clinical trial data in humans demonstrate that oral ingestion of dihydroberberine produces higher plasma berberine AUC (area under the curve) and Cmax compared to standard berberine, but at a magnitude of approximately 5-fold (for a 100 mg dose of DHB vs. a 500 mg dose of BBR, resulting in about a 5-fold to 6-fold increase in blood concentration relative to dose), rather than 40-fold. Additionally, transdermal administration of DHB in rats showed increased relative absorption compared to oral BBR, but no human or animal pharmacokinetic study demonstrates a 40-fold absorption advantage for oral dihydroberberine over oral berberine.
BPC-157 upregulates growth hormone receptor density.
"BPC has an effect on upregulating growth hormone receptor density, which means that you know, anyone who's doing any training, growth hormone is going to work a lot better and you're going to recover faster and preserve your muscle um a lot better from that one." (said at 0:54:26)
Evidence that BPC-157 upregulates growth hormone receptor expression comes strictly from preclinical laboratory models, primarily an in vitro study on isolated rat Achilles tendon fibroblasts showing dose- and time-dependent increases in growth hormone receptor mRNA and protein levels. There is no clinical trial data in humans demonstrating that BPC-157 increases growth hormone receptor density in vivo or that it enhances muscle preservation, recovery, or training adaptations in athletes.
BPC-157 upregulates VEGF and promotes angiogenesis (new blood vessel formation).
"Angiogenesis is one of the pathways that BPC upregulates. VEGF, angiogenesis, new blood vessel formation. That's fantastic for injury recovery for regeneration." (said at 0:58:01)
Preclinical evidence from animal models and cell cultures demonstrates that pentadecapeptide BPC-157 promotes angiogenesis (new blood vessel formation) and upregulates vascular endothelial growth factor (VEGF) and its receptor VEGFR2 during tissue healing (such as in injured tendons, muscles, and burn wounds). However, asserting this as a proven therapy for injury recovery in humans overstates the evidence, as all published data on BPC-157's angiogenic properties are derived strictly from in vitro assays and animal studies; no human clinical trials have established these effects or confirmed safety and efficacy in patients.
BPC accelerates injury recovery and connective tissue healing by acting on growth factors.
"the peptide works on all the all the growth factors and um accelerating the healing process. So that product is awesome for you know uh connective tissue injuries and helping with injury recovery." (said at 1:01:45)
Preclinical studies (primarily in vitro and rodent models) indicate that body protection compound-157 (BPC-157) modulates growth factors (such as VEGF, EGF, and growth hormone receptor expression) and can promote tendon, ligament, and muscle healing. However, claiming that it works on all growth factors and definitively accelerates connective tissue injury recovery in humans overstates the evidence. Systematic reviews emphasize that human clinical trials evaluating its efficacy and safety in musculoskeletal and connective tissue repair are currently lacking.
- partial: Gastric pentadecapeptide body protection compound BPC 157 and its role in accelerating mus… (Cell and tissue research 2019) · cited 45x in the literature
"Currently, all studies investigating BPC 157 have demonstrated consistently positive and prompt healing effects for various injury types, both traumatic and systemic and for a plethora of soft tissues. However, to date, the majority of studies have been performed on small rodent models and the efficacy of BPC 157 is yet to be confirmed in humans." (abstract, passage verified)
pubmedfull study (doi) - partial: Emerging Use of BPC-157 in Orthopaedic Sports Medicine: A Systematic Review. (HSS journal : the musculoskeletal journal of Hospital for Special Surgery 2025) · cited 14x in the literature
"The studies suggest that BPC-157 enhances growth hormone receptor expression and several pathways involved in cell growth and angiogenesis, while reducing inflammatory cytokines. In preclinical models, BPC-157 improved functional, structural, and biomechanical outcomes in muscle, tendon, ligament, and bony injuries... No clinical safety data were found." (abstract, results, passage verified)
pubmedfull study (doi) - partial: Injectable Peptide Therapy: A Primer for Orthopaedic and Sports Medicine Physicians. (The American journal of sports medicine 2026) · cited 11x in the literature
"BPC-157 demonstrated potential benefits in tendon and muscle repair, but these findings are largely unvalidated in human trials. A single human case series reported improvements in pain after intra-articular knee injections of BPC-157, although significant methodological flaws and a lack of controls limit its applicability and reliability." (abstract, results, passage verified)
pubmedfull study (doi)
BPC-157 can help preserve muscle mass while sealing the gut barrier to reduce lipopolysaccharide (LPS) leakage.
"The BPC's in it that's going to help preserve that could help preserve the muscle mass whilst it's sealing up the gut to reduce the LPS that's going to cause the liver issues" (said at 1:03:38)
The claim states that BPC-157 helps preserve muscle mass while sealing the gut barrier to reduce lipopolysaccharide (LPS) leakage. While BPC-157 has shown gastroprotective, mucosal healing, and muscle regenerative properties in animal models (such as rats subjected to transections, crush injuries, fistulas, and cachexia models), virtually all data supporting these mechanisms are derived from preclinical rodent studies. Systematic and scoping reviews confirm that there is an absence of robust randomized controlled clinical trials in humans evaluating muscle preservation or gut barrier restoration. Presenting these therapeutic effects as established human benefits overstates the existing evidence base.
- context: Emerging Use of BPC-157 in Orthopaedic Sports Medicine: A Systematic Review. (HSS journal : the musculoskeletal journal of Hospital for Special Surgery 2025) · cited 14x in the literature
"In preclinical models, BPC-157 improved functional, structural, and biomechanical outcomes in muscle, tendon, ligament, and bony injuries... Animal studies showed no harmful effects, but there is no clinical safety data in humans. Overall, BPC-157 could help heal musculoskeletal injuries, but there are potential risks due to unregulated production and lack of clinical safety data." (abstract, results)
pubmedfull study (doi) - context: Regeneration or Risk? A Narrative Review of BPC-157 for Musculoskeletal Healing. (Current reviews in musculoskeletal medicine 2025) · cited 19x in the literature
"BPC-157 demonstrates robust regenerative and cytoprotective effects in preclinical studies, positioning it as a potentially valuable tool in musculoskeletal medicine. Despite its growing popularity among athletes and its wide availability through non-regulated sources, there is minimal human data available. Until well-designed clinical trials are conducted, BPC-157 should be considered investigational, and its use approached with caution." (abstract, conclusions, passage verified)
pubmedfull study (doi)
5-Amino-1MQ produces a thermogenic effect.
"and I love the Longevity for what you all the reasons you said, but that 5-Amino-1MQ just kind of has that thermogenic effect as well." (said at 1:04:26)
5-Amino-1MQ (5-amino-1-methylquinolinium) is an experimental small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT). Preclinical studies in diet-induced obese mice and cultured adipocytes have shown that NNMT inhibition reduces adipose tissue mass, suppresses lipogenesis, and increases cellular energy expenditure without altering food intake. However, no human clinical trials evaluating 5-Amino-1MQ or other NNMT inhibitors for thermogenesis, metabolic rate, or weight loss have been published. Claiming a thermogenic effect in humans overstates evidence that is strictly limited to animal and cell models.
- partial: Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransfe… (Biochemical pharmacology 2018) · cited 84x in the literature
"Treatment of diet-induced obese mice systemically with a potent NNMT inhibitor significantly reduced body weight and white adipose mass, decreased adipocyte size, and lowered plasma total cholesterol levels. Notably, administration of NNMT inhibitors did not impact total food intake nor produce any observable adverse effects." (abstract, results, passage verified)
pubmedfull study (doi) - context: Roles of Nicotinamide N-Methyltransferase in Obesity and Type 2 Diabetes. (BioMed research international 2021) · cited 21x in the literature
"NNMT inhibition or NNMT knockdown significantly increases energy expenditure, reduces body weight and white adipose mass, improves insulin sensitivity, and normalizes glucose tolerance and fasting blood glucose levels. ... However, the exact mechanisms underlying these phenomena are not yet fully understood and clinical trials targeting NNMT have not been reported until now." (abstract, passage verified)
pubmedfull study (doi)
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.