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
4 Contradicted by research
GLP-1 receptor agonists ramp up AMPK, which can cause muscle wasting in people who do not consume adequate protein.
"Number two is wasting. Even if you're strength training, there is still this ramping up of AMPK, and it can lead to wasting in folks that are not consuming enough protein or not actually doing anything to mitigate or protect their muscle." (said at 0:05:30)
The speaker's claim bundles a known clinical phenomenon with an incorrect mechanistic claim. While clinical trials and systematic reviews confirm that glucagon-like peptide-1 receptor agonist (GLP-1 RA) therapy is accompanied by reductions in lean body mass—typically accounting for 25% to 30% of total weight loss during caloric restriction—this loss is primarily a consequence of hypocaloric weight reduction rather than AMPK-induced muscle proteolysis. In mechanistic and preclinical literature, GLP-1 RA–induced activation of AMP-activated protein kinase (AMPK) is actually associated with muscle protection, promoting mitochondrial biogenesis, suppressing inflammatory pathways, and decreasing the expression of proteolytic markers (such as MuRF1 and MAFbx), rather than causing muscle wasting.
- contradicts: Amelioration of inflammatory myopathies by glucagon-like peptide-1 receptor agonist via su… (Journal of cachexia, sarcopenia and muscle 2022) · cited 51x in the literature
"PF1801 inhibited necroptosis of the myotubes in an AMP-activated protein kinase (AMPK)-dependent manner. PF1801 activated AMPK and decreased the expression of PGAM5, a mitochondrial protein, which was crucial for necroptosis of the myotubes." (abstract, results, passage verified)
pubmedfull study (doi) - contradicts: Glucagon Like Peptide-1 Receptor Agonists for Sarcopenia and Muscle Wasting Disorders: A S… (Aging and disease 2025) · cited 4x in the literature
"Mechanistically, GLP-1RAs mitigate muscle wasting by upregulating myogenic factors (MyoD, MyoG), promoting mitochondrial biogenesis, and suppressing proteolysis (MuRF1, MAFbx) and inflammation via AMPK/SIRT1/NF-κB/Myostatin signaling." (abstract, results, passage verified)
pubmedfull study (doi) - context: Effect of Incretin-Based and Nonpharmacologic Weight Loss on Body Composition : A Systemat… (Annals of internal medicine 2026) · cited 12x in the literature
"Within the incretin groups across agents and measurement methods, the median proportion of total weight loss attributable to reductions in muscle-based indices was 28.3% (IQR, 15.9% to 39.9%), with 65% exceeding the benchmark of about 25%" (abstract, results, passage verified)
pubmedfull study (doi)
5-Amino-1MQ inhibits nicotinamide N-methyltransferase (NNMT), which preserves NAD levels.
"Its mechanistic way that it works is by inhibiting NNMT, which is the main enzyme that actually clears NAD out of your body into um nicotinic acid. So if you the 5-Amino inhibits that enzyme's function and basically preserves your NAD levels" (said at 0:43:56)
The speaker bundles two claims with an inaccurate biochemical mechanism: (1) 5-amino-1MQ is a small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT), which is supported in preclinical cell and animal studies; (2) NNMT functions by converting NAD into nicotinic acid to clear it from the body, which is contradicted by established biochemistry. NNMT does not metabolize NAD into nicotinic acid; rather, it transfers a methyl group from S-adenosylmethionine (SAM) to nicotinamide (NAM)—a product of NAD degradation and precursor in the NAD salvage pathway—generating 1-methylnicotinamide (MNA). By inhibiting NNMT, 5-amino-1MQ prevents the clearance of nicotinamide as MNA, allowing more nicotinamide to be salvaged back into NAD+. While NNMT inhibition by 5-amino-1MQ has been shown to support NAD+ levels in preclinical models, the stated mechanism of NAD conversion into nicotinic acid is incorrect, and clinical trial evidence in humans is lacking.
DNF-10 is a peptide ingredient that increases neuropeptide Y.
"I used peptides that increase neuropeptide Y. There's one called DNF-10." (said at 0:52:16)
DNF-10 is a commercial yeast hydrolysate (Saccharomyces cerevisiae hydrolysate below 10 kDa) marketed as an appetite suppressant and anti-obesity ingredient. Neuropeptide Y (NPY) is a potent orexigenic (appetite-stimulating) neuropeptide. Rather than increasing NPY, published studies examining low-molecular-weight yeast hydrolysates (<10 kDa) show that they decrease or downregulate NPY expression in hypothalamic appetite-regulating centers (such as the paraventricular nucleus and lateral hypothalamic area) to reduce food intake and body weight gain. The speaker inverted the claimed mechanism of action.
The peptide KPV is used as part of the Ritchie Shoemaker protocol to increase alpha-melanocyte-stimulating hormone (alpha-MSH) in cases of mold exposure and Chronic Inflammatory Response Syndrome (CIRS).
"It's part of the Ritchie Shoemaker protocol for increasing alpha-MSH. So that's why I love it for, you know, mold injury and CIRS uh not mold injury, mold exposure and CIRS" (said at 1:03:02)
The claim misidentifies both the biochemical nature of KPV and its therapeutic function. KPV (lysine-proline-valine) is the C-terminal tripeptide fragment of alpha-melanocyte-stimulating hormone (alpha-MSH) itself, not a molecule that stimulates or increases endogenous alpha-MSH levels. While KPV is studied in pre-clinical research for retaining some of the anti-inflammatory properties of alpha-MSH without causing pigmentation, published descriptions of the Ritchie Shoemaker protocol for Chronic Inflammatory Response Syndrome (CIRS) do not include KPV as an intervention to raise alpha-MSH. Published CIRS literature focuses on clearing sinonasal MARCoNS colonization, toxin binders, and vasoactive intestinal polypeptide (VIP).
- contradicts: Alpha-melanocyte-stimulating hormone and related tripeptides: biochemistry, antiinflammato… (Endocrine reviews 2008) · cited 323x in the literature
"Due to its preserved antiinflammatory effect but lack of pigmentary action, the C-terminal tripeptide of alpha-MSH, KPV, has been delineated as an alternative for antiinflammatory therapy." (abstract, results, passage verified)
pubmedfull study (doi) - contradicts: Terminal signal: anti-inflammatory effects of α-melanocyte-stimulating hormone related pep… (Advances in experimental medicine and biology 2010) · cited 34x in the literature
"Interestingly KPV, C-terminal tripeptide of α-MSH, which lacks the entire sequence motif required for binding to any of the known MC-Rs, retains almost all of the anti-inflammatory capacity of the full hormone, but in its activities display a lack of any pigmentory action." (abstract, results, passage verified)
pubmedfull study (doi) - context: Clearance of multiple antibiotic-resistant coagulase-negative staphylococci is selectively… (Frontiers in endocrinology 2026)
"Mixed-effects modeling revealed a significant timepoint-by-MARCoNS interaction for α-MSH, such that patients who were MARCoNS-negative at follow-up exhibited higher circulating α-MSH levels compared with those who remained positive." (abstract, results, 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.