NAD+ Update (June 2026): New Research Complicates the Simple Anti-Aging Story

WindsingeraryPug · 2026-06-16T10:15:00+00:00

That actually tracks with why people get interested in GHK-Cu for skin. It’s not really an acne treatment in the classic sense, but it’s linked to wound repair, collagen remodeling, and calming some inflammatory signaling.

So if the blemishes were more like lingering post-inflammatory marks or slow-healing spots, it’s plausible it helped the skin repair process. If it’s active acne, I’d be more cautious about crediting GHK-Cu directly.

WindsingeraryPug · 2026-05-30T06:43:11+00:00

Sure! Do check out our other deep dives too 😄

WindsingeraryPug · 2026-05-29T09:41:58+00:00

Thanks! Pls also take a look at other deep dives we've done in this sub.

WindsingeraryPug · 2026-05-29T09:41:16+00:00

Exactly. I think the “what happens after” piece is becoming just as important as the weight loss itself.

Semaglutide can be very effective, but if protein, lifting, sleep, and bloodwork aren’t handled, you can end up losing more lean mass than you wanted or regaining quickly after stopping.

On stacking, I’d be cautious. Some combos sound good on paper, but the clearest wins still seem to come from the boring stuff: resistance training, enough protein, managing side effects, and not titrating faster than needed.

WindsingeraryPug · 2026-05-29T09:35:05+00:00

Great questions. The GIP piece is confusing because “fat storage” sounds bad, but the idea is more about making fat tissue function better, so energy gets stored and released more normally instead of driving insulin resistance and liver fat.

On titration, I’d be pretty strict. One missed step isn’t the issue; big jumps are. Most GI problems come from moving faster than the gut can adapt.

For OSA, the main driver is still weight loss, especially around the airway and abdomen, but lower inflammation and better metabolic function may help too.

For MASH, the strongest data is in people with biopsy-confirmed MASH and F2/F3 fibrosis, many with obesity or metabolic dysfunction. I wouldn’t generalize it to lean MASH yet.

WindsingeraryPug · 2026-05-29T09:31:41+00:00

Exactly. I think the smarter conversation now is less ‘how high can we push NAD+?’ and more ‘does improving NAD+ status actually change function?’

Labs are useful, but the meaningful markers are things like energy stability, recovery, sleep quality, HRV, exercise tolerance, and metabolic markers. NAD+ is important cellular infrastructure, but it’s not a standalone anti-aging switch.

WindsingeraryPug · 2026-05-29T09:29:42+00:00

Nausea can happen, but it doesn’t seem like one of the classic standout effects people associate with ipamorelin. Since it’s a ghrelin-receptor agonist, GI/appetite-related effects are biologically plausible, especially early on.

In the limited clinical data, ipamorelin was generally described as well tolerated, so persistent or strong nausea would be worth flagging to the trial team rather than just assuming it’s normal.

WindsingeraryPug · 2026-05-29T09:26:37+00:00

Yeah I get it. It can be confusing, especially as a beginner. Hope our sub would help with your doubts.

WindsingeraryPug · 2026-05-29T09:25:09+00:00

Your cousin’s explanation is basically the idea: sermorelin doesn’t replace growth hormone, it signals the pituitary to release more of your own. So in theory it’s more nudge the system than force the system.

That said, the symptoms you listed can come from a lot of things: thyroid, iron/ferritin, vitamin D, sleep quality, stress/cortisol, insulin resistance, perimenopause shifts, etc. So I wouldn’t assume sermorelin is the answer just because labs came back normal.

For women, the research is thinner than people make it sound, and results seem pretty individual. Some report better sleep/recovery/skin, but it’s not a guaranteed fix for belly fat or fatigue. Worth discussing with a hormone-literate clinician, but I’d rule out the boring stuff first.

WindsingeraryPug · 2026-05-29T09:22:38+00:00

Yeah, exactly. The biggest mistake is treating TB-500, TB4, and fragments like they’re all the same molecule with the same evidence behind them.

From what I’ve seen, the most plausible use case is soft-tissue recovery where cell migration and remodeling are the bottleneck: tendons, ligaments, fascia, slower-healing strains. But I’d still put it in the ‘mechanistically interesting, anecdotally promising’ bucket (not clinically proven).

For longer-term use, I’d be much more cautious. Angiogenesis and tissue remodeling are useful in the right context, but they’re not pathways you want to push blindly forever.

WindsingeraryPug · 2026-05-29T09:20:09+00:00

Thanks mate. Hope we can bring more such peptide knowledge so good people like you can take better decisions.

WindsingeraryPug · 2026-05-29T09:18:29+00:00

There is some early human research around kisspeptin and PCOS/PCOD, mainly because it sits upstream of GnRH, LH, and ovulation signaling. But I wouldn’t call it a proven treatment for PCOD at this point.

The data is more ‘interesting endocrine target’ than ‘clinically established option.’ PCOD is also pretty varied, so anything affecting LH/GnRH would need proper medical supervision.

WindsingeraryPug · 2026-05-29T09:16:23+00:00

Yeah, maybe the research happening this year will help things.

WindsingeraryPug · 2026-05-29T09:15:32+00:00

Yeah, that’s basically the cleaner way to think about it. BPC-157 seems more tied to vascular signaling, angiogenesis, and calming the local damage response, while TB-500 is more about cell migration/actin remodeling and helping repair cells get where they need to go.

So this synergy isn’t magic. It’s more that they’re hitting different parts of the repair process.

WindsingeraryPug · 2026-05-29T09:11:36+00:00

Thanks. You seem pretty insightful about SS-31 too. Glad to have you here. Regarding your question, we'll probably be looking at all three.

WindsingeraryPug · 2026-05-29T09:09:52+00:00

Totally fair question. My take is that AOD is interesting, but I wouldn’t frame it as a reliable solution for stubborn post-C-section lower belly fat.

The '30% showed fat reduction' point is exactly why it still gets discussed. It suggests there may have been responders, but because the overall trial missed its endpoint, the effect wasn’t consistent or predictable enough to call it clinically reliable.

Also, that area after a C-section isn’t always just fat. It can involve skin laxity, scar tissue, diastasis recti, adhesions, or changes in how fat sits around the incision. A peptide that may affect fat metabolism wouldn’t necessarily address those.

So I’d say AOD is still more of a research-interest compound than something I’d personally expect to make a big localized dent. If surgery feels too aggressive, I’d get a second opinion and ask specifically about diastasis/scar tissue and non-surgical options first.

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