Do peptides actually fight inflammation better than any supplement?

What did @thecharlottemathis actually say?

The creator recommended two compounds as her "top anti-inflammatory peptides": NAD (nicotinamide adenine dinucleotide), which she described as "a peptide or coenzyme responsible for over 500 enzymatic reactions," and GLP-1 or GLP-1/GIP agonists. She said NAD decreases with age, contributes to fatigue, and is best supplemented via subcutaneous injection. For GLP-1, she cited patient-reported inflammation reduction and said it shows up in lab markers like sed rate and CRP. She then directed viewers to a telehealth partner where both could be prescribed and shipped.

That framing packs in several claims at once, and not all of them hold up to the same degree. The science on GLP-1 and inflammation is genuinely interesting. The claim that NAD is a peptide is just wrong.

Does the science back this up?

On GLP-1 and inflammation, yes, with caveats. On NAD as a peptide, no. And the idea that subcutaneous NAD injection is the definitively "best" delivery method is far from settled.

GLP-1 receptor agonists do appear to have anti-inflammatory effects beyond their glucose and weight effects. A 2021 meta-analysis by Rakipovski et al. in Cardiovascular Diabetology found significant reductions in CRP among patients on GLP-1 receptor agonists. The LEADER trial (Marso et al., 2016, NEJM) also observed cardiovascular benefit that researchers partly attribute to reduced systemic inflammation. The creator's reference to CRP and sed rate as measurable markers is reasonable clinical shorthand, though sed rate is a pretty nonspecific marker and isn't the standard readout in most GLP-1 inflammation research.

On NAD: it is a coenzyme, not a peptide. Peptides are short chains of amino acids. NAD is a dinucleotide, a structurally different class of molecule entirely. The "500 enzymatic reactions" figure is commonly cited and roughly plausible, but conflating NAD with peptides is a basic category error. Subcutaneous NAD+ injection does exist as a clinical modality, but evidence comparing it to oral NMN or NR precursors is limited. Yoshino et al. (2021, Science) showed oral NMN improved insulin sensitivity in postmenopausal women, but head-to-head injection versus oral data in humans is sparse.

What did they get wrong (or right)?

The biggest factual error is calling NAD a peptide. It isn't. This matters because the term "peptide" carries regulatory and clinical implications, and misusing it muddies informed consent for patients deciding whether to pursue treatment.

She got the GLP-1 inflammation narrative mostly right. Calling it "potent systemic anti-inflammatory" is a bit of an oversell since the mechanism is still being characterized, but the lab-value reference is grounded in real data. Researchers like Drucker (2018, Cell Metabolism) have documented anti-inflammatory signaling through GLP-1 receptors on immune cells, which gives the claim a legitimate scientific basis.

The claim that NAD decreases with age is accurate. Verdin (2015, Science) and others have documented age-related NAD+ decline in multiple tissues. The link to fatigue is biologically plausible but not definitively proven as a primary cause in otherwise healthy adults. The assertion that injection is the "best way" to supplement it is unsupported by comparative human trial data.

What should you actually know?

If you're considering either of these compounds, here's what the evidence actually supports, without the marketing framing.

• NAD is not a peptide. If a creator or clinic calls it one, that's either a mistake or a red flag about how rigorously they're vetting information.
• GLP-1 receptor agonists (like semaglutide or tirzepatide) do have real, measurable anti-inflammatory effects in clinical populations, particularly people with obesity, metabolic syndrome, or type 2 diabetes. Whether this extends to lean, otherwise healthy individuals is less clear.
• NAD+ precursors (NMN, NR) have more human trial data than injectable NAD+ at this point. Injection may have faster bioavailability but the clinical outcomes evidence hasn't caught up.
• CRP is a reasonable inflammation marker. Sed rate is much less specific and less commonly used in GLP-1 research. Citing both together sounds more comprehensive than it is.
• Both compounds are being actively researched. Neither has enough long-term human data to be called definitively "better than any other supplement." That's a marketing claim, not a clinical one.

Anyone seeing a telehealth provider for these compounds should ask specifically which peptide or compound is being prescribed, what the evidence base is for their specific condition, and whether the compounded version they're receiving has been third-party tested.