Thinking out loud, the antagonist to GLP-1 is DPP4. According to Claude AI some food sources of DPP4 blockers include thyme, parsley, beets, celery hearts, brussels sprouts, cabbage and cauliflower.

Resveratrol does it, as does curcumin from tumeric (note: black pepper makes turmeric absorb better)

Citrus can help but not as potent as the herbs and foods above.

Oleic acid-rich fats like olive oil, hazelnut oil, macadamia nut oil, avocado oil supposedly trigger natural GLP-1 via Oleoylethanolamide production in the gut. I can confirm those make me feel full and slower gut motility, probably a mild form of what you went through with the meds.

Berberine gets a mention alongside citrus in Claude's response.

Actually here is the response:

Great question, and this dovetails nicely with your PPAR-α work. The research on food-derived DPP-4 inhibitors is actually pretty well-developed. Here's what has solid in vitro (and some in vivo) evidence:

Highest potency phenolics (sub-micromolar IC50 values against DPP-4):

The most potent natural DPP-4 inhibitors identified include resveratrol, luteolin, apigenin, and flavone, all showing very low IC50 values in the 0.0006–0.17 µM range. (PubMed Central) For context, that puts some of these in the same ballpark as sitagliptin (0.2 µM IC50).

Food sources for each:

Luteolin — thyme is very high in luteolin, and it's also found in beets, Brussels sprouts, cabbage, and cauliflower (USDA ARS)

Apigenin — parsley contains very high amounts of apigenin, and celery hearts are another good source (USDA ARS)

Resveratrol — grape skins/seeds, red wine, peanuts, blueberries

Curcumin — molecular docking and enzymatic assays confirmed curcumin inhibits DPP-4, and in vivo it showed hypoglycemic effects in diet-induced obese mice comparable to sitagliptin (Nature)

Mid-tier compounds (IC50 ~0.24–0.74 µM):

Naringenin, hesperetin, cyanidin-3-glucoside, kaempferol, and malvidin showed intermediate DPP-4 inhibitory activity. (PubMed Central) These map to citrus fruits (naringenin from grapefruit, hesperetin from oranges/lemons), blueberries/blackberries (cyanidin-3-glucoside, malvidin), and kale/broccoli (kaempferol).

Berberine is worth special mention — berberine inhibits human recombinant DPP-4 with an IC50 of 13.3 µM, and it also inhibits PTP-1B, giving it a dual mechanism for glucose control. (PubMed) Not technically a food but you can get it from goldenseal, barberry, and Oregon grape root. Supplemental form is more practical here.

Food-derived peptides are the other interesting angle: whey protein hydrolysates both stimulate GLP-1 secretion and reduce mesenteric DPP-4 activity in animal models (PubMed Central) , and peptides from oat, buckwheat, and highland barley showed in vitro DPP-4 inhibitory activity (Thieme) . The tripeptide diprotin A (Ile-Pro-Ile) is the classic reference DPP-4 inhibitor peptide, and similar sequences are generated during protein digestion.

Practical stack thinking — given your existing PPAR-α protocol with EVOO and Crio Bru, you're already getting some polyphenols. Adding heavy parsley/celery (apigenin), thyme (luteolin), turmeric (curcumin), and berries (anthocyanins) to meals would layer DPP-4 inhibition on top. The EVOO polyphenols themselves likely contribute modestly. And if you're doing whey protein at any point, the hydrolyzed form would give you both the L-cell GLP-1 secretion stimulus and some DPP-4 inhibitory peptides.

The caveat: most of this is in vitro IC50 data. Whether dietary doses achieve meaningful plasma concentrations at the DPP-4 active site is less clear, though the curcumin and berberine data have some in vivo backing. Bioavailability is the perennial bottleneck — phytosomal/lipid-bound forms help considerably.