Is there herb or extract the increases Glp1 and gip
Executive summary
Multiple herbs and plant extracts have been reported to stimulate GLP‑1 secretion or activity in cell and animal studies, and a few small human trials show modest effects, but evidence for reliably increasing GIP is sparse and inconsistent; most claims rest on preliminary lab work, mixed human data, or commercial extrapolation [1] [2] [3] [4]. Clinically meaningful, reproducible increases comparable to pharmaceutical GLP‑1/GIP agonists are not established, and safety, dosing, and drug interactions remain major unresolved questions [5] [6].
1. Which herbs are tied to GLP‑1 increases in the literature?
Reviews and experimental papers list a set of phytochemicals and herbal extracts—berberine, green/black tea polyphenols, curcumin (turmeric), cinnamon, soybean/wheat components, resveratrol and gardenia—as agents that can influence GLP‑1 release or signaling in preclinical studies and some human contexts [1]. Specific extracts have mechanistic support: Gentiana scabra root extract stimulates GLP‑1 secretion from human enteroendocrine cells via a G‑protein βγ pathway and lowered glucose in diabetic mice, with loganic acid identified as an active bitter iridoid in vitro [2]. Gardenia compounds were computationally predicted to bind the GLP‑1 receptor and some in vitro work suggests gardenia‑containing formulas stimulate GLP‑1 secretion [7].
2. Are there human trials showing herbal GLP‑1 effects?
Human data exist but are limited and modest: a South American herbal combination (yerba mate, guarana and damiana, labeled “YGD”) raised post‑breakfast GLP‑1 AUC and reduced lunch energy intake in overweight women in a controlled trial, indicating a measurable hormonal and behavioral effect in people [3]. Other human‑facing sources report associations—like dark chocolate flavanols or Mediterranean dietary fats with higher postprandial GLP‑1—but these are dietary interventions rather than isolated herb/extract drug‑like effects and vary by study design [8] [9].
3. What about GIP—do herbs or extracts increase it too?
The literature compiled here emphasizes GLP‑1 far more than GIP; dual incretin activation (GLP‑1/GIP) is the basis for pharmaceutical agents like tirzepatide, but comparable herbal evidence for reliably raising GIP is scant [10]. Some in vitro work shows certain tastants and sweeteners can stimulate both GLP‑1 and GIP in cell lines, yet human trials often fail to replicate those findings for non‑nutritive sweeteners, underscoring a translational gap for GIP specifically [2]. Practical claims about herbs that boost GIP lack robust human evidence in the sources provided.
4. How strong is the evidence and what are the caveats?
Most positive signals come from in vitro assays, animal models or small human trials and systematic reviews caution that human efficacy and safety data are limited; reviews and clinical nutrition syntheses note that many botanical effects on glycemic control are only “limited” or “fair” in quality and that supplements can carry risks including interactions and liver injury [6] [1] [5]. Berberine exemplifies the tradeoff: it is repeatedly flagged as metabolically active with GLP‑1–related pathways in some reports but also causes gastrointestinal side effects and interacts with other drugs [5]. Commercial blends and branded extracts promise GLP‑1 boosts but often rest on small or non‑peer‑reviewed studies [11].
5. Practical interpretation: what can be concluded now?
Taken together, there are herbs and extracts—berberine, bitter melon, yerba mate, gardenia, Gentiana scabra and several polyphenol‑rich foods—that show signals for increasing GLP‑1 secretion in cells, animals, and isolated human studies [1] [2] [4] [3] [7]. Evidence that any herb reliably and safely elevates GIP in humans is weak in these sources [2] [10]. Clinical-grade GLP‑1/GIP agonists remain far more potent and predictable; the herbal literature supports further research but does not justify substituting plant extracts for prescribed incretin therapies or assuming equivalent effects [10] [6].