Feeling constantly hungry, battling random cravings, or feeling like your body is “working against you” is not a personal failing. GLP-1, a key hormone that regulates appetite, fullness, and blood sugar, plays an important role in these experiences.
It is released from intestinal L-cells after eating and helps stimulate insulin, reduce glucagon, slow stomach emptying, and promote satiety, making it central to metabolic health and a major target in obesity and type 2 diabetes care.
Medications like semaglutide and tirzepatide are designed to mimic or enhance GLP-1 activity, but everyday dietary choices can also help support your body’s own GLP-1 response.
Research suggests that people with higher natural GLP-1 responses may eat around 20–30% fewer calories after a meal, highlighting how powerful this hormone can be in shaping appetite. The following article focuses on six food categories rich in specific nutrients that may naturally stimulate GLP-1 release and help you feel more satisfied throughout the day.
Six Everyday Foods That May Naturally Boost GLP-1 Levels
Supporting your body’s natural GLP-1 response may be simpler than many people expect. Below are six food categories that research has linked with GLP-1 activity, along with practical ways they are commonly included in everyday diets.
Eggs
Starting the day with eggs is a common dietary choice in many balanced eating patterns. Eggs provide a source of high-quality protein and fats, nutrients that have been studied for their potential role in supporting feelings of fullness after meals.
Some research suggests that meals higher in protein, including those containing eggs, may be associated with improved post-meal blood sugar responses and increased satiety when compared with higher-carbohydrate breakfasts. These effects are thought to involve appetite-regulating hormones such as GLP-1 and peptide YY (PYY), which play a role in signalling fullness.
Including eggs as part of breakfast may help some people feel more satisfied for longer and support overall dietary balance. As with all foods, individual responses can vary, and eggs are best consumed as part of a varied, nutritious diet.
Certain Types of Nuts
Nuts such as almonds, pistachios, and peanuts provide a combination of protein, unsaturated fats, and dietary fibre that slows gastric emptying, supports insulin sensitivity, and is associated with increased GLP-1 release and satiety.
Regular nut intake has been linked with improved glycaemic control, greater fullness, and reduced risk markers for type 2 diabetes and cardiovascular disease in clinical and epidemiological studies.
Fermentation of nut fibre by gut bacteria produces short-chain fatty acids, which can stimulate GLP-1 secretion from intestinal L-cells through dedicated receptors and related metabolic pathways.
If you are not allergic to nuts, include a small handful of nuts as a snack or add them to meals like yoghurt, salads, or porridge as a practical way to support natural GLP-1 activity and promote fullness. Evidence suggests that nut-based snacks can enhance satiety and modulate appetite-regulating hormones, including GLP-1, compared with refined-carbohydrate options.
High Fibre Grains
Whole grains such as oats, barley, and whole wheat are rich in soluble fibre, which helps smooth out post-meal rises in blood glucose and is associated with increased GLP-1 secretion and improved satiety. Soluble fibre forms a gel-like texture in the gut that slows digestion and glucose absorption, providing a more gradual stimulus for appetite-regulating hormones like GLP-1 and PYY.
A key part of this effect comes from fermentation of fibre by gut bacteria into short-chain fatty acids (SCFAs) such as acetate, propionate, and butyrate, which can activate receptors on intestinal L-cells and promote GLP-1 release. Randomised controlled trials have shown that high-fibre, oat-based meals can increase GLP-1 and PYY levels, enhance fullness, and reduce subsequent energy intake compared with low-fibre cereals.
Choosing high-fibre grains like oats and barley in place of refined grains (for example, white bread or sugary cereals) is a practical, research-supported way to support natural GLP-1 activity and appetite regulation. People with coeliac disease or gluten intolerance should select certified gluten-free whole-grain options and seek personalised dietary advice where needed.
Avocado
Avocado is a source of monounsaturated fats and soluble fibre, nutrients that are commonly associated with supporting satiety and digestive comfort. Soluble fibre can contribute to slower digestion and more gradual nutrient absorption, while unsaturated fats are often included in dietary patterns linked with metabolic health.
Some research has explored the relationship between avocado consumption and post-meal hormonal responses, including appetite-regulating hormones such as GLP-1 and peptide YY (PYY). These studies suggest that meals containing avocado may be associated with greater feelings of fullness and more stable post-meal insulin responses in some individuals.
Including avocado in meals such as salads or sandwiches may help support satiety as part of a balanced diet. Individual responses can vary, and avocado is best consumed alongside a variety of other nutrient-rich foods.
Olive Oil
Olive oil is a key component of Mediterranean-style eating patterns and is a source of monounsaturated and polyunsaturated fats. Diets that include higher proportions of unsaturated fats are commonly associated with cardiometabolic health and may influence post-meal satiety responses.
Research examining Mediterranean dietary patterns has explored their relationship with appetite-regulating hormones, including GLP-1. Some studies suggest that meals rich in unsaturated fats, such as those containing olive oil, may be associated with differences in post-meal hormonal responses and markers of glycaemic control when compared with lower-fat dietary approaches. These effects are thought to involve interactions between dietary fats and gut-derived hormones, although the exact mechanisms are still being studied.
Using olive oil in cooking or as a salad dressing can be a practical way to include unsaturated fats as part of a balanced diet. As with all dietary choices, individual responses may vary, and olive oil is best consumed in moderation alongside a variety of nutrient-rich foods.
Vegetables
Non-starchy vegetables such as Brussels sprouts, broccoli, and carrots provide dietary fibre, vitamins, and a range of plant compounds that support overall nutritional quality. Fibre-rich foods are commonly associated with digestive health and may influence feelings of fullness after meals.
Some research has examined how the order in which foods are consumed -such as eating vegetables before carbohydrate-rich foods-may affect post-meal glucose responses and appetite-related hormones, including GLP-1. These studies suggest that prioritising vegetables earlier in a meal may be associated with more gradual rises in blood glucose and differences in satiety signals, particularly in certain populations. The underlying mechanisms are still being explored and may involve interactions between dietary fibre, digestion, and gut-derived signals.
Including non-starchy vegetables as part of the first course of a meal can be a practical way to increase fibre intake and support balanced blood sugar responses as part of an overall healthy eating pattern. Individual responses may vary.
How Food May Actually Trigger GLP-1?
The secretion of GLP-1 is closely linked to nutrient sensing by L-cells in the distal small intestine and colon. Specific nutrients, including proteins, peptides, fatty acids, and monosaccharides, interact with G-protein coupled receptors and transporters on L-cells, triggering intracellular signalling cascades that culminate in GLP-1 exocytosis.
Protein ingestion, for example, leads to the generation of peptides and amino acids that bind to calcium-sensing receptors and other nutrient sensors on L-cells, directly stimulating GLP-1 release. Similarly, mono- and polyunsaturated fats activate free fatty acid receptors (FFAR1 and FFAR4), while fibre-derived SCFAs interact with FFAR2 and FFAR3 to promote GLP-1 secretion.
Overall, protein, healthy fats, and dietary fibre represent the three main dietary triggers for endogenous GLP-1 release. Their combined presence in whole, minimally processed foods accounts for the satiety-enhancing and glucose-lowering effects observed in dietary intervention studies.
Fibre and Gut Health Synergy
The interplay between dietary fibre, gut microbiota, and GLP-1 secretion exemplifies the complex synergy underlying metabolic health. Fibre that escapes digestion in the upper gastrointestinal tract is fermented by colonic bacteria, resulting in the production of SCFAs such as acetate, propionate, and butyrate. These SCFAs serve as signalling molecules that activate FFAR2 and FFAR3 on L-cells, directly inducing GLP-1 release.
This gut microbiota-mediated mechanism not only enhances GLP-1 secretion but also confers additional metabolic benefits, including improved insulin sensitivity, reduced inflammation, and maintenance of gut barrier integrity. The inclusion of high-fibre foods such as whole grains, nuts, vegetables, and legumes thus represents a cornerstone of dietary strategies aimed at boosting GLP-1 and supporting overall metabolic health.
Conclusion
Dietary patterns that include adequate protein, fibre, and unsaturated fats are commonly associated with satiety, balanced blood sugar responses, and overall metabolic health. Foods such as eggs, nuts, high-fibre grains, avocado, olive oil, and non-starchy vegetables provide a range of nutrients that have been studied for their potential association with appetite-regulating hormones, including GLP-1. These foods contribute to feelings of fullness and may support steadier post-meal glucose responses as part of a balanced diet.
Research exploring GLP-1 has primarily focused on its role in appetite regulation and glucose metabolism. While diet alone is not a treatment for metabolic conditions, nutritional approaches that prioritise whole, fibre-rich, and protein-containing foods are widely recommended to support long-term health. Individual responses can vary, and dietary strategies are most effective when tailored to personal needs, preferences, and medical guidance.
For those exploring structured weight-management support, clinically supervised programmes can help integrate nutrition, lifestyle, and medical considerations in a safe and evidence-informed way.
If you would like to learn more about medically supported weight-management options, SheMed offers personalised programmes designed to align with individual health goals. Eligibility assessment is available online to help determine whether a programme may be suitable.
References
- Holst, J. J. (2007). The physiology of glucagon-like peptide 1. Physiological Reviews, 87(4), 1409-1439. https://doi.org/10.1152/physrev.00034.2006
- Ratliff J, Leite JO, de Ogburn R, Puglisi MJ, VanHeest J, Fernandez ML. Consuming eggs for breakfast influences plasma glucose and ghrelin, while reducing energy intake during the next 24 hours in adult men. Nutrition Research. 2010 Feb 1;30(2):96-103.https://www.sciencedirect.com/science/article/abs/pii/S0271531710000035
- Li TY, Brennan AM, Wedick NM, Mantzoros C, Rifai N, Hu FB. Regular consumption of nuts is associated with a lower risk of cardiovascular disease in women with type 2 diabetes. The Journal of Nutrition. 2009 Jul 1;139(7):1333-8.https://www.sciencedirect.com/science/article/pii/S00223166
- Esposito K, Maiorino MI, Ciotola M, et al. Effects of a Mediterranean-style diet on the need for antihyperglycemic drug therapy in patients with newly diagnosed type 2 diabetes: a randomised trial. Ann Intern Med. 2009;151(5):306-314. doi:10.7326/0003-4819-151-5-200909010-00004.
- Indarto D, Rochmah DN, Wiboworini B, Pratama YM, Wibowo YC. Effects of Vegetables Consumption Before Carbohydrates on Blood Glucose and GLP-1 Levels Among Diabetic Patients in Indonesia. Int J Prev Med. 2022;13:144. Published 2022 Nov 23. doi:10.4103/ijpvm.IJPVM_704_20
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The content on the SheMed blog is provided for general informational and educational purposes only. While SheMed provides professional weight loss services and strives to ensure the information shared is accurate and up to date, we make no representations or guarantees as to its accuracy, completeness, or timeliness. This content should not be taken as personal medical advice or a substitute for consultation with a qualified healthcare provider. Always speak with your doctor or licensed medical professional about your individual health or medical needs before starting any new treatment or programme. Never disregard or delay seeking professional medical advice because of something you have read on this site. SheMed is not responsible for any actions you may take based on the information provided in this blog.
Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), such as semaglutide (Wegovy) and liraglutide, are transforming the management of type 2 diabetes mellitus (T2DM) and obesity. Everyone is well-versed in their effects on blood sugar, weight, and the cardiovascular system.
One area of growing clinical interest is the impact of GLP-1 RAs on eye health, specifically their relationship with glaucoma, a progressive optic neuropathy that can lead to irreversible vision loss.
According to the National Health Service (NHS), glaucoma is a significant public health concern, with chronic open-angle glaucoma affecting approximately 480,000 people across the country.
Recent research supported by large-scale retrospective studies suggests that GLP-1 RAs are associated with a reduced risk of glaucoma incidence, particularly primary open-angle glaucoma (POAG), compared with other antidiabetic agents. This article provides a comprehensive, evidence-based analysis of the current state of knowledge regarding GLP-1 RAs and glaucoma risk.
GLP-1 RAs and Glaucoma
GLP-1 RAs, also known as incretin mimetics, are a class of drugs that enhance glucose-dependent insulin secretion, suppress glucagon release, delay gastric emptying, and promote satiety, making them effective treatments for T2DM and obesity. Semaglutide, in particular, has gained widespread attention due to its efficacy in both glycaemic control and weight reduction.
Glaucoma is an umbrella term for a group of optic neuropathies characterised by progressive loss of retinal ganglion cells (RGCs) and corresponding visual field defects, frequently but not exclusively associated with elevated intraocular pressure (IOP). The most common subtype, primary open-angle glaucoma (POAG), is a leading cause of irreversible blindness worldwide. Diabetes is a well-recognised risk factor for glaucoma, likely due to shared pathways involving vascular dysregulation, oxidative stress, and neurodegeneration.
The Current Clinical Evidence
Several robust observational studies have investigated the association between GLP-1 RA use and glaucoma risk. Population-based registry analyses from Denmark and large US cohort studies consistently demonstrate a protective signal. Research, like a Danish nationwide case control study, found that patients with T2DM initiating GLP-1 RA therapy had a 19–29% lower risk of developing POAG compared to those prescribed other anti-diabetic agents. These findings further suggest that the magnitude of risk reduction increases with the duration of GLP-1 RA exposure; patients using these agents for more than three years experienced the most pronounced benefits.
Importantly, emerging data indicate that the glaucoma-protective effect of GLP-1 RAs may extend beyond patients with diabetes. Observational analyses in obese, non-diabetic individuals prescribed GLP-1 RAs for weight management also show a reduced risk of incident glaucoma.
This suggests the benefit may not solely be attributabled to improved glycaemic control and may instead reflect a direct neuroprotective action. While these findings are compelling, it is crucial to acknowledge the limitations inherent in observational research, including residual confounding and potential selection bias.
Nevertheless, the consistency and magnitude of the association, alongside plausible biological mechanisms, strengthen the case for a genuine effect.
How GLP-1s Protect the Eye?
The mechanisms underlying the glaucoma-protective effects of GLP-1 RAs are under active investigation. The following pathways are most frequently proposed:
- Neuroprotection: GLP-1 receptors are expressed on retinal ganglion cells (RGCs), the primary targets in glaucoma. Agonism of these receptors may inhibit RGC apoptosis by modulating intracellular signalling pathways, enhancing cell survival, and reducing excitotoxicity. This is consistent with broader neuroprotective paradigms observed in stroke and neurodegeneration, where targeting multi-modal pathways (including inflammatory and apoptotic cascades) can yield meaningful protection.
- Anti-Inflammatory Action: GLP-1 RAs exert systemic and tissue-specific anti-inflammatory effects. In the eye, they may dampen microglial activation and inhibit the release of pro-inflammatory cytokines, reducing oxidative stress and interrupting the inflammatory cycles that drive glaucomatous damage.
- IOP Modulation (The Hypothesis): Some preclinical studies suggest that GLP-1 RAs may influence aqueous humour dynamics, potentially lowering IOP, although this effect appears less robust than their neuroprotective actions. The overall reduction in glaucoma risk observed in non-glaucomatous, normotensive populations supports the idea of a pressure-independent mechanism.
Collectively, these mechanisms align with contemporary theories of glaucoma pathogenesis as a neurodegenerative disease with vascular and inflammatory components, not simply one of elevated IOP.
Ocular Risks to be Vigilant About
While the evidence for a glaucoma-protective effect is encouraging, clinicians should balance this against specific ocular safety considerations associated with GLP-1 RAs. These include the potential for diabetic retinopathy progression and the rare but serious risk of non-arteritic anterior ischemic optic neuropathy (NAION).
Diabetic Retinopathy (DR) Progression
A paradox exists in the relationship among GLP-1 RAs, glycaemic control, and progression of diabetic retinopathy (DR). Long-term glycaemic improvement is unequivocally beneficial for retinopathy risk, yet rapid reductions in glycated haemoglobin (HbA1c), particularly greater than 2% over a short period, can transiently worsen pre-existing, advanced DR. This phenomenon was highlighted in the SUSTAIN-6 trial, where patients with advanced baseline DR who experienced rapid HbA1c declines on semaglutide had higher rates of retinopathy progression compared to controls.
Key clinical implications include:
- Baseline eye examination is essential before or shortly after initiating GLP-1 RA therapy, particularly in patients with advanced DR.
- Gradual titration and individualised glycaemic targets may mitigate the risk of rapid retinopathy progression.
- Ongoing surveillance is recommended, especially during the first year of treatment.
This emphasises the need for careful patient selection and counselling, as well as integrated care between diabetologists, general practitioners, and ophthalmologists.
Non-Arteritic Anterior Ischemic Optic Neuropathy (NAION)
NAION is characterised by sudden, painless visual loss due to infarction of the optic nerve head in the absence of giant cell arteritis. While rare, several post-marketing reports and some large database studies suggest a possible increased risk of NAION associated with certain GLP-1 RAs, including semaglutide.
The proposed mechanism involves systemic fluctuations in blood pressure and glucose, which, when superimposed on a “disc at risk” (an anatomically crowded optic nerve head), may precipitate ischemic events. Patients with diabetes, hypertension, hyperlipidaemia, and established small vessel disease are particularly susceptible.
Clinical recommendations include:
- Screening for NAION risk factors before and during GLP-1 RA therapy.
- Prompt evaluation of any new, sudden visual symptoms.
- Patient education regarding the signs and symptoms of NAION.
Mechanistic Parallels: Neuroprotection Beyond the Eye
The neuroprotective properties of GLP-1 RAs in glaucoma reflect a broader paradigm shift in the management of neurodegenerative diseases, emphasising multi-modal strategies that target not only acute injury but also the chronic processes underpinning neuronal loss. Lessons from preclinical and translational research in cerebral ischemia and stroke illuminate both the promise and challenges of neuroprotective therapy.
Amato and Arnold (2020) provided additional mechanistic clarity, modelling the activation of microglia and the balance between pro- and anti-inflammatory phenotypes (M1 and M2) in ischemic stroke. Their results suggest that early inhibition of M1 (pro-inflammatory) activation and support of M2 (anti-inflammatory) activation can shift the neuroinflammatory milieu towards tissue repair and recovery. By extension, GLP-1 RAs through their modulation of microglial activation may replicate these neuroprotective dynamics in the optic nerve, offering a biological rationale for the observed reduction in glaucoma risk.
Conclusion
Current research has examined a possible association between GLP-1 receptor agonist use and glaucoma-related outcomes, but the evidence remains limited and observational. Proposed neurobiological mechanisms have not been conclusively established, and no protective effect has been confirmed.
Existing literature highlights the importance of clinical awareness of ocular changes, particularly in people with diabetes, including transient changes in diabetic retinopathy and rare optic nerve events. Clinical decisions should continue to follow approved indications, individual patient factors, and established guidelines.
Further prospective and randomised studies are needed to clarify any relationship between GLP-1 receptor agonists and glaucoma, as well as their long-term ocular safety.
References
- Amato S, Arnold A. Modelling Microglia Activation and Inflammation-Based Neuroprotectant Strategies During Ischemic Stroke. Bull Math Biol. 2021 May 12;83(6):72. doi: 10.1007/s11538-021-00905-4. PMID: 33982158. https://pubmed.ncbi.nlm.nih.gov/33982158/
- Niazi, Siar et al.Association between Glucagon-like Peptide-1 Receptor Agonists and the Risk of Glaucoma in Individuals with Type 2 Diabetes. Ophthalmology, Volume 131, Issue 9, 1056 - 1063https://www.aaojournal.org/article/S0161-6420(24)00171
- NHS UK Glaucoma Prevalence Statistics NHS. (2023, October 13). Glaucoma.https://www.nhs.uk/conditions/glaucoma/
- Amaral DC, Guedes J, Cruz MRB, Cheidde L, Nepomuceno M, Magalhães PLM, Brazuna R, Mora-Paez DJ, Huang P, Razeghinejad R, Schuman JS, Myers JS. GLP-1 Receptor Agonists Use and Incidence of Glaucoma: A Systematic Review and Meta-Analysis. Am J Ophthalmol. 2025 Mar;271:488-497. doi: 10.1016/j.ajo.2024.12.024. Epub 2024 Dec 27. PMID: 39732312.https://pubmed.ncbi.nlm.nih.gov/39732312/
For most of my life, I knew something wasn’t right. I had every resource at my fingertips – access to specialists, a degree in nutrition, and a family with a background in healthcare, yet I was trapped in a body that didn’t make sense to me.
For years, I lived with excruciating pain, bloating, and cysts that would send me to the hospital time and time again. I had surgeries, ultrasounds, endless blood tests and still, no one could tell me why this was happening. It took nearly a decade before I finally received the diagnosis that explained everything: Polycystic Ovary Syndrome (PCOS).
Getting that diagnosis was both disheartening and liberating. Disheartening because I’d spent ten years fighting for an answer but liberating because, at last, I knew what I was up against. For the first time, I could treat the root cause instead of just the symptoms.
This is when my GLP-1 journey began and I was able to experience SheMed through a completely new lens; a member. It’s hard to put into words how much it changed my life. Within months, the chronic pain that had defined my every day; the sharp pelvic aches, the fatigue, the inflammation began to fade. For the first time in my adult life, I felt normal.
As someone who studied nutrition, played three sports, and still to this day works out five days a week, I’ve always lived an active and healthy lifestyle. Yet despite doing “everything right,” I couldn’t lose the extra weight brought on by my PCOS. On GLP-1s, my body finally responded. I shed 30 pounds in a healthy, steady way. But more importantly, I finally felt like my body was working with me instead of against me.
This medication has given me my life back. That’s why I plan to continue taking it for the foreseeable future, because for me it’s not about vanity or temporary results. It’s about treating a chronic condition that has caused years of pain and frustration. Stopping it would mean stopping the only treatment that has ever truly worked for me.
I know for many, GLP-1s are part of a weight loss journey, and that’s wonderful. But for me, and for so many others, this is about much more than the number on a scale. It’s about healing from the inside out. PCOS, endometriosis, and obesity are all examples of chronic conditions, and they all deserve compassion, understanding, and long-term care.
So wherever you are on your journey, listen to your body – really listen.
Not just to the number on the scale, but to your blood work, your hormones, your energy, and always your clinicians.
Do your research. Stay consistent. Keep taking your meds.
Because the most powerful transformation isn’t what people see, it’s what’s happening within.
💗 Olivia
Co-Founder, SheMed
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