
Finding the right dosage for any medication is essential, as everyone responds differently. This is equally true for GLP-1 medications. Our clinical team will work closely with you to determine the most suitable dose, balancing the desired effects with any side effects you may experience.
Mounjaro, for example, has three stable treatment doses: 5mg, 10mg, and 15mg. Additionally, there are intermediary doses of 2.5mg, 7.5mg, and 12.5mg, which help transition between these stable doses.
In practice, this means that treatment with Mounjaro will typically begin at 2.5mg per week for the first four weeks. If you tolerate this well and experience no significant side effects, we will generally increase the dose to 5mg from the second month. However, if you do experience side effects, we may keep you on 2.5mg for a longer period to allow your body time to adjust before increasing the dose.
Once you reach 5mg, we will usually maintain this dose for a few months unless your weight loss progress is minimal. While progress varies between individuals, a useful benchmark is a minimum weight loss of approximately 1% of your starting weight per month.
If you continue to make good progress at 5mg, we may agree that there is no need to increase the dose further. You can remain on this dose for as long as necessary. However, if progress slows, we may increase the dose to 7.5mg for a month or two before stepping up to the next stable dose of 10mg.
At this stage, we would typically maintain the 10mg dose for a few months. Together, we will keep an eye on your progress and decide whether to continue at this level or increase to the maximum dose if necessary.
Our goal is gradual and sustainable weight loss. GLP-1 treatment is not a "quick fix" but rather a long-term approach to improving your health and maintaining a healthy weight.
What happens when I reach my goal weight?
Once you achieve your target, we will work with you to determine the most appropriate dose to maintain your weight. For some, this will be the current dose, while others may step down to the next stable dose. Our clinical team will closely monitor your progress and help you find the right dosage to maintain a healthy weight and overall well-being.
Dr Matthew Noble

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.
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.
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.
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.
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 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 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.
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.
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.
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.
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.

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, 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.
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.
The mechanisms underlying the glaucoma-protective effects of GLP-1 RAs are under active investigation. The following pathways are most frequently proposed:
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.
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).
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:
This emphasises the need for careful patient selection and counselling, as well as integrated care between diabetologists, general practitioners, and ophthalmologists.
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:
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.
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.