top of page

How to make your own “Manjaro” and naturally boost your own GLP-1

  • Writer: A P
    A P
  • Oct 13
  • 7 min read

Updated: Oct 20

ree

By Dr Angus Perry.

GP & Founder of GeneralPractice.AI


This blog is for healthcare professionals looking for practical, evidence-based strategies to help patients who are struggling to lose weight, particularly those who may not qualify for, or have access to, GLP-1 based medications. It focuses on actionable lifestyle measures that can enhance satiety, improve metabolic health, and support sustainable weight loss.


GLP-1 receptor agonists have been transformative. They are delivering meaniful weight loss, better glycaemic control and significant reductions in cardiometabolic risk. Markably, their benefits appear not just confined to weight loss. They include reduced systemic inflammation; favourable shifts in blood pressure and lipids; slower progression of diabetic kidney disease and much more. They even appear to have neuroprotective effects and extend healthspan.


There are important considerations regarding GLP-1 based medications:


  • Without sustained lifestyle change, weight commonly rebounds once treatment stops. Appetite returns, old patterns re-emerge, and cardiometabolic risk can creep back. [1]

"Significant weight regain occurred 8 weeks after discontinuation of anti-obesity medication and was sustained through 20 weeks." [1]

  • Access is unequal. People with higher incomes are more likely to obtain and continue these medicines, while those with fewer resources face cost, supply, and service barriers. That gap risks deepening existing health inequalities.


  • Weight loss at the expense of skeletal muscle loss. Data from the STEP-1 and SURMOUNT-1 trails suggest that up to 45% of total weight loss may derive from skeletal muscle, leading to concerns about sarcopenia. [16]


Background.

From desert lizard🦎 to diabetes medication

The tale starts with the Gila monster, a slow, beaded reptile that gorges a few times a year yet keeps its blood glucose steady. In 1992, researchers isolated exendin-4 from its saliva, a peptide that activates the human GLP-1 receptor, shares ~53% sequence homology with human GLP-1, stimulates insulin, regulates glucose, and crucially resists rapid DPP-4 degradation, giving it a ~12-hour action. A synthetic version, exenatide, became the first GLP-1 receptor agonist approved for type 2 diabetes in 2005, opening the door to today’s agents. Subsequent GLP-1RAs have been engineered by modifying human GLP-1 to increase similarity, extend duration (once-weekly options).


Gut Signal ➡️ Brain Satiety ➡️ Better Glycaemia

GLP-1 is a meal-time hormone from intestinal L-cells. It boosts glucose-dependent insulin, suppresses glucagon, slows gastric emptying, and acts on brain circuits that govern appetite and reward, increasing fullness and reducing intake. The injectable drugs are GLP-1 receptor agonists engineered to resist DPP-4 enzyme breakdown and circulate for hours to days, so they sustain those same signals all day or all week. Clinically, that translates into smaller post-meal glucose rises, less hunger, and weight loss, with short-acting agents emphasising gastric-emptying effects and long-acting agents providing steady central and pancreatic actions. [2], [3]


Learn more

🧠 Brain (satiety & reward): boosts satiety circuits and dampens food-reward drive → less appetite & intake.

🩸 Pancreas: ↑ glucose-dependent insulin, ↓ glucagon, and supports β-cell function/survival.

🍽️ Stomach: slows gastric emptying, helping smaller post-meal glucose rises and earlier fullness.

🫀 Cardiovascular system: improves endothelial signalling and reduces inflammation/oxidative stress → cardioprotection beyond glucose control.

🧠🧬 Metabolic brain–liver axis: reduces hepatic gluconeogenesis/glycogenolysis and improves lipid handling → less hepatic steatosis.

🧈➡️🔥 Adipose & muscle: enhances insulin sensitivity and favours healthier lipid metabolism, aiding fat mass reduction over time.

🚰 Kidney: anti-inflammatory/anti-fibrotic signalling with renoprotective effects (e.g., lower albuminuria).

How to increase endogenous GLP-1 (“make your own Manjaro”)


🥦 Vegetables first, carbs last

  • Open with a fist-sized portion of non-starchy veg and your protein, leave starches to the end. This meal order tempers post-meal glucose/insulin and supports higher incretin (GLP-1) signalling. In clinic, teach a simple script: “Veg → protein → starch.” Works well for packed lunches (salad + chicken first, wrap last) and dinners (veg + fish first, potatoes last). [5]


🍗 Prioritise protein at every meal

  • Protein and certain peptides directly stimulate L-cells to release GLP-1 and PYY, improving fullness. A practical target for weight management is ~1.2–1.6 g/kg/day (e.g. 90–120 g/day for a 75-kg adult), spread across 3 meals (≈30–40 g each). What that looks like: 2 eggs + 170 g Greek yoghurt ≈ 35–40 g, 120–150 g chicken/salmon/tofu ≈ 30–35 g, Protein-rich legumes (lentil/bean bowls) + a scoop of protein powder in porridge to “top up.”Adjust for renal disease or other clinical constraints. [4], [7]


🥕 Chew more, keep foods solid when possible

  • Compared with blended/pureed forms, thorough chewing of vegetables enhanced post-prandial incretin responses (including GLP-1) in an RCT. Coach patients to slow down, put the fork down between bites, and aim for ~20–30 chews per mouthful of fibrous veg. [6]


🌿 Flavonoids: food-first approach

  • Polyphenols such as quercetin and myricetin (onions, capers, berries, kale) are linked to higher GLP-1 and may inhibit DPP-4 in preclinical models, potentially prolonging active GLP-1. Build a daily habit: half a plate of colourful veg/berries, sprinkle chopped red onion or capers onto salads, and swap sweets for a berry bowl with yoghurt. [4]


🍋 Citrus for a GLP-1 nudge

  • Citrus flavonoids (e.g., eriocitrin/hesperidin from lemon) have shown increases in GLP-1 and improvements in glycaemic markers in people with dysglycaemia/prediabetes in emerging clinical data. Practical idea: water with lemon, citrus-based dressings, and, when appropriate, standardised citrus-flavonoid nutraceuticals considered on a case-by-case basis. [8], [9]

Ultra-Processed Foods (UPFs): why they matter in health & weight management


UPFs (NOVA Group 4) are industrial formulations which include refined starches, reconstituted meats, sweetened beverages, flavour enhancers, emulsifiers, and cosmetic additives. A growing evidence base links higher UPF intake with obesity and worse health across multiple systems:


  • 🫀📉 Cardiometabolic & mortality risk: Umbrella review (~9.9M participants) links UPFs to 32 adverse outcomes including CVD mortality, T2D, depression, poor sleep, wheeze, obesity, and higher all-cause mortality (evidence ranges from convincing to suggestive). [10]


  • ❤️‍🔥🥤 Cardiovascular disease: Higher UPF intake = higher CVD/CHD/stroke risk; biggest culprits include meat-based ready-to-eat products and sugar-sweetened beverages. [11]


  • ⚰️📊 All-cause mortality (cohorts): In NHS/HPFS (31–34y follow-up), highest vs lowest UPF quartile → +4% all-cause mortality and +9% non-cancer/non-CVD mortality; strongest signal from ready-to-eat meat/poultry/seafood. [12]


  • 🧠⬇️ Cognition: Greater UPF % of energy linked to faster decline in global cognition and executive function over ~8 years. [13]


  • 🧪🍔➡️📈 Causality clue (mechanisms): NIH inpatient RCT (calories/macros/fibre matched): UPF diet led to ~+500 kcal/day intake and +0.9 kg in 2 weeks vs unprocessed—implicates palatability, eating rate, energy density, and structure, not just nutrients. [14]


Clinician takeaways: Audit UPF exposure (food diary/photo recall); replace high-risk categories first (processed meats, sweetened drinks, packaged desserts); rebuild meals around veg-first + protein structure; and teach “label red flags” (reconstituted meats, emulsifiers, artificial sweeteners + flavours, long ingredient lists).



Addendum - a note of caution on magnitude and duration 🚦


Your “make your own Manjaro” habits trigger brief pulses of native GLP-1; medications deliver a sustained, super-physiological signal. Native GLP-1 spikes around meals and is cleared fast (biological half-life ≈ 2 minutes). Effects last tens of minutes to a few hours, then fade until the next meal. GLP-1RAs are engineered to resist breakdown and bind proteins, so they keep receptors engaged 24 hours (daily agents) or all week (weekly agents). [15]


References


  1. Wu, H., Yang, W., Guo, T., Cai, X. and Ji, L. (2025) ‘Trajectory of the body weight after drug discontinuation in the treatment of anti-obesity medications’, BMC Medicine, 23, 398. https://doi.org/10.1186/s12916-025-04200-0

  2. Drucker, D.J. (2018) ‘Mechanisms of action and therapeutic application of glucagon-like peptide-1’, Cell Metabolism, 27(4), pp. 740–756. https://doi.org/10.1016/j.cmet.2018.03.001

  3. Zheng, Z., Zong, Y., Ma, Y., Tian, Y., Pang, Y., Zhang, C. and Gao, J. (2024) ‘Glucagon-like peptide-1 receptor: mechanisms and advances in therapy’, Signal Transduction and Targeted Therapy, 9, article 234. Available at: https://doi.org/10.1038/s41392-024-01931-z

  4. Hira, T., Trakooncharoenvit, A., Taguchi, H. and Hara, H. (2021) ‘Improvement of glucose tolerance by food factors having glucagon-like peptide-1 releasing activity’, International Journal of Molecular Sciences, 22(12), 6623. https://doi.org/10.3390/ijms22126623

  5. Shukla, A.P., Andono, J., Touhamy, S.H., Casper, A., Iliescu, R.G., Mauer, E., Zhu, Y.S., Ludwig, D.S. and Aronne, L.J. (2017) ‘Carbohydrate-last meal pattern lowers postprandial glucose and insulin excursions in type 2 diabetes’, BMJ Open Diabetes Research & Care, 5(1), e000440. https://doi.org/10.1136/bmjdrc-2017-000440

  6. Kamemoto, K., Tataka, Y., Hiratsu, A., Nagayama, C., Hamada, Y., Kurata, K., Chiyoda, M., Ito, M. and Miyashita, M. (2024) ‘Effect of vegetable consumption with chewing on postprandial glucose metabolism in healthy young men: a randomised controlled study’, Scientific Reports, 14, 7557. https://doi.org/10.1038/s41598-024-58103-w

  7. van der Klaauw, A.A., Keogh, J.M., Henning, E., Trowse, V.M., Dhillo, W.S., Ghatei, M.A. and Farooqi, I.S. (2013) ‘High protein intake stimulates postprandial GLP-1 and PYY release’, Obesity (Silver Spring), 21(8), pp. 1602–1607. https://doi.org/10.1002/oby.20154

  8. Ramos, F.M.M., de Sousa, A.R.A., Fogaça, I.E., et al. (2023) ‘Lemon flavonoids nutraceutical (Eriomin®) attenuates intestinal dysbiosis in prediabetes and increases GLP-1 production’, Journal of Functional Foods, 114, 105295. https://onlinelibrary.wiley.com/doi/10.1002/fsn3.3654

  9. César, T.B., Barbalho, S.M., Chermut, T.R., et al. (2023) ‘Citrus flavonoids and metabolic health: focus on Eriomin® and incretin pathways—a narrative review’, Nutrients, 15(1), 235. https://pmc.ncbi.nlm.nih.gov/articles/PMC12401686/

  10. Lane, M.M., Gamage, E., Du, S., Ashtree, D.N., McGuinness, A.J., Gauci, S., Barr, P., et al. (2024) ‘Ultra-processed food exposure and adverse health outcomes: umbrella review of epidemiological meta-analyses’, BMJ, 384, e077310. https://doi.org/10.1136/bmj-2023-077310.

  11. Mendoza, K., Smith-Warner, S.A., Rossato, S.L., Khandpur, N., Manson, J.E., Qi, L., Rimm, E.B., et al. (2024) ‘Ultra-processed foods and cardiovascular disease: analysis of three large US prospective cohorts and a systematic review and meta-analysis of prospective cohort studies’, The Lancet Regional Health – Americas, 37, 100859. https://doi.org/10.1016/j.lana.2024.100859.

  12. Fang, Z., Rossato, S.L., Hang, D., Khandpur, N., Wang, K., Lo, C-H., Willett, W.C., Giovannucci, E.L. and Song, M. (2024) ‘Association of ultra-processed food consumption with all cause and cause specific mortality: population based cohort study’, BMJ, 385, e078476. https://doi.org/10.1136/bmj-2023-078476.

  13. Gonçalves, N.G., Ferreira, N.V., Khandpur, N., Martinez-Steele, E., Levy, R.B., Lotufo, P.A., Bensenor, I.M., Caramelli, P., Matos, S.M.A., Marchioni, D.M. and Suemoto, C.K. (2023) ‘Association between consumption of ultraprocessed foods and cognitive decline’, JAMA Neurology, 80(2), pp. 142–150. https://doi.org/10.1001/jamaneurol.2022.4397.

  14. Hall, K.D., Ayuketah, A., Brychta, R., Cai, H., Cassimatis, T., Chen, K.Y., Chung, S.T., et al. (2019) ‘Ultra-processed diets cause excess calorie intake and weight gain: an inpatient randomized controlled trial of ad libitum food intake’, Cell Metabolism, 30(1), pp. 67–77.e3. https://doi.org/10.1016/j.cmet.2019.05.020.

  15. He, Y.L., Nosaka, K., Kometani, M. and Shikata, E. (2010) ‘Hormonal and metabolic effects of morning or evening administration of vildagliptin in patients with type 2 diabetes’, Clinical Drug Investigation, 30(11), pp. 713–721. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2909805/

  16. Sanchis-Gomar, F., Neeland, I.J. and Lavie, C.J. (2025) ‘Balancing weight and muscle loss in GLP1 receptor agonist therapy’, Nature Reviews Endocrinology, 21, pp. 584–585. Available at: https://www.nature.com/articles/s41574-025-01160-6

 
 
 
bottom of page