How to raise GLP-1 naturally: what your body can do
Your body builds the satiety hormone GLP-1 itself. It releases it after eating, mostly in response to protein, fibre and the fatty acids made by your gut bacteria. What you can eat to strengthen that response, what the studies show, and why natural Ozempic is still marketing.
Ever since the weight-loss injections took over the headlines, one promise pops up everywhere: natural Ozempic. The salad, the tea, the powder that supposedly does the same as the injection, just without a prescription. That is marketing, and I want to be honest with you. What is true: your body makes GLP-1 itself, every day, after every meal. And what you eat shapes how strong that response is. Protein, fermentable fibre and a well-fed microbiome can raise your body's own GLP-1 release. That is real and supported by good human studies. But the effect is clearly smaller and shorter than the medication. Here I show you what the body can really do, where the limit is, and why the natural route is still the sensible foundation.
This spoke belongs to the weight cluster and answers a question I am often asked in the practice: can I stimulate my satiety hormone through food instead of injecting it? We walk through what GLP-1 even is, how your gut makes it, which nutrients may strengthen the response, what the studies show, where the honest limit to the medication lies, and which three levers you can try. How the weight-loss injection works in detail is covered by its own spoke.
What GLP-1 actually is
Many people first hear of GLP-1 in connection with an injection. Yet it is an ancient body-own hormone. The name stands for glucagon-like peptide 1. It is made by special cells in your gut wall, the so-called L cells. Whenever food travels through the gut, these cells release GLP-1 into the blood. From there it sends two messages: to the pancreas, to release more insulin to match the sugar, and to your brain, that you are full.
GLP-1 is therefore not a foreign substance. It is a signal your body produces constantly to fine-tune satiety, blood sugar and appetite. The catch: your own GLP-1 does not last long. An enzyme breaks it down again within minutes. That is exactly why the question is interesting whether food can strengthen the body's own release.
What GLP-1 does in the body
Review Daniel Drucker and Jens Holst, two of the most important researchers in this field, summarised the biology of the incretin hormones in Diabetologia in 2023. Core message: GLP-1 from the L cells strengthens the insulin release to match the meal and dampens appetite via receptors in the brain. The GLP-1 receptors sit not only in the pancreas, but also in the brain, heart, gut and kidney. It is exactly this body-own satiety pathway that the weight-loss injections build on. They invent nothing new, they amplify an existing system.
Drucker DJ, Holst JJ. Diabetologia. 2023;66(10):1765-1779. doi:10.1007/s00125-023-05906-7 · PMID: 36976349
The weight-loss injection is not your body's enemy and not its replacement. It uses exactly the satiety switch your gut serves anyway. The real question is not injection or not, but: how well does your own GLP-1 system function, and what can you do to make it run better.
How your gut triggers GLP-1
There are two paths on which your food prompts GLP-1. The fast one and the slow one. Both matter, and you can influence both.
The fast path runs in the small intestine. As soon as food arrives there, the L cells sense what is passing by. Certain macronutrients, above all protein and fat, activate sensors on these cells and trigger the GLP-1 release. This happens within minutes to about two hours after eating.
The nutrient sensors of the L cells
Review Van Lu, Fiona Gribble and Frank Reimann described in Nutrients in 2021 how the L cells recognise individual nutrients. Via transporters, ion channels and special receptors on the cell surface, they register amino acids from protein, fatty acids and sugar and translate this into a GLP-1 signal. Their conclusion: because different nutrients address different sensors, the composition of a meal can shift the hormone response measurably. This is the scientific reason why WHAT you eat is not irrelevant.
Lu VB, Gribble FM, Reimann F. Nutrients. 2021;13(3):883. doi:10.3390/nu13030883 · PMID: 33803183
The slow path runs in the large intestine and is the more intriguing one. Fermentable fibre arrives there undigested. Your gut bacteria ferment it and in doing so produce short-chain fatty acids, above all acetate, propionate and butyrate. These fatty acids bind to two receptors on the L cells, FFA2 and FFA3, and may likewise prompt GLP-1. This path needs hours and an active microbiome.
How gut bacteria prompt GLP-1
Mechanism review Izumi Kaji and colleagues described the molecular path in Digestion in 2014. In the large intestine, the short-chain fatty acids from bacterial fermentation reach high concentrations. The receptors FFA2 and FFA3 on the enteroendocrine L cells recognise them and may prompt the release of GLP-1 and the related satiety hormone PYY. This describes a direct line: what your bacteria build from fibre may help steer your satiety hormones.
Kaji I, Karaki S, Kuwahara A. Digestion. 2014;89(1):31-36. doi:10.1159/000356211 · PMID: 24458110
The first lever: protein
Do you know the feeling of being full for a long time after a protein-rich meal, while a sweet breakfast sends you back to the fridge within an hour? That is no coincidence and not pure willpower. Protein addresses your satiety signals differently than sugar.
Protein is one of the strongest natural triggers of satiety. It acts through several routes at once: it can stimulate GLP-1, it slows gastric emptying, and it prompts further satiety hormones such as CCK. The evidence, honestly viewed, is nuanced, but the direction is clear.
A protein-rich breakfast and the satiety hormones
RCT, n=15 Wendy Blom and colleagues compared a protein-rich with a carbohydrate-rich breakfast in 15 healthy men in a crossover design, in The American Journal of Clinical Nutrition in 2006. The protein-rich breakfast lowered the hunger hormone ghrelin much more and slowed gastric emptying. The GLP-1 response tended to be higher, statistically borderline. The message: protein in the morning can shift the satiety signals favourably, even if not every single effect is statistically large.
Blom WAM, Lluch A, Stafleu A, et al. Am J Clin Nutr. 2006;83(2):211-220. doi:10.1093/ajcn/83.2.211 · PMID: 16469977
Protein and fat beat carbohydrates for GLP-1
RCT, n=18 Ehsan Parvaresh Rizi and colleagues tested three meals in 9 lean and 9 insulin-resistant men in PLoS One in 2018: protein-rich, fat-rich, carbohydrate-rich. Result: the protein- and the fat-focused meal produced a higher GLP-1 response than the carbohydrate-focused one, in lean and insulin-resistant men alike. Conversely, the carbohydrate-rich meal tended to dampen the satiety hormones. This supports a simple principle: if you want to strengthen your own GLP-1 response, you build meals around protein, not around fast carbohydrates.
Parvaresh Rizi E, Loh TP, Baig S, et al. PLoS One. 2018;13(1):e0191609. doi:10.1371/journal.pone.0191609 · PMID: 29385178
That leaves the question whether more GLP-1 even means less hunger. That is exactly what another study examined.
Higher GLP-1, less hunger
RCT, n=16 Catherine Gibbons and colleagues examined in 16 overweight adults how satiety hormones relate to hunger and eating behaviour, in the Journal of Clinical Endocrinology and Metabolism in 2013. Result: in the late satiety phase, GLP-1 was negatively linked with the sense of hunger and with the amount of energy consumed later. In other words: the higher the body's own GLP-1, the less hunger and the less was eaten. This shows that endogenous GLP-1 is not just a lab value, but genuinely relates to appetite.
Gibbons C, Caudwell P, Finlayson G, et al. J Clin Endocrinol Metab. 2013;98(5):E847-E855. doi:10.1210/jc.2012-3835 · PMID: 23509106
And a simple bonus lever that costs nothing: the order. Eating vegetables and protein before the starch may raise the GLP-1 response and flatten blood sugar, without changing the meal itself at all.
The order on the plate matters
RCT, n=16 Lijuan Sun and colleagues tested five isocaloric meals with different eating order of vegetables, protein and rice in 16 healthy adults, in Clinical Nutrition in 2019 (the PATTERN study). When vegetables and protein were eaten before the rice, GLP-1 release rose more strongly and the blood sugar rise was clearly flatter, without needing more insulin. The authors concluded: the order of food intake is a simple lever to influence the blood sugar and hormone response.
Sun L, Goh HJ, Govindharajulu P, Leow MK, Henry CJ. Clin Nutr. 2019;39(3):950-957. doi:10.1016/j.clnu.2019.04.001 · PMID: 31053510
The second lever: fibre and your microbiome
The protein path is fast and noticeable. The fibre path is the quieter one, but perhaps the more interesting. Because here your gut bacteria come into play, and they help decide how well the whole thing works.
Fermentable fibre is found in legumes, oats, psyllium, vegetables, unripe bananas and many unprocessed plant foods. It survives the small intestine undigested and is only fermented by bacteria in the large intestine. The product is the short-chain fatty acids that may stimulate your L cells. The strongest evidence for this comes from a particularly elegant study.
Short-chain fatty acids in the colon raise GLP-1
RCT, n=60 Edward Chambers and colleagues delivered a short-chain fatty acid, propionate, specifically into the human large intestine, packaged in a special fibre ester, in Gut in 2015. In a human colon cell model, propionate directly increased the release of PYY and GLP-1. In humans, an acute dose raised these satiety hormones and lowered the amount of energy consumed. Over 24 weeks, the daily intake slowed weight gain and the gain in belly fat in 60 overweight adults. This is the most convincing causal evidence so far that fatty acids from fibre may help steer GLP-1 and appetite in humans.
Chambers ES, Viardot A, Psichas A, et al. Gut. 2015;64(11):1744-1754. doi:10.1136/gutjnl-2014-307913 · PMID: 25500202
The right fibre feeds the right bacteria
RCT Liping Zhao and colleagues showed in people with type 2 diabetes, in Science in 2018, that a specifically fibre-rich diet promotes a certain group of bacteria that produce short-chain fatty acids. Where these good producers were present in greater diversity and abundance, long-term blood sugar (HbA1c) improved, and partly through increased GLP-1 production. The study makes clear: it is not the fibre alone that counts, but the interplay with a microbiome that converts it into the right fatty acids.
Zhao L, Zhang F, Ding X, et al. Science. 2018;359(6380):1151-1156. doi:10.1126/science.aao5774 · PMID: 29590046
Soluble fibre with a meal
RCT, n=19 Zhong Ye and colleagues gave 19 healthy people a meal with 0, 5 or 10 grams of a soluble fibre, in Nutrition Research in 2015. Only the 10-gram dose significantly raised GLP-1 and PYY and prolonged satiety by one and a half to two hours. 5 grams were not enough. This is an important practical insight: there is a threshold dose. A little fibre garnishes a meal, but only enough fibre moves the hormones noticeably.
Ye Z, Arumugam V, Haugabrooks E, Williamson P, Hendrich S. Nutr Res. 2015;35(5):393-400. doi:10.1016/j.nutres.2015.03.004 · PMID: 25823991
Not every fibre study shows an immediate GLP-1 rise. Two careful crossover studies did find more short-chain fatty acids after a single dose of inulin, but no acute GLP-1 rise (van der Beek 2018 in Metabolism, Rahat-Rozenbloom 2017 in the European Journal of Clinical Nutrition). This suggests: the gut has to get used to more fibre over weeks, and a single dose is no switch. Consistency beats the quick effect here.
„I drink a fibre shake and my GLP-1 rises like with an injection." It does not work that way. The fibre path is slow, microbiome-dependent and in scale far smaller than the medication. It is still worth it, but as a lasting habit, not as a miracle trick for the moment.
Why natural Ozempic is marketing
Now to the honest account that many advertising promises leave out. Yes, your body makes GLP-1. Yes, food shapes that response. But between what a meal triggers and what a weight-loss injection produces lie orders of magnitude.
Two things separate the medication from your breakfast. First, duration. Your own GLP-1 is broken down again within minutes. The active ingredients of the weight-loss injections are deliberately altered so that they escape this breakdown and stay active for days. Second, the height. The drug levels under the injection far exceed anything a meal ever reaches.
The scale of the medication
RCT, n=803 Domenica Rubino and colleagues showed in JAMA in 2021, in the STEP 4 trial with 803 adults with overweight, how strongly semaglutide influences weight. In the first 20 weeks alone, participants lost on average 10.6 percent of body weight. Those who continued the injection lost a further 7.9 percent, while those who switched to placebo regained 6.9 percent. No natural meal achieves such effects through the body's own GLP-1. Important to know: gastrointestinal side effects occurred frequently, and it is a prescription medication with medical supervision.
Rubino D, Abrahamsson N, Davies M, et al. JAMA. 2021;325(14):1414-1425. doi:10.1001/jama.2021.3224 · PMID: 33755728
The term promises an equation that does not add up. Food can support your body's own GLP-1 response. The medication delivers a manyfold higher, day-long stable drug level. Both use the same switch, but at completely different strength. Honestly: nutrition is the foundation, not the copy. Whoever sells it as natural Ozempic is selling you an expectation it cannot keep.
Four lenses on one hormone
In Clinical Psychoneuroimmunology I rarely look at just one molecule. GLP-1 is a good example of how several systems play together.
Nervous system
GLP-1 addresses the appetite centres directly via receptors in the brain. It tells your head that you have eaten enough. That is why satiety is not just a belly matter, but a message to your nervous system.
Metabolism
GLP-1 tunes the insulin release to the meal and slows gastric emptying. So the blood sugar stays flatter. A flatter blood sugar means fewer craving valleys afterwards.
Immune system and gut
The short-chain fatty acids that prompt GLP-1 also nourish the gut lining and may dampen low-grade inflammation. A calm, well-fed gut is the basis for a good hormone response.
Hormonal system
GLP-1 does not work alone. It plays together with ghrelin, PYY, insulin and leptin. Weight is a hormonal signal, not a pure arithmetic problem. GLP-1 is one instrument in this orchestra.
Three levers you can try
Enough theory. What can you concretely do to support your body's own GLP-1 response? Here are three directions that follow from the evidence. No recipes, no dosing plans, just basic habits.
Build meals around protein
A good portion of protein at every meal can shift the satiety hormones favourably and keeps you full longer than fast carbohydrates. Legumes, eggs, fish, meat, quark, tofu. Breakfast is often the biggest weak spot, because for many it consists almost only of sugar and starch.
Eat plenty of fermentable fibre
Legumes, oats, psyllium, vegetables, unprocessed plant foods. They feed the bacteria that produce the short-chain fatty acids. Important: increase slowly so your gut can adapt, and keep at it. The effect needs weeks, not a single dose.
Use the order and less processed food
Eating vegetables and protein before the starch may improve the GLP-1 response and blood sugar, without leaving anything out. And the less processed your foods, the better the hormone response. Highly processed products tend to dampen satiety rather than support it.
This text is educational and does not replace a medical examination or advice. Weight-loss injections (GLP-1 medications) are prescription-only and need medical supervision. They are not suitable for everyone and can have side effects. Please do not obtain such medications on your own. If you are thinking about weight, blood sugar or a possible therapy, speak with a doctor who knows your situation. If you have strong digestive complaints after a dietary change, have it medically checked.
Satiety is not a matter of willpower
When your body makes its own satiety signal well, you do not have to constantly hold yourself back. Then your appetite works with you, not against you. That is the core: not counting calories, but creating the conditions under which your body regulates its own satiety again. And now you know why WHAT and HOW you eat matters more than sheer amount.
Frequently asked questions
Can you really raise GLP-1 naturally?
Yes, within limits. GLP-1 is a hormone your own body makes, released by the L cells in your gut after every meal. How strong that response is depends on what and how you eat. Shown in human crossover studies: a protein- or fat-rich meal produced a higher postprandial GLP-1 response than a carbohydrate-rich one (Parvaresh Rizi 2018). Fermentable fibre may also stimulate GLP-1 via short-chain fatty acids from the gut microbiome (Chambers 2015). Important: the effect is real, but modest and short. It does not replace a medication, but it can be a sensible foundation.
Which foods stimulate GLP-1?
Mainly three groups. First, protein: a high-protein breakfast can lower ghrelin and tends to raise GLP-1 (Blom 2006). Second, fermentable fibre such as inulin, psyllium, legumes, oats and vegetables: gut bacteria ferment it into short-chain fatty acids that may prompt the L cells to release GLP-1 (Kaji 2014, Chambers 2015). Third, fermented foods that help feed the good producers in your gut. Order matters too: eating vegetables and protein before the starch raised GLP-1 release in one study (Sun 2019).
Is natural Ozempic real or marketing?
The term is marketing. It is true that your body makes GLP-1 itself and that food shapes that response. But the difference in scale is enormous. Your own GLP-1 has a half-life of just a few minutes. The weight-loss injection delivers a stable GLP-1 analogue over days and at far higher potency. In the STEP 4 trial (Rubino 2021), semaglutide led to about 10.6 percent weight loss in 20 weeks. No meal achieves such effects through the body's own GLP-1. Nutrition can support satiety regulation, it is the foundation, not a replacement for the injection.
How does fibre help the satiety hormone?
Fermentable fibre reaches the large intestine undigested. There, gut bacteria ferment it into short-chain fatty acids, mainly acetate, propionate and butyrate. These bind to the receptors FFA2 and FFA3 on the L cells and may prompt the release of GLP-1 and PYY (Kaji 2014). The strongest human evidence: when researchers delivered propionate specifically to the colon, PYY and GLP-1 rose, energy intake fell acutely, and over 24 weeks weight gain was slowed (Chambers 2015). Important: not every acute fibre dose raises GLP-1 immediately. The effect needs a healthy microbiome and some time.
Why is the effect weaker than the weight-loss injection?
For two reasons. First, amount and duration: your own GLP-1 is released briefly after eating and broken down within minutes. The medication is designed to escape this rapid breakdown and stay active for days. Second, the level of the peak: pharmacological GLP-1 levels far exceed anything a meal reaches. That is why the medication produces double-digit weight loss in RCTs (Rubino 2021), while nutrition supports satiety more subtly. This is not a criticism of nutrition, but an honest account of the scale.
Does protein raise GLP-1 reliably?
Protein is one of the strongest natural triggers of satiety signals, but the evidence is nuanced. Blom 2006 found a tendency towards a higher GLP-1 response after a high-protein breakfast and a clearly slower gastric emptying. Parvaresh Rizi 2018 showed that protein- and fat-rich meals triggered more GLP-1 than carbohydrate-rich ones. Gibbons 2013 found that higher GLP-1 went along with less hunger and less energy intake. In short: protein can shift the GLP-1 response favourably and also acts through other satiety signals such as CCK and slower gastric emptying.
Does the gut microbiome play a role?
Yes, a big one. The GLP-1 response to fibre depends on which bacteria live in your gut and how many short-chain fatty acids they produce. In a randomised study of people with type 2 diabetes, a fibre-rich diet selectively promoted the SCFA-producing bacteria, and where these were present in greater abundance, long-term blood sugar improved, partly through more GLP-1 (Zhao 2018). This explains why some people respond to fibre more strongly than others. A diverse, well-fed microbiome is the precondition for the fibre-GLP-1 pathway to work well.
How quickly does a GLP-1-friendly diet show an effect?
The protein effect on satiety is immediate, you feel it within the same meal. The fibre path through the microbiome takes longer. Acute studies with a single dose of inulin did find more short-chain fatty acids, but not always an immediate rise in GLP-1 (van der Beek 2018, Rahat-Rozenbloom 2017). This suggests the gut needs weeks to adapt to more fibre. Consistency beats speed here. A steadily fibre-rich, protein-focused way of eating is more effective than a single fibre dose.
Can I replace the weight-loss injection with this?
No, you cannot replace it, and that should be said honestly. Someone with a medical indication for GLP-1 therapy will not get the same effect from nutrition. But nutrition is the foundation every therapy stands on. It can support your body's own satiety regulation, keep blood sugar steadier and reduce low-grade inflammation. A sensible path starts with the basics: protein-focused meals, plenty of fermentable fibre, a well-tended microbiome. Whether and when an injection is added is a medical decision after an individual assessment.
Are weight-loss injections unnatural because GLP-1 is added artificially?
The mechanism itself is not unnatural. The weight-loss injections act through exactly the satiety pathway your body uses anyway, the GLP-1 system. They imitate a body-own hormone and make it more resistant to rapid breakdown. That is different from a foreign substance. Still, they are prescription medications with benefits and risks that need medical supervision. Neither blanket condemnation nor blanket cheering helps. Sensible for the right people, embedded in nutrition, muscle building, sleep and root-cause work.
Read on in the weight cluster
How semaglutide and tirzepatide act through the GLP-1 path, what RCTs show and where the limits are.
The interplay of ghrelin, leptin, GLP-1 and PYY. Why appetite is not a pure matter of willpower.
Why processed foods trick satiety and real food keeps you full longer.
How order, protein and fibre keep blood sugar flatter and prevent cravings.
Sources
- Drucker DJ, Holst JJ. The expanding incretin universe: from basic biology to clinical translation. Diabetologia. 2023;66(10):1765-1779. DOI: 10.1007/s00125-023-05906-7 · PMID: 36976349 [Review]
- Lu VB, Gribble FM, Reimann F. Nutrient-Induced Cellular Mechanisms of Gut Hormone Secretion. Nutrients. 2021;13(3):883. DOI: 10.3390/nu13030883 · PMID: 33803183 [Review]
- Kaji I, Karaki S, Kuwahara A. Short-chain fatty acid receptor and its contribution to glucagon-like peptide-1 release. Digestion. 2014;89(1):31-36. DOI: 10.1159/000356211 · PMID: 24458110 [Mechanism Review]
- Blom WAM, Lluch A, Stafleu A, et al. Effect of a high-protein breakfast on the postprandial ghrelin response. Am J Clin Nutr. 2006;83(2):211-220. DOI: 10.1093/ajcn/83.2.211 · PMID: 16469977 [RCT, n=15]
- Parvaresh Rizi E, Loh TP, Baig S, et al. A high carbohydrate, but not fat or protein meal attenuates postprandial ghrelin, PYY and GLP-1 responses in Chinese men. PLoS One. 2018;13(1):e0191609. DOI: 10.1371/journal.pone.0191609 · PMID: 29385178 [RCT, n=18]
- Gibbons C, Caudwell P, Finlayson G, et al. Comparison of postprandial profiles of ghrelin, active GLP-1, and total PYY to meals varying in fat and carbohydrate. J Clin Endocrinol Metab. 2013;98(5):E847-E855. DOI: 10.1210/jc.2012-3835 · PMID: 23509106 [RCT, n=16]
- Sun L, Goh HJ, Govindharajulu P, Leow MK, Henry CJ. Postprandial glucose, insulin and incretin responses differ by test meal macronutrient ingestion sequence (PATTERN study). Clin Nutr. 2019;39(3):950-957. DOI: 10.1016/j.clnu.2019.04.001 · PMID: 31053510 [RCT, n=16]
- Chambers ES, Viardot A, Psichas A, et al. Effects of targeted delivery of propionate to the human colon on appetite regulation, body weight maintenance and adiposity in overweight adults. Gut. 2015;64(11):1744-1754. DOI: 10.1136/gutjnl-2014-307913 · PMID: 25500202 [RCT, n=60]
- Zhao L, Zhang F, Ding X, et al. Gut bacteria selectively promoted by dietary fibers alleviate type 2 diabetes. Science. 2018;359(6380):1151-1156. DOI: 10.1126/science.aao5774 · PMID: 29590046 [RCT]
- Ye Z, Arumugam V, Haugabrooks E, Williamson P, Hendrich S. Soluble dietary fiber (Fibersol-2) decreased hunger and increased satiety hormones in humans when ingested with a meal. Nutr Res. 2015;35(5):393-400. DOI: 10.1016/j.nutres.2015.03.004 · PMID: 25823991 [RCT, n=19]
- van der Beek CM, Canfora EE, Kip AM, et al. The prebiotic inulin improves substrate metabolism and promotes short-chain fatty acid production in overweight to obese men. Metabolism. 2018;87:25-35. DOI: 10.1016/j.metabol.2018.06.009 · PMID: 29953876 [RCT, n=14]
- Rahat-Rozenbloom S, Fernandes J, Cheng J, Wolever TMS. Acute increases in serum colonic short-chain fatty acids elicited by inulin do not increase GLP-1 or PYY responses but may reduce ghrelin in lean and overweight humans. Eur J Clin Nutr. 2017;71(8):953-958. DOI: 10.1038/ejcn.2016.249 · PMID: 27966574 [RCT, n=25]
- Akhlaghi M. The role of dietary fibers in regulating appetite, an overview of mechanisms and weight consequences. Crit Rev Food Sci Nutr. 2024;64(10):3139-3150. DOI: 10.1080/10408398.2022.2130160 · PMID: 36193993 [Review]
- Rubino D, Abrahamsson N, Davies M, et al. Effect of Continued Weekly Subcutaneous Semaglutide vs Placebo on Weight Loss Maintenance in Adults With Overweight or Obesity: The STEP 4 Randomized Clinical Trial. JAMA. 2021;325(14):1414-1425. DOI: 10.1001/jama.2021.3224 · PMID: 33755728 [RCT, n=803]
This body of evidence rests mostly on controlled human studies. It shows: nutrition can measurably shape the body's own GLP-1 response. The effect is real, but in scale clearly smaller and shorter than the effect of prescription GLP-1 medications. I make this account transparent so that you can decide for yourself how much weight to give the statements. This text does not replace a medical examination.