Metformin for fatloss
Metformin (Glucophage) for Weight Loss and Bodybuilding
Metformin, sold under the trade name Glucophage, is used to treat diabetes, but several studies show that it also helps non-diabetics to lose weight by reducing hunger (1).
You may be overweight because your body makes too much insulin, especially if your store your fat primarily in your belly. When you eat, your blood sugar level rises. The higher it rises, the more insulin your pancreas releases. Insulin makes you fat by acting on your brain to make you hungry, your liver to manufacture fat, and the fat cells in your belly to fill with fat. So the treatment for this type of obesity is to avoid foods that cause the highest rise in blood sugar and to take medications that prevent your blood sugar levels from rising too high. Avoid bakery products, pastas and all foods made from flour, fruit juices and everything with added sugar. Eat fruits and root vegetables such as potatoes only with meals.
After you eat, sugar goes from your intestines into your bloodstream, and then immediately into your liver. Then your liver releases sugar back into your bloodstream to cause your blood sugar level to rise. To keep blood sugar levels from rising too high, your pancreas release insulin into your bloodstream. Insulin makes you hungry all the time and causes your liver to convert extra calories to fat and it constricts arteries to cause heart attacks. You need insulin to keep blood sugar levels from rising too high to cause diabetes, nerve damage, heart attacks, strokes and kidney damage. Glucophage reduces sugar release from your liver to prevents blood sugar levels from rising too high, so your body doesn't need to produce as much insulin that makes you hungry and causes your liver to make fat (3,13,14).
Glucophage lowers insulin levels (4), prevents many of the side effects of diabetes and can be used by people who want to lose weight. However, Glucophage is not effective when your blood is acidic from excess lactic acid and recent research shows that exercise, which raises lactic acid, does not cause blood acid levels to rise enough to reduce Glucophage's benefits (5). Glucophage, itself, does not raise blood lactate levels and is therefore considerably safer than doctors originally thought. Since Glucophage lowers insulin, diabetics should be placed on Glucophage to lower their requirements for all other medications used to treat diabetes (6).
A common cause of obesity in women is called polycystic ovary syndrome, which is caused by having high blood levels of insulin. Glucophage helps these women to lose weight (7-12).
Glucophage is a safe medication that prevents blood sugar levels from rising too high, but you defeat its effects by taking foods that cause rapid rises in blood sugar levels. So taking Glucophage after eating two bagels will not help you to lose weight. I prescribe 500 mg of Glucophage to be taken a few minutes before you eat, usually three times a day. You should not take it if you have kidney disease, heart failure or any medical condition that could make your blood acidic. There are many drugs that cannot be taken with Glucophage, so check with your doctor about all your medications. If you have nausea or diarrhea, take half a pill (250 mg) in the middle of a meal once a day, and if you then have no symptoms, try to work up to one half a pill before each meal.
Side effects: Metformin can initially cause nausea, upset stomach, and diarrhea — which may be partly responsible for weight loss. On the plus it lowers cholesterol.Glucophage should not be used for weight loss in athletes because it impairs competitive performance by lowering blood sugar. On rare occasions, during maximal effort, this can cause a person to pass out.
"During diet phases, bodybuilders have utilized Glucophage as a means of decreasing glucose production by the liver and glucose absorption by the intestines. This in itself decreases insulin secretion by the pancreas and increases the body's dependence upon fat stores for energy requirements. This was employed especially so during GH and PGF-2 use, and was synergistic with anabolic/androgenic steroids. SINCE cell insulin receptor sites are more sensitive and since there is an existing cross-over stimulation between IGF-1 and Insulin (and their opposing receptor-sites) lean mass retention was notablyincreased. This effect helped decrease the negative effects dieting has upon IGF-1 production endogenously" (Rea, p. 131).
1) G Paolisso, L Amato, R Eccellente, A Gambardella, MR Tagliamonte, G Varricchio, C Carella, D Giugliano, F Donofrio. Effect of metformin on food intake in obese subjects. European Journal of Clinical Investigation 28: 6(JUN 1998):441-446.
3) MB Davidson, AL Peters. An overview of metformin in the treatment of type 2 diabetes mellitus. American Journal of Medicine 102: 1 (JAN 1997):99-110.
4) T Sir, T Castillo, S Munoz, G Lopez, M Calvillan. Effects of metformin on insulin resistance in obese and hyperandrogenic women. Revista Medica de Chile 125: 12 (DEC 1997):1457-1463.
5) U Gudat, G Convent, L Heinemann. Metformin and exercise: No additive effect on blood lactate levels in healthy volunteers. Diabetic Medicine 14: 2 (FEB 1997):138-142.
6) F Abbasi, V Kamath, AA Rizvi, M Carantoni, YDI Chen, GM Reaven. Results of a placebo-controlled study of the metabolic effects of the addition of metformin to sulfonylurea-treated patients: Evidence for a central role of adipose tissue. Diabetes Care 20: 12 (DEC 1997):1863-1869.
7) J Holte, G Gennarelli, L Wide, H Lithell, C Berne. High prevalence of polycystic ovaries and associated clinical, endocrine, and metabolic features in women with previous gestational diabetes mellitus. Journal of Clinical Endocrinology and Metabolism 83: 4(APR 1998):1143-1150.
8) E Velazquez, A Acosta, SG Mendoza. Menstrual cyclicity after metformin therapy in polycystic ovary syndrome. Obstetrics and Gynecology 90: 3 (SEP 1997):392-395. Excellent editorial in The Lancet, January 31, 1998 351:305-6. lots of references.
9) LC Morinpapunen, RM Koivunen, A Ruokonen, HK Martikainen. Metformin therapy improves the menstrual pattern with minimal endocrine and metabolic effects in women with polycystic ovary syndrome. Fertility and Sterility 69: 4 (APR 1998):691-696.
10) Nestler JE et al. Effects of metformin on spontaneous and clomiphene-induced ovulation in polycystic ovary syndrome. NEJM, 1998(June 25);338:1876-1880.
11) N Mauras, et al. Ovarian hyperandrogenism is associated with insulin resistance to both peripheral carbohydrate and whole-body protein metabolism in postpubertal young females: A metabolic study. Journal of Clinical Endocrinology and Metabolism 83: 6(JUN 1998):1900-1905.
12) JE Nestler, DJ Jakubowicz, A Falcon, VC Brik, N Quintero, F Medina. Insulin stimulates testosterone biosynthesis by human thecal cells from women with polycystic ovary syndrome by activating its own receptor and using inositolglycan mediators as the signal transduction system. Journal of Clinical Endocrinology and Metabolism 83: 6(JUN 1998):2001-2005.
13) David Maggs of Yale University annual meeting of the American Diabetes association in Boston, November, 1997.
14) J Pugh. Metformin monotherapy for type II diabetes. Advances in Therapy 14: 6 (NOV-DEC 1997):338-347. sulfonureas: Unwanted effects such as hypoglycemia, weight gain, and increased fasting insulin levels have sometimes been associated with sulfonylureas. Metformin improves glucose intolerance without stimulating insulin release or causing hypoglycemia. Additional benefits associated with metformin include a favorable influence on body weight and plasma lipid profiles. Metformin is an important first-line alternative agent for patients with type II diabetes.
15)H YkiJarvinen, K Nikkila, S Makimattila. Metformin prevents weight gain by reducing dietary intake during insulin therapy in patients with type 2 diabetes mellitus. Drugs, 1999, Vol 58, Suppl. 1, pp 53-54.
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