Metformin 500 mg [30 Tabl]
Doctors and scientists want drug regulators and research funding agencies to consider medicines that delay ageing-related disease as legitimate drugs. Such treatments have a physiological basis, researchers say, and could extend a person’s healthy years by slowing down the processes that underlie common diseases of ageing — making them worthy of government approval. On 24 June, researchers will meet with regulators from the US Food and Drug Administration (FDA) to make the case for a clinical trial designed to show the validity of the approach.
Preliminary evidence shows metformin may decrease the risk of cancer. A direct action of metformin on cancer cells is suspected. Metformin exhibits a strong and consistent antiproliferative action on several cancer cell lines, including breast, colon, ovarian, pancreatic, lung, and prostate cancer cells. These cellular studies were generally completed by preclinical studies showing a reliable antitumoral effect in various mouse models. In addition, the first clinical trials demonstrated a beneficial effect in breast and colon cancer.
Malek, M; Aghili, R; Emami, Z; Khamseh, ME (2013). "Risk of Cancer in Diabetes: The Effect of Metformin.". ISRN endocrinology 2013: 636927. doi:10.1155/2013/636927. PMC 3800579. PMID 24224094.
Ben Sahra I, Le Marchand Brustel Y, Tanti JF, Bost F. Metformin in cancer therapy: a new perspective for an old antidiabetic drug?. Mol Cancer Therapeutics. May 2010;9(5):1092–99. doi:10.1158/1535-7163.MCT-09-1186. PMID 20442309.
Will the World’s First Anti-Aging Drug Help Humans Live to Be 120?
Studies in mammals have led to the suggestion that hyperglycemia and hyperinsulinemia are important factors in aging. Insulin/insulin-like growth factor 1 (IGF-1) signaling molecules that have been linked to longevity include daf-2 and InR and their homologues in mammals, and inactivation of the corresponding genes increases life span in nematodes, fruit flies and mice. It is possible that the life-prolonging effect of caloric restriction is due to decreasing IGF-1 levels. Evidence has emerged that antidiabetic drugs are promising candidates for both life span extension and prevention of cancer. Thus, antidiabetic drugs postpone spontaneous carcinogenesis in mice and rats, as well as chemical and radiation carcinogenesis in mice, rats and hamsters. Furthermore metformin seems to decrease cancer risk in diabetic patients.
Metformin hydrochloride is an oral antihyperglycemic medication. It is prescribed for the management of Type-II diabetes, sometimes also referred to as mature onset diabetes since it tends to develop later in life. The drug is typically utilized when dietary management and exercise alone have not been able to control the progress of the disease, yet injectable insulin is not an appropriate option. While the main activity of metformin HCL is the increased utilization of glucose, it does not directly mimic the action of insulin. While its precise mode of action is unknown, it is understood to reduce the output of glucose by the liver, decrease the intestinal absorption of glucose, and increase insulin sensitivity in certain organs and peripheral tissues. Use of this agent will lower the patient’s blood sugar, though its activity makes it less likely to cause a dangerous state of hypoglycemia if the dosage is accidentally misjudged (a concern with injectable insulin).
Insulin manipulation is common in sports due to the biological actions of this hormone. Insulin is involved in nutrient storage, helping to transport amino acids, fatty acids, and carbohydrates (glucose) into various cells. In the case of muscle cells, insulin also facilitates cellular anabolic (protein synthesizing) and anti-catabolic (protein sparing) actions. This hormone also directs nutrient storage to adipose cells, however, thus its manipulation has the potential to increase fat mass. Bodybuilders have found, however, that with intense weight training, insulin can show a much greater affinity for protein and carbohydrate storage in muscle cells. By manipulating insulin levels (or insulin sensitivity) under these conditions, muscle growth with minimal fat gain is possible. Injectable insulin can be risky however, as a mistake in dosage or carbohydrate intake has the potential to cause lifethreatening hypoglycemia (low blood sugar). Since this effect is rare with metformin, it is considered by some athletes to be an introduction to insulin manipulation. History: Metformin has a long and fairly complicated history in medicine. This drug was first synthesized in 1929 along with a series of other biguanides. Although some of its beneficial properties were elucidated at the time, it was not initially subject to human trials.It sat idle in the research books for nearly three decades after its creation. The first clinical study investigating its therapeutic potential as a glucose lowering medication was finally initiated in 1956.
hese trials were very successful, and metformin was selected for clinical development. It was given the trade name Glucophage, which translates to “glucose eater”. This, of course, refers to its ability to help the body dispose of blood glucose. Glucophage went on to be the most recognized trade name for metformin HCL.
This trade name is still being used to market the drug today, presently by the Bristol-Myers Squibb Company. Metformin was not initially the glucose-lowering agent of choice among clinicians. During the 1950s, it had been studied alongside phenformin and buformin, which had also been selected for commercial development. Metformin was initially pushed aside in favor of these two drugs, both of which had proven to be significantly more potent at lowering blood sugar levels. These drugs would remain the dominant biguanides for approximately 20 years. By the 1970s, however, it was being reported that phenformin and buformin were producing unacceptably high incidences of lactic acidosis, an oftenfatal metabolic disorder characterized by a rapid drop in pH. By the close of the 1970s, most governments had determined that these drugs were too risky to continue using. Phenformin and buformin were subsequently removed from most pharmaceutical markets worldwide. The structural and pharmacological similarity of metformin to phenformin and buformin held back its clinical potential for many years. Researchers were widely concerned that this agent would also present unfavorable risks.
While lactic acidosis is a legitimate concern, it occurs much less frequently than with the other biguanides (approximately 1 in 33,000 patients). Following much evaluation of its benefit-risk ratio, metformin eventually came to be regarded as the safest drug of the biguanide class. It was widely pushed back into clinical medicine during the mid-1990s. It was introduced to the United States in 1995, where it was an immediate success. In the years to follow, metformin continued to grab a stronger share of the global diabetes medication market. Today, it is estimated that metformin HCL is the most widely prescribed medication for the treatment of type-2 diabetes.
Metformin hydrochloride is most commonly supplied in oral tablets of 500, 850, and 1000 mg each. Structural Characteristics: Metformin is a synthetic derivative of the natural antidiabetic agent guanide. It is specifically the 1,1- dimethylated biguanide variant. Warnings: In rare cases, the use of metformin HCL is associated with lactic acidosis, an often-fatal metabolic disorder involving (among other factors) an increase in lactate levels (lactic) and a pronounced decrease in blood pH (acidosis). This risk increases with conditions such as sepsis, dehydration, excess alcohol intake, hepatic insufficiency, renal impairment, and acute congestive heart failure. Symptoms of lactic acidosis include malaise, muscle pain, respiratory distress, drowsiness, and abdominal distress. Laboratory abnormalities include low pH, increased anion, and elevated blood lactate. If lactic acidosis is suspected, metformin HCL should be discontinued and the individual should seek immediate medical attention. Side Effects: Common side effects of metformin HCL therapy include diarrhea (53.2%), nausea/vomiting (25.5%), flatulence (12.1%), weakness (9.2%), indigestion (7.1%), abdominal discomfort (6.4%), and headache (5.7%).731 Metformin must be used with caution in patients with renal dysfunction, and impaired creatinine clearance. A serum creatinine concentration above 1.5 mg/dL (men) or 1.4 mg/dL (women) is considered a contraindication to treatment. Metformin may also impair the absorption of vitamin B12. Hypoglycemia is uncommon with the use of metformin, though is sometimes noted when caloric intake is deficient, or when strenuous exercise is not compensated by caloric supplementation. Minor side effects often subside over time, or with use of a lower metformin HCL dosage. Lactic acidosis has been reported in approximately 32% of metformin HCL overdose cases (see: WARNINGS).
The oral absorption rate of metformin HCL is slow, with the body taking approximately six hours to absorb and distribute each dose. Extended release (XR) formulations are also made, which further delay the absorption of metformin HCL. Extended release tablets should be taken whole, and not crushed. In a clinical setting, the drug is given in divided doses with meals, except for extended release formulations, which are administered once daily with the evening meal. There is no set adult clinical dose, and the drug must be tailored to and the drug must be tailored to the individual needs of the patient. It is typically initiated at a low daily dosage, and slowly escalated by 500 mg each week or 850 mg every two weeks until the minimum daily dose required for adequate glycemic control has been established. The maximum recommended daily dose for type-2 diabetic patients in 2550 mg per day. Fasting plasma glucose is used to determine the therapeutic response to metformin HCL, and glycosylated hemoglobin levels are measured every three months. The goal of therapy is to decrease fasting plasma glucose and glycosylated hemoglobin levels to normal or near normal levels using the lowest effective dose of metformin HCL, either alone or in combination with another antihyperglycemic drug (sulfonylurea or insulin).
When used for physique or performance-enhancing purposes, the typical protocol is to take 850 mg once or twice per day. If a single application is desired, it is typically taken 1-2 hours before exercise, so that the drug can have its peak effect during the early stages of recovery. It is highly common to utilize a carbohydrate supplement during the hours metformin is active in the body, especially during the crucial 2-3 hour “nutrient uptake” window following intense training. The result of metformin treatment is typically not as dramatic as insulin, but the drug still does have a notable anabolic effect for many users. Most bodybuilders/athletes opt to use this drug for a limited duration, with cycles lasting 6-8 weeks in length. This would be followed by an equally long break (at a minimum) before metformin, insulin, or any other antihyperglycemic agent is used for physique or performance-enhancing purposes.
Metformin is readily available given its widespread use in clinical medicine. It is sold under many brand names, as both a standalone and combination medication. Bodybuilders and athletes tend to limit their use to preparations containing only metformin.
While the drug is not the subject of much interest by steroid counterfeiting or underground manufacturing operations, it is the target of many other general drug counterfeits given the ease in which it can be sold. As such, it should not be assumed that all packaged drug products labeled as metformin are legitimate. Care should be taken to ensure that all products bearing this ingredient have been acquired through legitimate pharmaceutical channels.
Metformin 500 mg [30 Tabl]
- Product Code: Metformin 500 mg [30 Tabl]
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