1. How much? 425mg 2x/day or 850mg 2x/day?

2. When? Obviously post-workout and when else?

3. Should I wait till I start my cycle or do it now so I know what it does without AS...I'm afraid I won't be able to tell when I'm sticking 500mg test and 300mg EQ in my ass.

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And, yes it would be very useful while dieting. Especially if you were using an extremely low carb diet. If I remember correctly, DocJ used it during a diet.

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Another good question...Take it before/with/after a high carb meal?

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Description: Metformin is an oral biguanide antidiabetic agent similar to phenformin, a drug that was withdrawn from US marketing in 1977 due to the development of lactic acidosis. The risk for this adverse reaction is considerably lower with metformin, however. Metformin represents a drug with actions that differ from, yet compliment, those of the sulfonylureas. Compared to glyburide in non-insulin-dependent diabetics, metformin was found to achieve similar glycemic control but metformin lead to a higher incidence of digestive complaints than glyburide.[713] Metformin was introduced in Europe in the 1950's but was not approved by the FDA until December 30, 1994. It is approved for use in the US for treatment of NIDDM (Type II diabetes mellitus) either as monotherapy or in combination with sulfonylureas, alpha-glucosidase inhibitors, or with insulin.

Mechanism of Action: Although its mechanism of action has not been clearly determined, decreased hepatic gluconeogenesis is thought to be the primary therapeutic effect of metformin in NIDDM.[1017] In addition, metformin appears to improve utilization of glucose in skeletal muscle and adipose tissue by increasing cell membrane glucose transport. This effect may be due to improved binding of insulin to insulin receptors since metformin is not effective in diabetics without some residual functioning pancreatic islet cells.[1156] Other mechanisms may include a decreased intestinal glucose absorption, however, this has only been observed in animals.[1156] Unlike the sulfonylureas, metformin rarely causes hypoglycemia since it does not significantly change insulin concentrations. An important distinction is that sulfonylureas increase insulin secretion thus making them useful in non-obese patients with NIDDM while metformin improves insulin resistance, a common pathophysiologic finding in obese patients with NIDDM.[1156] Metformin causes a 10�20% decrease in fatty-acid oxidation and a slight increase in glucose oxidation. Unlike phenformin, metformin does not inhibit the mitochondrial oxidation of lactate unless plasma concentrations of metformin become excessive (i.e., in patients with renal failure) and/or hypoxia is present.[1018]

Clinically, metformin lowers fasting and postprandial hyperglycemia. The decrease in fasting plasma glucose is approximately 25�30%. Unlike oral sulfonylureas, metformin rarely causes hypoglycemia. Thus, metformin demonstrates more of an antihyperglycemic action than a hypoglycemic action. Metformin does not cause weight gain and in fact, may cause a modest weight loss due to drug-induced anorexia. Metformin also decreases plasma VLDL triglycerides resulting in modest decreases in plasma triglycerides and total cholesterol. Patients receiving metformin show a significant improvement in hemoglobin A1c, and a tendency toward improvement in the lipid profile, especially when baseline values are abnormally elevated.

Pharmacokinetics: Metformin is administered as an oral tablet. The bioavailability of metformin is 50�60%. Food decreases the extent and slightly delays the absorption of metformin, however, it is recommended to be taken with meals.[1156] Metformin is distributed rapidly into peripheral body tissues and fluids and appears to distribute slowly into erythrocytes and to a deep tissue compartment (most likely GI tissues). The highest concentrations of metformin are found in the GI tract (10 times the concentrations in the plasma) and lower concentrations in the kidney, liver, and salivary gland tissue. Metformin does not bind to liver or plasma proteins. It is not metabolized by the liver and this fact may explain why the risk of lactic acidosis is much less for metformin than for phenformin (i.e., approximately 10% of patients have an inherited defect in the ability to metabolize phenformin).[1156] Metformin is excreted by the kidneys, largely unchanged, through an active tubular process. Approximately 30% of an oral dose is excreted in the feces, presumably as unabsorbed metformin and about 90% of a dose is excreted by the kidneys within 24 hours. The plasma half-life is approx. = 6.2 hours and the blood half-life is approx. = 17.6 hours in patients with normal renal function. Half-life is increased in patients with renal impairment. Metformin is removed with hemodialysis.

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"It's a good day to be alive, sir, It's a good day to be alive he said..."

DocJ...I haven't seen you around for a while.

So, should I wait until my cycle or use it now?

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BTW - I'm starting up a new clinic...been busy.

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"It's a good day to be alive, sir, It's a good day to be alive he said..."

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"It's a good day to be alive, sir, It's a good day to be alive he said..."