SHAKER OLIMP-PREZENT
Jak to podrabiałeś to zamiast "o" w profilu klubowym zrobiło Ci się "c" :)) ale jest git :) ------------------------------ Szukasz taniej odżywki białkowej i nie tylko?'Ovopol'-pytaj o szczególy pod nr.GG 1135964 Zamiast dać mi soga kliknij w pajacyka http://www.pajacyk.pl "Moderator w dziale Trening"
SHAKER OLIMP-PREZENT
czy szanowny pan z przepięknym bialym szalikiem raczy niep***ć głupot??? w okienku wysylania maila tez są dziwne literki a to dlatego ze przy zmniejszaniu zdjęcia sei to zrobilo, jak niedostane shakera to wysle olimpowi oryginał printscreena i juz, tutaj by sie niezmiescil(prawie 3mb) pozdrawiam ło czlonek-mafia.suple.hardcor.pl
(ELITE Ladies) 4nn/ Z czystej złośliwości i przez zazdrość %-)
Huanita może kiedyś zwierzę się publicznie 10x Trening A. A. Przysiad ze sztanga na plecach 30kg/40kg/45kgx9 B. RDL 40kg/50kg/60kgx8 C. wyciskanie sztangi skos góra 20kg/25kg/25kgx8 D. wiosło sztangą 25kg/30kg/30kgx5* E. wznosy z opadu max 12 F. plank 26sek *ayesiezabiłam mój brzuch, moje plecy, moje nogi, moje wszystko Micha: - owsiane, jaja, masło orzechowe, whey, tran - kaczka, ciecierzyca(!), jajko, ser żółty - syntha - serca drobiowe, ser żółty, makaron żytni Zmieniony przez - 4nn w dniu 2011-10-06 21:50:45
(ELITE Ladies) 4nn/ Z czystej złośliwości i przez zazdrość %-)
Cisnę, cisnę Ale to jeszcze nie jest ten etap, w którym mogę zrobić trening co 2 dzień Dzisiejsza micha: - jajecznica, razowiec, pasta z makreli, jajka i majonezu - whey, banan - śledzie - łosoś, masło, razowiec Trening 10x A. przysiad przedni 25kg/30kg/40kgx8 B. MC 50kg/60kg/65kgx8* C. WL 20kg/25kg/30kg D. Push Press 25kg/30kg/30kgx7** E. wypady F. pompki 1xmax: 10x *przetrenowałam mocno wymęczona ostatnia seria **j.w. Przywaliłam sobie w szczękę w drugiej serii PP aż przerwałam i sprawdzałam, czy mam wszystkie zęby
(ELITE Ladies) 4nn/ Z czystej złośliwości i przez zazdrość %-)
Anqua mi się marzą interwały w terenie bez wizji kalectwa a jeszcze bardziej miażdży dzień po Dvpa mnie boli Ale zrobiłam kolejny błąd: nie robi się czegoś takiego na noc Trening 5x Trening A. A. Przysiad ze sztanga na plecach 40kg/50kg/60kg B. RDL: 50kg/70kg/75kgx3 C. wyciskanie sztangi skos góra 30kg/35kg/40kgx3 D. wiosło sztangą 30kg/40kg/45kg E. wznosy z opadu 1x16,5 F. K2E x5/x3/x2 Przed każdym ćwiczeniem serie rozgrzewkowe. Pierwszy raz robiłam 5 powtórzeń w tak małej ilości serii i nie mogłam wyczuć ciężaru. W przysiadzie było ok, w RDL już poślady i dwugłowe rwały 4-tego powtórzenia już nie dałam rady dokończyć. Micha - omlet z owsianych, whey, masło orzechowe - udziec wołowy, plaster schabu, ser żółty - razowiec ze schabem i serem żółtym - pomidorowa z sercami drobiowymi, razowiec z masłem + wino Zmieniony przez - 4nn w dniu 2011-10-12 21:43:37
Masz pojedyńcze pytanie/pytania ?- reaktywacja 3
Zrób tą metodę na drążku.Efektywność wzrośnie o ponad połowę.Jeśli nie jesteś orłem zrób mechaniczny drop set: A Podciąganie szerokim nachwytem x 8/10 B Podciąganie pochwytem szerzej niż barki x max C Podciąganie chwytem neutralnym x max
Masz pojedyńcze pytanie/pytania ?- reaktywacja 3
Tak się zastanawiam, czy jesli cwiczymy planem typu : a) Push,b)Pull c)Nogi d) DNT to czy jest ważny fakt że trening Push jest pierwszy, przed Pullem? Domyślam się, że pewnie nie,ale czy można powiedzieć że po DNT umieścić się powinno trening priorytetowy? Czyli jeżeli zależy nam bardziej na progresji np w podciąganiu, to Pull powinien być po DNT, przed pushem... Dobrze kombinuję? Ok, może to brzmieć banalnie, ale jednak 90% osób z jakiegoś powodu najpierw robi Push. Spokojnie zatem możesz znaleźć się w tych 10%, którzy robią inaczej. Jeśli cały plan treningowy na mikrocykl tygodniowy ma ręce i nogi to będzie ok. Kolejność ustalasz Ty - a nie jakieś definicje czy ludowe przesądy.
Insulina ZA i PRZECIW
age - anagram godowej erekcji Metformin Description Metformin hydrochloride is an oral antihyperglycemic drug used in the management of type 2 diabetes. Metformin hydrochloride (N, N-dimethylimidodicarbonimidic diamide hydrochloride) is not chemically or pharmacologically related to any other classes of oral antihyperglycemic agents. The structural formula is as shown: Metformin hydrochloride is a white to off-white crystalline compound with a molecular formula of C4H11N5HCl and a molecular weight of 165.63. Metformin hydrochloride is freely soluble in water and is practically insoluble in acetone, ether, and chloroform. The pKa of Metformin is 12.4. The pH of a 1% aqueous solution of Metformin hydrochloride is 6.68. Each Metformin hydrochloride tablet, USP intended for oral administration contains 500 mg, 850 mg or 1000 mg Metformin hydrochloride. In addition, each Metformin hydrochloride tablet, USP contains the following inactive ingredients: colloidal silicon dioxide, corn starch, hypromellose, magnesium stearate, polyethylene glycol, polysorbate 80, povidone, sodium starch glycolate, and titanium dioxide. Metformin - Clinical Pharmacology Mechanism of Action Metformin is an antihyperglycemic agent which improves glucose tolerance in patients with type 2 diabetes, lowering both basal and postprandial plasma glucose. Its pharmacologic mechanisms of action are different from other classes of oral antihyperglycemic agents. Metformin decreases hepatic glucose production, decreases intestinal absorption of glucose, and improves insulin sensitivity by increasing peripheral glucose uptake and utilization. Unlike sulfonylureas, Metformin does not produce hypoglycemia in either patients with type 2 diabetes or normal subjects (except in special circumstances, see PRECAUTIONS) and does not cause hyperinsulinemia. With Metformin therapy, insulin secretion remains unchanged while fasting insulin levels and day-long plasma insulin response may actually decrease. Pharmacokinetics Absorption and Bioavailability The absolute bioavailability of a Metformin hydrochloride 500 mg tablet given under fasting conditions is approximately 50% to 60%. Studies using single oral doses of Metformin tablets 500 mg to 1500 mg, and 850 mg to 2550 mg, indicate that there is a lack of dose proportionality with increasing doses, which is due to decreased absorption rather than an alteration in elimination. Food decreases the extent of and slightly delays the absorption of Metformin, as shown by approximately a 40% lower mean peak plasma concentration (Cmax) a 25% lower area under the plasma concentration versus time curve (AUC), and a 35 minute prolongation of time to peak plasma concentration (Tmax) following administration of a single 850 mg tablet of Metformin with food, compared to the same tablet strength administered fasting. The clinical relevance of these decreases is unknown. Distribution The apparent volume of distribution (V/F) of Metformin following single oral doses of Metformin 850 mg averaged 654 ± 358 L. Metformin is negligibly bound to plasma proteins, in contrast to sulfonylureas, which are more than 90% protein bound. Metformin partitions into erythrocytes, most likely as a function of time. At usual clinical doses and dosing schedules of Metformin hydrochloride tablets, steady state plasma concentrations of Metformin are reached within 24 to 48 hours and are generally <1 mcg/mL. During controlled clinical trials of Metformin hydrochloride, maximum Metformin plasma levels did not exceed 5 mcg/mL, even at maximum doses. Metabolism and Elimination Intravenous single-dose studies in normal subjects demonstrate that Metformin is excreted unchanged in the urine and does not undergo hepatic metabolism (no metabolites have been identified in humans) nor biliary excretion. Renal clearance (see Table 1) is approximately 3.5 times greater than creatinine clearance, which indicates that tubular secretion is the major route of Metformin elimination. Following oral administration, approximately 90% of the absorbed drug is eliminated via the renal route within the first 24 hours, with a plasma elimination half-life of approximately 6.2 hours. In blood, the elimination half-life is approximately 17.6 hours, suggesting that the erythrocyte mass may be a compartment of distribution. Special Populations Patients with Type 2 Diabetes In the presence of normal renal function, there are no differences between single- or multiple-dose pharmacokinetics of Metformin between patients with type 2 diabetes and normal subjects (see Table 1), nor is there any accumulation of Metformin in either group at usual clinical doses. Renal Insufficiency In patients with decreased renal function (based on measured creatinine clearance), the plasma and blood half-life of Metformin is prolonged and the renal clearance is decreased in proportion to the decrease in creatinine clearance (see Table 1; also see WARNINGS). Hepatic Insufficiency No pharmacokinetic studies of Metformin have been conducted in patients with hepatic insufficiency. Geriatrics Limited data from controlled pharmacokinetic studies of Metformin in healthy elderly subjects suggest that total plasma clearance of Metformin is decreased, the half-life is prolonged, and Cmax is increased, compared to healthy young subjects. From these data, it appears that the change in Metformin pharmacokinetics with aging is primarily accounted for by a change in renal function (see Table 1). Metformin treatment should not be initiated in patients ≥80 years of age unless measurement of creatinine clearance demonstrates that renal function is not reduced. (See WARNINGS and DOSAGE AND ADMINISTRATION). Table 1. Select Mean (± S.D.) Metformin Pharmacokinetic Parameters Following Single or Multiple Oral Doses of Metformin * All doses given fasting except the first 18 doses of the multiple dose studies; † Peak plasma concentration; ‡ Time to peak plasma concentration; § Combined results (average means) of five studies: mean age 32 years (range 23 to 59 years). Kinetic study done following dose 19, given fasting. # Elderly subjects, mean age 71 years (range 65 to 81 years). Þ CLcr = creatinine clearance normalized to body surface area of 1.73 m2. Subject Groups: Metformin dose* (number of subjects) Cmax† (mcg/mL) Tmax‡ (hrs) Renal Clearance (mL/min) Healthy, nondiabetic adults: 500 mg single dose (24) 1.03 (± 0.33) 2.75 (± 0.81) 600 (± 132) 850 mg single dose (74)§ 1.60 (± 0.38) 2.64 (± 0.82) 552 (± 139) 850 mg three times daily for 19 doses (9) 2.01 (± 0.42) 1.79 (± 0.94) 642 (± 173) Adults with type 2 diabetes: 850 mg single dose (23) 1.48 (± 0.5) 3.32 (±1.08) 491 (± 138) 850 mg three times daily for 19 doses (9) 1.90 (±0.62) 2.01 (± 1.22) 550 (± 160) Elderly#, healthy nondiabetic adults: 850 mg single dose (12) 2.45 (± 0.70) 2.71 (± 1.05) 412 (± 98) Renal-impaired adults: 850 mg single dose Mild (CLcrÞ 61-90 mL/min) (5) 1.86 (± 0.52) 3.20 (± 0.45) 384 (± 122) Moderate (CLcr 31-60 mL/min) (4) 4.12 (± 1.83) 3.75 (± 0.50) 108 (± 57) Severe (CLcr 10-30 mL/min) (6) 3.93 (± 0.92) 4.01 (± 1.10) 130 (± 90) Pediatrics After administration of a single oral Metformin 500 mg tablet with food, geometric mean Metformin Cmax and AUC differed less than 5% between pediatric type 2 diabetic patients (12 to 16 years of age) and gender- and weight-matched healthy adults (20 to 45 years of age), all with normal renal function. Gender Metformin pharmacokinetic parameters did not differ significantly between normal subjects and patients with type 2 diabetes when analyzed according to gender (males = 19, females = 16). Similarly, in controlled clinical studies in patients with type 2 diabetes, the antihyperglycemic effect of Metformin hydrochloride tablets was comparable in males and females. Race No studies of Metformin pharmacokinetic parameters according to race have been performed. In controlled clinical studies of Metformin in patients with type 2 diabetes, the antihyperglycemic effect was comparable in whites (n = 249), blacks (n = 51), and Hispanics (n = 24). Clinical Studies In a double-blind, placebo-controlled, multicenter U.S. clinical trial involving obese patients with type 2 diabetes whose hyperglycemia was not adequately controlled with dietary management alone (baseline fasting plasma glucose of approximately 240 mg/dL), treatment with Metformin (up to 2550 mg/day) for 29 weeks resulted in significant mean net reductions in fasting and postprandial plasma glucose (PPG) and hemoglobin A1c (HbA1c) of 59 mg/dL, 83 mg/dL, and 1.8%, respectively, compared to the placebo group (see Table 2). Table 2. Metformin vs. Placebo Summary of Mean Changes from Baseline* in Fasting Plasma Glucose, HbA1c and Body Weight, at Final Visit (29-week study) * All patients on diet therapy at Baseline † Not statistically significant Metformin (n = 141) Placebo (n = 145) p-Value FPG (mg/dL) Baseline 241.5 237.7 NS† Change at FINAL VISIT -53.0 6.3 0.001 Hemoglobin A 1c (%) Baseline 8.4 8.2 NS† Change at FINAL VISIT -1.4 0.4 0.001 Body Weight (lbs.) Baseline 201.0 206.0 NS† Change at FINAL VISIT -1.4 -2.4 NS† A 29-week, double-blind, placebo-controlled study of Metformin and glyburide, alone and in combination, was conducted in obese patients with type 2 diabetes who had failed to achieve adequate glycemic control while on maximum doses of glyburide (baseline FPG of approximately 250 mg/dL) (see Table 3). Patients randomized to the combination arm started therapy with Metformin 500 mg and glyburide 20 mg. At the end of each week of the first four weeks of the trial, these patients had their dosages of Metformin increased by 500 mg if they had failed to reach target fasting plasma glucose. After week four, such dosage adjustments were made monthly, although no patient was allowed to exceed Metformin 2500 mg. Patients in the Metformin only arm (Metformin plus placebo) followed the same titration schedule. At the end of the trial, approximately 70% of the patients in the combination group were taking Metformin 2000 mg/glyburide 20 mg or Metformin 2500 mg/glyburide 20 mg. Patients randomized to continue on glyburide experienced worsening of glycemic control, with mean increases in FPG, PPG and HbA1c of 14 mg/dL, 3 mg/dL, and 0.2%, respectively. In contrast, those randomized to Metformin (up to 2500 mg/day) experienced a slight improvement, with mean reductions in FPG, PPG, and HbA1c of 1 mg/dL, 6 mg/dL, and 0.4%, respectively. The combination of Metformin and glyburide was effective in reducing FPG, PPG, and HbA1c levels by 63 mg/dL, 65 mg/dL, and 1.7%, respectively. Compared to results of glyburide treatment alone, the net differences with combination treatment were -77 mg/dL, -68 mg/dL, and -1.9%, respectively (see Table 3). Table 3. Combined Metformin/Glyburide (Comb) vs. Glyburide (Glyb) or Metformin (MET) Monotherapy: Summary of Mean Changes from Baseline* in Fasting Plasma Glucose, HbA1c and Body Weight, at Final Visit (29-week study) * All patients on glyburide, 20 mg/day, at Baseline † Not statistically significant Comb (n=213) Glyb (n=209) MET (n=210) p-values Glyb vs. Comb MET vs. Comb MET vs. Glyb Fasting Plasma Glucose (mg/dL) Baseline 250.5 247.5 253.9 NS† NS† NS† Change at FINAL VISIT -63.5 13.7 -0.9 0.001 0.001 0.025 Hemoglobin A1c (%) Baseline 8.8 8.5 8.9 NS† NS† 0.007 Change at FINAL VISIT -1.7 0.2 -0.4 0.001 0.001 0.001 Body Weight (lbs.) Baseline 202.2 203.0 204.0 NS† NS† NS† Change at FINAL VISIT 0.9 -0.7 -8.4 0.011 0.001 0.001 The magnitude of the decline in fasting blood glucose concentration following the institution of Metformin hydrochloride tablets therapy was proportional to the level of fasting hyperglycemia. Patients with type 2 diabetes with higher fasting glucose concentrations experienced greater declines in plasma glucose and glycosylated hemoglobin. In clinical studies, Metformin, alone or in combination with a sulfonylurea, lowered mean fasting serum triglycerides, total cholesterol, and LDL cholesterol levels and had no adverse effects on other lipid levels (see Table 4). Table 4. Summary of Mean Percent Change from Baseline of Major Serum Lipid Variables at Final Visit (29-week studies) Metformin Vs Placebo Combined Metformin/Glyburide Vs Monotherapy Metformin (N = 141) Placebo (N = 145) Metformin (n = 210) Metformin/ Glyburide (n = 213) Glyburide (n = 209) Total Cholesterol (mg/dL) Baseline 211.0 212.3 213.1 215.6 219.6 Mean % change at FINAL VISIT -5% 1% -2% -4% 1% Total Triglycerides (mg/dL) Baseline 236.1 203.5 242.5 215.0 266.1 Mean % change at FINAL VISIT -16% 1% -3% -8% 4% LDL-Cholesterol (mg/dL) Baseline 135.4 138.5 134.3 136.0 137.5 Mean % change at FINAL VISIT -8% 1% -4% -6% 3% HDL-Cholesterol (mg/dL) Baseline 39.0 40.5 37.2 39.0 37.0 Mean % change at FINAL VISIT 2% -1% 5% 3% 1% In contrast to sulfonylureas, body weight of individuals on Metformin tended to remain stable or even decrease somewhat (see Table 2 and 3). A 24-week, double-blind, placebo-controlled study of Metformin plus insulin versus insulin plus placebo was conducted in patients with type 2 diabetes who failed to achieve adequate glycemic control on insulin alone (see Table 5). Patients randomized to receive Metformin plus insulin achieved a reduction in HbA1c of 2.10%, compared to a 1.56% reduction in HbA1c achieved by insulin plus placebo. The improvement in glycemic control was achieved at the final study visit with 16% less insulin, 93.0 U/day vs 110.6 U/day, Metformin plus insulin versus insulin plus placebo, respectively, p=0.04. Table 5. Combined Metformin/Insulin vs Placebo/Insulin Summary of Mean Changes from Baseline in HbA1c and Daily Insulin Dose * Statistically significant using analysis of covariance with baseline as covariate (p=0.04). Not significant using analysis of variance (values shown in table) † Statistically significant for insulin (p=0.04) Metformin/ Insulin (n = 26) Placebo/ Insulin (n = 28) Treatment Difference Mean ± SE Hemoglobin A1c (%) Baseline 8.95 9.32 Change at FINAL VISIT -2.10 -1.56 -0.54 ± 0.43* Insulin Dose (U/day) Baseline 93.12 94.64 Change at FINAL VISIT -0.15 15.93 -16.08 ± 7.77† A second double-blind, placebo-controlled study (n=51), with 16 weeks of randomized treatment, demonstrated that in patients with type 2 diabetes controlled on insulin for 8 weeks with an average HbA1c of 7.46 ± 0.97%, the addition of Metformin maintained similar glycemic control (HbA1c 7.15 ± 0.61 versus 6.97 ± 0.62 for Metformin plus insulin and placebo plus insulin, respectively) with 19% less insulin versus baseline (reduction of 23.68 ± 30.22 versus an increase of 0.43 ± 25.20 units for Metformin plus insulin and placebo plus insulin, p<0.01). In addition, this study demonstrated that the combination of Metformin plus insulin resulted in reduction in body weight of 3.11 ± 4.30 lbs, compared to an increase of 1.30 ± 6.08 lbs for placebo plus insulin, p=0.01. Pediatric Clinical Studies In a double-blind, placebo-controlled study in pediatric patients aged 10 to 16 years with type 2 diabetes (mean FPG 182.2 mg/dL), treatment with Metformin (up to 2000 mg/day) for up to 16 weeks (mean duration of treatment 11 weeks) resulted in a significant mean net reduction in FPG of 64.3 mg/dL, compared with placebo (see Table 6). Table 6. Metformin vs Placebo (Pediatrics*) Summary of Mean Changes from Baseline† in Plasma Glucose and Body Weight at Final Visit * Pediatric patients mean age 13.8 years (range 10 to 16 years) † All patients on diet therapy at Baseline ‡ Not statistically significant Metformin Placebo p-Value FPG (mg/dL) (n=37) (n=36) Baseline 162.4 192.3 Change at FINAL VISIT -42.9 21.4 <0.001 Body Weight (lbs) (n=39) (n=38) Baseline 205.3 189.0 Change at FINAL VISIT -3.3 -2.0 NS‡ Ads by Google Renal Failure Treatment Holiday Dialyis Clinics in 14 Countries. Request Free Information www.DiaverumHolidayDialysis.com Airport VIP Lounges Escape Crowded Terminals - Relax in a Luxury Airport VIP Lounge. www.PriorityPass.com Tinea Versicolor Cured Tinea Versicolor Treatment Soap. Doctor Recommended. Guaranteed. BuyDermisil.co.uk/Tinea_Versicolor Indications and Usage for Metformin Metformin hydrochloride tablets, USP are indicated as an adjunct to diet and exercise to improve glycemic control in adults and children with type 2 diabetes mellitus. Contraindications Metformin hydrochloride tablets are contraindicated in patients with: Renal disease or renal dysfunction (e.g., as suggested by serum creatinine levels ≥1.5 mg/dL , ≥1.4 mg/dL or abnormal creatinine clearance) which may also result from conditions such as cardiovascular collapse (shock), acute myocardial infarction, and septicemia (see WARNINGS and PRECAUTIONS). Known hypersensitivity to Metformin hydrochloride. Acute or chronic metabolic acidosis, including diabetic ketoacidosis, with or without coma. Diabetic ketoacidosis should be treated with insulin. Metformin should be temporarily discontinued in patients undergoing radiologic studies involving intravascular administration of iodinated contrast materials, because use of such products may result in acute alteration of renal function. (See also PRECAUTIONS.) Warnings Lactic Acidosis Lactic acidosis is a rare, but serious, metabolic complication that can occur due to Metformin accumulation during treatment with Metformin; when it occurs, it is fatal in approximately 50% of cases. Lactic acidosis may also occur in association with a number of pathophysiologic conditions, including diabetes mellitus, and whenever there is significant tissue hypoperfusion and hypoxemia. Lactic acidosis is characterized by elevated blood lactate levels (>5 mmol/L), decreased blood pH, electrolyte disturbances with an increased anion gap, and an increased lactate/pyruvate ratio. When Metformin is implicated as the cause of lactic acidosis, Metformin plasma levels > 5 mcg/mL are generally found. The reported incidence of lactic acidosis in patients receiving Metformin hydrochloride is very low (approximately 0.03 cases/1000 patient-years, with approximately 0.015 fatal cases/1000 patient-years). In more than 20,000 patient-years exposure to Metformin in clinical trials, there were no reports of lactic acidosis. Reported cases have occurred primarily in diabetic patients with significant renal insufficiency, including both intrinsic renal disease and renal hypoperfusion, often in the setting of multiple concomitant medical/surgical problems and multiple concomitant medications. Patients with congestive heart failure requiring pharmacologic management, in particular those with unstable or acute congestive heart failure who are at risk of hypoperfusion and hypoxemia, are at increased risk of lactic acidosis. The risk of lactic acidosis increases with the degree of renal dysfunction and the patient’s age. The risk of lactic acidosis may, therefore, be significantly decreased by regular monitoring of renal function in patients taking Metformin and by use of the minimum effective dose of Metformin. In particular, treatment of the elderly should be accompanied by careful monitoring of renal function. Metformin treatment should not be initiated in patients ≥ 80 years of age unless measurement of creatinine clearance demonstrates that renal function is not reduced, as these patients are more susceptible to developing lactic acidosis. In addition, Metformin should be promptly withheld in the presence of any condition associated with hypoxemia, dehydration or sepsis. Because impaired hepatic function may significantly limit the ability to clear lactate, Metformin should generally be avoided in patients with clinical or laboratory evidence of hepatic disease. Patients should be cautioned against excessive alcohol intake, either acute or chronic, when taking Metformin hydrochloride tablets, since alcohol potentiates the effects of Metformin hydrochloride on lactate metabolism. In addition, Metformin should be temporarily discontinued prior to any intravascular radiocontrast study and for any surgical procedure (see also PRECAUTIONS). The onset of lactic acidosis often is subtle, and accompanied only by nonspecific symptoms such as malaise, myalgias, respiratory distress, increasing somnolence and nonspecific abdominal distress. There may be associated hypothermia, hypotension and resistant bradyarrhythmias with more marked acidosis. The patient and the patient’s physician must be aware of the possible importance of such symptoms and the patient should be instructed to notify the physician immediately if they occur (see also PRECAUTIONS). Metformin hydrochloride tablets should be withdrawn until the situation is clarified. Serum electrolytes, ketones, blood glucose, and if indicated, blood pH, lactate levels, and even blood Metformin levels may be useful. Once a patient is stabilized on any dose level of Metformin, gastrointestinal symptoms, which are common during initiation of therapy, are unlikely to be drug related. Later occurrence of gastrointestinal symptoms could be due to lactic acidosis or other serious disease. Levels of fasting venous plasma lactate above the upper limit of normal but less than 5 mmol/L in patients taking Metformin do not necessarily indicate impending lactic acidosis and may be explainable by other mechanisms, such as poorly controlled diabetes or obesity, vigorous physical activity or technical problems in sample handling. (See also PRECAUTIONS.) Lactic acidosis should be suspected in any diabetic patient with metabolic acidosis lacking evidence of ketoacidosis (ketonuria and ketonemia). Lactic acidosis is a medical emergency that must be treated in a hospital setting. In a patient with lactic acidosis who is taking Metformin, the drug should be discontinued immediately and general supportive measures promptly instituted. Because Metformin hydrochloride is dialyzable (with a clearance of up to 170 mL/min under good hemodynamic conditions), prompt hemodialysis is recommended to correct the acidosis and remove the accumulated Metformin. Such management often results in prompt reversal of symptoms and recovery. (See also CONTRAINDICATIONS and PRECAUTIONS). Precautions General Macrovascular Outcomes There have been no clinical studies establishing conclusive evidence of macrovascular risk reduction with Metformin or any other anti-diabetic drug. Monitoring of Renal Function Metformin is known to be substantially excreted by the kidney, and the risk of Metformin accumulation and lactic acidosis increases with the degree of impairment of renal function. Thus, patients with serum creatinine levels above the upper limit of normal for their age should not receive Metformin. In patients with advanced age, Metformin should be carefully titrated to establish the minimum dose for adequate glycemic effect, because aging is associated with reduced renal function. In elderly patients, particularly those ≥80 years of age, renal function should be monitored regularly and, generally, Metformin should not be titrated to the maximum dose (see WARNINGS and DOSAGE AND ADMINISTRATION). Before initiation of Metformin therapy and at least annually thereafter, renal function should be assessed and verified as normal. In patients in whom development of renal dysfunction is anticipated, renal function should be assessed more frequently and Metformin discontinued if evidence of renal impairment is present. Use of Concomitant Medications that May Affect Renal Function or Metformin Disposition Concomitant medication(s) that may affect renal function or result in significant hemodynamic change or may interfere with the disposition of Metformin, such as cationic drugs that are eliminated by renal tubular secretion (see PRECAUTIONS: Drug Interactions), should be used with caution. Radiologic Studies Involving the Use of Intravascular Iodinated Contrast Materials (for example, intravenous urogram, intravenous cholangiography, angiography, and computed tomography (CT) scans with intravascular contrast materials) Intravascular contrast studies with iodinated materials can lead to acute alteration of renal function and have been associated with lactic acidosis in patients receiving Metformin (see CONTRAINDICATIONS). Therefore, in patients in whom any such study is planned, Metformin should be temporarily discontinued at the time of or prior to the procedure, and withheld for 48 hours subsequent to the procedure and reinstituted only after renal function has been re-evaluated and found to be normal. Hypoxic States Cardiovascular collapse (shock) from whatever cause, acute congestive heart failure, acute myocardial infarction and other conditions characterized by hypoxemia have been associated with lactic acidosis and may also cause prerenal azotemia. When such events occur in patients on Metformin therapy, the drug should be promptly discontinued. Surgical Procedures Metformin therapy should be temporarily suspended for any surgical procedure (except minor procedures not associated with restricted intake of food and fluids) and should not be restarted until the patient’s oral intake has resumed and renal function has been evaluated as normal. Alcohol Intake Alcohol is known to potentiate the effect of Metformin on lactate metabolism. Patients, therefore, should be warned against excessive alcohol intake, acute or chronic, while receiving Metformin. Impaired Hepatic Function Since impaired hepatic function has been associated with some cases of lactic acidosis, Metformin should generally be avoided in patients with clinical or laboratory evidence of hepatic disease. Vitamin B12 Levels In controlled clinical trials of Metformin of 29 weeks duration, a decrease to subnormal levels of previously normal serum vitamin B12 levels, without clinical manifestations, was observed in approximately 7% of patients. Such decrease, possibly due to interference with B12 absorption from the B12 -intrinsic factor complex, is, however, very rarely associated with anemia and appears to be rapidly reversible with discontinuation of Metformin hydrochloride tablets or vitamin B12 supplementation. Measurement of hematologic parameters on an annual basis is advised in patients on Metformin and any apparent abnormalities should be appropriately investigated and managed (see PRECAUTIONS: Laboratory Tests). Certain individuals (those with inadequate vitamin B12 or calcium intake or absorption) appear to be predisposed to developing subnormal vitamin B12 levels. In these patients, routine serum vitamin B12 measurements at two- to three-year intervals may be useful. Change in Clinical Status of Patients with Previously Controlled Type 2 Diabetes A patient with type 2 diabetes previously well controlled on Metformin hydrochloride tablets who develops laboratory abnormalities or clinical illness (especially vague and poorly defined illness) should be evaluated promptly for evidence of ketoacidosis or lactic acidosis. Evaluation should include serum electrolytes and ketones, blood glucose and, if indicated, blood pH, lactate, pyruvate, and Metformin levels. If acidosis of either form occurs, Metformin must be stopped immediately and other appropriate corrective measures initiated (see also WARNINGS). Hypoglycemia Hypoglycemia does not occur in patients receiving Metformin alone under usual circumstances of use, but could occur when caloric intake is deficient, when strenuous exercise is not compensated by caloric supplementation, or during concomitant use with other glucose-lowering agents (such as sulfonylureas and insulin) or ethanol. Elderly, *****itated, or malnourished patients, and those with adrenal or pituitary insufficiency or alcohol intoxication are particularly susceptible to hypoglycemic effects. Hypoglycemia may be difficult to recognize in the elderly, and in people who are taking beta-adrenergic blocking drugs. Loss of Control of Blood Glucose When a patient stabilized on any diabetic regimen is exposed to stress such as fever, trauma, infection, or surgery, a temporary loss of glycemic control may occur. At such times, it may be necessary to withhold Metformin and temporarily administer insulin. Metformin may be reinstituted after the acute episode is resolved. The effectiveness of oral antidiabetic drugs in lowering blood glucose to a targeted level decreases in many patients over a period of time. This phenomenon, which may be due to progression of the underlying disease or to diminished responsiveness to the drug, is known as secondary failure, to distinguish it from primary failure in which the drug is ineffective during initial therapy. Should secondary failure occur with either Metformin or sulfonylurea monotherapy, combined therapy with Metformin and sulfonylurea may result in a response. Should secondary failure occur with combined Metformin/sulfonylurea therapy, it may be necessary to consider therapeutic alternatives including initiation of insulin therapy. Information for Patients Patients should be informed of the potential risks and benefits of Metformin and of alternative modes of therapy. They should also be informed about the importance of adherence to dietary instructions, of a regular exercise program, and of regular testing of blood glucose, glycosylated hemoglobin, renal function, and hematologic parameters. The risks of lactic acidosis, its symptoms, and conditions that predispose to its development, as noted in the WARNINGS and PRECAUTIONS sections, should be explained to patients. Patients should be advised to discontinue Metformin immediately and to promptly notify their health practitioner if unexplained hyperventilation, myalgia, malaise, unusual somnolence, or other nonspecific symptoms occur. Once a patient is stabilized on any dose level of Metformin, gastrointestinal symptoms, which are common during initiation of Metformin therapy, are unlikely to be drug related. Later occurrence of gastrointestinal symptoms could be due to lactic acidosis or other serious disease. Patients should be counselled against excessive alcohol intake, either acute or chronic, while receiving Metformin. Metformin hydrochloride tablets alone do not usually cause hypoglycemia, although it may occur when Metformin is used in conjunction with oral sulfonylureas and insulin. When initiating combination therapy, the risks of hypoglycemia, its symptoms and treatment, and conditions that predispose to its development should be explained to patients and responsible family members. (See PATIENT INFORMATION Printed Below.) Laboratory Tests Response to all diabetic therapies should be monitored by periodic measurements of fasting blood glucose and glycosylated hemoglobin levels, with a goal of decreasing these levels toward the normal range. During initial dose titration, fasting glucose can be used to determine the therapeutic response. Thereafter, both glucose and glycosylated hemoglobin should be monitored. Measurements of glycosylated hemoglobin may be especially useful for evaluating long-term control (see also DOSAGE AND ADMINISTRATION). Initial and periodic monitoring of hematologic parameters (e.g., hemoglobin/hematocrit and red blood cell indices) and renal function (serum creatinine) should be performed, at least on an annual basis. While megaloblastic anemia has rarely been seen with Metformin therapy, if this is suspected, vitamin B12 deficiency should be excluded. Drug Interactions (Clinical Evaluation of Drug Interactions Conducted with Metformin) Glyburide In a single-dose interaction study in type 2 diabetes patients, co-administration of Metformin and glyburide did not result in any changes in either Metformin pharmacokinetics or pharmacodynamics. Decreases in glyburide AUC and Cmax were observed, but were highly variable. The single-dose nature of this study and the lack of correlation between glyburide blood levels and pharmacodynamic effects, makes the clinical significance of this interaction uncertain (see DOSAGE AND ADMINISTRATION: Concomitant Metformin Hydrochloride and Oral Sulfonylurea Therapy in Adult Patients). Furosemide A single-dose, Metformin-furosemide drug interaction study in healthy subjects demonstrated that pharmacokinetic parameters of both compounds were affected by co-administration. Furosemide increased the Metformin plasma and blood Cmax by 22% and blood AUC by 15%, without any significant change in Metformin renal clearance. When administered with Metformin, the Cmax and AUC of furosemide were 31% and 12% smaller, respectively, than when administered alone, and the terminal half-life was decreased by 32%, without any significant change in furosemide renal clearance. No information is available about the interaction of Metformin and furosemide when co-administered chronically. Nifedipine A single-dose, Metformin-nifedipine drug interaction study in normal healthy volunteers demonstrated that co-administration of nifedipine increased plasma Metformin Cmax and AUC by 20% and 9%, respectively, and increased the amount excreted in the urine. Tmax and half-life were unaffected. Nifedipine appears to enhance the absorption of Metformin. Metformin had minimal effects on nifedipine. Cationic Drugs Cationic drugs (e.g., amiloride, digoxin, morphine, procainamide, quinidine, quinine, ranitidine, triamterene, trimethoprim, or vancomycin) that are eliminated by renal tubular secretion theoretically have the potential for interaction with Metformin by competing for common renal tubular transport systems. Such interaction between Metformin and oral cimetidine has been observed in normal healthy volunteers in both single- and multiple-dose, Metformin-cimetidine drug interaction studies, with a 60% increase in peak Metformin plasma and whole blood concentrations and a 40% increase in plasma and whole blood Metformin AUC. There was no change in elimination half-life in the single-dose study. Metformin had no effect on cimetidine pharmacokinetics. Although such interactions remain theoretical (except for cimetidine), careful patient monitoring and dose adjustment of Metformin and/or the interfering drug is recommended in patients who are taking cationic medications that are excreted via the proximal renal tubular secretory system. Other Certain drugs tend to produce hyperglycemia and may lead to loss of glycemic control. These drugs include the thiazides and other diuretics, corticosteroids, phenothiazines, thyroid products, estrogens, oral contraceptives, phenytoin, nicotinic acid, sympathomimetics, calcium channel blocking drugs, and isoniazid. When such drugs are administered to a patient receiving Metformin, the patient should be closely observed for loss of blood glucose control. When such drugs are withdrawn from a patient receiving Metformin, the patient should be observed closely for hypoglycemia. In healthy volunteers, the pharmacokinetics of Metformin and propranolol and Metformin and ibuprofen were not affected when co-administered in single-dose interaction studies. Metformin is negligibly bound to plasma proteins and is, therefore, less likely to interact with highly protein-bound drugs such as salicylates, sulfonamides, chloramphenicol, and probenecid, as compared to the sulfonylureas, which are extensively bound to serum proteins. Carcinogenesis, Mutagenesis, Impairment of Fertility Long-term carcinogenicity studies have been performed in rats (dosing duration of 104 weeks) and mice (dosing duration of 91 weeks) at doses up to and including 900 mg/kg/day and 1500 mg/kg/day, respectively. These doses are both approximately four times the maximum recommended human daily dose of 2000 mg based on body surface area comparisons. No evidence of carcinogenicity with Metformin was found in either male or female mice. Similarly, there was no tumorigenic potential observed with Metformin in male rats. There was, however, an increased incidence of benign stromal uterine polyps in female rats treated with 900 mg/kg/day. There was no evidence of a mutagenic potential of Metformin in the following in vitro tests: Ames test (S. typhimurium), gene mutation test (mouse lymphoma cells), or chromosomal aberrations test (human lymphocytes). Results in the in vivo mouse micronucleus test were also negative. Fertility of male or female rats was unaffected by Metformin when administered at doses as high as 600 mg/kg/day, which is approximately three times the maximum recommended human daily dose based on body surface area comparisons. Pregnancy Teratogenic Effects Pregnancy Category B Recent information strongly suggests that abnormal blood glucose levels during pregnancy are associated with a higher incidence of congenital abnormalities. Most experts recommend that insulin be used during pregnancy to maintain blood glucose levels as close to normal as possible. Because animal reproduction studies are not always predictive of human response, Metformin should not be used during pregnancy unless clearly needed. There are no adequate and well-controlled studies in pregnant women with Metformin. Metformin was not teratogenic in rats and rabbits at doses up to 600 mg/kg/day. This represents an exposure of about two and six times the maximum recommended human daily dose of 2000 mg based on body surface area comparisons for rats and rabbits, respectively. Determination of fetal concentrations demonstrated a partial placental barrier to Metformin. Nursing Mothers Studies in lactating rats show that Metformin is excreted into milk and reaches levels comparable to those in plasma. Similar studies have not been conducted in nursing mothers. Because the potential for hypoglycemia in nursing infants may exist, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother. If Metformin is discontinued, and if diet alone is inadequate for controlling blood glucose, insulin therapy should be considered. Pediatric Use The safety and effectiveness of Metformin for the treatment of type 2 diabetes have been established in pediatric patients ages 10 to 16 years (studies have not been conducted in pediatric patients below the age of 10 years). Use of Metformin in this age group is supported by evidence from adequate and well-controlled studies of Metformin in adults with additional data from a controlled clinical study in pediatric patients ages 10 to 16 years with type 2 diabetes, which demonstrated a similar response in glycemic control to that seen in adults (See CLINICAL PHARMACOLOGY: Pediatric Clinical Studies.) In this study, adverse effects were similar to those described in adults. (see ADVERSE REACTIONS: Pediatric Patients.) A maximum daily dose of 2000 mg is recommended. (See DOSAGE AND ADMINISTRATION: Recommended Dosing Schedule: Pediatrics.) Geriatric Use Controlled clinical studies of Metformin hydrochloride tablets did not include sufficient numbers of elderly patients to determine whether they respond differently from younger patients, although other reported clinical experience has not identified differences in responses between the elderly and younger patients. Metformin is known to be substantially excreted by the kidney and because the risk of serious adverse reactions to the drug is greater in patients with impaired renal function, Metformin should only be used in patients with normal renal function (see CONTRAINDICATIONS, WARNINGS, and CLINICAL PHARMACOLOGY: Pharmacokinetics). Because aging is associated with reduced renal function, Metformin should be used with caution as age increases. Care should be taken in dose selection and should be based on careful and regular monitoring of renal function. Generally, elderly patients should not be titrated to the maximum dose of Metformin (see also WARNINGS and DOSAGE AND ADMINISTRATION). Adverse Reactions In a U.S. double-blind clinical study of Metformin in patients with type 2 diabetes, a total of 141 patients received Metformin therapy (up to 2550 mg per day) and 145 patients received placebo. Adverse reactions reported in greater than 5% of the Metformin patients, and that were more common in Metformin- than placebo-treated patients, are listed in Table 7. Table 7. Most Common Adverse Reactions (>5.0%) in a Placebo-Controlled Clinical Study of Metformin Monotherapy* * Reactions that were more common in Metformin- than placebo-treated patients. Metformin Monotherapy (n=141) Placebo (n=145) Adverse Reaction % of Patients Diarrhea 53.2 11.7 Nausea/Vomiting 25.5 8.3 Flatulence 12.1 5.5 Asthenia 9.2 5.5 Indigestion 7.1 4.1 Abdominal Discomfort 6.4 4.8 Headache 5.7 4.8 Diarrhea led to discontinuation of study medication in 6% of patients treated with Metformin. Additionally, the following adverse reactions were reported in ≥1.0 to ≤5.0% of Metformin patients and were more commonly reported with Metformin than placebo: abnormal stools, hypoglycemia, myalgia, lightheaded, dyspnea, nail disorder, rash, sweating increased, taste disorder, chest discomfort, chills, flu syndrome, flushing, palpitation. Pediatric Patients In clinical trials with Metformin in pediatric patients with type 2 diabetes, the profile of adverse reactions was similar to that observed in adults. Ads by Google My Pump A web site designed to help people with Diabetes.Info/Reviews & more. www.MyPump.co.uk Diabetic Diet & Meals Free Diabetic Recipes > Breakfast, Lunch - Snack - Dinner - Dessert. www.diabetesinfocenter.org Diabetes Life Insurance We guarantee the most competitive premiums for clients with diabetes www.the-insurance-surgery.co.uk Overdosage Overdose of Metformin hydrochloride has occurred, including ingestion of amounts greater than 50 grams. Hypoglycemia was reported in approximately 10% of cases, but no causal association with Metformin hydrochloride has been established. Lactic acidosis has been reported in approximately 32% of Metformin overdose cases (see WARNINGS). Metformin is dialyzable with a clearance of up to 170 mL/min under good hemodynamic conditions. Therefore, hemodialysis may be useful for removal of accumulated drug from patients in whom Metformin overdosage is suspected. Metformin Dosage and Administration There is no fixed dosage regimen for the management of hyperglycemia in patients with type 2 diabetes with Metformin or any other pharmacologic agent. Dosage of Metformin must be individualized on the basis of both effectiveness and tolerance, while not exceeding the maximum recommended daily dose. The maximum recommended daily dose of Metformin hydrochloride tablets is 2550 mg in adults and 2000 mg in pediatric patients (10 to 16 years of age). Metformin should be given in divided doses with meals and should be started at a low dose, with gradual dose escalation, both to reduce gastrointestinal side effects and to permit identification of the minimum dose required for adequate glycemic control of the patient. During treatment initiation and dose titration (see Recommended Dosing Schedule), fasting plasma glucose should be used to determine the therapeutic response to Metformin and identify the minimum effective dose for the patient. Thereafter, glycosylated hemoglobin should be measured at intervals of approximately three months. The therapeutic goal should be to decrease both fasting plasma glucose and glycosylated hemoglobin levels to normal or near normal by using the lowest effective dose of Metformin hydrochloride tablets, either when used as monotherapy or in combination with sulfonylurea or insulin. Monitoring of blood glucose and glycosylated hemoglobin will also permit detection of primary failure, i.e., inadequate lowering of blood glucose at the maximum recommended dose of medication, and secondary failure, i.e., loss of an adequate blood glucose lowering response after an initial period of effectiveness. Short-term administration of Metformin may be sufficient during periods of transient loss of control in patients usually well-controlled on diet alone. Recommended Dosing Schedule Adults In general, clinically significant responses are not seen at doses below 1500 mg per day. However, a lower recommended starting dose and gradually increased dosage is advised to minimize gastrointestinal symptoms. The usual starting dose of Metformin hydrochloride tablets is 500 mg twice a day or 850 mg once a day, given with meals. Dosage increases should be made in increments of 500 mg weekly or 850 mg every 2 weeks, up to a total of 2000 mg per day, given in divided doses. Patients can also be titrated from 500 mg twice a day to 850 mg twice a day after 2 weeks. For those patients requiring additional glycemic control, Metformin may be given to a maximum daily dose of 2550 mg per day. Doses above 2000 mg may be better tolerated given three times a day with meals. Pediatrics The usual starting dose of Metformin tablets is 500 mg twice a day, given with meals. Dosage increases should be made in increments of 500 mg weekly up to a maximum of 2000 mg per day, given in divided doses. Transfer from Other Antidiabetic Therapy When transferring patients from standard oral hypoglycemic agents other than chlorpropamide to Metformin, no transition period generally is necessary. When transferring patients from chlorpropamide, care should be exercised during the first two weeks because of the prolonged retention of chlorpropamide in the body, leading to overlapping drug effects and possible hypoglycemia. Concomitant Metformin Hydrochloride and Oral Sulfonylurea Therapy in Adult Patients If patients have not responded to four weeks of the maximum dose of Metformin HCl monotherapy, consideration should be given to gradual addition of an oral sulfonylurea while continuing Metformin HCl tablets at the maximum dose, even if prior primary or secondary failure to a sulfonylurea has occurred. Clinical and pharmacokinetic drug-drug interaction data are currently available only for Metformin plus glyburide (glibenclamide). With concomitant Metformin HCl and sulfonylurea therapy, the desired control of blood glucose may be obtained by adjusting the dose of each drug. In a clinical trial of patients with type 2 diabetes and prior failure on glyburide, patients started on Metformin 500 mg and glyburide 20 mg were titrated to 1000/20 mg, 1500/20 mg, 2000/20 mg or 2500/20 mg of Metformin and glyburide, respectively, to reach the goal of glycemic control as measured by FPG, HbA1c and plasma glucose response (see CLINICAL PHARMACOLOGY: Clinical Studies). However, attempts should be made to identify the minimum effective dose of each drug to achieve this goal. With concomitant Metformin HCl and sulfonylurea therapy, the risk of hypoglycemia associated with sulfonylurea therapy continues and may be increased. Appropriate precautions should be taken. (See Package Insert of the respective sulfonylurea.) If patients have not satisfactorily responded to one to three months of concomitant therapy with the maximum dose of Metformin and the maximum dose of an oral sulfonylurea, consider therapeutic alternatives including switching to insulin with or without Metformin. Concomitant Metformin and Insulin Therapy in Adult Patients The current insulin dose should be continued upon initiation of Metformin therapy. Metformin therapy should be initiated at 500 mg once daily in patients on insulin therapy. For patients not responding adequately, the dose of Metformin should be increased by 500 mg after approximately 1 week and by 500 mg every week thereafter until adequate glycemic control is achieved. The maximum recommended daily dose is 2500 mg for Metformin. It is recommended that the insulin dose be decreased by 10% to 25% when fasting plasma glucose concentrations decrease to less than 120 mg/dL in patients receiving concomitant insulin and Metformin. Further adjustment should be individualized based on glucose-lowering response. Specific Patient Populations Metformin is not recommended for use in pregnancy. Metformin is not recommended in patients below the age of 10 years. The initial and maintenance dosing of Metformin hydrochloride tablets should be conservative in patients with advanced age, due to the potential for decreased renal function in this population. Any dosage adjustment should be based on a careful assessment of renal function. Generally, elderly, *****itated, and malnourished patients should not be titrated to the maximum dose of Metformin hydrochloride tablets. Monitoring of renal function is necessary to aid in prevention of lactic acidosis, particularly in the elderly. (See WARNINGS.) How is Metformin Supplied Metformin hydrochloride tablets, USP 500 mg are white, round, unscored, film-coated tablets, debossed GP 124 on one side and plain on the reverse side, and are supplied as follows: NDC 0781-5050-61 in bottles of 60 tablets, boxes of 12 NDC 0781-5050-01 in bottles of 100 tablets NDC 0781-5050-05 in bottles of 500 tablets NDC 0781-5050-10 in bottles of 1000 tablets Metformin hydrochloride tablets, USP 850 mg are white, round, unscored, film-coated tablets, debossed GP 127 on one side and plain on the reverse side, and are supplied as follows: NDC 0781-5051-61 in bottles of 60 tablets, boxes of 12 NDC 0781-5051-01 in bottles of 100 tablets NDC 0781-5051-05 in bottles of 500 tablets Metformin hydrochloride tablets, USP 1000 mg are white, oval-shaped, scored, film-coated tablets, debossed GP 128 on one side and plain on the reverse side, and are supplied as follows: NDC 0781-5052-61 in bottles of 60 tablets, boxes of 12 NDC 0781-5052-01 in bottles of 100 tablets NDC 0781-5052-05 in bottles of 500 tablets Store at 20°-25°C (68°-77°F) . Dispense in a light-resistant container with a child-resistant closure. PATIENT INFORMATION Metformin HYDROCHLORIDE TABLETS, USP Read this information carefully before you start taking this medicine and each time you refill your prescription. There may be new information. This information does not take the place of your doctor’s advice. Ask your doctor or pharmacist if you do not understand some of this information or if you want to know more about this medicine. What is Metformin? Metformin is used to treat type 2 diabetes. This is also known as non-insulin-dependent diabetes mellitus. People with type 2 diabetes are not able to make enough insulin or respond normally to the insulin their bodies make. When this happens, sugar (glucose) builds up in the blood. This can lead to serious medical problems including kidney damage, amputations, and blindness. Diabetes is also closely linked to heart disease. The main goal of treating diabetes is to lower your blood sugar to a normal level. High blood sugar can be lowered by diet and exercise, by a number of medicines taken by mouth, and by insulin shots. Before you take Metformin, try to control your diabetes by exercise and weight loss. While you take your diabetes medicine, continue to exercise and follow the diet advised for your diabetes. No matter what your recommended diabetes management plan is, studies have shown that maintaining good blood sugar control can prevent or delay complications of diabetes, such as blindness. Metformin helps control your blood sugar in a number of ways. These include helping your body respond better to the insulin it makes naturally, decreasing the amount of sugar your liver makes, and decreasing the amount of sugar your intestines absorb. Metformin does not cause your body to make more insulin. Because of this, when taken alone, they rarely cause hypoglycemia (low blood sugar), and usually do not cause weight gain. However, when they are taken with a sulfonylurea or with insulin, hypoglycemia is more likely to occur, as is weight gain. WARNING: A small number of people who have taken Metformin have developed a serious condition called lactic acidosis. Lactic acidosis is caused by a buildup of lactic acid in the blood. This happens more often in people with kidney problems. Most people with kidney problems should not take Metformin. (See “What are the side effects of Metformin?”) Who should not take Metformin? Some conditions increase your chance of getting lactic acidosis, or cause other problems if you take Metformin. Most of the conditions listed below can increase your chance of getting lactic acidosis. Do not take Metformin if you: have kidney problems have liver problems have heart failure that is treated with medicines, such as Lanoxinź (digoxin) or Lasixź (furosemide) drink a lot of alcohol. This means you binge drink for short periods or drink all the time are seriously dehydrated (have lost a lot of water from your body) are going to have an x-ray procedure with injection of dyes (contrast agents) are going to have surgery develop a serious condition, such as heart attack, severe infection, or a stroke are 80 years or older and you have NOT had your kidney function tested Tell your doctor if you are pregnant or plan to become pregnant. Metformin may not be right for you. Talk with your doctor about your choices. You should also discuss your choices with your doctor if you are nursing a child. Can Metformin hydrochloride tablets be used in children? Metformin has been shown to effectively lower glucose levels in children (ages 10 to 16 years) with type 2 diabetes. Metformin has not been studied in children younger than 10 years old. Metformin has not been studied in combination with other oral glucose-control medicines or insulin in children. If you have any questions about the use of Metformin hydrochloride tablets in children, talk with your doctor or other healthcare provider. How should I take Metformin hydrochloride tablets? Your doctor will tell you how much medicine to take and when to take it. You will probably start out with a low dose of the medicine. Your doctor may slowly increase your dose until your blood sugar is better controlled. You should take Metformin with meals. Your doctor may have you take other medicines along with Metformin to control your blood sugar. These medicines may include insulin shots. Taking Metformin with insulin may help you better control your blood sugar while reducing the insulin dose. Continue your exercise and diet program and test your blood sugar regularly while taking Metformin. Your doctor will monitor your diabetes and may perform blood tests on you from time to time to make sure your kidneys and your liver are functioning normally. There is no evidence that Metformin causes harm to the liver or kidneys. Tell your doctor if you have an illness that causes severe vomiting, diarrhea or fever, or if you drink a much lower amount of liquid than normal. These conditions can lead to severe dehydration (loss of water in your body). You may need to stop taking Metformin for a short time. plan to have surgery or an x-ray procedure with injection of dye (contrast agent). You may need to stop taking Metformin hydrochloride tablets for a short time. start to take other medicines or change how you take a medicine. Metformin can affect how well other drugs work, and some drugs can affect how well Metformin works. Some medicines may cause high blood sugar. What should I avoid while taking Metformin hydrochloride tablets? Do not drink a lot of alcoholic drinks while taking Metformin. This means you should not binge drink for short periods, and you should not drink a lot of alcohol on a regular basis. Alcohol can increase the chance of getting lactic acidosis. What are the side effects of Metformin? Lactic Acidosis. In rare cases, Metformin can cause a serious side effect called lactic acidosis. This is caused by a buildup of lactic acid in your blood. This buildup can cause serious damage. Lactic acidosis caused by Metformin is rare and has occurred mostly in people whose kidneys were not working normally. Lactic acidosis has been reported in about one in 33,000 patients taking Metformin over the course of a year. Although rare, if lactic acidosis does occur, it can be fatal in up to half the people who develop it. It is also important for your liver to be working normally when you take Metformin. Your liver helps remove lactic acid from your blood. Make sure you tell your doctor before you use Metformin if you have kidney or liver problems. You should also stop using Metformin and call your doctor right away if you have signs of lactic acidosis. Lactic acidosis is a medical emergency that must be treated in a hospital. Signs of lactic acidosis are: feeling very weak, tired, or uncomfortable unusual muscle pain trouble breathing unusual or unexpected stomach discomfort feeling cold feeling dizzy or lightheaded suddenly developing a slow or irregular heartbeat If your medical condition suddenly changes, stop taking Metformin and call your doctor right away. This may be a sign of lactic acidosis or another serious side effect. Other Side Effects. Common side effects of Metformin include diarrhea, nausea, and upset stomach. These side effects generally go away after you take the medicine for a while. Taking your medicine with meals can help reduce these side effects. Tell your doctor if the side effects bother you a lot, last for more than a few weeks, come back after they’ve gone away, or start later in therapy. You may need a lower dose or need to stop taking the medicine for a short period or for good. About 3 out of every 100 people who take Metformin have an unpleasant metallic taste when they start taking the medicine. It lasts for a short time. Metformin rarely cause hypoglycemia (low blood sugar) by themselves. However, hypoglycemia can happen if you do not eat enough, if you drink alcohol, or if you take other medicines to lower blood sugar. General advice about prescription medicines If you have questions or problems, talk with your doctor or other healthcare provider. You can ask your doctor or pharmacist for the information about Metformin that is written for healthcare professionals. Medicines are sometimes prescribed for purposes other than those listed in a patient information leaflet. Do not use Metformin for a condition for which it was not prescribed. Do not share your medicine with other people. Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088. 01-2011M 7400 4260090 Sandoz Inc. Princeton, NJ 08540 mg Label NDC 0781-5050-61 Metformin Hydrochloride Tablets, USP 500 mg Rx only 60 Tablets SANDOZ mg Label NDC 0781-5051-61 Metformin Hydrochloride Tablets, USP 850 mg Rx only 60 Tablets SANDOZ mg Label NDC 0781-5052-61 Metformin Hydrochloride Tablets, USP 1000 mg Rx only 60 Tablets SANDOZ Metformin HYDROCHLORIDE Metformin hydrochloride tablet, film coated Product Information Product Type HUMAN PRESCRIPTION DRUG NDC Product Code (Source) 0781-5050 Route of Administration ORAL DEA Schedule Active Ingredient/Active Moiety Ingredient Name Basis of Strength Strength Metformin HYDROCHLORIDE (Metformin) Metformin HYDROCHLORIDE 500 mg Inactive Ingredients Ingredient Name Strength COLLOIDAL SILICON DIOXIDE HYPROMELLOSES MAGNESIUM STEARATE POLYETHYLENE GLYCOL POLYSORBATE 80 POVIDONE SODIUM STARCH GLYCOLATE TYPE A POTATO STARCH, CORN TITANIUM DIOXIDE Product Characteristics Color WHITE Score no score Shape ROUND Size 11mm Flavor Imprint Code GP124 Contains Packaging # NDC Package Description Multilevel Packaging 1 0781-5050-61 12 BOTTLE In 1 CARTON contains a BOTTLE 1 60 TABLET In 1 BOTTLE This package is contained within the CARTON (0781-5050-61) 2 0781-5050-10 1000 TABLET In 1 BOTTLE None 3 0781-5050-05 500 TABLET In 1 BOTTLE None 4 0781-5050-01 100 TABLET In 1 BOTTLE None Marketing Information Marketing Category Application Number or Monograph Citation Marketing Start Date Marketing End Date ANDA ANDA075985 01/25/2002 Metformin HYDROCHLORIDE Metformin hydrochloride tablet, film coated Product Information Product Type HUMAN PRESCRIPTION DRUG NDC Product Code (Source) 0781-5051 Route of Administration ORAL DEA Schedule Active Ingredient/Active Moiety Ingredient Name Basis of Strength Strength Metformin HYDROCHLORIDE (Metformin) Metformin HYDROCHLORIDE 850 mg Inactive Ingredients Ingredient Name Strength COLLOIDAL SILICON DIOXIDE HYPROMELLOSES MAGNESIUM STEARATE POLYETHYLENE GLYCOL POLYSORBATE 80 POVIDONE SODIUM STARCH GLYCOLATE TYPE A POTATO STARCH, CORN TITANIUM DIOXIDE Product Characteristics Color WHITE Score no score Shape ROUND Size 13mm Flavor Imprint Code GP127 Contains Packaging # NDC Package Description Multilevel Packaging 1 0781-5051-61 12 BOTTLE In 1 CARTON contains a BOTTLE 1 60 TABLET In 1 BOTTLE This package is contained within the CARTON (0781-5051-61) 2 0781-5051-05 500 TABLET In 1 BOTTLE None 3 0781-5051-01 100 TABLET In 1 BOTTLE None Marketing Information Marketing Category Application Number or Monograph Citation Marketing Start Date Marketing End Date ANDA ANDA075985 01/25/2002 Metformin HYDROCHLORIDE Metformin hydrochloride tablet, film coated Product Information Product Type HUMAN PRESCRIPTION DRUG NDC Product Code (Source) 0781-5052 Route of Administration ORAL DEA Schedule Active Ingredient/Active Moiety Ingredient Name Basis of Strength Strength Metformin HYDROCHLORIDE (Metformin) Metformin HYDROCHLORIDE 1000 mg Inactive Ingredients Ingredient Name Strength COLLOIDAL SILICON DIOXIDE HYPROMELLOSES MAGNESIUM STEARATE POLYETHYLENE GLYCOL POLYSORBATE 80 POVIDONE SODIUM STARCH GLYCOLATE TYPE A POTATO STARCH, CORN TITANIUM DIOXIDE Product Characteristics Color WHITE Score 2 pieces Shape OVAL Size 19mm Flavor Imprint Code GP128 Contains Packaging # NDC Package Description Multilevel Packaging 1 0781-5052-61 12 BOTTLE In 1 CARTON contains a BOTTLE 1 60 TABLET In 1 BOTTLE This package is contained within the CARTON (0781-5052-61) 2 0781-5052-05 500 TABLET In 1 BOTTLE None 3 0781-5052-01 100 TABLET In 1 BOTTLE None Marketing Information Marketing Category Application Number or Monograph Citation Marketing Start Date Marketing End Date ANDA ANDA075985 01/25/2002 Labeler - Sandoz Inc (110342024) Establishment Name Address ID/FEI Operations Sandoz Inc 110342024 MANUFACTURE Establishment Name Address ID/FEI Operations Eon Labs, Inc. 012656273 MANUFACTURE Establishment Name Address ID/FEI Operations USV Limited 650434348 API MANUFACTURE
Insulina ZA i PRZECIW
ciekawa dyskusja sie rozwinela. Kazdy wali i robi to co chce kwestia priorytetow. Generalnie ciekaw jestem jak kolega vip wyglada. 6x 10 slinu ed to sporo tzn nieznam sie malo wiem o insulinie wiec moze dlatego. Bardzo mnie ciekawi czy jest mozliwe zdobycie suchej masy na takich dawkach a raczej jak mocno nas nie zaleje . Blx widzailem foty gadalem z gosciem i wyglada sie podchodzic do tematu z glowa . Ladowac slin po to zeby byc grubasem to troche bzdura. Pozatym te przyrosty spoko 15kg przyrostu ale dajcie spokoj po pierwsze jest to nie zdrowe dla organizmu ciezko przywzwyczaic sie do nowej wagi , niewiadomo ile z tego zostanie kolejna sprawa nie oszukujmy sie cykl 10 tyg przyrost 15kg miesnia z tego niech bedzie 3kg .Zrob 2 cykle rocznie do*** 30 kg to za kilka lat bedziesz potworem wiekszym od ruhla. Takie moje zdanie c*** z takiej masy gowno wartej zeby byc tlustym nie trzeba wcale insy grzac. No chyba ze ktos ma taka wiedze a zakladam ze vipa doswiadczenie i wiedza jest i robi relatywnie sucha mase to tylko i wylacznie szacunek.
Insulina ZA i PRZECIW
dobra ale wezme pod uwage co oni wiedza a co my wiemy . do tego co wala itd biora inse i maja prazki ale to inna liga . Zeby opanowac insuline moim zdaniem potrzeba lat zabawy z tym srodkiem. A nie 2 czy 3 cykli . Zazwyczaj jak ktos lapie za inse to c*** wielki z tego wychodzi . Pakuja mase ale jakosciowo lipa. Wszystko sie da tylko trzeba wiedziec jak. Wydaje mi sie ze malo osob wie . Bynajmniej tutaj w naszym gronie.
Insulina ZA i PRZECIW
chłopaki nie jeden z was na******la ostre imprezy co do dawek to na mnie inaczej działa 30mg a inaczej 50mg to samo ineczej 500mg tescia a inaczej 1000mg co do zdjecia to nikomu nie obiecywałem ze dam po za tym zle mnie odebraliscie nie uwarzam sie za eksperta po prostu mam swoje teorie jak wielu z tych co było na forum wchodziliscie na nich a za jakis czas pisaliscie ze cos wiedzieli a teraz sfd to c***nia jest z nikim nie chce wchodzić w spiny faktycznie zle sie zachowałem ale nie uważam ze napisałem jeśli chodzi o doping coś niezgodnego z prawdą Zmieniony przez - vipssclub w dniu 2011-08-23 08:39:48
Insulina ZA i PRZECIW
tak wpadlem poczytac widze tutaj juz bzdury leca wiec mimo ze juz kupe czasu nie cwicze ani silki nie widzialem nawet to : - kreatyna zayebiscie obciaza nerki, moj znajomy wyladowal po kretce w szpitalu (jadl bodajze 20-25g dziennie) - raz stworzona komorka tluszczowa pozostaje na cale zycie zwiekszajac badz zmniejszajac objetosc - w miejscu wbijania slina moga ulegac obumarciu/wypaleniu komurki tluszczowe lub odwrotnie moga sie tworzyc nowe (to z ulotki humaloga) - kazdy strzal slinu to krok w kierunku cukrzycy, wypalasz te wyepki i tyle.. niech nikt sie nie oszukuje ze nie, tu sie nic nie regeneruje etc to sa fakty nie mity pozdro koksy edit : myslal ktos nad pomiarem peptydu c po bombie i w sumie przed zeby zobaczyc ile tam wysp zostalo ? czy cale archipelagi czy juz tam tylko kilka ostro przpracowanych walcz zeby jakos to bylo ? Zmieniony przez - MICOOOLAI w dniu 2011-09-07 13:39:08
Insulina ZA i PRZECIW
sracie sie z ta insa i tym cukrem jak c*** . Tzn spoko rozumiem ze ktos tam sie boi itd i zre cukier ale.. Vips nie bije do Ciebie mowie ogolnie bo z tego co pamietam interesuje Cie ogromna masa. Ale jak chcesz robic dobra jakosc na slinie to niema opcji zeby na******lac tyle cukru. Walisz na pograniczu hipki troche , tzn jesz normalne posilki a nie ciagle gainer i gainer. Wstajesz wbijasz robisz zarcie i tyle dajesz mieszane wegle troche proste z zlozonymi ale tez bez przesady z prostymi. Mi sie podoba opcja posilku co 3h a w miedzy czasie jablko + izolat . Sprawdze jak sie zdecyduje moze w ta zime na slin. Ale mowie jak ja zrobilem a nie z teorii z***alem totalnie sprawe bo dalem za duzo wegli. Wiecej juz tak nie zrobie. Pozatym na tym poziomie powyzej 10 iu slinu to bzdura . stawiasz na jakosc im wiecej dobrej jakosci zarcia zjesz tym lepiej bedziesz wygladal i mniej sie otluszczal. To tak samo jak z redukcja i kiedys myslalem ze jak bede robil aero dwa razy dziennie i podjadal troche albo jadl nie tak czysto jakbym musial to bedzie git . Po czesci sie uda owszem. Ale jakbys dal tyle samo kcal a jakosciowo zarcie czyste na maxa to jeszcze bys byl w stanie budowac mieso . I to jest fakt. Dlatego odpuscilem sobie totalnie jakie kolwiek posilki oszukane na diecie tak dlugo bede cisnac az w koncu bede zadowolony. Zmieniony przez - Center88 w dniu 2011-09-20 13:11:23
Insulina ZA i PRZECIW
no a ja slyszalem wlasnie ale ile w tym prawdy to niewiem wlasnie. Bo to sa plotki osobiscie tej osoby nieznam. wy tutaj sie hipki boicie hipka to jest c*** trzeba niewiadomo ile walic i do tego byc idiota zeby od***ac numer i wyjechac na sygnale. Mnie bardziej interesuje tutaj mozliwosc zachorowania na cukrzyce dlatego podchodze do slinu z dystansem. Zmieniony przez - Center88 w dniu 2011-09-22 12:19:54
Insulina ZA i PRZECIW
juz tydzień na slinie dawka 5iu do posiłku przed treningowego i 6iu po w dni nie treningowe tylko do 1 posiłku 5iu, masa 2kg up glikogenu sie troche nadmagazynowało ale nie ulewa mnie narazie kable na ramionach napewno na plus na treningu juz konkret kable wychodzą, najbardziej mi sie podoba ta pompa na treningu człowiek odrazu inaczej wyglada, bez saa nie licze na duzo ale narazie dobrze jest, siłowo nic wiekszych zmian nie zauwazyłem bardziej wytrzymałosciowo i wieksza odpornośc na ból, mozna doje**ć do pieca ładnie na treningu a na drugi dzien mógł bym to powtórzyc he regeneracja swietna, co ktos mówił o wzroku to prawda znacznie sie pogarsza i dziury w głowie jak by sie upalonym chodziło codzien, ale to tez dziury spowodowane tym ze tylko siłownia 24h na dobe jesc trening jesc spać i o reszcie sie juz zapomina
L-tyrozyna
btw 3 g tyrozyny z 2-3 * TS naprawde pobudza podobnie do dawki standardowej E/C przynajmniej mnie przed treningiem silowym
Box Squats http://www.youtube.com/watch?feature=player_embedded&v=C-5u60CUTNc
Dzięki za odpowiedź. -Co do nóg...myślałem, że 3 razy w tygodniu bieganie jest lepsze niż katowanie raz w tygodniu na siłowni. -Jeżeli chodzi o liczbę serii to rozumiem, że podałeś łączną liczbę ze wszystkich ćwiczeń na daną partię w danym treningu. -Jak to jest z tym przedramieniem? Zmieniony przez - C-Shprot w dniu 2012-02-07 14:11:25
Metamorfoza z Mistrzem - adkens
18.12.2013 - Środa Trening: - bieganie(35min) - rozciąganie Jeszcze czuje nogi po poniedziałku ale trzeba to trzeba biegać ;) Dieta: 1. Posiłek -whey protein 81+ 40g -płatki owsiane -orzechów laskowych 25g 2. Posiłek -carbo 80g i bulk 70g 3-5. Posiłki - kasza gryczana/wafle ryżowe/ziemniaki : 80w/w - pierś z kurczaka/WPC 30g białka - słonecznik/oliwa z oliwek/orzechy 5-10g tłuszczu 6. Posiłek(wyczekiwany cały dzień najlepszy!) - good night 40g - masło orzechowe tu dałem jeszcze trochę mleka wszystko do blendera i smak nieziemski :) niedługo będą fotki itd Suplementacja: -crea force 5kaps. + pół miarki Bcaa+Glutamine rano na czczo -2kaps. C fit -pół miarki Bcaa+Glutamine + 5kaps. crea force -70g bulk mass + 80g carbo Naprawdę trening odczuwalne następnego dnia , duża ilość kcal . Może zakwasy nie powinny aż tak cieszyć bo wiadomo bolą , ale to znak , że dałem idealny bodziec na mięsień ! Dzięki Karol Zmieniony przez - adkens w dniu 2013-12-18 23:44:28
Metamorfoza z Mistrzem - adkens
1.01.01 - Środa Trening: Karol kazał zupełnie odpocząć , ale jestem nadgorliwy no i brzuch zrobiłem lekko z lekkim cardio bo grałem w piłkę trochę mam nadzieję , że to nie jest wielki błąd :) oprócz tego rozciąganie. Dieta: 1. Posiłek - płatki owsiane 115g - rodzynki 20g - jabłko 60g - wpc 40g 2. Posiłek( po gierce) - bulk 70g - ryż biały 100g(ze względu, że dzień nietreningowy dałem zamiast carbo ryż) 3-5 Posiłek - makaron/kasza gryczana/kasza jęczmienna : 4 paczki - pierś z kurczaka/jajka - orzechy laskowe/oliwa z oliwek 6. Posiłek - Good Night 60g - masło orzechowe 40g Suplementacja: -crea force 5kaps. + pół miarki Bcaa+Glutamine rano na czczo -2kaps. C fit -pół miarki Bcaa+Glutamine + 5kaps. crea force -70g bulk mass
