And it raises shbg, which reduces circulating free androgens, which obviously isn't a good thing.
This is a side i suffer when i was off but now on Test E, DBOL and EQ and some proviron.
Do you think this could make a difference?
Same for B 12 and folic acid deficient absorption...B vitamins are not a problem if you get 3 B complexs tabs per day + 1-2 multivitamins/mineral per day.(on Metformin of off).
I prefer old metformin who can improve my peripheral slin sensitivity (normally not very good as Endomorph) and down a bit androgens and high SHBG to Avandia risk of heart attack and HIGH price.
About lactic acidosis and his relation with Metformin:
http://www.ncbi.nlm.nih.gov/entrez/...ve&db=PubMed&list_uids=11412284&dopt=Abstract
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Lactic acidosis in metformin therapy: searching for a link with metformin in reports of 'metformin-associated lactic acidosis'.
Lalau JD, Race JM.
Service d'Endocrinologie-Nutrition, Hopital Universitaire, Amiens, France.
[email protected]
OBJECTIVE: The link between metformin and lactic acidosis in metformin therapy may be causal, associated or coincidental. Our objective was to investigate this link by studying and analysing published reports of so-called 'metformin-associated lactic acidosis'. RESEARCH DESIGN AND METHODS: systematically searched in the BIOSIS, DERWENT, EMBASE, MEDLINE, and PASCAL databases of the English language and non-English language literature for all reports of so-called 'metformin-associated lactic acidosis' published from May 1995 through January 2000. We did not include reports related to metformin overdose or contrast media-induced renal failure. Metformin accumulation and concurrent pathologies were critically reviewed as precipitating factors for metformin-associated lactic acidosis. Metformin accumulation was assessed in terms of the recorded measurement of metformin concentration in plasma or, if not available, by the presence of primary renal failure, i.e. renal failure that was not secondary to a shock syndrome. RESULTS: We found 21 reports describing a total of 26 patients. Criteria of lactic acidosis (lactate > 5 mmol/l, pH <or= 7.35) were not met in four patients. In the remaining 22 patients, plasma metformin concentration was determined in only four, of whom one had a normal value. In the 18 patients with lactic acidosis where plasma metformin concentration data was not available, the presence of primary renal failure was absent or unlikely in six patients, uncertain in two, and likely or proven in 14. With regard to these 14 patients, the precipitating factor was metformin in 12 patients (in the context of renal failure either chronic or acute) and intercurrent pathologies in two others. Overall, lactic acidosis was either absent (n = 4), precipitated by concurrent pathology (n = 8), precipitated by metformin without apparent associated pathology (n = 12) or of uncertain origin (n = 2). Death occurred 10 times but only once in the 12 patients with metformin-induced lactic acidosis and this was not related to metformin.
CONCLUSIONS: While the term 'metformin-associated lactic acidosis' is commonly used to depict all situations of lactic acidosis in metformin therapy, true metformin-associated lactic acidosis, i.e. one which refers to metformin and concurrent pathologies as co-precipitating factors, was never observed in the studied reports. As there was no mortality due to metformin alone, it is important that physicians are familiar with the range of other risk factors that contribute to lactic acidosis in patients treated with metformin.
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http://care.diabetesjournals.org/cgi/content/abstract/22/6/925
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Diabetes Care, Vol 22, Issue 6 925-927, Copyright © 1999 by American Diabetes Association
ARTICLES
Incidence of lactic acidosis in metformin users
M Stang, DK Wysowski and D Butler-Jones
Saskatchewan Health, Regina, Canada.
[email protected]
OBJECTIVE: The purpose of this study was to determine the incidence of lactic acidosis in a geographically defined population of metformin users. RESEARCH DESIGN AND METHODS: The study was based on a historical cohort from the Saskatchewan Health administrative databases. Individuals with a metformin prescription dispensed between 1980 and 1995 inclusive were eligible for the cohort. Person-years of exposure were calculated. Cases were defined by hospital discharge with a diagnosis of acidosis (International Classification of Diseases, Ninth Revision code: 276.2) and confirmation by chart review of a blood lactate level > or = 5 mmol/l. Death registrations of individuals dying within 120 days of a metformin prescription were also reviewed. RESULTS: During the study period, 11,797 residents received one or more metformin prescriptions, resulting in 22,296 person-years of exposure. There were 10 subjects who had hospital discharges with a diagnosis of acidosis.
However, primary record review revealed only two cases with laboratory findings of elevated blood lactate levels, for an incidence rate of 9 cases per 100,000 person-years of metformin exposure. In both cases, other factors besides metformin could have contributed to the lactic acidosis. No additional cases were found on review of death registrations. CONCLUSIONS: From 1980 through 1995, the incidence rate of lactic acidosis was 9 per 100,000 person-years (95% CI 0-21) in patients dispensed metformin in Saskatchewan, Canada. This incidence rate was derived from a population with complete ascertainment of hospitalizations and deaths associated with lactic acidosis in metformin users. It is similar to previously published rates based on passive reporting of cases, and it is well below the lactic acidosis rate of 40-64 per 100,000 patient-years in patients prescribed phenformin.
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