A new report from University of Louiseville describes 3 patients with resistant menopausal syndrome- hot flashes, fatigue and sweating- referred for endocrine workup; who proved to have hyperinsulinemia with normal glucose tolerance, and recovered on metformin 1gm/day.
This bears out
- that the average natural fat gain around the menopause- which is aggravated by oral estrogen-progestin(HT)- is perhaps more amenable to the co-hormone metformin (or numerous natural insulin-sensitizing equivalents) than to generally adverse risky oral HT;
- and the weight gain and insulin resistance are best reduced by metformin, which reduces the high risk of all the chronic degenerative diseases of aging that accelerate around menopause. If sex hormone replacement is still required, it is best used physiologically as non-oral balanced appropriate hormones based on restoration of average youthful blood levels eg with testosterone, estradiol and progesterone.
One must just remember that
- sensitivity to metformin varies greatly genetically as well as by size, so dose should always be started low eg ~125mg/day and titrated up over a few days to establish tolerance; (and the dose backtitrated if necessary to avoid symptoms eg nausea, diarrhoea. Metformin on it’s own with sensible diet never produces hypoglycemia;.
- Demonstration of insulin resistance let alone a raised blood glucose is often the extra motivation needed to persuade patients to stop using sugar and sugared foods/drinks, let alone cook fat-free .
- and that middle-aged patients who present should routinely have a fasting, and fed (at least eg 90mins after a can of Coke) blood glucose and insulin level, if not a full glucose-insulin tolerance test.
Another new study from Canada shows that even in patients around 77 years of age with diabetes and heart-failure, many are already being treated with metformin- a mean of about 1.7gm/day- indicating that there, there is no uncertainty about it’s safety and benefits under supervision. This is confirmed by a simultaneous publication from Albert Einstein College (Bronx) in which the use of lowdose metformin after experimental heartfailure in mice improves survival by 47%, through activation of AMPK- just as metformin improves thrombolysis, and energy uptake in all muscle (let alone improving bloodflow by lowering fibrinogen, inflammation, CRP).
Hence starting metformin preventively in the overweight / lipidemic – even before obesity, hypertension, lipidemia, depression, cancer, diabetes, vascular disease and heart failure supervene- can only be even better and safer.