Intended for healthcare professionals

Rapid response to:

Research

Prospective study of alcohol drinking patterns and coronary heart disease in women and men

BMJ 2006; 332 doi: https://doi.org/10.1136/bmj.38831.503113.7C (Published 25 May 2006) Cite this as: BMJ 2006;332:1244

Rapid Response:

“Biologically Plausible Mechanisms”

May 29, 2006

Tolstrup, et al, briefly address “biologically plausible mechanisms.”

Moderate amounts of alcohol suppress gluconeogenesis in the liver,
thus lowering the glucose load (total endogenous and exogenous glucose,
mostly glycogen stores - not the blood glucose level).

The desirable effects of moderate alcohol consumption result from
this reduction in glucose load as reflected in reductions in excessive
levels of glycogen storage in liver and then in consequent reductions in
VLDL production in the liver (VLDL production is triggered by a state of
overfull liver glycogen stores).

The VLDL reduction inhibits atherogenesis (VLDLs in the plasma
interact with CEPT, HDLs, and LDLs to produce small, dense atherogenic
LDLs and lower HDL levels).

The lower glucose load reduces beta cell destruction by reducing
insulin production demands (fuller glycogen stores require higher plasma
insulin to cram in new blood glucose via the glucose gradient - quite
separate from “insulin resistance”).

Note that both the mechanism of action of moderate alcohol and its
results parallel those of the diabetes drug metformin. Metformin’s
mechanism of direct action also is suppression of gluconeogenesis.

Of course, on modern diets gluconeogenesis only adds marginal amounts
of glucose while excessive glycogen levels are predominantly caused by
excessive dietary carbohydrate.

cfredc1@yahoo.com

Competing interests:
None declared

Competing interests: No competing interests

30 May 2006
Charles R. Fred
Electrical Engineer
Retired, New York City