Moderate Alcohol Consumption Increases Neurogenesis in the Adult Mouse

The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 9 No. 2 • April 2006


Moderate Alcohol Consumption Increases Neurogenesis in the Adult Mouse

A new paper reports the exciting news that in mice, moderate levels of voluntarily ingested ethanol (~6 g/kg·day) for ~10 weeks increased the proliferation of cells in the dentate gyrus of the brain, which survived and developed a neural phenotype.1 (This is about the amount of alcohol contained in 1 to 2 drinks per day for an adult human when calculated on a food-intake basis.) Moreover, the ethanol consumption at this level did not increase apoptosis (programmed cell death) or change differentiation or distribution patterns of the new cells. (It has previously been shown that binge ethanol administration for 1 and 4 days or via food for 6 weeks results in a decrease of neurogenesis in adult rats.1) After discontinuation of alcohol treatment in this study, it took 3 days for the proliferation rate to return to basal levels. Interestingly, the researchers report that in their study, female mice were investigated because they tend to consume more alcohol and that the mice were also kept one to a cage because group-housed animals do not consume much ethanol. Isolation is a social stress in both mice and humans. The authors suggest that “It is, thus, possible that ethanol had anxiolytic [anti-anxiety] effects in the present experiments, thereby counteracting a stress-induced depression of neurogenesis.”

Studies in alcoholics have found decreases in hippocampal size due to a reduction of white matter and numbers of astrocytes, though not in a reduction of neurons.1 Moderate alcohol consumption is thought to act as a mild stressor that results in upregulation of protective mechanisms, with consequent health benefits. For example, moderate alcohol consumption has been reported to increase cholesterol efflux in humans,2 inhibit advanced glycation end-product formation by acetaldehyde in diabetic rats,3 reduce the risk of total and cardiovascular disease mortality in hypertensive men,4 and increase HDL in men and women and reduce platelet aggregability in humans as well as animals.5

There is, in fact, a rather large scientific literature on substances (including ionizing radiation and ozone) that are toxic in large amounts but induce protective mechanisms for beneficial effects at low doses, a process called hormesis. Even caloric restriction is believed by some scientists6 to be a low-intensity stressor (hormetic agent) that induces various genetic and regulatory changes that result in life extension.

This study was partly funded by the National Institute on Drug Abuse. The agency must not have been very pleased with the results!

References

  1. Aberg et al. Moderate ethanol consumption increases hippocampal cell proliferation and neurogenesis in the adult mouse. Int J Neuropsychopharmacol 8:557-67 (2005).
  2. Beulens et al. Moderate alcohol consumption increases cholesterol efflux mediated by ABCA1. J Lipid Res 45:1716-23 (2004).
  3. Yousef Al-Abed et al. Inhibition of advanced glycation end product formation by acetaldehyde: role in the cardioprotective effect of ethanol. Proc Natl Acad Sci USA 96:2385-90 (1999).
  4. Malinski et al. Alcohol consumption and cardiovascular disease mortality in hypertensive men. Arch Int Med 164:623-8 (2004).
  5. Renaud and de Lorgeril. Wine, alcohol, platelets, and the French paradox for coronary artery disease. Lancet 339:1523-6 (1992).
  6. Masoro. Caloric restriction and aging: controversial issues. J Gerontol: Biol Sci 61A(1):14-9 (2006).

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