Ad hominem attacks are inappropriate. Ethanol is a neurotoxin at any dose, although its clinical significance increases with increasing doses. For people already suffering from a disposition to diabetic polyneuropathy, it seems reckless in the extreme to burden that pre-existing risk by drinking a neurotoxin like ethanol. Although its effects, such as melting the protective myelin sheath around nerve cells, will be more evident in more sensitive subjects, such as the developing fetus, it is still a substance toxic to all living things, as is abundantly illustrated by its widespread use to kill bacteria.
A Low Ethanol Dose Affects all Types of Cells in Mixed Long-Term Embryonic Cultures of the Cerebellum
Chris Pickering1,2, Grzegorz Wicher 3, Sofi Rosendahl3, Helgi B. Schiçth1 and sa Fex-Svenningsen3,4 1Functional Pharmacology, Department of Neuroscience, Uppsala University, Uppsala, Sweden, 2Addiction Biology Unit, Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden, 3Division of Developmental Genetics, Department of Neuroscience, Uppsala University, Uppsala, Sweden, and 4Anatomy and Neurobiology, Institute of Medical Biology, University of Southern Denmark, Odense, Denmark (Received 21 August 2009; Accepted 18 October 2009)
Abstract: The beneficial effect of the ‘1-drink-a-day’ lifestyle is suggested by studies of cardiovascular health, and this recommendation is increasingly followed in many countries. The main objective of this study was to determine whether this pattern of ethanol use would be detrimental to a pregnant woman. We exposed a primary culture of rat cerebellum from embryonic day 17 (corresponding to second trimester in humans) to ethanol at a concentration of 17.6 mM which is roughly equivalent to one glass of wine. Acutely, there was no change in cell viability after 5 or 8 days of exposure relative to control. By 11 days, a reduction in the numberof viable cells was observedwithout an accompanying change in caspase-3 activity (markerof apoptotic cell death), suggesting changes in cell proliferation. As the proportion of nestin-positive cells was higher in the ethanoltreated cultures after 5 days, we hypothesized that an increase in differentiation to neurons would compensate for the ongoing neuronal death. However, there were limits to this compensatory ability as the relative proportion of nestin-positive cells was decreased after 11 days. To further illustrate the negative long-term effects of this ethanol dose, cultures were exposed for 30 days. After this period, virtually no neurons or myelinating oligodendrocytes were present in the ethanol-treated cultures. In conclusion, chronic exposure to ethanol, even at small doses, dramatically and persistently affects normal development.