Could it be the end of one size-fits-all boozing guidelines as researchers finally get into their stride?
DOWN a few drinks, and then a few more, and do it again the next night and the next, and your liver may end up inflamed and scarred. But take the main type of liver cell, hepatocytes, and soak them alone in the lab in alcohol at the kinds of concentrations found in a drinker’s blood, and there are no signs of this kind of damage. So what is going on?
It turns out that it isn’t alcohol itself that destroys liver, but the toxic free radicals and inflammatory substances released as the body struggles to deal with it. What’s more, the severity of this response varies greatly from individual to individual. The efficiency of your alcohol-metabolising enzyme, your diet, your sex, the strength of your immune response and, most surprisingly of all, the number and type of bacteria that live in your gut may all determine whether you’ll succumb to liver disease or survive a lifetime of propping up the bar.
A third of heavy drinkers — loosely defined on both sides of the Atlantic as those who put away more than five or six drinks a day – develop alcoholic hepatitis, a life- threatening inflammatory condition, and a fifth get the fatal accumulation of scar tissue that is cirrhosis. But because there are few nerves in the liver, most people have no idea that alcohol is messing with theirs until the damage is in an advanced stage.
If you drink regularly for a few weeks, deposits of fat will build up in your liver. These are probably harmless, and disappear with abstinence. Yet continue drinking heavily, and for reasons that no one really understands, your liver may suddenly become inflamed, your abdomen will start to hurt all over, and you will feel sick. This is alcoholic hepatitis.
New Scientist, 27/11/99: 64
The Neurophysiology of Alcohol
*M. S. Berry and **V. W. Pentreath
Department of Zoology. University College of Swansea, Swansea SA2 SPP and Department of Biology, University of Salford. Salford, 315 4WT, United Kingdom
The principal effects of acute dosage of ethyl alcohol are observed in the nervous system, where there is a progressive and simultaneous impairment of function at many levels. It seems probable that the tolerance and dependence which develop from chronic dosage are also due to changes in central nervous function. However, considerable problems arise in studying these effects because of the complexity of the nervous system and also because of the diversity of the actions of alcohol on it. For example, the drug can increase or decrease the synthesis, storage, release, and inactivation of central neurotransmitter sub-stances, and increase or decrease resting membrane potential and resistance, neuronal excitability, and postsynaptic receptor sensitivity; in each case, certain cells only are affected, and different concentrations of alcohol may have opposite effects.
The actions of alcohol on the central nervous system (CNS) have been assessed by a variety of different electrophysiological measures, including spontaneous EEG, evoked potentials, multiple unit and single unit recording, intracellular recording, and electrical stimulation of specific brain areas. Ideally, the experimenter would like to correlate the actions of alcohol on known neuronal networks with particular changes in behaviour. However, our limited knowledge of normal brain function means that experimental data tends to be difficult to interpret. As a consequence, many investigators have utilized a variety of peripheral vertebrate or isolated invertebrate preparations where neuronal connectivity is simpler and better understood than in the CNS, high resolution techniques can be more readily applied, and interpretation of the actions of alcohol is more reliable. The value of these types of preparation as simple model systems and their relevance for mammalian CNS studies have frequently been questioned. For example, the concentrations of alcohol employed have often been well beyond those associated with the production of intoxication in mammals, suggesting fundamental differences in action and perhaps exaggerating the apparent role of the peripheral nervous system in the manifestations of intoxication.
from Sandler, M. (1980)
The Psychopharmacology of Alcohol. New York: Raven Press, p.43
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