Beer : Health and Nutrition

136 Chapter Six
Through adaptation, heavy drinkers probably metabolise alcohol more rapidly than
do non-drinkers, provided that their digestive system has not been damaged. Forsander
and Sinclair (1992) produced evidence based on studies with rats that rates of alcohol
elimination and alcohol consumption are partially determined by genetics. Rats displaying
higher rates of alcohol elimination or levels of ADH had higher voluntary intakes
of alcohol than rats with lower elimination rates. Although alcohol elimination itself
probably does not exert direct control over drinking, some factor related to the rate
of alcohol elimination appears to be among the mechanisms in uencing the level of
alcohol consumption.
Heavy drinkers commonly suffer from chronic gastritis, an in ammation of the stomach
lining (Figlie et al. 2002). It is a particular problem for those who also smoke. Alcohol
to excess also affects the blood supply to and motility of the small intestine (Chiba &
Phillips 2000). There is good evidence for a link between the organism Helicobacter
pylori and ulceration of the stomach and duodenum, as well as stomach cancer. It has
been reported that alcohol protects against infection by H. pylori (Brenner et al. 1997,
1999, 2001; Ogihara et al. 2000), in fact countering the effect of coffee. However, it
is also claimed that alcohol lessens the incidence of this organism in older people, but
appears to promote the growth of the organism in younger folk. Ohsugi et al. (1997)
showed that the hop β-acid lupulone could inhibit growth of H. pylori, so conceivably
it is not alcohol alone that is responsible for the effect.
There appears to be an increased risk of pancreatitis in heavy drinkers (Dreiling et
al. 1952; Haber et al. 1995; Sakorafas & Tsiotou 2000), with about 1 in 20 people suffering.
As this tissue is responsible for making digestive enzymes and also insulin, there
are attendant problems with digestion and diabetes. The reduced digestive ef ciency
leads to an increased level of triglycerides and therefore atheroma and increased risk of
cardiovascular disease (compare this statement with the observed upturn in the U-shaped
curve for high alcohol intake; see earlier). Schmidt (1991) suggests that the consumption
of distilled spirits, but not wine or beer, is a risk factor for pancreatitis.
Gall bladder activities are improved by alcohol. Its consumption speeds up the emptying
of the gall bladder after a meal and increases the rate of lling, too – so people with
reasonable alcohol intake develop fewer gallstones. Leitzmann et al. (1999) showed
that, after adjusting for other risk factors, an increased amount of alcohol consumed
correlated with a decreased risk of symptomatic gallstone disease. It seemed that frequency
of intake was an important factor, with intake 5–7 days per week leading to a
decreased risk, as compared with non-drinkers. In contrast, infrequent alcohol intake
(1–2 days per week) led to no change of risk. The nature of the alcoholic beverage did
not appear to be signi cant.
The Oxford Textbook of Medicine (Weatherall et al. 1996) suggests that consumption
rates of 80 g alcohol daily by a man and 50 g by a woman gives a 15% chance of liver
damage. These levels equate to more than 5 pints and 3 pints of average-strength beer,