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Beer : Health and Nutrition

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The liver <strong>and</strong> the digestive system<br />

The Impact of Alcohol on <strong>Health</strong> 135<br />

Heavy drinkers develop a poor <strong>and</strong> idiosyncratic appetite, which will focus on the ingestion<br />

of fats <strong>and</strong> proteins rather than carbohydrates (Roe 1979). Alcohol in moderation,<br />

however, stimulates the appetite (Hetherington et al. 2001).<br />

Alcohol suppresses the ow of saliva (Enberg et al. 2001), making the meal tend to<br />

be somewhat drier. Clearly beer would be expected to be better than wine in respect of<br />

hydrating the bolus. Swelling of the salivary gl<strong>and</strong>s (parotids) is a symptom of a heavy<br />

drinker (Santolaria et al. 1997).<br />

Very heavy drinkers may also occasionally be prone to oesophagitis (Seifert 1995),<br />

the re uxing of stomach hydrochloric acid into the oesophagus leading to ‘heart burn’<br />

<strong>and</strong> ‘acid brash’.<br />

<strong>Beer</strong> <strong>and</strong> to a lesser extent wine encourage the production of the hormone gastrin<br />

that switches on the ow of the gastric juices in the stomach (Chari et al. 1993). The<br />

stomach absorbs alcohol more ef ciently when it is full <strong>and</strong> it is metabolised more<br />

quickly (Sedman et al. 1976). Less alcohol then passes to the duodenum, from which<br />

alcohol is absorbed into the bloodstream very rapidly. Here is one explanation for the<br />

reduced feelings of lightheadedness when a drink accompanies the eating of a full meal,<br />

as opposed to nibbling.<br />

Fasting appears to reduce the level of alcohol dehydrogenase (ADH; Riveros-Rosas<br />

et al. 1997), a key enzyme involved in metabolising alcohol (Baraona et al. 1994), 90%<br />

of which is metabolised by the liver. ADH produces acetaldehyde, which is toxic if not<br />

adequately dealt with by the next enzymes in the cascade, aldehyde dehydrogenase.<br />

An accumulation of acetaldehyde causes hangovers <strong>and</strong> liver damage in the long term<br />

(Agarwal & Seitz 2001).<br />

In men, 80% of ADH is in the liver <strong>and</strong> the remainder in the stomach (Myerson 1973).<br />

Women produce less ADH, meaning that alcohol has more signi cant effects on them<br />

(Seitz et al. 1993), although ADH levels in women increase after the menopause, so<br />

that presumably older women are better able to deal with alcohol.<br />

A secondary alcohol-metabolising system in the body, known as the microsomal<br />

ethanol oxidising system (Lieber 1999), is probably stimulated to an increased extent by<br />

regular consumption of alcohol. When oxidised through this system, alcohol provides<br />

only two-thirds of calories that are generated when ADH deals it with.<br />

The ADH system is polymorphic – <strong>and</strong> different in Asians (Li & Bosron 1986; Yoshida<br />

et al. 1991). It is claimed that the genetic make-up of ADH impacts the response of<br />

individuals to alcohol in respect of the levels of acetaldehyde produced (Yin & Agarwal<br />

2001). Acetaldehyde may be the causative agent in several problems ascribed to excessive<br />

alcohol consumption. The Chinese <strong>and</strong> Japanese ush very readily, due to a mutation<br />

in one of the aldehyde dehydrogenases (Crabb et al. 1989).

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