Heavy drinkers develop a poor and idiosyncratic appetite, which will focus on the inges-tion of fats and proteins rather than carbohydrates (Roe 1979). Alcohol in moderation, however, stimulates the appetite (Hetherington et al. 2001).
Alcohol suppresses the ow of saliva (Enberg et al. 2001), making the meal tend to be somewhat drier. Clearly beer would be expected to be better than wine in respect of hydrating the bolus. Swelling of the salivary glands (parotids) is a symptom of a heavy drinker (Santolaria et al. 1997).
Very heavy drinkers may also occasionally be prone to oesophagitis (Seifert 1995), the re uxing of stomach hydrochloric acid into the oesophagus leading to 'heart burn' and 'acid brash'.
Beer and to a lesser extent wine encourage the production of the hormone gastrin that switches on the ow of the gastric juices in the stomach (Chari et al. 1993). The stomach absorbs alcohol more ef ciently when it is full and it is metabolised more quickly (Sedman et al. 1976). Less alcohol then passes to the duodenum, from which alcohol is absorbed into the bloodstream very rapidly. Here is one explanation for the reduced feelings of lightheadedness when a drink accompanies the eating of a full meal, as opposed to nibbling.
Fasting appears to reduce the level of alcohol dehydrogenase (ADH; Riveros-Rosas et al. 1997), a key enzyme involved in metabolising alcohol (Baraona et al. 1994), 90% of which is metabolised by the liver. ADH produces acetaldehyde, which is toxic if not adequately dealt with by the next enzymes in the cascade, aldehyde dehydrogenase. An accumulation of acetaldehyde causes hangovers and liver damage in the long term (Agarwal & Seitz 2001).
In men, 80% of ADH is in the liver and the remainder in the stomach (Myerson 1973). Women produce less ADH, meaning that alcohol has more signi cant effects on them (Seitz et al. 1993), although ADH levels in women increase after the menopause, so that presumably older women are better able to deal with alcohol.
A secondary alcohol-metabolising system in the body, known as the microsomal ethanol oxidising system (Lieber 1999), is probably stimulated to an increased extent by regular consumption of alcohol. When oxidised through this system, alcohol provides only two-thirds of calories that are generated when ADH deals it with.
The ADH system is polymorphic - and different in Asians (Li & Bosron 1986; Yoshida et al. 1991). It is claimed that the genetic make-up of ADH impacts the response of individuals to alcohol in respect of the levels of acetaldehyde produced (Yin & Agarwal 2001). Acetaldehyde may be the causative agent in several problems ascribed to excessive alcohol consumption. The Chinese and Japanese ush very readily, due to a mutation in one of the aldehyde dehydrogenases (Crabb et al. 1989).
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 P-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, respectively. However, consumption has to be regular and spread over many years (e.g. 15 years or more). It seems that the number of heavy drinkers who will actually develop cirrhosis is one in ten (Stuttaford 1997). Furthermore it needs to be recognised that there are various other causes of cirrhosis, such as in countries where hepatitis B is endemic.
Gruenewald and Ponicki (1995) reported a link between cirrhosis and excessive consumption of spirits, but not beer or wine. Similar results were reported by Kerr et al. (2000), based on data garnered from Australia, Canada, New Zealand, the UK and the US. Tverdal and Skurtveit (2003) observed an inverse relationship between the consumption of coffee and the instance of cirrhosis, including alcoholic cirrhosis.
Alcoholics, of course, tend to be malnourished (Lieber 2001). This has led to the concept in many critics' minds of alcoholic beverages representing merely 'empty calories' - i.e. they provide just energy (calories) without other nutrients. However, reference to Chapter 5 will illustrate why this can be refuted, at least for beer. Of course beer is de nitely not a meal in itself and it would be ridiculous to suggest it. There are people who abuse alcohol, and they will tend to be malnourished, at least in part because they do not have (or devote) money for the selection of a well-balanced diet. Somebody addicted to, say, chocolate would similarly be malnourished if they primarily consumed that and not the other key diet constituents described in Chapter 4. In abusers, though, alcohol will have a direct impact on metabolism (Bitsch 2003). High levels of ethanol impair the intestinal absorption and transport of some of the amino acids, e.g. isoleucine, arginine and methionine. There are also adverse impacts on the uptake of folate, and the oxidation product of ethanol (acetaldehyde) triggers the breakdown of that vitamin. This, together with the impact of high ethanol levels per se, causes damage to the intestinal mucosa, with attendant impairment of general nutrient uptake.
It is claimed that there is an increased risk of liver cancer from excessive consumption of alcohol; however, this is confounded by and perhaps related to the incidence of cirrhosis (Ohnishi 1992). Those imbibing alcohol to excess can also display fatty in ltration, a swelling of the liver and attendant lowered appetite and nausea (Kishi et al. 1996). Binge and prolonged drinking can cause alcoholic hepatitis (Maher 2002).
However, it would be wrong to conclude that there are no positive impacts of a food such as beer on the digestive system. Faist et al. (2002) showed that water-soluble melanoidins from roasted malt promoted the activity of detoxifying enzymes (NADPH-cytochrome c reductase and glutathione-S-transferase) in intestinal cells. Even at the very front end of the gut there may be bene ts. Tagashira et al. (1997) showed that hop polyphenols could inhibit growth of streptococci and delay the development of caries. Nakajima et al. (1998) found that dark beers (more so than paler beers) inhibited the synthesis of the polysaccharide that anchors streptococci to the teeth. They did not identify the inhibitory material(s), but suggested that all three stages of roasting, mashing and fermentation are signi cant in its development. On the other hand, beers that contain signi cant levels of residual sugar and unusually low pH (< 4.0) have potentially harmful effects on teeth (Nogueira et al. 2000).
Too much alcohol can affect absorption of all foods, but especially vitamins and other micronutrients through an effect on gastrointestinal motility and intestinal permeability (Knight et al. 1992). Once again we encounter the importance of balance in the diet. For example, some of the useful avonoids will not be available if essential vitamins are absent. In turn there is a requirement to have enough fat in the diet if these vitamins are to be utilised. An excess of one trace element can restrict the intake of another.
Alcohol may improve glucose tolerance (Baum-Baicker 1985a). It seems that alcohol attenuates the increase in blood glucose concentration in subjects given a glucose load, with an accompanying increase in the concentration of insulin in plasma (Facchini et al. 1994). The implication is that alcohol increases the sensitivity of susceptible cells to insulin. This in turn reduces demand on the pancreas. In a study of 735 'middle-aged' British men, moderate drinkers (16-24 units per week) displayed a reduced risk of developing non-insulin dependent diabetes (Perry et al. 1995).
Recently there have been some intriguing studies on the relationship between alcohol consumption and the development of type II diabetes mellitus. This is the type of diabetes that arises because the body does not make suf cient insulin and the system does not work properly to control glucose levels, leading to hyperglycaemia. It was formerly called 'adult-onset diabetes' and it accounts for 85-90% of diabetes in people over the age of 30. The biggest risk is obesity.
Wannamethee et al. (2002) found that heavy drinkers run a greater risk of type II diabetes. However, light and moderate drinkers did not run this risk. Stampfer et al. (1988b) found a lower incidence of non-insulin dependent diabetes in moderate drinkers (female nurses). Rimm et al. (1995) observed that moderate alcohol consumption among healthy people might be associated with increased insulin sensitivity and a reduced risk of diabetes. Moderate alcohol consumption may have a bene cial effect on the risk of death due to coronary heart disease in those people displaying type II diabetes (Valmadrid et al. 1999; Solomon et al. 2000). Tsumura et al. (1999) discovered that among men with a body mass index of 22.1 or more, moderate alcohol consumption was associated with a reduced risk of type II diabetes. However, among lean men (BMI below 22.1), heavy alcohol consumption was associated with an increased risk of type II diabetes.
If glucose accumulates through diabetic conditions then it is converted into sorbitol by aldose reductase, the accumulating sorbitol leading to damage of tissues such as eyes and kidneys. It has been shown that components of beer, including quercetin and the iso-a-acids, inhibit aldose reductase (Shindo et al. 2002).
Alcohol enhances the absorption of glucose and galactose (Carreras et al. 1992). There is little effect on fat absorption, provided there is an adequate intake of proteins.
Heavy drinking interferes with uptake of several nutrients (Chiba & Phillips 2000) including essential amino acids.
Thiamine de ciency is often claimed to be prevalent in heavy drinkers, and is frequently cited as a hallmark of malnutrition. Poupon et al. (1990), however, presented evidence to suggest that thiamine de ciency is either slight or absent in chronic drinkers. It is important to re-emphasise that a key reason why an alcohol abuser may have a substandard diet is because they do not have available funds to secure that diet, rather than a direct effect of alcohol on the ability to use the various components of the food intake.
Zinc is recommended as a dietary supplement for heavy drinkers (Zhou et al. 2002). There is evidence that excessive levels of alcohol deplete the body's reserves of this element, which is important for the reproductive systems of both sexes (Bedwal et al.
1991).
The bre content of beer is likely to be a contributor to atus in beer drinkers. Bolin and Stanton (1998) demonstrated a clear link between bre intake and frequency of daily emissions, which averaged 12.7 (range 2-53) for men and 7.1 (range 1-32) for women. There was also a correlation between men's beer drinking and the aroma of the resultant atus - indeed, men generally felt compelled to report more aromatic wind.
Beer, being produced from a cereal base, may present a dietary risk to those suffering from coeliac disease (Ellis et al. 1990; see later).
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