Dietary supplements may contain harmful or undesirable substances such as pesticides or heavy metals. Contaminants may be present before a substance is harvested for use as a dietary supplement or may be introduced during processing and packaging.
For example, coral calcium, a dietary supplement said to contain remnants of living coral reefs, may contain significant and harmful amounts of lead and other heavy metals. Consumption of excessive levels of lead can cause neurological problems, increased blood pressure, reproductive impairment, and hearing and sight problems. Scientists are also concerned that people who are allergic to shellfish may experience serious adverse events such as hives, swelling, and breathing problems, because of the presence of these allergens in coral reefs.
In 2003 the Sports Nutrition Working Group of the International Olympic Committee Medical Commission reported that approximately one in five dietary supplements commonly used by athletes were contaminated. Protein powders; amino acid supplements; creatine; pyruvate; and several vitamin, mineral, and herbal supplements were found to contain steroid-like chemicals that were not identified on product labels, caused positive doping tests, and were not known to be safe.
Dietary supplements may also contain controlled substances. Acetaminophen, aspirin, antihistamines, and cortico-steroids have been found in dietary supplements that did not list them as ingredients. In 2005 the FDA issued a warning about a dietary supplement that contains the antidiabetic agent glyburide after it caused hypoglycemia (dangerously low blood sugar) in several consumers. In 2006 the FDA warned consumers against using several weight-loss dietary
supplements that contain chlordiazepoxide HCl (the active ingredient in the drug Librium) and fluoxetine HCl (the active ingredient in the antidepressant Prozac).
Friday
The Safety of Dietary Supplements
Dietary supplement safety should be of primary concern to consumers. Because they are assumed to be safe unless proven otherwise, dietary supplements present special safety challenges. In 2000 the FDA received 500 dietary supplement adverse event reports; that number rose to 553 in 2001 and to 1214 in 2002. Adverse events caused by dietary supplements vary from mild to severe and may be influenced by individual health status (medical history and genetic makeup), dietary supplement composition and dosage (including levels of active and inactive ingredients), and concomitant consumption of other substances (including foods, beverages, over-the-counter and prescription drugs, and other dietary supplements).
Health Status
Dietary supplements may act differently in different people. As noted by Christine Lewis-Taylor, former director of the FDA's Office of Nutritional Products, Labeling, and Dietary Supplements, "one man's dose can be another man's poison." An individual's genes and health status help to explain this difference.
Nutritional genomics and metabalomics are growing areas of research that explain the relationship between genetic makeup and nutrition- and metabolism-related outcomes.
Certain relationships between nutrients and health outcomes are well characterized. Folate supplementation, for example, is recommended for all women of childbearing age to prevent fetal neural tube defects. By isolating and analyzing the function of the genes responsible for folate metabolism, however, scientists have identified a genetic variation that predisposes some women to give birth to babies with neural tube defects. This knowledge may eventually allow scientists to target folate supplementation to at-risk individuals.
Stage of life, medical history, and environmental factors such as diet and exercise can affect how a dietary supplement behaves in the body. Several populations are at increased risk of adverse effects of dietary supplements:
· children,
· people of smaller stature,
· elderly people,
· women who are pregnant or breastfeeding,
· people with immune disorders (for example, HIV or AIDS),
· people with cancer,
· malnourished people,
· people with existing or subclinical liver or kidney disease,
· people with a history of gastrointestinal health conditions (such as Crohn's disease) or surgery (such as gastric bypass surgery),
· people who are hospitalized,
· transplant recipients,
· surgical patients.
While research has revealed the unique nutritional needs in women of childbearing age (for example, 400 micrograms
of folate are recommended to prevent neural tube defects in offspring, and if pregnant, supplemental vitamins are recommended), information on the effects of dietary supplements during pregnancy and breastfeeding are extremely limited. This is largely due to ethical considerations: scientific studies are not conducted during pregnancy and breastfeeding because of potential risks to the women and their babies. Several herbal dietary supplements historically used during pregnancy have been identified as harmful
Health Status
Dietary supplements may act differently in different people. As noted by Christine Lewis-Taylor, former director of the FDA's Office of Nutritional Products, Labeling, and Dietary Supplements, "one man's dose can be another man's poison." An individual's genes and health status help to explain this difference.
Nutritional genomics and metabalomics are growing areas of research that explain the relationship between genetic makeup and nutrition- and metabolism-related outcomes.
Certain relationships between nutrients and health outcomes are well characterized. Folate supplementation, for example, is recommended for all women of childbearing age to prevent fetal neural tube defects. By isolating and analyzing the function of the genes responsible for folate metabolism, however, scientists have identified a genetic variation that predisposes some women to give birth to babies with neural tube defects. This knowledge may eventually allow scientists to target folate supplementation to at-risk individuals.
Stage of life, medical history, and environmental factors such as diet and exercise can affect how a dietary supplement behaves in the body. Several populations are at increased risk of adverse effects of dietary supplements:
· children,
· people of smaller stature,
· elderly people,
· women who are pregnant or breastfeeding,
· people with immune disorders (for example, HIV or AIDS),
· people with cancer,
· malnourished people,
· people with existing or subclinical liver or kidney disease,
· people with a history of gastrointestinal health conditions (such as Crohn's disease) or surgery (such as gastric bypass surgery),
· people who are hospitalized,
· transplant recipients,
· surgical patients.
While research has revealed the unique nutritional needs in women of childbearing age (for example, 400 micrograms
of folate are recommended to prevent neural tube defects in offspring, and if pregnant, supplemental vitamins are recommended), information on the effects of dietary supplements during pregnancy and breastfeeding are extremely limited. This is largely due to ethical considerations: scientific studies are not conducted during pregnancy and breastfeeding because of potential risks to the women and their babies. Several herbal dietary supplements historically used during pregnancy have been identified as harmful
The Ephedra Recall
In The Honest Herbal, Dr. Varro E. Tyler wrote that ephedra (Ephedra sinica) might have been the first Chinese herbal remedy to have been used significantly in western medicine. A potent central nervous system stimulator, ephedra (also known as ma huang) is effective as a nasal decongestant
and can provide relief of congestion and bronchiole constriction to people suffering from asthma. The man-made equivalents of ephedra, ephedrine and pseudoephedrine, have been added to many over-the-counter cold and asthma medications. Ephedra sinica stimulates the heart and causes constriction of the blood vessels, which raises blood pressure.
Ephedra began to be used as a weight-loss aid in the mid-1970s. This may have been the result of recommendations by natural health practitioners and/or the observation that ephedra had a "speed-like" effect on the body, which people might have interpreted as an ability to increase metabolism. Dietary supplements with ephedra often contained additional stimulants such as caffeine. Those products were marketed as weight-loss supplements that conveyed an "energy boost." In the 1990s, the dietary supplement industry estimated that as many as 3 billion servings of dietary supplements containing ephedra were being consumed each year in the United States.
Gradually, dietary supplement manufacturers and the FDA received numerous reports of adverse effects from consuming ephedra. Serious adverse effects of ephedra use include rapid heart rate, high blood pressure, arteriole constriction, seizure, stroke, and sudden death. In 1996 the FDA released a statement that consumers should avoid ephedra-containing dietary supplements. At that time, more than 800 deaths in the United States were attributed to their use.
In 1997 the FDA proposed revisions that would require all ephedra-containing products to be labeled with the following: "taking more than the recommended serving may result in heart attacks, seizures, or death." The FDA also proposed that all products be limited to 8 mg of active ingredient per serving, with a maximum daily dose of 24 mg; use should not exceed 7 days; and consumers should not use the supplement in combination with other specified substances that
exacerbate the effects, such as caffeine. In the summer of 1999, however, the U.S. General Accounting Office reported that, although the FDA was justified in voicing concerns over the safety of dietary supplements containing ephedra, more evidence was needed before regulations could limit dosage and duration of use. Several months later, despite 140 additional deaths attributed to ephedra, the FDA capitulated.
In response to growing concern among consumers and government entities, members of the Ephedra Committee of the American Herbal Products Association launched a public relations group called the Ephedra Education Council. In 2002 the council released a report of fifty-five clinical studies citing beneficial effects of ephedra when taken as directed, with zero studies showing evidence of adverse effects.
By 2003 additional studies had noted the risks of ephedra, including a report by the Rand Corporation, which conceded sufficient cause for concern regarding the relationship between consumption of ephedra and adverse events, including nausea, vomiting, heart palpitations, and psychiatric symptoms (anxiety and mood changes). When Steve Bechler, a 23-year-old pitcher for the Baltimore Orioles, died from an ephedra-related adverse event in February 2003, the national media began to report the risks of ephedra consumption.
Illinois banned the sale of products containing ephedra in 2003. Several other states considered similar legislation, restricted the sale to those over 18 years of age, or required products to have warning labels. Several sports organizations banned the use of dietary supplements containing ephedra, and General Nutrition Centers, the largest national dietary supplement store, discontinued the sale of products containing ephedra.
On February 6, 2004, the FDA issued a final rule that prohibited the sale of dietary supplements containing ephedra
(ephedrine alkaloids) because they presented a significant and unreasonable risk of illness or injury. This rule became effective 60 days after the date of publication. Since then, individual manufacturers of dietary supplements containing ephedra have challenged the FDA's ruling, and the FDA has developed analytical methods by which they can determine whether a dietary supplement contains ephedra. Dietary samples that test positive for ephedra undergo additional analysis to confirm those results.
In April 2005 a federal district court in Utah struck down the ban on the sale of ephedra, citing inconclusive evidence that it is harmful at lower doses (and therefore that the FDA lacked the authority to effect such a ban). While dietary supplement manufacturers were legally permitted to sell products containing ephedra (within certain limitations of potency and labeling), the company responsible for initiating this appeal elected to not reintroduce these products into the market. The FDA appealed this ruling, and a U.S. court of appeals ruled in their favor on August 17, 2006. However, ephedra-containing dietary supplements can still be purchased, mostly from Internet distributors.
While the FDA works to ensure that dietary supplement manufacturers adhere to the DSHEA, the volume of dietary supplements available makes this surveillance extremely difficult. In addition, the magnitude of evidence necessary for the FDA to effect any action against manufacturers of potentially harmful dietary supplements is so great, many people view the DSHEA as ineffective and, in fact, a deregulation.
and can provide relief of congestion and bronchiole constriction to people suffering from asthma. The man-made equivalents of ephedra, ephedrine and pseudoephedrine, have been added to many over-the-counter cold and asthma medications. Ephedra sinica stimulates the heart and causes constriction of the blood vessels, which raises blood pressure.
Ephedra began to be used as a weight-loss aid in the mid-1970s. This may have been the result of recommendations by natural health practitioners and/or the observation that ephedra had a "speed-like" effect on the body, which people might have interpreted as an ability to increase metabolism. Dietary supplements with ephedra often contained additional stimulants such as caffeine. Those products were marketed as weight-loss supplements that conveyed an "energy boost." In the 1990s, the dietary supplement industry estimated that as many as 3 billion servings of dietary supplements containing ephedra were being consumed each year in the United States.
Gradually, dietary supplement manufacturers and the FDA received numerous reports of adverse effects from consuming ephedra. Serious adverse effects of ephedra use include rapid heart rate, high blood pressure, arteriole constriction, seizure, stroke, and sudden death. In 1996 the FDA released a statement that consumers should avoid ephedra-containing dietary supplements. At that time, more than 800 deaths in the United States were attributed to their use.
In 1997 the FDA proposed revisions that would require all ephedra-containing products to be labeled with the following: "taking more than the recommended serving may result in heart attacks, seizures, or death." The FDA also proposed that all products be limited to 8 mg of active ingredient per serving, with a maximum daily dose of 24 mg; use should not exceed 7 days; and consumers should not use the supplement in combination with other specified substances that
exacerbate the effects, such as caffeine. In the summer of 1999, however, the U.S. General Accounting Office reported that, although the FDA was justified in voicing concerns over the safety of dietary supplements containing ephedra, more evidence was needed before regulations could limit dosage and duration of use. Several months later, despite 140 additional deaths attributed to ephedra, the FDA capitulated.
In response to growing concern among consumers and government entities, members of the Ephedra Committee of the American Herbal Products Association launched a public relations group called the Ephedra Education Council. In 2002 the council released a report of fifty-five clinical studies citing beneficial effects of ephedra when taken as directed, with zero studies showing evidence of adverse effects.
By 2003 additional studies had noted the risks of ephedra, including a report by the Rand Corporation, which conceded sufficient cause for concern regarding the relationship between consumption of ephedra and adverse events, including nausea, vomiting, heart palpitations, and psychiatric symptoms (anxiety and mood changes). When Steve Bechler, a 23-year-old pitcher for the Baltimore Orioles, died from an ephedra-related adverse event in February 2003, the national media began to report the risks of ephedra consumption.
Illinois banned the sale of products containing ephedra in 2003. Several other states considered similar legislation, restricted the sale to those over 18 years of age, or required products to have warning labels. Several sports organizations banned the use of dietary supplements containing ephedra, and General Nutrition Centers, the largest national dietary supplement store, discontinued the sale of products containing ephedra.
On February 6, 2004, the FDA issued a final rule that prohibited the sale of dietary supplements containing ephedra
(ephedrine alkaloids) because they presented a significant and unreasonable risk of illness or injury. This rule became effective 60 days after the date of publication. Since then, individual manufacturers of dietary supplements containing ephedra have challenged the FDA's ruling, and the FDA has developed analytical methods by which they can determine whether a dietary supplement contains ephedra. Dietary samples that test positive for ephedra undergo additional analysis to confirm those results.
In April 2005 a federal district court in Utah struck down the ban on the sale of ephedra, citing inconclusive evidence that it is harmful at lower doses (and therefore that the FDA lacked the authority to effect such a ban). While dietary supplement manufacturers were legally permitted to sell products containing ephedra (within certain limitations of potency and labeling), the company responsible for initiating this appeal elected to not reintroduce these products into the market. The FDA appealed this ruling, and a U.S. court of appeals ruled in their favor on August 17, 2006. However, ephedra-containing dietary supplements can still be purchased, mostly from Internet distributors.
While the FDA works to ensure that dietary supplement manufacturers adhere to the DSHEA, the volume of dietary supplements available makes this surveillance extremely difficult. In addition, the magnitude of evidence necessary for the FDA to effect any action against manufacturers of potentially harmful dietary supplements is so great, many people view the DSHEA as ineffective and, in fact, a deregulation.
Adverse Effects of Dietary Supplements
The FDA has the burden of proving that a dietary supplement is adulterated, that it "presents a significant or unreasonable risk of illness or injury." The FDA, however, must rely on the honesty of the industry to ensure safety. Through scientific studies, dietary supplement manufacturers determine that their ingredients present no significant or unreasonable risk to consumers and submit that information to the FDA. Although the FDA does not participate in or oversee the testing of dietary supplements for safety, the FDA is responsible for removing unsafe dietary supplements from the market.
Adverse or suspected adverse effects of dietary supplements should be reported to the FDA. Once the FDA receives such information, it generates alerts and warnings for consumers and letters notifying the manufacturer that their dietary supplement may be associated with harmful adverse events. The results of these actions may range from a consumer warning, labeling change, or product recall to a full-fledged product withdrawal. Dietary supplement manufacturers may voluntarily recall a product, as in the case of a labeling error, product mix-up, contamination, or questionable stability of the product or its components. The FDA may also request or order a product recall based on the above criteria.
Product recalls are expensive and done because there is something wrong with the product. The type of recall for dietary supplements depends on the severity of potential adverse effects. A class I recall means there is reasonable evidence to suggest that use of a product will cause serious adverse effects or death; a class II recall means a product may cause temporary or treatable adverse effects or that the risk of serious adverse effects is low; and a class III recall means the adverse effects are not likely to be serious.
Below is an adaptation of a letter from the FDA's Office of Nutritional Products, Labeling, and Dietary Supplements to the distributor of a hazardous dietary supplement.
Adverse or suspected adverse effects of dietary supplements should be reported to the FDA. Once the FDA receives such information, it generates alerts and warnings for consumers and letters notifying the manufacturer that their dietary supplement may be associated with harmful adverse events. The results of these actions may range from a consumer warning, labeling change, or product recall to a full-fledged product withdrawal. Dietary supplement manufacturers may voluntarily recall a product, as in the case of a labeling error, product mix-up, contamination, or questionable stability of the product or its components. The FDA may also request or order a product recall based on the above criteria.
Product recalls are expensive and done because there is something wrong with the product. The type of recall for dietary supplements depends on the severity of potential adverse effects. A class I recall means there is reasonable evidence to suggest that use of a product will cause serious adverse effects or death; a class II recall means a product may cause temporary or treatable adverse effects or that the risk of serious adverse effects is low; and a class III recall means the adverse effects are not likely to be serious.
Below is an adaptation of a letter from the FDA's Office of Nutritional Products, Labeling, and Dietary Supplements to the distributor of a hazardous dietary supplement.
Creation of New Government Entities
Appointed in 1995, the Commission on Dietary Supplements directs the labeling of dietary supplements, essentially to determine how to provide scientifically valid information about them. The first commission comprised scientists from various U.S. universities with expertise in dietary supplements, a member of the Council for Responsible Nutrition, a Seton Hall University School of Law professor, a public relations specialist, and a representative from the Herb Research Foundation.
Responsibilities carried out by the Commission on Dietary Supplements are now being performed by the Office of Nutritional Products, Labeling, and Dietary Supplements' Division of Dietary Supplement Programs, which comprises a regulations and review team, a compliance and enforcement team, and a clinical review team. Led by Dr. Susan Walker, the division creates policies, regulations, and guidance documents to ensure the safe manufacture and labeling of dietary supplements and reviews safety information submitted by dietary supplement manufacturers 75 days before the marketing of a product to ensure that it is reasonably expected to be safe.
The DSHEA also called for the creation of the Office of Dietary Supplements (ODS), which is housed within the National Institutes of Health and is responsible for facilitating
research into the role of dietary supplements in disease prevention and health promotion. The mission of ODS is to strengthen knowledge about dietary supplements by evaluating available research and stimulating and supporting more scientific trials, as well as by educating people about the current state of knowledge. As part of their mission, ODS hosted the 2000 National Nutrition Summit and created numerous resources, including Computer Access to Research on Dietary Supplements, International Bibliographic Information on Dietary Supplements, Annual Bibliographies of Significant Advances in Dietary Supplement Research, and Dietary Supplement Ingredient and Labeling databases (see Appendix D). The ODS's 2004-2009 strategic plan comprises five major goals: (1) expanding the evaluation of dietary supplements in reducing the risk for chronic disease; (2) fostering research on dietary supplements for optimal health and performance; (3) enhancing understanding of the basic effects of dietary supplements on biological systems; (4) improving methodologies; and (5) expanding outreach and education.
Responsibilities carried out by the Commission on Dietary Supplements are now being performed by the Office of Nutritional Products, Labeling, and Dietary Supplements' Division of Dietary Supplement Programs, which comprises a regulations and review team, a compliance and enforcement team, and a clinical review team. Led by Dr. Susan Walker, the division creates policies, regulations, and guidance documents to ensure the safe manufacture and labeling of dietary supplements and reviews safety information submitted by dietary supplement manufacturers 75 days before the marketing of a product to ensure that it is reasonably expected to be safe.
The DSHEA also called for the creation of the Office of Dietary Supplements (ODS), which is housed within the National Institutes of Health and is responsible for facilitating
research into the role of dietary supplements in disease prevention and health promotion. The mission of ODS is to strengthen knowledge about dietary supplements by evaluating available research and stimulating and supporting more scientific trials, as well as by educating people about the current state of knowledge. As part of their mission, ODS hosted the 2000 National Nutrition Summit and created numerous resources, including Computer Access to Research on Dietary Supplements, International Bibliographic Information on Dietary Supplements, Annual Bibliographies of Significant Advances in Dietary Supplement Research, and Dietary Supplement Ingredient and Labeling databases (see Appendix D). The ODS's 2004-2009 strategic plan comprises five major goals: (1) expanding the evaluation of dietary supplements in reducing the risk for chronic disease; (2) fostering research on dietary supplements for optimal health and performance; (3) enhancing understanding of the basic effects of dietary supplements on biological systems; (4) improving methodologies; and (5) expanding outreach and education.
The Regulation of Dietary Supplements
One hundred years ago, the dietary supplement industry was very different from today. Production and processing were not standardized, sanitation was questionable (manufacturers had little understanding of bacterial/microbial control and refrigeration was primitive), and distribution was unregulated. The twentieth century brought many changes in how dietary supplements were handled and transported, and several laws sought to improve supplement manufacturing practices.
The U.S. government has long concerned itself with regulation of the substances Americans consume. In the early 1900s, what we now consider to be dietary supplements were regulated as foods. While they are still technically considered foods today, dietary supplements are now regulated by the Dietary Supplement Health and Education Act (DSHEA) under the FDA.
Early Regulation of Dietary Supplements
During the late 1800s and early 1900s, concerns about the safety and purity of the American food supply were mounting. Farmers, millers, trade associations, and drug producers agreed that a government intervention was warranted, but each group was unwilling to compromise its own agenda in the interest of an agreement. In addition to concern about the
quality of food that was being sent to American troops fighting in the Spanish-American War, people had qualms about poisonous preservatives and dyes in food and were skeptical about the various health claims for worthless and potentially dangerous patent medicines. Widespread trepidation also came as a result of Upton Sinclair's The Jungle, which portrayed the graphic and gory details of Chicago's meat-packing industry.
In 1906 the Pure Food and Drug Act was passed by Congress and signed by President Theodore Roosevelt. The act was created to protect consumers and to provide them with education and choice of products. Essentially, the Pure Food and Drug Act prohibited interstate commerce in mis-branded or adulterated foods, beverages, and drugs. Adulteration included removal of valuable components, reduction of overall quality by substituting other ingredients, addition of harmful ingredients, and use of spoiled animal or vegetable products. The act also defined specific labeling requirements; foods and drugs could not be labeled with misleading or false statements, and doing so constituted misbranding. Although the concept of dietary supplements did not yet exist, the Act regulated as foods products that are now known as dietary supplements. Since this first Act, a number of laws have affected the regulation of dietary supplements The Supreme Court ruled that the 1906 Act did not prohibit false therapeutic claims; it only prohibited false and misleading statements about the ingredients or identity of drugs.
Overturned United States v. Johnson and prohibited labeling medicines with false therapeutic claims intended to defraud the consumer (a step in the right direction, but it created a standard that was extremely difficult to prove).
The Supreme Court's first ruling on food additives (ban on flour bleached with nitrite residues) placed the burden on the government to prove a food ingredient dangerous.
Extended the government's reach to cosmetics and therapeutic devices; eliminated the Sherley Amendment; required that drugs be demonstrated as safe by the manufacturer prior to marketing; standardized safe tolerances for unavoidable poisons; standardized product identity, quality, and how full a container must be for foods; authorized factory inspections; and introduced court injunctions for violators.
The U.S. government has long concerned itself with regulation of the substances Americans consume. In the early 1900s, what we now consider to be dietary supplements were regulated as foods. While they are still technically considered foods today, dietary supplements are now regulated by the Dietary Supplement Health and Education Act (DSHEA) under the FDA.
Early Regulation of Dietary Supplements
During the late 1800s and early 1900s, concerns about the safety and purity of the American food supply were mounting. Farmers, millers, trade associations, and drug producers agreed that a government intervention was warranted, but each group was unwilling to compromise its own agenda in the interest of an agreement. In addition to concern about the
quality of food that was being sent to American troops fighting in the Spanish-American War, people had qualms about poisonous preservatives and dyes in food and were skeptical about the various health claims for worthless and potentially dangerous patent medicines. Widespread trepidation also came as a result of Upton Sinclair's The Jungle, which portrayed the graphic and gory details of Chicago's meat-packing industry.
In 1906 the Pure Food and Drug Act was passed by Congress and signed by President Theodore Roosevelt. The act was created to protect consumers and to provide them with education and choice of products. Essentially, the Pure Food and Drug Act prohibited interstate commerce in mis-branded or adulterated foods, beverages, and drugs. Adulteration included removal of valuable components, reduction of overall quality by substituting other ingredients, addition of harmful ingredients, and use of spoiled animal or vegetable products. The act also defined specific labeling requirements; foods and drugs could not be labeled with misleading or false statements, and doing so constituted misbranding. Although the concept of dietary supplements did not yet exist, the Act regulated as foods products that are now known as dietary supplements. Since this first Act, a number of laws have affected the regulation of dietary supplements The Supreme Court ruled that the 1906 Act did not prohibit false therapeutic claims; it only prohibited false and misleading statements about the ingredients or identity of drugs.
Overturned United States v. Johnson and prohibited labeling medicines with false therapeutic claims intended to defraud the consumer (a step in the right direction, but it created a standard that was extremely difficult to prove).
The Supreme Court's first ruling on food additives (ban on flour bleached with nitrite residues) placed the burden on the government to prove a food ingredient dangerous.
Extended the government's reach to cosmetics and therapeutic devices; eliminated the Sherley Amendment; required that drugs be demonstrated as safe by the manufacturer prior to marketing; standardized safe tolerances for unavoidable poisons; standardized product identity, quality, and how full a container must be for foods; authorized factory inspections; and introduced court injunctions for violators.
The liver and the digestive system
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).
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).
The heart and the circulatory system
Lichtenstein (2003) states that 15 million deaths in the late 1990s could be attributed to cardiovascular disease. The American Heart Association has pointed out that coronary heart disease and the related cardiovascular disease is the number-one killer in the US, accounting for almost one in two deaths among Americans and more deaths than are caused by all the forms of cancer combined. The impact on disability and the attendant economic loss are enormous.
Atherosclerosis ('hardening of the arteries') is the term used to describe a number of pathological events occurring in arteries and which are responsible for coronary heart disease, stroke and diseases of the peripheral circulatory system (Fisher 1991).
Atheroma (from the Greek ather = porridge) comprises deposits of fatty material on the walls of arteries - a material comprising cholesterol, triglycerides, brous tissue and red blood cells. As it builds it restricts blood ow and if this is in the coronary artery then heart attack and death may follow, as the heart muscle does not receive suf cient oxygen. Atheroma has also been associated with the development of cataracts, macular degeneration in the retina and the development of cancers (Emerit et al. 1991; Tunick et al. 1994). If the atheroma accumulation (plaque) is ruptured a blood clot may form which not only can accelerate the blockage of the artery concerned but also may break loose and plug another artery, increasing the risk of heart attack or, if the newly blocked artery is in the brain, a stroke.
Plainly, the intake of saturated fats and cholesterol increases the risk, although it must be realised that four- fths of the cholesterol is made in our bodies and does not come through the diet. The quantity of cholesterol produced is increased in proportion to the level of saturated fatty acids in the diet (polyunsaturated fatty acids reduce blood cholesterol), and also the trans saturated fatty acids, i.e. those that are produced industrially by catalytic hydrogenation (Krisetherton 1995). High sugar intake can lead to high formation of saturated fats in the body. Indeed, any imbalance in metabolism such that there is an excess of calories over those needed to sustain the body will lead to an accumulation of fat. Obesity, hypertension, diabetes, sedentary living and the use of cigarettes all increase the risk of atherosclerosis.
As cholesterol and other lipids such as the triglycerides are insoluble in aqueous systems, they are transported through the body by combination with proteins, as lipo-proteins. The principal carrier of cholesterol is low-density lipoprotein (LDL) and there is a strong positive correlation between its level and the risk of atherosclerosis. Hence LDL is frequently referred to as 'bad cholesterol'.
A lower percentage (20-30%) of the blood cholesterol is in the form of high-density lipoprotein (HDL), which is responsible for transporting cholesterol away from the arteries to the liver where it is metabolised. This role has caused HDL to be named 'good cholesterol', such that high levels of HDL appear to afford protection against heart attack. Thus there is an inverse correlation between levels of HDL and atherosclerosis.
There is now a plethora of papers arguing that moderate consumption of alcohol counters coronary heart disease [see, for example, Dyer et al. 1977; Hennekens et al. 1978; Ramsey 1979; Marmot et al. 1981; Gordon & Kannel 1983 (the Framingham study); Kozarevic et al. 1983; Yano et al. 1984; Moore & Pearson 1986; Klatsky et al. 1992; Maclure 1993; Verschuren 1993]. Alcohol causes a lowering of LDL cholesterol in the plasma and an increased level of HDL cholesterol (HDL2 and HDL3) and apo-lipoproteins A-I and A-II (Clevidence et al. 1995; Goldberg et al. 1995; Jansen et al. 1995; Parker et al. 1996).
Alcohol also appears to lower the risk of blood clotting by reducing the level of brinogen in blood plasma (Stefanick et al. 1995) and lessening the tendency of blood platelets to aggregate (Renaud et al. 1992). The bene ts apply to both men and women
(Nanchahal et al. 2000).
Doyens of the eld have included Arthur Klatsky in Oakland, California, Norman Kaplan of the University of Texas Southwestern Medical Center, and Sir Richard Doll in Oxford, England.
The phenomenon has taken the name the 'French paradox', on account of the unexpectedly low risk of cardiovascular disease in a country noted for its intake of very fatty foods. We can look back nearly two centuries to the rst noting of this effect, when an Irish doctor, Samuel Black, remarked on the much greater incidence of angina in France as opposed to Ireland, which he believed was ascribable to 'the French habits and modes of living, coinciding with the benignity of their climate and the peculiarity of their moral affections' (Black 1819). The occurrence is now sometimes called the European Paradox because it re ects dietary characteristics beyond France alone
(Bellizzi et al. 1994).
Various laboratories have reported U-shaped curves (e.g. Doll et al. 1994) or J-shaped curves (e.g. Tsugane et al. 1999) (Fig. 6.1) to illustrate the impact of various intakes of alcohol on coronary heart disease and on all causes of mortality. For the most part it seems that the J shape relates to the relationship between alcohol intake and total mortality, with the U shape better describing that between alcohol consumption and coronary heart disease. The clear evidence is that the intake of some alcohol has a bene cial impact. In many instances consumption of between 1 and 3 units daily perhaps offers the best advantage, with higher intake progressively shifting the risk upwards again.
The low point (nadir) in these curves has been reported at various levels, for example, 69 g alcohol per week for men in the US (26 g per week for women), but 116 g per week for men in the UK (White 1999). It seems that bene ts for women are especially notable after the menopause (Fuchs et al. 1995; Nanchahal et al. 2000).
Even the American Cancer Society reported this type of effect (Boffetta & Gar nkel 1990). The study began in 1959 with 276,802 men between the ages of 40 and 59. Assigning 1.0 as a standard value for risk of death in non-drinkers, it was shown that the risk of death dropped to 0.84 (i.e. by 16%) for those taking one alcoholic drink per day. The risk of death for those claiming to consume six drinks per day was still lower than for abstainers, at 0.92.
Atherosclerosis ('hardening of the arteries') is the term used to describe a number of pathological events occurring in arteries and which are responsible for coronary heart disease, stroke and diseases of the peripheral circulatory system (Fisher 1991).
Atheroma (from the Greek ather = porridge) comprises deposits of fatty material on the walls of arteries - a material comprising cholesterol, triglycerides, brous tissue and red blood cells. As it builds it restricts blood ow and if this is in the coronary artery then heart attack and death may follow, as the heart muscle does not receive suf cient oxygen. Atheroma has also been associated with the development of cataracts, macular degeneration in the retina and the development of cancers (Emerit et al. 1991; Tunick et al. 1994). If the atheroma accumulation (plaque) is ruptured a blood clot may form which not only can accelerate the blockage of the artery concerned but also may break loose and plug another artery, increasing the risk of heart attack or, if the newly blocked artery is in the brain, a stroke.
Plainly, the intake of saturated fats and cholesterol increases the risk, although it must be realised that four- fths of the cholesterol is made in our bodies and does not come through the diet. The quantity of cholesterol produced is increased in proportion to the level of saturated fatty acids in the diet (polyunsaturated fatty acids reduce blood cholesterol), and also the trans saturated fatty acids, i.e. those that are produced industrially by catalytic hydrogenation (Krisetherton 1995). High sugar intake can lead to high formation of saturated fats in the body. Indeed, any imbalance in metabolism such that there is an excess of calories over those needed to sustain the body will lead to an accumulation of fat. Obesity, hypertension, diabetes, sedentary living and the use of cigarettes all increase the risk of atherosclerosis.
As cholesterol and other lipids such as the triglycerides are insoluble in aqueous systems, they are transported through the body by combination with proteins, as lipo-proteins. The principal carrier of cholesterol is low-density lipoprotein (LDL) and there is a strong positive correlation between its level and the risk of atherosclerosis. Hence LDL is frequently referred to as 'bad cholesterol'.
A lower percentage (20-30%) of the blood cholesterol is in the form of high-density lipoprotein (HDL), which is responsible for transporting cholesterol away from the arteries to the liver where it is metabolised. This role has caused HDL to be named 'good cholesterol', such that high levels of HDL appear to afford protection against heart attack. Thus there is an inverse correlation between levels of HDL and atherosclerosis.
There is now a plethora of papers arguing that moderate consumption of alcohol counters coronary heart disease [see, for example, Dyer et al. 1977; Hennekens et al. 1978; Ramsey 1979; Marmot et al. 1981; Gordon & Kannel 1983 (the Framingham study); Kozarevic et al. 1983; Yano et al. 1984; Moore & Pearson 1986; Klatsky et al. 1992; Maclure 1993; Verschuren 1993]. Alcohol causes a lowering of LDL cholesterol in the plasma and an increased level of HDL cholesterol (HDL2 and HDL3) and apo-lipoproteins A-I and A-II (Clevidence et al. 1995; Goldberg et al. 1995; Jansen et al. 1995; Parker et al. 1996).
Alcohol also appears to lower the risk of blood clotting by reducing the level of brinogen in blood plasma (Stefanick et al. 1995) and lessening the tendency of blood platelets to aggregate (Renaud et al. 1992). The bene ts apply to both men and women
(Nanchahal et al. 2000).
Doyens of the eld have included Arthur Klatsky in Oakland, California, Norman Kaplan of the University of Texas Southwestern Medical Center, and Sir Richard Doll in Oxford, England.
The phenomenon has taken the name the 'French paradox', on account of the unexpectedly low risk of cardiovascular disease in a country noted for its intake of very fatty foods. We can look back nearly two centuries to the rst noting of this effect, when an Irish doctor, Samuel Black, remarked on the much greater incidence of angina in France as opposed to Ireland, which he believed was ascribable to 'the French habits and modes of living, coinciding with the benignity of their climate and the peculiarity of their moral affections' (Black 1819). The occurrence is now sometimes called the European Paradox because it re ects dietary characteristics beyond France alone
(Bellizzi et al. 1994).
Various laboratories have reported U-shaped curves (e.g. Doll et al. 1994) or J-shaped curves (e.g. Tsugane et al. 1999) (Fig. 6.1) to illustrate the impact of various intakes of alcohol on coronary heart disease and on all causes of mortality. For the most part it seems that the J shape relates to the relationship between alcohol intake and total mortality, with the U shape better describing that between alcohol consumption and coronary heart disease. The clear evidence is that the intake of some alcohol has a bene cial impact. In many instances consumption of between 1 and 3 units daily perhaps offers the best advantage, with higher intake progressively shifting the risk upwards again.
The low point (nadir) in these curves has been reported at various levels, for example, 69 g alcohol per week for men in the US (26 g per week for women), but 116 g per week for men in the UK (White 1999). It seems that bene ts for women are especially notable after the menopause (Fuchs et al. 1995; Nanchahal et al. 2000).
Even the American Cancer Society reported this type of effect (Boffetta & Gar nkel 1990). The study began in 1959 with 276,802 men between the ages of 40 and 59. Assigning 1.0 as a standard value for risk of death in non-drinkers, it was shown that the risk of death dropped to 0.84 (i.e. by 16%) for those taking one alcoholic drink per day. The risk of death for those claiming to consume six drinks per day was still lower than for abstainers, at 0.92.
The Impact of Alcohol on Health
In this chapter we consider the effect that alcohol, including in the form of beer, might have on the overall state of healthfulness of the body. What harm might it do - and might it actually do some good? And let us start from a baseline statement that alcohol is relatively non-toxic, with an oral LD50 for the rat of 13.7 g/kg (i.e. the amount of ethanol which will kill half of the animals in an experimental population) (Bakalinsky and Penner 2003)
Increasingly the evidence is that there appear to be bene ts in drinking beer (and other types of alcoholic beverage). Guallar-Castillon et al. (2001) concluded that the consumption of total alcohol (wine and beer) was associated with a lower prevalence of sub-optimal health. Hospitalisation is less acute for daily moderate drinkers (Longnecker & McMahon 1988), especially for women who had consumed between 29 and 42 alcoholic beverages in the fortnight prior to lling in the questionnaire. Artalejo et al. (2000) found that moderate drinkers in Spain were less likely than abstainers to use healthcare services. Meanwhile Wiley and Camacho (1980) showed that moderate alcohol consumption (17-45 drinks per month) was associated with the most favourable adjusted health scores.
Beer drinkers were shown by Richman and Warren (1985) to have signi cantly lower rates of morbidity (sickness) than expected - one drink per day giving 15% less disability than was the case for the general population.
There will be those reading this who will not be able to countenance such ndings. If these people nd it hard to swallow that drinkers, imbibing in moderation, could be less ill, then they might note that they have certainly not been shown to be more sick. However, we must stress always that many of these studies are dealing with correlation, not necessarily causality. Some will argue that there may be other confounding factors not explored in the studies, and that those who tend to drink in moderation may have other lifestyle attributes that are the true reason for their enhanced healthiness. However, the sheer frequency of studies that have demonstrated the bene ts of restricted alcohol intake, which we will explore in this chapter, weigh heavily in support of the merits of sensible drinking.
In the mid-1990s, the Department of Health within the British government addressed the matter of recommended safe limits for drinking. After (we presume) careful consideration of the scienti c and medical evidence available up to that stage, they increased
the recommended limit for men from 21 units to 28 units per week, with the advice to women being to drink no more than 21 units per week (previously it had been 14). They stressed that the daily maximum should be 4 units and that binge drinking (the equivalent of taking all of the weekly allocation at one sitting) is absolutely undesirable.
Table 6.1 describes a unit of alcohol in terms of volume of beer and other alcoholic drinks in the UK. It should be noted that the de nition of a unit differs between countries . This table also indicates the recommendations concerning alcohol consumption in those countries. It must be stressed that beers can differ substantially in their alcohol content . Thus a mainstream ale or lager in most parts of the world is likely to contain between 3.5 and 5% alcohol by volume (ABV) and one unit is basically a half-pint (284 mL) of such a product. There are some beers
Increasingly the evidence is that there appear to be bene ts in drinking beer (and other types of alcoholic beverage). Guallar-Castillon et al. (2001) concluded that the consumption of total alcohol (wine and beer) was associated with a lower prevalence of sub-optimal health. Hospitalisation is less acute for daily moderate drinkers (Longnecker & McMahon 1988), especially for women who had consumed between 29 and 42 alcoholic beverages in the fortnight prior to lling in the questionnaire. Artalejo et al. (2000) found that moderate drinkers in Spain were less likely than abstainers to use healthcare services. Meanwhile Wiley and Camacho (1980) showed that moderate alcohol consumption (17-45 drinks per month) was associated with the most favourable adjusted health scores.
Beer drinkers were shown by Richman and Warren (1985) to have signi cantly lower rates of morbidity (sickness) than expected - one drink per day giving 15% less disability than was the case for the general population.
There will be those reading this who will not be able to countenance such ndings. If these people nd it hard to swallow that drinkers, imbibing in moderation, could be less ill, then they might note that they have certainly not been shown to be more sick. However, we must stress always that many of these studies are dealing with correlation, not necessarily causality. Some will argue that there may be other confounding factors not explored in the studies, and that those who tend to drink in moderation may have other lifestyle attributes that are the true reason for their enhanced healthiness. However, the sheer frequency of studies that have demonstrated the bene ts of restricted alcohol intake, which we will explore in this chapter, weigh heavily in support of the merits of sensible drinking.
In the mid-1990s, the Department of Health within the British government addressed the matter of recommended safe limits for drinking. After (we presume) careful consideration of the scienti c and medical evidence available up to that stage, they increased
the recommended limit for men from 21 units to 28 units per week, with the advice to women being to drink no more than 21 units per week (previously it had been 14). They stressed that the daily maximum should be 4 units and that binge drinking (the equivalent of taking all of the weekly allocation at one sitting) is absolutely undesirable.
Table 6.1 describes a unit of alcohol in terms of volume of beer and other alcoholic drinks in the UK. It should be noted that the de nition of a unit differs between countries . This table also indicates the recommendations concerning alcohol consumption in those countries. It must be stressed that beers can differ substantially in their alcohol content . Thus a mainstream ale or lager in most parts of the world is likely to contain between 3.5 and 5% alcohol by volume (ABV) and one unit is basically a half-pint (284 mL) of such a product. There are some beers
The Composition of Beer in Relation to Nutrition and Health
In Chapter 2 we encountered the changing opinions on the importance of beer as part of the diet. Seemingly on Captain Cook's ships beer contributed as many calories to the sailors' diets as biscuits (bread) and meat combined (Feeney 1997). Of course this a priori signi cance of beer is tilted rather differently nowadays; however, beer can still offer signi cant contributions to the diet, quite apart from its role as a thirst quencher and substantial contribution to the holistic dining experience.
Norris (1946) and Stringer (1946) contributed some of the earliest and most authoritative assessments of the worth of beer to the adult diet. These papers were based on presentations to a joint meeting of the Institute of Brewing and the Nutrition Panel of the Society of Chemical Industry in December 1945. World War II had just concluded and Norris observed that:
... there has been great activity on the nutrition front, largely as a result of the stress of war, and it is not unpro table to examine the position in regard to beer in the light of recently acquired knowledge of dietary requirements ...Norris (1946)
In the discussion recorded after that meeting, which was held at the historic Horse Shoe Hotel on Tottenham Court Road, Dr S.K. Kon was moved to offer his opinions, recorded as follows:
The two papers had underlined the nutritional importance of fermented beverages for a civilian community in war. He believed it was an open secret that when Dr Sydenstricker came here from the United States, in 1941, when nutritional problems were very dif cult, he found much less de ciency disease than was expected, and there seemed little doubt that the explanation, or part explanation, was the ribo-avin and nicotinic acid intake from beer, and possibly from tea. In that way this country seemed to have solved one or two nutritional problems more satisfactorily than the otherwise more fortunate USA. But the importance of beer becomes even greater when the nutrition is considered of the more primitive natives such as those of Africa. From the studies carried out there recently it would really seem that the local fermented native beer may be at times almost the sheet anchor of nutrition.
Norris (1946) and Stringer (1946) contributed some of the earliest and most authoritative assessments of the worth of beer to the adult diet. These papers were based on presentations to a joint meeting of the Institute of Brewing and the Nutrition Panel of the Society of Chemical Industry in December 1945. World War II had just concluded and Norris observed that:
... there has been great activity on the nutrition front, largely as a result of the stress of war, and it is not unpro table to examine the position in regard to beer in the light of recently acquired knowledge of dietary requirements ...Norris (1946)
In the discussion recorded after that meeting, which was held at the historic Horse Shoe Hotel on Tottenham Court Road, Dr S.K. Kon was moved to offer his opinions, recorded as follows:
The two papers had underlined the nutritional importance of fermented beverages for a civilian community in war. He believed it was an open secret that when Dr Sydenstricker came here from the United States, in 1941, when nutritional problems were very dif cult, he found much less de ciency disease than was expected, and there seemed little doubt that the explanation, or part explanation, was the ribo-avin and nicotinic acid intake from beer, and possibly from tea. In that way this country seemed to have solved one or two nutritional problems more satisfactorily than the otherwise more fortunate USA. But the importance of beer becomes even greater when the nutrition is considered of the more primitive natives such as those of Africa. From the studies carried out there recently it would really seem that the local fermented native beer may be at times almost the sheet anchor of nutrition.
The Basics of Human Nutrition
If we are to make reasoned judgements on the interrelationship of beer and human health, then it is important that we rst consider the key elements of nutrition.
Essentially our bodies require, in the correct balance, the key nutrients for healthy functioning and development. Additionally the diet should be devoid of materials that are damaging. In this context there may be components of our daily intake that, while not of themselves essential nutrients, may serve to counter negative impacts of adverse food constituents or materials present in the environment. For more detailed considerations of human nutrition the reader is referred to Boyle and Zyla (1996).
Our bodies need food to provide energy (calories) and the building blocks of our tissues (notably amino acids), for the most part taken into the body in the form of protein, carbohydrates, lipids, vitamins, minerals and water. Our wellbeing is therefore incon-trovertibly related to what we eat and drink, in terms of the content of the essentials, the form in which they are present in the food (e.g. carbohydrate in the form of bre acts bene cially in a way quite distinct from that carbohydrate that will overtly provide energy through digestion) and the presence or absence of molecules in the food that may be bene cial or damaging to the body.
If any individual component of the diet is present in excess or is insuf cient in quantity, then the diet is out of balance.
Energy
The main sources of energy for the human body are carbohydrates, fats and proteins. However, especially in the context of this book, we must stress that alcohol is a source of energy.
Energy in food is quanti ed on the basis of calories, one calorie being de ned as the amount of heat required to raise the temperature of one gram of water by one degree Celsius. It is customary to talk in terms of kilocalories (or Calories with a capital C) which equate to 1000 calories. These days it is more scienti cally correct to talk in terms of kilojoules, for the joule has replaced the calorie as the primary unit of energy under the international system of units (SI). (Incidentally, James Prescott Joule, 1818-89, after whom the unit of energy was named, was a member of a famous Staffordshire brew-
ing family.) One joule is de ned as the amount of energy exerted when a force of one newton is applied over a displacement of one metre. It is the equivalent to one watt of power radiated or dissipated for one second. However, calorie is so widely known and used as a term that I employ it here: the term calorie is proving impossible to shake from popular parlance. The reader should be warned that often calorie (without the capital C) is employed in the literature rather than kilocalorie.
The number of calories in a foodstuff can be determined in the laboratory by combustion. However the 'true' calori c content of a food as it pertains to the diet depends on the extent to which those calories are available to the body.
This applies to all components of the diet. Just because something is present in high quantity in a foodstuff it does not necessarily follow that it will get into the body to exert any effect. Many factors may impact, including the form in which the nutrient is present in a food. A metal such as iron may not be assimilated if it is attached to some other component of the diet that passes straight through the gut. Much of the modern work on antioxidants is awed in this way. For example, only if the speci c antioxidants get into the body will they get to the key site where they are able to act.
Returning to carbohydrates, those such as starch and sugar are almost completely digested and oxidised by the body and they are ascribed a calori c value of 3.75 kcal/g. Fats, which are digested up to 95%, afford a higher energy level (9 kcal/g) because they are less oxidised than the carbohydrates. The calori c value of protein is generally held to be similar to that of carbohydrate, at 4 kcal/g. Ethanol is ascribed a calori c value of 7 kcal/g, indicating that, molecule for molecule, it is an extremely rich source of energy, second only to fat.
If calories in excess of those needed to maintain the body in equilibrium are taken in, then the surplus will be built up in the form of fat, for the simple reason that, pound for pound, fat is a richer energy store than is starch or protein. The converse applies: enhanced energy demand through exercise will 'burn up' fat provided that the extra calorie requirement is not met from fresh food intake.
Phytonutrients
The importance of antioxidants is highlighted in the California pyramid, with the baseline here occupied by foodstuffs, notably fruits and vegetables, which are rich in these and other 'phytonutrients' (i.e. plant-derived nutrients). People living on plant-rich diets generally appear to have lower incidence of disease. This has prompted a search for the active ingredients, of which some are undoubtedly antioxidants. Others may regulate enzyme action and in uence the production or elimination of relevant components. Thus there has developed a large market for herbal supplements. It is in this context that attention has been paid to the hop (see Chapter 6).
Phytochemicals are de ned by the US Food Administration as substances of plant origin that may be ingested by humans daily in gram quantities and which exhibit the potential for modulating metabolism such as to be favourable for cancer prevention and cardiovascular protection (Rincon-Leon 2003). The word 'nutraceutical' has crept into common parlance.
For those preferring their phytonutrients in food - as opposed to supplement - form, Gollman and Pierce (1998) offer one useful recipe book. The authors endeavour to present their recipes from an underpinning scienti c perspective. Alas, beer is not featured. Wine is - yet we will discover in Chapter 6 that beer is likely at least the equal of wine from a health perspective.
Carbohydrate, fat and protein
Although carbohydrate, fat and protein are interchangeable through pathways of intermediary metabolism in the body, the relative amounts of each are not irrelevant. Carbohydrates, then, can 'spare' protein if they are present in adequate quantities. If they are not, then the body will use protein, which is a key component of muscles and other body tissues. Health experts suggest that about 60% of calorie intake should be as carbohydrate. Even within a category, there can be signi cant differences. More complex forms of carbohydrate, e.g. starch, will linger in the body longer than will simpler sugars, allowing the growth of microbes to take place and the attendant enrichment of vitamins in the uxing food. The converse can apply. Some individuals are lactose-intolerant, with this sugar being poorly absorbed and leading to attendant diarrhoea.
For proteins, a key feature of their value in the diet is their relative content of the various amino acids. The best proteins are those containing all of the essential amino acids (which the human body cannot synthesise) presupposing that those proteins are indeed taken up by the body. Meat, sh, milk and egg proteins are generally good. Barley protein is relatively de cient in two amino acids, lysine and (to a lesser extent) threonine, though high lysine variants have been developed (Kasha et al. 1993).
Of course most diets don't usually contain just a solitary source of protein, and generally there is an appropriate mix of animal and vegetable proteins.
The fats provide the essential fatty acid, linoleic acid, which the human body cannot synthesise. Unsaturated fatty acids of this type are associated with a lower incidence of coronary heart disease: they lower cholesterol levels. Beer is essentially fat free.
Vitamins are organic substances that the human body cannot synthesise itself and which must be provided in the diet (Finglas 2003). They have various functions in the body and are customarily divided into the water-soluble vitamins and the fat-soluble vitamins; they are summarised in Table 4.2. For the most part they are not required in very large quantities, but it must be borne in mind that the composition of the food matrix in which they are present can impact on their availability. One example is the higher requirement for thiamine if alcohol is present at high levels. It is equally important to stress that excessive intake of vitamins may have adverse effects. For the most part this pertains to two of the fat-soluble vitamins, A and D, though B6 at levels above 50 mg per day or nicotinic acid in excess of 2-6 g per day are of concern for neurological damage and liver damage respectively
Fibre
The term is unfortunate, for not all of the components generally considered under this heading are actually brous. Perhaps 'roughage' after all is no worse a term (Kritchevsky
& Bon eld 1995).
The majority of materials considered to be dietary bre are plant cell wall components including celluloses, hemicelluloses (such as are found in the cell walls of barley) and pectins. There can be a further division into soluble and insoluble fractions, though it must be remembered that this refers to what is solubilised in standard laboratory analytical procedures and not necessarily what happens in the gastrointestinal tract.
Insoluble components may serve to delay the digestion of other components via physical blocking. The soluble components, on the other hand, will afford increased viscosity if they are of high molecular weight, thereby lengthening transit time in the gut and also the rate at which digestion products (e.g. glucose) are taken through the gut wall. This may also explain the impact of dietary bre in reducing the absorption of cholesterol.
These materials hold water, lead to a softening of stools and accelerate the passage of the stool through the large intestine. Research in recent years has demonstrated the merits of bre in lowering plasma cholesterol levels, reducing cancer incidence, lessening the need for diabetics to take insulin, and so on. The understanding of the precise structural features in bre which lead to best effect is less than clear (see Johnson 2003). The beer carbohydrates comprising soluble bre (which will include the degradation products of barley cell wall polysaccharides and also the dextrins produced during starch degradation; see Chapter 3) escape absorption in the small intestine, thus becoming nutrients for bacteria located in the large bowel. The importance of these organisms to gut function and health has become well recognised in recent years and has led to the concept of probiotics and prebiotics. Probiotics are organisms, notably lactobacilli and bi dobacteria, which are added to diet to boost the ora in the large intestine. For example they are added to yoghurt (Young 1998). Prebiotics are nutrients that boost the growth of these organisms. These may include oligosaccharides that may promote the growth of the appropriate organisms (Gibson 1999; Roberfroid 2001). Microbes in the large intestine produce methane and other gases as a result of their metabolism, and the atulence experienced after drinking beer may relate to this activity .
It also needs to be borne in mind that materials capable of binding to the bre passing straight through the digestive system will also be less available to the body. This might include certain minerals and vitamins (Prosky 2003).
Water
The human body is almost two-thirds water. Loss of 5-10% of the body weight as water leads to symptoms of dehydration. Evidently the greater the risk of water loss, the greater the need for rehydration. Clearly if the water is also carrying away with it other nutrients, e.g. minerals, then these will need to be replaced in quantities that restore the status quo.
Balance
To reiterate: the diet needs to be in balance. And this includes 'trendy' food ingredients - the so-called functional food ingredients. Excessive bre can lead to problems with intestinal gas, perhaps intestinal obstruction, and a reduced absorption of essential minerals such as zinc, iron and calcium. Uptake of minerals can also be restricted by chelating agents such as phytate and oxalate. Polyphenolics can bind metals such as iron and so reduce uptake. Phosphates reduce the uptake of zinc while calcium interferes with assimilation of manganese. Another example is that high levels of antioxidants such as vitamin C can switch over and become pro-oxidants.
As is said more than once in this book, beer should be taken in moderation as part of a balanced diet. The same goes for all other foodstuffs.
Essentially our bodies require, in the correct balance, the key nutrients for healthy functioning and development. Additionally the diet should be devoid of materials that are damaging. In this context there may be components of our daily intake that, while not of themselves essential nutrients, may serve to counter negative impacts of adverse food constituents or materials present in the environment. For more detailed considerations of human nutrition the reader is referred to Boyle and Zyla (1996).
Our bodies need food to provide energy (calories) and the building blocks of our tissues (notably amino acids), for the most part taken into the body in the form of protein, carbohydrates, lipids, vitamins, minerals and water. Our wellbeing is therefore incon-trovertibly related to what we eat and drink, in terms of the content of the essentials, the form in which they are present in the food (e.g. carbohydrate in the form of bre acts bene cially in a way quite distinct from that carbohydrate that will overtly provide energy through digestion) and the presence or absence of molecules in the food that may be bene cial or damaging to the body.
If any individual component of the diet is present in excess or is insuf cient in quantity, then the diet is out of balance.
Energy
The main sources of energy for the human body are carbohydrates, fats and proteins. However, especially in the context of this book, we must stress that alcohol is a source of energy.
Energy in food is quanti ed on the basis of calories, one calorie being de ned as the amount of heat required to raise the temperature of one gram of water by one degree Celsius. It is customary to talk in terms of kilocalories (or Calories with a capital C) which equate to 1000 calories. These days it is more scienti cally correct to talk in terms of kilojoules, for the joule has replaced the calorie as the primary unit of energy under the international system of units (SI). (Incidentally, James Prescott Joule, 1818-89, after whom the unit of energy was named, was a member of a famous Staffordshire brew-
ing family.) One joule is de ned as the amount of energy exerted when a force of one newton is applied over a displacement of one metre. It is the equivalent to one watt of power radiated or dissipated for one second. However, calorie is so widely known and used as a term that I employ it here: the term calorie is proving impossible to shake from popular parlance. The reader should be warned that often calorie (without the capital C) is employed in the literature rather than kilocalorie.
The number of calories in a foodstuff can be determined in the laboratory by combustion. However the 'true' calori c content of a food as it pertains to the diet depends on the extent to which those calories are available to the body.
This applies to all components of the diet. Just because something is present in high quantity in a foodstuff it does not necessarily follow that it will get into the body to exert any effect. Many factors may impact, including the form in which the nutrient is present in a food. A metal such as iron may not be assimilated if it is attached to some other component of the diet that passes straight through the gut. Much of the modern work on antioxidants is awed in this way. For example, only if the speci c antioxidants get into the body will they get to the key site where they are able to act.
Returning to carbohydrates, those such as starch and sugar are almost completely digested and oxidised by the body and they are ascribed a calori c value of 3.75 kcal/g. Fats, which are digested up to 95%, afford a higher energy level (9 kcal/g) because they are less oxidised than the carbohydrates. The calori c value of protein is generally held to be similar to that of carbohydrate, at 4 kcal/g. Ethanol is ascribed a calori c value of 7 kcal/g, indicating that, molecule for molecule, it is an extremely rich source of energy, second only to fat.
If calories in excess of those needed to maintain the body in equilibrium are taken in, then the surplus will be built up in the form of fat, for the simple reason that, pound for pound, fat is a richer energy store than is starch or protein. The converse applies: enhanced energy demand through exercise will 'burn up' fat provided that the extra calorie requirement is not met from fresh food intake.
Phytonutrients
The importance of antioxidants is highlighted in the California pyramid, with the baseline here occupied by foodstuffs, notably fruits and vegetables, which are rich in these and other 'phytonutrients' (i.e. plant-derived nutrients). People living on plant-rich diets generally appear to have lower incidence of disease. This has prompted a search for the active ingredients, of which some are undoubtedly antioxidants. Others may regulate enzyme action and in uence the production or elimination of relevant components. Thus there has developed a large market for herbal supplements. It is in this context that attention has been paid to the hop (see Chapter 6).
Phytochemicals are de ned by the US Food Administration as substances of plant origin that may be ingested by humans daily in gram quantities and which exhibit the potential for modulating metabolism such as to be favourable for cancer prevention and cardiovascular protection (Rincon-Leon 2003). The word 'nutraceutical' has crept into common parlance.
For those preferring their phytonutrients in food - as opposed to supplement - form, Gollman and Pierce (1998) offer one useful recipe book. The authors endeavour to present their recipes from an underpinning scienti c perspective. Alas, beer is not featured. Wine is - yet we will discover in Chapter 6 that beer is likely at least the equal of wine from a health perspective.
Carbohydrate, fat and protein
Although carbohydrate, fat and protein are interchangeable through pathways of intermediary metabolism in the body, the relative amounts of each are not irrelevant. Carbohydrates, then, can 'spare' protein if they are present in adequate quantities. If they are not, then the body will use protein, which is a key component of muscles and other body tissues. Health experts suggest that about 60% of calorie intake should be as carbohydrate. Even within a category, there can be signi cant differences. More complex forms of carbohydrate, e.g. starch, will linger in the body longer than will simpler sugars, allowing the growth of microbes to take place and the attendant enrichment of vitamins in the uxing food. The converse can apply. Some individuals are lactose-intolerant, with this sugar being poorly absorbed and leading to attendant diarrhoea.
For proteins, a key feature of their value in the diet is their relative content of the various amino acids. The best proteins are those containing all of the essential amino acids (which the human body cannot synthesise) presupposing that those proteins are indeed taken up by the body. Meat, sh, milk and egg proteins are generally good. Barley protein is relatively de cient in two amino acids, lysine and (to a lesser extent) threonine, though high lysine variants have been developed (Kasha et al. 1993).
Of course most diets don't usually contain just a solitary source of protein, and generally there is an appropriate mix of animal and vegetable proteins.
The fats provide the essential fatty acid, linoleic acid, which the human body cannot synthesise. Unsaturated fatty acids of this type are associated with a lower incidence of coronary heart disease: they lower cholesterol levels. Beer is essentially fat free.
Vitamins are organic substances that the human body cannot synthesise itself and which must be provided in the diet (Finglas 2003). They have various functions in the body and are customarily divided into the water-soluble vitamins and the fat-soluble vitamins; they are summarised in Table 4.2. For the most part they are not required in very large quantities, but it must be borne in mind that the composition of the food matrix in which they are present can impact on their availability. One example is the higher requirement for thiamine if alcohol is present at high levels. It is equally important to stress that excessive intake of vitamins may have adverse effects. For the most part this pertains to two of the fat-soluble vitamins, A and D, though B6 at levels above 50 mg per day or nicotinic acid in excess of 2-6 g per day are of concern for neurological damage and liver damage respectively
Fibre
The term is unfortunate, for not all of the components generally considered under this heading are actually brous. Perhaps 'roughage' after all is no worse a term (Kritchevsky
& Bon eld 1995).
The majority of materials considered to be dietary bre are plant cell wall components including celluloses, hemicelluloses (such as are found in the cell walls of barley) and pectins. There can be a further division into soluble and insoluble fractions, though it must be remembered that this refers to what is solubilised in standard laboratory analytical procedures and not necessarily what happens in the gastrointestinal tract.
Insoluble components may serve to delay the digestion of other components via physical blocking. The soluble components, on the other hand, will afford increased viscosity if they are of high molecular weight, thereby lengthening transit time in the gut and also the rate at which digestion products (e.g. glucose) are taken through the gut wall. This may also explain the impact of dietary bre in reducing the absorption of cholesterol.
These materials hold water, lead to a softening of stools and accelerate the passage of the stool through the large intestine. Research in recent years has demonstrated the merits of bre in lowering plasma cholesterol levels, reducing cancer incidence, lessening the need for diabetics to take insulin, and so on. The understanding of the precise structural features in bre which lead to best effect is less than clear (see Johnson 2003). The beer carbohydrates comprising soluble bre (which will include the degradation products of barley cell wall polysaccharides and also the dextrins produced during starch degradation; see Chapter 3) escape absorption in the small intestine, thus becoming nutrients for bacteria located in the large bowel. The importance of these organisms to gut function and health has become well recognised in recent years and has led to the concept of probiotics and prebiotics. Probiotics are organisms, notably lactobacilli and bi dobacteria, which are added to diet to boost the ora in the large intestine. For example they are added to yoghurt (Young 1998). Prebiotics are nutrients that boost the growth of these organisms. These may include oligosaccharides that may promote the growth of the appropriate organisms (Gibson 1999; Roberfroid 2001). Microbes in the large intestine produce methane and other gases as a result of their metabolism, and the atulence experienced after drinking beer may relate to this activity .
It also needs to be borne in mind that materials capable of binding to the bre passing straight through the digestive system will also be less available to the body. This might include certain minerals and vitamins (Prosky 2003).
Water
The human body is almost two-thirds water. Loss of 5-10% of the body weight as water leads to symptoms of dehydration. Evidently the greater the risk of water loss, the greater the need for rehydration. Clearly if the water is also carrying away with it other nutrients, e.g. minerals, then these will need to be replaced in quantities that restore the status quo.
Balance
To reiterate: the diet needs to be in balance. And this includes 'trendy' food ingredients - the so-called functional food ingredients. Excessive bre can lead to problems with intestinal gas, perhaps intestinal obstruction, and a reduced absorption of essential minerals such as zinc, iron and calcium. Uptake of minerals can also be restricted by chelating agents such as phytate and oxalate. Polyphenolics can bind metals such as iron and so reduce uptake. Phosphates reduce the uptake of zinc while calcium interferes with assimilation of manganese. Another example is that high levels of antioxidants such as vitamin C can switch over and become pro-oxidants.
As is said more than once in this book, beer should be taken in moderation as part of a balanced diet. The same goes for all other foodstuffs.
Phenolic materials
In just the same way that the chemistry of the essential oil fraction of hops is enormously complex, so too is that of the phenolic materials contributed to beer by both barley and
hops (Verzele 1986).
We encountered ferulic acid above. Other monomeric phenolic species present in beer include catechin and quercetin. Catechin is rmly accepted as an antioxidant, through its ability both to scavenge oxygen radicals and to inhibit the enzyme lipoxygenase, which promotes the initial breakdown of unsaturated fatty acids to staling carbonyls.
Low molecular-weight contributors to beer aroma
Many people misguidedly believe that most of the avour of beer is derived from its taste. In fact they are detecting the avoursome materials by the nose, there being only four true characters detected on the tongue: bitterness, sweetness, sourness and saltiness
(Bamforth & Hughes 1998).
The confusion about what is detected by tongue and what by nose arises because there is a continuum between the back of the throat and the nasal passages. A beer's smell is the net effect of a complex contribution of many individual molecules. No beer is that simple as to have its aroma determined by one or even a very few substances. The perceived 'nose' is a balance between positive and negative avour notes, each of which may be due to more than a single compound from different chemical classes. Some of these volatile substances come from the malt and hops. A great many, though, are side products of the metabolism of yeast.
hops (Verzele 1986).
We encountered ferulic acid above. Other monomeric phenolic species present in beer include catechin and quercetin. Catechin is rmly accepted as an antioxidant, through its ability both to scavenge oxygen radicals and to inhibit the enzyme lipoxygenase, which promotes the initial breakdown of unsaturated fatty acids to staling carbonyls.
Low molecular-weight contributors to beer aroma
Many people misguidedly believe that most of the avour of beer is derived from its taste. In fact they are detecting the avoursome materials by the nose, there being only four true characters detected on the tongue: bitterness, sweetness, sourness and saltiness
(Bamforth & Hughes 1998).
The confusion about what is detected by tongue and what by nose arises because there is a continuum between the back of the throat and the nasal passages. A beer's smell is the net effect of a complex contribution of many individual molecules. No beer is that simple as to have its aroma determined by one or even a very few substances. The perceived 'nose' is a balance between positive and negative avour notes, each of which may be due to more than a single compound from different chemical classes. Some of these volatile substances come from the malt and hops. A great many, though, are side products of the metabolism of yeast.
Flavours from hops
Hops play several roles in the production ofbeer, but in particular they are crucial as a source of bitterness (from the hop resins) and aroma (from the essential oils) (Neve 1991).
The chemistry of hop resins is somewhat complex, but of most importance are the a-acids, which can account for between 2% and 15% of the dry weight of the hop, depending on variety and environment. The higher the a-acid content, the greater the bitterness potential. When wort is boiled, the a-acids are isomerised to form iso-a-acids. The latter are much more soluble and bitter than the a-acids. Isomerisation in a boil is not very ef cient, with perhaps no more than 50% of the a-acids being converted to iso-a-acids and less than 25% of the original bittering potential surviving into the beer.
Apart from imparting bitterness to beer, the iso-a-acids also promote foaming by crosslinking the hydrophobic residues on polypeptides with their own hydrophobic side-chains, rendering the foam almost solid-like and able to cling to ('lace') the walls of the drinking glass (Hughes & Simpson 1994). Furthermore they have strong antimicrobial properties and are able to suppress the growth of many Gram-positive bacteria (Fernandez & Simpson 1995). Beer is not entirely resistant to spoilage but certainly the bitter acids have a strong antimicrobial in uence. Other key factors that render beer extremely inhospitable to microbes are its very low pH (typically in the range 3.8-4.6), lack of oxygen, minimal levels of residual nutrients such as sugar and amino acids, its content of ethanol and perhaps the presence of some other antimicrobial constituents such as polyphenols. No pathogens will grow in beer, even alcohol-free beer. All too familiar food scares such as those due to Listeria, Escherichia coli O-157 and Clostridium botulinum cannot be caused by beer.
Increasingly used nowadays are isomerised resin extracts in which one or more of the side-chains of the iso-a-acids has been reduced, using hydrogen gas in the presence of a palladium catalyst (Hughes & Simpson 1993). This is because one of the side-chains is susceptible to cleavage by light, yielding a radical breakdown product that reacts with traces of sulphidic materials in beer to produce 3-methyl-2-butene-1-thiol (MBT), a compound that affords a reprehensible skunky aroma. If the side-chain is reduced, it no longer produces MBT. For this reason, beers that are likely to be exposed to light in package (e.g. by being sold in green or clear glass bottles) often contain these modi ed bitterness preparations, which have the added advantage of possessing increased foam-stabilising properties. Once again, these products are fully cleared for safe use.
Hops contain between 0.03% and 3% w/w of oil, which comprises a complex mixture of at least 300 compounds contributing to beer aroma (Gardner 1997).
The chemistry of hop resins is somewhat complex, but of most importance are the a-acids, which can account for between 2% and 15% of the dry weight of the hop, depending on variety and environment. The higher the a-acid content, the greater the bitterness potential. When wort is boiled, the a-acids are isomerised to form iso-a-acids. The latter are much more soluble and bitter than the a-acids. Isomerisation in a boil is not very ef cient, with perhaps no more than 50% of the a-acids being converted to iso-a-acids and less than 25% of the original bittering potential surviving into the beer.
Apart from imparting bitterness to beer, the iso-a-acids also promote foaming by crosslinking the hydrophobic residues on polypeptides with their own hydrophobic side-chains, rendering the foam almost solid-like and able to cling to ('lace') the walls of the drinking glass (Hughes & Simpson 1994). Furthermore they have strong antimicrobial properties and are able to suppress the growth of many Gram-positive bacteria (Fernandez & Simpson 1995). Beer is not entirely resistant to spoilage but certainly the bitter acids have a strong antimicrobial in uence. Other key factors that render beer extremely inhospitable to microbes are its very low pH (typically in the range 3.8-4.6), lack of oxygen, minimal levels of residual nutrients such as sugar and amino acids, its content of ethanol and perhaps the presence of some other antimicrobial constituents such as polyphenols. No pathogens will grow in beer, even alcohol-free beer. All too familiar food scares such as those due to Listeria, Escherichia coli O-157 and Clostridium botulinum cannot be caused by beer.
Increasingly used nowadays are isomerised resin extracts in which one or more of the side-chains of the iso-a-acids has been reduced, using hydrogen gas in the presence of a palladium catalyst (Hughes & Simpson 1993). This is because one of the side-chains is susceptible to cleavage by light, yielding a radical breakdown product that reacts with traces of sulphidic materials in beer to produce 3-methyl-2-butene-1-thiol (MBT), a compound that affords a reprehensible skunky aroma. If the side-chain is reduced, it no longer produces MBT. For this reason, beers that are likely to be exposed to light in package (e.g. by being sold in green or clear glass bottles) often contain these modi ed bitterness preparations, which have the added advantage of possessing increased foam-stabilising properties. Once again, these products are fully cleared for safe use.
Hops contain between 0.03% and 3% w/w of oil, which comprises a complex mixture of at least 300 compounds contributing to beer aroma (Gardner 1997).
Proteins, polypeptides and amino acids
The presence of polypeptide material in beer is important for the contribution it makes to foam (Bamforth 1985b). In the processes of malting and brewing, the native proteins of barley undergo considerable degradation and denaturation, such that those present in the nished beer bear little resemblance to those found in the barley kernel. While polypeptides can be bene cial for foaming, they are detrimental in another respect: they can crosslink with polyphenols to form hazes (McMurrough & Delcour 1994).
The amino acids in beer provide no real bene t to the beer. If present in excess, they potentiate infection of a product by acting as nitrogen sources for spoilage microorganisms. This is why brewers seek to optimise the level of amino acids in wort, so that the yeast uses up all that is readily assimilable.
Lipids
Barley contains about 3% w/w lipid, most of it congregated in the living tissues (embryo and aleurone) (Anness & Reed 1985). Very little lipid, however, survives into beer, making this beverage essentially a fat-free food. This is just as well, from an aesthetic point of view, because lipids are very bad news for beer foam (Bamforth 1985b).
The other adverse in uence of lipids is through their ability to act as precursors of stale avours in beer (Drost et al. 1971). The unsaturated fatty acids, such as linoleic acid, may get a good press for their health-giving properties; however, they can be oxidised, ultimately to yield carbonyl compounds that afford aged character to beer. For this reason many brewers try to ensure that as little lipid as possible survives the brewing process and therefore they are meticulous about eliminating solid material at all stages, because the insoluble lipid associates with solids.
The amino acids in beer provide no real bene t to the beer. If present in excess, they potentiate infection of a product by acting as nitrogen sources for spoilage microorganisms. This is why brewers seek to optimise the level of amino acids in wort, so that the yeast uses up all that is readily assimilable.
Lipids
Barley contains about 3% w/w lipid, most of it congregated in the living tissues (embryo and aleurone) (Anness & Reed 1985). Very little lipid, however, survives into beer, making this beverage essentially a fat-free food. This is just as well, from an aesthetic point of view, because lipids are very bad news for beer foam (Bamforth 1985b).
The other adverse in uence of lipids is through their ability to act as precursors of stale avours in beer (Drost et al. 1971). The unsaturated fatty acids, such as linoleic acid, may get a good press for their health-giving properties; however, they can be oxidised, ultimately to yield carbonyl compounds that afford aged character to beer. For this reason many brewers try to ensure that as little lipid as possible survives the brewing process and therefore they are meticulous about eliminating solid material at all stages, because the insoluble lipid associates with solids.
Water
As already stated, most beers comprise 90-95% water and so its composition is critical as a determinant of beer quality. Brewing demands much more water (5-20 times) than the amount which ends up in the beer (UNEP 1996). A lot is needed for cleaning and for raising the steam needed for heating vessels.
The water must contain no taints or hazardous components and a brewer may treat all water coming into the brewery by procedures such as charcoal ltration and ultra-ltration (Katayama et al. 1987). The water must also have the correct balance of ions (Taylor 1990). Traditionally ale brewing was established in towns such as Burton-on-Trent in England. The level of calcium in the water of the region is relatively high (about 350 mg/L), and it is claimed that this is good for ales, whereas low levels of calcium, such as the less than 10 mg/L in Pilsen, is best for bottom-fermented lagers. In many places in the world the salt composition of the water is adjusted to match that rst used by the monks in Burton in the year 1295, a process known as 'Burtonisation'. Often the brewer will simply add the appropriate blend of salts to achieve this speci cation. To match a Pilsen-type water it is usually necessary to remove existing dissolved ions by deionisation, perhaps by a ltration technique.
Carbohydrates
While most of the sugar found in wort is fermented to ethanol by yeast, some carbohydrates remain in the beer. Furthermore, extra sugars ('primings') may be added to sweeten the nal product.
The carbohydrates surviving into beer from wort are the non-fermentable dextrins and some polysaccharide material. The dextrins are remnants of starch degradation, whereas the polysaccharides derive from cell walls in barley.
Most of the starch in the endosperm of barley survives malting, because it is relatively resistant to enzymatic hydrolysis over anything other than prolonged contact times. However, if starch is gelatinised (which can be likened to melting) by heat treatment, then its constituent molecules, amylose and amylopectin, become much more accessible to enzymes. Thus the start of brewing involves gelatinisation, typically at 65°C, a stage known as 'conversion'. Other cereals, which may be used as adjuncts, have starches that need higher gelatinisation temperatures, e.g. rice and corn, in which starch gelatinises over the range 70-80°C. As stated above, amylase enzymes in the malt degrade the gelatinised starch to fermentable sugars; however, a proportion (usually around 20-25%) remains in the form of unfermentable dextrins. A range of beers is available, which are termed 'super-attenuated' but generally marketed as 'light', in which all of the available starch is converted into ethanol. To effect this, an exogenous heat-stable glucoamylase or pullulanase of microbial origin is often added to the mash or to the fermenter (Bamforth 1985a). It is not obligatory to approach the problem in this way. By judicious use of the mashing regime, and also perhaps the addition of an extract of lightly kilned or unkilned malt to the fermenter, the enzymes native to malt are suf cient to deal with all the dextrins.
The world's rst approved, genetically modi ed (GM) brewing yeast was transformed to express a glucoamylase; however, as yet this strain has not been used in any commercial operation (Hammond & Bamforth 1994). Indeed, no GM material is knowingly or deliberately introduced into beer by any brewer. The only commodities that are based overtly on products of gene technology are some of the commercial enzymes. However, most brewers do not use these and, where they are used, they are added to the mash, and are denatured and precipitated in the kettle boil. Even so, it needs to be stressed that GM commercial enzymes are themselves rigorously screened before approval for commercial use.
Another major carbohydrate component in brewing systems is in the cell walls of barley, a P-glucan comprising P 1-4 links (as in cellulose) but disrupted by occasional P 1-3 links. This molecule is very similar to the P-glucan that is found in oats and which is well known as the 'soluble bre' championed as part of oat-based breakfast cereals (Lasztity 1998). While one of the main purposes of malting is to degrade the cell walls through the action of P-glucanase enzymes during germination, in practice some glucan always survives into malt (Bamforth & Barclay 1993). Unless it is properly degraded it renders the wort extremely viscous, with attendant problems in the operations of separating the wort from the spent grains and with downstream beer ltration (Bamforth 1994). Thus some brewers mash-in at low temperatures (say 50°C) to allow the P-glucanase (which is sensitive to heat) to act. Additionally a heat-stable glucanase from bacteria (such as Bacillus subtilis) or fungi (such as Trichoderma reesei or Penicillium funicu-losum) may be employed (Bamforth 1985a). Barley has been transformed to express a heat-resistant P-glucanase, but it is not yet cleared for commercial use (Mannonen et al. 1993). All of these efforts to eliminate P-glucan are important if production problems are to be avoided, as well as quality problems, for the glucan can cause hazes and precipitates in beer. The beers that will contain the most residual glucan are those that are produced with a high charge of barley adjunct, for instance some well-known stouts. The products of P-glucan breakdown in malting and mashing are not fermentable by yeast, so they survive into beer. Even those beers in which most of the glucan has been converted to low molecular-weight oligosaccharides may be of some value as sources of bre, as it is now understood that any P-linked sugar, no matter how small, may retain some bene cial properties when they reach the lower gut (Schneeman 1999).
P-Glucan is not the only polysaccharide found in the cell walls of barley, the other being arabinoxylan. For reasons that are not entirely understood, this seems to survive malting and brewing more readily than does P-glucan, such that beers tend to contain more arabinoxylan than glucan (Schwarz & Han 1995). It also ranks as soluble bre. In the cell wall the arabinoxylan is covalently linked to ferulic acid (Ahluwalia & Fry 1986). This phenolic acid is released during mashing (McMurrough et al. 1996) and survives into beer (unless the beer is made with yeasts, such as those used in the fermentation of wheat-based beers, which contain an enzyme that can decarboxylate the ferulic acid to 4-vinylguiacol, a substance that gives the classic clove-like character to such products). There is huge interest in ferulic acid as an antioxidant (Kroon & Williamson 1999).
The water must contain no taints or hazardous components and a brewer may treat all water coming into the brewery by procedures such as charcoal ltration and ultra-ltration (Katayama et al. 1987). The water must also have the correct balance of ions (Taylor 1990). Traditionally ale brewing was established in towns such as Burton-on-Trent in England. The level of calcium in the water of the region is relatively high (about 350 mg/L), and it is claimed that this is good for ales, whereas low levels of calcium, such as the less than 10 mg/L in Pilsen, is best for bottom-fermented lagers. In many places in the world the salt composition of the water is adjusted to match that rst used by the monks in Burton in the year 1295, a process known as 'Burtonisation'. Often the brewer will simply add the appropriate blend of salts to achieve this speci cation. To match a Pilsen-type water it is usually necessary to remove existing dissolved ions by deionisation, perhaps by a ltration technique.
Carbohydrates
While most of the sugar found in wort is fermented to ethanol by yeast, some carbohydrates remain in the beer. Furthermore, extra sugars ('primings') may be added to sweeten the nal product.
The carbohydrates surviving into beer from wort are the non-fermentable dextrins and some polysaccharide material. The dextrins are remnants of starch degradation, whereas the polysaccharides derive from cell walls in barley.
Most of the starch in the endosperm of barley survives malting, because it is relatively resistant to enzymatic hydrolysis over anything other than prolonged contact times. However, if starch is gelatinised (which can be likened to melting) by heat treatment, then its constituent molecules, amylose and amylopectin, become much more accessible to enzymes. Thus the start of brewing involves gelatinisation, typically at 65°C, a stage known as 'conversion'. Other cereals, which may be used as adjuncts, have starches that need higher gelatinisation temperatures, e.g. rice and corn, in which starch gelatinises over the range 70-80°C. As stated above, amylase enzymes in the malt degrade the gelatinised starch to fermentable sugars; however, a proportion (usually around 20-25%) remains in the form of unfermentable dextrins. A range of beers is available, which are termed 'super-attenuated' but generally marketed as 'light', in which all of the available starch is converted into ethanol. To effect this, an exogenous heat-stable glucoamylase or pullulanase of microbial origin is often added to the mash or to the fermenter (Bamforth 1985a). It is not obligatory to approach the problem in this way. By judicious use of the mashing regime, and also perhaps the addition of an extract of lightly kilned or unkilned malt to the fermenter, the enzymes native to malt are suf cient to deal with all the dextrins.
The world's rst approved, genetically modi ed (GM) brewing yeast was transformed to express a glucoamylase; however, as yet this strain has not been used in any commercial operation (Hammond & Bamforth 1994). Indeed, no GM material is knowingly or deliberately introduced into beer by any brewer. The only commodities that are based overtly on products of gene technology are some of the commercial enzymes. However, most brewers do not use these and, where they are used, they are added to the mash, and are denatured and precipitated in the kettle boil. Even so, it needs to be stressed that GM commercial enzymes are themselves rigorously screened before approval for commercial use.
Another major carbohydrate component in brewing systems is in the cell walls of barley, a P-glucan comprising P 1-4 links (as in cellulose) but disrupted by occasional P 1-3 links. This molecule is very similar to the P-glucan that is found in oats and which is well known as the 'soluble bre' championed as part of oat-based breakfast cereals (Lasztity 1998). While one of the main purposes of malting is to degrade the cell walls through the action of P-glucanase enzymes during germination, in practice some glucan always survives into malt (Bamforth & Barclay 1993). Unless it is properly degraded it renders the wort extremely viscous, with attendant problems in the operations of separating the wort from the spent grains and with downstream beer ltration (Bamforth 1994). Thus some brewers mash-in at low temperatures (say 50°C) to allow the P-glucanase (which is sensitive to heat) to act. Additionally a heat-stable glucanase from bacteria (such as Bacillus subtilis) or fungi (such as Trichoderma reesei or Penicillium funicu-losum) may be employed (Bamforth 1985a). Barley has been transformed to express a heat-resistant P-glucanase, but it is not yet cleared for commercial use (Mannonen et al. 1993). All of these efforts to eliminate P-glucan are important if production problems are to be avoided, as well as quality problems, for the glucan can cause hazes and precipitates in beer. The beers that will contain the most residual glucan are those that are produced with a high charge of barley adjunct, for instance some well-known stouts. The products of P-glucan breakdown in malting and mashing are not fermentable by yeast, so they survive into beer. Even those beers in which most of the glucan has been converted to low molecular-weight oligosaccharides may be of some value as sources of bre, as it is now understood that any P-linked sugar, no matter how small, may retain some bene cial properties when they reach the lower gut (Schneeman 1999).
P-Glucan is not the only polysaccharide found in the cell walls of barley, the other being arabinoxylan. For reasons that are not entirely understood, this seems to survive malting and brewing more readily than does P-glucan, such that beers tend to contain more arabinoxylan than glucan (Schwarz & Han 1995). It also ranks as soluble bre. In the cell wall the arabinoxylan is covalently linked to ferulic acid (Ahluwalia & Fry 1986). This phenolic acid is released during mashing (McMurrough et al. 1996) and survives into beer (unless the beer is made with yeasts, such as those used in the fermentation of wheat-based beers, which contain an enzyme that can decarboxylate the ferulic acid to 4-vinylguiacol, a substance that gives the classic clove-like character to such products). There is huge interest in ferulic acid as an antioxidant (Kroon & Williamson 1999).
The chemistry of beer
As we shall see in Chapter 6, there is increasingly good evidence for the bene cial impact of moderate levels of ethanol on the body. There are several other effects of alcohol on the quality of beer. It contributes directly to avour, by impacting characters variously described as warming and sweet as well, of course, as alcoholic. It also moderates the contribution of other components to avour by in uencing their partitioning between the body of the beer and its headspace ('the nose'). Ethanol also in uences the foaming properties of beer (Brierley et al. 1996). It lowers surface tension, and so aids bubble formation, but it also competes with other surface-active molecules (notably proteins) for places in the bubble wall, thus detracting from stability of the head.
Beer strength is usually de ned in terms of alcohol by volume (ABV), i.e. the number of cm3 of ethanol per 100 cm3 of beer. Sometimes alcoholic strength is described in terms of weight per volume. As the speci c gravity of ethanol is 0.79, this means that a beer that contains 5% alcohol by volume has approximately 4% alcohol by weight. One of the most relevant examples to use by way of illustration is the so-called '3-2 beer' in Utah. Most of the beer in that US state is in this category, which refers to the fact that it contains no more than 3.2% by weight. This is of course 4% when quoted on the basis of volume.
Another way of describing the strength of a beer is on the basis of its 'original gravity' (known as 'original extract' in the US). This is variously quoted on the basis of speci c gravity or, increasingly commonly, degrees Plato. It is basically a measure of the strength (approximating to the sugar content) of the wort prior to fermentation. During fermentation, the fermentable sugars are converted into alcohol, leaving behind that proportion of the solubilised starch that is not fermentable. Sugar solutions have a high speci c gravity (weight per unit volume), as compared to water (1 mL of which weighs 1 g - i.e. the speci c gravity is 1.00) and to ethanol (speci c gravity 0.79). Thus there is a fall in speci c gravity during fermentation and the nal speci c gravity of a beer re ects the balance between ethanol and the residual unfermentable 'dextrins' (see later). By measuring the speci c gravity and ethanol content and putting the values into an equation, the brewer can calculate the original extract, that is, the original strength of the wort.
One degree Plato basically represents a 1% by weight solution of sugars. Thus a wort that is 10° Plato is the equivalent of a 10% sugar solution. A 12°P wort is a 12% sugar solution. If they contain the same proportion of fermentable sugars, then the latter would go on to give a more alcoholic beer. For most beers the sugars originate from malted barley, but some brewers use adjuncts. Thus, for instance, if the grist comprised 70% malt : 30% corn syrup, then, when compared to one of the same strength in degrees Plato derived from an all-malt grist, the former would contain less of the other components that are derived from malt (protein, vitamins, polyphenols, bre, etc.). Thus, although a knowledge of the original gravity of a beer is useful for 'normalising' analytical data on beers, it is important to bear in mind that the exact nature of the grist has a key role to play.
Beer strength is usually de ned in terms of alcohol by volume (ABV), i.e. the number of cm3 of ethanol per 100 cm3 of beer. Sometimes alcoholic strength is described in terms of weight per volume. As the speci c gravity of ethanol is 0.79, this means that a beer that contains 5% alcohol by volume has approximately 4% alcohol by weight. One of the most relevant examples to use by way of illustration is the so-called '3-2 beer' in Utah. Most of the beer in that US state is in this category, which refers to the fact that it contains no more than 3.2% by weight. This is of course 4% when quoted on the basis of volume.
Another way of describing the strength of a beer is on the basis of its 'original gravity' (known as 'original extract' in the US). This is variously quoted on the basis of speci c gravity or, increasingly commonly, degrees Plato. It is basically a measure of the strength (approximating to the sugar content) of the wort prior to fermentation. During fermentation, the fermentable sugars are converted into alcohol, leaving behind that proportion of the solubilised starch that is not fermentable. Sugar solutions have a high speci c gravity (weight per unit volume), as compared to water (1 mL of which weighs 1 g - i.e. the speci c gravity is 1.00) and to ethanol (speci c gravity 0.79). Thus there is a fall in speci c gravity during fermentation and the nal speci c gravity of a beer re ects the balance between ethanol and the residual unfermentable 'dextrins' (see later). By measuring the speci c gravity and ethanol content and putting the values into an equation, the brewer can calculate the original extract, that is, the original strength of the wort.
One degree Plato basically represents a 1% by weight solution of sugars. Thus a wort that is 10° Plato is the equivalent of a 10% sugar solution. A 12°P wort is a 12% sugar solution. If they contain the same proportion of fermentable sugars, then the latter would go on to give a more alcoholic beer. For most beers the sugars originate from malted barley, but some brewers use adjuncts. Thus, for instance, if the grist comprised 70% malt : 30% corn syrup, then, when compared to one of the same strength in degrees Plato derived from an all-malt grist, the former would contain less of the other components that are derived from malt (protein, vitamins, polyphenols, bre, etc.). Thus, although a knowledge of the original gravity of a beer is useful for 'normalising' analytical data on beers, it is important to bear in mind that the exact nature of the grist has a key role to play.
Styles of beer
One fundamental approach to classifying beers is based on whether they are generated by 'top fermentation' or 'bottom fermentation', i.e. whether the yeast congregates at the top of the vessel or sinks to the base. In modern fermenters with their high hydrostatic pressures the distinction is blurred. Top fermentation tends to be at relatively warm temperatures (15-25°C) with the yeast producing higher levels of avour volatiles such as esters, affording fruity characteristics. Bottom fermentation beers are produced at much lower temperatures (e.g. 6-15°C) and frequently possess signi cant sulphury notes.
The main top fermentation beers are the ales. Alcohol content will generally be in the range 3 to 7.5% by volume (ABV), and more frequently in the bottom half of the range. The major grist material will be well-modi ed malt, kilned to relatively high temperatures to impart a copper colour. 'Mild' is a sweeter, darker product, the colour being either due to caramel or in part to a low proportion of heavily kilned malt, though not so much as to impart burnt avours. It tends to have a lower alcohol content (less than 3.5% ABV) and when bottled may be referred to as 'Brown Ale'. 'Barley wines' are fermented at very high gravities and so develop much higher alcohol contents (up to 10% by volume). They are usually sold in smaller volumes, in bottles called 'nips'.
Porters (named after the main customers in eighteenth-century London) are traditionally very dark, due to the use of a proportion of roasted barley in the grist, and not overwhelmingly strong (about 5% ABV). Stouts are close relatives of porter, originating in Ireland, with intense colour and burnt, smoky avours due to the use of roasted barley adjuncts, and high bitterness. These robust avour characters are frequently mellowed by the use of nitrogen gas, which 'smoothes' the palate as well as affording the rich, white and creamy foam. Alcohol content may be between 4 and 7%, with up to 10% in Imperial stouts. Sweet stouts are a British variant, of lower alcohol content (up to 4% ABV), with less roast character (often due to the use of caramel and less roast barley as colourant). Trappist beers, from Belgium, are relatively dark, intensely bitter, acidic products of up to 12.5% alcohol by volume. Lambic and gueuze have very complex avours, owing to the use of a more complex micro ora than brewing yeast alone. They are sour (low pH) and usually hazy. Various avourants may be added, including cherries (Kriek) or raspberries (Framboise). The German wheat beers comprise a further class of top fermentation beers. Weizenbier is made from a grist of at least 50% wheat malt. The products are relatively highly carbonated, affording a refreshing nature alongside the fruity and phenolic (clove-like) characters. Often they are cloudy due to yeast, which is employed traditionally to carbonate the bottled product through 'natural conditioning'. The products are relatively lightly coloured (straw-like) and have alcohol contents of 5-6% by volume. Weissbier ('white beer') is much weaker (e.g. 2.8% alcohol by volume), made from a grist of less than 50% wheat malt, with the addition of lactic acid bacteria to generate a low pH of 3.2-3.4. Therefore such beers are quite sour, and may be taken with raspberry or sweet woodruff syrups.
The classic style of bottom fermentation beers originated in Pilsen and is known as Pilsner. It is quite malty with typically 4.8-5.1% ABV and a pale gold colour. Particularly important is the 'late hop character', which is introduced by retaining a proportion of the hops for addition late in the kettle boil. The term 'lager' is used by many, inaccurately, as a synonym for Pilsner. Lager as a term is really an umbrella description for relatively pale beers, fermented and dispensed at low temperatures.
Malt liquor is a term used to describe alcoholic products (6-7.5% ABV) which are very pale, very lightly hopped and quite malty and sweet.
Light beers comprise the most rapidly growing segment of the beer market. 'Standard' beers retain a proportion of carbohydrate that is not fermentable by yeast, whereas a light beer has most or all of this sugar converted into alcohol. These beers therefore have fewer calories, provided that the extra alcohol is diluted to the level found in 'normal' beers.
There are many de nitions worldwide about what constitutes low-alcohol products. Perhaps the most stringent is in UK, where non- and low-alcohol beers (NAB/LABs) contain less than 0.05% or 1.2% ABV, respectively. They are produced either by removing the alcohol from a full-strength brew (by techniques such as vacuum distillation or reverse osmosis), or by restricting the ability of yeast to ferment wort (either by making a wort containing very low levels of fermentable sugars or by ensuring that the contact between yeast and wort is at a very low temperature and for a relatively brief time).
The main top fermentation beers are the ales. Alcohol content will generally be in the range 3 to 7.5% by volume (ABV), and more frequently in the bottom half of the range. The major grist material will be well-modi ed malt, kilned to relatively high temperatures to impart a copper colour. 'Mild' is a sweeter, darker product, the colour being either due to caramel or in part to a low proportion of heavily kilned malt, though not so much as to impart burnt avours. It tends to have a lower alcohol content (less than 3.5% ABV) and when bottled may be referred to as 'Brown Ale'. 'Barley wines' are fermented at very high gravities and so develop much higher alcohol contents (up to 10% by volume). They are usually sold in smaller volumes, in bottles called 'nips'.
Porters (named after the main customers in eighteenth-century London) are traditionally very dark, due to the use of a proportion of roasted barley in the grist, and not overwhelmingly strong (about 5% ABV). Stouts are close relatives of porter, originating in Ireland, with intense colour and burnt, smoky avours due to the use of roasted barley adjuncts, and high bitterness. These robust avour characters are frequently mellowed by the use of nitrogen gas, which 'smoothes' the palate as well as affording the rich, white and creamy foam. Alcohol content may be between 4 and 7%, with up to 10% in Imperial stouts. Sweet stouts are a British variant, of lower alcohol content (up to 4% ABV), with less roast character (often due to the use of caramel and less roast barley as colourant). Trappist beers, from Belgium, are relatively dark, intensely bitter, acidic products of up to 12.5% alcohol by volume. Lambic and gueuze have very complex avours, owing to the use of a more complex micro ora than brewing yeast alone. They are sour (low pH) and usually hazy. Various avourants may be added, including cherries (Kriek) or raspberries (Framboise). The German wheat beers comprise a further class of top fermentation beers. Weizenbier is made from a grist of at least 50% wheat malt. The products are relatively highly carbonated, affording a refreshing nature alongside the fruity and phenolic (clove-like) characters. Often they are cloudy due to yeast, which is employed traditionally to carbonate the bottled product through 'natural conditioning'. The products are relatively lightly coloured (straw-like) and have alcohol contents of 5-6% by volume. Weissbier ('white beer') is much weaker (e.g. 2.8% alcohol by volume), made from a grist of less than 50% wheat malt, with the addition of lactic acid bacteria to generate a low pH of 3.2-3.4. Therefore such beers are quite sour, and may be taken with raspberry or sweet woodruff syrups.
The classic style of bottom fermentation beers originated in Pilsen and is known as Pilsner. It is quite malty with typically 4.8-5.1% ABV and a pale gold colour. Particularly important is the 'late hop character', which is introduced by retaining a proportion of the hops for addition late in the kettle boil. The term 'lager' is used by many, inaccurately, as a synonym for Pilsner. Lager as a term is really an umbrella description for relatively pale beers, fermented and dispensed at low temperatures.
Malt liquor is a term used to describe alcoholic products (6-7.5% ABV) which are very pale, very lightly hopped and quite malty and sweet.
Light beers comprise the most rapidly growing segment of the beer market. 'Standard' beers retain a proportion of carbohydrate that is not fermentable by yeast, whereas a light beer has most or all of this sugar converted into alcohol. These beers therefore have fewer calories, provided that the extra alcohol is diluted to the level found in 'normal' beers.
There are many de nitions worldwide about what constitutes low-alcohol products. Perhaps the most stringent is in UK, where non- and low-alcohol beers (NAB/LABs) contain less than 0.05% or 1.2% ABV, respectively. They are produced either by removing the alcohol from a full-strength brew (by techniques such as vacuum distillation or reverse osmosis), or by restricting the ability of yeast to ferment wort (either by making a wort containing very low levels of fermentable sugars or by ensuring that the contact between yeast and wort is at a very low temperature and for a relatively brief time).
Brewing
Brewing (and malting) is nowadays conducted in well-designed and highly hygienic facilities, for the most part fabricated from stainless steel. The equipment is repeatedly cleaned using regimes of acid or caustic, followed by thorough rinsing with clean water and perhaps a sterilant of the type that would nd use in the domestic kitchen.
In the brewery, the malted grain must rst be milled to generate relatively ne particles, which are then intimately mixed with hot water in a process called mashing. Mashes typically have a thickness of around three parts water to one part malt and contain a stand in the vicinity of 65°C. At this temperature the granules of starch are converted in a transition called gelatinisation into a 'melted' form that is much more susceptible to digestion by amylases. These enzymes are developed during malting, but only start to act once the gelatinisation of the starch has occurred in the mash tun. Some brewers will add starch from other sources, such as unmalted barley, maize or rice, to supplement that from malt. These other sources are called adjuncts. It may be necessary for the brewer to add extra enzymes at this stage, to help deal with some of these adjuncts. Many brewers, though, outlaw the adoption of such 'exogenous' enzymes, even though they are fully recognised as safe and are derived from harmless organisms, e.g. Aspergillus and Pencillium, which naturally thrive throughout nature, including on the surface of grain (Flannigan 2003).
After a period typically of one hour, the liquid portion of the mash, known as wort, is recovered in a 'lautering' or ltration operation and run to the kettle where it is boiled, again typically for an hour. Boiling serves various functions, including sterilisation of wort, precipitation as 'trub' of proteins and tannins (which would otherwise come out of solution in the rushed beer and cause cloudiness), and the driving away of unpleasant grainy characters that originate in the cereal. Many brewers add some adjunct sugars at this stage, and most brewers also introduce at least a proportion of their hops.
The hops have two principal components: resins and essential oils. The resins (so-called a-acids) are changed ('isomerised') during boiling to yield iso-a-acids, which provide the bitterness to beer. This process is rather inef cient. Nowadays, hops are often extracted with lique ed carbon dioxide and the extract is either added to the kettle or is isomerised outside the brewery for addition to the nished beer (thereby avoiding losses due to the tendency of bitter substances to stick on to yeast).
The oils in hops are responsible for the 'hoppy nose' on beer.
After the precipitate produced during boiling has been removed, the hopped wort is cooled and pitched with yeast. There are many strains of brewing yeast (Saccharomyces cerevisiae), and brewers carefully select and maintain their own strains because of their importance in determining brand identity. Yeast needs a little oxygen to trigger off its metabolism, but otherwise the alcoholic fermentation is anaerobic. Ale fermentations are usually complete within a few days at temperatures as high as 20°C, whereas lager fermentations at as low as 6°C can take several weeks. Fermentation is complete when the desired alcohol content has been reached and when an unpleasant butterscotch a-vour, which develops during all fermentations, has been mopped up by yeast. The yeast is harvested for use in the next fermentation. It may be washed with acid to eliminate contaminating microbes that can produce non-volatile nitrosamines (Simpson et al.
1988).
In traditional ale brewing the beer is now mixed with a small quantity of hops (to supplement hoppy avour), some priming sugars and isinglass nings, which settle out the solids in the cask. Isinglass is basically hydrolysed collagen, a protein found in many animal tissues. The collagen used for brewing comes from the swim bladders of certain species of sh that breed in the South China Seas. The swim bladders are dried, and then partially hydrolysed using sulphurous acid to generate a solution that has good capability for reacting with beer proteins to form large aggregates, which precipitate and settle. Under Draft Directive 2000/13/EC of the European Union it will in future be required that process aids or ingredients that are included in one of the major allergen groups be labelled. As sh and sh products are in the list that forms an annex to the Directive, this means that isinglass would need to be declared. Phillips (2003) has argued convincingly why this seems preposterous, for the collagen is vastly modi ed during processing and the levels that survive into beer are minimal.
In traditional lager brewing the 'green beer' is matured by several weeks of cold storage, prior to ltering. Filtration generally involves the use of lter aids that keep the lter bed loose and prevent it from clogging up. The two main types of lter aid are kieselguhr and perlite. They leave no residue in the beer.
Nowadays many beers, both ales and lagers, receive a relatively short conditioning period after fermentation and before ltration. This conditioning is ideally performed at -1°C for a minimum of three days, under which conditions more proteins drop out of solution, making the beer less likely to go cloudy in the package or glass. The long-term stability of beer may also be aided by the use of materials downstream that remove haze-forming protein or polyphenol. For the latter, the one choice is polyvinyl-polypyrrolidone. Protein may be removed in three ways: by adsorption on silica gels that are made from sand, by precipitation with tannic acid derived from gallnuts, or by hydrolysis with the enzyme papain from the pawpaw. This is the same enzyme that comprises meat tenderiser.
The ltered beer is adjusted to the required carbonation before packaging into cans, kegs or glass or plastic bottles. The packaging operations are rigorously designed to ensure that the product is delivered in secure (tamper-proof or at the very least tamper-evident) packages that minimise the opportunity for air ingress (oxygen promotes staling). Modern packaging lines incorporate highly ef cient systems to ensure that packages will not contain foreign bodies and furthermore that such items cannot be introduced during the packaging process itself.
Countries such as the UK have regulations which stipulate that packaging materials may not react with or alter the organoleptic properties of the food which they contact (Partington 2003). Aluminium or stainless steel cans, casks or kegs, therefore, are lined with epoxy lacquer coatings to prevent metal from leaching into the relatively low pH beer.
In the brewery, the malted grain must rst be milled to generate relatively ne particles, which are then intimately mixed with hot water in a process called mashing. Mashes typically have a thickness of around three parts water to one part malt and contain a stand in the vicinity of 65°C. At this temperature the granules of starch are converted in a transition called gelatinisation into a 'melted' form that is much more susceptible to digestion by amylases. These enzymes are developed during malting, but only start to act once the gelatinisation of the starch has occurred in the mash tun. Some brewers will add starch from other sources, such as unmalted barley, maize or rice, to supplement that from malt. These other sources are called adjuncts. It may be necessary for the brewer to add extra enzymes at this stage, to help deal with some of these adjuncts. Many brewers, though, outlaw the adoption of such 'exogenous' enzymes, even though they are fully recognised as safe and are derived from harmless organisms, e.g. Aspergillus and Pencillium, which naturally thrive throughout nature, including on the surface of grain (Flannigan 2003).
After a period typically of one hour, the liquid portion of the mash, known as wort, is recovered in a 'lautering' or ltration operation and run to the kettle where it is boiled, again typically for an hour. Boiling serves various functions, including sterilisation of wort, precipitation as 'trub' of proteins and tannins (which would otherwise come out of solution in the rushed beer and cause cloudiness), and the driving away of unpleasant grainy characters that originate in the cereal. Many brewers add some adjunct sugars at this stage, and most brewers also introduce at least a proportion of their hops.
The hops have two principal components: resins and essential oils. The resins (so-called a-acids) are changed ('isomerised') during boiling to yield iso-a-acids, which provide the bitterness to beer. This process is rather inef cient. Nowadays, hops are often extracted with lique ed carbon dioxide and the extract is either added to the kettle or is isomerised outside the brewery for addition to the nished beer (thereby avoiding losses due to the tendency of bitter substances to stick on to yeast).
The oils in hops are responsible for the 'hoppy nose' on beer.
After the precipitate produced during boiling has been removed, the hopped wort is cooled and pitched with yeast. There are many strains of brewing yeast (Saccharomyces cerevisiae), and brewers carefully select and maintain their own strains because of their importance in determining brand identity. Yeast needs a little oxygen to trigger off its metabolism, but otherwise the alcoholic fermentation is anaerobic. Ale fermentations are usually complete within a few days at temperatures as high as 20°C, whereas lager fermentations at as low as 6°C can take several weeks. Fermentation is complete when the desired alcohol content has been reached and when an unpleasant butterscotch a-vour, which develops during all fermentations, has been mopped up by yeast. The yeast is harvested for use in the next fermentation. It may be washed with acid to eliminate contaminating microbes that can produce non-volatile nitrosamines (Simpson et al.
1988).
In traditional ale brewing the beer is now mixed with a small quantity of hops (to supplement hoppy avour), some priming sugars and isinglass nings, which settle out the solids in the cask. Isinglass is basically hydrolysed collagen, a protein found in many animal tissues. The collagen used for brewing comes from the swim bladders of certain species of sh that breed in the South China Seas. The swim bladders are dried, and then partially hydrolysed using sulphurous acid to generate a solution that has good capability for reacting with beer proteins to form large aggregates, which precipitate and settle. Under Draft Directive 2000/13/EC of the European Union it will in future be required that process aids or ingredients that are included in one of the major allergen groups be labelled. As sh and sh products are in the list that forms an annex to the Directive, this means that isinglass would need to be declared. Phillips (2003) has argued convincingly why this seems preposterous, for the collagen is vastly modi ed during processing and the levels that survive into beer are minimal.
In traditional lager brewing the 'green beer' is matured by several weeks of cold storage, prior to ltering. Filtration generally involves the use of lter aids that keep the lter bed loose and prevent it from clogging up. The two main types of lter aid are kieselguhr and perlite. They leave no residue in the beer.
Nowadays many beers, both ales and lagers, receive a relatively short conditioning period after fermentation and before ltration. This conditioning is ideally performed at -1°C for a minimum of three days, under which conditions more proteins drop out of solution, making the beer less likely to go cloudy in the package or glass. The long-term stability of beer may also be aided by the use of materials downstream that remove haze-forming protein or polyphenol. For the latter, the one choice is polyvinyl-polypyrrolidone. Protein may be removed in three ways: by adsorption on silica gels that are made from sand, by precipitation with tannic acid derived from gallnuts, or by hydrolysis with the enzyme papain from the pawpaw. This is the same enzyme that comprises meat tenderiser.
The ltered beer is adjusted to the required carbonation before packaging into cans, kegs or glass or plastic bottles. The packaging operations are rigorously designed to ensure that the product is delivered in secure (tamper-proof or at the very least tamper-evident) packages that minimise the opportunity for air ingress (oxygen promotes staling). Modern packaging lines incorporate highly ef cient systems to ensure that packages will not contain foreign bodies and furthermore that such items cannot be introduced during the packaging process itself.
Countries such as the UK have regulations which stipulate that packaging materials may not react with or alter the organoleptic properties of the food which they contact (Partington 2003). Aluminium or stainless steel cans, casks or kegs, therefore, are lined with epoxy lacquer coatings to prevent metal from leaching into the relatively low pH beer.
Malting
The rst stage of malting comprises the steeping of barley in water at 14-18°C for up to 48 h, until it reaches a moisture content of 42-46%. Raising the moisture content allows the grain to start to germinate, a process that usually takes less than a week at 16-20°C. In germination, the enzymes break down the cell walls and some of the protein in the starchy endosperm (the grain's food reserve), rendering the grain friable. The amylases that break down the starch are produced (or released) in germination and these are important for the subsequent mashing process in the brewery, which is where they convert starch to fermentable sugars. Over the years a number of agents have been employed to assist the maltster to ef ciently produce malts that will satisfy the brewer in terms of quality and cost. In a great many markets these materials are banned, even though there is little or no evidence that they are harmful. Thus the natural gibberellin hormones of the barley, which have a key role in stimulating enzyme production, can be supplemented with gibberellic acid (GA), which is produced using industrial fermentation processes (Tudzynski 1999). GA is very closely similar to the native molecules in barley, but nonetheless is outlawed in the Scotch whisky industry and the North American brewing industry. Where it is used, its undesirable impact in excessively stimulating the production of rootlets (which is a waste of potentially fermentable material) has been countered by the use of potassium bromate. A detailed study showed that this latter molecule does not survive in signi cant quantities into beer (Brewing Research International, unpublished). Very few malting operations nowadays use bromate, but it is widely used in the baking industry where it is used to help bread rise.
There was a time, long ago, when maltsters experimented with the use of formaldehyde, as an agent to remove tannins from the surface of the grain and render the malt less prone to giving the beer a tendency to cloud (haze) formation (Macey 1970). I know of no maltster (or brewer) that has used this material for many years.
One recent development has been the proposal to seed barley with lactic acid bacteria during the malting process (Laitila et al. 2002). These bacteria are widely employed in the production of wholesome foodstuffs, e.g. sauerkraut and cheeses, and indeed natural infection of worts in German breweries has a very long history as an exercise in 'naturally' lowering the pH to a more favourable level. The rationale for using lactic acid bacteria in the maltings is that they will consume surface nutrients from the grain, thereby preventing undesirable organisms such as Fusarium from prospering.
Germination is arrested by kilning, in which there is a lowering of the moisture content. Regimes with progressively increasing temperatures over the range 50 to perhaps 110°C are used to allow drying to < 5% moisture, while preserving those enzymes that are particularly sensitive to heat. The more intense the kilning process, the darker the malt that is produced and the more roasted, coffee-like and smoky are the avour characteristics developed. Essentially, malts used for making very pale lager-style beers are kilned quite gently, whereas those going into the somewhat darker ales are subjected to more heating. The very dark colours in stouts come from the incorporation into the grist of a proportion of malt that is roasted intensely.
One of the biggest concerns with the intense heating of grain raised over 20 years ago was the risk of developing nitrosamines (Havery et al. 1981). These molecules have been demonstrated to be carcinogenic in model animal systems, but not so far for man. They are primarily produced when precursors in grain, notably hordenine, react under heat with oxides of nitrogen, which tend to be present in the atmosphere, especially in regions with heavy industry. The malting and brewing industries responded with tremendous alacrity to the 'scare' and within a very short period of time nitrosamine levels had been reduced to very low levels (Sen et al. 1996, and see Chapter 5). The key change in practice was the use of indirect kilning such that the nitrogen oxides no longer contacted the malt.
There was a time, long ago, when maltsters experimented with the use of formaldehyde, as an agent to remove tannins from the surface of the grain and render the malt less prone to giving the beer a tendency to cloud (haze) formation (Macey 1970). I know of no maltster (or brewer) that has used this material for many years.
One recent development has been the proposal to seed barley with lactic acid bacteria during the malting process (Laitila et al. 2002). These bacteria are widely employed in the production of wholesome foodstuffs, e.g. sauerkraut and cheeses, and indeed natural infection of worts in German breweries has a very long history as an exercise in 'naturally' lowering the pH to a more favourable level. The rationale for using lactic acid bacteria in the maltings is that they will consume surface nutrients from the grain, thereby preventing undesirable organisms such as Fusarium from prospering.
Germination is arrested by kilning, in which there is a lowering of the moisture content. Regimes with progressively increasing temperatures over the range 50 to perhaps 110°C are used to allow drying to < 5% moisture, while preserving those enzymes that are particularly sensitive to heat. The more intense the kilning process, the darker the malt that is produced and the more roasted, coffee-like and smoky are the avour characteristics developed. Essentially, malts used for making very pale lager-style beers are kilned quite gently, whereas those going into the somewhat darker ales are subjected to more heating. The very dark colours in stouts come from the incorporation into the grist of a proportion of malt that is roasted intensely.
One of the biggest concerns with the intense heating of grain raised over 20 years ago was the risk of developing nitrosamines (Havery et al. 1981). These molecules have been demonstrated to be carcinogenic in model animal systems, but not so far for man. They are primarily produced when precursors in grain, notably hordenine, react under heat with oxides of nitrogen, which tend to be present in the atmosphere, especially in regions with heavy industry. The malting and brewing industries responded with tremendous alacrity to the 'scare' and within a very short period of time nitrosamine levels had been reduced to very low levels (Sen et al. 1996, and see Chapter 5). The key change in practice was the use of indirect kilning such that the nitrogen oxides no longer contacted the malt.
The Basics of Malting and Brewing: Product Safety and Wholesomeness
The fundamental shape of the processes by which beer is made has not changed for many generations [see Bamforth (2003) for a general introduction and overview, and a full glossary of brewing terms]. However, the control and predictability of those processes has improved. Beer nowadays is invariably a highly consistent consumable, closely controlled for the ef ciency of its production and its safety. There is little that is hit-and-miss about the making of beer. Despite its reliance on agricultural products (barley, sometimes other cereals, and hops) the understanding of the process means that seasonal and regional vagaries can be overcome such that the taste, appearance and composition of a beer are generally consistent from batch to batch. There is no such thing as a vintage in brewing.
Accordingly, the customer should realise as they explore their local supermarket shelves that one of the most consistent and reliable products to be had is the beer. It is also one of the safest, as we shall see.
Chemical beer?
The brewing of beer is complicated. The vast majority of beers comprise at least 90% water, with ethanol (it is customary to use 'alcohol' synonymously for this one alcohol - although there are other alcohols in beer) and carbon dioxide being quantitatively the next major individual components (Table 3.1). Beers also contain a wide range of chemical species in relatively small quantities that determine the properties of the beer in respect of appearance and avour.
Malting and brewing are processes designed to maximise the extraction and digestion of starch and protein from barley, yielding a highly fermentable extract that is known as wort. The processes are also designed to eliminate materials that can have an adverse effect on beer quality, such as the haze-forming polyphenol from barley and hops and the lipids and oxygen that, together, can cause beer to stale.
Aflatoxins originate from some members of the genus Aspergillus, namely Aspergillus avus, A. parasiticus, A. nomius and A. ochraceoreseus (Moss 2003). (It will be noted that these don't include the strains such as A. oryzae that have a role in the production of alcoholic beverages such as sake or as a source of exogenous enzymes for brewers.) The most commonly a atoxin-contaminated foods are corn (maize) and peanuts, but all cereals may be affected. Infection is most commonly associated with post-harvest spoilage, when storage is under inapproporiate conditions of temperature and moisture.
Pesticides have real value in this context. Nonetheless there has been in-depth investigation of alternative ways of treating grain, particularly during storage, such that it does not develop infection. These studies have included the use of anaerobic storage (Baxter & Dawe 1990). Where pesticides are used much will be largely washed off the surface of the grain during steeping (Miyake et al. 2002).
It must be emphasised that authorities in most countries have regulations and systems for controlling the nature of pesticides that may be used, and those pesticides have been widely screened for their environmental and health impacts. Any perceived risks of using them are grossly outweighed by the very real problem that can accrue in any cereal from contamination with those micro ora capable of producing mycotoxins and ochratoxins (Petzinger & Weidenbach 2002). One such substance is deoxynivale-nol (DON), which is produced by the fungus Fusarium (Wolf-Hall & Schwarz 2002). Brewers (and therefore maltsters) set rigorous standards for the level of DON in barley
and malt, and will not use grain that contains it. Fusarium infection is a bigger risk in wetter climates. Thus it was virtually unheard of in North America until the mid-1990s, when a substantial problem was encountered. The reason was a movement away from the burning of straw stubble after grain had been harvested. This burning, outlawed for supposed environmental damage, had served the valuable function of destroying Fusarium spores. Once burning was banned, it meant that the Fusarium was enriched in the soil and readily available to spoil crops the subsequent year.
Woller and Marjerus (1982) and Marjerus and Woller (1983) failed to detect any mycotoxins in a diversity of beers (detection limit 1-2 ng/L). It is not impossible to nd nite levels of mycotoxins - see for example Payen et al. (1983). However, provided all parties adhere to the strictest standards of hygiene from eld to glass, and the grain is maintained under the appropriately low levels of moisture and temperature, then this is not an issue.
Accordingly, the customer should realise as they explore their local supermarket shelves that one of the most consistent and reliable products to be had is the beer. It is also one of the safest, as we shall see.
Chemical beer?
The brewing of beer is complicated. The vast majority of beers comprise at least 90% water, with ethanol (it is customary to use 'alcohol' synonymously for this one alcohol - although there are other alcohols in beer) and carbon dioxide being quantitatively the next major individual components (Table 3.1). Beers also contain a wide range of chemical species in relatively small quantities that determine the properties of the beer in respect of appearance and avour.
Malting and brewing are processes designed to maximise the extraction and digestion of starch and protein from barley, yielding a highly fermentable extract that is known as wort. The processes are also designed to eliminate materials that can have an adverse effect on beer quality, such as the haze-forming polyphenol from barley and hops and the lipids and oxygen that, together, can cause beer to stale.
Aflatoxins originate from some members of the genus Aspergillus, namely Aspergillus avus, A. parasiticus, A. nomius and A. ochraceoreseus (Moss 2003). (It will be noted that these don't include the strains such as A. oryzae that have a role in the production of alcoholic beverages such as sake or as a source of exogenous enzymes for brewers.) The most commonly a atoxin-contaminated foods are corn (maize) and peanuts, but all cereals may be affected. Infection is most commonly associated with post-harvest spoilage, when storage is under inapproporiate conditions of temperature and moisture.
Pesticides have real value in this context. Nonetheless there has been in-depth investigation of alternative ways of treating grain, particularly during storage, such that it does not develop infection. These studies have included the use of anaerobic storage (Baxter & Dawe 1990). Where pesticides are used much will be largely washed off the surface of the grain during steeping (Miyake et al. 2002).
It must be emphasised that authorities in most countries have regulations and systems for controlling the nature of pesticides that may be used, and those pesticides have been widely screened for their environmental and health impacts. Any perceived risks of using them are grossly outweighed by the very real problem that can accrue in any cereal from contamination with those micro ora capable of producing mycotoxins and ochratoxins (Petzinger & Weidenbach 2002). One such substance is deoxynivale-nol (DON), which is produced by the fungus Fusarium (Wolf-Hall & Schwarz 2002). Brewers (and therefore maltsters) set rigorous standards for the level of DON in barley
and malt, and will not use grain that contains it. Fusarium infection is a bigger risk in wetter climates. Thus it was virtually unheard of in North America until the mid-1990s, when a substantial problem was encountered. The reason was a movement away from the burning of straw stubble after grain had been harvested. This burning, outlawed for supposed environmental damage, had served the valuable function of destroying Fusarium spores. Once burning was banned, it meant that the Fusarium was enriched in the soil and readily available to spoil crops the subsequent year.
Woller and Marjerus (1982) and Marjerus and Woller (1983) failed to detect any mycotoxins in a diversity of beers (detection limit 1-2 ng/L). It is not impossible to nd nite levels of mycotoxins - see for example Payen et al. (1983). However, provided all parties adhere to the strictest standards of hygiene from eld to glass, and the grain is maintained under the appropriately low levels of moisture and temperature, then this is not an issue.
Temperance pressures
In the closing years of the eighteenth century less beer was brewed at home, with major brewing companies being spawned to supply beer to the millions employed in the newly developing industries. Only country folk retained their brewing traditions. The development of roads and railways provided distribution systems for the big brewers.
By 1810, there were 48,000 alehouses for some 8 million people in Britain (King 1947). Captains of industry were perturbed about wages being 'wasted' on excess drinking. This led to a tightening of licensing laws and many counties declared that public houses should be closed at 9 pm in winter and 10 pm in summer. Some were not satis ed even with that and the temperance movement developed. The rst pledge of 'teetotalism' was signed in Preston in 1832 (King 1947). [The word teetotal is said to have originated in an English temperance meeting, when a stammering man said 'We can't keep 'em sober unless we have the pledge total. Yes, Mr Chairman, tee-tee-total' (Fleming 1975).]
However, there were those who championed the merits of consuming beer. Savage (1866) wrote in the United States (where beer was very much the drink of moderation as compared to the much more prevalent distilled concoctions) that:
The most useful temperance lecturer is he who advocates the temperate use of beverages which custom has sanctioned and which . man will have. A reform may, and we trust will be effected in favour of healthful and comparatively mild drinks; but it is more than doubtful if hard working, energetic and withal social people, such as form the bone and sinew of the Republic, will or can be induced to give up all drink which custom, and the large majority of clergymen and physicians, have sanctioned as refreshing.
Savage reminded the reader that in Bavaria at the time the average frugally drinking labourer consumed a gallon per day. With reference to England, Savage championed beer thus:
With an impartial catholicity of palate the votary of the amber ale loves to see its 'beaded bubbles winking at the brim' and yet is never forgetful of the darker charms possessed by porter or stout. Boating men ... cricketers, and the whole of the manly English sporting community, are sensible alike to the charms of the long, thin, narrow glass, the simple and unassuming tumbler, and the thorough going pewter pot. The prudent and industrious mechanic prefers the wholesome brew of native malt and hops to the ery foreign distillations that madden the brain and shatter the nerves. The statistics of beer drinking are simply stupendous. Mr. Gladstone . computed that every adult male in England consumed the astounding quantity of six hundred quarts per annum. Despite all the arguments and invectives of the agitators who advocate what is paradoxically described as a 'permissive bill', on account of its prohibitory character, we adhere to our faith that sound honest malt liquor does far more good than harm; nor should we dream of opposing any system of nancial legislation which would make it cheaper without in icting an extra burden upon the community.
And the beer strength in England at the time was formidable (Dunn 1979). In 1843 Burton Ale had original gravities between 1077 (19.25°P) and 1120 (30°P), while Common Ale was 1073 (18.25°P) and Porter 1050 (12.5°P) (see Chapter 3 for de ni-tions of beer strength).
Early nineteenth-century diets, though, retained beer as an integral feature, indeed the recommended 'family economy' for 'moderate persons in a frugal family' for 1826 comprised (per person, per week):
6 pounds meat (undressed)
4 pounds bread (quartern loaf)
0.5 pounds butter
2 ounces tea
0.5 pound sugar
1 pint per day of beer (Porter)
By 1810, there were 48,000 alehouses for some 8 million people in Britain (King 1947). Captains of industry were perturbed about wages being 'wasted' on excess drinking. This led to a tightening of licensing laws and many counties declared that public houses should be closed at 9 pm in winter and 10 pm in summer. Some were not satis ed even with that and the temperance movement developed. The rst pledge of 'teetotalism' was signed in Preston in 1832 (King 1947). [The word teetotal is said to have originated in an English temperance meeting, when a stammering man said 'We can't keep 'em sober unless we have the pledge total. Yes, Mr Chairman, tee-tee-total' (Fleming 1975).]
However, there were those who championed the merits of consuming beer. Savage (1866) wrote in the United States (where beer was very much the drink of moderation as compared to the much more prevalent distilled concoctions) that:
The most useful temperance lecturer is he who advocates the temperate use of beverages which custom has sanctioned and which . man will have. A reform may, and we trust will be effected in favour of healthful and comparatively mild drinks; but it is more than doubtful if hard working, energetic and withal social people, such as form the bone and sinew of the Republic, will or can be induced to give up all drink which custom, and the large majority of clergymen and physicians, have sanctioned as refreshing.
Savage reminded the reader that in Bavaria at the time the average frugally drinking labourer consumed a gallon per day. With reference to England, Savage championed beer thus:
With an impartial catholicity of palate the votary of the amber ale loves to see its 'beaded bubbles winking at the brim' and yet is never forgetful of the darker charms possessed by porter or stout. Boating men ... cricketers, and the whole of the manly English sporting community, are sensible alike to the charms of the long, thin, narrow glass, the simple and unassuming tumbler, and the thorough going pewter pot. The prudent and industrious mechanic prefers the wholesome brew of native malt and hops to the ery foreign distillations that madden the brain and shatter the nerves. The statistics of beer drinking are simply stupendous. Mr. Gladstone . computed that every adult male in England consumed the astounding quantity of six hundred quarts per annum. Despite all the arguments and invectives of the agitators who advocate what is paradoxically described as a 'permissive bill', on account of its prohibitory character, we adhere to our faith that sound honest malt liquor does far more good than harm; nor should we dream of opposing any system of nancial legislation which would make it cheaper without in icting an extra burden upon the community.
And the beer strength in England at the time was formidable (Dunn 1979). In 1843 Burton Ale had original gravities between 1077 (19.25°P) and 1120 (30°P), while Common Ale was 1073 (18.25°P) and Porter 1050 (12.5°P) (see Chapter 3 for de ni-tions of beer strength).
Early nineteenth-century diets, though, retained beer as an integral feature, indeed the recommended 'family economy' for 'moderate persons in a frugal family' for 1826 comprised (per person, per week):
6 pounds meat (undressed)
4 pounds bread (quartern loaf)
0.5 pounds butter
2 ounces tea
0.5 pound sugar
1 pint per day of beer (Porter)
Beer: a nutritious dish for the whole family
By the late seventeenth century more than 12 million barrels of beer were drunk each year in Great Britain, when the population was only some 5 million. That's just about 2 pints per day per person. Even infants, who drank small beer, scarcely ever drank water. Although naturally there was no explanation for why it was the case, it was universally recognised that it was safer to drink beer. The boiling and the hopping were inadvertently water puri cation techniques.
In the era of Charles II, a family of seven in London would drink a barrel of small beer per week, this despite a tax of six pence a barrel (two shillings and sixpence for strong beer) (Savage 1866).
Tea seems rst to have arrived in Holland and Portugal in about 1610 and in Germany in the 1630s, but the rst public sale of tea in England was not until 1657 (Tannahill 1973). The rst coffeehouse in England was to be found in Oxford in 1650. Soon there were choices available for a wholesome beverage at mealtimes and it no longer needed to be alcoholic. The progressive growth in tea drinking led to brewers brewing weaker beer (small beer was now 2-3% alcohol, compared to the previous 4-5%) and having to keep lower prices (Drummond & Wilbraham 1958). Beer, though, retained a key place in the diet, and at the end of the seventeenth century the beer allowance at Christ's Hospital school was 30 barrels per week for 407 people (Drummond & Wilbraham 1958). These authors stress the nutritive value of the beer (additional to its safety dimension when compared to water to drink). They estimate that small beer will have had a calori c value of around 150-200 kilocalories per pint, so 3 pints per day for a small boy will have yielded some 20-25% of his energy needs. And furthermore it will have 'supplied a modest amount of calcium and appreciable quantities of ribo avin, nicotinic acid, pyridoxine, pantothenic acid and perhaps other vitamins' (Drummond & Wilbraham 1958).
This is not to ignore that the wholemeal bread still favoured in those days will also have supplied vitamins, including thiamine, which tends to be diminished in beer as it is readily consumed by yeast during fermentation.
It is certain, however, that home-brewed beer was a good, sound, healthful drink and one which could not possibly do any harm to children when drunk in reasonable amounts.
Drummond & Wilbraham (1958)
Moderation, however, was not universally displayed. And so the rst laws were already in place to reduce drunkenness, including xed hours when pubs must close at night, no opening on Sundays and a limit on any drinker of one hour at a time (King 1947).
In the era of Charles II, a family of seven in London would drink a barrel of small beer per week, this despite a tax of six pence a barrel (two shillings and sixpence for strong beer) (Savage 1866).
Tea seems rst to have arrived in Holland and Portugal in about 1610 and in Germany in the 1630s, but the rst public sale of tea in England was not until 1657 (Tannahill 1973). The rst coffeehouse in England was to be found in Oxford in 1650. Soon there were choices available for a wholesome beverage at mealtimes and it no longer needed to be alcoholic. The progressive growth in tea drinking led to brewers brewing weaker beer (small beer was now 2-3% alcohol, compared to the previous 4-5%) and having to keep lower prices (Drummond & Wilbraham 1958). Beer, though, retained a key place in the diet, and at the end of the seventeenth century the beer allowance at Christ's Hospital school was 30 barrels per week for 407 people (Drummond & Wilbraham 1958). These authors stress the nutritive value of the beer (additional to its safety dimension when compared to water to drink). They estimate that small beer will have had a calori c value of around 150-200 kilocalories per pint, so 3 pints per day for a small boy will have yielded some 20-25% of his energy needs. And furthermore it will have 'supplied a modest amount of calcium and appreciable quantities of ribo avin, nicotinic acid, pyridoxine, pantothenic acid and perhaps other vitamins' (Drummond & Wilbraham 1958).
This is not to ignore that the wholemeal bread still favoured in those days will also have supplied vitamins, including thiamine, which tends to be diminished in beer as it is readily consumed by yeast during fermentation.
It is certain, however, that home-brewed beer was a good, sound, healthful drink and one which could not possibly do any harm to children when drunk in reasonable amounts.
Drummond & Wilbraham (1958)
Moderation, however, was not universally displayed. And so the rst laws were already in place to reduce drunkenness, including xed hours when pubs must close at night, no opening on Sundays and a limit on any drinker of one hour at a time (King 1947).
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