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National Research Council (US) Committee on Diet and Health. Diet and Health: Implications for Reducing Chronic Disease Risk. Washington (DC): National Academies Press (US); 1989.

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Diet and Health: Implications for Reducing Chronic Disease Risk.

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Carbohydrates are the most important source of calories for the world's population because of their relatively low cost and wide availability. This chapter discusses the role of digestible (simple and complex) carbohydrates in the etiology and prevention of chronic diseases. The indigestible carbohydrates (components of dietary fiber) are considered in Chapter 10.

Simple carbohydrates are sugars and include monosaccharides, which consist of one sugar (saccharide) unit per molecule, and disaccharides, which contain two sugar units per molecule. The monosaccharides glucose and fructose and the disaccharides sucrose, maltose, and lactose occur naturally. Glucose and fructose are found in honey and fruits, whereas sucrose (common table sugar) is found in molasses, maple syrup, and in small amounts in fruits. Sucrose is made up of 1 unit each of glucose and fructose per molecule, whereas lactose (milk sugar) consists of 1 glucose and 1 galactose unit per molecule. Maltose consists of two glucose molecules and is present in sprouting grains, malted milk, malted cereals, and some corn syrups.

Sugars added during food processing include sucrose, fructose, and syrups that contain glucose or fructose. Ordinary corn syrups are made by hydrolyzing corn starch and contain glucose, maltose, and higher polymers of glucose. High-fructose corn syrups (HFCSs), which are made by the isomerization of glucose-containing syrups, contain both fructose and glucose in varying amounts. The most commonly used HFCSs contain from 42 to 55% fructose on a dry weight basis (Glinsmann et al., 1986).

Complex carbohydrates, or polysaccharides, are large molecules consisting of many sugar units. Starches (polymers of glucose) are the most abundant polysaccharides in the diet and occur in many foods, including cereal grains, legumes, and potatoes. Glucose, fructose, and galactose are produced during the digestion of the carbohydrate mixture found in the usual diet. After absorbtion, fructose and galactose are converted in the liver to glucose, the blood sugar. Although liver and muscles can store excess glucose as glycogen (animal starch), small amounts of glycogen remain in muscle meats after slaughter. Consequently, practically all dietary carbohydrates come from plant sources, except for lactose, which comes from milk.

Dietary Intake of Carbohydrates

Historical trends in the amounts of carbohydrates in the food supply since 1909 have been reported by the U.S. Department of Agriculture (Marston and Raper, 1987). These data do not represent the amount of carbohydrates actually consumed, however, because there are no estimates of losses or waste and no measurements of actual intake. Total carbohydrate availability has declined since 1909; per-capita amounts fell from 493 g/day during 1909-1913 to a low of 378 g/day during 1967-1969 and rose to 413 g/day in 1985 (Chapter 3, Table 3-3). The decline was due to decreased use of flour and cereal products.

From the early part of this century to the 1980s, there was a notable shift in the proportion of total carbohydrate derived from starch and sugars. During 1909-1913, 68% of total carbohydrates came from starch, in comparison to 47% in 1980. Conversely, the contribution of sugars increased from 32% during 1909-1913 to 53% in 1980 (Welsh and Marston, 1982).

Over the past 20 years, the relative contribution of sugars to the food supply has changed. In 1965, sucrose predominated, comprising 85% of total sugars; sugars in corn syrups comprised only 13%. There were no HFCS sweeteners at that time. By 1985, the use of all types of corn syrups had increased to 47% of total sugars but there was a concomitant decline in sucrose use. The marked increase in corn syrup use during the last decade was due chiefly to greater use of HFCS—a popular sweetener of soft drinks and other processed foods. In 1985, HFCS accounted for 30% of the total sugar supply (Glinsmann et al., 1986).

The 1977-1978 Nationwide Food Consumption Survey (NFCS) (USDA, 1984) indicated that carbohydrates furnished an average of 43% of calories, whereas the NFCS Continuing Survey of Food Intakes by Individuals (CSFII) (USDA, 1986, 1987, 1988) suggested that women and children derived closer to 47% of their calories from carbohydrates. Both surveys indicated that children had higher proportionate intakes of carbohydrates than did adults and that women had higher intakes of carbohydrates compared to men of the same age group. Because these surveys did not take into account the percentage of calories from alcohol, the reported percentages of calories from carbohydrates, fats, and proteins are inaccurate. Carbohydrate intake was not affected by region, urbanization, or season; however, it was higher for those below than above the poverty level (USDA 1984, 1987, 1988).

In 1986, the Food and Drug Administration (FDA) estimated that the average daily intake of all sugars by the U.S. population accounted for 21% of total calories—half coming from added sugars and half from naturally occurring sugars. On the average, approximately 4% of calories came from fructose, 9% from sucrose, and 5% from sugars in corn syrups (see Chapter 3, Tables 3-6 and 3-7, and Glinsmann et al. 1986).

Evidence Associating Carbohydrate Intake with Chronic Diseases

Noninsulin-Dependent Diabetes Mellitus

Epidemiologic Evidence

Most epidemiologic studies were conducted at the time when distinction was still made between juvenile-onset and adult-onset diabetes rather than the most recently adopted more distinct classifications of Type I, or insulin-dependent diabetes mellitus (IDDM), and Type II, or noninsulin-dependent diabetes mellitus (NIDDM), respectively. Although the studies referenced here generally concern adult-onset diabetes, it seems reasonable to extend the results to all cases of diabetes.

Increased intake of sugars or total carbohydrates is not associated with increased risk of NIDDM. In a prospective study of 9,494 male Israeli government employees who were nondiabetic and 40 years of age or older at baseline, Medalie et al. (1974) found no association between calories from sugars or intake of total carbohydrates and incidence of diabetes mellitus over a 5-year follow-up. In a cross-sectional study of 3,454 employed people in England, Keen et al. (1979) observed that intake of carbohydrates, fats, and protein tended to be inversely correlated with concentration of blood sugar and indices of glucose tolerance; they inferred that the correlations probably were confounded by caloric expenditure. Baird (1972) reported an inverse association between sugar intake and prevalence of previously undetected diabetes among the siblings of diabetic propositi. West et al. (1976) found no association between sugar consumption and occurrence of diabetes in 286 Plains Indians, whose intake of refined sugar ranged from less than 70 g/day to more than 200 g/day.

In a study involving 22 countries, Yudkin (1964) reported a correlation of 0.73 between mean per-capita supply of sugars from 1934 to 1938 and risk of death due to diabetes from 1955 to 1956. West (1978) pointed out that this result was not consistently observed; in a sample of 44 countries, the correlation was only 0.18 for sugar intake in 1951 and diabetes mortality in 1971. Furthermore, sugar consumption is high in several countries where rates of diabetes are low (Walker, 1977). In a correlation analysis study of data obtained from 1894 to 1934 in several countries, Himsworth (1935-1936) observed an inverse association between rates of death from diabetes and the mean percentage of total calories obtained from carbohydrates in the diets of urban working-class families. West (1978) reported an inverse correlation between prevalence of diabetes and mean percentage of calories from carbohydrates in surveys of persons 35 years of age and older in seven countries. To the extent that such correlations do exist, it seems reasonable to infer that they do not reflect direct associations but, rather, that they reflect confounding by variables such as caloric expenditure and obesity.

Clinical Studies

No long-term prospective studies have attempted to alter the incidence of NIDDM by changing the carbohydrate content of the diet. On the other hand, shifts in the proportion of carbohydrates in the diet have been used in the clinical management of both types of diabetes and have had a controversial history (Bierman, 1979). High-carbohydrate diets have been recommended for the management of diabetes, because they appear to improve glucose tolerance and insulin sensitivity, and with a change to such a diet, there is a concomitant reduction in the proportion of calories as fat, which reduces risk of atherosclerosis—a major cause of death among diabetics (American Diabetes Association, 1987). There have been no prospective studies on the influence of diet on the complications of diabetes, and the role of diet in the increased prevalence and severity of atherosclerosis among diabetics has not been documented. In studies of high-carbohydrate, low-fat diets given to people with NIDDM, investigators have observed reduced incidence of hyperglycemia, hypercholesterolemia, and hypertriglyceridemia, and decreased treatment requirements (Anderson and Ward, 1979; Blanc et al., 1983; Kiehm et al., 1976; Simpson et al., 1979a,b; Stone and Connor, 1963; Story et al., 1985). An increase in insulin sensitivity observed in vivo after high-carbohydrate diets (Kolterman et al., 1979) is consistent with enhanced insulin action at the cellular level (Olefsky and Saekow, 1978).

A change from a diet of average composition to a very-high-carbohydrate, low-fat diet (more than 60% of calories as carbohydrates and moderate to large amounts of sucrose, i.e., up to 220 g/day) is associated with short-term (2- to 4-week) increases in fasting plasma very-low-density lipoprotein (VLDL) and triglyceride levels in NIDDM patients (Emanuele et al., 1986; Jellish et al., 1984; Reaven, 1986) similar to those seen in nondiabetics. A 5-week study in which a diet high in complex-carbohydrates (65% of total calories) was substituted for saturated fat in NIDDM patients with normal lipid levels failed to show an increase in fasting serum triglyceride levels (Abbott et al., 1989). In a study by Reiser et al. (1981a,b), graded amounts of sucrose (up to 33% of total calories) were fed for 6 weeks in a gorging pattern (most of the daily calories at dinner) to subjects preselected on the basis of exaggerated insulin responses to a sucrose load. Higher fasting glucose, insulin, and triglyceride levels were observed at higher sucrose intakes. In contrast to fasting levels, postprandial triglyceride levels have been shown to decrease in hypertriglyceridemic NIDDM patients on high-sucrose, high-carbohydrate diets (Emanuele et al., 1986). However, in part based on their short-term metabolic studies (15-day periods comparing 60% and 40% carbohydrate diets in nine subjects), Reaven and colleagues (Coulston et al., 1987; Reaven 1988) have cautioned against using this type of diet for long-term management of NIDDM on the basis of observed increases in postprandial glucose and insulin levels and in basal triglyceride levels. Recently, these studies were repeated with longer (6-week) dietary periods yielding similar findings (Coulston et al., 1989). These diets were already reduced in saturated fat and cholesterol.

Studies in which smaller amounts of mixed carbohydrate (de Bont et al., 1981; Weinsier et al., 1974) or sucrose (Peterson et al., 1986) were substituted for fat in diets tested on diabetics failed to show elevations of fasting triglyceride levels. This was confirmed in a recent metabolic ward study comparing a 60% mixed-carbohydrate diet with a 50% carbohydrate baseline diet in 10 subjects with NIDDM, but fasting triglyceride levels were increased in comparison to a high monounsaturated (50% fat, 33% monounsaturated) fat diet (Garg et al., 1988). Thus, evidence from some short-term metabolic studies suggests that normolipidemic diabetics whose diet is changed from one that is high in saturated fat to a diet containing very high carbohydrate levels and moderate to large amounts of sucrose respond with an increase in fasting triglyceride levels but do not consistently have increased postprandial triglyceride levels. Lesser degrees of substitution of carbohydrate for saturated fat usually do not increase fasting triglyceride levels. The increase in fasting triglyceride levels in hypertriglyceridemic diabetics is exaggerated; after 2 weeks, these levels tend to revert toward control levels. High-carbohydrate, low-saturated fat diets lower both low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol levels (Abbott et al., 1989; Katan, 1984) and usually the degree of hyperglycemia as well.

Diabetic populations, such as those in Asia, that subsist on high-carbohydrate diets have lower levels of plasma cholesterol, LDL cholesterol, and plasma triglycerides and higher levels of HDL cholesterol and apolipoprotein A1 than do persons with diabetes in the United States (Pan et al., 1986). The relatively low frequency and severity of atherosclerotic disease among these diabetic populations compared to Western diabetics have long been known (West, 1978; WHO, 1985). Studies in migrant populations have shown that diabetic men adopting a higher-fat, lower-carbohydrate diet after moving from Japan to Hawaii have increased triglyceride and cholesterol levels and a higher incidence of cardiovascular diseases (Kawate et al., 1979). Nevertheless, although some diet-specific effects on the complications and severity of already diagnosed diabetes may continue to be suspected or remain controversial, there is little evidence to implicate dietary carbohydrates, either complex or simple, in the etiology of diabetes.

Animal Studies

Evaluation of the hypothesis that a high-carbohydrate diet is an independent risk factor in the development of glucose intolerance or diabetes is complicated by such factors as hyperphagia and meal patterns (ad libitum versus meal feeding), which can influence plasma insulin curves, body weight, and fat pad weight (Glinsmann et al., 1986). Data derived from studies in several animal species have been somewhat difficult to interpret and are frequently contradictory. For example, in a prediabetic line of female Yucatan miniature swine genetically selected for diminished glucose tolerance, a diet containing 42% of calories as sucrose or starch for 3 months appeared to improve glucose tolerance (Phillips et al., 1982). In contrast, a strain of the spiny mouse (Acomy cahirinus), a desert animal with pancreatic beta-cell hyperplasia and abnormal carbohydrate metabolism, developed decreased glucose tolerance, increased plasma triglycerides and cholesterol levels, and an increase in liver enzymes involved in lipid metabolism after consuming a diet containing 55% sucrose for 4 months (Obell, 1974).

In a study by Cohen (1978), genetically selected prediabetic rats (Hebrew University) were fed diets containing 72% (by weight) of sucrose, fructose, glucose, or starch for 8 months. Rats fed the high-sucrose and high-fructose diets had high glucose peaks, relatively higher tissue insulin resistance, and increased serum cholesterol, but those on the high-starch diet did not. The high-fructose diet also resulted in elevated triglyceride levels. None of these adverse effects was noticed in the normal rat strains used as controls. Prediabetic male rats developed proteinuria (nephropathy) and testicular atrophy and lost weight after eating these high-sucrose (72% by weight) diets (Rosenmann et al., 1974). In pregnant females, this diet caused an increase in fetal malformations (Ornoy and Cohen, 1980). Thus, although these studies suggest that glucose intolerance may be worsened or provoked in animals predisposed to that condition, their results have to be extrapolated with caution because of the very high levels of sugar used, which far exceed levels in the common U.S. diet, especially the usual diets of patients with diabetes.

The desert sand rat (Psammomys obesus) has been used as a laboratory model for both adult-onset diabetes and spontaneous obesity, since it overeats when given free access to food and becomes obese and hyperinsulinemic (Kalderon et al., 1986). In a study by Rice and Robertson (1980), sand rats fed a sucrose-rich (56%) diet for 18 months did not differ from sand rats fed a starch-rich (56%) diet in development of obesity and insulin resistance; diabetes was not reliably produced in either case.

A new rodent model of NIDDM was described by Ikeda et al. (1981). This Wistar rat (now designated WDF/Ta-fa/fa) was produced by transferring the mutant gene Fa (fatty) from the obese, hyperinsulinemic but normoglycemic Zucker fatty rat to a lean albino Wistar Kyoto background rat using a combination of inbreeding and backcrossing. Unlike the obese Zucker rat, which becomes insulin resistant and hyperinsulinemic but does not become hyperglycemic or glucosuric, the WDF/ Ta-fa/fa male becomes frankly diabetic. If the obese male is fed a diet high in sucrose, it becomes diabetic earlier and the hyperglycemia is worsened in the already hyperglycemic animal (Greenwood et al., 1988). The female WDF/Ta-fa/fa rat does not respond to the high sucrose diet by developing hyperglycemia. Thus, this new strain provides a sexually dimorphic rodent model in which to examine the interaction of diet with sex-associated obesity and diabetic traits.

Genetically obese young male SHR/N-cp/cp (corpulent) rats fed diets containing 54% (by weight) sucrose or cornstarch for 9 weeks had increased body weight, hyperlipidemia, hyperinsulinemia, and abnormal glucose tolerance. Their lean litter mates (+/cp) had increased blood insulin levels but were normoglycemic (Michaelis et al., 1984). Thus, it seems that obesity may be the most important dietary factor in the development of diabetes in this and other animal models.

In a study by Stearns and Smith (1985), female WDF/Ta-fa/fa rats were fed diets containing 77% (by weight) sucrose or cornstarch for 60 days. The sucrose-fed rats had increased body weight, but exhibited no differences from cornstarch-fed rats in their plasma glucose, insulin, or triglyceride levels, triglyceride secretion rates, or pancreatic insulin content. That study shows that hyperglycemia, hypertriglyceridemia, and hyperinsulinemia do not necessarily accompany sucrose feeding of rats.

Insulin-Dependent Diabetes Mellitus

Epidemiologic Evidence

The role of carbohydrates has not been examined in epidemiologic studies, at least in recent years, because there is considerable consensus that the etiology of IDDM is not diet dependent.

Clinical Studies

Alterations in carbohydrate intake have been used as an adjunct to the management of IDDM patients with the goal of preventing chronic diseases, especially atherosclerosis. As with NIDDM, increasing the proportion of total calories from carbohydrates improves insulin sensitivity; lowers glucose, triglyceride, and cholesterol levels; and decreases insulin requirements (Simpson et al., 1979b; Stone and Connor, 1963). Also, as with NIDDM, very-long-term clinical studies have not been performed.

Some short-term metabolic studies on high-carbohydrate diets have shown transient increases in basal triglyceride levels (Bierman and Hamlin, 1961; Hollenbeck et al., 1985), but others have not (Riccardi et al., 1984). Female patients with IDDM who were fed a 65% carbohydrate, low-cholesterol diet for 6 weeks had slightly increased triglyceride levels, reduced cholesterol, apolipoprotein B, and apolipoprotein A1 levels but did not have altered glycemic control (Hollenbeck et al., 1985). These observations are similar to those described for NIDDM patients and nondiabetics.

Animal Studies

In a diabetic strain of mice (C57BL/KsJ-db/db), pancreatic islet destruction results in insulin insufficiency and glucose intolerance, but the relevance of this model to humans is not yet known. Diets containing 60% (by weight) simple sugars (e.g., sucrose, fructose, or glucose) caused additional obesity, hyperglycemia, atrophy of pancreatic islets, and early death in this strain, whereas dextrin or meals without carbohydrates did not. In normal littermates (+/db), no adverse effects were observed (Leiter et al., 1983).

Other animal models of IDDM are created by chemical destruction of insulin-producing cells with streptozotocin, which produces moderate diabetes (hyperglycemia with glycosuria). Sucrose-rich diets fed to such animals usually produce increased adiposity and variable deterioration of glucose tolerance, making it difficult to determine whether observed effects are due to differences in adiposity or to specific effects of sucrose on glucose homeostasis (Goda et al., 1982; Gray and Olefsky, 1982; Hallfrisch et al., 1979). It appears that in animals, as in humans, carbohydrate-rich diets given in the untreated diabetic state may lead to further deterioration of glucose homeostasis. In contrast to studies of humans, few dietary studies have been conducted in animal models of IDDM during treatment of hyperglycemia.

Carbohydrates have been implicated in the development of microvascular changes in diabetic rodents. Studies of eye changes showed that there were increases in sorbitol, fructose, and lactate levels in the retina when either sucrose or cornstarch at 68% of the diet was fed for 15 days to streptozotocin-diabetic Wistar rats (Heath and Hamlett, 1976; Heath et al., 1975). Six months of feeding the same high-sucrose diet to normal Wistar rats produced retinopathy similar in severity to retinal changes in diabetic rats on high-starch diets (Papachristodoulou et al., 1976). Fructose alone was found to cause comparable retinal changes in the same strain of diabetic rats (Boot-Hanford and Heath, 1981). Thornber and Eckhert (1984) suggest that retinopathy following high-sucrose diets may be due to dietary deficiencies, since supplementation of experimental diets containing 68% (by weight) of sucrose with chromium, selenium, and corn oil prevented capillary damage.

Increased kidney weight and glomerulosclerosis were observed in streptozotocin-diabetic Wistar rats on cornstarch diets and in normal rats consuming 68% of their diet as sucrose or fructose for 6 months (Boot-Hanford and Heath, 1981). Other authors also reported kidney changes in diabetic rats fed high levels of sucrose or cornstarch and in normal rats fed high levels of sucrose (Kang et al., 1982; Taylor et al., 1980).

Streptozotocin-diabetic Sprague-Dawley rats, but not normal rats, fed diets containing 66% (by weight) sucrose for 13 weeks had elevated HDL, VLDL, and total cholesterol (Bar-On et al., 1981). Sucrose fed at 66% of the diet for 21 days caused hypertriglyceridemia in diabetic male Sprague-Dawley rats, but not when the rats exercised daily (Dallaglio et al., 1983). The presence of 12% bran in a high-sucrose (32 or 72%) diet fed to Sprague-Dawley rats for 14 to 32 days reduced the plasma triglyceride levels to normal (Lin and Anderson, 1977).

The effects of high-sucrose diets on serum triglyceride and cholesterol levels seem to depend on the animal model used. For example, diabetic Wistar rats had increased lipid levels, whereas genetically diabetic mice had no change (Gonnermann et al., 1982).

Caution needs to be exercised in extrapolating the results of these animal studies to humans because very high levels of sugars were used, species appeared to differ in their responses, chronic effects on glycemia and metabolic changes often were not monitored, metabolic responses were not tested for reversibility, and some of the reported changes may have been due to nutrient deficiencies that also produce glucose intolerance (Glinsman et al., 1986).

Atherosclerotic Cardiovascular Diseases

Variations in the prevalence of coronary heart disease (CHD) among populations correlate directly with the proportion of calories derived from fats (Chapter 7) and, therefore, inversely with the proportion of calories derived from carbohydrates. Yudkin (1964) compared the per-capita sugar consumption in various countries with mortality from CHD and proposed that sugar contributes to the occurrence of heart disease. However, several subsequent studies have failed to substantiate this. Recent animal and epidemiologic data were reviewed in the 1986 report of the Sugars Task Force of the FDA, Evaluation of Health Aspects of Sugars Contained in Carbohydrate Sweeteners (Glinsmann et al., 1986). This task force stated, ''There was no conclusive evidence that dietary sugars are an independent risk factor for coronary artery disease in the general population."

A change from a Western-type diet to a very-high-carbohydrate, low-fat diet (60% or more of calories from any type of carbohydrate, e.g., simple sugars or starches) has been shown in short-term studies to cause a reduction of HDL (Gonen et al., 1981; Katan, 1984) and LDL (Abbott et al., 1989; Nestel et al., 1979) and a transient increase in fasting plasma triglyceride levels (Jellish et al., 1984; Reaven, 1986). Glucose, sucrose, fructose, and starch appear to have comparable effects on fasting triglyceride levels in short-term metabolic studies (Dunnigan et al., 1970; Mann and Truswell, 1970; McDonald, 1972; Nikkilä and Kekki, 1972; Porte et al., 1966; Turner et al., 1979). The increased basal triglyceride levels decline after several weeks to months on the high-carbohydrate diets, whereas reduced HDL levels persist (Katan, 1984). A high mixed carbohydrate diet (65% of calories) fed to normolipidemic subjects did not increase basal triglyceride levels after 4 to 6 weeks (Grundy et al., 1988). The transient increase in basal circulating triglycerides may be exaggerated in hypertriglyceridemic people (Ahrens, 1986; Liu et al., 1983) regardless of the type of carbohydrate and appears to be greater in men than in women (McDonald, 1985). High-carbohydrate diets lead to a short-term increase in overnight triglyceride levels, whereas postprandial triglyceride levels are actually lower in normal and hypertriglyceridemic subjects given high-carbohydrate diets than when fed high-fat diets (Barter et al., 1971; Schlierf and Dorow, 1973; Schlierf et al., 1971).

On the other hand, long-term feeding of diets high in carbohydrates and soluble fiber (e.g., oat bran) do not raise and may actually lower fasting triglyceride levels in hypertriglyceridemic people (Anderson and Tietyen-Clark, 1986). Such effects have not been observed in hypertriglyceridemic subjects consuming high levels of insoluble fiber (e.g., wheat bran). High-complex-carbohydrate diets (60% of total calories) fed to hypertriglyceridemic subjects for as long as 3 months have also been shown to reduce fasting triglyceride levels (Cominacini et al., 1988). Increased levels of cholesterol-rich and triglyceride-rich lipoproteins are not found in some populations, such as vegetarians or people living in parts of Asia, who have adapted to very-high-carbohydrate and low-fat intakes (Cerqueria et al., 1979) and who also have low levels of HDL, LDL, and VLDL as well as a low prevalence of CHD. The low HDL levels (Connor et al., 1978; Katan, 1984; Knuiman et al., 1987) do not appear to adversely influence their low CHD prevalence rate.

A prospective study of the relationship of dietary intake to subsequent CHD was undertaken in Puerto Rico by Garcia-Palmieri et al. (1980). A 6-year follow-up of 10,000 men age 45 to 64 years in that study indicated that urban men who developed new CHD had significantly lower carbohydrate intakes. Similar results have been reported for populations in Framingham, Massachusetts (Gordon et al., 1981) and in Hawaii (Yano et al., 1978). In the Hawaii study, men who developed CHD during a 6-year follow-up consumed less total carbohydrates, starches, and sugars than did those without CHD. Thus the development of CHD does not appear to be associated with high-carbohydrate diets, and no differences among types of carbohydrate have been demonstrated.

Dental Caries

Epidemiologic Evidence

Experimental studies such as the classic 5-year cohort study of 436 institutionalized mental patients in Vipeholm, Sweden (Gustafsson et al., 1954), have established that sugars consumed in sticky form, particularly between meals, increases the risk of dental caries. Restricting the intake of sugars (Becks, 1950) or substituting a nonfermentable sugar alcohol (xylitol) for sucrose (Scheinin et al., 1975) decreases the incidence of caries.

Cross-sectional studies support the inference that consumption of sugars is an important determinant of the incidence of dental caries. In 47 countries from which data were available in the late 1960s and 1970s, Sreebny (1982) found a correlation of 0.72 between the prevalence of dental caries in 12-year-old children and the mean per-capita supply of sugars. For 6-year-olds in 23 countries, the correlation was 0.31. The prevalence of dental caries in Japanese children decreased precipitously during the 1940s in conjunction with the severe reduction in supply of sugars (Takeuchi, 1961). Similar changes were noted in Europe (Sognnaes, 1948; Toverud, 1957).

Clinical Studies

Many clinical studies of diet and its association with plaque formation and composition are confounded by such variations in oral hygiene as brushing of teeth (Glinsmann et al., 1986). The bulk of the evidence from clinical studies, however, is consistent, indicating that all dietary carbohydrates are potentially cariogenic (Brown, 1975).

Telemetry analysis of plaque in situ demonstrates that plaque pH is lowered not only after consumption of a sugar cube (Geddes et al., 1977) and after rinsing with sucrose solutions (Tenovuo et al., 1984) but also after ingestion of starch (Mormann and Muhlemann, 1981). Abelson and Pergola (1984) determined the effects of three sucrose concentrations (10, 40, and 70%) on in vivo plaque pH in caries-prone 18- to 26-year-old adults. Above a certain concentration, additional sucrose did not heighten the acidogenic response. Schachtele and Jensen (1983) inserted a pH electrode in teeth to measure oral pH after consumption of various foods and found that several foods high in starch produced a marked decline in oral pH. These foods (white bread, white rice, and cooked carrots) are notable in that they contain either none or only low levels of individual sugars such as sucrose, glucose, and fructose; most of their carbohydrate content is starch.

The preponderance of clinical evidence, however, indicates that dietary sugars are of major etiologic importance in caries formation. Sucrose in solution has been shown to stimulate plaque formation (Geddes et al., 1978) and to alter the composition of plaque and saliva to a form suggestive of increased mineral resorption from the teeth (Tenovuo et al., 1984). In five subjects, who frequently rinsed their mouths with a sucrose solution for 2 months, there were changes characteristic of early demineralization of tooth surfaces (Geddes et al., 1978). Slabs of bovine enamel mounted in the human mouth likewise underwent demineralization when frequently exposed to sucrose (Pearce and Gallagher, 1979; Tehrani et al., 1983).

Sucrose in foods has also been shown to be cariogenic. In one clinical trial (Scheinin et al., 1975), three groups consuming diets containing sucrose, frutose, or xylitol were followed for 2 years. By the study's end, the average number of decayed, missing, or filled teeth (DMFT) was higher in the sucrose group than in the fructose group. Subjects consuming only xylitol had virtually no DMFT. The authors attributed the low cariogenicity of xylitol to the fact that it is not metabolized by oral microbes (Scheinin, 1976; Scheinin et al., 1975). The inability of other studies to demonstrate a cariogenic effect of presweetened cereals in schoolchildren (Finn and Jamison, 1980; Glass and Fleisch, 1974) may reflect differences in the specific sugars added to the cereals (Glinsmann et al., 1986).

The form of dietary carbohydrates also appears to influence cariogenicity. Consumption of canned pears and apples, for example, lowers plaque pH to a greater degree than do sugars alone (Imfeld et al., 1978; Jensen and Schachtele, 1983). Edgar et al. (1975) found that there was a wide variation in the ability of different snack foods to increase plaque acid formation. However, the extent of plaque acid formation from foods does not necessarily indicate either the amount of enamel destruction that will occur or the number and severity of the related caries.

The sequence in which carbohydrate-containing foods and other foods are eaten also appears to influence caries formation. A sharp increase in oral hydrogen-ion concentration and in plaque scraped at regular intervals from the mouth has been noted after use of a sugar rinse; the concentration of hydrogen ions returns to baseline after approximately 30 minutes. If cheese is consumed 5 minutes after the sugar rinse, however, the sharp increase in hydrogen-ion concentration is diminished and the concentration returns quickly to baseline (Edgar, 1981; Edgar et al., 1982; Schachtele and Jensen, 1983). The frequency of carbohydrate consumption also appears to influence caries formation. In the Vipeholm study, caries activity in adult patients was monitored over several years while their diet and eating schedule were controlled. There were two important findings. First, the extent of caries activity appeared to be influenced more by the frequency of sucrose intake than by total amount consumed. Second, consumption of solid forms of sugar appeared to be more cariogenic than liquid forms (Gustafsson et al., 1954).

In summary, clinical evidence suggests that all carbohydrates are cariogenic to various degrees, but that the form of carbohydrate-containing foods, as well as their sequence and frequency of consumption, can substantially influence their cariogenicity. Beyond this observation, little is known about the cariogenic potential of specific carbohydrate-containing foods because of the complex and interactive role of diet in caries formation. Dental caries is a multifactorial bacterial disease; dietary factors, host resistance, fluoride exposure, and the nature of bacterial flora in the mouth all play important roles (Shaw, 1987). In addition, most clinical studies have involved adults whose teeth are much less caries-prone than those of children, which suggests caution in generalizing such findings.

Animal Studies

Rats exhibit a dose-dependent increase in caries formation as sucrose is added to the diet; a cariogenic effect is observed at dietary levels as low as 0.1% (by weight) of diet (Michalek et al., 1977). However, a saturation point on the dose-response curve has been noted at anywhere from 8% (Kreitzman and Klein, 1976) to 40% dietary sucrose (Hefti and Schmid, 1979); there is no increase in caries formation above these levels. The cariogenic potential of sucrose is greater than that of equivalent amounts of glucose, fructose, or invert sugars (mixture of dextrose and fructose obtained by hydrolyzing sucrose) (Birkhed et al., 1981; Horton et al., 1985).

Frequency, form, and composition of the diet appear to influence the cariogenicity of dietary carbohydrates in animals as in humans. For example, frequent consumption of carbohydrates markedly accelerates caries formation (Firestone et al., 1982; Skinner et al., 1982). Certain carbohydrate-containing foods, such as bananas, are much more cariogenic than sucrose alone or even frequently fed sucrose-topped chocolate (Shrestha and Kreutler, 1983). Consumption of an unsweetened cereal to which sucrose has been added has been shown to cause fewer caries than consumption of cereals presweetened with equal sucrose levels (McDonald and Stookey, 1977), and carbohydrates in the form of maize or wheat starch have virtually no cariogenic activity (Beighton and Hayday, 1984; Horton et al., 1985). With respect to dietary composition, addition of cheese to a cariogenic diet has been shown to be protective against buccal (cheek side) decay in some studies (Edgar et al., 1982; Harper et al., 1987) and against buccal as well as sulcal (toward the linear depression or valley in the occlusal surface of the tooth) caries in others (Rosen et al., 1984).

The rat is the most favored animal species in studies of dietary carbohydrates and dental caries. This is due to the rapidity with which it develops experimentally induced dental caries and to the similarity of its sulcal and smooth-surface carious lesions to those of humans (Glinsmann et al., 1986). Most findings in rats seem likely to be applicable to humans. Generalizations should still be made with caution, however, since feeding patterns and oral physiology differ. For example, microbial flora, oral pH, salivary composition, flow rate, and buffering capacity are known to differ between the two species (McDonald, 1985). Also, rats nibble throughout the day, and it is known that meal frequency correlates positively, and strongly, with caries formation in animals (Firestone et al., 1982; Skinner et al., 1982) and in humans (Gustafsson et al., 1954). Also, assessment of the cariogenicity of foods in animals is complicated by the fact that foods must be given in powdered form and not in the physical form usually consumed by humans (Krasse, 1985). Differences in oral physiology further complicate the issue. For example, most types of phosphates effectively reduce caries in rats when added to sucrose-containing diets, whereas phosphate supplemention of the human diet has been markedly unsuccessful in reducing caries incidence (Nizel and Harris, 1964). Although some caution is warranted in interpreting evidence obtained from the rat model, animal studies are essential to our understanding of the role of dietary carbohydrates in cariogenesis.


The cariogenic action of dietary sucrose is influenced by other dietary constituents. For animals (Edgar et al., 1982; Harper et al., 1987) and humans (Edgar, 1981; Edgar et al., 1982; Schachtele and Jensen, 1983), cheese exerts a protective effect by blunting the short-term increase in hydrogen-ion concentration characteristically associated with a cariogenic diet. Cheese extracts administered after sucrose rinses have also been shown to inhibit demineralization of bovine enamel blocks fitted into the mouths of volunteers (Silva et al., 1987). Dietary substances inhibiting sucrose cariogenicity in animals include cheddar cheese (Rosen et al., 1984); mineral concentrates containing protein, calcium, and phosphate (Harper et al., 1987); cocoa (Paolino, 1982); lycasin, a hydrogenated corn syrup product (Leach et al., 1984); xylitol (Leach and Green, 1981; Shyu and Hsu, 1980); and saccharin (Linke, 1980). The mechanisms by which these substances inhibit sucrose cariogenicity are not fully understood; they may include enzyme inhibition in oral bacteria (Paolino, 1982), the stimulation of saliva, which maintains plaque pH in a neutral range (Krasse, 1985), and, for cheeses, the influences of texture and the casein or calcium-phosphate content (Harper et al., 1987).


Epidemiologic and Clinical Studies

An inverse association between caloric intake and body fatness has been found in some epidemiologic studies (Baeke et al., 1983; Johnson et al., 1956; Keen et al., 1979; Keys et al., 1967; Kromhout, 1983a,b; Lincoln, 1972; Maxfield and Konishi, 1966; McCarthy, 1966; Stefanik et al., 1959; Wilkinson et al., 1977) but not in others (Morris et al., 1977). It is likely that variation in caloric intake along with variation in amount of physical activity are factors in the causation of obesity (Sopko et al., 1984). This issue is discussed in Chapter 6.

Studies in which the influence of calorie sources was assessed indicate that compared to lean people, fatter people generally have a lower mean intake of calories from all sources including carbohydrates (but excluding alcohol). Keen et al. (1979) found small inverse correlations (-0.01 to -0.31) of body mass index with intake of total energy, protein, fats, total carbohydrates, and sucrose in three samples of employed men and women in Great Britain. These results show that in the general population obese adults do not consume more sugars or more complex carbohydrates than lean people; in fact, they seem to consume less.

Psychophysical taste testing in obese and normal humans also consistently indicates that obese subjects do not have stronger preferences for sucrose or sweet solutions (Drewnowski et al., 1985; Grinker, 1978; Malcolm et al., 1980). Interpretation of the epidemiologic results is complicated, however, by the association of physical activity as well as total caloric intake with body fatness (see Chapter 6).

Animal Studies

In contrast to the clinical and epidemiologic data, studies in animals show that various types of high-carbohydrate diets can lead to obesity. For example, a diet containing sucrose produced greater weight gains in lean and corpulent (SHR/ N-cp/cp) rats than did a diet containing cooked cornstarch (Michaelis et al., 1984). Although the sweet taste of sugar has been thought to encourage overeating in rats, Hill et al. (1980) found no differences in carbohydrate or caloric intake when adult male rats were offered either a sweet-tasting sucrose solution or a bland dextrin powder in addition to a chow diet, but the sucrose group gained more weight. In a similar experiment, Sclafani and Xenakis (1984) compared solutions of sucrose, Polycose (a bland-tasting polysaccharide), or Polycose sweetened with saccharin. They concluded that sweetness was not essential for production of carbohydrate-induced obesity, although it did increase the intake of polysaccharide.

Kanarek and Hirsch (1977) have described a method of producing obesity in rats by feeding them sucrose solutions. In later experiments, Kanarek and Orthen-Gambill (1982) observed that obesity could also be induced by supplementing the standard diet with solutions of glucose or fructose. Rattigan and Clark (1984) reported that the effect of a sucrose solution depends on the composition of the solid diet. Body weight and body fat increased without a significant increase in total caloric intake in rats given a low-fat, high-carbohydrate diets and the sucrose solution. Body weight, body fat, and total caloric intake were all decreased, however, in rats given high-fat, low-carbohydrate diets and the sugar solution.


Epidemiologic and Clinical Studies

There is little epidemiologic evidence to support a role for carbohydrates per se in the etiology of cancer. No definitive conclusion is justified, however, because carbohydrates have often been reported in epidemiologic studies only as a component of total energy and not analyzed separately.

In several international correlation studies, investigators have evaluated the role of sugar and sometimes carbohydrates in the etiology of some cancers. Armstrong and Doll (1975) found that sugar intake was positively correlated with both the incidence of and mortality from cancer of the colon, rectum, breast, and ovary, and with the incidence of cancer of the corpus uteri. Similar positive correlations were found between sugar intake and the incidence of and mortality from cancer of the prostate, kidney, and nervous system and the incidence of cancer of the testes. Sugar intake was inversely correlated with liver cancer incidence, but positively correlated with mortality from pancreatic cancer in women. Armstrong and Doll (1975) also reported a weak association between liver cancer incidence and the intake of potatoes—a starch-rich vegetable. For most of the sites reported, however, particularly the colon, rectum, and breast, the positive correlations with fat intake were greater than for sugar intake. Other investigations have produced similar findings. For example, Hems (1978) and Carroll (1977) found a positive correlation between breast cancer and sugar intake. Subsequently, however, Carroll (1986) found that whereas breast cancer mortality is positively correlated with the percent of calories derived from dietary fat, it varies inversely with the percent of calories from carbohydrates. This mirrors an earlier finding by Hems and Stuart (1975), who also found an inverse relationship between breast cancer incidence and starch consumption.

Hakama and Saxen (1967) reported a strong correlation between the per-capita intake of cereal used as flour and mortality from stomach cancer. The possible association of carbohydrate intake with gastric cancer was further evaluated by Modan et al. (1974), who found that high-starch foods were consumed more frequently by cases than by controls. Similarly, in a case-control study of diet and stomach cancer in Canada, Risch et al. (1985) found an increasing risk with total carbohydrate consumption but the relative risk for each 100-g/day increase in carbohydrates was only 1.53.

The effect of monosaccharides was evaluated in two studies of colorectal cancer. In a case-control study conducted in Marseilles (Macquart-Moulin et al., 1986), there appeared to be no evidence of increasing risk with increasing consumption of monosaccharides. However, in another case-control study conducted in Belgium (Tuyns et al., 1987), with essentially the same dietary survey technique, increasing monosaccharide and disaccharide intake was related to increasing risk of both colon and rectal cancer. The relative risks for the highest compared to the lowest consumption level was 1.7 for colon cancer and 2.4 for rectal cancer.

Animal Studies

In an extensive survey of the literature, the National Research Council's Committee on Diet, Nutrition, and Cancer (NRC, 1982) found relatively few animal studies dealing with the effects of dietary carbohydrates on carcinogenesis, and those studies provided little evidence of significant effects. Two research groups investigated the effects of diets containing different starches and sugars on mammary tumors induced by 7,12-dimethylbenz(a)anthracene (Hoehn and Carroll, 1978; Klurfeld et al., 1984). The results provided some evidence that rats fed sucrose or dextrose developed tumors more readily than those fed lactose or starch. Gridley et al. (1983) found that mice had a much higher incidence of spontaneous mammary tumors when fed a diet containing sucrose than when given a diet with dextrin.

Two other studies focused on the effects of dietary carbohydrates on liver carcinogenesis. Hei and Sudilovsky (1985) used diethylnitrosamine to induce hepatocarcinogenesis and found more γ-glutamyltranspeptide-positive foci in rats fed a sucrose-containing diet compared to those on a diet containing glucose. In other experiments on liver carcinogenesis induced by 3'-methylaminoazobenzene in rats fed liquid or powdered diets, Sato et al. (1984) found that tumorigenesis was enhanced by reducing sugar intake.

Other Disorders


Several reports examined the effects on human behavior of reactive or postprandial hypoglycemia, which is defined by decreased blood glucose after eating coupled with a characteristic group of clinical symptoms. Hypoglycemia in children has been alleged to be associated with hyperkinesis, attention-deficit disorders, juvenile delinquency, and criminality (Harper and Gans, 1986; Kruesi and Rapoport, 1986; Milich, 1986). Furthermore, hypoglycemia has been specifically associated with the ingestion of sucrose. A review by Harper and Gans (1986) points to a lack of scientific experimentation or support of claims in this area.

There have been suggestions that dietary components, particularly sugars, cause changes in the behavior of children and adults. Some reports (e.g., Prinz et al., 1980) have linked sugar consumption to hyperactivity in children (hyperkinesis). This has some biologic plausibility, since experimental evidence in animals indicates that sugars as well as other dietary components may affect the level of brain neurotransmitters. Sugar consumption by humans, however, results in increased levels of serotonin (Crane and Ladene, 1983; Fernstrom and Wurtman, 1971), which should reduce activity levels.

Studies to determine whether there is a relationship between blood glucose levels and behavioral change failed to find any correlation (Behar et al., 1984; Brody and Wolinsky, 1983). The subjects of these studies included normal children as well as hyperactive children who, according to their parents, had behavioral deterioration following intake of sugars. Glucose and fructose were compared to a placebo (saccharin) by using standard tests for memory and attention as the dependent variables. There was no evidence for behavioral excitation and some weak evidence for a calming effect of sugars. These studies cast doubt on the hypothesized clinical significance of sugar intake in the etiology of behavioral disturbances (Prinz et al., 1980). A similar experimental design was used in a study by Wolraich et al. (1985) to test the effects of sucrose and aspartame on behavioral and cognitive parameters in 16 hyperactive boys. No differences were observed. Based on a review of the literature, several investigators (e.g., Kruesi and Rapoport, 1986; Milich, 1986) have concluded that there is no scientific basis for a relationship between sugar consumption and hyperactivity or other behavioral changes in children.


Some people claim that juvenile delinquency as well as aggressive, antisocial, and even criminal behavior can result from reactive or postprandial hypoglycemia following the ingestion of sucrose and other carbohydrates (Gray, 1987; Harper and Gans, 1986; Schauss, 1980). Schoenthaler (1982) contends that a high proportion (up to 90%) of prison inmates are hypoglycemic and attributes that to a particularly high consumption of refined sugar. Studies undertaken to support this contention are characterized by inadequate diagnosis of hypoglycemia and lack of valid control groups (Gray, 1987). Another set of studies of violent adult male habitual offenders in Finland failed to support a relationship between violent behavior and hypoglycemia (Virkunen, 1982; Virkunen and Huttunen, 1982). Thus, the claims that high sugar intake can cause aggressive, antisocial behavior are based largely on conclusions drawn from anecdotal evidence and inadequately designed studies (Gray, 1987; Harper and Gans, 1986).

Documented reactive hypoglycemia based on accepted criteria (American Diabetes Association, 1982) is an uncommon condition (Cahill and Soeldner, 1974; Yager and Young, 1974) and occurs only in a very small percentage of people who commit crimes (Gray and Gray, 1983; Jukes, 1986). Apparently, no objective studies have been published to support the contention that aggressive or criminal behavior is influenced by sugar or carbohydrate intake. Despite the absence of any supporting data, however, some prison authorities have altered their institutional diets (Gray, 1987).

Lactose Intolerance

Primary lactose intolerance is the inability to digest the disaccharide lactose (the main carbohydrate in milk), breaking it down into glucose and galactose. This results from a progressive decrease, early in childhood, of the enzyme lactase, which is normally present at birth. As described in Chapter 4, some adults maintain lactase activity, which is controlled by a single gene. Lactose ingestion (milk drinking) will not induce lactase activity after its decrease nor will lactose restriction reduce enzyme activity if still present. Thus, the ingestion of lactose plays no role in the genetic expression of primary lactose intolerance. However, symptoms of lactose intolerance can be ameliorated by restriction of lactose-containing dairy products. Total elimination of lactose is rarely necessary, since most affected individuals can tolerate 1 to 2 glasses of milk daily (Gray, 1983).

Secondary lactose intolerance is associated with chronic gastrointestinal disease in people with persistent lactase activity. This condition will lessen as the disease is reversed. Also, chronic alcoholics without malnutrition have an increase in lactase deficiency, which is reversible with alcohol abstinence (Perlow et al., 1977).

Sucrose intolerance due to sucrase deficiency is a rarer genetic disorder. Its symptoms are indistinguishable from those of lactose intolerance, except that they are elicited by table sugar rather than by milk. Starch is usually well tolerated and digested. Dietary sucrose plays no role in the expression of this disorder, but its restriction will ameliorate symptoms (Gray, 1983).


The role of sugar-containing foods in the etiology of a variety of disorders and disabilities in humans has generated considerable attention. Carbohydrates are still believed by some to be fattening beyond their contribution to total calories, and sugars themselves are sometimes regarded as contributors to diabetes and heart disease. Sugars have also been implicated in a variety of behavioral aberrations associated with hypoglycemia, but rarely confirmed by acceptable criteria as discussed earlier.

Epidemiologic studies have shown that populations eating high-carbohydrate diets usually have a lower prevalence of NIDDM and CHD compared to populations eating lower-carbohydrate and higher-fat diets. The role of carbohydrates has not been completely established, but it seems reasonable to infer that the correlations of NIDDM and CHD with carbohydrates do not reflect a direct association but, rather, are due to confounding by variables such as caloric expenditure and obesity. Paradoxically, obesity also is associated with lower caloric intake, including low carbohydrate intake, in population studies. Evidence supports the contention that consumption of sugars, in particular sucrose, is the major dietary factor associated with the incidence of dental caries. Population studies suggesting a link between carbohydrate intake and colorectal cancer have been inconclusive.

With the exception of dental caries, clinical studies of carbohydrate intake and chronic diseases have focused more on dietary management of chronic diseases than on the role of diet in causation. High-carbohydrate, low-fat diets have been recommended both for the management of diabetes mellitus and for lowering glucose and lipid levels and reducing insulin requirements. However, short-term metabolic studies suggest that for some individuals, such diets may raise glucose and triglyceride levels, thereby pointing to the need for further long-term population studies and for intervention trials.

The scientific data supporting beliefs that high-carbohydrate diets are associated with hypoglycemia, hyperactivity, or criminality are inadequate. Controlled clinical studies to test the carbohydrate-hypoglycemia-hyperactivity connection have been negative.

Directions for Research

  • Long-term prospective studies are needed to evaluate the effects of increasing the proportion of carbohydrate calories in the diet on morbidity and mortality from CHD among diabetics.
  • Longer-term clinical studies are needed to characterize the metabolic adaptive changes in lipoproteins associated with switching from a low-carbohydrate to a high-carbohydrate diet from various dietary sources.
  • Additional studies should be conducted to test for a possible link between intake of total or individual carbohydrates and the incidence of colorectal and other cancers.
  • Research on the effect of fluoridation on dental caries among people with a wide spectrum of carbohydrate intakes would help elucidate whether the contributory role of carbohydrates in the pathogenesis of caries can be effectively offset by fluoride.


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Copyright © 1989 by the National Academy of Sciences.
Bookshelf ID: NBK218753


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