Do high-carbohydrate diets increase the risk of death? | stapelholm.info
During a median follow-up of 25 years there were deaths in the ARIC despite incomplete and conflicting data regarding their long-term effects on health outcomes. .. in diet that could arise from the diagnosis of these diseases. .. However, the relationship between carbohydrate consumption and. Evidence of associations between carbohydrates and diseases comes from This is of profound public health importance because of the clearly defined in relation to diabetes, coronary heart disease and other chronic diseases of lifestyle. . growth, differentiation and selection of damaged cells for cell death ( apoptosis). Some will automatically assume a cause-and-effect relationship on the relationship between macronutrient intake and certain health outcomes. disease mortality, whereas replacing carbohydrates with saturated fat was.
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. 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. 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.
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 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. 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.
Glucose, sucrose, fructose, and starch appear to have comparable effects on fasting triglyceride levels in short-term metabolic studies Dunnigan et al. The increased basal triglyceride levels decline after several weeks to months on the high-carbohydrate diets, whereas reduced HDL levels persist Katan, The transient increase in basal circulating triglycerides may be exaggerated in hypertriglyceridemic people Ahrens, ; Liu et al.
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. On the other hand, long-term feeding of diets high in carbohydrates and soluble fiber e. Such effects have not been observed in hypertriglyceridemic subjects consuming high levels of insoluble fiber e.
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.
The low HDL levels Connor et al. A 6-year follow-up of 10, 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. 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 institutionalized mental patients in Vipeholm, Sweden Gustafsson et al.
Restricting the intake of sugars Becks, or substituting a nonfermentable sugar alcohol xylitol for sucrose Scheinin et al. 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 s and s, Sreebny found a correlation of 0. For 6-year-olds in 23 countries, the correlation was 0. The prevalence of dental caries in Japanese children decreased precipitously during the s in conjunction with the severe reduction in supply of sugars Takeuchi, Similar changes were noted in Europe Sognnaes, ; Toverud, 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.
The bulk of the evidence from clinical studies, however, is consistent, indicating that all dietary carbohydrates are potentially cariogenic Brown, Telemetry analysis of plaque in situ demonstrates that plaque pH is lowered not only after consumption of a sugar cube Geddes et al. Above a certain concentration, additional sucrose did not heighten the acidogenic response.
Schachtele and Jensen 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. 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.
Slabs of bovine enamel mounted in the human mouth likewise underwent demineralization when frequently exposed to sucrose Pearce and Gallagher, ; Tehrani et al. Sucrose in foods has also been shown to be cariogenic. In one clinical trial Scheinin et al. 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, ; Scheinin et al. The inability of other studies to demonstrate a cariogenic effect of presweetened cereals in schoolchildren Finn and Jamison, ; Glass and Fleisch, may reflect differences in the specific sugars added to the cereals Glinsmann et al. 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. 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, ; Edgar et al. 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. 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, 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.
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. 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. Certain carbohydrate-containing foods, such as bananas, are much more cariogenic than sucrose alone or even frequently fed sucrose-topped chocolate Shrestha and Kreutler, 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,and carbohydrates in the form of maize or wheat starch have virtually no cariogenic activity Beighton and Hayday, ; Horton et al.
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. 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. 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, 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.
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, 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, 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.
Interactions The cariogenic action of dietary sucrose is influenced by other dietary constituents. For animals Edgar et al. 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. Dietary substances inhibiting sucrose cariogenicity in animals include cheddar cheese Rosen et al. The mechanisms by which these substances inhibit sucrose cariogenicity are not fully understood; they may include enzyme inhibition in oral bacteria Paolino,the stimulation of saliva, which maintains plaque pH in a neutral range Krasse,and, for cheeses, the influences of texture and the casein or calcium-phosphate content Harper et al.
Obesity Epidemiologic and Clinical Studies An inverse association between caloric intake and body fatness has been found in some epidemiologic studies Baeke et al. 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. 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.
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.
Chapter 3 - Dietary carbohydrate and disease
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.
Although the sweet taste of sugar has been thought to encourage overeating in rats, Hill et al. In a similar experiment, Sclafani and Xenakis compared solutions of sucrose, Polycose a bland-tasting polysaccharideor 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 have described a method of producing obesity in rats by feeding them sucrose solutions. In later experiments, Kanarek and Orthen-Gambill observed that obesity could also be induced by supplementing the standard diet with solutions of glucose or fructose. Rattigan and Clark 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. Cancer 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 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 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 and Carroll found a positive correlation between breast cancer and sugar intake.
Subsequently, however, Carroll 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 Stuartwho also found an inverse relationship between breast cancer incidence and starch consumption.
Hakama and Saxen 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. Similarly, in a case-control study of diet and stomach cancer in Canada, Risch et al. The effect of monosaccharides was evaluated in two studies of colorectal cancer.
In a case-control study conducted in Marseilles Macquart-Moulin et al. However, in another case-control study conducted in Belgium Tuyns et al. The relative risks for the highest compared to the lowest consumption level was 1.
Animal Studies In an extensive survey of the literature, the National Research Council's Committee on Diet, Nutrition, and Cancer NRC, 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,dimethylbenz a anthracene Hoehn and Carroll, ; Klurfeld et al.
The results provided some evidence that rats fed sucrose or dextrose developed tumors more readily than those fed lactose or starch. Two other studies focused on the effects of dietary carbohydrates on liver carcinogenesis. In other experiments on liver carcinogenesis induced by 3'-methylaminoazobenzene in rats fed liquid or powdered diets, Sato et al. Other Disorders Hyperactivity 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, ; Kruesi and Rapoport, ; Milich, Furthermore, hypoglycemia has been specifically associated with the ingestion of sucrose. A review by Harper and Gans 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. 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, ; Fernstrom and Wurtman,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.
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. A similar experimental design was used in a study by Wolraich et al. No differences were observed. Based on a review of the literature, several investigators e. Criminality 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, ; Harper and Gans, ; Schauss, Studies undertaken to support this contention are characterized by inadequate diagnosis of hypoglycemia and lack of valid control groups Gray, Another set of studies of violent adult male habitual offenders in Finland failed to support a relationship between violent behavior and hypoglycemia Virkunen, ; Virkunen and Huttunen, 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, ; Harper and Gans, Documented reactive hypoglycemia based on accepted criteria American Diabetes Association, is an uncommon condition Cahill and Soeldner, ; Yager and Young, and occurs only in a very small percentage of people who commit crimes Gray and Gray, ; Jukes, 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, Lactose Intolerance Primary lactose intolerance is the inability to digest the disaccharide lactose the main carbohydrate in milkbreaking 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 4some 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, 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.
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, Summary 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. Increasing carbohydrate intake can assist in the reduction of saturated fat and many fruits and vegetables rich in carbohydrates are also rich in several antioxidants.
Cereal foods rich in non-starch polysaccharides have been shown to be protective against coronary heart disease in a series of prospective studies. There is no evidence for a causal role of sucrose in the etiology of coronary heart disease. The cornerstone of dietary advice aimed at reducing coronary heart disease risk is to increase the intake of carbohydrate-rich foods, especially cereals, vegetables and fruits rich in non-starch polysaccharide, at the expense of fat.
Among those who are overweight or obese it is more important to reduce total fat intake and to encourage the consumption of the most appropriate carbohydrate-containing foods.
There has been concern that a substantial increase in carbohydrate-containing food at the expense of fat, might result in a decrease in high-density lipoprotein and an increase in very low-density lipoprotein and triglycerides in the blood.
There is, however, no evidence that this occurs when the increase in carbohydrates results from increased consumption of vegetables, fruits and appropriately processed cereals, over prolonged periods. Certain non-starch polysaccharides for example b -glucans have been shown to have an appreciable effect in lowering serum cholesterol when consumed in naturally occurring foods, or foods which have been enriched by purified forms, or even when fed as dietary supplements.
Such polysaccharides may be used in the management of patients with existing hypercholesterolemia but their role, if any, in the prevention of coronary heart disease remains to be established. Less information is available concerning the role of carbohydrates in other cardiovascular diseases. Plant foods are good sources of potassium and reducing the sodium to potassium ratio may help to reduce the risk of hypertension.
Limited data suggest a protective effect of vegetables and fruit in cerebrovascular disease. There has been considerable debate in many developed countries which have high rates of coronary heart disease regarding the age at which children should start to reduce fat intake towards the recommended level for adults. Clearly children require an adequate intake of energy for growth, and it is important that this does not include an excessive intake of carbohydrates at a very young age.
It is generally accepted that dietary carbohydrate should gradually be increased and fat reduced after the age of two years, so that by the age of five years children should have reached a diet in the range of that recommended for adults. This advice should, of course, include the key dietary guidelines for children and adolescents, which suggest that nutritional adequacy should be achieved by eating a wide variety of foods and that energy intake should be adequate to promote growth and development, and to reach and maintain desirable body weight.
Cancer Diet is widely regarded as important in the etiology of colorectal cancer with meat and fat considered the primary risk factors, and fruit, vegetable and cereal foods considered to be protective. Cancer is a disease associated with well-recognized genetic abnormalities and for colorectal cancer in particular, defects in a number of genes have been clearly defined 67, These genes mostly code for proteins responsible for the control of either cell growth, cell-to-cell communication or DNA repair.
They are mainly oncogenes or tumor suppressor genes.
The Lancet Public Health: Moderate carbohydrate intake may be best for health
For the development of colorectal cancer an individual must acquire several of these genetic abnormalities in the same cell. The acquisition of gene defects in somatic cells is thought to be through DNA damage and a resultant failure of the DNA repair system or of apoptosis.
Dietary carbohydrate is thought to be protective through mechanisms involving arrest of cell growth, differentiation and selection of damaged cells for cell death apoptosis. This is probably achieved primarily through the action of butyric acid which is formed in the colon from fermentation of carbohydrates such as resistant starch and non-starch polysaccharides.
Such carbohydrates are found mostly in cereals, fruit and vegetables. The process of fermentation may protect the colorectal area against the genetic damage that leads to colorectal cancer through other mechanisms which include: These mechanisms, however, are much less well-established. Carbohydrate staple foods are a source of phytoestrogens which may be protective for breast cancer.
Cancer risk is increased for the obese. This applies especially to cancers of the breast and uterus. However, this is a general effect of total energy intake and not specifically of carbohydrates. Dietary carbohydrates do not have a known role in the etiology of lung, breast, stomach, prostate, pancreas, oesophagus, liver or cervical cancers. There is, however, some evidence that there is an increased risk of ovarian cancer in women with mild galactosemia 81, Gastrointestinal diseases other than cancer Intakes of non-starch polysaccharides and resistant starch are the most important contributors to stool weight.
Therefore, increasing consumption of foods rich in these carbohydrates is a very effective means of preventing and treating constipation, as well as haemorrhoids and anal fissures. Bran and other cereal sources containing non-starch polysaccharide also appear to protect against diverticular disease and have an important role in the treatment of this condition. Obesity is an important risk factor for gallstones.The Bittersweet Truth About What We Eat
High intakes of carbohydrate may facilitate the colonization of bifidobacteria and lactobacilli in the gut and thus reduce the risk of acute infective gastrointestinal illnesses. Dental caries The incidence of dental caries is influenced by a number of factors.
Foods containing sugars or starch may be easily broken down by a-amylase and bacteria in the mouth and can produce acid which increases the risk of caries. Starches with a high glycemic index produce more pronounced changes in plaque pH than low glycemic index starch, especially when combined with sugars However, the impact of these carbohydrates on caries is dependent on the type of food, frequency of consumption, degree of oral hygiene performed, availability of fluoride, salivary function, and genetic factors.
Prevention programmes to control and eliminate dental caries should focus on fluoridation and adequate oral hygiene, and not on sucrose intake alone.