Nutrition for some chronic diseases
Dental caries affects people predominantly in the first 25 years of life. Dental enamel is the hardest material in the body. Its weakness is that, because it is basically calcium phosphate, it is
dissolved by acid. Three factors together contribute to caries.
A specific species of viridans streptococci, Streptococcus mutans, metabolises sugars to lactic acid and also polymerises sugars to a layer of covering polysaccharide in which the bacteria are
shielded from saliva and the tongue. Some people harbour more of these bacteria than others.
Most sugars serve as substrate—sucrose, glucose, fructose, and lactose (not sorbitol or xylitol). Starches too, if they stay in the mouth, are split to sugars by salivary amylase. Consumption of
sugary foods between meals, especially if they are sticky and consumption is repeated, favours the development of caries. Brushing the teeth and flossing between them after meals reduces the likelihood of caries.
Resistance of the teeth
Caries is more likely in fissures. In older people the “mature” enamel is more resistant. An intake of 1-3 mg/day of fluoride— as occurs, for example, if drinking water is fluoridated at
a concentration of 1 mg/l—increases the enamel’s resistance, especially if taken while enamel is being laid down before the tooth erupts.
Most toothpastes now contain fluoride and this, rather than any change in children’s sugar consumption, seems the main reason for the decline where water is not fluoridated.
Mottling of the (anterior permanent) teeth occurs if the fluoride intake is too high in the first eight years of life. Young children should either be persuaded not to swallow their toothpaste or be provided with a “junior” product with half-strength fluoride.
Most gallstones are composed mainly (about 85%) of crystallised cholesterol with small proportions of calcium carbonate, palmitate, and phosphate. Cholesterol, which is excreted by the liver into the bile, would be completely insoluble in an aqueous fluid like bile if it were not kept in micelle microemulsion by the combined detergent action of the bile salts and phospholipids (chiefly lecithin) in bile.
Non-dietary risk factors include female sex, pregnancy, oral contraceptives, age, ileal disease, clofibrate therapy, and certain ethnic groups—for example, Pima Amerindians have a high
incidence of gallstones.
In obesity and during dieting (with rapid weight loss) cholesterol secretion into bile tends to increase. During fasting and on total parenteral nutrition the gall bladder does not contract normally. In people on vegetarian and high cereal fibre diets the pattern of biliary bile acids change favourably, with less deoxycholate and more chenodeoxycholate.
Moderate alcohol intake appears to be protective; decreased cholesterol saturation of bile has been reported. Regular exercise also appears to protect against gallstones.
Gallstones are more likely to form if:
Urinary tract stones
- biliary cholesterol is increased, or
- biliary bile acids are reduced, or
- the gall bladder is less motile, or
- factors in the bile favour nucleation of cholesterol crystals.
Dietary factors which tend to increase urinary calcium or have been associated with stones are high intakes of protein, sodium, refined carbohydrate, vitamin D, calcium (spread over the day),
alcohol, curry, spicy foods, and low intakes of cereal fibre and water. Since most patients with
hypercalciuria have intestinal hyperabsorption of calcium it has been common to recommend a low calcium diet or phytic acid or a resin to reduce calcium absorption. A diet providing usual calcium intake (1200 mg/day) but very low salt (50 mmol Na/day) and reduced animal protein (50 g/day) has reduced calcium stone recurrences significantly over five years compared with a low calcium diet (400 mg/day).6 The normal calcium, low protein, low salt diet reduced urinary excretion of both calcium and oxalate.
Associated dietary factors are high intakes of oxalate or vitamin C and low water intake.
Foods rich in oxalate :
Spinach, rhubarb, beetroots, cocoa, chocolate, currants, dried figs, tea, swiss chard, blackberries, oranges, turnip greens.
Uric acid stones
Uric acid stones are associated with an acid urine, a high purine diet, and low water consumption.
The one common dietary association with all the common types of stone—and with the rare ones also—is a low water intake. Drinking plenty of water is an important habit for anyone liable to stones, especially if the weather is hot. Last thing at night is the important time to take water.
Uric acid stones
- One dietary cause of acid urine is a high protein intake. The amino acids methionine and cystine are metabolised to urinary sulphuric acid.
- Foods traditionally rich in purines include liver, kidneys, sweetbreads, sardines, anchovies, fish roes, and yeast extracts, but there are no modern tables and dietary RNA may raise plasma urate more than DNA.
Insulin-dependent diabetes (Type 1) is usually caused by autoimmune damage to the beta -cells in the pancreatic islets, which lose their ability to secrete enough insulin. This type of diabetes typically starts in adolescents or younger adults.
Several epidemiological studies have reported that patients with type 1 diabetes were less often exclusively breast fed for the first 3-4 months of life than unaffected controls.
The prevalence of non-insulin dependent diabetes (Type 2) increases with age; overall it is about six times more common than Type 1. This type 2 diabetes is closely associated with overweight or obesity and with lack of exercise.
Diabetes is the complication of obesity whose incidence goes up at the steepest gradient with degree of overweight. The risk of developing diabetes is greater in people whose obesity is mainly intra-abdominal rather than on the hips or buttocks (subcutaneous)—people with a high ratio of waist:hip circumferences.
Diabetes is a multifactorial disease. There is a strong family influence, though this may be partly because eating habits and body weight are influenced by family behaviour. But a genetic factor is clear in some groups.
The popular belief that eating a lot of sugar predisposes to diabetes is not confirmed by several epidemiological and prospective studies. High fat intake is more likely to lead to
The risk of developing diabetes increased exponentially with increasing body mass index (BMI). Men with moderate physical activity had less than half the risk.
Moderate drinkers also developed less diabetes. On average those who developed diabetes had higher plasma triglycerides, higher blood pressures and higher casual blood glucose.
Another finding in people who will later develop type 2 diabetes has been an increased fasting insulin and/or insulin response to standard glycaemic stimulus, due to insulin resistance.
Alcoholic liver disease
Countries with high alcohol consumption per head have high mortalities from cirrhosis. Studies showed a lower incidence of cirrhosis than might be expected from the rate of alcohol consumption but mortality from cirrhosis has doubled. Where alcohol consumption is high most cases of cirrhosis are due to alcohol. Other causes—for example, viral hepatitis B or C,
account for important proportions of cases.
In heavy drinkers pre-cirrhotic liver disease—fatty liver or alcoholic hepatitis—is more common than cirrhosis. A fourth condition, primary liver cell cancer, is a complication of alcoholic cirrhosis.
Daily heavy drinking for years is the typical pattern—80g (eight drinks) a day in men, and usually well over this. A study found that cirrhosis appeared to be less likely in those who drank only with meals.
The essential treatment of alcoholic liver disease is complete and permanent abstinence from alcohol. Although alcoholics may become deficient in nutrients, those who develop cirrhosis are often socially organised and well nourished. There is no evidence that a high protein diet or
choline can prevent alcoholic cirrhosis in man. Even when cirrhosis is established, an improved clinical state and prognosis may be expected in those who manage to abstain completely.
No precise safe level of alcohol intake can be given—only a clinical impression—because people who drink heavily underestimate their consumption when asked about it, and no
prospective epidemiological study has been done. Women are more susceptible to hepatic damage from alcohol because they have smaller livers (where most metabolism of alcohol occurs) and also lower rates of gastric (first pass) oxidation of alcohol than men. Only a minority of heavy drinkers get cirrhosis; there is presumably a synergy between alcohol and hepatitis viruses.
Some types of cancer
Differences in diets are thought to account for more variation in the incidence of all cancers than any other factor (with smoking in second order). Our bodies have three routes of entry for foreign compounds: the skin, lungs, and intestines. There are countless natural non-nutrient substances
in foods and several are mutagens. The fact that they can induce mutations in a standard bacterial culture does not, however, establish that they are dangerous to man: there are many available protective mechanisms.
Poor diet may have a more decisive effect by weakening defence mechanisms than by supplying potent carcinogens. Epidemiologists estimate that synthetic chemical additives in food account for under 1% of all cancers. The cancers most clearly related to habitual diet are oesophageal, gastric, and large intestinal cancers.
In the focus of oesophageal cancer, nitrosamines have been found in mouldy food and there is a deficiency of molybdenum. Domestic fowl are affected too.
From present epidemiological data protective factors are fruits and vegetables, refrigeration of foods and vitamin C intake. Apparent causative factors are intake of salt, pickled and salted
foods, and smoking.
Cancer of the large intestine usually arises in a polyp. Different dietary factors may be involved in the successive stages: formation of polyps; malignant transformation; growth and spread of a
cancer. Having a halfway stage of polyps should make study of causative factors easier. In some epidemiological studies animal fat and meat have emerged as risk factors. But in the majority of
epidemiological studies meat has not been significantly associated. One possible mechanism is the formation of heterocyclic amines, which are potent mutagens, on the surface of well-cooked meat. Some types of beer have been associated with rectal cancer. Wheat fibre appears
the best established protective factor. It dilutes and moves on potential carcinogens in the lumen and promotes fermentation.
Vegetables also appear protective; they contain several anticancer substances and also folate, which may prevent hypomethylation of DNA, a characteristic change in this cancer. In a trial wheat bran plus low fat prevented polyp development. beta-Carotene or vitamin E have been
ineffective; other prevention trials are underway.
High fat intake increases the risk of breast cancer but prospective and case-control epidemiological studies have not confirmed a role for fat, unless it operates in childhood or
adolescence. Weight gain in adult life increases the risk of postmenopausal breast cancer. Adipose tissue is a major source of oestrogen after the menopause. Alcohol consumption also
shows some association but this is not dose related. Plant foods appear protective.
The two most promising of these are wheat fibre (which can bind oestrogens in the bowel, reducing reabsorption) and soya (which contains phytoestrogens, isoflavones).
Breast cancer :
In countries with a high incidence the majority of cases are postmenopausal. Early menarche
and/or late menopause increase the risk; bilateral oophorectomy protects, and endogenous plasma oestrogens are higher in patients with postmenopausal breast cancer.