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5. Population nutrient intake goals for preventing diet-related chronic diseases: Previous page | 1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27

Research relating to the association between NSP intake and type 2 diabetes is complicated by ambiguity with regard to the definitions used (the term dietary fibre and NSP are often incorrectly used interchangeably), different methods of analysis and, consequently, inconsistencies in food composition tables. Observations by Trowell in Uganda more than 30 years ago suggested that the infrequency of diabetes in rural Africa may be the result of a protective effect of substantial amounts of NSP in the diet (referred to as dietary fibre) associated with a high consumption of minimally-processed or unprocessed carbohydrate. The author also hypothesized that throughout the world, increasing intakes of highly-processed carbohydrate, depleted in NSP, had promoted the development of diabetes (46). Three cohort studies (the Health Professionals Follow-up Study of men aged 40-75 years, the Nurses’ Health Study of women aged 40-65 years, and the Iowa Women’s Health Study in women aged 55-69 years) have shown a protective effect of NSP (dietary fibre) (47-49) which was independent of age, BMI, smoking and physical activity. In many controlled experimental studies, high intakes of NSP (dietary fibre) have repeatedly been shown to result in reduced blood glucose and insulin levels in people with type 2 diabetes and impaired glucose tolerance (50). Moreover an increased intake of wholegrain cereals, vegetables and fruits (all rich in NSP) was a feature of the diets associated with a reduced risk of progression of impaired glucose tolerance to type 2 diabetes in the two randomized controlled trials previously described (22, 23). Thus the evidence for a potential protective effect of NSP (dietary fibre) appears strong. However, the fact that the experimental studies suggest that soluble forms of NSP exert benefit (50-53) whereas the prospective cohort studies suggest that it is the cereal-derived insoluble forms that are protective (47, 48) explain the “probable” rather “convincing” grading of the level of evidence.

Many foods which are rich in NSP (especially soluble forms), such as pulses, have a low glycaemic index.1 Other carbohydrate-containing foods (e.g. certain types of pasta), which are not especially high in NSP, also have a low glycaemic index. Low glycaemic index foods, regardless of their NSP content, are not only associated with a reduced glycaemic response after ingestion when compared with foods of higher glycaemic index, but are also associated with an overall improvement in glycaemic control (as measured by haemoglobin A1c) in people with diabetes (54-57). A low glycaemic index does not, however, per se, confer overall health benefits, since a high fat or fructose content of a food may also result in a reduced glycaemic index and such foods may also be energy-dense. Thus while this property of carbohydrate-containing foods may well influence the risk of developing type 2 diabetes, the evidence is accorded a lower level of strength than the evidence relating to the NSP content. Similarly, the level of evidence for the protective effect of n-3 fatty acids is regarded as “possible” because the results of epidemiological studies are inconsistent and the experimental data inconclusive. There is insufficient evidence to confirm or refute the suggestions that chromium, magnesium, vitamin E and moderate intakes of alcohol might protect against the development of type 2 diabetes.

A number of studies, mostly in developing countries, have suggested that intrauterine growth retardation and low birth weight are associated with subsequent development of insulin resistance (58). In those countries where there has been chronic undernutrition, insulin resistance may have been selectively advantageous in terms of surviving famine. In populations where energy intake has increased and lifestyles have become more sedentary, however, insulin resistance and the consequent risk of type 2 diabetes have been enhanced. In particular, rapid postnatal catch-up growth appears to further increase the risk of type 2 diabetes in later life. Appropriate strategies which may help to reduce type 2 diabetes risk in this situation include improving the nutrition of young children, promoting linear growth and preventing energy excess by limiting intake of energy-dense foods, controlling the quality of fat supply, and facilitating physical activity. At a population level, fetal growth may remain restricted until maternal height improves. This may take several generations to correct. The prevention of type 2 diabetes in infants and young children may be facilitated by the promotion of exclusive breastfeeding, avoiding overweight and obesity, and promoting optimum linear growth. The strength of evidence on lifestyle factors is summarized in Table 9.

Table 9. Summary of strength of evidence on lifestyle factors and risk of developing type 2 diabetes

Evidence

Decreased risk

No relationship

Increased risk

Convincing

Voluntary weight loss in overweight and obese people
Physical activity


Overweight and obesity
Abdominal obesity
Physical inactivity
Maternal diabetesa

Probable

NSP


Saturated fats
Intrauterine growth retardation

Possible

n-3 fatty acids
Low glycaemic index foods
Exclusive breastfeedingb


Total fat intake
Trans fatty acids

Insufficient

Vitamin E
Chromium
Magnesium
Moderate alcohol


Excess alcohol

1 NSP, non-starch polysaccharides.

a Includes gestational diabetes.
b As a global public health recommendation, infants should be exclusively breastfed for the first six months of life to achieve optimal growth, development and health (59).

5.3.5 Disease-specific recommendations

Measures aimed at reducing overweight and obesity, and cardiovascular disease are likely to also reduce the risk of developing type 2 diabetes and its complications. Some measures are particularly relevant to reducing the risk for diabetes; these are listed below:

  • Prevention/treatment of overweight and obesity, particularly in highrisk groups.
  • Maintaining an optimum BMI, i.e. at the lower end of the normal range. For the adult population, this means maintaining a mean BMI in the range 21-23 kg/m2 and avoiding weight gain (>5 kg) in adult life.
  • Voluntary weight reduction in overweight or obese individuals with impaired glucose tolerance (although screening for such individuals may not be cost-effective in many countries).
  • Practising an endurance activity at moderate or greater level of intensity (e.g. brisk walking) for one hour or more per day on most days per week.
  • Ensuring that saturated fat intake does not exceed 10% of total energy and for high-risk groups, fat intake should be <7% of total energy.
  • Achieving adequate intakes of NSP through regular consumption of wholegrain cereals, legumes, fruits and vegetables. A minimum daily intake of 20 g is recommended.

1 The glycaemic index is calculated as the glycaemic response to a quantity of food containing a set amount, usually 50 g, of carbohydrate, expressed as a percentage of the glycaemic response following ingestion of a similar quantity of glucose or of carbohydrate in white bread.

5. Population nutrient intake goals for preventing diet-related chronic diseases: 1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27 | Next page

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