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Extracts from
DIET, NUTRITION, AND THE PREVENTION OF CHRONIC
DISEASES
Report of a WHO Study Group
World Health Organization Technical Report Series 797
Articles
The World Health Report 2002, Reducing Risks..
Diet, Nutrition and the Prevention of Chronic Diseases
A WHO Study Group on Diet, Nutrition and Prevention of noncommunicable
Diseases met in Ceneva from 6 to 13 March 1989. The meeting was opened by Dr Hu
Ching-Li, on behalf of the Director-General, Dr Hiroshi Nakajima. He said that
the amount and type of food eaten were fundamental determinants of human health.
Since health was a fundamental determinant of the quality of each individual's
life, good health should be a primary social goal. Improvements in the
collective good health of a population- particularly the avoidance of chronic
diseases in adult life-also decreased the costs associated with both health care
and lost economic productivity. Good health was therefore an important economic
asset.
Changes in dietary habits towards the "affluent" diet that prevailed in many
developed countries had been followed by increases in the incidence of various
chronic diseases of middle and later adult life. Initially, those chronic
diseases coexisted with the long-standing and persistent problems associated
with nutritional deficiencies, which could affect all age groups. The continuing
public health importance of such deficiency disorders was recognized. However,
the task of the Study Group was to provide recommendations that would help to
prevent the chronic diseases that were related to the newly emerging dietary
changes in developing countries, and to help in reducing the impact of these
diseases in developed countries.
The Study Group's report would describe recent changes in the dietary and
health patterns of countries, define the relationship between the "affluent"
diet that typically accompanied economic development and the subsequent
emergence of chronic diseases, and explore the need for national food and
nutrition policies to prevent or minimize costly health problems in both
developing and developed countries.
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3.3 Cancer
The relationships between specific dietary components and
cancer are much less well established than those between diet and cardiovascular
diseases. This is reflected in reviews of diet and cancer (43-45). However, the
overall impact of diet on cancer: rates throughout the world appears to be
significant. For populations in developed countries, where cancer rates are
highest and account for approximately one-quarter of all deaths, some
epidemiologists estimate that 30-40% of cancers in men and up to 60% of cancers
in women are attributable to diet (46).
The evidence for the influence of diet on cancer risk is derived from several
sources. Correlations between national and regional food consumption data and
cancer rates, and studies of the changing rates of cancer in populations as they
migrate from a region or country of one dietary culture to another, have led to
many important hypotheses. Case-control studies of the dietary habits of cancer
patients and comparison subjects, and prospective studies of populations with
known dietary habits, provide stronger evidence for the effects of diet in
relation to major cancers. Many of these observations from human populations
have been supported by animal experimental data.
Studies of diet in relation to some cancers have been confined to relatively
homogeneous populations and have not been replicated across a range of cultural
and dietary settings; for other cancers, the research has been pursued over a
wider range of dietary intakes included among the cancers that have been linked
repeatedly to dietary factors in different populations are cancers of the oral
cavity. pharynx, larynx, oesophagus, stomach, large bowel, liver, pancreas,
lung, breast, endometrium, and prostate.
3.3.1 Cancers of the oral cavity, pharynx, larynx, and oesophagus
In developed countries, epidemiological studies clearly indicate that
drinking alcoholic beverages is causally related to cancers of the mouth,
pharynx, oesophagus, and upper part of the larynx (47). There is no indication
that the effect is related to the type of beverage. Smoking also causes cancers
at these sites. There is also some evidence that cancers of the mouth and throat
are increased by poor oral and dental hygiene.
In correlation studies conducted in different parts of the world.
investigators have found positive associations betweem oesophageal cancer and
several dietary factors, including (a) low intakes of lentils, green vegetables,
fresh fruits, animal protein, vitamins A and C, riboflavin, nicotinic acid,
magnesium, calcium, zinc, and molybdenum; (b) high intakes of pickles, including
salt-pickled vegetables, and mouldy foods containing N-nitroso compounds; and
(c) consumption of foods and beverages at very high temperatures. The reported
associations are consistent with the general hypothesis that certain nutrient
deficiencies, such as are found in many high-risk populations, including heavy
alcohol drinkers, might increase the susceptibility of the oesophageal
epithelium to neoplastic transformation. Case-control studies of oral and
laryngeal cancers have also shown an increased risk associated with infrequent
ingestion of fruit and vegetables.
3.3.2 Stomach cancer
A high incidence of stomach cancer is found in Japan and other parts of Asia
and in South America, but not in North America or Western Europe where the rates
are low and still decreasing. In the United States of America, stomach cancer
rates are now among the lowest in the world, whereas in 1930, this was the
leading cause of cancer death for men and the second leading cause in women.
Gastric cancer incidence is decreasing in Japan, and a gradual decline in
incidence over several generations has been noted among Japanese migrants to
Hawaii. It seems most likely that these trends are related to changes in food
consumption patterns, since several dietary factors have been implicated in
gastric cancer risk. Stomach cancer is associated with diets comprising large
amounts of smoked and salt-preserved foods (which may contain precursors of
nitrosamines) and low levels of fresh fiuits and vegetables (acting as possible
inhibitors of nitrosaminc formation). Dietary shifts away from this pattern
could explain the declines in stomach cancer mortality in industrialized nations
over the past 50 years, but the evidence is not conclusive.
3.3.3 Colorectal cancer
International comparisons indicate that diets low in fibre- containing foods
and high in fat increase the risk of colon cancer. the initial suggestion that a
lack of dietary fibre might increase the occurrence of large bowel cancer came
from observations of the virtual absence of this cancer in southern Africa. The
indigenous populations were known to eat a lot of plant foods, and to have much
higher faecal weights than populations fron industrialized countries.
Several studies also demonstrate positive assoaations between the risk for
colorectal (primarily colon) cancer and dietary fat. In general, the data
suggest that saturated rather than unsaturated fatty acids may be responsible
for this effect. In other studies, positive associations have been found between
meat consumption and this cancer, but many studies have also shown no
relationship between fat or meat intake and colorectal cancer. Several
case-control and cohort studies provide suggestive but inconclusive evidence
that drinking alcoholic beverages, in particular beer, has a causal role in the
development of rectal cancer.
The data relating dietary fibre per se to colorectal cancer are equivocal.
Although several studies have shown inverse relationships between the intake of
high-fibre foods and colon cancer risk, these foods (vegetables to a large
extent) are rich sources of other nutritive and non-nutritive constituents with
potential cancer- inhibiting properties. Lower rates of colorectal cancer in
Californian Seventh-Day Adventists, half of whom are vegetarians, support
protective effect of a vegetarian diet, although this group also abstains from
alcohol.
In summary, an increased risk of colorectal caner appears to be associated
with high fat intake (particularly saturated fats) and low vegetable intake. It
is not clear whether dietary fibre pev se is protective or whether the
apparent,ffect is due to other food constituents . Rectal cancer risk may be
increased by the consumption of beer.
3.3.4 Liver cancer
Primary liver cancer is relatively rare in North Alerica and most developed
countries, but it is common in sub-Sahran Africa and south-east Asia, where it
is associated primarily "the exposure to hepatitis B virus infection. Liver
cancer incidence and mortality, by geographical area,or among different
population groups, have been correlated with aflatoxin contamination of
foodstuffs in Africa. On the basis of evidence in developed, countries,
consumption of alcoholic beverages is causally related to liver cane, (47).
3.3.5 Lung cancer
In most industrialized countries, lung cancer is the leading cause of cancer
deaths among men, and it is rapidly approaching this status among women. The
most important causal factor is cigarette smoking. Luug cancer risk in males is
clearly increased by certain occupational exposures (e.g., to asbestos, nickel,
chromate, or gamma-radiation) several of which have been shown to interact
synergistically with smoking.
Studies in several different populations have shown an interactive effect
between smoking and a low frequency of intake or green and yellow vegetahles
rich in beta-carotene. These findings are consistent with experimental data
showing tumour inhibition by vitamin A and synthetic analogues. In prospective
studies, the frequency of consumption of beta-carotene-containing foods and the
concentration of beta-carotene in serum have been inversely associated with the
risk of lung cancer, but earlv reports of a similar inverse association for erum
retinol(vitamin A) have not been confirmed in subsequent studies. Detary fats
and dietary cholesterol have also been positively associated with lung cancer
risk.
3.3.6 Female breast cancer
Several lines of evidence support the importance of dietary factors in the
causation of breast cancer. The first derives from animal experimental studies,
which have demonstrated that, both with and without the presence of known
mammary carcinogens, the incidence of mammary tumours in rats increases
substantially with diets high in total and saturated fat, provided that the diet
contains a small amount of polyunsaturated fat. A role for fat and other dietary
factors is also supported by descriptive epidemiological studies, correlation
studies, case-control and cohort studies, and evaluations of nutrition-mediated
biological risk factors.
Correlation studies provide evidence of a direct association between breast
cancer mortality and the intake of energy, fats, and specific sources of dietary
fats, such as milk and beef (see, for example. Fig. 9, page 68). Several
case-control studies have associated breast cancer risk with dietary
constituents, especially fats. However, not all studies show these
relationships. There is epidemiological evidence--not fully consistent relating
alcohol consumption to the risk of breast cancer in women. It is, at present,
unclear whether this association is causal.
3.3.7 Endometrial cancer
A strong association between endometrial cancer risk and excess weight has
been reported in several studies, and a hormonal mechanism has been postulated
for this association. Specific dietary factors other than obesity have not been
identitied for this disease.
3.3.8 Prostate cancer
Internationa1 incidence and mortality data generally show a positive
correlation of prostate cancer with the incidence of other diet-related cancers,
including cancers of the breast, corpus uteri. and colon. Inter- and
intra-country analyses show positive correlations between mortality from
prostate cancer and per caput intake of total fat. These findings have been
supported in analytical studies showing an association of prostate cancer with
the intake of high-fat foods.
Although studies of certain other cancers suggest that vitamin A and, in
particular, beta-carotene may be protective factors, some case-control studies
indicate that beta-carotene may be a risk factor for prostate cancer, especially
among men aged 70 years and older. Increased weight or obesity has also been
positively associated with the risk of prostate cancer.
3.3.9 Summary and conclusions: major associations between diet and
cancer
Table 11 summarizes the strength of association between dietary components
and cancers at various sites. A review of the evidence indicates that a high
intake of total fat- and in some case-studies also saturated fat--is associated
with an increased risk of cancers of the colon, prostate, and breast. The
evidence is strongest for cancer of the colon, and weakest for breast cancer.
The epidemiological evidence is not totally consistent, but is generally
supported by laboralory data from studies in animals. The experimental data,
however, also point to an adverse effect of very high intakes of polyunsaturated
fats, at levels that are considerably above current intakes in human
populations.
Diets high in plant foods, especially green and yellow vegetables and citrus
fruits, are associated with a lower occurrence of cancers of the lung, colon,
oesophagus, and stomach. Although the mechanisms underlying these effects are
not fully understood, such diets are usually low in saturated fat anf high in
starches and fibre and several vitamins and minerals, including beta-carotene
and vitamin A. There is no conclusive evidence that these beneficial effects are
due to the high fibre content of such foods.
Sustained heavy alcohol consumption appears to be causally linked to cancer
of the upper alimentary tract and liver. Excessive hody weight is clearly a risk
factor for endometrial and postmenopausal breast cancers, but the association of
these cancers with excessive energy intake per se is less well established.
High fat intake is associated with cancer at several sites. Certainty about
the optimum intake of fat in relation to cancer must await future research, such
as controlled trials. In the meantime, international correlation analysis (Fig.
9) and other epidemiological data indicate that fat Intakes of less than 30% of
total energy will be needed to attain a low risk of fat-related cancers. A
reduction in risk is also likely when fat intake is reduced towards 30%,
especially if this dietary change is combined with a change in other dietary
components (Table 11).
Table 11. Associations between selected dietary components and cancer
(a)
Site of cancer |
Fat |
Body weight |
Fibre |
Fruits and vegetables |
Alcohol |
Smoked, salted and pickled foods |
Lung |
|
|
|
- |
|
|
Breast |
+ |
+ |
|
|
+/- |
Colon |
+ + |
|
- |
- |
|
Prostate |
+ + |
|
|
|
|
|
Bladder |
|
|
|
- |
|
|
Rectum |
+ |
|
|
- |
+ |
|
Endometrium |
|
+ + |
|
|
|
|
Oral cavity |
|
|
|
- |
+(b) |
|
Stomach |
|
|
|
- |
|
+ + |
Cervix |
|
|
|
- |
|
|
Oesophagus |
|
|
|
- |
+ +(b) |
+ | Key: + = Positive association; increased
intake with increased cancer. - = Negative association; increased intake with
decreased cancer. a Adapted and extended from reference 44. b Synergistic
with smoking.
In conclusion, although several lines of evidence indicate that dietary
factors are important in the causation of cancer at many sites and that dietary
modifications may reduce cancer risk, the contribution of diet to total cancer
incidence and mortality cannot be quantified on the basis of present knowledge.
Nevertheless, evidence indicates that a diet that is low in total and saturated
fat, high in plant foods, especiaIly green and yeIlow vegetables and citrus
fruits, and low in alcohol, salt-nickled, smoked, and salt-preserved loods is
consistent with a low risk of many of the current, major cancers, including
cancer of the colon, prostate, breast, stomach lung, and oesophagus.
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5.3 Derivation of population nutrient goals
The evidence is clear that
the risk of certain types of cancer is directly associated with the level of
total fat in the diet. At present the range over which the relationship holds is
not clear. It may extend across a range of total fat intakes from > 400% of
energy down to 20% or lower. There is suggestive evidence that obesity may he
associated with high total fat intake, but again there is no specific lower
level that marks the end of the relationship.
The Study Group noted
increasing evidence of specific beneficial effects of complex carbohydrates on
intestinal function, on the chemistry of the gut and the physiology of the gut
wall with a possible relationship to cancer, and on the absorption and
metabolism of carbohydrates and other energy sources (including short-chain
fatty acids formed by fermentation in the lower intestine) in relation to the
amelioration of diabetes and other metabolic diseases. At present, the available
evidence does not lead to the definition of specific population nutrient goals.
Rather, it argues in favour of maximizing the intake of this class of
carbohydrate, taking into account the energy provided by fat and protein. The
lower and upper limits were set on that basis.
For the purpose of this
recommendation, "fruits and vegetables" does not include potatoes, other tubers,
or cassava. The recommendation is made recognizing: the epidemiological evidence
of an increased risk of cancer with low intakes of certain fruits and
vegetables; the continuing problems of vitamin A deficiency and low availability
of dietary iron, which would be ameliorated with increased intakes of vitamin A
(or beta-carotene) and ascorbic acid, respectively, and the specific
contribution that these groups of foods make to micronutrient and protein
intakes. The population nutrient goals have bean set judgementally rather than
on the basis of specific evidence as to the necessary level of intake. The
recommended lower limit is higher than current intake in many populations and
much higher than current intake in some of the developed countries. No upper
limit has been suggested. The carbohydrate, lipid, and protein contributionsof
the fruits and vegetables are included within, not in addition to, the
previously stated goals.
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8. RECOMMENDATIONS
8.1 Recommendations to WHOThe Study Group recommended that WHO should
consider:
1.Developing a coherent nutrition and health policy with targets for
promoting the concept of healthy nutrition. This concept, which supplements the
long-standing concern with nutritional deficiencies and food shortages, takes
account of the increasecd risks of chronic diseases in later adulthood caused by
the "affluent" dietary pattern (i.e., high in fats and free sugars, and low in
starchy foods) that tends to accompany economic development.
2.Establishing a mechanism to ensure that the impact of diet upon a range of
health problems is recognized in all relevant WHO programmes.
3.Discussing with other United Nations and international agencies the major
implications for agriculture and trade of the nutritional needs ofboth
developing and developed countries, as described in this report. Commodity
analyses and the projections of FAO should be considered in relation to the
nutritional quality of the diet.
4.Communicating to the major trading organizations the consequences of
trading developments that might lead to adverse effects on health. The export of
subsidized saturated fat is an example of one potential problem.
5.Strengthening its programme to provide expert guidance the national
governments seeking to establish a nutrition and food policy, for example by
means of seminars for national governments and nongovernmental organizations.
6.Developing a basis for monitoring the progress of the initiatives described
in this report on diet and health, and setting targets for this work. In this
regard the development of surveillance programnes at country level should be
promoted.
7.Discussing with nongovernmental organizations how best to ensure that
communities throughout the world participate in activities to promote health by
eating an appropriate diet. The variety of diets consistent with the nutritional
goals should be recognized, and the nutritional goals translated into food needs
at national level.
8.Monitoring research developments and promoting international collaboration
in the study of the relationships between diet and health so that further
refinements to the Organization's nutrition policy can be made.
9.Involving the Coder Alimentarius Commission (1) in
establish- ing standards that will help to implement the proposals in this
report.
(1)The Codex Alimentarius Commission is an intergovernmental
body with a membership, in 1989, of 137 countries; it is charged with the
implementation of the FAO/WHO Food Standards Programme.
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8.2 Recommendations to national governments1O.Governments are
recommended to establish a national board for nutrition and food policy
involving, in addition to the ministry of health, the many government ministries
whose policies affect the production, distribution, and consumption of food.
11.Governments should ensure that experts are available to the ministry of
health to monitor the nutritional and health status of the population, as
assessed by a national surveillance system.
12.Ministries of health should initiate or strengthen professional training
programmes, at both undergraduate and postgraduate levels, to ensure that the
role of diet in the prevention of chronic diseases is understood by the medical
profession and other health care workers.
13.Each ministry of health should, as part of its health promotion programme,
establish regular contact with non governmental organizations, consumer
representatives, and the media to develop jointly a community-based programme.
This activity should be in addition to any government-sponsored healh promotion
campaign.
14.Governments should ensure that adequate nutritional com- petence exists
within the ministry of agriculture to allow full participation in a national
board for nutrition and food policy.
15.Governments should consider their investment and subsidy policies in both
agriculture and the food industryto ensure that they are consistent with the
nutritional concepts contained in this report. Policies should be geared to
promoting the growing of plant foods, including vegetables and fruits, and to
limiting the promotion of fat-containing products.
16.As part of a national policy, each government should set its own goals and
strategy for reducing the incidence of chronic diseases.
17.Governments are recommended to establish appropriate food standards, to
ensure the nutritional quality of foods that are substantial contributors to the
national diet.
18.Each government should consider all new legislation bearing on agriculture
and food, to ensure that it is compatible with the prevention of chronic
diseases.
19.Governments are recommended to establish, where possible, compulsory
labelling of food products based on the Codex Standardsand Guidelines for the
Labelling of Foods and Food Additives. (1) Labelling should
be clear and consistent and, to be understandable as well as scientifically
correct, information should be simply presented and expressed both graphically
and numerically. One method is proposed in Annex 6.
20.Discussions should be encouraged between the government, the food indusry,
and the consumers to ensure the development of food products that are low in
fat, free sugars, and salt.
21.Each government should examine its animal production policies and incentes
to ensure that they do not promote the production of excessive quantities of
saturated fats.
22.Ministriesof education should ensure that, as part of nutrition and health
education for teachers and children, due attention is given to ths prevention of
diet-related chronic diseases.
(1) CODEX ALIMENTARIUS COMMISSION. Codex Alimentarius, Volume
VI. Codex Standards and Guidelines for the Labelling of Foods and Food
Additives, 2nd ed. Rome, Food and Agriculture Organization of the United
Nations/World Health Organization, 1987.
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ACKNOWLEDGEMENTSThe Study Group wishes to acknowledge the
valuable contributions made to its work by: Dr K.V. Bailey, Regional Officer for
Nutrition, WHO Regional Office for Africa, Brazzaville, Congo; Dr H.W. Heiss,
University of Freiburg, Freiburg, Federal Republic of Germany; Dr E. Helsing,
Regional Officer for Nutrition, WHO Regional Office for Europe, Copenhagen,
Denmark; Dr F.K. Kaferstein, Chief, Food Safety, WHO, Geneva, Su;itzerland; Dr
E. Nicholls, Regional Adviser, Noncommunicable Diseases, WHO Regional Oflice for
the Americas, Washington, DC, USA; and Dr R. Saracci, Unit of Analytical
Epidemiology, International Agency for Research on Cancer, Lyon, France.
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