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Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging, Tufts University, Boston, MA 02111
2To whom correspondence should be addressed. E-mail: tucker{at}hnrc.tufts.edu.
| ABSTRACT |
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KEY WORDS: nutrition aging developing countries diet chronic disease nutrition transition
| INTRODUCTION |
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10% of the worlds population, or
600
million people, in 1999. They project that by the year 2050, this
proportion will increase to 20% and will include >2 billion people.
These changes will be most dramatic in the less developed countries,
where the population age structure will change rapidly from one that is
predominantly young, with few elderly, to one with more balanced
numbers across age groups (1)
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Nutritional status has a major impact on disease and disability and offers great promise for minimizing this oncoming burden. However, the current trend in developing countries is toward higher fat, more refined diets that contribute to increased risk of chronic disease, and the prevalence of chronic disease is already increasing rapidly. At the same time, social and demographic changes are placing elderly at even greater risk of food insecurity and malnutrition. This double burden of undernutrition and obesity in an aging population poses tremendous challenges for developing countries, whose policies and institutions are currently unprepared to handle the demands these changes will bring.
| The nutrition transition |
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| Dietary change |
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Analyses of the food supply in 21 Asian nations during 19751994
showed an overall decline in the availability of complex carbohydrates
and an increase in total fats (7)
. In addition,
hydrogenated fats increasingly replaced vegetable oils
(6)
. Similarly, data from the 1989 China Health and
Nutrition Survey showed a marked shift in the structure of the diet
toward greater proportions of fat intake from both animal and vegetable
sources (10)
. In both urban and rural populations, fat
consumption and use of animal products increased with per capita
income. In India, large community-based surveys showed that high
socioeconomic status
(SES)3
groups consumed an average of 32% of energy from fat, relative to 17%
of energy from fat in lower income groups, and that the prevalence of
coronary heart disease was three to four times greater for these high
versus lower SES groups (11)
.
Urban Africans have also increased their consumption of refined foods
and fats. Despite relatively low levels of economic development,
dietary shifts have begun to appear (5)
. In South Africa,
the transition to a Western diet is becoming evident in both rural and
urban areas. Bourne et al. (12)
compared the diet
composition of adults in 1990 with that in 1940, confirming a 14%
reduction in carbohydrate intake and an increase of 63% in fat intake
over this 50-y time span.
These dietary changes, combined with the rapid growth of the aging population, suggest that we can expect an escalating epidemic of chronic diseases, particularly obesity, diabetes and heart disease, in developing countries in the coming decades. Carefully designed nutrition interventions could have a major impact on future disease risk in these countries.
| Obesity |
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Obesity prevalence is particularly high in Latin America and the
Caribbean. In Chile from 1988 to 1997, the prevalence of obesity
increased from 14 to 23% in women and from 6 to 16% in men
(14)
. A recent analysis of subsets of the population
revealed that the Mapuche, the major aboriginal group in Chile, had a
much higher prevalence of obesity15% of men and 32% of women in the
rural areas, and 28% of men and 45% of women in the urban areas
(15)
. In the British Virgin Islands, >50% of adult
females and 25% of adult males were obese (defined as weight for
height > 120% ideal body weight) in 1984 (16)
. Although
prevalence of obesity is lower in less developed Latin American
countries like Brazil, a comparison of two national surveys showed an
increase in the proportion of obese adults (BMI > 30
kg/m2) from 5.7% in 1974 to 9.6% in 1989. The
greatest change was in the poorest 30% of women, from 3.6 to 9.7%
(9)
. More recently, data from the 1997 survey in Brazil
show that obesity prevalence has continued to increase rapidly among
the rural and low income urban populations. More optimistically,
obesity prevalence declined from 12.8% in 1989 to 9.2% in 1997 among
the upper income quartile of Brazilian urban women (17)
.
The authors suggest that an intense mass media campaign since 1992 may
be having a positive effect on this segment of the population.
In China, obesity has been clearly associated with higher income in
both rural and urban regions (18)
. However, a closer
evaluation of the impact of income on dietary change suggests shifts
that may lead to greater obesity among low income groups relative to
those with higher income in the urban areas (19)
. A
longitudinal study done in a small urban area of Southern Thailand
revealed an unexpectedly large proportion of overweight people. Among
2,703 men and 792 women living in urban areas, 26% of men and 21% of
women had BMI > 25.0 kg/m2 (20)
.
Data on obesity in Africa are limited and, due to lower development,
most African countries are behind other regions in terms of both the
demographic and the nutrition transition. Albeit, evidence of
transition is appearing. However, the 1997 Demographic Health Surveys
of maternal nutritional status reported that the prevalence of BMI >30
kg/m2 among women aged 1549 y ranged from <1%
in Burkina Faso and Malawi to 25% in Egypt. Recent reports on the
Tunisian and Moroccan populations in Northern Africa showed that women
were much more likely to be obese than men. In Tunisia and Morocco,
respectively, the prevalences of BMI >30 kg/m2
were 23 and 18% for women and 7 and 6% for men (21)
. In
South Africa, >44% of black females and 8% of males were recently
reported to have BMI > 30 kg/m2
(22)
. There have been very few studies of older Africans.
What is available on nutrition and aging in Africa is summarized and
discussed by Charlton and Rose, in this issue of the journal.
Obesity makes direct and powerful contributions to risk of chronic disease. Until very recently, the health systems in most developing countries have not focused on obesity prevention or treatment, and few programs are in place to address this rapidly growing problem. The experience in Brazil suggests that media campaigns can be effective, at least in some segments of the population.
| The epidemiologic transition: emerging chronic disease |
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33% were due to
infectious disease, 50% to vascular disease, and 12% to cancer
(23)
One of the clearest outcomes of the nutrition transition is the
epidemic growth of type 2 diabetes. Prevalence is currently higher in
developed than in developing countries, but the majority of people
affected already resides in developing countries, and prevalence is
increasing at a much more rapid rate in the developing countries.
Figure 3
shows the projected numbers of people in developed and developing
countries with diabetes in the years 1995 and 2025 (24)
.
In the developed countries, increases in prevalence during this period
will average
27%, from 6 to 7.6%, thus increasing from 51 to 72
million people. In the developing countries, a 48% increase in
prevalence, from 3.3 to- 4.9%, and a 170% increase in number, from 84
to 228 million, are projected. Figure 4
shows the relative prevalence projections for Latin America, India,
China and Africa. Among the developing countries, the greatest
prevalence of diabetes will continue to be in Latin America. The
greatest projected changes are for China and India, with expected
increases in prevalence of 68 and 59%, respectively. The fewest cases
will remain in the least developed regions of Africa, where this
transition has not yet progressed (24)
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Diabetes, hypertension and vascular disease have also been increasing
rapidly in Asia (30)
. In China the prevalence of diabetes
in adults aged 2564 y in 1994 (2.5%) was 300% greater than it had
been in 1984 (31)
. Diabetes incidence was associated with
age, income, family history, BMI and waist circumference, blood
pressure and physical inactivity (31)
. The prevalence of
adult diabetes has also doubled in many other Asian communities over
the past two decades, from 8 to 16% in Papua New Guinea, from 2 to 5%
in Hong Kong, and from 4 to -8% and 8 to 12% for adults in Singapore
of Chinese and Asian Indian origins, respectively (32)
.
Hypertension is also increasing rapidly in Asia. Stroke was the leading
cause of death in China in 1986 (33)
. A comparison of the
prevalence of hypertension in 1960 and 1990 showed that increases from
23% to 1520% in several Asian countries (34)
. This
report also found that hypertension and stroke occurred at relatively
younger ages and that hypertension was more prevalent at lower BMI in
Asia compared with other regions. In Pakistan, the prevalence of
hypertension in urban areas was nearly twice that of rural areas, and
in India adults from higher SES groups were three to four times more
likely to have coronary heart disease than those in lower SES groups
(34)
.
There have been few studies on chronic diseases in Africa, but limited
data suggest that the prevalence of diabetes is still <1% in most
countries in Africa. However, it has increased to >58% in South
Africa and 10% in Egypt, with up to 20% in urban areas. Many areas
with low diabetes prevalence are showing evidence of impaired glucose
tolerance, suggesting that increases in diabetes prevalence are likely
to follow (32)
. In South Africa, coronary heart disease
death rates in 1990 varied considerably by ethnicity. They were 165 and
101 per 100,000 population for whites and Asians, respectively,
considerably higher than that for the mixed race group (55 per 100,000)
or for black South Africans (5 per 100,000). In contrast,
cerebrovascular disease was greatest among the mixed race group (74 per
100,000), followed by whites and Asians (63 per 100,000) and blacks (37
per 100,000) (35)
. Although Africa is currently behind in
this transition, we can expect that changes in Africa will also occur
rapidly in the coming years.
| Theories linking earlier malnutrition with later chronic disease |
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Accumulating evidence supports the association between poor nutrition
and growth in utero or in early infancy and risk of type 2 diabetes and
cardiovascular disease later in life, especially when weight gain in
adulthood is added to early undernutrition (38)
. It has
been assumed that much of the difference in individual susceptibility
to disease that cannot be explained by environmental factors is due to
genetic causes. However, at least part of what has been regarded as the
genetic contribution to ischemic heart disease may be the effect of the
intrauterine or early postnatal environment (38)
. Several
studies have examined the relationship between birth weight and later
development of hypertension, diabetes and/or cardiovascular disease,
and results are remarkably consistent in demonstrating a positive
association between these conditions (39)
.
Another theory to explain these associations is that of the "thrifty
genotype." In 1962, James Neel, an American geneticist, postulated
the existence of the thrifty gene to explain the apparent paradox of
the high prevalence of diabetes in populations where it clearly had an
adverse effect on reproduction (40)
. He suggested that in
early life, a genotype predisposing to diabetes is "thrifty," or
efficient in the utilization of food. This genotype would have a
survival advantage in times of food shortage. In the nutrition
transition, with change from relative food scarcity to food
sufficiency, the thrifty genotype no longer confers a survival
advantage, but makes individuals more susceptible to obesity and
diabetes (38)
. Hattersley et al. (41)
have
also recently proposed that fetal genetics may explain the associations
used to support the Barker hypothesis. Their fetal insulin hypothesis
suggests that genetically determined insulin resistance may result in
both low insulinmediated fetal growth in utero and insulin
resistance, and thus, susceptibility to diabetes and heart disease in
later life.
It is possible that there is validity to each of these hypotheses. The observed associations are evident and further research should elucidate specific mechanisms. With the current rapidity of change in diet and lifestyle, the greater risk of obesity and chronic conditions in countries with poor intrauterine and infant nutrition means that a double burden of undernutrition and chronic disease will be increasingly faced simultaneously in those countries with the least resources to do so.
| Nutrition and food security |
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In most developing countries, few elder assistance programs currently exist. Elderly with declining functional ability will be at high risk for food insecurity, thereby placing them at even greater risk of progressing disease and disability. There are currently very few studies from which to understand the current and changing status of elderly in developing countries. As the size of this population grows, more documentation of the situation of elderly will be needed to formulate programs of prevention and emergency assistance.
| Nutrient status and requirements with aging |
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Recent research illustrates that protein adequacy is critical for
maintaining functional status with age. Casteneda et al.
(44)
found that older adults provided with diets
containing 0.45 g protein · kg body wt-1
· d-1 for 9 wk had significant losses in lean
tissue, immune response and muscle function. Recent studies suggest
that protein requirements to retard loss of muscle mass
(45)
and bone mass with aging (46)
in older
individuals may be greater than previously thought. Short-term
nitrogen balance results suggest that a safe recommended protein intake
for older men and women should be 1.01.25 g high quality protein ·
kg-1 · d-1
(45)
.
Aging is generally associated with a gradual decrease in muscle mass
(sarcopenia) (47)
. Loss of muscle mass poses significant
risks, including lower resting metabolic rate, reduced muscle strength
and increased functional dependency. In the combined New Mexico Aging
Process Study and the New Mexico Elder Health Survey (48)
,
the prevalences of sarcopenia and sarcopenic obesity (relatively high
ratios of body fat to muscle mass) were 15 and 2%, respectively, in
6069 y olds and 40 and 10%, respectively, in those >80 y of age.
Elders at greatest risk for disability and for several chronic diseases
in this population were those who were both sarcopenic and obese
(48)
. In addition to adequate protein intake, resistance
exercise has shown great promise in preventing sarcopenia. One study
demonstrated that nitrogen excretion decreased 1015% at the
beginning of resistance training and persisted for 12 wk
(45)
. Research on sarcopenia is still quite limited in
developing countries. New studies in China and Chile are presented in
articles by Stookey and Bunuot in this issue of the journal.
Micronutrient inadequacies are common among elderly, even in the most
developed countries, and they have increasingly been linked to risk of
chronic disease. For example, vitamins B-6, B-12, and folate are
required to prevent the accumulation of homocysteine, an amino acid
that has been consistently associated with risk of vascular disease
(49)
, and recent studies have also shown associations
between low concentrations of these B vitamins and cognitive decline
(50)
. In addition, vitamin B-12 is needed to maintain
neurological function (51)
. Data from several studies
suggest that inadequate blood concentrations of these B vitamins are
prevalent in older populations. In the Netherlands, 1045% of adults
aged 65 y and older were deficient in vitamin B-6
(52)
. Older persons have greater difficulty absorbing
vitamin B-12 because of atrophic gastritis, a degenerative stomach
condition estimated to affect 2540% of U.S. elderly
(53)
. Despite apparently adequate intakes of vitamin B-12,
relative to recommendations, >16% of elders in the U.S. Framingham
Study had low vitamin B-12 concentrations (54)
. One of the
few studies on B vitamins in elderly in Latin America (55)
found prevalences of folate deficiency (<7 nmol/L) of 51% in men and
33% in women and prevalences of vitamin B-12 deficiency (<148 pmol/L)
of 51% in men and 31% in women. On the other hand, in a small sample
of elderly in Bangkok, Thailand, folate deficiency was found for 21%
and vitamin B-12 deficiency was found for only 7% of cases
(56)
. More information is needed about the B vitamin
status of elderly in developing countries, where deficiency is likely
to be common.
Calcium and vitamin D are also nutrients of particular concern
for elderly populations. With age, declining renal function leads to
malabsorption of calcium and accelerated bone loss (57)
.
Requirements for vitamin D also increase with aging. Despite the
greater availability of sunlight in most developing countries, relative
to most developed countries, older individuals often have less exposure
than younger adults. Furthermore, with age, there is decreased ability
to form previtamin D-3- in skin with UV light exposure
(58)
. The low calcium and vitamin D in the diets of many
developing countries, together with the dietary and physical activity
changes associated with the nutrition transition, suggest that
osteoporosis will become an increasingly major problem as these
populations age.
Antioxidant vitamins, including vitamin C, vitamin E, and a variety of
phytochemicals, are important in maintaining effective antioxidant
defenses against oxidant stressrelated diseases, including cancer,
cataract and Alzheimers disease. Vitamin E has also been shown to be
effective in promoting immune function to fight infection
(59)
. Very few studies of antioxidant status in developing
countries are available. With the nutrition transition toward higher
fat, lower fiber diets, attention to maintaining and increasing intakes
of traditional fruits, vegetables and whole grains is of considerable
importance in helping to control the worldwide increases in incidence
of chronic disease.
Interestingly, the nutrients that have received the most
attention for maternal and child nutritioniron and vitamin Aare
required in lower amounts by elderly than by younger adults. There is
decreased clearance of vitamin A by hepatic and other peripheral
tissues with age (60)
. Similarly, iron stores accumulate
with age, and high serum ferritin has been associated with greater risk
of coronary heart disease (61)
. Consequently,
micronutrient fortification programs should consider the possible
effects on the growing elderly segment of their populations.
| Nutrition policy for aging populations in developing countries |
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This recommendation was followed with a joint consultation of the
World Health Organization with the Jean Mayer USDA Human Nutrition
Research Center on Aging at Tufts University in 1998, where these
issues were discussed in detail. An effort to utilize the growing
knowledge about aging in developed countries lead to a list of priority
concerns, for which more data are needed in developing countries
(Fig. 5
). Prominent on this list are the need to document the nutritional
status of elderly, to better determine nutrient requirements, and to
identify factors affecting dietary intake and nutrient absorption in
differing cultural and environmental settings. It was also recognized
that international dietary guidelines for older individuals are
lacking, and that these are needed to guide community awareness and
support of nutrition for elderly and for the development of
community-based interventions.
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Existing knowledge about nutrition and aging suggests that nutrition has the power to make a substantial impact on the health and functional status of older individuals. The size and rapidity of the ongoing demographic and nutrition transitions demand that nutrition for aging adults receive greater priority in developing countries. A common pattern observed in the nutrition transition demonstrates that diets improve in variety and nutrient content and then quickly pass this point to become higher in fat and refined grains and lower in fiber and micronutrient content. The extent to which more optimal diets can be maintained through the promotion of greater intakes of fruit, vegetables and whole grains and the discouragement of "fast food" culture are still unknown in many countries. However, nutrition intervention holds the promise of mitigating the impeding burden of chronic disease and disability and improving the quality of life of this rapidly growing segment of the worlds population.
| FOOTNOTES |
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3 Abbreviations: SES, socioeconomic status. ![]()
| LITERATURE CITED |
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1. World Health Organization (1999) Health and development in the 20th century 1999 World Health Report Geneva, Switzerland. .
2. United Nations (1999) Population Aging 1999 1999 Population Division United Nations .
3. World Health Organization (2001) Ageing and nutrition: a growing global challenge 2001.
4. Murray C. J. & Lopez A. D. (1997) Mortality by cause for eight regions of the world: Global Burden of Disease Study. Lancet 349:1269-1276.[Medline]
5. Popkin B. M. (1994) The nutrition transition in low-income countries: an emerging crisis. Nutr. Rev. 52:285-298.[Medline]
6. Vorster H. H., Bourne L. T., Venter C. S. & Oosthuizen W. (1999) Contribution of nutrition to the health transition in developing countries: a framework for research and intervention. Nutr. Rev. 57:341-349.[Medline]
7. Drewnowski A. & Popkin B. M. (1997) The nutrition transition: new trends in the global diet. Nutr. Rev. 55:31-43.[Medline]
8. Sinha D. P. (1997) Diet-related non-communicable diseases in the Caribbean and Latin America. Shetty P.S. McPherson K. eds. Diet, Nutrition and Chronic Disease: Lessons from Contrasting Worlds 1997:30-37 John Wiley & Sons Chichester, UK .
9. Monteiro C. A., Mondini L., Medeiros de Souza A. L. & Popkin B. M. (1995) The nutrition transition in Brazil. Eur. J. Clin. Nutr. 49:105-113.[Medline]
10. Popkin B. M., Keyou G., Zhai F., Guo X., Ma H. & Zohoori N. (1993) The nutrition transition in China: a cross-sectional analysis. Eur. J. Clin. Nutr. 47:333-346.[Medline]
11. Gopalan C. (1992) Nutrition in developmental transition in Southeast Asia 1992 World Health Organization New Delhi, India. .
12. Bourne L. T., Langenhoven M. L., Steyn K., Jooste P. L., Laubscher J. A. & Van der Vyver E. (1993) Nutrient intake in the urban African population of the Cape Peninsula, South Africa: the Brisk study. Cent. Afr. J. Med. 39:238-247.[Medline]
13. Caballero B. (2001) Introduction 2001 Symposium Obesity in developing countries biological and ecological factors. J. Nutr. 131 866S870S. .
14. Vio F. & Albala C. (2000) Nutrition policy in the Chilean transition. Pub. Health Nutr. 3:49-55.
15.
Uauy R., Albala C. & Kain J. (2001) Obesity trends in Latin America: transiting from under- to overweight. J. Nutr. 131:893S-899S.
16. Dinesh P. S. & Mclntosh C. E. (1992) Changing nutritional patterns in the Caribbean and their implications for health. Food Nutr. Bull. 14:88-96.
17. Monteiro C. A., DA Benicio M. H., Conde W. L. & Popkin B. M. (2000) Shifting obesity trends in Brazil. Eur. J. Clin. Nutr. 54:342-346.[Medline]
18. Du S., Bing K., Zhai F. & Popkin B. M. () The nutrition transition in China: a new stage of the Chinese diet. Pub. Health Nutr .
19. Guo S., Mroz T. A., Popkin B. M. & Zhai F. (2000) Structural changes in the impact of income on food consumption in China, 198993. Econ. Dev. & Cultural Change 48:737-760.
20. Tamphaichitr V., Kulapogse S., Pakpeankitvatana R. l., Leelahagul P., Tamwiwat C. & Lochaya S. (1991) Prevalence of obesity and its associated risks in urban Thais. Gomura Y. Tarui S. Inoue S. Shimazu T. eds. Progress in Obesity Research 1990 1991:649-653 Libbey London, UK .
21.
Mokhtar N., Elati J., Chabir R., Bour A., Elkari K., Schlossman N. P., Caballero B. & Aguenaou H. (2001) Diet culture and obesity in northern Africa. J. Nutr. 131:887S-892S.
22. Nube M., Asenso-Okyere W. K. & Boom G. L. M. (1998) Body mass index as indicator of standard of living in developing countries. Eur. J. Clin. Nutr. 52:136-144.[Medline]
23. World Health Organization (1998) Life in the 21st century: a vision for all 1998 Geneva Switzerland. .
24. King H., Aubert R. E. & Herman W. H. (1998) Global burden of diabetes, 19952025: prevalence, numerical estimates, and projections. Diabetes Care 21:1414-1431.[Abstract]
25. Castro V., Gomez-Dantes H., Negrete-Sanchez J. & Tapia-Conyer R. (1996) Chronic diseases in persons of 6069 years of age. Salud Publica Mex 38:438-447.[Medline]
26. Lerman I. G., Villa A. R., Martinez C. L., Cervantes Turrubiatez L., Aguilar Salinas C. A., Wong B., Gomez Perez F. J. & Gutierrez Robledo L. M. (1998) The prevalence of diabetes and associated coronary risk factors in urban and rural older Mexican populations. J. Am. Ger. Soc. 46:1387-1395.[Medline]
27. Oliveira J. E., Milech A. & Franco L. J. (1996) The prevalence of diabetes in Rio de Janeiro, Brazil. Diabetes Care 19:663-666.[Abstract]
28. Pan American Health Organization (1998) Diseases or health impairments. P.A.H. Organization eds. Health in the Americas 1998:102-209 Washington, D.C. .
29. World Health Organization (1999) The double burden: emerging and persistent problems. WHO eds. Full Report World Health Report 1999 1999:13-27 WHO Geneva, Switzerland .
30. Gupta R. & Singhal S. (1997) Coronary heart disease in India. Circulation 96:3785 (Comment).
31. Pan X. R., Yang W. Y., Li G. W. & Liu J. (1997) Prevalence of diabetes and its risk factors in China; 1994. Diabetes Care 20:1664-1669.[Abstract]
32. Bloomgarden Z. T. (1998) International Diabetes Federation meeting, 1997. Type 2 diabetes: its prevalence, causes, and treatment. Diabetes Care 21:860-865.[Medline]
33. Asian Acute Stroke Advisory Panel (2000) Stroke epidemiological data of nine Asian countries. J. Med. Assoc. Thailand 83:1-7.[Medline]
34. Singh R. B., Suh I. L., Singh V. P., Chaithiraphan S., Laothavorn P., Sy R. G., Babilonia N. A., Rahman A. R., Sheikh S., Tomlinson B. & Sarraf-Zadigan N. (2000) Hypertension and stroke in Asia: prevalence, control and strategies in developing countries for prevention. J. Hum. Hypertens. 14:749-763.[Medline]
35. Seedat Y. K. (1998) The prevalence of hypertension and the status of cardiovascular health in South Africa. Ethn. Dis. 8:394-397.[Medline]
36. Barker D. J., Winter P. D., Osmond C., Margetts B. & Simmonds S. J. (1989) Weight in infancy and death from ischaemic heart disease. Lancet 2:577-580.[Medline]
37. Barker D. J. (1990) The fetal and infant origins of adult disease. BMJ 301:1111 (Editorial).
38. McDermott R. (1998) Ethics, epidemiology and the thrifty gene: biological determinism as a health hazard. Soc. Sci. Med. 47:1189-1195.
39. Barker D. J., Bull A. R., Osmond C. & Simmonds S. J. (1990) Fetal and placental size and risk of hypertension in adult life. BMJ 301:259-262.
40. Barker D. J., Hales C. N., Fall C. H., Osmond C., Phipps K. & Clark P. M. (1993) Type 2 (non-insulin-dependent) diabetes mellitus, hypertension and hyperlipidaemia (syndrome X): relation to reduced fetal growth. Diabetologia 36:62-67.[Medline]
41.
Fall C. H., Osmond C., Barker D. J., Clark P. M., Hales C. N., Stirling Y. & Meade T. W. (1995) Fetal and infant growth and cardiovascular risk factors in women. BMJ 310:428-432.
42. Frankel S., Elwood P., Sweetnam P., Yarnell J. & Smith G. D. (1996) Birthweight, body-mass index in middle age, and incident coronary heart disease. Lancet 348:1478-1480.[Medline]
43. Martyn C. N., Barker D. J. & Osmond C. (1996) Mothers pelvic size, fetal growth, and death from stroke and coronary heart disease in men in the UK. Lancet 348:1264-1268.[Medline]
44.
Leon D. A., Koupilova I., Lithell H. O., Berglund L., Mohsen R., Vagero D., Lithell U. B. & McKeigue P. M. (1996) Failure to realise growth potential in utero and adult obesity in relation to blood pressure in 50 year old Swedish men. BMJ 312:401-406.
45. Stein C. E., Fall C. H., Kumaran K., Osmond C., Cox V. & Barker D. J. (1996) Fetal growth and coronary heart disease in south India. Lancet 348:1269-1273.[Medline]
46.
Rich-Edwards J. W., Stampfer M. J., Manson J. E., Rosner B., Hankinson S. E., Colditz G. A., Willett W. C. & Hennekens C. H. (1997) Birth weight and risk of cardiovascular disease in a cohort of women followed up since 1976. BMJ 315:396-400.
47.
Forsen T., Eriksson J. G., Tuomilehto J., Osmond C. & Barker D. J. (1999) Growth in utero and during childhood among women who develop coronary heart disease: longitudinal study. BMJ 319:1403-1407.
48. Neel J. V. (1962) Diabetes mellitus: a "thrifty" genotype rendered detrimental by "progress"?. Am. J. Human Genet 14:353-362.[Medline]
49. Hattersley A. T. & Tooke J. E. (1999) The fetal insulin hypothesis: an alternative explanation of the association of low birthweight with diabetes and vascular disease. Lancet 353:1789-1792.[Medline]
50. Martin L. G. & Kinsella K. (1994) Research on the demography of aging in developing countries. Martin L.G. Preston S.H.E. eds. Demography of Aging 1994 National Academy Press Washington, DC. .
51. Russell R. M. (1992) Micronutrient requirements of the elderly. Nutr. Rev. 50:463-466.[Medline]
52.
Castaneda C., Charnley J. M., Evans W. J. & Crim M. C. (1995) Elderly women accomodate to a low-protein diet with losses of body cell mass, muscle function, and immune response. Am. J. Clin. Nutr. 62:30-39.
53. Evans W. J. & Cyr-Campbell D. (1997) Nutrition, exercise, and healthy aging. J. Am. Diet. Assoc. 97:632-638.[Medline]
54. Hannan M. T., Tucker K. L., Dawson-Hughes B., Cupples L. A., Felson D. T. & Kiel D. P. (2000) Effect of dietary protein on bone loss in elderly men and women: the Framingham Osteoporosis Study. J. Bone Miner. Res. 15:2504-2512.[Medline]
55. Baumgartner R. N., Stauber P. M., McHugh D., Koehler K. M. & Garry P. J. (1995) Cross-sectional age differences in body composition in persons 60+ years of age. J. Gerontol. Med. Sci. 50A:M307-M316.[Abstract]
56.
Baumgartner R. N. (2000) Body composition in healthy aging. Ann. N. Y. Acad. Sci. 904:437-448.
57.
Selhub J., Jacques P. F., Bostom A. G., DAgostino R. B., Wilson P. W., Belanger A. J., OLeary D. H., Wolf P. A., Schaefer E. J. & Rosenberg I. H. (1995) Association between plasma homocysteine concentrations and extracranial carotid-artery stenosis [see comments]. N. Engl. J. Med. 332:286-291.
58. Selhub J., Jacques P. F., Bostom A. G., DAgostino R. B., Wilson P. W., Belanger A. J., OLeary D. H., Wolf P. A., Rush D., Schaefer E. J. & Rosenberg I. H. (1996) Relationship between plasma homocysteine, vitamin status and extracranial carotid-artery stenosis in the Framingham Study population. J. Nutr. 126:1258S-1265S.
59. Stampfer M. J., Malinow M. R., WIllett W. C., Newcomer L. M., Upson B., Ullmann D., Tishler P. V. & Hennekens C. H. (1992) A prospective study of plasma homocyst(e)ine and risk of myocardial infarction in US physicians. JAMA 268:877-881.[Abstract]
60.
Riggs K. M., Spiro A., 3rd, Tucker K. & Rush D. (1996) Relations of vitamin B-12, vitamin B-6, folate, and homocysteine to cognitive performance in the Normative Aging Study. Am. J. Clin. Nutr. 63:306-314.
61. Lindenbaum J., Healton E. B., Savage D. G., Brust J. C., Garrett T. J., Podell E. R., Marcell P. D., Stabler S. P. & Allen R. H. (1988) Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis. N. Engl. J. Med. 318:1720-1728.[Abstract]
62. Tolonen M., Schrijver J., Westermarck T., Halme M., Tuominen S. E., Frilander A., Keinonen M. & Sarna S. (1988) Vitamin B6 status of Finnish elderly: comparison with Dutch younger adults and elderly: the effect of supplementation. Int. J. Vitam. Nutr. Res. 58:73-77.[Medline]
63. Krasinski S. D., Russell R. M., Samloff I. M., Jacob R. A., Dallal G. E., McGandy R. B. & Hartz S. C. (1986) Fundic atrophic gastritis in an elderly population: effect on hemoglobin and several serum nutritional indicators. J. Am. Ger. Soc. 34:800-806.[Medline]
64.
Tucker K., Rich S., Rosenberg I., Jacques P., Wilson P., Dallal G. & Selhub J. (2000) Plasma vitamin B 12 concentrations relate to intake source in the Framingham offspring study. Am. J. Clin. Nutr. 71:514-522.
65. Olivares M., Hertrampf E., Capurro M. T. & Wegner D. (2000) Prevalence of anemia in elderly subjects living at home: role of micronutrient deficiency and inflammation. Eur. J. Clin. Nutr. 54:834-839.[Medline]
66. Prayurahong B., Tungtrongchitr R., Chanjanakijskul S., Lertchavanakul A., Supawan V., Pongpaew P., Vudhivai N., Hempfling A. A., Schelp F. P. & Migasena P. (1993) Vitamin B12, folic acid and haematological status in elderly Thais. J. Med. Assoc. Thailand 76:71-78.[Medline]
67.
Nordin B. E., Need A. G., Steurer T., Morris H. A., Chatterton B. E. & Horowitz M. (1998) Nutrition, osteoporosis, and aging. Ann. N. Y. Acad. Sci. 854:336-351.
68. Webb A. R., Kline L. & Holick M. F. (1988) Influence of season and latitude on the cutaneous synthesis of vitamin D3: exposure to winter sunlight in Boston and Edmonton will not promote vitamin D3 synthesis in human skin. J. Clin. Endocrinol. Metab 67:373-378.[Abstract]
69.
Meydani S. N., Barklund M. P., Liu S., Meydani M., Miller R. A., Cannon J. G., Morrow F. D., Rocklin R. & Blumberg J. B. (1990) Vitamin E supplementation enhances cell-mediated immunity in healthy elderly subjects. Am. J. Clin. Nutr. 52:557-563.
70. Krasinski S. D., Cohn J. S., Schaefer E. J. & Russell R. M. (1990) Postprandial plasma retinyl ester response is greater in older subjects compared with younger subjects: evidence for delayed plasma clearance of intestinal lipoproteins. J. Clin. Invest. 85:883-892.
71.
Turnlund J., Costa F. & Margen S. (1981) Zinc, copper, and iron balance in elderly men. Am. J. Clin. Nutr. 34:2641-2647.
72.
Bermudez O. I., Becker E. K. & Tucker K. L. (1999) Development of gender-specific equations for correction of stature of frail elderly Hispanics living in the Northeastern United States. Am. J. Clin. Nutr. 69:992-998.
73. Mazariegos M., Valdez C., Kraaij S., Setten C. V., Liurink C., Breuer K., Haskell M., Mendoza I., Solomons N. W. & Deurenberg P. (1996) A comparison of body fat estimates using anthropometry and bioelectrical impedance analysis with distinct prediction equations in elderly persons in the republic of Guatemala. Nutrition 12:168-175.[Medline]
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