Editorial. The thrifty genotype hypothesis: concepts and evidence after 30 years. Boyd Swinburn
Abstracts
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Overview of the thrifty genotype hypothesis
Kerin O'Dea
Asia Pacific Journal of Clinical Nutrition (1995) Volume 4, Number 4: 339-340
The thrifty genotype hypothesis was proposed by Neel in 1962 to explain the increasing incidence of diabetes in the western world. Since then it has been invoked frequently to explain the epidemics of obesity and non-insulin dependent diabetes (NIDDM) in populations all over the world as they have made the rapid transition to a westernised lifestyle in the twentieth century. An examination of the archaeological record indicates that human populations were exposed to nutritional stresses throughout history (both as hunter-gatherers and agriculturalists) which could have selected strongly for a "thrifty" metabolism. The metabolic basis of the "thrifty" genotype has been attributed to selective insulin resistance, in which the gluco-regulatory pathways of insulin action are affected primarily, thereby promoting compensatory hyperinsulinaemia and overstimulation of those pathways less affected by insulin resistance such as those involved in fat deposition. Both physical inactivity and an energy-dense diet high in saturated fat and fibre-depleted carbohydrate have been shown to increase insulin resistance. Thus, key components of the western lifestyle act to exacerbate insulin resistance and facilitate weight gain, which itself also worsens insulin resistance. Finally, Hales and Barker have argued provocatively for a "thrifty" phenotype as the major predisposing factor in NIDDM: that poor nutrition in the perinatal period is associated with increased risk of NIDDM in adulthood, mediated either through sustained effects on -cell function or insulin sensitivity. The difficulties in differentiating between "nature" and "nurture" in the aetiology of this complex condition cannot be overstated.
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"Civilisation" and the thrifty genotype
J 1000 ohn S Allen and Susan M Cheer
Asia Pacific Journal of Clinical Nutrition (1995) Volume 4, Number 4: 341-342
Over the past 30 years, Neel's "thrifty" genotype concept has received much support from investigators interested in diabetes and the health consequences of changing from traditional to more westernised diets. In many cases, the "thrifty" genotype was interpreted in a local context by people working in a limited geographical area. It is increasingly clear, however, that the "thrifty" genotype effects are present in populations throughout the world. In fact, there is a good chance that the majority of the world's population do indeed carry the "thrifty" genotype, although since a westernised diet is far from universally available, the negative consequences of the genotype have yet to be expressed.
Diabetes, obesity, and other diseases may indeed be the price paid for civilisation in the context of a "thrifty" genotype. We point out, however, that the negative consequences of the "thrifty" genotype seen in modernising populations with westernised diets today do not necessarily provide an explanation for why the "thrifty" genotype disappeared from some populations (mostly European and European-derived) in the past. Our assumption is that given its broad distribution today, the "thrifty" genotype was once universal in human populations; the problem then, is to explain the evolution of the "non-thrifty" genotype in those populations in which it is no longer seen.
The idea that "civilisation" has worked to select out (or relax selection for) the "thrifty" genotype is untenable, although this is the view accepted implicitly by most workers in the field. To be fair, it should be pointed out that they are mostly concerned with explaining the presence, not absence, of diabetes and other diseases in certain populations, and the "thrifty" genotype serves this purpose.
There are several reasons to not accept the face validity of the idea that civilisation has selected out the "thrifty" genotype:
In summary, the idea that civilised populations have provided a flush dietary environment for thousands of years is insupportable, and opportunities for the expression of negative sequelae of the "thrifty" genotype in European populations, for example, have occurred only relatively recently (less than l00 years). In other words, all things being equal, a typical consumer in the year 1650 say, no matter where he or she lived, would have benefited more from possessing a "thrifty" genotype, than from not possessing it. But given that today mos 1000 t European populations would appear to have a "thrifty" genotype frequency of less than 10% (and some much less), and the opportunities for strong selection against the genotype have been relatively rare over the past few hundred years, how can we explain the high frequency of the "non-thrifty" genotype in these populations? We see four possible explanations:
Besides the "thrifty" genotype, Europeans are out-of-step with most of the rest of the world in that they (or at least most of them) can digest lactose (the sugar found in mammalian milk) throughout their lifetimes, and do not turn off the production of the enzyme lactase at weaning as most normal mammals do. Selection for this ability is clearly associated with the herding of cows and other milk-producing animals, who provide a good, potentially steady nutritional source. More critically in the European context may be that lactose facilitates the absorption of calcium, and in high-latitude areas with low sunlight, acts as a substitute in calcium metabolism for vitamin D, which is normally synthesised with exposure to sunlight. Consumption of lactose therefore protects against rickets and other diseases or conditions associated with low calcium intake.
We have looked at more than 40 populations for which data are available concerning both lactose absorption rates and type II diabetes rates. Overall, there is an absence of populations exhibiting high lactose absorption rates and high diabetes rates. For the total sample, the (negative) correlation between lactose absorption and diabetes rate is significant although not particularly high. If we remove from consideration populations that were not likely to have had westernised diets (eg, in PNG, Africa, perhaps in Northern Canada) at the time of diabetes assessment, then the correlation is much stronger. Further, although the data for the Pima and Papago are in the "right" direction (ie, very low lactose absorption rates and high diabetes rates), their inclusion in the data set reduces the correlation as derived from the rest of the world's populations, 1000 since their diabetes rates are almost double that for any other population. In summary, diabetes rates and lactose absorption rates are highly negatively correlated in populations with a westernised diet.
Why should this be the case? At a metabolic level, there is no direct link between the two. Whether or not one produces lactase in adulthood has nothing directly to do with how one deals with glucose in blood. In individuals with type II diabetes, there is no correlation with lactose absorption ability. However, studies indicate that although lactose is a disaccharide (glucose-galactose; the galactose is converted to glucose in the liver), it is absorbed very quickly into the bloodstream and is metabolised essentially as a simple sugar. Furthermore, the insulin response to lactose in milk is five times higher than would be expected, and approaches that for straight glucose. If there is a primary difference between westernised and traditional diets, it is the substitution of simple sugars in the diet in place of complex carbohydrates.
Since the correlation between lactose absorption and the "non-thrifty" genotype cannot be explained physiologically, then perhaps an historical explanation is worth considering. The consumption of lactose was selected for in certain populations, perhaps due to the combined effects of milk availability, high latitude, and the facilitation of calcium uptake. Individuals who consume milk do have an increased simple sugar load relative to that typically seen in a hunter-gatherer diet. Thus the ability to consume lactose constituted a change in the environment in which the "thrifty" genotype was expressed. Although there was not necessarily an overall increase in the quality of the diet or in calories available in these populations, there was a dietary stress that could have lead to selection against the "thrifty" genotype, especially if the short-term benefits of consuming lactose (which would have a greater influence in early life) outweighed the long-term benefits of the "thrifty" genotype.
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Insulin resistance and low metabolic rate: do they cause obesity?
Boyd Swinburn
Asia Pacific Journal of Clinical Nutrition (1995) Volume 4, Number 4: 343-344
Insulin resistance and obesity have genetic determinants which are separate and probably polygenic. Under certain environmental conditions, both probably offer selective advantages for survival. Under modern environmental conditions, a genetic predisposition to both would result in marked insulin resistance and be a major risk for the development of NIDDM. A low relative metabolic rate and a high insulin sensitivity have been shown to predict weight gain. However, upon the weight gain these "metabolic risks" appear to normalise thus raising doubts about whether these factors are truly aetiological. The thrifty genotype hypothesis remains a valid construct to explain the presence of common, genetically-determined factors which are currently detrimental to health, however, the original mechanisms proposed by Neel of an "efficient" metabolism or hyperinsulinaemia need considerable rethinking in light of 30 years of evidence.
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Role of amylin in the regulation of energy metabolism in health and disease
Garth JS Cooper
Asia Pacific Journal of Clinical Nutrition (1995) Volume 4, Number 4: 345
Islet -cells play a central role in the regulation of most cells in the body through secretion of the hormone insulin. These cells are now known to secrete a second hormone-like protein, amylin, which is the major protein present in the islet amyloid which accumulates in almost all patients with non-insulin-dependent diabetes mellitus.
Amylin stimulates the breakdown of glycogen and opposes the actions of insulin in skeletal muscle and liver through alterations it evokes in the activity of key regulatory enzymes such as glycogen phosphorylase and glycogen synthase. It acts as a noncompetitive antagonist of insulin in skeletal muscle, and is able to induce a state of insulin resistance and suppressed insulin secretion when administered to living animals. It has also been shown to potently increase blood concentrations of glucose and lactate, probably through stimulation of the indirect Cori cycle. These actions of amylin are consistent with a view that it is a physiological regulator of carbohydrate metabolism, acting in concert with insulin to promote the redistribution of carbohydrate from muscle glycogen to long term stores in adipose tissue.
It has been postulated that amylin is a newly-recognised endocrine hormone which regulates fuel metabolism in association with other metabolic, endocrine and neural influences. Moreover, excessive pancreatic production leading to elevated blood concentrations of amylin has now been shown to occur in numerous animal models, as well as in humans with impaired glucose tolerance and obesity. This defect has been advanced as a mechanism underlying the insulin resistance which accompanies, and may well cause these conditions.
This presentation will review currently available evidence concerning the role of amylin in the physiological and pathological regulation of fuel metabolism. In it, the author submits that relative hyperfunction of pancreatic islet -cells, giving rise to hyperamylinaemia as well as hyperinsulinaemia, is a key mechanism underlying the metabolic changes which characterise and define the "thrifty" genotype.
Reference
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Ethnic comparisons in diabetes and insulin levels
David Simmons
Asia Pacific Journal of Clinical Nutrition (1995) Volume 4, Number 4: 346-348 1000
The prevalence of non insulin dependent diabetes mellitus (NIDDM) is increasing exponentially. While the genetic causes of NIDDM remain unclear, the differences in prevalence of NIDDM over time, between and within different ethnic groups highlight the importance of environmental factors in the development of NIDDM in any given individual. Besides the classical risk factors for NIDDM such as obesity and indolence, the role of intra-uterine over-exposure or deficit of nutrients is increasingly felt to be of importance in the aetiology of NIDDM. Indeed, ethnic differences in hyperinsulinaemia, can be detected at birth in some populations. In utero exposure to increased fuel supply may be of particular importance in Polynesian and American Indian populations. If this is so, efforts to control NIDDM will take several generations to be successful.
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Intrauterine nutrition and adult disease
Jane Harding
Asia Pacific Journal of Clinical Nutrition (1995) Volume 4, Number 4: 349
Professor Barker and colleagues have published a large series of epidemiological studies showing that body size and shape at birth are strong predictors of the subsequent risk of developing several adult diseases including coronary artery disease, hypertension, chronic lung disease and non-insulin dependent diabetes. These effects of birth phenotype are independent of other known risk factors, and grow stronger with increasing age. We have put forward the hypothesis that intrauterine nutrition determines birth phenotype, and it also determines the programming of a number of key homeostatic systems in a way which predisposes to adult disease. Thus the association between birth phenotype and adult disease is determined by nutrition of the fetus before birth. Although the mechanisms are not yet known, animal studies are beginning to demonstrate that intrauterine nutrition does affect fetal growth, cardiovascular and metabolic status. Intrauterine nutrition also may have effects that last over more than one generation.
There is extensive evidence from animal studies that intrauterine nutrition affects birth phenotype. In sheep, severe maternal undernutrition for just 10 days in late gestation (term = 145 days), results in fetuses with greatly enlarged hearts and kidneys, but small lungs. Maternal undernutrition around the time of conception results in a fetus that grows relatively slowly in late gestation and is partially protected from these effects. Development of coronary artery walls may also be altered by the same maternal nutritional insult.
We also have evidence in fetal sheep studies that intrauterine nutrition affects fetal metabolism and cardiovascular status. Slowly growing fetal sheep are relatively insulin resistant in utero. Fetuses undernourished for 10 days in late gestation develop hypertension during the 10 days of refeeding. Preliminary results also suggest that the relationship between birth size and blood pressure persists in lambs for at least the first few months after birth.
The effects of intrauterine nutrition are not just confined to later life of the affected fetus. Rats marginally undernourished for seven generations take three generations of nutri 1000 tional rehabilitation to reach the size of control animals. Those re-fed at weaning in the first generation may become obese. Similarly, in human studies severe maternal undernutrition in early pregnancy has been associated with an increased rate of obesity in the offspring. Reports from the Dutch famine suggest that baby girls exposed to undernutrition in utero in early gestation themselves give birth to small babies. Thus the effect of intrauterine undernutrition may extend over at least two generations, making interpretation of some genetic studies very difficult.
Intrauterine nutrition clearly affects fetal growth, metabolic and cardiovascular status before birth. These effects may persist after birth and even over subsequent generations. The mechanisms by which intrauterine nutrition predisposes to adult disease remain to be explored.
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Strong and weak linkages in the thrifty genotype hypothesis
Paul T Baker
Asia Pacific Journal of Clinical Nutrition (1995) Volume 4, Number 4: 350
Evidence for a substantial variability in the frequency of NIDDM among Pacific island populations is now well documented. Data from the published studies support the hypothesis that this variability is in part the result of genetic differences between the populations. In the past it has been hypothesised that these differences were the result of variation in a single gene. This hypothesis appears now to be abandoned. Hopefully the high level of research currently proceeding on the human genome will soon produce some clear loci linkages to the disorder.
Whether there are one or several genes involved in producing the population differences, a major evolutionary question is how natural selection processes resulted in such population differences. Indeed, major population variability in NIDDM frequency has been recently observed in a wide variety of identifiable populations and ethnic groups. Given the clear evidence that a reasonably affluent life style is a prerequisite for the high levels of NIDDM it seems probable that even more variability in population frequency rates will soon appear as new populations increase in affluence.
The close association of increased wealth to altered diets, increased body weight and rising rates of NIDDM has made James Neel's thrifty genotype hypothesis a very attractive explanation for the very high rate in such groups as Polynesians, Micronesians, Native Americans and Australian Aborigines. Neel has in recent years become more dubious of his own hypothesis and in a 1989 publication termed it a soft hypothesis noting that "non-insulin dependent diabetes mellitus is undoubtedly quite heterogeneous in aetiology".
In a 1984 publication I explored in a preliminary fashion the inter-relationship between the demographic and genetic history of the Pacific islanders and the degenerative disorders which had become common by that time. The conceptual structure of the "thrifty" genotype seemed to fit well with the rapid and massive weight gains demonstrable in Polynesians and Micronesians. However, the linkage of NIDDM to a feast and famine history fit only some of the groups. This evidence, along with the more recent studies which demonstrate a lack 1000 of consistent physiological and biochemical linkages, suggests that a detailed examination of the Pacific populations in terms of the postulated steps of the selected process is desirable.
It has been shown that the Polynesians, and to a lesser extent Micronesians, have very heavy weights and large BMIs. Indeed it appears that Samoans are, as a population, the heaviest group in the world with the greatest average BMI. Extensive studies of the possible causes for these high weights have been conducted and will be described in detail in the lecture. The evidence suggests an ability to gain weight with a rapidity which only occurs under conditions of forced feeding in other groups. Exercise reduction below critical levels and binge eating appear the most significant behaviour associations with high body weights.
The survival and reproductive advantages which are presumed to exist for individuals who can rapidly increase in fatness is that the energy stored will keep them alive and active during periods of food shortage. Such food shortage periods can be documented for small island groups in the typhoon areas of the Pacific and can be assumed to have occurred numerous times during voyaging.
A second advantage which has not been fully considered in relation to the level of fat is the insulative value during cold exposure. Data showing the insulation and calorie saving value of subcutaneous fat will be presented at the lecture. This may also be quite significant for the explanation of high fat levels in North American natives since their ancestors passed through quite cold areas and mortality from cold exposure was possible. However, for Pacific islanders the important aspect would have been the caloric savings gained during voyaging and fishing. It should be noted that sea mammals, including those restricted to tropical waters, have very heavy subcutaneous layers of fat which are used for insulation and for energy during travel without food.
These behavioural and physiological data provide strong evidence for the suggestion that evolutionary selection would have favoured genes that produced rapid fat and muscle gain. However, it is not obvious to me why this should result in high levels of NIDDM. Certainly there is an association between BMI and NIDDM in some populations, but the linkage appears to be weak. Thus the Nauru population which has a much lower average BMI than the Samoan group with a similar exposure to affluence and imported food have a frequency of NIDDM which is several times the Samoan rate. These findings do not mean that the unusually high levels of NIDDM among some Pacific populations lack a strong genetic basis but it is likely that the selection for the ability of some Pacific populations to rapidly increase body fatness is not a sufficient cause for the unusually high frequencies occurring in selected populations.
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Thrifty genotype concepts and health in modernising Samoans
Stephen T McGarvey
Asia Pacific Journal of Clinical Nutrition (1995) Volume 4, Number 4: 351-353
Thrifty genotype concepts are described and applied to the case of increasing overweight with modernisation. The prevalence of overweight (BMI 30 kg/m2) among American Samoans and Wes 1000 tern Samoans is increasing substantially as described in surveys conducted in 1976-82 and in 1990-91. There is a possible role of insulin and the sympathetic nervous system in weight gain and energy balance. The thrifty genotype concept provides important hypotheses which can be applied to concrete studies among modernising Samoans.
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Polynesian body size: an adaptation to environmental temperature?
Philip Houghton
Asia Pacific Journal of Clinical Nutrition (1995) Volume 4, Number 4: 354-356
A computer simulation of exposure at sea in the tropical Pacific supports the hypothesis that humans colonising this region have been subject to strong directional selection for a large muscular body. This is advanced as an explanation for the typical Polynesian phenotype, and suggestions are made linking this phenotype with the metabolic disorders of gout and non-insulin dependent diabetes mellitus.
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Cultural elaborations of obesity - fattening practices in Pacific societies
Nancy J Pollock
Asia Pacific Journal of Clinical Nutrition (1995) Volume 4, Number 4: 357-360
Fattening rituals in Pacific societies are examined within a discussion of the cultural aspects of obesity as a disease of modernisation. Those rituals contributed to a strong aesthetic value of large body size and light skin, while also incorporating the symbolic value of food. They may have enhanced survival value of a genetic potential in the face of irregular diet. Today with a more regular diet available only the negative aspects of large body size prevail.
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Patterns of colonisation and the "thrifty" genotype in Pacific prehistory
Alexandra A Brewis, Geoffrey Irwin and John S Allen
Asia Pacific Journal of Clinical Nutrition (1995) Volume 4, Number 4: 361-365
The seemingly distinctive markers of Polynesian biology - serologic, molecular, anatomical, and developmental - have been argued to have emerged from the special circumstances of colonisation and early sett 1000 lement of the region. Models point to the microevolutionary impact of mortality selection while voyaging, small founding group size forcing bottlenecking, and subsequent relative isolation of groups introducing heterogeneity through genetic drift within Polynesia. These ideas have drawn on a melange of ideas about the colonising experience to construct evolutionary narratives, including that of the "thrifty" genotype in Polynesia. The substantial problem is that there previously has been no independent theory of colonisation and inter-island contact for the region. We critically examine which microevolutionary forces would have impacted prehistoric Polynesians in terms of an independent navigational theory of colonisation, and map out the expected biological/ evolutionary sequelae. This theory suggests that Remote Oceania was settled by directed return voyages, that the tempo of population expansion was probably rapid, that voyaging continued after settlement, that whereas episodes of colonisation were directed to safety, subsequent inter-group voyages followed the pattern of mutual inter-island accessibility. The implication is that mortality selection would not have been the predominant force shaping the Polynesian genotype; the development of survival sailing strategies were designed to remove these very risks. This makes it unlikely that the specific experience of Polynesian colonisation would promote an efficient insulin mechanism, and so explain, for example, the high incidence of Type II diabetes mellitus in contemporary Polynesian groups.
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Body mass index and cardiovascular risk factors in Pacific Island Polynesians and Europeans in New Zealand
Judy McAnulty and Robert Scragg
Asia Pacific Journal of Clinical Nutrition (1995) Volume 4, Number 4: 366
Relationships between body mass index (BMI) and cardiovascular risk factors were compared between European and Pacific Island (Polynesian) New Zealand residents in a cross-sectional survey of 510 (279 European, 231 Pacific Island) Seventh-day Adventist church members. Participants were recruited while attending annual camp meetings or churches and response rates were 72% for Pacific Islanders and 95% for Europeans. The age range was 39-90 years. Age adjusted BMI was higher in Pacific Islanders than Europeans (mean(SE): 32.8(0.3) v 25.6(0.3), p=0.0001). Among Europeans, BMI was positively associated (p<0.05) with systolic and diastolic blood pressure, triglyceride, total cholesterol, LDL cholesterol and fasting glucose, and negatively associated with HDL cholesterol. In contrast, BMI was only significantly (p<0.05) associated with systolic and diastolic blood pressure, and with HDL cholesterol in Pacific Islanders. Associations were stronger in Europeans compared to Pacific Islanders, there being a significant difference (p<0.05) between Pacific Islanders and Europeans in ethnic specific regression coefficients for systolic blood pressure, triglyceride, and total cholesterol. We conclude that BMI has a weaker association with cardiovascular risk factors in Polynesians than Europeans. These results suggest that interventions to decrease BMI levels in Polynesian populations may not decrease risk of cardiovascular diseases to the same extent as in European populations.
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Body mass index: is it an appropriate measure of obesity in Polynesians?
B Swinburn, P Craig, B Strauss and R Daniel
Asia Pacific Journal of Clinical Nutrition (1995) Volume 4, Number 4: 367
The body mass index (BMI) is commonly used as an estimate of obesity with 20-25 kg/m2 being considered normal. Polynesians, as individuals and populations, are often described as overweight or obese based on BMI criteria. We derived body fat measurements by bioimpedance methods in 129 adult Cook Island Polynesians and a representative sample of 505 adult Caucasian Australians using the same equation (Lukaski). As a group, the Cook Islanders were heavier (91.5 2.5 kg for men, 78.9 2 kg for women) compared to the Caucasians (80.7 1 kg for men, 66.4 1 kg for women; p < 0.0001 for both). Heights were similar and therefore the BMI values (kg/m2) were also higher in the Cook Islanders (29.6 0.7 and 29.8 0.7 versus 26.4 0.2 and 25.3 0.2; p<0.0001). Body fat, however, was lower in Cook Island men (22.0 1.0% versus 25.2 0.4%; p<0.01) and similar in Cook Island women (31.2 1.0% versus 33.0 0.3%). The following table of body fat estimations at equivalent BMI values shows that across the range Polynesians are leaner on a weight for weight basis:
Body fat (%) for males |
Body fat (%) for females |
|||
At BMI |
Polynesian |
Caucasian |
Polynesian |
Caucasian |
20 kg/m2 |
4.9 |
7.1 |
15.9 |
25.9 |
25 kg/m2 |
13.7 |
21.4 |
23.7 |
32.5 |
30 kg/m2 |
22.5 |
1000 35.7 |
31.6 |
39.2 |
40 kg/m2 |
40 |
64.2 |
47.2 |
52.5 |
In conclusion, at any given BMI Polynesian men and women are leaner than Caucasians. If these data are confirmed with more definitive body composition studies, the BMI definitions may need to be altered for Polynesians, in which case a BMI of up to about 30 kg/m2 could be considered normal.
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Do Pacific Islanders still believe that "Big is Beautiful"? Body size perceptions among Cook Islanders.
H Matangi, B Swinburn, P Craig, T Matenga-Smith, G Vaughan
Asia Pacific Journal of Clinical Nutrition (1995) Volume 4, Number 4: 368
In the traditional Polynesian societies, obesity is a mark of beauty, prestige, good health, wealth and high social ranking. Previous studies have noted that very large body sizes were particularly common amongst families of chiefs and those of high status. However, Westernisation in Polynesian societies has brought with it not only the Western perception of body size where beauty, health and high status is equated with a thin body size, particularly for women, but also increasing problems of obesity and it's related diseases.
The main aim of this study was to determine the attitudes and perceptions of body size among Cook Islands Maori living in Rarotonga in comparison with a matched Australian Caucasian sample.
The survey took part in the Tutakimoa village in Rarotonga with a response rate of 74% (83 females, 49 males). Subjects were weighed and measured to obtain their body mass index (BMI = weight in kg/ (height in m2). Using a modification of the distorting camera technique, two graded sets of photographs (one female, one male) with calculated BMls were prepared. The photographs were laid out in order of increasing size and subjects were asked to indicate the body size which best represented their actual and preferred body size. Subjects were also asked to identify the most healthy and attractive sizes for their own and the opposite sex and the acceptable range of body size for each sex. The Australian sample were matched for sex, age and BMI.
Cook Islands (CI) women were the most accurate in their perception of their current size (measured BMI for both groups = 29.9, perceived by CI = 29.2, perceived by Aust = 34.7). All groups preferred to be smaller, particularly women (preferred BMI for CI women = 23.4, Aust women = 23.6, CI men = 27.8, Aust men = 25.2). Although Cook Islanders chose larger ideal sizes than Australians for both male and female body sizes, the ideal sizes tended to increase with age particularly for CI women.
Results in 1000 dicate that Cook Islanders perceive a larger body size as ideal which is probably quite appropriate given the greater lean body mass in Polynesians. However, of note is that younger CI women had similar perceptions of ideal body size to Australian women. This suggests that the gradual reduction in the ideal and acceptable body sizes experienced in Western societies is being adopted by young Cook Islands women.
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Metabolic markers of hyperinsulinaemia in normotensive Maori and Caucasian New Zealanders
T Maling, K van Wissen, R Toomath and R Siebers
Asia Pacific Journal of Clinical Nutrition (1995) Volume 4, Number 4: 369-370
New Zealand Maori are hyperinsulinaemic and insulin resistant, compared with age- and blood pressure-matched Caucasians and are therefore an important group in which to study previously described metabolic correlates of insulin resistance, including plasma urate, triglycerides and erythrocytic sodium. Only fasting triglycerides were associated with hyperinsulinaemia. Erythrocyte sodium and plasma urate were not correlated with fasting or stimulated insulin in either race. The reduced fractional urate clearance in Maori, compared with Caucasians, was positively correlated with fractional lithium clearance (proximal tubular sodium reabsorption), suggesting an ethnically expressed dependence of urate clearance on proximal tubular sodium reabsorption. Our findings indicate the need for caution in the generalisability of the variously described "markers" of hyperinsulinaemia.
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Cigarette smoking and socio-economic indicators as determinants of body fatness in three Southern Chinese communities of China
Linda Grievink, Bridget H-H Hsu-Hage, Xuxu Rao, Mark L Wahlqvist, Yi-He Li, Kuei Zhang, Tie Han Kuang, Dao Lin Zhang, Zong Rong Dai
Asia Pacific Journal of Clinical Nutrition (1995) Volume 4, Number 4: 376-383
Obesity is one of the major risk factors for cardiovascular disease and non-insulin dependent diabetes mellitus. This study describes cigarette smoking and the socio-demographic differences of body fatness in three sub-ethnic distinctive communities in Guangdong Province, China. In this study, 935 adult Chinese (Chauzhou - 203 men and 111 women; Meixian - 169 men and 140 women; Xinhui - 194 men and 118 women) were randomly sampled from three communities. A standard protocol was used to measure stature, body weight, waist and hip circumferences. Body mass index (BMI) and waist-to-hip circumference ratio (WHR) were calculated as measures of total body fatness and abdominal body fatness, respectively. The questionnaire was self-administered and demographic and lifestyle factors were assessed. WHR was positively 78a related to age in men (p=0.0001) and in women (p=0.0001) while BMI was associated with age only in women (p=0.0001). In women, WHR was significantly related to education levels after adjusting for age and BMI (p=0.0300). In men, BMI differed by educational level, after adjusting for age and WHR (p=0.0329). BMI was significantly associated with occupational status in men, after adjusting for age and WHR (p=0.0004). Gross household income was significantly associated with WHR in men, after adjusting for age and BMI (p=0.0469). Male smokers had a significantly lower mean BMI than the non-smokers, after adjusting for age and WHR (p=0.0037). Marital status was not related to body fatness measurements after adjusting for age and WHR. The differences in body fatness in Chinese living in Southern China can not be totally explained by educational level, occupational status, marital status, gross household income and cigarette smoking, particularly in women. Age was the only consistent predictor of abdominal body fatness in both men and women and also of total body fatness in women.
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Clinical Nutrition]. All rights reserved.
Revised: January 19, 1999.