Clinical Obesity in Adults and Children. Группа авторов
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Figure 1.1 Obesity prevalences in different regions of the world. Data for males are in the left block of data and females in the right‐hand series. Within each data set, the prevalences for 1980 are on the left and for 2008 on the right.
(Source: Reproduced from Finucane et al. [16].)
The INTERHEART international study later showed that waist size and W/H ratios were better indices of the risk of CHD than BMI [29]. W/H values showed marginally better statistical discrimination probably because higher hip values seem to be protective, perhaps relating to the body’s ability to safely store fat subcutaneously – on the hips. The importance of abdominal obesity as a predictor of morbidity has been shown many times, but the waist/height ratio expressed in metric units with a simple ratio cut‐off of 0.5, rather than hip circumference, seems a better and clinically more practical predictor of disease risk factors, e.g. dyslipidemia, increased blood glucose levels, or higher blood pressures [30] especially in children [31].
Different regional societal burdens of obesity with abdominal obesity
McKeigue et al. described in 1991 the propensity to abdominal obesity and thicker truncal skinfolds as being greater in South Asians than in British adults, and for each increment in waist/hip ratios, there was a greater increase in glucose intolerance, plasma insulin levels, diabetes, hypertension, and plasma triglyceride levels in the South Asians than in the British Caucasians [32]. These findings mirrored the concerns expressed by clinical researchers such as Misra et al. [33] from India, who highlighted the problem of abdominal obesity and its associated dyslipidemia at low BMIs in Indian slum dwellers. This was also noted by the subsequent WHO Singapore meeting [8] and then led the IOTF to assess whether these propensities to diabetes and hypertension were evident on a population basis by comparing Australasian data with large data sets derived from a series of studies across Asia. Iranian data were included in the reference data set from Australia and New Zealand as they were considered for practical purposes Caucasian. This addition may have been a mistake (see below), but their inclusion did not affect the overall conclusion, based on the analysis of 21 population groups with about 263,000 individuals, that those with abdominal obesity had a greater propensity to diabetes but not to hypertension, and that the Asian community was particularly prone to abdominal obesity and its hazardous consequences [30].
Genetic susceptibility could account for this Asian propensity to abdominal obesity and indeed to excess diabetes and lipid disorders at each increment of waist enlargement, or it could be attributed to other factors. A genetic basis is supported by the relatively new analyses of human evolution that have shown the different patterns of genetics as the human race evolved out of East Africa and then left Africa to evolve through the Middle East into Europe, Asia, and then across the Siberian/Alaskan link (now the Behring straits) into North America and down into Central and South America [34]. The most significant changes are those that involve the much more unstable mitochondrial DNA with its faster rate of mutation than nuclear DNA. There are very clear patterns of mitochondrial change, designated by different haplotypes, with a subset leaving Africa and subsequently evolving down multiple haplotype pathways and with some interbreeding with early hominids, the Neanderthals and Denisovans. There are mutations of mitochondrial DNA that are associated with diabetes, but as yet, there are no extensive population studies of genetics that also test for the prevalence of glucose intolerance and diabetes in populations across the world, as well as associated haplotype analyses.
This seemingly special Asian propensity to abdominal obesity and diabetes was then shown to be a more general feature when analyses of the 2006 national survey of Mexican adults found the same features – both a greater propensity to abdominal obesity and a greater prevalence of diabetes and hypertension at each increment of abdominal expansion [35] as shown in Figure 1.2. Furthermore, US studies showed that when ethnic differences were considered, Japanese Americans, as well as Hispanic Americans, were both more likely to have abdominal obesity and greater rates of diabetes at each increment of abdominal expansion than American Whites [36]. African Americans have higher BMIs than Whites or Hispanics, but their diabetes rates are even higher than one would expect for their greater size. However, attempts to identify a genetic basis for this excess diabetes in Africans have so far been unsuccessful [37], with studies of the African diaspora showing marked differences in glucose metabolism in different communities with different BMIs and degrees of abdominal obesity enhancing glucose intolerance but they were also eating different diets and with objectively measured differences in physical activity [38]. So there was no suggestion that dilution of the African genome in Jamaica and the United States had distinct weight independent effects as their results did not differ from those observed in Ghana and South Africa.
Figure 1.2 The prevalences of obesity in men and women in cohorts with over 263,000 adults either from Asia or from Australasia and Iran (depicted as Caucasians) [30]. Superimposed on this graph are data from the Mexican national survey in 2000 [35]. The Mexican study compared the national survey data with nationally representative data for US non‐Hispanic Whites, but these data are not shown in this graph as they were almost identical to those of the Australasian/Iranian data from the Asian study.
Furthermore, the seemingly genetically obesity‐prone Pima Indians from Mexico and Arizona in the United States show that with similar genetic profiles, there are big national differences in BMI and diabetes prevalences which are largely environmentally determined [39]. Very low obesity and diabetes rates occur in the hard‐working, home‐farming Pima Mexicans consuming a 25% fat, high fiber diet with a negligible sugar content [40]. So it is difficult to be sure what constitutes a greater genetic propensity to diabetes in different ethnic groups and how this relates to abdominal obesity without taking account of their prevailing diet and physical activity [41]. Indeed, the propensity to develop type 2 diabetes has been related to the duration of being overweight/obese, as well as the magnitude of excess weight [42].
The impression that Caucasians are relatively protected from diabetes associated with weight gain was further amplified by our findings in the Middle East. Carefully conducted randomly selected populations in each of the 21 countries covered by the WHO Eastern Mediterranean Region (EMR), i.e. including not only the Gulf countries, Lebanon, Syria, and the North African countries abutting the Mediterranean but also Djibouti, Somalia, Sudan, Afghanistan, and Pakistan showed (Fig. 1.3) that, despite the wide‐ranging levels of average BMI in both men and women, the national average diabetes rates are appreciably higher in the EMR than in the 28 countries of the Europe Union throughout the range of average BMIs.
Figure 1.3 The relationship between the prevalences of obesity and diabetes in each of the 21 WHO Eastern Mediterranean countries compared with equivalent data from the 28 countries of the European Union. Diabetes prevalence rates are about twice as high in the Eastern Mediterranean countries as in the European Union at equivalent obesity rates. These data are based on randomly selected adults with measured anthropometry and fasting blood glucose levels in each country undertaken according to a standard protocol (the WHO STEPS program).
(Source: Reproduced from Alwan et al. [43].)