Distribution and functional consequences of nucleotide polymorphisms in the 3'-untranslated region of the human Sep15 gene.

Selenium has been shown to prevent cancer in a variety of animal model systems. Both epidemiological studies and supplementation trials have supported its efficacy in humans. However, the mechanism by which selenium suppresses tumor development remains unknown. Selenium is present in known human selenoproteins as the amino acid selenocysteine (Sec). Sec is inserted cotranslationally in response to UGA codons within selenoprotein mRNAs in a process requiring a sequence within the 3'-untranslated region (UTR), referred to as a Sec insertion sequence (SECIS) element. Recently, a human Mr 15,000 selenoprotein (Sep15) was identified that contains an in-frame UGA codon and a SECIS element in the 3'-UTR. Examination of the available cDNA sequences for this protein revealed two polymorphisms located at position 811 (C/T) and at position 1125 (G/A) located within the 3'-UTR. Here, we demonstrate significant differences in Sep15 allele frequencies by ethnicity and that the identity of the nucleotides at the polymorphic sites influences SECIS function in a selenium-dependent manner. This, together with genetic data indicating loss of heterozygosity at the Sep15 locus in certain human tumor types, suggests that Sep15 may be involved in cancer development, risk, or both.

Maintenance of lower proportions of (n - 6) eicosanoid precursors in phospholipids of human plasma in response to added dietary (n - 3) fatty acids.

Competition between the (n - 3) and (n - 6) types of highly unsaturated fatty acids can diminish the abundance of (n - 6) eicosanoid precursors in a tissue, which in turn can diminish the intensity of tissue responses that are mediated by (n - 6) eicosanoids. The mixture of 20- and 22-carbon highly unsaturated fatty acids maintained in the phospholipids of human plasma is related to the dietary intake of 18:2 (n - 6) and 18:3 (n - 3) by empirical hyperbolic equations in a manner very similar to the relationship reported for laboratory rats (Lands, W.E.M., Morris, A. and Libelt, B. (1990) Lipids 25, 505-516). Analytical results from volunteers ingesting self-selected diets showed an inter-individual variance for the proportion of (n - 6) eicosanoid precursors in the fatty acids of plasma phospholipids of about 5%, but the variance among multiple samples taken from the same individual throughout the day was less (about 3%), closer to the experimental variance of the analytical procedure (about 1%). The reproducibility of the results makes it likely that analysis of fatty-acid composition of plasma lipids from individuals will prove useful in estimating the diet-related tendency for severe thrombotic, arthritic or other disorders that are mediated by (n - 6) eicosanoids. Additional constants and terms were included in the equations to account for the effects of 20- and 22-carbon highly unsaturated (n - 3) fatty acids in the diet. A lower constant for the 20- and 22-carbon (n - 3) fatty acids compared to that for the 18-carbon (n - 3) fatty acid in decreasing the ability of dietary 18:2 (n - 6) to maintain 20:4 (n - 6) in tissue lipids confirmed the greater competitive effectiveness of the more highly unsaturated n - 3 fatty acids in the elongation/desaturation process. Also, a lower constant for direct incorporation of 20-carbon fatty acids of the n - 6 vs. the n - 3 type indicated a greater competitive effectiveness of 20:4 (n - 6) relative to 20:5 (n - 3) in reesterification after release from tissue lipids. The equations may be used in reverse to estimate the dietary intakes of the (n - 3) and (n - 6) fatty acids by using the composition of the fatty acids that had been maintained in plasma lipids.

Dietary protein and weight reduction: a statement for healthcare professionals from the Nutrition Committee of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association.

High-protein diets have recently been proposed as a "new" strategy for successful weight loss. However, variations of these diets have been popular since the 1960s. High-protein diets typically offer wide latitude in protein food choices, are restrictive in other food choices (mainly carbohydrates), and provide structured eating plans. They also often promote misconceptions about carbohydrates, insulin resistance, ketosis, and fat burning as mechanisms of action for weight loss. Although these diets may not be harmful for most healthy people for a short period of time, there are no long-term scientific studies to support their overall efficacy and safety. These diets are generally associated with higher intakes of total fat, saturated fat, and cholesterol because the protein is provided mainly by animal sources. In high-protein diets, weight loss is initially high due to fluid loss related to reduced carbohydrate intake, overall caloric restriction, and ketosis-induced appetite suppression. Beneficial effects on blood lipids and insulin resistance are due to the weight loss, not to the change in caloric composition. Promoters of high-protein diets promise successful results by encouraging high-protein food choices that are usually restricted in other diets, thus providing initial palatability, an attractive alternative to other weight-reduction diets that have not worked for a variety of reasons for most individuals. High-protein diets are not recommended because they restrict healthful foods that provide essential nutrients and do not provide the variety of foods needed to adequately meet nutritional needs. Individuals who follow these diets are therefore at risk for compromised vitamin and mineral intake, as well as potential cardiac, renal, bone, and liver abnormalities overall.

Insulin-like growth factor I and low-density-lipoprotein cholesterol in women during high- and low-fat feeding.

In vitro studies suggest that insulin-like growth factor I (IGF-I) may modulate hepatic production and peripheral utilization of lipoproteins. We measured blood concentrations of IGF-I; total, high-density-lipoprotein, and low-density-lipoprotein (LDL) cholesterol; and apolipoproteins in 18 women with above average cholesterol after high- and low-fat diet periods. Total cholesterol fell 6% (P less than 0.02) during the low-fat diet because of reduced concentrations of LDL cholesterol (P less than 0.01). Serum concentrations of IGF-I were inversely correlated with total and LDL cholesterol and apolipoprotein B during both high-fat (r = -0.676, P less than 0.005; r = -0.745, P less than 0.001; and r = -0.504, P less than 0.04, respectively) and low-fat (r = -0.656, P less than 0.005; r = -0.757, P less than 0.001; and r = -0.695, P less than 0.001, respectively) diets. IGF-I increased with reduced fat intake in obese subjects only. Thus, IGF-I may contribute to the regulation of LDL cholesterol in mildly hypercholesterolemic women but may not mediate the beneficial response to reduced fat intake.

Differential reduction of plasma cholesterol by the American Heart Association Phase 3 Diet in moderately hypercholesterolemic, premenopausal women with different body mass indexes.

The ability of a low-fat, low-cholesterol diet to improve the risk-factor profiles of moderately hypercholesterolemic, premenopausal women was evaluated. Nineteen women were fed a typical American diet for 1 mo, after which a low-fat diet consisting of 21% of total energy (en%) as fat, 59 en% carbohydrates, 19 en% protein, and 96 mg cholesterol/d (P:S 1.8) was given. After 5 months, total and low-density lipoprotein (LDL) cholesterol was decreased by 7% and 11%, respectively, and total triglycerides increased by approximately 30%. High-density-lipoprotein (HDL) cholesterol was decreased by 12% at month 2 and 5% at month 5 (P less than 0.05). Although HDL2 cholesterol decreased progressively throughout the diet period to -35% by month 5, HDL3 cholesterol, which decreased to -5% at month 1, increased to +7% by month 5. Of the plasma apolipoproteins only apo A-II was altered (+15%) by the diet. Body mass index correlated to baseline values and affected response to diet; only the leanest women had significant decreases in total, LDL, and HDL2 cholesterol in response to the low-fat diet.

Changes in body weight, body composition, and energy intake in women fed high- and low-fat diets.

The effects of a 20%-fat diet (LF) on total body weight, lean body weight, and adiposity were studied in 18 premenopausal women with body mass index (BMI) of 18-44. Subjects were fed a 37%-fat (HF) control diet for 4 wk followed by the LF diet for 20 wk. Total body weight, lean body weight, and fat weight were measured at the end of the HF and LF dietary periods by hydrostatic weighing. Despite adjustments in energy intake to maintain weight throughout the study, subjects exhibited a 2.8% decrease in total body weight (P less than 0.0006), an 11.3% decrease in fat weight (P less than 0.0001), and a 2.2% increase in lean body weight (P less than 0.0149) by the end of the LF period. Similar changes were observed in obese (BMI greater than 30) and non-obese women (BMI less than 30). By the end of the LF period, energy intake had increased significantly in comparison with the HF diet (119% of the HF intake, P less than 0.0001). Results could not be explained by changes in daily activity levels and suggest that macronutrient composition plays a role in energy requirements for weight maintenance.

The influence of cigarette smoking on the association between body weight and mortality. The Framingham Heart Study revisited.

PURPOSE: To calculate for two measures of obesity, the Metropolitan Relative Weight (MRW) and body mass index (BMI), the value at which minimum mortality occurs. This was done to retest the hypothesis, in the Framingham Heart Study data, that the association between obesity and mortality can be obscured by an interaction between the measure of obesity and smoking. In the original analysis of the Framingham data it was suggested that there was a U- or J-shaped relationship between MRW and death in smokers but a linear relationship in nonsmokers. The design and setting were those of the NHLBI Framingham Heart Study. METHODS: The 5209 members of the Framingham Heart Study underwent a baseline examination in 1948-1952 (Exam 1) and they were reexamined at approximately two-year intervals over a 30-year period. The study included both men (n = 2336) and women (n = 2873) in the age range of 28 to 62 years. After excluding persons with missing baseline data, the analytic sample size was 5163. Additional analyses were conducted by deleting persons with cardiovascular disease (CVD) at baseline (n = 135), the sample used by the original paper by Garrison and colleagues, and persons who died within the first four years of follow-up (n = 62). The main outcome measures consisted of thirty-year survival through Exam 16, approximately in 1980, as influenced by MRW or BMI, age, and smoking status at baseline (Exam 1). RESULTS: We were able to show that the sample sizes of male nonsmokers were too small to test the hypothesis within age groups < 40 and 40-49 years. In men ages 50-62 there was a significant age-adjusted quadratic relationship between BMI or MRW, and risk of death. The estimated BMI at the minimum risk of death for smokers (24.5) and nonsmokers (23.8) were not statistically different. Identical results were found for MRW (minimum: smokers = 112.5, nonsmokers = 111.4). In men and women ages 28-62 there appeared to be a u- or j-shaped relationship between the 30-year crude mortality rate and MRW. After excluding persons with missing data, CVD at baseline, and persons who died within the first four years of follow-up, the age adjusted estimated BMI value at the minimum risk of death was nearly identical for men and women and for smokers and nonsmokers (Men: smokers = 22.8, nonsmokers = 22.8; Women: smokers = 22.9, nonsmokers = 23.3). Additionally, the estimates of the minimum were always below the mean. Identical results were found without deleting persons with CVD at baseline and deaths in the first four years of follow-up. Identical results were found for MRW. CONCLUSIONS: Reanalysis of the Framingham Heart Study data does not support the hypothesis that there is an interaction between smoking and measures of obesity. Moreover, the estimated BMI or MRW at the minimum risk of death was similar for men and women smokers and nonsmokers alike even after deleting prevalent cases of CVD and deaths within the first four years of follow-up.

Relative weight and mortality in U.S. blacks and whites: findings from representative national population samples.

PURPOSE: To examine the impact of relative weight on mortality in black and white men and women. METHODS: Two representative national populations samples were used: the NHANES-I Epidemiologic Follow-up Study (NHEFS), and the National Health Interview Survey (NHIS). The principal analysis focused on 13,242 participants in the NHEFS and 114,954 in the NHIS. Minimum mortality was estimated from both categorical analysis and a logistic model. RESULTS: Minimum mortality ranged from a body mass index (BMI) of 25 to 32 kg/m2. The model-estimated BMI of minimum mortality for NHEFS was 27.1 (24.8-29.4, 95% CI), 26.8 (24.7-28.9, 95% CI), 24.8 (23.8-25.9, 95% CI) and 24.3 (23.2-25.4, 95% CI); for black men, black women, white men and white women, respectively, whereas for NHIS the corresponding values were 30.2 (24.8-35.6, 95% CI) 26.4 (24.2-28.7, 95% CI), 27.1 (25.5-28.7, 95% CI), and 25.6 (24.2-27.0, 95% CI). In all groups the shape of the relative risk curve was virtually identical and a broad range of BMI values in the middle of the distribution was associated with low relative mortality risk. Averaging the results from both surveys, the observed BMI of minimum risk was 3.1 kg/m2 higher in black men and 1.5 kg/m2 higher in black women than in their white counterparts; when adjusted for covariates these differences were only of borderline statistical significance, however. CONCLUSIONS: Because of the wide range of BMI values associated with low risk, and the consistency of the point of the up-turn in risk, group specific definitions of optimal values do not appear to be warranted.

Abdominal adiposity and clustering of multiple metabolic syndrome in White, Black and Hispanic americans.

PURPOSE: The aim of this study was to evaluate the association of abdominal adiposity assessed by waist circumference (WC) with clustering of multiple metabolic syndromes (MMS) in White, Black and Hispanic Americans. MMS was defined as the occurrence of two or more of either hypertension, type 2 diabetes mellitus, dyslipidemia, hypertriglyceridemia or hyperinsulinemia. METHODS: The number of MMS and fasting insulin (a surrogate measure of MMS) were each used as dependent variables in gender-specific multiple linear regression models, adjusting for age, smoking and alcohol intake. The contribution of WC to interethnic differences in clustering of MMS and fasting insulin concentration was assessed in gender-specific linear regression models. The risk of MMS due to large waist was estimated by comparing odds ratio for men with WC >/= 102 cm with those with WC < 102, and women with WC >/= 88 cm with women with WC < 88 cm in the logistic regression model adjusting for age, smoking and alcohol intake. RESULTS: WC was positively and independently associated with clustering of MMS and increased fasting insulin concentration adjusting for age, smoking and alcohol intake in the three ethnic groups (p < 0.01). Black ethnicity was associated with clustering of MMS and fasting insulin concentration (p < 0.01). Hispanic ethnicity was also associated with clustering of MMS in men and associated with fasting insulin concentration in both men and women (p < 0.01). In both men and women, the risk of MMS clustering was strongly associated with increased WC in all ethnic groups independent of BMI. CONCLUSION: WC appears to be a marker for multiple metabolic syndromes in these ethnic groups. The results of this investigation lend support to the view that waist measurement should be considered as a clinical variable for assessing the risk of cardiovascular diseases.

Participation of minorities in cancer research: the influence of structural, cultural, and linguistic factors.

Overall, participation rates in cancer clinical trials are very low, ranging from 3 to 20% of eligible participants. However, participation rates are especially low among the socially disadvantaged and racial/ethnic minority groups that have been historically underrepresented in clinical research. Structural factors such as study duration, treatment or intervention schedule, cost, time, followup visits, and side effects represent more of a barrier to participation among these groups compared with white, non-Hispanics. Attitudes, beliefs, perceptions, and knowledge regarding clinical research, and cultural characteristics of underrepresented minorities pose additional barriers to participation. This article focuses on the structural, cultural, and linguistic factors that affect participation in clinical cancer research for each major U.S. racial/ethnic group. Low socioeconomic status, speaking a primary language other than English, differences in communication styles, mistrust of research and the medical system, fear, embarrassment, and lack of knowledge about the origin of cancer appear to have a negative impact on clinical cancer research participation rates. Much of the information about these factors comes from studies of cancer screening because little data is available on the factors that prevent and facilitate participation of minorities in clinical cancer trials specifically. Such research is needed, and, given the heterogeneity within and between minority populations, should occur in several different geographic settings and with as many different minority subpopulations as possible.

Abdominal obesity in the United States: prevalence and attributable risk of hypertension.

OBJECTIVE: The aim of this study was to determine the prevalence of abdominal obesity and its impact on the risks of hypertension in the US adult population. DESIGN AND METHODS: Data from the third US National Health and Nutrition Examination Surveys, 1988-1994, were utilised. Abdominal obesity was defined as waist circumference > or =102 cm in men and > or =88 cm in women. Hypertension was defined as mean diastolic blood pressure > or =90 mm Hg, systolic blood pressure > or =140 mm Hg or current treatment with prescribed hypertension medication. Prevalences of abdominal obesity were estimated in non-Hispanic White, non-Hispanic Black and Hispanic Americans. Gender-specific logistic regression analysis using empirical waist cut-off points was used to determine the risks of hypertension. The impact of abdominal adiposity on risk of hypertension was estimated from population-attributable risk adjusting for age, current smoking and alcohol intake. RESULTS: The prevalences of abdominal obesity were 27.1%, 20.2% and 21.4% in White, Black and Hispanic men, respectively. The corresponding values in women were 43.2%, 56.0% and 55.4%. Abdominal obesity was found to be associated with a two to three-fold increased risk of hypertension in this population. In men, the attributable risk percent ranged from 20.9% in Hispanics to 27.3% in Whites and in women ranged from 36.5% in Whites to 56.5% in Hispanics. We estimated that 24 million adult men and 40 million adult women of Hispanic and non-Hispanic Black and White ethnicity were suffering from abdominal obesity. CONCLUSIONS: In this population, hypertension appears to be associated with abdominal obesity. The estimates of population attributable risks suggest that the risk of hypertension could be potentially reduced if waist size were reduced to <102 cm in men and <88 cm in women.

One size fits all: implications for assessing dietary behavior.

Accurate assessment of dietary behavior is central to the design, implementation, and evaluation of intervention programs aimed at behavior change, and use of an Eating Behaviors Questionnaire (EBQ) has been suggested for measuring dimensions of dietary fat behavior. The EBQ has proven useful in characterizing fat-related dietary patterns among middle-class, highly educated, highly motivated white women. To investigate the generalizability of the instrument, we provide findings from a community-based sample of 235 African-Americans in Maywood, Illinois, a middle-class working community outside Chicago. The sample consisted of 159 women and 76 men with an average age of 47.4 +/- 13.8 years for women and 48.1 +/- 12.1 years for men (mean +/- standard deviation; range, 18 to 87 years). The EBQ is based on four broad behavioral domains (ie, avoidance, modification, substitution, and replacement) associated with fat-related eating patterns. These behavioral domains are composed of specific dietary behaviors (factors). Using a scoring system that allowed all participants to be included in all analyses, we identified a set of factors characterizing eating patterns in our sample that differed from those reported previously. When the factors were converted to scales using unit scoring, the average value suggested a tendency toward a higher fat eating pattern. Results indicate that although behavioral domains appear to be constant across populations, fat-related eating patterns are not. These observations have implications for understanding the diversity of fat-related dietary patterns across groups and for planning appropriate behavior change strategies.

Internal locus of control and social support associated with some dietary changes by elderly participants in a diet intervention trial.

OBJECTIVE: Measure relationships of locus of control and social support to diet changes in an intervention trial. DESIGN: Participants in the Polyp Prevention Trial (PPT) completed Multidimensional Health Locus of Control (MHLC) and Norbeck Social Support Questionnaires (NSSQ) and modified Block food frequency questionnaires. Data were collected at baseline and 1 year later. SUBJECTS/SETTING: A convenience sample of PPT intervention (N = 68) and control (n = 43) participants at 1 clinical center participated in this ancillary study. MAIN OUTCOME MEASURES: Mean daily dietary intakes after 1 year were compared with baseline values. Intervention participants' scores for MHLC internal locus of control and NSSQ total functional network were correlated with diet changes. STATISTICAL ANALYSES PERFORMED: Group percentages were compared using the Fisher exact test; means were compared by t test. RESULTS: Groups were comparable in demographics, baseline diet, and scores for internal locus of control and total functional network. Intervention group participants made greater diet changes than control participants in intake of fat (-27 g vs -8 g), fat as a percentage of kilocalories (-8% vs -2%), fiber as grams per 1,000 kcal (7 g vs 0.3 g), and daily fruit/vegetable servings (2.0 vs 0.2). Pearson correlations of diet changes with internal locus of control scores (all P > .05) were fat grams, r = 0.031; fat as percentage of kilocalories, r = 0.023; fiber grams per 1,000 kcal; r = 0.230; and fruit/vegetable servings, r = 0.186. Correlations with total functional network scores were: fat grams, r = 0.022 (P > .05); fat as percentage of kilocalories, r = -0.108 (P > .05); fiber grams per 1,000 kcal, r = 0.276, P < .05; and daily fruit/vegetable servings, r = 0.326, P < .05. APPLICATIONS/CONCLUSIONS: Intensive and skillful dietary intervention can succeed whether or not clients bring strong internal locus of control or social support to the diet change program.

The relation of central adiposity to components of the insulin resistance syndrome in a biracial US population sample.

The higher rates of type 2 diabetes mellitus, hypertension, and many others factors of the insulin resistant syndrome (IRS) often seen in African Americans compared to whites do not seem to be explained by differences in central obesity. Reasons for this may be due, in part, to the validity of the commonly used anthropometric surrogate of central adiposity. Recent findings have shown that waist circumference is a better surrogate of total body and visceral adipose tissue and is better correlated with CVD than the traditionally used anthropometric indexes of the body mass index or waist/hip ratios. In this study, waist circumference was employed to determine the association between central adiposity and components of the insulin resistance syndrome in blacks (N=1963) and whites (N=4894) from the US national population-based samples. Sex-specific correlation coefficients were used to estimate the association between waist circumference and factors of the IRS. Multiple linear regression analyses were used to determine racial differences in waist circumference and the independent association of waist circumference to some known factors of IRS adjusting for age, BMI, alcohol use, and smoking. Waist circumference was positively correlated with plasma glucose, DBP, SBP, LDL cholesterol, fasting insulin, serum triglyceride, total cholesterol and total cholesterol/HDL ratio in black and white men and women (P<0.01). In both biracial groups, waist circumference was significantly associated with increases in glucose, DBP, LDL cholesterol, total cholesterol, triglyceride and fasting insulin levels controlling for age, BMI, and behavioral risk factors, such as alcohol use and smoking (P<0.05). Our data shows that central adiposity assessed with waist girth did not wholly explain the higher prevalence of IRS components often seen among blacks. The results of this study reinforce the need to encourage the use of waist measure as a public health tool in screening for CVD risks.

Nutrient intake, lipids, and lipoprotein cholesterols in black and white children: the Lipid Research Clinics Prevalence Study.

Our specific aim was to assess differences in nutrient intake and in lipids and lipoprotein cholesterols between blacks and whites in 259 black children (129 boys, 130 girls) and in 811 white children (424 boys, 387 girls) ages 5-19. The nutrient intake data were obtained by 24-hr recall from the Houston and Cincinnati Lipid Research Clinics. The fundamental nutrient differences between blacks and whites were in total calories and in calories per kilogram of body weight, both of which were uniformly and significantly lower among black than white boys and generally, but less consistently and significantly, lower among black than white girls. No racial differences in total cholesterol or cholesterol intake per kilogram body weight were observed. After statistically controlling for education of the head of household, there were no consistent significant racial differences in Quetelet index. There was no significant independent effect of education of head of household on the children's caloric intake and racial differences in socioeconomic status did not appear to systematically account for differences in total energy intake. In aggregate, black children had lower triglyceride and very-low-density lipoprotein cholesterol levels, and higher levels of high-density lipoprotein cholesterol than whites; there were no significant differences by race in low-density lipoprotein cholesterol levels. Race was a significant independent explanatory variable for high-density lipoprotein cholesterol levels (higher in blacks) and for very-low-density lipoprotein and triglyceride levels (higher in whites) (P less than 0.005), after covariance adjusting for education of head of household, sex, age, Quetelet index, calories, saturated fat (g/day/kg body wt), and clinic. Lower caloric intake among blacks compared with whites, the major nutrient difference in the current study, did not account for differences in lipoprotein cholesterol levels between the two groups.

Relationship of serum immunoreactive somatomedin-C to dietary protein and energy in growing rats.

Protein-energy undernutrition has its most devastating consequences during growth. Postal somatic growth now appears to be regulated in large part by the somatomedins, a family of growth hormone-dependent peptide mitogens. This study, using growing rats as the model, was designed to determine the relationship between protein and energy intake and serum immunoreactive somatomedin-C. Four-week-old male Sprague-Dawley rats were fed ad libitum three levels of isoenergetic protein diets (5%, 10%, and 15% lactalbumin) at each of three levels of energy (ad libitum, 75% or 50% of ad libitum quantities). Dietary fat was held constant at 11.9% as cottonseed oil. At 5 weeks of age, serum somatomedin-C concentration was predominately influenced by the dietary protein and increased linearly as protein intake increased from 5% to 15%. at 6, 9, and 12 weeks of age, serum somatomedin-C concentration was influenced by both protein and energy intake, although protein intake appeared to be the more important variable. Serum somatomedin-C was highly correlated with both body weight (r = 0.84, P less than 0.001) and tail length (r = 0.74, P less than 0.01). These results indicate that measurement of immunoreactive somatomedin-C provides a valuable biochemical index of protein-energy nutriture.

Association of waist circumference with ApoB to ApoAI ratio in black and white Americans.

BACKGROUND: Although numerous studies have demonstrated obesity as an aspect of the insulin resistance syndrome in cardiovascular disease (CVD), the mechanism is not clear. Central adiposity, acting through many CVD risk factors, including, plasma glucose, insulin, total cholesterol, low density lipoprotein-cholesterol (LDL-C) and lipoprotein moities-apolipoprotein B (ApoB), apolipoprotein A-I (ApoAI), by atherogenic and thrombotic mechanisms has been proposed as a possible mechanism. In this study, we examined the relationship between central fat distribution (defined by waist circumference) and the ratio of these lipoproteins (ApoB/ApoAI). SUBJECTS AND METHODS: Association between ApoB/ApoAI ratio and waist circumference was compared in Blacks (n = 854) and Whites (n = 2552) using the NHANES III population-based samples. Correlation analyses and multiple regression analyses were used to determine the association between ApoB/ApoAI and waist circumference, controlling for age, body mass index (BMI), race, gender, plasma glucose, insulin, serum triglyceride and total cholesterol. RESULTS: Adjusting for age, ApoB/ApoAI was significantly correlated with waist circumference (Black men: r = 0.38, White men: r = 0.26, Black women: r = 0.20, White women: r = 0.36) (all P < 0.01). Adjusting for age and triglyceride or insulin, waist circumference was also positively correlated with CVD risk factors including, ApoB, LDL-C, plasma glucose and fasting insulin, and inversely correlated with ApoAI and HDL-C in Blacks and Whites (P < 0.05). Overall, triglyceride and total cholesterol were the strongest predictors of ApoB/ApoAI in Blacks and Whites adjusting for age, BMI and insulin, than waist girth (P < 0.01). CONCLUSIONS: The result of this study suggests the need to investigate ApoB/ApoAI as another possible facet in the insulin resistant syndrome.

Nutritional consequences of the African diaspora.

Along with their foods and dietary customs, Africans were carried into diaspora throughout the Americas as a result of the European slave trade. Their descendants represent populations at varying stages of the nutrition transition. West Africans are in the early stage, where undernutrition and nutrient deficiencies are prevalent. Many Caribbean populations represent the middle stages, with undernutrition and obesity coexisting. African-Americans and black populations in the United Kingdom suffer from the consequences of caloric excess and diets high in fat and animal products. Obesity, non-insulin-dependent diabetes mellitus, hypertension, coronary heart disease, and certain cancers all follow an east-to-west gradient of increasing prevalence. Public health efforts must focus not only on eradicating undernutrition in West Africa and the Caribbean but also on preventing obesity, hypercholesterolemia, and their consequences. Fortunately, a coherent and well-supported set of recommendations exists to promote better nutrition. Implementation of it founders primarily as a result of the influence of commercial and political interests.