Metabolic Syndrome Components in a Nondiabetic Afro-Caribbean Population: Influence of Gender and Age

Abstract

Background:

Our aim was to describe the prevalence of metabolic syndrome (MetS) and its components among Afro-Caribbean adults without diabetes and cardiovascular complications.

Methods:

Participants were recruited from a Health Center in Guadeloupe, French West Indies. MetS was defined according to the NCEP ATP III. Prevalence of MetS and MetS components were compared across age groups and sex. The odds ratios (ORs) and 95% confidence intervals were obtained using logistic regression.

Results:

There were 1011 participants (68.8% women, mean age 47.8 ± 11.8 years). Prevalence of MetS was 17.9% (21.1% women, 10.8% men) and increased by age in women. High blood pressure had the highest prevalence among men and among women ≥60 years. Prevalence of abdominal obesity (AbO) was higher in women than in men. High triglyceride levels were uncommon at all ages and, men and women <40 years, compared with the other groups had higher prevalence of low high-density lipoprotein cholesterol (HDL-C) levels. With multiple logistic regression, compared with adults <40 years, those ≥60 years had the highest OR for prevalent hypertension 7.8 (4.8–12.8); P < 0.001, AbO 2.1 (1.3–3.3); P = 0.002 and high fasting blood glucose levels 5.5 (3.1–9.8); P < 0.001. They also had lower odds for having low HDL-C than the younger ones (G1: age <40 years). Among persons ≥60 years, OR for MetS was 1.9 (1.1–3.6); P = 0.013 compared with the referent group. Compared with men, women had higher odds of MetS 2.2 (1.5–3.3); P < 0.001.

Conclusion:

Women were more likely to have MetS than men and persons ≥60 years were significantly more likely to have MetS than persons <40 years. Preventive measures are required to reduce the prevalence of MetS.

Introduction

Metabolic syndrome (MetS), also called insulin resistance syndrome is constituted by the clustering of several cardiovascular risk factors, including hypertension, central obesity, high fasting glucose, and dyslipidemia.^1

–4 This syndrome increases the risk of cardiovascular disease (CVD) and diabetes⁵ but, its prevalence is significantly influenced by various factors such as environment, sex, age, ethnicity, and also by the definition of MetS used.^3,6 In this line, older individuals frequently present various cardiovascular and metabolic risk factors that contribute to the increase of MetS prevalence with age. Ethnic and geographical differences in the prevalence of MetS and components in people of African ancestry (PAA) when compared with whites residing in similar locations have also been previously confirmed.^1,7

The prevalence of MetS has been assessed in various studies in PAA as the cross-sectional nationally representative health and nutrition examination survey (NHANES III),^6,8,9 which provides data for African Americans (AA) and White Americans (WA) or the Jackson Heart Study (JHS), a large prospective population-based study of African Americans¹⁰ and also in studies, including European and African-Caribbeans,¹¹ healthy Ghanaian adults,¹² or nondiabetic Ghanaians.¹³

Hypertension is found particularly prevalent among black individuals.¹⁴ A higher insulin resistance has also been reported in this ethnic group^15,16 with, paradoxically, higher high-density lipoprotein cholesterol (HDL-C) levels and lower serum triglyceride (TG) levels when compared with white counterparts.^16,17 These findings highlight the need to take gender, age, and ethnicity into account when assessing the prevalence of MetS.

In the French Caribbean Island of Guadeloupe where the majority of the population is Afro-Caribbean (about 85%), we hypothesized that the distributions of MetS and MetS components were close to those reported in other studies on PAA.

Our aim was to evaluate the prevalence of MetS and MetS components among Afro-Caribbean individuals, without diabetes and cardiovascular complications, according to gender and age while focusing on the elderly. Greater awareness of MetS, in this population, may also contribute to improve the management of risk factors and the determining of preventive measures against CVD and diabetes.

Methods

Study population

The present study included data from years 2017 to 2019, from research on cardio metabolic risk, in Guadeloupe, France. The subjects were recruited in the referral Health Center of Guadeloupe, among the individuals called by the Social Security for the performance of clinical and biological examinations.

The volunteers of 18 years of age and over, were recruited by a physician to constitute a control group, for studies on cardiometabolic risk. For this control group, pregnant women, individuals suspected of acute malignancies, inflammatory diseases, and previous cardiovascular complications (coronary artery disease, stroke, obliterating arteriopathy of the lower limbs) were not included. Within this control group, a total of 1211 Afro-Caribbean adults without known diabetes, living in Guadeloupe were selected, in which 200 individuals with fasting glucose ≥7 mmol/L and or with serum creatinine levels >1 mg/dL were also excluded. The final sample size was 1011 persons.

All participants were Afro-Caribbeans. The ethnic origin was defined whether the patient defined him/herself and his/her two first-degree relatives as Afro-Caribbeans. The protocol for studies on cardiometabolic risk was approved by the Ethics Committee (South West—Overseas III, France) (CPP: 2016 – A00241-50). All participants provided their written informed consent for this study.

Data collection

The individuals were interviewed by a physician using a standard questionnaire that required information on age, gender, history of CVDs, and use of antihypertensive or antihyperlipidemic or antidiabetic treatments.

Height and weight were measured with participants standing without shoes and lightly clothed. Body mass index was calculated as weight/height² (kg/m²). Waist circumference (WC) in centimeters was taken, with participants standing, above the iliac crests and below the lowest rib margin at minimal respiration. The measurements were made by trained nurses and physicians. Blood pressure (BP) was measured according to a standardized protocol with automatic sphygmomanometers. The retained values were the average of at least two readings.

Blood samples were obtained from participants after overnight fasting. Plasma cholesterol and TG were measured by enzymatic methods (Boehringer Mannheim).

All blood analyses were performed with standardized programs.

For MetS definition, we retained the NCEP ATP III criteria³ that includes three or more of the following abnormalities:

Hypertension: systolic blood pressure (SBP) ≥130 mmHg and/or diastolic BP ≥85 mmHg

Abdominal obesity (AbO): WC >102 cm in men or >88 cm in women,

Low high-density lipoprotein cholesterol (HDL-C) levels: HDL-C <1.04 mmol/L (40 mg/dL) in men or <1.29 mmol/L (50 mg/dL) in women,

High TG levels: TG ≥1.69 mmol/L (150 mg/dL)

High fasting blood glucose (FBG) levels: FBG ≥5.6 mmol/L (100 mg/dL).

For the purpose of this study, in individuals without diabetes, high FBG was defined as fasting glucose ≥5.6 mmol/L and <7 mmol/L.

Statistical analysis

Data are presented as numbers (percentages) for categorical variables and as mean ± standard deviations for continuous variables. Taking into account the recommendations in the NHANES Analytic Guidelines,¹⁸ the participants were stratified into three groups according to age: <40 years, 40–59 years, and ≥60 years.

The chi-squared test was used to test percentage differences between groups. To test mean differences, we used Student's t-test for comparison between genders in each age category and analysis of variance for comparison between age categories.

We used logistic regression to assess the association of hypertension, AbO, low HDL-C levels, high TG levels, high FBG levels, and MetS as binary dependent variables with sex and age categories as independent variables. Age <40 years was considered as the reference group. Adjusted odds ratios (ORs) and 95% confidence intervals (95% CI) were estimated.

The IBM SPSS Statistics software version 21.0 was used for data analyses. A P value <0.05 was considered as significant.

Results

Overall, 1011 individuals of both sexes were included in the study. The mean age of the study population was 41.4 ± 11.7 years and 68.8% were women. Participants were categorized as follows: Group 1 (G1 < 40 years; n = 260); Group 2 (G2 ≥ 40 years and <60 years; n = 604); and Group 3 (G3 ≥ 60 years; n = 147).

The clinical characteristics of participants and prevalence of MetS and MetS components, in the overall study population and by age are presented in Table 1.

Table 1.

Clinical Characteristics of Subjects and Prevalence of Metabolic Syndrome and Metabolic Syndrome Components, in the Overall Study Population and by Age Categories

N	Overall	Age
		<40 years	40–60 years	≥60 years	P
	1011	260	604	147
Continuous variables ^a
Age (years)	41.4 ± 11.7	32.5 ± 5.1	49.3 ± 5.3	66.2 ± 5.3	<0.001
SBP (mmHg)	133 ± 19	124 ± 14	135 ± 19	144 ± 23	<0.001
Diastolic BP (mmHg)	83 ± 12	79 ± 12	84 ± 12	85 ± 10	<0.001
BMI (kg/m²)	28.0 ± 6.1	28.1 ± 6.9	28.0 ± 5.9	27.9 ± 5.1	0.919
WC (cm)	89 ± 13	87 ± 14	89 ± 13	92 ± 12	0.008
HDL-C (mmol/L)	1.5 ± 0.4	1.3 ± 0.3	1.5 ± 0.5	1.5 ± 0.4	<0.001
TG (mmol/L)	1.0 ± 0.6	0.9 ± 0.7	1.0 ± 0.6	1.1 ± 0.5	<0.001
FBG (mmol/L)	1.0 ± 0.7	4.7 ± 0.6	5.0 ± 0.7	5.2 ± 0.7	<0.001
Categorical variables ^b
Sex (women) %	68.8	68.5	69.5	66.7	0.788
MetS components
Hypertension (%)	58.3	37.7	61.3	82.3	<0.001
AbO (%)	39.6	33.1	40.6	46.9	0.017
Low HDL-C (%)	27.0	39.2	22.8	22.4	<0.001
High TG (%)	8.4	7.3	8.6	9.5	0.721
High FBG (%)	16.5	7.7	16.7	31.3	<0.001
MetS (%)	17.9	15.4	17.2	25.2	0.037

Data are presented as ^amean ± SD or ^bcolumn percentage. P values: for differences between age groups.

For continuous variables: ANOVA for comparison between groups.

Significant P values are in bold.

ANOVA, analysis of variance; AbO, abdominal obesity; BMI, body mass index; BP, blood pressure; FBG, fasting blood glucose; HDL-C, high-density lipoprotein cholesterol; MetS, metabolic syndrome; SD, standard deviation; TG, triglycerides, WC, waist circumference.

Among the overall study population, prevalence of MetS was 17.9%. We noted the following prevalence for the MetS components: 58.3% for hypertension and 39.6%, 27%, 8.4%, and 16.5% for AbO, low HDL-C levels, high TG levels, and high FBG levels, respectively.

The prevalence of MetS according to age groups were as follows: 15.4% in G1, 17.2% in G2, and 25.2% in G3. Participants in G3 had higher prevalence of hypertension (P < 0.001), AbO (P = 0.017), and FBG (P < 0.001), but lower frequency of low HDL-C (P < 0.001) than the other groups.

Globally, in this population without diabetes and without cardiovascular complications, compared with women (data not shown), men were more likely to have elevated BP (65.4% vs. 55.0%; P = 0.002), high TG levels (13.0% vs. 6.3%; P < 0.001), high FBG (21.0% vs. 14.5%; P = 0.011), but less likely to have low HDL-C levels (18.1% vs. 31.0%; P < 0.001), AbO (10.8% vs. 52.6%; P < 0.001), and MetS (10.8% vs. 21.1%; P < 0.001). Overall, elevated BP was the most prevalent MetS component of the study population.

Table 2 presents the clinical characteristics of subjects and prevalence of MetS and MetS components, by age categories and gender. Prevalence of AbO and MetS were higher in women than in men in all age groups and prevalence of MetS increased with age in women but remained the same across age groups in men.

Table 2.

Clinical Characteristics of Subjects and Prevalence of Metabolic Syndrome and Metabolic Syndrome Components, by Age Categories and Gender

	<40 years			40–60 years			≥60 years
	Men N = 82	Women N = 178	P	Men N = 184	Women N = 420	P	Men N = 49	Women N = 98	P
Continuous variables ^a
Age (years)	32.5 ± 5.7	32.7 ± 4.8	0.861	50.0 ± 5.2	49.1 ± 5.4	0.054	66.0 ± 4.0	66.0 ± 7.0	0.521
SBP (mmHg)	128 ± 12	122 ± 14	0.001	136 ± 17	134 ± 19	0.236	144 ± 19	143 ± 25	0.790
Diastolic BP (mmHg)	80 ± 12	79 ± 11	0.354	84 ± 13	84 ± 12	0.732	84 ± 9	85 ± 11	0.488
BMI (Kg/m²)	26.8 ± 6.5	28.7 ± 7.0	0.033	25.8 ± 4.5	28.9 ± 6.1	<0.001	25.4 ± 3.9	29.1 ± 5.2	<0.001
WC (cm)	88 ± 14	87 ± 15	0.578	89 ± 12	89 ± 14	0.730	90 ± 10	92 ± 13	0.287
HDL-C (mmol/L)	1.3 ± 0.4	1.4 ± 0.3	0.116	1.4 ± 0.5	1.5 ± 0.5	0.009	1.4 ± 0.3	1.5 ± 0.4	0.041
TG (mmol/L)	1.1 ± 0.9	0.8 ± 0.4	0.001	1.1 ± 0.7	0.9 ± 0.5	<0.001	1.0 ± 0.5	1.1 ± 0.6	0.337
FBG (mmol/L)	4.8 ± 0.7	4.7 ± 0.7	0.273	5.1 ± 0.7	4.9 ± 0.6	0.004	5.3 ± 0.8	5.2 ± 0.7	0.449
Categorical variables ^b
MetS components
Hypertension (%)	51.2	31.6	0.002	68.5	58.1	0.016	77.6	84.7	0.285
AbO (%)	13.4	42.1	<0.001	9.8	54.0	<0.001	10.2	65.3	<0.001
Low HDL-C (%)	28.0	44.4	0.012	14.7	26.4	0.002	14.3	26.5	0.093
High TG (%)	13.4	4.5	0.010	14.1	6.2	0.001	8.2	10.2	0.691
High FBG (%)	7.3	7.9	0.878	22.3	14.3	0.015	38.8	27.6	0.166
MetS (%)	12.2	16.9	0.333	10.3	20.2	0.003	10.2	32.7	0.003

Significant P values are in bold.

Data are presented as ^amean ± SD or ^bcolumn percentage. P values: for differences between genders.

For continuous variables: Student's t-test for comparison between genders in each age category.

MetS, metabolic syndrome.

The distribution of MetS components in participants is presented in Fig. 1. High BP had the highest prevalence among men in three age groups (100% in G1, 95% in G2, and 100% in G3) and among women ≥60 years (97% in G3). The highest prevalence of AbO was observed among women in G1 (97%) and G2 (98%).

FIG. 1.

Prevalence of MetS components in men (black bars) and women (gray bars) having MetS. AbO, abdominal obesity; High BP, high blood pressure; High TG: high triglyceride levels; High FBG, high fasting blood glucose levels; Low HDL-C, low high-density lipoprotein cholesterol levels.

The most frequent combinations for individuals having MetS (three or more MetS components), were high BP, AbO, and low HDL cholesterol in both genders (26% in men and 55% in women) followed by high BP, AbO and high FBG for women (25%) and high BP, low HDL cholesterol, and high FBG for men (18%).

Table 3 presents the ORs for experiencing MetS components and MetS according to the NCEP ATP III MetS definition.

Table 3.

Odds Ratios of Metabolic Syndrome Components and Metabolic Syndrome for Gender and Age Categories

	Hypertension		AbO		Low HDL-C		High TG		High FBG		MetS
	OR (95% CI)	P	OR (95% CI)	P	OR (95% CI)	P	OR (95% CI)	P	OR (95% CI)	P	OR (95% CI)	P
Sex
Men	1		1		1		1		1		1
Women	0.6 (0.5–0.8)	0.002	9.4 (6.4–13.9)	<0.001	2.1 (1.5–2.9)	<0.001	0.4 (0.3–0.7)	0.001	0.6 (0.5–0.9)	0.012	2.2 (1.5–3.3)	<0.001
Age
<40 years	1		1		1		1		1		1
40–60 years	2.7 (2.0–3.6)	<0.001	1.4 (1.0–2.0)	0.034	0.5 (0.3–0.6)	<0.001	1.2 (0.7–2.1)	0.499	2.4 (1.5–4.0)	0.001	1.1 (0.8–1.7)	0.529
≥60 years	7.8 (4.8–12.8)	<0.001	2.1 (1.3–3.3)	0.002	0.5 (0.3–0.7)	0.001	1.3 (0.6–2.7)	0.455	5.5 (3.1–9.8)	<0.001	1.9 (1.1–3.6)	0.013

Significant P values are in bold.

OR (95% CI), odds ratio (95% confidence interval).

Individuals ≥60 years had the highest OR for prevalent hypertension 7.8 (4.8–12.8); P < 0.001, AbO 2.1 (1.3–3.3); P = 0.002, and high FBG 5.5 (3.1–9.8); P < 0.001. They also had a lower odds for having low HDL-C than the younger ones (G1: age <40 years). Among persons ≥60 years, OR for MetS was 1.9 (1.1–3.6); P = 0.013 compared with the referent group. Compared with men, women had lower odds of hypertension, high TG levels, and high FBG, but higher odds of low HDL-C levels, AbO, and MetS of 2.2 (1.5–3.3); P < 0.001.

Discussion

In the present study, in an Afro-Caribbean population, we investigated the variation in the prevalence of MetS and its components by gender and age. Prevalence of MetS increased with age in women. There was a gradual increase in prevalence of hypertension and high FBG with each succeeding age group, whereas prevalence of low HDL-C levels was higher in the younger individuals and that of high TG levels was relatively low and quite similar across the age groups. Prevalence of AbO and MetS were higher in women than in men in all age groups. This could explain, in part, the higher prevalence of diabetes among women (14% vs. 8% among men), in the population of Guadeloupe.¹⁹

Data for the prevalence of MetS components in individuals without diabetes and without known CVD are scarce in PAA. Thus, we put in parallel our data and those of previous studies, including AA, African-Caribbeans, and Africans.^6

–13 For these studies, we took into account results in agreement with MetS definition by the NCEP ATP III³ or the NCEP ATP III modified by the American Heart Association that includes pharmacological treatment for risk factors.²

High BP component

Overall, 58.3% of our study population had elevated BP versus 43.5% in WA and 51.3% in AA in NHANES III.⁶ In the JHS cohort, prevalence of elevated BP was 70.4% among the AA participants (including individuals with CVD).¹⁰ PAA are known to have high BP levels and to develop hypertension at an earlier age than whites.^14,20 Potential determinants of hypertension in PAA have been suggested, including higher salt sensitivity, low levels of plasma renin, abnormal vascular function, attenuated nocturnal decrease in BP, positive family history, and genetic predisposition.^14,21 In this line, heritability estimate of diastolic and SBP were 15% and 16% in AA.²²

AbO component

AbO is considered as a major contributor of insulin resistance and MetS. In this Afro-Caribbean population without diabetes, prevalence of AbO (39.6%) was much less compared with that of AA participants, including individuals with CVD, in the JHS cohort (64.6%).¹⁰ This discrepancy could be explained by cultural differences despite similar genetic background but also by the absence of other comorbidities in our participants. As in other studies on PAA, prevalence of AbO was higher in women than in men,^9,10 but this prevalence increased with age only in women. In NHANES 2003–2006, only prevalence of hypertension and hyperglycemia increased, in males, with each succeeding age group.⁶

Several possible explanations could be proposed for the observed trends, including differences in energy intake and physical activity. Genetic factors are also involved in AbO and, for AA, WC exhibited the highest heritability estimate (45%) among the MetS components.²²

High fasting glucose component

We noted a prevalence of 16.5% for high FBG. This prevalence was estimated at 31.3% in our individuals ≥60 years. Aging has been associated with declines in glucose tolerance, insulin sensitivity, and insulin secretion.^23
–25 In the elderly individuals, β cell function is impaired and compensatory hyperinsulinemia does not occur.²³ Additionally, the interaction of many diabetes risk factors associated with aging might contribute to the development of age-related glucose intolerance and increased insulin resistance.²³ Hyperinsulinemia appears to be a highly conserved trait in black African populations²⁶ and may be driven by both environmental and genetic factors.²⁷ Nevertheless, the heritability estimate of FPG was the lowest (14%) among the MetS components in AA participants.²²

Low HDL cholesterol and high TG components

We found prevalence of 27.0% and 8.4% for Low HDL-C levels and High TG levels, respectively, versus 37.2% and 16.6%, respectively, in nondiabetic AA of the JHS cohort.¹⁰ As in our study, some authors reported a lower prevalence of low-HDL-C levels in older patients (>60 years)⁶ but, this finding was inconsistent and may vary among different populations. In this line, low HDL cholesterol concentration was about equally prevalent across all AA age groups of the JHS cohort¹⁰ or was not linearly correlated with age in Chinese adults 20–79 years of age.²⁸

It is difficult to affirm that the lower prevalence of low-HDL-C concentrations in our older patients is related to the effect of lipid-lowering agents. About 4.2% of all the participants were taking lipid-lowering agents (0.4% in G1, 4.3% in G2, and 10.2% in G3, data not shown). However, data were available for cholesterol medication in general but not for specific treatment for hypertriglyceridemia or low HDL-C concentrations. In addition, statins, generally used in this population, have limited effects on HDL-C levels.

Higher TG levels in men than women were also found and have been reported in most studies and in different populations and ethnic groups as in AA and WA adults from the NHANES^6,9 or Chinese adults.²⁸ The more favorable lipid profile reported in PAA is in contrast with higher rates of unfavorable BP compared with whites²⁹ and might be explained by a higher lipoprotein lipase activity.³⁰ Genetic factors would also account for some of the observed differences between individuals of European and African ancestry.³¹ Heritability of TG (42%) and HDL-C (43%) were found relatively high and similar to the heritability of WC in AA individuals.²²

Metabolic syndrome

MetS prevalence with high FBG >5.6 mmol/L, in our Afro-Caribbean participants, was 17.9% (21.1% women and 10.8% men) and the highest in the elderly (25.2%). Various studies reported ethnic, gender, and geographical differences in MetS prevalence in PAA.^7,10,11,13

Our results are quite similar to those of a recent study in an African population of Ghana.¹³ A systematic review, including nine studies on “healthy” Ghanaian without CVD, reported a pooled MetS prevalence based on NCEP-ATP classification at 12.4% (19.2% women and 8.1% men).¹²

Prevalence of MetS increased with age only in women in our study population. This could be related to the fact that the frequency of AbO, a major contributor of insulin resistance and MetS, increased only in women and significantly with the succeeding age categories. This increased prevalence of MetS among older adults, also reported in other studies, may be explained by functional disability and decrease in physical activity.^8,9,32 However, some biological conditions,³³ such as chronic low-grade systemic inflammation,^33,34 hypoleptinemia,³⁵ and reduced serum magnesium levels^36,37 might link MetS and the aging process and be involved in the increase of MetS prevalence in the elderly.

The pathophysiology of MetS is very complex and not yet clear. The effects of weight, education, income, overeating, and sedentary lifestyle have been reported in various studies. There is also strong evidence, for the contribution of genetic factors to the phenotypic variability of MetS²² and, in the JHS cohort, the heritability of MetS among AA participants was 32%.²²

Genetic polymorphisms, especially those responsible for metabolism and transport of lipids, are often implicated.^38,39 Genome-wide association studies of MetS in Africans from Ghana and Nigeria followed by replication testing in other samples (African from Kenya and AA from the Atherosclerosis Risk in Communities study) found two African ancestry-specific variants that were significantly associated with MetS: SNP rs73989312[A], which conferred increased risk, and SNP rs77244975[C], which conferred protection against MetS.⁴⁰

Limitations and strengths of the study

Our study has some limitations, including the cross-sectional design, which did not let us draw any causality link between MetS components and gender and age. We were also limited by the relatively small number of subjects who were older than 60 years. Several other parameters, such as demographics, education, household income, lifestyle, and factors known to be involved in MetS, should have been considered but were not available. Nevertheless, this study provides useful information for a homogeneous population of Afro-Caribbeans without diabetes and without previous cardiovascular complications.

Conclusions

In our Afro-Caribbean individuals, the prevalence of MetS increased with age in women and, as consistently reported in PAA, a favorable lipid profile was present even in the elderly. The pattern of MetS was different for men and women and depending on age suggesting that MetS and each MetS components could have different effects on cardiovascular morbidity and mortality depending on the characteristics of the individuals.

MetS being a risk factor for diabetes and CVD, the management of each MetS component is a necessity notably in controlling hypertension, which seems to have a particular negative effect on cardiovascular morbidity in PAA. Nevertheless, the contribution of genetic factors linked to ethnicity should not be underestimated.

Footnotes

Acknowledgments

The authors would like to acknowledge all individuals who participated in the study. Great thanks to the nurses and physicians of the AGREXAM Health Center and to Dr. J. Plumasseau, the Head of the Health Center. The authors also thank Dr. T. Nyahuma and Dr. M. Nyahuma for language assistance.

Author Disclosure Statement

No conflicting financial interests exist.

Funding Information

This study was partly supported by grants from the University Hospital of Guadeloupe.

References

Ford

, Li

, Zhao

. Prevalence and correlates of metabolic syndrome based on a harmonious definition among adults in the US. J Diabetes, 2010; 2:180–193.

Grundy

, Cleeman

, Daniels

, et al. Diagnosis and management of the metabolic syndrome: An American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation, 2005; 112:2735–2752.

Expert Panel on

Detection

, Evaluation, and Treatment of High Blood Cholesterol in

Adults

. Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA, 2001; 285:2486–2497.

Reaven

. Role of insulin resistance in human disease (syndrome X): An expanded definition. Annu Rev Med, 1993; 44:121–131.

Ford

. Risks for all-cause mortality, cardiovascular disease, and diabetes associated with the metabolic syndrome: A summary of the evidence. Diabetes Care, 2005; 28:1769–1778.

Ervin

. Prevalence of metabolic syndrome among adults 20 years of age and over, by sex, age, race and ethnicity, and body mass index: United States, 2003–2006. Natl Health Stat Report, 2009; 13:1–8.

Gaillard

. Consequences of abdominal adiposity within the metabolic syndrome paradigm in Black people of African ancestry. J Clin Med, 2014; 3:897–912.

Aguilar

, Bhuket

, Torres

, et al. Prevalence of the metabolic syndrome in the United States, 2003–2012. JAMA, 2015; 313:1973–1974.

Moore

, Chaudhary

, Akinyemiju

. Metabolic syndrome prevalence by race/ethnicity and sex in the United States, National Health and Nutrition Examination Survey, 1988–2012. Prev Chronic Dis, 2017; 14:E24.

10.

Taylor

, Liu

, Wilson

, et al. Distinct component profiles and high risk among African Americans with metabolic syndrome: The Jackson Heart Study. Diabetes Care, 2008; 31:1248–1253.

11.

Tillin

, Forouhi

, Johnston

, et al. Metabolic syndrome and coronary heart disease in South Asians, African-Caribbeans and white Europeans: A UK population-based cross-sectional study. Diabetes Care, 2008; 31:1248–1253.

12.

Ofori-Asenso

, Agyeman

, Laar

. Metabolic syndrome in apparently “Healthy” Ghanaian adults: A systematic review and meta-analysis. Int J Chronic Dis, 2017; 2017:2562374.

13.

Annani-Akollor

, Laing

, Osei

, et al. Prevalence of metabolic syndrome and the comparison of fasting plasma glucose and HbA1c as the glycemic criterion for MetS definition in non-diabetic population in Ghana. Diabetol Metab Syndr, 2019; 11:26.

14.

Maraboto

, Ferdinand

. Update on hypertension in African-Americans. Prog Cardiovasc Dis, 2020; 63:33–39.

15.

Gaillard

, Schuster

, Osei

. Differential impact of serum glucose, triglycerides, and high-density lipoprotein cholesterol on cardiovascular risk factor burden in nondiabetic, obese African American women: Implications for the prevalence of metabolic syndrome. Metabolism, 2010; 59:1115–1123.

16.

Osei

. Metabolic syndrome in blacks: Are the criteria right?. Curr Diab Rep, 2010; 10:199–208.

17.

Kalk

, Joffe

. The metabolic syndrome, insulin resistance, and its surrogates in African and white subjects with type 2 diabetes in South Africa. Metab Syndr Relat Disord, 2008; 6:247–255.

18.

U.S. Department of Health and Human Services. NHANES 1999–2000 addendum to the NHANES III analytic guidelines, 2002. Accessed at www.cdc.gov/nchs/data/nhanes/guidelines1.pdf on March 1, 2021.

19.

ORSAG. Le Diabète en Guadeloupe, 2017. Accessed at https://wwworsagfr/wp-content/uploads/2018/06/ORSaG_DIABETE_KANNARI_rapport2017pdf on March 1, 2021.

20.

Ferdinand

, Townsend

. Hypertension in the US Black population: Risk factors, complications, and potential impact of central aortic pressure on effective treatment. Cardiovasc Drugs Ther, 2012; 26:157–165.

21.

Ortega

, Sedki

, Nayer

. Hypertension in the African American population: A succinct look at its epidemiology, pathogenesis, and therapy. Nefrologia, 2015; 35:139–145.

22.

Khan

, Gebreab

, Sims

, et al. Prevalence, associated factors and heritabilities of metabolic syndrome and its individual components in African Americans: The Jackson Heart Study. BMJ Open, 2015; 5:e008675.

23.

Chang

, Halter

. Aging and insulin secretion. Am J Physiol Endocrinol Metab, 2003; 284:E7–E12.

24.

Chia

, Egan

, Ferrucci

. Age-related changes in glucose metabolism, hyperglycemia, and cardiovascular risk. Circ Res, 2018; 123:886–904.

25.

Chen

, Bergman

, Pacini

, et al. Pathogenesis of age-related glucose intolerance in man: Insulin resistance and decreased beta-cell function. J Clin Endocrinol Metab, 1985; 60:13–20.

26.

Osei

, Schuster

, Owusu

, et al. Race and ethnicity determine serum insulin and C-peptide concentrations and hepatic insulin extraction and insulin clearance: Comparative studies of three populations of West African ancestry and white Americans. Metabolism, 1997; 46:53–58.

27.

Gower

, Fernandez

, Beasley

, et al. Using genetic admixture to explain racial differences in insulin-related phenotypes. Diabetes, 2003; 52:1047–1051.

28.

Weng

, Yuan

, Tang

, et al. Age- and gender dependent association between components of metabolic syndrome and subclinical arterial stiffness in a Chinese population. Int J Med Sci, 2012; 9:730–737.

29.

Gaillard

, Schuster

, Osei

. Metabolic syndrome in Black people of the African diaspora: The paradox of current classification, definition and criteria. Ethn Dis, 2009; 19(2 Suppl 2):S2-1–7.

30.

Sumner

, Vega

, Genovese

, et al. Normal triglyceride levels despite insulin resistance in African Americans: Role of lipoprotein lipase. Metabolism, 2005; 54:902–909.

31.

Deo

, Reich

, Tandon

, et al. Genetic differences between the determinants of lipid profile phenotypes in African and European Americans: The Jackson Heart Study. PLoS Genet, 2009; 5:e1000342.

32.

Denys

, Cankurtaran

, Janssens

, et al. Metabolic syndrome in the elderly: An overview of the evidence. Acta Clin Belg, 2009; 64:23–34.

33.

Dominguez

, Barbagallo

. The biology of the metabolic syndrome and aging. Curr Opin Clin Nutr Metab Care, 2016; 19:5–11.

34.

Grant

, Dixit

. Adipose tissue as an immunological organ. Obesity (Silver Spring), 2015; 23:512–518.

35.

Perry

, Zhang

, et al. Leptin reverses diabetes by suppression of the hypothalamic-pituitary-adrenal axis. Nat Med, 2014; 20:759–763.

36.

Barbagallo

, Di Bella

, Brucato

, et al. Serum ionized magnesium in diabetic older persons. Metabolism, 2014; 63:502–509.

37.

Dominguez

, Barbagallo

, Lauretani

, et al. Magnesium and muscle performance in older persons: The In CHIANTI study. Am J Clin Nutr, 2006; 84:419–426.

38.

Larifla

, Rambhojan

, Joannes

, et al. Gene polymorphisms of FABP2, ADIPOQ and ANP and risk of hypertriglyceridemia and metabolic syndrome in Afro-Caribbeans. PLoS One, 2016; 11:e0163421.

39.

Povel

, Boer

, Reiling

, et al. Genetic variants and the metabolic syndrome: A systematic review. Obes Rev, 2011; 12:952–967.

40.

Tekola-Ayele

, Doumatey

, Shriner

, et al. Genome-wide association study identifies African-ancestry specific variants for metabolic syndrome. Mol Genet Metab, 2015; 116:305–313.