IntroductionUncertainties exist on whether the main determinant of abnormal glucose tolerance (Abnl-GT) in Africans is β-cell failure or insulin resistance (IR). Therefore, we determined the prevalence, phenotype and characteristics of Abnl-GT due to β-cell failure versus IR in 486 African-born blacks (male: 64%, age: 38±10 years (mean±SD)) living in America.Research design and methodsOral glucose tolerance test were performed. Abnl-GT is a term which includes both diabetes and prediabetes and was defined as fasting plasma glucose (FPG) ≥5.6 mmol/L and/or 2-hour glucose ≥7.8 mmol/L. IR was defined by the lowest quartile of the Matsuda Index (≤2.98) and retested using the upper quartile of homeostatic model assessment of insulin resistance (HOMA-IR) (≥2.07). Abnl-GT-IR required both Abnl-GT and IR. Abnl-GT-β-cell failure was defined as Abnl-GT without IR. Beta-cell compensation was assessed by the Disposition Index (DI). Fasting lipids were measured. Visceral adipose tissue (VAT) volume was obtained with abdominal CT scan.ResultsThe prevalence of Abnl-GT was 37% (182/486). For participants with Abnl-GT, IR occurred in 38% (69/182) and β-cell failure in 62% (113/182). Compared with Africans with Abnl-GT-IR, Africans with Abnl-GT-β-cell failure had lower body mass index (BMI) (30.8±4.3 vs 27.4±4.0 kg/m2), a lower prevalence of obesity (52% vs 19%), less VAT (163±72 vs 107±63 cm2), lower triglyceride (1.21±0.60 vs 0.85±0.42 mmol/L) and lower FPG (5.9±1.4 vs 5.3±0.6 mmol/L) and 2-hour glucose concentrations (10.0±3.1 vs 9.0±1.9 mmol/L) (all p<0.001) and higher DI, high-density lipoprotein (HDL), low-density lipoprotein particle size and HDL particle size (all p<0.01). Analyses with Matsuda Index and HOMA-IR yielded similar results. Potential confounders such as income, education, alcohol and fiber intake did not differ by group.ConclusionsBeta-cell failure occurred in two-thirds of participants with Abnl-GT and may be a more frequent determinant of Abnl-GT in Africans than IR. As BMI category, degree of glycemia and lipid profile appeared more favorable when Abnl-GT was due to β-cell failure rather than IR, the clinical course and optimal interventions may differ.Trial registration numberNCT00001853.

The overall consensus is that foreign-born adults who come to America age < 20 y achieve economic success but develop adverse behaviors (smoking and drinking) that lead to worse cardiometabolic health than immigrants who arrive age ≥ 20 y. Whether age of immigration affects the health of African-born Blacks living in America is unknown. Our goals were to examine cultural identity, behavior, and socioeconomic factors and determine if differences exist in the cardiometabolic health of Africans who immigrated to America before and after age 20 y. Of the 482 enrollees (age: 38 ± 1 (mean ± SE), range: 20–65 y) in the Africans in America cohort, 23% (111/482) arrived age < 20 y, and 77% (371/482) arrived age ≥ 20 y. Independent of francophone status or African region of origin, Africans who immigrated age < 20 y had similar or better cardiometabolic health than Africans who immigrated age ≥ 20 y. The majority of Africans who immigrated age < 20 y identified as African, had African-born spouses, exercised, did not adopt adverse health behaviors, and actualized early life migration advantages, such as an American university education. Due to maintenance of cultural identity and actualization of opportunities in America, cardiometabolic health may be protected in Africans who immigrate before age 20. In short, immigrant health research must be cognizant of the diversity within the foreign-born community and age of immigration.

BackgroundEmerging data suggests that in sub-Saharan Africa β-cell-failure in the absence of obesity is a frequent cause of type 2 diabetes (diabetes). Traditional diabetes risk scores assume that obesity-linked insulin resistance is the primary cause of diabetes. Hence, it is unknown whether diabetes risk scores detect undiagnosed diabetes when the cause is β-cell-failure.AimsIn 528 African-born Blacks living in the United States [age 38 ± 10 (Mean ± SE); 64% male; BMI 28 ± 5 kg/m2] we determined the: (1) prevalence of previously undiagnosed diabetes, (2) prevalence of diabetes due to β-cell-failure vs. insulin resistance; and (3) the ability of six diabetes risk scores [Cambridge, Finnish Diabetes Risk Score (FINDRISC), Kuwaiti, Omani, Rotterdam, and SUNSET] to detect previously undiagnosed diabetes due to either β-cell-failure or insulin resistance.MethodsDiabetes was diagnosed by glucose criteria of the OGTT and/or HbA1c ≥ 6.5%. Insulin resistance was defined by the lowest quartile of the Matsuda index (≤ 2.04). Diabetes due to β-cell-failure required diagnosis of diabetes in the absence of insulin resistance. Demographics, body mass index (BMI), waist circumference, visceral adipose tissue (VAT), family medical history, smoking status, blood pressure, antihypertensive medication, and blood lipid profiles were obtained. Area under the Receiver Operator Characteristics Curve (AROC) estimated sensitivity and specificity of each continuous score. AROC criteria were: Outstanding: &gt;0.90; Excellent: 0.80–0.89; Acceptable: 0.70–0.79; Poor: 0.50–0.69; and No Discrimination: 0.50.ResultsPrevalence of diabetes was 9% (46/528). Of the diabetes cases, β-cell-failure occurred in 43% (20/46) and insulin resistance in 57% (26/46). The β-cell-failure group had lower BMI (27 ± 4 vs. 31 ± 5 kg/m2P &lt; 0.001), lower waist circumference (91 ± 10 vs. 101 ± 10cm P &lt; 0.001) and lower VAT (119 ± 65 vs. 183 ± 63 cm3, P &lt; 0.001). Scores had indiscriminate or poor detection of diabetes due to β-cell-failure (FINDRISC AROC = 0.49 to Cambridge AROC = 0.62). Scores showed poor to excellent detection of diabetes due to insulin resistance, (Cambridge AROC = 0.69, to Kuwaiti AROC = 0.81).ConclusionsAt a prevalence of 43%, β-cell-failure accounted for nearly half of the cases of diabetes. All six diabetes risk scores failed to detect previously undiagnosed diabetes due to β-cell-failure while effectively identifying diabetes when the etiology was insulin resistance. Diabetes risk scores which correctly classify diabetes due to β-cell-failure are urgently needed.

To identify determinants of daily life stress in Africans in America, 156 African-born Blacks (Age: 40 ± 10 years (mean ± SD), range 22–65 years) who came to the United States as adults (age ≥ 18 years) were asked about stress, sleep, behavior and socioeconomic status. Daily life stress and sleep quality were assessed with the Perceived Stress Scale (PSS) and Pittsburgh Sleep Quality Index (PSQI), respectively. High-stress was defined by the threshold of the upper quartile of population distribution of PSS (≥16) and low-stress as PSS < 16. Poor sleep quality required PSQI > 5. Low income was defined as <40 k yearly. In the high and low-stress groups, PSS were: 21 ± 4 versus 9 ± 4, p < 0.001 and PSQI were: 6 ± 3 versus 4 ± 3, p < 0.001, respectively. PSS and PSQI were correlated (r = 0.38, p < 0.001). The odds of high-stress were higher among those with poor sleep quality (OR 5.11, 95% CI: 2.07, 12.62), low income (OR 5.03, 95% CI: 1.75, 14.47), and no health insurance (OR 3.01, 95% CI: 1.19, 8.56). Overall, in African-born Blacks living in America, daily life stress appears to be linked to poor quality sleep and exacerbated by low income and lack of health insurance.