Sleep and Economic Status Are Linked to Daily Life Stress in African-Born Blacks Living in America.

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.

Non-invasive type 2 diabetes risk scores do not identify diabetes when the cause is ß-cell failure: The Africans in America study.

Background: Emerging data suggests that in sub-Saharan Africa ß-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 ß-cell-failure. Aims: In 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 ß-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 ß-cell-failure or insulin resistance. Methods: Diabetes 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 ß-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: >0.90; Excellent: 0.80-0.89; Acceptable: 0.70-0.79; Poor: 0.50-0.69; and No Discrimination: 0.50. Results: Prevalence of diabetes was 9% (46/528). Of the diabetes cases, ß-cell-failure occurred in 43% (20/46) and insulin resistance in 57% (26/46). The ß-cell-failure group had lower BMI (27 ± 4 vs. 31 ± 5 kg/m2 P < 0.001), lower waist circumference (91 ± 10 vs. 101 ± 10cm P < 0.001) and lower VAT (119 ± 65 vs. 183 ± 63 cm3, P < 0.001). Scores had indiscriminate or poor detection of diabetes due to ß-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). Conclusions: At a prevalence of 43%, ß-cell-failure accounted for nearly half of the cases of diabetes. All six diabetes risk scores failed to detect previously undiagnosed diabetes due to ß-cell-failure while effectively identifying diabetes when the etiology was insulin resistance. Diabetes risk scores which correctly classify diabetes due to ß-cell-failure are urgently needed.

The Africans in America study demonstrates that subclinical cardiovascular risk differs by etiology of abnormal glucose tolerance.

Abnormal-glucose tolerance (Abnl-GT) is due to an imbalance between ß-cell function and insulin resistance (IR) and is a major risk factor in cardiovascular disease (CVD). In sub-Saharan Africa, ß-cell failure is emerging as an important cause of Abnl-GT (Abnl-GT-ß-cell-failure). Visceral adipose tissue (VAT) volume and hyperlipidemia are major contributors to CVD risk when Abnl-GT is due to IR (Abnl-GT-IR). Yet, the CVD profile associated with Abnl-GT-ß-cell failure is unknown. Therefore, our goals in 450 African-born Blacks (Male: 65%; Age: 39 ± 10 years; BMI 28 ± 5 kg/m2), living in America were to: (1) determine Abnl-GT prevalence and etiology; (2) assess by Abnl-GT etiology, associations between four understudied subclinical CVD risk factors in Africans: (a) subclinical myocardial damage (high-sensitivity troponin T (hs-cTnT)); (b) neurohormonal regulation (N-terminal pro-Brain-natriuretic peptide (NT-proBNP)); (c) coagulability (fibrinogen); (d) inflammation (high-sensitivity C-reactive protein (hsCRP)), as well as HbA1c, Cholesterol/HDL ratio and VAT. Glucose tolerance status was determined by the OGTT. IR was defined by the threshold at the lowest quartile for the Matsuda Index (≤ 2.97). Abnl-GT-IR required both Abnl-GT and IR. Abnl-GT-ß-cell-failure was defined as Abnl-GT without IR. VAT was assessed by CT-scan. For both the Abnl-GT-ß-cell-failure and Abnl-GT-IR groups, four multiple regression models were performed for hs-cTnT; NT-proBNP; fibrinogen and hsCRP, as dependent variables, with the remaining three biomarkers and HbA1c, Cholesterol/HDL and VAT as independent variables. Abnl-GT occurred in 38% (170/450). In the Abnl-GT group, ß-cell failure occurred in 58% (98/170) and IR in 42% (72/170). VAT and Cholesterol/HDL were significantly lower in Abnl-GT-ß-cell-failure group vs the Abnl-GT-IR group (both P < 0.001). In the Abnl-GT-ß-cell-failure group: significant associations existed between hscTnT, fibrinogen, hs-CRP, and HbA1c (all P < 0.05), and none with Cholesterol/HDL or VAT. In Abnl-GT-IR: hs-cTnT, fibrinogen and hsCRP significantly associated with Cholesterol/HDL (all P < 0.05) and NT-proBNP inversely related to fibrinogen, hsCRP, HbA1c, Cholesterol/HDL, and VAT (all P < 0.05). The subclinical CVD risk profile differed between Abnl-GT-ß-cell failure and Abnl-GT-IR. In Abnl-GT-ß-cell failure subclinical CVD risk involved subclinical-myocardial damage, hypercoagulability and increased inflammation, but not hyperlipidemia or visceral adiposity. For Abnl-GT-IR, subclinical CVD risk related to subclinical myocardial damage, neurohormonal dysregulation, inflammation associated with hyperlipidemia and visceral adiposity. ClinicalTrials.gov Identifier: NCT00001853.