Background: Abnormal glucose tolerance (Abnl-GT) is a summary term for prediabetes and diabetes. The main etiologic determinant of Abnl-GT may be either β-cell failure or insulin resistance (IR). In African-born Blacks Abnl-GT may be predominantly due to β-cell failure rather than IR. Whether perceived and physiological stress profiles differ when Abnl-GT is due to β-cell failure rather than IR is uncertain. Aims: In 197 African-born Blacks living in the US (age: 38±11 (mean±SD); 58% men; BMI 28±5 kg/m 2 ) the perceived and physiological stress profiles were assessed based on Abnl-GT etiology. Methods: OGTT were performed. Abnl-GT was defined as FPG ≥100 mg/dL and/or glucose at 2h≥140 mg/dL. IR was defined by the lowest quartile of the Matsuda index (≤2.97). Abnl-GT-IR required Abnl-GT and IR. Beta-cell failure was defined as Abnl-GT without IR. The 10 question Cohen Perceived Stress Scale (PSS) was applied. Allostatic Load (ALS) included 10 variables: SBP, DBP, Pulse, cholesterol, HDL, homocysteine, BMI, A1C, Albumin, hs-CRP. Statistical analyses included t-tests, Chi-squares, and multiple regressions. Results: Abnl-GT occurred in 39% (77/197), with Abnl-GT-β-cell failure in 56% (43/77) and Abnl-GT-IR in 44% (34/77). The Abnl-GT-IR had higher BMI (31±5 vs 28±4) and WC (101±10 vs 90±11) vs Abnl-GT-β-cell failure, both P <0.01. PSS did not differ between groups. ALS was higher in Abnl-GT-IR vs the Abnl-GT-β-cell failure ( P <0.01). Yet, regression analyses, adjusted for age and sex, showed significant associations between PSS and ALS in the Abnl-GT-β-cell-failure-group ( P =0.01) ( Figure 1A ). However, PSS and ALS were insignificantly associated in the Abnl-GT-IR-group ( P =0.42) ( Figure 1B ). Conclusions: In Abnl-GT-β-cell failure, perceived stress may influence allostatic load. Reasons for the link between perceived stress and allostatic load in Abnl-GT due to β-cell failure need exploration.
Background: Africa is experiencing the most rapid rise of type 2 diabetes (T2D) in the world. In addition, Africa has the highest proportion of undiagnosed cases. If people with T2D are undiagnosed, then complications progress, outcomes are poor, and social and financial costs escalate. Our goal with this review is to determine whether Life-Style Intervention (LSI) as primary treatment can lead to remission of T2D. LSI generally includes some combination of dietary change, weight loss, exercise, and counseling. If LSI alone leads to high rates of T2D remission, this will provide both the impetus and justification for investing scarce health care resources in programs which would convert undiagnosed T2D into diagnosed T2D. Methods: PubMed, Embase, Cochrane and CINAHL were searched between September 1 st and September 13 th , 2021 for studies that assessed whether LSI, as the only treatment would lead to remission in either newly diagnosed or established T2D. Results: The search identified 1162 articles. After removal of duplicates (n=291), 871 are being screened for eligibility. To date, data have been extracted from 11 of the articles which met the inclusion criteria. None of the 11 studies were conducted in Africa. Three of the 11 studies reported on newly diagnosed T2D cases. All three were successful in achieving a high rate of T2D remission with LSI. Strategies which were successful in converting T2D to prediabetes included: (1) a caloric decrease of only 500 less than predicted maintenance; (2) a low carbohydrate diet; and (3) a 10% loss in baseline weight. Exercise and counseling regimens varied widely between the three trials. The eight articles which enrolled patients with known T2D focused largely on very low calorie diets and intensive psychologic support and counseling. Factors in these studies which were associated with success were: T2D duration less than 5 years, weight loss of >10% in the first year, and higher insulin concentrations at baseline. Conclusion: Literature review, even if scant, will provide currently known best practices. They will help us move forward in the design of culturally sensitive lifestyle interventions that would be acceptable to African participants and economically attractive to government and health care agencies.
Background: Five of the most important Type 2 Diabetes (T2D) prediction scores are: Cambridge, Finnish Diabetes Risk Score (FINDRISC), Rotterdam, Kuwaiti and Omani. These scores are based on the premise that Insulin Resistance (IR) is the primary cause of T2D. Yet, data in Africans suggest β-cell-failure without obesity is the most common cause of T2D. It is unknown whether these scores can identify undiagnosed T2D when the cause is β-cell-failure. Aims: Our aim was to compare in 514 African-born Blacks (age 38±10 (mean±SD); 68% male; BMI 28±5 kg/m 2 ) the ability of Cambridge, FINDRISC, Rotterdam, Kuwait and Omani scores to identify previously undiagnosed T2D due to either IR or β-cell-failure. Methods: Diabetes was diagnosed by OGTT. Insulin resistance was defined by the lowest quartile of the Matsuda index (≤2.97). Beta-cell failure was defined as T2D diagnosis in the absence of IR. Body mass index (BMI), waist circumference (WC) and visceral adipose tissue (VAT) was measured. Area under the Receiver Operator Characteristic curve (AROC) estimated sensitivity, specificity, and criteria for AROC were: 0.70-0.79=acceptable; 0.80-0.89=excellent; >0.90=outstanding. Logistic regression determined odds of T2D at the optimal cut-point for each score. Results: The prevalence of T2D was 7% (38/514). Of the T2D cases, IR occurred in 61% (23/38) and β-cell failure in 39% (15/38). Age did not differ by group, but the IR group had higher BMI (31±5 vs 27±4 kg/m 2 P <0.001) and WC (101±10 vs 91±10 cm P <0.001). This is supported by the higher VAT in the IR group (161±73 vs 106±62 cm 2 P <0.001), an important physiological correlate of insulin resistance. All scores showed acceptable to outstanding predictability for T2D due to IR, ranging from Cambridge at AROC=0.75, to the FINDRISC with AROC=0.92. Only weak to moderate predictability for all scores were shown in β-cell-failure (Cambridge at AROC=0.48 to FINDRISC with AROC=0.63). All models predicted significant odds of T2D due to IR, with FINDRISC≥10 OR=6.8 (95%CI, 2.6, 17.8) P<0 .001; Rotterdam≥7 OR=8.5 (95%CI, 3.1, 23.2) P<0 .001; Cambridge≥23 OR=11.4 (95%CI, 2.6, 50.0) P =0.001) proving most effective. Only the Cambridge score significantly predicted odds of T2D in β-cell-failure (OR=5.7 (95%CI 1.58, 20.54) P =0.001). Conclusions: All 5 diabetes risk scores effectively predicted undiagnosed T2D in Africans when the etiology was IR, but only the Cambridge score predicted T2D when the cause was β-cell failure. The Cambridge risk score rates overweight status, not just obesity status, which might explain why it was successful in predicting T2D in β-cell failure and the others were not. Existing scores which predict T2D might be modified, to effectively assess T2D risk when β-cell failure is the primary cause.
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