1.
Association Between Midlife Obesity and Kidney Function Trajectories: The Atherosclerosis Risk in Communities (ARIC) Study.
Yu, Z, Grams, ME, Ndumele, CE, Wagenknecht, L, Boerwinkle, E, North, KE, Rebholz, CM, Giovannucci, EL, Coresh, J
American journal of kidney diseases : the official journal of the National Kidney Foundation. 2021;(3):376-385
-
-
Free full text
-
Abstract
RATIONALE & OBJECTIVE Obesity has been related to risk for chronic kidney disease. However, the associations of different measures of midlife obesity with long-term kidney function trajectories and whether they differ by sex and race are unknown. STUDY DESIGN Observational study. SETTING & PARTICIPANTS 13,496 participants from the Atherosclerosis Risk in Communities (ARIC) Study. PREDICTORS Midlife obesity status as measured by body mass index (BMI), waist-to-hip ratio, and predicted percent fat at baseline. OUTCOMES Estimated glomerular filtration rate (eGFR) calculated using serum creatinine level measured at 5 study visits, and incident kidney failure with replacement therapy (KFRT). ANALYTICAL APPROACH Mixed models with random intercepts and random slopes for eGFR. Cox proportional hazards models for KFRT. RESULTS Baseline mean age was 54 years, median eGFR was 103mL/min/1.73m2, and median BMI was 27kg/m2. Over 30 years of follow-up, midlife obesity measures were associated with eGFR decline in White and Black women but not consistently in men. Adjusted for age, center, smoking, and coronary heart disease, the differences in eGFR slope per 1-SD higher BMI, waist-to-hip ratio, and predicted percent fat were 0.09 (95% CI, -0.18 to 0.36), -0.25 (95% CI, -0.50 to 0.01), and-0.14 (95% CI, -0.41 to 0.13) mL/min/1.73m2 per decade for White men; -0.91 (95% CI, -1.15 to-0.67), -0.82 (95% CI, -1.06 to-0.58), and-1.02 (95% CI, -1.26 to-0.78) mL/min/1.73m2 per decade for White women; -0.70 (95% CI, -1.54 to 0.14), -1.60 (95% CI, -2.42 to-0.78), and-1.24 (95% CI, -2.08 to-0.40) mL/min/1.73m2 per decade for Black men; and-1.24 (95% CI, -2.08 to-0.40), -1.50 (95% CI, -2.05 to-0.95), and-1.43 (95% CI, -2.00 to-0.86) mL/min/1.73m2 per decade for Black women. Obesity indicators were independently associated with risk for KFRT for all sex-race groups except White men. LIMITATIONS Loss to follow-up during 3 decades of follow-up with 5 eGFR assessments. CONCLUSIONS Obesity status is a risk factor for future decline in kidney function and development of KFRT in Black and White women, with less consistent associations among men.
2.
Adult weight gain and adiposity-related cancers: a dose-response meta-analysis of prospective observational studies.
Keum, N, Greenwood, DC, Lee, DH, Kim, R, Aune, D, Ju, W, Hu, FB, Giovannucci, EL
Journal of the National Cancer Institute. 2015;(3)
-
-
Free full text
-
Abstract
BACKGROUND Adiposity, measured by body mass index, is implicated in carcinogenesis. While adult weight gain has diverse advantages over body mass index in measuring adiposity, systematic reviews on adult weight gain in relation to adiposity-related cancers are lacking. METHODS PubMed and Embase were searched through September 2014 for prospective observational studies investigating the relationship between adult weight gain and the risk of 10 adiposity-related cancers. Dose-response meta-analyses were performed using a random-effects model to estimate summary relative risk (RR) and 95% confidence interval (CI) for each cancer type. All statistical tests were two-sided. RESULTS A total of 50 studies were included. For each 5kg increase in adult weight gain, the summary relative risk was 1.11 (95% CI = 1.08 to 1.13) for postmenopausal breast cancer among no- or low-hormone replacement therapy (HRT) users, 1.39 (95% CI = 1.29 to 1.49) and 1.09 (95% CI = 1.02 to 1.16) for postmenopausal endometrial cancer among HRT nonusers and users, respectively, 1.13 (95% CI = 1.03 to 1.23) for postmenopausal ovarian cancer among no or low HRT users, 1.09 (95% CI = 1.04 to 1.13) for colon cancer in men. The relative risk of kidney cancer comparing highest and lowest level of adult weight gain was 1.42 (95% CI = 1.11 to 1.81). Adult weight gain was unrelated to cancers of the breast (premenopausal women, postmenopausal HRT users), prostate, colon (women), pancreas, and thyroid. An increase in risk associated with adult weight gain for breast cancer was statistically significantly greater among postmenopausal women (P heterogeneity = .001) and HRT nonusers (P heterogeneity = .001); that for endometrial cancer was alike among HRT nonusers (P heterogeneity = .04). CONCLUSIONS Avoiding adult weight gain itself may confer protection against certain types of cancers, particularly among HRT nonusers.
3.
Adult weight gain and adiposity-related cancers: a dose-response meta-analysis of prospective observational studies.
Keum, N, Greenwood, DC, Lee, DH, Kim, R, Aune, D, Ju, W, Hu, FB, Giovannucci, EL
Journal of the National Cancer Institute. 2015;(2)
-
-
Free full text
-
Abstract
BACKGROUND Adiposity, measured by body mass index, is implicated in carcinogenesis. While adult weight gain has diverse advantages over body mass index in measuring adiposity, systematic reviews on adult weight gain in relation to adiposity-related cancers are lacking. METHODS PubMed and Embase were searched through September 2014 for prospective observational studies investigating the relationship between adult weight gain and the risk of 10 adiposity-related cancers. Dose-response meta-analyses were performed using a random-effects model to estimate summary relative risk (RR) and 95% confidence interval (CI) for each cancer type. All statistical tests were two-sided. RESULTS A total of 50 studies were included. For each 5 kg increase in adult weight gain, the summary relative risk was 1.11 (95% CI = 1.08 to 1.13) for postmenopausal breast cancer among no- or low-hormone replacement therapy (HRT) users, 1.39 (95% CI = 1.29 to 1.49) and 1.09 (95% CI = 1.02 to 1.16) for postmenopausal endometrial cancer among HRT nonusers and users, respectively, 1.13 (95% CI = 1.03 to 1.23) for postmenopausal ovarian cancer among no or low HRT users, 1.09 (95% CI = 1.04 to 1.13) for colon cancer in men. The relative risk of kidney cancer comparing highest and lowest level of adult weight gain was 1.42 (95% CI = 1.11 to 1.81). Adult weight gain was unrelated to cancers of the breast (premenopausal women, postmenopausal HRT users), prostate, colon (women), pancreas, and thyroid. An increase in risk associated with adult weight gain for breast cancer was statistically significantly greater among postmenopausal women (P(heterogeneity) = .001) and HRT nonusers (P(heterogeneity) = .001); that for endometrial cancer was alike among HRT nonusers (P(heterogeneity) = .04). CONCLUSIONS Avoiding adult weight gain itself may confer protection against certain types of cancers, particularly among HRT nonusers.
4.
A quantitative analysis of body mass index and colorectal cancer: findings from 56 observational studies.
Ning, Y, Wang, L, Giovannucci, EL
Obesity reviews : an official journal of the International Association for the Study of Obesity. 2010;(1):19-30
Abstract
To perform a systematic review of studies reporting on the association between body mass index (BMI) and the risk of colorectal cancer, we conducted a meta-analysis and meta-regression analysis. The identified 56 studies were conducted among 7 213 335 individuals including 93 812 cases. Compared with BMI < 23.0 kg m(-2), BMI of 23.0-24.9, 25.0-27.4, 27.5-29.9 and > or = 30.0 kg m(-2) were associated with 14%, 19%, 24% and 41% increased risks, respectively. Asians and premenopausal women had sharply increased risk from BMI < 23 kg m(-2) to general 'normal' range (23-25 kg m(-2)). Each 5 kg m(-2) increment was associated with 18% increased risk. Meta-regression analysis indicated that the association was stronger for colon than rectal cancer (P < 0.001), for men than women (P < 0.001), for self-reported BMI than directly measured BMI (P < 0.001), and for studies adjusting for physical activity than not adjusting (P < 0.001). The variation of the reported risk estimates for the association can be partly explained by cancer site, sex, women menopausal status, BMI assessment and adjustment of confounding variables.