Faculty Bibliography

BACKGROUND: Although high body mass index (BMI) is a risk factor for hypertension, diabetes, and cardiovascular disease, limited data exist on the association of overweight and obesity with early stages of kidney disease. METHODS: Cross-sectional data for 5083 participants of the nationally representative Third National Health and Nutrition Examination Survey with an estimated glomerular filtration rate > or = 60 mL/min/1.73 m(2) without micro- or macroalbuminuria were analyzed to determine the association between BMI and elevated serum cystatin C. Normal weight, overweight, class I obesity, and class II to III obesity were defined as a BMI of 18.5 to 24.9 kg/m(2), 25.0 to 29.9 kg/m(2), 30.0 to 34.9 kg/m(2), and > or = 35.0 kg/m(2), respectively. Elevated serum cystatin C was defined as > or = 1.09 mg/L (> or = 99th percentile for participants 20-39 years of age without diabetes, hypertension, micro- or macroalbuminuria, or stage 3-5 chronic kidney disease). RESULTS: The age-standardized prevalence of elevated serum cystatin C was 9.6%, 12.9%, 17.4%, and 21.5% among adults of normal weight, overweight, class I obesity, and class II to III obesity, respectively (P trend < .001). After multivariate adjustment for demographics, behaviors, systolic blood pressure, and serum biomarkers, and compared with participants of normal weight, the odds ratio (95% confidence interval) of elevated serum cystatin C was 1.46 (1.02-2.10) for overweight, 2.36 (1.56-3.57) for class I obesity, and 2.82 (1.56-5.11) for class II to III obesity. CONCLUSION: A graded association exists between higher BMI and elevated serum cystatin C. Further research is warranted to assess whether reducing BMI favorably affects elevated serum cystatin C and the development of chronic kidney disease.

To determine whether statin use leads to dietary indiscretion, this longitudinal cohort study examined the impact of statin initiation on saturated fat intake. We interviewed 71 patients who had received a new prescription for statins for primary prevention of cardiovascular disease, first at the time of prescription and then again 3 and 6 months later. Patients were asked about their beliefs regarding diet and medications as well as their diet during the past 24 hours in all interviews and about their adherence to statins in the 3- and 6-month follow-up interviews. At the time of statin prescription, 54 participants (76 percent) wanted to reduce dietary fat, 50 (70 percent) believed statin use could cure their hyperlipidemia, and 31 (44 percent) thought that physicians prescribed statins to them despite their preference to continue to try dietary changes. After 6 months of statin use, no significant change in saturated fat intake was noted

PURPOSE: Statins are potent drugs for reducing cholesterol and cardiovascular disease; however, their effectiveness is significantly compromised by poor adherence. This prospective study was designed to identify potentially modifiable patient factors including medication, disease, and diet beliefs related to statin adherence. METHODS: Veterans (n = 71) given their first prescription of a statin for primary prevention were interviewed at baseline, 3 months, and 6 months regarding medication, disease, and diet beliefs along with self-reported statin adherence. RESULTS: At 6-month follow-up, 55% of the cohort was non-adherent with 10% reporting never having started their statin, 50% reporting misconceptions about the duration of treatment and a median use of <2 months among those who discontinued their statin. Multivariate predictors of non-adherence were expected short treatment duration (OR = 3.6, 1.4-9.4), low perceived risk of myocardial infarction (OR = 3.1, 1.1-8.7), concern about potential harm from statins (OR = 2.5, 1.0-6.3), being Hispanic (OR = 3.9, 1.0-15.2), and younger age (OR = 4.2, 1.1-15.8). CONCLUSIONS: Poor adherence to statins was common in this primary prevention population with frequent early discontinuation despite access to low-cost medicines. Patient factors regarding the perception of risk, toxic effects of medication, expected treatment duration, as well as socio-demographic factors, were significant predictors of poor adherence and warrant further exploration

BACKGROUND: While lipid-lowering drugs reduce cardiovascular risk, there is concern that their use may discourage dietary restriction of saturated fat (SF). The purpose of this analysis was to evaluate the association between taking lipid-lowering drugs and SF intake. MATERIALS AND METHODS: We analyzed cross-sectional data on cholesterol and diet from 6,473 adult respondents in the National Health and Nutrition Examination Survey, 1999-2002. Respondents were classified into three groups: (1) no history of high cholesterol (Desirable Cholesterol or DC), (2) history of high cholesterol without current drug treatment (Non-Drug Treated or NDT), and (3) history of high cholesterol with active lipid-lowering medication use (Drug-Treated or DT). Regression models were used to compare the mean percentage of daily kilocalories from SF among the three groups while controlling for confounders. RESULTS: Unadjusted analyses revealed significantly lower mean daily intake of SF (% of Kcal/day) among DT respondents compared to both DC (-.40 SF; 95% Confidence Interval [CI], -0.71 to -0.08) and NDT respondents [-.36 SF; CI, -0.79 to 0.06]. The complete multivariate model controlling for all covariates (age, sex, education, race/ethnicity, current smoking, alcohol use, BMI, physical activity, cardiovascular disease, diabetes, hypertension) attenuated the relationship compared to D (-.35 SF, CI -0.7 to -0.01) and NDT (-.25 SF, CI -0.62 to 0.12) individuals. CONCLUSION: Taking lipid-lowering medications is associated with a lower intake of SF. However, a prospective study of diet and medication use is needed to definitively evaluate the relationship between lipid-lowering medications and SF intake

BACKGROUND.: It is unclear whether the coronary heart disease (CHD) mortality risk associated with obesity is mediated only through traditional CHD risk factors. This analysis evaluated the independent CHD mortality risk due to obesity and determined its population attributable risk (PAR). METHODS.: Using the NHANES I Epidemiologic Follow-up Study (1971-1992, n = 10,582), a diabetes-body mass index (BMI) variable was constructed. The hazard ratios (HR) for fatal CHD in the diabetes-BMI categories (adjusting for age, sex, race, exercise, education level, smoking, hypertension, cholesterol, and alcohol use) were determined and the PARs subsequently estimated. RESULTS.: Compared to lean non-diabetics, the HR (95% CI) for fatal CHD is 0.8 (0.7, 1.1) in overweight non-diabetics, 1.4 (1.3, 2.0) in obese non-diabetics, 2.2 (1.2, 4.0) in lean diabetics, 2.3 (1.4, 3.9) in overweight diabetics, and 3.3 (1.9, 8.9) in obese diabetics. The PAR% is -6.8 (-15.7, 1.8) in overweight non-diabetics, 6.1 (1.7, 11.1) in obese non-diabetics, 2.0 (0.3, 4.0) in lean diabetics, 2.2 (0.6, 4.3) in overweight diabetics, and 2.2 (0.8, 3.8) in obese diabetics. CONCLUSIONS.: Obesity is an independent risk factor for CHD mortality even after controlling for traditional CHD risk factors. The PAR for CHD death in obese non-diabetics is significant. Obesity should be aggressively treated in those without traditional CHD risk factors