Pao-Hwa Lin

Individuals with resistant hypertension (RH) have the greatest risk of cerebrovascular disease and cognitive impairment among individuals with hypertension. Elevated levels of pro-inflammatory cytokines may represent a critical yet unexamined factor influencing the impact of healthy lifestyle changes on cognitive function. We explored the influence of inflammation on changes in cognition following lifestyle modification among individuals with RH participating in the TRIUMPH clinical trial. One hundred forty participants with RH completed a battery of neurocognitive tests along with the inflammatory marker C-reactive protein (hsCRP) and were subsequently randomized to an intensive 4-month lifestyle modification intervention or to education and physician advice control. Results indicated that the effects of lifestyle modification on Executive Function and Learning were moderated by pre-intervention hsCRP levels (P = .049), with treatment efficacy increasing across levels of baseline inflammation levels (low: d = 0.12; mild: d = 0.43; moderate: d = 0.81). We conclude that inflammatory profiles may help identify individuals more likely to improve executive functioning resulting from lifestyle modification.

Objective: The dissemination of effective obesity interventions requires the documentation of key elements of the intervention. But outcome papers and other published manuscripts often lack detail that allow the replication of the intervention. The Behavior Change Technique (BCT) Taxonomy (BCTTv1) is a widely used approach to identify key elements of an intervention study. This study compares the extent to which BCTs and domains identified in studies' intervention protocol are concordant with detail from corresponding intervention design and study outcome papers. Methods: Data come from four obesity interventions with complete intervention protocols as well as published intervention design and outcome papers. The number of domains and BCTs was calculated for each treatment arm and stratified by coding source. Emphasis of domains and BCTs was determined using an Analytical Hierarchy Process (AHP). Results: A review of each study's intervention protocol showed the mean number of domains and BCTs used in treatment arms as 11.8 and 26.7, respectively. Primary outcome papers had a mean loss of 34% of the reported domains and 43% of BCTS as compared with intervention protocl. Design papers showed a loss of 11% and 21% of domains and BCTs, respectively. Conclusions: The results confirm the limitations of using the BCTTv1 coding of outcome papers to describe obesity-related interventions. The results also highlight the need for mechanisms that allow for a full description of intervention content such as inclusion in a supplemental section of an online journal or the use of intervention-focused consort guidelines.

BACKGROUND: High phosphorus (P) exposure may have negative effects on kidney function. Nutrient databases provide total P, but bioavailability varies by source. OBJECTIVES: We aimed to assess natural, added, and bioavailable P intake, and to relate these to estimated glomerular filtration rate (eGFR) in the Jackson Heart Study (JHS). METHODS: A total of 3962 African-American participants of the JHS, aged 21-84 y, with urine albumin:creatinine ratio < 30 mg/g, and eGFR ≥ 60 mL · min-1 · 1.73 m-2, and without self-reported kidney disease, were included. Diet was assessed by FFQ. We assigned P in foods as naturally occurring or added, and weighted intake by P bioavailability, based on published literature. Relations between P variables and eGFR were assessed using multivariable regression. RESULTS: Mean ± SE intakes were 1178 ± 6.7 mg and 1168 ± 5.0 mg for total P, 296 ± 2.8 mg and 291 ± 2.1 mg for bioavailable added P, and 444 ± 2.9 mg and 443 ± 2.2 mg for bioavailable natural P, in participants with eGFR = 60-89 and ≥90 mL · min-1 · 1.73 m-2, respectively. Major sources of total P included fish, milk, beef, eggs, cheese, and poultry; and of added P, fish, beef, processed meat, soft drinks, and poultry. After adjustment for confounders, P intakes, including total (β ± SE: -0.32 ± 0.15; P = 0.03), added (β ± SE: -0.73 ± 0.27; P = 0.01), bioavailable total (β ± SE: -0.62 ± 0.23; P = 0.01), and bioavailable added (β ± SE: -0.77 ± 0.29; P = 0.01), were significantly associated with lower eGFR. However, neither total nor bioavailable P from natural sources were associated with eGFR. CONCLUSIONS: Added, but not natural, P was negatively associated with kidney function, raising concern about P additives in the food supply. Further studies are needed to improve estimation of dietary P exposure and to clarify the role of added P as a risk factor for kidney disease.