Lifestyle Interventions for the Management of Hypertension in Adults: A Review of Reviews

Introduction: Hypertension is the most pervasive health concern in the U.S. with an estimated prevalence of 29.1–32.6%. Guidelines advise comprehensive treatment of hypertension that should include lifestyle changes. The objective of this review of reviews was to synthesize evidence on lifestyle interventions to reduce blood pressure in adults with essential hypertension and identify how race plays a role in determining which interventions are most effective. Methods: A systematic review of reviews was conducted in PubMed and CINAHL from January 2008 to October 2014 with the following search criteria: (1) major subject heading relating to the disease hypertension, (2) terms related to lifestyle and behavior modification interventions, and (3) systematic review or meta-analysis. Results: The literature search identified 652 citations, of which 10 met the selection criteria. These 10 reviews summarized evidence on 13 interventions that employed the following strategies: self-monitoring, professional support, education, diet, clinic reminders, problem solving, self-management, family involvement, or proactive delivery. The results demonstrated that although some individual strategies were successful in reducing blood pressure, combinations of strategies were the most successful. Discussion: Combinations of intervention strategies to reduce blood pressure are more successful than single strategies. No conclusions could be made about the differential effectiveness of based on race. Future studies need to evaluate which combinations of interventions are most successful to reduce blood pressure.Bachelor of Scienc

A Hybrid Implementation-Effectiveness Study of a Community Health Worker-Delivered Intervention to Reduce Cardiovascular Disease Risk in a Rural, Underserved Non-Hispanic Black Population: The CHANGE Study

Purpose To evaluate the implementation and effectiveness of the Carolina Heart Alliance Networking for Greater Equity (CHANGE) Program, an adapted evidence-based cardiovascular disease risk reduction intervention delivered by Community Health Workers (CHW) to rural adults. Design Hybrid implementation-effectiveness study with a pre–post design. Setting North Carolina Federally Qualified Health Center and local health department in a rural, medically underserved area. Sample Participants (n = 255) included 87% Non-Hispanic Black with a mean age of 57 years; 84% had diagnosed hypertension, 55% had diabetes, and 65% had hypercholesterolemia. Intervention A CHW-delivered, low-intensity, 4-month behavioral lifestyle intervention promoting a southern-style Mediterranean dietary pattern and physical activity. Measures We measured number and representativeness of participants reached and retained, intervention delivery fidelity, weight, blood pressure, and self-reported dietary and physical activity behaviors. Analysis Pre–post changes at 4 months were analyzed using paired t-tests. Results Study participants completed 90% of planned intervention contacts; 87% were retained. Intervention delivery fidelity measures showed participants receiving a mean of 3.5 counseling visits, 2.7 booster calls, and on average completing 1.7 modules, setting 1.8 goals, and receiving 1.3 referrals per visit. There were significant mean reductions in systolic (−2.5 mmHg, P < .05) and diastolic blood pressure (−2.1 mmHg, P < .01); the proportion of participants with systolic blood pressure <130 increased by 7 % points (P = .05), and diastolic pressure <80 by 9 percentage points (P < .01). Dietary behaviors improved significantly with average weekly servings of nuts increased by .5 serving (P < .0001), and fruits and vegetables by .8 daily serving (P < .0001). Physical activity also increased on average by 45 min./week (P < .001). Weight did not change significantly. Conclusions The CHANGE program showed both implementation and program effectiveness and adds to the evidence supporting CHW-delivered lifestyle interventions to reduce CVD risk among rural, Non-Hispanic Black, and medically underserved populations

A TRPA1-dependent mechanism for the pungent sensation of weak acids

Acetic acid produces an irritating sensation that can be attributed to activation of nociceptors within the trigeminal ganglion that innervate the nasal or oral cavities. These sensory neurons sense a diverse array of noxious agents in the environment, allowing animals to actively avoid tissue damage. Although receptor mechanisms have been identified for many noxious chemicals, the mechanisms by which animals detect weak acids, such as acetic acid, are less well understood. Weak acids are only partially dissociated at neutral pH and, as such, some can cross the cell membrane, acidifying the cell cytosol. The nociceptor ion channel TRPA1 is activated by CO2, through gating of the channel by intracellular protons, making it a candidate to more generally mediate sensory responses to weak acids. To test this possibility, we measured responses to weak acids from heterologously expressed TRPA1 channels and trigeminal neurons with patch clamp recording and Ca2+ microfluorometry. Our results show that heterologously expressed TRPA1 currents can be induced by a series of weak organic acids, including acetic, propionic, formic, and lactic acid, but not by strong acids. Notably, the degree of channel activation was predicted by the degree of intracellular acidification produced by each acid, suggesting that intracellular protons are the proximate stimulus that gates the channel. Responses to weak acids produced a Ca2+-independent inactivation that precluded further activation by weak acids or reactive chemicals, whereas preactivation by reactive electrophiles sensitized TRPA1 channels to weak acids. Importantly, responses of trigeminal neurons to weak acids were highly overrepresented in the subpopulation of TRPA1-expressing neurons and were severely reduced in neurons from TRPA1 knockout mice. We conclude that TRPA1 is a general sensor for weak acids that produce intracellular acidification and suggest that it functions within the pain pathway to mediate sensitivity to cellular acidosis

Polyclonal B Cell Differentiation and Loss of Gastrointestinal Tract Germinal Centers in the Earliest Stages of HIV-1 Infection

The antibody response to HIV-1 does not appear in the plasma until approximately 2–5 weeks after transmission, and neutralizing antibodies to autologous HIV-1 generally do not become detectable until 12 weeks or more after transmission. Moreover, levels of HIV-1–specific antibodies decline on antiretroviral treatment. The mechanisms of this delay in the appearance of anti-HIV-1 antibodies and of their subsequent rapid decline are not known. While the effect of HIV-1 on depletion of gut CD4+ T cells in acute HIV-1 infection is well described, we studied blood and tissue B cells soon after infection to determine the effect of early HIV-1 on these cells

Polyclonal B Cell Differentiation and Loss of Gastrointestinal Tract Germinal Centers in the Earliest Stages of HIV-1 Infection

BACKGROUND: The antibody response to HIV-1 does not appear in the plasma until approximately 2–5 weeks after transmission, and neutralizing antibodies to autologous HIV-1 generally do not become detectable until 12 weeks or more after transmission. Moreover, levels of HIV-1–specific antibodies decline on antiretroviral treatment. The mechanisms of this delay in the appearance of anti-HIV-1 antibodies and of their subsequent rapid decline are not known. While the effect of HIV-1 on depletion of gut CD4(+) T cells in acute HIV-1 infection is well described, we studied blood and tissue B cells soon after infection to determine the effect of early HIV-1 on these cells. METHODS AND FINDINGS: In human participants, we analyzed B cells in blood as early as 17 days after HIV-1 infection, and in terminal ileum inductive and effector microenvironments beginning at 47 days after infection. We found that HIV-1 infection rapidly induced polyclonal activation and terminal differentiation of B cells in blood and in gut-associated lymphoid tissue (GALT) B cells. The specificities of antibodies produced by GALT memory B cells in acute HIV-1 infection (AHI) included not only HIV-1–specific antibodies, but also influenza-specific and autoreactive antibodies, indicating very early onset of HIV-1–induced polyclonal B cell activation. Follicular damage or germinal center loss in terminal ileum Peyer's patches was seen with 88% of follicles exhibiting B or T cell apoptosis and follicular lysis. CONCLUSIONS: Early induction of polyclonal B cell differentiation, coupled with follicular damage and germinal center loss soon after HIV-1 infection, may explain both the high rate of decline in HIV-1–induced antibody responses and the delay in plasma antibody responses to HIV-1. Please see later in the article for Editors' Summar