Food insecurity, which affects >1 billion people worldwide, is inextricably linked to the HIV epidemic. We present a conceptual framework of the multiple pathways through which food insecurity and HIV/AIDS may be linked at the community, household, and individual levels. Whereas the mechanisms through which HIV/AIDS can cause food insecurity have been fairly well elucidated, the ways in which food insecurity can lead to HIV are less well understood. We argue that there are nutritional, mental health, and behavioral pathways through which food insecurity leads to HIV acquisition and disease progression. Specifically, food insecurity can lead to macronutrient and micronutrient deficiencies, which can affect both vertical and horizontal transmission of HIV, and can also contribute to immunologic decline and increased morbidity and mortality among those already infected. Food insecurity can have mental health consequences, such as depression and increased drug abuse, which, in turn, contribute to HIV transmission risk and incomplete HIV viral load suppression, increased probability of AIDS-defining illness, and AIDS-related mortality among HIV-infected individuals. As a result of the inability to procure food in socially or personally acceptable ways, food insecurity also contributes to risky sexual practices and enhanced HIV transmission, as well as to antiretroviral therapy nonadherence, treatment interruptions, and missed clinic visits, which are strong determinants of worse HIV health outcomes. More research on the relative importance of each of these pathways is warranted because effective interventions to reduce food insecurity and HIV depend on a rigorous understanding of these multifaceted relationships.

Background Cardiovascular disease (CVD) is an increasing cause of morbidity and mortality in HIV-infected patients. However, it is controversial whether HIV infection contributes to accelerated atherosclerosis independent of traditional CVD risk factors. Methods Cross-sectional study of HIV-infected and control subjects without pre-existing CVD from the study of Fat Redistribution and Metabolic Change in HIV Infection (FRAM) and the Multi-Ethnic Study of Atherosclerosis (MESA). Pre-clinical atherosclerosis was assessed by carotid intima-medial thickness (IMT) measurements in the internal/bulb and common regions in HIV-infected and control subjects after adjusting for traditional CVD risk factors. Results For internal carotid, mean IMT was 1.17±0.50mm for HIV-infected participants and 1.06±0.58mm for controls (p<0.0001). After multivariable adjustment for demographic characteristics, the mean difference of HIV-infected vs. controls was +0.188mm (95%CI 0.113-0.263, p<0.0001). Further adjustment for traditional CVD risk factors modestly attenuated the HIV association (+0.148mm, 95%CI 0.072-0.224, p=0.0001). For the common carotid, HIV infection was independently associated with greater IMT (+0.033mm, 95%CI 0.010, 0.056, p=0.005). The association of HIV infection with IMT was similar to that of smoking which was also associated with greater IMT (internal +0.173mm, common +0.020mm). Conclusions Even after adjustment for traditional CVD risk factors, HIV infection was accompanied by more extensive atherosclerosis measured by IMT. The stronger association of HIV infection with IMT in the internal/bulb region compared to the common carotid may explain previous discrepancies in the literature. The association of HIV infection with IMT was similar to that of traditional CVD risk factors, such as smoking.

Objective-To assess the association of HIV infection, HIV disease parameters (including CD4+ T-cell counts, HIV viral load, and AIDS) and antiretroviral medication use with subclinical carotid artery atherosclerosis.Design-Cross-sectional study nested within a prospective cohort study Methods-Among participants in the Women's Interagency HIV Study (1,331 HIV-infected women, 534 HIV-uninfected women) and Multicenter AIDS Cohort Study (600 HIV-infected men, 325 HIV-uninfected men), we measured subclinical carotid artery lesions and common carotid artery intima-media thickness (CIMT) using B-mode ultrasound. We estimated adjusted mean CIMT differences and prevalence ratios (PRs) for carotid lesions associated with HIV-related disease and treatments, with multivariate adjustment to control for possible confounding variables.Results-Among HIV-infected individuals, a low CD4+ T cell count was independently associated with an increased prevalence of carotid lesions. Compared to the reference group of HIV-uninfected individuals, the adjusted PR for lesions among HIV-infected individuals with CD4+ T-cell count <200 cells/mm 3 was 2.00 (95% confidence interval 1.22, 3.28) in women and 1.74 (95% confidence interval 1.04, 2.93) in men. No consistent association of antiretroviral medications with carotid atherosclerosis was observed, except for a borderline significant association between protease inhibitor use and carotid lesions in men (with no association among women). History of clinical AIDS and HIV viral load were not significantly associated with carotid atherosclerosis. The purpose of the present investigation was to assess the association of HIV infection, HIV disease parameters (including CD4+ T-cell counts, HIV viral load, and AIDS) and antiretroviral medication use with subclinical vascular disease. We report the results from two studies, conducted in parallel, within the Women's Interagency HIV Study (WIHS) and the Multicenter AIDS Cohort Study (MACS). WIHS and MACS are population-based US cohort studies that offer several important strengths, including large sample size, inclusion of HIVuninfected persons who were recruited from the same at-risk populations as the HIV-infected individuals, and extensive longitudinal, protocol-driven data collection on clinical, behavioral, and demographic variables. The present report describes data from the baseline phase of a WIHS-MACS Carotid Ultrasound Substudy, which features standardized image acquisition and measurement of carotid artery intima-media thickness, a quantitative measure of atherosclerosis burden. In April 2004, through coordinated efforts by the WIHS and MACS investigators, a vascular disease substudy was initiated in each cohort which included B-mode ultrasound imaging of the carotid arteries. All WIHS participants were eligible for the vascular substudy, while in MACS, eligibility was restricted to men who reported no history of coronary heart disease (CHD) (including angina, myocardial infarction [MI], or coronary revascularization). For the pres...

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Objective To determine the association of inflammatory markers, fibrinogen and C-reactive protein (CRP), with 5-year mortality risk. Methods Vital status was ascertained in 922 HIV-infected participants from the Study of Fat Redistribution and Metabolic Change in HIV infection. Multivariable logistic regression estimated odds ratios (OR) after adjustment for demographic, cardiovascular and HIV-related factors. Results Over a 5-year period, HIV-infected participants with fibrinogen levels in the highest tertile(>406mg/dL) had 2.6-fold higher adjusted odds of death than those with fibrinogen in the lowest tertile(<319mg/dL). Those with high CRP(>3mg/L) had 2.7-fold higher adjusted odds of death than those with CRP<1mg/L. When stratified by CD4 count category, fibrinogen (as a linear variable) remained independently associated [OR(95% confidence intervals) per 100mg/dL increase in fibrinogen: 1.93(1.57,2.37);1.43(1.14,1.79);1.43(1.14,1.81);and 1.30(1.04,1.63) for CD4 <200,200–350,>350–500, and >500cells/μL, respectively. Higher CRP also remained associated with higher odds of death overall and within each CD4 subgroup. Conclusion Fibrinogen and CRP are strong and independent predictors of mortality in HIV-infected adults. Our findings suggest that even in those with relatively preserved CD4 counts >500cells/μL, inflammation remains an important risk factor for mortality. Further investigation should determine whether interventions to reduce inflammation might decrease mortality risk in HIV-infected individuals.