Immune Activation: A Link Between Food Insecurity and Chronic Disease in People Living With Human Immunodeficiency Virus.

Persistent immune activation is a hallmark of human immunodeficiency virus (HIV) infection and thought to play a role on chronic diseases in people with HIV (PWH). Food insecurity is disproportionately prevalent in PWH and is associated with adverse health outcomes. We determined whether food insecurity was associated with increased plasma levels of soluble CD14, CD27, and CD163 in 323 antiretroviral-treated PWH from the Miami Adult Studies on HIV cohort. Nearly half (42.7%) of participants were food insecure, and 85.5% were virally suppressed (<200 copies/mL). Food insecurity was independently associated with higher levels of soluble CD14 and soluble CD27. Very low food security was associated with increased soluble CD163 levels among those with lower CD4+ cell counts. Food insecurity may promote immune activation in PWH, suggesting a biological link between food insecurity and chronic disease among PWH. Improving financial security and access to high-quality diets could reduce the burden of disease in this highly vulnerable population.

Food Insecurity and Cognitive Impairment in the Miami Adult Studies on HIV (MASH) Cohort.

BACKGROUND: Food insecurity is a social determinant of health associated with cognitive impairments in older adults and people living with HIV (PLWH). Few studies have examined this relation longitudinally, and no studies have explored how the frequency of food insecurity over time may impact cognitive impairment. OBJECTIVE: This study aimed to examine the impact of food insecurity on cognitive impairment over a 2-y follow-up period in a cohort of people living with and without HIV. METHODS: This was a 2-y longitudinal analysis of primarily economically disadvantaged, middle-aged, Black, and Hispanic participants from the Miami Adult Studies on HIV (MASH) cohort. Food insecurity was assessed with the USDA Household Food Security Module at baseline and 12- and 24-mo follow-ups. Food insecurity in all 3 assessments was considered persistent food insecurity. Cognitive impairment was assessed with the Mini-Mental State Examination. Statistical analyses consisted of logistic regressions. RESULTS: A total of 394 participants (247 HIV positive) with 2-y follow-up data were included in this analysis. At baseline, 104 (26.4%) were food-insecure and 58 (14.7%) had cognitive impairment. Very low food security was associated with cognitive impairment at baseline (OR: 3.23; 95% CI: 1.08, 9.65). PLWH not virally suppressed had higher risk for cognitive impairment compared with HIV-uninfected participants (OR: 2.87; 95% CI: 1.15, 7.18). Additionally, baseline food insecurity (OR: 2.28; 95% CI: 1.08, 4.81) and the frequency of food insecurity over time (OR: 1.50 per year; 95% CI: 1.08, 2.10), particularly persistent food insecurity (OR: 3.69; 95% CI: 1.15, 11.83), were associated with cognitive impairment at 2-y follow-up; the results were consistent after excluding cognitively impaired participants at baseline. CONCLUSIONS: Food insecurity is a significant risk factor for cognitive impairment, particularly among individuals who experience food insecurity frequently or persistently. Screening for food insecurity and interventions to secure access to sufficient, nutritious foods may help delay cognitive decline among socioeconomically disadvantaged individuals.

Heroin use is associated with liver fibrosis in the Miami Adult Studies on HIV (MASH) cohort.

BACKGROUND: People who use opioids and people living with HIV (PLWH) are at increased risk for liver-related morbidity and mortality. Although animal models suggest that chronic opioid use may cause liver damage, research in humans is limited. We aimed to determine whether opioid use, particularly heroin, was associated with liver fibrosis. METHODS: Cross-sectional analysis of 679 participants (295 HIV/HCV uninfected, 218 HIV mono-infected, 87 HCV mono-infected, 79 HIV/HCV coinfected) from the Miami Adult Studies on HIV (MASH) cohort. Liver fibrosis was assessed via magnetic resonance elastography (MRE) on a 3 T Siemens MAGNETOM Prisma scanner. RESULTS: A total of 120 (17.7 %) participants used opioids. Liver fibrosis was present in 99 (14.6 %) participants and advanced liver fibrosis in 31 (4.6 %). Heroin use (N = 46, 6.8 %) was associated with HCV-seropositivity, smoking, misuse of prescription opioids, and polysubstance use. The use of heroin, but not misuse of prescription opioids, was significantly associated with liver fibrosis (OR = 2.77, 95 % CI: 1.18-6.50) compared to heroin non-users, after adjustment for confounders including excessive alcohol consumption, polysubstance use and HIV and HCV infections. Both HIV and HCV infections were associated with liver fibrosis, whether virally suppressed/undetectable or viremic. CONCLUSIONS: Heroin use was independently associated with increased risk for liver fibrosis irrespective of the use of other substances and HIV or HCV infections. Both HIV and HCV were associated with higher risk for liver fibrosis, even among those with suppressed or undetectable viral loads. The exact mechanisms for opioid-induced liver fibrosis remain to be fully elucidated.

Food insecurity is associated with magnetic resonance-determined nonalcoholic fatty liver and liver fibrosis in low-income, middle-aged adults with and without HIV.

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is the most prevalent liver disease in the United States. Food-insecure individuals often depend on low-cost, energy-dense but nutritionally poor foods, resulting in obesity and chronic diseases related to NAFLD. OBJECTIVES: To determine whether food insecurity is associated with NAFLD in a cohort of HIV and hepatitis C virus (HCV) infected and uninfected adults. METHODS: We conducted a cross-sectional analysis of low-income, middle-aged adults from the Miami Adult Studies on HIV (MASH) cohort without a history of excessive alcohol consumption. Food security was assessed with the USDA's Household Food Security Survey. MRIs were used to assess liver steatosis and fibrosis. Metabolic parameters were assessed from fasting blood, anthropometrics, and vitals. RESULTS: Of the total 603 participants, 32.0% reported food insecurity. The prevalences of NAFLD, fibrosis, and advanced fibrosis were 16.1%, 15.1%, and 4.6%, respectively. For every 5 kg/m2 increase in BMI, the odds of NAFLD increased by a factor of 3.83 (95% CI, 2.37-6.19) in food-insecure participants compared to 1.32 (95% CI, 1.04-1.67) in food-secure participants. Food insecurity was associated with increased odds for any liver fibrosis (OR, 1.65; 95% CI, 1.01-2.72) and advanced liver fibrosis (OR, 2.82; 95% CI, 1.22-6.54), adjusted for confounders. HIV and HCV infections were associated with increased risks for fibrosis, but the relationship between food insecurity and liver fibrosis did not differ between infected and uninfected participants. CONCLUSIONS: Among low-income, middle-aged adults, food insecurity exacerbated the risk for NAFLD associated with a higher BMI and independently increased the risk for advanced liver fibrosis. People who experience food insecurity, particularly those vulnerable to chronic diseases and viral infections, may be at increased risk for liver-related morbidity and mortality. Improving access to adequate nutrition and preventing obesity among low-income groups may lessen the growing burden of NAFLD and other chronic diseases.

Cognitive Impairment among People Who Use Heroin and Fentanyl: Findings from the Miami Adult Studies on HIV (MASH) Cohort.

Background: Cognitive impairment is common in people living with HIV (PLWH). Opioid drugs exert direct and indirect effects on cognitive processes, which may contribute to cognitive dysfunction among PLWH. This study was designed to determine if opioid use is associated with cognitive impairment and whether the effect differs between PLWH and HIV-uninfected adults. Other neuropsychiatric symptoms, such as depression and apathy, were also examined. We conducted a cross-sectional analysis of 265 PLWH and 284 HIV-uninfected participants from the Miami Adult Studies on HIV (MASH) cohort. The Mini-Mental State Examination (MMSE) was used to assess cognitive impairment. Substance use was self-reported. Overall, 26.8% of PLWH and 15.1% of HIV-uninfected used opioids. Cognitive impairment was more frequent among people who used heroin and/or fentanyl than those who misused prescription opioids (31.6% vs. 10.5%, p = .005). The use of heroin/fentanyl was associated with increased odds for cognitive impairment (adjusted OR: 2.21, 95% CI 1.05-4.64, p = .036). Among PLWH only, the misuse of opioids was associated with a higher frequency of neuropsychiatric symptoms such as depression and apathy. A higher risk for cognitive impairment was seen among people who used heroin and fentanyl. PLWH who misuse opioids may be at an increased risk for neuropathology, but elucidation of mechanisms for opioid-induced cognitive deficits is needed.

Caffeine Intake and Its Association with Body Composition Measures and Macronutrient Intakes in People Living with HIV in the Miami Adult Studies on HIV Cohort.

Background: Caffeine acts as an anorexic agent, increases energy expenditures, and decreases total body fat mass, and could be detrimental to people living with HIV (PLWH). The objective of this study was to explore the relationship between caffeine consumption, body composition measures (fat mass, body mass index [BMI], and lean body mass [LBM]), nutrient intakes, CD4 counts, and HIV viral load in PLWH. Methods: A convenience sample of 130 PLWH was recruited and followed for 3 months. Caffeine intake, body composition measures, and nutrient intakes were collected using Modified Caffeine Consumption Questionnaire, bioimpedance analyses, and 24-hour dietary recalls. Linear regressions were used to analyze the baseline data for relationships between these variables. Linear mixed models (LMMs) were used to determine the overtime changes. Results: In baseline, linear regression analysis, higher caffeine consumption was associated with lower fat mass (ß = -0.994, p = 0.042). However, BMI and LBM did not show any significant association with caffeine intake. LMM analysis showed that the association between caffeine intake and fat mass strengthened overtime (ß = -1.987, p = 0.035). Baseline linear regression analysis showed that higher caffeine intake was significantly associated with lower caloric intakes from fat (ß = -1.902, p = 0.044) and lower total caloric intake (ß = -1.643, p = 0.042). However, LMM analysis showed that these associations diminished and lost significance overtime. There were no associations between body composition measures, nutrient intakes, CD4 counts, and HIV viral load. Conclusions: Caffeine intake adversely affected dietary intakes of macronutrients and total fat mass. Therefore, caffeine, a known anorectic, should be regulated in PLWH.

Caffeine and Insomnia in People Living With HIV From the Miami Adult Studies on HIV (MASH) Cohort.

We explored the relationship between caffeine consumption, insomnia, and HIV disease progression (CD4+ T cell counts and HIV viral loads). Caffeine intake and insomnia levels were measured using the Modified Caffeine Consumption Questionnaire and the Pittsburgh Insomnia Rating Scale (PIRS) in 130 clinically stable participants who were living with HIV, taking antiretroviral therapy, and recruited from the Miami Adult Studies on HIV cohort. Linear regressions showed that caffeine consumption was significantly and adversely associated with distress score, quality-of-life score, and global PIRS score. Linear regression analyses also showed that global PIRS score was significantly associated with lower CD4+ T cell counts and higher HIV viral loads. Caffeine could have precipitated insomnia in susceptible people living with HIV, which could be detrimental to their disease progression states.

The Relationship Between Caffeine Intake and Immunological and Virological Markers of HIV Disease Progression in Miami Adult Studies on HIV Cohort.

Although there are many studies on adverse health effects of substance use and HIV disease progression, similar studies about caffeine consumption are few. In this study, we investigated the effects of caffeine on immunological and virological markers of HIV disease progression. A convenience sample of 130 clinically stable people living with HIV/AIDS on antiretroviral therapy (65 consuming ≤250 mg/day and 65 consuming >250 mg/day of caffeine) were recruited from the Miami Adult Studies on HIV (MASH) cohort. This study included a baseline and 3-month follow-up visit. Demographics, body composition measures, substance use, Modified Caffeine Consumption Questionnaire (MCCQ), and CD4 count and HIV viral load were obtained for all participants. Multivariable linear regression and Linear Mixed Models (LMMs) were used to understand the effect of caffeine consumption on CD4 count and HIV viral load. The mean age of the cohort was 47.9 ± 6.4 years, 60.8% were men and 75.4% were African Americans. All participants were on ART during both the visits. Mean caffeine intake at baseline was 337.6 ± 305.0 mg/day and did not change significantly at the 3-month follow-up visit. Multivariable linear regressions after adjustment for covariates showed significant association between caffeine consumption and higher CD4 count (ß = 1.532, p = 0.049) and lower HIV viral load (ß = -1.067, p = 0.048). LMM after adjustment for covariates showed that the relationship between caffeine and CD4 count (ß = 1.720, p = 0.042) and HIV viral load (ß = -1.389, p = 0.033) continued over time in a dose-response manner. Higher caffeine consumption was associated with higher CD4 cell counts and lower HIV viral loads indicating beneficial effects on HIV disease progression. Further studies examining biochemical effects of caffeine on CD4 cell counts and viral replication need to be done in the future.

Low Plasma Zinc Is Associated with Higher Mitochondrial Oxidative Stress and Faster Liver Fibrosis Development in the Miami Adult Studies in HIV Cohort.

Background: Oxidative stress and reduced antioxidants may be a trigger for liver fibrogenesis. Reducing oxidative stress through higher antioxidant concentration may be a potential antifibrotic target.Objective: We aimed to investigate longitudinally whether plasma zinc, an antioxidant, is related to mitochondrial oxidative stress and the progression of liver fibrosis in the Miami Adult Studies in HIV (MASH) cohort.Methods: A prospective observational cohort study was conducted in 487 predominantly African American HIV-monoinfected and HIV/hepatitis C virus (HCV)-coinfected adults with a mean ± SD age of 47.08 ± 7.67 y from the MASH cohort and followed for a median of 34 mo. Blood was collected for plasma zinc and measures were used to calculate the fibrosis-4 (FIB-4) score (aspartate amino transferase, alanine aminotransferase, and platelets). Plasma zinc deficiency was defined as <0.75 mg/L. Total DNA was extracted from peripheral blood mononuclear cells and mitochondrial DNA (mtDNA) 8-hydroxyguanosine (8-oxo-dG) was determined. Adjusted mixed models were used to assess the relations between zinc, stage of liver disease, and oxidative stress over time and compared between HIV and HIV/HCV groups.Results: Zinc concentrations (ß: -0.368, SE = 0.172; P = 0.033) and deficiency were associated with lower FIB-4 scores over time (ß: 0.381, SE = 0.118; P = 0.001). Compared with those who were not zinc deficient, zinc-deficient participants had an increased risk of having more-progressed liver disease (OR: 1.91; 95% CI: 1.15, 3.16; P = 0.012). Higher mtDNA 8-oxo-dG was associated with zinc deficiency (ß: 0.049, SE = 0.024; P = 0.044) and higher FIB-4 scores over time (ß: 0.597, SE = 0.168, P < 0.001).Conclusions: Lower plasma zinc concentrations were associated with liver fibrosis progression and mitochondrial oxidative stress in the HIV and HIV/HCV groups. Zinc may play a role in the impact of liver disease outcomes.

Relationship of Oxidative Stress with HIV Disease Progression in HIV/HCV Co-infected and HIV Mono-infected Adults in Miami.

BACKGROUND: HIV and HCV infections are both characterized by increased oxidative stress. Information on the magnitude of this increase and its consequences in HIV/HCV co-infection and viral replication is limited. We investigated the relationship between oxidative stress and HIV-progression in HIV/HCV co-infected and HIV mono-infected adults. METHODS: 106 HIV/HCV co-infected and 115 HIV mono-infected participants provided demographic information and blood to determine 8-oxo-dG and percent oxidized glutathione. RESULTS: HIV/HCV co-infected subjects had higher percent oxidized glutathione, higher HIV viral load, lower mtDNA copies and higher liver fibrosis than mono-infected subjects. In a small sample of HIV/HCV co-infected participants with liver biopsy, 8-oxo-dG was significantly lower in participants with low fibrosis scores than those with high fibrosis scores, and the grade of inflammation was strongly associated with oxidized glutathione. CONCLUSIONS: HIV/HCV co-infection seems to diminish the capacity of the antioxidant system to control oxidative stress, and increases HIV replication.