Objective

To determine whether food insecurity, limited or uncertain food access owing to cost, is associated with greater health care expenditures.

Data source/study setting

Nationally representative sample of the civilian noninstitutionalized population of the United States (2011 National Health Interview Survey [NHIS] linked to 2012-2013 Medication Expenditure Panel Survey [MEPS]).

Study design

Longitudinal retrospective cohort.

Data collection/extraction methods

A total of 16,663 individuals underwent assessment of food insecurity, using the 10-item adult 30-day food security module, in the 2011 NHIS. Their total health care expenditures in 2012 and 2013 were recorded in MEPS. Expenditure data were analyzed using zero-inflated negative binomial regression and adjusted for age, gender, race/ethnicity, education, income, insurance, and residence area.

Principal findings

Fourteen percent of individuals reported food insecurity, representing 41,616,255 Americans. Mean annualized total expenditures were $4,113 (standard error $115); 9.2 percent of all individuals had no health care expenditures. In multivariable analyses, those with food insecurity had significantly greater estimated mean annualized health care expenditures ($6,072 vs. $4,208, p < .0001), an extra $1,863 in health care expenditure per year, or $77.5 billion in additional health care expenditure annually.

Conclusions

Food insecurity was associated with greater subsequent health care expenditures. Future studies should determine whether food insecurity interventions can improve health and reduce health care costs.

Objectives

Reducing utilization of high-cost healthcare services is a common population health goal. Food insecurity-limited access to nutritious food owing to cost-is associated with chronic disease, but its relationship with healthcare utilization is understudied. We tested whether food insecurity is associated with increased emergency department (ED) visits, hospitalizations, and related costs.

Study design

Retrospective analysis of a nationally representative cohort.

Methods

Adults (≥18 years) completed a food insecurity assessment (using 10 items derived from the US Department of Agriculture Household Food Security Module) in the 2011 National Health Interview Survey and were followed in the 2012-2013 Medical Expenditures Panel Survey. Outcome measures were ED visits, hospitalizations, days hospitalized, and whether participants were in the top 10%, 5%, or 2% of total healthcare expenditures.

Results

Of 11,781 participants, 2056 (weighted percentage, 13.2%) were in food-insecure households. Food insecurity was associated with significantly more ED visits (incidence rate ratio [IRR], 1.47; 95% CI, 1.12-1.93), hospitalizations (IRR, 1.47; 95% CI, 1.14-1.88), and days hospitalized (IRR, 1.54; 95% CI, 1.06-2.24) after adjustment for demographics, education, income, health insurance, region, and rural residence. Food insecurity was also associated with increased odds of being in the top 10% (odds ratio [OR], 1.73; 95% CI, 1.31-2.27), 5% (OR, 2.53; 95% CI, 1.51-3.37), or 2% (OR, 1.95; 95% CI, 1.09-3.49) of healthcare expenditures.

Conclusions

Food insecurity is associated with higher healthcare use and costs, even accounting for other socioeconomic factors. Whether food insecurity interventions improve healthcare utilization and cost should be tested.

Background

Cardiovascular disease is increased among HIV-infected patients, but little is known regarding ischemic stroke rates. We sought to compare stroke rates and determine stroke risk factors in HIV-infected versus non-HIV-infected patients.

Methods

An HIV cohort and matched non-HIV comparator cohort seen between 1996 and 2009 were identified from a Boston health care system. The primary endpoint was ischemic stroke, defined using International Classification of Diseases (ICD) codes. Unadjusted stroke incidence rates were calculated. Cox proportional hazards modeling was used to determine adjusted hazard ratios (HRs).

Results

The incidence rate of ischemic stroke was 5.27 per 1000 person-years in HIV-infected compared with 3.75 in non-HIV-infected patients, with an unadjusted HR of 1.40 [95% confidence interval (CI): 1.17 to 1.69, P < 0.001]. HIV remained an independent predictor of stroke after controlling for demographics and stroke risk factors (HR: 1.21, 95% CI: 1.01 to 1.46, P = 0.043). The relative increase in stroke rates (HIV vs. non-HIV) was significantly higher in younger HIV patients (incidence rate ratio: 4.42, 95% CI: 1.56 to 11.09, age 18-29; 2.96, 1.69-4.96, age: 30-39; 1.53, 1.06-2.17, age: 40-49), and in women [HR: 2.16 (95% CI: 1.53 to 3.04) for women vs. HR: 1.18 (95% CI: 0.95 to 1.47) for men]. Among HIV patients, increased HIV RNA (HR: 1.10, 95% CI: 1.04 to 1.17, P = 0.001) was associated with an increased risk of stroke.

Conclusions

Stroke rates were increased among HIV-infected patients, independent of common stroke risk factors, particularly among young patients and women.

Low blood dehydroepiandrosterone sulfate (DHEAS) levels have strong positive associations with stroke and coronary heart disease. However, it is unclear whether DHEAS is independently associated with cardiovascular risk factors. Therefore, we examined the association between cardiovascular risk factors and DHEAS concentration among a high-risk population of Latinos (Puerto Ricans aged 45 to 75 years at baseline) in a cross-sectional analysis of the Boston Puerto Rican Health Study. Of eligible participants, 72% completed baseline interviews and provided blood samples. Complete data were available for 1355 participants. Associations between cardiovascular risk factors (age, sex, total cholesterol, high-density lipid cholesterol, triglycerides, and glucose) and log-transformed DHEAS (μg/dL) were assessed. In robust multivariable regression analyses, DHEAS was significantly inversely associated with age (β = -12.4; 95% CI: -15.2, -9.7; per 5 years), being female (vs. male) (β = -46; 95% CI: -55.3, -36.6), and plasma triglyceride concentration (β = -0.2; 95% CI: -0.3, -0.1; per 10 mg/dL) and was positively associated with total cholesterol and plasma glucose levels (β = 1.8; 95% CI: 0.6, 3 and β = 0.2; 95% CI: 0.04, 0.3, respectively, per 10 mg/dL) after adjustment for smoking, alcohol, and physical activity and for postmenopausal hormone use in women. Estimates were unchanged after adjustment for measures of chronic disease and inflammation. Women exhibited a stronger age-related decline in DHEAS and a positive association with glucose in contrast to findings among men (P _interaction < 0.05). In conclusion, in this large study of Latinos with a heavy cardiovascular risk factor burden, we observed significant associations between cardiovascular disease (CVD) risk factors and DHEAS, with variations by sex. These findings improve our understanding of the role DHEAS may play in CVD etiology.

The new diagnostic threshold of hemoglobin A(1c) was made based on evidence from cross-sectional studies, and no longitudinal study supports its validity. To examine whether hemoglobin A(1c) of 6.5% or higher defines a threshold for elevated risk of incident retinopathy, we analyzed longitudinal data of 19,897 Japanese adults who underwent a health checkup in 2006 and were followed up 3 years later. We used logistic regression models and restricted cubic spline models to examine the relationship between baseline hemoglobin A(1c) levels and the prevalence and the 3-year incidence of retinopathy. The restricted cubic spline model indicated a possible threshold for the risk of incident retinopathy at hemoglobin A(1c) levels of 6.0-7.0%. Logistic regression analysis found that individuals with hemoglobin A(1c) levels of 6.5-6.9% were at significantly higher risk of developing retinopathy at 3 years compared with those with hemoglobin A(1c) levels of 5.0-5.4% (adjusted odds ratio, 2.35 [95% CI 1.08-5.11]). Those with hemoglobin A(1c) levels between 5.5 and 6.4% exhibited no evidence of elevated risks. We did not observe a threshold in the analysis of prevalent retinopathy. Our longitudinal results support the validity of the new hemoglobin A(1c) threshold of 6.5% or higher for diagnosing diabetes.

Objective

To compare rates of intracerebral hemorrhage (ICH) in HIV-infected and uninfected individuals in a large clinical care cohort and to assess risk factors associated with ICH.

Methods

We identified incident ICH in HIV-infected and uninfected control cohorts from the Partners Health Care system using ICD-9-CM codes. We constructed Cox proportional hazards models to estimate adjusted hazard ratios for HIV infection and other predictors of ICH.

Results

The incidence rate of ICH was 2.29 per 1,000 person-years in HIV-infected individuals compared with 1.23 per 1,000 person-years in uninfected individuals, with an unadjusted incidence rate ratio of 1.85 (95% confidence interval 1.37-2.47, p < 0.001). In a multivariable model, HIV infection was independently associated with a higher hazard of ICH, although its effect diminished with increasing age. Female sex was associated with a lower hazard of ICH in the uninfected cohort but not in the HIV cohort. CD4 count <200 × 10(6) cells/L and anticoagulant use were predictive of ICH.

Conclusions

HIV infection conferred an increased adjusted hazard of ICH, which was more pronounced in young patients and in women.

Importance

Increasing access to care may be insufficient to improve the health of patients with diabetes mellitus and unmet basic needs (hereinafter referred to as material need insecurities). How specific material need insecurities relate to clinical outcomes and the use of health care resources in a setting of near-universal access to health care is unclear.

Objective

To determine the association of food insecurity, cost-related medication underuse, housing instability, and energy insecurity with control of diabetes mellitus and the use of health care resources.

Design, setting, and participants

Cross-sectional data were collected from June 1, 2012, through October 31, 2013, at 1 academic primary care clinic, 2 community health centers, and 1 specialty center for the treatment of diabetes mellitus in Massachusetts. A random sample of 411 patients, stratified by clinic, consisted of adults (aged ≥21 years) with diabetes mellitus (response rate, 62.3%).

Main outcomes and measures

The prespecified primary outcome was a composite indicator of poor diabetes control (hemoglobin A1c level, >9.0%; low-density lipoprotein cholesterol level, >100 mg/dL; or blood pressure, >140/90 mm Hg). Prespecified secondary outcomes included outpatient visits and a composite of emergency department (ED) visits and acute care hospitalizations (ED/inpatient visits).

Results

Overall, 19.1% of respondents reported food insecurity; 27.6%, cost-related medication underuse; 10.7%, housing instability; 14.1%, energy insecurity; and 39.1%, at least 1 material need insecurity. Poor diabetes control was observed in 46.0% of respondents. In multivariable models, food insecurity was associated with a greater odds of poor diabetes control (adjusted odds ratio [OR], 1.97 [95% CI, 1.58-2.47]) and increased outpatient visits (adjusted incident rate ratio [IRR], 1.19 [95% CI, 1.05-1.36]) but not increased ED/inpatient visits (IRR, 1.00 [95% CI, 0.51-1.97]). Cost-related medication underuse was associated with poor diabetes control (OR, 1.91 [95% CI, 1.35-2.70]) and increased ED/inpatient visits (IRR, 1.68 [95% CI, 1.21-2.34]) but not outpatient visits (IRR, 1.07 [95% CI, 0.95-1.21]). Housing instability (IRR, 1.31 [95% CI, 1.14-1.51]) and energy insecurity (IRR, 1.12 [95% CI, 1.00-1.25]) were associated with increased outpatient visits but not with diabetes control (OR, 1.10 [95% CI, 0.60-2.02] and OR, 1.27 [95% CI, 0.96-1.69], respectively) or with ED/inpatient visits (IRR, 1.49 [95% CI, 0.81-2.73] and IRR, 1.31 [95% CI, 0.80-2.13], respectively). An increasing number of insecurities was associated with poor diabetes control (OR for each additional need, 1.39 [95% CI, 1.18-1.63]) and increased use of health care resources (IRR for outpatient visits, 1.09 [95% CI, 1.03-1.15]; IRR for ED/inpatient visits, 1.22 [95% CI, 0.99-1.51]).

Conclusions and relevance

Material need insecurities were common among patients with diabetes mellitus and had varying but generally adverse associations with diabetes control and the use of health care resources. Material need insecurities may be important targets for improving care of diabetes mellitus.

Objective

To determine if the greater risk of ischemic stroke observed in women living with HIV infection (WLWH) compared with HIV-uninfected women persists after accounting for both traditional and sex-specific stroke risk factors.

Methods

We performed an observational cohort study of WLWH (n = 1214) and demographics-matched HIV-uninfected women (n = 12 041) seen between 1996 and 2011 at two tertiary care hospitals in Boston. We used Cox proportional hazards regression analyses to model time to ischemic stroke, adjusting first for demographics and traditional stroke risk factors and then for sex-specific stroke risk factors, including menopause and estrogen use. We also constructed demographics-adjusted Cox models to identify HIV-related risk factors associated with ischemic stroke among WLWH.

Results

The incidence of ischemic stroke was higher among WLWH compared with HIV-uninfected women [incidence rate ratio 2.39, 95% confidence interval (CI) 1.62-3.43]. After adjusting for demographics and traditional stroke risk factors, HIV infection was associated with almost twice the risk of ischemic stroke (hazard ratio 1.93, 95% CI 1.31-2.85). The association of HIV with ischemic stroke persisted after inclusion of sex-specific stroke risk factors in the model (hazard ratio 1.89, 95% CI 1.28-2.81). Among WLWH, longer duration of antiretroviral therapy was associated with lower ischemic stroke risk (hazard ratio 0.86 per year, 95% CI 0.76-0.96).

Conclusion

The increased risk of ischemic stroke among WLWH compared with HIV-uninfected women persisted after adjusting for both traditional and sex-specific stroke risk factors. Further investigation into the mechanisms of elevated stroke risk among WLWH, including immunologic factors, will be key for developing targeted preventive strategies for this at-risk population.

Polygenic scores (PGSs) combine the effects of common genetic variants^1,2 to predict risk or treatment strategies for complex diseases^3-7. Adding rare variation to PGSs has largely unknown benefits and is methodically challenging. Here, we developed a method for constructing rare variant PGSs and applied it to calculate genetically modified hemoglobin A1C thresholds for type 2 diabetes (T2D) diagnosis^7-10. The resultant rare variant PGS is highly polygenic (21,293 variants across 154 genes), depends on ultra-rare variants (72.7% observed in fewer than three people) and identifies significantly more undiagnosed T2D cases than expected by chance (odds ratio = 2.71; P = 1.51 × 10^-6). A PGS combining common and rare variants is expected to identify 4.9 million misdiagnosed T2D cases in the United States-nearly 1.5-fold more than the common variant PGS alone. These results provide a method for constructing complex trait PGSs from rare variants and suggest that rare variants will augment common variants in precision medicine approaches for common disease.

Aims

Causal transcripts at genomic loci associated with type 2 diabetes (T2D) are mostly unknown. The chr8p23.1 variant rs4841132, associated with an insulin-resistant diabetes risk phenotype, lies in the second exon of a long non-coding RNA (lncRNA) gene, LOC157273, located 175 kilobases from PPP1R3B, which encodes a key protein regulating insulin-mediated hepatic glycogen storage in humans. We hypothesized that LOC157273 regulates expression of PPP1R3B in human hepatocytes.

Methods

We tested our hypothesis using Stellaris fluorescent in situ hybridization to assess subcellular localization of LOC157273; small interfering RNA (siRNA) knockdown of LOC157273, followed by RT-PCR to quantify LOC157273 and PPP1R3B expression; RNA-seq to quantify the whole-transcriptome gene expression response to LOC157273 knockdown; and an insulin-stimulated assay to measure hepatocyte glycogen deposition before and after knockdown.

Results

We found that siRNA knockdown decreased LOC157273 transcript levels by approximately 80%, increased PPP1R3B mRNA levels by 1.7-fold, and increased glycogen deposition by >50% in primary human hepatocytes. An A/G heterozygous carrier (vs. three G/G carriers) had reduced LOC157273 abundance due to reduced transcription of the A allele and increased PPP1R3B expression and glycogen deposition.

Conclusion

We show that the lncRNA LOC157273 is a negative regulator of PPP1R3B expression and glycogen deposition in human hepatocytes and a causal transcript at an insulin-resistant T2D risk locus.