Intimate Partner Violence and Breastfeeding Behaviors: Does the Source of Breastfeeding Information Affect the Associations Between Prepregnancy or Prenatal IPV and Breastfeeding Behaviors of Women in the United States? A PRAMS 2018 Study.

Background: Most countries do not meet World Health Organization's breastfeeding recommendations, and exposure to intimate partner violence (IPV) hinders positive breastfeeding behaviors. One in four U.S. women (43.6 million women) experiences IPV. This study aims to assess relationships between IPV, and breastfeeding initiation, duration, and early cessation among women in 42 U.S. states; and to evaluate possible modifying effect(s) of different breastfeeding information sources. Methods: Centers for Disease Control and Prevention's 2016-2018 Pregnancy Risk Assessment Monitoring System data (n = 105,230) were used to assess relationships between prepregnancy/prenatal IPV and breastfeeding initiation, duration, and early cessation; and modify effects of various breastfeeding information sources on study associations using multilogistic regression models. Results: About 1.4% of women experienced prenatal IPV with reduced odds of breastfeeding for 6 months or more (odds ratio [OR] = 0.74; 95% confidence interval = 0.58-0.94). Receiving breastfeeding information from baby's doctor modified early cessation (0.37 [0.18-0.78]) (p for interaction = 0.009) with prenatal IPV exposure. Among women exposed to prenatal IPV, breastfeeding initiation was stronger in women who received breastfeeding information from family/friends (2.46, [1.24-4.88]) (p for interaction = 0.010) or from breastfeeding support groups (3.03 [1.17-7.88]) (p for interaction = 0.023) compared to those who did not. Breastfeeding information from family/friends modified association between prepregnancy IPV and breastfeeding duration (0.67 [0.45-0.99]) (p for interaction = 0.042). Conclusions: Prenatal IPV is a risk factor for short-duration breastfeeding. Receiving information from doctors, nurses, support groups, and family/friends may improve breastfeeding behavior among IPV-exposed women. Interventions promoting breastfeeding information dissemination by family/friends, support groups, and doctors/nurses during hospital visits are encouraged.

Relation of plasma lipids to all-cause mortality in Caucasian, African-American and Hispanic elders.

OBJECTIVES: to investigate the relation of plasma lipids to all-cause mortality in a multi-ethnic cohort of non-demented elderly. SETTING: community-based sample of Medicare recipients, 65 years and older, residing in Northern Manhattan. PARTICIPANTS: about two thousand five hundred and fifty-six non-demented elderly, 65-103 years. Among participants, 66.1% were women, 27.6% were White/non-Hispanic, 31.2% were African-American and 41.2% were Hispanic. METHODS: a standardised assessment, including functional ability, medical history, physical and neurological examination and a neuropsychological battery was conducted. Vital status was ascertained through the National Death Index (NDI). We used survival analyses stratified by race and ethnicity to examine the relation of plasma lipids to subsequent all-cause mortality. RESULTS: hispanics had the best overall survival, followed by African-Americans and Whites. Whites and African-Americans in the lowest quartiles of total cholesterol, non-HDL cholesterol and low-density lipoprotein cholesterol (LDL cholesterol) were approximately twice as likely to die as those in the highest quartile (White HR: 2.2, for lowest total cholesterol quartile; HR: 2.3, for lowest non-HDL cholesterol quartile; and HR: 1.8, for lowest LDL cholesterol quartile. African-American HR: 1.9, for lowest total cholesterol, HR: 2.0, for lowest non-HDL cholesterol and HR: 1.9, for lowest LDL cholesterol). In contrast, plasma lipid levels were not related to mortality risk among Hispanics. CONCLUSIONS: hispanic ethnicity modifies the associations between lipid levels and all-cause mortality in the elderly.

Relationship between plasma lipids and all-cause mortality in nondemented elderly.

OBJECTIVES: To investigate the relationship between plasma lipids and risk of death from all causes in nondemented elderly. DESIGN: Prospective cohort study. SETTING: Community-based sample of Medicare recipients, aged 65 years and older, residing in northern Manhattan. PARTICIPANTS: Two thousand two hundred seventy-seven nondemented elderly, aged 65 to 98; 672 (29.5%) white/non-Hispanic, 699 (30.7%) black/non-Hispanic, 876 (38.5%) Hispanic, and 30 (1.3%) other. MEASUREMENTS: Anthropometric measures: fasting plasma total cholesterol, triglyceride, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and non-HDL-C, body mass index, and apolipoprotein E (APOE) genotype. clinical measures: neuropsychological, neurological, medical, and functional assessments; medical history of diabetes mellitus, heart disease, hypertension, stroke, and treatment with lipid-lowering drugs. Vital status measure: National Death Index date of death. Survival methods were used to examine the relationship between plasma lipids and subsequent mortality in younger and older nondemented elderly, adjusting for potential confounders. RESULTS: Nondemented elderly with levels of total cholesterol, non-HDL-C, and LDL-C in the lowest quartile were approximately twice as likely to die as those in the highest quartile (rate ratio (RR)=1.8, 95% confidence interval (CI)=1.3-2.4). These results did not vary when analyses were adjusted for body mass index, APOE genotype, diabetes mellitus, heart disease, hypertension, stroke, diagnosis of cancer, current smoking status, or demographic variables. The association between lipid levels and risk of death was attenuated when subjects with less than 1 year of follow-up were excluded (RR=1.4, 95% CI=1.0-2.1). The relationship between total cholesterol, non-HDL-C, HDL-C, and triglycerides and risk of death did not differ for older (>or=75) and younger participants (>75), whereas the relationship between LDL-C and risk of death was stronger in younger than older participants (RR=2.4, 95% CI=1.2-4.9 vs RR=1.6, 95% CI=1.02-2.6, respectively). Overall, women had higher mean lipid levels than men and lower mortality risk, but the risk of death was comparable for men and women with comparable low lipid levels. CONCLUSION: Low cholesterol level is a robust predictor of mortality in the nondemented elderly and may be a surrogate of frailty or subclinical disease. More research is needed to understand these associations.

Preservation of cognitive and functional ability as markers of longevity.

Longevity is a complex biological process for which the phenotypes have not been established. Preservation of cognitive and physical function may be important and preservation of these functions is, in part, inherited. We investigated the relation between rate of change in cognitive and functional abilities in probands and risk of death in their siblings. Probands were classified as showing no decline, slow, medium, or rapid rate of decline, based on the slope of change in cognitive and physical/functional factors over three or more assessments. Siblings of probands who did not decline on measures of memory, visuospatial/cognitive function or ADL skills were approximately half as likely to die as siblings of probands who had the most rapid decline. The reduction in risk of death in siblings of probands who did not decline in was primarily observed among siblings of probands who were older than 75 years, suggesting that genetic influences on life span may be greater at older ages. There was no association between probands' rate of change in language, IADL skills, upper or lower extremity mobility and risk of death in siblings. The results of the present study identify phenotypes associated with preserved cognitive and functional abilities which may serve as markers for longevity.

Exceptional memory performance in the Long Life Family Study.

Research to understand variability at the highest end of the cognitive performance distribution has been scarce. Our aim was to define a cognitive endophenotype based on exceptional episodic memory (EM) performance and to investigate familial aggregation of EM in families from the Long Life Family Study (LLFS). Using a sample of 1911 nondemented offspring of long-lived probands, we created a quantitative phenotype, EM (memory z ≥ 1.5), and classified LLFS families as EM and non-EM families based on the number of EM offspring. We then assessed differences in memory performance between LLFS relatives in the parental generation of EM families and those in non-EM families using multivariate analysis adjusted for APOE Apolipoprotein E genotype. LLFS relatives in the proband generation from EM families showed better EM performance than those from non-EM families (ß = 0.74, standard error = 0.19, p = 1.4 × 10(-4)). We demonstrated that there is a familial correlation of the EM endophenotype, suggesting that genetic variants might influence memory performance in long-lived families.

Cognitive function in families with exceptional survival.

The authors investigated whether cognitive function may be used as an endophenotype for longevity by assessing the cognitive performance of a family-based cohort consisting of 1380 individuals from 283 families recruited for exceptional survival in field centers in Boston, New York, Pittsburgh, and Denmark. Cognitive performance was assessed in the combined offspring of the Long Life Family Study (LLFS) probands and their LLFS siblings as compared with their spouses' cognitive performance. Our results indicate that the combined offspring of the LLFS probands and their siblings achieve significantly higher scores on both digit forward and backward tasks (p = 5 10(-5) and p = 8 10(-4) respectively) as well as on a verbal fluency task (p = 0.008) when compared with their spouse controls. No differences between groups were found for the other cognitive tests assessed. We conclude that LLFS family members in the offspring generation demonstrate significantly better performance on multiple tasks requiring attention, working memory, and semantic processing when compared with individuals without a family history of exceptional survival, suggesting that cognitive performance may serve as an important endophenotype for longevity.

A multi-center, randomized, double blind placebo-controlled trial of estrogens to prevent Alzheimer's disease and loss of memory in women: design and baseline characteristics.

BACKGROUND: Observational studies and small clinical trials suggested that hormone replacement therapy (HRT) decreases risk of cognitive loss and Alzheimer's disease (AD) in postmenopausal women and may have value in primary prevention. PURPOSE: A clinical trial was designed to determine if HRT delays AD or memory loss. This report describes the rationale and original design of the trial and details extensive modifications that were required to respond to unanticipated findings that emerged from other studies during the course of the trial. METHODS: The trial was designed as a multi-center, placebo-controlled primary prevention trial for women 65 years of age or older with a family history of dementia. Recruitment from local sites was supplemented by centralized efforts to use names of Medicare beneficiaries. Inclusion criteria included good general health and intact memory functioning. Participants were randomized to HRT or placebo in a 1:1 ratio. Assignment was stratified by hysterectomy status and site. The primary outcomes were incident AD and memory decline on neuropsychological testing. RESULTS: Enrollment began in March 1998. In response to the Women's Health Initiative (WHI) May 2002 report of increased incidence of heart disease, stroke, pulmonary embolism, and breast cancer among women randomized to HRT, participants were re-consented with a revised consent form. Procedural modifications, including discontinuation of study medication and a modification of the planned primary outcome based on a final enrollment below the target enrollment (N = 477), were enacted in response to the subsequent WHI Memory Study report of increased risk of dementia and poorer cognitive function with HRT. The mean length of treatment exposure prior to discontinuation was 2.14 years. Participants' mean age at baseline was 72.8; mean education was 14.2 years. Minority participation was 19% and 34% had a hysterectomy. The study continues to follow these participants for a total of 5 years blind to the original medication assignment. LIMITATIONS: Results reported from the WHI during the course of this study mandated extensive procedural modifications, including discontinuing recruitment before completion and halting study medication. Alternative strategies for study redesign that were considered are discussed.

Genetic influences on life span and survival among elderly African-Americans, Caribbean Hispanics, and Caucasians.

An investigation of the genetic influences on life span and survival was conducted among elderly African-Americans, Caribbean Hispanics, and Caucasians Medicare recipients (ages 65-104 years). Family history information on 13,161 parents and siblings was obtained. Heritability of life span varied by the age and by ethnic group being lowest for African-Americans. We recalculated the heritability coefficients for life span including only probands and their siblings, but the differences across ethnic groups persisted. In contrast the heritability of survival was more similar across ethnic groups but was similar to that for life span. Heritability coefficients for survival in probands and their siblings revealed little difference between ethnic groups and suggested that as much as 35% of the variation in survival may be genetically influenced. These results indicate that life span and survival are genetically influenced. Comparisons across generations and ethnic groups indicate that changes in environmental hygiene, social welfare, and health care systems are significant contributors to life span and survival, but genetic influences are also important. Identifying the genes associated with life span and survival will provide insight into how the genes interact with environment to influence aging in humans.