Explaining biological differences between men and women by gendered mechanisms

BackgroundAre the observed biological differences between men and women physiological, liked to sexual dimorphism, or can they be explained, at least in part, by social gender mechanisms ? We applied...

Toward understanding how early-life social experiences alter oxytocin- and vasopressin-regulated social behaviors

Although epidemiological data provides evidence that there is an interaction between genetics (nature) and the social and physical environments (nurture) in human development; the main open question remains the mechanism. The pattern of distribution of methyl groups in DNA is different from cell-type to cell type and is conferring cell specific identity on DNA during cellular differentiation and organogenesis. This is an innate and highly programmed process. However, recent data suggests that DNA methylation is not only involved in cellular differentiation but that it is also involved in modulation of genome function in response to signals from the physical, biological and social environments. We propose that modulation of DNA methylation in response to environmental cues early in life serves as a mechanism of life-long genome "adaptation" that molecularly embeds the early experiences of a child ("nurture") in the genome ("nature"). There is an emerging line of data supporting this hypothesis in rodents, non-human primates and humans that will be reviewed here. However, several critical questions remain including the identification of mechanisms that transmit the signals from the social environment to the DNA methylation/demethylation enzymes.

Early social environment, either positive or negative, shapes the adult brain. Communal nesting (CN), a naturalistic setting in which 2-3 females keep their pups in a single nest sharing care-giving behavior, provides high level of peer interaction for pups. Early social isolation (ESI) from dam and siblings represents, instead, an adverse condition providing no peer interaction. We investigated whether CN (enrichment setting) might influence the response to ESI (impoverishment setting) in terms of social behavior and glutamate system in the medial prefrontal cortex (mPFC) of adult and adolescent male and female rats. Pinning (a rewarding component of social play behavior) was significantly more pronounced in males than in females exposed to the combination of CN and ESI. CN sensitized the glutamate synapse in the mPFC of ESI-exposed male, but not female, rats. Accordingly, we observed (i) a potentiation of the glutamatergic neurotransmission in the mPFC of both adolescent and adult males, as shown by the recruitment of NMDA receptor subunits together with increased expression/activation of PSD95, SynCAM 1, Synapsin I and αCaMKII; (ii) a de-recruiting of NMDA receptors from active synaptic zones of same-age females, together with reduced expression/activation of the above-mentioned proteins, which might reduce the glutamate transmission. Whether similar sex-dependent glutamate homeostasis modulation occurs in other brain areas remains to be elucidated. CN and ESI interact to shape social behavior and mPFC glutamate synapse homeostasis in an age- and sex-dependent fashion, suggesting that early-life social environment may play a crucial role in regulating the risk to develop psychopathology.

We used data on children included in the UK Millennium Cohort Study. We described the social environment using area-level and material factors as well as socioeconomic position (SEP) at 9 months. EBV was measured at 3 years of age (n = 12 457). Lower rates of EBV infection were observed in children living in towns and rural areas compared with those living in cities. Lower SEP and overcrowding in the household increased the odds of being infected. Children whose parents were social tenants were more likely to be infected than homeowners. In the overall model, the strength of the association between material factors and EBV infection weakened. We showed that early life material deprivation was associated with a higher risk of EBV infection among 3-year-olds. Children living in more deprived social conditions may be more likely to become EBV carriers at an earlier age.

Season-specific carryover of early life associations in a monogamous bird species

Background: Air pollution is a leading cause of cardiovascular diseases including ischemic heart disease and stroke contributing to millions of deaths, with elevated blood pressure, endothelial dysfunction, and systemic inflammation being some of the most important underlying mechanisms. Various studies showed a promising beneficial effect of indoor air purification on various health outcomes, including blood pressure. We aimed to assess the effect of indoor air purification on systolic blood pressure (SBP) and Diastolic blood pressure (DBP) and provide a rationale for home use of these filters. Methods: We searched PubMed, Web of Science, Cochrane and Scopus for published literature up to May 2024. We included studies that assessed air purification, including HEPA filters or electrostatic air filters, as an intervention compared to no intervention. The primary outcome of interest was mean changes in blood pressure both systolic and diastolic. Secondary outcomes were biomarkers of inflammation and oxidative stress. Mean difference (MD) and 95% CI was used in a fixed-effect model to analyze the data. Results: A total of 21 studies were included in our meta-analysis with a total of 1955 participants. Air purification was associated with a significant reduction in systolic blood pressure (SBP) (MD: -2.42, 95% CI: -3.42, -1.41), and diastolic blood pressure (DBP) (MD: -1.11, 95% CI: -1.76, -0.46). However, there was no significant changes in levels of inflammatory biomarkers or oxidative stress. Conclusion: Indoor air purification was associated with significant reductions in systolic and diastolic blood pressure levels, but questions arise whether these reductions are clinically relevant or not. Further studies should assess these findings. Conclusion: Indoor air purification was associated with significant reductions in systolic and diastolic blood pressure levels, but questions arise whether these reductions are clinically relevant or not. Further studies should assess these findings.

BACKGROUND AND PURPOSEA number of experimental procedures require single housing to assess individual behaviour and physiological responses to pharmacological treatments. The endogenous opioids are closely linked to social interaction, especially early in life, and disturbance in the social environment may affect opioid peptides and thereby confound experimental outcome. The aim of the present study was to examine time-dependent effects of single housing on opioid peptides in rats.EXPERIMENTAL APPROACHEarly adolescent Sprague Dawley rats (post-natal day 22) were subjected to either prolonged (7 days) or short (30 min) single housing. Several brain regions were dissected and immunoreactive levels of Met-enkephalin-Arg6Phe7 (MEAP), dynorphin B and nociception/orphanin FQ, as well as serum corticosterone were measured using RIA.KEY RESULTSProlonged single housing reduced immunoreactive MEAP in hypothalamus, cortical regions, amygdala, substantia nigra and periaqueductal grey. Short single housing resulted in an acute stress response as indicated by high levels of corticosterone, accompanied by elevated immunoreactive nociceptin/orphanin FQ in medial prefrontal cortex, nucleus accumbens and amygdala. Neither short nor prolonged single housing affected dynorphin B.CONCLUSIONS AND IMPLICATIONSDisruption in social environmental conditions of rats, through single housing during early adolescence, resulted in time-, area- and peptide-specific alterations in endogenous opioids in the brain. These results provide further evidence for an association between early life social environment and opioids. Furthermore, the results have implications for experimental design; in any pharmacological study involving opioid peptides, it is important to distinguish between effects induced by housing and treatment.LINKED ARTICLESThis article is part of a themed section on Opioids: New Pathways to Functional Selectivity. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2015.172.issue-2

RESULTS: The mean ages of the 207 diabetic patients who were involved in the study was 54.5±33.5 years, and 56.5% (n = 117) of the patients were female. Higher levels control problems were related with the higher levels of blood pressure, total cholesterol, LDL cholesterol and body mass index. Higher levels of patients’ positive attitude were associated with lower diastolic blood pressure and fasting blood sugar levels. In contrast, higher levels of patients’ negative attitudes were associated with higher levels of fasting blood glucose, diastolic blood pressure and HDL cholesterol. Higher levels of patient care profi ciency were associated with the lower levels of blood glucose, systolic blood pressure, diastolic blood pressure, HDL cholesterol, LDL cholesterol and body mass index. Higher levels of self-care attitudes of the patients were associated with the lower levels of the fasting blood glucose, HbA1c, systolic blood pressure, diastolic blood pressure, LDL cholesterol and body mass index. Higher levels of strict adherence to diet were associated with lower levels of systolic blood pressure, diastolic blood pressure, total cholesterol, triglycerides and body mass index. Increased levels of barriers to reach the treatment were associated with higher levels of fasting blood glucose, systolic blood pressure, diastolic blood pressure, and the body mass index. The higher levels of barriers against physical exercise were associated with higher levels of body mass index and LDL cholesterol but lower levels of HDL cholesterol. Higher diabetes knowledge scores of patients were associated with lower systolic and diastolic blood pressure, and LDL cholesterol levels but higher triglyceride levels. Kafkas J Med Sci 2011; 1(2):57–63 • doi: 10.5505/kjms.2011.41736

Effects of the Social Environment and Stress on Glucocorticoid Receptor Gene Methylation: A Systematic Review

Background:Previous studies have observed associations between air pollution and heart disease. Susceptibility to air pollution effects has been examined mostly with a test of effect modification, but little evidence is available whether air pollution distorts cardiovascular risk factor distribution.Objectives:This paper aims to examine distributional and heterogeneous effects of air pollution on known cardiovascular biomarkers.Methods:A total of 1,112 men from the Normative Aging Study and residents of the greater Boston, Massachusetts, area with mean age of 69 years at baseline were included in this study during the period 1995–2013. We used quantile regression and random slope models to investigate distributional effects and heterogeneity in the traffic-related responses on blood pressure, heart rate variability, repolarization, lipids, and inflammation. We considered 28-day averaged exposure to particle number, PM2.5 black carbon, and PM2.5 mass concentrations (measured at a single monitor near the site of the study visits).Results:We observed some evidence suggesting distributional effects of traffic-related pollutants on systolic blood pressure, heart rate variability, corrected QT interval, low density lipoprotein (LDL) cholesterol, triglyceride, and intercellular adhesion molecule-1 (ICAM-1). For example, among participants with LDL cholesterol below 80 mg/dL, an interquartile range increase in PM2.5 black carbon exposure was associated with a 7-mg/dL (95% CI: 5, 10) increase in LDL cholesterol, while among subjects with LDL cholesterol levels close to 160 mg/dL, the same exposure was related to a 16-mg/dL (95% CI: 13, 20) increase in LDL cholesterol. We observed similar heterogeneous associations across low versus high percentiles of the LDL distribution for PM2.5 mass and particle number.Conclusions:These results suggest that air pollution distorts the distribution of cardiovascular risk factors, and that, for several outcomes, effects may be greatest among individuals who are already at high risk.Citation:Bind MA, Peters A, Koutrakis P, Coull B, Vokonas P, Schwartz J. 2016. Quantile regression analysis of the distributional effects of air pollution on blood pressure, heart rate variability, blood lipids, and biomarkers of inflammation in elderly American men: the Normative Aging Study. Environ Health Perspect 124:1189–1198; http://dx.doi.org/10.1289/ehp.1510044

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Design and rationale of penn medicine healthy heart, a randomized trial of effectiveness of a centrally organized approach to blood pressure and cholesterol improvement among patients at elevated risk of atherosclerotic cardiovascular disease

AHA 2012: Prevention a key focus of meeting

BackgroundAllostatic load (AL), reflecting cumulative biological stress, may contribute to Alzheimer's Disease (AD) risk. Biomarkers of AL may change during progression of cognitively unimpaired (CU) individuals as they develop Mild Cognitive Impairment (MCI) or AD. This study investigates change patterns in AL biomarkers in CU, MCI, and AD individuals.MethodsUsing the Alzheimer's Disease Neuroimaging Initiative (ADNI) database, we analyzed AL changes over 24 months in individuals cognitively unimpaired (CU), MCI and AD. Mean ALI and standard deviations were calculated, and biomarker changes were reported.ResultsAt baseline, mean ALI values were similar across groups (CU: 4.3 ± 2.1, MCI: 4.2 ± 2.3, AD: 4.3 ± 2.4, p = 0.781). Over 24 months, significant changes in neuroendocrine biomarkers were observed. Cortisol increased most in the MCI group (24, 72.73%), Prolactin in AD (19, 61.29%), and Luteinizing Hormone (LH) and Testosterone in CU (LH: 4, 57.14%; Testosterone: 5, 71.43%).Inflammatory biomarkers were highest in AD overall (81, 54.73%). Interleukin‐18 (IL‐18) and Tumor Necrosis Factor Alpha (TNF‐α) changes were most frequent in AD (IL‐18: 19, 76.00%; TNF‐α: 20, 76.92%), while IL‐6R increased mainly in MCI (14, 58.33%) and MCP‐3 in AD (17, 58.62%).ConclusionWhile baseline ALI was similar across cognitive statuses, longitudinal changes in specific neuroendocrine and inflammatory biomarkers, particularly Cortisol, Prolactin, IL‐18, and TNF‐α, were strongly associated with those with cognitive decline and AD progression. Future studies should identify clusters of AL biomarkers linked to cognitive decline across the AD continuum.Keywords: Alzheimer's Disease, Mild Cognitive Impairment, Allostatic Load, Inflammatory Biomarkers, Neuroendocrine Biomarkers.