Women are more susceptible to a range of detrimental diseases surrounding autoimmunity and inflammation, but the causes of this are largely unknown. Much of the current research investigating these patterns focus on a microscopic view of cellular and/or hormonal processes, but holistic perspectives incorporating sociology, psychology, physiology, and evolution are rarely considered. Through investigating interactions between a history of neglecting women’s research, evolutionary origins of sex differences in the immune system, and the impacts of society’s influences on stress, some sex-biased patterns of disease may emerge. The existing SS-SH-SS theory by Brown et al. (2022) describes the complex environmental, psychological, and biological mechanisms that interact to create a female sensitivity to stress-based inflammatory diseases. Using the foundations of this theory, in this study we used global disease and stress exposure data from the World Bank and Global Health Data Exchange project to investigate how the relationships between exposure to stress and prevalence of diseases differ by sex. Using principal component analysis and generalized linear mixed models, we demonstrated a complex relationship between certain stress factors and inflammatory diseases. Particularly, we found that levels of poverty, alcohol use and drug use had distinct, sex-specific impacts on rates of diseases that we studied. Female rates of disease were particularly sensitive to the changes in substance use and poverty, with an inverse relationship with poverty and a direct relationship with substance use. This study can serve as an example for investigating the correlates of sex-biased diseases and mental disorders, particularly about the role of sex-biased experiences of social stress in the origin of sex-biased mental illnesses. / Thesis / Master of Science (MSc) / Throughout history, women's health has been overlooked in research, leading to a lack of understanding regarding sex-related health disparities. Our project addresses this gap by exploring how stress impacts inflammation and its connection to the prevalence of diseases like rheumatoid arthritis and depression. We analyze data from international repositories, revealing that males and females respond differently to specific stressors, which may help explain why certain diseases are more prevalent among women. This insight strengthens our understanding of sex-based health outcomes and may lead to improved healthcare for women everywhere.

Thesis (M.S.)--Boston University / PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you. / 2031-01-01

Infertility impacts numerous individuals during their reproductive journey. Yet, there is little research and information available that examines if having a history of infertility goes on to have further implications after an individual conceives and gives birth. Thus, the current study aimed to examine if infertility impacts the postpartum period, and if there were any particular risk or resiliency factors that contributed to this relationship. In this study, women aged 18 to 50, who had given birth within the last 12 months, participated in an online survey that assessed a variety of physical and mental health constructs. Overall, results largely exemplified that infertility does not go on to impact postpartum adjustment within in this particular sample of women who identified as having higher levels of education, perceived SES, and income. However, many of the covariates, such as SES, did correlate with postpartum outcomes. Findings highlight the resilience of this sample of women, despite previously experiencing stressful events.

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Osteoarthritis (OA) is a prevalent and progressive musculoskeletal condition characterized by the degradation of the cartilage and bone and is often comorbid with cardiovascular disease (CVD), with both disease prevalence’s increasing with age. Several factors, such as the site of OA and the menopause transition, are known to independently influence both conditions. OA and CVD share overlapping risk factors and proposed mechanisms, though it is not well understood how these mechanisms influence the risk of comorbidity. This thesis examines the relationship of CVD risk factors, sites of OA, and menopausal variables on CVD risk in individuals with OA. The first aim of this thesis was to examine preclinical markers of CVD risk, namely the carotid intima-media thickness (cIMT) and cardiovascular risk scores, the Framingham risk score (FRS) and the InterHeart risk score (IHRS), in individuals with and without OA to examine differences in CVD risk profiles. Additional considerations were given to the site of OA, as well as non-specific CVD risk factors (such as social disadvantage and frailty). Risk factors were compared between age- and sex-matched individuals with and without OA and between weight-bearing and non-weight bearing OA. Individuals with OA had significantly greater cIMT, FRS, and IHRS, though no differences were found when comparing the site of OA. Unadjusted and multivariate adjusted odds ratios (OR) calculated odds of CVD at 3-year follow-up in the same cohorts. There was a significantly unadjusted (p<0.001, OR:1.70) and adjusted (p<0.001, OR ranging from 1.67-1.70) influence of OA diagnosis on odds of CVD at 3-year follow-up. There was no significant unadjusted or adjusted difference in odds of CVD at 3-year follow-up when comparing different sites of OA (p ranging from 0.24-0.75, OR ranging from 0.69-0.71). The second aim of this thesis was to study CVD risk in post-menopausal women. CVD risk factors and the IHRS were used to calculate differences between age-matched post-menopausal women. Unadjusted and multivariable adjusted ORs calculated odds of CVD at 3-year follow-up. There was a significant unadjusted influence of OA diagnosis (p=0.03, OR:1.34) on CVD outcomes, though the effect of OA diagnosis became non-significant after adjusting for the IHRS (p=0.25, OR:1.36) and the IHRS with menopausal variables (p=0.22, OR:1.40). Although OA is a multifaceted condition, it has often been viewed as a joint-centric disease. The elevated risk of CVD individuals with OA suggests that additional aspects of the OA pathology, such as inflammation and frailty, may drive the increase in risk of CVD independent of age, sex, or menopausal status. / Thesis / Master of Science (MSc) / Osteoarthritis (OA) and cardiovascular disease (CVD) are two of the most prevalent comorbidities that affect the aging population. Surrogate measures of CVD, such as CVD risk scores and carotid intima-media thickness, have rarely been examined in individuals with OA despite studies showing elevated CVD risk in individuals with OA. We used baseline and 3-year follow-up data collected by the Canadian Longitudinal Study on Aging to study CVD risk factors in older individuals with and without OA, with considerations given to the site of OA and to menopause, which are additional non-modifiable factors known to influence vascular outcomes. We hypothesized that individuals with OA have greater CVD risk and odds of developing CVD compared to individuals without OA. We found that individuals with OA have greater CVD risk and odds of developing CVD at 3-year follow-up, with no influence of OA site on CVD outcomes, and post-menopausal women with OA have greater odds of developing CVD than post-menopausal women without OA. Our findings suggests that aspects of the OA pathology play a role in increasing CVD risk, which are partially explained through shared risk factors and etiology.

Background: The composition of the vaginal microbiota (VMB) in the female genital tract (FGT) can impact the vaginal epithelium and protect against or increase risk of sexually transmitted viral infections. The VMB grows as a biofilm, a complex structure formed by bacteria for increased survival. When the VMB consists of a diverse bacterial community it correlates with pathogenic effects that lead to adverse health conditions and an increased risk of HIV infection. When the VMB contains Lactobacillus species, beneficial health effects and decreased susceptibility to infection are observed. The aim of this project is to optimize an in vitro model of biofilm formation for different bacteria associated with the VMB, identify the effects that biofilm has on vaginal epithelial cells and test biofilm treatment strategies. We hypothesize that a Lactobacillus biofilm will enhance barrier function and decrease cytotoxicity of vaginal epithelial cells whereas dysbiotic biofilm will decrease barrier function and induce cytotoxicity. We also hypothesize that various conditions, such as presence of estradiol and eubiotic short-chain fatty acids, will stimulate Lactobacillus biofilm growth and suppress dysbiotic biofilm growth in a vaginal epithelial cell model. Methods: For optimization of the biofilm model, VK2/E6E7 cells were grown in air-liquid interface (ALI) or liquid-liquid interface (LLI) cultures in presence or absence of L. crispatus, L. iners, G. vaginalis or P. bivia bacteria. Biofilm formation was assessed using FilmTracerTM SYPRO® Ruby biofilm matrix protein stain. Hormone effects were tested by adding estradiol (10-9 M) and progesterone (10-7 M) to culture media. Short-chain fatty acid (SCFA) effects were tested by adding lactic acid, acetic acid, succinic acid and butyric acid in varying concentrations to culture media. Enzyme effects were tested by adding sialidase to Vk2 cells before bacteria inoculation. Results: A novel in vitro model of biofilm formation on vaginal epithelial cells was created. Vk2 cells in ALI and LLI cultures remained viable in anaerobic conditions and showed mucin-1 production in aerobic and anaerobic conditions. Matrix protein staining provided a means to accurately visualize and quantify biofilm formation in this model. L. crispatus and L. iners biofilm growth maintained vaginal epithelial barrier integrity without cytotoxicity. G. vaginalis and P. bivia biofilm growth significantly reduced barrier integrity (p=0.0166, p=0.0115) and increased cytotoxicity (p=0.0024, p<0.0001). Estradiol significantly increased the growth of L. crispatus biofilm in the co-culture system (p<0.0001). Progesterone significantly increased G. vaginalis biofilm growth in the Vk2 cell co-culture (p=0.006). L. crispatus biofilm formation in the estradiol condition, G. vaginalis biofilm formation in the progesterone condition and P. bivia biofilm growth in the normal media condition were significantly decreased in the presence of sialidase (p<0.0001, p=0.0001, p=0.0380). Conclusion: A novel in vitro model of biofilm formation on a vaginal epithelial cell line that can be used to visualize and quantify biofilm growth was generated. This model was used to test various strategies for biofilm enhancement or dissociation. Estradiol enhanced beneficial Lactobacillus biofilm growth, while progesterone enhanced dysbiotic biofilm growth. Mucin- digesting enzyme sialidase was effective at dissociating all biofilms. This model can be used in the future to test different strategies of dysbiotic biofilm dissociation and enhancement of Lactobacillus biofilm in order to investigate treatments for Bacterial Vaginosis (BV) and reduce susceptibility to HIV transmission in women. / Thesis / Master of Science (MSc)