Background: Parents of NICU patients have high stress levels compared to other populations, which negatively impact their mental health. The kangaroo care (KC) method has been used for its numerous benefits for infants, but not as widely studied for its impacts on parental stress. The purpose of this integrative literature review is to examine and synthesize the existing evidence regarding kangaroo care and its impact on the stress levels of NICU parents. Methods: A literature search was conducted utilizing CINAHL Plus with Full Text, MEDLINE, and APA PsychInfo databases to identify relevant articles. Articles were included if they were published within the last five years (2018-2023), discussed parental subjective and/or objective measures of stress, and implemented a KC intervention in the NICU. A total of seven articles were analyzed and synthesized. Results: Key findings in this review included how KC is implemented and its effects on subjective and objective stress. Findings from all seven articles demonstrate that KC is effective in decreasing cortisol, increasing oxytocin, and decreasing subjective parental stress. Discussion: KC as an intervention for stress reduction for NICU parents showed an overall positive effect on parental stress measures. It may be beneficial for NICU providers to encourage KC not only for the positive benefits on the infant, but for the positive effects it can have on parental stress. However, additional research is necessary in subsequent populations, geographical locations, and with different measures of stress to improve generalizability of the results.

Bakgrund: Demens drabbar en stor del av den äldre befolkningen och antalet insjuknade väntas stadigt stiga. Det finns i dagsläget ingen sjukdomsbotande behandling och etiologin är oklar. Hypotalamus-hypofys-binjurebark (HPA)-axeln är ett neuroendokrint system som aktiveras vid exponering för endo- respektive exogena stressorer. Aktivering leder till frisättning av glukokortikoider från binjurebarken. Cirkulerande glukokortikoider (kortisol) påverkar kognitiva funktioner och verkar ha effekt på plasticiteten vid hippocampus, som är en region viktig för minnesfunktioner. Förhöjda kortisolhalter har korrelerats med snabbare kognitiv nedgång och pågående Alzheimers sjukdom. HPA-axeldysfunktion och förhöjda kortisolhalter har föreslagits vara en möjlig bidragande orsak till kognitiv funktionsnedsättning och demens. Syfte: Undersöka om HPA-axeldysfunktion med förhöjda kortisolhalter bidrar till demensutveckling. Metod: Systematisk litteratursökning med på förhand implementerade inklusions- respektive exklusionskriterier. Sökningar utfördes på databaserna Pubmed och Web of Science med sökorden ”dementia”, ”Alzheimer’s”, ”longitudinal”, ”cortisol”. Resultat: Av sex granskade artiklar kunde fem korrelera förhöjda kortisolhalter med senare nedsatt kognitiv förmåga eller demens. Resultaten varierade beroende på vilka effektvariabler som användes i samband med analys. Slutsats: Inkluderade studier uppvisade viss ökad förekomst av HPA-axeldysfunktion och förhöjda kortisolhalter i samband med senare demens eller kognitiv funktionsnedsättning. Det går dock inte att utesluta att förhöjda kortisolhalter orsakas av patofysiologiska förändringar i samband med det begynnande sjukdomsförloppet. / Background: Dementia affects a large part of the elderly population, and the incidence is expected to keep rising. However, there is no available disease-curing treatment nor is the etiology yet fully understood. The hypothalamus-pituitary-adrenal (HPA) axis is a neuroendocrine system that is activated under exposure to endo- and/or exogenous stressors. Activation leads to the release of glucocorticoids from the adrenal cortex. Circulating glucocorticoids (cortisol) affects cognitive functions including hippocampal plasticity. Elevated cortisol levels have been associated with ongoing Alzheimer’s disease and a more rapid cognitive decline. Thus, HPA axis dysfunction with elevated cortisol levels have been suggested as a possible contributor to cognitive impairment and dementia. Objective: To investigate if HPA axis dysfunction and elevated cortisol levels are a contributing cause of dementia. Method: Systematic literature search with pre-implemented inclusion and exclusion criteria. Searches were carried out on Pubmed and Web of Science using the words "dementia", "Alzheimer's", "longitudinal", "cortisol". Results: Associations between elevated cortisol levels and later cognitive decline or dementia was made in five out of six reviewed studies. The results varied depending on the effect variables used in connection with the analysis. Conclusion: Reviewed studies showed some degree of associations between high cortisol levels and later cognitive decline or dementia. It is however impossible to rule out the possibility of elevated cortisol levels as part of the initial disease progression, rather than a cause of disease.

Huntington Disease (HD) is a fatal neurodegenerative disorder that is characterized by motor, cognitive, and psychiatric symptoms. Although HD onset is determined by motor symptoms, psychiatric symptoms, like depression and aggression, can develop earlier, have a larger impact on quality of life, and are understudied due to stigma. Our lab has observed hyper aggression in our humanized HD mouse model (Hu97/18) compared to our knock-in HD mouse model (Q175FDN). We characterized these differences and found that the Hu97/18 mice overreact in neutral situations, behaving as if they are in threatening situations. We are now using this novel model of HD-related aggression to study its neurological basis. Increased reactive aggression has been linked to stress levels and the prefrontal cortex (PFC) due to its role in emotional regulation. This study seeks to determine if HD-related aggression is associated with increased stress levels and changes in the PFC. Our cortisol study shows that the Hu97/18 mice display significantly higher cortisol levels than baseline, suggesting a link between systemic stress and heightened aggression. Additionally, quantified PFC volumes show a moderate relationship between PFC volume and aggression in wild-type (WT) mice that is lost in the Hu97/18 mice. This data will help elucidate factors that modulate aggression in HD and may identify therapies with high potential to alleviate this devastating symptom in patients.

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The early adult years are critical as they provide the final window of opportunity to maximize peak bone mass and help prevent osteoporosis later in life. Dietary habits of young women are often molded by social pressures to be thin. Negative implications for cognitive eating restraint (CER) on bone health have been shown, but direct evidence to support such contentions is limited. Therefore, this study was conducted to further investigate the relationships between CER and bone health in young women. Women aged 18 to 25 years with normal body mass index and limited physical activity participated in this study. Body composition and anthropometric variables, dietary intake, endocrine factors, biomarkers of bone turnover, and measurements of bone mineral content (BMC) and bone mineral density (BMD) were examined cross-sectionally in women with high (n = 31) and low (n = 34) CER scores. High CER participants possessed more fat mass (FM) (p < 0.05) and percent body fat (BF%) (p = 0.01) and consumed a greater number of servings of fruits and vegetables (p < 0.05) per day than the CER participants. No differences in biochemical measurements, BMC or BMD were found between groups. Using similar methods, a study was conducted to compare high (n = 27) and low (n = 26) CER groups at baseline and after 6-months. At baseline, the high CER group possessed significantly higher FM (p < 0.05) and BF% (p = 0.01) and lower biochemical markers of bone formation (p < 0.05) than the low CER group; no other group differences were apparent at baseline. Using repeated measures ANOVA, a significant Group x Time interaction was identified for salivary cortisol concentrations (p < 0.05). Mean salivary cortisol concentrations were significantly lower at 6-months versus baseline in the high CER group (p < 0.05) but did not differ between time points in the low CER group. No other significant Group x Time interactions were found. Overall, despite finding a lower serum osteocalcin concentration in the high CER group at baseline, evidence of compromised BMC or BMD between women with high versus low CER scores over 6 months was not found. / Ph. D.