Abstract:Objective-Several Studies claim that psychophysical stress and depression contribute significantly to cardiovascular disease (CVD) development. The aim of our research is to discover and analyse a possible relationship between two psychosocial disorders (Depression and Perceived Mental Stress) and traditional cardiovascular risk markers.Methods-We selected 106 subjects (M:58, F:48), mean age 79,5 ± 3,8 years old, from The Massa Lombarda Project, an epidemiological study including 7000 north Italian adult subje… Show more
“…More specifically, for every unit increase in hA1c, CAs showed a 2.2 point increase in depressive symptomatology. While triglycerides also contributed to depressive symptomatology in this group, replicating previous work [25] the unit increase in the current study was marginal even when equated for meaningful change per measurement to hA1C; e.g., a 50 unit increase in triglyceride levels that equates to a move from borderline high (150 mg/dL) to high (200 mg/dL) only resulted in a 1 point increase in depressive symptomatology. No one individual disease contributed to depressive symptomatology in the AA group.…”
Section: Discussionsupporting
confidence: 87%
“…In contrast, some [22, 23], but not all [24] MetS studies suggests increasing depressive symptomatology in adults with MetS. This may be due, in part, to the fact that there may be a more selective relationship between depression and disease severity of individual MetS components, e.g., triglyceride levels, than between depression and MetS per se [25]. More work should be done investigating affective functioning as it relates to conflicting results suggesting MetS as well as individual MetS components may play a role in depressive symptomatology.…”
Metabolic syndrome (MetS), i.e., meeting criteria for any three of the following: hyperglycemia, hypertension, hypertriglyceridemia, low high-density lipoprotein and/or abdominal obesity, is associated with negative health outcomes. For example, MetS negatively impacts cognition; however, less is known about incremental MetS risk, i.e., meeting 1 or 2 as opposed to 3 or more criteria. We hypothesized incremental MetS risk would negatively contribute to cognition and relevant neuroanatomy, e.g., memory and hippocampal volumes, and that this risk extends to affective functioning. 119 non-demented/non-depressed participants (age=60.1±12.9; ~50% African American) grouped by incremental MetS risk–no (0 criteria met), low (1–2 criteria met), or high (3+ criteria met)–were compared across cognition, affect and relevant neuroanatomy using multivariable linear regressions. Exploratory analyses, stratified by race, consider the role of health disparities in disease severity of individual MetS component (e.g., actual blood pressure readings) on significant results from primary analyses. Incremental MetS risk contributed to depressive symptomatology (nolow=high) after controlling for age, race (n.s.) and IQ. Different indices of disease severity contributed to different aspects of brain structure and function by race providing empirical support for future studies of the impact distinct health disparities in vascular risk have on brain aging. MetS compromised mood, cognition and hippocampal structure with incremental risk applying to some but not all of these outcomes. Care providers may wish to monitor a broader spectrum of risk including components of MetS like blood pressure and cholesterol levels when considering brain-behavior relationships in adults from diverse populations.
“…More specifically, for every unit increase in hA1c, CAs showed a 2.2 point increase in depressive symptomatology. While triglycerides also contributed to depressive symptomatology in this group, replicating previous work [25] the unit increase in the current study was marginal even when equated for meaningful change per measurement to hA1C; e.g., a 50 unit increase in triglyceride levels that equates to a move from borderline high (150 mg/dL) to high (200 mg/dL) only resulted in a 1 point increase in depressive symptomatology. No one individual disease contributed to depressive symptomatology in the AA group.…”
Section: Discussionsupporting
confidence: 87%
“…In contrast, some [22, 23], but not all [24] MetS studies suggests increasing depressive symptomatology in adults with MetS. This may be due, in part, to the fact that there may be a more selective relationship between depression and disease severity of individual MetS components, e.g., triglyceride levels, than between depression and MetS per se [25]. More work should be done investigating affective functioning as it relates to conflicting results suggesting MetS as well as individual MetS components may play a role in depressive symptomatology.…”
Metabolic syndrome (MetS), i.e., meeting criteria for any three of the following: hyperglycemia, hypertension, hypertriglyceridemia, low high-density lipoprotein and/or abdominal obesity, is associated with negative health outcomes. For example, MetS negatively impacts cognition; however, less is known about incremental MetS risk, i.e., meeting 1 or 2 as opposed to 3 or more criteria. We hypothesized incremental MetS risk would negatively contribute to cognition and relevant neuroanatomy, e.g., memory and hippocampal volumes, and that this risk extends to affective functioning. 119 non-demented/non-depressed participants (age=60.1±12.9; ~50% African American) grouped by incremental MetS risk–no (0 criteria met), low (1–2 criteria met), or high (3+ criteria met)–were compared across cognition, affect and relevant neuroanatomy using multivariable linear regressions. Exploratory analyses, stratified by race, consider the role of health disparities in disease severity of individual MetS component (e.g., actual blood pressure readings) on significant results from primary analyses. Incremental MetS risk contributed to depressive symptomatology (nolow=high) after controlling for age, race (n.s.) and IQ. Different indices of disease severity contributed to different aspects of brain structure and function by race providing empirical support for future studies of the impact distinct health disparities in vascular risk have on brain aging. MetS compromised mood, cognition and hippocampal structure with incremental risk applying to some but not all of these outcomes. Care providers may wish to monitor a broader spectrum of risk including components of MetS like blood pressure and cholesterol levels when considering brain-behavior relationships in adults from diverse populations.
“…One mechanism was proposed in the Massa Lombarda Project, an epidemiological study including 7000 northern Italian adults (Bove et al 2010). In a subset of 106 men and women, selected for older age, psycho-emotional stress and depression disorder were associated with the development of metabolic syndrome, a cluster of multiple cardiovascular risk states.…”
The association between stress and cardiovascular disease (CVD) risk is becoming established. A mechanistic link clarifying the intermediate steps between the experience of stress and the development of CVD would support this association. We sought to examine the role of perceived stress as a factor associated with disturbed sleep with the goal of providing an explanation for the stress-CVD connection. We performed a cross-sectional analysis of data recorded by subjects at entry to our CVD prevention program. Data collection included questionnaire surveys, anthropometrics, and a CVD-relevant laboratory panel. Of 350 consecutively enrolled subjects (mean age 54.4 ± 12.4 [SD] years, 138 men, 39%), 165 (47%) scored above the mean for stress measures. These high-stress subjects displayed an increased cardiovascular risk profile including elevated body mass index (mean ± SD 31.1 ± 5.9 vs. 29.0 ± 5.9, r(s) = 0.175), increased waist circumference (102 ± 17 cm vs. 98 ± 14, r(s) = 0.135), and elevated high-sensitivity serum C-reactive protein (0.384 mg/dl vs. 0.356, r(s) = 0.109). High-stress subjects also demonstrated greater daytime sleepiness (Epworth Sleepiness Scale: 10.4 ± 5.0 vs. 7.8 ± 4.8, r(s) < 0.316), greater fatigue (fatigue scale: 5.4 ± 2.2 vs. 3.4 ± 2.4, r(s) = 0.484), poorer sleep quality (Pittsburgh Sleep Quality Index: 8.5 ± 4.4 vs. 5.9 ± 4.0, r(s) = 0.416), and shorter sleep duration (20 min less/24 h, r(s) = negative 0.177) with a higher risk for sleep apnea (60% at high risk vs. 40%, p = 0.003) than low-stress subjects. High stress was associated with significant disturbances in sleep duration and sleep quality. Stress levels also correlated with daytime consequences of disturbed sleep. The stress-sleep connection may be an important mechanistic mediator of the association between stress and CVD.
“…For example, the autonomic response (blood pressure) to acute stress varies as a function of baseline uric acid levels (Ohno et al, 2015). Low uric acid concentrations are also associated with anxiety and depression (Bove et al, 2010; Lyngdoh et al, 2013; Wen et al, 2012). Further, the social inhibition that characterizes certain stress, anxiety, and depressive disorders may be linked to low uric acid levels (Bove et al, 2010; Wen et al, 2012).…”
Uric acid is a naturally occurring, endogenous compound that impacts mental health. In particular, uric acid levels are associated with emotion-related psychopathology (e.g., anxiety and depression). Therefore, understanding uric acid’s impact on the brain would provide valuable new knowledge regarding neural mechanisms that mediate the relationship between uric acid and mental health. Brain regions including the prefrontal cortex, amygdala, and hippocampus underlie stress reactivity and emotion regulation. Thus, uric acid may impact emotion by modifying the function of these brain regions. The present study used functional magnetic resonance imaging (fMRI) during a psychosocial stress task to investigate the relationship between baseline uric acid levels (in saliva) and brain function. Results demonstrate that activity within the bilateral hippocampal complex varied with uric acid concentrations. Specifically, activity within the hippocampus and surrounding cortex increased as a function of uric acid level. The current findings suggest that uric acid levels modulate stress-related hippocampal activity. Given that the hippocampus has been implicated in emotion regulation during psychosocial stress, the present findings offer a potential mechanism by which uric acid impacts mental health.
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