Effects Of Allostatic Load Research Articles

Effects of Allostatic Load on Long-term Survival After Stroke (P1-5.014)

Effects of Allostatic Load on Long-term Survival After Stroke (P1-5.014)

Functional correlates of negative effects of allostatic load with long-term adaptation to labor factors

Under certain conditions of strong or prolonged external exposure, signs of either allostatic load or allostatic load are formed. The question of the different physiological nature of these states is discussed.

The Effects of Allostatic Load on Racial/Ethnic Mortality Differences in the United States

This study expands on previous findings of racial/ethnic and allostatic load (AL) associations with mortality by addressing whether differential AL levels by race/ethnicity may explain all-cause mortality differences. This study used data from the third National Health and Nutrition Survey public-use file, gathered between 1988 and 1994, with up to 18 years of mortality follow-up (n = 11,733). AL scores were calculated using a 10-biomarker algorithm based on clinically determined thresholds. Results of discrete-time hazard models suggest that AL is associated with increased mortality risks, independent of other factors, including race/ethnicity and SES. The results also suggest that the AL–mortality association is stronger for non-Hispanic blacks than for non-Hispanic whites, and that at low levels of AL observed mortality differences between non-Hispanic blacks and non-Hispanic whites are non-significant. These findings suggest that mortality differences between non-Hispanic blacks and non-Hispanic whites may be the result of how early life exposure causes premature aging and increased mortality risks. More attention to resource allocation and local environments is needed to understand why non-Hispanic blacks experience premature aging that leads to differential mortality risks compared to non-Hispanic whites.

The effect of allostatic load on hypothalamic–pituitary–interrenal (HPI) axis before and after secondary vaccination in Atlantic salmon postsmolts (Salmo salar L.)

The experiment consisted of three experimental groups: (1) "vaccine and stress", (2) "stress and vaccine" and (3) control. All groups have previously been vaccinated 6 months prior to the start of the experiment. At the start of the experiment, the "vaccine and stress" group was vaccinated with Pentium Forte Plus for the second time (25.02.2008) and then given a daily stressor (confinement stressor 267 kg m-3 in 15 min) for a period of 4 weeks. The "stress and vaccine" group was given a similar daily stressor for 4 weeks and then vaccinated for the second time. The control group was neither stressed nor vaccinated a second time. The results indicates that fish in the "stress and vaccine" group may have entered an allostatic overload type 2 due to oversensitivity to ACTH, a reduced efficient negative feedback system with elevated baseline levels of plasma cortisol and reduced immune response with pronounced effects on the well-being of the animal. The "vaccine and stress" group may likewise have entered an allostatic overload type 1 response, with oversensitivity to ACTH and transient reduced efficient negative feedback system. This study shows that if plasma cortisol becomes elevated prior to vaccination, it could perhaps instigate an allostatic overload type 2 with dire consequences on animal welfare. To reduce the risk of compromising the animal welfare during commercial vaccination of salmon, one propose to grade the fish minimum a week prior to vaccination or grade simultaneously with vaccination. This could reduce the overall allostatic load during handling and vaccination and secure a healthy fish with intact immune response and improved animal welfare.

Allostatic load and birth outcomes among white and black women in New Orleans.

As a marker of chronic stress, allostatic load has been theoretically recognized as a potential contributor to racial disparities in birth outcomes. The purpose of this investigation was to identify associations between allostatic load and birth outcomes and to assess differences in allostatic load and its relation to birth outcomes between white and black women. Blood samples from 123 women at 26-28 weeks gestation were assayed for cholesterol, glycosylated hemoglobin, dehydroepiandrosterone-sulfate, and cortisol, with 42 women having complete data on all biomarkers and birth outcomes. Together with systolic blood pressure, these biomarkers were combined to create an allostatic load index. Multiple linear regression models were used to evaluate associations between allostatic load index and gestational age, birth weight, birth weight ratio, birth length, and head circumference. Black women had a significantly lower allostatic load index than white women (P < 0.05). Gestational age was the only outcome significantly associated with allostatic load in both unadjusted and adjusted models (P < 0.05). Gestational age decreased significantly with increasing allostatic load (adjusted β -0.18, 95 % CI -0.35, 0.00). A significant interaction with age indicated that the effect was less strong at higher maternal ages (adjusted interaction β 0.04, 95 % CI 0.00, 0.08). There was no racial difference in the effect of allostatic load on birth outcomes. These findings represent possible evidence of the effect of stress age on gestational age. As a measure of cumulative disadvantage, allostatic load may prove to be a contributor to the racial disparities in birth outcomes.

The effects of allostatic load on neural systems subserving motivation, mood regulation, and social affiliation

The term allostasis, which is defined as stability through change, has been invoked repeatedly by developmental psychopathologists to describe long-lasting and in some cases permanent functional alterations in limbic-hypothalamic-pituitary-adrenal axis responding following recurrent and/or prolonged exposure to stress. Increasingly, allostatic load models have also been invoked to describe psychological sequelae of abuse, neglect, and other forms of maltreatment. In contrast, neural adaptations to stress, including those incurred by monoamine systems implicated in (a) mood and emotion regulation, (b) behavioral approach, and (c) social affiliation and attachment, are usually not included in models of allostasis. Rather, structural and functional alterations in these systems, which are exquisitely sensitive to prolonged stress exposure, are usually explained as stress mediators, neural plasticity, and/or programming effects. Considering these mechanisms as distinct from allostasis is somewhat artificial given overlapping functions and intricate coregulation of monoamines and the limbic-hypothalamic-pituitary-adrenal axis. It also fractionates literatures that should be mutually informative. In this article, we describe structural and functional alterations in serotonergic, dopaminergic, and noradrenergic neural systems following both acute and prolonged exposure to stress. Through increases in behavioral impulsivity, trait anxiety, mood and emotion dysregulation, and asociality, alterations in monoamine functioning have profound effects on personality, attachment relationships, and the emergence of psychopathology.

Racial/Ethnic Disparities in All-Cause Mortality in U.S. Adults: The Effect of Allostatic Load

We investigated the association between a cumulative biological risk or allostatic score and all-cause mortality risk. We used 13,715 records of participants aged 25 years and older from the Third National Health and Nutrition Examination Survey (NHANES III) linked to the National Death Index. We specified all-cause mortality using the underlying cause of death in the death certificate. We calculated time to death from interview date through December 31, 2000, as person-years of follow-up using the NHANES III interview month and year. We used Cox proportional hazards regression to estimate hazard ratios (HRs) relating all-cause mortality risk for those with an allostatic score of 2 and > or = 3 relative to those with an allostatic score of < or = 1. After controlling for age, gender, race/ethnicity, education, and income, mortality rates were 40% (HR = 1.40, 95% confidence interval [CI] 1.11, 1.76) and 88% (HR = 1.88, 95% CI 1.56, 2.26) higher for participants with an allostatic score of 2 and > or = 3, respectively, compared with those with a score of < or = 1. The death rate associated with allostatic score for each racial/ethnic group differed with age. The allostatic score increased the risk of all-cause mortality. Moreover, this increased risk was observed for adults younger than 65 years of age regardless of their race/ethnicity. Thus, allostatic score may be a contributor to premature death in the U.S.

Social disparities in periodontitis among US adults: the effect of allostatic load

BackgroundPeriodontitis has been shown to be associated with allostatic load, a measure of physiological instability across biological systems from cumulative or repeated adaptation to stressors. Minority racial/ethnic and low socioeconomic...

Effects of allostatic load on the social gradient in ischaemic heart disease and periodontal disease: evidence from the Third National Health and Nutrition Examination Survey

Introduction:Psychosocial stress and allostatic load have been postulated as a mechanism explaining socioeconomic inequalities in general and oral health. This study tested whether markers of allostatic load are associated with...

Psychobiology of childhood maltreatment: effects of allostatic load?

Facing an adverse physical or psychosocial situation, an individual is forced to adapt in order to survive. Allostasis is the term used to refer to adapting processes used to maintain the stability of an organism through active processes. When allostatic response is excessive or inefficient, the organism develops an allostatic load. The cascade of molecular and neurobiological effects associated with childhood abuse and neglect could be an example of allostatic response that could precipitate allostatic load in organism still vulnerable during its development. This article reviews the psychobiological consequences related to childhood abuse and neglect. A selective review with a systematic procedure was performed to investigate studies showing explicit association between childhood maltreatment and psychobiological/neurobiological consequences. We searched electronic database MedLine-PubMed to identify English-language articles from 1990 to 2007. From 115 articles we selected 55 studies from MedLine and 30 from their reference lists, in a total of 85 articles (JCR IF range: 1-31.4; median: 5.88). Only 29 studies showed direct and explicit association between them. Structural consequences of childhood maltreatment include disruptive development of corpus callosum, left neocortex, hippocampus, and amygdale; functional consequences include increased electrical irritability in limbic areas, frontal lobe dysfunctions and reduced functional activity of the cerebellar vermis; and neurohumoral consequences include the reprogramming activity of hypothalamo-pituitary-adrenal (HPA) axis and subsequently the stress response.