Elsevier

Physiology & Behavior

Volume 104, Issue 2, 3 August 2011, Pages 360-364
Physiology & Behavior

Allostatic load associations to acute, 3-year and 6-year prospective depressive symptoms in healthy older adults

https://doi.org/10.1016/j.physbeh.2011.02.027Get rights and content

Abstract

Allostatic load represents the strain that chronic stress exerts on interconnected biological systems. Associated algorithms are related to numerous deleterious physical outcomes in older populations, and yet few studies have assessed associations to mental health outcomes like geriatric depression. Using data from the Douglas Hospital Longitudinal Study of Normal and Pathological Aging, we assessed whether using an allostatic load index derived from seven biomarkers could detect self-rated depressive symptoms in 58 healthy older adults followed longitudinally over a 6-year period. Our results revealed that increased allostatic load was associated with increased depressive symptoms on the same year of assessment. After 3 years, AL was prospectively associated with depressive symptoms, but entering age and sex as covariates attenuated this effect to a trend. Only age emerged as a significant predictor of depressive symptoms over 6 years. These findings suggest that increased AL in older age is only associated with depressive symptomatology acutely. Over longer periods of time, however, the physical and psychological sequelae of advanced age may contribute to increased depressive symptoms via pathways otherwise undetectable using allostatic load indices of sub-clinical physiological dysregulations.

Research Highlights

► Chronic stress strains numerous biological systems as allostatic load linked to numerous diseases. ► Allostatic load was examined in relation to acute and prospective geriatric depressive symptoms. ► Allostatic load was associated with acute depressive symptoms but only as a trend after 3 years. ► Only increasing age was associated with depressive symptoms after six years.

Introduction

Depression currently affects 8–20% of older adults [1]. Aging populations worldwide need improved detection strategies that are sensitive to the antecedents of geriatric depression and associated physiological recalibrations that ensue. A promising framework is the allostatic load model [2], which posits a temporal physiological sequence whereby chronic stress renders individuals more susceptible to developing pathologies.

The term allostasis [3] refers to the adaptive physiological responses organisms activate when homeostasis is disrupted. For example during acute stress, real or interpreted threats to homeostasis initiate the sympathetic–adrenal–medullary (SAM) axis release of catecholamines and the hypothalamic–pituitary–adrenal (HPA) axis secretion of glucocorticoids that mobilize energy necessary for fight-or-flight responses [4]. When chronically activated, allostatic mechanisms become physiologically taxing — or an allostatic load (AL) — that consequently increase one's susceptibility to disease [5]. AL therefore represents the physiological strain organisms experience when allostasis is repeatedly activated [2].

Multiple allostatic mediators function as part of a non-linear network that contributes to the development of AL [6]. At first, over-activation of primary mediators such as stress hormones and pro- and anti-inflammatory cytokines exact primary effects on cellular activities [7], [8]. Subsidiary systems in turn recalibrate their own activities to compensate for the over and/or under production of primary mediators. This leads to secondary outcomes, whereby metabolic, cardiovascular, and immune biomarkers become dysregulated. AL becomes overloading when tertiary outcomes emerge with the manifestation of clinical endpoints such as mortality, cardiovascular disease, and depression.

By incorporating AL composite measures [9], a growing body of literature has demonstrated augmented prediction of numerous deleterious outcomes in comparison to traditional biomedical methods that focus almost exclusively on remediating clinically significant biomarker levels (for a review, see [35]). Because the AL index incorporates multiple biomarkers before they fall within clinical ranges, stronger prediction of pathological states is possible [10]. This is particularly the case for detecting physical conditions; although an alternative method is to use physiological recalibrations to assess impending psychiatric symptoms. To date, only a paucity of evidence links AL in association to psychiatric ailments, although mental health outcomes are postulated as important areas to explore further. Because exposures to life stressors contributes strongly to the pathogenesis of experiencing major depression [11], it follows that the AL model could theoretically be applied to detect emerging physiological recalibrations in older adults at risk of developing depressive symptoms.

A rich theoretical literature addressing AL and depression [12], [13], [14], [15], [16], [17], [18] has begun to be empirically substantiated in aging populations. Using the Taiwanese Social Environmental and Biomarkers of Aging Study (SEBAS), Seplaki and collaborators have found that dysregulation of AL biomarkers relate concurrently to higher self-reported depressive symptoms [19], [20], [21]. Using the same cohort, 3-year mortality risk, mobility limitations, cognitive declines, and depressive symptomatology were predicted by higher AL; however, these outcomes were driven differentially by traditional clinical risk-factors, neuroendoimmunological mediators, and attenuated by health controls [22]. These analyses suggest that AL is associated to acute and 3-year prospective symptoms of geriatric depression, yet this association is modulated by preexisting factors. Although encouraging, no studies have assessed whether increased AL levels can predict increased geriatric depressive symptoms beyond a 3-year timeframe, and whether the results obtained with the Taiwanese cohort can be applied to older individuals from Occidental societies.

In the present study, we used data from the Douglas Hospital Longitudinal Study of Normal and Pathological Aging [23], [24], [25], [26], [27] in order to assess whether AL indices are correlated with depressive symptoms acutely, 3 years later, and 6 years later in a cohort of 58 healthy older adults. We hypothesized that increased AL indices would be associated with increased symptoms of geriatric depression at all time points independently of sex or age effects.

Section snippets

Protocol

We analyzed data from the Douglas Hospital Longitudinal Study of Normal and Pathological Aging in affiliation with the World Health Organization previously reported in greater detail elsewhere [23], [24], [25], [26], [27]. Briefly, the medical status of each participant was continually assessed by complete physical examination, including ECG, EEG, CAT scan, and a battery of laboratory tests for kidney, liver, and thyroid functions, hemogram, vitamin B12, folate levels, as well as

Descriptive statistics

The AL indices at baseline (M = 2.21, S.E.M. = .22), 3 years (M = 2.19, S.E.M. = .2), and 6 years (M = 2.06, S.E.M. = .269, n = 32) did not differ according to paired-sample t-tests (ps > .20). Likewise, geriatric depressive symptoms measured acutely (M = 5.12, S.E.M. = .62) and 3 years later (M = 5.52, S.E.M. = .62) were similar (ps > .65). Repeated-measures ANOVAs assessing differences due to attrition revealed no group nor covariate effects on AL indices (ps > .30) nor depression scores (ps > .60), revealing no differences

Discussion

In the present study, we found that increased AL was associated with acute depressive symptoms in healthy older adults. While prospective 3-year depressive symptoms were significantly associated with AL indices entered alone, this effect was attenuated when entering sex and age. Consistently, only increased age predicted 6-year prospective depressive symptoms in half of the sample after attrition. The absence of a significant association between AL and depressive symptomatology in the cohort at

Disclosure statement

The authors unequivocally state no conflict of interests.

Acknowledgements

We would like to thank Drs. Joseph Rochford and Eric Loucks for their advice and mentorship. This study was funded by a grant (#134254) from the Canadian Institutes of Health Research to S.J.L. R.P.J. holds a doctoral scholarship from the Institute of Aging of the Canadian Institutes of Health Research. S.J.L. holds a senior investigator chair on Gender and Mental Health from the Canadian Institute of Gender and Health.

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