Social capital across the life course and functional somatic symptoms in mid-adulthood

Abstract

Aim: To examine social capital across life and functional somatic symptoms in middle-age, according to life-course models of cumulative risk and sensitive periods. Methods: Data from the 26-year prospective study the Northern Swedish Cohort enabled complete case analyses on 940 individuals (451 women and 489 men) participating in questionnaire surveys at ages 16, 21, 30 and 42. Social capital was operationalized at the individual level, comprising items on social participation, social influence and social support. Functional somatic symptoms were a summary measure of self-reported physical symptoms, palpitation and sleeping difficulties occuring during the 12 months prior to the data collection. Linear regression was used as the main statistical method, examining the relationship between functional somatic symptoms at age 42 and social capital across life. Results: Lower levels of social capital accumulated over the life course were associated with higher levels of functional somatic symptoms at age 42, for both women and men. Social capital was, especially among adolescent men, related to functional somatic symptoms at age 42, independently of social capital later in life and baseline material circumstances. Conclusions: The health impact of poor social capital may be due to accumulation across the life course and to adolescence being a particularly sensitive period. It is relevant for preventive work to acknowledge effects of social capital throughout life.

Keywords

Social epidemiology human development life course mental health midlife events models the Northern Swedish Cohort prospective study social capital somatic symptoms

Introduction

A large body of mainly cross-sectional research links individual social capital to physical and mental health in adolescence and adulthood [1 –4]. Whether social capital from earlier in life impacts health in adulthood is a central, but as of yet unresolved question within the field [5]. Following two life-course models, this prospective study examines if social capital, in adolescence and accumulated over the life course, relates to functional somatic symptoms in adulthood.

The concept of social capital originates from ideas by Bourdieu and Coleman about social networks [6] and social structures [7], respectively, combined with research by Putnam [8] on the importance of trust and reciprocity within communities. It can be described as “resources embedded in a social structure which are accessed and/or mobilized in purposive actions” [9], but due to its complexity, no consensus definition exists. Within research, social capital is generally differentiated as either social cohesion or networks, studied as a property of people or of communities and neighborhoods. Considering these differentiations, we studied social capital through its network aspects, approaching it as the integrated effects of social influence, social participation and social support at an individual level [10].

Social capital is assumed to benefit health by protecting against stress, creating a sense of belonging and providing information and material resources. Thus, the general assumption that social relations and networks generate symbolic, psychological and material recourses; and that these, via strengthening and buffering mechanisms, may protect people from the pathologic consequences of long-term stress, connects social capital to health [10,11]. But while a recent meta-analysis suggests cumulative associations and a strong relationship between social capital and self-rated health, as well as mortality [2], the effects on mental health remain inconclusive [12]. Still, social capital has been found to improve mental well-being [5], while associations between poor social capital and depression also have been revealed [13].

Longitudinal research is scarce within the field, making us unaware as to whether the impact of social capital on health early in life persists until adulthood. As suggested by a review from Nyqvist et al. [5], life-course studies on social capital are required, which would be especially beneficial if applied on mental health outcomes.

Generally defined as a clustering of physical symptoms with no or unknown pathology, functional somatic symptoms relate to mental health by being considered a measure of distress and by being closely linked to depression and anxiety [14,15]. But while this health problem is known to depend upon various social determinants [16], associations to social capital have been examined only in a few studies on adolescents [17]. In addition, although functional somatic symptoms are often a temporary state present early as well as later in life, it may be the subject of continuity along the life course, with enduring distress as a potential consequence [16,18].

Life-course epidemiology acknowledges not only contemporary exposures, but circumstances prior in life as having implications for health [19]. Through general theoretical models highlighting the importance of duration, magnitude and timing of exposure, this framework offers hypotheses on how health may develop over life. Thus, by following two conceptual life-course models, we analysed in what ways social capital across life may relate to functional somatic symptoms in adulthood. Applying the cumulative risk model, addressing whether factors act on health cumulatively [20], we proposed that social capital accumulates in number and/or severity (magnitude), but also across time (duration), with implications for mental health in mid-adulthood. This model focuses on amount of exposure, while timing of impact is ignored. In addition, the sensitive period model highlights exposure during certain life-course periods, especially childhood and adolescence as particularly critical, with enduring health effects independent from later conditions as a consequence [19]. Through this model, we hypothesized that functional somatic symptoms in adulthood were related to social capital during adolescence, independently of social capital further along the life course.

Aim

Contributing to the so far nonexistent knowledge about the life-course association between social capital and health, we especially focused on its relationship to mental health and functional somatic symptoms. The aim was to examine if an association between social capital across life and functional somatic symptoms in middle-age can be explained by the cumulative risk and/or sensitive period life-course models.

Methods

Sample and procedures

The Northern Swedish Cohort provides prospective data, collected five times (in 1981, 1983, 1986, 1995 and 2007) during 26 years, on all students whom attended or should have attended the 9^th grade of the Swedish compulsory school in the municipality of Luleå, in 1981 (at that time, aged 16) [21]. Out of 1071 students, 94.3% of those alive chose to participate across the entire period (n = 1010).

The present study used the self-administrated questionnaire data from the 1981, 1986, 1995 and 2007 surveys. Ethical approval was granted by the Regional Ethical Review Board in Umeå.

Outcome

Functional somatic symptoms during the last 12 months at age 42 formed an index (including 10 items scored 0–2; answered ‘no’, ‘yes light’ or ‘yes severe’) on different self-reported physical symptoms (headache/migraine, stomach ache, nausea, backache/hip pain/sciatica, fatigue, breathlessness, dizziness and overstrain), occurrence of palpitations and how often the respondent had suffered from difficulties sleeping. When summarized, Cronbach’s alpha revealed an internal consistency of 0.782 and the index ranged from 0–18 for women and 0–15 for men, where higher values equaled more somatic problems.

Exposures

Social capital was operationalized at the individual level, comprising items on social participation, social influence and social support; and aimed at broadly covering this a priori concept [10]. Items from questionnaires at ages 16, 21, 30 and 42 were combined (9, 6, 12 and 12 items selected for each age, respectively) into age-specific, as well as one cumulative measure of social capital.

Included items at age 16 were:

Social participation, items on involvement in associational and leisure activities;

Social influence, items on perceived opportunity to decide in school and at home; and

Social support, items on perceived contact with mother, father and friends.

Items selected at age 21 were:

Social participation involvement in associations;

Social influence, whether the respondent felt that he/she could decide sufficiently often, speak their mind, was appreciated by others and whether it was hard to get others to listen; and

Social support, (‘are you mostly alone or with friends during spare time’).

The items at age 30 and 42 were identical:

Social participation, involvement in associations;

Social influence, whether the respondent felt that he/she could decide sufficiently often, speak their mind, was appreciated by others and whether it was hard to get others to listen; and

Social support including seven questions on the number of and perceived support from close contacts.

All items had 4–6 Likert scale response options, coded from 1–6, where a higher value equaled less social capital. Each variable was then standardized and summarized into an index representing cumulative social capital. Although internal consistency was low (α < 0.05) the operationalization was guided by a theoretical framework; and an impact of exposure may still act on health through common pathways, despite a lack of co-occurrence.

Covariates

Functional somatic symptoms at age 16 were measured identically as at age 42, but based on questionnaires completed at age 16.

Socioeconomic disadvantage was operationalized based on parent(s)-reported occupation, separating between manual-working parents (blue-collar), at least one parent being a non-manual employee (white-collar) and self-employed. A high socioeconomic group contained those with non-manual and self-employed parents, while the manual work group represented low socioeconomic status.

Material adversity at age 16 was a measurement of unfavorable material circumstances, operationalized (for details, see Gustafsson, et al. [22]) as the count (0–3) of items on:

Parental unemployment;

Poor material standard of living; and

Residential crowding.

Data analysis

Descriptive statistics for all variables are displayed in Table I. Complete case analysis was possible for 940 participants (451 women and 489 men). We examined selection bias regarding missing data by using separate simple logistic regression with inclusion/exclusion as the outcome, and main variables as the predictors. The analysis revealed no evidence of systematic drop-out (p > 0.218) with regard to social capital measures (cumulative and at age 16, 21, 30 and 42), material adversity and socioeconomic disadvantage at age 16, or sex; although the functional somatic symptoms at age 16 was borderline significant (n = 52 excluded; p = 0.080).

Table I.

Descriptive statistics for levels of social capital at age 16, 21, 30 and 42, functional somatic symptoms at age 16 and 42, socioeconomic disadvantage and material adversities at age 16; in the full sample (n = 940), and between women (n = 451) and men (n = 489) Estimates are mean (SD).

	Full sample		Women		Men		Difference
	Range	Estimate	Range	Estimate	Range	Estimate	P-value
Social capital
Age 16	1–4.22	2.89 (0.411)	1–4.22	2.96 (0.380)	1–4.11	2.83 (0.429)	< 0.001^a
Age 21	1–3.83	2.20 (0.483)	1–3.83	2.23 (0.478)	1–3.83	2.16 (0.486)	0.022^a
Age 30	1–3.92	2.11 (0.479)	1–3.92	2.12 (0.463)	1–3.92	2.10 (0.494)	0.460^a
Age 42	1–4.33	2.09 (0.549)	1–4.18	2.09 (0.528)	1–4.33	2.10 (0.569)	0.852^a
Cumulative^c	−7.2–12.12	−0.004 (2.81)	−7.28–10.72	0.25 (2.73)	−7.04–12.12	−0.24 (2.87)	0.006^a
Functional somatic symptoms
Age 16	0.00–16.00	3.35 (2.540)	0.00–16.00	3.70 (2.510)	0.00–12.00	3.02 (2.526)	< 0.001^a
Age 42	0.00–18.00	4.24 (3.306)	0.00–18.00	4.77 (3.503)	0.00–15.00	3.75 (3.032)	< 0.001^a
Material adversities
Age 16	0.00–3.00	0.48 (0.677)	0.00–3.00	0.59 (0.726)	0.00–3.00	0.39 (0.614)	< 0.001^a
Socioeconomic disadvantage
Age 16	37.7% low		36.6% low		39.4% low		0.354^b

Based on t-test.

Based on chi-square test.

Index of standardized social capital variables.

All analyses were performed in SPSS 20 through linear regression on the full sample and stratified by sex, as both mental health problems and its determinants may differ between women and men [23]. We assessed the hypothesis of cumulative risk by regressing functional somatic symptoms at age 42 on cumulative social capital (Model 0); with additions of covariates sex, socioeconomic disadvantage and material adversity at age 16 (Model 1) and functional somatic symptoms at age 16 (Model 2). The sensitive period hypothesis tested the association between social capital at age 16 and functional somatic symptoms at age 42, with a successive introduction of social capital variables at later ages (age 21 (Model 1); 21 and 30 (Model 2); 21, 30 and 42 (Model 3)); as well as sex, socioeconomic disadvantage and material adversity at age 16 (Model 4), and baseline functional somatic symptoms (Model 5).

Multi-collinearity was at moderate levels; variance inflation factor (VIF) was < 1.51 in the full sample, < 1.61 for women and < 1.45 for men. Functional somatic symptoms at age 42 were slightly positively skewed, but considered to fulfill assumptions of approximate normality, after reviewing Q-Q plot and histogram, and analyzing the residuals.

Results

The descriptive analysis (Table I) showed stable, but slightly increasing levels of social capital across the life course, differing between the sexes at age 16 (p < 0.001) and 21 (p = 0.022), and with regard to cumulative social capital (p = 0.006); with men reporting significantly lower levels. Women presented higher levels (p < 0.001) of functional somatic symptoms at ages 16 and 42, but also a larger increase across life than men.

Zero-order correlations (by sex) presented in Table II reveal weak-to-moderate correlations between social capital at different periods and in relation to the covariates, indicating a measure of continuity of social capital from adolescence to mid-adulthood.

Table II.

Zero-order correlations (Pearson’s r) between all variables (SC, SD, MA and FSS) in women (above diagonal) and men (below diagonal).

Variable	SC	SC	SC	SC	SC	SD	MA	FSS	FSS
	age 16	age 21	age 30	age 42	Cum	age 16	age 16	age 16	age 42
SC	–	0.302^b	0.236^b	0.225^b	0.610^b	0.100^a	0.174^a	0.170^b	0.148^b
age 16
SC	0.244^b	–	0.392^b	0.347^b	0.724^b	0.154^b	0.139^b	0.103^b	0.174^b
age 21
SC	0.231^b	0.389^b	–	0.556^b	0.768^b	0.155^b	0.193^b	0.134^b	0.208^b
age 30
SC	0.208^b	0.316^b	0.490^b	–	0.746^b	0.111^b	0.087	0.085	0.393^b
age 42
SC	0.607^b	0.696^b	0.761^b	0.721^b	–	0.191^b	0.203^b	0.172^b	0.323^b
Cum
SD	0.077	0.125^b	0.085	0.070	0.134^b	–	0.190^b	0.021	0.027
age 16
MA	0.100^a	0.082	0.124^b	0.154^b	0.167^b	0.238^b	–	0.068	0.081
age 16
FSS	0.136^b	0.086	0.074	0.092^a	0.142^b	0.069	0.077	–	0.181^b
age 16
FSS	0.173^b	0.192^b	0.190^b	0.315^b	0.318^b	0.123^b	0.092^a	0.253^b	–
age 42

p < 0.05 (2-tailed)

p < 0.01 (2-tailed)

Cum: Cumulative; FSS: functional somatic symptoms; MA: material adversity; SC: social capital; SD: socioeconomic disadvantage

The cumulative risk model was examined by regressing functional somatic symptoms at age 42 on cumulative social capital (Table III). In the full sample, cumulative social capital significantly predicted higher levels of functional somatic symptoms at age 42, before (0.331, in Model 0) and after (0.287, in Model 2) controlling for sex, socioeconomic disadvantage, material adversities and baseline functional somatic symptoms. Stratifying the analysis by sex revealed similar results for women and men.

Table III.

Linear regressions of functional somatic symptoms at age 42 on cumulative social capital (Model 0), adjusted for sex, socioeconomic disadvantage and material adversity at age 16 (Model 1) and functional somatic symptoms at age 16 (Model 2) in the full sample (n = 940). Analysis stratified by sex: women (n = 451) and men (n = 489), excluding sex as a covariate (Model 1). Predictor estimates are standardized regression coefficients with 95% confidence intervals.

Estimate	Model 0	Model 1	Model 2
Full sample
Cumulative social capital,	0.331 (0.271–0.392)	0.312 (0.250–0.374)	0.287 (0.226–0.349)
age 16–42
Model R²	0.109	0.125	0.152
Model p	–	(0.001)	(<0.001)
Women
Cumulative social capital,	0.355 (0.260–0.451)	0.358 (0.259–0.457)	0.335 (0.236–0.435)
age 16–42
Model R²	0.107	0.108	0.122
Model p	–	(0.745)	(0.007)
Men
Cumulative social capital,	0.291 (0.215–0.368)	0.277 (0.199–0.355)	0.252 (0.175–0.329)
age 16–42
Model R²	0.102	0.111	0.154
Model p	–	(0.103)	(<0.001)

To examine the sensitive period hypothesis, functional somatic symptoms at age 42 was first regressed separately on social capital at ages 16, 21, 30 and 42, using simple regression. This analysis showed significant associations between lower levels of social capital at each age (Table IV, Model 0), with estimates being 0.180, 0.192, 0.199 and 0.346, respectively, in the full sample. Thereafter, by using multiple regression, we tested whether the relationship between social capital during adolescence and functional somatic symptoms in mid-adulthood existed independently of social capital across the life course.

Table IV.

Linear regressions in the full sample (n = 940). Social capital for each age, on functional somatic symptoms at 42, in simple regression (univariate). Using multiple regression when adjusting for social capital at age 21 (Model 1); age 21 and 30 (Model 2); age 21, 30 and 42 (Model 3); and adding sex, socioeconomic disadvantage and material adversity at age 16 (Model 4) and functional somatic symptoms at age 16 (Model 5). Analysis stratified by sex, women (n = 451) and men (n = 489), excluding sex as a covariate in Model 4. Predictor estimates are standardized regression coefficients with 95 % confidence intervals.

	Univariate		Model 1	Model 2	Model 3	Model 4	Model 5
Full sample	n
Age 16	977	0.180 (0.118–0.242)	0.143 (0.078–0.208)	0.128 (0.062–0.193)	0.107 (0.044–0.170)	0.082 (0.018–0.145)	0.060 (– 0.003–0.123)
Age 21	980	0.192 (0.130–0.254)	0.160 (0.095–0.225)	0.118 (0.049–0.187)	0.078 (0.011–0.145)	0.066 (– 0.001–0.133)	0.060 (– 0.005–0.126)
Age 30	962	0.199 (0.137–0.262)	–	0.119 (0.051–0.187)	− 0.021 (– 0.094–0.052)	− 0.023 (– 0.096–0.049)	− 0.031 (– 0.102–0.040)
Age 42	981	0.346 (0.288–0.405)	–	–	0.309 (0.239–0.379)	0.314 (0.244–0.383)	0.310 (0.242–0.379)
Model R²			0.058	0.070	0.139	0.157	0.186
Model p			<0.001	0.001	<0.001	<0.001	<0.001
Women	n
Age 16	471	0.170 (0.067–0.273)	0.127 (0.019–0.235)	0.106 (– 0.003–0.215)	0.075 (– 0.028–0.178)	0.068 (– 0.036–0.173)	0.048 (– 0.056–0.152)
Age 21	472	0.185 (0.090–0.280)	0.161 (0.060–0.262)	0.110 (0.003–0.217)	0.054 (– 0.048–0.157)	0.055 (– 0.048–0.157)	0.051 (– 0.051–0.153)
Age 30	463	0.230 (0.131–0.328)	–	0.150 (0.041–0.259)	− 0.053 (– 0.171–0.064)	− 0.059 (– 0.178–0.060)	− 0.077 (– 0.195–0.041)
Age 42	473	0.433 (0.341–0.525)	–	–	0.421 (0.307–0.535)	0.425 (0.311–0.539)	0.427 (0.314–0.541)
Model R²			0.045	0.061	0.160	0.162	0.181
Model p			0.002	0.007	< 0.001	0.542	0.002
Men	n
Age 16	506	0.153 (0.077–0.229)	0.125 (0.045–0.205)	0.111 (0.030–0.191)	0.093 (0.015–0.172)	0.089 (0.010–0.167)	0.066 (– 0.010–0.143)
Age 21	508	0.177 (0.098–0.256)	0.151 (0.068–0.234)	0.112 (0.023–0.200)	0.082 (– 0.005–0.168)	0.073 (– 0.014–0.160)	0.065 (– 0.020–0.150)
Age 30	499	0.169 (0.092–0.247)	–	0.104 (0.020–0.188)	0.002 (– 0.088–0.091)	− 0.001 (– 0.090–0.089)	0.000 (– 0.088–0.087)
Age 42	508	0.279 (0.206–0.352)	–	–	0.239 (0.153–0.325)	0.235 (0.149–0.321)	0.227 (0.142–0.311)
Model R²			0.057	0.068	0.122	0.131	0.174
Model p			<0.001	0.016	<0.001	0.099	<0.001

Our analysis revealed a significant association between social capital at age 16 and functional somatic symptoms at age 42, after controlling for social capital at ages 21, 30 and 42 (Models 1–3). The further addition of covariates (Model 4) did not alter the results substantially, whereas the final inclusion of baseline functional somatic symptoms (Model 5) caused a moderate attenuation with social capital at age 16 becoming borderline significant (confidence interval (CI) = -0.003-0.123). In addition, throughout the series of analyses, social capital at age 42 was found to be the main independent predictor with an estimate of 0.310 in the final model (5, top panel).

The stratified analysis revealed similar patterns for men (Table IV, lower panel). Social capital at age 16 was initially significantly associated with functional somatic symptoms at age 42, independently of later social capital, and after adjusting for socioeconomic and material conditions; whereas the addition of baseline functional somatic symptoms in the final model (Model 5) made the association drop to borderline significance (CI = − 0.010–0.143). The same progression was not evident for women, where only contemporary levels of social capital remained consistently significant, throughout the series of models.

Discussion

As far as we know, the present report is the first to examine the relationship between social capital over the life course and health, here exemplified by self-reported functional somatic symptoms in mid-adulthood. Our study suggested that social capital acts cumulatively on functional somatic symptoms across life, in both women and men. In addition, although contemporary levels of social capital seem to have the largest impact on adult mental health, our results indicated that adolescence may be a sensitive period for the health impact of social capital, particularly in men.

In light of the wealth of cross-sectional research concerning social capital and health, and in accordance with previous life-course research [24], our results suggested that the lower the levels of social capital that people experience, not only presently, but accumulated across life; the higher levels of mental health complaints they reported in adulthood. Furthermore, it seemed that social capital at age 16 could have more than a temporary influence on mid-life mental health; but also a direct association, existing independently of later social capital.

Considering the length of time between our measurements (26 years), even though the impact was minor, our sensitive period analysis suggested that the impact of poor social capital may have a small but not insignificant importance. Because adolescence is a period of change that tends to be particularly malleable [25], reduced social capital during this vulnerable period might contribute to a life trajectory that increases the risk of poor mental health in adulthood. Nevertheless, although it is interesting that an association could be observed at all after so many years, we found social capital at age 42 to be most strongly related to functional somatic symptoms, highlighting the importance of concurrent social capital.

When testing the hypothesis of adolescence being a sensitive period, baseline functional somatic symptoms were added in the final model, slightly attenuating social capital at age 16 to below significance. This indicated an interrelation between early functional somatic symptoms and social capital, partly explaining the association, either by health selection or functional somatic symptoms at age 16 acting as a mediator. Despite this result, the assumption of adolescent being a sensitive period in general terms remains, because regardless of which is the direction of causation the clustering and/or the mutually dependent relation between these two factors seemed to impact health later in life.

Differences between women and men were apparent with regard to functional somatic symptoms, and in social capital at ages 16 and 21 (with women scoring worse), but almost identical at ages 30 and 43. In the stratified analysis, while the significant association between social capital at age 16 and functional somatic symptoms at age 42 proposed a vulnerability to poor social capital and a potentially long-term effect for men, social capital at age 42 was higher for the women, suggesting that they might be somewhat more sensitive to the impact of poor social capital during adulthood; however, accumulation of social capital might affect the mental health of women and men approximately similarly, as indicated by comparable results revealed in the cumulative analysis.

The strengthening and buffering mechanism through which social capital is assumed to affect health has primarily been examined in a short-term perspective, through cross-sectional studies; therefore, our study added to the field by suggesting supplementary life-course mechanisms, given that the health impact of social capital may act cumulatively and continuously across life, with particular importance during adolescence.

Methodological considerations

The major strengths of this study are the prospective longitudinal data; the representativeness of the sample regarding the same age cohort as Sweden as a whole [21]; and a reduced risk of selection bias, due to a high response rate and lack of systematic drop-out. In addition, measuring functional somatic symptoms as a continuous variable entailed both methodological and conceptual benefits [26]; however, the likelihood of omitted factors limits this study. Within-household interaction was adjusted for by the inclusion of residential crowding in the material adversity measure [27], while other factors in the shared environment of the household that could be potentially confounding were not [28]. Moreover, there is a possibility that the health impact of social capital via stress-buffering mechanisms is caused by personal, rather than environmental factors that were not adjusted for in the present study. But rather than confounding, personality could also act by moderating the association [29]. Thus, although we adjusted for covariates relevant to social capital research [27], given the risk of residual confounding, causal interpretations should be made with causion.

Despite a lack of general consensus on how to measure social capital, scales exist; but due to our prospective design initiated in the early 1980s, only theoretically-grounded ad hoc operationalizations were feasible which we based on a synthesis by Kawachi et al. [10]. In line with Streiner [30], although internal consistency was low (which in combination with the main findings supported the idea that social capital is a holistic construct that might be empirically heterogeneous), the different dimensions could still act on mental health across life through common pathways.

Conclusions

Our study highlights social capital as a relevant determinant for understanding one aspect of self-reported mental health in adulthood by revealing a cumulative association over the life course and a potentially long-term impact of poor social capital during adolescence, especially in men. Taken together, although the results suggest that contemporary social capital in adulthood should be promoted; for health preventing reasons, particular attention ought to be placed upon interventions improving social capital early in life.

Footnotes

Conflict of interest

None declared. The funding bodies had no involvement in the research process.

Funding

This work was supported by The Swedish Research Council Formas (grant number 259-2012-37) and by the County Council of Västerbotten (grant number 355661). Per E Gustafsson was also supported by Umeå University (grant number 223-514-09).

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