Although earlier research has shown that a weak SOC can predict general morbidity and mortality [
11,
13,
19,
32], only little is known whether it can predict specific severe chronic diseases [
12]. As far as we know, there are no previous prospective studies of the relationship between SOC and diabetes. The results of this large scale longitudinal study among Finnish male employees showed that in a 18-year follow-up, initial weak SOC was associated with almost a 50% higher risk of diabetes in employees aged =<50 years at the start of the study. This result could not be explained by a variety of controlled baseline socio-demographic, psychosocial and health-risk behaviour variables. Therefore these results suggest that there can be a direct relationship between a weak SOC and physiological consequences affecting health. The result is in accordance with two earlier cross-sectional studies indicating a relationship between SOC and diabetes [
17,
18].
There are at least three processes that may explain the link between SOC and health [
33]. First, common genetic or physiological processes can determine both psychological attributes and disease. Second, individual differences (personality traits or attributes), such as SOC, can influence health promoting (e.g., regular exercise) or damaging (e.g., unhealthy diet) behaviours. Third, individual characteristics can influence the effective implementation of health-related coping behaviour and have an adverse effect on mental health.
Recent research supports Antonovsky's theory that SOC moderates (buffers) the health impacts of adverse life events [
34]. A weak SOC might increase experiences of overwhelming and negative stress through autonomous neural pathways, by neuroendocrinological or neuroimmmunological mechanisms [
35], and this could be reflected in a higher risk of diabetes. A weak SOC can be interpreted as a lower ability to cope with stressors [
7,
17]. Exposure to long-term stress affects the entire neuroendocrine system, activating the hypothalamic-pituitary-adrenal (HPA) axis and the central sympathetic nervous system [
36]. Increased cortisol levels following activation of the HPA axis could play a role in the development of decreased glucose tolerance. Cortisol has been shown to induce insulin resistance by increasing hepatic glucose production, suppressing glucose usage, and inhibiting insulin secretion [
37].
SOC is strongly linked with aspects of negative emotionality [
10,
38,
39]. Negative emotionality has been associated with higher body mass index and weight gain [
40] and hostility with the so-called 'metabolic syndrome'[
41], which are all risk factors for Type-2 diabetes. Additionally, people with a weak SOC can perceive their environment as nonsupportive. A weak SOC has been associated with low social support [
42], which has in turn been found to increase the risk of poor health [
43].
To sum up, a potential combination of stress inducing reactive tendency, inadequate coping systems and unhealthy lifestyle choices characterizing those with a weak SOC may help to explain the association between SOC and diabetes identified in this study.
Strengths and limitations
The cohort size of this study, our capacity to adjust for several traditional risk factors for diabetes, together with reliable prospective ascertainment of entitlement to drug imbursement due to diabetes from national registers provided a unique opportunity to test and confirm the hypothesis that a weak SOC is associated with an increased risk of diabetes. Non-response occurred randomly enough to limit the potential for selection bias. In addition, the observed effect size in employees =<50 years of age was relatively large, a 46% increase in the incidence of diabetes (after adjustment for several traditional risk factors). Further advantages include an exceptionally long the follow-up period. Earlier prospective studies on SOC and objective health outcomes have been based on less than 10 years follow-up periods. The use of long enough follow-up is important as the influence of SOC on severe health outcomes, such as diabetes, is slow to manifest itself.
However, our results should be interpreted in light of some limitations. First, even if a long follow-up can generally be considered as strength, on the other hand individuals can develop other health problems or poor health behaviours during this lengthy time period, and these problems and/or behaviours may have an impact on the eventual development of diabetes.
Second, some patients with Type-2 diabetes do not use medication but try to control their disease with a help of proper diet and exercise. These individuals would not have been identified in this study design. However, due to well developed health screening and occupational health care system in Finland, we can be fairly certain that most cases entitled to reimbursement of diabetes medication were detected in our study. It is possible, nevertheless, that employees who died during the follow-up, especially some of those employees who had a cardiovascular diagnosis (N = 185), may have had an undetected impaired glucose tolerance which may have contributed as a risk factor for death. If this is the case, the effect of weak SOC on diabetes incidence found in this study may be an underestimate.
Third, the Drug Imbursement Register was used as a means of determining the presence of diabetes and other chronic diseases at baseline. However, there are chronic diseases for which medications are not common or for which medications were developed only in recent years. In spite of this, the Drug Imbursement Register can be seen as a fairly reliable and objective data to use in determining a "healthy" status.
Fourth, in this study our outcome was disease even though theoretically SOC is promotive of health rather than illness.
Fifth, the SOC theory is not very specific about diagnoses, whereas our study was specific about the studied outcome. Individual characteristics such as SOC are typically generalised resistance resources, that is, their effects on health are non-specific [
44]. When encountering stressors and adverse life events, individuals can react differently and with different health outcomes because of their resources and other characteristics (e.g., work characteristics) [
44,
45]. However, in a medical study it is very difficult to include the incidences of diseases that have very different biomedical pathogenesis, such as for example type 2 diabetes and depression, in the same outcome variable. In our opinion, it is important to widen the scope of SOC theory towards various biomedical outcomes, such as coronary heart disease, diabetes or other conditions, and to further specify the psychomedical, psychosocial and psychobehavioral mechanisms through which SOC may affect various health and ill health outcomes, even though this is a dilemma in relation to traditional SOC research since Antonovsky's theory is not diagnosis-specific.
Sixth, the most serious epidemiological shortcoming of our study was that our questionnaire did not include questions about dietary habits, body mass index (BMI) and weight gain and therefore we were unable to examine their mediating role. In previous studies SOC has been associated with unhealthy lifestyles, such as unhealthy food choices [
16]. It is possible that the lack of weight-related variables in the analyses have affected the results. Further research needs thus to be conducted to test whether dietary habits, BMI or weight gain could be responsible for the association between SOC and diabetes.
Seventh, our physical activity measure was not optimal for this kind of study since the response options were not specific enough to separate sufficiently people with different frequency of weekly exercise. This shortcoming becomes even more significant since the study did not include data on BMI. Those participants exercising the most frequently are probably the most unlikely to be overweight.
However, regular physical exercise at least once a week has been associated with a reduced risk of type 2 diabetes in initially healthy 35–60-year-old men [
28]. Moreover, another study [
46] found that for those older adults who were physically active once a week, the risk of all-cause mortality was 40% lower than for those who were physically inactive. For those who were physically active more frequently, the reduction in all-cause mortality risk was about the same as for those who were physically active once a week.
Finally, assessing health behaviours only at baseline can be a limitation as these behaviours may change over 18 years. Finally, it can be assumed that individuals' health may influence their SOC, i.e., the causality between SOC and health may also operate in the other way around. Health represents one of the sources responsible for the maintenance of the level of SOC [
7]. However, in earlier research predictive relationships from health to SOC has not been found [
11].
Further studies in other countries and in other sectors are needed to confirm and develop our findings as well as determine their generalisability. More research is especially needed to examine the biopsychosocial mechanisms behind the association between SOC and diabetes, and investigate the associations of other individual difference variables with diabetes.