This study examined whether depressive symptoms could predict an increase in abdominal obesity over time in a large community-based sample of older persons. As hypothesized, depressed persons showed a significantly greater increase in abdominal obesity over 5 years, especially in visceral fat, than non-depressed persons. Such an association was not found for an increase in overall obesity and also appeared to be independent of changes in overall obesity, suggesting that depressive symptoms are rather specifically associated with fat gain in the visceral region.
To our knowledge, this is the first study to examine the association between depressive symptoms and increases in abdominal obesity over time in a large cohort. Our results are consistent with a study by Weber-Hamann et al.25
, which showed a larger accumulation of visceral fat mass over time in 29 depressed patients compared to 17 controls. Most studies so far have assessed the association between abdominal obesity and depression cross-sectionally, using either anthropometric measures alone, or CT measures in relatively small study samples19–24
. Most of these studies showed a positive relationship between depression and abdominal obesity, although one large epidemiological study could not demonstrate an association between waist circumference and depression34
. In our study, associations with waist circumference were also weaker than those with visceral fat, possibly due to the fact that waist circumference is only an indirect measure of visceral fat and is determined by both abdominal subcutaneous and visceral fat mass. Also, measuring waist circumference might be less precise than CT scanning. Stronger associations were found for sagittal diameter, which is considered a better indicator of visceral fat than waist circumference in older persons35
. Our results indeed show a higher correlation of sagittal diameter (r=0.75) than waist circumference (r=0.63) with visceral fat. Most pronounced, however, were the associations with visceral fat, which is in line with our hypothesis that depressive symptoms contribute to an accumulation of visceral fat specifically.
Although depression has been associated with weight loss30,31
, our results show an increase in visceral fat in persons with depressive symptoms, even in this aging population where decreases in fat mass are common36
. We found no evidence that depression would result in a loss of visceral fat. Even more, we found that depression was in fact negatively associated with a loss of visceral fat, indicating that depression is linearly linked with the accumulation of visceral fat and no u-shaped association exists. Furthermore, the results of this study show that depression appears to be specifically associated with abdominal obesity stronger than and independent of overall obesity. Associations between depressive symptoms and overall obesity were not found and adjusting abdominal obesity analyses for baseline BMI did not influence findings. Furthermore, we additionally adjusted for change in BMI which was partly an over-adjustment, because changes in BMI do also reflect changes in visceral fat. However, despite this relatively strict adjustment, the relationship between depression and change in visceral fat remained. Moreover, our results showed that across the whole range of weight change an association existed between depression and visceral fat suggesting that even in persons who lost weight, visceral fat was preferentially retained in those with depression. The finding that associations were specific for abdominal obesity, is in line with other studies showing that abdominal obesity, more than overall obesity, is associated with poor health outcomes, such as diabetes, CVD, and mortality15–18
. Because both depression and diabetes/CVD appear to be specifically associated with excess visceral fat, this could help explain the frequently found increased risk of diabetes and CVD among depressed persons.
Our results indicate that depression predicts increases in abdominal obesity in all but black women. Reasons for this exception are not entirely clear. One explanation may be that the black women in this older sample experienced a relatively large decrease in visceral fat, which might have obscured the association between depressive symptoms and the accumulation of visceral fat. Alternatively, this could have been a chance finding due to small sample sizes after stratification by sex and race. However, expected associations were found for the other 3 sex by race groups. Future research should explore sex and race differences further in younger samples.
What are the mechanisms by which depression may promote visceral fat accumulation? As suggested by Björntorp, stress activates the HPA-axis, which leads to an accumulation of visceral fat13
. Different studies show that chronic stress and depression are, at least in a subset of patients, associated with a dysregulation of the HPA-axis and elevated concentrations of cortisol7,8
. Visceral fat is highly sensitive to cortisol, due to a high density of glucocorticoid receptors14
. Cortisol promotes the accumulation of visceral fat by activating lipoprotein lipase and inhibiting lipid mobilization13
. Indeed, it has been shown that hypercortisolemic depression is associated with abdominal obesity20,37
. Moreover, these effects might be most pronounced when levels of sex steroid hormones, which have been found to reduce visceral fat mass and have a lipid-mobilizing effect13,38
, are low, as has been observed in late-life depression9
. Further, depression has been linked with high levels of inflammatory markers10
, which can activate the HPA-axis39
and therefore subsequently result in visceral obesity. Moreover, as described by Gold and Chrousos40
, even in persons with non-hypercortisolemic atypical depression, due to overeating, a cycling of weight gain and loss occurring throughout recurrent episodes of depression could preferentially distribute weight to visceral fat areas. An alternative explanation for why depression may lead to abdominal obesity is that depressed persons have an unhealthier lifestyle. Although we adjusted our analyses for some lifestyle behaviors (smoking, alcohol use, and physical activity), it is possible that depressed persons have a poorer dietary pattern. However, a poor diet in itself would likely lead to an increase in both overall and abdominal obesity41
. In combination with a hyperactive HPA-axis, however, it is possible that excess caloric intake is preponderantly stored into visceral fat depots42
. In addition, somatic comorbidities of depressed persons could have led to the increase in visceral fat, although our results were little affected by adjustment for diabetes, CVD, and general health status. Furthermore, weight gain in depressed persons has been associated with the use of antidepressants43
. However, in our study antidepressant use was not associated with increases in (abdominal) obesity, and therefore our findings can not be the result of antidepressant use.
Our results show that the link between depressive symptoms and increased abdominal obesity was stronger for the dichotomous indicator of depression than for the continuous CES-D score, suggesting that a certain amount of distress is needed before visceral fat starts to accumulate. On the other hand, we did not find evidence that the association between depression and an increase in abdominal obesity was specific for persons with persistent/recurrent depression compared to person with a single depression episode at baseline. However, most persons depressed at baseline did have an additional episode of depression during follow-up and it is very well possible that persons only depressed at baseline did experience additional depressive episodes in-between annual assessments.
Our study has some limitations. We did not have well-accepted criterion-based psychiatric diagnoses of depression. However, the CES-D is a commonly used scale to measure clinically relevant depressive symptoms. Our results might have been even stronger for persons with a diagnosis of major depressive disorder. Further, our sample showed low levels of depressive symptomatology at baseline and this aging population exhibited little change or even decrease in obesity, making it more difficult to detect associations with changes in obesity. Possibly, associations may be even stronger in a middle-aged population were visceral fat tends to increase over time. In addition, after 5 years of follow-up, there was drop-out due to mortality and non-response likely resulting in a relatively healthy sample, which could have led to an underestimation of the association between depression and change in abdominal obesity. On the other hand, studying the most healthy had the advantage that associations found were less likely confounded by somatic comorbidities. When missing values of persons without 5-year follow-up data were imputed, thereby including the less healthy, associations between depression and increase in abdominal obesity largely remained. Our study also has some important strengths, including use of a large community-based cohort followed for several years with repeated DXA and CT scans, which provide more direct assessments of total and visceral fat stores, as well as the more commonly used anthropometric measures.
In conclusion, our longitudinal results suggest that clinically relevant depressive symptoms give rise to an increase in abdominal obesity, in particular visceral fat, which seems to be stronger than and independent of overall obesity. Because of this specific accumulation of visceral fat, these results clearly suggest that there may be certain underlying pathophysiological mechanisms, plausibly involving the HPA-axis, which link depression with visceral fat. This could also help explain why depression is often followed by diabetes or CVD. Future research should further disentangle these mechanisms, since this will yield important information for prevention or treatment of depression-related health consequences.