Central adiposity, or deposition of body fat around the abdomen, is a risk factor for several negative health outcomes, including coronary heart disease, stroke, hypertension and non-insulin-dependent diabetes (Kissebah f& Krakower, 1994
; Lapidus, Bengtsson, Hallstrom, & Bjorntorp, 1984
). These associations are independent of body mass index (BMI). Additionally, central adiposity is associated with other risk factors for heart disease, such as hyperinsulinemia, insulin resistance, and increased plasma triglycerides (Despres et al., 1990
; Onat, Sansoy, & Uysal, 1999
). Central adiposity includes subcutaneous adipose tissue, found directly under the skin, and visceral adipose tissue, found between and around the internal organs. Non-invasive measurements of central adiposity include waist circumference (WC) and waist-to-hip-ratio (WHR), or waist circumference adjusted for hip size.
Arterial stiffness, or hardening of the arteries, is involved in the pathophysiology of cardiovascular disease (Boutouyrie et al., 2002
). Arterial stiffness is associated with aging, hypertension, and renal failure (Guerin, Blacher, Pannier, Marchais SJ, & London, 2001
; Munakata, Ito, Nunokawa, & Yoshinaga, 2003
; Ohnishi et al., 2003
). Hardening of the arteries results in a greater load on the heart and adversely affects heart function (Chang et al., 2006
). One measure of arterial stiffness is pulse wave velocity (PWV), which is distance traveled divided by time between pulse waves. Assuming the same distance, higher velocity is associated with stiffer vessels. Associations between arterial stiffness and central adiposity are apparent in adults (Choi et al., 2004
) and adolescents (Im, Lee, Shim, Lee, & Lee, 2007
Central adiposity and perhaps arterial stiffness in adolescence may pose later health risks. Research shows that central adiposity in childhood is associated with other cardiovascular risk factors in childhood, such as plasma lipid levels, glucose, insulin and blood pressure (Freedman, Srinivansan, Harsha, Webber, & Berenson, 1989
; Zonderland et al., 1990
; Zwiauer, Pakosta, Mueller, & Widhalm, 1992
). Central adiposity measured in adolescence tracks into adulthood (Eisenmann, Welk, Wickel, & Blair, 2004
). Consequently, central adiposity in adolescence sets up a trajectory of health risk across the life span. Adolescents with greater central adiposity have higher adulthood blood pressure, carotid intima-media thickness, and arterial stiffness (Eisenmann, Wickel, Welk, & Blair, 2005
; Ferreira et al., 2004
Several studies suggest that psychosocial variables are associated with central adiposity. Low social support may be one important factor. Wing and colleagues (1991)
found that social support was negatively correlated with WHR in women, after adjusting for body mass index (BMI). Another study showed that low levels of social support predicted WC over 5 years when controlling for baseline WC (Raikkonen, Matthews, & Kuller, 1999a
). A study that included adolescents (Ravaja, Keltikangas-Jarvinen, & Viikari, 1998
) reported that adolescent and young adult males who had declines in social support across 3 years had increases in WHR, adjusted for BMI. This relationship was independent of depression and hostility. However, results are not entirely consistent, as Kaye and colleagues (1993)
found null results for a relationship between social support and WHR in young adults.
Negative emotional traits have been more consistently linked to increased central adiposity. Several cross-sectional studies reported a positive association in adults between negative emotional traits, such as anger, anxiety, and hostility, and WHR (Ahlberg et al., 2002
; Kaye, Folsom, Jacobs, Hughes, & Flack, 1993
; Niaura et al., 2000
; Niaura et al., 2002
). Moreover, in a longitudinal investigation of women, anger, hostility, and depressive symptoms (although not anxiety) predicted an increase in central adiposity over time (Raikkonen et al., 1999a
; Raikkonen, Matthews, Kuller, Reiber, & Bunker, 1999b
). Another longitudinal study showed that negative emotional traits, particularly anger, anxiety, and components of hostility, predicted increased WHR (Nelson, Palmer, Pedersen, & Miles, 1999
). Specifically, cynicism and anxiety predicted higher WHR in both men and women, and anger predicted higher WHR in men, although lower WHR in women. However, this study did not control for baseline WHR, which minimizes the ability to confirm temporal sequence. Only one study has examined these relationships in adolescents. Mueller and colleagues (1998)
found that among 15–16 year olds, higher expressive anger was cross-sectionally associated with greater central body fat in boys but not girls.
Several cross-sectional studies link arterial stiffness and negative emotional traits. In the Baltimore Longitudinal Study of Aging, participants with suppressed anger had elevated carotid arterial stiffness measured in middle-aged adults (Anderson, Metter, Hougaku, & Najjar, 2006
). However, trait anger and anger expression were not correlated with arterial stiffness. In Atherosclerosis Risk in Community Study of black and white men and women, high trait anger was significantly associated with carotid arterial stiffness in men, but not in women (Williams, Din-Dzietham, & Szklo, 2006
). Yeragani and colleagues (2006)
showed that patients with anxiety disorders had higher PWV than did controls.
The purpose of our investigation was to examine the psychosocial correlates of central adiposity and arterial stiffness in black and white adolescents, both concurrently and longitudinally. We hypothesized that adolescents with less supportive social relationships and greater negative emotional traits would have greater central adiposity over time and greater arterial stiffness. We explored whether associations were stronger in blacks versus whites and males versus females, an important issue given the strong association of race and sex with cardiovascular risk. Should psychosocial factors be connected to central adiposity and arterial stiffness in adolescence, it would suggest the value of early prevention and intervention, identify susceptible subgroups, as well as inform understanding of the pathogenesis of cardiovascular disease.