2 research outputs found
Effect of short-term weight loss on mental stress-induced cardiovascular and pro-inflammatory responses in women
Epidemiologic evidence links psychosocial stress with obesity but experimental studies
examining the mechanisms that mediates the effect of stress on adiposity are scarce. The aim of
this study was to investigate whether changes in adiposity following minimal weight loss affect
heightened stress responses in women, and examine the role of the adipokine leptin in driving
inflammatory responses. Twenty-three overweight or obese, but otherwise healthy, women
(M age ¼ 30.41 ± 8.0 years; BMI ¼ 31.9 ± 4.1 kg/m2
) completed standardized acute mental stress
before and after a 9-week calorie restriction program designed to modify adiposity levels.
Cardiovascular (blood pressure and heart rate) and inflammatory cytokines (leptin and
interleukin-6; IL-6) responses to mental stress were assessed several times between baseline
and a 45-min post-stress recovery period. There were modest changes in adiposity measures
while the adipokine leptin was markedly reduced (27%) after the intervention. Blood pressure
reactivity was attenuated (3.38 ± 1.39 mmHg) and heart rate recovery was improved
(2.07 ± 0.96 Bpm) after weight loss. Blood pressure responses were inversely associated with
changes in waist to hip ratio post intervention. Decreased levels of circulating leptin following
weight loss were inversely associated with the IL-6 inflammatory response to stress (r ¼ 0.47).
We offered preliminary evidence suggesting that modest changes in adiposity following a brief
caloric restriction program may yield beneficial effect on cardiovascular stress responses. In
addition, reductions in basal leptin activity might be important in blunting pro-inflammatory
responses. Large randomized trials of the effect of adiposity on autonomic responses are thus
warranted
Disruption of multisystem responses to stress in type 2 diabetes: investigating the dynamics of allostatic load
Psychological stress-related processes are thought to contribute
to the development and progression of type 2 diabetes, but the
biological mechanisms involved are poorly understood. Here, we
tested the notion that people with type 2 diabetes experience
chronic allostatic load, manifest as dynamic disturbances in reactivity
to and recovery from stress across multiple (cardiovascular, neuroendocrine,
inflammatory, metabolic) biological systems, coupled
with heightened experience of chronic life stress. We carried out
an experimental comparison of 140 men and women aged 50–75 y
with type 2 diabetes and 280 nondiabetic individuals matched on
age, sex, and income. We monitored blood pressure (BP) and heart
rate, salivary cortisol, plasma interleukin (IL)-6, and total cholesterol
in response to standardized mental stress, and assessed salivary cortisol
over the day. People with type 2 diabetes showed impaired
poststress recovery in systolic and diastolic BP, heart rate and cholesterol,
and blunted stress reactivity in systolic BP, cortisol, cholesterol,
and IL-6. Cortisol and IL-6 concentrations were elevated, and
cortisol measured over the day was higher in the type 2 diabetes
group. Diabetic persons reported greater depressive and hostile
symptoms and greater stress experience than did healthy controls.
Type 2 diabetes is characterized by disruption of stress-related processes
across multiple biological systems and increased exposure to
life stress. Chronic allostatic load provides a unifying perspective
with implications for etiology and patient management