Also see:
The Streaming Organism
Stress, Portrait of a Killer – Full Documentary (2008)
Stress and Aging: The Glucocorticoid Cascade Hypothesis

“In experiments, progesterone was found to be the basic hormone of adaptation and of resistance to stress. The adrenal glands use it to produce their anti-stress hormones, and when there is enough progesterone, they don’t have to produce the potentially harmful cortisone. In a progesterone deficiency, we produce too much cortisone, and excessive cortisone causes osteoporosis, aging of the skin, damage to brain cells, and the accumulation of fat, especially on the back and abdomen.” – Ray Peat, PhD

“I think fat develops around the abdominal organs during stress as a defensive measure, similar to the padding effect that you mention, for walking, sitting, and moving. Around joints, fat pads fill in spaces between tendons, muscles, and bones. When stress becomes too generalized, for example when we live in a toxic environment and eat toxic foods, that produce inflammation, then fat deposition can lose its simple mechanical function, and, especially when the stored fat is highly unsaturated, it can become an internal source of inflammation and toxicity. The polyunsaturated fats that contribute to inappropriate fat storage, producing prostaglandins and toxic free radicals, also interfere with good muscle development, and eventually lead to the sarcopenia of aging, in which the body’s muscle content shrinks as the fat content increases. A good layer of abdominal muscle, subtly padded by fat, produces the most attractive body contour.” – Ray Peat PhD

“Fat does not provide substantial quantities of carbohydrate, but some of the latter is needed to maintain body functions. If it is not in the diet, then body protein catabolism will be accelerated for gluconeogenesis. In some individuals, sufficient protein destruction will result to provide glucose for synthesis of substantial quantities of new body fat.” -Constance Martin, PhD

The location of fat stores can provide feedback regarding hormonal regulation. The stress hormone, cortisol, is linked to the accumulation of belly fat.

Psychosom Med. 2000 Sep-Oct;62(5):623-32.
Stress and body shape: stress-induced cortisol secretion is consistently greater among women with central fat.
Epel ES, McEwen B, Seeman T, Matthews K, Castellazzo G, Brownell KD, Bell J, Ickovics JR.
OBJECTIVE:
Excessive central fat puts one at greater risk of disease. In animal studies, stress-induced cortisol secretion has been shown to increase central fat. The objective of this study was to assess whether women with central fat distribution (as indicated by a high waist-to-hip ratio [WHR]), across a range of body mass indexes, display consistently heightened cortisol reactivity to repeated laboratory stressors.
METHODS:
Fifty-nine healthy premenopausal women, 30 with a high WHR and 29 with a low WHR, were exposed to consecutive laboratory sessions over 4 days (three stress sessions and one rest session). During these sessions, cortisol and psychological responses were assessed.
RESULTS:
Women with a high WHR evaluated the laboratory challenges as more threatening, performed more poorly on them, and reported more chronic stress. These women secreted significantly more cortisol during the first stress session than women with a low WHR. Furthermore, lean women with a high WHR lacked habituation to stress in that they continued to secrete significantly more cortisol in response to now familiar challenges (days 2 and 3) than lean women with a low WHR.
CONCLUSIONS:
Central fat distribution is related to greater psychological vulnerability to stress and cortisol reactivity. This may be especially true among lean women, who did not habituate to repeated stress. The current cross-sectional findings support the hypothesis that stress-induced cortisol secretion may contribute to central fat and demonstrate a link between psychological stress and risk for disease.

Obes Res. 1999 Jan;7(1):9-15.
Stress-induced cortisol, mood, and fat distribution in men.
Epel EE, Moyer AE, Martin CD, Macary S, Cummings N, Rodin J, Rebuffe-Scrive M.
OBJECTIVE:
A previous study in our laboratory (Moyer et al., Obes Res. 1994;2:255-62 found that, in response to uncontrollable laboratory stress, women with a high waist-to-hip ratio (WHR) had higher cortisol reactivity, poorer coping skills, and lower anger responses than women with low WHR. We aimed to compare high WHR men’s stress responses to these women.
RESEARCH METHODS AND PROCEDURES:
The current study examined cortisol reactivity and psychological data of 27 healthy high WHR men exposed to the same laboratory challenges as the women from our previous study. Men’s data are discussed in relation to that of the high and low WHR women.
RESULTS:
Men responded to the stress with increases in both cortisol and blood pressure. In comparison with the high and low WHR women, men had significantly higher total cortisol on the stress day. However, when comparing a sub-sample of men and women matched in WHR’s, differences in cortisol secretion were greatly diminished and no longer significant. In addition, men had higher desire for control than both high and low WHR women, and lower mood reactivity than low WHR women. Despite the lower mood reactivity of high WHR groups, the high mood reactors among the high WHR women, and to a lesser extent, men, tended to have higher cortisol reactivity.
DISCUSSION:
These results suggest that the psychological differences and greater exposure to cortisol observed among the high WHR men and women may have played a role in contributing to their greater abdominal fat depots.

Obes Res. 1994 May;2(3):255-62.
Stress-induced cortisol response and fat distribution in women.
Moyer AE, Rodin J, Grilo CM, Cummings N, Larson LM, Rebuffé-Scrive M.
Recent studies have shown an association between uncontrollable stress and abdominal fat distribution. It has been suggested that changes in cortisol secretion might represent one possible mechanism for this relationship. This study investigated whether body fat distribution, determined by waist-to-hip ratio (WHR), is related to salivary cortisol levels in response to laboratory stressors. Subjects were 41 overweight women with a Low or a High WHR. Multiple measures of cortisol and mood were obtained during a session of stressful tasks (eg., timed arithmetic) and during a time-matched, control rest session. Also, background life stress and psychological trait variables were assessed. Compared to Low WHR subjects, High WHR subjects secreted significantly more cortisol during the stressful session after 60 minutes of stress, and considering the total area under the curve of secretion. This difference was not seen on the rest day. In terms of background and psychological measures, High WHR subjects were characterized by poorer coping skills and differences in mood reactivity. Specifically, although all subjects became more angry in response to the stressful session, High WHR subjects showed smaller increases in anger. This could indicate that they are more likely to evidence a helpless reaction to uncontrollable stress. These findings support the hypothesis that cortisol secretion might represent a mechanism for the observed association between stress and abdominal fat distribution. Furthermore, differences in coping and appraisal may suggest that a particular psychological pattern might influence the reactivity of the adrenal-cortical system to stress, and subsequent fat distribution.

Psychosom Med. 2010 May;72(4):357-64. Epub 2010 Apr 5.
Low calorie dieting increases cortisol.
Tomiyama AJ, Mann T, Vinas D, Hunger JM, Dejager J, Taylor SE.
OBJECTIVE:
To test the hypothesis that dieting, or the restriction of caloric intake, is ineffective because it increases chronic psychological stress and cortisol production–two factors that are known to cause weight gain; and to examine the respective roles of the two main behaviors that comprise dieting–monitoring one’s caloric intake and restricting one’s caloric intake–on psychological and biological stress indicators.
METHODS:
In a 2 (monitoring vs. not) x 2 (restricting vs. not) fully crossed, controlled experiment, 121 female participants were assigned randomly to one of four dietary interventions for 3 weeks. The monitoring + restricting condition tracked their caloric intake and restricted their caloric intake (1200 kcal/day); the monitoring only condition tracked their caloric intake but ate normally; the restricting only condition was provided 1200 kcal/day of food but did not track their calories, and the control group ate normally and did not track their intake. Before and after the interventions, participants completed measures of perceived stress and 2 days of diurnal saliva sampling to test for cortisol.
RESULTS:
Restricting calories increased the total output of cortisol, and monitoring calories increased perceived stress.
CONCLUSIONS:
Dieting may be deleterious to psychological well-being and biological functioning, and changes in clinical recommendations may be in order.

Am J Physiol Regul Integr Comp Physiol. 2007 Nov;293(5):R1864-74. Epub 2007 Sep 12.
Social stress and recovery: implications for body weight and body composition.
Tamashiro KL, Nguyen MM, Ostrander MM, Gardner SR, Ma LY, Woods SC, Sakai RR.
Social stress resulting from dominant-subordinate relationships is associated with body weight loss and altered body composition in subordinate (SUB) male rats. Here, we extend these findings to determine whether stress-induced changes in energy homeostasis persist when the social stress is removed, and the animal is allowed to recover. We examined body weight (BW), body composition, and relevant endocrine measures after one or two cycles of 14 days of social stress, each followed by 21 days of recovery in each rat’s individual home cage. SUB lost significantly more BW during social housing in a visible burrow system (VBS) compared with dominant (DOM) animals. Weight loss during social stress was attributable to a decrease in adipose tissue in DOM and SUB, with an additional loss of lean tissue in SUB. During both 21-day recovery periods, DOM and SUB regained lost BW, but only SUB were hyperphagic. Following recovery, SUB had a relatively larger increase in adipose tissue and plasma leptin compared with DOM, indicating that body composition changes were dependent on social status. Control animals that were weight matched to SUB or male rats exposed to the VBS environment without females, and that did not form a social hierarchy, did not exhibit changes in body composition like SUB in the VBS. Therefore, chronic social stress causes social status-dependent changes in BW, composition and endocrine measures that persist after repeated stress and recovery cycles and that may ultimately lead to metabolic disorders and obesity.

Psychoneuroendocrinology. 2013 Sep 2. pii: S0306-4530(13)00287-4. doi: 10.1016/j.psyneuen.2013.07.022. [Epub ahead of print]
Psychosocial stress induces hyperphagia and exacerbates diet-induced insulin resistance and the manifestations of the Metabolic Syndrome.
Sanghez V, Razzoli M, Carobbio S, Campbell M, McCallum J, Cero C, Ceresini G, Cabassi A, Govoni P, Franceschini P, de Santis V, Gurney A, Ninkovic I, Parmigiani S, Palanza P, Vidal-Puig A, Bartolomucci A.
Stress and hypercaloric food are recognized risk factors for obesity, Metabolic Syndrome (MetS) and Type 2 Diabetes (T2D). Given the complexity of these metabolic processes and the unavailability of animal models, there is poor understanding of their underlying mechanisms. We established a model of chronic psychosocial stress in which subordinate mice are vulnerable to weight gain while dominant mice are resilient. Subordinate mice fed a standard diet showed marked hyperphagia, high leptin, low adiponectin, and dyslipidemia. Despite these molecular signatures of MetS and T2D, subordinate mice fed a standard diet were still euglycemic. We hypothesized that stress predisposes subordinate mice to develop T2D when synergizing with other risk factors. High fat diet aggravated dyslipidemia and the MetS thus causing a pre-diabetes-like state in subordinate mice. Contrary to subordinates, dominant mice were fully protected from stress-induced metabolic disorders when fed both a standard- and a high fat-diet. Dominant mice showed a hyperphagic response that was similar to subordinate but, unlike subordinates, showed a significant increase in VO2, VCO2, and respiratory exchange ratio when compared to control mice. Overall, we demonstrated a robust stress- and social status-dependent effect on the development of MetS and T2D and provided insights on the physiological mechanisms. Our results are reminiscent of the effect of the individual socioeconomic status on human health and provide an animal model to study the underlying molecular mechanisms.