STRESS AND CARDIOVASCULAR-DISEASE

Authors
Citation
P. Bjorntorp, STRESS AND CARDIOVASCULAR-DISEASE, Acta Physiologica Scandinavica, 161, 1997, pp. 144-148
Citations number
14
Categorie Soggetti
Physiology
ISSN journal
00016772
Volume
161
Year of publication
1997
Supplement
640
Pages
144 - 148
Database
ISI
SICI code
0001-6772(1997)161:<144:SAC>2.0.ZU;2-T
Abstract
The statistical associations between stress and cardiovascular and oth er prevalent diseases have not been explained. Perceived stress, resul ting in an uncontrollable defeat reaction, has been shown by James Hen ry (Henry 1993) to be followed by specific endocrine abnormalities, in cluding sensitization of the hypothalamo-pituitary-adrenal (HPA) axis, and inhibited sex steroid and growth hormone secretions. With an elev ated waist/hip circumference ratio (WHR) - a simple, surrogate, measur ement of intraabdominal, visceral fat masses - combined with insulin r esistance, similar endocrine perturbations are found. Based on conside rable evidence, such endocrine abnormalities seem to be followed by ac cumulation of intraabdominal, visceral fat masses and insulin resistan ce, both powerful risk factors for cardiovascular disease, diabetes an d stroke. A postulated chain of events is therefore that the endocrine perturbations are primary factors, followed by visceral fat accumulat ion, insulin resistance and other risk factors dependent on the hyperi nsulinemia following insulin resistance. This highlights the importanc e of elucidating the cause(s) to the endocrine abnormalities. These ar e identical to those described by Henry (1993) to follow a stress reac tion of a defeat type. Findings of several psychosocial and socio-econ omic handicaps might provide a basis for such a reaction, supported by experimental studies in primates. Furthermore, depression, anxiety, a lcohol consumption and smoking, all known activators of the HPA axis, are also often found. The low sex steroid and growth hormone secretion s might be secondary to the hypersensitive HPA-axis. They could also b e caused by other factors, and are, each alone, capable of causing bot h visceral fat accumulation and insulin resistance. Visceral fat accum ulation is only an indirect, surrogate measurement of the underlying e ndocrine abnormalities, but is useful for screening purposes on a popu lation basis. Developments of novel techniques for sensitive, yet simp le measurements of HPA axis activity under undisturbed conditions seem to allow a better definition of pathogenetic factors. Utilizing such methods, subgroups of the syndrome including visceral fat accumulation , insulin resistance and other associated risk factors (Metabolic Synd rome), are beginning to emerge. A more detailed information on noxious factors in society leading to a defeat reaction to perceived stress, endocrine abnormalities and the Metabolic Syndrome, with increased ris k for prevalent disease may hopefully be developed by these new method s.