We now know that a body awash in stress hormones for years at a time is most likely to develop a range of diseases, such as cardiovascular disease, and loss of cognitive and physical functioning, all of which modern physicians consider common with advancing age.

A lifetime of job stress (high psychological demands and a lack of control) can accelerate the progression of atherosclerosis and heart failure (BMJ, 1997; 314: 553-8; Arterioscler Thromb Vasc Biol, 1996; 16: 363-7; BMJ, 1985; 291: 1312-4). Caring for a spouse or relative who is ill, say, with Alzheimer’s can also lead to a greater risk of coronary heart disease (Psychosom Med, 2002; 64: 418-35).

Higher cortisol levels have been recorded in patients at the onset of a myocardial infarction (Exp Clin Endocrinol, 1992; 99: 68-70; Clin Endocrinol, 1994; 40: 499-504). Stress can also raise blood pressure (Hypertension, 2002; 139: 184-8), create harmful free radicals and raise levels of homocysteine, which damages cell linings and arterial walls (Life Sci, 2000; 66: 2267-75; Life Sci, 1999; 64: 2359-65).

A nine-year study in Japan of 73,000 people showed that women who reported high mental stress were more than twice as likely to have a fatal stroke than those reporting low stress, and about two times as likely to have a deadly heart attack. Men who reported high mental stress were about 1.5 times more likely to die from a heart attack, but did not show significantly increased deaths overall due to stroke (Circulation, 2002; 106: 1229-36).

Although the women who reported high stress were more sedentary, more likely to have a history of hypertension or diabetes, smoked more and were more likely to work fulltime, the researchers noted that, even after adjusting for these factors, the association between stress and heart attacks in both women and men, and between stress and strokes in women, remained.

Stress can also lead to poor eating habits, poor glucose control and obesity (Prev Med, 2002; 34: 29-39; Psychosom Med, 1996; 58: 489-99) - cornerstones of many diseases later in life.

Indeed, a theory known as the ‘stress cascade’ suggests an interconnection between stress, diabetes, obesity, hypertension and altered lipoprotein metabolism (Clin Sci, 1989; 77: 453-61). The stress cascade results in the release of increasingly larger amounts of catecholamines and corticosteroids which, in turn, affect insulin regulation, glucose metabolism and fat storage. Sustained cortisol output due to stress increases insulin insensitivity, which tends to lead to a decreased tissue-glucose uptake. When this happens, insulin secretion increases to counteract the increased insulin insensitivity. The long-term elevations of cortisol and the secondary raised insulin levels also increase fatty acid, glycogen and lipoprotein lipase synthesis in fat tissues, creating ideal conditions for the development of high cholesterol and triglyceride levels in the blood - risk factors for atherosclerosis.

At the other end of the scale, Norwegian researchers have found that stress is a more influential factor in the development of Graves’ disease (an overactive thyroid) than genetics. In a study of 219 persons newly diagnosed with Graves’ disease and matched with 372 controls, those who were under stress had 6.3 times the risk of developing the disease compared with 3.6 times for those with a family history of the disease (Lancet, 1991; 338: 1475-9).

Immunity and cancer The ability of stress to alter immune function and to precipitate and aggravate infectious diseases has long been recognised (J Fla Med Assoc, 1993; 80: 409-11; Arch Psych Nurs, 1994; 8: 221-7). Today, suppressed immunity is recognised as a major problem associated with chronic exposure to stress hormones (Psychosom Med, 2002; 64: 15-28; Psychosom Med, 1992; 54: 680-5; Psychol Inquiry, 1991; 2: 249-51; Behav Immunol, 1988; 2, 67-78; Soc Neurosci, 1996; 22: 1350; N Engl J Med, 1991; 325: 606-12; JAMA, 1999; 281: 2268-70).