Is coronary heart disease caused by an environmentally-induced chronic metabolic imbalance?

The hypothesis is put forward that coronary heart disease (CHD) arises from a chronic imbalance between anabolism and catabolism in the body, induced by the psychosocial environment and mediated through the central nervous system (CNS) and neuroendocrine system. Psychosocial demands increase periods of waking arousal and reduce the periods of rest necessary to compensate for the catabolic and degradative effects of activity. This prevents the complete healing of repeated arterial damage caused by haemodynamic stress, and enhances the accumulation of lipids into damaged areas in the arterial wall. This hypothesis can account for the significance of known CHD risk factors. A high-fat diet exacerbates the problem by increasing the rate of lipid accumulation into the arterial lesions. Cigarette smoking increases CHD risk by acting as a stimulant of the arousal-inducing neuroendocrine mechanisms, and moderate alcohol consumption reduces CHD risk by depressing CNS arousal. Physical activity enforces subsequent inactivity and compensatory anabolism through feedback mechanisms, which "overshoots" and produces a net anabolic effect that increases cardiovascular strength and general resistance to physical strain.