Can circadian restriction of feeding modulate autonomic nervous system dysfunction and cardiometabolic risk?

Apart from the sympathetic and parasympathetic nerves, the pituitary and pineal glands and the suprachiasmatic nucleus are also involved in determining autonomic functions. Western diet, autonomic dysfunction and obesity are further associated with sympathetic activation that promotes atherosclerosis, end-organ damage, and hypertension. Experimental sites indicate that high-fatinduced weight gain in rats elevates plasma leptin at 1 to 3 days after the onset of calorie-dense diets, and that dietinduced overfeeding may increase sympathetic activity within 1 week after the onset of the regimen. It has been shown, for the first time, that the high-fat, cafeteria-style diet stimulates sustained increases in lumbar sympathetic neural drive in rats. Halberg demonstrated for the first time in 1973 that eating dinner was associated with relative weight gain, whereas eating the same amount of calories as breakfast was linked to relative weight loss in humans and death in animals. There appear to be independently variable effects on circadian physiology and metabolism in association with circadian restriction of feeding to a particular time of the day and during caloric restriction. Apart from these markers related to energy, circadian alteration in metabolism of nutrients, omega-3 fatty acids, flavonoids, B vitamins and coenzyme Q10 may be important in autonomic functions.