Pheromones cause disease: the exocrinology of anorexia nervosa.
The aetiology of anorexia nervosa is exocrinological. This notion is supported by physical evidence in animal models with directly comparable symptomatology. Anorexia nervosa (AN) syndrome would be a puberty delay caused by reception and autoreception of conspecific pheromone emissions: a pheromone-induced puberty delay (PIPD). As such, it would be amenable to medical treatment drawing from forty years of research in animals. This hypothesis is testable. For instance, since food ad libitum is a prerequisite for PIPD, occasional supervised fasting in healthy peripuberal subjects should prevent AN. Besides, tolerating an untestable thought disease (1,2) with symptoms of a curable well-understood animal condition would be anti-scientific and perpetuates medical disaster. Even their endocrinologies are identical. Pheromone feedback tunes animal appetites and immunity to available resources and prospects. In addition to timing puberty, pheromones regulate fertility. Pheromones will probably be implicated in the aetiology of the psychiatric and autoimmune diseases. This is the second in a series of twelve papers to explore this contention systematically.
Nicholson
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D000818:Animals; D000856:Anorexia Nervosa / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology; D005088:Exocrine Glands / Q000378:metabolism*; D005260:Female; D006801:Humans; D008297:Male; D008597:Menstrual Cycle; D012724:Sex Attractants / Q000502:physiology*; D012744:Sex Ratio
D012724:Sex Attractants