The etiopathogenesis of premenstrual syndrome as a consequence of altered blood rheology: a new hypothesis.
The multisystem symptoms of premenstrual syndrome (PMS), the variable nature of their occurrence and their relatively rapid disappearance with the onset of bleeding are highly suggestive of a systemic factor as the causal agent of the disorder. Reports of increased blood viscosity and enhanced red blood cell (RBC) hydration provide a basis for proposing that PMS is the consequence of an aberration of the change in blood viscosity which occurs in the third week of the normal menstrual cycle. The seriousness of the viscosity-impaired capillary blood flow will be greatest in organs and capillary beds with the smallest capillaries. Such an assumption implies that those women who suffer from PMS will be individuals whose capillaries are smaller in size than non-sufferers. The frequency of occurrence of fluid retention as a symptom suggests that the specific etiologic agent could be a reduction in RBC deformability as a consequence of impaired linoleic acid metabolism or high levels of noradrenaline or hypothyroidism or combinations of the three factors. If poorly deformable RBCs are involved then the use of agents such as evening primrose oil or fish oil to improve RBC deformability could ameliorate the symptoms of PMS. It is speculated that similar changes in RBC deformability should occur at other times of hormonal change. Health problems occurring during pregnancy, or after parturition, or after cessation of ovarian function might be caused by or exacerbated by reduced RBC deformability.
Simpson
L O
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Pathology Department, University of Otago Medical School, Dunedin, New Zealand.
D001794:Blood Pressure; D001809:Blood Viscosity; D004907:Erythrocyte Deformability; D005260:Female; D005836:Genitalia, Female / Q000098:blood supply; D012739:Gonadal Steroid Hormones / Q000502:physiology; D006801:Humans; D019787:Linoleic Acid; D008041:Linoleic Acids / Q000378:metabolism; D008597:Menstrual Cycle; D008833:Microcirculation; D008954:Models, Biological; D009638:Norepinephrine / Q000378:metabolism; D011293:Premenstrual Syndrome / Q000209:etiology* / Q000503:physiopathology; D013963:Thyroid Hormones / Q000502:physiology
D012739:Gonadal Steroid Hormones; D008041:Linoleic Acids; D013963:Thyroid Hormones; D019787:Linoleic Acid; D009638:Norepinephrine