I was intrigued by your hypothesis, partly for the inverse
possibility of yoga and type O's. Information which addresses your
hypothesis follows. Apparently vigorous exercise in type A's reduces
protection from very low density lipoprotein toxicity.
Biochemistry is like a plate of spaghetti; single syllogisms get lost in
the sauce of multiple factors.
Psychosom Med 1992 Sep;54(5):612-619
Effects of stress and blood type on cortisol and VLDL toxicity preventing
Neumann JK, Arbogast BW, Chi DS, Arbogast LY
Department of Veterans Affairs Medical Center, Johnson City, Tennessee 37684.
Past research has associated ABO blood type and mental stress with cardiovascular risk. We studied the effects of blood type (A vs. O) coupled with a mirror drawing stressor on very low density lipoprotein toxicity-preventing
activity (TxPA) and plasma cortisol levels. Exposure to the stressor significantly decreased TxPA and increased cortisol for the total group of 25 older adult males. However, the stress response patterns of the 15 blood type A
males were different from those of the 10 type O subjects. The blood type A group had higher initial levels of TxPA and cortisol as well as quicker stress recovery rates than the type O group. ABO blood type may be an important
behavioral hematologic variable to assess in studies concerning biochemical stress response or cardiovascular risk.
J Psychosom Res 1994 Nov;38(8):871-884
Transient loss of serum protective activity following short-term stress: a possible biochemical link between stress and atherosclerosis.
Arbogast BW, Neumann JK, Arbogast LY, Leeper SC, Kostrzewa RM
Department of Internal Medicine, James H. Quillen College of Medicine, East Tennessee State University, Johnson
City 37614-0622, USA.
Very low density lipoproteins (VLDL) are toxic to aortic endothelial cells in vitro, and toxicity preventing activity. (TxPA) inhibits this toxic effect of VLDL. Stress, an established arteriosclerosis risk factor, was examined for its effect on TxPA and on the ability of serum to protect endothelial cells from in vitro injury by VLDL. A standardized mirror tracing task with noise was administered to four healthy subjects. Blood samples were obtained at 0, 30, (stressor) 35, 50 and 80 min. Cortisol and non-esterified fatty acids increased during the stress period. TxPA significantly decreased following the stressor and had recovered by 80 min. When the ratio of non-TxPA/TxPA rose above 2, serum was no longer able to protect the cells from VLDL injury. If endothelial cells in vivo respond similarly to the endothelial cells in culture, the effect of stress on atherosclerosis may be mediated through these transient decreases in TxPA.