Cardiovascular System

Medical Studies on Pregnenolone – Cardiovascular System

Herz-Kreislauf-System

As a precursor hormone of DHEA (dehydroepiandrosterone) pregnenolone exerts important indirect effects on cardiovascular health. It improves blood flow within the blood vessels and also positively influences their degree of calcification; important factors in vascular heart disease.

Supporting Cellular Mechanisms

The protective effect of DHEA is due, among other things, to the activation of endothelial nitric oxide, which is involved as a messenger substance in vascular processes such as the regulation of blood pressure and the dilation of blood vessels. Studies have even shown that maintaining healthy physiological levels of pregnenolone, and thus also DHEA, can reduce the risk of vascular heart disease by half.

Steroid Hormones Support Heart Health

Furthermore, studies have shown that steroid hormones such as aldosterone also support cardiovascular health by maintaining healthy blood pressure and adequate water and salt balance. However, care should be taken to avoid overproduction, which can lead to hypertension. Cortisol also plays a role in blood pressure and also affects water and electrolyte balance.

Medical Studies on Pregnenolone – Cardiovascular System

Plasma dehydroepiandrosterone sulfate and cardiovascular disease risk in older men and women

2020-12 Jia X, Sun C, Tang O, Gorlov I, Nambi V, Virani SS, Villareal DT, Taffet GE, Yu B, Bressler J, Boerwinkle E, Windham BG, de Lemos JA, Matsushita K, Selvin E, Michos ED, Hoogeveen RC, Ballantyne CM

Lower dehydroepiandrosterone-sulfate (DHEA-S) levels have been inconsistently associated with coronary heart disease (CHD) and mortality. Data are limited for heart failure (HF) and association between DHEA-S change and events.

Sexual dimorphism following in vitro ischemia in the response to neurosteroids and mechanisms of injury

2020-01 Altaee R, Gibson C

Cerebral ischemic stroke is a significant cause of morbidity and mortality. Sex differences exist following stroke in terms of incidence, symptoms, outcomes and response to some treatments. Importantly, molecular mechanisms of injury, activated following ischemia may differ between the sexes and if so may account, at least in part, for sex differences seen in treatment response.

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