2 years ago

378

The latest human study into NMN has looked into its effect on hypertension, but maybe more importantly its effect on inhibiting the NAD killer CD38.
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Hypertension represents a major public health issue that is responsible for 8.5 million deaths due to stroke, coronary artery disease and renal disease worldwide. Endothelial dysfunction and arterial stiffness are considered hallmarks of hypertension, and they play a central role in the development of atherosclerotic cardiovascular diseases. In hypertensive patients, alterations to NAD+ levels, and their relationship with blood pressure (BP) elevation, and vascular damage have not yet been studied. Combining human clinical trial research, cellular analysis, and mouse studies, researchers published, in the Journal Nature, that they have discovered a relationship between NAD+, hypertension, and the immune signal CD38.
This research begins with a discussion around NAD+ and its nature as a fundamental aspect of human metabolism. In particular, the authors home in on the immune factor CD38, which has been previously found to suppress NAD levels. Previous research has found that the NAD+ precursor nicotinamide riboside (NR) may have positive effects on arterial stiffness in people. However, these researchers decided to use a different precursor, that being nicotinamide mononucleotide (NMN), to determine if this particular NAD Booster would help in the treatment of hypertension.
First, the researchers examined 102 people, 52 of whom were healthy and 50 of whom were recently diagnosed with hypertension.
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