It has been demonstrated in numerous human and animal studies that audiogenic stress (AS) can induce elevation of arterial blood pressure and cardiac damage and that noise –induced hearing loss may be associated with alterations in magnesium (Mg) metabolism. Our laboratories, over a period of approximately 40 years, have been investigating why AS causes high blood pressure and cardiac damage. This review focuses on a number of newer discoveries on why AS causes dysfunctions of the cardiovascular system (CVS) This review discusses the pivotal physiological and biochemical importance of Mg to body health and the fact that most Americans and Europeans are deficient in daily Mg intake which perforce can cause severe dysfunctions of the CVS. Our ongoing studies clearly provide a solid microcirculatory basis for how and why AS above 65dB(A) often induces elevated blood pressure and cardiac damage. We review a body of data that points to the fact that AS does the latter, but appears to do so because noise stress levels result in Mg deficiency followed by release of certain sphingolipids (e.g., ceramides) and generation and release of platelet- activating factor (PDF). It is our opinion that all people exposed to high degrees of noise stress should be monitored for cardiovascular functions, ionized Mg levels, blood ceramide levels and levels of PDF. Lastly, we believe all people exposed to high levels of AS (i.e., maintenance people and pilots on aircraft carriers, musicians [particularly at rock concerts], motorman and conductors on trains and subways, construction site workers, etc.) should have at least the equivalent daily intake of 500-600 mg of Mg/day.
Altura, B. M., Gebrewold, A., Carella, A., Shah, N. C., & Altura, B. T. (2018). Exposure to High Levels of Noise Poses Hazards and Risks for Development of Hypertension and Heart Disease: Potential Roles of Unrecognized Ionized Hypomagnesemia and Release of Ceramides and Platelet-Activating Factor. American Research Journal of Cardiovascular Diseases, 2 (1). https://doi.org/10.21694/2575-7601.17005
Originally published in the American Research Journal of Cardiovascular Diseases, 2(1). The original material can be found here.
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