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Postby doogles on July 24th, 2020, 7:43 pm 

This topic should be of interest to most people because of the widespread incidence of hypertension and its association with aging.


Progress in understanding the aetiology of benign essential hypertension appears to be at a standstill. Until the 1930s, and currently, the general consensus in medicine was, and still is, that benign essential hypertension is a primary disease entity of unknown cause, but probably of cardiac or vascular origin. It is regarded as a main risk factor for atherosclerosis and therefore of many end-organ degenerative diseases.

During the 1930s to the 1950s, when much research was conducted, one minority school of thought, dominated by the work of Moritz and Oldt, and by Harry Goldblatt, strongly suggested that renal ischaemia was the cause. In short, atherosclerosis of the main renal artery, and/or intrarenal arteriolosclerosis, resulted in the production of renin. This renin produced generalised vascular smooth muscle constriction via a further chain of biochemical processes, which in turn resulted in higher blood pressure. A majority of papers at that time questioned the minority renal arteriolosclerosis/ischaemia hypothesis, with the result that the older hypothesis appears to have maintained sway to this day.

My personal research and experience with vitamin K and atherosclerosis suggests that the minority opinion of the 1930s to 50s may be the better hypothesis. A number of the majority of contrarian papers of that era are critiqued in an Appendix.

No experimental evidence has been located indicating that hypertension does any harm in its own right, but several papers dated from 1998 have been cited to establish that the medical world currently regards it as a cause of other conditions in spite of the lack of such evidence. On the contrary, one study is available to indicate that it is not a cause of atherosclerosis.

The notion that hypertension causes end organ damage seems to have gained support by the number of papers associating lower mortality rates and end-organ conditions with the use of hypotensive pharmaceuticals. But several recent reviews suggest that there is high quality evidence that thiazide diuretics, acting as a symptomatic treatment, may be the main effective therapy, with low to moderate quality evidence that hypotensive pharmaceuticals are effective. One extensive 2-year study on elderly people actually suggests that the successful control of hypertension did more harm than good in that there were 4 times as many deaths during the period of study and twice as many cardiovascular events.

In line with the 1930s to 1950s minority opinion that atherosclerosis of renal arteries or intra-renal arterioles is associated with hypertension, a number of studies have been cited suggesting that low vitamin K status (the cause of atherosclerosis) is associated with chronic kidney disease.

In view of the evidence presented in the attachment, the aetio-pathogenesis and management of hypertension may need a re-think.
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