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Below, you will find the etiology and treatment for essential hypertension. It is very simple and most of the medications used today are contraindicated.

At 75, my BP is normal and I have no cholesterol in any arteries.
The full story can be found at the web site listed below.

R. M. Alford, MD

Essential Hypertension

What is hypertension?

Hypertension results from the induced constriction of the smaller arteries (arterioles) to produce an adequate circulatory/perfusion pressure for the kidneys.

What is its cause?

It is well established that exercise is beneficial for those patients having
hypertension, but to date no logical explanation has been ascribed. There are those that theorize that it is due to an adding to the tone of the
circulatory system. The beneficial component of exercise is the heat
generated which opens the peripheral capillary bed for heat diffusion, as is evidenced by the flushing that occurs in most people when they exercise. If heat production is the beneficial factor, there then logically has to be some degree of hypothermia/coldness present in the hypertensive patient, nature's most potent contractor of the peripheral circulation. Hypothermia in such cases is essentially always secondary to a decrease in the metabolic rate with its accompanying deficiency of heat production. As a corollary, has there ever been a reported case of comparable vascular diversion in a hyperthyroid patient?

What is the mechanism of hypertension?

As noted above, the core organs are designed to function optimally at a very narrow temperature range. When the temperature control center in the hypothalamus senses there is core hypothermia, the brain, being a part of the core, signals the shunting of the warmer arterial blood, in relative amounts directly back to the core via peripheral arterio-venous shunts, glomus bodies. (In the automobile there is no circulation of the engine coolant through the radiator until the engine warms to that critical point that opens the thermostat.) So it is in the human organism. The peripheral circulation will not open optimally until the core temperature rises to that optimal temperature that signals the heat control center to close the appropriate number of shunts. (All shunts are closed only when there is hyperthermia.) With the peripheral shunting there is a commensurate drop in blood pressure. With the steady decline in the metabolic rate that occurs as a part of the aging process in the hypothyroid individual, there is increased shunting with a continuing fall in blood pressure. (In over forty year of practice, this phenomenon was most prominently evidenced in the ectomorphic female, which, in itself, is a cardinal indication of hypothyroidism.) When the fall in blood pressure reaches the critical point at which the renal/kidney perfusion pressure is compromised, angiotensin is secreted to relatively constrict arterioles to raise the renal perfusion pressure. Thus is the evolution of hypertension.

Relative to the function of the glomus bodies, there is as yet discussion as to how are they controlled. Does the temperature control center communicate with them through a central connection or chemically? In the early stages of shunting, their presence is evidenced by mottling of the skin, primarily on the extremities, each blotch delineating the capillary distribution of one glomus body. The mottling shifts as the glomus bodies open and close, probably a result of the relative anoxia produced in the open shunt's capillary segment. By the time angiotensin enters the picture to any great degree, there is essentially a permanent state of shunting of all segments resulting in the pallor such patients evidence, producing a relatively constant state of anoxia of the skin.

Why are most of the presently used antihypertensive medications
contraindicated?

The medications used today in the treatment of hypertension are mainly aimed at reducing the arteriolar constrictive effect of angiotensin, that
protector of the renal perfusion pressure. This is especially true of the
Angiotensin Converting Enzyme (ACE) inhibitors and to a lesser extent with the calcium blockers and other antihypertensive medications. Any
medication that lowers the blood pressure and, in so doing compromises the renal perfusion pressure, is contraindicated. They are especially contraindicated when there is already compromised renal function secondary  to arteriosclerosis. In those patients having arteriosclerotic renal impairment, renal failure will progress even more rapidly.

Conclusion.

Thus, the most effective way in which to reverse the entire process, as
outlined above, is to increase the total body temperature to that
thermostatic level that ends peripheral shunting. With the early diagnosis and treatment of hypothyroidism, hypertension can be prevented and in its early stages effect a cure. Once atherosclerosis has begun, the rate of improvement is dependent on the stage to which it has progressed. When yet in the cholesterol phase, the cholesterol will be reabsorbed over time. If calcification has already occurred, improvement is less assured, but raising the core temperature can be beneficial with its enhancement of revascularization and development of collateral channels.

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