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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.
http://www.valint.net/php/rmalford
Dr.
med. Jochen Kubitschek , Wissenschaftsjournalist
LaHave
Media Services Limited
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