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Essential Hypertension

In the USA, an estimated one-in-four adults has hypertension. Of those 50 million Americans, 32 percent are unaware they have it, 26 percent are on medication but do not have their blood pressure under control, and 15 percent are not on medication. Essential hypertension is the common type of hypertension causing raised blood pressure. People with raised blood pressure are at a greater risk of coronary heart condition, heart failure, kidney failure, stroke and loss of vision. Raised blood pressure, probably from damaged organs, was known to the Chinese 4000 years ago but the cause of essential hypertension has remained unknown until now. Essential hypertension remains the greatest killer condition of advanced societies.

It is accepted that, in advanced societies, blood pressure rises with age. There are a wide variety of antihypertensive drugs designed to modify blood chemistry, and to interrupt or stimulate the otherwise normally regulated systems of the body. The whole current approach to the treatment of essential hypertension is based on the belief that its cause arises somewhere within the cardiovascular system. There is no evidence for this belief.

On the miliaria page we saw that blockage of sweat ducts causes skin inflammatory conditions. Where this blockage occurs near the surface of the skin the condition is called miliaria crystallina and if the blockage is a little deeper the condition is called miliaria rubra. These conditions are visible and irritating.

When the blockage of the sweat duct occurs in the lower skin, where the sweat leaves the gland and first enters the duct, the condition is called miliaria profunda. In this condition the duct rupture and dermal inflammation is not felt or seen, and goes unnoticed. In the area of the lower dermis where this inflammation occurs are numerous skin capilliary loops, thirty for each square millimetre of skin. These loops, with walls only one cell in thickness, connect many of the body arteries to the veins, and transfer oxygen and nutrients to the skin.

As the sweat liquid flows under pressure from the ruptured sweat ducts these fragile capillary loops are destroyed. Some of the connections between the arteries and the veins are lost and thus the blood pressure rises. This is the cause of essential hypertension. It is a skin condition.

Sweat duct blockage is progressive. As some ducts are blocked, failing to moisturise and cool the immediate surrounding skin, the speed of sweat output is increased in nearby glands. Thus the ducts of these glands become blocked, and so blood pressure continues to rise over long period of time. Recent research shows that loss of blood capillaries, known as rarefaction, starts at age twenty and that by age seventy as much as forty per cent of the capillaries may be lost.

As we have seen, in the absence of sufficient exercise or regular exposure to heat, the sweat glands go into adverse habituation and become blocked. The sweat glands which are least likely to be regularly stimulated are those of the lower legs. When we do output copious sweat, we do so from the head and upper back first, and then progressively further down, arising from our evolution under the African sun. The effect of sweat duct blockage in the lower legs, such as thread veins and pooling fluid, can be seen in many elderly people and even in some people of teenage years.

So in order to reverse esssential hypertension, and stop the other effects of sweat duct blockage, we have to treat the miliaria profunda. We can do this by signalling to the body that there are sufficient electrolytes (mostly chlorides) in the environment of the body. If we do this then the sweat ducts (Havards) will stop conserving electrolytes and the sweat anti-microbial peptides will prevent the entry of microbes, unblocking the duct.

We have to bring electrolytes into the environment of the body but not into the body. We can do this with ActiveSignalTM products, a new invention by Warren Ward, the first person to describe the true aetiology of essential hypertension. ActiveSignalTM products are carefully designed for smart cell signalling only and, unlike all other medicines, are not absorbed into the body. Also since they are required to signal against adverse habituation, the body must not become habituated to their use and thus ignore the signal. Fortunately, ActiveSignal products are very fast acting, and, since they are not absorbed and also have a consistent predictable action, they have no side effects. The first commercial ActiveSignal product is the very successful Equiwinner patch which reverses hypertension in horses. ActiveSignal products for humans are now under development.

ActiveSignalTM is very effective against essential hypertension and will return blood pressure to an optimum level after about two weeks.

This is not quite the complete story of essential hypertension. With ActiveSignalTM we can signal the body to stop conserving electrolytes from the sweat ducts. However the body may still have insufficient electrolytes in circulation, and so still continue to conserve electrolyte.

As we have said, the body defends osmolality above all else. Osmolality of the circulating blood is continually adjusted by the addition and subtraction of electrolyte, mostly sodium. Many substances contribute to serum osmolality such as haemoglobin, lipids and glucose. Many in advanced societies have become accustomed to a diet high in carbohydrate, including sugar. This diet gradually pushes up the level of glucose in the blood, which increases osmolality.

Even a slight increase in blood glucose levels (hyperglycaemia) causes a deficiency in sodium (hyponatremia) as the body subtracts sodium to adjust osmolality for the increased glucose. Thus in order to entirely prevent miliaria profunda, and thus essential hypertension, it is desirable to restore normal blood glucose. This may be achieved by a low carbohydrate diet and exercise, or, if necessary, the same drugs as are used against diabetes.

Many people do have raised blood glucose and thus are at risk of hypertension. Many studies have been done on the effect of alcohol on hypertension, often trying to find elusive beneficial substances in the drink. Now let us trace what happens to blood pressure when an individual intakes a little alcohol but not sugar, as with red wine or neat spirits. If the subject has slight hyperglycaemia, adding alcohol to serum lowers osmolality, and so additional electrolyte is added to serum by the body to correct the osmolality. The body senses it is replete with electrolyte, the sweat ducts unblock, the capillaries regenerate and blood pressure falls to normal.

Now let us suppose the subject continues to intake alcohol. Osmolality will fall further, and so more electrolyte is added to serum by the body. The sweat glands extract sweat directly from serum. As a higher level of alcohol in serum is reached the sweat will contain too much sodium, above the range of salinity for the effectiveness of the anti-microbial peptides. The sweat ducts block again and the destruction of the capilliaries causes the blood pressure to rise.

So a little alcohol confers a temporary benefit, but excess alcohol brings with it the disadvantage of hypertension until the excess alcohol is eliminated from circulation.

Even when serum electrolyte is normal, the body may still detect insufficient sodium because there is insufficient volume of serum. There are several factors related to serum volume. Certainly the expansion of blood vessels during heat or exercise helps to maintain volume, as does sufficient oestrogen. A common cause of loss of volume is vasoconstriction, the restriction of flow in the peripheral arteries. Vasoactive intestinal peptide (VIP) is an important mediator of vasodilation, as well as having many other functions in connection with the health of epithelial surfaces. However VIP has another function. Where persons eat a diet which is relatively low in protein over an extended period of time the stomach habituates to producing less acid for digestion. VIP mediates stomach acid production in a paracrine fashion, in other words less acid means less VIP is produced, and so vasoconstriction continues. Supplying additional acid to the stomach, such as unsweetened grapefruit or cranberry juice, restores the output of VIP. Loss of volume is unlikely to be a problem for persons on a low carbohydrate diet who are consuming relatively more protein.

During pregnancy even a slight rise in blood glucose can cause problems. As the pregnancy proceeds serum volume increases under the influence of oestrogen, thus the serum electrolyte level is maintained sufficiently to prevent the sweat ducts from conserving sodium and blocking. Thus the rise in volume can disguise the rise in blood glucose.

Later in the pregnancy the increase in volume slows, but if the blood glucose release set point of the liver is now habituated at a higher level, the body detects insufficient sodium, many sweat ducts are blocked as a result, and blood pressure can rise very suddenly. This is the aetiology of pregnancy hypertension. It is clearly very necessary to monitor and control blood glucose from the start of the pregnancy. This is not usually done.



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