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What causes high blood pressure? At a recent New York Heart Association conference, the 850 or so experts gathered there had to admit that 95 out of 100 times they did not know. There have been more than 20,000 scientific articles in the last 60 years on the subject of "primary" or "essential" or "idiopathic" hypertension, differing widely as to diagnostic criteria, estimates of its prevalence in the general population, and guesses as to its cause and mortality rate. However, it seems quite clear that most manifestations of the disease are the consequences of, or are made worse by, the presence of raised pressure. Also, the higher the arterial pressure, whether systolic or diastolic or mean, the higher the morbidity and mortality. There is probably a fair proportion of cases in which glomerulonephritis (a kidney disease) in childhood was a causative factor. Also, same cases in the adult are due to a pheochromocytoma (an operable type of benign blood vessel tumor) and can be surgically corrected. Same cases follow the toxemia of pregnancy. Hypertension, as a disease, affects about 10 million people in the U.S. Its victims eventually develop organic complications that cut their life expectancy by approximately 20 years. Heredity is vital, since if one parent has it, at least one of a large family will eventually become hypertensive, while if both parents have it, most of their children will also eventually develop it. In 1964, Dr. Irvine Page wrote accurately that, "Among the diseases of the heart and circulation, only arteriosclerotic disease of the blood vessels exceeds hypertension as a cause of death." Since that time, during the past five years, the incidence of high blood pressure has been on the increase, yet the mortality rate due to this cause has slowly been falling. In the past 15 years deaths from hypertensive heart disease have decreased by from 50 to 55 per cent. It is no small accomplishment; and thanks for it are due almost exclusively to pharmaceutical research and the development of remarkably effective new anti-hypertensive agents. In fact, it is these blood-pressure reducing agents that have solved what used to be the trickiest problem in vitamin E treatment of heart disease. The kind of large dosage, 400 to 1,600 units, of alpha tocopherol that has been found most effective in the treatment of coronary thrombosis and myocardial infarction, will usually improve the tone of the heart muscle and so raise the blood in the patient with hypertension. Immediately after a heart attack this may not represent a significant problem since one effect of the attack is to sharply lower the pressure. But where there has been a history of high blood pressure, as occurs in a very large proportion of these cases, in time the pressure will rise once more, and the greater strength of the beat of the improved heart muscle produced by vitamin E will tend to raise the pressure still higher. Formerly, we were faced constantly with this dilemma. The patient with obvious evidence of coronary heart disease, with a definite hypertension, must have an adequate dosage of the drug. However, in many cases the blood pressure, already too high, would rise still higher. This problem has been neatly resolved by the development of the anti-hypertensive medications. Of the range of these that have become available, I have found chlorothiazide and its derivatives the most useful. Where they are contraindicated, as with existing or latent diabetes, we use the Rauwolfia group, and sometimes if the pressure is high enough and the situation sufficiently critical, we will use the two in combination. The quick reduction in pressure obtained by use of these drugs and the continuing ability to control pressure with them makes it possible to safely embark at once on a large dosage (from 400 to 1,600 units) of alpha tocopherol and secure a rapid beneficial effect on the heart and the coronary arteries. Ultimately, when sufficient recovery has been made, we will eliminate the hypertensive drugs and find that, in many cases, the blood pressure remains normal or nearly normal without them. The ability to suspend the use of these drugs instead of continuing them perpetually is no small advantage. It is well known to all doctors that not only these, but all antihypertensive drugs, can sometimes be accompanied by serious complications, particularly under conditions of prolonged use. One seemingly common result of using the thiazide derivatives is a build-up of uric acid in the system. The excess of uric acid in the blood - hyperuricemia - may be without serious consequences in some patients, while in others acute gouty arthritis, kidney stones, or even kidney collapse may ultimately result. While we are aware of these potential complications, experience has shown that these dangers are minimal in the patient on a large dose of alpha tocopherol. Although the thiazides do not cause any glucose build-up in the nondiabetic patient, where diabetes exists even as only a tendency or a latency, the thiazides may bring on hyperglycemia, a concentration of glucose in the blood above the normal limit. ln as much as the frequent urination brought on by diabetes is easily mistaken for the simple diuretic effect of the drug, it is entirely possible for the diabetes to advance to the stage of severe ketosis before the diabetic condition becomes apparent. Fortunately, stopping use of the drug will quickly eliminate any enhancement of blood glucose levels that the drug has caused, and the chief danger is that the condition may go too long unnoticed because frequent urination is expected from a diuretic. Of course, when there is frequent urination and a dehydrating effect for any reason, there is always the possibility of severe depletion of the electrolytes sodium, potassium, and chloride. While this is ordinarily prevented by dietary means, prevention or correction of such deficiencies can become extremely difficult in the presence of a kidney disorder. There are mental changes that reportedly occur in about 15 to 25 per cent of those treated with Rauwolfia derivatives. They have been few in our own experience, because we do not continue the medication that long. But for those who keep patients more or less permanently on Rauwolfia, there is a high incidence of severe and lasting depression, which strongly resembles involutional melancholia or the depressed phase of manic-depressive psychosis. On occasion, the depressive effect of the drug has led to attempted suicides. Other mental changes due to Rauwolfia include marked lethargy, frequent nightmares, and sometimes a tremor like that of Parkinsonism. It is a decided problem that it sometimes takes from three to six months after withdrawal of the Rauwolfia for the mental changes to disappear. Rauwolfia also poses a very difficult problem at times when the need for surgery may arise. Anesthesia and even minimal losses of blood in such patients result in a profound drop in blood sugar, a danger at any time and marked danger to the patient with coronary heart disease. Angina pectoris, acute myocardial infarction, acute pulmonary edema, and cerebral thrombosis have been reported as the result of such hypotensive episodes following the administration of anesthesia. The side effects of these very good and highly effective drugs make it highly desirable that their use be discontinued as soon as possible. Before the advent of these antihypertensive drugs, we made the disconcerting discovery that the larger dosages of alpha tocopherol would elevate the blood pressure in about one-third of the hypertensive patients, of ten to a marked and, of course, dangerous degree. However, it would neither lower nor raise the pressure in another one-third and thus not reduce the dangers implicit in the hypertensive, while it would lower the blood pressure, occasionally to normal, in the other one-third. Obviously, then, if the full use of the blood-pressure lowering effect of these new drugs is added to alpha tocopherol, it is possible in all cases to initiate adequate treatment at once and so obtain the full benefit of the alpha tocopherol. However, those cases in which the pressure would drop to a lower or normal level were hidden by the use of the antihypertensive drugs, as were also the middle third in whom the blood pressure had not been elevated. Therefore, when the desired clinical improvement has been obtained, the cautious decrease in the dosage of the antihypertensive drugs will reveal the fact that they are no longer necessary in approximately two-thirds of the hypertensives treated. Where there is no emergency or the hypertensive drugs are contraindicated, it is possible to revert to a technique that we used to use before the advent of chlorothiazide and its companion drugs. it was based on the observation that small doses of alpha tocopherol will relieve spasms in the arteries and, by reducing the peripheral resistance in doing so, may lower an elevated blood pressure. We thus aimed at obtaining this effect first before increasing the dosage to the larger therapeutic levels that would benefit the heart itself. In this method, the initial dosage of alpha tocopherol is no more than 90 international units a day and, perhaps, even less for a period of one month. For the second month, the dosage is raised only slightly to 120 international units, succeeded by 150 units in the third month. Subsequent increases are handled very carefully until adequate therapeutic levels are reached. With this routine, many patients responded beautifully by a lowering of pressure, which did not become elevated again when therapeutic levels were reached. The treatment is obviously not as satisfactory as that which utilizes the hypertensive drugs, but there are cases in which the drugs would simply be too dangerous to use. In such a case, it is well worth trying. Results can be and have been very good at times.