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Hypertension - Nutritional Treatments for Hypertension
Nutritional Treatments for
Hypertension
Eric R. Braverman, M.D. and Ed Weissberg,
B.A.
Journal of Orthomolecular Medicine Vol 7, Number 4, 1992.
Introduction
Over the last 15 years, medicine has gone through a
revolutionary change. The medical dictum was that nutrition and lifestyle made
no contribution to chronic disease. Medicine has done a complete turnaround and
has started a war against bad lifestyle habits like smoking, fat consumption,
sedentary Behavior, etc. Modem medicine has accepted its responsibility to
direct the lifestyles of people toward health. Possibly no movement other than
orthomolecular medicine was shouting like a voice in the wilderness before the
rest of the profession identified the important role of nutrition. Although
orthomolecular physicians and scientists first touted the important role of
nutrition in mental health, mental health is actually now known to be the
foundation for all health. Indirectly, and often directly, orthomolecular
physicians and scientists have heralded the way for the complete nutrition
revolution in the United States. This nutritional revolution is most evident in
the transformation of the American doctor's treatment of hypertension. More than
any other illness, it is now accepted by mainstream medicine that nutritional
and dietary factors and therapies should be utilized by physicians in treating
hypertension. It is fitting, therefore, to bring this review to the readership
which helped begin the revolution that is now transforming all aspects of
American health.
Epidemiology
Hypertension is clinically
defined as systolic blood pressure greater than 140 mmHg and/or diastolic blood
pressure greater than 90 mmHg. It is a leading problem in the United States,
where nearly 20 percent of Americans are affected by this disease (Kaplan, 1984;
McCarron, 1984). More than ten million Americans are being treated for this
disease at a cost of over 2.5 billion dollars, the largest medical expenditure
for a single disease in the United States (Chobanian, 1986).
High blood
pressure afflicts over 60 million Americans and contributes to one million
deaths per year in the United States, adding 18 billion dollars per year to
United States health expenditures (Lavash, 1987). Genetic, psychological, and
environmental factors play a role in hypertension. In 1975, over half (54
percent) of all United States deaths were from cardiovascular disease.
Hypertension is the most significant and preventable contributing factor
(Froehlich, 1986). Hypertension is associated with an increased risk of heart
failure, kidney failure, and stroke. It is virtually an epidemic in the black
population (Check, 1980; Harburg et al., 1982; Schachter et al., 1984; Tyroller
and James, 1978). About 1/3 of blacks between 18 and 49 have hypertension and
2/3 over 50 have hypertension. However, the ratio of black to white
hypertensives is decreasing, probably due to the better treatment of high blood
pressure in blacks than in whites. American blacks are twice as likely to suffer
from kidney failure, and have the world's second highest incidence of stroke,
behind the Japanese (Williams, 1986; Check, 1986).
A study in Rochester,
Minnesota showed that controlling hypertension led to a decrease in the
incidence of stroke (Ganarrax and Whishant, 1957), In addition to increasing
incidence of stroke, high blood pressure appears as a contributing factor in
some cancer deaths as well (Journal of National Cancer Institute 77:1-63, 1986).
Vigorous treatment of elevated blood pressure reduces strokes (Daughtery, et
al., 1986). Another complication of hypertension in the portal system is that it
impairs nutrient absorption from the diet (Sarteh, et al, 1986). Hypertension is
also an increasing problem among children, possibly due to dietary factors, such
as high fat and refined carbohydrate consumption (Doheny, 1986). Hypertension
has been correlated to a diet high in calories, sodium, sodium/potassium ratio,
alcohol, low in protein, calcium, magnesium, micronutrients, and vitamins.
Hypertension increases with age and occurs more frequently in men. A study done
in Tel Aviv, Israel showed that 67 percent of the elderly population had some
degree of hypertension (Golan, et al., 1986). Women who get pregnant at a later
age (3 5 or over) have increased complications, especially essential
hypertension (Weisley, 1983). Paradoxically, one study supports the conjecture
that elevated systolic and/or diastolic blood pressure in the aged composes a
risk reduction factor (Burch, 1983).
Five percent of all hypertension has
been classified as "secondary", that is, associated with some other disease
(usually renal or adrenocortical tumor) (Chobanian, 1982). Ninety-five percent
of hypertension is classifed as "essential" hypertension, primarily related to
stress, nutrition and other lifestyle Iike factors (Chobanian, 1982; Davidman
and Opsahl, 1984). Most hypertension cases are probably due to arteriosclerosis.
Patients with sustained hypertension show increased peripheral resistance. This
is possibly due to a decrease in the number of arterioles and increased
viscosity. The physician should treat only after making an acceptable
benefit/risk ratio, and then involve the patient in his/her treatment (Bass,
1987).
Atherosclerosis formation is a very complex problem and may be
related to an intracellular deficiency in essential fatty acids. One study
suggests that them are four categories of hypertensive patients, each with a
different pathophysiology and pharmacological profile: The young patient often
has an increased cardiac output, the middle age patient's total peripheral
resistance is elevated, and the elderly patient's total peripheral resistance is
even further increased while their intravascular volume is contracted. Obese and
black patients have elevated total blood volume and cardiac output (Messerli,
1987).
Treatment
Our paper is devoted to the nutritional
treatment of essential hypertension. This is a very successful program and
should be the first approach to hypertension. A whole array of symptoms and
effects manifest themselves with the usage of standard hypertensive
pharmacological therapy (Curb, et al., 1986). Any regimen for hypertension may
have detrimental effects on the cerebral functioning of the aged (Middleton,
1984). Approximately 30-50 percent of elderly patients experience side effects
from antihypertensive therapy (Gifford, et al., 1986). Rapid treatment of
hypertension in the elderly can cause quick drops in blood pressure and possibly
lead to stroke (Jansen, et al., 1986). Antihypertensive drugs have been
postulated to be related to the genesis of acute, as well as chronic
pancreatitis (Weaver, 1987). Drug therapy for mild hypertension (systolic
140-150, diastolic 90100) will only help a small percentage of patients, and the
side effects may far outweigh the potential gain (Chobanian, 1986),
antihypertensive therapy should be matched to the underlying biochemical
problems. This would give more efficacious therapy than the standard stepped
care approach (Frohlick, 1987).
The financial cost of an antihypertensive
regimen should be considered for long-term patient compliance (Sahler, 1987).
Labartho (1986) further supports the use of nonpharmacological therapy in mild
hypertension while condemning drug use. The great many side effects of
antihypertensive medications for treating mild hypertension has caused many
cases of noncompliance and ineffective longterm therapy (Croog, et al., 1986).
It is becoming apparent that drug regimens for the treatment of hypertension
have become increasingly unsatisfactory to modem physicians. Even mild
hypertension poses risks in the long run and should be treated (Schoenlenger,
1986). This is where our nutritional and lifestyle program has a tremendous
input.
The Dangers of Drugs
Diuretics
There are
approximately five categories of drug treatments: diuretics, beta-blockers,
alpha blockers, angiotensin-2 inhibitors, and calcium channel blockers. The most
commonly used treatment is diuretics and continues to have a large variety of
side effects (Ames, et al., 1984; Reyes, et al., 1984; Morgan, et al., 1984;
Field and Lawrence, 1986; Weinberger, 1985; Kaplan, 1986). Patients who receive
diuretics as their sole therapy have an increased risk of mortality due to
myocardial infarction or sudden death (Morgan, et al., 1984). Diuretics deplete
magnesium and potassium (Reyes and Leary, 1984). Further support for early
plasma and urinary changes in potassium from diuretic treated patients comes
from the study of Papademetriou and colleagues. Potassium sparing diuretics can
cause serious hyperkalemia when administered, while hyponatremia can be a result
of thiazide diuretic therapy (Phan, 1986). Thiazide diuretic therapy in the
elderly leads to almost 50 percent of the patients displaying hypokalemia or
hypomagnesemia (Petri, et al., 19 86). Further support for intracellular
magnesium loss during diuretic therapy comes from Dyckner and Wester, 1983. They
demonstrate that 42 percent of patients with arterial hypertension had subnormal
levels of skeletal muscle magnesium. Potassium deficiency can usually be
corrected, but the loss of magnesium is rarely addressed. Red blood cell sodium
increased, the membrane sodium potassium ATPase activity decreased, and
potassium decreased when patients were studied who were receiving the diuretic
hydrochlorothiazide. Even at low doses, diuretics, like hydrochlorothiazide,
will have adverse effects on serum lipid levels but will not then produce
significant hypokalemia (Mokenney, et al., 1986). We have found decreased RBC
magnesium to be a common occurrence among patients using diuretics as well as
beta-blockers. Moreover, as Ames and Peacock (1984) have pointed out, serum
cholesterol as well as other serum lipids are increased during treatment with
diuretics. This includes triglycerides and LDL levels.
Diuretic drugs
prescribed for hypertension cause glucose intolerance and raise glycohemoglobin
concentrations as well as increase blood cholesterol and triglycerides. One
study showed that with up to one year of treatment with diuretics, plasma
cholesterol increased accordingly (Williams, 1986). The side effects of
diuretics are still disputed by some physicians (Freis, 1986). Hollifield
pointed out the problems of thiazide diuretics relative to potassium and
magnesium metabolism, and ventricular ectopy.
Beta-Blockers
The
second most commonly used therapy are beta-blockers. Beta-blockers have similar
side effects as diuretics. Weinberger has pointed out undesirable serum lipid
fractions in patients treated with beta blockers. At least 23 percent of all
patients using beta-blockers will develop a need for antidepressants (Avon,
1986). Moreover, they have negative inotropic effects which can cause an
increased risk of heart failure (Chobanian, 1982). Miettinen suggested that
patients on beta-blockers had an increased risk of coronary heart attacks, as
did patients on anticholesterol drugs or diuretics. Yet, Floras tried to argue
against the side effects of beta-blockers.
Beta-blockers, like most
antihypertensive drugs, can cause sexual dysfunction (Croog, at al., 1986),
Twenty-eight percent of patients on the beta-blocker timolol maleate experienced
adverse reactions which most commonly consisted of fatigue, dizziness, and
nausea. Lipid-soluble beta-blockers that cross the blood brain barrier have been
known to produce neurotoxic side effects as well as cold in the bodily
extremities (Thodani, 1983). Some evidence indicates that beta-blockers are more
effective in Caucasian than Negro hypertensives (Veiga and Taylor, 1986).
Longterm use of beta-blockers, more than two to three years, is probably
contraindicated for most patients,
Alpha
Blockers
Alpha-blockers such as Catapres have a significant amount of
side effects, notably hypotension, constipation, sedation, dry mouth, and
dizziness. I have not found them to be particularly helpful in long-term
treatment of hypertension.
Methyldopa and
Angiotension
Methyldopa, for instance, seems to lower work performance
and general well-being, as compared to other antihypertensive agents (Croog, et
al., 1986). In the same study, methyldopa was compared to Propranolol and
Captopril and rated worse in causing the following conditions: fatigue, sexual
disorder, headache, neck pressure, insomnia, and nightmares. Up to 50 percent of
patients on one of these three drugs experienced fatigue or lethargy; up to 30
percent bad some form of sexual disorder; and over 10 percent had sleep
disorder, nightmares, headaches, anxiety, irritability, palpitation, dry mouth,
dizziness, nausea, and muscle cramps (Croog, et al., 1986). Captopril, an
angiotensin inhibitor, is one of the safer drugs for hypertension, wherein it
does not affect a patient's glucose tolerance (Shinodin, 1987). Nevertheless,
angiotensin inhibitors seem to affect trace elements significantly. Selenium and
zinc are decreased and copper increased, which may be a problem in the
psychologically sensitive (Braverman and Pfeiffer, 1982). Calcium channel
blockers are seen to be more efficient and give fewer side effects as compared
to the traditional hypertension therapy of diuretics and/ or beta-blockers
(Tarazi and Tarazi, 1986).
Vasodilators
Vasodilators like
nitrates are frequently accompanied by headaches. Nitrates have been used for
the treatment of angina pectoris and congestive heart failure, but have not been
systematically studied for efficacy for clinical usage in hypertension (Simon,
et al., 1986). Drugs like Hydralazine also produce depression in 10 to 15
percent of the patients taking it. Dopamine-metabolite inhibitors (i.e.,
Methyldopa orAidomet) are frequently linked with depression and other negative
side effects. Hence, we have found virtually all drug regimens have side effects
significant enough to warrant searching for other modalities.
It has
become evident from articles in The New Scientist that treating hypertension
with drugs is not cost effective given the current efficacy of drug regimens
(Lesser, 1985; Kaplan, 1985). As Dr. Grimm and McAlister (1983) suggest, the
treatment of mild hypertension may not be beneficial. Mild hypertensive patients
have a diastolic blood pressure between90 and 104. Over the age of 80, there
seems to be little benefit from treating hypertension (Amery, et al., 1986). It
appears that once drug regimens are opted for, drug therapies will spiral.
However, the Framingham study indicates that a certain small percentage of
formerly treated hypertensives maintain normal blood pressure when treatment is
stopped. After abrupt withdrawal from antihypertensives, blood pressure usually
rebounds (Greenberg, 1986). The need for drugs continues to increase. This is
why a suitable nutritional program is necessary. Ironically, it has come from
places like the Annals of Internal Medicine and the AMA News to suggest that
dietary changes and not drugs are the best option (Kaplan, 1985; AMA News,
1986). The focus of treatment in hypertension should move towards elimination of
pharmacological side effects and reduction of risk factors for coronary heart
disease (Weinberger, 1987). A recent article in JAMA (1987) states that
"Nutritional therapy may substitute for drugs in a sizeable portion of
hypertensives, and if drugs are still needed it can lessen some unwanted
biochemical effects of drug treatment," A study in Finland where people
restructured their diet found that the mortality from coronary heart disease
decreased up to 49 percent in some segments of the population. In hypertensive
therapy, more than any other aspect of medicine, the role of dietary factors has
entered into orthodox medical thinking.
Lifestyle, Obesity, and
Dietary Considerations
Numerous lifestyle factors have been identified in
hypertension by McCarron and colleagues. A study in New York City, where school
children maintained ideal weight, decreased total and saturated fat,
cholesterol, and sodium while increasing consumption of complex carbohydrates
and fibers, showed improved blood pressure, plasma cholesterol, body mass index,
and overall cardiovascular fitness, Even men with a genetic history of familial
hypercholestemia can greatly reduce cardiovascular risks by eating a low fat
diet, doing regular aerobic exercise, strict avoidance of cigarettes, and
monitoring blood pressure and blood cholesterol (Williams, et al.,
1986),
The sympathetic nervous system, which is activated by stress,
isometrics, etc., plays an important role in creating hypertension (Tuck, 1986).
It has become increasingly clear that lifestyle changes can reduce excess
catecholamine levels, which are potentially harmful chemicals when
inappropriately distributed in the body and increase under stress (Eliasson, et
al., 1984; Maus, 1984). Nicotine from cigarette smoking causes small arterioles
to constrict, blocks the useful effects of antihypertensive medicines, and is
associated with malignant hypertension. A reduction of blood pressure was found
with exercise when hypertensive rats were given the opportunity to do so
(Fregly, 1984). A cold environment might correlate with higher blood pressure
levels. Differences between winter and summer blood pressure may be predictive
of future hypertension (Tanaka, 1989). There is some evidence that the roots of
hypertension are found in early childhood and preventive attention should begin
as early as adult blood pressures are achieved.
Obesity is the number one
lifestyle factor related to hypertension and probably overall health and
longevity. Therefore weight loss is an essential part of a high blood pressure
regimen (Garrison, et al., 1987). We do not, however, recommend appetite
suppressants. One of these, phenylpropanolamine, can induce significant
hypertension. Obesity is a major cardiovascular risk factor having a very
complex socioeconomic, cross-cultural interrelationship with various other risk
factors. One study established that long-term changes in blood Pressure
correlate with decreases in body weight (Dornfeld, at al., 1985). Hypertension
has been shown to be directly proportional to obesity and glucose intolerance.
In a study with Urban Bantus of Zaire, body weight and age were the major
predictors of systolic and diastolic blood pressure (M'Buyamba-Kabangu, et al.,
1986), There is a wide variability of blood pressures among black people in
Africa suggesting that factors other than race play a role. A simple genetic
explanation for the blood pres. sure differences between blacks and whites is
inadequate and socioeconomic issues must be considered (Anderson, 1989). Diet
and exercise such as walking, swimming, and biking have beneficial effects on
blood lipid levels. We always encourage our patients to exercise, if capable,
usually after an EKG, 24-hour blood pressure monitor, and echocardiogram have
been done, and, in some cases, after a stress Thallium test. Exercise has been
shown not to depress appetite but rather help to control it and is almost
essential in a weight loss plan for hypertension, Simple exercise such as
walking or swimming can add years to one's life. In a study where energy
expenditure per week approached 3500 calories, morbidity (illness) also
decreased significantly.
Seventh Day Adventist lactovegetarians were
compared with omnivorous Mormons theoretically matching groups for effects of
religiosity and abstention from alcohol, tobacco, and caffeine). The
lactovegetarians ad lower blood pressure, even after adjusting a for the effects
of weight. "Long-term adherence not to a vegetarian diet is associated with less
of a rise of blood pressure with age and a increased prevalence of hypertension.
Speciific mechanisms and nutrients involved have not been clarified." (Beillin,
Armstrong,Marqetts,Rouse, Vandongen, 1986).
Psychological emotional, and
environmental factors play a large role in cardiovascular disease, and this
knowledge can be used to complement treatment regimens. Psychosocial and
behavioral modification techniques are safe and somewhat effective in
hypertension therapy. Feedback monitoring of blood pressure at intervals of
several weeks was shown to be as effective as relaxation and biofeedback.
Cranial electrotherapy stimulation (CES) a stress and anxiety reduction
technique also probably liver, blood pressure. An Australian study showed that
after adjustment for different variables, the level of education was inversely
related to blood pressure levels. Learning and education correlates with better
lifestyle and lower blood pressure.
Serum cholesterol correlates very
closely to blood pressure levels and helps to identify the segment of the
population in need of treatment. Elevated serum cholesterol (above 240 mg/dl) is
the single, most important risk factor in coronary heart disease. In a study
with more than 360,000 men, cardiovascular mortality rises steadily with
increasing strum cholesterol levels (718 mg/dI). Aggressive dietary
modifications are very useful to lower blood cholesterol levels which are linked
to atherosclerotic vascular disease and coronary artery disease. Elevated serum
and arterial cholesterol is a major entity in hypertension and cholesterol and
can be reduced by dietary fibers such as bran and pectin, The positive role of
fiber in reducing cholesterol is further supported by Fletcher and Rogers.
Dietary fibers contained in foods such as carrots and other vegetables lower
body cholesterol levels by binding bile salts, Dietary fiber has an important
moderating effect on serum cholesterol. Insoluble dietary fibers such as guar
gum and pectin have been shown to be hypocholesterolemic and
hypertriglyceridemic.
High quality fresh and whole food sources of oils
and animal products are important, Fatty acids (including polyunsaturated fats
and cholesterol are susceptible to degradation by oxidation and free radical
reactions. Studies on animals show the resultant "oxy-cholesterols" have
atherogenic properties. Powers of egg and mouldy cheeses (found in many fast
foods) are especially susceptible .
Serum cholesterol and changes in
serum cholesterol were correlated to consumption of fats. However, serum
cholesterol levels are not significantly related to dietary cholesterol in
conjunction with a diet rich in polyunsaturated fats. A very high cholesterol
intake by rural South African blacks caused no meaningful blood lipid
fluctuations. The cholesterol synthesis-inhibiting drug lovastatin may have the
side effect of promoting cataracts.
Egg intake coupled with a diet low in
other saturated fats, high in polyunsaturated fats does not significantly raise
blood cholesterol, Polyunsaturated fats can be used to lower total serum
cholesterol and to raise HDL level, and thus can help to prevent
atherosclerosis. Therefore, up to 7 eggs per week are permitted for most
hypertensive patients (unless they have an extremely elevated or refractory high
cholesterol level). In one study with renal patients, egg consumption did not
significantly increase cholesterol or triglyceride levels. No significant
correlation between egg consumption and serum cholesterol level was suggested by
Pfeiffer.
Animal studies suggest that sucrose (found in cane sugar and
some fruits and vegetables) has the effect of raising blood pressure, At high
levels of carbohydrate consumption (50 to 80 percent) increased blood pressure
is also noted (McDonald, 1987). Kannel pointed out that the dietary factors in
hypertension may relate to the excess calories of saturated fat intake as well
as high cholesterol and salt intake.
Fruits, vegetables, whole grains,
and low fat dairy items protect against hypertension. An epidemiological study
showed that one Chinese group with a history of hypertension had a high intake
of added salt to their milk and tea, and consumed little starchy food, fresh
fruits, and vegetables. Consumption of proteins, animal fats, disaccharides,
animal products, refined foods, and high daily energy content of food were
directly related to congestive heart disease (CHD) morbidity, arteriosclerosis,
myocardial infarction, and arteriosclerosis mortality, whereas consumption of
vegetable fats, starch, cellulose, hemicellulose, pectin, vegetables and fruit
shared an inverse correlation.
Hypertensive patients may have impaired
glucose tolerance, especially when treated with diuretics. Glucose tolerance
tests in hypertensive patients are frequently abnormal. A high carbohydrate
(sucrose) diet has been shown to induce sodium retention. Sucrose Or glucose can
mediate a sodium retention effect, and thus, through this retention of sodium,
raise systolic blood pressure. A diet high in sucrose will raise blood pressure
in animals significantly, possibly due to a relative decrease in potassium
intake. Glucose intolerance, obesity, and blood pressure are tightly
interrelated, so a derangement in one will cause problems in the
others.
Significant decreases in the consumption of calcium, potassium,
vitamin A, and vitamin C have been identified as nutritional factors that
distinguish hypertensive from normotensive subjects. Calcium intake was the most
consistent factor in hypertensive individuals. Previous reports showed a
significant negative correlation between water hardness and mortality rates. A
study comparing the twin Kansas cities in the United States showed the opposite
to hold true; hard-watered Kansas City, Kansas had more cardiovascular problems
including a ten-fold higher serum cadmium level. Coffee has been shown to
increase coronary heart disease risk by almost 250 percent. Smoking and
hypertension are the two main risk factors for ischemic heart disease.
Youngsters who smoke even less than one pack of cigarettes per day increase
blood cholesterol and triglycerides.
Harlan and others have suggested
that alcohol plays a role in hypertension. Moderate use of alcohol may lower
blood pressure, but excessive use may elevate it. At moderate levels of one
drink per day, alcohol has been shown in some cases to be protective against
coronary artery disease. Alcohol in large doses may lead to rhythmic
disturbances in the electrophysiology of the heart (Greenspan and Schaal, 1983).
Alcohol use may lead to depression and increase carbohydrate consumption which
will lead to hypertension.
In light of these findings, we recommend the
following dietary guideline to most of our hypertensive patients: low sodium,
low saturated fat, and low refined carbohydrate intake, with high vegetable
intake from the starch group, high salad and protein intake (particularly fish).
Fresh cheeses are emphasized above aged cheeses. Simple sugar, alcohol,
caffeine, nicotine, and refined carbohydrates should be reduced drastically or
eliminated.
Saturated Fat and Fish Oil
Numerous researchers
have suggested that saturated fats can raise blood pressure, while Singer and
colleagues (1985), Knapp et al. (1986), and Nestel (1985) have suggested the
potential blood pressure-lowering effect of fish oil. Polyunsaturated fats can
be used to lower total serum cholesterol and to raise HDL level, and thus can
help to prevent atherosclerosis. Dietary fat modifications, such as an increase
in polyunsaturated to saturated fat ratio and an overall decrease in percentage
of fat in the diet, lower blood pressure and have favourable effects on serum
lipid levels. Greenland and Icelandic eskimos, whose diet is rich in saturated
fats, have a much lower incidence of coronary heart disease than controls
because of high fish consumption. An inverse relationship was found with fish
consumption and twenty-year mortality from coronary heart disease, Those who
consumed 30 grams or more of fish per day had a 50 percent lower cardiac
mortality rate than those who did not. Fish oils (Omega 3 fatty acids) reduce
high levels of plasma lipids, lipoproteins, and apolipoproteins in patients with
hypertriglyceridemia. They also have effects on serum lipid levels in healthy
humans (Gehily, et al., 1983, Experimental Nutrition, 1986). Eicosapentaenoic
acid (EPA or fish oil) lowers abnormal blood lipid levels and decreases blood
viscosity, Fish oil, like niacin, raises HDL and reduces risk from heart disease
(Messim, et al., 1983). Atherosclerosis formation is a very complex problem and
may, be related to an intracellular deficiency in essential fatty acids. Halberg
(1983) suggests that dietary lipid controls may be even more important than salt
restriction in the control of hypertension.
Polyunsaturates and
Hypertension
Mogenson and Box (1982) and Puska and colleagues (1985) have
suggested that both linoleic acid and dihomogammolinolenic acid (found in
evening primrose oil) can be extremely useful in the treatment of hypertension.
Fish oil, rich especially in Omega 3 fatty acids, has been shown to lower blood
pressure, Increasing consumption of monounsaturated fat is beneficial in
lowering high blood pressure (Williams, et al., 1987). Dietary fat modification
is an essential part of the treatment of hypertension. Saturated fats have been
definitively linked to high serum cholesterol. Dietary supplementation with
Iinoleic acid, gamma linoleic acid, or other polyunsaturated fatty acids is of
use in controlling hypertension, These agents lower blood pressure and have both
a diuretic effect (particularly linoleic acid and gamma linolenic acid) and a
prostaglandin-E2 inhibitory effect. A diet with fish, which is high in EPA, for
example mackerel, has been shown to lower high blood pressure, serum,
triglycerides, cholesterol, LDL, and raise HDL. A diet high in linoleic acid
lessened a rise in blood pressure in Nephrectornized rats (Izumi, et al., 1986).
Calcium supplementation may lower elevated blood pressure by increasing
naturesis (sodium excretion) (Gilland, et al, 1987). Linolenic acid, a
polyunsaturate, is helpful in the treatment and prevention of hypertension
probably due to its conversion to prostaglandins and/or other vascular
regulators (Benz and Hirsch, 1986). Linoleic and linolenic acids are both
prostaglandin precursers and are useful in hypertension therapy (Adam,
1985).
Cis-linoleic acid is converted to gamma linoleic acid and
eventually to prostaglandin E which is a vasodilator and inhibitor of platelet
aggregation (Fletcher and Rogers, 1985). Smith and Dunn (1985) of Case Western
Reserve University in Cleveland did at least eight different studies where
safflower oil, linoleic acid, cod liver oil, and eicosapentaenoic acid all
lowered blood pressure significantly. Fish oils, especially the Omega-3 fatty
acids, have been shown to decrease risk of coronary heart disease. A diet high
in fish or fish oil supplementation is recommended in patients with increased
risk of coronary heart disease (Neutze and Starlins, 1986). In doses of up to
16.5 grams, fish oil has been shown to significantly lower blood pressure and
cardiovascular risk factors (Norris, et al., 1980) .
Omega 3 fatty acids
prevent elevated triglycerides induced by carbohydrates by blocking VLDL and
triglyceride metabolism (Harris, et al., 1984), Angina patients showed a lower
ration of EPA to AA (arachidonic acid) (Kords, et al., 1986). The authors of the
study consider this a new cardiovascular risk factor. Six grams of fish oil per
day lowered VLDL and raised HDL while greatly decreasing plasma triglycerides
and cholesterol. A
diet high in fish as compared to one high in cold cuts or
meat lowered serum cholesterol, blood pressure, and raised HDL (Atherosclerosis,
1986). Fatty acids, especially linoleic, oleic, and arachidonic acids, have been
shown to reduce angiotensin receptor affinity (Good, Friend, and Ball, 1986). An
olive oil-rich diet has been shown to decrease non-HDL cholesterol while leaving
triglyceride levels constant (Mesink and Katan, 1987). Eicosapentaenoic acid in
the form of cod liver oil I or mackerel a an excellent polyunsaturate and lowers
cardiovascular risk factors (Singer, 1986).
Hence, all our patients were
treated with eicosapentaenoic acid (fish oils - Omega 3), linoleic acid
(safflower oil) or gamma linolenic acid (primrose oil) or all three (Smith and
Dunn, 1985). Dietary fatty acid intake is of particular importance in relation
to blood pressure when weight reduction is occurring (Katz and Knittle, 1985),
as is the case with our patients.
Calcium
Numerous studies
suggest that calcium may have an important role in hypertension (Bloomfield, et
al, 1986; Belizan, or al., 1983; McCarron, 1984; Schleiffer, et al., 1984; The
Lancet, 1982). An oral calcium load has been shown to decrease systolic and
diastolic blood pressure, elevate PGE2, decrease PTH, decrease norepinephrine,
and decrease 1,25 dihydroxy-Vitamin D (Yoshikatsu, et al., 1986). Hypertensive
patients showed significant deficiencies in dietary calcium, potassium, vitamin
A, and vitamin C with calcium being the most consistent dietary risk factor for
hypertension (McCarron, et al., 1984). Preliminary reports show that oral
calcium supplements (I to 2 grams per day) lower blood pressure in some
patients, particularly in young adults, possibly more so in women (Belizan,
1983). However, manipulation of dietary calcium may not be very useful in older
women (Schramm, or al., 1986). Oral calcium carbonate administration also seems
to have an effect on mild hypertensives (Bloomfield, 1986). Calcium citrate is
probably the best therapy. In one study, calcium supplementation reduced blood
pressure in young adults (Belizan, et al., 1983). Calcium supplementation of up
to 1000 grams has been shown to lower blood pressure in mild to moderate
hypertension (McCarron and Morris, 1985). Furthermore, surveys have shown a
positive relationship between blood pressure and serum calcium levels. Acute
elevation of circulating calcium levels during elevation of blood pressure,
chronic hypercalcemia or hyperthyroidism, and vitamin D intoxication are all
associated with increased chronic hypertension (Sewers, at al., 1985), Calcium
supplementation may lower elevated blood pressure by increasing natriuresis
(sodium excretion) (Gilland, et al,, 1987). Calcium can partially alleviate high
blood pressure in the spontaneously hypertensive rat due to its renal
productions of dopamine, a probable natriuretic factor (Felsiceita et.al.,
1986). Three clinically paradoxical findings in the relationship of calcium and
hypertension arc as follows: calcium mediates vascular smooth muscle; calcium
channel blockers lower blood pressure; and increased calcium intake can also
relieve hypertension (McCarron, et al., 1987). A recent hypothesis says that
there is a circulating plasma factor which increases intracellular platelet
coagulation in hypertension. This factor may on coils and thus increase
peripheral vascular resistance (Lindrer, et al., 1987).
In contrast,
several studies have shown that calcium can be a factor in elevating
hypertension, Therefore, we use calcium sparingly except in the case of a woman
suspected of having osteoporosis or in cases of/in normal plasma, ionized
calcium or red blood cell calcium (Schleiffer, et al., 1984; Bloomfield, et al,
1986; Cappuccio, et al., 1985; Nutrition Reviews, 1984; Belizan, or at,, 1983;
Kesteloot and Beboers, 1982; Sica, or al., 1984; Staessen, or al., 1983;
Weinsier and Norris, 1985; McCarron, at al., 1985; Johnson, or al,, 1985; Stem,
at al., 1984),
Furthermore, Schedl (1984) pointed out the need for
vitamin D in blood pressure control. Sewers et al. (1985) also correlates
vitamin D and calcium intake with blood pressure among women. When we use
calcium supplements, we use them with vitamin
D.
Magnesium
Magnesium, in contrast to calcium, is well known
to lower blood pressure, and has been used in the treatment of hypertension in
pregnancy for a number of decades (Lee, at al., 1984; Dyckner and Wester, 1983).
Magnesium, calcium, phosphorous, potassium, fiber, vegetable proteins, starch,
vitamin C, and vitamin D showed an inverse relationship with blood pressure.
with magnesium's correlation being the strongest (Joffrres, et al., 1987).
Magnesium is a vasodilator, according to Wallach and Verch (1986), and can at
high levels cause low blood pressure (Fassler, or al., 1985). The use of various
nutritional substances as pharmacological agents for hypertension has produced
many success stories. Nevertheless, magnesium therapy has been instituted for
hypertension to combat a deficiency state often inflicted by diuretic usage
(Braverman, 1987). In a study with Finish ewes, hypomagnesium was correlated
with hypertension (Weaver, 1986). Magnesium deficiency may relate to high blood
pressure by increasing microcirculatory changes or microcirculatory
arteriosclerosis (Altura, et at., 1984). Intracellular free magnesium levels are
inversely linked to blood pressure independent of calcium metabolism (Resnick,
at al., 1986). Direct lowering of blood pressure with magnesium in patients with
high blood pressure has been demonstrated by Dyckner and Wester (1983).
Magnesium works like a calcium channel blocking drug (i.e.,Verapamil, Diltiazem)
(Iseri and French, 1984; Sjogren and Edvinson, 1985; Platonoff, at al., 1985;
Flodin, 1985). Altura and colleagues suggested that magnesium supplements have a
valuable effect on diabetic and hypertensive rats (Altura and Altura, 1984).
Magnesium's use has been documented in cardiac situations, such as digitalis
toxic arrhythimas due to magnesium depletion and myocardial infarctions due to
decreases in potassium (Rasmussan, or al,, 1986; Cohen and Kitzes, 1983;
Delhumea, or al,, 1985; Cassadonte, et al., 1985). Magnesium may be an important
prophylaxis in hypertensive patients prone to arrythmia. Untreated hypertensives
showed lower levels of intracellular free magnesium which strongly correlates to
systolic and diastolic blood pressure (Resnick, et al., 1984). Sempos and
colleagues (1983) found that hypertensive patients using diuretics had a
magnesium level of 1.79 mg to 100 ml compared to normotensive patients with 1.92
mg to 1OO ml, a significant difference. Magnesium is also low in blood
mononuclear cells in intensive cardiac patients (Ryzen, 1986). Some magnesium
deficiency was noted as well in a medical ICU unit in Los Angeles County (Ryzen,
1985). Furthermore, we have shown in seven patients a significant decrease in
red blood cell magnesium (see Table 1, page 239) as compared to the mean of
nomotensive individuals. Type A personalities have been shown to lose red blood
cell magnesium under stress and thus show a correlation to their behavioral
tendency to eventually develop hypertension, ischemic heart disease, and
coronary vasospasms (Henrotte and Plovin, 1985). Further support for magnesium's
use in hypertension treatment is documented by Wester and Dyckner (1985) who
claim that magnesium acts by vasodilation or by a sodium potassium ATPase
metabolism. Magnesium metabolism was abnormal in the spontaneously hypertensive
rat (Berthelot, et al,, 1985). Hypomagnesia in acute myocardial infarction
patients was probably due to magnesium's migration from a cellular to
intracellular space and not from renal losses (Rassmussen, at al., 1986).
Magnesium deficiency has been shown to be sometimes related to dietary habits
(Sheehan, et al., 1984). Hence, many of our patients receive magnesium. In
addition, many of our hypertensive patients tend to have constipation which is
relieved by magnesium,
Sulfur Amino Acids
A study by Ogawa and
colleagues (1985) suggested that decreases in plasma taurine and methionine were
significant in patients with essential hypertension. Decreases in plasma serine
and threonine were also significant although not therapeutically relevant.
Taurine may lower blood pressure. Further. more, all sulfur amino acids - in
methionine, cysteine, and taurine - Iower heavy metals which are often factors
in hypertension. In our study we found a trend toward decreases in plasma
cystine probably due to B6 deficiency. Further studies, Paasonen et. al. (1980)
suggested there may be an elevation in platelet taurine. Hence, most of our
patients with hypertension receive supplemental sulfur amino acid treatment,
Three grams of taurine daily could elevate blood taurine levels 2 to 3 times
normal (Braverman and Lamola, 1986), We considered this an appropriate level to
reach for hypertensives. Paradoxically, plasma
taurine was elevated in our
patients (see Table 2, page 239).
Sodium and Potassium
The role
of dietary sodium in hypertension is long-standing and well-known (Liegman,
1985). It has been suggested that the average person consumes 10 to 12 grams of
sodium, which should be reduced to 2300 mg per day (Tufts University Diet and
Nutrition Letter, 1985). This can be counterbalanced by increasing potassium
intake (Emaley, 1984), which may lower blood pressure. A higher ratio of
potassium to sodium has been shown to lower moderately high blood pressure.
Potassium therapy is useful in lowering blood pressure induced by
diuretic-induced hypercalcemia (Carnegie, et al., 1983). An inverse relationship
between serum potassium and blood pressure was shown by Loft, et al., 1985. High
potassium intake greatly reduced brain hemorrahages, infarctions, and death rate
in spontaneous hypertensive rats (Tobian, 1986). A high potassium intake may
help to alleviate high blood pressure, the leading risk factor for smokers
(Khaw, Bamet-Carment, 1987). Biochemical abnormalities, including hypokalemia
and alkalosis due to amnesia, have been correlated with vascular headaches for
hypertensive patients (Colen, 1986). Linolenic acid is the precursor for
prostaglandins and omega 3 fatty acids and has a profound effect on blood
pressure (The American Journal of Clinical Nutrition, 1986). The hazards of high
sodium intake are beyond hypertension and include gastric cancer. Dietary sodium
affects urinary calcium and potassium excretion in men with regular blood
pressure and differing calcium intakes (Castermiller, 1985). Anderson (1984)
suggested that stress and salt are cyclical, meaning increased salt intake
produces stress and craving salt is a sign of stress, Dietary sodium and copper
have long-term effects on elevating blood pressure in the Long-Evans group of
rats (Wu, et al., 1984). Decreased sodium intake can decrease stress
(Castenmiller, et al., 1985; Richards, et al., 1984; Vollmer, et al., 1984;
Karppanen, et al., 1984; Kaplan, et al., 1985; Mantes or al., 1985; Treasure, et
al., 1983; Voors, et al., 1983).Some essential hypertensives have a low sodium
to potassium and/or a high lithium to sodium counterpart. One study shows that
hypertension in spontaneous hypertensive rats is caused by a circulating
hypertensive agent produced by the kidneys and adrenals whose secretion can be
suppressed by volume or salt depletion (Spieker, et al., 1986). Hence, all of
our patients are asked to restrict sodium as completely as possible and use salt
substitute, We suggest to all our patients that they use high potassium salt
substitutes.
Trace Elements and Hypertension
Numerous studies
have suggested that elevations in serum copper can raise blood pressure. Excess
dietary copper can increase systolic blood pressure in rats, according to Wu and
colleagues (1984) and Liu and Medeiros (1986). Elevations in serum copper and
cadmium have been found in smokers, which may be the reason why they have
elevated blood pressure, according to Davidoff and colleagues (1978) and
Kromhout, et al. (1985). Serum copper was inversely related to HDL level
(Kromhout, et al., 1985). Contraceptive pill users have elevations in serum
copper and elevations in arterial pressure (Staessen, et al., 1984). Patients
who suffered from myocardial infarctions had decreased levels of zinc and iron
but increased nickel levels (Khan, et al., 1984). Hypertensive subjects that use
diuretics have significantly higher serum copper levels. Increased serum copper
has a role in primary or pulmonary hypertension (Ahmed and Sackner, 1985). Zinc
lowers serum copper and may actually lower blood pressure (Ahmed, Sackner,
1985), Higher dietary zinc intake has been associated with lower blood pressure
(Pfeiffer, 1975; Medeiros and Brown, 1983). Zinc is depleted by diuretics
(Olness, 1985). Increased red cell content of zinc in essential hypertension has
been found by Frithz and Tonquist (1979) and Henrotte, et al. (1985). Zinc is a
well-known antagonist of heavy metals such as cadmium and lead (Pfeiffer, 1977),
which even in chronic dosages has been found to elevate blood pressure. Hence,
all our hypertensive patients receive zinc to lower copper, lead, cadmium, and
manganese. Studies suggesting that sub-acute elevations in cadmium and lead have
a role in the elevation in blood pressure have been done by Statessen, et al.,
1984; Hulon, et al., 1985; Perry, et al., 1979; and the AMA News, 1985. Blood
lead levels, which are elevated in chronic alcoholism, have been correlated with
increases in blood pressure (Dally, et al., 1986). The correlation of blood lead
to blood pressure is stronger for systolic than diastolic blood pressure
(Kromhout, et al., 1985), An overabundance of lead can lead to a form of
hypertension with renal impairment (Batuman, oral., 1983), The lead content of
the ventricles and aorta of myocardial infarction victims was consistently
greater than for normal patients though not significant. Further evidence for a
relationship between blood lead levels and blood pressure is presented by
Prickle and colleagues (1985). Serum zinc levels were significantly lower for
older hypertensive women and older men with high systolic readings (Medeiros and
Pellum, 1984; Harlan, et al., 1985). Elevations of lead and cadmium with
decreases in zinc are a factor in many inner city patients with hypertension.
Plasma zinc levels were significantly lower in patients having coronary heart
disease risk factors (Kushliedaite, et al., 1994). Furthermore, it has been
shown by Pfeiffer (1977) that vitamin C in combination with zinc maybe an even
more effective way of reducing subacute levels of lead and cadmium. Hence,
manganese levels are directly correlated to LDL and inversely correlated to HDL
(Kushliedaite, et al., 1984), We have had every patient follow a treatment plan
which included zinc therapy. It is a consistent clinical observation to see
rises in blood pressure with as little as 20 mg of manganese per day. A group of
hypertensive females has been shown to have decreased intake of phosphorous,
potassium, and magnesium (Karanja, et al., 1987).
Vitamin B6 and
Hypertension
It has been established by Dakshinamurti, et al. ( 1986)
that pyridoxine deficiency has a role in hypertension. Vitamin B6 inhibits
platelet aggregations through its metabolite pyridoxal 5' phosphate (Fletcher
and Rogers, 1985). Pyridoxine deficiencies which can cause hypothalamus 5-Ht and
GABA deficiencies (neurotransmitter involved in blood pressure regulation) as
well as general increases in sympathetic stimulation can cause blood pressure to
become elevated (Paulos, et al., 1986). Besides being a co-factor for
transamination, vitamin B6 seems to relieve edema and swelling and thus has mild
diuretic properties. It is known that pyridoxine (vitamin B6) has diuretic
properties; therefore, all of our patients receive
pyridoxine.
Niacin
Niacin, possibly because of its flush or
vasodilating producing properties, can lower blood pressure as a vasodilator and
can raise HDL fraction which is frequently reduced in hypertensive patients.
Niacin administration is a very effective agent against an increased level of
LDL in patients with type 11 hyperlipoproteinemia. It also significantly raises
HDL levels (Hoeg, et al., 1984). Niacin has also been shown to reduce the
average numbers of lesions per subject and block new atheroma formation. Niacin,
when used alone or in conjunction with the drug colestipol, can effectively
lower cholesterol and triglyceride levels to the normal physiological range
(Journal of Lipid Research, 198 1). Niacin is used as an adjunct therapy in our
treatment.
Selenium
Serum selenium of patients with acute
myocardial infarction was determined to be low before this condition occurred
and not as a result (Oster, et al., 1986). Further evidence for serum selenium
levels and cardiovascular death correlation comes from the work of Virtamo and
colleagues (1985). Chromium concentrations in aortas of patients dying from
atherosclerotic disease am significantly lower as compared to a control group.
Low plasma chromium was found in patients with coronary artery and heart
diseases (Somonoff et al., 1984). Both selenium and chromium may have a role in
the nutritional control of hypertension, at least in the protection from
myocardial infarction during a difficult dietary
period.
Tryptophane
Tryptophane may have a role in hypertension
too. It has been established by Feltkamp and colleagues (1984) and Wolf and Duhn
(1984) that tryptophan in dosages of 3.5 g/day can lower blood
pressure.
Other Nutrients
Vitamin C stabilizes vascular walls
and helps metabolism of cholesterol into bile acids. When elderly patients
receive 3 grams of inositol, their total blood lipid and cholesterol levels
decreased (Leinguard and Moore, 1949).Garlic has been shown to be of great
benefit in hypertension therapy, raising HDL and lowering both the total
cholesterol and LDL. Garlic oil decreases platelet aggregation, serum
cholesterol, and mean blood pressure, while it raises HDL and red blood cell
arachidonic acid. Thus garlic has been shown to be an antiatherosclerotic,
anti-thrombotic, and an anti-hypertensive agent (Banie, et al., 1987). Vitamin E
lowers cholesterol and effects prostaglandin synthesis (Fletcher and Rogers,
1985), yet vitamin E, by clinical observation, raises blood pressure (Sharma et.
al., 1976; Keyes, 1980; Bordia et al, 1977). Melatonin, according to Birau and
colleagues (1981) and Kawashima and colleagues (1984) may have a role in
regulating hypertension. Manipulation of dietary calcium may not be very useful
in older women (Schramm, et al., 1986). CoQIO has been deficient in
approximately 40 percent of hypertensives and has a possibly beneficial effect
on hypertensive therapy (Cardiovascular Research Ltd., 1985). One study has
shown that nutritional and hormonal treatments can enhance the sodium potassium
ATPase activity level and in turn helps to prevent or treat essential
hypertension (McCarty, 1984). One study has shown estrogen given to
postmenopausal women reduces heart attack risk (Healthline, 1986). Alcohol
abuse, lead poisoning, birth control pills (estrogen), licorice
(glycyrrhinzicals), diseases of the kidney, adrenal or pituitary glands,
pregnancy, and pre-eclampsia are some common causes of hypertension (Laragh,
1987). Although there are some things written on progesterone by Rylance (1995),
melatonin by Birau and colleagues (1981), and atrial peptides by Cantin and
Genest (1986), as hypertensive agents their use is unclear. Patki, et al., 1990
once again demonstrated the benefits of potassium 60 mg. a day in lowering
arterial blood pressure, Total body potassium content may be more useful in
producing and utilizing potassium in hypertension treatment. Abu Hamdon et al.,
1987, suggested that side effects of drugs like Captopril and angiotension 2
blockers might be helped by the addition of zinc. Saito et al., 1988, suggested
the benefits of magnesium therapy. Boulos et al., 1988, suggests warnings about
calcium supplements being contaminated. Numerous studies suggest the benefits of
24-hour blood pressure monitoring (Weber et al., 1988). This is an extremely
important breakthrough in the management of hypertension.
Chronic lithium
administration, because of its reduction in stress and increased secretion of
sodium, may also benefit blood pressure according to file et al., 1988.
Kestaltloot et al., 1988, suggests that the relationship of sodium, potassium,
calcium, and magnesium is critical to normal blood pressure. Cootman et al.,
1990, suggests the benefits of dietary treatment in hypertension. J, David
Spence et al., 1990, suggests the effect of any stress reduction technique on
blood pressure. Numerous studies suggest the benefit of doing body composition
analysis in patients with high blood pressure to monitor weight loss and fluid
retention such as Troisi et al., 1990. Body composition testing can help predict
and follow overall recovery from obesity and the natural approaches toward blood
pressure. lacona et al,, 1990 again show the detrimental effects of high fat
diets. Levinson et al., 1990 have again demonstrated the beneficial
antihypertensive effects of fish oil. Seelig et al., 1990, suggests the benefits
of magnesium therapy in numerous groups. Sauter and Rudin, 19 90 suggest once
again that if one has to use hypertension drugs, calcium antagonists may be the
best because they can reduce brain damage from stroke and damage to the heart
and other organs. Jule et al., 1990, has again suggested the benefits of non
pharmacological nutritional therapies in the treatment of hypertension. Digiesi
et al., 1990, suggested the benefits of 100 mg or more of CoQIO. Mills et al.,
1989, have suggested that the borage oil supplement may be even better than the
primrose oil supplement in lowering blood pressure. Hypertension and nutrition
research marches onward, Everyone with hypertension and/or a family history
needs a dietary and nutritional regimen.
Biochemical
Individuality/Genetic Differences
It is very important for both the
physician and hypertension patient to realize that every human being is
genetically, and thus, biochemically distinct. Dietary or drug regimens have
different effects on different patients. The influence of diet on blood lipid
levels is not predictable for each individual due to different genetic traits.
Sodium restriction is generally recommended in an anti-hypertensive diet, and
inmost cases, this reduces blood pressure through volume effects, Sodium
restriction is beneficial for the majority of hypertensives (Huddy, 1986). A
recent epidemiologic study showed sodium restriction to be of no value in a
small subgroup of the population at large (Cardiology Observer, 1987).
Furthermore, in a small group of patients, sodium restriction actually increases
the activity of the angiotensin system, and thus raises blood pressure.
According to Dr. Weinberger of Indiana University, dietary sodium restrictions
shows a heterogeneity of responses due to genetic differences in the
renin-angiotensin aldosterone system (Weinberger, 1996). Not all people respond
similarly to the same levels of electrolyte intake or patterns of multiple
electrolyte intake, hence biochemical individuality (Harlan and Harlan,
1986).
Dietary cholesterol, as found in eggs for example, usually does
not significantly raise serum cholesterol in most patients if the patient is on
a proper dietary regimen. Nevertheless, not all patients can consume large
quantities of eggs without an increase in serum cholesterol, The dietary
recommendations made in this paperwork exceptionally well in a vast majority of
the hypertensive population, but some trial and error might be needed to tailor
the program to a patient's specific biochemical needs. Clinical judgement of
which nutrient and diet to use can be refined by measuring, plasma fatty acids,
plasma amino acid, red blood cell trace elements, hair analysis and vitamin
levels. Following Sed rates, cholesterol epolepsoterms, and fibrinogen levels is
also useful.
New Data on Hypertension
Who will have a heart
attack? Does hypertension increase risk? We know that individuals who have a
high risk for heart attack have some of the following biochemical features:
elevated fibrinogen, elevated renin levels, elevated cholesterol, low HDL, low
apolipoprotein a.
Therapies for Hypertension, Updated
Patki et
al., 1990, once again demonstrated the benefits of potassium, 60 millimols a
day, in lowering arterial blood pressure. Total body potassium content may be
more useful in predicting and utilizing potassium in hypertension treatment,
Polert et al, 1990, has again shown the fact that blood sugar problems and
insulin resistance are characteristic of hypertension. Geyger et.al., 1999, bas
again shown the role of cadmium in contributing to high blood pressure.
Cappuccio et al., 1989 has again shown the benefits of calcium therapy in
hypertension, Rinner et al., 1989 has again shown the benefits of sodium,
Potassium, calcium, magnesium modifications in blood pressure. Lauten et al.
have also shown the benefits of dietary potassium in blood pressure. Marraccini
et al., 1989 have shown the dangers on overall health of hypertension. Hoffman
et al., 1988 have again shown the possible problems of increased sodium Morris
et al., 1989 have again shown how low level lead can raise blood pressure. Lind
et al., 1987 have again shown the benefits of vitamin D which can help the
absorption of calcium. Yuricomi et al, 1988 have again shown the role that
sulphur and amino acids can regulate blood pressure through changing brain
chemistry. Radek and Deck, et al., 1999 have again shown the roll of fish oil in
blood pressure. Bak et al,, have again shown the fact that caffeine can have an
impact on Word pressure. Stamler et al have again shown that overall approach to
hypertension must first be nutritional, dietary, and hygienic. Luft et al., 1989
have again shown that dietary interventions are critical to monitoring blood
pressure. Depet et al., 1990 suggested the possible benefits of calcium
supplementation to hypertension. Salvaggio et al 1990 has suggested the role of
caffeine in raising blood pressure. Steiner et al., 1989 suggested the benefit
of fish oil in hypertensive patients Ashry et al, 1989 suggested the benefit of
linoleic acid and safflower oil in lowering blood pressure. Baksi et al 1989
suggested a role for low calcium in elevated blood pressure. Tractman et al.,
1989 again suggested the role of taurine in lowering blood pressure Oberman et
al., 1990 again suggested of not pharmacological and nutritional treatments in
lowering blood pressure. Triber et al., 1989 has again shown the
relationship
between hostility and raising blood pressure, Rouse et al,, 1984
has again shown the role of vegetarian diet when all other approaches fail in
lowering blood pressure. Kaplan, 1990 has again shown the role and benefit of
nonpharmacological therapy, Multiple studies have shown the benefit of
nutritional and non pharmacological therapy and it is time to make use of
hypertensive nutrients,
Our antihypertensive nutrient called the heart
formula is the best nutritional supplement to date. Dyeetal., 1990 have show,
that sucrose and glucose ingestion can raise blood pressure. Golub et al., 1990
have suggested the possible benefits of bioflavonoids in lowering blood
pressure. Hsieh et al., 1990 suggested again the benefits of magnesium therapy
in hypertension. Jule et al., 1990, has again suggested the benefits of
nonpharmacological nutritional therapies in the treatment of hypertension.
Digiesi et al., 1990 suggested the benefits of 100 mg or more of CoQIO. Mills et
al., 1989 have suggested that the borage oil supplement may be even better than
the primrose oil supplement in lowering blood pressure. Hui et al., 1989 again
suggested the benefits of fish oil therapy,
Therapies for
Hypertension
Chronic lithium administration, because of its reduction in
stress and increased secretion of sodium lithium therapy, may, on occasion, also
benefit blood pressure according to Ideet et al, 1988. Kestaltloot et al., 1988
again suggests that the relationship of sodium, potassium, calcium, and
magnesium is critical to normal blood pressure. lacona et al., 1990, have again
shown the detrimental effects of high fat diets. Levinson et al., 1990 have
again demonstrated the beneficial anti hypertensive effects of fish oil. Seelig
et al., 1990 suggest the benefits of magnesium therapy. Boulos et al., 1988
suggests warnings about calcium supplements being contaminated by
lead.
Side Effects of Drugs
Abu Hamdon et al., 1987 suggested
that the side effects of drugs like Capropril and angiotensin 2 blockers might
be helped by the addition of zinc.
New Tests
Numerous studies
suggest the benefits of 24-hour blood pressure monitoring (Weber et al., 1988).
This is an extremely important breakthrough in the management of hypertension
because of the diagnostic accuracy of thirty blood pressure readings. Numerous
studies suggest the benefit of doing body composition analysis in patients, such
as Troisi et al., 1990 suggest the benefits of body composition testing in
predicting overall recovery from obesity and beneficial approaches toward blood
pressure. Drayer, 1985 and Pickering et al., 1988 have suggested at least 20
percent of hypertension patients are misdiagnosed because ambulatory blood
pressure monitoring is not used, O'Brien et al., 1990 has again shown the
benefits of 24-hour blood pressure monitoring in determining blood pressure.
Belini et al " 1990 has again shown the benefits of the influence of lowered
body composition on blood pressure. Sauter and Rudin, 1990 suggest once again
that if one has to use hypertension drugs, that calcium antagonists may be the
best because they can reduce brain damage from stroke and damage to the heart
and other organs.
Case Histories
1. Removal of Multiple
Drugs
G.F. is a 51-year-old male on multiple medications, weighing 265
pounds with a 25-year history of smoking 2 packs of cigarettes per day. He
stopped smoking 3 years ago. He had BP of 1501100 and 140/100 with a pulse of
74. He was taking Aldomet, Klotrix, Hydrochlomthiazide for 10 years and
Nitropatch nightly. He was put on a weight reducing, low carbohydrate diet and
started on a multivitamin, 6 per day; B6, 500 mg; magnesium orotate, 3 grams;
garlic, 1440 mg; taurine, 3 grams; primrose oil (dihomogammalinoleic acid), 3
grams; Max-EPA (eicosapentanoic acid), 6 grams; magnesium oxide, 1.5 grams per
day; and Klotrix, 4 per