High Blood Pressure 0

.4dditional studies suggest that even smaller reductions in sodium intake
over an extended period may reduce blood pressure, as discussed below.
In a 2-year controlled trial, 31 hypertensive patients were instructed to
reduce sodium intake by about 70 to 100 mEq. Although sodium excretion
declined only from 191 to 157 mEq, indicating a much smaller reduction in
intake, the average diastolic blood pressure fell by 7.3 mm Hg, a result
similar to that obtained by drug treatment (Morgan et al. 1978).

Similar results have been obtained in even shorter time periods. In a 12-
Lveek randomized trial, one-half of 90 drug-treated hypertensive patients
:vere placed on a no-added-sodium diet (estimated to be equivalent to a
maximum intake of about 100 to 150 mEq, or 2,300 to 3,450 mg of sodium).
Among the salt-restricted patients, sodium excretion decreased from 150
.o 37 mEq and diastolic blood pressure decreased by 6.3 mm Hg (compared
with a fall of 2.9 mm Hg in the drug-treated control group), and four of five
patients were able to discontinue or reduce medication (Beard et al. 1982).

In a randomized 8-week crossover study of 19 hypertensive patients,
dietary restriction was associated with a reduction in sodium excretion
`ram 191 to 83 mEq and a fall in mean blood pressure of 7.6 mm Hg
MacGregor, Markandu, et al. 1982). During a later double-blind phase of
.he trial, a level of sodium excretion of 76 mEq was associated with a mean
31ood pressure of 7.1 mm Hg lower than that of the control group (Mac-
Sregor, Smith, et al. 1982). Results of a nearly identical trial, however,
showed no difference in patients' blood pressures (Watt et al. 1983). The
.lifferences between these results may be related to a somewhat lower
llood pressure at entry, to a slight difference in average sodium excretion,
3r to chance variation.

4 recent review of 13 randomized clinical trials concluded that moderate
37 to 153 mEq/day) sodium restriction does reduce blood pressure, at least
:o some small extent, and that this practice is most effective for systolic
pressures, for older hypertensive patients, and for patients with higher
nitial blood pressures (Grobbee and Hofman 1986a).

3evention

The important question of whether reduction in sodium intake might
?revent the rise in blood pressure with age has been addressed in a few
short-term studies of adults, children, and infants with normal blood pres-
cures (normotensives). Blood pressure response to moderate sodium re-
itriction (to 60 mEq) for 3 months in 16 healthy normotensive husbands and
wives was associated with a decrease in sodium excretion from 152.7 to
59.5 mEq/day and significant decreases in systolic and diastolic blood

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pressure of 4 and 3 mm Hg, respectively (Miller et al. 1983). In a ran-
domized double-blind trial, 23 1 infants fed a diet reduced in sodium content
by two-thirds during the first 6 months of life had a mean systolic blood
pressure that was significantly lower (2.1 mm Hg) than that of 245 infants
fed a customary diet (Hofman, Hazebrock, and Valkenburg 1985). These
two studies indicate that apparently normal blood pressures can be re-
duced by dietary sodium restriction, and they suggest that this practice
might prevent age-related increases in blood pressure. To date, however,
no reported studies have tested this hypothesis directly.

Variability in Response

The disparate blood pressure responses to sodium intake in animals at-
tributed to genetic influence (Dahl, Heine, and Tassinari 1%2) have led to
the proposal that dietary sodium and blood pressure relationships are
controlled by similargenetic factors in humans (DahIl972). Support for the
concept of individual variability in human blood pressure response has
been provided by a study of 20 hypertensive patients in hospital metabolic
units who were fed daily sodium intakes of 9 mEq, 109 mEq, and 249 mEq.
Investigators were able to distinguish a salt-sensitive group, whose blood
pressures fell in response to sodium restriction, and a salt-resistant group,
whose blood pressures tended not to be influenced by changes in salt intake
(Kawasaki et al. 1978). It has not yet been possible, however, to identify a
way to consistently distinguish salt-sensitive from salt-resistant persons
other than by measuring the blood pressure response itself.

While acknowledging that there are some hype,tiensive individuals whose
blood pressures do not respond to sodium restriction, some investigators
believe that patients who continue to consume low-salt diets have a more
benign course than those who revert to a high salt intake (Dahl 1977).

Two dietary intervention studies suggest that weight loss or sodium restric-
tion or both can retard the return of high blood pressure in patients who
have achieved normal blood pressure levels through drug treatment. The
Dietary Intervention Study in Hypertension assessed whether hyperten-
sive patients whose hypertension was controlled with drugs could discon-
tinue these medications with or without dietary therapy. The 415 patients
who discontinued medications were randomized, stratified by body
weight, either to control, weight loss (mean loss of 10 lb), or sodium
restriction (mean decrease of 40 mEq/day). The patients in the dietary
intervention groups were more than twice as successful as those in the
control group in maintaining normal blood pressure. At the end of 56
weeks, 50 percent of these patients remained normotensive without medi-
cation. This success rate was higher for patients with pretreatment mild

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hypertension than for those with pretreatment severe hypertension. In the
former group, 71.5 percent in the weight loss group and 78 percent in the
nonobese sodium restriction group remained normotensive (Langford et
al. 1985).

Similar results were noted in a 4-year trial, the Hypertension Control
Program. Among patients with pretreatment mild hypertension who dis-
continued antihypertensive medications but who restricted calories and
sodium and alcohol intake, 39 percent maintained normal blood pressure
after 4 years. In contrast, only 4 percent of those patients who did not
receive nutritional intervention remained normotensive (Stamler et al.
1987).

It should be noted that in the two studies previously described, the patients
had relatively mild hypertension that had been controlled successfully with
drugs for the preceding 5 years. Although the long-term effectiveness of
dietary intervention in persons with more severe elevations in blood pres-
sure remains to be established, these studies have important implications
for the millions of Americans who are being treated for high blood pressure
or who have elevated diastolic blood pressure. Many persons who adhere
to a dietary regimen to control blood pressure can reduce or stop drug
therapy, with potential economic and health advantages.

Role of Alcohol in Hypertension

Epidemiologic studies have shown that individuals who regularly consume
large amounts of alcohol have higher blood pressure than people who
abstain from alcohol or who drink only moderate amounts. The epi-
demiologic literature for the existence and nature of an association be-
tween blood pressure and alcohol consumption has been reviewed (Mac-
Mahon 1987). In the 12 cross-sectional North American studies reviewed
(Table 3-6), with the exception of the Canada Health Study, all reports
showed a significant positive association that was independent of age,
relative body weight, exercise, and smoking status. In most U.S. studies, a
J-shaped or U-shaped association is observed between blood pressure and
alcohol consumption, with blood pressure greater in nondrinkers than in
those consuming one to two drinks per day. It is not clear whether this
might be partially explained by other factors, such as obesity. A more
consistent finding was elevation of blood pressure at levels of three drinks
or more per day. The prospective, observational studies of the association
of blood pressure with alcohol consumption (Table 3-7) have also been
reviewed (MacMahon 1987). In this group of investigators, only the Hono-
lulu Heart Study failed to show a positive association with either systolic or

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           Table 3-6
Studies of the Cross-Sectional Association of
Blood Pressure With Alcohol Consumption

Year       Studya

No. of       Male      Age
Subjects   Subjects (o/o)    (years)

1967    Los Angeles Heart         865        100
1977    Chicago W. Electric      1,899        100
1977    Kaiser-Permanente I     83,947        45
1980    Tecumseh           3,390        47
1981    Lipid Research Clinics     4,783        52
1981    Honolulu Heart        8,006        100
1983    Stanford Five City       1,842        48
1983    Framingham          5,209        42
1985    Canada Health         1,418         51
1985    NHANES           9,553         45
1986    Kaiser-Permanente II     66,510        44
1986    Albany             1,910        100

21+
40-55
15-79
18+
20+
46-68
20-74
29-62
20+
18-74

-
38-55

1974
1980
1982
1983
1984
1985
1985

European
Copenhagen          5,249
Yugoslavia          11,121
Lyon             1,134
North KarelialKuopio     8,479
Munich Blood Pressure    3,198
Wurttemberg         3,351
Zutphen               794

Australian and New Zealand

100       40-59
100       35-62
100       20-59
50       30-64
33       30-69
88       20-65
100       a59

1980
1981
1982
1982
1984
1984
1985
1985

Tasmania
CSIRO
Sydney Hospital
Perth
Medicheck
Australian RFPS
Milton
Auckland

Japanese

  85
350
20,920
491
11,000
5,550
901
1.429

loo
100
65
100
75
::
66

36"
23b
18-70
2Od5
43b
19+
19+
35-64

1984    OsakalAkita            887        100       40-69
1984    Minamikawachi         3,083         37       53b

North American

aCSlR0 = Commonwealth Scientific and Industrial Research Organization; NHANES =
National Health and Nutrition Examination Survey; RFPS = Risk Factor Prevalence
Study.
Wean age.

Source: Adapted from Macblahon 1987.

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             Table 3-7
Prospective Observational Studies of the Association of
   Blood Pressure Wii Alcohol Consumption

Year       Studv

No. of
Subiects

1977  Chicago People's Gas   1,340       100
1981  Chicago W. Electric     871       100
1982   Honolulu Heart      6,858      loo
1983  Framingham        5,209       42
1985  Zutphen             794      100
1986   Albanv            I .910      loo

Subjects (%)

Age   Followup
(years)   (years)

40-59
40-55   t
46-68      6
29-62      4
40-59     10
38-55     18

Source: Adapted from MacMahon 1987.

diastolic blood pressure at followup with alcohol intake either at baseline
or followup. This evidence, in summary, indicates the potential impor-
tance of alcohol restriction in blood pressure control.

Role of Other Minerals in Hypertension

Potassium

One of the earliest observations of the association of dietary potassium
with reduced blood pressure concluded that "potassium salt regularly
produced a decline in blood pressure, while sodium salt just as regularly
produced a rise" (Addison 1928). It was later observed that potassium
lowered blood pressure in individuals with hypertension even when dietary
salt intake remained high (McQuarrie, Thompson, and Anderson 1936).
This protective effect has also been observed in rats (Meneely, Ball, and
Youmans 1957). These inverse associations have been reviewed exten-
sively (Meneely and Battarbee 1976; Tannen 1983; Prineas and Blackbum
1985).

Population studies have shown both a positive relationship between so-
dium intake and blood pressure and an inverse relationship between po-
tassium intake and blood pressure (Maddocks 1967; Sinnett and Whyte
1973; Bulpitt et al. 1986). Although the Framingham study showed no
relationship between urinary potassium levels and blood pressure (Dawber
et al. 1%7), potassium intake was more strongly correlated than any other
dietary factor to blood pressure in a Hawaii study (Reed et al. 1985). In
disease prevalence studies in Evans County, Georgia, hypertension was
more strongly associated with lower potassium intake in black adults than
in white adults with similar sodium intakes (Grim et al. 1980). In a Southern
California cohort of 859 men and women ages 50 to 79 years, an inverse
relationship was observed between dietary potassium, estimated by 24-

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u Nutrition and Health

hour dietary recall at the baseline examination, and death from stroke,
identified by examination of death certificates, in the 1Zyear followup
(Khaw and Barrett-Connor 1987).

Intervention trials have attempted to lower blood pressure in hypertensive
patients with the use of potassium supplements. The effect of 60 mEq of
potassium supplementation was compared with that of placebo and was
documented in a double-blind 4-week crossover trial in 23 patients with
hypertension. A small but significant lowering of both systolic and diastolic
blood pressure occurred in the supplementation period compared with the
placebo period (MacGregor, Smith, et al. 1982). In another double-blind
crossover trial, 20 normotensive subjects taking a 64 mEq of potassium
supplement reduced diastolic blood pressure significantly (by 2.4 mm Hg)
in 2 weeks compared with subjects taking a placebo (Khaw and Thorn
1982). A double-blind clinical trial that enrolled 116 adults with mild
hypertension for 8 weeks found a 3.4 mm Hg greater decrease in systolic
blood pressure and a 1.8 mm Hg greater decrease in diastolic blood
pressure in the group taking potassium supplements of 120 mEq/day than in
the group taking placebo. A much greater decrease was observed in the five
black patients taking potassium compared with placebo (Svetkey et al.
1987). In a 15-week clinical trial that randomized 37 mildly hypertensive
patients, there was a mean difference (lower) of 14 mm Hg in systolic blood
pressure and 10.5 mm Hg in diastolic blood pressure in the patients taking
48 mEq/day of potassium compared with placebo (Siani et al. 1987). These
beneficial effects of potassium on blood pressure in hypertensive patients
have been confirmed in another randomized blinded crossover study of 19
hypertensive patients with diuretic-induced potassium depletion. Po-
tassium supplements of 60 mEq/day reduced mean blood pressures by 5.5
mm Hg (Kaplan, Carnegie, and Raskin 1985). In contrast to these findings,
an unblinded crossover study of 12 mildly hypertensive subjects showed
no influence of potassium supplementation on blood pressure (Richards et
al. 1984). One extensive review of the literature concluded that a high
potassium intake has no effect on blood pressure in normotensive animals
or humans, although a potassium intake of 120 to 175 mEq/day appears to
reduce blood pressure in hypertensive patients by 3 to 10 percent (Tannen
1983).

If potassium does have an effect, it is likely influenced by sodium. In a
randomized 12-week crossover study of increased sodium intake and
added potassium in hypertensive and normotensive adults, blood pressure
rose in both hypertensive and normotensive subjects who consumed in-
creased sodium, but among hypertensives who consumed supplemental
potassium, blood pressure fell (Parfrey et al. 1981).

I56


High Blood Pressure Ll

The relationship between sodium, potassium, and blood pressure in nor-
motensive adults has been found to be dependent on family history of
hypertension (Pietinen, Wong, and Altschull979). The response to dietary
potassium and sodium has been assessed in male medical students with and
without a family history of hypertension. In just the group with a positive
family history, diastolic blood pressure was reduced by about 11 mm Hg
when sodium intake was lowered in the presence of high potassium intake
compared with 7 mm Hg with reduced sodium intake alone (Parfrey et al.
1981). A reanalysis of these data confirmed this effect of potassium (Holly
et al. 1981). Also consistent with these data that show a lack of potassium
influence in those with a negative family history of hypertension are two
trials that failed to find a blood pressure-lowering effect of potassium in
those persons who achieved substantial reduction of sodium intake (Mor-
gan et al. 1983; Smith et al. 1985). Because the duration of the majority of
these studies has been only weeks or months, longer term intervention
studies have been recommended to evaluate the effects on blood pressure
of both increased potassium and reduced sodium (Prineas and Blackbum
1985).

Calcium

A possible role for dietary calcium in the regulation of blood pressure is
suggested by experimental studies in animals, epidemiologic studies, and
clinical studies, including clinical trials (Kaplan and Meese 1986).

Experimental studies in spontaneously hypertensive rats have suggested
that supplemental dietary calcium may prevent the development of hyper-
tension (Ayachi 1979; McCarron, Henry, and Morris 1982; Schleiffer et al.
1984). One study, however, reported no such effect (Stem et al. 1984).

An association between calcium and blood pressure was suggested by
reports that "hard" drinking water (containing calcium) was associated
with reduced prevalence of cardiovascular disease (Schroeder 1960). This
association between calcium and blood pressure is supported by observa-
tions from the Puerto Rico Heart Health Program that individuals who
drank no milk (which is high in calcium) had twice the prevalence of
hypertension as those who consumed a quart of milk or more per day
(Garcia-Pahnieri et al. 1984). An analysis of data for 5,050 adults in South-
em California surveyed for heart disease risk factors as part of a Lipid
Research Clinics population study indicated that hypertensive men, but
not hypertensive women, had a significantly lower intake of calcium from
milk than normotensive individuals; in men, diastolic blood pressure de-
creased significantly with reported increasing milk consumption (Ackley,
Barrett-Connor, and Juarez 1983). In a case-control study, dietary calcium

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0 Nutrition and Health

intake assessed by 24-hour dietary recall in 46 hypertensive patients and
normotensive controls showed that calcium intake was 22 percent less in
the hypertensive group (McCarron, Morris, and Cole 1982).

An analysis of the National Health and Nutrition Examination Survey I
(NHANES I) data found an inverse, although inconsistent, association
between dietary calcium and blood pressure; the lower blood pressures
were correlated with higher levels of serum calcium (Harlan et al. 1984).
Although a subsequent examination of a subset of NHANES I data also
suggested an inverse relationship between dietary calcium intake and
blood pressure (McCarron et al. 1984), the analysis was hindered by
methodological shortcomings: the salt added in food preparation and at the
table were excluded from dietary intake data; the results were examined
using only systolic blood pressure measures; and the analyses did not
control consistently for age, race, sex, and body mass index (Feinleib,
Lenfant, and Miller 1984). Subsequent analyses of both NHANES I and II
data have failed to identify a relationship between dietary calcium and
blood pressure except among black males in NHANES I (Sempos et al.
1986).

In a randomized placebo-controlled clinical trial, normotensive adults
taking 1,000 mg of calcium per day for 8 weeks had blood pressures that
were 6 to 9 percent lower than those receiving placebos (Belizan et al.
1983). In an uncontrolled clinical study, 2,000 mg of oral calcium carbonate
taken for 5 days lowered blood pressure in people with low plasma renin
activity (Resnick, Nicholson, and Laragh 1984). A blood pressure-lower-
ing effect of calcium has been noted after 5 months in an uncontrolled study
of individuals with mild-to-moderate hypertension (Resnick, Nicholson,
and Laragh 1984).

Another randomized placebo-controlled crossover trial provided 1,000 mg/
day of oral calcium for 8 weeks to 48 hypertensive and 32 normotensive
individuals. In the hypertensive group, standing systolic and diastolic
pressures were significantly reduced (by 6 and 2 mm Hg, respectively), as
was supine systolic (by 3 mm Hg)-but not diastolic-pressure. Among
normotensive persons, only supine diastolic blood pressure was signifi-
cantly lowered with calcium (McCarron and Morris 1985). Supplements of
1,500 mg of calcium per day produced modest (2 to 3 mm Hg) reductions of
systolic and diastolic pressures in both white and black normotensive men
in a recent study (Lyle et al. 1987). An oral calcium supplement of 10 or 20
mM/day was given for 2 months in a double-blind randomized crossover
study involving 5 1 hypertensive and 5 1 normotensive patients. There was
an apparent trend for lower systolic blood pressure. The diastolic blood


High Blood Pressure 0

pressure did not change significantly. In the normotensive group, there
were no significant changes in blood pressure (Nowson and Morgan 1986).
The effect of 1 g of calcium lactate gluconate or calcium carbonate in 23
patients with mild-to-moderate hypertension was observed for 8 weeks in
another double-blind crossover study. These investigators reported no
evidence that oral calcium supplements lowered blood pressure in these
patients (Zoccali et al. 1986).

Analyzed collectively, the preceding evidence suggests that a disturbance
in cellular calcium metabolism may contribute to the development of
hypertension, although the physiologic mechanism for this effect is as yet
unknown (Pak 1985). The possibility that calcium supplements may lower
blood pressure only in patients with mildly elevated levels of parathyroid
hormone that have occurred as a result of abnormally high kidney excre-
tion of calcium (and consequent lowering of blood calcium levels) has been
proposed on the basis of a study of 90 hypertensive patients (Grobbee and
Hofman 1986b). At present, the role of calcium in blood pressure regula-
tion must be considered uncertain and the clinical evidence considered
inconclusive (Kaplan and Meese 1986).

Chloride

In early studies, the blood pressure-raising effect of sodium chloride was
attributed to its chloride portion. Since the mid-1950's, however, the
sodium component of sodium chloride typically has been considered more
important (Dahl and Love 1954).

The effect of dietary chloride on the pathogenesis of sodium-dependent
hypertension has been examined in experimental animals. Steroid-treated
rats with one kidney removed developed hypertension when fed sodium
chloride but not when they were fed sodium bicarbonate. These different
responses could not be explained by differences in caloric intake, weight
gain, or the balance of sodium, water, or potassium (Kurtz and Morris
1983).

The observation that salt-sensitive hypertension depends on the presence
of both chloride and sodium has induced some investigators to suggest that
chloride-rather than sodium-induces hypertension. In one study of salt-
sensitive rats, for example, blood pressures were shown to be significantly
higher after 5 weeks of loading with sodium chloride, but they remained
normal when sodium bicarbonate was substituted for sodium chloride in
the diet (Kotchen, Luke, and Ott 1983). The effect of a nonchloride sodium
salt on blood pressure was recently tested in five hypertensive men. At 10
mEq/day of sodium chloride, blood pressure was normal. A 230 mEq of

159


0 Nutrition and Health

sodium chloride supplement induced a significant increase in blood pres-
sure, which was reversed with a supplement of an equimolar amount of
sodium as sodium citrate (Klutz, Al-Bander, and Morris 1987). This study
again raises the possibility that the chloride ion may independently contrib-
ute to the sodium chloride-induced increases in blood pressure. The need
for further investigation is reinforced by the report that chloride concentra-
tions and activity are decreased in erythrocytes of humans with essential
hypertension (Kurtz and Morris 1985).

Magnesium

An early study showed that clinical administration of magnesium salts
lowered blood pressure (Blackfan and Hamilton 1925), and recent epi-
demiologic data have rekindled an interest in this effect (Joffres, Reed, and
Yano 1987). Because magnesium, along with calcium, is present in "hard"
drinking water, an association between dietary magnesium and blood
pressure is also suggested by the finding of lower rates of cardiovascular
disease in hard-water areas. The possible association between magnesium
and blood pressure is supported to some extent by an observation that
magnesium-deficient rats had both higher blood pressure levels and re-
duced diameter of tiny blood vessels than control animals (Altura et al.
1984).

Among elderly people in Denmark, low serum magnesium concentration
has been associated with increased blood pressure (Petersen et al: 1977),
and magnesium intakes have been found to be reduced among hyperten-
sive patients (McCarron 1982). One randomized study of 18 patients taking
diuretic medications for hypertension or congestive heart failure showed
that magnesium supplementation was followed by a significant fall in both
systolic (by 12 mm Hg) and diastolic (by 8 mm Hg) blood pressure (Dyck-
ner and Webster 1983). As stated in the chapter on drug-nutrient interac-
tions, thiazide diuretics have been associated with magnesium depletion,
and this may be a factor in the blood pressure changes seen during magne-
sium supplementation. However, in another study in which patients with
mild to moderate hypertension not on diuretics were given either magne-
sium supplements or a placebo, blood pressures did not fall in either group,
despite a significant increase in plasma magnesium concentration and in
urinary magnesium in the group taking the supplement (Cappuccio, Mark-
andu, and Beynor 1985). The inconsistency of data regarding magnesium
and blood pressure levels indicates that there are many unanswered ques-
tions regarding the role of magnesium in hypertension.

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Trace Elements

Little is known about the role of trace elements in the regulation of blood
pressure. Because trace elements such as zinc, copper, and iron participate
in enzyme reactions related to blood pressure regulation, they could be
factors in the development of hypertension, although they are unlikely to
be its primary cause (Saltman 1983). In a comprehensive review of this
topic, cadmium was the only trace element that appeared to be related to
blood pressure (Mertz 1985), and experimental data from animals and the
results of some human studies are consistent with a potential causative role
for this element. This role, however, lacks confirmation and is complicated
by the many interactions of cadmium with selenium, copper, zinc, and
lead. Epidemiologic and animal data also suggest a direct relationship
between lead levels and blood pressure (Pirkle et al. 1985), but existing data
do not support a major role for this or any other trace element in the
pathogenesis of hypertension.

Role of Macronutrients in Hypertension

Carbohydrates

There is some evidence that carbohydrates may play a role in blood
pressure regulation. Studies in rats have indicated that dietary sucrose
increases blood pressure, whereas starch decreases it (Ahrens et al. 1980).
Normotensive humans who supplemented their diets with 200 g/day of
sucrose had diastolic blood pressures 5 mm Hg higher than those who
consumed no added sucrose (Ahrens 1974). Both a high sucrose and a high
glucose solution-but not galactose or lactose-consumed after an over-
night fast produce transient increases in blood pressure in normotensive
men. These observations suggest that carbohydrates might influence blood
pressure-regulating hormones in rats, but investigations conducted to date
have failed to find a similar effect in humans (Hodges and Rebello 1985).

Fiber

There is some indication that plant fiber may reduce blood pressure levels
(Anderson 1983; Anderson and Tietyen-Clark 19861, but it is uncertain
whether dietary fiber plays a role in blood pressure regulation that is
independent of other concomitant dietary changes, such as replacement of
fat or facilitation of lower sodium intake (Mendeloff 1985).

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Fat

The effect of dietary fats on blood pressure has been recently reviewed
(Sacks et al. 1987). Neither the effect of total fat content nor responses to
major changes in fatty acid intake have been sufficiently studied with
desirable methodology, controlling potentially confounding variables for
an adequate time period.

Polyunsaturated Fatty Acids. Considerable interest has focused on obser-
vational studies indicating that an increased intake of polyunsaturated fatty
acids is associated with lower blood pressure (Iacono, Puska, and Dough-
erty 1983; Puska et al. 1985). Although it is uncertain whether the lower
blood pressures were attributable to the change in the type of dietary fat, an
action of the fatty acids on blood pressure might be mediated through
changes in prostaglandin metabolism caused by increased intake of the
polyunsaturated fatty acid, linoleic acid. Some prostaglandin metabolites
influence salt and water excretion and can cause contraction or dilation of
small blood vessels, thereby affecting blood pressure (Iacono et al. 1981).
A single-blind randomized control experiment among hypertensive and
normotensive men and women in North Karelia, Finland, found that a low-
fat diet with a P/S ratio of 1 .O was associated with reductions in systolic and
diastolic blood pressure of 8.9 and 7.6 mm Hg, respectively, reductions
greater than those observed in parallel control groups receiving sodium
restriction or no dietary change (Puska et al. 1983). Another team of
investigators has shown that compared with the baseline diet, decreasing
saturated fats and increasing polyunsaturated fats are associated with
lower blood pressure (Iacono et al. 1975; Iacono et al. 1981; Iacono,
Dougherty, and Puska 1982).

No significant change in blood pressure was observed after feeding either a
low-fat diet (22 percent of calories from fat) or a diet high in polyunsatu-
rated fatty acids (19 percent of calories from polyunsaturated fatty acids-
compared with the U.S. average of about 7 percent) to 15 to 18 normoten-
sive young adults (Brussaard et al. 1981). A double-blind randomized
control trial of 6 weeks studying 21 mildly hypertensive patients found that
increasing the polyunsaturated fatty acid linoleate from 4.6 to 13 percent of
calories and reducing saturated fatty acids from 16 to 10 percent failed to
produce any significant changes in blood pressure (Sacks et al. 1987).

Monounsaturated Fatty Acids. An association between increased con-
sumption of the monounsaturate oleic acid and reductions in both systolic
and diastolic blood pressures has been observed recently in a cross-
sectional survey that examined 3-day food records and resting blood

162


High Blood Pressure O

pressure in 76 normotensive men. Although no physiologic explanation for
this association is evident, it is consistent with the lower prevalence of
hypertension among Mediterranean populations who consume diets rich in
oleic acid-containing olive oil; Mediterranean populations also have a high
carbohydrate intake and low saturated fatty acid intake compared with the
U.S. population (Williams et al. 1987).

Omega-3 Fatty Acids. The role of omega-3 fatty acids in blood pressure
lowering has also received attention. Investigators have reported that the
ingestion of enough fish to provide 5 g of omega-3 fatty acids per day for 2
weeks caused a significant fall in blood pressure, and the lower blood
pressure could be maintained subsequently by the weekly consumption of
20 oz of fish that provided 1.2 g/day of omega-3 fatty acids (Singer et al.
1986).

In summary, these results indicating that the type of fat intake may influ-
ence blood pressure level require further investigation to resolve inconsis-
tencies, confirm the observations, and establish their clinical significance
(Iacono, Dougherty, and Puska 1982).

Protein

The possibility of an effect of protein level on blood pressure regulation and
whether specific amino acids might have an antihypertensive role has
received little scientific study. In a study of spontaneously hypertensive
rats, those rats fed American rat chow containing 25.3 percent protein,
compared with rats fed Japanese rat chow containing 19.7 percent protein,
developed a lower incidence of stroke (30 percent versus 80 percent).
When the rats previously fed American rat chow were fed the Japanese
diet, an accelerated rate of cerebral lesions and stroke occurred. This
observation led to a search for specific amino acids in proteins that might
affect blood pressure; tryptophan and tyrosine, as well as total protein
intake, were cited as leading possibilities. Taurine has been demonstrated
as having an antihypertensive effect in patients with hypertension
(Kohashi et al. 1983) as well as in rats (Abe et al. 1987). One hypothesis is
that amino acids or protein may affect blood pressure either at the vascular
level or through changes in neuronal control of the cardiovascular system
(Yamori et al. 1984), but this idea has yet to be confirmed.

Role of Caffeine in Hypertension

The consumption of 150 mgof caffeine (two to three cups of brewed coffee)
may promote an increase in blood pressure by 5 to 15 mm Hg within 15

163


0 Nutrition and Health

minutes that is maintained for as long as 2 hours. These short-term effects
are primarily mediated by an increase in cardiac output, with systolic
pressure usually rising more than diastolic; they are demonstrable both in
individuals who do not habitually consume caffeine and in those who do
habitually ingest caffeine if they abstain for 12 hours or more. The cause of
these effects is uncertain; short-term effects are not directly attributable to
rises in plasma catecholamines, vassopressin, or renin activity (Izzo et al.
1983).

Chronic caffeine consumption, however, neither maintains high blood
pressure nor is it associated with increased rates of hypertension
(Robertson et al. 1984). Prolonged administration of caffeine-as much as
504 mg/day for 4 weeks-has not been associated with significant rises in
blood pressure either in normotensive (Ammon et al. 1983) or hypertensive
individuals (Robertson et al. 1984). Thus, there appears to be adaptation or
tolerance to the hemodynamic effects of caffeine.

Implications for Public Health Policy

Dietary Guidance

General Public

Dietary factors that clearly contribute to high blood pressure include
obesity and excessive intake of sodium and alcohol. The average daily
sodium consumption of 4 to 6 g by adult Americans is substantially above
the National Research Council's recommended range of 1.1 to 3.3 g for safe
and adequate intake and is 5 to 10 times higher than the amount required.
Many individuals are able to maintain normal blood pressure levels over a
large range of sodium intake; the lack of known harm from moderate
sodium restriction, however, and the potential benefit to people whose
blood pressures rise with increased sodium intake suggest that those who
ingest excess sodium-most Americans-should consider reducing their
dietary sodium intake.

The strong association between obesity and hypertension and the demon-
strated reduction in blood pressure that occurs with weight loss suggest
that maintenance of desirable body weight should be a goal for the popula-
tion.

Similarly, there is a direct association between blood pressure and alcohol
consumption beyond about two standard-sized drinks daily. (One stan-
dard-sized drink is defined as 12 oz of regular beer, 5 oz of wine, or 1 `/z oz of
distilled spirits.)

164


High Blood Pressure O

Some evidence indicates that a reduction in blood pressure is associated
with increased dietary intake of potassium, calcium, magnesium, and fiber.
This evidence is, as yet, too preliminary to recommend increased intake of
these factors for the general population for the purpose of hypertension
control. Likewise, although increased intake of certain lipids (e.g.,
omega-6 or omega-3 polyunsaturated fatty acids) may decrease blood
pressure, additional research is needed before any recommendations can
be made.

Special Populations

Achieving and maintaining desirable body weight and moderating sodium
and alcohol intake can lower blood pressure in patients with mild and
moderate hypertension and reduce the need for antihypertensive medica-
tions. Such patients should be informed of the likely benefit ofthese dietary
practices, along with the importance of adequate caloric expenditure
through exercise, and the moderation of fat intake, especially saturated
fatty acids, to reduce high blood cholesterol levels and the risk for heart
attack.

Nutrition Programs and Services

Food Labels

Evidence related to the role of dietary factors in hypertension supports the
need for nutrition labeling on a wide selection of foods so that the consumer
has the option of choosing foods with known amounts of calories and
sodium.

Food Services

Evidence related to the role of dietary factors in hypertension suggests that
food service programs should provide adequate choices of foods that
provide essential nutrients and energy to maintain desirable body weight
and should include foods that are low in sodium.

Food Products

Evidence related to the role of dietary factors in hypertension suggests that
food manufacturers should continue to reduce sodium in products and
continue the research and development of products low in calories and
sodium.

Special Populations

Counseling and assistance in the selection and preparation of foods low in
sodium and calories and assistance with the development of dietary pat-

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terns that control energy, sodium, and alcohol should be available to
individuals whose blood pressure places them in the mild-to-moderate as
well as high range of hypertension.

Research and Surveillance

Special priority is attached to the following research and surveillance tasks
related to the role of diet in hypertension:

o Development of practical methods for the rapid and reliable identifica-
tion of individuals at high risk for hypertension because they are salt
sensitive.

o Investigation of the interactions of sodium with other nutrients-such
as potassium, calcium, chloride, magnesium, fatty acids, and fiber-in
influencing blood pressure.

0 Investigation of the role of specific dietary factors, including po-
tassium, calcium, fatty acids, fiber, amino acids, trace elements, and
alcohol, in the cause and potential prevention of hypertension and the
mechanisms for these effects.

o Investigation of the mechanism of obesity-associated hypertension
and determination of the ratio of fat to lean body mass that might
prevent development of hypertension.

166


High Blood Pressure O

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