Salt : very good or bad ,how good or how bad?? That is the question which will continue chasing modern medicine!
Salt : very good or bad ,how good or how bad?? That is the question which will continue chasing modern medicine!
From the website of Graedon:[first article]
We have been told for decades that salt is sinful. Cut back on saltto lower blood pressure and reduce your likelihood of having a heart attack or suffering premature death. It has been a foundation of public health messages from the Centers for Disease Control and Prevention (CDC) and the National Institutes of Health (NIH). Challenge this conventional wisdom and you are likely to suffer the wrath of the medical establishment.
The trouble is that there are actual studies that suggest a very low-salt diet may have unexpected consequences. For one thing, sodium restriction may actually raise cholesterol, triglycerides and stress hormones (American Journal of Hypertension, Jan. 2012). A long-term study of over 3000 people revealed an unexpected finding: Those who consumed the least amount of salt were at the highest risk of dying during the study (Journal of the American Medical Association, May 4, 2011).
This goes against our core belief system, but could there be an explanation? Sodium restriction appears to increase stress hormones including adrenaline (epinephrine) renin and aldosterone. There is growing evidence that higher levels of renin have negative effects on the cardiovascular system and may lead to an increased risk of heart disease, heart attacks and death.
Nearly 30 years ago there was evidence that levels of the neurotransmitter norepinephrine jumped dramatically in healthy young men when they were put on an enforced low-salt diet (Journal of Clinical Endocrinology and Metabolism, March, 1983). A fascinating, but ignored finding from this research was that the low-sodium diet was linked to serious sleeping problems:
The researchers concluded:
"The low sodium diet was also associated with disturbed sleep patterns: decreased rapid eye movement and slow wave sleep and increased wakefulness."
What appears to happen when you restrict sodium intake is that the body tries to compensate. Not only does it churn out stress hormones, the whole "sympathetic" nervous system goes into high gear. When that happens, sleep patterns may be affected negatively.
As far as we can tell, this research disappeared without a trace. We suspect that very few health professionals are aware of this unintended consequence of a low-salt diet.
Should you wish to read more about salt restriction and blood pressure, we suggest our section about "The Salt Wars: Man Bites Dog" on page 287 in Best Choices From The People's Pharmacy. You might be surprised what the evidence actually shows.
H. Role of Macrominerals and Other Factors in Hypertension
Blood pressure (BP) is a measure of the pressure of the blood against the walls of the
blood vessels produced by the pumping action of the heart. When the BP is measured, two
readings are generally taken: systolic and diastolic pressure. The systolic reading indicates
the maximum pressure exerted on the arterial walls; this high point occurs when the left
ventricle of the heart contracts, forcing blood through the arteries. Diastolic pressure is a
measure of the lowest pressure in the blood vessel walls and happens when the left
ventricle relaxes and refills with blood. Healthy BP is considered 120 mm Hg systolic and
80 mm Hg diastolic (usually presented as 120/80).
Hypertension is defined as an elevated systolic BP, elevated diastolic BP, or both.
Many people can experience temporary increases in BP particularly under stressful
conditions. Some individuals experience ‘‘white coat’’ hypertension, which refers to an
elevated BP value measured in a clinical environment that is higher than the one obtained
outside of this environment. A clinical diagnosis of hypertension is made when the average
of two or more readings taken on two or more occasions consistently are elevated above
140/90. For systolic BP, values between 120 and 129 mm Hg are considered normal and
between 130 and 139 high normal. For diastolic BP, the corresponding value for normal is
between 80 and 84 and high normal is between 85 and 90. Most people (90–95%) suffering
from high BP have no identifiable cause for the disorder. This type of high BP is called
primary or essential hypertension. Patients have secondary hypertension when a specific
cause for elevated BP has been identified; about 5–10% of the people with hypertension
have a secondary cause. Hypertension is called a ‘‘silent’’ disease because unless BP is
measured periodically no one knows it is developing. An individual’s BP is influenced by
many factors including genetic predisposition, race, body weight, level of exercise,
cigarette smoking, insulin resistance, psychological stress, and diet.
High BP is a major health problem throughout industrialized world because of its
high prevalence and association with increased risk of cardiovascular disease, stroke and
renal disease. It can also affect vision, increase mortality and decrease longevity.
Estimates from the 1988–1991 National Health and Nutrition Examination survey
suggest that about 50 million Americans have hypertension. This represents approx-imately 25% of the adult American population. Only 47% have optimal or healthy BP.
Among adults 50 years of age or older a much higher proportion have hypertension and a
much lower proportion have optimal BP.
Role of Renin
Sodium is the main determinant of extracellularfluid volume. When the body contains
too much extracellular fluid the arterial pressure rises. The elevated pressure in turn has
a direct effect to cause kidneys to excrete the excess extracellularfluid, thus returning
the pressure back to normal. Located throughout the vascular system are volume or
pressure sensors that detect these changes and send either excitatory or inhibitory
signals to the central nervous system and/or endocrine glands to effect appropriate
responses by the kidneys.
The renin–angiotensin–aldosterone system (RAAS) plays an important part in the
regulation of arterial pressure. Decrease in BP and renal blood flow, volume depletion
or decreased sodium concentration [my remark: see my question mark below], and an activation of sympathetic nervous system
can all trigger an increased secretion of the enzyme, renin, from the juxtaglomerular cells in the kidney. Renin acts on angiotensinogen, a plasma protein synthesized in the liver, and forms angiotensin I. Angiotensin I is converted to angiotensin II by the action of angiotensin-converting enzyme present in the lungs. Angiotensin II is a potent vaso-constrictor and causes a rise inBP. It also triggers the adrenal glands to secrete aldosterone, which causes an increase in the reuptake of sodium by the kidneys, and because water
follows sodium, water retention increases as well. All of these processes work to restore BP and volume. The resultant increase in BP results in the suppression of renin release through negative feedback. Withsodium restriction, adrenal responses are enhanced and renal
vascular responses are reduced. Sodium loading has the opposite effect. [me:?????]
The range of plasma renin activities observed in hypertensive subjects is broader than
in normotensive individuals. Some patients have been defined as having low-renin and
others as having high-renin essential hypertension. Approximately 20% of patients with
hypertension have suppressed renin activity and higher plasma angiotensinogen levels.
This situation is more common in individuals of African descent than White patients.
There is historical basis for the assumption of a close relationship between salt intake
and BP. In the early years of the last century, no measures were available to decrease
BP other than a drastic reduction of dietary salt intake. The concept of dietary salt as
a major factor in reducing BP gained support from the work of Dahl in the 1950s
with a type of rat that was sensitive to salt. Since then an association between dietary
sodium and hypertension has been inferred from epidemiological studies, animal
experiments, and clinical trials. Data from population surveys are frequently cited as
primary evidence for a link between sodium intake and mean arterial pressure. The
highest incidence of hypertension occurs in Northern Japan where salt intake may be
as high as 20 g/day. A low incidence of hypertension has been found in societies with
low salt intake. There is substantial disagreement, however, as to how strong this
relationship is and whether the data support such an interpretation. This is because the
response of BP depends on variables such as genetic susceptibility, body mass,
mechanisms mediated by neuronal and hormonal system, and the kidneys. The most
comprehensive study on the role of sodium in hypertension was carried out by the
Intersalt Cooperative Research Group, based on 10,079 volunteers in 52 participating
centers in 32 countries.
The Intersaltfindings showed a weak positive association between urinary sodium
excretion, which reflects salt intake, and BP. Specifically, each 100 mmol sodium (6 g of
salt or 2.4 g sodium) per day increase in habitual intake was associated with a 2.2 mm Hg
increase in systolic BP. However, the association disappeared when four centers in
Brazil, Kenya, and New Guinea were excluded. The population in these specific centers
had unusually low salt intakes and BP and differed from the population of industrial
countries in many respects.
Evidence from randomized clinical trials has shown that a 4.9 mm Hg reduction in
systolic BP and a 2.6 mm Hg reduction in diastolic BP can be achieved with moderate
sodium restriction. However, the efficacy of sodium reduction in hypertensive patients
varies. Several clinical trials have shown significant BP lowering, but others have shown
minimal or no reduction. A recent meta-analysis of 56 trials in hypertensive and nor-motensive individuals demonstrated only a 3.7- and 1.0-mm Hg reduction in systolic and
diastolic BP, respectively, with sodium restriction. Compared with the overall population,
diabetics, African Americans, and elderly persons respond best to sodium restriction.
African Americans have a higher incidence of salt sensitivity that appears to be caused by
racially determined differences in renal handling of sodium.
Although the association between sodium intake and BP is weak, the evidence
suggests the general contention that habitual intake of salt is an important factor in the
occurrence of hypertension. Taste for salt is acquired and can be modified. On average,
Americans consume about 10 to 12 g salt/day, about 20 times the requirement of less than
0.5 g/day. Susceptibility to salt-induced hypertension (i.e., salt-sensitive individual)
cannot be identified easily for the entire population. Because there is no apparent risk
to mild sodium restriction, the most practical approach is to advise mild dietary sodium
restriction (up to 5 g salt/day), which can be achieved by eliminating all additions of salt
to food that is prepared normally.
Most studies assessing the role of salt on the hypertensive process have assumed that it is
the sodium ion that is important. However, some investigators have suggested that the
chloride ion may be equally important. This suggestion is based on the observation that
feeding chloride-free sodium salts to salt-sensitive hypertensive animal fails to increase
arterial pressure. In humans, BP is not increased by high dietary sodium intake with
anions other than chloride. These results suggest that chloride may also play a significant
role in the hypertensive effects observed with sodium chloride.
Potassium has been shown to be inversely related to BP. A moderate lowering of BP is
seen in humans by increasing potassium in the diet. Also, population surveys have
suggested that lower BPs exist in societies where dietary potassium intake is relatively
high. In some meta-analyses, dietary potassium supplementation of 50 to 120 mEq/day
reduced BP by about the same amount as salt reduction (by 6 mm Hg systolic and 3.4 mm
diastolic). Hypertensive patients should maintain adequate potassium intake (50 to 90
mmol/day) by adding fresh fruits and vegetables.
A number of observations in both experimental animals and humans suggests that there is
an inverse relationship between calcium intake and BP. In addition, analysis of the data
collected in a U.S. national survey shows that, as a group, hypertensive adults consume
less calcium per day than normotensive (573 vs. 897 mg). The association between
calcium intake and BP is supported by the findings that in communities with hard water,
there is lower cardiovascular mortality and BP. Calcium is the major determinant of
water hardness. Evidence from clinical trials on the antihypertensive effect of calcium
through dietary intake or supplements has been inconclusive. Although the effect of
calcium on BP is still controversial, the fact that a moderately high calcium intake (1.5 g/
day) probably also reduces the extent of age-related osteoporosis, indicating that it is
probably a useful adjunct.
Although an inverse association between magnesium intake and BP appears to exist, the
role of magnesium in hypertension is not well established. There are no compelling data
that recommend increased dietary intake of magnesium for lowering BP.
Preeclampsia is a pregnancy-specific condition, usually occurring after 20 weeks of
gestation, consisting of hypertension associated with edema, proteinuria, or both. Women
with preeclampsia may develop convulsions, a condition called eclampsia. Eclampsia has
a high mortality rate. Women with preeclampsia may unpredictably progress rapidly from
mild to severe preeclampsia and eclampsia within days and even hours. Magnesium
sulfate has been used for several years as an anticonvulsant to treat preeclampsia and
eclampsia, although its mode of action remains obscure. Magnesium sulfate is a potent
cerebral vasodilator and increases the synthesis of prostacyclin, an endothelial vaso-dilator. It also causes a dose-dependent decrease in systemic vascular resistance, which
may explain its transient hypotensive effect. Recently, in a large-scale clinical trial, which
included 10,000 women in 33 countries, magnesium sulfate given to pregnant women
with preeclampsia reduced the risk of eclampsia by 58% compared with a placebo.
Magnesium sulfate appears to have an important role in preventing as well as controlling
eclampsia, and the available evidence suggests that it is tolerably safe.
Calories Caloric intake may be the most important nutritional consideration in
the pathogenesis of hypertension. Epidemiological studies demonstrate a clear direct
relationship between an increase in body weight and BP. Overweight individuals have
increased incidence of hypertension and increased cardiovascular risk.Weight loss as small
as 10 lbs. of body weight in overweight patients may significantly lower BP. In overweight
hypertensive patients, the clinical data estimate that for every 1 kg of weight that is lost,
systolic and diastolic BP is lowered by 2.5 and 1.5 mm Hg, respectively. Weight is
potentially the most efficacious of all nonpharmacological measures to treat hypertension.
Weight loss also enhances the efficiency of antihypertensive drugs.
Alcohol Several large epidemiological studies have found that alcohol
consumption may increase BP. Whereas findings at moderate levels of alcohol intake
are inconsistent, heavy drinkers consistently exhibit higher BP than nondrinkers. Patients
who consume three to four drinks a day experience a 3 to 4 mm Hg increase in systolic
BP and a 1 to 2 mm Hg increase in diastolic BP over those who do not consume alcohol.
Alcohol consumption is not recommended for nondrinkers. For drinkers, intake should be
limited to 1 oz of alcohol (2 oz of 100 proof whiskey, 8 oz of wine, or 24 oz beer/day) in
most men and half that amount in most women.
Physical Activity Persons who are physically active have been shown to have
lower BPs than those who are less physically active. At least 30 min of moderate-intensity
physical activity such as brisk walking, bicycling, or yard work 3 times a week (preferably
once a day) can lower BP in both normotensive or hypertensive individuals. Regular
exercise can also promote weight loss and overall cardiovascularfitness.
Smoking Smoking is an independent risk factor for coronary heart disease.
Although smoking may not be related to chronic alterations in BP, it may interfere with
the response to certain antihypertensive drugs. In hypertensive patients cigarette smoking
cessation is probably the most significant and important modifiable risk factor.
DASH Combination Diet A few years back, a number of dietary approaches
were combined into a single intervention trial called Dietary Approaches to Stop
Hypertension (DASH). The participants were given a typical Western diet, a diet that
was rich in fruits and vegetables (to increase potassium and fiber), or fruit and
vegetable diet combined with low-fat dairy products (to increase calcium) coupled
with low saturated fat and total fat—DASH ‘‘combination’’ diet. The trial showed BP
reduction of 11.4/5.5 mm Hg in hypertensive persons receiving the DASH diet when
compared with hypertensive patients ingesting a so-called usual American diet, with
dietary sodium intake and body weight held constant. Furthermore, the DASH diet
produced reduction in BP of 3.5/2.1 mm Hg in subjects without hypertension. The
follow-up study to DASH (DASH-sodium) was recently reported. In this study, the
research group found that dietary sodium restriction on top of DASH combination diet
could be even more effective than DASH diet alone. Results of the DASH-sodium trial
confirm the earlier findings that the reduction of dietary sodium has a greater effect on
BP in African Americans than in Whites, in persons with hypertensive than in those
with high normal BP, and in women than in men. The DASH-sodium investigators
suggest that a reduction to about 3 g salt/day may be justified to all persons whether
they have hypertension or not. This will require cooperation from the food industry,
because much of the salt in the U.S. diet comes from prepared food, rather than salt
added in cooking.
The data from DASH studies provide strong support for a dietary approach to prevent
and control mild hypertension. Thus, in well-motivated patients, modifying the lifestyle
effectively lowers BP and may be more important than the initial choice of antihyperten-sive drugs. The same lifestyle-modification strategies that are effective in treating hyper-tensive patients may also be useful in the primary prevention of essential hypertension.
Lifestyle modifications for prevention and/or treatment of hypertension should
include: a) weight reduction, b) salt restriction, c) increased intake of fruits and vegetables
(potassium), d) increased intake of low-fat dairy products (calcium), e) moderation of
alcohol consumption, f) regular physical activity, and g) cessation of smoking. These are
all appropriate measures shown to produce significant reduction in BP while reducing