Intake of common salt is primarily related to the development of hypertension 9HT, which is a major risk factor for the development of heart attack called Coronary Heart Disease (CHD). For many diseases, the disease agent is still unidentified, e.g., CHD, Cancer, Peptic Ulcer, Mental illness, etc. In these conditions, the cause of the disease is generally discussed in terms of risk factors. Risk factors are ofter suggestive, but absolute proof of cause and effect between a risk factor and disease is usually lacking. The effect of risk factors is multiplicative rather than additive; thus, people with combination of risk factors (e.g., smoking, Hyper Tension, diabetes etc.) have the greater risk of developing CHD.
It is important to distinguish between relative risk and the absolute risk. Thus a person of 35 with high cholesterol level who smokes 40 cigarettes a day is relatively much more likely to die from CHD within the next decade tha a non-smoking woman of same age with normal cholesterol level.
But the absolute likelihood of his dying during this time is still small (high relative risk, low absolute risk). Even though a number of environmental factors have been implicated in the development of HT, salt intake has received the great attention. Even this factor illustrates the heterogeneous nature of the hypertensive populations, in that the BP in only 60% of hypertensives is responsible to the level of sodium intake. The cause of this special sensitivity to salt varies. In about half the patients, there is some primary pathology which accounts for the salt sensitivity.
In the remainder. the pathophysiology is still uncertain but postulated contributing factors include chloride intake, calcium intake, a generalized cellular membrane defect, insulin resistance and 'non-modulation' to rennin.
Most studies assessing the role of salt in HT 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 is based on the observation that feeding chloride free sodium salts to salt-sensitive hypertensive animals fails to increase arterial presure. A low calcium intake has also been asociated with an increase in blood pressire in epideemiological studies.
Since there is no easy test to distinguish salt responsive from salt resistant humans, the current emphasis on decreasing sodium intake in all humans makes some sense. However, the degree to which HT can be ameliorated or prevented (HT is a non-curable disease) will obviously vary with the salt sensitivity of the individual. Previously patients were instructed to curtail sodium intake drastically. But now investigators have suggested that this is not necessary. They base their conclusion on studies, which have documented that, mild sodium restriction significantly potentiates the efficacy of nearly all antihypertensive drugs.
Thus, by making it possible to control blood pressure with lower doses of drugs, sodium restriction leads to a reduction in side effects. In addition, it is quite proved that the level of sodium intake does influence the blood presure.