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Wellness and Rejuvenation Articles



  BONE MARROW (Bulalo)





Salt(both sea salt and rock salt) were well known to the ancient Greeks who noted that eating salty food affects basic body functions such as digestion and excretion (urine and stools). This led to salt being used medically. Even the healing methods of Hippocrates (460 BC) is made of frequent use of salt.  The Greeks, 2000 years ago, had already discovered topical use of salt for skin lesions, drinking salty or mineralized waters for digestive troubles and inhaling salt for respiratory diseases!
Paracelsus, a doctor and alchemist (1493–1541 A.D.) introduced an entirely new medical concept. He believed that external factors create disease and was the proponent of a chemically oriented medical system which is salt-based. To him salt is vital substance for human existence – "The human being must have salt, he cannot be without salt. Where there is no salt, nothing will remain, but everything will tend to rot." He prescribed salt water for the treatment of wounds and for use against intestinal worms. A hip bath in salt water was his superb remedy for skin diseases and itching – "This brine is better than all the health spas arising out of nature." He described the diuretic effect of salt consumption and recommended salt preparations of different strengths that were used for as remedies for different maladies, like for instance against constipation. He prescribed salt-based remedies as expectorant and a mixture of water, salt, and vinegar as an emetic. A mixture of two-thirds cow's milk and one-third salt-water, to be drank in the mornings, on an empty stomach was recommended as a cure for diseases of the spleen while a mixture of salt and honey applied topically is used to clean bad ulcers. Salt-water was also prescribed to be used externally against skin diseases and freckles.
According to Herman Aihara, the father of modern Macrobiotics, we carry our own inner sea within each of us in the form of a saline interstitial fluid which carries nutrients, messages, energy and even toxins to every part of our body, and also carries away the same toxic elements and more, as a result of the body’s daily metabolic process. An abundance of the ingredients in sea salt and salt mines are as synonymous with life today as they were a billion years ago. The limitation and even prohibition of salt intake will then be synonymous with birth defects, organ failure, decay, diseases, premature aging and death at a young age.  Regular table salt now a days, is mainly sodium chloride and not salt, devoid of the other ingredients of the original sea salt. With the advent of industrialization, our natural salt was "chemically cleaned" and reduced only to sodium and chloride. Most companies that produce salt, dry their salt in huge kilns with temperatures reaching 1200 degrees F, changing the salt's chemical structure, which in turn adversely affects the human body. 
Salt is an essential substance for the survival of all living creatures, particularly that of humans. Water and salt regulate the water content of the body. Water itself regulates the water content of the interior of the cell by working its way into all of the cells it reaches. It has to get there to cleanse and extract the toxic wastes of cell metabolisms. Salt forces some water to stay outside the cells and balances the amount of water that stays outside the cells. Good health depends on a most delicate balance between the water content of the interior and exterior of the cells, and this balance is achieved by salt – unrefined salt! 
When water is available to get inside the cells freely, it is first filtered from the exterior salty part of the cells and injected into interior of the cells that are being overworked despite their water shortage. This is the reason why in severe dehydration we develop an edema and retain water. The design of our bodies is such that the extent of the water outside the cells is expanded to have the extra water available for filtration and emergency injection into vital cells. The brain commands an increase in salt and water retention by the kidneys. This is how we get an edema when we don't drink enough water. 
The most natural way to treat edema is: (1) to put up the legs while lying down so that the collected water that pools mostly in the legs will be aided by the force of gravity to get the retained water onto the blood circulation; and (2) to drink enough water to be able to pass clear urine which will also pass out a lot of the salt that was held back. This way, we can get rid of edema fluid in the body; by drinking more water. Not taking diuretics, but more water!!  In cases where patient have an extensive edema and the heart is beginning to have irregular or very rapid beats with least effort, water intake should be increased gradually and spaced out, but not withheld from the body although salt intake should be limited for two or three days to let the body adjust from its overdrive mode to retain salt. Once the edema has cleared up, salt should not be withheld from the patient.
The following is an excerpt from the writing of Roy Moxham “Salt Starvation in British India – Consequences of High Salt Taxation in the Bengal Presidency, 1765 to 1878” with regards to our need for salt:
The Need for Salt  
In recent years there has been much publicity about the need to reduce salt consumption in societies where salt is added to many processed foods (Denton 1984, 584-7). [The health benefits of any general reduction in salt consumption are still being assessed, and contentious (Alderman, Cohen, and Madhavan 1998, 781-5). It has tended to be forgotten that some salt intake is absolutely necessary; that people need salt, sodium chloride, to survive:
The chemical requirements of the human body demand that the salt concentration in the blood be kept constant. If the body does not get enough salt, a hormonal mechanism compensates by reducing the excretion of salt in the urine and sweat. But it cannot reduce this output to zero. On a completely salt-free diet the body steadily loses small amounts of salt via the kidneys and sweat glands. It then attempts to adjust this by accelerating its secretion of water, so that the blood’s salt concentration can be maintained at the vital level. The result is a gradual desiccation of the body and finally death (Bloch 1963, 89).
Salt normally comprises about 1/400 of body weight (Marriott 1950, 6). In a 150-lb man this would be six ounces. In hot environments, especially when doing manual labour, people sweat heavily and lose considerable quantities of salt (Seavoy, Ronald E. 1986. Famine in peasant societies. New York; London: Greenwood). In tropical countries “salt deficiency is perhaps the commonest of all deficiency states” (Maccauly, Thomas. 1816. The Indian Trader’s Complete Guide. Calcutta).
The desire for salt is presumably in-built to ensure survival (Denton 1984, 604). Salt, up to a certain limit, is pleasurable to eat. Where it is plentiful, people eat more than they need – and if the body’s mechanism for secreting it is impaired, more than is desirable. Unlike hunger or thirst, however, the desire for salt does not increase when reserves are low (Marriott 1950, 22; Dill 1938, 82). For this reason people receiving too little salt will find food bland, but often not realise why they are feeling listless, or worse. Similarly, those whose salt reserves have been depleted by illness will experience no added desire to consume salt. Even doctors sometimes fail to recognise that patients are suffering from salt depletion. As Dr Marriott has written in Water and Salt Depletion: “their deaths are ascribed to ‘toxaemia’ or ‘uraemia’ or ‘circulatory failure’ when they have, in fact, died from simple lack of salt and could easily have been saved” (Marriott 1950, 3-5). Since he was writing of the situation in western hospitals in the middle of the twentieth century, it can be appreciated that deaths caused by salt depletion in eighteenth and nineteenth century Bengal would have been even less likely to be correctly attributed.
Illness is a major cause of salt depletion (Black 1953, 305-11). People who are already low on salt are particularly vulnerable. Large quantities of salt can be lost in fever-sweat, in vomit, and most of all in diarrhoea (Marriott 1950, 32-4). This should be continually replenished. Severe diarrhoeas can drain as much as 1 ¾ ounces of salt from the body in a single day, and thus quickly lead to severe dehydration. Without intravenous infusion of saline solution – not an option in the period being considered – recovery would have been unlikely (Souhami and Moxham 1990, 849). However, milder diarrhoeas, which as any traveller can relate are common in India, can over a few days also lead to severe depletion (Marriott 1950,33). Rehydration can only be effected with the intake of salt. Without this salt, however much water is drunk, recovery is impossible. Many diarrhoeas are self limiting – that is they terminate of their own accord, without drugs, after a few days. Rotavirus diarrhoea, which “is the commonest cause of diarrhoea in children up to 2 years old in the tropics” (Souhami and Moxham, 257), is an important example. It is essential to keep the body from dehydrating, and salt is necessary for this. The main ingredient of modern oral rehydration solutions is salt (Souhami and Moxham, 257).

Minimum Salt Requirement  
Exactly how much salt the inhabitants of the Bengal Presidency required to maintain health is difficult to estimate. Need would have depended on such variables as body weight, metabolism, the work environment, and local climate. Some people sweat more than others, and some have a higher concentration of salt in their sweat (Ladell, Waterlow, and Hudson 1944, 491-7, 527-531). Different researchers have come up with different minimum salt requirements (Robinson 1949, 218-31). Under constant conditions, some people seem able to reduce the loss of salt in their sweat to very low levels (Conn 1949, 373-93; Dahl 1958, 1152-7). Acclimatisation may reduce salt need (Collins 1963, 716-20). Some indigenous people in areas where salt has been scarce historically, seem to have a very low salt requirement (Denton 1984, 43-4). In contrast, for many others, living or working in hot environments, high levels of salt consumption seem to be essential (Ladell 1944, 492; McCance 1936a, 245-268; Haldane 1929, 469; Dill 1938, 83-4). As Knut Schmidt-Nielsen has pointed out, “sweat contains a variable amount of sodium chloride, but always enough to cause a considerable salt loss when sweat is produced in quantities. A relatively high intake of sodium chloride is therefore necessary” (Schmidt-Nielsen 1964, 21). It is difficult, he also observes, to collect sweat and other samples without altering the body’s environment, and impossible to give general rules for cutaneous salt loss, “but we can assume that, at high sweating rates, the total loss may easily run to 10 to 30 grammes [0.35 to 1.06 oz] of sodium chloride a day” (Bloch, M. R. 1963. “The Social Influence of Salt.” Scientific American 209: 89 – 98;  Brown, Judith Margaret. 1989. Gandhi: Prisoner of Hope. New Haven: Yale University Press;  Colebrooke, Henry Thomas. 1806. Remarks on the Husbandry and Internal Commerce of Bengal. Calcutta;  Collins, K. J. 1963. “Endocrine Control of Salt and Water in Hot Conditions.” Federation Proceedings 22: 716-20).
Salt depletion was reported among troops with heat exhaustion in Iraq (Ladell, Waterlow, and Hudson 1944). The daily hot station salt allowance was 21 grams, with another 10 grams estimated to be present in processed food, making a total of 31 grams, or 1.09 oz. Many other troops, it should be noted, found this intake adequate. In Iraq, a group of fit acclimatized men were subject to extensive tests in hot conditions. The average loss of salt in their sweat was calculated as 17.6 grams a day. There was also a loss of at least 3 grams a day in the urine, giving a total daily loss of 20.6 grams, or 0.73 oz.
Besides the avoidance of cholesterol-rich foods, one of the controversies in preventive medicine is, whether a general reduction in sodium intake can decrease the blood pressure of a population and thereby reduce cardiovascular mortality and morbidity. In recent years the debate continued and has even been extended by studies indicating that reducing sodium intake has effects on the hormone and lipid profile. Below is a Cochrane review abstract and plain language summary by Jürgens G and Graudal NA on the “Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterols, and triglyceride.” (Cochrane Database of Systematic Reviews 2004, Issue 1. Art. No.: CD004022. DOI: 10.1002/14651858.CD004022.pub2)

One of the controversies in preventive medicine is, whether a general reduction in sodium intake can decrease the blood pressure of a population and thereby reduce cardiovascular mortality and morbidity. In recent years the debate has been extended by studies indicating that reducing sodium intake has effects on the hormone and lipid profile.

To estimate the effects of low sodium versus high sodium intake on systolic and diastolic blood pressure (SBP and DBP), plasma or serum levels of renin, aldosterone, catecholamines, cholesterol and triglycerides.

Search strategy
"MEDLINE" and reference lists of relevant articles were searched from 1966 through December 2001.

Selection criteria
Studies randomising persons to low sodium and high sodium diets were included if they evaluated at least one of the above outcome parameters.

Data collection and analysis
Two authors independently extracted the data, which were analysed by means of Review Manager 4.1.

Main results
In 57 trials of mainly Caucasians with normal blood pressure, low sodium intake reduced SBP by -1.27 mm Hg (CI: -1.76; -0.77)(p<0.0001) and DBP by -0.54 mm Hg (CI: -0.94; -0.14) (p = 0.009) as compared to high sodium intake. In 58 trials of mainly Caucasians with elevated blood pressure, low sodium intake reduced SBP by -4.18 mm Hg (CI: -5.08; - 3.27) (p < 0.0001) and DBP by -1.98 mm Hg (CI: -2.46; -1.32) (p < 0.0001) as compared to high sodium intake. The median duration of the intervention was 8 days in the normal blood pressure trials (range 4-1100) and 28 days in the elevated blood pressure trials (range 4-365). Multiple regression analyses showed no independent effect of duration on the effect size. In 8 trials of blacks with normal or elevated blood pressure, low sodium intake reduced SBP by -6.44 mm Hg (CI: -9.13; -3.74) (p < 0.0001) and DBP by -1.98 mm Hg (CI: -4.75; 0.78) (p = 0.16) as compared to high sodium intake. The magnitude of blood pressure reduction was also greater in a single trial in Japanese patients. There was also a significant increase in plasma or serum renin, 304% (p < 0.0001), aldosterone, 322%, (p < 0.0001), noradrenaline, 30% (p < 0.0001), cholesterol, 5.4% (p < 0.0001) and LDL cholesterol, 4.6% (p < 0.004), and a borderline increase in adrenaline, 12% (p = 0.04) and triglyceride, 5.9% (p = 0.03) with low sodium intake as compared with high sodium intake.

Authors' conclusions
The magnitude of the effect in Caucasians with normal blood pressure does not warrant a general recommendation to reduce sodium intake. Reduced sodium intake in Caucasians with elevated blood pressure has a useful effect to reduce blood pressure in the short-term. The results suggest that the effect of low versus high sodium intake on blood pressure was greater in Black and Asian patients than in Caucasians. However, the number of studies in black (8) and Asian patients (1) was insufficient for different recommendations. Additional long-term trials of the effect of reduced dietary sodium intake on blood pressure, metabolic variables, morbidity and mortality are required to establish whether this is a useful prophylactic or treatment strategy.
Dr. Suzanne Oparil of the University of Alabama-Birmingham, past president of the American Heart Association, commented that the government may have been too quick to recommend that everyone cut back on salt as a solitary recommendation for the population for the prevention or the treatment of hypertension. An eight-year study of a New York City hypertensive population stratified for sodium intake levels found those on low-salt diets had more than four times as many heart attacks as those on normal-sodium diets – the exact opposite of what the “salt hypothesis” would have predicted (1995). Dr. Jeffrey R. Cutler documented no health outcomes benefits of lower-sodium diets in this study.

In a Joint Meeting with the Academy of Medical Sciences regarding “SALT AND DIET - TOO MUCH OR TOO LITTLE?” held at the Royal Society in April 24, 2001, the lectures referred to the evidence linking high blood pressure with the risk of coronary heart disease and strokes, and sodium intake with high blood pressure. They all noted that the picture was far from simple because as Professor Brown, in particular, drew attention to the fact that there exists a range of possible causes of high blood pressure, from genetic factors and to age-related differences in physiological responses. Professor Pickard on the other hand, also described some of the pitfalls in translating scientific evidence into practical dietary advice, and in particular the danger of focusing too much on a single factor and neglecting the importance of lifestyle. He argued that advice should be tailored to individual circumstances, not applied doctrinally to a heterogeneous population.