Blood sodium intake

The use of the potassium salt of benzoic acid is relatively new. Concerns regarding sodium intake and its possible relationship to high blood pressure have caused some soft drink manufacturers to switch to potassium benzoate. 

High levels of sodium in the diet are linked to high blood pressure. Doctors often recommend that individuals who need to lower their blood pressure limit their sodium intake, but the sodium in table salt is a big part of most people s diets. They can turn to salt substitutes instead. 

In addition to excess sodium intake, abnormal renal sodium retention may be the primary event in the development of hypertension, and it includes abnormalities in the pressure-natriuresis mechanism. In hypertensive individuals, this theory proposes a shift in the control mechanism preventing the normalization of blood pressure. The mechanisms behind the resetting of the pressure-natriuresis curve may include afferent arteriolar vasoconstriction, decreased glomerular ultrafiltration, or an increase in tubular sodium reabsorption.4 Other theories supporting abnormal renal sodium retention suggest a congenital reduction in the number of nephrons, enhanced renin secretion from nephrons that are ischemic, or an acquired compensatory mechanism for renal sodium retention.9... 

Limit daily sodium intake to 2.4 grams (6 grams of salt) for blood pressure control. 

It is extremely important to select the correct type of nutrition when feeding severely malnourished individuals or patients. The provision of food can be dangerous unless carefully controlled as it can lead to what is known as the refeeding syndrome . This is characterised by a rapid increase in extracellular volume, due to increased sodium intake, and decreased blood levels of phosphate and potassium due to increased levels of insulin which stimulate the entry of these into muscle. (The latter changes are also seen when type 1 diabetic patients in a severe hyper-glycaemic state are treated with insulin.) A recommended refeeding schedule is as follows ... 

Regular exercise helps in lowering blood pressure especially in obese patients. A sedentary lifestyle is often implicated in cardiovascular disease, such as hypertension. Other non-pharmacological methods that help reduce blood pressure include decrease in sodium intake, moderation of alcohol consumption, avoiding stress and stopping smoking for smokers. Healthy food... 

In addition to noncompliance with medication, causes of failure to respond to drug therapy include excessive sodium intake and inadequate diuretic therapy with excessive blood volume, and drugs such as tricyclic antidepressants, nonsteroidal anti-inflammatory... 

Vollmer WM et al Effects of diet and sodium intake on blood pressure Subgroup analysis of the DASH-Sodium trial. Ann Intern Med 2001 135 1019. [PMID 11747380]... 

A relatively new and promising area of research concerns the role of inadequate dietary calcium in the development of essential hypertension or high blood pressure (Villar et al. 1986 Karanja and McCarron 1986 Resnick 1985 NDC 1984A.B McCarron 1985, 1983, 1982 McCarron et al. 1982). While most reports relating diet to hypertension have emphasized sodium, it appears that only a small proportion of the U.S. population is genetically sodium sensitive and that for the majority, dietary sodium intake has little effect on blood pressure. As discussed below, inadequate calcium intake, either alone or in combination with other factors, appears to predispose to high blood pressure by a mechanism(s) as yet unknown. 

Sodium, potassium, and chloride are electrolytes found in cow s milk for which the Food and Nutrition Board has estimated safe and adequate daily dietary intakes for infants, children and adolescents, and adults (NAS 1980A). Sodium functions in the body to maintain blood volume and cellular osmotic pressure and to transmit nerve impulses (NAS 1980A). The estimated safe and adequate daily dietary intake of sodium is 1100-3300 mg (2.8-8.4 g sodium chloride) for healthy adults (NAS 1980A). The American Medical Association, Council on Scientific Affairs (1979), suggested 4800 mg sodium per day as a tentative definition of moderation in sodium intake. 

Elevated blood pressure is usually caused by a combination of several abnormalities (multifactorial). Epidemiologic evidence points to genetic inheritance, psychological stress, and environmental and dietary factors (increased salt and decreased potassium or calcium intake) as perhaps contributing to the development of hypertension. Increase in blood pressure with aging does not occur in populations with low daily sodium intake. Patients with labile hypertension appear more likely than normal controls to have blood pressure elevations after salt loading. 

The importance of maintaining precise concentration gradients is highlighted by the severe effects of metabolic disorders involving alkali metal cations. For example, high sodium intake is linked intimately with the development of high blood pressure on the other hand, aged... 

Some patients with elevated blood pressure must restrict the sodium intake in their diet. Which antacid would you recommend for such a patient ... 

Reduction in salt intake reduces blood pressure in both normotensive and hypertensive individuals (He and MacGregor 2004) and there is evidence that adding salt to food increases the risk of cerebral hemorrhage (Jamrozik et al. 1994). In contrast, a high intake of potassium may reduce stroke risk (Khaw and Barrett-Connor 1987 Whelton et al. 1997). It remains unclear whether reducing sodium intake lowers stroke risk. 

The antisalt zealots like to point to the famous International Intersalt Study, the most comprehensive effort undertaken in this field thus far. Researchers looked at blood pressure and sodium intake in thirty-two countries. For the most part, the results revealed few links between sodium intake and hypertension in people around the world. That said, however, people in countries that had extremely high salt intake tended to have higher levels of blood pressure, while individuals with very little salt in their diets had lower levels. But these are the extremes. For most people in most countries, there was little association between salt and sodium consumption and blood pressure. And, paradoxically, people in Thailand who traditionally eat very salty diets had relatively low blood pressure levels. 

How can you tell whether restricting your sodium intake will lower your blood pressure Experiment. Try testing yourself. Measure your blood pressure for a few days in a row. Cut back on processed foods, don t add salt when cooking, and put the salt shaker away. Do that for a few weeks and retest your blood pressure. See whether you benefit. If so, terrific. If not, there are other ways of lowering blood pressure. 

We ve heard a lot about how cutting back on salt and sodium is essential to blood pressure control. But take that advice with the proverbial grain of salt Yes, very high salt and sodium intake can raise blood pressure. And extreme restriction can lower it. But this approach isn t practical, and many men and women are not sensitive to the effects of salt and sodium. By all means, we should practice moderation. But most of the sodium in the modern diet comes not from the salt shaker or the salt on the rim of a margarita glass but, rather, from processed and canned foods and from fast food. 

Hypertension is often treated with diuretics. Diuretics are drugs that promote the Joss of sodium from the body, though some diuretics can cause the loss of potassium, resulting in hypokalemia. The use of dietary supplements of K to correct this hypokalemia has been shown to be of benefit and to result in decreases in blood pressure. The best source of potassium is plant food, as is strikingly apparent from the data in Table IG.l however, the interest in nonfood supplements of potassium continues. One problem with potassium salts is that they taste bad and can produce nausea. Hence, there has been some interest in the manufacture of aesthetically acceptable forms of potassium salts. One form, a mixture of NaCl and KCl, is useful for those who feel compelled to add sodium chloride to their food. One study revealed that NaCI-KCl mixtures are accepted and their use can result in a reduction of sodium intake. The study, which involved normotensive subjects, did not lead to any consistent change in blood pressure (Mickeisen rt nI., 1977). 

The importance of volume control in patients with renal insufficiency extends beyond its effect on blood pressure. Accordingly, the addition of hydrochlorothiazide can overcome the blunting by a high sodium intake of the therapeutic efficacy of ACE inhibition on proteinuria (42). This presumably relates to volume-related activation of the renin-angiotensin system. 

Thiazide diuretics have additional actions that may further explain their antihypertensive effects. Thiazides mobilize sodium and water from arteriolar walls. This effect would lessen the amount of physical encroachment on the lumen of the vessel created by excessive accumulation of intracellular fluid. As the diameter of the lumen relaxes and increases, there is less resistance to the flow of blood, and peripheral vascular resistance drops further. High dietary sodium intake can blunt this effect, and a low salt intake can enhance this effect. Thiazides also are postulated to cause direct relaxation of... 

Functional renal insufficiency is manifested as increases in serum creatinine and blood urea nitrogen. As cardiac output and renal blood flow decline, renal perfusion is maintained by the vasoconstrictor effect of angiotensin II on the efferent arteriole. Patients most dependent on this system for maintenance of renal perfusion (and therefore most likely to develop functional renal insufficiency with ACE inhibitors) are those with severe heart failure, hypotension, hyponatremia, volume depletion, and concomitant use of NSAIDs. - Sodium depletion (usually secondary to diuretic therapy) is the most important factor in the development of functional renal insufficiency with ACE inhibitor therapy. Renal insufficiency therefore can be minimized in many cases by reduction in diuretic dosage or liberalization of sodium intake. In some patients, the serum creatinine concentration will return to baseline levels without a reduction in ACE inhibitor dose. Since renal dysfunction with ACE inhibitors is secondary to alterations in renal hemodynamics, it is almost always reversible on discontinuation of the drug. ... 

The ability of the kidney to adjust to abrupt changes in sodium intake is greatly diminished in patients with severe CKD. Sodium restriction beyond a no-added-salt diet should not be recommended except in the face of hypertension or edema. The kidney maintains the ability to lower urinary sodium content to essentially zero, but this can only be accomplished by very gradual sodium restriction over a period of several days. Hospitalized patients should not routinely be sodium restricted because they have adapted to their outpatient intake. Negative sodium balance and its resultant volume contraction can result in decreased perfusion to the kidney and a subsequent further decline in GFR. Saline-containing IV solutions should be used cautiously in patients with CKD because the kidney s ability to excrete a salt load is impaired and such patients are prone to volume overload. Sodium retention and volume expansion contribute to hypertension in many patients with severe CKD, and diuretic therapy or dialysis may be necessary for control of edema or blood pressure. 

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