I know it’s taken for granted and is ingrained in the public mind as well as 99.9% of all doctors. But what is the proof of this relationship?
Except for a very small portion of patients with kidney problems, no.
And yes, most doctors know this. The thing is, patients like to “do something” when they’re ill, and letting people reduce their sodium intake is something they can do to take control of their diet. Furthermore, by reducing sodium, people tend to inadvertently make actually useful changes as a side effect, like choosing less processed foods which are high in sodium and more fresh vegetables low in sodium. Finally, reducing sodium is not going to hurt them. No one, simply no one, is actually *deficient *in sodium in our culture unless they’ve got some really rare disorder. Even “hyponatremia” (low serum sodium level) is not because of too little sodium, but because of too much water in the blood making the sodium hang out in the wrong place in the body.
So, it won’t hurt. It might, secondarily, lead people to make better food choices which will help. But no, for the vast majority of people, simply eating sodium isn’t going to cause hypertension.
http://www.health-report.co.uk/sodium_chloride_salt_myths2.html
http://www.ajcn.org/cgi/content/full/71/5/1013
While most people, 90% or more, are not salt sensitive and will not have their blood pressure increased by dietary sodium, if you are hypertensive, you’re probably in the group that is salt sensitive. If you don’t have hypertension, don’t worry about sodium, but if you do, cutting back couldn’t hurt.
I’m not so sure about reduced sodium being advisable for only those with kidney issues or salt-sensitivity. See this (my emphasis added):
Arterial hypertension and salt intake (2010)
From the abstract:
“High salt intake increases total peripheral vascular resistance, induces oxidative stress and inflammation, thus accelerating the atherosclerotic process. . . . Interventional studies have shown that salt intake reduction is associated with lower blood pressure and lower cardiovascular morbidity and mortality. Reducing salt intake in daily meals should be the main measure in primary prevention of cardiovascular and renal diseases, and it should be repeatedly emphasized not only to hypertensive patients, but also to the population at large.”
The effect of nutrition on blood pressure (2010)
From the abstract:
“. . . High sodium chloride intake strongly predisposes to hypertension. Increased alcohol consumption may acutely elevate blood pressure. High intakes of potassium, polyunsaturated fatty acids, and protein, along with exercise and possibly vitamin D, may reduce blood pressure. Less-conclusive studies suggest that amino acids, tea, green coffee bean extract, dark chocolate, and foods high in nitrates may reduce blood pressure. Short-term studies indicate that specialized diets may prevent or ameliorate mild hypertension; most notable are the Dietary Approaches to Stop Hypertension (DASH) diet, which is high in fruits, vegetables, and low-fat dairy products, and the DASH low-sodium diet. Long-term compliance to these diets remains a major concern.
Does the consumption of salt and food rich in sodium influence in the blood pressure of the infants? (2010)
From the abstract:
“ The medium consumption of salt found in this population was of 7.66 g (3098.81 mg or 133.86 mEq), which is above the recommended in the present literature. Canned food was related to be rich in sodium and to be associated with high levels of systolic blood pressure. In conclusion, as higher the salt consumption, higher the systolic blood pressure.”
Influence of Dietary Potassium and Sodium/Potassium Molar Ratios on the Development of Salt Hypertension (1972)
From the abstract:
“Among genetically hypertension-prone rats, dietary sodium (chloride) was demonstrably hypertensinogenic and potassium (chloride) antihypertensinogenic . . . At equivalent molar ratios, the respective effects of these two ions on blood pressure were dominated by that of sodium. It was concluded that the dietary Na/K molar ratio can be an important determinant for the severity, or even development, of salt-induced hypertension.”
Salt-sensitive hypertension is triggered by Ca2+ entry via Na+/Ca2+ exchanger type-1 in vascular smooth muscle (2004)
http://www.nature.com/nm/journal/v10/n11/abs/nm1118.html
From the abstract:
“Excessive salt intake is a major risk factor for hypertension.”
Effect of sodium loading/depletion on renal oxygenation in young normotensive and hypertensive men (2010)
From the abstract:
“These data demonstrate that dietary sodium intake influences renal tissue oxygenation, low sodium intake leading to an increased renal medullary oxygenation both in normotensive and young hypertensive subjects.”
Restriction of salt intake in the whole population promises great long-term benefits (2009)
From the abstract:
“Restricting salt intake not only leads to a decrease of blood pressure and a reduction in the incidence of arterial hypertension but also to a fall in cardiovascular morbidity and mortality. But high sodium intake is not only a risk factor for hypertension but also for cardiovascular diseases. “
The relationship between hypertension and salt intake in Turkish population (2010)
From the abstract:
“A positive linear correlation between salt intake and systolic and diastolic blood pressures was demonstrated (r = 0.450, p = 0.020; r = 0.406, p = 0.041; respectively), and each 100 mmol/day of salt intake resulted in 5.8 and 3.8 mmHg increase in systolic and diastolic blood pressures, respectively. Salt intake and systolic blood pressure was significantly correlated in normal weight individuals (r = 0.257, p < 0.01).”
Salt restriction for the prevention of cardiovascular disease (2010)
From the abstract:
“Restricting the dietary intake of sodium chloride is associated with a reduction of the arterial blood pressure by approximately 4/2 mm Hg in hypertensive patients and by approximately 1/0.6 mm Hg in normotensive persons. As the cardiovascular risk is known to rise steadily with systolic blood pressure values starting from 115 mm Hg, lowering the mean blood pressure of the general population by dietary salt restriction would seem to be a practicable form of primary prevention of cardiovascular disease.”
I find it hard to understand why it wouldn’t increase blood pressure. Your body likes to dilute its sodium. So if if you have a high sodium in your blood (where it must be if it is being filtered by the kidneys), the dilution is going increase the amount of blood produced, which, since it is at a fairly costant volume, will increase pressure.
The big thing is that reducing salt doesn’t help nearly so well, since the problem is usually the sodium content of other chemicals used in processing. Very little of the sodium in processed foods is used for adding saltiness.
One more thing–there are studies linking high sodium with lack of satiety. The one I found on Google says that salty foods actually have mild opiate properties.
You mean that reducing only the amount of salt that you consume in order to acheive a salty taste doesn’t work so well. But I think most people know that, if you need to reduce your salt intake, you need to reduce your consumption of food with a high salt content, whether or not it tastes salty to you.
Portwest, got anything about salt on hypotensive subjects? I’ve had to calm down both medical personnel and pharmacy techs when they saw my BP and claimed there was no way I could be upright with those numbers; the “quick and dirty” solution for when I’m feeling dizzy, as ordered by several doctors throughout the years is a handful of salty peanuts (if that doesn’t work, there are stronger measures, but that often makes the dizzy go away).
Barry Groves has this to say about salt and hypertension:
I’m loathe to enter this discussion (experience teaches me that some people seem to get very emotional about this subject), but let’s look at a bit of recent evidence.
In the British Medical Journal in 2009 a study examined data from over 177,000 patients collected in 13 separate studies. The results indicated that high salt intake increased the risk of stroke by more than 20 percent, and the risk of cardiovascular disease in general by about 15 percent. The authors noted that imprecision in determining salt intake likely makes these results an underestimate.
For those interested in computer simulations and projections, an article published this year in the New England Journal of Medicine concluded that:“Reducing dietary salt by 3 g per day is projected to reduce the annual number of new cases of coronary disease by 60,000 to 120,000, stroke by 32,000 to 66,000, and myocardial infarction by 54,000 to 99,000 and to reduce the annual number of deaths from any cause by 44,000 to 92,000. All segments of the population would benefit . . .” Note that 3 g of salt is a bit more than half a teaspoon - not very much at all. (“myocardial infarction” = heart attack)
There are approximately 4 zillion other studies purporting to demonstrate benefits of dietary salt restriction.
There is a lot of evidence. Find it by searching for “salt” and “hypertension.”
Part of the dilemma is the individual variation. Some folks can excrete excess salt and handle an acute or chronic salt load without problems. Others don’t.
Salt handling varies by individual and by large gene pools–i.e. different ethnic groups respond differently as an average for that group. See here, for instance. However the same article (and many others) shows benefit across all groups, so even though some groups are at higher risk for hypertension and even though that hypertension might be related to a higher prevalence of crappy salt-handling genes in that particular population, the reasonable thing is to recommend a more modest salt intake for everyone (recognizing that for some lucky individuals it won’t make a difference at all).
Nava, I did a quick search — note that I am not a doctor — as a matter of fact, I can hardly understand most of the abstract for the first item listed here below.
A search for “hypotension” and “sodium” didn’t appear to bring up anything relevant, but I used to have what my doctor labelled as “orthostatic hypotension” — where you get dizzy and nearly pass out if you rise too quickly from a reclining position — and so I used that term and found this:
Sodium paradoxically reduces the gastropressor response in patients with orthostatic hypotension (2006)
From the abstract:
Orthostatic hypotension (OH) can cause syncope that is difficult to treat. . . . OH patients are routinely advised to increase their sodium intake to augment their blood volume. . . . Both oral water and salt water increase BP in patients with OH.
Efficacy of high sodium intake in a boy with instantaneous orthostatic hypotension (2002)
We report the case of a 14-year-old boy with instantaneous orthostatic hypotension (INOH) with symptoms of orthostatic intolerance. . . . 48 hours after sodium intake, orthostatic tolerance was markedly improved with a concomitant increase in blood pressure in the orthostatic test. By measuring the patient’s body water before and after the high sodium intake, we were able to document the increase in plasma volume. We conclude that high sodium intake is an effective treatment for orthostatic hypotension in combination with vasoactive drugs.
Postural hypotension, hyponatremia, and salt and water intake: case reports (2004)
From the abstract:
In [quadriplegic patients with spinal cord injuries], severe [Postural Hypotension] PH was accompanied by avid conservation of water and impaired retention of sodium in the sitting position, as well as limited salt and water intake.
Dietary instead of pharmacological management to counter the adverse effects of physiological adaptations to space flight (2000)
Dietary sodium restriction has also been shown to improve calcium balance, bone mineralization, and the effectiveness of neurohumoral defenses against orthostatic hypotension. It is proposed that these simple alterations in the astronauts’ diets may be easily implemented to lessen the adverse effects of physiological adaptations to space flight, and to enhance or even replace prescribed pharmacological counter-measures.
In case you want to look further, all I did was go to PubMed and type in search terms such as “orthostatic hypotension” and “sodium”.
Hope that helps.
Reduce by 3g per day?
The current guidelines are to consume less than 1.5g / day - which shows just how much extra salt most people consume.
Does sweating via exercise help reduce salt levels?
IIRC, sweat is hypotonic, so if anything sweating would somewhat increase sodium concentration.
I have heard a general rule of thumb that if a food has more mgs of salt than calories, it has too much salt. That got me looking at labels. Turns out acceptable foods by that criterion are surprisingly difficult to find.
That’s why I’m on a celery and salted butter diet. (The latter: 100 calories per serving, 90 mg salt. Oh yeah!)
Sweat does have less salt than plasma, but exercise certainly can deplete your sodium levels. Here’sa relevant article
Thanks, on three counts:
for the specific info,
the info on where to look next time,
and because this provides evidence from the other end of the scale that yes, there appears to be a correlation between “salt intake” and “blood pressure”; enough to justify both telling people with high BP to lay off the salt and for us with low BP to claim our right to a salt shaker (“it’s what the doctor ordered”). People tend to focus on one end of the scale only, because it’s the end that has the reputation of being a killer.
You might be interested in the latest Cochrane Review, which completely debunks the studies you listed above.
http://onlinelibrary.wiley.com/o/cochrane/clsysrev/articles/CD009217/frame.html
My daughter has the same thing as you. After numerous specialists and a zillion tests, the final conclusion (or at least partially) was - intake salt before sporting events and if feeling faint, etc. It has made a huge difference.