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marylin monroe
Showing posts with label low salt. Show all posts
Showing posts with label low salt. Show all posts

Low Sodium Intake for Athletes? Good for Your Health, or Ergolytic Bogus & Hazardous Bullshit? 30g/Day Sodium Loss in "Hard Sweating" Athletes Speak for Themselves

Salt reduction is for "hard-sweating" athletes not.
Whenever I am browsing the latest studies, I see at least one of those hilarious "salt kills" papers citing official recommendations to reduce sodium intake, in order to lower your risk for hypertension, diabetes, stroke and what not. So, if everyone recommends it and scientists write about, it must be true, right? Well, I guess after reading today's SuppVersity article, you may question the way the average Westerner thinks: What the government suggests you should do is not always good for you.

You, a decently lean & insulin sensitive individual who works out at least thrice a week, and someone who takes the stairs instead of the elevator at least every other day, may in fact put himself / herself at risk of hampering your workout performance and eventually even your health if you reduce your salt intake too much.
Normal salt and sodium bicarbonate are not bad for athletes:

The Hazards of Acidosis

Build Bigger Legs W/ Bicarbonate

HIIT it Hard W/ NaCHO3

BA + Bicarb are Synergists

Bicarb Buffers Creatine

Creatine + Baking Soda = 2x Win!
And even if you weren't lean and athletic, it's questionable, whether you'd benefit. The latest Cochraine Review of the effects of reductions in dietary salt intake on the prevention of cardiovascular disease, for example says:
"Despite collating more event data than previous systematic reviews of RCTs (665 deaths in some 6,250 participants) there is still insufficient power to exclude clinically important effects of reduced dietary salt on mortality or CVD morbidity. Our estimates of benefits from dietary salt restriction are consistent with the predicted small effects on clinical events attributable to the small BP reduction achieved." (Taylor. 2011)
And there is more, as I've previously reported the low chloride intake that comes hand in hand with a reduction in dietary salt intake has been associated with +21% increased mortality risk.
Figure 1: Associations of serum chloride, natrium, potassium and HCO2 with systolic and diastolic blood pressure as well as risk of all-cause, cardiovascular disease, ischemic heart disease, stroke and non-CVD mortality risk (McCallum. 2013)
Scientists from the Incorporated Administrative Agency of Health and Nutrition a Japanese government institution that claims to have made "numerous contributions to improve nutrition and dietary habit and to advance the knowledge of health and nutrition science for the public," (Institute Website), say: "Low dietary Na may [...] be a risk factor for maintaining positive balances of Ca and Mg" (Nishimuta. 2005).
Figure 2: If exercising individuals follow the WHO recommendation for salt intakes, they will put themselves at risk of having negative magnesium and calcium balances (based on data from Nishimuta. 2005)
Nishimuta et al. base their assessment on analyses of the content of calcium (Ca) and magnesium (Mg) in sweat during exercise, which is considerably higher during a relatively low intake of sodium (Na) of 100 mmol/d than with an intake of 170 mmol/d. As the scientists point out in their 2005 paper, this is the reason that their subjects developed a negative calcium and magnesium balance, when their sodium intakes were below 61mg and 63mg per day, respectively.
Salt Reduction Kills! New Studies Suggest Cutting Back Below 3-5g Could Do More Harm Than Good! Scientists Say: Minimum Intake is Physiologically Set (King. 2014) -- Too much sodium remains a valid concern, but are current targets too low for optimal health?

Healthy salt intake physiologically determined - don't restrict, if you crave.
New research moves beyond sodium’s effect on the surrogate marker of blood pressure to examine the relation between sodium intake and cardiovascular morbidity and mortality. Results show that sodium intakes both less than and greater than ~3000–5000 mg/d increase the risk of negative health outcomes. Additionally, newly compiled sodium intake data across populations show a uniformity that suggests that intake is physiologically set. Perhaps not coincidentally, the observed intakes fall within the range related to lowest risk.

These findings are highly relevant to current efforts to achieve low sodium intakes across populations, because the data suggest that the efforts will be unsuccessful for healthy people and may cause harm to vulnerable populations. Remaining mindful of risks associated with both excessive and inadequate intakes is imperative with all nutrients, and sodium is no exception. Avoiding too much, and too little, sodium may be the best advice for Americans.
At first it may sound strange that a reduced salt intake would increase the calcium and magnesium loss during exercise, but when you look at it from a biochemical point of view you will realize that in the absence of sodium, other cations (like magnesium or calcium) will have to bind to the lactic acid molecule to form lactate and postpone the development of subchronic metabolic acidosis (Robergs. 2004).

Cramps could be a sign of severe sodium deficiency

The role of sodium during exercise takes us to another thing you should consider before you start restricting your sodium intake. If there is any mineral that is associated with exercise related cramping, it's not, as many people believe, magnesium or potassium, it's sodium! In his 2007 paper in Sports Medicine, Eichner points out that (Eichner. 2007)...
  • heat cramping in industrial workers is alleviated by saline, and in a self-experiment, salt depletion provoked muscle cramping
  • in tennis and football alike, heat-crampers tend to be salty sweaters
  • triathletes who cramp may lose more salt during the race than peers who do not cramp
  • practical experience with therapy and prevention indicates that untravenous saline can reverse heat cramping, and
  • lastly, more salt in the diet and in sports drinks can help prevent heat cramping
All this evidence clearly indicates that the most prevalent reason for cramping is a lack / loss of sodium, not magnesium of which you've just learned that it's excreted in your sweet in significant amounts only if you don't consume enough salt.
Salt is essential and covering your needs will reduce, not increase water retention: Salt is 40% sodium and 60% chloride and both are important for athletes. Sodium is the major cation of the extracellular fluidandone of its primary functions is to maintain fluid equilibrium in the body. Sodium is a criticalnutrient in the maintenance of normal physiologic function and optimal exercise performance (Valentine. 2007). Although the typical American diet often contains more sodium than is needed, this may not be true for the athlete. Significant sodium and water losses can occur during exercise, exceeding the dietary intake and adversely affecting the fluid balance.

Very low sodium can impair glucose uptake (learn more)
In that, sodium is particularly important because sodium is needed in the rehydration process. The ingestion of plain water causes a rapid fallin plasma sodium concentration and osmolarity, leading to decreased aldosterone and vasopressin production; this increases urine output.... in the short run. Chronic low salt and high water intakes will yet have the opposite effects. As previously discussed, studies by Luther et al. (2011) even suggest that reducing sodium too much will not just increase water retention, the consequent increase in aldosterone may even impair your glucose sensitivity (see Figure on the left).

Acute high sodium intakes, on the other hand, have no effect on the water retention in healthy individuals, where an increase in serum renin (increases sodium excretion) and urinary aldosterone excretion (lowers water retention) nullified the effects of high salt intakes on body water - without the need to increase the potassium intake, by the way (Kirkendall. 1976).
In 2005 Stofan et al. published a paper that investigated the correlation between sodium loss during exercise and the occurrence of heat cramps in NCAA football players. What they found was that sweat potassium was similar between groups, but the sodium loss in the sweat of those NCAA players who had cramps was two times higher than it was in the controls (54.6 ± 16.2 vs. 25.3 ± 10.0 mmol/L). As Stofan et al. point out, "[l]arge acute sodium and fluid losses (in sweat) may thus be a characteristic of football players with a history of heat cramping." (Stofan. 2005)
Figure 3: Football players may be the best studies, but they are certainly not the only athletes who lose tons of salt during an intense training session (data in the figure based on (Fowkes Godek. 2010)
Only recently, E. Randy Eichner, who has long been arguing that "salt is simplest, most effective antidote" against heat cramps in athletes (Eichner. 1999), highlighted in an article in Current Sports Medicine Reports that the current momentum of those who argue that we all need to drastically reduce our sodium intake could hurt those who would do better if they even increased their intakes: Athletes (Eichner. 2014).
I am not giving a one size fits it all recipe, but what I can do is to cite the following considerations from Valentine (2007): "An athlete exercising 4 hours a day who has a sweat rate of 3.0L/h with a sweat sodium concentration of 80mmol/L will lose 12 L of fluid and 960 mmol of sodium in 1 day. This equates to over 22 g of sodium or over 55 g of salt." I guess that's impressive enough to make you reconsider any efforts to reduce sodium - specifically in view of the fact that chronic low sodium can cause, not prevent water retentions in athletes due to its effects on aldosterone. And as I have pointed out previously, this will even worsen whole body glucose uptake.
Bottom line: I am not sure if you consider the previously presented evidence convincing, but if you want to give salt a try, I'd suggest you simply follow your appetite. Studies like the one Wald & Lesham conducted in 2003 clearly suggest that your appetite for salty foods after a workout will increase, if your salt stores are depleted (Wald. 2003). In view of the fact that Walt & Lesham found that this increase is astonishingly proportional to the amount of salt their subjects lost during a 90 minute workout, the average gymrat (not the ultramarthoner, though) will just have to follow his appetite for salt to make sure that a lack of sodium won't impair his performance and / or overall health.

Against that background and in view of the large inter-individual differences (Bergeron. 2003), the differences between different types of sports, exercise intensities and, of course, the environmental conditions, I am not stupid enough to try and make a general recommendation other than the aforementioned advise to simply follow your bodies lead - trust it, it knows it, when he needs salt | Comment on Facebook!
References:
  • Bergeron, M. F. "Heat cramps: fluid and electrolyte challenges during tennis in the heat." Journal of science and medicine in sport 6.1 (2003): 19-27.
  • Eichner, E. R. "Heat cramps: salt is simplest, most effective antidote." Sports Med Digest 21.8 (1999): 88. 
  • Eichner, E. Randy. "The role of sodium in ‘heat cramping’." Sports Medicine 37.4-5 (2007): 368-370.
  • Eichner, E. Randy. "The Salt Paradox for Athletes." Current sports medicine reports 13.4 (2014): 197-198.
  • Fowkes Godek, Sandra, et al. "Sweat rates, sweat sodium concentrations, and sodium losses in 3 groups of professional football players." Journal of athletic training 45.4 (2010): 364. 
  • King, Janet C., and Kristin J. Reimers. "Beyond Blood Pressure: New Paradigms in Sodium Intake Reduction and Health Outcomes." Advances in Nutrition: An International Review Journal 5.5 (2014): 550-552.
  • Kirkendall, Walter M., et al. "The effect of dietary sodium chloride on blood pressure, body fluids, electrolytes, renal function, and serum lipids of normotensive man." J Lab Clin Med 87.3 (1976): 411-434.
  • Luther JM, Brown NJ. The renin-angiotensin-aldosterone system and glucose homeostasis. Trends Pharmacol Sci. 2011 Dec;32(12):734-9.
  • McCallum L, Jeemon P, Hastie CE, Patel RK, Williamson C, Redzuan AM, Dawson J, Sloan W, Muir S, Morrison D, McInnes GT, Freel EM, Walters M, Dominiczak AF, Sattar N, Padmanabhan S. Serum Chloride Is an Independent Predictor of Mortality in Hypertensive Patients. Hypertension. 2013 Aug 26.
  • Nishimuta, Mamoru, et al. "Positive correlation between dietary intake of sodium and balances of calcium and magnesium in young Japanese adults--low sodium intake is a risk factor for loss of calcium and magnesium--." Journal of nutritional science and vitaminology 51.4 (2005): 265-270.
  • Palacios, C., et al. "Sweat mineral loss from whole body, patch and arm bag in white and black girls." Nutrition Research 23.3 (2003): 401-411.
  • Stofan, John R., et al. "Sweat and sodium losses in NCAA football players: a precursor to heat cramps?." International journal of sport nutrition and exercise metabolism 15.6 (2005): 641.
  • Taylor, Rod S., et al. "Reduced dietary salt for the prevention of cardiovascular disease: a meta-analysis of randomized controlled trials (Cochrane review)." American journal of hypertension 24.8 (2011): 843-853. 
  • Valentine, Verle. "The importance of salt in the athlete’s diet." Current sports medicine reports 6.4 (2007): 237-240.
  • Wald, N., and M. Leshem. "Salt conditions a flavor preference or aversion after exercise depending on NaCl dose and sweat loss." Appetite 40.3 (2003): 277-284.

Chloride & Heart Disease - Overlooked & Misunderstood? Low Chloride Levels (Below 100meq/L) Are Associated W/ 20% Increased All Cause Mortality in Hypertensive Subjects

Salt is a four-letter-word today - literally and figuratively; and so would be NaCl, if it was a word and not the combination of the acronyms for natrium, or as Americans like to all it "sodium", and chloride and that despite the fact that low Cl may put your life at risk.
From my previous articles and Facebook posts on the questionable usefulness of dietary salt restriction you will remember that several epidemiological studies have already shown that a very low salt intake can be associated with increases in cardiovascular and all cause mortality. In NHANES I, for example, total sodium intake was inversely associated with all-cause (p=0·0069) and CVD mortality (Alderman. 1998)

You may also have heard me say and write that some scientists have suggested that we should better focus on the chloride rather than the sodium atom in NaCl, if we wanted to rid ourselves of the hypertension problem we are facing these days. Against that background, it sounds somewhat surprising that Linsay McCallum and her colleagues from the BHF Glasgow Cardiovascular Research Centre at the University of Glasgow found that low (not as other scientists suggested high) chloride levels are associated with a +20% increase in all-cause, cardiovascular and noncardiovascular mortality in patients with (pre-)hypertension.

Na(+) >135 & Cl(−) >100 = best survival rate

Among the study subjects, those with Na+ values of more than 135mEq/L, but lower Cl- levels of less than 100mEq/L in the blood, were the ones with the highest (+21%) mortality risk:
Figure 1: Associations of serum chloride, natrium, potassium and HCO2 with systolic and diastolic blood pressure as well as risk of all-cause, cardiovascular disease, ischemic heart disease, stroke and non-CVD mortality risk (McCallum. 2013)
If you take a closer look at the data in figure 1, you as a well-versed SuppVersity reader will albeit also recognize that the main, because only correlate of both systolic (that's the upper value that's supposed to be below 130) and diastolic (that's the lower level that's supposed to be around 80) is neither sodium, nor chloride. It's  HCO3 - or bicarbonate!
Did you know that soccer players lose ~3.4g of chloride (ca. 6g NaCl = salt) and less than 500mg of potassium during a 90 minute pre-season training session (Maughn. 2004)?
Not surprising for you, I know, but still worth highlighting, also because it has been a couple of weeks since I have been writing about the benefits of sodium-bicarbonate and maintaining a healthy acid-base ratio.

There are still many questions to be answered

Excerpt from the researchers' press release: "Sodium is cast as the villain for the central role it plays in increasing the risk of high blood pressure, with chloride little more than a silent extra in the background. [...] However, our study has put the spotlight on this under-studied chemical to reveal an association between low levels of chloride serum in the blood and a higher mortality rate, and surprisingly this is in the opposite direction to the risks associated with high sodium [...] It is likely that chloride plays an important part in the physiology of the body and we need to investigate this further." (co-author Jeemon Panniyammakal)
As Mc Callum et al. point out, there is still a lot of research to be done (including whether similar associations can be observed in hitherto healthy individuals), but as of know it does in fact appear as if ...
"[...s]erum Cl − is a marker of risk that appears to be dissociated from serum Na +and HCO 3 − levels. The underlying mechanism for this risk is unclear. A simple explanation would be that serum Cl − reflects abnormal physiology better than serum Na + , levels of which are perhaps more homeostatically regulated than Cl−" (McCallum. 2013)
Against that background, it is somehwat unsettling that serum chloride levels are not part of the current routine clinical screening (not even in patients with hypertension), so that levels in the "danger zone" between the current lower limit of 95 mEq/L and 100mEq/L could go unnoticed unnoticed for years.

So what do these findings tell us? While the study has been done in hypertensive individuals, I personally feel that the results still support what I have been telling you before about the salt requirements of people who belong to the minority of those who are not yet living on convenience and fast food and work out (and sweat) regularly.

In this regard, the study at hand provides further evidence that falling for the "salt" (=NaCl) restriction propaganda you are exposed to on a daily basis will do more harm than good to someone like you, whose "paleo-ish" diet may cover your bicarbonate needs, but may put you in a similar position as our ancestors, when it comes to the availability of dietary salt - a scarcity that is at the heart of the "salty tooth" we have conserved till today.
References:
  • Alderman MH, Cohen H, Madhavan S. Dietary sodium intake and mortality: the National Health and Nutrition Examination Survey (NHANES I). Lancet. 1998 Mar 14;351(9105):781-5.
  • Maughan RJ, Merson SJ, Broad NP, Shirreffs SM. Fluid and electrolyte intake and loss in elite soccer players during training. Int J Sport Nutr Exerc Metab. 2004 Jun;14(3):333-46.
  • McCallum L, Jeemon P, Hastie CE, Patel RK, Williamson C, Redzuan AM, Dawson J, Sloan W, Muir S, Morrison D, McInnes GT, Freel EM, Walters M, Dominiczak AF, Sattar N, Padmanabhan S. Serum Chloride Is an Independent Predictor of Mortality in Hypertensive Patients. Hypertension. 2013 Aug 26. [Epub ahead of print] 

No Pump + Insulin Resistant? Maybe It's Your Healthy Low Salt Diet. Low Sodium Induced Increase in Aldosterone Has Direct Negative Impact on GLUT4 Mediated Glucose Uptake

A single Triple Whopper or about six whole steaks, what do you chose to get >75% of the 2g/sodium per day the feds are telling you you should maximally consume on a daily basis?
Today I felt kind of bored with covering only the latest studies. So I dug up one from 1999 that deals with the effects of dietary salt restriction on endothelial vasodilation (increased blood flow in the arteries) and insulin sensitivity by Ross D. Feldman and Nancy D. Schmidt. Yeah, the study is 14 years old, but when you've read today's SuppVersity article you'll probably still have learned something new - at least about "common wisdom".

If you also listen to the SuppVersity Science Round-Up on the Super Human Radio Network, you should be aware that very different rules apply with respect to salt consumption for athletes and physical culturists on a whole foods diet and the average sedentary inhabitant of the Western obesity belt (check out past episodes of the Science Round-Up).
Suggested Read: On "Clean Eating" being a myth - "A Tale of Macro- & Micro-Nutrient Modifi-cations" | read more
Talking about the ScienceRound-Up: In today's installment Carl and I will be talking about the latest meta-analysis on dairy and diabetes risk and how it's possible that only low fat dairy reduces the risk of diabetes. We will discuss how this relates to the differences in the fatty acid composition of milk which in turn depend on the feed the animals receive and whether there is in fact so much estrogen in milk that it can delay menopause. From there we will segue right into a discussion of the latest study on statins showing that they make you fat and diabetic and tell you which of the statins does what. If all works well, we will close the show by addressing Sarah M. Davis' question about a recently published and heavily discussed article that's titled "Why 'Clean Eating' is a Myth" (read it). I mean, is it really? Turn in live! at 12PM EST
What some of you may yet still not have on their radar is the fat that the "common wisdom" about salt being the root cause of all evil does not even apply to the majority of those guys and girls of whom you would expect they may in fact see benefits from a reduced salt consumption.

"Salt is bad, no matter what!"

In fact, Feldman & Schmidt were able to show that the provision of either normal or salt reduced diets to subjects aged 25 to 40 year.
Figure 1: Increased aldosterone levels during salt restriction will not only make you retain salt, but also reduce glucose uptake (Luther. 2011; my edits)
"Subjects were given a standardized diet that contained 75 mmol/L sodium chloride, 60 mmol/L potassium, and 20 mmol/L calcium for 14 days. Diets contained 16% protein, 54% carbohydrate, and 35% fat. Caloric intake was 2800 kcal/day. Subjects were advised to drink approximately 2L of water/day.

To assess the effects of dietary salt restriction independent of other dietary changes, subjects were randomized on a double blind cross-over basis to a daily supplement of 16 tablets of slow release sodium (Novartis, Mississauga, Ontario; 10 mmol/L sodium chloride/tablet) or matching placebo. Each were administered for 7 days." (Feldmann. 1999)
All of the participants had normal blood glucose levels, and were free of other abnormalities on history and physical examination. They did not smoke and their blood pressures levels ranged from normotensive to high normal/borderline. So, what would happen to the poor wretches consuming the additional sodium chloride tablets? Common wisdom tells us, their blood pressure will increase and they will develop metabolic abnormalities. Truth is (I quote from the study; Feldmann. 1999, my emphases), almost the exact opposite happened:
  • Did you know? Aldosterone increases are caused by falling blood pressure, increased potassium levels, a higher blood acidity and decreased sodium concentrations in the blood trigger, decreases occur when your blood pressure drops, the potassium levels get low and/or the sodium levels are high.
    Dietary sodium restriction was associated with a significant decrease in 24-h urinary sodium excretion. However, blood pressure (based on the average 24-h automatic ambulatory measurements) was not significantly decreased with dietary salt restriction.
  • Moderate salt restriction was associated with a significant increase in plasma norepinephrine concentrations. Dietary salt restriction was associated with a significant decrease in the glucose-to-insulin ratio, suggesting increased systemic insulin resistance. This decrease was primarily accounted for by an increase in plasma insulin concentration.
At the same time the researchers observed a significantly reduced effect of the vasculature to the insulin-mediated increase in blood flow, of which Hornstra et al. have shown only recently that it correlates negatively with blood pressure in overweight, but insulin sensitive individuals and may be the reason why those people don't suffer from the usual obesity related increases in blood pressure as well as its cardiovascular and renal consequences (Hornstra . 2013).

Most of you will remember the recent post about the ability of salt to block the negative effects of high intensity exercise on the cellular integrity of your heart and kidneys don't you?
Bottom line: If you are working out and sweating, even if it's not like a pig, SALT is the last thing to fear. In fact you can even increase your heart disease risk due to the negative impact on blood lipids (+10% total +12% LDL cholesterol in salt-sensitive and unsensitive normotensive subjects; Ruppert. 1991).

Now it is important to point out that it is not clear whether these effects are transient and a response to the abrupt changes in dietary salt in take that are characteristic of these short term intervention studies.

I am certainly not recommending you copy the salt intake of the average junk-food fanatic!

But let's be realistic, here: How much salt do you actually consume on a daily basis if you follow my advice and leave as much of the processed pre-packaged junk as you can right in the supermarket!? This will leave you with actually having to put salt on your foods and there really is no good reason for the average physical culturist not to so in a way that it's tasty and supplies you with one of the most important minerals in your body.

Suggest figure: Only obese people have increased risk of CVD with increasing sodium consumption | check it out the SuppVersity Facebook Wall

Reference:
  • Egan BM, Lackland DT. Biochemical and metabolic effects of very-low-salt diets. Am J Med Sci. 2000 Oct;320(4):233-9. Review.
  • Hornstra JM, Serné EH, Eringa EC, Wijnker MC, de Boer MP, Yudkin JS, Smulders YM. Insulin's microvascular vasodilatory effects are inversely related to peripheral vascular resistance in overweight, but insulin-sensitive subjects. Obesity (Silver Spring). 2013 Mar 20.
  • Luther JM, Brown NJ. The renin-angiotensin-aldosterone system and glucose homeostasis. Trends Pharmacol Sci. 2011 Dec;32(12):734-9.
  • Ruppert M, Diehl J, Kolloch R, Overlack A, Kraft K, Göbel B, Hittel N, Stumpe KO. Short-term dietary sodium restriction increases serum lipids and insulin in salt-sensitive and salt-resistant normotensive adults. Klin Wochenschr. 1991;69 Suppl 25:51-7.