Salt: Collateral Damage in the War on Fat
Caveman Doctor recently came upon a giant piece of pink rock salt while scaling the Himalayas. While trading salt normally gets him some decent meat for his family, the pink stuff will likely get him a prized cut of some fatty mammoth meat. Salt is a prized possession as it is well known to be vital for life and prized for its health benefits by fellow cavemen. While Caveman Doctor often gets his intake of salt from the blood present within his hunt, his coworkers have recently made him cut down on his blood intake, as it grosses them out. As a result he has had some serious cravings lately and has felt pretty run down, which always happens when he doesn’t get enough salt.
The Salty Truth
Salt has been a large presence within humanity from the dawn of time. Jesus referred to his followers as the salt of the earth, paying homage to the amount of salt in the caveman diet. Sabbath bread is dipped into salt to preserve the covenant with God in Judaism. Muhammad described four blessings sent down by God, iron, fire, water, and of course, salt. Salt has been an integral part of humanity since day one, and the health benefits have been known for centuries.
Fast-forwarding two million years or so from Caveman Doctor’s time, dietary restriction of salt has been a stalwart recommendation by health officials for several decades to aid in the prevention of high blood pressure and heart disease1. Salt’s increase in blood pressure is the commonly cited reason for recommending salt restriction, though we often hear of the overall negative health effects of salt. Interestingly, the Japanese, who are often cited as one of the healthiest cultures in the world (with the longest longevity), have the highest salt intake in the world.2 As is often the case in healthcare and dietary advice, there is a plethora of conflicting epidemiologic data, with some showing that a high salt intake, especially in the face of the carbohydrate-laden standard American diet, may have health detriment. Other data does not support such conclusions.
A large review of many trials (a meta-analysis) paid tribute to the recommendations of salt restriction, revealing a decrease in systolic blood pressure of 5 mmHg in those with high blood pressure and 2 mmHg in those with normal blood pressure. Considering a normal blood pressure is 120/80 (i.e. systolic 120 and diastolic 80), these changes are infinitesimally small. However, they were considered significant in this analysis due to the large number of individuals assessed (734 with elevated blood pressure and 2220 with normal blood pressure)3. The conclusion of this study was that salt reduction is an effective method of reducing blood pressure. Another study in patients with prehypertension revealed data showing a decrease in cardiovascular events (i.e. heart attacks, etc.) with salt restriction, however, there was no significant change in mortality.4
However, another extensive meta-analysis assessed 57 trials including 5,030 individuals, finding that a low-sodium diet reduces blood pressure by only 1%. The authors conclude that these findings do not support recommendations to consume less sodium5. In fact, the authors concluded that metabolic variables must be addressed to analyze the effects. The keywords here are metabolic variables…
Nevertheless, if changes in blood pressure alone, regardless of how minor, do not lead to changes in mortality, the question then becomes: “What is the point of changing a behavior if it doesn’t actually change your outcome?” Several studies observing salt intake and death have taken place to answer this question. Recently, European researchers have evaluated whether 24 hour urine sodium excretion predicts blood pressure and mortality.6 They used urinary secretion as a marker for sodium intake in the diet, which is considered the most accurate assessment of salt intake (i.e. the more salt consumed, the more excreted in the urine). The prospective study involved 3,681 participants, 2,096 of whom had normal blood pressure, for over 20 years. The researchers found that lower sodium consumption was associated with higher cardiovascular death. In other worlds, the less salt one ate the greater the chance of death from heart attacks, etc. While some studies may show a minor decrease in blood pressure, such changes are insignificant if death rate is increased. This study holds increased importance for those who do not have elevated blood pressure and are merely trying to construct the healthiest diet and lifestyle possible.
The National Health and Nutrition Examination Survey (NHANES) reported on three sequential studies analyzing sodium intake and mortality in thousands of individuals. However, the study evaluated sodium intake relying on dietary recall, which is fraught with error and bias and likely less accurate than measuring urinary levels. Regardless, these are some of the largest studies undertaken that assess salt intake and mortality. The results were as follows:
- NHANES I revealed a decrease in cardiovascular and all-cause mortality (i.e. dying from any cause) with increased salt consumption. 7
- NHANES II revealed similar findings that increased salt consumption led to a decrease in cardiovascular disease mortality, with the highest risk in those that limited their sodium to under 2300mg per day. 8
- NHANES III showed similar, but statistically non-significant increases in mortality with lower sodium consumption.9
Even recent data in patients with congestive heart failure, who often experience fluid overload and edema, have shown that a reduced salt diet results in increased hospitalizations and worse clinical outcomes.10 Patients with diabetes may fare no different as studies have revealed that diabetic patients with decreased sodium consumption experience increased all-cause and cardiovascular mortality.11 However, when many initial endpoints were removed from the NHANES I study, it was found that obese patients were found to have increased mortality with salt intake. 12 However, such statistical methods (and post hoc analysis) have been met with controversy.13 Whether this result was from salt intake, or the fact that the obese patients may have been less active with a poorer diet is difficult to assess due to the epidemiologic nature of this study.
Regardless, the topic of salt restriction remains one of stark controversy. While epidemiologic data shows salt intake may raise blood pressure, many studies have revealed lowering salt intake to have the opposite effect when it comes to death.
The Physiologic Function of Salt:
Sodium from salt is a vital nutrient within the diet. Table salt is 40% sodium and 60% chloride. Sodium helps the body maintain cellular water balance, blood volume, and pH. It is also vital in neuron (nerve cell) function by allowing them to send impulses from the brain to the muscles causing them to contract. When blood pressure or blood concentration of sodium decreases, the renin-angiotensin system causes the kidney to absorb more sodium, decreasing the amount lost in the urine. As a result, low dietary sodium causes our body to release several potentially harmful hormones like renin, aldosterone, and noradrenaline to compensate.14 The increase in sodium pulls water with it, thus supporting the circulatory system. This is also why increased salt intake can often cause swelling in individuals who are sensitive.
Sodium supports the circulatory system, and animal studies show that a low-salt diet leads to higher susceptibility of cardiovascular collapse and impaired ability to adjust to stress.15 In other words, sodium pulls water with it into our blood, allowing the circulatory system to function to its fullest while keeping fluid within the body. Dietary sodium largely comes into play, especially in those who exercise often and lose a significant amount of sodium through perspiration. Along these lines, studies show that vigorous exercise for one hour in the heat can result in salt loss that exceeds the recommended daily allowance16. Such data would favor much higher intake of sodium in athletes or those that work out vigorously or frequently.
What Causes the Kidneys to Retain Salt?
The issue of sodium within your body is not merely a factor of salt intake. As discussed above, the renal-angiotensin system regulates the reabsorption and excretion of salt based on the commands it receives from the body. Our sodium levels are based on a delicate interplay between salt intake in our diet, salt lost through our kidneys and in the urine (as well as sodium lost in sweat and the GI tract), and hormones acting on the kidney.
Much like with calcium and many other minerals and electrolytes in our diet, the kidney is constantly hard at work filtering our blood and keeping some substances in (reabsorbing them) and pushing others out with the urine. Viewing sodium as an in versus out equation, like calcium (and bone health)and calories, is shortsighted and incorrect. Insulin, the hormone within our body that is secreted by the pancreas to lower the blood sugar after a carbohydrate-rich meal, actually directly acts on the kidney telling it to reabsorb sodium.17 In fact, giving both normal patients and diabetics insulin almost immediately signals to the kidneys to stop secreting sodium. Interestingly, after prolonged fasting, carbohydrate intake leads to both an increase in serum glucose and insulin, and significant retention of sodium within the kidney.18 Once again insulin takes the blame, from obesity, to cancer, to sodium retention in the kidneys and it would appear that methods to minimize insulin levels will benefit health. It would appear that salt is merely collateral damage, as basing a diet on a food that causes the kidneys to retain sodium, falsely puts the blame on dietary sodium.
This is likely why changing to a low-carbohydrate diet often results in initial fluid loss. When insulin drops, it allows the kidneys to stop retaining as much sodium, thus explaining the initial water loss so often described in low-carb diets.
Not only do increased carbohydrates in the diet cause elevated levels of insulin and sodium retention, but studies show that low-salt diets actually inhibit the ability of insulin to lower our blood glucose and can actually lead to insulin resistance.19 In other words, a low-salt diet may leave the body in a physiologic state resembling that of a diabetic. Animal studies confirm this, revealing that low salt diets in rats leads to increased adiposity and insulin resistance.20 Even a moderate reduction of salt can negatively impact insulin sensitivity and the authors of one study stated that it “aggravates both systemic and vascular insulin resistance.”21 Perhaps this is a reason why low salt intake was associated with death in diabetic patients.11 While decreased salt intake has been shown to raise serum glucose levels, it has also been shown to activate our sympathetic nervous system13 (the fight or flight response), which of course will raise levels of chronic stress. Ironically, reducing salt has also been shown to raise LDL and overall cholesterol14, going directly against the goal of recommendations by the conventional wisdom to lower cholesterol.
Studies of a High-Fat, Low-Carb Diet:
In a study comparing a low-fat, calorie-reduced diet versus a low-carbohydrate diet with no restriction of calories, participants on the low-carbohydrate study were instructed to drink bouillon dissolved in water 2-3 times per day22, which roughly correlates to 1-2 grams of sodium. Knowing that a low-carbohydrate diet will decrease insulin significantly, which will lead to loss of sodium from the kidneys, the authors prophylactically raised the participants’ salt intake. How did they fare drinking this salty solution up to 3 times a day? Systolic blood pressure dropped by 17 points, while diastolic dropped by 8.
How can this be?
Partly was the improved metabolic status on a low-carb diet. The weight loss, decreased blood glucose, and decreased insulin levels likely lead to a drop in blood pressure. However, once again, we have to ask ourselves: Why would Mother Nature make the foods we have consumed for millions of years, including plenty of fat, moderate protein, low carbs, and salt, increase our blood pressure? Why would she pull such a cruel joke?
It is reassuring that Nature’s construction was correct, and when the experts like Dr. Westman put people on diets similar to the one she cooked up for us (including salt) high blood pressure and most other diseases improve.
Are Paleo, Low-Carb and Low-Salt Compatible?
From its onset Paleo has preached against salt intake. However, Paleo means switching to whole foods and eliminating processed foods. As a result, salt consumption drops drastically, as processed foods contain massive amounts of sodium. When we switch to lower amounts of dietary carbohydrates and drop grains and sugar, our serum insulin levels naturally drop. As a result, the kidney starts to secrete more sodium into the urine. This is often why Paleo advocates so often feel run down when they switch to a low-carb lifestyle. Finally, Paleo generally involves periodic, intense exercise, whether it is sprinting, crossfit, or other intense activity. This type of exercise often involves significant fluid and sodium loss, further adding to the net negative balance. Drinking excess fluid to replace the lost volume in sweat, further dilutes our salt balance resulting in hyponatremia (low blood sodium levels)23, which is often symptomatic.
We naturally must increase our salt consumption, or before long we will find ourselves in a negative balance of a substance that is vital for life and health. This is often described as “hitting the wall” in the Paleo world and more often confused with a need to carb-load, or worse yet, with thyroid dysfunction. Very often, these problems disappear with the addition of salt to the diet.
In fact thinking back to the past 2.5 million years, we ate mostly wild game, often raw and dripping with blood, including eating and drinking animal blood. The organs and blood contain high amounts of sodium, not present in the cooked muscle meat. It’s no surprise that we would need to supplement our modern caveman diet with sodium as the most salt-rich parts of the animal are often no longer consumed as we have in the past.
The Maasai eat around 3g of salt per day24, mostly from their intake of whole blood, and have very low blood pressure. Americans eat about 3.4g of sodium per day mostly in the form of processed table salt, which correlates to roughly double in salt25. However, the fact that the Maasai eat a diet of animal meat, blood, and milk (often fermented breaking down the milk sugar) and therefore a small fraction of the insulin-stimulating carbohydrates that dominate most American’s diets. As a result, they have less insulin signaling to their kidneys to retain sodium. The American Heart Association recommends limiting sodium to less than 1,500mg per day (roughly 4 g of salt), though evidence on this approach and the health benefits and safety has been called “weak, heterogeneous, inconclusive and inconsistent” by critics.26
What’s a salt loving modern caveman to do?
Final Thoughts: Is All Salt the Same?
No! The white salt that we commonly encounter is refined and processed removing trace minerals. Much like vegetable oils, refining is generally an unhealthy step in food preparation. After this salt is refined, several chemicals are added, including aluminum, ammonium, and ferrocyanide to minimize caking together of the salt and extend shelf life. The resulting compound is basically sodium, along with several chemicals and often iodine. Himalayan and natural sea salt are markedly different as they have all of their minerals if unrefined. They are not comparable to the factory made, chemically-laden white salt. These salts also have trace minerals, which is important as some studies have suggested that increasing salt intake that contains more potassium and magnesium may actually lower blood pressure.27 All studies generally look at consumption of salt in the form of processed table salt, or worse off, processed foods full of processed salt. If these studies assessed mineral-dense salt, a different picture would likely be painted.
- Reducing sodium in the diet does little to effect blood pressure.
- Reducing sodium in the diet may increase cardiovascular and all-cause mortality, especially in non-overweight healthy individuals.
- Low-salt diets may lead to decreased insulin sensitivity and increased adiposity.
- A low-carbohydrate lifestyle results in less circulating insulin, causing the kidneys to secrete more sodium in the urine.
- Strenuous exercise can result in loss of sodium greater than the recommended daily allowance.
- Those who exercise often and follow a low-carbohydrate lifestyle may want to think twice about reducing their sodium intake.
- Those who follow a very low-carbohydrate or Paleo diet may want to consider salt supplementation, especially if they are “hitting the wall”.
- Refined table salt is markedly inferior to mineral-rich Himalayan salt or natural sea salt.
Should we eat less salt? Maybe if we are on the standard American high-carbohydrate diet. But even then it likely doesn’t matter. If we are following a healthy low-carbohydrate diet that favors nutrient and calorically-dense foods, we not only may want to avoid limiting our salt, but actually increase our salt intake, especially around workout time. Also, once again we find that factory produced and processed foods pale in comparison to that with which Nature provides. Salt in its natural form provides a significant amount of minerals and has been shown to provide many health benefits. To purposely reduce it would be going against Nature’s design.
While we are at it, should we eat less fat and more carbohydrates? Sure, if we want our kidneys to retain more salt. This gives us something else to blame besides the dietary recommendations that are causing the problem in the first place. This merely leaves salt as collateral damage in the war against fat.
1. Chobanian AV, Bakris GL, Black HR, et al: Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 42:1206-1252, 2003, http://hyper.ahajournals.org/content/42/6/1206.abstract
2. Heaney RP: Role of Dietary Sodium in Osteoporosis. Journal of the American College of Nutrition 25:271S-276S, 2006, http://www.jacn.org/content/25/suppl_3/271S.abstract
3. He FJ, MacGregor GA: Effect of longer-term modest salt reduction on blood pressure. Cochrane database of systematic reviews:CD004937, 2004, http://www.ncbi.nlm.nih.gov/pubmed/15266549
4. Cook NR, Cutler JA, Obarzanek E, et al: Long term effects of dietary sodium reduction on cardiovascular disease outcomes: observational follow-up of the trials of hypertension prevention (TOHP). BMJ 334:885, 2007,
5. Jurgens G, Graudal NA: Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterols, and triglyceride. Cochrane database of systematic reviews:CD004022, 2004, http://www.ncbi.nlm.nih.gov/pubmed/14974053
6. Stolarz-Skrzypek K KTTL, et al.: FAtal and nonfatal outcomes, incidence of hypertension, and blood pressure changes in relation to urinary sodium excretion. JAMA: The Journal of the American Medical Association 305:1777-1785, 2011, http://dx.doi.org/10.1001/jama.2011.574
7. Alderman MH, Cohen H, Madhavan S: Dietary sodium intake and mortality: the National Health and Nutrition Examination Survey (NHANES I). Lancet 351:781-5, 1998, http://www.ncbi.nlm.nih.gov/pubmed/9519949
8. Cohen HW, Hailpern SM, Fang J, et al: Sodium intake and mortality in the NHANES II follow-up study. The American journal of medicine 119:275 e7-14, 2006, http://www.ncbi.nlm.nih.gov/pubmed/16490476
9. Cohen HW, Hailpern SM, Alderman MH: Sodium intake and mortality follow-up in the Third National Health and Nutrition Examination Survey (NHANES III). Journal of general internal medicine 23:1297-302, 2008, http://www.ncbi.nlm.nih.gov/pubmed/18465175
10. Paterna S, Gaspare P, Fasullo S, et al: Normal-sodium diet compared with low-sodium diet in compensated congestive heart failure: is sodium an old enemy or a new friend? Clinical science 114:221-30, 2008, http://www.ncbi.nlm.nih.gov/pubmed/17688420
11. Ekinci EI, Clarke S, Thomas MC, et al: Dietary Salt Intake and Mortality in Patients With Type 2 Diabetes. Diabetes Care 34:703-709, 2011, http://care.diabetesjournals.org/content/34/3/703.abstract
12. He J OLGVSBLALCWPK: DIetary sodium intake and subsequent risk of cardiovascular disease in overweight adults. JAMA: The Journal of the American Medical Association 282:2027-2034, 1999, http://dx.doi.org/10.1001/jama.282.21.2027
13. Alderman MH: Salt, Blood Pressure, and Human Health. Hypertension 36:890-893, 2000, http://hyper.ahajournals.org/content/36/5/890.abstract
14. Graudal Na GAMGP: Effects of sodium restriction on blood pressure, renin, aldosterone, catecholamines, cholesterols, and triglyceride: A meta-analysis. JAMA: The Journal of the American Medical Association 279:1383-1391, 1998, http://dx.doi.org/10.1001/jama.279.17.1383
15. Folkow B: Critical review of studies on salt and hypertension. Clinical and experimental hypertension. Part A, Theory and practice 14:1-14, 1992, http://www.ncbi.nlm.nih.gov/pubmed/1541030
16. Sharp RL: Role of Sodium in Fluid Homeostasis with Exercise. Journal of the American College of Nutrition 25:231S-239S, 2006, http://www.jacn.org/content/25/suppl_3/231S.abstract
17. Skøtt P, Hother-Nielsen O, Bruun N, et al: Effects of insulin on kidney function and sodium excretion in healthy subjects. Diabetologia 32:694-699, 1989, http://dx.doi.org/10.1007/BF00274259
18. DeFronzo RA: The effect of insulin on renal sodium metabolism. A review with clinical implications. Diabetologia 21:165-71, 1981, http://www.ncbi.nlm.nih.gov/pubmed/7028550
19. Garg R, Williams GH, Hurwitz S, et al: Low-salt diet increases insulin resistance in healthy subjects. Metabolism 60:965-968, 2011, http://www.sciencedirect.com/science/article/pii/S002604951000329X
20. Prada PO, Coelho MS, Zecchin HG, et al: Low salt intake modulates insulin signaling, JNK activity and IRS-1ser307 phosphorylation in rat tissues. Journal of Endocrinology 185:429-437, 2005, http://joe.endocrinology-journals.org/content/185/3/429.abstract
21. Feldman RD, Schmidt ND: Moderate dietary salt restriction increases vascular and systemic insulin resistance. American journal of hypertension 12:643-7, 1999, http://www.ncbi.nlm.nih.gov/pubmed/10371376
22. Westman EC, Yancy WS, Jr., Mavropoulos JC, et al: The effect of a low-carbohydrate, ketogenic diet versus a low-glycemic index diet on glycemic control in type 2 diabetes mellitus. Nutr Metab (Lond) 5:36, 2008, http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=19099589
23. Noakes TD: The hyponatremia of exercise. International journal of sport nutrition 2:205-28, 1992, http://www.ncbi.nlm.nih.gov/pubmed/1299494
24. Mtabaji JP, Nara Y, Moriguchi Y, et al: Diet and Hypertension in Tanzania. Journal of Cardiovascular Pharmacology 16:S3-S5, 1990, http://journals.lww.com/cardiovascularpharm/Fulltext/1990/06168/Diet_and_Hypertension_in_Tanzania.4.aspx
25. Americans Consume Too Much Sodium (Salt) http://www.cdc.gov/features/dssodium/, 2011
26. Logan AG: Dietary Sodium Intake and Its Relation to Human Health: A Summary of the Evidence. Journal of the American College of Nutrition 25:165-169, 2006, http://www.jacn.org/content/25/3/165.short
27. Geleijnse JM, Witteman JCM, Bak AAA, et al: Reduction in blood pressure with a low sodium, high potassium, high magnesium salt in older subjects with mild to moderate hypertension. BMJ 309:436-440, 1994
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