Salt May Not Be As Bad As They Say…Or Is It?

regulate salt intakeUsing a sufficiently large set of data, the Cochrane Library, a highly respected international collaboration of evidence-based medicine reviews, was able to draw startling conclusions about the association of salt intake with high blood pressure and cardiovascular risks. After looking at almost 6,500 people, comprising several well-conducted studies, Cochrane found that, for CVD mortality and all-cause mortality in persons with normal or elevated blood pressure, there is no strong evidence for restricting salt intake.

The American Journal of Hypertension reported Cochrane’s findings in July of 2011, stating that, “Although meta-analyses of randomized controlled trials of salt reduction report a reduction in the level of blood pressure, the effect of reduced dietary salt on cardiovascular disease events remains unclear.”  However, it was also found that salt reduction “was associated with reductions in urinary salt excretion…and reductions in systolic blood pressure between 1 and 4 mm Hg.”  Additionally, relative risk did not show evidence of any effect of salt reduction on cardiovascular episodes in people with normal BP, but noted that, “salt restriction increased the risk of all-cause mortality in those with heart failure.”

The Cochrane reviewers admitted that, despite collecting more data than ever before, there is still no definitive proof that salt reduction will have beneficial effects on all-cause mortality or on the risk of cardiovascular disease.  At the same time, Katherine Jenner, campaign director of the Consensus Action on Salt and Health (CASH), disputes these findings, adding that there are no trials to account for other chronic exposures, such as smoking and being overweight, and eating too few fruits and vegetables.  She stated strongly that it would be unethical to expose humans to a long period of high salt intake merely to satisfy the curiosity of researchers.  To add to this confusion, the Cochrane leader, Rod Taylor, said that large benefits were not seen because salt reduction was sufficiently minimal as to cloud significant effects on BP and heart disease.  Huh?

Prior to the development of refrigeration, salt was necessary for the preservation of food.  Milk was made into cheese using salt, and fish was salted to keep it for long periods.  Eating as we do, many of us accumulate more salt and water than the kidneys can handle.  Some folks have genes that control cellular channels, enzymes and hormones at various places in the kidneys, conserving salt to enable adaptation to hot and dry climates.  If water and salt were scarce, as would often be the case in mankind’s early days, the kidney would conserve salt to hold the water that would become sweat, which would evaporate from the skin and cool the body enough to keep temperature stable.  Without sweat the body would overheat.  These genes that were important to early mankind never stopped doing their job, regardless of climate.  About 20% of us will continue to reabsorb salt as long as excessive amounts are ingested.  Salt retains water through osmosis.  It also promotes thirst.  Why else would there be a bowl of salty pretzels or nuts on the bar?

Excess salt keeps circulatory volume higher than it needs to be, putting extra fluid pressure on blood vessel walls.  The walls react to this stress by getting thicker and narrower, leaving less space for the fluid already cramped inside, thereby raising resistance to flow and increasing the pressure needed to get it moving.  Because the heart has to pump against greater pressure, it can grow larger, just like the skeletal muscles subjected to heavy pressure from lifting weights.  Whatever excess pressure is exerted on the kidneys causes those organs to compromise their delicate filtration system, leading to disease.

Beyond reducing blood pressure, a low sodium intake improves the dilation of the blood vessels and consequently improves heart function.  Dilation of blood vessels is considerably greater in a low-sodium environment. (Dickinson. 2009)  Systolic pressure will drop, as well.

At a time when the U.S. advocates lowering salt intake from 2,300 mg a day to 1,500 mg a day, the Europeans are happy to see their intake lowered to 5,000 mg a day.  Considering that the typical European intake seems to be around 9,000 to 12,000 mg a day, that is quite a change.  Naturally, they would see a drop in blood pressure.  (He and Burnier. 2011)  Salt sensitivity is subjective, though, and not everyone would have a BP spike because of intake.

But now there might just be way to help control salt-induced blood pressure elevation. Researchers at Loyola University, under the direction of Dr. Paul Whelton, learned that the ratio of sodium to potassium is a more important indicator of cardiovascular problems than either salt or potassium alone.  (Whelton and Cook. 2009)  Little studied, potassium is the element on the other side of the cell membrane from sodium. Most of us are potassium deficient, consuming far less than the 4,700 mg a day that is suggested. The recommended 9 to 13 servings of fruits and vegetables a day, the most reliable sources of this mineral, is uncommon in the contemporary diet.  A high sodium to potassium ratio can be predictive of future coronary episodes; a low one, the opposite.  In his study, Dr. Whelton says that 2,300 milligrams should be the maximum sodium intake a day for those less than 30 years old, half that for those who are older.

Sodium is not salt, and salt is not sodium. About 40% of salt is sodium, the remainder being chloride, the chemical of which stomach acid is made.

For some of us, salt might be off the hook. For others of us, it might be a gremlin. It can be hidden in frozen dinners, some cereals, vegetable juice, canned vegetables and soups, sauces and marinades, snacks, and condiments. Potassium, on the other hand, is friendly to all. Jing Chen and his colleagues agree. (Chen. 2008)


Am J Hypertens. 2011 Jul 6. doi: 10.1038/ajh.2011.115. [Epub ahead of print]
Reduced Dietary Salt for the Prevention of Cardiovascular Disease: A Meta-Analysis of Randomized Controlled Trials (Cochrane Review). Taylor RS, Ashton KE, Moxham T, Hooper L, Ebrahim S.

Cochrane Database of Systematic Reviews 2011, Issue 7.
Reduced dietary salt for the prevention of cardiovascular disease.
Taylor RS, Ashton KE, Moxham T, Hooper L, Ebrahim S.

Am J Clin Nutr February 2009 vol. 89 no. 2 485-490
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He FJ, Burnier M, Macgregor GA.

Wolfson Institute of Preventive Medicine, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

MSG and Weight Gain

No MSGThe Body Mass Index (BMI) is a measure of the relative percentages of fat and muscle mass in the human body, based on a person’s weight and height, used to assess obesity. This barometer was used by researchers to determine the effect of the food additive, monosodium glutamate (MSG), on weight over a period of time. It was learned that those persons who consume MSG regularly experience changes in the part of the brain that controls appetite, thus having an influence on energy balance and consequent weight gain.

When researcher, Ka He, and his colleagues at the University of North Carolina began to look for a relationship between monosodium glutamate and weight gain, they hypothesized that it would be a positive one.  As a design element of the study, “…overweight was defined as a body mass index ≥ 25…based on World Health Organization recommendations for Asian populations.”  With an average MSG intake of 2.2 grams a day, and a five-year follow-up, the study population demonstrated that “MSG consumption was positively, longitudinally associated with overweight development…”

The better it tastes, the more we’ll eat.  That seems logical.  Most Americans eat so fast that their brains don’t have enough time to process the information that says they’re full.  Since that lag time is about twenty minutes, we should take at least that much time to eat.  But the school cafeteria, the incessant phone calls, the pressures of the job, and other lifestyle components disallow that.  Combine any of these facets of life with food additives that enhance flavor, and start looking for a longer belt.

Leptin is a hormone that plays an important role in energy intake and expenditure, and it tells us when to stop eating…if it works the right way.  It’s made by fat cells, oddly enough, but can also come from other parts of the body, such as the bones, stomach, and liver.  It acts on parts of the brain’s hypothalamus, where it inhibits appetite. If leptin is not appropriately received and taken up by the hypothalamus, appetite fails to shut off and food intake is uncontrolled.  Where does MSG fit into this picture?  It seems to be able to induce hypothalamic lesions and ensuing leptin resistance (He, et al. 2008).  The stage is now set for weight gain.

Glutamate is the major excitatory transmitter in the brain, meaning that it makes things happen, especially in cognition, memory and learning.  It also affects brain development, cellular survival and the manufacture of synapses.  Too much glutamate, though, can raise serious concerns because its excitatory nature becomes intensified by virtue of its accumulation, allowing excess calcium to enter a nerve cell and damage it beyond repair.  This is what happens in the hypothalamus.

Glutamate, sometimes as glutamic acid, is responsible for the tantalizing flavors of poultry, some fishes, and eggs, among other foods.  Its salt, MSG, was introduced to the United States after WW II as “Accent” flavor enhancer.  It can be made by the fermentation of beets, sugar cane, or molasses.  People began to experience adverse reactions to MSG after eating Chinese food prepared with it, thereby coining the expression “Chinese Restaurant Syndrome.”  Sensitivity to monosodium glutamate may present with headaches, asthmatic symptoms, hyperactivity (especially in children), and obesity.  Frequency of such responses is low, but if it happens in your family, it’s high enough to merit attention.

We all know that the world revolves around the dollar bill and the ball point pen, the latter often employed to guarantee the former.  As long as clandestine groups can get away with something, they’ll persist.  And so it is with MSG.  It has more disguises than Artemus Gordon and Sherlock Holmes combined.  Here are a couple handfuls of MSG aliases:  glutamic acid, monopotassium glutamate, magnesium, glutamate, monoammonium glutamate, yeast extract, hydrolyzed anything, calcium or sodium caseinate, yeast nutrient, gelatin, textured protein, soy protein isolate, soyprotein concentrate, whey protein, ajinomoto.

These ingredients often contain glutamic acid:  carrageenan, bouillon, stock, maltodextrin, barley malt, protease, malt extract, soy sauce, and any protein that is fortified or fermented.  Additionally, these work with MSG to further enhance flavor:  Disodium 5’-guanylate; Disodium 5’-inositate; and Disodium 5’-ribonucleotides.  Wherever these three abide, it’s almost guaranteed that MSG is a companion.

Individual amino acids are not generally listed on the ingredients labels of food or health care products.  Binders and fillers may or may not contain MSG.  Believe it or not, MSG may also appear in cosmetics, including shampoos, soaps and hair conditioners.  If the words “hydrolyzed,” “amino acids,” or “protein” appear on the label, MSG could be in it.  Live virus vaccines may also have it.  Even though reactions to MSG are dose-dependent, you could react to a very small amount all of a sudden, when you never did so before.  Yes, MSG is natural, but so is arsenic.  To most of us, MSG does not cause problems.  MSG might make you want to eat more.  It might affect the state of your hypothalamus.  On the other hand, it’s not likely to make you wash your hair more often.  Is it?


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Departments of Nutrition and Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC.

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*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Medium-Chain Triglycerides Effect Weight Loss

less-weightMedium-chain triglycerides (MCT) are a unique kind of dietary fat that lend a wide range of positive health benefits, weight loss among them. MCT’s have a fatty acid chain length that varies between six and twelve carbon atoms, which is only one characteristic that distinguishes them from the more familiar long-chain fatty acids, such as the highly-celebrated fish oil. MCT’s are transported through the blood by the portal system, which bypasses the usual route of digestion and sends them directly to the liver.

Medium-chain triglycerides do not require the modifications of long-chain and very-long-chain fatty acids.  Neither do they require bile salts for digestion.  These qualities enable them to be less susceptible to hormone-sensitive lipase and to deposition into adipose (fat) tissue storage.  A study from England’s Oxford Brookes University in 2010 announced that, because of their particular character, “MCT’s have been researched for both benefits to exercise performance and health.”  In the former application, MCT’s may be “a means to maximizing an athlete’s ability to maintain their glycogen stores so they can be more competitive.”  From the health angle, these substances “increase fat oxidation and energy expenditure as well as reduce food intake and beneficially alter body composition.”  (Clegg. 2010)

If you watch the lose-weight ads on TV, you might be driven to buy one of the untested, unproven, and maybe even unsafe products that promise the physique of champions.  Read the small print to learn that exercise and diet are part of the program, and your dreams of Roman god-hood (or goddess) are shattered.  Back to the chips and dip, right?  There might be something that’s been tested, and found to be safe and effective for at least a little drop in weight.

Because MCT’s don’t need energy for absorption, utilization or storage, they’ve been used to treat malabsorption conditions.  But weight management has evoked more interest.  The milks from humans, dogs, and guinea pigs contain mostly long-chain fats.  Those from goats, cows, and sheep are primarily short-chain.  Horse milk has lots of medium-chain fatty acids.  Data suggest that the milk of all species depends on a partial resynthesis of pre-formed glycerides. (Breckenridge. 1967)  (Since horses run faster than cows, their milk is hard to bottle, and because they have only two spigots, it takes longer to get it.)

Decades ago, MCT’s had been studied for body fat management in obese persons without diabetes, but more recent work has focused on those with Type 2 diabetes.  The findings showed that a diet containing MCT’s at 18 grams a day (about 2/3 ounce) brought about a reduction in body weight and waist circumference, a decrease in insulin resistance, and a drop in serum cholesterol concentration.  (Han. 2007)  Compared to the subjects ingesting long-chain fatty acids, the results are significant.  The MCT users also enjoyed increased dietary satiety, meaning that they felt full sooner, so they ate less.  Still another welcome benefit was realized by a cohort in 2009, when Chinese investigators noted a significant decline in serum triglycerides and LDL-cholesterol, both markers for cardiovascular complications, in those ingesting 25-30 grams (there are 28 grams in an ounce) of MCT’s a day. (Zhang. 2009).  (Xue. 2009)

The fast rate of oxidation of medium-chain fatty acids leads to greater energy expenditure—almost without doing any hard work.  It’s impressive that such can be the case, especially where weight gain is reduced and the size of body fat deposits diminishes.  Note that fat cells are not normally lost once they appear; they merely shrink in size.  They are, however, prepared to expand again at the drop of a hat.  (Xue. 2009)

Since the 1960’s MCT’s have been advocated for use in weight control.  Back then the research entailed other factors as well, including  the balance of energy intake, the nature of the diet, the ratio of MCT to LCT (long-chain triglycerides), and duration of the protocol.  Nonetheless, the presence of MCT’s as part of the regimen made a difference.  Although the exact mechanism hasn’t been fingered, MCT’s are able to increase energy outgo, hasten satiety at the table, and facilitate weight control when consumed as a replacement for fats containing LCT’s.  ( St-Onge. 2002)  Increased heat production, known as thermogenesis, is one of the activities by which MCT’s burn fat. (Baba. 1982)

Palm oil and coconut oil are major food sources of medium-chain fats.  The fact that these are saturated fats means little because all sat fats are not created equal, displaying differing cholesterolemic effects.  Therefore, when you see them listed on an ingredient label, have no fear.  The less weight you need to lose, the faster you will see results, so it’ll pay to get started now. (St-Onge. 2003)


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Clegg ME.
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Medium-chain triglycerides are advantageous in promoting weight loss although not beneficial to exercise performance

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Gallstones: An Ounce Of Prevention Is Worth…

basic-food-groupIf you have some gall, we hope it’s the kind that causes you to exasperate others, and not the kind that hurts in the center of your upper belly, under the ribs, and occasionally spreads to your right upper back or shoulder.  Gallstone disease is the most common and costly of all the digestive conditions in the United States, accounting for nearly a million hospitalizations a year.  It can interfere with breathing and become severe enough to wake you from sleep…if you can get there in the first place.  Sometimes a person will vomit and relieve the pain; at other times he’ll get feverish from an outright blockage of the bile duct that connects the liver and gall bladder to the small intestine.  With a blockage, urine turns dark, stools are clay-colored, and the whites of the eyes may yellow.  We hope it never gets this far.

While allopathic medicine preaches no sure way to prevent gallstones, it allows that there are means to reduce risk.  Staying close to your ideal weight is important.  A real concern with this is that, lately, everybody is jumping onto the “lose weight fast” bandwagon.  It seems that gallstones can form from such a regimen and even from gastric bypass surgery (Shiffman, 1991).   In obesity, bile tends to stand still and cholesterol saturation increases.  Stones can form within a month of severe caloric restriction, as much as twenty-five times more likely than in obese persons who lose weight gradually (Weinsier, 1993).  Once in a while a person gets lucky, and there are no symptoms, despite the fact that most middle-agers probably have small stones.

Whether it was intended to be a mnemonic or not, the association of the “Five F’s” with gallbladder disease has been around for a time.  Female, fair (hair and skin), forty-ish, fertile (gallbladder trouble is associated with high estrogen), and owning too much fat risk gallstones.  But alcohol intake, a high-fat diet (especially fried foods) and sedentary lifestyle are contributing factors.  In an acute gallbladder attack, people will generally go to the ER, where they will get antibiotics and medicine for the pain, which will probably go away.  If an obstruction is noted, surgery will be done.  In a chronic gallbladder condition, surgery, either traditional or laparoscopic, will remove the gallbladder.  In circumstances that can be pinpointed only by a physician, medications called chenodeoxycholic acids or ursodeoxycholic acids can be given to help dissolve the stones.  But this can take as long as two years and the stones often reappear after treatment is stopped.

It is advisable that, if you are prone to gallbladder problems, you eat a low-fat, low-sugar, high fiber diet.  Decreasing fat limits the amount of work the gallbladder has to do every day.  Increasing fiber helps the liver to eliminate toxins faster. Besides, anything that supports liver function also helps it to make more bile.  Alternative treatment of gallbladder disease relies on increased bile production, liquefaction of bile to help get rid of gallbladder sludge, and dissolution of stones so they can be reduced to a size that can pass naturally. Production of bile can be increased with foods that reduce toxic burden on the whole body, including beets, artichokes (Saénz Rodriguez, 2002), greens, and cruciferous vegetables (Tsai, 2006).  Acidulated water also stimulates liver function. Even a shot of unfiltered apple cider vinegar can help.

Since an ounce or prevention is worth more than a ton of cure, take a look at what coffee does for gallbladder disease.  Harvard scientists found that increased intake of caffeinated beverages reduces the risk of symptomatic gallbladder disease in men, while decaf demonstrated no such effect (Leitzmann, 1999).  In a ten-year study of male healthcare professionals, the incidence of gallbladder attacks was significantly lower in those consuming coffee regularly.   A novice coffee drinker might get the jitters and act like Barney Fife charging his cylinder, but the tradeoff is worth it.  Later study by the same researcher discovered a parallel benefit for women (Leitzmann, 2002).  Using ultra-sound to document gallbladder disease, the Third National Health and Nutrition Examination found that, among women, there was a decreased prevalence of previously diagnosed gallbladder disease with increased coffee drinking (Ruhl, 2000).

Primates and guinea pigs are unable to create vitamin C from diet, so supplementation is required.  The enzyme needed to convert glucose into ascorbic acid was lost eons ago.  Without vitamin C, even guinea pigs get gallstones, although we have never seen tiny guinea pig ambulances in our neighborhood.  From the same health and nutrition exam cited earlier, which ran from 1988 to 1994, researchers from the V.A. Center in San Francisco saw an inverse relationship between vitamin C intake and gallstones, strongly so among women, less so among men (Simon, 1998, 2000).  Vitamin C, by the way, affects the catabolism of cholesterol to bile acids.  Using guinea pigs as, well, guinea pigs, Swedish investigators learned that deficiency of vitamin C causes supersaturation of bile and the subsequent formation of cholesterol gallstones.  But they also found an interesting side story in humans.  Increasing ascorbic acid also increases phospholipid concentrations, leading to a strong inverse association with the conditions that lead to stone formation (Gstafsson, 1997).  German scientists came to the same conclusion about ascorbic acid when they found half the incidence of gallstones in a female population that supplemented with vitamin C regularly (Walcher, 2009) (Lammert, 2004).

So far, prevention has addressed measures that are readily available, off the shelf.  An important strategy to prevent stone formation if one is susceptible is to alter the conditions that promote it.  That can be done with phosphatidylcholine (PC), the chief phospholipid from which the cell membrane is made.  Enriching your diet with PC can directly affect cholesterol solubilization and reduce or eliminate the probability of gallstone formation (Kasbo, 2003) (Vakhrushev, 2005) (Lammert, 2004).

Anecdotal reports about healing protocols abound.  But some of them are surprisingly supportable.  When a person is hospitalized for gallbladder disease, his food is typically replaced with intravenous fluids.  In a while, the pain goes away, after which time you’re allowed to eat.  It’s believed that some foods invoke an allergic response that is at the root of gallbladder attacks.  In a casual test done in the late 1960’s, Dr. James Breneman, the chair of the Food Allergy Committee of the American College of Allergists, asked 69 people suffering from gallbladder pain to try an elimination diet to determine food allergies.  After the identified foods were taken from their diets, symptoms disappeared.  The offending foods were tagged.  Eggs, pork, onions, chicken and turkey, milk, coffee, and oranges were most bothersome, followed by corn, beans, nuts, spices, peanuts, fish and rye.  In addition to foods, twenty percent of the group had attacks caused by medications (Wright, 2004).

Pain and the fear of surgery will direct a person to the least invasive solution he can find, whether it’s clinically proven or not.  There is at least one such remedy for gallstone dissolution that seems to be popular outside the U.S.—a gallbladder cleanse purportedly designed by a Korean chemist named Dr. Lai Chiu Nan.  It entails drinking four glasses of apple juice (or eating four-five apples) daily for five days.  The juice is supposed to soften the stones.  Maintain a normal diet during this time.  On day six, no dinner is enjoyed.  At 6 PM, a teaspoon of Epsom salts in a glass of warm water is consumed, followed by a second such cocktail two hours later.  Magnesium sulfate opens the gallbladder ducts (Harvey, 1973).  At 10 PM, swallow a half cup of olive oil mixed with a half cup of fresh lemon juice, to lubricate the stones and to ease their passage.  Green stones are supposed to drop into the toilet the next day.  If they don’t, use the olive oil and lemon juice to make vinaigrette.  If they do, a gemologist might make you an offer.  Hey, sometimes folk medicine really works, as in the oatmeal baths for itchy skin or lemon juice and honey for a sore throat.

Bile synthesis has been improved and increased by taking essential fatty acids, most notably fish oil.  In a head-to-head contest with fibrates (drugs used to lower triglycerides and cholesterol), fish oil was found to up the ante on bile acids and to alter their distribution (Jonkers, 2006).  But this wasn’t the first time that fish oil stood in the limelight.  Gall bladder emptying increases with fish oil, as gall bladder motility improves and triglyceride levels drop (Jonkers, 2003).  And it sure works on monkeys (Scobey, 1991).  In prairie dogs, who must be kin to guinea pigs because they are prone to gallstones, menhaden oil (an occasional source of commercial fish oil) increased levels of EPA and DHA and reduced incidence of cholesterol crystals (Booker, 1990).

We normally think of solvents as able to dissolve things, but almost never relate them to the human body except in old Vincent Price movies.  Some scientists might disagree with this neglect because they have learned that gallstones can sometimes be dissolved by plant-sourced solvents, especially a terpene called limonene, common to citrus fruits and recognized as a safe flavoring agent in foods and beverages.  An unsaturated hydrocarbon from plants, limonene has been tried and proven to be a dissolver of cholesterol stones (Sun, 2007), while a welcome side effect is the relief of heartburn and GERD (Ibid.).  In a trial dating back to the 1970’s, a blend of limonene and polysorbate 80 (an emulsifier) was found safe and effective in the lab and the clinic (Igimi, 1976).  Occasionally following gallbladder surgery, stones are retained in the duct.  Injecting a limonene preparation directly to the biliary system was able to dissolve retained stones (Igmini, 1991).  Efficacy was enhanced when limonene was mixed with a medium-chain triglyceride in a Japanese study done toward the end of the last century (Shionogi, 1992).  Besides citrus, a readily available source of such solvent is peppermint oil.  Whether it works orally to dissolve gallstones is under investigation.  It’s doubtful that some of us can wait for the results to be printed.


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*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Salt’s At Fault? Now What?

too_much_saltFor years it was held that salt intake has a distinct influence on blood pressure and cardiovascular disease (CVD). In fact, in 2011 the American Heart Association issued a sweeping call for salt restriction (Appel, 2011), limiting intake of sodium to less than 1500 milligrams a day, which translates to approximately 3750 milligrams of sodium chloride. One teaspoon of salt, which is about 40% sodium and 60% chloride, has 2300 mg of sodium. Naturally found in most foods, sodium defies accurate measurement, but because men eat more food than women, they consume more. Nerve impulses depend on sodium for activation; otherwise you wouldn’t be able to open the link to this page. Overconsumption of sodium, however, can lead to calcium deficiency (Teucher, 2008). Once again, it’s a matter of balance…but not without at least a little controversy. Also in 2011, the Journal of the American Medical Association published a paper that discounts a relationship of salt intake to CVD. In a study that lasted for nearly eight years, researchers found the incidence of mortality and morbidity related to sodium intake to be minimal, with no translation to a greater risk of elevated blood pressure or CVD (Stolarz-Skrzypek, 2011). Contrary to conventional wisdom, low sodium was associated with elevated CVD risk. Now there, don’t jump for joy and a box of pretzels over one study. For every yin there’s a yang—potassium is the foil to sodium. Potassium is a mineral whose insufficiency is widespread. Most of us are fortunate if we get half the 4700 mg recommended every day. Maintaining the ratio, 2 to 1 in favor of potassium, offers considerable benefit to cardiovascular health (Yang, 2011). The bottom line in all this is that minerals need to be in, well, balance.

Still, excess salt intake is a way of life for some. In a fancy restaurant, you might be challenged to find salt and pepper shakers on a table, for fear of insulting the chef. At the corner diner, on the other hand… This temptation, or rather succumbing to the temptation, could be our downfall. Very recent papers published in the highly respected journal, Nature, deliver the news that salt intake may be associated with autoimmune diseases through a mechanism that turns certain of our immune cells into traitors. In autoimmune conditions, abnormal antibodies are produced and they attack the body’s own cells and tissues. Lupus, rheumatoid arthritis and type 1 diabetes are commonly known examples, but there are other disorders that have an autoimmune component. In each instance there will be a characteristic set of autoantibodies to attack normal cells. Sometimes the autoantibodies actually cause the tissue and organ damage; sometimes they’re only the markers of disease. Susceptibility to autoimmune disease could be blamed on environmental influences, genetic makeup, exposure to an infectious organism, or to a combination of these.

Newly identified in the study of autoimmune disease is a population of T cells called TH17, which produce an interleukin different from the run-of-the-mill T cells that assist other white cells in immunologic processes. Excessive numbers of TH17 cells are thought to play a vital role in autoimmune diseases (Harrington, 2005) (Stockinger, 2007), including multiple sclerosis, psoriasis, rheumatoid arthritis and Crohn’s disease. What these cells do is to fail to turn inflammation off. Inflammation is the body’s response to attack, whether from trauma, viral or bacterial infection, heat or whatever else might cause an insult. In this response a few things happen: blood vessels dilate, fluid may leak from the surrounding area and clot, cells swell, platelets get activated, macrophages show up to swallow damaged tissue, and the healing begins. We need inflammation to heal, but it has to stop before healing is complete. We take anti-inflammatory chemicals to stop the pain, but we also stop—or at least inhibit—the healing. TH17 cells are there to fight infections, normally targeting fungi and bacteria, but they need to control themselves. One of the factors found to instigate TH17 cells into aberrant activity is salt. In its presence, T helper cells are more likely to develop into TH17 cells that are pathogenic (Wu, 2013). Then they attack the body’s own cells.

Not surprising is that those who frequent fast-food joints were found to have elevated levels of TH17 cells. Why not, if this relationship is definitive?  Such establishments use salt to embellish flavor. Each of us has a gene that controls the physiological response to salt intake. In certain individuals, this gene is over-expressed by salt, leading to the pathogenicity of TH17 cells and subsequent inflammation (Wu, 2013). This effect is leading scientists to look more closely at low-salt diets in the treatment of autoimmune diseases. The good side of the original study is that several genes are implicated in the response, not just the one with the greatest impact. And it’s not likely that all are out of sync at the same time. Furthermore, the factors that initiate autoimmune disease need to be in concert. For most of us, they are not. For the rest, maybe hiding the salt shaker could make a difference. For those with type 2 diabetes, the difference would be substantial.


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Urinary sodium excretion, dietary sources of sodium intake and knowledge and practices around salt use in a group of healthy Australian women.
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Su M. Metcalfe
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John J. O’Shea & Russell G. Jones
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Fatal and nonfatal outcomes, incidence of hypertension, and blood pressure changes in relation to urinary sodium excretion.
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Teucher B, Dainty JR, Spinks CA, Majsak-Newman G, Berry DJ, Hoogewerff JA, Foxall RJ, Jakobsen J, Cashman KD, Flynn A, Fairweather-Tait SJ.
Sodium and bone health: impact of moderately high and low salt intakes on calcium metabolism in postmenopausal women.
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Chuan Wu, Nir Yosef, Theresa Thalhamer, Chen Zhu, Sheng Xiao, Yasuhiro Kishi, Aviv Regev & Vijay K. Kuchroo
Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1
Nature. 06 March 2013 doi:10.1038/nature11984

Yang Q, Liu T, Kuklina EV, Flanders WD, Hong Y, Gillespie C, Chang MH, Gwinn M, Dowling N, Khoury MJ, Hu FB.
Sodium and potassium intake and mortality among US adults: prospective data from the Third National Health and Nutrition Examination Survey.
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Nir Yosef, Alex K. Shalek, Jellert T. Gaublomme, Hulin Jin, Youjin Lee, Amit Awasthi, et al
Dynamic regulatory network controlling TH17 cell differentiation
Nature. 06 March 2013 doi:10.1038/nature11981

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.