Sodium

Why Are We So Scared of Salt?

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Over the past several decades, the general consensus of health professionals has been to recommend that all people lower their salt intake. Without the recognition of the effects of lifestyle and dietary choice differences, this avalanche of low salt advice hit the general public and as a direct result many became ill. Differences in individual genetic, lifestyle, and dietary factors have completely been ignored in the broad-brush campaign for lowering salt intake. Today, it is unmistakably obvious that a large segment of the population followed the low salt regimen with disastrous consequences.

The professionals who first introduced and propagated the low salt diets had good intentions. They did not know any better. Now we do know better and there is no excuse for not revising a failed treatment regimen in the face of new countervailing evidence. The process of correction needs to begin on a large scale. My work is part of this very much needed correction.

Why Are We Scared of Salt?

In the 1960’s, scientific studies linked salt consumption to hypertension and obesity. I am not quite sure why it was salt they picked on as “enemy number one.” I suspect the reason was the proliferation of precooked and canned food, all of which were salt preserved. To me, it was not logical that only salt was picked on. There were many other dangerous food items that could have been singled out: sugar, margarine, preservatives, pesticides, etc. The American Heart Association still has some of these salt reduction articles on their website. Even today, when waiting for an appointment at my medical institution, the forever-on TV was showing how to cut salt out of kids’ daily lunch to be “healthy.” Indeed, once something is ingrained in our brains, it is habit forming. Habits are very hard to break, particularly when the medical research relied upon showed that salt is something dangerous that may kill you.

Is Salt or Sugar the Enemy?

The problem is that hypertension and obesity are not and have never ever been caused by salt! They are caused by sugar—I am saving the sugar discussion for my next article.

Why not salt? Consider: human fetuses are floating in salt water and are typically not born with heart attack or hypertension. Our bodies are made of over 7% salt, our brains, heart, and all of our cells use salt to function. Humans have always consumed salt. Do they all have hypertension and heart attacks? No, they don’t. In fact, for some time now, studies have been surfacing suggesting that reduced salt does not eliminate the chances for hypertension and heart attack but may even contribute to the problem.

It is scientifically irresponsible to analyze biological processes in the human body involving salt without accounting for the effects of sugar and sugar substitutes and the amount of water consumed.

Probably not many of you have the handbook “Harrison’s Manual of Medicine” (18th edition McGraw Hill Medical by Longo et al.,) but I do. Page 4

…serum Na+ [sodium] falls by 1.4 mM for every 100-mg.dL increase in glucose, due to glucose-induced H2O efflux from cells.

Let me explain this sentence for you: Sodium is part of salt. Salt is Sodium (Na+) and Chloride (Cl-) where the + and – represent the ionic state in which there is either one extra or one fewer electron (electrons have negative charge) and so the atom is looking for another atom it can attach to and form a bond creating a molecule. According to the medical handbook, Na+ drops if glucose, which is blood sugar, increases. If you eat glucose, it causes “H2O efflux from cells” which means that sugar attracts water to the point that it pulls it out of the cells, thereby emptying the cells of sodium, and thus, the cells are dehydrated.

Sugar causes a very serious problem that can result in hypertension and heart attack. The volume of blood inside the cells reduces by dehydration of the sugar and higher pressure is required to pass the dehydrated blood to traverse the same route and be able to oxygenate organs at the same rate as hydrated blood cells. Think of a water hose when suddenly the pressure drops (unfortunately we cannot replicate reduced water molecule size the same way dehydrated cells become smaller). You instinctively squeeze the hose end to increase pressure so the water can continue to reach to the same distance. You have just given a hypertension to your water hose!

Note that if sodium (page 3 in same book) falls below 135 mmol/L, it is an electrolyte abnormality whose symptoms include “nausea, vomiting, confusion, lethargy, and disorientation”; if Na+ falls below 120 mmol/L it is a life threatening emergency that may cause “seizures, central herniation, coma, or death.” Not having enough salt (sodium) in the body is called hyponatremia and is “primarily a disorder of H2O homeostasis” meaning too much water and not enough salt. In common parlance, this is called water toxicity. Water toxicity can be caused by drinking too much water—e.g. drinking only water.

Interestingly, in the same book under the section of hypertension (page 834-835), the causes of hypertension are listed. Increased salt (or sodium) is not mentioned at all, but glucose intolerance is. However, under treatment, on page 836, it recommends lifestyle modifications that include lowering salt intake. So increased salt did not cause hypertension but lowering will cure it? I do not understand. Do you? Seems the authors of even this highly respected medical reference book could not escape the fallacy of the low salt campaign. Hypertension is clearly listed to be caused by sugar under the causes. So for heaven’s sake, if something is caused by sugar, treat it with removing sugar from our diet and not salt.

Confusion in the Ranks

In recent years a major fight started between the academic groups, not-for-profit organizations, and the government. Test after test shows that earlier hypotheses were all wrong about salt. Not only is added salt not hurting us, reduced salt does. Even the American Heart Association (AHA) and other heart organizations are in complete confusion. Next to the article of “lower your salt for health” are articles saying “that is all wrong and increase your salt.” I find this kind of funny. Here is an article from the AHA suggesting to increase salt. Here is another from the HealthAffairs organization; one from the American Journal of Hypertension, one from the Journal of the Association of American Medical Colleges, and there are now dozens more proving that indeed, reduced salt is actually bad for you.

How Bad is Reduced Salt on Health?

This particular article is my favorite because it shows how bad reduced salt diets really are on the heart. In detail, for a healthy individual reduced salt diet reduces BP by 1% (that means your systolic BP of 120 just dropped to oh my 118.5!!! gasp) and in patients with hypertension it reduced their BP by 3.5% (that is if it is say 160 systolic, which is high, it is reduced by a whopping 5.6 to 154.4! gasp again) but at the same time triglycerides, which contains the accurate measure of the sticky type of bad cholesterol in the LDL increased by 7% in people with hypertension (triglyceride should be less than 149). So if an individual with hypertension and triglyceride levels at 150 went on a low salt diet, that low salt diet would increase their triglycerides by 10.5 to 160.5, which is a significant jump for bad cholesterol. In a healthy individuals, the triglycerides jumped by 2.5%. Armed with such details, do you still believe that salt is bad for you?

Which Would You Rather Eat?

If I handed you 2 teaspoons: one was full of table sugar and the other full of table salt, which would you chose? For taste, we all would choose the sugar. What happens to our salt levels when we eat sugar? Refer back to the Harrison’s Medical Manual I mentioned earlier: eating glucose drops salt in our body because it sucks up all water and dehydrates. Eating a teaspoon of sugar will effectively dehydrate you and put you at risk of hyponatremia. By contrast, what will happen if you chose the teaspoon of salt? You will be thirsty, drink a couple of glasses of water and will feel like you are on top of the world.

My Recommendation

Stop being scared of salt and start being scared of sugar!

Sources

Longo et al., Harrison’s Manual of Medicine; 18th Edition, 2013; McGraw Hill Medicine

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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

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This article was first published on June 13, 2015.

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Hydration, Thirst, and Drinking Water

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Most of us equate the expression “hydrate extra” with drinking more water but – unfortunately – this is incorrect. In any online dictionary “to hydrate” means to create “…a substance that is formed when water combines with another substance…” In other words, water alone is not a hydrating fluid but it must be combined with something to become one. We do not have water in our body on its own; we have a substance we call electrolyte. I wrote substantially on the topic of hydration, mixing water with minerals, as part of the protocol that prevents migraines. However, a new problem has surfaced: when to drink water? Several articles have recently published water drinking instructions on the internet. Most of these articles consider it bad practice to drink water when one is not thirsty and recommend drinking water only when thirsty. There are several serious flaws with this argument.

Sweat

The first flaw is that most research is aimed at athletes, but athletes are not representative of the majority of the population. Furthermore, athletes should not be drinking “water” to hydrate. Drinking water cannot be absorbed by cells without adequate sodium to hold onto it. When athletes sweat, the content of sweat is not water but electrolyte. Many sports drinks aim at re-hydrating athletes but their problem is their sugar or sugar substitute content, defeating the purpose — see how much sports drink one needs to drink to make up the content of sweat for an athlete. Then add up the sugar in a typical sports drink: 1 teaspoon of sugar is 4 grams of carbs. An average serving of a typical sports drink provides between 14 grams to 54 grams of carbs, all sugar, which converts to 3.5 to 13.5 teaspoons of sugar per serving. Drinking sugar substitutes is even worse because sugar substitutes fool the body like it is receiving glucose so insulin spikes but there is no glucose. This creates insulin overflow in the blood causing you to become hungry! Sugar substitutes may lead to obesity and metabolic syndrome. Drinking sports drinks with sugar substitutes actually reduces muscle energy.

Moreover, anything that converts to glucose in the body removes both water and sodium from the cells1 so drinking/eating sugar with sodium (salt is the form in which sodium is available to us) and water is worse than not drinking anything at all. Many athletes have smartened up and drink pickle brine rather than water. Pickle brine is great, assuming the brine is of salt and water and not vinegar. Vinegar is fermented ethanol (alcohol). Thus, drinking vinegar-processed pickles will dehydrate further. Look for pickles made with salt rather than vinegar.

Best Hydrating Fluid

Whole milk is an ideal hydrating fluid because it has a perfect electrolyte balance in sodium, potassium, water, blood sugar (lactose), calcium, phosphorus, magnesium, and protein. Whole milk is THE perfect electrolyte. Some athletes drink water and take salt pills (also called electrolyte pills). That is also a great option, particularly since they are easy to carry around and take when needed.

The second flaw in the argument of “drink water when thirsty” is that many people feel thirst after eating sugar when it is the least advisable to drink water. Since about half of sugar converts to glucose, and glucose pulls water and sodium out of the cells1, if one is thirsty after eating sugar and drinks water, the metabolic process will remove more water from the cells. This can cause edema. Although most articles today blame salt for causing edema, the opposite is true.

While sodium retains water inside the cell, glucose removes water and sodium from the cell and forces the water to be retained in extracellular space2. Eating salt when one has edema reduces edema by the sodium bringing water back into the cell. This was easily demonstrated by a previous article showing how this works.

The problem with most studies that blame salt on retaining water is that no studies have ever controlled for both salt and sugar at the same time in the same experiment. All studies I could find only looked at the effects of salt on the body regardless of the amount of sugar, water, or protein the subjects had consumed before the experiment. Since the body can easily be tipped out of balance and is never in a vacuum for a pristine controlled experiment, one cannot say with certainty that one element makes a particular change without looking at what else is affecting the body. No such studies exist except in my migraine group where we control for all variables. We found that being thirsty often means the person does not have enough salt to keep water where it belongs3. A migraineur should never drink water when she is thirsty, particularly not if carbohydrates were consumed.

The final problem with only drinking water when thirsty is the population of people who have diabetes 2; they are always thirsty. Being thirsty can be a sign of diabetes mellitus and not the need for more water.

Should You Wait Until You Are Thirsty Before You Drink?

Absolutely not, and for sure drinking water alone will not get you hydrated. How much water you should drink is a question I will address in another article. Drinking the minimum 8 glasses of water is a myth; people vary in size, age, and activity, implying that each person needs a different amount of water. Many online water calculators go into detail of weight, climate, activity, altitude, your health, pregnancy, nursing, etc. For each person the amount of water and thus hydration needed (not just water) will differ and for that hydration level you need to make sure you drink adequate amounts of water as part of your hydration protocol.

Sources

  1. Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J. Harrison’s Manual of Medicine 18th Edition. New York: McGraw Hill Medical; 2013.
  2. Millar T. Biochemistry Explained: A Practical Guide to Learning Biochemistry. Vol reprint edition: CRC Press; 2002.
  3. Stanton, Angela A. Fighting The Migraine Epidemic: A Complete Guide: How To Treat & Prevent Migraines Without Medicine

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Pregnancy Toes – What Sugar Does to Feet

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Pregnancy toes are really swollen feet and swollen toes. The name stuck in my mind because one of my daughter-in-laws is pregnant and I was sent a photo from her winter vacation in her flip flops in the snow and winter coat—she was not able to put her boots on because of her swollen feet (swollen even in the cold!).

I did not think much about it until she came to visit me yesterday and I noticed the flip flops and her chubby toes. She had “pregnancy toes” again she said. It then suddenly all became clear. I asked her: did you by any chance have any sugar today? And she said “as a matter of fact, yes!”

I reached for my salt pills that I use for my migraines as do all members in my migraine group on Facebook and handed her one. I really should have photographed what happened but I did not think the effect was going to be so fast and so big. Less than 15 minutes after she took the salt pill and a glass of water, her toes went back to normal. We ended up laughing it away. Had she known this, she could have worn her boots in the snow after all!

So what did her pregnancy toes have to do with sugar and salt you may ask? Previously, I quoted from the Harrison’s Manual of Medicine an important paragraph that I repeat here:

…serum Na+ falls by 1.4 mM for every 100-mg/dL increase in glucose, due to glucose-induced H2O efflux from cells. (page 4)

The above means glucose (part of sugar) and sodium (part of salt) are in inverse relationship. As you increase sugar, salt drops and water is sucked out of your cells by sugar like a giant Slurpee machine. The water then collects on the outside of your cells rather than the inside, thereby dehydrating your cells and at the same time make your body swell. Edema is often associated with too much salt, but in fact, it is too much sugar. Being always thirsty is associated with Type 2 Diabetes but it is also associated with not having enough salt in the body since without salt the cells cannot get hydrated.

In light of this fragile balance between sodium and glucose in the blood, are we treating pregnancy edema, gestational diabetes, and other maternity complications, the way we should? Consider that with pre-eclampsia (gestational hypertension), women are told not to eat salt. You can see what happens when we reduce sodium: glucose increases and we also induce an ionic imbalance. This ionic level imbalance is visible (like the swollen toes) and may lead to further complications. There are two problems that we are facing here: first if she does not eat salt, her sodium-potassium pumps cannot work–this may cause migraines and headaches as I often see in my migraine group. Secondly, as you saw the fragile balance between the see-saw action of glucose and sodium, if she stops eating sodium her glucose may increase, causing swelling. This is an interesting theory to ponder – one that merits research.

Sodium and Glucose Work Together

Salt breaks up in the body into sodium and chloride. Sodium attracts water and holds onto it inside the cells. It keeps chloride outside of the cells to ensure proper voltage and electrolyte balance with the aid of potassium. When you eat sugar, the glucose part of it removes the water from the cells via osmotic channels that are too narrow for the sodium ions to exit. Thus, one ends up with a ton of water outside the cells with sodium inside hugging a tiny amount of water. Swelling occurs as the water leaves the cells but remains between cells.

Given the inverse nature of glucose and sodium in the blood, if one is swollen as a result of too much sugar, eating salt will take the water back from sugar and move it back into the cells–as it did for my daughter-in-law’s pregnancy toes. What is important in this information is this:

  1. If you feel swollen after eating sweets, you need to eat salt and drink a bit of water to reduce your swelling.
  2. If you have Type 2 Diabetes or are hypoglycemic, eating a salty meal can give you a major sugar crash and land you in the hospital!
  3. Eating sugar of any quantity will dehydrate your cells and you and make you run to the toilet every 30 minutes.

Because glucose takes water out of the cells, the edema that follows increases extra-cellular water and causes swelling in the body. This extra-cellular water needs to be reabsorbed into the circulation for the kidneys to be eliminated. To be reabsorbed, sodium is necessary since without sodium, the cells cannot operate their voltage gated sodium pumps and so the gates cannot open to grab glucose to take it into the cells and to get the water back into the cells. I think you can already see the contradictions in the logic of reduced salt: the mom-to-be is told to not eat salt, this causes extra-cellular water and swelling, which needs salt to be reabsorbed into her cells for clearance by the kidneys but which she is not allowed to eat. This way ionic level balance is not possible and chain reactions may occur with negative consequences. She may have protein leaching into her urine, extra hard kidney work, and a whole other long chain of complex events may kick in to make pregnancy a rather unpleasant experience risking the health of the fetus.

The amount of extra-cellular water is very hard for the body to get back into circulation without salt and may take days, taxing the kidneys with the volume of water leaving and increasing pressure on the blood vessels from the outside, causing high BP. However, as the volume of water is leaving the body finally, this reduces blood pressure. When a pregnant woman’s blood pressure drops as a result of all that water leaving, the dehydrated blood cells carry less oxygen. This indicates reduced oxygen for both her and the baby.

By telling mothers to reduce salt intake, glucose increases, which increases blood pressure (BP) rather than reduces it. The similar phenomenon happens in gestational diabetes. In gestational diabetes (and gestational hypoglycemia as well) the sugar level is unstable and is either too high or too low, respectively. Should the mother-to-be eat a salty pickle (as cravings always dictate pickles), she may end up in a major sugar crash and in the hospital for immediate treatment.

The balance between sodium and glucose is very fragile and extremely quick changing as you could see on my daughter-in-law’s foot. Interestingly we now also know that salt does not increase blood pressure but sugar does and so a reduced salt diet automatically increases blood pressure because of the glucose and sodium inverse connection and sugar’s dehydrating properties. Reduced salt also increases triglycerides (Graudal, 2011), causing a lot of problems for people with preexisting heart conditions. So by reducing the salt intake of the mothers to be, are we creating diabetic mothers and/or babies? Babies have been born with diabetes 2!

Is it possible that we are giving the wrong advise to pregnant women about salt and sugar? It’s an interesting question to pose and further research is badly needed. Knowing that salt and sugar are in inverse proportion in the blood, one may suggest eating them together. In fact, eating them together is a much better idea than eating sugar alone. It is best to not eat sugar at all but if you must eat sugar, consider eating salt too.

Sources:

Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol, and triglyceride. Graudal et al., Cochrane Database Syst Rev. 2011 Nov 9; (11).

This article was published originally on Hormones Matter on February 15, 2015. 

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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

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Why Academic Research is Dead

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The Perils of Academic Publishing

I am an avid student of cardiology since migraine, my field of interest, is connected to electrolyte imbalance, renin-angiotensin-aldosterone-system, blood pressure problems, and metabolic disorders, all of which collectively fall into the bucket of SyndromeX. SyndromeX is the disease researchers of the world have been trying to prevent and/or cure—or at least treat successfully—from the middle of the 20th Century through today and likely to continue for the next several decades. Why so long? There seems to be three trends in academic research:

  1. Poor study design and analyses often compromised by financial interests. 
  2. Only incremental findings are published.
  3. Paradigm shifting research is rarely, if ever published.  

Researchers who cannot publish often say the most important things.

These researchers are shifting the paradigm. When research goes against the current dogma, academic journal editors and reviewers have little interest in publishing. In these fields, particularly in the field of nutrition, researchers can lose their careers, face lawsuits and worse, when they dare to attempt to publish their work (see this page where I quickly saved a publication before it was removed–it is in PDF form) or here where a doctor (not a nutritionist) advised his patients on how to reverse metabolic syndrome by a new diet or here where one of the most famous researchers in the field of nutrition is sued by the same organization (Australian Health Practitioner Regulation Agency (AHPRA)). By contrast, those researchers who stand on false dogmatic premise always get published because their findings support the findings of the editors, reviewers, and the dominant industry (see here for or here for two sample articles that stand on completely erroneous research but support the dogma; and there are thousands more like these). An example of an historical review of the nutrition industry and how they misled us for over 60 years is published by the British Medical Journal here but it was not without an attack by (I counted) 199 academicians from the school of “Dogma” that demanded the article to be retracted by the journal. You can find their retraction demand here. Some of the signatories–if you are familiar with the nutrition war–will be familiar to you. Luckily the article was not retracted only one sentence was corrected. Another exception that published just two days ago is here. I have yet to see the comments and if it will stay published.

Historically, this has been the case too. Einstein, for example, could not publish any of his papers today–all his papers (except one) were published without the peer review process. Without his findings where would we be today? The one paper that went through peer review was not accepted in that journal and he published without peer review elsewhere. Today, a paper published without peer review is considered to be junk and equal to not having published anything at all. On the flip side, a published peer reviewed article in a top journal does not mean the paper is not junk. Published scientific papers are often junk even if published in the top journals.

In my research field of migraines and how increased dietary salt, for example, reduces migraines, I see this all the time. Migraines are preventable by increased sodium and thus research on sodium and health matters. Hundreds of studies show that it is sugar, and not salt, that increases blood pressure–implying safety in increased salt intake. I found no research that showed the effect of salt on blood pressure that discusses the magnitude of the shift by salt, only that there is a minor shift. The magnitude is tiny; only 2-8 systolic point changes are observed, while a normal daily blood pressure variation considers 39 such point changes as normal. Thus, the change of 2-8 points is statistically not significant at all. I submitted a paper stating this to The Lancet and received the message that “it is not a priority.” I published the paper elsewhere. Less than a year from the rejection, a paper was published in The Lancet along on the same subject, except that it contained an unexpected twist. The article tried to cross the dogmatic line of the “less dietary salt is healthier” while presenting findings supporting the notion that more dietary salt is actually better. Let me show you what I mean. Here is a portion of the abstract.

“Increased sodium intake was associated with greater increases in systolic blood pressure in individuals with hypertension (2·08 mm Hg change per g sodium increase) compared with individuals without hypertension (1·22 mm Hg change per g; pinteraction<0·0001). In those individuals with hypertension (6835 events), sodium excretion of 7 g/day or more (7060 [11%] of population with hypertension: hazard ratio [HR] 1·23 [95% CI 1·11–1·37]; p<0·0001) and less than 3 g/day (7006 [11%] of population with hypertension: 1·34 [1·23–1·47]; p<0·0001) were both associated with increased risk compared with sodium excretion of 4–5 g/day (reference 25% of the population with hypertension). In those individuals without hypertension (3021 events), compared with 4–5 g/day (18 508 [27%] of the population without hypertension), higher sodium excretion was not associated with risk of the primary composite outcome (≥7 g/day in 6271 [9%] of the population without hypertension; HR 0·90 [95% CI 0·76–1·08]; p=0·2547), whereas an excretion of less than 3 g/day was associated with a significantly increased risk (7547 [11%] of the population without hypertension; HR 1·26 [95% CI 1·10–1·45]; p=0·0009).” [Note they state they measured sodium all through the abstract but in the article they used these same numbers for salt. Sodium is 40% of salt. Salt is made of sodium chloride, so “7 gr sodium” would thus be equal to 17.5 gr salt, which is not something they measured or mentioned. Thus the abstract is misleading and confused]

Aside from the almost total incomprehensibility of the text, the abstract appears to suggest that less dietary salt intake is better, when in fact, if we translate and read the rest of the article, it indicates the exact opposite, that more salt is better. Here is my translation–replacing sodium with salt where it is due:

“This study found that increased sodium intake was associated with an increases in systolic BP in individuals with hypertension (2.08 mm Hg change per each gram of sodium increase) compared with healthy individuals. In hypertensive individuals, 7-gram salt [2.8 gr sodium] per day or higher amount, or less than 3-gram salt [1.2 gr sodium] a day were both associated with increased heart risk—meaning some heart event, such as a heart attack. Thus, the ideal daily sodium intake for a hypertensive individual has a definite lower end of 1.2 gr sodium and an upper end of 2.8 gr sodium, with the best outcome reached by hypertensive subjects at 4–5 gr salt [1.6 – 2.0 gr sodium] a day, which also did not harm the healthy population. Healthy individuals suffered when they excreted 3 grams salt [1.2 gr sodium] a day. Healthy individuals had a significantly increased risk of a negative heart outcome (heart attack or similar) from 1.2 gr sodium a day and also greater than 7 grams salt [2.8 gr sodium] a day.”

This was a sly move to suggest two things at once. The strategy worked. The article was published. Unfortunately, the evaluation of the data was flawed and since the presentation of said data obfuscated their real findings, the publication became a confused mess. Moreover, subsequent to the article’s publication, hundreds of other articles have referred to it, as if the findings were correct, deepening the damage this badly analyzed study created.

What the Data Actually Demonstrated

In order to fully illustrate the findings in this study (Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of data from four studies), I created two charts using their data.

Figure 1. Death rates per sodium change in hypertensive patients

Hypertensive death per sodium change

Figure 2. Death rates per sodium change in healthy individuals

Healthy Subjects Death per Change in Sodium

While Figure 1, shows the hypertensive and diabetic patients with a mixed curve-like relation to urinary salt, Figure 2 shows that healthy individuals tend to remain healthier the more salt they have in their urine. The two graphs show that both groups (healthy and hypertensive) tended to die or have cardiac events when less urinary salt was found. Thus, we may conclude that too little urinary salt is unhealthy and that for the healthy, the more salt in the urine the better. Do we know why the unhealthy had low or high urinary salt? No clue. Do we know why the healthy had low or high urinary salt? Nope. Can we conclude anything at all? Yes: in both groups, less urinary salt found in the urine meant earlier death.

The authors of the article did not publish these simple graphs. Why not? Perhaps because these graphs show that the data of the sick and the healthy cannot be combined. Instead, they ran a regression that cancels these differences to some degree, with which the whole article passes on a very confused message. Unfortunately, since The Lancet is the top academic journal, every single medical practitioner, cardiologist, and nutritionist who may gain some insight from an article like this will put it down and head for a walk instead.

These findings could have been important if properly analyzed, since they would represent a paradigm shift in medical understanding of the role of salt in our diet, why the sick are getting sicker and those on low salt diet die faster!

My Take on the Research

The study was flawed from the onset.

  1. The database they used, PURE, has data from thousands of individuals for general epidemiological analysis and so the control mechanism to conclude any causal relationship is impossible. In particular, reading salt amount in morning fasting urine samples tells nothing about how much salt the individual consumed the day before let alone in general. One cannot conclude a meaningful association between salt amount in urine and salt amount consumed because there are so many factors interfering with the clearance of salt from the body (1-9). Even correlation is dubious; deriving causation is impossible, yet that is precisely what this paper did.
  2. The authors combined findings of the sick and the healthy, regardless of what heart or diabetic medications the sick were taking (both alter urinary salt content), and created a combined graph representing the recommended daily dietary intake for all people (sick, healthy, children, elderly).

Back to the Perils of Academic Publishing

I wrote a commentary about the flaws and sent it to The Lancet. It was rejected after the editors sat on it for over two months. Why was it rejected? Interestingly, while most academic articles are followed by comments and debates, The Lancet did not allow any comments for or against this particular article. This is odd since without a healthy debate, science heads nowhere. When researchers discover errors or flaws and cannot publish these finding, less discerning readers will continue to misunderstand the research. In this case, most will think that less salt is better for cardiovascular health, when it is absolutely not.

References

  1. Unger T & Jun Li (2004) The role of the renin-angiotensin-aldosterone system in heart failure. Journal of Renin-Angiotensin-Aldosterone System 5(1 suppl):S7-S10.
  2. McQuarrie EP, et al. (2014) Association Between Urinary Sodium, Creatinine, Albumin, and Long-Term Survival in Chronic Kidney Disease. Hypertension 64(1):111-117.
  3. Christensen BM, et al. (2010) Sodium and Potassium Balance Depends on αENaC Expression in Connecting Tubule. Journal of the American Society of Nephrology : JASN 21(11):1942-1951.
  4. Ragot S, et al. (2016) Dynamic Changes in Renal Function Are Associated With Major Cardiovascular Events in Patients With Type 2 Diabetes. Diabetes Care 39(7):1259-1266.
  5. Mannucci E, et al. (Cardiac safety profile of rosiglitazone. International Journal of Cardiology 143(2):135-140.
  6. Longo DL, et al. (2013) Harrison’s Manual of Medicine 18th Edition (McGraw Hill Medical, New York).
  7. DiNicolantonio JJ & Lucan SC (2014) The wrong white crystals: not salt but sugar as aetiological in hypertension and cardiometabolic disease. Open Heart 1(1):e000167.
  8. Verbalis JG (Disorders of body water homeostasis. Best Practice & Research Clinical Endocrinology & Metabolism 17(4):471-503.
  9. Catterall WA (2000) From ionic currents to molecular mechanisms: the structure and function of voltage-gated sodium channels. Neuron 26.

 

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Happy Ending to Migraines: The Benefits of Milk

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Migraines and Electrolytes

In late June of 2015, I received a PM (personal message) on Facebook from a husband of a migraineur. The husband introduced himself and explained that his wife “suffered with migraines for 15 years (Oct. 2000) after hitting her head under a bathroom cabinet.” She had been through all kinds of typical migraine treatments – just about everything under the sun possible to try, including a neuronal stimulator placed in via surgery – but nothing has worked. As he was sitting in the hospital waiting for some results, he found me on Facebook and asked for help.

I have a standard questionnaire that I ask all migraineurs to fill and send the answers to me via PM so I can see what may be wrong. The first thing that hit me was that she was drinking 256 oz (32 glasses) water a day when the calculator suggested that her petite figure needed only 66 oz (just over 8 glasses) so something was terribly wrong. She also took a ton of medications, though the list he sent was already greatly reduced. Even with these medications, she suffered debilitating migraines every day.

The migraineur was Kristen Cassimatis. Her recovery was covered recently by a local television station on their news. You can watch it here: Raw milk helping woman relieve migraine pain.

What Do Electrolytes, Whole Milk, and Migraines Have in Common?

A lot actually. The very first article I published at Hormones Matter was on the importance of proper hydration to the body. Hydration is not water but a mix of electrolyte minerals with water, of which sodium and potassium (in proper balance) are the most important. An article I wrote somewhat later describes what excessive thirst means for the body and that sugar is really bad for you. Thus, if you look through some of the articles I published, you can see that a meal that is hydrating, contains no added sugar, has protein and some minimal carbs, electrolytes, and fat. Fat is good for you. I have also published several academic journal articles on the cause and treatment of migraine, based on statistical findings in the migraine group on Facebook.

I have not yet discussed fat and cholesterol in great detail but an article shall come about that in the near future. For now, since whole milk is full of saturated fat and cholesterol, I just want to mention a few important findings. It is important to note that over 70% of our brain is fat and 25% of all cholesterol in our body is found in our brain (1) in what is called the white matter where voltage transmitting axons are coated with cholesterol (myelinated). Thus, cholesterol and fat are important for us.

While there is a huge controversy over the benefit versus harm of saturated fats and cholesterol, more studies now show that saturated fats and higher levels of cholesterol are actually better for us, particularly for women. In fact, saturated fat is not associated with heart disease as suggested by many studies.

To add insult to injury, cholesterol is not actually made from fat but from acetoacetyl-CoA (2) by a 19-step process in the liver. We can choose to eat cholesterol but if we don’t eat enough, the liver has to make cholesterol. When we don’t eat cholesterol, the liver makes less cholesterol than each person’s optimal level (2). The only bad cholesterol our liver makes are triglycerides that do clog up arteries but they are made of sugar and under special circumstances. Thus, regardless in what stage studies are at now, something that every single cell is made of in our body – the membrane of each human cell is made of lipid bilayer – cannot possibly be bad for us: we are made of the stuff.

As in the story above, someone who feels the urge to drink a lot of water is usually not getting enough or the right balance of electrolytes. Moreover, the act of drinking too much water is harmful since it dilutes electrolytes. Drinking whole milk, which is full of electrolytes, on the other hand, is good for us migraineurs and others alike. Few people realize that milk is a great source of electrolytes, protein, and good cholesterol. Most of us were told from early on in our lives that milk is for cows and not people; milk is bad for us; it has puss in it; it causes puss; it makes one phlegm up; it makes us fat; it has too much fat; etc. We have been told not to drink milk, and as a result, many folks are having difficulty managing electrolyte and cholesterol balance.

I think that milk is a perfect food, assuming of course, that it is organic, whole milk, not treated with hormones and antibiotics, as in the story above. Raw milk is not legal everywhere so while drinking safe raw milk is healthier, it may not be available to everyone. Reduced fat milk does not have the benefits of whole milk and also contains added sugar and proteins that are not all that great for you. In fact, if you have no time to eat a meal, be it breakfast, lunch, or dinner, a glass of whole milk is an ideal replacement.

So, as Kristin recovered from her migraines and is also preparing to have her brain stimulator surgically removed, she joined the thousands of migraineurs who have joined our migraine community on Facebook. Enjoy Kristen’s story and join the several thousands who have been able to stop all their medicines and remained migraine free.

Sources

  1. Perlmutter D & Loberg K (2014) Grain Brain: The Surprising Truth About Wheat, Carbs, and Sugar – Your Brain’s Silent Killers (Hodder & Stoughton).
  2. Dr. Kendrick M (2007) The Great Cholesterol Con; The truth about what really causes heart disease and how to avoid it (John Blake Publishing, London, England) p 270.
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Sweet Death by Sugar

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We all know that sugar is bad for us but we cannot resist it. Why not? Expert Robert Lustig MD, reasoned on 60-Minutes that for humans in nature all sweet tasting things are edible and not poisonous. There are no toxins in nature that taste sweet, and thus, evolutionarily speaking, favoring sweet things is predetermined in our genes; we are born liking sweets. All of this is true with one major exception: sugar, the natural substance, can become poisonous when modified.

Sugar and Ethanol

Consider the simple modification of squeezing a fruit for its juice. The modification is not chemical: we merely separated the sugary liquid from the insoluble fiber in the fruit–some soluble fibers may remain. This little change makes no difference for most fruits or our taste buds, but it modifies how our body metabolizes sugar in it. According to Lustig’s book Fat Chance (a must read!), when we eat the fruit with insoluble fiber attached (typically the skin), the fructose in the fruit (most sugar in fruit is fructose) bypasses our metabolic digestive process (insoluble fibers are not digestible) and heads straight to the gut where the good bacteria digest the fructose as their food from the fibers, thereby producing more nutrients for us. But if we drink the juice alone without any insoluble fiber, the same amount of fructose now gets into the metabolic cycle and by a complicated process turns into ethanol and gets stuck in the liver. Ethanol is a toxin. Ethanol is an alcohol we also use to improve car mileage. Ethanol causes non-alcoholic “alcoholic” liver disease. In fact, ethanol is alcohol and those drinking apple juice (thinking of kids now) are in fact drinking alcohol in terms of the likely outcome of the metabolic process, as per Dr. Lustig.

So we all thought that feeding our kids fresh fruit juices is a good thing but we also knew that they should not be getting too much sugar because their behavior changes from it. Now it is clear why their behavior changes: the part of sugar that turns into ethanol is alcohol. The other parts of the fruit juice that do turn into digestible sugars (glucose and sucrose) do something else to the body.

What is Glucose?

Glucose is “blood sugar” meaning the sugar our body can use. Sucrose converts to glucose as well. What happens to the glucose?

Some stores sell glucose in a liquid gooey form—thicker than honey—that I recommend you taste. Take a small teaspoon, fill it with glucose and swallow. The first thing you will notice (yes, I did the tasting test) is that it is not that sweet. The second thing you will notice is that the moment you swallow it, you cannot count till 5 and you are hot. So you take your sweater off. Then you have the urge to do something—paint the house? Mow the grass? If you are a kid: bounce off the walls and drive the people around you nuts. This is normal. This is what glucose feels like.

Note, however, that when you eat a teaspoon of table sugar, you will neither feel so hot, nor will you have so much energy. What is the difference? What happens when you drink a diet drink or eat sugar substitutes? You will neither be hot nor have any energy. The difference in feeling hot and having energy versus not feeling hot and not having energy represents the difference in the metabolism of glucose versus fructose and the fake sugar stuff.

The Metabolism of Glucose versus Fructose

I will not get into deep chemical equations or models; for that please watch the video below by Dr. Lustig. Rather, I will reduce all complexity and simply tell you the end of the story with as minimal of the underlying process as possible.

When food arrives into the body, insulin is released to convert the food into fat and deposit it for later use as glucose. Glucose is used by our brain and muscles for energy. After insulin has done its conversion, all insulin is used up. When the brain is hungry, it fetches the hormone leptin to get some energy. Thus, leptin grabs a hold of the available glucose and serves it to the brain (this is highly simplified!). The brain is happy and full of energy.

Now consider the situation when the only food we eat is glucose. Insulin is released but it has nothing to convert. It is already in the final form (glucose for the brain) and so the glucose goes straight to the brain, the kids are popping off the wall, and you suddenly find yourself painting the house. Note, however, that the insulin is in the blood and it is waiting for the food to arrive so it can work and convert it to fat. But there is no food; we only ate glucose and it is already being used by the brain! So what is insulin in the blood to do? Insulin stays in the blood, circles around looking for food. It finds none. By staying in the blood, over time this is a “cry wolf” scenario and the body starts ignoring insulin announcing the arrival of food that isn’t there. This is how insulin resistance starts.

Now consider that instead of glucose, you drink a glass of apple juice. It has natural sugar in it, some vitamins (very little), no fiber, no protein. The sugar of fruit is mostly fructose but a small part of it is also sucrose. So insulin releases again to match the size of the apple juice drink we just had, but again, it faces a problem. While sucrose becomes glucose in our body and can be converted and stored as fat, fructose is not seen as sugar. So once again, insulin is looking for food but finds none; it keeps on circling in our blood looking for food. It is ignored and insulin resistance begins.

The Metabolism of Glucose versus Sugar Substitutes & “Natural” Sugars like Stevia

Now consider you eat a diet something—by diet I mean sugar substitutes with reduced or zero calories. It certainly tastes sweet (very sweet indeed) but again, there is no glucose or sucrose in it and while it does not become alcohol in the liver, it certainly makes insulin run around in circles looking for food to convert to fat and deposit. Cry wolf again and the insulin is ignored. Insulin resistance begins. Why is this important? Because insulin resistance is type II diabetes!

The Famine

Now let’s continue about the peril of our non-toxic sweets. The fact that insulin is out looking for glucose also signals leptin that energy is incoming! Leptin is a hormone that is in charge of messaging the brain that glucose is available. In the case when insulin is running around in our blood in search of food it can convert to fat for later use as glucose but there is no food to be found, leptin finds no glucose. Thus, leptin tells the brain that famine is here.

Famine for the Brain is Obesity for Your Body!

The famine message to the brain means one thing: conserve energy. It reduces all non-essential activities, and literally, will not let you get up from that couch! This is highly simplified of course, but pay attention to the outcome. You are actually eating and drinking and at the same time your brain is getting the message of famine. What will that lead to? When the brain thinks it is famine time, it is famine time. The fact that you are eating and drinking sugar or sugar substitutes with lots of calories is not noticed by the brain. As far as it is concerned, there is no glucose available so it must slow your metabolism. A slow metabolism leads to obesity.

Sugar Anyone?

So, while there are many people who think nothing of having sweets or a soda, consider what it does to your body! Consider that it slows down your activity and forces you into famine state even though you are well fed! Consider that it makes you obese and sets you up for type 2 diabetes.

Now tell me if you still think that sweets are not toxic poisons for us! They are. And there is one more thing to add to the story that no one talks about. I mention this because I deal with a group of migraineurs—I was one of them until I figured things out and wrote a book about it and several articles about it on Hormones Matter.

Consider this quote from the Harrison’s Manual of Medicine:

…serum Na+ falls by 1.4 mM for every 100-mg/dL increase in glucose, due to glucose-induced H2O efflux from cells. (page 4)

Na+ is sodium ion. Sodium is part of sodium-chloride, which is salt. Glucose-induced H2O efflux from cells represents water exiting the cells as a result of an increase of glucose. Why is that, you may ask? The answer is very simple: sugar is an amazing water soak-up device. It pulls water from everywhere it can. It holds onto water like its life depended upon it. Unfortunately for the body, sugar pulls the water from the cells leaving the cells empty on the inside and a lot of fluid tied to sugar on the outside. As long as that sugar is there, the cells are not able to hydrate in any fashion until the level of Na+ is increased beyond a threshold level where Na+ can take water away from the glucose. Na+ also attracts water. In fact, all saline electrolyte liquids provided by IV or for drinking in hospitals are Na+ heavy to rehydrate the cells.

Thus, sugar not only starts and enhances diabetes II and obesity; it also shuts down cell hydration. This may cause headaches or migraines depending on your propensity.

In conclusion, if someone asks you if you would prefer to eat a teaspoon of sugar or a teaspoon of salt, while your taste buds will undoubtedly scream for sugar, you should know better!

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References

  1. Sugar: The Bitter Truth https://www.youtube.com/watch?v=dBnniua6-oM
  2. Longo et al., Harrison’s Manual of Medicine. 18th edition. McGraw Hill. 2013.
  3. Artificial sweeteners could cause spikes in blood sugar by By Brady Dennis September 17, 2014
  4. Washington Post: http://www.washingtonpost.com/national/health-science/study-suggests-sweeteners-could-contribute-to-obesity-and-diabetes/2014/09/17/c3c04ea6-3dc2-11e4-b03f-de718edeb92f_story.html
  5. Artificial sweeteners could lead to obesity, diabetes. By Michelle Castillo CBS NEWS July 10, 2013, 4:28 PM
  6. CBS News: http://www.cbsnews.com/news/artificial-sweeteners-could-lead-to-obesity-diabetes/
  7. Artificial sweeteners may promote diabetes, claim scientists
  8. The Guardian: http://www.theguardian.com/science/2014/sep/17/artificial-sweeteners-diabetes-saccharin-blood-sugar
  9. Do Artificial Sweeteners Really Cause Diabetes? By Published: June 7, 2013 By Jessica Chia
  10. Women’s Health Magazine: http://www.womenshealthmag.com/health/artificial-sweeteners-cause-diabetes
  11. Could artificial sweetener CAUSE diabetes? Splenda ‘modifies way the body handles sugar’, increasing insulin production by 20% by Rachel Reilly Published: 12:27 Est, 30 May 2013 | Updated: 12:27 Est, 30 May 2013
  12. The Daily Mail: http://www.dailymail.co.uk/health/article-2333336/Could-artificial-sweetener-CAUSE-diabetes-Splenda-modifies-way-body-handles-sugar-increasing-insulin-production-20.html
  13. How To Starve Cancer To Death By Removing This One Thing From Your Diet
  14. Organic Health: http://organichealth.co/starve-cancer-to-death-by-removing-this/
  15. Is sugar a toxin? Experts debate the role of fructose in our obesity epidemic By Tamar Haspel, September 2, 2013
  16. Washington Post: http://www.washingtonpost.com/national/health-science/is-sugar-a-toxin-experts-debate-the-role-of-fructose-in-our-obesity-epidemic/2013/08/30/58a906d6-f952-11e2-afc1-c850c6ee5af8_story.html
  17. Scientific team sounds the alarm on sugar as a source of disease. By Barbara Sadick Chicago Tribune
  18. The Chicago Tribune: http://www.chicagotribune.com/lifestyles/health/sc-health-1210-sugar-metabolic-syndrome-20141205-story.html#page=1
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