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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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Let It Go! Forgiveness Is Part of a Healthy Diet

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As I pulled out of my neighborhood onto the main road in my town, a truck whipped up beside me the man leaning his head out the window, shooting me the bird. We were at a stop light but apparently I hadn’t sped to the stoplight fast enough for him. My initial reaction was to return the favor- two can play at the nasty, indignant driver game. But I was on my way to yoga class, so I decided to try practicing patience instead. It wasn’t easy. I was startled by the aggressiveness of his behavior over something so trivial. I knew I hadn’t done anything wrong but his anger and negativity affected me more than I was comfortable with. “Maybe he’s just having a terrible day,” I thought. “Who gets so hateful about something so insignificant?”

You may have heard the old chestnut, “Holding onto anger is like drinking poison and expecting the other person to die.” It’s often attributed to Buddha or Nelson Mandela though it’s not clear who said it first. Versions of this quote abound because of the profound truth that anger and resentment can make us physically ill. While many religions preach forgiveness as a model for salvation or enlightenment, the science actually agrees that letting go of blame can make us healthier.

Forgiving Others

There are many theories about why it’s so hard for humans to forgive. It may be that we are not very good at living in the present moment, always worried about the past where someone may have wronged us or anxious about the present where someone may wrong us again. Or perhaps it is that we are simply wired to remember what has hurt us so that we can avoid it. For whatever reason, and no matter how counterintuitive it may feel, letting go of anger and forgiving may be one of the best things we can do for ourselves.

This can be a real challenge for many of us. Especially depending upon the type of offense and the level of hurt. It didn’t take me long to forgive the man in the truck for his obscene gesture. But I wondered how long it would take him to forgive me for the offense of not driving exactly how he wanted me to.

“People who are hurt by others too often are hurt because someone is seeking power—power over you. Forgiveness, in contrast, concerns love—-loving those who are not loving you.” 

Loving people who are not loving to you is a tall order- sometimes a Herculean, or rather Mother Teresan, task. So why should we do it? Doesn’t it just make me a sucker to forgive someone who has wronged me?

According to the Mayo Clinic, “Forgiveness doesn’t mean that you deny the other person’s responsibility for hurting you, and it doesn’t minimize or justify the wrong. You can forgive the person without excusing the act.”

If being the better person isn’t enough for you, how about being a healthier person?

A study published in the American Heart Association Journal shows a link between coronary heart disease and anger, particularly in men. “In other words, we observed a gradient in CHD risk, with evidence of increased risk even among men with apparently “average” levels of anger.”

Florida State University found a correlation between forgiveness and improved cardiovascular function.

And the European Heart Journal published a meta-analysis that concluded that outbursts of anger are associated with the short-term risk of heart attacks, strokes, and disturbances in cardiac rhythm.

If that’s not convincing enough, letting go of anger and resentment can also help with anxiety and mental health. Concordia University found that anger has a powerful and serious health consequences “for millions of individuals around the world who suffer from generalized anxiety disorder, anger is more than an emotion; it’s an agent that exacerbates their illness.”

Forgiveness can also make your life feel easier. A study done at Erasmus University showed that holding onto grudges can literally weigh you down.

“Metaphorically, unforgiveness is a burden that can be lightened by forgiveness; we show that people induced to feel forgiveness perceive hills to be less steep (Study 1) and jump higher in an ostensible fitness test (Study 2) than people who are induced to feel unforgiveness. These findings suggest that forgiveness may lighten the physical burden of unforgiveness, providing evidence that forgiveness can help victims overcome the negative effects of conflict.”

How Can We Forgive?

One of the main things we can do to release the negative feelings associated with holding a grudge is to cultivate empathy. I tried to do that with the rude driver and I try to do this with anyone in my life exhibiting behaviors I don’t understand or find off-putting. I don’t know what the truck driver was going through that day. Perhaps his girlfriend had just broken up with him and he wanted to lash out at someone. Maybe the person who parked their car so terribly has a sick child at home and was too distraught and hurried to be more considerate. We never know what other people are going through. As another favorite old chestnut says, “Be kind, for everyone you meet is fighting a hard battle.”

Another way to practice forgiveness is to let go of expectations. Expectations are the root of all conflict. Expecting other people to think and act like you, to understand what you understand, to feel how you feel, to look at the world as you look at it- these are all ways we place unfair burdens on others.

Practicing empathy and letting go of expectations for others are just part of the forgiveness process. We must also learn how to do these things for ourselves.

Forgiving Yourself

If you’re anything like me, you may find forgiving yourself to be exponentially harder than forgiving others. According to University of California, Berkeley, “The ability to forgive oneself for mistakes, large and small, is critical to psychological well-being. Difficulties with self-forgiveness are linked with suicide attempts, eating disorders, and alcohol abuse, among other problems.”

This can be particularly difficult for women. According to study published in the Spanish Journal of Psychology, guilt is significantly higher in women. The same study claims that the problem is not that women feel more guilt but that men don’t feel enough. But that’s a topic for a different article. What can we do about all this guilt? Simply, we can forgive ourselves.

How exactly do we do that?

Steps to Forgiveness

Feel the feelings

The Greater Good website from the University of California, Berkeley explains, “Research suggests that criminal offenders who recognize that doing bad things does not make them bad people are less likely to continue engaging in criminal activity. And remorse, rather than self-condemnation, has been shown to encourage prosocial behavior. Healthy self-forgiveness therefore seems to involve releasing destructive feelings of shame and self-condemnation but maintaining appropriate levels of guilt and remorse—to the extent that these emotions help fuel positive change.”

Take responsibility and apologize if the situation warrants it

“In order to forgive ourselves, we first have to admit to ourselves that we blew it. We have to take ownership and acknowledge the flaw or mistake—and that feels almost counter to our sense of survival! It’s how we learn and grow.” – Psychology Today

Practice empathy for yourself and the person you wronged

You are human and make mistakes. The person you wronged is human and makes mistakes, too.

Learn from the experience. One of the great things about feeling bad is that we don’t like it. In fact, we go to great lengths to avoid feeling bad. And that’s exactly what makes feeling bad, making mistakes, such a powerful teacher. Our mistakes are painful so that we may learn from them. Try not to miss the lesson in whatever situation you find yourself in so that you don’t have to relearn it again in an even more painful situation.

Ask for help if you need it

According to Joretta L. Marshall, PhD, a United Methodist minister and professor of pastoral care at the Eden Theological Seminary in St. Louis, it can be done with or without formal therapy. “But not without community of some kind. It is in the context of our relationships (whether with therapists, pastors, counselors, churches, families, and friends) that we experience the grace of being forgiven and forgiving others.”

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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 published originally on August 11, 2016. 

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Heart Attacks in Women are Different: It Took Doctors Days to Diagnose Mine

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I guess I always knew it was coming, but I would never have banked on it being one month and one day after I turned 38!  I have a strong family history of heart disease and heart attack in my family, my Father passed suddenly at 49.  He was fit and healthy, never smoked, wasn’t a big drinker, played sports and generally lived a good life. My Aunt passed at 41 years of age. She was a big character who was full of life. My brother was 42, and like me, one of the lucky ones!

I suffer from chronic endometriosis and have had seven surgeries in eight years for this ugly disease, so I’m accustomed to pain, but the pain of the heart attack was something else!  It started unassumingly a week prior, with a horrid headache every day, behind my left eye, I put it down to hormonal changes and thought no more about it. I pushed on through.

I just didn’t feel myself on the Saturday, “off my eggs” as my Granny would say, I was so tired and out of sorts.  I was grateful when it was time to go to bed. I’d had “heartburn” and just wanted to sleep it off.  At 4:50am I was jolted awake with the searing, heavy pain in the center of my chest and an odd sensation in my throat area, like a squeezing.  “Bloody heartburn!”, so I got up and reached for more antacids and a glass of milk, and paraded around my lounge floor trying to pass wind and relieve the discomfort. After an hour it just wouldn’t relent, so I called the Healthline Service for some advice.  I was shocked when the Nurse at the other end said she was calling me an ambulance and began running through I was to do.  Feeling a bit silly, I put my dog outside, gathered my regular asthma medication and got dressed. My partner gave me 1000mg of dissolvable Asprin. They were here pretty swiftly and had me hooked up to the ECG machine, which I though odd for heartburn.

The pain was increasing, my blood pressure was elevated (nothing unusual for me when in pain), so I was given two sprays of GTN (Glycerin Spray) which lifted the pain almost immediately; finally the relief I had been looking for.  When I arrived at the Emergency Department, I was seen quickly by the team of Doctors and Nurses.  More ECG’s were taken, and my blood pressure was checked regularly.  I was given the results that my blood test had come back clear for tropinon, which would indicate a heart attack. Just to be sure, in came the ultrasound machine to take images of my heart. This was also given the all clear.  I was discharged with a prescription for Losec and Gaviscon and given a diagnosis of acid reflux. I felt so silly having been taken by ambulance and such a fuss having been made from just a bit of wind.

I was fine when I arrived home, just exhausted from being up all night in pain, but feeling reassured that my issue was gastric, not cardiac. I went about my day as normal, and headed over to see my Mum around 2 o’clock.  Just 5 minutes drive away from my Mum’s I had to stop in at a small shop and buy some milk and antacids, heartburn strikes again.  It came on quickly and intensely.  My pain increased, and all the other symptoms had come back, along with an aching in my arms and shoulders.  500mls of milk, and 5 fast acting antacids were quickly consumed while sitting in the car, and I waited for relief.   It didn’t come, and again the pain in the centre of my chest was starting to become overwhelming.  I drove quickly to the pharmacy just down the road, and asked for the strongest over-the-counter antacid, I again got back to the car and chewed my way through 3 chalky tablets praying for relief.  Still it didn’t come.  I had a sense I had to get to my Mums.

When I arrived she noticed immediately I looked off colour, and I explained about the trip to hospital and the diagnosis of acid reflux, and that I had just begun feeling very uncomfortable again.  She breaks out the Eno’s powder, so I knocked back 6 teaspoons worth, even doing star jumps to cause enough of a reaction to shift this dreaded wind! Of course I burped, who wouldn’t after that, but still, no real relief. I could see that I was upsetting my Mum so I pretended that it had improved and that I was going home to prepare dinner for that night. So again I drove the 20 minutes back home. I just couldn’t settle, parading up and down, rubbing my chest until my partner arrived home from work at 5.30pm.  I had little breaks from the pain, lasting 5 or 10 minutes but it just kept coming back.  By 9pm I was starting to worry a little so I called my Aunt who has been a nurse for over 40 years. She suggested that I go back to hospital again, so in the car I jumped telling my partner to stay home as he was up early the next day for work, and it was just a case of bad heartburn.

When arrived at the Emergency Dept at 10 pm, I was assessed quickly, my BP at that time being 211/142, which was initial cause for alarm.  Quickly taken through and again the process begun.  ECG ordered, which looked clear, bloods taken, then the wait.  The pain was still coming and going in waves, until I felt as if I had been punched in the back.  I was given morphine to address my pain levels.  My next BP was 238/157, but still my ECG was clear.  My blood results came back around midnight and again they were clear, but needing a further top up of pain relief by 2 am as I sat straddled the bed in my cubicle, grunting in pain, and rubbing my chest. I had one last set of bloods taken, and sent off to have a CAT scan with contrast taken, again the scan was clear and showing no signs of any issues.  I was asleep not long after and awoken around 5.30 am with the news I had a positive result.  “Great!” I thought, “So I can go home now?” I asked the young doctor. “No, you’re going directly to the Cardiac Unit, your blood test is positive for a heart attack”.

It all happened pretty quickly from there. I was taken in to Theatre to have an angiogram, and have a stent fitted into my right coronary artery.  I’m one week post-surgery and still coming to terms with the situation.  I feel so blessed that I have had the opportunity to survive my heart attack, it certainly puts a new spin on what life means to me, and what I want out of it. There’s one thing I’ve learned from both this experience and my endometriosis, sometimes we know our bodies better than any doctor, sometimes we need to ask questions, and most importantly we are always our own best advocate, so I’m now a great believer in speaking up for myself.

I asked the doctors why my heart attack took so long to diagnose. I was told that it can take hours, in my case days, for the enzyme to build up in the blood. Even when the enzyme does finally build up, in women those enzymes are sometimes much lower than in men. My tropinin levels were only 178-243, whereas in the case of a man’s heart attack those readings can be in the thousands. Another reason my heart attack didn’t show on the ECG reading was because the damage was not in the main area of the heart, so it didn’t cause any redirection of the current.

I am grateful for the young ER doctor who recognized the symptoms of my heart attack and pushed for one more set of tests before releasing me again. I am especially grateful that those blood tests finally revealed the elevated cardiac enzyme. Had another test come back positive, I am certain they would have sent me home and I would not be here writing about my story.

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This article was published originally on Hormones Matter on February 25, 2014.

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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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