Central arterial blood pressure - Kendrick

What is your blood pressure (BP)?

 

http://drmalcolmkendrick.org/2013/09/09/what-is-your-blood-pressure-bp/

 

Central arterial blood pressure

(What is it, don’t like it. Pay attention it could save your life)

 

It is a pressure that is measured, almost exclusively, by placing a cuff around one arm – usually the left. The cuff is then inflated to a point whereby all blood flow is stopped. If you have placed a stethoscope over the brachial artery (artery in the arm) you will hear nothing at this point. Because there is no blood flow, and nothing to hear.

 

As the pressure in the cuff is lowered, a noise will be heard as the blood first starts to squeeze through. This is defined as the systolic blood pressure i.e. the point of highest arterial pressure, just after the heart contracts. A sharp tapping noise would be the best description.

 

As you lower the pressure in the cuff, the noise changes and muffles. Eventually, there will come a point where the blood is flowing through the brachial artery all the time …the point of ‘lowest’ blood pressure. Once this pressure is reached, the noises in the brachial artery cease. This is defined as the diastolic blood pressure. (The pressure does not reach zero, because the heart pumps once again to boost the pressure again).

 

All of this means that your blood pressure is presented as two figures. The highest recorded pressure (systolic) over the lowest (diastolic).

 

Historically, blood pressure measured in millimetres of mercury. Because, in the good old days, blood pressure meant how many millimetres of mercury could be pushed up a tube by the force of the cuff being inflated round the arm. If you used water in the tube, instead of mercury, we would measure in metres, not millimetres.

 

Despite the fact that mercury has nothing to do with the process any more, the measurement is still called mmHg (millimetres of mercury that can be pushed up a narrow tube). A normal blood pressure is around 120/70. If you are an Olympic weightlifter, the blood pressure can reach over 300mmHg during a lift. Which is pretty high.

 

In a nutshell that is what your blood pressure is…. but what does it mean? The pressure in your arm is certainly not the same as the pressure in your finger, or your brain. The pressure will be different in the right and left arms, as the blood has further to go before it reaches your right arm. It will be different if the cuff is put in a slightly different place on the arm. It will also be different if you are stressed, if the cuff is a bit small – or slightly too big.

 

In short, your blood pressure can be all over the place. Which is why a single measurement is not used to define high blood pressure. You need at least three. In fact, this is not nearly enough either. To diagnose someone with high blood pressure you really need to monitor the blood pressure over a twenty four hour period – using ambulatory monitoring. This helps to get rid of ‘white coat’ hypertension (high blood pressure). A phenomenon whereby the act of a healthcare professional wrapping a cuff round your arm sends your blood pressure sky high.

 

Because of the difficulties of measuring the blood pressure, it is estimated that around twenty five per cent of people diagnosed as having hypertension – do not actually have high blood pressure at all. Which means that they are taking drugs that they do not need. Costing the NHS at least a billion a year, and a great deal more around the world (yes, this truly is an international blog).

 

The other major problem with measuring the blood pressure at the arm is that it may not reflect the blood pressure just after the blood leaves the heart. The central arterial pressure. This is important, because this is the most critical pressure of all. There are a number of reasons why this is so.

Firstly, the central arterial pressure is the pressure in the aortic arch (the U bend in the aorta (biggest artery in the body)). This represents the pressure that sends blood straight up the carotid arteries and into the brain, which is clearly important with regard to stroke risk. [This where two, critically important, small BP sensing organs sit]

 

It is also the pressure that has the greatest impact on the kidneys. The renal arteries branch directly from the aorta itself. Therefore the central arterial pressure is closely monitored by the kidneys, which are the primary organs of blood pressure control. In addition, the central pressure has the greatest impact on the aorta itself. A relatively common cause of death is a ‘ballooning’ of the aorta (aortic aneurysm).  Such aneurysms can burst, with obviously catastrophic results.

 

Now, there is no doubt that the pressure at the arm is related to the central arterial pressure. It must be – to a certain degree. And for most people measuring at the arm is probably a good enough estimate of the ‘true’ blood pressure.

 

However, if your blood pressure measurement is high, or low, or you are on blood pressure medication….then the pressure measured in the arm becomes increasingly unreliable. It can even become misleading i.e. your pressure seems to be going down in the arm – but it is not going down as much centrally¹. (It may even be going up.)

 

‘The results of the Conduit Artery Functional Endpoint (CAFE) study also suggest that the central aortic blood pressure may be more predictive of cardiovascular events, such as stroke and heart attack, than traditional peripheral (brachial) blood pressure measurements. CAFE was the first study to repeatedly measure central aortic pressure in a major clinical outcomes trial and the first to show that central aortic pressure is a plausible mechanism to explain the better clinical outcomes seen in patients treated with amlodipine-based therapy in ASCOT.’

 

Of course, central arterial blood pressure is somewhat difficult to measure. Up till fairly recently you had to insert a catheter, with a measuring device, into to the femoral artery, and push it up to the aortic arch. This would not be highly practical during a consultation with a GP. So central BP is very rarely measured. But it would be best if it could…

 

The anomalies of blood pressure trials

Now to introduce another thread to this discussion. Which is the fact that, if you choose to look at the clinical trials on blood pressure lowering with an objective eye, there is almost no correlation between the amount the blood pressure is lowered (at the arm) – and any clinical outcomes. By which I mean that the rate of heart attacks and strokes do not relate to the degree of blood pressure lowering.

To quote a series of bullet point in the European Journal of Cardiology entitled ‘There is a non-linear relationship between mortality and blood pressure’:

• Drugs that lower the blood pressure by about the same amount have very different effects on outcomes
• Cardiovascular benefits of ACE-inhibitors (Angiotensin Converting Enzyme – Inhibitors), independent of blood pressure, are not observed with calcium antagonists, despite the latter having more pronounced effects on blood pressure.
• HOPE (Heart Outcomes Prevention Evaluation study) demonstrated that ACE inhibitors provided diverse and profound cardiovascular benefits, with only trivial differences in blood pressure between the treatment and control groups
• ALLHAT (Antihypertensive and Lipid Lowering treatment to prevent Heart Attack Trial) showed a dramatic difference in cardiovascular risk between alpha blockers and diuretics, with essentially no difference in their effect on blood pressure. The investigators of ALLHAT concluded ‘blood pressure lowering is an inadequate surrogate marker for health benefits in hypertension.’

This is extremely important, because for many years, most of the ‘evidence’ on blood pressure treatment has been based on a statistical model known as the ‘log-linear’ model. This model states that ‘the relation of blood pressure to risk of death is continuous, graded, and strong, and there is no evidence of a threshold.’ (Stamler). The model itself, and that statement, were almost entirely based on evidence from the Framingham Heart Study. The study that your doctors will use to calculate your risk of dying of heart disease.

Essentially, according the log-linear model, the lower your blood pressure (measured at your arm), the better. And the more that drugs lower it, the better. At least this is the thinking that is currently used.

However, thirty years ago Ancel Keys (yes, him) concluded that the linear model, in terms of the relationship of overall and coronary heart disease death to blood pressure was ‘unjustified’. Ten years ago, the authors of the article ‘There is a non-linear relationship between mortality and blood pressure’ further concluded (after reviewing the Framingham data – the data upon which your doctor will determine your future risk of dying of CVD)…the following:

‘Shockingly, we have found that the Framingham data in no way supported the current paradigm to which they gave birth. In fact, these data actually statistically rejected the linear model. This fact has major consequences. Statistical theory now tells us that the paradigm MUST be false ….’ (Their italics and capital letters).

In short, the blood pressure model that is used worldwide is simply, plain damned wrong. The reality is that the amount the blood pressure is lowered in the arm bears little, or no, relationship to any benefit on heart attacks and stroke.  How can this be? Well, there are two major reasons for this. One of which I am covering in this article. The other, later. Now to introduce another thread.

How do blood pressure lowering drugs work?
I am going to avoid being too technical here – which is tricky. I am also, only focussing on the four most commonly used blood pressure lowering agents/classes.

1: Diuretics. These drugs make you pass more urine, by blocking sodium re-absorption by nephrons in the kidney. This means that you pass a lot of urine (diuresis). This puts you into a state of mild dehydration, thus reducing blood volume. Exactly why this lowers your blood pressure is a moot point. (You may think you know. However, it is almost certainly far more complicated that what you are thinking – I certainly don’t understand it)

2: Beta-blockers: These, effectively, slow your heart rate and also decrease the pumping force of your heart. An unwanted effect is that they also cause peripheral blood vessel constriction.

3: Calcium channel blockers: These reduce the force of contraction of the heart, dilate blood vessels (arteries not veins), and slow the heart rate at bit. All of which lowers the blood pressure.

4: ACE-inhibitors: (a bit more explanation is required to explain how they work). The kidneys are the primary organs that control blood pressure. If they pick up that the BP is too low, they release a substance called renin. Renin triggers a whole series of other hormones into action. Ending up with increased angiotensin II levels.

This hormone has multiple effects. It reduces urine production, by increasing sodium absorption. It causes constriction of arteries, and stimulates the pituitary gland to produce anti-diuretic hormone (ADH) – thus reducing urine output.  It does several  other things too, all of which result in the blood pressure going up.

As is the complex way of the body, the kidney doesn’t actually produce angiotensinogen II  when the blood pressure drops(which would seem logical). The kidney produces renin, the liver produces angiotensinogen. When these two hormones met, angiotensinogen is converted into angiotensin I. Then angiotensin I is further converted to angiotensin II by an enzyme called Angiotensin Converting Enzyme (ACE). (There will be an exam later)

All of this means that angiotensin II is the main, active, substance. Once it has been produced, angiotensin II goes off to do all its blood pressure lowering things. If, however, you give an ACE-inhibiting drug (ACE-inhibitor), angiotensin II production is blocked, and the blood pressure will fall.
Anyway, as I hope has now become clear, the blood pressure lowering classes of drugs all work though very different mechanism. They all lower the blood pressure at the arm, but what else are they doing?

Beta blockers tend to constrict peripheral blood vessels. Calcium channel blockers and ACE-inhibitors tend to dilate them. Diuretics are mainly neutral on blood vessel diameter.  ACE-inhibitors also do something else that is extremely important. They stimulate Nitric Oxide synthesis in the blood vessels themselves, which both dilates arteries, and increases blood vessel flexibility.
In short, the effect on central and peripheral blood pressure of various BP lowering medications will be very different.

Bringing these thoughts together
You may think, why now? Why is he quoting articles, and research, from many years ago? Well, you have to bear in mind that it is a long time since anyone did a placebo controlled blood pressure lowering study. It would be considered unethical to do so now (such are the alleged enormous benefits of BP lowering). So, there isn’t really any fresh information. Just the monitoring of one drug vs. another, and assuming benefit based on the degree of BP lowering – using the log-linear scale.
However, it has now become possible to measure central blood pressure by simply using a cuff placed round the arm. I have had this process explained to me many times, and cannot really understand how it is done. But the results are repeatable, and accurately reflect central blood pressure. Which is all that really matters.

When you do this, you can also measure the velocity of the pulse wave, which is an accurate indicator of arterial flexibility – and thus arterial health. If your arteries are stiff this is a worrying sign, and reflects poor arterial health. The more flexible your arteries are, the better.

At last, hoorah, instead of wrapping a simple cuff round people’s arms, we can use a complicated cuff to look at two more, really important things. The central blood pressure, and arterial flexibility. This gives us far more information.

Perhaps most importantly, we can monitor the effects that different blood pressure lowering medications have, beyond their impact on the BP measured at the arm. We can see if central pressure is increased, or decreased, or if arterial compliance (flexibility) is improved.

I think that this is a major breakthrough in medical practice. So much so, that I have acquired a machine for myself, and will be using it on a regular basis. I fear it will take the wider medical profession about twenty years or so for this to become an accepted way of measuring blood pressure. This is about the normal lead time for new ideas to become standard practice.

It may, of course, take longer. Or never happen at all. At the risk of going off on a major tangent, I remember looking at pictures of roads Sweden in 1967. This was when they switched from driving on the left, to driving on the right. 3^rd Sept 1967


As you can see from the picture, a bit of a mess. But imagine if any country tried to do it now, with the extra number of cars and lorries, and roads, and signs. This would probably be just too difficult.
How about changing the way we look at measuring blood pressure. We have always measured blood pressure using a simple cuff on the arm. All the clinical studies on BP lowering were done using this technique. All the data, all the guidelines….everything, is now based on doing BP measurement in this way.

Just imagine what happens if someone now says. Hold on, this is not good enough. The measurement is inaccurate and potentially confusing, and it doesn’t’ really tell us what we need to know. Let us start again. Let us drive on the right, not the left.

In the meantime, whilst the medical world grapples (or chooses not to grapple) with a trillion dollar problem, you can do yourself a favour and get your blood pressure measured centrally.

More on this later.

1: http://www.medscape.org/viewarticle/518570
2: Port S, et al: ‘There is a non-linear relationship between mortality and blood pressure.’ European Heart Journal (2000) 21, pp. 1635 – 1638
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Read the complete article here.

Another article here and here.

Preventing Glucose-Induced Cardiovascular Damage - Michaels

Preventing Glucose-Induced Cardiovascular Damage

Conditions Associated With Elevated Blood Glucose and Advanced Glycation End Products

Elevated cholesterol and atherosclerosis49,50 Symptoms of carotid artery atherosclerosis (major risk for stroke)51 Risk of developing high risk cardiac rhythm disturbances following heart attack52 Cataracts of the eye35 Overall risk of developing cancer53 Risk of developing fatal cancer54 Increased prostate size in benign prostatic hyperplasia (BPH)55 Abnormal elevation in liver enzymes, markers of liver damage56 Incidence and severity of obstructive sleep apnea57

Blood vessels are lined by a thin layer of cells called the endothelium which constantly regulates blood pressure and flow. Damage to the endothelium, which occurs in response to elevated glucose levels, is an important first step in producing heart attacks, heart failure, and stroke.

Studies now show that benfotiamine can prevent endothelial dysfunction and substantially improve blood vessel and heart muscle function, even in the face of glucose-induced tissue damage.

The process of healthy endothelial cell replication is vital to maintaining healthy arteries. Excess levels of glucose can reduce endothelial cell replication. The addition of benfotiamine to endothelial cells grown in a high-glucose environment corrects the defective replication. Benfotiamine accomplishes this through normalization of advanced glycation end product production.

High glucose levels also trigger early death of endothelial cells through the process called apoptosis; benfotiamine supplementation reverses increased apoptosis in cultures of endothelial cells by several mechanisms.

The body produces toxic alcohol-like compounds called polyols during periods of high blood sugar. Polyols disrupt endothelial and cardiovascular cell function. Benfotiamine reduces production of polyols, accelerates the rate of glucose breakdown, and reduces free glucose levels within cells. All of these effects further contribute to protection of endothelial cell function.

After a heart attack, or as a result of persistently high blood pressure, heart muscle cells beat more weakly than they should, resulting in heart failure. High glucose levels and advanced glycation end products substantially contribute to this diminished heart muscle function. Studies show that benfotiamine abolishes many of the abnormalities in heart muscle cell contractility, which may "rescue" impaired heart muscle and improve its ability to pump blood effectively. Benfotiamine activates important cell survival signaling pathways in heart muscle cells failing under the effects of elevated glucose.

Atherosclerosis

Not all advanced glycation end products (AGEs) are produced internally in the body. Consuming a meal rich in AGEs (such as one abundant in browned meats or caramelized sugars) can increase blood levels of AGEs and impair endothelial function. Supplementation with benfotiamine, 1,050 mg/day for 3 days, completely prevented the changes in endothelial function and blood flow produced by such a meal in a group of human subjects.

In addition to its effective control of AGE-related endothelial dysfunction, benfotiamine exerts powerful direct antioxidant effects. In rats with experimentally induced vascular endothelial dysfunction, benfotiamine reduced oxidative stress and enhanced favorable generation of nitric oxide, a compound that contributes to blood vessel relaxation.33,34 The result was an improvement in endothelial integrity and function.

All of these endothelium-protecting effects make benfotiamine an essential nutrient in your fight against the devastating effects of elevated blood glucose on your cardiovascular system.
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Read the complete article here.

Salt intake What of Nuns? - Kendrick

Salt intake – What of Nuns?

 

Excess salt intake is one of the great issues in preventative medicine. Last year I watched a bus go by, with an advert for reducing salt plastered all over the side. Some restaurants have taken salt cellars off their tables, to protect customers. Many foodstuffs now have their salt content clearly labeled, with high salt content given a red sticker.

Given all of this you would think, would you not, that the case for excess salt consumption causing cardiovascular disease had been made beyond even the slightest possibility of doubt. One of the arguments in support of the dangers of salt consumption (the one that I am looking at in this article), comes from the native peoples living in the Amazon

The Amazon is an extremely low salt environment, and the average salt consumption of those living there is at very low. Several studies have found that the tribes people living in the Amazon have very low blood pressure which does not increase with age. They also have very little in the way heart disease and strokes.

‘Primitive societies who ingest little or no salt have no hypertension¹’

Proof, the anti-salt lobby cry, that it is excess salt intake that causes our blood pressure to rise dangerously.

Or is it? When presented with ‘proof’ like this I tend to look for contradiction, rather than confirmation. Are there, I wondered, other populations that fail to demonstrate a rise in blood pressure with age, that do not have a low salt consumption. My attention was drawn to nuns, living in Italy.

‘The powerful effect of psychosocial and acculturating influences on population blood pressure trends seems to be confirmed, through longitudinal observations, in the nuns in a secluded order. After initial observations had been made on culture, body form, blood pressure, diet, and other variables in 144 nuns and 138 lay women, included as a control group, a 30-year follow-up study was undertaken. Most striking were opposite trends noted between the two groups in blood pressure trend. During the follow-up period, blood pressure remained remarkably stable among the nuns. None showed an increase in diastolic blood pressure over 90 mm Hg.’

So, nuns do not develop high blood pressure as they age. What happened to the control women in this study?

‘By contrast, the control women showed the expected increase in blood pressure with age. This resulted in a gradually greater difference (delta>30/15 mm Hg) in systolic and diastolic blood pressure between the two groups, which was statistically significant.’

No difference in diet or salt consumption, yet one population developed the ‘normal’ Western rate of hypertension whilst the other did not. What did the authors of this thirty yearlong study think was the reason for this finding?

‘In conclusion, it seems reasonable to attribute much of the difference in blood pressure and cardiovascular events, to the different burden in psychosocial factor and to the preserved peaceful lifestyle of the nuns².’

Now I do not know for sure if those living in the Brazilian rain forests have managed to preserve a traditional peaceful lifestyle – but it seems a reasonable assumption to make.

However, the main point I am trying to make here is that you do not need a low salt diet in order to prevent hypertension. You can find populations with a normal salt diet who do not develop hypertension either.

What factor, or factors, appears to link these two populations? The factor appears to be living a preserved peaceful lifestyle. This would suggest that stress is the cause of hypertension and cardiovascular disease, and not salt. Whilst association cannot prove causation, a lack of association disproves it.

1: Freis ED. The role of salt in hypertension. Blood Pressure 1992; 1: 196-200.
2: Timio M, et al: ‘Blood pressure in nuns in a secluded order: A 30-year follow-up.’ Miner Electrolyte Metab. 1999 Jan-Apr;25(1-2):73-9

JAMA on salt HERE.
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Read the complete article here.
Another article here.

Salt guidelines raised ... as Canadian experts cite existing targets as ‘not feasible’

More data in the Salt Wars - Aug 14, 2014; http://www.medpagetoday.com/Cardiology/Hypertension/47203

An article by Marion Nestle - http://www.foodpolitics.com/2014/08/its-salt-arguments-again-new-research-arguments-over-public-health-recommendations-and-issues-of-conflicts-of-interest/

Are We Over-Treating High Blood Pressure? - Peter Lipson

Forbes is not my usual go-to for my medical posts here but I thought this was an article worthy of note. Here is a small quote from the article. Please read the complete

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Are We Over-Treating High Blood Pressure?
By: Peter Lipson,

Heath argues that this is too aggressive, and that we over-treat people whose BPs run in the 140-160/90s range. She bases her opinion on a recent review published by the Cochrane Collaboration, an evidence-based medicine group that keeps an eye on such things. The review included data from four studies (they use fairly strict selection criteria).

Cochrane’s conclusions were fairly clear: when data from the four studies were analyzed,  the treatment of mild hypertension did not prevent important outcomes such as heart attack and stroke, but did cause side-effects.

At what level to treat high blood pressure is a hugely important question, given it’s impact on the nation’s health. As I said above, we’re talking about people who don’t already have other heart risks, and we’re talking about whether or not to commit them to long-term treatment. We’re also talking about patients who have not been able to bring their pressures down through proper diet and exercise (which, unfortunately, is a whole lot of people).

So what evidence is there to treat so-called low risk people with mild high blood pressure?

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Read the complete article here.

Is salt really so bad for you? - Fenster

Is salt really so bad for you?

Decades of science show NO conclusive evidence that cutting back on dietary sodium reduces cardiovascular morbidity

By Michael S. Fenster                     
                        

Enlarge

(Credit: This piece originally appeared on Pacific Standard.

 

No salt, low salt, salt free, heart-healthy salt substitution–any added salt will hurt your constitution. It reads like some bizarre, Seussian tale. Excepting that we’ve heard it not from the good Dr. Geisel but from the medical community and public health advocates everywhere. We watch as celebrity chefs take the salt elimination cooking challenge to prepare an “improved healthy” cuisine. Self-anointed “experts” cadge, coax, and cajole us to decrease our salt, or, more specifically, sodium intake. If that doesn’t work then the specter of heart attacks and strokes is unleashed upon us, along with a dash of fire and brimstone for good measure. It is, after all, clearly in our best personal and the greater public interest.
The hypothesis is sound and the supporting data is impeccable, right?

The theory goes as follows: Salt acts to make us retain fluid. When we retain more fluid it increases our blood pressure (albeit temporarily). Increased blood pressure is hypertension. Hypertension is a risk factor for cardiovascular disease like heart attacks and stroke. Heart attacks and strokes are bad. Therefore, hypertension is bad. Thus, sodium must be bad; A causes B which causes C, therefore A causes C. Get rid of A and you get rid of C—simple basic arithmetic, no? Reduce sodium intake and you will reduce blood pressure and thus reduce the incidence of stroke and heart attack. Reducing sodium intake is good—simple, effective, and undeniably the prevailing conventional wisdom these days.

Except… one thing is missing.

The conclusive data—or any data-that definitively shows that cutting back on dietary sodium reduces mortality or significantly reduces cardiovascular morbidity. For over half a century, starting in the 1960s, there has been a vehement and salty exchange just out of public earshot involving respected scientists on both sides of this line. But with the advent of an aggressive public policy to reduce dietary sodium intake for presumed public health benefit and studies emerging suggesting negative consequences of a low-sodium diet, the clamor of dissension is heating up.
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JAMA on salt HERE.
Read the complete article here.

Here is an article from The Kennebec Journal on the division regarding the salt controversy. Here are a couple of quotes:

"Four months after an Institute of Medicine report said reducing salt to the lowest recommended level doesn't improve health and may harm it, the U.S. Centers for Disease Control and Prevention said they disagree. In an article published Monday in the American Journal of Hypertension, the CDC and New York City health officials said getting Americans to eat less salt remains a key objective with the potential to save thousands of lives."

and

"Lowering sodium to the extent required to lower blood pressure has a variety of other effects," including some that boost heart attacks, strokes and death, he said. "It's just not that simple. The message from the evidence is we don't know."

Here is another article from Food Politics by Marion Nestle.
Another article on salt here.

More data in the Salt Wars - Aug 14, 2014; http://www.medpagetoday.com/Cardiology/Hypertension/47203

An article by Marion Nestle - http://www.foodpolitics.com/2014/08/its-salt-arguments-again-new-research-arguments-over-public-health-recommendations-and-issues-of-conflicts-of-interest/
 

http://www.zoeharcombe.com/2013/03/salt-awareness-week-10-things-to-be-aware-of/

Salt Awareness Week – 10 things to be aware of

Written by Zoë on March 11, 2013
  

March 11-17 2013 is “Salt Awareness Week” in the UK – what exactly might we like to be aware of?
Let’s get some definitions out of the way first. Salt can be unrefined or refined. Unrefined salt is also known as sea salt. Unrefined (sea) salt comes with many valuable minerals and natural elements. Refined salt is also known as table salt. This is made up of sodium and chloride. There are approximately 2.4g of sodium in 6g salt. This means that approximately 40% of salt is sodium. You’ll see sodium on food labels, rather than salt.

Here are 10 things that you may find interesting about salt…

1) Like every other government target, the salt dictat has no evidence base

The NHS wants us to eat “no more than 6g salt per day.” (Ref 1) (which equates to 2,400mg sodium). Why? I have no idea and nor does the NHS. Why not 7? Why not 5? Why have a target at all? Goodness only knows. Just like 5-a-day, 14/21 alcohol units, 20-30g saturated fat, 18g fibre – none of these precise targets has precise evidence.

The NHS web site is supposed to provide evidence for government policy. Here is “Salt – the facts” which opens with “Many of us in the UK eat too much salt. Too much salt can raise your blood pressure, which puts you at increased risk of health problems such as heart disease and stroke” and then it goes on to tell you how to cut your salt intake. I don’t know about you but I found those ‘facts’ quite underwhelming.

2) We need to consume salt (and potassium) or we die

We die without salt. It’s as simple as that. Unlike cholesterol, which is also utterly life vital, our body doesn’t make salt. The term “essential nutrient” in nutrition mean that it is essential that we consume the nutrient. Salt is thus an essential nutrient. Fortunately it is in the majority of real foods, including water, and so ingestion of this vital mineral is not difficult.

Potassium is another essential dietary mineral. The potassium/sodium balance, is absolutely critical to the overall functioning of every cell in the human body. If salt levels fall too low, a condition called Hyponatremia can develop, which can be fatal. (Ref 2)

3) Salt has nothing to do with obesity

The inclusion of salt in the Academy of Royal Colleges obesity report (Ref 3) was quite bizarre because salt has nothing directly to do with obesity. It has no calories, no macronutrients (no fat, no protein, no carbohydrate) and therefore cannot directly impact obesity.

There may be an indirect argument that salt could encourage people to eat things. However, I would argue that people may desire doughnuts or biscuits (combinations of flour, sugar and salt), but that they would be unlikely to crave, say, anchovies, unless salt deficient for some reason. I would then expect a salt-deprived person to stop consuming anchovies once any salt deficiency were corrected and not to binge on them. The ‘but for’ test therefore points to the refined carbohydrates, containing salt, being substances of desire and not salt per se.

4) CASH has it in for salt

A charity called Consensus Action on Salt and Health (CASH) exists purely to campaign against salt. As the web site says: “CASH was set up in 1996 as a response to the refusal of the Chief Medical Officer (CMO) to endorse the COMA recommendations to reduce salt intake.” (COMA stands for Committee On Medical Aspects of Food Policy).

The COMA report merely says (and I quote) “The panel recommends that the dietary intake of common salt should not be increased further and that consideration should be given to ways and means of decreasing it.”

The worst thing that the COMA report could say about salt was: “High salt intakes have frequently been linked with the prevalence of high blood pressure in communities but a mechanism whereby salt could lead to the development of essential hypertension has not been established.”

Hang on a second – so there are alleged “frequent links”, for which no evidence is presented and we don’t even know how salt could impact hypertension (high blood pressure)… (I’ll answer this for them in a minute – we’ve known how since Carl Von Voit’s work in 1860).

The COMA report continues “Cross-cultural studies show a statistical association between estimates of salt intake and the average blood pressure of a community but detailed investigations within a single community frequently fail to demonstrate such a relationship.” And CASH was set up because the CMO failed to take action against salt?!

5) ‘High’ blood pressure is in fact normal

If you look at figures 1 and 2 in this highly referenced article, the actual population normal/average blood pressure is 140/86. The European Society of Hypertension and the World Health Organisation both define blood pressure of 140/90 as the baseline for high blood pressure. So normal has been redefined as high. This enables drug companies to medicate many more people.

6) Salt can increase blood pressure, but so what?

There is a very simple mechanism by which salt can increase blood pressure (of which the COMA report didn’t seem to be aware). Salt provides sodium. The normal concentration of sodium in blood plasma is 136-145mM (mmol/Litre). One of the easiest ways for the body to maintain the concentration of sodium is to increase fluid levels if sodium rises. If we consume salty food, we want to drink more (that’s why bars put free bowls of peanuts on the counter) so step 1 is for the increased intake of sodium to lead to an increase in fluid intake. Step 2 means that the additional fluid is more likely to be retained because the body is back in sodium concentration equilibrium, albeit with more sodium and more water.

Water retention in the human body can raise blood pressure. However, there are three points to make here:

i) Raised blood pressure is a symptom. It’s not a problem per se. What the salt antagonists fail to provide is any evidence for a substantial and/or sustained increase in blood pressure as a direct result of any defined level of salt consumption.
ii) Salt opponents also fail to provide any direct causation between salt consumption and end point disease (e.g. heart disease) regardless of whether or not salt impacts blood pressure.
iii) A completely overlooked point is that any rise in water retention from consuming even a couple of grams of salt is incomparable to the impact of consuming 100g of carbohydrates – which we are encouraged to consume (a few times a day) in illogical parallel with the discouragement of salt intake.

We can store up to 500g of glycogen if we consume carbohydrates that are not used up for energy. We know that each gram of glycogen is accompanied by four grams of water. Hence we can gain 2.5kg (c. 5lb) overnight by consuming carbohydrates above human need. This is way more significant in terms of water retention and blood pressure than any impact of a couple of grams of salt – and yet carb consumption is recommended and salt consumption is demonised. Yet another example of our completely incomprehensible dietary advice.

7) Even if salt impacts blood pressure, and even if this matters, reducing salt intake substantially would have negligible impact

The 1994 COMA report (Ref 4) states: “Its [The review group] recommendation was to reduce salt consumption by an average of 3g/day. It has been estimated that this would reduce average systolic blood pressure by about 3.5mm Hg.” [systolic blood pressure is the first of the two numbers we get].
Gary Taubes noted the same in The Diet Delusion: “cutting our average salt intake in half, for instance, which is difficult to accomplish in the real world – will drop blood pressure by perhaps 4 to 5 mm Hg in hypertensives and 2 mm Hg in the rest of us.”

So, halve your salt intake and your blood pressure may go from 130/X to 127/X?

If you have ever had your blood pressure read frequently (while in hospital or getting ready for an operation or a baby), or if you have one of those blood pressure machines at home, you will know that you hardly ever get the same reading twice in a row. Even within a couple of minutes, your blood pressure can vary by more than a handful of points – more than the amount it could possibly change by if you managed to halve your salt intake.

8) CASH’s evidence on “Salt & Health” is completely lacking

For the seven years after its formation, Consensus Action on Salt & Health was relying upon the 1994 COMA report. Since 2003 they have relied upon a Scientific Advisory Committee on Nutrition (SACN) report, called “Salt and Health”. (Ref 5)

Feel free to read the 134 page document. The summary will give you the key elements. The summary opens by saying: “Increased blood pressure, or hypertension, is the most common outcome that has been associated with high levels of salt intake. Hypertension is a major risk factor in the development of cardiovascular disease. The relative risk of cardiovascular disease increases as blood pressure rises even within what is considered the normal range of blood pressure, indicating that large numbers of people are at risk.”

i.e. the most common (the only?) outcome that salt intake has been associated with is increased blood pressure. If there were any direct association between salt intake and any actual disease, it would have been claimed.

Increased blood pressure in turn is then claimed to be a “major risk factor in the development of cardiovascular disease.” I disagree. High blood pressure (BP) (even when properly defined as actual high BP and not normal BP i.e. 140/86) is a symptom, not a cause. This makes blood pressure a condition observed at the same time as heart disease and not a risk factor. (It is far more likely the opposite direction of causation – heart disease causes high blood pressure – hence the symptom).
Notwithstanding this – the argument against salt still boils down to – we think salt is associated with blood pressure and we think blood pressure causes heart disease. So, by inference, they want us to think that salt causes heart disease.

The jewel in the crown of the anti-salt lobbyists is “The International Study of Salt & Blood Pressure” (Intersalt Co-operative Research Group, 1988). This study collected data on 24-hour urinary sodium excretion and blood pressure of over 10,000 adults in 52 population samples from 32 countries. Associations (note, not causation) were found between sodium excretion and blood pressure readings – until the four populations with very low salt intakes were removed from the analysis and then any statistical significance disappeared. (That latter point about the statistical significance disappearing was the view of the SACN Salt and Health report to give credit for honesty – it wasn’t my playing with numbers that led to this finding.)

Dr David Brownstein’s book Salt your way to health noted the findings from the Intersalt study as follows: “Although there was a slight relationship between blood pressure and sodium excretion in INTERSALT, a ‘smoking gun’ could not be found. This study showed a mild decrease in blood pressure (3-6mmHg systolic and 0-3mmHg diastolic) when there was a dramatic decrease in salt excretion.”

9) There is no evidence that salt causes heart disease; there is evidence that low salt is associated with heart attacks

A study of approximately 3,000 hypertensive subjects (men with high blood pressure) found that there was a 430% increase in myocardial infarction (heart attack) in the group with the lowest salt intake versus the group with the highest salt intake. (Ref 6) Knowing how vital salt is for human health, this should not be surprising – low-sodium diets have been shown to cause multiple nutrient deficiencies, including nutrients vital for heart health (calcium, magnesium, potassium and B-vitamins). (Ref 7)
The SACN report concluded: “There are insufficient reliable data on long-term effects of salt on cardiovascular disease outcomes to reach clear conclusions.” Quite.

c

p.s. The interesting twist to researching salt is that the motive for attacking this substance has not been as obvious as usual. The motive in the anti-fat movement is clear – it gives the ‘food’ industry the green light to make highly lucrative fake low-fat food. The motive in the anti-cholesterol movement is clear – it gives the drug industry the green light to make drugs worth tens of billions of dollars and ‘food’ companies can make spreads and other ‘cholesterol-lowering’ fake foods.

The common bad relationships between the ‘food’ industry and health campaigners can be found in the salt world. Check out p12 of the April 2012 Action on Salt annual report – the usual suspects from the ‘food’ industry are warmly thanked for their support.

Who gains by demonising salt? The lo-salt company clearly does. The founder of Consensus Action on Salt & Health, Professor Graham MacGregor, has personally done well out of founding the organisation. MacGregor is now chairman of action on salt. MacGregor is also chairman of the Blood Pressure Association. He sits on the board for the World Hypertension League and recently served as President of The British Hypertension Society. MacGregor was awarded 37th place on the Independent on Sunday’s list of people who have made Britain a “much, much better place.” (Ref 9) Salt has given MacGregor’s life purpose – I believe that he believes that salt is a bad thing. I also think that he is wrong.

As a final thought – have you heard of the expressions “salt of the earth” or “worth his/her salt”? We describe someone as the salt of the earth when they are as good and worthy as anyone can be. The word salary comes from the Latin word salarium and has the root sal or salt. In ancient Rome, salary meant the amount of money given to a Roman soldier to buy salt, which was an expensive but essential commodity. This explains the “worth his salt” expression. Our language is telling us the truth, our government is sadly not.


References
1) http://www.nhs.uk/Livewell/Goodfood/Pages/salt.aspx
2) http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001431/
3) http://www.aomrc.org.uk/about-us/news/item/doctors-unite-to-deliver-prescription-for-uk-obesity-epidemic.html
4) http://www.actiononsalt.org.uk/salthealth/Recommendations%20on%20salt/42491.pdf
5) http://www.sacn.gov.uk/pdfs/sacn_salt_final.pdf
6) Alderman “Low urinary sodium is associated with greater risk of myocardial infarction among treated hypertensive men.” Hypertension. 1995
7) Engstrom et al “Nutritional consequences of reducing sodium intake.” Ann. Intern. Med. 1983.
8) http://www.charity-commission.gov.uk/Accounts/Ends18/0001098818_AC_20100430_E_C.PDF
9) http://www.independent.co.uk/news/people/news/the-ios-happy-list-2012–the-100-7661358.html?action=gallery&ino=37
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Read the complete article here.
Another article here.

More data in the Salt Wars - Aug 14, 2014; http://www.medpagetoday.com/Cardiology/Hypertension/47203

An article by Marion Nestle - http://www.foodpolitics.com/2014/08/its-salt-arguments-again-new-research-arguments-over-public-health-recommendations-and-issues-of-conflicts-of-interest/

Potassium, your invisible friend - Kendrick

Poatassium, your invisible friend Dr. Malcolm Kendrick

 

I recognise that I spent a lot of time telling people what does not cause heart disease, and what does not protect against heart disease. My sister told me… ‘well, what advice would you give people, then?’ I usually shrug my shoulders and reply ‘there is no shortage of advice around, I don’t think I need to add to the daily bombardment.’

However, I shall break the habit of a lifetime and, with slight trepidation, announce that I strongly believe that Potassium is good for you. If you consume more of it you will, most likely, live both longer and in better health.

How much should you consume? A couple of extra grams a day should do the trick. Having said this, I do recognise that most people will not have the faintest idea how much potassium they consume and, frankly, neither do I. But you are probably not consuming enough, and your kidneys will easily get rid of any excess.

For those who are not keen on bananas, spinach and broccoli, and other foods high in potassium, you could take it as a tablet. Potassium bicarbonate or potassium citrate appears to be the best formulation. Depending on which brand you decide to buy, it should cost about £15 – 20/year.

Why this sudden potassiumophilia? Well, there is a growing body of research which points to the fact that potassium is very good for you. The first time I became aware that it might be good for you was when I first looked at the Scottish Heart Health study. The researchers looked at twenty seven different ‘factors’ they thought might cause, or protect against, heart disease – and overall mortality.

  The authors noted that:
“[There was] an unexpectedly powerful protective relation of dietary potassium to all-cause mortality,” the study concluded.

The paper showed that:

• Men consuming an average of 5400 mg of potassium per day vs 1840 mg were 55% less likely to die during 7.6 year study (the highest one-fifth of men vs the lowest one-fifth of men)

• Men consuming an average of 5400 mg of potassium per day vs 3350 mg were 22% less likely to die during 7.6 year study (the highest one-fifth of men vs the second highest one-fifth of men)

• Women consuming an average of 4500 mg of potassium per day vs 1560 mg were 59% less likely to die during 7.6 year study (the highest one-fifth of women vs the lowest one-fifth of women)

• Women consuming an average of 4500 mg of potassium per day vs 2700 mg were 15% less likely to die during 7.6 year study (the highest one-fifth of women vs the second highest one-fifth of women

The study can most easily be found here http://www.ncbi.nlm.nih.gov/pubmed/9314758
I immediately liked this finding. Mainly because it was almost completely unexpected, and unexpected findings are always far more likely to be correct than expected findings. Also, this was a very large effect indeed. It turned out that increased potassium consumption was very nearly as protective as smoking was damaging.

Of course, this was an observational study, so I filed it under – most interesting – but did nothing much more about it. As the authors said themselves: ‘ Potassium excretion was very significantly related to risk of death from all causes, having a protective role, whereas its role in coronary events was weaker and that of sodium excretion weak and even paradoxical. These results are unifactorial, without correction other than for age and sex. Our findings need corroboration from elsewhere and more detailed analysis with more events from longer follow-up.’

Since then, a large number of other studies have followed up, and appear to have confirmed that potassium has considerable health benefits. Some of these studies were not just observational, they were interventional. Here is summary of the potential beneficial effects. Potassium:

• lowers blood pressure
• lowers the risk of arrhythmias
• lowers the risk of cardiovascular disease
• lowers the risk of stroke
• lowers the risk of heart attacks
• lowers the risk of cancer, and
• lowers the risk of death

These benefits have been confirmed in a number of different studies. However, as this is a blog, I am not going to turn it into a medical paper and provide references for every statement, so I will stick to a couple of referenced studies. (If enough people are interested I can point you at additional papers).
With regard to blood pressure, a study published in 1997 found that adding roughly 2 grams (2000 mg) of potassium per day lowered blood pressure in older people by 15/8 mm Hg. As good, if not better, than any antihypertensive drug¹. And with no side-effects at all.

When it comes to stroke, it has been found that having a low potassium level is a very potent risk factor for both bleeding (haemorrhagic) and clotting (ischaemic strokes). In an American study it was found that in those with low potassium levels the relative risk of ischaemic stroke increased by 206%. The relative risk increased by 329% for haemorrhagic stroke².

Admittedly, these two studies were done in people with high blood pressure to start with, but these effects are also found in healthy people. However, to my mind, the most important thing about potassium is that I cannot find any study, anywhere, which suggests that increasing potassium consumption may be harmful. In short, it seems to be something that does only good.

I do recognise that a lot of doctors will shudder at the thought of adding potassium to the diet, as they have all been taught that a high potassium level is something terribly dangerous. A condition that needs immediate treatment, or else it will cause arrhythmias and death.

It is true that you need to be careful of adding potassium to the diet of patients taking medications that can raise potassium levels. These are mainly drugs used to lower blood pressure. However, even in this group the risk of overdosing on potassium is exceedingly small. For everyone else the risk seems to be zero. This is why I now recommend potassium supplementation as a good way to live a longer, healthier life.

My goodness, I think this is the first time I have ever recommended a dietary supplement. Must go and lie down.


1: ‘Long term potassium supplementation lowers blood pressure in elderly hypertensive subjects’ Fotherby M.D. et al: Int J Clin Practice 1997 41(4): 219 – 222)
2: Smith NL, et al: ‘Serum potassium and stroke risk among treated hypertensive adults.’ Am J Hypertens. 2003 Oct;16(10):806-13

I recognise that I spent a lot of time telling people what does not cause heart disease, and what does not protect against heart disease. My sister told me… ‘well, what advice would you give people, then?’ I usually shrug my shoulders and reply ‘there is no shortage of advice around, I don’t think I need to add to the daily bombardment.’

 

However, I shall break the habit of a lifetime and, with slight trepidation, announce that I strongly believe that Potassium is good for you. If you consume more of it you will, most likely, live both longer and in better health.

 

How much should you consume? A couple of extra grams a day should do the trick. Having said this, I do recognise that most people will not have the faintest idea how much potassium they consume and, frankly, neither do I. But you are probably not consuming enough, and your kidneys will easily get rid of any excess.

 

For those who are not keen on bananas, spinach and broccoli, and other foods high in potassium, you could take it as a tablet. Potassium bicarbonate or potassium citrate appears to be the best formulation. Depending on which brand you decide to buy, it should cost about £15 – 20/year.

 

Why this sudden potassiumophilia? Well, there is a growing body of research which points to the fact that potassium is very good for you. The first time I became aware that it might be good for you was when I first looked at the Scottish Heart Health study. The researchers looked at twenty seven different ‘factors’ they thought might cause, or protect against, heart disease – and overall mortality.

 

 The authors noted that:

“[There was] an unexpectedly powerful protective relation of dietary potassium to all-cause mortality,” the study concluded.

 

The paper showed that:

• Men consuming an average of 5400 mg of potassium per day vs 1840 mg were 55% less likely to die during 7.6 year study (the highest one-fifth of men vs the lowest one-fifth of men)

• Men consuming an average of 5400 mg of potassium per day vs 3350 mg were 22% less likely to die during 7.6 year study (the highest one-fifth of men vs the second highest one-fifth of men)

• Women consuming an average of 4500 mg of potassium per day vs 1560 mg were 59% less likely to die during 7.6 year study (the highest one-fifth of women vs the lowest one-fifth of women)

• Women consuming an average of 4500 mg of potassium per day vs 2700 mg were 15% less likely to die during 7.6 year study (the highest one-fifth of women vs the second highest one-fifth of women

The study can most easily be found here http://www.ncbi.nlm.nih.gov/pubmed/9314758

I immediately liked this finding. Mainly because it was almost completely unexpected, and unexpected findings are always far more likely to be correct than expected findings. Also, this was a very large effect indeed. It turned out that increased potassium consumption was very nearly as protective as smoking was damaging.

 

Of course, this was an observational study, so I filed it under – most interesting – but did nothing much more about it. As the authors said themselves: ‘ Potassium excretion was very significantly related to risk of death from all causes, having a protective role, whereas its role in coronary events was weaker and that of sodium excretion weak and even paradoxical. These results are unifactorial, without correction other than for age and sex. Our findings need corroboration from elsewhere and more detailed analysis with more events from longer follow-up.’

 

Since then, a large number of other studies have followed up, and appear to have confirmed that potassium has considerable health benefits. Some of these studies were not just observational, they were interventional. Here is summary of the potential beneficial effects. Potassium:

• lowers blood pressure
• lowers the risk of arrhythmias
• lowers the risk of cardiovascular disease
• lowers the risk of stroke
• lowers the risk of heart attacks
• lowers the risk of cancer, and
• lowers the risk of death

These benefits have been confirmed in a number of different studies. However, as this is a blog, I am not going to turn it into a medical paper and provide references for every statement, so I will stick to a couple of referenced studies. (If enough people are interested I can point you at additional papers).
With regard to blood pressure, a study published in 1997 found that adding roughly 2 grams (2000 mg) of potassium per day lowered blood pressure in older people by 15/8 mm Hg. As good, if not better, than any antihypertensive drug¹. And with no side-effects at all.

When it comes to stroke, it has been found that having a low potassium level is a very potent risk factor for both bleeding (haemorrhagic) and clotting (ischaemic strokes). In an American study it was found that in those with low potassium levels the relative risk of ischaemic stroke increased by 206%. The relative risk increased by 329% for haemorrhagic stroke².

Admittedly, these two studies were done in people with high blood pressure to start with, but these effects are also found in healthy people. However, to my mind, the most important thing about potassium is that I cannot find any study, anywhere, which suggests that increasing potassium consumption may be harmful. In short, it seems to be something that does only good.

I do recognise that a lot of doctors will shudder at the thought of adding potassium to the diet, as they have all been taught that a high potassium level is something terribly dangerous. A condition that needs immediate treatment, or else it will cause arrhythmias and death.

It is true that you need to be careful of adding potassium to the diet of patients taking medications that can raise potassium levels. These are mainly drugs used to lower blood pressure. However, even in this group the risk of overdosing on potassium is exceedingly small. For everyone else the risk seems to be zero. This is why I now recommend potassium supplementation as a good way to live a longer, healthier life.

My goodness, I think this is the first time I have ever recommended a dietary supplement. Must go and lie down.

1: ‘Long term potassium supplementation lowers blood pressure in elderly hypertensive subjects’ Fotherby M.D. et al: Int J Clin Practice 1997 41(4): 219 – 222)
2: Smith NL, et al: ‘Serum potassium and stroke risk among treated hypertensive adults.’ Am J Hypertens. 2003 Oct;16(10):806-13

Poatassium, your invisible friend

March 4, 2013Dr. Malcolm KendrickLeave a commentGo to comments

I recognise that I spent a lot of time telling people what does not cause heart disease, and what does not protect against heart disease. My sister told me… ‘well, what advice would you give people, then?’ I usually shrug my shoulders and reply ‘there is no shortage of advice around, I don’t think I need to add to the daily bombardment.’

However, I shall break the habit of a lifetime and, with slight trepidation, announce that I strongly believe that Potassium is good for you. If you consume more of it you will, most likely, live both longer and in better health.

How much should you consume? A couple of extra grams a day should do the trick. Having said this, I do recognise that most people will not have the faintest idea how much potassium they consume and, frankly, neither do I. But you are probably not consuming enough, and your kidneys will easily get rid of any excess.

For those who are not keen on bananas, spinach and broccoli, and other foods high in potassium, you could take it as a tablet. Potassium bicarbonate or potassium citrate appears to be the best formulation. Depending on which brand you decide to buy, it should cost about £15 – 20/year.

Why this sudden potassiumophilia? Well, there is a growing body of research which points to the fact that potassium is very good for you. The first time I became aware that it might be good for you was when I first looked at the Scottish Heart Health study. The researchers looked at twenty seven different ‘factors’ they thought might cause, or protect against, heart disease – and overall mortality. The authors noted that:

“[There was] an unexpectedly powerful protective relation of dietary potassium to all-cause mortality,” the study concluded.

The paper showed that:

• Men consuming an average of 5400 mg of potassium per day vs 1840 mg were 55% less likely to die during 7.6 year study (the highest one-fifth of men vs the lowest one-fifth of men)

• Men consuming an average of 5400 mg of potassium per day vs 3350 mg were 22% less likely to die during 7.6 year study (the highest one-fifth of men vs the second highest one-fifth of men)

• Women consuming an average of 4500 mg of potassium per day vs 1560 mg were 59% less likely to die during 7.6 year study (the highest one-fifth of women vs the lowest one-fifth of women)

• Women consuming an average of 4500 mg of potassium per day vs 2700 mg were 15% less likely to die during 7.6 year study (the highest one-fifth of women vs the second highest one-fifth of women

The study can most easily be found here http://www.ncbi.nlm.nih.gov/pubmed/9314758

I immediately liked this finding. Mainly because it was almost completely unexpected, and unexpected findings are always far more likely to be correct than expected findings. Also, this was a very large effect indeed. It turned out that increased potassium consumption was very nearly as protective as smoking was damaging.

Of course, this was an observational study, so I filed it under – most interesting – but did nothing much more about it. As the authors said themselves: ‘ Potassium excretion was very significantly related to risk of death from all causes, having a protective role, whereas its role in coronary events was weaker and that of sodium excretion weak and even paradoxical. These results are unifactorial, without correction other than for age and sex. Our findings need corroboration from elsewhere and more detailed analysis with more events from longer follow-up.’

Since then, a large number of other studies have followed up, and appear to have confirmed that potassium has considerable health benefits. Some of these studies were not just observational, they were interventional. Here is summary of the potential beneficial effects. Potassium:

• lowers blood pressure
• lowers the risk of arrhythmias
• lowers the risk of cardiovascular disease
• lowers the risk of stroke
• lowers the risk of heart attacks
• lowers the risk of cancer, and
• lowers the risk of death

These benefits have been confirmed in a number of different studies. However, as this is a blog, I am not going to turn it into a medical paper and provide references for every statement, so I will stick to a couple of referenced studies. (If enough people are interested I can point you at additional papers).
With regard to blood pressure, a study published in 1997 found that adding roughly 2 grams (2000 mg) of potassium per day lowered blood pressure in older people by 15/8 mm Hg. As good, if not better, than any antihypertensive drug¹. And with no side-effects at all.
When it comes to stroke, it has been found that having a low potassium level is a very potent risk factor for both bleeding (haemorrhagic) and clotting (ischaemic strokes). In an American study it was found that in those with low potassium levels the relative risk of ischaemic stroke increased by 206%. The relative risk increased by 329% for haemorrhagic stroke².
Admittedly, these two studies were done in people with high blood pressure to start with, but these effects are also found in healthy people. However, to my mind, the most important thing about potassium is that I cannot find any study, anywhere, which suggests that increasing potassium consumption may be harmful. In short, it seems to be something that does only good.
I do recognise that a lot of doctors will shudder at the thought of adding potassium to the diet, as they have all been taught that a high potassium level is something terribly dangerous. A condition that needs immediate treatment, or else it will cause arrhythmias and death.
It is true that you need to be careful of adding potassium to the diet of patients taking medications that can raise potassium levels. These are mainly drugs used to lower blood pressure. However, even in this group the risk of overdosing on potassium is exceedingly small. For everyone else the risk seems to be zero. This is why I now recommend potassium supplementation as a good way to live a longer, healthier life.
My goodness, I think this is the first time I have ever recommended a dietary supplement. Must go and lie down.
1: ‘Long term potassium supplementation lowers blood pressure in elderly hypertensive subjects’ Fotherby M.D. et al: Int J Clin Practice 1997 41(4): 219 – 222)
2: Smith NL, et al: ‘Serum potassium and stroke risk among treated hypertensive adults.’ Am J Hypertens. 2003 Oct;16(10):806-13

Dr Blanchet podcast 20121219

Listen to an excellent podcast to learn about stroke and heart disease prevention by having tests to measure presence of disease before a catastrophic event happens. Wish I had known this before 1994!

http://tuesdaytalkshow.podomatic.com/entry/2012-12-19T08_01_16-08_00

Dr Davis was interviewed by Wellness Mama  recently. The full interview can be seen here. I have shown only the part that specifically addresses heart disease.
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2. How is wheat consumption linked to heart health?

Wheat consumption causes heart disease. It’s not cholesterol, it’s not saturated fat that’s behind the number one killer of Americans; it’s wheat.

The nutrition community has been guilty of following a flawed sequence of logic: If something bad for you (white processed flour) is replaced by something less bad (whole grains) and there is an apparent health benefit, then a whole bunch of the less bad thing is good for you. Let’s apply that to another situation: If something bad for you—unfiltered Camel cigarettes—are replaced by something less bad—filtered Salem Cigarettes—then the conclusion would be to smoke a lot of Salems. The next logical question should have been: What is the health consequence of complete removal? Only then can you observe the effect of whole grains vs. no grains . . . and, from what I witness every day, you see complete transformations in health.

Consumption of wheat, due to its unique carbohydrate, amylopectin A, triggers formation of small, dense LDL particles more than any other common food. Small, dense LDL particles are the number one cause for heart disease in the U.S. The majority of adults now have an abundance of small LDL particles because they’ve been told to cut their fat and “eat plenty of healthy whole grains.” This situation of excessive small LDL particles can appear on a conventional cholesterol panel as higher levels of LDL (“bad”) cholesterol, along with low HDL cholesterol and higher triglycerides that often leads to statin drugs. When more sophisticated lipoprotein testing is obtained, then the explosion of small LDL particles becomes obvious.

Compound this with the increased appetite triggered by the gliadin protein in wheat that acts as an appetite-stimulant, and you gain weight. The weight gained is usually in the abdomen, in the deep visceral fat that triggers inflammation, what I call a “wheat belly.” Wheat belly visceral fat is a hotbed of inflammation, sending out inflammatory signals into the bloodstream and results in higher blood sugar, blood pressure, and triglycerides, all adding up to increased risk for heart disease.
Say goodbye to wheat and small LDL particles plummet, followed by weight loss from the wheat belly visceral fat. Inflammation subsides, blood sugar drops, blood pressure drops. In short, elimination of wheat is among the most powerful means of reducing risk for heart disease.

Salt, We Misjudged You

By GARY TAUBES

Published: June 2, 2012   Oakland, Calif.

THE first time I questioned the conventional wisdom on the nature of a healthy diet, I was in my salad days, almost 40 years ago, and the subject was salt. Researchers were claiming that salt supplementation was unnecessary after strenuous exercise, and this advice was being passed on by health reporters. All I knew was that I had played high school football in suburban Maryland, sweating profusely through double sessions in the swamplike 90-degree days of August. Without salt pills, I couldn’t make it through a two-hour practice; I couldn’t walk across the parking lot afterward without cramping.

While sports nutritionists have since come around to recommend that we should indeed replenish salt when we sweat it out in physical activity, the message that we should avoid salt at all other times remains strong. Salt consumption is said to raise blood pressure, cause hypertension and increase the risk of premature death. This is why the Department of Agriculture’s dietary guidelines still consider salt Public Enemy No. 1, coming before fats, sugars and alcohol. It’s why the director of the Centers for Disease Control and Prevention has suggested that reducing salt consumption is as critical to long-term health as quitting cigarettes.

And yet, this eat-less-salt argument has been surprisingly controversial — and difficult to defend. Not because the food industry opposes it, but because the actual evidence to support it has always been so weak.

When I spent the better part of a year researching the state of the salt science back in 1998 — already a quarter century into the eat-less-salt recommendations — journal editors and public health administrators were still remarkably candid in their assessment of how flimsy the evidence was implicating salt as the cause of hypertension.

“You can say without any shadow of a doubt,” as I was told then by Drummond Rennie, an editor for The Journal of the American Medical Association, that the authorities pushing the eat-less-salt message had “made a commitment to salt education that goes way beyond the scientific facts.”

While, back then, the evidence merely failed to demonstrate that salt was harmful, the evidence from studies published over the past two years actually suggests that restricting how much salt we eat can increase our likelihood of dying prematurely. Put simply, the possibility has been raised that if we were to eat as little salt as the U.S.D.A. and the C.D.C. recommend, we’d be harming rather than helping ourselves.

WHY have we been told that salt is so deadly? Well, the advice has always sounded reasonable. It has what nutritionists like to call “biological plausibility.” Eat more salt and your body retains water to maintain a stable concentration of sodium in your blood. This is why eating salty food tends to make us thirsty: we drink more; we retain water. The result can be a temporary increase in blood pressure, which will persist until our kidneys eliminate both salt and water.

The scientific question is whether this temporary phenomenon translates to chronic problems: if we eat too much salt for years, does it raise our blood pressure, cause hypertension, then strokes, and then kill us prematurely? It makes sense, but it’s only a hypothesis. The reason scientists do experiments is to find out if hypotheses are true.

In 1972, when the National Institutes of Health introduced the National High Blood Pressure Education Program to help prevent hypertension, no meaningful experiments had yet been done. The best evidence on the connection between salt and hypertension came from two pieces of research. One was the observation that populations that ate little salt had virtually no hypertension. But those populations didn’t eat a lot of things — sugar, for instance — and any one of those could have been the causal factor. The second was a strain of “salt-sensitive” rats that reliably developed hypertension on a high-salt diet. The catch was that “high salt” to these rats was 60 times more than what the average American consumes.

Still, the program was founded to help prevent hypertension, and prevention programs require preventive measures to recommend. Eating less salt seemed to be the only available option at the time, short of losing weight. Although researchers quietly acknowledged that the data were “inconclusive and contradictory” or “inconsistent and contradictory” — two quotes from the cardiologist Jeremiah Stamler, a leading proponent of the eat-less-salt campaign, in 1967 and 1981 — publicly, the link between salt and blood pressure was upgraded from hypothesis to fact.

In the years since, the N.I.H. has spent enormous sums of money on studies to test the hypothesis, and those studies have singularly failed to make the evidence any more conclusive. Instead, the organizations advocating salt restriction today — the U.S.D.A., the Institute of Medicine, the C.D.C. and the N.I.H. — all essentially rely on the results from a 30-day trial of salt, the 2001 DASH-Sodium study. It suggested that eating significantly less salt would modestly lower blood pressure; it said nothing about whether this would reduce hypertension, prevent heart disease or lengthen life.

While influential, that trial was just one of many. When researchers have looked at all the relevant trials and tried to make sense of them, they’ve continued to support Dr. Stamler’s “inconsistent and contradictory” assessment. Last year, two such “meta-analyses” were published by the Cochrane Collaboration, an international nonprofit organization founded to conduct unbiased reviews of medical evidence. The first of the two reviews concluded that cutting back “the amount of salt eaten reduces blood pressure, but there is insufficient evidence to confirm the predicted reductions in people dying prematurely or suffering cardiovascular disease.” The second concluded that “we do not know if low salt diets improve or worsen health outcomes.”

The idea that eating less salt can worsen health outcomes may sound bizarre, but it also has biological plausibility and is celebrating its 40th anniversary this year, too. A 1972 paper in The New England Journal of Medicine reported that the less salt people ate, the higher their levels of a substance secreted by the kidneys, called renin, which set off a physiological cascade of events that seemed to end with an increased risk of heart disease. In this scenario: eat less salt, secrete more renin, get heart disease, die prematurely.

With nearly everyone focused on the supposed benefits of salt restriction, little research was done to look at the potential dangers. But four years ago, Italian researchers began publishing the results from a series of clinical trials, all of which reported that, among patients with heart failure, reducing salt consumption increased the risk of death.

Those trials have been followed by a slew of studies suggesting that reducing sodium to anything like what government policy refers to as a “safe upper limit” is likely to do more harm than good. These covered some 100,000 people in more than 30 countries and showed that salt consumption is remarkably stable among populations over time. In the United States, for instance, it has remained constant for the last 50 years, despite 40 years of the eat-less-salt message. The average salt intake in these populations — what could be called the normal salt intake — was one and a half teaspoons a day, almost 50 percent above what federal agencies consider a safe upper limit for healthy Americans under 50, and more than double what the policy advises for those who aren’t so young or healthy. This consistency, between populations and over time, suggests that how much salt we eat is determined by physiological demands, not diet choices.

One could still argue that all these people should reduce their salt intake to prevent hypertension, except for the fact that four of these studies — involving Type 1 diabetics, Type 2 diabetics, healthy Europeans and patients with chronic heart failure — reported that the people eating salt at the lower limit of normal were more likely to have heart disease than those eating smack in the middle of the normal range. Effectively what the 1972 paper would have predicted.

Proponents of the eat-less-salt campaign tend to deal with this contradictory evidence by implying that anyone raising it is a shill for the food industry and doesn’t care about saving lives. An N.I.H. administrator told me back in 1998 that to publicly question the science on salt was to play into the hands of the industry. “As long as there are things in the media that say the salt controversy continues,” he said, “they win.”

When several agencies, including the Department of Agriculture and the Food and Drug Administration, held a hearing last November to discuss how to go about getting Americans to eat less salt (as opposed to whether or not we should eat less salt), these proponents argued that the latest reports suggesting damage from lower-salt diets should simply be ignored. Lawrence Appel, an epidemiologist and a co-author of the DASH-Sodium trial, said “there is nothing really new.” According to the cardiologist Graham MacGregor, who has been promoting low-salt diets since the 1980s, the studies were no more than “a minor irritation that causes us a bit of aggravation.”

This attitude that studies that go against prevailing beliefs should be ignored on the basis that, well, they go against prevailing beliefs, has been the norm for the anti-salt campaign for decades. Maybe now the prevailing beliefs should be changed. The British scientist and educator Thomas Huxley, known as Darwin’s bulldog for his advocacy of evolution, may have put it best back in 1860. “My business,” he wrote, “is to teach my aspirations to conform themselves to fact, not to try and make facts harmonize with my aspirations.”

A Robert Wood Johnson Foundation Independent Investigator in Health Policy Research and the author of “Why We Get Fat.”
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Read the full article here.

More data in the Salt Wars - Aug 14, 2014; http://www.medpagetoday.com/Cardiology/Hypertension/47203

An article by Marion Nestle - http://www.foodpolitics.com/2014/08/its-salt-arguments-again-new-research-arguments-over-public-health-recommendations-and-issues-of-conflicts-of-interest/