About Keir Watson

Researcher and lecturer in Nutrition & Human Evolution, (rosemarycottageclinic.wordpress.com), Tutor ( physics), Permaculturist: fruit tree training; garden building construction; green roofs (www.herbidacious.wordpress.com)

Salt and cardio-vascular disease: Policy and Science clash

The recent video we posted of Dr SalimYusuf’s PURE study had a section on sodium intake, where he showed that the lowest risk of cardiovascular events, cardiovascular deaths and all-cause mortality was associated with an intake between 3000 and 6000 mg of sodium per day (equivalent to 7 to 15g salt per day). The current US average sodium intake is 3800 mg placing the general population nicely within this sweet spot, although towards the lower end.

Current US and UK dietary recommendations recommend an upper limit at 2300mg of sodium (6g of salt) whilst cardiovascular recommendations by bodies such as the American Heart Association aim to reduce sodium intake to 1500 mg per day (approx 3.75 g salt). If the PURE study is right (and it is not alone in questioning the current guidelines), then these aspirations would do more harm than good.

How did such discrepancy arise? The problem may be the use of surrogate markers. The thinking goes like this: Salt raises blood pressure. Raised blood pressure increases CVD risk, so salt increases CVD risk. This kind of thinking was evident in 2011 when the American Heart Association (AHA) called for salt targets to be reduced to 1500mg per day.At the time MedPage Today explained:

The evidence linking salt intake with blood pressure — and the major adverse outcomes of heart disease, stroke, and kidney disease — is “impressive,”…

That evidence includes more than 50 trials assessing the blood pressure effects of salt, as well as a meta-analysis showing that cutting salt intake by about 1,800 mg per day lowered blood pressure by 5 mm Hg systolic and 2.7 mm Hg diastolic.

This is a “critically important public health issue,” according to Appel and colleagues, and this AHA advisory must be considered “a call to action.”

On the basis of this ‘A leads to B leads to C, therefore A leads to C’ thinking initiatives were instigated all round the world to reduce public consumption of salt. A task force of concerned scientists even formed a lobby group to put pressure on food manufacturers, which successfully led to reductions in added salt in manufactured foods.

However, within a short time of the AHA call to action reports started coming in contradicting this advice.

Over this period it is clear that scientists were becoming more and more irritated with the dogmatic approach of the AHA and government bodies, and by the last article were publicly calling the AHA anti-scientific!

Despite all of the research questioning the validity of further salt reduction US and UK policy remains stubbornly wedded to the ‘less is best trajectory’. In their 2016 survey the UK government reported proudly that average sodium consumption fell from 3500mg in 2005 to 3200 mg in 2014.

Their report claimed “Too much salt in the diet can raise blood pressure which increases the risk of heart disease and stroke. A reduction in average salt intake from 8g to 6g per day is estimated to prevent over 8000 premature deaths each year and save the NHS over £570million annually.”

Yet contrary evidence from studies including PURE would suggest that this is not simply futile but probably harmful. You would think that with the swathe of research challenging the low salt dogma that public policy would be questioning the wisdom of further reductions. Not a bit of it. Dr Alison Tedstone, chief nutritionist at Public Health England, makes no bones about it:

Our analysis makes clear that there is a steady downward trend in salt consumption. While people are having less salt than 10 years ago, we are still eating a third more than we should.

Many manufacturers and retailers have significantly reduced the salt levels in everyday foods. However, more needs to be done, especially by restaurants, cafes and takeaways.

The intransigence of health policy makers leads researchers to exasperation and despair. As one writer put it:

…the ‘salt hypothesis’ is rather like a monster from a 1950s B movie. Every time you attack it with evidence it simply shrugs it off and grows even stronger. – Malcolm Kendrick

In an interview with MedPage today researchers who found that patients with heart failure who ate more salt did better than those who ate less made the following statement which we have published before, but is such a gem it deserves another outing:

“We have had no basis for any of our recommendations regarding sodium restriction during the past 50 years, although these recommendations have changed a great deal (for no good reason). After this report, we still have no basis for any of our recommendations regarding sodium restriction. We were ignorant before; we are not any smarter now. Did we really need this report to tell us that we lack evidence for our recommendations regarding dietary sodium in patients with heart failure?”
Milton Packer, Professor in the Division of Cardiology, UT Southwestern

Further reading:

Salt vs sodium measurements

We made a boo-boo in out recent post (Cardiologist attacks diet dogma at 2017 symposium) where we summarised the findings from the PURE study regarding salt intake. We originally stated that 3 to 6 grams of salt per day appeared optimal but this should have read 3 to 6 grams of sodium per day.

What’s the difference?

Salt is a simple compound sodium chloride, NaCl, composed of sodium and chlorine atoms in a 1:1 ratio. Sodium has an atomic mass of 23 and chlorine a mass of 35, so the the fraction by weight of sodium in salt is 23/58 = 40%; or said the other way round, 1 gram of sodium is found in 2.5g of salt. To make things even more confusing, sodium is often quoted in milligrams (mg) whilst salt is given in grams, so the conversion becomes: 1000mg sodium = 2.5g salt

Let’s put this to the test with a confusing pair of health policies: UK guidelines recommend you eat no more than 6g of salt per day, whereas US guidelines place the limit at 2,300 mg of sodium per day. How do these compare?

First, converting the US 2,300 mg of sodium to grams gives 2.3 g of sodium. Next, convert this to the equivalent amount of salt by multiplying by two and a half: 2.3g x 2.5 =  5.75g. This figure rounds to 6g. i.e. they are essentially recommending the same thing, but expressing them in different ways. (That’s the special relationship for you!)

Here is a handy table for converting between sodium, salt and teaspoons:

Salt in
Sodium in mg Approx. equivalent to                Guidelines – daily limit
0.5 200 Average pinch of salt
2.5 1000 Half a teaspoon salt
3.75 1500 ¾ a teaspoon salt Recommended (AHA)
5 2000 One teaspoon salt
6 2400 1¼ teaspoons salt Upper limit (UK / US)
10 4000 2 teaspoons salt Current average consumption
15 6000 3 teaspoons salt Upper limit (PURE study*)

*The PURE study found that the lowest risk of cardiovascular and all-cause mortality was associated with a sodium intake of 3000 to 6000 mg per day. A concern I will look at in the next post is that public health policy does not take into account the lower limit, and assumes that less salt is always better. PURE and other studies suggest otherwise!

This sodium/salt mistake crops up a little too often and leads to confusion. For example MedPage Today, a respected medical news site, reported in 2011 that the American Heart Association had called for salt intake to be limited to 1,500 Mg. (I will write more about the conflict between this figure and the findings of the PURE study in my next post)

First off, I’m sure they meant milligrams (mg), not mega grams (Mg). Autocapitalising their title, put them out by a ‘trifling’ factor of one billion, but that’s forgivable. Where they really sowed confusion was by muddling up sodium and salt like I did. The AHA were calling for sodium intake to be reduced from 2300mg per day to 1500 mg per day (for adults), but MedPage reported these figures as salt not sodium.

One bemused commenter wrote “This article suggests 1 1/2 gms of salt a day, in the UK we are told 6gms per day”

So to clarify, the UK and US recommended upper limit is 2300 mg sodium per day (= 6 g salt), and the AHA recommendation is 1500 mg sodium (=just under 4g of salt). In contrast the PURE study found the ideal range was 3000 to 6000 mg sodium (=between 7.5 and 15g of salt per day).

Why then do researchers and nutrition labels quote sodium, not salt quantities? Because in principle at least, you could get sodium from sources other than sodium chloride. In practice non-salt sources of sodium are insignificant.

Anyway, hope that clears up the confusion about measuring sodium levels.

Next up I’ll tackle how the national guidelines are pushing us in the opposite direction to that suggested by the PURE study.

Kids eat sugar. But no one knows how much. Apparently.

The headline drew me in. I couldn’t resist. My Sword of Irony was twitching eager for a fight. It was going to be a blood bath…

Children’s sugar intake equals five doughnuts a day, campaigners say.

The Guardian, 24/02/17

So sugar is measured in donuts now? How much is one donut of sugar? Are we talking metric donuts or imperial? Couldn’t we just say it in tea spoons or sugar lumps? I read on hoping for clarification… “Children and young people are consuming the equivalent of 20 chocolate chip biscuits a day in sugar, according to anti-obesity campaigners.” Right. That’s cleared that up. Metric donuts obviously.

I press on being told that much of their sugar intake is ‘hidden’ in drinks and food. Hidden? How? Do you mean to say that parents don’t realise a can of coke contains sugar? Is the sugar in fruit juice really hidden? Have we all lost the ability to tell that sweet tasting foods contain sugars? OK, granted, some savoury kids’ staples like baked beans contain a bit of sugar, but you’d have to eat a hell of a lot to reach even five imperial donuts worth, let alone five metric ones.

Ah! This looks better: “Children and young people aged between 11 and 18 typically have an intake of 73.2 grams of sugar a day, far in excess of the 30g – or seven teaspoons – maximum recommended in official health advice”.

Woah! The sugar measuring system just swung from the hopelessly vague to the impossibly precise: 73.2 grams? One wonders why the point two was needed – is it somehow relevant? Call me cynical, but I suspect it’s so that after intensive government intervention and millions of tax payers money they can claim success when it is announced that intake has fallen to 73.1 grams.

Anyway, the article finishes with the promise extracted under duress from big name brands including Tesco, Waitrose, Nestlé, Lucozade, Ribena and Kellogg’s (whose sugar content has never been particularly occult to my knowledge), who have announced plans to reduce their use of sugar as part of a ‘reformulation drive’ ahead of the government’s sugar tax coming into force in 2018.

Damn right! They should get on with driving that reformulation and drive it hard. And while they are at it they should stop hiding donuts in kids food. Disgraceful.

As for the Guardian’s sloppy metrology, I am writing to them to insist they stick to units everyone recognises: the size of Wales.

Whole grains? Not a health food say these researchers

heart-health-whole-grainsIn the conclusion to their study examining the links between cardiovascular disease (CVD) and food consumption across 42 European countries, Pavel Grasgruber et al. make this bang-on-the-money statement about the propaganda surrounding so-called “heart healthy whole grains”:

A very important case is that of cereals because whole grain cereals are often propagated as CVD prevention. It is true that whole grain cereals are usually characterised by lower glycaemic index and insulin index values than refined cereals, and their benefits have been documented in numerous observational studies, but their consumption is also tied with a healthy lifestyle. All the available clinical trials have been of short duration and have produced inconsistent results indicating that the possible benefits are related to the substitution of refined cereals for whole grain cereals, and not because of whole grain cereals per se.

To use an analogy with smoking, a switch from unfiltered to filtered cigarettes can reduce health risks, but this fact does not mean that filtered cigarettes should be propagated as part of a healthy lifestyle.

In fact, even some unrefined cereals [such as the ‘whole-meal bread’ tested by Bao et al.] have high glycaemic and insulin indices, and the values are often unpredictable. Therefore, in the light of the growing evidence pointing to the negative role of carbohydrates, and considering the lack of any association between saturated fat and CVDs, we are convinced that the current recommendations regarding diet and CVDs should be seriously reconsidered

Source: Grasgruber et al.,Food consumption and the actual statistics of cardiovascular diseases: an epidemiological comparison of 42 European countries, Food and Nutrition Research, Sep 2016

Acrylamide – is it really a risk?

profile-keirAcrylamide is a potentially cancer causing compound produced when starches are browned during cooking. As reported in our Jan 2017 News Round Up concern about dietary acrylamide has led the Food Standards Agency to recommend the public ‘go for gold’ – avoiding medium and heavily browned toast, potatoes and pastries. But is this advice overblown?

‘Risk’ is always a slippery subject and human evolution does not appear to have equipped us to deal with it intuitively. The very word ‘risk’ is enough for many of us worry, or exclude a food ‘just to be on the safe side’. Hopefully, the following will put to bed any such concerns about the risk from acrylamide.

This graphic shows the commonest sources of acrylamide exposure:


One of the highest sources is coffee. Coffee consumprion, however, is associated with reduced all-cause mortality. The benefits across a huge range of measures from heart disease to dementia, increases with consumption, up to six cups per day, and has been shown to be independent of caffein. [See our post on coffee here]

If the risk from acrylamide was significant you would expect to see the reverse, with more coffee consumption linked to more cancer. As the data does not show this then the risk from acrylamide must be very small. Small enough to be countered by the beneficial phytonutrients in a cup of coffee.

Ah! If only all risks in life were so easily neutralised!

Looking again at the table above, apart from the coffee there are plenty of reasons to avoid the junk on that list: oxidised oils, gluten, n6 PUFAs… Acrylamide would be a long way down my list of concerns.

Heart disease trials: Low-fat diet fails. Nuts and olive oil succeed.


In brief

  • This post focuses on two of the largest intervention trials ever undertaken to assess the effects of diet on heart disease. Together they cover 1.5 million person-years of follow up and show that fats from high quality foods can be protective, whilst low fat diets failed to change heart disease outcomes. 
  • In the first study, The Women’s Health Initiative, an intensive decade long trial of a low fat diet failed to produce any difference in heart disease between the control and intervention arms, despite participants reducing their calories from fat by 10%
  • A second large scale intervention trial, PREDIMED, compared the standard low fat diet to an energy-unrestricted Mediterranean diet supplemented with nuts or olive oil. Despite an increase in fat consumption of 4.5% a distinct benefit was identified with 30% fewer cases of heart disease or death compared to the control group.
  • Between them they demonstrate the futility of low-fat diets and point to the importance of including sources of high quality fats, from unprocessed food in the diet, such as nuts, extra virgin olive oil and oily fish. 

Read time: 7 minutes (1400 words)

1. The WHI (Women’s Health Initiative) – low fat diet and heart disease

In 1991 the US National Institutes of Health (NIH) initiated The Women’s Health Initiative (WHI). It was the largest intervention study ever undertaken, focusing on 160,000 postmenopausal women aged 50–79 years over 15 years. The study included three large scale clinical trials and one observation study covering cardiovascular disease, cancer, and osteoporosis.

The Dietary Modification Eating Pattern is the trial we are interested in here, as it aimed to determine the effect of a low-fat eating pattern on coronary heart disease incidence. The question it was tasked with answering was “can a low-fat diet reduce heart disease?”

The diet group consisted of 19541 women who underwent intensive intervention consisting of:

  • initial training in eating a low-fat diet
  • ongoing group meetings and consultations to keep participants on track
  • dietary fat target of 20% of daily caloric intake
  • Increasing the consumption of fruits, vegetables, and grains

The control group (29294) were given no advice and left to eat their habitual diets. The trial lasted eight years, meaning that this was a very large, long, expensive intervention. Trials like this only come along once in a lifetime. To ensure the participants stuck to the diet the ongoing support and monitoring was unusually thorough.

The study group achieved a reduction in fat intake of 10.7% in the first year, compared to the control group. By year 6 the difference had only dropped slightly to 8.2% so long-term compliance was good. They also increased

Yet for all the success of the study design, there was no significant reduction in coronary heart disease, stroke or cardiovascular disease events as the graph below shows:


Along with the failure to affect heart disease there was also no significant reduction in colorectal or breast cancer incidence which were secondary outcomes of the trial.

Despite all of these failures to affect disease progression, the intervention group did have significant improvements in biomarkers. This is an important point as biomarkers are usually treated as surrogates for disease risk. The logic is that if A causes B and B is associated with C then A causes C. You can see this in the following advice from the NHS:

Eat less Saturated fat… Eating a diet that is high in saturated fat can raise the level of cholesterol in the blood. Having high cholesterol increases the risk of heart disease. NHS Choices, Nov 2016

Saturated fat (A) raises cholesterol (B) and high cholesterol (B) is associated with increased risk of heart disease (C). Implying that saturated fat (A) causes heart disease (C). It’s a compelling argument. It seems so rational. But… it’s wrong.

The Women’s Health Initiative showed that this logic does not hold. The women on the low fat diet did reduce saturated fat, they did have improved cholesterol, but damn them they had just as much heart disease as ever. What were they playing at? Didn’t anyone tell them what was supposed to happen?

The complete failure of a low-fat diet to modify disease progression should have been the nail in the coffin for low fat diets. These results were published at the turn of the century, yet we are still waiting for government recommendations to catch up. In deed, instead of relaxing the recommendations on dietary fat restrictions, the UK government in its latest revisions have doubled down on

Likewise the The World Health Organisation advocate a diet with less than 30% calories from fat overall. The NHS pages on fats states “Current UK government guidelines advise cutting down on all fats” Then goes on to explain how to eat a low fat diet. They say “If you want to cut your risk of heart disease, it’s best to reduce your overall fat intake and swap saturated fats for unsaturated fats.” yet this is not what the highly expensive and extensive WHI study showed.

2. The PREDIMED trial (Prevención con Dieta Mediterránea) – an unrestricted Mediterranean diet with increased fat from olive oil or walnuts

The PREDIMED trial began in 2003. The 7447 participants were men (55 to 80 years of age) and women (60 to 80 years of age) with no cardiovascular disease at enrollment, who had either type 2 diabetes mellitus or at least three of the following major risk factors: smoking, hypertension, elevated low-density lipoprotein cholesterol levels, low high-density lipoprotein cholesterol levels, overweight or obesity, or a family history of premature coronary heart disease.

They were split into three groups: A control group who received the standard of care advice to eat a low-fat diet. The other two groups were advised to eat a Mediterranean dietary pattern: moderate consumption of ethanol (mostly from wine), low consumption of meat and meat products, and high consumption of vegetables, fruits, nuts, legumes, fish, and olive oil. These two groups were then provided with either extra-virgin olive oil or nuts (walnuts, hazelnuts and almonds) as regular, free food items.


Supplementary table S2 from the PREDIMED trial showing the main changes in dietary patterns between the control and Mediterranean diet groups (click image to enlarge)

Despite regular counselling to eat a Mediterranean dietary pattern the only significant differences with the control group (apart from a rather obvious increase in consumption of  extra virgin olive oil and nuts), was a modest increase in fish and legume consumption amounting to aproximately half a portion per week. The main difference in macronutrients was an average 4.5% increase in consumption of calories from fat mainly due to the olive oil and nuts. This additional fat would be primarily monounsaturated and polyunsaturated.

What is remarkable, when compared to the Women’s Health Initiaive is the clear benefits of these high-fat foods. On average there were 30% fewer cases of heart disease or death among those eating the extra virgin olive oil or nuts. The graph below shows the distinct and increasing separation between the mortality lines of the control and intervention groups.


Considering the relatively modest dietary changes involved the size of the protective effect is quite remarkable.


  1. High Fats v Low Fat
    The PREDIMED intervention clearly produced cardiovascular benefits despite being higher in fat, whereas the low fat WHI failed to produce any such benefits.
  2. Plant v Animal fats
    The main source of the additional fats in the PREDIMED diet was from plants (olive oil and nuts). However, there would have been a small contribution from animal fats via moderatly increased fish consumption. The benefits observed were not from reduced meat consumption, as these remained similar between both control and intervention groups.
  3. Type of Fatty acids
    The types of fat in the PREDIMED diet varied between the two intervention groups: In the olive oil group the main increase came from monounsaturated fatty acids (MUFAs) whilst in the nut group the main increase came from polyunsaturated (PUFAs). As both groups benefitted equally it seems unlikely that either MUFAs or PUFAs are uniquely beneficial. Saturated fat decreased slightly across all groups (including the control group), so cannot account for the observed benefits. Omega 3 PUFAs (α- linolenic acid or marine long chain fatty acids) are considered cardio protective, but these varied little between the groups, and were most different between the nut and olive oil groups. Overall it seems unlikely that changes in individual fatty acids accounts for the benefits. This suggests that other factors in nuts and olive oil are significant. Interestingly, the trial used extra virgin olive oil, as this contains a range of micronutrients and phytochemical not found in more refined and heat treated oils. 
  4. Diet Quality
    In a 2016 comprehensive review in Circulation, the journal of the American Heart Association, Dariush Mozaffarian suggests that it is time to move away from considering diet in terms of isolated nutrients as they appear to behave differently depending on the particular food matrix they are found in as well as the other foods they are eaten with. He suggests that the benefits observed in the PREDIMED diet come not from individual nutrients, but rather differences in overall foods across the diet as a whole. The Mediterranean diet pattern includes more fish, legumes, nuts and whole foods generally, and it may be this that contributed most to the improvements seen in this trial.I think he is right: don’t avoid fats and aim to include low or minimally processed foods like these:



Howard BV et al, Low-fat dietary pattern and risk of cardiovascular disease: the Women’s Health Initiative Randomized Controlled Dietary Modification Trial. JAMA, 2006 [Full Text, PubMed]

Ramón Estruch, et al, Primary Prevention of Cardiovascular Disease with a Mediterranean Diet. 2013 [Full Text, PubMed]

Dariush Mozaffarian. Dietary and Policy Priorities for Cardiovascular Disease, Diabetes, and Obesity. Circulation, Jan 2016 [Full text, PubMed]

Red light phototherapy (3/3): Hair regrowth, Pain reduction, Wound healing and Practical applications

red-light-hair-pain-woundThis is the third and final post looking at the huge body of research that is uncovering the remarkable health benefits of red light.


Part 1: Skin (click to read)
• Red light and skin rejuvenation, collagen production and wrinkle reduction
• Red light protects skin from photo-aging

Part 2: Brain, Muscles and Eyes (click to read)
• Red light and brain health
• Red light enhances muscle performance and exercise recovery
• Red and infra-red light protect the retina

Part 3: Hair regrowth, Pain, Wound Healing and Practical Ideas (this post)
• Red light increases hair regrowth
• Red-light for pain relief
• Red-light for wound healing
• Practical ways to make use of these ideas


In researching these three posts I have been constantly surprised that red light exposure demonstrates measurable effects at very low doses and durations: it seems just a few minutes per day with standard LED lamps are enough to produce measurable hair regrowth, exercise enhancement or speed up wound healing. The greatest length of exposure in the papers I looked at was for brain stimulation where the duration required 30 to 60 minutes per day for approximately ten days. But in such cases a sinlge LED placed in one nostril appears to be sufficient! Continue reading

Male fertility ~ a fishy business


The extraordinary decline in male fertility over the last century has coincided with a major shift in our dietary polyunsaturated fatty acids intake away from omega-3’s (found in seafood) towards omega 6’s (found in vegetable seed oils). In this post I cast my net wide and haul in a boat-load of evidence linking PUFAs to sperm function.  Continue reading