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.

Cardiologist attacks diet dogma at 2017 Symposium



Dr Salim Yusuf speaking at the Cardiology Update 2017 symposium gives preliminary findings from the PURE study which followed 140,000 people in 17 countries, designed to address causation of cardiovascular disease.

He explains that the results indicate:

  • Greater fat intake is protective
  • Carbohydrates are harmful
  • High fat dairy is beneficial
  • Saturated fat from meat is neutral
  • Fruit is beneficial, but no additional benefit over 2 portions per day
  • Legumes are beneficial
  • 3 to 6 g/day sodium* intake optimal (vs US guidelines of 1.5g)
  • Eggs, fish and vegetables were neutral

*Edit 10/03/2017
Correction: I previously wrote 3 to 6 grams of salt per day, but have corrected this to 3 to 6 grams of sodium per day. This is equivalent to 7.5 to 15 g of salt per day.

Gluten – what we learned in 2016 (part 2) – the Great Imitator

20+ conditions related to gluten – a review of some 2016 papers

gluten-related-disorders-2016-20🔍 Please feel free to share this infographic or the whole post!

In part 1 we looked at some of the key developments in understanding gluten sensitivity (coeliac and non-coeliac gluten sensitivity) that emerged in 2016. In part 2 now we take a look at some case studies, and small trials that link gluten to a wider range of conditions.

Read time: 18 minutes (2400 words)

Some of the conditions that were linked to gluten in 2016

When I did my medical training I was examined on clinical diagnostic skills. We students of herbal medicine, like other medical students, were taught that whatever symptoms a patient presented with, our list of possible diagnoses we could always include tuberculosis and syphilis. These two systemic diseases were called the great imitators due to their potential for affecting any tissue or organ. From back pain, to skin rashes and mental illness, these ancient adversaries of Man could be the cause. Misdiagnosis could be serious in that the wrong treatment might be pursued, and the effective treatment missed. What we are seeing with gluten related disorders is another great imitator at play. The conditions that follow will leave you in no doubt that gluten and/or other factor in cereal grains, can play havoc with every corner of the body and should always be considered, properly tested for,m and ruled out by the responsible and updated clinician.

In reading this post there are several points to bear in mind: (1) This is far from an exhaustive list, even of 2016 papers. (2) Gluten related disorders often go unsuspected, undiagnosed and therefore untreated for many many years and 80% of coeliacs remain undiagnosed! (3) Gluten can affect any system or tissue type of the body and should always be considered as part of a differential diagnosis even if there are no intestinal symptoms. A full gluten blood test, not just the standard NHS coeliac tests, should be used, or a minimum of a 6 week exclusion diet. (4) The true extent of the gluten iceberg’s sub-surface volume has yet to be established. These reports give some insight into the extent of the murky mass.

I have seperated these reports into those related to coeliac – where there is adaptive immunity and/or autoimmune factors involved and non coeliac gluten sensitivity (NCGS) – where the innate immune system is principally involved. The latter is particularly important as it indicates the propensity of gluten to affect potentially anyone.

1. Coeliac (autoimmune) related

Coeliac hepatitis: hepatic fibrosis, advanced steatohepatitis and cirrhosis
In a Nov 2016 case study, a 20 year old woman with coeliac disease and severe liver cirrhosis had a near complete reversal once placed on a gluten-free diet.The author called this a “hepatomiracle” [Gaur, Nov 2016]
An Iranian study published in Jul 2016 found that the prevalence of coeliac disease among patients with epilepsy was 6% – about five times higher than in the general population. [Bashiri, Jul 2016]
Chronic Hepatitis C Virus (CHV)
CHV infection can lead to autoimmune diseases and shares one of the same genetic loci as coeliac disease (HLA-DQ2). Liver disease also leads to anti-tissue transglutaminase antibodies (anti-tTG). Some CHV patients develop coeliac disease during interferon therapy. There is a complex relationship with many overlapping features between these two conditions, although it is not yet clear whether the incidence of coeliac disease is higher in CHV or not [Association between celiac disease and chronic hepatitis C, 2016].
Distal Renal Tubular Acidosis Associated with Celiac Disease and Thyroiditis
A case report of a 12 year old girl with a particular form of kidney disease, (distal renal tubular acidosis, RTA) with autoimmune diseases, which is extremely rare in children. [Indian Pediatrics, Nov 2016] “Despite resolution of acidosis on bicarbonate, she continued to have poor growth and delayed puberty. Investigations revealed autoimmune thyroiditis and celiac disease. Levothyroxine and gluten-free diet were initiated. Child gained height and weight and had onset of puberty after gluten withdrawal.”
Psychiatric Case
The BMJ recently published a case study of a girl admitted to a psychiatry ward suffering with suicidal behaviours who then developed an agitated catatonic state. She was unresponsive to antidepressants, anxiolytics, antipsychotics and electroconvulsive therapy, but improved significantly when a gluten-free diet was started [Oliveira-Maia, Dec 2016]. Another recent paper The progression of coeliac disease: its neurological and psychiatric implications, Campagna G, Dec 2016, explores the current understanding of the neurological implications of coeliac disease.
Burning Tongue
An elderly woman presented with complaints of a burning tongue for the past two years as well as occasional loose stools and fatigue. Tests revealed iron deficiency anemia, zinc deficiency and an abnormal celiac panel. Ten weeks on a gluten free diet led to complete symptom resolution [Sherman, Jun 2016].
Macrophage activation syndrome
A case report in Pediatric Rheumatology Online Journal, reports on a six year old girl who was diagnosed with Macrophage activation syndrome – an autoinflammatory or rheumatic disease involving hyper inflammation and an ineffective immune response. Serology indicated coeliac disease and symptoms stabilised with the introduction of a gluten-free diet. Authors state that “Clinicians should have a low threshold for screening children with other autoimmune diseases for coeliac disease.” [Palman, Dec 2016].
Coeliac like disease in dogs
The Veterinary Record [Lowrie, Dec 2016] reports on a case of “gluten-sensitive dyskinesia (previously termed canine epileptoid cramping syndrome) is a condition of Border terriers in which the leading manifestation is neurological… responsive to a gluten-free diet.” As such, the authors suggest that gluten sensitivity in Border terriers “may manifest as a multisystem disease in a similar manner to that seen in human beings.” There is another paper on this topic: Gluten exposure and multisystem disease in dogs [Davies M, Dec 2016], but I have been unable to access it.
Gluten free diet in pregnancy and type 1 diabetes in offspring
As we have previously discussed, gluten has a significant role in the development of type 1 diabetes. A study in the Journal of Diabetes Research [Antvorskov JC, Aug 2016] investigated the a mouse model of type 1 diabetes. Withholding gluten during pregnancy prevented the subsequent development of type 1 diabetes in offspring, even when exposed to gluten after birth. However, the effect disappeared if the mother received a gluten-free diet prior to pregnancy.
Aortic stiffness may explain increased cardiovascular risk
Many studies show an increased risk of cardiovascular disease in coeliac patients which cannot be explained by traditional risk factors. A study from Antalya, Turkey used echocardiograms to compare the aortic function of 81 coeliac patients with that of 63 healthy volunteers. They found an increased level of aortic stiffness and inflammation in coeliac patients. Whilst inflammation decreased with adherence to a gluten free diet, aortic stiffness did not, suggesting that increased cardiovascular risk may persist despite a gluten-free diet. [Bayar, Mar 2016]
Hemophagocytic lymphohistiocytosis
Hemophagocytic Lymphohistiocytosis and is a life-threatening immunodeficiency. It affects people of all ages and ethnic groups. Common symptoms are fevers, enlarged spleen, low blood counts and liver abnormalities. [ref] A recent paper [Fordham NJ Sep 2016] reports a case that did not respond to standard treatment, but following blood tests established undiagnosed coeliac disease. “She initially responded to chemoimmunotherapy specific for hemophagocytic lymphohistiocytosis but relapsed within a few months of cessation of treatment and then achieved complete remission on gluten withdrawal alone.”
Down’s Syndrome
A study in Poland identified high levels of diagnosed coeliac disease among patients with Down’s syndrome (5.4% vs 1% in general population). The authors emphasise that tests for coeliac disease should be carried out in all (Polish) patients with Down’s syndrome, regardless of the clinical picture. [Szaflarska-Popławska, 2016]
Multiple autoimmune syndrome with celiac disease
Reumatologia published a case report of a 32 year old woman who had four co-existing autoimmune diseases: autoimmune hypothyroidism, Sjögren’s syndrome, systemic lupus erythematosus (SLE) and celiac disease which leads to the final diagnosis of multiple autoimmune syndrome type 3 with celiac disease. The authors point out that patients with single autoimmune disorders are at 25% risk of developing other autoimmune disorders. The case emphasises the need for continued surveillance for the development of new autoimmune disease in predisposed patients. [Harpreet, Dec 2016]

2. Non-coeliac Gluten Sensitivity (NCGS)

NOTE: I am using NCGS as a looser category than is currently accepted to include any studies where withdrawal of gluten or wheat showed clinical benefit.

Intestinal cell damage and systemic immune activation in NCGS
A study published in the BMJ’s journal Gut at the end of 2016, examined serum from 80 individuals meeting the criteria for NCGS (although the authors use the term Non Celiac Wheat Sensitivity). They found increased levels of lipopolysaccharide binding protein – indicating that these patients had raised levels of gut bacteria products passing through a damaged gut wall, known as ‘leaky gut’. Associated with this was raised markers of systemic immune activation. The researchers went on to find raised levels of fatty acid binding protein, indicative of intestinal cell damage. As NCGS patients do not have villous atrophy (which is characteristic of celiac disease) it had been assumed that there is no intestinal damage taking place in NCGS, however, this study shows that damage is indeed taking place. The authors speculate that damage in NCGS may be taking place in the mid section of the small intestine, the jejunum, rather than the first section, the duodenum, from which biopsies are usually taken. Finally, these markers were found to improve with the initiation of a gluten free diet. [Melanie Uhde, 2016]
Psychotic Illness
Schizophrenia has previously been linked to raised kynurenine and reduced tryptophan [Chiappelli, Nature, 2016], both of which are related to the production of Vitamin B3. Researchers hypothesised that this imbalance could be caused by inflammatory immune mediators such as gluten. They found schizophrenic patients had raised levels of anti-gliadin antibodies (IgG) which correlated with kynurenine/tryptophan ratios. They concluded “Our results connect nonceliac gluten sensitivity with the KYN pathway of TRP metabolism in psychotic illness” [Okusaga, 2016]. This links to an long used treatment of schizophrenia which is goodly doses of Vitamin B3 (niacin), the production of which may be getting interfered with by gluten in these patients.
Atopic Dermatitis (Eczema)
A recent study sent 169 atopic dermatitis patients a 61-question survey asking about dietary modifications they had tried and their perceptions and outcomes of such trials. The most common foods eliminated were ‘junk foods’ (68%), dairy (49.7%), and gluten (49%). The best improvement in skin was reported when removing white flour products (37 of 69, 53.6%), gluten (37 of 72, 51.4%) and the nightshade family of vegetables, i.e. potatoes, tomatoes, aubergines, peppers, chilli and paprika (18 of 35, 51.4%). [Nosrati, 2017]
Lymphocytic colitis
(This condition is characterised by chronic watery diarrhoea yet with normal colon cells when sent to the histology lab, but with an accumulation of lymphocytes in the colonic epithelium/lining)
A study in the journal PLoS One found that 91% of lymphocytic colitis patients who were identified as NCGS responded to a double blind gluten challenge indicating a causative role for gluten in these patients. [Rosinach M, Jul 2016]
Nephrotic Syndrome
This is a rare condition in childhood that presents with proteinuria, hypoalbuminemia, and oedema. Kidney function is usually normal however. Most children (>90%) respond to an initial course of oral steroids and are designated as having steroid-sensitive nephrotic syndrome (ssNS). A study in Pediatrics placed 8 children with difficult-to-manage disease (characterized by steroid dependence or frequent relapses) on a gluten-free diet. They all had clinical improvement enabling reduction or discontinuation in steroids. The role of gluten in this condition was confirmed through relapse following re-exposure to gluten. The authors conclude “Elimination of gluten from the diet, may reduce the need for potentially toxic immunosuppressant therapies” [Lemley KV, Jul 2016]
Microscopic colitis
– A new clinical and pathological entity (“lymphocytic enterocolitis”)?
Of patients with Marsh 1 duodenal damage, but no coeliac serology (i.e. negative for anti-endomysium and anti-tissue transglutaminase), half were found to have microscopic colitis. Although this study was not specifically looking at gluten, 14 patients tried a gluten free diet for at least one month and 3 of them (21%) had improvements. [Bonagura, Nov 2016]
Postural orthostatic tachycardia syndrome (POTS)
A study published in the European Journal of Gastroenterology and Hepatology found that 4% of PoTS patients had coeliac antibodies, yet 42% reported gluten sensitivity, suggesting that many POTS patients are NCGS. [Penny HA, Dec 2016]
Eosinophilic oesophagitis
Eosinophilic oesophagitis (also called EoE for those who spell oesophagus without the ‘o’) is a chronic inflammatory oesophageal disease triggered predominantly by food antigens. Although considered a food allergy, EoE is unique in not involving the immunoglobulin IgE antibody response. A recent review identifies milk and gluten elimination as the most promising cure strategies. [Molina-Infante, Dec 2016] How is EoE caused? Until recently it was considered that the oesophagus was relatively impermeable to food antigens and allergic diseases of the oesophagus were unknown. Researchers from the Mayo Clinic wondered if food antigens were present in the oesophageal tissue of sufferers. In a recently published paper they report finding increasing levels of gliadin (gluten) in the oesophageal tissue with increased severity of disease, whilst none was present amongst controls. This suggests a direct causative role of gluten in EoE.


Comparison of total anti-gliadin staining (y-axis) in patients on a gluten free diet (GFD), control patients and patients with inactive and active EoE on gluten (x-axis, 63x). E. V. Marietta, AP&T Nov 2016

Effect of a gluten-free diet in children with autism spectrum disorders
In this randomised clinical trial [Ghalichi F, Nov 2016] 80 children with ASD were randomised to gluten-free diet [40] or regular diet [40].

“In the GFD group, the prevalence of gastrointestinal symptoms decreased significantly (P<0.05) after intake of GFD (40.57% vs. 17.10%) but increased insignificantly in the RD group (42.45% vs. 44.05%). GFD intervention resulted in a significant decrease in behavioral disorders (80.03±14.07 vs. 75.82±15.37, P<0.05) but an insignificant increase in the RD group (79.92±15.49 vs. 80.92±16.24).”

Alcohol related cerebellar degeneration
Alcohol-related cerebellar degeneration is one of the commonest acquired forms of cerebellar ataxia, however, the mechanism by which alcohol causes this damage is unknown. The cerebellum is the back part of the brain, responsible for many basic things including walking. ‘Ataxia’ is difficulty in walking. In a recent study from Royal Hallamshire Hospital, Sheffield, England, a group of 38 patients with ataxia were studied. 34% were found to have circulating antigliadin antibodies vs. 12 % in healthy controls, and 39 % were found to have antibodies to transglutaminase 6 (which are neurological antibodies) vs. 4 % of healthy controls. The authors suggest that chronic alcohol abuse increases gut permeability exposing the immune system to increased levels of gluten peptides to which these two antibodies are raised. They conclude “Alcohol induced tissue injury to the central nervous system leading to cerebellar degeneration may also involve immune mediated mechanisms, including sensitisation to gluten.” [Shanmugarajah PD, Oct 2016]


We are in the middle of an epidemic of gluten related disease that have crept up on us over the last few decades. Our European culture has lived with wheat and its associated diseases, for thousands of years, and we have named and described them, yet only now are we becoming aware of the true cost to our health. At the same time, many Central America countries (Guatemala, El Salvador, Honduras, Nicaragua, Costa Rica, and Panama), which historically have had very low rates of coeliac disease, are transitioning from a diet based on maize to one increasingly centred around wheat. Maize too has its problems but the prolamine in maize, zein, is less likely to cause immune reactions than is the prolamine in wheat, namely gluten.

A paper published in the journalNutrients  [Amado Salvador Peña* and Jakob Bart Arie Crusius, Sep 2015] provides a salutary reminder of the scope of the problem:

[these] changes permit a prediction of an increase of celiac disease and other autoimmune diseases such as type I diabetes and thyroid disease.

The aim of this review is to… alert authorities responsible for the planning of education and health, to find possibilities to avoid a rise in these disorders before the epidemics start.

– Amado Salvador Peña and Jakob Bart Arie Crusius, Central America in Transition: From Maize to Wheat. Challenges and Opportunities (Nutrients, Sep 2015)

Gluten – what we learned in 2016 (part 1)

toast-head-by-rysunek-kuczynski▲ Image: Pawel Kuczynski

“Give us this day our daily bread (…) but deliver us from evil”

—Matthew 6:11, 13

This is an update on our previous series of articles “Why No One Should Eat Grains” which were published in 2015; we recommend you read them too if you want to get your brain around this topic (before gluten makes toast of it!):


  • Introduction – “deliver us from evil”
  • Gluten related disorders on the rise – but why?
  • Amylase Trypsin Inhibitors – activate myeloid cells
  • Type 1 diabetes – gluten affects the pancreas of even healthy mice
  • Grain globulins – contain coeliac and T1 diabetes reactive proteins
  • Oats – evidence that they should be avoided in coeliac disease
  • IBS and gluten sensitivity – gluten is often the problem
  • New coeliac auto-antibodies identified – linked to autoimmune polyneuropathies
  • Neurological effects of gluten – Simiar in coeliac and NCGS
  • Gluten in Latin America – high levels of self reported gluten avoidance.

Read time: 11 minutes (2200 words)

Continue reading

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]

5 everyday ancestral foods with proven health benefits

supermarket-ancestral-nutritionThe Weston A Price Foundation and the wider Ancestral Health movement have long advocated the use of traditional food processing methods such as fermentation, soaking and sprouting. It is claimed that these steps, honed over generations, improve the nutritional properties of certain foods, whilst reducing or neutralising toxic and anti-nutritive components.

As a result many people have taken to making keffir, fermenting their own vegetables or baking sprouted seed loaves. However, several such ancestral foods have found their way down the centuries and quietly entered the industrialised market. I’m talking about common or garden staples like tea, coffee, chocolate, cheese and olives.

It’s easy to forget the ancient origins of these shopping basket basics, and the complex processing they go through before reaching the supermarket shelves. So lets put the WAPF and Ancestral Health thesis to the test and check out the health credentials of these once-exotic commodities. 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