According to advocates of low carbohydrate diets a key benefit is the effect on triglycerides in the blood. The argument goes that a high level of triglycerides is linked to increased risk for coronary heart disease; low carb diets lower triglycerides; so low carb diets should lower the risk for heart disease. Sounds plausible enough, but is it true?
Blood lipids and heart disease risk
The approach to managing blood lipids to lower heart disease risk has evolved over time as our understanding of this complicated field has grown. Decades ago the focus was on lowering total cholesterol but this was later narrowed down to LDL-cholesterol – ‘bad’ cholesterol for the lay person. ‘Good’ HDL-cholesterol was considered protective and the balance between the bad and the good – the LDL/HDL ratio – came into use. More recently, the total cholesterol/HDL ratio has been considered to be a better measure as all non-HDL-cholesterol appears to increase heart disease risk.
What about triglycerides?
If you are interested in how triglycerides affect the risk for heart disease and how diet affects blood triglycerides look no further than the American Heart Association’s scientific statement Triglycerides and Cardiovascular Disease. You may need to allocate an afternoon as the paper is very comprehensive and has over 500 references.
Pete Evans, Sarah Wilson and some international speakers were involved in the recent series of Low Carb Downunder presentations. It was a very slick exercise. And very expensive, but who footed the bill?
In August and September the Low Carb Downunder road show came to Sydney and Melbourne. I went along to the Sydney presentation and was certainly impressed by the organisation of the event. Great venue, a big audience, big celebrities and an international speaker – the Melbourne program had three!
Pete Evans is quite a performer. He moved confidently around the stage engaging his lay audience with his passion for The Paleo Way of eating and they lapped it up. If you have ever seen one of those American motivational speakers at work and their star struck audiences hanging off every word, it was a bit like that.
But something was not quite right. The usual rhythm of things is that nutrition professors sell nutrition messages and celebrities sell products. So what were these celebrity presentations on nutrition all about?
As the focus of public health nutrition switches from fats to carbohydrates there is uncertainty about how carbohydrates actually affect the risk for chronic diseases, such as type 2 diabetes and coronary heart disease. Early dietary advice on fats was based on effects on blood cholesterol but what mechanisms are driving the risk associated with carbohydrate?
Glycaemic response or fructose?
One view is that the key driver of carbohydrate-related risk is glycaemic response i.e. the degree to which carbohydrates raise blood glucose and insulin levels. If glycaemic response is the critical factor then the dietary measure of interest would be glycaemic load, which takes into consideration both the amount of carbohydrate consumed and its potential to raise blood glucose.
An alternative view is that fructose drives the chronic disease risk associated with dietary carbohydrate. If so, we should expect fructose or perhaps sucrose (the major dietary source of fructose) to be associated with risk for chronic disease in large population studies. And, importantly, glycaemic load would not be linked with risk.
Let’s look at the epidemiology and see if it supports one argument or the other.
Glycaemic load and coronary heart disease risk
Four meta-analyses of prospective cohort studies of glycaemic load and risk for coronary heart disease have been published in the last couple of years (Dong 2012, Fan 2012, Ma 2012, Mirrahimi 2012). The findings are essentially the same – glycaemic load is associated with heart disease in women but not men. In two of the meta-analyses the links between glycaemic load and heart disease were stronger in overweight subjects. Fan (2012) also found an association with stroke incidence, as did Sieri (2013) in a recent cohort study. In all four meta-analyses the relative risks for heart disease in men were positive – they just failed to reach statistical significance, perhaps due to smaller numbers.
A study in a Chinese cohort published last year found glycaemic load was associated with coronary heart disease risk in both genders (Yu 2013). Compared to studies in western populations carbohydrate intake was high (68% of calories) but sugar intake was relatively low. Most of the carbohydrate was starch, 87% of which came from white rice and refined wheat products.
Recently the Weekend Australian (19-20 July) published an article ‘The six foods I never stock at home’ by celebrity chef Pete Evans. Although the newspaper acknowledged ‘his downright fanaticism’, some basic fact checking would have revealed many false claims and inaccuracies.
There is no substantial evidence that proves we need to consume grains to be healthy
I have to disagree with Mr Evans on this point – he seems unaware of grains’ contribution to thiamin intake and the importance of this essential B vitamin.
The healthy diets modelled for the latest Australian Dietary Guidelines contained plenty of thiamin, well above the Recommended Dietary Intake (RDI), but nearly two-thirds of it came from just one food group – grains. If grains were removed from the otherwise optimal diets the thiamin content would fall to well below the RDI. As no other food group is a major source of thiamin it is unlikely that replacement foods could correct the thiamin deficit. If the population adopted Mr Evans ‘no grains’ advice the likely consequence would be the emergence of the thiamin deficiency disease beri beri in vulnerable groups.
Those who strictly follow Mr Evans advice should be on the lookout for the early symptoms of beri beri which include tingling, burning or numbness in the fingers and toes, strange eye movements and vomiting. There may also be loss of appetite and severe constipation. As the heart failure starts to develop you can expect to experience shortness of breath and swelling in the lower part of the legs. In the final stages there will be mental confusion, problems with speech, difficulty walking, coma and death.
Alternatively, you could eat some wholegrain cereal at breakfast and have a sandwich for lunch and live a healthy life, just like normal people.
Over the last year or so two senior Australian nutritionists have been subjected to a sustained social media campaign to denigrate them and their research. Their alleged crime? Daring to say what they believed to be true.
In 2011, Professor Jennie Brand-Miller from the University of Sydney and Dr Alan Barclay, Chief Scientific Officer at the Glycaemic Index Foundation and Head of Research at the Australian Diabetes Council published a paper on the Australian Paradox – the apparent fall in sugar consumption that occurred over a period when rates of obesity in this country increased. The paper was obviously intended to stir the pot a little.
The narrative in the United States at the time was that the increase in obesity prevalence in that country had coincided with increasing sugar intake, so perhaps sugar was a causative factor. In their paper Barclay and Brand-Miller pointed out that while that may well be the case in the United States, sugar intakes had remained fairly constant in the United Kingdom over the same period and had actually fallen by 16 per cent in Australia. However, both countries had experienced an increase in rates of obesity, hence the Australian Paradox.
Under normal circumstances this simple paper may have dissolved away into the vast ocean of scientific literature and never been heard of again. However, a member of the public took exception to the finding that sugar intakes in Australia were falling. Despite not having any qualifications in nutrition or science he had formed a view that sugar intakes in Australia were in fact rising. A social media campaign was initiated to attack the nutrition researchers and their findings and a formal complaint was lodged with the University of Sydney.
Credible nutrition scientists have opposing views on whether omega 6 in vegetable oils is good for heart health. But who is right?
Part 1 of this series examined claims that omega 6 in vegetable oils causes ill health by increasing the risk for cancer, macular degeneration, Parkinson’s disease and inflammatory conditions, such as rheumatoid arthritis, ulcerative colitis and asthma. These claims, frequently expressed on the internet and in social media, were found to be baseless.
Part 2 will consider whether omega 6 increases or decreases the risk for coronary heart disease. Unlike the wild social media claims about omega 6, this issue is argued in the scientific literature with credible scientists on both sides. Whose argument is stronger?
The conventional wisdom
Leading heart health agencies such as the Heart Foundation, the American Heart Association and the World Health Organisation assert that polyunsaturated fats (mainly omega 6) are heart healthy and that they may be the ideal replacement for saturated and trans fats in the diet. The case appears to be strong:
• Polyunsaturated fat (mainly omega 6) has a beneficial effect on blood lipids. When saturated fat is replaced by polyunsaturated fat the level of serum LDL-cholesterol and the total cholesterol/HDL cholesterol ratio both fall, which is consistent with lower risk for coronary heart disease.
• Epidemiological studies indicate that polyunsaturated fat (mainly omega 6) is heart friendly. A pooled analysis of 11 prospective cohort studies conducted in Europe and the United States shows that replacing saturated fat with polyunsaturated fat lowers coronary risk more than other macronutrients.
• In randomised controlled trials coronary heart disease risk falls when saturated fat is replaced by polyunsaturated fat (mainly omega 6) – see Harvard’s meta-analysis.
So the conventional wisdom is based on three consistent lines of evidence with a rare meta-analysis of randomised controlled dietary trials sitting on top. Impressive. How could you argue against it?
Following the publication of the latest national dietary survey it is clear that sugar intake has fallen since 1995. But mere facts are unlikely shake the resolve of the non-nutritionists driving the lucrative sugar scare.
The trend in sugar consumption in Australia has been a contentious issue in recent years, especially as nutritionists and lay people have sought dietary explanations for the obesity epidemic. On one side of the argument is the view that the intake of sugar, or perhaps fructose, has increased in recent decades and that this has been the driving force behind the epidemic. This argument emerged in the United States where sugar intakes are undoubtedly high.
In the Australian context it has been argued that sugar intake hasn’t increased at all and is actually in steady decline. Proponents of this argument include Dr Alan Barclay and Professor Jennie Brand-Miller who published an assessment of trends in intakes of sugars and obesity rates in Australia, the United Kingdom and the United States between 1980 and 2003. In this paper the authors identified an ‘Australian Paradox’ – increased rates of obesity despite an apparent fall in sugar intake.
The recent publication of new data from the Australian Health Survey (AHS) has provided some clarity on this issue.
Sugar data from the Australian Health Survey
The AHS was conducted by the Australian Bureau of Statistics, which also conducted Australia’s last national dietary survey of adults and children in 1995, so now we have insights into how the diet of Australians has changed over the intervening period of approximately 16 years. Here are some of the top-line results relating to sugar.
• Intake of total sugars has fallen in men, women and children.
• The percentage of dietary energy from total sugars has also fallen.
• Carbohydrate intake has fallen, both in absolute terms and as a percentage of energy. Total energy intake has also fallen.
More than six months after it broadcast two misleading Catalyst programs about diet, medication and heart disease the ABC has admitted there were problems with impartiality and has undertaken corrective action. But there is still something fishy about this.
In October last year ABC television’s science program Catalyst ran two controversial programs purporting to expose myths about diet, medication and cardiovascular disease. In the first program Catalyst presenter Dr Maryanne Demasi challenged the role of dietary saturated fat in affecting risk for coronary heart disease and in the second she questioned the efficacy of statin medication. Essentially, the Catalyst program argued that the world’s leading nutrition organisations and cardiovascular researchers had got it wrong over the last four decades.
Heart Foundation outraged
In an interview on the ABC radio program PM, Maryanne Demasi even stated that the Heart Foundation was ‘certainly supportive’ of the Catalyst program’s evidence. In fact, the Heart Foundation was livid, took offence and submitted a formal complaint. They weren’t alone – the ABC received a total of 146 complaints. To their credit, journalists within the ABC, such as health reporter Dr Norman Swan and Media Watch front man Paul Barry, challenged the accuracy of the programs and the standard of the journalism on display, respectively. For more of detail see my two posts on the Catalyst programs here and here.
Results of independent review
Yesterday, the results of a review of the Catalyst programs by the ABC’s Audience and Consumer Affairs Unit were made public and included findings that standards of impartiality had been breached. Here are some excerpts from the review:
Omega 6 in vegetable oils stands accused of causing ill health by increasing the risk for cancer, macular degeneration, Parkinson’s disease, inflammation and heart disease. Sounds bad, but is any of it true?
What is omega 6?
All fats – animal or vegetable – are made up of building blocks called fatty acids which generally fall into three main groups called saturated, monounsaturated and polyunsaturated. There are two classes of polyunsaturated fatty acids – omega 6 and omega 3. The omega 3 in vegetable oils is called α-linolenic acid and the omega 6 is linoleic acid. The concern about omega 6 relates to linoleic acid which is the most common polyunsaturated fatty acid in the diet.
Do omega 6 fats cause cancer?
In the early 1980s it was thought that fat intake may affect the risk for cancer of the breast and bowel. This hypothesis was based on very basic evidence i.e. different cancer incidence in countries with differing fat intakes, but worth investigating nevertheless.
Several prospective cohort studies were commenced around this time. Data from seven of these studies were pooled in the definitive breast cancer study by Hunter and colleagues. Breast cancer risk was not associated with intake of total fat, animal fat, vegetable fat or polyunsaturated fat. Another pooled analysis of cohort studies published five years later confirmed that polyunsaturated fat was not associated with breast cancer. So omega 6 was off the hook.
Addressing the obesity epidemic by taxing sugary soft drinks sounds good in theory but it appears to fall down in practice. How could a taxation strategy be made to work?
Obesity is proving to be an intractable public health problem demanding innovative solutions and one idea that is attracting attention is the taxation of sugar-sweetened beverages. The theory is simple enough. Basic economics tells us that if the price of sugary soft drinks were to rise, their consumption would fall; lower intake should mean lower calorie intake which would lead to lower body weights. But would it work in practice?
The Ohio experience
A recent research study conducted in the United States provided some interesting insights. Taxing soft drinks has a long history in the US and occurs in many states today, though historically the rates have been low and the purpose has been to raise revenue. But there was an interesting exception. In 1992, the state of Ohio introduced high taxation of sugary soft drinks which was then repealed at the end of 1994. This provided an opportunity to test the effect of taxation of soft drinks on body weights over a period of two years. The researchers compared changes in body weights in Ohio over this period to (1) all other states that had no increased taxation and (2) a bundle of states with the same mean BMI as Ohio. The researchers found:
… very little evidence that the large tax imposed in Ohio had any detectable effect on population weight … our results cast serious doubt on the assumptions that proponents of large soda taxes make on its likely impacts on population weight.
How come? Why didn’t quite high taxation of sugary soft drinks affect body weights?