Big fat debate in NZ 2/2 – what does the evidence say?


Part 2 – previous post (part 1) here

Just to sum up where we (and the others) are at, I’ve paraphrased the main arguments with counter points below.

 There is no long-term evidence of low carb high fat (LCHF) not harming people

We would respond that in the short and medium term LCHF is at least equivalent to the best other approaches (non-inferiority) and for some sub groups – like the insulin resistant it is superior.  Long term RCTs are unlikely to ever be done, but anthropology suggests this approach is healthful in the context of whole foods. The epidemiology is limited because the questions around high fat intake in the context of equal (and adequate/moderate) protein and replacement of carbohydrate with extra fat haven’t been asked, but could be answered with more subtle analysis (see below in discussion of meta-analyses).

We also maintain that the burden of proof in a diet that is superior on every metabolic measure to the current best practice, with no evidence of harm is not to have 40 year mortality data. By their own arguments, (Te Morenga last week “RCTs shouldn’t be used in nutrition research because long term adherence is low”). We don’t agree that RCTs are suddenly out (just because they keep looking good for LCHF?) but do agree that the 40 year LCHF RCT will never get done. If risk factors mean as much as the experts say they do, then the experts need to explain how the improvements in risk factors seen on various LCHF diets are predicting future harm.

The “totality of evidence” and everyone agrees

We respond – since when is science a democracy? Plausible hypotheses are fair game for public discussion, especially in the face of good evidence and substantial and unresolved public health issues. This is just old school ivory tower stuff. They’ll also argue that others aren’t qualified to talk about food.

Mann has also argued that this science was settled in the 1970-80s and he himself has studied low carb diets and shown them to be inferior. His definition of low carb back then was appalling – a 40% carb diet of mainly refined and processed high GI foods pitted against a low GI 60% carb diet.  The diabetics in this study showed small differences in glycemic control and none in insulin load – both groups were still hyperglycaemic and hyperinsulinemic the whole day (unlike diabetics on properly defined low carb diets). Mann pegs these very studies at Oxford as convincing, which we don’t agree with

Reference: Simpson Hcr, Simpson Rw, Lousley S., Carter Rd, Geekie M., Hockaday Tdr, Mann Ji. A high carbohydrate leguminous fibre diet improves all aspects of diabetic control. Lancet 1981; i: 1-5

The meta-analyses are very clear that SFA is dangerous and causes CVD.  

These are studies that combine all of the available high quality evidence. In support of the saturated fat hypothesis, they will quote the Hooper et al Cochrane review of 48 randomized controlled trials, and usually another of a pooled analysis of 11 cohort studies by Jakobsen et al. Both show effects of substituting polyunsaturated fats for SFA on CVD mortality.

That sounds like good evidence, but in context they also show no evidence of any effect of the same thing on overall mortality (usually claiming the studies are underpowered to detect this – although if somehow this were true, and we are missing an effect it must be very small because the risks are close to 1.0 and the CIs up to +/-0.1. In other words, people still die on the same day but from something else presumably.

Second, the Hooper et al analyses showed no benefit for substituting carbs for SFA. The Jakobsen et al analysis showed a small harm. So I assume you can use the reverse logic and say there is no harm or possibly a small benefit in adding extra SFA to replace carbs?

No study showed any effect of total fat. Interesting as the nutrition guidelines for almost every developed country emphasis lean and low fat products.

Most important, they also never asked the most important question which is “what happens if you hold SFA constant and replace carbs with other (mono or poly) fats?”. The logic of this question in context is crucial. I say this because the analyses are biased towards finding an effect of reducing SFA when in fact any effect could be extra fat from polyunsaturated fatty acids (many of which are essential). There could be deficiencies in these fats or other mechanisms we do not yet know about. There is no way of having a totality of evidence without answering this question.

This question was asked in the Kuopio Ischaemic Heart Disease Risk Factor Study (KIHD). (Virtanen et al. 2014) where 1981 men (21.4 year follow-up from median age 52) suffered 183 fatal and 382 non-fatal CHD events. They stated Our results suggest that SFA intake is not an independent risk factor for CHD, even in a population with higher ranges of SFA intake. Consumption of polyunsaturated fatty acids was linked to reduced risk of dying of heart disease, no matter whether they replaced saturated fats, trans fats, or carbohydrates in the diet. However, replacing saturated fats with carbohydrates did not affect the risk of heart disease. Furthermore, the quality of carbohydrates, measured by GI, was irrelevant in these replacement models.”

They also showed that the protective effect of the polyunsaturates did not significantly increase above 5% of energy (meta-analysis shows this effect is stronger for n-3 plus n-6 than for a preponderance of n-6m – Skeaff and Miller, 2009).

This is important and it is supportive of a more parsimonious hypothesis – that the small increases in polyunsaturated fats are the protective mechanism not the displacement of the saturated fats. It’s a small cohort study, but they at least asked the obvious question.

BTW, there are numerous other meta-analyses showing no effects whatsoever in the saturated fats. But there are arguments about funding, conflicts, analysis techniques and much more. I have just pulled out the two quoted in support of reducing saturated fat.

 LCHF – you might get away with if you are lean and very fit

Professor Mann also asserts (at least he has twice in the media) that low carb high fat diets might be alright if you are highly active and burn lots of energy and you might get away with it (“Anyone trying these diets may well lose weight. Some might exercise like mad, get very lean and fit”).

This of course, is ridiculous and I assume, this “fit and athlete” thing is a reaction against my and Tim Noakes’ backgrounds in the field of exercise science and human performance. It shows no understanding of the differential outcomes in LCHF diet studies for the high risk people who benefit – and do not in low fat diets.

The people who stand to benefit the most health wise from a diet restricting carbs are the people who have least tolerance to processing and moving those carbs out of the blood stream – the insulin resistant population which is the bulk of the high risk groups.  It includes everyone who has elevated blood sugars. I’d also include in this group those who have impaired insulin homeostasis but normal glucose response to carbs.

The LDL cholesterol argument – that saturated fat raises LDL cholesterol and that is associated with higher CVD. A then B, B then C, therefore A causes C.

The data from the LCHF research doesn’t support this view.  Feeding studies, RCTs and the mechanisms all support the idea that there are more nuanced explanations to understanding lipids and arteriosclerosis. Particle size, HDL and triglycerides are all part of this. Dietary carbs drive at least part of this process.

Carbohydrate quality

The idea that most apparently healthy “wholegrain carbs” are nothing more than a bag of glucose, especially if you are insulin resistant seems to be an area of some common ground.

Professor Mann’s assertion is that “most dietitians are telling people to eat whole grains, and most wholegrain breads are no better than a bag of glucoseEASD conference Europe last year, and that “Vogel’s bread doesn’t cut it as a whole grain” Listener this year are interesting – we agree of course, but then what is left in the supermarket –only All Bran cereal and that’s about it?

“Vogel bread is a higher fibre bread in NZ and Aussie supermarkets.”

Summing up

In the end, what matters above all, is that the people who most need low carbohydrate, high fat diets have access to them. If this means using olive oil rather than coconut oil, we have no problems with this. The question about the health effects of saturated fat, although an important scientific question and undoubtedly a health and performance question in individual cases, is not as important in the public health context as the freedom to replace carbohydrates with good-quality fats when necessary.

However we feel that giving people %E targets for saturated fat in a low-carbohydrate context is counterproductive. Advice to eat a variety of fatty foods including those low in saturated fat and high in MUFA and PUFA (chicken, fish, nuts, olive oil and so on) as well as some meat and dairy is effective in randomized controlled trials. Advice which revives fears about the macronutrient switch which is the whole point of the intervention – fats for carbs – is unlikely to improve results, whereas encouraging a healthy variety of foods will improve both compliance and overall nutrition.

7 Comments on “Big fat debate in NZ 2/2 – what does the evidence say?

  1. I think the biggest ‘trip-over’ is not having evidence of the effects of LCHF in the years to come. But lets see it this way – ever since we’ve had an increase carb intake thanks to Ancel Keys claiming that saturated fat was the problem, our obesity rates had gone off the roof. So, what else have we got to lose? If there’s current evidence out there that shows positive changes in people’s health and lifestyle, I think it only makes sense to try LCHF and try it out on yourself. I’m glad I did, and I don’t regret it one bit. If in 40 years time if I still manage to develop some kind of chronic disease or have any metabolic conditions due to LCHF, then so be it. With the current scientific evidence though, I really doubt it and I fully agree to the new research. Perhaps it might be some other disease emerging instead! I’m sure as hell not going back to high carb, low fat. I hate being sleepy and hungry the entire day and be a slave of food!

  2. The comment in the summing up “If this means using olive oil rather than coconut oil, we have no problems with this.” is that a cost consideration or do you think olive oil is preferable to coconut oil?

  3. I am a medical specialist (ICU and Anaesthesia) and have worked in cardiac anaesthesia since 1984. The cardiologists/nutritionists are claiming a lower incidence of Ischaemic Heart Disease (IHD)since the 1970s’ from low fat diets, when in fact they are using mortality data. This is blatantly incorrect and scientifically dishonest. If anything the incidence of IHD is rising but treatment with stents, anticoag drugs and other pharmaceuticals are responsible for the longer lifespans (or as others have said the decades of dying slowly that people now experience) The change in smoking habits during that period is probably the other key factor in survival both from cardiovascular disease and cancer.

    In addition there is a very significant population of obese insulin resistant patients who have never been investigated for IHD or other vascular disease. Their high sugar/carb/transfat diets are certainly not going to offer any protection against these diseases. Caloric restriction and a ‘normal’ diet with increased physical activity have also repeatedly been shown to have minimal effect in this group of patients. Only bariatric surgery produces significant improvement. However as a public health measure it is enormously expensive. The benefits and cost of a low carb, moderate to high fat diet for this population seem obvious to all but our ‘experts’!

  4. Just to add to that the Heart Foundation lists the incidence of IHD as rising and this paper from Auckland estimates 1 in 5 NZ (and they excluded higher risk Pacific Island and Maori subjects in their study) will need pharmacological intervention for IHD–so much for our declining prevalence of IHD!!

    Vol 119 No 1232 ISSN 1175 8716
    NZMJ 21 April 2006, Vol 119 No 1232 Page 1 of 8
    URL: © NZMA
    Estimated prevalence of cardiovascular disease and
    distribution of cardiovascular risk in New Zealanders: data
    for healthcare planners, funders, and providers
    Susan Wells, Joanna Broad, Rod Jackson
    Aims New Zealand cardiovascular risk management guidelines advocate targeted risk
    assessment based primarily on age, gender, and ethnicity—and recommend drug
    management for people with a 5-year absolute cardiovascular disease (CVD) risk
    greater than 15%. To inform service planning and healthcare delivery for district
    health boards and primary healthcare organisations in New Zealand, we have
    produced population estimates of CVD prevalence and 5-year absolute CVD risk.
    Methods The 1993 Auckland Heart and Health Study provided the data for estimating
    CVD prevalence and absolute CVD risk distributions using the Framingham CVD
    risk prediction equation. These estimates were applied to population projections for
    2005 based on 2001 New Zealand Census data.
    Results Of the projected 2.09 million people aged over 35 years in New Zealand in
    2005, approximately 1.5 million (72%) meet national criteria for formal CVD risk
    assessment. About 151,000 (7%) are estimated to have suffered a non-fatal heart
    attack or stroke or have angina. A further 262,000 (13%) are estimated to have a 5-
    year CVD risk greater than 15% based on New Zealand CVD risk charts. This
    represents around 1 in 5 adults over the age of 35 years in New Zealand for whom
    pharmacological interventions are recommended according to the New Zealand CVD
    risk guidelines for the prevention of new or further CVD events.
    Conclusions The latest published data available on the burden of CVD risk in New
    Zealand is now over 10 years old and does not include Maori, Pacific, and other non-
    European ethnic groups. Current data on the risk profile of adult New Zealanders is
    required for more accurate service planning. However the information reported here
    provides a reasonable estimate of the magnitude of the task. Although systematic
    identification and management of CVD risk in New Zealanders with raised CVD risk
    will be a major undertaking for healthcare services, it has the potential to produce
    significant health-gains while reducing health disparities.
    Cardiovascular disease (CVD) is the leading cause of death and hospitalisation in
    New Zealand.1 There are major disparities in CVD between ethnic groups and
    significant under-treatment of high-risk patients. Age-specific death rates are two to
    three times higher for Maori compared with non-Maori in those aged less than 75
    years.2 CVD prevention and management and the reduction of health inequalities have
    been targeted as priorities in the New Zealand Health Strategy,

  5. Heart Foundation stats off their website today:


    General heart statistics for New Zealand

    Cardiovascular disease (heart, stroke and blood vessel disease) is still the leading cause of death in New Zealand, accounting for 30% of deaths annually [1]
    Every 90 minutes a New Zealander dies from coronary heart disease [1]
    Many of these deaths are premature and preventable
    One in twenty adults have been diagnosed with coronary heart disease. That’s 176,000 New Zealand adults [2]
    It is estimated that 5,000 people die prematurely from smoking each year – this equates to around 12 people a day dying from smoking. [3]

    How much you move, what you eat and whether you smoke are important factors that influence your risk of heart disease. Current figures show that [2]:

    One in six New Zealanders older than 15 smoke
    Almost half of adults are not physically active for more than 30 minutes per day
    One in three adults do not eat three or more servings of vegetables per day
    Two in five adults do not eat two or more servings of fruit per day
    About one million adults are now obese in New Zealand.

    Women’s Heart Disease

    Globally, cardiovascular disease, often thought to be a ‘male’ problem, is the number one killer of women. [4]

    Nearly two-thirds of the deaths from heart attacks in women occur among those who have no history of chest pain [5]
    Women who smoke cigarettes are three times as likely to have a heart attack as women who don’t smoke. [5]

    In 2011, 2600 women died of heart disease in New Zealand. That’s more than 7 women a day – or about 50 each week. [1]


    [1] Ministry of Health (2014) Mortality and Demographic data 2011. Wellington: Ministry of Health
    [2] Ministry of Health (2013) NZ Health Survey: Annual update 2012-2013. Wellington: Ministry of Health.
    [3] Ministry of Health (2009) Implementing the ABC approch for Smoking Cessation. Framework and Work Programme. Wellington: Ministry of Health.
    [4] World Health Organisation (2013) Women’s health fact sheet N334: World Health Organisation.

    [5] Oestreicher Stock, E., Redberg, R. (2012) Cardiovascular disease in Women. Curr Probl Cardiol,37(11), 45-526.

  6. Just in case you missed it that is the same Prof Rod Jackson who in the above 2006 NZMJ paper highlights the very high prevalence of IHD–so what has the ‘healthy’ diet they support done for us over the last 3.5 decades?

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