Eating more saturated fats raises risk of early death; yeah, right.


Behold, a new diet-health observational paper appears! (What, this one, again?)

There are two long term observational studies of diet and health that get more press coverage than all the others combined. New papers on these studies, which say the same things with minor variations, are published every few months in high-impact journals. The editors of these journals don’t seem to mind that the papers they get are unoriginal and the repetitive choice of the same studies amounts to cherry picking, because the authors are the rock stars of the nutritional establishment, and their university, Harvard, has a cachet that guarantees publication, just as an education at Eton guarantees influence in the British political establishment no matter how much of an idiot one happens to be.

Was that too critcal? You be the judge.

The studies are the Nurses Health Study (NHS), which had run for 30 years and is all-women (being a male nurse must have been an exclusion criteria for this study) and the Health Professionals Follow-up Study (HPFS) which had run for 26 years (and, you guessed it, included no female health professionals) when the results were analysed yet again to create this new paper.

Association of Specific Dietary Fats With Total and Cause-Specific Mortality
Dong D.Wang, MD, MSc; Yanping Li, PhD; Stephanie E. Chiuve, ScD; Meir J. Stampfer, MD, DrPH; JoAnn E. Manson, MD, DrPH; Eric B. Rimm, ScD; Walter C. Willett, MD, DrPH; Frank B. Hu, MD, PhD.
JAMA Intern Med. Published online July 05, 2016. doi:10.1001/jamainternmed.2016.2417

The mortality rate in these two studies, given their long duration, was quite high – 33 304 deaths among 126233 people. After adjustment for known and suspected risk factors, dietary total fat compared with total carbohydrates was inversely associated with total mortality (hazard ratio [HR] comparing extreme quintiles, 0.84; 95% CI, 0.81-0.88; P < .001 for trend). The HRs of total mortality comparing extreme quintiles of specific dietary fats were 1.08 (95% CI, 1.03-1.14) for saturated fat, 0.81 (95% CI, 0.78-0.84) for polyunsaturated fatty acid (PUFA), 0.89 (95% CI, 0.84-0.94) for monounsaturated fatty acid (MUFA), and 1.13 (95% CI, 1.07-1.18) for trans-fat (P < .001 for trend for all).

Taken at face value, this tells us that people who ate a higher-fat, lower-carb diet overall were less likely to die, over three decades, than people who didn’t. The amount of saturated fat people ate didn’t have much, if anything, to do with this.

So how was this reported in the media?

People who eat more saturated fat have a higher risk of an early death, according to a large study that contradicts recent claims that “butter is back”.

The study from the Harvard TH Chan School of Public Health in the United States has been following 126,000 people for three decades to assess the impact of their diet on their health and lifespan. The researchers claim it is the most detailed and powerful examination to date of the effects of eating different types of fats.

Its findings run counter to those of a study published by the National Obesity Forum in May, which said people should eat more fat and fewer carbohydrates and rubbished the nutritional guidelines from Public Health England, which recommend that people should eat less butter and red meat.

According, that is, to The Guardian. Last time we read the National Obesity Forum document, it was recommending that people at risk of diabetes and obesity eat more fat, mainly from wholefoods, while using olive oil and butter for cooking, and restrict carbohydrates, especially refined carbohydrates.

This is a dietary pattern that, if eaten by the people in the NHS and HPFS, would have increased fat in place of carbs (HR 0.84), increased MUFA (HR 0.89), increased PUFA (0.81), and decreased trans fats (HR 1.13). In other words, following the National Obesity Forum recommendations should have significantly decreased mortality. In this context, the HR 1.08 for SFA (a tiny 8% increased risk) is relatively meaningless. We’ll have a look at how it was arrived at next (spoiler, it was arrived at poorly).
But first it’s worth talking about trans fats. Trans fats are formed when unsaturated vegetable oils are partially hardened by hydrogenation to create spreads and shortenings that can be used in place of animal fats like butter, lard, and tallow. These industrial trans fats (mainly elaidic acid, the trans isomer of oleic acid) are associated with an increased risk of CVD mortality at relatively small intakes and are probably best considered toxic in all but naturally occurring trace amounts.
Industrial trans fats only exist in the food supply because of the widespread fear of natural saturated fat and animal fats. The people who warn us against trans fats today include some of the same people who made us eat them in the first place.

How does the Guardian article get around this inconvenient truth? By treating trans fats and saturated fats as if they are part of the same problem.

The new paper, published in the prestigious US journal Jama Internal Medicine, says eating trans-fats and saturated fats, including those from red meat and butter, is linked to higher mortality rates compared with the same number of calories from carbohydrates.

More importantly, they say, they found that death rates dropped by between 11% and 19% among people who substituted saturated fats such as butter, lard and red meat for unsaturated fats such as olive oil, canola oil and soybean oil.

The first claim is false; the trans fats in red meat and dairy are widely believed to be beneficial and weren’t the trans fats measured in the studies. Let’s look at that latter claim – it might surprise you to know that no-one in this study substituted any food for any other food (or rather, if they did, this wasn’t looked at). This is all imagination; and when these substitutions were tested for real, they didn’t result in lower mortality. Also, there’s a lot of unsaturated fat in butter, meat and lard. The unsaturated fat that’s supposed to be good for people in this study. It’s also important to note that Americans eat very little butter (it was 4.8% of total fat in 1955, before the scare started); the contribution of butter and lard to saturated fat intake in these studies would have been small, and in a recent meta-analysis of butter alone, the first ever done, it has zero correlation with cardiovascular disease.

How were the data analysed?

But how were the results obtained? (If interested, you can find detailed, and somewhat scathing, critiques, by other experts, of the methods used here on the PubPeer website, which go into much more depth). Participants in the study were asked, every few years, to remember what food items they had eaten in the previous year. Really. “In each SFFQ, we asked how often, on average, the participant had consumed a specified portion size of each food during the preceding year.” Oh dear. The NHS participants have reported, by this method, eating only an average ~1,500 kcal a day for 32 years. For the purposes of our analysis, we’ll have to reluctantly take these data at face value, but seriously? (an ongoing problem in nutrition research really, especially these types of cohort studies)

In the raw NHS data, women in the lowest quintile for saturated fat intake (average age 48.2 years) had more than double the death rate of women in the highest quintile (average age 45.9 years) (5852 vs 2332). So saturated fat intake was spread unevenly by age; younger women ate more of it (and people with low cholesterol ate more); or so it seems from the raw data (though the paper says otherwise); but would an extra 2.3 years really make such a huge difference? When both studies were combined, and the deaths were adjusted for age, the HR for saturated fat was 1.71 (1.65-1.78). This is quite a correlation – but there were a lot of differences, besides age, between the upper and lower quintiles for saturated fat intake. More smokers and less exercise in the upper quintile for saturated fat, for instance. When the data were adjusted for “known and suspected risk factors” the correlation was bumped down to the minimal HR of 1.08. The difference between 1.08 and 1.71 is +0.63. That is, there are things here that are associated with a 63% increase in mortality, and the authors had to pare those away to arrive at something associated with an 8% increase, which is what they decided to warn us about.
I don’t know about you, but I’m more interested in this 63% risk, which dwarfs anything any of these fats might be doing to us.

After age, these adjustments were made; this was the 63%.

Adjusted for white race, marital status, body mass index, physical activity, smoking status, alcohol consumption, multivitamin use, vitamin E supplement use, current aspirin use, family history of myocardial infarction, family history of diabetes, family history of cancer, history of hypertension, history of hypercholesterolemia, intakes of total energy and dietary cholesterol, percentage of energy intake from dietary protein, and menopausal status and hormone use in women.


Smoking  (for example) wasn’t evenly distributed among quintiles, and passive smoking, which was among the many possible “known and suspected” risk factors not measured, probably has a similar distribution to smoking. So does sugar consumption; though measured in these studies and previously associated with both saturated fat consumption and CVD mortality, this also wasn’t adjusted for. What’s interesting here is that these authors think that vitamin E supplement use is worth adjusting for. Polyunsaturated vegetable oils are the main source of vitamin E in modern SAD-type diets.

Why do smoking, inactivity, and no doubt sugar consumption and other unhealthy behaviours associate with saturated fat intake? After all, there’s no natural explanation for this. Steak doesn’t make you crave cigarettes, coconut oil doesn’t make people stop exercising. But this is a study involving two groups of health professionals, followed during the years 1980-2012. These people were TOLD, over and over again, that foods that were sources of saturated fat were unhealthy and foods that were sources of polyunsaturated fat were healthy.  We ask whether it’s ever possible to do statistical adjustments to model the independent associations of single variables (e.g., saturated fat) by various statistical techniques, given the public health messaging over the decades which inextricably confounds these results?
The people who cared about being healthy ate less butter and red meat, and used polyunsaturated oils and spreads. They exercised more and probably did many other things we don’t measure well or even at all. The people who couldn’t be bothered made less of these changes, were more likely to keep smoking and care less about second-hand smoke, probably drank too much and for all we know were more likely to have unprotected sex and use drugs – and on the list can go. They included the risk-takers, the contrarian ignorers of advice, the fun-lovers, and the pessimists and fatalists. This is called “healthy user bias”, and it’s always a problem when analysing observational studies of behaviours that society has strong opinions about.

Can we show that healthy user bias or residual confounding or the considerable potential for error built into the SFFQ system accounts for the 1.08, the remaining 8% of risk not seen in better quality studies of less easily biased populations? Saturated fat is believed to increase heart disease risk (the largest part of CVD mortality) by raising LDL cholesterol, you know the story. This is not a mechanism that anyone thinks plays a role in other causes of death; yet the Harvard study also found a positive correlation between respiratory disease mortality and saturated fat (HR 1.56; 95% CI, 1.30-1.87) and an inverse correlation with PUFA. This is a condition we’d expect to relate directly to smoking and air quality, even more so than CVD. It is likely to be an indicator of residual confounding (the authors describe this association as “novel”, so there’s no support for it in any other studies). The study also found this same pattern of associations (SFA mildly bad, MUFA and PUFA good) with all of the diverse causes of death studied, including cancer and neurodegenerative diseases; this is impossible to explain in terms of the lipid hypothesis, but easy to explain if high saturated fat consumption in this Standard American Diet population was associated with lower micronutrient and antioxidant intake, greater risk taking (including exposure to infections), higher sugar and refined grain intake, and greater exposure to smoking and environmental pollutants.

This reminds us of the study that found red meat consumption was significantly associated with accidental death in men. So beef makes you clumsy, or drive too fast, or not wear a seatbelt. D’you think? It’s much more likely that this indicates some residual confounding around risk-taking behaviours that weren’t properly measured and accounted for, men being overall bigger risk-takers than women. Unfortunately, there’s no accidental death data in the Harvard paper to compare.

We also found an earlier 20-year follow up study from the NHS alone which found no correlation between saturated fat and heart disease incidence in this group – HR 0.97 (95% CI 0.73, 1.27).

Is canola oil consumption associated with cancer mortality?

If you look at supplement 1 for this new Harvard study, which gives the results for men (HPFS) and women (NHS) separately, they are sometimes quite different, and are less significant, than the correlations in the main paper. A really interesting result that’s in the supplementary data is that omega-3 alpha linolenic acid (ALA) consumption is significantly associated with cancer mortality.
The HR for cancer mortality between low and high quintiles of ALA intake (table 14, p62) is 1.12 (1.04, 1.20), which is greater than the HR between saturated fat and all-cause mortality. ALA is in healthy foods like leafy green veges, pulses, some nuts and seeds, and whole grains, in small amounts. It’s not likely that eating these increases the risk of cancer. But ALA is present in larger amounts in canola oil and soybean oil, and these are the main sources of ALA in the US diet.
Go figure, there could be many reasons for this, but it’s odd that this correlation, which runs against the grain of any likely healthy user bias or residual confounding, appears tucked away in the supplement to a paper which is being used to support the idea that we should replace butter and lard with canola spread and soybean oil.
The correlation is mentioned briefly (without figures) in the main paper, which tries to minimise it by saying that the correlation in the “most recent” fat consumption table (table 7) is non-significant. But surely the whole point of a 32-year study like this is to try to capture the effect of dietary factors over a significant part of the lifespan.

It’s predictable that Harvard are beginning to confirm the benefits of a high-fat diet (yes, even in the context of the confounders of this study), but annoying that they harp on the evils of the saturated fat found in naturally occurring and nutritious foods, and continue to promote industrially refined vegetable oils and spreads (which is how trans fats got in our diet in the first place), based on evidence collected by methods which don’t seem that reliable to begin with. In the USA they don’t require labelling of trans fats in oils and spreads and even in NZ this is still voluntary. Even going by Harvard’s own research into the NHS and HPFS cohorts, there’s a better way to get any health benefits of PUFA and vitamin E.

Overall ? Just eat real food with a mixture of fatty acids. Avoid trans-fats and advocate for more funding for intervention research, where cause and effect is more easily determined and confounding exists less because of randomisation.


All That Fat – A Guide for the Perplexed


By George Henderson, a member of the Human Potential Centre Research team at AUT University 

An updated version of this post is available in PDF “All That Fat” – Factors influencing the choice of fats in a high fat diet; A Guide for the Perplexed for your use as you see fit

This blog is a bit longer than usual, and a little more science focused than usual. Its aimed to help you understand where the talk about fat and health comes from, and where the field is moving.

The question I hear most often when introducing audiences to low carb high fat (LCHF) or Paleo concepts is some variant of “aren’t you worried about all that fat?” The idea that fat is fattening is the easy one to address, plenty of people have lost weight publically on high-fat diets, the fattening carbohydrate was never really forgotten, and contrary ideas have a degree of attractiveness.

The question of cholesterol and heart disease, or other diseases presumably involving lifelong processes that are mysterious to the average person  and far from clear to scientists), is a harder one to answer. My purpose here is not to answer it conclusively, but to place it in context. There are four basic positions when it comes to dietary saturated fat, cholesterol, and animal fat as dietary risk factors (note that I include dietary cholesterol).

The classic view, developed by Ancel Keys and promoted widely, is that these dietary risk factors (DRF) promote the development of coronary heart disease, and that replacing them with other foods – mainly carbohydrate and polyunsaturated vegetable fat, but also some additional fibre and long-chain omega 3s (it is arguable that neither of these latter two actually supplies enough energy to be taken seriously as a “substitution”, being rather in the nature of “supplements”) – reduces this risk. A secondary assumption often tacked onto the classic view in popular science writing, and which had some official backing until recently, is that the DRFs play a role in other diseases, such as cancers. The first claim is supported by extreme epidemiological studies involving populations such as vegetarians who sedulously avoid the DRF, and have lower incidence of CHD. However these same populations have higher rates of non-CHD mortality, contradicting the secondary assumption. Avoiding the DRF is not “good for you” but seems to trade one type of disease risk for a raft of others.[1]

The contrary view, held by the cholesterol skeptics, is that there is no causal link between the DRF and CHD. This is supported by a wide range of evidence that contains findings contradictory to the classic view. Meta-analyses of saturated and polyunsaturated fat consumption within standard dietary patterns (as opposed to the extreme DRF avoidance patterns supportive of the classic theory) do not support the link. Controlled trials (RCTs) in which polyunsaturated fats or carbohydrate replace saturated fats do not produce strong or consistent benefits and sometimes produce increased harms in terms of both CHD and other causes of mortality.[2]

The Paleo view is that the DRF are not risk factors in the context of an evolutionarily appropriate diet and lifestyle (lifestyle aspects include sleep and other aspects of circadian rhythm, exercise, avoidance of environmental risk factors, healthy gut bacteria, and intermittent fasting); that the studies supporting the classic view are confounded by inclusion of trans fats, processed meats, and refined carbohydrates. This is supported by the logic of evolutionary theory and a wide range of circumstantial evidence; for example that traditional cultures do not experience the DRF as risk factors for any disease, but do so experience modern foods – sugars, refined starches, and vegetable oils.[3]

The LCHF or low-carb view is that DRF are not risk factors in a carbohydrate restricted diet, which creates a unique metabolic state in which biomarkers shift towards those associated with protection against CHD. This is supported by clinical trials and by the logic of the biochemistry of metabolism and human physiology, as well as by epidemiological and experimental evidence that sugars and high-GI carbohydrates are also DRF, without the protective associations against non-CHD mortality seen with the classic DRF. [4]

Is there common ground between the opposing views?
All these views have some supportive evidence, and when this evidence is viewed in detail they are not completely incompatible. At a time when the classic view is, generally with good reason, coming under sustained attack among the scientific community, and is rapidly losing support among the public, it is prudent to remember that there are likely to be babies floating in its dirty bathwater – observations that will remain true under any paradigm, which still beg for explanations, and which may point the way to new truths.
For example, in epidemiology correlating DRF with CHD there is an exception in that dairy fat, which is rich in the DRF, has protective associations with CHD.[5] This is consistent with the so-called French Paradox, wherein France has relatively low rates of CHD yet the world’s highest butter consumption per capita, as well as an appetite for other fatty dairy foods; when Ancel Keys collected evidence to support his hypothesis, that saturated fat consumption was linked to heart disease, American butter consumption only contributed 4.8% of that nation’s total fat intake.[6] At the other extreme, processed meat products are the high-DRF foods with the strongest correlations with disease.[7] Similarly, nuts are rich in polyunsaturated fats, and nut consumption is associated with health benefits (reductions in both CHD and non-CHD mortality) not seen with polyunsaturated oils.[8] This difference between nuts and polyunsaturated vegetable oils is particularly striking in the epidemiology of the eye disease age-related macular degeneration (AMD).[9] These examples illustrate why attempts to influence disease risk by replacing animal fat with vegetable fat (for example, in commercial deep fryers, in shortenings, and in the spreads used on breads) have not produced the benefits Ancel Keys predicted (to put it mildly). The DRF – dietary cholesterol, saturated fat, and animal fat – are also protective factors, especially when associated with nutrient-dense unprocessed foods; and the polyunsaturated oils, which look like protective factors in the context of evolutionarily appropriate foods such as nuts, become DRF when isolated; in much the same way as high intakes of some vitamins, once removed from the foods that supply them, do not produce benefits and begin to be associated with harm.

Risk of disease, both CHD and non-CHD, can be also predicted by metabolic risk factors not directly influenced by the classic DRF in the way that serum cholesterol is said to be – blood pressure, blood glucose, fasting triglyceride, CRP, body fat %, and so on. These are the markers that improve when carbohydrate is restricted (and when fatty fish is consumed) but that tend to worsen or stay the same when animal fat is replaced with carbohydrate or vegetable oil. They are also improved by exercise and the other lifestyle adjustments of the Paleo approach. The impact of even moderate exercise on heart attack risk dwarfs the benefits claimed for replacing saturated fat with polyunsaturated fat by those basing their predictions on the lipid hypothesis.[10] In which case, it is worth asking, what stops people at risk from exercising? This will often turn out to be factors such as pain and fatigue – inflammatory and metabolic symptoms which are reliably reduced by carbohydrate restriction, and which may be exacerbated by high intakes of omega 6 PUFA.

The rationale behind the low-carbohydrate Mediterranean diet.

It sometimes happens – reportedly in about 20% of cases – that LDL cholesterol rises significantly on a low-carb paleo diet rich in DRF, even as all the other risk markers improve. Whether or not this is significant in terms of long term risk of CHD (primary prevention), which is debatable, it is not seen as desirable in the management of pre-existing CHD (secondary prevention) or in high-risk patients (those with family history of CHD or with established medical conditions that increase risk). Best practice in these cases currently seems to be a carbohydrate-restricted version of the dietary pattern invented by Ancel Keys, liberalised to contain sufficient of the DRF to maintain health.[11] For example, cardiologist Aseem Malhotra, who famously wrote that “saturated fat is not the major issue” in the British Medical Journal, and who is skeptical about the benefits of cholesterol-lowering statins for primary prevention of CHD, recommends a low-carbohydrate Mediterranean diet that includes full-fat dairy, and excludes oils other than olive oil.[12] (The various Mediterranean Diets seem to resemble what Mediterranean peoples actually ate in much the same way as the various Paleolithic Diets resemble what Paleolithic peoples actually ate). Whether this partial restriction of red meat and higher wholefood PUFA intake is necessary for secondary prevention in the context of a low-carb diet, it seems to be the “best guess” available from reading the epidemiology available around non-carbohydrate restricted diets. It involves a “hedging of bets” that balances the relative risks of CHD and non-CHD deaths in secondary prevention cases.[13]

Why are DRF both risk factors and protective factors?
Animal fat, dietary cholesterol and saturated fat, as well as red meat, tend to be associated together (vegetable fats can be highly saturated, but never contain cholesterol). Animal fats can also contain large amounts of PUFA, which, like cholesterol, can be oxidised or otherwise adversely affected by heat. Red meat also forms carcinogenic heterocyclic amines (HCA) when scorched. Meat, especially cheaper meats like pork, is subject to processing in various ways that deplete its nutritional value, denature its lipids and proteins, and add unwanted non-food chemicals of unknown safety. The ways in which livestock is fed and medicated can also affect the health of consumers, and animals (especially pork) can carry parasites able to infect humans. For this reason many meat products (unlike dairy products) need to be well-cooked before consumption. The high heme iron content of red meat is another possible risk factor, but is also a protective factor, depending on one’s iron status.
If these considerations are valid, then clearly the best way to include meat in the diet is to source high quality unprocessed meats from pasture-fed animals, mainly ruminants, and as much as possible cook it at lower temperatures (for example, in soups and stews) or for shorter times (as with steak).

Fatty animal foods are the only source of retinol and vitamin D3, and the main source of vitamin K2 in the diet. These are vitamins that play important roles in maintaining healthy blood vessels.[14] They are also (ruminant fats including dairy) sources of rumenic acid, the main isomer of conjugated linoleic acid (CLA), a naturally-occurring trans fatty acid which can perhaps best be characterised as analogous in its anti-inflammatory, anti-atherogenic and fat-burning effects to omega-3 fats.[15] The anti-diabetic effect of CLA in clarified butter (ghee) in the Indian diet may be responsible for health benefits which have been lost with that subcontinent’s modern switch to low-fat, high-PUFA diets.[16] Ruminant meat fat from pasture-fed animals is also a source of DHA. Fatty animal foods, especially those richest in cholesterol, are also the main dietary source of choline, which is removed from vegetable oils, and which is essential for the prevention of fatty liver disease, a precursor of both cirrhosis and diabetes.[17] Dietary cholesterol and individual saturated fatty acids may by themselves have protective effects in specific cases, for example this is well-documented in alcoholic liver disease.[18] Red meat is also an important source of zinc and iron.
The argument is that saturated fats are thus a relatively neutral source of energy in health terms, as meta-analysis suggests, but may in individual studies have been sometimes damned, sometimes blessed, by the company they keep – that is, by their association with many other factors that are not usually taken into account by epidemiologists, such as cooking and food processing methods, additive or micronutrient content, lifestyle choices, and so on.

Intrinsic fats vs added fats
While some perceptions of the LCHF diet include large amounts of added cream, butter, extra virgin olive oil and coconut oil, this is not always the case, because many wholefoods that are suitable for LCHF diets are intrinsically high in fat, e.g. nuts, salmon, avocado, coconut, lamb and other meats, eggs, cheeses, olives. These foods are rich sources of protein, vitamins, and minerals and it is possible for many people – those with low bodyweight or low energy requirements – to be well nourished without ever eating added fats in amounts greater than the relatively small amounts needed in cooking, or to dress vegetables. Added fats provide what are called discretionary calories – the extra energy that someone needs after the core nutritional requirements of the body have been realised. This can be a relatively small amount of energy, even if one is trying to maintain a high fat-to-carbohydrate ratio, and in many cases is easily supplied by wholefoods, while those with larger frames or greater energy outputs can benefit from the energy density and high digestibility of added fats. This often appears as a gender difference, with women having less need for added fats to maintain a LCHF or even a ketogenic diet.[19] Sometimes added fats are consumed for medicinal as well as nutritional reasons; the neuroprotective effects of coconut oil, the gut-healing effects of coconut, butter or ruminant fats, or the cardioprotective effects of olive oil polyphenols may be given as reasons for preferring specific fats.

The vitamin E content of wholefood vegetable fats, e.g. nuts, seeds, avocadoes and olives, supplements the low vitamin E concentrations in animal fats, which by themselves are unlikely to supply optimal levels of this vitamin for everyone.

How much fat do you need to eat on a LCHF diet?
Persons eating a modern diet of processed and takeaway food, high in refined carbohydrates, are often unaware of the high fat content of such a diet, because fat is hidden in foods not usually considered fatty (such as bread) and because polyunsaturated vegetable fats are not perceived as being as greasy, satiating, or nourishing as the more saturated animal fats. Because a primary benefit of LCHF diets is an improvement in appetite control, due to greater satiety from the current meals and easier ability to access the energy already stored in the body from previous meals, any increase in fat intake is often small in terms of real amounts eaten, and can be offset by an improvement in the quality of fat and its nutritional content.[20] An exception is the case of athletes with high energy requirements who trade high carbohydrate intakes for high fat intakes on LCHF diets. Athletes are highly aware of their fitness, and follow LCHF diets either because their fitness and performance improves, or because other aspects of health improve, and fitness and performance do not suffer.

LCHF, and Paleo, are nutritional principles, or templates, that can be used in the design of diets, and are not absolutely rigid prescriptions. The key is adaptability; dietary needs can change over time, and the ability to adjust and vary the amounts and types of foods eaten on a LCHF diet, including the amounts, types, and sources of fat and carbohydrate, provides a form of nutritional insurance, if such is needed.


[1] Dietary determinants of ischaemic heart disease in health conscious individuals, Mann J. et al. Heart 1997

[2] The Questionable Role of Saturated and Polyunsaturated Fatty Acids in Cardiovascular Disease, Ravnskov U. J Clin Epidemiol Vol. 51, No. 6, pp. 443–460, 1998

[3] Cardiovascular Disease Resulting From a Diet and Lifestyle at Odds With Our Paleolithic Genome: How to Become a 21st-Century Hunter-Gatherer. O’Keefe, J.H., Cordain, L. Mayo Clin Proc. 2004;79:101-108

[4] Dietary carbohydrate restriction induces a unique metabolic state positively affecting atherogenic dyslipidemia, fatty acid partitioning, and metabolic syndrome. Volek, J. et al. Prog Lipid Res. 2008 Sep;47(5):307-18. doi: 10.1016/j.plipres.2008.02.003

[5] Dietary intake of saturated fat by food source and incident cardiovascular disease: the Multi-Ethnic Study of Atherosclerosis de Oliveira Otto, M. et al. Am J Clin Nutr. Aug 2012; 96(2): 397–404. doi: 10.3945/ajcn.112.037770

[6] Atherosclerosis and the diet, Keys SAMJ 1955

[7] Red meat and processed meat consumption and all-cause mortality: a meta-analysis. Larsson S.C. Am J Epidemiol. 2014 Feb 1;179(3):282-9. doi: 10.1093/aje/kwt261

[8] Association of Nut Consumption with Total and Cause-Specific Mortality. Bao, Y. et al. N Engl J Med 2013; 369:2001-2011November 21, 2013DOI: 10.1056/NEJMoa1307352

[9] Progression of age-related macular degeneration: association with dietary fat, transunsaturated fat, nuts, and fish intake. Seddon, J.M. et al. Arch Ophthalmol. 2003 Dec;121(12):1728-37.

[10] Leisure-Time Running Reduces All-Cause and Cardiovascular Mortality Risk. Lee, D. et al. J Am Coll Cardiol. 2014;64(5):472-481. doi:10.1016/j.jacc.2014.04.058

[11] See, for example, the Low-Carb Mediterranean Diet designed for diabetics by Dr Steven Parker M.D.

Low-Carb Mediterranean Diet

[12] Saturated fat is not the major issue, Malhotra, A. BMJ 2013;347:f6340

[13] New insights into the health effects of dietary saturated and omega-6 and omega-3 polyunsaturated fatty acids. De Lorgeril, M. and Salen, P. BMC Medicine 2012, 10:50 doi:10.1186/1741-7015-10-50

[14] Vitamins D and K as pleiotropic nutrients: clinical importance to the skeletal and cardiovascular systems and preliminary evidence for synergy. Kidd, P.M. Altern Med Rev. 2010 Sep;15(3):199-222.

[15] Dietary Conjugated Linoleic Acid In Health: Physiological Effects and Mechanisms of Action, Belury, M.A. Annu. Rev. Nutr. 2002. 22:505–31 doi: 10.1146/annurev.nutr.22.021302.121842

[16] Significance of the N-6/N-3 Ratio for Insulin Action in Diabetes. Raheja B.S. Ann N Y Acad Sci. 1993 Jun 14;683:258-71.

[17] Choline Metabolism Provides Novel Insights into Non-alcoholic Fatty Liver Disease and its Progression. Corbin, K.D. and Zeisel, S.H. Curr Opin Gastroenterol. Mar 2012; 28(2): 159–165. doi: 10.1097/MOG.0b013e32834e7b4b

[18] Dietary fat and alcoholic liver disease, Mezey, E. Hepatology Volume 28, Issue 4, pages 901–905, October 1998

[19] See for example this blog post by itsthewooo October 15th 2013

[20] Nutrient Intake of Subjects on Low Carbohydrate Diet Used in Treatment of Obesity. Stock, A.L. and Yudkin, J.

The real food guidelines


It’s a food fight.

The time has finally come where a deep and important line needs to be drawn in the sand.  No more throwing bad science and bad advice around.  Stop!

The “food pyramid” guidelines are still alive (and well?) in New Zealand (see here). They are outdated, old school and quite simply wrong. Recently they were up for review…

Unfortunately, they came back more or less the same – saturated fat and fats in general are bad for us ….blah blah blah.

So our team felt we had to put all the science out there publicly for everyone to have a look at. So here it is for your scrutiny.

MOH dietary guidelines feedback REVISED Appendix 9.5.14


This is our response to the draft nutrition guidelines.

The timing could not be better actually as tonight I go head to head with the very people who advised on these guidelines.  The 3rd Degree piece will be available here (its rightly called “Food fight” after 8.30 tonight NZ time.

Please take the time to read at least the lay summary, and even the full scientific document. I think you will be shocked just how little there is to back up the current and future nutrition guidelines.

It’s time for a full and robust scientific analysis of what we are told to eat to be presented to government health officials (who have it now), and the lay, scientific, and health communities.

We have also proposed a new set of guidelines called the Real food guidelines – real food, for real people, based on real evidence.  It’s time to get real people!  Here they are for the first time :

The real food guidelines
Real food for real people, based on real evidence

  1. Enjoy nutritious foods everyday including plenty of fresh vegetables and fruit.
  2. Buy and prepare food from whole unprocessed sources of dairy, nuts, seeds, eggs, meat, fish and poultry.
  3. Keep sugar, added sugars, and processed foods to a minimum in all foods and drinks.
  4. If you drink alcohol, keep your intake low. Don’t drink if you are pregnant or planning to become pregnant.
  5. Prepare, cook, and eat minimally processed traditional foods with family, friends, and your community.
  6. Discretionary calories (energy foods) should:
    a) Favour minimally refined grains and legumes, properly prepared, over refined or processed versions, and boiled or baked potatoes, kumara or taro over deep fried or processed potato fries and chips.
    b) Favour traditional oils, fats and spreads over refined and processed versions.

We welcome feedback and scrutiny of our scientific analysis. This is open source and for the people. We are constantly trying to improve our understanding of  the science of human nutrition. The evidence changes all the time. Our scientific statement is another iteration in the right direction but should by no means be where we stop.  It’s a start..

Thanks to everyone in our team who contributed (see below).  Also Dee Holdsworth-Parks for tirelessly keeping my life organised and our team working smoothly.

Dr Caryn Zinn PhD
NZ Registered Dietician. Senior lecturer Human Potential Centre, AUT University

Dr Nigel Harris PhD, BRmgmt
Senior lecturer, Human Potential Centre, AUT University

Dr Mikki Williden PhD
Registered Nutritionist, Senior lecturer Human Potential Centre, AUT University

Catherine Crofts MPS M.Phil
Research Assistant, Human Potential Centre, AUT University

Dr Simon Thornley BHB, MBChB, MPH (Hons), FAFPHM.
Professional Teaching Fellow & Research Fellow, Section of Epidemiology & Biostatistics, University of Auckland

Cliff Harvey ND
Holistic Performance Nutrition

George D. Henderson
Research Assistant, Human Potential Centre, AUT University

LCHF success, but will protein kill me?


Here’s a great letter about LCHF success but with an important question. I hope you enjoy Norman’s story – it’s a nice one about improved weight, energy and health.  Great blood results, but some concern about protein. In fact, its been a big week for protein.  The story about two research papers lead to headlines like “High protein as bad as smoking” (see detailed comments I’ve made at the end of this blog).

So today we’ll look at Norman’s story, and think about the role of protein.

Hi Grant,

Following the recent post on your blog from Andrew, I thought I would share my indicators and also raise a question.

I am a 51-year-old male and switched to a LCHF diet just over 6 months ago. When I started the new eating regime I weighed 93kg with a BMI of 27.5, now I weigh 86kg and have a BMI of 25.4. I lost weight rapidly at first, losing 5kg in the first 2 months. Weight loss then slowed, and rose slightly over the Christmas holidays (Mince tarts and Christmas pudding being my undoing!) but since late January has again continued a slow downward trend.  In terms of getting a healthy BMI I would like to get down to about 80kg, which would place my BMI at 23.7.

While weight loss was my first goal, I was also concerned about my overall health because I have always had a ‘sweet tooth’. When my older brother was diagnosed as pre-diabetic a couple of years ago, I was concerned about going the same way. Two years ago I had a badly infected gall bladder removed, a 4-week period of my life when I quickly lost 10kg (From 98kg to 88kg). I had hoped to keep that weight off, but despite being ‘good’ about portion sizes and snacking between meals I found my weight just crept up again over the ensuing year and a half. Then I discovered LCHF.

For breakfasts I have settled on a fruit salad with a sprinkling of nuts (Pure Delish’s “No Grain-ola” is my current favourite) and cream. While the fruit has a relatively high amount of sugar, I consider the nutrients in fresh fruit outweighs the disadvantages, and this sets me up for the day. About twice a week I have fried bacon and eggs for breakfast instead.  For lunch I have a handful of nuts, or about 100gm of hot roast meat from the local deli. Occasionally I have salami and cheese or similar. For dinner I usually have a home-cooked meat-and-veg meal, with only low carbohydrate veges. During the day I seldom snack, but have a couple of coffees with cream. I also drink 500ml of full-cream milk mid-afternoons (which causes many comments at work!). About twice a week I will have an Atkins-diet snack bar, which has high fat and a few grams of sugar. I also succumb to iced coffee’s a few times a week (despite knowing they are high in sugar!). So I probably have slightly more sugar than the ideal, but as long as I feel good and the weight is very slowly still dropping I am happy.

What has amazed me about the past six months is how my ‘sweet tooth’ has disappeared. When people at work bring cakes or chocolate I have actually no desire to have any, and that is not just self-discipline. When I was coerced into eating some chocolate some weeks ago I found it unbearably sweet and stopped after a single piece. Like Andrew, I am not hungry during the day (in fact am seldom hungry at all, even at mealtimes. I eat meals because it is mealtimes, not because my stomach is grumbling). During the day I find myself having to avoid snacking just for something to do – the mid-morning coffee break and muffin was a welcome distraction, and is not quite as distracting with just a coffee. Yet I have plenty of energy and have eliminated the three-thirty-itis that for years has been a common feature of my working days. I feel great, and enjoy my meals.

I have just recently had a full set of blood tests done as part of an insurance medical , and was able to compare them to the results I had from 2011. My indicators are as follows:

Oct 2011 Feb 2014
Total Cholesterol 4.8 5.0
Triglyceride 2.6 1.2
HDL: 1.11 1.31
LDL: 2.5 3.1
Chol/HDL Ratio: 4.3 3.8
TG/HDL ratio 2.34 0.92
Hba1C: 34 35

All of which are well within the ‘good’ limits, especially my TG.HDL ratio. The biggest change I note is my triglycerides have halved, and as a result my TG/HDL ratio is also dramatically better.

However, during my medical exam this morning I also had a urine test. This showed some evidence of proteins in my urine. My GP said that some recent studies had showed that higher protein levels have been shown to have long-term health issues. Although I am not specifically increasing my protein intake on LCHF, the nature of it means for example that for lunch I may have a slice of hot roast ham (with crackling!) whereas before I would perhaps have had a carb-laden muffin.So it is conceivable that my protein intake has increased overall, since most high fat snacks also contain a fair amount of protein.

Any comments on the protein indicator in the urine test? My GP is not convinced that LCHF is necessarily a good diet, although concedes my weight loss and all the indicators show it is working well for me. I have to say he is a bit old-school, like much of the medical fraternity, but I am working on him.


Norman Holtzhausen

First up – nice work Norman.  Love it and thanks for sharing. Let’s have a think about protein.

So what about protein?

What we do know about protein:

  1. Protein is essential for life. We need to derive most of it from diet including at least some animal sources
  2. Over consuming protein means extra glucose as the liver, through gluconeogenesis, turns that protein into carbohydrate. This may be a factor in some people stalling or not losing weight on LCHF diets – they are over-consuming protein and still giving the body a high glucose load, raising insulin and all the downstream metabolic effects.
  3. Protein is associated with the production of Insulin-like Growth Factor 1 (IGF-1). IGF-1 is necessary for life, but over  production may be part of the causal pathway for all metabolic diseases.
  4. People with kidney disease may need to be careful about over consuming protein as this can cause protein toxicity. Protein toxicity occurs when the body is unable to get rid of the potentially toxic wastes that are generated as a result of protein metabolism. Several studies, however, have found no evidence of protein toxicity due to high protein intakes on kidney function in healthy people.

So, I think that all means that if you are on a low carb eating plan, it’s best to be careful about overeating protein if you are prone to being insulin resistant. If you have any kidney disease then its even more important. I keep an eye on my intake from time to time using online apps like easy diet diary. I  have a tendency to eat too much protein and need to watch this.

What about the recent research showing that high protein intake is “as dangerous as smoking”?

There’s been a big deal in the last 10 days made about two studies in the journal “Cell Metabolism”. It’s all about the over-consumption of protein and mortality, especially from cancer.

The first was titled “Low Protein Intake Is Associated with a Major Reduction in IGF-1, Cancer, and Overall Mortality in the 65 and Younger but Not Older Population

They claim to show that:

  • High protein intake is linked to increased cancer, diabetes, and overall mortality
  • High IGF-1 levels increased the relationship between mortality and high protein
  • Higher protein consumption may be protective for older adults
  • Plant-derived proteins are associated with lower mortality than animal-derived proteins

My take: First, this is a cross sectional study and can never show cause and effect.  It may be that higher protein intake produces more IGF-1 and affects tumour growth and the development of other metabolic issues. That’s one reason why we advocate an adequate protein diet (around a gram of protein/kg per day plus a bit more if your are very active or doing resistance training).  Second, carbs also raise IGF-1.  So the logical best diet to reduce levels of IGF-1 being chronically high is a low carb high fat diet with adequate protein (exactly what I advocate for).

That said, this study can build a hypothesis which can be tested in trials.  It’s not the basis for public health recommendations. Another example of nutrition science headlines going beyond the data. Remember that across the WHOLE population in this study, there was NO effect of protein, AND only an ASSOCIATION in a sub-group analysis. Let’s not draw too much out of this study.  They probably are onto something about excessive IGF-1, which is great to see as we have been talking about that for a while.

The second was  titled “The Ratio of Macronutrients, Not Caloric Intake, Dictates Cardiometabolic Health, Aging, and Longevity in Ad Libitum-Fed Mice

They claim to show that:

  • Food intake is regulated primarily by dietary protein and carbohydrate
  • Low-protein, high-carbohydrate diets are associated with the longest lifespans
  • Energy reduction from high-protein diets or dietary dilution does not extend life
  • Diet influences hepatic mTOR via branched-chain amino acids and glucose

This study was a mouse model and in my opinion went well beyond their data and made conclusions that were simply not robust.  A few things worth noting. First. hidden in the supplementary material we see that they only report 25 of the 30 diets because they culled diets for mice who “failed to thrive” and were removed from the study (see more below).  Second, they fed them synthetic food made from soybean oil, two amino acids, sucrose and dextrose. Third, they didn’t report median life expectancy as the main outcome when they should have.  Last, mice have a different carbohydrate and protein metabolism to humans so extrapolating to human life expectancy is a long shot.

Here are some comments on the  study spotted by the vigilant (and more robust apparently) lay peer review process (Rory Robertson from the in this case).

  • Why were 100+ sick mice – all on low-protein diets – excluded from longevity results?
  • The original study reportedly involved 30 diets and nearly 1000 mice: see here. Yet the published paper reports the results for – amongst other things – “…longevity in [only 858] mice fed one of [only] 25 diets ad libitum”.
  • I’m trying to understand why five of the 30 original diets – all low-protein diets – were excluded from the final results.
  • Specifically, “These diets were discontinued due to weight loss (≥ 20%), rectal prolapse or failure to thrive”: Table S1, p. 7 
  • Failure to thrive! Imagine the disappointment of those 100+ sick/dying mice – ALL on low-protein diets – when they were told that, sorry, we’re going to euthanize you and then exclude you from this longevity study.
  • It’s a longevity study – sick and dying mice are the main thing we are looking for! Yet they were excluded. Why?
  • My observation is that the study’s high-profile “finding” – that lower-protein diets boost longevity in mice – is NOT ROBUST when the analysis is properly REBALANCED – by excluding the five most-unhealthy high-protein diets – to properly adjust the design for the low-profile exclusion of the most-unhealthy low-protein diets.
  • Moreover, to properly capture the underlying reality of the published results, it makes sense to focus on MEDIAN not maximum lifespans.
  • Checking the medians for the remaining 20 diets, the claimed boost to mouse longevity from low-protein diets has disappeared: the TOP-2 diets now are HIGH-protein, as are FOUR of the TOP-7 diets.
  • And LOW-protein diets now represent THREE of the Bottom-6 diets. (This information is via Table S2 in the link above.)
  • Doesn’t ditching those five obviously unhealthy low-protein diets – involving 100+ sick/dying mice! – by itself invalidate the paper’s claim that low-protein diets boost longevity in mice (and so humans)?
  • In my opinion, the study’s longevity “findings” should be re-written to properly reflect the underlying results from ALL of those original 30 diets, including the longevity of ALL those nearly 1000 mice.
  • As things stand, the public is being misinformed by this research claims and interpretation.

Take homes:

  • Science media is a mess, especially in nutrition, and you will have to do some research to make any informed choice.
  • Protein is essential for life, but over-consumption might be an issue – we still don’t have the full answer.
  • In my view, eating whole plants and animals provides about adequate protein and nutrient dense food to make thinsg work for most people most of the time. This is also lowish in carbs, and higher in fat.

Dr Caryn Zinn talks LCHF and dietetics – a must watch

This is an outstanding 15 min presentation by our own Dr Caryn Zinn, Registered Dietician, about her growth , development, practice and ethics of LCHF practice.  Recorded at the recent Low Carb Down Under conference in Auckland, she is the first of the videos released. Enjoy.  Send this to your dietician friends (and even the ones who are not friends!). Click here or below.

NZ’s health leaders respond to our research publicity: Saturated fat…its bad, low carb radical and unsafe

Screen Shot 2013-10-31 at 2.19.56 PM
It was no surprise to see this one coming.  A perfect storm for the old powers that be in New Zealand obesity research and practice. The BMJ paper on why we got the saturated fat thing wrong, the ABC Catalyst series, and me out and about in the media talking about low carb high fat. I just noticed another one the NZ Herald just now by a NZ dietitian.
Looks like I (and those associated with me, sorry everyone) are now officially on the outer after this press release today (see this Experts decry fat diet – press release from the University of Otago (Professor Jim Mann)). It’s undersigned by key members of virtually every health organisation in the country.
I guess they are thinking that this document will shut everyone up, calm the uneducated masses, and we can continue our solution to the world’s problem with chronic disease?  How’s that going by the way?
I know you’d like me and my team to go away, but it’s not happening. Sorry for the inconvenience. Oh, and because of the Internet and open access science, the public is now able to do its own research.  And guess what? It has decided that the evidence isn’t convincing either. The world has changed.
The science of nutrition and chronic disease, and the public health approaches to nutrition are not solved. Let’s just get that straight – we (my team) don’t have all the answers, and neither do you.  I’ve been wrong before and could be wrong again, the reverse also applies guys.  Things will change.  Change is happening now.  It will happen again in the future.
Jim, do you recall being the younger scientist taking on the older ones in the BMJ 1979 in “Fats and atheroma: A retrial?”  Back then you were arguing about the complexity of nutrition and the need to go beyond fat and think about refined and processed carbohydrates. Everyone here has more in common than not.
For the record, I did correspond with Jim Mann yesterday.  Here’s part of what I sent him.  I think it puts down a reasonable position.
Jim…….My take is that I haven’t particularly been walking around promoting saturated fat (although to be fair I haven’t been talking about reducing it).  I have been walking around talking about diets higher in fat and lower in refined and processed carbohydrates.  I think I have some sound scientific reasons for this.  I will continue the line of research for the foreseeable future. I haven’t done much on athletes as they said in the paper.  Most of the recent work is secondary analysis of a few very large datasets we have from the US in hyperinsulinaemia. Also some basic work in low carb high fat eating.  So don’t believe everything you read in the newspaper. We do have a reasonable line of research going across this topic.
 What, in my view, we (all) have in common:
  1. That whole plants and animals are likely to be good for you and your chronic disease risk
  2. That foods which reduce inflammation are good for reducing chronic disease
  3. That sugar and processed carbs are not good, especially if you are insulin resistant (most of the vulnerable populations)
  4. That hyperinsulinaemia and chronic inflammation (both highly inter-related and can cause one another) are a problem and part of the mechanism for developing CVD and other chronic diseases.
  5. The Standard American industrial food diet and lifestyle is toxic, and much of the research showing different ways of eating show benefits simply because this diet is so bad.
  6. Trans fats and high omega 6 seed oils are inflammatory
  7. The interplay between hormonal physiology, built environment, food, and physical activity is complex.  This influences catabolic and anabolic states and therefore human energy homeostasis.  We don’t know exactly how the system works.  We have made the mistake (using Einstein’s words “make it as simple as possible but no simpler”) to describe the calories in and calories out dogma which we need to move on from.
What we seem to disagree on is:
  1. That SFA from whole healthy animals has any proven negative effect on human health in the context of the above (whole food eating).
  2. Attributing changes in populations to specific nutrients in a complex multifactorial disease using epidemiology which measures eating is fraught and is giving answers the opposite to those observed in decent robust RCTs.
  3. That low carb high fats diets are safe, efficacious, and useful for the public.

My response to the technical points in the media release asking for evidence today

  1. The actual trials showing SFA reduction and health improvements are fraught because they are still mainly in the Standard American Diet (SAD) paradigm with small dietary modifications.  I agree that SFA intake in the context of the SAD might be problematic.  What I still have a problem with, in these trials, is that many (most) still use a control group eating the same old food.  Putting anyone on a diet different from the SAD will probably help.  Here’s the latest meta analysis.  In fact, the reality is that consuming SFA has positive effects on HDL cholesterol and reduces triglycerides.
  2. I’m not bothering with an in-depth rebuttal of the population studies.  There’s just too much (uncontrolled and unmeasured) going on there, with poor food measurement to say saturated fat causes anything.
  3. I particularly draw to your attention to the bit in the media release directed straight at me (just say my name guys I am comfortable with that). “However, the group suggests that those who advocate for radical new dietary approaches have a responsibility to provide convincing peer-reviewed evidence of long term benefit as well as absence of harm. Such evidence does not exist for diets high in saturated and total fat, and very low in carbohydrate”. I have tried to address these issues in depth below. But first, how a diet full of whole plants and animals, similar to what humans have eaten the whole time they have been on the planet (up until recently, when human life expectancy halved (agricultural revolution) and then got full of disability from chronic disease (last few decades)) is radical is beyond my reasoning.  Read the latest nutritional biochemistry and draw your own conclusions.
  4. Low carbohydrate diets being safe, efficacious and useful? RCT and mechanistic evidence shows that dietary saturated fat alone, in the context of a low carb diet doesn’t have the proposed cardio-metabolic risk effects of being harmful.  In fact, things all go the other way (improve) which is a very good sign.  I have put some references below, but also here’s a  recent meta analysis of the clinical trials of low carb high fat diets and their metabolic effects. People generally do better metabolically, adhere better, and control blood glucose and insulin better on low carb high fat diets than other diets.  Much of the reason for this (expanded below) is that when you become insulin resistant then a lower fat diet will provoke high insulin which only adds to the problem. Here is an excellent summary of the 23 RCTs on low carb high fat
  5. More on long term safety – Jim Mann’s main point on the article and media release about low carb high fat was around long term efficacy and safety. He does have a point – you can study this through RCTs, but the long term epidemiology isn’t there for eating actual whole plants and animals (short of the work on healthy indigenous populations, and that this is the sort of diet humans have eaten for 99.9% of the time they have been on the planet). There is certainly no evidence of harm – some people like to quote the Swedish women’s study to show there is harm of a high fat, high protein diet. I am not promoting this combination of eating. The epidemiology in this study is woeful because the lowest decile of population carb eaters was still getting 40 percent of their calories from carbs who also had to be in the highest decile of protein eaters – again not what I suggest – had poorer health outcomes.  Again if the cardio- metabolic risk factors are worth anything – then people do better.  Here’s a good dissection of this Swedish paper.

     I think this shows how epidemiology sometimes gives us what we want to see.  I agree that more work needs to be done.  My starting hypothesis is to look at human nutrition through an evolutionary biology lens – what food environments are humans adapted to? And what is the physiology around this?   I think we have to understand how and why insulin resistance happens and how that relates to chronic disease through inflammatory processes. I particularly recommend to you this paper which has a brilliant and comprehensive take on the evolutionary nutritional biochemistry and chronic disease development.  BTW – the 40% CHO diet and high protein combination in the Swedish study showing the highest CVD is very much the type of mix Professor Mann has advocated (to me at least) he would support.

  6. Some longer-term data on Type 1 diabetics and low carb high fat diets – good efficacy and safety.
  7. Mechanistically high SFA doesn’t translate to high plasma SFA in the context of low carb diets – see reference.
  8. I agree that people respond differently to different diets. Insulin resistance is important as to what diet we can tolerate.  Hyperinsulinaemia induces the direct and indirect effects for the major chronic diseases.  Impaired glucose tolerance doesn’t catch this until end stage.  Many many people get glucose into their cells at the right rate, but with hyperinsulinaemia.  Complex carbs may not help, and in fact be even worse because the carbs are digested slowly provoking longer hyperinsulinaemia – a reference. We will publish our analysis of this soon. But in the meantime see the work of Dr Joseph Kraft.
  9. The only way to diagnose this is a dynamic glucose tolerance test measuring insulin.  We have a database of 15,000 of these with insulin for up to five hours post OGTT. You will see the pattern of hyperinsulinaemia with normal glucose tolerance decades before impaired glucose tolerance.
  10. I contend that virtually every CVD risk factor either causes insulin resistance through inflammatory or other processes e.g. Sleep, stress, sugar, alcohol, smoking, pollution and so on.  Obviously some have other effects too (e.g. smoking). But also that age and ethnicity affect Insulin sensitivity – Maori and Pacific are likely to be more prone to the above.
  11. Here’s the kicker for me – in terms of health inequalities the current dietary guidelines probably perpetuate health inequities because the least at risk do the best and stay healthy. So even if the two types of dietary guidance are efficacious – which they are – albeit not equally distributed in their efficacy AND there seems to be no evidence of harm from a lower carb high fat – then we have no option but to go the high fat route because of the inequalities – although I acknowledge we need more work to understand this. That’s the reason I am pursuing this.

Extra references to 23 RCTs showing good outcomes for low carb diets compared to other diets. Actual data summarised here very nicely too

1. Foster GD, et al. A randomized trial of a low-carbohydrate diet for obesity. New England Journal of Medicine, 2003.

2. Samaha FF, et al. A low-carbohydrate as compared with a low-fat diet in severe obesity. New England Journal of Medicine, 2003.

3. Sondike SB, et al. Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factor in overweight adolescents. The Journal of Pediatrics, 2003.

4. Brehm BJ, et al. A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. The Journal of Clinical Endocrinology & Metabolism, 2003.

5. Aude YW, et al. The national cholesterol education program diet vs a diet lower in carbohydrates and higher in protein and monounsaturated fat. Archives of Internal Medicine, 2004.

6. Yancy WS Jr, et al. A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia. Annals of Internal Medicine, 2004.

7. JS Volek, et al. Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body composition in overweight men and women. Nutrition & Metabolism (London), 2004.

8. Meckling KA, et al. Comparison of a low-fat diet to a low-carbohydrate diet on weight loss, body composition, and risk factors for diabetes and cardiovascular disease in free-living, overweight men and women. The Journal of Clinical Endocrinology & Metabolism, 2004.

9. Nickols-Richardson SM, et al. Perceived hunger is lower and weight loss is greater in overweight premenopausal women consuming a low-carbohydrate/high-protein vs high-carbohydrate/low-fat diet. Journal of the American Dietetic Association, 2005.

10. Daly ME, et al. Short-term effects of severe dietary carbohydrate-restriction advice in Type 2 diabetes. Diabetic Medicine, 2006.

11. McClernon FJ, et al. The effects of a low-carbohydrate ketogenic diet and a low-fat diet on mood, hunger, and other self-reported symptoms. Obesity (Silver Spring), 2007.

12. Gardner CD, et al. Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women: the A TO Z Weight Loss Study. The Journal of The American Medical Association, 2007.

13. Halyburton AK, et al. Low- and high-carbohydrate weight-loss diets have similar effects on mood but not cognitive performance. American Journal of Clinical Nutrition, 2007.

14. Dyson PA, et al. A low-carbohydrate diet is more effective in reducing body weight than healthy eating in both diabetic and non-diabetic subjects. Diabetic Medicine, 2007.

15. Westman EC, et al. The effect of a low-carbohydrate, ketogenic diet versus a low-glycemic index diet on glycemic control in type 2 diabetes mellitus. Nutrition & Metabolism (London), 2008.

16. Shai I, et al. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. New England Journal of Medicine, 2008.

17. Keogh JB, et al. Effects of weight loss from a very-low-carbohydrate diet on endothelial function and markers of cardiovascular disease risk in subjects with abdominal obesity. American Journal of Clinical Nutrition, 2008.

18. Tay J, et al. Metabolic effects of weight loss on a very-low-carbohydrate diet compared with an isocaloric high-carbohydrate diet in abdominally obese subjects. Journal of The American College of Cardiology, 2008.

19. Volek JS, et al. Carbohydrate restriction has a more favorable impact on the metabolic syndrome than a low fat diet. Lipids, 2009.

20. Brinkworth GD, et al. Long-term effects of a very-low-carbohydrate weight loss diet compared with an isocaloric low-fat diet after 12 months. American Journal of Clinical Nutrition, 2009.

21. Hernandez, et al. Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a high-fat, low-carbohydrate diet. American Journal of Clinical Nutrition, 2010.

22. Krebs NF, et al. Efficacy and safety of a high protein, low carbohydrate diet for weight loss in severely obese adolescents. Journal of Pediatrics, 2010.

23. Guldbrand, et al. In type 2 diabetes, randomization to advice to follow a low-carbohydrate diet transiently improves glycaemic control compared with advice to follow a low-fat diet producing a similar weight loss. Diabetologia, 2012.

Low carb high fat lecture full, so we are doing another

NEW DATE due to popular demand 22 October

Thanks to the many who have registered and shown interest in this seminar at AUT Millennium on October 16th.  Its been wildly over subscribed to the point we have decided to do a second seminar.  So please if you are interested, its filling very fast, get registered today.

Event Details
Date:   Tuesday, 22 October 2013
Time:   7.00pm – 8.30pm
Venue: AUT Millennium Institute, 17 Antares Place, Mairangi Bay, Auckland

Free public parking is available


6.00pm – 6.50pm       Registrations open
7.00pm – 7.45pm       Event commences.  Keynote presentation from Professor Grant Schofield
7.45pm – 8.30pm       Q&A session and open discussion followed by refreshments

Note, we will also be taking registrations on the night for a series of corresponding paid workshops that will be held in November. Details about the workshops will be posted on this site once confirmed.

RSVP to attend the event by providing your name, email, and contact number REGISTER

For those international and out of town, we will video and make available online.

We’re doing a public lecture on Low Carb High Fat

Low Carb High Fat_16 Oct 2013

Click here for the full PDF version of the invite Low Carb High Fat_16 Oct 2013

Join me and my research team to see the latest in the world of Low Carb HIgh Fat (LCHF) research and practice.  We will look at what the research shows, what we are doing, and what this means in practical terms.  We will be discussing both health (weight loss, diabetes, and chronic disease), and athletic performance.

Get in quick to register if you are in Auckland as seats are free but limited.

When: Wednesday October 16th 7-8.30 PM

Where: AUT Millennium INstitute, Mairangi Bay Auckland

Register by emailing

Joseph Kraft: Why hyperinsulinemia matters

Joseph Kraft MD
Dr Joseph Kraft MD, pathologist and author of “Diabetes Epidemic and You” and unsung pioneer in insulin responses and early diagnosis of diabetes

Science has a history of ignoring some of the most important and astonishing work for a long time, then coming to its senses and celebrating it. It is time now to celebrate the work of Dr Joseph Kraft MD, a pathologist now in his nineties. Dr Kraft is the author of “Diabetes Epidemic and You” which is still available, at least in hard copy. He defines what he calls “Diabetes in situ” which is borrowed from his cancer pathology background. He has written several good papers, none of which have ended up being cited that highly.  A nice, free summary of his work is available here. Kraft has carried out more than 14,000 oral glucose tolerance tests over a few decades. Normally we measure the glucose response to drinking glucose.  This response can tell us the degree to which we metabolize and remove glucose from our blood.  Very important for diabetes diagnosis and other metabolic issues. Kraft’s test are different though.  He is way more thorough than normal.  First, rather than monitoring glucose for 2 hours post test, he monitors it for at least 5 hours.  Second, he also measures insulin, as well as glucose, over the course of the test. From his test results and the other literature, as well as his pathology and direct autopsy observations, he concludes that:

  1. We may be able to diagnose diabetes much much earlier than we do
  2. Abnormal insulin levels (high) are directly and indirectly damaging to the vascular system, and therefore almost every organ in the body
  3. This high insulin (hyperinsulinemia) is a condition in its own right and really the causal mechanism behind most of the metabolic and chronic diseases we experience today.

He calls the abnormal insulin response, with normal glucose response “Diabetes In SituWhat is Diabetes In Situ? Here’s the deal – you go to your doctor.  You get a series of tests to see how well you are functioning metabolically. This is a really important series of tests because metabolic functioning is what will determine almost all of our quantity and quality of life. I would go as far as to at least hypothesize (there’s enough evidence) that problems in carbohydrate metabolism are implicated in virtually every chronic disease from head to foot, and most of the organs in between.  This includes Alzheimer’s and vascular dementia, peripheral vascular disease and everything in between, from common obesity to diabetes to fatty liver disease to cardiovascular disease…and the list goes on. The trouble is that your doctor will look for metabolic markers which are either flawed as predictors, or mostly are markers of end stage dysfunction. Things like elevated blood glucose, high blood pressure, vascular blockages (arterial sclerosis) etc. If your doctor is really interested in your health and suspects you aren’t doing that well, they might order an oral glucose tolerance test. Kraft shows us that there are five typical patterns of insulin response to the glucose which characterize disease state.  As mentioned earlier, these are really what we should be considering in early identification of metabolic problems. Unfortunately, the glucose tolerance test is rarely run long enough, nor is insulin (key to this) measured concurrently.  In fact, in New Zealand, insulin measurement can only be ordered and covered under the public hospital system by a handful of specialist endocrinologists. Insulin is not considered as useful in the diagnosis of early stage chronic disease. That’s a shame really because Dr Kraft shows it certainly is useful. Let’s look at Kraft’s five patterns….. Here’s what we consider a normal insulin response to a glucose bolus in an oral glucose tolerance test. Kraft calls this “Pattern 1”. Pattern 1 insulin peaks after a 75 or 100 g glucose load after 30 to 60 min at 50-70 units. Everything is almost back to baseline after 2 hours, certainly after 3 hours. This is what we regard as a normal insulin response to a glucose load. It’s also likely that slower release carbs (lower GI) like beans might provoke an even lower area under the curve for the same total CHO load. Pattern 1

Pattern 2 (below) is the first sign of insulin resistance, but things will likely look fine if you simply look at the glucose responses. We see a similar time to peak, but a much higher peak. Insulin hasn’t returned to close to baseline until 4 hours or so after the initial load.  The area under the insulin curve is very large.  The total stress on pancreatic beta cells is high simply because of the overall demand for insulin. Many (most) people with this pattern present normal glucose curves and are told they are doing “just fine”.

Pattern 2

Pattern 3 (below) is a delayed and high peak.  This is indicative of some beta cell function, but some functional loss.  In essence we are seeing the beginning of beta cell burn out.  People can eventually move glucose into their cells, but they take a long time to produce enough insulin.

Pattern 3

Pattern 4 (below) is the same as Pattern 3 except the fasting level of insulin is much higher.

Pattern 4

Pattern 5 (below) is beta cell failure. In other words, there is little or no ability to move the glucose into cells because the pancreas can’t produce insulin. Patients will need exogenous insulin injected at that point to get the same result. Interestingly, Kraft also shows that sometimes people on low carb diets can show this pattern temporarily. It’s not that they are unable to produce insulin, it’s just more likely that they can take up glucose into cells (eg, brain) without insulin in the first instance.  These people return to Pattern 1 after a period on a higher carb diet. I think this is also consistent with the finding that people on LCHF diets typically have a temporary diagnosis of peripheral insulin resistance which is resolved after a large carb meal. It’s likely that the body adapts to preferentially shunt the available glucose to the brain first.  So Pattern 5 with a low carb diet is OK, its jus the same physiology as Pattern 1 but adapted to low carb. Pattern 5

Take-home messages, implications for practice, and questions

  • Dr Kraft was onto it decades ago – that we should measure glucose and insulin concurrently for an extended period in the glucose tolerance test to identify those people who are at risk early.
  • This early detection is both ethical and necessary.
  • Instead current best practice sends people away who are insulin resistant until they present with end stage disease markers.  Only then will we take them seriously.
  • Why haven’t we taken Dr Kraft’s excellent work more seriously?

Finally here is a link to a letter I received from Dr Kraft recently. He outlines is overall approach and ideas from his results of several thousand OGTTs over several decades.  It’s interesting stuff – page 1 click herepage 2 click here

As usual, for all my blog thanks so much to Helen Kilding who tirelessly edits and corrects my terrible typing!