The Science of Human Potential

Response to Freedhoff and Hall – the differences between diets do matter.

In the latest Lancet, Yoni Freedhoff and Kevin Hall have an opinion piece about diet trials, in which they argue that it’s not helpful to know that an ad lib low-carb diet results in more weight loss than a calorie-restricted low-fat “dietary guidelines” type diet, because the weight loss differences are not clinically significant, a claim which we think is both false, and overlooking other benefits of carbohydrate restriction.[1]

They then go on to ask that more effort go into identifying ways to ensure that people can adhere to diets long term, a reasonable request and something we’re very much interested in ourselves. However, they spoil this a bit by talking about “hype” (short for hyperbole) and “society’s endless parade of fad diets”. If you want to improve adherence to diets and you think that there is little to choose between them, why use the word “fad”, which is normally used to devalue people’s dietary choices?
Further, is there even an endless parade of diets these days? Aren’t there a just few variations on and recombinations of the same timeless themes, such as vegan or vegetarianism, calorie restriction, carbohydrate restriction, ancestral, and so on? The only really original idea is fasting, yet this ancient therapy only seems original because we’ve just been led through such an intensive era of round-the-clock eating.

Freedhoff and Hall concentrate their argument on one trial, the DIRECT study (sometimes better known as Shai et al.) which was a 24-month workplace intervention in Israel, with ad lib low-carb, low-fat calorie restricted, and Mediterranean diet calorie restricted arms. “The low-carbohydrate, non–restricted-calorie diet aimed to provide 20 g of carbohydrates per day for the 2-month induction phase and immediately after religious holidays, with a gradual increase to a maximum of 120 g per day to maintain the weight loss…the [low carb] participants were counseled to choose vegetarian sources of fat and protein and to avoid trans fat. The diet was based on the Atkins diet.” The Mediterranean diet (at 40% fat, mainly from olive oil and nuts) was based on a 2001 book by Walter Willett and PJ Skerrett, and the low-fat diet was based on American Heart Association dietary guidelines. All dieters had access to the same food in the workplace cafeteria, but the food suitable for each different diet was colour coded.
In this study, people in the low carb group (not very low carb after induction, it varied between 87g/day at 6 months and 120g/day reported CHO intake over the first 12 months) lost on average 1.8 Kg more weight than the low fat dieters overall.[2]
Well as Freedhoff and Hall say, that’s not a lot of weight in the grand scheme of things. So does it support their claim that we should stop caring about the results of these studies?
Not so fast. The average weight loss includes all the people who drop out of the study; this is “intention to treat” (ITT) analysis, designed to keep the randomisation of baseline characteristics stable.
But what you might want to know if you were choosing a weight-loss diet, is, what will happen to me if I follow the diet? There were more drop-outs (22% vs 10%) in this study in the low carb arm, who found it hard to resist the biscuits and cakes in the cafeteria (interestingly, this caused their intake of saturated fat to increase over the study, even as their total fat intake went down), and self-reported complete adherence to low-carb was 57% at month 24.[3] The superiority of the low carb diet in DIRECT includes the effect of including this higher drop-out rate, and those extra cakes and biscuits. The per-protocol analysis only gives us a stratified comparison of completers vs non-completers (i.e. minus drop-outs, but including those with weak adherence to diets) at 24 months, but we do know from other studies that when non-completers are excluded, the long-term difference between diets at 12 months becomes larger.[4]


So compliance is important, sticking to the diet is critical of course, but what diet you stick to matters more than Freedhoff and Hall are saying. In the DIRECT study, people who completed 24 months of the low-carb diet lost a mean 5.5 +/- 7.0 Kg, and those who completed the low fat diet lost 3.3 +/- 4.1 Kg. The biggest loser in the DIRECT study lost 35% of their body weight, but all we know about the most successful dieters is, that they weighed more at baseline, lost weight more rapidly in the early stages, and ate a bit less protein and cholesterol at baseline (but overall the protein intakes in this population were, and remained, quite high). Rapid weight loss early in a diet is usually associated with success, and of course it’s a feature of the ketogenic diet, or the induction phase of the Atkins diet here.

But wait, there’s more. Weight loss isn’t the only effect of diet, and overweight people often suffer from increased cardiometabolic risk owing to insulin resistance and the metabolic syndrome.

Freedhoff and Hall for some reason don’t mention this, but it’s the evidence we have about the “long term safety” of any diet. In all parameters the ad lib low carb diet does better than the calorie-restricted low-fat diet, even at 24 months, and even including the drop-outs.

“Among the participants with diabetes, the proportion of glycated hemoglobin at 24 months decreased by 0.4±1.3% in the low-fat group, 0.5±1.1% in the Mediterranean-diet group, and 0.9±0.8% in the low-carbohydrate group. The changes were significant (P<0.05) only in the low-carbohydrate group (P=0.45 for the comparison among groups).”[2] In fact, as far as we know, carbohydrate-restricted diets are the only diets that can produce some of these benefits without weight loss.[5]

There’s a curious extra point in the chart below – LDL rose slightly at 6 months in the low-carb arm, when adherence was good and polyunsaturated fat intake was high, and dropped at 24 months when polyunsaturated fat intake decreased and carbohydrate, but also saturated fat, intake increased.

Shai markers

But wait, there’s more. Something else that Hall and Freedhoff didn’t mention is the very long-term effects of this diet trial, because there was a four-year follow-up study. And the results here are very interesting, because there is less of a rebound effect for the ad lib low carb diet and the Mediterranean diet than for the low-fat, calorie restricted AHA diet.[6]

Shai figure 1
In the low-fat diet group (which had the fewest drop-outs) most of the improved metabolic parameters, including weight, are back to baseline levels. In the low-carb group, weight and the LDL/HDL cholesterol ratio are still improved. This is four years after the end of a 2-year study – six years in all. Quite a different result from Hall’s Biggest Loser study, where severe rebound weight gain from CICO “eat less move more” energy restriction was the order of the day.[7]

After the completion of intervention, the participants were invited once a year to the clinic for a regular check-up and were encouraged to pursue a healthy diet. Although diet-group color coding and nutrition labeling in the workplace cafeteria were stopped at the end of the intervention, the cafeteria continued to serve suitable meals according to the guidelines of the 3 diets, suggesting that the workers could still consume their specific dishes, which continued to be regularly served, as they were during the trial. We did not continue with the dietary sessions or any other activity encouraging adherence. We used one question: Are you still dieting? The question had three possible answers to choose from: 1. “Yes, with my original diet” 2. “Yes, but I switched to another diet” 3. “No, I am not dieting”. No differences were observed in response to this question between the 3 assigned diet groups (p=0.36).


Perhaps there are a few people in this group who were so happy with their results that they stuck with the low-carb diet for 6 years, and their results are carrying the rest – or perhaps the 2 years of low-carb diet (or the 2 months of ketogenic dieting) had lasting benefits. These questions weren’t really answered by the questionnaire quoted above, which kind of refutes Freedhoff and Hall’s suggestion that we have nothing more to learn from diet comparisons. Good post hoc analysis of the data from weight loss trials can seek to develop further hypotheses about what baseline markers, characteristics, and responses predict success, and that should inform the design of further trials and interventions. It’s also possible to tweak the diets to improve them for both effect and ease of compliance – (e.g. what if the AHA diet had been lower-GI, the Med diet lower carb, and the low-carb diet lower carb, with more Mediterranean and real food elements? Something like this probably went on during the 4-year follow-up among the people still interested in the diets).
But in the meantime, we needn’t let ourselves get confused about how to proceed.

As Prof Richard Feinman says, “remind me again why we have a medical science literature?” Comparative trials of diets and drugs are designed and published so that we know what is the most effective option between two or more choices for any given diagnosis. The intention is that the best treatment, determined by experiment, will be the one to be offered first. The patient may not like it, or it may not work, in which case it will be time to try something else, but the evidence is there to inform the discussion.

Instead we are stuck in this Catch 22 where the evidence about the best treatment for overweight and diabetes, collected over decades at great expense, is ignored (or worse) because its results contradict cherished beliefs about (in this case) the pre-eminence and equivalence of the calorie, or (at other times) the health effects of saturated fat.

Fortunately some people are brave enough to follow the existing evidence while applying themselves to solving the question of adherence. David Unwin and colleagues in the UK have worked on the psychological aspects of motivating and supporting people in low carb diets for type 2 diabetes and NAFLD with great success,[8] and recently a multicenter LCHF approach in Canada has also reported good adherence and impressive results.[9]


A thought experiment

The DIRECT study had no control group, i.e. no group of people from the same population eating a normal (whatever they are normally eating)  diet ad lib.

Imagine there was a fourth arm randomised to an ad lib version of one of the 3 diets.
Without calorie restriction, it seems less likely that the AHA-approved, last-year’s dietary guidelines diet would have made any difference from baseline. It’s possible that nothing would have improved and plausible that things would have continued to get worse overall.
Without calorie restriction, it’s likely that the Mediterranean diet (the modern, updated dietary guidelines diet) would still have been better than the AHA-approved, last-year’s model dietary guidelines diet.There may well have been some smaller improvements, and things would be unlikely to get worse.

Now imagine an ad lib version of the LCHF diet (the controversial, alternative-dietary guidelines diet). The results would still be exactly the same, because the experimental diet was ad lib.

[1] Freedhoff Y, Hall KD. Weight loss diet studies: we need help not hype. The Lancet , Volume 388 , Issue 10047 , 849 – 851.

[2] Shai, I, Schwarzfuchs, D, Henkin, Y et al. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. N Engl J Med. 2008; 359: 229–241

[3] Greenberg, I, Stampfer, MJ, Schwarzfuchs, D, and Shai, I. Adherence and success in long-term weight loss diets: the dietary intervention randomized controlled trial (DIRECT). J Am Coll Nutr. 2009; 28: 159–168

[4] Feinman RD. Intention-to-treat. What is the question? Nutr Metab (Lond). 2009 Jan 9;6:1. doi: 10.1186/1743-7075-6-1. Full text:

[5] Gannon MC, Nuttall FQ. Control of blood glucose in type 2 diabetes without weight loss by modification of diet composition.  Nutrition & Metabolism 2006 3:16 DOI: 10.1186/1743-7075-3-16. Full text:

[6] Schwarzfuchs D, Golan R, Shai I. Four-year follow-up after two-year dietary interventions. N Engl J Med. 2012 Oct 4;367(14):1373-4. doi: 10.1056/NEJMc1204792.
Full text:

[7] Fothergill, E, Guo, J, Howard, L et al. Persistent metabolic adaptation 6 years after “The Biggest Loser” competition. Obesity (Silver Spring). 2016; DOI: (published online May 2.)

[8] Unwin DJ, Cuthbertson DJ, Feinman R, Sprung VS (2015) A pilot study to explore the role of a low-carbohydrate intervention to improve GGT levels and HbA1c. Diabesity in Practice 4: 102–8. Full text:

[9] Mark S, Du Toit S, Noakes TD, Nordli K, Coetzee D, Makin M, Van der Spuy S, Frey J, Wortman J. A successful lifestyle intervention model replicated in diverse clinical settings. S Afr Med J. 2016 Jul 3;106(8):763-6. doi: 10.7196/SAMJ.2016.v106i8.10136.
full text:

Australia’s response to the diabetes epidemic – shooting the messenger.


On the Sunday current affairs program in New Zealand there was a report on the diabetes epidemic in South Auckland. This is our largest (and growing) health problem, and two of the players in this tragedy had messages that stood out. An elderly woman, overweight and now condemned to thrice-weekly dialysis, told us “I didn’t do anything wrong”.

How right she was. The Ministry of Health website still offers this “healthy eating” advice – “Fill up on breads, cereals, pasta and rice.”

Junk epidemiology and junk food

The epidemiologists from Harvard recently grabbed headlines with claims that polyunsaturated fats are the healthiest fats, that chicken is one of the healthiest animal proteins, and that plant proteins are healthier than animal proteins. In South Auckland, a staple food is Kentucky Fried Chicken. Chicken is a meat naturally high in polyunsaturated fat, KFC is fried in “healthy” polyunsaturated vegetable oils, and therefore a good source of these, and it even comes with a bean salad – plant protein. This junk food meal, eaten wherever diabetes is rampant (the franchise only came to New Zealand in the 1970’s), actually ticks most of the boxes thrown up by junk epidemiology.

With this sort of dangerous misinformation on official government websites and in the media, how can anyone know what is “right” or “wrong” when it comes to their risk of type 2 diabetes?

The look of success?

One chap in the Sunday program, Kim, had it figured out. He’d reversed his diabetes by, firstly, losing weight rapidly on a low calorie diet (like the Newcastle diet, but with real food instead of Optifast), by exercising regularly, and by eating a diet described as “lots of vegetables” – we saw a delicious looking stir-fry – “no bread, potatoes, rice, pasta” – he didn’t even need to mention sugar.

Incidentally, what is a “fast-acting” carbohydrate? Previously, it was assumed that fast-acting carbohydrates were sugars or juices. It is now known that this is not true, and if there were a fast-acting carbohydrate, it would probably be a starch. “Fast-acting carbohydrate” is a term we need to eliminate from our diabetes vocabulary. – Marion J. Franz, MS, RD, LD, CDE

“So what’s left?” asked the interviewer. “Eggs, meat?” “You’d be surprised how much there is left that’s good to eat!”

Now, the direct end result of type 2 diabetes is a series of complications which include cardiovascular disease, retinopathy, neuropathy, kidney disease and gangrene (caused when vascular damage cuts of blood supply to the extremities, usually the feet, compounded by neuropathy preventing pain warning of injury, and infections fed by high sugar levels and suppressed immune function). Gangrene often requires the amputation of the affected parts, and the surgeon who has to perform this procedure is an orthopedic surgeon.

The case of Dr Gary Fettke

Gary Fettle is a friend of mine. He’s also an orthopedic surgeon in Tasmania, Australia who performs dozens of these operations on patients with type 2 diabetes every year. “I used to do one amputation every 6 to 12 months and now I’m doing one a week”. Seeing, as anyone can who has eyes in their head, the link between diet and diabetic blood sugars and the risk of complications (hardly controversial), he had dared to make a study of nutrition and diabetes literature – something which, as a highly trained medical professional, he was well able to do – and advise his patients, and the public, about how to eat to beat, and avoid type 2 diabetes and/or its complications.

Now Dr Fettke has been banned from giving any diet advice, to patients or in any media, until further notice.

Why? What he is advising is plainly good sense as well as evidence-based. It’s the same message Kim gave on the Sunday program, except that Dr Gary Fettke is a highly trained medical professional with hundreds of hours of clinical experience.

Here’s a great response to the silencing of Dr Fettke, written by Tyler Cartwright for the Ketogains website, that puts the case better than we can.

Meanwhile the Australian authorities continue to allow Associate Prof Sof Andrikopoulos to give diet advice, despite his telling the Australian public to eat sugar with burgers – based on his experience with mice. (I guess that also makes the soft drinks at KFC part of the healthy menu now).

Gary’s not the first and won’t be the last

In 2005 the Swedish dietetics authorities tried to silence Dr Annika Dahlqvist. Their heavy-handed actions led to a court case in 2008 which Dr Dahlqvist won, publicising the benefits of LCHF all over Sweden, and as a result  a significant proportion of the Swedish population soon knew about the diet, and butter sales went up – leading to much hand-wringing around the world among people committed to outdated bad advice, but no adverse effects in the Swedish population – according to the Swedish government’s health data base, heart attacks are now at an all-time low.

20-85+ 39,418 38,846 37,150 34,780 34,140 32,814 32,149 29,823 28,783

Heart attacks in Sweden by year, 2006-2014.



In this recent Australian TV series, The Saving Australia Diet, Dr Fettke is seen advising the patient Tony on how to treat diabetes with the LCHF diet, with the help of chef Pete Evans. For no good reason that we can see, other than some virulent local strain of the Tall Poppy syndrome, the Australian establishment hates Pete Evans, and this has made some scientists who should know better indulge in bottom-of-the-barrel stunts like Ass Prof Sof Andrikopoulos’s “Paleo mouse” attacks on low carbohydrate diets. It is almost certainly his association with Pete Evans that has drawn the complaint that has led to Dr Fettke being silenced.

Of course, this kind of heavy-handed, bloody-minded action is only possible because Dr Fettke is a health professional, and therefore subject to the discipline of a regulatory body, even if it is being abused for unworthy personal ends and is clearly not in the public interest. Pete Evans, on the other hand, is a member of no such body, so he can’t be silenced, thank goodness.

This is why it’s important for everyone who speaks on nutrition to have a proper qualification – so they can be silenced when they embarrass the authorities, for example by being right about something the government and its appointed experts have been consistently wrong about. Especially in the middle of an epidemic, when damage control is the order of the day.

Well, here’s an idea – instead of “damage control” being about saving reputations, can’t we have damage control that will mean saving feet, eyes, and kidneys?

We don’t always say good things about Aussies (us New Zealanders, and vice versa), but they are our mates really and Gary Fettle is one of the good ones.  Shame on you Australia and the Australian Medical Authorities for allowing this to happen.

Intro to low carb and fasting seminar

MIL154729 HPC Facebook Post (1200 x 1200)We are doing a seminar Sept 8th, AUT Millennium Auckland

Presenters – me (Grant Schofield), dietician Dr Caryn Zinn, and Jimmy Moore all the way form the USA talking about his experiences with fasting.

It’s definitely an intro night, so well suited to those just getitng into or supporting others getting into this lifestyle

Limited space – book online here

  • Date: Thursday 8th September
  • Location: AUT Millennium, The Finish Line,
  • 17 Antares Place,Mairangi Bay, Auckland
  • Time: 6.30pm –8.30 pm
  • Tickets: $25, limited to the first 150 people
  • Buy your tickets online at
  • Sorry no door sales

PDF flyer here MIL154729 HPC Flyer 8.9.16 2



The “thrifty” gene found in Samoa and what it means

SamoaThis (very technical) paper has made a big splash on the internet and in the media, not just in New Zealand but all around the world.

A thrifty variant in CREBRF strongly influences body mass index in Samoans
Ryan L Minster, Nicola L Hawley, Chi-Ting Su, Guangyun Sun, Erin E Kershaw, Hong Cheng, Olive D Buhule, Jerome Lin, Muagututi‘a Sefuiva Reupena, Satupa‘itea Viali, John Tuitele, Take Naseri, Zsolt Urban, Ranjan Deka, Daniel E Weeks, & Stephen T McGarvey
Nat Genet. 2016 Jul 25. doi: 10.1038/ng.3620. [Epub ahead of print]

Samoans are a unique founder population with a high prevalence of obesity, making them well suited for identifying new genetic contributors to obesity. We conducted a genome-wide association study (GWAS) in 3,072 Samoans, discovered a variant, rs12513649, strongly associated with body mass index (BMI) (P = 5.3 × 10−14), and replicated the association in 2,102 additional Samoans (P = 1.2 × 10−9). Targeted sequencing identified a strongly associated missense variant, rs373863828 (p.Arg457Gln), in CREBRF (meta P = 1.4 × 10−20). Although this variant is extremely rare in other populations, it is common in Samoans (frequency of 0.259), with an effect size much larger than that of any other known common BMI risk variant (1.36–1.45 kg/m2per copy of the risk-associated allele). In comparison to wild-type CREBRF, the Arg457Gln variant when overexpressed selectively decreased energy use and increased fat storage in an adipocyte cell model. These data, in combination with evidence of positive selection of the allele encoding p.Arg457Gln, support a ‘thrifty’ variant hypothesis as a factor in human obesity.

Samoa gene

How the variant gene correlates with BMI in Samoa

This is a big deal because the thrifty gene hypothesis – that some people are prone to obesity because their ancestors evolved to store energy more effectively in times of plenty – had been dead in the water for lack of convincing evidence. Genes are complicated things and previous studies hadn’t turned up anything with this sort of effect size (obesity is common today, yet these “thrifty” genes are normally quite rare). The thinking is that the gene variant (technically a “missense” mutation where a particular amino acid in a protein has been replaced with a different amino acid that reduces its function) was selected for during long sea voyages, where starvation and hypothermia weeded out individuals who had been less effective at storing and/or holding onto fat.

These genes are not destiny

Stephen McGarvey, the senior author, was quick to point out in all his interviews that this genetic evidence doesn’t mean that such genetics destine Pasifika people to be obese independently of environment, that is, diet, lifestyle, and exercise. (Though the study only looked at Samoa, it is almost certain that the gene will be found to be similarly common in other Pasifika populations). It is unlikely that the va’a tele or waka that carried the Polynesian explorers round the Pacific basin carried any obese individuals even when they set out; the stored energy advantage that the gene variant gave in these times was probably a few Kg and barely noticeable. If we look online for historical photographs of Samoa, we find that Samoa has a rich political history – it was the meeting place of the German, British, and U.S. Empires in the late 19th century – which resulted in much photographic documentation. But even as recently as 1930, during the period of the Mau independence movement, there is no evidence of obesity in photos.
These are pupils of Vaipouli school, a Samoan secondary school, ca 1930.


And these (photo at top) are leaders of the Mau movement at the same time.


Regardless of genetics, indigenous populations rarely if ever experience obesity eating their traditional diets, and always experience a high rate of obesity and/or diabetes, as well as the other diseases of Western civilisation (tooth decay, heart disease, cancer, appendicitis), after transitioning to Western processed and refined foods – foods with a high Human Interference (HI) factor. Traditional Samoan staple foods are taro and coconut, breadfruit and banana, turtle, pork and fish; this is never a question of fat vs carbs, or of saturated fat vs unsaturated fat, nor even of fructose vs glucose (the Ti root prepared in much of polynesia is very high in fructose) – it’s a question of natural foods with their fibre, micronutrients, fats and protein intact, vs refined starch, sugar, and refined oils, including the soybean oil used to pack canned fish in the case of Polynesia.[1]

Obesity prevents diabetes? Come again?

A really interesting finding from this study from our point of view is that the “obesity” gene variant is strongly protective against type 2 diabetes.

Higher BMI and adiposity are usually associated with greater insulin resistance (higher fasting insulin levels and homeostatic model assessment–insulin resistance (HOMA-IR)), an atherogenic lipid profile (especially higher serum triglyceride and lower HDL cholesterol levels), and lower adiponectin levels. We therefore expected the BMI-increasing A allele of rs373863828 to also be associated with these metabolic variables. However, even though the A allele was consistently associated with higher BMI and adiposity in both the discovery and replication cohorts, the expected associations with the above obesity-related comorbidities were not observed and, in some cases, were even in the opposite direction to that expected (Table 2 and Supplementary Table 2).
Notably, when considering all subjects, the risk of diabetes was actually lower (OR = 0.586 for the discovery cohort, P = 6.68 × 10−9) or trended lower (0.742 for the replication cohorts, P = 0.029) in carriers of the A allele. Likewise, even in non-diabetic subjects, the variant was associated with moderately but significantly lower fasting glucose levels in both the discovery and replication cohorts (1.65 mg/dl (P = 9.5 × 10−5) and 1.54 mg/dl (P = 8.8 × 10−4) lower for each copy of the A allele, respectively). These effects became even more significant after adjusting for BMI (2.25 mg/dl, P = 6.9 × 10−8 and 2.09 mg/dl, P = 7.6 × 10−6), suggesting an independent effect of the variant on glucose homeostasis and diabetes risk.

How can this be? Obesity is associated with, and plausibly causal in, diabetes, yet a gene variant that increases obesity halves the rate of diabetes?
This is in fact strongly supportive of the ectopic fat hypothesis of diabetes causation, and the personal fat threshold hypothesis of Professor Roy Taylor of Newcastle Diet fame.

“We hypothesize that each individual has a personal fat threshold (PFT) which, if exceeded, makes likely the development of T2DM. Subsequent weight loss to take the individual below their level of susceptibility should allow return to normal glucose control. Crucially, the hypothesized PFT is independent of BMI.”[2]

“A key reason for the greater increase in diabetes risk per unit increase in BMI in South Asians compared with Europeans may be due to a reduced capacity in South Asians to store fat in the primary superficial subcutaneous adipose tissue compartment, leading to earlier `overflow’ into secondary deep subcutaneous and visceral fat compartments, and potentially the liver.” [3]


(Professor Taylor’s research also pinpoints the pancreas as a target for this “overflow”).
Imagine the body as a house in which rainwater (energy stored as fat) is collected in a tank; if the water is not used, and the tank fills, the water will overflow into the walls and floors of the house; the house will be at risk of rotting and the electrics might short out. The larger the tank, the less risk of damage there will be in a downpour. But no matter how big the tank, the house can still be damaged if it fills to overflowing. This tank is the capacity to store energy (fat, and the fat produced from carbohydrate) subcutaneously (in the folds of fatty tissue under the skin).
So it is not a paradox that while weight gain increases the risk of type 2 diabetes, some of the people who are most prone to obesity for genetic reasons will have a lower risk of type 2 diabetes at a given BMI.

Take-home messages:

1) about 1 in 4 people in Samoa, and possibly similar numbers in other Pacific populations, have a variant gene that makes it easier to store fat and become obese. This strengthens the “thrifty gene” hypothesis of obesity, at least with regard to these populations.

2) This gene is also associated with a significantly reduced risk of diabetes, a fact which strengthens the “ectopic fat” and “personal fat threshold” hypotheses of type 2 diabetes.

3) Variant genes or their lack did not result in obesity or diabetes in Samoan populations living their traditional lifestyles and eating their traditional diets of unrefined, nutritious animal and vegetable foods. Western processed foods and refined high-energy ingredients have been a disaster for these peoples. This strengthens the “gene – environment mismatch” theory of modern diseases, and the Paleolithic diet hypothesis.


[1] Behavioral risk factors for obesity during health transition in Vanuatu, South Pacific.
Kelsey Needham Dancause, Miguel Vilar, Michelle Wilson, Laura E Soloway, Christa DeHuff, Chim Chan, Len Tarivonda, Ralph Regenvanu, Akira Kaneko, J Koji Lum, and Ralph M Garruto. Obesity (Silver Spring). 2013 Jan; 21(1): E98–E104. (full-text link)

[2] Normal weight individuals who develop Type 2 diabetes: the personal fat threshold. Roy Taylor, Rury R. Holman. Clinical Science Apr 01, 2015, 128 (7) 405-410; DOI: 10.1042/CS20140553

[3] Type 2 diabetes as a disease of ectopic fat?
Naveed Sattar and Jason MR Gill. BMC Medicine 2014:12(123) (full-text link)

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.


The timing of carbs in meals makes a diference!



The spirit of science is not merely faith in the power of reason; it is also a belief that our problems may be simpler than they appear to be.

– Colin Wilson, The Strength to Dream

This recent pilot study is an example of good science for two reasons – it suggests that a minor change in behaviour can be a shortcut to important health benefits, and it raises more questions than it answers.

Alpana P. Shukla, Radu G. Iliescu, Catherine E. Thomas, and Louis J. Aronne.
Diabetes Care 2015;38:e98–e99 | DOI: 10.2337/dc15-0429

The authors looked at the effect of food order, using a typical Western meal (628 kcal:
55 g protein, 68 g carbohydrate, and 16 g fat), incorporating vegetables, protein, and carbohydrate, on postprandial glucose and insulin excursions in overweight/obese adults with type 2 diabetes. There were only 11 subjects (5 male, 6 female), which is why it’s a pilot study; the numbers were small, so any effect, to be statistically significant, actually had to be clinically significant too. But these people could be exceptions, the effect of metformin may be necessary for the response, it might vary when different foods are eaten, the effect might not be seen with larger meals, or in free-living populations, and the long-term effect on fasting glucose and insulin wasn’t investigated; so it’s a “proof of concept” type of experiment that tells us, loud and clear, that further investigations are certainly warranted.

The study was a cross-over design, meaning that both meal orders were tested in all subjects, a week apart. The meals were made up of ciabatta bread and orange juice (the carbohydrate part) and a chicken salad with low fat vinaigrette, plus broccoli and butter (the vegetable and protein part) and these two parts were eaten, separated by 15 minutes, in 2 different orders. Insulin and glucose were measured just before the meal and at 30, 60, and 120 minutes after the start of the meal.

When the vegetable and protein part of the meal was consumed first, mean postmeal glucose levels were decreased by 28.6%, 36.7%, and 16.8% at 30, 60, and 120 min, respectively, and the incremental area under the curve (iAUC) was 73% lower. Postprandial insulin levels at 60 and 120 min and the insulin iAUC were also significantly lower when protein and vegetables were consumed first.

Meal Order

The authors commented that “the magnitude of the effect of food order on glucose levels is comparable to that observed with pharmacological agents that preferentially target postprandial glucose. Moreover, the reduced insulin excursions observed in this experimental setting suggest that this meal pattern may improve insulin sensitivity.”

How can this be? The same food was eaten, and 15 minutes is not a very long time; it’s a sedate meal, but not a long-drawn out one.

No mechanism is offered in the paper, but we would like to suggest one. After a meal, and especially in people with type 2 diabetes, glucose does not only appear from the food eaten. Glucose is released from glycogen (the liver’s carbohydrate stores) in the fasting state, and this appearance of glucose may continue or even increase after eating carbohydrate, likely because of the post-prandial spike in glucagon, which is released from cells in the gut, as we described in an earlier post. This rise in glucagon in people with type 2 diabetes following carbohydrate consumption has not always been seen experimentally, but it appears as a significant effect in most studies, especially when carbohydrate is fed in a meal; it can clearly be seen here, where the diet is 55% carbohydrate (designed according to AHA and USDA Dietary Guideline recommendations, and represented by the circles – the triangles represent the baseline American diet, which had almost identical effects).
Nuttal 2004 HiCHO glucagon
(from Effect of a High-Protein, Low-Carbohydrate Diet on Blood Glucose Control in People With Type 2 Diabetes. Mary C. Gannon and Frank Q. Nuttall. Diabetes 53:2375, 2004

(This study also says “We and others also have reported that even short-term starvation (hours) results in a dramatic decrease in the blood glucose concentration in people with type 2 diabetes. This seems to be due largely to a rapid, progressive decrease in the rate of glycogenolysis.” Even when you’re fasting, glycogen release slows down once insulin drops and you start burning more fat.)

We suggest that feeding the vegetable and protein part of the meal first blunts the glucagon response to the carbohydrate portion. There could be multiple reasons for this – a delayed appearance of glucose in the gut, or the pre-emptive ability of the insulin, somatostatin 28, and incretins released in response to the protein part of the meal to suppress glucagon release, resulting in lower insulin release overall, because there is both less glucose from glycogenolysis and less glucagon, both of which require extra insulin.
This is only one possible explanation – we’d like to hear others – and verifying or refuting it will take (among other things) accurate measurement of glucagon and other peptides at many time points over the immediate post-prandial period, which is not easy.

Why might eating carbohydrate trigger the release of glucose from glycogen in some circumstances?

Imagine our early human ancestors; they didn’t eat all the time, and sources of dense and easily digestible carbohydrates were rare in some environments. It’s likely that these hominids adapted to hoard glycogen, saving it for an emergency, like sprinting from Pachycrocuta, the giant prehistoric hyena that hunted Homo erectus. And this meant that glucose, which can be used to fuel growth, and to store fat, glucose which we take for granted today, was usually restricted. In this context it made sense if, as soon as an appreciable amount of glucose was detected in the gut, some extra glucose from the glycogen store was released into the blood as well; this extra could be used wisely, and replaced later – the analogy is dipping into your savings for something special when you know there’s going to be lots of money coming in, then being a lot tighter in between paydays.
This (if it’s true) would be the adaptive system, and work when appropriate; and type 2 diabetes, by definition, means that adaptive systems of blood glucose control have become dysregulated and are poorly controlled. It’s a model that does help to explain why fasting and low carb diets can help to bring post-prandial glucose under control, but it’s a highly conjectural one, a “just-so story”.

Takeaways –

  • post-meal release of glucose from glycogen can make an important contribution to post-prandial blood glucose spikes
  • post-meal glycogen release can be triggered by eating carbohydrate
  • very low carb diets and fasting cause the body to conserve glycogen
  •  in this study, eating the carbohydrate portion 15 minutes after the protein and vegetable portion in a high-carbohydrate meal resulted in significantly lower post-prandial glucose and insulin spikes

We note that the carbohydrate timing study of Shukla et al. was “supported by the Clinical and Translational Science Center at Weill Cornell Medical College (UL1 TR000457) and the Dr.Robert C. and Veronica Atkins Curriculum in Metabolic Disease at Weill Cornell Medical College Grant” and that Dr David Ludwig, who was not an author, is thanked for helping to formulate the study hypothesis.

The new BMJ review of high cholesterol and mortality in the elderly


High cholesterol ‘does not cause heart disease’ new research finds, so treating with statins a ‘waste of time’ – or at least that’s the headline in the UK papers following the Just published paper in the BMJ . This, the latest study to question the established view that high cholesterol is always a bad thing, looked at the relationship between serum LDL-cholesterol and mortality in observational studies of people aged 60 and older

“We identified 19 cohort studies including 30 cohorts with a total of 68 094 elderly people, where all-cause mortality was recorded in 28 cohorts and CV mortality in 9 cohorts. Inverse association between all-cause mortality and LDL-C was seen in 16 cohorts (in 14 with statistical significance) representing 92% of the number of participants, where this association was recorded. In the rest, no association was found. In two cohorts, CV mortality was highest in the lowest LDL-C quartile and with statistical significance; in seven cohorts, no association was found.”[1]

In other words, in free-living populations without pre-existing disease, higher LDL-cholesterol predicts a lower risk of death in those over 60, and (with more limited evidence) does not predict an increased risk of death from heart disease or stroke.

This has been known for a long time – this review, which collated these studies for the first time, should not have been controversial. To be more exact, it has been known for a long time that higher levels of total cholesterol are protective in the elderly, and this knowledge predates the use of statins (which, if they are given to elderly with high cholesterol, and do prevent heart attacks, have been proposed as a confounder). Data about LDL-cholesterol levels in the elderly is more recent in most cases, and that is specifically what this review investigates.

The results are not just academic; old people are medicated, and are fed poorly in rest homes and hospitals, on the premise that high cholesterol is bad for them and everything must be done to lower it if it is high. As Professor R.D. Feinman says, “remind me again why we have a medical literature?” – because it’s obviously not there so that anyone can learn from it!

The latest review was published in the UK. Meanwhile the reigning monarch, Queen Elizabeth II, now 90 years old, remains healthy and hard-working on a completely different diet to that recommended and fed to her elderly subjects. She likes her food cooked in butter and cream, eats meat regularly, and skips the carbs.


Her Majesty knows what’s good for her – LCHF!

Criticisms of the study

So, how solid is the latest review? Are there other explanations for the correlations, or lack thereof? The Committee for Evidence Based Medicine launched an attack on Ravnskov et al’s review when it was published, in the form of a post-publication peer review. This is worth reading as it gives insights into possible confounders and errors in interpretation.
Yet it does not really disagree with the evidence or refute or overturn the conclusions.
The main issues are:

Limitations of the study: the search was restricted by being limited to PubMed and English-language publications.

Our response: PubMed is a large data resource, and as can be seen the search turned up many relevant studies. It is not usual to include foreign-language papers in, for example, Cochrane collaboration meta-analyses. The search also retrieved the references from the papers found, a process which would have turned up most of the relevant papers stored outside the PubMed archive.

The limitations of the review are probably related to the limited resources available for research which is merely a matter of public interest.

HDL cholesterol: “only three out of the 19 included studies appear to have controlled for HDL-C level in their analyses. It is highly possible that the observed inverse association for LDL-C and mortality is entirely mediated by a high HDL-C in the included cohorts.”

Our response: the 3 papers that controlled for HDL all found that high LDL-C was significantly associated with reduced mortality.

Statins: “The issue is that those who have high LDL-C are much more likely to be prescribed statins during the period of observation than the low LDL-C group. This would lead to an overall protective effect in the group with high LDL-C, making it appear that LDL-C is correlated with reduced all-cause mortality, when, in fact, it may be the effect of statin therapy.”

Our response: observational studies showing a protective effect of high cholesterol in the elderly date from before the statin era. Statins are expected to reduce cardiovascular mortality; there is no evidence from RCTs that they reduce death from other causes. It is total mortality, not cardiovascular mortality that is most strongly negatively associated with serum LDL-C in this review.  Of the three studies we found in Ravnskov et al. that controlled for statin use, two found a strong protective effect of higher LDL-C and one found no association, a pattern typical of the review as a whole.

Data extraction errors: The reviewers identified a small number of data extraction errors. Unfortunately these are common occurrences; almost all the diet-heart meta-analyses, for example, contain such errors. Hopefully the errors in this review can be corrected. However, using the correct figures does not alter the conclusions of the review.

The CEBM review asks us to reject the conclusions of Ravnskov et al, but fails to supply alternative evidence to support a different conclusion.

More insight:

We pulled up at random one of the studies used in Ravnskov et al’s review to see whether it gives more insight into lipids and risk. This study followed people 50+, so may be of interest to more readers.[2]

Bathum L, Depont Christensenc RD, Engers L et al. Association of lipoprotein levels with mortality in subjects aged 50 + without previous diabetes or cardiovascular disease: A population-based register study. Scandinavian Journal of Primary Health Care. Volume 31, Issue 3, 2013. full-text:  DOI:10.3109/02813432.2013.824157

Objective. This study aimed to investigate the association of lipoprotein and triglyceride levels with all-cause mortality in a population free from diabetes and cardiovascular disease (CVD) at baseline. The European Guidelines on cardiovascular disease prevention state that in general total cholesterol (TC) should be < 5 mmol/L (190 mg/dL) and low-density lipoprotein cholesterol (LDL-C) should be < 3 mmol/L (115 mg/dL).

Design. A population-based register study in the period 1999–2007 including 118 160 subjects aged 50 + without statin use at baseline. All-cause mortality was related to lipoprotein and triglyceride levels and adjusted for statin use after inclusion.

Results. All-cause mortality was lower in the groups with TC or LDL-C above the recommended levels. Compared with subjects with TC < 5 mmol/L, adjusted hazard ratios for the group aged 60–70 years ranged from 0.68 (95% confidence interval (CI) 0.61–0.77) for TC 5–5.99 mmol/L to 0.67 (95% CI 0.59–0.75) for TC 6–7.99 mmol/L and 1.02 (95% CI 0.68–1.53) for TC ≥ 8 mmol/L in males and from 0.57 (95% CI 0.48–0.67) to 0.59 (95% CI 0.50–0.68) and 1.02 (95% CI: 0.77–1.37) in females. For triglycerides, ratios compared with the group < 1 mmol/L in the females aged 60–70 years ranged from 1.04 (95% CI 0.88–1.23) to 1.35 (95% CI 1.10–1.66) and 1.25 (95% CI 1.05–1.48) for triglycerides 1–1.39 mmol/L, 1.4–1.69 mmol/L, and ≥ 1.7 mmol/L, respectively. Statin treatment after inclusion provided a survival benefit without correlation to cholesterol level.

Conclusion. These associations indicate that high lipoprotein levels do not seem to be definitely harmful in the general population. However, high triglyceride levels in females are associated with decreased survival.


In Bathum et al, higher LDL-cholesterol is associated with lower mortality in all age groups over 50.

Our comment: Bathum et al was a study of a Danish population, and the Danes have access to good quality dairy and other animal foods. Thus higher LDL-C, in as far as this has anything to do with diet, may mainly distinguish the well-fed from those subsisting on the ersatz concoctions of the budget food industry. Very high HDL was not protective in “younger” men, but this is something you mainly see in those drinking lots of alcohol. This research does not suggest that the lipid patterns associated with LCHF diets (low TG, high HDL, moderate or high LDL-C) will lead to an increased rate of mortality as people age (which is, of course, when most mortality occurs).

So in the end, we will go with the British headlines – yes High LDL cholesterol isn’t a problem in normal older people – unless it’s low! There are a group of epidemiologists, and nutrition scientists in New Zealand and around the world, who have based their whole career around the idea that high LDL cholesterol is a problem.  What do you have to say?

And, the queen got at least one thing right – low carb.


[1] Ravnskov U, Diamond DM, Hama R. Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review. BMJ Open 2016;6:e010401. full-text: doi:10.1136/bmjopen-2015-010401

[2] Bathum L, Depont Christensenc RD, Engers L et al. Association of lipoprotein levels with mortality in subjects aged 50 + without previous diabetes or cardiovascular disease: A population-based register study. Scandinavian Journal of Primary Health Care. Volume 31, Issue 3, 2013. full-text:  DOI:10.3109/02813432.2013.824157



UK charity comes out with LCHF Real Food Guidelines

A British charity called the National Obesity Forum, in association with the Public Health Coalition, is in the news today for attacking the low-fat dietary guidelines and food industry manipulation of science (in the UK known as the Eatwell Guide), and suggesting a way out of our growing public health crisis in this document. The Public Health Coalition earlier came out with LCHF guidelines for the prevention and control of obesity and diabetes, and with real food, healthy fat guidelines for the rest of the population. You can download this document, Healthy Eating Guidelines & Weight Loss Advice For The United Kingdom, here.

They’ve even created some cool graphics to counter Public Health England’s dire grain-based Eatwell Guide:


The National Obesity Forum/Public Health Collaboration report has had excellent coverage in the UK media, their recommendations are in all the major newspapers, news websites, and TV news programs.

This has stirred up the usual backlash from experts, many from the UK organizations that have sweetheart deals with the food industry.

For example,

Dr Tedstone of Public Health England responded to the publication by saying: “In the face of all the evidence, calling for people to eat more fat, cut out carbs and ignore calories is irresponsible.”

She said thousands of scientific studies were considered as part of the official guidance adopted throughout the UK, whereas the National Obesity Forum quoted just 43 studies, some of which were comment pieces.

She added: “It’s a risk to the nation’s health when potentially influential voices suggest people should eat a high fat diet, especially saturated fat. Too much saturated fat in the diet increases the risk of raised cholesterol, a route to heart disease and possible death.”

You get the picture. Let’s all get lost in the “totality of the evidence” and leave things as they are, with the Food Industry in charge of our diets in a token partnership with these expert bodies it sponsors.

So who are these irresponsible people at the Public Health Collaboration? They include GP David Unwin, who has published several papers about the effectiveness of LCHF in treating obesity, type 2 diabetes, and non-alcoholic fatty liver disease in his Southport practice. Dr Unwin’s practice has been reported as saving £45,000 per year on drugs for type 2 diabetes compared to the average in his area. (If you want a guide as to how to introduce the LCHF diet into clinical practice in an affordable, practical way, we recommend Dr Unwin’s work)
The PHC also includes cardiologist Aseem Malhotra, who promotes a low carb, high-fat Mediterranean diet as an effective way of managing coronary heart disease, plus a dietitian, a diabetologist and several more GPs. Of particular interest is the presence of a psychiatrist and psychologist, showing a holistic understanding of the importance of not only finding solutions, but motivating and helping people as individuals.


All these people have considerable experience between them, often working in deprived areas and with seriously ill patients; they are reporting back from the front lines in the war on diabesity and the health problems caused by poor nutrition, and it would be foolish not to take them seriously just because they have produced a short, readable document.

The PHC’s Healthy Eating Guidelines & Weight Loss Advice For The United Kingdom joins the ranks of Real Food Guidelines globally – including our own Real Food Guidelines from 2014, as well as the Brazilian dietary guidelines and the Canadian Government report on obesity.

It’s the Real Food Revolution and it’s not going to be won in a day, but when you get a group of well-qualified people leading by example and ignoring the nay-sayers to show that the LCHF approach works, as the members of the PHC are doing in Britain, it’s no longer just a battle of words. The public are impressed by results, rather than by hearing opinions, or by reading thousands of peer-reviewed papers. Which we still do, because reading peer-reviewed papers is necessary, useful, and often rewarding, but by golly it’s nice to see people helped by LCHF to a better life on TV, as in the recent Aussie TV show The Saving Australia Diet.

Let’s not diet like it’s 1999. How a Generation of nutritionists and dietitians was taught to make weight loss more difficult than it needs to be.

Diet advice is so varied today, and nutrition science is changing so fast, that it’s easy to forget how monolithic low-fat weight loss advice was only a few years ago.

We recently discovered a US nutrition textbook from 1999. This book has a good claim to represent the orthodoxy. It contains the views of multiple experts in the various areas of nutrition.


By far the bulk of the book is sound nutrition science, and still worth learning – but there are areas where it wanders away from science fact and stakes a position that seems questionable today.

It’s the section on Energy Balance and Weight Control that’s the real eye opener.

It’s very much about calories in vs calories out. Well, of course it is, but with the 1999 diet plan, food intake and activity level need to be focused on to a high degree.

“1. The plan should meet nutritional needs, except for energy. To do that, it should follow the Food Guide Pyramid, emphasizing low-fat and nonfat choices and adequate fluids (6-8 cups per day). Overall this controlled eating should remain a satisfying and pleasurable experience.”

[Note that this book does include mention of the novel 1994 Mediterranean Pyramid, but because it can supply more fat – 25-35% shock horror – and one or two full-fat dairy foods, weight gain is considered a possible risk, so it’s kept out of the Energy Balance section!)

“2. Slow and steady weight loss, rather than rapid weight loss, should be stressed. A loss of 1 or so pounds of fat storage per week is desirable. Once about 10% of excess weight is lost, maintenance of that loss for 6 months is recommended before more weight loss is attempted”

“Total fat intake for the day is the focus. This approach makes sense, because a lifelong restriction of energy intake is almost impossible, whereas a low-fat diet is easy to follow indefinitely if it allows consumption of enough foods – especially fruits, vegetables, and whole grains – to satisfy hunger. However, this method will only work if high-calorie fat-free foods – such as fat-free cakes and cookies – are not overeaten.”

What is the Food Guide Pyramid of 1999? In terms of the weight loss diet, it is 6 servings of bread, cereals, rice or pasta (serving = 1/2 cup or 1 slice), 2-4 servings of fruit, 3-5 servings of vegetables, 2-3 servings of nonfat or low-fat milk/dairy products (serving = 1 cup), and 4-6 oz lean meat or alternatives [this category includes dried beans, which might have been more usefully deployed as cereal alternatives]

Why so much carbohydrate over the more satiating fat (in an earlier section of “hard science” it is explained that chylomicrons are satiating)?

The reason given for preferring a high-carbohydrate diet is slightly gob-smacking today; because carbohydrate stimulates energy expenditure. This is the old metabolic advantage argument sometimes used by both sides of the carb vs fat debate..

The following are listed among “practices that can stimulate metabolism while dieting”.

  • “- Fidget when sitting and standing [Seriously? This seems pretty desperate! Try telling a person who fidgets NOT to fidget, and you’ll see how practical this advice is.]
  • – Eat breakfast, so food intake is spread throughout the day. Each time food is consumed, metabolism increases
  • – Follow a carbohydrate-rich diet; much of this is further processed by the liver, which uses energy.”

So the conversion of glucose to fat by the liver is one of the advantages of a high-carb diet, while the conversion of fat to ketones on low carb diets is a problem?

We know that the low-fat diet will produce weight loss in people who are satisfied enough by it, or have enough willpower, to restrict calories.
The problem is, what happens to people who become hungrier on such a diet, and what happens when such Food Pyramid diet advice is applied to the whole population without calorie restriction, and in the presence of sweet treat foods, in the belief that this will also help with energy balance and weight control? The frequent high-carbohydrate meals stimulate high insulin levels, and the processing of carbohydrate by the liver results in increased ectopic fat and insulin resistance, tending to promote increased fat storage and appetite and higher blood sugars.

Further, some forms of calorie restriction can produce a lasting drop in the metabolic rate, which then makes it hard to avoid regaining weight. This is why the low-fat diet plan has you eating all the time, losing weight slowly (if at all), and trying to fidget; to keep up the metabolism. But low carb diets, and plain fasting, don’t depress the metabolic rate. They don’t set you up to fail as the Biggest Loser diet, which is Eat Less, Move More taken to its (il)logical extreme, does. This is explained very neatly by Jason Fung in a recent post at Diet Doctor, using the evidence from 3 recent metabolic studies by Kevin Hall.
This is the real “metabolic advantage” of LCHF – not a boost to metabolism as once thought, but its protection.

The problem with the 1999 advice is not the low—fat diet as such, but the lack of respect for and serious scientific consideration of alternative ways of eating, which is explicable here by the predominating fear of animal fat and cholesterol, and the higher calorie-per-gram value of fats. The existence of an officially-sanctioned Food Guide Pyramid must also have tied the hands of textbook writers – if they presented a convincing case for an alternative, what publisher would take a risk on their work? Perspectives In Nutrition gives several pages for experts to debate, sometimes hotly, divergent views on undecided topical issues such as the use of vitamin E supplements, but fails to provide the diversity of expert opinion about weight control that surely (?) still existed in 1999. The failure to consider the role of insulin in the energy balance response to diet, and to look into the contradictions and controversies around diet, cholesterol and health, undermines all the good science and good intentions in this book and results in the building of a massive structure of difficult-to-follow advice on a shaky foundation. A whole generation of today’s nutritionists and dietitians were given no reasons to think that carbohydrate restriction might be a safe and useful strategy, and were, it seems, trained to dismiss it out of hand as a ‘fad diet’.

The one-size-fits-all low fat, high carbohydrate diet plan, which has now been shown to be, on average, less effective than just about anything else you could try, really did preside over nutrition teaching during the obesity epidemic, however much this might be denied today.

Yudkin NS

Yudkin’s experiments with prebiotics – from a 1961 profile in New Scientist

It is a relief to turn from the Energy Balance section of Perspectives in Nutrition to the sound sense of John Yudkin, writing in 1963.

“The ability to separate palatability from nutritional value leads to the consumption of increasing amounts of food, chiefly rich in carbohydrate, in circumstances in which one would have expected a reduction in the intake of carbohydrate [i.e. in periods of increased income, when one would reasonably expect intake of fat and protein to increase]. There is evidence that this distortion of the diet plays a part in the increased incidence of obesity and dental caries, and also perhaps in the increased incidence of myocardial infarction, peptic ulcer, diabetes, and other diseases.”

“Another consequence of the increase in food consumption and the decrease in physical activity can be seen in the rise of the number of obese children and adults. The thesis that food intake is high chiefly because of the high palatability of modern carbohydrate-containing foods is supported by the fact that very effective weight reduction follows simple omission from the diet of a large part of these foods, with unrestricted eating of carbohydrate-free foods such as meat, fish, eggs, cheese, butter, and cream. We have shown that, in this sort of diet, the reduction in caloric intake is associated with a negligible increase in protein intake, but no increase -sometimes a fall- in fat intake. It is sometimes supposed that obesity is usually caused by an uncontrollable desire to eat. The fact is that those who cannot keep to their carbohydrate-restricted diet have, rather, an uncontrollable desire to eat highly palatable sugar-containing foods, to which they have, it seems, become addicted.”

This was, although not the only advice available, a very well-accepted and uncontroversial explanation of obesity and weight loss in the 1960’s, as seen in part 3 of this public information film about childhood obesity.

A Cruel Kindness 1967

Part 1

Part 2

Part 3

People were not told to restrict fat or animal fats in the 1960’s. (The subjects in Yudkin’s studies ate about 100 grams of fat a day, both before and after restricting carbohydrate). Once animal fat in the diet was reduced by public decree, and carbohydrate intake increased, the numbers of those who were overweight increased. By 1999 the problem was recognised and great intellectual effort went into proposing solutions, but the simplest classical solution was overlooked, perhaps because the problem in 1999 seemed much more complex than it had in 1963 (or in 1825, when Brillat-Savarin first introduced the idea of the “fattening carbohydrate”), thanks in no small measure to Ancel Keys and the diet-heart hypothesis.

It became a case where “The weakness of the remedy lies in its simplicity”. The growth of the academic nutrition establishment after Ancel Keys’ huge success, and the need to keep that workforce employed, meant that arguments as simple as Yudkin’s became unwelcome, even if their basic truth could be demonstrated. In 1999, simple propositions were what defined quacks and fad diets. Yet complex instructions have a limited utility to the general public.

Surely, rather than always glamourising the complexity of science and the “multifactoral” nature of disease, it is a better approach to some public health problems to find the most true of the simple propositions, and make sure everyone knows them?




Will the Paleo diet increase heart disease again?

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Grant Schofield and George Henderson

On the same day that our low carb and diabetes paper was published in the New Zealand Medical Journal, a new analysis of the correlation between New Zealanders’ fat intakes and cholesterol levels from the public health epidemiology team at Otago University was published in the Australian and New Zealand Journal of Public Health.

Trends in serum total cholesterol and dietary fat intakes in New Zealand between 1989 and 2009.  Jody C. Miller, Claire Smith, Sheila M. Williams,  Jim I. Mann, Rachel C. BrownWinsome R. ParnellC. Murray Skeaff.
Aust NZ J Public Health. 2016; Online; doi: 10.1111/1753-6405.12504

It contains this passage:

Reduction in saturated fat, a key component of public health nutrition measures aimed at IHD risk reduction, has in the past been achieved as a result of near universal acceptance of the nutrient disease link and by collaboration among health and nutrition educators, regulators, the media, the public and food providers. This consensus has recently been threatened by a movement advocating benefits of a diet low in carbohydrate and high in fat, including saturated fat (e.g. the ‘paleo’ diet). Despite the questionable scientific basis for such a nutritional approach, it appears to have widespread appeal – to the extent that it has been shown to be associated with an increase in mean population cholesterol levels in some areas where uptake of the advice has been high.(42)

Reference 42 is a Swedish paper from 2012 showing that increased uptake of low carb diets and an increase in butter (and oil) sales and decrease in sales of “cooking margarine” has indeed been associated with an increase in cholesterol there.[1]

However, the Swedish data on heart disease shows that its incidence continues to decline (most recently in 2014). Indeed, heart attack (AMI) mortality in women had plateaued, and only began to decline again following the increase in butter sales around 2008. Going by the official Swedish health data, available here in an easy-to-search interactive database, there doesn’t seem to be anything to worry about.

But what about New Zealand? The new study compares fat intakes from dietary surveys taken in 1989 (n=1,618), 1997 (n=4,636), and 2008/2009 (n=4,721) with the mean non-fasting cholesterol levels in those populations.

So it only looks at fat, and no other dietary factor, and only looks at total cholesterol. Which is a marker even your doctor is unlikely to find very revealing these days. There is a supplementary table about HDL, which increased in young males, but not those 55 and over between 1997 and 2008/2009, and also increased in women of both age groups. But no news about triglycerides, ApoB, small dense LDL particles or any of the other atherogenic and protective factors we see in other studies about heart disease.

There’s also no mention of blood glucose and HbA1c. We know the incidence of diabetes and pre-diabetes, significant risk factors for heart disease, have increased in the study period. Does this correlate with the decrease in saturated fat intake and reduction in cholesterol? You bet it does, but you’re not going to find it mentioned here.

This narrow focus on confirming one belief about the causes of heart disease and ignoring other evidence in the same data set is a flaw in this study.

What did they find? A decrease in saturated fat intake from 15.9% of energy in 1989 to 13.1%E in 2008/2009 correlated with a decrease in cholesterol from 6.15 mmol/L in 1989 to 5.39 mmol/L in 2008/09, some of which was due to statin use by older New Zealanders.

miller 2

The paper states “Although some meta-analyses have not demonstrated a convincing reduction in cardiovascular mortality and saturated fat when macronutrient substitution is ignored,(40) cardiovascular risk is reduced when saturated fat is replaced with polyunsaturated fat.(41)”

Their ref 41 is the Hooper et al 2015 meta-analysis showing a small reduction in combined CHD events (after statistical adjustment because there is no such effect for the raw data), but no reduction in heart attacks or cardiovascular or total mortality, when saturated fat is replaced with polyunsaturated fat in RCTs (the people told to eat less SFA in these RCTs were told to change their diets to be “healthier” in multiple ways,  including eating less refined grains and sugar, exercising more etc, so it’s not that great a test of the hypothesis, but anyway).[2]

So if there is such an effect, was saturated fat replaced with polyunsaturated fat in New Zealand? According to this study polyunsaturated fat intake as a % of energy declined in all groups between 1989 and 2008/2009.  The effect of replacing saturated fat with polyunsaturated fat is irrelevant for this paper – it just didn’t happen in New Zealand.

This means that New Zealanders replaced saturated fat with something else. Maybe protein, maybe starch, maybe sugar – none of this is in the paper.


How that is supposed to have reduced heart disease we don’t know.

All the reduction in saturated fat intake in this study is from people eating less dairy – less butter, whole milk, and cheese. Of course, these are the very foods associated with lower incidence of diabetes, and even lower rates of cardiovascular disease, in recent studies.[3,4,5].Under these circumstances – less fat, less saturated fat, and less polyunsaturated fat – it is hard to see how dietary factors can account for the increase in HDL between 1997 and 2008/2009. However, cigarette smoking decreased significantly between 1997 and 2008/2009 (though it actually rose a bit between 1989 and 1997) and smoking is associated with lower HDL (and, indeed, higher LDL), so this might be the explanation.[6]

There’s another contradiction at the heart of this evidence. We’ve been told often that prospective cohort epidemiological studies don’t show a link between saturated fat and heart disease because the range of saturated fat intakes in most populations is too small – everyone is exposed to too much saturated fat to see the benefit from reducing it, and people in RCTs don’t usually reduce it enough.

The old “you’re just not trying hard enough” argument!

However, in this study, the range of saturated fat intake is very small – from ~16%E in 1989 to ~13%E in 2008/2009 – still “well above internationally recommended ranges of intake” as the authors state. This is a fraction of the variation seen in cohort epidemiology – it’s like the difference between two quintiles in many studies. Yet, now we’re supposed to accept that this small variation has produced a major benefit, one which is not seen in real outcomes such as heart attacks when we compare people in larger populations whose saturated fat intakes differ much more for long periods of time [4] or indeed in RCTS where this is achieved.


If the evidence from New Zealand nutritional surveys is to be used meaningfully, it needs to be analysed for all trends for which data was collected, not just fat and cholesterol. You’ll never see the correlations you don’t look for.
One interesting finding from 2008/2009 was that reported caloric intake had decreased since 1997, from 2866 calories for men to 2479, while women’s reported caloric intake had declined from 1911 calories to 1815, though this last change wasn’t significant. Yet BMI continues to increase.

Miller 1997

This graph from the 1997 survey report by the same authors might still have some relevance.

The claim that if some people are now eating more saturated fat (but also more polyunsaturated fat from nuts, fish, lard, and olive oil) and less carbohydrate, and eating real foods instead of processed foods, because it improves their well-being, controls their weight, and improves their TG/HDL ratio and blood sugar, then this is therefore going to increase the risk of heart disease because of the prospect of a relatively small increase in total cholesterol in the population, needs a lot more evidence than is presented in this paper.

It’s certainly possible that there are people on the fringes of comprehension who might just use a paleo news item as an excuse to double up on their meat pie with coke. Just as there were many who bought into the high-sugar low-fat yoghurt craze, and still do.
It would be good if there weren’t conflicting messages out there, but it’s in the nature of science that hypotheses are easy to generate, but can be a lot harder to lay to rest.

This study has gone way beyond what the data say. In fact, they claim things their data do not say.  The data certainly say nothing about the possible benefits or harms of people eating paleo or LCHF.


[1] Johansson I, Nilsson LM, Stegmayr B, Boman K, Hallmans G, Winkvist A. Associations among 25-year trends in diet, cholesterol and BMI from 140,000 observations in men and women in Northern Sweden. Nutr J. 2012;11:40.

[2] Hoenselaar B. Letter to the Editor: Further response from Hoenselaar. Br J Nutr. 2012 Sep;108(5):939-42.

[3] Ericson, U, Hellstrand, S, Brunkwall, L, Schulz, C-A, Sonestedt, E, Wallström, P, et al. Food sources of fat may clarify the inconsistent role of dietary fat intake for incidence of type 2 diabetes. AJCN 2015;114.103010v1

[4] Praagman J, Beulens JWJ, Alssema M, et al. The association between dietary saturated fatty acids and ischemic heart disease depends on the type and source of fatty acid in the European Prospective Investigation into Cancer and Nutrition–Netherlands cohort.
Am J Clin Nutr ajcn122671

[5] Mohammad Y. Yakoob, Peilin Shi, Walter C. Willett, Kathryn M. Rexrode, Hannia Campos, E. John Orav, Frank B. Hu, Dariush Mozaffarian. Circulating Biomarkers of Dairy Fat and Risk of Incident Diabetes Mellitus Among US Men and Women in Two Large Prospective Cohorts. Circulation AHA.115.018410
Published online before print March 22, 2016

[6] He BM, Zhao SP, Peng ZY. Effects of cigarette smoking on HDL quantity and function: Implications for atherosclerosis. J Cell Biochem. 2013 Jul 15.