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

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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 stuff.co.nz 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.

Awkward? Food blogger calls me “socially awkward”!

Me, Grant Schofield standing up for the high fat diet and good science
Me, Grant Schofield standing up for the high fat diet and good science

How is one supposed to feel?  Good, I think as friend, food blogger, and academic Dr Mikki Williden wrote a blog about me and others.  Read here.

Of note:

  1. She stands up for me, and the fact that challenging conventional nutrition science is worthwhile.  Thanks, as frankly I have hardly impressed the public health people I usually interact with in New Zealand.  They mostly assume I am either mad, stupid, ignorant or a combination of the three.  I, of course, think I’m on the right track.  And now at least Mikki does.  TICK
  2. She describes me as “He’s a strange mix of charismatic and socially awkward – which are not uncommon character traits for an academic“. I was giving this a big tick on the basis of the charismatic bit, but socially awkward – who knew?  I asked a few people about this, and pretty everyone except the ones I regard myself as socially awkward agreed and said that everyone knows this!  Oh well, that’s that.
  3. She writes “While he hasn’t devoted his entire academic life to studying the area, what I don’t think people realise is that Grant has literally spent the last year living and breathing the literature around insulin, carbohydrates and health (as anyone within earshot of him over this time can attest to). I would conservatively estimate he has crammed the same amount of information in that time that would take another person five years to learn.”  TICK and thanks for that.  You have to do your reading, its as simple as that.  I’m more impressed by Catherine Crofts my doctoral student who has read probably 1500 research papers in the last several months.
  4. Most importantly. she writes this which I really really like and agree with “He’s not always right – far from it, and he’s the first to say he is wrong when he is wrong. And his belief that the foundation of what we’ve hung our hat on in terms of health is flawed makes for some uncomfortable conversations. But, without people like Grant, we would not be having the conversations to begin with. In terms of public health I think we should be questioning – particularly with the health problems that most western nations suffer from today. And hopefully, instead of dismissing what he has to say as being uninformed, people will be doing their best to prove him wrong if they truly believe that what he has to say is inaccurate and misleading.

That last one is just so important, and as I have talked more and more about human metabolism and how our conventional dietary approaches have little scientific basis for the most afflicted – the obese and the diabetic – I have copped a bit (a lot?) of criticism.  But I not yet seeing is the compelling arguments from these public health (scientists).  Just criticisms.

Thanks Mikki for raising the attention to the cause of good nutrition and metabolic science.  We want good science and good debate.  I’m up for that.

Hopefully it won’t be too awkward!

 

 

What if I ate less?

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What would happen if I ate less?  Here’s a theoretical question from a reader.  I’ve been mulling it over as it is really fundamental to what I am talking about. Here’s the question:

Professor Schofield, I have a situation for you and I would love to hear how you respond.

Given three identical 100-kg individuals (assume they are a model of a human that experiences no natural desires or whims to suppress or appease) who all burn kilocalories at a rate of exactly 2500 per day. Assigning letters ‘A’, ‘B’ and ‘C’ to these individuals.
‘A’ consumes exactly 2000-kcal per day eating nothing but candy.
‘B’ consumes exactly 2000-kcal per day eating nothing but vegetables.
‘C’ consumes exactly 2000-kcal per day eating nothing but meats.
How are the bodies of ‘A’, ‘B’, and ‘C’ going to change in 60-days?

I have read many of the points made on this blog that a calorie is not a calorie and I also understand that all three of the above diets are pretty unrealistic; however, my math background wants to align myself with the law of the conservation of energy and say that they would all lose approximately the same amount of weight.

Your response is appreciated.

OK here’s what I think would happen, and there is some evidence around this, although as usual, more metabolic wards studies would confirm it.

What happens in the eating vegetables only and eating meat only feeding regimes probably depends a little on the exact composition of the meals and the insulin sensitivity of the individual.  But I would say that for both of these regimes, it is almost certain they will lose significant weight, and stay mostly healthy.  It is possible that a vegetable diet of almost exclusively starches and frequent meals, combined with someone who is highly insulin resistant, would result in constantly elevated insulin. This of course would result in some metabolic dysregulation, where energy expenditure is down regulated and insulin shunts some carbs into fat through de novo lipogenesis. I think this is unlikely to be what a vegetable only diet would look like.  It’s most likely that they will just lost weight.  They might not be that satisfied with their food, but all should be OK at least in the short term. In the longer term, B12, essential fatty acids, and amino acid deficiencies from vegetarianism should be considered.

Overall predictions for:

  1. Meat only diet – good weight loss, good energy, reasonable regulation of energy expenditure.  Need vegetables in the longer term for fiber and other micronutrients.
  2. Vegetable only diet – weight loss, although not as great as the meat only diet.  Some down regulation in energy expenditure depending on the metabolic health of the individual and the amount of starch eaten.  Not recommended long term because of lack of essential nutrients.

Now what we really want to consider is this one.  Someone eats just candy for six weeks. They are eating less than their daily energy requirements, so given you can’t defeat the first law of thermodynamics, then the weight loss should be predictable?

Not so fast I say.  I predict a few things will happen and the extent of this will depend on the metabolic health and the individual’s susceptibility to metabolic dysregulation.  This will depend on genes, age, and metabolic history.

So for the most insulin resistant person, a candy only diet will provoke constant hyperinsulinemia.  That is to say insulin, the fat storage hormone, will constantly be elevated. That means:

  • Fat burning is switched off
  • Carbs and fat are stored as fat
  • Energy expenditure is down regulated
  • Insulin probably blocks leptin, so they still feel constantly hungry

These factors can at least theoretically conspire to reduce energy expenditure and preferentially partition energy into fat. As time goes by, the sugar and fat combination in candy makes the insulin resistance and general metabolic dysfunction worse and worse.

My prediction is that it is possible to gain fat mass and therefore weight even on a calorie restricted diet because of the dysregulation that sugar provokes.

A good example of this in action is the OB OB mouse model. These are animals bred to be leptin deficient. That means they cannot send or receive a signal from the fat cells to down regulate hunger and to increase physical activity. That’s really the model which has shown us that leptin changes energy out and partitions energy into fat at the expense of other uses.

The thing is in humans, obese people become leptin resistant, which is a similar outcome to being leptin deficient.  Either way the brain can’t see leptin and down-regulate hunger and start expending not storing energy.

High insulin and the inflammatory pathways through sugar and so forth are highly implicated in leptin resistance.

In other words, I am saying that sometimes it is at least theoretically possible to eat a lot less and still get fat. The OB OB mouse eating exactly the same food as a normal leptin producing mouse gets obese, while the normal mouse stays lean. The OB OB mouse stops moving and stores a higher amount of food as fat.  When the OB OB mouse gets leptin injections it moves more and gets leaner.  The leptin injections have no effect on the lean mouse.

The solution? Stay off the junk carbs.

The cause of obesity – opportunistic voracity?

ObesityOK, here’s some real evidence of why the science of nutrition and metabolism is in such a mess. It’s an email discussion between myself and Professor Boyd Swinburn about the role of insulin and other metabolic factors in overweight and obesity, including weight loss.
It gets scientific and technical in places, but I think it’s an interesting debate to have. It’s also long (3000 words..).
The reality is, we both (Boyd and I) want the same thing – a healthier and happier population – but differences in our beliefs around the underlying causes of the problem make a big difference to how we approach the solutions.
Boyd argues that the reason we are so fat is because we are in a “hypercaloric environment”. There’s just too much food laying around, the exact type (carbs, fat etc) doesn’t matter. That drives “opportunistic voracity” (great words!). That means that there’s heaps of food around and we just gobble up too many calories. Metabolic partitioning and macronutrient intake has very little to do with it, although in Boyd’s words “the science of the particular dangers of saturated fat is long since settled”. He is not only adamant, but convincing and speaks strongly about exactly this.
His argument is a calorie is a calorie. My argument is that this isn’t the case at all. Human energy metabolism is controlled by hormones, specifically insulin and leptin as the main drivers. These are affected by several factors, a main one is dietary carbs.
Boyd is a highly accomplished academic in public heath obesity work. He also has a background in metabolism as you will see. He’s an MD and Professor of Population Nutrition and Global Health at the University of Auckland AND is the Alfred Deakin Professor, and Co-Director of the WHO Collaborating Centre for Obesity Prevention at Deakin University in Melbourne.
I also asked Prof Tim Noakes (Professor of Exercise and Sports Science at the University of Cape Town, and well known in the new nutrition paradigm) to have a read and see what he made of the debate.
It all started with a discussion on a flight to Rotorua about insulin and weight. Boyd pointed me to a couple of papers he authored in the 1990s where they looked at the metabolic state of weight gainers in Pima Indians. These were detailed metabolic studies. See this description of how the most insulin resistant Pima Indians gained the least weight (counter intuitive to what I would argue). The trouble is that the cross sectional and the (uncontrolled) longitudinal findings are completely opposite to each other.
At baseline, the most obese people tended to have high absolute resting metabolic rate, low RQ (high amount of fat oxidation), and insulin resistance. After 3 years, the ones who put on the most weight were the highest carb burners (higher RQ), had the lowest resting metabolic rate, and were the most insulin sensitive.
Note: RQ (Respiratory Quotient measures how much fat you burn for fuel v how much carbohydrate you burn. Low RQ=fat burner, high RQ=carb burner
So what do you make of all of this, and why should anyone care?
Well, it is a very important metabolic argument about what happens in the body to dysregulate your homeostasis of energy balance and cause weight gain. I say that the food we eat drives subsequent fat storage or fat burning. Hunger and fullness from food depends on the interaction between the carbs, fat, and protein in the food and the person eating it. High carbs means less satiation, more overeating and more fat storage; less carbs results in the opposite.
Anyway, if you like a bit of hardcore science, here’s the discussion Boyd (BS) and I (GS) had. It gives you a feel for how far apart obesity researchers actually are on very important topics – like what causes us to get fat.
Opportunistic voracity or hormonal energy homeostasis?

To: Boyd Swinburn

Subject: Re: papers

GS=Grant Schofield, BS=Boyd Swinburn, GS=Gnant second response

GS: The debate then in the discussion [of your Pima Indian paper] isn’t around the fact that RQ is modifiable by macronutrient composition, but that fat mass drives RQ?

BS: I THINK RQ IS AFFECTED BY MANY THINGS AND ACUTELY OF COURSE IT IS THE NUTRIENT LOAD AND NUTRIENT MIX. CHRONICALLY, AS I REMEMBER, IT IS MAINLY ENERGY BALANCE AND FAT MASS

GS: Given that industrial food [or Std American] diets are moderate carb at least, many who eat them are hyperinsulinemic most of the day. What I am arguing is that RQ is mostly to a point which turns off lypolysis, most of the time. Fasting insulin may be a different story, but less important because of the continual high insulin from carb ingestion. Sugar probably provides a mechanism to increase insulin resistance further.

GS: I maintain that eating sufficiently low dietary carbs and high fat reduces RQ.

BS: YES SURE

GS: LCHF is known to be more effective for weight loss maintenance in free living trials ad lib, than calorie restricted low fat diets.

BS: GENERALLY, ALL DIETS WORK TO REDUCE WEIGHT IF THE RULES OF THE DIET ARE ABLE TO BE FOLLOWED AND IF FOLLOWED ARE HYPOCALORIC. ALL DIETS ALSO SHOW THE SAME RETURN TO PREVIOUS WEIGHT (METABOLIC BRAKES ON WEIGHT LOSS PLUS RETURN TO THE OBESOGENIC ENVIRONMENT AND OLD HABITS). THE ONLY ‘METABOLIC’ EFFECT THAT I AM CONVINCED OF IS THE EFFECT OF PROTEIN ON SATIATION.

YOU HAVE TO BE CAREFUL ABOUT IMPLYING METABOLIC MECHANISMS FROM AN EDUCATIONAL INTERVENTION, I THINK. THE STUDY THAT WAS INFLUENTIAL FOR ME WAS THE KENDALL STUDY OF 11 WEEKS OF SURREPTITIOUS HIGH FAT V HIGH CHO.

KENDALL AM J CLIN NUTR 1991 http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=2021123

GS: Here’s what these guys did and found “Thirteen females were randomly assigned to either a low-fat diet (20-25% of calories as fat) or a control diet (35-40% fat) for 11 weeks. After a 7-wk washout period, the conditions were reversed for another 11 weeks. Energy intake on the low-fat diet gradually increased by 0.092 kJ/wk, resulting in a total caloric compensation of 35% by the end of the 11-wk treatment period. This failure to compensate calorically on the low-fat diet resulted in a deficit of 1.22 kJ/d and a weight loss of 2.5 kg in 11 weeks, twice the amount of weight lost on the control diet. These results demonstrate that body weight can be lost merely by reducing the fat content of the diet without the need to voluntarily restrict food intake.”

Yes, caloric deficit and short term weight loss on a low fat diet is seen. Plenty of research on that. Yes, eventually most people return to previous weights, but this is in an environment which is overrun by dietary carbs and processed ones at that. The problem is over-exposure to food as you say it is the processed carbs that are the problem in the food though not the fat.

The Kendall paper pits a low fat diet against a moderate fat.moderate carb diet which is nothing to do with a LCHF diet.

Good points though about problems with diet and weight loss research. Educational lead programs – where we tell them what to do and some lose weight – is how much research is conducted. Of course, we don’t understand the metabolic effects of it clearly because people vary in their application and adherence. We could do more metabolic ward, respiratory chamber diet studies. We will never get the funding to do those in my country though, at least not through our Health Research Council, which funds a max of $1.2 million for a three year project, much of which is kept centrally by university administration as the salary overheads are 100%.

On the other hand, public health recommendations should be based on what people will do and find sustainable, so we do need to find the best weight loss and metabolic health programs people can actually follow. LCHF diets offer more promise than other regimes at this point. The 18+ RCTs to date show better weight loss, better cardio-metabolic parameter improvements, and better adherence wins in the short and medium term. I agree, long term outcomes are a problem for all diets, mostly because of the obesogenic environment. We all agree on that, but we don’t agree on what that actually is. I say it’s the processed carbs, you say its just food in general.

I’d also put forward a hypothesis that all diets work because they sufficiently lower serum insulin allowing lipolysis. You said I would lose weight on a hypocaloric high CHO/sugar diet in a previous conversation. Would I? I probably would as I am insulin sensitive. Would someone who isn’t?

GS: The hypothesis is that different macronutrient’s compositions have different metabolic effects, mainly through stimulating insulin more or less. Insulin directly affects RQ.

BS: INSULIN DOES ENORMOUSLY AFFECT RQ. MACRONUTRIENT COMPOSITION HAS A LOT OF DIFFERENTIAL METABOLIC EFFECTS ON LIPIDS AND HORMONES ETC. BUT FOR MACRONUTRIENT COMPOSITION TO AFFECT ENERGY BALANCE, IT NEEDS TO AFFECT EI OR EE – THE FACT THAT IT AFFECTS FFA FLUX, RQ ETC IS NOT GOOD ENOUGH. THERE ARE CLEAR MECHANISMS FOR HIGH FAT INCREASING EI THROUGH ENERGY DENSITY AND IT SLIPPING ‘UNDER THE ENERGY-BALANCE DETECTION RADAR’. ALSO, HIGH CHO DIETS FROM REAL FOODS ARE BULKY AND TEND TO REDUCE EI. IN ISOCALORIC STUDIES I DID IN METABOLIC WARDS IN OVERWEIGHT/OBESE PEOPLE, GETTING THEM TO FORCE DOWN ENOUGH FOOD ON A HIGH CHO (REAL FOOD, HIGH FIBRE) DIET TO KEEP THEM ISOCALORIC WAS HARD WORK.

GS: My understanding is that RQ has effects on lipolysis and fat storage. High RQ makes you store dietary carbs as fat and fat as fat if there is no high energy flux. All the research on the other clear mechanisms are in the context of a modern at least moderate carb diet. Using a LCHF approach, these mechanisms may not act the same way. In other words, when RQ is low because carbs are low you won’t store fat as easily, as the main mechanism isn’t activated. That’s the practical and experimental experience of people exposed to these (LCHF) regimes.

A couple of other points we discussed…

GS 1: Every low carb high fat trial [18 RCTs] shows favourable improvements in every CVD risk factor with big increases in saturated fat intake. That is not consistent with saturated fat being an important risk factor. There’s quite a bit published on this.

BS: IT HAS BEEN A WHILE SINCE I LOOKED AT ALL THIS STUFF. I UNDERSTAND THAT HIGH SIMPLE CHO HAS NEGATIVE EFFECTS ON TRIGLYCERIDES AND HDL AND THAT HIGH SAT FAT HAS A NEGATIVE EFFECT ON LDL. I BET THERE ARE A SERIOUS NUMBER OF META-ANALYSES OR POOLED ANALYSES ON THIS

GS: Yes the debate has moved on I think. All correct above, the fuller understanding of LDL particle size and number has increased our understanding of how this affects CVD risk. I’m not convinced that the saturated fat debate has done any public good and may have caused harm. There are prospective meta-analyses (see http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2824152) and experimental studies showing the lack of evidence for saturated fat harm.

You will be aware of the main mechanism identified in CVD and other metabolic disorders. It’s chronic inflammation. I contend that hyperinsulinemia is inflammatory. A high CHO diet is therefore inflammatory.

GS 2: The assumption that every calorie has the same metabolic effect I think should be under scrutiny.

BS: I DON’T THINK ANYONE SAYS THAT MACRONUTRIENT COMPOSITION DOES NOT INFLUENCE METABOLISM (IN ITS BROAD SENSE). THE QUESTION NEEDS TO BE TIGHTER – IF YOU ARE TALKING ABOUT ENERGY BALANCE AS THE METABOLIC EFFECT, THEN YOU NEED TO DO SURREPTITIOUS ALTERATIONS TO REMOVE THE COGNITIVE/KNOWLEDGE EFFECTS.

GS: This sounds like you are saying we can only feed people either liquid bland meals, or meals identical in look and feel but with different macronutrient compositions, before you would take the results seriously. Surely we overcome almost all of your problems with eating actual food using RCT protocols or, in my experience, subjects as their own controls in ABAC. Or crossover designs? Your method lacks validity of being actual food, which of course is what humans usually eat. It’s not translatable into public policy or anything else really.

You should also really have a look at a more recent paper out of your previous NIH lab using the same Pima Indians and others. They show how carb burners eat more and gain more weight than fat burners. See here.

GS: Different macronutrients affect humans differently and the magnitude of effects varies depending on total meal composition and genetic and metabolic history.

BS: THIS IS A DIFFERENT QUESTION AGAIN – WITH EVERYTHING THAT AFFECTS A GROUP AS A WHOLE THERE IS HETEROGENEITY IN RESPONSE. THIS HETEROGENEITY INTERESTS SOME PEOPLE AND THOSE ARE THEIR RESEARCH QUESTIONS? THIS IS VERY DIFFERENT FROM THE AVERAGE AFFECT ON A GROUP OR POPULATION

GS: We should be interested in how the responders and non-responders differ in experimental trials. After all, some people stay healthy metabolically on an industrial food diet and others suffer. What is it about those who suffer? That’s where the term carbohydrate intolerance came from and we should take that term and investigation of it seriously.

GS 3: Do you recall the paper regarding weight loss in low fat v high fat? I predict in advance, if indeed low fat had better weight loss, then the high fat was not low carb (i.e. at least under 100g per day, and hopefully under 50g CHO/day). If it was, I would have more serious food for thought. What we are talking about is reducing massively the area under the daily insulin curve.

BS: CHECK IT OUT ABOVE. INSULIN IS A GREAT HORMONE WITH ITS FINGERS IN SO MANY METABOLIC PIES, BUT I THINK TOO MANY PEOPLE ATTRIBUTE TOO MUCH TO IT IN RELATION TO ENERGY BALANCE. ONLY SMALL RISES IN INSULIN ARE ENOUGH TO TURN OFF LIPOLYSIS, MORE IS NEEDED TO TURN OFF GLUCONEOGENSIS, MORE FOR GLUCOSE TRANSPORT INTO THE CELL AND EVEN MORE FOR DE NOVO LIPOGENESIS.

I agree, the problem is most people on a high carb diet are hyperinsulinemic the whole day.

SORRY TO QUOTE ALL THIS OLD STUFF BUT SEE KEVIN ACHESON’S PAPER AM J CLIN NUTR 1987http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=3799507

GS: As I expected, the Kendall paper wasn’t LCHF so isn’t relevant. The Acheson paper shows that subjects had a highly insulinemic response to dextrose – obese and non-obese alike. They showed very little de novo lipogenesis, even with large carb loads. OK. But, insulin still dials down lipolysis and promotes fat storage. De novo lipogenesis might only be a minor part in this. But that doesn’t mean insulin doesn’t promote weight gain through modifying energy metabolism, storage, and output.

Look, when insulin is raised a bit you turn off lipolysis and you store any fat floating around. That is exactly what happens in the standard industrial moderate carb moderate fat diet. Sugar through fructose increases insulin resistance. Other inflammation sets in making the problem worse. Leptin gets blocked. Hyperinsulinemia ensues well before actual glucose control is evident. Weight gain is a downward spiral and you are permanently stuck in the seasonal metabolic weight storage situation humans are well designed for.

GS: Thanks for talking to me about this. I am thinking about this very carefully. In some ways, I would like you to be right then I can carry on with what my career has followed so far, which is mostly environmental determinants of physical activity and obesity. But if the alternative hypothesis turns out then we have to rethink obesity prevention and treatment. At least that’s my view. If macronutrients, namely dietary carbs, overwhelm our biological capacity to deal with them in loads way beyond that which our ancestors (and therefore we) were designed for, then we should think carefully about that.

BS: THE HYPERCALORIC FOOD ENVIRONMENT (WHICH INCLUDES A HELL OF A LOT OF SIMPLE CARBS FOR SURE) IS WHAT OVERWHELMS US IN MY VIEW – SUGAR, FAT AND SALT MAKE FOOD MUCH EASIER TO OVERCONSUME. I DON’T THINK WE NEED TO HYPOTHESIZE SUCH FINE GRAINED MACRONUTRIENT EFFECTS

GS: I think we all agree that the industrial food culture and environment is toxic. Your argument has been that it’s too much food laying around, period. I disagree. That certainly doesn’t help. But simply processed carbs, especially sugar, are the active ingredient in this. Yes, taste added with fat and salt heightens palatability and promotes fatness. This is because it’s the carbs that stimulate the fat to be stored not burned. There are obviously issues about seed oils, trans fats etc as well. This is especially so in inflammation. Microbiome issues in absorption, gut permeability and inflammation are all mechanisms that are likely to be involved. Current literature puts dietary carbs, especially sugar and wheat (also highly processed oils), at the top of the list of suspects here, not saturated fat.

Again have a look at a later paper from your previous lab showing just how carbohydrate balance affects weight gain through subsequent food intake.

GS: I understand you think it almost certain I’m wrong, but that’s science and it might just be true.

BS: A HELL OF A LOT HAS ALREADY BEEN DONE IN THIS SPACE BUT I AM NOT REALLY UP WITH THE PLAY – JUST STICKING TO OLD IDEAS

GS: I think we can easily both agree that nutritional science and metabolism isn’t fully understood yet. Where we seem to disagree is how that rolls into public health. I SAY WE NEED TO THINK MORE CAREFULLY BECAUSE CARBS AFFECT SOME PEOPLE VERY ADVERSELY. You say that it’s just the presence of food in general. There seems to be a gap there in what this will mean for the person on the street. I say we need to think about nutrient composition and how this affects different people.

GS: It wouldn’t be the first time science got something wrong. I’d also challenge you in the spirit of medical self experimentation to try a LCHF diet, with ad lib quantities, for three weeks. Control dietary carbs to 50g/day and judge your own metabolic changes. I did for sceptic reasons and decided it needed more investigation….just a thought.

BS: I THINK IF I PAID ATTENTION TO MY DIET IN REDUCING CARBS OR FAT OR ALCOHOL I WOULD BE BETTER OFF. IF YOU TAKE STUFF THAT REPRESENTS ABOUT 30 OR 40% OF OUR DIET (IE BREAD, PASTA, RICE, SPUDS, ROOT VEGE, BISCUITS, CAKES, PASTRIES ETC) THEN MY GUESS IS THAT I WOULD DEFINITELY LOSE WEIGHT AND I WOULD FEEL BETTER FOR HAVING DROPPED A FEW KG.

GS: Medicine has a long history of self experimentation. Are you remotely curious about the possible physiologies of carbs and how that might affect you personally? As well, I am saying remove these and replace them. I’m saying replace them with fat. It’s not deprivation and undereating. It’s tasty and fun. More importantly it sets humans into an energy homeostasis that allows control over eating. What I don’t think you are considering is that different dietary intakes affect satisfaction, satiation, and health in different ways because they affect energy homeostasis in different ways. LCHF is quite different and has a biological mechanism for being different to other diets. It also is not a fad diet as it is the only one based on evolution by natural selection as a principal of shaping our human genome’s response to different macronutrients.

BS: GREAT TALKING WITH YOU BUT I HAD BETTER GET OUT OF THIS ENJOYABLE STUFF AND GET BACK TO MY NHMRC REVIEWS

GS: Did you see the paper written about NHMRC writing and reviewing showing the cost to the Australian tax payer compared to the investment? Something like 600 person years spent grant writing alone in the last round!

Subsequent comment form Tim Noakes, after reading the correspondence

Hi Grant,

Just a very quick comment. You burn what you eat. This is where the alternate argument breaks down. Carb burners eat high carb diets. If they get fat it is because they eat too much carbs (carb addiction) and are insulin resistant. Place them on a high fat diet (by removing ALL addictive carbs) and they lose weight and become powerful fat burners. Problem solved.
Boyd needs to get into clinical practice. Once he sees it happen once, he will understand. My best case – 80kg lost in 7 months. New man but same “metabolism”. So what changed? Learned to control his carb addiction.
From the literature you can select anything you want to support your argument. But when you are in practice, the evidence is absolutely clear. The only people who don’t understand are those who have never tried it.
Will respond more fully in due course.
Warm regards,
Tim

Do diabetes specialists have learning resistance?

The healthy diabetes plate is a peer-reviewed “evidence based guidelines for healthy eating for Type 2 diabetics”.PCD41A12s01

Here’s my rant around what I consider to be a gaping hole in sensible logic.

Here’s the biological logic:

  1. You have become metabolically dysregulated. In mainstream medicine, your doctor will call you “insulin resistant”.
  2. That means your body is having difficulty getting glucose out of your blood stream into your cells.
  3. Your body still needs to get rid of this glucose, so your pancreas produces more insulin to get the glucose into the cells.
  4. Chronically high insulin makes you more insulin resistant, requiring you to produce more and more insulin. It gets worse and worse. Fat oxidation is turned off, and adipocyctes (fat cells) take up extra glucose and fat.
  5. No matter how much insulin you produce, you can’t move all the glucose into cells. Your blood glucose is high which damages the body irreparably.
  6. Sometimes, because of the stress of overproduction of insulin, the pancreas will have burnout in the beta cells which produce the insulin. Then you’ll need extra insulin, like a Type 1 diabetic.

Here’s your choice:

  1. Take mainstream diabetes treatment advice and follow their dietary guidelines (see above and below). That will be a low fat, moderate carb diet, where you should probably restrict calories. This will result in continued high blood glucose and insulin as you are eating quite a lot of carbs. Whole grains and beans are suggested as they are higher quality and absorbed more slowly. That just means high insulin the whole day for the insulin resistant person. I’ve written about the evidence for this previously.
  2. OR Here’s a novel idea…..or am I missing something here all you diabetes specialists and dieticians? RESTRICT YOUR DIETARY CARBS to very low amounts (<50g/day), eat more fat, and everything will improve. Here’s the outcomes when you do this.
    Just a thought. A glaringly obvious solution to the problem of being unable to tolerate carbs and move them into cells……don’t eat them!

    Take a look at the diabetes food pyramid below…..a low fat diet will be a high carb diet, even with high lean protein, because excess protein ends up being dealt with in exactly the same way as carbs. I contend the only way that a diet like this can work to help a diabetic is if somehow they have enough will power to semi-starve themselves into a very low calorie diet. That diet now works because it too is now a low carbohydrate diet. Why does mainstream medicine seem to be so resistant to even considering this possibility? Who’s right here? Do I have learning resistance, or do the current guidelines just make no sense in the light of the evidence? Insulin resistance or learning resistance?

    pyramid

TEDMED Peter Attia

Is the “obesity crisis” just a disguise for a deeper problem?

Dr Peter Attia’s TEDMED talk is out. He articulates very nicely, in good conservative medical speak, just what the alternative insulin resistance hypothesis is, and why we get fat and sick. The more detailed hypothesis I have covered in “Why some people stay skinny and others get fat.”  Well done Peter, we need to get this video out there, so please like it, pass on my blog, whatever to help with this.

Peter writes the blog eatingacademy and is President and Co-founder with Gary Taubes of the Nutrition Science Initiative (NUSI), who we will see way more often in the future. The non-profit has raised many millions now to fund state of the art nutrition research.

Full version here http://www.tedmed.com/talks/show?id=18029

Why some people must restrict carbs

Spot the difference
OK, I will start this by saying that this is a more academic piece about metabolic control in type 2 diabetics, and the ethics of feeding them low fat diets. It is a bit technical in places and deals directly with original research. Read on if you are interested!
The key message is that in my opinion, when you are insulin resistant, really the first option you should consider is restricting carbs. I hear a lot about “it’s the processed carbs, not the starchy veges that are the problem”, that “vegetarian and vegan approaches are good at reversing type 2 diabetes”, that “fibre solves everything” and so on.
Look, I agree that healthy humans can eat a wide variety of macro-nutrients that may contain plenty of carbs and nothing adverse will happen, but it’s likely that processed carbs will help metabolically well regulated healthy people into insulin resistance and a downward cycle of getting fatter and sicker. The mechanisms by which fructose (sucrose – table sugar is half fructose) work are being understood more clearly by modern science. The way fructose stirs up inflammation, blood lipids, liver fat deposition, addictive pathways in the mesolimbic system in the brain, and causes leptin resistance (the off switch hormone) are all important factors.
Once, or if, you become insulin resistant, I believe that macro-nutrient profiles are very important. Mainly, I am talking about restricting dietary carbs. Remember, if you are insulin resistant then you will have a problem getting dietary carbohydrate into your cells. The pancreas needs to produce more insulin to help do this. In the early stages of insulin resistance, all this means is you end up being hyperinsuliemic – having constantly high insulin – if you eat even moderate amounts of any dietary carbohydrate.
Hyperinsulinemia is known to have multiple direct and indirect effects on the body, making things significantly worse. Insulin is directly inflammatory. Insulin turns off fat oxidation and promotes fat storage and conversion of carbs into fat (de novo lipogenesis). Insulin probably blocks the hormone leptin in the brain (off switch not working again!). High insulin is directly implicated in many cancers, especially breast and prostate cancers. The list is growing all the time as we understand more about this essential hormone, which causes havoc when out of whack.
Interestingly, the treatment approach of most endocrinologists, dieticians and diabetes specialists is to advise those with insulin resistance to have a low fat, moderate protein, high fruit and vegetable diet. Taken correctly, and iso-calorically for weight maintenance, for even consistent small weight loss, this wil be a moderate or high carbohydrate diet. True, the carbs have some fibre and you could avoid all processed carbs. Nonetheless, it is overall carb load that is important here for the insulin resistant person.
Here’s the kicker – some of the “best” carbs recommended for these people by health professionals, because they are low glycemic index, don’t help. This is because these carbohydrates are absorbed slowly into the system; but because the insulin resistant person is so easily overwhelmed by even moderate carb loads, the result is day-long hyperinsulinemia. There’s plenty of evidence for this too.
The evidence comes, in the main, from feeding studies comparing normal metabolically functioning people, with type 2 diabetics.
Here are a few examples:
1. First, I have written about this before in less detail, the study with beans and glucose. The main thing about this paper is that it compares diabetics with healthy non-diabetic controls. This is very important to see the differential insulin response provoked by the same carb load. This study shows how the insulin responses to several types of beans are high and prolonged for Type 2 diabetics compared with controls.
2, This study in Diabetic Medicine in 1989 shows how rolled oat meals in diabetics result in massive hyperinsulinemia and hyperglycemia compared to the healthy controls after 3 hours. It seems to me that any of these meals are the last thing you would want to feed to a Type 2 diabetic.
Rasmussen et al (1989). Postprandial glucose and insulin responses to rolled oats ingested raw, cooked or as a mixture with raisins in normal subjects and type 2 diabetic patients.
Cooking and processing of food may account for differences in blood glucose and insulin responses to food with similar contents of carbohydrate, fat, and protein. The present study was carried out to see if short-term cooking of rolled oats caused an increase in blood glucose. Furthermore, we wanted to see if dried fruit could substitute for some of the starch without deterioration of the postprandial blood glucose response. We therefore compared the blood glucose and insulin responses to three isocaloric, carbohydrate equivalent meals in 11 normal subjects and 9 Type 2 diabetic patients. Meals composed either of raw rolled oats, oatmeal porridge or a mixture of raw rolled oats with raisins were served. In normal subjects, the three meals produced similar glucose (75 +/- 22, 51 +/- 16 and 71 +/- 23 (+/- SE) mmol l-1 180 min, respectively) and insulin response curves (3160 +/- 507, 2985 +/- 632 and 2775 +/- 398 mU l-1 180 min, respectively). Type 2 diabetic patients also showed similar postprandial blood glucose (515 +/- 95, 531 +/- 83 and 409 +/- 46 mmol l-1 180 min, respectively) and insulin (5121 +/- 850, 6434 +/- 927 and 6021 +/- 974 mU l-1 180 min, respectively) responses to the three meals. Thus, short-term cooking of rolled oats has no deleterious effect on blood glucose and insulin responses, and substitution of 25% of the starch meal with simple sugars (raisins) did not affect the blood glucose or insulin responses.
3. Here’s another paper in Diabetes Care from 1987. In this study they fed diabetics 50g of starch contained in various foods. The foods were neither isocaloric, nor matched for other marco-nutrients (see table). The insulin response was greater for many of the foods than predicted by the glucose response. There were no comparison controls though.
fig 3
The glucose and insulin areas under the curve are shown below. A few comments – while the lentils and kidney beans provoked a lower peak glucose, the rise took longer and the response was still increasing at 2 hours. Second, the results show that all foods produced hyperinsulinemia for several hours afterwards.
Untitled
fig2.1
4. And then this paper in Diabetes Care from 1998. Look at the insulin curve responses to three different meals below – a standard American meal, a low starch/high fibre meal, and a high starch meal. You’ll notice a few things. First, the subjects are hyperinsulinemic after all meals. Second, the low starch meal appears to do much better than the higher starch meal. This research is flawed because the macronutrient compositions of the two meals are different – so it’s not the carbs that define the different insulin responses. There are no healthy controls either – so who knows what the difference is between meals and insulin resistant/insulin sensitive subjects.
The “high starch” diet is 55% carbs, 15% protein, and 30% fat. The “low starch” meal is 43% carbs, 22% protein, and 34% fat. So we see here that people have better insulin responses on lower carb, higher protein, higher fat diets! Just reduce the carbs a bit more and you might have something that resembles a healthy diet for a Type 2 diabetic. Another example of poorly conducted research reaching the wrong conclusions about dietary carbs.
5. Finally, heres a paper in the Archives of Internal Medicine from 2005. The figure shows the day long insulin response of the same subjects (they are their own control) on a low carb diet. The low carb diet is ketogenic. To be fair, the diets are not isocaloric because the subject spontaneously ate less food, as is usual for a low carb diet. They were not restricted and ate to fullness though.
Boden-Insulin51
Take home message:
If you are insulin resistant, you are by definition carbohydrate intolerant. Conventional treatment is to reduce fat, eat less processed carbohydrate, but still at least a moderate carb diet. That will result in chronic hyperinsulinemia and make things worse. The best and most sustainable approach is to restrict carbs and to eat moderate protein with fat as needed to fill you up. You can achieve the same result on a vegan diet or a vegetarian diet, it doesn’t matter, although more difficult. I would hypothesize that any diet in which the symptoms of diabetes are reversed is a carb restricted diet, whether it be through carb retsriction alone or an overall very low calorie diet.
Call to action? Understanding that dietary carbs affect some people very negatively is very important but not understood at all by mainstream medicine. Start telling your doctor about this! Pass on this blog, email people, get on Facebook or Twitter – do what you can. This will be a ground up movement in changing public health nutrition.

Curing Type 2 Diabetes

I’m writing this post and getting these videos out there after a conversation with a diabetes nurse who was very happy to go around telling her diabetic patients, and anyone else who would listen, that “you can’t cure type 2 diabetes”. Really? No chance of completely reversing all the symptoms?

First is an interview with Dr Jay Wortman by the Diet Doctor (one of my favorite bloggers in the LCHF field)

The second is Dr Wortman’s film about curing diabetes in Canadian first nations’ people. It’s called “My Big Fat Diet“. It comes in three parts.

Enjoy

Will sweeteners make you fat or sick?

sweeteners

Now here’s a very controversial topic: aspartame and other artificial sweeteners. My conversations with (usually) men on sugar and substitutes usually go something like this:

Me: ‘Have you thought about replacing your fizzy drinks with diet drinks like Coke Zero or Diet Coke?’

‘No.’

Me: ‘Why not?’

‘I don’t drink that shit.’

Me: ‘What do you mean?’

‘It’s full of that artificial crap, like those sweeteners and other chemicals. They cause cancer. Diet Coke is a girls’ drink, as well.’

Me: ‘So you’d rather drink that 500 ml of Coke, which has 12 teaspoons of sugar in it?’

‘Yep.’

Me: ‘Even though half of that Coke will send your blood sugar through the roof, raise your insulin, and leave you hungrier than before you had it, while the other half that is fructose will go straight to your liver and screw you up in several other ways? And even though there is no evidence for negative outcomes, especially cancer, in the artificial sweeteners like aspartame, one of the most tested and long-standing additives to the human food supply?’

‘What are you talking about, [usually some profanity starting with d or f and ending with -head]?’ (Returns to drinking, laughing at me.)

Okay, my overall approach was probably fundamentally flawed and really misses the mark on the ‘how to win friends and influence people’ scale, but this is very typical of the responses I hear from men. I’m not a promoter of diet drinks for their own sake, but if you want a sweet drink I think the choice is a no-brainer. Sugary drinks – and fruit juice is in this category as it contains exactly the same amount of sugar as regular Coke – are a worse choice than a diet drink. Sugar is relatively toxic to the body. Aspartame is probably not.

What the heck does “probably not” mean? That’s a very good question. The answer is that there isn’t much evidence, especially experimental evidence with humans, showing adverse health outcomes.

Don’t you hate it when researchers sit on the fence and say that sort of stuff? There isn’t convincing evidence that sweeteners don’t harm you either. So it’s a double edged sword. The reality is that you would be better off drinking water. But that’s not the social and environmental reality of the world we live in. I’m saying that all things being equal, I’d prefer the diet drink to the full sugar version.

OK, I hear all the paleo, whole foods guys screaming – and I hear you. But how do you balance that approach with the pragmatism of public health? (clue: think about our approaches to reducing smoking which is obviously bad for you).

Here’s why I would take a more pragmatic approach to sweeteners. First, all foods are made of chemicals. Nutrients are chemicals. Too much or too little of any nutrient has adverse effects. In other words, when we exceed our biological capacity to deal with a nutrient it is almost always a problem. This is why high carb diets are a problem for some people. Aspartame, when synthesised, breaks down into phenylalanine (an amino acid), aspartic acid, and methanol – all of which are found naturally in foods. So I think it’s a matter of perspective and harm with sweeteners. We can deal with these substances in small amounts.

This isn’t everyone’s view, but I think there is now enough evidence to make this recommendation a public health one. In other words, on the continuum of water being the best and sugary drinks the worst, sweetened drinks and meals fit somewhere in between. That’s different than a personal health choice. It might be considered “harm minismisation”. Some people will say that by drinking sweet (even artificially sweetened) drinks you are giving people a taste for sweet stuff. My response is that we already like sweet stuff and no amount of abstinence from sugar will completely cure our taste for it. That being said, lower carb, sugar free diets do go a long way to curing the actual addition many people develop. Through sweeteners, food technology allows us to enjoy sweetness without the sugar.

Besides aspartame, which can have an aftertaste that some people find off-putting (and was originally developed as a fly spray which is even more off putting), there are two other popular sweeteners available in New Zealand: Splenda and Stevia.

Splenda is sucralose, which is made from sucrose (normal sugar), but with a refining process that reduces the calories. Because sucralose is inert (not metabolised) in the body it is calorie free. This product looks and feels a bit more like actual sugar and doesn’t have the same aftertaste as aspartame sweeteners, so it is much better for cooking and baking.

Stevia is a natural plant extract. In New Zealand it is sold under the name Sweete in 2 g sachets, which contain 1 calorie. Compared with sugar, the onset and duration of sweetness is slower and longer. Stevia is, however, about 16 times sweeter than sugar, the 2 g sachet providing the same sweetness as a teaspoon of sugar. So if you are worried about being natural, this plant-extract additive is pretty good.

On balance, I much prefer the Stevia sweetener.

A few comments about research on these sweeteners:

  1. None are likely to stimulate an insulin response on their own.
  2. I acknowledge that actual experimental trials with these substances on humans will never happen because that research is unethical. So we are left with only some prospective study showing no harm. That’s not that convincing.
  3. A study out last week in the journal “Diabetes Care” showed something very interesting. The paper by Pepino et al was entitled “Sucralose Affects Glycemic and Hormonal Responses to an Oral Glucose Load“. So you can see from the title that Sucralose (Splenda), although on its own doesn’t stimulate an insulin response, combined with glucose does magnify the glycemic and insulin response and area under the insulin curve. That’s interesting. I have no idea why that would happen, whether it happens with other sweeteners, how much glucose is required for this response, or whether it applies in slimmer subjects (average BMI was 42). In any case, it is a bit of a warning about Splenda in particular. Not sure about the others.
  4. Watch out for emotional claims about research in this space. Here’s a great example of one about the above paper which is titled “Splenda and Sucralose shown to contribute to the development of diabetes“. That seems to happen all the time in this field. Let’s agree that absence of evidence isn’t the same as evidence of absence. But let’s also agree that the evidence just isn’t their yet for the outright harm of these substances.

So will they make you fat and sick? They might, but sugar is more likely to do so. Are they harm free? Probably not entirely, but in an obesity epidemic let’s be pragmatic in public health.

Diet wars: Can you really eat fat and get lean?

Grant Schofield doing the weekly LCHF shopping sans vegetables
Grant Schofield doing the weekly LCHF shopping sans vegetables, still to be purchased

There’s a food fight cooking…

In the red corner, we have the national nutrition guidelines, with its support crew of dietitians and most of the conservative medical and scientific community. They are the reigning public health champions. They are undefeated, but then they haven’t been seriously challenged. Until now.  In the blue corner, we have a new challenger. He’s been around a while but till now he’s just been shadow boxing. For some reason he strikes fear in those around him. I present to you…..Fat.

We’ve been told for decades now that saturated fat is the major enemy in the battle against obesity and chronic disease. Reduce your fat intake and eat more carbs instead we’re told.  Carbs are essential for human health we’re told.  Eat less, move more we’re told and you’ll stay in shape.  Here are the National Nutrition guideline for New Zealand.:

  1. Maintain a healthy body weight by eating well and by daily physical activity.*
  2. Eat well by including a variety of nutritious foods from each of the four major food groups each day:
  • Eat plenty of vegetables and fruits.
  • Eat plenty of breads and cereals, preferably wholegrain.
  • Have milk and milk products in your diet, preferably reduced or low-fat options.
  • Include lean meat, poultry, seafood, eggs or alternatives.
  1. Prepare foods or choose pre-prepared foods, drinks and snacks:
  • with minimal added fat, especially saturated fat
  • that are low in salt; if using salt, choose iodised salt
  • with little added sugar; limit your intake of high-sugar foods.

As well:

  1. Drink plenty of liquids each day, especially water.
  2. If choosing to drink alcohol, limit your intake.
  3. Purchase, prepare, cook and store food to ensure food safety.

* At least 30 minutes of moderate intensity physical activity on most if not all days of the week and if possible add some vigorous exercise for extra health and fitness.

Yep, that’s the advice and what I have been preaching publicly for the last 15 years, and practicing privately for my whole adult life.

So what’s the problem? The guidelines seem sensible right?  They’re evidence based, and the evidence is extensive right? Yes, sort of, and no.

Let’s deal with the Yes’s first:

Yes, there is extensive and compelling evidence that the type of diet described above is better for you than the Standard American Diet, henceforth known as the SAD :(.  This evidence is from randomized controlled trials, detailed longitudinal studies, and correlational studies.  There are plausible and known mechanisms for some of it, especially whole foods and meats. The important and convincing data around exercise and health is reflected in the guidelines too.

But that’s compared to the SAD.  It’s like saying that because studies show that smoking filtered, low tar cigarettes results in better health, less lung cancer, stroke, and heart disease than smoking roll your own cigarettes, that we should all smoke low-tar cigarettes. Bogus logic. 

The Sort Of’s

  • Sort Of: The part about maintaining a healthy body weight is true – that is good for you. And eating healthily certainly is the way to do this. A low fat diet could make this possible but in the 18 randomized controlled trials to date, where low fat diets have been pitted against low carb high fat (LCHF) diets, there is no instance where the low fat diet has outperformed the LCHF diet. Weight loss and risk profiles, including lipids, are all better with the LCHF. It’s been a knockout in every fight so far.
  • Sort Of: Salt raises blood pressure simply by increasing blood volume.  Equally, low salt is a risk for insulin resistance. Anyone who has ever completed a well formulated LCHF diet is aware of the importance of salt supplementation to prevent low blood pressure and cramps. The same is true for indigenous cultures who eat LCHF diets; they all add about 1.5-2.0 g salt a day.

The No’s

  • No: Where is the convincing evidence to say that saturated fat on its own is a health risk?  Here’s a recent meta-analysis of the longitudinal studies in the American Journal of Clinical Nutrition. There is no evidence of an association between saturated fat intake and cardiovascular outcomes in a combined cohort of more than 347,000 adults followed up for between 5 and 25 years.
  • No: Eat plenty of breads and cereals, preferably wholegrain, and limit your intake of high-sugar foods. Really? How about going with the more plausible mechanism for how we store fat in fat cells via raised insulin.  Insulin, you recall, is raised by carbs, even the so called healthy whole grains.  Sugar is an extra baddie – we all agree on that.  But the language is so lame, it almost condones anything other than high sugar.  Sugar and other insulin raising carbs promote hyperinsulemia, inflammation, glycation, oxidative stress, and fat storage. Because the inevitable outcome of a low fat diet is either starving yourself and keeping insulin under control that way, or a high carbohydrate diet. Either way, this regime is neither sustainable nor healthy in the long run. A low fat diet with sufficient calories for normal living is going to have to also be a high carb diet. Even if you eat lots of extra protein to avoid the extra starchy carbs, you end up with glucose anyway because excess protein will be converted, albeit inefficiently, into glucose in the liver via gluconeogenesis. 
  • No: A calorie is not a calorie.  Calories from different sources have profoundly different metabolic and hormonal effects in the body. Starchy and easily digested carbs raise insulin and insulin chronically blocks leptin. Protein raises insulin but the effect is short lasting and therefore satiating.  Fat is metabolically benign in the absence of chronically elevated insulin. This is why an “eat as much as you feel like” LCHF diet out-performs a low fat high carb diet. The way you get weight homeostasis is by controlling insulin. Perversely, the healthy food guidelines most governments push are likely to negatively affect the people who are highest risk the most; i.e. those who are less carbohydrate tolerant and therefore predisposed to excessive weight gain and insulin resistance in the presence of high carb diets. 

In the end, it looks a bit like the story about the time I was in a long distance ocean swim. The support kayaker taps me on the shoulder and says “You are going to need a change of strategy”.  “Why, I’m swimming flat out already” I reply.  “Because you haven’t made forward progress in an hour, in fact I think you are going backwards….”.  “I see, let’s talk about our options” I say.

We have to accept that we are making no progress in reducing the epidemic of obesity and chronic disease and we need to consider why. We need a discussion about our strategy.  This is the start of that discussion. We all agree that our industrialized food supply is bad but we don’t agree on how to change it and what nutrients are causing the damage.  We all mostly agree that sugar is a bad guy, but we can’t all agree that it is the effect of sugar on insulin and insulin resistance that is the problem. Yes sugar has fructose as well which has problems through other pathways. But, whether it’s loads of insulin-raising simple or complex carbs, it doesn’t matter – both need to be given the boot from the healthy food guidelines. In fact, perversely in my view, we ignore the fact that obesity is a metabolic disorder caused by any type of carb.  Sure, trans fats and the like don’t help. But let’s name the real VILLAIN here and now. It’s not saturated fat….it’s high carbs.

So what’s the answer?

  1. Stop doing nutrition research which tests one thing – the low fat dogma against the SAD. This is fundamentally bogus.
  2. Start doing research which has a start point in biology and evolution by natural selection.  That means start with some sort of paleo/primal LCHF as the “probably healthiest option” hypothesis.  Humans are omnivores = we eat plants and meat.  In human evolution, insulin was hardly ever raised excessively, and if it was, it was probably near the end of summer when man needed to pack away fat to survive the winter.
  3. Stop pretending we know everything about nutrition.  We don’t and we shouldn’t trust anyone who says they do. It’s a science in its infancy with a good deal of poor research behind it and an industry which has infiltrated research and public policy for its own benefit and not ours.
  4. Start to consider that like many other instances in human history, almost the opposite of what we have preached might be true.  Think Galileo, Hormone Replacement Therapy, causes of stomach ulcers, and dozens of times when medicine had it completely wrong.  It’s obvious that at least a few of the assumptions behind current healthy eating guidelines are bogus.

If you end up eating too many carbs in the presence of fat, no matter how paleo plant and meat based the rest of your diet, then all bets are off, you will get fat.

I’m writing this expecting to draw the wrath of colleagues, academia, government and medical and research conservatism. Hopefully first though they carefully consider points 1-4 above. What we need to start with is good science. I could be wrong, but so could you.

So let the diet wars commence; we’re in the ring and we’re ready to fight. We’re starting with the hypothesis that carbs make you fat, and that fat keeps you lean.  Bring it!

Footnote: There are typically three types of diet commonly and currently discussed; the LCHF diet, a low fat high carb diet and a moderate fat moderate carb diet (SAD). I want to reiterate that the SAD is the deadliest. A well formulated LCHF diet is not high protein, it is only adequate protein.  Low carb has nothing to do with dietary percentages.  It’s a total carb intake of <100g/day, maybe even <50g/day, or up to 150g/day for athletes. The LCHF approach is often confused by researchers and clinicians because I often see this regime criticised as either high protien, high fat, or the maount of carbohydrate quoted being far too high. Total daily carbs are what are important.

Thanks again to Helen Kilding in writing this blog