Saturated fat is bad for you…….really???

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by Grant Schofield and Helen Kilding

Addendum note from Grant: This post has generated an enormous amount of debate – see the comments section.  Its interesting as the authors of this study came back into the debate early.

Another study, this time it’s my colleagues much closer to home in New Zealand, and they received quite a bit of media space from it. The authors sought to estimate the potential impact on cardiovascular health of modifying dietary intake of saturated fat across the New Zealand population, and whether this would be appropriate and feasible.

They decided that while there was no evidence that fat intake affected health, substituting saturated fats with polyunsaturated fats would be of use and is “feasible” for the health of New Zealanders.

Here’s the paper. “Review of the evidence for the potential impact and feasibility of substituting saturated fat in the New Zealand diet (Rachel H. Foster, Nick Wilson, Burden of Disease, Epidemiology, Equity and Cost-Effectiveness (BODE3) Programme, Department of Public Health, University of Otago – Wellington, New Zealand).

They concluded that “Replacing 5% of daily energy consumed as saturated fat with polyunsaturated fats would be expected to reduce cardiovascular events by about 10%.”

Here’s what the media made of it – The New Zealand Herald, and Stuff.co.nz

And I got more than a few questions from readers….for example:

Hi Grant

What’s your take on this study? (see attached)

Many of the fats they mention as bad I have been eating for the past two months and have lost weight and improved cholesterol! This is an actual result and if anything by default resulted in me consuming less of their so called good fats i.e canola oils, polyunsaturated oils etc.

No wonder it  is hard for people to make informed decisions about diet with so much conflicting information. End of the day I decided to see for myself and make myself the test subject on a LCHF diet and continue to be thankful I did.

So what do we make of all this? First, they actually found no association between fat intake and disease outcomes in their meta-analysis. So great, fat isn’t a risk. But they did conclude that because replacing saturated fat reduces risk, that saturated fat must therefore be a risk factor.

I guess they haven’t considered the latest meta analysis in the American Journal of Public Health (2013)  “Food Sources of Saturated Fat and the Association With Mortality: A Meta-Analysis “. This specifically looks at saturated fats. They show very limited evidence for most saturated fats foods having any association with CVD or cancer. Probably processed meat is the strongest association. In this sort of food product, saturated fat isn’t the only metabolic ingredient.

Nor have they considered that actual experimental evidence through randomized controlled trials (there are more than 20 now) does not show a harm for increasing saturated fat intake in LCHF diets. All the “established” cardio-metabolic risk markers show very favorable outcomes compared with all other diets. No long term outcomes, but these are well known and regarded proxies.

The recently published Sydney Heart study data shows that exactly the opposite happened back in the 1970s, when they replaced saturated fat with polyunsaturated fat and saw things get worse. Here’s the BMJ editorial on this. And here are some results:

“Participants were randomly divided into two groups. The intervention group was instructed to reduce saturated fats (from animal fats, common margarines and shortenings) to less than 10% of energy intake and to increase linoleic acid (from safflower oil and safflower oil polyunsaturated margarine) to 15% of energy intake. Safflower oil is a concentrated source of omega-6 linoleic acid and provides no omega-3 PUFAs. The control group received no specific dietary advice.

Both groups had regular assessments and completed food diaries for an average of 39 months. All non-dietary aspects of the study were designed to be equal in both groups.

The results show that the omega-6 linoleic acid group had a higher risk of death from all causes, as well as from cardiovascular disease and coronary heart disease, compared with the control group.”

Nor have they considered almost all of the growing mechanistic evidence that metabolic issues, including CVD, are inflammatory based and the evidence points strongly to a myriad of interacting pathways, from gut microbiome, to sugar, to simple carbs, to the stress axis, to VLDL and triglycerides through the liver etc etc. The direct effect of dietary saturated fat is not clear in any of these mechanisms and unlikely to be a factor.

Overall, the evidence from the association studies is weak, equivocal, or inconsistent, depending on what term you like best.  Experimentally and mechanistically it doesn’t stack up.  Come on guys, are you doing your reading? It’s not good enough when there is such a broader amount of evidence. Your study doesn’t lead to a rationale for reducing saturated fat and replacing it with polyunsaturated.

Worse still, you’re promoting the use of manufactured vegetables oils which are high in Omega 6 and likely to be inflammatory, adding further to the problem.  These oils are also quite unstable and easily oxidized further, adding to metabolic problems. Saturated fat is not.

Avoiding fat will likely mean eating more carbohydrate.  For many, this will further dysregulate their carbohydrate metabolism and make them more insulin resistant resulting in a downward cycle with all the direct and indirect effects of hyoerinsulinemia.  These guys just haven’t even thought that the active metabolic ingredient in their weak epidemiology might be something else which they haven’t or can’t control for…..insulin-raising carbs.

WHAT I THINK WE SHOULD THINK ABOUT WITH FAT:

  1. Fat contains loads of calories
  2. Fat is an essential nutrient
  3. Highly processed fats are inflammatory
  4. Good quality whole foods, including loads of vegetables, are good for you.  Their fat content appears not to harm you.
  5. Omega 3 fats are good for you. These are poly unsaturated so if that is what they are talking about then great.  But these guys go on to talk specifically about manufactured seed oils – these are not good.
  6. In high carb, insulin-provoking diets, fat seems to add to the insulin response.  This seems to be worse in people who are insulin resistant.  By itself, fat is metabolically benign, at least as far as insulin response is concerned. A good reason to avoid the standard American diet.
  7. Processed meats are likely to be bad for you.  I’m not sure if it’s the actual fat and I’m not sure what the mechanisms might be – inflammatory? We may never know if they are for sure because no one is likely to run an experimental trial where people get a long dose of processed meat.

Take home messages:

  • Don’t believe everything you see in a scientific paper.  Sometimes they go past the evidence.
  • Carry on eating fat, hopefully in the absence of processed and simple carbs as they may harm you in combination.

How did fat get such a bad name in the first place?

We’ve been brainwashed in to thinking that when we eat saturated fat it goes straight into our bloodstream, instantly bonding to the inside of our arteries, eventually clogging them up completely. This is bullshit. Atherosclerosis is caused by oxidised LDL particles penetrating our arterial walls, inciting inflammation and damaging the arterial tissue. And what increases LDL particle number?

  1. Insulin resistance and metabolic syndrome
  2. Poor thyroid function
  3. Infections
  4. Leaky gut
  5. Genetics

Let’s look at that list again…..no mention of dietary intake of saturated fat.

And when we talk about saturated fat, everyone always wants to talk about cholesterol. Dietary cholesterol does not affect total blood cholesterol. In fact, when we do eat cholesterol, our body makes less of it to keep our blood levels in balance.

So even if eating fat doesn’t result in CVD, won’t eating fat make us fat?

No again. As we’ve said before, fat doesn’t make you fat. Fat is very satisfying, especially when paired with low-carb eating. A nice steak rippled with fat is far more filling than some crusty bread spread with butter. You’ll eat a decent piece of the former and be satisfied but could easily polish off half a loaf of the bread with a good helping of butter and still be hungry. It’s difficult to overeat on a high-fat, low-carb diet.

Our bodies want to use fat for energy, but when we eat fat in the presence of large amounts of dietary carbohydrates, it makes it difficult to access fat for energy. On the flip side, dietary fat in the presence of low levels of dietary carbohydrates makes it easier to access fat for energy. It’s also easy to overeat fat and carbs together – think hot chips, buttered toast, milk chocolate.

And let’s think about farming for a second….how do you fatten cattle? You feed them lots of lots of grass (a carbohydrate). According to a recent post on Christine Cronau’s Facebook page, “70 years ago, farmers tried to fatten their livestock with saturated fat. It backfired! The pigs lost weight and became more active. Of course, the farmers weren’t silly enough to persist with something that didn’t work, yet our conventional health professionals have insisted on doing so!” I’ve tried to source more detail on this but have drawn a blank so far.

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.

Does carb burning age you?

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Grant was out for his weekly hill ride with his old mate Stephen. Stephen was now in his nineties and Grant just about to turn 90. The day was sunny and warm. At halfway, they stopped and had a coffee and talked about their grandchildren, each showing off a bit to the other. On the last high hill Grant took off and lead out a sprint. It was all good until just as they hit the top, Grant felt a sudden pain in his chest and dropped dead. Stephen, after a lifetime of never quite winning the hill sprints, seeing him falter took his chance and rode past him – at the exact moment he finally won a sprint, he too felt a sudden pain and dropped dead.

Neither man even had the chance to pull over and unclip from their carbon racing bikes. They lay turtle up, each having won the final sprint to the line.

As Mark Sisson puts it, “they lived long and dropped dead”. Good quantity and great quality.

Anyway, that’s my little fantasy and thought experiment about how I should die along with my long time mate Stephen Farrell, who strangely thrashes me at everything except hill climbs.

Two things are inevitable in life, death and taxes.

I’m here to talk about the first one. I am assuming we want both quantity and quality of life. How do you get the most “bang for your buck” so to speak? The first clue might be in the caloric restriction data – eat less live longer. Sounds feasible, and some data support this idea. The unappealing thing, to me at least, is that eating is fun, enjoyable, and perhaps in the end the trade off isn’t worth it because you are alive but had to go hungry the whole time so life was just way less fun. But there are new data and new hypotheses about how glucose metabolism may be the driver, not caloric restriction.

How glucose metabolism fits in

I want to spend the main part of this blog summarizing (at least as well I can summarize a complex neurophysiology paper) how glucose metabolism controls the aging process, mainly through the brain. I’m talking about a paper just published in Trends in Endocrinlogy and Metabolism called “Metabolic mystery: aging, obesity, diabetes, and the ventromedial hypothalamus” available here. First, its hardly light bedtime reading, unless you quickly want to fall asleep. Second, there is so much complex genetics, animal study material, and hormonal and neuronal mechanistic stuff it takes a very long time to get through it. So I’ll spare you all the challenge and get straight to the major hypotheses and practical implications.

They start by revisiting the well known phenomenon that caloric restriction can increase lifespan, in at least some animals. Possibly humans and primates, although the jury is still out on that, and the only decent primate study wasn’t a decent study after all because of the high sugar diets for both caloric restriction and ad lib feeding groups.

Major findings of this review

  1. The energy mediating centre in the brain (the ventromedial hypothalamus) has specific glucose and FFA (free fatty acid) sensors.
  2. These sensors directly affect hepatic (liver) and peripheral (muscle and organ) glucose metabolism in opposite ways.
  3. High glucose in the blood drives a decrease in liver glucose production and an increase in glucose metabolism in other tissues. It’s vice versa for lower glucose and increased FFAs in the blood.
  4. Increased oxidation of glucose in peripheral tissues requires less oxygen to metabolise but results in more oxidative stress (i.e. damage) to the tissues. This damage is directly implicated in aging. Increased availability of insulin and insulin-like growth factor 1 (IGF-1) are also implicated in this process.
  5. Glucose on its own may not be enough. Increased mortality of Type 2 diabetics who are aggressively treated with exogenous insulin is evidence for this.
  6. Take home message – there is direct evidence that high dietary glucose load (read CARBOHYDRATE) Continue reading “Does carb burning age you?”

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

How ketogenic (low carb high fat) diets work

A really nice paper was just published by Paoli, Rubini, Volek and Grimaldi in the European Journal of Clinical Nutrition titled “Beyond weight loss: a review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets”

You won’t see a better review paper for summarizing the latest in how we think carbohydrate restriction affects various aspects of metabolic health; from weight loss to neurological issues to acne (yes acne!).

A second excellent review article was also published in Nutrition Today by Volek (again!) and Phinney, the low carb gurus. This one is called “A New Look at Carbohydrate-Restricted Diets: Separating Fact From Fiction”. Again this is an excellent scientific review paper.

What I should be doing in this blog is simply drawing your attention to this good work and you can go and check it out for yourself.

Except I’m aware that unless you work at a university, that’s easier said than done. You’d have to buy the papers, which means that most of the people who stand to benefit from the knowledge won’t.

Actually, copyright publishing is a scam of the highest order. What happens is that guys like Volek and Phinney put in heaps of work, often that work is paid for by either public institutions, or by research grants gained through public funds. They then (usually) slave away in the degrading process of blinded peer review, often having to respond to inane comments and endless rebuttals. When they are done, they then sign all of their IP over to a journal, which keeps it all for no cost (and all profit) in perpetuity. Can you imagine anywhere else in the business world that would happen besides academia? It’s laughable, but it is actually what happens to us academics everyday and frankly, we no longer find it funny.

Anyway, I digress. What I really want to do here is summarize the two reviews.

Let’s start with the Nutrition Today paper by Volek and Phinney, which is a nice synthesis of the available evidence for the biology of human energy regulation and homeostasis, and how a carbohydrate restricted diet operates. The main points here are:

  1. Saturated fat levels in the blood are not associated with dietary saturated fat intake, but dietary carbohydrate intake. They show evidence from both randomized controlled trials and population data for this.
  2. They discuss in detail what the keto-adapted (fat adapted) state is; how this comes about, including increased beta oxidation of fat, decreased hyperinsulinemia, and a reorchestration of substrate utilization in the body, including the use of ketones to fuel brain function. It is interesting that the majority of practicing dietitians, endocrinologists, cardiologists, and public health physicians have never heard of any of this.
  3. They point out what is a very important and obvious set of outcomes, which are well documented in the scientific literature; that treating a patient with insulin resistance with a low fat/high carb diet is palliative and going to make the problem worse. If you are having trouble getting glucose into your cells, then reduce the glucose load stupid!
  4. They show a nice little diagram, which I have reinterpreted and redrawn below, to show the role of dietary carbohydrate in metabolic (dys)function. To quote the authors “The major point is that SFA (saturated fatty acids), and the response to eggs, has a totally different metabolic behavior when consumed in the context of a low carbohydrate diet.”Slide1
  5. They show a meal plan for a typical low carb daily meal. This is excellent as it shows what real and tasty foods we are talking about.

2500 kcal daily food intake restricting carbs

Breakfast (scrambled eggs with sides of spinach and sausage)

  • Scrambled eggs: 2 large + 1 tbsp palm oil
  • Mozzarella cheese: 1 oz
  • Pork sausage: 2 links (48 g)
  • Chopped frozen spinach, boiled: 3/4 cup (142.5 g) + 1.5 tbsp butter

Snack

  • 1/2 Avocado: 67 g
  • Swiss cheese: 2 oz (56 g)

Lunch (broiled salmon and a side salad)

  • Broiled Atlantic salmon: 4 oz + 1 tbsp butter
  • Mixed baby greens: 2.5 cups
  • Diced tomatoes: 1/4 cup
  • Chopped onion: 1/8 cup
  • Feta cheese: 1 oz
  • Black and green olives: 4 each
  • Blue cheese dressing: 1.5 tbsp

Snack

  • Peanuts, oil-roasted: 1 oz
  • Hood Calorie Countdown milk: 1/2 cup

Dinner (sirloin with sauteed mushrooms and cauliflower ‘‘mashed” potatoes)

  • Beef sirloin tips: 3 oz
  • Olive oil: 1.5 tbsp
  • Sauteed mushrooms: 1/4 cup
  • Olive oil cooking spray
  • Cauliflower ‘‘mashed potatoes’’: boiled cauliflower 1 cup + shredded cheddar cheese 1 oz + Butter 1 tbsp
  • Sugar-free jello: 1/2 cup (121 g)

Macronutrients:

  • Protein: 134 g
  • Carbohydrates: 42 g, Fiber 20 g
  • Fat: 204 g
  • Cholesterol: 853 mg
  • SFA: 81 g
  • MUFA: 78 g
  • PUFA: 28 g

Reproduced from Volek and Phinney (2013), Nutrition Today

Now on to the second paper in the European Journal of Clinical Nutrition titled “Beyond weight loss: a review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets”. This is a comprehensive scientific review of the evidence and emerging evidence for the treatment and prevention of a range of chronic diseases with carbohydrate restricted (ketogenic) diets. I have adapted one of their figures into two new ones, showing the state of scientific evidence (strong and emerging separately) for “therapeutic uses of the ketogenic diet”. Hopefully these figures are self-explanatory.

I draw your attention to the “suggested mechanisms” under each one. I’m not going to go into these in detail but it is worth looking at these two figures and noting a few things:

  1. Carbohydrate restricted diets are a legitimate and well documented approach to the treatment of a wide range of issues.
  2. There are common mechanisms, mostly about reducing the load of insulin the body has to deal with. This is because the body has to dispose of less dietary carbohydrate. This point is seemingly lost on most in the field of chronic disease prevention and treatment. Hyperinsulinemia is a problem in itself, reducing it helps.
  3. As well, there are associated mechanisms associated with high insulin. There are problems in the IGF pathway, mitochondrial function, and inflammation.

Slide1

Slide2

There is now strong evidence to show that low carbohydrate diets are safe and effective treatments for several conditions, and have some likely positive effects for other conditions.

So that’s it. Two great papers. Hopefully I have captured the essence of what they are saying and where the evidence is at. This is important to get out there into the public and health community. While it’s all behind the paywalls of journals it won’t. So hopefully this helps.

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

Why beans could make you fat…and cheese won’t

Beans

This post is about how different people react, metabolically, to different foods, especially carbohydrates.  How you personally respond to dietary carbohydrate should help you make some decisions about what and how you eat.

It gets scientific but the science is important.

Several researchers have tried to quantify how we process different types of carbs.  These include the glycemic index, the glycemic load and the less known insulin index.  These are all really interesting and occasionally useful to tell an individual about how rapidly the carbs they consume are likely to be absorbed into their body and the possible glycemic and insulin response.

The insulin index, in particular, offers some promise. The insulin index quantifies the typical insulin response to various foods. That’s great because that’s what’s we are particularly interested in; our insulin response to foods.

The alternative hypothesis (also known as the carbohydrate theory of obesity) suggests that high levels of insulin are responsible for us getting fat. I think this alternative hypothesis should be the default one as the most likely mechanism of obesity.  I’m basing this on the available evidence and logic through evolutionary biology.  This means that the insulin index, in particular, offers some promise. The insulin index quantifies the typical insulin response to various foods and shows some foods will cause more insulin to be released than other foods.

The trouble is that the Index is based on the average effect of particular foods on metabolically functional (insulin sensitive) humans, not the specific effect on a given individual.  I’m not alone in thinking that individuals vary enormously in their ability to move carbohydrates out of their blood stream into cells.  The cells might be muscle, other body, or fat cells.  It all depends on your genetics, your age, and your personal eating and exercise history. In other words, depending on who you are and how you have treated your body, you will respond very differently to the same load of carbs.

This is nothing new of course. That is the whole point of the Oral Glucose Tolerance test.  You drink 75g of pure glucose and we monitor your glucose response over time. More insulin sensitive people will clear the glucose load more quickly. Although not normally measured, we know the area under the insulin curve will be less in these people. Less insulin = more fat burning, less fat storage and a greater propensity to move and exercise.

So what about other foods and how we react to them? The conventional advice is to eat more carbohydrates with fibre, especially plant fibre. These are released into the blood stream more slowly. This provokes a much smaller glucose and insulin response, thus the insulin resistant cells of metabolically dysfunctional (insulin resistant) people can much more easily deal with the reduced load, even if the total amount of carbs eaten is the same.

That’s why our dietary guidelines at least warn us away from refined (no fibre) dietary carbs and steer us toward “healthy whole grains” and “fibrous” (non-starchy) vegetables. Legumes (beans) are a good example of this. They are absorbed much more slowly.

But what if for some people, like those with Type 2 Diabetes, slow digestion simply means high insulin for a longer time? These people have insulin resistant cells. To get any carbs into the cells, insulin might have to be really high.  Legumes may not be as bad as pure glucose in causing a high insulin response, but the response may be high compared to someone who is insulin sensitive. So beans might just add to the metabolic problems and make them fatter.

So what we should do is feed people a range of different carbohydrate-rich food; from glucose to beans and other things in between. We should measure their glucose and insulin responses before they eat, and for several hours afterwards.

The questions are:

  1. How much does the individual’s area under the glucose and insulin curves vary for different foods?
  2. How much do the absolute amounts of insulin secreted vary between individuals?
  3. How do the insulin curves for the simplest carbs for the most insulin sensitive, compare with the most complex carbs for the least insulin sensitive? Could it be possible that beans provoke a glucose-like response in some, but hey, it just lasts longer in some people?

For me, the idea was planted after a conversation with well-known and highly respected nutrition expert and endocrinologist, and a mentor to me, Professor Jim Mann. For those of you who don’t know this guy, he is simply a legend in New Zealand public health medicine.  His contribution has been and is massive. He is clearly way more experienced than I am in public health nutrition. I have a huge respect for his knowledge, and a readiness to learn from him, but also I hope to generate some healthy debate at the same time.

Anyway, our conversation around carb metabolism was a little bit awkward.  After all, Jim really goes for the “plenty of plant-based carbs, low saturated fat, lean protein” diet.  To be fair, he certainly promotes the importance of at least some fats.  Anyway, despite some differences in the starting hypothesis, what I think I finally got down to was Jim’s assertion that “more complex carbohydrates, like legumes, are digested in the small bowel and have been shown to have lower glycemic and insulin responses”.

Fair enough. I just don’t know that much about beans.

So Catherine Crofts (a doctoral student) and I planned a study to test this. We want to know if high loads of carbohydrate are OK  as long as they are absorbed slowly?  It will hopefully allow us to understand more clearly how individuals could be metabolically profiled, at least for their response to carbs of different sorts.

Of course, any scientist starts by reviewing the literature in the field. And so be it. Talk about having to hunt for research papers.  Catherine, also a pharmacist sick of handing out diabetes medication, has been an absolute legend at digging up research papers on carbohydrate metabolism.  I think she had reviewed some 1600 papers at last count.

Then she found this little cracker from 1989, only cited 18 times since. These citations all, in my view, incorrectly cite what the original researchers actually found. People citing this paper all claim that the glycemic response to beans is so good in diabetics that we should all start eating more beans (the data shows the opposite in fact).

The paper is by Indian researchers Viswanathan et al, in Nutrition Reports International (1989) titled “Responses To Legumes In Niddm Subjects: Lower Plasma Glucose And Higher Insulin Levels.”

The blood glucose and corresponding insulin responses to five different isocaloric (300 kcal) legume preparations were assessed, along with 75 g of glucose (also 300 kcal). They concluded “..the study indicates that the legume preparations are useful in the management of diabetes on account of the lower glycaemic and higher insulin responses produced. The factors responsible for these changes need to be evaluated in greater detail.” 

OK, fair enough, except for a few things:

  1. Their data (see figure below) shows the glucose (top panels) and insulin responses (bottom panels) for healthy controls (left panels) and type 2 diabetics (right panels). The glucose units are not matched on the upper panels – they show that the glucose response to BOTH legumes and glucose is much higher in the diabetics.
  2. The area under the insulin curve for the legumes is comparable to that for glucose for the diabetics.
  3. The insulin curve for the legume-fed diabetics is high and still high at the conclusion of measurement at 2 hours. Also, the insulin curve for glucose and one of the lentils is still climbing!

On the basis of these data, I think we have a case for our study and questioning why we would expose people with insulin resistance to large loads of carbohydrate ever. Surely the logic is faulty?  It is as I see it, faulty logic because while some carbs do get absorbed more slowly from the intestines into the bloodstream, the cells still need large amounts of insulin to get the glucose into the cells.

Insulin is a metabolically useful hormone, but chronic hyperinsulinamia (insulin is high all the time) isn’t good for you.

Promoting even “healthy carbs” in larger loads may not be good for the most metabolically vulnerable. They raise insulin, they raise it high, and for a long time. That’s a poor combination because fat burning is off, and fat storage is on, for a long time.  Something a little more metabolically benign, say cheese, although higher in calories, won’t stuff your hormonal energy regulation up nearly as much.

Eaten on their own, beans could make you fat. Cheese, well we still need to look at how insulin responses vary.  Cheese has zero carbs, some protein and some fat. We probably do get a smaller and shorter insulin response to the protein in  cheese. We should test cheese!

Data from Viswanathan et al, Nutrition Reports INternational (1989) RESPONSES TO LEGUMES IN NIDDM SUBJECTS: LOWER PLASMA GLUCOSE AND HIGHER INSULIN LEVELS.
Data from Viswanathan et al, Nutrition Reports International (1989) RESPONSES TO LEGUMES IN NIDDM SUBJECTS: LOWER PLASMA GLUCOSE AND HIGHER INSULIN LEVELS.

Thanks to Helen Kilding, Catherine Crofts, and Mikki Williden in writing this post