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

6 comments

  1. I tend to come down on yours and Tim Noakes side in this. I am not a scientist but I have been involved with health and fitness for many years. I have been fat. I struggled with all the various diets over the years. It was only when I was diagnosed with cancer that I eventually solved the problem for myself. I A diet of whole natural foods high in unprocessed fats. I effortlessly went from 14 1/2 stone (203lb) to 11 stone (154lb). No hunger, better mood throughout the day. Ditching sugar and high sugar alcohol was key.

    The difficulty all public health obesity researchers will have is until they consider the emotional and psychological effect of food, macronutrients will mean nothing. The food manufacturers have known this for years. Spend a month analysing food ads (especially those where the products have some form of sugar or sugar substitute in them) and you’ll see that it is feelings and emotions that are targeted as well as taste.

    To make a profit in selling food you need people to keep wanting it, addiction being the perfect outcome. The food manufacturers understand the human psyche and thus are able to provide the appropriate emotional cues in tandem with the foods (high carb, high sugar with or without processed fats) that satisfy our emotional and psychological needs temporarily (fix?) but also trigger further repeated hunger. I have seen this repeatedly in my own business where the language of people referring to processed carbs (bread especially), cakes, sweets and chocolates is that of addicts. A typical comment i receive is when I suggest lowering intake of this list of foods is “but I have to have some enjoyment in life”.

    Back to my case, my change in mental approach to the foods I previously loved meant I was easily able to change to a diet that benefited my health and maintain that 4 years later.

  2. interesting dialogue, carbs are not the bad guy neither is fat or protein, whatever diet you follow if it lacks certain nutrients that your body needs and your body is thrifty, it will be interpreted as a famine (with weight loss) and feasting (weight regain) always will be the result.low quality fats and carbs are problem because you get hte caloires you need but not the nutrients you need to metabolise andhandle it properly. so you body has all these caloires to deal wit but not the vitamines and minerals and fiber to handle it. for me all the different low fat low cal low carb diets didn’t work for me, low carb works best now that I am supplementing with vitad3, if you lack this nutrient you can’t handle glucose very well, vitad3 lowers glucose setpoint, thus you can eat less carbs and stay satiated and not hve hypo symptoms between meals. obesity is a natural adapation to a poor quality or low quantity diet. it has little to do with self controlor will power, that is a myth that is like saying you need willpower ot drink enough water or breath enough oxygen or not breath to much oxygen. I mean really? obesity has been given a moral failure problem when it is a physical problem,

  3. 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.

    1. What an awesome question. I think I have a good answer, so will write a full blog this week on it. Thanks for the insightful “what if”

    2. Why do you impose that they “all burn kilocalories at a rate of exactly 2500 per day”?
      Will they lose fat mass, muscle mass or glycogen?

      I have a couple of questions, and I also would like answers aligned with the law of the conservation of energy.

      I want to increase my muscle mass in 2 kg. Assuming I don’t change my physical activity levels, how many calories (e.g. in the form of cakes) should I eat to achieve my goal?

      I have one more question: is it good or bad for the goal of increasing the energy accumulated as muscle mass to increase my energy expenditure (e.g. more physical activity)? Should I exercise more or less?

      I insist, answers to my questions should be aligned with the law of energy conservation.

  4. or, ‘D’ consumes 3000-kcal per day eating nothing but ethanol
    I see this often; excessive alcohol calorie consumption in place of other food does not produce classic obesity, but, if there is weight gain at all, a phenotype close to that of diabetes; pot belly, thin legs.

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Richard David Feinman

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