Slightly updated (11/05/2015).

Prepare to be grossly disappointed.

Brief Intro

If you follow my blog you know this entry has been a long-time coming. And in fact this entry will signify the re-starting of this series, since I now have a lot more information that I did originally, I know a lot more about it, and therefore I have to set the record straight with my previous entries.

I was delayed in doing this entry partly because I submitted an academic essay for a public health unit at uni that talked about obesity policy here in Australia with a strong focus on the science. And I didn’t want to duplicate anything that was in it, lest I get done for plagiarising my blog! The tutor really liked my essay and I got 92% this is what he had to say about it: “It was really impressive – one of the few that took a critical perspective on policymaking. It was very well written, clear, well referenced and persuasive. You got a 46 out of 50 (one of the highest marks in the class).” I’ve uploaded the essay now here on my blog if you’d like to read it (click here). Again the essay is on the topic of public health policy in Australia and what I primarily critique is the decision not to class obesity as a disease and the direct mass-marketing campaigns that have been run since 2008. But I also talk about some of the science that was directly relevant to policy. Note though that I didn’t specifically talk about the important role that insulin plays – but that it does have a long-term effect on weight. Much as I would have liked to, I did not get to fully cover the science of obesity, which is what this blog post aims to do! I will do a blog post on obesity policy another time, but I suggest taking a look at my essay if you’re wanting to know about obesity policy in Australia.

I have now researched this topic thoroughly, and I’ve read a lot of peer review science. There is a lot of misinformation out there on diets, and weight maintenance, and almost none of it is based on actual science. And when I say a lot, I mean an awful lot. So although some of the things I have to say may seem implausible, they are 100% scientifically valid and reflect the general academic thinking by the experts on obesity. If you haven’t studied it, some of these facts will surprise you.

What is the cause of obesity?

Obesity is caused by homoeostatic imbalance of the hunger hormones: ghrelin, leptin, insulin, and to a lesser extent glucagon. Your hunger hormones physiologically control the quantity of energy you consume from food. This process is incredibly precise, so much so that a 20-year study done in the USA (Mozaffarian et al. 2011) that followed 120,000 non-obese people found that the average long-term weight gain in the people they studied to be 0.38 kilograms per year. Over 20 years that’s a total of 7.6 kilos. But what should shock you is that the average amount of energy a person needs to consume per day is 2,000 kcal for women and 2,500 kcal for men. By the formula that 1lb of fat roughly equals 3555 kcal, that is an upset in the homoeostatic equilibrium that equals just 7 kcal per day. That is just 0.28-0.35% of the total daily requirements. 7 kcal is equal to just one single McDonald’s French fry. No one has that precision of conscious control over their diet. Obesity is caused by an upset to the homoeostatic equilibrium that is supposed to keep weight down, it is most certainly not caused by overeating.

How is fat stored in the body?

Ask yourself this question: have you ever heard the diet industry explain this to you, or do you simply take it for granted that 1lb of fat yields 3500 kcal? Fat cells are called adipocytes, and adipocytes form a connective tissue called adipose tissue. Adipose tissue is for all intents and purposes a permanent structure of the human body. Now the number I hear a lot is that on average human adipose tissue that is used for fat storage is 87% lipid by volume. We do also have some adipose tissue we use for other purposes besides fat storage (eg it makes the walls of our kidneys).

When a person gains weight and becomes pre-obese they generally are storing more fatty lipids (i.e. mostly triglycerides) in their pre-existing adipocyte cells. When that person loose weight they are in fact only burning the stored lipids, and the cells are never destroyed – like I said they’re essentially permanent. They can grow in size substantially to store more fatty lipids, but there is a limit. And the limit is actually different for different people, but generally speaking once a person becomes obese their body start to build more permanent adipose tissue. This person’s physiology has now changed, and if they loose the weight to go back to where they started they still have all that additional adipose tissue – but now it no longer contains 87% lipid by volume. And what we now know happens is that weight is controlled by the brain, and following weight loss the hunger hormones change their effect in such a way as to give people a “terrible hunger” as Joe Proietto puts it, and cause them to regain the weight.

What about the formula that 1lb of fat equals 3500 kcal?

It’s wrong. Plain and simple. It’s true that 1lb of adipose tissue will roughly yield 3,555 kcal in total – however only the lipids are easily catabolised by the body. The rest of the fat cell remains – it does not get broken down, end of story. Furthermore lipids yield an average of 9kcal per gram, so you in fact need to burn 4,082 kcal to lose 1lb of body fat. That’s substantially more than the 3500 number you often hear, and the horrible truth is that it’s far from permanent weight loss especially for obese people: your body will want to regain the weight. And if you really try to stop it you could end up with a serious eating disorder.

Next time you see someone claim this number – whether it’s a qualified personal trainer or a “health coach” or someone in the diet industry trying to peddle diet products, ask them where they got the figure from and to defend it scientifically. They won’t be able to do it.

Jenny Craig, Weight Watchers, other diets, diet products – do they work?

NO. They do not. They may work for some non-obese people, but non-medical intervention is not able to reverse obesity long term, and all the experts agree on this – Robert Lustig, Joe Proietto, etc. I originally believed otherwise, but it’s been proven well beyond any doubt. Let me ask you this: how is it possible that a large proportion of people who get bariatric surgery re-stretch their stomachs if weight gain is not driven by a biochemical process? How can you explain the rise in the rate of obese 6-months olds if the cause is anything but biochemical? Or just ask yourself this question: what kind of legitimate product blames the consumer when it fails to deliver what is promised?

What the diet industry does is provide a product that does not work to reverse obesity long term. Although the product doesn’t work, consumers blame themselves and not the product! Think about this, comedian Magda Szubanski was made a main spokesperson for Jenny Craig here in Australia – she lost 36kg and was looking healthy. Then she regained the weight and she was dropped by the company who blamed her!

If you want another example, think of David Elmore Smith – the “650 pound virgin”. He spent 2 years with a personal trainer who became his best friend losing the weight. He then had surgery to remove the excess skin. Then he regained 300 of the 400 lbs that he had lost in just 2 years, his friend decided he was no longer worth their friendship, and so he also lost his best friend. And then he blamed himself. It took him some 30 years or so to grow to 650 lbs, so how is it mathematically possible that he re-gained 300 lbs in only 2 years? Surely it should have taken at least 15 years, under the theory that weight gain is caused by overeating.

Do some genes make some people more susceptible to becoming obese?

Yes. Some people as mentioned will build more adipose tissue more easily and this can snowball into long-term permanent weight gain. Some people are more resistant to putting on weight and their body will instead increase their metabolism when excess kcal are consumed.

Are you really saying that food intake is controlled physiologically and cannot be reversed through dieting?

Yes. You don’t get to choose how many kcal per day to consume, it’s controlled by a negative feedback mechanism that keeps your energy intake from food in homoeostasis (equilibrium). I have a pretty good way of explaining this – think of type-2 diabetes. This is caused by over production of insulin (due to eating too much sugar), which ultimately leads to the cells that insulin work on shutting down their receptors. We know that diabetes is non-reversible, but we now know that pre-diabetes, the medical condition that leads to type-2 diabetes, is reversible. The exact same principle is true for obesity: the leptin hormone losses its effectiveness to suppress hunger, even though it’s still produced in the correct amount. Pre-obesity is generally reversible without medical intervention. Obesity is not reversible long-term without medical intervention. People who lose the weight experience a “terrible hunger” (Proietto’s words) and regain the weight over time.

Lustig says that sugar causes obesity, and Cordain says that cereal grains cause obesity – who is right?

The simple answer to this is I do not know. No one knows for certain. These are both two popular hypothesis. Lustig’s proposal that fructose in particular is responsible is based on what happens to flush it out of the blood – fructose has to be converted by the liver to glucose, and this does stimulate the production of triglycerides – i.e. fatty lipids. You need lipids in your blood, but excess lipid gets stored in the adipose tissue as body fat. Cordain, and some other researchers, think that it is cereal grain consumption that causes us to develop chronic diseases (I’m not even sure Cordain himself specifically links it to obesity, but certainly there are others who do). They argue that humans have eaten domesticated grains for less than 8,000 years – and some people have only just started eating them (e.g. Aboriginal Australians who never had agriculture prior to the arrival of the Europeans). Both hypothesis are interesting – I do not come down firmly on one side or the other of this argument, it may be a combination of the two. Japan seems to do very well eating a lot of rice, so it may be that the grains that are bad for us are limited to wheat and corn (and also potato see Mozaffarian et. al 2011), and that rice is much healthier.

Is obesity a disease in its own right, and what is the scientific definition of obesity?

Yes it is a disease, according to the World Health Organisation and to American Medical Association. It is not recognised as a disease in Australia at this time. There is no one precise definition of obesity, but generally speaking it refers to a condition associated with an abnormal amount of abdominal adipose tissue.

But isn’t the body designed to store excess fat for times of famine?

That is a theory as to why we can become overweight (pre-obese). It may well be true – but it’s not true for obesity. Obesity is a chronic disorder, there’s no biological benefit in it and ancient people were not becoming obese to save themselves in times of famine, they were only becoming overweight. Obesity leads to less mobility, sleep apnoea and difficulty in breathing, type 2 diabetes, arthritis and chronic pain. All of those issues would certainly have been relevant to all ancient humans even when life expectancy was much younger. There was an interesting study done in the UK that found that non-obese people respond differently to increased energy intake from food – some absorb it completely by speeding up their metabolism and gain no weight at all, others gain most of the excess kcal in stored weight but then some of those people stored it as muscle and not fat. Our bodies actually have quite a range of different ways it can behave and the explanation that the body is just “doing what it is supposed to do” is not really a valid explanation for obesity.

Selected References

1. ABC News. (2014). Is obesity a disease? Retrieved from http://www.abc.net.au/news/2014-10-10/is-obesity-a-disease-fact-check-special/5766114
2. Baxter, D. (2014). Obesity in Australia. Retrieved from https://blog.aractus.com/obesity-public-policy-essay.pdf
3. Cordain, L. 1999. Cereal grains: Humanity’s double-edged sword. Evolutionary Aspects of Nutrition and Health, 84, 19-73.
4. Enriori, P. J., Evans, A. E., Sinnayah, P. and Cowley, M. A. (2006). Leptin resistance and obesity. Obesity, 14(S8), 254S-258S. http://dx.doi.org/10.1038/oby.2006.319
5. Mozaffarian, D., Hao, T., Rimm, E. B., Willett, W. C. and Hu, F. B. (2011). Changes in diet and lifestyle and long-term weight gain in women and men. New England Journal of Medicine, 346(25), 2392-2404. http://dx.doi.org/10.1056/NEJMoa1014296
6. Proietto, J. (2011). Why is treating obesity so difficult? Justification for the role of bariatric surgery. The Medical journal of Australia, 195(3), 144-146.
7. Wargo, R. (Producer), & Ford, J. (Producer). (2013). The complete skinny on obesity . Retrieved from http://youtu.be/moQZd1-BC0Y