A few days ago under the title ‘Good calories bad calories – what we know’ I posted my notes on the main points of the ‘Good Calories, Bad Calories’ (GCBC) book as I saw them while I was reading it. Long before I actually read the whole book I had read a rebuttal by Stephan Guyenet, an obesity researcher. I didn’t want to re-read his scientific critique before actually finishing the entire book first (I didn’t want to be subjective while reading it). I also wanted to post my observations before I re-read Stephan’s blog post (actually two posts – here and here).
Today I re-read Stephan’s critique and wanted to write another post that I think represents the stance of the scientific community spoken by this obesity researcher (he has made a great summary of the science on obesity in the last 60 years and that’s why I feel that he is speaking on behalf of the entire community of obesity scientists).
This post, just like the last one will contain minimal comments from me. The reason for this is I don’t feel I am in a position to comment while making observations on the science. I am just a guy who has a passion for health sciences and logic and has experimented with his own body fat levels quite a bit – both as a competitive athlete and as just an individual who wants to know how the body responds to changes in lifestyle but who doesn’t have access to lab rats.
Here is what we know so far that comes directly from the obesity research community:
- The first law of thermodynamics still applies (energy in vs. energy out). If more energy enters the body and less is expended – we become fat (but some individuals tend to store more fat, some less – all other things being relatively equal). Both, GCBC and the research community agree on this.
- Fat tissue itself, as an organ, does not regulate the fat levels in the body. Neither does the pancreas (the insulin-secreting organ). The brain regulates it.
- Insulin is not the hormone that orchestrates the whole process of becoming fat (and obese). Leptin is – in concert with other hormones and systems.
- High-carbohydrate meals may be more satisfying than high-fat meals (protein being the same). High-carbohydrate meals may even cause less subsequent food intake than high-fat meal. That despite the fact that after a high-carbohydrate, low-fat meal (protein is the same) the insulin response is greater after a high-protein, high-fat, low-carbohydrate meal.
- For many protein foods protein elicits greater insulin response than carbohydrates. Yet a high-protein, low-carbohydrate diet has a greater fat loss potential compared to other macro nutrient ratios diets. This suggests that insulin may even aid fat loss.
- The fat tissue in obese individuals is insulin resistant. Since insulin suppresses the release of fats from the fat cells and obese individuals have fat that’s insulin resistant they release as much or even more fat from their fat cells into the blood stream (to be used as fuel by other tissues in the body). If these individuals stay obese it is because the energy coming in continues to exceed the energy released from the fat cells and used as fuel — and not because chronically elevated insulin levels ‘lock’ the fat into the fat cells and do not allow its use as fuel.
- Hyperinsulinemia (elevated insulin levels) is not a cause of obesity – it’s an effect of obesity.
- Obese people have higher metabolic rate (burn more calories during the day) but they also consume more calories, which compensates and overcompensates for the increased levels of calories burned.
- Both glucose and fructose cause fat gain – glucose to a slightly higher degree (not fructose as commonly thought). Fructose causes fat gain primarily in the belly region and less in other places in the body.
- High food palatability/food reward hypothesis has gained traction as a possible explanation of why we eat calories in surplus (and thus become overweight and obese).
- Human genetics tells us that obesity is dominated by malfunctioning of genes that regulate leptin signaling in the brain. Insulin signaling does not appear to be a cause of obesity, genetics tells us.
- Common obesity isn’t a function of insulin only. It is a function of a complex of hormonal and anatomic systems. These include: amylin, glucagon, GLP-1, ghrelin, leptin, melanocortins, neuropeptide Y, dopamine, stomach distension, and more. The regulation of fat levels happens in the brain and it is controlled by the interaction of these (and possibly other) systems.
- The total carbohydrate intake in 1909 was just as high as in 2000 but the obesity didn’t exist in ratios it does today (1 out of 3 in the US). This suggests that carbohydrate intake cannot be singularly blamed for the obesity epidemic.
- Obesity researchers know that positive energy balance (more energy in, less energy out) causes obesity. However, they don’t know exactly what is causing the energy imbalance.
My comments on these notes:
- On the second to the last bullet point above – carbohydrate levels the same in 1909 as in 2000 – I know for a fact that the simple carbohydrates (sugar, HFCS, etc.) have about doubled during this period, so simple sugars probably play a role in the obesity epidemic. How exactly? We only know that it isn’t by messing up insulin. It’s more complex than this.
- In my previous post, containing my notes from the GCBC book I mentioned exercise and its limited role in combating obesity. The obesity research community does not mention anything about how calorie burning activities influence fat gain/fat loss. This is understandable – the research is focused on how food affects the brain and its signaling pathways. We only know that the ‘eat less, move more’ type of advice isn’t very practical due to the fact that we don’t exactly know what is causing the positive energy balance (for example you may eat less – but mainly from the wrong foods, and exercise more and still not lose fat).
Finally, there is still no clear answer as to why we become obese. To borrow the words of one commenter on Stephan’s blog: ‘we know that pizza makes us fat… we don’t know why’.
In any case, Stephan Guyenet himself has a good working hypothesis as to what is causing the energy imbalance – and from there obesity. Here is a paragraph from his blog post ‘Roadmap to obesity‘:
...in genetically susceptible people, excessive food reward/palatability/availability and inactivity cause overconsumption and an increase in the body fat setpoint, followed by the eventual accumulation of fat metabolites and inflammation in the hypothalamus, which exacerbate the problem and make it more difficult to treat. Other factors, such as micronutrients, gut flora, fiber, fat quality, polyphenols, sleep and stress, may also play a role.
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