Off the back of episode 84 of the podcast there was a lot of follow-up discussion from the SNR listenership. In that episode Dr. Jason Fung was on to discuss his perspective on what drives fat gain and hence obesity development,
One of the primary questions I was getting was around my thoughts on this whole issue of obesity development, CICO, insulin and hormonal drivers of fat gain. So first, thanks to everyone who send in their thoughts and questions via email and social media. The whole purpose of the show is to promote critical thinking.
We know there is an obesity epidemic that’s ever-increasing and never before have more people been overweight. This has led to many hypotheses as to why this is and hence what we should do about it.
The purpose of this commentary is not to attempt to explain the obesity epidemic, or offer a solution. I simply want to lay out what I think is fair to conclude from current understanding and research.
Carbohydrate-Insulin Hypothesis vs. Insulin Hypothesis
The first port of call is to first address the carbohydrate deal as this is often the sole focus of those looking at this issue from the CHO-insulin hypothesis perspective.
I’ve already clearly outlined on the blog before why I think carbohydrates are not to blame (I’ll link to that post in the show notes THIS POST). If you do believe carbohydrates are the cause of all this then please go and read that post before closing yourself off to the remainder of my points.
Now, I’m not saying we all should be going around eating high amounts of carbohydrates all day everyday. All I’m saying that carbohydrates can NOT drive fat gain unless they promote an energy imbalance.
Low-carb diets can be awesome for lots of people. But for people to avoid becoming overweight, carbohydrates do not *NEED* to be avoided. How anyone can still deny this in the face of so much contradictory evidence to the ‘carbs make you fat’ argument is beyond me.
I believe carbohydrate restriction can be an exteremely effetive tool for fat loss. I believe many people can improve metabolic health on LC diets. I believe many people can feel a lot better on a LC diet. In fact, I shouldn’t say “believe”, I should say “know”, as I’ve seen it first-hand. But I’ve never said any different. What I do NOT believe is the cause of obesity is simply the effect of carbohydrates on elevating insulin.
Also as of yet, there is nothing in the literature to suggest that LCHF/ketogenic diets hold a metabolic advantage for preventing fat gain, over diets that are matched for both calories and protein. And please no one send me that Feinman paper. Yes, I’ve seen it. Yes, I’ve read it. There are too many inaccuracies and assumptions in it to even start listing.
Usually when people claim a metabolic advantage for low-carb (LC) diets over low-fat (LF) diets in terms of fat loss (i.e. isocaloric diets will see LC give more fat loss OR it’s possible to lose fat on a higher number of calories when LC), studies they point to are not matched for protein. And generally, embarking on a LC diet will lead to a subconscious, almost automatic increase in protein intake. Comparing isocaloric diet that are NOT equivalent (or at least close to it) in protein intake is a big confounder.
So to make a fair comparison from a physiological perspective, there shouldn’t be wild differences in protein intakes between the diets we are comparing.
HOWEVER, on the flip side, when we consider things from a pragmatic perspective, one critical piece that “anti-LC” people miss when they dismiss anything that is not protein-matched is something I just mentioned:
“… generally, embarking on a LC diet will lead to a subconscious, almost automatic increase in protein intake.”
And so if we take the case of someone who is not receiving nutrition coaching (i.e. going it alone) and decides not to track calories, then “going low-carb” could prove more effective in practice:
Reduce CHO intake –> Subconsciously increase protein intake –> Increased Satiety –> Subconsciously decrease total caloric intake –> Fat loss
I’ve written about this before in a post: Just How Effective is Low-Carb Dieting?. As well as talking about it in a previous podcast: Are Low-Carb Diets More Effective For Fat Loss?. Either of those will give you more context to the conclusions I’m drawing on the carbohydrate hypothesis of obesity. I don’t think I have to cover old ground by regurgitating all that again. So let’s move onto what I think is a more interesting discussion…
CICO vs. Hormonal/Metabolic Dysfunction: A False Dichotomy
The real crux of this debate for me has centered around discussions over two things driving fat gain; namely energy balance (i.e. the calories-in/calories-out model) and hormonal/metabolic dysfunction. To me the polarization of these two concepts makes no sense. Having to pick whether obesity is an energy balance problem or a hormonal problem is a false dichotomy.
This was one of the things I hoped to iron out by having Dr. Fung on the podcast. Previous to that, we had a public discussion over a Facebook post I posted, in which I listed some bullet points that I felt related to obesity development. In that post I listed, among others, these few points:
- In order for fat gain to occur an energy imbalance must be present, where calories in (CI) > calories out (CO).
- But when asking “why do we get fat?”, even though CI > CO in such a scenario, the reason driving this is the true cause. This is where the several hypotheses of obesity come in: hypothalamic injury, food reward/palatability, hormones causing a lowering of CO (e.g. thyroid), etc.
- The hormonal basis of obesity has always been accepted by pretty much every researcher on the planet. Saying energy balance still determines body weight gain/loss, doesn’t conflict with this at all. In that they are not mutually exclusive.
Dr. Fung: “Are you arguing point #3 – calories make you fat, or point #5 – hormones make you fat? You can’t have both.”
Hormones influence energy balance. And changing energy input or energy expenditure will affect various hormones.
Frank Greenway, who’s a researcher out of the Pennington Biomedical Research Center, wrote a nice paper on the mechanisms underpinning weight regain, which was published in the International Journal of Obesity a couple of months back.
From that paper, Greenway discusses how body weight maintenance is regulated by the interaction of both homoeostatic processes, as well as environmental and behavioural factors.
So if we think about homeostatic regulation of energy, we’re essentially talking about hormones controlling calories in and calories out. The hypothalamus has a central role here in integrating signals related to food intake and energy balance, as well as body weight itself. For example, we know hormones like NPY, GIP and Ghrelin can influence energy intake. While if we turn to hormones that exert a role on energy expenditure, we’d be talking about ones such as leptin, insulin, GLP-1, PYY, etc.
So yes, of course, there is a hormonal basis to obesity. There is disregulation of these homeostatic controls. BUT calories-in/calories-out still holds true. The first law of thermodynamics is not being violated. When bodyweight gain is occurring, someone is in a state of positive energy balance. When bodyweight loss is occurring, someone is in a state of negative energy balance.
Now, then the argument is raised about the validity of calorie restriction as a treatment. But before I get to that, let me state that I think there is a major problem with the position of some of the “anti-CICO” crowd on this. They create a presumptuous straw man argument; claiming that anyone who discusses energy balance is clueless because they’re just telling people to eat less and move more. Quite rightly, that advice is useless in nearly all cases. Anyone that I see doing a good job in this industry is NOT doing that.
However, that does not mean that a situation where calories in being less than calories out can be avoided. You want to lose weight, negative energy balance must be in place.
Saying that the CICO model is correct and that telling people to eat less is the solution to obesity are NOT the same thing.
CICO and a hormonal basis of obesity are not mutually exclusive ideas. In fact, there both intertwined.
Commentary on Calories, Insulin & Obesity
In order to answer people’s questions surrounding how my viewpoint compares to the insulin hypothesis presented by Dr. Fung in the previous episode, I feel it’s important to first to be clear on exactly what we agree and disagree on.
Points of agreement
- The CHO-insulin hypothesis is not accurate (or as Dr. Fung termed it; “at the very least incomplete”)
- There is a hormonal basis to obesity
- The solution isn’t as simplistic as getting everyone on a LCHF/ketogenic diet. That doesn’t work for everyone.
- The solution also isn’t telling an obese patient to eat less and move more. It’s not helpful & likely won’t work.
- Calories in and calories out are not independent variables. Calories in affects calories out. Interestingly, there is research to show that high insulin levels are associated with higher resting energy expenditure, even after controlling for body fat (e.g. Weyer et al.)
Things I’ve learnt from Dr. Fung and our conversations
- Simply focusing on blood glucose in insulin resistant patients or type 2 diabetics is misguided. Addressing the underlying insulin resistance is more important.
- Fasting can be amazingly effective in a clinical setting with diabetic and obese patients.
Points I Disagree With
- First, while I understand the usefulness of analogies in explaining topics to a wide audience, the comparisons of obesity and CICO to alcoholism and alcohol in/alcohol out is misleading.
- While of course insulin is important, I don’t agree that it is the ultimate cause of obesity. As I’ve said in numerous comments over the past week, I think insulin is a piece of the puzzle for sure. I just don’t think it is the puzzle itself.
- Calories are irrelevant and that calorie restriction doesn’t work. That the reason any calorie restricted diet works is because of lowered insulin, as opposed to simply inducing a negative energy balance.
- If insulin is the ultimate cause of obesity, what is the mechanism? Now of course the pathology of obesity is far from simple. Obesity is a distinct metabolic state that is not equal to simply having too much body fat. And so while Dr. Fung admitted that he (or anyone else) can’t completely explain the exact mechanisms underlying obesity, saying that discussing mechanisms is irrelevant, made it difficult to bring many of the counter-points to the insulin hypothesis up. One example being that higher RMR I mentioned a minute ago. I also think that unless we have at least some mechanistic explanation for how insulin is the ultimate cause of obesity, it’s not accurate to be confident in it’s complete damnation. For example, we know insulin doesn’t trap fat in fat cells. In fact, in obese folks their fat cells are no poorer at releasing fat from fat cells than lean people, and in some cases may even be more lipolytic.
And’s that pretty much concludes my quick summary of some thoughts on 1-2 issues brought up in recent discussions, emails and the last podcast.
I’d love for you to leave a comment with your thoughts either on social media or on the show notes page at sigmanutrition.com/episode85. And if you enjoyed this episode, I’d really appreciate you sharing the link on social media or tagging someone in the comments.
In a couple of days time, Mike T Nelson will be on the show. For those of you not familiar with Mike T Nelson’s work, he’s brilliant. He did his own PhD. research on metabolic flexibility and continues to look deep into that area and various substrate use during exercise. In the next episode I’m going to chat with Mike about advanced metabolic flexibility, different substrate use, fasting, keto-adaptation, etc.
Until then, have a great day and I will talk to you in episode 86!