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Set point Settling points and Bodyweight Regulation Part 1

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Having explained why the separation of psychology and physiology is a false separation in Dieting Psychology vs. Dieting Physiology, I want to discuss quickly some of the physiology behind diet failures. This is a topic that I discuss in detail in nearly all of my recent books and I’m not going to spend endless time on it here (trying to eventually get back to the psychological factors behind diet failures).

A long standing debate in the world of obesity research revolves around the idea that bodyweight (or perhaps body fat) is regulated. What does that mean exactly?

Think about your thermostat (yes, this is the example I always use): you set it to keep the house at 80 degrees and it continually senses the temperature (via a thermometer). If the temperature goes above 80 degrees, the air conditioning comes on; if it drops below 80, the heat comes on. This is a regulated system. Your cruise control in the car works the same way: you set the speed you want to maintain and it either gives more or less gas to the engine in an attempt to maintain that level.

For some 50 odd years, it’s been thought that bodyweight/body fat are regulated similarly; that is the body is attempting to maintain some set level (called the set point) and is adjusting things like appetite, behavior, movement, etc. to do so.

A great deal of animal research supports this model: starve a rat and its metabolic rate slows, it moves around less (conserving energy), it’s appetite goes up such that when you give it free access to food again it will eat until it reaches its starting weight at which point things go back to normal. The same occurs when you fatten it up, metabolic rate goes up, activity goes up, appetite/hunger go down and it rapidly returns to its starting weight when you stop force feeding it. The rat is, somehow, trying to maintain weight at a set level.

Quick note: and this ties into that research review I did on homeostatic vs. hedonic pathways a few weeks back: exposed to certain types of diets (in rat lingo, this is called a cafeteria diet and consists of calorically dense tasty foods), most rats will readily maintain a weight that is above their set point (when exposed to a more typical rat diet). That is, the tastiness of the food can overcome any homeostatic attempts to prevent weight gain. This is important and something I’ll come back to later in this series.

Some research has found a similar effect in humans although the studies tend to be very mixed on this (I’ll address why in a later blog post): when you diet down a human being, often you see metabolic rate decreasing far more than you’d expect based on the loss of body weight alone. That is, based on the weight loss, say you expected metabolic rate to drop by 200 calories; but when you measure it it really drops by 300. That extra 100 calories is more than predicted and suggests that the body is ‘adapting’ to the weight loss in an attempt to not only slow further fat loss but also to get bodyweight/body fat back up when food becomes available again.

There are other adaptations, folks often decrease their activity levels (conserving energy), fat burning goes down and fat storage goes up, appetite often goes up so that people eat more when food is made available. In common parlance, this is often referred to as the ‘starvation response’ and, yes, there is something to it. Unfortunately, it’s basically the price that has to be paid for losing body fat to any significant level. People talk constantly about avoiding the starvation response and things of that nature but the only way to avoid it completely is to never lose fat.

In any case, perhaps the classic study in this regards is the Minnesota semi-starvation study, a 6 month study undertaken during the mid 20th century where a number of lean male war objectors were placed on 50% of their maintenance calories for the entire time while forced to engage in quite a bit of daily activity (5-6 miles walking per day).

In that study, after reaching the lower limits of human body fat levels (about 5%) and showing a host of adaptations (including an obsession with food), the men showed uncontrolled hunger when food was made available and rapidly ate themselves back up beyond their initial body fat level.

This has been termed post-starvation hyperphagia (a technical word that means overeating). Of course, it’s crucial to realize just how lean these men got; the response to less severe diets or fat loss is exactly that: less severe. A lot of this also depends on the nature of the intervention (e.g. type of diet) and the population studied. Initial body fat percentage plays a huge role here for reasons you’ll learn about in future blog posts.

Unlike in rats however, in humans, overfeeding doesn’t have nearly as reliable an impact in terms of increasing metabolic rate and it looks increasingly like any bodyweight regulation system present in humans is assymetrical: that is it protects against weight loss far more so than it protects against weight gain.

Put a bit differently and most realize this on some level: for most it’s far harder to lose weight than it is to gain it.

The reasons for this are a bit obscure but it’s thought that since humans never had any real evolutionary pressure to not get fat (e.g. we had no real predators and, during evolution, few could have gotten or stayed fat for extended periods), the body never had to develop defenses against weight gain. In contrast, starving to death was a very real reality in our evolutionary past and the body developed a number of ways of ‘defending’ against weight loss.

Moved into modern times (where food is readily available and activity levels continue to drop), this is a bad bad thing.

For completeness, I should note that there are exceptions, some people appear to show a pronounced response to overfeeding which is now being called NEAT (non-exercise activity thermogenesis) or SPA (spontaneous physical activity); some folks ramp these up to high levels when subjected to increased caloric intakes, burning off the excess calories instead of storing them as fat.

These are the people for whom gaining weight is often difficult: invariably when they try to increase food intake, not only do they sub-conciously start moving around more (burning off the excess calories), their hunger shuts off. You probably had one of these guys in your high school, the one who was always fidgeting and bouncing his leg and all of that; it turns out that the caloric expenditure from that type of activity adds up significantly over a day.

Hunger also seems to shut off more rapidly in these folks as well. They are often the folks who also claim “I eat a ton and can’t gain weight” but when you look at their food intake, they either aren’t eating much at all or they eat a single big meal and get so full that they don’t eat much else for the rest of the day (or next day).

Unfortunately, NEAT seems to be quite genetic and researchers still haven’t really figured out the exact causes or if this can be applied to help in any practical way. It probably has to do with not only the various hormones involved in all of this (which I’ll discuss in a later blog post) but how the brain responds to them.

In any case, all of the above supports the basic idea of a set point in humans: human metabolic rate, etc. clearly adapts (and does so more than weight loss alone would predict) to caloric restriction and weight/fat loss.

Unfortunately, it doesn’t appear to adapt nearly as well to overfeeding and weight gain.

Even more unfortunately, this isn’t the end of the story and determining exactly what sets the setpoint or whether or not it can change in the long-term is an area of continuing debate. Most of what I’ve seen suggests that, if setpoint can change, it only goes up. I’ve seen nothing to suggest that it ever comes back down, even over years of maintaining a lowered body weight.

Additionally, not everyone agrees with the idea of a biological setpoint anyhow, some researchers feel that a settling point is a better description of what’s going on.

Read Part 2

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