Why It Looks Like Overweight People Eat Too Much

By Steve Anthony

We have all been out somewhere and have seen an overweight person eating what seems to be too much food. But while objectively it might be a lot of food, I hope after reading this article you will understand that it’s not, necessarily, “too much food.” While I think you’ll find this article easy to read, you might find it difficult to wrap your head around, because it looks at weight gain/loss from a perspective we aren’t used to seeing it from.

The body has several homeostatic processes that keep us going, day after day, without us needing to think about them. Body temperature, for example, is kept at about 98.6 degrees Fahrenheit (37 degrees Celsius). On a hot day, our bodies make us perspire to help cool ourselves; on a cold day, we will be made to shiver in order to warm up. These are things we don’t need to think about — and we really would have a difficult time trying to prevent them from happening, as they are largely out of our conscious control.

Our weight is also regulated by a homeostatic process and is largely controlled by hormones — the king of which is insulin. Insulin performs many functions within the body but has a few key roles in weight management.

Insulin is secreted by the pancreas into the blood when we eat carbohydrate and, to a lesser extent, protein. It is insulin that makes glucose and its denser form, glycogen, available to cells in our body. When our cells are full of glucose and/or glycogen, insulin stuffs what’s left into adipose (fat) tissue.

Under conditions of a heavy intake of carbohydrate, which creates a spike in blood glucose, we get a corresponding spike of serum insulin to manage that glucose. The spike in serum insulin also inhibits the hormone glucagon from doing its job of directing the metabolism of body-fat for energy. So, essentially, fat metabolism drastically slows or stops and the body looks to use the glucose before turning back to fat for energy. Unfortunately, for many people, these insulin spikes also make their cells less sensitive to insulin (insulin resistant). That is, over time, it takes more and more insulin to manage the same amount of glucose in the blood.

We always have some glucose in our blood, so we also always have some base level of serum insulin to manage it. If our cells become insulin resistant, our base level of serum insulin goes up.

But what does this have to do with how much people eat?

Our homeostatic process for weight management works to strike a balance between our energy input and our energy output from day to day. These two ends of the balance are linked to each other — changing one impacts the other.

Eating more than usual one day leads to not being so hungry later on (or to being more active or just warmer) as the body works off the extra energy ingested earlier, in an attempt to maintain a balance around the body’s basal metabolic rate (BMR); eating less than usual (or moving more than usual) causes you to feel hungrier than usual — again, to get to that energy balance.

It’s important to note here that the “extra energy ingested earlier” exists in the body largely as stored fat. Even if you don’t overeat, a portion of the energy you ingest at a meal is likely stored as fat to be used later in the day and when you are asleep. It’s also important to remember that if the base level of serum insulin is above a certain threshold, the burning of “extra energy ingested earlier” will not occur. And, without the availability of that “extra energy ingested earlier,” the body will send hunger signals to the person to get them to ingest more energy, now.

Here’s the perspective we aren’t used to thinking about: Eating according to the USDA dietary guidelines, in terms of how many calories we should eat a day and the macronutrient composition of those calories, puts an enormous amount of glucose into the blood. If the body becomes insulin resistant and the base level of serum insulin rises above the fat-usage threshold, body fat becomes less available (or unavailable) for daily energy.

The rest will be easier to see via example — it’s oversimplified to convey the overall “plot;” there are other sub-plots going on as well, but this will give you a practical overview.

Let’s say Guy A needs 2000 calories a day to function (he’s 35 years old, 6’0″, 226 pounds). The USDA recommends as much as 65% of his daily calories come from carbohydrate — so, 1300 calories from carbs. Guy A is NOT insulin resistant so when he eats 2000 calories a day according to the suggested macronutrient ratios in the USDA guidelines, he maintains his 226 pounds. He will store some fat at meal-time, but will use that fat for energy when he’s not eating between meals and while sleeping. For the sake of the example, let’s say 600 of his 2000 calories get stored as fat and used up throughout the day and while he sleeps. So Guy A uses all 2000 calories over the course of the day and maintains his weight of 226 pounds.

Guy B is also 226 pounds, with the same physical stats as Guy A. His story, however, is quite different because he just pasted the threshold of being insulin resistant (by bad luck in the DNA department). Like Guy A, a portion of Guy B’s 2000 calories will get stored as fat. Let’s say it’s also 600 calories. The difference with Guy B is that he’ll never get to use those 600 calories because his elevated serum insulin won’t allow the fat burning process within his body to work.

The end result is that Guy B is living on 600 calories below his BMR requirement of 2000. As we saw above, this will make Guy B hungrier than Guy A — and will make Guy B eat more food in order to get those extra 600 calories. And Guy B will need to eat more than 600 calories to recover the ones locked in fat storage, because 65% of those extra calories will be carbohydrate and some will likely be sent to fat storage — so maybe he’ll need to eat 650 or 700 calories more than Guy A to get the same amount of available energy Guy A’s diet gives him.

This is why it seems that overweight people eat too much. We see Guy B eating more than Guy A and over time Guy B gets fatter and fatter — we assume Guy B gets fatter because he’s “eating too much.” What we can’t see is that both Guy A and Guy B are obeying the same hunger signals to get them to have 2000 calories of available energy each day, to live on. But because Guy B doesn’t have access to stored fat, he needs to eat more than 2000 calories to get 2000 calories of usable energy. So yes, Guy B is eating more than Guy A— but from a metabolic perspective, he is NOT eating “too much.”

And if we look deeper, we see that Guy B wasn’t eating “too much” on his way to becoming insulin resistant, either. It turns out he was just eating too much carbohydrate for his system — but this wasn’t something his doctor or nutritionist or his government clued him in on or warned him about. In fact, we’ve all been encouraged to eat a diet rich in grains and other carbohydrates.

Why we haven’t been clued in on the potential impact large amounts of carbohydrate can have on our weight (and other aspects of our health) is a topic for another article! Teaser: it’s not because the relationship between carbohydrate and weight gain wasn’t known…

References used in writing this article include:

Dokken, BB and Tsao, T-S, (2007) “The Physiology of Body Weight Regulation: Are We Too Efficient for Our Own Good?” Diabetes Spectrum, Vol 20, Number 3: 166–170.

Morton GJ, et al. (2006) “Central nervous system control of food intake and body weight,” Nature, 443:289–295.

Rosenbaum M, Leibel RL (1998) “The physiology of body weight regulation: relevance to the etiology of obesity in children,” Pediatrics, 101:525–539.

Leibel RL, Rosenbaum M, Hirsch J (1995) “Changes in energy expenditure resulting from altered body weight,” New England Journal of Medicine, 332:621–628.

Wadden TA (1993) “Treatment of obesity by moderate and severe caloric restriction: results of clinical research trials,” Annals of Internal Medicine, 119:688–693.

Keesey RE, Powley TL (1986) “The regulation of body weight,” Annual Review of Psychology, 37:109–133.

Sims EA, et al. (1973) “Endocrine and metabolic effects of experimental obesity in man,” Recent Progress in Hormone Research, 29:457–96.