Why a calorie isn't a calorie; what I wish I'd known about how the body processes energy

 It is so often an argument, does calorie counting work, is a calory of sugar more fat inducing than a calory of celery. I’ve never really understood why one source would be more energy inducing than another given that they have the same amount of energy.

Well, I’d like in this post to present what I have found recently starting with sugar.

When learning biology back in my GCSEs we were taught that the body uses glucose as a fuel and that glucose was sugar. Now although I’m sure the commutativity of that equality was never explicitly confirmed I had presumed that if glucose was sugar then sugar must be glucose right?

Kind of.

Sugar is made of a disaccharide called sucrose, this is a molecule made up of one glucose and one fructose. The body starts breaking this down in the saliva and then more so in the small intestine, where the glucose and fructose molecules are absorbed into the blood.

Now unlike glucose, most of the cells in the body can’t use fructose as fuel. That means that the sugar rush you feel come only from the glucose component of the sugar. Only half the calories, the other half don’t contribute to the “energy” you feel after having sugar.

What happens to the fructose?

Since most things that have died, in the history of life have died of a lack of energy the body will not let something that it could use as energy go to waste. Once in the blood, the fructose gets absorbed by the liver. The liver then converts this to glucose. However because the same amount of fructose was in the sugar as glucose, but whereas the glucose is used body-wide, is in the liver; that is a lot of glucose being built up in a single place. Too much glucose in the cells is a really bad thing as it will try to bond to all sorts of things causing damage to the cell. The body has a defence to this, it can turn the glucose into glycogen. It can only store so much glycogen so when its glycogen is full it starts to convert the free glucose of which there is still a very high amount (remember all that fructose is turned into glucose in the liver). Not to be deterred the body has another solution, the production of fatty lipids. As a result of the concentration of energy the conversion of fructose to glucose causes in the liver this can readily lead to non-alcoholic fatty liver desis.

The reason it’s called non-alcoholic (apart from it being caused by excess sugar and not from alcohol) is because most cases of excessive fat in the liver is seen in alcoholics. The reason is very similar. Alcohol can be processed by the body to make glucose too. This is also done in the liver, and when consumed in high or consistent amounts the alcohol causes the same local fatty build-up. This localised overconcentration of energy is one of the reasons for the beer belly.

This locally high concentration of energy also causes more of an insulin response that would happen from the glucose alone leading to a larger crash as the locally high level of glucose are absorbed into the nearby muscles and fat cells.

Why complex carbohydrates are better than sugar for a feeling of energy?

Complex carbohydrates, which are basically carbohydrates that aren’t sugar are broken down in the small intestine into glucose that is then absorbed into the blood. This, as explained in the last section, doesn’t lead to a very high local concentration of glucose although it may (normally 2 hours after eating) lead to high blood sugar. This is the reason that type 1 diabetics need to consume insulin after a meal.

Just because the complex carbs don’t go through the same damaging cycle that fructose and alcohol do doesn’t mean you can’t get fat off them. It does however mean that you will feel the energy from them before that energy becomes fat as opposed to fructose and alcohol which become fat before the glucose gets to the brain to allow you to feel the energy.

Fat then?

Fat as a group can be quite complex to understand. We lump saturated, unsaturated and all the other ways of subdividing these molecules into this one group of “fat”. It’s also an intuitive mistake to think dietary fat -> body fat. You are what you eat after all.

It is so much more complicated than that. Oils (generally labelled as fat) play an irreplaceable role in the functioning of the body. Like protein, they are not just used for energy but many other cellular processes. These processes more often than not require specific kinds of oil. Sometimes the body can make these specific kinds from its own supplies of fat and fat derivatives and sometimes it can’t. When it can’t it becomes very important that we include them as a part of our diet. Like most things in biology, it’s also rarely as clear cut as, can be produced, can’t be produced. There are many things the body can produce if its dietary source is depleted but will only do so sparingly. For these things, it’s generally advised that the dietary source should be the way your body sources the particular oil (the same applies for amino acids).

Although going any deeper into how the body handles fats is beyond the scope of this particular post it is worth noting something else I’ve recently learned. The muscle cells in our body can take in triglyceride to use as energy from the blood whereas the brain is far pickier and will only use glucose. Triglyceride is what the body digests fats into for transport around the body in the blood.


Protein is the hardest of the groups mentioned here for the body to use as a fuel and as such, it takes much more energy for the body to digest and then converts to glucose (if needed).

It also has the benefit of making you feel more full.

Starvation mode

When people talk about dieting they often talk about how the body will go into starvation mode. This is said to decrease metabolism and increase the bodies absorption of energy from the diet.

I’ve recently been curious about the mechanics of this starvation mode. Is it something that is controlled in the bodies neural system or does the body use chemical signals to notify all the cells that calories are scarce?

I was inclined to believe that it must be the latter as I can’t think of a mechanism by which neural signals would be able to affect the rate of metabolism inside the cells of the body.

It turns out it was only in the 1990s that the hormone leptin was discovered. The hormone is released by fat cells to notify the brain of their fullness. As the fat cells increase in size they release more leptin. This notifies the brain that there is no longer any need to be hungry. 

At least it should do.

 Originally it was thought that supplementary leptin would signify to the brain that it was full. That an injection a day would be a great cure for those with obesity. Unfortunately, the cure to obesity was not to be found so easily. It turns out that obese people already have ample leptin in their body. The issue is that over time the brain will become resistant to leptin. Much like how people develop a resistance to caffeine over time, or any drug really.

That means that although an obese person will have a concentration of leptin that should be signifying fullness, much like how a single coffee should be sufficient for anyone, the brain no longer recognises the current level of leptin as full instead considering it normal. A decrease in leptin from a diet will then be treated by the brain as the fat cells being empty. This alert will make the brain crave food, particularly food it knows to be high in energy.

Over time the mind will recover its leptin sensitivity but that isn’t going to help someone who has been overweight for years and is only months into a diet.

As with how abstaining from caffeine to regenerate your sensitivity takes seemingly far longer than developing that caffeine resistance, the same is true for leptin.

In the intervening decades since the hormone was discovered treatments using knowledge of leptin have been developed. One, a drug that is injected daily, uses a mechanism to increase leptin sensitivity, rather than simply increase the leptin levels further.

It is unclear from my own online searches if there is a baseline level of leptin for which a given individuals body cannot become sensitive of, making it harder to get to a body fat percentage that yields the washboard abs.

As with everything in the body the true mechanisms are far more complicated than x performs function y.

For one thing, there are many other hormones involved in the cycle of hunger and metabolism.

Solving obesity and ageing in a single change

The bird is the word.

I recently read a fascinating book with a captivating title: “Power, Sex, Suicide”. It explores the world around these powerhouses of our cells and how they are the major source of oxidants. It talks about how in birds the mitochondria are arranged differently such that they are constantly using up more energy. It seems the reason this was permitted on the evolutionary stage is that flight requires such a surge of effort that the cells needed to be able to deliver that effort on demand. The current architecture of bird mitochondria seems to be the way evolution has squared that circle.

To produce useful energy the mitochondria flow ATP through a chemical process that results in proton gradients (As aside it is fascinating how the body uses the most primitive unit of positive charge for its processes often in a similar way to how we use the most primitive unit of negative charge with electricity). When more energy is available than the body actually uses, birds will dump this energy into body heat. For humans it is conserved but the mechanism of conservation leads to “free radicals” building up in the cells. These free radicals over time cause issues with the cell’s epigenetic code. This could be somewhat exclusively what causes the major process of ageing. It is at least the major cause of epigenetic degradation which seems to be the main biological factor in ageing.

The fact that birds burn through unused energy means they have a much higher metabolism for a given bodyweight. It also reduces epigenetic damage. This results in birds having a 5 times increase in their natural lifespan when compared to mammals of similar weight class. 

If humans could move over to this mechanism for energy generation we would not only be able to eat more energy-rich foods we would also likely increase our life expectancy 5 fold.

This is a very first world solution to a very first world problem. Increasing human metabolism would also make starvation much more common and it is much more likely that the poorest even in rich societies would be on or below the bread line. 

Even so, there are currently more obese people than starving people and so killing two stony problems with one bird solution might be something that is pursued.


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