Food affects the body in various ways and sugar only affects it by making it fat.

Sugar (sucrose) and high fructose corn syrup contain two molecules: glucose and fructose.

Glucose is absolutely vital for life and is an integral part of our metabolism. Our bodies produce it and we have a constant reservoir in our bloodstream.

Every cell in the body can use glucose for energy.
If we don’t get enough glucose in our diet, our bodies make what we need from protein and fat.

Fructose, however, is very different. This molecule is not a natural part of metabolism and is not produced by humans.

In fact, very few cells in the body can make use of fructose, except for liver cells.

When we eat a large amount of sugar, most of the fructose is metabolized by the liver. There it is converted to fat, which is then secreted into the blood.

1. Fructose Causes Insulin Resistance

Have you ever heard of the hormone insulin?

It is one of the key hormones that regulate human metabolism and energy use.

Insulin is secreted by the pancreas, then travels in the blood to peripheral cells such as muscle cells.

Insulin signals these cells to put glucose transporters on their surface, allowing glucose to enter cells where it can be used.

When we eat a high carbohydrate meal, glucose levels rise. Excess glucose is toxic so insulin rises rapidly to move glucose out of the bloodstream and into the cells.

If we didn’t have insulin or it wasn’t working properly, blood glucose would reach toxic levels.

In healthy people, this mechanism works very well, allowing us to eat carbohydrate-rich meals without making our blood glucose levels too high.

However, this mechanism tends to break down. Cells become resistant to the effects of insulin, causing the pancreas to have to secrete even more insulin to drive glucose into the cells.

Basically, when cells become resistant to insulin, you will have more insulin in your blood all the time (until it all breaks down and leads to type II diabetes, which can happen over time).

But insulin also has other functions. One of them is to send signals to our fat cells. Insulin tells fat cells to pick up fat from the bloodstream, store it, and avoid burning the fat they’re already carrying.

When insulin levels are chronically elevated, much of the energy in our bloodstream is selectively deposited in fat cells and stored.

Excess fructose consumption is a known cause of insulin resistance and elevated blood insulin levels.

When this happens, the body has a hard time accessing stored fat and the brain starts to think it’s hungry. So we eat more.

Mechanism # 1 in which sugar consumption leads to having more fat and gaining weight:

Eating a lot of sugar chronically increases blood insulin levels, which selectively deposit energy from food into fat cells.

Learn more about “fructose” in our article: The 4 Dangers of the Sweetest Poison: Fructose .

2. Fructose causes resistance to a hormone called leptin

Fructose also causes weight gain through its effects on a hormone called leptin.

Leptin is secreted by fat cells. The larger the fat cells, the more leptin they secrete. This is the signal the brain uses to determine how much fat you have stored for a rainy day.

When we eat food, some of it is stored in fat cells. This causes the fat cells to grow larger and secrete more leptin.

When the brain detects the increase in leptin, it “sees” that we have enough stored fat and that we don’t need to eat.

This is the elegant mechanism designed by nature to make us stop being hungry and eat less when there is a lot of fat in our fat cells, which is supposed to prevent us from becoming obese.

More fat = more leptin = we have enough energy = no need to eat. Easy.

The increase in leptin also makes us release more fat from our fat stores and increases the metabolic rate.

This is how it is supposed to work, but if the brain becomes leptin resistant (not “seeing” leptin in the blood), then this regulatory process will not work.

If the brain doesn’t see leptin, it won’t know that the fat cells are full and there won’t be any signals to tell the brain that it needs to stop eating.

Low leptin = we don’t have enough stored energy = we need to eat more and burn less.

This is how leptin resistance leads us to store fat. The brain thinks the body is starving and makes us eat more and burn less.

Trying to “willpower” over the powerful leptin-driven hunger signal is nearly impossible. This is why most people can’t just “eat less, move more” and live happily ever after.

In order to be able to eat less, we have to get rid of leptin resistance, so that our brain “sees” all the fat we have stored.

A high fructose diet can cause leptin resistance. One mechanism is that fructose raises blood triglyceride levels, which blocks the transport of leptin from the blood to the brain.

This is how excess sugar disrupts the regulation of body fat, causing the brain to think it needs to keep eating.

Mechanism #2:

Fructose makes the brain leptin resistant, which means the brain can’t “see” all the fat stored in the body and thinks it’s starving. This causes a powerful leptin-induced biochemical drive to keep eating even when we don’t need to.

3. Fructose does not induce satiety in the same way as glucose

The way in which the body and brain regulate food intake is extremely complex, involving multiple hormones and neural circuitry.

There is a region in the brain called the hypothalamus, where all these signals are interpreted.

This is where leptin (mentioned above) works in the brain, along with various neurons and other hormones.

A relatively new study published in 2013 examined the effects of fructose versus glucose on satiety and food intake.

They gave 20 healthy volunteers either a glucose-sweetened drink or a fructose-sweetened drink, scanned their brains, and asked them a bunch of questions.

It turned out that the glucose drink reduced blood flow and activity in the hypothalamus (where food intake is controlled), while the fructose drink did not.

The glucose drinkers felt less hungry and more full compared to those who drank the fructose drink, who did not feel full at all and were still somewhat hungry.

This implies that the fructose-sweetened drink, despite having the same calories as the glucose drink, did not influence satiety as much.

Another important hormone is called ghrelin, the “hunger” hormone. The more ghrelin produced, the hungrier we feel.

Another study showed that fructose did not reduce blood levels of ghrelin nearly as much as glucose.

These studies suggest that fructose does not make you feel full after a meal in the same way that glucose does, even with the same number of calories.

Mechanism #3:

Fructose does not make you feel full after a meal in the same way that glucose does, leading to an increase in total calorie intake.

4. Sugar can cause addiction in some people.

Sugar triggers opiate and dopamine activity in the reward centers of the brain, as do drugs of abuse such as cocaine.

In a large review article published in 2008 in the journal Neuroscience and Biobehavioural Reviews, researchers examined the evidence for the potential addictiveness of sugar.

These studies were done on rats, which are good representatives of humans because they become addicted to abusive drugs in the same way that we do.

This is a quote we took from the study:

“The evidence reviewed supports the theory that, in some circumstances, intermittent access to sugar can lead to behavioral and neurochemical changes that mimic the effects of a substance of abuse.”
The evidence that frankly demonstrates that sugar is addictive is very strong. It makes perfect sense since sugar affects the same neural pathways as drugs of abuse.

Eating sugar gives us “high” and releases opiates and dopamine into the brain’s reward system, specifically in an area called the Nucleus Accumbens. These are the same areas stimulated by drugs of abuse like nicotine and cocaine.

For certain individuals with a certain predisposition, this can lead to addiction outright.

People who have strong cravings for sugar and are unable to stop or reduce their intake despite negative physical consequences (such as weight gain) are addicted to sugar.

Mechanism #4:

Sugar, due to its powerful effects on the reward system in the brain, leads to the classic signs of addiction comparable to drugs of abuse. This activates a powerful reward behavior that can lead to overeating.

Learn more about “lowering sugar” in our article: How to Lower Blood Sugar in 8 Steps .

The perfect recipe to gain fat

Okay, so let’s take a step back and review what we’ve covered on fructose and fat gain.

Fructose causes insulin resistance and increases insulin levels in the body, which increases fat deposition in fat cells.
Fructose causes resistance to a hormone called leptin, which prevents the brain from “seeing” that fat cells are full of fat. This leads to increased food intake and decreased fat burning.
Fructose does not make you feel full after meals. It does not decrease levels of the hunger hormone ghrelin and does not reduce blood flow to the appetite control centers of the brain. This increases overall food intake.
Sugar, with its powerful effect on the reward system, is addictive in certain individuals. This activates a powerful reward behavior that also increases food intake.
Therefore, excessive consumption of fructose throws off short-term energy balance on a meal-to-meal basis and throws off long-term energy balance.

The more sugar you eat and the longer this process is allowed to continue, the more powerful it becomes. Insulin and leptin resistance increase over time and reward-seeking behavior becomes stronger.

In this way, sugar sets up an extremely powerful biochemical drive to make you eat more, burn less fat, and gain weight. Trying to maintain willpower on this powerful unit can be next to impossible.

I would like to point out that this does not apply to whole fruits, which are real foods with fiber and low energy density. Fruits are a relatively minor source of fructose in the diet.