So why is sugar bad again?

Instead of being very vague in order to sound knowledgeable, I’m writing down my current understanding of the science behind the explanations. Consequently, as forewarning, there are definitely some lapses in fact.

First, sugar is composed of 50% glucose (which is the essential energy component of life) and 50% fructose (which is what makes sugar sweet)

When we consume sugar, the glucose portion is metabolized normally and reaches the cell as energy. More on the normal process later.

However, the fructose is problematic since it does not metabolize normally, and most of it ends up going to the liver to be metabolized there. Fructose does not stimulate insulin secretion from pancreatic cells (insulin regulates how glucose gets delivered to and metabolized in cells), thus also somehow leading to insulin resistance in cells*** (when something goes wrong between the insulin hormone in the bloodstream and the its receptor on the cell)

Insulin resistance thus leads to several different harmful pathways. Because insulin resistant cells are not able to take in glucose, amino acids, or fatty acids, it inhibits glycolysis and thus energy production, and results in increased glucose levels in the blood, which directly leads to diabetes. (I’m actually unsure of that process as well). Insulin resistance in fat cells results in increased mobilization of stored lipids and fatty acids in one’s blood.

Because cells become insulin resistant, the body is misinformed and thinks that it needs to produce more insulin, and it thus signals the pancreas to produce more. At some point, the pancreas won’t be able to produce insulin to the needed levels, and the person becomes diabetic. But, increased insulin also blocks leptin, which is a hormone that regulates the positive/negative feedback system to the brain’s hypothalamus. Thus, if we have less leptin circulating, our bodies think that we are actually in starvation, resulting in the urge to eat even more, and ultimately the continuation of a vicious cycle of obesity.

Fructose is also metabolized as fat in the liver. I don’t know how or why, but the effects are serious. Once the liver is fatty, it overproduces LDL (Low Density Lipoprotein) and other cardiovascular risk factors.

Despite the fogginess on the biochemistry behind these interactions to explain causation (and my own dearth of knowledge), the important thing scientists do know is that there is a strong correlation. Liver fat is known to predict type 2 diabetes and to be extremely prevalent in obese individuals. I think that alone justifies identifying fructose as the enemy. Plus, the more obvious correlation is there. Obesity levels have risen drastically over the past thirty years, and so has the dietary intake of fructose (it’s more than doubled)


***I did find an article that hypothesized a solution to the missing explanation for the link between fructose and insulin resistance.

The article in essence: Caveat, this study was only conducted on mice in a lab. Nevertheless, researchers found that the gene PGC-1b was responsible for the building of fat in the liver because it boosted SREBP-1 levels, which is a gene that is a master regulator of the manufacturing of lipids in the liver.


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