Nutrition / Health

Public health issues and sugar metabolism

By November 8, 2019 November 15th, 2019 No Comments

Never before have we had these levels of metabolic syndrome (obesity, diabetes, hypertension, high triglycerides) as we have today.

Back in the 70s there has been a strong propaganda against dietary fat. People have been led to believe that dietary fat makes us store more fat, that it increases cholesterol levels, and so on..

Coincidentally, this was the time HSCS has been invented and, naturally, people only started consuming more sugar, to make up for the, now reduced, calories from fat.

So did the high sugar consumption lead to mentioned diseases? We can’t say for sure, but there is a strong positive correlation between the two.

To understand this, we need to take a step back and understand sugar metabolism.

Ok so: The primary fuel for our bodies is GLUCOSE. From all the glucose we eat, 80% will get to cells around our body (upon Insulin release) where only 20% will hit the liver. This isn’t a bad thing because a large % will go towards replenishing the glycogen storage. Now many complicated enzymatic process will here occur, and the end point of it is that only about 0.4% of original calories will via SRABP1 (sterol receptor binging protein number 1) goes to form LDL (‘bad cholesterol’)

What about white sugar/ table sugar? This is SUCROSE which is in fact 50% glucose and 50% fructose. Glucose part is as above, but the let’s see what happens with the FRUCTOSE part!

Well, 100% of the fructose will hit the liver, as it does not spike insulin and doesn’t go to any other cell in the body. Again, complicated enzymatic process occur – eventually high as 30% from original number of calories eaten from sucrose even up stored as FAT!!!!

📖6 medical students were given a huge amount of group a)GLUCOSE and group b) FRUCTOSE. Group a developed NO FAT, group b stored 30% more fat (Helleestein et al., Annual rev.nutr.,1996)

In another study the acute administration of FRUCTOSE resulted in elevated triglycerides compared to the control group (Parks et al., Journal of nutrition, 2008).

Third study showed doubled triglycerides, 5 fold increase in de novo lipogenesis (new fat formation from sugar) and insulin resistance (Faeh and Schwartz, Diabetes, 2005).

The hormonal effects are quite straightforward. Glucose spikes insulin, insulin triggers leptin – so the brain gets signal that we are FULL.

FRUCTOSE doesn’t spike insulin, so no leptin response is induced. Consequently, the brain doesn’t get signal we are fed.

Another pathway is by not signalling GHRELIN and another is via the VEGAL nerve. So it would appear that FRUCTOSE doesn’t satisfy us, no matter how much we eat.

This can be one of the reasons HFCS and table sugars contribute to metabolic diseases.

Take home note is that wether sugar consumption is the main cause of mentioned conditions – we can’t say but it certainly is correlated and reducing the amount of refined sugars we consume as a society must be a priority, not a choice.