Sugar – Part 1
Composition:
Sucrose or table sugar, is a disaccharide (two monosaccharides) synthesized by plants thanks to photosynthesis. The monosaccharides that make up sugar are glucose and fructose.
Each of these monosaccharides can be relatively healthy, but only in moderate amounts and when they come from real unadulterated foods. Table sugar being one of the worst way to obtain them, since in this refined form, glucose creates very pronounced insulin peaks and refined fructose, a series of dysfunctions that we will describe after we delve into the first one.
Glucose:
Since the body does not waste anything, glucose can take three routes:
- Be used immediately as energy.
- Being stored as glycogen (carbohydrate reserve), which is the short-term energy reserve.
- Being stored as adipose tissue (fat), which is the long-term energy reserve.
The route it takes has a direct relationship with the speed at which it is released into the blood, and this speed depends on the type of food from which that glucose is obtained.
When we eat, the food travels through the esophagus to the stomach, where acids and enzymes break it down and then pass to the intestine, where it is finished digesting before reaching the bloodstream.
As we have mentioned in the previous blog, if the glucose comes from foods rich in fibrous complex carbohydrates such as non-starchy vegetables, or those rich in resistant starches with a low glycemic index, the slowness that this process would take would cause it to be released little by little, so this scenario, may be ideal for people who decide to get much of their energy intake from carbohydrates.
This way of obtaining glucose is the slowest and most gradual, maintaining stable levels in the blood and, therefore, healthy levels of insulin.
The slower the release of glucose, the more likely it is that it can be used as energy by the tissues or stored as a short-term reserve (glycogen), but when refined flours and especially sugar are consumed, this changes radically.
Low-quality carbohydrates quickly raise blood glucose levels and therefore, the insulin response and, since the body does not waste anything, it is most likely that this glucose is stored as a long-term reserve (fat).
Glucose- Insulin resistance:
A continuous high intake of low-quality carbohydrates and vegetable seed oils, have the closest relationship with the development of the pathologic insulin resistance.
Low-quality carbohydrates such as simple sugars and refined flours, complicate blood glucose homeostasis and table sugar, is the one that produces the largest insulin peaks (1,2).
Once the cells start being resistant and glucose remains in the blood, the pancreas will release larger amounts of insulin in order to maintain a normal glycemic level.
This situation, where whatever is that stops working between the insulin receptor and the PI3K is compensated by an even greater secretion of this hormone, could last for years before being reflected in blood sugar levels.
(Note: We’ll see more about the PI3K in future blogs)
Glucose – Hyperglycemia:
If this situation continues, cells become so insensitive, that even with high insulin secretions, blood glucose levels will be higher and higher, which will finally be reflected in the analysis as “high sugar” and then, is when insulin resistance is finally diagnosed, something that could be prevented if in the annual analysis, fasting insulin levels and not only glucose, were requested. Because this way, we’ll know that insulin resistance is happening way before it’s reflected in the fasting glucose.
But this does not end there. If this situation is maintained long enough, the following is type 2 diabetes.
In most cases, type 2 diabetes is essentially the result of not remedying this downward spiral and yes, except in some exceptional cases (that I’ve never seen), this disease is self-inflicted (more about diabetes in future blogs called “lipids”).
(Note: Refined fructose is also related to insulin resistance, only through different mechanisms, which will be described later.)
Fructose, the other half:
Plants have developed defense mechanisms such as natural pesticides or lectins (more about lectines in future blogs called “Proteins”) to defend themselves from their predators.
Even vegetables considered healthy have some level of toxicity because like all living things, they do not want to be eaten and have no other form of defense.
However, the fruit seems to have been designed to invite us to eat it, since it is striking, colorful, tasty and falls directly into our hands. Almost as if the plant does not want any animal to miss them.
In her infinite wisdom, nature created an irresistible natural delicacy that makes that in our symbiotic relationship, both the plant and animal kingdoms have benefits.
On the one hand, the plants would have their seeds scattered in other areas by the defecation of the animals and on the other, thanks to the lipogenic (fat-generating) capacity of fructose, the animals would obtain long-term energy reserves (body fat), for the times of fasting that entails the shortage of food of the following seasons.
Today, we still get fructose in its natural form from honey, fruits and vegetables, but we also consume it in its refined form (mainly through table sugar), something that evolution did not prepare us for.
When eating a fruit, a large amount of nutrients and a small portion of fructose are ingested, which are slowly absorbed as it is accompanied by a high amount of fiber, as well as antioxidants, flavonoids, minerals and vitamins (3,4).
In a healthy person, eating honey or organic fruits in season and in moderation should not bring complications, but as we will see in the development of this blog, when eating refined fructose such as that contained in table sugar, the body does not respond in the same way.
Among other things, the consumption of refined fructose is particularly related to metabolic syndrome, hypertension, insulin insufficiency, lipogenesis, diabetes, inflammation and kidney disease (3,5,6,7,8).
Metabolic pathways of glucose and fructose:
Glycolysis is the metabolic pathway used to obtain energy from glucose.
Most of the glucose in the blood does not remain in the liver, but is immediately mobilized by all tissues to be used immediately as energy or stored as glycogen or fat (11).
Fructose can be catabolized into fructose 6-phosphate (phosphorylation at position six by hexokinases as with glucose) or, much more likely (based on animal studies), become fructose 1-phosphate in the liver (phosphorylation at position one by fructokinases).
This means that when fructose reaches the liver, it is phosphorylated at position one directly, without phosphorylation at position six. As a consequence, it becomes a substrate for aldolase, collaborating with higher levels of ATP and citrate, which manufacture fatty acids (9,10,7). In other words, this means that instead of being metabolized and used for energy throughout the body, fructose is almost entirely processed in the liver with the potential to be stored as fat. In addition to that, in this process it has the potential to intoxicate this organ in a way similar to alcohol (12).
Fructose doesn’t seem to be an efficient source of energy, and even if a part could be used as fuel it is not a direct source, but has to be converted into glucose, lactate or fatty acids in the liver (13,14,7).
If fructose avoids the first step of glycolysis in humans like we see in the animal model, it may explain why sugar is directly related to increased rates of nonalcoholic fatty liver disease and associated insulin resistance (9,15). In addition, by not producing significant increases in blood glucose and hormones involved in satiety (16,17), consumption tends to be excessive (this is a theme that we will also develop later).
Fructose – Insulin resistance:
Since fructose does not directly raise insulin, it is generally believed that it may be better in this regard, but refined fructose may also lead to insulin resistance, only through different mechanisms and with a much wider spectrum of complications.
As we have seen (at least in animal studies), unlike glucose, fructose is almost entirely metabolized in the liver, turning into an alcohol-like toxin (12) and creating a series of dysfunctions.
Fructose-induced insulin resistance is due to several direct and indirect mechanisms, including activation of protein kinase C, stimulation of lipogenesis, inhibition of mitochondrial β-oxidation of long-chain fatty acids, fructosylation of proteins, formation of reactive oxygen species, stress in the endoplasmic reticulum, formation of triglycerides and fatty liver (18,19,15,20,21,22).
“In conclusion, supplementation with fructose, but not glucose, causes fatty liver without inflammation and oxidative stress and alters insulin signaling in the three main tissues that respond to insulin, regardless of the increase in energy intake”
Miguel Baena et al. Sci Rep. 2016 (15)
The worst thing about table sugar is that it contains one molecule of each (glucose and fructose). Therefore, a high intake may collaborate with the pathology of insulin resistance both directly through the creation of insulin spikes by high glucose levels, as well as through the indirect mechanisms of fructose, which in the context of an overstimulated Growing Mode, may make table sugar one of the main promoters of insulin resistance.
Fructose vs. glucose:
As we mentioned, the high consumption of starches (especially refined flours), can bring health complications by creating spikes in blood glucose, but table sugar is more harmful.
By replacing starches (glucose) with sugar or fructose, both in animal and human studies are observed:
- Increased levels of insulin (1).
- Reduced sensitivity of receptors (23,24).
- Increased fasting glucose (25).
- Increased glucose and insulin response to sucrose loading (1,2).
On the contrary, when fructose is replaced by glucose (starches) in the diet of obese children (26,27), all the symptoms of metabolic syndrome improve, including:
- Insulin sensitivity.
- Fatty liver.
- Lipogenesis.
- Diastolic blood pressure.
- Triglycerides.
(TakeAway: Both glucose and fructose can contribute to insulin resistance, but while glucose takes various pathways (energy, glycogen, or fat) throughout the body, fructose may be absorbed by the liver and immediately converted to fat and even if some can be used as fuel, it is not a direct source of energy.
Calorie for calorie, the consumption of refined fructose such as that contained in sugar, is much more harmful than starch when it comes to metabolic syndrome, including blood pressure, triglycerides and fatty liver, but glucose can also be problematic if it is consumed from refined carbohydrates continuously.
For these reasons, if you decide to incorporate both fructose and glucose in your diet, they should come from the only form for which we are designed, that is, from a variety of vegetables and a moderate consumption of honey and seasonal fruits.)
Next blog…is sugar addictive?
References:
3 – The effect of two energy-restricted diets, a low-fructose diet versus a moderate natural fructose diet, on weight loss and metabolic syndrome parameters: a randomized controlled trial. 4 – Vitamin C intake and serum uric acid concentration in men.
5 – Increased fructose associates with elevated blood pressure.
6 – Added fructose: a principal driver of type 2 diabetes mellitus and its consequences.
7 – Fructose and cardiometabolic health: what the evidence from sugar-sweetened beverages tells us.
11 – Glucose: Chemistry and Dietary Sources.
12 – Fructose: it’s “alcohol without the buzz”
14 – Normal roles for dietary fructose in carbohydrate metabolism.
18 – The role of fructose in the pathogenesis of NAFLD and the metabolic syndrome.
19 – Fructose and hepatic insulin resistance
20 – Metabolic effects of fructose and the worldwide increase in obesity.
21 – Fructose as a key player in the development of fatty liver disease.
22 – Role of Dietary Fructose and Hepatic de novo Lipogenesis in Fatty Liver Disease.