★What if Your Body Is Being Programmed to Store Fat?
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What if Your Body Is Being Programmed to Store Fat?
Many people blame calories or willpower, but a different signal may be quietly reshaping how the body uses and stores energy.
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Just the Gut Speaking, back when we were tied to the Natures Seasons anything with much Fructose would be hard to find in late Fall, Winter, Spring. Today, anything and everything no matter what the time of year is available. Here, what a great treat when the Strawberry's came into season. Or, apples, the berry's and all. Once a looked forward too time of year, now just one more thing on the menu. Still good, but now doesn't have the same antipipated bang. As pointed out in the article; "Fructose tricks your body into thinking winter is coming — It evolved as a signal of seasonal fruit abundance; a cue to eat heavily and store fat before food disappeared. In a modern food environment where that signal fires dozens of times a day, your body doesn't get the message that the harvest is over. It just keeps storing."
So many body function ques disrupted or interfered with. Cautious diets with whole fruits and berries throughout winter are likely just fine, it's just that as the article also points out there is a constant and heavy overload of Fructose from sources outside of foods too encouraging us to crave more than we should.
Not to worry though, we have a pill/shot for that!
Added sugars are included in various processed foods, such as sugary drinks, sweets and candies, desserts and sweet snacks, cereals and breakfast bars, coffee and tea, whole milk, and yogurts. They are associated with an increased risk of obesity, tooth decay, fatty liver disease, cancer, and cardiovascular disease. The amount of added sugars is also associated with all-cause mortality. This association with all-cause mortality has been shown to be significant and dose-dependent, particularly for added sugars in beverages.
An interesting point reported by Dr. Mercola is that the body can produce fructose endogenously, even without consuming sugar or fruit. This occurs through the so-called polyol pathway.
Previously, it was believed that fructose was primarily metabolized in the liver; however, plasma fructose levels are much lower than those in the portal vein and intestinal lumen. Recent findings have shown that the gut also plays a significant role in fructose metabolism. Recently, it was demonstrated that fructose is converted into glucose derivatives in the intestine. Recent findings on the metabolism of exogenous and endogenous fructose are topics of great interest. While the relationship between fructose intake and various metabolic diseases has been reported, the fact that the small intestine acts as a barrier to fructose and that fatty liver occurs despite a low concentration of fructose in the portal vein after fructose ingestion suggests the involvement of metabolites such as pyruvate, which is metabolized from fructose in the small intestine.
1. Glucose is converted into sorbitol by the enzyme aldose reductase.
2. Sorbitol is then converted into fructose by sorbitol dehydrogenase.
This pathway is especially activated when there is:
• Hyperglycemia (poorly controlled diabetes).
• Diets very high in refined carbohydrates.
• Ischemia or lack of oxygen in some tissues.
• Dehydration or high salt concentrations, as the body uses this pathway as a response to osmotic stress.
Mitochondrial dysfunction favors the process and is supported by experimental studies, but the strongest evidence establishes that there is a bidirectional feedback loop:
1) Mitochondrial dysfunction → more oxidative stress and greater activation of the polyol pathway under certain circumstances.
2) More fructose (dietary or endogenous) → greater mitochondrial damage and oxidative stress.
That is, researchers currently consider that both processes enhance each other, rather than a purely one-way cause-and-effect relationship.
Interestingly, internally produced fructose can have similar effects to that from the diet if it is generated in large quantities. Several researchers, including nephrologist Richard Johnson, have proposed that this endogenous production can contribute to:
• Fat accumulation in the liver.
• Insulin resistance.
• Increased uric acid. • Metabolic syndrome.
It is therefore important to follow Dr. Mercola's advice because in healthy individuals with normal glucose levels and a balanced diet, the amount of fructose produced is usually small and is part of normal physiology. The greatest concern arises when this pathway is chronically activated, for example, in obesity, diabetes, or habitual consumption of large amounts of refined carbohydrates, and other factors mentioned by Dr. Mercola.
Mitochondrial dysfunction increases oxidative stress and promotes metabolic alterations that can activate the polyol pathway, increasing the production of endogenous fructose in certain tissues.
In turn, fructose metabolism (especially when excessive) can deplete ATP, increase uric acid production, generate reactive oxygen species (ROS), and worsen mitochondrial function, creating a vicious cycle.
Emerging evidence also links fructose to cancer and dementia. In the devastating pancreatic ductal adenocarcinoma, fructose exhibits remarkable metabolic plasticity, enabling tumor cells to survive and proliferate under conditions of extreme nutrient deprivation and oxidative stress. This review systematically integrates the latest evidence confirming that fructose metabolism functions not only as an alternative carbon source but also as a coordinated and actively regulated survival strategy in pancreatic cancer. By integrating dietary intake of exogenous fructose with endogenous fructose synthesis via the polyol pathway, we reveal a multi-level regulatory network.
Fructose drives the pentose phosphate pathway flux, lipid biosynthesis, and AMPK-mTORC1 signaling, thereby maintaining redox balance, suppressing excessive autophagy, and promoting
https://pubmed.ncbi.nlm.nih.gov/31166222/ (2019)
https://pmc.ncbi.nlm.nih.gov/articles/PMC10096667/ (2023)
https://www.nature.com/articles/s42255-026-01506-y (2026)
https://www.nature.com/articles/s42255-024-01198-2 (2025)
https://link.springer.com/article/10.1186/s43556-025-00287-2 (2025)
https://www.frontiersin.org/journals/medicine/articles/10.3389/fmed.2026.1794440/full (2026)