High fat diet + glycation = obesity

Glycation, obesity, ageing and metabolic disease


Is glycation the cause of today's obesity and degenerative disease epidemic?

A new study published last month has shown that a high-fat diet rich in AGEs (advanced glycation end-products) induces overweight / obesity faster than an equivalent high-fat but low-AGE diet.

This study shows that AGEs accelerate fatty liver and obesity, when combined with a high fat diet, but similar results should be expected with a AGE-rich, high carb diet, as it seems both diets are fattening and glycation plays the role of accelerator of fattening.


What are AGEs / advanced glycation end-products?

Advanced glycation end-products are produced when sugar reacts with protein, either during cooking or inside the body. Sugar-rich foods and overcooked protein-rich foods, both lead to the creation of AGEs.


The evils of dry-heated protein and of sugary food

For example, dry-cooked meat, i.e. barbecued, fried, grilled, broiled or over-roasted meat, is extremely high in AGEs. Caramelised or crispy protein is exactly a glycated protein. Fried bacon, for example, contains 38,985% more AGEs than smoked ham! Other dry-heated, high-protein foods are also quite high in AGEs. Conversely, protein cooked in moist heat produces very few AGEs.

Furthermore, high-temperature, dry-heated food also  lead to the formation of heterocyclic amines, benzopyrenes, and polycyclic aromatic hydrocarbons, which are known carcinogens. In addition, fried food leads to the creation of lipid peroxidation products and advanced oxidation protein products (AOPP), also very detrimental to health, especially cardiovascular health and skin ageing.

Over-grilled, charred food, so popular in the UK, is one of the richest sources of AGEs, benzopyrenes, lipid peroxidation products and AOPPs.

On the other hand, sugar-rich foods, cooked or uncooked, produce AGEs inside the body, as opposed to dry-heated protein where AGEs are produced during cooking.

AGEs are known to contribute to ageing, diabetes, cardiovascular disease and cellulite, and this new study has shown that they also lead to faster weight gain and fatty liver disease. From this perspective, a low-AGE diet seems to be essential in the fight against overweight, obesity and degeneration diseases that plague people the modern world.


"What can I practically do?"

It's simple:

  • Keep to low-heat, moist-cooked food, rather than high-heat, dry-cooked or fried food. Marinated meat or meat cooked with a little water in the oven and covered (not wrapped) with some aluminium foil is far better than broiled, grilled, charred or fried meat. The same applies to all other protein-rich foods. This may sound boring, but with some nice marinade, food can be as tasty as grilled food, so try to become an expert cook in marinades, instead of a barbecue expert. Besides, skin ageing, obesity, diabetes, heart disease and cellulite is far more boring...
  • Avoid sugar and all sugary food, at all costs
  • Have a diet rich in vegetables and fruit, both known to contain substances that fight glycation. The antioxidant chlorogenic acid, for example, found in numerous vegetables, herbs and green coffee, helps fight glycation. Moreover, the flavonoid quercetin has recently been found to reduce glycation by 60%. More and more natural chemicals from fruit and veg are discovered every year that can fight glycation, so you can't go wrong by increasing your intake!
  • The aminoacid carnosine is the strongest natural anti-glycation agent we currently know. Take 500-2,000mg of carnosine daily to help mitigate some of the effects of glycation (always consult a healthcare professional first)
  • On skin, use a quality, concentrated cream that is rich in chlorogenic acid and carnosine for topical protection against glycation



Paper: Advanced Glycation End Products Induce Obesity and Hepatosteatosis in CD-1 Wild-Type Mice.

Abstract: AGEs are a heterogeneous group of molecules formed from the nonenzymatic reaction of reducing sugars with free amino groups of proteins, lipids, and/or nucleic acids. AGEs have been shown to play a role in various conditions including cardiovascular disease and diabetes. In this study, we hypothesized that AGEs play a role in the "multiple hit hypothesis" of nonalcoholic fatty liver disease (NAFLD) and contribute to the pathogenesis of hepatosteatosis. We measured the effects of various mouse chows containing high or low AGE in the presence of high or low fat content on mouse weight and epididymal fat pads. We also measured the effects of these chows on the inflammatory response by measuring cytokine levels and myeloperoxidase activity levels on liver supernatants. We observed significant differences in weight gain and epididymal fat pad weights in the high AGE-high fat (HAGE-HF) versus the other groups. Leptin, TNF-α, IL-6, and myeloperoxidase (MPO) levels were significantly higher in the HAGE-HF group. We conclude that a diet containing high AGEs in the presence of high fat induces weight gain and hepatosteatosis in CD-1 mice. This may represent a model to study the role of AGEs in the pathogenesis of hepatosteatosis and steatohepatitis.