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Glykation – wie Zucker und Hitze den Körper still altern lassen

Glycation – how sugar and heat cause the body to age silently

We are all familiar with the outward signs of aging: wrinkles, gray hair, and reduced mobility. But in parallel, a silent, invisible process takes place inside the body that significantly determines our biological age: glycation. This is a chemical reaction in which sugar molecules bind to proteins and fats, causing lasting damage. Modern research shows that this process is far more than just a cosmetic issue – it affects the aging of skin, brain, and blood vessels and can be significantly influenced by diet and lifestyle.

What is glycation?

Glycation is a non-enzymatic reaction in which sugar molecules (such as glucose or fructose) bind to proteins or lipids. . Unlike enzymatically controlled processes in the body, glycation occurs uncontrollably – and that is precisely what makes it so problematic.

This reaction produces so-called advanced glycation end products (AGEs) . These AGEs are highly reactive compounds that accumulate in tissues and can cause significant damage. Particularly insidious: Once formed, AGEs persist and accumulate over the lifespan.

The two sources of AGEs

The body is confronted with AGEs in two ways:

1. Endogenous AGEs (formed in the body): These are produced wherever elevated blood sugar levels persist for extended periods. People with diabetes or insulin resistance are particularly affected, but any significant fluctuation in blood sugar levels also contributes to AGE formation. .

2. Exogenous AGEs (from food): AGEs can also be formed when food is heated – namely through the Maillard reaction, the chemical reaction that gives roasted meat, toasted bread or fried foods their typical brown color and aroma. AGE levels are particularly high when exposed to dry heat, such as grilling, frying, deep-frying, or roasting. .

The effects of AGEs in the body

Destruction of collagen and elastin

Perhaps the best-known and most thoroughly researched effect of AGEs concerns the skin. Collagen and elastin – the two proteins responsible for the skin's firmness, elasticity, and resilience – are among the main targets of glycation. .

When sugar binds to these structural proteins, cross-links are formed between the collagen fibers. As a result, the normally flexible collagen becomes stiff and brittle. The skin loses elasticity, becomes thinner, and more prone to wrinkles. Dr. Ross Perry, a cosmetic doctor in London, describes the process as follows: "Normally, collagen plumps up the skin, giving it a younger, fuller appearance. Elastin gives the skin its ability to bounce back. If you consistently consume a high-sugar diet, collagen and elastin become stiffer, wrinkles form more easily, and cells are less able to repair normal damage." .

A particularly alarming finding: A study conducted by Leiden University Medical Center in the Netherlands with 600 men and women between the ages of 50 and 70 showed a direct correlation between blood sugar levels and perceived age. For every 1 mmol/l increase in blood sugar, perceived age increased by up to five months. .

Inflammation promotion via RAGE

AGEs bind to specific receptors on the cell surface, the so-called RAGE (Receptor for Advanced Glycation End Products). This binding triggers a cascade of inflammatory responses, including the activation of the pro-inflammatory NF-κB signaling pathway and the production of oxidative stress. This chronic, low-grade inflammation – also called "inflammaging" – accelerates the aging process in many ways.

Brain damage

A particularly current area of research is the link between glycation and neurodegenerative diseases. A study published in Biomaterials in January 2026 shows that AGEs accumulate in brain tissue and colocalize there with the typical protein deposits of Alzheimer's disease (amyloid-beta and tau). .

The researchers developed a model of the aged brain and were able to show that AGEs lead to **endothelial dysfunction** in the brain and to the activation of microglia (the brain's immune cells) – both factors that drive neuroinflammation and neurodegeneration. Particularly noteworthy: They discovered that the effects of AGEs are mediated via epigenetic mechanisms, specifically via the histone-modifying enzyme KMT2A. This opens up entirely new perspectives for potential therapeutic interventions. .

Impairment of memory function

Another recent study, published as a preprint on PubMed in January 2026, investigated the effects of dietary AGEs on memory. The researchers fed rats during adolescence – a critical phase of brain development – a diet rich in AGEs, which was produced by heat treatment.

The results are alarming:

  • The AGE-rich diet impaired the hippocampus-dependent memory function of the animals.

  • Changes were observed in the gut microbiome , even in the absence of obesity or other behavioral deficiencies.

  • The memory deficits were accompanied by impaired glutamatergic synaptic transmission in the hippocampus.

  • Important: The memory impairments could be prevented by administering the AGE inhibitor Alagebrium and by supplementing with an AGE-inhibiting bacterial strain (Lactococcus lactis).

This study demonstrates a direct functional link between early AGE exposure, the microbiome and memory disorders – and opens up possible preventive approaches.

Bone health: A nuanced picture

The Rotterdam Study, one of Europe's largest population-based long-term studies, investigated the relationship between skin AGEs (measured as skin autofluorescence) and bone health. The analysis, published in Bone in January 2026 and involving over 2,500 participants, reached a nuanced conclusion: no significant association was found between AGEs and changes in bone density over time. .

However, an interesting exception emerged: In people with type 2 diabetes, a higher AGE concentration was associated with lower bone density at the femoral neck. The authors suggest that AGEs influence bone health more likely through other mechanisms—such as bone quality or fall risk—and not primarily through bone density. .

The interaction with UV radiation

A particularly important finding of recent research is the interaction between glycation and UV radiation. UV light significantly accelerates the formation of AGEs in the skin by promoting oxidative stress and inflammatory processes. Conversely, AGEs intensify the harmful effects of UV radiation via RAGE activation – a dangerous vicious cycle.

In practical terms, this means that even those with a healthy diet cannot completely prevent glycation if their skin is exposed to the sun without protection. And those who use sunscreen but have persistently high blood sugar levels will also accumulate AGEs. The combination of both is particularly potent. .

How can glycation be slowed down?

The good news: We can significantly influence AGE formation through targeted measures.

Stabilize blood sugar

Since endogenous AGE formation depends directly on the level and duration of blood sugar levels, a blood sugar-stabilizing diet is the most important lever. :

  • Build meals from protein + fiber + healthy fats

  • Prefer whole-food carbohydrates to refined sugar (oatmeal, legumes, whole grains)

  • Replace sugary snacks with protein-rich alternatives (Greek yogurt, nuts, berries)

  • In cases of existing insulin resistance or diabetes: medically supervised blood sugar optimization.

Adapt cooking methods

The choice of preparation method has a huge influence on the AGE content of food. :

Low AGE formation:

  • Dampening

  • Cook

  • Poach

  • braising / slow cooking

High AGE formation (use sparingly):

  • Grilling / searing

  • Deep frying

  • Roasting at very high temperatures

Sufficient protection against UV radiation

Daily sun protection factor (even in the office and on cloudy days) is essential to slow down UV-driven AGE formation. .

Supportive nutrients

Certain micronutrients may reduce AGE formation:

  • Carnosine-containing foods (such as beef) or carnosine as a supplement are being discussed.

  • Antioxidants (vitamin C, vitamin E) can reduce oxidative stress, which promotes AGE formation.

  • In the animal study , Lactococcus lactis showed promise as an AGE-inhibiting bacterial strain.

Conclusion

Glycation is a silent but powerful driver of the aging process. It ages our skin, damages our blood vessels, impairs our memory, and contributes to the development of neurodegenerative diseases. However, current research also shows that we are not helplessly at the mercy of this process.

Stabilizing blood sugar levels, reducing high-heat cooking methods, and protecting skin from UV radiation can effectively slow down AGE formation. Combining these strategies is particularly effective – and has the added benefit of not only inhibiting glycation but also providing numerous other positive health effects. It's never too early – and never too late – to start.


Official sources & studies:

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