Glycation, skin aging, cellulite and diet: what is the connection?
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What is glycation and how can it cause skin looseness and cellulite?
It is already known for decades that glycation causes skin and whole body ageing, and consequently cellulite
It’s official: Advanced glycation end-products end up straight into the skin and other body tissues, leading to skin damage and aging
Reduce glycation to reduce whole body ageing, skin ageing, cellulite and skin looseness
The Association Between Dietary and Skin Advanced Glycation End Products: The Rotterdam Study
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What is glycation and how can it cause skin looseness, skin aging and cellulite?
Very few people have ever heard of the term “glycation” and what it does to the body.
Glycation is the process of sugar molecules reacting with proteins and consequently damaging them.
Glycation is one of the main causes of age-related diseases as it leads to skin and blood vessel damage, which results in whole body ageing and, in particular, skin aging, cellulite and loose skin.
The products of the reaction between sugar molecules and proteins are called advanced glycation end-products, or AGE in short.
Advanced glycation end-products are found in carbohydrate-rich foods, especially those cooked at high-temperatures (fried, heavily grilled, toasted, caramelised etc).
AGEs are also produced inside the body, when high levels of carbs/sugars are consumed. As expected, with insulin resistance/diabetes, body glycation is extremely high.
A measure of glycation in the body is provided by a blood test marker called glycated haemoglobin, glycosylated haemoglobin or HbA1c, useful in checking insulin resistance, blood glucose levels and diabetic status.
Tests that measure glycation in the skin (skin autofluorescence) also exist.
It is already known for decades that glycation causes skin and whole body ageing, and consequently cellulite
We know for a few decades now about the detrimental role of glycation on body ageing, blood vessel aging, skin aging and, consequently, cellulite.
Glycation is a major cause of aging and an important cause of cellulite too.
(Of course, you will never read that in any “beauty” article in high-end consumer magazines. For them anti-aging is all about using using SPF 50 even in your sleep, exfoliating three times a day and having lots of botox and fillers…)
We also know that heavily cooked carbohydrate foods do contain high amounts of advanced glycation end-products.
And we know that some AGEs do get detoxified by the body but also that the body produces its own AGEs, especially in people with metabolic syndrome / insulin resistance (pre-diabetes) or full-blown diabetes.
But we did not know with certainty:
If those unhealthy chemical compounds already found in foods even before ingestion and metabolism accumulate in the skin
If those compounds are fully detoxified by the body
Or if perhaps the body itself creates and deposits more AGEs than it receives from food, even in healthy people without insulin resistance
It’s official: Advanced glycation end-products end up straight into the skin and other body tissues, leading to skin damage and aging
A research paper published in the American Journal of Clinical Nutrition has answered some of these questions.
In a study called The Rotterdam Study, scientists looked into the dietary intake and AGE concentration of 2515 people. A percentage of them suffered from diabetes and chronic kidney disease (CKD), which are known to accumulate AGEs in the body.
After analysis of the data the researchers found that AGEs found in unhealthy foods, especially the most common AGE chemical carboxymethyl-lysine (CML), do accumulate in the tissues of healthy people.
In fact, when measurement of dietary AGEs was time-wise close to measurement of skin AGEs, the link between diet and skin AGE accumulation was even clearer.
This means that dietary AGEs get absorbed and deposited into the skin very quickly and then only very slowly detoxified.
On the other hand, in people with diabetes or chronic kidney disease there was no clear temporal link between higher dietary AGE intake and higher AGE skin content.
This is explained by high AGE formation in diabetes and decreased AGE kidney elimination in chronic kidney disease or perhaps by different diets in these disease groups in relation to a healthy population.
This all practically means that glycated food components end up in the skin where they contribute to skin aging, inflammation, cellulite and skin laxity.
Reduce glycation to reduce whole body ageing, skin ageing, cellulite and skin looseness
Glycation is known to cause ageing in various tissues, including the skin, regardless of where and how it is produced, i.e. in our bodies or by high temperature cooking.
However, we can minimise the glycation load in our bodies by:
Eating healthier foods, with less sugars and less carbohydrates overall
Specifically avoiding high fructose corn syrup, fructose, table sugar, agave and apple juice, all rich sources of fructose (fructose causes much more glycation than glucose)
Cooking foods at lower temperatures, i.e. no frying (of any kind, even stir frying for more than a few seconds) and no heavy grilling / toasting / broiling / roasting / charring / caramelising
Eating lots of vegetables, berry and citrus fruits and herbs, which contain natural chemicals that fight glycation
Supplementing with the dipeptide carnosine, the most effective anti-glycation natural compound
Applying a body cream with known anti-glycation natural chemicals, such as green coffee extract, centella asiatica extract, green tea extract, turmeric extract and carnosine, among others
This in turn will help prevent age-related diseases, skin ageing and even skin looseness and cellulite (glycation is a major factor in cellulite and skin laxity).
The Association Between Dietary and Skin Advanced Glycation End Products: The Rotterdam Study
Research paper link: https://academic.oup.com/ajcn/article/112/1/129/5846050
Abstract: Background: Advanced glycation end products (AGEs) accumulate in tissues with age and in conditions such as diabetes mellitus and chronic kidney disease (CKD), and they may be involved in age-related diseases. Skin AGEs measured as skin autofluorescence (SAF) are a noninvasive reflection of long-term AGE accumulation in tissues. Whether AGEs present in the diet (dAGEs) contribute to tissue AGEs is unclear. Objectives: Our aim was to investigate the association between dietary and skin AGEs in the Rotterdam Study, a population-based cohort of mainly European ancestry. Methods: In 2515 participants, intake of 3 dAGEs [carboxymethyl-lysine (CML), N-(5-hydro-5-methyl-4-imidazolon-2-yl)-ornithine (MGH1), and carboxyethyl-lysine (CEL)] was estimated using FFQs and the content of AGEs measured in commonly consumed foods. SAF was measured 5 y (median value) later using an AGE Reader. The association of dAGEs with SAF was analyzed in linear regression models and stratified for diabetes and chronic kidney disease (CKD, defined as estimated glomerular filtration rate ≤60 mL/min) status. Results: Mean ± SD intake was 3.40 ±0.89 mg/d for CML, 28.98 ±7.87 mg/d for MGH1, and 3.11 ±0.89 mg/d for CEL. None of them was associated with SAF in the total study population. However, in stratified analyses, CML was positively associated with SAF after excluding both individuals with diabetes and individuals with CKD: 1 SD higher daily CML intake was associated with a 0.03 (95% CI: 0.009, 0.05) arbitrary units higher SAF. MGH1 and CEL intake were not significantly associated with SAF. Nevertheless, the associations were stronger when the time difference between dAGEs and SAF measurements was shorter. Conclusions: Higher dietary CML intake was associated with higher SAF only among participants with neither diabetes nor CKD, which may be explained by high AGE formation in diabetes and decreased excretion in CKD or by dietary modifications in these disease groups. The dAGE–SAF associations were also modified by the time difference between measurements. Our results suggest that dAGEs can influence tissue AGE accumulation and possibly thereby age-related diseases.
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