Feature articles

Sugar and skin health

Women’s magazines, numerous websites and even some dermatologists warn against eating sugar because of its adverse effects on skin. They say it ages skin, making it look dull and tired. We investigate these claims and examine the evidence.

CLAIM: eating sugar ages the skin.

The term ‘sugar sag’ was proposed in a 2015 skin therapy journal. The hypothesis suggests that sugar in food irreversibly binds to collagen, which is important for skin structure and without its reinforcement the skin becomes saggy, much like the effect of aging.  This hypothesis is detailed in a paper from 2010 describing how glucose and fructose link with collagen proteins in the skin to form Advanced Glycation End products (AGEs) rendering them difficult to repair.

What are AGEs?

AGEs are a heterogenous group of compounds formed through a non-enzymatic reaction between sugars and amino acids, lipids and nucleic acids. They are formed endogenously in the body and exogenously in food. Endogenous AGE formation is akin to the Maillard reaction in food. AGEs from both sources appear to have detrimental effects.

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Endogenous AGE production

The formation of AGEs is a normal part of metabolism, but excessively high levels are believed to contribute to oxidative stress and inflammation. AGEs have been implicated in several aging-related and diabetes-related chronic diseases such as cardiovascular disease, chronic kidney disease, insulin resistance, Alzheimer’s disease, connective tissue disease and skin aging.

Production of AGEs increases when blood glucose levels are high (hyperglycemia), during oxidative stress, when skin is exposed to UV light, and generally increases as we get older- even in healthy adults.  Research is emerging, but there are still many questions about the effects of AGEs, and how levels could be reduced including via dietary means. Diets with high glycemic index (GI) and high glycemic load (GL) have been associated with oxidative stress, and therefore may also increase AGE production, however this research has not yet been completed.

Reducing endogenous AGEs

The evidence for dietary manipulation of endogenous AGEs production is sparse and unconvincing. Possible mechanisms whereby dietary sugars might contribute have been suggested, however evidence is mostly in-vitro and in animal studies and results cannot be directly applied to humans.

“The involvement of endogenous glycation in dietary sugar-induced dysmetabolism is far from being demonstrated in humans.” – Arastro & Mastrocola

In animal models, feeding very high amounts of fructose has produced higher tissue levels of AGEs. Ninety five percent of Australians consume less than 60g fructose a day. Read more here about fructose in a previous Issue.

Besides normal aging and sun exposure, diabetes, insulin resistance and hyperglycemia increase AGE production (including glycated haemoglobin, or HbA1C), yet what causes these is a complex mix of individual genetic, metabolic as well as dietary risk factors.

When it comes to diet, GL is the best predictor of postprandial glycemia and insulinemia. An analysis of the Australian Health Survey (2011-12) found the biggest contributors to the GL of the diet were bread, cereal based dishes (like pasta and rice dishes), and breakfast cereals.

Sugary drinks, however, may be uniquely problematic, especially in the USA due to their high consumption. High sugary drink consumption has been found to be the main contributor of GL in the USA and studies suggest it may increase metabolic risk, alter glucose handling and insulin sensitivity. However, there is no evidence linking sugary drink consumption and increased AGE production in humans.

Exogenous AGEs in food

AGEs can be elevated in foods containing protein and carbohydrate. Cooking methods can influence AGE content and grilled, fried or roasted foods have higher levels. There is a dietary AGEs (dAGE) database of 549 foods now available and a practical guide to reducing AGE intake published by the American Dietetic Association. In summary:

  • Dry heat cooking produces 10-100 times more AGEs than in the uncooked state across all foods.
  • Animal foods high in fat and protein are generally AGE rich and form new AGEs during cooking.
  • Carbohydrate-containing foods such as vegetables, fruits, whole grains and milk contain relatively few AGEs, even after cooking.
  • Strategies to reduce AGE formation include using moist-heat cooking methods, shorter cooking times, lower temperatures, and using acidic ingredients. These cooking methods also reduce formation of Heterocyclic Amines (HCA) and Polycyclic Aromatic Hydrocarbons (PAH) when cooking meat, which are known carcinogens.
  • While population data is limited on AGE intake, a high intake is suggested at more than 15,000 kU AGE. People who consume a diet high in roasted meats, fats and highly processed foods could consume more than 20,000 kU. An optimal dAGE for disease prevention is not known, however a 50% reduction of usual consumption has been shown to reduce oxidative stress in animal studies.
  • A diet high in protein and fat and lower in carbohydrate may substantially raise dAGE intake and adversely affect health in the long term.

 AGE content of a range of foods

Food  Serving size (g) AGE kU/serve
Fried bacon 13 11905
Deep fried crumbed chicken breast 90 8750
Fried beef burger 90 4974
Sautéed tofu 90 4251
Grilled salmon fillet 90 3012
Greek feta cheese 30 2527
French fries 100 1522
Roasted almonds 30 1995
Donut, choc iced, crème filled 30 541
Chocolate chip cookie 30 505
Sunflower oil 5 197
McDonalds apple pie 30 191
Sugar frosted corn flakes 30 128
Oat and honey granola 30 128
Scrambled egg 30 35
Wholewheat bread 30 16
Banana 100 9
Sugar, white 5 0

 

Reducing dietary AGEs in a nutshell

The USA Academy of Nutrition and Dietetics concludes:

A significantly reduced intake of dAGEs can be achieved by increasing the consumption of fish, legumes, low-fat milk products, vegetables, fruits, and whole grains and by reducing intake of solid fats, fatty meats, full-fat dairy products, and highly processed foods”.

Does the evidence support ‘sugar sag’ in the skin?

There are numerous evidentiary gaps undermining the ‘sugar sag’ theory.

  • Evidence is lacking for any direct relationship between endogenous AGEs and diet and how to reduce them.
  • Hyperglycemia increases endogenous AGE formation but eating sugar per se does not.
  • AGEs can be consumed pre-formed from a wide variety of foods. Sugar itself has zero AGEs and processed sweet foods are on the lower end of the AGE content range.

In summary, eating too many AGE rich foods may contribute to inflammation and aging and it may be prudent to limit dry-cooked animal foods as they contain the highest amounts of exogenous AGEs. Perhaps ‘sugar-sag’ should be renamed ‘roast meat-sag’.  Sugar intake causing endogenous AGE formation is not supported by the evidence. The GI and GL of the diet are possible promoters of AGEs but there is no evidence for this to date and is a worthy future research topic. 

NEXT: Milk intake in Australian children

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