In the past seven years, sugar consumption worldwide has increased by nearly twenty million metric tons. 1 This is an alarming statistic considering sugar’s deleterious role in the development of obesity, diabetes, gastrointestinal issues, cardiovascular disease, and cancer.
Dietary sugar may also be involved in creating advanced glycation end products (AGEs). AGEs are formed when glucose attaches to proteins (specifically, the amino acids lysine and arginine) within the body. Microvascular and macrovascular damage, seen in diabetes, is attributed to the accumulation of AGEs in tissues.2
AGEs role in disease
The accumulation of AGEs over time in vivo contributes to changes in the structure and function of the cardiovascular system. It is suggested that AGEs disrupt collagen fibres responsible for adding elasticity to and protecting the integrity of arterial walls. Therefore, this produces stiffness of the blood vessels. One study looked at twenty-seven post-mortem aortas from people with diabetes and found a correlation between AGEs accumulation and aortic stiffness.3
AGEs may also contribute to sarcopenia, which is a loss of muscle mass and strength, by increasing oxidative stress and inflammation. Studies have found that a decline in muscular function observed in ageing and increased muscle weakness have been connected to higher levels of AGEs. 4, 5
In the skin, glycation is associated with the ageing process and negatively affects endothelial cells and fibroblasts and structural proteins such as collagen and elastin.6 In the elderly, the accumulation of AGEs modifies the mechanical properties of human skin by decreasing elasticity and increasing stiffness.6
Dietary consumption of AGEs
AGEs are not only found in our bodies but can also be sourced from food. Highly processed foods, especially foods that are processed by using high levels of heat, contain AGEs. Also, the way in which food is prepared may also affect the amount of AGEs found in it. Meat that is grilled or charred contains high levels of AGEs.
Scientific evidence suggests that eating a higher amount of AGEs from a more processed diet can contribute to insulin resistance. A study done in Diabetes Care showed that implementing a diet restrictive in AGEs improved insulin resistance. Two groups of diabetes patients, who both followed the standard protocol of care for diabetes, were randomised to either a high- or low- AGE diet. The group that followed the low-AGE diet showed improved insulin resistance, as restricting AGE consumption may help preserve the body against oxidative stress.7
Another study in Current Diabetes Reports found that higher increased circulation of AGEs was found in the bodies of subjects who consumed a meal with high AGE content. Also, the authors concluded that by lowering AGE intake, hyperinsulinemia could improve by 40 percent in type 2 diabetes patients and that excessive intake of AGE may be a potential cause of diabetes.8
Sugar Intake and AGE progression
A large amount of the research that has been done on how AGEs affect the body has been focused on diabetes patients. This is so because people with diabetes do not process sugar efficiently, creating an environment in which glycation can occur.
In a review of AGEs and diabetes, the authors state that “the most important pathway involved in the pathogenesis of the accelerated atherosclerosis in diabetes is most likely the increase in non-enzymatic glycation of proteins and lipids, with the irreversible formation and deposition of reactive AGEs.”9 The authors continue to describe how AGEs do this by breaking down collagen, which creates plaque within arterial walls. Therefore, there is evidence to conclude that AGEs are responsible for the deterioration of collagen in diabetic patients.
According to Dr. Ellen Marmur, dermatologic surgeon and associate clinical professor of dermatology at The Mount Sinai Medical Center, “the only testing that has been done on glycation and the skin has been in vitro (in a Petri dish in a laboratory), so there’s a long way to go before it’s proven that eating carbohydrates and sugars can destroy the collagen in the dermis. Can sugars do equally damaging things to collagen in the skin, even in people who don’t suffer from diabetes? It’s a very interesting theoretical question and a strong argument could be made, but there are as yet no human controlled studies to show the relevance of glycation to the skin.”10
Although there is limited evidence to conclude that eating sugar could theoretically increase AGEs in the skin, there is research to support sugar’s role in disease development, especially type 2 diabetes (which has been proven to increase AGEs).
Research has shown that increased sugar intake can lead to the formation of diabetes. 11, 12 This is so because eating too much sugar increases insulin resistance. Insulin is the hormone that is responsible for clearing excess sugar from the blood and placing it into the cells, which use it to perform metabolic activities. However, when the body is overloaded with sugar, the cells become less sensitive to insulin, not allowing sugar to enter. This causes a build-up of sugar in the bloodstream and other tissues. The build-up of sugar increases glycation activities and causes oxidation and inflammation.
Sugar intake is also associated with a weakened immune system13, an increased risk of ulcerative colitis and Crohn’s disease14, cardiovascular disease15, and cancer16. All of these diseases are associated with biomarkers that show increased inflammation, all of which can contain an environment in which AGEs can do more damage. Therefore, indirectly, dietary sugar can contribute to the formation of AGEs and increased inflammation within the body.
Interesting research on a fruit that can decrease AGEs within the skin
Akebia quinata is a creeping woody vine that comes from East Asia. The dry ripe fruit of A. quinata is used as an analgesic, an antiphlogistic and a diuretic in traditional Chinese medicine. In Korean medicine, it is used to treat obesity.
In a 2015 in vitro study looking at how the fruit extracts of A. quinata affects skin ageing, A. quinata was able to inhibit AGE activity and significantly decreased the appearance of wrinkles after eight weeks.17 More human studies need to be conducted in order to have more conclusive recommendations; however, this study shows promise as to how A. quinata could be an effective anti-ageing agent.
Dietary recommendations to decrease AGE formation
- Decrease sugar consumption. Although further research needs to be done to confirm sugar’s role in AGE progression, it is safe to say that sugar should be decreased in the diet in order to decrease the risk of diseases that are associated with increased levels of AGEs (like diabetes).
- Avoid highly refined and processed foods. A good rule of thumb to follow is to avoid packaged foods that have more than four ingredients. Include real, whole foods from a variety of fruits and vegetables, grass-fed and organic meats, poultry and dairy, wild-caught fish, legumes, lentils, nuts, and seeds. If you notice, the only sugar you would consume on this type of diet would be from fruit, which also provides a wide range of vitamins and phytonutrients.
- Be wary of hidden sugars. Foods that may seem healthy can contain hidden added sugars. Examples are store-bought tomato sauces, low-fat food products, bread and baked goods, dried fruit, and fruit juices. Be sure to check the nutrition label to see if sugar is in the first three ingredients on the ingredients label. If it is, the food product is high in sugar and should be avoided.
- Avoid foods that are processed with heat. Foods like roasted coffee beans and nuts, cooked meats like boiled hot dogs and fried bacon are high in AGEs. Make sure to shop for foods with minimal heat processing as heat increases the AGEs of foods.
- Stop grilling and start steaming. The way in which you cook your food is a very important factor in reducing AGE formation. Grilling and charring foods on the grill or frying drastically increase AGEs found in foods. Safer methods of cooking include steaming and boiling.
Although further research needs to be done to determine whether or not sugar intake directly affects increased AGE levels and deterioration of the skin, it is widely recognised that higher sugar consumption increases the risk of many inflammation-related diseases like diabetes. It is imperative to adopt a lifestyle that not only protects the skin but enhances the health and functioning of the body. Taking measures to reduce sugar intake and increasing real, whole foods within the diet will not only keep you feeling healthy, but will keep you looking young from the inside out.
References and Sources:
- Total sugar consumption worldwide from 2009/2010 to 2016/2017 (in million metric tons) https://www.statista.com/statistics/249681/total-consumption-of-sugar-worldwide/ [Accessed March 13, 2017].
- Luevano-Contreras, Claudia, and Karen Chapman-Novakofski. “Dietary advanced glycation end products and aging.”Nutrients 2, no. 12 (2010): 1247-1265. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257625/ [Accessed March 13, 2017].
- Sims, T. J., L. M. Rasmussen, H. Oxlund, and A. J. Bailey. “The role of glycation cross-links in diabetic vascular stiffening.”Diabetologia 39, no. 8 (1996): 946-951. https://link.springer.com/article/10.1007%2FBF00403914?LI=true [Accessed March 13, 2017].
- Haus, Jacob M., John A. Carrithers, Scott W. Trappe, and Todd A. Trappe. “Collagen, cross-linking, and advanced glycation end products in aging human skeletal muscle.”Journal of applied physiology 103, no. 6 (2007): 2068-2076. http://jap.physiology.org/content/103/6/2068.short [Accessed March 13, 2017].
- Dalal, Mansi, Luigi Ferrucci, Kai Sun, Justine Beck, Linda P. Fried, and Richard D. Semba. “Elevated serum advanced glycation end products and poor grip strength in older community-dwelling women.”The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 64, no. 1 (2009): 132-137. https://doi.org/10.1093/gerona/gln018 [Accessed March 13, 2017]
- Pageon, Hervé, Marie-Pascale Técher, and Daniel Asselineau. “Reconstructed skin modified by glycation of the dermal equivalent as a model for skin aging and its potential use to evaluate anti-glycation molecules.”Experimental gerontology 43, no. 6 (2008): 584-588. http://dx.doi.org/10.1016/j.exger.2008.04.004 [Accessed March 13, 2017]
- Uribarri, Jaime, Weijing Cai, Maya Ramdas, Susan Goodman, Renata Pyzik, Xue Chen, Li Zhu, Gary E. Striker, and Helen Vlassara. “Restriction of advanced glycation end products improves insulin resistance in human type 2 diabetes.”Diabetes care 34, no. 7 (2011): 1610-1616. https://doi.org/10.2337/dc11-0091 [Accessed March 13, 2017].
- Vlassara, Helen, and Jaime Uribarri. “Advanced glycation end products (AGE) and diabetes: cause, effect, or both?.”Current diabetes reports 14, no. 1 (2014): 1-10. https://link.springer.com/article/10.1007/s11892-013-0453-1 [Accessed March 13, 2017]
- Basta, Giuseppina, Ann Marie Schmidt, and Raffaele De Caterina. “Advanced glycation end products and vascular inflammation: implications for accelerated atherosclerosis in diabetes.”Cardiovascular research 63, no. 4 (2004): 582-592. https://doi.org/10.1016/j.cardiores.2004.05.001 [Accessed March 13, 2017].
- What is glycation? https://www.sharecare.com/health/functions-of-skin/what-is-glycation [Accessed March 13, 2017].
- Beck-Nielsen, H., O. Pedersen, and N. Schwartz Sørensen. “Effects of diet on the cellular insulin binding and the insulin sensitivity in young healthy subjects.”Diabetologia 15, no. 4 (1978): 289-296. https://link.springer.com/article/10.1007%2FBF02573821?LI=true [Accessed March 13, 2017].
- Reiser, Shelton, Judith Hallfrisch, Meira Fields, Andrea Powell, W. Mertz, E. S. Prather, and J. J. Canary. “Effects of sugars on indices of glucose tolerance in humans.”The American journal of clinical nutrition 43, no. 1 (1986): 151-159. http://ajcn.nutrition.org/content/43/1/151.short [Accessed March 13, 2017].
- Sanchez, Albert, J. L. Reeser, H. S. Lau, P. Y. Yahiku, R. E. Willard, P. J. McMillan, S. Y. Cho, A. R. Magie, and U. D. Register. “Role of sugars in human neutrophilic phagocytosis.”The American journal of clinical nutrition 26, no. 11 (1973): 1180-1184. http://ajcn.nutrition.org/content/26/11/1180.long [Accessed March 13, 2017].
- Persson, Per-Gunnar, Anders Ahlbom, and Göran Hellers. “Diet and inflammatory bowel disease: a case-control study.”Epidemiology 3, no. 1 (1992): 47-52. http://journals.lww.com/epidem/Abstract/1992/01000/Diet_and_Inflammatory_Bowel_Disease__A.9.aspx [Accessed March 13, 2017].
- Vaccaro, Olga, Karen J. Ruth, and Jeremiah Stamler. “Relationship of postload plasma glucose to mortality with 19-yr follow-up. Comparison of one versus two plasma glucose measurements in the Chicago Peoples Gas Company Study.”Diabetes Care 15, no. 10 (1992): 1328-1334. http://care.diabetesjournals.org/content/15/10/1328.short [Accessed March 13, 2017].
- Bui, Thi, and Craig B. Thompson. “Cancer’s sweet tooth.”Cancer cell 9, no. 6 (2006): 419-420. DOI: http://dx.doi.org/10.1016/j.ccr.2006.05.012 [Accessed March 13, 2017].
- Shin, Seoungwoo, Dahee Son, Minkyung Kim, Seungjun Lee, Kyung-Baeg Roh, Dehun Ryu, Jongsung Lee, Eunsun Jung, and Deokhoon Park. “Ameliorating effect of Akebia quinata fruit extracts on skin aging induced by advanced glycation end products.”Nutrients 7, no. 11 (2015): 9337-9352. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4663606/ [Accessed March 13, 2017].