Glycation is a natural process that occurs in your body, but certain environmental and lifestyle factors — your diet, especially — can amp up its effects in ways that are detrimental to health. In this guide, we'll answer "what is glycation," explore the connection between glycation and chronic diseases, as well as glycation and skin aging, and provide steps to help prevent glycation in excess.

What is glycation?

The definition of glycation refers to the chemical reaction, known as the Maillard reaction, that occurs when reducing sugars react nonenzymatically with amino groups in proteins, lipids, or nucleic acids. When this reaction occurs, new chemical compounds are formed (see AGEs, below). Glycation can occur in your body (in vivo) in two ways: as a part of the normal metabolic process, or endogenously; or deriving from external sources (exogenously), such as your diet. Scientists also study glycation when it occurs in vitro, or outside the body, whether that be within food sources, in a test tube, or in animal test subjects. 

What are AGEs?

Advanced glycation end-products (AGEs) are the chemically heterogeneous compounds formed by glycation. (However, while the majority of AGEs are produced by the non-enzymatic Maillard reaction, it has become understood more recently that some AGEs are formed via alternative pathways, such as autoxidation of glucose.) Since glycation is an irreversible reaction, AGEs accumulate in the blood and tissues over time. As we age, this buildup of AGEs is considered a normal part of physiological decline; AGEs are directly involved in the pathogenesis of degenerative musculoskeletal conditions in older people, such as osteoporosis, osteoarthritis, and sarcopenia. 

However, an increase in AGE accumulation, particularly related to modern dietary practices, has also been implicated in the dramatic rise in the prevalence of non-communicable diseases — such as diabetes, kidney disease, and mental health conditions — in younger as well as older people. 

What are RAGE and MAGE?

While we’re describing acronyms such as AGE, you might also hear some similar-sounding acronyms, such as RAGE and MAGE, when the process of glycation is being discussed. An AGE, as we discussed above, is essentially the end product of glycation. MAGE stands for melibiose-derived glycation product, and it is a newer class of AGEs, first described in a 2021 Nature study, that appears highly associated with elevated blood pressure (hypertension) and a lowering of HDL (your “good” cholesterol) — suggesting that MAGE may be a marker of arteriosclerosis in diabetic (and likely other) patients.

Understanding receptors to AGEs

RAGE is one of the most important of the many “receptors” to AGEs. When AGEs “do their damage,” if you will, one way that they do it is by binding to specific receptors on the surface of various cells, including phagocytes and endothelial cells. The interaction of AGEs and their receptors (such as  RAGE) causes oxidative stress and inflammatory reactions that can result in tissue damage of varying types. RAGE belongs to the immunoglobulin superfamily, capable of binding a broad repertoire of ligands. The affinity of RAGE to AGEs is high, leading to constant stimulation of cells and consequent irreversible tissue damage during pathological states — including immune reactions, diabetic complications (such as heart failure and stroke), chronic kidney disease (CKD), end-stage renal diseases (ESRD), Alzheimer’s disease, atherosclerosis, cataracts, Parkinson’s disease, sarcopenia, vascular dementia, and aging. 

Other significant receptors include the so-called scavenger receptors (SR-AI, SR-BI, CD36, CD6816), a superfamily of membrane-associated proteins that bind many ligands, including endogenous proteins and pathogens, and are found on hepatocytes, phagocytes, endothelial cells, vascular walls and smooth muscle, as well as on nervous system cells. These receptors are involved in lipid metabolism, platelet aggregation, and oxidative stress, among other processes; thus, they are implicated in the many disorders that stem from the aging of and damage to blood vessels (such as cardiovascular and, in fact, most other vascular complications, including retinopathy).

AGER1 is another receptor of much interest, as it is involved in aiding the clearance of AGEs. Thus, if its presence is “downregulated,” there is an association with increased incidence and severity of several chronic disorders (diabetes, CKD, and autoimmune diseases). 

The harmful effects of excessive glycation and high AGE levels 

Glycation occurs naturally as a part of your body's metabolism, and the process accelerates as you age. Thus, over time, your body becomes less efficient at removing AGEs, leading to a higher accumulation of these compounds. However, factors other than natural aging appear to be involved in glycation rates: Lifestyle (especially diet) and environmental factors, as well as your overall health profile and genetic makeup, play significant roles in how glycation occurs and progresses given your particular, individualized physiology. 

While the contribution of dietary AGEs to various pathologies has yet to be fully elucidated, researchers now believe that high levels of AGEs brought on by glycation are involved in the onset and exacerbation of a variety of diseases, including the following:

Chronic non-communicable diseases: Research has confirmed that AGEs are involved in the pathogenesis of diabetes and other degenerative diseases, including cardiovascular and kidney diseases as well as neurodegenerative diseases (e.g., Alzheimer’s disease, ALS and Parkinsons), as well as the secondary stages of traumatic brain injury (TBI). While the exact mechanisms are still being studied, it appears that the detrimental impact of AGEs relates to their ability to promote oxidative stress and inflammation by binding with cell surface receptors or cross-linking with body proteins, altering their structure and function. 

Cardiovascular and vascular complications: There is considerable evidence that the interaction of AGEs and their receptors cause the formation of areas of calcification and the formation of blood clots in the walls of the arteries. In this way, AGEs are involved in the aging of blood vessels and their numerous damages, such as atherosclerosis, hypertension and other cardiovascular complications, as well as other vascular complications (such as retinopathy) — and all are common complications of advanced diabetes. 

Increased risk of heart failure even without preexisting chronic disease: Damage caused by excessive glycation and resultant high levels of AGEs also appears to affect the cardiovascular health of individuals who have not been diagnosed with a chronic degenerative disorder such as diabetes or CVD (cardiovascular disease). As discussed in a the 2021 Nature review, stiffening of arterial vessels and increased blood pressure are the main risk factors for cardiovascular disease in the elderly, and AGEs act directly and through receptors to change the function of many intracellular and extracellular proteins, including metabolic enzymes and calcium channels, which then causes endothelial dysfunction, inflammation, and oxidative stress. The result: stiffness of blood vessels and increased blood pressure, both of which raise risks for cardiovascular disease and death.

Digestive disorders: While research in this area is scant to date, it does appear that AGEs negatively affect the gut and overall health directly through their effects on gut architecture; as well as indirectly through their interactions with the gut microbiota. Specifically, a 2023 review declares that AGEs markedly alter the gut structure, “leading to increased intestinal permeability and reduced expression of enteric neurons, as well as to reshaping the microbiota composition.” Researchers further postulate that inflammatory bowel disease (IBD), an umbrella term that encompasses both ulcerative colitis and Crohn’s disease, is one of the major gut disorders that is likely exacerbated (if not directly caused by) the direct effects of AGEs, although IBD’s causes are likely multifactorial. 

Acceleration of aging: While less medically serious than diabetes and other chronic, degenerative disorders, skin conditions can also be impacted by the “aging effects” of AGEs. In other words, with glycation and skin aging, higher AGE levels appear to contribute to the formation of wrinkles, sagging skin, and age spots. This is because AGEs can cross-link collagen and elastin fibers, which are responsible for maintaining the skin's elasticity and firmness.

What causes excessive glycation?

Much remains unknown about what causes glycation, and less about why certain individuals are more adversely affected by the process than others. Clearly, genetics plays a significant role, as does age. In addition, the following factors appear at play

1. High blood glucose: It has become clear that elevated levels of blood sugar (glucose), often associated with conditions like diabetes, can lead to increased glycation, as those with diabetes typically have high levels of AGEs, while diabetics put on an AGE-restricted diet have shown improvements in insulin sensitivity and other biomarkers of improved disease management. In other disease states, including kidney disease, AGE levels are also often elevated; however, whether AGEs “cause” kidney disease, or the disease causes high AGE levels, remains uncertain. (The causation may be bidirectional.)

2. Diet — especially the modern “Western diet”: As mentioned previously, the contribution of dietary AGEs to various pathologies remains to be fully elucidated. However, a consensus of researchers has demonstrated that the intake of dietary AGEs affects oxidative stress (OS) and inflammatory mediators, which are known to contribute to various disease states and disorders. The Western diet — commonly defined as a diet high in animal protein, saturated- and trans-fats, sugar and salt; while low in fruits, vegetables, fiber, and other essential nutrients — has particular features that are highly associated with the excessive production of AGEs. But what part(s) of the modern Western diet are most to blame?

• High-heat animal foods: As described in a 2010 review, the modern diet is largely heat-processed, which has contributed to high levels of advanced glycation end products (AGEs). Dry heat promotes new AGE formation by >10- to 100-fold above the uncooked state across food categories. Animal foods that are high in fat and protein are the most susceptible to AGE formation during cooking. Topping the list are overly charred grilled, broiled, seared, roasted or fried meats, red meat producing the highest levels of AGEs after cooking, followed by chicken and egg yolks fried in butter. In contrast, carbohydrate-rich foods such as vegetables, fruits, whole grains, and milk contain relatively few AGEs, even after cooking. ‍
• Processed foods: Deli meats, potato chips, and ketchup are but a few examples of highly processed foods that contain high quantities of added fats and sugars — and they also tend to be very high in AGEs. Beyond the dietary AGEs that they contain, increased consumption of energy dense, nutrient poor foods, which are high in sugars and salt, and low in essential nutrients, actively contribute to hemodynamic and metabolic abnormalities, culminating in hypertension, obesity, and T2D which, in turn, facilitate endogenous AGE production. See our report, The Truth About Processed Foods, for details on which foods are ultra-processed (and therefore the least healthy) versus those that are minimally processed (e.g., a can of beans or a loaf of whole wheat bread) and so still considered relatively healthy.‍
• Unhealthy fats: High-fat spreads, particularly of animal origin (including butter, cream cheese, margarine, and mayonnaise), are also among the foods highest in AGEs. Even certain plant-based fats, considered healthy for numerous reasons, contain somewhat high levels of AGEs (although far less than animal fats); certain oils and nuts, including peanut butter, are in this group, even in their uncooked forms. This may be due to various extraction and purification procedures involving heat, in combination with air and dry conditions, however mild they are. The jury is still out, however, about whether or not the healthy polyunsaturated fats, such as nuts and oils, produce the same ill effects as other high-AGE food products such as red meat; it may very well be that the plant-sourced fats are absorbed, taken up, or cleared differently. This is an active area of research.
• Sugars: Normally, glucose is either metabolized to generate energy, or stored for later use (fat). However, when there's excessive glucose in the bloodstream, it becomes more likely that glucose molecules will interact with proteins and lipids –– i.e., more glycation and more AGEs. Because of this high correlation between hyperglycemia (above-normal blood glucose levels) and elevated AGEs, a diet high in sugars is implicated in excessive glycation. In particular, foods that have a high glycemic index (GI) score are more likely to cause blood glucose spikes, and could ultimately contribute to chronically high blood sugar levels, corresponding high levels of AGEs and the development of type 2 diabetes. (Learn more: The Link Between Diabetes and Blood Sugar.) High-GI foods score in the 70s or 80s; (pure sugar is a 100.) Worse yet are high-GI foods that are also processed, such as sugar-sweetened beverages (SSBs), white rice, and high-sugar/high-fat sweets such as cookies, cakes and other desserts. Even “natural” sources of fructose, such as agave, contain high levels of dietary AGEs.‍
• Certain cheeses: Whereas cooking is known to drive the generation of new AGEs in foods, it is interesting to note that even uncooked, animal-derived foods such as cheeses can contain large amounts of AGEs. This is likely due to pasteurization and/or holding times at ambient room temperatures (e.g., as in curing or aging processes). Culprits include high-fat cheeses such as Parmesan and American cheeses. Lower-fat cheeses, such as reduced-fat mozzarella, 2% milk cheddar, and cottage cheese, contain far lower AGE levels. 

3. Obesity: Individuals who are overweight or obese are at considerably higher risk for the production of high levels of endogenous AGEs within the body.

4. Tobacco smoke: Exposure to tobacco products can be a significant source of exogenous AGEs. Tobacco smoke contains compounds known as xenobiotics that induce the formation of large amounts of free radicals, substances which the body is unable to detoxify that consequently lead to the formation of AGEs and resultant damage to cells and tissues. 

How to prevent glycation

Here are some tips to prevent glycation in excess:

Dietary changes to reduce glycation

Making dietary modifications is an effective way to reduce glycation and mitigate its impact on our health:

• Refrain whenever possible from heating animal fats/proteins, particularly meats, to high temperatures. Cooking with moist heat, using shorter cooking times, cooking at lower temperatures, and by adding acidic ingredients (such as lemon juice or vinegar) all appear to be effective at reducing the AGEs produced after consumption of these same foods.
  
• Limit consumption of processed foods of all kinds: Second to dry-heated meats, foods that are produced with highly industrialized processes — such as cookies and cakes, but also processed deli meats, potato chips, hot dogs, sugar-sweetened breakfast foods and drinks — contain the highest AGE content.
  
• Avoid consumption of unhealthy fats, particularly saturated fats, typically abundant in so many processed foods. Unhealthy fats are associated with dyslipidemia — elevated triglycerides, low high-density lipoprotein cholesterol (HDL-C; “good cholesterol”), and high LDL (“bad cholesterol”). Dyslipidemia, which is especially common as a co-morbidity of type 2 diabetes, is a major link to cardiovascular disease and stroke, the diabetic complications so feared for their correlation with earlier death rates. Recent research indicates that hyperlipidemia, along with hyperglycemia, leads to the formation of AGEs; and vice versa, higher AGE levels drive hyperlipidemia and hyperglycemia. On the other hand, diets containing healthy, plant- or fish-derived fats (e.g., avocados, olive oil, fatty fish) — such the Mediterranean diet — have been shown to be low in AGEs.
  
• Limit consumption of foods high in added sugars, especially if also processed; but also limit consumption of natural, simple sugars (agave, honey, table sugar) and replace them with whole-food, natural alternatives such as fruits to help better regulate blood sugar levels and so also contain the production of AGEs. 
• Up your consumption of high-fiber, low-glycemic fruits and vegetables, which also tend to be high in phytochemicals (such as polyphenols), which have strong  antioxidant properties believed to help reduce glycation. Antioxidants neutralize free radicals that promote glycation reactions, thus reducing the formation of AGEs. Berries, dark green leafy vegetables, and green tea are examples of foods high in beneficial polyphenols.
  
• Grains, legumes, whole-grain breads, and milk are also among the lowest items in AGEs, unless prepared with added fats. (For instance, biscuits had more than 10 times the amount of AGEs found in low-fat breads, rolls, or bagels.)
  

Lifestyle modifications to combat glycation

While diet plays a significant role, lifestyle modifications complement dietary changes in combating glycation:

• Avoidance of tobacco smoke is vital, not just by refraining from smoking, but by avoiding exposure to secondary smoke.
  
• Maintain a healthy weight: As concluded in many studies, summed up well in a 2023 systematic review, weight loss (from an overweight or obese level) reduces the oxidative stress that is associated with and likely exacerbated by high levels of AGEs.
  
• Exercise regularly: Regular exercise not only helps you lose weight, with its aforementioned beneficial impact upon AGEs and consequent oxidative stress levels, but physical activity (even simple movements) can help regulate blood sugar levels, promote healthy circulation, and may reduce the risk of complications associated with glycation, as demonstrated in this 2015 study. More specifically, study authors concluded that exercise activates molecular mechanisms that improve insulin sensitivity and glucose tolerance in peripheral tissues; consequently, this reduces cellular glucotoxicity and exposure to lipid peroxidation.

Glycation for those with diabetes (or at high risk for it) 

Because AGEs are so notably elevated in individuals with diabetes (and renal disease), and their impact upon downstream cardiovascular complications seem so pronounced, much of the AGE and glycation research now underway is endeavoring to better understand (a) how to measure AGEs and (b) how to determine what therapeutic interventions, pharmacological and non-pharmacological (e.g., diet, lifestyle, environment factors), could help combat elevated AGE levels for individuals with diabetes and those at risk for diabetes and other non-communicable, chronic degenerative disorders.

Put simply, diabetes is caused by abnormal glucose levels or inappropriate tolerance, accompanied by an insufficient insulin response. However, “the causes behind the causes” of diabetes, if you will, are still being studied and elucidated, especially since type 2 diabetes (T2D) is such a complex and multifactorial metabolic disease. As an aside: the notion that sugar is the only causative factor in the onset of type 2 diabetes, or T2D, is inaccurate. Many other factors are at play, including genes, weight gain and waist circumference gains irrespective of dietary causes, a sedentary lifestyle, the effects of other disease states one may have or have had — including high blood pressure, high triglycerides, high cholesterol, polycystic ovary syndrome, gestational diabetes, and a whole cascade of other physiological variables relating to complex processes involving immunity, inflammation, oxidative stress and more. That being said, it seems clear that high blood sugar, or hyperglycemia, is the main cause of diabetic complications that decrease life quality and expectancy. 

Oxidative stress has an important role in hyperglycemia-induced tissue injury as well as in early events relevant for the development of T2D. The formation of AGEs is one contributing factor. On the one hand, it has been reported that AGEs increase reactive oxygen species formation and impair antioxidant systems; on the other hand, the formation of some AGEs is induced per se under oxidative conditions. Thus, AGEs contribute at least partly to chronic stress conditions in diabetes. 

The impact of dietary choices affects AGEs and diabetes disease progression

As AGEs are not only formed endogenously, but also derive from exogenous sources, i.e., food, they have been assumed as risk factors for T2D. As summarized in a 2022 review, in individuals with T2D and renal failure, excessive AGE intake positively correlates with serum biomarkers of oxidative stress, inflammation, endothelial dysfunction, hyperglycaemia and hyperlipidaemia. Conversely, dietary AGE restriction in healthy individuals and those with T2D have demonstrated favorable outcomes in circulating 8-isoprostanes and tumor necrosis factor alpha (TNFα), improvements in cognitive function, and insulin sensitivity. The effects of dietary AGEs on insulin sensitivity is vitally important, since abnormalities in glucose homeostasis are potent risk factors for CKD development and progression. 

Dietary choices also affect non-diabetics

A 2022 study found that even in young, non-diabetic individuals, there is a significant association between the levels of α-dicarbonyls (a type of compound that can lead to the formation of AGEs) and insulin resistance. This suggests that the process of AGE formation can occur even in the absence of diabetes and may contribute to the development of insulin resistance. Similarly, a 2011 study determined that the circulating level of AGEs is associated with insulin resistance even in non-obese, non-diabetic subjects.

Low-AGE diets and related dietary guidance

So what are the best strategies for accomplishing glycation/AGE mitigation for those with diabetes or at risk for the disease? 

• Generally, adoption and adherence to the dietary guidance we outlined previously (see previous section, Dietary changes to reduce glycation) should be the starting strategy: Avoidance of high-heat meats and limited consumption of other animal fats/proteins; avoidance of processed foods, especially those containing unhealthy fats and added sugars; increased intake of high-fiber and high-polyphenol fruits and vegetables; and caution with consumption of high-fat dairy, especially certain cheeses.
  
• Ironically, the heightened interest in therapeutic diets that are higher in protein and fat (Keto, Paleo) and lower in carbohydrate for weight loss, diabetes, and cardiovascular disease may run counter to the new AGE research findings, since the combination of animal protein and fat, at high heat, substantially raises serum AGE levels. This is one reason why leading medical centers are leaning more toward the recommendation of the Mediterranean and other plant-forward diets, as they appear less likely to contribute to numerous health problems, including diabetes, over the long term.‍
• A specifically formulated low-AGE diet, structured with the guidance of a nutritionist or other medical provider, may be notably beneficial for those with diabetes. Two independent randomized crossover dietary intervention studies found that low AGE diets improve insulin sensitivity and renal function. 
• While your medical provider may continue to recommend “carb-counting” as a part of a healthier diabetic diet, in line with guidance from the American Diabetes Association, bear in mind that that prebiotic-rich fruits and vegetables, as well as whole grains, appear to be very low in dietary AGEs — despite the fact that these foods are carbohydrates, and they are also high in phytochemicals (e.g., polyphenols), which are being studied for their ability to reduce AGE levels. Accordingly, the plant-forward Mediterranean diet, so high in fruits and vegetables, is low in AGEs. ‍
• Prebiotic, probiotic and synbiotic supplementation may be of benefit: A 2021 meta-analysis found that pre-, pro- and symbiotic-supplementation reduces fasting insulin levels, hyperinsulinemia and circulating AGEs in individuals with diabetes, suggesting the link between the microbiome, glucose homeostasis and AGE burden is an important one. (However, a 2022 review citing this 2021 meta-analysis cautions, appropriately, that whether this occurs through modulation of enteroendocrine factors, inflammation or gut-barrier permeability remains to be fully elucidated.) 

Of course, as with any disease state, and notably with diabetes, the impact of food intake (and its effect on your blood glucose levels and insulin sensitivity) is highly individualized. Everyone’s biology and lifestyle is different, so it’s impossible to give a simple one-size-fits-all answer on exactly how many carbs, fats or protein you should eat. Similarly, what foods most impact your level of AGEs can’t easily be determined with current disease monitoring/testing technology, which we discuss in a later section of this report.

Other lifestyle strategies benefiting AGE levels in the diabetes population

Beyond diet, the other lifestyle factors affecting AGE levels, discussed previously, apply with equal (if not greater) importance to those with diabetes: weight management, exercise, and refraining from smoking are three of the most significant factors that help diabetics better regulate blood sugar levels while reducing the oxidative stress associated with (and likely exacerbated by) high levels of AGEs.

The importance of monitoring blood sugar levels for glycation

Clearly, monitoring to determine if blood glucose levels are rising or high is of the utmost importance for those with diabetes or even those at risk. The advent of the continuous glucose monitor (CGM), a wearable device that continuously tracks interstitial fluid (where your glucose moves after it has been through your blood vessels and capillaries), enables the wearer to receive an estimate of glucose levels throughout the day and night. The January AI app integrates such data with personal dietary, exercise, and other factors that can provide new insights into which particular factors most affect a person’s blood glucose levels, assisting in the effort to modify such variables and thereby keep blood glucose levels within a target range. The lower the blood glucose levels, in all probability the lower the AGEs level will likely be. And so monitoring and controlling your blood sugar could be a key part of glycation and skin aging.

Although various AGE biomarkers are being studied and used in research settings, measuring AGE levels, per se, is not yet a common component of current clinical medical practice. However, scientists (such as the authors of the 2021 Nature paper) explain that the A1c test (known also as HbA1c) — the gold standard for confirming a prediabetes or diabetes diagnosis — measures a compound formed in the glycation process; its high level proves not only chronic hyperglycemia, but also correlates well with its risk. Moreover, it is considered to be an independent risk factor for coronary heart disease and stroke, obesity-related metabolic disorders and carotid atherosclerosis even in non-diabetic individuals.

Because A1c tests are administered in a medical office, and rarely more than once per quarter, combining CGM use with prescribed A1c tests (and other tests merited by your medical team) provides a more complete picture of blood glucose patterns and likely AGE elevation. If you'd like to monitor your blood sugar, with or without a CGM, give January AI a try here.

Pharmacological therapies 

While it is not within the scope of this report to provide pharmacological advice, it is clear that many drugs currently in wide use, especially for the treatment of advanced T2D, have demonstrated an ability to reduce circulating levels of AGEs. The 2021 Nature paper cites anti-inflammatory drugs with anti-glycation properties (diclofenac, acetylsalicylic acid); metabolically active drugs and vitamins with anti-AGE properties (pyridoxamine, metformin); antioxidants and free radical scavengers (herbal extracts rich in flavonoids, carnosine); AGE inhibitors with chelating properties (pyridoxamine, acarbose); substances inhibiting excessive aggregation of platelets (clopidogrel); and a group of compounds capable of producing endogenous insulin, e.g. sulfonylurea.

Additionally, drugs that target specific pathways involved in glycation, such as inhibitors of the receptor for AGEs (RAGE), are being explored as potential therapeutic options. These advances open new doors for preventing and managing glycation-related health issues.

Whether or not antioxidant-rich supplements, like alpha-lipoic acid, have demonstrable positive impacts on AGE accumulation and improving markers of glycation remains to be well studied.

Key takeaways

Glycation, a natural process in your body, can have detrimental effects on your health when certain factors amp up the process in a negative way. By understanding what glycation is, recognizing its impact on your health, and becoming more aware of diet, lifestyle, environmental, and medical strategies to help combat its potentially concerning effects, you may be able to lead a healthier and longer life. Key among these strategies: Adherence to a diet limiting high-heat animal/fat foods, other highly processed foods, and high-sugar foods; increased intake of polyphenol-rich, high-fiber fruits, vegetables, legumes and whole grains; maintenance of a healthy weight and waist circumference; regular exercise; and avoidance of tobacco smoke. In the case of those with diabetes (and those at risk), that same dietary/lifestyle  guidance applies, together with additional strategies to help ensure the most optimal management of blood glucose levels as a way to mitigate AGE elevation. Blood glucose monitoring, already of vital importance for the diabetic population, can also provide insights valuable to non-diabetics concerning the impact of particular high-AGE foods. Consult with your physician for further guidance.