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Avoid Dry Cooking to Prevent AGEs and Diabetes

Dean Pomerleau

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Here is an useful new study [1] (press release) for folks concerned about risk of impaired glucose tolerance, insulin insensitivity, and diabetes.


It was a one-year randomized control trial of obese folks with metabolic syndrome, but not overt diabetes. Half the participants (the Reg-AGE group) ate their normal diet and used their normal cooking methods for the year. The other half (the Low AGE or L-AGE group) were told not to change what or how much they ate, but simply  to use cooking techniques known to minimize the formation of Advanced Glycation End-products (AGEs). In particular, they were instructed as follows:


L-AGE participants prepared their own food at home after being individually instructed on how to reduce dietary AGE intake by modifying the cooking time and temperature without changing the quantity, quality or composition of food. They were specifically instructed to avoid frying, baking or grilling, and they were encouraged to prepare their food by boiling, poaching, stewing or steaming.


Below is a sample daily diet for both the Reg-AGE and the L-AGE diets. Note these are just examples given to the L-AGE subjects for how to model their own, self-selected low AGE diet. They were given phone calls twice per week from a dietitian to encourage and facilitate compliance:




Based on diet questionnaire responses, compliance was good. The AGE intake was about 65% lower in the L-AGE group compared with the Reg-AGE group by the end of the study. Both groups lost a modest, nearly comparable amount of weight (1-3 lbs on average) - not enough to explain the following differences. 


Here are the dramatic main results, in graphical form (black bars represent the L-AGE group and the white bars represent the Reg-AGE group):



 As you can see from the first graph, insulin sensitivity (HOMA-IR - a measure of pancreatic β-cell function) improved, and fasting leptin and insulin dropped on the L-AGE diet.


While glucose area-under-the-curve in response to an OGTT didn't improve, the second graph shows that the L-AGE group used dramatically less insulin to clear the same amount of glucose, indicating that their insulin sensitivity was much improved. 


The third graph shows that important markers of circulating AGEs and markers of systemic inflammation (e.g. TNFα) came down dramatically in the L-AGErs, but rose across the board in the Reg-AGE group. 


The opposite was true for pro-health and longevity markers like the level of SIRT1 and adiponectin - which went up in L-AGE folks by the end of the study, and stayed flat or dropped in the Reg-AGE group.


The authors conclude the paper with:


L-AGE [diet] is effective against insulin resistance in obese individuals with the metabolic syndrome.


Here is more good color commentary by the authors from the popular press interview (my emphasis):


The investigators believe that daily AGE consumption in the standard Western diet is at least three times higher than the safety limit for these oxidants. This could, in part, explain the changes seen in disease demographics.

Dr. Vlassara cautioned, "Even though the AGEs pose a more immediate health threat to older adults, they are a similar danger for younger people, including pregnant women and children, and this needs to be addressed. AGEs are ubiquitous and addictive, since they provide flavor to foods. But they can be controlled through simple methods of cooking, such as keeping the heat down and the water content up in food and by avoiding pre-packaged and fast foods when possible. Doing so reduces AGE levels in the blood and helps the body restore its own defenses."


Sorry to rain on your Labor Day cookouts, but you, your family and friends may want to skip the barbie (not to mention the fry pan, oven and toaster) to reduce your risk of impair glucose metabolism, insulin resistance, not to mention cancer [2]. 





[1] Diabetologia. 2016 Jul 29. [Epub ahead of print]

Oral AGE restriction ameliorates insulin resistance in obese individuals with the
metabolic syndrome: a randomised controlled trial.
Vlassara H(1,)(2), Cai W(1), Tripp E(1), Pyzik R(1), Yee K(1), Goldberg L(1),
Tansman L(1), Chen X(1), Mani V(3), Fayad ZA(3), Nadkarni GN(4), Striker
GE(1,)(4), He JC(4), Uribarri J(5).
AIMS/HYPOTHESIS: We previously reported that obese individuals with the metabolic
syndrome (at risk), compared with obese individuals without the metabolic
syndrome (healthy obese), have elevated serum AGEs that strongly correlate with
insulin resistance, oxidative stress and inflammation. We hypothesised that a
diet low in AGEs (L-AGE) would improve components of the metabolic syndrome in
obese individuals, confirming high AGEs as a new risk factor for the metabolic
METHODS: A randomised 1 year trial was conducted in obese individuals with the
metabolic syndrome in two parallel groups: L-AGE diet vs a regular diet,
habitually high in AGEs (Reg-AGE). Participants were allocated to each group by
randomisation using random permuted blocks. At baseline and at the end of the
trial, we obtained anthropometric variables, blood and urine samples, and
performed OGTTs and MRI measurements of visceral and subcutaneous abdominal
tissue and carotid artery. Only investigators involved in laboratory
determinations were blinded to dietary assignment. Effects on insulin resistance 
(HOMA-IR) were the primary outcome.
RESULTS: Sixty-one individuals were randomised to a Reg-AGE diet and 77 to an
L-AGE diet; the data of 49 and 51, respectively, were analysed at the study end
in 2014. The L-AGE diet markedly improved insulin resistance; modestly decreased 
body weight; lowered AGEs, oxidative stress and inflammation; and enhanced the
protective factors sirtuin 1, AGE receptor 1 and glyoxalase I. The Reg-AGE diet
raised AGEs and markers of insulin resistance, oxidative stress and inflammation.
There were no effects on MRI-assessed measurements. No side effects from the
intervention were identified. HOMA-IR came down from 3.1 ± 1.8 to 1.9 ± 1.3
(p < 0.001) in the L-AGE group, while it increased from 2.9 ± 1.2 to 3.6 ± 1.7
(p < 0.002) in the Reg-AGE group.
CONCLUSIONS/INTERPRETATION: L-AGE ameliorates insulin resistance in obese people 
with the metabolic syndrome, and may reduce the risk of type 2 diabetes, without 
necessitating a major reduction in adiposity. Elevated serum AGEs may be used to 
diagnose and treat 'at-risk' obesity.
TRIAL REGISTRATION: ClinicalTrials.gov NCT01363141 FUNDING: The study was funded 
by the National Institute of Diabetes and Digestive and Kidney Diseases
DOI: 10.1007/s00125-016-4053-x 
PMID: 27468708
[2] Diabetes Metab Syndr Obes. 2015 Sep 1;8:415-26. doi: 10.2147/DMSO.S63089.
eCollection 2015.
Current perspectives on the health risks associated with the consumption of
advanced glycation end products: recommendations for dietary management.
Palimeri S(1), Palioura E(1), Diamanti-Kandarakis E(1).
Author information: 
(1)Endocrine Unit, Medical School University of Athens, Athens, Greece.
Advanced glycation end products (AGEs) constitute a complex group of compounds
produced endogenously during the aging process and under conditions of
hyperglycemia and oxidative stress. AGEs also have an emerging exogenous origin. 
Cigarette smoke and diet are the two main exogenous sources of AGEs
(glycotoxins). Modern Western diets are rich in AGEs which have been implicated
in the pathogenesis of several metabolic and degenerative disorders. Accumulating
evidence underlies the beneficial effect of the dietary restriction of AGEs not
only in animal studies but also in patients with diabetic complications and
metabolic diseases. This article reviews the evidence linking dietary glycotoxins
to several disorders from diabetic complications and renal failure to liver
dysfunction, female reproduction, eye and cognitive disorders as well as cancer.
Furthermore, strategies for AGE reduction are discussed with a focus on dietary
DOI: 10.2147/DMSO.S63089 
PMCID: PMC4562717
PMID: 26366100
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Dietary Advanced Glycation End Products and Aging




Advanced glycation end products (AGEs) are a heterogeneous, complex group of compounds that are formed when reducing sugar reacts in a non-enzymatic way with amino acids in proteins and other macromolecules. This occurs both exogenously (in food) and endogenously (in humans) with greater concentrations found in older adults. While higher AGEs occur in both healthy older adults and those with chronic diseases, research is progressing to both quantify AGEs in food and in people, and to identify mechanisms that would explain why some human tissues are damaged, and others are not. In the last twenty years, there has been increased evidence that AGEs could be implicated in the development of chronic degenerative diseases of aging, such as cardiovascular disease, Alzheimer’s disease and with complications of diabetes mellitus. Results of several studies in animal models and humans show that the restriction of dietary AGEs has positive effects on wound healing, insulin resistance and cardiovascular diseases. Recently, the effect of restriction in AGEs intake has been reported to increase the lifespan in animal models. This paper will summarize the work that has been published for both food AGEs and in vivo AGEs and their relation with aging, as well as provide suggestions for future research."




Assessment of the Concentrations of Various Advanced Glycation End-Products in Beverages and Foods That Are Commonly Consumed in Japan


"In humans, two major sources of advanced glycation end-products (AGEs) have been identified, exogenous and endogenous AGEs [15]."




Advanced Glycation End Products in Foods and a Practical Guide to Their Reduction in the Diet


"Modern diets are largely heat-processed and as a result contain high levels of advanced glycation end products (AGEs). Dietary advanced glycation end products (dAGEs) are known to contribute to increased oxidant stress and inflammation, which are linked to the recent epidemics of diabetes and cardiovascular disease. This report significantly expands the available dAGE database, validates the dAGE testing methodology, compares cooking procedures and inhibitory agents on new dAGE formation, and introduces practical approaches for reducing dAGE consumption in daily life. Based on the findings, dry heat promotes new dAGE formation by >10- to 100-fold above the uncooked state across food categories. Animal-derived foods that are high in fat and protein are generally AGE-rich and prone to new AGE formation during cooking. In contrast, carbohydrate-rich foods such as vegetables, fruits, whole grains, and milk contain relatively few AGEs, even after cooking. The formation of new dAGEs during cooking was prevented by the AGE inhibitory compound aminoguanidine and significantly reduced by cooking with moist heat, using shorter cooking times, cooking at lower temperatures, and by use of acidic ingredients such as lemon juice or vinegar. The new dAGE database provides a valuable instrument for estimating dAGE intake and for guiding food choices to reduce dAGE intake."

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From table 1 in Advanced Glycation End Products in Foods and a Practical Guide to Their Reduction in the Diet

I didn't realize nuts and olive oil were so high in AGEs.  Or that bread, even end crust pieces or a toasted bagel, were that low in AGEs.  Also a little surprised that dried figs are so high, I just planted 3 fig trees this year  :(xyz I wish they had fresh figs tested for comparison, I wonder how much of the drying process causes this? Avocados and dark chocolate also a little on the high side.  Of course grilled meats are high in AGEs but I didn't realize how crazy high fried bacon is or that by microwaving it you'd get 1/10th the AGEs (and yet at 1/10th it is still very high in AGEs).

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Does the type of AGE matter? E.g. the type found in coffee or nuts? Does it depend on whether other nutritients are adjacent to the AGEs in coffee/nuts? Most of the studies only show positive benefits to coffee/nuts, but this may be in the context of the shitty diets found in most American diets (whereas idealized diets in CR practitioners may never have been studied..)

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