Start Here for Glycation and AGEs

If you are looking for my writings on glycation and AGEs, you should start with
this article:

Where Do Most AGEs Come From? O Glycation, How Thy Name Hast Deceived Me! For a more technical and comprehensive introduction, I recommend chapter 2 of my doctoral dissertation.

For the importance of insulin and glucose to protect against AGEs, see my Examine.Com Editorial with the slightly hyperbolic but not ironic title, Sugar is the Ultimate Antioxidant and Insulin Will Make You Younger: Appreciating a Few Poorly Recognized but Critical Contributions of Carbohydrate.

For the ability of methylglyoxal, the most important source of AGEs in the body, to contribute to the physiologically important role of glucose production, see We Really Can Make Glucose From Fatty Acids After All! O Textbook, How Thy Biochemistry Hast Deceived Me!

For major problems with the idea that AGEs contribute to disease by binding to the so-called “Receptor for AGEs” (RAGE), see Is the “Receptor for AGEs (RAGE)” Really a Receptor for AGEs?

For major problems with the high-profile papers purporting to measure the “AGE” content of foods, see Is Butter High in AGEs? and The Trouble With Measuring AGEs — Butter and More.

These are my podcasts about glycation:

• The Daily Lipid Podcast Episode 6: Why “Glycation” Is a Bad Reason to Restrict Carbs 

• The Daily Lipid Podcast Episode 12: What is Measuring Our Hba1c REALLY Telling Us About Our Blood Glucose and Diabetes Risk?

• The Daily Lipid Podcast Episode 13: Wait a Second, Is Glycation Actually GOOD For You?

These are my peer-reviewed articles related to AGEs:

• γ-Tocopherol abolishes postprandial increases in plasma methylglyoxal following an oral dose of glucose in healthy, college-aged men.

• Acute glutathione depletion induces hepatic methylglyoxal accumulation by impairing its detoxification to D-lactate.

• Dietary fructose feeding increases adipose methylglyoxal accumulation in rats in association with low expression and activity of glyoxalase-2.