Guard Your Precious Proteins Against Premature AgingApril 2008
By Steven Joyal, MD
It may seem inconceivable, but scientists long ago learned why aging people suffer so many disorders related to their eyes, kidneys, brain, and vascular system.
While these pathological processes are accelerated in diabetics, they affect all aging people to one degree or another.
In a startling revelation, Steven Joyal, MD, lays out an innovative, but remarkably simple program to enable both diabetics and normal aging humans to avoid these horrendous biological consequences.
The article you are about to read is a summary of Dr. Joyal’s new book titled What Your Doctor May Not Tell You About Diabetes.
In fact, this book contains vital information for every aging person. The reason is that most aging people suffer pre-diabetic pathologies and should therefore follow similar strategies to protect against common age-related diseases.
Diabetes Is a Form of Accelerated Aging
For decades, scientists have been trying to uncover the root causes of premature aging. The fact that diabetes is a form of accelerated aging comes as a surprise to most people. In fact, life expectancy for people with diabetes is four to eight years less than for non-diabetics. Both aging and diabetes share two important biological processes that damage the body: glycation, which results in damage to protein and lipid molecules, and oxidative stress, characterized by increased free-radical activity and damage to tissues by molecules like reactive sugar aldehydes. And many signs and symptoms of diabetes also commonly occur with aging, including:
Given that diabetes and aging share so many characteristics, it’s not surprising that they also respond to many of the same prevention and treatment strategies.
Glycation and Glycotoxins: AGEs Age You Faster
When patients hear that glycation is one of the major consequences of diabetes and a contributing factor in diabetic complications, their typical response is, “I’ve never heard of it. Is it something new?” When they hear that scientists have known about glycation since at least 1912 and of its major impact on diabetes and diabetic complications since the 1980s, their typical response is, “Why haven’t I heard about it? Why isn’t my doctor talking about it?”
Glycation is a biochemical process that involves a series of non-enzymatic reactions (those that don’t require enzymes to make them happen) between proteins and/or certain lipids (fats) and glucose.
The result is the formation of toxic substances known as AGEs—advanced glycation end products—and ALEs—advanced lipoxidation end products.
If you’ve ever made toast, then you’ve experienced glycation firsthand. Toasting bread involves the Maillard reaction—the browning reaction that occurs when food is heated and cooked at high temperatures. This reaction is also commonly observed when we grill lamb chops, broil salmon steaks, and make French fries.
Levels of AGEs and ALEs increase as people grow older, and those levels are fueled by the foods we eat.
In the past, scientists underestimated the impact of food-derived glycotoxins’ damage on human cells, organs, and tissues. Recent groundbreaking research, however, has uncovered startling evidence of the critical role that food-derived glycotoxins play in contributing to glycation in the body. Furthermore, recent research indicates AGEs play an important role in the aging process as well as in diseases such as diabetes, heart disease, kidney disease, cancer, Alzheimer’s disease, and certain types of neuropathy.
Glycotoxin levels increase dramatically in people who have elevated blood glucose levels because these noxious substances thrive in high-glucose environments. Thus, glycotoxins are especially prevalent in individuals who have metabolic syndrome, predia-betes, or diabetes. Sites in the body that are especially susceptible to the accumulation of glycotoxins include the renal glomerulus (in the kidney), the retina (the membrane at the back of the eye that helps you see), and important blood vessels like the coronary arteries (the arteries that supply blood to the heart). We also know that glycotoxins play a significant role in causing chronic diseases that are associated with underlying inflammation, such as heart disease and neuropathy.
How Glycotoxins Are Formed in Food
Food-derived glycotoxins are formed during a series of chemical reactions that occur between glucose and the proteins, lipids, and nucleic acids derived from food. Glycotoxins trigger cells to send messages that lead to the production of inflam-matory substances called cytokines, which cause tissue damage in the body. Experimental studies show that this is exactly what happens in glycotoxin-induced vascular (blood vessel) damage often seen in diabetes. Hemoglobin A1c (HbA1c) is an AGE that is created when glucose molecules bind to hemoglobin, a protein in blood. Measurement of this factor in the blood is very helpful in monitoring the level of glycation damage in prediabetes and diabetes.
An important strategy to reduce the level of glycation damage is to keep blood glucose levels within a healthy range (below 100 mg/dL premeal or after a fast). We also know from extensive research in this area that fasting blood sugar readings in the 70 to 85 mg/dL range appear optimal for disease prevention and longevity.
Glycotoxins are also formed during food production and preparation. Food manufacturers use various heating processes to enhance flavor, color, and texture; to improve food safety (sterilization and pasteur-ization); and to extend shelf-life. Unfortunately, glycotoxins are a byproduct of these processes. Foods as varied as cola drinks, baked goods, caramel, and brewed products contain glycotoxins.
Foods high in fat and protein (such as meat and poultry) typically have the highest glycotoxin levels. How you prepare your food (or have it prepared for you if you eat out) can also have a significant impact on the formation of glycotoxins.
Glycotoxins are especially harmful to people with diabetes, in whom these molecules are associated with retinopathy (glycotoxins accumulate in the retinal blood vessels), neuropathy (they accumulate in peripheral nerves, resulting in nerve damage), kidney failure (they are found in kidney tissue), heart disease, and blood vessel disease.
High blood glucose levels also invite damage from another source—oxidative stress.
You may remember from high-school chemistry that molecules are composed of atoms, which in turn each consist of a nucleus, protons, neutrons, and electrons. The atoms of a molecule are held together by chemical bonds. When these bonds are broken—which occurs naturally as part of metabolism, for example—highly reactive molecules called free radicals can be produced. Exposure to environmental toxins (pollution, food additives, radiation, pesticides, and cigarette smoke, for example) also stimulates the production of free radicals.
The body can often ward off the damage these free radicals may cause by sending in antioxidants, substances to prevent the oxidative damage that free radicals can inflict on the body’s tissues. If, however, the body is under stress, which can be caused by failing to follow a diet that contains enough antioxidants (in other words, lots of fresh fruits and vegetables), the body may not be able to neutralize these damaging molecules. When this happens, the end result may be damage to the body’s cells, tissues, and organs. This damage has been associated with several complications of diabetes, including injury to the heart and blood vessels. In addition, free-radical damage is a well-known cause of the accelerated aging of tissues in the body.
Oxidative Stress and Metabolism
There are many different types of free radicals, but those that play a critical role in cardiovascular and metabolic problems are called superoxide radicals and peroxynitrite. Research has shown that hyperglycemia (high levels of glucose in the blood) promotes the formation of free radicals, especially superoxide radicals, and therefore oxidative stress as well.
Situations that can promote oxidative stress include:
Oxidative stress, in turn, stimulates the development and progression of complications from diabetes. Some research even suggests that oxi-dative stress serves as a key trigger for diabetes.
In fact, sophisticated experiments on insulin resistance show that repeated exposure of insulin-resistant tissue to oxidative stress can result in hyper-glycemia.
As we can see, therefore, reducing food-derived glycotoxins in the diet as well as oxidative stress can have a significant, positive impact on our health.