How's your Athero?

The Little-Known Culprit Behind Clogged Arteries

If I talk about atherosclerosis most people will glaze over. “Oh.. ah.. it’s some sort of heart disease isn’t it?”

If I asked people to name the disease condition responsible for four out of ten deaths in the US, I’m confidently guessing the same people will say cancer.

But it’s not cancer. It’s atherosclerosis so perhaps it’s time to learn a little about it and what can be done now to jump the queue to health beyond that forty percent line.

I’m also guessing that of the people who don’t know about it, almost all of them will not know about its primary causes – especially one that is happening in their bodies right now.

So let’s ‘clear the deck’ with a little definition.

Atherosclerosis is the condition in which an artery wall thickens as the result of a build-up of fatty materials such as cholesterol. It is a syndrome affecting arterial blood vessels, a chronic inflammatory response in the walls of arteries, in large part due to the accumulation of macrophage white blood cells and promoted by low density (especially small particle) lipoproteins (plasma proteins that carry cholesterol and triglycerides) without adequate removal of fats and cholesterol from the macrophages by functional high density lipoproteins (HDL). It is commonly referred to as a hardening or furring of the arteries. It is caused by the formation of multiple plaques within the arteries.

See, you DID know what it was. It’s hardening of the arteries, and EVERYONE has heard of that!

So what is happening in virtually everybody’s body right now is a process called advanced glycation. And that means we need another definition moment.

Advanced Glycation is a non-enzymatic glycoxidation process involving sugars and basic amino acids of various proteins. The end products (AGEs) are chemically diverse, stable and implicated in various diseases in which deposits are formed, including amyloidosis, atherosclerosis and rheumatoid arthritis.

Simple answer; it’s sugar attaching itself to naturally occurring proteins and fats in the body.

These end products are what reside in our body right now. They are molecules formed by a process called glycosylation in which excess sugars attach themselves to your body’s proteins and lipids. And once formed, these AGEs are completely irreversible—wreaking havoc on your body, where they damage cells and tissues while prematurely aging your body.

Under normal circumstances, this isn’t a problem—a healthy body is equipped to remove these toxic molecules on a regular basis.

But in the all-too-common case of prolonged oxidative stress - A.K.A acidosis – A.K.A. modern ifestyle (caused by high blood sugar, a diet rich in processed food or an environment steeped in toxins and stress), you may not be so lucky. In cases like these, AGEs build up at a faster rate than your body can handle—and studies show that the damage they can do to your tissues… and especially your arteries, kidneys and retinas… is severe.

Research says that AGE accumulation occurs in the small arteries in the heart muscle and arteries that have lost their normal elasticity due to diminished nitric oxide levels, increased plaque formation and inflammation—all of which directly contribute to the risk of serious cardiac events like heart attacks and strokes.6-7
What’s worse, these artery-hardening and clogging effects have been shown to be completely independent of risk factors like age, high blood pressure and hyperglycemia—which means that when AGEs are involved, even otherwise healthy people may be at risk.8-10
So let’s break all this down to some simple 1-2-3 points that a typical overstressed busy modern ‘glycolator’ can use.

1. Glycolation comes from excess sugars, and toxic and stressful lifestyle
2. Glycolation causes excess acidification and oxidation and its toxic byproducts cannot be removed.
3. To prevent glycolation and its toxic end products we need to change our diet.
- Less acid-forming foods, especially sugars, and more alkalinizing food and water sources.
- More anti-oxidation products in the form of greens or antioxidant water.

Oh, and there is a fourth action point. Because it’s non-reversible, and happening now, the last and most important point is to DO IT NOW.

References:
1. Centers for Disease Control and Prevention. Potential Infectious Etiologies of Atherosclerosis: A Multifactorial Perspective. Available at: http://www.cdc.gov/ncidod/eid/vol7no5/oconnor.htm#1. Accessed on: 8-10-09.
2. Forbes JM, Soldatos G, Thomas MC. Below the radar: advanced glycation end products that detour “around the side”. Is HbA1c not an accurate enough predictor of long term progression and glycaemic control in diabetes? Clin Biochem Rev. 2005 Nov;26(4):123-34.
3. Tan D, Wang Y, Lo CY, et al. Methylglyoxal: its presence and potential scavengers. Asia Pac J Clin Nutr. 2008;17 Suppl 1:261-4.
4. Wendt TM, Tanji N, Guo J, et al. RAGE drives the development of glomerulosclerosis and implicates podocyte activation in the pathogenesis of diabetic nephropathy. Am J Pathol. 2003 Apr;162(4):1123-37.
5. Ahmed N. Advanced glycation endproducts--role in pathology of diabetic complications. Diabetes Res Clin Pract. 2005 Jan;67(1):3-21.
6. Zieman SJ, Kass DA. Advanced glycation endproduct crosslinking in the cardiovascular system: potential therapeutic target for cardiovascular disease. Drugs. 2004;64(5):459-70.
7. McNulty M, Mahmud A, Feely J. Advanced glycation end-products and arterial stiffness in hypertension. Am J Hypertens. 2007 Mar;20(3):242-7.
8. McNulty M, Mahmud A, Feely J. Advanced glycation end-products and arterial stiffness in hypertension. Am J Hypertens. 2007 Mar;20(3):242-7.
9. Semba RD, Najjar SS, Sun K, et al. Serum carboxymethyl-lysine, an advanced glycation end product, is associated with increased aortic pulse wave velocity in adults. Am J Hypertens. 2009 Jan;22(1):74-9.
10. Vlassara H, Fuh H, Donnelly T, et al. Advanced glycation endproducts promote adhesion molecule (VCAM-1, ICAM-1) expression and atheroma formation in normal rabbits. Mol Med. 1995 May;1(4):447-56.
11. Loske C, Neumann A, Cunningham AM, et al. Cytotoxicity of advanced glycation endproducts is mediated by oxidative stress. J Neural Transm. 1998;105(8-9):1005-15.
12. Hipkiss AR. Would carnosine or a carnivorous diet help suppress aging and associated pathologies? Ann N Y Acad Sci. 2006 May;1067:369-74.
13. Reddy VP, Garrett MR, Perry G, et al. Carnosine: a versatile antioxidant and antiglycating agent. Sci Aging Knowledge Environ. 2005 May 4;2005(18):pe12.
14. Guiotto A, Calderan A, Ruzza P, et al. Carnosine and carnosine-related antioxidants: a review. Curr Med Chem. 2005;12(20):2293-315.
15. Hipkiss AR, Chana H. Carnosine protects proteins against methylglyoxal-mediated modifications. Biochem Biophys Res Commun. 1998 Jul 9;248(1):28-32.
16. Hsieh CL, Yang MH, Chyau CC, et al. Kinetic analysis on the sensitivity of glucose- or glyoxal-induced LDL glycation to the inhibitory effect of Psidium guajava extract in a physiomimic system. Biosystems. 2007 Mar;88(1-2):92-100.
17. Lunceford N, Gugliucci A. Ilex paraguariensis extracts inhibit AGE formation more efficiently than green tea. Fitoterapia. 2005 Jul;76(5):419-27.
18. Mosimann AL, Wilhelm-Filho D, da Silva EL. Aqueous extract of Ilex paraguariensis attenuates the progression of atherosclerosis in cholesterol-fed rabbits. Biofactors. 2006;26(1):59-70.
19. Yamagishi S, Matsui T, Takenaka K, Nakamura K, Takeuchi M, Inoue H. Pigment epithelium-derived factor (PEDF) prevents platelet activation and aggregation in diabetic rats by blocking deleterious effects of advanced glycation end products (AGEs). Diabetes Metab Res Rev. 2009 Mar;25(3):266-71.
20. Suji G, Sivakami S. DNA damage during glycation of lysine by methylglyoxal: assessment of vitamins in preventing damage. Amino Acids. 2007 Nov;33(4):615-21.
21. Du X, Edelstein D, Brownlee M. Oral benfotiamine plus alpha-lipoic acid normalises complication-causing pathways in type 1 diabetes. Diabetologia. 2008 Oct;51(10):1930-2.
22. Hammes HP, Du X, Edelstein D, et al. Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med. 2003 Mar;9(3):294-9.