Living in the 21st century affords you many luxuries. High-speed computers… cell phones… air conditioning and LCD TVs. But the chemicals and industrial solvents that make them possible are poisonous. We’re now floating in a sea of space-age, lab-created, synthetic molecules. And they’re flowing through your blood as you read this letter.
They’re a part of life today, and we now have a new way of measuring their effect.
One of the things that happened is the environment is causing your telomeres to shorten.
Let me give you the example of the number-one risk factor for heart disease – high homocysteine levels.1
High homocysteine is a way to measure the inflammation that’s going on inside your body that’s being caused by all these foreign substances. High homocysteine then does more damage by blocking blood flow across your body and damaging the lining of your arteries.
And most doctors know nothing about another damaging effect of high homocysteine. It shortens your telomeres.
High homocysteine in your blood can triple the speed at which your telomeres shorten.2
One of the reasons homocysteine has such a damaging effect on these tiny tips to your DNA is that homocysteine cuts off telomerase.
Telomerase is the enzyme your body uses to rebuild the telomere. So the environment is giving you a double whammy. First homocysteine shortens telomeres, then it cuts off the enzyme your body uses to repair the damage.
Short telomeres are so prevalent in people with heart disease that having critically short telomeres is now an independent risk factor for heart disease.3
In a study published in the prestigious journal The Lancet, researchers found an association between short telomeres and atherosclerosis.4 The people with short telomeres had accelerated aging of their blood vessels and had a buildup of plaque that correlated to arteries that acted 8.6 years older.
This increased risk extends into the very fiber of your heart muscle. In a study published in the Journal of the American College of Cardiology, researchers discovered that people with heart failure had telomeres that were 40% shorter than normal.5
High homocysteine can cause strokes and heart attacks as well.6
One way to know if you’re at risk is by getting your homocysteine checked with a simple blood test from your doctor. I personally like to keep my patients’ levels at 7 or below.
The natural way to help keep your homocysteine in check and protect yourself from heart disease is to ramp up your levels of vitamin B.
Vitamins B6, B9 (also known as folic acid or folate) and B12 all help to convert homocysteine into methionine, the good guy. B9 also restores the action of telomerase, counteracting the worst effect of homocysteine.7
Methionine is one of the building blocks of protein. And without enough levels of B vitamins in your system, your body can’t convert homocysteine to methionine efficiently. This can lead to an overload of homocysteine racing through your blood.
To boost your B vitamins, here’s what I recommend:
Another way to turn homocysteine into methionine is with choline.
You may remember I’ve written to you about choline as a brain booster. But choline is also essential in the process that breaks down homocysteine into helpful amino acids like methionine.
Studies show that the more choline you have, the lower your homocysteine will be.8 In one study, people who took in the most choline had almost 10% lower homocysteine.9
The best way to get more choline is to eat one of the “taboo” foods modern nutritionists tell you to stay away from – animal meat and eggs. You can also find smaller amounts of choline in cod, cauliflower, avocados, and bananas.
To supplement, look for choline citrate. In my view, it’s the best way to get high levels of choline, and there are no side effects. You need at least 425 mg of choline a day as a woman; 550 mg if you’re a man.
To Your Good Health,
Al Sears, MD
1. Levy D, Hwang S, et. al. “Associations of plasma natriuretic peptide, adrenomedullin, and homocysteine levels with alterations in arterial stiffness: the Framingham Heart Study,” Circulation 2007; 115(24):3079-85
2. Richards J, et. al. “Homocysteine levels and leukocyte telomere length.” Atherosclerosis. 2008;200(2):271-7.
3. Zhang W, Hui R, Yang S. “Telomeres, cardiovascular aging, and potential intervention for cellular senescence.” Sci China Life Sci. 2014;57(8):858-62.
4. Samani NJ, et al. “Telomere shortening in atherosclerosis.” Lancet. 2001;358(9280):472-3.
5. van der Harst P, et al. “Telomere length of circulating leukocytes is decreased in patients with chronic heart failure.” J Am Coll Cardiol. 2007; 49(13):1459-64.
6. McCarty M, Thomas C. “The Vascular Toxicity of Homocysteine and How to Control It.” Linus Pauling Inst. lpi.oregonstate.edu. Retrieved Nov 6, 2014.
7. Zhang D, Wen X, Wu W, Xu E, Zhang Y, Cui W. “Homocysteine-related hTERT DNA demethylation contributes to shortened leukocyte telomere length in atherosclerosis.” Atherosclerosis. 2013;231(1):1739.
8. Imbard A, et. al. “Plasma choline and betaine correlate with serum folate, plasma S-adenosyl-methionine and S-adenosyl-homocysteine in healthy volunteers.” Clin Chem Lab Med. 2013;51(3):683-92.
9.Lee J, Jacques P, Dougherty L, Selhub J, Giovannucci E, Zeisel S, Cho E. “Are dietary choline and betaine intakes determinants of total homocysteine concentration?” Am J Clin Nutr. 2010;91(5):1303-10.