What Blocks Your Anti-Aging Enzyme?
August 2014, Xtend-Life Expert
Some of you are familiar with the claim that telomeres - the DNA at the end of each chromosome - are a key determinant of aging. There are telomeres in every cell of your body. The shorter they get, the older you look and feel. But when telomeres are prevented from becoming shorter, or they are lengthened, the body is programmed to create younger cells. Telomerase is the enzyme which is critical in the process of rebuilding telomeres and rejuvenating cells (ref. 1). Unfortunately, telomerase can be easily ‘blocked’ or ‘de-activated’. This blog looks at what causes the blockage, and how you can prevent it.
Some of you are familiar with the claim that telomeres - the DNA at the end of each chromosome - are a key determinant of aging.
There are telomeres in every cell of your body. The shorter they get, the older you look and feel. But when telomeres are prevented from becoming shorter, or they are lengthened, the body is programmed to create younger cells. Telomerase is the enzyme which is critical in the process of rebuilding telomeres and rejuvenating cells (ref. 1).
Unfortunately, telomerase can be easily ‘blocked’ or ‘de-activated’. This blog looks at what causes the blockage, and how you can prevent it.
What Causes Telomerase to become Blocked?
The key cause is an excess of cytokines.
Cytokines are inflammatory molecules. Studies show how they shorten telomere length and may lead to degenerative disorders such as frailty, loss of muscle mass, stroke, diabetes, and Alzheimer’s disease (ref. 2-3)
People with short telomeres were seen to have high levels of three cytokines: interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-a), and interferon type 1 (IFN-a).
The evidence also suggests that cytokines not only shorten telomeres through inflammation, but they also directly block telomerase production. (ref. 4)
Even worse, cytokines appear to create free radicals which literally kick telomerase out of the cell! (ref. 5)
It’s like a triple hit to your body. First, your tissues become inflamed. Then your telomeres get shorter, making your cells older and weaker. And in the process, free radicals ‘export’ telomerase out of the cell.
So what can you do to prevent, or even control cytokines, so they don’t cause so much degenerative damage?
How to Reduce the Degenerative Effects of Cytokines
Based on the above, you will not be surprised to hear that the key to reducing the degenerative effects of cytokines is to address systematic chronic inflammation. We have described how to do this here (ref 6)
In essence, the chronic inflammatory process is heavily influenced by a combination of factors such as toxins, oxidative stress, free radicals, injury, infections, lack of exercise, heredity and, especially, diet.
Indeed, a poor diet can increase and prolong inflammation while a good diet can reduce it. There are two nutrients which are especially powerful in fighting the degenerative effects of cytokines:
Perhaps the most widely studied, and acknowledged anti-cytokine nutrient is Omega-3 fatty acid.
1. Diet and Omega 3 Fatty Acids
Studies show how people who get more DHA andEPA, the two main Omega-3s, produce fewer cytokines (ref. 7). One of the best foods containing Omega-3s is cold water fish. Researchers followed over 3,000 Greek men and women. Those who ate 10 ounces of fish per week had up to 33% fewer cytokines than those who didn’t eat fish.
Try to eat the smaller oily fish like sardines or herring. Sardines are at the bottom of the ocean’s food chain. They only feed on plankton, so they don’t accumulate heavy metals and other contaminants in their flesh like many larger fish do.
Whether or not you are a fish-eater, supplementation is your next option. Our pure and potent Omega 3 fish oil formulas (ref. 8) not only have a very high DHA content. But also, according to lab tests, they contain greater inflammation fighting properties than highly concentrated Omega 3 fish oil.
A less well known, but powerful way to stop the telomerase-blocking action of cytokines, is with Beta-Carotene.
2. Diet and Beta Carotene
Beta-carotene is a red-orange pigment found in plants and fruits, especially carrots and colourful vegetables. The human body converts beta-carotene into vitamin A (retinol).
Research shows how people who eat the most vegetables have significantly longer telomeres… and that vegetables with the most beta carotene help to optimise telomere health. (ref. 9)
Also, do you remember I told you earlier that cytokines ‘kick’ telomerase out of the cell? Well, one of the ways anti-oxidants like beta-carotene benefits telomerase is that they block this effect. (ref 5)
Xtend-Life’s Total Balance products all include high quality natural Beta-Carotene.
Perhaps now you have a glimmer of The Fountain of Youth?!
1. For a simple explanation of the relationship between aging and telomeres please see www.lifelength.com/pdf/Aging_and_the_Telomere_Connection-Dr.Jerry_Shay-A4M-Orlando-April_2013.pdf
2. This study shows how chronic inflammation can shorten telomere length. www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0019687
3.The effects of inflammatory cytokines on aging and age-related diseases are shown in this study www.ncbi.nlm.nih.gov/pubmed/23792036
4. This research shows how the cytokine, tumour necrosis factor alpha, inhibits telomerase production
5.Free radicals appear to ‘export’ telomerase out of the cell as seen in this study www.docphin.com/research/article-detail/243909/PubMedID-14963003/Antioxidants-inhibit-nuclear-export-of-telomerase-reverse-transcriptase-and-delay-replicative-senescence-of-endothelial-cells
6. To read our blog describing the facts about chronic inflammation please see www.xtend-life.com/Blog/11-01-20/Are_You_Inflamed.aspx
7. These studies show how people who get more EPA and DHA, produce fewer cytokines
8. To find out more about our Omega 3 fish supplements please see www.xtend-life.com/product/Omega_3_Fish_Oil_Supplements.aspx
9. This research shows the beneficial effects of vegetables, antioxidants and beta-carotene on telomere health www.ncbi.nlm.nih.gov/pubmed/21857007