Volume 3, Issue 15
April 15, 2010
The surprising therapy that makes postmenopausal women live longer
Are you doing everything you can to live a long healthy life? If you're a postmenopausal woman, you may not be. That's because many women are avoiding one of the best ways to increase their life span.
I've told my readers many times the fundamental secret to slowing down aging and preventing disease. All you have to do is maintain youthful levels of cellular energy production. And earlier this year, a new study revealed one of the most effective ways for women to do this. All you have to do is maintain youthful estrogen levels.
The researchers wanted to look at the effect of estrogen on mitochondrial biogenesis. Remember that phrase "mitochondrial biogenesis." It refers to the ability of the cells to replace old and worn out mitochondria with new ones. Mitochondrial biogenesis is essential for maintaining vitality, strength, and optimal cellular function.
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As you may know, the mitochondria make almost all of the energy in your cells. The mitochondria are tiny bubbles that are found throughout your cells. Every cell in the body has thousands of mitochondria. The problem is as you get older your cells start losing mitochondria because of decreased mitochondrial biogenesis. And as we lose mitochondria, we lose the ability to make energy. This is at the center of what makes us so susceptible to disease and frailty as we get older.
The fact that we lose mitochondria from decreased biogenesis is well established in medical circles. But why we lose them is another matter. But these researchers figured it out. They knew that our cells have fewer mitochondria as we get older. They also knew that our bodies become deficient of hormones during the same time. So they wondered if hormone deficiency could be responsible for the loss of mitochondria. Here's what they did:
They looked at three different kinds of thyroid cells. In some of the cells, they inhibited the function of an estrogen receptor called "estrogen-related receptor alpha (ERRa)." Keep in mind that hormones exert their influence on cells by activating certain receptors in the cells in the same way that the right key can open up a lock. By blocking ERRa in these cells, they blocked the effect that a particular estrogen called estradiol could have in them. What happened when they did this was astounding. All of the cells began to lose mitochondria at an accelerated rate. Then they took the experiment a step further.
They took the same cell lines and did the opposite — they increased the number of ERRas.ÿ This increased the effect of estradiol on the cells.
When they did this, the opposite thing happened. The cells started making more mitochondria. And at the end of the experiment, they had many more mitochondria than the cells with the normal number of ERRas. In other words, they were able to show that estrogen, particularly the estrogen estradiol, is a potent stimulator of mitochondrial biogenesis.
All of the estrogen stimulated cells produced greater amounts of cellular energy. No wonder women who replace their sagging estrogen levels with bioidentical hormones live longer and are more vital and resistant to disease.
But isn't estrogen replacement dangerous? This study and many others that look at that question strongly suggest just the opposite. It not only isn't dangerous to replace deficient estrogen levels, it is dangerous not to replace them. All of the published studies that show increased risks from taking "hormones" use synthetic drugs with hormone-like effects. They don't use real bioidentical hormones. My best advice to women is to find a doctor well versed in prescribing bioidentical hormones. Replace them as soon as they start to become deficient. This will typically start to happen in your late 40s to early 50s.
You can find a doctor well-versed in bioidentical hormones at www.acam.org.
Finding your Real Cures,
Frank Shallenberger, MD
REF: Mirebeau-Prunier D, Le Pennec S, Jacques C, et al. Estrogen-related receptor alpha and PGC-1-related coactivator constitute a novel complex mediating the biogenesis of functional mitochondria. FEBS Journal Volume 277 Issue 3, Pages 713 - 725. Published Online: 11 Jan 2010.
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