Life Extension Magazine®

Issue: Mar 2014

Mitochondria And Aging Conference On The Canary Islands

The Mitochondria, Metabolic Regulation, and the Biology of Aging Conference featured discoveries on the links between mitochondria and insulin resistance, between fat cells and aging, and between air pollution and cardiovascular disease. The 2013 conference demonstrated how mitochondria play key roles in the cause and potential cures of aging and associated diseases.

By Ben Best, BS, Pharmacy.

Mitochondria And Aging  

Mitochondria And Aging

Mitochondria are the source of most energy in living organisms.1 Muscle, which requires significant amounts of energy, typically has over a hundred mitochondria in every cell.1 Sugar, fat, and protein are eventually converted to energy-rich ATP molecules by mitochondria, but free radicals are often an unfortunate by-product.2

Over 40 years ago Denham Harman, Professor Emeritus at the University of Nebraska Medical Center, proposed that because mitochondria are the main source of free radicals, mitochondria are the major determinants of aging and life span.3 Harman’s theories on the cause of aging have been extremely influential.

Mitochondria were the subject of many of the presentations at the Mitochondria, Metabolic Regulation, and the Biology of Aging Conference held on the Canary Island of Lanzarote, February 10-13, 2013. The conference was organized by UK-based Zing Conferences, which specializes in organizing scientific conferences.

Mitochondrial Dynamics And Insulin Resistance


Antonio Zorzano, PhD (Professor of Biochemistry and Molecular Biology at the University of Barcelona, Barcelona, Spain) has been studying the effects of mitochondrial dynamics. Mitochondria are generally depicted as static oval-shaped organelles within cells, but with varying degrees of frequency, mitochondria will fuse with and then separate from other mitochondria within the same cell.2,4 Dynamic networks of mitochondria are important for mitochondrial maintenance and quality control. Damaged mitochondria that cannot be rehabilitated by fusion cease to fuse with other mitochondria, and are digested by the cell’s incinerators (lysosomes). More than 10 years ago Dr. Zorzano demonstrated that a protein responsible for mitochondrial fusion is often reduced as much as 40% in the muscle of obese rats.5 Two years later he showed that the expression of a gene that encodes this fusion protein in muscle is directly proportional to insulin sensitivity (the degree to which a given amount of insulin causes glucose to enter cells).6 Recently, he has determined that reduced mitochondrial fusion protein is not simply associated with insulin resistance, but causes insulin resistance―and he has proposed that this is a potential target for diabetes drug development. 7 Dr. Zorzano’s team has shown that although obese non-diabetics can increase their production of mitochondrial fusion protein (and production of new mitochondria) through aerobic exercise, type II diabetics have lost their capacity to do so.8

Fat Stem Cells And Aging


Werner Zwerschke, PhD (Team Leader, Institute of Biomedical Aging Research, Austrian Academy of Sciences, Innsbruck, Austria) cited a study indicating that although total body fat may decrease in old age, lean tissue may decrease even more―resulting in the possibility of an increase in percentage of body fat. 9 With age, fat increasingly tends to accumulate where it does not belong—in muscle, liver, and bone marrow―rather than in adipose tissue (fat cells), which contributes to dysfunction of those tissues.9 Adipose progenitor cells (fat stem cells) are extremely diligent at retaining the same number of adipocytes (fat cells) throughout adulthood, contributing to the difficulties obese people have in losing weight.10 Dr. Zwerschke has been studying the mechanisms controlling fat cell replenishment by fat stem cells in the hope of finding therapies for weight loss.11 He has identified resveratrol as a substance that reduces the activity of fat stem cells.12

Autophagy Of Mitochondria


Nektarios Tavernarakis, PhD (Professor of Molecular Systems Biology, Medical School of the University of Crete, Greece) has been focused on the degradation of dysfunctional mitochondria (autophagy). Parkinson’s disease patients are thought to have particularly damaged mitochondria in the substantia nigra (the brain region that is most affected in Parkinsonism). Damage to a protein that causes defective mitochondria to be degraded by autophagy results in an inherited form of Parkinson’s disease.13 Dr. Tavernarakis gave evidence for a similar defect contributing to other brain diseases of aging, namely Alzheimer’s disease and Huntington’s disease.14 He believes that removal of defective organelles by autophagy, particularly mitochondria, is an important reason for the life extension benefits seen for rapamycin, resveratrol, and spermidine in model organisms.15


Frank Madeo, PhD (Professor, Institute of Molecular Biosciences, University of Graz, Graz, Austria) has been working with Dr. Tavernarakis in studying the means by which degradation of damaged or unnecessary cellular components (autophagy) increases life span in model organisms (yeast, nematode worms, and fruit flies). Their team found that resveratrol and spermidine increase autophagy by different mechanisms, and that one tenth of the optimal dose of resveratrol or spermidine can be highly effective when the two substances are given in combination rather than separately.16 Dr. Madeo has also shown that spermidine increases resistance to free radicals and stress in fruit flies by means that are dependent upon as well as by means that are independent of autophagy.17 Spermidine has been shown to be enriched in the blood of healthy humans who have lived to be over 90 years of age. 18 Dr. Madeo told me that he eats foods that are high in spermidine. Spermidine content is particularly high in cooked soybeans, green peas, pears, lentil soup, and mushrooms (listed in descending order).19

Telomerase Protection Of Mitochondrial DNA


Judith Haendeler, PhD (Team Leader, Molecular Cell & Aging Research, University of Duesseldorf, Duesseldorf, Germany) has been studying telomerase, the enzyme that repairs the ends of chromosomes. Telomeres protect the ends of chromosomes just as caps on shoelaces protect shoelaces from becoming frayed. The telomerase enzyme elongates chromosomes, helping to protect nuclear DNA.20 Like the cell nucleus, mitochondria contain DNA, but the DNA in mitochondria is circular, and thus has no ends, has no telomeres, and has no need for telomerase. Nonetheless, Dr. Haendeler has shown that the active portion of the telomerase enzyme can bind to and thereby protect mitochondrial DNA.21 She has also shown that the mechanisms for activation of the telomerase enzyme are similar in the nucleus and in the mitochondria.22 Most recently, she has shown that these mechanisms can be interfered with by ultra-fine carbon black particles in the air as well as by a combination of high levels of dietary fructose and fat.23 The consequences of this harm contribute to both lung disease and cardiovascular disease, with ultra-fine particles from air pollution damaging the linings of blood vessels along with the lungs.23


Although aging theories have been modified considerably since Denham Harman proposed his mitochondrial free radical theories, the researchers at this conference presented much evidence that mitochondria continue to be of major significance in the cause, and possible cures, of aging and aging-associated diseases.

If you have any questions on the scientific content of this article, please call a Life Extension® Health Advisor at 1-866-864-3027.


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