Free Power Up Your Brain by David Perlmutter M. D., Alberto Villoldo Ph.d.

cancer cells don’t know they need to undergo apoptosis, and, without that message from the mitochondria, they would continue to reproduce, out of control, until they endanger the host—you.
    THE PROBLEM WITH FREE
RADICALS AND CELL DEATH
     
    While cellular suicide, as described above, is generally positive, it becomes a negative situation when mitochondrial function becomes impaired and sends signals that tell normal cells to die. In fact, this is the fundamental flaw in the mitochondrial mechanism that leads to the destruction of brain cells in essentially every neurodegenerative condition, including Alzheimer’s, multiple sclerosis, Parkinson’s, and Lou Gehrig’s disease, to name just a few. However, this brain cell apoptosis is not limited to just these diseases. The process occurs throughout your lifetime and is responsible for a general decline in brain function, even if not categorized as a disease per se.
    And the catalysts—or culprits—are free radicals. Free radicals are chemicals that cause oxidative damage to tissues, essentially causing them to rust like a piece of iron left exposed to the weather. They can also damage proteins, fat, and even DNA. In fact, damage to your tissues by free radicals is thought to underlie the process of aging, a theory first described by Denham Harman, a biogerontologist who was then a research associate at the Donner Laboratory of Medical Physics at the University of California, Berkeley. His much-cited article, now considered to be a landmark work, appeared in 1956. 5
    Dr. Harman also stated that free radicals are “quenched” by antioxidants and thus laid the groundwork for an understanding of the positive effects of ingesting antioxidants, which we will learn more about later in the book.
    MITOCHONDRIAL DNA
     
    Mitochondria play a far more interesting role than simply being an energy factory and the source of ROS. Indeed, there are many characteristics of the mitochondria that serve to differentiate them from all the other structural parts of our cells. For instance, mitochondria possess their own DNA (referred to as mt-DNA), which is distinctly separate from the far more familiar and more often studied DNA in the nucleus of the cell (known as n-DNA).
    While the nucleus of the cell contains exactly two copies of its DNA, mitochondria may have anywhere from two to ten copies of DNA. Interestingly, the mt-DNA, unlike n-DNA, is arranged in a ring, a configuration much like that seen in bacteria. Furthermore, in addition to similarities in the shape of their DNA, mitochondria and bacteria both lack the protein surrounding their genetic code that helps protect it from free radical damage, while in contrast, nuclear DNA is invested with protective proteins called histones, which also serve to regulate its function.
    These similarities led the biologist Lynn Margulis to propose an important new theory of the origin of mitochondria. 6 She posited that mitochondria evolved hundreds of millions of years ago from aerobic (oxygen-breathing) bacteria that gradually entered into an “endosymbiotic” relationship with anaerobic bacteria, which means they began to live inside the bodies of these other organisms. This symbiosis enabled the anaerobic organisms to survive in an oxygen-rich environment. Over time, the mitochondria assumed the primary function of energy production, intracellular signaling, apoptosis regulation, and perhaps communicating with the biosphere. Human mt-DNA contains only 37 genes, while n-DNA has thousands, and it is possible that, over time, n-DNA has been taking on more of the functions of mitochondria, allowing other organelles in the cell to specialize in such activities as protein building, waste elimination, and reproduction.
    Eventually, one bacterium engulfed another. The result was that these formerly free organisms now reside within each of your cells. Because of their role in energy metabolism, we might expect larger numbers of mitochondria in the