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August 2018 (Vol. 3 Issue 6)

Mitochondria: small but mighty

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Lynne McTaggart is co-editor of WDDTY. She is also a renowned health campaigner and the best-selling author of The Field, The Intention Experiment and The Bond.

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Mitochondria: small but mighty

July 31st 2018, 13:54
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Everybody's talking about them as the new hope for overcoming every condition from chronic fatigue to Alzheimer's disease. 'They' are the mitochondria of our cells—microscopic 'organs' in their own right that act like a teensy digestive system to convert the nutrients absorbed by the cell into energy, or 'respiration,' which the cell requires to carry out its business. These little 'organelles' even have their own DNA, and besides producing energy, they play an active role in monitoring and maintaining regular communication between neurons.

Where they differ from an ordinary digestive system is that each cell requires anywhere from hundreds to thousands of these little 'stomachs,' depending on the cell's job.

One of the body parts that requires the highest number of mitochondria to power its cells is the brain. Not surprisingly, nerve cells require a great deal of energy to do all they do, including maintaining communication around the body. They're also particularly vulnerable to free-radical damage, and woefully underdefended in that regard, particularly as free-radical production is highest within these cellular power plants.

The latest evidence shows that small changes in mitochondria caused by DNA and free-radical damage ultimately lead to neurological degeneration, which in turn may lead to one of a number of conditions from Alzheimer's to attention deficit/hyperactivity disorder (ADHD).

The reason for this has to do with energy burnout. When neurodegeneration occurs, mitochondria are continuously called upon to produce ever more energy—far more than is needed by the brain—which itself causes free-radical damage. But new evidence shows that much like a trusty sentinel, these mitochondria must be present for nerve cells to have optimum communication.

This holds all sorts of implications for any condition in which nerve communication is impaired.

It also suggests that the original theories about the cause of Alzheimer's, for instance, may be incomplete. The neurofibrillary tangles and plaques so characteristic of Alzheimer's may simply be a by-product of the condition—not its cause.

Indeed, the latest evidence in our cover story this month (see page 28) is that the plaques are in fact the body's way of attempting to defend itself against Alzheimer's. Rather than counting plaques, gauging energy production within brain cells is a better way of determining the extent of the disease.

Alzheimer's is not the only serious neurological illness caused by faulty mitochondria. Energy deficits in brain cells may also be behind other serious conditions like Parkinson's, Huntington's disease, and even amyotrophic lateral sclerosis (ALS, or motor neuron disease, which afflicted the late Dr Stephen Hawking). There's also evidence that the extent of energy deficit appears to determine the extent of the disease.

If all this is true, we may be treating all these diseases with the wrong medicine. For Parkinson's we focus on L-dopa, a brain chemical deficient in people with the condition, and never consider the role of the cells' energy supply. Small wonder that L-dopa often makes Parkinson's worse, and also why no drug for Alzheimer's, ADHD or motor neuron disease has made much of an impact on outcomes.

Medicine is convinced that these serious conditions require a heroic batch of chemicals to make much of a difference, but we're not only looking in the wrong place, we're trying too hard. In fact, it's not difficult to power up flagging mitochondria. New evidence shows that that an all-purpose nutrient, co-enzyme Q10, has miraculous effects on mitochondria, as does a newly identified type of B vitamin called PPQ, copiously present in many healthy foods but also available as a simple supplement.

Other simple supplements also demonstrate the ability to regenerate the mitochondria in neurons. In fact, one of the most promising is a supplement made up of a giant molecule—one of the largest pure carbon molecules in nature—called buckminsterfullerenes after the famous architect and inventor, Buckerminster Fuller, because they resemble his geodesic domes. These 'fullerenes' have the capacity to continuously stabilize free radicals in the mitochondria like a reusable sponge.

Not surprisingly, these carbon molecules, called C60 after their chemical formula, are being investigated for a number of illnesses, but most particularly as an anti-aging supplement against a range of conditions resulting from oxidative damage.

Once again, the latest science shows us that medicine has it all wrong when it comes to attempting to fix neurological damage. Instead of turning to harsh chemicals to fix the by-products of the condition, we need to look to the source—the power supply. As with most areas of biology, everything—including medical solutions—is energy.

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