What Is Coenzyme Q 10? Why Was It Used In The Small Alzheimer’s Study? What is Oxidative Stress? Statins and Coenzyme Q 10.

“Hi Terri… I love hearing about diet and lifestyle changes reversing disease. Lately I read about coconut oil and its usefulness in Alzheimers – Alzheimer’s Disease: What If There Was a Cure?   Terri, can you tell me why the methylcobalamin and CoQ10 were used?  What were their specific roles?”

Please refer to last post for the article this question refers to.

wpid-IMAG1043.jpgIn medical school, the basic science classes are usually contained to the first two years of study, classes like physiology, biochemistry, and histology. The last two years of school we don short white coats and run around wards and clinics learning how to take care of patients.  We put basic science behind us as we forge forward, identifying diseases in actual patients and learning what our staff doctors do about it.  When we transition to “real doctor-hood,” we all like to roll our eyes and refer to the basic science stuff as “minutiae.”  It is in this “minutiae” that I am learning how food is the best medicine but can be the worst disease.

Co Q 10 ( also Coenzyme Q 10 or ubiquinone) helps make our energy and is highest in our mitochondria:

Where specifically do you find Co Q 10 in the body? It’s everywhere!  Ubiquitous.  But it’s super high in our mitochondria because one of its main functions is helping to generate energy (ATP) via the electron transport chain.  (Egads.  I thought my test on ATP production was over 12 years ago.  This blog is a hobby?)  Mitochondria are the “power-houses” of cells and make our energy, which comes from ATP.  Co Q 10 is therefore highest in organs that are “highly active,” such as the heart and liver, but it is present in every cell since every cell needs energy.  Mitochondria need Co Q 10 to make energy, and you need mitochondria and Co Q 10.

Co Q 10 is also an extremely important, well-placed anti-oxidant our body can make:

Co Q 10 has the ability to easily transfer electrons back and forth in different situations, and so it can block free radical formation. Free-ruh-form-WHAT?  Free radicals.  Free radicals can also just be simply called “radicals.”  Free radicals are unstable molecules and will “steal” electrons from the proteins and fats that make up our cells in order to stabilize themselves.  Good for them.  Bad for the cell (us).  Even in a perfect world, free radicals are actually made in our bodies as a by-product of all the reactions going on, especially in our mitochondria, who are busy, busy making us energy to live.  (Living is good.)  You cannot escape free radical formation.  It’s a fact of life, although our food choices can definitely drastically increase the load of free radicals in our body.  (Eat right.  Eat right.)  Co Q 10 has the ability to give or take electrons to help these free radicals calm down.  I find it amazing that co Q 10 functions in both the production of ATP and the protection from by-products of ATP production; it is a pretty darn cool design.  (Never lose your awe of life.)

An aside on why getting off of statins if a person can is ultra-important:

Co Q 10 can be (and is) made by the body. (Three things I want you to know about this.  One, it takes a lot of other nutrients to make it, so you must eat right.  Two, you can also eat it to get it.  Three, production slows down drastically as we age.)  Because the body doesn’t like to waste effort, it builds cholesterol and Co Q 10 along the same assembly line.  (Cholesterol is not bad.  It is absolutely, positively necessary to live.)  For those who have had biochemistry and pharmacology, statins are made to block cholesterol formation by blocking HMG-CoA Reductase, a necessary enzyme to take acetoacetyl co-A to mevalonate, which then goes on to become either Co Q 10 or cholesterol.

So in our efforts to block cholesterol formation, we are blocking one of the cofactors necessary for energy production and intense anti-oxidant protection! (Through my study of food, I very clearly see that everything in the body is a path that leads right back to the beginning. We must be careful when mucking with the system.  It is best to try to RESTORE the system, the point we conventional doctors and modern patients don’t really want to accept.  We CANNOT beat the design.)  Some patients can actually “feel” this lack of Co Q 10, and they get muscle aches and have to stop the medicines so freely handed out.  To combat this loss of Co Q 10 levels, many physicians advocate for Co Q 10 supplementation for statin patients, particularly as they age.  None of my friends and family members who are on statins has been told to take Co Q 10.  Regardless, their Co Q 10 production is being blocked, and they could probably benefit from Co Q 10—and a strict diet of real food low in grains, sugar, and detrimental vegetable/grain oils.

How does this relate to Alzheimer’s?

It is now suspected that Alzheimer’s disease is due, in part, to damage to the brain’s proteins, fats, and DNA by free radicals. The mitochondria are hit particularly hard, and because they are damaged, they create even more of these free radicals, thus damaging themselves further.  If you know much about Alzheimer’s disease, you may have heard of the amyloid plaques and tau tangles in the brain of Alzheimer’s patients.  It is felt these changes occur after the mitochondria are damaged.

Mitochondria work extensively with oxygen to make our energy. You will see the words “oxidative stress” associated with Alzheimer’s disease and other diseases.  Let’s manipulate the phrase oxidative stress to “oxygen stress.”  What?  I thought oxygen was good!  Well, it is, but when processed it makes some nasty reactive byproducts.  When the mitochondria use oxygen to make our energy (ATP) the oxygen is made into a reactive oxygen species (ROS) (a kind of free radical).  The ROS free radical goes to scavenge electrons from fully-functioning proteins, fats, and DNA which are sitting there minding their own business and quite content with their electrons just the way they are.  When there is increasing ROS without a counter-balance, it damages structure and function of cells.  In the brain, that’s neurons.

Enter Co Q 10 to act as an anti-oxidant. Not just any anti-oxidant, but an anti-oxidant which shoots like a bullet to a target—right to the mitochondria.  Co Q 10 is more specific to mitochondria than, say, vitamin C, a perfectly good anti-oxidant, is.  Struggling mitochondria play a large role in the development of Alzheimer’s, so using Co Q 10 is a way to boost mitochondrial function and halt damage.  Animal studies support that Co Q 10 reduces oxidative stress, reduces amyloid plaques, and improves behavior in mice with induced Alzheimer’s disease.

Closing:

My hobby site here is not intended as medical advice or treatment advice. You should consult with your healthcare practitioner regarding your health.  This site is only my story of what I am learning in my journey through food.  I am learning that deep nutrition counts.  Taking out foods which lead to inflammation and oxidative stress in the body (sugars, ill-prepared and excessive grains, and vegetable/processed oils) and putting in nutrient-dense foods (vegetables, greens, seafood, organ meats, and fruits).  If you’re wondering where you can get your Co Q 10, you won’t like the answer.  I don’t always like the foods I eat, but “Let food be they medicine…”  Anyhow.  The answer to that question is beef heart.  (And less but still fair quantities in liver, kidney, and muscle meats.)  However, a healthy, young, well fed body can make its own Co Q 10.  As we age or as we acquire deficits, that may not be enough and supplementation via strong food sources or vitamins may be indicated.  Read up.  Talk with your doc.

Methylcobalamin next.  Thank you for the question.

~~Terri

 

Antioxidant Therapies for Alzheimer’s Disease. Ye Feng and Xiaochuan WangOxidative Medicine and Cellular Longevity.  April 2012.

Coenzyme Q10 Decreases Amyloid Pathology and Improves Behavior in a Transgenic Mouse Model of Alzheimer’s Disease. Magali Dumont, Khatuna Kipiani, […], and M. Flint Beal. Journal of Alzheimer’s Disease. 2011.  27(1): 211-223

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