Mitochondrial Dysfunction

Mitochondrial Dysfunction is a functional diagnosis, for which conventional medicine has identified no causative mechanism. It appears to be associated with a variety of different diseases, including:

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  Parkinson's disease,
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  Alzheimer's,
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  Autism,
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  Low thyroid function,
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  Chronic fatigue syndrome,
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  Fibromyalgia.
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  Bipolar disorder,
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  Schizophrenia,
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  Diabetes,
• Asthma
• Kidney problems
• Heart problems
• GI problems
• Seizures

Please see conventional, complimentary and alternative medical treatments for important background information regarding the different types of medical treatments discussed on this page. Naturopathic, Complementary and Alternative treatments that may be considered include:

Among the possible causes of mitochondrial dysfunction that have been advanced, the following appear to be most important:

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  Low thyroid function -
T4 and T3 thyroid hormones increase the number and activity of mitochondria [Guyton2000, pg 861], [Starr2005, pg 55] Mitochondria are the primary source of energy in most cells of the human body.
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  Heavy metal toxicity
•        Functional deficiency of D-ribose (building block of ATP).
•        Functional deficiency of carnitine (needed to carry fatty acids into mitochondria to be converted to energy).
•        Functional deficiency of CoQ-10
(essential to the operation of the electron transport chain inside mitochondria). Note that statin drugs that are used to lower cholesterol levels in the blood also suppress the body's production of CoQ-10.
•        Genetic deterioration of mitochondrial DNA due to reduction in evolutionary pressure
[Starr2005, pg 56].
Note that mitochondrial DNA is distinct from the 23 pair of somatic chromosomes inherited from the mother and the father - since sperm cells have no mitochondria, all the child's mitochondrial DNA is derived from the mother's ovum. Studies of mitochondrial DNA across racial groups suggests that mitochondrial DNA is quite stable, which argues against significant genetic deterioration over the course of a few generations.

• Basal Body Temperature (depressed if hypothyroid)
• Heavy metal urinalysis with provocation.
• Dr. Weyrich hypothesizes: Organic Acid Test (elevated markers for gut dysbiosis).
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  LDH (part of Complete Metabolic Panel, CMP)
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  Translocator protein studies

Naturopathic, Complementary and Alternative Treatments

Dr. Weyrich notes that many disorders, including chronic fatigue and fibromyalgia are associated both with hypothyroidism and yeast dysbiosis.

The Organic Acid Test described by Great Plains Laboratory and [Shaw2008] suggests a link between dysbiosis and mitochondrial dysfunction. In particular, the following metabolites of yeast or fungal metabolism may be elevated in cases of dysbiosis:

• Tartaric acid (3-hydroxymalic acid or 2,3-hydroxy-succinic acid) - An analog of the Krebs cycle intermediate malic acid that inhibits the Krebs cycle enzyme fumarase that converts fumaric acid to malic acid.
• Citramalic (methylmalic) acid - An analog of the Krebs cycle compound malic acid; may interfere with the production of malic acid in the Krebs cycle.
• 3-Oxoglutaric acid - An analog of the Krebs cycle compound 2-oxoglutaric (alpha-ketoglutaric) acid; may interfere with the Krebs cycle.

The important point here is that the Krebs cycle is found exclusively in the mitochondria and is critical to the function of the mitochondria in production of ATP. Thus, one of the direct consequences of yeast or fungal dysbiosis may be mitochondrial dysfunction.

It follows that dysbiosis may be the underlying cause of mitochondrial dysfunction, and the protocol [Starr2005] describes for treatment of what he calls type-II hypothyroidism is compensating for impaired mitochondrial function by inducing proliferation of mitochondria through the use of supraphysiological levels of thyroid hormone. While this approach may have the benefit of boosting the immune system to help the body clear the dysbiosis, a naturopathic approach to treating the root cause must not lose sight of the underlying cause - dysbiosis.