Dr Charles Forsyth

Integrated Medicine


Mitochondrial Function Tests & Chronic Fatigue Syndrome

There is now good evidence that the central problem in many people with chronic fatigue syndrome (and many other chronic diseases) is reduced efficiency of the microscopic sausage shaped structures present in every cell of the body, called mitochondria.  One of the main functions of mitochondria is to act as the power station for each cell, producing a molecule called ATP (adenosine triphosphate).  The cell releases energy from ATP by converting it to ADP (adenosine diphosphate).  The ADP is then recycled - it is taken back into the mitochondria where it is reconverted to ATP, which is then exported back to the cell - and so the cycle continues.  This biochemical processes that recycle ADP to ATP are called the citric acid cycle, the tricarboxylic acid cycle or the Kreb’s cycle and oxidative phosphorylation,.  This recycling is a far more efficient and rapid process than the mitochondria making ATP from scratch.  It is now thought that this is one of the factors that determines the rate of the ageing process.

Mitochondrial inefficiency may result from:

  1. Deficiencies of the substrates/nutrients required by mitochondria, especially magnesium, vitamins B3, B1, B2, biotin, zinc, manganese, L-carnitine, coenzyme Q10, d-ribose and short chain fatty acids.

  2. Toxins - substances that block mitochondrial functioning, eg:

  3. Environmental pollutants, eg. pesticides, mercury, nickel, dyes, etc.

  4. Microbial toxins, DNA & RNA.

  5. Endogenous toxins:

  6. Normal substances in the wrong places, eg. copper

  7. Those produced by our own faulty metabolism, eg. lipid peroxidation products(diolein, and complex aldehydes, including malondialdehyde) and peptide complexes (such as resulting from leaky gut syndrome). 

  1. Genetic - inherited.

Acumen has developed a number of investigations of mitochondrial function:

ATP Profile

This measures certain key aspects of mitochondrial functioning in neutrophils (one type of white blood cell):

  1. The total amount of ATP in the neutrophil and the fraction of this that is available for energy supply.

  2. The efficiency of ADP to ATP recycling and also the degree of blocking (by toxins) of this process.

  3. The efficiency of translocator protein - this is the mechanism by which ADP & ATP are transported across the mitochondrial membrane. 

Mitochondrial Membrane & Translocator Protein Studies

This examines mitochondria in much more detail and specifically identifies any toxins that are blocking oxidative phosphoryation, translocator protein and mitochondrial DNA.

Cardiolipin Profile

Cardiolipin is a lipid that is exclusive to mitochondrial membranes and is vitally important to mitochondrial function. The enzyme that makes cardiolipin (cardiolipin synthase) is manganese dependent and is very susceptible to being blocked by other metals.

Mitochondrial Respiration Studies

This tests is able to identify when oxidative phosphorylation is uncoupled from the electron transport chain.  When uncoupling is present, it is due to toxins.  Uncoupling may be present even when the ATP Profile and Translocator Protein Studies appear normal.

These tests enable much more precise diagnosis and treatment of a whole range of conditions, especially chronic fatigue syndrome.

See: www.ijcem.com/files/IJCEM812001.pdf for the first scientific publication (January 2009) of research conducted using the ATP Profile.

For more information concerning these and other related investigations, download “Mitochondrial Tests” from: Downloads.


Mitochondrial Investigations

   INVESTIGATIONS: Nutritional  Gut  Toxins  Microbial  Mitochondrial  DNA Adducts