Friday, November 04, 2016

CFS is still a mystery

Chronic Fatigue syndrome better known as Myalgic Encephalomyelitis, is now thought to be a metabolic dysfunction with the result that not enough energy is being produced.  There is mounting evidence to suggest that the blood metabolites of CFS patients are very different from the products of metabolism in healthy controls (Naviaux et Al, Davis; Fluge and Mella.....)
In humans, energy comes from the complete oxidation of glucose to carbon dioxide and water. The digestive system does the first part, it produces glucose, glycerol and fatty acids, and amino acids (Myhill et al)

Impaired digestion is going to result in impaired energy production at a very base level (eg iron-deficient anaemia) and these problems are usually ruled out by running a few blood tests.  At the next step in energy
production is when the glucose and lipids are fed into the blood stream where, together with oxygen bound to haemoglobin in erythrocytes (red blood cells), they are transported to every cell in the body (MYHILL et al).  Those with CFS are
tested to determine if the lungs and circulatory system are functioning correctly and if so then it can be assumed that the energy deficit is coming from problems with cellular respiration and ATP production.  Without ATP, there is no energy!!!
With a little ATP formation there is a little energy and with the required level of ATP production there is more than enough energy to cover the functions of everyday living.  The problems in people with CFS are caused by not having enough ATP to produce the
energy required for maintaining a healthy body at the cellular level and in terms of the energy requirements of movement.  Unfortunately for patients, it seems as if the energy required to move is the first kind of problem they notice or at least the desire for a lot more sleep
(why can't I keep up with my peers and pull all-nighters?).  Others notice too and the word "lazy" can be the first accusation that motivates patients to seek help (if they are old enough).  The accusers cannot see the extra effort that is required to hear through all the background
noise that they can effortlessly block out for instance.  Without enough energy, everything becomes harder than it was.  Similarly without enough sleep. 

For people with CFS, the energy deficit is coming from within single cells even though they are being supplied with adequate oxygen and nutrients because their digestive system and circulatory systems are working with no sign of malfunction. 
The cellular performance is mostly invisible to others so the words "invisible disease" are used to describe the condition and for some unknown reason, testing for mitochondrial function is rarely considered unless your doctor happens to specialise in CFS.  The
 functioning or dysfunctioning of the energy producers called mitochondria seems like an obvious place to start for someone who is complaining about life-altering fatigue unless they have a known existing condition which would explain it.
Scientists have known about the structure within cells that handles ATP production for a long time and they called
the ATP energy producers "mitochondria".  Another way of looking at it is by thinking about your metabolism.  Someone with a fast metabolism makes lots of ATP energy and quickly enough to keep the supply going.  A slow metabolism is usually what is blamed
for people putting on weight and some people have the privilege of watching their own metabolic rate change over the years.  Mitochondria and metabolism go hand-in-hand; so that when you see a CFS study talking about patients having a hypometabolic disorder
 or having a slow (hypo means slow) metabolism, you will know why.  But even that seems to give the wrong idea because the kind of 'slow' the recent studies are talking about is designed for creatures who are going into a low-powered state "on purpose" as a matter of survival.
As a result of detecting a threat, which is quite often a lack of food supply triggering something like calorie restriction (not getting enough carbs usually).  This means that the CFS patients body is going into an altered state as a matter of survival,
after detecting a threat to life itself as in the state of dauer.  Your body is doing what it can to help when you have CFS and you had best follow its lead for now until further research uncovers what the threat to survival is.  Some are saying that the persistent threat is biotoxins and until
the threat is eliminated (aka cleaning up the environment or leaving the environment), the body will continue to protect itself in this strange way (Erikson & .  ............)  This means that the initial virus or trauma that appeared to trigger the CFS is totally incidental to the continuing
symptoms.  An infection for example, may well have been the event that triggered the need for more ATP which the body could not supply but it was an overloaded body system in the first place as a result of something even more sinister, like mould.  Black mould that is not
visible because it is on the inside of the wall or inside a pipe.

The other main theory seems to involve chronic, stealth or reactivating viruses and bacteria like EBV, mycoplasmas, Borreliosis to name a few and perhaps we can throw in the bugs we call probiotics because microbiome changes (Ref in Evernote I hope) are also noted in people with
CFs as compared to healthy controls and some have even suggested that feeding ourselves live bacteria is risk-taking behaviour when it is taking place in people who have dysfunctional immune systems (reference, I forgot). Others are explaining psychological
and neurological symptoms
 by the fact that evidence of many of these invaders including worms are being found in the brain and central nervous system. Similarly the heart and sexual organs.  These microinvaders are hiding in biofilm and plaques and they have been photographed under the microscope,
especially the spirochaetes (cork-screw-shaped bacteria)

J Clin Exp Med. 2009; 2(1): 1–16.
Published online 2009 Jan 15.
PMCID: PMC2680051
Chronic fatigue syndrome and mitochondrial dysfunction
Sarah Myhill, Norman E. Booth, and John McLaren-Howard.

Not finished

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