The Connection Between
Mitochondria and Autoimmune Disease
I
wrote about the connection between mitochondrial issues and autoimmune
dysfunction in the new book, “The Periodic Paralysis Guide And Workbook: Be All
You Can Be Naturally.” I did not go into the research and the information that
led me to my findings. Although I had written about this for the members in our
PPNI Support Group, I felt it was important to add that information to our blog
for others to read about and understand.
I am now posting what I wrote last year.
November 3, 2013
Yesterday
I spent a great deal of time researching the connections between Periodic
Paralysis and lactic acidosis. I did this because of several reasons, but
mostly due to the results of a set of tests done a few years ago, that no
doctor seems to know what it means or what to do about it.
I
posted these a few weeks ago but I am posting it again in order to further
explain what I discovered yesterday which may be a major break through for us
all !
The
following is the results of the Amino Acid Plasma Quantitative Test :
Aspartic
Acid (<2, 0-6) and 3 Methylhistidine (<;6, 0-64) were low and Proline
Plasma (501, 110-360), Alanine Plasma (744, 230-510), Valine (331, 150-310)
Plasma, Tyrosine Plasma (107, 45-74), Homcysteine Plasma (11.9, 4.0-12.0), and
Pyruvic Acid (0.146, 0.030-0.107) were all high. Lactic Acid was high also
(1.8, .5-1.6)
"The
high Alanine Plasma indicates: Primary or Secondary Lactic Acidosis or
Hyperammonemic Syndrome. Clinical findings may be episodic. Further workup may
be warranted."
"Hyperprolinemia
is consistent with Mitochondrial Dysfunction or may indicate Type 1 or Type 2
Hyperprolinemia. Further analysis may be warranted."
"Recommend
measurement of blood lactate and repeat of the Plasma Amino Acid
Analysis."
These
test results indicate "primary or secondary lactic acidosis" and
Mitochondrial Dysfunction.
My
real eye opener came when I read this:
"Metabolic
dysregulation can also cause mitochondrial dysfunction. Vitamins, minerals, and
other metabolites act as necessary co-factors..." So, wanting to understand how I
could have Periodic Paralysis, over 10 autoimmune condition diagnoses AND
Mitochondrial Dysfunction, I set out to find some answers. The discovery I made
was unbelievable. Karen Carr has mentioned mitochondrial issues on this board
for as long as I can remember. I have read through the complicated articles,
etc. and I never quite understood the connection. I will try to put this in an
easy to understand format, though it may be a little difficult to follow.
First
of all...a biology lesson: There are many mitochondria in a cell. Mitochondria
can became damaged for many reasons and then mutate or change. When this
happens we can then have "Mitochondrial Dysfunction", leading to
things such as lactic acidosis.
There
are of course, Mitochondrial Disorders that can be present at birth also which
I knew. I had no idea that we can "develop" them.
“…..for
the synthesis and function of mitochondrial enzymes and other compounds that
support mitochondrial function (see Table 4 ), and diets deficient in
micronutrients can accelerate mitochondrial decay and contribute to
neurodegeneration (Ames, 2004)"
However,
since symptoms vary from case to case, age of onset, and rate of progression,
mitochondrial dysfunction can be difficult to diagnose when it first appears.
According to Cohen, who wrote a July 2001 article in the Cleveland Clinic
Journal of Medicine, “The early phase can be mild and may not resemble any
known mitochondrial disease. In addition, symptoms such as fatigue, muscle
pain, shortness of breath, and abdominal pain can easily be mistaken for
collagen vascular disease, chronic fatigue syndrome, fibromyalgia, or
psychosomatic illness”
http://www.nbihealth.com/publications/Mitochondrial_dysfunction.pdf
Periodic
Paralysis is a 4th Class Metabolic Dysregulation (Disorder)!!!!!! Periodic
Paralysis can cause Mitochondrial Dysfunction!!!!!!!!! Obviously the potassium
shifting can cause the damage to the mitochondria in the cells!!!!!! We already
know there seems to be an issue with autoimmune issues....Here is the
connection!!!!
"…diets
deficient in micronutrients can accelerate mitochondrial decay"
THIS
IS WHY THE BALANCED DIET IS SO IMPORTANT TO US AND WE SEE DIFFERENCES WHEN WE
CUT OUT THE JUNK AND ADD SUPPLEMENTS!!!!!!!
"…symptoms
such as fatigue, muscle pain, shortness of breath, and abdominal pain can
easily be mistaken for collagen vascular disease, chronic fatigue syndrome,
fibromyalgia, or psychosomatic illness”
(MUSCLE PAIN, SHORTNESS OF BREATH, FIBROMYALGIA, CONVERSION
DISORDER??????)
"Mitochondrial
dysfunction is at the core of a surprising range of very common illnesses and
conditions...Even autoimmune diseases such as multiple sclerosis, Sjogrens
syndrome, lupus and rheumatoid arthritis appear to have a mitochondrial basis
to illness.
Mitochondrial
dysfunction has been associated with a wide range of solid tumors, proposed to
be central to the aging process, and found to be a common factor in the
toxicity of a variety of physical and chemical agents."
http://www.umdf.org/site/pp.aspx?c=8qKOJ0MvF7LUG&b=7934637
"EVEN
AUTOIMMUNE DISEASES"!!!!!!!!!!!!!
"…toxicity
of a variety of physical and chemical agents" (The ISSUES WE HAVE WITH ALLERGIES AND PROBLEMS WITH
MEDICATIONS????)
Table
1
Signs,
symptoms, and diseases associated with mitochondrial dysfunction
(Cohen
and Gold, 2001)
Organ system: Possible symptom or disease
Muscles: Hypotonia, weakness, cramping, muscle pain,
ptosis,
opthalmoplegia
Brain: Developmental delay, mental retardation, autism, dementia, seizures,
neuropsychiatric disturbances, atypical cerebral palsy, atypical migraines,
stroke, and stroke-like events
Nerves: Neuropathic pain and weakness (which may be intermittent), acute and
chronic inflammatory demyelinating polyneuropathy,
absent deep tendon reflexes, neuropathic
gastrointestinal problems (gastroesophageal reflux, constipation,
bowel pseudoobstruction), fainting, absent or
excessive sweating, aberrant temperature regulation
Kidneys: Proximal renal tubular dysfunction (Fanconi syndrome); possible loss
of protein (amino acids), magnesium, phosphorus, calcium, and other
electrolytes
Heart: Cardiac conduction defects {(electrical system)} (heart blocks),
cardiomyopathy
Liver: Hypoglycemia, gluconeogenic defects, nonalcoholic
liver
failure
Eyes: Optic neuropathy and retinitis pigmentosa
Ears: Sensorineural hearing loss, aminoglycoside sensitivity
Pancreas: Diabetes and exocrine pancreatic failure
Systemic:
Failure to gain weight, short stature, fatigue, and respiratory problems
including intermittent air hunger
http://www.nbihealth.com/publications/Mitochondrial_dysfunction.pdf
"Exercise
intolerance is a well recognized clinical feature of mitochondrial respiratory
chain defects due to pathogenic mutations of mitochondrial or nuclear DNA.
Severely impaired muscle oxidative phosphorylation results in disabling
exercise limitations in which trivial exertion produces muscle fatigue and
lactic acidosis. In such patients, low levels of exercise cause prominent
tachycardia and dyspnoea (shortness of breath) due to increases in cardiac
output and ventilation that exceed the capacity of skeletal muscle to utilize
the increase in oxygen delivery mediated by these physiological responses"
".....results
in disabling exercise limitations in which trivial exertion produces muscle
fatigue and LACTIC ACIDOSIS."
EXERCISE
INTOLERANCE and LACTIC ACIDOSIS!!!!! from the Mitochondrial Dysfunction!!!!!
"Oxygen utilization and
Lactic Acidosis”
“Latic
acidosis has often been used as an indicator of impaired oxidative metabolism
and as a clinical marker for mitochondrial disorders…elevated lactate values at
rest strengthen the possibility of a mitochondrial disorder."
http://ghr.nlm.nih.gov/mitochondrial-dna
LACTIC
ACIDOSIS a cause of low oxygen levels.....
"In
such patients, low levels of exercise cause prominent tachycardia and dyspnoea
(shortness of breath) due to increases in cardiac output and ventilation that
exceed the capacity of skeletal muscle to utilize the increase in oxygen
delivery mediated by these physiological responses"...........
So...could
this be abortive attacks or what we may be mistaking for PP episodes in normal
ranges or it just happens and we wonder why...we cannot figure out a
trigger????? We take potassium when we do not need to and it causes side
effects, hyperkalemia???
"In
conclusion, this study reveals a wide spectrum of oxidative limitations and
exercise capacities........It illuminates the relationship between severity of
muscle oxidative defects and symptoms of exercise intolerance in MM patients.
Furthermore, it provides insight into the regulatory mechanisms responsible for
characteristic physiological responses to exercise in these patients,"
http://ghr.nlm.nih.gov/mitochondrial-dna
"oxidative
limitations" problems with oxygen...fluctuating oxygen levels....going
down upon exertion.......
Most
of the body's cells contain thousands of mitochondria, each with one or more
copies of mitochondrial DNA. These cells can have a mix of mitochondria
containing mutated and unmutated DNA (heteroplasmy). The severity of many
mitochondrial disorders is thought to be associated with the percentage of
mitochondria with a particular genetic change.
http://ghr.nlm.nih.gov/mitochondrial-dna
So
there may be varying degrees and severity among us and I suspect that, of
course, as we age the symptoms worsen such as the permanent muscle weakness,
breathing issues, etc....Thus the importance of stopping the attacks with diet,
avoiding triggers, etc as soon as possible when we are young...hopefully
avoiding the damage to the mitochondria over a long period of time.....
MY
THEORY: Periodic Paralysis, a mineral metabolic disorder, can cause damage to
the mitochondria in the cells due to the atypical shifting of potassium. This
damage to the DNA of the mitochondria, in turn contributes to the development
of autoimmune disorders.
The
longer a person with Periodic Paralysis goes with out a diagnosis and without
proper treatment and continual atypical potassium shifting, the more chance
there is for damage to the mitochondria, which then creates autoimmune diseases.
Periodic
Paralysis is difficult to diagnose. Mitochondrial dysfunction is difficult to
diagnose. Symptoms of both appear similar to "conversion
disorders". More time passes.
Autoimmune diseases develop further clouding the picture of the basic
disease...Periodic Paralysis. Damage is irreversible and becomes progressive
causing permanent muscle weakness, oxygen issues, cardiac issues...etc.
November 5, 2013
Good Morning Everyone!
This is about Exercise Intolerance......
When I wrote about my discovery yesterday, I forgot
to mention how our exercise intolerance may play into this. So, today I will
discuss that connection with:
"MY THEORY: Periodic Paralysis, a mineral
metabolic disorder, can cause damage to the mitochondria in the cells due to
the atypical shifting of potassium. This damage to the DNA of the mitochondria,
in turn contributes to the development of autoimmune disorders."
This is based on the fact that metabolic disorders and
other issues can cause damage to the mitochondria in cells (probably due to the
atypical shifting of potassium). The DNA of the mitochondria gets damaged.
Damaged mitochondria then may begin to develop autoimmune disorders. This is
all factual except what is in the parentheses...I am not sure of the process
for the damage.
This is all related to how the complicated oxygen cycle
works in our cells and bodies. That being said, this is the part forgot:
"Exercise intolerance is a well recognized
clinical feature of mitochondrial respiratory chain defects due to pathogenic
mutations of mitochondrial or nuclear DNA. Severely impaired muscle oxidative
phosphorylation results in disabling exercise limitations in which trivial
exertion produces muscle fatigue and lactic acidosis. In such patients, low
levels of exercise cause prominent tachycardia and dyspnoea due to increases in
cardiac output and ventilation that exceed the capacity of skeletal muscle to
utilize the increase in oxygen delivery mediated by these physiological
responses (Haller and Bertocci, 1994). "
This says that exercise intolerance is related to
mutations of the mitochondria. The oxygen cycle does not work properly and then
we are unable to do anything in which we must exert ourselves, even the
smallest amount of exertion causes muscle weakness and lactic acidosis and then
tachycardia and shortness of breath set in. This is because the heart must work
harder to try to keep up with a lack of oxygen the muscles are receiving and
(our body is not expelling the carbon dioxide as it should).
"......in patients .......peak oxygen uptake and
mitochondrial capacity for oxidative phosphorylation decreased in proportion to
increasing mutation load in muscle. "
"This study is the first to relate the severity of
the skeletal muscle oxidative defect to the severity of mismatch between the
exercise increase in cardiac output and oxygen uptake."
As we exert ourselves and need more oxygen, we do not
get it. The more exertion, the less amount of oxygen.
"This study demonstrates for the first time that
exaggerated ventilation relative to oxygen utilization ........ is related to
the degree of oxidative impairment. Hyperventilation was more pronounced in
patients with more severe oxidative defects, consistent with symptoms of
exertional dyspnoea experienced by many patients. The mechanism underlying this
hyperventilatory exercise response may relate to excess carbon dioxide
production due to lactate buffering, as suggested by the finding of a
correspondingly exaggerated respiratory exchange ratio..."
http://brain.oxfordjournals.org/content/126/2/413.long
The more we exert ourselves the more carbon dioxide
builds up.
This may be the reason for our exercise intolerance.
This may be why also, when you go to the doctor and
they take your blood oxygen level with the finger oximeter it is just fine,
because you are sitting and have been for awhile, but you know you are having
problems with your breathing, etc they do not think you need oxygen. They need
to test you with an overnight or 24 hour recording oximeter. It should show
oxygen level decreases during exercise and episodes of paralysis, etc....any
exertion.
I am on oxygen 24/7 because my oxygen drops any time I
exert myself, even talking on the telephone, going to the bathroom, etc at the
same time, my heart rate increases and breathing gets difficult. This is
happening even with my oxygen. I can only imagine how bad it would be without
my oxygen.
Before I was on it, I could not even sit up to a meal
at the table. It was too much exertion. Even now, sitting up straight for any
length of time is too taxing...why I have a reclining feature on my power
wheelchair.
I hope this information is helpful to you. It explains
a lot of what we are all experiencing everyday and not fully understanding it
or how it relates to Periodic Paralysis.
I do not know if anyone has put this together like this. I did it quite
accidentally. It does seem to make sense. I forgot to mention that the lactic
acidosis thing is also something that would be intermittent and may not show up
on tests each time. It also needs to be tested using a very rare test: Amino
Acid Plasma Quantitative Test it is only interpreted at a few places in the
country. One is: Duke Children's Hospital and Health Center in North Carolina
A thought.....If our body is in stress from the lack of appropriate
oxygen to the muscles and build up of lactic acidosis and carbon
dioxide...would the STRESS be the CAUSE of the paralysis from exercise or
exertion and why it happens after we begin to rest after our running around,
walking, shopping, cooking dinner, doing dishes, etc?? As we begin to rest,
the adrenaline will be released from the stress?? The adrenaline causes
paralysis for most of us.
Until later...
