Dr. Sarah Myhill
<p>From: Dr Goode lecture transcription, and 'Diagnosis and Treatment of Chronic Fatigue Syndrome and Myalgic Encephalitis: It's Mitochondria, Not Hypochondria' This section to be updated</p>
<p>Thyroid and Adrenals</p>
<p>Many people specifically come to me because they want help with their
thyroid. The thyroid is a popular topic in the health world because
dysfunction in the thyroid is typically associated with weight gain (an
abnormal metabolism), body temperature dysregulation (including cold hands
or even hot flashes), a lack of energy, thinning hair, dry skin, and sleep
problems. Research is even linking thyroid problems with plaque
accumulation in the arteries.15</p>
<p>A leading thyroid doctor, Dr. Broada Barnes MD of the Broada Barnes
Institute, says that 90% of American men and women have subclinical
hypothyroid (symptomatic but undiagnosed). 80% of diagnosed thyroid
conditions are in women and 80% of that group have an autoimmune thyroid,
meaning that their immune system mistakenly attacks healthy tissue in an
attempt to protect itself from a perceived threat.16</p>
<p>According to the American Association of Clinical Endocrinologists (AACE),
27 million Americans suffer from a thyroid condition. Out of the 27
million, only half have been diagnosed. Therefore over 13 million people
are likely experiencing symptoms related to their dysfunctioning thyroid
but don’t know what is wrong. Being properly evaluated is essential because
it affects your quality of life and thyroid disease leaves you predisposed
to many other degenerative dysfunction. Look at these statistics:
• People with thyroid disease are twice as likely to have a blocked aorta
or experience a heart attack.</p>
<p>• 50% of all depression could be caused by an undiagnosed thyroid condition.</p>
<p>• Types of autoimmune diseases such as Hashimoto’s Disease can lead to
psychosis, seizures, dementia, and mood changes.</p>
<p>• People with thyroid disease often suffer from other hormone problems,
especially women during perimenopause and menopause.17</p>
<p>The thyroid impacts more than just your metabolism. Clinically, a low
functioning thyroid seems to be common in women who have fertility problems
or have suffered miscarriages. Increased thyroid activity is common when
the body releases progesterone (the hormone that prepares the uterus for
pregnancy).18 If the thyroid is malfunctioning before a pregnancy, the
change in activity after conception often exacerbates the situation. A low
functioning thyroid also causes intestinal motility to slow down.19 Thyroid
dysfunction can even negatively affect the liver’s ability to detoxify!20
It’s incredible how one small gland has such an impact on the entire body!
Interestingly enough, 80% of the Vitamin C your body stores is in the
adrenal glands!21 This is why I always recommend Vitamin C supplements in
an adrenal repair program.</p>
<p>Hypothyroid
Foods to avoid for hypothyroidism, Charanya Vijay Health & Lifestyle
Thursday, November 19, 2015
If you are hypothyroid, choosing the right food is essential to stay
healthy and undoubtedly there are certain foods to avoid for
hypothyroidism. . Hypothyroidism is known as under active thyroid, where
the thyroid gland is under producing the thyroid hormones which is not
sufficient for your body. Consuming some foods may not be friendly for
your thyroid gland and that may end up in further aggravating low thyroid.
Choosing the right food and eliminating the food which is not good for your
thyroid is significant for a wholesome well being. This article helps you
with a list of foods to avoid for hypothyroidism.
Soy
It is believed that soy can infringe your thyroid function and sometimes it
can also create trouble in absorption of thyroid hormones (pills) if
consumed within some hours of taking the pills. Avoiding or restraining soy
from your diet is extremely good for a healthy thyroid.
Broccoli, Brussels sprouts, cabbage, cauliflower, kale, turnips, raddish
and bok choy.:
These are called cruciferous vegetables that potentially interfere with
secretion of thyroid hormones. Having these foods may enlarge your thyroid
gland causing goiter. So it is better to completely get rid of these
veggies in your diet.
Wheat, barley, semolina, rye, malt & spelt
These are some of the foods that come with gluten content. Gluten
containing foods may be detrimental to your thyroid health and it is
considered as a key trigger for endocrine diseases. Go for a gluten-free
diet to guard your thyroid health.
Fatty foods
Consuming fatty foods can worsen your thyroid conditions as poly
unsaturated fat is linked with complication of the under active thyroid
gland. Butter, mayonnaise, margarine, and fatty cuts of meat, crackers,
cookies, cakes, pastries and French fries are some of the fatty foods that
not only affect thyroid but also can increase your cholesterol levels and
the risk of weight gain.
Sugary foods
Added sugar foods can disrupt with your thyroid functioning leading
difficulty in managing your weight, appetite and energy. Sugar, syrups,
sweeteners, soft drinks, candies, dry fruits, cookies, cakes, pies, jams,
sauces are some of the sugary foods to avoid for hypothyroidism.
Processed foods
Consumption of processed foods such as pasta, pizza, bread, cakes,
pretzels, cookies can be harmful for your thyroid gland as it contains high
carbohydrates, sugar and gluten.
Too much fiber
Excess fiber in your diet can impede with absorption difficulties if you
are in the hypothyroidism synthetic pills treatment. Though dietary fiber
is necessary, it is recommended to avoid too much fiber in your diet.
Caffeine
Extra dosage of caffeine intervenes with thyroid function and result in
enlarged thyroid gland. Having more cups of coffee can cause problem in
absorbing T4 hormones and affects the conversion of T4 to T3 hormones. It
is wise to avoid coffee, tea, chocolates and other caffeine based products
are the harmful foods to avoid for hypothyroidism.
Alcohol
Alcohol directly impacts the thyroid health thereby leading to lot of
negative effects to the thyroid gland. Say no to alcohol and adopt a
healthy lifestyle for an optimal thyroid health.
If chosen right, food can be your best medicine. Considering these
categories of foods to avoid for hypothyroidism can help you to prevent and
manage the condition.
Five steps to boosting your thyroid function almost immediately
Learn more:
http://www.naturalnews.com/037147_thyroid_function_boosting_remedies.html#ixzz3mfVArg8L</p>
<p>Best foods to eat to kick-start a sluggish thyroid
Learn more:
http://www.naturalnews.com/036632_thyroid_foods_remedies.html#ixzz3mfWAsg7o
many articles here
http://www.planbeforedo.com/search?updated-max=2015-11-11T23%3A27%3A00%2B05%3A30&max-results=6
Are all CFS patients low thyroid?
As explained in our previous articles, it is clear there is a distinct
hormonal disturbance in Chronic Fatigue Syndrome (CFS) patients, with a
general suppression of the hypothalamic – pituitary – adrenal axis (HPA
axis). It is the pituitary which is the “conductor of the endocrine
orchestra.†If the pituitary is malfunctioning like in CFS patients, then
this will affect the thyroid gland, adrenal gland, sex hormones, possibly
the pineal (produces melatonin for normal sleep), as well as hormones for
growth and urine production.
Symptoms Of An Underactive Thyroid
Hypothyroidism symptoms are very similar to the ones experienced by CFS
sufferers. Lethargy, sensitivity to cold, heat intolerance, mood swings and
depression, poor memory and concentration, joint pains and morning
stiffness, headaches, vertigo and deafness, pre-menstrual tension, voice
changes, loss of libido and susceptibility to viral infections are all
found with both conditions.
Visible signs experienced by hypothyroid sufferers are: weight gain, fluid
retention, puffy face, puffy eyes, hair loss (classically the outer third
of the eyebrows), cold extremities and dry skin, rashes, eczema and boils
and enlargement of the tongue. One may also suffer from hoarse voice,
hypoglycaemia, constipation, menstrual problems, skin problems and tendency
to infections, slow pulse, goitre, infertility, digestive problems, slowed
Achilles tendon reflex and carpal tunnel syndrome.
The Connection Between Chronic Fatigue Syndrome And Low Thyroid
Studies demonstrate that in addition to an increased incidence of primary
hypothyroidism in CFS, there is a combination of secondary, tertiary and
thyroid resistance in the overwhelming majority of CFS patients, despite
having normal thyroid tests. Why is this happening?
These latter forms of tissue hypothyroidism are not detected by standard
thyroid function tests. Thus, many CFS patients are erroneously told that
their thyroid levels are fine. In fact, standard thyroid tests fail to
detect tissue hypothyroidism 80-90% of the time in patients with CFS.
There are multiple abnormalities in CFS that result in undetectable tissue
hypothyroidism, such as :
* TSH is secreted by the pituitary and stimulates the thyroid to produce
T4, the non-active thyroid hormone. However, hypothalamic dysfunction
results in the production of TSH that has diminished biological activity so
there are lower T4 and T3 levels for any given level of TSH. T3 is the
active thyroid hormone. In addition, the pituitary dysfunction results in a
diminished secretion of TSH, masking low tissue thyroid levels as the TSH
is usually in the normal range. Very few doctors understand the
significance of this and incorrectly state that the thyroid is fine based
on a normal TSH level.
* diminished T4 to T3 conversion and a relatively increased T4 to reverse
T3 conversion result in low tissue levels of active thyroid hormone levels
despite having a normal TSH.
type II deiodinase that converts T4 to T3 is down regulated in CFS, while
the type III deiodinase enzyme that increases T4 to reverse T3 (rT3) is
unregulated in these conditions.
there has been shown to be a peripheral thyroid hormone resistance found
in these patients, meaning that there is a diminished thyroid effect for a
given amount of thyroid hormone in the blood.
As you see, the combination of factors present in CFS, including
hypothalamic and pituitary dysfunction, diminished T3/rT3 production ratios
and thyroid resistance, results in most, if not all, CFS patients having
inadequate tissue thyroid effect.
What Is An Adequate Treatment For Low Thyroid in CFS?
T4 preparations such as Synthroid and Levoxyl rarely work and Armour
thyroid, a pig glandular product, is somewhat better, but definitely not
adequate for most patients. The treating physician must know when to use a
T4/T3 combination or straight T3. T3 works the best for many of these
patients, but Cytomel, a very short acting T3 available at normal
pharmacies, is also a poor choice, because the varying blood levels can
cause significant side effects.
Compounded timed release T3 is usually the best treatment. However, to
achieve significant improvement, the treating physician must be very
knowledgeable about T3 and must realize that when on T3, standard blood
test will lead one to dose incorrectly and not obtain significant benefits.
This includes doctors who previously felt that they were thyroid experts
and had been using thyroid in CFS patients for a long time.
Ultimately, it is the expertise and dosing of the T3 or T4/T3 combinations
and the makeup of the medications that determines the optimal treatment
regimen and is one major component in the treatment of CFS. The experts at
Holtorf Medical Group can help with your CFS and thyroid treatment.
– Holtorf Medical Group
Resources: Are All Chronic Fatigue and Fibromyalgia Patients Low Thyroid?
Hypothyroidism – A Common Hormonal Problem in CFS
How to treat thyroid naturally, Charanya Vijay Health & Lifestyle
Tuesday, November 17, 2015
Once you become hypothyroid, you think of how to treat thyroid naturally.
Hypothyroidism is a state where in your thyroid hormones level is
significantly low and this deficiency obstructs your physical and mental
health. This post suggests some natural home remedies which will answer
your question how to treat thyroid naturally.
Coconut oil
People wonder how to treat thyroid naturally using coconut oil. You can use
coconut oil for cooking as it raises your metabolism and improves your
thyroid functioning. You can also add a spoon of virgin coconut oil to your
morning cup of milk or fry your eggs using it.
Ginger
Ginger has compounds that help in stimulating thyroid function. Ginger can
be simply peeled and chopped to add on to your dishes. It can be grounded
or can also be used in powder forms.
Pears and apples
Pears and apples contains nutrients that will balance your hormones and
nourish thyroid functioning. You can make a scrumptious fruit salad,
delicious juices or just eat it as whole fruit.
Eggs
Including one or two large eggs a day is good to regulate your thyroid
function as eggs contain three rich nutrients required for a healthy
thyroid namely tyrosine, iodine and selenium.
Avocados
Avocados are good sources of copper, iron, selenium and also contain
essential fatty acids that help your thyroid to function better. You can
add some avocados to your salad or make a flavorsome smoothie.
Kelp
Kelp is seaweed rich in iodine, potassium, magnesium, calcium and iron and
also contains abundant vitamins. Adding it in to your diet promotes a
healthy thyroid functioning. But doctors recommend to 158 to 175 micro
grams of kelp a day and not more than that.
Fish oil
Fish oil comes with essential fatty acids and intake of fish oil boosts the
thyroid function. Recommended dosage is not more than 3-4 grams.
Apple cider Vinegar
Apple cider vinegar helps to detox your body and stimulates the thyroid
function. You can add few drops of apple cider vinegar in your diet regime
or mix 2 spoons of it in warm water along with some honey for taste.
Carrot juice
A glass of carrot juice a day perks up your thyroid function as it is the
rich source of Vitamin A.
Mushroom
Mushroom is loaded with essential nutrients that benefit your thyroid
gland. It also promotes your immune functions and just taking 3 mushrooms
can get you a daily requirement.
Now you are very much apparent about how to treat thyroid naturally and
these home remedies are so easy and you can simply include in your everyday
food regime.
Common hormonal disturbances in CFS – hormones are the controllers - in
this case the accelerator pedal and the gearbox!
It is now quite clear there is a distinct hormonal disturbance in CFSs with
a general suppression of the hypothalamic-pituitary-adrenal axis. It is the
hypothalamus-pituitary which is the “conductor of the endocrine orchestraâ€.
If the pituitary is malfunctioning then this has knock on effects for the
thyroid gland, adrenal gland, sex hormones, growth hormone and possibly the
pineal (produces melatonin for normal sleep).
In practice I invariably measure thyroid hormones (TSH, T4 and T3), often
prescribe melatonin and often check adrenal function. I very rarely use sex
hormones. Many CFSs are substantially improved by correcting thyroid
hormones and I insist all my CFS patients get fully tested. A useful book
on the subject is The Thyroid Solution by Prof Ridha Arem ISBN
0-345-42920-6.
Underactive thyroid gland
Low levels of thyroid hormones in the blood means the “accelerator pedalâ€
is set slow so the body will go slow. This can be underactive for three
reasons – either the gland itself has failed (primary thyroid failure), or
the pituitary gland which drives the thyroid gland into action is
under-functioning (secondary hypothyroidism), or there is failure to
convert inactive hormone T4 to active T3. The symptoms of these three
problems are the same.
In primary thyroid failure, the blood tests show high levels of thyroid
stimulating hormone (TSH) and low levels of T4 and T3.
In pituitary failure, the blood tests show low levels of TSH, T4 and T3. In
conversion problem, TSH and T4 may be normal, but T3 is low.
There is another problem too which is that the so-called “normal range†of
T4 is probably set too low and TSH set too high. I know this because many
patients with low normal T4 often improve substantially when they are
started on thyroid supplements. Indeed Dr Skinner, who is a consultant
virologist at Birmingham, has shown how many patients with CFS have low
normal levels of thyroxine (T4) and do well when their levels are increased
to average levels. The laboratory I use has a normal range of 12-22 pmol/l
and I am finding many levels coming back at 9-14. In these patients there
is an indication for trying T4, especially if symptoms suggest this.
Furthermore the normal range for TSH is set too high. In UK the normal
range is up to 4.4mIU/l and often higher. In America anyone with a TSH
above 3.0 is now started on thyroid hormones – this is because a high TSH
is a risk factor for arterial disease.
Symptoms and signs of an underactive thyroid
Chronic fatigue syndrome may be a symptom of hypothyroidism – that’s why
all sufferers need their thyroid checking!
Other symptoms: weight gain, lethargy, sensitivity to cold, heat
intolerance, fluid retention, mood swings and depression, poor memory and
concentration, hair loss, joint pains and morning stiffness, skin problems
and tendency to infections, headaches, vertigo and deafness,
hypoglycaemia, constipation, menstrual problems, pre-menstrual tension,
digestive problems, infertility and loss of libido.
Signs: puffy face, puffy eyes, hair loss (classically the outer third of
the eyebrows), cold extremities and dry skin, rashes, eczema and boils,
enlargement of the tongue, hoarse voice, soft pulse or bradycardia, goitre,
slowed Achilles tendon reflex. Further useful information is the basal body
temperature. Use a mercury thermometer to take the temperature in the
armpit over 10 minutes immediately on wakening. Temperatures consistently
below 97.8°F (36.6°C) indicates slow metabolic rate, which may be due to
hypothyroidism.
Treatment of an underactive thyroid
This depends on the bloods tests and the clinical symptoms.
If the T4 is low and T3 commensurate with a low T4 - I would start with
thyroxine 50mcgms (25mcgms for a small person or child or someone very
debilitated) and increase in 25mcgms increments every month up to 100mcgms
(or 75 mcgms in a small person or child or debilitated person) at which
point the blood needs retesting. The aim is to get into the middle or upper
half of the “normal†range. If I had a patient who was very small or very
debilitated I might even start with 12.5mcgms.
If the T3 is low, and T4 normal, then I would use generic thyroid, which is
a physiological mix of T4 and T3. I would start with ½ grain daily for one
month, then ½ grain twice daily for one month, then 1 grain plus ½ grain
daily for the third month at which point the blood need retesting. Take the
second dose not later than 4pm or it may interfere with sleep. Some people
like to take the second dose at lunch time to get an afternoon boost.
If the dose of thyroid was too high, then side effects would develop -
hotness and sweating, fine tremor and palpitations. In this event, stop the
thyroid supplement immediately. Taking additional thyroid will clearly make
this situation worse. If in doubt, please phone in. Some of my patients do
seem to get the symptoms of over-activity despite the blood levels being
normal. This may be due to receptor hypersensitivity. In this event cut the
tablet into smaller doses and build up slowly.
Thyroxine is only available on prescription and I am able to supply if your
GP is not happy to prescribe. However I do insist on the patient being seen
by a doctor to ensure there are no signs or symptoms of thyrotoxicosis and
obviously I need to write to the GP to tell them what I am prescribing.
Once stabilised I like to check levels once a year. Obviously, your GP
needs to be informed.
If you are taking thyroid supplements at any time, it is always possible
that you could become thyrotoxic – not through any fault of the tablet but
because the thyroid gland suddenly decides to. This is unusual! If you
suspect this because you develop symptoms of toxicosis such as hotness and
sweating, anxiety, fine tremor, palpitations and possibly sleeplessness,
then stop the thyroid supplement immediately and get your levels rechecked.
Treatment with thyroid hormones is nearly always for life.
For more information see: “Understanding thyroid disorders†by Dr Anthony
Toft; ISBN: 1 903474 19 1, available from http://www.familydoctor.co.uk/
Also see my information handout THYROID – THE CORRECT PRESCRIBING OF
THYROID HORMONES – AND WHY THIS IS NOT HAPPENING IN THE UK
Underactive Adrenal Gland (DHEA and cortisol) – the gear box of the car
The adrenal gland is responsible for the body’s hormonal response to
stress. It produces adrenaline, which stimulates the instant stress hormone
response (fight or flight reaction). It also produces cortisol and DHEA,
which create the short and long term stress hormone responses. Cortisol
suppresses the immune system, breaks down tissues and has a generally
catabolic effect. However, these effects are balanced out by DHEA, which
has the opposite effect – activating the immune system and building up
tissues. All these hormones are made from cholesterol – just one reason why
running a low cholesterol is not necessarily a good thing! The sequence or
events is as follows:
Cholesterol
¯
pregnenolone ® progesterone ® cortisol
¯ ¯
DHEA ® androstenedione ® testosterone</p>
<p>¯ ¯
Oestrone ® Oestrodiol</p>
<p>Both cortisol and DHEA are essential for life – too little cortisol causes
the life threatening disease Addison’s disease, too much causes the
debilitating condition Cushing’s syndrome. Then name of the game is to get
the right balance. To achieve this both hormones must be measured. This can
be done with the adrenal stress index (ASI) test. By measuring and
supplementing within the physiological range, with biologically identical
hormones, one is not going to get any unpleasant side effects i.e. we are
trying to copy Nature and restore normality.
The ASI test looks at cortisol and DHEA levels over 24 hours. This test
entails taking salivary samples through the day (yippee, no needles!).
Indeed, salivary sampling is felt to be the most accurate way of assessing
steroid hormone levels.
An abnormal result may be a symptom of other problems or it may cause
problems in its own right. The response of the body to stress (any stress –
infectious, nutritional, emotional, physical etc) is to increase the output
of stress hormones. This gears the body up for action by raising blood
pressure, increasing heart rate, improving mental alertness (which can
cause anxiety), increasing energy supply and so on. It is actually
metabolically very inefficient because it uses up lots of energy, but
totally desirable if one has to fight for one’s life! This reaction is
essential for short term stress, but unsustainable long term. So time for
rest and recovery is equally essential.
Problems arise when the stress is unremitting because eventually the output
of the adrenal gland will reduce making one far less able to tolerate
stress. Indeed this is often a complaint of my CFS patients – they simply
do not tolerate stress at all well.
The pattern of the result from the adrenal stress test gives some idea
where one is along the stress response time line.
A typical CFS adrenal stress profile test result showing low levels of
cortisol and DHEA.</p>
<p>chart
Interpretation of the Adrenal Stress Index test for DHEA and cortisol
levels
Levels of DHEA and cortisol vary according to the level of stress and for
how long that stress has been applied. Increasing cortisol production is
the normal response to stress and is highly desirable, so long as the
stress is removed and the adrenal glands can recover. On-going, unremitting
stress means the adrenal gland and the whole body is in a constant state of
alert, does not get time to recover and eventually packs up. So, there are
several stages of adrenal function gradually leading to failure:
1. Normal levels of cortisol and DHEA. Normal result. Normal adrenal gland
2. Raised cortisol, normal DHEA. This indicates a normal short term
response to stress.
3. Raised cortisol and raised DHEA. The adrenal gland is functioning
normally but the patient is chronically stressed. So long as the stress is
removed, the adrenal gland will recover completely.
4. High levels of cortisol, low levels of DHEA. The body cannot make enough
DHEA to balance cortisol. This is the first sign of adrenal exhaustion.
This is the first abnormal response to chronic stress. The patient needs a
long break from whatever that chronic stress may be – the commonest chronic
stress is HYPOGLYCAEMIA, but also consider insomnia, mental, physical or
emotional overload or whatever. DHEA can be supplemented to make the
patient feel better, but it must be part of a package of recovery without
which worsening can be expected.
5. Cortisol levels low, DHEA levels low. The gland is so exhausted it can’t
make cortisol or DHEA. By this time patients are usually severely fatigued.
6. Cortisol levels low, DHEA borderline or normal. This probably represents
the gland beginning to recover after a long rest. DHEA may be used to help
patients feel better whilst they continue their programme of rest and
rehabilitation.</p>
<p>In Addison’s disease there is complete failure of the adrenal gland not
because of chronic stress but because of autoimmunity. This too is a life
threatening disorder and the patient is severely ill. The main clinical
symptom is severe postural hypotension and chronic hypoglycaemia. Addison’s
disease is tested for by a short synacthen test in which cortisol levels
are measured before and after an adrenal gland stimulant ACTH. Many
patients with CFS are given this test, which is found to be normal
resulting in the patient being told their adrenal gland is fine and no
action is required. The problem with this test is it only shows where the
adrenal gland is completely non-functioning, it does not diagnose partial
adrenal failure or adrenal stress and no measurements of DHEA are made.
This makes it potentially misleading.</p>
<p>Treatment
The idea with treatment with cortisol and DHEA is to stay within
physiological ranges. By doing this there are no side effects in the short
or long term. Many doctors and patients recoil at the prospect of taking
steroid hormones. Remember all the side effects of steroid hormones are
created by the dose. Using physiological as opposed to pharmacological
doses avoids all these problems.
A normal adrenal gland produces about 10-50mgs of DHEA daily and 20-25mgs
of hydrocortisone daily. Steroid side effects would appear after a few
weeks of 100mgs a day or a few months at 50mgs a day.</p>
<p>DHEA is available over the counter in the USA, where the FDA has classified
it as a food supplement up to a daily dose of 25mgs. It is also available
from www.pharmwest.co.uk. It is better absorbed taken sublingually – ie
allow it to dissolve in the mouth. I start my patients on 12.5mgs for small
people and 25mg for larger people of DHEA a day taken in the morning. I
like to recheck a single DHEA after 3 months to make sure I am staying
within physiological ranges and because a few patients need 50mg.</p>
<p>Cortisol again needs to be used in sub-physiological doses – ie. up to, but
not more than 10mgs a day. (Please note that the usual steroid most often
used is prednisolone. 5mgs of prednisolone is equivalent to 20mgs of
hydrocortisone). Both these are prescription only drugs.
After 3 – 6 months if the patient wishes to continue taking DHEA then
levels need to be re-checked by doing a single sample salivary DHEA (you
can order this test from my website – “DHEA (saliva) singleâ€. Cortisol
levels replete reliably well and it is not necessary to recheck levels.</p>
<p>As the patient improves, usually hydrocortisone can be stopped typically
after 1-2 years. I suspect DHEA is an acquired metabolic dyslexia – that is
to say as we age we get less good at making it. Young people can often stop
DHEA as they improve and maintain levels, but older people often benefit
from taking DHEA long term.</p>
<p>A New Hydrocortisone Trial
Another randomised, controlled, crossover trial of low-dose hydrocortisone
treatment for CFS has recently been published. 32 participants, fulfilling
both the Oxford and CDC 1994 criteria, completed this short-term trial.
Participants received 5mg or 10mg of hydrocortisone for 28 days and placebo
for 28 days.
The results revealed modest, statistically significant improvements in
fatigue with this low-dose hydrocortisone treatment compared with placebo.
The degree of disability was also reduced with hydrocortisone treatment but
not with placebo. There was no significant difference in changes in fatigue
score when 5mg and 10mg doses were compared. The authors suggest that, in
view of the lack of dose response in this study, 5mg is a sufficient low
dose of hydrocortisone.
Participants who responded to this hydrocortisone treatment did not differ
from ‘non-responders’ in terms of their pre-treatment cortisol levels.
Although none of the participants in this study had a current psychiatric
illness, those who responded to hydrocortisone treatment had fewer
psychiatric symptoms prior to treatment.
Based on the results of the insulin stress test, this short-term, low dose
hydrocortisone treatment was not found to cause significant suppression of
adrenal gland function. None of the participants dropped out of the study
and only minor side effects were reported.
The authors conclude that this low-dose hydrocortisone treatment resulted
in “significant reduction in self-rated fatigue and disability in patients
with chronic fatigue syndromeâ€.</p>
<p>Comment
This study sheds interesting light on the possible role of low cortisol
levels in the disease processes involved in CFS. Caution is required,
however, in interpreting the results. Participants’ baseline cortisol
levels could not predict their response to hydrocortisone treatment and
participants appeared to have baseline cortisol levels within the normal
reference range.
In another randomised controlled trial of hydrocortisone therapy ( see
Interaction 29, page 21 for a review), McKenzie at al., used a higher
‘low-dose’ hydrocortisone treatment of 25 - 35mg daily. They found that
this dose was associated with some improvements in symptoms but caused
significant adrenal suppression. Neither of these research teams currently
recommended the use of hydrocortone as a treatment for CFS. The present
study assessed the effects of hydrocortisone treatment in the short-term
only. As the authors point out, further studies, involving longer durations
of treatment and follow-up are required to assess the long-term
effectiveness and safety of this treatment.
Reference: Cleare et al; The Lancet, 1999, Vol. 353 February 6, p455-458
Also see: THE ROLE OF HUMAN GROWTH HORMONE (HGH) AND SECRETOGOGUES TO
IMPROVE PITUITARY FUNCTION</p>
<p>6g) Improper Functioning of Thyroid and Adrenal Glands and/or Sluggish
Metabolism
Iodine levels, thyroid, adrenals and other glands and hormone levels
Fluoridated water could be attacking your thyroid
Lack of iodine
Radiation from Fukishima
Japan herbivore men low drive, estrogen n disruptors
Hormones
It is possible I have 'burned out' my adrenal and/or other glands.
Article on Thyroid and Sluggish Metabolism
http://www.besthealthnutritionals.com/blog/category/thyroid-2/</p>
<p>M.A.T. Is Just 5.4% Of Your Bodyweight, But Burns More Than 50% Of ALL Your
Daily Calories!
Are You IGF-1 Deficient? IGF-1 RESETS YOUR BIOLOGICAL CLOCK
Researchers recently “re-discovered†how to stimulate this natural compound
found inside all humans.</p>
<p>It suffocates fat cells, and triggers a whole-body calorie burn like
nothing seen before.
This enhanced calorie burn shifts your key organs into a higher gear:
-Your brain process information faster, remembers better and focuses
longer...
-Your heart pumps more blood, carrying precious nutrients to starving
cells...
-Your lungs process more oxygen, enhancing your energy levels...
-Your bones, ligaments and cartilage strengthen, allowing you to move
more freely...
-Your aging skin rejuvenates while saggy muscle tones and tightens...
-Plus, your metabolism accelerates as your thyroid produces more
fat-burning hormones...</p>
<p>Everything just works better. And you look and feel 10 years younger.
However, Its Metabolic Power is Silenced in Most of Us...
By the time you’re 40, levels of this compound have dropped 25%... and a
full 56% by your 60s.</p>
<p>Plus, studies show that environmental toxins, our inactive lifestyle, and
certain foods act like metabolic vampires, sucking the life out of this
powerful compound.
That’s unfortunate because studies also show that low levels of this
compound not only block calorie burning, but also increase your risk for
heart attack, stroke, Alzheimer’s and diabetes.
How to Unleash Its Power Inside You...Now, researches have worked out how
you can boost levels of this calorie-burning compound naturally.</p>
<p>A very specific combination of foods, eaten at the right times, commands
your body to produce more. Surprisingly, some of these foods are the very
foods you’ve been told to stay away from.</p>
<p>Prescription medications for hypothyroidism are very common in the United
States. According to the American Association of Clinical Endocrinologists
studies have shown that as many as 10 percent of women and 3 percent of men
have hypothyroidism (low thyroid activity). The thyroid gland is located at
the base of your neck below your Adam’s apple. It secretes thyroid hormones
that have pronounced effects on the cells of your body.</p>
<p>The two main thyroid hormones include T3 (liothyronine) and T4 (
L-thyroxine). Another thyroid hormone known as thyroid stimulating hormone
(TSH) regulates the secretion of T3 and T4. This hormone is secreted by the
pituitary gland when it senses blood levels of thyroid hormones are getting
low. It also receives messages from the brain (hypothalamus) that
influences TSH secretion. When the hypothalamus senses blood levels of
thyroid hormones it signals the pituitary gland to release more TSH. It is
secreted by the pituitary and then signals the thyroid gland to release
more of T4 and T3 hormone.</p>
<p>Thyroid hormones control the metabolic activity in every cell. This is
important for temperature control, weight regulation, heart rate, and
energy production. Thyroid activity even influences one’s mood and
neurotransmitter balance and affects the balance of other hormones in the
body. Hypothyroidism occurs when the thyroid gland is under active. This
leads to a shortage of thyroid hormones. The most common cause is a disease
known asHashimoto’s thyroiditis.This is an autoimmune condition where the
body’s immune system produces antibodies to the thyroid gland. This attack
on the thyroid gland leads to the suppression of thyroid hormone production
and secretion. Other reasons for hypothyroidism may include iodine and
other nutritional deficiencies, stress, pregnancy, medications such as
lithium or estrogen therapy, and an under functioning pituitary gland.</p>
<p>Hypothyroidism is most common in middle-aged and older women. It can occur
at any age though, including infants and teenager. Untreated hypothyroidism
can be life threatening.</p>
<p>Thyroid damage caused by fluoride in the water
Posted by: Dr. Mark Stengler on March 10, 2015
Thyroid destroying toxin dumped into your drinking water</p>
<p>Reach a certain age, and it hits you like an oncoming train. You’re drained
of energy… flabby around the middle… and sadder than a country song about a
girl who left you and took your dog.</p>
<p>Complain to a mainstream doc, and he’ll say you’re just getting older. But
I know the REAL reason, and it’s got nothing to do with your age.</p>
<p>It’s your thyroid — the “master gland†in charge of energy, metabolism and
your overall wellbeing. And right now, it’s coming under constant attack
from a toxic metal in your own home.</p>
<p>Most American communities deliberately pollute their water with fluoride,
and you don’t have to be a card-carrying conspiracy theorist to believe
it’s wrecking your body from the inside.</p>
<p>Read more…
Categories: Thyroid.
---------
Metformin linked to thyroid dysfunction
Posted by: Dr. Mark Stengler on October 16, 2014</p>
<p>Risky diabetes drug does a number on your thyroid
You don’t have to be a diabetic to get a prescription for the diabetes drug
metformin.
These days, docs are passing out this bad-news drug like candy on
Halloween. Pre-diabetic? Docs claim it can prevent full-blown diabetes (it
can’t).</p>
<p>Heart disease? Some docs say it can protect your ticker (it won’t).
Read more…
Categories: House Calls, Thyroid.
Boost energy and focus and lose weight with Thyroid Performance Plus
Posted by: Dr. Mark Stengler on October 3, 2014
--------
Feeling fat and sluggish? Here’s why
It happens to the best of us. You’re chugging along full of zip, sharp as a
tack and lean as a rail when suddenly — out of nowhere — the tables turn.
You’re left feeling tubby, a bit fuzzy, and ready to hit the hay by 8:00…
and you have no idea why.
If you go to see your doc he’s likely to tell you this is to be expected,
that we all slow down as we age. But the truth is for many of us who find
ourselves suddenly feeling sluggish and fat there’s a lot more to it than
that. There’s a REASON we feel this way.
Read more…
Categories: Energy, House Calls, Thyroid.
----------
Sluggish Thyroid? Take These 4 Steps and Improve Your Thyroid Function Today
Posted by: Allison Davis on August 12, 2014
If you’re suffering from a sluggish thyroid, you probably want to improve
your thyroid function — so you can have more energy and avoid feeling tired
all the time. And because you strive for overall health, you want to do so
naturally, without turning to chemicals that may do more harm than good.
That’s why Dr. Mark Stengler created Thyroid Performance Plus, your latest
weapon against feeling fat, sluggish, and unmotivated.
Read more…
Categories: Adrenal, Energy, Herbs and Supplements, Thyroid.
----------
Thyroid Performance Plus Reviews – Real Information You’re Looking For
Posted by: Allison Davis on July 30, 2014
Thyroid Performance Plus energy supportYou’re feeling fat and sluggish and
you are over it!
So you’re looking for Thyroid Performance Plus reviews to hear from other
people who wanted more from life, in order to find out if Thyroid
Performance Plus really worked for them.</p>
<p>You want more energy that keeps you more active. You want to feel better
and you want it fast. That’s exactly what the people who wrote in with
these Thyroid Performance Plus reviews were looking for, too – and they
found it!
Read more…
Categories: Energy, Herbs and Supplements, Thyroid.</p>
<p>From phoenixrising user Ian H: <a href="http://forums.prohealth.com/forums/index.php?threads/recently-started-a-new-regimen-for-cfs-iodine-making-me-feel-awful-i-have-questions.265339/">http://forums.prohealth.com/forums/index.php?threads/recently-started-a-new-regimen-for-cfs-iodine-making-me-feel-awful-i-have-questions.265339/</a></p>
<p>Firstly the regime is a reasonable one at face value.
the iodine is not essential so drop it for now and see how you go.
You have not stated any doses. Doses are important for some of the items. Can you list your doses please?
You are basically missing the methylation support items (which also support mitochondrial function):
folate as in MTHF (methyltetrahydrofolic acid)
a sulphur containing antioxidant (glutathione substrates) such as NAC (N-acetyl cysteine) or S-adenosyl methionine or glutathione sublingual
These two (folate and glu substrates) are more important than the D-ribose or the niacin, however D-ribose and niacin are not unimportant.
I have noticed before that Sarah Myhill misses folate and glutathione substrates but they are important.
Why are you taking magnesium by spray? Is it a transdermal spray because if it is these are not very effective at delivering the required magnesium. Also if you can afford it Magnesium Threonate is by far the best form.
You are also missing vitamin K2 complex. <strong>Very</strong> important to go along with your vitamin D.
You are also missing zinc which is critical in immune system modulation and again goes with the vitamin D. Also taking magnesium without zinc is not advisable for too long and this is a long term regime.
Lastly, it is critical to reduce sugar intake. I don't know what your sugar intake is like but normally I would assess sugar intake. the less sugar you take in the better. It is also important not to replace sugar with sugar substitutes because most of them induce some pro inflammatory markers and alter gut balance.
*
From : 'HIP's Overview of Dr. Myhill's ATP Work in Chronic Fatigue Syndrome (ME/CFS)' <a href="https://www.healthrising.org/forums/resources/hips-overview-of-dr-myhills-atp-work-in-chronic-fatigue-syndrome-me-cfs.390/">https://www.healthrising.org/forums/resources/hips-overview-of-dr-myhills-atp-work-in-chronic-fatigue-syndrome-me-cfs.390/</a>
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<div>Metabolomics<em> studies providing evidence of severe energy depletion and mitochondrial dysfunction in chronic fatigue syndrome (ME/CFS)</em></div>
<strong> The ME/CFS Energy Metabolism Studies of Dr. Sarah Myhill et al.</strong>
With recent metabolomic studies from <a class="externalLink" href="http://forums.phoenixrising.me/index.php?threads/new-mella-talk-exciting-reveals.47329/" target="blank"><strong>Fluge and Mella</strong></a> as well as <a class="externalLink" href="http://www.openmedicinefoundation.org/2016/09/09/updated-metabolic-features-of-chronic-fatigue-syndrome-q-a-with-robert-naviaux-md/" target="blank"><strong>Robert Naviaux et al</strong></a> finding defects in the energy metabolism of ME/CFS patients, perhaps now we should more closely examine the three very incisive studies of <strong>Dr Sarah Myhill</strong>, <strong>Norman E. Booth</strong> and <strong>John McLaren-Howard</strong>(published in <a class="externalLink" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2680051/" target="blank"><strong>2009</strong></a>, <a class="externalLink" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3403556/" target="blank"><strong>2012</strong></a> and <a class="externalLink" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3515971/" target="blank"><strong>2013</strong></a>) on the dysfunctional energy metabolism of ME/CFS.
<a class="externalLink" href="http://www.drmyhill.co.uk/" target="blank"><strong>Dr. Sarah Myhill</strong></a> is a GP with a lot of research interest and expertise in treating ME/CFS. <a class="externalLink" href="https://www.researchgate.net/profile/Norman_Booth" target="blank"><strong>Norman E. Booth</strong></a> is a physicist and molecular biologist. <a class="externalLink" href="http://www.neurolipid.org/who-we-are/medical-advisory-board/dr-john-mclaren-howard-phd/" target="blank"><strong>John McLaren-Howard</strong></a> is cofounder of Biolab Medical Unit, and medical director of Acumen Labs, UK.
<strong>Summary Points</strong>
• The experimental results of these studies <strong>strongly implicate mitochondrial dysfunction as an intermediate cause of ME/CFS</strong> symptoms (by "intermediate," I think the authors mean not the primary cause of ME/CFS, which may for example be viral and/or autoimmune, but an intermediate pathophysiology that is induced by the primary cause).
• The studies used the "<a class="externalLink" href="http://www.drmyhill.co.uk/wiki/Mitochondrial_Function_Profile" target="blank"><strong>ATP Profiles</strong></a>" test (Acumen Laboratory, UK) to measure the <strong>efficiency of five metabolic pathways</strong> involved in energy production. The "ATP Profiles" test provides five numerical figures that indicate the functional efficiency of each of the five energy pathways.
Using this "ATP Profiles" test in their studies, the authors found that almost <strong>all ME/CFS patients in their cohorts had defective energy production</strong> (the studies examined ~200 ME/CFS patients). However, out of the five metabolic pathways, each patient had their own particular pathways that were at fault (ie, running at low efficiency), and their own particular pathways that were working fine (running at normal efficiency). So all patients had defective energy production, but there were patient subsets according to which particular energy metabolism pathways were dysfunctional.
• Because the studies discovered that defects in energy metabolism are not found in just in one pathway, but found in up to five different pathways, the authors combined the individual efficiency figures for each of the five pathways into one single efficiency figure, which they call the <strong>Mitochondrial Energy Score</strong> (MES). The MES is thus a single numerical value that gives the overall efficiency of a patient's energy production.
• The authors found there is a high degree of correlation between the Mitochondrial Energy Score and the degree of severity of ME/CFS (severity as measured on the <a class="externalLink" href="http://drmyhill.co.uk/wiki/CFS_Ability_Scale-a_rough_measure_of_how_disabled_you_are" target="blank"><strong>Bell scale</strong></a>).
• Furthermore, the Mitochondrial Energy Score value was able to successfully <strong>distinguish between ME/CFS patients and healthy controls</strong> in nearly all cases. So the Mitochondrial Energy Score could be a good potential biomarker for ME/CFS (although the authors do not claim a low MES is unique to ME/CFS, because there are other neurological illnesses and metabolic syndromes which are also associated with mitochondrial dysfunction).
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• The authors do not mention this in their studies, but other research I came across indicates that defects in two energy metabolism pathways at fault in ME/CFS (namely the two translocator protein pathways) may be caused by an <strong>autoantibody</strong> that targets and disables <strong>translocator protein</strong>. This translocator protein autoantibody appears to be triggered by coxsackievirus B, as the autoantibody has been found in CVB myocarditis. As far as I can see, this virally-associated autoantibody may well in part explain how viral infection causes ME/CFS.
• Most impressively, the authors pinpoint what may be the physiological mechanism behind <strong>post-exertional malaise</strong> (PEM). Briefly, they suggest PEM occurs when adenosine triphosphate (ATP) molecules, whose role it is to convey energy, inadvertently in effect get flushed out of the body in the urine, via a particular set of metabolic circumstances; this results in a temporary shortage of ATP molecules, and a temporary inability to transport energy in the cell — a situation which they posit causes PEM. Full explanation coming up next.
<strong>Sarah Myhill et al's Theory of PEM</strong>
Rather than jumping straight into the 5 energy pathways that were found at fault in ME/CFS, we are going to start with Myhill et al's biochemical explanation of how PEM arises, as this is quite easy to understand, and makes a nice introduction the studies.
So we begin with the studies' findings that ME/CFS involves a poor, low-efficiency energy metabolism. There are knock-on effects arising from this poor energy metabolism — knock-on effects that occur in periods of exertion when the energy demands of the body are high, and the blocked energy metabolism is thus overtaxed and put under stress. Dr Myhill explains:
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<div class="quote">Problems arise when the system is stressed. If the CFS sufferer asks for energy faster than he can supply it (and actually most CFS sufferers are doing this most of the time!), ATP is converted to ADP faster than it can be recycled.
This means there is a build up of ADP. Some ADP is inevitably shunted into adenosine monophosphate (AMP). But this creates a real problem, indeed a metabolic disaster, because AMP, largely speaking, cannot be recycled and is lost in urine.
Indeed this is the biological basis of poor stamina. One can only go at the rate at which mitochondria can produce ATP. If mitochondria go slow, stamina is poor.
If ATP levels drop as a result of leakage of AMP, <strong>the body then has to make brand new ATP</strong>. ATP can be made very quickly from a sugar D-ribose, but D-ribose is only slowly made from glucose (via the pentose phosphate shunt for those clever biochemists out there!). This takes anything from one to four days. <strong>So this is the biological basis for delayed fatigue</strong>.
Source: <a class="externalLink" href="http://www.drmyhill.co.uk/wiki/CFS-The_Central_Cause:Mitochondrial_Failure" target="blank"><strong>CFS - The Central Cause: Mitochondrial Failure</strong></a></div>
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In other words, Dr Myhill is saying that delayed fatigue and presumably post-exertional malaise arise when some of the ADP molecules, which are normally very quickly recycled back to ATP, instead get converted to ATP in a desperate attempt to harvest energy; and because ATP is not easily recycled, this ATP is flushed right out of the body, thereby causing a permanent loss of the ADP molecules that the ATM was derived from.
So then you get an acute shortage of ADP molecules, which is a major problem, because ATP/ADP recycling is the main basis of the body's energy creation and distributing system, responsible for carrying more than 90% of our cellular energy.
As a consequence of this shortage, more of these ATP/ADP molecules then have to be manufactured by the body from scratch, to replace the lost ATP/ADP molecules. And efficient energy distribution can only be resumed once these lost molecules are manufactured. But it takes 1 to 4 days for the body to rebuild its stock of ATP/ADP molecules, as it takes a lot longer to rebuild the ATP molecule from scratch (this called <a class="externalLink" href="https://en.wikipedia.org/wiki/De_novo_synthesis" target="_blank"><strong>de novo synthesis</strong></a>), rather than simply making ATP by recycling ADP molecules.
Dr Myhill et al. think this 1 to 4 days of novo synthesis of ATP may explain the PEM period: you get PEM and delayed fatigue for several days after physical exertion, as your body struggles to rebuild its stock of ATP and ADP molecules.
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Note: to be clear, when Dr. Myhill is referring to a shortage of ATP/ADP molecules during the PEM period, this not so much a shortage of energy itself (although energy supply may also be poor), but rather an acute shortage of the ATP/ADP molecules that carry and convey the energy generated in the mitochondria.
This is analogous to saying there is not so much a shortage of electricity, but rather a shortage of rechargeable batteries for storing and carrying that electricity to where it is needed. The ATP/ADP molecules are analogous to a rechargeable battery: ATP is like a fully charged battery, and ADP likes an empty battery. ADP can be quickly recharged back to ATP at any time, using energy from the mitochondria.
Dr. Myhill is saying that PEM results when the body inadvertently dumps many of its ATP/ADP rechargeable batteries, and so then the body has too few batteries to distribute the energy made by the mitochondria. You only get over the PEM period when your body makes more rechargeable batteries (makes more ATP/ADP molecules).
So this is a compelling theory of how PEM arises (and I believe it is the first theory proposed to explain the mystery of PEM and delayed fatigue).
I was thinking that Dr. Myhill's ATP/ADP molecule restocking theory of PEM suggests that <strong>D-ribosesupplementation</strong> <em>specifically during the PEM period </em>might help mitigate PEM, since Myhill points out that the ATP molecule is easily synthesized from D-ribose (by de novo synthesis). So taking D-ribose specifically during PEM may help you to more quickly rebuild your stock of ATP molecules.
Dr. Myhill then goes on to explain how in ME/CFS high levels of <strong>lactic acid</strong> arise during physical exertion, as a direct result of this ATP molecule shortage:
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<div class="quote">However there is another problem. If the body is very short of ATP, it can make a very small amount of ATP directly from glucose by converting it into lactic acid.
This is exactly what many CFS sufferers do and indeed we know that CFS sufferers readily switch into anaerobic metabolism. However this results in two serious problems — lactic acid quickly builds up especially in muscles to cause pain, heaviness, aching and soreness ("lactic acid burn"), secondly no glucose is available in order to make D-ribose! So new ATP cannot be easily made when you are really run down. Recovery takes days!
When mitochondria function well, as the person rests following exertion, lactic acid is quickly converted back to glucose (via-pyruvate) and the lactic burn disappears. But this is an energy requiring process! Glucose to lactic acid produces two molecules of ATP for the body to use, but the reverse process requires six molecules of ATP. If there is no ATP available, and this is of course what happens as mitochondria fail, then the lactic acid may persist for many minutes, or indeed hours causing great pain. (for the biochemists, this reverse process takes place in the liver and is called the Cori cycle).
Source: <a class="externalLink" href="http://www.drmyhill.co.uk/wiki/CFS-The_Central_Cause:Mitochondrial_Failure" target="blank"><strong>CFS - The Central Cause: Mitochondrial Failure</strong></a></div>
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So Myhill et al. are saying that as a consequence of this shortage of ATP/ADP molecules (the rechargeable batteries), the body desperately tries to manufacture new ATP molecules (make more rechargeable batteries) by any route it can. One route is to manufacture ATP via the conversion of glucose to lactic acid (<a class="externalLink" href="http://www.hussmanfitness.org/html/TLEnergySystems.html" target="blank"><strong>anaerobic glycolysis</strong></a>), which takes place in the cell cytosol rather than the mitochondria. But by making ATP in this way, you get a build up of lactic acid.
So this would explain why ME/CFS patients generate far higher levels of lactic acid during physical exertion: it's the result of the desperate attempt to make more ATP, which the body needs in order to convey the energy generated by the mitochondria.
This lactic acid build-up then further compounds the energy shortage problem of PEM, because clearing lactic acid by converting it back to glucose, requires considerably more energy than was originally gained from the conversion of glucose to lactic acid. (Glucose to lactic acid yields two molecules of ATP for the body to use, but the reverse process uses up six molecules of ATP).
Obtaining energy by the conversion of glucose to lactic acid is an act of desperation by the body: it's like being desperate for money and going to a loan shark, only to find that you have to pay back a lot more than you were originally lent.
So Myhill et al. are theorizing that the production of lactic acid further contributes to the energy shortage issue that we know as PEM.
Incidentally, the idea that lactic acid build up further exacerbates PEM in this way nicely ties up with the fact that nearly all the <a class="externalLink" href="http://forums.phoenixrising.me/index.php?threads/acetyl-l-glutathione-atp-baking-soda-sam-e-catalase-no-pem-after-exercise.34446/#post-536633" target="blank"><strong>"PEM Buster" supplements</strong></a>(which members of this forum have found significantly mitigate PEM) appear to reduce lactic acid. This seems to support the idea that lactic acid build up is part of the problem in PEM.
In summary: Myhill et al are theorizing that PEM may be due to an acute shortage of ATP/ADP molecules (which were dumped out of the body in the urine through the AMP route), which is then further compounded by the body desperately lending energy from the lactic acid loan shark.
So a combination of D-ribose (to help restock the body with ATP molecules) plus some of these PEM Buster supplements (to neutralize lactic acid) might work for combating PEM.
<strong>The Dysfunctional Energy Metabolism at the Root of ME/CFS</strong>
Let's now delve into the five energy pathways whose efficiencies are measured by the "ATP Profiles" test, and which were found to be poorly functioning in ME/CFS.
These five energy metabolism pathways are as follows:
<strong>(1) ATP Concentration = the quantity of ATP present in the cell </strong>
This one is very straightforward: ATP is created in the mitochondria (recycled from ADP), and created in the cell cytosol via glycolysis. This ATP then supplies energy to the cell. Mitochondria supply around 90% of the cells ATP energy needs; whereas glycolysis only supplies around 10%.
The ATP Concentration measured in the "ATP Profiles" test is simply the total amount of ATP molecules present in the cell.
<strong>(2) ATP Ratio = the fraction of ATP in the cell that is complexed with magnesium </strong>
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The majority of ATP molecules present in cells are bonded onto magnesium ions, to create a complex known as Mg-ATP. This bonding to magnesium is necessary in order for ATP to yield its energy; ATP molecules that are not bound to magnesium are not able to liberate the energy they carry. Thus an important factor in energy metabolism efficiency is the percentage of ATP in the cell that is bonded to magnesium, as only this percentage can supply energy. This percentage is given by the ATP Ratio. The ATP Ratio is also an indication of the amount of magnesium in the cell.
<a class="externalLink" href="https://www.ncbi.nlm.nih.gov/pubmed/1672392" target="blank"><strong>One study</strong></a> found ME/CFS patients have low levels of intracellular magnesium, which may cause a shortage of magnesium for ATP to bond to, and thereby reduce the amount of ATP in the cell available to supply energy.
I wonder if this may in part explain why magnesium injections or high dose transdermal magnesium cream has been found helpful in ME/CFS. Presumably, though, such magnesium treatment might only be useful for ME/CFS patients who have a poor ATP Ratio, as measured by the "ATP Profiles" test.
Note that if you are going to try magnesium injections or high dose transdermal magnesium cream, it might be an idea to also take cofactors that promote the absorption of magnesium into cells, such as: vitamin B6 and vitamin B1 (see <a class="externalLink" href="http://forums.phoenixrising.me/index.php?threads/cofactors-for-magnesium-absorption-into-cells.26885/#post-410700" target="blank"><strong>this</strong></a> and subsequent posts).
<strong>(3) Oxidative phosphorylation = efficiency of oxidative phosphorylation </strong>
Oxidative phosphorylation is the mitochondrial process by which ADP is recycled back to ATP. This recycling is achieved by adding phosphate to the adenosine diphosphate (ADP) molecule, which has two phosphates, to convert it to adenosine triphosphate (ATP), which has three phosphates.
Myhill et al found that around half the ME/CFS patients in their studies had oxidative phosphorylation running normally (these they labeled Group A patients), but the other half of patients had their oxidative phosphorylation partially blocked and running at low efficiency (these they labeled Group B patients).
In ME/CFS patients whose oxidative phosphorylation is running normally (Group A), they found cellular metabolism uses increased glycolysis to partially compensate for the overall energy metabolism dysfunction.
Whereas for patients whose oxidative phosphorylation was partially blocked (Group B), these patients use an alternative route to increased glycolysis, most likely the adenylate kinase reaction in which two molecules of ADP combine to make one of ATP and one of AMP. This creation of AMP is the same process detailed earlier, in which exertion led to the loss of ATP/ADP molecules via dumping AMP in the urine, thereby creating PEM. Ref: <a class="externalLink" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3515971/" target="blank"><strong>Myhill 2013</strong></a>.
In <a class="externalLink" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3403556/" target="blank"><strong>Myhill 2012</strong></a> the authors state:
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<div class="quote">This division into 2 distinct groups, A and B, appears to correlate with the 2 groups observed in some exercise studies.
Recycling by Group A patients of the lactate generated by glycolysis into glucose and glycogen takes place on a shorter time scale, but Group A patients will suffer from increased acidosis due to build-up of H+ ions from ATP hydrolysis which are not recycled by the ETC, and will also exhibit excess lactate in the blood.
Group A patients will have large PCr [creatine phosphate] depletion, excess lactate production and high acidosis (depressed pH). Group B patients will have low PCr depletion (the shuttle is not needed for the ADK reaction), no excess lactate production and less acidosis for the same work load.
For repeat exercise tests patients of Group B will have great difficulty in reaching the same maximal voluntary contraction not because of the behavioral reason of exercise avoidance, but because the lost substrate has not been replaced. These predictions are close to what is observed in this recent exercise study [<a class="externalLink" href="https://www.ncbi.nlm.nih.gov/pubmed/21749371/" target="_blank"><strong>23</strong></a>].</div>
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Note that <strong>co-enzyme Q10</strong> is a vital factor in oxidative phosphorylation, and deficiency in Q10 may cause oxidative phosphorylation to go slow.
<strong>(4) Translocator Protein Out = efficiency of ADP transport out from the cell </strong>
One job of translocator protein, which is located on the mitochondrial membrane, is to transport ADP in the cell across the mitochondrial membrane, and into the mitochondrion, for recycling back to ATP.
<strong>(5) Translocator Protein In = efficiency of ATP transport into the cell </strong>
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The other job of translocator protein is to transport the energy-carrying ATP molecules created in the mitochondria (from recycled ADP) across the mitochondrial membrane and into the cell, where their energy is used for cellular functioning. The efficiency of this ATP transport process across the mitochondrial membrane is another important factor in the efficiency mitochondrial energy production.
Dr. Myhill says that translocator protein could be malfunctioning as a result of xenobiotic stress (e.g. organochlorine or organophosphate pesticide exposure), poor antioxidants status (lipid peroxides), and various other factors. See: <a class="externalLink" href="http://drmyhill.co.uk/wiki/Translocator_protein_studies" target="blank"><strong>Translocator protein studies - DoctorMyhill</strong></a> for a list of factors that can disrupt translocator protein.
Out of the five energy metabolism pathways, Translocator Protein In (TL IN) is unusual, as in some ME/CFS patients its efficiency is actually <em>higher</em> than it is for all of the control group. Thus some ME/CFS patients appear to be transporting super-normal amounts of ATP from their mitochondria into the cell cytosol. In <a class="externalLink" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3403556/" target="blank"><strong>Myhill 2012</strong></a> they say that these super-normal values of TL IN are:
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<div class="quote">most likely due to below normal ATP levels in the mitochondria due to shortage of substrate, either the well-known substrates of the Krebs cycle or those of the ETC, principally ADP and inorganic phosphate, Pi, but also the essential co-factors CoQ10, reduced Niacinamide (NADH) and Mg.Note</div>
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that the Krebs cycle substrates are: succinate, glutamate, malate, pyruvate and fatty acids.
In <a class="externalLink" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3403556/" target="_blank"><strong>Myhill 2012</strong></a> they state:
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<div class="quote">Clearly, <strong>the partial blocking of the TL sites is a very important aspect of the mitochondrial dysfunction</strong> and this has not been considered in any other study.
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One of us (JMH) is making further studies of TL function and has found chemical blocking in those cases with subnormal values. Possible sources of blocking agents are byproducts of viral or bacterial pathogens, cellular debris due to oxidative damage, and some environmental chemicals. Results from molecular level fluorescence microscopy, and the identification of the blocking agents by Micro Raman Spectroscopy and Fourier Transform Infrared Spectroscopy, will be the subject of a further paper.</div>
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<strong>Viruses, Autoimmunity and the Translocator Protein</strong>
I came across a very interesting <strong>connection between coxsackievirus B, autoimmunity and translocator protein</strong>: <a class="externalLink" href="https://www.ncbi.nlm.nih.gov/pubmed/8974071" target="_blank"><strong>this study</strong></a> found autoantibodies that target and disable translocator protein in patients with myocarditis and dilated cardiomyopathy (DCM), which they then reproduced in a murine model infected with coxsackievirus B3. This seems very significant, because the chronic infections in coxsackievirus B myocarditis and dilated cardiomyopathy are very similar to the chronic coxsackievirus B infections of ME/CFS. The study authors said:
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<div class="quote">We were able to identify autoantibodies against the adenine nucleotide translocator [another name for translocator protein] in the sera of patients suffering from myocarditis and DCM .... These antibodies show cross-reactivity to the VP protein of Coxsackie B3 virus known to induce myocarditis in humans and animals.So</div>
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they are proposing a molecular mimicry-type autoimmunity, where antibodies that target the virus VP protein also, unfortunately, target the translocator protein — thus in fighting the virus, the immune system antibodies inadvertently attack the crucial translocator protein on mitochondria. And indeed, it is known that energy metabolism in myocarditis and dilated cardiomyopathy is running at low efficiency, due to translocator protein dysfunction. The same autoimmune-mediated disruptions to translocator protein could thus also be happening in ME/CFS.
As long ago as 1985, ME/CFS researchers <a class="externalLink" href="https://www.ncbi.nlm.nih.gov/pubmed/2993423" target="_blank"><strong>Behan et al</strong></a> thought something like may be the case in ME/CFS, when they suggested that:
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<div class="quote">an autoantibody, such as the anti-mitochondrial antibody recently identified in patients with viral myocarditis, might be involvedAnti-mitochondrial</div>
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autoantibodies of various sorts have been found in a number of diseases, including lupus, Sjögren’s, myocarditis, cardiomyopathy, tuberculosis and leprosy. See: <a class="externalLink" href="https://en.wikipedia.org/wiki/Anti-mitochondrial_antibody" target="_blank"><strong>Anti-mitochondrial antibody - Wikipedia</strong></a>.
If ME/CFS does indeed involve an energy metabolism dysfunction caused by mitochondrial autoantibodies, and if those autoantibodies do indeed derive from an autoimmune state triggered by viral infection, that would neatly tie together and explain three known features of ME/CFS pathophysiology:
<ol>
<li>the fact that ME/CFS is associated with infection from certain viruses, particularly coxsackievirus B;</li>
<li>the fact that ME/CFS likely involves autoimmunity,</li>
<li>the fact that energy metabolism appears to be dysfunctional in ME/CFS. <strong>A coxsackievirus B-triggered translocator protein autoantibody could explain all these features</strong>.</li>
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In terms of treatment possibilities, it occurred to me that since translocator protein autoantibodies need to cross the cellular membrane in order to get into the cell and disable the translocator protein, any supplements or drugs that can modify the cellular membrane or its receptors in a way that inhibits the ferrying of antibodies across the cell membrane may have the potential to treat ME/CFS, because this would block the ill effects of these translocator protein autoantibodies.
Perhaps that could be one reason why supplements like fish oil (especially high EPA fish oil such as VegEPA®) which affect cellular membranes benefit some ME/CFS patients.
<strong>Study Results: Defects in 5 Energy Metabolism Pathways in ME/CFS</strong>
For the 71 ME/CFS patients in the <a class="externalLink" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2680051/" target="blank"><strong>Myhill 2009</strong></a> study, <a class="externalLink" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2680051/figure/fig02/" target="blank"><strong>figure 2</strong></a> below shows how their five metabolic energy pathways (labeled A to E) were functioning in terms of efficiency, as determined by the "ATP Profiles" test.
If you glance at the second column, you can see that the blue bars, which represent ME/CFS patients' energy pathway efficiencies, are generally lower down (= less efficient) on the vertical axis of energy efficiency, compared to the gray bars in the third column, which represent the energy pathway efficiencies of the healthy controls.
This shows that these 5 energy pathways in ME/CFS patients are generally functioning at a reduced output compared to healthy people. Similar low energy pathway efficiencies were found in the 138 ME/CFS patients of the <a class="externalLink" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3403556/" target="blank"><strong>Myhill 2012</strong></a> study.
<strong>The Five Energy Pathway Efficiencies of ME/CFS Patients and Health Controls</strong>
<img src="/fb3251d6-d077-592b-8483-151dd2d94deb.png" />
<a class="externalLink" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2680051/figure/fig02/" target="blank"><strong>Figure 2</strong></a> from Myhill 2009
<strong>The Mitochondrial Energy Score (MES)</strong>
As the above figure 2 shows, defects in ME/CFS patients' energy metabolism are found not just in one area, but in up to five different energy pathways. So in the study, the authors combined the efficiency figures for each of the five energy pathways into one overall efficiency figure, called the Mitochondrial Energy Score (MES). The Mitochondrial Energy Score thus provides a single numerical value that indicates the overall efficiency of energy production.
In the <a class="externalLink" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2680051/" target="blank"><strong>Myhill 2009</strong></a> study, in <a class="externalLink" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2680051/figure/fig04/" target="blank"><strong>figure 4a</strong></a> shown below, they plot a graph of the Mitochondrial Energy Score against the severity of ME/CFS, as measured by the <a class="externalLink" href="http://drmyhill.co.uk/wiki/CFS_Ability_Scale-a_rough_measure_of_how_disabled_you_are" target="blank"><strong>Bell scale</strong></a>.
<strong>Mitochondrial Energy Score vs ME/CFS Severity</strong>
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<a class="externalLink" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2680051/figure/fig04/" target="blank"><strong>Figure 4a</strong></a> from Myhiil 2009
It is immediately apparent from this graph that the Mitochondrial Energy Score clearly separates ME/CFS patients from healthy controls in almost all cases; and furthermore, that the MES strongly correlates with the severity of ME/CFS.
<strong>Some References and Further Reading</strong>
<strong>Sarah Myhill, Norman E. Booth and John McLaren-Howard's three studies on mitochondrial failure in ME/CFS</strong>:
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<li><a class="externalLink" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2680051/" target="_blank">Chronic fatigue syndrome and mitochondrial dysfunction</a> (2009)</li>
<li><a class="externalLink" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3403556/" target="_blank">Mitochondrial dysfunction and the pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)</a> (2012)</li>
<li><a class="externalLink" href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3515971/" target="_blank">Targeting mitochondrial dysfunction in the treatment of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) - a clinical audit</a> (2013)</li>
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<strong>Dr. Myhill's book (2014)</strong>:
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<li><a class="externalLink" href="https://www.amazon.co.uk/Diagnosis-Treatment-Chronic-Fatigue-Syndrome/dp/1781610347" target="_blank">Diagnosis and Treatment of Chronic Fatigue Syndrome: Mitochondria, Not Hypochondria (Diagnosing & Treating)</a></li>
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<strong>A summary of Myhill et al's energy metabolism defect research can be found on Dr. Myhill's website</strong>:
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<li><a class="externalLink" href="http://www.drmyhill.co.uk/wiki/CFS-The_Central_Cause:Mitochondrial_Failure" target="blank">CFS - The Central Cause: Mitochondrial Failure</a></li>
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<strong>A Dr Myhill video explaining the mitochondrial dysfunctions in ME/CFS, and detailing the "ATP Profiles" test</strong>:
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<li><a class="externalLink" href="https://www.youtube.com/watch?v=BG_v6-U1a8g" target="_blank">Clinical management of chronic fatigue syndrome (CFS/ME) by Dr. Sarah Myhill</a></li>
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An example of the results of the "ATP profiles" test can be seen in <a class="externalLink" href="http://forums.phoenixrising.me/index.php?threads/mitochondrial-function-profile-acumen-laboratories-biolab-via-dr-myhill.13921/" target="blank"><strong>this post</strong></a>, from a forum member who took this test.
A summary of Myhill, Booth and McLaren-Howard's mitochondrial dysfunction ME/CFS research, testing and treatment can be found on <a class="externalLink" href="http://www.me-ireland.com/diag/10.htm" target="blank">www.me-ireland.com</a>.[/fright]</blockquote>
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