Hypothyroidism Misdiagnosed as Depression
So we have an interesting
medical conundrum, do we not? On one hand, doctors are more than eager to
prescribe antidepressants at the drop of a hat, based entirely on the patients
reported symptoms. No need for any blood tests, and no evidence that they work
for the vast majority of people. --Dr. Malcom Kendrick
Here is an imagined, but
not far off the truth, conversation between a doctor and a patient.
‘Why can’t I have T3 doctor? I
feel so much better when I do?’
‘Because I say so, now go
away.’
Nowadays doctors, at least
when they are in training, are repeatedly told that they must NEVER be
paternalistic. To do so will result in immediate censure. In the UK it is also
a very rapid way of failing the GP entrance exams. We are told that we must
explore the patients’ expectations, listen to their worries and fears, and work
with them in partnership to lead to a therapeutic partnership…. or some such
left wing bollocks. [Joke]
How exactly that fits
within the National Institute of Health and Care Excellence (NICE) guidelines
is up for grabs. For those who don’t know, NICE decide on which drugs and
interventions can be prescribed, or paid for, within the NHS. So you can
explore expectations with your patient till the cows come home, only to find
that you cannot prescribe what the patient wants, even requires. Even if it
makes them feel much better and costs very little. Would you call this
paternalism? Oxford entrance exam, discuss.
Don’t get me wrong, I think
rationing is increasingly vital for healthcare provision, and at one point I
supported NICE. I now realise how naïve and misguided I was…but that is a
discussion for another day.
Where was I? Oh yes, T3.
Most people have never heard of it. But I am willing to bet that if youhave heard of it, and you are a patient, you will
certainly know all about this particular hormone. You will definitely know
about a thousand times as much as your GP, who may nod sagely when you mention
T3. But frankly they are unlikely to have any idea what it is, or does.
To be honest, until about a
year ago I had no real idea what T3 was either, but I have learned quite a lot
since. Wikipedia states that: ‘The thyroid hormones,
triiodothyronine (T3) and its prohormone, thyroxine (T4), are tyrosine-based
hormones produced by the thyroid gland that are primarily responsible for
regulation of metabolism.’ I would like to draw your attention to
the fact that, in Wikipedia, at least, T3 is mentioned before T4 – which makes
it more important?
In reality, in a physiological
sense at least, T4 comes before T3, in that T4 is produced almost exclusively
by the thyroid gland in a ratio of about 17:1 T4 to T3. Once inside various
tissues and organs T4 is then converted to T3, where it becomes the
biologically active hormone.
Whichever does come first,
it can be argued that T3 that is the key thyroid hormone, because T4 is
basically a ‘prohormone.’ From Wikipedia again: ‘A prohormone refers to a
committed precursor of a hormone, usually having minimal hormonal effect by itself.
The term has been used in medical science since the middle of the 20th century.
Though not hormones themselves, prohormones amplify the effects of existing
hormones.’ Although the figures are not absolutely clear cut,
it is usually stated that T3 is five times more biologically active than T4.
Therefore, if someone is
hypothyroid, which is normally taken to mean that the thyroid gland is not
producing a sufficient quantity of thyroid hormone, you would want to prescribe
the active hormone T3, would you not?
This is a rather rhetorical
question because what doctors do, at least since the 1960s, is to prescribe
synthetic T4 (levothyroxine). Once T4 is in the body it is converted to T3
(through the kidneys, liver, spleen and brain – and numerous other thyroid
hormone receptors throughout the body) and does its thing. In most cases this
is a perfectly good treatment. However, there is a kicker, which I will get to.
At this point I feel I need
to add that hypothyroidism is a very, very common condition. By the age of 60,
10% of people have ‘lab’ test abnormalities that would define them as
having subclinical hypothyroidism. At least 2% of the population has overt,
clinical, symptoms. Which means that we are talking about millions of people in
the UK, possibly tens of millions in the EU and US.[It affects women ten times
as much as men].
TSH
I now need to bring in
another player called Thyroid Stimulating Hormone (TSH). As with all systems in
the human body, a negative feedback loop controls the function of the thyroid
gland, and it works something like this:
If you have a high T4
level, this is detected by the pituitary gland, which sits deep within your
brain. At which point the pituitary gland reduces the production of Thyroid
Stimulating Hormone. As TSH is the hormone that instructs the thyroid gland to
produce T4/T3, production of T4/T3 falls. [There are actually a couple of other
steps, but this is essentially what happens].
If T4 falls too far, the
pituitary gland swings into action to produce more TSH. In turn stimulating the
thyroid gland to manufacture more T4…and so it goes. Up and down, up and down,
up and down. Endlessly until, of course, you get too old and drop dead. And
there ain’t no feedback loop for that.
TSH is also important in
that it is usually the substance you measure to decide whether or not someone
is hypothyroid. If TSH is very high this means it is trying to ‘drive’ the
thyroid gland into action – and failing. You also use the TSH level to
determine the dose of T4 that is required as replacement therapy. If the level
of TSH is low, this suggests you may be giving too much T4. If the level of TSH
is high, this suggests you may be giving too little.
As you may have noticed, at
this point I have slipped into talking about TSH and T4, with T3 getting very
little mention. That is because this is where the medical profession now
stands. Hypothyroidism means high TSH and low T4. You are getting adequate
thyroid replacement hormone if TSH in the ‘normal’ range. End of.
Here is what the Royal
College of Physicians (RCP) and the British Thyroid Association (BTA) have to
say on the matter. Key points only
- The only validated method
of testing thyroid function is on blood, which must include serum TSH and
a measure of free thyroxine (T4).
- Overwhelming evidence
supports the use of Thyroxine (T4) alone in the treatment of
hypothyroidism. Thyroxine is usually prescribed as levothyroxine. We do
not recommend the prescribing of additional Tri-iodothyronine (T3) in any
presently available formulation, including Armour thyroid, as it is
inconsistent with normal physiology, has not been scientifically proven to
be of any benefit to patients, and may be harmful. [Then again, it may not be – harmful,
that is]
An aside – (Additional
information, as provided to me)
I should mention here that I
have been told that the RCP has been asked on numerous occasions to cite
references to research/studies showing “overwhelming evidence supports the
use of thyroxine (T4 alone)”, but to date, they have provided none. A
Freedom of Information (FOI) request that the RCP provide such evidence – again
met with no response. A request was made via the ‘Ask for Evidence’ website,
run in association with ‘Sense About Science’ asking for evidence on the safety
and efficacy of L-T4 as a treatment for hypothyroidism. This request was directed
to the RCP who eventually responded stating “The RCP’s guidance is based on
the opinion of an expert panel which was temporarily formed for this
purpose. The evidence they used to form their individual opinions has
not been collated and therefore the RCP cannot provide any evidence list”1 (Jolly, as
they say, good)
Restricting the diagnosis
and treatment of hypothyroidism to measuring T4 and TSH, and nothing else, is
the approach that seems to be used by conventional medicine in the rest of the
World. I recently received an e-mail from someone in Singapore telling me that
their doctor was about to be struck off for prescribing T3 to patients- against
Singaporean medical rules. In the UK, T3 testing is virtually banned, and the
medical authorities are making it virtually impossible to prescribe T3 in any
form.
In the UK, a doctor called
Gordon Skinner was repeatedly dragged in front of the General Medical Council
(GMC) for prescribing thyroxine to patients whose T4 and TSH levels were in the
‘normal range’. He was also attacked for prescribing natural thyroid extract (NDT)
(a combination of T4 and T3) to his patients – who he felt would benefit. He is
now dead. It has been suggested that constant and repeated efforts to strike
him off the medical register may have had an impact on his health. I couldn’t
possibly say.
Now, there is no doubt that
this area is highly complex and for those who know this area, you will be aware
that I am keeping things as simple as possible. But I think it is important to
make a few points:
The lab tests, especially
for TSH, are far from 100% reliable, to say the very least. In fact the man who
developed the test in the UK, at Amersham International in Wales, has told me
that the test is virtually worthless in many cases (especially continuous
testing when patients are taking thyroid hormone replacement).
The conversion of T4 into
T3 can be significantly reduced in some people. So these individuals can have
normal T4 and TSH, but they are still effectively hypothyroid. For those who
are interested in a bit more detail, there is a population with a defective
DIO2 gene. This blocks T4 to T3 conversion, and results (amongst other things)
in reduced T3 levels in the brain, which can lead to mood disorders2. I mention this single example to make it clear that
there is solid scientific evidence to back up the conjecture that it is
possible to be functionally ‘hypothyroid’ with normal blood tests.
A lot of people have
reported significant improvements in their health through taking thyroxine,
with normal blood tests, and also natural thyroid extract when their laboratory
tests were ‘normal’. Please look at this article in the Daily Telegraph3…then look at the comments section – which is very, very
telling. A cry of despair!
I am not going into further
detail of how T4 binding and conversion in various organs can be affected by
stress hormones, inflammation, trauma, adrenal insufficiency, lack of
converting enzymes in tissues, and infection of various sorts. I shall just
keep this simple by stating that it is possible to have enough T4, even T3 in
your bloodstream, but these hormones have reduced ‘bioavailability’. This is
not crank ‘woowoo’ stuff. This is real and measurable and you can find studies
on this in peer-reviewed medical journals.
Far more telling, from my
point of view, is the fact that hundreds, indeed thousands of patients report
that, although their blood tests were normal, they felt terrible, and that they
have felt so much better when they have been given ‘excess’ T4 and/T3, or NDT
(natural desiccated thyroid). Whilst there is no doubt that some of them are,
to quote a medical colleague, ‘not tightly wrapped.’ I have spoken to many,
many, people who are calm, rational and reasonable, and their stories are
compelling. A hellish existence that was ‘cured’ by Dr Skinner and his like. I
refuse to believe that all of these patients are ‘somatising’ fruitcakes.
Comparing the use of SSRIs and
‘Unconventional’ Treatments for Hypothyroidism
At this point I will change
tack slightly. For I think it is fascinating to compare and contrast the
treatment of depression using SSRIs, with hypothyroid patients who complain
that they are unwell, despite ‘normal’ T4 and TSH tests.
Today, almost all doctors
you speak to believe that depression is due to a low level of serotonin in the
brain. This is why they prescribe SSRIs (Selective Serotonin Reuptake
Inhibitors) by the lorry-load. Drugs such as Prozac, Zoloft, Paxil etc.To quote
from a recent article in the BMJ ‘Serotonin and depression, the marketing of a
myth’4.
‘…the number of antidepressant
prescriptions a year is slightly more than the number of people in the Western
World.’
This all happens despite
the fact that:
‘There was no correlation
between serotonin reuptake inhibiting potency and antidepressant efficacy. No
one knew if SSRIs raised or lowered; they still don’t know. There was no
evidence that treatment corrected anything.’
In short, with depression,
there is no lab test, no way of measuring the impact of anti-depressants. They
are prescribed purely and simply on the basis of the patient history. Equally,
there is no doubt at all that SSRIs have significant side-effects, some of
which are very, very serious e.g. increased suicidal tendency. They are also
addictive and patients can end up stuck on them for years. So, they do cause
harm.
Equally, as you may be
aware, clinical trial data in this area have been horribly distorted….
“…That said, the fact that the class of antidepressants known as the
selective serotonin reuptake inhibitors (SSRIs), are basically useless in
treating depression in children and adults is not news to the FDA. Back on
September 23, 2004, during testimony at a hearing before the House Oversight
and Investigations Committee on Energy and Commerce, Dr Robert Temple, the
FDA’s Director of the Office of Medical Policy, discussed the agency’s review
on the efficacy of SSRIs with the children.”
He noted that it was
important in a risk-benefit equation to understand the benefit side. “Of the seven products studied in pediatric MDD (Prozac,
Zoloft, Paxil, Celexa, Effexor, Serzone and Remeron),” he
testified, “FDA’s reviews of the effectiveness data resulted in only one
approval (Prozac) for pediatric MDD.”
“Overall,” Dr Temple said, “the
efficacy results from 15 studies in pediatric MDD do not support the
effectiveness of these drugs in pediatric populations.”
Also in 2004, a study of
previously hidden unpublished data as well as published studies on five SSRIs,
was conducted by Tim Kendall, deputy director of the Royal College of
Psychiatrists’ Research Unit in London, to help analyze research to draw up the
clinical guidelines for British regulators, and published in the Lancet.
Following his evaluation,
Mr Kendall stated: “This data confirms what we found in
adults with mild to moderate depression: SSRIs are no better than placebo, and
there is no point in using something that increases the risk of suicide.”
In 2005, the British
Medical Journal published another study that concluded that SSRIs are no more
effective than a placebo and do not reduce depression.
In December 2006, at the
most recent FDA advisory committee meeting held to review studies on SSRI use
with adults, SSRI expert, Dr David Healy, author of, “The
Antidepressant Era,” told the panel that the efficacy of SSRIs has been greatly exaggerated, while the
actual studies reveal that only one in ten patients responds specifically to an
SSRI rather than a nonspecific factor or placebo.
In February 2008, Irving
Kirsch’s study at the Department of Psychology at the University of Hull is the
first to examine both published and unpublished evidence of the effectiveness
of selective serotonin reuptake inhibitors (SSRIs), which account for 16
million NHS prescriptions a year. The largest study of its kind concluded that
antidepressant drugs do not work. More than £291 million was spent on
antidepressants in 2006, including nearly £120 million on SSRIs. 4
Critics complain that
industry funded studies are presented in ways to exaggerate benefits and
obscure side effects. “These include failure to publish
negative results, the use of multiple outcome measures, and selective
presentation of ones that are positive, multiple publication of positive study
results, and the exclusion of subjects from the analysis,” according
to the paper, “Is Psychiatry For Sale,” by Joanna Moncrieff, in People’s Voice.”5
So we have an interesting
medical conundrum, do we not? On one hand, doctors are more than eager to
prescribe antidepressants at the drop of a hat, based entirely on the patients
reported symptoms. No need for any blood tests, and no evidence that they work
for the vast majority of people.
On the other hand, if a patient
dares to say that they feel better taking T4 when their blood tests are normal,
or if they say they feel better taking a combination of T3 and T4/NDT, they are
dismissed as ‘somatising.’ Which is a posh medical way of saying, you are
making your symptoms up and we don’t believe you. Equally, if a patient
complains of continuing symptoms and that they don’t feel better when they are
taking T4 (or T3 and T4) and their blood test results show ‘normal’ they are
again accused of ‘somatising’6
The world, my friends, has
gone nuts and, in a bitter irony, the medical profession – at least in this
area – has become institutionally paternalistic. ‘You cannot be feeling better, because your blood tests say you
were never unwell. So you cannot have treatment. And you, Dr Skinner and your
like. If you dare treat patient’ symptoms you will be attacked and struck off
from medical practice.’ Now I have looked long and hard, and I have
found no evidence, from anywhere, that giving T3, in the dose that’s needed,
causes any significant medical problems, and I have listened to repeated
testimony from people who feel they have greatly improved.
As for antidepressants,
these mostly useless addictive drugs that can increase suicide risk. ‘Have as many as you like for as long as you like. Because we fully
believe everything you say about your symptoms….’ No need for any
silly tests, or anything like that.
Compare and contrast, then
try to make some sense of the medical world that we now live in.
Sigh.
P.S. Because I am considered
to have alternative views about medical matters, many people contact me to help
promote their ‘alternative’ ideas. Some I believe to be completely whacko, I
smile sweetly and move on. Some I cannot decide. Other issues, once I start
looking into the evidence, I find the evidence compelling.
I certainly find the
evidence that a large number of people are effectively hypothyroid, with
‘normal’ thyroid blood tests, to be virtually overwhelming. Both from a
scientific/physiology basis, and also from a patient testimonial basis.
I now firmly believe that
the medical profession is currently doing these people a great disservice, and
that the guidelines on the treatment of ‘hypothyroidism’ are rigid, autocratic,
and just plain wrong (for a significant minority).
As with all medical matters
that I write about, I have no axe to grind, no horse in the race, no financial
links to anyone or anything with regard to treating thyroid patients. I simply
hope this article can have some positive impact. For it seems very clear to me
that many thousands, hundreds of thousands, of people are suffering
unnecessarily. And I would like it to stop.
References:
4. Serotonin and Depression, the marketing of a
myth.’ BMJ2015;350:h1771
Further postscript
Malcolm – we need to clear
up the fact regarding the definition of ‘hypothyroidism’ which is
“underactivity of the thyroid gland” according to the RCP Policy Statement on
the diagnosis and management of hypothyroidism. Hypothyroidism is easily
diagnosed and more often than not, easily treated with L-thyroxine only.
However, what is being missed by everybody is that over 300,000 UK citizens
(15% of the thyroid community – millions worldwide) have a normally functioning
thyroid GLAND, but the hormone it is secreting is not getting into the cells
where it does its work. These are the folk who need T3, in combo. with T4, T3
alone or in NDT. The RCP teaching curriculum makes no mention of the
possibility of a non-thyroidal condition where patients suffer the same
symptoms and signs of hypothyroidism that may need to be treated with a
different medication or hormone. When these patients complain of continuing
symptoms when treated with L-T4 monotherapy, many are given an incorrect
diagnosis of ME, CFS, FM, depression, functional somatoform disorder – or even
old age blah, blah, blah – and sent on their way without further investigation
or treatment. This is a serious business, which the RCP and BTA choose to
ignore.