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Hypothyroidism - The Other Side of the Story

To quickly access the various sections of this article just click on the following links

My Experiences

Hypothyroidism: symptoms and signs

Diagnostic Dilemmas

But aren't Thyroid Tests Perfect?

Wilson's Disease and Euthyroid Sick Syndrome

When the Treatment is Not Working

Thyroxine Intolerance

Optimising the Dose of Thyroid Hormone

Nutrition and Thyroid Function

T4, T3, T2, T1: when T4 is not enough

Hypothyroidism, the Adrenal Glands, and Chronic Fatigue Syndrome

Conclusion

Links and References

Hypothyroidism - an introduction

This article deliberately adopts a patient orientated approach whereby the success of treatment is judged by how the patient actually feels rather than by the results of blood tests and laboratory data which, after all, are only of secondary importance. Those who are more interested in laboratory data rather than the well being of their patient/s will no doubt disapprove of such an unscientific approach.

Since my interest in this topic is the result of my experiences since I was diagnosed with Hashimoto's disease (hypothyroidism) about nine years ago, I will commence this discussion by briefly detailing some of those experiences. This will be followed by supportive medical and scientific evidence.

My Experiences with Thyroid Disease

Right from the outset my Hashimoto's disease was complicated by severe thyroxine intolerance. Although my starting dose of T4 was only 50mcg, the ill effects were so severe that this was quickly reduced to 25mcg daily. Even on 25mcg I experienced severe restlessness, insomnia, sweating, diarrhea, "overheating", tremor, palpitations and even pain and tightness around the heart upon exertion. These symptoms were so intense that for many months I could not take thyroxine continuously, but would have to cease taking it for a few days every week or so. These symptoms occurred even when thyroid tests revealed that my dosage of thyroxine was insufficient.

I also learned rather quickly that a change in my T4 dosage would have rather rapid and dramatic effects. While an increase in dose would effect me within 24 hours, a reduction in dose would take a little longer, around 48-72 hours. Many doctors, believing that it takes at least two weeks for a change of dose to have any noticeable effect, could not believe the rapidity of the effect in my case. 

Even after my body eventually adjusted to the thyroxine and I ceased having side effects, these problems could all return if I contracted a significant infection such as influenza, whooping cough or glandular fever. Such infections would necessitate that I dramatically reduce my thyroxine dosage because of the sudden onset of severe thyroxine intolerance. If for instance I had been stable on a dose of 250mcg daily for six months, the onset of a significant infection would normally require me to reduce this dose to 25-50mcg daily. Even at this reduced dosage I would experience signs of hyperthyroidism which were absent, prior to the infection, when I was taking the higher dose. 

This situation could continue, although sometimes with fluctuations, for many months or even years, following an infection. Blood tests performed when I was taking the high dose, or on the other hand, the low dose, would usually, but not always, confirm the appropriateness of the dose. Notable exceptions to this did occur however. For instance, on one occasion when I was taking 25mcg daily for months because of severe thyroxine intolerance (even though prior to this I had been stable on a much higher dose), I was medically diagnosed as suffering from all the symptoms of hyperthyroidism and told I should not be taking any thyroxine at all.  However after obtaining the results of a blood test which was done to confirm the diagnosis, the doctor claimed I was taking insufficient thyroxine and I should increase the dose.

Eventually, as I recover from the infection, I would reach a point when I would begin to tolerate the reduced dosage and feel considerably better. This would then be followed by a sudden and sometimes very dramatic attack of hypothyroidism. I would then have to begin to restore my thyroxine dosage to its correct, pre-infection level.

I should also point out that exposure to infections which aggravate my CFS, in addition to causing a sensitivity to the ill effects of thyroxine, also simultaneously cause me to become partially resistant to the good effects of this hormone. Following an infection, in other words, I sometimes appear to suffer from the effects of both hypothyroidism and hyperthyroidism, something which is not unusual in cases of thyroxine resistance. Only when I fully recover from the infection, which may take months or years, do these anomalies return to normal.

The following facts emerge from my experiences.

• Any infection which aggravates my CFS will cause both erratic thyroid test results and erratic response to thyroxine.
• Although conventional thyroid tests do not reveal the precise mechanism underlying this thyroid disturbance, these erratic responses have been repeatedly observed by various doctors.
• Medical theories advanced to explain these phenomena include thyroxine resistance or CFS caused disturbance of mitochondrial transport of thyroxine.

From my experience conventional T4 treatment is frequently only partially effective. It is no substitute for the thyroid gland's natural hormones, a fact which underlines the primitive nature of current thyroid therapies.

Hypothyroidism: symptoms and signs

Hypothyroidism has been described as the "great masquerader" ( 33 ) because of the many vague symptoms it may cause which resemble symptoms of numerous other diseases. Although there are various "classical" hypothyroid symptoms related to the general slowing of metabolism such as tiredness, fatigue,  depression, coldness, reduced sweating and slowed thinking, speech and movements, there are also many other lesser known or paradoxical symptoms. These symptoms, which include mania, hyperactivity, anxiety, palpitations and insomnia, may be related to deficiency of T3 in brain cells. Perhaps even more important however, is the fact that hypothyroidism may cause stimulation of the adrenal gland and the sympathetic nervous system with increased levels of cortisol, adrenalin, and noradrenalin (112). It is interesting to note a recent report that hypothyroidism may effect brain size ( 100 ). A more comprehensive list of symptoms is as follows.

Symptoms and Signs ( 11, 12, 32, 33, 46, 50, 82, 102,112 )

Diagnostic Dilemmas with Hypothyroidism

According to Arem ( 11 ): 

According to the recent Colorado Thyroid Disease Prevalence Study ( 3, 4, 5  ), 10% of Americans, or 13 million adults have an undiagnosed thyroid disorder. Brownstein ( 13 ) claims that the figure of 10% seriously understates the problem since conventional medical tests fail to diagnose around 30% of those with hypothyroidism. This makes the true incidence of hypothyroidism in America around 40% or 52 million adults ( 13, 32, 33 ). 

Clearly, many doctors today have considerable difficulty diagnosing hypothyroidism. Dommisse for instance, reported that his thyroid condition remained undiagnosed for 36 years ( 1 ) while another case was medically diagnosed as suffering from "growing pains" ( 9 ). The correct diagnosis in this latter case was finally made by a naturopath. Other cases are falsely diagnosed as suffering from psychiatric disorders such as depression ( 2, 3, 11, 12, 13, 25, 26 ), or even pregnancy ( 3 ). While one recent case of severe hypothyroidism with ascites was misdiagnosed as suffering from an "intra-abdominal malignancy" ( 102 ). Misdiagnosed hypothyroid patients have even been led to believe by psychiatrists that all their various thyroid symptoms may be due to depression ( 26 ).

Unfortunately, the poor thyroid patient's problems do not necessarily end even if he or she is successfully diagnosed and treated. According to Arem ( 11 ) some general practitioners take their patients off their thyroid medication when their tests become normal, completely overlooking the fact that the only reason the tests have become normal is because of the medication. One particular patient cited by Arem who was taken off her thyroid medication by her GP subsequently developed severe depression and other symptoms of hypothyroidism. Upon returning to her GP however, she was "diagnosed" as suffering from "stress". It is absolutely astonishing that doctors, who are supposedly trained in a scientific approach to health care, can make such blatant errors with such amazing frequency. Sadly, a diagnosis" of "stress", "anxiety", or "depression" is frequently no more than a delusion of the diagnostically destitute. It is a diagnosis which commonly says more about the doctor than the patient.

The reasons for the common misdiagnosis of hypothyroidism are twofold. Firstly, as I have already indicated, the many vague and perhaps psychological symptoms of thyroid failure leads many physicians to erroneously make a psychiatric or psychosomatic diagnosis ( 2,11, 12, 15, 19, 27 ). This matter has been adequately addressed by Wilson ( 27 ):

The scientific reductionist approach to medicine clearly encourages physicians not to consider the whole body but rather simplistically reduce illness to a disturbance in a particular organ or tissue ( see Is Illness Holistic? ). In such a diagnostic environment vague systemic symptoms such as fatigue, general aches and pains, lack of motivation, and general slowness or "brain fog" will be too difficult to accurately diagnose and will commonly be reduced by physicians to a psychiatric problem such as depression, even though the effects of hypothyroidism are well known. As has been pointed out by Arem ( 11 ), psychiatrists frequently misdiagnose thyroid disorders because they fail to consider any possibility that mental symptoms may be caused by a physical illness. Arem notes ( 11 ) that 50% of a group of hyperthyroid patients were misdiagnosed by psychiatrists as suffering from depression or an anxiety disorder. What enables such attitudes to be validated and perpetuated is the reductionist philosophy of modern medicine ( see The Reductionist Philosophy ) and the fact that doctors are taught that they know everything there is to know and what they do not know simply does not exist ( 27 ).

Wilson ( 27 ) empathises admirably with frustrated undiagnosed thyroid patients who are unable to convince doctors to take their complaints seriously:

Any attempt to explain the frequent misdiagnosis of hypothyroidism as depression on the basis of the apparently common nature of depression ( 11 ) and the occurrence of stressful events in the lives of patients is totally without logic or justification. Since depression only effects 10% of the population ( 11 ) while undiagnosed hypothyroidism has an estimated incidence of 10%-40% ( 5, 13, 32, 33 ) , and may also be related to stress ( 11, 12 ), there is considerably more scientific evidence for doctors to assume that all patients with emotional disturbances need thyroid treatment. The vital lesson to be learned here is that depression is merely a symptom, not a cause. How can an illness possibly be caused by a symptom? Preoccupation with treatment of "depression" is an inevitable result of an interventionist symptomatic reductionist approach to health care where the cause or "big picture" is relatively unimportant. Medicine should not be based upon assumptions nor on a fragmented symptomatic tunnel vision approach to health care. As has been noted by Shames and Shames ( 12 ), " in a medical system geared to catastrophic illness and crisis intervention, the common milder cases of low thyroid generally go undiagnosed." While this is obviously true, although depression is not a catastrophic illness the milder cases of depression rarely seem to go undiagnosed. Unfortunately, notwithstanding the fact that depression is merely a symptom, the frequency with which depression is diagnosed is directly proportional to the diagnostic inefficiency of modern medicine.

The second reason why hypothyroidism is so frequently misdiagnosed is because of excessive reliance upon imperfect medical tests and the fact that conventional or non-holistic doctors commonly prefer to treat a series of test results rather than an individual patient. However I shall consider this matter in more detail below.

Hypothyroidism then, is a disease which many doctors not only find very difficult to diagnose with any degree of accuracy, but furthermore, even after correct diagnosis, effective treatment may be difficult to obtain.

But aren't Thyroid Tests Perfect?

Although many doctors still rely exclusively upon laboratory tests to assess thyroid status, such tests can be quite unreliable and misleading. According to Rothfeld and Romaine (109):

There are many reasons why thyroid tests, and medical tests generally, are a long way from perfection( 6, 7, 8, 27, 29, 30, 31, 46, 109 ). These reasons include the following:

• blood levels do not necessarily detect defects in cellular transport and utilisation
• unscientific "normal ranges" - what is normal?
• limitations of the sensitivity of the test
• hormonal variations
• the presence of antagonistic or inhibitory chemicals and hormones
• other interfering factors
• variations in target cell sensitivity

Undoubtedly the two biggest problems when it comes to the reliability of thyroid tests is the imprecise nature of normal ranges and the inability of current tests to detect exactly what is happening inside cells. Measurements of thyroid hormone levels may also be particularly misleading in the presence of autoimmune disorders such as Hashimoto's disease. The presence of thyroid antibodies in such diseases may displace thyroxine from cellular receptors and prevent it from working thus causing hypothyroidism in the presence of normal hormone levels ( 48, 49 ). The ability of cellular receptors to bind thyroid hormones is also believed to be influenced by genetics (109).

It is generally considered that the TSH test is the single most sensitive and reliable laboratory test for diagnosing hypothyroidism ( 11, 24, 35, 48 ). Yet, in spite of this, modern medical science has yet to determine what is a normal level of TSH. While some doctors will declare that the maximum permissible level for TSH is 5 ( 7, 30 ), or perhaps even 10 ( 7, 30, 31 ), increasing medical evidence suggests that this limit should be lowered to 1.5-2.00 ( 7, 17 ), the "optimum" value being between 1.3 and 1.8 ( 39 ), values above these figures being indicative of hypothyroidism ( 7, 17 ). 

As has been pointed out by Arem ( 11 ), and also Rothfeld and Romaine (109), it is not the absolute TSH level per se that is of utmost importance, but rather the change in level in each particular individual. Arem points out that a patient who normally has a TSH of 0.6 may experience symptoms of hypothyroidism at a level of 3.0 even though this would be diagnosed as normal. Clearly, although Arem lists the "normal range" for TSH as being from 0.4 to 5.0, it seems that many people whose TSH lies within this range are in fact hypothyroid. According to Arem in fact ( 11 ), "if your TSH is close to the upper limit of the normal range set by laboratories, you have a higher risk of being low-grade hypothyroid." But Arem goes even further claiming that "even if the TSH is in the lower segment of the normal range, a person may still be suffering from low-grade hypothyroidism." The term low-grade hypothyroidism of course, which is based upon laboratory data, is one of theoretical if not unscientific convenience, and may be quite divorced from the severity of the symptoms the patient is experiencing in the real world.

According to Brownstein ( 13 ), there is some evidence to suggest that thyroid laboratory tests may only detect 2%-5% of hypothyroid patients. Brownstein comments:

When it comes to interpreting TSH test results, commonly considered the gold standard of thyroid tests, it seems that many people whose laboratory results are "normal", may well be decidedly abnormal. It is no wonder that hypothyroidism is so commonly misdiagnosed!!

The unreliability of the TSH test is further underlined by the fact that this test is not specific for hypothyroidism since adrenal insufficiency may also cause elevated TSH levels which are corrected by appropriate adrenal therapy ( 105, 106 ) .

The difficulty of interpreting TSH test results is also a significant factor in the treatment of hypothyroidism. Shames and Shames ( 12 ) point out that doctors should aim to achieve a level of TSH around the lower limit of normal ( 0.4 ) or perhaps even lower than normal ( 0.1-0.2 ). These workers draw attention to the fact that some of their patients do not feel well until their TSH is lowered to 0.1, considerably below what is regarded as "normal". Shames and Shames comment ( 12 ): "the patient feels good, but only at a TSH level that feels bad to the doctor." This raises a very important point, namely, what is the goal of thyroid treatment? Is the goal simply to "normalise" laboratory test results or is the goal to normalise the health of the patient and enable him/her to have total freedom from thyroid symptoms? Is the doctor treating a set of laboratory data or an individual human being?

Various practitioners, especially practitioners of holistic medicine, have emphasised the need to give top priority to the attainment of optimum health for their patients rather than simply the normalising of laboratory data ( 12, 13, 16, 27, 32, 33, 109 ). The degree to which these two goals differ is a measure of the different interests of patients and doctors, patients being exclusively concerned about their health rather than being preoccupied with laboratory data. It is odd that a patient is forced to seek out an holistic practitioner if he/she requires a practitioner whose perspective is more in tune with the needs of patients. It is this concern for patients, combined with the exceedingly poor track record of conventional thyroid laboratory tests, that has led to increasing interest in alternative methods of diagnosing and treating hypothyroidism.

One such alternative method of diagnosis is based upon measuring the body temperature, temperatures consistently below 97.8ºF being suggestive of hypothyroidism ( 12, 13, 16, 27, 29, 32 ). The use of body temperature has been outlined in some detail by Wilson ( 16, 27, 29 ), Barnes ( 32 ), Langer ( 33 ) and  Rind ( 40 ). 

Rind ( 40 ) makes the point that significant reductions in body temperature reflect a reduced metabolic rate and therefore may also be due to other factors such as adrenal insufficiency which, unlike hypothyroidism, produces a more unstable temperature pattern ( click image at left ). Since holistic practitioners do not rely upon body temperature alone but also give a much higher priority to clinical history and symptoms than do conventional practitioners, they are more equipped to distinguish between different causes of reduced temperature patterns. They care more about how the patient FEELS. Although often forgotten by conventional practitioners, it is the clinical picture which is of absolutely paramount importance, abnormal laboratory test results only being significant insofar as they indirectly and imprecisely reflect the patients clinical condition.

Temperature Graphs Reproduced courtesy of Dr. Bruce Rind http://www.drrind.com

To assist in providing an accurate clinical assessment of the various causes of low metabolic rate Rind also uses a detailed and informative "metabolic scorecard" . While total diagnostic dependence upon pathology tests may be simpler and less time consuming for the practitioner, from a patients perspective it is the actual real life effects of his/her illness, the symptoms and signs, which are of primary concern.

Arem ( 11 ) has recently criticised the use of body temperature and clinical history to diagnose hypothyroidism on the basis that such methods lead to false diagnosis. Clearly, no system of diagnosis is perfect, however the track record of conventional thyroid laboratory tests is, according to overwhelming scientific evidence, exceedingly poor. From a scientific point of view, if we wish to abandon misleading tests then perhaps it is the thyroid laboratory tests, such as the TSH test, which should be abandoned ( 41 ). After all, a misleading and inaccurate test is not only a hazard to the well being of patients, it may in many cases be worse than no test. Those who are obsessed with laboratory test results tend to overlook the most important test, namely, how the patient actually feels.

Since, according to Rothfeld and Romaine (109) it is estimated that one third of hypothyroid patients have normal blood test results, it is the welfare of these patients which should be of grave concern to the medical profession. While some may argue that even this estimated 66% efficiency of current thyroid tests justifies a dependence upon such tests, it should be noted that those persons who are successfully diagnosed owe their initial diagnosis to obvious thyroid symptoms and hence the need for tests. Tests are merely used to confirm the diagnosis. What is not often discussed by the medical profession is the fate of those hypothyroid patients whose test results are normal. When most doctors receive a negative test result any consideration of thyroid disease may be ruled out for years. 

Typically the hypothyroid patient with normal test results is forced to go from doctor to doctor, diagnosis to diagnosis, and treatment to treatment. Undoubtedly such patients frequently fall into the hands of other specialists such as psychiatrists and are subjected to inappropriate and harmful treatments. Patients who are insistent that they have thyroid disease may even be humiliated and falsely labelled as hypochondriacs. The use of psychoactive drugs and other psychiatric therapies to treat such patients is to be deplored. If doctors are to learn the truth, and if we are to move forward, the tragic plight of these patients, instead of being ignored by doctors, should be publicised. 

As if to underline how misleading and dangerous conventional thyroid laboratory tests may be, Arem ( 11 ) cites the case of a patient who was insistent that her symptoms were due to hypothyroidism although all her thyroid tests indicated she was in perfect health. Because she threatened to go to another doctor if she did not receive thyroid treatment, Arem relented and commenced low doses of thyroxine. Arem comments ( 11 ): "to my surprise, most of her symptoms went away, and she has continued to do fine." Arem notes that he has also had other patients with normal test results who responded positively to thyroxine. Other doctors such as Wilson ( 16, 27, 29 ), Barnes ( 32 ) and Langer ( 33 ) have also shared the experiences of Arem. Langer makes the point that many of his patients, and also those of Barnes, who had normal thyroid laboratory tests were subsequently found to be "conclusively hypothyroid according to the basal temperature test, symptoms and medical history."

There are some interesting issues here. How is it possible for a patient to be so right about a diagnosis while both the endocrinologist and the most sophisticated available scientific testing technology are so wrong? How many other patients, who were not so insistent, are currently on the medical merry-go-round receiving incorrect treatment simply because of excessive reliance on inaccurate tests? What happens if we extrapolate the experiences of Dr's Arem, Barnes, Langer and Wilson to other doctors throughout the world? It is not difficult to see why excessive reliance upon laboratory tests has correlated with such widespread misdiagnosis. Why is there such reliance upon laboratory tests when they are so unreliable? It is foolishness to assume that all thyroid disorders must necessarily occur within the full view of pathology laboratories.

What is needed are clinical trials comparing the various systems of diagnosis rather than simplistic criticisms and suggestions that the use of body temperature tests should be abandoned ( 11 ). Bearing in mind that the yardstick for evaluating any test should be how the patient feels, we could do no better than examine the results of real life clinical trials performed by doctors throughout the world on their patients. These clinical trials, as discussed above, are far from impressive.  Laboratory tests are merely an indirect and imprecise aid to attaining this end. Shames and Shames ( 12 ) advise patients to make the following query of their doctors: "listen, the goal of therapy is not to have a normal TSH or normal T4. The goal of therapy is to have a normal patient. Can't you work with me on this?"

Arem ( 11 ) further criticises the use of body temperature readings on the basis that depression also causes disturbances in temperature. However, Arem points out that almost 20% of patients hospitalised for severe depression were found to have Hashimoto's disease and 52% of patients with untreatable major depression have hypothyroidism. Arem also cites a recent study which revealed that 86% of patients with chronic depression had an enlarged thyroid gland whereas only 25% of non depressed people had an enlarged gland. Given the fact that so many hypothyroid patients remain undiagnosed, much of the current epidemic of depression may simply be the result of hypothyroidism ( 12 ). Furthermore, according to Arem ( 11 ), some cases of depression are due to a local deficiency of T3 in the brain even though there is no detectable malfunction of the thyroid gland. Such cases are successfully treatable with T3 supplements.

I should make the point here that the suggestion that a local deficiency of T3 in the brain does not constitute a thyroid disorder hardly seems tenable. Since these disorders are correctable by taking additional T3 there is clearly an insufficient production ( or conversion ) of T3 to ensure optimum health. The fact that such disorders are not detectable by current thyroid lab tests is a different issue. If a new test is developed tomorrow then these non-thyroid disorders may suddenly become thyroid disorders. Such is the nature of conventional medicine. As always, those who dare to think beyond the square will always be the ones who pave the way for groundbreaking new developments.

The other vital issue here is that depression is only a symptom. Depression is simply a disturbance of the chemicals in the brain. Preoccupation with symptoms diverts our attention from the fact the cause is the underlying chemical disturbance. It is now known for instance, that depression may be just one symptom of numerous disturbances in the levels of various hormones. Depression may also result from various nutritional deficiencies including deficiencies of vitamins B1, B3, B5, B6, B12, and folate ( see B vitamins page ). It is indeed interesting to note that nutritional deficiencies, like thyroid disorders, have traditionally been misdiagnosed because of excessive reliance upon imperfect laboratory data. It is now known that nutritional deficiencies are extremely common although still largely unrecognised by the medical community at large ( see B vitamins, Nutrition is for the Birds ). In spite of all this, depression is frequently blamed for all manner of symptoms, from tiredness to heart disease( 36, 37, 38 ) . Although we know that hypothyroidism and adrenal overactivity may both cause heart disease and depression, as is also the case with vitamin B6 deficiency, heart disease which occurs in a "depressed" person may even be attributed to depression ( 36, 37, 38 ). The eagerness with which modern medicine regards depression as simultaneously being both a cause as well as a symptom makes it absolutely unique amongst modern medical disorders.

We should not be satisfied to treat symptoms such as depression as if they are causes. If we do, we may find that many hormonal or nutritional problems are misdiagnosed as depression!!! There is a lesson here for those who are concerned about the astonishing increase in the incidence of iatrogenic diseases.

I must also take issue with the claim by Arem that ( 11 ) "a decrease in body temperature is not sensitive enough to diagnose hypothyroidism" because "only profound, severe hypothyroidism causes low temperature." This is certainly not consistent with my own experiences. I have described above the effects certain infections have upon my thyroid condition. Following severe infections my tolerance of thyroxine changes, my response to thyroxine becomes erratic with long periods of low grade symptoms of hypothyroidism interspersed with symptoms of hyperthyroidism. During these changes the results of conventional thyroid tests are also erratic and certainly do not reflect the nature of my symptoms. However, during the course of all these changes my body temperature is often consistently low, around 96.5º-97º F . When my temperature becomes consistently normal my thyroid symptoms also disappear and my response to thyroxine normalises. My body temperature corresponds with the course of these events much more accurately than thyroid lab tests.

The other major problem with thyroid lab tests is that they do not detect defects in the peripheral utilisation and cellular activity of thyroxine.

The inability of blood tests to detect problems involving the peripheral utilisation of thyroid hormones is probably the biggest problem associated with excessive reliance upon such tests. Although it is well known that it is the intracellular T4/T3 conversion and the utilisation of T3 within cells or mitochondria which is responsible for the energy producing effects of thyroid hormones ( 11, 12, 13, 16, 27, 29, 32 ), there remains a widespread assumption within orthodox medicine that normal blood levels ensures normal cellular utilisation. It is important to note that this belief has no basis in science but rather is simply an assumption, an assumption which probably owes its existence to the belief that whatever cannot be measured by blood tests simply does not exist - irrespective of the suffering of patients. In fact, since it is within the mitochondria that the numerous energy producing reactions occur which are responsible for determining our metabolic rate, it is here also that there are numerous opportunities for things to go wrong. Unfortunately however, it is inconvenient for things to go wrong beyond the detection of blood tests.

The possibilities of improper utilisation of thyroxine include the following.

• Peripheral T4/T3 conversion problems.
• Thyroxine resistance where cells fail to respond properly to thyroxine.
• Cellular transport problems where there is faulty transport of T4 into mitochondria.
• Displacement of thyroid hormones from cellular receptors by rT3, anti-thyroid antibodies, or other substances.

It should be noted that the popular TSH test will not detect defects in cellular utilisation of thyroxine as long as the blood levels of T4 are "normal". This is because the pituitary gland is suppressed by feedback from T4 levels in the blood ( 13 ). An exception to this may occur in cases of thyroxine resistance, especially if the pituitary gland is resistant to the feedback effects of T4.

Disorders such as thyroxine resistance ( 10, 13, 34, 42, 43, 44, 45, 47, 50 ), or cellular deficits of T3 may present a unique diagnostic challenge. This is especially true of those forms of thyroxine resistance which present with normal thyroid lab tests or varying degrees of thyroxine resistance in the different organs of the body. Such patients may be simultaneously hypothyroid and hyperthyroid ( 10 ) (in different organs). Although thyroxine resistance is usually considered a genetic disorder, there may well be some similarities with thyroid disorders which occur in CFS ( see CFS section below ).

According to evidence cited by Brownstein ( 13 ) and Lowe ( 45 ), thyroxine resistance is quite common, especially amongst sufferers of fibromyalgia or CFS. Victims of these disorders who have symptoms of hypothyroidism but normal laboratory tests may experience a positive response to thyroid therapy ( 13 ).

The other common problem concerning the cellular utilisation of thyroxine involves faulty conversion of T4 to the much more active T3 ( 11,12, 13, 16, 27, 29, 46, 47, 50 ). Even a minor deficiency of T3 in the cells of the body, especially the brain, can cause dramatic and diverse symptoms ( 11, 16, 27, 29 ). Deficiency of T3 in brain cells has been related to numerous "mental" illnesses, from depression and anxiety to mania, hyperactivity and ADD ( 11 ). Thyroid laboratory tests may fail to reveal cellular deficits of T3 in spite of the presence of severe symptoms of hypothyroidism.

There are many factors which may interfere with thyroxine utilisation or peripheral T4/T3 conversion. These include: stress, chronic illness, heavy metals, drugs ( HRT, beta blockers, steroids, antidiabetic drugs, cholesterol lowering drugs, oestrogen etc. ), cigarette smoking, carnitine, alpha lipoic acid, consumption of soy products, and nutritional deficiencies such as selenium, zinc, and vitamin B6 ( 11, 12, 13, 46, 109 ). It must be noted also that adrenal hormones play an important role in T4/T3 conversion and the peripheral utilisation of thyroxine ( 12, 13, 46 ). According to Shames and Shames ( 12 ): "some adrenal hormones assist in the conversion of T4 to T3 and perhaps assist in the final effect of T3 on the tissues. Some scientists believe that even the entrance of thyroid hormone into our cells is under the influence of adrenal hormones." While low levels of cortisol may cause a deficiency of T3 because of reduced conversion from T4 ( 46, 109 ), excessive amounts of cortisol on the other hand, or an elevation of the cortisol/DHEA ratio, causes T4 to be converted to reverse T3 ( 46, 52 ). Reverse T3 ( rT3 ) displaces normal T3 from receptors in cells and causes a T3 deficiency ( 46, 52, 53, 109 ). The adrenal hormone DHEA is also involved with the conversion of T4 to T3 ( 51, 52 ). 

It is encouraging to see some laboratories, such as Meridian Valley Laboratories (110) and Great Smokies Diagnostic Laboratory (111), now including the measurement of rT3 and also the T3/rT3 ratio as a standard part of their thyroid tests. 

The bottom line when it comes to thyroid tests is, to be sufficiently dependable as a means of diagnosing thyroid conditions, a thyroid test must detect not only the level of free T3 and T4 inside and outside all cells in the body, but furthermore, it must also be capable of detecting any other problem or substance in the body which may influence the way in which thyroid hormones are transported and utilised. It must do this with 100% accuracy.  Until we attain this ideal, laboratory values should be "optimised", as suggested by Rind ( 39 ), and used only as a guide.

If test results are interpreted with the above limitations in mind, they may be a useful guide. However, if, as more often appears to be the case, test results are accepted as being conclusive, then they may be dangerously misleading. Since excessive and inappropriate reliance on imperfect medical tests may actually delay, or even prevent the reaching of a correct diagnosis, such reliance may be one of the greatest obstacles faced by patients in their quest for correct diagnosis and treatment. This is especially true of course, for those patients who are suffering from less severe or less common forms of thyroid disease rather than  a severe textbook case of typical hypothyroidism. In the words of Wilson ( 27 ): "if obvious* cases with abnormal* blood tests are easily overlooked, how much more easily overlooked are cases with normal blood tests*?"  

In my own case for instance, a doctor who diagnoses me as suffering from all the symptoms of hyperthyroidism, subsequently suggests, on the basis of a blood test result, that I should increase my dose of thyroxine as I am not taking anywhere near enough. These types of errors which result from excessive reliance upon imperfect tests must be positively eliminated.

When it comes to the reliability of thyroid laboratory tests, Brownstein concludes ( 13 ): 

When all is said and done there is only one question that is important when it comes to the use of thyroid tests, namely: are the tests perfect and incapable of error or misdiagnosis? If the answer is "no", then the tests should be treated accordingly and not relied upon. It would be both foolish and unscientific to exclusively depend upon tests which, because of their known imperfections, are guaranteed to result in misdiagnosis and incorrect treatment of thyroid disorders. There is an absolutely massive chasm between normal medical test results and normal health. But there is a far greater chasm between normal medical test results and optimum health.

* Wilson's emphasis

Wilson's Disease and the Euthyroid Sick Syndrome

In some cases however, according to Wilson ( 16, 27, 29 ), the blockage in T3 formation does produce symptoms and continues even after the causative illness or stress has resolved. In other words the system does not automatically "reset" after the underlying non-thyroidal illness has disappeared ( 16, 27, 29 ). This condition has been termed "Wilsons's Syndrome" ( 16, 21, 27, 29, 109 ).

Unlike Euthyroid Sick Syndrome, Wilson's Syndrome may be characterised by completely normal thyroid blood test results, although there may be an increase in reverse T3 levels (Wilson's Syndrome can of course, also coexist with clinical thyroid disease). This is because the T3 deficiency occurs inside cells where most of the T4-T3 conversion takes place. As a result, Wilson's Syndrome is normally diagnosed by clinical history and subnormal body temperature readings ( 16, 21, 27, 29 ). Since the body temperature is proportional to the basal metabolism or rate of cellular heat production, it reflects more closely what is actually happening inside cells. 

Another interesting aspect of Wilson's Syndrome is the effect of T4 upon sufferers of this condition. The Wilson's Syndrome patient will normally  experience partial or temporary response to T4 but when the effect wears off the dose must be continually increased in order to further boost the failing conversion of T4 to T3 ( 16, 27, 29 ). Wilson claims that correct T3 replacement therapy with a special time release T3 preparation, may permanently correct this disorder and permit the cessation of T3 treatment ( 16, 27, 29 ). It is important to note however, that T3 is a very potent medication which may not be tolerated as well as the less potent and slower acting T4. It is for this reason that Wilson uses a special time release T3 preparation.

Arem ( 11 ) has recently expressed doubt about the existence of Wilson's syndrome and its treatment with T3. Arem claims that the symptoms of Wilson's syndrome are symptoms of depression and in "these patients there seems to be no scientific basis for true hypothyroidism in organs other than the brain." Whether there is "scientific evidence" or not, and whether there is "true hypothyroidism" or not, is hardly the issue. People are continuing to suffer because of misdiagnosis of diseases affecting the thyroid system. While conventional non-holistic practitioners only tend to be concerned about the level of thyroid hormones in the blood, as Wilson points out ( 16, 27, 29 ), disorders of the thyroid system also include the effects of thyroid hormones inside target cells. Because such disorders are beyond current "scientific" tests does not detract from the reality of their existence. The simple question here is: should we ignore the suffering of such patients until the matter becomes legitimised by science? While conventional practitioners would normally answer "yes", the reverse is true of holistic practitioners.

While Arem ( 11 ) indicates that symptoms of Wilson's syndrome - "fatigue, depression, headaches, migraines, premenstrual syndrome ( PMS ), anxiety, panic attacks, irritability, hair loss, decreased motivation and ambition, inappropriate weight gain, decreased memory and concentration, insomnia, and intolerance to heat and cold - are symptoms of depression", he also acknowledges the fact that doctors frequently continue to misdiagnose hypothyroid disorders as "stress" or "depression". Indeed, Arem suggests that "the logical explanation for Wilson's observations is that, during and following stressful events, a person may begin to suffer from depression ( resulting in low brain T3 levels because of impaired conversion of T4 to T3 )."

To a lay person the reasoning here seems very confusing. Firstly, according to Arem, depression is a symptom of depression. Secondly, depression, which Arem describes as a "symptom", causes a deficiency of T3 in the brain. Finally, a deficiency of T3 in the brain causes depression. 

Whatever the merits of Wilson's syndrome per se, Wilson has been unfairly demonised and ostracised by a medical profession which is absolutely obsessed with maintaining the strict introversion and rigidity of established medical dogma. At a time when conventional medicine has made misdiagnosis of thyroid disease into a highly developed art, Wilson has paid the penalty for daring to try and help patients who have been misdiagnosed and mistreated by conventional thyroid practitioners. While conventional medical practitioners were displaying an obsession with T4 treatment and the alleged infallibility of thyroid blood tests , Wilson has drawn attention to the frequent superiority of T3 treatment and the inability of blood tests to detect cellular T3 deficits. Rather than disprove the beliefs of Wilson, medical science is increasingly acknowledging their accuracy. While Wilson attempted to help patients with apparent cellular T3 deficiency, the medical profession has displayed more interest in punishing the doctor rather than helping the patients.

We owe our progress in science and health care to those who dared to think beyond the square in spite of the inevitable condemnation they receive from their more conservative less progressive colleagues. Important discoveries are always made by those who dare to be different, by those whose allegiance is to the pursuit of truth rather than preservation of the status quo. Holistic practitioners continue to set the standards for individuality, open-mindedness, humility, and their self sacrificing nature.

When Thyroid Treatment is not Working

The modern doctor is very skilled in treating and normalising thyroid hormone levels in the blood but perhaps not quite so adept at treating patients with hypothyroidism. Many patients, in spite of modern technology, fail to respond fully to modern thyroid treatment. Even patients who receive "correct" thyroid replacement therapy may not fully respond and may remain unwell ( 3, 11, 12, 13, 16, 27, 29, 32, 33, 99, 101, 109 ). Although doctors have expressed little interest in researching the quality of life of treated thyroid patients (113), recent research has confirmed that current treatments do leave much to be desired (113). It seems that doctors are constantly confronted with thyroid patients who are unhappy with the results of their thyroid treatment even though their blood test results may be perfectly "normal". ( 11, 12 ). In the words of Arem ( 11 ):

Similarly, according to Rothfeld and Romaine (109):

I should perhaps add here that an even worse scenario is when these symptoms of hypothyroidism are treated with antidepressants and mood altering drugs simply because the doctor can find no laboratory explanation.

Rothfeld and Romaine continue (109):

These frank accounts of Arem, and also Rothfeld and Romaine, are indeed commendable and should serve to alert other practitioners about the frequency with which difficulties occur during the diagnosis and treatment of thyroid disorders. Let us examine some of these difficulties.

As medicine continues to realise the limitations of a reductionist approach to health care and the advantages of a holistic approach it is increasingly being realised that many cases of hypothyroidism, perhaps 50%, also involve other endocrine glands, particularly the adrenal glands (109). According to Rothfeld and Romaine (109): "doctors are beginning to believe that it is nearly impossible for thyroid balance, particularly underactive thyroid, to exist without a corresponding imbalance in adrenal function." Rothfeld an Romaine continue: "increasingly, doctors are finding that adrenal function in particular is the culprit when your symptoms paint one picture and your lab results paint another." In this connection it is indeed interesting to note that "T3 supplementation does seem to improve symptoms related to underactive thyroid, especially when adrenal fatigue is also a factor."

For further information about the adrenal glands and hypothyroidism see below under the following subsection - Hypothyroidism, the Adrenal Glands, and Chronic Fatigue Syndrome.

Thyroxine intolerance
Commencement of thyroid therapy can represent an exceedingly difficult part of the recovery process. To suddenly accelerate the sluggish metabolism of a hypothyroid person may be quite challenging, especially if there has been relatively severe longstanding thyroid disease, anaemia, heart disease or some degree of adrenal weakness ( 75, 76, 77, 105, 106, 107 ). While the thyroid hormone may seek to bring the body ( and mind ) "up to speed" quickly, there may be dramatic objections from the heart, muscles, nervous system and the body generally. In fact, until the body adapts to the dose of thyroxine and the increased metabolic rate it is possible to experience typical symptoms of hyperthyroidism, even though test results suggest normal or below normal levels of thyroid hormones. From my experience, this adaptive period may be very uncomfortable and prolonged, even though it seems to be little discussed by doctors.

While there may be various factors which may accentuate the length and severity of this adaptive period, there are three factors which are of particular significance. Firstly, as I have already indicated, more severe or longstanding cases of undiagnosed hypothyroidism are likely to experience a more severe and prolonged adaptive period. Secondly, if there is any coexistent reduction in adrenal capacity then thyroxine intolerance will also be greatly exacerbated ( 78, 79, 105, 107 ). In fact adrenal insufficiency can cause elevated TSH levels and a false diagnosis of hypothyroidism ( 105 ). As is so often the case when there is a dependence upon imperfect medical tests, the milder or subclinical forms of adrenal deficiency would be expected to pose much more of a problem in this regard than the much more easily recognised and less common cases of full blown Addison's disease. Finally, the early stages of Hashimoto's disease may be characterised by unstable and inconsistent thyroid function, perhaps with swings from hypothyroidism to hyperthyroidism.

In order to prevent or reduce such reactions experts suggest that thyroxine therapy should be commenced at a small dosage and increased slowly as tolerance permits ( 78, 79 ). Additionally, it may be necessary to utilise adrenal supplements, although such treatments need to be carefully supervised by a practitioner. I have also found that various herbal YIN tonics ( 80, 81 ) may assist in counteracting the ill effects of thyroxine. Yin tonics, such as lily bulb ( Lilium brownii; Bai He ), dwarf lilyturf root ( Ophiopogon japonica; Mai Men Dong ), and dendrobium ( Dendrobium nobile; Shi Hu ) are mild but strengthening herbs which help to counteract the stimulating and heating effects of thyroxine. If stronger colder herbs are required then herbs such as water plantain root ( Alisma orientalis; Ze Xie ), Anemarrhena ( Anemarrhena asphodeloides; Zhi Mu ), and American ginseng ( Panax quinquefolius; Xi Yang Shen ), could also be added. Best results will be obtained by an individualised mixture prescribed by a TCM practitioner.

I should emphasise here that in addition to the more transient forms of thyroxine intolerance mentioned above, it is possible to experience more chronic or recurring forms of intolerance. In my own case for instance, I have experienced ( fluctuating ) thyroxine intolerance for months or years following various infectious illnesses. The common factor with these various infections is that they must be sufficiently severe to aggravate ( or cause) CFS. Mild infections which have no effect upon my CFS also have no effect upon my tolerance of thyroxine. It is important to note that those infections which do alter my thyroxine tolerance appear to set up chronic metabolic changes which may be quite persistent and quite resistant to treatment. I should also indicate that this form of thyroxine intolerance is not generally as acute or severe as that which occurred when I first commenced thyroxine treatment for my thyroid condition. Some of the severe symptoms I experienced at that time ( ie. severe overheating and drenching sweats ) tend to be conspicuously lacking in this later more chronic form of thyroxine intolerance. Interestingly, when I begin to recover from the infection and my CFS begins to improve, these more acute symptoms do tend to return. However this is only temporary and is followed by the cessation of thyroxine intolerance and completely normal response to thyroxine - until I get another infection!

Since the actual cause of this syndrome is unknown, its treatment is also exceedingly difficult. In view of the involvement of the adrenal gland in CFS ( see CFS page ) and the well known interactions between adrenal hormones and thyroid hormones it is tempting to speculate that the answer to this mysterious syndrome may be explained by some kind of hormonal interaction. In order to consider this possibility it is necessary to first outline the types of hormonal changes which may be expected to occur in CFS ( for more details see also CFS, Stress and the Adrenal Glands ).

The available evidence suggests that CFS is characterised by a genetic adrenal weakness and excessive compensatory stimulation of the HPA axis in response to a significant stressor, usually an infection or toxin ( see CFS, Stress and the Adrenal Glands ). According to Poesnecker ( 68 ) it is the combination of adrenal weakness and excessive hypothalamic-pituitary stimulation that causes a symptom pattern which is "unique to CFS." It is during the second or resistance stage of adaptation that this unique syndrome becomes prominent in CFS patients ( 68 ). If there is a correlation between stress and altered thyroid function then perhaps anti-stress treatments such as Relora could be useful.

If, as the available evidence suggests, CFS is characterised by a degree of genetic adrenal weakness, then it would be expected that hypothyroid CFS patients would be more likely, as a group, to be hypersensitive to thyroxine. In fact, since CFS patients tend to display a hypersensitivity to a broad range of substances this would hardly be surprising. The question arises however, what impact do the HPA axis abnormalities which occur in CFS have upon thyroid function and tolerance of thyroxine?

Those who require extra support or information about thyroxine intolerance are referred to the various chat groups such as the thyroid hormone intolerance group at http://health.groups.yahoo.com/group/thyroid_hormone_intolerance/ .

Optimising the Dose of Thyroid Hormone
According to overwhelming evidence the correct dose of thyroid medication is best determined by consideration of the entire clinical picture and symptoms combined with blood tests and measurements of body temperature ( 12 ). Since no one system of diagnosis is perfect, diagnostic errors can only be minimised by utilising the full range of diagnostic tools ( 12 ). Not to do so will clearly increase the risk of errors. 

Interpretation of the TSH test is obviously a continuing problem for conventional doctors and pathology laboratories. While there is an increasing trend to regard TSH levels above 2 as being indicative of possible hypothyroidism, even this low level may not allow a sufficient margin of safety when individualities in metabolism are taken into account ( 11, 12, 109 ). Perhaps the best solution is that recommended by Shames and Shames ( 12 ) which involves keeping the TSH level at 0.5 or even less, the final decision being determined predominantly by the symptoms and clinical response. Although blood tests may be used as a guide they are far too unreliable to be used as the sole criteria for determining the correct dose of thyroid medication. As has been noted by Shames and Shames ( 12 ), "thyroid testing, by itself, should dictate neither thyroid diagnosis nor thyroid treatment."

Since many doctors still will not diagnose hypothyroidism unless the TSH is above 5 it is clear that excessive reliance upon this test remains a major cause of misdiagnosis. There are urgent reforms needed here to ensure that doctors become more determined to avoid false negative test results by adopting a less rigid approach to the interpretation of "normal" ranges and give much more priority to the patients clinical condition and how the patient actually feels. The TSH test should not be used to erroneously diagnose "depression".

Nutrition and Thyroid Function
Nutrition is involved with every aspect of thyroxine metabolism, from hormone production in the thyroid gland through to cellular transport, utilisation and conversion to T3. Zinc, iodine, vitamins A, B2, B3, B6 and C, and the amino acid tyrosine are all necessary for the production of thyroxine ( 83, 108, 109 ). Also necessary for the cellular utilisation of thyroxine or the conversion of T4 to T3 are copper, zinc, vitamin B12 and selenium, the latter being particularly important for conversion of T4 to T3 ( 11, 12, 13, 109 ). Deficiencies of any of these nutrients may adversely effect the function of the thyroid system although caution must be exercised in the use of iodine in particular. Dosages of iodine in excess of 150mcg daily may have an adverse effect on thyroid function, perhaps having an inhibitory effect on thyroid function or aggravating autoimmune thyroid diseases such as Hashimoto's disease ( 11, 12 ). According to Arem ( 11 ), excess dietary iodine intake, which may result from consumption of iodised salt, kelp supplements or certain drugs such as dyes used for X-rays, may also cause thyroiditis or thyroid cancer.

Since mitochondria are of vital importance for utilisation of thyroxine and energy production ( 91, 109 ), and there seems to be some evidence that occasionally thyroxine is impeded from entering cells or mitochondria because of damage to cell membranes or a failure of cellular transport mechanisms ( 84 ), nutrients that are involved in these processes may also be useful in some cases of hypothyroidism. Such nutrients include essential fatty acid containing oils such as fish oil and flaxseed oil ( 86, 87 ), the amino acid taurine ( 85, 88 ), coenzyme Q10 ( 89 ), and L-carnitine ( 90 ). Mitochondria are of such fundamental importance in thyroid metabolism that it has recently been suggested that a new field of research, namely, mitochondrial endocrinology, be established ( 98 ).

T4, T3, T2, T1: when T4 is not enough
The bottom line when it comes to the treatment of hypothyroidism is that cellular T3 must be restored to optimum levels, something which cannot be guaranteed by the taking of T4 supplements ( 11, 12, 13, 109 ). There is also no way that the attainment of this goal can be confirmed by blood tests.

There is abundant evidence that T3, or a combination of T4/T3, is much more effective for treating hypothyroidism than T4 alone ( 11, 12, 13, 16, 22, 23, 27, 29, 92, 93, 99, 109 ). T3 has been particularly effective in reversing the mental effects of hypothyroidism ( 11, 22, 23, 99 ), deficiency of T3 in brain cells having been related to quite a range of mental illnesses ( 11 ). Case history after case history has demonstrated that hypothyroid patients who do not respond satisfactorily to T4 respond much better when a small dose of T3 is added ( 11, 12, 13, 16, 22, 23, 27, 29, 99 ). Arem ( 11 ) claims that combined T4/T3 treatment is the "state-of-the-art treatment for hypothyroidism and a viable alternative to the most widely accepted current medical approach, which has been to prescribe T4." Similarly, according to Wiersinga ( 99 ), "recent animal experiments indicate that only the combination of T4 and T3 replacement, and not T4 alone, ensures euthyroidism in all tissues of thyroidectomized rats. It is indeed the experience of many physicians that there exists a small subset of hypothyroid patients who, despite biochemical euthyroidism, continue to complain of tiredness, lack of energy, discrete cognitive disorders and mood disturbances." In view of these facts, and the more potent nature of T3 as compared to T4, there is an urgent need for a more readily available supply of delayed absorption forms of T3 ( 99 ).

According to Arem ( 11 ), the most effective way of using T3 therapy is to initiate treatment with T4 until the patient's condition is stabilised before adding a small amount of T3. Since the optimum amount of T3 is around 10mcg daily ( 11 ), and since this is apparently equivalent to around 38mcg of T4, the procedure used by Arem is to subtract 38mcg from the total T4 dose when the 10mcg of T3 is added. The T3 should then be given in divided doses to prevent any sudden surges from excess T3.

Perhaps the ultimate form of thyroxine for difficult patients is whole thyroid extracted from animals, such as Armour thyroid tablets ( 94, 95, 96, 97 ). Whole thyroid extracts not only contain T3 and T4 but they also contain T1 and T2 ( 12, 13 ) which apparently also have some hormonal activity ( 13, 109 ). According to Brownstein ( 13 ) natural thyroid extracts such as Armour also contain, in addition to T1 and T2, a diuretic constituent which corrects the fluid accumulation which occurs in hypothyroidism. Although doctors have long assumed that T2 is simply an inactive by product which is of no consequence it has recently been suggested by Rothfeld and Romaine (109) that T2 "might be the most significant form of thyroid hormone in the body." It is now believed that deficiencies of T2 and T3 may interfere with mitochondrial energy production and cause complex mitochondrial disorders (109).

Although the availability of whole thyroid extracts in Australia is limited to specialist suppliers and compounding chemists ( 103, 104 ), their long history of successful use in America has seen these products successfully compete with the heavily promoted synthetic preparations of T3 and T4. Not only are whole glandular extracts often superior to T4 for the treatment of hypothyroidism ( 12, 13 ), but furthermore, there is some evidence to suggest that such products are also superior to combined T4/T3 preparations. Shames and Shames ( 12 ) report a patient who was treated unsuccessfully with a combination of T4 and T3 who experienced a dramatic improvement when switched to Armour whole thyroid extract. Interestingly, when synthetic T4 and T3 first became available, Arem ( 11 ) reports the considerable difficulties he experienced when switching patients from whole thyroid extracts to the new synthetic preparations. According to Arem, "the new treatment was seldom entirely successful." Arem continues ( 11 ):

Since at least a third of treated hypothyroid patients whose blood tests have been restored to "normal" continue to have symptoms ( 11, 101, 109 ), modern thyroid treatment is often unsuccessful, a fact which is hardly surprising given the fact that T2 and T3 seem to be the most important thyroid hormones. This underlines the urgent need for reforms to current methods of thyroid treatment. Clearly, much greater priority must be given to a symptomatic approach and the importance of how the patient feels. The relative ineffectiveness of T4 and the unreliability of blood tests should form a fundamental part of the medical curriculum. Since thyroid replacement therapy should aim to reproduce as closely as possible the natural secretions of the thyroid gland, there should be more support for the use of whole thyroid extracts. To this end the effectiveness of whole thyroid extract versus synthetics should be compared in clinical trials, especially involving difficult patients.

Hypothyroidism, the Adrenal Glands, and Chronic Fatigue Syndrome

In view of the numerous symptoms and signs which are common to both CFS and hypothyroidism it is hardly surprising that it has long been suspected that there is a connection between these two disorders ( 14, 109 ). However, if we are to rely on conventional thyroid tests clinical thyroid disease is rather uncommon in CFS ( 13, 54 ) although a minority of CFS patients do develop autoimmune thyroid disease ( Hashimoto's disease ) or T3 deficiency during the course of CFS ( 12, 54, 55, 109 ). Evidence suggests that CFS is also an autoimmune disorder ( 54, 56, 57, 58, 64 ).

In my case Hashimoto's disease was diagnosed around 10 years after commencement of CFS. Although I have now had clinical thyroid disease for around 9 years, my thyroid symptoms, especially after diagnosis of Hashimoto's disease, have often occurred in spite of normal thyroid laboratory tests. Having an awareness of clinical thyroid symptoms because of my Hashimoto's disease, there is absolutely no doubt that these continuing symptoms are due to a thyroid disorder, irrespective of the results of medical tests. Furthermore, these thyroid symptoms deteriorate every time I experience a significant infection which aggravates my CFS. From my experience, although CFS has the ability to cause clinical biochemical thyroid disease, it more commonly causes a vague and variable thyroid disorder which is not detectable by medical tests. Additionally, T4 treatment is only partially effective as a treatment for this CFS caused thyroid syndrome. In my case, the suggestion has been made that CFS has caused a defect in cellular transport resulting in improper transport of thyroxine into the mitochondria. Not only is there evidence of possible cellular transport defects  ( 59, 60, 61 ) and mitochondrial dysfunction ( 62, 64 ) in CFS, but furthermore, it is also known that stress, which forms a fundamental part of CFS, may cause thyroxine conversion problems ( 16, 27, 29 ) (see above). The vital importance of mitochondria for energy production is also well known ( 63, 65 ).

When it comes to the connection between CFS and thyroid disease there seems little doubt that CFS has the ability to significantly alter the metabolism of thyroxine. Although some workers have reported that some CFS patients respond positively to thyroid treatment ( 12, 13, 66, 67 ), even in the absence of laboratory evidence of thyroid disease ( 13, 66, 67 ), others have found the results of thyroid treatment disappointing ( 54 ). In the latter case it has been suggested that CFS may be characterised by resistance to thyroid hormone or an inability to convert T4 to T3 ( 13, 54, 109 ). Bell ( 54 ) has noted that elevated levels of cytokines may block the metabolism of thyroxine.

Interestingly, reduced adrenal function, which is common in CFS ( see CFS page ), may cause hypothyroid symptoms by blocking the conversion of T4 to T3 ( 12, 13, 46, 51, 52, 53, 68 ). Additionally, the adrenal hormone DHEA which stimulates the conversion of T4 to T3 is commonly deficient in both CFS and hypothyroidism ( 68, 69 ). In view of the well known adrenal abnormalities which may occur in CFS, thyroid changes which occur in this disorder may be the result of CFS rather than the cause of it. Increasingly, evidence seems to suggest that many cases of hypothyroidism, particularly those that are more difficult to diagnose and treat, also involve a degree of adrenal hypofunction. In view of the fact that T3 therapy may be more effective when there is adrenal involvement (109) and in view of the fact that around 50% of hypothyroid patients also suffer from adrenal fatigue (109), conventional T4 therapy is rapidly becoming outdated.

It is also interesting to note that elevated cortisol levels may also adversely effect the metabolism of thyroxine ( 46, 52 ). Victims of Cushing's syndrome ( excess production of cortisol ) also have "a remarkably high prevalence of primary thyroid disease" ( 70 ) while resolution of the Cushing's syndrome is associated with the onset of autoimmune thyroid disease ( 70 ). What makes these observations even more interesting is that a deficiency of DHEA may cause the same features as elevated cortisol levels even when cortisol levels are normal ( 72, 73, 74 ). While DHEA supplements may enhance immunity ( 69 ), deficiency of DHEA has been linked to autoimmune diseases ( 69 ). It has also been suggested recently that the "Metabolic Syndrome" or "Syndrome X" may actually be caused by a form of Cushing's syndrome in which cortisol levels are normal ( 71 ).

Conclusion

When it comes to the treatment of hypothyroidism, patients should seek a practitioner whose aim is to optimise the health of patients rather than simply normalise the results of blood tests. The patient's desire and determination to obtain optimum health should be supported by the practitioner. Any practitioner who is up to date with proper treatment will also readily acknowledge the superiority of T3 treatment, combined T4/T3 treatment, or treatment with whole thyroid extracts. Such practitioners will not rigidly adhere to outdated T4 treatment if their patients are not progressing satisfactorily. In view of the reluctance of many within orthodox medicine to embrace treatment with T3 or whole thyroid extracts there seems to be a remarkable scarcity of clinical trials comparing these treatments, especially in regard to treatment of more difficult patients. Given the multitude of clinical trials conducted upon all manner of drugs this is a deficiency that needs to be rectified immediately.

In view of all these facts, anyone who suspects they may be suffering from thyroid disease would be well advised to maximise their chances of obtaining an accurate diagnosis and effective treatment by consulting a holistic practitioner who is prepared to openly acknowledge the limitations of conventional thyroid blood tests. The practitioner should also have a determination to avoid unnecessary false negative test results because of the unscientifically rigid interpretation of "normal ranges". The responsible practitioner will not simply dismiss the results of clinical examination and history, and consistently subnormal body temperature, merely because of the result of blood tests. 

It should be borne in mind that although the conventional doctor may be highly skilled in the science of medicine, the holistic practitioner on the other hand is highly skilled in the art of healing. The patient should make an informed choice.

Other Useful Links
www.dcnutrition.com/problems/Detail.CFM?RecordNumber=234
www.thyroid-info.com/
http://thyroid.about.com/cs/basicinformation/index_2.htm

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This page was last updated on 18/05/09
Copyright © 2000 Graham Williamson
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