Chronic Fatigue Syndrome and Fibromyalgia
By Robyn Koumourou 2000
A question that is frequently asked is “Is there a connection between Chronic Fatigue Syndrome (CFS), or Fibromyalgia Syndrome (FMS), and thyroid function disorders?” For some people diagnosed with CFS or FMS the answer is definitely “Yes”. When a doctor has run relevant tests to rule out the possibility of other conditions and has not found any particular cause for a person’s ill health, the diagnosis of chronic fatigue may be made. The symptoms that arise when a person is suffering with CFS are almost identical to the most classic symptoms of hypothyroidism. Thyroid function test results often appear completely normal (within the reference ranges) in many cases and then no further investigation of thyroid dysfunction is considered.
Could various thyroid disorders be a possible cause or co-factor in the development of CFS and fibromyalgia in some individuals?
A significant proportion of people diagnosed as having CFS do have undiagnosed thyroid disease. In many cases thyroid function tests are not ordered or are not extensive enough to rule out thyroid disease as a possible cause.
At present, CFS and FMS are classified as syndromes, rather than diseases, due to the fact they do not have a known cause, and cannot be identified with a single laboratory test. They are diagnosed by exclusion of all other potential causes. For each person diagnosed with CFS and FMS the causative factors will be different. It may be possible that multiple causes occurring simultaneously contribute to the signs and symptoms present in a person suffering with chronic fatigue.
Chronic fatigue syndrome (CFS) and fibromyalgia (FMS) are debilitating conditions, which need to be taken seriously. Current medical research has demonstrated that people suffering with these conditions have definite alterations in biochemical pathways and interference with chemical processes related to the endocrine, nervous and immune systems. The actual cause for these abnormalities is not yet fully known, although it is more than likely that multiple health conditions occurring simultaneously contribute to an abnormally functioning body. Some of the possible triggering factors established include: imbalanced gut flora due to over-use of antibiotics, viruses and other infectious agents, toxic and chemical substances (e.g. pesticides, aluminium, mercury), hereditary disorders, autoimmune conditions, injury or accident affecting brain function and the nervous system, drugs and their side-effects, allergies and intolerances, severe nutritional deficiencies, and sometimes severe trauma or prolonged stress. Any one of these factors or a combination of these can be the recipe for the development of a chronic health condition. The development of one condition, such as imbalanced gut flora, can set the stage for more problems developing and a vicious cycle of abnormal body functioning continues.
The Signs and Symptoms
The signs and symptoms of chronic fatigue syndrome and fibromyalgia can be many and varied, and often differ slightly from one individual to another. CFS is a disorder usually characterized by unrelenting fatigue or exhaustion, generalized muscle aches and pains, poor memory and concentration, mood swings and sleep disorders, balance and visual disturbances, digestive complaints, poor temperature control, headaches and reduced circulation. Fibromyalgia is predominantly characterized by ongoing musculoskeletal pain and fatigue, often together with other symptoms of CFS. Fibro means fibre, my means muscle, and algia means pain. Patients with fibromyalgia may initially be diagnosed with arthritis, usually because they ache all over, sleep poorly, and remain stiff, sore and tired all day. The pain can be mild to severe, affecting a number of muscles, tendons, ligaments and soft tissues. Individuals with FMS are also prone to headaches, memory and concentration problems, dizziness, numbness and tingling, itching, fluid retention, cramping abdominal or pelvic pain, diarrhoea, and chest pain - just to mention a few.
Many doctors and researchers have discovered that the majority of people presenting with the symptoms of chronic fatigue and muscle/joint pain are hypometabolic (have poorly functioning cell and tissue metabolism). Blood flow, oxygen and nutrient transport are reduced to all parts of the body, including the brain, and energy production is hindered. The brain, muscle and nerve cells can be particularly affected as normal cell function is undermined. The causative factors that impede the metabolism of cells and specific tissues may be numerous, and will differ from one individual to the next. However, one possible cause of hypometabolism that should never be overlooked is thyroid hormone deficiency.
Possible Thyroid Connection
Any person, who is diagnosed with CFS or fibromyalgia, should explore the possibility that a thyroid disorder could be the cause or a co-factor in the development of their condition. Thyroid hormone deficiency can account for the various signs and symptoms present in these illnesses. A thyroid disorder may be easily overlooked using conventional methods of assessment and the correct diagnosis may be missed. Laboratory blood tests are often poorly interpreted, and frequently not all thyroid hormones are assessed to establish a more accurate picture of thyroid function. Many people who have been diagnosed with chronic fatigue or fibromyalgia have suffered for years unnecessarily before finally being told that they have a thyroid condition, in particular autoimmune hypothyroidism (Hashimoto’s thyroiditis). Treatment with thyroid hormone replacement has been life saving for many, as their debilitating symptoms have slowly disappeared, or have been greatly relieved.
Similarly, there have been many thyroid patients on thyroid hormone therapy who have, over time, developed more and more muscular and joint aches and pains, only to be told that they are also suffering with arthritis or fibromyalgia. In many of these cases their symptoms are the result of inadequate thyroid hormone replacement (under-dosing). Some patients may simply need to increase their thyroxine dose, while others may benefit from a combination of T4 and T3 hormones in a synthetic or natural form. Treatment for hypothyroidism should be aimed at normalizing tissue metabolism, not simply normalizing thyroid hormone levels to somewhere within the reference ranges. When it comes to thyroid hormone replacement, the fine-tuning of dosage is vital as everyone has a personal set point for their TSH and thyroid hormone levels within the normal reference ranges. Even a slight deviation away from that personal set point can result in symptoms of thyroid dysfunction.
In the Medical Journal of Australia (2001), Dr John Walsh and Dr Bronwyn Stuckey discussed what the optimal treatment for hypothyroidism was according to the latest research:
"There is evidence that individuals have different set points in the relationship between serum thyroxine, T3 and TSH concentrations. The reference range for TSH is wide (typically 0.3-4.0mU/L) and not normally distributed, with a mean and median in the lower part of the range, at about 1.5mU/L. Thus, a serum TSH concentration of 4.0mU/L, although within the reference range, might reflect significant undertreatment for a patient whose optimal thyroxine replacement dose would result in a serum TSH concentration of 0.4mU/L."
Professor Jim Stockigt, head of Endocrinology at the Alfred and Epworth Hospitals, stated in an interview with Sigma Pharmaceuticals, March 2001,
"When we have normal population data for serum TSH we need to log-transform the values in order to get the familiar bell-shaped curve that defines a normal distribution. The normal range is usually quoted as about 0.4 to 4mU/L (milliunits per litre), but the log transformation introduces one peculiarity - it moves the mean and median values for TSH down towards the lower end of the range - at about 1mU/L. The upward tail between 2 and 4mU/L is rather thin, and there is room for doubt as to whether values in this range are actually normal or not. The important point is that when normalizing TSH by treatment, our target (the mean and median) TSH value should generally be around 1mU/L. If we simply aim for TSH values in the middle of the range, some individuals will remain under-treated."
Patients on thyroid hormone replacement need to work closely with their doctors to ensue that their thyroid hormone levels are optimised individually. Under replacement may result in continued symptoms of hypothyroidism that may be mistaken as CFS or fibromyalgia.
Some researchers and innovative doctors have chosen to treat primarily CFS and FMS patients. They have incorporated various treatment protocols to better the health of these individuals. These include nutritional supplementation, immune system enhancers (antioxidants, herbs), consideration of infectious agents, relaxation and exercise, and thyroid hormone replacement therapy where indicated. Interestingly, a large percentage of their patients responded and improved dramatically when they were given thyroid hormone replacement. This has lead some doctors to believe that many people suffering with CFS or FMS actually have inadequate thyroid hormone regulation, either due to high thyroid antibody levels, thyroid hormone deficiency, or poor utilization of thyroid hormones at the cellular level. These abnormalities can account for the wide range of symptoms experienced by people with these chronic conditions.
In the article “Fine-needle aspiration cytology of the thyroid in chronic fatigue”, The Lancet (Volume 357, No’ 9260, 24 March 2001), https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(05)71654-8/fulltext Swedish researchers investigated 219 patients complaining of suffering with chronic fatigue for more than 1-year duration. Using a fine needle aspiration biopsy (FNAB), they studied a small sample of tissue taken from the volunteer’s thyroid gland, and found that 87 of these patients had definite cytological lymphocytic thyroiditis (autoimmune thyroid disease).
In addition to the FNAB findings, conventional biochemical thyroid function tests were performed. Of the 87 patients, 50 had a TSH level within the normal reference range, while 37 were outside of the reference range indicating an obviously poorly functioning thyroid gland. All 87 of these patients were then given thyroid hormone replacement, irrespective of their initial TSH level, and monitored carefully. The clinical response to taking thyroxine proved to be equally favourable among all of the patients who had been diagnosed with lymphocytic thyroiditis, and their chronic fatigue symptoms resolved.
Conventional laboratory blood tests sometimes reveal very little, and often appear perfectly normal when conventionally interpreted, even when symptoms indicate a metabolic problem. It is still not the standard protocol in many countries to test for autoimmune thyroiditis (by assessing levels of thyroid antibodies) in patients presenting with chronic fatigue symptoms. A positive result revealing high antibody levels may be the only abnormality found, long before thyroid hormone levels become abnormal. Positive thyroid antibodies confirm the diagnosis of autoimmune thyroiditis and may be the cause of the person’s chronic fatigue symptoms. The conclusions drawn from the 2002 Whickham study stated that high antibody levels are a strong predictor of later overt hypothyroidism. See chapter 12.
The processes in various autoimmune conditions can have quite a profound effect upon the body. The immune system, endocrine and nervous systems are all involved, causing a cascade of chemical reactions. These can present themselves as flu-like symptoms, such as unrelenting fatigue, muscle/joint pain and weakness and a generalized brain-fog. Further investigation into autoimmune thyroiditis should always be considered with any individual presenting with the classic symptoms of hypothyroidism or CFS and FMS. Any family history of autoimmune disorders is also a strong indicator of the possible cause of a person’s ill health.
Another complication that can occur in some individuals is the poor utilization of thyroid hormones at the cellular level. Thyroid hormone levels in the blood stream may appear within normal limits, but their effects at the cellular level may be hindered. Hypothyroidism due to faulty cellular metabolism may be difficult to establish. In rare individuals, the receptor sites for thyroid hormones in the cell nucleus are abnormal, and the hormones cannot be used effectively by the cell to regulate cellular metabolism. This is often referred to as generalized resistance to thyroid hormone. It is due to a genetic defect, and usually discovered at birth, although unfortunately, not in all cases. More commonly, enzyme deficiency, and poor conversion of T4 into T3 hormone in peripheral tissues and target organs may be responsible for cellular hypothyroidism. The less active T4 needs to be converted into the highly active T3, to maintain cellular function. Acute or chronic stress, fasting, illness, infectious agents, and elevated adrenal hormones can all have a profound affect on our cells’ abilities to function normally. It is known that the conversion of T4 into T3 can be inhibited by other hormonal imbalances, major surgery, B-blockers, Lithium, corticosteriods, and mercury toxicity. It is also medical fact that in times of stress the body protects itself by slowing down the metabolism, less T4 is converted into free T3, and T3 levels drop.
For those with hypothyroidism as a result of faulty cellular processes, the difficulty comes when a diagnosis is being made, as conventional thyroid function tests may reveal nothing unusual. Regular testing of free T3 levels may be of value here and reveal a problem if consistently low.
Treatment for individuals with faulty cellular metabolism may involve removing hindering factors (such as various interactive drugs, infectious agents, allergic substances, stressful situations) or correcting other hormonal imbalances (adrenal or ovarian hormones). Larger than normal doses of thyroid hormone replacement (T4), may be required to correct the imbalance in some patients. For others, small doses of T3 hormone are sometimes necessary. These have been used successfully alone, or in conjunction with T4 therapy.
Following the publication of the article by Robertas Bunevicius et al, “Effects of Thyroxine as Compared with Thyroxine plus Triiodothyronine in Patients with Hypothyroidism”, there has been a great debate amongst thyroid patients around the world about the benefits (or not) of using T3 as well as T4 for thyroid hormone replacement. This article, published in the New England Journal of Medicine (February 11, 1999 -- Vol. 340, No. 6), reported that:
“a combination of thyroxine and triiodothyronine, approximating the ratio normally secreted by the thyroid gland, resulted in significant improvements in mood and neuropsychological function, as compared with a higher dose of thyroxine alone, in the same patients”.
Since this article was published an Australian double-blind randomised trial was conducted, and appeared in the Journal of Clinical Endocrinology and Metabolism.  https://pubmed.ncbi.nlm.nih.gov/14557419/ Researchers sought to compare the effects of T4 therapy alone and T4/T3 combination therapy on the symptoms of hypothyroidism and quality of life. The conclusion from this trial was that combination therapy as administered in the study was no better than T4 alone in restoring quality of life and cognitive functions. However, the authors admit that this experimental trial did have its faults in that a fixed quantity of T3 was used in substitution of T4 and was administered in a single dose. The amount of T3 used was standardised and there was no consideration of personal T3 dose requirements. There is clearly need for more investigation and carefully controlled studies on this issue. So far some studies seem to confirm the benefits of combined hormone therapy, and it may be particularly important for those individual’s who do not feel well on thyroxine alone. https://pubmed.ncbi.nlm.nih.gov/15705921/
Overall, there are many factors that come into play where CFS and FMS are concerned. Every individual is biochemically unique, and throughout their lifetime will be influenced by different things and experiences. When sickness and disease take hold, it is difficult to establish what the triggering factors may have been; as a result, the cause may never be fully realized. For some patients with CFS and FMS, low dose antibiotics have resolved their health problems when a bacterial cause has been found. Some patients and doctors have been able to pinpoint allergies and intolerances to various substances and foods, which when eliminated have brought relief of symptoms. For others, chronic fatigue symptoms have slowly disappeared with time, simply by having adequate rest, a healthy, well balanced diet and correcting any nutritional deficiencies. Again, others have been shown to have problems with pituitary and hypothalamus function or hormonal imbalances related to different endocrine glands. Whatever the causative factors, a multifaceted treatment protocol will more than likely be required if a person’s health and well-being are to be restored.
“A major and often overlooked cause of chronic fatigue syndrome is an underactive thyroid gland (located in the neck), a condition known as hypothyroidism. Although, according to conventional medicine, hypothyroidism is a separate illness from CFS and a diagnosis of one precludes a diagnosis of the other, many people with CFS have not been properly tested for thyroid problems. Since thyroid hormones are integral to maintaining optimal body energy and are required for proper immune system function and nearly all aspects of body function, hypothyroidism can be central among the multiple factors involved in creating CFS. If that is the case, successfully reversing the syndrome will require discovering the hidden thyroid imbalance along with all the other contributing factors”.
Relevant Article: 'Pure T3 Thyroid and Stories of Recovery from ME/CFS and Fibromyalgia: An Overview' - HEALTH RISING
 Drs John P Walsh and Bronwyn G A Stuckey, "What is the optimal treatment for hypothyroidism?" Medical Journal of Australia, 2001;174:141-143 [Thyroid Australia, Thyroid Flyer, 2:4, October 2001.] https://7c6d4c62-9d52-4bd0-a2e4-c3a8bcb1fe50.filesusr.com/ugd/a3a40a_beb8ae4abbda4133b250ace9ab7dad88.pdf
 Prof Jim Stockigt. “Subclinical hypothyroidism or Mild thyroid failure: How important is early diagnosis and what treatment is optimal?, Sigma Pharmaceuticals, March 2001. [Thyroid Australia, Thyroid Flyer, 2:3, July 2001.]
 Dr Anthony D. Toft. M.D. Royal Infirmary. “Thyroid Hormone Replacement -- One Hormone or Two?”, The New England Journal of Medicine, Feb 11, 1999 – Vol.340, No.6. file://D:\Articles\Hypothyroidism\Editorials – NEJM 1999: 340 469-470.htm
 John P Walsh and others, “Combined thyroxine/liothyronine treatment does not improve well-being, quality of life or cognitive function compared to thyroxine alone: a randomized controlled trial in patients with primary hypothyroidism”, Journal of Clinical Endocrinology and Metabolism; 88(10): 4543-4550. https://pubmed.ncbi.nlm.nih.gov/14557419/
 Burton Goldberg. “Chronic Fatigue, Fibromyalgia and Environmental Illness”. Future Medicine Publishing Inc, Tiburon, California 94920, 1998. Pg. 164 (no longer available). Relevant link: 'Illness from low levels of environmental chemicals: relevance to chronic fatigue syndrome and fibromyalgia' https://pubmed.ncbi.nlm.nih.gov/9790486/
© 2000 by Robyn Koumourou
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