Hypothyroidism is due either to:
A. Deficiency of thyroid hormone production, or
B. Failure of thyroid hormone to reach the tissues.
Both may operate together in varying degrees.
Deficiency of hormone production is due to:
1. Environmental toxins/deficiencies2. Genetic thyroid failure
3. Thyroid failure secondary to pituitary insufficiency
4. Thyroid surgery
5. Treatment of previous over-activity
6. Major surgery
7. Tonsillectomy
8. Major trauma
9. Glandular fever
Failure of hormone to reach the tissues results from:
1. Receptor resistance, or failure2. Dysfunction of T4-T3 conversion
3. Adrenal insufficiency
Dealing in turn with the therapeutic management of these problems, we may turn first to (A)Thyroid hormone production failure. This will be due to:
1. Environmental toxins and deficiency
a)Toxins
-A number of chemical agents tend to interfere with the manufacture of thyroid hormone. Notables among these are:
-Poly chlorinated Biphenyls (Paints and wood preservatives)-Resorcinol (Millet)
-Phthylate Esters (Plastics)
-Thiouracil (Cabbages, Turnips, Cassava)
-Anthracin
-Bromoform
-Cyanides (Barbiturates
-Fluorides
-Thiocyanates (Smoking)
-Caffeine
-Aspirin
-Lithium
-Amiodarones
The elimination of these from the diet may be desirable, if not always practical.
b)Nutritional Deficiencies
(i) Iodine. Endemically absent in certain inland areas, e.g., Peak District, UK.
(ii)Minerals, in particular:
-Selenium-Iron
-Magnesium
-Zinc
(iii) Vitamins
Vit A - Conversion of Carotene to Vit A is inhibited by low thyroid states, and may cause yellow pigmentation. It controls uptake of Iodine into the thyroid gland. Deficiency also reduces TSH
Vit B Riboflavin, Niacin, Pyridoxine play a role in thyroid hormone manufacture.
Vit C and Vit E - Deficiency has been shown to cause hyperplasia at cellular level in the thyroid. Clearly, part of the management of hypothyroidism requires some dietary advice; the provision of iron and vitamins and other minerals is simple and obvious.
2. Genetic Thyroid Failure
This will have become apparent soon after birth; but may not be obvious cretinism. A sickly child, with poor weight gain, frequent infections, lethargy, or oddly enough, hyperkinesia, and is a candidate for genetic poor thyroid function. Thyroid replacement is mandatory as early as possible.
3. Pituitary Failure
This is a more common problem than is recognized, and apart from its specific clinical features, it may be a cause of secondary hypothyroidism. The pituitary may have a genetic deficiency, when it will have been probably recognized early. Not uncommon is Sheehan’s Syndrome, resulting from major trauma from accidents or surgery. Adenomas of the pituitary may cause pressure atrophy and / or abnormal hormone outputs. But the pituitary may be involved in the general multiple deficiency state, and more specifically in low thyroid states. This partial failure in hypothyroidism may well be a cause of low TSH, so that a vicious spiral may slip into being. The danger of a low or normal TSH in this situation being misinterpreted when thyroid function tests are carried out is quite clear. In this situation, correction of the thyroid state will bring benefits to the pituitary; and may explain why some patients on thyroid replacement therapy begin to need lesser doses as time passes. Correction of the thyroid deficiency is clearly necessary; but adrenal insufficiency, considered in more detail later, as a consequence of lowered ACTH output, may require cortisone and Dehydroepiandrosterone (DHEA) in addition.
4. Thyroid Surgery
This is undertaken as a treatment for pathology of the thyroid itself, or as a treatment for over-activity, discussed below. Thyroid cysts, adenomas or carcinomas are necessarily removed by surgery; and it is sometimes necessary to remove goiters where the size is causing respiratory or oesophageal embarrassment. Hashimoto’s disease may come into this category.
Replacement by thyroid hormone is an obvious consequence.
5. Treatment of previous thyroid over-activity, by surgery or I131 ablation
Grave’s disease is widely treated, where medical methods are deemed unsatisfactory, by partial thyroidectomy, or Radioactive Iodine ablation. This is often unsatisfactory, since it is very difficult to get it right. Either too much is removed or destroyed; (in which case replacement therapy is a permanent necessity) or too little, and it may have to be done again.
For such patients, replacement therapy is an obvious no-option requirement.
6. Major Surgery
Most particularly in this context comes cholecystectomy and hysterectomy. Many doctors are aware that women may suffer weight gain and loss of well being after this surgery; and this will be found to be due to early loss of thyroid function. Replacement therapy is required.
7. Tonsillectomy
Quite why in adults, tonsillectomy may result in slow running down of thyroid function is not clear, but may be the result of interruption of the blood supply. The present writer has noted a number of cases of young adults misdiagnosed as M.E sufferers in this situation. Replacement therapy provides a most satisfactory return to normal.
8. Major Trauma
Major road traffic accidents, and surgical accidents are known to precipitate thyroid and/or pituitary insufficiency. In this category have been noted the major psychic trauma of certain life events. Replacement indicated, with regard given to pituitary/adrenal function.
9. Glandular Fever
This is an often met with cause of failure of the thyroid/adrenal axis. Evidence has pointed to pituitary damage causing secondary hypothyroidism, but progressive loss of thyroid-producing cells within the thyroid has been noted. In either event, replacement is required. Discussion of failure of uptake at tissue level may be conveniently dealt with in the section below on therapeutic options. Consideration should now be given to the aims of replacement therapy.
The overall purpose is to restore metabolism to normal, so as to eliminate all hypothyroid symptoms, and to secure a sense of normal well being. This implies that thyroid hormone levels in each and every cell are nominal; that all the exchange reactions are taking place, as they should be. Sadly, this ideal is at least as often as not, simply not reached, often by a long way. Residual tiredness, lack of drive, or depression is frequently admitted to. Menstrual dysfunction may remain a feature. Skin problems, fluid retention, digestive problems, or arthralgia may remain in some degree. Many patients will continue to complain of weight gain, or great difficulty in losing it, and receive scant sympathy.
In this situation, the physician may estimate thyroid function by Free Thyroxine Index (Free T4), or Thyroid Stimulating Hormone (TSH) and be confronted by normal readings. It is the present writer’s view that these estimations may be seriously flawed, and their value fundamentally limited. The most popular, at the moment, is the TSH. This may be much affected by poor pituitary function itself due to hypothyroidism; it may be low or normal, rather than raised. The Free T4 test is subject to several errors. Poor tissue uptake is probably the most telling. If the actual use by the tissues is reduced by poor conversion of T4 to T3 (see below) and/or receptor block, then high or normal Free T4 blood tests will result. Haemoconcentration may be an additional factor.
There can be no substitute for proper clinical appraisal. If the patient sounds and looks hypothyroid, then probably that is the problem, irrespective of pathological testing.
The net result very much too often in clinical practice is to under-dose. To provide full remission of symptoms, the level in the tissues of thyroid hormone should be as high as possible, short of too much. (The patient/doctor monitoring to achieve this is described later). The situation is worsened by a tightly held misapprehension in many quarters that there are grave risks associated with overdose. These are largely apocryphal and must be corrected. Probably most widely held, is that thyroid overdose is bad for the heart. The risk is there if coronary artery insufficiency, previous M.l or incipient failure already compromises the heart; the risk of over working a damaged heart is obviously undesirable. The healthy heart will not be damaged by minor degrees of overdose, whether by accident or design; and is rarely much affected even by high levels of thyroid hormone, as in Grave’s Disease.
Another anxiety is osteoporosis. There is a risk in sustained overdose, and untreated hypothyroidism, but this is still not certain. There is NO risk of osteoporosis in thyroid supplementation in correct, physiological doses obviously; and in any inadvertent minor overdose is rapidly detected by monitoring, and therefore of no consequence either.
Suppression of the thyroid gland as a result of treatment is another frequently expressed anxiety. There is a sensitive negative feedback operating through the hypothalamus and the pituitary Overdose will suppress the thyroid; but this will come back to normal at once when the dose is adjusted. Not treating a patient with an under-active thyroid for tear of promoting further depression is quite unrealistic.
Vague fears that thyroid is like "speed"; that any deliberate or accidental overrunning of the metabolism will result in early "burn out" have been expressed. All that can be said is that is simply not true.
The correct management of thyroid replacement requires a flexible approach; full explanation to the patient, and monitoring, relying as much on the patient’s assessment as the physician’s own clinical impression. One may often be obliged to deal with partial response to replacement therapy, with failure to respond to an increase of dose; and more wrongly, some symptoms of overdose on small levels of treatment. These will include raised pulse rate, tremor, breathlessness, headaches. Sometimes an encouraging response levels off and drops back.