Hypothyroidism - the disregarded epidemic

Tom Stockdale is a past chair of the Scottish branch of the MacCarrison Society, a retired farmer and farm recorder for ICI, and a long time sufferer from selenium deficiency. He adds his thoughts on the 'Great Thyroid Debate'

The thyroxine molecule is activated when either of two enzymes removes one of its four iodine atoms. Deiodinase is a seleno-protein but deiodinase II is not. When the supply of deodinase I is restricted by selenium deficiency the release of thyroid stimulating hormone from the pituitary is increased and this produces an inhibitory effect upon deiodinase II . Thus, hypothyroidism can be induced by either iodine or selenium deficiency.

By depressing the rate of metabolism hypothyroidism lowers the basal rate of ATP synthesis so that when the stress upon a particular tissue is increased by environmental, nutritional, pathological or emotional factors the tissue is handicapped in its response: it is like an athlete who is made to start a race from behind the usual starting line. I identify the brain, the immune system the gonads, breast tissue and the pancreas as tissues which usually fail to function normally in individuals who are suffering from hypothyroidism. Typical symptoms are depression, increased susceptibility to infection, infertility, cancer and indigestion.

Because the gluten in white wheat flour is potent in stimulating the production of gastric acid, and because it takes less energy to produce gastric than pancreatic bicarbonate, the material entering the duodenum of those who are suffering from hypothyroidism is not properly neutralised. This induces reflux, which can lead to the formation ulcers as well as stomach and oesophageal cancers.

Moreover when the material entering the small intestine is too acidic the digestive enzymes are unable to act efficiently and digestive upsets together with food intolerances follow. When incompletely digested and potentially toxic material has been absorbed into the blood stream the autonomic nervous system is activated and increasing amounts of adrenal cortical hormones are released. In addition the autonomic nervous system causes celiac disease by enabling serotonin to be released into the crypts of the villi of the small intestine.

One of the many effects produced by adrenal cortical hormones takes place in the liver and is known as gluconeogenesis. This process, by destroying amino acids, and especially tryptophan, decreases their availability to brain tissue. 

Within the brain trytophan is synthesised into serotonin, niacin and melatonin. More of the latter is produced in winter than in summer and so less tryptophan is available for synthesis into serotonin and niacin. Shortages of either of these, by restricting the rate of ATP synthesis, can cause Seasonial Affective Disorder or a more general depression.

Because the endogenous synthesis of niacin is inhibited by oestrogens women are more subject to depression than men. This, together with the long winters in the north of the UK, explains why it is that women are more susceptible to multiple sclerosis than men and why there is more of this disease in the north of the UK than in the south. An inadequate supply of tryptophan to the brain, when associated with the low rate adenosine synthesis is that results from folate deficiency, can cause Alzheimer’s, and failure to synthesise sufficient GTP when associated with tryptophan deficiency can lead to Parkinson’s.

Much of the ATP that is synthesised is used to move ions and nutrients across plasma membranes and this is a major factor is maintaining body temperature. Selenium deficiency causes cold feet because as deficiency develops it is concentrated in the thyroid gland, but iodine deficiency makes all external tissues cold sensitive. Under production of ATP depresses the rate of recovery of essential elements by the kidneys and this may explain the excessive salt consumption which is today so common. Under-production of ATP is associated also with an increase in the concentration of intracellular calcium ions. But, because calcium ions stimulate ATP synthesis and ATP is needed to expel an excess of intercellular calcium ions, under production of ATP leads to a loss of homeostatis, which presents as Attention Deficit Hyperactivity Disorder. Girls usually do not suffer from this condition because the inhibition of niacin synthesis by oestrogens and the consequent shortage of NAD+ prevents the level of ATP synthesis required to cause hyperactivity being reached.

In order for prostaglandins, leukotrienes and thromboxane to be synthesised from arachidonate the latter to be released from the phospholipids within the cells by an enzyme which is activated by calcium ions. Normally the concentration of these ions  is insufficient to activate the enzyme, but the more deficient in iodine or selenium an individual may be the more likely it is that the enzyme will be activated inappropriately. The presence of this situation appears to provide the basis for most  autoimmune disease. For instance in asthma the mast cells degranulate in response to a stimulus provided by  an allergen which increases their intracellular calcium ion concentration. When the intracellular calcium ion concentration within these mast  cells is already abnormally high, due to the failure of the cells to synthesise sufficient ATP, inappropriate and large-scale deregulation will follow.


Many hormones and drugs increase the flow of calcium ions into cells and when they are not promptly expelled they can accumulate until they destroy the cells, as happens in Alzheimer’s and Parkinson’s. Osteoporosis may be caused by the presence of too many calcium ions in cells preventing the synthesis of the most active form of vitamin D. In the glands and breast tissues the intracellular concentration of calcium ions is increased by pituitary sex hormones and, in individuals who suffer from hypothyroidism, the abnormally high concentration instead of being used to stimulate metabolism may be used to stimulate cancerous growth. Conceivably, the desmolase reaction is slowed in some of those with hypothyroid problems. This reaction involves the first stage in the synthesis of adrenal cortical steroid hormones, testosterone and oestrogens. The decreased production of these hormones could explain the incidence of homosexuality, premature birth and the delayed failure by adolescents to close their bone epiphyses which results in increased height

The low spirits and decreased physical activity associated with hypothyroidism may act as an incentive for some to take drugs. It needs also to be kept in mind that heavy metals can decrease the availability of both iodine and selenium. Mercury combines with both, so is it possible that autism is an iatrogenic form of cretinism when it develops following vaccination with MMR?

As hypercholesterolemia, diabetes and obesity are classic symptoms of hypothyroidism is it surprising that so many unsatisfactory explanations have been offered to explain these conditions. Hypothyroidism adversely affects the formation of oleic acid in the liver and presumably also certain polyunsaturated fatty acids. The absence of sufficient oleic acid in low density lipo-protein causes free cholesterol to accumulate in cells. The presence of this uncombined cholesterol inhibits low-density lipoprotein receptor synthesis and causes the lipoprotein to accumulate in blood. This deprives the tissues of the amino acids and unsaturated fatty acids, which would otherwise be used by cells for maintenance purposes. Membranes become thin and blood vessels more likely to haemorrhage, especially on the backs of the hands and in the brain where they cause strokes.

This paper is not intended to be a scholarly, comprehensive or detailed account of the consequences of hypothyroidism. It is an attempt to bring together a range of information, which will encourage investigation and stir up complacency. I think it fair to state that of the many diseases referred to above there is not one that has been properly researched and understood. Yet few of these diseases were common in the UK sixty years ago. The present situation is lamentable and should stimulate vigorous criticism of the leadership of the medical profession and the system by which research grants are rewarded. One scientist has complained of being unwilling to write a grant application to enable an aspect of selenium deficiency to be investigated because the usual response by the research council to such requests is to state that there is insufficient evident to prove that such work is needed.

How much evidence is needed, and how is to be obtained without a research grant? The problem lies within the research council and with the failure of its members to understand what is happening in every hospital and surgery. Diseases which are caused by vitamin or mineral deficiencies cannot be cured by the use of drugs and attempts to cure them with drugs are inevitably expensive failures.

 

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First Published in 2007

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