What Doctors Don't Tell YouGeneral practitioners are in a good position to spot major failings of the medical options available to us. High on the list is the inadequate way we deal with heart disease risk. In 1980, I came across the work of Dr Broda Barnes (Solved: The Riddle of Heart Attacks, Fort Collins, Colorado: Robinson Press Inc, 1976) and quickly realised how large a contribution he had made to our understanding of thyroid deficiency.
Barnes was a thyroid physiologist who subsequently trained as a doctor and practised medicine from 1937 until the late 1960s. He questioned the validity of thyroid hormone measurements and advocated a return to functional tests of the effects of those hormones, of which the basal temperature is both the easiest and (in his view) the most reliable (JAMA; 119: 1072-4).
As a scientist, Barnes demonstrated that around 10 per cent of the US population had a subnormal basal temperature due to lowered metabolic rate, and worked out the pathological implications of this greater susceptibility to tuberculosis (TB) and coronary artery degeneration. People who began surviving TB in the 1950s suffered early heart attacks instead from the 1970s onwards, which Barnes the doctor aimed to prevent. The clinical research of his contemporaries Drs W. Kountz, M. Chieffi (Geriatrics, 1947; 2: 6, 344) and J. Wren (J Am Geriatr Soc, 1968; 16: 696- 704) suggested that some 80-90 per cent of heart attacks and related deaths could be prevented in this way.
Meanwhile, the standard treatment for thyroid deficiency was changing. Until around 1970, Dried Thyroid Tablets BP, a standardised preparation composed of the thyroid glands of slaughtered food animals, was the usual medication. This treatment contained known amounts of iodine and thyroid hormones together with other proteins. Its potency varied somewhat between batches and weakened appreciably as it aged so that physicians welcomed the introduction of pure sodium l-thyroxine (T4) which rapidly superseded it. Although triiodothyronine (T3) is sometimes used as well as or instead of thyroxine, the latter remains the standard treatment for thyroid deficiency. Although few doctors had any doubts about this transition, it is apparent that something had been lost.
One of the features of lowered thyroid activity is an increase in the level of cholesterol in the blood, which returned permanently to normal as long as appropriate supplementation with Thyroid BP was maintained. T4 does not achieve this. At best, the cholesterol comes down initially, but creeps back up to the raised level within three months (The Lancet, 1961; i: 783-6). Many patients treated with T4 continue to feel unwell even when their thyroid hormone levels are within the normal range. Their views have been strongly represented to the medical profession and Health Authorities in both Great Britain and the US, but without any tangible response so far.
These dissatisfied patients still have a depressed metabolism, according to their basal temperature.
I began prescribing Thyroid BP alongside T4 to correct this, with good results. But I started to doubt the validity of the basal temperature method because so many other people (without known thyroid problems) had low temperatures. Many were convinced their thermometers were wrong because all of the members of their family showed low results. Altogether, about one in three of the people I tested gave a subnormal result and, of those who were checked, all had low normal T4 and T3, but had been told that these must be okay for them because they also had a normal TSH value.
TSH (thyroid stimulating hormone) is how the pituitary gland regulates thyroid output. If T4 were pathologically low, TSH would rise and that was not happening.
Among the dissatisfied patients who have tried in vain to change medical practice, half were in this category with normal TSH levels. The reason for this occurred to me after a chance remark by a Finnish friend that everybody in Finland has a low temperature. Finns have a notorious tendency to heart attacks and have made strenuous efforts to deal with this problem by dietary changes. They are unlikely to all be thyroid deficient, but could they have used a limited form of hibernation to cope with their long, dark, cold winters?
Examinations of the Inuit inhabitants of Alaska by the US Department of Public Health confirmed that low body temperature is universal among them. These sturdy people cannot all be ill, and hibernation would have been a useful adaptation to life within the Arctic Circle.
Modern peoples with Arctic ancestors may be able to partially hibernate. This is prompted by low physical activity, cold temperature, meagre diet (these people are permanently trying to reduce weight) and low light levels. The pituitary lets thyroid action dwindle without raising TSH so everything looks normal.
But susceptibility to coronary disease radically increases. Most of the accepted risk factors for heart disease (apart from diabetes) are themselves in part the results of depressed metabolism and only correlate with heart disease about half as well as their root cause. If we want to beat heart disease, it is the root cause we should aim for. The numbers of people affected depend on the closeness of the ancestral tie which is far greater in northern Europe (and perhaps northern Asia) than in the more mixed polyglot populations of North America.
If this is so, we should be asking how to switch off hibernation. Starting from Thyroid BP, it should be possible to devise a hormonal switch with minimal adverse effects which would be patentable an essential attractor for pharmaceutical research. Meanwhile, European Thyroid BP is available inexpensively in Great Britain for any doctor who is willing to prescribe it.
!ADr Peter Mansfield
Daniel Redwood DC
Tom Ferguson MD
