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The Diagnosis and Treatment of an Endemic Illness (Thyroid and Adrenal Dysfunction)





by Dr Barry Durrant-Peatfield


The first quarrel many people may have – but most especially doctors – may well be in the title. The use of the word endemic. To read a number of learned articles would leave the impression that thyroid dysfunction was a matter of a few percent of the general population; and adrenal dysfunction much less than this.


I have to say now, right at the outset, that this widely held view, held by establishment medicine, is quite wrong, disgracefully so. It is in the profession politically correct to believe that thyroid dysfunction is not common at all, and the symptoms are due to other things, notably depression. If you are really learned, you will speak of maladaption to one’s environment due to a personality dysfunction.


Adrenal dysfunction fares worse, and is believed to be about as rare as hens’ teeth. In any event, the argument goes, Addison’s disease by definition, hardly occurs.


I cannot emphasise strongly enough that both thyroid and adrenal dysfunction are so commonly met with as indeed to be endemic; and disgraceful diagnostic failure is the rule. I speak after more than a quarter century of practical study and treatment of both conditions, and I have suffered in the hands of an ignorant establishment for daring to diagnose and treat these problems.


If you take away from here nothing else, you must take this fact away: thyroid dysfunction, and its partner in crime, adrenal dysfunction are all around us, every day, in our clients/patients and even our colleagues. So common are they that whenever your opinion as a practitioner is asked on an apparently complex illness, you must ask yourself first – could there be an underlying thyroid and adrenal problem? (For the moment I shall not consider over-activity of either, but only sub-optimal activity.)


Thyroid and adrenal dysfunction usually come together but in varying degrees of emphasis. They cause a down-regulation of all metabolic processes; these clients/patients are all hypometabolic. Metabolism, as I need not remind you, may be defined as the rate at which energy is produced and consumed by the tissues. Glucose, oxygen in; carbon dioxide, water, energy out. For everything to work properly this process has to be optimally regulated, and it is the thyroid hormone which does this.


Thyroid hormones ensure that the cell membrane is actively and positively involved in the transport of the raw materials of energy production – not just oxygen and glucose but all the required enzymes and cofactors passing into the cell; and equally the passage out of the waste products once the energy has been released. The activity of the Krebs cycle where the mitochondrion is equally thyroid dependent.


It’s helpful to think of the whole organism as an incredibly complex and intricate electric machine, which is built and wired up for 240 volts. If we try to run it at 190 volts it’s not going to work properly. The lights flicker, and grow dim. A down-regulated metabolism affects the organism in the same way. This means nothing works properly. Every tissue, every organ, every biological process, suffers. Some pieces of the equipment are affected more than others, and differently, depending on the original design.


In ourselves, probably the most sensitive organ to metabolic down-regulation is the brain. Not far behind is the highly metabolically active liver, then the kidneys, then digestive processes, then our temperature control; and the intricate working of our immune system. Point is, you see; you name it, it doesn’t work properly. Our clients/patients may have lots of different things wrong with them, so many, that even they think they are hypochondriacs, never mind the doctor who came to that conclusion some time earlier.


It is essential to understand that a downgraded metabolism has a global effect. You cannot, you must not, focus on one or two symptoms; they must all be considered as a whole. How difficult this is in today’s environment. There’s never enough time, it’s all got to be written down, quick decision, then out. Another symptom? – Ah! Make another appointment and we will talk about it later. Here is the advantage many of us have who practise away from the mainstream – we have time.


Let’s take hypothyroidism first; probably the most common misdiagnosis of all common illnesses. A decent history soon gives us a few facts. Fatigue, weight gain, brain fog, depression, cold/heat intolerance, arthralgic aches and pains, fluid retention, bad skin, menstrual problems and infertility, hair loss, intractable constipation and lots of others. If you take these separately, how easily it is to narrow the focus and go for the wrong thing.


Fatigue: well, go to bed early, don’t work so hard, you are depressed, anaemic – some Prozac and iron pills, and you’ll be OK. Weight: you eat too much – try this diet. Brain fog: well, none of us are getting any younger, are we – too much stress. Depression. Ah! We can help you there, no trouble. Cold/heat intolerance: your age – wear warmer things. Arthralgia: bit of arthritis here I’m afraid – try these NSAIDs. Fluid retention – lovely pills here, make you pee, no trouble. Skin: bad diet, hormones. Bad periods: one of the crosses you women all have. Hair loss: age, diet – better hairdresser. Constipation: got something for that or try the chemist.


All the time the underlying problem is being missed. A simple examination can pick out the thyroid deficiency in minutes. And we’ll come to the tests later.



Now, as to why the thyroid goes wrong. It may be due to control failure – dysfunction in the hypothalamus or pituitary. It may be failure of conversion of T4 into T3, due to enzyme failure and poor adrenal function. There may be failure or resistance to binding of T3 at the receptor sites damaging gene expression – the Gq/11 proteins may be activated to switch off this response. And, most of all, it may be primary failure, in the gland itself. Primary failure in the gland may be:


(1) Genetic, appearing at, or soon after, birth. A baby with thyroid failure is true cretinism.


(2) It may be due to environmental deficiencies, like iodine, or the presence of toxins such as fluoride, PCB, dioxins and endless others.


(3) Trauma – general surgery, especially in the ladies; for example, cholecystectomy, hysterectomy. Or damage to the gland from whiplash.


(4) Glandular fever.


(5) Autoimmune disease.


(6) Pregnancy and childbirth.


A word about the over-active thyroid. Again, more common in women, but you don’t see that many; probably 2 for every 100 under-active. Not a difficult diagnosis; the patient is hot, terribly nervy, has loose bowels, is losing weight, has a racing pulse. Only real differential diagnosis is an anxiety state.


Now for adrenal dysfunction. The glands can go wrong in two ways: too much or too little. Too much and we have Cushing’s disease. Only three causes really; too much cortisone for the asthma, rheumatoid arthritis or whatever; an adenoma on the gland itself; or one on the pituitary. We are all familiar with the moon face, thin skin, obesity, buffalo hump, so it shouldn’t be difficult. A lot of people are checked out for Cushing’s just because they are a funny shape, but unless iatrogenic, it isn’t very common at all.


Adrenal hypo-function is a different kettle of fish entirely. The diagnosis is missed more decisively even than hypothyroidism, because most clinicians only seem to think of it in terms of Addison’s disease. In fact, the adrenals can malfunction in degrees. A failure in pituitary control may play a role, often as a spin off from a generally low metabolic state; but usually the failure is the result of long-term stress. Hans Selye recognised, didn’t he, three major stages in adrenal hypo-function, which he called the General Adaption Syndrome (GAS).


Stage I is the stressed phase, where, due to illness or other stress, the adrenals mobilise cortisol and DHEA to help the body deal with the problem. This is an acute phase; the stress settles, and the adrenals settle down.


Stage II, resistance, is where it all goes on and on, and the adrenals enlarge and increase their hormone output on a longer-term basis. This can go on for weeks, months, or even years; but eventually they can’t take it any more, and start to regress into exhaustion, stage III. The degree of exhaustion, is reflected in their output and balance of their two chief hormones, cortisol and DHEA, which is where the Adrenal Stress Index (ASI) comes in.


The last phase of the GAS is what we will often see if we are looking for it. Important causes, of course, are major life-events, trauma, operations, and the general and prolonged ghastliness of existence. But for our purposes, the big cause is persistent and chronic illness. In the attempt to help the body deal with, and compensate for, the illness, adrenal exhaustion starts to take over. An example of a persistent and chronic illness untreated, or mistreated, is hypothyroidism.


So now you see why thyroid and adrenal hypo-function have to be considered together. Here’s a precept for you. Anyone with undiagnosed or unsatisfactorily treated hypothyroidism will sooner or later inevitably slip into adrenal exhaustion. May take months, or years, but it will happen. Symptoms of adrenal exhaustion exaggerate pre-existing thyroid symptoms. There will be ongoing and endless fatigue, even less tolerance to cold, depression, dizziness (postural hypotension), body hair loss, pigmentation (especially in skin folds), poor response to treatments generally, and an obviously weak immune system.


Most particularly, if there is an adrenal malfunction – I still like to call this low adrenal reserve – the patient responds poorly to thyroid hormone, or rapidly gets ill and toxic on even quite small doses of thyroxine.


And now I want to broaden my sweep even further because we have to consider chronic fatigue. Something else to remember: all clients/patients suffering from chronic fatigue, CFS, ME, Fibromyalgia, have a number of features in common. Most importantly, they are metabolically down-regulated. Whatever else is wrong, their thyroid and adrenal function is damaged. It’s not as simple as that, of course, because the illness brings in its train other problems too.


There is likely to be viral load. This may follow from the original event that started it all off, a nasty flu, or glandular fever. If there has been a deficiency in EFAs at any time, there may have been a lower than normal eicosapentaenoic acid (EPA) level since some of these big nasty viruses can damage the 6-delta-desaturase enzyme which makes EPA from linolenic acid; and EPA is viracidal and makes interferon.


There may be systemic candida. Because it’s systemic and lurking in the gut, it may not have been thought of; but will be producing toxins and allowing all the problems of dysbiosis and a leaky gut. This must be looked for and treated.


There may be sex hormone imbalance, especially around the menopause; oestrogen dominance, which interferes with thyroid hormone, transport, production and receptor uptake. Intervention may be considered here if there is marked deficiency or imbalance. Food allergies can be an associated problem, especially if dysbiosis has been marked. There is often deficiency of essential minerals and vitamins which have to be sought for, especially if malabsorption is a feature, as is likely.


Prof Basant Puri’s work has focused on EPA and virgin EPO as a method of clearing the viral load, which has had some success; and Dr Sarah Myhill uses D-ribose, L-carnitine, magnesium, co-enzyme Q10 and high dosage B12 as another approach.


I am going to pull together later the diagnostic approach to the detection of thyroid and adrenal dysfunction; so before we do, it’s time to consider our treatment strategies.


First thyroid. There are 3 levels of approach. The first is nutritional. To manufacture thyroid hormone there needs to be tyrosine, selenium and iodine, together with vitamin and mineral cofactors. We are most especially thinking of the B Complex – B6 is crucially important – and magnesium, zinc, manganese and chromium. A number of companies make excellent thyroid support products – an example is Thyrocomplex from Nutri Ltd.


The next level is the use of natural glandular concentrates. In this country, they are successfully produced as nutritional supplements. Nutri make Nutri Thyroid, which contains 130 mg of glandular concentrate and enzymes, and enough thyroid hormones to greatly improve thyroid levels. A dose of 1 up to 4 tablets daily is recommended.


The third level is thyroid hormone replacement. Many of you are aware of the prescription medication, natural desiccated thyroid; Armour is the most well known. This is available on-line in 30 mg, 60 mg, 120 mg and 240 mg tablets, and may be used with confidence where the glandular concentrate has not provided significant improvement. A usual starting dose would be either 30 or 60 mg.


Then there is the use of synthetic thyroxine or levothyroxine. Because the generics appear to vary in potency (an accusation thrown quite unfairly and wrongly at Armour thyroid), clients/patients may not be doing awfully well on them, firstly because the dose is managed purely on the outcome of blood tests. (Instead of asking the patient and actually listening to them as an alternative to blood tests, which is actually not just frowned upon; it is now a hanging offence. Thus far has evidence based medicine brought us.) And secondly, there is often an adrenal problem which if not dealt with, will cause T4 toxicosis and/or an adrenal crisis.


Adrenal dysfunction may be detected clinically without difficulty – the Raglan test, Romberg test, pupillary reflex are most helpful, and the Adrenal Stress Index, will confirm the diagnosis. Treatment of low adrenal reserve has, like the thyroid three levels, and if hypothyroidism is present must be put in place before thyroid supplementation is begun.


Nutritionally, the adrenals need Vitamin C, 4 grams or more daily; they need pantothenic acid (B5), and benefit from the use of liquorice (wood or tincture), Siberian ginseng and coenzyme Q10.


Extremely valuable is the adrenal glandular concentrate; that made by Nutri Ltd is widely available (I recommend them because I have found their products to be very efficacious). One product contains 80 mg of the concentrate alone, and another, 221 mg together with a number of vitamins and minerals.


If this proves unsatisfactory, which is uncommon and usually because the adrenals have been badly damaged over a period of time, the use of the adrenal hormone cortisol (hydrocortisone), 2.5 mg up to 25 mg may be considered by the practitioner, together with DHEA 25 mg or 7-keto DHEA 50 mg.


These measures will remedy the underlying damage, but intervention may be necessary to balance low progesterone or high oestrogen – the use of natural transdermal creams is the best method.


Systemic candida must be treated where present, using a fungicide (fluconazole can be helpful), together with grapefruit seed extract, caprylic acid, horopito etc, along with an effective pre- and probiotic.


Food allergies have to be dealt with on their merits, usually by simple avoidance; and malabsorption may require the use of Betaine HCl and/or pancreatic enzymes.


A viral load may respond to VegEPA, the EPA – EPO formulation I mentioned earlier.


Treatment of thyroid and adrenal insufficiency along these lines can be extremely rewarding and successful, and a similarly broad approach in dealing with CFS has been proving very helpful also.


Now we’ve got a working knowledge of diagnosis and treatment, it is right to discuss the use of available pathological aids to diagnosis. Long recognised by many practitioners as an invaluable indication of thyroid deficiency is the waking temperature, as described by Dr Broda Barnes.


Thyroid first of all. Standard NHS testing tends to be restricted to TSH usually, with Free T4 thrown in if you’re lucky. The full range, which includes T4, T3, TSH and TPO & TgAb antibodies will not usually be done, even at knifepoint, and so clients/patients will usually seek the help of private laboratories.


This if possible should always be done, but you must remember that the TSH is often unreliable if the pituitary is suffering from a hypometabolic state, and there are other reasons which can affect its reliability. If it’s high, well and good; if it’s at normal levels, it proves nothing. T4 if low, again good, if it’s normal, it may mean that it is not being properly used; is building up, and causing a false result. The same argument applies to the T3, but the antibody test may be relied upon.


Thyroid tests should always be considered against the clinical findings, and remember clinical observation is very much more reliable than tests. As you may have observed I have a deep-rooted cynicism about the politically correct obsession with evidence-based medicine. Surely, it should be observation first, tests second.


Where doubt continues to exist, this may be resolved by the 24 hour urine test. As far as is known only IWDL do this test in the UK; ELN do it in The Netherlands. It relies on the findings of Hertoghe & Baisier who showed the greatly increased reliability of the 24 hour urine, which after all, measures the thyroid production over a whole day, as opposed to the blood test, which is a snapshot of a single moment of levels that can vary widely with time of day and other variables. The test demonstrates the amount of T4 and T3 actually used and passed through the tissues. It is much more useful than other tests, and will show even minor degrees of low thyroid function.


In an ideal world both the full serum thyroid screen and the 24 hour urine should be done, but there are logistic and financial difficulties that have to restrain one’s enthusiasm. While interpretation of the 24 hour urine is perfectly straight forward, the blood thyroid screen has to be carefully assessed.


The first stumbling block is the TSH; a rise of TSH indicates poor thyroid response; but the level considered to be indicative of this can be a matter of different interpretation by laboratories and doctors. The recent guidelines issued by the British Thyroid Association suggesting that treatment should not be offered below 10 units is quite unbelievable. The American Association of Clinical Endocrinologists have recently considered a level of 3.2 to be the cut off point, and in my view anything over this, combined of course with a clinical appraisal pointing to the diagnosis, should demand intervention. Labs seem to vary between about 4 and 6; but I say again, anything over 2 should arouse suspicion, and anything over 2.5 should result in a trial of treatment at the very least.


The trouble with the TSH is that it may not be a proper response to thyroid uptake since there are four types of thyroid receptor and a metabolically challenged pituitary can’t respond properly anyway. So a high level is valuable; a low level may mean nothing.


Measurement of T4 and T3 has always been very much subject to error. The obvious difficulty is that it is only, as I said earlier, a snapshot of a level which may vary a lot during the day, but it goes deeper than that. Failure of uptake by exhausted and missing receptors will allow levels to be normal or even high in the bloodstream, simply since thyroid hormone isn’t being used; and conversion deficits can further distort the picture.


The presence of thyroid antibodies (TPO & TgAb) shouldn’t usually cause much difficulty: either they are well raised or they are not, allowing an immediate diagnosis of Hashimoto’s or Graves’ disease to be made. It should be borne in mind that the levels fall away with the passage of time.


Reverse T3 is sometimes of help; high levels may indicate poor T3 receptor uptake, with the system trying to rid itself of surplus T3. General illness, malnutrition, trauma will also raise the T3.


We come now to the tests for adrenal function. Once again, one simply must place foremost the clinical picture; if the blood and salivary tests don’t necessarily agree – why, rely on your clinical judgement. Happily IWDL do not offer a serum cortisol as greatly relied on by establishment medicine. It is almost useless. Similarly the Synacthen (long or short) seems to be of significance only where the adrenal insufficiency is plainly Addisonian.


More helpful by far is the salivary Adrenal Stress Index (and ASI Comprehensive) which measures SigA as well as cortisol and DHEA output in 24 hours. Clearly illustrated in the graphics, and helpfully commented on, the true picture of adrenal stress may be recognised, and the three stages of the General Adaption Syndrome clearly shown.


High levels of cortisol and DHEA show adrenals under stress. Sometimes the cortisol pathway starts to fade as exhaustion sets in, with DHEA still reasonably present. Less commonly, there may be a really high DHEA – a response to ACTH stimulation but the cortisol pathways responding poorly. Erratic levels in both are evidence of strain and uneven response.


The 21 Hydroxylase and 17 hydroxylase enzyme deficiencies may be apparent here; really weak cortisol, with high androgenic output enough to cause virilisation. Where cortisol levels are obviously weak, and DHEA response is weak and flat, the diagnosis of adrenal insufficiency (low adrenal reserve) slowly heading towards Addison’s disease may be made.


We have to consider the sex hormones in more depth. Many of us are aware that in the ladies hypothyroidism may start with, and parallel, the menopause. One scenario is the progressive loss of progesterone often some years before the menopause itself. Apart from the obvious increased risk of osteoporosis, the imbalance will lead to oestrogen dominance – with weight gain, bloating, mastalgia, heavy painful periods. And this will increase thyroid-binding globulin, thus taking some thyroid out of use; it will adversely affect thyroid manufacture, and receptor uptake. All the symptoms are put down to the menopause of course; when actually the increasing deficiency of thyroid is the main problem.


Later, both hormones run down, and under the principle of permissive action, where hormone production requires the other players in the endocrine orchestra to play their parts well and in tune, thyroid production and processing may be affected adversely. So being able to detect oestrogen dominance is pretty helpful – one can correct the balance with natural transdermal progesterone. If levels of both are low careful use of natural progesterone and oestrogen can be very valuable. So, we should consider most carefully the menopause profile, or at the very least, a spot check of a day’s output of progesterone and oestrogen. In menstruating women thought may be given to assessment of both throughout a month. In general, however, getting the thyroid and adrenal status right will often provide welcome correction in much of the menstrual difficulties, and it may perhaps be considered at a later date.


The lads must not be left out of the equation. The male menopause most certainly happens – we can call it the andropause – but is usually an altogether more gradual and insidious affair. Ideally, the testosterone panel or the male hormone profile should be carried out if the slightest doubt exists.


The role of candida I have considered earlier, and it’s so common that its presence must be sought for. The old-fashioned nutritionist spit in a glass test should be done, I think, as a routine. The presence of a miniature Medussa means that the candida antibody profile simply must be carried out, and if active candida antibodies are present, treatment is essential. I find it in rather more than half of my clients/patients.


To sum it all up, I am here making a plea for the recognition of the very common syndrome of thyroid and adrenal deficiency, using observation and medicine practised as an art, as the primary diagnostic method, with the lab playing a secondary role. Further, that the syndrome has global effects, with imbalance of other hormones, the likely presence of systemic candida and dysbiosis, malabsorption and food allergy all playing a probable role.


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People in this conversation

  • Great article. I have been telling my symptoms for 2-3 years. The standard thyroid test is done and appears within normal range. I finally asked to have the TPO antibody tests and my level was 465. I also have the buffalo hump but was told it was not Cushings due to the cortisol level resulting within normal range.
    Thank you for the information.

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