In producing this document in addition to the earler one I’m well aware of the resistance it will meet in the medical profession. A completely new understanding is needed to better diagnose and treat thyroid patients. However, based on the dogmatic statements I see from various posts, that endocrinologists and doctors will feel some degree of humiliation if they have to accept they have been practicing and treating wrongly for many years. This the medical profession will not bear and deaf ears will be turned to those like me who question their whole basis of action.
However, even though the immediate likelihood of success in getting the newer ideas accepted is not high, it is absolutely important to air them in public. If they are not publicized, no-one will know of their existence and no progress can be made at all. It has to be admitted that a whole generation of “specialists” will have to retire/die to allow the better ideas to percolate through. That is a sad but necessary admission, and won’t cheer those who read this. But the marker has to be put down to change things.
I’ve put my two posts through simply to make the new ideas available to patients who can then use them to try to influence their diagnosticians. This is purely transferring the ideas from my particular point of view as a representative of our group to a general forum. How individuals use them is up to them.
The basic problem has been that present-day GP’s and endocrinologists have been brought up on a 30 year old mistaken simplistic idea of how the pituitary, hypothalamus , thyroid and body talk chemically to each other. This has implications for when the thyroid fails and treatment is required. That the situation is much more complicated (and we haven’t got right down to the bottom of it yet) means explanations and actions coming from those concepts have to be much more sophisticated than understood at present. The prominence of the individual over the group in deciding treatment, and the realigning of biochemistry to its real, flexible but not dominant role is the overarching message. It may be that the ordinary GP is no longer suited in a diagnostic/treatment role and that like diabetes treatment, specialists must play a much larger part. But of course they too must up their game.
I hope at least some sufferers will be able to use these ideas to advantage.
To the doctor
You and I are meeting to discuss my health problem that I suspect (know) is associated with hypothyroidism. I’m sure we both want to come to a conclusion and treatment that best suits my particular state of health. Therefore before we start, I’d like to put in front of you the ideas and concepts that modern thinking on thyroid function has developed. These have radically changed the understanding of the relationship of TSH with thyroid hormones T4 and T3, and the way in which these all interact together. At the moment, TSH alone is used initially to detect the onset of hypothyroidism. That this test is useful and highly sensitive is not denied, but the interpretation of the test is highly controversial when deciding on relevant action. An important part of this is a decision when, and at what TSH level, therapy by oral thyroid hormone is indicated. In this regard I put the following points to you:
1)The reference range for healthy subjects is generally accepted at 0.5-4 mIU/L. However unlike the symmetrical distribution of values for free thyroxine (FT4) and free triiodothyronine (FT3), the distribution of so-called healthy values for TSH is severely skewed towards the upper end of the scale, so that relatively few patients deemed euthyroid have TSH values above 2.5 mIU/L. It has been suggested that in such patients, the thyroid is showing the beginning of strains which may herald difficulties later on. TSH values above the top of the reference range up to 10 mIU/L are assigned to subclinical hypothyroid subjects, currently perceived not at the time to require medication.
2)Individuals maintain health through unique combinations of TSH, FT4 and FT3 applicable only to them. But for me, we do not know what these are, because I have had these been measured in health. Therefore, when thyroid disease strikes, it usually does so surreptitiously with only a gradual progressive change to overt hypothyroidism requiring treatment. Because of my individual makeup of thyroid hormones, the point at which indications of a thyroid under strain, but not yet obviously compromised, move into an overt state requiring treatment will be unique to me. However as I said, my start point from health is not known. Therefore diagnosing me by “shoehorning” TSH values into categories defined by ranges is not correct. It assumes that everyone will respond equivalently within that range, and that decisions to treat or not can be made purely on statistical, rather than on personal, grounds.
3)Diagnosing purely by TSH has to take account of a) my particular makeup as regards thyroid function and b) the symptoms I am displaying:
4)hair loss/limpness, loss of outer part of eyebrows, thickening facial skin, feeling cold, sluggish- THESE ARE JUST EXAMPLES –USE YOUR OWN HERE.
I realise that symptoms can be misleading, being nonspecific to thyroid problems, but combined with my results, it is more likely that they result from developing problems with my thyroid.
5)A TSH above the reference range but below 10 mIU/L therefore can have many meanings. For some individuals, given obvious symptoms of hypothyroidism, it can strongly indicate the need for treatment. For others with exactly the same value, it may not require treatment at present. However the magic number of 10 mIU/L should not be used as a decision point as to whether to treat or not. There cannot be a hard and fast cut-off point for treatment given patient individuality.
6)Are there any useful blood test pointers that can aid in deciding whether to treat or not that are independent of thyroid function tests? One useful test is blood cholesterol and triglycerides. If hypothyroidism is at a significant level, then these will be raised. On treatment with thyroxine, the levels should fall back to lower values if the treatment is appropriate. Thyroid antibody tests should also determine whether or not I have autoimmune thyroiditis.
7)Another useful approach is to measure FT4 and FT3 and obtain a FT4/FT3 ratio. If I am seriously on the path to hypothyroidism then my FT4/FT3 ratio will be significantly lower than 3/1, In health, this ratio is usually between 3/1 and 4/1, The reduction in the ratio is due to my thyroid failing to produce enough T4, while my body is trying to maintain T3 levels to a level normal for it in health.
8)I realise that deciding the exact point when and how to treat hypothyroidism is a difficult area, but decisions on my future based on hard diagnostic dividing lines cannot be the best way forward given my individuality. My individual presentation is at least as important as the biochemical numbers. The recently defined category of subclinical hypothyroidism (i.e. not requiring treatment) has been a retrograde step in diagnosis, as it has consigned individuality in disease progress into a statistically defined mass-based decision resulting in the arbitrary cut-off of 10 mIU/L. Incidentally, this situation seems not to be mirrored in other countries where treatment begins at a much lower TSH level.
9)It may possibly be that I display hypothyroid symptoms, when TSH is still within its reference range. In which case, FT4 should be measured to see if it is very low within this range or even below. If this turns out to be the case, it may be that I am suffering from central hypothyroidism (pituitary insufficiency rather than thyroid disease). In this case, unlike thyroid failure, both FT4 and FT3 will be reduced but the ratio will remain typical of health.
10) If in the event, treatment with T4 is indicated, 50 ug should be a starter dose (omit this if over 65 years when 25 ug might be a better more cautious start). When treatment is begun, FT3 should be used as a determinant of successful treatment, realising that neither TSH nor FT4 are adequate in this regard. This is because T3, not T4 or TSH is the determinant of health.
11)You will note that I have emphasised that TSH cannot be the only arbiter of diagnosis. Using it in the way done at present takes no regard of my individuality as to how my disease develops.
12) I hope by combining presentation with biochemical measurements in a considered and personal way, treatment can be begun. A problem with delaying treatment is that irreversible changes in the thyroid axis can occur which will be difficult to reverse in the future. This is the more problematic, the longer I am left without treatment as irreversible epigenetic effects can alter how I respond. This is another dilemma that we should discuss together.
Links:
1) TSH Measurement and Its Implications for Personalised Clinical Decision-Making December 2012 Journal of Thyroid Research 2012(2):438037
DOI: 10.1155/2012/438037
2) Recent Advances in Thyroid Hormone Regulation: Toward a New Paradigm for Optimal Diagnosis and Treatment
December 2017 Frontiers in Endocrinology DOI: 10.3389/fendo.2017.00364
Suggestions regarding the elimination of hypothyroid symptoms
lost in translation...
