Health, Thyroid and TSH.

Increasingly health is defined by a bunch of arbitrary numbers. High cholesterol? That’s not normal take a pill. Low iron? Here take this iron supplement. In Ivan Illich’s book, Limits to Medicine- Medical Nemesis, Illich makes the reader fully aware of his disdain of medical check ups –

” The medicalisation of prevention thus becomes another major symptom of social iatrogenesis. It tends to transform personal responsibility for my future into my management by some agency.”

Instead of heavily reliant systems on numbers and markers. Should we not look to improve qualitative and quantitative pairings to get a better picture of health and improve outcomes? The last ten weeks of my life have been wrapped up in a post graduate diploma in endocrinology. Getting a better picture of how clinicians tackle complex areas has been a rewarding but at the same time frustrating area of study.

Sometimes the questioning has been a down the lines of – This patient has this endocrine feature, what are the medication used, which medications interfere, what surgical options can be pursued and what is the follow up? What is frustrating for me is there is little effort to understand why? Why? Why Donald why? Diet, stress and environmental aspects of hormonal health are often forgotten about, because the goal of getting that client back into the window of numerical health takes priority. But what if we took a better look at the why? Might it not yield better long-term outcomes for the patient?

I have a special interest in thyroid function, motivated by the writings of Ray Peat, Broda Barnes, Mark Starr and others. There’s a significant amount of work discrediting the role of combined T4/T3 therapy and in particular natural desiccated thyroid (NDT). In many endocrine textbooks the elevation of the active form of thyroid hormone, T3 was elevated significantly post NDT treatment.

A confounding factor in this assumption was based upon a previously incorrect conversion which can still be found in endocrine textbooks stating that 1mg of NDT was equivalent to 1ug of LT-4. There is recent evidence available showing a patient preference for NDT, which showed improved outcomes to weight loss, energy, happiness, sleep and memory (Hoang, Olsen, Mai, Clyde, & Shakir, 2013).

A reliance on TSH, T3 and T4 levels alone may be ineffective at analysing the effectiveness of combination therapy in comparison to synthetic monotherapy treatment of hypothyroidism. Additionally this study highlights the inaccuracy of the assumed conversion of 1mg: 1ug. Using more accurate 3rd generation TSH assays yields a suggested ratio of 1.47 mg’s to 1ug. This may explain the lack of effectiveness in previously conducted trials and the conclusion that increased transient T3 levels were decided as unacceptable. NDT in many cases may offer a better solution than synthetic thyroid hormone after all

Potential mechanisms of improvement may also lie in the actions of T1 and T2 and assumptions based solely on TSH, T3 and T4 may not explain the benefits recorded in this and other studies.     Thyroid pic

Another pitfall of number reliance is well known in the reference of thyroid stimulating hormone (TSH). TSH is considered the gold standard for hypothyroid diagnosis but its limitations have become increasingly prevalent due to its production via the stimulating centers from TRH (thyroid releasing hormone) from the hypothalamus and then TSH from the pituitary, if a problem exists at the periphery the likelihood of getting an accurate assessment is diminished. A normal TSH reading is defined as 0.4-4.5 mU/L but generally many Doctors do not consider someone hypothyroid unless they present with a TSH over 4 mU/L.

Increasingly some Doctors are becoming aware of the reduction of hypothyroid symptoms when TSH is kept below 1mU/L and some evidence suggests that even at 0.5 mU/L (lowered but suppressed) is ideal to ensure that hypothyroid symptoms are decreased (Pantalone & Nasr, 2010).

Me? I am going to go back and contradict myself and say that numbers are useful. The basal temperature test with a cheap thermometer, as championed by Broda Barnes still suggests a good window of function of the thyroid test. 36.5 to 37 degrees is considered normal and reflects a well functioning metabolism. Couple that with a pulse rate test and you can also get a good indication of cortisol. So I am not against the numbers. I just think we need to ask better questions before we accept them as absolutes.

References:

Hoang, T. D., Olsen, C. H., Mai, V. Q., Clyde, P. W., & Shakir, M. K. M. (2013). Desiccated thyroid extract compared with levothyroxine in the treatment of hypothyroidism: A randomized, double-blind, crossover study. Journal of Clinical Endocrinology and Metabolism, 98(5), 1982–1990. http://doi.org/10.1210/jc.2012-4107

Illich, I. Limits to Medicine – Medical Nemesis. Marion Boyars. 1976.

Pantalone, K. M., & Nasr, C. (2010). Approach to a low tsh level: Patience is a virtue. Cleveland Clinic Journal of Medicine. http://doi.org/10.3949/ccjm.77a.10056

 

Muscles, pain, hormones and other stuff.

As a therapist who works within the fields of pain, movement, energy and digestion I have seen my share of pain and muscle dysfunction in clients. As my exposure to these situations increase, I realise more than ever, that the muscles are very rarely the problem.

Specific muscle dysfunction usually boils down to spindle cell

Thyroid pic

Muscle pain and thyroid hormone

dysfunction and notably Nuclear Bag Fibres (NBF) and Nuclear chain Fibres (NCF). The primary roles of these structures are related to stretch and contraction of muscle function. There can be other factors involving neuro transmitters, involved in nocicpetion such as glutamate, utilised in the withdrawal reflex and often referred to as first pain, (also known as Neospinalthalamic tract located in the Anterolateral system or ALS) and lasting, less than a tenth of a second. Problems can arise when the following pain pathway, called second pain (or Paleospinalthalmic tract also part of the ALS) has problematic feedback with first pain, this is mediated by Bradykinin.

Further complexities arise with serotonin and other structures associated with pain such as the Amygdala and Peri Aqueductal Gray (PAG) that are beyond the scope of this short blog. However a common, over looked feature of pain, may arise with hypothyroidism .

Low thyroid function can be classified effectively with assessment of a basal temperature test and a reading of between 36.6 and 37 degrees. Most blood tests designed to measure thyroid hormones such as TSH, T3, T4 and others, often do not reflect accurate function of thyroid hormone. This is often due to feedback loops between cellular function and the Pituitary gland. Some of the regular hallmarks of hypothyroidism are poor energy, weight gain, poor sleep, hair thinning, digestive dysfunction (constipation and also alternating loose stools), cold hands and feet and pain. Here’s an old blog on thyroid and adrenalin issues.

Another assessment of thyroid function is the Achilles return reflex. When stimulating the myotactic reflex a hammer hits the Achilles tendon stimulating, the dorsi flexors or calf muscles. The response should be a quick return of the foot to it’s resting position but with low thyroid the foot returns slowly. Low thyroid output equals low ATP (Adenosine Tri Phosphate – the energy used by the mitochondria/cells). This low energy state does not allow for optimal contraction and relaxation. This is where we can see specific issues with NCF and NBF’s within the muscle spindle cell.

Muscle tendons and associated ligaments provide a feedback loop via the Golgi Tendon Organs or GTO’s. There’s potential for pre-existing GTO dysfunction to drive muscle dysfunction and vice versa. As far back as the 1960s symptoms associated with muscle disorder from low thyroid were.

* Weakness

* Cramps pain and stiffness

* Hypertrophy

* Myotonoid features.

A well-documented feature of hypothyroidism is muscular hypertrophied calf muscles and despite their size may often test weak to stimulation.

Muscle pain, may indeed not be muscle related, it may be due to many factors, suggested above and these may even be related to hormones and neurotransmitters. Many people often deal with muscle aches and pains by constantly focusing on mobility work but these structures continually return to their pre mobility work status (although this could also be an underlying stability issue). In reality there can be many factors that create dysfunction such as crude touch, vibration, nociception, Golgi, Pacini-pressure related structures and many more. But even after seeing a skilled therapist, these still don’t appear to get better, then addressing the chemical aspects of pain and function might be the next sensible thing to do.

References:

Armour Laboratories. The Thyroid Gland and Clinical Application of Medicinal Thyroid. 1945.

Ramsay I. Thyroid disease and Muscle Dysfunction. William Heinemann Medical Books. 1974.

Purves, D. et al. Medical Neuroscience. 5th Edition. Sinauer Assocates Inc. 2001

Starr, M Hypothyroidism Type II. Mark Starr Trust 2013.

http://raypeat.com/articles/articles/hypothyroidism.shtml