I’ve seen a number of assumptions from doctors suggesting that there’s no optimal diet for improving thyroid function. If that were the case there would be no optimal diet for heart disease, cancer or autoimmune disease but there are many proposed guidelines of certain foods that should be avoided.
If you want to slow down the thyroid eating plenty of cruciferous vegetables, fish oils and exposure to oestrogens (environmental pollution, contraception and other medical drugs) seems to inhibit thyroid function dramatically and large amounts of anti-thyroid (goitregens) foods are certainly linked with thyroid cancer. Often an individual’s perceived healthy choices can suppress thyroid function and therefore be resolved with nutrition alone. A functionally suppressed thyroid state that’s treated with thyroid hormone may not yield the best results.
Sub clinical hypothyroidism (SCH) is an issue that divides endocrinology but when you look at the process of thyroid dysfunction there are some clear indicators that should suggest that it’s treatment would be the most sensible (but not the most money making) action in the long run. Let’s start with defining what SCH is.
SCH is usually defined as an asymptomatic state in which free T4 is normal but TSH (thyroid stimulating hormone or TSH is the pituitary stimulator of thyroid hormone) is elevated. If serum TSH is >10mU/L there is consensus that the patient should be treated with thyroxine because of the likelihood that the patient will develop overt hypothyroidism with subnormal T4 and because this degree of SCH predisposes to cardiovascular disease. When the TSH is in the range of 4.5 to 10 mU/L, there is controversy about the efficacy of T4 therapy (Lavin, N, Ali, Omar., Beall, M.U., Bhutto, 2016).
Although many people with most forms of thyroid disease often present with diverse symptoms due to the systemic effects of thyroid hormone action but are often ignored through reductionist observation. The table below lists most of the major actions of thyroid function and deficits created by a hypothyroid state.
Here’s a short history of some of the contrasting opinions on treating SCH. Biondi cites the original controversies of Wartofsky and Dickey (2005) who favoured a narrower TSH range (Wartofsky & Dickey, 2005), which was in contrast to the opposition to a lower TSH suggested by Surks et al. (2005) (Biondi, 2013).
The latter authors stated ‘that there was little evidence supporting the treatment of SCH, citing a single small study by Kong et al. treating 40 women with SCH (Kong et al., 2002). The main findings demonstrated that thyroxine treatment had no impact on lipids, energy expenditure, weight gain or composition despite decreases in TSH levels in the treatment group (8.0 +- 1.5 mU/L change from baseline -4.6 +-2.3 mU/mL compared to 7.3 +- 1.6 -1.7 +-2.0 mU/L in the placebo). However this study, perhaps like many others (Laurberg et al., 2011) (Surks et al., 2005), failed to assess the nutritional status of this small group of patients. For example, if calorific excess were present, these markers may show little change, as weight loss requires a calorie deficit. Conversely if a patient were chronically undernourished through a low nutrient intake, attempting to enhance metabolic rate and weight loss with TH replacement may be negated when adrenaline, glucagon and cortisol are produced to regulate blood sugar levels.
Problems associated with some of the smaller seemingly positive older studies, is often the lack of control groups for comparison. A smaller RCT (treatment n-22 control n-19) comparing treatment of subjects with biochemically euthyroid TFTs yet clinical hypothyroidism with thyroxine, found the intervention no more successful than placebo (Pollock et al., 2001). Whilst the effect of placebo cannot be discounted, the study only focused on cognitive function and wellbeing, factors that are a limited component of thyroid function. A friend of mine also pointed out that the use of T4 alone and female cohort with an increased weight some 20kgs over the control group are also problematic issues in studies like this.
More studies trickle through that builds upon previous suggestions that measuring TSH is a poor way to accurately assess thyroid function, primarily due to the facts that stress, environmental pollutants and nutrition can cause biochemistry and in particular thyroid blood tests to present as normal. The problem with ignoring SCH is the following scenario.
You have isolated or a number of hypothyroid symptoms such as weight gain, high blood pressure, high cholesterol, hair loss, fatigue, low libido, altered menstrual cycle, anxiety or depression, poor sleep, constipation, brain fog, inflammation of the brain, altered heart contraction, dry skin etc.
Good news Mrs X you have normal thyroid function as your blood tests came back within the normal ranges. The symptom/s you have must be in your head. Here you have high blood pressure take this anti-hypertensive medication.
The pituitary should be considered a source of evaluation that could be useful but should be treated with suspicion. There are many factors that alter thyroid feedback which include the disparity between the enzymes in the pituitary (deioidinase 2 supports the conversion of thyroid hormone in the pituitary and can appear normal) and other tissues, thyroid receptor and mitochondrial damage. Recent meta analysis and other studies support the role of treating SCH to prevent cardiovascular disease, high cholesterol, hypertension (Ochs et al., 2008)(van Tienhoven-Wind & Dullaart, 2015)(Udovcic, Pena, Patham, Tabatabai, & Kansara, 2017) (Sun et al., 2017) and there’s a strong possibility that hypothyroidism in the central nervous system in areas like the prefrontal cortex are associated with dementia and Alzheimer’s (Pasqualetti, Pagano, Rengo, Ferrara, & Monzani, 2015)(Davis et al., 2008).
Temperature, pulse and symptoms can be a useful indicator of function when bloods appear to support the notion of sub clinical hypothyroidism
It’s worth suggesting that endocrinologists should be well aware of all of the factors that can create the perception of normal blood tests, especially when individual’s present with clinical findings of hypothyroidism as suggested above. My previous posts on assessing thyroid function through body temperature and Ray Peat’s well written post should also be considered an integral part of assessment of thyroid evaluation. The concept of SCH is really only related to the blood test, because the other findings should give the game away. Treating SCH shouldn’t be problematic when a thorough understanding of nutrition and environmental stimulus are known, and the only people at risk from taking a gradually increased dose of thryroxine would be individuals at risk of an immediate heart attack who generally would present with a certain set of symptoms.
If Broda Barnes, an MD in the last century found that his patients didn’t succumb to heart disease when taking thyroid hormone. Shouldn’t we be looking for the more global implications of health improvements? Rather than treat high cholesterol, blood pressure, blood sugar, menstrual irregularities, metabolic syndrome (and many others) which all have a substantial relationship with thyroid function, with many studies that show substantial improvements when treated with thyroxine. Call me a cynic but perhaps a more detailed understanding of nutrition, environmental pollutants and their effects on thyroid physiology is probably more challenging to integrate into practice than completing genetic analysis with the proposed mutation driving a specific dysfunction.
BARNES, B. O. (1973). On the Genesis of Atherosclerosis. Journal of the American Geriatrics Society. http://doi.org/10.1111/j.1532-5415.1973.tb01239.x
Biondi, B. (2013). The normal TSH reference range: What has changed in the last decade? Journal of Clinical Endocrinology and Metabolism. http://doi.org/10.1210/jc.2013-2760
Davis, J. D., Podolanczuk, A., Donahue, J. E., Stopa, E., Hennessey, J. V, Luo, L. G., … Stern, R. A. (2008). Thyroid hormone levels in the prefrontal cortex of post-mortem brains of Alzheimer’s disease patients. Curr Aging Sci.
Kong, W. M., Sheikh, M. H., Lumb, P. J., Freedman, D. B., Crook, M., Doré, C. J., & Finer, N. (2002). A 6-month randomized trial of thyroxine treatment in women with mild subclinical hypothyroidism. American Journal of Medicine. http://doi.org/10.1016/S0002-9343(02)01022-7
Laurberg, P., Andersen, S., Carlé, A., Karmisholt, J., Knudsen, N., & Pedersen, I. B. (2011). The TSH upper reference limit: where are we at? Nature Reviews Endocrinology, 7(4), 232–239. http://doi.org/10.1038/nrendo.2011.13
Lavin, N, Ali, Omar., Beall, M.U., Bhutto, A. et al. (2016). Manual of Endocrinology and Metabolism (4th Editio). Lippincott Williams and Wilkins.
Ochs, N., Auer, R., Bauer, D. C., Nanchen, D., Gussekloo, J., Cornuz, J., & Rodondi, N. (2008). Meta-analysis: subclinical thyroid dysfunction and the risk for coronary heart disease and mortality. Annals of Internal Medicine, 148(11), 832–845.
Pasqualetti, G., Pagano, G., Rengo, G., Ferrara, N., & Monzani, F. (2015). Subclinical Hypothyroidism and Cognitive Impairment: Systematic Review and Meta-Analysis. The Journal of Clinical Endocrinology & Metabolism, 100(11), 4240–4248. http://doi.org/10.1210/jc.2015-2046
Pollock, M. A., Sturrock, A., Marshall, K., Davidson, K. M., Kelly, C. J., McMahon, A. D., & McLaren, E. H. (2001). Thyroxine treatment in patients with symptoms of hypothyroidism but thyroid function tests within the reference range: randomised double blind placebo controlled crossover trial. BMJ (Clinical Research Ed.). http://doi.org/10.1371/journal.pone.0098254
Sun, J., Yao, L., Fang, Y., Yang, R., Chen, Y., Yang, K., & Limin, T. (2017). The relationship between subclinical thyroid dysfunction and the risk of cardiovascular outcomes: a systematic review and meta-analysis of prospective cohort studies. International Journal of Endocrinology, 2017(2017). http://doi.org/10.1007/s00774-017-0828-5
Surks, M. I., Goswami, G., & Daniels, G. H. (2005). The thyrotropin reference range should remain unchanged. Journal of Clinical Endocrinology and Metabolism, 90(9), 5489–5496. http://doi.org/10.1210/jc.2005-0170
Udovcic, M., Pena, R. H., Patham, B., Tabatabai, L., & Kansara, A. (2017). Hypothyroidism and the Heart. Methodist DeBakey Cardiovascular Journal, 13(2), 55–59. http://doi.org/10.14797/mdcj-13-2-55
van Tienhoven-Wind, L. J. N., & Dullaart, R. P. F. (2015). Low-normal thyroid function and the pathogenesis of common cardio-metabolic disorders. European Journal of Clinical Investigation. http://doi.org/10.1111/eci.12423
Wartofsky, L., & Dickey, R. A. (2005). The evidence for a narrower thyrotropin reference range is compelling. Journal of Clinical Endocrinology and Metabolism. http://doi.org/10.1210/jc.2005-0455