Thyroid Health

​Thyroid Dysfunction.
Why so many of us get it wrong, and why it goes undetected for years. 

What is the answer to autoimmunity?

   Diving in the deep end has always been my best learning tactic. I do not leave a chance for my brain to suspect, hesitate, or be complacent. 
My brain does not see a thing coming...

   Why, would you say?
   The answer, for me, is simple. A know-it-all approach is not only negative but can become an extraordinary obstacle in learning a new skill or keeping on top of current research. Hesitating brings procrastination, and confidence may be lacking as one is thinking about it more and more. 
   I also love to get to different places, this brings new challenges for my brain. For example, one day, I will be doing my research at the Wellcome Library and the next at the British Library, as long as I can find what I am looking for. Then, I may browse the internet for the missing links. 
   This allows me to broaden my scope of knowledge but also the access to original studies. 

   Today, when it comes to nutrition, anyone can claim to know it all, pretending to be an expert, and yet, most statements are not built upon strong foundations, sound nutritional knowledge, or actual qualifications. 
   This is not the only problem. Read below the latest email from Mark Hyman, on of the pillars of the Institute of Functional Medicine:

"Eating the right food is also the single biggest thing you can do to prevent heart disease, type 2 diabetes, cancer, dementia, autoimmune disease, allergies, digestive problems, AND it can make you feel better RIGHT NOW. 

At the same time, some readers and patients have told me eating healthy can feel confusing. If you’re confused by what to eat, you’re not alone. 

So why are we all so confused?

It’s not your fault. In fact, it is by DESIGN—the food industry, our government, and the media are all sending us conflicting messages. And all the contradictory science doesn’t help either! Here’s the bottom line: Money is corrupting science, our government’s food policies, and the media.

Where’s the money coming from?

There is a multi-trillion dollar global food industry that is growing, processing, manufacturing, marketing, and serving food like substances that are making us sick and fat. They are cheap to make and rake in big profits for ”Big Food”.

They put private profit over public good, harming us all. They privatise profits and socialise costs. We taxpayers are footing the bill for the growing of processed foods (through agricultural subsidies for the raw materials of processed food—namely wheat, corn, and soy), and for providing the poor quality processed food and soda to the poor (through our food stamps program).

Then, we also pay for the costs of obesity and chronic disease caused by that food through Medicaid and Medicare. Not to mention the costs of soil degradation, depletion of our water supplies, climate change, and the widespread damage to humans and ecosystems from pesticides."

   And now you are wondering why the next blogger is spreading misinformed articles, which are, most of the time, never referenced, and a patchwork of various other blogs. You are never able to know where they sourced their information, and if you do not know any better can take their word for truth.
   As a guide, always read articles that have references, and that are checkable. Many bloggers copy and paste other articles, never checking that the reference is actually active. So you may think they have done the hard work, when, in fact, they haven't.
   Click on any reference and see if they indeed point into a study or a research paper, and not a previous blog they have written or to another blog. 

   The reason why I am "ranting", ever so slightly, is because when I had to write my paper on Hypothyroidism (Hashimoto's and Ord's thyroiditis), it took me months to write, and subsequently came up with 4 pages of references for a 200-page work. I was attributed the highest mark in the entire history of my school, and my work had circulated in all the branches, before being handed to me. 

   Now, I take this blog very seriously, because my "job" as a naturopath is to educate people, and empower them with the knowledge they need to make up their mind about nutrition. How could I possibly do this if I am circulating false information?  

​    I am in a way echoing Robyn Openshaw:

"Thyroid Health and Nutrition: Is The Autoimmune Protocol the answer?

Another common problem in the way thyroid patients are treated is that many of the practitioners, including the “functional” (or more holistic) ones, can’t take the time necessary to educate their patients about the role of their diet and nutrition.
So, they often plug the patient into whatever fad diet is ruling, at the time.

The practitioner may prescribe you the Autoimmune Protocol (AIP), which may help identify foods thyroid patients are sometimes reactive to, such as lectins in beans, or oxalates or goitrogens in greens.

Two things about the AIP are of significant concern to me, as I continue to study thyroid health, overall health, and trends in functional medicine.
A growing body of evidence documents that, in fact, the “anti-nutrients” may be friends, with supporting roles in your health, rather than foes.

One, the AIP is a temporary way of eating while you heal, but avoiding all legumes (chickpeas, black beans, kidney beans, split peas and the like) over a lifetime is counter to a massive body of evidence showing these foods to be an important part of the diet of the healthiest people around the world.
Two, the Internet-popularised idea that crucifers and greens (high in two goitrogens and oxalates) should be avoided, does not seem to have solid science underpinning it. It appears to be a theory, that has been spread mostly on the internet, and is not tested.

One of the reasons this theory is problematic is that some under-educated thyroid practitioners assume that an “anti-nutrient” is bad for you, and a growing body of evidence documents that, in fact, the “anti-nutrients” may be friends, with supporting roles in your health, rather than foes.
Another reason suggesting that the idea that avoiding greens isn’t a good strategy, for most thyroid patients, is that our thyroid-disease-free primate cousins forage for greens all day, every day, and the healthiest populations in the world, for thousands of years, have mostly eaten significant or even massive quantities of greens.

I fail to find any significant or published or controlled-study evidence that greens are anything but highly nourishing and healing to the vast majority of thyroid patients. In fact, there are dozens of micronutrients in virtually all greens, that have known therapeutic effects for regulating and balancing hormone function.

This suggests that to laser in on goitrogens in broccoli and cabbage, or oxalates in spinach and kale, and ban them from your diet, is anywhere from unhelpful to tragic, at least as a long-term strategy."

I am so grateful for such statements, as I personally believe that your practitioner knows only what he knows. Your general practitioner only has 9 minutes to deal with you and your complaints. It is humanly impossible to care for that many people in a day. This is why over 75% of GPs hate their job and wish they studied something else (The evolution of Medicine by James Maskell). If a GP comes across something he is unsure, he would rarely refer you to a colleague, he will instead go for what his training is calling for: medicine, and most often antibiotics. the 9 minutes are up... "NEXT...!!!!"
 
"The good news is that the truth about nutrition, the basic guiding principles of how and what to eat to promote health, weight loss, and longevity—AND to prevent, treat and reverse most chronic disease—is pretty simple.
​
I have read thousands of papers on nutrition and tried and recommended various ways of eating with tens of thousands of patients over 20 years. And I’ve seen the effects of food on weight, health, diabetes, gut issues, autoimmune disease, and lots more." concludes Mark Hyman in his email. 

    I may not be there yet, but I hope, that one day I will. In the time being, I am still researching all that I can to increase my knowledge and keep on the current development in nutrition and medicine to offer protocols that are truly validated by evidence-based research and, indeed, individualised to the person in front of me. ​

    Back to the subject of this article: 

---

   Hypothyroidism

​   In the last decades, Hypothyroidism has exploded exponentially. (Vanderpump, MPJ. 2011. p. 42)
   The symptoms, however, can develop over many years and may be left unchecked:
   "An underactive thyroid gland (hypothyroidism) is where your thyroid gland doesn't produce enough hormones. Most cases are caused either by the immune system attacking the thyroid gland and damaging it, or by damage to the thyroid that occurs during some treatments for an overactive thyroid or thyroid cancer.  

   Symptoms of an underactive thyroid are often similar to those of other conditions, and they usually develop slowly, so you may not notice them for years." (NHS. 2015)

Pathophysiology

​   "Some degree of hypothyroidism is common in the elderly. It affects 5–20% of women and 3–8% of men. The occurrence varies with genetics with a high prevalence in caucasians, and the disease is more common in population with a high iodine intake" (Laurberg, P. et al. 2005. p. 23).

   "The incidence of hypothyroidism increases steeply with age, 45% of all patients newly diagnosed with hypothyroidism are 70 yr or older" (Carlé, A. et al. 2008. p. 23), "it affects 15 in every 1,000 women and 1 in 10,000 men." (NHS. 2015)

   Pregnancy leads to marked changes in thyroid hormone physiology, increasing in size by 10% (thyroxine production is increased by 50%). Requirements for iodine are also increased. Many women are euthyroid (normal functioning of the thyroid) but have immunological evidence of thyroid autoimmunity or are iodine deficient (Stagnaro-Green, A. et al. 2011; Negro, R. et al. 2010). This occurs in 10–20% of all pregnant women in the first semester of pregnancy (higher rate of obstetrical complications: impaired development and increased foetal mortality, and postpartum thyroiditis). (Negro, R. et al. 2010; Negro, R. et al. 2006; Alexander, EK, et al. 2004) 

   Primary TSH screening in newborns has become standard to prevent retardation, poor brain development, and improve developmental outcomes in adults with congenital hypothyroidism. (Rose, SR. et al. 2006). "The frequency of congenital hypothyroidism is about one in 7,000 births" (Dussault, JH. et al. 1975. p. 670), which has now increased to "about one newborn in 3,500–4,000 births." (Vanderpump, MPJ. 2011. p. 41; NHS UK; Tran, M. Odle, TG. 2005).  

​

Pathogenesis and Aetiology

​   "Congenital hypothyroidism (CH) is a condition of thyroid hormone deficiency present at birth and is the most common inborn endocrine disorder." (Bona, G. et al. 2015. p. 27)
   Peripheral Thyroid Hormone Resistance can also be inherited, characterised by reduced end-organ responsiveness to thyroid hormone (elevated Free T4 and T3, normal TSH), goitre, and signs of subclinical hypothyroidism. (Sodano, WL, Grisanti, R. 2011; Agrawal, NK. et al. 2008; Lamberg, BA , Liewendahl, K. 1990) 

   Subclinical or Primary Hypothyroidism “often remains undetected,” diagnosed by assessing TSH level (High TSH, normal Free T4); but insufficient if Secondary or “Central Hypothyroidism is either present or suspected”. (Garber, JR. et al. 2012. p. 990; Vanderpump, MPJ. 2011; Mandel, SJ. et al. 1993).
   Symptoms include: Myxoedema (swelling of face, hands and feet), inflammation and thickening of the skin, intolerance to cold, weight gain, weakness, lethargy, fatigue, irregular menses, impaired memory and depression.
   Primary Hypothyroidism accounts for 95% of cases, while Central Hypothyroidism is often the result of Hypothalamic-Pituitary tumour, its treatment, or other Pituitary dysfunctions, and will show very low levels of TSH, along with low TH.  (Dieffenbach, S. 2015; Yamada, M. Mori, M. 2008)
​

   Triiodothyronine (T3) and Thyroxine (T4), which respectively contain three and four atoms of Iodine, are known as Thyroid Hormone (TH): required for normal functioning of numerous tissues in the body (see presentation). T3 and T4 are synthesised from Tyrosine and Iodine in the Thyroid Gland, process controlled by the Thyroid-Stimulating Hormone (TSH), secreted by the Pituitary. Production of TSH is stimulated by Thyrotropin-releasing hormone (TRH), released from the hypothalamus. Production of TSH and TRH is decreased by Thyroxine via negative feedback. Not enough TRH, can lead to low TSH, and subsequently, to reduced thyroid hormone production. (Dieffenbach, S. 2015; Persani, L. 2012)
 
   Because most body cells have receptors for thyroid hormones, T3 and T4 exert their effects throughout the body. TH increases metabolic rate (maintaining normal body temperature), is involved in intracellular pH regulation, cell volume regulation, and stimulate formation of blood vessels and cell growth. (Cheng, SY. Leonard, JL. Davis, PJ. 2010; Bobulescu, IA. Moe, OW. 2006) 
   Over 99% of both T3 and T4 are bound to transport proteins in the blood; however, only the free unbound TH is biologically active (Garber, JR. et al. 2012). When T4 enters a body cell, it is converted to T3.
   In hypothyroidism, metabolism is decreased at the cellular level, with every tissue in the body functioning at suboptimal level. (Zaidi, S. 2014), and is often due to an increase production of Reverse T3, the body’s emergency break(Holtorf, K. 2016). T3 is often replaced by T3 in response to chronic and heightened state of stress/anxiety/depression. 


  Risk factors: Hashimoto’s Thyroiditis, recent treatment with radioactive iodine, cancer treatment, treatment with Lithium, recent pregnancy and child delivery.
   Other causes: nutrient malabsorption (including IBS, starvation and fasting, Gliadin cross-reaction - gluten), medication, nutritional deficiencies, and iodine excess. (Sodano, WL, Grisanti, R. 2011)

Epidemiology

   “The standardized incidence of primary hypothyroidism varied between 3.90 and 4.89 per 1000 women per year between 1993 and 2001. The incidence of hypothyroidism in men significantly increased from 0.65 to 1.01 per 1000 per year” (Vanderpump, MPJ. 2011. p. 45 – UK data), and it is also higher in patients with Diabetes (Jia, F. et al. 2015), HIV (Tran, M. Odle, TG. 2005), Coeliac Disease (Collins, D. et al. 2012; McDermott, JH. et al. 2005), and other autoimmune conditions (Boelaert, K. et al. 2010).
​
​

Allopathic Treatment

​Hypothyroidism results from insufficient production of TH (Murray, M. Pizzorno, JE. 2012; Tran, M. Odle, TG. 2005). Treatment, therefore, involves hormones replacement. L-T4 (Levothyroxine) is usually recommended (few side effects, long serum half-life). L-T3 has many side effects, and is not recommended (Duntas, LH. Wartofsky, L. 2016; Dieffenbach, S. 2015; Escobar-Morreale, HF. et al. 2015; Laurberg, P. et al. 2005). Thyroid hormone replacement therapy maintains normal TH levels, and “reduces risk of cardiac disease, particularly from atherosclerosis.” (Tran, M. Odle, TG. 2005. p. 1043)
 
  The number of pregnant women initiated on L-T4 has increased over the years, aiming to correct maternal thyroid function and to decrease the rate of undesired obstetrical events. (Alexander, EK. et al. 2004).
   Treatment may carry postpartum and checked after 6 weeks. (Stagnaro-Green, A. 2015; Negro, R. et al. 2006). 

Drug/Nutrients–Drug/Drug interaction:

   Soya, and High-fibre diets, decreases absorption of Levothyroxine. (Bell, DSH. Ovalle, F. 2001)
   Calcium Carbonate, Ferrous sulfate, Sucralfate, Bile Acid Sequestrants, Antacids decrease T4 absorption. 
Phenytoin (Dilantin), Carbamazepine (Tegretol), and Sertraline (Zoloft) increase disposal of T4. (Singh, N. et al. 2000)

Naturopathic and functional medicine explanation
 
   Research gives a direct link between Insulin and Thyroid function.
   “There is convincing evidence for a major impact of thyroid function on all components of the metabolic syndrome, reflecting profound alterations of energy homeostasis at many levels.” (Iwen, KA. et al. 2013. p. 83), adding: “Thyroid dysfunctions and the metabolic syndrome are the two most common endocrine disorders with a substantial overlap.” 

Classification of obesogens

   Hyperglycaemia,  HDL/ŸLDL cholesterol, Ÿtriglycerides, hypertension, Hyperlipidemia, Diabetes Mellitus, obesity, gastrointestinal disturbances (and Dysbiosis), and visceral fat, are components of the metabolic syndrome with Insulin resistance as the main causative factor, proposing an imbalance in homeostasis, an increase in free radical production and inflammation, the leading causes of Cardiovascular Disease. (Van Tienhoven-Wind, LJN. Dullaart, RPF. 2015; Iwen, KA. et al. 2013; Longhi, S. Radetti, G. 2013; Sodano, WL, Grisanti, R. 2011; Balch, PA. 2010). “Hypothyroidism may be a leading cause of diabetes.” (Balch, PA. 2010. p. 516–518; Tran, M. Odle, TG. 2005) 

   Taddei, S. et al. (2006. p. 5076) explain that in patients with SHT: “low-grade chronic inflammation causes endothelial dysfunction and impaired NO availability by a COX-2-dependent pathway, bringing about increased production of oxidative stress.” Boelen, A. et al. (2011. p. 670) go further to explain that inflammation leads to “overall down-regulation of metabolism in order to save energy”: inhibiting thyroid metabolism and increasing the production of Reverse T3 from T4. (Holtorf, K. 2016)

   Longhi, S. Radetti, G. (2013. p. 40) give the final clue: “Hypothyroidism causes a weight increase together with a decrease in basal metabolic rate and Thermogenesis,” adding: “Body composition and thyroid hormones appear to be closely related since the latter is known to be involved in the regulation of basal metabolism and Thermogenesis, playing an important role in lipid and glucose metabolism, food intake and fat oxidation.”
   This leads to hypothesise that inflammation leads to Hypothyroidism and Hypothyroidism to inflammation, generating a vicious circle, with cardiovascular disease as an end result. (Holtorf, K. 2016; Balch, PA. 2010)

Functional Medicine University's Approach to Assess the Cause of Thyroid Dysfunction

   Sodano, WL, Grisanti, R. (2011), add that Hypothyroidism can find its root cause in gastrointestinal dysfunction (e.g. Dysbiosis) and, possibly, is the result of opportunistic bacterial/viral infections: “recurrent vaginal infections or a history of treatment with antibiotics, oral contraceptive or systemic glucocorticoids” (p. 12); they also include: “high intake of sugar”, “milk and other dairy products”, “hypochlorydia”, and “food allergies” (p. 14).   

   Bacterial lipopolysaccharides can trigger autoimmune Thyroiditis. (Bajaj, JK. et al. 2016)
Current research also links Epstein Barr virus to Hypothyroidism. A virus of the herpes family. Recent studies suggest that 95% of the entire population is infected by the virus. (www.ncbi.nlm.nih.gov/pmc/articles/PMC5099387/pdf/CEJI-41-28581; www.ncbi.nlm.nih.gov/pubmed/25931043)
 
   Hypothyroidism can find its source in IgA/IgG-led reactions (immune cells), often from a cross-reaction, which originates in the gut, between anti-Gliadin antibodies (core molecule of gluten), and Autoantibodies to thyroid Peroxidase (TPO-AB) (Briania, C. et al. 2008; Naiyer, AJ. et al. 2008). This reaction is also present in Autoimmune Diabetes (Szyper-Kravitza, M. et al. 2005). Confirming the hypothesis that autoimmune conditions are linked. (Boelaert, K. et al. 2010; KUČERA, P. et al. 2003)
 
   Environment, endocrine disrupters (e.g. PCBs, PBDEs, Thiocyanates (tobacco smoking), Percholarates (used in batteries, cars, etc), and Nitrates, affect thyroid function in many ways:

• Alteration of TH metabolism,
• Direct toxic effect on the gland, changing function and regulation,
• Production of thyroid antibodies,
• Interaction with thyroid protein carriers,
• Decreased iodine absorption in the GIT,
• Blocking iodine uptake by the thyroid gland (affecting the Pituitary-Thyroid axis, similarly to iodine deficiency),
• Increasing liver metabolism of the hormone, and affecting carrier proteins production synthesised by the liver,
• Interrupting reception in cells,
• Causing goitre, and tumours,
• Suppressing hormone production, and
• Increased urinary iodine excretion.

(Sodano, WL, Grisanti, R. 2011; Ward, MH. et al. 2010; Kostogrys, RB. et al. 2006; Eskiocak, S. et al. 2005; Tran, M. Odle, TG. 2005).

Note: Serum pollutant concentration can be aggravated by weight loss, since they tend to bioaccumulate in adipose tissue. (Lim, JS. et al. 2011; Sodano, WL, Grisanti, R. 2011)


   High oestrogen levels in the blood can prevent TH to enter the target cells, which can be exacerbated by pregnancy, OCP (pill), oestrogen therapy, but also Dysbiosis, by returning detoxified oestrogen into circulation. (Sodano, WL, Grisanti, R. 2011)
  
   “The thyroid gland has several mechanisms to resist oxidative stress. The thyroid cells (thyrocytes) are protected by the enzymes, Catalase (CAT), glutathione Peroxidase (GPx) and Superoxide Dismutase (SOD), both of which are selenium containing enzymes” (Sodano, WL, Grisanti, R. 2011. p. 38); a deficiency in Selenium can therefore lead to Hypothyroidism due to the damage impacted on follicular cells.
   T3 has pro-oxidant effect: increase oxygen consumption by mitochondria, to produce energy – generating Reactive Oxygen Species, and the use of cellular antioxidants to prevent oxidative damage. 

The Thyroid Gland and Oxidative Stress

Thyroid-Friendly Smoothie

​
​Why nutrient-density matters...
​
... and not restriction!

Get your free recipe

The Thyroid and Adrenal Connection

   Chronic stress and high levels of Cortisol show to cause thyroid and adrenal dysfunction (Sodano, WL, Grisanti, R. 2011); decrease of thyroid activity by converting T4 into Reverse T3 instead of T3, effectively shutting down the body (Patients in such case might benefit from T3 only); lower transportation of T4 into the cells. (Holtorf, K. 2016)

HPA (Hypothalamus-Pituitary-Adrenals)-HPT (Hypothalamus-Pituitary-Thyroid) Axes

   Recording basal body temperature can be an indicator of basal metabolic rate. “Hypofunction of the Thyroid gland and adrenal function are common causes of low metabolic energy” (Sodano, WL, Grisanti, R. 2011. p. 51). This is done first thing in the morning, and 2–3 times per day at the same time everyday, and recorded on a graph, such as below. 

Therapeutics

   Using Levothyroxine might be the sole treatment given in conventional medicine; however, a more holistic approach may be more appropriate. “Hypothyroidism diagnostic relies heavily on TSH levels, which is only an indication of what is going on at the level of the Pituitary, but not in peripheral tissues, including skin, muscles, bones and main organs. Hypothyroidism may be disregarded if TSH levels are within the range, despite patients experiencing most, or all, signs and symptoms.” Zaidi, S (2014)
   Since neonatal screening was introduced, treatment and dosage have increased dramatically, but “there are possible adverse effects of high-dose regimens and elevated T4 levels on temperament and behaviour in later childhood.”  (Hrytsiuk, I. et al. 2002. p. 485)
 
   “Alternative treatments are aimed primarily at strengthening the thyroid gland and will not eliminate the need for thyroid hormone medications. They include nutritional therapy, herbal therapy, and exercise” (Tran, M. Odle, TG. 2005. p. 1042)
 
    The association of Thyroid and Adrenal function prompts a specific protocol, and must be analysed beforehand. “In patients in whom hypothyroidism and severe hypoadrenalism coexist, administration of thyroid hormone prior to correcting adrenal insufficiency can trigger an ‘adrenal crisis’.”  (Sodano, WL, Grisanti, R. 2011. p. 68)
​   This is echoed by Yamada, M. Mori, M. (2008. p. 692): “Most cases of central hypothyroidism are accompanied by other hormone deficiencies, which should be examined, particularly those of the Adrenocorticotropic hormone–adrenal axis.” 
​

​

Naturopathic Treatment: Hypothyroidism (Hashimoto's), other thyroid dysfunction, Metabolic Syndrome and autoimmunity. 

​   Want to consult a practitioner that will listen to you and will guide you on your path to optimum health, then contact me today, and book your initial consultation. 

Book your consultation

Agrawal, NK. et al. (2008). Thyroid hormone resistance. Postgraduate Medical Journal. 84, pp. 473–477.
Available at: http://cmcendovellore.org/publications/Thyroid-hormone-resistance.pdf. Last accessed: 23th May 2016.
 
Ajjan, RA. Weetman, AP. (2015). The Pathogenesis of Hashimoto's Thyroiditis: Further Developments in our Understanding. Hormone and metabolic research. 47 (10), pp. 702–710.
 
Alexander, EK. et al. (2004). Timing and Magnitude of Increases in Levothyroxine Requirements during Pregnancy in Women with Hypothyroidism. The New England Journal of Medicine. 351, pp. 241–249.
 
Armanini, D. et al. (2016). Interrelationship Between Vitamin D Insufficiency, Calcium Homeostasis, Hyperaldosteronism, and Autoimmunity. The Journal of Clinical Hypertension.  Early View (Online Version of Record published before inclusion in an issue). Available at: http://onlinelibrary.wiley.com/doi/10.1111/jch.12822/full. Last accessed: 26th May 2016.
 
Bajaj, JK. Salwan, P. Salwan, S. (2016). Various Possible Toxicants Involved in Thyroid Dysfunction: A Review. Journal of Clinical and Diagnostic Research. 10 (1), FE01-FE03.
 
Balch, PA. (2010). Hypothyroidism. In: Bell, S Prescription for Nutritional Healing: A practical A-to-Z Reference to Drug-Free Remedies Using Vitamins, Minerals, Herbs and Food Supplements. 5th ed. London: Penguin Group. pp. 516–518.

Basch, E. et al. (2003). Therapeutic Applications of Fenugreek.Alternative Medicine Review. 8 (1), pp. 20–27.
Available at: http://inconnate.com/Download/Fenugreek/document3.pdf. Last accessed: 25th May 2016
 
Bell, DSH. Ovalle, F. (2001). Use of Soy Protein Supplement and resultant need for increased dose of Levothyroxine. Endocrine Practice. 7 (3), pp. 193–194.
 
Bland, J. (2002). Breakthrough Approaches for Improving Adrenal and Thyroid Function. Nutritional Endocrinology. Syllabus pp.82–167 
 
Bobulescu, IA. Moe, OW. (2006). Na+/H+ Exchangers in Renal Regulation of Acid-Base Balance. Seminars in Nephrology. 26 (5), pp. 334–344. Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2878276/pdf/nihms-194791.pdf. Last accessed: 9th May 2016.
 
Boelaert, K. et al. (2010). Prevalence and Relative Risk of Other Autoimmune Diseases in Subjects with Autoimmune Thyroid Disease .The American Journal of Medicine. 123 (2), pp. 183.e1–183.e9.
 
Boelen, A. Kwakkel, J. Fliers, E. (2011). Beyond Low Plasma T3: Local Thyroid Hormone Metabolism during Inflammation and Infection. Endocrine Reviews. 32 (5), pp. 670–693. Available at: http://press.endocrine.org/doi/pdf/10.1210/er.2011-0007. Last accessed: 18th May 2016.
 
Bona, G.et al. (2015). Etiology of Congenital Hypothyroidism. In: Bona, G. De Luca, F. Monzani, A Thyroid Diseases in Childhood. Recent advances from basic science to Clinical Practice. Switzerland: Springer International Publishing. pp. 27–32.

Carlé, A. et al. (2008). Thyroid Volume in Hypothyroidism due to Autoimmune Disease Follows a Unimodal Distribution: Evidence against Primary Thyroid Atrophy and Autoimmune Thyroiditis Being Distinct Diseases - See more at: h. The Journal of Clinical Endocrinology & Metabolism. 94 (3), pp. 833–839. 
Available at: http://press.endocrine.org/doi/pdf/10.1210/jc.2008-1370. Last accessed: 9th May 2016.
 
Cheng, SY. Leonard, JL. Davis, PJ. (2010). Molecular aspects of thyroid hormone actions. Endocrine Reviews. 31 (2), pp. 139–70.
 
Christianson, A (2014). Adrenal Reset Diet, the: Strategically Cycle Carbs and Proteins to Lose Weight, Balance Hormones, and Move from Stressed to Thriving. New York: Harmony Books.
 
Collins, D. et al. (2012). Celiac Disease and Hypothyroidism . The American Journal of Medicine. 125 (3), pp. 278–282.
 
Holtorf, K. (2016). Thyroid disorders. In: Elsegood, L The LDN Book: How a Little-Known Generic Drug — Low Dose Naltrexone — Could Revolutionize Treatment for Autoimmune Diseases, Cancer, Autism, Depression, and More. Vermont: Chelsea Green Publishing. pp. 81–98.

Murray, M. Pizzorno, JE. (2012). Hypothyroidism. The Encyclopaedia of Natural Medicine. 3rd ed. New York: Atria Paperback. pp. 716–723.
 
Murray, M. Pizzorno, JE. Pizzorno, L. (2006). The Encyclopaedia of Healing Foods. The Most Comprehensive, user-friendly A-Z Guide available on the Nutritional Benefits and Medicinal Properties of Food. London: Piatkus Books Ltd.
 
Naiyer, AJ. et al. (2008). Tissue Transglutaminase Antibodies in Individuals with Celiac Disease Bind to Thyroid Follicles and Extracellular Matrix and May Contribute to Thyroid Dysfunction. Thyroid. 18 (11), pp. 1171-1178.
 
Negro, R. et al. (2010). Universal Screening Versus Case Finding for Detection and Treatment of Thyroid Hormonal Dysfunction During Pregnancy. the Journal of Clinical Endocrinology and Metabolism. 95, pp. 1699 –1707.
Available at: http://cfpcwp.com/MCDG/wp-content/uploads/2013/02/Thyroid-Screening-in-Preg-J-Clin-End-Metab2010.pdf. Last accessed: 9th May 2016. (see annexes)
 
Negro, R. et al. (2010). Increased Pregnancy Loss Rate in Thyroid Antibody Negative Women with TSH Levels between 2.5 and 5.0 in the First Trimester of Pregnancy. The Journal of Clinical Endocrinology and Metabolism. 95 (9), E44 –E48.
Available at: http://press.endocrine.org/doi/pdf/10.1210/jc.2010-0340. Last accessed: 9th May 2016. (see annexes)
 
Negro, R. et al. (2006). Levothyroxine Treatment in Euthyroid Pregnant Women with Autoimmune Thyroid Disease: Effects on Obstetrical Complications. The Journal of Clinical Endocrinology & Metabolism. 91 (7), pp. 2587–2591.
Available at: http://press.endocrine.org/doi/pdf/10.1210/jc.2005-1603. Last accessed: 13th May 2016.
 
NHS UK. (2015). Underactive thyroid (hypothyroidism). 
Available: http://www.nhs.uk/conditions/Thyroid-under-active/Pages/Introduction.aspx. Last accessed 1st May 2016.
 
Odle, TG. (2005). Dementia. In: Longe, JL The Gale Encyclopedia of Alternative Medicine. 2nd ed. Farmington Hills: Thomson Gale. pp. 851–852.

Sodano, WL, Grisanti, R. (2011). Functional Medicine Approach to Diagnosis and Treatment of Thyroid Dysfunction. Functional Medicine University's Functional Diagnostic Medicine Training Program. Greer: Functional Medicine University. pp. 1–76.
(see annexes)
 
Stagnaro-Green, A. (2015). Postpartum Management of Women Begun on Levothyroxine during Pregnancy. Frontiers in Endocrinology. 6 (83), (A183) pp. 1–5. Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4663256/pdf/fendo-06-00183.pdf. Last accessed: 13th May 2016.
 
Stagnaro-Green, A. et al. (2011). Pregnancy and Foetal Development. Thyroid. 21 (10), pp. 1081–1125.
Available at: http://online.liebertpub.com/doi/pdf/10.1089/thy.2011.0087. Last accessed: 9th May 2016.
 
Tran, M. Odle, TG. (2005). Dementia. In: Longe, JL The Gale Encyclopedia of Alternative Medicine. 2nd ed. Farmington Hills: Thomson Gale. pp. 597–600, pp. 1040-1044.
 
Yamada, M. Mori, M. (2008). Mechanisms related to the pathophysiology and management of central hypothyroidism. Nature Clinical Practice Endocrinology & Metabolism. 4, pp. 683–694. 
Available at: http://www.readcube.com/articles/10.1038/ncpendmet0995. Last accessed: 9th May 2016