Overview

Low thyroid function, called hypothyroidism, is associated with a wide variety of disorders, including: Often these disorders resolve when hypothyroidism is treated [Starr2005].

Far more people in the United States have hypothyroidism than is commonly diagnosed, due to over-reliance on the TSH blood test as the definitive diagnostic tool in mainstream medicine [Starr2005]. Basal body temperature appears to be the most reliable indicator of functional thyroid capacity.

Please see conventional, complimentary and alternative medical treatments for important background information regarding the different types of medical treatments discussed on this page. Naturopathic, Complimentary and Alternative treatments that may be considered include:

Etiology

Hypothyroid disease may be due to a number of causes, including poor adrenal function, environmental toxicity, inadequate nutrition, autoimmune disease, and genetic predisposition.

Prolonged treatment with supraphysiological doses of corticosteroids such as prednisone can also lower thyroid function [Starr2005, pg 158].

Starr has identified two types of hypothyroid disease, which he refers to as Type I and Type II. In analogy with Diabetes Types I and II, Hypothyroidism Type I is due to a failure of the thyroid gland to produce adequate thyroid hormone, while Hypothyroidism Type II is attributed to cellular resistance to circulating thyroid hormone [Starr2005].

There are many causes for inadequate thyroid hormone being produced, which may result from a failure of the hypothalamus to produce Thyroid Releasing Hormone (TRH), failure of the pituitary to produce Thyroid Stimulating Hormone (TSH), failure of the thyroid gland to produce T4, or failure of the liver and kidneys to convert the T4 to the most active form of the thyroid hormone, T3. In some cases the peripheral tissues convert T4 to an inactive form called reverse-T3. Blood tests can help identify the nature of these failures in Type I Hypothyroidism.

On the other hand, when hypothyroidism is due to lack of cellular response to adequate levels of T3 (i.e. Type II Hypothyroidism), blood tests may appear to be normal and the diagnosis must be made based on signs and symptoms [Starr2005].

Some practitioners have noted an association with inflammatory process mediated by homocysteine [Rogers2008, pg 9]. Note that the common diuretic hydrochlorothiazide (HCTZ) increases homocysteine levels [Westphal2003  🕮 ].

Diagnosis

One study has shown that patient medical history (signs and symptoms) was more reliable (76%) than either physical examination (12%) or lab tests (11%) in diagnosing hypothyroidism [Starr2005, pg 72], [Peterson1992  🕮 ].

Differential Diagnosis

  •  >   
    Hashimoto's (Autoimmune) Thyroiditis [Kharrazian2010].
  •  >   
    Iodine deficiency (check urine) [Brownstein2009].
  • Chronic fatigue syndrome
  • Anemia
  • Euthyroid sick syndrome
  • Depression
  • Congestive heart failure
  •  >   
    Adrenal Deficiency (leads to intolerance of thyroid supplements)
  •  >   
    Adrenal Excess (shuts down thyroid) [Hill1950  🕮 ],
  • Primary Amyloidosis [Domino2017]
  • Dementia not due to hypothyroidism [Domino2017]
  • Thyrotropin-secreting pituitary adenoma [Domino2017]
  •  >   
    Selenium deficiency (check RBC selenium) [Pelter1999].
  •  >   
    Magnesium deficiency (check RBC magnesium) [Starr2005, pg 183].
  •  >   
    Zinc deficiency (check plasma zinc) [SpectraCell seminar 5/2010].
  •  >   
    Iron deficiency (check ferritin) [Barnes_Research_Foundation],
  • Estrogen causing overproduction of thyroid binding globulin, which reduces free-T3 [Kharrazian2010, pg 5].
  • Myxedema (hydrated mucin) must be distinguished by palpable texture from subcutaneous fat in skinfold measurements, e.g. on the lateral arm.
  • Copper toxicity can cause hypothyroidism; This may especially be a problem in "red-rock" areas of Arizona, where the soil/water may be high in copper.
  • Toxins: Fluorine (toothpaste, water), Bromine (polybrominated biphenyls = PBBs, hot spas, some carbonated beverages, fire retardants), Perchlorates (rocket fuel), Phthalates and Bisphenol A (in some plastics), Pyridines (cigarette smoke), PCBs, UV screens (sunblocks), cosmetics, pesticides, VOCs (volatile organic compounds) [Myhill2018, pg 81]
  • Viral thyroiditis [Myhill2018, pg 81]
  • Thyroid hormone receptor resistance [Myhill2018, pg 81]
  • Natural goitrogens (e.g. cruciferous vegetables and soy. Fermented soy may be less of a problem) [Myhill2018, pg 81]

Treatment

Naturopathic, Complimentary and Alternative Treatments

It is important to treat the patient's symptoms rather than their labs. Resolution of symptoms is more important than "normalization" of lab values. However, it is even more important to find and treat the cause, since if left untreated the underlying cause can cause further damage and result in even worse symptoms arising [Kharrazian2010].

Some symptoms of hypothyroidism will respond to treatment within a few months (thyroid replacement must be titrated up slowly), while it may take years for other symptoms (such as symptoms due to mucin deposition) to respond fully.

  • When treating hypothyroidism, it is important to also address adrenal dysfunction if present, due to the interaction between thyroid hormones and cortisol. Boosting thyroid function in a patient with hypoadrenalism can further stress the adrenals, and contrariwise, poor adrenal function can impact thyroid function. This requires a careful balancing of thyroid and adrenal aspects of the treatment with frequent evaluation and adjustments to the treatment protocol.
  • While Dr. Barnes typically started thyroid hormone first and then addressed adrenal insufficiency if necessary, Dr. Starr suggests starting with a course of iodine/iodide supplementation for one to four weeks to boost adrenal function before beginning thyroid hormone. Other doctors start with a 4 to 7 day course of low dose corticosteroids before beginning thyroid hormone [Starr2005, pg 186].
  • Provide nutritional support to the thyroid as indicated by testing.
  • Conventional medicine tends to prescribe only T4 (levothyroxine, Synthroid, Levoxyl, Unithroid), and occasionally T3 (Cytomel). There is also a product named Thyrolar that contains both T4 and T3.
  • Dr. Sonkin suggests starting with a dose of 50mcg T4 and titrating dose up to 150mcg T4 over several weeks, and then adding 5mcg T3 and titrating T3 up to 25mcg in 5mcg increments until symptomatic picture resolves [Sonkin1997  🕮 ], [Starr2005, pg 172].
  • Naturopaths more often supplement with a bioequivalent blend of T4 and T3 hormones in a sustained release formulation from a compounding pharmacy (the FDA frowns on using the word bio-identical).
  • Dr. Barnes and others argue that the most effective approach is a natural product such as desiccated pork thyroid gland (Armour Thyroid) [Barnes_Research_Foundation], [Barnes1972], [Barnes1976a], [Baisier2001], [Barnes1999], [Starr2005, pg 174].
  • Dr. Barnes recommended starting a relatively healthy adult with 1 grain desiccated thyroid and titrating up to 5 grains in increments of 0.5 grain/month until symptomatic relief is obtained or side effects develop. When treating children, start with one-quarter grain for children under three, or one-half grain in children over six, and titrate up more slowly by increments of one-quarter grain per two months. Dr. Barnes suggests a very slow rate of increase for persons with existing heart disease with a maximum of 2 grains for persons with a history of heart attack (other practitioners will go up to 2.5 grains). Dr. Barnes recommended not starting thyroid treatment until 2 months after a heart attack.
  • Dr. Starr suggests starting all patients with one-quarter grain of desiccated thyroid [Starr2005, pg 178].
  • When converting a patient from T4 to desiccated thyroid, Dr. Starr recommends maintaining the existing level of T4 and titrating desiccated thyroid up, and then titrating the T4 down [Starr2005, pg 178].
  • Generally speaking, stop titrating up when the patient's heart rate rises 10-15 beats per minute (BPM) above baseline [Starr2005, pg 179].
  • Response to thyroid replacement therapy is slow - typically 6 to 12 months [Starr2005, pg 178].
  • Doctors Sonkin, Cohen, and Rawson also used T3-propionate, which is no longer commercially available in the United States. T3-propionate is slowly released into the blood stream and is better tolerated by some individuals. Apparently, since this product is not patentable, pharmaceutical companies have no interest in developing this product [Starr2005, pg 173].
  • Note that 100mcg T4 is equivalent to 1 grain of desiccated thyroid (1 grain = 64.8mg).
  • When titrating a patient up, if symptoms worsen, this is a signal that there may be an adrenal deficiency, iodine deficiency, or environmental toxicity that needs to be dealt with before increasing thyroid supplementation [Starr2005, pg 179].
  • Overdosing thyroid supplements tends to elevate heart rate, but not affect blood pressure much [Starr2005, pg 190].
  • Regardless of the type, thyroid supplements are best taken on an empty stomach, first thing in the morning at least 20-30 minutes before eating.
  • When treating hypothyroid conditions, onset of any of the following symptoms may be a signal that too much thyroid hormone has been administered, and the patient should discontinue taking the medication and contact the prescribing physician immediately [Starr2005, pg 181]:
    • Increase of basal body temperature above 98.2 degrees F.
    • Increase of heart rate above age/gender norms or 15 BPM above baseline.
    • Nervousness, tremor, or increased problems sleeping.
    • Weight loss.
    • Excessive sweating.
  • Treat iodine deficiency if present.
  • Treat selenium deficiency if present (200-400mcg/day) [Pelter1999].
  • Treat iron deficiency if present (ferrous glycine is well tolerated) [Barnes_Research_Foundation], [Starr2005, pg 182].
  • Treat magnesium deficiency if present.
  • Treat dyslipidemia (cholesterol imbalance) if present; however Dr. Weyrich notes that correcting T4 levels will often correct dyslipidemia without further intervention.

Low Dose Naltrexone (LDN)

[LdnResearchTrust_conditions] reports that hypothyroidism is a condition that LDN could help. Dr. Weyrich has been trained in the use of Low Dose Naltrexone (LDN), and has treated one patient with Hashimoto's thyroiditis with LDN.

Please see What is Low Dose Naltrexone? for more information.

Pathophysiology

Myxedema results from an accumulation in the tissues of a substance called mucin. Mucin is a jelly-like substance that absorbs water, resulting in a boggy swelling of the tissues. This is unlike the pitting edema seen in congestive heart failure, in that the water is bound to the mucin instead of being mobile. Other tissues throughout the body are also affected, which results in impaired function of many organ systems [Starr2005, pp 2-3].

See [Holtorf2014] [Holtorf2014a]

Hypotheses

In some cases, patients exhibit a paradoxical sign/symptom picture that is often associated with hyperthyroidism, except that these patients also have low body temperature and respond well to treatment of hypothyroid. It has been proposed that in these cases, the body is compensating for low thyroid status by increasing sympathetic tone (adrenaline or other adrenal hormones) [Starr2005, pg 15].

Armour Thyroid may give better results with fewer side effects because the glandular product contains a mixture of T4, T3, T2, and T1 [Starr2005, pg 174]. It is known that T1 slows the heart rate and induces hypothermia [Scanlan2004  🕮 ], so it may moderate side effects by balancing the effects of T3. Note however that some studies show that T3 is converted to T2 and T1 primarily in the peripheral tissues, which raises questions regarding how much T2 or T1 is found in desiccated thyroid [Kelly2000  🕮 ].

Dr. Weyrich notes published data shows hypothyroid patients treated with T4 only have symptom scores and urinary T3 levels comparable to controls, whereas when these same patients are treated with natural desiccated thyroid, their symptom scores drop dramatically and their urinary T3 levels rise dramatically [Baisier2001]. This suggests that the "peripheral resistance to thyroid hormone" that [Starr2005] refers to as "type-II hypothyroidism" is at least in large part due to the inability of these patients to convert T4 to the more active T3 form.

ICD-9 Codes

ICD-9 CodeDescriptionComments
244.0Hypothyroid, Post-surgical 
244.1Hypothyroid, Other post-ablative 
244.2Hypothyroid, Iodine 
244.8Hypothyroid, Other acquired (specify) 
244.9Hypothyroid, Unspecified 
780.79Fatigue and malaise 
783.9Hypometabolism 

References