Thyroid

Hashimoto’s patients fluctuate between hypo and hyper thyroidism.  This is why TSH (thyroid stimulating hormone) alone is not a good measurement of thyroid function.

 

Prevalence:  1 in 5 women.  Women are 5 to 8 times more affected than males. 50% go undiagnosed.

                                             

How does Hashimoto’s develop?

1. Body develops “leaky gut” or a permeable gut: Molecules that are meant to stay in gut leak into the blood stream.  The body’s immune system launches an attack on these molecules and the thyroid gland.

2. Genetic predisposition: Having the gene may or may not predispose one to the disease.

3. Trigger event: genes are expressed.

 

Recommended lab tests: *TSH (this may take years to elevate) *TPO antibodies  *Free T3     *Free T4 (T4 alone won’t tell you if the patient T3 is converting to T4).

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T4 is a prohormone that can roll to make T3 (active hormone) or reverse T3 (inactive hormone). If you only give T4 the patient may not improve because they have impaired T4 to T3 conversion.  This is why some practitioners prefer Nature Thyroid which is desiccated thyroid from a pig.  This type of thyroid contains T3 & T4.  

                   

What inhibits T4 from going to T3? 

• Stress  

• nutrition

• oxidative stress

• lifestyle factors

• medications     

• genetics    

• blood sugar regulation

              

Nutrients that help T4 to go to T3?

• Vitamin A         

• Vitamin B    

• Iodine (less than 250mg)   

• Iron  

• Selenium 200 mcg

• tyrosine      

• selenium 200mcg     

• potassium   

• zinc

 

You cannot help a patient with Hashimoto’s without also addressing their stress levels. 

Stress is the root cause of most diseases.  90% of patients with Hashimoto’s have an adrenal issue.  Thyroid symptoms equal adrenal symptoms.  Patient is started on a thyroid medicine …. initially feels great but then symptoms return.

  

General strategies for stress reduction:

• Adaptogens   

• Balance blood sugar   

• Address nutrient depletion  

• Rest

• eliminate inflammation

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Conventional Standard of Care                 

• disease is labeled: treated as one size fits all               

• only test TSH                                                              

• use outdated reference range                                      

• all thyroid disease is treated the same                        

• write a prescription                              

• give Synthroid (T4 only)                                              

• diet & nutrition are rarely considered                          

Functional Medicine Approach

• patient centered: customize treatment

• test TSH, free T3/T4 and antibodies

• use optimal range/look at symptoms

• treat autoimmunity & its root cause

• educate the patient

• give T3 & T4 and supplements

• use food & nutrition as medicine

• empowering … you can get better

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Simple way to check your thyroid:  is to do a basal temperature test: Place a digital thermometer by the bed.  In the morning, with as little movement as possible take temperature   Normal: 97.8-98.2 | less than 97.8: hypothyroid | more than 98.2: hyperthyroid or infection.

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The Thyroid Solution: Ridha Arem M.D.  

Bestselling book with a functional medicine approach.  Minimal thyroid imbalances have an important effect on mental and physical health.

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Doctors continue to treat thyroid dysfunction as a simple physical disorder rather than what it is: a complex blow to the body and brain.  Some doctors may give antidepressants, and a pep talk instead of blood tests, proper medication and counseling on how to cope with their problems.  Thyroid imbalance can quickly escalate into a destructive brain chemistry disorder.  Many physicians perceive the symptoms of hypothyroidism as trivial…… tiredness, lack of interest in life, and weight gain.  A doctor may feel uncomfortable dealing with the patient’s mental anguish and instead stick to the familiar territory of performing a physical examination, obtaining lab test results and writing a prescription.

• an underactive thyroid causes depression

• an overactive thyroid causes anxiety

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Stress and thyroid imbalance, which comes first?  The biochemical cascade that links the brain to the immune system is at the root of how mental stress triggers thyroid imbalance.  The two most common underlying causes of thyroid dysfunction are disorders of the immune system.  

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Hashimoto’s thyroiditis: a thyroid deficiency         

Graves’ disease: excess thyroid

Both are auto immune … body is attacking self.  Stress management should become a central part of any strategy for treating thyroid patients.  

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The greater the excess of thyroid hormone, the lower the TSH will be; the greater the deficit the higher the TSH will be. 

These drugs increase TSH:                                                   

• amiodarone

• haloperidol                                                     

• metoclopramide

• lithium              

 

These drugs decrease TSH:

• heparin

• somatostatin 

• cortisone 

• dopamine     

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If a patient is on too high a thyroid dose his TSH becomes low.  If less than 0.5 then we see a 712% increase in cognitive impairment.  

 

Merck Manuel: A bestselling mainstream medical textbook.

The thyroid regulates the metabolic rate of the body.  The gland itself should be the shape of a bowtie which cannot be seen and can barely be felt.  Hypothyroidism is common, especially among older people, particularly women.  It affects about 10% of older women.  Severe hypothyroidism is called myxedema.  Can be diagnosed with one simple blood test: TSH.  In rare cases that are caused by inadequate secretion of TSH, a second blood test is needed to measure the level of the thyroid hormone T4 that is not bound by protein (free).  A low level confirms the diagnosis of hypothyroidism.  Preferred preparations are synthetic T4.  Start low with the dose and gradually increase until the TSH returns to normal.

The Wisdom of Menopause: bestselling book by Dr. Christiane Northrup.  

Thyroid problems are very common during peri and postmenopausal years.  Some women are completely asymptomatic, and others may have a wide variety of symptoms.  The most common symptoms are mood disturbances (depression and irritability), low energy level, weight gain, mental confusion and sleep disturbances.  26% of women in or near perimenopause are diagnosed with hypothyroidism.  Dr John Lee thought there was a cause-and-effect relationship between inadequate levels of thyroid hormone and estrogen dominance.  When estrogen is not properly counterbalanced with progesterone, it can block the action of the thyroid hormone.  The American Association of Clinical Endocrinologists says the upper limit for TSH should be about 3.0 whereas Dr. Northrup thinks the upper limits of TSH should be 2.5.

The role of iodine in thyroid disease: iodine is an essential element that your body needs to produce thyroid hormones.  If your T3 and T4 levels are normal but your TSH is elevated, you may be suffering from an iodine deficiency.  Other signs of iodine deficiency include apathy, depression, and reduced mental function.  Currently 13% of US citizens are iodine deficient.  It used to be 3% back in 1974.  Ironically, too much iodine in your body can shut down the production of thyroid hormone which will lead to a lower level, so don’t overdo it.  If you are taking thyroid hormones, the introduction of iodine often increases the body’s capacity to produce thyroid on its own.  So, if you are taking thyroid and start iodine you may increase the body’s capacity to produce thyroid hormone on its own…shakiness, rapid heart rate, and nervousness may occur.  Note that this entire topic of iodine supplementation is highly controversial.

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Natural ways to help your thyroid level recover?   Balance out your   

1. adrenal stress  

2. glycemic stress       

3. iodine deficiency        

4. estrogen dominance

 

Factors That Inhibit T4 to T3 Conversion:  Dr. John Monaco, MD 

Medications Include:

• glucocorticoids beta blockers  

• low progesterone  

• SSRI                                                                     

• opiates   

• phenytoin   

• theophylline   

• lithium         

• excess iodine

 

Applied Therapeutics: Mary Ann Koda-Kimball, Clinical Pharmacy Textbook

T3 is four times more potent than T4 but its serum concentration is lower.  T4 is the major circulating hormone secreted by the thyroid.  In contrast, about 80% of the total daily T3 production results from the peripheral conversion of T4 to T3 through deiodination of T4.  T4 has intrinsic biological activity and does not function solely as a prohormone.  35 to 40% of secreted T4 is converted peripherally to T3, another 45% of secreted T4 undergoes peripheral conversion to inactive reverse T3 (rT3).  Certain drugs and diseases can modify the conversion rate of T4 to T3 and decrease the serum T3 levels.

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99.7% of circulating T4 is bound to plasma proteins which accounts for T4’s slow metabolic degradation and long half-life of seven days.  In contrast T3 is less strongly bound to plasma proteins which accounts for its threefold greater metabolic potency and its shorter half-life of 1 ½ days.

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Hypothyroidism can be caused by either primary (thyroid gland) or secondary (hypothalamic pituitary) malfunction.  Primary is more common.

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Hashimoto’s thyroiditis, an autoimmune disorder, is the most frequent cause of primary hypothyroidism and appears to have a strong genetic disposition.  The destruction of thyroid cells by circulating thyroid antibodies produces a defect or block in the intrathyroidal binding of iodide.  Clinical presentation depends upon the time of patient diagnosis.  Typical presentations are hypothyroidism and goiter.  Hashimoto’s can be related to Graves’ disease (hyperthyroidism).  Both diseases share similar clinical features: positive antibody titers, a goiter, a familial tendency, and predilection for women.  Both diseases can exist in the same gland manifesting themselves in different ways…. thyrotoxicosis can precede the onset of Hashimoto’s hypothyroidism, and Graves’ hyperthyroidism can lead to hypothyroidism.  

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Typical symptoms: weight gain, fatigue, sluggishness, cold intolerance, constipation, heavy menses and muscle aches. A goiter may or may not be present.

 

Diagnostic lab findings:

• Overt hypothyroidism: elevated TSH and low FT4 (free thyroxine levels)

• Subclinical or early hypothyroidism: elevated TSH and normal free thyroxine level.

• Levothyroxine seems to be the drug of choice.  dose is 1.6 to 1.7micrograms/kg/day

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However, with elderly, severe hypothyroidism and cardiac toxicity …. start low and gradually increase.

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Over-replacement of levothyroxine (with resulting low serum concentrations of TSH) causes osteoporosis & cardiac changes.   It will take 6 to 8 weeks to get to steady state dosage.  Once a patient is euthyroid test every 3 to 6 months the first year and then yearly thereafter.  Medications that interfere with thyroxine absorption (iron, aluminum HCl) should be avoided.  

 

Synthroid’s (levothyroxine) Drug Interactions: taken from Synthroid’s package insert and Medscape.

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amitriptyline: Concurrent use of tricyclic (e.g., amitriptyline) antidepressants and Synthroid may increase the therapeutic and toxic effects of both drugs, possibly due to increased receptor sensitivity to catecholamines. Toxic effects may include increased risk of cardiac arrhythmias and central nervous system stimulation. Synthroid may accelerate the onset of action of tricyclics. Administration of sertraline in patients stabilized on Synthroid may result in increased Synthroid requirements.  

 

propranolol: Synthroid may decrease conversion of T4 to T3.  Potential impact: Administration of enzyme inhibitors decreases the peripheral conversion of T4 to T3, leading to decreased T3 levels. However, serum T4 levels are usually normal but may occasionally be slightly increased.

 

metformin: levothyroxine decreases the effects of metformin by pharmacodynamic antagonism.

 

omeprazole:   Gastric acidity is an essential requirement for adequate absorption of levothyroxine. Sucralfate, antacids and proton pump inhibitors may cause hypochlorhydria, affect intragastric pH, and reduce levothyroxine absorption.

 

phenytoin: Phenytoin and carbamazepine decrease the serum protein binding of levothyroxine, leading to a 20% to 40% reduction in total and free T4 levels. However, most patients maintain normal serum TSH levels and exhibit clinical euthyroidism.

 

furosemide: has been shown to inhibit the protein binding of T4 to TBG and albumin, causing an increase in free T4 fraction in serum. Furosemide competes for T4-binding sites on TBG, prealbumin, and albumin, so that a single high dose can acutely lower the total T4 level. 

 

heparin: levothyroxine increases the effects of heparin by pharmacodynamic synergism.  Avoid.  

 

digoxin: levothyroxine decreases effects of digoxin by an unknown mechanism.  Use caution and monitor.

 

warfarin: levothyroxine increases the effects of warfarin

 

birth control pills:  These drugs may increase serum thyroxine-binding globulin (TBG) concentration.  More of your thyroid is bound?  Less thyroid is active.