Background of hypothyroidism
Hypothyroidism is the most common thyroid disorder prevalent in the United States. Currently, hypothyroidism affects around 0.1-0.2% of the population. Hypothyroidism is caused by a deficiency of thyroid hormone (TH) production from the thyroid gland. The thyroid gland is a butterfly shaped gland found on the anterior surface of your neck.
Hypothyroidism affects women 5-8 times more than men. Hypothyroidism has been implicated as one of the greatest factors in clinical depression amongst depressive patients.
Diagnosing hypothyroidism can be done by your primary care provider along with treatment as well. Increasingly, many patients are diagnosed with hypothyroidism while being screened for other medical conditions.
Pathophysiology of hypothyroidism
Before we can discuss hypothyroidism one must be knowledgeable about the negative feedback system. To simplify the operation of the negative feedback system think of this scenario — your thermostat is set to 71 degrees however the house is currently 69 degrees. When your house’s temperature reaches 71 degrees the thermostat will shut off. When the temperature falls below 71 degrees the thermostat will kick back on until 71 degrees is once again achieved.
Now, let’s compare the thermostat scenario to your body’s hormonal regulation using negative feedback. The hypothalamus releases thryotropin-releasing hormone (TRH) and sends it to the pituitary gland. The pituitary gland releases thyroid stimulating hormone (TSH), which in turn is sent to the thyroid gland. When the thyroid gland detects the TSH the thyroid gland responds by releasing TH; the THs are T3 and T4. When TH levels rise and become sufficient, they will then send a negative feedback message to the hypothalamus to stop releasing TRH. When TH levels fall TRH is once again released signaling for the thyroid gland to increase TH levels.
Hypothyroidism is also classified as primary or secondary. Primary hypothyroidism is characterized by insufficient TH release directly from the thyroid gland. Secondary hypothyroidism, which is a very uncommon form of hypothyroidism, are conditions that impair hypothalamic-pituitary function, which can be manifested as failure of TRH or TSH release.
Types of primary hypothyroidism
Hashimoto’s thyroiditis. Hashimoto’s is the most common form of hypothyroidism. It is sometimes referred to as autoimmune thyroiditis and is the result of an immune-mediated injury. In other words, at some point during your life your body starts to synthesize antibodies against your thyroid gland.
Postpartum hypothyroidism. Postpartum hypothyroidism is considered another variant of Hashimoto’s affecting ~5% of women during the postpartum period. This presentation is preceded by a very short period of hyperthyroidism which may present as “a state of increased tension” followed by a brief period of hypothyroidism which peaks around 3-4 months postpartum and its presentation can be attributed to an increase in antibody production from the pregnancy. Symptoms resolve spontaneously within ~2 months, but the presentation tends to reoccur with subsequent pregnancies.
Screening for hypothyroidism
Screening can be achieved through a few avenues however the gold standard is done by obtaining your TSH and free T4. Since TSH is released from your pituitary obtaining this measurement will determine if the hypothyroidism originates from within the hypothalamic-pituitary pathway or not. If your TSH levels come back normal, then you can rule out a pituitary problem and consider that the problem is originating within the thyroid gland itself.
Remember, TSH stimulates your thyroid gland to release T3 and T4. If TSH levels are low, then there’s a good chance that your thyroid isn’t “getting the message.”
Obtaining your T3 and free T4 levels will identify if the problem is stemming from an inability of your thyroid gland itself to produce enough T3 or T4. However, T3 tests tend to be more expensive therefore we will focus only on obtaining your TSH and free T4.
I mention free T4 instead of total T4 because it is not bound to thyroid-binding globulin, which is a protein that binds T4 (“bound T4”). Total T4 includes T4 which is bound to protein AND free T4 whereas free T4 is not bound to protein. Free T4 is readily usable since it hasn’t been bound to protein, therefore you want to know the amount of usable free T4 instead. Think of free T4 as empty parking spaces ready to be used by your body.
To understand your results it is important to remember how negative feedback works. If your TSH levels are HIGH and your free T4 levels are LOW that tells us that your hypothalamus is trying to compensate for low T4 levels by pumping out increased levels of TSH in an effort to get your T4 levels up. This can be diagnosed as hypothyroidism.
To make a long story short (for you math geeks): TSH high + free T4 low = hypothyroidism
Management of hypothyroidism
Drug therapy. Medication management of hypothyroidism will be achieved using a drug called Synthroid (levothyroxine). Synthroid is essentially a synthetic T4.
For healthy adults under 65 your primary care provider will usually start you on around 50-75 micrograms, unless you have a cardiac condition or are over 65.
Therapy begins by getting your baseline TSH and free T4 and then getting the same readings in about 6 weeks (since steady state concentration of the drug takes about 6 weeks). If your follow up labs show high TSH and low T4, then you can expect them to increase your levothyroxine dose. If your labs show low TSH, high T4, then they will decrease your levothyroxine dose. After you have reached a steady state you will recheck labs about every 6-12 months.
Remember to take the med on an empty stomach and avoid taking it with the following foods since they disrupt absorption: soy, coffee, calcium supplements, antacids, iron and PPI meds (e.g. Nexium, Prilosec).
Dietary implications. Contrary to what you may have heard there isn’t a specific thyroid-curing diet. I’ve scoured Uptodate and PubMed yet have to find one. However, you should avoid consumption the aforementioned as they may interfere with your thyroid medication. Also, stay a bit on the cautious side when consuming soy as it may precipitate hypothyroidism in a patient with Hashimoto’s.
Although there isn’t a hypothyroidism diet per se you should be more cognizant of making smarter decisions when eating. Since your metabolism will be somewhat suppressed you may gain some weight however some research indicates that most people with hypothyroidism gain no more than 10lbs. But if you were already 10lbs overweight, then adding another 10lbs only increases how much you have to lose in addition to increasing your cardiovascular health risks.
Exercise. Since the person with hypothyroidism will have a slower metabolism and heat response it is best to wait until the person is a few weeks into their medication therapy to ensure that they are responding in the correct way. Upon beginning an exercise program the hypothyroidism patient should start off with a rather long warm-up period to adjust their core temperature. Due to hypothyroidism their cardiovascular rate may be somewhat depressed, therefore having them jump right in may not be the wisest decision.
After the initial break-in period the patient with hypothyroidism should build up gradually until they reach a solid “steady state” level of fitness. In other words, to play it safe….make SLLOOWWW progress. Your goal isn’t to make leaps and bounds as would someone without hypothyroidism instead focus on making slow progression while seeing how your body responds to medication therapy.
When you reach a steady state of medication therapy, then you can start focusing on them gainz. Until then, build slowly and focus on consistency.
Putting it all together
- Focus on making smarter decisions with your dietary intake as your metabolism will be suppressed
- Avoid certain foods (as mentioned earlier) as they can interfere with medication therapy
- Your exercise program should start off slowly — only focus on making leaps and bounds in your program AFTER you have reached a steady state of medication therapy
Goroll, A. and Mulley, A. (2009). Primary care medicine: Office evaluation and management of the adult patient (6th ed.). Philadelphia, PA: Wolters Kluwer
McCance, K. and Huether, S. (2014). Pathophysiology: The biological basis for disease in adults and children (7th ed.). St. Louis, MO: Saunders Elsevier.
Ross, D. and Cooper, D. (2014). Treatment of hypothyroidism. J. Mulder. (Ed.), UpToDate. Retrieved from www.UpToDate.com.
No author (2013). Uncontrolled thyroid: Exercise, diet risks. Retrieved from http://health.clevelandclinic.org/ 2013/10/uncontrolled-thyroid-exercise-diet-risks/ on December 16, 2014.
No author (2014). Can hypothyroidism lead to fat gain? Retrieved from http://examine.com/faq/can-hypothyroidism-lead-to-fat-gain.html on December 16, 2014.