Allison Rogers
King University
HYPOTHYROIDISM 2
must first understand how the organ normally functions. The thyroid contains follicular cells,
which are responsible for producing thyroid hormone (Ain & Rosenthal, 2011). According to
Ain and Rosenthal (2011) and Ross (2014), these cells join together to form a sphere-shaped
cluster, with the center called the follicular lumen. The lumen is filled with colloid, mainly
thyroglobulin, which is an early form of thyroid hormone (Ain & Rosenthal, 2011; Ross, 2014).
the endoplasmic reticulum of the follicular cells (p. 201). Circulating levels of hormones are
distributed throughout the body, however only certain cells with receptors for those hormones are
affected (Brashers et al., 2014a). The follicular cells contain receptors for hormones that help to
control the thyroid gland, such as thyroid stimulating hormone (TSH) (Ain & Rosenthal, 2011).
According to Ain and Rosenthal (2011), when TSH docs on the receptor, a chain of events
initiate. The nucleus of the follicle is stimulated to begin thyroid hormone synthesis (Ross,
2014). Iodine pumps are formed and iodide, the inorganic form of iodine, is transported from the
bloodstream into the cell (Ain & Rosenthal, 2011; Brashers et al., 2014a; Ross, 2014). Iodide
oxidative metabolism (Ross, 2014, p. 2). The iodide is then joined with thyroglobulin on
tyrosyl deposits (Ain & Rosenthal, 2011; Ross, 2014). According to Ain and Rosenthal (2011),
these places then detach forming the thyroid hormone, thyroxine (T4). Thyroglobulin and T4 are
then released into the bloodstream, leaving some of the thyroglobulin behind in the follicular
cells (Ain & Rosenthal, 2011). According to Ain and Rosenthal (2011), once the thyroid
HYPOTHYROIDISM 3
hormones enter circulation, approximately 99.97% are bound to proteins called thyroid hormone
transport proteins, making them unable to enter the cells in this form. The remaining 0.03% are
not bound to proteins, making them free (free T4), which allows the hormone to be taken up and
used by the bodys cells (Ain & Rosenthal, 2011; Ross, 2014).
According to Ain and Rosenthal (2011) and Ross (2014), T4 is exclusively produced in
the thyroid gland, whereas triiodothyronine (T3) is converted from T4 inside the cell. This takes
place all throughout the body, although a large amount through the liver and kidneys (Ross,
2014). According to Ain and Rosenthal (2011), each cell regulates how much T3 it will need,
and converts the correct amounts according. The hormone T3 is the active thyroid hormone, and
is responsible for binding to, activating, and influencing genes inside of the cell (Ain &
Rosenthal, 2011; Brashers et al., 2014a). The thyroid hormones, T4 and T3, are attached to
thyroglobulin, where they are synthesized and stored in the colloid of the follicular cells until
needed (Brashers et al., 2014a; Ross, 2014). When the thyroid gland is stimulated, the follicular
cells become columnar and release their accumulation of thyroglobulin, then the process is
According to Brashers et al. (2014a), feedback systems, such as the negative feedback
system seen with the thyroid gland, monitor and control the cellular environment and help to
thyrotropin-releasing hormone (TRH), which promotes TSH secretion from the anterior pituitary,
resulting in the synthesis and release of thyroid hormones, T3 and T4 (Brashers et al., 2014a).
Increased levels of T3 and T4 generate negative feedback on the pituitary and hypothalamus in
order to take a break from production and release of TSH and TRH (Ain & Rosenthal, 2011;
When the negative feedback system fails to maintain balance for any reason, dysfunction
will occur (Brashers et al., 2014a). When serum levels of thyroid hormones, T3 and T4,
decrease, even by very small amounts, TSH secretion increases, as seen with thyroid gland
dysfunction in primary hypothyroidism (Brashers, Jones, & Huether, 2014b; Ross, 2014).
synthesize proper amounts of TSH causing lack of negative feedback to the hypothalamus to stop
releasing TRH, in turn bringing about low levels of TSH and thyroid hormones and high levels
TRH, causing a domino effect, resulting in low levels of TRH, TSH, and thyroid hormones
According to Ain and Rosenthal (2011) and Brashers et al. (2014b), the primary cause of
iodine are essential for the thyroid to be able to produce enough thyroid hormones (Ain &
Rosenthal, 2011). Other causes of primary hypothyroidism are seen with conditions resulting in
loss of functional thyroid tissue, ultimately leading to decreased amounts of thyroid hormones
prevention in some means for the pituitary or hypothalamus to do its job correctly (Brashers et
al., 2014b). Congenital hypothyroidism results from thyroid hormone deficiency often seen with
absent thyroid tissue or a hereditary defects in thyroid hormone synthesis (Brashers et al.,
2014b).
HYPOTHYROIDISM 5
Thyroid hormones affect most cells of the body, therefore affecting many, if not all, body
systems in some manner (Ain & Rosenthal, 2011; Bello & Bakari, 2012; Brashers et al., 2014a).
According to Bello and Bakari (2012), systemic effects are due to either derangements in
According to Bello and Bakari (2012), growth and development can be greatly affected
system, and skeletal system. The fetal hypothalamic-pituitary axis develops and functions on its
own, although maternal iodine supply is still essential for the placenta to convert T4 for use
The largest reported and earliest recognized symptoms originate from the metabolic
system (Bello & Bakari, 2012). According to Brashers et al. (2014a), thyroid hormones affect
cell metabolism by altering protein, fat, and glucose metabolism (p. 702). Thyroid hormone
deficiency leads to reduction of the bodys metabolic processes, resulting in a number hallmark
symptoms discussed in the paragraphs below (Bello & Bakari, 2012; Brashers et al., 2014b;
Surks, 2015).
Apparent changes caused by decreased circulation to the skin include cold intolerance,
cool, pale, dry, and flaky skin, as well as coarseness, brittleness, and reduction in growth of both
hair and nails, decreased sweating and sebaceous gland secretion (Brashers et al., 2014b; Surks,
2015) and slow wound healing (Brashers et al., 2014b). Some forms of thyroiditis manifest with
According to Brashers et al. (2014a), T3 stimulates the synthesis of certain contractile proteins,
bradycardia, decreased contractility and stroke volume, and decreased cardiac output, potentially
resulting in fatigue, decreased exercise tolerance and shortness of breath on exertion (Surks,
2015). As well as, prolonged circulation time and decreased blood flow to tissues (Brashers et
al., 2014b). A variety of electrocardiogram changes may be present, including sinus bradycardia,
QRS changes (Brashers, et al., 2014b). Other cardiovascular abnormalities normally occurring
dysfunction may include hypoventilation due to respiratory muscle weakness and reduced
pulmonary responses to hypoxia and hypercapnia. Sleep apnea occurs in some patients due to
Brashers et al. (2014b) explains that the musculoskeletal and neurologic systems are
altered as a result of decreased rate of muscle contraction and relaxation, as well as decreased
cerebral blood flow and reduced intracellular processes, related to decreased beta-adrenergic
activity. Neurologic signs include headache, vertigo, tinnitus, relaxation of deep tendon reflexes
(Bello & Bakari, 2012). Other neurologic symptoms include visual disturbances, hearing loss,
lethargy, slowed speech and thinking, slow clumsy movements, and decreased desire for food
myalgia, stiffness occurring in both muscles and joints (Bello & Bakari, 2012; Brashers et al.,
HYPOTHYROIDISM 7
2014b; Surks, 2015), and an increase in bone density (Brashers et al., 2014b). Carpal tunnel
Gastrointestinal and renal symptoms are common, including constipation, weight gain,
fluid retention, decreased absorption of nutrients, decreased glucose absorption and delayed
glucose uptake, and elevated levels of serum lipids, decreased renal excretion of water therefore
an increase in total body water causing weight gain, dilutional hyponatremia, increased serum
creatinine levels, and decreased production of erythropoietin (Brashers et al., 2014b; Surks,
2015). Surks (2015) reports that pernicious anemia is present in ten percent of patients with
hypothyroidism caused by chronic autoimmune thyroiditis, and celiac disease is four times more
alterations manifest due to reduced intake and peristalsis, increased water reabsorption due to
decreased peristalsis, depressed insulin degradation, and depressed lipid synthesis and
degradation. Renal changes are caused by reduced renal blood flow and glomerular filtration
rate and hemodynamic alterations related to reduced blood flow and filtration (Brashers et al.,
2014b).
estrogens and androgens as well as decreased levels of sex hormone-binding globulin (Brashers
et al., 2014b). According to Brashers et al. (2014b) and Surks (2015), females may experience
resulting in decreased fertility, increased risk of spontaneous abortion, and decreased libido.
Males may experience decreased libido, erectile dysfunction, delayed ejaculation, and
oligospermia (Brashers et al., 2014b; Surks, 2015). Surks (2015) goes on to state that some men
According to Garber et al. (2012), in the United States and countries where iodine is
Autoimmunity of the thyroid gland is thought to be inherited and often accompanied by other
and TSH receptor), therefore ultimately bringing about the production of antibodies for each
(Aziz kan, Al-Jameil, Khan, Al-Rashid, & Tabassum, 2015; Garber et al., 2012).
According to Aziz kan et al. (2015), Bello and Bakari (2012), Brashers et al. (2014b), and
Garber et al. (2012), when immune tolerance is lost to thyroid auto-antigens, the thyroid is
infiltrated with lymphocytes. Aziz kan et al. (2015) goes on to explain, antigen-presenting cells
belonging to the major histocompatibility complex II, such as macrophages and dendritic cells,
introduce specific thyroid antigens to the lymphocytes. Aziz kan et al. (2015), reports studies
have revealed that cytokines have shown pro-inflammatory tendencies on the follicular cells of
the thyroid, therefore initiating the inflammatory response, activating B and T lymphocytes. This
specifically Th1, Th2, and Th17, inducing the formation of cytotoxic cluster of differentiation
eight (CD8+) T cells and activation of B cells (Aziz kan et al., 2015). Th1 initiates cell mediated
immunity, resulting in apoptosis of the follicular cells, while Th2 activates the humoral response,
lymphocytes (Aziz kan et al., 2015). Studies have shown increased amounts of plasma Th17
cells present with autoimmune thyroiditis (Aziz kan et al., 2015). Bello and Bakari (2012)
explain that chronic inflammation of the gland [as seen in thyroiditis] causes progressive
HYPOTHYROIDISM 9
destruction of the functional tissue (p. 64). According to Aziz kan et al. (2015), TPO antibodies
are the key enzyme for iodination and coupling reaction in thyroid hormone synthesis (p.
6678).
According to Rote and McCance (2014), immune function decreases as one ages,
especially over the age of 60. T-cell function diminishes and B-cell function is altered by
and circulating autoantibodies (Rote & McCance, 2014). This may explain why there is an
According to Bello and Bakari (2012) and Brashers et al. (2014b), silent, or painless,
thyroiditis and postpartum thyroiditis are additional forms of thyroiditis, similar to autoimmune
thyroiditis. These conditions result in elevated anti-TPO antibodies (Bello & Bakari, 2012).
Inflammatory conditions of the thyroid, often seen following viral infections, have the potential
deQuervain thyroiditis (Bello & Bakari, 2012; Brashers et al., 2014b). These conditions usually
Treatment Identification
The ultimate treatment goal is to restore euthyroid state and reverse clinical signs and
symptoms of hypothyroidism, in order to decrease further harm from the disorder and make the
patient more comfortable (Bello & Bakari, 2012; Ross, 2016). There are many pharmaceutical
containing both T4 and T3, and desiccated (animal derived) thyroid extract (Ain & Rosenthal,
HYPOTHYROIDISM 10
2011). Many over the counter thyroid dietary supplement preparations are also available (Garber
et al., 2012).
to Garber et al. (2012) and Ross (2016), as a result of the extreme sensitivity of TSH to slight
increase or decrease in thyroid hormones, monitoring of serum TSH levels should be considered
with any change in formulary of the medication, such as change in manufacturer or switching
from brand name to generic formulation, due to possible variances in amount of bioavailability.
Because of this, patients should be monitored and instructed to notify their healthcare provider of
Worldwide the most common cause of hypothyroidism is from lack of dietary iodine (Ain
& Rosenthal, 2011; Brashers et al., 2014b; Garber et al., 2012; Ross, 2014). In this case holistic,
natural treatment with dietary supplement of iodine rich foods, such as kelp, may be sufficient
(Axe, 2016b). According to Robinson (2015), eating a well-balanced diet, including not too
much or too little of any foods, consuming a variety of colorful fruits and vegetables, and limited
amount of meats, is key to maintaining a healthy lifestyle that aids in treatment of most any
disease process. In the United States, for the most part hypothyroidism does not originate from
lack of iodine in the diet, therefore foods that are high in iodine, such as kale, broccoli, spinach,
kelp, and seaweed should be treated like all other foods in the diet, eaten in moderation
(Robinson, 2015). According to Ross (2016), selenium is required for deiodinase of T4 to T3.
Selenium supplementation has been shown to reduce anti-thyroid peroxidase antibody levels
(Ross, 2016). Heavy metal buildup in the body can cause hypothyroid symptoms (Axe, 2016b).
Using a combination of foods and herbs such as milk thistle, turmeric, chlorella, and cilantro, as
HYPOTHYROIDISM 11
well as having silver fillings in teeth replaced with non-metallic fillings, may help detoxify and
remove excess heavy metals from the body (Axe, 2016a). According to Axe (2016a), certain
food intolerances and allergies to hybridized proteins found in gluten and dairy products
containing a1 casein, causes leaky gut syndrome, which is associated with inflammation of the
thyroid, impairing its function. Eliminating gluten and a1 casein in the diet will eliminate this
problem (Axe, 2016a). Axe (2016a) states, bisphenol A (BPA), found in plastic, can disrupt the
endocrine system, effecting the thyroid, therefore using glass, stainless steel, or BPA free
materials is recommended. Axe (2016a) goes on to report, increased cortisol levels caused by
stress, to many carbohydrates and too little fat in the diet can also effect thyroid hormone levels.
decrease cortisol, as well as decreased intake of sugars and grains along with increased intake of
relaxation include, acupuncture, yoga, and meditation (Robinson, 2015). According to Robinson
(2015), contrast therapy, which involves placing alternating heat and cold items such as towels
on the neck in order to help to stimulate the thyroid gland is a theory but has not been tested for
effectiveness.
Treatment Argument
I feel that monotherapy supplement with synthetic T4 is the best treatment option for
is the initial recommended treatment (Brashers et al., 2014b; Garber et al., 2012). Synthetic T4,
such as levothyroxine, is preferred over desiccated thyroid, such as Armour Thyroid (Ain &
HYPOTHYROIDISM 12
Rosenthal, 2011; Brashers, et al., 2014b; Garber et al., 2012). Desiccated preparations contain
dried animal thyroid gland, which contain T4, T3, and thyroglobulin, making it very hard and
often inaccurate to measure potency and bioavailability with each preparation (Ain & Rosenthal,
recommended for hypothyroidism due to the half-life of T3 being one day, therefore leaving the
patient with a peak followed by too little of the hormone for the remainder of the day. It is
believed that due to the bodys conversion of T4 into, its active form, T3, that treatment with
synthetic form of T4 should be adequate (Garber et al., 2012; Ross, 2016). Treatment with
combination of L-thyroxine and L-triiodothyronine has been studied, but at this time studies are
unable to prove benefit of combination therapy over monotherapy with L-thyroxine alone,
therefore T4 monotherapy remains to be the treatment of choice at this time (Bello & Bakari,
According to Axe (2016a; 2016b), one can benefit from a more natural, holistic approach
to regulating thyroid hormone function by altering diet. For example, an increase in selenium
containing foods (such as Brazil nuts, salmon, sunflower seeds, beef, mushrooms and onions) is
one natural way of helping to relieve hypothyroid symptoms (Axe, 2016a). However, Ross
(2016) reports that increasing selenium has not been proven effective in improving thyroid
function in hypothyroid patients. Garber et al. (2015) states that dietary supplements fail to meet
a level of scientific evidence proven necessary to treat the disease. Robinson (2015) goes on to
say, natural treatments cannot replace traditional hormone replacement therapy, but they can help
relieve some symptoms and assist in feeling better. Therefore the mainstay of treatment remains
supplementation with thyroid hormone, L-thyroxine (Ain & Rosenthal, 2011; Bello & Bakari,
HYPOTHYROIDISM 13
2012; Brashers et al., 2014b; Grarber et al., 2012). According to Ross (2016), although treatment
administered and levels of TSH and thyroid hormones return to normal state, some patients still
the healthcare provider, natural approaches used in conjunction with thyroid hormone
Complications
Myxedema, an alteration in the composition of the dermis and other connective fibrous
tissues, is seen with severe or long-standing hypothyroidism (Brashers et al., 2014b). According
to Brashers et al. (2014b), severe hypothyroidism can lead to an emergent medical condition
called myxedema coma, and is often seen with discontinuation of thyroid supplements, overuse
of narcotics or sedatives, or after infection or acute illness. Symptoms associated with this
hypoventilation, hypotension, hypoglycemia, lactic acidosis, and coma (Brashers et al., 2014b).
Cretinism is a condition seen with untreated congenital hypothyroidism (Brashers et al., 2014b).
Classic signs, such as dwarfism with short limbs and delayed dentition are thought to be
associated with somatic and linear bone growth, and mental retardation is due to lack of thyroid
hormone to allow proper brain growth and differentiation occurring after birth, as approximately
hypertension and hypercholesterolemia, are major risk factors of cardiovascular disease (Ain &
Rosenthal, 2011; Bello & Bakari, 2012; Surks, 2015). Also according to Surks (2015), clearance
of medication may be slowed with hypothyroidism. Care should be taken and teaching
HYPOTHYROIDISM 14
hypnotic and opioid medications (Surks, 2015). Treatment with L-thyroxine should be initiated
with caution in persons with known or suspected cardiac history, a sudden increase in thyroid
hormones may cause an increase in myocardial oxygen demand, which has the potential to cause
adverse effects, such as heart attack, in the presence of underlying cardiac problems (Bello &
Bakari, 2012). Many of the cardiovascular symptoms and complications caused by untreated
hypothyroidism resolve soon after euthyroid state is reached (Ain & Rosenthal, 2011).
According to Brashers et al. (2014b) and Surks (2015), decreased fertility or infertility
have been linked to hypothyroid disorders. A study revealed that sperm morphology was
abnormal in sixty four percent of men with hypothyroidism (Surks, 2015). Bello and Bakari
(2012) report, higher miscarriage rate with autoimmune thyroiditis related to anti-thyroid
during pregnancy increases the risk of low-weight or stillborn infant, preterm delivery, maternal
Summary
Iodine is essential for thyroids production of the thyroid hormone T4 (Ain & Rosenthal,
2011; Brashers et al., 2014a; Ross, 2014). Inside the cells of the bodys tissues, T4 is converted
to the active form of thyroid hormone, T3 (Ain & Rosenthal, 2011; Ross, 2014). Negative
feedback systems are in place in order to help regulate and maintain euthyroid levels, when this
system fails to maintain balance thyroid dysfunction occurs (Brashers et al., 2014a).
thyroid gland and manifests with decreased thyroid hormone levels and increased TSH levels
(Brashers et al, 2014b). Secondary, or central, hypothyroidism can originate from a pituitary
HYPOTHYROIDISM 15
malfunction, resulting in low levels of TSH and thyroid hormones and high levels of TRH, or
from a hypothalamic malfunction results in low levels of TRH, TSH, and thyroid hormones
(Brashers et al., 2014b). Congenital hypothyroidism results from absent thyroid tissue or defects
in thyroid hormone synthesis resulting in thyroid hormones deficiency (Brashers et al., 2014b).
Thyroid hormones affect every cell and organ of the body, therefore hypothyroidism has
many manifestations (Ain & Rosenthal, 2011; Bello & Bakari, 2012; Brashers et al., 2014a).
Some of the most common signs and symptoms experienced include feeling tired and fatigued,
forgetfulness, difficulty concentrating, bradycardia, arthralgia and myalgia, cool, pale, dry, flaky
skin, dry and brittle hair, intolerance to cold, weight gain, constipation, and menstrual
irregularities (Axe, 2016a; Bello & Bakari, 2012; Brashers et al., 2014b; Surks, 2015).
In areas where dietary iodine is sufficient, autoimmune thyroiditis is the most common
antigens (Aziz kan et al., 2015; Garber et al., 2015). According to Aziz kan et al. (2015), Bello
and Bakari (2012), Brashers et al. (2014b), and Garber et al. (2012), there is an infiltration of the
thyroid gland with lymphocytes. Cytokines initiate the inflammatory process, activation of B
and T lymphocytes as well as T-helper cells initiate cell mediated immunity and humoral
response, resulting in apoptosis of follicular cells and death of cytotoxic lymphocytes (Aziz kan
et al., 2015). Chronic inflammation causes progressive destruction of functional thyroid tissue
According to Bello and Bakari (2012), Garber et al. (2012), and Ross (2016), L-thyroxine
triiodothyronine (Bello & Bakari, 2012; Garber et al., 2012; Ross, 2016). There are many
HYPOTHYROIDISM 16
holistic treatments that may be beneficial as adjuvant therapy with L- thyroxine supplementation
especially in patients that still have symptoms although euthyroid levels of thyroid hormones
have been achieved. These therapies include consuming foods rich in iodine and selenium,
eliminating gluten and a1 casein from the diet, decreasing sugars and grains from the diet,
incorporating healthy fats, consuming adaptogen supplements, eliminating heavy metals from the
body, and using BPA free products (Axe, 2016a; Axe, 2016b). Complimentary treatments
include acupuncture, yoga, and meditation and help with relief of symptoms by promoting
Complications are often caused by the systemic effects of hypothyroidism. The most
severe conditions associated with hypothyroidism include myxedema, myxedema coma, and
cretinism (Brashers et al., 2014b). An increased risk for cardiovascular disease is caused by
hypercholesterolemia and hypertension (Ain & Rosenthal, 2011; Bello & Bakari, 2012; Surks,
hormone (Bello & Bakari, 2012). Decreased fertility or infertility have also been associated with
hypothyroidism (Brashers et al., 2014b; Surks, 2015). Other reproductive complications include
References
Ain, K., & Rosenthal, M. S. (2011). The complete thyroid book (2nd ed.). New York, New York:
McGraw-Hill.
Axe, J. (2016a). 8 natural hypothyroidism treatments that work. In Dr.Axe.com. Retrieved from:
http://draxe.com/8-secrets-to-cure-hypothyroidism-and-other-hormone-
problems/
Axe, J. (2016b). Is your thyroid the cause of your health problems? In Dr.Axe.com. Retrieved
from: http://draxe.com/is-your-thyroid-the-cause-of-your-health-problems/
Aziz khan, F., Al-Jameil, N., Khan, M. F., Al-Rashid, M., Tabassum, H. (2015). Thyroid
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4509150/pdf/ijcem0008-6677.pdf
Bello, F. & Bakari, A. G. (2012). Hypothyroidism in adults: A review and recent advances in
10.5897/JDE11.017
Brashers, V. L., Jones, R. E., & Huether, S. E. (2014a). Mechanisms of hormonal regulation. In
The biologic basis for disease in adults and children (7th ed.) (pp. 689-716). Saint Louis,
Brashers, V. L., Jones, R. E., & Huether, S. E. (2014b). Alterations of hormonal regulation. In
The biologic basis for disease in adults and children (7th ed.) (pp. 717-767). Saint Louis,
Garber, J. R., Cobin, R. H., Gharib, H., Hennessey, J. V., Klein, I., Mechanick, J. I., Woeber,
http://www.webmd.com/women/features/low-thyroid-alternative-therapy
Ross, D. S. (2014, April 18). Thyroid hormone synthesis and physiology. In Cooper, D. S. &
http://www.uptodate.com/contents/thyroid-hormone-synthesis-and-physiology?
source=search_result&search=thyroid+hormone+synthesis+and+physiology&selectedTit
le=1~150
hypothyroidism?
source=search_result&search=treatment+of+hypothyroidism&selectedTitle=1%7E150
Rote, N. S. & McCance, K. L. (2014). Adaptive Immunity. In McCance, K. L., Huether, S. E.,
Brashers, V. L. & Rote, N. S. (Eds.), Pathophysiology: The biologic basis for disease in
adults and children (7th ed.) (pp. 224-261). Saint Louis, MO: Elsevier Mosby.
HYPOTHYROIDISM 19
http://www.uptodate.com/contents/clinical-manifestations-of-hypothyroidism?
source=search_result&search=clinical+manifestations+fo+hypothyroidism&selectedTitle
=1%7E150