Running head: HYPOTHYROIDISM 1

A Closer Look at Hypothyroidism- Part 2

Allison Rogers

King University
HYPOTHYROIDISM 2

A Closer Look at Hypothyroidism- Part 2

Pathophysiology: Cellular Level

In order to better understand a dysfunction of the thyroid, such as hypothyroidism, one

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).

According to Brashers, Jones, and Huether (2014a), uniodinated thyroglobulin is produced by

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

transport is linked to transport of sodium, is energy-dependent and saturable, and requires

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

permitted to begin again (Ross, 2014).

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

maintain hormone concentrations within a certain range. The hypothalamus produces

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;

Brashers et al., 2014a; Ross, 2014).

HYPOTHYROIDISM 4

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).

According to Brashers et al. (2014b), secondary, or central, hypothyroidism can be caused by

either a pituitary or hypothalamic dysfunction. Pituitary malfunction results in failure to

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

of TRH (Brashers et al., 2014b). Hypothalamic malfunction causes a decrease in release of

TRH, causing a domino effect, resulting in low levels of TRH, TSH, and thyroid hormones

(Brashers et al., 2014b).

According to Ain and Rosenthal (2011) and Brashers et al. (2014b), the primary cause of

hypothyroidism is caused by an insufficient intake of iodine in ones diet. Adequate amounts 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

(Brashers et al., 2014b). Secondary hypothyroidism is usually associated with injury or

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

Pathophysiology: Systemic/Body System

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

metabolic processes or direct effects by myxedematous infiltration (that is, accumulation or

glucosaminoglycans in the tissues) (p.58).

According to Bello and Bakari (2012), growth and development can be greatly affected

by hypothyroidism, ultimately affecting proper development of central nervous system, auditory

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

(Bello & Bakari, 2012).

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

a goiter (Brashers et al., 2014b).

HYPOTHYROIDISM 6

The cardiovascular and respiratory systems are also affected by hypothyroidism.

According to Brashers et al. (2014a), T3 stimulates the synthesis of certain contractile proteins,

such as sodium-potassium-ATPase pump, calcium ATPase pump and beta-adrenergic receptors.

Cardiovascular symptoms associated with decreased T3, as seen in hypothyroidism, include

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,

prolonged PR interval, depressed P waves, flattened or inverted T waves, and low-amplitude

QRS changes (Brashers, et al., 2014b). Other cardiovascular abnormalities normally occurring

with hypothyroidism are pericardial effusion, hypertension, hypercholesterolemia, and

hyperhomocystemia (Surks, 2015). According to Surks (2015), associated respiratory

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

macroglossia, and rhinitis is also a reported as a common problem (Surks, 2015).

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

(Brashers et al., 2014b). Many experience musculoskeletal symptoms such as arthralgia,

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

syndrome is often experienced in patients with hypothyroidism (Surks, 2015).

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

common in persons with hypothyroidism. Brashers et al. (2014b) states, gastrointestinal

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).

Lastly, the reproductive system experiences alterations due to altered metabolism of

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

menstrual irregularities such as oligo-menorrhea or amenorrhea, menorrhagia, anovulation

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

experience low serum free testosterone levels.

HYPOTHYROIDISM 8

Immunity: Role of Immune Response

According to Garber et al. (2012), in the United States and countries where iodine is

sufficient, chronic autoimmune thyroiditis is the most common cause of hypothyroidism.

Autoimmunity of the thyroid gland is thought to be inherited and often accompanied by other

autoimmune disorders (Garber et al, 2012). Autoimmune thyroiditis is caused by a decreased

immune susceptibility of three main thyroid auto-antigens (thyroglobulin, thyroid peroxidase,

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

results in antigen-specific T-helper cluster of differentiation four (CD4+) lymphocytes,

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,

increasing B cell autoantibody production, ultimately resulting in the death of cytotoxic

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

decrease in specific antibody productions, resulting in increased circulating immune complexes

and circulating autoantibodies (Rote & McCance, 2014). This may explain why there is an

increase in hypothyroidism and autoimmune thyroiditis with age.

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

to cause transient hyperthyroidism followed by hypothyroidism, called subacute thyroiditis or

deQuervain thyroiditis (Bello & Bakari, 2012; Brashers et al., 2014b). These conditions usually

resolve over time (Brashers et al., 2014b).

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

preparations available for treatment including: monotherapy of L-thyroxine (synthetic T4

supplementation) or L-triiodothyronine (synthetic form of T3), as well as combination therapy

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).

Regardless of the preparation, consistency with treatment should be followed. According

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

any indications of hyperthyroidism, common signs and symptoms manifest as nervousness,

tachycardia, insomnia, and unexplained weight loss (Axe, 2016b).

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.

As a result adaptogen supplements, such as ashwagandha and tulsi, in an attempt to help

decrease cortisol, as well as decreased intake of sugars and grains along with increased intake of

healthy fats should be implemented to balance hormone levels (Axe, 2016a).

Additional complimentary treatments that may aid in relief of symptoms by promoting

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

hypothyroidism. Hypothyroidism has many different etiologies, depending on where the

disorder originates. Regardless of the type of hypothyroidism, supplementation with L-thyroxine

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,

2011; Garber et al, 2012).

According to Ain & Rosenthal (2011), monotherapy with L-triiodothyronine is not

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,

2012; Garber et al., 2012; Ross, 2016).

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

experience clinical symptoms of hypothyroidism. Therefore in my opinion, after consulting with

the healthcare provider, natural approaches used in conjunction with thyroid hormone

replacement therapy may be of great benefit in reducing symptoms that T4 supplementation

alone may not relieve.

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

condition include diminished level of consciousness, hypothermia without shivering,

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

two-thirds of this occurs after birth (Bello & Bakari, 2012).

Adverse effects on the cardiovascular system caused by hypothyroidism, such as

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

implemented when administering or prescribing drugs such as antiepileptic, anticoagulant,

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

peroxidase or thyroperoxidase antibodies. Inadequate thyroid hormone replacement therapy

during pregnancy increases the risk of low-weight or stillborn infant, preterm delivery, maternal

hypertension, and postpartum hemorrhage (Bello & Bakari, 2012).

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).

Hypothyroidism manifests in many forms. Primary hypothyroidism results from dysfunction of

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

cause of hypothyroidism, and is caused by a decreased immune susceptibility of thyroid auto-

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

(Bello & Bakari, 2012).

According to Bello and Bakari (2012), Garber et al. (2012), and Ross (2016), L-thyroxine

monotherapy supplementation is the mainstay of treatment for hypothyroidism. Current studies

have failed to prove effectiveness of combination therapy with L-thyroxine and L-

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

relaxation (Robinson, 2015).

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,

2015). Underlying cardiovascular disease can be adversely affected by fluctuations in thyroid

hormone (Bello & Bakari, 2012). Decreased fertility or infertility have also been associated with

hypothyroidism (Brashers et al., 2014b; Surks, 2015). Other reproductive complications include

miscarriage, increased risk of low-weight or stillborn infant, preterm delivery, maternal

hypertension, and postpartum hemorrhage (Bello & Bakari, 2012).

HYPOTHYROIDISM 17

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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-

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Aziz khan, F., Al-Jameil, N., Khan, M. F., Al-Rashid, M., Tabassum, H. (2015). Thyroid

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10.5897/JDE11.017

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