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Mikaela Mohr

What is Hashimotos Disease, and how does it affect a persons body and mind?
The endocrine system is made up of eight major glands in the body. The endocrine glands
include the pineal gland, thyroid gland, pituitary gland, thymus, adrenal gland, pancreas, ovaries
or testes, parathyroid gland, hypothalamus, and the gastrointestinal tract, which is not a gland but
plays a major part in the system. Hormones send chemical messages through the bloodstream to
tissues and organs. They work slowly to affect the body and its processes. If a persons hormones
are too far from normal, they can have an endocrine disorder (Endocrine Diseases).
Hashimotos Disease is an autoimmune disorder that affects the endocrine system. In this
condition, the immune system attacks the thyroid gland. The immune system creates antibodies
against the thyroid, leading to inflammation. It disrupts the thyroids ability to make thyroid
hormone. Thyroid hormones affect the bodys overall metabolism and other body processes.
Hashimotos often leads to hypothyroidism: reduced thyroid function, where the body is unable
to make the amount of hormones it needs. Iodine deficiency is the most common cause of
hypothyroidism worldwide, but in the United States, Hashimotos is the most common cause of
hypothyroidism (National Institute of Diabetes and Digestive and Kidney Diseases). It most
often appears in middle-aged women, but it can also appear in men and women of any age,
including children.
There are many factors that play into Hashimotos. Genes, gender, pregnancy, too much
iodine intake and some drugs, or radiation exposure. If a parent or family member has
Hashimotos, a person is likely to develop the disease. People who have other autoimmune
diseases, such as arthritis, type 1 diabetes, graves disease, and lupus, are much more likely to
develop Hashimotos. If someone in their family has an autoimmune disease, they are also more

likely to develop Hashimotos. Women are seven times more likely to develop Hashimotos than
men (Womens Health). Pregnancy can trigger Hashimotos in some women, as well as excess
iodine intake, some drugs, and radiation exposure, such as an atomic bomb or certain radiation
treatments.
Many people with Hashimotos do not notice any symptoms, at first. As it worsens, and
the thyroid becomes less active, people can have many different symptoms, but the classic signs
include: fatigue, unexplained weight gain (mostly fluid retention of ten to twenty pounds), cold
intolerance, unexplained joint or muscle pain, hair loss and dryness, depression, infertility,
hoarse voice, puffy face, long menstrual cycles and memory fog. Symptoms vary depending on
the person and severity of the disease. Some unofficial, nonmedical lists have forty or more
symptoms that can be caused by hypothyroidism.
Hypothyroid pregnant women and hypothyroid women trying to conceive have to be
monitored for their thyroid levels during pregnancy every three to six weeks. During pregnancy,
a hypothyroid patient may need her dosage of medication raised in order to maintain proper
thyroid function. After birth, it may be lowered back to her dosage before she was pregnant. If
Hashimotos goes untreated during pregnancy, many complications can arise, for the mother and
the baby. Underactive or undertreated hypothyroidism from Hashimotos can lead to the
following problems for the mother: preeclampsia, anemia, miscarriage, placental abruption, and
postpartum bleeding. It can also cause the following problems for the baby: preterm birth, low
birth weight, stillbirth, birth defects, and thyroid problems (Womens Health). During
breastfeeding, thyroid medication does pass to the baby, but it isnt harmful. Some women can be
physically unable to make breast milk if their thyroid is underactive.

About one in every three thousand to four thousands babies born in the United States is
born with congenital hypothyroidism, which is rare. About eighty to eighty five percent of
congenital hypothyroidism cases is because the thyroid gland is underdeveloped, missing or too
small to make hormones. The other fifteen percent of cases are from a genetic cause, and both
parents have to have the gene and pass it on to the child for congenital hypothyroidism to occur.
In very rare cases, iodine deficiency in the mother during pregnancy is the cause. Any pregnant
woman who doesnt take in enough iodine during pregnancy can put her baby at risk of
developing it. Antithyroid drugs taken by the mother can also put the baby at risk. Babies born
with congenital hypothyroidism begin showing signs about three to four weeks after birth,
including jaundice, sleeping longer or more often, constipation, weak muscle tone, swelling
around the eyes, swollen tongue, cool or pale skin, large belly with a navel that sticks out, a
hoarse-sounding cry, and delayed growth and weight gain. It can be treated with hormone
replacement therapy. If treatment is started soon after birth, babies can be healthy and
development normally, although some may still have trouble in school or delayed growth, even
with treatment. They will be on thyroid medication for their whole life. Delayed treatment puts
babies with congenital hypothyroidism at risk of intellectual disabilities, learning disabilities,
developmental delays, and delayed growth (Babys First Test).
Hashimotos disease is the most common cause of hypothyroidism in the United States,
particularly in children and teens. Usually, the disease appears later in life. Kids with a genetic
predisposition, such as a parent with it or any other autoimmune disease, can develop it much
sooner. Undiagnosed children can experience slowed growth rate, and without treatment early on
in life, can lead to stunted physical growth and mental retardation.

Treatment for Hashimotos depends on the on the severity of the disease, the doctor, and
which route the patient chooses. It can be treated using synthetic hormones and/or supplements.
If a patient starts synthetic hormones, they will likely be on it for the rest of their life. Some
doctors will not prescribe hormones if a patients Thyroid-Stimulating Hormone (TSH) is within
normal range, and the definition of normal will vary depending on the doctor. However, even is
someones TSH is within normal range, they can still experience symptoms if their antibodies are
high. Doctors dont want to over medicate people, even if it can fix their symptoms. Some
patients may opt for a more holistic approach, using supplements, diet and other alternative
methods for treating their condition. People can find improvement in their condition by taking
supplements such as iron, calcium, low cholesterol medications, and medications that prevent
high blood potassium levels (Mayo Clinic). Patients should be tested to see if they have vitamin
deficiencies that can contribute to their autoimmune disease.
There has been an uproar of outrage in the Hashimotos patients community, particularly
about treatment in an online presence. Online blogs like Hypothyroid Mom and Stop The
Thyroid Madness have advocated the importance of proactive treatment, which is treating people
who have high antibodies and normal TSH with thyroid medications to stop the onset and
severity of the disease, which helps patients feel much better. Hashimotos patients taking
medications feel much better when their dosage is high enough to get rid of their symptoms,
which can be the most important part to the patients suffering in their everyday lives. Many
conventional doctors dont agree with this, but some patients are lucky enough to find a doctor
who will proactively treat them by treating their symptoms, not just their TSH. More research on
Hashimotos patients and clinical trials will drastically help the people suffering from the
disease, as well as reform in the medical community regarding treatment discrepancies.

Works Referenced
Trentini, Dana. "Hashimotos: Your Body Is Not Supposed To Destroy Itself Right?"
Hypothyroid Mom. N.p., 3 Dec. 2012. Web. 22 Sept. 2015.
"Hashimotos - The Autoimmune Thyroid Attack - Stop The Thyroid Madness." Stop The
Thyroid Madness. Stop the Thyroid Madness, 2015. Web. 24 Sept. 2015.

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