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Thyroid Diseases and Diet Control
Tan Kar Soon* and Poh Wei Ting
Microbiology and Fish Disease Laboratory, Borneo Marine Research Institute, University Malaysia Sabah, Jalan UMS, 88400, Kota Kinabalu, Sabah, Malaysia
*Corresponding author: Tan Kar Soon, Microbiology and Fish Disease Laboratory, Borneo Marine Research Institute, University Malaysia Sabah, Jalan UMS, 88400,
Kota Kinabalu, Sabah, Malaysia, Tel: +6088-320000; Fax: +6-088-320261; E-mail: tankarsoon@ums.edu.my
Received date: February 07, 2018; Accepted date: February 09, 2018; Published date: February 16, 2018
Copyright: © 2018 Soon TK, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted
use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Thyroid diseases are major problem of modern society and are classified as diseases of civilization. Unhealthy
lifestyle, stress and exposure to chemical are believed to increase the risk of developing thyroid disorders.
Medication and surgery are commonly used to address thyroid diseases. Despite the advancement in medical
technology, it was unfortunate that there had not yet to be any potential cure for hypothyroidism. Treatment in the
form of synthetic thyroid hormone cause patients to suffer from the symptoms of hypothyroid, despite their thyroid
hormone levels being balanced. Whereas the limitation of surgery is patient might need to rely on synthetic thyroid
hormone for their lifetime after the thyroid gland is removed. Approaching thyroid disease and autoimmunity from a
holistic level and seeing the body as an interconnected system is the better way to address disease. Many recent
studies show dietary intervention offer a promising result in treating thyroid diseases. Therefore, a strict eliminating
diet to soothe gut inflammation, restore digestive health, and address autoimmune diseases from a holistic approach
could be the best way to prevent or treat thyroid diseases.
Keywords: yroid diseases; Causative factors; Treatment; Diet
control
Introduction
yroid disease is triggered by the immune system initiating an
attack on own molecules due to the deterioration of immunologic
tolerance to auto- reactive immune cells [1]. yroid gland is
commonly targeted by autoimmune diseases, where the most common
dysfunctions of the thyroid gland are hypothyroidism, lymphocytic
thyroiditis (Hashimoto’s thyroditis), and hyperthyroidism (Graves’s
disease) [2]. Among the thyroid diseases, Craves’ disease is the
dominant and accounts for 50 to 80% of cases of thyroid disease in
dierent regions of the world [3].
yroid disease is substantially greater prevalence in old age than in
those of younger age and are oen covert, being masked by co-
morbidities. e majority of cases of thyroid diseases are diagnosed in
patients aged 45 to 65 years, but they can also aect children [4].
Moreover, thyroid disease is a sex related disease where women are
biologically more prone to thyroid disorders [5]. yroid disease is
estimated to aects 2% of female and 0.2% of male worldwide [6]. In
addition, tobacco smoking [7], heavy metal and toxic chemical
exposure [8], and stress [9] can signicantly increase the risk of
developing thyroid disorders.
Diagnosis of thyroid diseases particularly hypothyroidism and
Hashimoto’s thyroiditis usually leads a long journey of
supplementation with synthetic thyroid hormone thyroxin [10].
However, this is does not address the true cause of hypothyroidism and
Hashimoto’s thyroiditis. In fact, despite the advancement in medical
technology, it was unfortunate that there had yet to be any potential
cure for hypothyroidism and Hashimoto’s thyroiditis. erefore, this
paper aims to uncover some of the existing research about
autoimmune disease with attempt to identify an eective way to
address thyroid diseases.
yroid diseases
yroid diseases are caused by an abnormal immune response to
auto-antigens present in the thyroid gland. e three main types of
autoimmune thyroid diseases are hypothyroidism, lymphocytic
thyroiditis (Hashimoto’s thyroiditis), and hyperthyroidism [2].
Hypothyroidism is a condition in which the thyroid gland is under-
active and produces too little thyroid hormone [11]. Typical symptoms
of hypothyroidism include: hoarse voice; slowed speech; puy face;
drooping eyelids; intolerance of cold conditions; constipation; weight
gain; dry hair; dry skin; and depression. Patient with hypothyroidism
have a greater risk of cardiovascular disease, osteoporosis, overweight,
celiac disease and diabetes [12].
Hashimoto’s yroiditis (HT) is an autoimmune disorder in which
the body immune system attacks the thyroid [13]. is will cause
decrease in thyroid function and eventually lead to the clinical disorder
known as hypothyroid. Untreated hypothyroid can cause patients mild
to severe symptoms ranging from hair loss, cold sensitivity, sleep
disturbances, weight gain, depression, constipation, brain fog, fatigue,
goiters (enlargement of the thyroid gland) and thyroid cancer [12].
Women are 10 to 20 times more likely to be aected by HT disease
than man [14].
Hyperthyroidism also known is a condition in which the thyroid
gland is overactive and produces too much thyroid hormone [3].
Typical symptoms of hyperthyroidism include: high blood pressure;
fast heartbeat; moist skin; increased sweating; tremor; nervousness;
increased appetite with weight loss; diarrhea and/or frequent bowel
movements; weakness; eyeballs appear to be protruding; and sensitivity
of the eyes to light [15]. Hyperthyroidism occurs in approximately 2 to
3% of the adult population [16]. Hyperthyrodism occurs about ten
times more frequently in women than men [3]. e average age at
diagnosis of hyperthyroidism is 48 years [6,17].
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ISSN: 2161-0509
Journal of Nutritional Disorders &
Therapy Soon and Ting, J Nutr Disorders Ther 2018, 8:1
DOI: 10.4172/2161-0509.1000224
Review Article Open Access
J Nutr Disorders er, an open access journal
ISSN:2161-0509
Volume 8 • Issue 1 • 1000224
Factors aecting the risk to thyroid diseases
Several factors have been identied which increases the risk of
developing thyroid disorders which include gender [18], tobacco
smoking [7], heavy metal and toxic chemical exposure [8], gluten and
stress [9].
Most thyroid diseases are more prevalent in women than in men
[5,18]. Sex specic dierences in the microbiota composition are found
only aer puberty [19,20]. e main dierences between female and
male immune systems are the sex hormones, the presence of two X
chromosomes versus one X and one Y chromosome [21]. To avoid
double dosage of X chromosome-derived proteins, one of the X
chromosomes is randomly silenced in female in the early stages of
embryogenesis. However, X chromosome inactivation is not complete
and about 15% of the genes are still active, which leading to over
expression of some X-linked genes in females [22]. Moreover, sex
hormones such as estrogens, progesterone, androgens and pro-lectin
can inuence dierent aspects of immune system function and
potentially aect the risk, activity and progression of thyroid diseases.
is is due to present of hormones receptors on immune cells [5].
Generally, estrogens, in particular 17-ᵦ estradiol (E2) and prolactin, act
as enhancers at least of humeral immunity, and testosterone and
progesterone as natural immune-suppressants [23]. Prolactin in
particular increases antibody production, regulates the development of
CD4+ T cells and triggers pro-inammatory cytokine production [24].
Tobacco cigarette smoking is a risk factor for the development of
systemic lupus erthematosus, where the ratios for current smokers
versus individuals who have never smoke is 1.5 [25]. Smoking causes
tissue damage and increases apoptosis through high production of free
radicals, release of metalloproteinase, and the induction of Fas
expression on lymphocytes which associated with autoantibody
production. In addition, smoking also provokes inammation as it
causes an increase in brinogen levels, induces leucocytosis, and
elevates levels of C-reactive protein, intercellular adhesion molecule-I
and E-selectin [7].
Heavy metals contamination can result in acute heavy metal
intoxications in human through accumulations of metals in food chain
[26]. Heavy metals such as mercury, cadmium, lead, arsenic, nickel and
other metals can stimulate autoantibodies, which in turn, may result in
thyroid diseases [8]. Mycotoxins produced by heavy metals are very
volatile that wreak havoc on immune system. In addition, chemical
toxins such as pestisides, industrial chemicals, hair dyes and some
household cleaners can also be link to thyroid diseases [27].
Glutens, made up of two main fractions, gliadins and glutenins, are
the main storage proteins of wheat and are comprised of about 100
dierent proteins in a given wheat cultivar (variety) [28]. Gluten
contributes to thyroid disease in three ways. First, it is the primary
cause of leaky gut because gliadin triggers the release of zonulin in
intestines, a chemical that trigger the opening of gut lining [9]. Second,
gluten is highly inammatory and it stresses immune system [29].
irdly, the gluten protein has a similar chemical structure to some of
thyroid tissues, which can lead to molecular mimicry, where body
mistakes thyroid tissues for gluten and attacks it [30]. In addition,
casein in milk (dairy products) also mimicks gluten hence causes
inammation [9].
Stress may aect the immune system either directly or indirectly
through the nervous and endocrine systems [31,32]. Stressful
situations cause body to release cortisol and activate an acute phase
response, which is a part of the innate immune inammatory response
[9]. In order to maintain homeostasis during stress, activation of the
hypothalamic- pituitary- adrenal axis and of the sympathoadrenal
system leads to an increased secretion of glucocorticoids and
catecholamine’s, respectively. e neuroendocrine hormones triggered
during stress may lead to immune dysregulation or to amplify cytokine
production, resulting in atopic thyroid disease (Tsatsoulis, 2006).
Moreover, the stress hormones acting on antigen- presenting immune
cells, which may inuence dierentiation of bipotential helper T-cells
away from 1 phenotype and towards a 2 phenotype [32].
Treatments
Medication and surgery: Hyperthyroid diseases could be addressed
through medication. e main approach is to reduce the hormone via
drugs, which act to stabilise the hormone level. Treatment duration is
usually between one-and-half to two years, depending on cases. Once
the treatment starts, the level of thyroid hormones would gradually
reduce towards stabilization, and so would the dosage [33].
Nevertheless, there had been cases where the patients did not respond
well to the treatment. Under such circumstances, there was another
more aggressive treatment, the radiation iodine [16]. However, this
treatment should consider as the last option and needed the patient’s
consent as it involved radioactivity. Female patient who is at child-
bearing age is best to avoid undertaking the radiation iodine
treatment, unless she is really in critical condition. is is because once
the patient undergoes the radiation iodine treatment; she needs to
postpone any plan to have children until it is completed [34]. Besides
that, hyperthyroid diseases could also be addressed through surgery, in
which the swelling parts of the gland are removed [15]. is could only
be performed if the thyroid functions were stable.
Unlike hyperthyroidism, patients with hypothyroidism would need
to depend on ongoing medication. Treatment for hypothyroidism
focuses on replacing the thyroid hormone in the body, and one of the
natural ways is by increasing salt-iodine in the patients’ diet [11].
Treatment comes in the form of synthetic thyroid hormone thyroxin,
leaving many patients of hypothyroidism and Hahimoto’s thyroiditis to
suer from the symptoms of hypothyroid, despite their thyroid
hormone levels being balanced [10,35]. erefore, more studies are
required to fully understand the mechanisms of hyperthyroidism, in
order to come out with an eective medicine to address not just the
symptom of hypothyroid, but to cure the cause of HT entirely.
Although there is no medication for this condition so far, surgery
would be suggested as an option should the goiter grow larger [36].
However, surgery should consider as the last option as patients will
need to rely on synthetic thyroid hormone for their lifetime aer the
thyroid gland is removed.
Gut healing: Gut imbalance, or leaky gut is believed to be the root
cause of most thyroid disease [30]. e leaky gut not only reduces the
eectiveness of intestines in absorbing nutrients, but also allows toxins
and microbes that are not supposed to be in the gut in and provoke an
immune response [9]. e causative factors that can lead to a leaky gut
to begin with, underlying food allergies, regular usage of antibiotics,
some medications and lifestyle factors can all lead to yeast and/or
bacterial overgrowths that cause lining of the gut to be disturbed and
lead to autoimmune diseases down the road[37]. Childhood factors
such as frequent ear infections or lack of proper bacteria from breast
feeding can also lead to a pre-disposal to leaky gut [9].
In general, there are four steps to gut healing processes including;
1) removing any elements (cadmium (Cd), mercury (Hg), arsenic (As),
lead (Pb) etc) that are disrupting the digestive environment, 2)
Citation: Soon TK, Ting PH (2018) Thyroid Diseases and Diet Control. J Nutr Disorders Ther 8: 224. doi:10.4172/2161-0509.1000224
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J Nutr Disorders er, an open access journal
ISSN:2161-0509
Volume 8 • Issue 1 • 1000224
restoring good digestive enzymes into digestive system, 3) rebuilding
probiotics bacterial in the gut, and 4) restoring the gut lining.
Eliminating inammatory foods such as gluten, grains, dairy, eggs,
nuts, and legumes allow gut to heal [29]. Once the digestive system is
healthy and able to process these foods properly, then these foods can
be reintroduced.
Restoring good digestive enzymes into digestive system is important
in preventing nutrients deciency diseases. Enzymes level can be
increased naturally by four ways including eat raw foods, eat low
calories, chew food thoroughly and avoid chewing gum. Raw foods are
enzyme-rich, and consuming them decreases your body's burden to
produce its own enzymes [30]. erefore, it is ideally to eat at least 75%
of foods at raw to supply our body with the amino acids and the
enzyme co-factors needed to boost our own natural enzyme
production. In fact, diets heavy in cooked, processed, and sugary
foods, combined with overuse of pharmaceutical drugs such as
antibiotics, deplete body's ability to make enzymes. Another way to
lower body's demand for enzymes is to reduce caloric intake. Reducing
overall consumption will reduce the need for digestive enzymes, which
allows body to put more of its energy into producing metabolic
enzymes. In addition, there are important physiological reasons to
chew food well. Chewing stimulates saliva production and activate
digestive system by stimulates a reex that sends a message to pancreas
and other digestive organs. Increasing in chewing time caused saliva
enzymes work longer in mouth which lessening the workload of
stomach and small intestine. However, chewing gum fools our body
into believing it is digesting something, so it wasted those enzymes by
pumping out digestive enzymes unnecessarily.
Intestinal micro biome plays an important role in the function and
integrity of the gastrointestinal tract, maintenance of immune
homeostasis and host energy metabolism [38]. Probiotics help
replenish good bacteria in the gut. Keep the harmful bacteria
population in check, inhibit yeast overgrowth, support positive
communication between the brain and intestinal tract, reduce
inammation, and provide an overall healthy environment for body.
Probiotics particularly
Lactobacillus
strains enhance the integrity of
the intestinal barrier, which may result in maintenance of immune
tolerance, decreased translocation of bacteria across the intestinal
mucosa, and disease phenotypes such as gastrointestinal infections,
inammatory bowel disease and irritable bowel syndrome [39].
Moreover, probiotics can modulate the intestinal immunity and alter
the responsiveness of the intestinal epithelia and immune cells to
microbes in the intestinal lumen [40,41].
e nal step in gut healing processes is to heal the damaged
intestinal lining. Gut lining restoration can be done by consuming an
unprocessed diet and giving your body time to rest by providing it with
substances that are known to heal the gut, like L-glutamine, omega-3
fatty acids, licorice, antioxidants (in the form of vitamins A, C, and E),
quercitin, aloe vera, sh oil and turmeric. L-glutamine helps to heal
and seal the gut [29], whereas omega-3, licorice and aloe can help
soothe inammation and can help to relax the gastrointestinal tract
[9]. In addition, sh oil helps reduce inammation, balance hormones,
and supports the immune system. Turmeric is a potent astringent that
contracts the proteins in the bowel lining, squeezing the spaces
between the cells and reducing gut permeability.
Foods that disrupting the digestive environment
Eggs and dairy: Egg whites contain enzymes intended to protect the
yolk during embryo development. ese enzymes can break up protein
chains rendering the smaller chains useless. Lysozyme has the ability to
pass through the digestive system and will latch on carrying other
proteins and bacteria to cross the gut-barrier, leading to a leaky gut
syndrome [29].
On the other hand, dairy products contain protease inhibitors
which contribute to leaky gut, and it is insulin-genic causing spikes in
blood insulin levels [29]. Moreover, dairy products contain A1 casein
which can cause leaky gut syndrome and increase inammation in the
thyroid gland and ultimately aect its function [9].
Gluten: Gluten is a protein found in wheat, barley, rye, kamut, oats,
quinoa, buckwheat, and millet [30]. Gluten contains high levels of
lectins, saponins, and protease inhibitors [9]. Gluten intakes by a
patient with gluten sensitivity will cause the gluten go through the
stomach, into the small intestine and force the body to produce a
chemical called zonulin, which opens up the intestinal walls, allowing
particles and liquids to ow. When this happens, over time the body
becomes chronically inamed, leaving one susceptible to developing an
autoimmune disorder, such as thyroid disease and other serious
conditions. In addition, gluten closely resembles many of the tissues in
our body, therefore gluten that get into the bloodstream due to leaky
gut will trigger body to produce antibodies to attack the gluten, but
also attack our own tissues [30].
Nightshades, nuts, seeds, grains and legumes: Nightshades
vegetables, nuts, seeds, grains and legumes contain high levels of
lectins. Lectins are not broken down during the digestive process
because our bodies’s natural digestive enzymes are unable to digest the
lectin proteins, and because they contain protease inhibitors. Lectins
cause leaky gut by rst tricking the gut lining enterocytes into treating
it like a simple sugar, allowing it to pass from the inner-gut to the
outer-gut, activating immune response and causing the immune
system to attack not long the lectin but also enterocytes, creating holes
in the gut lining [29].
Nightshades in particular the tomatoes have particular lectin,
agglutinin, which stimulates the production of antibodies [9], and it
can get into bloodstream quickly and contribute to leaky gut. In
addition, nightshades contains saponins, particularly glycoalkaloids
which can feed bad bacterias in the gut and destroy the red blood cell
membranes when enter the bloodstream [9]. Nuts and seeds in
particular contain phytic acid and amylase inhibitors which prevent
the breakdown of seeds and cause inammation, stress out the gut and
active the immune system [9].
Additionally, grains and legumes are high in saponins, which can
create holes in the surface membrane of the gut and cause
inammation. Protease inhibitors neutralize enzymes in an attempt to
avoid digestion, so the body’s response is to secrete more digestive
enzymes throwing o the balance of enzymes and potentially leading
to the destruction of the enterocytes creating a pathway for leaky gut
and provolke an immune response.
Sugars and sweeteners: Natural sweeteners such as agave are pure
fructose, which can tease the body into thinking because it is sweet,
that it needs to release insulin to digest the glucose before realizing
there is no glucose to digest [29]. erefore, in the event of sugars are
desired, it is best to gain them from natural sugar sources such as
honey, maple syrup, or molasses as they all maintain glucose-fructose
levels that the body is able to easily digest. It is important to consider
that in case of any sort of overgrowth, bacterial or yeast, sugars should
be avoided entirely, even fruit based and starchy vegetables that are
Citation: Soon TK, Ting PH (2018) Thyroid Diseases and Diet Control. J Nutr Disorders Ther 8: 224. doi:10.4172/2161-0509.1000224
Page 3 of 5
J Nutr Disorders er, an open access journal
ISSN:2161-0509
Volume 8 • Issue 1 • 1000224
converted to glucose as these can feed the overgrowth and lead to
further battles to ght them o.
Alcohol: Hypothyroidism and Hashimoto’s patients are
oen developing intolerance to alcohol. is is because alcohol causes
direct cellular toxicity on thyroid cells, thereby causing thyroid
suppression and reducing thyroid volume [42]. Moreover, continuously
high alcohol intake can inhibits thyroid hormones T3 and T4 and may
reduce the activity of type II 5’-deiodinase, which resulting in reduced
levels of Free T3 with ongoing symptoms.
It has also been found that alcohol creates tiny holes in the epithelial
cells which can allow some endotoxins into the body [29]. Alcohol
feeds on negative bacteria, and can allow them to get into the
bloodstream through the holes and create an autoimmune response
even in very small amounts.
Discussion and Conclusion
e dietary intake, as well as lifestyle and environmental factors play
a huge role in overall wellness. yroid problems seem to be more
prevalent these days, in fact, thyroid cancer is the most rapidly
increasing cancer in the United States [43]. is could be contributed
by the less healthy lifestyle, stressful environments and higher exposure
to chemicals which elevated the risk of developing thyroid disorders.
Stress is a fact of modern life and it has in fact become an unavoidable
part of today’s fast-paced, competitive world [44]. Study showed that in
stressful conditions, such as sickness or death in the family, nancial
problems, loss of job, and the unstable political situation caused
considerable anxiety which link to autoimmune diseases in many
patients [45]. Stress can prevent the body from healing itself and
encourage more of an autoimmune inammatory response. Moreover,
exposure to toxins through polluted air or water can wreck the body.
Although it is clear that the chemical toxins are a major cause of
thyroid disease, yet synthetic compounds with estrogenic activity
particularly xenoestrogens are present in cosmetics and personal care
products (makeup, hair dyes, soaps, and perfume) that are more
commonly used by woman [46]. In addition, caeine-lled food such
as coee is getting popular in busy life. In fact, caeine should be
avoided because it could increase the heart rate, which might make the
condition worse. However, we also do not rule out that increasing
number of reported thyroid diseases cases could also be due to more
people are being tested, and the tests themselves are better at detecting
irregularities.
For treatment, it is important to treat the whole body as a system
rather than seeing individual parts working separately. Diet and
lifestyle factors formed a key component in the overall treatment of a
patient with thyroid diseases. Laboratory study found that four months
gluten free diet with supplements of vital minerals and vitamins was
able to reverse the Hasimoto’s thyroiditis [13]. A 49-year-old man
presented with a typical celiac disease with malabsorption, anemia and
osteoporosis. e patient received nutritional counseling and was put
on a gluten-free diet. A follow-up examination aer four months
revealed complete remission of the abnormal clinical and laboratory
ndings with partial remission of endoscopic and histologic changes
(reduced to Marsh stage 2 from stage 3a) [13]. erefore, the treatment
of thyroid diseases should start from practicing gluten free diet which
allows the gut to heal. At the same time, adopting healthy lifestyle
habits such as regular exercise and using natural products to avoid
exposure toxic chemicals can facilitate the process of healing the
thyroid disease. On the other hand, social factors such as the quality of
relationship between patient and his family, are useful prognostic
factors in patient with thyroid disease [45,47-49]. Moreover, stress
management and behavioral interventions such as weight
management, adequate balanced diet, and a healthy home
environment indeed will help in recovering from thyroid disease
[47,48,50]. Coping strategies are important for daily routine and for
physiological well-being of chronic patients. ey enable the patients
to adapt to problems and stressors arising from the disease, such as
pain, fatigue, limitation in mobility, diculties in daily life activities,
and threats to the patient’s self-esteem [50-52].
In conclusion, with this understanding, it is possible to see the
positive synergic eects of healthy diet and healthy lifestyle factors in
addressing thyroid disease. Although there is clear and increasing
evidences that practising healthy lifestyle, gluten free diet, and use of
probiotics look promising in treating thyroid diseases. However, more
researches are needed before it can be used therapeutically to heal
leaky gut and indirectly cure thyroid diseases. In addition, further
understanding about the root causes of thyroid diseases is necessary, to
nd an eective solution to address not just to cure, but to prevent the
cause of thyroid diseases entirely. e bottom-line is regardless of the
conditions, annual health check-ups and blood tests are important for
early detection [53,54].
Acknowledgments
is work was nancially supported by University Malaysia Sabah.
References
1. Invernizzi P, Gershwin ME (2009) e genetics of human autoimmune
disease. Journal of Autoimmunity 33: 290-299.
2. Przybylik-Mazurek E, Hubalewska-Dydejczyk A, Huszno B (2007)
Autoimmune hypothyroidism. Immunulogia 3-4: 64-69.
3. Brent GA (2008) Clinical practice. Graves’ disease. New Eng J Med 358:
2594-2605.
4. Bjoro T, Holmen J, Kruger O, Midthjell K, Hunstad K, et al. (2000)
Prevalence of thyroid disease, thyroid dysfunction and thyroid peroxidise
antibodies in a large, unselected population. e Health Study of Nord-
Trondelag (HUNT). European J Endocin 143: 639-647.
5. Merrill S, Mu Y (2015) yroid autoimmunity as a window to
autoimmunity: an
6. explanation for sex dierences in the prevalence of thyroid
autoimmunity. Journal of eoretical Biology 375: 95-100.
7. Kahaly GJ, Grebe SK, Lupo MA, McDonald M, Sipos JA (2011) Grave’s
disease: diagnostic and therapeutic challenges (multimedia activity). Am
J Med 124: S2-S3.
8. Shoeneld Y, andman-Goddard G, Stojanovich L, Cutolo M, Amital H, et
al. (2008) e mosaic of autoimmunty: hormonal and environmental
factors involved in autoimmune diseases 10: 12.
9. Samuchiwal SK (2017) Autoimmune disease: backring of an otherwise
unerring defence. MOJ Autoimmune Disease 2: 00008.
10. Myers A (2015) e autoimmune solution. New York, New York: Harper
Collins Publications.
11. Baron-Faust, R, Buyon J (2003) e autoimmune connection. New York
McGraw-Hill: New York.
12. Jonklaas J, Bianco AC, Bauer AJ, Burman KD, Cappola AR, et al. (2014)
Guidelines for the treatment of hypothyroidism: prepared by the
American yroid Association task force on thyroid hormone
replacement. yroid 24: 1670-1751.
13. Rugge JB, Bougatsos C, Chou R (2015) Screening and treatment of
thyroid dysfunction: an evidence review for the U.S. Preventive services
task force. Annals of Internal Medicine 162: 35.
Citation: Soon TK, Ting PH (2018) Thyroid Diseases and Diet Control. J Nutr Disorders Ther 8: 224. doi:10.4172/2161-0509.1000224
Page 4 of 5
J Nutr Disorders er, an open access journal
ISSN:2161-0509
Volume 8 • Issue 1 • 1000224
14. Schreiber F, Zolb T, Veith M, Elsbernd H (2011) A typical cellac disease in
a patient with type 1 diabetics mellitus and Hashimoto’s thyroiditis.
DeutsheMedizinischeWochenschrit 136.
15. Intidhar LS, Chaabouni AM, Kralem T, Attia N, Gritli S, et al. (2006)
yroid carcinoma and Hashimoto thyroiditis. Ann Otolaryngol Chir
Cerviofac 123: 175-178.
16. Yi KH, Moo JH, Kim IJ, Bom HS, Lee J, et al. (2013) e diagnosis and
management of hyperthyroidism consensus: report of the Koran yroid
Association. J Korean yroid Assc 6: 1.
17. Moon JH, Yi KH (2013) e diagnosis and management of
hyperthyroidism in Korea: Consensus report of the Korean thyroid
association. Endocrinology and Metabolism 28: 275.
18. Tunbridge WMG, Evered DC, Hall R, Appleton D, Brewis M, et al. (1977)
e spectrum of thyroid disease in community: the Whickman survey.
Clinical Endocrinology 7: 481-493.
19. Quintero OL, Amador-Patarroyo MJ, Montoya-Ortiz G, Rojas-Villarraga
A, Anaya JM (2012) Autoimmune disease and gender: Plausible
mechanisms for the female predominance of autoimmunity. Journal of
Autoimmunity 38: 109-119.
20. Frieri M (2003) Neuroimmunology and inammation: implications for
therapy of allergic and autoimmune diseases. Annals of Allergy, Asthma
and Immunology 90: 34-40.
21. Murphy ED, Roths JB (1979) A Y chromosome associated factor in strain
BXSB producing accelerated autoimmunity and lymphoproliferation.
Arthritis and Rheumatology 22: 1188-1194.
22. Pierdominici M, Maselli A, Colasanti T, Giammarioli AM, Delunardo F,
et al. (2010) Estrogen receptor proles in human peripheral blood
lymphocytes. Immunology Letters 132: 79-85.
23. Selmi C, Brunetta E, Raimonda MG, Meroni PL (2012) e X
chromosome and the sex ratio of autoimmunity. Autoimmunity Reviews
11: A531-537.
24. Zandman-Goddard G, Peeva E, Shoenfeld Y (2006) Gender and
autoimmunity. Autoimmun Rec 6: 366-372.
25. Shelly S, Boaz M, Orbach H (2011) Prolactin and autoimmunity.
Autoimmunity Reviews 11: A465-470.
26. Costenbader KH, Karlson EW (2006) Cigarette smoking and
autoimmune disease: what can we learn from epidemiology? Lupus 15:
737-745.
27. Tan KS, Denil DJ, Ransangan J (2016) Temporal and spatial variability of
heavy metals in Marudu Bay, Malaysia. Oceanological and Hydrological
Studies 45.
28. Viswanath D (2013) Understanding autoimmune disease- A review.
Journal of Dental and Medical Sciences 6: 8-15.
29. Jabri B, Kasarda DD, Green PH (2005) Innate and adaptive immunity: the
yin and yang of celiac disease. Immunol Rev 206: 219-231.
30. Ballantyne S (2013) e Paleo Approach: Reverse autoimmune disease
and heal your body, Victory Belt Publishing, USA.
31. Blum S (2013) e immune system recovery plan. New York: Scribner.
32. Tsatsoulis A (2006) e role of stress in the clinical expression of thyroid
autoimmune disease. Autoimmune Review 7: 209-213.
33. Wu LI, El-Kaissi S, Wall JR (2004) Stress and thyroid autoimmunity.
yroid: O J Am yroid Assoc 14: 1047-1055.
34. Cooper DS (2005) Antithyroid drugs. N Engl J Med 352: 905-917.
35. Nazarpour S, Ramezni R, Simbar M, Azizi F (2016) yroid antibodies
and the eect on pregnancy outcomes. Journal of Obstetrics and
Gynecology 36: 3-9.
36. Vita R, Saraceno G, Trimarchi F, Benvenga S (2013) A novel formulation
of L-thyroxine (L-T4) reduces the problem of L-T4 malabsorption by
coee observed with traditional tablet formulations. Endocrine 43:
154-160.
37. Colucci P, Yue CS, Ducharme M, Benvenga S (2013) A review of the
pharmacokinetics of levothyroxine for the treatment of hypothyroidism.
European Endocrinology 40-47.
38. Fasano A (2011) Leaky gut and autoimmune diseases. Clinic Review
Allergy and Immunology 42: 71-78.
39. Pughoe K, Versalovic J (2012) Human microbiome in health and
disease. Annual Reviews Pathology 7: 99-122.
40. Lee B, Bak Y (2011) Irritable bowel syndrome, gut microbiota and
probiotics. Journal of Neurogastroenterology and Motility 17: 252-266.
41. omas C, Versalovic J (2010) Probiotics-host communication:
modulation of signaling pathways in the intestine. Gut Microbes 1:
148-163.
42. Bron P, Van Baarlen P, AndKleerebezem M (2011) Emerging molecular
insights into the interaction between probiotics and the host intestinal
mucosa. Nature Reviews Microbiology 10: 66-78.
43. Ozsoy S, Esel E, Izqi HB, Sofuoqlu S (2006) yroid function in early and
late alcohol withdrawal: relationship with aggression, family history, and
onset age of alcoholism. Alcohol Alcohol 41: 515-521.
44. Lim H, Devesa SS, Sosa JA, Check D, Kitahara CM (2017) Trends in
thyroid cancer incidence and mortality in the United States,
1974-2013. JAMA 317: 1338.
45. Dahiya S (2015) Occupational stress and personality trait in the Indian
manufacturing sector: An analytical study. ELK Asia Pacic Journal of
Human Resources Management and Organisational Behaviour 1: 69-88.
46. Stojanovieh L (2010) Stress and autoimmunity. Autoimmunity Reviews 9:
271-276.
47. Ortona E, Pierdominici M, Maselli A, Veroni C, Aloisi F, et al. (2016) Sex-
based dierences in autoimmune diseases. Annalidell’ Istituto Superiore
di Sanita 52: 205-212.
48. Maefarlane GJ, Pallewatte N, Paudya P, Blyth FM, Coggon D et al. (2008)
Evolution of work related psychosocial factors and regional
museuloskeletal pain: results from a EUIAR task force: Annals of the
Rheumatic Diseases 68: 885-891.
49. Stojanovieh L, Marisavlkeveh D (2008) Stress as a trigger of autoimmune
diseases. Autoimmune Review 7: 209-213.
50. Herrmann M, Sholmerich J, Straub RH (2000) Stress and rheumatic
disease. Rheumatic Diseases Clinics of North America 26: 737-763.
51. Persson IO, Berglud K, Saliberg D (1999) Psychological factors in chronic
rheumatic diseases- a review. e case of rheumatoid arthritis, current
research and some problems. Scandinavian Journal of Rheumatology 28:
137-144.
52. Wilder IR (2002) Neuroimmunoendocrinology of the rheumatic diseases
past, present and future.Annals of the New York Academy of Sciences
960: 13-19.
53. Cuolo M, Straub RH (2006) Stress as a risk factor in the pathogenesis of
rheumatoid arthritis. Neuroimmunomodulation 13: 277-282.
54. Shoenfeld Y, Isenberg D (1989) e mosaic of autoimmunity. Research
Manographs in Immunology Amsterdam. e Netherlands: Elsevier
Science Publishers: 1989.
Citation: Soon TK, Ting PH (2018) Thyroid Diseases and Diet Control. J Nutr Disorders Ther 8: 224. doi:10.4172/2161-0509.1000224
Page 5 of 5
J Nutr Disorders er, an open access journal
ISSN:2161-0509
Volume 8 • Issue 1 • 1000224