ArticlePDF Available

Thyroid Diseases and Diet Control

Authors:
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
dierent regions of the world [3].
yroid disease is substantially greater prevalence in old age than in
those of younger age and are oen 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 aect 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 aects 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 signicantly increase the risk of
developing thyroid disorders.
Diagnosis of thyroid diseases particularly hypothyroidism and
Hashimotos 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
Hashimotos 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 eective 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 (Hashimotos 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; puy 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].
Hashimotos 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 aected 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].
J
o
u
r
n
a
l
o
f
N
u
t
r
i
t
i
o
n
a
l
D
i
s
o
r
d
e
r
s
&
T
h
e
r
a
p
y
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 aecting the risk to thyroid diseases
Several factors have been identied 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 specic dierences in the microbiota composition are found
only aer puberty [19,20]. e main dierences 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 inuence dierent aspects of immune system function and
potentially aect 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- 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-inammatory 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 inammation 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
dierent 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 inammatory 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
inammation [9].
Stress may aect 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 inammatory 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 inuence dierentiation 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
suer 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 eective 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 aer 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
eectiveness 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
Page 2 of 5
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 inammatory 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 deciency 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 reex 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
inammation, 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,
inammatory 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 inammation and can help to relax the gastrointestinal tract
[9]. In addition, sh oil helps reduce inammation, 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 inammation in the
thyroid gland and ultimately aect 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 inamed, 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 inammation, 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
inammation. 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
oen 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 inammatory 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, caeine-lled food such
as coee is getting popular in busy life. In fact, caeine 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 aer 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, diculties 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 eects 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 eective 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 dierences 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. Shoeneld 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: backring 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.
DeutsheMedizinischeWochenschrit 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 inammation: 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 proles 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 eect 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
coee 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. Pughoe 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 Pacic 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 dierences 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
... Often known as hyperthyroidism is a disorder in which the thyroid gland is overactive, producing too much thyroid hormone [102]. Typical hyperthyroidism signs include elevated blood pressure, fast heartbeat, damp skin, excessive sweating nervousness, increased appetite and weight loss, diarrhea and/or irregular bowel movements, weakness, protruding eyeballs and sensitivity of the eyes to light [103]. ...
... Typical hyperthyroidism signs include elevated blood pressure, fast heartbeat, damp skin, excessive sweating nervousness, increased appetite and weight loss, diarrhea and/or irregular bowel movements, weakness, protruding eyeballs and sensitivity of the eyes to light [103]. In women, hyperthyroidism around tem times is more common than in men [102]. ...
... The results of X-ray diffraction of the pure zinc oxide model deposited on the glass substrates and the laser energy (950mJ) at RT showed, as shown in the Fig. (4-12). There are four separate peaks for the growth of crystalline granules and in the directions (002), (100), (101), (102), and (103 ) with distinct growth in direction (002) and this corresponds to (JCPDS00-004-0831), and the appearance of these vertices indicates that the obtained composition is polycrystalline and also indicates that the prepared membrane is good due to the high intensity. This result is in good agreement with (Sahar .F et. ...
... Підхід до лікування автоімунного тиреоїдиту і розладів автоімунітету з позиції сприйняття організму як взаємопов'язаної та цілісної системи -це кращий спосіб боротьби із захворюванням [17]. Під час лікування ТХ важливо ставитися до всього організму як до системи, а не як до окремого її органа. ...
... Під час лікування ТХ важливо ставитися до всього організму як до системи, а не як до окремого її органа. На сьогодні деякі автори вважають, що фактори дієти, відновлення здорового травлення, усунення запалення кишечника та імунної дисфункції є ключовими компонентами загального лікування хворих на ТХ [10,17]. ...
... Лікування НЩК передбачає зменшення впливу або і ліквідацію механізмів, які її спри-чиняють, нормалізацію мікрофлори кишечника, відновлення кількісного та якісного складу ферментів травної системи, лікування запалення стінки кишечника, виключення з раціону харчових інгредієнтів, що є факторами розвитку НЩК і автоімунної агресії. У нормалізації мікрофлори кишечника провідного значення надають пребіотикам і пробіотикам [17,35,36]. Важливо відновити чи врівноважити фізіологічний склад флори кишечника [37]. ...
Article
Резюме. На сьогодні питання щодо лікування тиреоїдиту Хашимото (ТХ) залишається невирішеним. Згідно з даними літератури, ефективний вплив на автоімунний процес у щитоподібній залозі може мати нормалізація порушених функцій кишечника. У цьому відношенні важливого значення надають дієтичному харчуванню. Проте чітко не обґрунтовано доцільності призначення дієтичного харчування пацієнтам із ТХ і вимог до нього для забезпечення фізіологічного функціонування щитоподібної залози та кишечника. Мета дослідження – проаналізувати і систематизувати дані літератури, що присвячені дієтичному харчуванню в комплексному лікуванні хворих на тиреоїдит Хашимото. Матеріали і методи. У дослідженні використано публікації світової наукової літератури, присвячені ТХ, зокрема причинам та механізмам розвитку, лікуванню, ускладненням і його наслідкам. Результати. В огляді звернено увагу на патогенетичне обґрунтування дієтичного харчування, вимоги до нього та проаналізовано запропоновані дієти. Висновки. Проаналізовані дані літератури дають підстави вважати, що правильно збалансоване харчування, яке забезпечує організм усіма необхідними поживними речовинами, позитивно впливає на перебіг ТХ і самопочуття пацієнтів.
... A hoarse voice, slurred speech, pudgy face, drooping eyelids, intolerance to cold weather, constipation, weight gain, dry skin, dry hair, and depression are typical signs of hypothyroidism. Cardiovascular disease, osteoporosis, being overweight, celiac disease, and diabetes are all more common among hypothyroid patients [4,5]. According to estimates, 0.2% of men and 2% of women globally suffer from thyroid illness. ...
Article
Full-text available
In regions of the world where iodine is abundant, Hashimoto's thyroiditis, also known as Hashimoto's disease or autoimmune thyroiditis, is the most prevalent cause of hypothyroidism. It is a chronic inflammation of the thyroid gland. It is characterized by autoimmune-mediated thyroid gland destruction, which results in progressive thyroid failure, either with or without goitre formation. In young to middle-aged women, Hashimoto's thyroiditis typically starts as a painless, diffuse, firm thyroid gland enlargement those progresses to hypothyroidism. Many people don't initially exhibit hypothyroidism, and some don't even have goitre or may have an atrophic thyroid gland. Hashimoto's thyroiditis (HT), also known as chronic autoimmune thyroiditis, is an inflammatory condition that is characterized by parenchymal atrophy, fibrosis, and diffuse lymphocytic infiltration. Being the main source of primary hypothyroidism in regions with adequate iodine. With the help of various criteria, such as physical examination, blood tests for thyroid hormone levels (TSH is low, T3 and T4 are tall, for example), serum cholesterol and triglycerides, blood glucose, and radioactive iodine uptake, it is possible to distinguish between infections and clutter. According to estimates from several thyroid disease studies, 42 million persons in India are estimated to have the ailment. The pathogenesis, causes, risk factors and combination therapy linked to Hashimoto's thyroiditis are discussed in this review study.
... Thyroid diseases can also caused by an abnormal immune response to auto-antigens present in the thyroid gland. Study by Soon, et al 10 All articles did not conducts an experiment. 9. Analogy PFOA does not specifically cause thyroid disease only. ...
Article
Full-text available
Background: Perfluorooctanoic Acid (PFOA) is one of the Perfluoroalkyl acids family that can affect human health. It can act as an endocrine disruptors which interfered the hypothalamus–pituitary–thyroid (HPT) axis and targeted the biosynthesis and secretion of thyroid hormones, which can caused thyroid diseases. To determine the causal relationship between PFOA and thyroid diseases, it is necessary to look for some evidence regarding this relationship. The search for evidence is also complemented by a seven-step occupational disease assessment to establish occupational diseases.Methods: The literature searching using the electronic database “PubMed”, “Cochrane”, and “Scopus” search engine. The keyword is “PFOA” “perfluoroalkyl substances” “perfluorooctanoic acid” “perfluorooctanoate” AND “thyroid disease” “thyroid function” “thyroid parameters” combined with MeSH and Title/Abstract terms. The inclusion criteria are research on humans, English language, free full article and the exclusion is duplicate articles.Result: From the five literature obtained, there are differences in results. Four articles stated that there are association between PFOA and thyroid diseases but one articles stated PFOA concentrations measured in this study were not associated with thyroid hormones.Conclusion: Althought most articles stated there are associations between PFOA and thyroid disease but it does not mean that PFOA can caused thyroid disease so it is still not clear the causal relationship between PFOA and thyroid disease especially in occupational setting.
... Furthermore, the protocol of stretching exercises was developed based on recommendations from the Guidelines for Exercise Testing and Prescription proposed by the American College of Sports Medicine (39). When encountering medical related scenarios with self-reported hyperthyroidism, hyperuricemia, or urinary stones, the servicelearning students consulted supervisors, who were experienced registered nurses, regarding foods not to recommend and/or increase in amount, such as iodine-rich foods (40,41), purinerich foods (42,43), and diets high in salt, purine, and oxalate (44,45), respectively. In addition, pork was not to be suggested for Muslims due to religious reasons. ...
Article
Full-text available
Background: Risks attributed to chronic diseases, cancer, musculoskeletal discomfort, and infectious diseases among Indonesians were found to be associated with lifestyle behaviors, particularly in rural areas. The aim of this study was to examine the outcomes of a home-visiting lifestyle modification program on improving health risk behaviors among Indonesians living in rural areas. Methods: A total of 160 Indonesians living in rural hamlets in the Yogyakarta Region of Indonesia participated in the program in the period of June 21 to July 21, 2019. In the pre-intervention home interview, learning needs of diet, exercise, hand hygiene, and substance use were identified by using structured assessment tools. In the next home visit, the visitors provided health education and facilitated lifestyle planning based on the related affective and cognitive domains of learning. Subsequent follow-up interviews were conducted 3 weeks after intervention. Results: The results showed that the self-reported intake of vegetables, fruits, meat and salt, cooking with less oil, hand hygiene before eating, number of cigarettes smoked, and symptoms of muscle stiffness significantly improved after the intervention. The lifestyle modification program consisted of the affective and cognitive domains of learning, and could lead to the target behavioral changes in self-reported and observable measures over 1 month. Conclusions: The findings contributed to the framework of community-based health education for health risk reduction and behavioral modification in developing rural communities where health care resources were limited. Further studies with control groups and vigorous objective measures were recommended to elucidate its long-term impacts. The factors leading to its sustainability concerning collaborative care partnerships between community residents and faculty resources are worthy of continued exploration.
... Omega-3s can help to reduce inflammation in the body, as well as boost immunity. [25] Iron deficiency is common in thyroid disease; so iron-rich diet is also recommended. [26] Pumpkin seeds are remarkably high in zinc, a nutrient that is commonly low for thyroid patients. ...
Article
Full-text available
Old age refers to ages nearing or surpassing the life expectancy of human beings. Older people are an important and distinct yet sometimes the heterogeneous group of persons living with thyroid diseases. They have a unique biomedical, psychological, and social constitution. Their needs are different from those who are young adults. This implies that special care must be taken while planning, implementing, and evaluating nursing care for them. Management of different thyroid diseases in the elderly should provide attention on limitation of geriatric syndromes (medical conditions encountered in elderly persons) and neurocognitive dysfunction (impairment in the functioning of the brain and nervous system). This review takes a practical approach to the assessment, medical intervention along with nursing care for the elderly with thyroid diseases. It highlights major challenges and suggests solutions to these commonly encountered clinical nursing problems.
... Thyrocytes will be destroyed by cells and antibody mediated immune processes. This will cause a decrease in thyroid function and eventually lead to the clinical disorder known as hypothyroidism [18,19]. in female patients agree with Ruggeri, et al. [21] whom founded that serum IL-23 concentrations increased significantly in HT patients in comparison with both Grave's disease patients and healthy subjects. As well as with Konca et al. [22] who indicated that there is an increased concentration of IL-23 level in HT patients in comparison with control. ...
Article
Full-text available
Background: Hashimoto's thyroiditis and Hypothyroidism play a distinct role in the suppression and reactivation of herpes viruses. Herpes simplex virus infections have been assumed as one of the factors that may trigger autoimmune thyroid diseases; however, IL-23 has an important role in the pathogenesis of several inflammatory and autoimmune conditions. Objective: This study aimed to investigate the association between thyroid hormones in hypothyroid state and the Herpes simplex virus status in such patients; besides detecting the role of IL-23 in these cases. Materials and Methods: The present study included 65 Iraqi female hypothyroid patients with age ranged between 26-54 years and 25 healthy controls with age ranged between 25-50 years. Serum samples were collected from the study groups. Levels of thyroid hormones (TSH, T4, and T3) were determined by using automated Chemiluminescence Immunoassay (CLIA) analysis system. The detection of herpes simplex virus IgG and IL-23 levels in the serum samples were determined by an enzyme linked immunosorbent assay (ELISA) kits. Results: The current study results revealed that serum IL-23 and HSV levels are increased significantly (P<0.001) in the hypothyroid patients group as compared with control. There was a significant positive correlation between TSH and (IL-23, HSV); also between IL-23 and HSV (P<0.01). Moreover, there was a significant negative correlations (P<0.01) between IL-23 with (T4, T3) and between HSV with (T4, T3). Conclusion: The present study pointed to the association between thyroid hormones deficiency in Hashimoto thyroiditis cases and IL-23 levels through disruption of the patient ' s immune system; and with Herpes simplex viruse-1by their role in the replication.
Article
Background: In India, 42 million people are suffering from thyroid disorders, out of which hypothyroidism is most common with a prevalence of 5.4%. It is more prevalent among females with the male-female ratio being 1:6. Hypothyroidism is a clinical syndrome resulting from a deficiency of thyroid hormones, which in turn results in a generalized slowing down of metabolic processes. Impaired metabolism can be compared with vitiation of Agni causing Agnimandhya according to Ayurveda. Agnimandhya further hampers the formations of Ahara Rasa and consecutive Dhatus Nirmana, diminishing the metabolism, thereby causing features similar to hypothyroidism. The objective of the Study: To assess the impact of diet & lifestyle on the prevalence of Hypothyroidism in Females. Materials and Methods: It is a cross-sectional survey study. A total of 150 female subjects were selected for the study. With the help of a validated pre-designed and pre-tested questionnaire, the interview was conducted on female subjects diagnosed with Hypothyroidism to assess the impact of diet and lifestyle on the prevalence of Hypothy- roidism in and around Mysuru city. Result: In the survey study, the majority of the hypothyroidism diagnosed subjects followed unhealthy daily regimes and the majority percentage of them practised unwholesome diet, food habits and lifestyle. Diet and lifestyle have a direct influence on the occurrence of hypothyroidism. Conclusion: Hypothyroidism is a metabolic disorder is mainly caused by Agni Mandhya and Rasa Pradoshaja as a result of faulty diet and lifestyle. One should follow Dincharya, Rutucharya and other Ayurveda principles to protect the Agni and thereby prevent Hypothyroidism. The practice of Ahita Ahara Vidhi and Ahita Vihara in the manifestation of Agnimandhya, followed by the development of features of hypothyroidism was substantiated by the result of the survey. Keywords: Hypothyroidism; Diet; Lifestyle; Agnimandhya; Rasa Pradoshaja Vikara.
Article
Full-text available
ZET Hipotiroidi, temel olarak vücutta tiroid hormonlarının yeter-sizliği, nadiren de hedef dokulara etki edememesi nedeniyle meydana gelen endokrin bir bozukluktur. Tiroid hormonları metabolizmanın devamı için büyük önem taşıdığından, ye-tersizliği durumunda vücuttaki pek çok sistem etkilenmekte ve hastalığın düzeyine göre şiddeti değişebilen bulgular meydana gelmektedir. Enerji harcamasında azalma ile mey-dana gelen ağırlık artışı ve obezite, kan basıncında yüksel-me, lipit profilinde olumsuz değişiklikler, insülin direnci, konstipasyon ve çölyak hastalığı hipotiroidi ile birlikte görü-lebilen metabolik bozukluklardır. Diyetle iyot, selenyum ve demir alımının yeterli olmasına ek olarak, bu metabolik etkilere yönelik beslenme tedavisi de hastalığın yönetiminde önem taşımaktadır. Bu derlemenin amacı, hipotiroidi ile birlikte vücutta meydana gelen metabolik değişiklikler ve bunların beslenme ile ilişkisini değerlendirmektir. ABSTRACT Hypothyroidism is an endocrine disorder that occurs mainly due to inadequacy of thyroid hormones in the body and rarely due to the decreased effects on the target tissues. Because of great importance of thyroid hormones for the metabolism, in deficiency states, many systems in the body are affected and many symptoms which may vary depending on the severity of the disease occur. Weight gain and obesity due to the reduction in energy expenditure, increased blood pressure, negative changes in lipid profile, insulin resistance, constipation and celiac disease are metabolic disorders those may be associated with hypothyroidism. In addition to adequate intake of iodine, selenium, and iron in the diet, nutrition therapy for these metabolic effects is also important for the management of the disease. The aim of this review is to evaluate the metabolic changes in the body with hypothyroidism and their relationship with nutrition.
Article
Full-text available
Importance Thyroid cancer incidence has increased substantially in the United States over the last 4 decades, driven largely by increases in papillary thyroid cancer. It is unclear whether the increasing incidence of papillary thyroid cancer has been related to thyroid cancer mortality trends. Objective To compare trends in thyroid cancer incidence and mortality by tumor characteristics at diagnosis. Design, Setting, and Participants Trends in thyroid cancer incidence and incidence-based mortality rates were evaluated using data from the Surveillance, Epidemiology, and End Results-9 (SEER-9) cancer registry program, and annual percent change in rates was calculated using log-linear regression. Exposure Tumor characteristics. Main Outcomes and Measures Annual percent changes in age-adjusted thyroid cancer incidence and incidence-based mortality rates by histologic type and SEER stage for cases diagnosed during 1974-2013. Results Among 77?276 patients (mean [SD] age at diagnosis, 48 [16] years; 58?213 [75%] women) diagnosed with thyroid cancer from 1974-2013, papillary thyroid cancer was the most common histologic type (64?625 cases), and 2371 deaths from thyroid cancer occurred during 1994-2013. Thyroid cancer incidence increased, on average, 3.6% per year (95% CI, 3.2%-3.9%) during 1974-2013 (from 4.56 per 100?000 person-years in 1974-1977 to 14.42 per 100?000 person-years in 2010-2013), primarily related to increases in papillary thyroid cancer (annual percent change, 4.4% [95% CI, 4.0%-4.7%]). Papillary thyroid cancer incidence increased for all SEER stages at diagnosis (4.6% per year for localized, 4.3% per year for regional, 2.4% per year for distant, 1.8% per year for unknown). During 1994-2013, incidence-based mortality increased 1.1% per year (95% CI, 0.6%-1.6%) (from 0.40 per 100?000 person-years in 1994-1997 to 0.46 per 100?000 person-years in 2010-2013) overall and 2.9% per year (95% CI, 1.1%-4.7%) for SEER distant stage papillary thyroid cancer. Conclusions and Relevance Among patients in the United States diagnosed with thyroid cancer from 1974-2013, the overall incidence of thyroid cancer increased 3% annually, with increases in the incidence rate and thyroid cancer mortality rate for advanced-stage papillary thyroid cancer. These findings are consistent with a true increase in the occurrence of thyroid cancer in the United States.
Article
Full-text available
The current study was conducted to estimate the baseline concentration of heavy metals in the surface sediment of Marudu Bay. Environmental parameters were measured at the seafloor and samples of the surface sediment were collected at monthly intervals for the period of 12 months. The organic content, total N, total P and concentration of 16 trace metals in the surface sediment were analyzed. The baseline concentration of metals was estimated by geochemical normalization. Anthropogenic inputs of metals were then estimated by calculating the enrichment factor for each element. The result demonstrated that the C/N ratio of sediment at Marudu Bay varies from 15 to 342, which indicates the dominance of terrestrial organic matter. The baseline concentration of V, Fe, Mn, Zn, Ti, Rb and Sr were 26.74 mg kg
Article
Full-text available
Autoimmune disorder is an umbrella term for a variety of painful conditions involving a malfunction in the body's complex immune system. In a normal immune response to an infection or invasion, the immune system causes a temporary inflammation while it kills off the invader cells. In autoimmune disorders, this inflammation becomes chronic, causing pain and permanent changes or damages the involved tissues. There is no specific cause for autoimmune disorders; they show patterns of remission and recurrence and they are difficult to diagnose because the specific disorders have different possible symptoms and individual symptoms varies. This article introduces a number of autoimmune diseases and inflammatory myopathies. It includes a definition of autoimmune diseases as well as a short explanation of immunity.
Article
Full-text available
Background: A number of recent advances in our understanding of thyroid physiology may shed light on why some patients feel unwell while taking levothyroxine monotherapy. The purpose of this task force was to review the goals of levothyroxine therapy, the optimal prescription of conventional levothyroxine therapy, the sources of dissatisfaction with levothyroxine therapy, the evidence on treatment alternatives, and the relevant knowledge gaps. We wished to determine whether there are sufficient new data generated by well-designed studies to provide reason to pursue such therapies and change the current standard of care. This document is intended to inform clinical decision-making on thyroid hormone replacement therapy; it is not a replacement for individualized clinical judgment. Methods: Task force members identified 24 questions relevant to the treatment of hypothyroidism. The clinical literature relating to each question was then reviewed. Clinical reviews were supplemented, when relevant, with related mechanistic and bench research literature reviews, performed by our team of translational scientists. Ethics reviews were provided, when relevant, by a bioethicist. The responses to questions were formatted, when possible, in the form of a formal clinical recommendation statement. When responses were not suitable for a formal clinical recommendation, a summary response statement without a formal clinical recommendation was developed. For clinical recommendations, the supporting evidence was appraised, and the strength of each clinical recommendation was assessed, using the American College of Physicians system. The final document was organized so that each topic is introduced with a question, followed by a formal clinical recommendation. Stakeholder input was received at a national meeting, with some subsequent refinement of the clinical questions addressed in the document. Consensus was achieved for all recommendations by the task force. Results: We reviewed the following therapeutic categories: (i) levothyroxine therapy, (ii) non-levothyroxine-based thyroid hormone therapies, and (iii) use of thyroid hormone analogs. The second category included thyroid extracts, synthetic combination therapy, triiodothyronine therapy, and compounded thyroid hormones. Conclusions: We concluded that levothyroxine should remain the standard of care for treating hypothyroidism. We found no consistently strong evidence for the superiority of alternative preparations (e.g., levothyroxine-liothyronine combination therapy, or thyroid extract therapy, or others) over monotherapy with levothyroxine, in improving health outcomes. Some examples of future research needs include the development of superior biomarkers of euthyroidism to supplement thyrotropin measurements, mechanistic research on serum triiodothyronine levels (including effects of age and disease status, relationship with tissue concentrations, as well as potential therapeutic targeting), and long-term outcome clinical trials testing combination therapy or thyroid extracts (including subgroup effects). Additional research is also needed to develop thyroid hormone analogs with a favorable benefit to risk profile.
Article
Autoimmune diseases are characterized by an exaggerated immune response leading to damage and dysfunction of specific or multiple organs and tissues. Most autoimmune diseases are more prevalent in women than in men. Symptom severity, disease course, response to therapy and overall survival may also differ between males and females with autoimmune diseases. Sex hormones have a crucial role in this sex bias, with estrogens being potent stimulators of autoimmunity and androgens playing a protective role. Accumulating evidence indicates that genetic, epigenetic and environmental factors may also contribute to sex-related differences in risk and clinical course of autoimmune diseases. In this review, we discuss possible mechanisms for sex specific differences in autoimmunity with a special focus on three paradigmatic diseases: systemic lupus erythematosus, rheumatoid arthritis, and multiple sclerosis.
Article
Incidences of autoimmune diseases are rising; the numbers of cases are tripled over the last few decades. There are more than eighty illnesses caused by autoimmunity. It has been estimated that autoimmune diseases are among the ten leading causes of death among women in all age groups up to 65 years. The etiology of autoimmune diseases is multifactorial: Genetic, hormonal, environmental, immunological factors, together with host susceptibility are all considered important in their development. The cause of this worldwide epidemic lies primarily in our environment and the toxic world in which we live, as various stressors have been implicated in the induction and perpetuation of many autoimmune diseases. Various stressors including physical, chemical, biological, and psychological have been shown to be responsible for this growing epidemic. Understanding the pathogenic modes of actions of various stressors e.g. molecular mimicry, role of cytokines, Toll-like receptors signaling pathways, role of stress proteins (heat shock proteins), role of reactive species, in addition to neuroendocrine immune systems interactions foster the advent in targeted therapeutic era. New strategies have been introduced and are being studied to overcome effects of oxidative stress at the cellular level for subsequent use as new therapies for autoimmune diseases e.g. targeting intracellular signaling pathways for various proinflammatory cytokines, DNA vaccines, anti-inflammatory neuropeptides, and more. The better understanding of these etiopathogenetic mechanisms can move us from the era of controlling or treating autoimmune diseases to a new era of preventing these diseases.
Article
Thyroxine hormone has been recognised since the early part of the nineteenth century and levothyroxine has been available since the mid-nineteenth century as a replacement for deficient thyroid hormones. While levothyroxine remains the staple treatment for hypothyroidism even to this day, its optimal use can be challenging. As is often the case with older drugs, the pharmacokinetics of levothyroxine is often under-appreciated or misunderstood and many factors influence the optimal dosing of levothyroxine. This article will review the pharmacokinetics of levothyroxine in the treatment of hypothyroidism and highlight major concepts that should aid both clinicians and researchers.
Article
Background: In 2004, the U.S. Preventive Services Task Force found insufficient evidence to recommend thyroid screening. Purpose: To update the 2004 U.S. Preventive Services Task Force review on the benefits and harms of screening and treatment of subclinical and undiagnosed overt hypothyroidism and hyperthyroidism in adults without goiter or thyroid nodules. Data sources: MEDLINE and Cochrane databases through July 2014. Study selection: Randomized, controlled trials and observational studies of screening and treatment. Data extraction: One investigator abstracted data, and a second investigator confirmed; 2 investigators independently assessed study quality. Data synthesis: No study directly assessed benefits and harms of screening versus no screening. For subclinical hypothyroidism (based on thyroid-stimulating hormone levels of 4.1 to 11.0 mIU/L), 1 fair-quality cohort study found that treatment of subclinical hypothyroidism was associated with decreased risk for coronary heart disease events versus no treatment. No study found that treatment was associated with improved quality of life, cognitive function, blood pressure, or body mass index versus no treatment. Effects of treatment versus no treatment showed potential beneficial effects on lipid levels, but effects were inconsistent, not statistically significant in most studies, and of uncertain clinical significance (difference, -0.7 to 0 mmol/L [-28 to 0 mg/dL] for total cholesterol levels and -0.6 to 0.1 mmol/L [-22 to 2 mg/dL] for low-density lipoprotein cholesterol levels). Treatment harms were poorly studied and sparsely reported. Two poor-quality studies evaluated treatment of subclinical hyperthyroidism but examined intermediate outcomes. No study evaluated treatment versus no treatment of screen-detected, undiagnosed overt thyroid dysfunction. Limitation: English-language articles only, no treatment study performed in the United States, and small trials with short duration that used different dosage protocols. Conclusion: More research is needed to determine the clinical benefits associated with thyroid screening. Primary funding source: Agency for Healthcare Research and Quality.