Did You Know?

7 causes of hypothyroidism
Only ONE of which requires thyroid drugs, if even then
Hashimoto’s autoimmune thyroid disease
Hypothyroidism caused by mental or metabolic stress
Primary hypothyroidism
Under-conversion to active thyroid hormone
Over-conversion to active thyroid hormone
Too many proteins bind to thyroid hormone so it can’t get inside cells
Cells become resistant to thyroid hormone
Finally — the book that provides real answers for those still suffering from hypothyroidism or Hashimoto’s!

Get Dr. Kharrazian’s (my mentor) new book at www.thyroidbook.com

Journal of Clinical Endocrinology & Metabolism , doi:10.1210/jc.2008-0798

Celiac Disease
Thyroid Diseases

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The Journal of Clinical Endocrinology & Metabolism Vol. 93, No. 10 3915-3921
Copyright © 2008 by The Endocrine Society

Risk of Thyroid Disease in Individuals with Celiac DiseasePeter Elfström, Scott M. Montgomery, Olle Kämpe, Anders Ekbom and Jonas F. Ludvigsson
Department of Pediatrics (P.E., J.F.L.) and Clinical Research Centre (S.M.M.), Örebro University Hospital, SE-701 85 Örebro, Sweden; Clinical Epidemiology Unit (S.M.M., A.E., J.F.L.), Department of Medicine, Karolinska Institutet, Karolinska University Hospital, SE-17176 Stockholm, Sweden; Department of Medical Sciences (O.K.), Uppsala University, University Hospital, SE-75123 Uppsala, Sweden; and Department of Primary Care and Social Medicine (S.M.M.), Charing Cross Hospital, Imperial College, W6 8RF London, United Kingdom

Address all correspondence and requests for reprints to: Peter Elfström, Department of Pediatrics, Örebro University Hospital, SE-701 85 Örebro, Sweden. E-mail: peter.elfstrom@orebroll.se.

Background: It has been suggested that celiac disease is associated with thyroid disease. Earlier studies, however, have been predominately cross-sectional and have often lacked controls. There is hence a need for further research. In this study, we estimated the risk of thyroid disease in individuals with celiac disease from a general population cohort.

Methods: A total of 14,021 individuals with celiac disease (1964–2003) and a matched reference population of 68,068 individuals were identified through the Swedish national registers. Cox regression estimated the risk of thyroid disease in subjects with celiac disease. Analyses were restricted to individuals with a follow-up of more than 1 yr and with no thyroid disease before study entry or within 1 yr after study entry. Conditional logistic regression estimated the odds ratio for subsequent celiac disease in individuals with thyroid disease.

Results: Celiac disease was positively associated with hypothyroidism [hazard ratio (HR) = 4.4; 95% confidence interval (CI) = 3.4–5.6; P < 0.001], thyroiditis (HR = 3.6; 95% CI =1.9–6.7; P < 0.001) and hyperthyroidism (HR = 2.9; 95% CI = 2.0–4.2; P < 0.001). The highest risk estimates were found in children (hypothyroidism, HR = 6.0 and 95% CI = 3.4–10.6; thyroiditis, HR = 4.7 and 95% CI = 2.1–10.5; hyperthyroidism, HR = 4.8 and 95% CI = 2.5–9.4). In post hoc analyses, where the reference population was restricted to inpatients, the adjusted HR was 3.4 for hypothyroidism (95% CI = 2.7–4.4; P < 0.001), 3.3 for thyroiditis (95% CI = 1.5–7.7; P < 0.001), and 3.1 for hyperthyroidism (95% CI = 2.0–4.8; P < 0.001).

Conclusion: Celiac disease is associated with thyroid disease, and these associations were seen regardless of temporal sequence. This indicates shared etiology and that these individuals are more susceptible to autoimmune disease.

Global Physiological Effects of Thyroid Hormone
An estimated 27 million Americans suffer from thyroid-related illness, the majority of them women. Yet thyroid-related diseases are often ill diagnosed, and there is much about their treatment that bears greater clarification and study. In Dr. Datis Kharrazian’s book “Why do I still have thyroid symptoms When all my labs are normal?” he presents a revolutionary breakthrough in understanding Hashimoto’s and hypothyroidism and supporting people who have these conditions. There are 7 patterns of of low thyroid function that can be indentified using blood tests. Only one of the patterns responds to thyoid replacement therapy.

Global Physiological Effects of the Thyroid
1. GI Motility. Generally gastrointestinal motility is decreased in hypothyroid states. A decrease in gastrin leads to a decrease in HCL acid which is necessary to breakdown food.

2. Anemias. Due to a decrease in absorption of nutrients, iron defiency anemia is often present. Also, pernicious anemia is common in about 12% of all hypothyroid patients due to autoimmune attacks against the parietal cells in the gut responsible for producing intrinsic factor.

3. IGF1. IGF1 is decreased in hypothyroid states which helps in the anabolic repair/rebuilding of the body.

4. Epinepherine/Norepinepherine. These 2 neurotransmitters lose their function in hypothyroid states and lead to loss of motivation and depression. They are also responsible for lypolysis, which is the breakdown of fat, this leads to difficulty losing weight.

5. Hepatic clearance. Phase 2 conjugating enzymes can’t mature in a hypothyroid state and this inhibits the clearance of toxins.

6. Progesterone. Progesterone receptor sites lose their sensativity to take in progesterone and often times we will see a spike or increase in serum progesterone, yet a patient has symtoms of decreased progesterone.

7.SHBG. Sex hormone binding globulin is increased in hypothyroid states and this decreases the ability of testosterone and estrogen to get into the cells, causing symptoms of defiecency.

As you can see, the thyroid has a dramatic effect of many physiological sysytems.

Most, (80-90%), of all hypothyroid conditions are autoimmune in origin, meaning the body is attacking itself. In these instances, replacement therapy (natural or synthetic) will have very little effect on the long term success in management of these conditions. In our office, after a comprehensive blood panel, (including a breakdown and dissection of the white blood cells) we determine if it is in fact an autoimmune condition. If it is, we have specific management protocols that address the autoimmune component and help to modulate the genetic expression of the condition.

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