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WWW.IHPMAGAZINE.COM WINTER 2016

Natural Options in Thyroid Disease

CAM in Europe

THYROID HEALTH

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contents

DEPARTMENTS

FEATURES

WINTER 2016 • IHPMAGAZINE.COM 4

5 Publisher’s Letter

6 Editorial Board

8 Bits and BitesIndustry and Research News

22 Product Pro�les

24 Clinic Pro�leDarou Wellness

38 Post Scriptum

20 The 12th International Conference of the Society of Integrative Oncology: A Canadian perspective

28 Evidence for novel, therapeutic, natural options in thyroid disease

32 Emotional Effects of Thyroid Cancer and Patient Needs

34 Complementary and Alternative Medicine in Europe

�nd us on348

28

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publisher’s letter

O ver the years, I have always found

that one of the best ways to meet

fellow industry members is at a

trade show or convention. I recently attended

the 2016 Canadian College of Naturopathic

Medicine (CCNM) student event, and I caught

up with some old friends—and met some

new ones.

At the show itself, there was a sense of

excitement in the air. It was a pleasure to

meet graduating students and future natu-

ropathic doctors who are stoked on starting

their own clinics. I met with many exhibitors

who were excited to showcase their new

and innovative products. I also liased with

some old friends, who after years in the

business, are still very passionate about

homeopathic medicine. All this buzz and

excitement made me proud to be part of

this fantastic industry.

The ever-changing regulation also brings

forth a sense of excitement. Last year,

naturopathic medicine in Ontario acquired

a new status. With the Naturopathy Act, 2007,

proclaimed in June, the naturopathic pro-

fession became self-regulated, which brings

it to the next level in terms of integration.

New doctors, new clinics, new and inno-

vative products, experienced—and very

passionate—doctors are all ingredients of a

growing and vibrant industry. Now, that is

something to be excited about.

Please don’t forget to download

your IHP App to have access to

exclusive content and full-length

reference material.

Founder Sanjiv Jagota

Publisher & Editor-in-Chief Olivier Felicio

Senior Managing Editor Phill Feltham

Managing Editor Inna Levchuk

Art Director Scott Jordan

Graphic Designer Kaitlin Yep

Contributors

Rita Banach, Jason Boxtart, Julie Ennis, Rochelle Fernandes,

Hannah Lemke, Ellen McDonell, Marie-Jasmine Parsi, Susanne

Schunder-Tatzber

IHP Magazine Inc.

President Olivier Felicio

General Manager Melanie Seth

General Customer Care Manager Lucy Holden

Subscription RatesCanada $80 (gst included) for six issues | International $120

Canada Post Canadian Publication Mail Agreement Number 4067800 The pub-lisher does not assume any responsibility for the contents of any advertisement and any and all representations or warranties made in such advertising are those of the advertiser and not of the publisher. The publisher is not liable to any advertiser for any misprints in advertising not the fault of the publisher and in such an event the limit of the publisher’s liability shall not exceed the amount of the publisher’s charge for such advertising. No portion of this publication may be reproduced, in all or part, without the express written permission of the pub-lisher. ihp magazine is pleased to review unsolicited submissions for editorial consideration under the following conditions: all material submitted for edito-rial consideration (photographs, illustrations, written text in electronic or hard copy format) may be used by ihp Media Inc. and their af�liates for editorial pur-poses in any media (whether printed, electronic, internet, disc, etc.) without the consent of, or the payment of compensation to, the party providing such mate-rial. Please direct submissions to the Editor, ihp magazine.

Published by IHP Magazine

CirculationIHP Magazine Inc.1235 Bay St., Suite 700; Toronto, Ontario, M5R 3K4Email: [email protected]

Advertising Olivier Felicio Weng Ng(416) 203-7900 x 6107 (416) 203-7900 x [email protected] [email protected]

WINTER 2016 • Volume 9 Issue 1

Olivier Felicio

Publisher/Editor-in-Chief

EXCITEMENT IN THE AIR

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feature

INTRODUCTIONThyroid disorders affect about 200 million people in the

world (0.8-5% of the population), and are four to seven

times more common in women (Mircescu, 2010). These

disorders are ubiquitous in the context that they are the

root of many other diseases. Thyroid conditions include

hyper/hypothyroidism, goiter, thyroid cancer, Graves’

disease (GD) and Hashimoto’s thyroiditis. Conventional

treatment option for nodules and cancer is surgery.

Medications are also used for many thyroid conditions.

Pharmaceutical medications that are common for hypo-

thyroid status include Synthroid and Cytomel.

Hyperthyroidism is treated by radioactive iodine or anti-thy-

roid medications, such as Methimazole. There are several

natural options available to treat thyroid conditions that

can be used in conjunction with these medications or on

their own, such as selenium (Se), kelp and zinc. However,

more recent attention has been drawn to other options,

such as magnesium, vitamin D and carnitine. The following

is a summary of the current evidence on these natural

treatment options.

MAGNESIUMMagnesium (Mg) is a vital part of cellular reactions; it is

involved in metabolism, DNA replication, repair, transport

mechanisms and cell proliferation. Food sources that are

high in magnesium are whole and unrefined grains, seeds,

cocoa, nuts, almonds, green leafy vegetables, avocados

and fish (Blaszczyk, 2013). Magnesium has been used in a

wide array of diseases, such as arrhythmia, hypertension,

high cholesterol, premenstrual syndrome, asthma, diabetes

and attention deficit hyperactivity disorder (ADHD), in

doses of 100-400mg on average taken with meals

(Micromedex, 2015). More recently, the relationship between

Mg abnormalities and the development of thyroid disorders

has been considered.

EVIDENCE FOR MAGNESIUMA growing body of evidence has shown the role and pattern

of magnesium levels in thyroid disorders, including thyroid

cancer and autoimmune thyroid disease. For example,

after factoring out ethnicity, one meta-analysis showed a

significant association between serum Mg and thyroid

cancer. This retrospective analysis found that individuals

with thyroid cancer had lower serum levels of Se and Mg,

but higher levels of copper (Cu) than the healthy controls

(Shen, 2015). Further benefit from these findings in a future

study would be to understand the results in the context of

ethnicity. Another study on metabolic disorders indicated

that mineral deficiencies, including Mg, were found in

patients with autoimmune thyroid disease, alongside

protein and vitamin deficiencies (A, B’s and C). It suggests

that an improved diet via maintenance of required daily

intakes of vitamins and minerals could help decrease symp-

toms and prevent recurrence of malnutrition-induced

thyroid disease (Kawicka, 2015). Although this study was

Evidence for novel, therapeutic, natural options in thyroid

diseaseBy Rochelle Fernandes (MSc., ND (cand))

Peer reviewed by Jason Boxtart (ND), Hannah Lemke (ND (cand)), Marie-Jasmine Parsi (ND (cand))

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feature

done on a malnourished population, it offers unique results

that warrant further exploratory studies to see if the effect

to correct the thyroid diagnosis is maintained in a non-mal-

nourished population. One prospective cohort study showed

no evidence of association between thyroid cancer and

micronutrient levels, including Mg, however this may have

been partly attributed to the low statistical power of the

study and lack of detail surrounding the population studied

(O'Grady, 2014). Additionally, details were obtained via a

food frequency questionnaire; it is possible that numerical,

measurable outcomes could have different results if utilized

in further study.

A well designed, cross sectional study divided patients

into five groups: 1) subclinical-hypothyroid (SHY), 2)

overt-hypothyroid (OHY), 3) subclinical-hyperthyroid (SHE),

4) overt-hyperthyroid (OHE), 5) patients under thyroxine

therapy (EU), and normal controls. It showed that overtly

hypothyroid patients had reduced serum Mg levels-OHY

group, among other abnormal serum levels of nutrients

(Abdel Gayoum, 2014), thus suggesting the need for diet

modification and supplementation with this micronutrient.

It would also be beneficial to do an extension of this type

of study to examine whether this effect changes and/or is

maintained past six months. A study examined the effects

of Mg levels after treatment with thyroid medication; exam-

ining Mg as a pathology marker. The study demonstrated

that using Methimazole in the treatment of hyperthyroidism

due to Graves’ Disease led towards normalizing Mg levels

(Klatka, 2013). These results are useful with further inves-

tigation on whether, in addition to Mg as a pathology marker,

it could be used therapeutically, and a correction of Mg

deficiency could be beneficial towards correcting thyroid

abnormalities.

VITAMIN DVitamin D is a fat soluble vitamin that is found in certain

foods and can be produced internally when ultraviolet rays

hit the skin. It is inactive and has to go through two trans-

formations to be biologically active: primarily, the liver

converts vitamin D to 25-hydroxyvitamin D (calcidiol), and

secondly, the kidney converts calcidiol into 1,25 dihydroxyvi-

tamin D (calcitriol) (NIH, 2015). The function of vitamin D

in the body is for bone and cell growth, neurological func-

tion, normal inflammatory response and thyroid optimiza-

tion. Food sources of vitamin D include cod liver oil,

swordfish, salmon, milk and liver.

EVIDENCE FOR VITAMIN DThe role that vitamin D plays in the development and

treatment of thyroid conditions, such as Graves’ disease

and thyroid cancer, remains to be uncovered. One study

showed that the prevalence of vitamin D deficiency was

significantly higher in GD patients when compared to

control subjects (56.25 vs. 10.00 %, p < 0.001). The same

study also demonstrated that GD radioactive iodine therapy

(RIT) failed in 27 (37.50 %) of patients whose serum 25(OH)

D levels were < 20 ng/ml (Li, 2015). This suggests that

vitamin D deficiency might be an independent risk factor

for predicting failure of RIT in GD subjects. Another study

found that low vitamin D was associated with three types

of autoimmune thyroid disease (Ma, 2015).

Although the study of molecular mechanisms of vitamin

D are beyond the scope of this article, the following should

be noted as it illustrates the potential for future vitamin D

therapy. The mortality due to anaplastic thyroid cancer

(ATC) is high because of fast progression of the disease

and its high metastatic potential with no effective treatment

existing. The active form of vitamin D3, 1α,25(OH)2D3, has

been shown to thwart metastases in pre-clinical studies,

but has not been used clinically because of its potential to

create a state of hypercalcemia. A recent study unveiled

that a category of less-calcemic vitamin D analogs,

19-nor-2α-(3-hydroxypropyl)-1α ,25-dihydroxyvitamin D3

(MART-10), is more potent than 1α,25(OH)2D3 in repressing

cancer growth and metastasis in a variety of cancers. The

study showed that both 1α,25(OH)2D3 and MART-10 could

effectively inhibit the migration and invasion of ATC cells,

suggesting hopeful future clinical application (Chiang,

2015). Another emerging supplement for thyroid disorders

is carnitine.

Evidence has suggested a relationship pattern between lower Mg levels and their potential

correlation that could help in treating thyroid autoimmune and other thyroid-related diseases.

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CARNITINECarnitine is found in different forms. L-Carnitine (LC) is

made up of methionine and lysine. It is part of an effective

shuttling mechanism that transports long chain acyl groups

into the mitochondrial matrix to produce energy from fat

(Olpin, 2005). LC metabolism within the body occurs via

dietary intake, synthesis, and reabsorption in the kidney.

It is absorbed by the jejunum, through a sodium dependent

transporter (Gross, 1986). This transporter takes up LC,

while Acetyl LC (ALC) requires the removal of the acetyl

group before absorption. The levels of absorption are dose

and source dependent. Usual therapeutic dosage ranges

are between 500 to 2000 milligrams per day depending

on the use (Malaguarnera M, 2011). It has been used for

diabetes, osteoporosis, kidney and liver disease, and more

recently, for thyroid diseases.

EVIDENCE FOR CARNITINEResearch suggests that diminished fatty acid oxidation

can be corrected by carnitine supplementation. One ran-

domized, double blind, placebo controlled study consisted

of women who were given thyroid hormones to treat benign

thyroid nodules. They were divided into three groups; a)

those who received placebo for six months, b) those who

had placebo for two months followed by carnitine 2 or 4

g/day for two months, then back to placebo, and c) those

who got carnitine 2 or 4 g/day for four months and then,

placebo. The placebo group displayed symptoms of hyper-

thyroidism, such as muscle weakness, shortness of breath,

heart palpitations, nervousness, and insomnia, amongst

others. The second group had hyperthyroid symptoms

during the two months of placebo, but those symptoms

disappeared after two months of carnitine supplementation,

and returned again during the last two months of placebo.

The last group had no hyperthyroid symptoms until they

stopped receiving carnitine at the end of the first four

months (Benvenga, 2001). The results, although not reaching

statistical significance, were still meaningful from a clinical

standpoint, and showed a time-sensitive benefit of carnitine

supplementation in hyperthyroidism.

The basis of why carnitine supplementation is useful

for many clinical thyroid settings derived from the under-

standing that hyperthyroidism lowers tissue carnitine

levels. It was shown that urinary excretion of carnitine is

increased in hyperthyroid individuals (Maebashi, 1977).

One study showed that there were no differences found

in the serum ALC profiles between hypo-, hyper- and euthy-

roid states before and after treatment with thyroxine or

Thionamide therapy (Wong, 2013). Despite this, most

evidence has shown a significant reduction in carnitine

(mostly esterified portion) in hyperthyroid individuals, with

a return to normal levels as euthyroid status was achieved

(Sinclair, 2005). This indicates that further investigation

is needed to better understand the mechanisms by which

thyroid conditions could result or cause a deficiency in

carnitine. So far, LC is thought to inhibit both triiodothy-

ronine (T3) and thyroxine (T4) entry into the cell nuclei,

and thus supplementation could be beneficial to increase

tissue levels (Benvenga S. A., 2004).

Other thyroid diagnoses, such as thyroid storm, were

successfully treated with a combination of conventional

treatment, such as Methimazole and LC (Benvenga S. L.,

2003). Another study showed an awakening from a coma

caused by thyroid storm after intravenous administration

of LC (Kimmoun, 2011). The methods by which carnitine

elicits these effects on the thyroid is not fully understood.

Some studies have shown that LC can also modulate thyroid

hormone action in peripheral tissues, most often through

inhibition (Benvenga S. , 2005)

See table 1 on your IHP app for further details on clinical

studies with magnesium, carnitine and vitamin D in associa-

tion with thyroid diagnoses that were discussed in this text.

CONCLUSION Overall, given that thyroid conditions can be detrimental if

they are not treated and overlap with other diagnoses, it is

imperative that several effective treatment options be con-

sidered, including conventional and natural ones. Evidence

has suggested a relationship pattern between lower Mg

levels and their potential correlation that could help in

treating thyroid autoimmune and other thyroid-related

diseases. Vitamin D has shown efficacy in preventing migra-

tion of certain thyroid cancer cells, helping predict the

success of certain conventional thyroid treatments. Carnitine

effectively modulates thyroid metabolites in peripheral

tissues and can correct inherent carnitine deficiencies

caused by hyperthyroidism. These three powerful supple-

ments have recently shown promise as potential effective

therapeutic targets in thyroid disease, enabling a greater

spectrum of choice of natural treatments for practitioners

and patients.

View the table and references on your tablet.

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