Herbs: Bayberry,black cohosh,gentian, mugwart,and goldenseal are supposed to help.
Food: eat molasses,egg yolks,parsley,apracots,dates and prunes.Eat fish or chicken and raw milk and cheeses.
Avoid sugar,prossesed foods and white flour.
Homeopathy: cal carb.1m is affective in treating Hypothyroidism and improving thyroid function.
Infusions of the herb bladderwack will help regulate thyroid funtion.
Herbs:Ifustions of the herb Bugleweed three times aday may help slow the action of the gland.
Homeopathy:a homeopath may persribe Iodum 30c twice a day for two weeks.
FOOD :eat plenty of Broccoli,brussel sprouts,cabbage cauliflour,kale,mustard greens,peaches pears,rutabagas,soybeans,spinach,and turnips these help to suppress thyroid funtion.
AVOID DAIRY PRODUCTS FOR AT LEAST 3 MONTHS
ALSO AVOID STIMULANTS<COFFEE,TEA,NICOTINE AND SOFT DRINKS.
FOR GOITERS: Try reflexology there are areas that relate to the thyroid which are found in the big toe and the arch of the foot.
Acupuncture is also supposed to help.
HOMEOPATHY: specific remadies might include,Iodum 30c,
spongia 30c,calcarea 30c and fluoric ac.30c.
I have found repetative mention of these two amino acids good for all thyroid problems.
L-tyrosine is important in the treatment of anxiety,depression,allergies and headaches.It aids in the production of melanin(pigment of the skin nd hair)and in the funtions of the adreanal,thyroid and pituitary glands.Low plasma levels of tyrosine have been associated with hypothyroidism.It acts as a mood elevator suppresses appetite,and reduces body fat.
A lack of tyrosine triggers a deficiency of the hormone
norephinephrine at a specific brain location,which results in depression and mood disorders.L-tyrosine is also used to sythasize epinephrine and dopamine.It has been used for withdraw from drugs aswell.
1,000mg aday is recomended.
LCYSTEINE: L-CYSTEINE has a high sulfur content .This amino acid is formed from L-methionine in the body;however vitamin B6
is necessary for this conversion.L-cysteine help to detoxify harmful toxins,thereby protecting and perserving the cells Cysteine is a precursor to L-glutathione. one of the best free radical destroyers,it works best when taken with Selenium and vitamin E(avoid exess amounts of vitamin E with any thyroid problem).In addition to protecting the cells from the harmfull afect of radiation,it protects the liver and brain from damage due to alcohol and cigarette smoke.It is recomended forteatment of Rheumatiod arthritis.It removes exess copper from the body and promotes the burning of fat and the building of muscle.Also L-cystein is used for bronchitis,emphysema and tuberculosis.
These aminos work best when taken on an empty stomache. Also brewers yeast is good for thyroid.
These are not meant to be an alternatives to your medication ;however for Herbs and Homeopathy it is best to cunsult with a homeopath or a Herbologist.
Regarding the food don't change your diet unless you know for sure wether your hypo or hyper.
These are safe to take for eanyone:
L-tyrosine and L-cystein
Take vitamin B complex it realy helps with depression and tremmors.
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Hashimoto's Thyroiditis is an autoimmune disorder in which antithyroid antibodies attack the thyroid gland tissue and prevent it from producing hormone.
Doctors typically test for two types of Antithyroid Antibodies: AntiThyroglobulin Antibodies - which attack the thyroglobulin protein -- a protein necessary to produce thyroid hormone) and Antithyroid Microsomal Antibodies - measured by the Antithyroid Peroxidase ("TPO") assay and also referred to as Anti-TPO antibodies.
Elevated levels of TPO antibodies confirm the diagnosis of Hashimoto's thyroiditis. Elevated AntiThyroglobulin Antibodies are also related to thyroiditis and, if you have had thyroid cancer with a total thyroidectomy, the presence of AntiThyroglobulin antibodies means that the Thyroglobulin blood test (typically used as a post-surgery annual follow-up study) will be inaccurate and you may need annual thyroid scans instead.
Additional thyroid antibodies can also be tested, including Thyroid Stimulating Immunoglobulins (which can make a person Hyper). A person can have any combination of antibodies at any time.
The ANA also measures antibodies related to autoimmune disorders, but while an elevated ANA level may occur along with thyroid disease, it does NOT always indicate thyroiditis. This is why doctors typically conduct the thyroid-specific tests.
Antibody-related Thyroiditis generally causes symptoms that fluctuate between Hypo and Hyper (or sometimes presents a combination of both). It is quite common for the symptoms to occur BEFORE the blood levels become abnormal; the presence of antibodies explain why the patient isn't "normal." Laboratory reference ranges for "normal" vary, but most adult females feel best when their TSH is at or below 1.0 and their Free T3 and Free T4 levels are in the middle of the lab's ranges. Adult males may feel best when their TSH is much lower (some prefer below 0.1).
Treatment typically consists of thyroid medication (as appropriate for the patient's blood levels and symptoms). It is best to see an Endocrinologist who specializes in Thyroid Disease and who is familiar with Antibody-related thyroiditis so that you will have a doctor who listens and treats your overall symptoms (rather than telling you that your blood levels are normal and that's all that matters).
Treatment is important because persistent antibodies will destroy the thyroid gland and may cause growth of additional tissue (nodules or cysts) as the gland tries to overcompensate for the missing hormone.
Supplements that may help include Selenium (maximum dose 200 mcg/day) and Maca. Recent studies have shown that Selenium may help fight thyroid antibodies while also helping the body to metabolize and absorb thyroid hormone. Maca (a type of Peruvian turnip) helps balance all the body's hormones and also supports the adrenals, which tend to become stressed during flare-ups of thyroiditis. These supplements typically help the "residual" symptoms that may linger even after your meds are balanced, such as body ache, fatigue, brain fog, and libido.
See the post about Thyroiditis Flare-ups (this page, 8/18/02) for details about what to do with the intermittent imbalances of Hashi's.
[This message has been edited by ArtfulD (edited 11-16-2002).]
If possible, call your doctor and ask him/her to explain your FNA biopsy results in layperson’s terms. You may also want to ask for follow-up tests, such as an Iodine Uptake Scan to determine if your nodule is hot (producing more thyroid hormone than normal), warm (producing the same amount of thyroid hormone as normal thyroid tissue), or cold (not producing thyroid hormone). Cold nodules require a closer watch.
I've gleaned this information from a variety of medical websites so, unfortunately, it's still pretty technical. Hopefully, I've interpreted them properly.
TERMS YOU MAY SEE IN THE FNA RESULTS
Adenoma - Clustered cells forming a growth or nodule. Can be benign or malignant.
Capsule infiltration - an indication that the thyroid gland cell "capsule" has been breached, suggesting malignancy (thyroid cancer). Benign cells have no capsule invasion.
Carcinoma - A malignant adenoma, indicating the presence of thyroid cancer.
Colloid - Colloid is a a gelatinous or mucinous substance found in tissues that naturally surrounds the follicular epithelial cells. In a normal thyroid gland, colloid should predominate with clusters or sheets of follicular cells with wispy cytoplasm (cellular fluid) and indistinct cell borders. Abnormal FNA results may identify nodules or cysts filled with colloid.
Colloid phagocytosis – a condition where phagocytes take in colloid
Epithelium or Epithelial Cells - Epithelium is the type of glandular tissue that is sampled in an FNA Biopsy.
Follicular and Microfollicular Adenoma – A benign thyroid nodule. The nodule shows microfollicles, is sharply circumscribed by a delicate even fibrous capsule, and there is no invasion of the capsule or blood vessels by the tumor. The cells that have grown to form this follicular neoplasm remain contained within a thin capsule of tissue that surrounds it.
Follicular Carcinoma – A malignant thyroid nodule, representing a form called follicular thyroid cancer. The cells in this follicular neoplasm have grown to penetrate the capsule of tissue to invade normal thyroid tissue or blood vessels within the thyroid gland. NOTE: It is not possible to distinguish a follicular adenoma from follicular thyroid cancer on the basis of a fine needle aspiration biopsy sample. To make a definitive diagnosis, it is necessary to surgically remove the nodule so that it can be cut into sections and examined under a microscope to look for any evidence of invasion of normal thyroid tissue or blood vessels.
Follicular Epithelium - Follicles are the type of cells (with nuclei) that compose the thyroid gland. "Normal" thyroid tissue would have follicles that are evenly dispersed; An FNA of normal tissue would reveal low columnar follicular cells surrounding pink colloid (containing thyroglobulin produced by follicular cells).
Follicular Neoplasm - Follicular neoplasms are thyroid nodules that may be benign or may be a form of thyroid cancer. The FNA Biopsy reveals clusters of increased numbers of epithelial cells grouped together in specific patterns with small amounts of colloid present.
Hemosiderin - a yellowish brown granular pigment that is formed in some phagocytic cells by the breakdown of hemoglobin and is probably essentially a denatured form of ferritin (a form of iron found in the blood).
Hemosiderosis – A condition where iron in the form of hemosiderin is found in the tissues
Hyperplasia, Hyperplasm, Hyperplastic - an abnormal or unusual increase in the cells composing a tissue.
Macrofollicle – a type of clustered follicular cells. Colloid nodules contain macrofollicles.
Macrophages - a cell (typically a white blood cell) that engulfs and consumes foreign material (as microorganisms) and debris. Phagocytes are macrophages.
Microfollicle - a type of clustered follicular cells. Hurthle cells contain microfollicles.
Neoplasm or Neoplastic - a new growth of tissue serving no physiological function (such as a nodule)
Nuclei Size – Follicular Cells typically have large nuclei. Cells with small nuclei may suggest an abnormal degeneration in the cells.
Phagocyte or Phagocytic Cells – see "Macrophage."
Polsters or Papillations - papillary infoldings that lack vascular cores and appear as round, bump-like protrusions.
Thyroglobulin - an iodine-containing protein of the thyroid gland that is the precursor of thyroxine (T4 hormone) and triiodothyronine (T3 hormone). The body uses Thyroglobulin to produce thyroid hormone.
Here are some Technical Descriptions from FNA Biopsy results as they correlate to diagnoses as found in the Powerpoint presentation at
There is much more information in the source website NOT included here, including tissue and cellular pathology descriptions for the various forms of thyroid cancer.
Various Types of Euthyroid (healthy thyroid) non-neoplastic conditions:
1. Indications of a Hematoma/Hemorrhage into the Thyroid - The sampled fluid includes Brownish fluid "chocolate" (old blood) that disappears with aspiration but may reaccumulate over time. FNA shows Red cells predominate with numerous macrophages. Results may show ingested debris and/or hemosiderin should lack ciliated or columnar epithelium; may have sparse degenerative follicular cells.
2. Simple Colloid Goiter - The tissue shows generally enlarged thyroid cells with glistening/waxy cut surface. The tissue consists of huge colloid filled follicles. FNA biopsy shows cells with abundant colloid of both thick and thin types; scant uniform follicular cells.
3. Colloid Cyst or Nodule - Benign epithelial cells filled with colloid. FNA Biopsy would reveal ciliated columnar epithelium (tall cells with hairlike protrusions), colloid, occasional macrophages, proteinaceous debris with variable inflammation and old blood, sometimes crystalline material (ie: cholesterol), occasional multinucleated giant cells.
"Colloid nodules" display macrofollicles lined by flattened thyroid epithelial cells. The nodules are circumscribed (self-contained) and do not have a fibrous capsule. Colloid cyst material may fall off the slide during processing, leaving the lab with an inadequate sample.
NOTE: the color of the fluid extracted from a Colloid Cyst during an FNA Biopsy is NOT an indicator of malignancy (or potential likelihood for the presence of thyroid cancer).
4. Adenomatous (Multinodular) Goiter (nontoxic) - Multiple nodules varying from solid, cystic degeneration or hemorrhagic. FNA biopsy shows tissue with pseudo-papillations (round, bump-like protrusions) lack true vascular core; macrofollicular containing colloid rare microfollicle; no true capsule. Cells are variable colloid; may have numerous follicular cells but still in a "honeycomb" pattern; ill defined cell borders; nuclei normal; easily confused with follicular neoplasms especially if cellular.
FNA Results for patient with Hyperthyroidism or Thyroid Storm:
Hyperthyroid FNA results are not neoplastic and rarely malignant. FNA frequently reveals pseudo-neoplastic features (described as: follicular cells with colloid, nuclear overlap, nuclear membrane irregularities). If the patient has been treated (with thiouracil, thiamidazole, or radiation), results may be atypical. Diagnoses may include - Diffuse toxic goiter (Grave’s Disease), Toxic nodular goiter (Plummer’s syndrome), and Autonomous hyperfunctioning "Hot" adenoma.
Typically, Grave's is diagnosed by clinical signs/symptoms & thyroid function tests. FNAs are typically given only to evaluate "cold" nodules.
The tissue is diffuse, "beefy red" and shows Hyperplasia of follicular cells; colloid thin with vacuolations "scalloping" at periphery of colloid; "polsters" which are papillary infoldings (lack vascular cores); variable lymphoid hyperplasia with some follicle formation; no chromatin clumping; occasional degeneration, giant cells, and Hurthle cells.
The cells appear with usually lots of fresh blood due to vascularity of condition; sparse "thin" colloid; moderate to numerous follicular cells; increased "flame cells" (metachromatic vacuoles at outer edge of cells on modified Giemsa stain giving the hyperplastic cells a "dark-wavy" edge (2* to dilated endoplasmic reticulum), pseudo-neoplastic features are common (follicular cells more frequent than colloid, nuclear overlap, nuclear membrane irregularities, anisonucleosis), occasional degenerative changes (macrophages and giant cells); occasional Hurthle cell.
1. Acute Thyroiditis - Neck is generally tender when touched, there is a sudden onset and variable mass (grows and shrinks). The FNA fluid sometimes contains pus at aspiration (if nodular) and the sample is sent for culture. FNA Biopsy shows cells with Neutrophils (type of white blood cell) and necrotic debris (debris from dead cells); intracellular bacteria (seen on DQ stain) Identifiable thyroid tissue in background.
2. Subacute Thyroiditis (De Quervain’s) - May be due to a virus. Neck is Tender and may develop nodules. Tissue shows Giant cells and granulomas; variable fibrosis; mixed inflammatory response; lymphoid follicles and Hurthle cells are unusual. FNA Biopsy shows that cells are sometimes scanty return due to fibrosis; multinucleate giant cells-large and numerous epithelioid histiocytes; mixed inflammatory cells and macrophages; degenerating follicular cells; follicular center lymphocytes and Hurthle cells are uncommon.
3. Hashimoto’s (Auto-immune) Thyroiditis - Neck has a moderately enlarged thyroid (usually 2-4x). Nodules are large, confined, rubbery or hard. Patient's blood levels may indicate Hypothyroidism
FNA Biopsy shows tissue with numerous lymphoid follicles; Hurthle cells; variable degenerative changes. Lymphoid nodules will be pale (white to tan) and solid with "fish-flesh" texture.
Cells are in moderate numbers of mainly small lymphocytes and scattered plasma cells with occasional follicular center cells in florid cases, moderate Hurthle cells (oncocytic appearance = enlarged; grey-blue cytoplasm on modified Giemsa stain; well defined cytoplasmic borders; nuclei enlarged, smooth membrane; prominent enlarged nucleoli), few multinucleate giant cells; epithelioid histiocytes (variable). Normal follicular epithelium to slightly hyperplastic, fibrosing variant of Hashimoto’s may be confused with Riedel’s thyroiditis or malignant neoplasm.
Secondary neoplasia: There is an increased incidence of malignant neoplasms within background of Hashimoto’s (both epithelial and lymphomas); therefore cold nodules arising within Hashimoto’s must be evaluated separately.
4. Riedel’s Thyroiditis - Extremely rare; more likely underlying malignancy or fibrosing variant of Hashimoto’s. Nodule is small and extremely hard. Blood tests are typically within normal laboratory range. FNA Biopsy reveals cells that include eosinophils, mature lymphocytes and fibrous stroma. Hurthle cells are rare but there are increased leukocytes.
Selenium: The Good, the Bad and the Ugly
Selenium is useful in helping the body convert T4 to T3, and may also help fight
against thyroid antibodies. However, the recommended dose for thyroid
disease is 200 mcg/day. For anyone concerned about potential overdosing on
this mineral, here is a breakdown of where you can find it nutritionally, plus
symptoms of overdose:
Brazil nuts, brewer’s yeast, broccoli, brown rice, chicken, dairy products, garlic,
liver, molasses, onions, salmon, seafood, vegetables, wheat germ, and
whole grain breads and cereals contain selenium.
Herb sources of selenium include alfalfa, burdock root, catnip, cayenne,
chamomile, chickweed, fennel, fenugreek, garlic, ginseng, hawthorn berry,
hops, horsetail, lemongrass, milk thistle, nettle, oat straw, parsley,
peppermint, raspberry leaf, rose hops, sarsaparilla, uva ursi, yarrow and
Note: The selenium content of food is dependent on the selenium content of the
soil in which the food is grown. Washing, cooking, improper storage or processing
and refining can result in a loss of selenium content of the food.
Acute overdose: Fatigue and irritability, nausea, vomiting, abdominal
cramps, diarrhea, rash and garlicky breath.
Chronic overdose: Tooth decay, tooth loss, cancer, hair loss, white streaking
or thickening of the fingernails, loss of nails, and tenderness and swelling of
What to do: For an acute overdose, call your doctor, emergency medical
services (EMS), or the nearest poison control center immediately. For symptoms
of chronic overdose, contact your doctor.
Note: These toxicity symptoms MAY appear in individuals whose daily intakes
are greater than 750mcg.
Following the Posting Policy in the FAQ is your responsibility.
Email contact - firstname.lastname@example.org
Please read the FAQ before emailing.
Last edited by Administrator; 11-17-2003 at 02:59 AM.
On the deficiencies of the TSH test for diagnosing and monitoring
Copyright 2002 Kevin G. Rhoads, permission to copy in whole is
granted in accordance with any of the following public licenses: GNU
Public Licence 2.0, (a.k.a., GPL2), GNU Lesser Public License 2.0,
(a.k.a., LGPL2) or any successor licences issued by the GNU
organization to GPL2 or LGPL2. Any copying in part is prohibited
unless permission is granted by the author in writing.
Disclaimer: The author is not a medical doctor, this writing is not
intended as medical advice or to prescribe treatment. This is
supplied solely for informational purposes and to raise issues for
discussion. This is supplied free, and while the author has
attempted to make it as accurate as possible, it is supplied "as-is"
as is detailed further in both the GPL2 and LGPL2.
History Once upon a time, in the middle of the 20th century, doctors
diagnosed thyroid disease by the symptoms of the patient. For
hypo-thyroidism, treatment typically involved supplementation of
thyroid hormone(s) from either animal sources or synthesized
hormones. Hormone supplementation was provided to levels at which
relief of symptoms was apparent, while avoiding the appearance of
symtoms of hyper-thyroidism. Tests for TSH were known, but were not
sensitive enough to adequately measure levels as needed for diagnosis
and treatment monitoring. Then the "ultra-sensitive" TSH test was
developed. And its use became widespread, on assumptions that TSH
testing was meaningful. But the assumptions needed for TSH testing
to be meaningful are many and questionable.
Assumptions about TSH testing
In applying the results of the TSH test to diagnosis and monitoring
of treatment there are several assumptions that have been made. (1)
First, for diagnosis it is assumed that when TSH is outside the
normal range that there is a problem with the thyroid system. (2)
Next, the converse is also assumed, that if TSH is within the normal
range that there is no problem with the thyroid system. (3) Once
treatment has been started, it is assumed that if TSH is outside the
normal range, adjustment of the treatment regime or additional
treatment is needed. (4) But if TSH is in normal range, many doctors
assume treatment is adequate and does not need further adjustment.
(5) There is the assumption that the techniques used by diagnostic
laboratories to calibrate their lab's normal range are valid,
adequate and result in properly calibrated normal ranges. (6) There
is the assumption that the normal range for TSH of people without
thyroid disease is the normal range for TSH in people with thyroid
disease when treatment is adequate. (7) And although it is well
known in medical research that in normal people TSH varies by at
least 2 to 1 over the course of a 24 hour day, most doctors assume
that they can measure TSH at one randomly chosen time and
meaningfully interpret that even unto the decimal level, e.g., 5.6 is
abnormal but 5.4 is normal. (8) Finally, in using TSH to manage dose
levels for thyroid disease, it is assumed that the part of the
thyroid system that sets TSH is acting normally and correctly, even
though other parts of the thyroid system are broken.
Let us examine the first two assumptions. For diagnosis, TSH out of
range means there is thyroid disease, TSH in range means no thryoid
disease. The first assumption is generally valid, if the TSH is
outside the actual normal range, the thryoid system is not acting
normally. However, there are other things that can result in
temporary changes in the TSH which do not mean that a permanent
thyroid disorder is present. The converse is not valid. It is
known, for example, that in central hypothyroidism, the TSH levels
can be within normal range, even though the person is hypo-. Most
doctors assume that central hypothyroidism is rare. Since it is
presumed rare, the doctors rarely test for it. I must ask, is the
rarity of this a result of it actually being rare or an artifact of
rarely looking for it. For you will not find something that you are
not looking for.
Assumption three is that once treatment has been started, it is
assumed that if TSH is outside the normal range, adjustment of the
treatment regime or additional treatment is needed. This is almost
certainly a trivial truth. However, its converse, "if TSH is in
normal range with treatment, then treatment is adequate and does not
need further adjustment" is clearly false. Even the dosing
directions for at least some kinds of thyoid supplement clearly state
that dose levels can be increased even if TSH is in range already, so
long as symptoms remain and TSH levels do not go out of range.
But there is a further problem with assumption four. It is dependent
upon the further assumption (number 6) that TSH ranges in healthy
people are the ranges for people with thyroid disease indicating
correct management of the disorder and relief of symptoms. This
assumption has never been proven, and there is considerable evidence
to show it is utterly false. The normal ranges for TSH in people
with thyroid disease being properly treated have never been
researched. The medical community has no idea what TSH ranges should
be for people with properly managed thyroid diseases. They don't
even know if the TSH ranges for people with hypo- that is being
properly treated and the range for those with hyper- which is being
properly treated are the same or different.
Further, many biological systems are as or more sensitive to peak
levels than average levels, so if the glands involved in the TRH/TSH
setting act that way, we can be certain that TSH levels in normal
people have NO relation to TSH levels in people with properly managed
thyroid disease. The thyroid gland itself is known to have such a
peak sensitivity, it resonds to the the nighttime surge of TSH, which
is often absent in central hypothyroidism. So to assume there is no
such peak sensitivity elsewhere in the thryoid system seems to me to
be the height of folly. But that is a necessary assumption
underlying assumption number six.
Assumption five, that labs' TSH normal ranges are properly set, has
come under fire. There are good reasons to believe that the method
used to set TSH normal range includes results from many people with
thyroid disease in the input data used by the statistical process for
setting "normal" ranges. How can the result be a true measure of the
normal range, if significant numbers of input data are from
thyroidally abnormal people? They can't.
Assumption seven, that the TSH can be measured at one randomly
selected time during the day, and still be interpreted to the limit
of significance in the reported numbers, is prima facia false. That
is like saying I can measure the outdoor temperature at randomly
different times of day and compare the figures to fractional degrees
to a standard range. So if the doctor measured at one time of day
you are normal, but if he measured at another you are not. Really?
Assumption eight, that even though it is known that part of the
thryoid system is broken in thyroid disease, it can be assumed that
the part that sets TSH is still correct - this really bothers me. As
an engineer, if I know that some system is broken, I do not trust any
part of it.
TSH as a diagnostic is limited to showing the existence of disease.
If TSH is outside normal range, then the thyroid system is out of
kilter. But TSH is not useful as a means of monitoring wellness.
TSH in range proves NOTHING. It does not prove that someone not
under treatment is free of thryoid disease. And it certainly does
not prove adequacy of treatment in general for thyroid disease, and
it may not prove adequacy of treatment for any specific case of
thyroid disease. TSH is sort of useful as a quick screen, but
nothing more. If doctors wish to use TSH for other purposes beyond a
quick screening, then they need to prove by double-blind testing what
is provable from the eight assumptions listed above. And some can be
clearly proven false, based on the limited information known to us
This is a great article that explains how thyroid hormones work in the body, what systems they effect, and different things that enhance or inhibit T4 and T3 like stimulants, depressants, other hormones, etc. Also, something I found interesting is a mention of alcohol and opiates inhibiting the breakdown of T3 in the brain thus increasing T3 levels and lifting the mood which may be one reason why these substances are so addictive.
FLAX AND THYROID
Flax oil, flaxseeds, and flax meal are not often mentioned on lists of goitrogen foods. One might assume that's because flax isn't as commonly ingested in North America as are other more common goitrogen foods such as cabbage family vegetables. Consumption levels of flax are changing, as the seed and oil become more aggressively marketed as an excellent source of omega-3 essential fatty acids, which have been proven to reduce cholesterol levels [common to thyroid sufferers], heart disease, and cancer.
My own recent toxic reaction to flax has lead me to research why it happened to me. Here's my lay interpretation of what occurred:
Flaxseed is a cyanogenic goitrogen, which means it contains a substance that converts to thiocyanate in the body. Thiocyanate effectively blocks iodine concentration by the thyroid gland and thus causes thyroid dysfunction.
Flax is also a rich source of lignan, a phytochemical which converts after digestion into a phytoestrogen-like substance. Phytoestrogens are known to suppress thyroid function.
Edited to add:
I received this information in an e-mail today from the mill where the flax I bought was processed:
" I'm sorry we do not have much information on flaxseed meal and the effects on the thyroid gland. The only information we have been able to obtain is from the Flax Council of Canada. In a book labeled "Flaxseed, Health, Nutrition and Functionality", there is a paragraph that has a
mention of the Thyroid gland. It is labeled under Cyanogenic Glucosides. Here it is in its entirety.
'Cyanogens are natural toxicants that occur in foods like lima beans and cassava as well as in flaxseed. In the body, they are hydrolysed to release hydrogen cyanide which is rapidly converted enzymatically to thiocyanate (SCN). SCN is also a breakdown product
from glucosinolates in common vegetable like cabbage and rutabaga. SCN inhibits the uptake of iodine by the thyroid gland and, at high levels in the blood for a sustained time when iodine intake is limited, goiter
can result. This hazard is offset where iodine consumption is adequate.
In Canada, table salt has been iodized since the 1930's to eliminate endemic goiter in inland regions where dietary iodine was inadequate. The addition of iodine to table salt is required in Canada and is
permitted in the United States. We are not in a position to make nutritional or dietary recommendations
for any medical condition. We suggest that you consult your doctor on this specific subject concerning our product.'
If you wish to consult the Flax Council of Canada, their web site is [url="http://www.flaxcouncil.ca"]www.flaxcouncil.ca[/url] and their e-mail contact is email@example.com."
[This message has been edited by midwest1 (edited 03-05-2003).]
[This message has been edited by midwest1 (edited 04-27-2003).]
__________________ "We can complain because rose bushes have thorns, or rejoice because thorn bushes have roses." Abraham Lincoln
A complete and easy-to-read primer on hypothyroidism from the University of California at Davis Med Center: (Be sure to click on all the page links at the bottom of the first one.) [url="http://www.ucdmc.ucdavis.edu/ucdhs/health/a-z/38Hypothyroidism/doc38.html"]U.ofCalif_Davis[/url]
[This message has been edited by midwest1 (edited 06-13-2003).]
[This message has been edited by midwest1 (edited 10-10-2003).]
__________________ "We can complain because rose bushes have thorns, or rejoice because thorn bushes have roses." Abraham Lincoln
There is an article titled THE DIAGNOSIS AND TREATMENT OF HYPOTHYROIDISM by Michael Schachter M.D.,
F.A.C.A.M. (Fellow of the American College for Advancement in Medicine) that says:
"If a patient has a normal TSH and a normal free T4, he is told by the conventional physician that he does not
have hypothyroidism, no matter how many symptoms or signs of hypothyroidism he has. This is the fatal error
because these tests only pick-up the most severe cases of hypothyroidism and miss virtually all of the milder cases
that would respond favorably to thyroid hormone treatment."
As we are all pretty much aware the optimal TSH levels are believed to be between 1 and 2, and levels above that
may in fact represent an abnormaility. Yet it's the levels above 5.0 that are generally considered abnormal by
practitioners. Some of us have said we feel best with a TSH below 1. So you see there is a huge disparity here as
to what is normal and abnormal. It's clear that what constitutes a normal TSH level urgently needs attention by the
There is another interesting Danish study reported in the JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM earlier in 2002 that summarized that individuals all have different variations of their thyroid
function and tended to fluctuate slightly within their own range over the course of a studied 12 month period. These
findings led the researchers to conclude that a thyroid test result within a lab's reference limit - or "normal range"
---is not necessarily normal for a particular individual.
These studies make it pretty clear that we cannot rely on lab ranges and even though they look normal by
lab standards, we could still be extremely symtomatic and be told that everything looks fine. So if you are told your
labs look normal and it's evident that you have fatigue, lethargy, problems with body weight, intolerance to cold,
hair loss, dry skin/hair, etc. then I can only say I would press on and try to convince the practitioner that
thyroxine treatment may be appropriate.
[This message has been edited by blondegal (edited 05-15-2003).]
Women With Thyroid Cancer at Increased Risk for Breast Cancer
According to a retrospective study conducted at the University of Texas MD Anderson Cancer Center, younger women with thyroid cancer have an increased risk of developing breast cancer later in life. The study establishes a relationship between the post-surgical use of radioactive iodine (RAI) I31I treatments for thyroid cancer, and later development of breast cancer.
The authors of the study, "The Development of Breast Cancer in Women with Thyroid Cancer," are all from the The University of Texas MD Anderson Cancer Center Houston, TX. Their findings are being presented at the annual meeting of the American Academy of Otolaryngology--Head and Neck Surgery Foundation Annual Meeting in Washington, D.C.
Using the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) database, the researchers found that young women (30-34 years) with thyroid cancer exhibited the greatest risk of developing breast cancer. Women who were between the ages of 40 and 44 at initial diagnosis of thyroid cancer were also at significantly elevated risk. The data suggested that the greatest risk appears 15-20 years after the thyroid cancer.
The study concluded that premenopausal adult Caucasian women who are treated for differentiated thyroid cancer are at increased risk to develop breast cancer five to 20 years later. Breast cancer, however, does not increase the risk of subsequent thyroid cancer. This finding suggests that the increased risk of breast cancer after thyroid cancer is related to the thyroid cancer treatment. In particular, the RAI treatment is suspected to be the agent involved in increasing the cancer risk.
The authors' recommendation is for regular follow-up of all women patients with thyroid cancer and "judicious use of radioactive iodine as a treatment regimen."
What This Means for Thyroid Patients
It would seem prudent for women who have received RAI to pay particular attention to preventive factors for breast cancer, including diet, exercise, and healthy body weight. You should incorporate some form of regular screening - i.e., monthly breast self-exams, regular professional breast examinations, and/or mammograms - into your health care.
In my opinion, of critical importance to women who have had RAI treatment for Graves' Disease is the need for a definitive study looking at whether the lower levels of RAI used to ablate the thyroid also pose an increased risk of breast cancer. Given that RAI is the preferred treatment for hyperthyroidism in the U.S., this is an important question. It's already thought by some researchers that having an autoimmune thyroid disorder contributes to increased risk of breast cancer. But given that researchers are suggesting that the RAI is the factor that is the likely cause of the subsequent breast cancer in thyroid cancer patients, this question warrants further research.
That was wonderful Tree Frog!! Thank you so much, even though I am undiagnosed I feel better because as I stated earlier I think my doctor thinks its all in my head or doesn't care!
I know it isn't in my head, I suffer from so many of the symptoms you named!! I need a better doctor who cares, and who will listen.
I found this board by surfing around, thank goodness, and I passed it on to a couple of friends as well!
[This message has been edited by moderator1 (edited 10-07-2003).]
13.08 Thyroid Hormones and the Thyroid Gland
13.08.01 Free Thyroxine Index (FTI T-7 Thyroid Hormone Binding Ratio)
13.08.02 Thyrotropin-Releasing Hormone (TRH) Test
13.08.03 Triiodothyronine-to-Thyroxine Ratio
13.08.05 Estimate of Thyroid Volume from Body Weight and Age
13.08.06 Estimate of Thyroid Volume from Urinary Iodine Excretion
13.08.07 WHO Classification of Goiter Size
13.08.08 WHO Stage and Endemic Goiter in the Community
13.08.09 Thyroid Testing Algorithm
13.08.10 Clinical Diagnostic Index of Crooks et al for Thyrotoxicosis
13.08.11 Clinical Score of Zulewski et al for Hypothyroidism
13.08.12 Clinical Index of Billewicz et al for Hypothyroidism
13.08.13 Thyrotoxicosis Factitia and Serum Thyroglobulin Levels
13.08.14 Color Flow Doppler Sonography (CFDS) Patterns for the Thyroid Gland
13.08.15 Classification of Amiodarone-Induced Thyrotoxicosis