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Reverse T3 Ratio – Should it be Greater than 20?

Posted on April 9, 2013 by barb

Some thyroid internet groups insist that a reverse T3 (rT3) ratio > 20 is required for good health.  The ratio is the calculation of Free T3/Reverse T3.  The problem is, very few people can meet that ratio, so nearly everyone is told they must then go on the T3-only protocol to “clear their blocked receptors.”  Some people do need more T3 than others, so they may see initial improvements on this protocol.  Others may have a low ratio because they were taking too much T3 (from desiccated thyroid) in the first place, so the T3 protocol only makes them worse.  Different reasons for high rT3 are explained in more detail at http://tiredthyroid.com/rt3.html#3

Who invented this ratio?  According to these groups, it comes from Dr. Kent Holtorf, who prescribes very expensive time-released T3 at his clinics.  If you are considering this protocol, you owe it to yourself to read some reviews from his patients, where the negative reviews far outnumber the positive:  http://www.yelp.com/biz/holtorf-medical-group-torrance

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Iodine Protocol—Thyroid Cure or Curse?

Posted on February 14, 2013 by barb

Iodine appears to have polar opposite effects in people with thyroid problems.  The pros:  some people say iodine cured their cancer, eliminated fibrocystic breasts, or allowed them to reduce their thyroid medication dose or even eliminate their medication.  The cons:  others say iodine induced permanent hypothyroidism or hyperthyroidism in them, their hair fell out, or they developed horrible skin reactions that looked like boils.  Iodism is the term for iodine poisoning, iododerma the term for toxic skin reactions.

As far as I can tell, there’s no way to tell which camp anyone will fall into, although people with long-standing iodine deficiency or any kind of thyroid gland abnormalities (nodules) will be more at risk.  Iodine proponents say that negative side effects are from bromine toxicity, and supplemental iodine is just pushing out the bromide toxins.  But some of the effects I see people reporting are hyperthyroid or hypothyroid symptoms.  A steady heart rate of 120+ beats per minute, 24/7, is a sign of hyperthyroidism and needs immediate attention; thyroid storm can be fatal.  Yes, bromide toxicity causes skin reactions, but I don’t believe it affects the heart that way.  And the required companion nutrients (supplements) of sea salt, selenium, magnesium, and Vitamin C cannot cure Graves’ disease.  Likewise, hair loss, dry skin, fatigue, and weight gain are hypothyroid symptoms.

Iodine in high doses will induce the Wolff-Chaikoff effect, where thyroid hormone synthesis and release stops.  This is why Lugol’s iodine solution is given in high doses to hyperthyroid Grave’s patients before thyroidectomies—they become less hyper and surgery has less complications.  But this shutdown is often only temporary, which is why surgery has to be performed shortly after starting Lugol’s.  With time (1 week to 3 months), the body adapts to high doses of iodine and thyroid function should return to normal (which would be hyperthyroid for someone with Graves’ disease).  For some hyperthyroid patients, the iodine protocol may appear to induce a remission, but it can be followed by an exacerbation of symptoms, even if the iodine is stopped.  The Wolff-Chaikoff effect can make someone hyperthyroid normal (temporarily or permanently), but it can also make someone fairly normal hypothyroid (temporarily or permanently).  There are enough case studies to prove the effect is real, but because it’s unpredictable (sometimes permanent, sometimes temporary) it remains controversial.  Someone who still has hypo or hyperthyroid symptoms after three months should get complete thyroid labs for an accurate diagnosis.  Here’s a link to the thyroid and antibody tests that should be requested.

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Hair Loss—a Hyperthyroid & Hypothyroid Symptom

Posted on October 24, 2012 by barb

Hair loss is brought up on both hyperthyroid and hypothyroid forums, and those who have been both, like me, have noticed their hair coming and going.  So what exactly is required for good hair?  There are few human studies to cite, but there’s a lot of anecdotal evidence that I can report, and some of my own theories.

Hair cycles through a growth phase called anagen, a regression stage called catagen, a resting phase called telogen, and finally, the hair is shed in the last stage called exogen.  I believe that when someone is hypothyroid, their whole body is in slow motion, so their hair stays in the resting phase far longer than normal.  That means no new hair grows until there’s enough energy to start the growth phase again.  Where does energy come from?  T3!  So some amount of T3 is necessary (a normal human secretes, on average, about 6 mcg of T3 daily).  If you’re only on T4 or levothyroxine, then you might need to add a small amount of T3 to get your hair growing again.  But T3 cannot be tolerated in those with insufficient iron or cortisol levels, so those need to be tested and addressed too.  Cortisol, iodine, iron, selenium, zinc, and Vitamin A are all required for normal thyroid metabolism.

Hair loss is also reported by people with Graves’ Disease who are hyperthyroid, or on the T3-only protocol, or even on high doses of desiccated thyroid.  They’ve got plenty of T3, so what’s the problem?  Well unlike the hypothyroid body that’s in slow motion, a hyperthyroid body is moving at warp speed.  Each strand of hair has a limited lifespan, and it progresses through all the stages sequentially.  But the rate of the progression would be greatly increased in someone with too much T3.  Maybe hair cycles too quickly with too much T3 and finishes the growth stage and enters the resting stage prematurely.  My hairdresser noted that my hair strands were thinner when I was on too much T3.  The other possibility is that too much T3 simply overwhelms the hair follicles, in the same way that it causes damage to other parts of the body.  Excess T3 causes bone loss and muscle wasting, so the same type of mechanism may be at work that causes hair loss too.

T4, or levothyroxine, seems to have a positive effect on many patients’ hair.  I know my hair improved when I went from 100% desiccated thyroid to a combo with T4.  My hairdresser said my individual hair strands are thicker now.  And I have heard multiple anecdotal accounts reporting the same thing.  While some cells pull T3 straight out of the bloodstream, other cells prefer to get their T3 by conversion from T4.  That way, the cells are never overwhelmed with an excess of T3.  I believe hair follicles prefer T4 and know people on 100% T4 who have full heads of hair, but the lack of T3 causes other problems for them, like weight gain.

Hair loss may also be caused by androgenic hormones like DHEA or testosterone, which contribute to androgenetic alopecia or male pattern baldness.  Even pregnenolone can convert into testosterone in some women.  This is a male pattern type of hair loss, which consists of a receding hairline and hair loss at the temples.  Low thyroid hair loss is usually a general thinning throughout the entire scalp.

Vitamin D has positive effects on skin and hair too, so don’t ignore that supplement if your levels are low.  Of course, as with all supplements mentioned, be aware of adverse reactions.  People have had negative reactions to Vitamin D, iodine, iron, zinc, and hydrocortisone (for cortisol), even though they are all found in the human body.

Both thyroid hormones, T3 and T4, need to be at good levels for an individual to have healthy hair.  Hair and eyebrows are really non-essential, and if there’s a deficit of thyroid hormone, the body will skimp on the hair’s portion and allocate it to more important organs where it’s needed.  In general, good health is found when both Free T3 and Free T4 are in the upper half of the range.  If raising T3 has not helped your thin hair and in fact made it worse, perhaps you need more T4 instead of more T3.  Read more about optimal thyroid labs and misleading reference ranges.

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High T3 Levels affect Memory, Language, and Math Ability

Posted on September 2, 2012 by barb

Can’t remember anything lately?  Having problems recalling the right words or performing simple math like adding and subtracting?  Taking longer to perform simple cognitive tasks?  You may be on too much T3 if you’re on a high dose of desiccated thyroid or on the T3-only protocol.  The brain has a very narrow range of what it considers optimal T3, and it achieves this by converting any T4 to rT3 if there’s too much T3 coming in, or by converting more T4 to T3 if there isn’t much T3 coming in.  But someone taking no T4 or too much T3 can literally short circuit this mechanism, resulting in severe memory problems.

In one study, females with previous thyroidectomies who were stopping their levothyroxine dose (for more tests) were given cognitive tests when mildly hyperthyroid, normal, and profoundly hypothyroid.  They took the longest to perform the same task when mildly HYPERthyroid, longer, in fact, than when they were profoundly HYPOthyroid!  Graves’ hyperthyroid patients also tend to have problems with attention, memory, and complex problem solving.  [References and more info on this topic at http://tiredthyroid.com/rt3.html#7]

I know I could not do simple subtraction when I was taking T3 + desiccated thyroid, but my math skills returned when I dropped back to just desiccated thyroid.  I feel my memory and thinking have improved even more since I’ve lowered the desiccated thyroid and added some T4.

Has anyone else noticed any changes in their brain power with different levels of T3?  Please share your story.

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High T3 May Induce Insulin Resistance and High Blood Sugar

Posted on July 30, 2012 by barb

The T3-only protocol and/or high doses of desiccated thyroid can cause high blood sugar, which causes A1C to rise to levels that warrant treatment.  Thyroid levels, both too high or too low, have a direct impact on blood glucose.  High doses of T3 have induced severe insulin resistance and type 2 diabetes in some patients, who are now on drugs like Metformin to control the condition.

High T3 levels stimulate the liver to produce excess glucose and the pancreas to produce excess insulin.  This causes high blood glucose and insulin resistance. [8]

A comparison between the T3/rT3 ratios of insulin resistant and insulin sensitive subjects found a significantly higher T3/rT3 ratio in insulin resistant subjects. [9] Since a high ratio is actually the goal of the T3-only protocol, the protocol itself may induce insulin resistance as a side effect in some people.

A suppressed TSH is also expected on the T3-only protocol or on desiccated thyroid, but a low TSH has been shown to correlate to insulin resistance, higher insulin levels, and lower insulin sensitivity.  This positive correlation holds even when Free T4 and T3 are within the reference range.  In short, as T3 rises, so does insulin resistance. [10]

References and more info at:  http://tiredthyroid.com/insulin-resistance.html

Please share your story if you’ve had problems controlling your blood sugar while either hypo or hyperthyroid or on any protocols.

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T3-only or Hydrocortisone (HC) Treatment May Induce Osteoporosis

Posted on June 4, 2012 by barb

The T3-only protocol often results in high SHBG levels, and high SHBG is correlated with poor bone mineral density, osteoporotic fractures of the vertebra and peripheral bones (especially the femur or thigh bone) [14], and hip fractures [19].  SHBG appears to have a bone wasting effect on post-menopausal women, while estradiol has a bone preserving effect. [18]

Hydrocortisone (HC) supplementation at 30 mg/day can also adversely affect bones, because corticosteroids like HC not only decrease bone formation, they also increase bone resorption. In one study, patients reduced their 20-30 mg daily hydrocortisone doses to 10-15 mg/day. None of the patients reported low cortisol symptoms.  Instead, 10/11 subjects lost weight (specifically abdominal fat), total cholesterol and triglycerides decreased, and Quality of Life scores improved. [17]  Another study found a negative correlation with osteocalcin (a protein involved with bone formation) as the hydrocortisone dose was increased.  In other words, as the HC dose increased, bone formation decreased.  Since bone loss would be induced at a daily hydrocortisone dose of 30 mg, the study recommended 15 to 20 mg of HC instead. [20]

The T3-only protocol combined with hydrocortisone treatment may have adverse effects on bone health and bone density scans are highly recommended. Vitamin D levels should also be tested and treated if low. [15]

If you have been on either the T3-only protocol or HC treatment and have had a bone density scan after being on this therapy, please share your story.   There are people who take HC at these lower doses, in combination with estradiol and testosterone, who have not suffered from bone loss.  I hope people with both positive and negative experiences will share their stories.

More information and references at:  http://tiredthyroid.com/osteoporosis.html

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TSH Test Results are often Normal even with Hypothyroid Symptoms (Depression, Insomnia, Fatigue, Hair Loss, Constipation, Coldness, and Memory Problems)

Posted on May 5, 2012 by barb

Thyroid medications often do not relieve typical hypothyroid symptoms such as depression, insomnia, fatigue, hair loss, constipation, coldness, and memory problems.  Is it possible patients are underdosed because of “normal” TSH test results?

Thyroid function is typically measured with a TSH (Thyroid Stimulating Hormone) lab test, even though TSH is a pituitary hormone and not a thyroid hormone.  The actual thyroid hormones, T3 and T4, can also be measured with lab tests, yet the T3 test is often not ordered.  Doctors often declare a patient “normal” if their TSH level falls within the laboratory reference range, meaning their TSH level was neither above nor below the specified range.  But two people can have the exact same TSH level (below the reference range), yet one person will be hypothyroid while the other will be hyperthyroid.  Measurement of a thyroid hormone, T3, will confirm that one person is actually hypothyroid (low T3–T3 below or near the bottom of the reference range), while the other is hyperthyroid (high T3–T3 above or near the top of the reference range).

TSH is like the gas gauge on a car.  The gauge is a measure of gas levels, but the gauge itself doesn’t provide any energy.  The actual gas in the car’s tank provides the car’s energy.  Likewise, T3 and T4 are the “gas” for the thyroid.  A faulty gas gauge may say the tank is full (TSH low or normal), but a look inside will show it’s nearly empty (low T3 and low T4).  If it’s empty, it makes sense to fill the tank and ignore the gauge, because the gauge is obviously broken.  Unfortunately, doctors are taught to follow the gauge (TSH), with little concern for whether the tank is actually empty or full (of T3 and T4).  Even more frustrating is that Free T3, the thyroid hormone that correlates most with symptoms, is rarely even measured!

TSH is not a reliable diagnostic measure for multiple reasons–it varies with time of day, time of year (season), fasting, and is affected by head injuries, autoimmune antibodies, pregnancy, diabetes, trauma, renal disease, liver disease, and cardiac conditions.  Medical journal references and more discussion of the TSH can be found at: http://tiredthyroid.com/tsh.html

Free T4 is sometimes measured along with TSH to make diagnosis and dosing decisions.  But Free T3 (not Free T4) is the only thyroid hormone level that has shown any correlation with symptoms.  Studies that compared the common thyroid function tests (Free T3, Total T3, Free T4, Total T4, TSH and reverse T3) found that only Free T3 correlated with symptoms.  Ideally, both Free T3 and Free T4 levels should be tested, because both hormones are present, at good levels, in healthy people without thyroid disease.  More discussion on relevant diagnostic tests can be found at: http://tiredthyroid.com/what-labs.html

Thyroid reference ranges are also so broad, that they are of little help in diagnosing and dosing someone who is hypothyroid.  According to one of the major laboratory testing companies, the T3 graph does not follow a normal bell curve (the majority of the people in the middle of the range, with a symmetrical, equal, decreasing number of people on either side of this midpoint).  Rather, T3 levels of the general population form a negatively skewed curve, with most people having T3 levels in the upper half of the range.  Only a few have T3 levels below the midpoint, so the left side of the curve follows a steep rise and peaks to the right of the midpoint, and then gradually decreases to the right, as T3 levels go higher.  Logically, it would make sense to change the ranges so they reflected the majority of the values; in other words, the bottom of the range should move up to what is currently the midpoint.  These overly broad ranges result in many hypothyroid patients (with obvious hypothyroid symptoms) being told that their thyroid is normal and “just fine” when they have levels in the lower half of the range.  Thyroid reference ranges and optimal thyroid levels are discussed further at: http://tiredthyroid.com/optimal-labs.html

To summarize, hypothyroid patients have three major obstacles working against their getting properly diagnosed and medicated:

  1. TSH, the hormone commonly tested, does not measure actual thyroid levels.
  2. Free T3, the only thyroid hormone level that correlates with symptoms, is often not tested.
  3. The normal range for thyroid hormone levels is so broad that patients who test at the bottom of the range with multiple hypothyroid symptoms are still classified as “normal.”

This explains why so many suffer from such common hypothyroid symptoms as depression, insomnia, fatigue, hair loss, constipation, coldness, and memory problems. With their “normal” TSH, it couldn’t possibly be their thyroid!  Sadly, many hypothyroid patients already on thyroid medications also complain of these same hypothyroid symptoms because they are actually undermedicated.  These symptoms only disappear on the correct dose of thyroid hormone, which cannot possibly be determined by the TSH.

 

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Osteoporosis Correlates with Thyroid Levels, not low TSH

Posted on April 30, 2012 by barb

From: http://tiredthyroid.com/osteoporosis.html

Osteoporosis, osteopenia, or bone loss can be caused by thyroid levels (Free T3 and Free T4) that are too high.  What is not well known is that osteoporosis can also develop from low thyroid levels (low Free T3 and Free T4), which are not always reflected in the TSH. [TSH levels do not reflect thyroid levels]  High thyroid levels upregulate the genes involved with bone resorption or bone loss.  But thyroid hormone also upregulates the genes involved with bone matrix formation and collagen maturation (bone generation), so if thyroid levels are kept too low, bone generation is impaired. [1]  Healthy bone metabolism requires thyroid levels that are neither too high nor low.  

Doctors believe that a low TSH always indicates a hyperthyroid state and will thus lead to osteoporosis.  There are, however, many exceptions to this TSH rule, and many with a low TSH actually have low thyroid levels.  Because of the misleading TSH, patients are maintained on a thyroid replacement dose that is so low they still remain hypothyroid, and with time, they eventually develop low thyroid symptoms such as osteoporosis, gingivitis, periodontitis, high cholesterol, heart disease, depression, etc.

From:  http://www.rxlist.com/synthroid-drug/warnings-precautions.htm

Effects on bone mineral density- In women, long-term levothyroxine sodium therapy [T4] has been associated with increased bone resorption, thereby decreasing bone mineral density, especially in post-menopausal women on greater than replacement doses or in women who are receiving suppressive doses of levothyroxine sodium.

Osteopenia or osteoporosis in patients taking T4-only drugs may be from the lack of T3, not from the T4 itself.  A normal thyroid gland produces 6+ mcg of T3 daily, so this lack of direct T3, over time, could contribute to osteopenia/osteoporosis.  There are anecdotal reports on thyroid internet forums where women switching from T4 to desiccated thyroid have reported improved bone density.  Also, the warning above noted decreased bone mineral density “especially in post-menopausal women” on T4.   A woman who is post-menopausal is lacking in estrogen and progesterone, two other hormones involved in healthy bone metabolism.  Perhaps a lack of estrogen, progesterone, T3, and T4 creates the perfect environment for osteopenia and osteoporosis.

If you currently have osteopenia or osteoporosis and have been on T4-only drugs, please share your story.   Or if you found that adding T3 or desiccated thyroid improved your bone mineral density, please share the details, such as your current and previous doses.  Thank you.

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Desiccated Thyroid contains T4, T3, and rT3, but little T2 or T1

Posted on March 31, 2012 by barb

Myth:  Natural Desiccated Thyroid is superior to T4 meds because it contains the same hormones that your own thyroid would produce–T4, T3, T2, T1 and calcitonin.  I have heard some variation of this statement on nearly every thyroid forum, and it is repeated all over the internet, even on some doctors’ websites.

The problem with this statement is that it is only partially correct.  Yes, T4 and T3 are components of natural desiccated thyroid, but T2 and T1 are not produced in the thyroid gland, according to thyroid physiology textbooks.  Studies show only trace amounts of T2 inside the thyroid, because T2 and T1 are actually produced by peripheral deiodination (conversion) outside of the thyroid gland.  Reverse T3 is produced within the thyroid and by peripheral deiodination.  Calcitonin is not a thyroid hormone at all, but is produced by the parafollicular cells, which happen to also reside in the thyroid.

An excellent description of calcitonin from: http://www.britannica.com/EBchecked/topic/594629/thyroid-gland

The thyroid gland is also the site of the production of calcitonin, a hormone
that can lower serum calcium concentrations. The cells that produce calcitonin,
which are called C cells, or parafollicular cells arise, separately from the
thyroid and migrate into it during development of the embryo. The C cells end up
nestled in the spaces between the follicles. Because these cells have a separate
embryological origin from the thyroid follicular cells, and because they secrete
calcitonin, they in essence form a separate endocrine organ. (In some animals
the C cells remain separate from the thyroid.)

Calcitonin is secreted in response to high serum calcium concentrations, and it lowers the concentrations acutely by inhibiting the resorption of bone. However, its action wanes within days, so calcitonin therapy is not an effective treatment for high calcium levels.


From http://tiredthyroid.com/medications.html (references and more information  can be found at this link)

Most people on the forums who have been on synthetic T4 and then switched to desiccated thyroid report feeling better, especially if they have no thyroid gland.  So it’s a popular medication, it’s just difficult to find a doctor to prescribe it.  Desiccated thyroid is made from whole pig thyroids and therefore contains all the components found in a thyroid gland:  T4, T3, rT3, diiodotyrosine (DIT), monoiodotyrosine (MIT), thyroglobulin, thyroperoxidase enzyme (TPO), hydrogen peroxide (H2O2), iodide, tyrosyl residues, and calcitonin (a hormone involved in calcium and bone metabolism). [7]  Calcitonin is not a thyroid hormone, but another hormone produced by the parafollicular cells, which just happen to be located within the thyroid.  Prescription calcitonin is administered by nasal spray or injection, because it is not absorbed well orally, so its effect in desiccated thyroid may be minimal. However, there is probably a synergy with all these additional components that make desiccated thyroid a more complete and effective replacement therapy for some than the synthetic replacements.  People on desiccated thyroid tend to have healthier bones, but I believe that is from the T3, not the calcitonin.  Studies show T3 is essential to bone health.

T2 and T1 are supposedly the special ingredients in desiccated thyroid, but thyroid physiology textbooks say that only T4, T3, MIT, and DIT are produced in the thyroid.  Only trace amounts of T2 have ever been measured in thyroglobulin in the thyroid [10], and T1 cannot be formed by the available iodotyrosine building blocks, MIT (1 iodine) and DIT (2 iodine).  1+1 = T2, 1+2 = T3, and 2+2 = T4.  When a pair of iodotyrosines (MIT and DIT) couple together, they form a thyroid hormone, also known as an iodothyronine.  Perhaps the confusion is because one of the precursors is called diiodotyrosine (DIT), while T2 is also known as diiodothyronine. The words are similar but they are two different things:  DIT is a precursor with only one tyrosine ring, while T2 has two tyrosine rings and has measurable effects as a thyroid hormone.  Diiodotyrosine (DIT), like T4 and T3, has been found in the thyroid and in serum. [8]

It is not my intent to discredit desiccated thyroid; I am merely pointing out that some of the benefits attributed to it are actually false.  I myself take both generic T4 and desiccated thyroid, because I believe that comes closest to natural replacement for me.

Has anyone had their antibodies (TPO, Tg, TRab) increase after starting desiccated thyroid?  And then decrease after returning to synthetics?

Has anyone shown a positive or negative change in bone density after switching to desiccated thyroid?

I’d love to hear your story.

 

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LDN (Low Dose Naltrexone) for Graves’ and other Autoimmune Diseases

Posted on February 20, 2012 by barb

From:  http://tiredthyroid.com/graves.html

There is a prescription substance called low dose naltrexone, or LDN, which has helped some Graves’ patients significantly reduce their antibodies.   Positive first person testimonies can be found on Graves’ and LDN chat groups throughout the internet, and there are a few medical journal studies on LDN that showed positive results in autoimmune conditions like Crohn’s, multiple sclerosis, and fibromyalgia.  Low Dose Naltrexone and LDNScience are two websites with a great deal of information that one could share with their doctor.  

Lately, the positive effects of LDN have come up on several thyroid forums.  I cannot share any personal experiences with LDN since I myself have never tried it, but I have heard positive testimonies from several Graves’ patients who are using LDN as a treatment for Graves’ disease, and thought they should be shared.

Graves’ patient #1 feels much more stable since starting LDN treatment.  In the past, her tapazole (anti-thyroid drug) dose was frequently adjusted up or down in response to life stressors, which seemed to trigger her Graves’; this left her with fluctuating, erratic thyroid levels where she sometimes felt hyper, yet at other times hypo.  Later, a modified block and replace regimen of 5 mg. tapazole + 25 mcg levothyroxine left her with other hypo symptoms like high cholesterol, weight gain, rising glucose, and just feeling hypo, even though she had no TSH, and her FT4 and FT3 were mid-range.

After starting on a very small dose of LDN (1.12 mg, or ¼ of the typical 4.5 mg dose), her LDN dose was raised a month later to 2.25 mg., and feeling more hypo, her tapazole was slowly reduced until she now takes no tapazole and no levothyroxine either.  After only 6 months on LDN, she now has measurable TSH, although it’s still on the low side.  And while she still has other health issues she is working on, she feels the LDN treatment has stabilized her constantly fluctuating thyroid levels and has vastly improved her health.  She has more energy, her thoughts are clearer, she’s lost 4 lbs, is handling stress better, and does not feel hyper.

Graves’ patient #2 (who takes the full 4.5 mg LDN dose in addition to low dose block and replace) reports better and deeper sleep, more energy, and noticed that her seasonal allergies and arthritic pain disappeared.  She no longer needs Albuterol or Advair for her allergies.  Her antibodies have come down since starting LDN treatment.

Graves’ patient #3 suffered debilitating muscle pain 24/7 that disappeared only 3 weeks after starting 1.5 mg LDN.  She feels her immunity has improved since her entire family got sick this year and she didn’t, when she normally caught every bug going around.  Her digestive system has also improved to the point that she recently had a slice of cheese pizza with no reaction, where previous to LDN treatment, she would feel sick to her stomach and have bloating, cramps, constipation, and nausea.  Her skin is also much clearer today.  She feels her mental clarity has improved and hopes to see further improvement with a higher LDN dose.

Is LDN treatment the cure for all autoimmune diseases?  That is probably too much of a blanket statement, and some on the LDN internet forums have reported side effects.  Some may not be Graves’ patients, but current theories are that a genetic MTHFR mutation is responsible for some cases of intolerance, while low IGF-1 (insulin-like growth factor) is another cause.  In any case, LDN is a prescription drug that must be obtained from a compounding pharmacy, so one must work closely with a doctor while following this protocol.  I urge everyone who suffers from an autoimmune disease to do further research on LDN, to see if they might benefit from a trial dose.

My initial impression is that LDN treatment should be tried as a first option for someone with Graves’, given that all the other options are either difficult to manage, or can have serious, irreversible side effects.  Anti-thyroid drugs (ATDs) like tapazole, methimazole, or propylthiouracil can be difficult to dose, because many with Graves’ have fluctuating thyroid levels, requiring frequent dose adjustments.  But an increase in dose to offset a hyper episode may leave them hypo as soon as it settles down, requiring another adjustment.  High doses of ATDs are not recommended because they can cause liver damage, so there is a limit to how much one can take.  In difficult cases, LDN can be used in combination with the anti-thyroid drugs, and may even result in a lower dose of the ATD, which would be safer and less stressful to the body.  A thyroidectomy cannot be undone, nor can radioactive iodine (RAI), and RAI has caused permanent, debilitating, lifelong side effects like TED (thyroid eye disease) in some, so really should not be a first choice of treatment.

If you are using LDN to treat Graves’ disease, please share your story, positive or negative, by leaving a comment.

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