Armour Thyroid Medication Reformulation Part III

http://www.hospitalsoup.com/health-conditions/thyroid/thyroid-medication-nature-throid-vs-armour-thyroid

If you’ve been following along with this series on how Armour Thyroid Medication was reformulated, you’ll know that it came as a surprise to patients, including myself, that a medication could simply be reformulated without informing patients, physicians or pharmacists. So, to pick up after the last update, I had a resurgence of all the hypo-thyroid symptoms that I had previously been managing so well while on the naturally desiccated thyroid hormone, Armour Thyroid, and found out that Forest Laboratories, the drug company producing Armour Thyroid had changed the fillers. Since I was obviously not doing well on the new reformulation, the new task at hand became on what to do about replacing Armour Thyroid.

First of all, it’s not that easy to change medications. Especially, if you’re taking a naturally desiccated or non-synthetic thyroid hormone. Most doctors, especially if they don’t have a good understanding of thyroid issues, or simply believe everything that their drug rep tells them, will prescribe a synthetic medication which contains only T4 hormone. Other synthetic hormone preparations may have only T3, but the bottom line is that your body produces both T3 and T4, so many thyroid patients will do better taking a medication that more closely resembles the hormones that your body would produce naturally if it could do so. The other argument that some medical practitioners use is that they will tell patients that it is perfectly acceptable to take a synthetic T4 hormone supplement only because the thyroid gland will convert some of the synthetic T4 to T3. This is a problem for many of us with thyroid disorders because if you are relying on an already malfunctioning thyroid gland to do conversions of hormones for you, it can be problematic to expect that you will get the proper conversions with a thyroid gland that is not working optimally. Not to mention the fact if you talk to a group of thyroid patients, most likely the ones most satisfied with their treatment are those who are taking non-synthetic type/s of hormone replacement. Not all, because the thyroid is a complex organ, and of course, everyone’s body is different, thus the need to adjust dosages and pay attention to patient’s symptoms. But most patients I have interviewed and the thousands of news group postings online seem to reflect a common denominator in that most will feel much better by taking a naturally desiccated thyroid hormone.

Alright, we’ll talk more about the different types of naturally desiccated thyroid hormones in another segment, but for this time, we’re going to focus on Nature-Throid™. After finding out that the thyroid medication that I relied on every day to keep me functioning no longer worked, I got busy and found that there were many thyroid patients who were switching over to Nature-Throid. So I called my pharmacists and explained the situation and found out that because Nature-Throid and Armour are essentially the same active ingredients, that they could most likely just refill my prescription with Nature Throid without my having to schedule another doctor’s visit. My pharmacy actually ended up making a call to my doctors office for me and my doctor just went ahead and wrote out a new prescription and faxed it to the pharmacy and I was able to pick up my new Nature-Throid medication the very next day. It took some adjustment in order to get my dosage correct. Even though theoretically, the Nature Throid is the same “active” ingredients because it has different fillers my body does process it differently and I am now taking 1/4 of a grain less than what I was taking using the Armour Thyroid. But so far, it’s been a few weeks and things are finally getting back to normal in terms of my energy, memory and other symptoms. And no more headaches which is great.

As always if you’re on any type of medication, make sure to listen to the signals your body is telling you and don’t ignore any new side effects even if you think that it “couldn’t be an issue with your medication” because you’ve taken it for years.

And no, there’s not a mis-spelling with the words “Nature-Throid” . The “y” has been left off the word Thyroid, so please make note of this if you’re trying to have your pharmacy order it in for you if it is not in stock and you want to try it as an alternative to Armour Thyroid.

Armour Thyroid Medication Reformulation Part II

http://www.hospitalsoup.com/health-conditions/thyroid/armour-thyroid-medication-reformulation-part-ii

When Forest Labs changed how Armour Thyroid Medication was formulated, there apparently was no announcement made to physicians, pharmacists or patients taking the drug. Forest has not responded to my request for information or an interview regarding this issue although their Pharmaceutical Customer Service Telephone Number (866-927-3260) states that there are “unexpected production delays” with certain strengths of Armour Thyroid.

When my hypo-thyroid symptoms re-appeared after getting my thyroid prescription refilled, and it was the second time that this had happened, I went online to research possible causes. And imagine my amazement when I discovered I was not the only one having difficulty with the new Armour. I found hundreds of other patients with similar stories reporting brain fog, tiredness, muscle and joint pain, hair falling out, feeling cold, weight gain. All symptoms I was all too familiar with and which were associated with improper levels of thyroid hormone in my body.

According to sources who have been able to speak to someone at Forest Labs, the laboratory changed the fillers in Armour Thyroid. The changes that were reported to have been made include the following: increasing cellulose (this has made Armour more difficult to dissolve), and reducing the amount of dextrose (which was the ingredient which gave it a slightly sweet taste). The “active component” of Armour has said to have remained the same.

Why you must stay vigilant regarding any medications that you take: Medications are made up of “active ingredients” which is the actual part of the tablet containing the specific “medicine” and in-active ingredients which can be flavors, fillers, and dyes. This is why you may have a brand name medication that is similar to a generic version of a drug, but generic versions may work differently for individuals. Because all of us are unique in how we respond to medications, certain fillers or non-active components of a medicine may help or hinder your body from absorbing or responding to a particular medication. That is one reason why in certain cases some physicians will not allow substitution of a generic drug for a brand name, or perhaps vice-versa. In the case of the Armour reformulation it has nothing to do with generic vs. brand names but it is important to understand how fillers, dyes and flavors can effect your response to a medication. From the hundreds of e-mails I’ve received from thyroid patients who had read my first post regarding Armour Thyroid’s reformulation it appears that there are many of us whose bodies are not responding properly to the medication change.

If you are taking Armour Thyroid and have comments about this issue please enter your thoughts below. Let me know if you are experiencing any problems or if the medication is still working for you. One way to tell if you have the “old” Armour or new formulation is that the old formulation had a stronger smell, whereas the new one is less pungent. If you’ve taken Armour before you will understand.

In the next installment, I’ll explain what thyroid medication I am now using, and the good news is that I am slowly getting back to my old self, and the hypo-thyroid symptoms are slowly disappearing.

Armour Thyroid Medication Reformulation Causing Some Patients Problems

http://www.hospitalsoup.com/health-conditions/thyroid/armour-thyroid-medication-reformulation-causing-some-patients-problems

Thyroid Medication Reformulation – Some Patients Report Armour Thyroid No Longer As Effective

Patients taking the thyroid medication Armour Thyroid, which is a naturally desiccated thyroid hormone drug, are reporting problems with the medication after the manufacturer, Forest Laboratories, changed some of the fillers of the medicine.

What was reportedly changed: According to Forest Labs the only thing that has changed in the new formulation of Armour is the fillers. More specifically they say that they have increased the amount of cellulose, added cornstarch and decreased the amount of dextrose in the Armour Thyroid tablets. Unfortunately, for many thyroid patients, this change has resulted in patients reporting that their hypothyroid symptoms, or problems with too little thyroid hormone, have returned when they receive their new prescriptions filled with the new formulation of Armour.

We’ll talk more about this in upcoming articles, but what was most striking maybe the fact that I cannot find any announcements to physicians, pharmacists, or even the general public from the manufacturer, Forest Labs, advising anyone that the medication was changed.

Can you imagine how it feels to be taking the very same medication you had been taking for months or years and suddenly having symptoms start returning and then calling your doctor or pharmacist and being told that “everything is the same” with your medication when it’s not?

Stay tuned as we’ll share the story of one of our readers who had that very same experience. Thyroid medication can sometimes take months to regulate, and once you are on an optimum dose it gives many patients the feeling of having their energy and sense of self back. To suddenly lose this with no warning and then perhaps worst of all to be told that it is “all in your head” when there is really something changed with your medication is not a good thing. Another reason, dear readers, to trust your judgment when it comes to your body, your medications, and how you feel. More on Armour Thyroid and our reader’s stories coming up soon.

T3 Thyroid Hormone Helps with Major Depression Treatment

Mary Shomon

http://thyroid.about.com/cs/thyroiddrugs/l/blt3depression.htm

April, 2003 — Israeli experts have found that as many as half of all patients experiencing unipolar and non-psychotic major depression do not respond to initial selective serotonin reuptake inhibitor (SSRI) antidepressant treatment. As a result, the researchers have developed a formula of progressively increased doses of prescribed antidepressant drug, usually Prozac (fluoxetine). And those who are unresponsive also receive triiodothyronine (T3), from 25 to 50 micrograms per day.

In research reported on in the International Journal of Neuropsychopharmacology, 81 patients were started on fluoxetine 20 mg; and 9 patients received paroxetine, and at four weeks, 74 completed treatment, and at that time, 44 0– or 48.9% — responded to the regimen. An additional 5 patients (16.6%) responded when the SSRI dose was raised to 40 mg two weeks. Patients who did not respond to SSRI treatment were evaluated at the onset to be far more depressed.

T3 was added, and found to be effectiver among 10 out of 16 women patients (62.5%), but was not effective in any of the 9 male patients who received it. Although values were within the normal range, patients who responded to T3 had higher serum thyroid-stimulating hormone (TSH) levels than those who did not.

The researchers speculate that the effect of T3 may be related to thyroid function even within the normal range.

Source: “Algorithm-based treatment of major depression in an outpatient clinic: clinical correlates of response to a specific serotonin reuptake inhibitor and to triiodothyronine augmentation” Int J Neuropsychopharmacology 2003;6:41-49.

Autoimmune Thyroid Disease and Depression Linked

http://thyroid.about.com/cs/depression/a/autoimmune.htm

Jun 19 2006

by Mary J. Shomon, with Dr. William Cline

In a fascinating new study coming out of Greece, researchers have found that depression can be linked to autoimmune thyroid disease. The study findings were published in the March 15 issue of BMC Psychiatry. According to the lead author, Dr. K.N. Fountoulakis, “unipolar depression might be characterized by a ‘low-thyroid function syndrome.’”

This small study involved 60 control subjects and 30 patients experiencing major depression. Among the patients with depression, 20 female and 10 male, and they ranged in age from 21 to 60.

None of the people studied had abnormal TSH levels, or abnormalities in free T3 or free T4 — they would be considered to have no evidence of thyroid disease by many physicians. Yet all of the depressive patients had significantly higher levels of one particular measure of thyroid function, kinown as thyroid binding inhibitory immunoglobulins, than the control subjects. And among the 10 out of 30 patients who had an “atypical” form of depression, all ten were found to have significantly higher levels of thyroid microsomal antibodies — a measure of autoimmune thyroid disease — than the control subjects.

This study found was that there was a relationship between good response to the treatment for depression, and the level of detectably thyroid dysfunction. Those with less thyroid dysfunction had greater likelihood of a good response to treatment for depression. Additionally, In addition, the atypical depressives – those who had significantly higher levels of thyroid microsomal antibodies — were found to be less responsive to treatment than the other people in this study.

Overall, the researchers concluded that the fact that depressed patients in this study had increased Thyroid Binding Inhibitory Immunoglobulins was suggestive of some sort underlying autoimmune process in depression, and that this is independent of the type of depression. Additionally, they found that response to treatment for depression can be predicted on the basis of certain thyroid indicators, with better responses being noted when these indices were closer to normal values.

The authors acknowledge that this study was restricted by the number of patients included as well as by limitations of the methodology employed. They considered their findings exploratory and suggest that additional studies involving more patients need to be conducted to establish what relationships might exist between various types of unipolar depression, thyroid function, and clinical outcome.

What Does This Study Potentially Tell Us?

What this study potentially tells us is there appears be a relationship between the presence of thyroid antibodies and immunological dysfunction in the thyroid that predisposes us, or perhaps even triggers, various forms of depression.

It also reinforces the fact that measure of the thyroid’s immunological factors, including thyroid antibodies, is part of a complete thyroid evaluation, and symptoms cannot be dismissed solely on the basis of normal TSH, T4 and T3 levels.

Thyroid Hormone Helps Treatment-Resistant Bipolar Depression

Kimberly Read & Marcia Purse

http://bipolar.about.com/b/2009/08/07/thyroid-hormone-helps-treatment-resistant-bipolar-depression.htm

You’ve tried 10, 12, even 14 or more medications for your bipolar depression and they just haven’t worked well enough. Well, maybe your doctor should consider adding another type of treatment altogether. The thyroid hormone triiodothyronine – better known as T3 – has been shown to be effective for treatment-resistant depression in patients with bipolar disorder.

A study published in the Journal of Affective Disorders was a chart review of about 160 patients, mostly with bipolar II disorder, who had tried an average of 14 different drugs for their depression, who were given T3 from 2002 to 2006. The results were impressive: a whopping 84% of the patients experienced improvement, and 33% full remission. Not one experienced a switch into mania. Although the doses were higher than normal for many patients, the researchers report that the medication was well-tolerated, although 16 patients (10%) dropped out because of side effects.

The authors do point out that a chart review study has its limitations, but this is still exceedingly hopeful news for those of us whose depression stubbornly hangs on.

Depression Explored, With Dr. Barry Durrant-Peatfield

http://thyroid.about.com/b/2003/11/19/depression-explored-with-dr-barry-durrant-peatfield.htm

Having just read the tragic news item from India about the depressed thyroid lady who committed suicide and preparing as I am at present a lecture about thyroid and depression, which I shall shortly give to London’s Insitute of Optimum Nutrition’s Mind Conference, I felt it might be appropriate to remind people of the strong link and frequency of depression and hypothyroidism…

Depression causes untold misery and destroys lives. Perhaps one in five people will suffer from it sometime in their lives. A huge industry has arisen around the treatment of depressive illness and psychiatrists are gainfully employed in their thousands. Whether it is more widespread than it was is perhaps difficult to answer. There are more of us to be depressed; we have more to be depressed about, and we are more likely to seek help. But there certainly seems to be more people troubled by depression and the great panoply of antidepressant medication tells its own story.

Before having a look at thyroid deficiency and its link to depression, we should learn a bit about it, and how it is caused and why. People who are depressed are sad, unmotivated most of the day and are usually worse in the morning. They sleep poorly, and wake up tired; they feel worthless, they have a poor self-image. They may eat more or less and put on or lose weight. Sir Winston Churchill used to call it his Black Dog. In his case, as with many, it was self-limiting: probably an extra cigar and brandy banished itâ?¦

There are two sorts of depression fundamentally: the exogenous kind, which is the result of circumstance, and the endogenous form, an illness from within ourselves. It is the second form we are to deal with. Maintenance of mood resides in part of the brain called the hippocampus. Here brain cells release neurotransmitter hormones, which are taken up by receptors; the amount released and the number of receptors responding, governs whether we are depressed or not.

Probably the most important of these mood neuro transmitter substances are serotonin and noradrenalin, and treatment is directed at preventing the decay of these substances at the receiving nerve endings. This is what Monoamine Oxidase Inhibitors (MAOIs) antidepressants, Tricyclic antidepressants and Selective Serotonin Reuptake Inhibitors (SSRIs) do. However, thyroid hormone deficie ncy acts on the receptor sites and hastens the recycling of these neurotransmitters at the nerve endings or reduces the amount being secreted. The result is that the neurotransmitters that are responsible for maintaining mood do not work at optimum efficiency. Depression then takes over.

It has been estimated that more than one third of people suffering from depression are hypothyroid. Some are in hospital. They receive, over long periods, antidepressants of one sort or another when actually the problem is deficiency of thyroid hormones. It is simply that no one thought of thyroid deficiency as a cause when their illness began; or the simplistic tests failed to reveal it.

Any patient suffering from depression should be routinely assessed for hypothyroidism. There should be no exceptions; half to one third will be found to be hypothyroid, and as a result of treatment, their depression will begin to lift in weeks. Conventional medicine will turn with little thought to psychotropic antidepressants. The problem with these is that they are sometimes difficult to stop taking. Of the SSRIs, Seroxat in particular has a poor reputation in this respect; Prozac has attracted unfavourable reports and moreover contains a fluoride compound. Tricyclic antidepressants (eg Tryptizol, Imipramime) often have unpleasant sedating side effects, and the MAOIs (eg Parnate, Nardil) clash with a number of drugs and foodstuffs. St John’s Wort is an altogether simpler and safer alternative.

Hypothyroidism should not be considered in isolation. It is more than likely that there are other deficiencies at work and cortisol, testosterone, oestrogen, DHEA and progesterone deficiencies should be looked for and corrected. It is now clear that nutrition plays a much greater role in mental illness than conventional medicine would have us believe.

The brain and its neurotransmitters simply don’t work properly without the proper raw materials. An obvious one is that there should be a constant, even supply, of its fuel glucose. Hypoglycaemia is certainly associated with depression. The essential amino acids must be provided for the manufacture of the protein neurotransmitters; so must essential fatty acids, especially the omega 3 group, which make up the structure of the brain and the neurones releasing the neurotransmitters. The vitamin B complex, folic acid, vitamin C are needed to allow the amino acids to form complex proteins and the other mineral micronutrients have to be there.

Get the nutrients right (also ensuring thyroid manufacture and uptake), provide thyroid supplementation if required, perhaps as naturally as possible from glandular extracts, and we can fight the black tide of mind altering drugs that threatens to overwhelm so many of us.

Kind regards,

Barry Peatfield

Hypothyroidism In Women Associated With Liver Cancer

http://www.medicalnewstoday.com/articles/148903.php

Hypothyroidism is the most common thyroid disorder among U.S. adults, affecting between 8 and 12 percent of the U.S. population, and more women than men. The condition can cause hyperlipidemia and weight gain and may play a role in the development of nonalcoholic steatohepatitis which can progress to more severe liver disease. Studies have also suggested a clinical association between hypothyroidism and hepatitis C, which is contributing to the country’s rising rate of liver cancer.

Researchers, led by Manal Hassan of Anderson Cancer Center at the University of Texas, designed a case-control study to better understand the association between hypothyroidism and the development of liver cancer, also known as hepatocellular carcinoma (HCC), in the U.S.

They included 420 patients with liver cancer and 1,104 healthy controls. From each subject, the researchers gathered demographic data and information about liver cancer risk factors, like smoking, alcohol consumption and family cancer history. The participants were also asked about their history of thyroid conditions and obesity. They provided blood samples that were tested for hepatitis B and hepatitis C.

About 15 percent of the liver cancer patients had a history of thyroid disease, compared to about 12 percent of the healthy controls. Subjects with a history of hypothyroidism had twice the risk of liver cancer; however the relationship was only significant for females.

Women who had a prior history of hypothyroidism for more than 10 years had a threefold higher risk of liver cancer compared to women without a history of thyroid disorders. Adjusting for obesity did not change the association.

“Whether and why hypothyroidism causes HCC is not clear,” the authors write. “However, the association between hypothyroidism and NASH can be explained by the underlying hyperlipidemia, decreased fatty acid oxidation insulin resistance and lipid peroxidation in patients with hypothyroidism.” And these conditions may make the patient susceptible to HCC development.

“Further studies among different populations are warranted to confirm the association between hypothyroidism and HCC and to identify the underlying biological mechanisms and the genetic predisposition factors that may contribute to susceptibility to HCC development in the presence of thyroid disorders,” the authors conclude.

Article: “Association Between Hypothyroidism and Hepatocellular Carcinoma: USA Case-Control Study.” Hassan, Manal; Kaseb, Ahmed; Li, Donghui; Patt, Yehuda; Vauthey, Jean-Nicolas; Thomas, Melanie; Curley, Steven A.; Spitz, Margaret; Sherman, Steven; Abdalla, Eddie; Davila, Marta; Lozano, Richard; Hassan, Deena; Chan, Wenyaw; Brown, Thomas; Abbruzzese, James. Hepatology; May 2009.

Source:

Sean Wagner

Wiley-Blackwell

Another Call for Early Treatment

http://www.thyroidscience.com/

A study report we published in Thyroid Science this past week is well worth announcing.[1] It stirs a hope in us—that the report will motivate more clinicians to provide subclinical hypothyroid patients with early thyroid hormone treatment. Early treatment is likely to relieve the patients’ suffering, enable them to maintain normal function, and reduce their overall costs for health care services. In addition, early treatment will—if assertively engaged in—halt incipient functional and structural abnormalities, or reverse the frank pathology that has already developed, such as the muscle abnormalities reported by the authors of the report we published this week.

Four of the researchers and authors of the report (Drs. Michael Dunn, Arthur Cosmas, Linda Lamont, and Thomas Manfredi) are from the Department of Kinesiology, University of Rhode Island. The fourth (Dr. James Hennessey) is from the Division of Endocrinology, Rhode Island Hospital, Brown University School of Medicine.

To qualify a patient to enter their study, Dunn et al. used the conventional criteria for the diagnosis of subclinical hypothyroidism, the mildest form of hypothyroidism. The criteria included an above-range TSH level and an in-range free T4 level.

Their study shows that among subclinical hypothyroid patients, muscle symptoms may be underlain by objectively verifiable structural muscle abnormalities. The study is the first to document with light and electron microscopy, pathological structural changes in the skeletal muscles of subclinical hypothyroid patients. The researchers note that their findings indicate a progression of such changes from subclinical to overt hypothyroidism.

The structural muscle pathology that Dunn et al. report is consistent with other researchers’ reports of other muscle-related abnormalities in subclinical hypothyroid patients. (To read the specific findings of Dunn et al., detailed on pages 4 through 6 of their paper,[1,pp.4-6] must be compelling to clinicians who are committed to the well-being of their patients.) Hekimsoy and Oktem,[2] for example, reported elevated creatine kinase levels in subclinical patients. The patients’ levels were not significantly elevated. Overall, however, the TSH and creatine kinase levels were positively correlated; that is, the higher the TSH levels, the higher the creatine kinase levels. Conversely, creatine kinase levels and free T3 and free T4 levels were inversely correlated; higher creatine kinase levels were associated with lower free T3 and free T4 levels.

Monzani et al. reported that during exercise, the average blood lactate level of subclinical hypothyroid patients was significantly higher than in controls “from the third exercise step onward.”[3] The researchers wrote that the patients’ mean increase of blood lactate during exercise was positively related to the duration of their subclinical hypothyroidism. “We conclude,” they wrote, “that muscle energy metabolism is impaired in [subclinical hypothyroidism] in rough proportion to the known duration of the disease.” This finding has an important practical implication: among subclinical hypothyroid patients, the energy-related biochemical abnormality of elevated blood lactate may progressively worsen when patients fail to undergo early therapy hormone therapy.

As Dunn et al. point out,[1] the muscle pathology they found is among a range of possible adverse health consequences when hypothyroid patients go untreated. They note that some of the adverse effects (“coronary heart disease, osteoporosis, atrial fibrillation, cognitive impairment, and depression”) are among the nation’s most common causes of illness, death, and diminished quality of daily life among older adults.[1,p.1]

But older adults aren’t the only people adversely affected by untreated hypothyroidism. In more than two decades of working clinically with hypothyroid patients, I’ve regularly seen subclinical hypothyroid patients—ranging in age from the teens through the fifties—in an unfortunate circumstance: their clinicians cavalierly denied them thyroid hormone therapy, preferring to wait until the patients’ subclinical condition progressed to an overt and, in some cases, disabling stage.

The delayed treatment was, to me, patently unjustified. The patients had multiple classic hypothyroid symptoms. These included different combinations of fatigue, depression, cognitive dysfunction, cold intolerance, constipation, dry skin, hair loss, exercise intolerance, and chronic muscle pain and tension. The patients also had test results consistent with hypothyroidism, such as high cholesterol and LDL levels despite wholesome diets and regular exercise. Many patients had high thyroid peroxidase and thyroglobulin antibodies. The first of these subclinical hypothyroid patients I worked with suffered from treatment-resistant myofascial pain syndromes. The patients had failed to get more than palliation, even with high-quality physical treatment.

Most of my patients—perhaps because they were younger than the more commonly afflicted older adults—responded quickly, often dramatically, to thyroid hormone therapy; they had either complete or nearly-complete recovery from their symptoms and signs. On the other hand, I observed that in general, when clinicians had allowed their patients’ hypothyroidism to progress from subclinical to overt, the patients’ health problems had become compounded and complicated. As a result, more time and greater effort were needed for them to recover their health. Observing the results of delayed treatment were troubling to witness and worse for the patients. Hence, I’m especially appreciative of the report of the muscle pathology found by Dunn et al. in that it may lead to earlier treatment for many subclinical hypothyroid patients.

The muscle pathology that Dunn et al. report add to other types of muscle abnormalities that researchers have previously reported. Together, the different research groups’ findings make clear to us ominous possibilities for subclinical hypothyroid patients whose clinicians deny them early treatment. If treatment is delayed, some of the patients are highly likely to undergo more advanced muscle pathology with associated worsening of their muscle symptoms and signs. It’s highly likely that early treatment will prevent the proliferation of muscle pathology, reverse incipient muscle abnormalities, and relieve the patients’ suffering from muscle tension, cramps, energy-deficiency contractures, and treatment-resistant myofascial pain.[10]

Early treatment for subclinical hypothyroidism will prevent clinicians from diagnosing some patients as having “fibromyalgia.” Nowadays this diagnosis leads to FDA-approved “fibromyalgia” drug therapies (Cymbalta and Lyrica) that are inappropriate, unnecessary, and “effective” only in the most liberal sense of the term. We regularly hear complaints of adverse effects from patients who have undergone treatment with the drugs. The muscle abnormalities Dunn et al. report are similar to those of patients with a diagnosis of fibromyalgia.[4,5,6,7,8] The muscle abnormalities among fibromyalgia patients, along with other similarities to hypothyroidism, led Eisinger et al. in France[7,8] and me in the U.S., separately but almost simultaneously in the early 1990s,[10,11,12] to conclude that fibromyalgia is a metabolic disorder; in most respects, it is virtually identical to hypothyroidism. The hypothyroid-like muscle abnormalities of fibromyalgia patients were among the research findings that led my colleagues and me to conclude that the main underlying mechanism of fibromyalgia is inadequate thyroid hormone regulation.[9,10] The findings of Dunn et al. add carbon to our already-steel hard conclusion about the etiology of fibromyalgia.[9,10]

When Monzani et al. reported high lactate levels in subclinical hypothyroid patients, they concluded, “Early [thyroid hormone] therapy may be useful not only to provide specific treatment for such metabolic changes, but also to avoid progression to frank hypothyroidism.” This humane proposal—early thyroid hormone treatment—is echoed by Dunn et al.[1,pp.7-8] For emphasis, I’ll quote their conclusion:

“Establishing consistent morphological markers of subclinical hypothyroidism prior to disease progression could justify an earlier, more efficacious treatment with thyroid hormone. This treatment strategy may diminish morbidity by preventing disease progression from subclinical to overt hypothyroidism. Earlier initiation of this therapy may ultimately translate into an improvement in patients’ lifestyle.”[1,pp.7-8]

References

1. Dunn, M.E., Hennessey, J.V., Cosmas, A.C., Lamont, L.S., and Manfredi, T.G.: Clinical Case Report: Ultrastructural Evidence of Skeletal Muscle Mitochondrial Dysfunction in Patients With Subclinical Hypothyroidism. Thyroid Science, 4(6):CLS1-8, 2009.

2. Hekimsoy, Z. And Oktem, I.K.: Serum creatine kinase levels in overt and subclinical hypothyroidism. Endocr. Res., 2005;31(3):171-175, 2005.

3. Monzani, F.,Caraccio, N., Siciliano, G., et al.: Clinical and biochemical features of muscle dysfunction in subclinical hypothyroidism. J. Clin. Endocrinol. Metab., 82(10):3315-3318, 1997.

4. Kalyan-Raman, U.P., Kalyan-Raman, K., Yunus, M.B. and Masi, A.T.: Muscle pathology in primary fibromyalgia syndrome: a light microscopic, histological and ultrastructural study. J. Rheumatol., 11:808-813, 1984.

5. Awad, E.A.: Pathological changes in fibromyalgia. First International Symposium on Myofascial Pain and Fibromyalgia. Minneapolis, Minnesota, May 9, 1989.

6. Awad, E.A.: Histopathological changes in fibrositis. In Advances in Pain Research and Therapy, Vol.17. Edited by J.R. Fricton and E.A. Awad, New York, Raven Press, Ltd., 1990, pp.249-258.
7. Eisinger, J., Plantamura, A., and Ayavou, T.: Glycolysis abnormalities in fibromyalgia. J. Am. Coll. Nutr., 13:144-148, 1994.

8. Eisinger, J., Clairet, D., Zakarian, H., and Ayavou, T.: ATP érythrocytaire et apparel locomoteur: action de la calcitonine. Lyon Méditerranée Med., 26:326-328, 1990.

9. Lowe, J.C.: The Metabolic Treatment of Fibromyalgia. Boulder, McDowell Publishing Co., 2000.

10. Lowe, J.C. and Yellin, J.: Inadequate Thyroid Hormone Regulation as the Main Mechanism of Fibromyalgia: A Review of the Evidence. Thyroid Science, 3(6):R1-14, 2008.

11. Lowe, J.C.: Improvement in euthyroid fibromyalgia patients treated with T3 (tri-iodothyronine). J. Myofasc. Ther., 1(2):16-29, 1994.

12. Lowe, J.C.: T3-induced recovery from fibromyalgia by a hypothyroid patient resistant to T4 and desiccated thyroid. J. Myofasc. Ther., 1(4):21-30, 1995.

Are You Pregnant and Suffering from Depression?

http://www.mentalpro.com/2009/07/are-you-pregnant-and-suffering-from.html

Thyroid testing identifies the levels of several hormones, including T4 and T3, which are the most active of the thyroid hormones; and thyroid-stimulating hormone, produced by the pituitary gland that controls the production and secretion of thyroxine. When T3 and T4 levels rise, the pituitary secretes less TSH, which causes production ofT3 and T4 to decline, restoring balance. If T3 and T4 levels fall, secretion of TSH again increases, which boosts production ofT3 and T4.

Testing for T3, T4, and TSH levels is a good start if you have symptoms of hypo- or hyperthyroidism, but because the normal range for these blood tests is wide, it’s possible to have thyroid dysfunction with so-called normal test results. Measurement of thyroid antibodies can provide additional information about the risk of depression and treatment prognosis. One report, for example, found that women with high levels of antithyroid peroxidase (anti-TPO) antibodies are more likely to become depressed than those without these antibodies. A subsequent study concluded that testing for antibody levels “seems necessary,” especially in the elderly and in individuals who do not respond to depression treatment

While women are more likely to have thyroid hormone imbalance (especially hypothyroidism) than men are, a subgroup of women are at particular risk. Up to 10 percent of new mothers develop postpartum thyroiditis, chronic inflammation of the thyroid gland, and concurrent depression. This condition can be diagnosed with tests that check for antibodies against the thyroid. Research has shown that up to 50 percent of women who have high levels of thyroid antibodies during their first trimester develop postpartum thyroiditis and are subsequently at risk for postpartum depression. These women may be iodine-insufficient and will probably respond to iodine supplementation. Women who are significantly iodine insufficient and then become pregnant will become much more insufficient, because iodine is preferentially transported to the fetus. As the woman becomes more insufficient, she is likely to develop anti thyroid antibodies, and after delivery is more likely to develop postpartum depression.

In recent years, studies of depression have shown that some people who take antidepressants respond better if they also take T3. In one particular study of patients who had hypothyroidism, those who took a combination ofT3 and T4 had better results in regard to mental and emotional symptoms than those who took T4 alone. Unfortunately, most patients with hypothyroidism who are treated conventionally usually take only T4. Occasionally patients are given T3 (as the medication Cytomel), which must be taken several times a day and can cause mood and energy swings. To prevent these problems, a physician could prescribe long-acting T3, which is available from compounding pharmacies. Today, however, I would certainly try therapeutic doses of iodine before prescribing long-acting T3.