Re: Thyroid Treatment of FM/ Long

January 12, 2004

I have been diagnosed with Hypothyroidism. Seeing my doctor tomorrow to see what he is going to do about it. I am really hoping a pill is required and then I can finally look for a job again.

Thyroid Treatment of FM/ Long

Hi all:Here's an explanation of the treatment I'm on and a link to my doctor's website. In case link doesn't work, I posted article below.http://www.integrativecarecenters.com/index2.htmThyroid Regulation and Fibromyalgia Berndtson, MDEvolving Medical Perspectives on HypothyroidismHistorians note a recurring phenomenon in the evolution of human ideas over the centuries. When an established, mainstream way of thinking is challenged by a new and different way of thinking, the mainstream often responds with "that's absurd." If the new way of thinking picks up steam, the mainstream changes its opinion to, "okay, it's not absurd, but it's not that relevant." Finally, when the new way of thinking has picked up enough converts to make it more than relevant, the mainstream declares, "we thought of it first." This sets the stage for an ongoing battle of ideas concerning the diagnosis and treatment of hypothyroidism, and a gathering medical debate that revolves around the following questions: What are the subtle mechanisms by which abnormal thyroid hormone system regulation slows down metabolism? What roles might these mechanisms play in chronic illnesses? How should we sort those who suffer from subtle forms of abnormal thyroid regulation? How should we treat subtle forms of hypothyroidism? While there is little room for disagreement about the basic mechanisms that produce primary or central hypothyroidism, there are differing opinions about the best ways to treat them, even within mainstream practice.1,2 The true paradigm-shifting potential of the debate has to do with how we should identify and manage something referred to as "partial peripheral cellular resistance to thyroid hormone" (referred to hereafter in this paper as "thyroid resistance syndrome"). Forcing this debate with mainstream thinkers is a new wave of integrative medicine clinicians and researchers, led by Lowe and his team, whose book, The Metabolic Treatment of Fibromyalgia, is changing the way patients and physicians think about the thyroid hormone system, and about metabolic health.3Based on their clinical research and practice experience, Lowe and colleagues contend:An estimated 90% of patients with fibromyalgia suffer from one form or another of abnormal thyroid hormone system regulation. Up to one-third of these patients appear to have some form of thyroid resistance syndrome.4, 3 (p. 295-338)Most of these patients are affected by one or more of the following additional metabolism-slowing factors: Poor diet (one that produces glucose-insulin imbalance, fatty acid imbalance, excess oxidative stress, etc.) Nutritional deficiencies Low physical fitness Adrenal and sex hormone imbalances Use of drugs that also impair metabolism To fully recover, these patients must be treated with the proper dose and form of thyroid hormone, but they must also control any other factors adding to the slowing of their metabolism. Thyroid hormone alone, even a proper form and dose, will not work if other metabolism-slowing factors are left unaddressed.Thyroid blood tests do not accurately identify patients who have thyroid resistance syndrome. In addition, in patients with a thyroid resistance syndrome, thyroid blood tests are of little use in monitoring the full range of metabolic responses to thyroid hormone therapy.In patients with thyroid resistance, levothyroxine (T4) therapy alone is not as effective as triiodothyronine (T3) therapy alone. In primary or central hypothyroidism, T4 therapy is not as effective as T3-T4 combination therapy.Current mainstream practice guidelines on the diagnosis, treatment, and monitoring of clinical hypothyroidism are short-sighted; they steer physicians away from the diagnosis and management of thyroid resistance syndrome, and from the use of T3, or combination T3-T4 therapies in cases of c One response from mainstream thinkers is that the symptoms of hypothyroidism are non-specific, and should therefore not be treated as clinical hypothyroidism unless blood tests establish the diagnosis of hypothyroidism. As Lowe makes clear, this claim rests on the shaky assumption that current laboratory evaluations of clinical hypothyroidism do an adequate job of sorting those who have thyroid-related metabolic slowing from those who do not.3 (p. 993-994)Mainstream thinkers also invoke a precautionary principle, claiming that treating patients with T3, or with any form thyroid hormone when blood tests are normal, may cause osteoporosis, adrenal crisis, atrial fibrillation, and heart attack. Lowe's review of the literature pertaining to these risks shows:scant support for the claim that T3, or T3-T4 therapy causes osteoporosis (there is a stronger claim that using these therapies in patients with thyroid-related slowing of metabolism improves bone density).3 (p. 866-875) reports of adrenal crisis related to T3 therapy are exceedingly rare, and preventable with careful baseline evaluation and monitoring5 (p.173-174) reports of atrial fibrillation or heart attack related to the use of T3 therapy involved only debilitated, elderly patients; there is no evidence for these risks in patients of middle age or younger who have appropriate baseline evaluation and monitoring.3 (p.875-880) Mainstream medicine prides itself on taking a rigorously scientific and logical approach to medical care. Recently, the American Association of Clinical Endocrinologists (AACE), published its clinical practice guidelines for the diagnosis and management of hypothyroidism.6 Concerning diagnosis, the guidelines state that "A TSH assay should always be used as the primary test to establish the diagnosis of primary hypothyroidism.6 (p. 463-4) On the treatment and management of clinical hypothyroidism, the guidelines state that "…all physicians will treat clinical hypothyroidism with levothyroxine [T4] replacement therapy."6 (p. 464).Regarding recent interest in the use of T3-containing preparations to treat clinical hypothyroidism:Recent studies have shown a resurgence of interest in the possible benefits of treatment of hypothyroidism with combinations of T4 and T3 or with natural thyroid preparations. The small-scale study that seems to have sparked this interest treated patients for only 5 weeks, focused on mood changes, used a T4 plus T3 combination that differs substantially from that found in natural thyroid products, and have found a benefit in only a subset of patients, and has not been replicated.36,37[36=reference #2 in this paper] Insufficient evidence is available to know which patients with hypothyroidism, if any, would be better treated with a combination of T4 plus T3 rather than T4 alone6 (p. 464).The AACE's advice reads more like a dogmatic edict than a set of guidelines for clinicians. A mere paragraph is devoted to the possible role for T3-containing preparations in treating clinical hypothyroidism, and that paragraph appears to be included for the sole purpose of brushing off the idea that T3 has any useful role to play. There is not so much as a word about thyroid resistance syndrome, let alone an analysis of clinical studies on the subject. Clinical practice guidelines presented by medical professional groups in a position of authority have a responsibility to those physicians and patients who stand to be influenced by them. For patients with symptoms of clinical hypothyroidism, but whose blood tests are within the normal range, or for those patients with symptoms of clinical hypothyroidism who fail to respond fully to T4 therapy alone, there is a great deal at stake. For physicians in the trenches who are called upon to evaluate and manage such patients, nothing less than the trustworthiness of their professionalism is at stake. To take full advantage of the scientific information that is available, physicians and patients looking for guidance on the diagnosis and treatment of clinical hypothyroidism will have to dig deeper than the AACE guidelines.The Effects of Thyroid Hormone on Cell Structure and FunctionThe effects of thyroid hormone on cell metabolism are sweeping and profound. Thyroid hormone regulates protein interactions within the cytoplasm of the cell, and gene expression by the nucleus of the cell. Thyroid hormone's interactions with cytoplasmic proteins influence the function of cell membranes, the synthesis and breakdown of proteins, and the production, storage, and consumption of energy, including the burning of fats and carbohydrates.7 In the nucleus of the cell, T3 binding to T3 receptors alters gene expression in a range of DNA sequences referred to as thyroid response elements.8 The activation of nuclear T3 receptors controls the expression of genes that influence central and peripheral activity of norepinephrine, dopamine, serotonin, growth hormone, corticotrophin releasing hormone, and other key regulators of energy, mood and metabolism.9Unlike steroid hormones, thyroid hormones pass freely through cell membranes without need for specialized transport mechanisms. Thyroid hormone is also unusual among the body's hormones in that it regulates both catabolic (breakdown) and anabolic (restoration) pathways.Categories of Abnormal Thyroid Regulation Primary and Central HypothyroidismPrimary hypothyroidism occurs when the thyroid gland does not make enough thyroid hormone. Central hypothyroidism occurs when the hypothalamus fails to sufficiently stimulate the pituitary gland, or when the pituitary gland fails to sufficiently stimulate the thyroid gland. Both forms result in decreased availability of thyroid hormone. Lowe and colleagues conclude that roughly 50 to 60% of fibromyalgia patients suffer from primary or central hypothyroidism.10 They also find that the use of T4 alone to treat these forms of clinical hypothyroidism is a fatally flawed approach to correcting the abnormal thyroid hormone regulation found in these conditions.5 (p. 311) Thyroid Resistance SyndromeHormone resistance syndromes generally refer to conditions caused by abnormal interactions between a hormone and its receptors.8 According to Lowe, who has written the most comprehensive review ever published on the subject of thyroid resistance, syndromes of partial peripheral cellular resistance to thyroid hormone may be common, occurring in roughly 30 to 40% of patients with fibromyalgia, and perhaps responsible for metabolic slowing in a variety of other chronic illnesses.3 (p. 295-338) In addition, the mechanisms capable of causing thyroid resistance can involve factors other than abnormal hormone-receptor interactions.Potential Causes of Thyroid Resistance SyndromeThere are many potential points in the cellular metabolism of the body's various tissues where thyroid system regulation can go wrong. Proposed mechanisms for causing thyroid resistance syndrome include:>Mutations in the â thyroid receptor gene, causing mutant T3 nuclear or cellular receptors which abnormally bind thyroid hormone, resulting in a decreased thyroid signal.8 Increased rate of T3 efflux from cells.11 Abnormal DNA sequences in thyroid hormone response elements.12 Decreased ability of thyroid hormone to control nitric oxide release by endothelial cells.13 Undetermined abnormal cofactors in thyroid metabolism.14 Defective transport of T4 across cell membranes.15 Defects in the conversion of T4 to T3.16 Antibodies against circulating thyroid hormone.17 Cytomegalovirus infection.8 Mercury, PCB, dioxin, and other potential heavy metal and chemical contaminants interfering with thyroid system metabolism.3 (p. 226-232; ) Current research into the molecular biology of thyroid function suggests that most of the defective mechanisms capable of causing thyroid resistance syndrome take place at the level of intracellular thyroid receptors, or in the pathways activated when thyroid hormone binds to these receptors.18 There may also be factors causing thyroid hormone's blocked access to endothelial cell mediators. This could occur when stealth infections (such as cytomegalovirus) upregulate immune system function, in turn triggering a cascade of coagulation proteins that in some people results in a hypercoagulable state.19,20Abnormal Thyroid Regulation and FibromyalgiaLowe interprets the symptoms of fibromyalgia as manifestations of abnormal thyroid hormone regulation.3 (p.341-768) In their program, 50 to 60% of fibromyalgia patients have primary or central hypothyroidism, and their treatment plan includes T3-T4 combination therapy, along with a carefully monitored effort to control symptoms by addressing any additional metabolism-slowing factors that apply to a given patient. The metabolic rehabilitation factors included by Lowe and colleagues are poor diet, nutritional deficiencies, low physical fitness, adrenal or sex hormone imbalances, and the use of drugs that impair metabolism. This is not an exclusive list of factors potentially critical to successful metabolic rehabilitation. Other potential obstacles to metabolic rehabilitation include hypercoagulation (and protein accumulation), poor sleep, poor stress management, lack of appropriate physical therapy, and problems with digestion and assimilation, chemical or heavy metal contamination, or detoxification. Any of these problems, left unaddressed, could cause appropriate thyroid hormone therapy to fail. A case series performed at Integrative Care Centers indicates that hypercoagulation and protein accumulation is another factor worthy of attention in patients with fibromyalgia.21 In this series, anti-coagulants or enzymes are thought to have induced improvements in microcirculatory flow in the blood and lymphatics of patients with fibromyalgia, resulting in decreased pain and increased energy in nearly two-thirds of patients. It is possible that the reduced pain and increased energy reported by fibromyalgia patients using enzymes were in part produced by enhanced thyroid regulation of endothelial cell function, given the link between thyroid and endothelial cell nitric oxide release.13 Clearing fibrin and protein debris from endothelial cell membranes could enhance thyroid hormone's ability to regulate nitric oxide release, improving microcirculatory dynamics, thereby enhancing downstream tissue responsiveness to thyroid hormone.The bottom line for fibromyalgia patients is this: correcting thyroid regulation and taking active steps to remove existing obstacles to metabolic rehabilitation currently has an estimated 80 to 90% success rate for obtaining a nearly full health recovery. The paradigm for diagnosing and treating abnormal thyroid regulation is changing.22Detecting and Treating Abnormal Thyroid Regulation in FibromyalgiaThe clinical thyroid protocol outlined by Lowe and colleagues5 serves as a reasonable starting point for fibromyalgia evaluation and treatment. Added to the thyroid protocol must be a systematic effort to identify and graph therapeutic responses to a patient's most debilitating symptoms, as well as an action plan for addressing any co-existing obstacles to re-establishing metabolic balance.Baseline studies include a thyroid hormone profile (at a minimum including TSH, free T4, and free T3,) and screening for evidence of a hypercoagulable state. Baseline labs may also include assessments of adrenal and sex hormone function, as well as any other tests that could shed light on the presence of co-existing obstacles to recovery. Baseline bone density and electrocardiogram tests may also be considered.If evidence for primary or central hypothyroidism is found, thyroid treatment will begin with a T3-T4 combination, with dose increases every two weeks correlated with self-monitoring of symptom changes (on a 10-point scale), using a connect-the-dots line graph for each symptom over time. If thyroid resistance is suspected, thyroid treatment will begin with a T3 preparation, with dose increases every week, again, correlated with a symptom graph. Thyroid hormone therapy will be combined with additional clinical support for co-existing metabolic imbalances, and must be combined with aggressive lifestyle changes and self-care where needed.Symptoms common to hypothyroidism and fibromyalgia include low energy, widespread aches and pains, depressed mood, decreased ability to concentrate, puffiness, constipation, cold intolerance, poor sleep, low exercise tolerance, and difficulty getting going in the morning. Other symptoms, such as difficulty losing weight, heightened susceptibility to infection, menstrual cycle abnormalities, low body temperature, indigestion, and irritable bowel may also be present in patients with either diagnosis. Physical signs of hypothyroidism include a delayed Achilles tendon relaxation phase, dry or yellowish skin, low basal body temperature, and high cholesterol. Symptoms of excess thyroid hormone also need to be monitored. They include jitteriness, racing pulse, irritability, difficulty sleeping, chest pain, heat intolerance, frequent loose stools, and decreased appetite.Factors Affecting the Response to Thyroid Hormone SupplementationLow levels of adrenal function, as reflected by a low serum DHEA-S level, or low adrenal reserves (as assessed by an ACTH stimulation test), may further aggravate low levels of thyroid function, as well as interfere with a successful response to thyroid treatment.24 For this reason, we will often evaluate adrenal status when considering an empirical trial of thyroid supplementation. Low thyroid patients may also have low estrogen, progesterone, and testosterone activity in the body. T3 is thought to help stimulate the liver's production of the proteins that carry these sex hormones to the cells of the body.24 Monitoring and balancing thyroid, adrenal, and reproductive hormones as a group is often required for an empirical trial process to succeed in restoring health.Iron and calcium can block the absorption of thyroid hormone. Soy protein may interfere with thyroid metabolism, so limit your intake if this is a concern. It is best to take your thyroid supplement on an empty stomach with water, thirty minutes before a meal or taking vitamin supplements. Most patients keep their thyroid supplements in the bathroom and take it just after they get out of bed. That way, by the time you hit the kitchen, it's absorbed. To exert its many effects on human metabolism, thyroid hormone relies on enzyme pathways that, in turn, rely upon several key vitamins, minerals, and micronutrients. These include thiamine (B1), riboflavin (B2), niacin (B3), biotin, pantothenic acid (B5), pyridoxine (B6), cobalamin (B12), folic acid, magnesium, zinc, selenium, manganese, alpha lipoic acid, malic acid, essential fatty acids, and coenzyme-Q-10. The use of nutritional supplements can help maximize the efficiency thyroid hormone activity. Supplementation of your diet with these, or other important nutritional co-factors is typically part of an overall treatment plan.Use of certain medications, especially those that stimulate norepinephrine or endorphin pathways, may interfere with a normal response to thyroid hormone.5 (p. 312-318) Appropriate physical therapy and chiropractic treatments are also critical to the success of a metabolic rehabilitation effort.5 (275-286) Incomplete digestion, intestinal hyperpermeability, gut-derived toxicity and immune system overactivation, chemical or heavy metal contamination, and sluggish detoxification may also block metabolic rehabilitation efforts.The safety and effectiveness of the clinical thyroid protocol largely depends on accurate dosing and careful monitoring, including use of symptom graphs to document improvement and to minimize the risk of thyrotoxicity. At Integrative Care Centers, you can trust that detecting and effectively treating subtle forms of hypothyroidism is a high priority. ReferencesToft AD. T3/T4 combination therapy. Endocrine Abstract 2002; 3(S40).Bunevicius R, Kazanavicius G, Zalinkevicius R, Prange AJ. Effects of thyroxine as compared with thyroxine plus triiodothyronine in patients with hypothyroidism. New England Journal of Medicine 1999;340(6):424-29.Lowe JC. The Metabolic Treatment of Fibromyalgia. Boulder:McDowell, 2000.Lowe JC. Garrison RL, Reichman AJ, Yellin J. Effectiveness and safety of T3 therapy for euthyroid fibromyalgia: a double-bline placebo-controlled response-driven crossover study. Clinical Bulletin of Myofascial Therapy 1997; (2(2/3):31-58.Honeyman-Lowe G, Lowe JC. Your Guide to Metabolic Health, Boulder:McDowell, 2003.AACE Thyroid Task Force. American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Endocrine Practice 2002; 8(6):457-467. PJ. Cellular actions of thyroid hormone. In Werner and Ingbar's The Thyroid: a Fundamental and Clinical Text, 6th edition. Edited by LE Braverman and RD Utiger, New York:JB Lippincott, 1991, p.190-203.Refetoff S, Weiss RE, Usala SJ. The syndromes of resistance to thyroid hormones. Endocrinological Reviews 1993; 14(3):348-399.Oppenheimer JH. The nuclear receptor-triiodothyronine complex: relationship to thyroid hormone distribution, metabolism, and biological action. In Molecular Basis of Thyroid Hormone Action. Edited by JK Oppenheimer and HH s, New York:Academic Press, 1983, p.1-35.Lowe JC. Thyroid status of 38 fibromyalgia patients: implications for the etiology of fibromyalgia. Clinical Bulletin of Myofascial Therapy 1997; 2(1):47-64.Ribeiro RCJ et al. Thyroid hormone export regulates cellular hormone content and response. Journal of Biological Chemistry 1996; 271(29):17147-17151.Ikeda M, Wilcox EC, Chin WW. Different DNA elements can modulate the conformation of thyroid hormone receptor heterodimer and its transcriptional activity. Journal of Biological Chemistry 1996; 271(38):23096-23104.Taddei S et al. Impaired endothelium-dependent vasodilatation in subclinical hypothyroidism: beneficial effect of levothyroxine therapy. Journal of Clinical and Endocrinological Metabolism 2003; 88(8):3731-3737.Weiss RE et al. Dominant inheritance of resistance to thyroid hormone not linked to defects in the á or â thyroid hormone receptor genes may be due to a defective cofactor. Journal of Clinical Endocrinology and Metabolism 1996; 81(12):3239-3245. Wortsman J, et al. Familial resistance to thyroid hormone associated with decreased transport across the plasma membrane. ls of Internal Medicine 1983; 98:904-909.Schimmel M, Utiger RD. Thyroidal and peripheral production of thyroid hormones. ls of Internal Medicine 1977; 87:760-768.Ginsberg J et al. Inappropriate T3 and T4 radioimmunoassay levels secondary to circulating thyroid hormone autoantibodies. Clinical Endocrinology 1978; 8:133-139.Yen PM. Molecular basis of resistance to thyroid syndrome. Trends in endocrinology and metabolism 2003(Sept); 14(7):327-333.Sutherland MR et al. Coagulation initiated by herpes viruses. Proceedings of the National Academy of Sciences 1997; 94(25):13510-13514.Berndtson K. Hypercoagulation, protein accumulation, and fibromyalgia. Unpublished analysis. Integrative Care Centers, 2003. <www.integrativecarecenters.com>Berndtson K. Results of heparin self-injection, and of oral fibrinolytic and proteolytic enzyme therapy in fibromyalgia. Unpublished case series. Integrative Care Centers, 2003. <www.integrativecarecenters.com>Garrison RL, Breeding PC. A metabolic basis for fibromyalgia and its related disorders: the possible role of resistance to thyroid hormone. Medical Hypotheses 2003; 61(12):182-189.Simoncini T et al. Dehydroepiandrosterone modulates endolthelial nitric oxide synthesis via direct genomic and nongenomic mechanisms. Endocrinology 2003; 144(8):3449-3455.Sarne DH, Refetoff S, Rosenfeld RL, Farriaux JP. Sex hormone-binding globulin in the diagnosis of peripheral tissue resistance to thyroid hormone: the value of changes after short-term triiodothyronine administration. Journal of Clinical Endocrinology and Metabolism 1988; 66:740-6 Copyright © 2003 Integrative Care Centers

January 13, 2004

Just keep in mind, unless your doctor is willing to give you more thyroid t=

han a test

says you should, your FM won't be treated properly. I would print out the t=

hyroid

article and take with to the Dr.

-- In Fibromyalgia_Support_Group , " Nor " <dolphinlady58@c...=

>

wrote:

> I have been diagnosed with Hypothyroidism. Seeing my doctor tomorrow to =

see

what he is going to do about it. I am really hoping a pill is required and =

then I can

finally look for a job again.

> Thyroid Treatment of FM/ Long

>

> Hi all:

>

> Here's an explanation of the treatment I'm on and a link to my

> doctor's website. In case link doesn't work, I posted article below.

>

> http://www.integrativecarecenters.com/index2.htm

>

> Thyroid Regulation and Fibromyalgia

> Berndtson, MD

>

> Evolving Medical Perspectives on Hypothyroidism

>

> Historians note a recurring phenomenon in the evolution of human

> ideas over the centuries. When an established, mainstream way of

> thinking is challenged by a new and different way of thinking, the

> mainstream often responds with " that's absurd. " If the new way of

> thinking picks up steam, the mainstream changes its opinion

> to, " okay, it's not absurd, but it's not that relevant. " Finally,

> when the new way of thinking has picked up enough converts to make it

> more than relevant, the mainstream declares, " we thought of it

> first. "

>

> This sets the stage for an ongoing battle of ideas concerning the

> diagnosis and treatment of hypothyroidism, and a gathering medical

> debate that revolves around the following questions:

>

> What are the subtle mechanisms by which abnormal thyroid hormone

> system regulation slows down metabolism?

> What roles might these mechanisms play in chronic illnesses?

> How should we sort those who suffer from subtle forms of abnormal

> thyroid regulation?

> How should we treat subtle forms of hypothyroidism?

> While there is little room for disagreement about the basic

> mechanisms that produce primary or central hypothyroidism, there are

> differing opinions about the best ways to treat them, even within

> mainstream practice.1,2 The true paradigm-shifting potential of the

> debate has to do with how we should identify and manage something

> referred to as " partial peripheral cellular resistance to thyroid

> hormone " (referred to hereafter in this paper as " thyroid resistance

> syndrome " ). Forcing this debate with mainstream thinkers is a new

> wave of integrative medicine clinicians and researchers, led by

> Lowe and his team, whose book, The Metabolic Treatment of

> Fibromyalgia, is changing the way patients and physicians think about

> the thyroid hormone system, and about metabolic health.3

>

> Based on their clinical research and practice experience, Lowe and

> colleagues contend:

>

> An estimated 90% of patients with fibromyalgia suffer from one form

> or another of abnormal thyroid hormone system regulation. Up to one-

> third of these patients appear to have some form of thyroid

> resistance syndrome.4, 3 (p. 295-338)

>

> Most of these patients are affected by one or more of the following

> additional metabolism-slowing factors:

> Poor diet (one that produces glucose-insulin imbalance, fatty acid

> imbalance, excess oxidative stress, etc.)

> Nutritional deficiencies

> Low physical fitness

> Adrenal and sex hormone imbalances

> Use of drugs that also impair metabolism

> To fully recover, these patients must be treated with the proper dose

> and form of thyroid hormone, but they must also control any other

> factors adding to the slowing of their metabolism. Thyroid hormone

> alone, even a proper form and dose, will not work if other metabolism-

> slowing factors are left unaddressed.

>

> Thyroid blood tests do not accurately identify patients who have

> thyroid resistance syndrome. In addition, in patients with a thyroid

> resistance syndrome, thyroid blood tests are of little use in

> monitoring the full range of metabolic responses to thyroid hormone

> therapy.

>

> In patients with thyroid resistance, levothyroxine (T4) therapy alone

> is not as effective as triiodothyronine (T3) therapy alone. In

> primary or central hypothyroidism, T4 therapy is not as effective as

> T3-T4 combination therapy.

>

> Current mainstream practice guidelines on the diagnosis, treatment,

> and monitoring of clinical hypothyroidism are short-

> sighted; they steer physicians away from the diagnosis and management

> of thyroid resistance syndrome, and from the use of T3, or

> combination T3-T4 therapies in cases of c

> One response from mainstream thinkers is that the symptoms of

> hypothyroidism are non-specific, and should therefore not be treated

> as clinical hypothyroidism unless blood tests establish the diagnosis

> of hypothyroidism. As Lowe makes clear, this claim rests on the

> shaky assumption that current laboratory evaluations of clinical

> hypothyroidism do an adequate job of sorting those who have thyroid-

> related metabolic slowing from those who do not.3 (p. 993-994)

>

> Mainstream thinkers also invoke a precautionary principle, claiming

> that treating patients with T3, or with any form thyroid hormone when

> blood tests are normal, may cause osteoporosis, adrenal crisis,

> atrial fibrillation, and heart attack. Lowe's review of the

> literature pertaining to these risks shows:

>

> scant support for the claim that T3, or T3-T4 therapy causes

> osteoporosis (there is a stronger claim that using these therapies in

> patients with thyroid-related slowing of metabolism improves bone

> density).3 (p. 866-875)

> reports of adrenal crisis related to T3 therapy are exceedingly rare,

> and preventable with careful baseline evaluation and monitoring5

> (p.173-174)

> reports of atrial fibrillation or heart attack related to the use of

> T3 therapy involved only debilitated, elderly patients; there is no

> evidence for these risks in patients of middle age or younger who

> have appropriate baseline evaluation and monitoring.3 (p.875-880)

> Mainstream medicine prides itself on taking a rigorously scientific

> and logical approach to medical care. Recently, the American

> Association of Clinical Endocrinologists (AACE), published its

> clinical practice guidelines for the diagnosis and management of

> hypothyroidism.6 Concerning diagnosis, the guidelines state that " A

> TSH assay should always be used as the primary test to establish the

> diagnosis of primary hypothyroidism.6 (p. 463-4) On the treatment

> and management of clinical hypothyroidism, the guidelines state

> that " .all physicians will treat clinical hypothyroidism with

> levothyroxine [T4] replacement therapy. " 6 (p. 464).

>

> Regarding recent interest in the use of T3-containing preparations to

> treat clinical hypothyroidism:

>

> Recent studies have shown a resurgence of interest in the possible

> benefits of treatment of hypothyroidism with combinations of T4 and

> T3 or with natural thyroid preparations. The small-scale study that

> seems to have sparked this interest treated patients for only 5

> weeks, focused on mood changes, used a T4 plus T3 combination that

> differs substantially from that found in natural thyroid products,

> and have found a benefit in only a subset of patients, and has not

> been replicated.36,37[36=reference #2 in this paper] Insufficient

> evidence is available to know which patients with hypothyroidism, if

> any, would be better treated with a combination of T4 plus T3 rather

> than T4 alone6 (p. 464).

>

> The AACE's advice reads more like a dogmatic edict than a set of

> guidelines for clinicians. A mere paragraph is devoted to the

> possible role for T3-containing preparations in treating clinical

> hypothyroidism, and that paragraph appears to be included for the

> sole purpose of brushing off the idea that T3 has any useful role to

> play. There is not so much as a word about thyroid resistance

> syndrome, let alone an analysis of clinical studies on the subject.

>

> Clinical practice guidelines presented by medical professional groups

> in a position of authority have a responsibility to those physicians

> and patients who stand to be influenced by them. For patients with

> symptoms of clinical hypothyroidism, but whose blood tests are within

> the normal range, or for those patients with symptoms of clinical

> hypothyroidism who fail to respond fully to T4 therapy alone, there

> is a great deal at stake. For physicians in the trenches who are

> called upon to evaluate and manage such patients, nothing less than

> the trustworthiness of their professionalism is at stake. To take

> full advantage of the scientific information that is available,

> physicians and patients looking for guidance on the diagnosis and

> treatment of clinical hypothyroidism will have to dig deeper than the

> AACE guidelines.

>

> The Effects of Thyroid Hormone on Cell Structure and Function

>

> The effects of thyroid hormone on cell metabolism are sweeping and

> profound. Thyroid hormone regulates protein interactions within the

> cytoplasm of the cell, and gene expression by the nucleus of the

> cell. Thyroid hormone's interactions with cytoplasmic proteins

> influence the function of cell membranes, the synthesis and breakdown

> of proteins, and the production, storage, and consumption of energy,

> including the burning of fats and carbohydrates.7

>

> In the nucleus of the cell, T3 binding to T3 receptors alters gene

> expression in a range of DNA sequences referred to as thyroid

> response elements.8 The activation of nuclear T3 receptors controls

> the expression of genes that influence central and peripheral

> activity of norepinephrine, dopamine, serotonin, growth hormone,

> corticotrophin releasing hormone, and other key regulators of energy,

> mood and metabolism.9

>

> Unlike steroid hormones, thyroid hormones pass freely through cell

> membranes without need for specialized transport mechanisms. Thyroid

> hormone is also unusual among the body's hormones in that it

> regulates both catabolic (breakdown) and anabolic (restoration)

> pathways.

>

> Categories of Abnormal Thyroid Regulation

>

> Primary and Central Hypothyroidism

>

> Primary hypothyroidism occurs when the thyroid gland does not make

> enough thyroid hormone. Central hypothyroidism occurs when the

> hypothalamus fails to sufficiently stimulate the pituitary gland, or

> when the pituitary gland fails to sufficiently stimulate the thyroid

> gland. Both forms result in decreased availability of thyroid

> hormone. Lowe and colleagues conclude that roughly 50 to 60% of

> fibromyalgia patients suffer from primary or central

> hypothyroidism.10 They also find that the use of T4 alone to treat

> these forms of clinical hypothyroidism is a fatally flawed approach

> to correcting the abnormal thyroid hormone regulation found in these

> conditions.5 (p. 311)

>

> Thyroid Resistance Syndrome

>

> Hormone resistance syndromes generally refer to conditions caused by

> abnormal interactions between a hormone and its receptors.8

> According to Lowe, who has written the most comprehensive review ever

> published on the subject of thyroid resistance, syndromes of partial

> peripheral cellular resistance to thyroid hormone may be common,

> occurring in roughly 30 to 40% of patients with fibromyalgia, and

> perhaps responsible for metabolic slowing in a variety of other

> chronic illnesses.3 (p. 295-338) In addition, the mechanisms capable

> of causing thyroid resistance can involve factors other than abnormal

> hormone-receptor interactions.

>

> Potential Causes of Thyroid Resistance Syndrome

>

> There are many potential points in the cellular metabolism of the

> body's various tissues where thyroid system regulation can go wrong.

> Proposed mechanisms for causing thyroid resistance syndrome include:

>

> >Mutations in the â thyroid receptor gene, causing mutant T3 nuclear

> or cellular receptors which abnormally bind thyroid hormone,

> resulting in a decreased thyroid signal.8

> Increased rate of T3 efflux from cells.11

> Abnormal DNA sequences in thyroid hormone response elements.12

> Decreased ability of thyroid hormone to control nitric oxide release

> by endothelial cells.13

> Undetermined abnormal cofactors in thyroid metabolism.14

> Defective transport of T4 across cell membranes.15

> Defects in the conversion of T4 to T3.16

> Antibodies against circulating thyroid hormone.17

> Cytomegalovirus infection.8

> Mercury, PCB, dioxin, and other potential heavy metal and chemical

> contaminants interfering with thyroid system metabolism.3 (p. 226-

> 232; )

> Current research into the molecular biology of thyroid function

> suggests that most of the defective mechanisms capable of causing

> thyroid resistance syndrome take place at the level of intracellular

> thyroid receptors, or in the pathways activated when thyroid hormone

> binds to these receptors.18 There may also be factors causing

> thyroid hormone's blocked access to endothelial cell mediators. This

> could occur when stealth infections (such as cytomegalovirus)

> upregulate immune system function, in turn triggering a cascade of

> coagulation proteins that in some people results in a hypercoagulable

> state.19,20

>

> Abnormal Thyroid Regulation and Fibromyalgia

>

> Lowe interprets the symptoms of fibromyalgia as manifestations of

> abnormal thyroid hormone regulation.3 (p.341-768) In their program,

> 50 to 60% of fibromyalgia patients have primary or central

> hypothyroidism, and their treatment plan includes T3-T4 combination

> therapy, along with a carefully monitored effort to control symptoms

> by addressing any additional metabolism-slowing factors that apply to

> a given patient.

>

> The metabolic rehabilitation factors included by Lowe and colleagues

> are poor diet, nutritional deficiencies, low physical fitness,

> adrenal or sex hormone imbalances, and the use of drugs that impair

> metabolism. This is not an exclusive list of factors potentially

> critical to successful metabolic rehabilitation. Other potential

> obstacles to metabolic rehabilitation include hypercoagulation (and

> protein accumulation), poor sleep, poor stress management, lack of

> appropriate physical therapy, and problems with digestion and

> assimilation, chemical or heavy metal contamination, or

> detoxification. Any of these problems, left unaddressed, could cause

> appropriate thyroid hormone therapy to fail.

>

> A case series performed at Integrative Care Centers indicates that

> hypercoagulation and protein accumulation is another factor worthy of

> attention in patients with fibromyalgia.21 In this series, anti-

> coagulants or enzymes are thought to have induced improvements in

> microcirculatory flow in the blood and lymphatics of patients with

> fibromyalgia, resulting in decreased pain and increased energy in

> nearly two-thirds of patients.

>

> It is possible that the reduced pain and increased energy reported by

> fibromyalgia patients using enzymes were in part produced by enhanced

> thyroid regulation of endothelial cell function, given the link

> between thyroid and endothelial cell nitric oxide release.13

> Clearing fibrin and protein debris from endothelial cell membranes

> could enhance thyroid hormone's ability to regulate nitric oxide

> release, improving microcirculatory dynamics, thereby enhancing

> downstream tissue responsiveness to thyroid hormone.

>

> The bottom line for fibromyalgia patients is this: correcting

> thyroid regulation and taking active steps to remove existing

> obstacles to metabolic rehabilitation currently has an estimated 80

> to 90% success rate for obtaining a nearly full health recovery. The

> paradigm for diagnosing and treating abnormal thyroid regulation is

> changing.22

>

> Detecting and Treating Abnormal Thyroid Regulation in Fibromyalgia

>

> The clinical thyroid protocol outlined by Lowe and colleagues5 serves

> as a reasonable starting point for fibromyalgia evaluation and

> treatment. Added to the thyroid protocol must be a systematic

> effort to identify and graph therapeutic responses to a patient's

> most debilitating symptoms, as well as an action plan for addressing

> any co-existing obstacles to re-establishing metabolic balance.

>

> Baseline studies include a thyroid hormone profile (at a minimum

> including TSH, free T4, and free T3,) and screening for evidence of a

> hypercoagulable state. Baseline labs may also include assessments of

> adrenal and sex hormone function, as well as any other tests that

> could shed light on the presence of co-existing obstacles to

> recovery. Baseline bone density and electrocardiogram tests may also

> be considered.

>

> If evidence for primary or central hypothyroidism is found, thyroid

> treatment will begin with a T3-T4 combination, with dose increases

> every two weeks correlated with self-monitoring of symptom changes

> (on a 10-point scale), using a connect-the-dots line graph for each

> symptom over time. If thyroid resistance is suspected, thyroid

> treatment will begin with a T3 preparation, with dose increases every

> week, again, correlated with a symptom graph. Thyroid hormone

> therapy will be combined with additional clinical support for co-

> existing metabolic imbalances, and must be combined with aggressive

> lifestyle changes and self-care where needed.

>

> Symptoms common to hypothyroidism and fibromyalgia include low

> energy, widespread aches and pains, depressed mood, decreased ability

> to concentrate, puffiness, constipation, cold intolerance, poor

> sleep, low exercise tolerance, and difficulty getting going in the

> morning. Other symptoms, such as difficulty losing weight,

> heightened susceptibility to infection, menstrual cycle

> abnormalities, low body temperature, indigestion, and irritable bowel

> may also be present in patients with either diagnosis. Physical

> signs of hypothyroidism include a delayed Achilles tendon relaxation

> phase, dry or yellowish skin, low basal body temperature, and high

> cholesterol. Symptoms of excess thyroid hormone also need to be

> monitored. They include jitteriness, racing pulse, irritability,

> difficulty sleeping, chest pain, heat intolerance, frequent loose

> stools, and decreased appetite.

>

> Factors Affecting the Response to Thyroid Hormone Supplementation

>

> Low levels of adrenal function, as reflected by a low serum DHEA-S

> level, or low adrenal reserves (as assessed by an ACTH stimulation

> test), may further aggravate low levels of thyroid function, as well

> as interfere with a successful response to thyroid treatment.24 For

> this reason, we will often evaluate adrenal status when considering

> an empirical trial of thyroid supplementation. Low thyroid patients

> may also have low estrogen, progesterone, and testosterone activity

> in the body. T3 is thought to help stimulate the liver's production

> of the proteins that carry these sex hormones to the cells of the

> body.24 Monitoring and balancing thyroid, adrenal, and reproductive

> hormones as a group is often required for an empirical trial process

> to succeed in restoring health.

>

> Iron and calcium can block the absorption of thyroid hormone. Soy

> protein may interfere with thyroid metabolism, so limit your intake

> if this is a concern. It is best to take your thyroid supplement on

> an empty stomach with water, thirty minutes before a meal or taking

> vitamin supplements. Most patients keep their thyroid supplements in

> the bathroom and take it just after they get out of bed. That way,

> by the time you hit the kitchen, it's absorbed.

>

> To exert its many effects on human metabolism, thyroid hormone relies

> on enzyme pathways that, in turn, rely upon several key vitamins,

> minerals, and micronutrients. These include thiamine (B1),

> riboflavin (B2), niacin (B3), biotin, pantothenic acid (B5),

> pyridoxine (B6), cobalamin (B12), folic acid, magnesium, zinc,

> selenium, manganese, alpha lipoic acid, malic acid, essential fatty

> acids, and coenzyme-Q-10. The use of nutritional supplements can

> help maximize the efficiency thyroid hormone activity.

> Supplementation of your diet with these, or other important

> nutritional co-factors is typically part of an overall treatment plan.

>

> Use of certain medications, especially those that stimulate

> norepinephrine or endorphin pathways, may interfere with a normal

> response to thyroid hormone.5 (p. 312-318) Appropriate physical

> therapy and chiropractic treatments are also critical to the success

> of a metabolic rehabilitation effort.5 (275-286) Incomplete

> digestion, intestinal hyperpermeability, gut-derived toxicity and

> immune system overactivation, chemical or heavy metal contamination,

> and sluggish detoxification may also block metabolic rehabilitation

> efforts.

>

> The safety and effectiveness of the clinical thyroid protocol largely

> depends on accurate dosing and careful monitoring, including use of

> symptom graphs to document improvement and to minimize the risk of

> thyrotoxicity. At Integrative Care Centers, you can trust that

> detecting and effectively treating subtle forms of hypothyroidism is

> a high priority.

>

> References

>

> Toft AD. T3/T4 combination therapy. Endocrine Abstract 2002; 3(S40).

>

> Bunevicius R, Kazanavicius G, Zalinkevicius R, Prange AJ. Effects of

> thyroxine as compared with thyroxine plus triiodothyronine in

> patients with hypothyroidism. New England Journal of Medicine 1999;340

> (6):424-29.

>

> Lowe JC. The Metabolic Treatment of Fibromyalgia. Boulder:McDowell,

> 2000.

>

> Lowe JC. Garrison RL, Reichman AJ, Yellin J. Effectiveness and safety

> of T3 therapy for euthyroid fibromyalgia: a double-bline placebo-

> controlled response-driven crossover study. Clinical Bulletin of

> Myofascial Therapy 1997; (2(2/3):31-58.

>

> Honeyman-Lowe G, Lowe JC. Your Guide to Metabolic Health,

> Boulder:McDowell, 2003.

>

> AACE Thyroid Task Force. American Association of Clinical

> Endocrinologists medical guidelines for clinical practice for the

> evaluation and treatment of hyperthyroidism and hypothyroidism.

> Endocrine Practice 2002; 8(6):457-467.

>

> PJ. Cellular actions of thyroid hormone. In Werner and Ingbar's

> The Thyroid: a Fundamental and Clinical Text, 6th edition. Edited by

> LE Braverman and RD Utiger, New York:JB Lippincott, 1991, p.190-203.

>

> Refetoff S, Weiss RE, Usala SJ. The syndromes of resistance to

> thyroid hormones. Endocrinological Reviews 1993; 14(3):348-399.

>

> Oppenheimer JH. The nuclear receptor-triiodothyronine complex:

> relationship to thyroid hormone distribution, metabolism, and

> biological action. In Molecular Basis of Thyroid Hormone Action.

> Edited by JK Oppenheimer and HH s, New York:Academic Press,

> 1983, p.1-35.

>

> Lowe JC. Thyroid status of 38 fibromyalgia patients: implications for

> the etiology of fibromyalgia. Clinical Bulletin of Myofascial Therapy

> 1997; 2(1):47-64.

>

> Ribeiro RCJ et al. Thyroid hormone export regulates cellular hormone

> content and response. Journal of Biological Chemistry 1996; 271

> (29):17147-17151.

>

> Ikeda M, Wilcox EC, Chin WW. Different DNA elements can modulate the

> conformation of thyroid hormone receptor heterodimer and its

> transcriptional activity. Journal of Biological Chemistry 1996; 271

> (38):23096-23104.

>

> Taddei S et al. Impaired endothelium-dependent vasodilatation in

> subclinical hypothyroidism: beneficial effect of levothyroxine

> therapy. Journal of Clinical and Endocrinological Metabolism 2003; 88

> (8):3731-3737.

>

> Weiss RE et al. Dominant inheritance of resistance to thyroid hormone

> not linked to defects in the á or â thyroid hormone receptor genes

> may be due to a defective cofactor. Journal of Clinical Endocrinology

> and Metabolism 1996; 81(12):3239-3245.

>

> Wortsman J, et al. Familial resistance to thyroid hormone associated

> with decreased transport across the plasma membrane. ls of

> Internal Medicine 1983; 98:904-909.

>

> Schimmel M, Utiger RD. Thyroidal and peripheral production of thyroid

> hormones. ls of Internal Medicine 1977; 87:760-768.

>

> Ginsberg J et al. Inappropriate T3 and T4 radioimmunoassay levels

> secondary to circulating thyroid hormone autoantibodies. Clinical

> Endocrinology 1978; 8:133-139.

>

> Yen PM. Molecular basis of resistance to thyroid syndrome. Trends in

> endocrinology and metabolism 2003(Sept); 14(7):327-333.

>

> Sutherland MR et al. Coagulation initiated by herpes viruses.

> Proceedings of the National Academy of Sciences 1997; 94(25):13510-

> 13514.

>

> Berndtson K. Hypercoagulation, protein accumulation, and

> fibromyalgia. Unpublished analysis. Integrative Care Centers, 2003.

> <www.integrativecarecenters.com>

>

> Berndtson K. Results of heparin self-injection, and of oral

> fibrinolytic and proteolytic enzyme therapy in fibromyalgia.

> Unpublished case series. Integrative Care Centers, 2003.

> <www.integrativecarecenters.com>

>

> Garrison RL, Breeding PC. A metabolic basis for fibromyalgia and its

> related disorders: the possible role of resistance to thyroid

> hormone. Medical Hypotheses 2003; 61(12):182-189.

>

> Simoncini T et al. Dehydroepiandrosterone modulates endolthelial

> nitric oxide synthesis via direct genomic and nongenomic mechanisms.

> Endocrinology 2003; 144(8):3449-3455.

>

> Sarne DH, Refetoff S, Rosenfeld RL, Farriaux JP. Sex hormone-binding

> globulin in the diagnosis of peripheral tissue resistance to thyroid

> hormone: the value of changes after short-term triiodothyronine

> administration. Journal of Clinical Endocrinology and Metabolism

> 1988; 66:740-6

>

January 13, 2004

Well, I am very happy to announce that my doctor has prescribed synthroid for me. I am keeping my fingers crossed and looking to God for relief. I am desperate to get back to work.

What I did was I took the document, the blood test report, and a document that I have attached here.

Thyroid Treatment of FM/ Long> > > Hi all:> > Here's an explanation of the treatment I'm on and a link to my > doctor's website. In case link doesn't work, I posted article below.> > http://www.integrativecarecenters.com/index2.htm> > Thyroid Regulation and Fibromyalgia> Berndtson, MD> > Evolving Medical Perspectives on Hypothyroidism> > Historians note a recurring phenomenon in the evolution of human > ideas over the centuries. When an established, mainstream way of > thinking is challenged by a new and different way of thinking, the > mainstream often responds with "that's absurd." If the new way of > thinking picks up steam, the mainstream changes its opinion > to, "okay, it's not absurd, but it's not that relevant." Finally, > when the new way of thinking has picked up enough converts to make it > more than relevant, the mainstream declares, "we thought of it > first." > > This sets the stage for an ongoing battle of ideas concerning the > diagnosis and treatment of hypothyroidism, and a gathering medical > debate that revolves around the following questions: > > What are the subtle mechanisms by which abnormal thyroid hormone > system regulation slows down metabolism? > What roles might these mechanisms play in chronic illnesses? > How should we sort those who suffer from subtle forms of abnormal > thyroid regulation? > How should we treat subtle forms of hypothyroidism? > While there is little room for disagreement about the basic > mechanisms that produce primary or central hypothyroidism, there are > differing opinions about the best ways to treat them, even within > mainstream practice.1,2 The true paradigm-shifting potential of the > debate has to do with how we should identify and manage something > referred to as "partial peripheral cellular resistance to thyroid > hormone" (referred to hereafter in this paper as "thyroid resistance > syndrome"). Forcing this debate with mainstream thinkers is a new > wave of integrative medicine clinicians and researchers, led by > Lowe and his team, whose book, The Metabolic Treatment of > Fibromyalgia, is changing the way patients and physicians think about > the thyroid hormone system, and about metabolic health.3> > Based on their clinical research and practice experience, Lowe and > colleagues contend:> > An estimated 90% of patients with fibromyalgia suffer from one form > or another of abnormal thyroid hormone system regulation. Up to one-> third of these patients appear to have some form of thyroid > resistance syndrome.4, 3 (p. 295-338)> > > Most of these patients are affected by one or more of the following > additional metabolism-slowing factors: > Poor diet (one that produces glucose-insulin imbalance, fatty acid > imbalance, excess oxidative stress, etc.) > Nutritional deficiencies > Low physical fitness > Adrenal and sex hormone imbalances > Use of drugs that also impair metabolism > To fully recover, these patients must be treated with the proper dose > and form of thyroid hormone, but they must also control any other > factors adding to the slowing of their metabolism. Thyroid hormone > alone, even a proper form and dose, will not work if other metabolism-> slowing factors are left unaddressed.> > > Thyroid blood tests do not accurately identify patients who have > thyroid resistance syndrome. In addition, in patients with a thyroid > resistance syndrome, thyroid blood tests are of little use in > monitoring the full range of metabolic responses to thyroid hormone > therapy.> > > In patients with thyroid resistance, levothyroxine (T4) therapy alone > is not as effective as triiodothyronine (T3) therapy alone. In > primary or central hypothyroidism, T4 therapy is not as effective as > T3-T4 combination therapy.> > > Current mainstream practice guidelines on the diagnosis, treatment, > and monitoring of clinical hypothyroidism are short-> sighted; they steer physicians away from the diagnosis and management > of thyroid resistance syndrome, and from the use of T3, or > combination T3-T4 therapies in cases of c > One response from mainstream thinkers is that the symptoms of > hypothyroidism are non-specific, and should therefore not be treated > as clinical hypothyroidism unless blood tests establish the diagnosis > of hypothyroidism. As Lowe makes clear, this claim rests on the > shaky assumption that current laboratory evaluations of clinical > hypothyroidism do an adequate job of sorting those who have thyroid-> related metabolic slowing from those who do not.3 (p. 993-994)> > Mainstream thinkers also invoke a precautionary principle, claiming > that treating patients with T3, or with any form thyroid hormone when > blood tests are normal, may cause osteoporosis, adrenal crisis, > atrial fibrillation, and heart attack. Lowe's review of the > literature pertaining to these risks shows:> > scant support for the claim that T3, or T3-T4 therapy causes > osteoporosis (there is a stronger claim that using these therapies in > patients with thyroid-related slowing of metabolism improves bone > density).3 (p. 866-875) > reports of adrenal crisis related to T3 therapy are exceedingly rare, > and preventable with careful baseline evaluation and monitoring5 > (p.173-174) > reports of atrial fibrillation or heart attack related to the use of > T3 therapy involved only debilitated, elderly patients; there is no > evidence for these risks in patients of middle age or younger who > have appropriate baseline evaluation and monitoring.3 (p.875-880) > Mainstream medicine prides itself on taking a rigorously scientific > and logical approach to medical care. Recently, the American > Association of Clinical Endocrinologists (AACE), published its > clinical practice guidelines for the diagnosis and management of > hypothyroidism.6 Concerning diagnosis, the guidelines state that "A > TSH assay should always be used as the primary test to establish the > diagnosis of primary hypothyroidism.6 (p. 463-4) On the treatment > and management of clinical hypothyroidism, the guidelines state > that ".all physicians will treat clinical hypothyroidism with > levothyroxine [T4] replacement therapy."6 (p. 464).> > Regarding recent interest in the use of T3-containing preparations to > treat clinical hypothyroidism:> > Recent studies have shown a resurgence of interest in the possible > benefits of treatment of hypothyroidism with combinations of T4 and > T3 or with natural thyroid preparations. The small-scale study that > seems to have sparked this interest treated patients for only 5 > weeks, focused on mood changes, used a T4 plus T3 combination that > differs substantially from that found in natural thyroid products, > and have found a benefit in only a subset of patients, and has not > been replicated.36,37[36=reference #2 in this paper] Insufficient > evidence is available to know which patients with hypothyroidism, if > any, would be better treated with a combination of T4 plus T3 rather > than T4 alone6 (p. 464).> > The AACE's advice reads more like a dogmatic edict than a set of > guidelines for clinicians. A mere paragraph is devoted to the > possible role for T3-containing preparations in treating clinical > hypothyroidism, and that paragraph appears to be included for the > sole purpose of brushing off the idea that T3 has any useful role to > play. There is not so much as a word about thyroid resistance > syndrome, let alone an analysis of clinical studies on the subject. > > Clinical practice guidelines presented by medical professional groups > in a position of authority have a responsibility to those physicians > and patients who stand to be influenced by them. For patients with > symptoms of clinical hypothyroidism, but whose blood tests are within > the normal range, or for those patients with symptoms of clinical > hypothyroidism who fail to respond fully to T4 therapy alone, there > is a great deal at stake. For physicians in the trenches who are > called upon to evaluate and manage such patients, nothing less than > the trustworthiness of their professionalism is at stake. To take > full advantage of the scientific information that is available, > physicians and patients looking for guidance on the diagnosis and > treatment of clinical hypothyroidism will have to dig deeper than the > AACE guidelines.> > The Effects of Thyroid Hormone on Cell Structure and Function> > The effects of thyroid hormone on cell metabolism are sweeping and > profound. Thyroid hormone regulates protein interactions within the > cytoplasm of the cell, and gene expression by the nucleus of the > cell. Thyroid hormone's interactions with cytoplasmic proteins > influence the function of cell membranes, the synthesis and breakdown > of proteins, and the production, storage, and consumption of energy, > including the burning of fats and carbohydrates.7 > > In the nucleus of the cell, T3 binding to T3 receptors alters gene > expression in a range of DNA sequences referred to as thyroid > response elements.8 The activation of nuclear T3 receptors controls > the expression of genes that influence central and peripheral > activity of norepinephrine, dopamine, serotonin, growth hormone, > corticotrophin releasing hormone, and other key regulators of energy, > mood and metabolism.9> > Unlike steroid hormones, thyroid hormones pass freely through cell > membranes without need for specialized transport mechanisms. Thyroid > hormone is also unusual among the body's hormones in that it > regulates both catabolic (breakdown) and anabolic (restoration) > pathways.> > Categories of Abnormal Thyroid Regulation > > Primary and Central Hypothyroidism> > Primary hypothyroidism occurs when the thyroid gland does not make > enough thyroid hormone. Central hypothyroidism occurs when the > hypothalamus fails to sufficiently stimulate the pituitary gland, or > when the pituitary gland fails to sufficiently stimulate the thyroid > gland. Both forms result in decreased availability of thyroid > hormone. Lowe and colleagues conclude that roughly 50 to 60% of > fibromyalgia patients suffer from primary or central > hypothyroidism.10 They also find that the use of T4 alone to treat > these forms of clinical hypothyroidism is a fatally flawed approach > to correcting the abnormal thyroid hormone regulation found in these > conditions.5 (p. 311) > > Thyroid Resistance Syndrome> > Hormone resistance syndromes generally refer to conditions caused by > abnormal interactions between a hormone and its receptors.8 > According to Lowe, who has written the most comprehensive review ever > published on the subject of thyroid resistance, syndromes of partial > peripheral cellular resistance to thyroid hormone may be common, > occurring in roughly 30 to 40% of patients with fibromyalgia, and > perhaps responsible for metabolic slowing in a variety of other > chronic illnesses.3 (p. 295-338) In addition, the mechanisms capable > of causing thyroid resistance can involve factors other than abnormal > hormone-receptor interactions.> > Potential Causes of Thyroid Resistance Syndrome> > There are many potential points in the cellular metabolism of the > body's various tissues where thyroid system regulation can go wrong. > Proposed mechanisms for causing thyroid resistance syndrome include:> > >Mutations in the â thyroid receptor gene, causing mutant T3 nuclear > or cellular receptors which abnormally bind thyroid hormone, > resulting in a decreased thyroid signal.8 > Increased rate of T3 efflux from cells.11 > Abnormal DNA sequences in thyroid hormone response elements.12 > Decreased ability of thyroid hormone to control nitric oxide release > by endothelial cells.13 > Undetermined abnormal cofactors in thyroid metabolism.14 > Defective transport of T4 across cell membranes.15 > Defects in the conversion of T4 to T3.16 > Antibodies against circulating thyroid hormone.17 > Cytomegalovirus infection.8 > Mercury, PCB, dioxin, and other potential heavy metal and chemical > contaminants interfering with thyroid system metabolism.3 (p. 226-> 232; ) > Current research into the molecular biology of thyroid function > suggests that most of the defective mechanisms capable of causing > thyroid resistance syndrome take place at the level of intracellular > thyroid receptors, or in the pathways activated when thyroid hormone > binds to these receptors.18 There may also be factors causing > thyroid hormone's blocked access to endothelial cell mediators. This > could occur when stealth infections (such as cytomegalovirus) > upregulate immune system function, in turn triggering a cascade of > coagulation proteins that in some people results in a hypercoagulable > state.19,20> > Abnormal Thyroid Regulation and Fibromyalgia> > Lowe interprets the symptoms of fibromyalgia as manifestations of > abnormal thyroid hormone regulation.3 (p.341-768) In their program, > 50 to 60% of fibromyalgia patients have primary or central > hypothyroidism, and their treatment plan includes T3-T4 combination > therapy, along with a carefully monitored effort to control symptoms > by addressing any additional metabolism-slowing factors that apply to > a given patient. > > The metabolic rehabilitation factors included by Lowe and colleagues > are poor diet, nutritional deficiencies, low physical fitness, > adrenal or sex hormone imbalances, and the use of drugs that impair > metabolism. This is not an exclusive list of factors potentially > critical to successful metabolic rehabilitation. Other potential > obstacles to metabolic rehabilitation include hypercoagulation (and > protein accumulation), poor sleep, poor stress management, lack of > appropriate physical therapy, and problems with digestion and > assimilation, chemical or heavy metal contamination, or > detoxification. Any of these problems, left unaddressed, could cause > appropriate thyroid hormone therapy to fail. > > A case series performed at Integrative Care Centers indicates that > hypercoagulation and protein accumulation is another factor worthy of > attention in patients with fibromyalgia.21 In this series, anti-> coagulants or enzymes are thought to have induced improvements in > microcirculatory flow in the blood and lymphatics of patients with > fibromyalgia, resulting in decreased pain and increased energy in > nearly two-thirds of patients. > > It is possible that the reduced pain and increased energy reported by > fibromyalgia patients using enzymes were in part produced by enhanced > thyroid regulation of endothelial cell function, given the link > between thyroid and endothelial cell nitric oxide release.13 > Clearing fibrin and protein debris from endothelial cell membranes > could enhance thyroid hormone's ability to regulate nitric oxide > release, improving microcirculatory dynamics, thereby enhancing > downstream tissue responsiveness to thyroid hormone.> > The bottom line for fibromyalgia patients is this: correcting > thyroid regulation and taking active steps to remove existing > obstacles to metabolic rehabilitation currently has an estimated 80 > to 90% success rate for obtaining a nearly full health recovery. The > paradigm for diagnosing and treating abnormal thyroid regulation is > changing.22> > Detecting and Treating Abnormal Thyroid Regulation in Fibromyalgia> > The clinical thyroid protocol outlined by Lowe and colleagues5 serves > as a reasonable starting point for fibromyalgia evaluation and > treatment. Added to the thyroid protocol must be a systematic > effort to identify and graph therapeutic responses to a patient's > most debilitating symptoms, as well as an action plan for addressing > any co-existing obstacles to re-establishing metabolic balance.> > Baseline studies include a thyroid hormone profile (at a minimum > including TSH, free T4, and free T3,) and screening for evidence of a > hypercoagulable state. Baseline labs may also include assessments of > adrenal and sex hormone function, as well as any other tests that > could shed light on the presence of co-existing obstacles to > recovery. Baseline bone density and electrocardiogram tests may also > be considered.> > If evidence for primary or central hypothyroidism is found, thyroid > treatment will begin with a T3-T4 combination, with dose increases > every two weeks correlated with self-monitoring of symptom changes > (on a 10-point scale), using a connect-the-dots line graph for each > symptom over time. If thyroid resistance is suspected, thyroid > treatment will begin with a T3 preparation, with dose increases every > week, again, correlated with a symptom graph. Thyroid hormone > therapy will be combined with additional clinical support for co-> existing metabolic imbalances, and must be combined with aggressive > lifestyle changes and self-care where needed.> > Symptoms common to hypothyroidism and fibromyalgia include low > energy, widespread aches and pains, depressed mood, decreased ability > to concentrate, puffiness, constipation, cold intolerance, poor > sleep, low exercise tolerance, and difficulty getting going in the > morning. Other symptoms, such as difficulty losing weight, > heightened susceptibility to infection, menstrual cycle > abnormalities, low body temperature, indigestion, and irritable bowel > may also be present in patients with either diagnosis. Physical > signs of hypothyroidism include a delayed Achilles tendon relaxation > phase, dry or yellowish skin, low basal body temperature, and high > cholesterol. Symptoms of excess thyroid hormone also need to be > monitored. They include jitteriness, racing pulse, irritability, > difficulty sleeping, chest pain, heat intolerance, frequent loose > stools, and decreased appetite.> > Factors Affecting the Response to Thyroid Hormone Supplementation> > Low levels of adrenal function, as reflected by a low serum DHEA-S > level, or low adrenal reserves (as assessed by an ACTH stimulation > test), may further aggravate low levels of thyroid function, as well > as interfere with a successful response to thyroid treatment.24 For > this reason, we will often evaluate adrenal status when considering > an empirical trial of thyroid supplementation. Low thyroid patients > may also have low estrogen, progesterone, and testosterone activity > in the body. T3 is thought to help stimulate the liver's production > of the proteins that carry these sex hormones to the cells of the > body.24 Monitoring and balancing thyroid, adrenal, and reproductive > hormones as a group is often required for an empirical trial process > to succeed in restoring health.> > Iron and calcium can block the absorption of thyroid hormone. Soy > protein may interfere with thyroid metabolism, so limit your intake > if this is a concern. It is best to take your thyroid supplement on > an empty stomach with water, thirty minutes before a meal or taking > vitamin supplements. Most patients keep their thyroid supplements in > the bathroom and take it just after they get out of bed. That way, > by the time you hit the kitchen, it's absorbed. > > To exert its many effects on human metabolism, thyroid hormone relies > on enzyme pathways that, in turn, rely upon several key vitamins, > minerals, and micronutrients. These include thiamine (B1), > riboflavin (B2), niacin (B3), biotin, pantothenic acid (B5), > pyridoxine (B6), cobalamin (B12), folic acid, magnesium, zinc, > selenium, manganese, alpha lipoic acid, malic acid, essential fatty > acids, and coenzyme-Q-10. The use of nutritional supplements can > help maximize the efficiency thyroid hormone activity. > Supplementation of your diet with these, or other important > nutritional co-factors is typically part of an overall treatment plan.> > Use of certain medications, especially those that stimulate > norepinephrine or endorphin pathways, may interfere with a normal > response to thyroid hormone.5 (p. 312-318) Appropriate physical > therapy and chiropractic treatments are also critical to the success > of a metabolic rehabilitation effort.5 (275-286) Incomplete > digestion, intestinal hyperpermeability, gut-derived toxicity and > immune system overactivation, chemical or heavy metal contamination, > and sluggish detoxification may also block metabolic rehabilitation > efforts.> > The safety and effectiveness of the clinical thyroid protocol largely > depends on accurate dosing and careful monitoring, including use of > symptom graphs to document improvement and to minimize the risk of > thyrotoxicity. At Integrative Care Centers, you can trust that > detecting and effectively treating subtle forms of hypothyroidism is > a high priority. > > References> > Toft AD. T3/T4 combination therapy. Endocrine Abstract 2002; 3(S40).> > > Bunevicius R, Kazanavicius G, Zalinkevicius R, Prange AJ. Effects of > thyroxine as compared with thyroxine plus triiodothyronine in > patients with hypothyroidism. New England Journal of Medicine 1999;340> (6):424-29.> > > Lowe JC. The Metabolic Treatment of Fibromyalgia. Boulder:McDowell, > 2000.> > > Lowe JC. Garrison RL, Reichman AJ, Yellin J. Effectiveness and safety > of T3 therapy for euthyroid fibromyalgia: a double-bline placebo-> controlled response-driven crossover study. Clinical Bulletin of > Myofascial Therapy 1997; (2(2/3):31-58.> > > Honeyman-Lowe G, Lowe JC. Your Guide to Metabolic Health, > Boulder:McDowell, 2003.> > > AACE Thyroid Task Force. American Association of Clinical > Endocrinologists medical guidelines for clinical practice for the > evaluation and treatment of hyperthyroidism and hypothyroidism. > Endocrine Practice 2002; 8(6):457-467.> > > PJ. Cellular actions of thyroid hormone. In Werner and Ingbar's > The Thyroid: a Fundamental and Clinical Text, 6th edition. Edited by > LE Braverman and RD Utiger, New York:JB Lippincott, 1991, p.190-203.> > > Refetoff S, Weiss RE, Usala SJ. The syndromes of resistance to > thyroid hormones. Endocrinological Reviews 1993; 14(3):348-399.> > > Oppenheimer JH. The nuclear receptor-triiodothyronine complex: > relationship to thyroid hormone distribution, metabolism, and > biological action. In Molecular Basis of Thyroid Hormone Action. > Edited by JK Oppenheimer and HH s, New York:Academic Press, > 1983, p.1-35.> > > Lowe JC. Thyroid status of 38 fibromyalgia patients: implications for > the etiology of fibromyalgia. Clinical Bulletin of Myofascial Therapy > 1997; 2(1):47-64.> > > Ribeiro RCJ et al. Thyroid hormone export regulates cellular hormone > content and response. Journal of Biological Chemistry 1996; 271> (29):17147-17151.> > > Ikeda M, Wilcox EC, Chin WW. Different DNA elements can modulate the > conformation of thyroid hormone receptor heterodimer and its > transcriptional activity. Journal of Biological Chemistry 1996; 271> (38):23096-23104.> > > Taddei S et al. Impaired endothelium-dependent vasodilatation in > subclinical hypothyroidism: beneficial effect of levothyroxine > therapy. Journal of Clinical and Endocrinological Metabolism 2003; 88> (8):3731-3737.> > > Weiss RE et al. Dominant inheritance of resistance to thyroid hormone > not linked to defects in the á or â thyroid hormone receptor genes > may be due to a defective cofactor. Journal of Clinical Endocrinology > and Metabolism 1996; 81(12):3239-3245. > > > Wortsman J, et al. Familial resistance to thyroid hormone associated > with decreased transport across the plasma membrane. ls of > Internal Medicine 1983; 98:904-909.> > > Schimmel M, Utiger RD. Thyroidal and peripheral production of thyroid > hormones. ls of Internal Medicine 1977; 87:760-768.> > > Ginsberg J et al. Inappropriate T3 and T4 radioimmunoassay levels > secondary to circulating thyroid hormone autoantibodies. Clinical > Endocrinology 1978; 8:133-139.> > > Yen PM. Molecular basis of resistance to thyroid syndrome. Trends in > endocrinology and metabolism 2003(Sept); 14(7):327-333.> > > Sutherland MR et al. Coagulation initiated by herpes viruses. > Proceedings of the National Academy of Sciences 1997; 94(25):13510-> 13514.> > > Berndtson K. Hypercoagulation, protein accumulation, and > fibromyalgia. Unpublished analysis. Integrative Care Centers, 2003. > <www.integrativecarecenters.com>> > > Berndtson K. Results of heparin self-injection, and of oral > fibrinolytic and proteolytic enzyme therapy in fibromyalgia. > Unpublished case series. Integrative Care Centers, 2003. > <www.integrativecarecenters.com>> > > Garrison RL, Breeding PC. A metabolic basis for fibromyalgia and its > related disorders: the possible role of resistance to thyroid > hormone. Medical Hypotheses 2003; 61(12):182-189.> > > Simoncini T et al. Dehydroepiandrosterone modulates endolthelial > nitric oxide synthesis via direct genomic and nongenomic mechanisms. > Endocrinology 2003; 144(8):3449-3455.> > > Sarne DH, Refetoff S, Rosenfeld RL, Farriaux JP. Sex hormone-binding > globulin in the diagnosis of peripheral tissue resistance to thyroid > hormone: the value of changes after short-term triiodothyronine > administration. Journal of Clinical Endocrinology and Metabolism > 1988; 66:740-6 > > > > Copyright © 2003 Integrative Care Centers > > > >

January 13, 2004

Well, I am very happy to announce that my doctor has prescribed synthroid for me. I am keeping my fingers crossed and looking to God for relief. I am desperate to get back to work.

What I did was I took the document, the blood test report, and a document that I have attached here.

Thyroid Treatment of FM/ Long> > > Hi all:> > Here's an explanation of the treatment I'm on and a link to my > doctor's website. In case link doesn't work, I posted article below.> > http://www.integrativecarecenters.com/index2.htm> > Thyroid Regulation and Fibromyalgia> Berndtson, MD> > Evolving Medical Perspectives on Hypothyroidism> > Historians note a recurring phenomenon in the evolution of human > ideas over the centuries. When an established, mainstream way of > thinking is challenged by a new and different way of thinking, the > mainstream often responds with "that's absurd." If the new way of > thinking picks up steam, the mainstream changes its opinion > to, "okay, it's not absurd, but it's not that relevant." Finally, > when the new way of thinking has picked up enough converts to make it > more than relevant, the mainstream declares, "we thought of it > first." > > This sets the stage for an ongoing battle of ideas concerning the > diagnosis and treatment of hypothyroidism, and a gathering medical > debate that revolves around the following questions: > > What are the subtle mechanisms by which abnormal thyroid hormone > system regulation slows down metabolism? > What roles might these mechanisms play in chronic illnesses? > How should we sort those who suffer from subtle forms of abnormal > thyroid regulation? > How should we treat subtle forms of hypothyroidism? > While there is little room for disagreement about the basic > mechanisms that produce primary or central hypothyroidism, there are > differing opinions about the best ways to treat them, even within > mainstream practice.1,2 The true paradigm-shifting potential of the > debate has to do with how we should identify and manage something > referred to as "partial peripheral cellular resistance to thyroid > hormone" (referred to hereafter in this paper as "thyroid resistance > syndrome"). Forcing this debate with mainstream thinkers is a new > wave of integrative medicine clinicians and researchers, led by > Lowe and his team, whose book, The Metabolic Treatment of > Fibromyalgia, is changing the way patients and physicians think about > the thyroid hormone system, and about metabolic health.3> > Based on their clinical research and practice experience, Lowe and > colleagues contend:> > An estimated 90% of patients with fibromyalgia suffer from one form > or another of abnormal thyroid hormone system regulation. Up to one-> third of these patients appear to have some form of thyroid > resistance syndrome.4, 3 (p. 295-338)> > > Most of these patients are affected by one or more of the following > additional metabolism-slowing factors: > Poor diet (one that produces glucose-insulin imbalance, fatty acid > imbalance, excess oxidative stress, etc.) > Nutritional deficiencies > Low physical fitness > Adrenal and sex hormone imbalances > Use of drugs that also impair metabolism > To fully recover, these patients must be treated with the proper dose > and form of thyroid hormone, but they must also control any other > factors adding to the slowing of their metabolism. Thyroid hormone > alone, even a proper form and dose, will not work if other metabolism-> slowing factors are left unaddressed.> > > Thyroid blood tests do not accurately identify patients who have > thyroid resistance syndrome. In addition, in patients with a thyroid > resistance syndrome, thyroid blood tests are of little use in > monitoring the full range of metabolic responses to thyroid hormone > therapy.> > > In patients with thyroid resistance, levothyroxine (T4) therapy alone > is not as effective as triiodothyronine (T3) therapy alone. In > primary or central hypothyroidism, T4 therapy is not as effective as > T3-T4 combination therapy.> > > Current mainstream practice guidelines on the diagnosis, treatment, > and monitoring of clinical hypothyroidism are short-> sighted; they steer physicians away from the diagnosis and management > of thyroid resistance syndrome, and from the use of T3, or > combination T3-T4 therapies in cases of c > One response from mainstream thinkers is that the symptoms of > hypothyroidism are non-specific, and should therefore not be treated > as clinical hypothyroidism unless blood tests establish the diagnosis > of hypothyroidism. As Lowe makes clear, this claim rests on the > shaky assumption that current laboratory evaluations of clinical > hypothyroidism do an adequate job of sorting those who have thyroid-> related metabolic slowing from those who do not.3 (p. 993-994)> > Mainstream thinkers also invoke a precautionary principle, claiming > that treating patients with T3, or with any form thyroid hormone when > blood tests are normal, may cause osteoporosis, adrenal crisis, > atrial fibrillation, and heart attack. Lowe's review of the > literature pertaining to these risks shows:> > scant support for the claim that T3, or T3-T4 therapy causes > osteoporosis (there is a stronger claim that using these therapies in > patients with thyroid-related slowing of metabolism improves bone > density).3 (p. 866-875) > reports of adrenal crisis related to T3 therapy are exceedingly rare, > and preventable with careful baseline evaluation and monitoring5 > (p.173-174) > reports of atrial fibrillation or heart attack related to the use of > T3 therapy involved only debilitated, elderly patients; there is no > evidence for these risks in patients of middle age or younger who > have appropriate baseline evaluation and monitoring.3 (p.875-880) > Mainstream medicine prides itself on taking a rigorously scientific > and logical approach to medical care. Recently, the American > Association of Clinical Endocrinologists (AACE), published its > clinical practice guidelines for the diagnosis and management of > hypothyroidism.6 Concerning diagnosis, the guidelines state that "A > TSH assay should always be used as the primary test to establish the > diagnosis of primary hypothyroidism.6 (p. 463-4) On the treatment > and management of clinical hypothyroidism, the guidelines state > that ".all physicians will treat clinical hypothyroidism with > levothyroxine [T4] replacement therapy."6 (p. 464).> > Regarding recent interest in the use of T3-containing preparations to > treat clinical hypothyroidism:> > Recent studies have shown a resurgence of interest in the possible > benefits of treatment of hypothyroidism with combinations of T4 and > T3 or with natural thyroid preparations. The small-scale study that > seems to have sparked this interest treated patients for only 5 > weeks, focused on mood changes, used a T4 plus T3 combination that > differs substantially from that found in natural thyroid products, > and have found a benefit in only a subset of patients, and has not > been replicated.36,37[36=reference #2 in this paper] Insufficient > evidence is available to know which patients with hypothyroidism, if > any, would be better treated with a combination of T4 plus T3 rather > than T4 alone6 (p. 464).> > The AACE's advice reads more like a dogmatic edict than a set of > guidelines for clinicians. A mere paragraph is devoted to the > possible role for T3-containing preparations in treating clinical > hypothyroidism, and that paragraph appears to be included for the > sole purpose of brushing off the idea that T3 has any useful role to > play. There is not so much as a word about thyroid resistance > syndrome, let alone an analysis of clinical studies on the subject. > > Clinical practice guidelines presented by medical professional groups > in a position of authority have a responsibility to those physicians > and patients who stand to be influenced by them. For patients with > symptoms of clinical hypothyroidism, but whose blood tests are within > the normal range, or for those patients with symptoms of clinical > hypothyroidism who fail to respond fully to T4 therapy alone, there > is a great deal at stake. For physicians in the trenches who are > called upon to evaluate and manage such patients, nothing less than > the trustworthiness of their professionalism is at stake. To take > full advantage of the scientific information that is available, > physicians and patients looking for guidance on the diagnosis and > treatment of clinical hypothyroidism will have to dig deeper than the > AACE guidelines.> > The Effects of Thyroid Hormone on Cell Structure and Function> > The effects of thyroid hormone on cell metabolism are sweeping and > profound. Thyroid hormone regulates protein interactions within the > cytoplasm of the cell, and gene expression by the nucleus of the > cell. Thyroid hormone's interactions with cytoplasmic proteins > influence the function of cell membranes, the synthesis and breakdown > of proteins, and the production, storage, and consumption of energy, > including the burning of fats and carbohydrates.7 > > In the nucleus of the cell, T3 binding to T3 receptors alters gene > expression in a range of DNA sequences referred to as thyroid > response elements.8 The activation of nuclear T3 receptors controls > the expression of genes that influence central and peripheral > activity of norepinephrine, dopamine, serotonin, growth hormone, > corticotrophin releasing hormone, and other key regulators of energy, > mood and metabolism.9> > Unlike steroid hormones, thyroid hormones pass freely through cell > membranes without need for specialized transport mechanisms. Thyroid > hormone is also unusual among the body's hormones in that it > regulates both catabolic (breakdown) and anabolic (restoration) > pathways.> > Categories of Abnormal Thyroid Regulation > > Primary and Central Hypothyroidism> > Primary hypothyroidism occurs when the thyroid gland does not make > enough thyroid hormone. Central hypothyroidism occurs when the > hypothalamus fails to sufficiently stimulate the pituitary gland, or > when the pituitary gland fails to sufficiently stimulate the thyroid > gland. Both forms result in decreased availability of thyroid > hormone. Lowe and colleagues conclude that roughly 50 to 60% of > fibromyalgia patients suffer from primary or central > hypothyroidism.10 They also find that the use of T4 alone to treat > these forms of clinical hypothyroidism is a fatally flawed approach > to correcting the abnormal thyroid hormone regulation found in these > conditions.5 (p. 311) > > Thyroid Resistance Syndrome> > Hormone resistance syndromes generally refer to conditions caused by > abnormal interactions between a hormone and its receptors.8 > According to Lowe, who has written the most comprehensive review ever > published on the subject of thyroid resistance, syndromes of partial > peripheral cellular resistance to thyroid hormone may be common, > occurring in roughly 30 to 40% of patients with fibromyalgia, and > perhaps responsible for metabolic slowing in a variety of other > chronic illnesses.3 (p. 295-338) In addition, the mechanisms capable > of causing thyroid resistance can involve factors other than abnormal > hormone-receptor interactions.> > Potential Causes of Thyroid Resistance Syndrome> > There are many potential points in the cellular metabolism of the > body's various tissues where thyroid system regulation can go wrong. > Proposed mechanisms for causing thyroid resistance syndrome include:> > >Mutations in the â thyroid receptor gene, causing mutant T3 nuclear > or cellular receptors which abnormally bind thyroid hormone, > resulting in a decreased thyroid signal.8 > Increased rate of T3 efflux from cells.11 > Abnormal DNA sequences in thyroid hormone response elements.12 > Decreased ability of thyroid hormone to control nitric oxide release > by endothelial cells.13 > Undetermined abnormal cofactors in thyroid metabolism.14 > Defective transport of T4 across cell membranes.15 > Defects in the conversion of T4 to T3.16 > Antibodies against circulating thyroid hormone.17 > Cytomegalovirus infection.8 > Mercury, PCB, dioxin, and other potential heavy metal and chemical > contaminants interfering with thyroid system metabolism.3 (p. 226-> 232; ) > Current research into the molecular biology of thyroid function > suggests that most of the defective mechanisms capable of causing > thyroid resistance syndrome take place at the level of intracellular > thyroid receptors, or in the pathways activated when thyroid hormone > binds to these receptors.18 There may also be factors causing > thyroid hormone's blocked access to endothelial cell mediators. This > could occur when stealth infections (such as cytomegalovirus) > upregulate immune system function, in turn triggering a cascade of > coagulation proteins that in some people results in a hypercoagulable > state.19,20> > Abnormal Thyroid Regulation and Fibromyalgia> > Lowe interprets the symptoms of fibromyalgia as manifestations of > abnormal thyroid hormone regulation.3 (p.341-768) In their program, > 50 to 60% of fibromyalgia patients have primary or central > hypothyroidism, and their treatment plan includes T3-T4 combination > therapy, along with a carefully monitored effort to control symptoms > by addressing any additional metabolism-slowing factors that apply to > a given patient. > > The metabolic rehabilitation factors included by Lowe and colleagues > are poor diet, nutritional deficiencies, low physical fitness, > adrenal or sex hormone imbalances, and the use of drugs that impair > metabolism. This is not an exclusive list of factors potentially > critical to successful metabolic rehabilitation. Other potential > obstacles to metabolic rehabilitation include hypercoagulation (and > protein accumulation), poor sleep, poor stress management, lack of > appropriate physical therapy, and problems with digestion and > assimilation, chemical or heavy metal contamination, or > detoxification. Any of these problems, left unaddressed, could cause > appropriate thyroid hormone therapy to fail. > > A case series performed at Integrative Care Centers indicates that > hypercoagulation and protein accumulation is another factor worthy of > attention in patients with fibromyalgia.21 In this series, anti-> coagulants or enzymes are thought to have induced improvements in > microcirculatory flow in the blood and lymphatics of patients with > fibromyalgia, resulting in decreased pain and increased energy in > nearly two-thirds of patients. > > It is possible that the reduced pain and increased energy reported by > fibromyalgia patients using enzymes were in part produced by enhanced > thyroid regulation of endothelial cell function, given the link > between thyroid and endothelial cell nitric oxide release.13 > Clearing fibrin and protein debris from endothelial cell membranes > could enhance thyroid hormone's ability to regulate nitric oxide > release, improving microcirculatory dynamics, thereby enhancing > downstream tissue responsiveness to thyroid hormone.> > The bottom line for fibromyalgia patients is this: correcting > thyroid regulation and taking active steps to remove existing > obstacles to metabolic rehabilitation currently has an estimated 80 > to 90% success rate for obtaining a nearly full health recovery. The > paradigm for diagnosing and treating abnormal thyroid regulation is > changing.22> > Detecting and Treating Abnormal Thyroid Regulation in Fibromyalgia> > The clinical thyroid protocol outlined by Lowe and colleagues5 serves > as a reasonable starting point for fibromyalgia evaluation and > treatment. Added to the thyroid protocol must be a systematic > effort to identify and graph therapeutic responses to a patient's > most debilitating symptoms, as well as an action plan for addressing > any co-existing obstacles to re-establishing metabolic balance.> > Baseline studies include a thyroid hormone profile (at a minimum > including TSH, free T4, and free T3,) and screening for evidence of a > hypercoagulable state. Baseline labs may also include assessments of > adrenal and sex hormone function, as well as any other tests that > could shed light on the presence of co-existing obstacles to > recovery. Baseline bone density and electrocardiogram tests may also > be considered.> > If evidence for primary or central hypothyroidism is found, thyroid > treatment will begin with a T3-T4 combination, with dose increases > every two weeks correlated with self-monitoring of symptom changes > (on a 10-point scale), using a connect-the-dots line graph for each > symptom over time. If thyroid resistance is suspected, thyroid > treatment will begin with a T3 preparation, with dose increases every > week, again, correlated with a symptom graph. Thyroid hormone > therapy will be combined with additional clinical support for co-> existing metabolic imbalances, and must be combined with aggressive > lifestyle changes and self-care where needed.> > Symptoms common to hypothyroidism and fibromyalgia include low > energy, widespread aches and pains, depressed mood, decreased ability > to concentrate, puffiness, constipation, cold intolerance, poor > sleep, low exercise tolerance, and difficulty getting going in the > morning. Other symptoms, such as difficulty losing weight, > heightened susceptibility to infection, menstrual cycle > abnormalities, low body temperature, indigestion, and irritable bowel > may also be present in patients with either diagnosis. Physical > signs of hypothyroidism include a delayed Achilles tendon relaxation > phase, dry or yellowish skin, low basal body temperature, and high > cholesterol. Symptoms of excess thyroid hormone also need to be > monitored. They include jitteriness, racing pulse, irritability, > difficulty sleeping, chest pain, heat intolerance, frequent loose > stools, and decreased appetite.> > Factors Affecting the Response to Thyroid Hormone Supplementation> > Low levels of adrenal function, as reflected by a low serum DHEA-S > level, or low adrenal reserves (as assessed by an ACTH stimulation > test), may further aggravate low levels of thyroid function, as well > as interfere with a successful response to thyroid treatment.24 For > this reason, we will often evaluate adrenal status when considering > an empirical trial of thyroid supplementation. Low thyroid patients > may also have low estrogen, progesterone, and testosterone activity > in the body. T3 is thought to help stimulate the liver's production > of the proteins that carry these sex hormones to the cells of the > body.24 Monitoring and balancing thyroid, adrenal, and reproductive > hormones as a group is often required for an empirical trial process > to succeed in restoring health.> > Iron and calcium can block the absorption of thyroid hormone. Soy > protein may interfere with thyroid metabolism, so limit your intake > if this is a concern. It is best to take your thyroid supplement on > an empty stomach with water, thirty minutes before a meal or taking > vitamin supplements. Most patients keep their thyroid supplements in > the bathroom and take it just after they get out of bed. That way, > by the time you hit the kitchen, it's absorbed. > > To exert its many effects on human metabolism, thyroid hormone relies > on enzyme pathways that, in turn, rely upon several key vitamins, > minerals, and micronutrients. These include thiamine (B1), > riboflavin (B2), niacin (B3), biotin, pantothenic acid (B5), > pyridoxine (B6), cobalamin (B12), folic acid, magnesium, zinc, > selenium, manganese, alpha lipoic acid, malic acid, essential fatty > acids, and coenzyme-Q-10. The use of nutritional supplements can > help maximize the efficiency thyroid hormone activity. > Supplementation of your diet with these, or other important > nutritional co-factors is typically part of an overall treatment plan.> > Use of certain medications, especially those that stimulate > norepinephrine or endorphin pathways, may interfere with a normal > response to thyroid hormone.5 (p. 312-318) Appropriate physical > therapy and chiropractic treatments are also critical to the success > of a metabolic rehabilitation effort.5 (275-286) Incomplete > digestion, intestinal hyperpermeability, gut-derived toxicity and > immune system overactivation, chemical or heavy metal contamination, > and sluggish detoxification may also block metabolic rehabilitation > efforts.> > The safety and effectiveness of the clinical thyroid protocol largely > depends on accurate dosing and careful monitoring, including use of > symptom graphs to document improvement and to minimize the risk of > thyrotoxicity. At Integrative Care Centers, you can trust that > detecting and effectively treating subtle forms of hypothyroidism is > a high priority. > > References> > Toft AD. T3/T4 combination therapy. Endocrine Abstract 2002; 3(S40).> > > Bunevicius R, Kazanavicius G, Zalinkevicius R, Prange AJ. Effects of > thyroxine as compared with thyroxine plus triiodothyronine in > patients with hypothyroidism. New England Journal of Medicine 1999;340> (6):424-29.> > > Lowe JC. The Metabolic Treatment of Fibromyalgia. Boulder:McDowell, > 2000.> > > Lowe JC. Garrison RL, Reichman AJ, Yellin J. Effectiveness and safety > of T3 therapy for euthyroid fibromyalgia: a double-bline placebo-> controlled response-driven crossover study. Clinical Bulletin of > Myofascial Therapy 1997; (2(2/3):31-58.> > > Honeyman-Lowe G, Lowe JC. Your Guide to Metabolic Health, > Boulder:McDowell, 2003.> > > AACE Thyroid Task Force. American Association of Clinical > Endocrinologists medical guidelines for clinical practice for the > evaluation and treatment of hyperthyroidism and hypothyroidism. > Endocrine Practice 2002; 8(6):457-467.> > > PJ. Cellular actions of thyroid hormone. In Werner and Ingbar's > The Thyroid: a Fundamental and Clinical Text, 6th edition. Edited by > LE Braverman and RD Utiger, New York:JB Lippincott, 1991, p.190-203.> > > Refetoff S, Weiss RE, Usala SJ. The syndromes of resistance to > thyroid hormones. Endocrinological Reviews 1993; 14(3):348-399.> > > Oppenheimer JH. The nuclear receptor-triiodothyronine complex: > relationship to thyroid hormone distribution, metabolism, and > biological action. In Molecular Basis of Thyroid Hormone Action. > Edited by JK Oppenheimer and HH s, New York:Academic Press, > 1983, p.1-35.> > > Lowe JC. Thyroid status of 38 fibromyalgia patients: implications for > the etiology of fibromyalgia. Clinical Bulletin of Myofascial Therapy > 1997; 2(1):47-64.> > > Ribeiro RCJ et al. Thyroid hormone export regulates cellular hormone > content and response. Journal of Biological Chemistry 1996; 271> (29):17147-17151.> > > Ikeda M, Wilcox EC, Chin WW. Different DNA elements can modulate the > conformation of thyroid hormone receptor heterodimer and its > transcriptional activity. Journal of Biological Chemistry 1996; 271> (38):23096-23104.> > > Taddei S et al. Impaired endothelium-dependent vasodilatation in > subclinical hypothyroidism: beneficial effect of levothyroxine > therapy. Journal of Clinical and Endocrinological Metabolism 2003; 88> (8):3731-3737.> > > Weiss RE et al. Dominant inheritance of resistance to thyroid hormone > not linked to defects in the á or â thyroid hormone receptor genes > may be due to a defective cofactor. Journal of Clinical Endocrinology > and Metabolism 1996; 81(12):3239-3245. > > > Wortsman J, et al. Familial resistance to thyroid hormone associated > with decreased transport across the plasma membrane. ls of > Internal Medicine 1983; 98:904-909.> > > Schimmel M, Utiger RD. Thyroidal and peripheral production of thyroid > hormones. ls of Internal Medicine 1977; 87:760-768.> > > Ginsberg J et al. Inappropriate T3 and T4 radioimmunoassay levels > secondary to circulating thyroid hormone autoantibodies. Clinical > Endocrinology 1978; 8:133-139.> > > Yen PM. Molecular basis of resistance to thyroid syndrome. Trends in > endocrinology and metabolism 2003(Sept); 14(7):327-333.> > > Sutherland MR et al. Coagulation initiated by herpes viruses. > Proceedings of the National Academy of Sciences 1997; 94(25):13510-> 13514.> > > Berndtson K. Hypercoagulation, protein accumulation, and > fibromyalgia. Unpublished analysis. Integrative Care Centers, 2003. > <www.integrativecarecenters.com>> > > Berndtson K. Results of heparin self-injection, and of oral > fibrinolytic and proteolytic enzyme therapy in fibromyalgia. > Unpublished case series. Integrative Care Centers, 2003. > <www.integrativecarecenters.com>> > > Garrison RL, Breeding PC. A metabolic basis for fibromyalgia and its > related disorders: the possible role of resistance to thyroid > hormone. Medical Hypotheses 2003; 61(12):182-189.> > > Simoncini T et al. Dehydroepiandrosterone modulates endolthelial > nitric oxide synthesis via direct genomic and nongenomic mechanisms. > Endocrinology 2003; 144(8):3449-3455.> > > Sarne DH, Refetoff S, Rosenfeld RL, Farriaux JP. Sex hormone-binding > globulin in the diagnosis of peripheral tissue resistance to thyroid > hormone: the value of changes after short-term triiodothyronine > administration. Journal of Clinical Endocrinology and Metabolism > 1988; 66:740-6 > > > > Copyright © 2003 Integrative Care Centers > > > >

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