Friday, June 29, 2012

What happened to all those children who were saved by modern antibiotics?

We know that around the turn of the Century infant mortality was high.  It was 50% in the US and higher in other countries.  

We cheated Mother Nature's “Survival of the Fittest” protocol with the discovery of antibiotics, but to what end?  What happened to the population we started saving with antibiotics?  What happened to the infants and young children that were rescued from diseases and infections that would normally have killed them?  After several generations of saving people who would not have survived childhood without intervention, how do they fare as adults?  

According to several researchers those (weak) individuals were mostly born with genetic defects in their mitochondria.  “Mitochondria are the energy factories that convert the food we eat into the chemical currency that our bodies use to function.  Mitochondria are responsible for 90% of the production of energy that our tissues, organs, and bodies require for metabolism.  The Textbook of Physiology, states, “It seems almost to be an obvious deduction that the principal function of thyroxine (thyroid hormone) might be simply to increase the number and activity of mitochondria.” ” (1)(55) 

“Mitochondrial mutations appear to be largely responsible for metabolic defects at the cellular level, which results in a hypothyroid like condition.  Modern thyroid blood tests do not detect this because thyroid hormones levels may be normal, but they are not high enough to stimulate the genetically defective mitochondria into normal activity. The increased basal temperature that results from administering desiccated thyroid is a direct result of enhanced mitochondrial activity.” (1)(59)

The trait for mitochondria is passed from the mother (only) through special DNA that is separate from the 46 chromosomes that dictate humans inherited traits.  The father contributes nothing to the inheritance of mitochondria.

Dr. Mark Starr calls the multiple hypothyroid like symptoms resulting from this mitochondrial defect “Type 2 Hypothyroidism.”  Type 2 Hypothyroidism therefore cannot be determined by standard Thyroid blood tests since the problem is not hormone related.  People with Type 2 Hypothyroidism typically have normal Thyroid blood tests.  The term used to refer to defective mitochondria has been “Thyroid Hormone Resistance,” but the name “Type 2 Hypothyroidism” seems to fit this condition a little better.

It seems the average doctor is not equipped to deal with Type 2 Hypothyroidism.  They have been wrongly told that all “Thyroid Hormone Resistance” is rare, and always results from a bad gene that occurs in 1 in 50,000 live births.  “Usually dominantly inherited, RTH is associated with diverse, heterozygous THRB gene mutations impairing hormone binding and/or transcriptional activity of receptors (3–5).” (2) This information comes from statistics collected in the 1960’s and refers only to “General” Thyroid Hormone Resistance where the Pituitary Gland is resistant to thyroid hormones and Thyroid blood tests show a High TSH reading.  In “Peripheral” tissue Thyroid Hormone Resistance the Pituitary Gland is NOT involved and reacts normally to Thyroid Hormones, so Thyroid blood tests will show normal TSH with normal levels of all Thyroid Hormones.  “Peripheral Tissue Thyroid Hormone Resistance” is the type of Tissue Resistant Hypothyroidism that Dr. Starr is talking about that presents as “Type 2 Hypothyroidism” where all blood tests are normal. It is NOT rare!  Current estimates indicate that at least half the population has it because it is always inherited through the mother.  

Remember that 50% mortality at the turn of the Century?  Several generations of those saved 50%, and many more saved accumulated annually, have now reproduced this trait consistently for the last 60 years!  These people now make up the majority of our population that suffer from Coronary Artery Disease, Diabetes, High Blood Pressure, High Cholesterol, Obesity, Chronic Fatigue, Fertility and Reproductive Problems, Skin Disorders, Liver disease, Gastrointestinal disorders including IBS and Constipation, Fibromyalgia and other Pain disorders, Sleep disorders, Depression and assorted Mental Illness’.  Defective mitochondria cause massive problems at the cellular level! 

(1) Starr, Mark. Hypothyroidism Type 2: The Epidemic. 4th printing. Published by Mark Starr Trust; 2010
(2)  Multiple Authors, American Society for Clinical Investigation, Published in Volume 120, Issue 4, (April 1, 2010);120(4):1345–1354. doi:10.1172/JCI38793
Retrieved from:    http://www.jci.org/articles/view/38793

Thursday, June 28, 2012

Women-- Just Say No to Statin Drugs

Cholesterol Lowering Statin Drugs for Women

 Just Say No to Statin Drugs

 by Jeffrey Dach MD

"The reality is that there is no mortality benefit from lowering cholersterol with statin drugs: Both lines on the mortality chart below are superimposed meaning the number of deaths in the statin drug group was identical to the number of deaths in the placebo group. Chart Courtesy of (Eddie Vos).

Lipitor Mortality Chart

Just say NO When Your Doctor Prescribes a Statin Drug. 

The truth is that NO woman should ever be given Lipitor or any other statin drug for elevated cholesterol. Dr. Rose says, "There are no statin trials with even the slightest hint of a mortality benefit in women and women should be told so". (5). In other words, statin drugs don’t work for women. 

No Female Should Ever Take A Statin Drug 

Let me repeat that so this is very clear: No female should ever take a statin drug to lower cholesterol for primary prevention of heart disease. They don’t work for women. Women who take Lipitor or any other statin drug to lower cholesterol do not live any longer than women who don’t take the drug. There is no benefit in terms of prolonging your life for women. 

Adverse Side Effects of Statin Drugs:

On the other hand, there are plenty of adverse side effects which include muscle pain, cognitive impairment, neuropathy, congestive heart failure, transient global amnesia, dementia, cancer and erectile dysfunction (impotence).Read about Statin Drug adverse side effects on this message board and this message board.  The side effects are thought to be caused by Co-Enzyme Q10 depletion.

Are you still not convinced that women should NOT take Statin Drugs? Don’t take my word for it. Take the word of Judith Walsh MD who wrote this in JAMA, 4 years ago in an article entitled, Treatment of Hyperlipidemia in Women: "For women without cardiovascular disease, lipid lowering does not affect total or CHD (Cardiovascular Heart Disease) mortality. Lipid lowering may reduce CHD events, but current evidence is insufficient to determine this conclusively. For women with known cardiovascular disease, treatment of hyperlipidemia is effective in reducing CHD events, CHD mortality, nonfatal myocardial infarction, and revascularization, but it does not affect total mortality."(8) 

Translation: Cholesterol lowering with statin drugs does not reduce total mortality in women, PERIOD. It doesn’t reduce mortality in women without heart disease, called primary prevention. It doesn’t reduce mortality in women with heart disease, called secondary prevention." 
See more at:

Tuesday, June 26, 2012

Dr. Mark Starr quotes Dr. Broda O. Barnes work in his book "Hypothyroidism Type 2: The Epidemic


“Dr. Barnes presented his research on the coexistence of diabetes and hypothyroidism at a 1971 American Medical Association meeting.”
“He also met with prominent doctors…”
“Unfortunately, he found no sympathetic ears, despite the wealth of evidence he had gathered from the autopsies, his own patients, and Dr. Eaton’s report.”
“In my opinion, every diabetic patient seen in my practice has suffered hypothyroidism.”
Contact Information
Dr. Starr’s Contact Information
Here is contact information for Dr. Starr.
Mark Starr, MD
21st Century Pain & Sports Medicine
10565 N. Tatum Blvd Suite B-115
Paradise Valley, AZ 85253
(480) 607-6503
(480) 607-6533 fax
http://21centurymed.com
http://type2hypothyroidism.com

Sunday, June 24, 2012

Type 2 Hypothyroidism, my search for help

Well so far no luck in finding someone to treat me for my Peripheral (tissue) Thyroid Hormone Resistance.  Pac Med failed to have someone who has even heard of it and the Poly Clinic had someone who has heard of it but has no idea how to manage, or diagnose it.  The UW is pretending it doesn’t exist.  Probably because they receive lots of money for Drug research from pharmaceutical companies. http://sop.washington.edu/porpp

Thyroid Hormone Resistance is called Type 2 Hypothyroidism and it is claimed to be an untreated epidemic in the US.  


"blood tests do not detect Type 2 hypothyroidism." "The pervasiveness of Type 2 hypothyroidism has yet to be recognized by mainstream medicine but is already in epidemic proportions."
http://www.type2hypothyroidism.com/Type1VsType2.html


Thyroid hormones transport essential Iodine to all cells of your body (called Iodine uptake). Thyroid Hormones are made by the thyroid gland and are called: T4, T3, T2, T1, and calcitonin.  The thyroid gland also produces Reverse T3 (RT3) to regulate T3 uptake.  The ratio of RT3 to T3 is about 60:40. Thyroid hormone T3 is the active hormone in metabolism regulation. The storage hormone T4 is converted to the usable hormone T3 in the liver. The other hormones--T2, T1 and Calcitonin--help regulate the effects of T3 on the body. 

Here is what Dr. Jarvis has to say about the Halogen's, one of which is Bromine, and their effect on displacing Iodine in the body: "There is a well-known law of halogen displacement. The halogen group is made up as follows:
Halogen’s     Relative Atomic Weight  (found primarily in)
Fluorine                   19.                 (drinking water and dental products)
Chlorine                  35.5             (drinking water)
Bromine                   80.               (agricultural pesticides)
Iodine                    127.                (Kelp and Sea Salt)
The critical activity of any one of these four halogens is in inverse proportion to its atomic weight. This means that any one of the four can displace the element with a higher atomic weight, but cannot displace an element with a lower atomic weight. For example, fluorine can displace chlorine, bromine and iodine because fluorine has a lower atomic weight than the other three. Similarly, chlorine can displace bromine and iodine because they both have a higher atomic weight. Likewise, bromine can displace iodine from the body because iodine has a higher atomic weight. But a reverse order is not possible. A knowledge of this well-known chemical law brings us to a consideration of the addition of chlorine to our drinking water as a purifying agent. We secure a drinking water that is harmful to the body not because of its harmful germ content but because the chlorine content now causes the body to lose the much-needed iodine."
http://www.jcrows.com/hypothyroidism.html

US Gov medical site: "A metabolic basis for fibromyalgia and its related disorders: the possible role of resistance to thyroid hormone."
http://www.ncbi.nlm.nih.gov/pubmed/12888300

"Fibromyalgia, Hypothyroidism and the Theories of Dr. John Lowe"
http://thyroid.about.com/cs/fibromyalgiacfs/a/drlowe.htm

"In some patients, the inadequate tissue regulation by thyroid hormone results from cellular resistance to thyroid hormone.  In others, the inadequate regulation results from a thyroid hormone deficiency.  So, when I refer to fibromyalgia, I'm referring to a certain set of symptoms and signs of too little thyroid hormone regulation of tissues."
http://www.thyroid-info.com/articles/drlowefms.htm

"Some experts believe that like most cases of hypothyroidism, fibromyalgia is also autoimmune in nature. Others believe that fibromyalgia may be one manifestation of an underactive metabolism – hypometabolism – and is therefore one variation on thyroid dysfunction."
http://thyroid.about.com/cs/fibromyalgiacfs/a/fibrothyroid.htm

FYI - There are a several million people on the web complaining about the lack of good diagnosis and treatment of Hypothyroidism and its related Adrenal issues, which I suffer from as well.

This next site, The National Academy of Hypothyroidism is the best one I have found that explains how the Thyroid Hormones get to their intended location.  It is NOT by diffusion as was previously thought.

“Changes in pituitary conversion of T4 to T3 are often opposite of those that occur in the liver and kidney under similar circumstances. The presence of this pathway of T3 production indicates that the pituitary can respond independently to changes in plasma levels of T4 and T3…Given these results, it is not surprising that a complete definition of thyroid status requires more than the measurement of the serum concentrations of thyroid hormones. For some tissues, the intracellular T3 concentration may only partially reflect those in the serum. Recognition that the intracellular T3 concentration in each tissue may be subject to local regulation and an understanding of the importance of this process to the regulation of TSH production should permit a better appreciation of the limitations of the measurements of serum thyroid hormone and TSH levels (148).”
http://nahypothyroidism.org/deiodinases/9

Book:   Lowe, J.C.: The Metabolic Treatment of Fibromyalgia. Boulder, McDowell Publishing Co., 2000. The only definitive test I have found for Peripheral Tissue Thyroid Hormone Resistance (it's listed in all the pharmacy and hospital computers by the way) is "TSH suppressed  to Zero, and patient can take 125mcg of, T3, liothyronine and it doesn't hurt them, but makes them better,"  as referred to in "The Metabolic Treatment of Fibromyalgia" by Dr. John C. Lowe.  
http://www.goodreads.com/book/show/679258.The_Metabolic_Treatment_of_Fibromyalgia

"At a dose of 125 mcg per day, she began feeling better, her skin and hair improved, and she lost 20 pounds over two months."  Dr. Jacobs
http://www.neuroendocrinology.org/thyroid-hormone-resistance.html  

Book: "In Dr. Starr's description of Type 2 Hypothyroidism, he presents overwhelming evidence showing a majority of Americans suffer this illness, which is due to environmental and hereditary factors." Mark Star MD
http://www.ei-resource.org/related-conditions-books/thyroid-disorders/hypothyroidism-type-2:-the-epidemic/

I have talked to Alan R. Jacobs, M.D., neuroendocrinologist, Mark Star MD, and several fibromyalgia clinics that take Cash only.  Apparently they are all a step ahead of the endocrinologists that I have already seen at Pac Med and the Poly Clinic who can't help me. There are also several Naturopaths that are treating this disorder, but I am curious as to why they all take Cash only, or very limited insurance in some cases? Unfortunately, I have no money due to the lifelong struggle with this disorder that destroyed my life.

Because of what I have learned from my own intensive research in an effort to save my own life, I have come to the conclusion that this is an area of medicine (thyroid hormone resistance - Type 2 hypothyroidism) that is grossly ignored, and very misunderstood.

It is important to note that there are 3 types of Thyroid Hormone Resistance. 'General' Thyroid Hormone Resistance (RTH) is the one that has been identified as most often (85% of the time) having a Genetic cause, however there is also 'Peripheral" (tissue) Thyroid Hormone Resistance (PRTH), and Partial 'Peripheral" (tissue) Thyroid Hormone Resistance (partial PRTH).  The statistics of 1 in 50,000 live births (less than 10,000 people using 2010 population statistics) are about the prevalence of 'General' Thyroid Hormone Resistance and the numbers are from the 1960's.  This informations seems to be what the community of practitioners is relying on.  Yet, current information indicates there may be as many as half the US population affected by 'Peripheral' Thyroid Hormone Resistance and it is genetic, but may also be environmental!  So, not enough attention is being paid to this phenomena.  

"Defects in THRB are the cause of selective pituitary thyroid hormone resistance (PRTH) [MIM:145650]; also known as familial hyperthyroidism due to inappropriate thyrotropin secretion. PRTH is a variant form of thyroid hormone resistance and is characterized by clinical hyperthyroidism, with elevated free thyroid hormones, but inappropriately normal serum TSH. Unlike GRTH, where the syndrome usually segregates with a dominant allele, the mode of inheritance in PRTH has not been established."
http://www.uniprot.org/uniprot/P10828

"Resistance to thyroid hormone (RTH) is an uncommon disorder, characterized by elevated circulating thyroid hormones with non-suppressed thyrotropin (TSH) levels, reflecting resistance within the hypothalamic-pituitary-thyroid axis but variable refractoriness to hormone action in peripheral tissues (2). Usually dominantly inherited, RTH is associated with diverse, heterozygous THRB gene mutations impairing hormone binding and/or transcriptional activity of receptors (3–5). In addition, mutant receptors inhibit the action of their wild-type counterparts in a dominant-negative manner when they are coexpressed (6, 7). The clinical phenotype of RTH is variable: most subjects are either asymptomatic or have nonspecific symptoms and are deemed to be in a compensated euthyroid state termed generalized RTH (GRTH); in contrast, a subset of affected individuals can exhibit some clinical features of hyperthyroidism, suggesting greater central or pituitary RTH (PRTH) than in peripheral tissues. Although imprecise, this clinical distinction may remain useful in the management of the disorder (8). The basis of and mechanisms underlying variable tissue resistance in RTH are not fully understood."  
http://www.jci.org/articles/view/38793

I need someone who understands the nature of Peripheral Thyroid Hormone Resistance and is willing to treat me with the supraphysiologic doses of liothyronine (125mcg) I need, according to my symptoms, to help me stay alive and well. Someone who will listen to me, and provide assistance in the management of this tricky disorder and the Adrenal Fatigue that goes with it.  Preferably someone I can see in person and takes my insurance. (I have plenty of offers for Cash.)

In my research I came across a lot of evidence indicating that Insulin Resistance is strongly linked to Thyroid Hormone Resistance in obese diabetics.  These two conditions may have the same cause.

Thursday, June 21, 2012

UW Medical Center and Thyroid Hormone Resistance

I was told by the office staff that the Medical Director of the University of Washington Medical Center said, "There is no such thing as a Type 2 Hypothyroidism epidemic."  "Tissue resistance to Thyroid Hormones is very rare" "We can't help you with the supraphysiologic doses of thyroid you need."   

Please read the book:  "Hypothyroidism type 2 : the epidemic" by Starr, Mark, M.D. In Dr. Starr's description of Type 2 Hypothyroidism, he presents overwhelming evidence showing a majority of Americans suffer this illness, which is due to environmental and hereditary factors."

http://www.ei-resource.org/related-conditions-books/thyroid-disorders/hypothyroidism-type-2:-the-epidemic/


The UW is supposed to be a leader in Medicine, but they don't BELIEVE a problem exists.  The last time I checked belief was NOT required for a thing to exist!  You must apply some time to Research and Observation to verify if something exists or not. Could this be because the UW gets Pharmaceutical Company Money (to make the truth go away)  for RESEARCH ???


"The University of Washington Pharmaceutical Outcomes Research and Policy Program (PORPP) conducts research and provides graduate and external training in health outcomes and policy research on health care technologies, with a focus on drugs,"  "PORPP is a nationally and internationally recognized center for pharmaceutical economics,"  http://sop.washington.edu/porpp


So, it is obvious they are in it to help the Pharmaceutical Company's economics, NOT the health interests of the people!

Please let them know how you feel about this.  DEPARTMENT OF MEDICINE
University of Washington School of Medicine Administrators Contact Link:

http://depts.washington.edu/medweb/directory/admin.html








Reposted: by Pain Center of Orlando, Inc. Saturday, June 13, 2009


Hypothyroidism: The Silent Epidemic

by Pain Center of Orlando, Inc. on Saturday, June 13, 2009 at 11:56am ·
Hypothyroidism: The Silent Epidemic

Hypothyroidism can be loosely defined as a medical condition that results from the under-secretion of Thyroid Hormone. The difficulty with this traditional approach to diagnosis of hypothyroidism is that it relies on ‘normal values,’ or reference ranges that are defined by the population itself. It has been estimated that as many as 50 million American suffer from undiagnosed hypothyroidism.

Fact #1: Thyroid hormone is necessary to maintain basal metabolic rate, or the amount of fuel that is consumed to sustain health. The manifestation is that of temperature.

a. When a person is generating too little thyroid hormone, or if the individual has an imbalance that involves thyroid metabolism, body temperatures will fall.

b. These persons may be told that they ‘normally have low temperatures.’

c. This bit of nonsense is causing tremendous problems for society.

d. The result is weight gain, depression and elevations in cholesterol levels.

Fact #2: The traditional approach to the diagnosis of hypothyroidism involves measurement of a hormone released by the pituitary gland, TSH. If the central nervous system senses that there is inadequate thyroid hormone in the blood stream, TSH levels will increase. Increase in TSH should lead to increases in the release of Thyroid Hormone from the Thyroid Gland. As levels of Thyroid Hormone reach adequate levels, TSH release decreases.

Problem #1: Unfortunately, a lot can go wrong between the brain, pituitary gland and the thyroid gland, itself. Inadequate levels of thyroid hormone can persist, and the brain will ‘reset’ to new and lower levels of this hormone. Factors that can cause this include:

1. chronic stress

2. pregnancy

3. trauma

4. chronic disease states.

5. autoimmune conditions

6. fasting or famine conditions.

As TSH levels drop back to normal, the diagnosis of hypothyroidism becomes more difficult, if all the practitioner relies upon is the TSH level. Unfortunately, this is the case more times than not.

Problem #2: Thyroid Hormone does not work alone. It requires adequate levels of estradiol, estrone, progesterone, testosterone, cortisol, insulin, DHEA and a host of other hormones, peptides, fatty acids and humoral elements. If any one of these necessary pieces are missing, out of balance, or in excess, thyroid hormone may not work properly, leading to a state of ‘functional hypothyroidism.’

TSH levels, thyroid hormone levels are ‘normal,’ but the body does not function properly and resembles the hypothyroid condition.

Problem #3: Thyroid Hormone replacement may be inadequate or improper for the patient. That is, not all thyroid replacement works for all patients. There are chemicals in some of the commercially available thyroid preparations that cause all manners of problems. One such substance is ‘Acacia,’ which is a family of shrubs and trees, and portions of this plant are used in some medications to provide form and shape to tablets. Lactose is also used in the most popular of the Thyroid Replacement Hormones. Not only is Lactose an allergic trigger for people with lactose intolerance, but it may actually block the absorption of the thyroid replacement, itself. Signs of lactose intolerance include nausea, cramps, bloating, gas, and diarrhea.

It is very common to hear patients tell the doctor that the thyroid medicine that they are receiving is ‘making me sicker.’ Unfortunately, the practitioner does not often make the effort to figure out why this might be the case.

Problem #4: Certain foods make thyroid conditions worse. Patients with auto-immune disorders may be more sensitive to soy-protein than other persons. Soy contains two chemicals that inhibit an important enzyme that is necessary for thyroid hormone replacement. If a person is already ‘on the edge,’ taking soy protein can make the condition worse. To a lesser extent, peanuts, pinto beans do this, as well.

Recommendations:

1. In order to sort through the diagnosis of thyroid related problems, it is important to determine not only the levels of thyroid hormones and TSH, but it is important to determine the presence of antibodies to the binding protein and converting enzymes.

2. If you suspect that you have hypothyroidism, it is necessary to cease eating anything that contains soy, soy lecithin, peanuts and pinto beans.

3. Replacement of thyroid hormone should be accomplished with products that do not contain lactose, Acacia, and artificial colorations.

4. Thyroid hormone must be taken on an empty stomach.

5. Determination of hormone imbalances that affect thyroid metabolism must be accomplished.

David S. Klein, MD, FACA
Pain Center of Orlando, Inc.
225 W. SR 434 Suite #205

Longwood, Florida 32750 dsklein@earthlink.net

www.suffernomore.com

www.stages-of-life.com

Facebook: https://www.facebook.com/note.php?note_id=110687236795

Monday, June 4, 2012

The truth about thyroid testing is finally told


An article form the National Academy of Hypothyroidism   Copyright ©   2012 about Thyroid Hormone Transport


Thyroid hormone transport is an extremely important topic. It must be clearly understood by any physician who hopes to accurately evaluate an individual’s thyroid status and to appropriately treat thyroid dysfunction. Unfortunately, only a small fraction physicians and endocrinologists understand even the basics of thyroid transport, because what they have learned in medical school and continue to be taught regarding this topic is incorrect. When one understands the physiology involved with thyroid hormone transport, it becomes clear that standard blood tests, including the TSH and T4 levels, cannot be used to accurately determine intracellular and tissue thyroid level in the presence of a wide range of common conditions, including chronic and acute dieting, anxiety, stress, insulin resistance, obesity, diabetes, depression and bipolar disorder, hyperlipidemia (high cholesterol and triglycerides), chronic fatigue syndrome, fibromyalgia, neurodegenerative diseases (Alzheimer’s, Parkinson’s and multiple sclerosis), migraines, cardiomyopathy, and aging.
http://nahypothyroidism.org/thyroid-hormone-transport/

“It is clear that serum thyroid hormone and thyroid stimulating hormone concentrations cannot be used with any degree of confidence to classify patients as receiving satisfactory, insufficient, or excessive amounts of thyroxine replacement…The poor diagnostic sensitivity and high false positive rates associated with such measurements render them virtually useless in clinical practice…Further adjustments to the dose should be made according to the patient’s clinical response.” (121)
http://nahypothyroidism.org/thyroid-hormone-transport/

In a study published in the British Medical Journal, Meir et al also investigated the correlation of TSH and tissue thyroid effect. It was shown that the TSH level had no correlation with tissue thyroid levels and could not be used to determine a proper or optimal thyroid replacement dose. The authors concluded that “TSH is a poor measure for estimating the clinical and metabolic severity of primary overt thyroid failure. … We found no correlations between the different parameters of target tissues and serum TSH.” They stated that signs and symptoms of thyroid effect and not the TSH should be used to determine the proper replacement dose (122).
http://nahypothyroidism.org/thyroid-hormone-transport/

In a study published in the Journal of Clinical Endocrinology and Metabolism, Zulewski et al also investigated the accuracy of TSH to determine proper thyroid replacement. The study found that the TSH was not a useful measure of optimal or proper thyroid replacement, as there was no correlation between the TSH and tissue thyroid levels. Serum T4 and T3 levels had some correlation, with T3 being a better indictor than T4. In contrast, a clinical score that involved a thorough assessment of signs and symptoms of hypothyroidism was shown to be the most accurate method to determine proper replacement dosing. The authors also agreed that it is improper to use the TSH as the major determinant of the proper or optimal doses of thyroid replacement, stating “The ultimate test of whether a patient is experiencing the effects of too much or too little thyroid hormone is not the measurement of hormone concentration in the blood but the effect of thyroid hormones on the peripheral tissues [symptoms] (124).”
http://nahypothyroidism.org/thyroid-hormone-transport/

From The Journal of Clinical Endocrinology & Metabolism 2005; 90(12):6403–6409
This study showed that increased T4 and RT3 levels and decreased T3 levels are associated with hypothyroidism at the tissue level with diminished physicial func­tioning and the presence of a catabolic state (breakdown of the body). This study adds to the mounting evidence that giving T4 preparations such as Synthroid and Levoxyl are inadequate for restoring tissue euthyroidism and that a normal TSH cannot be relied upon as as an indication of euthyroidism, as it has a very low sensitivity and specificity for hypothyroidism. This poor sensitivity and specificity is further decreased with the presence of one or more systemic illnesses, including diabetes, heart disease, hypertension, systemic inflammation, asthma, CFS, fibro­myalgia, rheumatoid arthritis, lupus, insulin resistance, obesity, chronic stress and almost any other systemic illness. 
http://www.holtorfmed.com/index.php?section=downloads&file_id=12