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Thyroflex Questionaire:

The following is an excerpt from Chapter 17: Hypothyroidism:The Undiagnosed Epidemic from 13 Secrets to Optimal Aging: How Your Hormones Can Help You Achieve a Better Quality of Life and Longevity, by Kelly Miller DC NMD FASA FBAARM CFMP.*

*Licensed in Chiropractic and Acupuncture in Missouri. “Certified Health Coach” in Florida.

Chapter 17: Hypothyroidism : The Undiagnosed Epidemic

By far, the most difficult hormones to accurately assess are the thyroid hormones. When I attended Logan University of Health Sciences in 1980 I was taught that an initial screening for the thyroid consisted of TSH, T4, and T3. This procedure has changed through the years for the worse, in my opinion. TSH has become the sole standard marker to screen for hypothyroidism. Today’s doctors have been brainwashed to believe this, most probably because the standard treatment now for hypothyroidism is with synthroid or levothyroxine to be determined by TSH only. If the TSH is above the reference range, one of the two drugs above is prescribed. As soon as the TSH comes back into range they are declared cured of the hypothyroidism as long as they continue with the medication. I wish this was the case but it is not. It would be so much simpler if it was true, but it is not. The fact of the matter is that this methodology does not work for the majority of hypothyroid patients because the TSH does not demonstrate the hypothyroidism in most people. Furthermore, even when an individual is prescribed a medication, approximately half of these patients still exhibit multiple overt signs and symptoms of hypothyroidism but the doctor points to the TSH on the report and tells the patient there is nothing wrong with their thyroid. I have heard this story from one my patients hundreds of times. Unfortunately, this is the standard of care despite patients exhibiting numerous signs and symptoms of hypothyroidism. This protocol prevents millions of patients from being treated and millions others under-treated for hypothyroidism.

Over fifty years of research in monitoring basal body temperatures by Dr. Broda Barnes demonstrates that there are many people with hyothyroidism that are being missed by TSH. The clinical experience and writings of Dr. David Brownstein also echo the opinions of Dr. Barnes of widespread hypothyroidism in the population based on signs, symptoms, and lowered basal body temperatures. My personal thirty-seven years of clinical experience of examining and treating patients with hypothyroid symptoms by monitoring their basal body temperature despite a normal reference range of TSH has convinced me of the efficacy. These patients often exhibited temperatures as low as 96 degrees vs. the expected 98.6 degrees. Their thermostats were way off. No wonder they felt tired, fatigued, and could not lose weight. I treated these patients for hypothyroidism and they made improvements in function even though their TSH was within reference range. My conclusions after many patients and many years in clinical practice is that using reference range of TSH, T4, and T3 as determining factors for hypothyroidism is practically worthless. Even patients who had reference ranges in the upper quartile of free T3 often had hypothyroid symptoms. This was all before I discovered the thyroflex.

In November, 2016, one of my mentors, Dr. Paul Ling Tai, told me about an exciting FDA cleared device that detects intracellular T3 levels with a 98.5 % accuracy. My investigation of the device and its implementation in my practice has changed the way I analyze and treat the endocrine system forever.

Before we discuss the thyroflex in more detail let us go over the increased risks for subclinical, also known as type II hypothyroidism, in the literature. There are numerous studies demonstrating significant increased cardiovascular, diabetes, arthritis, inflammatory, and neurological risks for hypothyroid patients.

Several investigations have shown an increase in dyslipidemia (elevated cholesterol and triglycerides), homocysteine, c-reactive protein, coronary disease, hypertension, and ischemic heart disease in people with subclinical hypothyroid.1-11 Several investigators have also found hypercoagulability (sticky platelets and red blood cells), endothelial dysfunction, and peripheral artery disease.12-16 One researcher found a correlation between hypothyroidism and cardiac output. 12

Research from McCluskey showed that disruption of a substance called GLP-1 (glucagon like peptide-1) which signals the pancreas to produce insulin adversely affected cortisol levels and thyroid function in mice.18 Another researcher, Schultes, demonstrated that hypoglycemic episodes in humans caused a decrease in TSH, free T4, and free T3 lasting up to eighteen hours.19 This probably accounts for the reason all people trying to lose weight hit a plateau at 30-90 days. Another researcher showed that beta cell productivity and insulin resistance and triglyceride/HDL ratios all increased with hypothyroidism.20 Research also demonstrates that insulin sensitivity, insulin clearance, and glucose uptake and oxidation increased with normal thyroid function.21-22 Risk of blood sugar dysregulation seems to be reduced with normal thyroid function. 21-22

Dessein showed that in rheumatoid arthritis patients, subclinical hypothyroid patients had dysfunction of glucose metabolism and insulin resistance.19 Innocencio showed that 52% of systemic sclerosis and 32% of rheumatoid arthritis patients also had antibodies for Hashimoto’s disease. The finding of undiagnosed Hashimoto’s disease in these two populations may contribute to low thyroid symptoms in people with other autoimmune disease.20-23

Many musculoskeletal and neurological risks are associted with hypothyroidism. Caskir showed an increase in Dupuytren’s contracture, carpal tunnel syndrome, and decreased joint mobility in people who were subclinically hypothyroid. 26 A polymyositis-like syndrome has been demonstrated in hypothyroid patients.28 Tandeter showed an increased incidence of subclinical hypothyroidism in Parkinson’s patients.27 Davis showed increased hearing loss in hypothyroid patients.25 Other researchers have found abnormal EEG (brain) readings in subclinical hypothyroid patients.30 Several researchers have shown an association between anxiety and depression and hypothyroidism. 29,34 Research from Valpoto demonstrated in 628 women older than 65 years old there was a 1.97 (approximately 2x) relative cognitive loss risk in subclinical hypothyroid women. These multiple findings of abnormal brain functions related to subclinical hypothyroidism is disturbing news as Alzheimer’s disease is now the fastest growing cause of death in the US.

There is research that demonstrates a three-fold increase in placenta previa and a two-fold increase in premature delivery in pregnant women with subclinical hypothyroidism.35 Undiagnosed hypothyroidism could very well be the leading cause of infertility in women.

Had these researchers had the thyroflex at their disposal for analysis I suspect all these patients classified as having sub-clinical hypothyroidism through bloodwork would have been clearly confirmed as hypothyroid. The data base on thyroflex-tested patients is now over 100,000. The findings confirm approximately eighty per cent of those tested exhibit varying degrees of hypothyroidism. This is a percentage proposed by Dr. David Brownstein. We now have objective confirmation with the thyroflex on this clinical finding by Dr. Brownstein as determined by basal body temperature.

The thyroflex measures the speed of the brachioradialis reflex in milliseconds. The observation of diminished or absent reflexes in the hypothyroid patient was made over 100 years ago. This is something most doctors were taught in school but forgotten by many. The original study validating the thyroflex was conducted on 563 patients who were evaluated by measuring thyroid symptoms, age, gender, height, weight, body mass index, calculated RMR (resting metabolic rate), measured RMR with the Douglas Breathing Apparatus (the gold standard), brachioradialis reflex intervals, and serum measurements of TSH, T4,T3, total cholesterol, LDL, HDL, and triglycerides. Some patients had free T4, free T3, and TPO and thyroglobulin antibodies, ACTH, and prolactin measurements as well.

Those patients testing hypothyroid and that were already on thyroid medication received a dosage increase of the same medication if tested abnormal on the thyroflex. People not on medication were given a choice of thyroid treatments including both prescriptive and non-prescriptive choices. All patients were re-evaluated at 30 day intervals and dosages were increased until the brachioradialis reflex interval was < 66 milliseconds.

Subsequent data was gathered on additional patients until 2200 were in the data pool. After that the mathematicians went to work crunching the numbers with cross correlation between the basal body temperature, RMR, and reflex speed. A speed of 50-100 milliseconds was arrived at for optimum thyroid function. A speed of 100-120 milliseconds was considered satisfactory, but marginal. The predictability of correlating thyroid function with brachioradialis reflex speed is 98.5 % accurate. This is far more accurate than bloodwork because it is demonstrating the level of bio-active T3 within the cell not in the serum.

Having this information is invaluable in helping a patient achieve optimum thyroid function and better health. With optimum thyroid function, the sex hormones produced by the adrenals and gonads ae more likely to be higher. If the thyroid is functioning optimally, less dosing may be necessary for the sex hormones to achieve balance.

Call today at 816-210-6913 in Missouri and 813-985-5190 in Florida for your thyroid evaluation.