Wall Street Journal Reporter Helps Bring Clarity to Thyroid Treatment Controversy


On April 11, 2016 an article, Doctors Hear Patients’ Calls for New Approaches to Hypothyroidism, appeared in the Wall Street Journal regarding the growing influence of patient preference on treatment selection for hypothyroidism (sluggish thyroid). The article was written by the WSJ health columnist Melinda Beck. I might have missed it but thanks to a motivated patient I received a copy within a week after its publication.  With a glance I knew this report could be a highly significant addition in the on-going debate between specialists treating hypothyroidism (endocrinologists) and advocates of alternative approaches. (more…)

HCG is a Hairy Hormone

By Gary Pepper, M.D.
Editor, Metabolism.com
In the first article in this series, The HCG-Cancer Connection, I explained how HCG is made by some types of cancer and can serve as a marker for cancer activity. Now I want to explore another effect of HCG, the stimulation of male hormone (testosterone) production.
Just to review, there is no evidence that HCG will cause cancer although conceivably certain cancer responsive tumors may grow faster due to its effect to increase estrogen and testosterone. Every woman who has had a normal pregnancy has been exposed to high HCG levels for many months so if it did cause cancer that effect would be very obvious.
What concerns me is how HCG can influence the normal ovary and its hormone metabolism. HCG is a promiscuous hormone. It will hook up with different hormone “receptors” and masquerade as these other hormones. In the previous article I explained how at very high levels HCG can stimulate the thyroid to make thyroid hormone resulting in hyperthyroidism. Another hormone effect of HCG is to mimic LH (leutinizing hormone) which turns on the production of the sex hormones by the testicle in men and ovary in woman. Surprisingly the normal ovary makes testosterone which it then converts to estrogen. FSH (follicle stimulating hormone) from the pituitary helps the ovary change testosterone to estrogen. What happens when the ovary gets a lot of LH but not FSH? This is the situation when a woman gets HCG. Testosterone levels will rise more than estrogen levels. Research shows that after a single HCG injection a rise of 20% in testosterone levels occurs in normal women, confirming this theory. During pregnancy with HCG pumping in the blood from the placenta, testosterone levels can double, resulting in acne, oily skin and (in some women) an increase in sex drive. The situation would be far worse for a pregnant woman if the placenta wasn’t also pumping out 100 times the normal amount of estrogen to counteract all the male hormones.
So why should women care if HCG makes their testosterone levels go up? Acne, oily skin and horniness are one thing but there are other effects which might be less acceptable. Testosterone is a mischievous hormone. While it causes hair growth where you don’t want it, it causes hair loss in places you want to keep it. Testosterone stimulates hair growth on the face, chest, back and abdomen. At the same time it causes hair loss from the scalp particularly at the temples and crown. This is referred to as male pattern baldness. Other effects of testosterone in women are the growth of the clitoris, known as clitoromegaly. A clitoris the size of a man’s thumb has been described in a woman due to excess testosterone exposure. Generally this degree of clitoromegaly is seen only in more extreme cases. So you may want to think twice before starting an HCG diet unless looking like Bruce Willis is your thing.
In the final installment on the hazards of HCG I will focus on other possible nasty hormone effects of HCG such as fibroids, infertility and bulging muscles.

Will T-3 Help Dana with her weight, hair, skin and mood?

Although we often speak of the metabolic effects of thyroid hormone, we are really referring to the fact that this hormone helps to regulate the function of every system in the body. A system that is often a source of concern is known as the integument; the hair, skin and nails. The effects of disease is often first noticed due to effects on the integument and thyroid disease is one of the most likely to show up here. Brittle hair that sheds easily, and skin that is dry, itchy and flaky are often noticed early in hypothyroidism. Here is Dana’s story and I’m hoping that the addition of T3 will help her lose her excess weight and also reverse the deterioration she is experiencing in her integument, and her nervous system (mood).

Dana writes:

I was diagnosed as hypo a few years ago and my doctor just added 25 mcg of liothyronine (Cytomel) along with 100 mcg of Synthroid. In the past year I have gained 35+ pounds and it’s been alomost impossible to take it off. Last year I competed in my very first fitness/ figure competion. At 135lbs I came in 2nd place. I play softball and basketball on competitve level teams for the psat 15 years and I run about 3-4 times a week. I eat relatively healthy and have recent gone gluten-free, soy free, and nitrate free. Today is my very first day on the combined T3/T4 thereapy. I steppeed on my scale and it said 174lbs. Im hopeful that not only my weight will decrease but my hair will stopp shedding, dry skin/ scalp, joint pain, hopelessness and depression, and fatigue will all go away. I know patience is the key so I will be patient and wait.

My response:

Hi Dana

As you read here, some people are unable to return to normal thyroid equilibrium on t4-treatment alone; this may be due to an inherited form of enzyme defect preventing the normal conversion of the t4 hormone into the more potent t3 hormone; I am happy you found a doctor who will prescribe T3. Sometimes this needs to be given twice daily since t3 is a short acting hormone and the benefit may wear off within 6 to 8 hours. Some people don’t notice this while others definately do.
Good luck with your treatment. Also remember, thyroid hormone allows you to lose weight normally but doesn’t make weight “melt off”. You still have to do the right things with diet and exercise but at least your efforts should start paying off.
Good luck.

Gary Pepper, M.D.
Editor-in-chief, metabolism.com

Obama Not to Blame for Armour Shortage, Says New Member

Will S., a new member of metabolism.com, offers these sensible comments on who to blame for the sad state of FDA oversight of prescription drugs like Armour Thyroid.

Will argues:

Gatekeeper: Just a suggestion to do a little more research on this situation before blaming it on Obama. It was several years ago, at the end of the Clinton and beginning of the Bush administration, that the FDA began to investigate and reveal that Armour Thyroid had never been officially approved by the regulatory agency. Membership on the FDA consists partially of highly paid executives that came from pharmaceutical companies. It makes sense that they have an interest in making sure that only the big pharmaceutical companies have the money to get their drugs approved. Situations like this are why we need health care reform now. Yes, you certainly can and should bring this issue to the attention of the current administration, but please place blame where it is due, as finger pointing in the wrong direction is unhelpful to those who are suffering.

Major Revision Possible in Guidelines for Diagnosing and Treating Hypothyroidism

In a suprise announcement a prominent leader in the field of thyroid disease, Dr. Leonard Wartofsky, suggested that a new lower level of TSH be utilized when attempting to evaluate and treat hypothyroidism.

When diagnosing hypothyroidism (low thyroid function) most physicians are trained to obtain a TSH measurement. TSH (thyroid stimulating hormone) is produced by the pituitary gland not the thyroid. The pituitary’s job is to act like a thermostat regulating the amount of thyroid hormone in the blood. When the pituitary senses thyroid hormone deficiency this “master gland” releases TSH into the blood to stimulate the thyroid to make more thyroid hormone. TSH therefore increases when thyroid hormone levels are low.

According to good medical training, it is appropriate to diagnose hypothyroidism and give thyroid hormone replacement only if the TSH level is above normal. The normal TSH level is generally recognized to be between 0.4 up to 4 or 5 (microIU/ml) depending on the lab where the assay is done.

I have found that relying strictly on the normal TSH range may fail to render a correct diagnosis of hypothyroidism. Take the situation in which an individual’s TSH level a year ago was 1.0 but this year is 2.8. Both of these TSH levels are within the normal range. Hasn’t something changed, however? Why is the pituitary releasing more TSH this year? My thought is in this situation the pituitary is sensing thyroid hormone deficiency and is trying to compensate by releasing more TSH. In such a case it may be appropriate to try thyroid hormone supplementation if there are also complaints compatible with low thyroid function.

The major flaw in the TSH measurement stategy is to fail to recognize how much variation in thyroid function can be hidden within the TSH normal range. To explain this I like to use the analogy of shoe sizes (you heard it here first!). It is common knowledge that although most people have normal foot size, only one shoe size is appropriate for each person. Similarly with TSH, for each individual there is very likely to be a particular level that is the “best fit”. Recall the normal TSH range is between 0.4 and 4.5. This is equivalent to a normal range of shoe size from 4 to 45! How difficult is it then to find the “best fit”?

For years, endocrinologists have debated what level of TSH is appropriate for the diagnosis of hypothyroidism. In a suprise announcement Dr. Wartofsky from Washington Hospital Center suggested lowering the upper limit of TSH to 2.5 (microIU/ml). This was after an analysis showed that 97% of the population had TSH levels below 2.5. In comparison the official American Association of Clinical Endocrinologists (AACE) statement recognizes the upper normal limit as 5.0, although dissenting members of this organization have been using 3.0 as the upper limit. By recognizing that a TSH level of 2.5 may signify thyroid hormone deficiency, Dr. Wartofsky and his colleagues legitimatize treatment with thyroid hormone replacement for a much broader range of patients then ever before. Public action groups have for years been seeking this reform in the medical community’s method for diagnosing and treating thyroid hormone deficiency.

My comments are intended as informational only, not to diagnose and treat medical conditions. Consult your own physician for individual advice on diagnosis and treatment of medical conditions.

Gary Pepper, M.D. Editor-in-Chief, metabolism.com

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