Hypothyroidism & extreme weight gain

Posters, please do not offer medical advice. Stick to non-medical responses

dudara

No problems in asking for a doctor. By the way, I think that this thread is better suited to the Biology & Medicine forum, so I'll move it there.

dudara

Individual people need individual levels of thyroxine - yours might need tweaked, but only your own doctor can do that.

That's the one! Let me know how you're getting on!

This guy is my doctor and he actually tests and treats the thyroid properly. He tests all the stuff that should be tested such as free T3 and free T4 and does not worship the TSH test like so many doctors do. For years I was told that I was fine because my TSH was "normal". Well turns out my Free T4 and Free T3 were both really low and my antibodies very high. Turns out I have had Hashimotos thyroiditis all along. There are so many undertreated thyroid patients around that it is criminal. There are many, many people who do not convert their T4 (storage hormone) into the actual ACTIVE thyroid hormone T3. Therefore eltroxin is useless to them.

This site is brilliant http://www.stopthethyroidmadness.com/site-map/

DrIndy wrote: »

This site is advocating using armour thyroid which is pig thyroid extract over other therapies and I am concerned there is product sponsored bias.

Desiccated pig thyroid is not a good product. It is not licensed in Europe and it is not advocated by the British Thyroid Association.

http://www.british-thyroid-association.org/Guidelines/Docs/Armour_nov_07.pdf

Product sponsored bias? So the millions of patients around the world who still suffer lingering hypothyroid symptoms and/or go undiagnosed are not afflicted by the product sponsored bias of the T4 only meds? These companies have gone so overboard in marketing spin that they have in fact had to pay out $41.8 million dollars in a class action lawsuit http://thyroid.about.com/cs/synthroid1/a/mfrsettlement.htm. You do realise that if people were offered a choice between T4 only meds and desiccated thyroid; more people would improve. Many of them would not need weight loss dugs, statins or anti depressants. Site such as Stop the Thyroid Madness started because so many of us thyroid patients remained ill and untreated/undertreated. We started using desiccated thyroid and we got better. Why would a doctor object to that?

There are MAJOR problems with the BTA's statements and a suspicion that it is the one that is in bed with the pharmaceutical industry. These intelligent rebuttals to it's infamous statements can be found here: http://www.tpa-uk.org.uk/rcp_statement_v_goals.pdf and here http://www.tpa-uk.org.uk/resp_bta_armour.pdf. Not all patients can convert from T4 to T3 and not all patients will display a high TSH. Before the 1970's many patients were diagnosed on clinical grounds and symptoms only. Why allow patients to suffer? Why do you offer your patients a choice between different brands of anti depressants, different antibiotics etc? I assert it is because you realise each patient is unique. So why not offer them a choice between T4 only, synthetic combined T3/T4 or desiccated thyroid extract?

DrIndy wrote: »

The above site is biased and should be taken with a shovel of salt. It ascribes virtually every symptom under the sun as attributed to hypothyroidism and subsequently advocates only one cure to alleviate them.

Yes because it was created by a poor patient who was sick for years on T4 only treatment http://www.stopthethyroidmadness.com/my-story/. So much so that she had to give up working and go on disability benefit. She switched and got better as have millions of us all around the world. Of course she is biased. Those of us who were very sick and are now getting better tend to be that way.

Obviously you have never been hypothyroid. Believe me if you had and T4 only meds did not work for you, you would consider it nothing short of a miracle if another medicine alleviated all your other symptoms. Also, the fact is hypothyroidism does cause many, many symptoms. Personally when any disorder is present, I like to find the root cause rather than a band aid solution for each individual symptom.

Have you ever heard of Broda Barnes? He was able to reduce heart disease incidence in his almost 2,000 patients by 90% for starters, a mark few physicians, if any, have ever matched. He did this without counselling on diet, smoking, or any of that. How did he achieve this? Desiccated thyroid extract.

DrIndy wrote: »

In addition, you are taking a product extracted from another species who's naturally containing proteins are unknown. This was how BSE was originally cross-transmitted from sheep to cows and hence to humans.

This BSE link you consistently refer to has nothing to do with armour. Armour meets the very strict standards advocated by the US Pharmacopeia http://www.tpa-uk.org.uk/:

"The United States Pharmacopoeia (USP) web site states: "Federal law requires prescription and non-prescription medicines sold in the U.S. to meet USP standards, if such standards are available. Manufacturers independently ensure that their products conform to USP standards, where applicable. When medicines meet USP standards, it means that they are pure, consistent in ingredients and strength, and properly labelled and stored. The Food and Drugs Administration (FDA) approves drugs based on manufacturers' own standards. USP sets public standards for products already approved by the FDA. Once USP standards become official, manufacturers must comply with them and the FDA can enforce the standards".

Also here: http://books.google.ie/books?id=LhDchTKf2e4C&pg=PA65&lpg=PA65&dq=desiccated+thyroid+and+BSE&source=bl&ots=AK-pJeSUHF&sig=uggRMxGymIglwUY6wZ1VRXzoEJ8&hl=en&ei=DHTOSazrEYaZjAeujNTqCQ&sa=X&oi=book_result&resnum=2&ct=result#PPA65,M1

Armour has a 100 year history of safe usage so I don't know how you can suggest it is dangerous.

As a doctor I just don't understand why you can't open your mind and read up on the other side of the story. Don't you want your patients to get better?? There are many great authors on the thyroid out there such as Broda Barnes, Mark Starr, Barry Durant-Pietfield and Janie Bowthorpe.

There are now thyroid groups all around the world fighting for our rights as patients to get adequate treatment. You might find them to be of interest:
http://www.tpa-uk.org.uk/index.php
http://www.thyroiduk.org/
http://www.kit-online.org/
http://www.geocities.com/thyroide/

Tallaght01

If you read those links you will see that the papers I link to include multitudes of references http://www.tpa-uk.org.uk/rcp_statement_v_goals.pdf and here http://www.tpa-uk.org.uk/resp_bta_armour.pdf. They are not simply opinion based.

It is also a fact that Synthroid have had to pay out $41.8 million dollars for going overboard on marketing spin. Armour has had fewer FDA citations for potency and quality problems than T4-only medications. Again, another fact.

The only agendas these sites have is getting people well and offering them options. Why is it okay to post the biased BTA statements? There are millions of us around the world who cried with frustration when we read that statement. We have experienced ourselves that what they write is not true so why should we be put on anti depressants or statins for our symptoms when we could just get to the root cause and treat our hypothyroidism? I have a friend on a T4 only med who is still losing her hair, still battling weight and still suffering high cholesterol. Yet I and others that have been switched to armour find that these symptoms go away. What is wrong with letting people have options? That's what bugs me. I believe armour is the best but if others feel well on T4 only meds or synthetic T3/T4 only combos I am happy for them. I just want people to have a choice.

So you want direct references. Okay here we go. I can offer you lots more on specific aspects of the thyroid if you wish:

1) Michalopoulou G, Alevizaki M, Piperingos G, Mitsibounas D, Mantzos E, Adamopoulos P, Koutras DA. High serum cholesterol levels in persons with ‘high-normal’ TSH levels: should one extend the definition of subclinical hypothyroidism? Eur J Endocrinol 1998 Feb;138(2):141-5.

2) Colin M Dayan, Ponnusamy Saravanan, Graham Bayly Whose normal thyroid function is better—yours or mine? Commentary The Lancet 2002 Aug 03; 360 (9330): 353. http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(02)09602-2/fulltext (You have to pay to see this but I am sure students can access it through their library).

3) Elder J, McLelland A, O’Reilly DS, Packard CJ, Series JJ, Shepherd J. The relationship between serum cholesterol and serum thyrotropin, thyroxine and tri-iodothyronine concentrations in suspected hypothyroidism. Ann Clin Biochem. 1990 Mar;27 ( Pt 2):110-3

4) Robertas Bunevicius, M.D., Ph.D., Gintautas Kazanavicius, M.D., Ph.D., Rimas Zalinkevicius, M.D., and Arthur J. Prange, M.D. Effects of Thyroxine as Compared with Thyroxine plus Triiodothyronine in Patients with Hypothyroidism, http://content.nejm.org/cgi/content/short/340/6/424

5) Nicoloff JT, Spencer CA. The use and misuse of the sensitive thyrotropin assay. J Clin Endocrinol Metab. 1990;71:553-8.

6) And of course the infamous Hunt Study:
Thyrotropin Levels and Risk of Fatal Coronary Heart Disease: The HUNT Study
Arch Intern Med. 2008;168(8):855-860. http://archinte.ama-assn.org/cgi/content/abstract/168/8/855

Re: bias it is almost impossible to have no bias whatsoever on any topic. You seem to be a pretty opened minded guy and I know you are just following the board rules. I moderate in a paid capacity myself so am aware of the difficulties. However as a doctor it would be great if you read the other side of the story thoroughly before you denounced it as biased and wrong. There are many respected authors on the thyroid out there such as Broda Barnes, Mark Starr, Mary Shamon, Barry Durant-Peatfield and Ray Peat. Or pay a visit to any thyroid patient group and listen to their stories of mis diagnosis, ill health and under treatment before you decide that I and other armour supporters are wrong.

I think every individual is different and what works for some will not work for others. Quinnie, if you could let us know how you get on that would be great

"Normal" thyroid levels are based on standard devaitions around mean. It therefore stands to reason that there are peolpe out there who are either hypo- or hyper-thyroid but have "normal" blood tests. These are undoubtedly under diagnosed. Great care should be used when dealing with high normal or low normal results especially with contributory symptoms.
That been said most people who have normal thyroid function tests have normal results because they do not have a thyroid problem.

tallaght01 wrote: »

One of the biggest mistakes the public make is thinking that if something gets published, it's true and irrefutable.

Firstly, I certainly do NOT think that. There are a multitude of badly designed studies around. Ancel Keys and his data manipulation comes to mind. Secondly, I know how to read research. Anyway...

I shall elaborate on the Hunt Study. This study was published in 2007 and can be read in detail here http://www.eje-online.org/cgi/content/full/156/2/181

What's our understanding of the issue currently?

Currently, thyroid function is assessed using the TSH (Thyroid Stimulating Hormone) assay. This test came into routine clinical use in the 1970's. It is one in a long line of thyroid function tests that have been utilised since the discovery of hypothyroidism. Such tests have included the basal metabolism test and the protein bound iodine test amongst others. The TSH test has been criticised by certain medical professionals for two specific reasons. One criticism lobbied at the TSH test is that the range is set too high, and that clinically hypothyroid patients are not diagnosed.

Dr. A P Weetman, professor of medicine, wrote in the article "Fortnightly review: Hypothyroidism: screening and subclinical disease," which appeared in the 19 April 1997 issue of the British Medical Journal, the following statement:

". . . even within the reference range of around 0.5-4.5 mU/l, a high thyroid stimulating hormone concentration (>2 mU/l) was associated with an increased risk of future hypothyroidism. The simplest explanation is that thyroid disease is so common that many people predisposed to thyroid failure are included in a laboratory's reference population, which raises the question whether thyroxine replacement is adequate in patients with thyroid stimulating hormone levels above 2 mU/l."

Another criticism lobbied at the TSH is that it is fundamentally a useless diagnostic tool of thyroid function. The TSH is a measure of the feedback mechanism operating between the pituitary gland (TSH is actually a pituitary hormone) and the thyroid. Theoretically, when the body runs low in thyroid hormones, the TSH rises in order to send a message that more thyroid hormones are needed. However, like many theories this has not panned out. The failure of the TSH test in diagnosis is particularly evident in the case of Hashimotos thyroiditis where a person can swing from being hyperthyroid to being hypothyroid. The hyperthyroidism period is caused by the release of thyroid hormones into the blood due to the destruction of the thyroid gland. The hypothyroidism is caused by the lessening function of the thyroid due to the attack. The TSH test also does not measure the actual free unbound thyroid hormones levels.

In a response to the aforementioned article David Derry M.D., Ph.D., a thyroid expert and researcher said:

"Why are we following a test which has no correlation with clinical presentation? The thyroidologists by consensus have decided that this test is the most useful for following treatment when in fact it is unrelated to how the patient feels. The consequences of this have been horrendous. Six years after their consensus decision Chronic fatigue and Fibromyalgia appeared. These are both hypothyroid conditions. But because their TSH was normal they have not been treated. The TSH needs to be scrapped and medical students taught again how to clinically recognize low thyroid conditions."

In 2003 the American Association of Clinical Endocrinologists called for the TSH range to be lowered from 0.5 to 5.0 to 0.3 to 3.04. They stated:

"In the future, it is likely that the upper limit of the serum TSH euthyroid reference range will be reduced to 2.5 mIU/L because >95% of rigorously screened normal euthyroid volunteers have serum TSH values between 0.4 and 2.5 mIU/L."

It appears that the TSH range will continue to be lowered.

The Study:

30,656 people from Nord-Trøndelag County in Norway participated in this study. The group excluded those with known and confirmed thyroid disease, as well as those with cardiovascular disease and diabetes. Levels of total serum cholesterol, HDL, LDL and triglycerides were measured in this population to give a baseline. The participants were followed up for cardiac incidents and mortality rates.

Study design:

This was an observational study. Observational studies tend not to be as powerful as controlled clinical trials; however this study certainly presents an interesting case.

Results:

During median follow-up of 8.3 years, 228 women and 182 men died of CHD. Of these, 192 women and 164 men had TSH levels within the clinical reference range of 0.50 to 3.5 mIU/L. Overall, TSH levels within the reference range were positively associated with CHD mortality (P for trend = .01); the trend was statistically significant in women (P for trend = .005) but not in men. Compared with women in the lower part of the reference range (TSH level, 0.50-1.4 mIU/L), the hazard ratios for coronary death were 1.41 (95% confidence interval [CI], 1.02-1.96) and 1.69 (95% CI, 1.14-2.52) for women in the intermediate (TSH level, 1.5-2.4 mIU/L) and higher (TSH level, 2.5-3.5 mIU/L) categories, respectively.

This is a very recent study so it has not been included in large meta- analyses.

Conclusion:

The findings of this observational study suggest that the ranges of TSH usually regarded as normal contributes to cardiovascular disease, abnormal lipid patterns and death. While several other studies have likewise shown a relationship of higher TSH/lower thyroid function with lipid abnormalities and heart disease, no previous study has plumbed the depth of TSH to this low level and on such a large scale.

These findings may be enough cause to begin thinking seriously about monitoring thyroid function more seriously to uncover "borderline" TSH increases in the "normal" range.

Perhaps it is time to use clinical observations, basal temperatures and free thyroid hormones as tests of thyroid function in patients?

Or maybe it is best to leave the TSH as a test of pituitary function since it is a pituitary hormone rather than a thyroid hormone. TSH has merit as a tool for diagnosing hypopituitarism but not hypothyroidism.

DrIndy wrote: »

Can someone have subclinical hypothyroidism with a normal TSH? Yes seems to be consensus from this evidence. What can be done is the next question.

There seems to be many, many doctors who will REFUSE point blank to offer any treatment options to a person who falls within the standard range. I LOVE my normal GP but I went to her a few years ago because I could not lose weight I had gained despite rigorous exercise and a VERY strict diet; I was cold ALL THE TIME; I had high cholesterol and my waking temperature tended to be around 35.8. I begged her to test my thyroid function so she tested TSH and total T4 only. Naturally my TSH was totally normal along with my total T4. I was basically told that medical science hadn't figured out all the answers to my problems. A year later, after having battled the same symptoms all this time I decided to go to someone who would investigate ALL my hormones as I knew there was something wrong. My TSH remained normal but my antibodies were very high and my Free T3 and Free T4 very low. So finally, I got diagnosed and treated.

My answer to your question then is:
1) Go back to the old ways and diagnose hypothyroidism on clinical grounds.
2) Utilise the basal temperature test which has proven to be VERY effective in catching cases of sub clinical hypothyroidism. Personally I find it strange that one can have a temperature of 39C and a doctor will have no qualms in saying there is a problem. Yet going to a doctor with symptoms and a waking temperature of 35C somehow means nothing???
3) Use labs wisely. Current thyroid experts such as Dr. Mark Starr, Dr. David Derry and Dr. Barry Durant-Peatfield all have suggested that one should have a free T3 at least in the top third of the lab range (even over it) and the free T4 at least mid range. Antibodies of course should be as low as possible but it takes time to reduce them. While we are at it T3 should always be measured instead of just T4 only. After all T3 is the active thyroid hormone.
4) Throw out the TSH test as a measure of thyroid function.

Part of the problem is that doctors and the lay public do not realise how common hypothyroidism is. Whether it is due to toxins in the environment, people living longer, or people's lifestyles being unhealthy I don't know. In the case of Ireland, we are certainly not helped by having our water supply contaminated by fluoride (a known thyroid suppressor that used to be used to treat hyperthyroidism). Since doctors do not think of it as common they are less likely to be on the lookout for it. However depression and weight problems are seen as common so doctors accept that and are willing to prescribe band-aid solutions for those problems. In fact, those patients with excess weight and depression could be just undiagnosed hypothyroid patients. However most of these people will not be diagnosed. I am not blaming doctors. Most are just not educated enough about the thyroid. Perhaps some thyroid experts need to give talks at medical schools around the globe or some very famous person with hypothyroidism needs to speak out about it. I don't know.

As for armour, the ratio of T3:T4 between Armour and human thyroid production is not the same, but it's not hugely different. Isn't a synthetic medication a xeno as well? It's not exactly bio-identical either. Bear in mind that medical students ALWAYS dissect a pig. Every time, never fails. Why? Because their endocrine systems are nearly identical to humans. There has to be a reason for that. In addition, if there were such controversies surrounding using different species - why do surgeons use valves from PIG hearts on heart surgeries? Why do they use whale blubber in lipstick and perfumes if it's such a danger to use organic products from other species on human beings? I have read of a paper (Gaby AR.”Sub-laboratory hypothyroidism and the empirical use of Armour thyroid”. Altern Med Rev. 2004 Jun;9(2):157-79 http://www.ncbi.nlm.nih.gov/pubmed/15253676?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum) where the doctor reported on her own patients' finding desiccated thyroid relieved their symptoms greatly, however I have not been able to locate the entire paper anywhere. Again, I am aware that it is not a double blind, placebo controlled clinical trial, but you might find it interesting.

True Thyroid T3/T4 in the Serum is 1:4. However the Thyroid Gland & the Cells have aT3/T4 ratio of 1:3, the same as Armour has. Note that the brain has T3 concentrations up to six times higher than serum levels & that T4 is usually expelled by the Brain. Note too that high T4 levels (such as when taking T4 only) can cause the brain to produce Rt3. So Thyroxine (T4) meds are certainly not "natural". Nor are the T3/T4 combos of 1:4. The closest to a healthy Thyroid Gland is Armour at 1:3.

So Thyroxine (T4) meds are certainly not "natural". Nor are the T3/T4 combos of 1:4. The closest to a healthy Thyroid Gland is Armour at 1:3. I have highlighted the pertinent facts in the excerpts below.

As for Armour possibly containing pathogens, do you remember when everyone with insulin-dependent diabetes took bovine or porcine insulin? It's not so long ago (15 years or so only) and there are many who continue to take it as their endos have determined that the synthetic human insulin wasn't working for them and put them back on animal insulin.

The dessicated thyroid in Armour and similar products actually goes through a lot of processing, like the bovine insulin. The thyroid glands are soaked in an acetone bath for defatting, for one thing - and acetone is a virucidal, fungicidal and bactericidal agent. It's far safer than eating meat, in terms of pathogens.

Prion risk is very, very small to nonexistent - prion disease is very rare in pigs, there's currently no evidence of porcine-human prion transmission, and there's been some decent research done in that area because of attempts to transplant porcine islet cells to humans. You have more risk of prion disease eating a steak than you do taking Armour regularly.

Armour is to pig thyroid glands as a handful of poppyseeds is to codeine or morphine, or willowbark and aspirin. :-) Highly processed, standardised, and safe.
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Excerpts from....

Thyroid: Therapies, Confusion, and Fraud

http://raypeat.com/articles/articles/thyroid.shtml

Years ago it was reported that Armour thyroid, U.S.P., released T3 and T4, when digested, in a ratio of 1:3, and that people who used it had much higher ratios of T3 to T4 in their serum, than people who took only thyroxine.

The argument was made that thyroxine was superior to thyroid U.S.P., without explaining the significance of the fact that healthy people who weren’t taking any thyroid supplement had higher T3:T4 ratios than the people who took thyroxine, or that our own thyroid gland releases a high ratio of T3 to T4.

The fact that the T3 is being used faster than T4, removing it from the blood more quickly than it enters from the thyroid gland itself, hasn't been discussed in the journals, possibly because it would support the view that a natural glandular balance was more appropriate to supplement than pure thyroxine.

The serum’s high ratio of T4 to T3 is a pitifully poor argument to justify the use of thyroxine, instead of a product that resembles the proportion of these substances secreted by a healthy thyroid gland, or maintained inside cells.

About 30 years ago, when many people still thought of thyroxine as "the thyroid hormone," someone was making the argument that "the thyroid hormone" must work exclusively as an activator of genes, since most of the organ slices he tested didn't increase their oxygen consumption when it was added.

In fact, the addition of thyroxine to brain slices suppressed their respiration by 6% during the experiment. Since most T3 is produced from T4 in the liver, not in the brain, I think that experiment had great significance, despite the ignorant interpretation of the author. An excess of thyroxine, in a tissue that doesn’t convert it rapidly to T3, has an antithyroid action (see Goumaz, Et Al, 1987). This happens in many women who are given thyroxine; as their dose is increased their symptoms get worse.

The brain concentrates T3 from the serum, and may have a concentration 6 times higher than the serum (Goumaz, et al., 1987), and it can achieve a higher concentration of T3 than T4. It takes up and concentrates T3, while tending to expel T4. Reverse T3 (RT3) doesn’t have much ability to enter the brain, but increased T4 can cause it to be produced in the brain. These observations suggest to me that the blood's T3:T4 ratio would be very "brain favourable" if it approached more closely the ratio formed in the thyroid gland, and secreted into the blood. Although most synthetic combination thyroid products now use a ratio of four T4 to one T3, many people feel that their memory and thinking are clearer when they take a ratio of about three to one. More active metabolism probably keeps the blood ratio of T3 to T4 relatively high, with the liver consuming T4 at about the same rate that T3 is used.

Since T3 has a short half life, it should be taken frequently. If the liver isn't producing a noticeable amount of T3, it is usually helpful to take a few micrograms per hour. Since it restores respiration and metabolic efficiency very quickly, it isn't usually necessary to take it every hour or two, but until normal temperature and pulse have been achieved and stabilized, sometimes it's necessary to take it four or more times during the day. T4 acts by being changed to T3, so it tends to accumulate in the body, and on a given dose, usually reaches a steady concentration after about two weeks.

An effective way to use supplements is to take a combination T4-T3 dose, e.g., 40 mcg of T4 and 10 mcg of T3 once a day, and to use a few mcg of T3 at other times in the day. Keeping a 14-day chart of pulse rate and temperature allows you to see whether the dose is producing the desired response. If the figures aren't increasing at all after a few days, the dose can be increased, until a gradual daily increment can be seen, moving toward the goal at the rate of about 1/14 per day.


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With thyroid patients everyone's dose is different, because we are aware that the amounts of T4 and T3 we need are not set in stone. No one knows exactly how much of each we should be having because everyone's situation is different - some can't convert T4 to T3 properly so the doses have to be calibrated. Trial and error and symptom monitoring is the best way to treat.

I do have one question for you though: Where and how did you form your opinion of armour? Were you taught this during your medical degree?

With respect,

Lynnsback