A Question Regarding Lithium

During the past 24 hours a Natural Health News reader was searching for information about the use of lithium and any connection it may have with Alzheimer's Disease.

Lithium is often used in mental health for people with the alleged diagnosis of Bipolar dis-order or also referred to as manic-depressive illness.

Using lithium has some serious side effects to consider, the major one leading to severe thyroid problems. Regular blood testing is required. Lithium toxicity is a risk as is retention with diuretic use or kidney function issues.

Proper function of the thyroid is important in aging and memory issues. I have mentioned many times that in the past those physicians who were well educated about aging and dementia routinely prescribed vitamin B12 shots and natural thyroid.  Dementia was very infrequent during this time, about 40-60 years ago.  Some more informed physicians today are returning to this protocol.

Acute Lithium Intoxification

Thyroid and Heart Connection: Known for Decades

UPDATE 3 July, 2010
Larry Frieders, the compounder, THYROID MADNESS DEFINITION:

1.Treating hypothyroid patients solely with T4-only meds (synthroid)
2.Dosing solely by the TSH and the total T4, or using the outdated "Thyroid Panel"
3.Prescribing anti-depressants in lieu of evaluating and treating the free T3
4.Telling thyroid patients that desiccated natural thyroid like Armour is "unreliable", "inconsistent", "dangerous" or "outdated".
5.Making lab work more important than the hypo symptoms which scream their presence
6.Failing to see the OBVIOUS symptoms of poorly treated thyroid, and instead, recommending a slew of other tests and diagnoses.

9/23/08 - I am pleased to see this topic in the medical article arena. I'd like it more if I saw it in mainstream news. This way there might be some hope that patients would pressure their doctors to run annual thyroid panels, especially for the over 35 crowd, as the AMA recommended about 15 years ago or more.

Endocrine function is closely related to heart function. This is very true for good thyroid health and good gallbladder health, among related issues.

I don't agree that the TSH alone is sufficient for good thyroid evaluation. A Free T3 and a Free T4 are very necessary. If you've never had a reverse T3 (rT3) it's not a bad idea to add that in for baseline, as it does relate to autoimmune issues that are becoming more common today.

Does Your Doctor Know About the New TSH Lab Standards?

I'd be happier too if providers would get current on the TSH et al ranges: The Clinical Endocrinologists (AACE) are currently suggesting that TSH is 0.3-3.0 mU/L.
Over 13 Million Americans with Thyroid Disease Remain Undiagnosed

It is also a good idea to refer to the National Academy of Clinical Biochemistry, part of the Academy of the American Association for Clinical Chemistry (AACC), Laboratory Medicine Practice Guidelines: Laboratory Support for the Diagnosis and Monitoring of Thyroid Disease

"It is likely that the current upper limit of the population reference range is skewed by the inclusion of persons with occult thyroid dysfunction."

"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."

"A serum TSH result between 0.5 and 2.0 mIU/L is generally considered the therapeutic target for a standard L-T4 replacement dose for primary hypothyroidism."

"Thyroxine requirements increase during pregnancy. Thyroid status should be checked with TSH + FT4 during each trimester of pregnancy. The L-T4 dose should be increased (usually by 50 micrograms/day) to maintain a serum TSH between 0.5 and 2.0 mIU/L and a serum FT4 in the upper third of the normal reference interval."

Optimally, cardiologists have a lot to gain by talking cross-specialty.

Patients have much more to lose if they don't.

From this article, ranges not current with ACCE recommendations. "Normal thyroid function (euthyroid; TSH 0.45 - 4.5 mU/L), those with subclinical hypothyroidism (divided into moderate, TSH 4.5 - 9.9 mU/L, and severe, ≥ 10.0 mU/L), and those with subclinical hyperthyroidism (TSH < 0.45 mU/L)."

3 July, 2010 - And consider this article on thyroid and heart health

From Heartwire — a professional news service of WebMD

September 22, 2008 — A new study has found that older adults with severe subclinical hypothyroidism had almost double the risk of developing heart failure (HF) compared with those with normal thyroid function over a 12-year follow-up period [1]. Dr Nicolas Rodondi (University of Lausanne, Switzerland) and colleagues report their findings in the September 30, 2008 issue of the Journal of the American College of Cardiology.

Rodondi told heartwire that these results were in line with those of the only other study to have looked at subclinical hypothyroidism and HF incidence, which also found an increased HF risk only in those with high levels of thyroid-stimulating hormone (TSH).

The findings are important to inform the debate about subclinical hypothyroidism, he says. "There is a big controversy about whether we should screen and treat people with subclinical hypothyroidism. We know that people with overt hypothyroidism with symptoms need to get treated, but about those with no symptoms and just subclinical disease, there is debate. And within this debate about whether to treat or not is another controversy about the threshold at which you should treat."

These and other results from prior studies support the recommendations of several guidelines that those with subclinical hypothyroidism and no symptoms should be treated with thyroxine only if their TSH is 10.0 mU/L or more, Rodondi says. However, he points out that some endocrinologists disagree and advocate treating such patients at lower TSH levels. The debate is important, he says, because it is has been shown that monitoring of TSH levels under thyroxine is not always accurate in clinical practice, with overtreatment having its own attendant risks.

"Indirect evidence" that thyroxine might prevent HF

Rodondi and colleagues studied 3044 adults who were 65 or older participating in the Cardiovascular Health Study, all of whom were free of HF at baseline. They compared adjudicated HF events over a mean of 12 years of follow-up and changes in cardiac function over the course of five years among those with normal thyroid function (euthyroid; TSH 0.45 - 4.5 mU/L), those with subclinical hypothyroidism (divided into moderate, TSH 4.5 - 9.9 mU/L, and severe, ≥ 10.0 mU/L), and those with subclinical hyperthyroidism (TSH < 0.45 mU/L).Over the follow-up period, 736 people developed HF events. Those with TSH 10.0 mU/L or more had a greater incidence of HF compared with euthyroid participants (adjusted HR 1.88, p=0.01). No such increased risk was seen in those with TSH 4.5 - 9.9 mU/L or in those with subclinical hyperthyroidism compared with euthyroid participants.Baseline peak E velocity — an echocardiographic measure of diastolic function associated with incident heart failure in the cohort — was also greater in those with TSH 10.0 mU/L or more compared with euthyroid participants (0.80 m/s vs 0.72 m/s; p=0.002). And over the course of five years, left ventricular mass increased among those with TSH 10.0 mU/L or more, although other echocardiographic measures were unchanged. In a further exploratory analysis, the researchers stratified people with TSH 10.0 mU/L or more into those who received thyroxine replacement therapy and those who didn't. They found that those who got thyroxine did not have an increased risk of HF, "providing indirect evidence that [thyroxine] might work to prevent development of HF in those with TSH 10.0 mU/L or more," said Rodondi. He stressed, however, that "to definitively prove a link between subclinical thyroid dysfunction and HF, a randomized clinical trial would be needed in which one group is treated with thyroxine vs placebo to see if the former reduces the risk. That would be proof of concept, but it has not been done as yet." Overtreatment with thyroxine has risks too Rodondi said their findings — that those with less severe subclinical hypothyroidism do not seem to be at risk of HF — are "important," because a high proportion of older adults fit into this category and are treated with thyroxine in clinical practice, without consistent evidence that this is of benefit. Monitoring of TSH levels under thyroxine is not always accurate in clinical practice, he explains, and it is estimated that around 20% to 30% of people receiving thyroxine are overtreated. This in itself has risks, as subclinical hyperthyroidism has been associated with atrial fibrillation and increased fracture risk. "In aggregate, our findings might help refine a treatment threshold at which clinical benefit would be expected and demonstrate a subpopulation at risk for a life-threatening condition," he and his colleagues say in their paper."Clinical trials should examine the efficacy of screening for and treating subclinical thyroid dysfunction and assess whether the risk of HF might be ameliorated by thyroxine replacement in individuals with TSH levels above 10 mU/L," they conclude.Source: Rodondi N, Bauer DC, Cappola AR, et al. Subclinical thyroid dysfunction, cardiac function and the risk of heart failure. The Cardiovascular Health Study. J Am Coll Cardiol. 2008;52:1152-1159.

Your Eyes and Cell Phone Damage

Many years ago, perhaps in the mid 90s, an attorney I know, and a HAM radio operator, was talking with me about EMF. He pointed out that for a very long time the FCC has had on its licensing exam a question regarding the fact that EMF (radio waves) are a known cause of cataract.

This article looks at the issue again and also points out the importance of keeping the cell phone as far away from you as possible.

This is the same concern in regard to cell phone effect on your thyroid gland and function.

Nutrients 4 Eye Health

Cell phones can damage eyes: Study
Prashant Rupera, TNN, Jun 23, 2010

VADODARA/ANAND: While scientists across the globe are still debating whether usage of cell phones results in heart diseases, a new study carried out by scientists at Charotar University of Science and Technology (CHARUSAT) has revealed that mobile phones also affect eyes.

The scientists, who have studied the impact of electromagnetic waves on human eye, say that usage of mobile can also lead to early cataract in lens apart from affecting retina, cornea and other ocular systems of the eye.

"We are in ocean of electromagnetic signals and hundreds of signals are hitting human body every moment. It is affecting all our body parts, but we are not realising it," says professor Ved Vyas Dwivedi, head of department of ECE at CHARUSAT, who along with dean of the faculty of engineering and technology Y P Kosta and lecturer Dhara Patel carried out the study based on a mathematical model.

"The wavelength of wireless signals (which is about 2 to 2.5 cm) used for mobile phones and other wireless terminals matches with that received by the human eye. The dielectric constant (absorption capacity) of eye tissues is around 70 which is greater than unity (above 50). This means that the eye can absorb electromagnetic energy very quickly," explains Dwivedi.

During the study, scientists computed the specific absorption rate (SAR) and maximum temperature increase in the eye because of electromagnetic radio frequency fields generated by wireless terminals such as a mobile phones. SAR and temperature rise depend on the distance between eye and radio frequency transceiver (the mobile phone) and the angle between the line of sight and shortest normal path.

"The problem is not that the eye absorbs the energy, but that the heat absorbed by the eye does not get transmitted or radiated out of the body," says Dwivedi, adding that prolonged usage of mobile phones can affect retina, sclera, lens, cornea as well as vitreous humour which are parts of the human eye.

These scientists have also recommended that a mobile handset should be kept as far as possible from the eye. "It should not be used more than is necessary. A user should avoid use of mobile in rural areas or a car where the cell phone uses more power and the SAR value can be ten or hundred times higher than the normal," they suggest. This group of scientists is also planning to approach the government in collaboration with a hospital to get license to conduct tests on human to further study mobiles affect on human eye.

prashant.rupera@timesgroup.com
THE TIMES OF INDIA

Experts make Down syndrome and Alzheimer`s eye link

ODDLY IN BOTH DOWN SYNDROME AND ALZHEIMER'S, HIGH INCIDENCE OF THYROID PROBLEMS EXIST AS WELL

Eye problems can be a symptom of thyroid imbalance

Contact Lenses News :: Experts make Down syndrome and Alzheimer`s eye link

Taking Too Many Pills

There is a recent TV commercial for Crestor that has a woman explaining about how her doctor put her on the drug to help her reduce LDL, or what is marketed as " bad cholesterol".

When I hear this commercial I want to have equal time to explain something very important to doctors and to women.   Since I don't have the gazillions of disposable income that the PhRMA companies have, I don't have a snowflake's chance in hell of this, so I'll address it here.

One of the most problematic health issues today is thyroid function.  Part of the problem is that it is not only overlooked as important in today's Big Insurance+Big PhRMA controlled medical care, but it is also porrly diagnosed.

Yes, folks, the TSH test won't tell you " squat" !

What also is missing is that thyroid dysfunction cause your cholesterol level to rise.

Since this concept is basic physiology why is your doctor pushing a drug on you to lower cholesterol when properly evaluating thyroid function is a much better place to start?

This is also very much related to gall bladder function which can be resolved without "cutting it out" !

Another generally overlooked is the vital part sound nutrition plays in the prevention and treatment of disease, yet mainstream media continues to ignore this vital concept.

Recently, the New York Times also looked at the issue of pushing pills, especially as the vultures from PhRMA and the buzzards from Big Insurance begin their efforts to round you up for the kill, following the passing of the so-called "health" bill. (Just recall that HillaryCare wanted everyone to be taking Prozac, and we know what a disaster the SSRI drugs have become.)

Risks Seen in Cholesterol Drug Use - "With the government’s blessing, a drug giant is about to expand the market for its blockbuster cholesterol medication Crestor to a new category of customers: as a preventive measure for millions of people who do not have cholesterol problems."
http://www.nytimes.com/2010/03/31/business/31statins.html?partner=rss&emc=rss

And so did the London Daily Mail

D. Mail 29.3.10 "A NATION OF PILL-POPPERS"
Dept of Health data reveals we each pick up more than 16 prescriptions a year on average, twice as many as 20 years ago. The boom is partly put down to a profit-hungry pharma industry inventing & exaggerating ailments & then blitzing doctors to boost sales. The NHS spent £22million a DAY on prescription drugs in England in 06 - a 60% rise in real terms on 10 years earlier.
-
(A colleague's comment: Prof. Michael Oliver, emeritus professor of Cardiology at Edinburgh University, wrote in the British Medical Journal in March last year that healthy older people are being turned into patients by GPs who are too quick to prescribe pills for high blood pressure, cholesterol & mild diabetes. The standard for these is based on much younger people's needs. The professor stated that few older people are allowed to enjoy being healthy as a bureaucractic demand for documentation can lead to over-diagnosis, over-treatment & unnecessary anxiety - known as "the medication of health." GPs are pressurised by the government to hit targets & this has overtaken personal advice from GPs. Incentives known as "Quality & Outcomes Framework" mean a proportion of GP practice-income is dependent on hitting targets. He questions whether patients are warned about medications' side-effects & whether older people could be allowed to return to their previous unencumbered & reasonably fit lives.

Please note that our organization offers an excellent thyroid testing kit, and health and nutrition counseling,
http://leaflady.org/detect.html

Thyroid Concerns, again

I pulled out this paragraph of Fox's article to point out an error in "standard of care" currently.

No one can effectively determine your thyroid function by only a measurement of TSH.

An no lab worth its salt should be using the old TSH range of up to 5 or in some cases up to 8.

The current standard was lowered by the clinical endocrinologists 4-5 years ago and the "high" end of the range is now about 3.

And if you don't by my argument on the 'just TSH' approach, read what John Lowe has to say about it.

And skip the Synthoid unless you want to be foreced on to a bisphosphonate fluoride based bone destroying drug to add to what is already harmed by Synthroid. Just in case your doctor failed to explain to you.
"The thyroid, located in the neck, is a kind of master gland, secreting hormones that affect metabolism. Doctors usually check its activity by an indirect measure -- looking at levels of TSH, or thyroid stimulating hormone."

Low thyroid? Maybe you're an "elephant"By Maggie Fox, Health and Science Editor Fri Jun 12, 6:31 pm ET

WASHINGTON (Reuters) – Low thyroid activity, one of the most treated conditions in the United States, may actually be a sign of longevity, researchers reported on Friday.

While they said it was far too soon for people taking thyroid pills to stop, they will be looking to see if the thyroid may hold the key to a long life, at least for some people.

Dr. Martin Surks and colleagues at the Montefiore Medical Center and the Albert Einstein College of Medicine in New York studied hundreds of people who had lived to be 100, and found evidence that people with low thyroid activity were more likely to be in that group.

"We studied a large group of Ashkenazi Jews with exceptional longevity," Surks told a news conference at a meeting of the Endocrine Society, specialists in human hormones.

They used a large national survey of health to see what the average hormone levels are for people of various ages.

The thyroid, located in the neck, is a kind of master gland, secreting hormones that affect metabolism. Doctors usually check its activity by an indirect measure -- looking at levels of TSH, or thyroid stimulating hormone.

High TSH levels suggest the thyroid is underactive, a condition known as hypothyroidism. Low levels suggest it is overactive, known as hyperthyroidism.

People with low thyroid function may lose hair, gain weight and feel sluggish, while those with overactive thyroids may lose weight, feel their hearts race and have trembling hands Both can be easily treated with a daily pill.

Surks and colleagues found 15 to 20 percent of people over the age of 60 had TSH levels that suggest an underactive thyroid gland. He told the meeting he believed that may be normal for older people and may in fact be a sign of longevity.

"We estimate that 70 percent of old people whose TSH was minimally elevated and who were considered to have hypothyroidism were actually in their age-specific limits," Surks said in a telephone interview.

OLD AGE

They singled out 200 Jews who had lived to be 100, and 400 of their children. Two genetic changes were linked with low thyroid function but also with extreme old age.

Metabolic rate affects life span in animals. For instance, elephants have slow metabolic rates, slow heartbeats, and can live for decades, as opposed to mice, which have fast metabolisms and live for just months.

It may be, Surks said, that people with low thyroid function in old age were "elephants" with a slow metabolism who can live longer, as compared to 'mice" with fast metabolic rates who may have shorter natural life spans.

"If you are an older person with high TSH, this suggests you are on the road to a long life," Surks said.

What worries him is that millions of people in the United States are being treated for hypothyroidism. "In North America, thyroid hormone is used at the drop of a hat," he said.

His group is seeking to see if that might interfere with a person's natural life span.

Surks noted that having a low thyroid function before about age 50 is a separate condition and appropriately treated with hormones.

He also plans studies to see what the biological function of having high TSH levels might mean for cells and aging.

(Editing by Peter Cooney)

Use Current Standards for Accurate Diagnosing

Read More about thyroid, radiation exposure and cancer: Keep in mind that your mobile phone radiates the region in your neck surrounding the very important thyroid gland.

Originally posted 9/23/08 -

From time to time people are searching for information on results of the TSH
(thyroid stimulating hormone) test.

The correct range currently and for the last several years for TSH is 0.3 to 3 or 3.2 mU/L. Even some whose TSH result is in this narrowed range may still be suffering with symptoms realted to abberation in thyroid function.

One medical naturopath overlooked low thyroid in a client and focused on getting cholesterol down, not the low thyroid that raises cholesterol.

A reader of NHN this morning seems to have been told a level of 6+ is "normal".

The old range used to be up to 8, some have been using 5. Both are invalid.

From this article, ranges not current with ACCE recommendations. "Normal thyroid function (euthyroid; TSH 0.45 - 4.5 mU/L), those with subclinical hypothyroidism (divided into moderate, TSH 4.5 - 9.9 mU/L, and severe, ≥ 10.0 mU/L), and those with subclinical hyperthyroidism (TSH < 0.45 mU/L)"

From Heartwire — a professional news service of WebMD

September 22, 2008 — A new study has found that older adults with severe subclinical hypothyroidism had almost double the risk of developing heart failure (HF) compared with those with normal thyroid function over a 12-year follow-up period [1]. Dr Nicolas Rodondi (University of Lausanne, Switzerland) and colleagues report their findings in the September 30, 2008 issue of the Journal of the American College of Cardiology.

Rodondi told heartwire that these results were in line with those of the only other study to have looked at subclinical hypothyroidism and HF incidence, which also found an increased HF risk only in those with high levels of thyroid-stimulating hormone (TSH).

The findings are important to inform the debate about subclinical hypothyroidism, he says. "There is a big controversy about whether we should screen and treat people with subclinical hypothyroidism. We know that people with overt hypothyroidism with symptoms need to get treated, but about those with no symptoms and just subclinical disease, there is debate. And within this debate about whether to treat or not is another controversy about the threshold at which you should treat."

These and other results from prior studies support the recommendations of several guidelines that those with subclinical hypothyroidism and no symptoms should be treated with thyroxine only if their TSH is 10.0 mU/L or more, Rodondi says. However, he points out that some endocrinologists disagree and advocate treating such patients at lower TSH levels. The debate is important, he says, because it is has been shown that monitoring of TSH levels under thyroxine is not always accurate in clinical practice, with overtreatment having its own attendant risks.

"Indirect evidence" that thyroxine might prevent HF

Rodondi and colleagues studied 3044 adults who were 65 or older participating in the Cardiovascular Health Study, all of whom were free of HF at baseline. They compared adjudicated HF events over a mean of 12 years of follow-up and changes in cardiac function over the course of five years among those with normal thyroid function (euthyroid; TSH 0.45 - 4.5 mU/L), those with subclinical hypothyroidism (divided into moderate, TSH 4.5 - 9.9 mU/L, and severe, ≥ 10.0 mU/L), and those with subclinical hyperthyroidism (TSH < 0.45 mU/L).

Over the follow-up period, 736 people developed HF events. Those with TSH 10.0 mU/L or more had a greater incidence of HF compared with euthyroid participants (adjusted HR 1.88, p=0.01). No such increased risk was seen in those with TSH 4.5 - 9.9 mU/L or in those with subclinical hyperthyroidism compared with euthyroid participants.

Baseline peak E velocity — an echocardiographic measure of diastolic function associated with incident heart failure in the cohort — was also greater in those with TSH 10.0 mU/L or more compared with euthyroid participants (0.80 m/s vs 0.72 m/s; p=0.002). And over the course of five years, left ventricular mass increased among those with TSH 10.0 mU/L or more, although other echocardiographic measures were unchanged.

In a further exploratory analysis, the researchers stratified people with TSH 10.0 mU/L or more into those who received thyroxine replacement therapy and those who didn't. They found that those who got thyroxine did not have an increased risk of HF, "providing indirect evidence that [thyroxine] might work to prevent development of HF in those with TSH 10.0 mU/L or more," said Rodondi.

He stressed, however, that "to definitively prove a link between subclinical thyroid dysfunction and HF, a randomized clinical trial would be needed in which one group is treated with thyroxine vs placebo to see if the former reduces the risk. That would be proof of concept, but it has not been done as yet."

Overtreatment with thyroxine has risks too

Rodondi said their findings — that those with less severe subclinical hypothyroidism do not seem to be at risk of HF — are "important," because a high proportion of older adults fit into this category and are treated with thyroxine in clinical practice, without consistent evidence that this is of benefit.

Monitoring of TSH levels under thyroxine is not always accurate in clinical practice, he explains, and it is estimated that around 20% to 30% of people receiving thyroxine are overtreated. This in itself has risks, as subclinical hyperthyroidism has been associated with atrial fibrillation and increased fracture risk.

"In aggregate, our findings might help refine a treatment threshold at which clinical benefit would be expected and demonstrate a subpopulation at risk for a life-threatening condition," he and his colleagues say in their paper.

"Clinical trials should examine the efficacy of screening for and treating subclinical thyroid dysfunction and assess whether the risk of HF might be ameliorated by thyroxine replacement in individuals with TSH levels above 10 mU/L," they conclude.

Source: Rodondi N, Bauer DC, Cappola AR, et al. Subclinical thyroid dysfunction, cardiac function and the risk of heart failure. The Cardiovascular Health Study. J Am Coll Cardiol. 2008;52:1152-1159.

Thyroid care off base in the US too...

Thyroid concerns are perhaps a greater health concern that realized. This may be related to low selenium levels in food, the thyroid suppressing effect of water fluoridation, the rise in the number and use of fluoride based prescriptions drugs, and increased presence of drug waste in water. Rising impact of EMF-ELF proliferation and depleted uranium are environmental concerns.

HOT NEWS

DID YOU KNOW: Thyroid therapy was used to cure polio and breast cancer, as well as prevent dementia?

There is quite a substantial body of science regarding thyroid health on the web. Just as with anything, some of the information may be incorrect, however the majority of valuable data comes from longtime researchers and providers like Dr. Barnes, Dr. Wilson, Dr. Lowe and others.

Once again on a trip back to the future, people with thyroid problems and the thyroid were not disregarded as "flakes". And it seemed that doctors knew what tests to order and how to properly interpret them s well. They also had no fear of natural thyroid products such as Armour.

Today, it seems as if the thyroid is some taboo gland that will, if not functioning very well on the hypothyroid side, lead you only to the following scenario - a TSH only test - or if you are lucky you might get a TSH and a T4 - and maybe if your result is outside the old range up to 5 or even 8, you might get Synthroid.

Synthroid is synthetic T4 and it usually does not effectively address the physiological issues present. It also can lead to osteoporosis in long term treatment.

One problem is that several years ago the range for TSH results were redefined at 0.3 to 3.2. So if your doctor, NP, or lab is still relying on the old scale, get a new one.

And if they rely on the old scale, maybe they don't even know how to interpret the results.

Some people may need T3, like Cytomel, but with compounding pharmacies being attacked maybe this is herd to come by where you live.

Many people do not do well on Synthroid and really need natural glandular products, or a combination product like Thyrolar.

And you can have normal appearing lab results and still have a problem, which indicates more testing like an rT3 and/ or a TRH, and not to overlook both Free T3 and Free T4.

On the other side of the coin is a group of people with hyperactive thyroid conditions who are "radiated" to "kill" the gland and then require supplementation, usually Synthroid. This group of people should know that there are effective ways to address this situation, as hypothyroid as well, using natural therapy or in combination with drugs; usually you do not hear this too.

Of course it is worthwhile to consider that adrenal function might be evaluated first, and corrected if needed, before addressing thyroid concerns. Its that TPA (Thyroid-Pituitary-Adrenal) axis thing you know...

"The prevailing dogma says that all you need to know is that the TSH test is the gold standard for diagnosis, and the only treatment is T4-replacement/levothyroxine. Even then, the dogma usually stipulates that you use Synthroid, the top-selling levothyroxine drug, the most expensive of all the brands, the one that has legions of drug reps in its employ, and the one that not coincidentally spreads around millions in research money, grants, honoraria, freebies, samples, and support to doctors, endocrinologists, professional groups and patient organizations each year.

People deserve to know that:
there are other brands of levothyroxine than Synthroid, and despite a doctor's allegiance to one brand, another brand may work better for you (not to mention cost you far less)
some patients will not be relieved of their hypothyroidism symptoms -- such as fatigue, depression, weight gain -- despite treatment to the so-called "normal range," and will need additional treatment to regain their health
patients deserve to know that there are other thyroid medicines that for some, may better relieve their symptoms -- additional T3 as Cytomel or time-released T3, a synthetic T4/T3 combination Thyrolar, or the natural desiccated prescription thyroid drugs Armour and Nature-throid
the TSH test itself is one part of diagnosing thyroid problems, but T4, T3, free T4, free T3 tests, antibodies tests, clinical evaluation of signs and symptoms, and consideration of medical and family history, should also be part of a thorough diagnostic process for thyroid disease
The TSH "normal" range that is used to rule thyroid disease in and out may not be relevant on an individual basis, it may be flawed, and it is subject to change, making it a rocky foundation on which to base an entire diagnosis and treatment regimen"

from David Odom, MD, a UK physician: "Of course, this move in Britain is politically based. This document is no more than ossified opinion. This is in a country that has 'cookbook' medicine. So, politics rules! Likely, this our future, approaching rapidly. In my practice, I have the patient supplement Thyroid USP, so as to maintain relief from low thyroid symptoms while maintaining a youthful Free T3 (& coincidentally suppressing TSH). It is ironic that the British medical literature has pointed out 'the emperor's new clothes' regarding treatment of hypothyroidism. It turns out that suppression of the TSH is an expected consequence of thyroid supplementation that has no adverse health consequences, moreover the TSH has no specific or reliable correlation with thyroid function. The large majority of medical practitioners follow the system of prescribing synthetic levothyroxine to regulate the TSH, even though this practice has no scientific foundation. Doctors who practice Natural Hormone Replacement therapy, on the other hand, prescribe Thyroid USP or compounded T4/T3 combinations, seeking symptom reversal without regard to the TSH and find success with great benefit for patients."

Thyroid disorders 'misdiagnosed'
People with suspected thyroid disorders are being mistreated and misinformed, experts have warned.

British Thyroid Association doctors say some people are being given the wrong tests and the wrong treatment.

NHS doctors abide by expert guidelines - but the BTA says the problem comes when patients go outside the NHS.

Around 3% of the UK population has an underactive thyroid, which should be diagnosed with a blood test and treated with a synthetic hormone.

An under-active thyroid, or hypothyroidism, develops when the thyroid gland produces too little thyroxine, and it is becoming more prevalent because of the ageing population.

Symptoms can include being very tired, feeling the cold, having difficulties with memory or concentration, weight gain and fertility problems.

These are symptoms that can mimic other conditions, and experts warn an incorrect diagnosis could mean some patients could suffer harmful effects from excess thyroid hormones, while other serious conditions may go undiagnosed.

The Royal College of Physicians (RCP) recently set out guidance for how hypothyroidism should be diagnosed and treated in the UK.

It says the only accurate way to diagnose a thyroid disorder is via a blood test which measures hormone levels, and the only scientifically proven way of treating the condition is by topping up a patient's natural thyroxine levels with a synthetic form of the hormone.

But the BTA warns that information on the web and in the media about alternative ways of diagnosing and treating the condition are leading people to turn to alternative methods of diagnosis and treatments.

It says urine tests, saliva tests and measuring body temperature are not reliable ways of diagnosing the condition.

Confusion

Dr Amit Allahabadia, the secretary of the BTA who wrote the editorial, said: "This is potentially an enormous problem, given that in any one year, one in four people in the United Kingdom have their thyroid function checked.

He added: "I think it is essentially doctors who are outside the NHS [who] may be misdiagnosing the condition.

"Patients may go to see them when they think they have an under-active thyroid, or when tests have shown they have normal hormone levels but they still feel ill."

Dr Allahabadia said he believed a "significant minority" of patients were affected, either directly through misdiagnosis or mistreatment or because they were being confused by inaccurate information.

Professor Peter Trainer, who chairs the clinical committee of the Society for Endocrinology which represents the specialists who treat thyroid disorders, said: "Our sympathy has to lie with the patient because there is potentially misleading information available on the web.

"It can be confusing for patients, and it can be difficult for GPs when they are confronted with that information, which is why the RCP guidance was published."

Story from BBC NEWS:http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/7965417.stm
Published: 2009/03/27 © BBC MMIX

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Alzheimer's drugs double death risk

Use of Fluoride containing anti-psychotics included in this study. Another issue to consider above most for problems with Alzheimer's disease.

Fluoride suppresses proper function of the thyroid gland. As I have mentioned elsewhere, 67% of people in Alzheimer's care facilities in 1998 had a thyroid disorder. Anyone on long term use of a fluoride containing drug, in an area where fluoride is forced into the municipal water system, is already on fluoride overload.

I guess I wonder where are those asking the right questions...

Alzheimer's drugs double death risk in elderly
By MARIA CHENG, AP Medical Writer
Thu Jan 8, 2009

LONDON – Anti-psychotic drugs commonly used to treat Alzheimer's disease may double a patient's chance of dying within a few years, suggests a new study that adds to concerns already known about such medications.

"For the vast majority of Alzheimer's patients, taking these drugs is probably not a worthwhile risk," said Clive Ballard, the paper's lead author, of the Wolfson Centre for Age-Related Diseases at King's College London.

"Would I want to take a drug that slightly reduced my aggression but doubled my risk of dying? I'm not sure I would," Ballard said.

The research was published Friday in the medical journal, Lancet Neurology.

Alzheimer's disease is the most common cause of dementia and causes symptoms including aggression, delusions and hallucinations. Previous studies have shown anti-psychotic drugs, which can help control the aggression and hallucinations for a few months raise the risk of death in older patients with dementia. There are other side effects, including respiratory problems and stroke.

Ballard and colleagues followed 165 patients aged 67 to 100 years with moderate to severe Alzheimer's disease from 2001 to 2004 in Britain. Half continued taking their anti-psychotic drugs, which included Risperdal, Thorazine and Stelazine. The other half got placebos.

Of the 83 receiving drugs, 39 were dead after a year. Of the 82 taking fake pills, 27 were dead after a year. Most deaths in both groups were due to pneumonia.

After two years, 46 percent of Alzheimer's patients taking the anti-psychotics were alive, versus 71 percent of those not on the drugs. After three years, only 30 percent of patients on the drugs were alive, versus 59 percent of those not taking drugs.

In the United Kingdom and the United States, guidelines advise doctors to use anti-psychotic drugs cautiously and temporarily. But in many nursing homes in Europe and North America, up to 60 percent of patients with dementia are routinely given the drugs for one to two years.

"The drug regimen for any person with Alzheimer's needs to be personalized," said William Thies of the Alzheimer's Association in the U.S. Thies was not connected to the study. "At some points, some people will be better off with no medication."

Simon Lovestone of the Institute of Psychiatry at King's College in London said psychiatrists should try environmental or behavioral therapies instead of anti-psychotics.

Experts aren't sure how the anti-psychotics increase patients' risk of dying. But they think the drugs could be damaging to the brain and their sedative effects make patients less able to exercise and more susceptible to deadly infections.

The study was paid for by the U.K. Alzheimer's Research Trust. Ballard reported receiving grants from various pharmaceutical companies which make drugs used to treat Alzheimer's patients.
___

On the Net: http://www.lancet.com
Copyright © 2009 The Associated Press. All rights reserved

The Lancet Neurology, Early Online Publication, 9 January 2009
doi:10.1016/S1474-4422(08)70295-3
Longterm Risk of Death for Alzheimer's and Use of Antipsychotics
Editors' note: Antipsychotics do not improve cognitive or neuropsychiatric outcomes in most patients with dementia, and serious concerns have been raised about their side effects in the very old. Increased mortality rate and risk of cerebrovascular events have been reported by previous studies of relatively short duration (usually 12 weeks). In this article, the DART-AD investigators report long-term mortality rates among patients with Alzheimer's disease in residential care after 12-months of neuroleptic treatment, adding to the growing evidence against the use of antipsychotics in this vulnerable population.

The dementia antipsychotic withdrawal trial (DART-AD): long-term follow-up of a randomised placebo-controlled trial.

Original Text: Clive Ballard MD a , Maria Luisa Hanney PhD b, Megan Theodoulou MRCPsych c, Simon Douglas BSc d, Rupert McShane MRCPsych e, Katja Kossakowski BSc a, Randeep Gill MBBS a, Edmund Juszczak MSc f, Ly-Mee Yu MSc f, Robin Jacoby DM c, for the DART-AD investigators

Background: Data from 12-week placebo-controlled trials have led to mounting concerns about increased mortality in patients with Alzheimer's disease (AD) who are prescribed antipsychotics; however, there are no mortality data from long-term placebo-controlled trials. We aimed to assess whether continued treatment with antipsychotics in people with AD is associated with an increased risk of mortality.

Methods: Between October, 2001, and December, 2004, patients with AD who resided in care facilities in the UK were enrolled into a randomised, placebo-controlled, parallel, two-group treatment discontinuation trial. Participants were randomly assigned to continue with their antipsychotic treatment (thioridazine, chlorpromazine, haloperidol, trifluoperazine, or risperidone) for 12 months or to switch their medication to an oral placebo. The primary outcome was mortality at 12 months. An additional follow-up telephone assessment was done to establish whether each participant was still alive 24 months after the enrolment of the last participant (range 24—54 months). Causes of death were obtained from death certificates. Analysis was by intention to treat (ITT) and modified intention to treat (mITT).

This trial is registered with the Cochrane Central Registry of Controlled Trials/National Research Register, number ISRCTN33368770.

Findings: 165 patients were randomised (83 to continue antipsychotic treatment and 82 to placebo), of whom 128 (78%) started treatment (64 continued with their treatment and 64 received placebo). There was a reduction in survival in the patients who continued to receive antipsychotics compared with those who received placebo. Cumulative probability of survival during the 12 months was 70% (95% CI 58—80%) in the continue treatment group versus 77% (64—85%) in the placebo group for the mITT population. Kaplan—Meier estimates of mortality for the whole study period showed a significantly increased risk of mortality for patients who were allocated to continue antipsychotic treatment compared with those allocated to placebo (mITT log rank p=0·03; ITT p=0·02). The hazard ratio for the mITT group was 0·58 (95% CI 0·35 to 0·95) and 0·58 (0·36 to 0·92) for the ITT population. The more pronounced differences between groups during periods of follow up longer than 12 months were evident at specific timepoints (24-month survival 46% vs 71%; 36-month survival 30% vs 59%).

Interpretation: There is an increased long-term risk of mortality in patients with AD who are prescribed antipsychotic medication; these results further highlight the need to seek less harmful alternatives for the long-term treatment of neuropsychiatric symptoms in these patients.

Funding: UK Alzheimer's Research Trust.

Sjogren's Fatigue and Cancer Drugs

UPDATE: 26 January, 2009. Related article.
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Rituximab is a (monoclonal antibody genetically engineered) drug mainly used as a treatment for Non-Hodgkin's Lymphoma. It may also be used for the treatment of Rheumatoid Arthritis. Now you may receive it if you have fatigue from a thyroid related (generally thought of as auto-immune) dis-order called Sjogren's.

Make sure if this is proposed to you that you get this information that the drug may cause

severe and sometimes fatal infusion reactions. Tell your doctor right away if you develop blurred vision, cough, dizziness, drowsiness, headache, hives, itching, swelling, trouble breathing, or wheezing, while you receive or after you receive Rituximab .

Severe and sometimes fatal kidney problems and skin reactions may also occur during treatment with Rituximab . Tell your doctor right away if you experience decreased urination; red, swollen, peeling, or blistered skin; or skin or mouth sores or ulcers.

Rarely, a severe and sometimes fatal viral infection of the brain has been reported with the use of Rituximab in certain patients. Tell your doctor right away if you notice new or worsening medical problems such as changes in thinking (eg, confusion, disorientation), loss of balance or coordination, muscle weakness, trouble walking or talking, or unusual eye movements or vision changes.

You might also pursue proper thyroid testing, as thyroid dysfunction often is associated with fatigue.

And it now might be related to low levels of vitamin D-

Researchers at UCLA tried to show that low vitamin D would make an autoimmune thyroid problem worse. Their experiment was based on the idea that vitamin D has a dampening effect on an excessive and inappropriate immune response in many areas of your body, so they figured this was likely to apply to the thyroid as well. This turned out not to be the case, but what they did find was rather surprising.

First they created two groups of mice, one with vitamin D in their diet and the other with none. Even before they started their experiment they found that the vitamin D deficient mice had low levels of thyroxine (t4), meaning they were actually hypothyroid prone when the experiment was conducted. When the experiment was performed, vitamin D lacking mice did not have an excessive immune response as expected. Rather, they developed persistent hyperthyroidism because their thyroid glands were less able to withstand the stress of the experiment and were more sensitive to the autoimmune antibodies that both sets of mice were being exposed to. Simply put, a lack of vitamin D makes your thyroid more susceptible to injury that could result in hyperthyroidism.

While this is an animal study, the findings are important. First, it means that a lack of vitamin D contributes to the possibility of low thyroid. Second, it means that many irritants are likely to aggravate your thyroid to a greater extent if you lack vitamin D. For example, there are many chemical irritants in the environment that irritate your thyroid gland, such as perchlorate and fluoride. If you lack vitamin D you are more likely to be adversely affected by them.

This may be part of the reason that so many people feel metabolically worse and gain weight as the winter months move along. It is simple to make sure you take some extra D in the winter and doing so may help you keep your metabolism and thyroid from suffering the winter blues. Courtesy Wellness Resources.

Rituximab May Ease Fatigue in Sjogren's Syndrome By David Douglas

NEW YORK (Reuters Health) Nov 06 - Results of a pilot study suggest that rituximab may reduce fatigue in patients with Sjogren's syndrome and thus may improve quality of life, UK researchers report in the November issue of the Annals of the Rheumatic Diseases.

Dr. Paul Emery of Allerton Hospital, Leeds, and colleagues studied 17 patients with a fatigue score of more than 50 on a 100-mm visual analogue scale. They were randomized in a double-blind fashion to receive 2 infusions of rituximab 1 g or placebo. All patients also received oral and intravenous steroids.

At 6 months, 7 of the 8 patients receiving rituximab showed a greater than 20% improvement in the VAS for fatigue. This was true of only 5 of the 9 patients who had placebo.

Overall, there was a significant 36.8% improvement in fatigue VAS in the rituximab group compared to a non-significant 17.9% improvement in the placebo group. General health was also significantly improved in the active treatment group, but not in the placebo group.

There was also a significant difference in measures of social functioning and a trend towards improved mental health scoring in the rituximab group.

Commenting on the findings, Dr. Emery told Reuters Health that "this was the first randomized controlled trial in Sjogren's syndrome to show benefit, in particular a significant improvement in fatigue, a major issue for patients. This pilot study will now be followed by a more definitive study."

Ann Rheum Dis 2008;67:1541-1544.

IODINE AND SJOGREN'S SYNDROMEWe encourage - especially in darker and colder seasons - the use of iodine supplementation. This need is increased with fluoridated municipal water supplies and use of fluoride based drugs in the antibiotic, antidepressant, anticholesterol and antiosteoporosis drugs et al. We also encourage the proper use of selenomethionine in the support of proper thyroid function.

Thyroid dysfunction in primary Sjogren's syndrome: a long-term followup study.
D'Arbonneau F, Ansart S, Le Berre R, Dueymes M, Youinou P, Pennec YL.

Arthritis Rheum. 2003 Dec 15;49(6):804-9.

"OBJECTIVE: To evaluate the prevalence of thyroid dysfunction and related autoantibodies in patients with primary Sjogren's syndrome (pSS), and to determine whether these abnormalities develop over time. METHODS: pSS patients (n = 137) and controls (n = 120) were investigated for thyroid dysfunction and for the presence of anti-thyroid peroxidase antibody (anti-TPO) and antithyroglobulin antibody (ATG). Followup time for patients was 1-16 years, and 72 of the 120 controls were reevaluated 3 years after initial evaluation. RESULTS: Thyroid disease was more frequent in the pSS patients than in the controls (30% versus 4%; P < 10(-4)), as were anti-TPO and ATG (11% versus 3%; P < 0.02, and 3% versus 1%, not significant). Ten of 107 euthyroid pSS patients dropped out of the study, and thyroid dysfunction became apparent at followup in 12 of the remaining 97. Most of the patients with thyroid-related autoantibodies at entry developed autoimmune thyroid disease thereafter. CONCLUSION: Thyroid dysfunction is frequent in pSS patients, and those prone to develop thyroid disorders are identified by thyroid-related autoantibodies, or by rheumatoid factor and anti-Ro/SSA activity."

Thyroid disease in primary Sjogren syndrome. Study in a series of 160 patients.
Ramos-Casals M, Garcia-Carrasco M, Cervera R, Gaya J, Halperin I, Ubieto I, Aymami A, Morla RM, Font J, Ingelmo M.

Medicine (Baltimore). 2000 Mar;79(2):103-8.

"We studied 160 consecutive patients (147 female and 13 male) with primary Sjogren syndrome (SS) to determine the prevalence and clinical significance of thyroid disease in a large series of patients with primary SS from our unit and to compare the prevalence and significance with those in 75 individuals without SS from a primary care center. Serum levels of thyroid hormones (free thyroxine, triiodothyronine, and thyroid-stimulating hormone) and autoantibodies against thyroglobulin (TgAb) and thyroid peroxidase (TPOAb) were measured in all SS patients and in 75 control patients. Fifty-eight (36%) of the 160 patients with primary SS had evidence of thyroid disease. Autoimmune thyroid disease (ATD) was diagnosed in 32 (20%) patients and nonautoimmune thyroid disease (NATD) in 26 (16%). No significant differences were found when these prevalences were compared with those in control patients. On the other hand, comparing those patients with altered hormonal profiles, patients with NATD showed mainly hyperthyroidism (10/17, 59% versus 2/20, 10% in patients with ATD, p = 0.001). Finally, when clinical and immunologic manifestations of SS were analyzed in patients with and without thyroid disease, respectively, we found that patients with thyroid disease had a higher prevalence of female gender (98% versus 88%, p = 0.03), antiparietal cell autoantibodies (33% versus 12%, p = 0.002), TgAb (30% versus 5%, p < 0.001), and TPOAb (40% versus 5%, p < 0.001). In conclusion, thyroid disease occurred in more than one-third of patients with primary SS; the main cause was ATD, which was present in 20% of the patients studied. We note that no significant differences were observed when the prevalence of thyroid disease (either ATD or NATD) was compared with that in a control group of similar age and gender. Our results indicate that middle-aged women (with or without SS) should be screened periodically for thyroid function."

Autoimmune thyroid disease in primary Sjogren's syndrome.
Perez B, Kraus A, Lopez G, Cifuentes M, Alarcon-Segovia D.

Am J Med. 1995 Nov;99(5):480-4.

"PURPOSE: To evaluate the prevalence of autoimmune thyroid disease and thyroid dysfunction in patients with primary Sjogren's syndrome. PATIENTS AND METHODS: Thyroid function of 33 patients with primary Sjogren's syndrome was clinically and biochemically evaluated. Thyroid hormones and autoantibodies against thyroid peroxidase, thyroglobulin, and thyroid hormones were measured. RESULTS: Autoimmune thyroid disease and thyroid dysfunction were found in 15 cases (45%): autoimmune thyroiditis in 8 (24%); autoimmune hyperthyroidism in 2 (6%); and reversible iodine-induced hypothyroidism in the remaining 5 (15%). One or more of the evaluated autoantibodies were detected in 8 euthyroid patients (24%). Overall, the prevalence of autoantibodies against thyroid peroxidase, thyroglobulin, thyroxine, and triiodothyronine was 45%, 18%, 42%, and 36%, respectively. CONCLUSIONS: The high prevalence of autoimmune thyroid disease and thyroid dysfunction found in primary Sjogren's syndrome, using sensitive immunologic and thyroid function tests, suggest that both diseases are more frequently associated than it was previously thought, and should be sought clinically and by laboratory tests in all patients with primary Sjogren's syndrome."