Synthroid and breathing problems

[Guest guest]

Hi all,

I have been having breathing problems while on synthroid. I a don't

take it, I don't have the problem. I take it again and have the

breathing problem again, especially at night.

Here is an amazing article that someone from another thyroid group

posted. It has information that most of you have never heard before,

I am sure.

http://www.drlowe.com/jcl/comentry/breathingproblems.htm

Air Hunger to Death:

Breathing Problems from

too Little Thyroid Hormone Regulation

Dr. C. Lowe

February 25, 2005

Last week I consulted long distance with a young

hypothyroid woman who had a distressing

symptom—trouble getting a deep enough breath. She told

me, " I just can't seem to get in enough air. " She said

her doctor doesn't believe her hypothyroidism is the

cause of her breathing problem.

I referred the patient to sections of my book The

Metabolic Treatment of Fibromyalgia.[1] In those

sections, I explain that her labored breathing is a

troubling symptom for which some hypothyroid patients

seek medical care.[2, 11-13, 15-24] Medical journals

contain many reports that some patients with

hypothyroidism or thyroid hormone resistance have

labored breathing. The difficult breathing is called

" air hunger " or " dyspnea. " Air hunger, however, isn't

the worst of the breathing troubles of some patients

with too little thyroid hormone regulation.

In The Metabolic Treatment of Fibromyalgia,[1] I

explain mechanisms of these patients' air hunger, all

of which result from too little thyroid hormone

regulation. One mechanism is weakness of their

respiratory muscles, including the diaphragm[22][23]

Another is impairment of the phrenic nerves that

innervate the diaphragm. When impaired, the nerves

send too few nerve signals to the diaphragm for it

contract normally.[23] Researchers call this weakness

of respiratory muscles " hypothyroid myopathy. " A third

mechanism is decreased " central drive of respiration. "

This means that brain centers that regulate breathing

are impaired by too little thyroid hormone regulation.

Still another mechanism is abnormal heart and lung

function.[14][15][20] Some patients suffer from air

hunger only when they exert themselves; others do so

even at rest.

The young hypothyroid woman I consulted with had been

on T4-replacement for three months. She had been

troubled with hypothyroid symptoms, including air

hunger, for a year before her doctor diagnosed her

hypothyroidism. The T4-replacement had slightly

improved her fatigue and dry skin, but not her air

hunger. Her dose of T4 was 100 mcg (0.1 mg) per day.

I was not surprised that the patient was still

suffering from hypothyroid symptoms, including air

hunger. To illustrate, consider study data reported by

a group of endocrinologists in 1997.[30] They measured

nine hypothyroid patients TSH levels and their resting

metabolic rates in relation to their doses of T4. I

analyzed their data from a different perspective from

which they did.

At one point in the study six of the endocrinologists'

nine patients had used 100 mcg (0.1 mg) of T4. For

three of the six patients, this dose provided normal

metabolic rates, although the rates of two patients

were low normal. These two patients' metabolic rates

were 7% and 9% below the calculated average rate. (We

consider a rate abnormally low only if it's 10% or

more below the calculated average rate). For the other

three patients, however, the 100 mcg of T4 was

woefully inadequate: One patient's metabolic rate was

18% below normal, and another's was 23% below, and a

third patient's was 26% below normal.

The endocrinologists didn't report this finding. I

found it by analyzing at their data from a different

perspective. This perspective shows that some

hypothyroid patients are kept hypometabolic on 100 mcg

of T4. We find this regularly in our clinic when we

measure the metabolic rates of patients on

T4-replacement. And 100 mcg of T4 is obviously not

working for this young woman, whose main troubling

symptom is air hunger.

Doctor-Caused Lifelong Breathing Problem. Yesterday I

consulted long distance with a woman in her seventies

whose breathing troubles have been far worse than

those of the young woman I mentioned above. In the

early 1970s—before the tyranny of the TSH began—an

endocrinologist treated her for hypothyroidism.

Through trial-and-error, he found that her safe and

effective dose of Armour Thyroid was 6 grains (360

mg).

She remained well on that dose until, years later, a

second endocrinologist found her TSH level suppressed.

The patient had no symptoms of overstimulation, but

despite that, this endocrinologist insisted that she

reduce her dose of Amour. She complied, lowering it to

4.5 grains (270 mg).

" Soon, " she told me, " I simply was not functional. I

was gasping for air and coughing so bad that I felt

like I was damaging my lungs. " For eight weeks, she

had to sit upright on a sofa and couldn't put her head

back to rest it. If she did, she couldn't breathe.

When her daughter, a nurse, phoned the

endocrinologist, he denied that the patient's

breathing problem was related to her lower dose of

Armour. He advised her to consult an

ear-nose-and-throat specialist. She saw a lung

specialist instead, and he prescribed 40 mg of

cortisone and an inhaler. The inhaler enabled her to

get through her days. But even with the help of the

inhaler, she couldn't walk up a short flight of stairs

without gasping for air. Her voice was so badly

affected that she could no longer sing, which she had

always enjoyed. " I could only croak, " she said.

In March of 2004, she located the first

endocrinologist who in the early 1970s had put her on

6 grains of Armour. Her put her back on that dose. " It

took me the rest of the year to get off the cortisone

and get well, " she told me. " Before the second

endocrinologist lowered my Armour dose, I'd never had

any asthma or other breathing problems. Now I'm left

with a lifelong breathing problem. " She's largely over

the breathing problems that began on the lower dose,

but she still has to use an inhaler one or two times

each day.

I admire this woman's strength of character in

wresting control of her health from her doctors. Some

of them have recently tried to persuade her to lower

her dose again. " They simply don't listen when I tell

them what happened to me on the lower dose. I feel

that I'm up against a wall of idiocy, " she said. " I

don't have too many years left to fool around with

their book theories, and I'm not going to let them

kill me. " The tragic fact is, of course, that many

doctors today would sacrifice her health and, indeed,

even her life; like fanatics in other walks of life,

any price the patient might pay is worth achieving

their chief aim—keeping the patient's TSH " in range. "

Asthma. Studies show that thyroid hormone increases

the activity of beta2-adrenergic receptors and, as a

result, increases responsiveness of brochial tissues

to adrenaline and noradrenaline.[28] Patients

stimulate these receptors with some inhalants to

relieve their asthmatic symptoms. An alternative to

using the inhalers is to take an effective daily dose

of thyroid hormone to increase the activity of the

receptors. T3 is especially useful for this purpose.

In 1991, Egyptian researchers treated 23 children with

chronic bronchial asthma with T3.[29] The children had

normal thyroid test results. During the 30 days of

treatment, they continued to use their usual

anti-asthma drugs as need, but they reduced the doses

as low as they could.

The researchers wrote, " They all reported at the end

of the 30 days an obvious subjective improvement of

their asthmatic conditions with a decrease in the

number of exacerbations. Seven patients stopped their

usual anti-asthmatic medicines, being maintained on T3

only and 3 have decreased the amount of

bronchodilators needed. A significant improvement of

pulmonary function tests was noted in all patients. "

According to the researchers, " All patients tolerated

well the T3 regimen without any adverse effect. " They

concluded that T3 induced beneficial effects: T3

" proves to be a useful adjuvant to classic anti-asthma

therapy, and may reduce the amount of bronchodilators

needed. "

Other researchers reported that patients with asthma

became hypothyroid from using an iodine-containing

expectorants. When they became hypothyroid, their

asthma worsened. The asthma improved, however, when

they stopped using the expectorants and their thyroid

function became normal again.[27]

Another group of researchers took hypothyroid children

off thyroid hormone for a month. By the end of the

month, the children's brochial tubes became more

reactive than before to antigens. Heightened

reactivity of the bronchial tubes to antigens, of

course, is the mechanism of allergy-induced asthma.

The children then resumed their thyroid hormone

therapy. However, their bronchial tubes remained more

reactive to antigens for two more months. Then, twenty

days later, their bronchial tubes became normally

reactive to antigens.[26]

Other researchers sensitized the airways of rats to an

antigen (ovalbumin) by injected it beneath the mucous

membranes. Two weeks later, the rats inhaled the

antigen to see if it provoked an allergic response.

Hypothyroid rats had an abnormal response, largely

because they had a markedly reduced level of

immunoglobulin E(IgE). The IgE level became normal

after the researchers treated the rats with thyroid

hormone. The researchers reported that by impairing

production of IgE, hypothyroidism can impair the

inflammatory component of asthma.[25]

Respiratory Failure and Other Breathing Problems. In

2004, doctors described a 36-year-old male admitted to

the hospital for progressive respiratory failure.[3]

His chest

X-ray and CT scan were normal, but he had a severely

slow heart rate (bradycardia) and his cognitive

function was slow. His TSH was over 150 microU/ml (in

the US, the current upper limit for a " normal " TSH is

2.5 or 3.03). After the man began thyroid hormone

treatment, his respiratory function steadily improved.

The doctors who reported this patient's case listed

five other respiratory disorders common among

hypothyroid patients: dysfunction of the diaphragm,

poor respiration from low central nervous system

drive, obstruction of the airways, pleural effusion,

and sleep apnea. They advised doctors to evaluate

patients with respiratory problems for hypothyroidism.

Hypothyroidism and Obstructive Sleep Apnea. Hudgel

recommended thyroid hormone as a " ventilatory

stimulant " for hypothyroid patients with

sleep-disordered breathing.[5] He explained that in

1964, Massumi and Winnacker reported the association

of sleep-disordered breathing with hypothyroidism.[6]

Their report was about two hypothyroid patients who

had obstructive sleep apnea. In 1981, Orr reported the

results of polysomnograms (recordings of physiology

during sleep) of three hypothyroid patients.[7] The

tests showed repetitive obstructive apneas during

sleep. Further testing by Rajagopal tightly linked

hypothyroidism to obstructive sleep apnea.[8] Nine of

his 11 consecutive hypothyroid patients had apnea.

Not all hypothyroid patients, of course, have

obstructive sleep apnea. Lin found that among 25

hypothyroid patients, only 25% had sleep apnea. The

patients who had apnea were older and more obese than

patients without apnea. And not all patients with

obstructive sleep apnea are hypothyroid. Lin found

that only 3% of patients with apnea were hypothyroid.

For most hypothyroid patients with sleep apnea, the

consequences can be troubling. For example, because

they don't sleep deeply long enough, they can be

severely fatigued through the day. But as the section

below shows, for at least one hypothyroid patient,

apnea wasn't troubling; it was terminal.

First Reported Death From Hypothyroidism and Sleep

Apnea. In 1999 doctors reported the first case of a

hypothyroid patient who suddenly died from sleep

apnea.[4] The patient was a 48-year old man who was

short and slightly overweight. He had hypothyroidism

that doctors had previous failed to diagnose.

For several years, the patient suffered from air

hunger at night. In the previous few weeks, his air

hunger had worsened. In the hospital, doctors noted

that he was lucid, but his mental and physical

functions were slow. They found that he had a

multinodular goiter, and the goiter had move his

windpipe (trachea) from its normal position. His

tongue was enlarged, and his pharynx (the cavity that

connects the mouth and nasal passages to the

esophagus) was swollen with edema. His blood was 97%

saturated with oxygen.

Doctors treated the man with T3 and hydrocortisone.

They doubted that he had sleep apnea syndrome (SAS),

but they applied pulse oximetry. (Pulse oximetry is a

monitor, usually with a finger sensor, used during

anesthesia and critical care. It measures oxygen

saturation of arterial blood.) The man suddenly died

seven hours later.

The oximetry record showed that over the seven-hour

period, the patient had prolonged episodes of sleep

apnea. These episodes had caused deep drops in oxygen

saturation of his blood. The doctors who reported the

man's death urged other doctors to promptly diagnose

hypothyroidism that's associated with obstructive

sleep apnea. They noted that the condition can become

serious and require intensive care with continuous

nasal airway positive pressure. They wrote that some

patients may need tracheal intubation with assisted

ventilation. They cautioned, " Continuous cardiac

monitoring should also be carried out, given the risk

for acute coronary complications and ventricular

arrhythmias in the early phases of substitutive

therapy with thyroid hormone. "

Conclusion: The studies I've cited in this report show

that too little thyroid hormone regulation can cause a

variety of breathing problems. These range from mere

frustrating air hunger to death from sleep apnea. If

you have a breathing problem and your doctors can't

find the cause, ask him or her to evaluate you for

hypothyroidism or thyroid hormone resistance. If

you're being treated for hypothyroidism with

T4-replacement, ask your doctor to consider that this

thyroid hormone therapy leaves almost 50% of patients

suffering from chronic hypothyroid symptoms,[31] and

you may need to switch to a more effective approach,

such as a T4/T3 combination product or T3 alone. At

minimum, if your doctor isn't aware that too little

thyroid hormone regulation can cause breathing

problems, share this special report with him or her.

The doctor may use the information to relieve your

breathing problem and other patients, too.