Some of the most common questions that I get from people who reach out to me are about antibodies.
There seems to be a good deal of confusion about them and also a good deal of emotion and expectation attached to these numbers going up or down.
In this post, we examine thyroid antibodies and, hopefully, dispel some of the myths around them.
First of all, what are antibodies, exactly? I like to use military analogies when describing the immune system. And antibodies are like military intelligence (hold the oxymoron jokes).
They are the part of the immune system that gathers information on the bad guys (bacteria, viruses, fungus, parasites, etc.) and then they label those bad guys. Kind of like putting a red flag on them.
The invader is called an antigen. Antibodies bind to these antigens like a lock and a key. Every cell has antigens and these are what the immune system recognizes. And every cell in our body has a self-antigen which are supposed to let the immune system know that our own tissue isn’t a bad guy.
Once the bad guys have been labeled, other parts of the immune system are signaled and they attack and, in most cases, kill the bad guys. In some cases these antibodies can neutralize the bad guys all by themselves and not have to wait for reinforcements.
With autoimmune disease these antigen signals get confused and the immune system ends up attacking our own tissue.
Over the last 50 years there has been a lot of research in this area.
There is a region on cells located on some of our genes called the HLA (or Human Leucocyte Antigen) System. Many of these are located on chromosome 6 (for those of you keeping count).
Mutations or defects of HLA has been linked to many different autoimmune diseases. Exactly what happens is not known, there are numerous theories, but the end result is that our own tissue gets attacked and destroyed by the immune system.
There is a specific class of HLA (class II) that has been linked to autoimmune thyroid diseases like Hashimoto’s and there are also specific antibodies that are important in the disease.
There are 2 autoantibodies that are important:
Thyroid Peroxidase Antibody (TPO Ab): This antibody is the one that is usually high in autoimmune thyroid conditions like Hashimoto’s. It is also known as microsomal antibody.
Thyroglobulin Antibodies (TgAb): These aren’t seen high as often as TPO Ab. They are usually ordered when thyroid lab results seem strange because these antibodies can interfere with thyroid hormone production.
TgAb is also used to monitor progress after surgery for removing the thyroid in thyroid cancer.
In Hashimoto’s, TPOAbs are present in nearly all (>90 %) patients, while TgAbs can be seen in approximately 80%.
Antibodies against TPO (TPOAbs) and Tg (TgAbs) are of immunoglobulin G class, (IgG) and both are really good buddies with their antigens.
For TPO, it is for the enzyme thyroid peroxidase, which frees iodine and helps in the production of T4 and T3.
And for TgAb it is for Thyroglobulin, which is also used by the thyroid to produce T3 and T4.
When these 2 things get destroyed, over time, the body can’t make enough thyroid hormone.
This results in hypothyroidism and all the familiar problems of Hashimoto’s: fatigue, constipation, depression, hair loss, cold hands and feet, brain fog, memory issues and lots more.
Unlike TgAbs, TPOAbs can activate certain parts of the immune system (complement) and are able to cause damage to thyroid cells.
However, there isn’t much evidence that both antibodies have a major role in the formation of Hashimoto’s or in the destruction of thyroid cells.
It seems a lot more likely that other parts of the immune system are signaled and that they bring in the Navy Seals of the immune system which attack and kill thyroid cells.
TPO and TgAb antibodies, however, are considered the definitive test for whether or not you have Hashimoto’s. Basically, if either one or both of these are found to be above the lab range values, then you are positive for the disease.
Most labs have the high end at about 25 to 35. Numbers vary considerably, but it is not unusual for people who have been diagnosed to have antibodies above 1,000.
As I stated above, in most cases these antibodies, themselves, do not attack and kill thyroid cells.
What’s also important to understand is that there are various stages of autoimmune disease and depending on where you are in the progression, you will have different degrees of thyroid tissue destruction and, therefore, different symptoms.
According to Dr. Datis Kharrazian, there are 3 stages of autoimmune disease. While these stages are not recognized by conventional doctors, they are very useful in determining exactly where you are in the progression of the disease.
And realizing that there are stages and that the stages get worse and worse, is also helpful for motivating you to do as much as you can to stop the progression. (Hopefully!)
You can read more about these stages here.
The antibodies are really involved in signaling the immune system and in setting off a series of events that results in the attack and destruction of the thyroid.
I have written extensively about what happens in this previous post.
The important thing to understand here is that the amount of antibodies don’t necessarily directly correspond to how severe the Hashimoto’s is.
There are many reasons for this, but one simple way to look at it is this: The amount of destruction that is done by the army (the immune system) depends on the strength and number of the soldiers.
As I said earlier, the antibodies are really like the CIA or some intelligence gathering part of the army. The front line soldiers are the killers. If you have lots of soldiers and they are all revved up and ready to dance, then you get more destruction.
If your army is weak and there aren’t that many soldiers, then the CIA tells them to kill, kill, kill, but they can only do so much damage.
On the other hand, even if there are only a few CIA agents and there is a large, aggressive army, you will still have massive destruction (and loss of thyroid function).
Where am I going with all this? The amount of destruction, which really is the cause of how crappy you feel, depends on the strength and number of soldiers, not on the number of CIA agents in the field.
This is why antibodies are not a good measure of progress and often don’t correspond with how well people feel.
Antibody numbers don’t correspond, directly, with tissue destruction. As I mentioned above, in some cases TPO antibodies have been linked to tissue destruction, but more often, this is not the case.
Many patients and doctors or practitioners track these numbers and use them as a measure of whether or not what they are doing is working. And many times, they will find that there is no correspondence.
Obviously, getting antibody numbers to drop is not a bad thing. But it is also not necessarily such a good thing, because it may not be an indication that the destruction or the progression of the disease has slowed.
In conventional lab testing there really aren’t tests that are done to look at this. One theory with Hashimoto’s is that the ratio between the CIA and the soldiers is important.
The soldiers are also known as the TH-1 system, the cytokines or immune proteins associated with this part of the immune system are the killers.
The CIA is known as the TH-2 part of the immune system and you can test for ratios between TH-1 and TH-2 cytokines.
If there is a lot more of the soldiers than CIA agents, then the prognosis is not good and the disease tends to be more severe.
With Hashimoto’s there is a tendency towards more TH-1 than Th-2, but this is not always the case.
On the other hand if the CIA is more numerous or more balanced and the control and command part of the immune system (TH-3 or the regulatory part of the immune system- what we can call the General) is also strong, then, usually the prognosis is better and you can calm the attack and slow or stop the progression of the disease.
In reality, the immune system isn’t linear and this is an oversimplification. Testing is available to look at the cytokines that represent these different parts of the immune system, but there are many other factors that make current tests for this unreliable and not that helpful.
However, you can use these ideas to help figure out what you need to do in order to calm the attack, slow the progression of the disease and, most importantly, feel better.
The major cause of thyroid tissue destruction is something called apoptosis. This is programmed cell death.
Lots of crazy things happen on a molecular level (like cytoskeletal disruption, cell shrinkage, chromatin condensation, nuclear fragmentation, membrane blebbing, and DNA fragmentation – membrane blebbing, people!) to make this happen, but the easiest way to grok the root of it is to understand that it is initiated by inflammation.
The best way to slow the progression and minimize destruction is to do everything you can to stop inflammation and to strengthen the regulatory part of the immune system.
2 important anti-inflammatory agents are: Vitamin D and glutathione. These supplements strengthen the regulatory part of the immune system (TH-3 or the General).
(One important thing to note is that some people with Hashimoto’s have a defect with vitamin D receptors and may need to take more than is usually required by normal individuals.)
These are important anti-inflammatories.
Another player in the complicated drama of Hashimoto’s is TH-17. This is like a rouge agent that when numerous and aggressive can do major damage. TH-17 is highly inflammatory.
Natural supplements that reduce TH-17 include Turmeric and Resveratrol. Some Chinese herbs that have been shown to reduce TH-17 are Chang Shan or dichroa root and Huang Lian and Huang Qin whose active compound is berberine.
Also, it is very important to reduce the causes of inflammation in your diet. The three most inflammatory foods in our diet are gluten, dairy and soy.
Gluten has been extensively hybridized and deamidated and has been linked to the initiation and progression of thyroid autoimmunity.
Dairy products when commercially produced are full of antibiotics, hormones and god knows what else. They have also been linked to the initiation of various autoimmune diseases.
Soy is one of the most heavily genetically modified foods in our diet and is also quite difficult to digest.
Some research has indicated that thyroid replacement hormone can reduce TPO antibodies, though there is also some indication that natural desiccated hormone can raise antibodies in some individuals (it seems to be those who have a particularly severe immune reactivity – i.e., they have lots of inflammation).
Selenium has been found to reduce TPO antibodies in a number of studies.
Thyroid antibodies are important for determining whether or not you have Hashimoto’s but are not always a good indicator of how well what you are doing is working.
Do not get too excited if antibody numbers go up or down. It’s not the antibodies that are the problem as much as the other parts of the immune system that are attacking and destroying the thyroid.
Get excited about reducing inflammation. That should be your daily obsession. Really, its that important.
Thyroid replacement hormone and selenium have been shown to reduce TPO antibodies, but this may not work for everyone.
Hashimoto’s is complicated. It is a multi-system disorder that requires a multi-system approach. That’s why created my program: Healing Hashimoto’s: The 5 Elements of Thyroid Health. Click here to learn more.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3271310/– Technichal, but great info on what happens in Hashimoto’s
The human body is a wonderfully complex playground where hormones, immune cells, neurotransmitters, red and white blood cells, bacteria, and more all frolic.
With Hashimoto’s that playground gets invaded by a hurricane of inflammation and this disrupts many of the systems that produce these things.
In today’s post, we focus on how blood sugar problems can impact the thyroid and how Hashimoto’s and hypothyroidism can also make blood sugar problems worse.
It’s a two way street, people.
The endocrine gland that is responsible for helping maintain blood sugar balance is the pancreas. The poor, dear, much beleaguered pancreas.
What does the pancreas do? Quite a lot actually, we really should be nicer to it. It does endocrine stuff and non-endocrine or exocrine stuff.
On the endocrine side it produces insulin, glucagon and somatostatin. Insulin and glucagon are involved in blood sugar metabolism and somatostatin is involved in intestinal absorption.
The exocrine functions include secreting digestive enzymes into the small intestines. These breakdown proteins, fats and carbs in the diet.
Studies have found pancreatic function was significantly reduced in patients with hypothyroidism.
And, in many people today, the pancreas is under siege.
Americans are addicted to sugar. In some measure, it’s their own doing. In other ways, it is the food industry and public health officials who decided that fat was evil when it was discovered that cholesterol was linked to heart disease in the 1980s. The National Academy of Science made sweeping recommendations at that time to get rid of dietary fat.
So fat was taken out of many processed, fast foods and in an effort to make it taste less like an old ping pong table, it was replaced with sugar.
Carb Roller Coaster
What has since developed is a nation of carb and sugar addicts riding the roller coaster of sugar highs and crashes.
On average, Americans hammer about 200 pounds of sugar a year, and diabetes is a serious threat to bankrupt our healthcare system in the next 20 years.
It is estimated that almost half the population born after 2000 will become diabetic.
This is almost entirely due to diet. As Thomas Edison said, “We’re digging our graves with our teeth.”
Health is really all about balance. And nowhere is this idea more evident than when you look at blood sugar balance.
There are really 2 different kinds of blood sugar problems and many people have a mixture of both. These are hypoglycemia (or too little sugar in the blood) and insulin resistance (or too much sugar in the blood).
With Hashimoto’s either one or both of these blood sugar problems can make things worse. And just to remind you that this goes in both directions; its important to understand that hypothyroidism can also cause blood sugar problems all by itself.
(We have the makings of a vicious cycle.)
Your body is programmed to recognize low blood sugar as a threat because severe or long term hypoglycemia can cause seizures, coma, and death.
When your blood sugar levels drop below normal, your adrenal glands respond by secreting cortisol. Cortisol then tells the liver to make more glucose, bringing blood sugar levels back to normal.
Hypoglycemia is a condition in which there is not enough cortisol to raise blood sugar into the normal range.
The problem is that cortisol (along with epinephrine) is also a sympathetic nervous system stimulant involved in the “flight or fight” response. This can end up wearing out the adrenals.
In fact, we often see adrenal fatigue and hypoglycemia together.
Cortisol’s job is to increase the amount of glucose available to the brain, enhance tissue repair, and slow other functions – like digestion, growth and reproduction – that aren’t so important when you are running from hungry lions on the African Savannah (flight).
Unfortunately for these people, repeated cortisol release caused by low blood sugar can also suppress pituitary function.
And the pituitary is the master gland that instructs the thyroid. If this function isn’t working properly, then “Houston, we have a problem.”
And where do we have a problem? In the thyroid.
Cortisol directly inhibits the enzyme (5’-deiodinase) which converts inactive T4 into active T3. This can lead to low T3 levels.
In addition, elevated cortisol will cause thyroid hormone receptor insensitivity meaning that even if T3 levels are high enough, they may not be able to bind normally to receptor sites. And when this happens it doesn’t get into the cells.
Cortisol will also increase the production of reverse T3 (rT3) which is inactive. (It’s kind of like the anti-hormone.)
rT3 can cause an increase in the production of substances known as thyronamines that can cause hypothyroid symptoms (like, low basal body temperature,fatigue, depression, etc.) along with insulin resistance symptoms of increased blood sugar.
Cortisol can also lower the levels of protein that binds to thyroid hormone so it can circulate in a stable structure.
And finally, elevated cortisol will slow TSH production by messing with hypothalamic-pituitary feedback leading to lower TSH production.
In my previous post on the adrenal glands we learned about the HPA (hypothalmus-pituitary-adrenal) axis.
Well, there is also an HPT (hypothalmus-pituitary-thyroid) axis.
And much like wires going through a transformer on an electric grid, the HPT and HPA axis are very closely related and problems in one area can affect the other.
“When things go wrong, wrong with you, it hurts me too.” sings the HPA to the HPT axis.
Common symptoms of hypoglycemia include (These come from a form called a Metabolic Assessment Form that I use in my practice that I got from studying with Dr. Datis Kharrazian):
(Many of these symptoms improve when you eat )
*Irritable if meals are missed
*Depend on coffee or other kinds of caffeine for energy
*Eating relives fatigue
*Feel shaky, or jittery
*Feel agitated or nervous
*Get upset easily
*Poor memory, forgetful
It’s important for hypoglycemics to eat often throughout the day and not skip meals. Each meal should be a combination of protein, carbohydrates and fats. And, for these people, too many carbs will often cause serious problems with their blood sugar levels.
When you eat too many carbs and too much sugar, the pancreas secretes insulin to move extra glucose from the blood into the cells where glucose is used to produce energy.
But over time, the cells lose the ability to respond to insulin. It’s like insulin is a little dog barking outside the cell, but the cell won’t let it in.
“I hear you barking, but you can’t come in.”
The pancreas responds by pumping out even more insulin (barking louder) in an effort to get glucose into the cells, and this eventually causes insulin resistance.
Studies have shown that the repeated insulin surges that come with insulin resistance increase the destruction of the thyroid gland in people with autoimmune thyroid disease.
Let me repeat that, insulin resistance increases the destruction of the thyroid gland in autoimmune thyroid disease (Hashimoto’s).
As the thyroid gland is destroyed, what happens? Thyroid hormone production falls. And this causes hypothyroidism. Not good.
Insulin resistance can also cause a reduced conversion of T4 to T3 hormones.
When this is addressed, the cells can once again start using glucose for energy and T3 production picks up.
So for a person who is insulin resistant, a lower carbohydrate diet may help restore better T4 to T3 conversion and often these people lose weight in the process ( a nice side effect).
For other people, other things like long-term chronic stress may be affecting their response to low carb diets. As we have seen in my previous post, chronic stress can interfere with thyroid hormones in several ways.
(These are also from that form mentioned above):
(Eating generally doesn’t improve these symptoms )
* Fatigue after meals (this is the hallmark symptom)
* General fatigue
* Constant hunger
* Craving for sweets that isn’t relieved when you eat sweets
* Must have sweets after meals
* Waist girth equal to or larger than hip girth
* Frequent urination
* Increased appetite and thirst
* Difficulty losing weight
* Migrating aches and pains
Life is not a textbook. Many people are somewhere in the middle of this blood sugar odyssey and they have some symptoms of hypoglycemia and some symptoms of insulin resistance.
I put this question to my Facebook Support Group and of the 66 respondents with Hashimoto’s, 24 reported symptoms of hypoglycemia and 14 reported symptoms of insulin resistance.
16 reported some symptoms of both.
While this is hardly a scientific study, it does demonstrate how common this problem is in this population.
On thing that’s important to understand is that whether you have high or low blood sugar, you probably have some amount of insulin resistance.
I explained how high blood sugar causes insulin resistance above, but insulin resistance can also cause low blood sugar.
This condition, called reactive hypoglycemia, happens when the body secretes excess insulin in response to a high sugar and carbohydrate meal.
For example: A burger on a sesame seed bun, french fries and a soda – causing blood sugar levels to spike and then drop below normal. (I’m not lovin’ it!)
If you eat like this and you have Hashimoto’s (and hypothyroidism), you are setting yourself up for a world of hurt.
Hypo-function of the thyroid can cause everything we just talked about because:
These mechanisms present clinically as hypoglycemia. When you’re hypothyroid, your cells aren’t very sensitive to glucose (they are resistant).
So although you may have normal levels of glucose in your blood, you’ll have the symptoms of hypoglycemia (fatigue, headache, hunger, irritability, etc.).
And since your cells aren’t getting the glucose they need, your adrenals will release cortisol to increase the amount of glucose available to them.
This causes a chronic stress response, as I described in a previous post, that suppresses thyroid function.
Does this sound familiar?
In another post on Synthroid, TSH and T4, I wrote about how some people are functionally hypothyroid. In other words, they have enough thyroid hormone, but it’s not getting into the cells.
Many of these people also have enough sugar in their blood but its not getting into the cells. Its another vicious cycle.
And let me tell you this from clinical experience. It is really, really, really, really, really, really, really, hard to manage a Hashimoto’s patient or someone with functional hypothyroidism if he or she doesn’t stop this sugar happy carb fest.
In fact, I’m going to say it. It’s a deal breaker.
If this high sugar diet isn’t stopped, you might as well throw in the towel, pack it in, wave the white flag, say “Uncle”, hear the fat lady sing, and give up, because you’re done.
All the money you’re spending on supplements and therapies won’t work. Instead, the first thing you need to do is to balance your blood sugar.
When balancing blood sugar, there are two things to consider. The first is fasting blood glucose, which can be measured first thing in the morning before eating or drinking anything.
In functional medicine we define normal range for fasting blood glucose as 75 – 95 mg/dL. Although 100 is often considered the top of the range for normal, studies have shown that fasting blood sugar levels in the mid-90s may set the table for future diabetes a decade later.
And although 80 mg/dL is often defined as low end of the range, plenty of healthy people have fasting blood sugar in the mid-to-high 70s (especially if they follow a low-carb diet – all you Paleo fans- time to do the wave).
The second, and more important thing to measure is post-prandial blood glucose. This is measured 1-2 hours after a meal.
Several studies have shown that post-prandial blood glucose is the most accurate predictor of future diabetes and is the first marker (before fasting blood glucose and Hb1Ac) to indicate blood sugar imbalances.
Normal post-prandial blood sugar one to two hours after a meal is 120 mg/dL, but most normal people are under 100 mg/dL two hours after a meal.
How does this apply to you? If you’re hypoglycemic, your challenge is to keep your blood sugar above 75 throughout the day.
The best way to do this is to eat a low-to-moderate carbohydrate diet (to prevent the blood sugar fluctuations I described above), and to eat frequent, small meals every 2-3 hours (to ensure a continuous supply of energy to the body.
If you’re insulin resistant, your challenge is to keep your blood sugar below 120 two hours after a meal.
The only way you’re going to be able to do this is to restrict carbohydrates.
Everyone should buy a blood glucose meter. The technology has gotten to the point where they are very precise and quite inexpensive.
How low-carb do you need to go?
Its different for everyone. (But, for most people with Hashimoto’s it is recommended to reduce carbs significantly.)
First, figure out your carbohydrate tolerance by buying a blood glucose meter and testing your blood sugar after various meals.
If you’ve eaten too many carbs, your blood sugar will remain above 120 mg/dL two hours after your meal.
Finally, if you have Hashimoto’s, it’s also important that you take steps to make sure your thyroid is properly balanced as well.
As you have seen, this thing works in both directions.
Sugar problems can mess with thyroid function, and thyroid disorders like Hashimoto’s can cause sugar problems and put you at greater risk for hypoglycemia, insulin resistance and if nothing is corrected, diabetes.
As you can also see, there are layers and layers here that may need to be addressed and worked on.
Hashimoto’s is so much more than a thyroid problem. Its a multi-system problem and it requires a multi-system approach.
That’s why I created my program: Healing Hashimoto’s: The 5 Elements of Thyroid Health.
In it you will discover how all these systems interact and cause vicious cycles and you will also learn how to correct these imbalances and heal.
In the meantime, put down the happy meal and step from away from the counter! 🙂
http://www.ncbi.nlm.nih.gov/pubmed/16530289: Study on insulin resistance and inflammation
http://www.eje-online.org/content/134/1/21.extract : Cytokines and autoimmune disease
http://www.ncbi.nlm.nih.gov/pubmed/3500324: Impact of immune cells on TSH
http://care.diabetesjournals.org/content/24/8/1448.full: Study on Glucose Tolerance and Neuropathy
http://www.ncbi.nlm.nih.gov/pubmed/939192 : Study on impact of thyroid hormone on insulin secretion.
http://www.ncbi.nlm.nih.gov/pubmed/2013384 : Influence of the thyroid on pancreatic function
http://diabetes.diabetesjournals.org/content/16/9/643.full.pdf+html: Effects of thyroid function on insulin secretion
http://www.ncbi.nlm.nih.gov/pubmed/19364696 : Excess thyroid hormone and carbohydrate metabolism
The Thyroid: A Fundamental and Clinical Text, Lewis E. Braverman & Robert D. Utiger, Ninth Edition, Lippincott, Williams & Wilkins, 2005
Why Do I Still Have Thyroid Symptoms? (When My Lab Tests Are Normal), Dr. Datis Kharrazian, Elephant Printing 2010
Hashimoto’s is the most common cause of hypothyroidism in the United States. An estimated 20 million people suffer from some form of thyroid disease.
Up to 60 per cent have no idea that they have a thyroid problem.Women are five to eight times more likely than men to have thyroid issues.
Fibromyalgia is a multi-symptom disorder that affects an estimated 5 million Americans 18 or older. Between 80 and 90 percent of people diagnosed with fibromyalgia are also women.
This week, I was thinking about the number of patients that I have seen that have been diagnosed with both conditions.
I put the question to my Facebook support group and 74 people with Hashimoto’s responded.
Almost all of them confirmed that they had been diagnosed with both or had all of the symptoms of fibromyalgia.
This is hardly a scientific study, but it does give us some evidence that there is a lot of overlap between the 2 conditions.
As I said, several patients have come to me with a pre-existing diagnosis of fibromyalgia, or FMS, for which they have received little effective treatment or relief.
Many doctors treat these symptoms using drugs rather than uncovering the root cause of the patient’s issues.
Diagnosing fibromyalgia is admittedly difficult. For years it has involved assessing the presence in the patient of multiple symptoms that indicate the syndrome.
Currently, there are three main symptoms which must be present for a fibromyalgia diagnosis. They are:
1. Widespread pain
2. Sleep problems
The only existing blood test available is the FM/a, which tests for a lowered cytokine level suggestive of fibromyalgia, but the test is controversial and not yet considered definitive.
I do not mean to diminish or discount a diagnosis of fibromyalgia. What I am curious about is the link between FMS and Hashimoto’s.
Studies have come to indicate there is a component of thyroid dysfunction associated with FMS. A 2007 study by the Division of Rheumatology at the Department of Internal Medicine at the University of Pisa looked into a possible link between fibromyalgia and Hashimoto’s Hypothyroidism. It concluded that the presence of thyroid autoimmunity may predispose one to fibromyalgia.
This opens up the possibility that the opposite may be true: what if in some cases the various symptoms that point to a diagnosis of fibromyalgia are, in fact, just Hashimoto’s (which is often undiagnosed)?
In my own experience, I can tell you that a lot of fibromyalgia symptoms are present in my Hashimoto’s patients.
Is there a connection between the two?
In a review published in Thyroid Science by John C. Lowe and Jackie Yellin at the Fibromylgia Research Foundation, the authors wrote that, based on the available research, “inadequate thyroid hormone regulation is the most likely underlying mechanism of the symptoms and objective abnormalities of patients who meet the criteria for FMS.”
In the authors’ view, only hormone therapy has been seen to result in the mitigation of fibromyalgia symptoms. This, obviously, points to a connection between fibromyalgia and thyroid autoimmunity.
In fact, 2 neuroscientists at Stanford (Dr. Ian Carroll, MD and Dr. Jarred Younger PhD) are currently doing a clinical trial investigating T3 treatment for fibromyalgia.
So, at the very least, FMS and Hashimoto’s share a great number of symptoms. If you are diagnosed with FMS, it is highly advisable that you be tested for Hashimoto’s.
If you aren’t familiar with which tests to order for Hashimoto’s, check out my previous blog post for an in depth discussion on this.
Since there is so much overlap, I have decided to illustrate how virtually all the common symptoms of fibromyalgia can be caused by hypothyroidism (and, often, Hashimoto’s).
According to WebMD the most common symptoms of fibromyalgia are those in italics below. We will examine how hypothyroidism leads to each group of symptoms and why.
• Chronic muscle pain, muscle spasms, or tightness: Muscle-related symptoms are common with patients with hypothyroidism. The symptoms vary, but in a recent series of studies 79% of patients reported some kind of myopathy (muscle pain).
The exact reasons why are not known, theories include impaired glycogenolysis (the breakdown of glycogen to glucose – a reminder of why blood sugar balance is so important), reduced mitochondrial activity (mitochondria are the cell’s energy producers) and a decrease in production of ATP (Adeosine triphosphate), the actual fuel in the cell.
A recent study also showed increased lactate production during exercise with hypothyroid patients – this is also consistent with mitochondria problems.
• Tension or migraine headaches: Any of the causes above or below can lead to tension and headaches.
• Jaw and facial tenderness: Jaw and facial tenderness can also be caused by the same factors that lead to other muscle pain.
• Moderate or severe fatigue and decreased energy: Fatigue and decreased energy are some of the most common symptoms of hypothyroidism and Hashimoto’s.
There are many factors that lead to this including too little thyroid hormone production, the affect of too little thyroid hormone on the adrenals and blood sugar metabolism and the problems with ATP and mitochondria mentioned above.
• Insomnia or waking up feeling just as tired as when you went to sleep: Sleep issues are also incredibly common with hypothyroidism. Instability of thyroid hormone levels due to poorly managed autoimmunity, T3 building up and being released into the bloodstream, and the thyroid’s affect on the adrenals can all lead to insomnia.
With hypothyroidism, too little T4 can lead to a slower breakdown of cortisol. It then builds up in the body and this impacts the HPA axis (hypothalmus-pituitary-adrenal axis). See my past blog post for an in depth look at this.
• Stiffness upon waking or after staying in one position for too long: Hypothyroidism tends to cause a slower relaxation of tendons and some studies have shown high serum creatinine kinase levels. The levels are almost invariably in the MM isoenzyme that is the type of creatinine kinase found in skeletal muscles.
High levels of this enzyme are normally found in people who have been under extreme stress or who have just completed heavy exercise.
• Reduced tolerance for exercise and muscle pain after exercise: This certainly could be caused by what we just discussed. In addition, there are a host of issues that hypothyroidism can cause that relate to reduced tolerance for exercise. Check out my previous post on this.
• Difficulty remembering, concentrating, and performing simple mental tasks (“fibro fog”): According to Dr. Datis Kharrazian, the role of the thyroid on the brain is profound. Thyroid function impacts brain inflammation, plasticity, neurotransmitter activity and general brain function.
Thyroid hormone impacts all neurotransmitter receptors in men and women.
All of them.
So hypothyroidism can impact serotonin, dopamine, acetylcholine and gaba levels.
These neurotransmitters have a huge influence on memory, concentration and mood. Especially acetylcholine. Hypothyroidism can lead to acetylcholine deficiency and inefficient nerve firing.
This can cause memory loss and poor concentration.
Brain fog is brain inflammation, plain and simple. It is really important not to ignore it, like many doctors do. The consequences can be really bad.
• Feeling anxious or depressed: As we just discussed, thyroid hormone impacts all neurotransmitter receptors. Gaba is an inhibitory neurotransmitter, it keeps you calm.
Hypothyroidism can impact gaba synthesis, release and reuptake. All of this can lead to increased anxiety.
Dopamine and serotonin are responsible for enabling us to experience joy and enjoy activities in our life and to get pleasure out of what we do. Hypothyroidism can also impact these neurotransmitters and can lead to deficiencies in both serotonin and dopamine.
• Increase in urinary urgency or frequency (irritable bladder): Acetylcholine deficiency can impact urinary urgency and frequency.
• Abdominal pain, bloating, nausea, and constipation alternating with diarrhea (irritable bowel syndrome): Studies in human and dogs of hypothyroid patients have demonstrated a decrease in the electric and motor activity of the esophagus, stomach, small intestine and colon.
Digestive dysfunction is also incredibly common with hypothyroid patients. Leaky gut has been implicated in the formation and progression of various autoimmune diseases including Hashimoto’s.
Neuropathic symptoms including parasthesias (tingling or prickling sensation caused by issues with peripheral nerves) and painful dysthesias (an abnormal, uncomfortable sense of touch) are also common with hypothyroidism.
The most common type of neurological symptom in hypothyroid patients is carpal tunnel syndrome.
• Sensitivity to one or more of the following: odors, noise, bright lights, medications, certain foods, and cold: Neuropathies involving the cranial nerves (those that control smell, hearing, vision) have all been reported. Hearing loss due to hypothyroidism is the most common and has been reported in 31%-85% of patients.
There are many theories on how hypothyroidism impacts nerves, but some studies have shown demyelination (the loss of the coating around nerve fibers), and axonal degeneration (degeneration of the nerve branches).
• Numbness or tingling in the face, arms, hands, legs, or feet: Certainly, this can be caused by what we just discussed.
• A feeling of swelling (without actual swelling) in the hands and feet: This could be neurological or it could simply be caused by the destructive inflammatory process that is at the root of Hashimoto’s.
As you can see, there is a plausible argument to be made that almost all of the symptoms of fibromyalgia could be rooted in hypothyroidism and Hashimoto’s.
Of course, this begs the question of what to do.
As with all things related to this disease, we are once again reminded that this is a multi-system disorder.
It’s much more than just a thyroid problem and it requires a multi-system approach if you want to manage it successfully.
This is exactly why I created my program: Healing Hashimoto’s: The 5 Elelments of Thyroid Health.
In it, I teach a step by step strategy for finding and healing your issues in all of these systems.
For more information, check out my program here.
http://www.thyroid.org/media-main/about-hypothyroidism/ : Statistics on thyroid disease
https://med.stanford.edu/clinicaltrials/trials/NCT00903877 : Clinical study using T3 to treat fibromyalgia
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1856434/?tool=pubmed : Paper on leaky gut
: A review of the evidence on the link between fibromyalgia and hypothyroidism
http://www.ncbi.nlm.nih.gov/pubmed/21085966 : Study linking fibromyalgia and autoimmune thyroid disease
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Monzani F, Caraccio N, Siciliano G, et al. Clinical and biochemical features of muscle dysfunction in subclinical hypothyroidism. J. Clinical Endocrinol Metab 1997;82:3315
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Kowalewski K, Kolodej A. Myoelectrical and mechanical activity of the stomach and intestine in hypothyroid dogs. Am J Dig Dis 1977;22;235
Bhatia PL, Gupta DP, Agrawal MK, et al. Audiological and vestibular function tests in hypothyroidism. Laryngoscope 1977;87:2082
Dyck PJ, Lambert ED. Polyneuropathy associated with hypothyroidism. J Neuropathl Exp Neurol 1970;29:631
The Thyroid: A Fundamental and Clinical Text, Lewis E. Braverman & Robert D. Utiger, Ninth Edition, Lippincott, Williams & Wilkins, 2005
Why Isn’t My Brain Working? Dr. Datis Kharrazian, Elephant Press, 2013