You’re Not Crazy, It’s Your Genes
Hashimoto’s is a complicated condition. It’s not just a thyroid problem. It’s an autoimmune disease, it’s progressive and over time it can impact many different parts of your body.
This is true on the macroscopic where it affects major organs like the thyroid, liver, adrenal glands, brain, pancreas, stomach, small intestine, gall bladder and more.
And this is also true on the microscopic level where it affects immune cells, hormones, neurotransmitters, enzymes, proteins and even DNA and specific genes.
And with many of these influences, it is not a one way street.
One thing affects another and you sometimes have the creation of vicious cycles and problems and its hard to tell where they started.
In this post we will examine one of these vicious cycles on the microscopic level called the MTHFR gene.
MTHFR sounds a little scary and I like to think of it as the MotherFR gene because it can cause so many problems.
MTHFR is an abbreviation for a gene with a very long name, methylenetetrahydrofolate reductase.
(MotherFR is so much easier to remember.)
Basically, what the MTHFR gene does is produce an enzyme with the same really long name (methylenetetrahydrofolate reductase).
Genes produce enzymes and these enzymes do all the heavy lifting, they do the work.
They make stuff happen in the body. Without enzymes we wouldn’t have physiological function.
The job for the MTHFR enzyme is to convert one form of folate into the most active and usable form of folate in the human body – in every cell in the body.
This type of folate is called methyltetrahydrofolate or more commonly by it’s nickname methylfolate.
Methylfolate Does 2 Important Jobs:
Firstly, it helps make neurotransmitters in your brain.
Neurotransmitters are our molecules of emotion.
They are what enable us to think, reason, laugh, cry, be happy, sad, love, learn, crave and have crushes.
When methylfolate levels are low, so are your neurotransmitters.
And low levels of neurotransmitters like serotonin, dopamine, GABA and acetylcholine cause all kinds of unpleasant feelings and behavior.
Like depression, anxiety, bipolar disorders, ADHD, addictive behavior, irritability, insomnia, learning disorders and more.
With Hashimoto’s we often see depletions in these neurotransmitters.
This can be caused by too little thyroid hormones (both T3 and T4) and/or MTHFR defects.
The second thing methylfolate does is it allows us to make something called s-adenosylmethionine better known by its nickname SAMe.
SAMe is important because it helps regulate 200+ enzymes in the human body, its influence is second only to ATP which is every cell’s power source.
Basically what SAMe does is to take what is called a “methyl group” and give it away to these 200+ enzymes and this is what allows them to do their jobs.
Jobs like protect DNA, reduce histamine levels, maintain T and B cell responses, produce key components of cell membranes and about 196 other things.
Because SAMe is so important, when we are deficient in it, we are at higher risk for a lot of different diseases like: autoimmune disease, cancer, infertility, autism, down’s syndrome, thrombosis, high blood pressure and more.
And with autoimmune diseases, studies demonstrate the central role of SAM-dependent methylation ( I’ll explain this in a second) associated with T cell function and it is a key factor in maintaining T and B cell immune responses.
New T cell synthesis is needed in order for T cell clones to expand and respond properly to an immune assault. T cells are needed to help to control the B cells and to balance TH1 and TH2 responses.
If there are methylation cycle problems or mutations, you may have trouble making the bases that are needed for new DNA synthesis.
If you cannot make new DNA, then you cannot make new T cells and as a result you may lack immune system regulatory cells. This is like having a weak and ineffective general who can’t control his troops.
The immune system has many arms, but the B cell “arm” that makes antibodies, known as humoral immunity. I like to think of this part of the immune system as the C.I.A. It gathers intelligence and labels the bad guys.
There is also the T cell “arm” known as cellular immunity, these are like the elite soldiers of the front line. They do the attacking and killing. These are the cells that are often overzealous in Hashimoto’s.
For an in depth discussion on this, check out this post.
If you are having trouble making new T cells, in particular, T suppressor cells, then the immune response may become more heavily weighted in the direction of B cells.
B cell skewed individual has the ability to respond by making antibodies (or autoantibodies) in high numbers to attempt to overcome the T cell deficiency that fights infection.
This is one of the factors in high antibody counts in autoimmune disease.
Methylation is how we get to Oz.
It is the act of taking a single carbon and 3 hydrogens – a methyl group – and attaching itself to an enzyme.
When this happens, the enzyme can do it’s thing.
One common example of this is the breakdown of histamine.
What happens here is a methylation group is made by the methylation pathway and it hangs around until it finds a specific enzyme to bind to.
In the case of histamine, when the methyl group binds to it, the histamine falls apart and goes bye bye.
On the other hand, if your methyl pathway is not making enough methyl groups, then histamine doesn’t break apart and this causes some pretty intense allergic reactions.
For some this may mean running nose and itchy eyes, for others it is full on hives and intolerable itching.
One thing I have observed clinically is that there is a sub-group of people with Hashimoto’s who have histamine intolerance.
This can really complicate recovery and make some of the solutions that help others not work for them.
For example, the Paleo and Autoimmune Paleo diets both have a number of foods that are high in histamine, like bone broth.
So these people eat these foods, thinking that they are doing the right thing (and they are in theory) and they wind up feeling really crappy and just not getting better.
And the people with the most intense reactions may have higher levels of histamine and decreased methyl groups.
What is also interesting is that research has shown some correlation between more severe Hashimoto’s and some of these methylation defects.
Which kind of makes sense, because, as we have seen, SAMe is responsible for maintaining immune responses. And with autoimmune disease, these responses are out of control.
Well, this could be one reason why.
Another key area where this is a concern is brain health. We’ve already seen the impact of methylation on neurotransmitters.
They also play a key role in keeping your myelin healthy.
Myelin coating on nerves is important for proper function of those nerves. Methylation of amino acids in myelin basic protein helps to stabilize it against degradation.
When you lose myelin or it starts to break down then your nerves and brain can’t communicate as well. Myelin is like the coating on the outside of a copper wire.
If a wire isn’t coated it can short out or get major interference from other electrical impulses. In you body this can lead to poor memory or more severe losses in function like those seen in Multiple Sclerosis ( an autoimmune disease caused by the breakdown of myelin).
But, wait there’s more! Methylation is also really important for glutathione production.
Glutathione is our body’s body guard. It is involved in controlling inflammation and in getting every environmental toxins you can think of out of our systems through a process known as direct conjugation.
It is a major anti-oxidant, it regulates the nitric oxide cycle, it is essential for the immune system to operate properly.
It affects how antigens present to immune cells, it can strengthen the regulator part of the immune system.
It is involved in every major biochemical activity, especially those systems most impacted by Hashimoto’s: the immune system, the nervous system and the gastrointestinal system.
It’s importance can not be overstated.
With Hashimoto’s and hypothyroidism, some people develop a sluggish MTHFR enzyme.
This happens because thyroxine (T4) helps produce the body’s most active form of vitamin B2, flavin adenine dinucleotide know by its nickname FAD.
Vitamin B2 must be converted into active FAD by T4 so that the body can use it.
And, the MTHFR enzyme must have enough FAD in order to do its job. If FAD levels are low due to too little T4, then the MTHFR enzyme slows down, which leads to low methylfolate which leads to low neurotransmitters, which leads to low SAMe.
No bueno!
This becomes a vicious cycle.
Another really common finding that I see in analyzing blood test results from Hashimoto’s patients is that they have high levels of homocysteine.
As it turns out, low activity of the MTHFR enzyme may also lead to this. High homocysteine is a major risk factor for heart disease, inflammation, difficult pregnancies, birth defects, and more.
Nutrient deficiencies in Folate B6, and B12 have been linked to high homocysteine.
To matters more complicated, people with MTHFR issues may have a difficult time processing certain types of folic acid like those found in processed food and cheap supplements.
A better source is real food: asparagus, spinach, and liver. Both B12 and B6 are found in meat. And alcohol can deplete the body of B6.
Betaine is also helpful in metabolizing homocysteine.
If you are found to have the MTHFR gene variations and/or you have high homocysteine a better way to supplement is to use the activated version of folate, B6 and B12.
These are:
Methylfolate: (also known as L-5-MTHF Folate)
Pyridoxyl-5-Phosphate (P5P): B6
Methylcobalamine: B12
(Thanks to Vicki Ross for sending me an email to help clarify this very important point.) Not everyone can tolerate methylcobalamine (B12). Just like not everyone can tolerate caffeine, some people don’t do with with methyl cobalamine. And the MTHFR results provide clues to how to determine who may not respond well.
The COMT & VDR genotypes determine WHICH B12 you should take. Most people can handle Hydroxocobalamin or Adenosylcobalamin, but may have problems with methyl B12.
Here is a breakdown of the 4 types of B12:
1. Methylcobalamin
This is the most active form in the human body. It converts homocysteine into methionine, which helps protect the cardiovascular system. Methylcobalamin also offers overall protection to the nervous system. This B12 form can also cross the blood-brain barrier–without assistance–to protect brain cells. It contributes essential methyl groups needed for detoxification and to start the body’s biochemical reactions.
2. Cyanocobalamin
This synthetic version of vitamin B12 is created in a lab, which makes it the cheapest supplement option. It offers the most stable form of B12, although it does so through the presence of a cyanide molecule. While the amount of cyanide is not dangerous, it does require the body to expend energy to convert and remove it.
3. Hydroxocobalamin
Bacteria naturally creates this form of vitamin B12, making it the main type found in most foods. It easily converts into methylcobalamin in the body. Hydroxocobalamin is commonly used via injection as a treatment for B12 deficiency as well as a treatment for cyanide poisoning.
4. Adenosylcobalamin
The energy formation that occurs during the Citric Acid cycle requires this form of B12. Although naturally occurring, it is the least stable of the four types of B12 outside the human body and does not translate well into a tablet-based supplement. It can be difficult to find this one in supplement form, although some supplements, like Vegansafe™, have been able to stabilize it.
Well, firstly, we have to do all the other stuff we do to insure that we are thyroid healthy. And, as all of us who have Hashimoto’s know, this is sometimes easier said than done with all the different systems affected and involved.
Key nutrients for thyroid function are magnesium, iodine (no end to the controversy there – more on this in a future post), selenium, zinc and tyrosine.
Methylfolate, produced by the MTHFR enzyme is also needed to convert tyrosine into active thyroid hormone.
So you can se, we have all the ingredients of a vicious cycle.
Where hypothyroidism leads to MTHFR not working as well, which leads to thyroid hormone not being converted properly and on and on.
Here are some basic tips to correct these challenges:
1. Consider supplementing with glutathione and Vitamin D.
2. Take the active forms of B vitamins mentioned above.
3. Incorporate organic grass fed meats and good fats into your diet.
4. Avoid processed foods and environmental chemical that compete for iodine receptors like fluoride, chlorine and bromine (bromide).
5. Avoid gluten, dairy and soy 100%
6. Avoid GMO foods.
7. Consider testing for homocysteine and the MTHFR gene mutations and defects.
Testing for homocysteine and the MTHFR gene variation is available through many labs. 23andme.com offers a test for the MTHFR gene and many individuals can get the tests from their physicians covered by insurance.
However, some people may be concerned ( and with good reason) with this genetic information getting reported on insurance or to employers.
A MTHFR variation or elevated homocysteine levels may affect future insurance coverage especially with the advances in personal data mining and sharing.
To find out more information about MTHFR testing – along with the ethical considerations of it – visit: MTHFR test options
http://www.jimmunol.org/cgi/content/meeting_abstract/188/1_MeetingAbstracts/116.13 -SAMe and Autoimmune disease
http://www.ncbi.nlm.nih.gov/pubmed/23039890 – Severity of Hashimoto’s corresponds with defect
MTHFR Basics, Benjamin Lynch, ND
http://www.thyroidpharmacist.com/blog/mthfr-hashimotos-and-nutrients
http://mthfr.net/mthfr-test-optins-oral-swab-blood-test-orsaliva/2013/06/26/
http://www.globalhealingcenter.com/natural-health/four-types-vitamin-b12/
Polycystic ovaries and Hashimoto’s have a lot in common.
Hashimoto’s is the most common cause of hypothyroidism worldwide and research has shown that it also has many similarities to PCOS or Polycystic Ovarian Syndrome.
What’s really interesting about these 2 interacting health challenges is what they reveal about how interconnected everything in the body is.
In this post we explore these connections and how, once again, Hashimoto’s is so much more than a thyroid problem.
In order to be diagnosed with PCOS you must have 2 of the 3 following criteria.
(These are what is known as the Rotterdam criteria)
1) No period (Anovulation) or Irregular Periods
2) High levels of testosterone (Hyper-androgenism)
OR
Clinical hyper-androgenism: adult acne, hirsutism (a male pattern of body or facial hair), or hair loss (androgenic alopecia)
3) Polycystic (multiple cysts) appearing ovaries on ultrasound, containing multiple small follicles
Many women with PCOS are overweight, find it difficult to lose weight, and suffer with fatigue, depression and anxiety and either have excess hair or hair loss.
Many women who suffer from Hashimoto’s are also overweight, find it difficult to lose weight, suffer from fatigue, depression and/or anxiety and they struggle with hair loss.
Is it a coincidence? Well, in a word, no.
There is a clear connection between Hashimoto’s thyroiditis and PCOS.
A 2013 meta-analysis found that in a total of 6 studies involving 1605 women, there was a significant increase in the prevalence of Hashimoto’s, increased serum TSH, increased anti TPO antibodies, and anti TG antibodies in women with PCOS when compared to control groups.
A 2012 study found that women with PCOS had a 65% increase in thyroid peroxidase antibodies, and a 26.6% increase in the incidence of goiter, when compared to other subjects in the same age group.
Both Hashimoto’s and PCOS can also lead to infertility and another recent study showed that women suffering with PCOS-related infertility who also had high anti-TPO levels were significantly more likely to not respond to treatment.
There are a number of common causes that make both PCOS and Hashimoto’s worse and they reveal some important clues into treatment strategies.
Here are some common factors:
1. Blood sugar imbalances
2. Low progesterone
3. High Estrogen
4. Hypothyroidism
5. Inflammation: The Root of All Evil
I have written extensively about how sugar imbalances can be major triggers for Hashimoto’s and if you don’t take this seriously you won’t get better. It’s just that simple.
If you missed my previous blog post on this check it out here.
50-70% of women suffering from PCOS have blood sugar issues.
And one of the most common is insulin resistance.
This is basically caused by too much sugar in your blood. Or your classic high carbohydrate diet.
Insulin is a hormone that tells muscle and fatty tissue to take up glucose (sugar) from the bloodstream and to store it as fat or energy.
When the body tissues are “resistant” to insulin, the pancreas simply pumps out more to try and keep the blood sugar levels controlled.
And a woman with PCOS will often have much higher insulin levels in their blood than normal for this reason.
With PCOS, even though other tissues in the body are resistant to insulin, the ovaries and pituitary gland remain very sensitive to it.
The pituitary is a master endocrine gland and it must read and make decisions on many important organs including the adrenals, the thyroid, ovaries and lots more.
It is very sensitive to many different hormones and has been shown to absorb these hormones differently than many other cells in the body.
This is one of the reasons why TSH testing can be so inaccurate – it comes from the pituitary.
A recent research study looked at the role of the pituitary-ovary, adrenal, and thyroid axes in PCOS.
The researchers found through testing TRH (Thyroid Releasing Hormone) that PCOS groups had higher TSH and prolactin and lower free T4.
And adrenal stress may contribute to both high testosterone and insulin resistance, in part because of the impact of this pituitary axis .
High insulin levels also cause the pituitary gland to make too much luteinizing hormone (LH), and too much LH causes the overproduction of testosterone, which causes problems with ovulation.
In addition, insulin surges cause an enzyme (17, 20 lyase) to increase activity and this promotes the development of cysts and more production of testosterone.
What is also interesting is that estrogen is transformed into testosterone in fat cells by an enzyme called aromatase.
This is very common in overweight women who are insulin resistant and who are hypothyroid.
Drugs that lower insulin levels like metformin have been shown to be beneficial in the treatment of PCOS in some women because of this connection.
They lower insulin and aromatase levels which helps lower testosterone levels and, thus, cyst formation.
As part of a vicious cycle, the high testosterone in PCOS sparks even more insulin resistance.
And research has shown that this is not a one way street.
Low thyroid function (higher TSH) actually makes insulin resistance worse in women with PCOS.
Boil this all down to one thing?
Too much sugar is like adding gasoline to the flame of both PCOS and Hashimoto’s.
(If you get nothing else from this post, burn that into your brain.)
Also, it is interesting to note that one of the most common factors of hair loss in women with Hashimoto’s is blood sugar imbalances and insulin resistance.
Low progesterone is another thing that is very common in both PCOS and Hashimoto’s.
It is difficult to know which came first, but there are some common factors.
Usually in their mid-thirties, women’s progesterone levels begin to fall more quickly than their estrogen levels, creating what is known as “estrogen dominance”.
If left uncorrected, this imbalance of progesterone and estrogen can get worse over time and all kinds of issues can appear, including: premenstrual headaches (often migraine-like) fluid retention, fibrocystic breast disease, uterine fibroids, heavy, painful menstrual periods, endometriosis and functional hypothyroidism.
Estrogen dominance also causes the liver to produce high levels of a protein called “thyroid binding globulin”, which, you guessed it, binds to thyroid hormone.
When this happens the amount of thyroid hormone that can be used by the cells of the body goes down.
What does this lead to? Low thyroid function and all of the negative side effects that come along with it.
A 2009 study looked at a group of 337 women with PCOS. All of the women were assessed for the key markers of PCOS, including hirsutism, acne, and menstrual irregularity.
What the researchers found was that women with the highest TSH levels tended to have the most severe insulin resistance. Interestingly, this was not related to weight: hypothyroidism caused insulin resistance in women in all weight categories.
The study concluded that a TSH above 2 miU/L was associated with insulin resistance in PCOS.
It seems that for women with PCOS, an optimal TSH range may be below 2-2.5 mIU/L.
While the research on this topic is generally focused on TSH, it is also makes sense that an optimal range also exists for free T3 and free T4 in PCOS.
In my practice, I have found that values at the top part of the range may provide benefit for some women with PCOS.
And, once again, this is not a one way street.
Low thyroid function leads to low progesterone and high estrogen.
This can lead to weight gain and insulin resistance which can lead to estrogen getting transformed into testosterone and too much LH which can all lead to PCOS.
And correcting hypothyroidism can improve and sometimes resolve PCOS.
Do you see how this is all connected into a massive vicious cycle?
Dear reader, if you know me and my work, you know where I’m going with this.
The root of all evil is inflammation.
Both Hashimoto’s and PCOS are driven by inflammation.
Nodules and thyroid inflammation and cysts on the ovaries are both caused by inflammation.
We’ve seen how sugar and inflammation go together like gamblers and con men.
Well, inflammation, Hashimoto’s and PCOS go together like gamblers, pick pockets and con men.
Recent research has shown that there are common inflammatory markers in both PCOS and Hashimoto’s.
(Read this post to learn more about what is happening with the immune system and Hashimoto’s.)
C-reactive protein levels are 96% higher in PCOS patients than in healthy controls. It has also been found to be significantly elevated in patients with subacute thyroiditis.
Interleukin 18 (IL-18) is high with obesity and insulin resistance. IL-18 is a major culprit in the initiation and progression of Hashimoto’s, especially those with severe symptoms that don’t respond to levothyroxine treatment.
Polymorphisms (genetics variations) of the IL-1a, IL-1b and IL-6 genes have also been associated with PCOS.
IL-6 is also elevated with insulin resistance, PCOS and Hashimoto’s and is thought to be a major factor in the initiation and progression of both disorders.
PCOS and Hashimoto’s have many common factors and symptoms and when you boil it all down have very similar origins.
They are made worse by blood sugar imbalances, especially insulin resistance and by inflammation.
So the best way to treat them is?
Conventional treatment for PCOS is to prescribe oral contraceptives to shrink cysts and falsely normalize menstrual patterns.
But many times, this is not a good long term solution because it does not address the underlying causes of the problem.
If the underlying causes are thyroid related, then proper thyroid management will often resolve the cysts.
In addition, the following strategies should be implemented:
Balance blood sugar, improve insulin receptor sensitivity and reduce systemic inflammation.
This is the holy trinity.
Hashimoto’s is an progressive autoimmune disease and, over time, it becomes way more than a thyroid problem.
As this post clearly demonstrates, many different systems of the body get involved and affect each other.
When these start to malfunction, they can cause a web of problems that result in a downward spiral that causes you to get worse and worse.
It is possible to turn this downward spiral on it’s head.
But you need an understanding of what is going on, you need an approach that can help you deal with everything and fix it and you need support in making all these changes.
That’s why I created my program, the 5 Elements of Thyroid Health. It is 3 pronged approach that:
1. First, teaches you what is happening in your body,
2. Then we work with you to create an action plan to fix those problems, and
3. Finally, we also work on creating a lifestyle that will sustain and support those changes to give you the best chances for success.
Click this link to watch a video to learn more.
(The European Society for Human Reproduction and Embryology (ESHRE) and the American Society for Reproductive Medicine (ASRM) cosponsored the Rotterdam polycystic ovary syndrome (PCOS) consensus workshop to come up with the Rotterdam Criteria in 2004).
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3683210/ – Thyroid disorders in PCOS
http://www.ncbi.nlm.nih.gov/pubmed/24260593 – 2013 meta-analysis
http://www.ncbi.nlm.nih.gov/pubmed/21866332 – 2012 study
http://www.ncbi.nlm.nih.gov/pubmed/20638057 – poor response to treatment
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3002408/ – Origins of PCOS
http://www.ncbi.nlm.nih.gov/pubmed/12477517 – Metformin treatment in PCOS
http://www.ncbi.nlm.nih.gov/pubmed/19654109 – High TSH leads to more insulin resistance
http://www.ncbi.nlm.nih.gov/pubmed/22553983 – PCOS and Chronic Inflammation
http://www.jofamericanscience.org/journals/am-sci/am0706/175_6025am0706_1156_1162.pdf – IL-6 and IL-15 elevated in hashimoto’s
As many of you know, all I do is treat Hashimoto’s and over the last 4 years I have worked and spoken with over 2,000 people with Hashimoto’s.
Most of these conversations have happened during my consultations. In these, people share with me their struggles and I offer advice that helps them right away.
By far, the most common theme of these conversations is that they have normal lab results (this usually means TSH and T4 – to learn more about what are better tests to order read this post) and yet they have all the common hypothyroid symptoms.
In other words, they are fatigued, they have brain fog and memory issues, their hair is falling out, the may have depression, constipation, difficulty sleeping and muscle weakness or joint pain and more.
While researchers sometimes claim that this is rare, clinical experience and empirical data prove otherwise. I put this question to my Facebook support group on 2 occasions and over 300 people responded that they have some or all of the symptoms above and “normal” lab test results.
This situation isn’t rare, it’s very common.
And the vast majority of these people are taking some type of thyroid replacement hormone. The prescriptions vary from Synthroid to Armour to Levothyroxine and sometimes there’s some Cytomel thrown in or they’re taking Naturethroid or Tyrosint.
But often, regardless of the prescription or the dosage, they still have all the hypothyroid symptoms. And some people are over-medicated so they have hyper symptoms, as well. Like, palpitations, insomnia, tachycardia, anxiety, etc.
And after a while you have to ask: What is going on here?
It’s the same story over and over again. The medications are different, the constellation of symptoms are different, but the basic pattern is the same.
People are getting plenty of thyroid hormone, but it’s not getting into their cells and having the effect it is supposed to.
If it were, they’d have no hypothyroid symptoms. But virtually everyone does have hypothyroid symptoms.
In this post we examine why thyroid hormone conversion doesn’t happen the way it’s supposed to and what to do about it.
Let’s Review the Physiology
First of all, let’s look at basic physiology. In the body, normally, the thyroid is signaled by the pituitary with TSH (Thyroid Stimulating Hormone). The purpose of this is to goose the thyroid into producing more thyroid hormone.
This occurs because of signals from the body that it needs more. If it’s cold or you need your heart rate to increase, or your metabolism to rev up or you needs to get things moving for sex, etc.
When this happens the thyroid releases T4 (about 97%) and a little bit of T3 (do the math – yup, 3%).
And this is the basic premise of thyroid replacement hormones like Synthroid. It’s synthetic T4. The theory is that you just give it to the patient and tell them to call you in 6 months. An everything should be hunky dory.
And the reason it doesn’t work is that thyroid hormone must be converted from T4 into T3 in order for the body to utilize it. This conversion happens differently in different parts of the body.
The problem with TSH only testing to determine thyroid hormone levels in the entire body is that the pituitary, which releases TSH, converts thyroid hormone differently than the rest of the body.
This is why you often see normal TSH with lots of hypothyroid symptoms.
Many doctors, somehow, are ignorant of this fact and instead of truly understanding what is happening physiologically, blame the patient for having symptoms when their lab tests say that they should be fine.
There is an enzyme that is largely responsible for thyroid hormone conversion. It is called 5′ deodinase. And it actually comes in 3 forms: deodinase type I (D1), deodinase type II (D2)and deodinase type III (D3).
D1 converts inactive T4 to active T3 throughout the body. In the pituitary, D2 controls this conversion. These two forms behave very differently and are affected by different things.
D1 is suppressed and down-regulated (which means it decreases T4 to T3 conversion and increases reverse T3 levels) in response to stress (both physiologic and emotional), depression, dieting, weight gain and leptin resistance, insulin resistance, obesity and diabetes, inflammation from autoimmune disease or systemic illness, chronic fatigue syndrome and fibromyalgia, chronic pain, and exposure to toxins and plastics.
What did we just describe? Your average Hashimoto’s patient living in the modern world! Most people with Hashimoto’s have the majority of conditions mentioned above.
In addition, D1 activity is also lower in females, making women more prone to tissue or functional hypothyroidism.
Sound familiar? Normal lab results but hypothyroidism at the cellular level.
And when you have these conditions, there are reduced tissue levels of active thyroid hormone in all tissues except the pituitary because D2 does not behave like this, at all.
D2 is 1,000 times more efficient at converting T4 to T3 than D1 in the rest of the body. And it isn’t suppressed and down regulated by any of the things we mentioned.
So TSH is within normal range because the pituitary is getting plenty of thyroid hormone, but the rest of the body is hurtin’ for certain.
D3 converts T4 into reverse T3. There is none of it in the pituitary. D3 also competes with D1. T4 can go either way. It can be converted to T3 which the body can use or into reverse T3 which is not active.
And reverse T3 blocks the effect of T3. It blocks T3 from binding to receptors and when this happens it doesn’t work. So your metabolism slows, and D1 is suppressed so it can’t do it’s job and convert T3 to T4. And D3 blocks T3 and T4 from getting absorbed into cells.
So the result is you have low T3 levels in the cells of your body and you get all the hypothyroid symptoms.
Like most things related to Hashimoto’s the solution is not simple and it requires a multi-prong approach.
As I have said and written many times, Hashimoto’s is way more than a thyroid problem and way more than a thyroid and autoimmune problem. It is a multi-system disorder that can only be healed using a multi-system approach.
Nowhere is this more evident than in trying to fix poor thyroid hormone conversion.
There are 5 important areas that need to be assessed and addressed if you want better conversion of T4 to T3.
Let’s break it down:
1. Liver Detoxification and Other Metabolic Pathways
2. Increasing T3 and Lowering Reverse T3 Levels
3. The Gut and Thyroid Hormone Conversion
4. Adrenal Stress Can Cause Lower T3 and Higher Reverse T3
5. Systemic Inflammation Lowers T3
And as a bonus we’ll look at key nutrients that support better thyroid hormone conversion.
In the liver D1 is involved in converting T4 into T3 and selenium is an important part of this process. Reverse T3 is also broken down there.
So having enough selenium is essential. (It is recommend to take from 200 to 400 mcg. (micrograms) per day. Make sure you do not take selenium supplements that contain dairy or gluten based fillers.)
Other important factors that can prevent T4 to T3 conversion include stress (both emotional and physiological), poor nutrition, chronic illness and exposure to heavy metals like cadmium, mercury and lead.
Another important factor is lipid peroxidation and antioxidants in the liver. One of the most important in helping the body deal with the damage caused by these heavy metals and to nourish antioxidant enzyme systems is glutathione.
The best form to take orally is S-Acetyl-L-Glutathione. It can also be taken in liposomal cream form or in an IV.
In addition, there are 2 metabolic pathways in the liver that can have an impact on thyroid hormones. One such pathway is the glucoronidation pathway. This pathway is supported by B vitamins, magnesium, and glysine.
The second is sulfation. Sulfation involves binding things partially broken down in the liver with sulfur containing compounds. It is one of the major detoxification pathways for neurotransmitters, toxins, and hormones (like thyroid hormones).
Vitamin B6 and magnesium are important for sulfur amino acid metabolism, as are foods containing sulfur such as: eggs, meat, poultry, nuts and legumes. (Eggs, nuts and legumes might be a problem if you are on the Autoimmune diet.)
Lowering reverse T3 levels and increasing T3 levels is not a simple thing. There are so many variables and other factors that may hinder this process that it’s hard to offer general things that will help.
To really do this properly, one must be tested, evaluated and treated according to what results, symptoms and patterns present themselves.
That being said, let’s look at some general things that may help.
Glucoronidation, mentioned above, has been shown to degrade reverse T3.
The addition of T3 to your thyroid replacement hormone regimen may also be helpful. There are those in the thyroid community that strongly advocate T3 only treatment. Some suggest doing with natural cortisol rhythms, some with time released T3 and others with slow and deliberate increases in T3 therapy.
This may or may not work and what they fail to say is that T3 can also be toxic to the liver in high doses. Again, proper assessment and treatment is required to determine if this course of action is a good idea for you.
Elevations in cortisol, catecholamines, and some cytokines (IL-6, TNF-a, and IFN-a), and low serum albumin levels have also been associated with low T3 syndrome.
Gut bacteria is important for converting T4 into T3.
About 20 percent of T4 is converted to T3 in the GI tract, in the forms of T3 sulfate (T3S) and triidothyroacetic acid (T3AC). The conversion of T3S and T3AC into active T3 requires an enzyme called intestinal sulfatase.
Intestinal sulfatase comes from healthy gut bacteria. (Sulfur is an important nutrient for this, as well).
When you have an imbalance between good and bad bacteria in the gut, this may significantly reduce the conversion of T3S and T3AC to T3. This is one reason why people with poor gut function may have thyroid symptoms but normal lab results.
Inflammation in the gut also reduces T3 by raising cortisol. Cortisol decreases active T3 levels while increasing levels of inactive T3.
Studies have also shown that cell walls of intestinal bacteria, called lipopolysaccharides (LPS), negatively effect thyroid metabolism in several important ways.
LPS:
• reduce thyroid hormone levels;
• dull thyroid hormone receptor sites;
• increase amounts of reverse T3;
• decrease TSH; and
• promote autoimmune thyroid disease (AITD).
With stress, cortisol levels often go up. The increased cortisol levels contribute to this disconnect in the body between the TSH and peripheral tissue T3 levels.
Stress reduces T3 levels in the tissues and increases reverse T3 and this results in tissue hypothyroidism and potential weight gain, fatigue, and depression.
This vicious cycle of weight gain, fatigue, and depression that is associated with stress may be prevented with supplementation with timed-released T3 according to some studies.
The reduced immunity from chronic stress has also been thought to be due to excess cortisol production; but the associated reduction in tissue thyroid levels are shown to play a larger role in the decreased immunity seen with stress.
As with stress, treatment with prednisone or other glucocorticoid will suppress D1 and stimulate D3, reducing T4 to T3 conversion and increasing T4 to reverse T3, causing a relative tissue hypothyroidism that is not detected by TSH testing.
This low cellular thyroid level certainly contributes to the weight gain and other associated side-effects with such treatment. Thus, in stressed patients or those treated with corticosteroids, there are reduced tissue T3 levels that are not reflected by the TSH level, making the TSH an inappropriate marker for tissue levels of T3.
So making sure that you have proper levels of DHEA and cortisol is very important.
As is changing the things in your life that cause you stress. With Hashimoto’s we have emptied our stress savings accounts. We have so much physiologic stress that added emotional stress is incredibly destructive. And one area, in particular, is in the impact of stress on tissue levels of T3.
Hashimoto’s is, at it’s root, a disease of inflammation. And research has found that the inflammatory immune cells (cytokines) and proteins like IL-1, Il-6, C-reactive protein (CRP), and TNF-alpha will significantly decrease D1 activity and reduce tissue T3 levels. Any person with an inflammatory condition – Hashimoto’s – will have a decreased T4 to T3 conversion in the body and a relative tissue hypothyroidism.
These immune proteins will, however, increase the activity of D2 and suppress the TSH despite reduced peripheral T3 levels; again, making a normal TSH an unreliable indicator of normal tissue thyroid levels.
There is also a direct inverse correlation between CRP and reduced tissue T3, so individuals with elevated CRP (greater than 3 mg/l) or other inflammatory cytokines may have a significant reduction in cellular T3 levels.
The suppression of T3 levels inside the cells is linked with the degree of elevation of CRP, despite serum thyroid tests being “normal”.
So, if any inflammation is present, the body will have lower T3 levels in the cells and this can impact function; but the pituitary will have increased levels of T3, resulting in a lowering of the TSH so that, once again test results appear normal. (Have I made this point enough times?)
This really emphasizes the importance of anti-inflammatory strategies to improve T3 levels in the tissues. Anti-inflammatories like Turmeric, ginger, resveratrol, glutathione, and Vitamin D are all helpful.
Sometimes these are needed in rather high dosages.
Eliminating foods that cause inflammation is also absolutely critical: gluten, dairy, soy, sugar, alcohol, processed foods, pesticides and chemical additives should all be strictly eliminated.
The Autoimmune Paleo approach is an excellent diet for reducing systemic inflammation and increasing tissue T3 levels.
Commiphora muku guggulu (Myrrh resin) Guggul produces a resinous sap known as gum guggul. The extract of this gum, called gugulipid, guggulipid or guglipid, has been used in Ayurvedic medicine, a for nearly 3,000 years in India. The active ingredient in the extract is the steroid guggulsterone. This has been shown to stimulate healthy synthesis of T3.
Selenium is a major cofactor for the enzyme 5′ deiodinase which is responsible for converting T4 into T3 as well as degrading reverse T3.
Low zinc status has been shown to compromise T3 production. Zinc can improve thyroid hormone production and play a role in reducing antibodies.
Lipid peroxidation and antioxidant enzyme systems have been shown to play a profound role peripheral thyroid hormone conversion. Glutathione is extremely effective in supporting peroxidation.
Lastly, it is essential to work with someone who understands the complexity of this situation and who can evaluate what is going on properly and who can determine which course of action and combination of things may be best for you.
http://nahypothyroidism.org/deiodinases/
http://www.aaqm.org/Downloads/doc-qmuAUG08.pdf
http://www.chiro.org/nutrition/FULL/Peripheral_Metabolism_of_Thyroid.html
Bianco AC, Salvatore D, Gereben B, Berry MJ, Larsen PR. Biochemistry, Cellular and Molecular Biology, and Physiological Roles of the Iodothyronine Selenodeiodinases Endocrine Reviews 2002;23 (1):38-89.
Koenig RJ, Leonard JL, Senator D, Rappaport N, Regulation of thyroxine 5’-deiodinase activity by 3,5,3’-triiodothyronine in cultured rat anterior pituitary cells. Endocrinology 1984;115(1):324-329.
Silva JE, Dick TE, Larsen PR. The contribution of local tissue thyroxine monodeiodination to the nuclear 3,5,3’-triiodothyroinine in pituitary, liver and kidney of euthyroid rats. Endocrinology 1978;103:1196. location of D2
Kaplan MM. The Role of Thyroid Hormone Deiodination in the Regulation of Hypothalamo-Pituitary Function Progress in Neuroendocrinology. Neuroendocrinology 1984;38:254-260.
Peeters RP, Geyten SV, Wouters PJ, et al. Tissue thyroid hormone levels in critical illness. J Clin Endocrinol Metab 2005;12:6498–507.
Bartelena L, Brogioni S, Grasso L, et al. Relationship of the increased serum interleukin-6 concentration to changes of thyroidal function in nonthyroidal illness. J Endocrinol Invest 1994;17:269-274.
St Germain DL, Galton VA. The deiodinase family of selenoproteins. Thyroid 1997;7:655-668.
Moreno M, Berry MJ, Horst C, et al. Activation and inactivation of thyroid hormone by type I iodothyronine deiodinase. FEBS Lett 1994;344:143-146.
Gupta P, Kar A. Cadmium induced thyroid dysfunction in chicken: hepatic type I iodothyronine 5′-monodeiodinase activity and role of lipid peroxidation. Comp Biochem Physiol C Pharmacol Toxicol Endocrinol 1999;123:39-44.
Chaurasia SS, Kar A. Protective effects of vitamin E against lead-induced deterioration of membrane associated type-I iodothyronine 5′-monodeiodinase (5’D-I) activity in male mice. Toxicology 1997;124:203-209.
Barregard L, Lindstedt G, Schutz A, Sallsten G. Endocrine function in mercury exposed chloralkali workers. Occup Environ Med 1994;51:536-540.
Brzezinska-Slebodzinska E, Pietras B. The protective role of some antioxidants and scavengers on the free radicals-induced inhibition of the liver iodothyronine 5′-monodeiodinase activity and thiols content. J Physiol Pharmacol 1997;48:451-459.
Visser TJ, Kaptein E, van Toor H, et al. Glucuronidation of thyroid hormone in rat liver: effects of in vivo treatment with microsomal enzyme inducers and in vitro assay conditions. Endocrinology 1993;133:2177-2186.
Visser TJ, Kaptein E, van Raaij JA, et al. Multiple UDP-glucuronyltransferases for the glucuronidation of thyroid hormone with preference for 3,3′,5′-triiodothyronine (reverse T3). FEBS Lett 1993;315:65-68.
Gueraud F, Paris A. Glucuronidation: a dual control. Gen Pharmacol 1998;31:683-688.
Wyatt I, Coutts CT, Elcombe CR. The effect of chlorinated paraffins on hepatic enzymes and thyroid hormones. Toxicology 1993;77:81-90.
van Raaij JA, Kaptein E, Visser TJ, van den Berg KJ. Increased glucuronidation of thyroid hormone in hexachlorobenzene-treated rats. Biochem Pharmacol 1993;45:627-631.
Kester MH, Kaptein E, Roest TJ, et al. Characterization of human iodothyronine sulfotransferases. J Clin Endocrinol Metab 1999;84:1357-1364.
Visser TJ. Role of sulfation in thyroid hormone metabolism. Chem Biol Interact 1994;92:293-303.
Schuur AG, Brouwer A, Bergman A, et al. Inhibition of thyroid hormone sulfation by hydroxylated metabolites of polychlorinated biphenyls. Chem Biol Interact 1998;109:293-297.
Visser TJ, Kaptein E, Glatt H, et al. Characterization of thyroid hormone sulfotransferases. Chem Biol Interact 1998;109:279-291 .
Wu SY, Huang WS, Chopra IJ, et al. Sulfation pathway of thyroid hormone metabolism in selenium-deficient male rats. Am J Physiol 1995;268:E572-E579.
Kaptein E, van Haasteren GA, Linkels E, et al. Characterization of iodothyronine sulfotransferase activity in rat liver. Endocrinology 1997;138:5136-5143.
Panda S, Kar A. Gugulu (Commiphora mukul) induces triiodothyronine production: possible involvement of lipid peroxidation. Life Sci 1999;65:PL137-141.
Panda S, Kar A. Changes in thyroid hormone concentrations after administration of ashwagandha root extract to adult male mice. J Pharm Pharmacol 1998;50:1065-1068.
Burger AG, Engler D, Sakoloff C, Staeheli V. The effects of tetraiodothyroacetic and triiodothyroacetic acids on thyroid function in euthyroid and hyperthyroid subjects. Acta Endocrinol (Copenh) 1979;92:455-467.
Arthur JR, Nicol F, Beckett GJ. Selenium deficiency, thyroid hormone metabolism, and thyroid hormone deiodinases. Am J Clin Nutr 1993;57:236S-239S.
Kralik A, Eder K, Kirchgessner M. Influence of zinc and selenium deficiency on parameters relating to thyroid hormone metabolism. Horm Metab Res 1996;28:223-226.
Olivieri O, Girelli D, Stanzial AM, et al. Selenium, zinc, and thyroid hormones in healthy subjects: low T3/T4 ratio in the elderly is related to impaired selenium status. Biol Trace Elem Res 1996;51:31-41.
Olivieri O, Girelli D, Azzini M, et al. Low selenium status in the elderly influences thyroid hormones. Clin Sci (Colch) 1995;89:637-642.
Strain JJ, Bokje E, van’t Veer P, et al. Thyroid hormones and selenium status in breast cancer. Nutr Cancer 1997;27:48-52.
Calomme M, Vanderpas J, Francois B, et al. Effects of selenium supplementation on thyroid hormone metabolism in phenylketonuria subjects on a phenylalanine restricted diet. Biol Trace Elem Res 1995;47:349-353.
Fujimoto S, Indo Y, Higashi A, et al. Conversion of thyroxine into tri-iodothyronine in zinc deficient rat liver. J Pediatr Gastroenterol Nutr 1986;5:799-805.
Nishiyama S, Futagoishi-Suginohara Y, Matsukura M, et al. Zinc supplementation alters thyroid hormone metabolism in disabled patients with zinc deficiency. J Am Coll Nutr 1994;13:62-67.
Kuang AK, Chen JL, Chen MD. Effects of yang-restoring herb medicines on the levels of plasma corticosterone, testosterone and triiodothyronine. Chung Hsi I Chieh Ho Tsa Chih 1989;9:737-778, 710. [Article in Chinese]
Winterhoff H, Gumbinger HG, Vahlensieck U, et al. Endocrine effects of Lycopus europaeus L. following oral application. Arzneimittelforschung 1994;44:41-45.
Winterhoff H, Sourgens H, Kemper FH. Antihormonal effects of plant extracts. Pharmacodynamic effects of lithospermum officinale on the thyroid gland of rats; comparison with the effects of iodide. Horm Metab Res 1983;15:503-507.
Tahiliani P, Kar A. Role of moringa oleifera leaf extract in the regulation of thyroid hormone status in adult male and female rats. Pharmacol Res 2000;41:319-323.
Forsythe WA 3rd. Soy protein, thyroid regulation and cholesterol metabolism. J Nutr 1995;125:619S-623S.
Potter SM, Pertile J, Berber-Jimenez MD. Soy protein concentrate and isolated soy protein similarly lower blood serum cholesterol but differently affect thyroid hormones in hamsters. J Nutr 1996;126:2007-2011.
One of my favorite organizations, the Environmental Working Group, released their 2014 list of produce with highest amount of pesticides.
This is a real concern for those of us with Hashimoto’s and hypothyroidism because studies have linked pesticide concentrations with a significant increase in thyroid disease.
They found an association of organochlorines and fungicides with hypothyroidism. And a 12.5% higher increase in thyroid disease than in the general population.
According to the study “Exposure to these classes of pesticides and thyroid dysfunction is plausible given that the main effects of these compounds are thought to be elevation of TSH levels and reduction of circulating thyroid hormone (T3 and T4).”
An Apple A Day Doesn’t Keep The Doctor Away Anymore
Nonorganic apples once again topped The EWG’s Shopper’s Guide to Pesticides in Produce report, making it the fourth year in a row that the fruit that has the reputation of keeping the doctor away, may now be having the opposite effect thanks to better living through chemistry.
Kale, collard greens, and hot peppers were frequently contaminated with insecticides that are particularly toxic to human health, prompting their “Dirty Dozen Plus” status.
The moral of the story? Grow your own in an organic garden and/or buy organic at your local farmer’s market.
1. Apples
2. Strawberries
3. Grapes
4. Celery
5. Peaches
6. Spinach
7. Sweet Bell Peppers
8. Nectarines (Imported)
9. Cucumbers
10. Cherry Tomatoes
11. Snap Peas (Imported)
12. Potatoes
+ Hot Peppers
+ Kale/Collard Greens
It’s not all bad news! This produce contained the lowest pesticide levels.
1. Avocados
2. Sweet Corn
3. Pineapples
4. Cabbage
5. Sweet Peas (Frozen)
6. Onions
7. Asparagus
8. Mangoes
9. Papayas
10. Kiwi
11. Eggplant
12. Grapefruit
13. Cantaloupe
14. Cauliflower
15. Sweet Potatoes
This pill may not be the answer.
Some of the most common questions I receive via phone, email, Facebook, and yelled across the street concern thyroid replacement hormone.
The question usually goes something like, “Hey, what’s the best thyroid hormone?”
And like most things with Hashimoto’s, this is a super difficult, complicated question disguised as a simple one.
All I can do is mumble, “It depends”
In addition, the problem is that, in reality, many, many people don’t feel better after taking thyroid replacement hormone.
Or they feel better for a while, then they feel worse again.
And a lot of Hashimoto’s patients get fixated on this drug.
Some have to change to natural desiccated. Some are told they have to get on a synthetic. Others have to add T3 or only be on T3. Or they have to raise the dosage, then lower it, then change to something else.
And doctors also share this fixation because thyroid hormone is really important physiologically and for most, thyroid replacement hormone is the only tool in their tool box. And many refuse to budge from the myth that synthetic T4 is the only safe option.
So we wind up with dueling and intractable obsessions resulting in people being pissed off at their doctors, doctors refusing to prescribe anything except Synthroid or the generic equivalent and, unfortunately for the patient, little or no improvement in their hypothyroid symptoms.
There has got to be a better way.
In this post, we will look past this obsession and help break down and demystify thyroid replacement hormone.
The first question, and one that is controversial, is do you really need to be on thyroid replacement hormone?
This is an important question and, of course, the answer is….(wait for it)…it depends.
On what?
Really, it depends on how much thyroid function you have left.
Hashimoto’s is an autoimmune disease in which your immune system slowly destroys your thyroid.
If enough of your thyroid gets destroyed and it stops producing sufficient amounts of thyroid hormone, you can not be without replacement hormone. End of conversation.
On the other hand, if you do have enough thyroid function (and a lot of people do), then the problem may lie elsewhere.
Often the problem is an out of control immune system impacting thyroid function or problems with breakdowns in thyroid pathways that are causing the hypothyroidism.
It’s not the lack of thyroid replacement hormone.
If you focus on properly managing the autoimmune disease part of the equation and on properly evaluating and improving the pathways that make thyroid hormone work, then you may not need extra thyroid hormone at all.
(To complicate matters, once you start taking replacement hormone it impacts the amount of thyroid hormone your body is producing.
So if you have been on it for many years, chances are you may have compromised the thyroid’s ability to produce it alone.)
Even when thyroid hormone replacement is used, it is still very important to manage the autoimmune condition.
This will make the medication work better, slow the destruction of the thyroid gland, and prevent the progression of the autoimmune condition into attacks on other parts of the body like the brain, which comes in really handy, at times.
This is where we should really be fixated. Slowing or stopping the progression of the autoimmune part of this disease should be our obsession. (Ok, I admit it, it’s mine.)
Let’s Look At The Options
That being said, let’s take a look at what the options are and how you can make the best decision for you and your unique set of circumstances.
First there are 2 important factors to consider:
* Bio-identical versus Synthetic
* T3
Bio-identical Versus Synthetic
Bio-identical, as the name suggests, is more like what your body actually produces. The most popular of these are Armour or Nature-throid. The advantage to these is that we can actually test their levels in your system using laboratory testing other than TSH.
The disadvantage is that some people with Hashimoto’s will feel worse on these because their immune system can attack T3 and T4 because they actually have antibodies against them.
Unfortunately, we do not yet have laboratory tests available to test these antibodies.
The advantage of synthetic drugs like Synthroid and levothyroxine is that they are synthetic and the immune system will not attack them.
The disadvantage is that TSH is the only test to measure levels of these drugs and there are many reasons why TSH is an unreliable marker of thyroid hormone levels.
The criticism by doctors leveled against bio-identical hormones is that the dosage varies from batch to batch. A frequently perpetuated myth (from the marketers of Synthroid) is that the dosages and ratio of T4:T3 in Armour aren’t consistent.
That’s just not true, studies have shown otherwise. Armour contains a consistent dose of 38 mcg T4 and 9 mcg T3 in a ratio of 4.22:1. As does Nature-throid.
T3 to the Rescue
Many patient advocates and thyroid support groups sing the praises of T3. And for some, there is no question, T3 is the answer. For others, it’s a nightmare.
T3 is the active form of thyroid hormone, this is what has the greatest impact on our bodies. This is what gives you energy, gets the bowels moving, makes you feel happier and helps you think more clearly. For some this is what helps their hair grow better and their skin get that blood flow back into it.
These people may have trouble converting T4 to T3 because their cells develop thyroid hormone resistance.
On the other side of this are the people who get hyperthyroid with the addition of T3. Think anxiety, insomnia, palpitations, weirdness, a strong desire to vacation at the funny farm.
This is also the case with people who are not managing the autoimmune part of this disease. The attacks against the thyroid causes more thyroid hormone to be released into the bloodstream.
For these people, synthetic T4 might be the better choice along with a concerted focus on managing the causes of these inflammatory incidents (like eliminating gluten, dairy, soy, stress and environmental toxins).
2 Common Things Make You Feel Worse
There are also 2 important factors that can make you feel much worse on thyroid replacement hormone:
Fillers and Adrenal Issues.
Fillers: These are extra things added to the drugs by the manufacturers. Many popular thyroid medications contain common allergens such as cornstarch, lactose and, in some cases, even gluten.
Most Hashimoto’s patients have issues with gluten, and many of them also react to corn and dairy (which contains lactose).
Synthroid has both cornstarch and lactose as a filler. Cytomel, which is a popular synthetic T3 hormone, has modified food starch – which contains gluten – as a filler.
Even the natural porcine products like Armour use fillers. In 2008, the manufacturers of Armour reformulated the product, reducing the amount of dextrose & increasing the amount of methylcellulose in the filler.
This was great for some patients who were sensitive to dextrose and a disaster for others who were sensitive to the methylcellulose.
Nature-throid is considered the most hypo-allergenic of the bio-identicals.
The best choice may be to ask your doctor to have a compounding pharmacy fill the prescription using fillers you aren’t sensitive to. This can be more expensive and unfortunately, some insurance companies refuse to cover it.
Adrenal Issues: If you take Synthroid or even a bio-identical and feel so horrible on the drug that you just can’t continue taking it, one thing to check right away is your adrenals.
The warning label of Synthroid states explicity “Patients with concomitant adrenal insufficiency should be treated with replacement glucocorticoids prior to initiation of treatment with levothyroxine sodium.”
This can cause an acute adrenal crisis in the most extreme cases.
But even in less extreme cases, like those people who have adrenal fatigue and/or exhaustion, taking this drug can result in the patient feeling really lousy.
The adrenals should always be evaluated whenever a patient is prescribed thyroid replacement hormone. (Ideally, this should happen before it is prescribed. Good luck with that.)
Let’s take a look at some other common clinical situations and look at why these things happen.
Normal TSH, But Still Feel Like Crap
This is by far the most common scenario for people with Hashimoto’s. Chronic inflammation can prevent thyroid hormone from getting absorbed in to the cells of the body. This the root of autoimmune disease, but can also come from other things (like infections, surgery, obesity, overtraining, poor diet, etc.).
This can:
*Inhibit thyroid receptors on cells from responding to thyroid hormone.
*Prevent T4 from converting to T3.
*Interfere with the communication between the pituitary and the thyroid (and the adrenals).
Felt Better With Bio-Identical
Some people truly do feel better with bio-identicals. It’s not true of everyone but the addition of T3 can sometimes be the answer because these people:
*May need T3 due to problems with the thyroid hormone receptors on cells
* Were unable to convert T4 to T3 when using T4-only medication
*Had sensitivities to dyes or fillers in synthetic compounds that are not in bio-identical compounds
*Have receptor sites on cells that simply respond better to bio-identical than synthetic hormones
Did Better With T3 Only
As we have seen, some people improve with the addition of T3, while others do their best with T3 only. And these can be synthetic or bio-identical.
This can happen for a couple of reasons:
* Their receptor sites are resistant to thyroid hormone because of high cortisol, high homocysteine, inflammation, low progesterone, vitamin A deficiency and more.
* Difficulty in converting T4 to T3
Didn’t Feel Better With T3 or Bio-identical Hormones
In both cases, more T3 is introduced. These people often don’t have too little T3, they have an active and uncontrolled autoimmune process causing the release of thyroid hormone.
These are also the people who often vacillate from hyper to hypo. They have an immune flare up, more hormone is released and then they crash, it calms done and they are hypo again.
In some cases, these people can have excess adrenal hormones caused by too much nicotine, caffeine, stress or exercising too much.
Feel Better on Synthetic Hormones
Some people actually feel better on synthetic hormones. These can be people who are converting well, have an overactive metabolism and just don’t need more T3.
These are people who also really benefit from an approach that will calm the autoimmune attacks that cause their thyroid to be revved up in the first place.
In every single case described above addressing the underlying autoimmune process first will result in a better clinical outcome (you will feel better) because by reducing the inflammation which is the root of this problem you can:
Improve thyroid receptor site sensitivity
Prevent further destruction of the thyroid
Slow the progression of the autoimmune disease so it doesn’t spread to other parts of the body.
Once again, there are so many variables with Hashimoto’s. The best approach involves a full thyroid work-up and exam, followed by trial and error of different types of replacement medications.
Such a work-up includes more than just TSH, it also has a more complete thyroid panel (including antibodies), other important blood markers (glucose, lipids, CBC with diff, electrolytes, iron, etc.) and additional inflammatory markers like homocysteine, vitamin D, CRP, ferritin, etc.
A history must be taken with attention paid to the patient’s past responses to replacement hormones. With Hashimoto’s patients what a patient feels is clinically relevant and diagnostically important.
Unfortunately, this rarely happens in the conventional model, where the standard of care is to test only for TSH and, if you’re lucky T4.
If TSH is elevated, the patient will get whatever hormone that particular doctor or practitioner is fond of prescribing and that’s the end of it.
Then they are told, “Come back in 6 months to a year and get your TSH tested again. Buh bye.”
And all too often, as many of you know, this approach is doomed to failure. But there is a better way and we are practicing it here at Hashimoto’s Healing.
We offer a complete work up and we focus…, ok, I’ll say it…rather obsessively on reducing the inflammation at the root of this disease and at doing other things to calm, slow and prevent the advancement of autoimmunity to other parts of your body.
This is not just a thyroid problem and there is a lot at stake here. If we’re going to be obsessive, let’s obsess about the things that are at the root of the problem.
I set aside time every week to talk to people with Hashimoto’s about what’s going on with them. In the last year, I have had over 500 of these conversations.
I offer a free 30 minute Hashimoto’s Healing Discovery Session.
In it you can share where you are and where you want to be, I can give you some advice that will help right away and we can discuss how else I may be able to get you feeling better.
If you want to talk with someone who gets it, someone who has been there and who has devoted his life to help people with Hashimoto’s, then I suggest you schedule a time to chat with me.
You might just learn something. Here’s the link to schedule.
http://www.ncbi.nlm.nih.gov/pubmed/23072197 T3 to T4 ratios
http://www.womensinternational.com/pdf/thyroid_hormone_therapy_options.pdf T3 to T4 ratios
http://www.medscape.com/viewarticle/722086_1 Full on medical discussion
http://www.ncbi.nlm.nih.gov/pubmed/15767619 Interesting study on the difference additional T3 therapy makes
http://chriskresser.com/3-steps-to-choosing-the-right-thyroid-hormone
http://thyroidbook.com/blog/which-thyroid-hormone-is-right-for-you/
http://www.rxlist.com/synthroid-drug.htm
http://www.rxlist.com/armour-thyroid-drug.htm
http://www.rxlist.com/cytomel-drug.htm
http://www.nature-throid.com/what_is_nature_throid.php
http://tpauk.com/main/?page_id=1054 Argument against marketing propaganda
The Thyroid, A Fundamental and Clinical Text, Braverman and Utiger, 9th Edition, 2005
Why Do I Still Have Thyroid Symptoms When My Lab Tests Are Normal? Dr. Datis Kharrzian, Elephant Printing 2010
Hey People!
Wow, it’s been a year since I launched my website and Facebook support group. SO MUCH HAS HAPPENED!
I am a big proponent of looking back at the data and the experiences and analyzing what we learned. And, hopefully, we can build from that and improve what we are trying to do.
And that is to help and educate people to heal their Hashimoto’s.
Over the course of this year, I have had over 500 consultations with people with this disease.
I’ve listened as people described their symptoms and their health histories and I’ve also taken a number of surveys and polls at our Facebook support group which has now reached 10,000 Likes.
I want to thank everyone who has joined us for their continued love and support! This is something we could not have achieved without you.
In this blog post I’m going to summarize the top 5 things that I think are really important (from a clinical and practical point of view) and I’ll share a few odds and ends that are just really interesting to me.
Here are my top 5 clinical pearls and a little discussion on each and why I believe it matters to you.
By far, the most common thing I have seen is that many, many people taking thyroid replacement hormone are functionally hypothyroid.
What does that mean?
Well, they are taking thyroid replacement hormone (and it doesn’t seem to matter whether it’s Synthroid, Armour, or Synthroid and Cytomel, or Naturethroid, etc.), their lab test results (usually this means TSH and if we’re lucky TSH and T4) are normal.
However, they have all the common hypothyroid symptoms: they are tired all the time, they are frequently depressed and/or they have anxiety, they have trouble losing weight, their hair is falling out, they have brain fog and memory issues, etc.
Since there is such a consistency of symptoms despite the thyroid replacement hormone, then you have to look at the possibility that the solution can be found in something other than thyroid replacement hormone.
Many people really focus on switching hormones or switching back or switching dosage up and down and for a few, the change works, for others it works for a little while and stops working and for the majority it doesn’t matter because it doesn’t work at all.
For some the addition of T3 can help tremendously, for others it helps for a little while and then stops working. And for others it doesn’t seem to help very much either.
So, if it’s not the thyroid replacement hormone, then what’s the problem?
The problem that I have seen repeatedly is that they are not converting and/or absorbing the replacement hormone.
One reason for this is that TSH is produced by the pituitary which absorbs thyroid hormone differently than the rest of cells in the body.
The pituitary can register thyroid hormone levels when the rest of the body is resistant or just not absorbing it.
There are lots of other reasons why this can happen, but the most important thing to understand is that it’s not always the choice of thyroid hormone, it’s a problem somewhere along the process of getting that hormone into the cells of your body.
What this means is that this becomes a systemic problem and trying to solve that kind of problem by just adding more thyroid hormone is like trying to fix global warming by driving a hybrid.
It might help a little, but there’s a whole lot more that needs to be done.
For example, I worked with one woman who as taking both Levothyroxine and Cytomel. She had the exact symptoms described above. Normal TSH and T4 and all the hypothyroid symptoms I described.
After doing a compete panel we discovered that she had high cholesterol, LDL and triglycerides (because she was functionally hypothyroid) and she wasn’t converting or absorbing well.
We focused on cleaning up her diet, giving her targeted nutrition to help her liver and we worked on improving conversion. She contacted me a month later in total disbelief because her cholesterol had dropped by a little more than 50 points and she noticed that she had a lot more energy.
No cholesterol medication, no changes in thyroid replacement hormone. We just made everything work better and this caused her liver to convert more efficiently. In addition, the changes to her diet help reduce the systemic inflammation and this allowed her cells to better absorb thyroid hormone.
Check out this post on T4 that goes into detail about what is happening here.
This is really a “no brainer”, but I am continually surprised at how many people refuse to accept this or want to negotiate a kinder, gentler half way approach that doesn’t involve them changing their diet and, of course, their lives.
Hashimoto’s is an autoimmune disease and that means that your immune system is attacking your your own tissue. Tissue attack and destruction is induced by immune system stimulation.
Where is your immune system? An estimated 70% lives in your digestive tract. So everything that passes through there interacts with your immune system.
Also, there is a lot of research evidence that shows a clear link between “leaky gut” or intestinal permeability and autoimmune disease.
The breakdown of your intestines is a breakdown in the barrier to your immune system and this clearly is a factor in the initiation of autoimmune disease, but it is also an important factor in people’s symptoms because if this is not addressed you have constant immune stimulation and constant tissue attack.
My advice is always get off of gluten, dairy and soy 100% and for many, because of the state of their intestines, this is not enough. They need to do more. For them we recommend a version of the Paleo diet designed for autoimmune disease and Hashimoto’s, in particular.
I have gotten messages on Facebook and emails from at least a dozen different women who have credited this change alone with completely transforming their lives.
If you’re on the fence about your diet, you’re just prolonging your misery needlessly. It’s such a simple part of the solution.
This is another common area of dysfunction that is often overlooked. However, in my experience and in the experience of many of my colleagues (including my teacher and mentor, Dr. Datis Kharrazian,) this is one of the first steps that needs to be taken.
There are a couple of different types of blood sugar dysfunction. Hypoglycemia, which means your fasting glucose is generally too low and Insulin Resistance, which can be a whole combination of symptoms but is generally brought on by too much sugar in the diet.
And, in reality, lots of people have a mix of both.
The reason this can wreck the whole show is because of the impact of sugar fluctuations on the entire endocrine system.
Blood sugar and insulin spikes impacts cortisol and thyroid hormone levels. This creates a vicious cycle that impacts the pancreas and the pituitary and winds up driving you down.
And to add insult to injury, many people use sugar to get energy to overcome their fatigue.
This is like smoking cigarettes to help your asthma, it does way more harm than good.
For example, I worked with a woman who really had supplement fatigue. She had been put on so many different things that she had spent what amounted to a small fortune on supplements.
She sent me two full pages of things she had been prescribed. This was giving her very expensive urine, but wasn’t helping her feel a whole lot better.
The one thing that no one had told her was that she needed to balance her blood sugar. She had what amounted to a pretty serious case of insulin resistance. She had really bad fatigue, brain fog and memory issues and depression. She just felt like she had lost her life.
One of the main reasons that she had developed this was that her fatigue was so oppressive that sugar was the thing she relied on to get her through the day. Well, what she didn’t realize was that this was intensifying the fatigue and actually making her feel worse and worse.
So we focused on normalizing her blood sugar by getting her to stop the sugar habit and start using protein and good fats and by giving her targeted nutrition that helped to improve insulin receptor sensitivity.
And lo and behold, she felt like a new person. That was the one missing link for her. It restored her energy, it improved her brain fog and memory issues, it helped her to start feeling like her old self again.
Check out this post to get an in depth look at what happens with blood sugar issues.
The next area that is really crucial to evaluate and treat, if necessary, is the adrenals.
There are various stages of adrenal issues from adrenal fatigue to exhaustion and if your adrenals are compromised it can dramatically impact the way you feel when you take thyroid replacement hormone.
In fact, the warning label for Synthroid reads:
“Patients with concomitant adrenal insufficiency should be treated with replacement glucocorticoids prior to initiation of treatment with levothyroxine sodium.
Failure to do so may precipitate an acute adrenal crisis when thyroid hormone therapy is initiated, due to increased metabolic clearance of glucocorticoids by thyroid hormone.”
What this means, in plain English, is that in cases of hypothyroidism, the adrenals need to be evaluated before putting patients on thyroid replacement hormone.
How many people with Hashimoto’s and hypothyroidism do you think have adrenal insufficiency?
I put this question to my Facebook support group and 100% of the 85 respondents with Hashimoto’s said they had most of the symptoms of adrenal insufficiency such as:
* Fatigue, also a thyroid symptom
* Headaches, splitting headaches especially
* Decreased immunity
* Sleep issues. Difficulty falling asleep, staying asleep and waking up feeling exhausted even after you had enough sleep.
* Mood swings
* Sugar and caffeine cravings, (have a hankering for a Red Bull? It could be your adrenals)
* Irritability or lightheadedness between meals, a blood sugar and adrenal problem
* Eating to relieve fatigue, another blood sugar problem
* Dizziness when moving from sitting or lying to standing, it affects your blood pressure
* Gastric ulcers, ulcers in the stomach can be caused by the adrenals
Granted, that’s not a scientific study, but it certainly is emblematic of this problem.
Unfortunately, many doctors dismiss adrenal insufficiency as one of those make believe disorders. It’s not make believe at all, it’s very real.
For example, I had a patient who had developed Hashimoto’s after having a baby. She was diagnosed after lab tests revealed antibodies above the normal range and elevated TSH. Her doctor immediately put her on Synthroid.
She had a terrible reaction and felt so sick that she literally could not continue with the drug. The doctor dismissed this reaction and insisted that she get back on the drug.
She dismissed her doctor and eventually found me. We did a number of different things including getting her on the autoimmune diet, cleaning up her liver and we worked on restoring her adrenals and helping her body adapt to stress.
After three moths of following this protocol she went back to her doctor and asked him to reorder the tests. He grudgingly did saying there wouldn’t be any change he was sure of it.
The lab test all came back normal, TSH was within normal range and the antibodies were undetectable. Naturally, she felt vindicated and was overjoyed.
This doesn’t happen with everyone, but this was a perfect example of a case that illustrates this point.
Here’s a post I wrote that goes into the adrenal thyroid connection in much greater detail.
I think my last important observation is one that I had to learn myself the hard way. I struggled for years before I was diagnosed with Hashimoto’s.
Largely because I didn’t really know what was happening, I kept making excuses for not fully committing to what I have now come to call the Hashimoto’s lifestyle.
Once I got diagnosed and got obsessed with learning about this disease and seeing the damage it can cause in people’s bodies, I started to realize what was at stake and went all in.
After that, things really started to turn around for me in a big way. And I have seen the exact same thing in many, many people I have worked with.
Those that aren’t successful in getting this under control are usually the ones who are unwilling to give up certain things in their lives in order to save their health.
These include stressful jobs and relationships that are repeatedly causing flare ups of their condition. Foods like gluten, dairy and soy that are in virtually every processed and fast food. (You can’t eat like the average American if you have Hashimoto’s, you just can’t).
In addition, you really need to understand that this becomes a systemic problem over time. It progresses into other systems of the body and these can include the liver, the stomach, the gall bladder, the intestines, the cardiovascular system, the brain and nervous system, the muscles and joints and more.
And sometimes you need to go through every system and evaluate it and fix what’s not working.
So you have to go all in. You have adopt a lifestyle that includes diet, includes eliminating triggers like stress and toxic (chemical and emotional) situations.
You know, I was the co-owner of large and lucrative medical practice which it took me 2 years to close. I was so stressed out running that place that it totally fired up my autoimmunity.
I am now a couple of years into an entirely new life and this life is richer, happier and it has far less stress in it.
Plus, I really love what I do. Honestly, I believe that my higher power has a plan for me and that is to help people with Hashimoto’s.
That’s why I’ve gone all in and have devoted both my personal and professional life to bringing hope, help and healing to people who suffer from Hashimoto’s.
These were some interesting observations I have made:
1. More than 80% of the people I worked with had Mono and were exposed to the Epstein Barr Virus.
Clearly this virus is somehow involved in Hashimoto’s. How? The research is far from definitive. Theories include activation of NF Kappa Beta, activation of rouge B cells and proteins like IL-8.
This is an area I intend to explore in much greater depth this year.
2. The most common symptom is fatigue.
Of all the many potential symptoms of Hashimoto’s fatigue is by far Public Enemy #1. And fatigue is often brain based which means it is the result of neurodegeneration caused by hypothyroidism and autoimmunity in the brain. Read more about this here.
3. The disease is progressive. My teacher and mentor, Dr. Datis Kharrazian and others have identified 3 stages. Read this post to learn more about this.
4. Many people have more than one autoimmune disease or at the very least antibodies to other tissues.
One of the most common places for these additional antibodies is to brain tissue, especially cerebellar tissue.
A lot of people don’t understand this and they just dismiss cognitive issues as “aging”. Well, with Hashimoto’s your brain is at serious risk of degenerating rapidly. This is something that really needs to be taken seriously.
Well, that’s all for now. I can’t wait to see what this next year will bring!
And if you’re not aware of it, I offer a free 30 minute Hashimoto’s Healing Discovery Session. In it you can share your story with me. Tell me where you are and where you want to be.
I’ll make some recommendations that I think will help right away and we can discuss how else I might be able to help.
I set aside time every week to talk with people who have Hashimoto’s and I’d love to talk to you.
You can schedule a free session by clicking here.
With Hashimoto’s: How Much Is Too Much?
People often ask me about exercise. What’s the best kind of exercise for Hashimoto’s?
There are 2 types and both can be beneficial. But the real key is not to overdo it. If you do too much you defeat the purpose of exercise and you wind up doing more harm than good.
The first type is simple and slow.
Walking, slow jogging, slow cycling or other exercises like yoga, tai chi or qigong that involve endurance can support your adrenals. This type of exercise can decrease cortisol, help with blood flow and circulation and normalize blood pressure.
Something like this should be part of your routine a few times a week.
The second type involves high intensity for short duration. This should also be part of the mix.
According to research, the optimal exercise level to achieve all the health benefits described above is high intensity: when doing this you will:
* Break a sweat after 3-5 minutes
* Breathe deeply and rapidly
* Only talk in short phrases while you are doing this.
You want to go hard enough to achieve 70% or greater of your maximum heart rate. This can be calculated by this simple equation: 220 – your age in years = your maximum heart rate.
There is a fine line between the right amount of exercise which can really improve health and too much which can actually cause more health problems.
The key point is this: The more intense the exercise, the greater the potential for health benefits that include everything mentioned above, but also the greater risk of doing too much and this results in the loss of all those benefits.
This is especially true if you suffer from an autoimmune disease like Hashimoto’s because you may not be able to exercise like a normal person and you may reach the threshold of maximum benefit sooner than people who do not have this condition.
So the best thing to do is to start slow and gradually build. And the objective is not to “feel the burn” or “pain is gain”. You are in enough pain. The object is to feel better, feel energized and feel the beneficial effects of exercise. If you are wiped out after your workout, you’ve gone too far.
Start small and only increase when you feel like what you are doing is physically not demanding enough. A high intensity workout can be beneficial if you doing as little as 5 minutes per day. Err on the side of too little, if you’re not sure.
Here’s a longer blog post that really goes into detail and provides a great 7 minute high intensity work out. Check it out and try it!
Immune Cells Directly Impact the Thyroid
Hey people! Today’s post in about how the immune system and the thyroid interact.
In researching this week’s content I stumbled on something fascinating that I just have to share with you.
Did you know that the immune system actively modulates thyroid hormone levels and TSH?And I do not mean indirectly, I mean directly.
Check this out! TSH is not only produced in the pituitary. 20 years ago, it was discovered by researchers that immune cells actually produce TSH.
Where? In the bone marrow where immune cells are born, by white blood cells and also in the intestines, when exposed to a virus, or when exposed to bacterial toxins like lipopolysaccharide (LPS), which can end up in the blood stream when you have leaky gut or intestinal permeability issues.
LPS exposure also increases conversion of T4 to T3 causing a local surge of T3. This in can result in a lower output of thyroid hormone.
And 2 immune proteins, IL-18 and IL-12, both of which have been implicated as proteins that may make flare ups and inflammation worse with Hashimoto’s also produce TSH.
I was working with someone the other day, who is a perfect example of this.
Her lab tests say her TSH is too high, yet she is having all these hyper symptoms (she should be hypo). Anxiety, palpitations, mood swings, she’s going nuts.
One possible explanation? She isn’t gluten or dairy free. She has some gluten and dairy, it causes a massive immune response in her intestines, maybe she’s exposed to a bovine virus or viral fragments, these immune cells produce TSH. It looks high because of this, but she’s functionally hyperthyroid because the immune system has overcompensated.
And this works both ways, a hypothyroid state creates impaired immune function. There is still a lot that is not known about this, but one of the theories is that immune cells produce this local surge of T3 and this causes a systemic decline in TRH and TSH production.
One theory on this is that in times of infection and immune induced inflammation (which autoimmune disease is a chronic state of) the immune system shuts down thyroid function and then at some point kicks it back in again.
Well, with Hashimoto’s, this endocrine-immune communication is out of whack. The immune system may not be able to kick things in again. Or may not know when the “infection” is over due to chronic inflammation and tissue attack. The antigen is the tissue of the body. The fight never stops, you understand what I’m saying?
So the immune system is actively throwing the body’s thyroid hormone levels out of whack trying to keep the body in a lower metabolic state so that it can recover from this infection. But there may be a chronic state of infection, or ongoing chronic infections in the body.
Food for thought. Heal your gut. Address chronic infections. This is not just a thyroid problem!
The truth hurts
In this post we’re going to break down the stomach, stomach acid, and, of course, it’s relationship to the thyroid and Hashimoto’s.
What does the stomach do?
It’s role is really to take food that has been chewed (hopefully well) and mixed with saliva and to break it down.
Break it down! Like James Brown!
Break it down, stomach! Do the mashed potato. Ok, what breaks all this food down?
Hydrochloric acid. This is vitally important for breaking down vitamins, minerals (like iron) and vital nutrients so that they can be absorbed by your small intestine.
A lot of people, misled by advertising, think that stomach acid is bad. 2 of the top 10 most prescribed drugs in the US are Nexium and Prevacid.
These are designed to block the production of stomach acid and are called proton pump inhibitors.
These proton pump inhibitors work by completely blocking the production of stomach acid. They do this by inhibiting (shutting down) a system in the stomach known as the proton pump.
Because we don’t need that.
No, actually, it’s hugely important.
Having enough stomach acid prevents food poisoning, parasites and other critters from taking over your digestive tract.
Enough hydrochloric acid also stimulates gall bladder and pancreas function to complete digestion and keep everybody in the digestive tract happy, happy, happy.
Proton pump inhibitors also affect thyroid hormone absorption and a study from Endocrinology Practice, the official journal of the Endocrine Society of America found their impact is so significant that patients taking these drugs and thyroid hormone may need to adjust their dosage.
What I’m saying is you actually do need hydrochloric acid or HCL and it’s production depends on the hormone gastrin.
And guess what else has an impact on gastrin? Thyroid hormone.
So hypothyroidism causes less gastrin to be produced, which leads to lower amounts of hydrochloric acid which, in turn leads to heartburn, bloating, gas and..wait for it…….!
Why, yes I did.
But didn’t you also say too little hydrochloric acid?
Why, yes I did.
Let me explain…mechanisms, people. It’s how things work.
It turns out, having enough stomach acid actually prevents heartburn by helping to thoroughly digest your food.
The burning is felt in the lower esophagus.
The burning sensation that people feel from heartburn is actually from the poorly digested food rotting in your gut and shooting up into your esophagus, where there is no protection from the acid.
Even a small amount of acid will cause problems there.
In an editorial published in the journal Gastroenterology first published online in 2009, the author remarked:
Treating gastroesophageal reflux disease with profound acid inhibition (which the popular drugs are) will never be ideal because acid secretion is not the primary underlying defect.
You see, there is the truth rearing it’s ugly little head. Another study referenced below suggests the actual cause of GERD is pressure on the abdomen (often made worse by weight gain and obesity) not too much acid.
For decades the medical establishment has been directing its attention at how to reduce stomach acid secretion in people suffering from heartburn and GERD, even though it’s well-known that these conditions are not caused by excess stomach acid.
Advertising, people. Great for making money, not so good for healing.
Another thing that HCL is important for is the absorption of vital nutrients like B12, iron, and calcium and for breaking down and absorbing protein.
Too little HCL can also lead to inflammation, lesions and infections in the intestines.
All of that leads to poor absorption of thyroid hormone, leading to…this one is a gimmee….(yup, you guessed it) normal lab tests but hypothyroid symptoms.
With too little stomach acid, also called hypochlorhydria, 2 important factors lead to GERD and acid reflux.
The first is bacterial overgrowth. Stomach acid acts like the police of the digestive tract. It keeps the riff raff out. When you don’t have enough you can get overgrowth of bacterial species that cause problems like copious amounts of gas. (Whew!)
The second problem that too little stomach acid causes is that it can lead to poor digestion, especially of carbohydrates. And these 2 problems feed each other because these problem bacteria really like to feed on carbohydrates.
So you wind with yet another vicious cycle.
This is also why people with acid reflux often feel better after going off of gluten (and other carbs). You stop feeding the problem.
I am very fortunate to have a robust community of Hashimoto’s folks at our Facebook support group.
I asked them how many of them experienced symptoms of acid reflux or GERD. And of the 75 respondents, virtually all of them had symptoms related to issues involving stomach acid.
Here’s a chart that illustrates their symptoms.
3 Symptoms of Acid Reflux – SURVEY TABULATION – January 13 2
And a second chart that looks at what helped.
3 Symptoms of Acid Reflux – SURVEY TABULATION – January 13 4
While this is hardly a scientific study, it is emblematic of how common these problems are among this population. Notice how many people improved by going off of gluten and wheat and/or going Paleo. All approaches that limited the number of carbs. Also notice how many are on proton pump inhibitors.
Too little stomach acid also leads to anemia because you can’t absorb B12, and you can’t properly absorb iron.
Couple this with heavy bleeding during your cycle which can also be caused by too little thyroid hormone (more on that in an upcoming post) and you have a recipe for iron deficiency anemia.
The stomach is important for breaking down and digesting foods and for allowing the body to absorb important vitamins, minerals and protein.
Too little stomach acid can lead to a host of problems: like heartburn (counter-intuitive but true), anemia, iron and protein deficiency.
All of this creates a vicious cycle of less conversion and utilization of thyroid hormone and lower stomach acid. Not good.
So glad you asked.
Let’s use logic, even though it can be counter intuitive. If you have too little stomach acid and this is the cause of the problem then….yup, that’s right, do something to increase the stomach acid when you eat.
Some simple natural solutions include:
* Going gluten free or Paleo (to cut out the carbs)
* Apple cider vinegar (to increase stomach acid)
*Lemon or Lime juice in some water (to increase stomach acid)
*Fresh Ginger or ginger tea (to increase stomach acid secretion)
*HCL supplements (to boost HCL levels)
How much really depends on how bad you’ve got it and on whether or not there are other things going on. And all the things that increase stomach acid should be done with your meal, not on an empty stomach.
H. Pylori
There are some other things that can make resolving this more difficult. One of the most common is the bacteria Heliobactor Pylori also known as H. Pylori.
This little critter can take over when there is not enough stomach acid in your stomach. So be sure to test for it to rule it out if you have these symptoms.
Alkaline Water
This stuff is often marketed as the answer. “Cancer can’t grow in an alkaline environment.”
Here’s the thing. Different parts of your body have different acid and alkaline requirements. Your stomach needs to be acidic.
When you drink lots of alkaline water, especially if it’s with your meal, you may wind up causing everything I have just described.
Don’t believe the hype, acid ain’t all bad.
Once again we see how there is an explanation for what’s gong on and the conventional medical approach or the multi-marketed hype, while profitable, is actually counterproductive to healing.
I envision a day, sometime in the future when medicine actually becomes about healing and resolving people’s issues.
Wait! It’s here… at Hashimoto’s Healing where we provide hope, help and healing for Hashimoto’s and the varied ways that it wreaks havoc on our bodies. For example check out my program The 5 Elements of Thyroid Health.
Please, please, please! Give your body a chance to heal by learning the truth. Question the drug companies and the marketers who are talkin’ loud and sayin’ nothin’.
(I will give a free 30 minute consultation to anyone who can identify the numerous allusions to James Brown songs and/or dances that I have in this post.)
http://www.natap.org/2009/HIV/070409_02.htm :Article on how proton pump inhibitors actually cause the problem they are supposed to fix
http://www.gastrojournal.org/article/S0016-5085(07)01843-4/preview : The real cause of GERD
http://www.ncbi.nlm.nih.gov/pubmed/9079271 : Study showing how antibiotics can improve gastric reflux
http://www.ncbi.nlm.nih.gov/pubmed/16871438 : An interesting study showing that a low carb diet improves acid reflux
http://www.ncbi.nlm.nih.gov/pubmed/17669709 : Study showing how proton pump inhibitors affect thyroid hormone absorption
The Thyroid, A Fundamental and Clinical Text, Ninth Edition. Lewis E. Braverman and Robert D. Utiger 2005
Hey, People!
Hypothyroidism and Blood Sugar Problems Go Together Like a Big Boy and A Big Gulp
This week’s tip involves blood sugar issues and Hashimoto’s. This is one of those vicious cycles where one thing leads to another and together they make a downward spiral.
Did you know that both high blood sugar and low blood sugar levels can make your Hashimoto’s worse?
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.
Well, diabetes doesn’t happen overnight, it’s progressive. And often that progression passes through something called metabolic syndrome and insulin resistance on its way to diabetes.
According to Chris Kresser, L.Ac., Metabolic Syndrome is defined as a group of bad things appearing together, including:
▪ abdominal fat; “the muffin top”
▪ high cholesterol and triglycerides (caused by sugar being stored as fat in the liver)
▪ high blood pressure (caused by plaque build up in the arteries that comes from excess sugar and cholesterol)
▪ insulin resistance
▪ tendency to have blood clots (because sugar makes the blood more prone to clotting)
▪ our good friend, inflammation (the root of all evil – well, at least the root of autoimmune diseases like Hashimoto’s)
Metabolic syndrome is caused by a chronic state of too much sugar in the blood.This is caused by eating too many carbohydrates.
So really, metabolic syndrome could be called “hammering too many carbs disease”.
Because that’s what it is.
When you eat too many carbs, 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 knocking on the door, but the cells won’t let it in.
“I hear you knocking but you can’t come in.”
The pancreas responds by pumping out even more insulin (knocking louder, “Please, let me in!”) in an effort to get glucose into the cells, and this eventually insulin receptors get tired of it all and this leads to insulin resistance.
Studies have shown that the repeated insulin spikes that come with insulin resistance increase the destruction of the thyroid gland in people with autoimmune thyroid disease. Read all about them in this detailed post on blood sugar.
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? Less thyroid hormones are made by the thyroid and you get all the hypothyroid symptoms like fatigue, weight gain, brain fog, depression, joint pain, hair loss and on and on.
Low blood sugar or hypoglycemia can also cause problems with the thyroid.
Your body sees low blood sugar as a threat because severe or long term hypoglycemia can cause seizures, coma, and death. Not good things.
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.
The problem is that cortisol is involved in the “flight or fight” response. This response includes speeding up your heart rate and lung action, increasing blood flow to the muscles to get us ready to fight or to scream and run for the hills.
Cortisol’s job is to increase the amount of glucose available to the brain, help with healing, and to slow down certain things – like digestion, growth and reproduction – that aren’t so important when we were running from hungry lions on the African Savannah (flight).
Unfortunately for hypoglycemics, repeated cortisol release caused by episodes of low blood sugar makes the pituitary gland not work as well.
The pituitary is in charge of the thyroid and when it isn’t working properly, this can cause problems with the thyroid.
So either too much or too little sugar can mess with thyroid function and cause problems.
And, check this out. Hypo-function of the thyroid can cause everything we just talked about because:
▪ it slows the rate of glucose uptake by cells;
▪ it decreases rate of glucose absorption in the gut;
▪ it slows response of insulin to elevated blood sugar; and,
▪ it slows the clearance of insulin from the blood.
These mechanisms present clinically as hypoglycemia. When you’re hypothyroid, your cells aren’t very sensitive to glucose.
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 described above, that suppresses thyroid function.
A vicious cycle. If you want to heal your Hashimoto’s, you need to deal with blood sugar issues. And that means dealing with your sugar habit.