Osteoporosis can be a problem for people with Hashimoto’s and hypothyroidism.
Osteoporosis is a medical condition in which the bones break down and loose tissue. This can make them brittle and fragile and can make the people who suffer from it more susceptible to fractures, breaks and chronic pain.
The National Osteoporosis Foundation reported that by 2020, about 14 million people over the age of 50 are expected to have osteoporosis and over 47 million are expected to have low bone mass.
The most important risk factor for bone loss in midlife women is menopause. Women lose about 50% of their trabecular or spongy bone (found at the ends of long bones as well as in the skull, ribs, pelvic bone and in the bones of the spine.
And they lose about 30% of their cortical bone (the dense outer surface of the bone that protects the inside of the bones) during the course of their lifetime, about half of which is lost during the first 10 years after menopause.
Approximately 40% of all postmenopausal women will eventually experience fractures.
To further complicate matters, women in menopause who are taking thyroid hormone (levothyroxine) have a higher incidence of osteoporosis and low TSH and low bone density go hand in hand. ( hyperthyroid = low bone density).
Physiologically when you increase levels of thyroid hormone, you also increase bone turnover which can result in loss of bone density. It is very important to factor this in and to treat both hypothyroidism and bone loss at the same time.
In this post, I dig into the problem of osteoporosis and how it affects people with Hashimoto’s and hypothyroidism.
I explore why it’s happening, why conventional treatments may or may not help and, in Part II I will share with you lots of things you can do to treat and prevent it.
Bones provide the architecture of our bodies, like the steel beams in a building they provide the structural support for the body and work with the muscles and joints to allow us to move freely.
The skeleton is one of the first things to begin growing in the developing fetus, it’s growth begins as early as a few weeks after conception.
By the eighth week of pregnancy, most of the skeleton is already in place in the form of cartilage and connective tissue.
These tissues form the foundation for the transformation into actual bone know as ossification.
There are two ways that bones grow and mature in the body and the type of growth depends upon what type of bone is needed.
Types of bones include:
Flat bones like ribs, and the bones in the skull
Irregular bones like the vertebrae
Long bones like arm and leg bones
Short bones like the small bones in the wrists
Irregular, long and short bones grow by a process where cartilage is replaced by bony tissue. Most bones are made this way. Flat bones, like those in the skull are made when sheet-like connective tissue membranes are replaced with boat tissue.
Normal healthy bones develop during childhood and teen years as bone is absorbed by the body and rebuilt. Your bones continue to grow and become larger and heavier until about age 30 when they reach their peak density (bone mass).
After age 30, people lose a little bit of bone mass every year. Osteoporosis is the thinning of bones to the point they can become brittle, lose strength and fracture or break.
To Understand Osteoporosis You Need to Understand Bone Cells
The loss of bone density is the result of dysfunction of the certain bone cells. Proper bone function requires a complex interaction of hormones, calcium balance and bone maintenance.
There are three specialized cells that are unique to bones:
Osteoblasts: these are cells that form new bone. They come from the bone marrow and are related to structural cells. These cels work in teams to build bone. They control calcium and mineral depositing and are found on the surface of new bone.
When a team of osteoblasts finish building a bone cavity, the cells change and become flat like little pancakes. They then line the surface of the bone. Old osteoblasts are also called “lining cells”.
These lining cells regulate the passage of calcium into and out of the bone and they respond to hormones by making special proteins that activate osteoclasts.
Osteoclasts are large cells that break down bones. They come from the bone marrow and are related to immune cells (white blood cells). They are found on the surface of the bone.
So osteoblasts control the absorption of calcium and osteoclasts control the deportation of calcium (remember this, it’s going to be important as we continue).
What’s critically important to understand is that in order to have healthy bone you must have a healthy balance of both osteoblasts and osteoclasts. If this balance is lost and there are more osteoclasts (which which cause bone loss) than osteoblasts (which build bone) then you will wind up with more bone loss.
The third kind of bone cells are called osteocytes and these are cells inside the bone. They also come from osteoblasts. Some osteoblasts turn into osteocytes when new bone is being built and they get surrounded by new bone.
They form the matrix of the bone and connect out to other osteocytes. They also have a certain innate intelligence and the can sense cracks or fractures and help direct osteoclasts by telling them where to dissolve bones.
There’s an interesting relationship between thyroid hormone and bone density.
Thyroid hormones are necessary for the development of bones and the establishment of peak bone mass.
When children have hypothyroidism, their bones are still developing this can result in slower bone growth with delayed skeletal development. If they have hyper-thyroid symptoms this can accelerate bone development.
In adults, T3 regulates bone turnover and bone mineral density. So normal levels are required for optimal bone strength.
Too little T3 can result in slower bone turnover and breakdown, whereas too much T3 can result in increased turnover and loss of bone density.
However, both hyper and hypo-thyroid patients can experience bone related issues. It seems that in adult patients with hypothyroidism, bone density increases but bone quality is poor (possibly due to low turnover), thus this may cause increased fracture risk in these patients.
This study showed showed that at the time of diagnosis of hypothyroidism, Bone Mineral Density (BMD) was not significantly different from normal subjects.
Interestingly, the patients that received 2 years of levothyroxine replacement therapy had lower bone density. As I mentioned previously, it’s really important to think about treating bone loss when treating hypothyroidism.
How often is this done? Unfortunately, not very often or not until significant BMD loss has been discovered. (Why wait?)
There is clearly evidence that menopause and the resulting decline in estrogen can result in more bone loss.
Estrogen performs lots of functions in the body and one of those is functions is to slow bone loss (interestingly, increasing estrogen increases thyroid binding globulin which makes less thyroid hormone available, less thyroid hormone = less bone loss).
If more calcium is absorbed into the bones, which can happen when estrogen levels decline the production of both osteoblasts (which control calcium absorption) and osteoclasts (which control calcium deportation) is increased.
When a lot of calcium is absorbed, the body will compensate and lots of calcium will also be deported. However, 50-70% of bone building osteoblasts die in the building of new bone.
The more their activity is stimulated (as with increased thyroid hormone), the more osteoblasts may die. And since estrogen inhibits the uptake of calcium, estrogen actually acts to slow the death of these cells.
It’s kind of like the brakes on the bone loss system. Whereas, adding more calcium can be like the gas pedal.
In some cases, as long as you are consuming plenty of calcium replacement osteoblasts are being made all the time. And many people are successful in increasing bone mineral density by consuming more calcium.
However, the problem is that you can reach a point where replacement capacity is full or another way to look at it is that you have exhausted the body’s ability to absorb so much.
In this study it was observed that people with consistently high lifetime calcium intake and high BMD may actually end up wearing out bone health.
When you increase osteoblast production by increasing calcium intake, you also increase osteoblast apoptosis (cell death). The body always seeks balance.
So, to put it another way, the greater the intake of calcium, the greater the osteoblast activity, the greater the osteoblast cell death rate.
With age this whole cycle can get exhausted. And the increased rate of osteoblast cell death leads to a decrease in the ability for new cells to be made. It’s like you wear out the workers at the bone building factory.
And what happens then is that less bone matrix is made and without matrix calcium can’t help new bone be made and since old bone is constantly getting broken down, the end result is less bone replacement.
When less bone is being replaced you get more porous holes in the bone structure. This is exactly what happens in osteoporosis. Osteoblasts are getting made or they are impaired, dead cells aren’t getting replaced and micro-fractures don’t get repaired.
The reason why osteoporosis risk is greater in women than in men, regardless of menopause and calcium consumption is because of monthly estrogen and parathyroid hormone levels (remember the parathyroid glands control the body’s calcium levels).
In a woman’s cycle estrogen levels are lowest around menstruation and parathyroid hormone levels peak which increases deportation of calcium from the bones and the absorption of calcium into bones.
So for women, the lifetime bone turnover is increased. The workers in the bone making factory have to do more work every month. Over a lifetime, this may lead to their exhaustion.
The important other part of the equation is the relationship between osteoporosis and autoimmunity and inflammation (the root of all evil).
One question that researchers have recently begun to ask is: Is osteoporosis caused by an inflammatory process?
Clinical observation has shown that osteoporosis is also found with other inflammatory diseases (like autoimmune disease, rheumatoid arthritis, inflammatory bowel diseases, etc.)
Conditions like gout, osteomyelitis, rheumatoid arthritis, ankylosing spondylitis, and psoriatic arthritis, are tall commonly linked with inflammation in the joints.
And links between high HS-CRP (a marker that is linked to systemic inflammation) levels and bone mineral density has been seen in some research.
There is also some other research that notes a connection between cytokines (immune cells) and bone reabsorption.
Two cytokines in particular IL-6 and IL-11 (which are both commonly high with Hashimoto’s patients) have been found to play an important role in the formation of osteoclasts (which you will recall break down bone).
Also cytokines can impact nitric oxide synthesis. Nitric oxide is an important mediator of inflammation and it has been shown to be involved in osteoporosis.
“The activation of the inducible NO synthesis (iNOS) pathway by cytokines, such as IL-1 and TNF-α, inhibits osteoblast function in vitro and stimulates osteoblast apoptosis.”
In other words, these immune proteins slow the function of osteoblasts and increase their destruction. Again, leading to possible imbalance of osteoblasts to osteoclasts.
The important take away here is more inflammation means potentially more osteoclasts and when this results in an imbalance between these and osteoblasts (which make bone) the the end result is more bone loss.
One common argument for prescribing Hormone replacement therapy (HRT) for post menopausal women is that it will help prevent further bone loss.
This is true to some extent, but not in the way that many doctors argue.
Basically, as I discussed previously, estrogens are the brakes on this system that help minimize erosion. (remember, extra calcium is the gas-pedal)
Calcium is absorbed into the bones due to osteoblasts, which increase free phosphate level in the bones, which causes the ‘passive’ influx of calcium to restore the calcium-phosphate ratio.
The osteoblasts also compose the matrix upon which the calcium can build bone. They build bone.
Oesteoclasts break down bone. Deportation of calcium from the bones by osteoclasts is a more direct process.
Structurally, estrogen does not stimulate osteoblasts. It protects the bones against excessive bone turnover and osteoblasts against apoptosis.
Post-menopausal bone loss is associated with a high bone remodelling rate, as indicated by increased numbers of both osteoclasts and osteoblasts.
And since women naturally tend to build bone more slowly as they age (i. e., make fewer osteoblasts), the resulting balance between osteoblasts and osteoclasts can be lost.
If this balance is lost, the result is the same, more bone loss. This is why HRT doesn’t always result in better bone mineral density (BMD). It doesn’t affect the numbers of osteoclasts.
This process is explained here.
What About Corticosteroid Use?
A common treatment for joint and back pain is corticosteroid injections. Corticosteroids are also prescribed for inflammation in many inflammatory diseases.
THIS HAS TREMENDOUS CONSEQUENCES WITH BONES AND CARTILAGE.
This is one of those areas that drives me completely insane. Injecting corticosteroids into an already weakened joint capsule is almost a guarantee for bone destruction and development of more severe problems.
This study looks at this problem in detail.
And here is there opening statement: “Glucocorticoid-induced bone disease is characterized by decreased bone formation and in situ death of isolated segments of bone (osteonecrosis) suggesting that glucocorticoid excess, the third most common cause of osteoporosis, may affect the birth or death rate of bone cells, thus reducing their numbers.”
Let’s unpack this sentence. First of all glucocorticoids are known to cause bone disease. Secondly, excess use of them is the third most common cause of osteoporosis(!!!!), and this treatment affects the birth and death rate of bone cells – something that results in reducing their numbers.
And as we have seen (and I hope you understand by now) fewer osteoblasts means less bone formation, fewer osteocytes means less bone matrix on which to build bone.
So here’s the big takeaway, if you have an older relative, friend, parent or you yourself are starting to get up in age, getting steroid injections for pain is a really bad idea for the bones in that area.
It may be a good way to make sure that they need a knee or hip replacement, but it’s not good for their osteoporosis.
This is one of those things that everyone who is concerned about osteoporosis does. The common thought is: Worried about bone loss? Take more calcium.
Ok, that’s a good idea in theory, but is it really a good idea?
It turns out that it might not be in excess. As with most things there is a point where too much calcium may do the opposite of what you had hoped.
Consuming high amounts of calcium may increase osteoblasts, however, you can get to the point where you have too much calcium in your bloodstream ( A calcium level of 10.0 is considered high normal, more than that can cause health problems.)
Too much calcium in your blood can weaken your bones, create kidney stones, and interfere with the way your heart and brain works. This is a condition called hypercalcemia and it can be caused by overactive parathyroid glands.
The body normally absorbs all the calcium it needs from our food. Only about 200 mg is absorbed into the blood. And the absorption rate actually declines when we consume more than we can absorb.
The body naturally compensates in order to prevent blood calcium levels from getting too high.
This happens because our muscles can only function if calcium from inside muscle cells can be deported to outside the cells. If there’s already too much calcium in the bloodstream, this process may be hampered.
Excessively high levels of calcium can actually be life threatening, so to save your life, excessive amounts of calcium are stored in the bones. The problem is that this extra calcium is processed by osteoblasts and osteoclasts.
This extra calcium is absorbed due to actions of the osteoblasts. When they process excess calcium they die sooner, when they die sooner and faster this can result in the balance being lost between osteoblasts and osteoclasts and too little bone matrix is made.
Without the matrix, the calcium can not be used effectively and new bone can’t be made. But the old bone is still being broken down. And this results in porous holes in the bone matrix.
Again, this is exactly what happens in osteoporosis. In people who have osteoporosis, osteoblasts may not be replaced as they should be, and less are available or their activity is compromised and low bone mineral density is the result.
1. Osteoporosis is the result of an imbalance of bone cell production and bone cell breakdown. If more bone is broken down than is created you end up with bone loss.
2. Osteoporosis happens because of an inflammatory process. Treating systemic inflammation will benefit people with osteoporosis and may actually slow bone loss.
3. Supplementing with estrogen may not be successful if you ignore other issues, like inflammation.
4. Supplementing with thyroid hormone has consequences for bone health. Excessive T4 and/or T3 supplementation can lead to faster bone loss.
5. Excessive calcium supplementation can have long term consequences and result in more, not less bone loss.
6. Corticosteroids can be a really bad idea when you have osteoporosis, especially injecting it into areas that are already compromised, like the hips, for example.
In Part II, I will go into all the many things we can do to improve bone health naturally. You definitely want to stay tuned for that.
Can’t wait? Book a consultation with Marc to get some immediate advice about how you can prevent and treat osteoporosis.
Click here to learn more.
https://www.iofbonehealth.org/facts-and-statistics/index.html#category-299 Statistics
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2266953/ Bone loss in menopause
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4199196/ TSH and Levothyroxine and Bone Loss
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279063/ High prevalence of oesteoporosis in women with subclinical hypothyroidism treated with levothyroxine
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4199196/ Effects of levothyroxine and TSH on bone loss
http://www.ncbi.nlm.nih.gov/pubmed/18981975: Bone loss in worse in post menopausal women treated with levothyroxine
https://ostelin.com.au/bones-grow-develop/
https://depts.washington.edu/bonebio/bonAbout/bonecells.html
https://www.ncbi.nlm.nih.gov/pubmed/19885809 Actions of thyroid hormone in bones
Bone loss in worse in post menopausal women: http://www.ncbi.nlm.nih.gov/pubmed/18981975
Bone Loss and Autoimmunity: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1308846/
Osteoimmunology -link between immune system and bone loss http://www.ncbi.nlm.nih.gov/pubmed/23457765
Cytokines and Bone Loss: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC294166/pdf/jcinvest00033-0178.pdf IL-11 and bone loss
http://www.ncbi.nlm.nih.gov/pubmed/8275387 Cytokines and bone reabsorption
http://www.nature.com/nrd/journal/v11/n3/fig_tab/nrd3669_F3.html Inflammatory bone loss illustration
http://www.ncbi.nlm.nih.gov/pubmed/18992710 NfKb and osteoclasts
http://www.ncbi.nlm.nih.gov/pubmed/18365831 Osteoclasts, innate immune cells of the bones
http://www.ncbi.nlm.nih.gov/pubmed/16831928 Autoimmunity and bone
https://www.researchgate.net/publication/281395069_Journal_of_Autoimmunity Bone erosion and autoimmunity
http://www.4.waisays.com/ExcessiveCalcium.htm
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With Hashimoto’s, sometimes the things that cause the most problems are the things we are most attached to. Dairy certainly falls into this category.
In this post we’ll look at the potential problems caused by dairy and Hashimoto’s. And, yes, that may include cheese and ice cream.
There are 2 distinctly different problems that can be caused by dairy consumption. The first is caused by milk proteins, the second is caused by milk sugars.
Let’s take a look at both.
Milk Proteins Have A Similar Structure to Gluten
Unless you’ve been living under a rock, you’ve probably heard about the benefits of going gluten free for people with Hashimoto’s. If this is a new concept to you, check out my previous post on this here.
Well, milk based products have a host of proteins that also can and do cause immune reactions. These include casein (alpha & beta), casomorphin (a protein that closely resembles morphine), milk butyrophilin, and whey.
These proteins are known as “cross-reactors” because they closely resemble gluten proteins and can cause a similar immune response in the body.
In a lot of cases these are undiagnosed and people continue to eat these foods and/or are advised to eat these foods and they end up hurting themselves by damaging their intestines and robbing themselves of important nutrients.
There are different parts of the immune system that react to these foods; IgE, IgA and IgG reactions.
Food allergies are mediated by the IgE part of the immune system. These generally casue an immediate reaction and are often what is called a “true allergy” by doctors and other medical professionals. However, this is not the only type of food reaction your body can have.
IgA and IgG systems can also lead to hypersensitivities. These are sometimes termed “food intolerance” or “food sensitivity.”
The important thing to understand is that they are much different in their mechanism and ability to wreak havoc in your body.
IgA Food Reactions
IgA food intolerance is the more severe reaction and happens mostly in the intestines. It is an abnormal response of the intestines to certain foods in genetically predisposed individuals. The intolerances may manifest themselves early in childhood, or later in life.
IgA food intolerance results in irritation and inflammation of the intestinal tract every time that particular food is consumed. This results in damage to the intestines, and eventually it hurts your ability to absorb nutrients, and can increase the risk of autoimmune diseases, cancer, and accelerate aging through increased intestinal permeability or leaky gut.
IgA food intolerances can also vary in their symptoms considerably. They may be asymptomatic, may be neurological or they may present with the following symptoms: diarrhea, loose stools, constipation, acid reflux, malabsorption of nutrients from foods, and increased intestinal permeability.
They can cause IBS, gas, nausea, skin rashes (including eczema), acne, respiratory conditions such as asthma, nasal congestion, headache, irritability, cognitive problems and vitamin/mineral deficiencies.
The most famous IgA food reaction is “celiac” disease, and it is an intolerance to gluten, the protein found in wheat. We have looked into how this impacts Hashimoto’s extensively. Check out our previous post here.
However, dairy protein, egg, and soy protein IgA intolerances are also extremely common in people with Hashimoto’s. These intolerances do not have a specific name, and may be confused with other, less severe food absorption syndromes.
IgG Food Reactions
These are antibodies that provide long-term resistance to infections, called Immunoglobulin G (IgG), and they have a much longer half-life than the traditional IgE allergy. These reactions can be much more subtle and people can live with them for years, if not their entire lives.
Symptoms, ranging from headache and nausea to seizure and hyperactivity, or simply just fatigue, bloating, mood changes brain fog, memory problems or dark circles under the eyes. They may occur hours or even days after the problem food has been ingested.
Food allergy tests like the ALCAT test, test both IgA and IgG reactions to foods. A positive or equivocal finding of IgG against foods may indicate that the person has been repeatedly exposed to food proteins recognized as foreign by the immune system.
This matters with thyroid autoimmunity because this process can fire up the very same parts of the immune system that are already attacking our own tissue. In fact, Antithyroglobulin antibodies (TgAb) and antithyroperoxidase antibodies (TPOAb), predominantly of the immunoglobulin (Ig) G class, are hallmarks of Hashimoto’s.
Researchers have recently discovered that there are 2 types of IgG proteins, IgG4-positive and IgG4-negative. Further studies are needed to determine exactly what the difference between them is. But this may have clinical and treatment ramifications.
The degree and severity of symptoms vary greatly because of the genetic makeup of the individual. The complete elimination of IgG positive foods may bring about important improvements in Hashimoto’s symptoms because this can be a key factor in calming autoimmunity.
Often people confuse the food immune reactions to dairy mentioned above and milk intolerance which is caused by milk sugars known as lactose.
One thing that people don’t always realize is that even tiny amounts of lactose can have a major impact on our ability to absorb thyroid medications. Worst of all, some thyroid medications actually contain lactose, defeating their own purpose!
Lactose Can Make Thyroid Hormone Not Work As Well
A recent study published in 2014 by Asik and colleagues found that lactose intolerant Hashimoto’s patients who were taking levothyroxine showed a decrease in TSH after lactose restriction.
In other words, removing lactose improved how their levothyroxine was working.
Another study from August 2014 had a similar finding. This was published in the Journal of Clinical Endocrinology and Metabolism by Cellini and colleagues and found that lactose intolerance increased the need for more thyroid medications.
The researchers found that the average person with Hashimoto’s required an average dose of 1.31 mcg/kg/day of levothyroxine to get to an average TSH right around 1 mU/L (that would be right around 75 mcg of levothyroxine for a 125 pound person), while a person with Hashimoto’s and lactose intolerance who continued to consume lactose needed a dose of 1.72 mcg/kg/day to reach the same goal (that would be like 100 mcg of levothyroxine for the same 125 pound person- that’s quite a bit more).
In addition, patients who had other gut disorders in addition to lactose intolerance required an even higher dose to get to their goal TSH 2.04 mcg/kg/day, or around 116 mcg for a 125 pound person. So you can see, the more gut related issues the higher the dose to achieve the same effect.
If your TSH levels are jumping up and down and you’re having a hard time controlling them, dairy protein immune responses and lactose intolerance should be top on your list of suspects.
Lactose intolerance rates in Caucasians have been reported to be between 7% to 20%, and much higher those in those of Asian and African descent. Lactose intolerance can be secondary to other conditions and reversible or it can be genetic and permanent.
A recent 2014 study by Asik and colleagues tested 83 Hashimoto’s patients for lactose intolerance and found lactose intolerance in 75.9% of the patients. I’d say that would qualify as pretty darn common!
38 of those patients were instructed to start a lactose free diet for 8 weeks, and the researchers found that over this time, the patients’ TSH dropped, meaning, they were absorbing their thyroid medication better.
For some lactose intolerant people, even tiny amounts of lactose that are found in thyroid medications can be an issue, causing impaired absorption of thyroid medications. Yes, what we’re saying is that thyroid medications could be undermining their own absorption if they contain even teeny amounts of lactose.
So if you are someone that can’t get his/her TSH into your “Goldilocks zone” – where it’s just right (there is much debate about where this is, but general consensus is that TSH should be somewhere between 0.5-2 mU/L for people to feel best) despite taking higher and higher doses of thyroid medications, consider lactose intolerance and the possibility that the lactose in your diet or even in your thyroid medication may be hindering its absorption.
And here’s the thing, the reality is you could have both lactose intolerance and be having an immune reaction to diary proteins. This is a potent and destructive double whammy for people with Hashimoto’s. Which, as you should know, is an autoimmune disease of the thyroid!
So dairy can potentially wind up autoimmune tissue destruction and prevent thyroid hormone from working. The result is a rapidly accelerating decline in thyroid function.
Some people will ask, “What about Lactaid?” They sometimes ask this because they can’t bear the idea of living without dairy products such as cheese and ice cream. And the logic makes sense to some degree. The problem is it doesn’t really solve the long term damage and potential problems.
It’s a little bit like an alcoholic taking the drug Antabuse and continuing to drink. The real problem is alcohol. And the real problem for some people is dairy.
As far as diet, I have seen tremendous improvements in my own health and the health of my clients and readers on a dairy free diet, so this is something that I strongly recommend for everyone with Hashimoto’s.
If you weren’t aware of it, here are some common medications that contain lactose as a filler and some that are lactose free.
· Synthroid
· Euthyrox
· WP Thyroid
· Nature-Throid
· Most generic brands of levothyroxine
· Some compounded medications- check with your pharmacist
· Tirosint
· Armour Thyroid
· Cytomel
· Levoxyl
· Some compounded medications may use lactose as a filler – check with your pharmacist
Of all of the T4 containing medications, Tirosint has the fewest fillers that may affect absorption, and this medication was designed for people with these types of intolerance. This medication is recommended if you suspect you may have problems with dairy and lactose.
Of course, some people do better with the addition of T3. Of all of the T4/T3 combination medications, WP Thyroid has the fewest fillers that can impair absorption. However, it does contain trace amounts of lactose, as well.
Armour thyroid does not contain lactose, but contains corn derived ingredients that can be problematic in corn sensitive individuals and can trigger a gluten like reaction.
When they changed their formulation a few years ago, some people did very poorly with the new mixture, and one of the reasons was this corn based filler.
Another really interesting research finding is that high TSH can simply be caused by absorption disorders like lactose intolerance, celiac disease, atrophic gastritis, H. Pylori infections, inflammatory bowel disease and/or parasites.
All of these issues commonly prevent people from getting their Hashimoto’s into remission, as well. These are more positive feedback loops and they cause vicious cycles that lead to poor results in different systems of the body.
This is a perfect example of how this is not just a thyroid problem. Thyroid hormone metabolism is dependent on other systems of the body.
A 2012 Polish study by Ruchala and colleagues reported that thyroid patients who need more that 2 mcg/kg/day of levothyroxine with an increased TSH should be suspected of having an absorption disorder like the ones mentioned above.
Get off of dairy 100%. Treat it the same way you treat gluten and understand that the misery it can cause if not worth the buzz of an ice cream cone or some cheese on crackers.
Also understand that having “just a little bit” is not really solving the problem at all. A tiny amount can be a tsunami to your immune system and can lead to a whole cascade of problems.
Being “sort of dairy free” is like being “sort of pregnant”. It’s not a real thing.
http://www.ncbi.nlm.nih.gov/pubmed/23992023 IgG proteins in Hashimoto’s
http://www.researchgate.net/publication/271022933_Thyroxine_softgel_capsule_in_patients_with_gastric-related_T4_malabsorption – The influence of lactose intolerance and other gastro-intestinal tract disorders on L-thyroxine absorption. Endokrynol Pol. 2012;63(4):318-23.
http://www.ncbi.nlm.nih.gov/pubmed/24078411 Asik, et al study
http://press.endocrine.org/action/doSearch?AllField=lactose+intolerance+and+thyroxine – Systematic appraisal of lactose intolerance as cause of increased need for oral thyroxine. J Clin Endocrinol Metab. 2014 Aug;99(8):E1454-8. doi: 10.1210/jc.2014-1217. Epub 2014 May 5. PMID: 24796930
http://www.ncbi.nlm.nih.gov/pubmed/17123345 Lactose intolerance revealed by severe resistance to treatment with levothyroxine. Thyroid. 2006 Nov;16(11):1171-3.
http://labeling.pfizer.com/ShowLabeling.aspx?id=688&mc_cid=3f79b51f37&mc_eid=c1f303f62b Levoxyl – Levoxyl
http://www.rxlist.com/tirosint-drug.htm – Tirosint
http://www.pdr.net/full-prescribing-information/wp-thyroid?druglabelid=3202 – WP Thyroid
Some of the most common questions that I get from people who reach out to me are about antibodies.
There seems to be a good deal of confusion about them and also a good deal of emotion and expectation attached to these numbers going up or down.
In this post, we examine thyroid antibodies and, hopefully, dispel some of the myths around them.
First of all, what are antibodies, exactly? I like to use military analogies when describing the immune system. And antibodies are like military intelligence (hold the oxymoron jokes).
They are the part of the immune system that gathers information on the bad guys (bacteria, viruses, fungus, parasites, etc.) and then they label those bad guys. Kind of like putting a red flag on them.
The invader is called an antigen. Antibodies bind to these antigens like a lock and a key. Every cell has antigens and these are what the immune system recognizes. And every cell in our body has a self-antigen which are supposed to let the immune system know that our own tissue isn’t a bad guy.
Once the bad guys have been labeled, other parts of the immune system are signaled and they attack and, in most cases, kill the bad guys. In some cases these antibodies can neutralize the bad guys all by themselves and not have to wait for reinforcements.
With autoimmune disease these antigen signals get confused and the immune system ends up attacking our own tissue.
Over the last 50 years there has been a lot of research in this area.
There is a region on cells located on some of our genes called the HLA (or Human Leucocyte Antigen) System. Many of these are located on chromosome 6 (for those of you keeping count).
Mutations or defects of HLA has been linked to many different autoimmune diseases. Exactly what happens is not known, there are numerous theories, but the end result is that our own tissue gets attacked and destroyed by the immune system.
There is a specific class of HLA (class II) that has been linked to autoimmune thyroid diseases like Hashimoto’s and there are also specific antibodies that are important in the disease.
There are 2 autoantibodies that are important:
Thyroid Peroxidase Antibody (TPO Ab): This antibody is the one that is usually high in autoimmune thyroid conditions like Hashimoto’s. It is also known as microsomal antibody.
Thyroglobulin Antibodies (TgAb): These aren’t seen high as often as TPO Ab. They are usually ordered when thyroid lab results seem strange because these antibodies can interfere with thyroid hormone production.
TgAb is also used to monitor progress after surgery for removing the thyroid in thyroid cancer.
In Hashimoto’s, TPOAbs are present in nearly all (>90 %) patients, while TgAbs can be seen in approximately 80%.
Antibodies against TPO (TPOAbs) and Tg (TgAbs) are of immunoglobulin G class, (IgG) and both are really good buddies with their antigens.
For TPO, it is for the enzyme thyroid peroxidase, which frees iodine and helps in the production of T4 and T3.
And for TgAb it is for Thyroglobulin, which is also used by the thyroid to produce T3 and T4.
When these 2 things get destroyed, over time, the body can’t make enough thyroid hormone.
This results in hypothyroidism and all the familiar problems of Hashimoto’s: fatigue, constipation, depression, hair loss, cold hands and feet, brain fog, memory issues and lots more.
Unlike TgAbs, TPOAbs can activate certain parts of the immune system (complement) and are able to cause damage to thyroid cells.
However, there isn’t much evidence that both antibodies have a major role in the formation of Hashimoto’s or in the destruction of thyroid cells.
It seems a lot more likely that other parts of the immune system are signaled and that they bring in the Navy Seals of the immune system which attack and kill thyroid cells.
TPO and TgAb antibodies, however, are considered the definitive test for whether or not you have Hashimoto’s. Basically, if either one or both of these are found to be above the lab range values, then you are positive for the disease.
Most labs have the high end at about 25 to 35. Numbers vary considerably, but it is not unusual for people who have been diagnosed to have antibodies above 1,000.
As I stated above, in most cases these antibodies, themselves, do not attack and kill thyroid cells.
What’s also important to understand is that there are various stages of autoimmune disease and depending on where you are in the progression, you will have different degrees of thyroid tissue destruction and, therefore, different symptoms.
According to Dr. Datis Kharrazian, there are 3 stages of autoimmune disease. While these stages are not recognized by conventional doctors, they are very useful in determining exactly where you are in the progression of the disease.
And realizing that there are stages and that the stages get worse and worse, is also helpful for motivating you to do as much as you can to stop the progression. (Hopefully!)
You can read more about these stages here.
The antibodies are really involved in signaling the immune system and in setting off a series of events that results in the attack and destruction of the thyroid.
I have written extensively about what happens in this previous post.
The important thing to understand here is that the amount of antibodies don’t necessarily directly correspond to how severe the Hashimoto’s is.
There are many reasons for this, but one simple way to look at it is this: The amount of destruction that is done by the army (the immune system) depends on the strength and number of the soldiers.
As I said earlier, the antibodies are really like the CIA or some intelligence gathering part of the army. The front line soldiers are the killers. If you have lots of soldiers and they are all revved up and ready to dance, then you get more destruction.
If your army is weak and there aren’t that many soldiers, then the CIA tells them to kill, kill, kill, but they can only do so much damage.
On the other hand, even if there are only a few CIA agents and there is a large, aggressive army, you will still have massive destruction (and loss of thyroid function).
Where am I going with all this? The amount of destruction, which really is the cause of how crappy you feel, depends on the strength and number of soldiers, not on the number of CIA agents in the field.
This is why antibodies are not a good measure of progress and often don’t correspond with how well people feel.
Antibody numbers don’t correspond, directly, with tissue destruction. As I mentioned above, in some cases TPO antibodies have been linked to tissue destruction, but more often, this is not the case.
Many patients and doctors or practitioners track these numbers and use them as a measure of whether or not what they are doing is working. And many times, they will find that there is no correspondence.
Obviously, getting antibody numbers to drop is not a bad thing. But it is also not necessarily such a good thing, because it may not be an indication that the destruction or the progression of the disease has slowed.
In conventional lab testing there really aren’t tests that are done to look at this. One theory with Hashimoto’s is that the ratio between the CIA and the soldiers is important.
The soldiers are also known as the TH-1 system, the cytokines or immune proteins associated with this part of the immune system are the killers.
The CIA is known as the TH-2 part of the immune system and you can test for ratios between TH-1 and TH-2 cytokines.
If there is a lot more of the soldiers than CIA agents, then the prognosis is not good and the disease tends to be more severe.
With Hashimoto’s there is a tendency towards more TH-1 than Th-2, but this is not always the case.
On the other hand if the CIA is more numerous or more balanced and the control and command part of the immune system (TH-3 or the regulatory part of the immune system- what we can call the General) is also strong, then, usually the prognosis is better and you can calm the attack and slow or stop the progression of the disease.
In reality, the immune system isn’t linear and this is an oversimplification. Testing is available to look at the cytokines that represent these different parts of the immune system, but there are many other factors that make current tests for this unreliable and not that helpful.
However, you can use these ideas to help figure out what you need to do in order to calm the attack, slow the progression of the disease and, most importantly, feel better.
The major cause of thyroid tissue destruction is something called apoptosis. This is programmed cell death.
Lots of crazy things happen on a molecular level (like cytoskeletal disruption, cell shrinkage, chromatin condensation, nuclear fragmentation, membrane blebbing, and DNA fragmentation – membrane blebbing, people!) to make this happen, but the easiest way to grok the root of it is to understand that it is initiated by inflammation.
The best way to slow the progression and minimize destruction is to do everything you can to stop inflammation and to strengthen the regulatory part of the immune system.
2 important anti-inflammatory agents are: Vitamin D and glutathione. These supplements strengthen the regulatory part of the immune system (TH-3 or the General).
(One important thing to note is that some people with Hashimoto’s have a defect with vitamin D receptors and may need to take more than is usually required by normal individuals.)
These are important anti-inflammatories.
Another player in the complicated drama of Hashimoto’s is TH-17. This is like a rouge agent that when numerous and aggressive can do major damage. TH-17 is highly inflammatory.
Natural supplements that reduce TH-17 include Turmeric and Resveratrol. Some Chinese herbs that have been shown to reduce TH-17 are Chang Shan or dichroa root and Huang Lian and Huang Qin whose active compound is berberine.
Also, it is very important to reduce the causes of inflammation in your diet. The three most inflammatory foods in our diet are gluten, dairy and soy.
Gluten has been extensively hybridized and deamidated and has been linked to the initiation and progression of thyroid autoimmunity.
Dairy products when commercially produced are full of antibiotics, hormones and god knows what else. They have also been linked to the initiation of various autoimmune diseases.
Soy is one of the most heavily genetically modified foods in our diet and is also quite difficult to digest.
Some research has indicated that thyroid replacement hormone can reduce TPO antibodies, though there is also some indication that natural desiccated hormone can raise antibodies in some individuals (it seems to be those who have a particularly severe immune reactivity – i.e., they have lots of inflammation).
Selenium has been found to reduce TPO antibodies in a number of studies.
Thyroid antibodies are important for determining whether or not you have Hashimoto’s but are not always a good indicator of how well what you are doing is working.
Do not get too excited if antibody numbers go up or down. It’s not the antibodies that are the problem as much as the other parts of the immune system that are attacking and destroying the thyroid.
Get excited about reducing inflammation. That should be your daily obsession. Really, its that important.
Thyroid replacement hormone and selenium have been shown to reduce TPO antibodies, but this may not work for everyone.
Hashimoto’s is complicated. It is a multi-system disorder that requires a multi-system approach. That’s why created my program: Healing Hashimoto’s: The 5 Elements of Thyroid Health. Click here to learn more.
References:
http://en.wikipedia.org/wiki/Apoptosis
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC555850/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3271310/
http://www.thyroidmanager.org/chapter/hashimotos-thyroiditis/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3271310/– Technichal, but great info on what happens in Hashimoto’s
http://www.ncbi.nlm.nih.gov/pubmed/15307940
http://www.ncbi.nlm.nih.gov/pubmed/7878464
http://www.ncbi.nlm.nih.gov/pubmed/20477110
http://www.medicalnewstoday.com/releases/241571.php
http://www.jimmunol.org/content/185/3/1855.full
http://www.cambridgemedicine.org/news/1299069648
http://jcem.endojournals.org/content/87/4/1687.long
The human body is a wonderfully complex playground where hormones, immune cells, neurotransmitters, red and white blood cells, bacteria, and more all frolic.
With Hashimoto’s that playground gets invaded by a hurricane of inflammation and this disrupts many of the systems that produce these things.
In today’s post, we focus on how blood sugar problems can impact the thyroid and how Hashimoto’s and hypothyroidism can also make blood sugar problems worse.
It’s a two way street, people.
The endocrine gland that is responsible for helping maintain blood sugar balance is the pancreas. The poor, dear, much beleaguered pancreas.
What does the pancreas do? Quite a lot actually, we really should be nicer to it. It does endocrine stuff and non-endocrine or exocrine stuff.
On the endocrine side it produces insulin, glucagon and somatostatin. Insulin and glucagon are involved in blood sugar metabolism and somatostatin is involved in intestinal absorption.
The exocrine functions include secreting digestive enzymes into the small intestines. These breakdown proteins, fats and carbs in the diet.
Studies have found pancreatic function was significantly reduced in patients with hypothyroidism.
And, in many people today, the pancreas is under siege.
Americans are addicted to sugar. In some measure, it’s their own doing. In other ways, it is the food industry and public health officials who decided that fat was evil when it was discovered that cholesterol was linked to heart disease in the 1980s. The National Academy of Science made sweeping recommendations at that time to get rid of dietary fat.
So fat was taken out of many processed, fast foods and in an effort to make it taste less like an old ping pong table, it was replaced with sugar.
Carb Roller Coaster
What has since developed is a nation of carb and sugar addicts riding the roller coaster of sugar highs and crashes.
On average, Americans hammer about 200 pounds of sugar a year, and diabetes is a serious threat to bankrupt our healthcare system in the next 20 years.
It is estimated that almost half the population born after 2000 will become diabetic.
This is almost entirely due to diet. As Thomas Edison said, “We’re digging our graves with our teeth.”
Health is really all about balance. And nowhere is this idea more evident than when you look at blood sugar balance.
There are really 2 different kinds of blood sugar problems and many people have a mixture of both. These are hypoglycemia (or too little sugar in the blood) and insulin resistance (or too much sugar in the blood).
With Hashimoto’s either one or both of these blood sugar problems can make things worse. And just to remind you that this goes in both directions; its important to understand that hypothyroidism can also cause blood sugar problems all by itself.
(We have the makings of a vicious cycle.)
Hypoglycemia
Your body is programmed to recognize low blood sugar as a threat because severe or long term hypoglycemia can cause seizures, coma, and death.
When your blood sugar levels drop below normal, your adrenal glands respond by secreting cortisol. Cortisol then tells the liver to make more glucose, bringing blood sugar levels back to normal.
Hypoglycemia is a condition in which there is not enough cortisol to raise blood sugar into the normal range.
The problem is that cortisol (along with epinephrine) is also a sympathetic nervous system stimulant involved in the “flight or fight” response. This can end up wearing out the adrenals.
In fact, we often see adrenal fatigue and hypoglycemia together.
Cortisol’s job is to increase the amount of glucose available to the brain, enhance tissue repair, and slow other functions – like digestion, growth and reproduction – that aren’t so important when you are running from hungry lions on the African Savannah (flight).
Unfortunately for these people, repeated cortisol release caused by low blood sugar can also suppress pituitary function.
And the pituitary is the master gland that instructs the thyroid. If this function isn’t working properly, then “Houston, we have a problem.”
And where do we have a problem? In the thyroid.
Cortisol directly inhibits the enzyme (5’-deiodinase) which converts inactive T4 into active T3. This can lead to low T3 levels.
In addition, elevated cortisol will cause thyroid hormone receptor insensitivity meaning that even if T3 levels are high enough, they may not be able to bind normally to receptor sites. And when this happens it doesn’t get into the cells.
Cortisol will also increase the production of reverse T3 (rT3) which is inactive. (It’s kind of like the anti-hormone.)
rT3 can cause an increase in the production of substances known as thyronamines that can cause hypothyroid symptoms (like, low basal body temperature,fatigue, depression, etc.) along with insulin resistance symptoms of increased blood sugar.
Cortisol can also lower the levels of protein that binds to thyroid hormone so it can circulate in a stable structure.
And finally, elevated cortisol will slow TSH production by messing with hypothalamic-pituitary feedback leading to lower TSH production.
In my previous post on the adrenal glands we learned about the HPA (hypothalmus-pituitary-adrenal) axis.
Well, there is also an HPT (hypothalmus-pituitary-thyroid) axis.
And much like wires going through a transformer on an electric grid, the HPT and HPA axis are very closely related and problems in one area can affect the other.
“When things go wrong, wrong with you, it hurts me too.” sings the HPA to the HPT axis.
Common symptoms of hypoglycemia include (These come from a form called a Metabolic Assessment Form that I use in my practice that I got from studying with Dr. Datis Kharrazian):
(Many of these symptoms improve when you eat )
*Craving sweets
*Irritable if meals are missed
*Depend on coffee or other kinds of caffeine for energy
*Eating relives fatigue
*Feel shaky, or jittery
*Feel agitated or nervous
*Get upset easily
*Poor memory, forgetful
*Blurred vision
It’s important for hypoglycemics to eat often throughout the day and not skip meals. Each meal should be a combination of protein, carbohydrates and fats. And, for these people, too many carbs will often cause serious problems with their blood sugar levels.
When you eat too many carbs and too much sugar, the pancreas secretes insulin to move extra glucose from the blood into the cells where glucose is used to produce energy.
But over time, the cells lose the ability to respond to insulin. It’s like insulin is a little dog barking outside the cell, but the cell won’t let it in.
“I hear you barking, but you can’t come in.”
The pancreas responds by pumping out even more insulin (barking louder) in an effort to get glucose into the cells, and this eventually causes insulin resistance.
Studies have shown that the repeated insulin surges that come with insulin resistance increase the destruction of the thyroid gland in people with autoimmune thyroid disease.
Let me repeat that, insulin resistance increases the destruction of the thyroid gland in autoimmune thyroid disease (Hashimoto’s).
As the thyroid gland is destroyed, what happens? Thyroid hormone production falls. And this causes hypothyroidism. Not good.
Insulin resistance can also cause a reduced conversion of T4 to T3 hormones.
When this is addressed, the cells can once again start using glucose for energy and T3 production picks up.
So for a person who is insulin resistant, a lower carbohydrate diet may help restore better T4 to T3 conversion and often these people lose weight in the process ( a nice side effect).
For other people, other things like long-term chronic stress may be affecting their response to low carb diets. As we have seen in my previous post, chronic stress can interfere with thyroid hormones in several ways.
(These are also from that form mentioned above):
(Eating generally doesn’t improve these symptoms )
* Fatigue after meals (this is the hallmark symptom)
* General fatigue
* Constant hunger
* Craving for sweets that isn’t relieved when you eat sweets
* Must have sweets after meals
* Waist girth equal to or larger than hip girth
* Frequent urination
* Increased appetite and thirst
* Difficulty losing weight
* Migrating aches and pains
Life is not a textbook. Many people are somewhere in the middle of this blood sugar odyssey and they have some symptoms of hypoglycemia and some symptoms of insulin resistance.
I put this question to my Facebook Support Group and of the 66 respondents with Hashimoto’s, 24 reported symptoms of hypoglycemia and 14 reported symptoms of insulin resistance.
16 reported some symptoms of both.
While this is hardly a scientific study, it does demonstrate how common this problem is in this population.
On thing that’s important to understand is that whether you have high or low blood sugar, you probably have some amount of insulin resistance.
I explained how high blood sugar causes insulin resistance above, but insulin resistance can also cause low blood sugar.
This condition, called reactive hypoglycemia, happens when the body secretes excess insulin in response to a high sugar and carbohydrate meal.
For example: A burger on a sesame seed bun, french fries and a soda – causing blood sugar levels to spike and then drop below normal. (I’m not lovin’ it!)
If you eat like this and you have Hashimoto’s (and hypothyroidism), you are setting yourself up for a world of hurt.
Hypo-function of the thyroid can cause everything we just talked about because:
These mechanisms present clinically as hypoglycemia. When you’re hypothyroid, your cells aren’t very sensitive to glucose (they are resistant).
So although you may have normal levels of glucose in your blood, you’ll have the symptoms of hypoglycemia (fatigue, headache, hunger, irritability, etc.).
And since your cells aren’t getting the glucose they need, your adrenals will release cortisol to increase the amount of glucose available to them.
This causes a chronic stress response, as I described in a previous post, that suppresses thyroid function.
Does this sound familiar?
In another post on Synthroid, TSH and T4, I wrote about how some people are functionally hypothyroid. In other words, they have enough thyroid hormone, but it’s not getting into the cells.
Many of these people also have enough sugar in their blood but its not getting into the cells. Its another vicious cycle.
And let me tell you this from clinical experience. It is really, really, really, really, really, really, really, hard to manage a Hashimoto’s patient or someone with functional hypothyroidism if he or she doesn’t stop this sugar happy carb fest.
In fact, I’m going to say it. It’s a deal breaker.
If this high sugar diet isn’t stopped, you might as well throw in the towel, pack it in, wave the white flag, say “Uncle”, hear the fat lady sing, and give up, because you’re done.
All the money you’re spending on supplements and therapies won’t work. Instead, the first thing you need to do is to balance your blood sugar.
When balancing blood sugar, there are two things to consider. The first is fasting blood glucose, which can be measured first thing in the morning before eating or drinking anything.
In functional medicine we define normal range for fasting blood glucose as 75 – 95 mg/dL. Although 100 is often considered the top of the range for normal, studies have shown that fasting blood sugar levels in the mid-90s may set the table for future diabetes a decade later.
And although 80 mg/dL is often defined as low end of the range, plenty of healthy people have fasting blood sugar in the mid-to-high 70s (especially if they follow a low-carb diet – all you Paleo fans- time to do the wave).
The second, and more important thing to measure is post-prandial blood glucose. This is measured 1-2 hours after a meal.
Several studies have shown that post-prandial blood glucose is the most accurate predictor of future diabetes and is the first marker (before fasting blood glucose and Hb1Ac) to indicate blood sugar imbalances.
Normal post-prandial blood sugar one to two hours after a meal is 120 mg/dL, but most normal people are under 100 mg/dL two hours after a meal.
How does this apply to you? If you’re hypoglycemic, your challenge is to keep your blood sugar above 75 throughout the day.
The best way to do this is to eat a low-to-moderate carbohydrate diet (to prevent the blood sugar fluctuations I described above), and to eat frequent, small meals every 2-3 hours (to ensure a continuous supply of energy to the body.
If you’re insulin resistant, your challenge is to keep your blood sugar below 120 two hours after a meal.
The only way you’re going to be able to do this is to restrict carbohydrates.
Everyone should buy a blood glucose meter. The technology has gotten to the point where they are very precise and quite inexpensive.
How low-carb do you need to go?
Its different for everyone. (But, for most people with Hashimoto’s it is recommended to reduce carbs significantly.)
First, figure out your carbohydrate tolerance by buying a blood glucose meter and testing your blood sugar after various meals.
If you’ve eaten too many carbs, your blood sugar will remain above 120 mg/dL two hours after your meal.
Finally, if you have Hashimoto’s, it’s also important that you take steps to make sure your thyroid is properly balanced as well.
As you have seen, this thing works in both directions.
Sugar problems can mess with thyroid function, and thyroid disorders like Hashimoto’s can cause sugar problems and put you at greater risk for hypoglycemia, insulin resistance and if nothing is corrected, diabetes.
As you can also see, there are layers and layers here that may need to be addressed and worked on.
Hashimoto’s is so much more than a thyroid problem. Its a multi-system problem and it requires a multi-system approach.
That’s why I created my program: Healing Hashimoto’s: The 5 Elements of Thyroid Health.
In it you will discover how all these systems interact and cause vicious cycles and you will also learn how to correct these imbalances and heal.
In the meantime, put down the happy meal and step from away from the counter! 🙂
http://www.ncbi.nlm.nih.gov/pubmed/16530289: Study on insulin resistance and inflammation
http://www.eje-online.org/content/134/1/21.extract : Cytokines and autoimmune disease
http://www.ncbi.nlm.nih.gov/pubmed/3500324: Impact of immune cells on TSH
http://care.diabetesjournals.org/content/24/8/1448.full: Study on Glucose Tolerance and Neuropathy
http://nahypothyroidism.org/insulin-resistance-can-trigger-hashimotos-disease/
http://chriskresser.com/thyroid-blood-sugar-metabolic-syndrome
http://diabetes.niddk.nih.gov/dm/pubs/statistics/
http://www.ncbi.nlm.nih.gov/pubmed/939192 : Study on impact of thyroid hormone on insulin secretion.
http://www.ncbi.nlm.nih.gov/pubmed/2013384 : Influence of the thyroid on pancreatic function
http://diabetes.diabetesjournals.org/content/16/9/643.full.pdf+html: Effects of thyroid function on insulin secretion
http://www.ncbi.nlm.nih.gov/pubmed/19364696 : Excess thyroid hormone and carbohydrate metabolism
http://www.huffingtonpost.com/t-colin-campbell/low-fat-diets-are-grossly_b_740543.html
The Thyroid: A Fundamental and Clinical Text, Lewis E. Braverman & Robert D. Utiger, Ninth Edition, Lippincott, Williams & Wilkins, 2005
Why Do I Still Have Thyroid Symptoms? (When My Lab Tests Are Normal), Dr. Datis Kharrazian, Elephant Printing 2010
In my last post I looked at 6 different systems and how they were affected by the thyroid and, how that affected Hashimoto’s patients. This is part 2 of that post. And, as I stated in that post, some of this material comes from Dr. Datis Kharrazian, one of the world’s leading experts in the treatment of thyroid issues using functional medicine and from another book called The Thyroid, A Fundamental and Clinical Text, by Braverman and Utiger.
The reason this is important is because the things that you are feeling are not a coincidence or some random group of symptoms. They are caused by your thyroid not functioning properly.
And often, there is a back and forth relationship where a problem or weakness in one of these systems can actually make the problem in your thyroid worse. This is why a holistic approach that treats these various systems is so important.
In our last post, we looked at these systems:
1. Bones and bone growth
2. Blood sugar metabolism
3. Brain
4. Cholesterol and other fats in the blood
5. Gallbladder
6. Cardiovascular system
7. Intestines
8. Liver
9. Maintaining Weight
10. Protein metabolism
11. Red blood cell metabolism
Thyroid hormone has a direct affect on movement through the entire gastrointestinal tract. Thyroid hormones increase intestinal neurotransmitters, increase blood flow to the intestines and support the repair and regeneration of the intestines.
Hypothyroidism can slow movement through the esophagus, can affect muscle function in this area and can affect the nerves that cause movement. Hypothyroidism also has an affect on the vagus nerve and this can lead both directly and indirectly to slowing movement through the intestines.
This can lead to 3 common problems:
1. Constipation: One of the most common complaints of Hashimoto’s and hypothyroid patients is constipation. When the bowels slow and it takes more time to empty.
2. Malabsorption: People with hypothyroid problems and Hashimoto’s can have difficulty absorbing important vitamins, minerals and nutrients from their foods. This can lead to a host of health problems including, low protein, anemias, and vitamin deficiencies. Hyperthyroid patients can experience diarrhea that can also lead to poor absorption.
3. Dysbiosis: Hashimoto’s and hypothyroid people often have issues involving problems in the intestinal tract with overgrowth of yeast, harmful species of bacteria and fungus.
When you add the problems caused by gluten and cross reactivity to the slowing of movement and repair in the intestines you have a recipe for a really vicious cycle. Gluten causes breakdown of the lining, slow transit and slower repair and this means that the damage done is compounded and each makes the other worse.
T4 that is secreted by the thyroid gland is converted by the liver into T3 which then has effects on the body. Patients with liver diseases, like cirrhosis have problems converting T4 into T3. High TSH has also been found to cause an abnormal response in the pituitary gland, which signals the thyroid to release more hormones.
Hypothyroid and Hashimoto’s patients also experience issues involving the liver. A hypothyroid state can lead to problems with detoxification pathways, especially phase II detoxification. This can lead to a clogged liver and more problems with converting T4 to T3. This is the reason why liver detoxification is so important for Hashimoto’s patients whether or not they are taking thyroid hormones.
Many Hashimoto’s patients have issues maintaing a proper weight. For some it is due to a low thyroid state, for others it is due to a hyperthyroid status.
For those who are unable to lose weight, there are several different reasons for this. Thyroid hormones are responsible for metabolic activity, a slower metabolism means an inability to lose weight or, in some cases, weight gain. A hypothyroid state can also slow the the body’s ability to use free fatty acids, when this happens fat can not be broken down.
A slower metabolism and fat not breaking down can both lead to fatigue. Hypothyroidism can also cause less growth hormone to be produced, this can lead to loss of muscle mass and the inability to build muscles.
For Hashimoto’s people who have difficulty gaining weight, their problem is that their thyroid is undergoing an immune attack and is in hyperthyroid state. This can last for an extended period of time. Eventually, in Hashimoto’s patients, they get to a hypothyroid state due to thyroid tissue destruction.
If a patient stays in a hyperthyroid state, then Grave’s disease should be considered and a tissue biopsy should be ordered. Also, in Graves disease TSH autoantibodies will be very high. In Hashimoto’s TPO (thyroid peroxidase) antibodies will be highest, with or without TSH antibodies.
When someone is hypothyroid, serum protein levels may be increased because capillaries dilate and allow larger proteins into the bloodstream. Albumin also breaks down more slowly. This can be seen in elevated protein in both the blood and the urine.
A hypothyroid state can lead to several different types of anemia.
Normocytic normochromic anemia: Hypothyroidism can cause a decrease in the production of the hormone erythropoeitin and this may cause this type of anemia. There are about 14 different kinds. For this treatment should be focused on the thyroid.
Macrocytic anemia: Low thyroid activity can lead to this because of a decrease in absorption of vitamin B12 and folic acid caused by a decrease in hydrochloric acid. For this, one must rule out the autoimmune condition below and if it is not autoimmune supplement with B12, folic acid and, possibly hydrochloric acid.
Pernicious anemia: This is an autoimmune disease caused by an autoimmune attack on intrinsic factor which is responsible for helping the body break down and absorb vitamin B12. One of the realities of autoimmune disease is that there are sometimes multiple tissues being attacked.
In about 12% of Hashimoto’s patients, there is also an autoimmune attack on intrinsic factor. If you suspect this type of anemia, an Intrinsic Factor Autoantibody test can be ordered. (IF ab). If this is positive, then they have pernicious anemia. These people respond better to B12 injections.
Iron deficiency anemia: Hypothyroidism can also affect iron absorption because of decreases in stomach acid and excessive blood loss from progesterone receptor site resistance. If iron is deficient, TIBC (total iron binding capacity) should be checked. This will be elevated in iron deficiency and is a good marker to see early iron deficiency. For this, supplement with iron, hydrochloric acid and, possibly, vitamin C to enhance absorption.
Whenever you see an abnormal pattern in a CBC (complete red and white blood cell count) then the thyroid should be evaluated. And when someone sees a thyroid issue, a CBC should always be evaluated.
And here is why this matters: if a patient is anemic, they are not getting enough oxygen to their cells and nothing you do is going to be effective. If you don’t fix this, all the treatments that you attempt will be exercises in futility because the cells of the body are not being powered properly.
Bottom Line:
The body is not a machine with a series of unrelated parts. It is a group of inter-related ecosystems that all affect one another. When treating Hashimoto’s, it is important to understand these relationships and to work on healing and balancing the body. This will lead to faster, better and more long lasting results. This is why I created Hashimoto’s Healing: The 5 Elements of Thyroid Health. This system gives you the tools to do this and to radically improve your results in managing and healing your Hashimoto’s.
References:
Kharrazian, Datis, DC Mastering the Thyroid, 2011
The Thyroid, A Fundamental and Clinical Text, Ninth Edition, Lewis E. Braverman & Robert D. Utiger, 2005, Lippincott Williams & Wilkins
Green JR, Diminished TSH repines to TRH stimulation in patients with hepatic cirrhosis dispute subnormal T3 levels. Z. Gastroenterol. 1979:17(7):447-51
Saha B, Maity C. Alteration of serum enzymes in primary hypothyroidism. Clin Chem Lab Med. 2002;40:609-611