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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Intermittent fasting is an approach to timing your meals that has grown in popularity. Recently a number of people have asked my opinion about doing it if you have Hashimoto’s.
Like all things Hashimoto’s related, this is a complicated question masquerading as a simple one.
IF is not really a diet, it’s more of an eating pattern where you cycle between your regular meal pattern and fasting (not eating at all).
The focus is not on what foods you should eat, it’s more on when you should eat whatever is you choose to eat.
If you have been following me for any period of time you will know that I believe what you eat makes a huge difference if you are trying to heal. And the reason is simple: Hashimoto’s is an autoimmune disease and an estimated 70-80% of our immune system lives in our digestive tract.
So what you eats matters, in a big way. It also turns out that deciding not to eat can also have major impacts on your health.
The question today is what are the pros and cons of intermittent fasting with regards to Hashimoto’s and hypothyroidism.
The reason IF has become popular is that it has been shown in some research to have a number of health benefits.
Basically, there are three major mechanisms that have been identified as benefits of intermittent fasting:
Before you get all excited, it’s important to understand that people with Hashimoto’s are not normal subjects.
They often don’t have normal insulin responses, their immune systems are hyper-vigilant, and they rarely have a normal capacity for handling additional stress.
It’s important to understand is that intermittent fasting can help you under some circumstances and can actually do some harm in others.
The more I study physiology and look at the connections between systems of the body, the more I realize how incredibly important respecting your body’s natural clock is.
This is one of those areas that can have a profound impact on your health and well being and on the progression of your Hashimoto’s.
Your body’s natural clock regulates your hormones, affects your ability to digest food and absorb nutrients, affects immune function, eliminates toxins, and helps regulate your insulin and stress responses.
If this system is out of whack it can result in you not sleeping properly, having digestive issues and constipation, craving sweets and carbs, having trouble losing weight and having a really hard time handling stress (Sound familiar? These are super common Hashimoto’s symptoms).
These chronic disruptions of your circadian rhythms are pretty much ignored by proponents of intermittent fasting.
Eating times are either random or just plain wrong. This can have huge consequences when you have Hashimoto’s and autoimmunity. You can not overlook the relationship between meal times and your body’s internal clock, especially if you need to restore that rhythm.
Your body is actually programmed to eat at night. The Autonomic nervous system operates around your circadian clock.
During the day your sympathetic nervous system puts your body into an energy burning mode, whereas at night your parasympathetic nervous system puts your body into an energy replenishing relax and sleep mode.
This is why normal cortisol peaks in the morning and gradually diminishes and melatonin peaks at night.
Unfortunately, this system is highly sensitive to getting disrupted, especially when you have autoimmunity and hypothyroidism and none of your body’s systems are functioning properly.
So, if you eat at the wrong times when having a large meal during the day, you can cause insulin surges and this can totally mess up your autonomic nervous system.
This can result in you inhibiting your sympathetic nervous system and turning on your parasympathetic nervous system which makes you feel tired and fatigued during the day.
And instead of spending energy and burning fat, you’ll store energy and gain more fat. This is a downward spiral and the ultimate no win situation.
The problem with many intermittent fasting programs is that they don’t pay any attention to this at all.
Another thing that is really important with Hashimoto’s is blood sugar balance. I have written pretty extensively about this here.
The impact of fasting on a pre-existing blood sugar imbalance must be considered whenever you’re considering doing IF. I CANNOT OVERSTATE HOW IMPORTANT THIS IS!!!!
Let’s Breakdown Some Common IF Programs. Here are the most common approaches that I could find:
ALTERNATE DAY FASTING: Followers of this program eat on some days and don’t eat at all on others. This is really hard to do and can result in a major surge in hunger (obviously).
If you do this and then binge eat, you are pretty much guaranteeing a massive insulin surge. This will cause a cortisol surge which can result in LH and FSH suppression by the pituitary, problems with liver detoxification, under conversion of T4 into T3, thyroid hormone receptor resistance and suppression of SIgA and a breakdown of immune barriers.
If you are hypoglycemic, your blood sugar will crash dangerously and you might wind up feeling major fatigue, having insomnia, getting irritable and/or depressed, slowing your metabolism so that losing weight will be harder, getting headaches and hormonal imbalances. Not good.
There are reports from people who have tried this that they experience sleeping disorders, constipation and persistent fatigue. In other words, an absolute disaster for people with Hashimoto’s.
ONCE A WEEK OR TWICE A WEEK FASTING: A little easier to do than alternate day fasting, but the problems mentioned above still persist. Coming off of it can generate massive insulin surges and hypoglycemics will suffer in a big way.
FASTING EVERY OTHER WEEK OR EVERY MONTH: This is even worse than once or twice a week and basically it’s an attempt to create an easy fast program. Half measures almost never result in half successes in my experience, they result in disappointment and failure.
SKIPPING DINNER: This totally goes against your body’s natural rhythms. If you’re hypoglycemic you’re just prolonging the punishment and the damage.If you are insulin resistant you may once again wind up with an insulin surge when you have breakfast.
This can also make sleep problems worse. People who are in favor of this approach say that breakfast is a very important meal and should not be skipped.
I agree, but most Americans have a breakfast that is heavily weighted towards sugar and carbohydrates. That is a recipe for insulin surges and a day filled with misery.
SKIPPING BREAKFAST: Some people feel that this is better than skipping dinner. Especially if you exercise in the morning. But this also can cause problems.
Again, if you are hypoglycemic you will not have had anything for 6-9 hours – fasting is technically the gap between meals minus digestion time – so even though you don’t eat for 12-16 hours you’re actually fasting for 6-9 hours.
No matter how you calculate it, that’s just too long.
For hypoglycemics or people with Hashimoto’s who have a mixed presentation of hypoglycemia and insulin resistance, I think it’s far more important to work to balance blood sugar and to restore and preserve circadian rhythms.
In my experience that will make you feel much better, help you to have enough energy to exercise and be active and get you in a position to actually lose weight.
And your choice of foods is also very important. Eating foods that are high in nutrient density and avoiding inflammatory foods like gluten, dairy and non-fermented soy is also much more important than fasting for reducing systemic inflammation.
It really depends on how bad things are and where you are in the progression of the disease. If you have major disruptions in your circadian rhythms and you have major imbalances in blood sugar, I would strongly discourage attempting the intermittent fasting programs.
In my experience most people who have Hashimoto’s that come for treatment are advanced enough where intermittent fasting just doesn’t give you enough benefits for all the serious downsides that may result.
If you have healed to the point where you have restored your circadian rhythms and you blood sugar is well balanced then perhaps the One Meal Per Day Fast could be something that you could attempt.
The is really the only viable option for keeping balance of your body’s clock and maximizing the beneficial effects of intermittent fasting. If you exercise, you’ll need to feed your muscles post workout with a low glycemic index recovery meal to avoid the dangers of insulin surges.
And having proteins and carbs before your workout that are quickly assimilated can help load glycogen in your muscles, nourish the fast fibers in those muscles and help boost max strength and performance.
With Hashimoto’s, however, this is another potential land mine as the most commonly recommended form of protein is good quality whey protein and while whey is refined and filtered it can contain trace amounts of casein which can cause major immune flare ups in some Hashimoto’s folks.
Check out this post to learn more.
In my opinion, intermittent fasting can have some health benefits for people whose Hashimoto’s is very well managed and who have balanced blood sugar and well respected and preserved circadian rhythms.
Unfortunately, the reality is that most people with Hashimoto’s have not achieved anything close to that in their lives and many have some degree of circadian disruption and some degree of blood sugar dysfunction.
For them, working to restore their body’s natural clock and to keep their blood sugar stable throughout the day is much more important than jumping on the IF bandwagon.
Daily focus on those two goals (body clock maintenance and blood sugar balance) is a much better use of your money, time, and energy and will yield much better long and short term results like more energy, better sleep, better digestion and a happier mood and outlook on life.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3680567/ IF research overview
http://www.nature.com/ijo/journal/v35/n5/full/ijo2010171a.html IF and insulin sensitivity
http://ajcn.nutrition.org/content/86/1/7.full Review of trials IF
http://fitness.mercola.com/sites/fitness/archive/2012/09/14/intermittent-fasting-benefits.aspx
Hey people!
I get a lot of requests for advice on diet and though it can be really tricky and complicated, I decided to create an infographic to give you a Hashimoto’s diet in 5 steps for reducing systemic inflammation.
As I am fond of saying, when it comes to Hashimoto’s and hypothyroidism, inflammation is the root of all evil. And diet is a big player in inflammation.
Here’s the entire 5 steps in an easy to follow infographic. Feel free to download it and share.
The diet is pretty straight forward, but for some people it can be a radical departure from what you are used to.
Let’s break down some of the most important elements.
Not to eat ;), but to keep track of everything you are doing. Some of us operate under the delusion that we are good at remembering things. When it comes to your diet and reactions to what you eat, you aren’t. There are way to many variables and things going on, you can’t possibly remember it all.
And why does it matter? Your immune system lives in your digestive tract (an estimated 70-80% is found there) and when you have autoimmunity, interactions with your immune system can have consequences.
When you react to certain foods or herbs or supplements, this can cause an immune response, which can lead to more inflammation and it can promote an attack on your own tissue.
So it’s really important to identify what foods in your diet cause responses. And some of these responses are digestive and others may be emotional or neurological. That’s why we need the journal to look for patterns.
If you’re just starting out. It’s time to simplify. Too many variables means that you don’t know what’s causing what. You need to simplify things (often in more than one part of your life).
Start with your diet. And start with the foods that can have the biggest impact. These are: gluten, dairy and soy.
There are reams of research on gluten and thousands of success stories from people who have gotten off of it and feel significantly better. If you doubt that this is true, here’s a post where I looked into this topic and a metric ton of research.
Same is true of dairy, Both lactose and casein (a protein found in milk) can be problematic for Hashimoto’s folks. They can hamper conversion and absorption of thyroid hormone. Still not convinced? Read this post that also looks at tons of research.
And soy is a goitrogen and can also hamper thyroid hormone behavior in the body. Go off of all three for 30 to 60 days minimum, 100%. Note all the symptoms you have in your journal before, during and after. Then review the journal and see how many remain.
The next step is to take this to the next level. The reality is that gluten, dairy and soy may just be the tip of the iceberg.
Other foods like refined sugars, alcohol, grains, nuts and seeds, and nightshades (tomatoes, eggplants, peppers and white potatoes) can also cause inflammation. This is basically the Autoimmune Paleo Diet, you can learn more about it in this post.
You can test to see whether or not you have sensitivities to these foods, but sometimes these tests are inaccurate and you may react to those foods any way.
The best way to find out is to eliminate these foods for a period of time (usually 30 to 60 days) and then reintroduce them in a systematic way, one food at a time (More on that in a moment).
Here, again, your journal is a very important tool. Note all the symptoms you had when you started this phase of your recovery and keep track before, during and after.
During this period, it’s also a great time to detoxify your liver, work on healing leaky gut, boost stomach acid, balance blood sugar and work on all the systems of your body that may be compromised.
Once you’ve gone through this process, you need to re-evaluate. This is where your journal becomes worth it’s weight in gold. You took the time to keep track of what you did, now go back over it and analyze the data.
What improved and what didn’t? Where did you cheat? What happened when you did? How much better are you know than when you began?
If you like many of the people I work with, chances are you got some improvement from this process. But if you still aren’t satisfied with your results, the it may be time to dig a bit deeper and do some testing (this can also be done at the beginning, of course).
You might want to rule out SIBO (Small Intestine Bacterial Overgrowth), candida, H.pylori, blastocystis, parasites and more. Most of these can ordered in a single stool test.
The final step is to go through the re-introduction process. Again, you’ll need your journal. Introduce one food at a time as the only variable. Start small and keep track of your reactions.
This will give you invaluable information on what foods you react to and it will help you create a solid foundation for healing.
Once you go through this, you will be able to identify what works and what doesn’t. Double down on what works and tweak or experiment with variations of what didn’t.
Awesome! Great job! Now you are on your way to getting your Hashimoto’s into remission. Remember remission is a journey a destination, you are now on the right path in your journey.
P.S. Staying on a restrictive diet for too long a period of time also can have consequences. Read this post to learn what I mean.
Feeling a little overwhelmed by all this? No worries, reach out to Marc and set up a consultation to help guide you on your way.
Hey people!
Here’s an awesome recipe for one of my favorite dishes called Kichari.
It’s a delicious dish, traditionally made in India that is easy to digest, detoxifying and anti-inflammatory.
It’s really easy to make too!
I like to make a big batch and then eat it for the rest of the week. It can also be eaten as a fast to detoxify the body and lose weight.
It’s not exactly AIP perfect, but it’s still quite beneficial. (This is better after you’ve gone through the elimination phase and have reintroduced foods.)
One of the ingredients is mung bean. If you aren’t familiar with it, it’s small green bean is used in Chinese Medicine to clear heat and toxins and was used traditionally as an effective antidote for overdose from a variety of toxins.
This dish is also flavored with turmeric, a fantastic anti-inflammatory.
Ingredients:
Equal parts:
Powdered turmeric, cumin and coriander. (1 tbsp or so of each)
1 cup white basmati rice
1 cup mung beans (if you feel ambitious you can sprout these first)
ghee or coconut oil (1-2 tbsp)
1 tbsp fresh grated ginger
Coconut yoghurt
Cilantro and lime to garnish
Yum!
Damn that looks good!
This is my partner, Olesia Farberov’s (she also took the photos!), take on the famous chicken pot pie but Autoimmune-Paleo style. This labor of love will definitely make an impression on your guests and kids.
What can be better than a perfectly wrapped, edible present!
4 medium or 6 small Pumpkins, scraped of seeds and strings
3 lbs Chicken breast, cut in bite-size pieces
¼ lb Uncured Bacon
4 Carrots, cut in thin rounds
1 large or 2 small Yucca root (optional)
1 large yellow onion, chopped
4 Bay leaf
4 Savory sprigs, thinly sliced
2 Oregano sprigs, thinly sliced
2 Sage leaves, thinly sliced
½ tsp Salt
½ tsp Pepper
1 ½ cup Cranberries, fresh
1. Give your pumpkins a bath with soap and water to rid of any loose dirt. Using a small knife, cut out a hole 4-5” in diameter around the stem and open the “lid”. Scrape the insides of seeds and gooey strings and discard. Set pumpkins aside.2. Peel and cut yucca root into 2” rounds. Cook, covered in water, until easily pierced with fork. Drain and leave it to cool. Once cool enough to handle, cut each piece into bite-size pieces, eliminating the hard, rope-like core. Set aside.
3. In a large pot, fry bacon until golden and crisp. Take out bacon and reserve for later.
4. Preheat oven to 395F.
5. Into the pot of bacon fat, throw in onion and cook until browned. Add chicken, yucca, bay leaf, herbs, salt & pepper and cook over medium-high heat, stirring occasionally, until chicken is cooked through, about 15-20 min. In the last 5 minutes of cooking, add cranberries and stir to distribute evenly.
6. Stuff each pumpkin with chicken mixture, including liquid. Cover with pumpkin “lid”. Place on a large sheet, covered with foil, and bake on middle rack at 395F for approximately 1hr or until pumpkin can be pierced easily with a fork.
7. Let pumpkins cool for at least 10 minutes with “lid” slightly open. Before serving, remove lid and sprinkle crumbled bacon into each pumpkin then place the “lid” back on.
Each pumpkin can be served whole or cut into either half (for adults) or quarter size (for kids).
Have Fun & Enjoy!!
Recipe and photos by Olesia Farberov, L.Ac.
What?
This week we are looking into the earth element which involves the spleen and pancreas and how this relates to thyroid and autoimmune disease.
A new study in the news this week has found that drinking soda and other sweet beverages (2 or more per day) doubles the risk for getting diabetes regardless of whether or not it is an artificial sweetener or not.
This was a case-control study within a population-based Swedish cohort study that aimed to see whether consumption of sweetened drinks was associated with risk of a lesser known form of diabetes called latent autoimmune diabetes in adults (LADA).
LADA is sometimes called Type 1.5 diabetes because has features of both type 1 diabetes, where the body’s own immune cells destroy the insulin-producing cells in the pancreas and type 2 diabetes, which usually develops later in life and is most commonly caused by eating too much sugar.
But unlike type 1 diabetes, which normally develops in childhood, in LADA the cell destruction is much slower.
Also, the condition often develops later in life and shares many features with type 2 diabetes. For example, the person doesn’t always need treatment with insulin straight away. This study reports that in the Swedish diabetes registry, LADA accounts for 5% of all cases.
Data was available for 1,136 people with type 2 diabetes, 357 people with LADA, and 1,371 diabetes-free controls.
Average age was 59 for people with LADA and controls, and 68 for those with type 2 diabetes.
Just under two-thirds of all people reported consuming sweetened (including artificially sweetened) drinks.
In general they found that consumption of sweetened drinks was linked with higher body mass index (BMI) and other poor lifestyle factors like smoking, low physical activity and consumption of processed meat and sugary foods. (Birds of a feather flock together, as do unhealthy habits.)
One problem with the study is that, as you can see, there are many other potential factors that could also lead to poor health and the development of diabetes, so it’s hard to say it’s just soda and other sweet beverages, though these are certainly very high in sugar.
How does this relate to Hashimoto’s?
There are few interesting links between these two diseases.
Firstly, as we noted in a previous post, when you have one autoimmune disease there is a higher risk of developing others.
What’s interesting is that insulin resistance has been found to increase destruction of the thyroid in thyroid autoimmunity, and it can also clearly be a trigger for Hashimoto’s.
These don’t usually develop at the same time and often take years to progress, just like other autoimmune diseases.
In one study of autoimmune polyendocrine diseases it was found that type I diabetes manifested first in half the cases and autoimmune thyroid disease manifested first in 17% of the cases.
And the most common combination was type I diabetes and autoimmune thyroid disease at 33%.
So, it’s another reminder of how important sugar balance and sugar control is for people with Hashimoto’s.
We explore this idea in depth in this post.
Something else that is really fascinating is that candida is also a common denominator in many autoimmune polyendocrine disorders.
What does candida thrive on?
Sugar.
Adding another layer of reasons why sugar should be taken seriously. It can not only lead to more autoimmunity, it can also lead to secondary conditions that are both causes of the disease and hindrnaces to getting better.
Finally, I think what’s also an interesting revelation from this is that there is a kind of myth that diet soda is a safer alternative.
Well, various research reviews and a case study have found this not to be true.
In fact, here’s one case study that showed dramatic improvement in Hashimoto’s symptoms when the patient stopped drinking diet soda.
BOTTOM LINE IS THIS
Excessive sugar consumption (and this includes artificial sugar substitutes) is a potential threat not just for Type II Diabetes or LADA, but also for autoimmune thyroid and polyendocrine thyroid diseases.
It can also foster secondary infections like candida and SIBO (Small Intestine Bascterial Overgrowth).
Treat sugar like the potentially dangerous substance that it is.
References:
https://www.ncbi.nlm.nih.gov/pubmed/15182509 LADA and Thyroid autoimmunity
http://www.eje-online.org/content/175/6/605.abstract?sid=93eb363b-97d3-4f35-92cd-11e7c2ed5ee4 sweet
beverage consumption and LADA
http://www.medicalnewstoday.com/articles/313612.php Diabetes risk doubled with soda consumption-diet doesn’t change anything
https://www.ncbi.nlm.nih.gov/pubmed/18800291 Sucralose alters microbiome
https://www.ncbi.nlm.nih.gov/pubmed/20693348 Previous research on soda and type 2 diabetes
http://media.aace.com/press-release/cause-and-effect-case-report-shows-association-between-sugar-substitutes-and-common-th Case study on artificial sweeteners and Hashimoto’s
https://www.sav.sk/journals/endo/full/er0301e.pdf LADA and Autoimmune Thyroiditis
http://www.diabetesforecast.org/2010/may/the-other-diabetes-lada-or-type-1-5.html?referrer=https://www.google.com/ LADA or Type 1.5 diabetes
http://www.diabetesselfmanagement.com/diabetes-resources/definitions/type-1-5-diabetes/ More on LADA
Low Carb Diet Lowers Thyroid Antibodies
Hey people! I’m always astonished when people share with me that their doctor said, “Diet doesn’t matter, there’s nothing you can do except take thyroid hormone.”
I have literally heard variations of that one sentence over 500 times. I really don’t understand it because in my (and many of my colleagues) clinical experience this is the single most important factor in achieving long term success.
In today’s post I want to share a new research study that suggests otherwise. This was published in the Drug Design, Development and Therapy Journal, Volume 10, 2016.
This study, entitled, Effects of low-carbohydrate diet therapy in overweight subject with autoimmune thyroiditis: possible synergism with ChREBP , looked at “…a total of 180 patients, 84 males and 96 females, aged 30–45 years. All the subjects did not present celiac disease, but Hashimoto’s disease was detected. Moreover, each patient showed others autoimmune symptoms, they are typical Hashimoto’s disease.”
(This isn’t huge cohort, but it’s certainly enough people to give us some decent data.)
All patients had elevated antibodies.
TSH, free T3, free T4 and levels of anti-microsomal, anti-thyroglobulin, and anti-peroxidase Abs were measured. (Which is interesting since anti-microsomal and anti-TPO antibodies are essentially the same ).
They were put on the following: a diet program based on the following proportions: carbohydrates 12%–15%, proteins 50%–60%, and lipids 25%–30%. These patients were instructed to eat large leafy and other types of vegetables and only lean parts of red and white meat, avoiding goitrogenic food. The following items were also excluded from the diet: eggs, legumes, dairy products, bread, pasta, fruits, and rice.
This protein-rich diet plan was implemented for 3 weeks, at the end of which bioimpedance tests, bodyweight measurements, and blood tests (TPO Ab, anti-microsomal Ab, thyroglobulin [TG] Ab, and thyroid hormones) were performed.
There was also a control group that didn’t make any dietary changes and were also tested.
Initial (pre-diet) levels of FT3, FT4, and TSH were not significantly different between the two groups.
In just 3 weeks, these were the results: patients treated as above showed a significant reduction of antithyroid (-40%,P<0.013), anti-microsomal (-57%, P<0.003), and anti-peroxidase (-44%, P<0,029) Abs. Untreated patients had a significant increase in antithyroid (+9%, P<0.017) and anti-microsomal (+30%,P<0.028) Abs. Even the level of anti-peroxidase Abs increased without reaching statistical significance (+16%, P>0064).
In other words, there was a 40% reduction in anti-thyroid, a 57% anti-microsomal and a 44% ant-TPO antibodies. While people in the control group who made no changes showed an in crease of 9% anti-thyroid, 30% anti-microsomal and 16% increase in anti-TPO antibodies.
There was also some weight loss noted about a 5% reduction and a 4% reduction in BMI.
Those antibody reduction numbers are HUGE differences. If they were develop a drug that could do that, it would be a multi-billion dollar discovery.
So, I think it’s safe to say that this type of diet is, at least, worth trying.
I also think there are few things that came up in this study that interesting and worth pointing out. These researchers had the dieters remove goitrogenic vegetables. I have looked into the research on this and I don’t think they have the impact that we have been led to believe.
In my opinion, as long as you steam or blanch or cook them in some way, most of those properties are not an issue. Here’s a good discussion on this.
Basically, with the exception of soy, these vegetables have far more health benefits than problems.
The other thing I thought was fascinating about this study was the discussion of why this may be (I’m a geek when it comes to this and I’m forever curious to learn WHY?)
First thing the researchers note is that “… the aim of this type of diet is to reduce the overall inflammatory state and consequently inflammation of the thyroid gland.” This is an anti-inflammatory diet and test results confirm that.
Also, they note that these results may be “related to the role of the thyroid hormone receptor-α (TRα), found mainly in the liver and white adipose tissues.”
This receptor is involved in fat metabolism and balance. It causes certain genes to be expressed ( such as ChREBP or Carbohydrate-responsive element-binding protein which interacts with carbohydrate expression in DNA.)
In addition, they note “It has also been suggested that TRα could be involved in the transcriptional regulation of lipogenesis in the liver. Activation of these genes determines an increase in the expression of anti-microsomal Abs, which occurs mainly in the REL of hepatocytes, and it has a fundamental role in inflammatory processes.”
In other words, this receptor is involved in fat production in the liver (which is the result of sugar and carbohydrate consumption) AND it increases anti-microsomal antibodies AND it is is important in inflammation.
I have often noted how important blood sugar regulation is for Hashimoto’s patients and I frequently express this to my patients and we work diligently to balance their blood sugar. And this is why it is so important!
They also note” that 83% of patients with a high level of autoantibodies are breath test positive to lactase with a lactase deficit higher than 50%…” This is one of the reasons dairy can be problematic for Hashimoto’s patients as well.
And one final point that was really interesting and which emphasizes the importance of making sure your liver is functioning properly is that “Chronic inflammation of the thyroid gland can also be due to the presence of environmental contaminants that are suspected to disturb activity against the endocrine system, known as endocrine disrupting chemicals.”
These chemicals like PCBs are known endocrine disruptors and have been shown to disrupt thyroid function. These researchers suggest that a rise in anti-microsomal antibodies may be a way for our bodies to defend the thyroid and prevent it from being further destroyed.
What these chemicals do is to disrupt the thyroid receptor that we looked at earlier. And this all happens in the liver. What this study makes us more curious about is how the thyroid gland is involved in lipid metabolism (yes, those of you who know me may see the light going off in my brain- more blog posts to come!).
Bottom Line? A diet based on the reduction of carbohydrate content leads not only to a weight loss, but also a decrease in fat mass and a significant drop of autoantibodies in Hashimoto’s thyroiditis.
So, dear doctor, DIET DOES MATTER!!!!!
Try it people.
Have a great day, unless you have other plans!
Edit:
I recently conducted an informal survey on my Facebook page (http://facebook.com/hashimotoshealing)
I asked people about what worked for them the most in treating their Hashimoto’s symptoms.
The results were rather telling and, I feel, are relevant to this post. Many of them talked about dietary changes being one of the most significant factors in helping to alleviate their symptom.
Here’s a graph of the results:
Hey people!
Here’s a real story about the huge difference diet can make. This was submitted to us by Hillary Bergh, a contributor and recipe-author at furtherfood.com
“Throughout my childhood, I suffered from psoriasis, various skin issues, extreme fatigue, digestive distress, migraines, mood swings, thinning hair, weak nails, and had trouble regulating my body temperature. I saw multiple doctors before I was finally diagnosed with Hashimoto’s Thyroiditis in my teens. I was put on synthetic thyroid and estrogen hormones to manage my condition. While some of the symptoms were reduced, my skin and digestive issues became much worse.
They all told me food was not a factor
My general practitioner, my endocrinologist, and my dermatologist all continued to tell me food was not and could not be a factor–which was a relief. I wanted to believe them because food was my life. My parents owned restaurants, and I was passionate about cooking and wanted a career in food. When I was a teen, my mom did take me to see a naturopath, who suggested I eliminate wheat and gluten. I simply couldn’t do it back then; it was too hard.
I went on to fulfill my dreams of going to culinary school, then baking/pastry school, and then obtained my business degree. Yet, I continued to be plagued by my health issues. I saw various western trained doctors over the years, took medications, used creams – yet saw no improvement, and more often than not, my symptoms worsened.
Hit rock bottom, and started a strict elimination diet
I got so sick that I was forced to spend weeks in bed, and was having increasingly painful symptoms. Finally, a very good friend covered the cost for me to see an acupuncturist for six months, four times per week. I was put on a very strict elimination diet and drank 4oz of a horribly bitter tonic after every meal. Within two weeks, I saw results that exceeded my wildest dreams!
Getting better, reducing meds
As the six month mark approached, I noticed my nails getting stronger, my hair getting thicker, skin issues reducing, no headaches, and had increased energy. I was able to reintroduce many foods, reduce my thyroid dosage, and eliminate my estrogen dosage.
Finding my life’s purpose
Since then, I have received an integrative nutrition health coaching certificate and expanded my knowledge of food as healing. I have been able to combine this newfound knowledge with my culinary education and be a coach to others. It is my life’s purpose to be an example and inspiration to others who are suffering. My health journey is an ongoing adventure and now I can enjoy the ride!”
Awesome! Another great example of why we need to be our own advocates and why the right food choices should be the foundation of any treatment strategy.
Hashimoto’s and other autoimmune diseases have multiple causes. There is no single origin and, therefore, to date there is no single solution.
Instead, successful healing requires exploration into the multiple causes of the disease and healing the areas that need attention.
One such area that has recently been discovered to have a major impact on health and disease is the microbiota or the tiny living organisms that populate our bodies.
These various different species of bacteria, viruses and fungi make up the lion’s share of our DNA and are more a part of us than we realized.
In this post we explore the role of bacteria in the formation and healing of autoimmunity and Hashimoto’s.
One of the fundamental things to understand regarding the world of microbes is that they are not separate from us. We are one. And I don’t mean this is a woo woo, philosophical sense.
I mean this is a very real, practical sense.
The Human Microbiome Project
The Human Microbiome Project (HMP) was a United States National Institute of Health (NIH) sponsored project whose goal was to identify and study the microorganisms (little critters) that are found in association with both healthy and diseased humans.
Launched in 2008, it was a five-year project, with a total budget of $115 million. The ultimate goal was to test how changes in the human microbiome are associated with human health or disease.
Here’s some of the things that they discovered:
• No two people have the same microbiome, not even identical twins.
• There are approximately 10 trillion bacteria in (and on) our bodies vs. only 1 trillion human cells. You read that correctly. We have 10x more bacterial cells than we do human cells.
• Bacterial genes outnumber human genes 150:1.
• Our cells have incorporated and use bacterial DNA.
• There are over 1,000 species of bacteria found inside our GI tract alone.
• There are over 1,000 different proteins made by bacteria in the gut which are essential to optimal body function.
• Several diseases are directly associated with a disruption to the microbial ecosystem of the gut. These include, but are not limited to: Asthma, Allergies, Crohn’s, IBS, Obesity and, in my humble opinion, Hashimoto’s.
• Pathogenic bacteria/organisms like candida, h.pylori, etc. have evolved to be natural inhabitants of our gut, and under ideal conditions don’t always lead to illness or cause disease. On the contrary, sometimes they provide vital functions and we’re worse off without them.
• Destroying these pathogens completely has physiological consequences that we’re just beginning to understand. (Remember when the appendix didn’t matter? Oh yeah, we were wrong about that, too. It has been found to be a store house of good bacteria.)
One thing that looking at this research makes abundantly clear is how potentially destructive antibiotic therapy is, especially for children (for whom it is often prescribed).
Of course, these drugs have saved countless lives, when they are used appropriately. But they have been abused and overused and we are now seeing the consequences in new bacteria resistant strains, as well as a wide variety of diseases like digestive disorders and autoimmune disease.
Giving a child or adult antibiotics every time they get an upper respiratory infection (most of which are caused by viruses not bacteria) is often doing little more than setting the table for future disease and a decline in natural immunity and actually makes them more susceptible to infections.
This also has physiological consequences in our guts and it makes us more vulnerable to pathogens because the beneficial bacteria that are killed play an important role in our immune system.
It’s time we stopped looking at medicine as, simply, a war between invading pathogens and our body. It’s more nuanced than that.
As I have written in the past, we are a collection of interacting ecosystems and researchers now know that these ecosystems are composed of a wide variety of friendly organisms.
Just like we need to learn to be good stewards of the earth and our external environment, we also need to view the insides of our bodies in this way and start caring for these internal ecosystems in the same way.
The lesson here is that we can’t just eradicate ourselves to good health. We see this time and time again with pesticides, herbicides and antibiotics.
Lots of patients and practitioners still have mind set that says, “All we need to do is kill ___________(choose your favorite pathogen), then you’ll be healthy.” And many of us have been trained to think and treat this way, whether it is with drugs or herbs and natural supplements.
Well, a lot of times this approach can result in a disruption of the ecosystem of the gut (and sometimes overgrowth of other pathogens). And this doesn’t just happen with drugs like antibiotics, it also happens with natural products like herbs that kill pathogens in our bodies.
It’s time we create a new way of doing things. Figuring tht out is beyond the scope of this post. So, first let’s try and figure out what a “healthy” microbial ecosystem is.
Here’s the thing about your digestive tract, it’s not just one ecosystem. Really, there are several distinct ecosystems that overlap and interact with one another.
Let’s break it down:
There’s your mouth, your esophagus, your stomach, your upper and middle small intestine, your lower small intestine and your colon. The bacteria that populate each of these ecosystems is quite different.
And to complicate things, there’s the intestinal mucosa and lining which has distinctly different species than the space in side the intestine .
In addition, no two people have the same microbiota. Early research on this subject came up with the idea of “enterotypes” which are microbiota types like blood types, but they only looked at a small group of people.
After looking at a lot more people from different cultures researchers determined that it wasn’t so clear cut and there’s so much variation that it’s really hard to be definitive about this. (It’s more nuanced – I think that’s my new motto 🙂 ).
In the following diagram you can get a sense of the number and the diversity of bacteria that populate these various ecosystems.
from http://physrev.physiology.org/content/90/3/859
Frankly, this makes the claims and marketing of probiotics pretty ridiculous (more on that in a moment). No one or two strains of bacteria are going to properly populate your entire digestive tract. Nor does everyone need the same strains.
Furthermore, diversity is more important than overall population of certain strains. A diverse microbiome is the very definition of good health. With diversity comes proper function, more resistant to pathogens, infections, and overgrowth from other species of bacterial, yeast, etc.
Here’s what we have learned about this:
• During vaginal childbirth, we are exposed to our mother’s microbiome. This occurs via the birth canal, and exposure to feces during the birth process.
• We receive between 400-600 different species via breast milk. Also, breast milk contains a powerful prebiotics (which feed good bacteria). This helps these strains to proliferate and colonize inside our GI tract.
This means that births via C-Section and feeding babies formula (rather than breast milk) can have a very real impact on the diversity and overall population of a person’s microbiome.
• An infant’s microbiome reflects the mother’s vaginal bacteria initially, and then it begins to resemble the mother’s mouth, skin, and gut after that.
• After the very early stages of life, the microbiome is generally populated via environmental and food exposure.
• Skin-to-skin contact with parents provides some of the strains comprising a healthy microbiome.
This means that anti-bacterial soap, hand sanitizers and overall germ-phobia can also have a very real ( and not so beneficial) impact on the development of healthy GI flora – especially related to diversity. You want your infants and kids exposed to dirt and grime ( this news will be liberating for some parents and horrifying for others).
Environment also really matters when it comes to a healthy microbiome.
• Those who live in rural environments generally have much greater microbiome diversity than those who live in urban environments. (Working the earth is not just good for the soul, it turns out.)
There is a good deal of evidence to support the idea that the microbiome has a profound impact on the immune system and that it is involved with the prevention as well as initiation and progression of autoimmune disease.
But the idea that probiotics are always good for people with autoimmunity is not supported in the research, at all. On the contrary, there is some evidence that opposite is true and that certain strains of bacteria cause different types of immune responses and affect different autoimmune diseases differently.
And there are many complicating factors here including genetics, environment and type of disease. And mutations and changes in the microbiome can also result in different outcomes.
Like most things, the reality is that there is enormous individual variation and determining whether or not probiotic therapy is beneficial and which probiotics are appropriate is not an easy thing to do.
The reality is that we are only beginning to understand this complex interaction between our immune systems and the microbiome. However, there are two theories about how the microbiota can help protect against autoimmune disease.
The first is known as “specific lineage hypothesis” and it says that in genetically predisposed animals or humans, the microbiota could provide signals that calm our body’s immune responses.
As a result, the microbiota stays in a homeostatic (balanced) relationship with us.
Basically, the microbes are saving themselves and we have acquired these lineages from our mother and they have been passed down.
When a specific microbial lineage is expanded, it blocks the development of autoimmunity. It does so to improve its own odds of staying in this expanded state by suppressing our inflammatory and adaptive responses.
Autoimmunity is calmed as a side effect of this microbial self-preservation.
The second theory is called the “balanced signal hypothesis” this says that the host’s interactions with microbiota are independent of the precise microbiota composition and that the host’s genetics plays a critical role in the conversation with microbes.
So that your genetic profile is more important.
Whereas a balanced host response to good bacteria and this bacteria’s effort to reduce this response do not affect disease development, the inability of the host to control the microbiota properly results in stronger negative signaling provided by the microbiota and a reduction of autoimmunity.
Again, the microbes are looking out for themselves and sending out signals that result in calming autoimmunity.
(Both theories predict that the increase of tolerance would be lost in germ-free conditions without the microbes.)
There is also evidence that the microbiota behaves in different ways depending on the circumstances. It’s not static, it adapts to changing conditions.
Here’s the thing, the microbiota always faces 2 competing problems:
So there’s this constant balancing act that we and our microbiome must do to keep each other healthy.
Bottom line is this, you need to be cautious when using probiotics with autoimmunity and don’t just assume that any variety is going to help.
They might, in fact, not help or make things worse. So, like everything else, you need to carefully assess your need for them and then experiment and keep track to see if they are, in fact, giving you the desired result.
One question I frequently get is “which probiotic is a good one?” As with all things Hashimoto’s related you can see that this is not a simple question and there is so much individual variability that it really depends.
Probiotics are big business. Global probiotics market was valued at $32.06 billion dollars in 2013.
There are literally hundreds of brands and many make outrageous health claims. I’ve experimented with a number of different brands both personally and professionally. For some patients the results have been good, in others, there’s been little or no noticeable effect and for some they’ve actually had adverse reactions.
Some manufacturers and proponents might say these are “die off” reactions and they may be, but it could also be that in that particular individual with that particular genetic makeup and immune profile that they were inappropriate. ( I think that sometimes practitioners use “die off” to cover incompetence).
When deciding which type of probiotic to choose there are a few things that are really important to determine.
Will the strain actually survive digestion to be of any help?
Are the strains actually found in nature?
Are they good quality?
Let’s take a look at these issues:
In order to have any benefit, a probiotic must be able to reach the desired location within your GI tract alive (and the large intestine is by far the most populated bit of real estate in the GI tract).
Many strains of bacteria included in probiotic supplements today are very fragile, some requiring refrigeration. The human gut, on the other hand, is not a hospitable environment. It has very low pH (extremely acidic) environments, it’s body temperature, and it has evolved to keep out invading critters.
A large study done on this subject was done by the Food Standards Agency (FSA), along with Reading University, in the UK. They tested 35 popular commercial probiotic products, mostly comprised of lactobacillus and bifidobacterium strains.
Here’s what they found:
Those 6 were put through survival tests to determine survivability in the large intestine, and only 4 survived the large intestines.
So, at the end of the day, only 4 of the 35 strains showed any chance of survival, and even that was at, or around 50%.
These are not very good odds of survival.
It’s safe to say that many of the probiotic products on the market don’t deliver on their claims because they don’t live long enough to do anything.
This is important and often overlooked. In our arrogance, man has made the false assumption that we can improve upon and do better than billions of years of evolution. Time and time again this has been proven wrong. Remember the Biosphere 2? That experiment didn’t go well.
Mother nature is infinitely more experienced and developed than we are. If we survive as a species, it will only be because we learn to leverage that truth.
(Bacteria are among the earliest forms of life that appeared on Earth billions of years ago. Many believe that more complex cells developed as once free-living bacteria took up residence in other cells, eventually becoming the organelles in modern complex cells. The mitochondria that make energy for our body’s cells is one example.)
Those strains found in nature have a very long track record of survival and adaptation. Those manufactured in laboratories do not. It’s important that the strains you take are found in the human microbiome.
In addition, this also highlights the importance of diversity. Having variety in the gut matters. Taking high doses of a few specific strains, and eating large amounts of the same fermented foods every day can result in self-induced bacterial overgrowth where a couple of species dominate.
This is the same principle that applies to any ecosystem. When you overload a particular species, things get out of balance and it compromises the entire system.
Because probiotics are such big business and are unregulated, this is an important concern. I looked at a study from Consumerlabs, which was a thorough review of many popular probiotic products and strains.
They found that two products did not have the amount of organisms that they claimed. Essential Formulas Dr. Ohira’s Probiotics and Jameison Probitoics were 2 brands that had significantly less number of organisms than advertised. Click here to read the full report.
One type of probiotic I have been experimenting with is called spore form bacteria. These are organisms that survive the stomach and small intestines quite well. They have evolved to be very stable in the environment and also to colonize the GI tract very effectively.
These check all the boxes of the questions we just looked at. They survive digestion, are found in the natural world and they are of superior quality.
What do we know about spores?
• They are found all over the environment (in soil, vegetation, aquatic environments, and the digestive systems of many living species like insects, marine life, mammals, etc.) what this means is that as a probiotic they have evolved to be very resilient.
• Spores remain dormant until they get to the intestinal tract and then they colonize the bowel. They pass through the stomach and upper GI and survive.
• They are normal organisms of our digestive tract and are part of the human biome.
• They have been used in industries where efficacy is closely monitored, for example the pharmaceutical and agriculture industries.
• Human studies have proven spores to be safe and effective.
Why choose spore form bacteria over others?
What’s interesting about these bacteria is that they have been shown to be effective in several ways.
In a previous post I investigated oral tolerance and since then I’ve been looking for supplements to help improve it. These spore form bacteria have been shown to do this in a number of ways:
What brand has these?
The brand that I’ve been experimenting with with promising results thus far is called Megaspore Biotic. 
This is not available in retail stores because it is pharmaceutical grade and really requires some understanding and clinical know how in order to administer it.
It contains five bacillus spore probiotics– the value of each strain is supported by numerous studies and scientific publications. All strains are produced in a GMP facility under drug manufacturing guidelines.
It’s a very powerful spore probiotic formulation, and it delivers more than four billion live probiotic cells daily – a dose that matches and exceeds many other products on the market.
Are there any downsides?
Nothing is perfect. There are some indications that some strains in this product may be histamine producing.
But this is not only true of these strains. There are a number of different bacterial species that produce histamine. For example, these common probitoic species are all histamine producers: E. coli, Klebsiella pneumoniae, Lactobacillus bulgaricus, Lactobacillus casei, Lactobacillus helveticus, Lactobacillus reuteri. And many of these are found in yogurt and other probiotic products.
So, be aware if you have histamine intolerance that you may have to be very careful about the probiotics you choose. These species have been found to degrade histamine: Bifidobacterium infantis, Bifidobacterium longum, Lactobacillus gasseri, Lactobacillus rhamnosus, Lactobacillus plantarum, Lactobacillus salivarius
Bottom line is this. A healthy microbiome is essential to good health. I can help increase oral tolerance, help you fight infections and overgrowth of destructive species, it can help you lose weight and can also help heal autoimmunity.
However, more is not always better and different species populate different parts of the ecosystem of the gut. So varying different products and different foods that feed those species is essential.
Furthermore, using spore based probiotics can be a beneficial part of your strategy.
Finally, it’s time we stop thinking of the gut as a battlefield of the enemy. Like a farm, it must be weeded, cultivated and nurtured.
If you’re not sure what to do, feel lost or are not getting the results from probiotics that you hoped for, I’m available for a consultation to discuss testing and treatment options.
Click here to book a consultation: Yes! I’d like to speak with Marc.
In the meantime, take good care of your microbiome.
http://physrev.physiology.org/content/90/3/859 Gut microbiome in health and disease.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4528021/ Role of natural microbiota
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3145058/ Role of microbiota in health and disease
http://www.sciencedirect.com/science/article/pii/S1931312811002927 Microbiota and autoimmune disease
http://www.ncbi.nlm.nih.gov/pubmed/24763536 Diet, gut and autoimmunity
http://cshperspectives.cshlp.org/content/5/3/a007294.full.pdf+html Microbiota and autoimmunity
http://www.cell.com/cell-host-microbe/fulltext/S1931-3128%2811%2900292-7 Microbiota and autoimmune disease
http://www.nature.com/cmi/journal/v8/n2/full/cmi201067a.html Role of microbiota in cancer and autoimmune disease
http://bmcimmunol.biomedcentral.com/articles/10.1186/s12865-015-0083-2 Systemic effects of gut microbiota, relationship with disease and immunomodulation
http://www.discoverymedicine.com/Kouki-Mori/2012/11/27/does-the-gut-microbiota-trigger-hashimotos-thyroiditis/ Gut Microbiota and Hashimoto’s
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4036413/ Autoimmunity and the gut
http://gut.bmj.com/content/early/2014/11/28/gutjnl-2014-308514.short?g=w_gut_ahead_tab Does microbiome play a role in autoimmune disease?
http://www.naturalendocrinesolutions.com/articles/intestinal-dysbiosis-thyroid-health/ Self-explanatory
http://press.endocrine.org/doi/abs/10.1210/jc.2007-0606 Hypothyroidism and SIBO
http://www.bpgastro.com/article/S1521-6918%2813%2900057-7/abstract Fecal transplants for treating autoimmunity
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2904693/ Gut bacteria and TH-17
http://www.nature.com/articles/nmicrobiol201515 Assessment of Microbiome Research
http://www.newyorker.com/magazine/2012/10/22/germs-are-us Self Explanatory
https://hsbjournalclub.files.wordpress.com/2012/02/microbiota-article.pdf What are the consequences of the disappearing microbiota?
https://www.researchgate.net/publication/51577921_The_human_gut_microbiome_Are_we_our_enterotypes
http://www.nature.com/news/gut-microbial-enterotypes-become-less-clear-cut-1.10276
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3159383/ Has the microbiome played a critical role in the development of the adaptive immune system?
http://www.grandviewresearch.com/industry-analysis/probiotics-market Value of probiotics market
http://www.ncbi.nlm.nih.gov/pubmed/17241350 Adhesion of 31 actobaccilus strains
http://www.naturalevo.com/uncategorized/the-evolution-of-probiotics/
https://www.bulletproofexec.com/why-yogurt-and-probiotics-make-you-fat-and-foggy/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3316997/ Probiotics that degrade histamine
As many of you know, for the last several years I have focused solely on treating people with Hashimoto’s.
This has given me a tremendous opportunity to explore this health issue in considerable depth. I have had the honor and the privilege to work with over 1,000 people with Hashimoto’s and I’ve been privy to some cutting edge research from colleagues like Dr. Datis Kharrazian and Dr. Izabella Wentz.
Dr. Kharrazian first introduced me to the concept of oral tolerance and I’ve spent a good deal of time combing through the medical literature learning about it’s significance with regard to Hashimoto’s and reactions to foods.
In doing so, I recently had an epiphany and it has changed my way of thinking about how we can use diet to heal this disease.
In this post, I’m going to go deep into what I have learned about oral tolerance and it’s relationship to Hashimoto’s, autoimmunity and the Autoimmune Paleo Diet.
One thing I have learned is that diet is the foundation of success. And the reason this is true, in my opinion, is that the digestive tract is ground zero for autoimmunity.
An estimated 70% of the immune system is found there, and a breakdown of the gut and the intestinal lining leads to the systemic inflammation that is at the root of diseases like Hashimoto’s.
According to Dr. Alessio Fasano, MD, an expert on the origins of autoimmunity, the cause of this disease in the intestines.
In a paper published in the Clinical Review of Allergy Immunology February 2012 , he noted that,
“Together with the gut-associated lymphoid tissue and the neuroendocrine network, the intestinal epithelial barrier, with its intercellular tight junctions, controls the equilibrium between tolerance and immunity to non-self antigens.
Zonulin is the only physiologic modulator of intercellular tight junctions described so far that is involved in trafficking of macromolecules and, therefore, in tolerance/immune response balance. When the zonulin pathway is deregulated in genetically susceptible individuals, autoimmune disorders can occur.”
What that means in plain English is that the breakdown of the barrier of the intestines is the pathway to autoimmune disease.
This is by no means the whole story. Yes, the breakdown of the intestinal lining is a causative factor for the development of autoimmune disease, however, it’s just the gateway.
This is kind of like getting a view of the door, but there is an entire landscape of immune reactions that go on beyond that door.
And what lies beyond the doorway is what we are going to explore here today.
What’s happing with autoimmunity? Our immune system has lost the ability to differentiate between our own cells and foreign invaders, like bacteria, viruses and other pathogens.
And this confusion leads to our immune system attacking our body’s own proteins. This is caused by our immune systems losing the ability to have tolerance to our own tissue (made of these proteins).
The entire digestive tract is made up of multiple little ecosystems and these ecosystems are always battling with this problem of tolerance.
Because the gut is, essentially, one long open tube and lots of pathogens in the form of bacteria, viruses, fungi and parasites pass though there along with proteins that we need to ingest and get nourishment from.
An important part of this process of the ebb and flow of tolerance is something called “oral tolerance”.
Oral tolerance is defined as your immune system NOT REACTING locally and systemically to antigens such as food proteins.
In other words, oral tolerance is when you eat a certain protein and you become tolerant to that protein.
We can think about this in terms of our own evolution. If you are eating something (a protein) all the time, it would be a really good thing for you to develop a tolerance to it and not attack it.
If we’re only eating certain kinds of foods, we‘d be more likely to survive if we could build tolerance to them.
Proteins are the things we are most often exposed to. (They’re the building blocks of life, after all.)
And it turns out that tolerance to ingested proteins is also really important for the barrier function of the intestines i.e. to prevent leaky gut.
As we saw above, when this tolerance breaks down, chronic diseases follow; like celiac, Crohn’s, ulcerative colitis (these all occur locally in the intestines) and other systemic autoimmune disease like Multiple Sclerosis and even Hashimoto’s.
In other words, oral tolerance is a kind of dimmer switch, it turns down the attack. Both in the intestines and in the rest of the body.
When you have oral tolerance, your immune system doesn’t attack as aggressively.
When you lose oral tolerance you wind up with things like celiac disease (which is an autoimmune disease – not just a food intolerance).
We don’t fully understand this, yet.
However, what we do know is that oral tolerance works by deactivating T and B cells that target our tissues – either by clearing them out and getting rid of them or by making them not respond to proteins anymore with something know as “anergy”.
Anergy is the lack of a normal immune response to a particular antigen or allergen.
Oral tolerance also works by Tregs directly suppressing these cells.
Tregs is another name for regulatory T cells (also called suppressor T cells). They are T cells which modulate the immune system, maintain tolerance to self-antigens, and discourage the development of autoimmune disease.
Of course, with autoimmune disease this may be a really important thing to achieve, if possible.
The question is this: If you can establish or re-establish or at the very least improve oral tolerance, can you remove or at least diminish the autoimmune attack?
Some researchers believe the answer is “yes”. There is some evidence that this may be an achievable goal.
That’s a very, very important question. Because this is potentially a dangerous game. By no means is this a easy, risk free process.
For example, should we attempt to establish oral tolerance to things like gluten and dairy? (Dietary proteins with tremendous destructive potential.)
In my opinion, the answer is a resounding NO!
They have been implicated in the destruction of brain tissue such as cerebellar tissue and myelin. (I’d like to keep my brain for as long as possible, wouldn’t you?)
So what does that leave us with?
A lot, actually. (More on this in Part 2 of this post).
But before we attempt to answer that, another thing the research has shown us is that simply establishing tolerance alone is not enough.
We must also do other things like reduce inflammation and strengthen the regulatory part of the immune system and work to calm and/or eliminate stress, restore integrity and balance to the ecosystem of the gut, etc. while we do this to achieve the best results.
So first, let’s look at the big picture.
What are the steps to first calming the immune system and then, secondly, trying to improve oral tolerance?
First off, if you’re looking for a quick and easy solution, click away. This isn’t quick and it isn’t easy.
This is a long term project that may take several months and it may be riddled with unexpected outcomes (welcome to the immune system).
That being said, it can also yield profoundly positive long term results.
If you are just starting out this is the place to begin.
The Autoimmune Paleo/Lectin Avoidance Diet removes the following foods:
Grains, nuts, seeds, legumes, nightshades, gluten, dairy, soy and eggs.
I’m not going to spend time on the how or the why of this diet in this post, but this is a very effective approach for reducing systemic inflammation and for calming the immune system.
In addition, in many cases with Hashimoto’s this will yield improvements in virtually all important thyroid markers including antibody levels, TSH, etc.
And it often results in a (sometimes dramatic) improvement in weight, brain fog, mood and energy.
With my patients, I also assess all the other systems of the body and when it is called for we work on healing the gut (almost always called for), detoxifying the liver, healing the adrenals and reducing inflammation in the brain while we are on this diet.
This is also beyond the scope of this particular post, but suffice it to say that this is a systemic, multi-organ problem and we need to heal every part of the body that is impacted if we hope to get this into remission.
Also, the fact is that being on this diet provides a tremendous opportunity to aggressively reduce inflammation and to clean up the liver, heal the gut and calm compounding factors.
Clinical Pearl: One thing I have observed with some people who tried the Autoimmune Paleo Diet (myself included) is that it can actually increase your sensitivity to foods that you are sensitive to.
A food that you had a reaction to in the past (like gluten) will often cause a much more severe reaction once you have eliminated it for a prolonged period of time.
And in some cases, the elimination can increase sensitivity to foods across the board. (And I have observed it seems to increase not decrease with time. Meaning the longer some people are on the strict elimination diet, the more sensitive they become.)
One theory is that what may be happening here is that the elimination of these antigens can lead to a decrease in oral tolerance.
This makes logical sense because oral tolerance requires exposure to the antigens ( in this case, dietary proteins).
And there is some evidence of this in the medical literature. Some researchers claim that the elimination diet is a potential cause of anaphylaxis or a severe and life threatening allergic reaction.
And many researchers and health professionals are now questioning the wisdom of NOT exposing children to things like peanuts in early childhood because the LACK of exposure can lead to a massive immune response when they do get exposed.
The question is, why?
If this is the case, what is the mechanism that could lead to the decline of oral tolerance?
I think the simple answer is that elimination of multiple immune stimulating antigens changes the entire landscape of your immune system. It has a major impact.
And while some of this is really good and, arguably, absolutely necessary, (especially in circumstances like autoimmunity) it may have some unintended consequences.
This is also a great illustration of the complexity of the immune system. It has multiple parts that move in multiple directions, all the time. And overly simplistic linear thinking doesn’t work when trying to understand and balance the immune system.
Another important observation about this process is that having to worry about food all the time and having an increasingly smaller and more restricted diet is very stressful. It makes it difficult (if not impossible) to go out with friends and relatives. It can create anxiety over what to eat and it can make you feel further alienated and frustrated.
And stress is a really big deal for people suffering from autoimmune diseases like Hashimoto’s. The body is already under a great deal of physiological stress, to add further daily stresses regarding what to eat and where to find the right food can be really counter-productive to the process of healing.
So, if we can tweak this process to make it less stressful, than that is a very valuable innovation.
Once you have done the elimination phase of the Autoimmune Paleo diet (usually for 30 to 60 days), the next phase involves reintroducing foods, one food at a time to see if you react to them.
In some cases, people react to an awful lot of stuff, precisely because they have been so good at eliminating these foods and have accomplished some really good things with regard to calming their immune systems.
My understanding of this phase of the Autoimmune Paleo approach is that this is essentially a test to see what you can and can not eat.
Proponents of the Autoimmune Paleo Approach rationalize this increase in sensitivity by saying, essentially, this is part of the healing process. And they assert that once you heal your gut you’ll have fewer sensitivities.
But this isn’t always true, there are people who have spent several years healing their guts and still find that they are sensitive to a number of foods.
Obviously, everyone is a little different and some people do better than others. And some people find they can re-introduce all sorts of things, while others can introduce just a few and still others find their diets becoming more and more restrictive.
If you’re one of these people, this process can be really demoralizing because here you have worked your butt off to be super compliant and follow the plan and the end result is that your diet consists of fewer and fewer foods.
It’s the living embodiment of the expression, “No good deed goes unpunished.”
What I have come to see is that instead of just eliminating and seeing what happens during re-introduction, what we have is an amazing opportunity.
And that is to work to re-establish or improve oral tolerance and create a much more hospitable immune environment.
How do we do that?
Great question! (And one that needs a good deal more experimentation and exploration than this one post can provide).
I’m not going to pretend to have all the answers on this, but here is what the research suggests.
In autoimmune disease research, the goal with oral tolerance seems to be to suppress the Th1/Th17 response (for most autoimmune diseases).
There are two ways that researchers have tried to do this.
The first is by giving a high dose of a protein once. (This, obviously, is the heavy handed approach.) From an immune system standpoint, when it works this can result in a anergy or complete shutdown of both TH-1 and TH-2 responses.
Problem is that it doesn’t always work and obviously with autoimmunity the risk here is that you can cause a massive flare ups and discomfort.
The second approach is to take the protein at a lower dosage multiple times, which has been found to increase Tregs.
The multiple dose approach is gentler and from an immune standpoint, a lot better suited for autoimmune disease.
Here’s the real difference in approach. You shouldn’t think of this phase as simply a testing phase.
It could be much more than that.
However, before you get all excited, understand that we are wading into uncharted waters and if we are going to challenge the immune system, there is bound to be some reactions.
And not all of them will be good.
In addition, maybe it’s time to view reactions differently. Maybe not every reaction is just simply “bad”.
And maybe total elimination of reactions isn’t totally “good”.
It may be a bit more nuanced than that.
That being said, there are two things to consider during this process:
1. What helps induce or improve oral tolerance? (This would include supplements, life style changes, etc.)
2. Which proteins do you want to create oral tolerance for? (This would include the approach to diet and reactions)
Both are important because we want to do everything we can to make this a successful experiment.
Actually, there is also a third thing to consider and that is, what can we do to minimize the discomfort and immune system flare ups during this process?
(I don’t know about you, but I prefer to suffer as little as possible.)
Before we look at what to do to improve oral tolerance, let’s take a look at some of the mechanisms for establishing and improving it.
IL-10 and Oral Tolerance: IL-10 is anti-inflammatory cytokine because it decreases various immune cells such as Th1 AND Th2 cells. It also inhibits NF kappa beta, which is important in destructive inflammation. It inhibits COX 2 and mast cells and it decreases insulin and leptin resistance. IL-10 is something we want to increase.
IL-12 and Oral Tolerance: IL-12 is part of the TH-1 family of cytokines and it can block oral tolerance in TH-1 conditions. It is responsible for helping cytotoxic lymphocytes, natural killer cells mature and it also supplies growth factor to help certain cells grow into the killers that they are.
IL-12 is also involved in turning on genes that result in attacks on specific organs and has been implicated as an important player in Hashimoto’s. IL-12 is something we want to reduce.
Tregs and Oral Tolerance: Tregs comprise ∼5%–10% of T helper cells.
There are two types of Tregs: ‘induced’ (iTregs) and ‘natural’ (nTregs). Both types are anti-inflammatory. Induced means that they are created outside the thymus. (There are 2 kinds of induced Tregs: (Th3 and Tr1). Natural means that they are part of the cells naturally produced in our thymus gland.
Tregs calm and suppress Th1, Th2, Th17 cells and their cytokines, as well as many other immune cells and proteins such as, basophils, eosinophils, mast cells, and IgE and they also influence migration of inflammatory cells to tissues.
Tregs inhibit immune activation by direct cell to cell contact. This means that they are directly anti-inflammatory.
Tregs need to be ‘activated’ in order to have their suppressor functions. Exposure to a dietary protein or an antigen is one of the ways that they get activated. Obviously, increasing Tregs in a balanced way is a good idea with autoimmunity.
But, as with all things, if you do this too aggressively, there is the risk of becoming less able to defend against some infections. And unfortunately, one of those infections is a viral infection like herpes and Epstein Barr. (You can read more about the herpes/Hashimoto’s connection in this post.)
Mucous in the Intestines and Oral Tolerance: researchers have found that mucous plays an important role in maintaing the barrier of the gut and in modulating homeostasis (or balance) in the gut. Having a healthy amount of mucous in the gut is also a good idea.
Dendritic Cells and Oral Tolerance: Dendritic cells (DCs) are antigen-presenting cells(also known as accessory cells) of the immune system of mammals. Their main function is to process antigen material and present it on the cell surface to the T cells of the immune system. They act as messengers between the innate and the adaptive immune systems.
Dendritic cells are important for immune tolerance because they can adapt to proteins or enhance the attack on them. At low levels these proteins help dendritic cells to adapt, but if proteins become excessive and aren’t cleared this can result in dendritic cells attacking and consuming the protein (and in some cases our own tissue). With dendritic cells we want to encourage as much variety as we can and make sure that intestinal transit and protein clearance is functioning well.
cAMP and Tolerance: cAMP is a signaling molecule that relays messages to T cells to not respond and proliferate to a protein. This, essentially, trains the immune cells to not respond. Increasing cAMP may be beneficial.
Intestinal Health and Tolerance: A healthy ecosystem in your gut, with good blood flow, motility and transit time and healthy amounts of enzymes, bile and stomach acid are all important for improving oral tolerance. A healthy gut ecosystem is extremely important.
Commensal Bacteria and Tolerance: Oral tolerance is dependent on good bacteria in the gut. The more we learn about intestinal bacteria, the more valuable they become and the more irresponsible excessive antibiotic treatment becomes. Gut bacteria should be treated like an endangered species and be tended to and watched over carefully.
High protein diets and Oral Tolerance: This was a very interesting finding in the research. Diets that are lower in protein reduced both TH-1 and Th-2 and were effective in helping promote oral tolerance. Reducing dietary protein may help to reduce sensitivity.
Things that Cause Declines in Oral Tolerance: There are a number of things that may lead to declines in oral tolerance. Obviously, these are things we want to avoid:
In summary, you can see that many factors contribute to the development and maintenance of oral tolerance. And that it is critically important for dampening immune reactions.
And the loss of loss or decline of tolerance may be an important factor in autoimmunity and in sensitivity reactions to dietary proteins.
But, as with everything, carefully balancing oral tolerance is critically important when dealing with autoimmune disease and reactions to dietary proteins.
In part 2 of this series, we’ll take a look at specific herbs, supplements, dietary and lifestyle approaches for improving and maintaining healthy oral tolerance.
Let’s talk! Schedule an appointment with me to discuss these and other health issues. Click Here
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3578149/ Mechanisms of oral tolerance
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3376463/ Boosting IL-10
http://science.sciencemag.org/content/342/6157/447.abstract Mucous and oral tolerance
http://www.hindawi.com/journals/jir/2013/972865/ Dendritic cells and oral tolerance
http://www.sciencedirect.com/science/article/pii/S0008874996902749 cAmp and Tolerance
http://www.news-medical.net/news/20110211/Blocking-interleukin-15-may-help-restore-oral-tolerance-to-gluten.aspx
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC27123/ Dendritic cells induce anergy in autoimmunity
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2857757/ Model of Oral Tolerance: Suppress TH1 and TH-17, but not TH-2
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3076704/ Keys to success
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC44268/pdf/pnas01136-0446.pdf Oral tolerance determined by dosage
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2270752/pdf/CDI-13-143.pdf Oral tolerance, therapeutic implications for autoimmune disease.
http://www.nature.com/mi/journal/v5/n3/full/mi20124a.html Oral tolerance to food protein
http://www.nature.com/mi/journal/v2/n1/full/mi200875a.html Celiac disease as an example of the destructive potential of loss of oral tolerance.
http://www.hindawi.com/journals/ad/2014/437231/ Link between environmental factors and auotimmunity
https://www.drmcdougall.com/misc/2009nl/jan/ms.htm MS and dietary protein
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3741914/ Celiac and cerebellar autoimmunity
http://circ.ahajournals.org/content/129/Suppl_1/AP354 Lectin Avoidance study
http://www.nature.com/nri/journal/v9/n5/full/nri2515.html Microbiata shapes intestinal immune responses
http://cshperspectives.cshlp.org/content/4/6/a006957.full T cell tolerance
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1628850/ Anaphlaxis during elimination diet
http://www.ncbi.nlm.nih.gov/pubmed/21333554 Intestinal tolerance requirements
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3376463/ Boosting Treg function (IL-10)
http://www.ncbi.nlm.nih.gov/pubmed/15681753 IL-10 Creates Tolerance
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3222333/ Having Lots of an Allergic Protein will create tolerance
http://www.ncbi.nlm.nih.gov/pubmed/12026189 Low Protein diet induces tolerance, boosts IL-4
http://www.ncbi.nlm.nih.gov/pubmed/12887157 Low protein reduces Th-1 cytokines.
http://naglerlab.bsd.uchicago.edu/documents/Caoetal2014.pdf Role of commensal bacteria in oral tolerance
http://www.ncbi.nlm.nih.gov/pubmed/22339388 Skin Sensitization and oral tolerance
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3563838/?report=classic Medium Chain Triglycerides and tolerance
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC187370/ H. Pylori’s impact on oral tolerance
http://www.ncbi.nlm.nih.gov/pubmed/17034584 Alcohol and oral tolerance
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3103798/ Apendectomy and oral tolerance
http://www.ncbi.nlm.nih.gov/pubmed/9921278 Palimate and oral tolerance
http://www.ncbi.nlm.nih.gov/pubmed/21307853 Retinoic acid and oral tolerance