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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Rodriguez JP, Abnormal osteogenesis in osteoporotic patients is reflected by altered mesenchymal stem cells dynamics. J. Cell. Biochem. 1999 / 75 (3) / 414-423. ,
Gazit D, et al, Bone loss (osteopenia) in old male mice results from diminished activity and availability of TGF-beta. J. Cell. Biochem. 1998 / 70 (4) / 478-488. ,
Ikeda T, et al, Age-related reduction in bone matrix protein mRNA expression in rat bone tissues: application of histomorphometry to in situ hybridization. Bone1995 / 16 (1) / 17-23. ,
Parfitt AM, et al, Relations between histologic indices of bone formation: implications for the pathogenesis of spinal osteoporosis. J. .Bone Miner. Res.1995 / 10 (3) / 466-473. ,
Neidlinger-Wilke C, et al, Human osteoblasts from younger normal and osteoporotic donors show differences in proliferation and TGF beta-release in response to cyclic strain. J. Biomech. 1995 / 28 (12) / 1411-1418. ,
Marie PJ, Decreased DNA synthesis by cultured osteoblastic cells in eugonadal osteoporotic men with defective bone formation. J Clin Invest 1991 Oct;88(4):1167-1172.
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Hey people!
Earlier this week I shared a post I wrote that looks into some questions around the influenza vaccine.
We had quite a few reactions and they were distinctly different.
Some people reported getting the flu vaccine and it was no problem for them. Others reported terrible reactions and said they’d never get it again.
Well, as always, I’m curious about why this might be.
So I took a look at the research and I’ve come up with a plausible theory.
I’ll get to it in a moment, but, first, I think it’s important to understand something about the immune system.
The Immune System Is Incredibly Complex
The immune system is made of many different parts, and much of it is still a mystery to researchers.
One thing that we do know is that these different parts can behave differently in different situations and trying to over simplify and assign “good” or “bad” attributes to the different parts often results in frustration.
And the reason for this is that sometimes it does things that are “good” for the body (like defend it from pathogens like the flu virus) and sometimes it does things that are not so beneficial (like develop autoimmunity).
But even autoimmunity comes from a necessary and “good” process, the body needs to dispose of old dead cells or we’d become a toxic stew of cell fragments and mutations.
Sometimes these processes get thrown out of balance and “bad” things happen such as autoimmunity and one of the possible reasons for this has to do with the way the body tries to deal with and dispose of viruses.
And examining this process can give us insights into why some people with autoimmunity have such a bad reaction to the flu (and sometimes, other viruses, as well.)
In reality, everyone is a little different and we all have different immune profiles. Even among people with Hashimoto’s there is a good deal of variety in terms of how their immune system is functioning (or dysfunctioning).
Autoimmunity and Influenza Reactions Have One Thing In Common
The one common denominator in both bad reactions to the flu and the development of autoimmunity is that, in both cases, there is a deficiency in certain immune cells.
One thing that both autoimmunity and influenza infection have in common is that a deficiency of CD8+ cells can be found in autoimmune disease and it can also be a factor in having a more intense reaction to the influenza virus.
CD8+ cells are important for immune defense against bacteria and viruses and they also help the body monitor for tumors.
Some researchers have theorized that the Epstein Barr virus plays an important role in autoimmunity because it can ultimately leads to a decline in CD8+ cells.
This is a bit complicated and I have written about it in more depth here: https://www.hashimotoshealing.com/the-herpes-virus-and-has…/
How to Boost CD8+ Cells
For this post I thought it might be helpful to give you some suggestions for boosting CD8+ cells, which may help reduce your susceptibility and reaction to colds and flus.
Butyrate, which is important food for good bacteria and for cell lining in the intestines has been found to be helpful in restoring CB8+ cells that were depleted by viral infections.
These are short chained fatty acids and can be found in resistant starches. Butyrate can also be purchased as a supplement on it’s own.
The Chinese herb Chuan Xin Lian, or Andrographis can also boost CD8+ cells and is an excellent herb for sore throats and colds and flus. ( This is herb is contraindicated in pregnancy and must be used with caution. It is available in capsule and tablet form). More information can be found here: http://examine.com/supplements/Andrographis+paniculata/
Another Chinese herb called Jiao Gu Lan or Gynostemma has been shown to boost CD8+ cells and to have anticancer and cholesterol lowering properties: https://www.ncbi.nlm.nih.gov/pubmed/24832985
Finally, Wu wei zi, or Schizandra is another herb that has been shown to boost CD8+ cells after radiation exposure: http://www.egh.net.cn/EN/abstract/abstract2207.shtml
(Note: Herbs are medicine too, so use caution when taking them and be sure to do your own research or consult an experienced physician on proper dosage and contraindications).
References:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC136883/ CD8+ def. and influenza
https://www.hindawi.com/journals/ad/2012/189096/#B47 CD8+ def. in autoimmunity
https://wwwnc.cdc.gov/eid/article/12/1/pdfs/05-1237.pdf Cell mediated Protection in Influenza
http://bitesized.immunology.org/cells/cd8-t-cells/ Good explanation of CD8+ cells
https://www.hindawi.com/journals/jir/2015/979167/ Immune disorders and Hashimoto’s
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4196144/ Butyrate boosts CD8+ cells
Thyroid Levels Impact Dementia Risk
A new study published in the journal Neurology has found that high and high-normal thyroid levels are linked to greater risk of developing dementia, but not vascular brain disease.
This is a very interesting finding because (as this previous post illustrates) cognitive decline has been linked with hypothyroidism and high TSH.
This study shows that having too low TSH can also be risk factor (we’ll explore why this might be in a moment). What this also shows us is just how important balance is. There may be a “Goldilocks” zone of TSH and free T4 that’s “just right”.
In this study, researchers led by Layal Chaker, MD, MSc, of Erasmus University Rotterdam, the Netherlands investigated the role of thyroid function in dementia, cognitive decline, and vascular brain disease.
They examined a subgroup of 9446 people (mean age 65) enrolled into this Rotterdam Study. Researchers looked into the link between thyroid-stimulating hormone (TSH) and free thyroxine (free T4) and incidents of dementia.
Here’s what they found: Over the course of follow-up (mean 8 years), 601 patients developed dementia (Alzheimer’s dementia n=487). Higher levels of TSH were found to be associated with lower dementia risk for both the full and normal ranges of thyroid function, independent of cardiovascular risk factors (hazard ratio [HR] 0.90, 95% confidence interval [CI] 0.83–0.98; and HR 0.76, 95% CI 0.64–0.91, respectively).
Participants with higher levels of free thyroxine were found to have greater dementia risk (HR 1.04, 95% CI 1.01–1.07).
Higher levels of TSH were associated with better cognitive scores (P =.021), and in older women, a 5% decrease in absolute 10-year dementia risk. Notably, thyroid function was not found to be associated with subclinical vascular brain disease.
The results, the authors concluded, suggest that thyroid hormone impacts dementia risk through nonvascular pathways.
The researchers offered a couple of other ideas about why this might be including the possibility that excess free thyroxine may affect the way that genes are expressed in important pathways in the brain or that destruction to nerves my be caused by oxidative stress which can cause destruction of brain tissue (which, frankly, makes a lot of sense to me – more on this in a moment).
Also, participants with early signs of dementia may have changes in behavior, like diet, which may alter thyroid function. (As we know diet and behavior are extremely important for maintaining a healthy brain).
“In other words, we may not be observing a true effect of thyroid hormone on dementia risk but rather the opposite,” the authors concluded.
This is one of those instances when looking at research can make you crazy. Too high TSH and hypothyroidism is clearly a potential problem and too low TSH may also be a potential problem.
Age is another factor to consider when trying to wind yourself through this maze. Thyroid hormone is absolutely essential for the developing brain, so if your are pregnant or if you are an infant or young child, it may be more important to have your TSH a little lower (In fact, the American Endocrine Society has recommendations for TSH in each trimester and they can be found in this post.)
As we age, the brain becomes becomes more vulnerable to certain processes and, I think, the chief concern here may be the role of oxidative stress on the mitochondria in the brain.
In thyrotoxicosis (excessively low TSH or a hyperthyroid state), glucose uptake and utilization by muscle is increased as is the breakdown of glycogen (glycogenolysis) and glycogen (a substance that stores carbohydrates) depletion is seen in muscle biopsy samples.
Also, mitochondrial oxidation is increased and lipid oxidation, protein and purine breakdown all occur and this results in lower ATP (our cells energy sources).
And being naturally a little hypothyroid might actually protect your brain from this (but, it can also cause it’s own problems – damned if you do and damned if you don’t!)
And mitochondria are smack dab in the middle of this whole process because they are involved in both energy production and cell death.
Mitochondria are unique in that they both produce energy and make free radicals. They do this in order to monitor cellular health and to make a rapid decision (if necessary) to initiate programmed cell death.
When this process goes haywire in the brain, it can have devastating impacts on nerve cells. And too much free T4 can be one of the factors that drives this.
From http://www.sciencedirect.com/science/article/pii/S0925443909002427
Ironically, mitochondria in the brain are really of victims of their own amazing abilities.
If the amount of free radical species produced by them overwhelms the neurons in the brain’s ability to neutralize them, oxidative stress occurs, followed by mitochondrial dysfunction and neuronal damage.
Reactive species generated by mitochondria have several cellular targets including mitochondrial components themselves (lipids, proteins, and DNA). The lack of histones in mitochondrial DNA (mtDNA) and the diminished capacity for DNA repair render the mitochondria an easy target to oxidative stress events.
So, they are especially vulnerable to their own attacks. (There has to be a lesson there. 🙂 )
All of this can translate into destruction of brain tissue due to this oxidation which produces free radicals. (In fact, many symptoms of aging are due to these free radicals).
Basically, this all comes down to electrons. These reactive oxygen species are untethered electrons flying around breaking up cells, and wreaking havoc (think bullet in a tin can).
And really, at the end of the day, this mitochondrial dysfunction is a causal link between neurodegeneration caused by both hypo and hyperthyroidism.
So, obviously, this begs the question, How do we preserve and heal the mitochondria in our brains (and the rest of our bodies?)
Stay tuned. We’ll be exploring this in a future post in considerable depth.
Want to Banish Brain Fog and Heal Your Brain? Check out Dr. Datis Kharrazian’s Banish Brain Fog Program ($50 off if you purchase before 10/3/2016).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4923401/ Endocrine Risk factors for Cognitive Impairment
https://www.ncbi.nlm.nih.gov/pubmed/17353866 Hypothyroidism and reversible cognitive decline
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3496329/ Review of 23 studies on subclinical hyperthyroidism and cognitive decline
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3872098/ Role of Thyroid Hormone in Oxidative Stress and Neurodegeneration
http://joe.endocrinology-journals.org/content/176/3/321.full.pdf Hypothyroidism alters mitochondria
http://www.sciencedirect.com/science/article/pii/S0925443909002427 Mitochondria Dysfunction and Alzheimer’s
We’ve had a few posts covering the adrenals this week. In this one, I talk about how they can affect your kidneys and what you can do about it.
Well something that is often overlooked with hypothyroidism and Hashimoto’s is it’s impact on the kidneys (the Water Element in Chinese Medicine)
I’ve had a lot of questions this week about why blood pressure goes up in people who have low blood pressure for years.
Read this post and you’ll learn why.While this is one area that is not often discussed, Hashimoto’s and hypothyroidism can have a big impact on kidney function.Hypothyroidism can cause:
(This can cause creatinine to build up and not be excreted. Creatinine is a chemical waste molecule that is generated from muscle metabolism. )
The kidneys fail to filter waste products from your body properly when your pressure is low, and “angiotensin” is produced, which raises your blood pressure.
Also, a rise in cortisol from your adrenals can raise your blood pressure.
Hypothyroidism can also cause edema.
You can see this swelling under the eyes, or as mild swelling of the hands and feet.
This is caused by several things: decreased kidney function, capillaries becoming more permeable-, poor lymphatic drainage and salt and water retention by the kidneys.
Another area that’s important to think about is the amount of protein in your diet.
As many of you know, we advocate the Autoimmune Paleo approach because this diet can be so effective in healing the gut and calming an overactive immune system.
One problem with this diet with regard to the kidneys is that some people have a tendency to focus too much on the meat. It becomes the all-meat-all-day diet.
This is really hard on the kidneys because they are responsible for filtering out the metabolic wastes that are created when protein is broken down.
So, it’s really important to make sure that you have plenty of vegetables and fruit (preferably organic and if you’re ambitious – grown in your garden).
You don’t need to eat meat with every meal. It’s perfectly fine to have some meals that are vegetable and/or vegetable and a good starch only.
Your kidneys will thank you for it!
A new study from the Journal Chemical Research in Toxicology has released some interesting research on how household dust may contain chemicals that bind to thyroid hormone receptors.
When this happens, of course, it may block your thyroid’s own thyroid hormone or thyroid hormone medication from binding and working properly in your body.
What these researcher did was use compounds already known to bind to human thyroid receptors to help predict which other chemicals might also bind to receptors.
They found five chemicals and one of them, an herbicide, bonded most strongly to thyroid receptors.
According to toxipedia.org, this chemical called 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) in no longer registered for use in the US and was discontinued as an herbicide in 1985. However, like many chemicals it can persist in the environment long after it has been discontinued (http://bit.ly/2cIQAJ2)
It also gained infamy by being one of the compounds in Agent Orange, used in the Vietnam War to destroy the forests of Vietnam where guerrillas were thought to be hiding.
It was used for selective control of weeds in cereal crops and lawns, nettles in pasture and woody weeds in forestry, particularly with conifers since 1945.
Some products that contained it are: Dacamine, Ded-Weed, Farmco Fence Rider, Forron, Inverton 245, Line Rider, T-Nox, Transamine, Brushwood Killer, Brush-Rhap, Brushtox, Esterone, Fruitone A, Reddon, Spontox, Tormona, Tributon, Veon 245, Verton 2T, Visko Rhap Low Volatile Ester, Amine 2,4,5-T for Rice, Super D Weedone, Trinoxol, Weedar, Weedone
And this is just one chemical found in household dust. The research showed that common dust particulars could have an impact on the brain, cardiovascular system, metabolism and other systems regulated by thyroid hormones.
A study released last summer found that certain dust chemicals could be a major factor in obesity.
So what do we do about it?
Obviously, vacuuming your house and dusting with something that catches dust and doesn’t just make it airborne, like a wet rag is a good idea.
Using an air filter might also be an excellent idea. This with HEPA filters are effective in removing airborne particles. I have one in my office (that I just paused to turn on :)) made by IQ Air, that is very effective.
Lastly, glutathione is an antioxidant found in virtually every cell of your body and it is used by the body to help rid itself of many environmental toxins.
It is most effective in IV or lioposomal cream form and can also be taken orally in the form of S-acetyl-L Glutathione, which is mostly absorbed by the liver.
Cordyceps is a Chinese herb that helps the body make and reuse glutathione and pharmacologically it is antibiotic, anticancer, it relieves asthma, stimulates immune function, it stimulates the adrenals, and has been found to increase platelets.
In short, it’s the perfect answer to the scourge of household dust.
That’s all for today, be good, be kind and remember to have compassion for everyone (including yourself!)
Comments, questions, observations, shares, and likes are all encouraged!
References:
Chinese Medical Herbology and Pharmacology by John and Tina Chen, 2004 Art of Medicine Press
http://pubs.acs.org/doi/abs/10.1021/acs.chemrestox.6b00171?source=cen&
https://en.wikipedia.org/wiki/Persistent_organic_pollutant
https://chemicalwatch.com/30214/house-dust-chemicals-activate-receptor-linked-to-obesity?
The Heart and Thyroid Connection
Hey people!
In the last few days there’s been lots of news coverage of the influence of thyroid hormone and thyroid hormone levels on the heart. All of these news outlets had stories:
This is all because of a new study out of the Netherlands in a medical journal called Circulation. The study found that elevated levels of free T4 may result in an increased risk (1%-4%) of sudden cardiac death, even in normal patients.
When asked why, the theory was that “Our hypothesis was that thyroid hormone levels could increase the risk of sudden cardiac death by affecting cardiovascular risk factors such as blood pressure levels,” said Dr. Layal Chaker, research fellow in endocrinology and epidemiology at Erasmus University Medical Center Rotterdam in the Netherlands, lead author of the study.
I’ve done a bunch of research on this area and I covered it in my book, Roadmap to Remission. One thing I discovered was that the heart is very sensitive to thyroid hormone, especially T3.
This is an excerpt 9IN ITALICS) from the section on the Fire Element, which includes the cardiovascular system. It includes a good, easy to understand explanation for exactly what might cause all of this to happen.
The heart circulates nutrients by pumping blood throughout the body.
When blood is pumped through your body, it puts pressure against the walls of your blood vessels.
Right? This is your blood pressure.
When doctors describe blood pressure, they use two numbers like “120 over 70”. These numbers describe the pressure when your heart pumps blood into your blood vessels (the high number) and the pressure when your heart relaxes (the low number).
Imagine squeezing a ketchup bottle. When you squeeze it to ‘pump’ ketchup onto your plate, the pressure is high. When you stop squeezing, the pressure is low.
Blood pressure can change a lot during the day. It is usually lower while you are relaxing and higher when you are active. Other things like pregnancy, smoking, medication, being stressed and thyroid hormone levels can change your blood pressure.
Usually, with hypothyroid conditions, you’re blood pressure is low and with hyperthyroid conditions it tends to be high. But there are many reasons why this is not always the case, in fact, many Hashimoto’s people actually have high blood pressure.
This is because even though many thyroid patients, or those being treated with T4 meds like Synthroid, can start out with low blood pressure, factors related to having functional hypothyroidism can actually create hypertension and high blood pressure over time.
For example, as we saw when we looked at the Water Element hypothyroidism leads to a host of problems physiologically that cause kidney and cardiovascular problems.
For example, there’s less blood flow to the kidneys, this causes the kidneys to not filter waste products like creatinine from your body properly.
In addition, when your blood pressure is low, and “angiotensin” is produced, this raises your blood pressure.
Also when you are hypothyroid, blood is taken from the extremities into the body, which tends to raise pressure by forcing the same volume of blood into a smaller network of vessels.
This process is brought about by a constriction of peripheral vessels.
Hypothyroid patients produce an excess of noradrenalin from the adrenal gland, which constricts blood vessels all over the body, another effort of the body to deal with the low blood pressure.
This in turn is partly related to the effort by the body to raise blood sugar levels when low. We’ve already discussed this, as well.
These problems may or may not be caused by being overmedicated.
Anxiety, tachycardia (fast heart rate), and high blood pressure that people with Hashimoto’s experience is not always from being hyperthyroid or overmedicated, it may also be from noradrenaline that the body is secreting for energy to compensate for the lack of thyroid hormone.
Unfortunately, what often happens is that they’re prescribed blood pressure medications (such as beta blockers) and/or anti-anxiety medications (such as benzodiazepines).
Neither of these drugs corrects the underlying functional hypothyroidism (low thyroid condition) that caused the symptoms in the first place, and both have side effects. In one study, noradrenaline was three times higher in hypothyroid subjects than normal controls when lying down.
So what was once low blood pressure, now takes a nasty turn towards hypertension, or high blood pressure.
Another….you guessed it, vicious cycle.
Obviously, too high blood pressure can be dangerous. It means that there is too much stress on your blood vessels. This makes the vessels weak and can damage them. Imagine squeezing a ketchup bottle really hard and fast until it breaks.
High blood pressure is a major cause of heart disease.
Ok, so let’s take a look at how else the thyroid impacts cardiovascular function. Firstly, thyroid hormone has a direct impact on cholesterol; with hypothyroidism serum cholesterol increases.
Thyroid hormone stimulates an enzyme called HMG-CoA reductase, the same enzyme that statin drugs inhibit. This speeds up the synthesis and utilization of cholesterol by the body.
Thyroid hormone stimulates the removal of cholesterol by the liver using LDL receptors. In a hypothyroid state, this whole process is slowed and the result is that cholesterol builds up and isn’t cleared as quickly.
Hypothryoidism can also cause homocysteine levels to rise. High homocysteine can lead to inflammation of the arteries and can make you more prone to blood clots, heart attacks and strokes.
We talked about that in the last chapter too, because nourishing certain pathways in the liver can really help bring down high homocysteine.
CRP, another risk factor and inflammatory marker for inflammation in the arteries is also often high with hypothyroidism.
Another odd thing that too little thyroid hormone can cause is lower plasma volume. This is caused by capillaries becoming more permeable and when this happens albumin and water leak into the interstitial spaces.
So here again, we have the makings of a particular dangerous vicious cycle.
In the chapter on the Earth Element, we spoke about how blood sugar problems like metabolic syndrome can create a lot of conditions that make you more likely to develop heart disease.
Well, when you combine that with hypothyroidism, you have a very potent combination that can put you at risk for heart attack and stroke.
Another area that does not get the attention it deserves is the impact of thyroid hormone on the heart and cardiac tissue. One of the things that research is starting to reveal is that thyroid hormone is absorbed differently by different tissues of the body.
In other words not every part of you body is affected the same way by T4 and T3. For example, the pituitary is different than every cell in the body with different deiodinase enzymes and it has more sensitive to thyroid hormone receptors.
Many physicans assume, incorrectly, that thyroid hormone is simply absorbed via diffusion (which is basically like the cell sucking hormone in through a biochemical straw).
However the reality is that the process is energy dependent and called active transport which means it requires the body to use energy to push it into the cells.
In addition, different parts of the body respond differently to T3 and T4. 90% of T3 is absorbed by the stomach while T4 is much less efficient (50 – 90%) and T4 requires much more energy to get absorbed.
T3 affects cardiac muscle cell (myocyte), it affects contraction, T3 also affects the performance of sodium, potassium and calcium channels in the heart.
And what this new study concluded was that “Higher FT4 levels are associated with an increased risk of SCD (sudden cardiac death), even in euthyroid (normal thyroid) participants.” This was an increased risk of 1% – 4%, so don’t panic, that’s not a huge increase.
What this means is that just throwing more thyroid hormone at the problem may not be the answer and can have unintended consequences.
And something else the research has identified is that thyroid autoimmunity can affect the valves of the heart. So, if you have Hashimoto’s and have been diagnosed with heart murmur, an echocardiogram might be a really good idea.
What this also tells us that this is way more than a thyroid problem and issues in other systems of the body must be treated, as well.
And where your heart is concerned it’s super important to take steps to reduce all the risk factors that contribute to cardiovascular disease. And sugar, inflammation and lack of exercise are the big three that put you at risk.
It’s all connected people!
Everything we do or don’t do has consequences. Properly managing and treating your thyroid may also heal your heart and properly managing and treating heart disease may also heal your thyroid.
Not sure what to do? Set up a consult and we’ll discuss how to create a heart healthy program for you.
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
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Slide from presentation by Dr. A. Vojdani on LDN
Hashimoto’s is the most common autoimmune disease of the thyroid and if affects millions of people globally. The most common treatment for this condition is synthetic T4 (usually Synthroid or a generic equivalent).
For many this treatment is ineffective and for some it only makes their symptoms worse. There are many reasons for this, but one of the important ones is that synthetic T4 does not sufficiently address the autoimmunity that is at the root of this disease.
In addition, unfortunately, many doctors ignore autoimmunity and pretend that it isn’t there. This is an abdication of responsibility and it can result in poor outcomes and poor clinical results.
And, unfortunately, it is the patients who suffer most from this approach. In this post, which is part of a new series, we will explore alternatives to just giving synthetic T4. One that shows promise with very few side effects is Low Dose Naltrexone, also known as LDN.
Naltrexone is a drug that was originally approved in the 1980’s as a treatment for opiate and alcohol addiction. The drug is an opiate antagonist and it blocks opiate receptors on cells. So it blocks the effects of legal and illegal opiates like morphine, codeine, oxycontin and heroin and opium.
With alcohol, it acts to block endogenous opiates which are opiates our bodies naturally produce. These include endorphins, enkephalin and other hormones we produce naturally.
When these natural opiates are blocked, there are more of them in the system and it can result in less craving and consumption of alcohol by alcoholics.
It is also this effect of blocking our natural opiates that also may provide benefit by calming and modulating the immune system in autoimmunity.
Naltrexone was approved in 1984 by the FDA in a 50 mg dose as a treatment for heroin addiction. When it was licensed, Dr. Bernard Bihari, then involved in running programs for treating addiction, tried it with more than 50 heroin addicts.
None of the patients stayed on the drug because of side effects experienced at the 50 mg dosage such as insomnia, depression, irritability and loss of feelings of pleasure, (all due to the effect of the drug at this dose in blocking endorphins which are involved in many of these activities and emotions).
Physicians treating heroin addicts with this approach got frustrated and many stopped prescribing naltrexone. Then, in the 1980s, a large number of heroin addicts began to get sick with AIDS (studies from that time have shown that about 50% of heroin addicts were HIV Positive).
Dr. Bihari and his colleagues decided to shift their research focus to AIDS, in particular studying ways of strengthening the immune system. Since endorphins are involved in supporting and regulating the immune system, levels of endorphins were measured in the blood of AIDS patients. They were found to average only 25% of normal.
Naltrexone became the focus of Dr. Bihari’s research group because they observed that when given to mice and people at high doses, the body raises endorphin levels to compensate for the naltrexone blockade.
The group discovered that endorphins are almost all produced in the middle of the night, between 2 AM and 4 AM, and the studies focused on small doses (1.5-4.5 mg at bedtime) with the hope that a brief period of endorphin blockade before 2 AM might induce an increase in the body’s endorphin production.
In fact, it was discovered that the drug was able to do this in this lower dosage range. It had no effect below 1.5 mg and too much endorphin blockade at doses over 5 mg. A placebo-controlled trial in AIDS patients showed a much better outcome in patients on the drug as compared with those on placebo.
By coincidence, during the research trial, a close friend of Dr. Bihari’s daughter had three acute episodes of multiple sclerosis over a nine-month period with complete spontaneous recovery from each.
Because of his knowledge of MS as a neurologist and of recent evidence that naltexone might have impact on autoimmunity, Dr. Bihari decided to start his daughter’s friend on the drug at 3 mg every night at bedtime.
She took it for five years with no further attacks. At that point, when her supply ran out, she stopped it because she thought she no longer had MS.
About a month later, she developed an episode of weakness, numbness, stiffness and spasms in her left arm ( all common symptoms of MS) and resumed LDN, which she then stayed on for 12 years. During that time she reportedly had no further disease activity.
The exact mechanism of how naltrexone works with immune related diseases is not fully understood. But here’s what we do know.
LDN Works in Several Ways:
A small dose of the drug taken nightly at bedtime increases endorphin levels in the body the following day.
Since endorphin levels are often low in people with autoimmunity, immune function is impaired and the normal immune regulatory function of CD4 cells is affected.
These cells include proteins in the TH-1, TH-2 and TH-17 families that can cause so much damage with autoimmune disease. These cells and proteins that are related to them are what create antibodies to our own tissue, signal attacks on that tissue and, ultimately lead to the destructive inflammatory process that destroys it.
If the T regulatory part of the immune system is weak, these other parts of the immune system can get out of control and cause more significant damage.
The anti-inflammatory effect of LDN has been studied and using it resulted in suppressed TNF-alpha, IL-6, MCP-1, and other inflammatory agents in peripheral macrophages.
It also has strong effect on calming glial cells and given the wide variety of inflammatory factors produced by activated microglia (e.g., proinflammatory cytokines, substance P, nitric oxide, and excitatory amino acids) this is also a significant effect of the treatment.
Opioid growth factor (OGF; [Met5]-enkephalin) is a natural peptide that has been shown to inhibit growth of certain cancer cells. LDN has shown promise in treating liver and pancreatic cancers.
LDN is an opioid receptor antagonist that acts at classical and non-classical opioid receptors including the opioid growth factor receptor (OGFr).
Animal models of type 1 and type 2 diabetes, as well as normal rodents, have shown that topical naltrexone enhances the healing rates of corneal epithelium and full-thickness cutaneous wounds. The mechanism of this general opioid antagonist on growth, and in particular the specific receptor pathway involved, is not understood.
Neuropeptides may play a role in irritable bowel syndrome and these molecules (e.g., enkephalins and endorphins) are present in the gastrointestinal tract and these modulate immune responses.
Upregulation of met-enkephelin (opioid growth factor-OGF) and opioid receptors can all be induced by low dose naltrexone.
LDN displaces endogenous endorphins bound to the OGF receptor. Affected cells become low in OGF which results in more receptors being made.
Receptor sensitivity is increased to capture more OGF and production of OGF is also increased to compensate for the perceived shortage of this molecule.
Higher levels of endogenous opioids and receptors inhibit cell proliferation which suppresses B and T lymphocyte responses. Naltrexone has been shown to reverse a mouse colitis model by decreasing the pro-inflammatory interleukins 6 and 12.
LDN has been shown to stimulate certain parts of the immune system and suppress and down-regulate others. It has been shown to inhibit IL-17, a protein that is part of the TH-17 family. It can also down regulate IL-10 and TGF beta (Transforming Growth Factor beta).
What’s interesting to observe here is that not everyone has the same immune cell profiles and LDN may work better on those that have a profile that best fits the things that it enhances and suppresses.
(Note: If the part of your immune system that is causing problems is not suppressed but rather stimulated by LDN, then you might feel worse after taking it.
Once again, this is very complicated and not everyone with Hashimoto’s and autoimmunity has the same immune configuration. This may explain why some people do well with the drug and others seem not to.)
There is no real consensus on how this all works and considerable debate about how LDN does what it does.
One such question is whether or not immune cells have opiate receptors.
There is some debate in the scientific community about whether or not the effect of opioids on the immune system are due to the fact that immune cells have opiate receptors.
Researchers have not been able to find these receptors, yet there is no doubt that opiates have a powerful effect on immune cells. And there is ample evidence of the functional influence of opioids on these cells.
In fact, in many ways opiates behave like immune cells, themselves. They impact the production of immune cells by acting locally, and inside cells, they affect gene expression and these influences both depend on dosage and time.
One thing that’s also important to understand is that the endogenous opiates in our bodies do not behave the same as drugs like morphine, heroin and other exogenous opiates.
What’s also interesting is that immune cells themselves contain endogenous opiate proteins. They actually carry them to sites of inflammation.
Immune cells have been shown to contain numerous opioid peptides such as β-endorphin (END), met-enkephalin (ENK), and dynorphin-A (DYN), although the most common appears to be END.
These opioid-containing immune cells travel to inflamed tissues and once there, opioid peptide is released from the immune cells upon stimulation with corticotrophin-releasing factor (CRF), noradrenaline, and interleukin 1β (IL-1β), and then the immune cells return to the local lymph node depleted of this peptide.
Which means if you can increase the amount of these endogenous opiates (which LDN does) you have more of them available to be delivered.
It’s also interesting to note that research found that endogenous opiates can raise TSH.
So if you can follow the logic of this, systemic immunosuppression (which is the standard approach used to treat autoimmune diseases) may affect the body’s ability to regulate immune cells that are important for the release of endogenous opioid peptides within inflamed tissue.
To further complicate matter it is know that exogenous opioids may impair immune cell function, something not shared by endogenous opioid peptides.
This means that giving pain relieving medication that are opiates may also impair immune system function.
So if you have autoimmune disease and you are using immunosuppresant therapy and opiates for pain relief, you are setting yourself up for failure and may be making the disease progression worse and more severe.
Another really interesting thing that the research reveals is the role of glial cells in the brain and central nervous system on opioids.
This research has shown that these cells can become activated and they can make the opioids not work as well.
This happens via numerous mechanisms, including directly affecting receptors, upregulation of excitatory amino acid receptor function, downregulation of GABA receptor function, etc.
The downstream effects of glial activation result in increased pain, suppressed acute opioid pain relief, increased tolerance, and the development of opioid dependence.
Conditions such as fibromyalgia may involve chronic glial cell activation and subsequent production of pro-inflammatory factors.
And Hashimoto’s and fibromyalgia have many symptoms that are identical. See this post I wrote on this.
In addition, it is widely known that T3 has important and dramatic effects on the microglia and hypothyroidism, “functional hypothyroidism” and “low T3 syndrome” can all result in glial cell activation, making all of this worse.
One theory is that LDN, itself, is a glial cell modulator. It may calm theses glial cells and prevent them from exerting the damage that they do.
What’s also really interesting is that CBD (Cannabanoid) has also been found to calm glial cells. I’ll be exploring this more in an upcoming post.
Naltrexone taken at low doses has virtually no side effects. According to lowdosenaltrexone.org, occasionally, during the first week’s use of LDN, patients may complain of some difficulty sleeping.
This rarely persists after the first week. Should it do so, dosage can be reduced from 4.5mg to 3mg nightly.
LDN Will Interfere With Narcotic Medication
Because LDN blocks opioid receptors throughout the body for three or four hours, people using narcotic medication — such as Ultram (tramadol), morphine, Percocet, Duragesic patch or codeine-containing medication — should not take LDN until such medicine is completely out of one’s system.
Patients who have become dependent on daily use of narcotic-containing pain medication may require 10 days to 2 weeks of slowly weaning off of such drugs entirely (while first substituting full doses of non-narcotic pain medications) before being able to begin LDN safely.
LDN May Impact Thyroid Hormone Dosage
Patients who are taking thyroid replacement hormone for Hashimoto’s with hypothyroidism ought to begin LDN at the lowest range (1.5mg for an adult).
Be aware that LDN may lead to a prompt decrease in the autoimmune disorder (and less inflammation within the thyroid and the rest of the body), which then may require a reduction in the dose of medication in order to avoid symptoms of hyperthyroidism.
LDN Should Not Be Taken With Immunosuppresant Medication
People who have received organ transplants and who therefore are taking immunosuppressive medication on a permanent basis are cautioned against the use of LDN because it may act to counter the effect of those medications.
The same is also true for people who have been prescribed immunosuppresant medications. As we learned above, the long term consequences of this medication may be increased severity and progression of the disease.
There are several important takeaways from this post:
1. LDN is safe and has few side effects
2. Dosage really matters, less is absolutely more!
3. There is ample evidence that it can be beneficial in calming the immune system in autoimmunity, though how it works is not yet fully understood.
There is evidence that it calms TH-1, TH-17 and other cytokines and that it can help calm glial cells in the brain and CNS (Central Nervous System).
3. It is not the magic bullet. If you don’t have an immune system profile that fits the way LDN works in your body, it may not work for you as effectively as it does for others.
And you can’t take it and ignore all the other things we must do to heal Hashimotos such as:
Healing your brain, and calming glial cells, healing your adrenals, healing your gut and doing all of the other things we advocate.
But LDN may be a good option and could give you the upper hand in dealing with immune system dysfunction.
http://www.ldnresearchtrust.org
http://www.lowdosenaltrexone.org/ldn_and_ai.htm
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC95944/ Opiates receptors on immune cells
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3962576/ LDN and pain treatment
http://www.ncbi.nlm.nih.gov/pubmed/22850250 TLR4 Receptors
http://www.ncbi.nlm.nih.gov/pubmed/22826216 TLR4 Receptors promote autoimmunity
http://www.ncbi.nlm.nih.gov/pubmed/23188075 LDN for Crohn’s disease in children (safety)
http://www.ncbi.nlm.nih.gov/pubmed/17222320 LDN improves Crohn’s disease
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1857294/ Glial cells as “bad guys” opioids and glial cell modulation
Endogenous opioids and immune modulation
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1661636/ Endogenous opioid analgesia
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3912755/ Mu opiod receptor
http://www.scielo.br/scielo.php?pid=S0034-70942012000500010&script=sci_arttext&tlng=en Opioids and the Immune system
http://bja.oxfordjournals.org/content/111/1/80/T1.expansion.html Table of impact of endogenous opioids on the immune system. ENDOGENOUS OPIATES INCREASE TSH!
http://bja.oxfordjournals.org/content/111/1/80.full Opioids and immune modulation
http://www.nature.com/icb/journal/v78/n5/full/icb200077a.html Effect of neuropeptides on the immune system
http://www.ncbi.nlm.nih.gov/pubmed/9610674 Opioid cytokine connection
http://www.jimmunol.org/content/186/9/5078.full.pdf Relationship of T cells and pain relief
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4407783/ Endogenous opioids inhibit TH-1 and TH-2
http://link.springer.com/article/10.1007/s12026-008-8018-0 Microglial Cells and Parkinson’s
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1661636/ Endogenous opioid analgesia
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2096733/ Endogenous neurotransmitters function as retrograde inhibitory neurotransmitters
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4452882/ T3 and microglia
http://www.ldnscience.org/opioid-growth-factor-ogf/51-ogf/ogf-explanatory
Like most health conditions, Hashimoto’s has no single cause.
It is the result of the perfect storm of factors that include a genetic predisposition, exposure to some pathogen (often a herpes virus), the breakdown of the gut and barrier systems (without or without the help of gluten), exposure to gluten, environmental toxins like radiation, mercury and other toxic chemicals and often, some particularly stressful event.
In this post we explore one of those causes, the herpes virus.
As many of you know, I have Hashimoto’s and have made it my life’s work to understand everything I can about the causes, treatment and management of this disease.
I also have herpes simplex 1 (along with 90% of the population). While this is not a life threatening disease it can be the cause of shame and embarrassment, especially when I get a more serious outbreak on my face or lips.
As a health care practitioner, there are times when having an outbreak of herpes has made me feel like I’m not very good at my job because it can look much worse than it is.
But the reality is that there are few other biological entities as resilient and unstoppable as the herpes virus. All the technology at our disposal is pretty useless when it comes to trying to eradicate this infection.
And I suppose one blessing of having it is that I can not venture too far from the things I know I need to do to stay healthy. The virus will rear it’s ugly head and remind me to get back in line.
In addition, one thing I have observed in my own life is that an outbreak of herpes can also affect my Hashimoto’s, resulting in a debilitating double whammy that can affect me emotionally, physically and psychologically.
So I thought I would explore this in more depth, and look at the relationship between herpes and Hashimoto’s. You may be surprised by the information and the impact that these various herpes diseases can have.
There are 8 different herpes viruses known to infect human beings. These include herpes simplex 1 & 2, varicella zoster (which causes chicken pox) also known as herpes 3, Epstein Barr virus (herpes 4), Cytomegalovirus (herpes 5), Human Herpes Virus 6 & 7 and Human Herpes Virus 8 found in people with complications due to HIV.
While the whole herpes family is believed to be linked to autoimmune disease, there is more research into the link between herpes simplex 1 & 2, Epstein Barr, and Cytomegalovirus and autoimmune thyroid disorders like Hashimoto’s.
The common factors that unite them is that all of them remain in the body forever, they can remain dormant for years and then get reawakened (often by stress or stressful events) and they all have the potential to do harm to the brain because the herpes virus has an affinity to nerve tissue.
Herpes simplex virus (HSV) infections are very common worldwide. HSV-1 is the main cause of herpes infections on the mouth and lips, including cold sores and fever blisters. It is transmitted orally (through kissing or sharing drinking glasses and utensils). HSV-1 can also cause genital herpes, although HSV-2 is the main cause of genital herpes.
HSV-2 is spread through sexual contact. You may be infected with HSV-1 or HSV-2 but not show any symptoms. Often symptoms are triggered by exposure to the sun, fever, menstruation, emotional stress, a weakened immune system, or an illness (like Hashimoto’s).
While most herpes infections do not cause serious complications, infections in infants and in people with weakened immune systems, or herpes infections that affect the eyes, can be life threatening. In addition, herpes virus attack nerves so they can do damage to the brain by attacking the ganglia.
In fact, Herpes simplex encephalitis (HSE) is an acute or subacute illness that causes both general and focal signs of cerebral dysfunction. Brain infection is thought to occur by means of direct neuronal transmission of the virus from a peripheral site to the brain via the trigeminal or olfactory nerve. The exact pathway is unclear, and factors that precipitate HSE are unknown.
Epstein-Barr is the virus that causes mononucleosis and is part of the herpes family. Even if you didn’t come down with it in high school or college, you were very likely infected with it, an estimated 95% of US adults have been infected with this virus.
It can present without any symptoms and has been linked to both Hashimoto’s and Graves’ disease. In my own patient population about 80% of the people I have worked have been diagnosed with EBV.
I surveyed our Facebook group and asked how many also had the Epstein Barr virus. Of the 131 (and counting) people with Hashimoto’s who responded 85% were aware that they had been exposed to the Epstein Barr virus.
This is obviously not a rigorous study, but it does show you just how prevalent this infection is in this patient population.
It has also been linked to other autoimmune diseases, such as Multiple Sclerosis, Lupus, and Sjogren’s syndrome. In addition, both fibromyalgia and chronic fatigue syndrome are also linked to EBV.
Epstein Barr can also lead to inflammation of the brain (viral encephalitis). This is a serious concern with Hashimoto’s because it can also have a profound impact on the brain and this inflammation has the potential to lead to neurodegeneration and cognitive decline.
Most people infected with CMV do not have any symptoms. Acute CMV infection can cause mono-like symptoms such as fever, enlarged lymph nodes, sore throat, muscle aches, loss of appetite and fatigue.
In people with compromised immune function, CMV infections can attack different organs and systems in the body and can lead to blurred vision and even blindness (CMV retinitis), lung infection, diarrhea, inflammation of the liver, inflammation of the brain (encephalitis). In more severe cases it can lead to behavioral changes, seizures and coma (again highlighting the impact of the virus on the brain).
It is not believed that the herpes viruses directly cause autoimmune disease. But they do play a part in it’s initial onset and progression and they can certainly make symptoms more intense and be a barrier to healing and feeling better.
There are many reasons for this and I will discuss them in a moment, but first let’s take a look at antigens and antibodies so that you can understand how these viruses cause problems in the body.
Antigens Trigger an Immune Response, Antibodies Bind to Antigens
An antigen is a substance that produces an immune response. So for example, foreign substances such as chemicals, bacteria, or viruses are all considered antigens. Foods can also be seen as antigens by the immune system.
However, an antigen can also be produced inside of the body, and even the tissue cells can be considered to be an antigen at times, which is what happens with autoimmune conditions such as Graves’ Disease and Hashimoto’s.
An antibody is a protein which is produced by the immune system, and this antibody binds to a specific antigen. Once the antibody binds to the antigen other immune system cells (i.e. macrophages) attempt to engulf and destroy the antigen.
There are number of theories about the different mechanisms that can lead viruses to trigger autoimmune disease. A couple examples are: direct bystander activation, and molecular mimicry.
Direct bystander activation: This describes an indirect or non-specific activation of autoimmune cells caused by the inflammatory environment present during infection. Think of this as being in the wrong place at the wrong time, just like being caught in a drive by shooting.
In this case, one part of the immune system becomes activated and this turns on other parts which can kill both viral-infected cells, and healthy cells as well.
So, for example, virus-specific T cells might migrate to the areas of a viral infection, and when these T cells encounter virus infected cells they sound the alarm and release immune proteins (called cytokines), which not only kill the infected cells, but also leads to “bystander killing” of other healthy cells nearby.
Molecular mimicry: This is a process where a foreign antigen shares an amino acid sequence or has a similar structure to self-antigens. So for example, a certain virus can have an amino acid sequence that is very similar to the amino acid sequence of human cells.
This can result not only in the production of antibodies against the virus, but can also lead to auto-antibodies against the human cells due to the similarities in the proteins.
Something else that can occur is that viral fragments can attach to human tissue and result in a hybrid that is part virus and part human and this can also be attacked by the immune system.
The mechanisms mentioned above really the end of a series of potential steps that lead to autoimmunity. There are some interesting theories about how this happens. This matters because if we can figure out how it is happening, it can help us figure out what how to treat it.
And what’s also interesting is that this same process takes place with all herpes viruses, it’s not unique to the ones that we’re looking at as examples.
It Starts with CD8+ T-cells
CD8+ T-cells are a kind of cell which inhibits viruses. Basically, once activated they kill bad cells.
Cells infected with the virus are used to make more virus.
Cells which viruses have infected are one example. These cells will be used by the virus to make more virus, so they must be killed by the immune system.
Having a deficiency of them is a common characteristic of virtually every chronic autoimmune disease (including: multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, Sjögren’s syndrome, systemic sclerosis, dermatomyositis, primary biliary cirrhosis, primary sclerosing cholangitis, ulcerative colitis, Crohn’s disease, psoriasis, vitiligo, bullous pemphigoid, alopecia areata, idiopathic dilated cardiomyopathy, type 1 diabetes mellitus, Graves’ disease, Hashimoto’s thyroiditis, myasthenia gravis, IgA nephropathy, membranous nephropathy, and pernicious anaemia).
Some scientists believe that this CD8+ T-cell deficiency may be partially responsible for the formation of these chronic autoimmune diseases, as well. And one reason is that they aren’t able to control the Epstein-Barr virus (EBV) or other herpes infection.
If EBV isn’t controlled, it can cause all kinds of problems in the body. When EBV infects B cells it can make them “auto-reactive”, which means its products (antibodies) target our own tissues.
According to a paper called “CD8+ T-Cell Deficiency, Epstein-Barr Virus Infection, Vitamin D Deficiency, and Steps to Autoimmunity: A Unifying Hypothesis” by Michael P. Pender, one theory is that autoimmunity occurs in the following steps:
1. First you have CD8+ T-cell deficiency – this has a genetic component.
2. Then, EBV (or other herpes virus) infection and spread of EBV because of CD8+ T-cell deficiency (there aren’t enough of these cells to kill these virus infected cells).
3. Increased antibodies against EBV (kind of like a second line of defense), your body responds and tries to bring in more help.
4. EBV infects a specific organ – and, particularly, B Cells in that organ. This corrupts the B cells to attack our own tissue. (One theory is that since viruses and bacteria have proteins similar to our own proteins, we mistakenly attack our own proteins. This confusion by our immune system is the ‘molecular mimicry’ I described above.)
5. B Cells proliferate in the infected organ (your antibody numbers increase)
6. T cells are drawn into the organ and also attack our tissue. Antibodies signal the attackers.
7. Development of ‘structures’ in the target organ, which causes B cells to attack our tissues. (This is dependent on Th17 cells ) This process repeats and builds on itself.
Some common factors that push autoimmunity are:
Low Vitamin D
High Estrogen
High Chronic Stress
Low Vitamin D
Vitamin D and sunlight are very important for CD8+ T cells production, which may explain why countries that get less sunlight have a higher occurrence of autoimmunity. People with Hashimoto’s commonly have low Vitamin D levels.
High Estrogen
Estrogen also decreases CD8+ T cells, which may explain the higher incidence of autoimmunity in females. Women with estrogen dominance and/or impairment of detoxification pathways in the liver may have too much circulating estrogen and this can cause problems with the immune system.
High Chronic Stress: High Cortisol/Low Pregnanolone
Chronic stress can cause reactivation of EBV, probably by downgrading the TH1 immune response. (TH1 are T helper cells that sound the alarm and also induce destruction. They are like the elite soldiers of the immune system.)
When you have chronic stress, your body keeps pumping out cortisol. Cortisol is made from cholesterol and a hormone that helps make cortisol is known as pregnenolone.
Pregnenolone is a neurosteroid and is important in the creation of other hormones like cortisol.
When your body is under constant stress (which is the state of living with an autoimmune disease like Hashimoto’s) and needs to keep producing more and more cortisol something called the “pregnenolone steal” can happen.
This is where cortisol is ‘stealing’ or diverting pregnenolone for cortisol production and depleting it. When pregnenolone is depleted, there will, of course, be less of it to produce more cortisol in the future.
Viruses Hijack the Mevalonate Pathway
When a viral infection becomes active it takes control over what’s known as the “mevalonate pathway.” Viruses use this pathway to make their protective outer coats.
In answer to this, your body makes interferon, which shuts down the mevalonate pathway, which in turn suppresses the virus. However, inhibiting this pathway may also lead to a reduction in synthesis of pregnenolone and Co-enzyme Q10 (which also may be depleted in Hashimoto’s).
One of the most common viruses that causes this pathway to be inhibited is Epstein-Barr Virus (EBV).
There’s also another problem.
When you’re under high stress the body releases cortisol, which suppresses your immune system.
Specifically, the TH1 (or T Helper 1) part of the immune system is suppressed by chronic stress. This aspect of the immune system (Th1) protects us from viral reactivation. Cells and proteins in this family sound the alarm and kill viruses.
When this part of the immune system is suppressed, viral infections can then reactivate- including EBV, herpes and a host of other viruses.
What’s really interesting about this is that Hashimoto’s was originally thought to be a TH-1 dominant disease and some people with Hashimoto’s do have TH-1 dominance.
And here’s where it gets tricky. If you stimulate TH-1, then you may risk firing up the part of the immune system that is destroying your thyroid. So this requires some real skill in dealing with with both Hashimoto’s and EBV or other herpes viruses at the same time.
There are some other things that EBV can cause problems with and these are really significant because they are also common problems with Hashimoto’s.
EBV can cause problems with serotonin, methylation, and can compromise the blood brain barrier and, as we have already seen, lead to neurodegeneration.
This is really interesting because with Hashimoto’s and hypothyroidism, serotonin can also become depleted. This one of the reasons why some people with Hashimoto’s experience depression and a lack of motivation and enjoyment in things. So the combination of Hashimoto’s and EBV can lead to some serious emotional issues.
Methylation issues are also quite common with Hashimoto’s and some people have MTHFR gene mutations which can exacerbate this problem. In addition, dominance of the TH1 part of the immune system can lead to methylation problems, as well.
And, finally leaky gut and intestinal permeability are the hallmark of virtually all autoimmune diseases and this is sometimes the sign of a larger systemic problem involving all the barrier systems of the body.
The gut and the brain are very closely related and the same proteins that protect the barrier of the intestines also line the blood brain barrier. When one area is compromised the other can be as well.
So, the combination of EBV and Hashimoto’s certainly has all the ingredients of a potent vicious cycle that can create a downward spiral of difficult to resolve physical and psychological health problems.
Treating both EBV (and other herpes viruses) and Hashimoto’s at the same time can be tricky because herbs and supplements that are known to prevent reactivation of the virus can also stimulate parts of the immune system.
And if these parts of the immune system are causing tissue destruction and flare ups of your symptoms, then you are simply trading problems. And this approach may actually make matters worse.
So, let’s take a look at some obvious and less obvious treatment strategies that can keep EBV or other viruses at bay and not stoke the fires of autoimmunity.
One of the most important treatments for EBV (and other herpes viruses) is having stress relieving hobbies. Many people are aware of the destructive power of stress, but it always amazes me how little they are willing to do about it.
If you have Hashimoto’s and EBV and you don’t do things to reduce stress daily, you are setting yourself up for failure. It’s like walking into oncoming traffic and expecting not to be hit by a car or truck. You are going to be in a world of hurt if you don’t have daily habits for reducing stress.
These include meditation, yoga, qi gong, music, art, relaxation, massage, acupuncture, spa days, mineral baths, etc. These are not luxuries, they are necessities for someone living with Hashimoto’s and EBV.
I’m giving you permission to indulge yourself. If you need a note from your doctor for this, email me and I’ll be happy to write one for you. 🙂
Another thing to be conscious of are foods and supplements that can feed and encourage the herpes virus. The most common are foods that are low in lysine and high in arginine.
These include:
• chocolate
• coconut (coconut oil is fine since it has no amino acids)
• seeds and nuts
• orange juice
• wheat products and products containing gluten
• oats
• lentils
• protein supplements: casein, the protein found in milk may also increase arginine levels.
• gelatin
What’s interesting to note here is that some of these foods are foods we commonly avoid with Hashimoto’s while others are staples of the Paleo and Autoimmune Paleo diets. (This emphasizes the importance of being flexible and of the highly individualized nature of the problem.)
Highly acidic foods and those laden with chemicals can also exacerbate viral infections and lead to outbreaks.
• alcohol
• caffeine
• all junk food
• too much red meat
• processed/white flour products
• food additives
• artificial sweeteners.
These are all also foods that can exacerbate your Hashimoto’s. So there’s no love lost here. Caffeine can potentiate or increase the utilization of arginine so that should be done in moderation.
There are several different strategies for treating EBV and other herpes viruses. Novice herbalists will often throw lots of immune stimulating herbs at the problem like astragalus, ashwaganda and medicinal mushrooms like maitake and reishi.
These are great herbs, but can be a really bad idea for some people with autoimmune disease.
Instead a more targeted approach of attacking the virus and strengthening different parts of the immune system with a more nuanced approach is a much, much better idea. The Chinese Herbal Materia Medica is full of herbs that can accomplish these tasks beautifully.
Here are some herbs that specifically attack EBV and other herpes viruses:
Anti-EBV Herbs:
Angelica sinensis, chrysanthemum, citrus, lithosperum, milletia, paedria, picrorhiza
Anti-Cytomegalovirus:
Isatis root, baphicacanthes, cnidium, lithosperum, forsythia, gardenia, chrysanthemum, vitex, dandelion, epimedium, lonicera
Anti-Herpes Herbs:
Belamcanda, clove, crataegous, dandelion, epimedium, houttuynia, inula, lonicera, portulaca, prunella, rhubarb, salvia, scrophularia
It’s important to note that many of these herbs have multiple pharmacological properties and can therefore be used to accomplish more than one thing if combined properly.
It’s important to strengthen the immune system to treat these herpes viruses, as well, but it must be done carefully.
As we saw before, Vitamin D is important for strengthening CD8+ T cells, as is glutathione and superoxide dismutase, EPA and DHA.
Turmeric is helpful because of it’s anti-inflammatory properties.
Also, there are couple of essential oils that I have found are very effective for first attacking the virus and, then healing the sores.
Ravensara is an excellent anti-viral oil that may applied topically directly on the lesions. Heliochrysum is an oil that helps regenerate flesh and can help to heal the sores more quickly.
My partner, Olesia Farberov makes a fantastic herbal salve with some of Chinese herbs mentioned above and both these essential oils called The Healer.
The Healer, made with anti-herpes herbs and essential oils
This is an absolute must for your purse, pocket and medicine cabinet. I prescribe it to all of my patients with herpes and use it myself because it just plain works.
Vitamins, Minerals and Supplements:
Research has shown that a daily intake of at least 1250 mg of lysine supplements can help control herpes outbreaks.
Zinc, Vitamin C and B vitamins may also be helpful.
Other supplements that can help increase CB8+ cells include:
N-Acetyl-Cysteine (NAC), butyrate, andrographis, and gynostemma
Western Medication
One area where I actually advocate using Western pharmaceutical drugs is in the treatment of these viruses. Acyclovir is a potent anti-viral and for some people who have really stubborn hard to treat outbreaks, it can be an effective tool in your arsenal.
Another drug to consider is Low Dose Naltrexone (LDN). It has the ability to modulate immune function and calm physiological stress. It can also be effective in helping the body to deal with the herpes virus.
At the end of the day, the reality is that these viruses are here to stay. They are remarkably adaptable and persistent and they have there own insidious intelligence.
We can not hope to defeat them, we have to accept them, live with them and adapt our lives to them. And the good news is, the most effective treatments for them like stress relieving hobbies and a healthy diet are also important ingredients in our long term health, happiness and well being.
Notes from Studying with Dr. M.M. Van Benschoten, O.M.D.
http://www.ncbi.nlm.nih.gov/pubmed/24008857: herpes and Hashimoto’s 3 case studies
http://www.hindawi.com/journals/tswj/2013/867389/: Role of herpes 6 as a trigger for autoimmune thyroid disease
http://jidc.org/index.php/journal/article/viewFile/22169789/645: Role of viruses in Autoimmune disease
http://www.virologyj.com/content/6/1/5: Viruses and thyroiditis
http://www.dana.org/Media/GrantsDetails.aspx?id=38800: herpes and MS
https://umm.edu/health/medical/altmed/condition/herpes-simplex-virus: good general info on herpes
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2654877/ : Viruses and thyroiditis
http://www.cellandbioscience.com/content/1/1/24 Affects of thyroid hormone on HSV-1 gene regulation
http://dx.doi.org/10.4236/health.2013.58162 Large cohort on TH levels and HSV 1 activation
EBV and Hashimoto’s
http://www.ncbi.nlm.nih.gov/pubmed/8750577: Elevated Epstein Barr titers in AIT
http://www.ncbi.nlm.nih.gov/pubmed/20404456: Immune responses to EBV in AITD patients
http://www.bioline.org.br/request?mb10037: EBV activation in AID patients
http://www.hindawi.com/journals/ad/2012/189096/: Hypothesis of how this all happens
http://www.ncbi.nlm.nih.gov/pubmed/16055563 Serotonin and EBV
http://www.ncbi.nlm.nih.gov/pubmed/21289059 EBV and methylation
http://www.ncbi.nlm.nih.gov/pubmed/20826008 EBV and the blood brain barrier
Infections and Autoimmune disease:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2665673/ role of infections in AID
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1360274/ Molecular mimicry
http://www.direct-ms.org/sites/default/files/FujinamivirusMS.pdf
http://medicalxpress.com/news/2014-10-scientists-link-viral-infection-autoimmune.html
http://www.ncbi.nlm.nih.gov/pubmed/12699597 T3 autoantibodies can cause latent EBV activation!
Molecular mimicry
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3266166/
Neurological impact of herpes:
http://www.nature.com/nrneurol/journal/v3/n2/full/ncpneuro0401.html Neurological impact of herpes
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3437531/ Herpes infections in the CNS
http://www.herpes.org/whitepaper-the-psychological-effects-of-herpes/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4175921/ Anxiety and depression and viral disease
http://medind.nic.in/daa/t12/i1/daat12i1p188.pdf Viral infections and depression
http://www.naturalendocrinesolutions.com/articles/which-viruses-can-trigger-thyroid-autoimmunity/ Good descriptions and solutions
http://www.ncbi.nlm.nih.gov/pubmed/11572634 virus induced autoimmunity
http://www.ncbi.nlm.nih.gov/pubmed/22095454 molecular mimicry as autoimmune intitiation
http://www.ncbi.nlm.nih.gov/pubmed/25445494 B cell epitope spreading
http://www.ncbi.nlm.nih.gov/pubmed/11140461 Epitope spreading
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1360274/ Bystander activation
http://justherpes.com/facts/foods-to-avoid-with-herpes-diet/ Herpes food