Hey, people!
I’ve been getting a boat load of questions about the Covid-19 vaccines. As with all things Covid related, unfortunately, there seems to be lots of bogus misinformation.
I have created this post to look at the actual facts regarding the vaccines produced by Pfizer and Moderna.
It’s been really interesting to watch how many practitioners and thought leaders in the alternative medicine realm and others in the “New Age” community have aligned themselves with conspiracy theories and outright nonsense regarding the pandemic.
The very same things that are being pushed by the alt-right. It’s an odd and dangerous marriage of right and left wing “conspirituality” that has resulted, in my opinion, in the US becoming the epicenter of an out of control pandemic.
It didn’t have to be this way. What we are living through now is the consequences of this irresponsible, self serving behavior. And while there is reason for optimism, the truth is it’s not going to be over for any time soon.
If you’re looking for someone to pander to the legions of anti-mask and anti-vaccine conspiracy theorists, I’m not your man.
I’m frankly disgusted by some of my colleagues who have irresponsibly pushed conspiracy theories and made simple methods of prevention like mask wearing and social distancing into some sort of political game.
Of course, there are many important things we can do to keep ourselves healthy and less likely to get seriously ill such as take Vitamin D and zinc, and other herbs and essential oils. (I have written about these in the past.)
We should all also let this be a wake up call about the importance of good diet and exercise and how vulnerable we are when we have pre-existing conditions. That’s just common sense. As is taking simple precautions like wearing a mask, social distancing and washing hands.
I think conspiracy mongering is nothing but a form of narcissism and it should be called out as such. Here’s a good article that looks at this in depth and really does a good job of calling out this dangerous phenomenon.
As of writing this the death toll in the US is 626,713. Covid-19 is not a hoax or a grand plot to control humanity. It’s a deadly, novel virus that is lethal for some and, unfortunately, we don’t yet know enough about it to know why. So, that means anyone can be at risk of dying or of having long term effects from the virus.
The focus of this piece is to look at the pros and cons of the COVID-19 vaccines that are currently being made available via the emergency use authorization from the FDA. There are two vaccines that have been authorized at this time, one made by Pfizer and one made by Moderna.
Both are mRNA vaccines. What does this mean?
mRNA technology was discovered 30 years ago. And it has been studied for vaccine purposes for nearly two decades. Scientists were working on vaccines for both SARS and MERS, but funding was cut and they didn’t develop them until recently, when due to the pandemic we had a great deal more urgency and money to help develop these more quickly.
Clinical trials for mRNA vaccines have been conducted for influenza, Zika, rabies, and cytomegalovirus (CMV). Advances in technology in RNA biology and chemistry as with delivery systems has improved the stability, safety and effectiveness of these vaccines.
RNA and DNA are not the same. Without getting too far into the weeds, let’s say they are both some of the most important molecules for cell biology and they are used to store and share information about every cell, organ and tissue in the body.
DNA encodes the information, RNA is the reader that decodes that information. (Here’s an in-depth look at this:)
That being said, RNA vaccine development is relatively new and we just do not have much data on the long term effects of this technology. And the reality is that we won’t for some time. We are all living through a large global experiment right now involving COVID-19 and treatment and prevention strategies for it.
One concern that many people have is in the ingredients of what’s in the vaccines. This is also an area of misinformation and outright lies. Both manufacturers of these vaccines have been transparent about what is in them.
These vaccines do not use the live virus that causes COVID-19. They also do not interact with our DNA. These vaccines work by providing instructions to our immune cells by introducing fragments of the spike protein which is found on the surface of the virus (that’s what the virus uses to enter our cells).
The vaccines also do not contain fetal stem cells. Some of the vaccines being studied in clinical trials used cells originally isolated from fetal tissue. These come from historical cells lines that were derived in the 1970’s and 1980’s from two elective abortions.
The fetal cell lines that were used to produce some of the potential COVID-19 vaccines are from two sources:
HEK-293 A kidney cell line that was isolated in 1972
Per.C6 A retinal cell line that was isolated in 1985
The mRNA COVID-19 vaccines produced by Pfizer and Moderna do not require the use of fetal cell cultures in order to manufacture the vaccine.
Early in the development of these vaccines they were used for “proof of concept” to show how a cell could take up mRNA and produce the COVID spike protein or to characterize the spike protein.
In fact, both vaccines have been deemed ethically uncontroversial by pro-life policy organizations like The Charlotte Lozier Institute and the Catholic Health Association of the United States.
The vaccine is injected into the muscle in the upper arm. Once in the muscle cell the cells follow the instructions from the mRNA fragment and make a piece of protein. After this is made the cells break break down these instructions and destroy them.
Next, the cell displays this protein piece on it’s surface. Our immune system recognizes this protein as something foreign and it makes antibodies against it. The development of these antibodies by our immune system gives us protection against future infection.
The obvious benefit of doing this versus actually getting COVID-19 is that you gain protection without having to go through the potentially dangerous consequences of getting the virus. However, we do not yet know how long this protection lasts.
In addition, there has been some research done by Dr. Kharrazian and Dr. Vojdani on cross-reactivity of the spike protein to some of our own tissues and this is an area of potential concern.
This may have implications for the development of autoimmune disease, but we just don’t know yet. It’s not clear whether the fragments used in the vaccines are proteins that cross react, not all of them do.
Another area of misinformation is the ingredients. There is no formaldehyde, no aluminum, and no mercury. These are sometimes used in other vaccines, they are not used in these.
When the Pfizer COVID-19 vaccine was granted an EUA from the FDA, its ingredients list was published online along with other safety data. The list includes:
What are the Moderna COVID-19 vaccine ingredients?
Moderna has also been given emergency use authorization for their vaccine. Moderna also recently released its ingredients list through the FDA:
OTHER FACTS
| Pfizer | Moderna |
| 95% effective 30 mcg doses given 21 days apart Must be diluted with 0.9% sodium chloride Must be stored at -112 to -76 degrees F 36,621 people took part in the clinical trial Approved for age 16 and over Published safety and final efficacy results from Phase 3 on 12/10/20 | 94.5% effective 100 mcg doses given 28 days apart No dilution required Stored at -13 to -5 degrees F 30,350 people took part in clinical trial Approved for age 18 and over Announced primary efficacy analysis on Phase 3 on 11/30/20 |
One concern that many people have is whether or not this vaccine is safe for people with autoimmunity and in our case, thyroid autoimmunity.
The CDC guidelines on this are pretty vague:
“People with autoimmune conditions may receive an mRNA vaccine. However, they should be aware that no data are currently available on the safety of mRNA COVID-19 vaccines for them. Individuals from this group were eligible for clinical trials.”
Not much help.
As I mentioned previously, Dr. Kharrazian and Dr. Vojdani’s research into cross reactivity of the COVID-19 spike protein and some of our tissues revealed that some (not all of the) proteins are cross reactive to human tissue. This has implications for the development of autoimmunity from the virus.
But, I could not find data on whether or not these proteins are the proteins used in the mRNA vaccines.
Something else that has been studied is the impact of COVID-19 on the thyroid.
There is evidence that COVID-19 may result in post-infection thyroid disease. Sub-acute thyroiditis is a common finding.
This is pretty common for any virus that affects the upper respiratory system. Epstein Barr can also do this as can the flu, the mumps and other viral infections.
There is also some evidence of that thyroid disease is associated with severe COVID-19 infections.
Pre-existing hypothyroidism is not associated with increased hospitalization or ventilator use in patients with COVID-19. One study looked at 3703 COVID-19 patients (251 had pre-existing hypothyroidism, 22 had Hashimoto’s. 68% of the COVID-19 positive patients with hypothyroidism needed hospitalization. But apparently, this is not higher than other groups.
At the end of the day, there are potential consequences to the thyroid if you contract COVID-19. And while I have not seen any evidence that people with Hashimoto’s are more vulnerable to COVID, getting it may complicate the disease. How much? We still don’t know.
We do not have a lot of data on people with Hashimoto’s who got the vaccine. As you know we have a wonderful and supportive community online and I was able to survey my Facebook (51,000) and Instagram (14,000) followers and I got responses from 23 people with Hashimoto’s, all mostly frontline workers who got the vaccine.
All but two got the the first shot of the Pfizer vaccine. Of that group, none reported any severe reactions. 6 reported some soreness in the arm around the injection site which went away in a day or two. Two others reported fatigue and body aches.
Everyone else reported no reaction at all that they were aware of. None have gotten the second dose of the vaccine yet. I will be following up and asking them about this.
Whenever making a decision of this magnitude, we have to look at risk and benefit. I am not for or opposed to the vaccine. But I am opposed to misinformation and lies.
Here’s what we know:
Covid can be fatal and can cause long term damage to many parts of the body ( the lungs, the cardiovascular system, the brain and nervous system and the thyroid and more).
We don’t know who it will be fatal for, but it kills more men, and those with pre-existing conditions and people of color.
Also, the pandemic’s economic and social destruction will not end until we have some type of herd immunity. This can happen if enough people get sick (and lots, lots more will die) or we get vaccinated to such a degree as a society that the virus peters out.
Some combination of that will probably occur over the next year. The vaccine is an important part of achieving that (and ultimately saving lives).
These mRNA vaccines do not contain mercury, formaldehyde, or aluminum. Nor are fetal stem cells used to manufacture the vaccine.
So far, from the small sample size we have, there were few side effects. We don’t know about the long term effects of the vaccine, but we do know about the long term effects of COVID-19.
Vaccines have also worked historically for other diseases.
I hope this was helpful and that it can be used to help you make a better, more well informed decision about whether or not to get the vaccine.
I intend to get it as soon as I am able.
Sincerely, Marc
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
With Hashimoto’s, sometimes the things that cause the most problems are the things we are most attached to. Dairy certainly falls into this category.
In this post we’ll look at the potential problems caused by dairy and Hashimoto’s. And, yes, that may include cheese and ice cream.
There are 2 distinctly different problems that can be caused by dairy consumption. The first is caused by milk proteins, the second is caused by milk sugars.
Let’s take a look at both.
Milk Proteins Have A Similar Structure to Gluten
Unless you’ve been living under a rock, you’ve probably heard about the benefits of going gluten free for people with Hashimoto’s. If this is a new concept to you, check out my previous post on this here.
Well, milk based products have a host of proteins that also can and do cause immune reactions. These include casein (alpha & beta), casomorphin (a protein that closely resembles morphine), milk butyrophilin, and whey.
These proteins are known as “cross-reactors” because they closely resemble gluten proteins and can cause a similar immune response in the body.
In a lot of cases these are undiagnosed and people continue to eat these foods and/or are advised to eat these foods and they end up hurting themselves by damaging their intestines and robbing themselves of important nutrients.
There are different parts of the immune system that react to these foods; IgE, IgA and IgG reactions.
Food allergies are mediated by the IgE part of the immune system. These generally casue an immediate reaction and are often what is called a “true allergy” by doctors and other medical professionals. However, this is not the only type of food reaction your body can have.
IgA and IgG systems can also lead to hypersensitivities. These are sometimes termed “food intolerance” or “food sensitivity.”
The important thing to understand is that they are much different in their mechanism and ability to wreak havoc in your body.
IgA Food Reactions
IgA food intolerance is the more severe reaction and happens mostly in the intestines. It is an abnormal response of the intestines to certain foods in genetically predisposed individuals. The intolerances may manifest themselves early in childhood, or later in life.
IgA food intolerance results in irritation and inflammation of the intestinal tract every time that particular food is consumed. This results in damage to the intestines, and eventually it hurts your ability to absorb nutrients, and can increase the risk of autoimmune diseases, cancer, and accelerate aging through increased intestinal permeability or leaky gut.
IgA food intolerances can also vary in their symptoms considerably. They may be asymptomatic, may be neurological or they may present with the following symptoms: diarrhea, loose stools, constipation, acid reflux, malabsorption of nutrients from foods, and increased intestinal permeability.
They can cause IBS, gas, nausea, skin rashes (including eczema), acne, respiratory conditions such as asthma, nasal congestion, headache, irritability, cognitive problems and vitamin/mineral deficiencies.
The most famous IgA food reaction is “celiac” disease, and it is an intolerance to gluten, the protein found in wheat. We have looked into how this impacts Hashimoto’s extensively. Check out our previous post here.
However, dairy protein, egg, and soy protein IgA intolerances are also extremely common in people with Hashimoto’s. These intolerances do not have a specific name, and may be confused with other, less severe food absorption syndromes.
IgG Food Reactions
These are antibodies that provide long-term resistance to infections, called Immunoglobulin G (IgG), and they have a much longer half-life than the traditional IgE allergy. These reactions can be much more subtle and people can live with them for years, if not their entire lives.
Symptoms, ranging from headache and nausea to seizure and hyperactivity, or simply just fatigue, bloating, mood changes brain fog, memory problems or dark circles under the eyes. They may occur hours or even days after the problem food has been ingested.
Food allergy tests like the ALCAT test, test both IgA and IgG reactions to foods. A positive or equivocal finding of IgG against foods may indicate that the person has been repeatedly exposed to food proteins recognized as foreign by the immune system.
This matters with thyroid autoimmunity because this process can fire up the very same parts of the immune system that are already attacking our own tissue. In fact, Antithyroglobulin antibodies (TgAb) and antithyroperoxidase antibodies (TPOAb), predominantly of the immunoglobulin (Ig) G class, are hallmarks of Hashimoto’s.
Researchers have recently discovered that there are 2 types of IgG proteins, IgG4-positive and IgG4-negative. Further studies are needed to determine exactly what the difference between them is. But this may have clinical and treatment ramifications.
The degree and severity of symptoms vary greatly because of the genetic makeup of the individual. The complete elimination of IgG positive foods may bring about important improvements in Hashimoto’s symptoms because this can be a key factor in calming autoimmunity.
Often people confuse the food immune reactions to dairy mentioned above and milk intolerance which is caused by milk sugars known as lactose.
One thing that people don’t always realize is that even tiny amounts of lactose can have a major impact on our ability to absorb thyroid medications. Worst of all, some thyroid medications actually contain lactose, defeating their own purpose!
Lactose Can Make Thyroid Hormone Not Work As Well
A recent study published in 2014 by Asik and colleagues found that lactose intolerant Hashimoto’s patients who were taking levothyroxine showed a decrease in TSH after lactose restriction.
In other words, removing lactose improved how their levothyroxine was working.
Another study from August 2014 had a similar finding. This was published in the Journal of Clinical Endocrinology and Metabolism by Cellini and colleagues and found that lactose intolerance increased the need for more thyroid medications.
The researchers found that the average person with Hashimoto’s required an average dose of 1.31 mcg/kg/day of levothyroxine to get to an average TSH right around 1 mU/L (that would be right around 75 mcg of levothyroxine for a 125 pound person), while a person with Hashimoto’s and lactose intolerance who continued to consume lactose needed a dose of 1.72 mcg/kg/day to reach the same goal (that would be like 100 mcg of levothyroxine for the same 125 pound person- that’s quite a bit more).
In addition, patients who had other gut disorders in addition to lactose intolerance required an even higher dose to get to their goal TSH 2.04 mcg/kg/day, or around 116 mcg for a 125 pound person. So you can see, the more gut related issues the higher the dose to achieve the same effect.
If your TSH levels are jumping up and down and you’re having a hard time controlling them, dairy protein immune responses and lactose intolerance should be top on your list of suspects.
Lactose intolerance rates in Caucasians have been reported to be between 7% to 20%, and much higher those in those of Asian and African descent. Lactose intolerance can be secondary to other conditions and reversible or it can be genetic and permanent.
A recent 2014 study by Asik and colleagues tested 83 Hashimoto’s patients for lactose intolerance and found lactose intolerance in 75.9% of the patients. I’d say that would qualify as pretty darn common!
38 of those patients were instructed to start a lactose free diet for 8 weeks, and the researchers found that over this time, the patients’ TSH dropped, meaning, they were absorbing their thyroid medication better.
For some lactose intolerant people, even tiny amounts of lactose that are found in thyroid medications can be an issue, causing impaired absorption of thyroid medications. Yes, what we’re saying is that thyroid medications could be undermining their own absorption if they contain even teeny amounts of lactose.
So if you are someone that can’t get his/her TSH into your “Goldilocks zone” – where it’s just right (there is much debate about where this is, but general consensus is that TSH should be somewhere between 0.5-2 mU/L for people to feel best) despite taking higher and higher doses of thyroid medications, consider lactose intolerance and the possibility that the lactose in your diet or even in your thyroid medication may be hindering its absorption.
And here’s the thing, the reality is you could have both lactose intolerance and be having an immune reaction to diary proteins. This is a potent and destructive double whammy for people with Hashimoto’s. Which, as you should know, is an autoimmune disease of the thyroid!
So dairy can potentially wind up autoimmune tissue destruction and prevent thyroid hormone from working. The result is a rapidly accelerating decline in thyroid function.
Some people will ask, “What about Lactaid?” They sometimes ask this because they can’t bear the idea of living without dairy products such as cheese and ice cream. And the logic makes sense to some degree. The problem is it doesn’t really solve the long term damage and potential problems.
It’s a little bit like an alcoholic taking the drug Antabuse and continuing to drink. The real problem is alcohol. And the real problem for some people is dairy.
As far as diet, I have seen tremendous improvements in my own health and the health of my clients and readers on a dairy free diet, so this is something that I strongly recommend for everyone with Hashimoto’s.
If you weren’t aware of it, here are some common medications that contain lactose as a filler and some that are lactose free.
· Synthroid
· Euthyrox
· WP Thyroid
· Nature-Throid
· Most generic brands of levothyroxine
· Some compounded medications- check with your pharmacist
· Tirosint
· Armour Thyroid
· Cytomel
· Levoxyl
· Some compounded medications may use lactose as a filler – check with your pharmacist
Of all of the T4 containing medications, Tirosint has the fewest fillers that may affect absorption, and this medication was designed for people with these types of intolerance. This medication is recommended if you suspect you may have problems with dairy and lactose.
Of course, some people do better with the addition of T3. Of all of the T4/T3 combination medications, WP Thyroid has the fewest fillers that can impair absorption. However, it does contain trace amounts of lactose, as well.
Armour thyroid does not contain lactose, but contains corn derived ingredients that can be problematic in corn sensitive individuals and can trigger a gluten like reaction.
When they changed their formulation a few years ago, some people did very poorly with the new mixture, and one of the reasons was this corn based filler.
Another really interesting research finding is that high TSH can simply be caused by absorption disorders like lactose intolerance, celiac disease, atrophic gastritis, H. Pylori infections, inflammatory bowel disease and/or parasites.
All of these issues commonly prevent people from getting their Hashimoto’s into remission, as well. These are more positive feedback loops and they cause vicious cycles that lead to poor results in different systems of the body.
This is a perfect example of how this is not just a thyroid problem. Thyroid hormone metabolism is dependent on other systems of the body.
A 2012 Polish study by Ruchala and colleagues reported that thyroid patients who need more that 2 mcg/kg/day of levothyroxine with an increased TSH should be suspected of having an absorption disorder like the ones mentioned above.
Get off of dairy 100%. Treat it the same way you treat gluten and understand that the misery it can cause if not worth the buzz of an ice cream cone or some cheese on crackers.
Also understand that having “just a little bit” is not really solving the problem at all. A tiny amount can be a tsunami to your immune system and can lead to a whole cascade of problems.
Being “sort of dairy free” is like being “sort of pregnant”. It’s not a real thing.
http://www.ncbi.nlm.nih.gov/pubmed/23992023 IgG proteins in Hashimoto’s
http://www.researchgate.net/publication/271022933_Thyroxine_softgel_capsule_in_patients_with_gastric-related_T4_malabsorption – The influence of lactose intolerance and other gastro-intestinal tract disorders on L-thyroxine absorption. Endokrynol Pol. 2012;63(4):318-23.
http://www.ncbi.nlm.nih.gov/pubmed/24078411 Asik, et al study
http://press.endocrine.org/action/doSearch?AllField=lactose+intolerance+and+thyroxine – Systematic appraisal of lactose intolerance as cause of increased need for oral thyroxine. J Clin Endocrinol Metab. 2014 Aug;99(8):E1454-8. doi: 10.1210/jc.2014-1217. Epub 2014 May 5. PMID: 24796930
http://www.ncbi.nlm.nih.gov/pubmed/17123345 Lactose intolerance revealed by severe resistance to treatment with levothyroxine. Thyroid. 2006 Nov;16(11):1171-3.
http://labeling.pfizer.com/ShowLabeling.aspx?id=688&mc_cid=3f79b51f37&mc_eid=c1f303f62b Levoxyl – Levoxyl
http://www.rxlist.com/tirosint-drug.htm – Tirosint
http://www.pdr.net/full-prescribing-information/wp-thyroid?druglabelid=3202 – WP Thyroid
Gliadin, a gluten protein
However, because of misinformation and the inconvenience of going gluten free, many people ignore these warnings or don’t think this really applies to them.
I have had a number of people write me and tell me during consultations that they need to see “peer reviewed studies” about gluten and Hashimoto’s before they are going to commit to going gluten free.
In this post we examine a boat load of research on this subject and we seek to demonstrate, once and for all, why eating gluten is not a luxury you and your thyroid (and lots of other important parts of your body – like your brain) can afford.
Celiac Disease is an Autoimmune Disorder
According to the Celiac Support Association “Celiac disease, also known as celiac sprue or gluten-sensitive enteropathy, is a genetically linked autoimmune disorder that can affect both children and adults…”
Yes, celiac disease is an autoimmune disease. It’s not just a food allergy or sensitivity.
What do we know about autoimmune disease?
When you have one, it’s easy to get others.
Like Hashimoto’s, for example.
To read more about this, check out my previous post that looks into this in depth.
“…In people with celiac disease, eating certain types of grain-based products sets off an immune mediated response that causes measurable damage to the small intestine.”
Another key point. I and many other specialists in this field believe that the small intestine is ground zero for autoimmune diseases of all kinds.
This damage to the small intestines has systemic consequences.
These include the immune system, the endocrine system, the nervous system and the brain. This is no small matter (pun intended).
“…This, in turn, interferes with the small intestine’s ability to absorb nutrients in food, leading to malnutrition and a variety of other complications.”
Yes, the other complications include an inability to convert and absorb thyroid hormone, major deficiencies in important vitamins and minerals like iodine, iron, selenium, magnesium and vitamins like B, D and plenty more.
Pretty much guaranteeing hypothyroidism and thyroid gland dysfunction.
“…The offending amino acid sequences are collectively called “gluten” and are found in wheat, barley, rye, and to a lesser extent, oats* (WBRO). Related proteins are found in triticale, spelt, and Kamut.”
Indeed, these “offending amino acid sequences” are not just found in these grains, they are found in many foods like dairy, soy, coffee, corn, potatoes, and lots more.
The reality is gluten may just be the tip of the iceberg and going gluten free may not be enough to effectively treat autoimmune disease.
Some people do not get better by only going gluten free. This is not because they don’t have a problem with gluten.
There are many other foods that have a similar amino acid sequence to gluten and these may also be a problem.
Because it is these amino acid sequences that the immune system attacks and that resemble our own tissues. (To learn more about this, check out this previous post).
Tissue transglutaminase is an enzyme that repairs damage in the body. People with celiac disease often make antibodies that attack this enzyme.
Well, studies have shown that people with transglutaminase and gliadin antibodies also have a much higher levels of TPO and TgAB antibodies.
Celiac Disease and autoimmune thyroid disorders share a common genetic link, namely, the DQ2 allele.
This is a subtype of a region of cells called the HLA (or Human Leucocyte Antigen) System.
There is a region on cells located on some of our genes called the HLA. Many of these are located on chromosome 6 (for those of you keeping count).
Mutations or defects of HLA have been linked to many different autoimmune diseases.
Exactly what happens is not known, there are numerous theories, but the end result is that our own tissue gets attacked and destroyed by the immune system.
With Celiac disease and autoimmune thyroid diseases we see an increase in both types of antibodies that lead to attack on these tissues.
Collin et al found 5.4% of 335 adult celiac patients, of whom 83% complied with a gluten-free diet, had autoimmune thyroid disease (autoimmune hypothyroidism or Graves’ disease).
Counsell et al found that 14% (15 out of 107) of celiac patients had thyroid disorders (3.7% hyperthyroid and 10.3% hypothyroid).
The same authors also noted a high prevalence of thyroglobulin antibodies (11%) and thyroid microsomal (TPO) antibodies (15%) in their CD patients.
Likewise, Velluzzi et al found the prevalence of thyroid peroxidase antibodies to be higher in CD (29.7%, 14 out of 47 patients) than in healthy controls (9.6%).
This is another area of misinformation. Most doctors test for 2-4 gluten antibodies.
Current testing for Gluten-Reactivity and Celiac disease (CD) includes serum IgG and IgA against gliadin and tissue transglutaminase-2 (tTG2).
These antibodies are measured against minor components of a wheat protein called alpha-gliadin.
Here’s the thing, wheat consists of multiple proteins and peptides including, alpha-gliadin, omega-gliadin, glutenin, gluteomorphin, prodynorphin, and agglutinins.
And there are many we still do not know about.
And the important thing to understand is that any of these antigens can cause an immune response.
So, even if you tested negative to celiac, you could still have gluten sensitivity or silent celiac disease because you may not have tested for the right thing.
This is a really interesting question that is controversial and no one really knows.
But, here’s what we do know.
Autoimmunity doesn’t just happen for no reason. It is the result of a perfect storm of factors.
You need the genetic predisposition (like the HLA DQ2 allele mentioned above), you need exposure to some antigen (Often Yersenia, Epstein Barr, Coxsackie, Lyme disease or some other pathogen), these produce antibodies and somehow you get the breakdown of mucosal IgA and tight junction proteins.
Ground zero is the intestinal mucosa.
One theory is that gluten, which is sticky and invasive (like a thief who can get into anywhere it wants), gets into the intestines, into the spaces between the intestines (the tight junctions) and eventually into the bloodstream.
Then the immune system kicks in.
Antigen presenting cells like macrophages (those Pac man cells that munch the bad guys) start attacking and they stimulate the T helper cells.
These are either TH-1 or Th-2 (check out this previous post that describes this works with Hashimoto’s in detail) and these lead to pro-inflammatory immune cells and proteins, more antibodies, cross reactions – generally, all hell breaking loose.
And, finally as this plays out and is repeated over and over again every time you eat a piece of bread, a pastry, some cake, a doughnut, etc. you are unknowingly pushing your body further and further into autoimmunity.
Your immune system is so juiced it doesn’t know which way is up and eventually, you loose self tolerance.
And loss of self tolerance means the immune system starts attacking your own tissue.
Another problem caused by gluten is that it makes thyroid hormone less effective.
An interesting study published by the American Thyroid Association found “…This study examined 68 patients with Hashimoto’s thyroiditis alone and 35 patients with Hashimoto’s thyroiditis and celiac disease.
The average dose of levothyroxine needed to treat patients with Hashimoto’s thyroiditis alone was lower than the average dose required to treat patients with Hashimoto’s and celiac disease.
When the patients with celiac disease went on a gluten-free diet while staying on the same dose of thyroxine, their TSH level decreased, indicating that their absorption of thyroxine had improved.”
We see this clinically all the time.
When patients go gluten free, they often must reduce their dosage of thyroid replacement hormone because it starts to work so much better.
Well, thyroid hormone produced by your thyroid and thyroid replacement hormone have the same structure.
Gluten prevents thyroid hormone produced by your thyroid from being absorbed, as well.
One idea that is often discussed in this context is something called molecular mimicry.
This is what happens when the immune system identifies certain proteins or protein fragments (amino acid sequences) and then attacks everything that has that amino acid sequence.
With autoimmunity, when the immune system attacks a virus like Epstein Barr, for example, it activates certain kinds of B cells.
These differentiate into plasma cells and one theory is that these may also stimulate anti-self B cells.
These are present in normal people and are there because our immune system constantly gets rid of old dead cells from our body.
But somehow these viral fragments cause other immune proteins called complement to stick to our own tissue and when they accumulate the immune system starts attacking that living tissue as well.
Viruses may also down regulate the T suppressor cells that call off the attack and this keeps the carnage going.
This is what happens to the thyroid. Thyroid cells get attacked as does the enzyme thyroid peroxidase and the protein thyroglobulin.
There is plenty of evidence that gluten is involved with firing up autoimmunity, but I could not find any actual research to support the claim that gliadin proteins closely resemble thyroid tissue (which is something that many bloggers in this area repeat).
There is no question exposure to gluten leads to autoimmunity, destruction of the small intestine, systemic inflammation and destruction of the thyroid.
But whether this type of molecular mimicry is at play is not clear. (I invite any readers to show me this actual research.)
However, at the end of the day, this hardly matters. There are so many other reasons not to eat gluten. And here’s another really big one.
Another really good reason to stay far away from gluten is that it has been linked to destruction of the brain, especially the cerebellum.
The brain is profoundly impacted by Hashimoto’s.
Check out this video (SAVE YOUR BRAIN (FROM HASHIMOTO’S) to learn more.
This is the reason why the second most common symptom for people with Hashimoto’s is brain fog and memory issues. (The most common symptom is fatigue.)
A condition of advanced neurodegeneration that results from Hashimoto’s is called Hashimoto’s Encephalopathy.
This destroys parts of the brain in much the same way that Alzheimer’s does.
And this is caused by autoimmunity in the brain.
One area of the brain that can be impacted is the cerebellum. And a common symptom of impairment to the cerebellum is ataxia.
Ataxia is uncoordinated movement is due to a muscle control problem.
It leads to a jerky, unsteady, to-and-fro motion of the middle of the body (trunk) and an unsteady gait (walking style). It can also affect the limbs.
You can test this by doing the DUI test. Close your eyes and imagine you are walking on a tight rope, put one foot in front of the other.
If you lose your balance or fall over, this may indicate some impairment of the cerebellum.
Guess what else causes ataxia?
Gluten.
In fact, a study from Brain a Journal of Neurology, 2003 found “Gluten ataxia is therefore the single most common cause of sporadic idiopathic ataxia.”
The most common cause of ataxia that has no known explanation.
So when you combine Hashimoto’s with brain autoimmunity and gluten, you have a recipe for really bad things.
The final pièce de résistance of this post is something that is related to gluten but adds a whole other layer of badness.
That is glyphosate or Monsanto’s marquee product Roundup.
Glyphosate is sprayed on wheat and many other grain crops just before harvesting to make them dry out more uniformly.
Well, it turns out that this chemical also does a number on the small intestine, may be responsible all by itself for the destruction of the intestinal lining and the initiation of a host of diseases.
Fish exposed to glyphosate develop digestive problems that are a lot like celiac disease.
Celiac disease is associated with imbalances in gut bacteria that can be fully explained by the known effects of glyphosate on gut bacteria.
Characteristics of celiac disease point to impairment in many cytochrome P450 enzymes, which are involved with detoxifying environmental toxins, activating vitamin D3, catabolizing vitamin A, and maintaining bile acid production and sulfate supplies to the gut.
Glyphosate is known to inhibit cytochrome P450 enzymes.
Deficiencies in iron, cobalt, molybdenum, copper and other rare metals associated with celiac disease can be attributed to glyphosate’s strong ability to chelate these elements.
Deficiencies in tryptophan, tyrosine, methionine and selenomethionine associated with celiac disease match glyphosate’s known depletion of these amino acids.
Celiac disease patients have an increased risk to non-Hodgkin’s lymphoma, which has also been implicated in glyphosate exposure.
So Let’s Review:
Here are 5 reasons to never touch gluten as long as you live that are supported by about 30 peer review studies listed below.
1. Celiac Disease is an Autoimmune Disease with striking similarities to Autoimmune Thyroid Disease.
2. People with Celiac, and Gluten Sensitivity have higher levels of thyroid antibodies and visa versa.
3. Gluten can destroy your small intestines and cause deficiencies in important nutrients, vitamins, and minerals absolutely necessary for proper thyroid function.
4. Gluten and Celiac Disease block the absorption of thyroid hormone.
5. Gluten can cause neurodegeneration in your brain.
And a Bonus
6. Commercial wheat also has lots of glyphosate, a chemical that can make all of what we have just mentioned a whole lot worse.
In life we must always make decisions based on risk and benefit.
The risk of the destruction that gluten can cause in people with Hashimoto’s so far outweighs the benefit that it is really no contest.
http://www.csaceliacs.org/celiac_disease_defined.jsp
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2111403/ Celiac Disease and Autoimmune thyroid disease
http://www.ncbi.nlm.nih.gov/pubmed/18176874 North Italian prevelance of CD in autoimmune thyroid
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC96126/: CD and autoimmune endocrinopathies
http://www.eje-online.org/content/130/2/137.abstract Autoimmune thyroid disorders and celiac disease
http://www.ncbi.nlm.nih.gov/pubmed/15244201 Antigliadin antibodies in celiac disease
http://www.ncbi.nlm.nih.gov/pubmed/9872614 Autoimmune thyroid diseases and celiac disease
http://www.ncbi.nlm.nih.gov/pubmed/12919165 Risk factors of thyroid autoimmunity
http://www.ncbi.nlm.nih.gov/pubmed/11768252 Autoimmune thyroid disease in celiac patients
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3725235/ Celiac disease and autoimmunity: excellent overview
http://cvi.asm.org/content/8/4/678.full Celiac related autoimmune endocrinopathies
http://www.direct-ms.org/pdf/LeakyGutMS/Fasano%20Celiac%20other%20autoimmune%20disease.pdf Systemic Autoimmune disease and celiac
http://en.wikipedia.org/wiki/Anti-transglutaminase_antibodies EMA and transglutaminase antibodies
http://www.thyroid.org/patient-thyroid-information/ct-for-patients/vol-5-issue-6/vol-5-issue-6-p-3-4/ The effect of celiac disease on levothyroxine dosage
http://www.nature.com/cmi/journal/v8/n2/full/cmi201065a.html Antibodies in Celiac disease, implications beyond diagnosis
http://www.wjgnet.com/1007-9327/13/1715.asp Dutch study of patients with Hashimoto’s and Celiac disease
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2730948/ Celiac disease and autoimmunity in the gut and elsewhere
http://jeffreydachmd.com/2014/01/hashimotos-thyroid-disease-molecular-mimicry/
http://www.todaysdietitian.com/newarchives/110310p52.shtml Research connects Celiac and Hashimoto’s
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1808742/ Gliadin, TPO and other antibodies in latent autoimmune diabetes patients
https://www.enterolab.com/StaticPages/EarlyDiagnosis.aspx Before the Villi Are Gone
http://en.wikipedia.org/wiki/Human_leukocyte_antigen Define HLA
http://thyroidbook.com/eating-gluten-increases-need-thyroid-hormones/
http://www.hindawi.com/journals/ijad/2011/865432/ Transglutaminase enzyme involved in Alzheimer’s
http://www.csaceliacs.org/celiac_disease_defined.jsp
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2077662/ Hashimoto’s Encepheopathy and Cerebellar Ataxia
http://www.ncbi.nlm.nih.gov/pubmed/12566288 Gluten Ataxia
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3945755/ Glyphosate, pathways to modern disease: Celiac sprue and gluten intolerance
https://www.cyrexlabs.com/Portals/0/Docs/ClinicalApplications/ClinicalAppArray3.pdf
“Why Isn’t My Brain Working”, Dr. Datis Kharrazian, 2013 Elephant Press
You’re Not Crazy, It’s Your Genes
Hashimoto’s is a complicated condition. It’s not just a thyroid problem. It’s an autoimmune disease, it’s progressive and over time it can impact many different parts of your body.
This is true on the macroscopic where it affects major organs like the thyroid, liver, adrenal glands, brain, pancreas, stomach, small intestine, gall bladder and more.
And this is also true on the microscopic level where it affects immune cells, hormones, neurotransmitters, enzymes, proteins and even DNA and specific genes.
And with many of these influences, it is not a one way street.
One thing affects another and you sometimes have the creation of vicious cycles and problems and its hard to tell where they started.
In this post we will examine one of these vicious cycles on the microscopic level called the MTHFR gene.
MTHFR sounds a little scary and I like to think of it as the MotherFR gene because it can cause so many problems.
MTHFR is an abbreviation for a gene with a very long name, methylenetetrahydrofolate reductase.
(MotherFR is so much easier to remember.)
Basically, what the MTHFR gene does is produce an enzyme with the same really long name (methylenetetrahydrofolate reductase).
Genes produce enzymes and these enzymes do all the heavy lifting, they do the work.
They make stuff happen in the body. Without enzymes we wouldn’t have physiological function.
The job for the MTHFR enzyme is to convert one form of folate into the most active and usable form of folate in the human body – in every cell in the body.
This type of folate is called methyltetrahydrofolate or more commonly by it’s nickname methylfolate.
Methylfolate Does 2 Important Jobs:
Firstly, it helps make neurotransmitters in your brain.
Neurotransmitters are our molecules of emotion.
They are what enable us to think, reason, laugh, cry, be happy, sad, love, learn, crave and have crushes.
When methylfolate levels are low, so are your neurotransmitters.
And low levels of neurotransmitters like serotonin, dopamine, GABA and acetylcholine cause all kinds of unpleasant feelings and behavior.
Like depression, anxiety, bipolar disorders, ADHD, addictive behavior, irritability, insomnia, learning disorders and more.
With Hashimoto’s we often see depletions in these neurotransmitters.
This can be caused by too little thyroid hormones (both T3 and T4) and/or MTHFR defects.
The second thing methylfolate does is it allows us to make something called s-adenosylmethionine better known by its nickname SAMe.
SAMe is important because it helps regulate 200+ enzymes in the human body, its influence is second only to ATP which is every cell’s power source.
Basically what SAMe does is to take what is called a “methyl group” and give it away to these 200+ enzymes and this is what allows them to do their jobs.
Jobs like protect DNA, reduce histamine levels, maintain T and B cell responses, produce key components of cell membranes and about 196 other things.
Because SAMe is so important, when we are deficient in it, we are at higher risk for a lot of different diseases like: autoimmune disease, cancer, infertility, autism, down’s syndrome, thrombosis, high blood pressure and more.
And with autoimmune diseases, studies demonstrate the central role of SAM-dependent methylation ( I’ll explain this in a second) associated with T cell function and it is a key factor in maintaining T and B cell immune responses.
New T cell synthesis is needed in order for T cell clones to expand and respond properly to an immune assault. T cells are needed to help to control the B cells and to balance TH1 and TH2 responses.
If there are methylation cycle problems or mutations, you may have trouble making the bases that are needed for new DNA synthesis.
If you cannot make new DNA, then you cannot make new T cells and as a result you may lack immune system regulatory cells. This is like having a weak and ineffective general who can’t control his troops.
The immune system has many arms, but the B cell “arm” that makes antibodies, known as humoral immunity. I like to think of this part of the immune system as the C.I.A. It gathers intelligence and labels the bad guys.
There is also the T cell “arm” known as cellular immunity, these are like the elite soldiers of the front line. They do the attacking and killing. These are the cells that are often overzealous in Hashimoto’s.
For an in depth discussion on this, check out this post.
If you are having trouble making new T cells, in particular, T suppressor cells, then the immune response may become more heavily weighted in the direction of B cells.
B cell skewed individual has the ability to respond by making antibodies (or autoantibodies) in high numbers to attempt to overcome the T cell deficiency that fights infection.
This is one of the factors in high antibody counts in autoimmune disease.
Methylation is how we get to Oz.
It is the act of taking a single carbon and 3 hydrogens – a methyl group – and attaching itself to an enzyme.
When this happens, the enzyme can do it’s thing.
One common example of this is the breakdown of histamine.
What happens here is a methylation group is made by the methylation pathway and it hangs around until it finds a specific enzyme to bind to.
In the case of histamine, when the methyl group binds to it, the histamine falls apart and goes bye bye.
On the other hand, if your methyl pathway is not making enough methyl groups, then histamine doesn’t break apart and this causes some pretty intense allergic reactions.
For some this may mean running nose and itchy eyes, for others it is full on hives and intolerable itching.
One thing I have observed clinically is that there is a sub-group of people with Hashimoto’s who have histamine intolerance.
This can really complicate recovery and make some of the solutions that help others not work for them.
For example, the Paleo and Autoimmune Paleo diets both have a number of foods that are high in histamine, like bone broth.
So these people eat these foods, thinking that they are doing the right thing (and they are in theory) and they wind up feeling really crappy and just not getting better.
And the people with the most intense reactions may have higher levels of histamine and decreased methyl groups.
What is also interesting is that research has shown some correlation between more severe Hashimoto’s and some of these methylation defects.
Which kind of makes sense, because, as we have seen, SAMe is responsible for maintaining immune responses. And with autoimmune disease, these responses are out of control.
Well, this could be one reason why.
Another key area where this is a concern is brain health. We’ve already seen the impact of methylation on neurotransmitters.
They also play a key role in keeping your myelin healthy.
Myelin coating on nerves is important for proper function of those nerves. Methylation of amino acids in myelin basic protein helps to stabilize it against degradation.
When you lose myelin or it starts to break down then your nerves and brain can’t communicate as well. Myelin is like the coating on the outside of a copper wire.
If a wire isn’t coated it can short out or get major interference from other electrical impulses. In you body this can lead to poor memory or more severe losses in function like those seen in Multiple Sclerosis ( an autoimmune disease caused by the breakdown of myelin).
But, wait there’s more! Methylation is also really important for glutathione production.
Glutathione is our body’s body guard. It is involved in controlling inflammation and in getting every environmental toxins you can think of out of our systems through a process known as direct conjugation.
It is a major anti-oxidant, it regulates the nitric oxide cycle, it is essential for the immune system to operate properly.
It affects how antigens present to immune cells, it can strengthen the regulator part of the immune system.
It is involved in every major biochemical activity, especially those systems most impacted by Hashimoto’s: the immune system, the nervous system and the gastrointestinal system.
It’s importance can not be overstated.
With Hashimoto’s and hypothyroidism, some people develop a sluggish MTHFR enzyme.
This happens because thyroxine (T4) helps produce the body’s most active form of vitamin B2, flavin adenine dinucleotide know by its nickname FAD.
Vitamin B2 must be converted into active FAD by T4 so that the body can use it.
And, the MTHFR enzyme must have enough FAD in order to do its job. If FAD levels are low due to too little T4, then the MTHFR enzyme slows down, which leads to low methylfolate which leads to low neurotransmitters, which leads to low SAMe.
No bueno!
This becomes a vicious cycle.
Another really common finding that I see in analyzing blood test results from Hashimoto’s patients is that they have high levels of homocysteine.
As it turns out, low activity of the MTHFR enzyme may also lead to this. High homocysteine is a major risk factor for heart disease, inflammation, difficult pregnancies, birth defects, and more.
Nutrient deficiencies in Folate B6, and B12 have been linked to high homocysteine.
To matters more complicated, people with MTHFR issues may have a difficult time processing certain types of folic acid like those found in processed food and cheap supplements.
A better source is real food: asparagus, spinach, and liver. Both B12 and B6 are found in meat. And alcohol can deplete the body of B6.
Betaine is also helpful in metabolizing homocysteine.
If you are found to have the MTHFR gene variations and/or you have high homocysteine a better way to supplement is to use the activated version of folate, B6 and B12.
These are:
Methylfolate: (also known as L-5-MTHF Folate)
Pyridoxyl-5-Phosphate (P5P): B6
Methylcobalamine: B12
(Thanks to Vicki Ross for sending me an email to help clarify this very important point.) Not everyone can tolerate methylcobalamine (B12). Just like not everyone can tolerate caffeine, some people don’t do with with methyl cobalamine. And the MTHFR results provide clues to how to determine who may not respond well.
The COMT & VDR genotypes determine WHICH B12 you should take. Most people can handle Hydroxocobalamin or Adenosylcobalamin, but may have problems with methyl B12.
Here is a breakdown of the 4 types of B12:
1. Methylcobalamin
This is the most active form in the human body. It converts homocysteine into methionine, which helps protect the cardiovascular system. Methylcobalamin also offers overall protection to the nervous system. This B12 form can also cross the blood-brain barrier–without assistance–to protect brain cells. It contributes essential methyl groups needed for detoxification and to start the body’s biochemical reactions.
2. Cyanocobalamin
This synthetic version of vitamin B12 is created in a lab, which makes it the cheapest supplement option. It offers the most stable form of B12, although it does so through the presence of a cyanide molecule. While the amount of cyanide is not dangerous, it does require the body to expend energy to convert and remove it.
3. Hydroxocobalamin
Bacteria naturally creates this form of vitamin B12, making it the main type found in most foods. It easily converts into methylcobalamin in the body. Hydroxocobalamin is commonly used via injection as a treatment for B12 deficiency as well as a treatment for cyanide poisoning.
4. Adenosylcobalamin
The energy formation that occurs during the Citric Acid cycle requires this form of B12. Although naturally occurring, it is the least stable of the four types of B12 outside the human body and does not translate well into a tablet-based supplement. It can be difficult to find this one in supplement form, although some supplements, like Vegansafe™, have been able to stabilize it.
Well, firstly, we have to do all the other stuff we do to insure that we are thyroid healthy. And, as all of us who have Hashimoto’s know, this is sometimes easier said than done with all the different systems affected and involved.
Key nutrients for thyroid function are magnesium, iodine (no end to the controversy there – more on this in a future post), selenium, zinc and tyrosine.
Methylfolate, produced by the MTHFR enzyme is also needed to convert tyrosine into active thyroid hormone.
So you can se, we have all the ingredients of a vicious cycle.
Where hypothyroidism leads to MTHFR not working as well, which leads to thyroid hormone not being converted properly and on and on.
Here are some basic tips to correct these challenges:
1. Consider supplementing with glutathione and Vitamin D.
2. Take the active forms of B vitamins mentioned above.
3. Incorporate organic grass fed meats and good fats into your diet.
4. Avoid processed foods and environmental chemical that compete for iodine receptors like fluoride, chlorine and bromine (bromide).
5. Avoid gluten, dairy and soy 100%
6. Avoid GMO foods.
7. Consider testing for homocysteine and the MTHFR gene mutations and defects.
Testing for homocysteine and the MTHFR gene variation is available through many labs. 23andme.com offers a test for the MTHFR gene and many individuals can get the tests from their physicians covered by insurance.
However, some people may be concerned ( and with good reason) with this genetic information getting reported on insurance or to employers.
A MTHFR variation or elevated homocysteine levels may affect future insurance coverage especially with the advances in personal data mining and sharing.
To find out more information about MTHFR testing – along with the ethical considerations of it – visit: MTHFR test options
http://www.jimmunol.org/cgi/content/meeting_abstract/188/1_MeetingAbstracts/116.13 -SAMe and Autoimmune disease
http://www.ncbi.nlm.nih.gov/pubmed/23039890 – Severity of Hashimoto’s corresponds with defect
MTHFR Basics, Benjamin Lynch, ND
http://www.thyroidpharmacist.com/blog/mthfr-hashimotos-and-nutrients
http://mthfr.net/mthfr-test-optins-oral-swab-blood-test-orsaliva/2013/06/26/
http://www.globalhealingcenter.com/natural-health/four-types-vitamin-b12/
Hashimoto’s Thyroiditis: An Autoimmune Disease
I’ve worked with an awful lot of people with Hashimoto’s (this is all I do) and I’ve spent years studying and looking at research on how this condition impacts the body. And I’ve also lived with the disease, myself, for many years.
WHAT I’VE LEARNED FROM LIVING WITH & TREATING HASHIMOTO’S
By far, the most important thing I have learned is that Hashimoto’s is much more than a thyroid problem. It’s an autoimmune disease, but it’s not just an immune system problem either. It’s an all-over-your-body problem.
Your body is not a machine. Like the earth, it’s a complex group of ecosystems that all interact. And these ecosystems can all be adversely affected by Hashimoto’s. When this happens you get a downward spiral of vicious cycles all feeding on one another.
With Hashimoto’s and hypothyroidism you often wind up with a multi-system disorder. It creates webs that can lead to problems with virtually all the major systems of the body.
These include issues with the brain, the adrenals, the liver and gall bladder and problems with the digestive tract like acid reflux, leaky gut, as well as body wide pain and inflammation and more.
All of this can result in anxiety and depression, gall stones and poor liver detoxification, poor absorption of vitamins and nutrients, poor conversion of thyroid hormone, blood sugar imbalances, terrible fatigue and immune responses to various triggers from foods to environmental toxins and chemicals.
Hashimoto’s is not a simple condition that can just be fixed by some thyroid replacement hormone and/or a surgical removal of the thyroid. This works for some, but millions of others have done one or both of these things and don’t feel any better at all.
You have to be able to see the big picture. Then you have you have to isolate each system and look at the interactions and start working on healing the whole body. This requires several steps.
The first thing you must do is find the most destructive triggers and eliminate them. After that, you need to identify which systems are involved and start repairing them.
When you do this, something magical happens. All of those vicious cycles get turned on their head and start having a positive impact on the other systems. When that happens, you can stop triggering the immune system and start to restore balance. Then the body can heal itself.
In the beginning, this will give you glimpses of more good days than bad ones and if you stay the course and work on the big picture you can even sometimes get this condition into a state that resembles remission. (But remember that’s not permission to go back to everything that got you sick in the first place.)
To put it another way. You must adopt a Hashimoto’s lifestyle. That is what I teach my patients and what I try to share about in my Facebook support group and here on my blog. Healing Hashimoto’s requires you to go all in.
1. Step One: Understand Which Systems Are Impacted
The first step is to get a proper diagnosis that will lead you to understanding which systems make up your unique web of vicious cycles. The key is to work with someone who understands this.
In my practice, I specialize in treating people with Hashimoto’s. I know which diagnostic tests are appropriate and I have worked with hundreds of people with this disease and lived through it myself so I’ve seen a lot of permutations and variations.
2. Step Two: Take Your Diet Seriously
Hashimoto’s is an autoimmune disease. 70% of the immune system is found in your digestive tract. What you eat has a huge impact on the state, quality and severity of your autoimmune disease. Anyone who tells you otherwise has no idea what they are doing, plain and simple.
Some foods serve you, some cause you harm. In my practice I prescribe a special Hashimoto’s diet that is the foundation of the work we do. I have found that people who won’t make the dietary changes that they need to heal are just setting themselves up for failure.
3. Step Three: Heal Your Adrenals
For a lot of people with Hashimoto’s the adrenals are a critical piece of the puzzle. Did you know that the label on Synthroid and other thyroid replacement hormone warns that if a patient has adrenal insufficiency they should not be prescribed the drug?
That’s how important the adrenals are. They can be the difference between you turning this thing around and you treading water and not improving or just continuing to get worse. In my practice we do proper testing evaluation and treatment of the adrenals.
4. Step Four: Heal Your Gut
This is really closely related to Step Two. The gut is where your immune system lives. Many really smart people believe that issues in the gut like intestinal permeability (leaky gut) are actually one of the root causes of Hashimoto’s and other autoimmune diseases.
When you heal your gut, you heal everything else: your brain, your immune system, your thyroid, your adrenals and more.
5. Step Five: Remove the Triggers
You have to find and eliminate the triggers that drive your autoimmune flare ups and the progression and destruction of this autoimmune disease. We’ve already mentioned the dietary triggers. Where are the other ones?
Environmental toxins and chemicals (these include some drugs) can be triggers. Blood sugar imbalances can be another important trigger.
Stress can be another trigger and if ignored can torpedo your progress.
In my practice we take you through all of these steps and we teach you along the way how to identify what your unique set of issues, triggers and solutions are.
Then we create an action plan and help guide you out of the woods. You can heal your Hashimoto’s, but healing requires acceptance, and it requires adopting a new lifestyle that will support your body and your immune system and that will provide you with the foundation to get lasting results.
And last but not least, remember to have fun. To laugh and enjoy the life you have. There is a lot in this struggle that is not fun, but what we try to do is to empower you with the knowledge you need, but also make it enjoyable and entertaining.
Because there’s nothing worse than doing all this work and not being able to enjoy the process. A sense of humor can be healing all by itself.
Lastly, I offer a 30 minute Hashimoto’s Healing Discovery Session. In it you can share where you are and where you want to be. I can help by giving you some suggestions that will help right away and we can discuss which other programs or services may help you reach your goals.
Here’s a link to set up a time to chat.
I look forward to chatting with you!
Best,
Marc
In today’s health tip, I’d like to talk about remission from Hashimoto’s.
Remission should be the goal for all of us. We should all strive to get Hashimoto’s to a place that can allow us to have our lives back.
And we should all work hard to stop the progression and the proliferation of the underlying autoimmune process.
The stakes of not doing this are just too high.
But how do you define remission? And what happens when you get there?
The problem with focusing on this as a goal is that this implies that once we reach it, we’re done.
And this begs the question: How do we know when we get there?
One way that some people define remission is normal blood work including normal or undetectable antibodies.
There are several problems with this.
Many, many people have normal blood test results and feel awful.
And antibody numbers are not static, they are changing all the time. Getting them into a normal range is not a guarantee that they will stay there.
And there are lots of reasons why blood tests can look normal and you can still feel terrible. The immune system can release TSH and thyroid hormones all by itself, and this can throw off your results and make them less meaningful.
Also, your pituitary absorbs thyroid hormone differently than the cells in the rest of your body, so it may be getting enough thyroid hormone while the rest of your body is not.
Again making your blood test results less meaningful.
So, blood test results aren’t a great measure of success. As I have said repeatedly, how you feel, on the other hand, is diagnostically important and clinically relevant with Hashimoto’s.
This is actually a really important measure of success.
And the other problem with viewing remission as an end point is that if we do get there, it is a natural tendency to get complacent and to just go back to the same old behavior and diet that contributed to you being sick in the first place.
That’s just human nature.
So, I invite you to see remission as a journey and not as a destination. And to view it as a path and not a place you reach.
If you think about it his way, it involves a higher level of acceptance and commitment. Because it’s not conditional and it’s not something you’re ever finished with.
Remission is an ever evolving journey and if you are committed and vigilant and open to the possibilities of personal growth and transformation then it becomes like a kind of garden that just keeps rewarding you with new gifts.
Because here’s the other thing, you never know how good it could be and if you just settle for normal blood test results, then you might be putting a cap on this that stops you from going to a much higher place.
The possibilities are endless, people, when you think of it this way.
What we need to do is to create a lifestyle that supports healing and remission every single day. And strive to do that at every opportunity.
That’s a whole different ball game.
What are your thoughts on this? Please share them with us.
This pill may not be the answer.
Some of the most common questions I receive via phone, email, Facebook, and yelled across the street concern thyroid replacement hormone.
The question usually goes something like, “Hey, what’s the best thyroid hormone?”
And like most things with Hashimoto’s, this is a super difficult, complicated question disguised as a simple one.
All I can do is mumble, “It depends”
In addition, the problem is that, in reality, many, many people don’t feel better after taking thyroid replacement hormone.
Or they feel better for a while, then they feel worse again.
And a lot of Hashimoto’s patients get fixated on this drug.
Some have to change to natural desiccated. Some are told they have to get on a synthetic. Others have to add T3 or only be on T3. Or they have to raise the dosage, then lower it, then change to something else.
And doctors also share this fixation because thyroid hormone is really important physiologically and for most, thyroid replacement hormone is the only tool in their tool box. And many refuse to budge from the myth that synthetic T4 is the only safe option.
So we wind up with dueling and intractable obsessions resulting in people being pissed off at their doctors, doctors refusing to prescribe anything except Synthroid or the generic equivalent and, unfortunately for the patient, little or no improvement in their hypothyroid symptoms.
There has got to be a better way.
In this post, we will look past this obsession and help break down and demystify thyroid replacement hormone.
The first question, and one that is controversial, is do you really need to be on thyroid replacement hormone?
This is an important question and, of course, the answer is….(wait for it)…it depends.
On what?
Really, it depends on how much thyroid function you have left.
Hashimoto’s is an autoimmune disease in which your immune system slowly destroys your thyroid.
If enough of your thyroid gets destroyed and it stops producing sufficient amounts of thyroid hormone, you can not be without replacement hormone. End of conversation.
On the other hand, if you do have enough thyroid function (and a lot of people do), then the problem may lie elsewhere.
Often the problem is an out of control immune system impacting thyroid function or problems with breakdowns in thyroid pathways that are causing the hypothyroidism.
It’s not the lack of thyroid replacement hormone.
If you focus on properly managing the autoimmune disease part of the equation and on properly evaluating and improving the pathways that make thyroid hormone work, then you may not need extra thyroid hormone at all.
(To complicate matters, once you start taking replacement hormone it impacts the amount of thyroid hormone your body is producing.
So if you have been on it for many years, chances are you may have compromised the thyroid’s ability to produce it alone.)
Even when thyroid hormone replacement is used, it is still very important to manage the autoimmune condition.
This will make the medication work better, slow the destruction of the thyroid gland, and prevent the progression of the autoimmune condition into attacks on other parts of the body like the brain, which comes in really handy, at times.
This is where we should really be fixated. Slowing or stopping the progression of the autoimmune part of this disease should be our obsession. (Ok, I admit it, it’s mine.)
Let’s Look At The Options
That being said, let’s take a look at what the options are and how you can make the best decision for you and your unique set of circumstances.
First there are 2 important factors to consider:
* Bio-identical versus Synthetic
* T3
Bio-identical Versus Synthetic
Bio-identical, as the name suggests, is more like what your body actually produces. The most popular of these are Armour or Nature-throid. The advantage to these is that we can actually test their levels in your system using laboratory testing other than TSH.
The disadvantage is that some people with Hashimoto’s will feel worse on these because their immune system can attack T3 and T4 because they actually have antibodies against them.
Unfortunately, we do not yet have laboratory tests available to test these antibodies.
The advantage of synthetic drugs like Synthroid and levothyroxine is that they are synthetic and the immune system will not attack them.
The disadvantage is that TSH is the only test to measure levels of these drugs and there are many reasons why TSH is an unreliable marker of thyroid hormone levels.
The criticism by doctors leveled against bio-identical hormones is that the dosage varies from batch to batch. A frequently perpetuated myth (from the marketers of Synthroid) is that the dosages and ratio of T4:T3 in Armour aren’t consistent.
That’s just not true, studies have shown otherwise. Armour contains a consistent dose of 38 mcg T4 and 9 mcg T3 in a ratio of 4.22:1. As does Nature-throid.
T3 to the Rescue
Many patient advocates and thyroid support groups sing the praises of T3. And for some, there is no question, T3 is the answer. For others, it’s a nightmare.
T3 is the active form of thyroid hormone, this is what has the greatest impact on our bodies. This is what gives you energy, gets the bowels moving, makes you feel happier and helps you think more clearly. For some this is what helps their hair grow better and their skin get that blood flow back into it.
These people may have trouble converting T4 to T3 because their cells develop thyroid hormone resistance.
On the other side of this are the people who get hyperthyroid with the addition of T3. Think anxiety, insomnia, palpitations, weirdness, a strong desire to vacation at the funny farm.
This is also the case with people who are not managing the autoimmune part of this disease. The attacks against the thyroid causes more thyroid hormone to be released into the bloodstream.
For these people, synthetic T4 might be the better choice along with a concerted focus on managing the causes of these inflammatory incidents (like eliminating gluten, dairy, soy, stress and environmental toxins).
2 Common Things Make You Feel Worse
There are also 2 important factors that can make you feel much worse on thyroid replacement hormone:
Fillers and Adrenal Issues.
Fillers: These are extra things added to the drugs by the manufacturers. Many popular thyroid medications contain common allergens such as cornstarch, lactose and, in some cases, even gluten.
Most Hashimoto’s patients have issues with gluten, and many of them also react to corn and dairy (which contains lactose).
Synthroid has both cornstarch and lactose as a filler. Cytomel, which is a popular synthetic T3 hormone, has modified food starch – which contains gluten – as a filler.
Even the natural porcine products like Armour use fillers. In 2008, the manufacturers of Armour reformulated the product, reducing the amount of dextrose & increasing the amount of methylcellulose in the filler.
This was great for some patients who were sensitive to dextrose and a disaster for others who were sensitive to the methylcellulose.
Nature-throid is considered the most hypo-allergenic of the bio-identicals.
The best choice may be to ask your doctor to have a compounding pharmacy fill the prescription using fillers you aren’t sensitive to. This can be more expensive and unfortunately, some insurance companies refuse to cover it.
Adrenal Issues: If you take Synthroid or even a bio-identical and feel so horrible on the drug that you just can’t continue taking it, one thing to check right away is your adrenals.
The warning label of Synthroid states explicity “Patients with concomitant adrenal insufficiency should be treated with replacement glucocorticoids prior to initiation of treatment with levothyroxine sodium.”
This can cause an acute adrenal crisis in the most extreme cases.
But even in less extreme cases, like those people who have adrenal fatigue and/or exhaustion, taking this drug can result in the patient feeling really lousy.
The adrenals should always be evaluated whenever a patient is prescribed thyroid replacement hormone. (Ideally, this should happen before it is prescribed. Good luck with that.)
Let’s take a look at some other common clinical situations and look at why these things happen.
Normal TSH, But Still Feel Like Crap
This is by far the most common scenario for people with Hashimoto’s. Chronic inflammation can prevent thyroid hormone from getting absorbed in to the cells of the body. This the root of autoimmune disease, but can also come from other things (like infections, surgery, obesity, overtraining, poor diet, etc.).
This can:
*Inhibit thyroid receptors on cells from responding to thyroid hormone.
*Prevent T4 from converting to T3.
*Interfere with the communication between the pituitary and the thyroid (and the adrenals).
Felt Better With Bio-Identical
Some people truly do feel better with bio-identicals. It’s not true of everyone but the addition of T3 can sometimes be the answer because these people:
*May need T3 due to problems with the thyroid hormone receptors on cells
* Were unable to convert T4 to T3 when using T4-only medication
*Had sensitivities to dyes or fillers in synthetic compounds that are not in bio-identical compounds
*Have receptor sites on cells that simply respond better to bio-identical than synthetic hormones
Did Better With T3 Only
As we have seen, some people improve with the addition of T3, while others do their best with T3 only. And these can be synthetic or bio-identical.
This can happen for a couple of reasons:
* Their receptor sites are resistant to thyroid hormone because of high cortisol, high homocysteine, inflammation, low progesterone, vitamin A deficiency and more.
* Difficulty in converting T4 to T3
Didn’t Feel Better With T3 or Bio-identical Hormones
In both cases, more T3 is introduced. These people often don’t have too little T3, they have an active and uncontrolled autoimmune process causing the release of thyroid hormone.
These are also the people who often vacillate from hyper to hypo. They have an immune flare up, more hormone is released and then they crash, it calms done and they are hypo again.
In some cases, these people can have excess adrenal hormones caused by too much nicotine, caffeine, stress or exercising too much.
Feel Better on Synthetic Hormones
Some people actually feel better on synthetic hormones. These can be people who are converting well, have an overactive metabolism and just don’t need more T3.
These are people who also really benefit from an approach that will calm the autoimmune attacks that cause their thyroid to be revved up in the first place.
In every single case described above addressing the underlying autoimmune process first will result in a better clinical outcome (you will feel better) because by reducing the inflammation which is the root of this problem you can:
Improve thyroid receptor site sensitivity
Prevent further destruction of the thyroid
Slow the progression of the autoimmune disease so it doesn’t spread to other parts of the body.
Once again, there are so many variables with Hashimoto’s. The best approach involves a full thyroid work-up and exam, followed by trial and error of different types of replacement medications.
Such a work-up includes more than just TSH, it also has a more complete thyroid panel (including antibodies), other important blood markers (glucose, lipids, CBC with diff, electrolytes, iron, etc.) and additional inflammatory markers like homocysteine, vitamin D, CRP, ferritin, etc.
A history must be taken with attention paid to the patient’s past responses to replacement hormones. With Hashimoto’s patients what a patient feels is clinically relevant and diagnostically important.
Unfortunately, this rarely happens in the conventional model, where the standard of care is to test only for TSH and, if you’re lucky T4.
If TSH is elevated, the patient will get whatever hormone that particular doctor or practitioner is fond of prescribing and that’s the end of it.
Then they are told, “Come back in 6 months to a year and get your TSH tested again. Buh bye.”
And all too often, as many of you know, this approach is doomed to failure. But there is a better way and we are practicing it here at Hashimoto’s Healing.
We offer a complete work up and we focus…, ok, I’ll say it…rather obsessively on reducing the inflammation at the root of this disease and at doing other things to calm, slow and prevent the advancement of autoimmunity to other parts of your body.
This is not just a thyroid problem and there is a lot at stake here. If we’re going to be obsessive, let’s obsess about the things that are at the root of the problem.
I set aside time every week to talk to people with Hashimoto’s about what’s going on with them. In the last year, I have had over 500 of these conversations.
I offer a free 30 minute Hashimoto’s Healing Discovery Session.
In it you can share where you are and where you want to be, I can give you some advice that will help right away and we can discuss how else I may be able to get you feeling better.
If you want to talk with someone who gets it, someone who has been there and who has devoted his life to help people with Hashimoto’s, then I suggest you schedule a time to chat with me.
You might just learn something. Here’s the link to schedule.
http://www.ncbi.nlm.nih.gov/pubmed/23072197 T3 to T4 ratios
http://www.womensinternational.com/pdf/thyroid_hormone_therapy_options.pdf T3 to T4 ratios
http://www.medscape.com/viewarticle/722086_1 Full on medical discussion
http://www.ncbi.nlm.nih.gov/pubmed/15767619 Interesting study on the difference additional T3 therapy makes
http://chriskresser.com/3-steps-to-choosing-the-right-thyroid-hormone
http://thyroidbook.com/blog/which-thyroid-hormone-is-right-for-you/
http://www.rxlist.com/synthroid-drug.htm
http://www.rxlist.com/armour-thyroid-drug.htm
http://www.rxlist.com/cytomel-drug.htm
http://www.nature-throid.com/what_is_nature_throid.php
http://tpauk.com/main/?page_id=1054 Argument against marketing propaganda
The Thyroid, A Fundamental and Clinical Text, Braverman and Utiger, 9th Edition, 2005
Why Do I Still Have Thyroid Symptoms When My Lab Tests Are Normal? Dr. Datis Kharrzian, Elephant Printing 2010
Some of the most common questions that I get from people who reach out to me are about antibodies.
There seems to be a good deal of confusion about them and also a good deal of emotion and expectation attached to these numbers going up or down.
In this post, we examine thyroid antibodies and, hopefully, dispel some of the myths around them.
First of all, what are antibodies, exactly? I like to use military analogies when describing the immune system. And antibodies are like military intelligence (hold the oxymoron jokes).
They are the part of the immune system that gathers information on the bad guys (bacteria, viruses, fungus, parasites, etc.) and then they label those bad guys. Kind of like putting a red flag on them.
The invader is called an antigen. Antibodies bind to these antigens like a lock and a key. Every cell has antigens and these are what the immune system recognizes. And every cell in our body has a self-antigen which are supposed to let the immune system know that our own tissue isn’t a bad guy.
Once the bad guys have been labeled, other parts of the immune system are signaled and they attack and, in most cases, kill the bad guys. In some cases these antibodies can neutralize the bad guys all by themselves and not have to wait for reinforcements.
With autoimmune disease these antigen signals get confused and the immune system ends up attacking our own tissue.
Over the last 50 years there has been a lot of research in this area.
There is a region on cells located on some of our genes called the HLA (or Human Leucocyte Antigen) System. Many of these are located on chromosome 6 (for those of you keeping count).
Mutations or defects of HLA has been linked to many different autoimmune diseases. Exactly what happens is not known, there are numerous theories, but the end result is that our own tissue gets attacked and destroyed by the immune system.
There is a specific class of HLA (class II) that has been linked to autoimmune thyroid diseases like Hashimoto’s and there are also specific antibodies that are important in the disease.
There are 2 autoantibodies that are important:
Thyroid Peroxidase Antibody (TPO Ab): This antibody is the one that is usually high in autoimmune thyroid conditions like Hashimoto’s. It is also known as microsomal antibody.
Thyroglobulin Antibodies (TgAb): These aren’t seen high as often as TPO Ab. They are usually ordered when thyroid lab results seem strange because these antibodies can interfere with thyroid hormone production.
TgAb is also used to monitor progress after surgery for removing the thyroid in thyroid cancer.
In Hashimoto’s, TPOAbs are present in nearly all (>90 %) patients, while TgAbs can be seen in approximately 80%.
Antibodies against TPO (TPOAbs) and Tg (TgAbs) are of immunoglobulin G class, (IgG) and both are really good buddies with their antigens.
For TPO, it is for the enzyme thyroid peroxidase, which frees iodine and helps in the production of T4 and T3.
And for TgAb it is for Thyroglobulin, which is also used by the thyroid to produce T3 and T4.
When these 2 things get destroyed, over time, the body can’t make enough thyroid hormone.
This results in hypothyroidism and all the familiar problems of Hashimoto’s: fatigue, constipation, depression, hair loss, cold hands and feet, brain fog, memory issues and lots more.
Unlike TgAbs, TPOAbs can activate certain parts of the immune system (complement) and are able to cause damage to thyroid cells.
However, there isn’t much evidence that both antibodies have a major role in the formation of Hashimoto’s or in the destruction of thyroid cells.
It seems a lot more likely that other parts of the immune system are signaled and that they bring in the Navy Seals of the immune system which attack and kill thyroid cells.
TPO and TgAb antibodies, however, are considered the definitive test for whether or not you have Hashimoto’s. Basically, if either one or both of these are found to be above the lab range values, then you are positive for the disease.
Most labs have the high end at about 25 to 35. Numbers vary considerably, but it is not unusual for people who have been diagnosed to have antibodies above 1,000.
As I stated above, in most cases these antibodies, themselves, do not attack and kill thyroid cells.
What’s also important to understand is that there are various stages of autoimmune disease and depending on where you are in the progression, you will have different degrees of thyroid tissue destruction and, therefore, different symptoms.
According to Dr. Datis Kharrazian, there are 3 stages of autoimmune disease. While these stages are not recognized by conventional doctors, they are very useful in determining exactly where you are in the progression of the disease.
And realizing that there are stages and that the stages get worse and worse, is also helpful for motivating you to do as much as you can to stop the progression. (Hopefully!)
You can read more about these stages here.
The antibodies are really involved in signaling the immune system and in setting off a series of events that results in the attack and destruction of the thyroid.
I have written extensively about what happens in this previous post.
The important thing to understand here is that the amount of antibodies don’t necessarily directly correspond to how severe the Hashimoto’s is.
There are many reasons for this, but one simple way to look at it is this: The amount of destruction that is done by the army (the immune system) depends on the strength and number of the soldiers.
As I said earlier, the antibodies are really like the CIA or some intelligence gathering part of the army. The front line soldiers are the killers. If you have lots of soldiers and they are all revved up and ready to dance, then you get more destruction.
If your army is weak and there aren’t that many soldiers, then the CIA tells them to kill, kill, kill, but they can only do so much damage.
On the other hand, even if there are only a few CIA agents and there is a large, aggressive army, you will still have massive destruction (and loss of thyroid function).
Where am I going with all this? The amount of destruction, which really is the cause of how crappy you feel, depends on the strength and number of soldiers, not on the number of CIA agents in the field.
This is why antibodies are not a good measure of progress and often don’t correspond with how well people feel.
Antibody numbers don’t correspond, directly, with tissue destruction. As I mentioned above, in some cases TPO antibodies have been linked to tissue destruction, but more often, this is not the case.
Many patients and doctors or practitioners track these numbers and use them as a measure of whether or not what they are doing is working. And many times, they will find that there is no correspondence.
Obviously, getting antibody numbers to drop is not a bad thing. But it is also not necessarily such a good thing, because it may not be an indication that the destruction or the progression of the disease has slowed.
In conventional lab testing there really aren’t tests that are done to look at this. One theory with Hashimoto’s is that the ratio between the CIA and the soldiers is important.
The soldiers are also known as the TH-1 system, the cytokines or immune proteins associated with this part of the immune system are the killers.
The CIA is known as the TH-2 part of the immune system and you can test for ratios between TH-1 and TH-2 cytokines.
If there is a lot more of the soldiers than CIA agents, then the prognosis is not good and the disease tends to be more severe.
With Hashimoto’s there is a tendency towards more TH-1 than Th-2, but this is not always the case.
On the other hand if the CIA is more numerous or more balanced and the control and command part of the immune system (TH-3 or the regulatory part of the immune system- what we can call the General) is also strong, then, usually the prognosis is better and you can calm the attack and slow or stop the progression of the disease.
In reality, the immune system isn’t linear and this is an oversimplification. Testing is available to look at the cytokines that represent these different parts of the immune system, but there are many other factors that make current tests for this unreliable and not that helpful.
However, you can use these ideas to help figure out what you need to do in order to calm the attack, slow the progression of the disease and, most importantly, feel better.
The major cause of thyroid tissue destruction is something called apoptosis. This is programmed cell death.
Lots of crazy things happen on a molecular level (like cytoskeletal disruption, cell shrinkage, chromatin condensation, nuclear fragmentation, membrane blebbing, and DNA fragmentation – membrane blebbing, people!) to make this happen, but the easiest way to grok the root of it is to understand that it is initiated by inflammation.
The best way to slow the progression and minimize destruction is to do everything you can to stop inflammation and to strengthen the regulatory part of the immune system.
2 important anti-inflammatory agents are: Vitamin D and glutathione. These supplements strengthen the regulatory part of the immune system (TH-3 or the General).
(One important thing to note is that some people with Hashimoto’s have a defect with vitamin D receptors and may need to take more than is usually required by normal individuals.)
These are important anti-inflammatories.
Another player in the complicated drama of Hashimoto’s is TH-17. This is like a rouge agent that when numerous and aggressive can do major damage. TH-17 is highly inflammatory.
Natural supplements that reduce TH-17 include Turmeric and Resveratrol. Some Chinese herbs that have been shown to reduce TH-17 are Chang Shan or dichroa root and Huang Lian and Huang Qin whose active compound is berberine.
Also, it is very important to reduce the causes of inflammation in your diet. The three most inflammatory foods in our diet are gluten, dairy and soy.
Gluten has been extensively hybridized and deamidated and has been linked to the initiation and progression of thyroid autoimmunity.
Dairy products when commercially produced are full of antibiotics, hormones and god knows what else. They have also been linked to the initiation of various autoimmune diseases.
Soy is one of the most heavily genetically modified foods in our diet and is also quite difficult to digest.
Some research has indicated that thyroid replacement hormone can reduce TPO antibodies, though there is also some indication that natural desiccated hormone can raise antibodies in some individuals (it seems to be those who have a particularly severe immune reactivity – i.e., they have lots of inflammation).
Selenium has been found to reduce TPO antibodies in a number of studies.
Thyroid antibodies are important for determining whether or not you have Hashimoto’s but are not always a good indicator of how well what you are doing is working.
Do not get too excited if antibody numbers go up or down. It’s not the antibodies that are the problem as much as the other parts of the immune system that are attacking and destroying the thyroid.
Get excited about reducing inflammation. That should be your daily obsession. Really, its that important.
Thyroid replacement hormone and selenium have been shown to reduce TPO antibodies, but this may not work for everyone.
Hashimoto’s is complicated. It is a multi-system disorder that requires a multi-system approach. That’s why created my program: Healing Hashimoto’s: The 5 Elements of Thyroid Health. Click here to learn more.
References:
http://en.wikipedia.org/wiki/Apoptosis
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC555850/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3271310/
http://www.thyroidmanager.org/chapter/hashimotos-thyroiditis/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3271310/– Technichal, but great info on what happens in Hashimoto’s
http://www.ncbi.nlm.nih.gov/pubmed/15307940
http://www.ncbi.nlm.nih.gov/pubmed/7878464
http://www.ncbi.nlm.nih.gov/pubmed/20477110
http://www.medicalnewstoday.com/releases/241571.php
http://www.jimmunol.org/content/185/3/1855.full
http://www.cambridgemedicine.org/news/1299069648
http://jcem.endojournals.org/content/87/4/1687.long