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.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
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 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 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.
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.
• coconut (coconut oil is fine since it has no amino acids)
• seeds and nuts
• orange juice
• wheat products and products containing gluten
• protein supplements: casein, the protein found in milk may also increase arginine levels.
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.
• 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:
Angelica sinensis, chrysanthemum, citrus, lithosperum, milletia, paedria, picrorhiza
Isatis root, baphicacanthes, cnidium, lithosperum, forsythia, gardenia, chrysanthemum, vitex, dandelion, epimedium, lonicera
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.
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
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.ncbi.nlm.nih.gov/pubmed/12699597 T3 autoantibodies can cause latent EBV activation!
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.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
This last weekend, I had the honor and the privilege to be invited to a mastermind in Boulder Colorado that was hosted by Michael and Izabella Wentz. It was a meeting of some of the top people in our field and we gathered together to share some of the things we have learned with each other.
In today’s post, I wanted to share some of my initial thoughts (while they are still fresh in my mind) about some of the important takeaways from the event both for deepening our understanding of how to heal Hashimoto’s and also of how we can better serve each other and our world.
If you aren’t familiar with a mastermind (I wasn’t until last year) the basic idea is that you bring together a group of people with similar goals and collectively the brain power of everyone’s minds creates a kind of quantum up-leveling of ideas and understanding on your topic. The sum becomes greater than the individual parts.
For those of us working in the world of thyroid health and autoimmunity, the purpose of this event was two-fold. To share ideas about what we have learned in working with this unique patient population and, also, how we can have successful businesses so that we can have a bigger impact, help more people and improve patient care for the millions struggling with these diseases.
In this post, I’m going to focus on my top five takeaways from the event.
Here they are:
1. The profoundness of your “why”
2. It’s all about the proteins
3. Diet matters times infinity
4. Root cause is plural
5. Hashimoto’s isn’t the end of your life, it’s the beginning of your journey
At the event there were quite a few speakers (the Wentzs have a wonderful, generous spirit and wanted to highlight as many people’s brilliance as they could) and it made for a very rich weekend of content (far too much for me to cover in this single post – which means there’s a lot more to come, stay tuned 🙂 ).
But time and time again, in smaller groups and as introductions to the different talks people shared their “why”. And by that I mean the experiences and struggles that motivates them.
It was truly inspiring to hear story after story of people overcoming some really serious adversity and illness and taking the momentum and mind shift resulting from that and going on to do some really amazing work.
On my way there, I read a book because (being a knucklehead) I missed my flight. I had brought a box full of copies of my book to give to everyone and long story short, I didn’t give myself enough time to check the box and get to my flight.
So I had some time to kill and I finished reading The Obstacle is the Way by Ryan Holiday. (You have to read this book!) It’s all about using obstacles, disappointments and adversity to transform the world. And not just in a “glass half empty or half full” accentuate-the-positive sort of way.
This book takes it to a whole new level and it points out the incredible blessing of failure, illness, and disappointment. And, essentially, some of the greatest inventors, thinkers and doers of history weren’t defeated by hard times, pain and struggle they were made possible by it. And instead of fighting it, they embraced it and used it to their advantage to do great things.
And this event was a real life example of this. Everyone there has overcome something major and now they are motivated by it. And the common thread was that we are all inspired to help others and do whatever we can to make the world a better place. And that difficulty is daily being transformed into action.
So I encourage you to really spend some time finding your “why” and if you are feeling defeated and discouraged know that you are not alone is this and that the opportunity is there for you to accept it, embrace it and use it to create great things of your own.
The other part of your “why” that you really need to explore, in my opinion, is the physiological “why” of your signs and symptoms. What this event reminded me of, once again, is how complicated this all is and how many different layers they are to these health challenges.
If we can find at least some of the “why”, then we can find important clues to getting you better, faster and more deeply. This brings me to my next takeaway (see how I did that?):
The keynote speaker of the event was Dr. Datis Kharrazian, who has been a longtime teacher and mentor of mine (and many others in the group). He shared his “why” which was poignant, heart breaking and deeply personal and involved his mother’s health struggles. And it has motivated him to become an extraordinary clinician and researcher.
(I don’t know if you guys are aware of this, but people are going to be talking about the research that he is doing for generations. That’s how important this is. He and Dr. Vajdani of Cyrex Labs are helping to unravel the mystery of autoimmunity – I am not exaggerating when I say this could be Nobel Prize level research in the way that it will transform our understanding of autoimmunity.)
Dr. K shared some of this research he has been doing over the last year or so, which was funded entirely on his dime (and we’re talking a serious pile of dimes) because these issues that are so important to us with autoimmune diseases are not really seen as that important to the powers that be.
There are many layers to this research and it’s going to be released soon, and he’d have to kill me if I revealed the details because it could compromise the study, but here’s the big takeaway: It’s all about the proteins.
Autoimmune reactions are reactions by your immune system to various proteins. Or, really, protein fragments – the sequences of amino acids that make up those proteins.
They are what cause the immune reaction that destroys our tissue.
Proteins are the building block of life. So these proteins and the amino acid patterns that make them up are everywhere. In lots of different foods (and many you don’t think of as proteins like grains and vegetables) and in meat and in the tissues of our body.
And these proteins are the “on switch” for autoimmune destruction. They turn on the antibodies (which don’t destroy tissue) that signal other parts of the immune system to attack, kill and destroy.
And because these amino acid sequences repeat all over the place, all kinds of different tissue can get destroyed. Really important stuff. One example of this is the affinity of thyroid antibodies (like antibodies to TPO and T3) to tissues in our brain.
Proteins don’t just signal destruction of the thyroid, they can also signal other parts of our immune system to destroy our cerebellum and myelin, the sheath that protects our nerves. (Destruction of myelin is what causes Multiple Sclerosis (MS)
This is one of the reasons “why” some people with Hashimoto’s will develop encephalopathy. Their brain is being attacked and, in some cases, it’s being signaled by TPO. The most common symptoms of this process? Memory loss, fatigue and depression!
These proteins are a really big deal!!! Which leads me to my next takeaway (see how I did that again? 🙂 )
The single largest source of these proteins is the food we eat. This is why it makes me insane when doctors say things like “Diet doesn’t matter”.
That is a very dangerous lie.
Not only does diet matter, ignoring the role of diet can literally destroy you. What did we just talk about? These proteins leading to destruction of parts of your brain.You lose your brain, you’re done. You have no life.
Much of the research that Dr. Kharrazian and Dr. Vajdani have done involves testing the effects of these various proteins on the thyroid axis and the brain. And the results are going to be available to us soon and it’s going to radically transform how we can help you, but for right now here’s what we can tell you.
Dr. Izabella Wentz did a very interesting study of 2, 322 Hashimoto’s patients and she collected some really important data on just how important and effective dietary changes are.
Here are some of the results:
This illustration reveals just how effective diet is in improving symptoms and lowering antibody levels.
And here’s some more important information on some common foods that may cause problems:
Highly reactive foods per IgG test sampling:
100% – Cottage cheese, brewer’s yeast
90%- cola, safflower, whey, baker’s yeast
80%- casein, blue cheese, chicken, cow milk, goat milk, rosemary, yogurt
70%- corn, cheddar, Swiss, licorice, mushroom, sugar cane
60%-pineapple, pinto bean, ginger, oregano, oyster, white potato, sesame, walnut
For myself and my patient population I know that tomatoes can also be a problem. And as we know gluten, dairy and soy proteins can also wreak havoc.
Spinach can also be a problem. One thing I’ve observed with spinach is that it can actually reduce iron levels. I had a patient who was eating spinach salad 3 times a day and she was severely iron deficient.
I tried everything and nothing worked and finally I said stop eating spinach and that turned out to be the problem. Once she stopped, we were able to successfully restore her iron levels to the normal range.
One important thing to understand about these foods is that you may or may not react to them. As I said this is highly individualized. You can use the percentages to make an educated guess about what you might react to, but you are unique and you may not have these same reactions.
Here’s another quick tidbit that’s really helpful: One important thing you can do to strengthen the T regulatory or the “good guy” part of your immune system is to feed them fiber: here’s what Dr. Vajdani drinks every morning: Pay attention to this, this is the guy who probably has done more research on autoimmunity than anyone on the planet:
Hemp or chia seed pwder
Flax seed powder
Almond milk (You can substitute coconut milk if you are sensitive to almonds.)
As I said above, an important thing to understand about all of this is that there is tremendous variability and millions of possible permutations of this. So everyone doesn’t have sensitivities to all these foods. But, you really need to figure out which foods you have a problem with.
Cyrex labs has a lab test called Array #10 that tests about 200 different dietary proteins and tests them the way we actually eat them. For example, many labs test for IgG and IgA reactions for raw chicken and turkey. When’s the last time you ate raw chicken? I hope it wasn’t recently.
Array 10 tests for reactions to cooked chicken, turkey and other foods because cooking changes the proteins.
And here’s a clinical pearl: Since the problem is these amino acid sequences, the affinity that is formed is based on longer sequences. If you can break down those sequences into smaller pieces, then you can can slow or stop the destruction.
Digestive enzymes that break down protein have the ability to do this. They break apart the amino acid connections and can render the protein harmless or at least less harmful.
But, here’s the bottom line: This is whole thing is highly individualized and there are a million different causes and variations of causes. Which leads me to my next point ( see how I did that a third time?):
I love Izabella’s main theme of finding your root cause because it’s so simple and obvious, yet it’s so profound. Find the root cause and fix it.
But here’s the thing. You probably have thousands of root causes and you need to keep searching for them. Because they are the root of all your physical, mental and psychological problems.
One example that came up in Dr. Kharrazian talk was the patients we all have to do everything right, take all the right supplements, fix their adrenals, get their thyroid working properly, clean up the inflammation, detox their livers, heal their leaky gut and do the Autoimmune Paleo diet perfectly, but they still don’t get the results we had hoped for.
The problem? Leaky gut is only part of it. There’s the levels of bacteria in the gut. There’s the fact that the dendtritic cells in the intestines can be primed and over excited, the Kupffer cells in the liver can also be primed and over excited.
Another interesting clinical pearl: The dendtritic cells in the intestines actually produce TSH. Another presenter Dr. Allen Christianson shared a case study with a patient whose TSH was all over the place, upend down, up and down.
Well, he discovered that when they treated her for a chronic sinus infection her TSH went done. Dendritic cells are found in tissue that has contact with the outside environment such as the over the skin (present as Langerhans cells) and in the linings of the nose, lungs, stomach and intestines.
I discovered in researching my book that these cells can actually produce TSH. Here’s the study.
See? It totally makes sense if you understand the “why”.
All of this stuff is connected and there are many levels. One of the things that Dr. Kharrazian also brought up was that leaky gut can lead to the loss of something known as “oral tolerance”.
I’m going to explore this a lot more in a future post, this one is getting long :). But, basically, here’s why it matters.
Oral tolerance is what keeps us from having hypersensitivity reactions. This is from an interesting article on this.
Let me translate parts of the abstract:
Oral tolerance is the state of local and systemic immune unresponsiveness that is induced by oral administration of innocuous antigen such as food proteins. (That’s saying you don’t respond to harmless things like proteins., which we have just learned are not so harmless. Because if you lose oral tolerance, they aren’t innocuous anymore).
The local and systemic effects of these regulatory T cells prevent potentially dangerous hypersensitivity reactions to harmless antigens derived from the intestine and hence are crucial players in immune homeostasis.
(In a perfect gut, regulatory T cells, the “good guys” of our immune system prevent potentially dangerous hypersensitivity reactions. Yeah, Hashimoto’s is a an example of a “potentially dangerous hyper-sensitivity reaction”.)
This is just another level of our growing understanding of what is going in our bodies. Which brings me to the last point which Stacey Robbins so eloquently out for us:
The first presenter at the event was Stacey Robbins and she shared something beautiful: Hashimoto’s is not the end of your health (or life as you know it), it’s the beginning of your journey.
The good news is that we are all traveling this journey together and there are some really amazing people working on this.
But the reality is we are only in the infancy of understanding what is going on and what we need to do about it.
But there is reason for optimism because there are some great minds and some incredibly devoted people who are working day and night to help you.
So let me end on a positive note and say how grateful I am am to all the people who attended the Thyroid Mastermind and to say our work now has just begun!
The obstacle is our way and the journey is our path and together we will find hope, help and healing.
I can’t wait to see where this journey takes us. I have a feeling it might just be historic, and just think, we all get to be part of it!
Please share this with whomever you can think of. There’s some really valuable stuff in here!
Have a great day! (Unless you have other plans.)
My chicken scratch from the Thyroid Mastermind, Boulder Colorado, 2015. Hosted by Dr. Izabella Wentz and her husband Michael Wentz.
http://www.nature.com/mi/journal/v5/n3/full/mi20124a.html – article on oral tolerance
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2768616/ – paper on the immune system as regulator of thyroid activity
Hey, people! Here’s a post I originally wrote for Hypothyroidmom as a guest post. I decided to make a video of it, as well for all you video fans.
As I’m sure you know, one of the most common concerns for people with Hashimoto’s and hypothyroidism is maintaining proper body weight.
For people with Hashimoto’s (the most common cause of hypothyroidism) this comes in 2 varieties. They gain weight and can’t lose it or they have trouble keeping it on.
In this post we will examine the many reasons why a lot of people with hypothyroidism have difficulty losing weight.
One of the obvious things that people think about with hypothyroidism and weight gain is the fact that the thyroid has an impact on the body’s metabolic rate.
What is metabolism, anyway? In technical terms, its the amount of oxygen used by the body over a particular amount of time. When this measurement is made at rest, it is called the basal metabolic rate or BMR.
Testing BMR was, once upon a time, used to assess a patient’s thyroid status. Those with lower BMRs were found to have underactive thyroids and those with overactive thyroids were found to have high BMRs.
Later studies showed that low thyroid hormone levels were linked to low BMRs. Then, most physicians decided to scrap testing BMR in favor of simply testing thyroid hormone levels because it is easier and it was found that the thyroid was not the only thing to influence metabolism.
High or low BMRs are associated with changes in energy balance. Energy balance comes down to the difference between how many calories one eats and how many calories one’s body burns.
Things that create a high BMR, like amphetamines for example, often cause a negative energy balance which results in weight loss. (This is one reason why you tend not to see many overweight speed freaks.)
Based on this, many people originally assumed that changes in thyroid hormone levels which can lead to changes in BMR should lead to the same changes and the same weight losses (Minus the lost teeth and paranoia).
Well, as with most things related to the body, it turns out that its more complicated than that. Other hormones, proteins and neurotransmitters have also been found to be part of the mix and these all also have influence on energy, food intake and body weight.
Some of them that are worth taking a look at and dealing with are leptin, insulin, neuropeptide Y, serotonin and inflammatory proteins like interleukin 6 (IL-6).
Physiologically, evolution takes quite a long time (relative to our sweet, short lives). And our ancestors evolved in a calorie poor environment where fat was pretty hard to come by.
As a hunter gatherer on the open plains of Africa, our forefathers (and foremothers) had to expend a lot of energy to get food and there wasn’t a whole lot of fat around.
Most prey was pretty lean and grass fed and there weren’t too many fast food joints (The fossil record has yet to reveal a single Mickey D’s).
As a result, our bodies developed a natural tendency to store whatever fat was available. And that fat got programmed with some pretty ingenious innate intelligence.
One of those ingenious adaptations from the clever mind of fat is the hormone leptin.
Leptin is a hormone that is made in your fat cells and it is involved in maintaining body weight. Interestingly enough, it also has influence on the thyroid.
Leptin acts as an important control system that communicates to other organs about the state of your fat balance and whether to eat more or stay in low-metabolism survival state. (Where, oh where, have all the wildebeest gone?)
When you have more fat cells, you get higher leptin levels.
The high leptin lets your hypothalamus (a kind of master endocrine gland in your brain) know that you don’t need to eat as much, so metabolism slows (and this signals you to make more Thyrotropin-releasing hormone (TRH), and this raises TSH) and the TSH tells your thyroid to make more thyroid hormone.
This is what happens when everything is working properly. But with Hashimoto’s and hypothyroidism, lots of things are often not working properly and many people develop leptin resistance.
You may have heard of insulin resistance (if you haven’t, read about it here). Well, leptin resistance is similar and often co-exists. In fact, both are consequences of obesity.
With insulin resistance your body’s insulin receptors get fatigued because they have to deal with so much sugar. (They just give up and say “Uncle”). A lot of people in the US, today, has some degree of this.
With hypothyroidism, people often become overweight and use less energy. The increased amounts of fat and the lower energy use can result in leptin resistance and you wind up with a vicious cycle where leptin stops doing its job.
Its stops telling you when to eat and it stops signaling your thyroid.
Of course, many people’s natural inclination when they gain weight is to go on a diet to try and lose it. Often these people will keep dieting and fail and then diet again and get all stressed out about it because its not working.
And guess what? Chronic dieting and/or major stress are common causes of leptin resistance.
As a result, leptin no longer signals your hypothalamus and your metabolism slows down.
Leptin resistance makes the hypothalamus believe that you are in starvation mode, and you make more fat, and slow down thyroid hormone production.
So, TSH goes down, you don’t convert as much T3 from T4, and your reverse T3 goes up. And, in what can only be described as unfair and cruel, your appetite actually increases, you can also become insulin resistant, and fat breakdown (lipolysis) slows down.
So a vicious cycle is created in which more fat accumulates, you’re hungrier and your thyroid is slower.
Over time, you gain weight, especially around the mid-section, and it becomes more difficult to lose the weight and accumulated fat.
With Hashimoto’s (and hypothyroidism) one of the most serious problems is inflammation. In fact, a destructive inflammatory process is really what is at the root of all autoimmune diseases (of which Hashimoto’s is one.)
Leptin controls and influences the immune system, too. It is chemically very similar in structure to IL-6, which is an inflammatory cytokine (immune protein) that studies have shown to be significantly elevated in women with Hashimoto’s.
One of the places where can find high concentrations of IL-6 is in the fat that accumulates around the abdomen. This adipose tissue is highly inflammatory and can, itself, lead to the progression and more aggressive proliferation of many diseases.
Low vitamin D has also been associated with both insulin and leptin resistance. And vitamin D is an important anti-inflammatory that is often low in people with hypothyroidism.
Your perception of hunger is intimately linked to your brain chemistry. Normally, when things are working properly, your hypothalamus gets signals that you need energy and a brain neurotransmitter called neuropeptide Y (NPY- not to be confused with NYPD) is released.
It makes you you want to eat more carbohydrates (think overwhelming urge to finish that can of Pringles). That surge is what makes you feel cravings and hunger.
Once your body has had enough carbohydrates, the brain releases serotonin which is your brain’s way of saying, “Put down the bag and step away from the counter.”
Studies have shown that NPY is an important go between of leptin in the central nervous system and the hypothalamus. And that giving people NPY suppressed circulating levels of thyroid hormone (T(3) and T(4)) and resulted in an inappropriately normal or low TSH.
So, high levels of NPY can actually lead to functional hypothyroidism. And leptin’s job is to suppress NPY. So once again, we have the makings of another vicious cycle.
This also may be yet another reason why TSH testing can be unreliable in circumstances involving leptin and insulin resistance and weight gain due to hypothyroidism. (A set of circumstances that is ridiculously common.)
Another neurotransmitter that is impacted by hypothyroidism is serotonin. As we saw above, one of the many roles of serotonin is to tell you to stop eating those crazy carbohydrates.
Thyroid hormone and serotonin have an intimate relationship and many studies have shown that thyroid hormones impact virtually all neurotransmitters in the brain.
So, with hypothyroidism you also may have less serotonin production and all the accompanying emotional and physiological problems related to that, like depression and minimized signaling that tells you to stop eating.
The cravings don’t go away, they intensify with weight gain and hypothyroidism. And this is all accompanied by emotional discomfort that makes you want to reach for that high carb comfort food.
Naturally, we can’t leave you there. Let’s talk about what to do about all of this.
In a simple sense the root of all of this can be summed up with one word: inflammation. Being overweight is a problem of inflammation. So is Hashimoto’s, the most common cause of hypothyroidism.
So the most important thing to do is to reduce inflammation. And if you do that you can start to unwind many of these hormonal and neurotransmitter disruptions that are leading you down the road to feeling really crappy a lot of the time.
One place to start is with some version of the Paleo diet. There are many versions, with my patients I use a version that is tailored for people with autoimmune disease.
This is also called the elimination diet and is very restrictive. But it is also very effective. Desperate times call for desperate measures.
If you want to unwind all of these vicious cycles and to reset leptin and insulin you can’t mess around and use half measures. When things get bad, half measures do not result in half results. They result in disappointment or worse, no results.
This diet involves the elimination of virtually everything that is inflammatory in your diet and it removes almost all of the carbohydrates that lead to most of the problems we have described, too.
This allows your body to convert from a sugar burning leptin and insulin resistant machine to a happy fat burning ecosystem. It also reduces systemic inflammation.
This is absolutely essential, but often, the diet is not enough. As we have seen here, many systems are involved (and this is just the tip of the iceberg).
Over time, these various systems start to break down because of the influence of thyroid hormone on virtually every aspect of our physiology -link. The impact of hypothyroidism is felt everywhere.
This can cause problems in all the other systems of your body including your adrenals, your liver, your heart, your pancreas, your brain, your blood and much more.
Other things to add to the mix are natural anti-inflammatories like Vitamin D, turmeric, glutathione and lots of fruits and vegetables high in anti-oxidants.
Also, it should be noted that the Paleo diet recommended here is not the all meat all the time variety.
It is a diet that consists of meat, and lots of vegetables, healthy fats like coconut oil, olive oil and fat from grass fed, organic animals and a healthy amount of fruit (featuring low glycemic varieties).
In addition, it is super important to eliminate from your diet other foods that are inflammatory like gluten, dairy products, soy, artificial sweeteners and processed foods.
The other important ingredient is exercise. If you have Hashimoto’s or hypothyroidism this can be a real challenge because many people don’t have the energy to do anything.
But it’s really important that you do and that you do it consistently and at a relatively high intensity. For some people you may only be able to do high intensity for a few minutes a few times a week. Here’s a post I did on this that discusses how to exercise with Hashimoto’s.
But gradually, as your lose the weight and the inflammation you will have more efficient energy reserves and distribution and you will turn this oppressive trend of downward spirals on its head and create a positive upward momentum towards weight loss and healing.
It can be done. It takes commitment and it takes perseverance. But, the results are well worth the effort.
I was asked by a Turkish Hashimoto’s support group to answer some questions.
They had a lot of them (41 to be exact).
Many of these questions are universal and they will benefit you no matter where you live. And I also go into much more detail in my new book, Roadmap to Remission.
One thing this showed me was that Hashimoto’s knows no borders and the quality of care worldwide is pretty poor.
Yet another reason why we are here.
Please check it out and share it with anyone you think might benefit.
And if you don’t have a copy of my new book, what are you waiting for?
Here are some of the reviews that have been coming in:
“This is the definitive book on how YOU can get your Hashimotos into remission–and stay there. Although the book contains tons of information, it is surprisingly an easy, digestible read.
Something you can refer to again and again. It answered all of my many questions from both a conventional and alternative medical perspective. You can tell the author has been there, done that, and is willing to share the whole journey.
It’s like having a conversation with a compassionate, slightly quirky genius, who only wants you to feel better because he understands the nightmare you are going through. If you have Hashimotos, then this book will be the best investment you will ever make. You’ll save yourself from years of confusion, pain, suffering, financial drain, and ill health. What have you got to lose?” D
“If you, or anyone you love, is living with Hashimoto’s thyroiditis, this guide is a must have. There is so much wisdom packed into this book – I am happy I bought it, so that I can read it time and again. I also have had my highlighter out to notate the nuggets of wisdom that pop out of each section.
The other thing I love about it, is the tone of the writing. Marc Ryan has taken clinical information and made it accessible, all while making the whole thing somewhat funny. Not belittling the scenario with the humor, but sprinkling much appreciated levity over a sometimes too heavy subject. I found myself chuckling throughout the read.
I highly recommend reading this guide. The angle of Chinese medicine that is included is quite interesting, and different than any of the other thyroid books out there. You will not be disappointed.” Amanda Baker
“Rescue Remedy is what I call this book.Rescue from the myriad of medical practitioners that have poor knowledge base of Hashimoto’s Disease, rescue from tons of misinformation, rescue from believing there’s no hope and you must live the rest of your life feeling horrible.
Remedy because there’s a “potion” that will heal you if you are brave enough to try it. The information does take time to absorb, but that’s ok because review of concepts and ideas are right there at your finger tips.” Julie
Click the link above and get a copy for yourself. You just mind find hope, help and healing.
Hypothyroidism affects nearly 10% of the US population. That’s upwards of 35 million people. And Hashimoto’s is believed to be the leading cause.
In actuality, hypothyroidism can be caused by many other factors, as well. And to complicate matters, both of these conditions can lead to the other.
Prolonged, chronic hypothyroidism can become Hashimoto’s and virtually everyone with Hashimoto’s becomes hypothyroid eventually because their thyroids are gradually destroyed by their immune system.
One common factor that we see with both patient populations is deficiencies of important micronutrients such as selenium, zinc, iron, Vitamin D, B Vitamins, Vitamin A and Vitamin E.
(Iodine is also an important nutrient that is sometimes deficient, but it is also quite controversial due to it’s ability to rapidly cause an increase in both TSH and antibody levels, and in some cases, increase in hypothyroid symptoms. People with Hashimoto’s, MUST, therefore be extra cautious hen supplementing with iodine. As a general rule you should test first, then, if you need to supplement, work with someone who knows what they are doing.)
In this 2 part post we will first explore some of the causes of nutrient deficiencies, and, then in part 2, best practices for supplementing and correcting them. And of course, as always, why it matters.
If you are a follower of our blog, you know that I’m always interested in why things happen, so before we look at the actual nutrients, let’s look at the most common causes of nutrient deficiencies in the body.
1. Low Stomach Acid
2. Leaky Gut or Intestinal Permeability
3. Soda Consumption
4. Tea and Coffee
5. MTHFR and VDR Gene Mutations
With Hashimoto’s and hypothyroidism, a very common problem is that too little gastrin and stomach acid (hydrochloric acid or HCL) are produced. This can result in a number of things that can lead to micronutrient deficiencies.
(For an in depth read on this problem, check out this post.
For example, one thing that HCL is important for is the absorption of vital nutrients like B12, iron, and calcium and for breaking down and absorbing protein.
Too little HCL can also lead to inflammation, lesions and infections in the intestines.
All of that leads to poor absorption of these nutrients and thyroid hormone, leading to a vicious cycle that leads to more hypothyroidism and more nutrient deficiencies.
It’s a positive feedback loop of repeated deficiencies making each other worse.
The following micronutrients depend on proper stomach acid levels in order to be absorbed in the small intestine:
Selenium (selenite form is not pH dependent)
And it’s also important to note that medication that reduces and/or eliminates acid reflux like proton pump inhibitors and antacids, may also cause poor absorption of these vitamins and minerals.
When the lining of the digestive tract is inflamed, the connections between the pieces of lining known as “tight junctions” break down and allow large, undigested compounds—toxins and bacteria—to leak into the bloodstream.
These substances all react with the intestine’s immune system and cause an exaggerated immune response. This over-reaction by the immune system becomes another vicious cycle that leads to more intestinal damage.
And as this problem grows, diet, lifestyle, medications, and infections can cause further intestinal inflammation that can ultimately lead to more serious problems.
In addition, after the intestinal lining becomes damaged, the damaged cells become unable to properly digest food and produce the enzymes necessary for digestion.
This damage can lead to micronutrient deficiencies, malnourishment, hypothyroidism and more autoimmune disease.
It’s another positive feedback loop perpetuating further damage and further deficiencies. This is a problem because so many things are absorbed in the gut, mostly through the small intestines.
Approximately 80% of water is absorbed by the small intestine, 10% by the large intestine and the remaining 10% excreted in the feces.
All of the important electrolytes are absorbed in the small intestine: chloride, iodine, calcium (these are absorbed with the help of vitamin D), iron, magnesium and potassium.
Vitamins including fat soluble ones (Vitamins A, D, E and K) are absorbed together with dietary fats.
Water soluble vitamins like vitamins B and C are absorbed by diffusion. Vitamin B12 combined with intrinsic factor (from the stomach) is absorbed by active transport.
Of these iron is absorbed in the duodenum, most are absorbed in the jejunum and Vitamin B12 and bile salts are absorbed in the later part of the ileum.
So you can see, when this process is damaged or impaired there are a lot of potential consequences.
There are several micronutrient deficiencies that a recent Brazilian review published in 2012 by Teixeira TF et al found to be associated with leaky gut and obesity, specifically vitamin A, magnesium, zinc, vitamin D, and calcium.
Vitamin A, zinc, and magnesium all help maintain tight junctions in the intestine and regulate endothelial cells in the gut, while vitamin D stimulates intestinal lining rebuilding and it can slow the damage by calming and regulating the immune system.
Vitamin D and calcium play a joint role in maintaining the protective barrier of the intestines by helping ATP (the cell’s energy source) mechanisms in the intestinal cells.
In obesity (which is found in some hypothyroid and Hashimoto’s patients), intake of these micronutrients is sometimes low, so deficiencies could play a major role in making leaky gut conditions worse, especially when combined with an unhealthy intestinal ecosystem and poor food choices.
What that all means is that having a good intake of these micronutrients could be protective against the development of leaky gut and the inflammation and eventual obesity it can cause.
Most popular sodas (like Coke, Pepsi, Dr. Pepper and Mountain Dew, etc.) are loaded with sugar, and caffeine and this mixture is suspended in phosphoric acid, which actually allows you digest it.
Here’s what happens in your body when you drink one of these drinks:
First, about 10 teaspoons of sugar hit your system (roughly 100% of what you’re supposed to consume in a day). This causes a massive spike in insulin and your liver freaks out and turns all of this excess sugar immediately into fat.
Then the caffeine kicks in and causes a massive burst of stress hormones to be released from the adrenals, which causes the liver to kick all that sugar into your bloodstream and causes a massive release of cortisol to try and deal with it.
This cortisol release also reduces stomach acid levels, impairs your immune response and, ultimately, causes your intestinal lining to be further compromised.
Sugar, caffeine and phosphoric acid all impair absorption of vital nutrients like iron, calcium and zinc. And the phosphoric acid actually binds to these minerals.
Then the diuretic properties of caffeine kick in and you pee all these valuable nutrients out.
This is pretty much the same as soda, minus the added problems caused by phosphoric acid.
Let’s take a look at how caffeine can lead to deficiencies in important micronutrients.
As we discussed above, caffeine is a diuretic. It makes you pee. Caffeine causes calcium to be excreted in the urine and feces. According to “Effects of caffeine on health and nutrition: A Review” by Tsedeke Wolde, for every 150 mg of caffeine ingested, about the amount in one cup of coffee, an estimated 5 mg of calcium is lost.
Caffeine also inhibits the amount of calcium that is absorbed through the intestinal tract and depletes the amount retained by the bones. In fact, one study of postmenopausal women found that those who drank more than 300 mg of caffeine lost more bone in their spines than women who did not drink as much.
Caffeine also inhibits vitamin D receptors, which means less may be absorbed. Because vitamin D is important in the absorption and use of calcium in building bone, this could also decrease bone mineral density, resulting in an increased risk for osteoporosis.
Caffeine interferes with the body’s absorption of iron (sugar does too), which is important for many processes in the body like red blood cell production, and carrying thyroid hormone to the cells.
Tea reduces iron absorption significantly more than coffee, but both impair absorption. Tannins in tea can also bind to iron, and prevent absorption of calcium and thyroid hormone, as well.
Water soluble vitamins, such as the B-vitamins, can be depleted by the fluid loss caused by the diuretic effects of caffeine. In addition, it interferes with the metabolism of some B-vitamins, such as thiamine (vitamin B1).
Caffeine may also reduce the absorption of manganese, zinc and copper. It also increases the excretion of the minerals magnesium, potassium, sodium and phosphate. There is also evidence that caffeine interferes with the action of vitamin A.
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.
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.
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.
VDR gene defects can lead to poor absorption and utilization of vitamin D in the body, which can lead to a more active immune system, worse symptoms and a faster progression of Hashimoto’s and hypothyroidism.
You see, more positive feedback loops resulting in more vicious cycles reinforcing an existing problem.
The big takeaway here is that all the factors mentioned in this article can lead to positive feedback loops or repeated problems that make each other worse. So if you have low stomach acid, leaky gut and you drink sodas, coffee and tea, you may be, unwittingly, causing your own health to decline.
And in this situation, taking supplements containing these vitamins and minerals may not do much good if you don’t address the root causes of the problems (like the low stomach acid and leaky gut) and start working on reducing the positive feedback loops that lead to this in the first place.
Because here’s the thing, these positive feedback loops can be reversed and you can achieve positive healing momentum if you get to the bottom of this and correct the underlying imbalances. I write all about how to do this in my new book, Roadmap to Remission.
In part 2 of this post, we’ll explore these micronutrients and look at best practices for correcting the causes of deficiencies and for supplementing them with food and supplements.
http://www.ncbi.nlm.nih.gov/pubmed/18341376 -Coffee interferes with T4 absorption
Benvenga, S. et. al. “Altered Intestinal Absorption of L-Thyroxine Caused by Coffee.” Thyroid. Volume 18 Issue 3, pages 293-301. March 2008 Abstract.
Mazzaferri, MD MACP, Ernest. “Thyroid Hormone Therapy,” Clinical Thyroidology for Patients: Summaries for Patients from Clinical Thyroidology. August 2008 Vol 1, Iss 1.
Sindoni, Alessandro et. al. “Case Report: Coffee Impairs intestinal Absorption of Levothyroxine: Report of Additional Cases,” Hot Thyroidology, Article 5/09
http://www.ncbi.nlm.nih.gov/pubmed/23039890 – Severity of Hashimoto’s corresponds with genetic defect
http://www.ncbi.nlm.nih.gov/pubmed/17669709 Effect of proton pump inhibitors on absorption of levothyroxine
http://www.ncbi.nlm.nih.gov/pubmed/23084636 Obesity and nutrient deficiencies linked to leaky gut
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2084394/ -Intestinal crosstalk, very interesting article on how this is all connected
http://www.ncbi.nlm.nih.gov/pubmed/7599455 caffeine and calcium
http://www.ncbi.nlm.nih.gov/pubmed/1564564 calcium, coffee and oesteoporisis
http://www.ncbi.nlm.nih.gov/pubmed/16758142 Swedish cohort on oesteoporosis and caffeine
http://www.ncbi.nlm.nih.gov/pubmed/6402915 inhibition of food iron by coffee
http://www.ncbi.nlm.nih.gov/pubmed/6896705 Effects of various drinks on iron absorption
Effects of caffeine on health and nutrition: A Review, Tsedeke Wolde Lecturer of Nutrition, Department of Public Health, College of Medical and Health Sciences, Wollega University, Nekemte, Ethiopia
The Thyroid, A Fundamental and Clinical Text, Ninth Edition. Lewis E. Braverman and Robert D. Utiger 2005
Menopause is an important time of transition for every woman, but when you also have Hashimoto’s it can be particularly challenging.
I recently attended a lecture called the Neuroendocrine Immunology of Perimenopause written by Dr. Datis Kharrazian. I learned a ton and I’ll share some of it, but I must say I was disappointed by the lack of references to Hashimoto’s and hypothyroidism. Fortunately, that disappointment led me to explore these topics further with Hashimoto’s in mind.
In this post we examine the physiological changes that women go through during this time of their lives and we show how these changes can be impacted by Hashimoto’s and hypothyroidism. And, as always, we explore why it matters.
For many women in the US and in cultures that have adopted our diet and lifestyle, menopause has become something to dread. It is associated with physical, emotional and psychological decline and for some also brings with it an increased risk of numerous other conditions.
And these other conditions are not minor. They include:
Cardiovascular disease and stroke
Dementia and Alzheimer’s disease
Autoimmune disease (Yes, that includes Hashimoto’s)
However, this is not true for everyone. And it is a relatively new phenomena, for much of recorded history and in many other cultures throughout the world menopause is just another transition in life.
Like the transitions from childhood to adolescence and adolescence to adulthood, the transition to menopause is just a transition. It lasts about a year and life goes on without major declines in health and well being.
Studying menopause across cultures is difficult, but the research has shown some possible differences in different countries and ethnic groups.
For example, Japanese women may report fewer hot flashes because they have a diet high in soy (which includes phytoestrogens) (Freeman & Sherif, 2007).
Within the medical literature there are different views on the relationship between body mass index (BMI) and hot flashes, with some studies linking a protective effect of body fat, others the opposite, and some finding no connections (Andrikoula & Prevelic, 2009; Chedraui et al., 2007; Freeman et al., 2001; Schwingl et al., 1994; Whiteman et al., 2003).
However more recently, Thurston et al. (2009) have found that body fat gains during the menopause, rather than high or low BMI, were associated with hot flash symptoms.
Women who smoke and have sedentary lifestyles have been found to report more menopausal symptoms. And this makes sense when you look at what is happening physiologically which we will explore shortly.
Reproductive history may also be relevant; for example, in the Mayan culture women marry between the ages of 14 and 18 years, have many children and few repetitive menstrual cycles.
Mayan women usually enter the menopause in their early to mid 40s, which is about 10 years earlier than women in the UK and North America (Beyene, 1989).
Regardless of your cultural background, there are some important changes that take place in the body during peri-menopause and menopause and these can be amplified when you also have Hashimoto’s.
Of course, everything in the body happens for a reason and is caused by specific mechanisms. For example, in a moment I’ll explore the most common perimenopausal symptoms and the mechanisms or causes that lead to them.
But before I do, I want to share an observation that is a really important mindset for making the transition to menopause far gentler and less destructive.
After looking at all this research, one thing I realized is that the problems and more severe symptoms that are caused by this transition are entirely preventable if you prepare for them and take action before they happen.
And even if you have already gone through this transition, taking these preventative measures will also reduce your risk of developing some of the serious conditions we mentioned above.
Here’s a simple way to think about it: treat your body in the years leading up to perimenopause just like you would when you are pregnant. Don’t smoke, don’t drink excessive amounts of alcohol, don’t over indulge in refined sugars and junk food.
Reduce stress, get moderate amounts of exercise and heal the parts of your body that may be compromised. In particular, focus on healing your brain, your gut, your adrenals and do everything you can to reduce inflammation.
If you have read any of our other materials or my new book, Roadmap to Remission, you will notice that these are all important areas to heal when you have Hashimoto’s, as well.
Here’s an overview of the most common symptoms of perimenopause and some of their potential causes.
1. Systemic inflammation and pain: This is caused by surges in certain immune cells and proteins called cytokines. Cytokines like IL-6, IL-1 and TNF-alpha are all implicated in Hashimoto’s, as well.
2. Multiple food sensitivities, gastrointestinal symptoms. These are often caused by Intestinal permeability or “leaky gut”: This maybe caused by declines in estrogen, increases in cortisol production, hypothyroidism and dysfunction in the gut. Intestinal permeability is ground zero for autoimmunity, as well.
3.More stress, poor sleep, fatigue during the day. The adrenals have to do additional work when other female hormones, like estrogens decline. Adrenals issues are also very common with Hashimoto’s.
4. Poor circulation, cold hands and feet, poor nails beds, fungal overgrowth in nail beds. This is caused by problems with peripheral circulations, especially in the small vessels. And may be due to altered nitric oxide function. These symptoms are also very common with Hashimoto’s.
5. Brain fog, depression, memory loss and poor cognitive function. This is due to inflammation in the brain and deficiencies or declines in neurotransmitters. These are some of the most common symptoms of Hashimoto’s.
6. Hot flashes, night sweats. A hallmark of perimenopause caused by altered FSH (follicle stimulating hormone) and feedback from the ovaries. This is a less common symptom of Hashimoto’s but something many women experience.
7. Poor bone density. This is caused by problems in osteoclast or bone cell formation and other issues. It is also a very real concern for Hashimoto’s patients, as well. One of the major causes of this breakdown in bone health is the cytokines that we spoke about above.
Now, let’s dive a little deeper and look at what to do about each of these symptoms.
Hashimoto’s is, as we all know, an autoimmune disease. One of the hallmarks of autoimmunity is an overly excited immune system and this can be seen in high levels of substances called cytokines.
The root of autoimmunity and the damage it causes in the body is inflammation. many of these cytokines help promote this inflammation.
When you go through the changes of menopause, estrogen levels decline and estrogen calms inflammation. So if you already have an overexcited immune system producing lots of cytokines, you may have a major surge during peri-menopause and menopause.
Other signs of cytokines include:
1. Brain inflammation: brain fog is a clear sign
2. Body fat: adipose tissue produces cytokines
3. Free radicals: this causes inflammation
4. Stress: it’s very inflammatory
Declines in estrogen can lead to cells being more responsive to cytokines and more receptors and messengers that just amplify this inflammation. This can stay elevated even after estrogen replacement therapy.
In my opinion, the breakdown of the intestinal lining that results in leaky gut and intestinal permeability is an important battlefield in healing Hashimoto’s.
Well, declines in estrogen production can lead to breakdowns in the gut, as well. When this happens you may develop leaky gut, as wells leaks in the blood brain barrier.
And these leaks cause the immune system to get all fired up and it creates more of the cytokines we just mentioned above.
It’s a classic vicious cycle made worse by estrogen levels declining.
During and after the transition of menopause the adrenal glands step in and take over for the ovaries.
Essentially, what happens is this.
FSH (Follicle Stimulating Hormone) receptors in the ovaries begin to lose sensitivity during perimenopause. This leads to changes in levels of FSH and estradiol.
The adrenals, in turn, step in and create more adrostenedione, a steroid hormone and this is converted to estrogen by adipose (fat) tissue. It’s the body’s way of compensating for declines in estrogen.
Obviously, there is a potential problem here if the adrenals are already taxed or exhausted. A lot more demands are made on them in perimenopause.
So adrenal health is very important prior and during this transitional time.
Circulatory issues are very common with patients with Hashimoto’s. This is due to many factors including systemic inflammation, and the tendency for the body to compensate for hypothyroidism by bringing blood from the extremities into the body.
This sometimes occurs because the body is trying to regulate blood pressure and hypothyroidism, at least at first, can cause low blood pressure.
Another issue that leads to poor circulation in the extremities is lower plasma volume. This is caused by the capillaries becoming more permeable and when this happens albumin and water can leak from the vessels into the intestinal spaces.
This causes swelling from edema and water retention, often in the ankles and lower legs. Of course increased swelling is going to impact circulation, as well.
I have written quite a bit about the profound impact of Hashimoto’s on the brain and it is an area that I am very passionate about. If you aren’t familiar with this, here’s a previous post on brain fog.
In a nutshell, hypothyroidism and autoimmunity can both lead to inflammation in the brain. This is caused by many things including breakdowns in the blood brain barrier, blood sugar imbalances, adrenal stress and more. In addition, as estrogen declines during menopause and peri-menopause the body loses it’s anti-inflammatory effects.
The result of all of this is a massive reaction by the brain’s immune cells, the microglia. These cells have no real off switch so once they get activated it can be difficult to calm them down. And when they are called into action they can cause more inflammation and destruction of brain cells and neurons.
All of this results in that all too familiar feeling of brain fog, difficulty concentrating, focus problems and all the associated emotional issues of isolation, depression and anxiety.
The exact mechanism for hot flashes is not known. But there are many interesting theories.
Robert R. Freedman has studied hot flashes for 25 years. He and his colleagues measured skin temperature, blood flow, and skin conductance (an electrical measure of sweating) in menopausal women before, during, and after hot flashes.
They found that women who have hot flashes have a lower tolerance for small increases in the body’s core (innermost) temperature than women who don’t have hot flashes. The body tries to keep its core temperature within a comfortable “thermoneutral zone.” When our core temperature rises above the zone’s upper threshold, we sweat; when it drops below the lower threshold, we shiver.
Women who don’t have hot flashes have a thermoneutral zone of several tenths of a degree centigrade. But in women with hot flashes, this thermoneutral zone is so narrow, it’s “virtually nonexistent,” according to Freedman.
As a result, small variations in core body temperature — by as little as one-tenth of a degree centigrade — that don’t trouble some women trigger hot flashes (and chills) in others.
What causes the thermoneutral zone to narrow? One theory is that elevated levels of the brain chemical norepinephrine are involved. Norepinephrine has been shown to reduce the thermoneutral zone in animals.
Interestingly, patients with hypothyroidism often have elevated levels of norepinephrine. One theory is that hypothyroidism can cause changes in blood flow (hemodynamics). One thing the body does to compensate for less blood flow is to release more norepinephrine. So you can see, hypothyroidism could make this symptom worse.
Oesteoporosis is a major concern for both Hashimoto’s and menopausal women. One common factor in both is the IL-6. This cytokine is a major predictor of bone loss in women, especially in the first decade of menopause.
These pro-inflammatory immune proteins are also involved in the body’s reabsorption of bone. In addition, one of the roles of estrogen is to slow the break down of bones.
What the research seems to suggest is that the combination of increased cytokines and decreased estrogen leads to more bone loss. It’s a perfect storm of inflammation and natural transitions.
With thyroid disorders bone loss is also a major issue. Too much thyroid hormone can lead to to increased bone mineral resorption and calcium loss through kidneys. (One reason why it’s so important to not take too much thyroid hormone.)
Also, hypothyroidism can lead to problems with the bones. It seems that there is increase in bone density in adult subjects with hypothyroidism, but the bone quality is poor which is responsible for the possible increase in fracture in these patients.
Isn’t that always the million dollar question?
Well, if you’ve read any of my writing you’ll know my answer it, “It depends.” And it does, you have to address the problems.
So, let’s review the problems and look for common issues. That will tell us what we should do.
Here are the main issues we identified:
Ok, well we identified that inflammation and pro-inflammatory cytokines are at least partly responsible for brain fog, hot flashes, bone loss and, of course systemic inflammation.
So, dealing with inflammation, the root of all evil is pretty darn important.
What can we do for inflammation?
Well, boosting Vitamin D is super important, especially because of it’s role in bone health. Other anti-inflamatories like turmeric, glutathione, resveratrol, and also avoiding foods that are pro-inflammatory like gluten, dairy and soy.
2. Declines in Estrogen:
We also noted that declines in estrogen can lead to all of the above, plus leaky gut. And there are 2 ways to deal with this. Heal and empower the adrenals to take over, or supplement with hormone replacement therapy.
Hormone replacement therapy comes with it a number of risks. Breast and ovarian cancer being top of the list.
Also, according to a study in the New England Journal of Medicine, June 7th 2001 on women treated for thyroid cancer found that about 40% of women taking thyroid hormone had decreases in their blood levels of thyroxine. These levels were low enough to trigger hypothyroid symptoms, such as low energy and feeling tired, sluggish, and cold, or to put them at risk for regrowth of thyroid cancer.
In addition, estrogen has also been linked to increased metastasis of thyroid cancer. And radioactive iodine therapy has been linked to a increased risk of breast cancer in some studies.
Some herbs that are helpful for healthy estrogen metabolism are: tribulus, panax ginseng, dang guy, black cohosh, redeliver leaf, isoflavones from soy (sometimes called phytoestrogens may also help, but must be used cautiously with Hashimoto’s patients), cruciferous vegetables can also helpful in estrogen metabolism, and vitamins that support methylation like B6, B12 and folic acid are also helpful for clearing out dangerous estrogen metabolites.
3. Leaky Gut
In my opinion, leaky gut is ground zero for autoimmunity and Hashimoto’s. It also happens to be a major factor in preimenopause. Estrogen reduces permeability of the intestines by strengthening the tight junctions of the intestinal walls.
As etsrogen levels decline, intestinal permeability risk increases. Add Hashimoto’s and hypothyroidism to the mix and you have a potent recipe for leaky gut.
To heal leaky gut avoid the foods that can make it worse: eliminate gluten, dairy and soy. Consider trying a diet like the Autoimmune Paleo diet. Drink bone broth, kombucha tea and water keifer.
4. Adrenal Health
If you elect not to do estrogen replacement therapy, then your adrenals become very important for your health and well being.
And stress management becomes absolutely essential.
For the adrenals: phosphatidylserine, adaptogenic herbs like Siberian ginseng, holy basil, rhodiala are beneficial. As is licorice root, DHEA, B vitamins, B 1 and B 2 and more.
All of these herbs and vitamins shouldn’t be taking randomly in what I like to call “the supplement lottery”. You should first do a proper assessment of each system of the body and then determine which supplements may be appropriate.
Also, having a real stress strategy and not just an abstract understanding of the destructive effects of stress is also critical. Yoga, qi gong, meditation, prayer, massage therapy, acupuncture, walking in Nature, having fun are effective for treating stress.
Any and all of these activities must become a regular part of your life. In fact, if you do anything you should err on the side of too much relaxation and stress treatment. Stress is very inflammatory, not treating it is just not an option.
I provide a detailed discussion of proper assessment in my new book, How to Heal Hashimoto’s: An Integrative Roadmap to Remission,published by Hay House.
The Neuroendocrine Immunology of Perimenopause, 2015, Dr. Datis Kharrazian
http://www.natural-menopause-journey.com/perimenopause-symptoms-and-culture.html: menopause differences in different cultures
Freeman, E.W., Sammel, M.D., Grisso, J.A. et al. (2001). Hot flashes in the late reproductive years: Risk factors for African American and Caucasian women. Journal of Women’s Health & Gender-Based Medicine, 10(1), 67–76.
Freeman, E.W., Sammel, M.D., Lin, H. et al. (2005). The role of anxiety and hormonal changes in menopausal hot flashes. Menopause, 12(3), 258–266.
Freeman, E. & Sherif, K. (2007). Prevalence of hot flushes and night sweats around the world. Climacteric, 10, 197–214.
Andrikoula, M. & Prevelic, G. (2009). Menopausal hot flushes revisited. Climacteric, 12, 3–15.Avis, N.E., Crawford, S.L. & McKinley, S.M. (1997). Psychosocial behavioural and health factors related to menopause symptomatology. Womens Health, 3, 2, 103–120.
Avis, N.E., Stellato, R., Crawford, S. et al. (2001). Is there a menopausal syndrome? Menopausal status and symptoms across racial/ethnic groups. Social Science and Medicine, 52, 345–356.
Hunter, M.S., Gupta, P., Papitsch-Clark, A. & Sturdee, D.W. (2009). Mid–aged health in women from the Indian subcontinent (MAHWIS): A further quantitative and qualitative investigation of experience of menopause in UK Asian women, compared to UK Caucasian women and women living in Delhi. Climacteric, 12(1), 26–37.
Thurston, R.C., Sowers, M.F.R., Sternfeld, B. et al. (2009). Gains in body fat and vasomotor symptom reporting over the menopausal transition. The Study of Women’s Health Across the Nation. American Journal of Epidemiology, 170(6), 766–774.
Beyene, Y. (1989). From Menarche to menopause: Reproductive lives of peasant women in two cultures. Albany, NY: State University of New York Press.
Freedman, RR. Seminars in Reproductive Medicine 2005; 23 (2): 117-125.
http://www.ncbi.nlm.nih.gov/pubmed/19433574 Estrogen and Leaky gut
http://www.ncbi.nlm.nih.gov/pubmed/11844745 Changes in proinflammatory cytokine activity after menopause
http://www.ncbi.nlm.nih.gov/pubmed/9507566 Changes in enzymatic antioxidant defense system of women after menopause
http://www.ncbi.nlm.nih.gov/pubmed/11344203 IL-6 as a predictor of bone loss
http://www.ncbi.nlm.nih.gov/pubmed/6467635 : Plasma elevations of norepinephrine
http://hyper.ahajournals.org/content/5/1/112.full.pdf Hypothyroidism and hypertension
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3169869/ Thyroid disorders and Bone Loss
http://www.hindawi.com/journals/ije/2013/941568/ Estrogen and Thyroid Cancer metastasis
http://www.ncbi.nlm.nih.gov/pubmed/12182054 : Hormone Replacement therapy after thyroid surgery
Hashimoto’s affects so many different systems of the body. One of the main reasons is that thyroid hormone affects so many different activities.
One of the most complex areas of interaction is that of the thyroid and female hormones.
Having some idea of these relationships can be helpful in understanding what is happening in your body. And may help shed light on some symptoms you are having.
Also, once you understand, then you can start working on a plan to fix them.
(But fair warning, your doctor, even your endocrinologist may not understand these interactions and may have even less of idea of what to do about them.)
In the body there are 2 different kinds of feedback loops: positive feedback and negative feedback. These can both play a major role with Hashimoto’s and hypothyroidism.
And the irony is that positive feedback can result in really negative outcomes, while negative feedback generally helps to keeps things in balance which results in positive outcomes.
Positive Feedback Isn’t So Positive
Positive feedback is the feedback of repetition and reinforcement. You get something created from a behavior, habit or health issue and it keeps reinforcing itself.
Take progesterone and Hashimoto’s, for example.
If you take progesterone AND you’ve got Hashimoto’s, taking external progesterone may stimulate your thyroid gland to become more active–increase levels of TPO–and fan the flames of that autoimmune attack on TPO.
What are the signs that progesterone is worsening the Hashimoto’s, or maybe even triggering it?
You could have more fatigue, more hair loss, more depression. You could actually make the symptoms that you thought you were treating with the progesterone worse.
Many women go into a doctor’s office, be it a acupuncturist or a medical doctor or naturopath, complaining of symptoms like depression, hair loss, low libido…and the doctor thinks that that person has a hormonal problem such as a progesterone “deficiency” or “estrogen dominance”.
And the well-meaning practitioner may prescribe creams or oral progesterone and then—the symptoms get worse.
If your symptoms get worse with progesterone that’s a good sign you probably DO NOT have a progesterone deficiency or estrogen dominance.
Instead, it may have caused a flare up of Hashimoto’s.
Adding more progesterone just added to the positive feedback loop.
This whole thing is reinforced and repeated and just builds on itself. This is how vicious cycles are born and how they continue to progress and make things worse. Adding insult to injury.
Negative Feedback Isn’t That Negative
Negative feedback is your body’s way of course correcting.
For example, with thyroid hormone, when too much thyroid hormone is produced, the body responds and signals the thyroid to stop making so much.
Neurons in the hypothalamus secrete thyroid releasing hormone (TRH), which tells cells in the anterior pituitary to secrete thyroid-stimulating hormone (TSH).
TSH binds to receptors in the thyroid gland, stimulating the making and release of thyroid hormones, which affect virtually all the cells in the body.
When blood concentrations of thyroid hormones increase above a certain threshold, TRH-secreting neurons in the hypothalamus are inhibited and stop secreting TRH.
One of the things we often see when working with Hashimoto’s people is the complex nature of feedback loops causing a web of problems.
Positive feedback or the feedback of reinforcement leads to one system breaking down and causing a domino effect in others.
The only way to alter these feedback loops is to address all the different parts simultaneously.
That way you can reverse the negative trends and create positive healing momentum.
To add another layer of complication the endocrine system has a number of negative feedback loops that help to regulate and balance other things.
For example, high levels of estrogen suppress the secretion of FSH (follicle stimulating hormone).
So there are naturally occurring positive (reinforcing) and negative (suppressing or counterbalancing) feedback loops happening all the time.
Endocrine function does not go in just one direction. The various female hormones affect thyroid metabolism and thyroid hormone affects how these hormones work in the body too.
So fasten your seat belts because it’s going to get complicated, but I’m going to make as easy as I can.
Let’s Review Some Physiology
First thing we should do before we dive in is to review what happens in a woman’s cycle hormonally. Then we can look how each hormone is impacted by Hashimoto’s and hypothyroidism.
Follicular Phase: Days 1-5: Estrogen Drops and FSH Rises
Menstrual bleeding begins on day 1 and normally lasts about 5 days. During the last few days leading up to day 1 there is a sharp fall in levels of estrogen and progesterone. This signals the uterus that pregnancy has not occurred during the cycle.
This signals starts the shedding of the endometrial lining of the uterus. Since estrogen suppresses FSH, when estrogen levels drop FSH levels rise. Follicle stimulating hormones, stimulate, yup, you guessed it the follicles.
By day 5-7 of the cycle, one of the follicles responds to FSH and becomes the dominant follicle.
When it does it starts releasing lots of estrogen.
Midcycle: Days 6-14: Estrogen Rises and FSH Falls
All good things must come to pass so the large amounts of estrogen released by the follicle during this phase has several important effects.
The endometrial lining of the uterus becomes thicker and is prepared for the fertilized egg. When this happens FSH gets suppressed (through negative feedback).
At about midcycle, this estrogen spike and FSH fall leads to the release of luteinizing hormone (LH).
This is known as an LH surge and this leads to a sudden rise in body temperature which is a sign that ovulation is about to happen.
This LH surge causes the follicle to break and send an egg into the fallopian tube.
Luteal Phase: Days 14-28 Estrogen and Progesterone First Rise, Then Fall
After the follicle frees the egg, its walls collapse and this is called the corpus luteum.
Right after ovulation, the corpus luteum begins secreting large amounts of progesterone, which also helps prepare the lining of the endometrium to accept and nurture the fertilized egg.
If the egg is fertilized, a small amount of a hormone called human chorionic gonadotropin (HCG – the hormone that is used in a popular diet treatment) is released.
HCG keeps the corpus luteum strong so it can keep pumping out estrogen and progesterone. This keeps the endometrial lining strong and intact.
By about week 6 to 8, if pregnancy has occurred then the newly formed placenta takes over and starts secreting progesterone.
Thyroid hormone affects all of this and all of this affects thyroid hormone.
Hypothyroidism Messes with All of This
When women have hypothyroidism, a common problem is an increase of another hormone called prolactin.
This causes less of a release of LH, and a loss of progesterone receptor site sensitivity, and a loss in sensitivity to FSH in the follicle.
All of these losses lead to problems with ovulation, and they also mess with the communication to the pituitary gland.
Hypothyroidism can lead to lower levels of LH. Which means you don’t get an LH surge, which means ovulation may not happen properly.
Using birth control pills on top of this can further harm the communication and feedback loops in this system.
Using herbs to stimulate the ovaries or the reproductive system may also not work unless the hypothyroid issues are corrected.
Studies have found that even mild hypothyroidism may cause ovarian problems.
Testing thyroid function is very important with women who suffer from infertility, especially if they have elevated prolactin or they can’t ovulate.
Also, hypothyroidism can cause the development of ovarian cysts.
We looked at that in detail in a previous post where we look at the connection between PCOS and Hashimoto’s.
Hypothyroidism may also lead to low FSH levels, which may lead to immature follicles and infertility.
Suppressed LH levels will often lead to problems with ovulation in timing or abnormal luteal phase progesterone levels.
These changes may cause miscarriage, depression in the second half of your cycle, or migraines in the second half of your cycle.
To summarize, hypothyroidism can cause:
* A decrease in FSH release and FSH receptor sensitivity, this leads to problems with the development of the follicle and infertility
* Suppressed LH which leads to problems with ovulation and abnormal progesterone levels, this leads to abnormal cycles and infertility
* Progesterone receptor insensitivity which also leads to abnormal cycles and infertility
* Increased Prolactin, which leads to problems with ovulation, abnormal menstrual cycles and infertility
Prolactin has a very close relationship to dopamine, thyroid hormone, progesterone and serotonin.
All of these hormones and neurotransmitters affect each other. For example, low dopamine and progesterone can suppress TSH.
Also, hypothyroidism can affect the adrenals directly. It can cause too much cortisol to be released or over time exhaust the adrenals.
And this also suppresses TSH. So what happens is you get weird mixed test results and symptoms.
Mixed Messages and Confusing Signs
The presentation looks like this: TSH is normal or even slightly low, but you have a ton of hypothyroid symptoms and your T4 is low.
It doesn’t make sense. Everyone is confused. Well, it’s this complex dance of hormones that may be causing this.
Something else that is interesting to note is that high cortisol, which can be caused by hypothyroidism can dampen the activity of the enzyme that converts T4 into T3 (5 alpha deodinase).
So what happens is high cortisol causes low T3.
Estrogen increases thyroid binding globulin levels. These are the proteins that bind to thyroid hormone and keep it from working.
We see this with normal TSH and low free thyroid hormones (free T3 and free T4). This can happen with birth control pills.
This also explains why some women with hypothyroidism and Hashimoto’s experience tachycardia, tremors and hypothermia every month before their cycle.
Progesterone up-regulates TPO (the enzyme thyroid peroxidase). This is why when women ovulate, their temperature goes up.
During ovulation, the surge of progesterone stimulates TPO.
When this happens there is a surge in thyroid hormones produced, that makes the temperature rise.
Women with low progesterone can also have less thyroid hormone than their body needs (even thought this isn’t always visible on a lab test.)
But they might have both low thyroid and low progesterone symptoms.
Symptoms of low progesterone include heavy menstrual cycle, inability to lose weight, mid-cycle luteal phase depression, headaches, etc.
It is interesting to note that problems with progesterone are often not caused by your body being unable to make enough progesterone, rather they are caused by some sort of problem with the pituitary gland.
There are a number of axises involved with the pituitary, the adrenal-pituitary, thyroid-pituitary and ovarian-pituitary connections can all affect each other and can lead to problems with this communication system.
This is always a better place to attempt treatment before adding external progesterone which can actually make Hashimoto’s symptoms worse.
Obviously, this is not something that a single pill is going to correct. Rather than look for the drug or supplement to solve the problem let’s look at how hormones behave and see how we can improve that.
The physiologic effects of hormones depend largely on their concentration in blood and extracellular fluid. Disease and health problems happen when hormone concentrations are too high or too low.
First thing to do is to test to determine whether or not you have enough hormone in your body. As we saw above with progesterone therapy, this can make matters worse if you supplement when you already have enough.
If there isn’t enough, you should consult your physician to help your body get or make more.
This can be done naturally or with supplementation and involves many different treatment options that are beyond the scope of this post.
If there is enough of a given hormone in the body how do we get them to work better?
Well we need to get enough hormone to the target tissue so that it can work. The concentration of hormones is determined by 3 things:
1. The rate of production. How do you improve the rate of production? Well, firstly make sure you have enough of the raw materials in the body to make them.
Many important reproductive hormones are made from cholesterol.
While cholesterol often gets a bad rap, when it comes to hormone production and synthesis it’s critical.
A cholesterol lower than 150 means you may not have enough of the raw materials to make estrogen, progesterone, cortisol and many other important hormones in the body.
Here are some foods high in cholesterol: eggs (especially fish eggs), liver, fish, shellfish, shrimp, bacon, sausages, red meat, and brain which has the highest amounts (all you zombies, take notice).
Then look to improve the feedback mechanisms. Positive feedback can improve this.
2. The rate of delivery. Blood flow makes a huge difference for hormone delivery. If you are anemic and/or have low blood pressure you can pretty much guarantee that you won’t be able to deliver optimal amounts of hormones to your body’s tissues.
High blood flow delivers more hormone than low blood flow. This is a very important fact that is often ignored or disregarded, yet it makes a huge difference physiologically.
3. Rate of degradation and elimination.
Hormones all break down and are reabsorbed by the body, but things like a clogged liver and enhanced negative feedback loops can affect the amount of hormones that are released.
Thyroid hormones are basically a “double” tyrosine with the critical incorporation of 3 or 4 iodine atoms.
The circulating halflife of thyroid hormones is on the order of a few days. They are inactivated primarily by intracellular deiodinases.
Systemic inflammation, out of control blood sugar and high cortisol can all affect the activity of these enzymes.
As we stated above, female hormones like estrogen and progesterone are steroid hormones derived from cholesterol.
The thing that can limit the production of these hormones is the conversion of cholesterol to pregnenolone. Chronic stress can cause something called a “pregnenolone steal” where pregnenolone is siphoned off to make cortisol and is not available for other steroid hormone production.
So reducing stress and balancing blood sugar are also critical for the production of estrogen and progesterone.
Obviously, this is not easy to fix nor is it simple to figure out and correct.
However, doing a proper workup, and working with someone who understands positive and negative feedback interactions and creating an action plan that will use your body’s natural tendencies to your advantage are all important factors in getting better results.
At Hashimoto’s Healing we off a free 30 minute Discovery Session where we’d be happy to discuss this process with you. (Fair warning these are very popular and are currently booked 3 to 4 months out)
If you would like to speak to Marc sooner please contact us here.
http://www.ncbi.nlm.nih.gov/pubmed/25750078 : L/T4 supplementation : These findings suggest that the thyroid gland and peripheral tissues are integrated in the physiological process of T3 homeostasis in humans via a feed-forward TSH motif, which coordinates peripheral and central regulatory mechanisms. Regulatory and capacity deficiencies collectively impair T3 homeostasis in L-T4-treated patients.
http://www.ncbi.nlm.nih.gov/pubmed/1585690 : Higher free T3 levels with birth control?
http://www.ncbi.nlm.nih.gov/pubmed/3107297 : Value of measuring free fractions
http://www.ncbi.nlm.nih.gov/pubmed/23184912: TSH testing not adequate
http://www.ncbi.nlm.nih.gov/pubmed/15588378 : short feedback
http://www.ncbi.nlm.nih.gov/pubmed/15481810: TRH feedback regulation
http://www.ncbi.nlm.nih.gov/pubmed/16876577: TRH Neurons
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3520819/ Elevated TSH and elevated cortisol: These studies all taken together suggest a physiologic feedback loop where lower thyroid function increases cortisol, but cortisol feeds back to reduce TSH; this hypothesis is consistent with the observations that in the case of primary hypothyroidism (elevated TSH) cortisol is elevated, but in the setting of primarily elevated cortisol TSH is suppressed.
http://www.ncbi.nlm.nih.gov/pubmed/16793944 – The effects of sex-steroid administration on the pituitary thyroid axis
Ben-Rafael Z, Mastroianni L, Strauss JF, Flickinger GL, Arendasch-Durand B. Changes in thyroid function tests and sex hormone binding globulin associated with treatment of gonadotropin. Fertil Steril. 1987: 48;318-320
Malarkey WB, Strauss Rh, Leizman DJ, et al. Endocrine effects in female weight lifters who self administer testosterone and anabolic steroids. Am J Obstet Gynecology. 1991;165:1385-90
Knopp RH, Bergelin RO, Wahl PW, Walden CE, Chapman MB. Chemical alterations in pregnancy and oral contraceptive use. Obstet Gynecol 1985;5;66:682-90
The Thyroid, A Fundamental and Clinical Text, Ninth Edition, Braverman and Utiger, 2005
Functional Endocrinology, Dr. Datis Kharrazian, 2007
Pearl Thomas and Fabienne Heymans have both worked with me to get their Hashimoto’s into remission. I knew that they were both in New York and I suggested that they meet and support one another.
A short time later they contacted me about their passion to create a non-profit dedicated to people suffering from Hashimoto’s Thyroiditis.
I knew without hesitiation that this was an organization I wanted to support. I am proud to be on the Advisory Board of Hashimoto’s Awareness, the organization that they created.
Here are their stories:
Pearl and I were simultaneously raising awareness of the disease individually, holding our own support groups, had active Facebook pages, and we were exploring ways to expand.
At the time, Marc Ryan L.Ac. and functional practitioner, was giving us both consultations separately. One day, he suggested that we connect because we were both living in New York City and had the same passion to be of service to the Hashimoto’s Community.
On March 16, 2014, we met in Hu-Kitchen; now, our favorite paleo diet restaurant on 5th Ave. We immediately saw the possibility of creating something bigger than ourselves together! Our combined energy was effervescent and both of our big dreams coincided with each others.
We were both in remission from Hashimoto’s and passionate about sharing our journey with all who were still struggling with the disease. It was simply serendipitous! We became teammates and dear friends to-be. Together, we became unstoppable.
We immediately filed for a non-profit organization known as HA! Today, we have launched a campaign on Crowdrise.com and with the funds we are starting to organize the very first National Conference for Hashimoto’s Thyroiditis!
It is truly by accident that I was diagnosed after being sick nearly all my life. I experienced highs and lows, as you all know, I am sure! The symptoms included brain fog, extreme fatigue, joint pain, hair loss, thinning skin, sensitivity to perfumes, just to name a few.
By February 2012, my immune system was at its worst! Menopause only made matters worse. I was scheduled for surgery to remove one of my parathyroid glands which was inflamed to twice its normal size!
The scan of the thyroid gland showed many patches on the tissue and a biopsy confirmed Hashimoto’s Thyroiditis. Yeahh, thank you God!!
Ironically, one of the best days of my life!! I finally had an answer to my question about why I had all these symptoms. I finally confirmed that, “NO, I wasn’t crazy” all these years!
The surgery was supposed to be a minor procedure. But, my body, after fighting all these years, on every level of my being, was emotionally, psychologically and physically exhausted.
After the surgery, I was not waking up from the anesthesia. The entire day went by and still I wasn’t coming back from the place between life and death.
To keep the story short, I finally woke up with the determination to make a difference for all the people that are in despair, struggling with Hashimoto’s, and who don’t know how or where to look for support.
All my life, the medical field insisted that all my lab tests were normal and therefore they claimed that my symptoms must be of psychological origin. I promised myself that no one should ever be in this position ever again and from there everything changed!
After reading Dr. Datis Kharrazian’s book, Why Do I Still Have Thyroid Symptoms? When My Lab Tests Are Normal I researched and found a Functional Practitioner in NYC. I learned the critical importance to stop eating gluten completely.
I started taking the right supplements according to Dr. Kharrazian’s protocol and I started feel significantly better.
Although the journey is ongoing, I have a strong support system and a great community as a resource when I need it. Today, I live a productive life in NYC and dedicate my days to empowering others with Hashimoto’s to live a symptom-free life.
I was diagnosed with Hashimoto’s Thyroiditis in February of 2012. I was fortunate enough to have been referred to a wonderful integrative physician who gave me proper testing for early diagnosis. Months leading up to my appointment, my personal trainer noticed my energy levels going down in our high intensity workouts.
I was cranky, my hairline was thinning and I was experiencing 2-3 inch hives on my calves, that were itchy, brown colored and stuck around up to three weeks. I took action and made an appointment for blood work.
Two weeks later, at my follow-up appointment, I was diagnosed. My TSH and TPO levels were off the charts. I was instructed to start a natural hormone medication Nature-throid, stop eating gluten, wheat, soy, and dairy and was instructed to start adding supplements such as Liquid D3, B-12, Omega 3’s, probiotics, and meditation. (Speak to your doctor before trying supplements to be sure they are right for you.)
At the time, I realized this was a serious condition and it was time to act NOW. I chose to start doing some research.
Fortunately, I stumbled across a book by Dr. Datis Kharrazian, who some call, the Functional Medicine Guru, the book is called, Why Do I Still Have Thyroid Symptoms? When My Lab Tests Are Normal and I started reading.
I found out that Hashimoto’s disease was killing my immune system, brain function, and circulatory system. Everything he wrote about from vitamin deficiencies to recommending a diet free of gluten, soy, wheat, corn and eggs; I was dumbfounded.
This book was my best friend. His research gave me hope that I could put this disease in remission quickly. I followed his protocol diet and began my journey to remission.
Six months later after following Datis’s protocol diet, I was sleeping better, finally losing weight, my hair was thicker, and I was no longer depressed or experiencing anxiety attacks. It was working. Changing my diet was working! I then went for my next round of blood work and my results came back, my TSH and TPO were now in normal range!
My doctor stated, “You are a miracle walking. I have not yet seen someone’s levels go up so quickly.” I was in full remission from the disease. And in that moment, I knew this was possible for others.
Today, after three years in remission, I’ve dedicated my life to being of service in the Hashimoto’s community. And through that, I am the Co-Founder and Co-Creative Director of the not-for-profit, Hashimoto’s Awareness.
I work alongside an incredibly talented and driven friend and kindred spirit, Fabienne Heymans, who is also in remission from the disease.
As we work with some of the top experts in the community, we have a great vision for this organization and how we might be of service in many ways to others.
We are committed to bringing clarity to the community that is in need of education on this serious disease and we believe we will make the difference worldwide.
What I will share with others struggling with the disease is that you are not alone. Remission is possible if you’re willing to do the work.
We are here to support you in an empowering way and we promise your journey to remission will be inspiring, powerful, and supported by a community that stands as your greatest fans.
About Hashimoto’s Awareness
We are committed to bringing clarity to the community of people suffering from the auto-immune disease, Hashimoto’s Thyroiditis. According to the AACE, 30 million people in the United States are diagnosed with hypothyroidism and 90 percent of those people have Hashimoto’s Disease.
HA is a registered 501(c)(3) non-profit organization.
We invite you to join us on our campaign page HASHIMOTO’S AWARENESS CAMPAIGN: “HEALING TOGETHER”!
Your donation allows HA to drive diagnosis and treatment of Hashimoto’s Thyroiditis through education, advocacy and advancing research.
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.
· WP Thyroid
· Most generic brands of levothyroxine
· Some compounded medications- check with your pharmacist
· Armour Thyroid
· 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://www.rxlist.com/tirosint-drug.htm – Tirosint