November 2015 – Hashimotos Healing

Archive Monthly Archives: November 2015

Guest Post: Shannon Garrett and Her Hashimoto’s Success Story

Shannon Garrett Fall 2015 Headshot Cream Blouse_Final

My Personal Story
One of the responsibilities of a nurse is to educate patients about their medication(s) and to assess and monitor for symptoms of adverse reactions or side effects.

As a previous cardiac nurse, I’ve observed my share of medications that cause significant side effects, many of which were severe.

One of the reasons I became a holistic and integrative nurse in private practice was to help people discover how they could take care of their health, mind, body, spirit, and emotions through healthy lifestyle choices and eating real food.

My second reason is because after 8 long years of seeing several doctors, I was diagnosed with 3 autoimmune diseases: Hashimoto’s thyroiditis, pernicious anemia, and celiac disease.

My only knowledge with respect to medication for use in autoimmune disease at that point was of immune system suppressants such as Remicade, prednisone, Imuran and others.

As a nurse, I knew I didn’t want those because they carry significant health risks. So I set up business not only to help my clients, but also to help myself in the process.

I decided to follow many of the suggestions commonly recommended by functional medicine practitioners today. I was tested for food sensitivities, underlying co-infections such as H. pylori, Epstein-Barr virus, Lyme disease, Yersinia entercolitica and Candida overgrowth. I was also tested for adrenal fatigue, vitamin deficiencies, and had the Genova gut health test.

I had eliminated gluten and dairy within one week of receiving my diagnoses simply because I knew they wreaked havoc on the system and their potential for inflammation.

I was pleased when my kidney filtration rate increased by 20 points after 60 days simply by eliminating these two proteins from my diet!

Fortunately, I did not have any underlying co-infections to deal with. I did have an adrenal fatigue issue. However, after approximately 9 months of commitment to lifestyle changes, healthy eating and reducing stress, my thyroid antibodies hadn’t really moved much.

I was devoted to an anti-inflammatory diet based on my test results, healing my gut, reducing stress, optimizing vitamin & mineral deficiencies, and balancing my hormones.

Although I felt slightly better, I hadn’t really lost the weight I’d expected, and I knew with an immune system that was still “confused” about what was my tissue and what was foreign was the perfect storm for additional autoimmune illnesses.

In the past, I’ve cared for patients in the clinical setting who struggled with multiple autoimmune diseases (some 8 and 9) and their daily quality of life was null. I knew I wanted to prevent this for myself.

Within 6 months I was experiencing what I believed to be MS-type symptoms and this scared me. My doctor made arrangements for me to see a specialist.

One day I was sharing my issues with another nurse and she asked me if I’d ever heard of low-dose naltrexone (LDN) and as I listened to her explain how it basically cured her father’s autoimmune illness, I knew I had to learn more.

To make a long story short, I researched LDN, gathered the information and presented it to my physician in a way I thought he would be open to listening…very methodical and with research to back up what I was saying.

We consulted with LDN literate pharmacists and both agreed I didn’t have anything to lose; however I didn’t start it immediately. I continued to work on healing my body an additional 9 months.

LDN has changed my life and I’ve seen it change others for the better…however, it is not a stand-alone treatment, and for autoimmune thyroid disease, there is a specific protocol to follow.

Today I am an independent autoimmune/thyroid wellness nurse consultant, certified nurse-nutritionist, holistic lifestyle & wellness coach and nurse educator. I am also a LDN nurse educator and love to share my knowledge with physicians and pharmacists on its use in a variety of autoimmune diseases.

What is LDN?

LDN modulates the immune system and has been shown to help patients with autoimmune disease, cancer, and other neurodegenerative disorders. It is relatively inexpensive and is available by prescription only and dispensed by a compounding pharmacy. I recommend LDN only be compounded by a LDN approved compounder.

It has been recognized that in many diseases the body may be lacking endorphins. The discovery of LDN is somewhat of a miracle, e.g. it is derived from naltrexone which has been available in generic forms for many years; however in low doses, it has been shown to modulate the immune system by blocking opiate receptors during sleep resulting in an increase of endorphins.

The therapeutic effect is believed to be achieved by increasing the body’s production of bea-endorphin and metenkephalin which are important regulators of the immune system.

These endorphins can increase circulating natural killer cells and lymphocyte-activated CD-8 cells, both of which are important to immunity. They also help regulate T-helper 1 and T-helper 2 (Th-1/Th-2, respectively) balance in the immune system.

(For more in depth look at how LDN works read Marc’s previous post.)

Many physicians are not familiar with LDN, or what they do know about it is very limited. Big Pharma does not have a vested interested in marketing a drug unless they can hold a patent on it. The patent for naltrexone expired a long time ago so it’s not profitable for them.

This means that their best-dressed sales reps will never be knocking on the doors of physicians-at-large to educate them on the miracle of LDN. Sadly, it’s simply never going to happen!

What they might know about LDN is limited to generic naltrexone in 50 mg doses which is used for alcohol, opiate withdrawal and heroin addiction.

That’s not what we’re talking about here, at all. LDN used for autoimmune disease including Hashimoto’s is not prescribed higher than 4.5 mg – and we start at a much lower dose than that before landing on a maintenance dose.

LDN and Autoimmune Disease

As previously stated, LDN is not a stand-alone treatment; however it is an amazing adjunct with the potential to trick the body into healing itself. The people who experience the most success with LDN are those who have optimized thyroid hormone levels, corrected nutrient deficiencies (especially iron, ferritin, vitamins D & B12, selenium, magnesium, zinc, and folate, etc.), healed their adrenals, eliminated infections such as Candida (Candida will block LDN), or Lyme, and healed leaky gut and low stomach acid if that was an issue.

SIDENOTE: Candida must be healed to a level within normal limits prior to starting LDN or it will not work.

When LDN is prescribed for a patient with Hashimoto’s, we start very low with the dose and slowly titrate over two months prior to a 6 month period of what we refer to as the modulating dose.

When a physician refers a patient to me who has LDN in mind as their ultimate goal, not only do I work with them on lifestyle changes to get their body ready, I also teach them how to monitor their vitals at home when starting LDN and educate them on what to watch out for and what to report, etc.

Depending on a patients progress (believe it or not, going hyper is a sign that LDN is working) they will be taught how to titrate down their thyroid hormone. One of the biggest mistakes we see patients (and physicians) making when a patient reports hyper symptoms is that they will abruptly discontinue LDN.

This is the wrong course of action…what is necessary however, is to titrate down slowly on thyroid hormone (and of course lab tests are done to validate this action).

LDN and Medication Concerns

Since LDN blocks opiate receptors, it cannot be taken with any narcotic medication. Naltrexone is a pure opioid antagonist and will block the action of narcotics. In other words, pain medication won’t work if you’re taking LDN.

I recently temporarily had to discontinue my LDN due to surgery and I knew that pain medication was going to be prescribed for a few days after the procedure.

LDN will not work if you are taking medications that suppress the immune system like prednisone or others. LDN is an immune system modulator and steroids suppress – both will antagonize the other and neither will work.

Examples of narcotic-based medications include morphine, Percocet, duragesic patch and any medication that contains codeine.

LDN and Potential Side Effects

The main side effects I’ve observed and experience personally are mild and usually disappear within two weeks while the immune system is responding to the blocking of opiate receptors. Most common are:

  • Disturbed sleep
  • Vivid, colorful dreams
  • Tiredness or fatigue

Again, these typically go away within two weeks of starting LDN and given the potential LDN offers, are well worth the effort.

Tips if you are Interested in LDN

  • It is important to get your body in the best shape possible prior to going on LDN. I devoted 9 months to healing my body even further before going on LDN.
  • Be sure to work with a LDN-approved compounding pharmacy. I cannot tell you how important this is and we’ve found that not all compounding pharmacies follow the correct LDN protocol. For resources on approved pharmacists and new research you can check here: http://www.lowdosenaltrexone.org
  • Seek a physician who is either very open to LDN or is already LDN-literate for its use in autoimmune thyroid disease. The way LDN is dosed and monitored in autoimmune thyroid disease differs greatly than how it is prescribed for any other autoimmune disease. You can contact me HERE for resources, or check with the LDN Research Trust-England

This article focused on LDN for use in autoimmune thyroid disease. However, LDN is used successfully in a variety of autoimmune diseases as well as in cancer and Lyme disease. Given its potential, it’s very sad to me that drug companies aren’t interested.

LDN has changed my life! I now live a life full of vitality, and I have my body and my brain back. I’ve been in remission for 3 years as of this writing and I’m passionate about helping other women find this same level of healing…whether it be through natural lifestyle changes or LDN, my goal is to help them succeed.

To read more about my story, I invite you to read my eBook Hashimoto’s: Finding Joy in the Journey available on Amazon as a Kindle book and soon it will be available in paperback!

Hashi eBook Cover Web Image

I invite you to also check out my Facebook page (Holistic Thyroid Care) and website for resources to help you live your best thyroid life!


Shannon Garrett, BS, RN, CHLC, CNN

Low Dose Naltrexone (LDN) and Hashimoto’s


                                            Slide from presentation by Dr. A. Vojdani on LDN

Hashimoto’s is the most common autoimmune disease of the thyroid and if affects millions of people globally. The most common treatment for this condition is synthetic T4 (usually Synthroid or a generic equivalent).

For many this treatment is ineffective and for some it only makes their symptoms worse. There are many reasons for this, but one of the important ones is that synthetic T4 does not sufficiently address the autoimmunity that is at the root of this disease.

In addition, unfortunately, many doctors ignore autoimmunity and pretend that it isn’t there. This is an abdication of responsibility and it can result in poor outcomes and poor clinical results.

And, unfortunately, it is the patients who suffer most from this approach. In this post, which is part of a new series, we will explore alternatives to just giving synthetic T4. One that shows promise with very few side effects is Low Dose Naltrexone, also known as LDN.

What is Naltrexone?

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.

A Little History: Dr Bernard Bihari

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).

AIDS Changed Everything

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.

Naltrexone Seemed to Work with MS

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.

How Does LDN Work?

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:

  1. It increases endogenous opiates
  2. It inhibits pro-inflammatory cytokines
  3. It promotes nuclear opioid growth factor
  4. It blocks opiate receptors in the GI tract
  5. It regulates T-reg cells like IL-10 and TGF

Increases Endogenous Opiates

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.

Inhibits Pro-Inflammatory Cytokines

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.

Promotes Opioid Growth Factor

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.

Blocks Opiate Receptors in the GI Tract

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.

Down Regulates TH-17

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.

Do Immune Cells Have Opiate Receptors?

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.

Endogenous Opiates Are Not the Same as Drugs

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.

The Standard Therapy for Autoimmune Disease May Make Things Worse

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.

Glial Cells in the Brain and Central Nervous System Affect Opioids

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.

Is LDN Safe?

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.

Caution: LDN May Cause Adverse Effects in These Circumstances

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.

Bottom Line: LDN is Worth Trying

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.

References and (A Boatload of) Research:



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