Hashimoto’s and the COVID-19 Vaccine

Hey, people!

I’ve been getting a boat load of questions about the Covid-19 vaccines. As with all things Covid related, unfortunately, there seems to be lots of bogus misinformation.

I have created this post to look at the actual facts regarding the vaccines produced by Pfizer and Moderna. 

It’s been really interesting to watch how many practitioners and thought leaders in the alternative medicine realm and others in the “New Age” community have aligned themselves with conspiracy theories and outright nonsense regarding the pandemic. 

The very same things that are being pushed by the alt-right. It’s an odd and dangerous marriage of right and left wing “conspirituality” that has resulted, in my opinion, in the US becoming the epicenter of an out of control pandemic. 

It didn’t have to be this way. What we are living through now is the consequences of this irresponsible, self serving behavior. And while there is reason for optimism, the truth is it’s not going to be over for any time soon.

If you’re looking for someone to pander to the legions of anti-mask and anti-vaccine conspiracy theorists, I’m not your man.

I’m frankly disgusted by some of my colleagues who have irresponsibly pushed conspiracy theories and made simple methods of prevention like mask wearing and social distancing into some sort of political game.

Of course, there are many important things we can do to keep ourselves healthy and less likely to get seriously ill such as take Vitamin D and zinc, and other herbs and essential oils. (I have written about these in the past.)

We should all also let this be a wake up call about the importance of good diet and exercise and how vulnerable we are when we have pre-existing conditions. That’s just common sense. As is taking simple precautions like wearing a mask, social distancing and washing hands.

I think conspiracy mongering is nothing but a form of narcissism and it should be called out as such. Here’s a good article that looks at this in depth and really does a good job of calling out this dangerous phenomenon.

As of writing this the death toll in the US is 626,713. Covid-19 is not a hoax or a grand plot to control humanity. It’s a deadly, novel virus that is lethal for some and, unfortunately, we don’t yet know enough about it to know why. So, that means anyone can be at risk of dying or of having long term effects from the virus.

The focus of this piece is to look at the pros and cons of the COVID-19 vaccines that are currently being made available via the emergency use authorization from the FDA. There are two vaccines that have been authorized at this time, one made by Pfizer and one made by Moderna.

mRNA VACCINES

Both are mRNA vaccines. What does this mean?

mRNA technology was discovered 30 years ago. And it has been studied for vaccine purposes for nearly two decades. Scientists were working on vaccines for both SARS and MERS, but funding was cut and they didn’t develop them until recently, when due to the pandemic we had a great deal more urgency and money to help develop these more quickly.

Clinical trials for mRNA vaccines have been conducted for influenza, Zika, rabies, and cytomegalovirus (CMV). Advances in technology in RNA biology and chemistry as with delivery systems has improved the stability, safety and effectiveness of these vaccines.

RNA and DNA are not the same. Without getting too far into the weeds, let’s say they are both some of the most important molecules for cell biology and they are used to store and share information about every cell, organ and tissue in the body.

DNA encodes the information, RNA is the reader that decodes that information. (Here’s an in-depth look at this:)

That being said, RNA vaccine development is relatively new and we just do not have much data on the long term effects of this technology. And the reality is that we won’t for some time. We are all living through a large global experiment right now involving COVID-19 and treatment and prevention strategies for it.

One concern that many people have is in the ingredients of what’s in the vaccines. This is also an area of misinformation and outright lies. Both manufacturers of these vaccines have been transparent about what is in them.

FACTS ABOUT COVID-19 mRNA VACCINES

These vaccines do not use the live virus that causes COVID-19. They also do not interact with our DNA. These vaccines work by providing instructions to our immune cells by introducing fragments of the spike protein which is found on the surface of the virus (that’s what the virus uses to enter our cells).

The vaccines also do not contain fetal stem cells. Some of the vaccines being studied in clinical trials used cells originally isolated from fetal tissue. These come from historical cells lines that were derived in the 1970’s and 1980’s from two elective abortions. 

The fetal cell lines that were used to produce some of the potential COVID-19 vaccines are from two sources:

HEK-293 A kidney cell line that was isolated in 1972

Per.C6 A retinal cell line that was isolated in 1985

The mRNA COVID-19 vaccines produced by Pfizer and Moderna do not require the use of fetal cell cultures in order to manufacture the vaccine.

Early in the development of these vaccines they were used for “proof of concept” to show how a cell could take up mRNA and produce the COVID spike protein or to characterize the spike protein.

In fact, both vaccines have been deemed ethically uncontroversial by pro-life policy organizations like The Charlotte Lozier Institute and the Catholic Health Association of the United States.

HOW THE VACCINE WORKS

The vaccine is injected into the muscle in the upper arm. Once in the muscle cell the cells follow the instructions from the mRNA fragment and make a piece of protein. After this is made the cells break break down these instructions and destroy them.

Next, the cell displays this protein piece on it’s surface. Our immune system recognizes this protein as something foreign and it makes antibodies against it. The development of these antibodies by our immune system gives us protection against future infection.

The obvious benefit of doing this versus actually getting COVID-19 is that you gain protection without having to go through the potentially dangerous consequences of getting the virus. However, we do not yet know how long this protection lasts.

In addition, there has been some research done by Dr. Kharrazian and Dr. Vojdani on cross-reactivity of the spike protein to some of our own tissues and this is an area of potential concern.

This may have implications for the development of autoimmune disease, but we just don’t know yet. It’s not clear whether the fragments used in the vaccines are proteins that cross react, not all of them do.

INGREDIENTS

Another area of misinformation is the ingredients. There is no formaldehyde, no aluminum, and no mercury. These are sometimes used in other vaccines, they are not used in these.

When the Pfizer COVID-19 vaccine was granted an EUA from the FDA, its ingredients list was published online along with other safety data. The list includes:

• mRNA
• Lipids ((4-hydroxybutyl)azanediyl)bis(hexane-6,1-diyl)bis(2-hexyldecanoate), 2 [(polyethylene glycol)-2000]-N,N-ditetradecylacetamide, 1,2-Distearoyl-sn-glycero-3- phosphocholine, and cholesterol)
• Potassium chloride
• Monobasic potassium phosphate
• Sodium chloride
• Dibasic sodium phosphate dehydrate
• Sucrose

What are the Moderna COVID-19 vaccine ingredients?

Moderna has also been given emergency use authorization for their vaccine. Moderna also recently released its ingredients list through the FDA:

• mRNA
• Lipids (SM-102, 1,2-dimyristoyl-rac-glycero3-methoxypolyethylene glycol-2000 [PEG2000-DMG], cholesterol, and 1,2-distearoyl-snglycero-3-phosphocholine [DSPC]),
• Tromethamine,
• Tromethamine hydrochloride
• Acetic acid
• Sodium acetate
• Sucrose

OTHER FACTS

Pfizer	Moderna
95% effective 30 mcg doses given 21 days apart Must be diluted with 0.9% sodium chloride Must be stored at -112 to -76 degrees F 36,621 people took part in the clinical trial Approved for age 16 and over Published safety and final efficacy results from Phase 3 on 12/10/20	94.5% effective 100 mcg doses given 28 days apart No dilution required Stored at -13 to -5 degrees F 30,350 people took part in clinical trial Approved for age 18 and over Announced primary efficacy analysis on Phase 3 on 11/30/20

POTENTIAL SAFETY ISSUES

One concern that many people have is whether or not this vaccine is safe for people with autoimmunity and in our case, thyroid autoimmunity.

The CDC guidelines on this are pretty vague:

“People with autoimmune conditions may receive an mRNA vaccine. However, they should be aware that no data are currently available on the safety of mRNA COVID-19 vaccines for them. Individuals from this group were eligible for clinical trials.”

Not much help.

As I mentioned previously, Dr. Kharrazian and Dr. Vojdani’s research into cross reactivity  of the COVID-19 spike protein and some of our tissues revealed that some (not all of the) proteins are cross reactive to human tissue. This has implications for the development of autoimmunity from the virus.

But, I could not find data on whether or not these proteins are the proteins used in the mRNA vaccines. 

Something else that has been studied is the impact of COVID-19 on the thyroid. 

There is evidence that COVID-19 may result in post-infection thyroid disease. Sub-acute thyroiditis is a common finding.

This is pretty common for any virus that affects the upper respiratory system. Epstein Barr can also do this as can the flu, the mumps and other viral infections.

There is also some evidence of that thyroid disease is associated with severe COVID-19 infections.

Pre-existing hypothyroidism is not associated with increased hospitalization or ventilator use in patients with COVID-19. One study looked at 3703 COVID-19 patients (251 had pre-existing hypothyroidism, 22 had Hashimoto’s. 68% of the COVID-19 positive patients with hypothyroidism needed hospitalization. But apparently, this is not higher than other groups.

At the end of the day, there are potential consequences to the thyroid if you contract COVID-19. And while I have not seen any evidence that people with Hashimoto’s are more vulnerable to COVID, getting it may complicate the disease. How much? We still don’t know.

REACTIONS TO THE VACCINES

We do not have a lot of data on people with Hashimoto’s who got the vaccine. As you know we have a wonderful and supportive community online and I was able to survey my Facebook (51,000) and Instagram (14,000) followers and I got responses from 23 people with Hashimoto’s, all mostly frontline workers who got the vaccine.

All but two got the the first shot of the Pfizer vaccine. Of that group, none reported any severe reactions. 6 reported some soreness in the arm around the injection site which went away in a day or two. Two others reported fatigue and body aches.

Everyone else reported no reaction at all that they were aware of. None have gotten the second dose of the vaccine yet. I will be following up and asking them about this.

Bottom Line:

Whenever making a decision of this magnitude, we have to look at risk and benefit. I am not for or opposed to the vaccine. But I am opposed to misinformation and lies.

Here’s what we know:

Covid can be fatal and can cause long term damage to many parts of the body ( the lungs, the cardiovascular system, the brain and nervous system and the thyroid and more).

We don’t know who it will be fatal for, but it kills more men, and those with pre-existing conditions and people of color.

Also, the pandemic’s economic and social destruction will not end until we have some type of herd immunity. This can happen if enough people get sick (and lots, lots more will die) or we get vaccinated to such a degree as a society that the virus peters out. 

Some combination of that will probably occur over the next year. The vaccine is an important part of achieving that (and ultimately saving lives).

These mRNA vaccines do not contain mercury, formaldehyde, or aluminum. Nor are fetal stem cells used to manufacture the vaccine.

So far, from the small sample size we have, there were few side effects. We don’t know about the long term effects of the vaccine, but we do know about the long term effects of COVID-19.

Vaccines have also worked historically for other diseases.

I hope this was helpful and that it can be used to help you make a better, more well informed decision about whether or not to get the vaccine.

I intend to get it as soon as I am able.

Sincerely, Marc

References:

1. https://www.nature.com/articles/nrd.2017.243
2. https://www.technologynetworks.com/genomics/lists/amp/what-are-the-key-differences-between-dna-and-rna-296719
3. https://www.health.nd.gov/sites/www/files/documents/COVID%20Vaccine%20Page/COVID-19%20Vaccine%20Fetal%20Cell%20Handout.pdf
4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7246018/
5. (https://www.fda.gov/media/144414/download
6. https://www.cdc.gov/coronavirus/2019-ncov/vaccines/recommendations/underlying-conditions.html
7. https://www.endocrineweb.com/amp/63098
8. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7387272/
9. https://www.frontiersin.org/articles/10.3389/fendo.2020.00565/full)
   

CBD, THC and Hashimoto’s

In today’s post, I examine a boatload of research on CBD, THC and Hashimoto’s and autoimmunity. While there are lots of claims about it’s effectiveness, I was really surprised by how little critical analysis there is of the research that is out there.

So, naturally, I took it upon myself to dig in and see what I could find. And I’m posting this on 420 day for all you fans.

What Are Cannabinoids Anyway?

With the movement of many states here in the US legalizing marijuana for both recreational and medical uses, there has been a lot of attention over the last few decades on why this plant may be so effective in treating certain types of health issues.

One of the main reasons for the therapeutic value of marijuana is cannabinoids.

Scientists have identified close to 500 phytochemicals in hemp plants. Hundreds of them are compounds called terpenoids.

Terpenoids give fruits, flowers and herbs many of their pleasant aromas, flavors and other special properties. Cannabinoids are a sub-class of these terpenoids.

There are over 60 cannabinoids found in hemp and cannabis — it’s the only place they are found. This is one of the many reasons hemp stands alone in the plant kingdom as a potent repository of nutrition.

The Endocannabinoid System

What’s interesting to note about cannabinoids is that, for some reason, our bodies evolved with receptors for them. We have our own endogenous cannabinoid system.

These endocannabinoids and their receptors are found throughout the body: in the brain, organs, connective tissues, glands, and immune cells.

In each tissue it seems that cannabinoids perform different tasks, but one thing that seems to be consistent is that they help promote homeostasis or balance within the body.

And this ability to promote balance exists on various levels of biological life, from the macrocosm to the microcosm.

For example, autophagy, the process where cells isolate parts of themselves to be self-digested and recycled is mediated by the cannabinoid system.

This is an area of extreme interest for those of us with autoimmunity because this is the very system that has gone haywire. In fact researchers are currently looking into find drugs that affect this system to improve outcomes for patients with autoimmunity.

Endocannabinoids Help Different Systems Talk to Each Other

Another interesting notion is that endocannabinoids and cannabinoids are important players in the communication and coordination between different systems of the body. And this occurs on both the macro and micro levels.

For example, at the site of an injury,  cannabinoids can be found decreasing the release of compounds from injured tissue, stabilizing the nerve cell to prevent excessive firing, and calming nearby immune cells to prevent release of pro-inflammatory substances.

Three very different mechanisms of action on three different cell types all working together for a single purpose: to minimize the pain and damage caused by the injury.

Cannabinoids are really effective in reducing pain and are a viable alternative to opiate based painkillers and have far fewer downsides. They are also clearly effective in helping to reduce inflammation systemically.

Again, this has important implications for autoimmune disease and Hashimoto’s. As I have said repeatedly in my writing and in my presentations.; Autoimmunity is a systemic problem, many systems of the body are impacted and begin losing balances.

This is why Hashimoto’s is literally a mind, body and spirit condition. And the endocannabinoid system, with its complex actions in our immune system, nervous system, and all of the body’s organs, is also a kind of bridge between body and mind.

By understanding this system we can see a mechanism that explains how things that affects the mind and spirit can promote health or disease.

THC and CBD (Cannabinoid) Receptors Are Everywhere

Virtually every species, from all vertebrae on down to tiny nematodes (worms), share the endocannabinoid system.

Cannabinoid receptors are present throughout the body, embedded in cell membranes, and are believed to be more numerous than any other receptor system.

When cannabinoid receptors are stimulated, a whole bunch of physiologic processes follow.

Researchers have identified two cannabinoid receptors: CB1, predominantly present in the nervous system, connective tissues, gonads, glands, and organs; and CB2, predominantly found in the immune system and its associated structures.

Many tissues contain both CB1 and CB2 receptors, each linked to a different action. And emerging research has found that immune cells may express both CB1 and CB2 receptors.

These receptors can be acted upon by our own natural cannabinoids (ends cannabinoids) or by plant based (phytocannabinoids)

Delta-9-tetrahydrocannabinol, or THC, is the most psychoactive and certainly the most famous of these substances, but other cannabinoids such as cannabidiol (CBD) and cannabinol (CBN) are have become more popular with researchers due to a variety of healing properties. Here’s a good breakdown of a number of different cannabinoids.

Most phytocannabinoids have been isolated from cannabis sativa, but other medical herbs, such as echinacea purpura, have been found to contain non-psychoactive cannabinoids as well.

Some studies show that treatment with endocannabinoids leads to increases in certain types of immune proteins (like IL-10) and that they help to diminish others (like IL-17), this can result in suppressing delayed type hypersensitivity response.

Both of these immune proteins have been found to play important roles in Hashimoto’s. IL-10 can block other destructive immune proteins and IL-17 is a kind of immune instigator that can make tissue destruction more intense.

If you aren’t familiar with these proteins, check out this post for detailed discussion of them in a Hashimoto’s context.

These studies also suggest that endogenous cannabinoid system is one of the homeostatic mechanisms that the body uses to down-regulate immune response to foreign antigens as well as combat autoimmunity.

Targeting of this system could yield valuable therapeutics in the future.

Let’s take a look at a few of these in the context or Hashimoto’s and autoimmunity.

The Cannabinoid System and Immune Regulation

In general, there seems to be a big connection between the brain and immune system and cannabinoids. As I have written about on many occasions, Hashimoto’s has a profound impact on the brain and much of autoimmunity’s impact on the body can be found in both the brain and the gut.

And the cannabinoid system seems to be firmly in the middle of this axis. For the purposes of this post, I have focused mostly on the THC and CBD research.

CBD and THC can have opposite effects on regional brain function, which may be why they cause different symptomatic and behavioral effects.

CBD is also known to be able to block the psychoactive effects of Δ-9-THC.

While THC promotes sleep, CBD may actually have the opposite effect and promote wakefulness or make it more difficult to sleep.

In gerneral, there seems to be a kind of yin and yang effect with THC and CBD, they appear to balance and counteract one another.

They also behave a little differently in the way that they influence the immune system.

Immune System Effects of THC

Studies have shown that THC increases TH-2 and suppresses TH-1 by inhibiting IFN and IL-12 and it affects IL-12 receptors. IL-12 can turn on genes that cause destruction of certain tissues, like the thyroid. So, inhibiting it can be a good thing for people with Hashimoto’s.

In addition it promotes IL-4. This is not always a good thing. IL-4 can activate IgE which is involved with allergic reactions and some sensitivities.

Also, the fact that both CB1 and CB2 receptors have been found on immune cells suggests that cannabinoids play an important role in the regulation of the immune system.

Recent studies demonstrated that administration of THC into mice triggered apoptosis (cell death) in T cells and dendritic cells, resulting in immunosuppression.

In addition, several studies showed that cannabinoids downregulate cytokine and chemokine production and, in some models, upregulate T-regulatory cells (Tregs) as a mechanism to suppress inflammatory responses.

This is a very good thing for Hashimoto’s. Boosting T-regs is an important goal for calming the immune system and in maintaining health and balance in the gut ecosystem.

Later studies using activated peripheral blood T-cell cultures showed that treatment with THC inhibited cell growth and the generation of Th1 cytokines, including IL-12, by CB2-mediated mechanisms. Again demonstarting that THC can be a TH-1 suppressant.

So how does this relate to Hashimoto’s?

Hashimoto’s was originally thought to be a TH-1 dominant autoimmune disorder, but has since been shown to be an over simplification and some people have overactive TH-2 systems.

So while THC can definitely be anti-inflammatory, it may not be if you are TH-2 dominant or already have an over active TH-2 response. Context always matters when you make decisions on what is right for you.

That being said, there is ample evidence that it can help calm TH-1.

Negative side effects of THC

The most common side effects seem to be anxiety, potential for addiction, short term memory loss, loss of motivation.

Like any herb, or drug you can overdo it and this can result in adverse reactions.

Some people get really anxious and paranoid after consuming THC. CBD can help counter act this.

THC also has a profound effect on the brain and the hippocampus and cerebellum are both rich with cannabinoid receptors. These are both important parts of the brain for memory, learning and integration.

This can suffer with excessive THC consumption.

I also think the potential for addiction and abuse is also a real concern. Much of the hype around THC is that it is not physically addictive like opiates and this is true.

However, as anyone who lives in the 21st century knows, some people get hooked and smoke weed pretty religiously. It may be easier to quit, but it can still be habit forming if you are predisposed to addiction.

Next, let’s take a look at CBD and the immune system.

The Immune Effects of CBD (Cannabidiol)

CBD acts not only through the endocannabinoid system, but also has an impact on serotonin receptors.

Cannabidiol has also been found to calm glial cells in the brain. These are the immune cells in the brain and they are very easily excited and the body has no natural way to calm them down. So this is a very valuable outcome.

CBD has also been found to treat Type I diabetes by decreasing TH-1 and increasing TH-2.

However, In another study of the medical literature, the action of CBD was summed up this way:

“On the whole, our results and data from the literature indicate that cannabidiol can exert different effects on the macrophages. It seems to inhibit the precocious steps of the inflammatory process throughout reduction of chemotaxis and NO (nitric oxide) production, whereas it can activate the following phases of macrophage activation, by increasing IL-12 and decreasing IL-10 production therefore favoring the development of a Th1 response.”

Hold on what? This suggests that CBD increases TH-1 response. IL-12 is also involved in turning on genes that result in attacks on specific organs and has been implicated as an important player in Hashimoto’s. And this is clearly the opposite of what we just learned about THC.

They go on to say: “However, the inhibition of chemotaxis can also be interpreted as a signal of arrest, a fundamental step for the macrophage cell to fully express its antimicrobial and pro-inflammatory potential once it has reached the appropriate tissue. Indeed, it is possible that cannabidiol, by enhancing the efficacy of the macrophagic response, could lead to a faster resolution of an inflammatory/infective process.”

Or that this may mean that CBD speeds up the resolution of the immune response. This may be beneficial, but it could also be a problem if you have an overzealous TH-1 response in your body.

Certainly, this should give you pause if you are considering taking CBD supplements alone as these will not have the TH-1 reducing powers of THC.

However, CBD has been shown to be quite effective as a pain reliever, especially topically and it’s ability to clear out these circulating immune cells and proteins may be one of the reasons why.

Potential Negative Side Effects of CBD

This is one area that gets almost no attention and it took some digging for me to find it and I think it’s important to look at the whole picture.

In this paper, they looked at a number of studies and deduced:

“Several studies suggest that CBD is non-toxic in non-transformed cells and does not induce changes on food intake, does not induce catalepsy, does not affect physiological parameters (heart rate, blood pressure and body temperature), does not affect gastrointestinal transit and does not alter psychomotor or psychological functions.”

All good things, obviously.

“Also, chronic use and high doses up to 1,500 mg/day of CBD are reportedly well tolerated in humans. Conversely, some studies reported that this cannabinoid can induce some side effects, including inhibition of hepatic drug metabolism, alterations of in vitro cell viability, decreased fertilization capacity, and decreased activities of p-glycoprotein and other drug transporters.”

So let’s unpack that:

Inhibition of hepatic drug synthesis means CBD may impact how some drugs are metabolized. This is probably caused by CBD’s effect on the enzyme P450. Over 60% of medication that is prescribed is metabolized by this pathway including thyroid hormone.

In vitro cell viability: it seems that CBD helps promote apoptosis or the destruction of cells. This can good if they are cancer cells and not so good if they cells that you need. This property induced by CBD in normal lymphocytes (immune cells) could contribute to the immunosuppressive effects induced by this cannabinoid.

Decreased fertilization capacity: Suppression of follicular steroidogenesis (production of testosterone, progesterone and estradiol-17) has been demonstrated in vitro at a wide range of CBD concentrations (100-200μM).

Luteinizing hormone (LH)-stimulated accumulation of progesterone and testosterone decreased, while estradiol accumulation was only slightly affected. Low progesterone is a common problem for women with hypothyroidism, so this is a real concern is you are struggling with infertility issues or low progesterone.

A probable mechanism is that cannabinoids modulate the release of cholesterol from its ester storage in lipid droplets and, thus, limit the availability of the substrate for steroidogenesis.

Many people with Hashimoto’s have altered cholesterol metabolism because of the effects of thyroid hormone on this process. Some have high cholesterol and others have low cholesterol. If your is low, CBD might make that problem worse.

It has also been found to decrease Testosterone and lower sperm count. Of course dosage matters and this is less significant in lower doses.

Bottom Line:

All in all, I think there are some significant potential benefits for to using THC and CBD, but like anything there are risks of over doing it.

As in all decisions regrading your body, context really matters. You need to look at your underlying issues and weaknesses and then look at how THC and CBD behave.

The do a risk/benefit analysis. Are you TH-1 or Th-2 dominant? If you’re TH-1, then strains with more THC might better for you.

If you are TH-2 dominant, then strains with more CBD might be better for you.

If you are low in cholesterol or low progesterone, then CBD might cause more problems. If you are high in cholesterol, it could be beneficial.

Finally, I think, in moderation, and applied in the appropriate context both THC and CBD could be beneficial for some of the underlying issues of Hashimoto’s.

Particularly for important issues like pain, anxiety and some types of immune system imbalances.

Here’s a cool infographic that summarizes some of the pain relieving effects of both. This is courtesy Greencamp.com.

greencamp.com

References:

http://norml.org/library/item/introduction-to-the-endocannabinoid-system 

https://www.ncbi.nlm.nih.gov/pubmed/26054920 Autophagy and autoimmunity

http://journal.frontiersin.org/article/10.3389/fimmu.2013.00088/full Autophagy and autoimmunity crosstalk

http://www.medicalnewstoday.com/articles/269432.php THC alters gene expression and can help calm autoimmunity.

https://www.sciencedaily.com/releases/2014/06/140602150914.htm THC suppresses immune function

CBD, THC and the Immune System:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2828614/

http://www.ncbi.nlm.nih.gov/pubmed/?term=cannabinoid

http://www.ncbi.nlm.nih.gov/pubmed/?term=endocannabinoid

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3448900/ CBD calms glial cells and makes opiates more potent!

http://www.medicalnewstoday.com/articles/269432.php Marijuana for autoimmune disease

http://www.sciencedaily.com/releases/2014/06/140602150914.htm THC and immune functions

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2270485/ CBD arrests Type I Diabetes

http://www.medicaljane.com/2012/12/20/cannabidiol-cbd-medicine-of-the-future/

http://files.iowamedicalmarijuana.org/science/cancer/Klein%202003.pdf The cannabinaoid system and immune regulation FASCNATING!

http://www.nature.com/nature/journal/v394/n6690/full/394277a0.html Control of pain by endogenous cannabanoids

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2828614/ Cannabanoids as novel anti-inflammatory drugs

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1576166/ CB2 receptors, cannababoids IL12 and IL10

http://www.jneurosci.org/content/23/16/6470.full.pdf IL-1 and Cannabanoids

http://www.febsletters.org/article/S0014-5793%2898%2900851-5/abstract Cannabanoids potentiate IL6

http://www.ukcia.org/research/CannabidiolModulatesChemotaxis.pdf Cannabanoids other than THC and IL10 and IL12

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3974854/ Cannabanoids reduce IL 17 and Increase IL10

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2828293/

https://www.zamnesia.com/content/260-cbd-thc-cbg-exploring-cannabinoids different types of cannabinoids

General Information:

http://hypothyroidmom.com/reefer-madness-or-a-promising-treatment-for-thyroid-disease/

http://www.ncbi.nlm.nih.gov/pubmed/22625422 Mechanism of action of CBD

http://www.leafscience.com/2014/02/23/5-must-know-facts-cannabidiol-cbd/

http://www.medicalcannabis.com/wp-content/uploads/centonze_et_al_2007_inflammatory_neuro.pdf

http://www.medicalcannabis.com/wp-content/uploads/di_marzo_1998_endocannabinoids.pdf

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4023456/ CBD as a sleep deterrrent

http://www.medicinalgenomics.com/wp-content/uploads/2013/01/Bergamaschi_2011.pdf safety and side effects of CBD

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3055598/ Opposite effects of CBD and THC

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2697699/ Cannabanoids as treatment for motor dysfunction

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3579248/#b98 Cannabanoids for neurdegenerative disorders

http://www.health.harvard.edu/mind-and-mood/medical-marijuana-and-the-mind

http://www.21stcenturysciencetech.com/articles/marijuana/Medical_effects.pdf

Osteoporosis and Hashimoto’s: Part I of A 2 Part Series

Osteoporosis is a medical condition in which the bones break down and loose tissue. This can make them brittle and fragile and can make the people who suffer from it more susceptible to fractures, breaks and chronic pain.

The National Osteoporosis Foundation reported that by 2020, about 14 million people over the age of 50 are expected to have osteoporosis and over 47 million are expected to have low bone mass.

Menopause and Thyroid Medication Can Make It Worse

The most important risk factor for bone loss in midlife women is menopause. Women lose about 50% of their trabecular or spongy bone (found at the ends of long bones as well as in the skull, ribs, pelvic bone and in the bones of the spine.

And they lose about 30% of their cortical bone (the dense outer surface of the bone that protects the inside of the bones) during the course of their lifetime, about half of which is lost during the first 10 years after menopause.

Approximately 40% of all postmenopausal women will eventually experience fractures.

To further complicate matters, women in menopause who are taking thyroid hormone (levothyroxine) have a higher incidence of osteoporosis and low TSH and low bone density go hand in hand.          ( hyperthyroid = low bone density).

Physiologically when you increase levels of thyroid hormone, you also increase bone turnover which can result in loss of bone density. It is very important to factor this in and to treat both hypothyroidism and bone loss at the same time.

In this post, I dig into the problem of osteoporosis and how it affects people with Hashimoto’s and hypothyroidism.

I explore why it’s happening, why conventional treatments may or may not help and, in Part II I will share with you lots of things you can do to treat and prevent it.

Quick Review of How Bones Grow

Bones provide the architecture of our bodies, like the steel beams in a building they provide the structural support for the body and work with the muscles and joints to allow us to move freely.

The skeleton is one of the first things to begin growing in the developing fetus, it’s growth begins as early as a few weeks after conception.

By the eighth week of pregnancy, most of the skeleton is already in place in the form of cartilage and connective tissue.

These tissues form the foundation for the transformation into actual bone know as ossification.

There are two ways that bones grow and mature in the body and the type of growth depends upon what type of bone is needed.

Types of bones include:

Flat bones like ribs, and the bones in the skull

Irregular bones like the vertebrae

Long bones like arm and leg bones

Short bones like the small bones in the wrists

Irregular, long and short bones grow by a process where cartilage is replaced by bony tissue. Most bones are made this way. Flat bones, like those in the skull are made when sheet-like connective tissue membranes are replaced with boat tissue.

What Happens with Osteoporosis?

Normal healthy bones develop during childhood and teen years as bone is absorbed by the body and rebuilt. Your bones continue to grow and become larger and heavier until about age 30 when they reach their peak density (bone mass).

After age 30, people lose a little bit of bone mass every year. Osteoporosis is the thinning of bones to the point they can become brittle, lose strength  and fracture or break.

To Understand Osteoporosis You Need to Understand Bone Cells

The loss of bone density is the result of dysfunction of the certain bone cells. Proper bone function requires a complex interaction of hormones, calcium balance and bone maintenance.

There are three specialized cells that are unique to bones:

Osteoblasts: these are cells that form new bone. They come from the bone marrow and are related to structural cells. These cels work in teams to build bone. They control calcium and mineral depositing and are found on the surface of new bone.

When a team of osteoblasts finish building a bone cavity, the cells change and become flat like little pancakes. They then line the surface of the bone. Old osteoblasts are also called “lining cells”.

These lining cells regulate the passage of calcium into and out of the bone and they respond to hormones by making special proteins that activate osteoclasts.

Osteoclasts are large cells that break down bones. They come from the bone marrow and are related to immune cells (white blood cells). They are found on the surface of the bone.

So osteoblasts control the absorption of calcium and osteoclasts control the deportation of calcium (remember this, it’s going to be important as we continue).

What’s critically important to understand is that in order to have healthy bone you must have a healthy balance of both osteoblasts and osteoclasts. If this balance is lost and there are more osteoclasts (which which cause bone loss) than osteoblasts (which build bone) then you will wind up with more bone loss.

The third kind of bone cells are called osteocytes and these are cells inside the bone. They also come from osteoblasts. Some osteoblasts turn into osteocytes when new bone is being built and they get surrounded by new bone.

They form the matrix of the bone and connect out to other osteocytes. They also have a certain innate intelligence and the can sense cracks or fractures and help direct osteoclasts by telling them where to dissolve bones.

What Happens with Hashimoto’s and Hypothyroidism?

There’s an interesting relationship between thyroid hormone and bone density.

Thyroid hormones are necessary for the development of bones and the establishment of peak bone mass.

When children have hypothyroidism, their bones are still developing this can result in slower bone growth with delayed skeletal development. If they have hyper-thyroid symptoms this can accelerate bone development.

In adults, T3 regulates bone turnover and bone mineral density. So normal levels are required for optimal bone strength.

Too little T3 can result in slower bone turnover and breakdown, whereas too much T3 can result in increased turnover and loss of bone density.

However, both hyper and hypo-thyroid patients can experience bone related issues. It seems that in adult patients with hypothyroidism, bone density increases but bone quality is poor (possibly due to low turnover), thus this may cause increased fracture risk in these patients.

This study  showed showed that at the time of diagnosis of hypothyroidism, Bone Mineral Density (BMD) was not significantly different from normal subjects.

Interestingly, the patients that received 2 years of levothyroxine replacement therapy had lower bone density. As I mentioned previously, it’s really important to think about treating bone loss when treating hypothyroidism.

How often is this done? Unfortunately, not very often or not until significant BMD loss has been discovered. (Why wait?)

What Happens in Menopause?

There is clearly evidence that menopause and the resulting decline in estrogen can result in more bone loss.

Estrogen performs lots of functions in the body and one of those is functions is to slow bone loss (interestingly, increasing estrogen increases thyroid binding globulin which makes less thyroid hormone available, less thyroid hormone = less bone loss).

If more calcium is absorbed into the bones, which can happen when estrogen levels decline the production of both osteoblasts (which control calcium absorption) and osteoclasts (which control calcium deportation) is increased.

When a lot of calcium is absorbed, the body will compensate and lots of calcium will also be deported. However, 50-70% of bone building osteoblasts die in the building of new bone.

The more their activity is stimulated (as with increased thyroid hormone), the more osteoblasts may die. And since estrogen inhibits the uptake of calcium, estrogen actually acts to slow the death of these cells.

It’s kind of like the brakes on the bone loss system. Whereas, adding more calcium can be like the gas pedal.

Wait What?

Calcium Can Act As Gas Pedal For Bone Loss?

In some cases, as long as you are consuming plenty of calcium replacement osteoblasts are being made all the time. And many people are successful in increasing bone mineral density by consuming more calcium.

However, the problem is that you can reach a point where replacement capacity is full or another way to look at it is that you have exhausted the body’s ability to absorb so much.

In this study  it was observed that people with consistently high lifetime calcium intake and high BMD may actually end up wearing out bone health.

When you increase osteoblast production by increasing calcium intake, you also increase osteoblast apoptosis (cell death). The body always seeks balance.

So, to  put it another way, the greater the intake of calcium, the greater the osteoblast activity, the greater the osteoblast cell death rate.

With age this whole cycle can get exhausted. And the increased rate of osteoblast cell death leads to a decrease in the ability for new cells to be made. It’s like you wear out the workers at the bone building factory.

And what happens then is that less bone matrix is made and without matrix calcium can’t help new bone be made and since old bone is constantly getting broken down, the end result is less bone replacement.

When less bone is being replaced you get more porous holes in the bone structure. This is exactly what happens in osteoporosis. Osteoblasts are getting made or they are impaired, dead cells aren’t getting replaced and micro-fractures don’t get repaired.

The reason why osteoporosis risk is greater in women than in men, regardless of menopause and calcium consumption is because of monthly estrogen and parathyroid hormone levels (remember the parathyroid glands control the body’s calcium levels).

In a woman’s cycle estrogen levels are lowest around menstruation and parathyroid hormone levels peak which increases deportation of calcium from the bones and the absorption of calcium into bones.

So for women, the lifetime bone turnover is increased. The workers in the bone making factory have to do more work every month. Over a lifetime, this may lead to their exhaustion.

Wait, There’s More! Autoimmunity and Bone Loss

The important other part of the equation is the relationship between osteoporosis and autoimmunity and inflammation (the root of all evil).

One question that researchers  have recently begun to ask is: Is osteoporosis caused by an inflammatory process?

Clinical observation has shown that osteoporosis is also found with other inflammatory diseases (like autoimmune disease, rheumatoid arthritis, inflammatory bowel diseases, etc.)

Conditions like gout, osteomyelitis, rheumatoid arthritis, ankylosing spondylitis, and psoriatic arthritis, are tall commonly linked with inflammation in the joints.

And links between high HS-CRP (a marker that is linked to systemic inflammation) levels and bone mineral density has been seen in some research.

There is also some other research that notes a connection between cytokines (immune cells) and bone reabsorption.

Two cytokines in particular IL-6 and IL-11 (which are both commonly high with Hashimoto’s patients) have been found to play an important role in the formation of osteoclasts (which you will recall break down bone).

Also cytokines can impact nitric oxide synthesis. Nitric oxide is an important mediator of inflammation and it has been shown to be involved in osteoporosis.

“The activation of the inducible NO synthesis (iNOS) pathway by cytokines, such as IL-1 and TNF-α, inhibits osteoblast function in vitro and stimulates osteoblast apoptosis.”

In other words, these immune proteins slow the function of osteoblasts and increase their destruction. Again, leading to possible imbalance of osteoblasts to osteoclasts.

The important take away here is more inflammation means potentially more osteoclasts and when this results in an imbalance between these and osteoblasts (which make bone) the the end result is more bone loss.

What About Hormone Replacement Therapy and Osteoporosis?

One common argument for prescribing Hormone replacement therapy (HRT) for post menopausal women is that it will help prevent further bone loss.

This is true to some extent, but not in the way that many doctors argue.

Basically, as I discussed previously, estrogens are the brakes on this system that help minimize erosion. (remember, extra calcium is the gas-pedal)

Calcium is absorbed into the bones due to osteoblasts, which increase free phosphate level in the bones, which causes the ‘passive’ influx of calcium to restore the calcium-phosphate ratio.

The osteoblasts also compose the matrix upon which the calcium can build bone. They build bone.

Oesteoclasts break down bone. Deportation of calcium from the bones by osteoclasts is a more direct process.

Structurally, estrogen does not stimulate osteoblasts. It protects the bones against excessive bone turnover and osteoblasts against apoptosis.

Post-menopausal bone loss is associated with a high bone remodelling rate, as indicated by increased numbers of both osteoclasts and osteoblasts.

And since women naturally tend to build bone more slowly as they age (i. e., make fewer osteoblasts), the resulting balance between osteoblasts and osteoclasts can be lost.

If this balance is lost, the result is the same, more bone loss. This is why HRT doesn’t always result in better bone mineral density (BMD). It doesn’t affect the numbers of osteoclasts.

This process is explained here.

What About Corticosteroid Use?

A common treatment for joint and back pain is corticosteroid injections. Corticosteroids are also prescribed for inflammation in many inflammatory diseases.

THIS HAS TREMENDOUS CONSEQUENCES WITH BONES AND CARTILAGE.

This is one of those areas that drives me completely insane. Injecting corticosteroids into an already weakened joint capsule is almost a guarantee for bone destruction and development of more severe problems.

This study looks at this problem in detail.

And here is there opening statement: “Glucocorticoid-induced bone disease is characterized by decreased bone formation and in situ death of isolated segments of bone (osteonecrosis) suggesting that glucocorticoid excess, the third most common cause of osteoporosis, may affect the birth or death rate of bone cells, thus reducing their numbers.”

Let’s unpack this sentence. First of all glucocorticoids are known to cause bone disease. Secondly, excess use of them is the third most common cause of osteoporosis(!!!!), and this treatment affects the birth and death rate of bone cells – something that results in reducing their numbers.

And as we have seen (and I hope you understand by now) fewer osteoblasts means less bone formation, fewer osteocytes means less bone matrix on which to build bone.

So here’s the big takeaway, if you have an older relative, friend, parent or you yourself are starting to get up in age, getting steroid injections for pain is a really bad idea for the bones in that area.

It may be a good way to make sure that they need a knee or hip replacement, but it’s not good for their osteoporosis.

What About Calcium Supplementation?

This is one of those things that everyone who is concerned about osteoporosis does. The common thought is: Worried about bone loss? Take more calcium.

Ok, that’s a good idea in theory, but is it really a good idea?

It turns out that it might not be in excess. As with most things there is a point where too much calcium may do the opposite of what you had hoped.

Consuming high amounts of calcium may increase osteoblasts, however, you can get to the point where you have too much calcium in your bloodstream ( A calcium level of 10.0 is considered high normal, more than that can cause health problems.)

Too much calcium in your blood can weaken your bones, create kidney stones, and interfere with the way your heart and brain works. This is a condition called hypercalcemia and it can be caused by overactive parathyroid glands.

The body normally absorbs all the calcium it needs from our food. Only about 200 mg is absorbed into the blood. And the absorption rate actually declines when we consume more than we can absorb.

The body naturally compensates in order to prevent blood calcium levels from getting too high.

This happens because our muscles can only function if calcium from inside muscle cells can be deported to outside the cells. If there’s already too much calcium in the bloodstream, this process may be hampered.

Excessively high levels of calcium can actually be life threatening, so to save your life, excessive amounts of calcium are stored in the bones. The problem is that this extra calcium is processed by osteoblasts and osteoclasts.

This extra calcium is absorbed due to actions of the osteoblasts. When they process excess calcium they die sooner, when they die sooner and faster this can result in the balance being lost between osteoblasts and osteoclasts and too little bone matrix is made.

Without the matrix, the calcium can not be used effectively and new bone can’t be made. But the old bone is still being broken down. And this results in porous holes in the bone matrix.

Again, this is exactly what happens in osteoporosis. In people who have osteoporosis, osteoblasts may not be replaced as they should be, and less are available or their activity is compromised and low bone mineral density is the result.

Bottom Line: Here’s A Summary of the Takeaways

1. Osteoporosis is the result of an imbalance of bone cell production and bone cell breakdown. If more bone is broken down than is created you end up with bone loss.

2. Osteoporosis happens because of an inflammatory process. Treating systemic inflammation will benefit people with osteoporosis and may actually slow bone loss.

3. Supplementing with estrogen may not be successful if you ignore other issues, like inflammation.

4. Supplementing with thyroid hormone has consequences for bone health. Excessive T4 and/or T3 supplementation can lead to faster bone loss.

5. Excessive calcium supplementation can have long term consequences and result in more, not less bone loss.

6. Corticosteroids can be a really bad idea when you have osteoporosis, especially injecting it into areas that are already compromised, like the hips, for example.

In Part II, I will go into all the many things we can do to improve bone health naturally. You definitely want to stay tuned for that.

Can’t wait? Book a consultation with Marc to get some immediate advice about how you can prevent and treat osteoporosis.

Click here to learn more.

References:

https://www.iofbonehealth.org/facts-and-statistics/index.html#category-299 Statistics

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2266953/ Bone loss in menopause

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4199196/ TSH and Levothyroxine and Bone Loss

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279063/ High prevalence of oesteoporosis in women with subclinical hypothyroidism treated with levothyroxine

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4199196/ Effects of levothyroxine and TSH on bone loss

http://www.ncbi.nlm.nih.gov/pubmed/18981975: Bone loss in worse in post menopausal women treated with levothyroxine

https://ostelin.com.au/bones-grow-develop/

https://depts.washington.edu/bonebio/bonAbout/bonecells.html

https://www.ncbi.nlm.nih.gov/pubmed/19885809 Actions of thyroid hormone in bones

Bone loss in worse in post menopausal women: http://www.ncbi.nlm.nih.gov/pubmed/18981975

Bone Loss and Autoimmunity: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1308846/

Osteoimmunology -link between immune system and bone loss http://www.ncbi.nlm.nih.gov/pubmed/23457765

Cytokines and Bone Loss: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC294166/pdf/jcinvest00033-0178.pdf IL-11 and bone loss

http://www.ncbi.nlm.nih.gov/pubmed/8275387 Cytokines and bone reabsorption

http://www.nature.com/nrd/journal/v11/n3/fig_tab/nrd3669_F3.html Inflammatory bone loss illustration

http://www.ncbi.nlm.nih.gov/pubmed/18992710 NfKb and osteoclasts

http://www.ncbi.nlm.nih.gov/pubmed/18365831 Osteoclasts, innate immune cells of the bones

http://www.ncbi.nlm.nih.gov/pubmed/16831928 Autoimmunity and bone

https://www.researchgate.net/publication/281395069_Journal_of_Autoimmunity Bone erosion and autoimmunity

http://www.4.waisays.com/ExcessiveCalcium.htm

A Metric Ton of Additional Research

Erben RG, et al, Androgen deficiency induces high turnover osteopenia in aged male rats: a sequential histomorphometric study. J. Bone Miner. Res. 2000 / 15 (6) / 1085-1098. ,

Yeh JK, et al, Ovariectomy-induced high turnover in cortical bone is dependent on pituitary hormone in rats. Bone1996 / 18 (5) / 443-540. ,

Garnero P, et al, Increased bone turnover in late postmenopausal women is a major determinant of osteoporosis. J. Bone Miner. Res.1996 / 11 (3) / 337-349.

Taguchi Y, et al, Interleukin-6-type cytokines stimulate mesenchymal progenitor differentiation toward the osteoblastic lineage. Proc. Assoc. Am. Physicians 1998 / 110 (6) / 559-574. ,

Jilka RL, et al, Loss of estrogen upregulates osteoblastogenesis in the murine bone marrow.

Evidence for autonomy from factors released during bone resorption. J. Clin. Invest. 1998 / 101 (9) / 1942-1950. ,

Tau KR, et al, Estrogen regulation of a transforming growth factor-beta inducible early gene that inhibits deoxyribonucleic acid synthesis in human osteoblasts. Endocrinology1998 / 139 (3) / 1346-1353. ,

Hietala EL, The effect of ovariectomy on periosteal bone formation and bone resorption in adult rats. Bone Miner. 1993 / 20 (1) / 57-65. ,

Egrise D, et al, Bone blood flow and in vitro proliferation of bone marrow and trabecular bone osteoblast-like cells in ovariectomized rats. Calcif. Tissue Int. 1992 / 50 (4) / 336-341.

Jilka RL, et al, Osteoblast programmed cell death (apoptosis): modulation by growth factors and cytokines. J. Bone Miner. Res. 1998 / 13 (5) / 793-802.

Mogi M, et al, Involvement of nitric oxide and biopterin in proinflammatory cytokine-induced apoptotic cell death in mouse osteoblastic cell line MC3T3-E1. Biochem. Pharmacol. 1999 / 58 (4) / 649-654. ,

Kobayashi ET, et al, Force-induced rapid changes in cell fate at midpalatal suture cartilage of growing rats. J. Dent. Res.1999 / 78 (9) / 1495-1504.

Vegeto E, et al, Estrogen and progesterone induction of survival of monoblastoid cells undergoing TNF-alpha-induced apoptosis. FASEB J.1999 / 13 (8) / 793-803. ,

Tomkinson A, et al, The role of estrogen in the control of rat osteocyte apoptosis. J. Bone Miner. Res. 1998 / 13 (8) / 1243-1250.

Boot AM, et al, Bone mineral density in children and adolescents: relation to puberty, calcium intake, and physical activity. J Clin Endocrinol Metab 1997 Jan;82(1):57-62. ,

Hu JF, et al, Dietary calcium and bone density among middle-aged and elderly women in China. Am J Clin Nutr 1993 Aug;58(2):219-27.

Weinstein RS, et al, Apoptosis and osteoporosis.Am. J. Med. 2000 / 108 (2) / 153-164. , Manolagas SC, Birth and death of bone cells: basic regulatory mechanisms and implications for the pathogenesis and treatment of osteoporosis. Endocr. Rev. 2000 / 21 (2) / 115-137. ,

Rodriguez JP, Abnormal osteogenesis in osteoporotic patients is reflected by altered mesenchymal stem cells dynamics. J. Cell. Biochem. 1999 / 75 (3) / 414-423. ,

Gazit D, et al, Bone loss (osteopenia) in old male mice results from diminished activity and availability of TGF-beta. J. Cell. Biochem. 1998 / 70 (4) / 478-488. ,

Ikeda T, et al, Age-related reduction in bone matrix protein mRNA expression in rat bone tissues: application of histomorphometry to in situ hybridization. Bone1995 / 16 (1) / 17-23. ,

Parfitt AM, et al, Relations between histologic indices of bone formation: implications for the pathogenesis of spinal osteoporosis. J. .Bone Miner. Res.1995 / 10 (3) / 466-473. ,

Neidlinger-Wilke C, et al, Human osteoblasts from younger normal and osteoporotic donors show differences in proliferation and TGF beta-release in response to cyclic strain. J. Biomech. 1995 / 28 (12) / 1411-1418. ,

Marie PJ, Decreased DNA synthesis by cultured osteoblastic cells in eugonadal osteoporotic men with defective bone formation. J Clin Invest 1991 Oct;88(4):1167-1172.

Weinstein RS, et al, Apoptosis and osteoporosis.Am. J. Med. 2000 / 108 (2) / 153-164. , Manolagas SC, Birth and death of bone cells: basic regulatory mechanisms and implications for the pathogenesis and treatment of osteoporosis. Endocr. Rev. 2000 / 21 (2) / 115-137. ,

Rodriguez JP, Abnormal osteogenesis in osteoporotic patients is reflected by altered mesenchymal stem cells dynamics. J. Cell. Biochem. 1999 / 75 (3) / 414-423. ,

Gazit D, et al, Bone loss (osteopenia) in old male mice results from diminished activity and availability of TGF-beta. J. Cell. Biochem. 1998 / 70 (4) / 478-488. ,

Ikeda T, et al, Age-related reduction in bone matrix protein mRNA expression in rat bone tissues: application of histomorphometry to in situ hybridization. Bone1995 / 16 (1) / 17-23. ,

Parfitt AM, et al, Relations between histologic indices of bone formation: implications for the pathogenesis of spinal osteoporosis. J. .Bone Miner. Res.1995 / 10 (3) / 466-473. ,

Neidlinger-Wilke C, et al, Human osteoblasts from younger normal and osteoporotic donors show differences in proliferation and TGF beta-release in response to cyclic strain. J. Biomech. 1995 / 28 (12) / 1411-1418. ,

Marie PJ, Decreased DNA synthesis by cultured osteoblastic cells in eugonadal osteoporotic men with defective bone formation. J Clin Invest 1991 Oct;88(4):1167-1172.

(9) Byers RJ, et al, Differential patterns of osteoblast dysfunction in trabecular bone in patients with established osteoporosis. J. Clin. Pathol. 1997 / 50 (9) / 760-764. ,

Mullender MG, et al, Osteocyte density changes in aging and osteoporosis. Bone1996 / 18 (2) / 109-113. ,  Ikeda T, et al, Age-related reduction in bone matrix protein mRNA expression in rat bone tissues: application of histomorphometry to in situ hybridization. Bone1995 / 16 (1) / 17-23. ,

Hills E, et al, Bone histology in young adult osteoporosis. J. Clin. Pathol. 1989 / 42 (4) / 391-397.

Kassem M, et al, Demonstration of cellular aging and senescence in serially passaged long-term cultures of human trabecular osteoblasts. Osteoporos. Int. 1997 / 7 (6) / 514-524. ,

de Vernejoul MC, Bone remodelling in osteoporosis. Clin. Rheumatol.1989 / 8 Suppl. 2 / 13-15.

Delany AM, et al, Osteopenia and decreased bone formation in osteonectin-deficient mice. J. Clin. Invest. 2000 / 105 (7) / 915-923. ,

Gazit D, et al, Bone loss (osteopenia) in old male mice results from diminished activity and availability of TGF-beta. J. Cell. Biochem. 1998 / 70 (4) / 478-488. ,

Arlot M, et al, Impaired osteoblast function in osteoporosis: comparison between calcium balance and dynamic histomorphometry. Br. Med. J. (Clin. Res. Ed.) 1984 / 289(6444) / 517-520.

Namkung-Matthai H, et al, Osteoporosis influences the early period of fracture healing in a rat osteoporotic model. Bone2001 / 28 (1) / 80-86. ,

Dunstan CR, et al, Bone death in hip fracture in the elderly. Calcif. Tissue Int. 1990 / 47 (5) / 270-275.

Intermittent Fasting and Hashimoto’s

Intermittent fasting is an approach to timing your meals that has grown in popularity. Recently a number of people have asked my opinion about doing it if you have Hashimoto’s.

Like all things Hashimoto’s related, this is a complicated question masquerading as a simple one.

How does Intermittent Fasting (IF) Work?

IF is not really a diet, it’s more of an eating pattern where you cycle between your regular meal pattern and fasting (not eating at all).

The focus is not on what foods you should eat, it’s more on when you should eat whatever is you choose to eat.

If you have been following me for any period of time you will know that I believe what you eat makes a huge difference if you are trying to heal. And the reason is simple: Hashimoto’s is an autoimmune disease and an estimated 70-80% of our immune system lives in our digestive tract.

So what you eats matters, in a big way. It also turns out that deciding not to eat can also have major impacts on your health.

The question today is what are the pros and cons of intermittent fasting with regards to Hashimoto’s and hypothyroidism.

What’s the Point of IF?

The reason IF has become popular is that it has been shown in some research to have a number of health benefits.

Basically, there are three major mechanisms that have been identified as benefits of intermittent fasting:

• 1. Increased insulin sensitivity and mitochondrial energy efficiency – Fasting increases insulin sensitivity and improves energy production from mitochondria (your body’s energy factories), this slows aging and disease and helps with weight loss.
• 2. Increased capacity to resist stress, disease and aging – stress isn’t always bad. Fasting causes a stress response inside cells (kind of like exercise). This causes genes to be expressed that help your body better cope with stress.
• 3. Reduced oxidative stress – fasting helps reduce free radicals inside your cells and prevents damage from them.

This All Happens in People Who Don’t Have Hashimoto’s

Before you get all excited, it’s important to understand that people with Hashimoto’s are not normal subjects.

They often don’t have normal insulin responses, their immune systems are hyper-vigilant, and they rarely have a normal capacity for handling additional stress.

It’s important to understand is that intermittent fasting can help you under some circumstances and can actually do some harm in others.

Preserving Your Circadian Rhythm Trumps Everything Else

The more I study physiology and look at the connections between systems of the body, the more I realize how incredibly important respecting your body’s natural clock is.

This is one of those areas that can have a profound impact on your health and well being and on the progression of your Hashimoto’s.

Your body’s natural clock regulates your hormones, affects your ability to digest food and absorb nutrients, affects immune function, eliminates toxins, and helps regulate your insulin and stress responses.

If this system is out of whack it can result in you not sleeping properly, having digestive issues and constipation, craving sweets and carbs, having trouble losing weight and having a really hard time handling stress (Sound familiar? These are super common Hashimoto’s symptoms).

These chronic disruptions of your circadian rhythms are pretty much ignored by proponents of intermittent fasting.

Eating times are either random or just plain wrong. This can have huge consequences when you have Hashimoto’s and autoimmunity. You can not overlook the relationship between meal times and your body’s internal clock, especially if you need to restore that rhythm.

When Are the Best Times To Eat?

Your body is actually programmed to eat at night. The Autonomic nervous system operates around your circadian clock.

During the day your sympathetic nervous system puts your body into an energy burning mode, whereas at night your parasympathetic nervous system puts your body into an energy replenishing relax and sleep mode.

This is why normal cortisol peaks in the morning and gradually diminishes and melatonin peaks at night.

Unfortunately, this system is highly sensitive to getting disrupted, especially when you have autoimmunity and hypothyroidism and none of your body’s systems are functioning properly.

So, if you eat at the wrong times when having a large meal during the day, you can cause insulin surges and this can totally mess up your autonomic nervous system.

This can result in you inhibiting your sympathetic nervous system and turning on your parasympathetic nervous system which makes you feel tired and fatigued during the day.

And instead of spending energy and burning fat, you’ll store energy and gain more fat. This is a downward spiral and the ultimate no win situation.

The problem with many intermittent fasting programs is that they don’t pay any attention to this at all.

Another thing that is really important with Hashimoto’s is blood sugar balance. I have written pretty extensively about this here.

The impact of fasting on a pre-existing blood sugar imbalance must be considered whenever you’re considering doing IF. I CANNOT OVERSTATE HOW IMPORTANT THIS IS!!!!

Let’s Breakdown Some Common IF Programs. Here are the most common approaches that I could find:

ALTERNATE DAY FASTING: Followers of this program eat on some days and don’t eat at all on others. This is really hard to do and can result in a major surge in hunger (obviously).

If you do this and then binge eat, you are pretty much guaranteeing a massive insulin surge. This will cause a cortisol surge which can result in LH and FSH suppression by the pituitary, problems with liver detoxification, under conversion of T4 into T3, thyroid hormone receptor resistance and suppression of SIgA and a breakdown of immune barriers.

If you are hypoglycemic, your blood sugar will crash dangerously and you might wind up feeling major fatigue, having insomnia, getting irritable and/or depressed, slowing your metabolism so that losing weight will be harder, getting headaches and hormonal imbalances. Not good.

There are reports from people who have tried this that they experience sleeping disorders, constipation and persistent fatigue. In other words, an absolute disaster for people with Hashimoto’s.

ONCE A WEEK OR TWICE A WEEK FASTING: A little easier to do than alternate day fasting, but the problems mentioned above still persist. Coming off of it can generate massive insulin surges and hypoglycemics will suffer in a big way.

FASTING EVERY OTHER WEEK OR EVERY MONTH: This is even worse than once or twice a week and basically it’s an attempt to create an easy fast program. Half measures almost never result in half successes in my experience, they result in disappointment and failure.

SKIPPING DINNER: This totally goes against your body’s natural rhythms. If you’re hypoglycemic you’re just prolonging the punishment and the damage.If you are insulin resistant you may once again wind up with an insulin surge when you have breakfast.

This can also make sleep problems worse. People who are in favor of this approach say that breakfast is a very important meal and should not be skipped.

I agree, but most Americans have a breakfast that is heavily weighted towards sugar and carbohydrates. That is a recipe for insulin surges and a day filled with misery.

SKIPPING BREAKFAST: Some people feel that this is better than skipping dinner. Especially if you exercise in the morning. But this also can cause problems.

Again, if you are hypoglycemic you will not have had anything for 6-9 hours – fasting is technically the gap between meals minus digestion time – so even though you don’t eat for 12-16 hours you’re actually fasting for 6-9 hours.

No matter how you calculate it, that’s just too long.

What’s the Best Approach?

For hypoglycemics or people with Hashimoto’s who have a mixed presentation of hypoglycemia and insulin resistance, I think it’s far more important to work to balance blood sugar and to restore and preserve circadian rhythms.

In my experience that will make you feel much better, help you to have enough energy to exercise and be active and get you in a position to actually lose weight. 

And your choice of foods is also very important. Eating foods that are high in nutrient density and avoiding inflammatory foods like gluten, dairy and non-fermented soy is also much more important than fasting for reducing systemic inflammation.

Is There A Fasting Approach That Can Work for People With Hashimoto’s?

It really depends on how bad things are and where you are in the progression of the disease. If you have major disruptions in your circadian rhythms and you have major imbalances in blood sugar, I would strongly discourage attempting the intermittent fasting programs.

In my experience most people who have Hashimoto’s that come for treatment are advanced enough where intermittent fasting just doesn’t give you enough benefits for all the serious downsides that may result.

If you have healed to the point where you have restored your circadian rhythms and you blood sugar is well balanced then perhaps the One Meal Per Day Fast could be something that you could attempt.

The is really the only viable option for keeping balance of your body’s clock and maximizing the beneficial effects of intermittent fasting. If you exercise, you’ll need to feed your muscles post workout with a low glycemic index recovery meal to avoid the dangers of insulin surges.

And having proteins and carbs before your workout that are quickly assimilated can help load glycogen in your muscles, nourish the fast fibers in those muscles and help boost max strength and performance.

With Hashimoto’s, however, this is another potential land mine as the most commonly recommended form of protein is good quality whey protein and while whey is refined and filtered it can contain trace amounts of casein which can cause major immune flare ups in some Hashimoto’s folks.

Check out this post to learn more. 

Bottom Line:

In my opinion, intermittent fasting can have some health benefits for people whose Hashimoto’s is very well managed and who have balanced blood sugar and well respected and preserved circadian rhythms.

Unfortunately, the reality is that most people with Hashimoto’s have not achieved anything close to that in their lives and many have some degree of circadian disruption and some degree of blood sugar dysfunction.

For them, working to restore their body’s natural clock and to keep their blood sugar stable throughout the day is much more important than jumping on the IF bandwagon.

Daily focus on those two goals (body clock maintenance and blood sugar balance) is a much better use of your money, time, and energy and will yield much better long and short term results like more energy, better sleep, better digestion and a happier mood and outlook on life.

References:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3680567/ IF research overview

http://www.nature.com/ijo/journal/v35/n5/full/ijo2010171a.html IF and insulin sensitivity

http://ajcn.nutrition.org/content/86/1/7.full Review of trials IF

http://fitness.mercola.com/sites/fitness/archive/2012/09/14/intermittent-fasting-benefits.aspx

Hashimoto’s Diet in 5 Steps

Hey people!

I get a lot of requests for advice on diet and though it can be really tricky and complicated, I decided to create an infographic to give you a Hashimoto’s diet in 5 steps for reducing systemic inflammation.

As I am fond of saying, when it comes to Hashimoto’s and hypothyroidism, inflammation is the root of all evil. And diet is a big player in inflammation.

Here’s the entire 5 steps in an easy to follow infographic. Feel free to download it and share.

Hashimoto’s Diet in 5 Steps

The diet is pretty straight forward, but for some people it can be a radical departure from what you are used to.

Let’s break down some of the most important elements.

1. First of all, get a journal. 

Not to eat ;), but to keep track of everything you are doing. Some of us operate under the delusion that we are good at remembering things. When it comes to your diet and reactions to what you eat, you aren’t. There are way to many variables and things going on, you can’t possibly remember it all.

And why does it matter? Your immune system lives in your digestive tract (an estimated 70-80% is found there) and when you have autoimmunity, interactions with your immune system can have consequences.

When you react to certain foods or herbs or supplements, this can cause an immune response, which can lead to more inflammation and it can promote an attack on your own tissue.

So it’s really important to identify what foods in your diet cause responses. And some of these responses are digestive and others may be emotional or neurological. That’s why we need the journal to look for patterns.

2. Simplify Your Diet

If you’re just starting out. It’s time to simplify. Too many variables means that you don’t know what’s causing what. You need to simplify things (often in more than one part of your life).

Start with your diet. And start with the foods that can have the biggest impact. These are: gluten, dairy and soy.

There are reams of research on gluten and thousands of success stories from people who have gotten off of it and feel significantly better. If you doubt that this is true, here’s a post where I looked into this topic and a metric ton of research.

Same is true of dairy, Both lactose and casein (a protein found in milk) can be problematic for Hashimoto’s folks. They can hamper conversion and absorption of thyroid hormone. Still not convinced? Read this post that also looks at tons of research.

And soy is a goitrogen and can also hamper thyroid hormone behavior in the body. Go off of all three for 30 to 60 days minimum, 100%. Note all the symptoms you have in your journal before, during and after. Then review the journal and see how many remain.

3. Remove Inflammatory Foods

The next step is to take this to the next level. The reality is that gluten, dairy and soy may just be the tip of the iceberg.

Other foods like refined sugars, alcohol, grains, nuts and seeds, and nightshades (tomatoes, eggplants, peppers and white potatoes) can also cause inflammation. This is basically the Autoimmune Paleo Diet, you can learn more about it in this post.

You can test to see whether or not you have sensitivities to these foods, but sometimes these tests are inaccurate and you may react to those foods any way.

The best way to find out is to eliminate these foods for a period of time (usually 30 to 60 days) and then reintroduce them in a systematic way, one food at a time (More on that in a moment).

Here, again, your journal is a very important tool. Note all the symptoms you had when you started this phase of your recovery and keep track before, during and after.

During this period, it’s also a great time to detoxify your liver, work on healing leaky gut, boost stomach acid, balance blood sugar and work on all the systems of your body that may be compromised.

4. Re-evaluate and Test

Once you’ve gone through this process, you need to re-evaluate. This is where your journal becomes worth it’s weight in gold. You took the time to keep track of what you did, now go back over it and analyze the data.

What improved and what didn’t? Where did you cheat? What happened when you did? How much better are you know than when you began?

If you like many of the people I work with, chances are you got some improvement from this process. But if you still aren’t satisfied with your results, the it may be time to dig a bit deeper and do some testing (this can also be done at the beginning, of course).

You might want to rule out SIBO (Small Intestine Bacterial Overgrowth), candida, H.pylori, blastocystis, parasites and more. Most of these can ordered in a single stool test.

5. Re-introduce and Double Down

The final step is to go through the re-introduction process. Again, you’ll need your journal. Introduce one food at a time as the only variable. Start small and keep track of your reactions.

This will give you invaluable information on what foods you react to and it will help you create a solid foundation for healing.

Once you go through this, you will be able to identify what works and what doesn’t. Double down on what works and tweak or experiment with variations of what didn’t.

Awesome! Great job! Now you are on your way to getting your Hashimoto’s into remission. Remember remission is a journey a destination, you are now on the right path in your journey.

P.S. Staying on a restrictive diet for too long a period of time also can have consequences. Read this post to learn what I mean.

Need help?

Feeling a little overwhelmed by all this? No worries, reach out to Marc and set up a consultation to help guide you on your way.

Click here to set up a consulting call with Marc.

Lots of Things Impact Thyroid Hormone Absorption

Hey people,

I had a question recently from someone asking what foods can hamper thyroid hormone absorption. This is an important question, so I thought I’d take this opportunity to answer it.

How Hormones Bind

The first thing to understand about thyroid hormone is that it behaves a little differently than many of it’s hormone cousins and binds quite easily to stuff.

Let me break it down for you:

The ability of a hormone to bind to a receptor inside or outside a cell depends on the chemical makeup of that hormone and how compatible it is to the cell’s fatty outer membrane.

Some hormones can go easily into cells to find receptors. For example, fat based steroid hormones like estrogen, progestins, etc. belong to this category. They prefer fatty surroundings (fat or lipid soluble) and they don’t like water.

As a result they can pass easily through the cell membrane, but they need proteins to help them through the watery bloodstream (these are the binding globulins that you may have heard of).

Receptors for these steroid hormones are found in several different places: the cells outer membrane, the cytoplasm and/or the nucleus inside the cell.

Other hormones stay outside the cell and attach to receptors found in the outer membrane. Insulin, growth hormone and other protein based peptide hormones prefer water (water soluble) and don’t like fat (fat insoluble).

The cell’s fatty membrane makes it difficult for these messengers to enter the cell. This keeps these peptide hormones outside the cell where they only bind with receptors found there.

Thyroid Hormone Is Unique

Thyroid hormones, which are derived from amino acids, behave more like steroids than its peptide cousins and can actually bind to receptors both inside and outside the cell.

Which means they are very adaptable and flexible and it can also mean that they are able to bind to other things as well, like food, chemicals and minerals.

Many Drugs and Supplements Bind to Thyroid Hormone

Many commonly used medications or supplements like iron, calcium, estrogen, proton pump inhibitors, and statins can cause affect thyroid hormone absorption or binding to plasma proteins.

Sometimes, if the doctor is paying attention, this may require making changes in dosage of levothyroxine. If you have been prescribed any of these drugs with your thyroid medication, you need to be aware of this.

Alcohol

Alcohol can disrupt thyroid function in a number of different ways. There are some indications that it may lower peripheral T4 and T3 levels.

In addition, it has a toxic effect on thyroid cells and ethanol is actually used to treat thyroid nodules in some cases. It can also, potentially, reduce the risk of certain types of thyroid cancer.

On the flip side, alcohol is very hard on the digestive tract and can also lead to destruction of the gut lining and make leaky gut worse.

I generally recommend avoiding alcohol, especially if you are trying to heal the gut.

Coffee and Tea

Coffee also impacts the absorption of levothyroxine; this is why thyroid patients need to take their hormone replacement pill at least an hour before drinking coffee.

Caffeine found in coffee can also increase blood sugar levels . This is especially bad for people with hypoglycemia (or low sugar levels) because it can lead to complications.

For example, blood sugar fluctuations can cause cortisol spikes, which not only exhaust the adrenals, but also can wreak havoc on the immune system. Obviously, this is not a good thing for those of us with adrenal fatigue, and/or Hashimoto’s.

I recommend avoiding coffee if you have adrenal issues or hypoglycemia.

Black and green tea also has caffeine (though in lesser amounts than coffee), and it contains tannins which can hamper iron absorption and many teas also contain fluoride which blocks iodine absorption and may hamper thyroid function.

Green and Black tea are also Th2 stimulants. Drinking it in moderation may be ok for some and not good for others. If you drink a lot of tea, you may want to eliminate it for a period of time to see if it has an impact on your symptoms.

High doses of green tea have also been found to cause a significant decrease in serum T3 and T4 and increase in TSH levels has been reported along with decreased TPO and deiodinase activity in response to dietary green tea extract in rats.

Gluten 

There is ample evidence that gluten can lead to poor absorption of thyroid hormone. This is true for a couple of reasons; it can lead to destruction of the intestinal lining (which can hamper absorption), and it can cause systemic inflammation (which can clog receptors) This can lead to hypothyroidism and/or poor results from medication.

If you follow this page, you know I recommend eliminating gluten 100%. (For an in depth look at this read this post.)

Dairy

Lactose has also been found to hamper thyroid hormone absorption. And casein, a protein found in milk is similar in protein structure to gluten and can also cause gluten like problems.

I also recommend eliminating dairy 100%. (Grass fed butter is one possible exception) (For an in depth look at this read this post.)

Soy

Soy is rich in phytoestrogens and affect levels of thyroid binding globulin (creating more of it). It can also hamper thyroid hormone absorption. Soy can also be goitrogenic in large quantities.

Soy protein and isoflavones doesn’t seem to harm people with sufficient levels of iodine, but it still may interfere with absorption of thyroid medication.

I generally recommend avoiding soy with the occasional exception of miso and fermented soy products like tempeh.

Sugar

As mentioned above, the adrenals release cortisol to compensate for low blood sugar levels.

Cortisol directly inhibits the enzyme (5’-deiodinase) which converts inactive T4 into active T3.  This can lead to low T3 levels.

In addition, elevated cortisol will cause thyroid hormone receptor insensitivity meaning that even if T3 levels are high enough, they may not be able to bind normally to receptor sites. And when this happens it doesn’t get into the cells.

Cortisol will also increase the production of reverse T3 (rT3) which is inactive. (It’s kind of like the anti-hormone.)

rT3 can cause an increase in the production of substances known as thyronamines that can cause hypothyroid symptoms (like, low basal body temperature,fatigue, depression, etc.) along with insulin resistance symptoms of increased blood sugar.

Cortisol can also lower the levels of protein that binds to thyroid hormone so it can circulate in a stable structure.

And finally, elevated cortisol will slow TSH production by messing with hypothalamic-pituitary feedback leading to lower TSH production.

Sugar should be treated as the addictive drug that it is. Use with extreme caution.

Processed Foods

Processed foods tend to be high in both sodium, sugar and saturated fat. High sodium levels have been linked to autoimmunity and to thyroid disease. Sodium is important for getting iodide into thyroid cells.

Excess amounts of sodium can lead to higher amounts of iodine in the thyroid which can lead to a more aggressive autoimmune attack.

We have already discussed problems caused by low sugar. High blood sugar levels can lead to insulin resistance. This can also cause a reduced conversion of T4 to T3 hormones.

Eat real whole food. Processed food has little or no nutritional benefit. Don’t eat it.

Fat

Diets high in polyunsaturated fat caused significant thyroid dysfunction in rats. High triglycerides, decreased total T4 and free T4 levels and elevated TSH were all noted.

Goitrogens

Naturally Found in found in legumes, plants, amiodarone, lithium, as well as cabbage, cauliflower, broccoli, turnip, forms of root cassava. These may reduce T4 absorption if iodine and/or selenium levels are low.

Generally, I think these foods have so many health benefits that they should be eaten. Goitrin is an active goitrogen present in plants of Rutabaga, turnip and Brassicae seeds.

Steam or blanch the vegetables as cooking destroys the enzyme responsible for activation of progoitrin to goitrin thus negating its anti-thyroid effects.

So, eat these vegetables, but don’t eat wheel barrels’ full. Normal moderate amounts are fine, in my opinion.

Millet

This common gluten free ingredient contains C-glycosylflavones which may inhibit TPO activity. Be cautious with millet. In moderate amounts it is probably ok.

Environmental Toxins

Pesticides can lead to decreased half life of T4.

BPA (bisphenol-A) has been found to be an endocrine disruptor and may have direct action on thyroid receptors.

Percolates found in rocket fuel, thiocyanates and nitrates interfere with iodine uptake. A study in California on pregnant women found a strong association between urinary percolate levels and decreased total and free T4 and increased TSH.

Heavy metals like cadmium and lead are also known to affect thyroid function. In a study on pregnant women, those from lead exposed town had lower mean free thyroxine (FT4), higher mean TPO antibodies along with higher lead concentration suggesting stimulation of auto-immunity by prolonged lead exposure.

Bottom Line:

As you can see, there are many things that can bind to thyroid hormone both natural and chemical. All must be considered when deciding on dosage and when trying to improve thyroid hormone function in the body.

References:

https://www.ncbi.nlm.nih.gov/pubmed/25040647 Drugs and thyroid hormone interactions

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3743356/ Alcohol and the thyroid axis

https://www.ncbi.nlm.nih.gov/pubmed/9846599 Affects of caffeine on glucose levels

http://www.thyroid.org/patient-thyroid-information/ct-for-patients/vol-5-issue-6/vol-5-issue-6-p-3-4/ Gluten, celiac and thyroid hormone absorption.

https://www.researchgate.net/publication/230762976_The_influence_of_lactose_intolerance_and_other_gastro-intestinal_tract_disorders_on_L-thyroxine_absorption

https://www.ncbi.nlm.nih.gov/pubmed/16571087 Soy and Thyroid hormone absorption

https://www.ncbi.nlm.nih.gov/pubmed/15642784 Sodium and thyroid hormone

https://www.ncbi.nlm.nih.gov/pubmed/20561943 Green tea and thyroid function

in rats

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4220075/ Fat and rats

https://www.ncbi.nlm.nih.gov/pubmed/26485730 California Percolate study

https://www.ncbi.nlm.nih.gov/pubmed/24866691 Lead exposure and thyroid function

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4740614/#b52 Possible Toxicants Involved in thyroid dysfunction

Kichari: Cleansing, Detoxifying & Delicious

Hey people!

Here’s an awesome recipe for one of my favorite dishes called Kichari.

It’s a delicious dish, traditionally made in India that is easy to digest, detoxifying and anti-inflammatory.

It’s really easy to make too!

I like to make a big batch and then eat it for the rest of the week. It can also be eaten as a fast to detoxify the body and lose weight.

It’s not exactly AIP perfect, but it’s still quite beneficial. (This is better after you’ve gone through the elimination phase and have reintroduced foods.)

One of the ingredients is mung bean. If you aren’t familiar with it, it’s small green bean is used in Chinese Medicine to clear heat and toxins and was used traditionally as an effective antidote for overdose from a variety of toxins.

This dish is also flavored with turmeric, a fantastic anti-inflammatory.

Ingredients:

Equal parts:

Powdered turmeric, cumin and coriander. (1 tbsp or so of each)

1 cup white basmati rice

1 cup mung beans (if you feel ambitious you can sprout these first)

ghee or coconut oil (1-2 tbsp)

1 tbsp fresh grated ginger

Coconut yoghurt

Cilantro and lime to garnish

1. Wash and soak the rice and beans separately.
2. Cook each separately and set aside. (I like to use a rice cooker for the rice.)
3. In a deep pan, heat the ghee or coconut oil until it is melted. Add the spices and mix altogether until all the spices meld together and you smell the aroma. Add the fresh grated ginger.
4. Add the cooked rice and beans.
5. You can also mix in cubed, cooked winter squash (butternut or kabocha) and/or some sautéed vegetable like spinach or kale.
6. Garnish with a few sprigs of cilantro, a spoonful of coconut yoghurt and a lime wedge and enjoy!

Yum!

The Earth Element: Emotions and Spheres of Influence

In previous a previous post, we looked at the role of blood sugar imbalances on the thyroid and the thyroid axis. The endocrine gland that is in control of sugar balance in the body is, of course, the pancreas.

The pancreas is part of the Earth Element in Chinese Medicine. In this post, which is an excerpt from my book, Roadmap to Remission, we explore some of the important concepts related to the Earth Element and how they affect the thyroid axis.

The Spleen/Pancreas: It’s a Hybrid

Okay, so now let’s take a look at the Earth Element and its sphere of influence. As I said, the yin organ is the spleen, and the yang organ is the stomach.

The endocrine gland associated with the Earth Element is the pancreas. In fact, a lot of what the ancient Chinese ascribed to the spleen sounds, in my opinion, very much like the pancreas.

The other parts of the system that represent the Earth Element are the mouth, saliva, flesh, or muscles. It governs the sense of taste.

The spleen governs digestion and keeps the blood circulating. We know that it is also responsible for cleaning old and dead red blood cells from the bloodstream. It also stores platelets that aid in clotting and coagulation.

The ancient Chinese recognized the spleen as an important organ for immune function. We know now that it also stores monocytes—the Pacman white blood cells—and that B and T cells are made and mature in the spleen.

Remember in the last chapter when we spoke about certain immune cells producing TSH? Well, some of those cells come from the spleen.

The sense organ associated with the spleen is the mouth and health issues involving the spleen sometimes manifest on the lips and the corners of the mouth.

The negative emotion of the spleen is worry or obsessive thinking, and the energy or vitality of the Earth Element is intent.

This energy is linked with mental and physical activity of the body. Lack of desire or difficulty with coordination and movement of the body may reveal an issue with intent and, therefore, the spleen.

This difficulty with coordination is a problem with moving and articulating the limbs, and it is associated with poor utilization of nutrients by the muscles.

What are they talking about? It could be insulin utilization—the state of insulin resistance that we spoke about in the last chapter.

Almost all cells in the body have insulin receptors. So intent involves a major mental component and is also under the influence of insulin, but not always for the purpose of just utilizing glucose. Insulin can also help with the uptake of certain amino acids.

Serotonin Is a Great Example

One interesting example of this relationship involves serotonin.

The brain’s ability to absorb serotonin is enhanced by insulin. If you become insulin resistant, what happens emotionally? You lose this intent, you become depressed, and you crave carbs to try and make you feel better.

Do you see how this is all connected? These are examples of spheres of influence.

In a spiritual sense, this intent affects the digestive functions of thought that allows for the processing and assimilation of our life experiences in a nourishing way.

Unbalanced function leads to brooding, worry, and excessive thought patterns, such as obsessive compulsive disorders. People who think obsessively can become stuck in a pattern of thinking for thinking’s sake alone, and they don’t get nourished by their experiences, because they can’t move on.

One of the health issues that is problematic for the spleen is dampness. Internally, this can take the form of phlegm. Phlegm is made in the spleen and then sent up to the lung.

Metaphorically, dampness is an accumulation of everything that should be nourishing, but instead has become a burden. In a psychological sense, it manifests as lethargy, boredom, mental sluggishness, obsessive thinking, and brooding.

On a physical level, phlegm dampness accumulates in the spleen, stomach, lungs, and large intestines. Sweetness is the flavor of the Earth Element. We’ve seen the problems excess sugar can cause.

Well, from a spiritual/psychological standpoint, this phlegm dampness represents the excessive need to give or receive sympathy. Therefore, it’s spiritual phlegm. It is giving too much and not taking care of yourself or demanding too much so that it becomes a burden to others.

 That’s the beauty of Chinese Medicine. It looks at the connection between things, mind, body and spirit are not separate. They all influence one another.

Pumpkin Pot Pie With Cranberry Chicken

PUMPKIN POT PIE with CRANBERRY CHICKEN

This is my partner, Olesia Farberov’s (she also took the photos!), take on the famous chicken pot pie but Autoimmune-Paleo style. This labor of love will definitely make an impression on your guests and kids.

What can be better than a perfectly wrapped, edible present!

Happy Holidays!

Ingredients:

4 medium or 6 small Pumpkins, scraped of seeds and strings

3 lbs Chicken breast, cut in bite-size pieces

¼ lb Uncured Bacon

4 Carrots, cut in thin rounds

1 large or 2 small Yucca root (optional)

1 large yellow onion, chopped

4 Bay leaf

4 Savory sprigs, thinly sliced

2 Oregano sprigs, thinly sliced

2 Sage leaves, thinly sliced

½ tsp Salt

½ tsp Pepper

1 ½ cup Cranberries, fresh

1. Give your pumpkins a bath with soap and water to rid of any loose dirt. Using a small knife, cut out a hole 4-5” in diameter around the stem and open the “lid”. Scrape the insides of seeds and gooey strings and discard. Set pumpkins aside.2. Peel and cut yucca root into 2” rounds. Cook, covered in water, until easily pierced with fork. Drain and leave it to cool. Once cool enough to handle, cut each piece into bite-size pieces, eliminating the hard, rope-like core. Set aside.

3. In a large pot, fry bacon until golden and crisp. Take out bacon and reserve for later.

4. Preheat oven to 395F.

5. Into the pot of bacon fat, throw in onion and cook until browned. Add chicken, yucca, bay leaf, herbs, salt & pepper and cook over medium-high heat, stirring occasionally, until chicken is cooked through, about 15-20 min. In the last 5 minutes of cooking, add cranberries and stir to distribute evenly.

 

6. Stuff each pumpkin with chicken mixture, including liquid. Cover with pumpkin “lid”. Place on a large sheet, covered with foil, and bake on middle rack at 395F for approximately 1hr or until pumpkin can be pierced easily with a fork.

7. Let pumpkins cool for at least 10 minutes with “lid” slightly open. Before serving, remove lid and sprinkle crumbled bacon into each pumpkin then place the “lid” back on.

Each pumpkin can be served whole or cut into either half (for adults) or quarter size (for kids).

 Have Fun & Enjoy!!

Recipe and photos by Olesia Farberov, L.Ac.

Health News: New Study on Sweet Beverages and Diabetes Risk

This week we are looking into the earth element which involves the spleen and pancreas and how this relates to thyroid and autoimmune disease.

A new study in the news this week has found that drinking soda and other sweet beverages (2 or more per day) doubles the risk for getting diabetes regardless of whether or not it is an artificial sweetener or not.

This was a case-control study within a population-based Swedish cohort study that aimed to see whether consumption of sweetened drinks was associated with risk of a lesser known form of diabetes called latent autoimmune diabetes in adults (LADA).

LADA IS TYPE 1.5 DIABETES

LADA is sometimes called Type 1.5 diabetes because has features of both type 1 diabetes, where the body’s own immune cells destroy the insulin-producing cells in the pancreas and type 2 diabetes, which usually develops later in life and is most commonly caused by eating too much sugar.

But unlike type 1 diabetes, which normally develops in childhood, in LADA the cell destruction is much slower.

Also, the condition often develops later in life and shares many features with type 2 diabetes. For example, the person doesn’t always need treatment with insulin straight away. This study reports that in the Swedish diabetes registry, LADA accounts for 5% of all cases.

WHAT DID THE STUDY FIND?

Data was available for 1,136 people with type 2 diabetes, 357 people with LADA, and 1,371 diabetes-free controls.

Average age was 59 for people with LADA and controls, and 68 for those with type 2 diabetes.

Just under two-thirds of all people reported consuming sweetened (including artificially sweetened) drinks.

In general they found that consumption of sweetened drinks was linked with higher body mass index (BMI) and other poor lifestyle factors like smoking, low physical activity and consumption of processed meat and sugary foods. (Birds of a feather flock together, as do unhealthy habits.)

One problem with the study is that, as you can see, there are many other potential factors that could also lead to poor health and the development of diabetes, so it’s hard to say it’s just soda and other sweet beverages, though these are certainly very high in sugar.

LINK BETWEEN TYPE II DIABETES, LADA AND AUTOIMMUNE THYROID DISEASE

How does this relate to Hashimoto’s?

There are few interesting links between these two diseases.

Firstly, as we noted in a previous post, when you have one autoimmune disease there is a higher risk of developing others.

What’s interesting is that insulin resistance has been found to increase destruction of the thyroid in thyroid autoimmunity, and it can also clearly be a trigger for Hashimoto’s.

These don’t usually develop at the same time and often take years to progress, just like other autoimmune diseases.

In one study of autoimmune polyendocrine diseases it was found that type I diabetes manifested first in half the cases and autoimmune thyroid disease manifested first in 17% of the cases.

And the most common combination was type I diabetes and autoimmune thyroid disease at 33%. 

So, it’s another reminder of how important sugar balance and sugar control is for people with Hashimoto’s.

We explore this idea in depth in this post.

CANDIDA ALSO A  FACTOR IN POLYENDOCRINE DISORDERS

Something else that is really fascinating is that candida is also a common denominator in many autoimmune polyendocrine disorders. 

What does candida thrive on?

Sugar.

Adding another layer of reasons why sugar should be taken seriously. It can not only lead to more autoimmunity, it can also lead to secondary conditions that are both causes of the disease and hindrnaces to getting better.

DIET SODA DOESN’T PROTECT YOU FROM ANYTHING

Finally, I think what’s also an interesting revelation from this is that there is a kind of myth that diet soda is a safer alternative.

Well, various research reviews and a case study have found this not to be true.

In fact, here’s one case study that showed dramatic improvement in Hashimoto’s symptoms when the patient stopped drinking diet soda.

BOTTOM LINE IS THIS

Excessive sugar consumption (and this includes artificial sugar substitutes) is a potential threat not just for Type II Diabetes or LADA, but also for autoimmune thyroid and polyendocrine thyroid diseases.

It can also foster secondary infections like candida and SIBO (Small Intestine Bascterial Overgrowth).

Treat sugar like the potentially dangerous substance that it is.

References:

https://www.ncbi.nlm.nih.gov/pubmedhealth/behindtheheadlines/news/2016-10-21-sweetened-drinks-including-diet-drinks-may-raise-diabetes-risk-/

https://www.ncbi.nlm.nih.gov/pubmed/15182509 LADA and Thyroid autoimmunity

http://www.eje-online.org/content/175/6/605.abstract?sid=93eb363b-97d3-4f35-92cd-11e7c2ed5ee4 sweet

beverage consumption and LADA

http://www.medicalnewstoday.com/articles/313612.php Diabetes risk doubled with soda consumption-diet doesn’t change anything

https://www.ncbi.nlm.nih.gov/pubmed/18800291 Sucralose alters microbiome

https://www.ncbi.nlm.nih.gov/pubmed/20693348 Previous research on soda and type 2 diabetes

http://media.aace.com/press-release/cause-and-effect-case-report-shows-association-between-sugar-substitutes-and-common-th Case study on artificial sweeteners and Hashimoto’s

https://www.sav.sk/journals/endo/full/er0301e.pdf   LADA and Autoimmune Thyroiditis

http://www.diabetesforecast.org/2010/may/the-other-diabetes-lada-or-type-1-5.html?referrer=https://www.google.com/ LADA or Type 1.5 diabetes  

http://www.diabetesselfmanagement.com/diabetes-resources/definitions/type-1-5-diabetes/ More on LADA