In this first post of this series we will examine different Hashimoto’s types and explore the possibility of different types or subtypes of the disease in women.
Autoimmune thyroid disease is the most common autoimmune disease in the US and it affects an estimated 2% of the female population and an estimated 0.2% of the male population.
That’s roughly 3.08 million women in the US. Yet, for some reason all of these cases are treated the same way in the conventional medical model.
If it is determined that they are hypothyroid (their TSH is high and their total T4 is low), then they are prescribed synthetic T4 (Synthroid or a generic equivalent). From there, their TSH and total T4 is monitored and managed and kept within a certain range (which many doctors don’t agree on). That’s the full extent of care.
Actually there are many problems with this approach, but the biggest one is that it ignores two fundamental truths.
Firstly, not all of these people are at the the same stage of progression of the disease. Hashimoto’s is a progressive disease, if untreated or poorly managed it can progress and advance and cause widespread damage in the body. (More on this in a moment.)
Secondly, not everyone who has Hashimoto’s is at the same place in their lives. Women, in particular go through major changes in their lives in adolescence, pregnancy, peri-menopause and in their later years of menopause.
It is common knowledge that the endocrine system, the immune system and the central nervous are all impacted by these changes of life.
Why, then, wouldn’t Hashimoto’s be effected, also?
Well, the truth is, that Hashimoto’s is impacted by different stages in life and these changes can provide important clues on how to better manage the disease and how to prioritize and focus care.
Let’s examine this theory and review the different stages of autoimmune disease and Hashimoto’s.
3 Stages of Hashimoto’s:
In the medical literature several different researchers have identified 3 stages of Hashimoto’s disease.
Dr. Datis Kharrazian has proposed 3 stages of autoimmunity and researchers Arvin Parvathaneni, Daniel Fischman and Pramil Cheriyath has identified 3 stages of Hashimoto’s, as well.
Both theories overlap and this matters because the further the disease progresses the more it impacts other systems of the body.
Here’s an excerpt from my book, Roadmap to Remission which details this progression:
Stage 1: Silent Autoimmunity
In this stage, the body has lost tolerance to its own tissue, but there are no symptoms yet and it doesn’t really affect the way that the system functions. This stage can, however, be identified by lab tests that show elevated antibodies. People can stay in this stage for years.
This is the best place to begin some sort of treatment aimed at prevention, because your odds of getting good results are highest.
Physiologically, in this stage thyroid specific antigens are presented to antigen presenting cells (APCs) by thyroid cells, often after some kind of insult or environmental stressor(s). (For example, infection(s), excessive iodine, pregnancy, toxins in cigarette smoke, etc.)
Stage 2: Autoimmune Reactivity
In this stage, the destruction of the target tissue has begun. Elevated antibodies and some symptoms appear. However, the destruction is not significant enough to actually be labeled autoimmune disease because 70–90 percent of the target tissue has not yet been destroyed. This stage is where a lot of Hashimoto’s patients are.
They may or may not have been placed on thyroid replacement hormone, and that may or may not have normalized their thyroid lab results. However, the destructive autoimmune process is active and is progressing.
This is a very important stage for treating the immune dysfunction, because you have a greater chance to slow or stop the destruction of that tissue and slow the progression to other autoimmune diseases.
Physiologically, this is the stage where APCs (Antigen Presenting Cells) differentiate into T cells and B cells and begin the process of destruction.
Stage 3: Autoimmune Disease
This stage is where Western medicine finally acknowledges the autoimmune disease. And it takes this long, because you need significant destruction of tissue in order to see the destruction with an MRI or ultrasound.
Other findings include elevated antibodies, serious and significant symptoms, lab results, and special studies that all confirm a loss of function. Unfortunately, this is really late in the game. With Hashimoto’s, this stage is where the thyroid is almost completely destroyed.
Luckily, most people don’t reach this stage before they have been given thyroid replacement hormone, because the symptoms have already become so serious that they will have sought out a doctor to help them before they got here.
Finally, this is the stage, physiologically, where positive feedback has led to massive destruction of the thyroid gland and major loss of function in other systems of the body. T cells have induced cytotoxicity, and B cells have produced antibodies that have led to apoptosis or programmed cell death of thyroid cells, and macrophages have infiltrated the thyroid and started producing the interleukin proteins we spoke about earlier.
The reality is that Hashimoto’s can begin at any time in a woman’s life and during the different changes that her body goes through there are different challenges and stressors that can exacerbate or complicate the disease.
In studying the medical literature and in examining my patient population (at the time of writing this blog post I have spoken with over 2,000 people with Hashimoto’s, 99% them have been women, and I have treated over 500 women).
I have identified five different times of life for the onset and/or exacerbation of Hashimoto’s that could represent “types” or “subtypes” of Hashimoto’s patients.
The onset for this age group is most commonly mid-puberty. (Although we are seeing an increase in the prevalence of children diagnosed with the disease.)
Of course, puberty is a time of many hormonal changes, which can also impact the immune system and the nervous system and brain.
These young women have many of the common symptoms of Hashimoto’s and hypothyroidism and may also have developmental disorders if the disease has gone undiagnosed or it began earlier in childhood.
Common symptoms include:
According to an Italian study, the evaluation of these patients, according to their final outcome, revealed that subjects with deteriorating thyroid function had significantly higher anti-TG antibodies, TSH concentrations, and greater thyroid volume at presentation. And after 5 years, more than 50% of the patients remained or became euthyroid (meaning they had a normally functioning thyroid gland).
So this can resolve, and never be a problem again or it can resurface later in life. One of the life events that leads to it resurfacing and/or is a cause for onset all by itself is pregnancy.
In pregnancy, a woman’s body goes through many hormonal changes and the immune system makes large adjustments in order to preserve the fetus and not reject it as a foreign invader.
During the third trimester a pregnant woman becomes TH-2 dominant, then TH-1 dominant after giving birth. This is thought to be due more to the body naturally suppressing TH-1, rather than boosting TH-2.
The Th-1 suppression ends after birth and this causes the immune system to surge. If it is already unstable, this can result in the onset of Hashimoto’s.
This is inflammation in the thyroid that comes on after pregnancy in about 5 to 7 % of women, usually within two to four months after giving birth.
Interestingly, this is also a form of autoimmune disease. (In fact, these two disorders are very hard to distinguished from one another.)
This usually presents as a painless, small, firm enlargement of the thyroid or goiter. And it can cause either hyper or hypothyroid symptoms.
As noted, this can also lead to postpartum depression because of it’s impact on thyroid function.
During postpartum thyroiditis, there are, potentially two phases. The inflammation and release of thyroid hormone may first cause signs and symptoms similar to those of a hyperthyroid condition, including:
Hyperthyroid symptoms usually happen two to ten months after delivery—most commonly at three months—with recovery taking place over the next two to three months after it begins. It is important to figure out if it’s postpartum thyroiditis or Graves’ disease with proper lab testing.
Later, as thyroid cells are attacked, signs and symptoms of a hypothyroid condition may develop, including:
Hypothyroid symptoms usually happen two to twelve months after delivery—most commonly at six months. About eighty percent of women with postpartum thyroiditis return to normal thyroid function around the one-year mark, however, 30 to 50 percent develop permanent hypothyroidism within nine years.
So again, it can resolve and then resurface later after another pregnancy or another stressful time of life or other life change (see below).
Pregnancy and the Pituitary
Another thing that can cause hypothyroidism with pregnancy is the pituitary becoming depressed. Chronic stressors like food intolerances, blood sugar imbalances, gut infections and out of whack hormones can all depress the function of the pituitary.
And the pituitary is responsible for signaling the thyroid, so when it’s depressed it can fail to send enough TSH to the thyroid. Which means this isn’t a thyroid problem at all. It’s really a pituitary issue. For many women this can result in low thyroid function and depression.
And, of course, proper thyroid hormone levels are also essential for the healthy development of the fetus and infants. Some researchers believe that one factor in the development of autism is severe hypothyroidism in their mothers.
In addition, TPO andtibodies have been found to be a risk factor for complications during pregnancy and beyond.
Another possible type are women who have difficulty conceiving and suffer one or more miscarraiges due to Hashimoto’s and hypothyroidism.
When women have hypothyroidism, a common problem is an increase of another hormone called prolactin. This causes less of a release of LH, and a loss of progesterone receptor site sensitivity, and a loss in sensitivity to FSH in the follicle. All of these losses lead to problems with ovulation, and they also may hamper communication to the pituitary gland.
Using birth control pills on top of this can further harm the communication and feedback loops in this system. Using herbs to stimulate the ovaries or the reproductive system will also not work unless the hypothyroid issues are corrected.
Studies have found that even mild hypothyroidism may cause ovarian problems. Testing thyroid function is very important with women who suffer from infertility, especially if they have elevated prolactin or they can’t ovulate.
Hypothyroidism may lead to low FSH levels, which may lead to immature follicles and infertility. Suppressed LH levels will often lead to problems with ovulation in timing or abnormal luteal phase progesterone levels. These changes may cause miscarriage, depression in the second half of your cycle, or migraines in the second half of your cycle.
To summarize, hypothyroidism can cause:
There are a number of important issues to address when trying to conceive, here’s a post I wrote on this that goes into more depth on this.
The changes of life leading up to and during the transition to menopause are another time of life when Hashimoto’s can come on, resurface or progress.
As the ovaries retire and reproductive hormones decline, the adrenal glands step in and take over.
Essentially, what happens is this: FSH (Follicle Stimulating Hormone) receptors in the ovaries begin to lose sensitivity during perimenopause. This leads to changes in levels of FSH and estradiol.
The adrenals, in turn, step in and create more adrostenedione, a steroid hormone and this is converted to estrogen by adipose (fat) tissue. It’s the body’s way of compensating for declines in estrogen.
Obviously, there is a potential problem here if the adrenals are already taxed or exhausted. A lot more demands are made on them in perimenopause.
So adrenal health is very important prior and during this transitional time.
Here are some of the common symptoms of peri-menopause and how they are connected to Hashimoto’s:
Common Symptoms and their Causes During Perimenopause
1. Systemic inflammation and pain: This is caused by surges in certain immune cells and proteins called cytokines. Cytokines like IL-6, IL-1 and TNF-alpha are all implicated in Hashimoto’s, as well.
2. Multiple food sensitivities, gastrointestinal symptoms: These are often caused by Intestinal permeability or “leaky gut”: This maybe caused by declines in estrogen, increases in cortisol production, hypothyroidism and dysfunction in the gut. Intestinal permeability is ground zero for autoimmunity, as well.
3. More stress, poor sleep, fatigue during the day: The adrenals have to do additional work when other female hormones, like estrogens decline. Adrenals issues are also very common with Hashimoto’s.
4. Poor circulation, cold hands and feet, poor nails beds, fungal overgrowth in nail beds: This is caused by problems with peripheral circulations, especially in the small vessels. And may be due to altered nitric oxide function. These symptoms are also very common with Hashimoto’s.
5. Brain fog, depression, memory loss and poor cognitive function: This is due to inflammation in the brain and deficiencies or declines in neurotransmitters. These are some of the most common symptoms of Hashimoto’s.
6. Hot flashes, night sweats: A hallmark of perimenopause caused by altered FSH (follicle stimulating hormone) and feedback from the ovaries. This is a less common symptom of Hashimoto’s but something many women experience.
7. Poor bone density: This is caused by problems in osteoclast or bone cell formation and other issues. It is also a very real concern for Hashimoto’s patients, as well because osteoporosis can be a side effect of thyroid medication . (One of the major causes of this breakdown in bone health is the cytokines that we spoke about above.)
Here’s a previous post I wrote on this subject that looks into all of these factors in more depth.
The important take away here is to see that all of these issues must be addressed. As I am fond of repeating, this is way more than a thyroid problem.
If these other areas are not addressed, the result is the perfect recipe for compounded problems and more aggressive symptoms and progression of the disease.
As women enter their later years the symptoms of long standing hypothyroidism and Hashimoto’s become harder to separate from other aging symptoms.
Analysis of patients with long term hypothyroidism due to Hashimoto’s thyroiditis suggested that metabolism of thyroxine (T4), including conversion (via deiodination) to triiodothyronine (T3), was reduced in the elderly. Consequently, low-T3 syndrome is also common in this population.
Another serious concern is that there are real risks of long term treatment with levothyroixine. Adults aged ≥70 years treated with it have a significantly increased risk of fractures, with a strong dose-response relationship, a Canadian research group has found.
Although autoimmune thyroiditis is the most common cause of hypothyroidism in elderly subjects, other things, such as medications can also cause complications. Unfortunately, many elderly women have been prescribed a number of medications and often doctors to not communicate with one another to determine if there are problems that may result from these different prescriptions.
Medications Can Complicate Hypothyroid Symptoms
A small subset of medications including dopamine agonists, glucocorticoids and somatostatin analogs affect thyroid function through suppression of TSH.
Other medications that may affect TSH levels are metformin, antiepileptic medications, lithium carbonate and iodine-containing medications.
In addition, other drugs can alter T4 absorption, T4 and T3 transport in serum and metabolism of T4 and T3, such as proton-pump inhibitors and antacids, estrogens, mitotane and fluorouracil, phenobarbital and rifampin. Amiodarone administration is also associated with hypothyroidism.
The Immune System Also Ages
As the body ages, many systems of the body also age. The immune system is no exception. Aging of the immune system, or immunosenescence, is characterized by a decline of both T and B cell function, and paradoxically the presence of low-grade chronic inflammation.
Chronic inflammation is at the root of Hashimoto’s and autoimmunity and many other disease such as cardiovascular disease and Alzheimer’s. So, this can have serious health impacts over time and be a factor in the progression of these other diseases.
Other Systems Also Decline
Other systems of the body also decline as the body ages, stomach acid levels tend may lessen, the intestinal lining can break down and commensal bacteria may decline and all of this this can impact thyroid hormone absorption and conversion.
In addition, there are numerous cardiovascular symptoms. These include:
There are also a host of psychological issues that are related to the impact of hypothyroidism and autoimmunity on the brain. These include:
Finally there are also pulmonary issues. These include:
Here’s the important take away from this post. Women with Hashimoto’s at different stages of life are not all the same. And treating them all the same way does not make sense.
When you are diagnosed, the stage you have progressed to and where you are in your life are all important factors in determining the best course of treatment. It’s time we start acknowledging this and looking more deeply into the nuances of patient care.
In the next few posts of this series I will examine how the most common challenges for Hashimoto’s patients (weight gain, fatigue/exhaustion, brain fog and memory/cognitive issues and diet) may be different for these different “types” and how the treatment strategies and priorities might also be different.
We will begin by looking at how the brain is impacted in each of these Hashimoto’s “types”.
http://www.thyroidmanager.org/chapter/hashimotos-thyroiditis/ Stages of disease
http://cdn.intechopen.com/pdfs-wm/28726.pdf 3 Stages of Disease referenced
20 and Under:
http://adc.bmj.com/content/83/3/207.short Prevalence and etiology of hypothyroidism in the young
http://www.hindawi.com/journals/jtr/2011/675703/#B2 Autoimmune Thyroid disease in children
P. Saravanan and C. M. Dayan, “Thyroid autoantibodies,” Endocrinology and Metabolism Clinics of North America, vol. 30, no. 2, pp. 315–337, 2001.
http://www.ncbi.nlm.nih.gov/pubmed/24756046 Natural course of Hashimoto’s in children
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4338651/ Thyroid function in pregnancy
http://www.ncbi.nlm.nih.gov/pubmed/17137901 Natural history of euthyroid in Hashimoto’s patients
http://www.ncbi.nlm.nih.gov/pubmed/11305796 Clinical course of Hashimoto’s in children and adolescents a 6 year follow up.
http://www.ncbi.nlm.nih.gov/pubmed/2189331 51 cases of children and adolescents with Hashimoto’s
http://annals.org/article.aspx?articleid=691332 14 Cases of Transient Postpartum thyroiditis
http://arbl.cvmbs.colostate.edu/hbooks/pathphys/endocrine/thyroid/thyroid_preg.html Changes in thyroid function during pregnancy
http://www.indianjmedsci.org/article.asp?issn=0019-5359;year=2003;volume=57;issue=6;spage=252;epage=258;aulast=Kumar Thyroid function tests in pregnancy
http://www.ncbi.nlm.nih.gov/pubmed/9588218 Shifts in TH-1 and Th-2 during pregnancy
http://www.hindawi.com/journals/mi/2012/416739/ TH-1 suppression rather than TH-2 dominance
Stagnaro-Green A. Clinical review 152: postpartum thyroiditis. J Clin Endocrinol Metab. 2002;87:4024-7.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4518419/ TPO antibodies and risk for pregnancy complications
http://www.ncbi.nlm.nih.gov/pubmed/1427622 The role of thyroid hormone in ovulation
http://ttvps.com/saegre/revista/numeros/2010/n2/act_efectos_de_hormonas_tiorideas_n2.pdf Effects of thyroid hormone on ovarian function
Perimenopause and Hashimoto’s:
http://www.ncbi.nlm.nih.gov/pubmed/9356978 Perimenopause and thyroid issues (lipid and weight)
Hashimoto’s in the Elderly:
http://www.ncbi.nlm.nih.gov/pubmed/9893482 Hashimoto’s and the elderly
http://www.ncbi.nlm.nih.gov/pubmed/1987440 Thyroid disease in the elderly
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2889224/ Aging and the immune system
Nature Reviews Endocrinology 7, 435 (August 2011) | doi:10.1038/nrendo.2011.99 Pharmacotherapy: Levothyroxine in the elderly—finding the breaking point by Linda Koch
Hashimoto’s and other autoimmune diseases have multiple causes. There is no single origin and, therefore, to date there is no single solution.
Instead, successful healing requires exploration into the multiple causes of the disease and healing the areas that need attention.
One such area that has recently been discovered to have a major impact on health and disease is the microbiota or the tiny living organisms that populate our bodies.
These various different species of bacteria, viruses and fungi make up the lion’s share of our DNA and are more a part of us than we realized.
In this post we explore the role of bacteria in the formation and healing of autoimmunity and Hashimoto’s.
One of the fundamental things to understand regarding the world of microbes is that they are not separate from us. We are one. And I don’t mean this is a woo woo, philosophical sense.
I mean this is a very real, practical sense.
The Human Microbiome Project
The Human Microbiome Project (HMP) was a United States National Institute of Health (NIH) sponsored project whose goal was to identify and study the microorganisms (little critters) that are found in association with both healthy and diseased humans.
Launched in 2008, it was a five-year project, with a total budget of $115 million. The ultimate goal was to test how changes in the human microbiome are associated with human health or disease.
Here’s some of the things that they discovered:
• No two people have the same microbiome, not even identical twins.
• There are approximately 10 trillion bacteria in (and on) our bodies vs. only 1 trillion human cells. You read that correctly. We have 10x more bacterial cells than we do human cells.
• Bacterial genes outnumber human genes 150:1.
• Our cells have incorporated and use bacterial DNA.
• There are over 1,000 species of bacteria found inside our GI tract alone.
• There are over 1,000 different proteins made by bacteria in the gut which are essential to optimal body function.
• Several diseases are directly associated with a disruption to the microbial ecosystem of the gut. These include, but are not limited to: Asthma, Allergies, Crohn’s, IBS, Obesity and, in my humble opinion, Hashimoto’s.
• Pathogenic bacteria/organisms like candida, h.pylori, etc. have evolved to be natural inhabitants of our gut, and under ideal conditions don’t always lead to illness or cause disease. On the contrary, sometimes they provide vital functions and we’re worse off without them.
• Destroying these pathogens completely has physiological consequences that we’re just beginning to understand. (Remember when the appendix didn’t matter? Oh yeah, we were wrong about that, too. It has been found to be a store house of good bacteria.)
One thing that looking at this research makes abundantly clear is how potentially destructive antibiotic therapy is, especially for children (for whom it is often prescribed).
Of course, these drugs have saved countless lives, when they are used appropriately. But they have been abused and overused and we are now seeing the consequences in new bacteria resistant strains, as well as a wide variety of diseases like digestive disorders and autoimmune disease.
Giving a child or adult antibiotics every time they get an upper respiratory infection (most of which are caused by viruses not bacteria) is often doing little more than setting the table for future disease and a decline in natural immunity and actually makes them more susceptible to infections.
This also has physiological consequences in our guts and it makes us more vulnerable to pathogens because the beneficial bacteria that are killed play an important role in our immune system.
It’s time we stopped looking at medicine as, simply, a war between invading pathogens and our body. It’s more nuanced than that.
As I have written in the past, we are a collection of interacting ecosystems and researchers now know that these ecosystems are composed of a wide variety of friendly organisms.
Just like we need to learn to be good stewards of the earth and our external environment, we also need to view the insides of our bodies in this way and start caring for these internal ecosystems in the same way.
The lesson here is that we can’t just eradicate ourselves to good health. We see this time and time again with pesticides, herbicides and antibiotics.
Lots of patients and practitioners still have mind set that says, “All we need to do is kill ___________(choose your favorite pathogen), then you’ll be healthy.” And many of us have been trained to think and treat this way, whether it is with drugs or herbs and natural supplements.
Well, a lot of times this approach can result in a disruption of the ecosystem of the gut (and sometimes overgrowth of other pathogens). And this doesn’t just happen with drugs like antibiotics, it also happens with natural products like herbs that kill pathogens in our bodies.
It’s time we create a new way of doing things. Figuring tht out is beyond the scope of this post. So, first let’s try and figure out what a “healthy” microbial ecosystem is.
Here’s the thing about your digestive tract, it’s not just one ecosystem. Really, there are several distinct ecosystems that overlap and interact with one another.
Let’s break it down:
There’s your mouth, your esophagus, your stomach, your upper and middle small intestine, your lower small intestine and your colon. The bacteria that populate each of these ecosystems is quite different.
And to complicate things, there’s the intestinal mucosa and lining which has distinctly different species than the space in side the intestine .
In addition, no two people have the same microbiota. Early research on this subject came up with the idea of “enterotypes” which are microbiota types like blood types, but they only looked at a small group of people.
After looking at a lot more people from different cultures researchers determined that it wasn’t so clear cut and there’s so much variation that it’s really hard to be definitive about this. (It’s more nuanced – I think that’s my new motto 🙂 ).
In the following diagram you can get a sense of the number and the diversity of bacteria that populate these various ecosystems.
Frankly, this makes the claims and marketing of probiotics pretty ridiculous (more on that in a moment). No one or two strains of bacteria are going to properly populate your entire digestive tract. Nor does everyone need the same strains.
Furthermore, diversity is more important than overall population of certain strains. A diverse microbiome is the very definition of good health. With diversity comes proper function, more resistant to pathogens, infections, and overgrowth from other species of bacterial, yeast, etc.
Here’s what we have learned about this:
• During vaginal childbirth, we are exposed to our mother’s microbiome. This occurs via the birth canal, and exposure to feces during the birth process.
• We receive between 400-600 different species via breast milk. Also, breast milk contains a powerful prebiotics (which feed good bacteria). This helps these strains to proliferate and colonize inside our GI tract.
This means that births via C-Section and feeding babies formula (rather than breast milk) can have a very real impact on the diversity and overall population of a person’s microbiome.
• An infant’s microbiome reflects the mother’s vaginal bacteria initially, and then it begins to resemble the mother’s mouth, skin, and gut after that.
• After the very early stages of life, the microbiome is generally populated via environmental and food exposure.
• Skin-to-skin contact with parents provides some of the strains comprising a healthy microbiome.
This means that anti-bacterial soap, hand sanitizers and overall germ-phobia can also have a very real ( and not so beneficial) impact on the development of healthy GI flora – especially related to diversity. You want your infants and kids exposed to dirt and grime ( this news will be liberating for some parents and horrifying for others).
Environment also really matters when it comes to a healthy microbiome.
• Those who live in rural environments generally have much greater microbiome diversity than those who live in urban environments. (Working the earth is not just good for the soul, it turns out.)
There is a good deal of evidence to support the idea that the microbiome has a profound impact on the immune system and that it is involved with the prevention as well as initiation and progression of autoimmune disease.
But the idea that probiotics are always good for people with autoimmunity is not supported in the research, at all. On the contrary, there is some evidence that opposite is true and that certain strains of bacteria cause different types of immune responses and affect different autoimmune diseases differently.
And there are many complicating factors here including genetics, environment and type of disease. And mutations and changes in the microbiome can also result in different outcomes.
Like most things, the reality is that there is enormous individual variation and determining whether or not probiotic therapy is beneficial and which probiotics are appropriate is not an easy thing to do.
The reality is that we are only beginning to understand this complex interaction between our immune systems and the microbiome. However, there are two theories about how the microbiota can help protect against autoimmune disease.
The first is known as “specific lineage hypothesis” and it says that in genetically predisposed animals or humans, the microbiota could provide signals that calm our body’s immune responses.
As a result, the microbiota stays in a homeostatic (balanced) relationship with us.
Basically, the microbes are saving themselves and we have acquired these lineages from our mother and they have been passed down.
When a specific microbial lineage is expanded, it blocks the development of autoimmunity. It does so to improve its own odds of staying in this expanded state by suppressing our inflammatory and adaptive responses.
Autoimmunity is calmed as a side effect of this microbial self-preservation.
The second theory is called the “balanced signal hypothesis” this says that the host’s interactions with microbiota are independent of the precise microbiota composition and that the host’s genetics plays a critical role in the conversation with microbes.
So that your genetic profile is more important.
Whereas a balanced host response to good bacteria and this bacteria’s effort to reduce this response do not affect disease development, the inability of the host to control the microbiota properly results in stronger negative signaling provided by the microbiota and a reduction of autoimmunity.
Again, the microbes are looking out for themselves and sending out signals that result in calming autoimmunity.
(Both theories predict that the increase of tolerance would be lost in germ-free conditions without the microbes.)
There is also evidence that the microbiota behaves in different ways depending on the circumstances. It’s not static, it adapts to changing conditions.
Here’s the thing, the microbiota always faces 2 competing problems:
So there’s this constant balancing act that we and our microbiome must do to keep each other healthy.
Bottom line is this, you need to be cautious when using probiotics with autoimmunity and don’t just assume that any variety is going to help.
They might, in fact, not help or make things worse. So, like everything else, you need to carefully assess your need for them and then experiment and keep track to see if they are, in fact, giving you the desired result.
One question I frequently get is “which probiotic is a good one?” As with all things Hashimoto’s related you can see that this is not a simple question and there is so much individual variability that it really depends.
Probiotics are big business. Global probiotics market was valued at $32.06 billion dollars in 2013.
There are literally hundreds of brands and many make outrageous health claims. I’ve experimented with a number of different brands both personally and professionally. For some patients the results have been good, in others, there’s been little or no noticeable effect and for some they’ve actually had adverse reactions.
Some manufacturers and proponents might say these are “die off” reactions and they may be, but it could also be that in that particular individual with that particular genetic makeup and immune profile that they were inappropriate. ( I think that sometimes practitioners use “die off” to cover incompetence).
When deciding which type of probiotic to choose there are a few things that are really important to determine.
Will the strain actually survive digestion to be of any help?
Are the strains actually found in nature?
Are they good quality?
Let’s take a look at these issues:
In order to have any benefit, a probiotic must be able to reach the desired location within your GI tract alive (and the large intestine is by far the most populated bit of real estate in the GI tract).
Many strains of bacteria included in probiotic supplements today are very fragile, some requiring refrigeration. The human gut, on the other hand, is not a hospitable environment. It has very low pH (extremely acidic) environments, it’s body temperature, and it has evolved to keep out invading critters.
A large study done on this subject was done by the Food Standards Agency (FSA), along with Reading University, in the UK. They tested 35 popular commercial probiotic products, mostly comprised of lactobacillus and bifidobacterium strains.
Here’s what they found:
Those 6 were put through survival tests to determine survivability in the large intestine, and only 4 survived the large intestines.
So, at the end of the day, only 4 of the 35 strains showed any chance of survival, and even that was at, or around 50%.
These are not very good odds of survival.
It’s safe to say that many of the probiotic products on the market don’t deliver on their claims because they don’t live long enough to do anything.
This is important and often overlooked. In our arrogance, man has made the false assumption that we can improve upon and do better than billions of years of evolution. Time and time again this has been proven wrong. Remember the Biosphere 2? That experiment didn’t go well.
Mother nature is infinitely more experienced and developed than we are. If we survive as a species, it will only be because we learn to leverage that truth.
(Bacteria are among the earliest forms of life that appeared on Earth billions of years ago. Many believe that more complex cells developed as once free-living bacteria took up residence in other cells, eventually becoming the organelles in modern complex cells. The mitochondria that make energy for our body’s cells is one example.)
Those strains found in nature have a very long track record of survival and adaptation. Those manufactured in laboratories do not. It’s important that the strains you take are found in the human microbiome.
In addition, this also highlights the importance of diversity. Having variety in the gut matters. Taking high doses of a few specific strains, and eating large amounts of the same fermented foods every day can result in self-induced bacterial overgrowth where a couple of species dominate.
This is the same principle that applies to any ecosystem. When you overload a particular species, things get out of balance and it compromises the entire system.
Because probiotics are such big business and are unregulated, this is an important concern. I looked at a study from Consumerlabs, which was a thorough review of many popular probiotic products and strains.
They found that two products did not have the amount of organisms that they claimed. Essential Formulas Dr. Ohira’s Probiotics and Jameison Probitoics were 2 brands that had significantly less number of organisms than advertised. Click here to read the full report.
One type of probiotic I have been experimenting with is called spore form bacteria. These are organisms that survive the stomach and small intestines quite well. They have evolved to be very stable in the environment and also to colonize the GI tract very effectively.
These check all the boxes of the questions we just looked at. They survive digestion, are found in the natural world and they are of superior quality.
What do we know about spores?
• They are found all over the environment (in soil, vegetation, aquatic environments, and the digestive systems of many living species like insects, marine life, mammals, etc.) what this means is that as a probiotic they have evolved to be very resilient.
• Spores remain dormant until they get to the intestinal tract and then they colonize the bowel. They pass through the stomach and upper GI and survive.
• They are normal organisms of our digestive tract and are part of the human biome.
• They have been used in industries where efficacy is closely monitored, for example the pharmaceutical and agriculture industries.
• Human studies have proven spores to be safe and effective.
Why choose spore form bacteria over others?
What’s interesting about these bacteria is that they have been shown to be effective in several ways.
In a previous post I investigated oral tolerance and since then I’ve been looking for supplements to help improve it. These spore form bacteria have been shown to do this in a number of ways:
What brand has these?
The brand that I’ve been experimenting with with promising results thus far is called Megaspore Biotic.
This is not available in retail stores because it is pharmaceutical grade and really requires some understanding and clinical know how in order to administer it.
It contains five bacillus spore probiotics– the value of each strain is supported by numerous studies and scientific publications. All strains are produced in a GMP facility under drug manufacturing guidelines.
It’s a very powerful spore probiotic formulation, and it delivers more than four billion live probiotic cells daily – a dose that matches and exceeds many other products on the market.
Are there any downsides?
Nothing is perfect. There are some indications that some strains in this product may be histamine producing.
But this is not only true of these strains. There are a number of different bacterial species that produce histamine. For example, these common probitoic species are all histamine producers: E. coli, Klebsiella pneumoniae, Lactobacillus bulgaricus, Lactobacillus casei, Lactobacillus helveticus, Lactobacillus reuteri. And many of these are found in yogurt and other probiotic products.
So, be aware if you have histamine intolerance that you may have to be very careful about the probiotics you choose. These species have been found to degrade histamine: Bifidobacterium infantis, Bifidobacterium longum, Lactobacillus gasseri, Lactobacillus rhamnosus, Lactobacillus plantarum, Lactobacillus salivarius
Bottom line is this. A healthy microbiome is essential to good health. I can help increase oral tolerance, help you fight infections and overgrowth of destructive species, it can help you lose weight and can also help heal autoimmunity.
However, more is not always better and different species populate different parts of the ecosystem of the gut. So varying different products and different foods that feed those species is essential.
Furthermore, using spore based probiotics can be a beneficial part of your strategy.
Finally, it’s time we stop thinking of the gut as a battlefield of the enemy. Like a farm, it must be weeded, cultivated and nurtured.
If you’re not sure what to do, feel lost or are not getting the results from probiotics that you hoped for, I’m available for a consultation to discuss testing and treatment options.
Click here to book a consultation: Yes! I’d like to speak with Marc.
In the meantime, take good care of your microbiome.
http://physrev.physiology.org/content/90/3/859 Gut microbiome in health and disease.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4528021/ Role of natural microbiota
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3145058/ Role of microbiota in health and disease
http://www.sciencedirect.com/science/article/pii/S1931312811002927 Microbiota and autoimmune disease
http://www.ncbi.nlm.nih.gov/pubmed/24763536 Diet, gut and autoimmunity
http://cshperspectives.cshlp.org/content/5/3/a007294.full.pdf+html Microbiota and autoimmunity
http://www.cell.com/cell-host-microbe/fulltext/S1931-3128%2811%2900292-7 Microbiota and autoimmune disease
http://www.nature.com/cmi/journal/v8/n2/full/cmi201067a.html Role of microbiota in cancer and autoimmune disease
http://bmcimmunol.biomedcentral.com/articles/10.1186/s12865-015-0083-2 Systemic effects of gut microbiota, relationship with disease and immunomodulation
http://www.discoverymedicine.com/Kouki-Mori/2012/11/27/does-the-gut-microbiota-trigger-hashimotos-thyroiditis/ Gut Microbiota and Hashimoto’s
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4036413/ Autoimmunity and the gut
http://gut.bmj.com/content/early/2014/11/28/gutjnl-2014-308514.short?g=w_gut_ahead_tab Does microbiome play a role in autoimmune disease?
http://press.endocrine.org/doi/abs/10.1210/jc.2007-0606 Hypothyroidism and SIBO
http://www.bpgastro.com/article/S1521-6918%2813%2900057-7/abstract Fecal transplants for treating autoimmunity
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2904693/ Gut bacteria and TH-17
http://www.nature.com/articles/nmicrobiol201515 Assessment of Microbiome Research
http://www.newyorker.com/magazine/2012/10/22/germs-are-us Self Explanatory
https://hsbjournalclub.files.wordpress.com/2012/02/microbiota-article.pdf What are the consequences of the disappearing microbiota?
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3159383/ Has the microbiome played a critical role in the development of the adaptive immune system?
http://www.grandviewresearch.com/industry-analysis/probiotics-market Value of probiotics market
http://www.ncbi.nlm.nih.gov/pubmed/17241350 Adhesion of 31 actobaccilus strains
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3316997/ Probiotics that degrade histamine