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.
The Conventional Approach Ignores Hashimoto’s Types
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?
Hashimoto’s Can Be Different at Different Stages
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.
You Can Be at Any Stage at Any Time in Your Life
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).
Five Hashimoto’s “Types”
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.
1. Age 22 and under: “Hashi-Tweens”
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:
- Poor linear growth (thyroid disorders usually effect height more than weight)
- Delayed bone maturation
- Puberty disorders
- Irregular menstrual periods
- Lethargy and/or impaired school performance
- Bradycardia and decreased cardiac output
- Cold intolerance/Hypothermia
- Fluid retention and weight gain (due to impaired renal free water clearance)
- Puffiness of the face
- Dry skin
- Increased body hair
- Delayed deep tendon reflexes
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.
2. After Pregnancy: “Hashi-Moms”
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:
- Increased sensitivity to heat
- Rapid heartbeat or palpitations
- Unexplained weight loss
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:
- Lack of energy
- Increased sensitivity to cold
- Dry skin
- Difficulty concentrating
- Aches and pains
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.
4. Infertility: “Hashi-Heartbreak”
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:
- A decrease in FSH release and FSH receptor sensitivity, this leads to problems with the development of the follicle and infertility
- Suppressed LH which leads to problems with ovulation and abnormal progesterone levels, this leads to abnormal cycles and infertility
- Progesterone receptor insensitivity which also leads to abnormal cycles and infertility
- Increased Prolactin, which leads to problems with ovulation, abnormal menstrual cycles and infertility
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.
3. Peri-Menopause: “Hashi – Hormone Hurricane”
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.
Women 60 and over: “Hashi – Sage”
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:
- Diminished cardiac output
- Diastolic hypertension
- Increased LDL
- Pericardial effusion
There are also a host of psychological issues that are related to the impact of hypothyroidism and autoimmunity on the brain. These include:
- Sleep disturbances
- Poor concentration
- Cognitive impairment
- Madness (confusion, paranoia) in severe disease
Finally there are also pulmonary issues. These include:
- Shortness of breath
- Sleep apnea
- Increased susceptibility to lung infections
Bottom Line: There are Unique Circumstances at Different Times of Life
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