Osteoporosis can be a problem for people with Hashimoto’s and hypothyroidism.
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.
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.
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.
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.
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?)
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.
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.
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.
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.
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.
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.
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
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 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.
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.
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:
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.
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.
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.
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.
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.
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.
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