Stress and Your Thyroid

Stress is vital for our survival; it is the body’s natural defense against danger and predators.

Stress flushes your body with hormones that activate the “fight-or-flight” mechanism.

When we deal with stressful situations and challenges in everyday life, a part of our response to that situation is physical.

The body produces stress hormone cortisol and other chemicals that improve your ability to respond to the given challenge. While stress helps us overcome different problems in life, too much of it is not a good thing.

When left unresolved, stress causes a number of health problems and it affects the function of thyroid gland. What can stress do to your thyroid? Let’s find out.

How stress contributes to hypothyroidism?

It’s impossible to avoid stress. Not only it is the body’s response to challenging situations, but life itself brings both good and bad times.

Too much stress is a major problem today. Figures show that 77% of people regularly experience physical symptoms caused by stress while 73% report psychological symptoms due to this problem. About 33% of people live with extreme stress while 48% reported lying awake at night due to stress[i].

Chronic stress contributes to sleep deprivation, decreases energy levels, and it also contributes to hypothyroidism or underactive thyroid gland.

How does stress contribute to this common thyroid disorder?

It takes a multifaceted approach, which will be discussed below.

Stress impairs the HPA axis

Hypothalamic-pituitary-adrenal (HPA) axis is our central stress response system; it is a complicated network of interaction between the hypothalamus and two types of glands (pituitary and adrenal).

The HPA axis helps regulate digestion, body temperature, mood, immune system, energy levels, and even your sexuality.

Hypophysiotropic neurons from the medial parvocellular division of the paraventricular nucleus (PVN) of hypothalamus secrete and synthesize corticotropin-releasing factor (CRF). The CRF is the primary regulator of HPA axis.

As a part of body’s response to stress, CRF gets released into hypophysial portal vessels that access pituitary gland.

When CRF binds to its receptor in your pituitary, it promotes the release of adrenocorticotropic hormone (ACTH) in your system circulation.

The main target for ACTH is adrenal cortex, where it stimulates glucocorticoid synthesis. Glucocorticoids are considered downstream effectors of HPA axis and they play a vital role in regulating magnitude and duration of HPA axis activation.

During stress exposure, higher glucocorticoid levels inhibit the activity of this axis[ii].

Since stress has a major impact on the function of hypothalamus and pituitary, it also affects thyroid since these parts of your body contribute to the overall functioning of this gland.

A team of scientists at the University of Texas Health Science discovered that the inflammatory cytokines that are released during stress (IL-1 beta, IL-6, and TNF-alpha) tend to down-regulate the HPA axis and decrease levels of thyroid stimulating hormone (TSH)[iii].

Pang X.P. and a team of scientists carried out a study where they administered synthetic TNF-alpha, involved in stress, into male rats. They found that a single injection decreased serum TSH, T3, free T3 and T4, and hypothalamic TRH for about five days[iv].

In addition, TNF-alpha reduces the conversion of T4 to T3 hormone, decreases thyroid uptake, and decreases the sensitivity of the gland to TSH.

Basically, stress has a negative impact on HPA axis and its effects expand to decreasing the function of the gland and hormone production.

Decreased T4 to T3 conversion

As mentioned above, the stress acting on the HPA axis can also lead to the decreased conversion of hormone T4 to T3 and thus contribute to hypothyroidism.

Despite the fact that 93% of hormone produced by the thyroid gland is T4 it is inactive or unusable until your body converts it to T3. The inflammatory cytokines are also involved in stress response and they have the tremendous potential to affect the conversion of one hormone to another.

A growing body of evidence confirms that stress decreases levels of thyroid hormones[v] and higher levels of inflammatory cytokines lead to rapid decline in TSH and T3 and an increase in the inactive reverse T3 (rT3)[vi].

Thyroid hormone resistance

Thyroid and its hormones are truly complex. Hormones produced by this gland participate in many processes in your body, but to do their job it’s not enough for the thyroid to simply make these hormones and get it over with. To exhibit their effects, hormones have to activate receptors on cells.

Researchers at the Johns Hopkins School of Medicine found that inflammatory cytokines suppress site sensitivity of thyroid receptors[vii].

This becomes even more severe if you bear in mind the evidence that stress impairs the immune system’s response to anti-inflammatory signals[viii], thus contributing to the rise of inflammatory cytokines which affect thyroid function.

If this seems complicated, let’s take insulin resistance as an example. Your pancreas produces insulin which allows the cells to use glucose or sugar for energy. In people with insulin resistance, cells lose their insulin sensitivity and are unable to use insulin effectively; they have trouble absorbing glucose which only leads to accumulation of blood sugar in your blood.

Thyroid hormone resistance functions in a similar manner. Cells gradually lose their sensitivity which is why it becomes difficult to activate receptors.

At this point, some practical way to assess receptor site sensitivity in a clinical setting is lacking, but this problem could be due to a result of problems with the immune system too.

Of course, thyroid hormone resistance makes it difficult for your body to obtain sufficient amount of hormones produced by this gland, which only aggravates hypothyroid disorders particularly Hashimoto’s, an autoimmune condition.

Cortisol and thyroid

Cortisol belongs to the group of glucocorticoid hormones; it regulates many processes in your body including immune response and metabolism.

However, cortisol is primarily known as the stress hormone. Most of us tend to associate stress with higher cortisol levels although the entire process is more complex.

The Journal of Clinical Endocrinology and Metabolism published a study showing that cortisol decreases TSH, thus lowering thyroid hormone production. In the study, daytime TSH levels decreased by 39% compared to baseline. The highest TSH suppression was recorded during the time when cortisol levels were the highest[ix].

Stress hormone inhibits the conversion of T4 to T3, thus contributing to hypothyroidism. Another way cortisol aggravates symptoms of hypothyroidism is through its impact on blood sugar.

Both low and high levels of cortisol can cause a disturbance in blood sugar balance and lead to hypoglycemia and hyperglycemia.

Hypoglycemia is a condition when levels of blood sugar fall below normal, while hyperglycemia indicates blood sugar concentration is excessive. For example, one study showed that hypoglycemia is closely associated with hypothyroidism[x].

As it was mentioned above, stress takes a multifaceted approach to affect thyroid function or symptoms associated with thyroid disorders. Weight gain could be one of them. A study from the journal Obesity found that higher levels of cortisol are positively associated with larger waist circumference and higher BMI.

Basically, science confirmed stress contributes to weight gain. Not only that, but chronic high-level cortisol also plays a role in obesity maintenance[xi] which could explain why someone’s efforts to slim down fail.

Weight gain is strongly associated with thyroid disorders, particularly hypothyroidism. Evidence confirms that due to low metabolic rate, patients with longstanding overt hypothyroidism tend to be overweight and their body weight increases as their condition becomes more severe[xii]. Hypothyroid patients who are also under stress can find it difficult to manage their weight.

Thyroid autoimmunity and stress

Thyroid autoimmunity is the disease wherein a patient’s immune system is attacking the thyroid gland. Two types of autoimmune thyroid conditions are identified: Hashimoto’s thyroiditis and Graves’ disease. See the common thyroid questions and answers article if you’re not sure what either mean exactly.

The first condition is the primary cause of hypothyroidism while the latter leads to hyperthyroidism or overactive thyroid gland.

Although more research on this topic is necessary, studies show that stress affects the immune system directly or indirectly through nervous and endocrine systems. Through immune modulations, stress contributes to autoimmune thyroid disorders and increases the risk of these conditions in genetically predisposed individuals.

What’s more, stress poses as one of the biggest environmental risk factors for thyroid autoimmunity. Due to the onset and course of Hashimoto’s thyroiditis, the effect stress on this autoimmune condition tends to be overlooked[xiii].

Current studies on this topic focus on Graves’ disease. For instance, stressful life events may contribute to the precipitation of Graves’ disease.

Patients with this disease had significantly more negative events and they experienced a greater negative impact from them than they did before the onset of this condition[xiv]. The University of London researchers discovered that stressful and negative life events and hereditary factors are risk factors for Graves’ disease[xv].

Stress management tips

Unfortunately, we can’t avoid stress and prevent it from happening ever again. This doesn’t mean you’re powerless.

There are plenty of solutions to manage stress and learn how to overcome negative situations that cause it, even if you have some thyroid disorder. We have become a society that takes stress for granted and expects things to go away on their own.

That’s not how it works!

Let’s take a look at some useful stress management tips that will help you prevent its negative effects on your thyroid and overall health:

  • Get enough good night’s rest – sleep deprivation is a major cause of stress and high cortisol levels. Therefore, the solution is logical – you should strive to get enough sleep regularly. Go to bed and wake up every morning at the same time. Establishing a regular sleep schedule will take a while, but if you’re persistent you can do it
  • Limit or avoid alcohol, cigarettes, and caffeine – caffeine and nicotine are stimulants meaning they increase stress rather than reduce it. Although alcohol is depressant in larger qualities it also acts as stimulant in smaller amounts, so using alcoholic beverages to relieve stress doesn’t work and puts your health in jeopardy
  • Exercise regularly – not only is physical activity beneficial for individuals with thyroid disorders, it can also help tackle stress by metabolizing excessive stress hormones and restoring body and mind to a calmer state
  • Keep a stress diary – since stress has a big impact on thyroid conditions, then keeping a diary is a great idea. It’s simple, just write down when you’re under stress and describe the entire situation. Do it regularly for a few weeks and read everything from the beginning. The diary will help you identify situations that induce stress the most and allow you to develop a plan to avoid or tackle these situations

Conclusion

Stress is a natural process that occurs in our body and it is mandatory for our survival, but too much stress is never a good thing.

When your body is under stress, thyroid gland suffers too. Evidence shows that stress affects thyroid function in many ways including through reduced conversion of T4 to T3, hormone suppression, resistance, and many other factors.

Find a unique way to manage stress and consult your doctor about this problem if you can’t find relief on your own. Perhaps supplementation can also help.

References

[i] What is stress? American Institute of Stress https://www.stress.org/daily-life/

[ii] Smith SM, Vale WW. The role of the hypothalamic-pituitary-adrenal axis in neuroendocrine responses to stress. Dialogues in Clinical Neuroscience. 2006;8(4):383-395. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181830/

[iii] Rettori V, Jurcovicova J, McCann SM. Central action of interleukin-1 in altering the release of TSH, growth hormone, and prolactin in male rat. Journal of Neuroscience Research 1987;18(1):17-83. Doi: 10.1002/jnr.490180125 https://www.ncbi.nlm.nih.gov/pubmed/3500324

[iv] Pang XP, Hershman JM, Mirell CJ, Pekary AE. Impairment of hypothalamic-pituitary-thyroid function in rats treated with human recombinant tumor necrosis factor-alpha (cachetin). Endocrinology 1989 Jul;125(1):76-84. Doi: 10.1210/endo-125-1-76 https://www.ncbi.nlm.nih.gov/pubmed/2500334

[v] Helmreich DL, Tylee D. Thyroid Hormone Regulation by Stress and Behavioral Differences in Adult Male Rats. Hormones and behavior. 2011;60(3):284-291. doi:10.1016/j.yhbeh.2011.06.003. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3148770/

[vi] Corssmit EP, Heyligenberg R, Endert E, et al. Acute effects of interferon-alpha administration on thyroid hormone metabolism in healthy men. Journal of Clinical Endocrinology and Metabolism 1995 Nov,80(11):3140-4. Doi: 10.1210/jcem.80.11.7593416 https://www.ncbi.nlm.nih.gov/pubmed/7593416

[vii] Kimura H, Caturegli P. Chemokine orchestration of autoimmune thyroiditis. Thyroid 2007, Oct;17(10):1005-11. Doi: 10.1089/thy.2007.0267  https://www.ncbi.nlm.nih.gov/pubmed/17910527/

[viii] Miller GE, Cohen S, Ritchey AK. Chronic psychological stress and the regulation of pro-inflammatory cytokines: a glucocorticoid-resistance model. Health Psychology 2002 Nov;21(6):531-41 https://www.ncbi.nlm.nih.gov/pubmed/12433005

[ix] Samuels MH. Effects of variations in physiological cortisol levels on thyrotropin secretion in subjects with adrenal insufficiency: a clinical research center study. Journal of Clinical Endocrinology and Metabolism 2000 Apr;85(4):1388-93. Doi: 10.1210/jcem.85.4.6540 https://www.ncbi.nlm.nih.gov/pubmed/10770171

[x] Kalra S, Unnikrishnan AG, Sahay R. The hypoglycemic side of hypothyroidism. Indian Journal of Endocrinology and Metabolism. 2014;18(1):1-3. doi:10.4103/2230-8210.126517. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3968713/

[xi] Jackson SE, Kirschbaum C, Steptoe A. Hair cortisol and adiposity in population-based sample of 2527 men and women aged 54 to 87 years. Obesity 2017 Feb,25(3):539-544. Doi: 10.1002/oby.21733 http://onlinelibrary.wiley.com/doi/10.1002/oby.21733/abstract;jsessionid=6136F0ADEFF8C1CA684505F598286D16.f04t02

[xii] Laurberg P, Knudsen N, Andersen S, Carlé A, Pedersen IB, Karmisholt J. Thyroid Function and Obesity. European Thyroid Journal. 2012;1(3):159-167. doi:10.1159/000342994. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3821486/

[xiii] Mizokami T, Wu Li A, El-Kaissi S, Wall JR. Stress and thyroid autoimmunity. Thyroid 2014 Dec;14(12):1047-55. Doi: 10.1089/thy.2004.14.1047 https://www.ncbi.nlm.nih.gov/pubmed/15650357

[xiv] Santos AM, Nobre EL, Costa J, et al. Graves’ disease and stress. Acta Medica Portuguesa 2002 Nov-Dec;15(6):423-7 https://www.ncbi.nlm.nih.gov/pubmed/12680288

[xv] Harris T, Creed F, Brugha TS. Stressful life events and Graves’ disease. British Journal of Psychiatry 1992 Oct;161:535-41 https://www.ncbi.nlm.nih.gov/pubmed/1393342

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