As much as 90% of thyroid diseases are autoimmune (AITD). Hashimoto’s Thyroiditis (HT) is the most common cause of thyroid disorder and affects about 1 in 50 people in the US. It is an autoimmune disease caused when a particular white cell (lymphocytes) invades the thyroid tissue. The cells cause tissue inflammation and thyroid dysfunction, which is gradually replaced by scarring changes (fibrosis). For a deeper dive into HT, refer to this YHF article.
The result of Hashimoto’s is overt hypothyroidism when the thyroid can no longer secrete the hormones T3 and T4.
Is it possible to identify HT at an earlier stage and reverse or reduce the process of deterioration and loss of thyroid functioning? Are there any ways we can effectively reverse thyroid disease?
Table of Contents
Answer: Probably, but it depends on how early.
The intuitive answer is yes; it is likely to reverse a disease early on. We tell aphorisms like “a stitch in time, saves nine.”
Evolution: Survival of the Fittest and Adaptation
A deeper exploration of the question requires an overview of the theory of evolution and how integral the environment is to our genetic expression. Certain inherited genetic risk factors are related to autoimmune diseases like Hashimoto’s, vitiligo, Crohn’s disease, and diabetes. However, environmental factors like diet, exposures to toxins, infections, and stress events likely play a role in how our body manifests our genome. This is known as epigenetics.
Darwin proposed the theory of evolution in On the Origin of Species in 1859, selling out on the 1,250 copies its first day. However, other ideas were espoused during the era. Jean Baptiste de Lamarck (1744-1829) proposed that environmental adaptations are inheritable. He described an “inner want” of an organism that led to changes in size or other characteristics. His theory was a prevailing thought that he held was commonplace and self-apparent (Burkhardt, 2013).
He used an example of how a giraffe stretched its neck and passed this down through generations, leading to its current long neck. Darwin would apply his theory and state that the pressure of access to food selected the animals with longer necks. Over time, those traits were passed as longer-necked ancestral giraffes mated with similar giraffes – as they were able to survive.
Although the Lamarckian theory was disproven and found to be categorically wrong, the concept of how the environment shapes humans has been appealing to understanding and treating disease. The new science of epigenetics informs us that our environment influences the expression of our genome.
Epigenetics: Giving New Meaning to “Survival of the Fittest.”
The Life expectancy in the United States is 79.1 years. While this seems an incredible achievement, when life expectancy was 58 years a century ago, the US is ranked 46th. If a child were born today in the top-ranked (country) Hong Kong, it could expect to live to 85.29 years. On the other hand, the life expectancy in the Central African Republic is 54.36 years.
What accounts for such a variation? More so, people live long lives within one country, while others live shortened lives with chronic diseases.
The environment holds the key to how we adapt. Toxins from our environment lead to inflammation which fuels cellular changes that lead to disease, including Hashimoto’s disease.
Epigenetics is defined literally as “in addition to changes in genetic sequence” or “changes to the genome that do not involve changes in DNA sequence” (Brunet, 2014). The genome is not the regulator of adaptation of an organism as much as the epigenome. Brunet illustrates that a “queen” and “worker” honeybee has nearly indistinguishable genomes yet have lifespans that are 10-fold different. In humans, we need to look no further than the varied lifespans of identical twins.
Our genome goes through changes that impact its genetic expression as we age. Epigenetic changes occur from environmental exposures, such as diet, stress, and lifestyle factors. The alterations over time can hurt the production of proteins. For example, an epigenetic change known as DNA methylation has been linked to the development of cancer (Weinhold, 2006). Multiple other diseases, such as Barrett’s esophagus, cirrhosis, inflammatory bowel disease, have been associated with epigenetic harm.
Epigenetic modifications are heritable between mother (initial) and daughter cells. Therefore, there is an accumulation of changes over time. Less epigenetic changes occur in a healthier lifestyle. Since these changes impair the future production of proteins, the lifestyle that one chooses indeed can increase one’s lifespan.
| Chromatin Modification | Acetylation of histone groups tied in with DNA; microRNAs and other RNAs can modify chromatin structure. | |
| DNA Methylation Changes | Methyl group to a cytosine nucleotide. | |
| Loss of Imprinting | Normally, imprinted genes only have expression on 1 copy (one of two). In loss of imprinting, either both copies are expressed or both are not expressed. | |
| Non-coding RNA | MicroRNA (miRNA). The miRNA binds to mRNA and degrades it. |
Epigenetics and How to Reverse Thyroid Disease
Epigenetic changes, including many of those listed in the table above, may be responsible for autoimmune processes, including the thyroid diseases like Grave’s disease and Hashimoto’s thyroiditis (Coppede, 2017). Although the evidence is now clear, future studies will show potential ways to diagnose and treat this process. Genomic testing may even become an instrumental part in the future of medicine.
A compelling observation is that obesity and aging are associated with common epigenetic changes, and there is an increased level of inflammation in these conditions. Exercise comes with benefits in methylation. In this situation, higher methylation meant less inflammation and a lower incidence and mortality of stroke and heart disease (Alegria-Torres J, 2013). Less inflammation means less disease.
Hashimoto’s disease progresses over time until there is thyroid failure and a need to take thyroid replacement. After lymphocytes invade the thyroid tissue, there may be a period of one to two decades before overt thyroid disease requires replacement. Thyroid disease may be able to be delayed or even reversed.
The complete reversal of a disease would be a hard case to prove. Autoantibodies correlate with disease activity, and levels go down in the setting of a healthy lifestyle. The more difficult task is to make thyroid screening a routine process of everyone’s health screening. The American Thyroid Association (ATA) recommends a thyroid function test in all adults starting at 35 and screening every five years. Some groups, including the American College of Physicians, advise screening with bloodwork beginning in women older than 50. The US Preventive Services Task Force (USPSTF) did not find compelling data that detecting thyroid disease earlier would have a major impact.
My Recommendations:
- A Healthy Lifestyle Enriches Someone’s Life in many ways: Work toward a whole foods plant-based diet. Stress reduction strategies and plenty of sleep area fundamental.
- Screening bloodwork seems reasonable beginning at the age of 35. A thyroid stimulating hormone (TSH) blood test can be ordered and toggle further work-up to include a thyroid peroxidase Ab and thyroglobulin Ab.
- Having elevated thyroid peroxidase Ab and thyroglobulin Ab are very sensitive and specific for Hashimoto’s. There are also characteristic findings on ultrasound thyroid, but it is not clear if this will ever represent a method to staging.
Bibliography
Alegria-Torres J, Baccarelli A, Bollati V. Epigenetics and Lifestyle. Epigenomics. 2011. 3(3): 267-277.
Brunet A, Berger S. Epigenetics of Aging and Aging-related Disease. J Gerontol A Biol Sci Med Sci. 2014. 69(Suppl 1): S17-S20.
Burkhardt, R. Lamarck, Evolution, and the Inheritance of Acquired Characters. Genetics. 2013. 194(4): 793-805.
Coppede F. Epigenetics and Autoimmune Thyroid Diseases. Front Endocrinol (Lausanne). 2017; 8: 149.
Hamilton J. Epigenetics: Principles and Practice. Dig Dis. 2011; 29(2): 130-135.
Weinhold B. Epigenetics: The Science of Change. Environ Health Perspect. 2006. 114(3): A160-A167.
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