Article at a Glance
- While diet alone likely cannot cure hypothyroidism, learning about how your genetics affect hypothyroidism and adjusting your nutrition accordingly may help. Genetics account for about 70% of all autoimmune thyroid conditions. Genetic variants of interest include those of the MTRR and MTHFR genes, which affect DNA methylation.
- DNA methylation relies on enough of the right vitamins, but not too much. Scientists are still working to fully understand these interactions, but those that may affect people with hypothyroidism include B vitamins, vitamin D, selenium, iodine, and goitrogens (substances that interfere with iodine intake).
- While iodine is essential for good thyroid health, it may also be dangerous, with too much of it causing thyroid damage. Be sure not to take an iodine supplement — or any supplement — without first consulting a health care practitioner if you have an autoimmune thyroid condition.
Is it possible to “fix” hypothyroidism by diet alone? The short answer is no — there’s no dietary factor that can cure every case of hypothyroidism. There are, however, specific nutrients such as iodine and selenium that we need for healthy thyroid function. Too little or too much of these nutrients can cause serious thyroid problems. In most cases, however, the interplay between nutrition and thyroid function is not so clear-cut.
In recent years, scientists have discovered a variety of ways in which diet and genetics can conspire to either increase or decrease your risk of developing autoimmune thyroid disease (AITD). Before we look at this interaction and possible ways to manage the risk of hypothyroidism through diet, let’s quickly review hypothyroidism.
What is hypothyroidism?
Thyroid issues affect an estimated 300 million people worldwide. (R) Hypothyroidism is a condition where the thyroid gland (in the neck) does not make enough thyroid hormone to properly regulate essential physiological processes. In a healthy system, thyroid hormone (thyroxine) is produced by the thyroid in response to thyroid stimulating hormone (TSH), itself produced by the pituitary gland in the brain. Thyroxine is transported in the blood to regulate metabolism, growth, and development.
People with an underactive thyroid often experience symptoms caused by a slowing down of metabolism, including:
- Feeling tired all the time
- Sensitivity to cold
- Weight gain
- Dry, cool skin
- Slow healing
- Hair loss
- Poor concentration
- Goiter (a lump in the neck)
Hypothyroidism can be congenital (present at birth) or a result of having too many or two few chromosomes (such as in Down syndrome and Turner syndrome). The most common cause of hypothyroidism worldwide, however, is iodine deficiency, because the body needs iodine to produce thyroid hormone. Iodine deficiency isn’t all that common in North America and many parts of Europe, though, because most countries fortify salt with iodine. Instead, autoimmune thyroid disease is the most common cause of hypothyroidism in North America and many parts of Europe. Genetics are said to account for around 70% of the risk in the autoimmune thyroid conditions, with environmental factors making up the rest. (R)
What is autoimmune thyroid disease?
An autoimmune condition is one where the body falsely identifies normal cells and tissues as a foreign invader and attacks them, resulting in dysfunction and disease. Autoimmune conditions include type 1 diabetes, lupus, Multiple Sclerosis, Hashimoto’s thyroiditis and Graves’ disease.
Graves’ disease is an autoimmune thyroid disease (AITD) where immune system dysfunction results in the production of an antibody called thyrotropin receptor antibody (TRAb). This antibody acts like thyroid stimulating hormone (TSH), meaning that the thyroid gland produces more thyroxine than is necessary. This causes a dangerous increase in metabolism, leading to symptoms such as:
- Rapid and irregular heartbeat
- Sweating and heat intolerance
- Anxiety and irritability
- Difficulty maintaining body weight
- Bulging eyes (caused by excessive tissue growth)
- Bulging neck
Hashimoto’s thyroiditis (HT) is an AITD with the opposite effects to Graves’ disease. In HT, the immune system attacks the thyroid gland resulting in decreased production of thyroid hormone. Metabolism becomes sluggish and leads to symptoms of hypothyroidism as described above. HT is the most common cause of hypothyroidism in North America and most frequently affects women in middle age. People who have a personal or family history of autoimmune disease are more likely to develop autoimmune thyroid disease, as are people exposed to high levels of environmental radiation.
Genetics and hypothyroidism
Several genes have been implicated in the development of autoimmune conditions. In recent years, several genes have also been identified as being uniquely involved in Hashimoto’s thyroiditis. For instance, the genetic variant MTRR+66AA appears to be more frequent in people with severe HT than in those with mild HT. (R) This variant of a gene encoding for methionine synthase reductase (MTRR) affects the carrier’s ability to methylate DNA.
DNA methylation is an epigenetic mechanism that cells use to regulate the expression of genes. In many cases, epigenetic factors use DNA methylation to “switch off” genes. Impaired DNA methylation has been identified as a factor in autoimmune thyroid disease, and epigenetic modifications are increasingly recognized as playing a significant role in the development of autoimmune disorders, including Hashimoto’s thyroiditis and Graves’ disease. (R)
Environmental, lifestyle, and dietary factors may also influence the risk of hypothyroidism in other ways. For instance, epigenetic mechanisms can silence genes by non-coding RNA molecules. RNA is a messenger that relays genetic information to assist DNA. RNA also selects the correct amino acids needed by each ribosome to build proteins. Put simply, non-coding RNAs are functional RNA molecules that send a blank message when transcribed from DNA, meaning that they are not translated into proteins. These RNAs include microRNAs (miRNAs), which make up about 60% of all genes. miRNAs interact with DNA methylation and histone tail modifications and essentially regulate the entire gene expression profile. (R)
Histones are DNA scaffold proteins. Histone tail modifications involve the addition of acetyl groups to histones which enhances gene transcription (basically doing the opposite of DNA methylation which tends to reduce gene transcription). As such, it’s possible that environmental, dietary, and lifestyle factors that influence acetylation may play a role in conditions like AITD.
Studies have so far found evidence that Hashimoto’s thyroiditis might be linked to increased levels of miR-22, miR-375, and miR-451 and differential expression of miR-200a and miR-155. In terms of histone tail modifications, epigenetics research has so far only identified links with Graves’ disease and not hypothyroidism. (R)
Nutrigenomics and autoimmune thyroid disease
Scientists are yet to fully understand the complex interactions between genes, epigenetics, and autoimmune diseases like Hashimoto’s thyroiditis. Knowing that DNA methylation is involved, however, does suggest an opportunity for nutrigenomics to modulate an individual’s risk of developing the condition. That’s because DNA methylation relies on an adequate supply of bioavailable nutrients including folate and other B vitamins.
Other nutritional factors may also play a role in modulating the risk or progression of autoimmune conditions, although there is little clinical evidence to support specific interventions at this time.
Folate, choline, betaine, methionine, and vitamins B2, B6, and B12 are needed for the production of S-adenosylmethionine (SAMe), a compound that acts as a donor for methyl groups in the process of DNA methylation. (R) As such, low levels of these nutrients in the diet can result in low SAMe synthesis and reduced DNA methylation, which appears to translate into a higher risk of autoimmune conditions.
Ensuring a good intake of methyl donors including folate and other B vitamins, in forms that you can absorb and use, is essential for robust health throughout life. This includes supporting thyroid health and healthy immune system activity. B vitamins won’t, by themselves, cure or prevent hypothyroidism, but deficiencies of these nutrients could, it seems, raise your risk of thyroid trouble.
Vitamin D is another important nutrient increasingly implicated in the development of autoimmune conditions. The active form of vitamin D, 1,25(OH)2D, directly and indirectly controls the expression of over 200 genes, including several involved in immune system activity. Several studies have found that vitamin D deficiency (25(OH)D level < 25 nmol/L) is much more likely in people with AITD. In one study, 72% of people with AITD were vitamin D deficient, compared to 30.6% of healthy controls. (R) In another study, 92% of people with Hashimoto’s disease had vitamin D insufficiency (25(OH)D level < 75 nmol/L), compared to 63% of health controls. (R)
As with B vitamins, taking a vitamin D supplement isn’t a foolproof way to prevent hypothyroidism, but it does seem that having low levels of vitamin D raises the risk of thyroid disease. As vitamin D is stored in the body, it’s best to have your levels tested before taking a supplement.
Selenium also plays a role in thyroid health as it is essential for the proper production of thyroid hormones. This trace mineral is incorporated into the amino acid selenocysteine (Sec) which is a key part of a group of proteins known as selenoproteins. These proteins include important antioxidant enzymes such as glutathione peroxidase (GPx) and thioredoxin reductase (TrxR), as well as iodothyronine deiodinases (DIO). DIO enzymes are instrumental in the regulation of metabolism as they control the activity of thyroid hormones thyroxine (T4), 3,5,3’-triodothyronine (T3), and reverse-3,5,3’-triiodothyronine (rT3).
Selenium is toxic in high doses, so it’s best not to exceed 400 mcg per day. Brazil nuts are a great source of selenium and just a handful of these nuts every few days can help meet most people’s minimum need for the mineral when eaten as part of a healthy, balanced diet.
Iodine is something of a double-edged sword when it comes to thyroid health. While it is essential for thyroid hormone production, too much iodine can actually cause thyroid damage. Taking an iodine supplement without first consulting a health care practitioner could prove harmful and may even lead to hyperthyroidism and Graves’ disease.
In genetically susceptible individuals, excess iodine can trigger thyroiditis. This is because highly iodinated thyroglobulin is more immunogenic than poorly iodinated thyroglobulin. Iodine may also be directly toxic to the thyroid, causing damage via free radicals and immunogenic activity. (R)
Most people in North America get enough iodine from dietary sources, with two key exceptions: anyone eating a predominantly plant-based diet (which is often low in iodine) and anyone who is pregnant (because pregnancy increases iodine demands to fuel fetal growth).
Many multivitamin and mineral formulas, as well as formulas featuring seaweeds (such as kelp), and those formulated to support skin, hair, and nails, often contain iodine. As such, it is important that individuals tally the total amount of iodine in all supplements they’re taking, as well as likely intake from dietary sources including iodized salt and seaweeds, as well as medicines such as amiodarone and some topical antiseptics and contrast dyes. Anyone taking thyroid medications needs to be especially careful about natural supplements that may contain iodine as this may interfere with the effectiveness of medications.
Just as certain nutrients help support thyroid health, some dietary constituents can hinder thyroid function. Goitrogens are foods or substances that interfere with iodine uptake in the thyroid gland, leading to reduced production of thyroid hormones. Common goitrogens include:
- Bok choy
- Brussel sprouts
- Mustard and mustard greens
Goitrogens are also found in legumes, cassava root, turnip, amiodarone, and lithium, and soy foods can worsen thyroid issues by reducing thyroxine absorption and thyroid hormone function. As such, soy has been associated with an increased risk of auto-immune thyroid disease. (R)
Again, the situation is more complex than these associations initially suggest. For example, epigallocatechin-3-gallate (EGCG), polyphenols in green tea, and genistein (an isoflavone in soy) appear to inhibit the activity of DNA methyltransferase, which may decrease DNA methylation. (R) In some cases, this effect may be beneficial as it could help suppress the growth of certain cancers. However, in people with a propensity for autoimmune thyroid problems, the effect may have negative consequences, suggesting that it may be helpful for people with a family or personal history of autoimmune conditions to minimize intake of soy, green tea, and sources of phenolic compounds, including hesperetin, naringin, apigenin, and luteolin.
In summary, we have a lot to learn about the involvement of genes in autoimmune hypothyroidism, and even more to uncover about the complex interplay of epigenetics in Hashimoto’s thyroiditis. The good news is that, once diagnosed, most cases of hypothyroidism can be effectively managed with medications and/or by correcting nutritional deficiencies.
If you’re concerned about thyroid health, don’t try to self-medicate with supplements as you may do yourself more harm than good. Instead, talk to your health care practitioner about your concerns and have a full thyroid test panel where appropriate.