Category Archives: Triggers for Graves’ disease

Effects of Cadmium on thyroid gland

Effects of Cadmium on thyroid gland

What is the connection between cadmium metal and thyroid?

Cadmium (Cd) is a silvery metal sitting next to zinc on a periodic table. The metals often appear together in nature. Unfortunately, unlike zinc, cadmium is a toxic and carcinogenic. Even though cadmium release into environment is closely controlled by government legislation, cadmium is impossible to avoid. More and more people are getting closer to reaching toxic levels, especially with increased age and those who had occupations exposing them to cadmium or exposed to cigarette smoke. Cadmium accumulates in the body and is difficult to excrete. Cadmium is found in soils (especially those industrially polluted), artists’ paints (orange, yellow and red), pigments, bake ware, nickel cadmium batteries, phosphorous fertilizers, plastics stabilizers, corrosion-resistant metal plating, metal alloys, brake lining of cars, pollution from power plants, mining and smelting and from production of some foods like margarine. Cd may be present in some plants (especially grown on soils contaminated with industrial pollution, green leafy plants tend to uptake it more easily), some organ meats (liver and kidneys), molluscs and other shellfish in some areas (as they tend to accumulate it) and large ocean fish. Some plants such as tobacco, marijuana and rice tend to uptake Cd more readily. Coffee and black tea may also contain some cadmium. Cigarettes are a significant source of cadmium exposure as lungs take up cadmium more readily than the digestive system. It is considered a substantial source of cadmium toxicity in humans. It generally doubles the cadmium intake. We also have to remember that cigarette smoke also contains other substances including thiocyanate that inhibits iodine uptake by the thyroid gland. Nicotine in cigarettes increases the synthesis of T3 from T4 in the brain, which might explain the difficulty in quitting smoking as higher T3 levels correspond to higher serotonin (feel good chemical) levels in the brain. However since cadmium is such a toxic metal, its influence on thyroid cannot be overlooked. Thyroid is one of organs that tends to accumulate cadmium.

What is the relationship between cadmium, thyroid and autoimmunity?

Cadmium and other toxins present in cigarettes interfere with thyroid gland function and thyroid hormone T4 to T3 conversion; they may cause damage to the thyroid resulting in the generation of autoantibodies. Cadmium exposure is associated with thyroid autoimmunity (both Graves’ disease and Hashimoto’s thyroiditis) in genetically predisposed people. A study of 132 pairs of twins showed that cigarette smoke exposure was connected with thyroid autoimmunity with higher rates (about 2.5X higher) for Graves’ disease than Hashimoto’s thyroiditis. It was also less significantly associated with non-autoimmune thyroid diseases (simple goiter and nodular toxic goiter) (17).

There is some suggestions in literature that Hashimoto’s thyroiditis may be triggered by cadmium especially when iodine and selenium levels are low. People with Graves’ disease may have adequate iodine levels (although not always) but are also usually low in selenium.

Graves’ disease is strongly connected to cadmium toxicity. It is especially connected to Graves’ disease with TED (eye involvement). Smoking has been connected with higher incidence of GD in females (26). It is believed that cigarette smoke may increase the risk of GD as much as two fold. Acropachy association with TED tends to represent the most severe form of autoimmune thyroid disease, with patients having very high levels of thyroid stimulating antibody. Cigarette smoking rates were found to be high in these individuals. Cd disrupts the ratio of copper and zinc which are vital for thyroid function. It contributes to copper deficiency, condition which accelerates thyroid function. Copper deficiency can occur when the body uses copper very fast (perhaps when children and teens get Graves’ disease) or when it cannot use copper efficiently and stores it in unusable form. Cadmium also interferes with zinc metabolism and competes with copper and zinc for binding on a transport protein called metallothionein. Also, in the cause of adrenal exhaustion, due to chronic stress for example, metallothonein is not produced in sufficient quantities. When this happens, copper is not metabolized properly. Copper deficiency affects the immune system and can also result in hyperactivity, high blood pressure and overuse of the sympathetic nervous system. According to Dr. Willson (9) cadmium toxicity may contribute to violent human behavior. Cd exposure may cause GABA imbalances (calming molecule in the brain). Cd also interferes with metabolism of vitamin D which is important for the balance of the immune system. It also decreases magnesium levels (common deficiency with autoimmune thyroid conditions). Cadmium can also induce iron deficiency anaemia. Cadmium damages mitochondria, organelles where energy is produced. Dysfunctional mitochondria are connected to autoimmunity. Cd toxicity has also been connected to rheumatoid arthritis and Multiple sclerosis. Cadmium may also bind to glutathione making it ineffective. Glutathione is a free radical scavenger, important for the health of the thyroid gland.

Reducing Cadmium levels may be important for some people in achieving a remission from thyroid autoimmunity.

Do some people absorb Cd more easily?

This predisposition to accumulate those specific metals might be connected to individual’s genetics. It is also relates to a poor stress management. Females tend to absorb Cd more easily due to higher levels of oestrogen hormone (necessary for ovulation and pregnancy). Oestrogen may act as an accelerator of mineral uptake into the body; it may act to enhance cadmium absorption. Women who have insufficient levels of progesterone to balance oestrogen may accumulate Cd more easily. People with low iron stores are especially vulnerable to the adverse effects of cadmium. As cadmium tends to accumulate with age (it is difficult to get rid of), it causes lowered levels of zinc which is needed for thyroid hormonal binding to their receptors. This may explain higher risks of hypothyroidism in older people, especially women. Also, older cells have a reduced capacity to produce Metallothioneins (MTs) which is are protective against Cd toxicity and proper levels of zinc and copper. Adrenals glands need to strong for sufficient production of this molecule.

Stress and cigarette smoke exposure can induce Graves’ disease as it lowers production of metallothioneins and increased Cd exposure. This trigger might be especially powerful in younger people as they tend to use copper fast. Copper deficiency accelerates thyroid function and damages the energy producing mitochondria. It was found to interfere with Coenzyme A, which helps to transport free fatty acids to mitochondria for energy production.

What Cadmium does in the body?

Cadmium tends to accumulate in the thyroid gland and therefore may cause thyroid damage due to its toxicity. It is one of the triggers for thyroid autoimmunity in individuals who are genetically predisposed to autoimmunity. In significant levels, it depletes selenium mineral which is extremely important for the health of the thyroid gland as it important for the glutathione peroxidase system which removes free radicals from the thyroid gland. In the thyroid gland, free radicals are produced continuously due to oxidation of iodine by hydrogen peroxide for the production of thyroid hormones. If free radicals are not properly controlled by glutathione peroxidase in the thyroid, they damage the thyroid cells and the lipid membranes. Cadmium toxicity increases free radicals in the body overall. Cd was shown to inhibit superoxide dismutase (copper, zinc based), two antioxidant enzymes. Cd toxicity may therefore play a role in other autoimmune disorders.

Cd was found to decrease T4 levels and increase T3 levels in a Japanese study comparing residents of the Cd-polluted Kakehashi River basin with residents of a nonpolluted area (1). Therefore Cd can induce T3 thyrotoxicosis and hyperthyroidism which was also demonstrated in animal studies (5). In people predisposed to autoimmunity, it can cause thyroid autoimmunity. High levels of cadmium exposure were associated with changes to thyroid hormonal levels. A large human study (29) showed that blood Cd was positively associated with FT3 and urinary Cd was positively associated with FT4.

It may also lower levels of both T4 and T3 (perhaps if iodine and selenium are low) which was shown in animal studies. Obviously as Cd levels accumulate, eventually T3 levels will be decreased due to lowered levels of T4 and selenium resulting in hypothyroidism. A study in children demonstrated that Cd increases TSH levels and decreases thyroid hormone T4 (15).

People who had a thyroidectomy might be more vulnerable to lung damage by exposure to Cd (11). Smoking would not be recommended.

Other thyroid changes and thyroid cancer (22) may also be seen with cadmium toxicity. Cancer may also be more advanced with cadmium toxicity.

“The accumulation of cadmium in thyroid tissue may be one of important etiologic factors for the thyroid cancer progression and aggravation in Korean women.”(21)

“Colloid cystic goiter, adenomatoid follicular hyperplasia with low-grade dysplasia and thyroglobulin hypo- and asecretion, and parafollicular cell diffuse and nodular hyperplasia and hypertrophy are often found in chronic cadmium toxicity.” (20)

Test for Cadmium:

Comprehensive Urine Profile (better for detection of long time Cd exposure), serum Cadmium and mineral hair analysis

How to reduce Cadmium in the body:

The medical system uses chelators such as DMPA for cadmium removal from the body in case of detected toxicity.

However, there are ways to decrease Cd uptake and increase removal in the body and they are:

  • Consider stopping smoking, avoid secondary cigarette smoke
  • Limit occupational/environmental exposure
  • Support glutathione production in the body (glutathione requires selenium and precursors such as glycine, glutamine, cysteine).
  • Support glutathione conjugation in liver which detoxifies body from heavy metals. The nutrients required for this step are methionine, amino acids cysteine and taurine, glycine, vitamin C and vitamin B6. Brassica vegetables, such as cabbage, cauliflower, kale, and broccoli and allium vegetables, such as onions, garlic, shallots also help. Vitamin E, N-acetyl cysteine (NAC), bioflavonoids supplementation and fermented vegetables may also be helpful to improve glutathione conjugation. Brewers’ yeast has glutathione building nutrients. One of the best ways is to consume fermented vegetables with liver cleansing herbs. Dandelion root, milk thistle, coriander herb, horseradish and wasabi may also be helpful. Probiotics may also help.
  • Avoid environmental exposure in food (organic diet, increasing fibre, detoxifying vegetables, herbs, avoiding refined food). Fibre removes toxins by binding to them.
  • Chlorella, sea algae may help but since it is high in iodine, it can aggravate Graves’ disease but may help people with low iodine. Selenium levels needs to be adequate. MetalAway is one of the products a holistic doctor may prescribe in case of metal toxicity.
  • Hormone balancing (for example, insufficiency of thyroid hormones compromises liver function and detoxification).
  • Adrenal support, stress reduction and better stress management may help.
  • Coenzyme Q10 may play a positive role as an agent for treatment of CD poisoning (6)
  • Carotenoids were found to increase Cd excretion from the body in study in rats (7), (present in red and orange vegetables, if you use carrots for carotenoids source, use organic carrots and peel them before use)
  • Diet which includes selenium and glutathione producing nutrients.
  • Vitamin C (28)
  • Vitamin D
  • Correcting iron deficiency
  • Checking zinc and copper levels
  • Reducing alcohol consumption as alcohol can increase cadmium uptake
  • Alpha-lipoic acid
  • Fruit pectin (soluble fibre), psyllium
  • Olive leaf supplement
  • Willson recommends near infrared sauna for cadmium removal
  • Milk consumption may increase Cd uptake (as it is rich in hormones), especially with iron deficiency.

 

This post is for educational purposes only. Consult your doctor in regards to cadmium and before taking any supplements and dietary changes.

References:

  1. Nishijo M, Nakagawa H, Morikawa Y, Tabata M, Senma M, Miura K, Tsuritani I, Honda R, Kido T, Teranishi H. A study of thyroid hormone levels of inhabitants of the cadmium-polluted Kakehashi River basin]. Nihon Eiseigaku Zasshi. 1994 Jun; 49(2):598-605.
  2. Hammouda F, Messaoudi I, El Hani J, Baati T, Saïd K, Kerkeni A. Reversal of cadmium-induced thyroid dysfunction by selenium, zinc, or their combination in rat. Biol Trace Elem Res. 2008; 126(1-3):194-203.
  3. S Salminen, et al. Probiotic bacteria as potential detoxification tools: assessing their heavy metal binding isotherms. Can J Microbiol. 2006 Sep; 52(9):877-85.
  4. JN Bhakta, et al. Characterization of lactic acid bacteria-based probiotics as potential heavy metal sorbents. J Appl Microbiol. 2012 Jun; 112(6):1193-206.
  5. Ghosh N; Bhattacharya S. Thyrotoxicity of the chlorides of cadmium and mercury in rabbit. Department of Zoology, Visva-Bharati University, Santiniketan, India. Biomed Environ Sci, 1992 Sep; (3):236-40.
  6. Patrick J. Kennedy, Ajay A. Vashisht, Kwang-Lae Hoe, Dong-Uk Kim, Han-Oh Park, Jacqueline Hayles, and Paul Russell6. A Genome-Wide Screen of Genes Involved in Cadmium Tolerance in Schizosaccharomyces pombe Toxicol Sci. 2008 Nov; 106(1): 124–139
  7. El-Missiry, M.A. and F. Shalaby, 2000. Role of β-carotene in ameliorating the cadmium-induced oxidative stress in rat brain and testis. J. Biochem. Mol. Toxicol., 14: 238-243.
  8. A. Bashandy and I. M. Alhazza. The Hepatoprotective Effect of β-Carotene against Cadmium Toxicity in Rats. Science Alert. URL: http://scialert.net/fulltext/?doi=jpt.2008.457.463&org=10
  9. http://drlwilson.com/Articles/CADMIUM.htm
  10. Sharma G; Sandhir R; Nath R; Gill K. Effect of ethanol on cadmium uptake and metabolism of zinc and copper in rats exposed to cadmium. Department of Biochemistry, Postgraduate Institute, Medical Education and Research, Chandigarh, India. 1991 Jan; J Nutr. 121(1):87-91
  11. Palmer KC; Mari F; Malian MS. Cadmium-induced acute lung injury: compromised repair response following thyroidectomy. 1986 Dec Environ Res, 41(2):568-84
  12. Nishiyama S; Onosaka S; Taguchi T; Konishi Y; Tanaka K; Kinebuchi H Stimulation of cadmium uptake by estradiol in the kidney of male rats treated with cadmium. Department of Environmental and Occupational Health, Kochi Medical School, Japan. 1988 Aug 15. Biochem Pharmacol, 37(16):3091-6.
  13. Fiala J; Hrub´a D; R´ezl P. Cadmium and zinc concentrations in human placentas. Institute of Preventive Medicine, Faculty of Medicine, Masaryk University, Brno, Czech Republic. Cent Eur J Public Health, 1998 Aug; (3):241-8.
  14. Soldatovi´c D; Matovi´c V; Vujanovi´c D; Stojanovi´c Z. Contribution to interaction between magnesium and toxic metals: the effect of prolonged cadmium intoxication on magnesium metabolism in rabbits. Department of Toxicological Chemistry, Faculty of Pharmacy, University of Belgrade, Yugoslavia. Magnes Res, 1998 Dec.11(4):283-8
  15. Osius N, Karmaus W, Kruse H, Witten J. Exposure to polychlorinated biphenyls and levels of thyroid hormones in children. Environ Health Perspect 1999 Oct; 107(10):843-9.
  16. Sumathi R, Baskaran G, Varalakshmi P. Relationship between glutathione and DL alpha-lipoic acid against cadmium-induced hepatotoxicity. Jpn J Med Sci Biol 1996 Apr; 49(2):39-48.
  17. Thomas Heiberg Brix, MD; Pia Skov Hansen, MD; Kirsten Ohm Kyvik, MD, PhD; Laszlo Hegedüs, MD Cigarette Smoking and Risk of Clinically Overt Thyroid Disease. A Population-Based Twin Case-Control Study. Arch Intern Med. 2000 Mar 13; 160(5):661-6.
  18. Z Ernahrungswiss The toxicological estimation of the heavy metal content (Cd, Hg, Pb) in food for infants and small children 1990 Mar;29(1):54-73.
  19. Stohs SJ, Bagchi D, Hassoun E, Bagchi M. Oxidative mechanisms in the toxicity of chromium and cadmium ions. J Environ Pathol Toxicol Oncol. 2000; 19(3):201-13.
  20. Jancic SA, Stosic BZ. Cadmium effects on the thyroid gland. Vitam Horm. 2014; 94:391-425.
  21. Chung HK, Nam JS, Ahn CW, Lee YS, Kim KR. Some Elements in Thyroid Tissue are Associated with More Advanced Stage of Thyroid Cancer in Korean Women. Biol Trace Elem Res. 2016 May;171(1):54-62
  22. John Kovach, Maisie Shindo, Sharon Liang, Jingxuan Liu, Joy Roelfs, John Chen, David Bellis and Patrick Parsons. Environmental cadmium as a potential risk factor for thyroid cancer. Cancer research. URL: http://cancerres.aacrjournals.org/content/68/9_Supplement/5593
  23. Yangho Kim, MD and Sangkyu Park, MD. Iron deficiency increases blood concentrations of neurotoxic metals in children. Korean J Pediatr. 2014 Aug; 57(8): 345–350
  24. Ithyroid.com Cadmium. URL: http://www.ithyroid.com/cadmium.htm
  25. Oualid Hamdaoui. Removal of cadmium from aqueous medium under ultrasound assistance using olive leaves as sorbent. Chemical Engineering and processing: process intensification. Volume 48, Issue 6, June 2009, Pages 1157-1166.
  26. Yoshiuchi K, Kumano H, Nomura S, Yoshimura H, Ito K, Kanaji Y, Ohashi Y, Kuboki T, Suematsu H. Stressful life events and smoking were associated with Graves’ disease in women, but not in men. Psychosom Med. 1998 Mar-Apr; 60(2):182-5.
  27. Hegedus, T.H. Brix and P. Vestergaard. Relathionship between cigarette smoking and Graves’ ophthalmopathy. J. Endocrinol. Invest. 2004. 27:265-271.
  28. Gupta P, Kar A. Role of ascorbic acid in cadmium-induced thyroid dysfunction and lipid peroxidation. J Appl Toxicol. 1998; 18:317–20.
  29. Aimin Chen, Stephani S. Kim, Ethan Chung, and Kim N. Dietrich. Thyroid Hormones in Relation to Lead, Mercury, and Cadmium Exposure in the National Health and Nutrition Examination Survey, 2007–2008. 2013. Volume 121. Issue 2. URL: https://ehp.niehs.nih.gov/1205239/

 

 

 

 

 

Autoimmune Thyroid Disease and gluten. Is there a connection?

 Autoimmune Thyroid Disease and gluten. Is there a connection?

Our digestive system is like a plants’ root system. If a plant is grown in a barren soil deprived of soil bacteria and nutrients, it will not be healthy.

A ‘leaky gut’ allows to filter out undigested larger food molecules instead of just simple fatty acids, amino acids, minerals and vitamins, the building blocks and simple molecules our body needs to function. These simple molecules go through the cell of the intestinal lining into the outside fluid and bloodstream.

However when a person has a leaky gut, unwelcome components can pass through spaces between the intestinal cells to the outside. The junctions between the cells of intestinal lining supposed to be tight and nothing should get through between the cells. However in leaky gut some of the junctions are not closed enough. These components can be undigested molecules, toxins and pathogens. About ¾ of our immune system is associated with our gut. This relationship is extremely important as digestive system is the main contributor to the health of our immune system. Leaky gut is associated with autoimmunity problems but not all leaky gut problems cause autoimmune disorders. Genetic components are also important. Gluten sensitivity is linked to a leaky gut and vice versa, a leaky gut can make a person more sensitive to gluten.

There are many reasons why a person may have an unhealthy gut. They include: poor nutrition (too much sugar, not enough vegetables, too much processed food), lack of fiber in diet, infections, food poisonings, frequent use of antibiotics, illness (including thyroid autoimmunity and thyroid problems, pancreatic insufficiency, etc.), certain medications such as NSAIDS (non-steroidal anti-inflammatory drugs such as aspirin or ibuprofen), stress, toxins (such as food chemicals, pesticides, other additives), food allergies and sensitivities such as sensitivity to gluten. A low stomach acid may play a role in how well gluten is digested and the health of the gut.

Gluten is a protein, a large molecule composed of amino acids. ‘Gluten’ comes from a Latin language and it means glue. It is what gives dough its elasticity. It is found in gluten containing grains. The proteins in gluten are: prolamines and glutelins, folded and coiled and connected by disulphide bridges. Wheat contains prolamine – gliadin and glutelin- glutenin. The prolamine of rye is secalin, prolamine of barley is hordein and oats is avenin. Allergy to gluten is usually strongest to gliadin (in wheat).

Gluten containing food include: wheat bran, wheat, rye, barley (both whole grains and flours) and oats. Wheat flour white bread, cakes, pastries and pasta contain high amounts of gliadin. It is also found as a filler in many products. Modern wheat is different to the wheat our ancestors ate. It has been hybridized and selected for higher yields. The modern farming technology involves using pesticides and fertilizers and bleaching the flour. The flour our ancestors ate was organic, grind whole and unbleached. There are questions regarding the effects of modern wheat on our health which are still awaiting clear answers. Nevertheless, some people are sensitive to gluten containing products.

Good gluten free grains are:  brown/white rice, buckwheat, quinoa and amaranth. Quinoa contains lots of iron and methylated folate, which is beneficial.

Gluten is a complex molecule, which is difficult to digest as some of the bonds between amino acids in gluten are uncommonly seen in other proteins. Some sections of undigested gluten can have immuno-modulatory activities in individual people.

Some people are able to dispose of the undigested parts of gluten through their gut easier than others. They can also digest it better. There are individuals in which their overall health is strongly impacted by their gastrointestinal system and it is the key for their well being.

There is an enzyme in human cells called transglutaminase. It is important for linking proteins to collagen in extracellular matrix (outside of cells). Gliadin molecule in gluten looks similar to transglutaminase enzyme and can confuse the immune system in genetically predisposed people. This may result in Coeliac Disease where antibodies to transglutaminase and components of collagen (what holds cells together) are generated.

Gluten, especially gliadin part also shares similarity to thyroid molecules. Therefore, when leaky gut is present, the immune system of genetically predisposed individual can get confused and generate faulty antibodies to thyroid tissues. Also, the auto-antibodies directed against transglutaminase (anti-TGase II antibodies) bind to thyroid cells and the collagen components outside of the thyroid cells and thus could be implicated directly in thyroid autoimmunity which can explain an increased correlation of Coeliac Disease and thyroid autoimmunity.

Gluten sensitivity is associated with Hashimoto’s thyroiditis and Graves’ Disease and other autoimmune disorders. Gluten sensitivity seems to be more strongly associated with Hashimoto’s thyroiditis than Graves’ Disease. Apart from possible gluten sensitivity, casein in cow’ milk products may be a problem for people with thyroid autoimmunity. It seem to be more strongly connected to Grave’s Disease.

Coeliac disease (CD) is an autoimmune disorder, severe allergy to gluten with auto- antibodies to tissue components which can damage intestinal finger-like projections (villi) which absorb nutrients from food. It can co-occur with thyroid autoimmunity. Coeliac disease may sometimes precede thyroid autoimmunity. The links between autoimmune thyroid disease and Coeliac Disease were shown in many scientific research studies (1, 2, 3, and 4). The immune system in people with autoimmunity in general shares common genetic components and can get confused easier. The presence of Coeliac Disease in patients with Autoimmune Thyroid Disorder ranged from 3.3% – 5.5%. There were also few cases of laboratory diagnosis of Coeliac Disease in Autoimmune Thyroid Patients who did not have symptoms of Coeliac Disease (4).

The presence of Autoimmune Thyroid Disease was also 11.8% higher in coeliac patients when compared to controls in a study (4). It is worth mentioning that the diagnosis of Coeliac Disease requires more tests than blood anti-gliadin antibody test. This test is not 100%. Stool analysis is one more sensitive method to detect antibodies produced in the digestive tract rather than blood. Dr. Kenneth Fine at the Intestinal Health Institute had shown that a high percentage of his patients had IgA anti-gliadin antibodies in stool samples and not in blood, 60% and 75% positive versus 11% in the blood (7). Some asymptomatic people have these antibodies. Tissue biopsy and antibody testing to tissue components such as anti-endomysial antibodies or EMA and transglutaminase autoantibodies (TGAA) confirms CD diagnosis. Patients need to be on a gluten containing diet at the time of testing.

It may be beneficial to get tested for Coeliac Disease if you experience a lot of gastrointestinal issues. Coeliac Disease affects 1 in 70 Australians but many others may be not be diagnosed because many symptoms can be unrecognized and some people may be asymptomatic as mentioned before, perhaps in early stages of an illness. Genetic screening for the HLA DQ2/8 gene (present in a half of population) can also be a useful test especially with a family history of an illness. People not carrying this gene are very unlikely to have Coeliac disease. People with Coeliac Disease cannot have any gluten in their food. They need to have gluten-free grains like rice or quinoa, otherwise they get very sick and have symptoms such as bloating, irritable bowel, diarrhea, constipation, gas, abdominal pain, nausea, joint and muscle pain, headaches, skin rashes, tiredness, brain fog, sleep disturbances, anxiety, depression, iron deficiency and emotional issues. In Coeliac Disease secretory IgA antibody binds gliadin and transports it on the outside of the intestinal cell. The immune system generates antibodies to gliadin (in gluten) and the connective tissue in the gut (endomysium), specifically tissue transglutaminase or tTg (also abbreviated as TG2 or TG).

However one does not need to have Coeliac Disease, antibodies and classical changes in gut villi to be sensitive to gluten. Negative coeliac panel tests do not necessary mean that a person is not sensitive to gluten. People with autoimmune thyroid illness may not have Coeliac Disease (as it only co –occurs in about 3-5% of people with thyroid autoimmunity), they may just be sensitive to gluten. Allergic and autoimmune reactions are not present in gluten sensitivity. A study reported that about 6.8% of population were diagnosed in Non-Coeliac Gluten Sensitivity –NCGS (15). More specifically, patients have negative serological tests for Coeliac Disease (endomysial and/or tissue transglutaminase antibodies) but antigliadin antibodies may be present. They may have other antibodies to various wheat and tissue components (15, 17). This was demonstrated in a patient with Crohn’s Disease (17) who also had NCGS. The immune system mechanisms of gluten sensitivity are not clearly understood. People with gluten sensitivity may also have symptoms triggered by other molecules present in rye or barley. This sensitivity may possibly be connected to stress, toxins, low stomach acid, hormonal imbalances and other factors. People who are sensitive to gluten might have symptoms similar to Irritable Bowel Syndrome. They might experience discomfort, gas and burping after they eat gluten containing food. A research study showed that heartburn, stomach ulcers, GERD may be linked to gluten sensitivity. Complete stool diagnostic test can determine the health of the digestive system.

 Dr. Alessio Fasano, a leading expert in Celiac Research and Gastroenterology has done a lot of research into non-celiac gluten sensitivity. It was noted by Dr Fasano and other health practitioners that people with IBS (Irritable Bowel Syndrome) like symptoms such as bloating, abdominal pain, constipation and diarrhea and no Coeliac Disease improved their gastrointestinal symptoms on a gluten free diet. Some people report feeling generally better and happier as gluten sensitivity may affect brain and other tissues.

People, sensitive to gluten, have an immune response to undigested parts of gluten molecules, which causes inflammation although exact mechanism are yet to be understood. The nervous system influences the permeability of tight junctions to macromolecules, thus modifying mucosal barrier of the digestive system through neuropeptides. Thus stress plays a big role in the gastrointestinal health. It is important to have a balanced but flora. The beneficial bacteria in our gut ‘educate’ the immune system how to function properly. A healthy gut flora reduces the over-activity to some food antigens and prevents allergies.

Gluten intolerance can cause low levels of diamine oxidase (DAO) in the digestive system, which breaks down histamine. Histamine is an immune system modulating molecule, which causes an immediate inflammatory response. The intestinal lining can become more permeable to certain toxic molecules, which leak through it and enter the blood system. Inflammatory molecules can be released as a reaction to gluten sensitivity, opening passages between the cells of gastrointestinal tract, allowing toxic molecules to leak through these passages. Dr. Alessio Fasano and his team of researchers had discovered a molecule called zonulin (10), a protein that can be triggered by gluten and other molecules, which is expressed in all autoimmune conditions and is associated with leaky gut. Dr. Fasano’s and his research team are working on a new medication which inhibits zonulin.

Gluten sensitivity may play a big part in some people. As mentioned previously, the gut is closely connected to the immune system and as gluten can mimic some molecules of the thyroid, subsequent attack on thyroid attack is possible.

Personally, I do not have Coeliac Disease. I was tested for blood anti-gliadin antibodies when I had experienced a lot of IBS like symptoms while on sub optimal thyroid hormonal treatment after my thyroid removal. This is not surprising as the luck of T3 hormone creates lots of negative effects on the gastrointestinal system. Without adequate T3 a person suffers from a low stomach acid and poor digestion of proteins such as gluten. People with a low stomach acid can have vitamin B12 or iron deficiency. My issues subsided with the introduction of Natural desiccated thyroid to my levothyroxine hormonal replacement. I was skeptical in regards to gluten for years until my integrative doctor suggested to try to lower my inflammation levels by avoidance of gluten. I thought that it is possible that I may have gluten sensitivity and a gluten free trial would help me determine that. I had gone on a complete gluten free diet for six months and I did see improvements in my well- being, less bloating, better digestion and feeling better. The markers of my inflammation had decreased (anti-nuclear antibodies- ANA). When people lower their inflammation, T3 hormone works better in their body. However I am not sure if the markers of inflammation went down specifically due to gluten as I had made some other positive changes. I personally feel that I am more sensitive to cow’s milk products than wheat. These days, I am still limiting gluten products and a light gluten exposure works for me. I feel better when I limit gluten and will continue to do so.

However, every situation is unique and the power of your personal observation is important. Gluten free diet may benefit people with autoimmunity problems. We know that there is a connection between thyroid autoimmunity and Coeliac Disease. We also know that some people with autoimmunity have Non Coeliac Gluten Sensitivity. A Case Report in Non-Coeliac Gluten Sensitivity and Autoimmunity (18) says that: “Non-coeliac gluten sensitivity can be associated with autoimmune manifestations and, more importantly, that the finding and treatment of non-coeliac gluten sensitivity can be critical for the management of an otherwise refractory patient.”

One of the important observation derived diet tips for Hashimoto’s thyroiditis and Graves’ disease suggested in literature is the avoidance of gluten. It was found in a study (12) that gluten withdrawal may in distinct cases, reverse thyroid abnormality.

Apart from thyroid autoimmunity, some people who have coeliac disease may also suffer from sub clinical non-immune hypothyroidism which may be due to malabsorption of nutrients.

Bone broths, foods containing gelatin, organic food which includes lots of vegetables, apple cider vinegar, fermented vegetables and stress reduction may also improve the health of gastrointestinal system. It is also important to avoid any other food your body reacts negatively to.

Speak to your doctor if you have any digestive issues.

This blog is for educational purposes only.

References:

  1. Pekka Collin, Jorma Salmi, Olavi Hällström, Timo Reunala and Amos Pasternack. Autoimmune thyroid disorders and coeliac disease. Eur J Endocrinol 1994; 130:137–40.
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  3. Chin Lye Ch’ng, MRCPI, M. Keston Jones, MD, FRCP, and Jeremy G. C. Kingham, MD, FRCP. Celiac Disease and Autoimmune Thyroid Disease. Clin Med Res. 2007 Oct; 5(3): 184–192.
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  5. Hakanen M, Luotola K, Salmi J, Laippala P, Kaukinen K, Collin P. Clinical and subclinical autoimmune thyroid disease in adult celiac disease. Dig Dis Sci. 2001 Dec; 46(12):2631-5.
  6. Ruuskanen A, Kaukinen K, Collin P, Huhtala H, Valve R, Mäki M, Luostarinen L. Positive serum antigliadin antibodies without celiac disease in the elderly population: does it matter? Scand J Gastroenterol.2010 Oct; 45(10):1197-202.
  7. Carlo Catassi and Alessio Fasano. Tempters and Gluten- Free Diet. Nutrients. 2016 Dec; 8(12): 786.
  8. Chin Lye Ch’ng, MRCPI, M. Keston Jones, MD, FRCP, and Jeremy G. C. Kingham, MD, FRCP. Celiac Disease and Autoimmune Thyroid Disease. Clin Med Res. 2007 Oct; 5(3): 184–192.
  9. Fasano A. Leaky Gut and autoimmune disease. Clin Rev Allergy Immunol. 2012 Feb; 42(1):71-8.
  10. Fasano A. Zonulin and Its Regulation of Intestinal Barrier Function: The Biological Door to Inflammation, Autoimmunity, and Cancer. Physiol Rev. Vol 91. Jan 2011. 151-175.
  11. Naiyer AJ, Shah J, Hernandez L, Kim SY, Ciaccio EJ, Cheng J, Manavalan S, Bhagat G, Green PH. Tissue transglutaminase antibodies in individuals with celiac disease bind to thyroid follicles and extracellular matrix and may contribute to thyroid dysfunction. Thyroid. 2008 Nov; 18(11):1171-8.
  12. Sategna-Guidetti C, Volta U, Ciacci C, Usai P, Carlino A, De Franceschi L, Camera A, Pelli A, Brossa C. Prevalence of thyroid disorders in untreated adult celiac disease patients and effect of gluten withdrawal: an Italian multicenter study. The American Journal of Gastroenterology. 2001; 96(3): 751–757.
  13. Carlo Catassi, Julio C. Bai, Bruno Bonaz, Gerd Bouma, Antonio Calabrò, Antonio Carroccio, Gemma Castillejo, Carolina Ciacci, Fernanda Cristofori, Jernej Dolinsek, Ruggiero Francavilla, Luca Elli, Peter Green, Wolfgang Holtmeier, Peter Koehler, Sibylle Koletzko, Christof Meinhold, David Sanders, Michael Schumann, Detlef Schuppan, Reiner Ullrich, Andreas Vécsei, Umberto Volta, Victor Zevallos, Anna Sapone, and Alessio Fasano. Non-Celiac Gluten Sensitivity: The New Frontier of Gluten Related Disorders. Nutrients. 2013 Oct; 5(10): 3839–3853.
  14. Geoffrey Holmes. Non coeliac gluten sensitivity. Gastroenterol Hepatol Bed Bench. 2013 Summer; 6(3): 115–119.
  15. Capannolo A, Viscido A, Barkad MA, Valerii G, Ciccone F, Melideo D, Frieri G, Latella G. Non-Celiac Gluten Sensitivity among Patients Perceiving Gluten-Related Symptoms. Digestion. 2015; 92(1):8-13.
  16. Imran Aziz and David S. Sanders (2012). Emerging concepts: from coeliac disease to non-coeliac gluten sensitivity. Proceedings of the Nutrition Society, 71, pp 576-580.
  17. Aristo Vojdani and David Perlmutter. Differentiation between Celiac Disease, Nonceliac Gluten Sensitivity, and Their Overlapping with Crohn’s Disease: A Case Series. Case Reports in Immunology.Volume 2013 (2013), Article ID 248482, 9 pages. URL: https://www.hindawi.com/journals/crii/2013/248482/
  18. Carlos Isasia, Isabel Colmenerob, Fernando Cascoc, Eva Tejerinad, Natalia Fernandez-Pugae. Non-Coeliac Gluten Sensitivity and Autoimmunity: A Case Report. URL: http://ejcrim.com/index.php/EJCRIM/article/view/156/206
  19. Grain brain David Perlmutter, MD. Little, Brown and Company. Hachette Book Group. 2013 New York.
  20. Diagnosing coeliac disease – the key facts URL: http://www.coeliac.org.au/uploads/65701/ufiles/Fact_sheets/DiagnosingCoeliacDisease.pdf
  21. An Interview with Dr. Kenneth Fine of EnteroLab.com and the Intestinal Health InstituteCeliac.com. URL: https://www.celiac.com/articles/23428/1/An-Interview-with-Dr-Kenneth-Fine-of-EnteroLabcom-and-the-Intestinal-Health-Institute/Page1.html.)
  22. Sarah Wilson. URL:http://www.sarahwilson.com/2015/11/should-i-be-eating-gluten-if-i-have-hashimotos-i-mean-really/
  23. Chris Kresser. The gluten thyroid connection. URL:https://chriskresser.com/the-gluten-thyroid-connection
  24. MTHFR support. Australia. URL:https://www.mthfrsupport.com.au/dao-deficiency-and-histamine-the-unlikely-connection/URL:
  25. Gluten Free Society. URL:https://www.glutenfreesociety.org/gluten-sensitivity-induces-acid-reflux/#QbsgUG90I4WtrY5g.99

 

 

 

 

 

 

 

 

Aspartame and thyroid autoimmunity

Aspartame and thyroid autoimmunity

Aspartame is an artificial sweetener used since 1980s. It was made accidently in 1965 by James M. Schlatter while doing a research in a laboratory. It is therefore not a naturally occurring substance. It is commonly known as NutraSweet, Equal, NatraTaste Blue or number E951. There are many other artificial sweeteners but I will focus on aspartame in this blog. Aspartame is about 200 times sweeter than sugar so very little is needed to achieve the same sweetness as sugar. It is approved for human consumption by FDA and is present in thousands of products including common diet soft drinks, chewing gums, vitamins, some medications (even sugar free cough lozenges) and many other foods ( jellies, confectionary, desserts, yoghurts).

While we all know that high sugar diet is bad for us but what about aspartame?

There is a controversy about the safety of aspartame and the efficacy of aspartame studies. Aspartame breaks down to toxic products in the body. The products are phenylalanine, aspartic acid, methanol (which is then metabolised to a neurotoxin formaldehyde and formic acid). The amounts generally consumed by people are believed to be acceptable and safe. However, as a scientist who worked on DNA, I can tell you that methanol and formaldehyde are still mutagenic substances. Aspartame contains aspartic acid and amino acid phenylalanine, which our body can convert to tyrosine, a building block or thyroid hormone and other hormones. Aspartic acid is a nerve cell stimulant. Even though aspartic acid and phenylalanine occur naturally in protein food, they do not occur by themselves but are balanced with other amino acids. There is a observational study linking consumption of diet soda daily was associated with significantly greater risks of select incident metabolic syndrome components and type 2 diabetes (1). Another scientific study linked consumption of artificial sweeteners with obesity (3). There are many other diseases possibly linked to aspartame consumption (6, 7).

The article published in The American Journal of Industrial medicine in 2014 urges for urgent need for regulatory evaluation of Aspartame and raises serious questions about its safety for human consumption and possible link to cancer development. “On the basis of the evidence of the potential carcinogenic effects of APM herein reported, a re-evaluation of the current position of international regulatory agencies must be considered an urgent matter of public health.”

Even though I will focus on thyroid autoimmunity in this blog, it is important to mention the questions raised about aspartame as our body works as a whole system and to focus on thyroid alone would be irrational.

In my opinion, the research on thyroid autoimmunity and aspartame is insufficient to properly establish a definite link between thyroid autoimmunity and aspartame. Larger population studies would be needed and beneficial. The link between aspartame and GD is not proven as such so far. However Dr. H. J. Roberts described cases of aspartame-related Graves’ disease in four weight-conscious women with hyperthyroidism who had experienced dramatic remissions within several weeks to 3 months of avoiding aspartame. He also had noticed that four other women who had been treated previously for Graves’ disease developed symptoms after beginning aspartame consumption and their symptoms subsided after cessation (4, 5). The power of observation is important and it is great that Dr Roberts is putting those issues into a light and raising questions. Artificial sweeteners were also tentatively linked to Hashimoto’s thyroiditis (8). Dr Janet Starr Hull, managed to cure herself of Graves’ disease by detoxifying from aspartame (10). Those correlations have been noticed by nutritionists as well. It is therefore best to avoid aspartame for people with thyroid autoimmunity. Having regular food and drinks containing aspartame may contribute to thyroid autoimmune illness.

Some individuals may be more sensitive to aspartame damage and may include pregnant women, growing foetus, children and older people who might not tolerate it well. For people with the disease phenylketonuria, ingesting aspartame may cause damage to their brain.

How do you then satisfy your sweet tooth and stay healthy? Limiting sugar is important, especially the white and refined sugar.

I can only talk about my personal choices only. I am not a dietician but I do not like including anything artificial in my food. I made my personal choices in regards to sugar and its artificial substitutes. I avoid foods containing high fructose corn syrup. I do not have any diet or sugar free foods with artificial sweeteners. I try hard to limit sugar. In my belief, sugar is inflammatory (especially refined, white) for someone with autoimmunity problems. It should be limited definitely. I stopped using sugar to sweeten my drinks in my twenties. Over time, I got used to that and never looked back. I do not use stevia (plant derived sweetener) as personally, I do not tolerate it well. I bake cakes or biscuits for special occasions and use brown unrefined sugar, coconut sugar in baking but only with less than a third of the recommended amount and limit the amount I eat. Unrefined brown sugar comes from natural sources like sugar beets and cane and not from a laboratory so I believe it is still better in small amounts than artificial sweeteners. I sometimes use small amount of honey, blackstrap molasses or maple syrup in baking also. Blackstrap molasses is a thick, brown liquid which also contains B vitamins, iron, chromium and other minerals. The presence of chromium in blackstrap molasses is very beneficial as chromium deficiency is connected to increased sugar cravings. Maple syrup also contains minerals. Aspartame may deplete chromium nutrient, which is important for hormonal balance and it may make you crave sugar more. Both blackstrap molasses and maple syrup are believed to have some antioxidant and anti-inflammatory qualities. They have a lower glycaemic index than plain sugar. Raw honey is high in sugar but also has antimicrobial and other beneficial properties so it is a better alternative to plain white sugar when used in small amounts.

I had noticed that some tricks can reduce my sugar cravings, which I usually have after dinner. Good adrenal support day formula works well for me if I notice experiencing lots of sugar cravings. Eating something fatty (few nuts or small piece of feta cheese) or sour (pickled or fermented vegetables) after a main meal has helped me personally. The trick for me is to be strong and wait 10-15 minutes after that and the craving go away. A teaspoon of apple cider vinegar in some water before a meal also lowers my blood sugar and helps. Including foods containing chromium and B vitamins in your diet such as some Brewer’s yeast helps with sugar cravings. Also, having lots of green, organic salads every day help with sugar cravings as they provide plenty of minerals such as potassium and magnesium which support adrenal glands. Finally, a small piece of dark 70-80% chocolate with unsweetened coffee helps me if everything else fails. Naturally decaffeinated, organic coffee would be better for people with Graves’ disease. Dealing with sugar cravings and emotions may help some. Emotional freedom technique (tapping on some acupuncture points) is a gentle technique that may be useful.

Please note my blogs are for educational purposes only.

 

Bibliography

  1. Jennifer A. Nettleton, PHD, Pamela L. Lutsey, PHD, Youfa Wang, MD, PHD, João A. Lima, PHD, Erin D. Michos, MD and David R. Jacobs, Jr., PHD. Diet Soda Intake and Risk of Incident Metabolic Syndrome and Type 2 Diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA). Diabetes Care 2009 Apr; 32(4): 688-694.
  2. Morando Soffritti, MD, Michela Padovani, MPH, Eva Tibaldi, PhD, Laura Falcioni, DMV, Fabiana Manservisi, PhD and Fiorella Belpoggi, PhD. The carcinogenic effects of aspartame: The urgent need for regulatory re-evaluation. American Journal of Industrial Medicine. 2014: 57(4):383-397.
  3. Endocrine Society. Low-calorie sweeteners promote fat accumulation in human fat. April 03, 2017. URL: https://www.endocrine.org/news-room/current-press-releases/low-calorie-sweeteners-promote-fat-accumulation-in-human-fat
  4. J. Roberts, MD, FACP, FCCP. Aspartame Disease. A Possible Cause for Concomitant Graves’ Disease and Pulmonary Hypertension. Tex Heart Inst J. 2004; 31(1): 105
  5. Roberts HJ. Aspartame and hyperthyroidism: a presidential affliction reconsidered. Townsend Letter for Doctors & Patients 1997; May: 86–8.
  6. http://www.blatantpropaganda.org/propaganda/articles/is-aspartame-a-dangerous-toxic-poison-doctors-link-it-to-diseases-illnesses.html
  7. https://www.livescience.com/36257-aspartame-health-effects-artificial-sweetener.html
  8. 22nd Annual Scientific & Clinical Congress of the American Association of Clinical Endocrinologists: Hashimoto’s Hypothyroidism Induced by Artificial Sweeteners. https://www.endocrineweb.com/professional/meetings/hashimotos-hypothyroidism-induced-artificial-sweeteners
  9. http://articles.mercola.com/sites/articles/archive/2011/08/03/just-how-bad-is-aspartame.aspx
  10. Janet Starr Hull. Sweet Poison. New Horizon Press. 1999. USA.

 

 

Imprint of stress on thyroid – Angel’s wing

Imprint of stress on thyroid – Angel’s wing

You might wonder about a strange photo I included in my blog. I call it “Angel’s wing”. I took this picture myself after I had noticed an imprint of bird’s wing on my window. The bird must have hit my window very hard to leave such an imprint. However it must have recovered and flew away as it was nowhere to be seen. I thought this picture would be a great metaphor for my blog. Sometimes life presents us with unexpected stresses we were not prepared for or stresses which are chronic, origin of which can be difficult to define. The stresses leave imprints on our health like the wings of unknown bird on my window.

Genetics (this includes personality traits), together with specific epigenetics factors (factors originating from outside of the body) such as toxins, radiations, nutrition, infections, hormonal imbalances, emotions and stress can cause autoimmunity. I will focus on stress specifically in this blog. It is one of the triggers of autoimmunity in genetically predisposed people. Stress can affect many functions in the body and may be connected to chronic infections, food intolerance and allergies. From scientific research, we know that even identical twins do not both necessary get Grave’s disease (GD) and so the environmental factors are at play. If you lose yourself in stress, then your immune system will lose itself too, it will stop distinguishing self from non self. The most difficult stressful events are the sudden loss of a loved one. However stresses can be chronic. Those cannot be easily solved sometimes due to particular circumstances of life. Stress itself is not the only culprit; it is important how stress is handled. If an emotionally sensitive person is constantly exposed to GD triggers and cannot effectively react to them, autoimmune thyroid illness may start. Our genes direct our personality. People predisposed to Graves’ disease may be more vulnerable to negative emotions. It has nothing to with being weak or emotional but just being more genetically sensitive to stress.

I had always been interested in psychology of an illness and understanding my own personal journey. Today, I believe that specific stresses are connected to specific body symptoms. Different people are sensitive to different stresses and experiences.

I would like to share the things I had learned about stress and thyroid autoimmunity relationship. The knowledge is not my own vague hypothesis. It comes from observations of medical practitioners, researchers and psychologists who collected data from their patients.

Medical doctors in their descriptions of Graves’ disease in past decades attributed it to stress. It was noted that there were more cases of GD during war times. The correlation of GD and stress was noticed by Doctor Parry, who originally described the illness. Large population studies indicated that negative life events, their increased number and impact can definitely be a factor in GD (1, 2, 3, and 4). Despite the fact that stressful life events often correlate with GD and there seems to be plenty of data to support it, the link still remains controversial. It is difficult to measure stress or an individual reaction to it. We should be careful tough of dismissing the power of observation. Emotions, such intense fear, has been connected to GD as early as 1825 by doctor Caleb Perry, who described case of a young woman developing GD after falling from her wheelchair while coming down the hill too fast. GD used to be called ‘Shock-Basedow’.

The thyroid gland is located at the level of the fifth energy centre called the throat chakra in Oriental spiritual books that has to do with expression and creativity. It is believed that when this energy centre does not flow properly, thyroid problems may arise. Dr Christiane Northrup, in her book: ‘The wisdom of menopause’ (6) talks about the connection between emotions and physical anatomy. The energy center of thyroid is connected with communication. It suffers when a person fears expression. The person who is unable to self-express, has an inability to communicate personal needs and express hostility, is treated as insignificant or denied their self- expression might suffer from thyroid issues. Thyroid gland likes free expression of feelings, telling personal truths and it does not like secrets. My personal understanding is that when a person has a problem processing some inner conflict, which is difficult to word or express, that person can metaphorically ‘slow down or speed up time’ by changes to the thyroid function by the immune system, as seen in Graves’ disease or Hashimoto’s thyroiditis. Those two alternating thyroid functions can fluctuate in thyroid autoimmune disease. Hyperthyroidism often proceeds Hashimoto’s disease. Imagine a person saying’ I cannot deal with it and it is hard for me to word what I am missing so ‘I let time pass quickly’ and then realizing ‘I need more time to sort this out’. Nervous energy, never enough time and time is precious and should not be wasted may be emotions of a person with autoimmune thyroid disease.

Austin W. Bennet and Charles Glenn Cambor in a clinical study of hyperthyroidism (7) reference previous studies indicating that hyperthyroid patients tend to bind close to their mothers by caring for them and by winning their love by caring for others. They also struggle against fear, have problems expressing hostility, have care taking behavior, premature self-sufficiency, ambition and exhausting work obligation.

The thyroid autoimmunity stress is also connected with feeling of being unloved, loss of love and security in love. Svetla Bankova, psychologist and a fellow sufferer from GD, who managed to cure herself with lifestyle changes, calls Graves’ disease: ‘a missed call for love’ (9). Childhood is an important time and growing up in a stressful environment of a dysfunctional family where a child has to fight for parental attention or is experiencing some neglect or economic hardship, selective parents focusing on the youngest sibling, premature responsibilities, unresolved trauma and post-traumatic stress disorder may all render the immune system more susceptible to thyroid autoimmunity. One of the factors occurring in a dysfunctional family can relate to child who was unwanted and feels that from the parents even on subconscious level (22) making the child more fearful. An unwanted child’s system may subconsciously try to ‘self-destroy’ because that was what the parents once wanted, which is exactly what autoimmunity is, an immune system trying to destroy its own cells (23). Some studies indicate that the development of a child during pregnancy can be affected by maternal stress hormones. In fact, autoimmunity can arise from stress and poor expression of thyroid molecule in the thymus during a child development as discussed in my previous blog. I came across this information while listening to fascinating and thought provoking Polish presentations by a Magdalena Dembowska who is a consultant in Total Biology.

There is a link between a parent/s with autoimmune BPD and a child/adult with autoimmunity problems. Children brought up by Borderline Personality Disorder (BPD) parents have a higher rate of autoimmune disorders due to invalidating, confusing, controlling and stressful environment they grew up in. This was noted through the observation of a psychologist, while dealing with adult children of BPD parents (10). Interestingly, BPD is also associated with autoimmunity, hypothyroidism and anti-thyroid antibodies (anti-thyroglobulin antibodies) (11, 19 and 20). Stress has been linked to anti thyroid antibodies, autoimmune Borderline Personality Disorder (BPD) and fluctuating mood. Stress can be a factor for both a parent and a child and therefore autoimmunity can possibly be passed through ‘stressful growing up conditions’ to a next generation. Interestingly, when a child develops Graves’ disease, it has been linked to a father’s thyroid autoimmunity and anti TPO antibodies. The imprint of stress on a parent (one example is stressful childhood of the parent) can imprint child’s health too. Not every neglected or stressed child will get BPD and autoimmunity. Of course genetic predisposition plays a role too but we know that triggers has to be there for autoimmunity to develop and stress is one of those triggers. Awareness of this link can help to modify the behavior of a parent and break a chain of suffering for future generations. Childhood stress affects the limbic part of the brain, in which thyroid hormones play a major role. An early negative conditioning (often subconscious) from a parent can create illness in the future if a person is not able to reverse some of the programming.

The loss of a mother or a mother figure in childhood or infancy was a common factor precipitating GD in many studies. Cases of children, who developed GD after a death or separation from the mother figure were described by Morillo and Gardner in a clinical report (8). The onset of Graves’ disease can be followed by a significant life-altering event like death of a loved one (loss of love), separation from a loved one or a divorce. Many studies indicate that these children, who lost their mother figure before teenage years are at a higher risk of behavioral changes and depression in a later life.

An interrupted maternal care during childhood and poor mother-child relationships create dysfunctions in the hypothalamic-pituitary-adrenal (HPA) axis for life. Also, a maternal stress, anxiety, and fatigue have similar consequences on a child. Some children with interrupted maternal care are often diagnosed with ADHD (13). These disruptions can affect cortisol production in a person for life can be a factor in a development of GD.  Some children diagnosed with ADHD may be found later to have hyperthyroidism.

It is stipulated that people predisposed to GD might have a poor coordination between the thyroid and adrenal glands. Dr Wilson (15), who studied hair mineral pattern in people with GD, believes that Grave’s disease is linked to an ineffective stress response in which the adrenal glands do not participate much and the thyroid overcompensates and becomes hyperactive. Lowered levels of cortisol are often seen in people with GD and generally in autoimmune disorders as its production is impaired in chronically exhausted adrenal glands.

Forteza states that stress is indeed a factor in development of hyperthyroidism by demonstrating that 65% of his younger patients, who developed the disease, had psychological stress. Physical stress was a factor in older patients (12).  Stress (emotional or physical) is also associated with lower vitamin D levels, which affects the immune system negatively. On top of that, stress affects neurotransmitters in the body, detoxification processes and depletes B vitamins, especially B1. Deficiency of that vitamin can express itself as a nervous tension and vivid nightmares. Stress produces real chemical changes in the body. It affects the immune system.  Scientific studies found that certain immune system molecules which control autoimmunity were significantly reduced in lymphocytes from stressed animals compared to non-stressed control animals (17). Scientists have looked at the role of B lymphocytes in autoimmune diseases and uncovered that the production of B cell activating factor (BAFF) is related to immune responses affected by stress. When there is too much BAFF, harmful B cells live longer than they can damage healthy tissue (18). Chronic or severe stress alters how minerals in our body are distributed and retained. The first reaction to stress is to excrete zinc and magnesium and accumulate sodium, which is needed to make aldosterone hormone by adrenal glands. Aldosterone prepares body for flight or fight response and increases our blood pressure. Low levels of zinc and magnesium affect the thyroid gland. Some scientists believe that the increased level of thyroid hormone production due to stress may be the culprit to changes of immune system leading to autoimmunity.

I believe that symptoms of illness and autoimmunity, ’angel’s wing’ are the wake up calls to look at unresolved issues. It is our time to act, to become more aware and connect with our outside environment. We should be aware why we feel nervous or fearful sometimes. If we are not in an immediate physical danger, we might need to look into our past experiences for answers. Therefore, resolution is important. However we have to live in here and now, not in the past and not in the future. I believe the resolution of our negative feelings can came through awareness of ourselves. Relaxation, meditations, understanding of our life, lives of others and forgiveness are all important. It is helpful to aim at replacement of anger, pain with peace, forgiveness, gratitude and love. It is also important to remember that our loved ones who had passed would not want us to become sick due their passing. Those are difficult processes but necessary for our health. The best conflict resolutions are practical but they can also be done within us. It is ideal when a conflict resolutions in relationships involve the related parties but that is not always possible. You might consider slowing down, relaxing more, going easy on yourself, expressing your emotions and doing things that make you happier.

It is important to say that nobody should be blamed for your illness, including yourself. Emotions and self- awareness are important for us to grow. We are all learning. Once we are aware of our personal stress triggers and the science behind them, they would be easier for us to handle when encountered again.

Please note this blog is for educational purposes only.

References:

  1. Harris T, Creed F, Brugha TS. Stressful life events and Graves’ disease. Br. J. Psychiatry. 1992 Oct; 161:535-41.
  2. Sonino N, Girelli ME, Boscaro M, Fallo F, Busnardo B. Fava GA. Life events in the pathogenesis of Graves’ disease. A controlled study.Acta Endocrinol (Copenh). 1994 Apr; 128(4):293-6.
  3. Radosavljević VR, Janković SM, Marinković JM. Stressful life events in the pathogenesis of Graves’ disease. Eur J Endocrinol. 1996 Jun; 134(6):699-701.
  4. Kung AW. Life events, daily stresses and coping in patients with Graves’ disease. Clin. Endocrinol (OXF).1995 Mar; 42(3):303-8.
  5. Geraldine Falgarone, Hassan M Heshmati, Regis Cohen and Gerard Reach. Role of emotional stress in the pathophysiology of Graves’ disease. European Journal of Endocrinology. 2013; 168 R13–R18
  6. Wisdom of menopause; the complete guide to women’s health and wellbeing. Christiane Northrup, MD. Piatkus Book. London 2001.
  7. Austin W. Bennett, M.D.; Charles Glenn Cambor M.D. Clinical Study of Hyperthyroidism. Comparison of Male and Female Characteristics. Arch Gen Psychiatry. 1961; 4 (2):160-165.
  8. Edgar Morillo, MD and Lytti. Gardner, MD. Clinical report. Bereavement as an Antecedent Factor in Thyrotoxicosis of Childhood: Four Case Studies with Survey of Possible Metabolic Pathways Psychosomatic Medicine. 1979 November; 41(7): 547.
  9. Svetla Bankova. Life manual for Graves’ disease and hyperthyroidism. Cafepress. USA 2011.
  10. Kimberlee roth and Freda B. Friedman. Surviving a borderline parent. New Harbinger Publications, Inc. 2003. Oakland, CA.
  11. Geracioti TD Jr, Kling MA, Post RM, Gold PW. Antithyroid antibody-linked symptoms in borderline personality disorder. Endocrine. 2003 Jul; 21(2):153-8.
  12. Forteza ME. Precipitating factors in hyperthyroidism. Geriatrics. 1973 Feb; 28(2):123-6.
  13. Corinne Rees. Childhood attachment. Br. J. Gen Pract. 2007 Nov 1; 57(544): 920–922.
  14. http://www.gdatf.org/about/about-graves-disease/children-graves/
  15. Lawrence Wilson. Thyroid disease and its healing.URL: http://drlwilson.com/Articles/thyroid.htm
  16. Falgarone G, Heshmati HM, Cohen R, Reach G. Mechanisms in endocrinology. Role of emotional stress in the pathophysiology of Grave’s disease. Eur J Endocrinol 2012 Dec; 168(1) R13-8. URL: http://www.eje-online.org/content/168/1/R13.full.pdf
  17. Weiss JM, Sundar SK, Becker KJ, Cierpial MA. Behavioral and neural influences on cellular immune responses: effects of stress and interleukin-1. J Clin Psychiatry; 1989 May; 50:43–55.
  18. Crupi Rosalia, Cambiaghi Marco, Spatz Linda, Hen Rene, Thorn Mitchell, Friedman Eitan, Vita, Giuseppe, Battaglia Fortunato. Reduced adult neurogenesis and altered emotional behaviors in autoimmune-prone B-cell activating factor transgenic mice” Biological psychiatry; 2010 March 15; 67(6):558-566.
  19. Geracioti TD Jr, Kling MA, Post RM, Gold PW. Endocrine. Antithyroid antibody-linked symptoms in borderline personality disorder. 2003 Jul; 21(2):153-8.
  20. M. A. Iddah and B. N. Macharia. Stress and anti TPO antibodies. Autoimmune Thyroid Disorders. Published online 2013 Jun 26. doi: 10.1155/2013/509764. URL: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3710642/
  21. Seqni M. Pani MA. Pasquino AM. Badenhoop K. Familial clustering of juvenile thyroid autoimmunity: higher risk is conferred by human leukocyte antigen DR3-DQ2 and thyroid peroxidase antibody status in fathers. J. Clin. Endocrinol. Metab.2002 Aug: 87(8):3779-82.
  22. http://www.euro.who.int/__data/assets/pdf_file/0005/270689/Adverse-childhood-experiences-survey-among-university-students-in-Turkey-study-report-2013_Eng.pdf

23.Int. J. Prenatal and Perinatal Psychology and Medicine. Moscow2007.Coordinated Congress Summaries.  Vol. 20 (2008) No. 1/2, pp. 42–76 http://www.mattes.de/buecher/praenatale_psychologie/PP_PDF/PP_20_1-2_Moscow2007.pdf

  1. http://porozmawiajmy.tv/zakazana-medycyna-uzdrawiajaca-skutecznie-magdalena-dembowska/