Summary: Borderline levels of TSH (thyroid stimulating hormone) still within the reference ranges typically printed in laboratory reports can indicate low thyroid function (and predict hyperthyroid on the other end of the scale). A thorough assessment of the more than two dozen patterns of thyroid dysfunction is necessary for an accurate diagnosis.

Clinicians and patients may often be misled by TSH levels that appear normal, but experienced practitioners know that they can mask the presence thyroid disorders. Because hypothyroidism affects function globally, a study just published in the Journal of Clinical Endocrinology & Metabolism that practitioners in all specialties should be vigilant. The authors state:

“Serum TSH in the upper part of the reference range may sometimes be a response to autoimmune thyroiditis in early stage and may therefore predict future hypothyroidism. Conversely, relatively low serum TSH could predict future hyperthyroidism…The objective of the study was to assess TSH within the reference range and subsequent risk of hypothyroidism and hyperthyroidism.”

The authors examined 10,083 women and 5,023 men without previous thyroid disease who had a baseline TSH of 0.20–4.5 mU/liter for the predictive probabilities of developing hypothyroidism or hyperthyroidism according to categories of baseline TSH during follow-up 11 years later. Their data drew a strong result:

“During 11 yr of follow-up, 3.5% of women and 1.3% of men developed hypothyroidism, and 1.1% of women and 0.6% of men developed hyperthyroidism. In both sexes, the baseline TSH was positively associated with the risk of subsequent hypothyroidism. The risk increased gradually from TSH of 0.50–1.4 mU/liter [women, 1.1%; men, 0.3%] to a TSH of 4.0–4.5 mU/liter (women, 31.5%; men, 14.7%). The risk of hyperthyroidism was higher in women with a baseline TSH of 0.20–0.49 mU/liter (3.9%) than in women with a TSH of 0.50–0.99 mU/liter (1.4%) or higher (∼1.0%).”

Too many patients with thyroid dysfunction fall between the cracks of routine care. This evidence strongly supports the importance of a complete assessment of thyroid function when these disorders, especially autoimmune thyroid disease, are suspected. The authors conclude:

“TSH within the reference range is positively and strongly associated with the risk of future hypothyroidism. TSH at the lower limit of the reference range may be associated with an increased risk of hyperthyroidism.”

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Although autoimmune diseases are labeled as separate diagnostic entities, it’s important to bear in mind that this nomenclature masks the fact that they are like branches growing from the same trunk. While the tissue targets of autoimmune inflammatory attack differ according to the individual, the underlying causal factors are similar. Moreover, if one tissue is under autoimmune attack, it is almost always that others are too. A report published in the Journal of Clinical Rheumatology draws attention to the association of autoimmune thyroid disease and Sjögren syndrome. The authors state:

“The thyroid, salivary, and lacrimal glands are susceptible to immunologic damage, which can be expressed as an organ-specific autoimmune disease such as thyroiditis, or a systemic autoimmune disease such as primary Sjögren syndrome (pSS). Sjögren syndrome is characterized by the progressive destruction of the exocrine parotid and lacrimal glands, causing mucosal and conjunctival dryness (sicca syndrome). The serology of patients with pSS often shows elevated levels of antibodies including antinuclear antibody, rheumatoid factor, Ro (SS-A), and La (SS-B). There is a growing body of literature suggesting an increased risk of autoimmune thyroid disease (AITD) in individuals with pSS and an increased risk of pSS in individuals with AITD.”

They continue to describe the case of a 41-year-old man suffering from autoimmune hypothyroid disease who was also found to have pSS after thyroid hormone replacement therapy was initiated. They elaborate the salient implications:

“Patients with one autoimmune disease are often at increased risk for developing another autoimmune disease. In the case of 170 Hungarian subjects with Hashimoto thyroiditis (HT), 17% had Sjögren syndrome. In a group of 176 Spanish patients with AITD…the prevalence of keratoconjunctivitis was 23% and that of xerostomia was 37%. In 2 smaller studies of patients with autoimmune thyroiditis and hypothyroidism, 22% to 58% had salivary gland abnormalities as demonstrated by parotid scintigraphy, sialometry, and/or salivary gland biopsies showing lymphocytic involvement.”

Furthermore…

“…patients with pSS may show higher rates of AITD. The largest retrospective study to date included 479 patients from Hungary with pSS, who had thyroid function testing every 3 to 6 months. The frequency of HT was 6%, which was greater than the 1% to 2% frequency in the general population…In other smaller studies, the prevalence of HT in patients with pSS ranged from 11% to 50%.”

The authors note a study in which the sera from 26 patients with pSS and 7 patients with hypothyroid were tested for antihuman thyroglobulin (antihTg) antibody activity. Interestingly, all of the pSS sera contained IgG and IgM antihTg autoantibodies, the antihTg autoantibodies in patients with pSS and HT overlapped in their reaction with a certain region on the thyroglobulin molecule. They conclude:

“As demonstrated in this case, primary Sjögren syndrome and AITD are often associated. Although not all studies consistently demonstrated an increased association, the number of positive studies and the larger studies suggest a true association…Rheumatologists and endocrinologists may miss the presence and association of these 2 autoimmune conditions, given several nonspecific and overlapping symptoms such as fatigue, weight gain, and diffuse myalgias. We therefore recommend that rheumatologists consider assessing patients with Sjögren syndrome with periodic thyroid function testing.”

Moreover, clinicians managing any autoimmune disease should be alert to the presence of autoimmune activity involving additional target sites. And of course we must bear in mind the necessity of going beyond symptom management to investigate and treat the underlying causal factors. Those with a particular interest may wish to read the earlier post on Sjögren syndrome.

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It may not be recognized widely enough that recurrent canker sores (aphthous stomatitis) is an autoimmune disorder. A study just published in the Journal of the European Academy of Dermatology and Venereology investigates the association between recurrent canker sores and autoimmune thyroid disease (the most common cause of low thyroid function in developed countries). The authors state:

“Recurrent aphthous stomatitis (RAS) is an autoimmune disorder characterized by the periodic appearance of aphthous lesions on the oral mucosa. TH1 cytokines plays a key role in the aetiopathogenesis. Autoimmune thyroid disease (ATD) is the most common autoimmune disease and is frequently accompanied by various other autoimmune diseases.”

They examined ninety patients and 30 healthy volunteers by measuring thyroid stimulant hormone (TSH), free and total triiodothyronin (fT3, TT3), free and total thyroxin (fT4, TT4), thyroglobulin, and the most common antibodies found in autoimmune thyroiditis, anti-thyroid peroxidase antibody (anti-TPO) and anti-thyroglobulin antibody (anti-TG. They also performed thyroid ultrasonography. Their data showed a connection:

“The anti-thyroid antibody was positive in 31.11% of the patients with RAS, and in only 10% of the individuals in the control group. The mean anti-TG level was also higher in the RAS group. Ultrasonography revealed nodules in 28.8% of the patients with RAS and in 16.7% of the individuals in the control group. The sT4 levels were lower and the TSH, anti-TPO and anti-TG levels were significantly higher in the RAS patients with thyroid nodules than the RAS patients without nodules.”

Rarely is there only one tissue target in an autoimmune state. Personally, I feel that an important question for any practitioner confronting a condition characterized by chronic inflammation is: “to what degree is there an autoimmune component?” The authors conclude:

“The frequency of thyroid autoimmune-related problems was higher in patients with RAS. It would be worthy of searching autoimmune thyroid disorders in patients with RAS.”

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Ionizing radiation damages DNA and other proteins directly, but does most of its dirty work through oxidative damage when a storm of free radicals are generated by the effect of radiation on water molecules inside the cells. That makes the best protection from ionizing radiation a comprehensive approach that optimizes intrinsic resources for ameliorating oxidative and mutagenic damage. Additionally, it is well known that iodine (potassium iodide) can help to protect the thyroid gland by displacing radioactive forms of the element, but should it be taken preventively? In fact, there is a substantial amount of scientific evidence that great care must be taken when recommending iodine for any health concern. Most clinicians that practice according the functional model are aware that the widespread surge in autoimmune disease presents a specific risk because iodine supplementation can trigger latent or aggravate pre-existing autoimmune thyroiditis (Hashimoto’s disease), as illustrated by a paper published recently in the journal Hormones. The authors state:

“Epidemiological studies have linked increased iodide intake from dietary or other sources to the development of hypothyroidism, and it appears that in several—though not all—cases, this phenomenon has an autoimmune basis.”

They further note:

“Within an immunological context, iodine may mediate thyroiditis induction via at least two mechanisms: a) by increased post-translational modification of thyroglobulin (Tg), an event which may enhance the immunopathogenicity of this molecule as detailed further in this review; and b) via apoptotic/necrotic effects of thyrocytes, a step that could initiate presentation of thyroid antigens at immunostimulatory levels.”

All clinicians who manage conditions for which supplemental iodine therapy is contemplated should bear in mind the authors’ conclusion:

“High dietary iodide intake may lead to the development of thyroid autoimmunity via at least two pathways. First, iodide may epigenetically modify the Tg molecule and create iodinated neoantigenic determinants to which immune tolerance has not been established or alter the processing of Tg to facilitate generation of pathogenic but cryptic Tg determinants that may not contain iodine. Second, iodine may precipitate apoptotic/necrotic effects on thyrocytes, thus releasing increased amounts of thyroid antigens that can activate autoreactive T cells in situ or in thyroid-draining lymph nodes. The genetic background of the host may be permissive to one or both of these pathways that may act in synergy or independently of each other.”

The authors of a study published in the Journal of Clinical Endocrinology & Metabolism also weigh in on the subject of hypothyroid due to thyroiditis from high iodine intake:

“Twenty-two patients with spontaneously occurring primary hypothyroidism were studied to evaluate the spontaneous reversibility of the hypothyroid state. Twelve (54.5%) became euthyroid [normal thyroid] after restriction of iodine intake for 3 weeks (reversible type).”

Of particular interest is the finding that:

“Seven patients with the reversible type were given 25 mg iodine daily for 2–4 weeks; all became hypothyroid again...The patients with reversible hypothyroidism had focal lymphocytic thyroiditis changes in the thyroid biopsy specimen, whereas those with irreversible hypothyroidism had more severe destruction of the thyroid gland.”

Their conclusion is consonant with those of the previously mentioned study, and implies that milder forms of thyroiditis may recover if iodine is discontinued:

“These results indicate the existence of a reversible type of hypothyroidism sensitive to iodine restriction and characterized by relatively minor changes in lymphocytic thyroiditis histologically. Attention should be directed to this type of hypothyroidism, because thyroid function may revert to normal with iodine restriction alone.”

Another study published in the journal Biological Trace Element Research finds more evidence for the role of iodine in promoting hypothyroidism. The authors first state:

“Excessive iodine intake is known to induce hypothyroidism in people who have underlying thyroid disorders. However, few studies have been performed on subjects with normal thyroid function without a history of autoimmune thyroid disease. We hypothesized that high iodine intake may cause a subtle change in thyroid function even in subjects with normal thyroid function.“

They examined 337 subjects with normal levels of thyroid antibodies for urinary iodine excretion, free T4 (FT4), and thyroid-stimulating hormone (TSH).

“The results showed urinary iodine excretion had negative correlation with FT4 and showed a positive trend with TSH. We found that 61.7% of subjects had circulating TPO-Ab within normal reference range. In all subjects, TPO-Ab levels were negatively correlated with FT4 and positively with TSH.”

In other words, as iodine went up the thyroid hormone free T4 went down and TSH (thyroid stimulating hormone)—bother markers for hypothyroid disease. Additionally, while 38.3% had high levels of thyroid peroxidase antibody (proof of autoimmune thyroiditis), for everyone higher levels of TPO-Ab correlated with lower free T4 and higher TSH. (Personally, I have observed that the standard reference ranges for thyroid antibodies are too ‘generous’.) They authors summarize the implications of their data:

“In conclusion, high iodine intake can negatively affect thyroid hormone levels in subjects with normal thyroid function.”

I have heard the Japanese consumption of seaweed cited as evidence for allowing higher levels of iodine intake, but a study published in the Endocrine Journal (of the Japanese Endocrine Society) contradicts this assumption.

“The effect of ingesting seaweed “Kombu” (Laminaria japonica) on thyroid function was studied in normal Japanese adults. Ingesting 15 and 30 g of Kombu (iodine contents: 35 and 70 mg) daily for a short term (7-10 days) significantly increased serum thyrotropin (TSH) concentrations, exceeding the normal limits in some subjects…During long term daily ingestion of 15 g of Kombu (55-87 days), the TSH levels were elevated and sustained while the FT4 and FT3 levels were almost unchanged. Urinary excretion of iodine significantly increased during ingestion of Kombu. These abnormal values returned to the initial levels 7 to 40 days after discontinuing the ingestion of Kombu.”

In other words, a diet  heavy on the seaweed Kombu can introduce enough iodine to suppress thyroid function. The authors conclude by recommending:

“Based on these findings that thyroid function was suppressed during ingestion of Kombu, though the effect was reversible, we recommend Japanese people avoid ingesting excessive amounts of seaweed.”

Their findings are echoed in a paper published recently in The Medical Journal of Australia which reports…

“…a series of cases of thyroid dysfunction in adults associated with ingestion of a brand of soy milk manufactured with kombu (seaweed), and a case of hypothyroidism in a neonate whose mother had been drinking this milk. We also report two cases of neonatal hypothyroidism linked to maternal ingestion of seaweed made into soup. These products were found to contain high levels of iodine.”

Happily, in both cases the TSH returned and the patients recovered after discontinuing the seaweed enriched soy milk. The conclude with this alert:

“Despite increasing awareness of iodine deficiency, the potential for iodine toxicity, particularly from sources such as seaweed, is less well recognised.“

Another paper just published in the Journal of Paediatrics and Child Health reports a similar phenomenon and offers a balanced conclusion:

“Mild iodine deficiency is a recognised problem in Australia and New Zealand. However, iodine excess can cause hypothyroidism in some infants. We highlight two cases which illustrate the risks of excess dietary iodine intake during pregnancy and breastfeeding. They also describe a cultural practice of consuming seaweed soup to promote breast milk supply. Although most attention recently has been on the inadequacy of iodine in Australian diets, the reverse situation should not be overlooked. Neither feast nor famine is desirable.“

Caution should be used even when applying topical iodine as an antiseptic as reported in a paper published in the journal Anales española de pediatría. They note that iodine-containing antiseptics are still common in obstetrics and neonatology, and that…

“Topical iodine given both to the mother before delivery and to the neonate causes iodine overload. The absorption of maternal iodine through the skin is so fast that iodine in the blood of the umbilical cord increases by 50% a few minutes before delivery. Iodine overload also occurs in the mother. Urinary and breast-milk iodine are increased more than 10-fold in the days after delivery if providone-iodine is used in episiotomy. The overload in the neonate is even higher if breast-fed….this overload can produce thyroid blockade…”

The effects of thyroid blockade in the infant are potentially very serious, especially considering the importance of thyroid function for brain development. The authors conclude with a warning:

“Attention should be drawn to the undesirable effects of iodine antiseptics and their use in the perinatal period should be avoided.“

Of course there is a place for iodine supplementation in cases of deficiency conditions (which can manifest in a variety of ways) along with prophylaxis for disastrous exposure to ionizing radiation, but generally speaking, how much is enough? A very nice study on a chronically iodine-deficient population was recently published in the journal Endokrynologia Polska (Polish Journal of Endocrinology):

“Until 1997, Poland was one of the European countries suffering from mild/moderate iodine deficiency. In 1997, a national iodine prophylaxis programme was implemented based on mandatory iodisation of household salt with 30 ± 10 mg KI/kg salt, obligatory iodisation of neonatal formula with 10 μg KI/100 mL and voluntary supplementation of pregnant and breast-feeding women with additional 100-150 μg of iodine. Our aim in this study was to evaluate the iodine status of pregnant women ten years after iodine prophylaxis was introduced.“

They examined 100 healthy pregnant women between the fifth and the 38th week of pregnancy for serum TSH, fT(4), fT(3), thyroglobulin (TG), anti-peroxidase antibodies (TPO-Ab), anti-thyroglobulin antibodies (TGAb), urinary iodine concentration (UIC) and thyroid volume and structure by ultrasonography. This really was an iodine-deficient population—28% of the subjects had a goiter. What did their data show?

“Median UIC was significantly higher in the group receiving iodine supplements than in the group without iodine supplements…Serum TSH, fT(3) and fT(3)/fT(4) molar ratio increased significantly during pregnancy while fT(4) declined. Median serum TG was normal: 18.3 ng/mL (range 0.4-300.0 ng/mL) and did not differ between trimesters. Neonatal TSH performed on the third day of life as a neonatal screening test for hypothyroidism was normal.”

Thus the authors concluded:

“Iodine supplements with 150 μg of iodine should be prescribed for each healthy pregnant [Polish] woman according to the assumptions of Polish iodine prophylaxis programme to obtain adequate iodine supply.”

Here is a point worth noting for those who are aware of a recent trend for prescribing extremely high doses of supplemental iodine, as high as 50 mg per day and sometimes more: 50 mg = 50,000 μg (micrograms). That’s 333 times the amount recommended by the Polish study. This is not to say that there are never cases where megadoses of iodine may be indicated, but clinicians should maintain a biological perspective and exercise caution.

Regarding tools to support the practitioner’s thoughtful efforts to structure a careful approach to thyroid case management and iodine supplementation, can we rely on urinary iodine concentration (UIC) as a metric? A study published in Clinical Endocrinology suggests that we can’t. The authors set out to…

“…measure breast milk iodine (MI) and urinary iodine (UI) concentrations in healthy newborns and their nursing mothers from an iodine-sufficient region to determine adequacy and to relate these parameters to thyroid function tests in mothers and infants.”

Their study cohort included 48 healthy neonates of 37 to 42 weeks’ gestation and their mothers. Serum thyroid function tests and urinary iodine excretion were measured for infants and mothers, and maternal milk iodine concentration were measured. What did their data show?

“Neonatal and maternal UI did not correlate with serum thyroid function tests…Among euthyroid neonates, UI was adequate despite low median maternal UI and MI concentrations. There were no significant correlations between UI or MI and thyroid function tests in the mothers and infants.“

What about in cases where there is documented thyroid dysfunction? Is urinary iodine a correlative marker in this patient population. An interesting study published in the journal Endocrine implies that it is not. The authors state:

“The prevalence of thyroid dysfunction varies in different populations. The aim of this cross-sectional study was to analyze the prevalence of undiagnosed thyroid dysfunction and thyroid antibodies and their relationship with urine iodine excretion in a representative sample of 1,124 (55.5% women; mean age: 44.8 ± 15.2 years) non-hospitalized Mediterranean adults, in Catalonia (Spain).”

They measured free thyroxine (fT4), thyroid-stimulating hormone (TSH), thyroperoxidase and thyroglobulin antibodies, and urine iodine. Interestingly, they found thyroid dysfunction in 8.9% of their subjects with 5.3% previously undiagnosed (13.61% and 9.8% in those over age 60). Rough indicators of autoimmune thyroiditis were present: thyroperoxidase antibodies in 2.4% of men and 9.4% of women and thyroglobulin antibodies in 1.3% of men and 3.8% of women. What about the correlation with urine iodine?

“No differences were observed in urine iodine between groups with thyroid dysfunction and euthyroidism, or between subjects with positive or negative antibodies.“

In other words, urine iodine completely failed to discriminate between those with normal and abnormal thyroid function.

Here’s what the evidence boils down to: iodine supplementation has its place when used with sound clinical judgment and a biological perspective in the hands of a practitioner with the knowledge and experience to assess the need and tolerance of each individual patient with care. As for protection from harmful doses of ionizing radiation, clinicians who employ a functional medicine perspective are well equipped to evaluate your resources for ameliorating oxidative and mutagenic stresses.

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A study just published in the Archives of Internal Medicine presents evidence that taking levothyroxine (T4, thyroid hormone) before bed raises levels more effectively. But it also illustrates the important practical point that it still doesn’t help most patients to feel better anyway (because of the autoimmune dynamics of most hypothyroid cases). The authors state:

“There is consensus that levothyroxine should be taken in the morning on an empty stomach. A pilot study showed that levothyroxine intake at bedtime significantly decreased thyrotropin levels and increased free thyroxine and total triiodothyronine levels…To ascertain if levothyroxine intake at bedtime instead of in the morning improves thyroid hormone levels, a randomized double-blind crossover trial was performed.”

Patients at Maasstad Hospital Rotterdam in the Netherlands took a capsule in the morning and at bedtime. One was levothyroxine and the other placebo. After three months the capsules were ‘reversed’. The authors followed thyroid hormone levels, creatinine, lipids, body mass index, heart rate, and quality of life. What did the data show?

“Ninety patients completed the trial and were available for analysis. Compared with morning intake, direct treatment effects when levothyroxine was taken at bedtime were a decrease in thyrotropin [TSH, due to increase thyroxine] level of 1.25 mIU/L, an increase in free thyroxine level of 0.07 ng/dL, and an increase in total triiodothyronine level of 6.5 ng/dL.”

BUT…

“Secondary outcomes, including quality-of-life questionnaires (36-Item Short Form Health Survey, Hospital Anxiety and Depression Scale, 20-Item Multidimensional Fatigue Inventory, and a symptoms questionnaire), showed no significant changes between morning vs bedtime intake of levothyroxine.”

The authors concluded:

“Levothyroxine taken at bedtime significantly improved thyroid hormone levels. Quality-of-life variables and plasma lipid levels showed no significant changes with bedtime vs morning intake.“

Why? Because most hypothyroid in developed countries is autoimmune in nature. The background inflammatory activity impairs thyroid receptor function and upregulation of the relevant genes. For those interested in the functional medicine approach to thyroid conditions see Dr. Kharrazian’s Why Do I Still Have Thyroid Symptoms under Useful Links on the right.

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It has come to my attention that many are still not aware that vitiligo, a condition that causes skin to lose its normal pigmentation, is an autoimmune disorder and must be treated as such. A cursory review of the literature turns up an abundance of evidence:

Frontiers and controversies in the pathobiology of vitiligo: separating the wheat from the chaff

“There is a body of interlocking, compelling evidence supporting an autoimmune basis for most or all cases of generalized vitiligo. The development of an autoimmune disease generally involves three components; the immune system, environmental triggers and other exogenous precipitating factors, and the target tissue. In vitiligo, precipitating factors could induce melanocyte damage in genetically susceptible individuals and consequent cell death, loss of tolerance, and induction of melanocyte-directed autoimmunity.”

Immunological pathomechanisms in vitiligo

“Briefly, circulating autoantibodies and autoreactive T cells that recognise pigment cell antigens have been detected in the sera of a significant proportion of vitiligo patients compared with healthy individuals. In addition, vitiligo is often associated with other disorders that have an autoimmune origin, including Hashimoto’s thyroiditis, Graves’ disease, type 1 insulin-dependent diabetes mellitus and Addison’s disease.”

Autoimmune Etiology of Generalized Vitiligo

“Vitiligo is characterized by progressive skin depigmentation resulting from an autoimmune response targeting epidermal melanocytes…Type I cytokine-mediated immunity to melanocytes in vitiligo involves T cells reactive with melanosomal antigens…”

Autoimmune Destruction of Skin Melanocytes by Perilesional T Cells from Vitiligo Patients

“Our data show that perilesional cytotoxic T cells eradicate pigment cells, the characteristic hallmark of vitiligo, thereby providing evidence of T cells being able to mediate targeted autoimmune tissue destruction.”

Prediction and prevention of autoimmune skin disorders

“Autoimmune diseases can be preceded by a symptom-free phase which is defined by the presence of autoantibodies, and may last for many years…Characteristic autoantibodies and susceptible genes have been identified in many autoimmune systemic and mucocutaneous diseases such as systemic lupus erythematosus, pemphigus, vitiligo, dermatitis hepretiformis and even psoriasis…Prevention of overt disease may be achieved once high-risk individuals are identified and triggering factors are avoided. Numerous environmental factors, such as vitamin D deficiency, ultraviolet light, smoking, drugs, etc., that may trigger autoimmunity have been found.”

Moreover, an interesting and important connection with conditions such as autoimmune thyroiditis and type 1 diabetes has been observed:

Autoimmune Aspects of Vitiligo

“In brief, the disease is frequently associated with other disorders which have an autoimmune origin such as autoimmune thyroiditis and insulin-dependent diabetes mellitus. Furthermore, circulating antibodies and T lymphocytes which react against melanocyte antigens are present in the sera of a significant proportion of vitiligo patients compared with healthy individuals.”

High frequency of thyroid dysfunction in patients with vitiligo

“An association between vitiligo and autoimmune thyroid disease has previously been suspected…There appears to be an increased frequency of clinical as well as subclinical thyroid disease in patients with vitiligo. Our findings support the theory of vitiligo being an autoimmune disease and indicate a need for screening vitiligo patients for thyroid disease.”

Of keen interest and significance is the overlap with genes involved in gluten sensitivity:

HLA-DQA1*0301-Associated Susceptibility for Autoimmune Polyglandular Syndrome Type II and III

“We determined the HLA-DR and HLA-DQA1 association in 112 unrelated patients with APS II (n = 29), APS III (n = 83) and 184 unrelated patients with single-component diseases without further manifestations of APS: Graves’ disease, Hashimoto’s thyroiditis, autoimmune Addison’s disease, vitiligo and alopecia…”

Due to its prevalence, treating the causes of autoimmunity is a major part of a functional medicine practice.

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This important paper was published in the American Journal of Psychiatry. The authors state, “Thyrotoxicosis, celiac disease, acquired hemolytic anemia, interstitial cystitis, and Sjögren’s syndrome had higher prevalence rates among patients with schizophrenia,” and further conclude, “Schizophrenia is associated with a larger range of autoimmune diseases than heretofore suspected. Future research on comorbidity has the potential to advance understanding of pathogenesis of both psychiatric and autoimmune disorders.” In my experience, the autoimmune component must be recognized and treated. A couple related studies:

1. Vitamin D deficiency and schizophrenia published in Schizophrenia Bulletin in April, 2009
2. Gluten sensitivity and schizophrenia also in Schizophrenia Bulletin in June, 2009

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Most Lapis Light patients understand that when the genes for autoimmune disease are turned on, rarely is there only one tissue target for the inflammatory immune reaction. This paper from the journal Pediatric Endocrinology, Diabetes and Metabolism concludes: “Autoimmune thyroid disease and celiac disease occur more frequently in children with T1DM, therefore screening at an onset and repeated measurements are recommended.”

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This paper from the journal Clinical Medicine & Research is an extensive review of the strong association between celiac disease and autoimmune thyroid disease. Two things to bear in mind: (1) most thyroid disease is autoimmune; (2) this paper does not encompass the more widespread non-celiac gluten sensitivity. They conclude: “Treatment of CD with a gluten-free diet should reduce the recognized complications of this [autoimmune thyroid] disease and provide benefits in both general health and perhaps life expectancy. It also improves glycemic control in patients with type 1 diabetes mellitus…”

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Numerous studies have noted the association of autoimmune thyroid disease and celiac disease (not to mention the more widespread non-celiac gluten sensitivity). This recent paper in Nature Reviews Endocrinology asserts that “Clinicians should screen for autoimmune thyroiditis in all patients with celiac disease.”

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