Notice: Undefined index: extension in /home/drsoszka/public_html/wp-content/themes/Divi/epanel/custom_functions.php on line 1319
The Viral - Hashimoto’s Connection
Hashimoto’s Thyroiditis is the most common form of thyroid dysfunction in the “modern world”. It is an autoimmune disease in which our own white blood cells attack the thyroid. It has long been puzzling why one part of the body would suddenly turn upon another, however research has found a link to autoimmune thyroid conditions such as Hashimoto’s and Grave’s disease and stealth viral infections such as Epstein-Barr and Cytomegalovirus. As a possible cause, it is very important to look to your medical history for clues of ongoing viral infection.
Understanding Thyroid Function and Disease
The thyroid is a small, 2-inch-long, butterfly-shaped gland located in the front of the neck below the adam’s apple. The thyroid has two lobes, one on either side of the trachea (windpipe). As a important part of the endocrine system, it produces vital hormones that affect practically every cell in the body.
The thyroid uses iodine to make two thyroid hormones, triiodothyronine (T3) and thyroxine (T4), the numbers associated each hormone indicate how many iodine atoms are attached to the hormone. T3 is the active form of thyroid hormone and is converted from T4 in the liver and digestive tract. Thyroid hormones affect every aspect of body function including metabolism, brain development and function, breathing, heart and nervous system function, body temperature regulation, muscle strength, skin dryness, menstrual cycles, weight, and even cholesterol levels.
One of the commonly performed blood test to measure thyroid activity is the thyroid-stimulating hormone (TSH), which is not direct measurement of the thyroid but rather a hormone made by the pituitary gland in the brain which regulates thyroid hormone production. It operates on feedback loop, so when thyroid hormone levels in the blood are low, the pituitary releases more TSH. When thyroid hormone levels are high, the pituitary decreases TSH production. There can be dysfunction in this feedback loop, but this is for another post on a later date.
Low functioning thyroid has long been associated with malnutrition, especially low iodine intake. This remains the main cause of thyroid disease in developing countries. In developed countries, iodine deficiency isn’t nearly as common. Most cases of low-functioning thyroid in the USA, Canada and the UK are associated with this autoimmune condition.
Hashimoto’s Thyroiditis, also known as chronic lymphocytic thyroiditis was first discovered in 1912 by Hakaru Hashimoto MD, a Japanese surgeon working in Berlin, Germany. He discovered a high number of white blood cells called lymphocytes in thyroid tissue of patients from whom he had removed swollen thyroid glands (goiters). These lymphocytes make the antibodies that start the autoimmune process. The two most common antibodies in this condition target thyroglobulin, which is a protein found in the thyroid gland, and an important enzyme used to make thyroid hormone called peroxidase. These antibodies are called anti-thyroglobulin antibodies and anti-thyroid peroxidase (anti-TPO) antibodies, respectively.
There appears to be a progressive increase in the number of cases of this autoimmune thyroid condition, which is 15 times more common in women than men. Currently, Hashimoto’s thyroiditis believed to affect 3.5 out of 1,000 women and 0.8 out of 1,000 men. While seen in adolescents and younger women, the average age of diagnosis is between 30 and 50, and men 45 to 65. A number practitioners, holistic and conventional find this condition usually begins without any symptoms. Keep in mind, this condition is often diagnosed after symptoms are present, and have progressed significantly.
More concerning, is that autoimmune thyroiditis is often found alongside other autoimmune conditions such as rheumatoid arthritis, lupus, type 1 diabetes, or Sjogren’s disease.
What are the Symptoms of Hashimoto’s Thyroiditis?
In the early stages of the disease commonly reported symptoms include fatigue, constipation, and dry skin. Some report weight gain as another symptom, but research has found that weight gain isn’t always linked directly to thyroid function. In fact, I’ve seen weight gain more common in adrenal fatigue syndrome and late stage hypothyroidism. Later stage symptoms include cold intolerance, voice hoarseness and pressure symptoms in the neck from thyroid enlargement, decreased sweating, slowed movement and loss of energy, diminished hearing, poor memory, hair loss and/or coarse, brittle hair, joint pains and muscle cramps, menstrual irregularities, numbness (neuropathy) in the hands and feet (not caused by diabetes), depression, anxiety, and mood swings, and sleep apnea along with feeling sleepy during the day.
Infection and Hashimoto’s Thyroiditis
Before going further, it’s important to clarify that our topic in this article is different from subacute viral thyroiditis, which is a temporary inflammation of thyroid as a result of viral infection of the nose and throat.
The cause of autoimmune thyroid conditions have remained a mystery for many years. Viruses are not the only contributors to autoimmune disease, there are a number of other possible causative factors including bacteria, vitamin D receptor dysfunction, chronic stress, barrier breakdown, yeast, parasites, Lyme disease positive, food allergies, and environmental toxins (especially mercury). It is important to look at the complete medical history to find clues as to cause. Each of these causes will be reviewed in future posts, today’s focus is focused on the role of viruses.
What is often confusing about looking at Epstein-Barr virus (EBV) and its role in Hashimoto’s thyroiditis is its universal presence in the human body. Its estimately between 90 to 95% of adults have been exposed to and are life-long carriers of EBV which tends to live in immune cells. In fact, this infection is almost certain to be present in the human body by age 3 in developing countries and only half the children by age 10 in the developed world. Symptoms of an infection at an early age are typically minimal, if at all. When exposure occurs in adolescence, the infection is more symptomatic, and is called Infectious Mononucleosis.
EBV Tricks the Immune System
The virus lives within a specific line of immune cells called “B lymphocytes”. It is these cells that create antibodies that identifies “self” from “nonself” and tags any foreign bodies found in the tissues for destruction. EBV must play a delicate balancing act to keep these B cells alive, but the longer these infected cells live, the more likely they are of becoming “autoreactive” meaning they produced antibodies to themselves which can in turn, result in antibodies attacking other tissues in the body.
Genetic Predisposition and Gender
Normally, a EBV infection can limited by CD8+ cells which find and destroy these infected cells. However, new evidence suggests that certain genetic variance can result lower production of these CD8+ cells which then tips the scales in favor of the EBV. Those who are vitamin D deficiency produce fewer CD8+ cells. Such a deficiency is either due to insufficient sun exposure (fairly common) and/or due to genetic polymorphism (minor mutation) in the Vitamin D receptor. resulting in poor binding of vitamin D to its receptor (your humble author just such a genetic variance, and I keep my vitamin D supplement within arm’s reach).
Furthermore, between the genders, females tend to have fewer CD8+ which is one reason women are more prone to autoimmune diseases. Age also plays a role in likelihood of autoimmunity. As mentioned above, early exposure to EBV results in a minimal symptom picture due to a higher level of CD8+ cells in younger children. A typical 2 year old has three times as many CD8+ cells as a 15 year old.
Combine these various factors and its not difficult to imagine a hypothetical female living in the relatively hygienic developed part of the world, being exposed to EBV as a teen, resulting in a linger EBV infection that can spread to other tissues. Add in the prevalence of sunscreen use and the resultant vitamin D deficiency and we see a higher likelihood of an autoimmune condition developing.
Keep in mind, that the model of autoimmunity isn’t limited to the thyroid, as studies have found the same findings in rheumatoid arthritis, lupus, multiple sclerosis, among others.
If you have been diagnosed with Hashimoto’s thyroiditis, it is important to look at vitamin D levels, as low levels often make the autoimmune process much worse. If you had mononucleosis earlier in your life, then EBV may a contributor to your autoimmunity and testing to determine if its still active may be appropriate.
The information on this website is not intended to replace a one-on-one relationship with a qualified healthcare professional and is not intended as medical advice. It is intended as a sharing of knowledge and information from the research and experience of Dr. Soszka, who encourages you to make your own health care decisions based upon your research and in partnership with a qualified healthcare professional.
Understanding Small Intestine Bacterial Overgrowth
Small Intestine Bacterial Overgrowth (SIBO) is a condition that can often be overlooked as so many of it symptoms are similar to other more recognized digestive disorders. However, when typical holistic treatments do not improve, or worsen, gastrointestinal symptoms, then we should strongly consider SIBO.
What is SIBO?
Small Intestine Bacterial Overgrowth is a chronic bacterial infection of the small intestine. Normally, the small intestine should have very little bacteria present. However SIBO occurs in three different ways; 1) when friendly bacteria which is normal in the large intestine finds its way into the small intestine, 2) non-pathological bacteria from the mouth and throat colonize the small intestine, or 3) the normally small amount of bacteria found in the small intestine grows out of control.
The body normally has mechanisms to keep the small intestine bacteria under control. Mechanisms include the acid of the stomach to control bacteria from the mouth, nose, and throat; bile from the liver and gallbladder; the digestive enzymes from the pancreas, and movement rhythms of the small intestine itself. When functioning normally, these different mechanisms keep the small intestine bacteria in check.
It is interesting to see that the bacteria associated with SIBO can be “body-friendly” and not always a pathological strain which is more likely to cause acute gastroenteritis (think cholera or salmonella poisoning). Ultimately, small intestine bacterial overgrowth is matter of too much bacteria being in the wrong place.
The main reason SIBO is overlooked clinically, is because so many of the symptoms are identical to the symptoms of Irritable Bowel Syndrome (IBS). SIBO symptoms include: abdominal bloating/distension, belching, flatulence, abdominal pain, cramps, constipation, diarrhea, or alternating forms of both. All of these symptoms are also seen in IBS.
The other symptoms seen in SIBO include heartburn, nausea, food sensitivities, greasy stools, and even non-GI symptoms like headaches, joint pain, skin rashes, poor concentration and memory, etc. Its easy to see why SIBO might be diagnosed as a disease. There are several significant indications that SIBO might be the underlying cause of the symptoms: 1) when all the symptoms either improve or dramatically worsen when taking oral antibiotics - which kills gut flora, and 2) when normally beneficial probiotics such as acidophilus worsens the symptoms, 3) taking fiber worsens constipation and other GI symptoms.
What Causes SIBO?
There are several theories about what causes Small Intestine Bacterial Overgrowth. Surgery and damage to the small intestine can be a trigger for SIBO as the change in structure can reduce the normal movement of the small intestine. Additional causes include opiate medication such as pain killers, non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin and acetaminophen can also trigger SIBO.
Decreased stomach acid should always be considered as a cause, as stomach acid acts as a barrier (much like a moat around a castle) designed to prevent bacteria colonizing the small intestine. Interestingly enough, recent research has linked past episodes of food poisoning to an increased risk of SIBO. Certain strains of virulent bacteria can actually damage the clusters of nerve cells called the Migrating Motor Complex (MMC) that live deep in the small intestine tissue. Injury to the MMC results abnormal small intestine movement and emptying.
In some cases, the source of the small intestine dysfunction may exist in the brain. In well documented cases, a brain trauma such as a head injury from an accident, can trigger digestive dysfunction. Research is indicating that there is a close relationship between the brain and the highly developed, enteric nervous system of the digestive tract. I’ve seen cases of patients who with a significant medical history of brain trauma experience seemingly unrelated digestive symptoms.
Ultimately, colonization of the otherwise nearly pristine small intestine by bacteria that would otherwise not be found in the part of the digestive tract results in the symptoms of SIBO. As these colonies of bacteria (and sometimes yeast) gain a foothold, nutrients that would normal be absorbed by the small intestinal cells are hijacked by the bacteria resulting in malabsorption, triggering conditions such as fatigue, iron-anemia, and other vitamin and mineral deficiency.
How Do You Test for SIBO?
Testing for SIBO is relatively simple with appropriate testing. Unfortunately, neither a stool, blood or urine test can accurately detect SIBO. The only means to detect SIBO is through the SIBO Lactulose Breath Test. This is a timed test in which a patient drinks lactulose before the test. Lactulose is a sugar molecule that isn’t absorbed into the body, instead the bacteria consumes this substance and produces gas as a byproduct.
The SIBO breath test a timed test as the small intestine transit time is about 120 minutes (2 hours) when consuming lactulose on an empty stomach. Ten breath samples are collected in glass tubes over a 3 hours period, spaced every 30 minutes apart. Normally, such a test would detect a spike in gas production once this substance reaches the colon (large intestine) which is full intestinal flora. Remember, a healthy small intestine should have very little bacteria as its main job is absorbing our food. Theses glass tubes are tested for two types of gas, hydrogen and methane. If the amount of either gas meets the required threshold within the first 120 minutes, then the SIBO breath test is positive and the diagnosis of SIBO is given.
In part 2, treatment options will be discussed, including some fascinating work being done with bacteriophages.
The Parasite-Mental Health Connection
Interesting new research has recently revealed the unexpected effect a common parasite has on the human brain. It is becoming abundantly clear that certain microorganisms such as yeast, bacteria, and now parasites can directly and indirectly negatively impact both mood and even our ability to engage in reality itself. This is an important topic that often goes undiscussed in the conventional medical and psychiatric world. Sadly, many of the people affected by this parasite go undiagnosed and untreated.
What is Toxoplasma gondii?
Toxoplasma gondii (or T. gondii), is a parasitic organism commonly found in cat feces, in undercooked meat (pork, lamb, venison) and on unwashed vegetables. In fact, the increased risk of infection affecting both mother and fetus is why pregnant women are instructed to avoid cleaning cat boxes.
This particular parasite prefers our feline friends as its host of choice, as the intestine of the cat is the only place it can reproduce. The parasite can survive quite well in humans as well. The CDC estimates that 20% of people in the U.S. are carrying T. gondii in their bodies, most in a dormant state.
The active infection called toxoplasmosis is typically found in infected pregnant women and their newborns and immunocompromised people, with symptoms of swollen lymph nodes, fever, night sweats, weakness, fatigue, headache, body aches, and a sore throat in some cases.
As research continues into this parasite, a more sinister picture comes into focus. Its presents trigger a progressive inflammatory response in the brain due to toxic chemicals the parasite produces which are absorbed into the central nervous system.
The Parasite - Suicide Risk Connection
As the brain becomes more and more inflamed, the affected person is more likely to experience not just depression, but also suicidal thoughts and intentions. As stated by Lena Brundin Ph.D., M.D. about a study published in 2012: “In our study, we found that if you are positive for the parasite, you are seven times more likely to attempt suicide.”¹
This astounding finding adds a missing piece to the inflammatory model of depression, which is slowly overtaking the previous serotonin theory of depression. But the effects on mental health do not stop there.
It turns out that while T. gondii often lives in the muscle tissue of its host, it has been found brain tissue as well. The location of the infection within the brain can influence which cluster of symptoms appear.
Highjacking Dopamine Production
The parasite is thought to trigger the overproduction of dopamine², an important neurotransmitter affecting movement thought, and behavior. While low dopamine is associated with neurological diseases such as Parkinson’s; excess production of dopamine has long been held as a cause behind schizophrenia. Excess levels of dopamine negatively influence mood, sociability, mental concentration, and the sleep/wake cycle. These same behaviors are disrupted in schizophrenia.
Based on the research thus far, it is suspected that about 20%, or 1 in 5 people with schizophrenia are infected with, and therefore psychological impaired by T. gondii³. The direction in which research is headed suggests that other “mental illnesses” may have parasitic or dysbiotic origins.
While this information may be alarming, there are simple blood tests that can be performed to determine if a person has been, or is currently infected by the Toxoplasma gondii parasite. A blood sample is taken, and the presence of IgM and IgG antibodies to the parasite is identified confirming the diagnosis. If healthcare providers who work with schizophrenic patients would test for this parasite in these instances, I believe we begin to see a positive change in the mental health landscape. There are several therapies both pharmaceutical and herbal that are effective in treating this parasitic infection.
- Michigan State University. “Common parasite may trigger suicide attempts: Inflammation from T. gondii produces brain-damaging metabolites.” ScienceDaily. ScienceDaily, 16 August 2012.
- Emese Prandovszky, Elizabeth Gaskell, Heather Martin, J. P. Dubey, Joanne P. Webster, Glenn A. McConkey. The Neurotropic Parasite Toxoplasma Gondii Increases Dopamine Metabolism. PLoS ONE, 2011; 6 (9): e23866.
- Gary Smith. Estimating the population attributable fraction for schizophrenia when Toxoplasma gondii is assumed absent in human populations. Preventive Veterinary Medicine, 2014.
The information on this website is not intended to replace a one-on-one relationship with a qualified health care professional and is not intended as medical advice. It is intended as a sharing of knowledge and information from the research and experience of Dr. Soszka, who encourages you to make your own health care decisions based upon your research and in partnership with a qualified healthcare professional.