gardasil and hashimotos

Vitamin D Plays an Integral Role in Adaptive Immunity

6310 views

Severe Adverse Reactions Include Vitamin D Deficiency and Autoimmunity

Hormones Matter researchers discovered that, inter alia, severe adverse reactions to any of the surveyed drugs trigger significant but varying autoimmune responses. Moreover, the research revealed an underlying consistency involving all reviewed drugs: vitamin D deficiency.

Vitamin D Helps Regulate the Adaptive Immune System

The adaptive immune system comprises the body’s intricate network of antibodies and special types of white blood cells (called sensitized lymphocytes ) to thwart new and previous invaders including viruses, bacteria, and drugs. When the adaptive immune system is not strong enough to endure external disruptions such as severe side effects of drugs, it can go awry by signaling antibodies and sensitized lymphocytes to attack healthy cells. This response is called autoimmunity—when the adaptive immune system’s cells do not recognize previous invaders and designate healthy cells as those invaders. In other words, the body’s immune cells attack its own healthy cells.

Scientific research over the past three decades solidifies the connection between vitamin D and autoimmunity. Vitamin D plays an integral role in the regulation of the adaptive immune system. Adequate vitamin D in our bodies can protect us from autoimmunity because adaptive immune cells contain vitamin D receptors (VDRs). These receptors are attached to the surface of the adaptive immune system’s antibodies and sensitized lymphocytes. The VDRs act as “gate keepers” by signaling what external substances, e.g., components of medications, can enter a cell. The VDRs must be replete with vitamin D to effectively regulate adaptive immunity. When the VDRs receive adequate amounts of vitamin D, they enable the adaptive immune system to function properly by attacking new and previous invaders.

When the VDRs attached to the adaptive immune system’s cells do not contain sufficient vitamin D to attack invaders, autoimmunity may kick in, causing the death of healthy immune cells. Thus, low vitamin D levels can lead to autoimmune diseases including thyroid disorders such as Hashimoto’s and demyelinating diseases including multiple sclerosis (MS).

Vitamin D and Hashimoto’s Autoimmune Thyroid Disease

The Real Women, Real Data research also uncovered another consistency among severe adverse reactions to the reviewed drugs: Hashimoto’s thyroiditis, an autoimmune disease caused by abnormal cells constantly assaulting the thyroid gland
.
Vitamin D receptors are present in the thyroid as well as the pituitary, the pea-shaped gland that controls the thyroid. Not surprisingly, low levels of serum vitamin D have been linked to Hashimoto’s thyroiditis, according to recent Turkish medical research:

Published in a 2013 issue of the journal Endocrine Practice, a study conducted at a training and research hospital in Ankara demonstrated that serum vitamin D levels of female chronic Hashimoto’s patients were significantly lower than healthy subjects. Furthermore, the researchers discovered a direct correlation between serum vitamin D levels and thyroid volume as well as an inverse correlation to the antibodies involved in the thyroid.

Researchers at Medeniyet University’s Goztepe Education and Research Hospital in Istanbul learned that 92 per cent of their 161 Hashimoto’s thyroiditis cases had serum vitamin D levels lower than 30 ng/mL (12 nmol/L), a value characterized as “insufficient.” Published in a 2011 issue of the journal Thyroid, the study reports an association between vitamin D insufficiency and Hashimoto’s thyroiditis.

Vitamin D and Demyelinating Disorders

Another disturbing outcome of the Real Woman, Real Data research is the reporting of neurological and neuromuscular symptoms, many which of are consistent with demyelinating disorders such as MS, an autoimmune disease. The development of MS occurs when a poorly functioning, adaptive immune system gradually attacks the protective covering of the nerve cells (called the myelin sheath) of the brain and spinal cord. This potentially debilitating process is called demyelination.

Scientific—primarily epidemiological—research indicates an association between vitamin D levels and the risk of developing a demyelinating disorder such as MS. VDRs exist on nerve cells and the myelin sheath. When the VDRs receive adequate amounts of vitamin D, they help protect the integrity of the myelin sheath. However, when the VDRs do not contain sufficient vitamin D, autoimmunity may occur, resulting in the death of healthy nerve cells. Numerous clinical trials are underway to assess the connection between vitamin D status and the likelihood of developing demyelinating disorders.

Low Vitamin D: The Chicken or the Egg?

The connection between low vitamin D status and the development of autoimmune disease is genuine. However, medical research has not yet determined if vitamin D deficiency plays a role in the development of autoimmune disease, if low vitamin D levels are a consequence of the disease itself, or if vitamin D deficiency acts as both a cause and effect. The authors of the aforementioned 2013 Hashimoto’s study concluded,

“Finally, our results suggested that there may be a causal relation between vitamin D deficiency and development of Hashimoto’s thyroiditis. On the other hand, there might be a possible relation between severity of vitamin D deficiency and progression of thyroid damage. However, further studies are needed especially about the effects of vitamin D supplementation on prevention and/or progression of autoimmune thyroid disease.”

Proactive Protection against Severe Adverse Reactions

We could wait years (or decades) to garner the results of further scientific studies and clinical trials to define the exact relationship between vitamin status and severe adverse reactions to vaccines and medications that culminate in autoimmune disorders. Or we could be proactive by taking daily vitamin supplements and enjoying moderate sunlight exposure to increase our vitamin D levels.

It is imperative to take enough vitamin D3 so this essential nutrient will be stored in your cells to help regulate your immune system. The greater your serum vitamin D level (easily obtained from a simple blood test called 25(OH) D, the more likely you will benefit from a stronger immune system that protects your body’s cells from attacking one another.

No one wants to endure severe adverse reactions to drugs such as Gardasil and Lupron, let alone an autoimmune disease. Attaining and maintaining adequate supplementation provides a safe, easy, and inexpensive approach to improved preventive health. By empowering yourself with adequate vitamin D, you may reap the benefits of avoiding disease and enjoying better quality of life.

Copyright © 2013 by Susan Rex Ryan. All rights reserved.

This article was published previously on Hormone Matter in September 2013.

We need your help.

Hormones Matter needs funding now. Our research funding was cut recently and because of our commitment to independent health research and journalism unbiased by commercial interests, we allow minimal advertising on the site. That means all funding must come from you, our readers. Don’t let Hormones Matter die.

Yes, I’d like to support Hormones Matter.

Adverse Reactions, Hashimoto’s Thyroiditis, Gait, Balance and Tremors

69742 views

One of the things I most love about social media and health research is the opportunity to identify patterns of illness across different patient groups. Here is an example of finding research from one patient group, ThyroidChange, that likely spans many others (Gardasil injured, post Lupron Hashimoto’s, and Fluoroquinolone reactions – to name but a few) and offers clues to a perplexing array of symptoms. The research, is about a little known association between movement and balance disorders and Hashimoto’s thyroiditis: Ataxia associated with Hashimoto’s disease: progressive non-familial adult onset cerebellar degeneration with autoimmune thyroiditis.  Some background.

Hashimoto’s Disease

Hashimoto’s is the most common causes of hypothyroidism afflicting women at a rate of 10 to 1 compared to men. It is an autoimmune disorder in which antibodies attack the thyroid gland and destroy its ability to maintain normal thyroid hormone concentrations. The most common symptoms include: fatigue, muscle pain, weight gain, depression, cognitive difficulties, cold intolerance, leg swelling, constipation, dry skin. If left untreated, goiter – a swollen thyroid gland, appears. If left untreated for an extended period, cardiomyopathy (swelling of the heart muscle), pleural (lung) and pericardial (heart) effusion (fluid), coma and other dangerous conditions develop.

Hashimoto’s and Cerebellar Degeneration

A little known risk in Hashimoto’s is cerebellar degeneration. The cerebellum is the cauliflower looking section at the base of the brain that controls motor coordination – the ability to perform coordinated tasks such as walking, focusing on a visual stimuli and reaching for objects in space. The walking and balance disturbances associated with cerebellar damage or degeneration have a very distinct look, a wide gait, with an inability to walk heel to toe. Cerebellar ataxia looks like this:

In recent years, cerebellar involvement in attention and mood regulation have also been noted. The physicians reporting the Hashimoto’s – ataxia connection present case studies of six patients with Hashimoto’s disease, presumably controlled with medication and a progressive and striking shrinkage of the cerebellum (see report for MRI images) along with progressively debilitating ataxia (walking and balance difficulties) and tremors. Here’s where it becomes interesting.

Hashimoto’s: Medication Adverse Reaction and Misdiagnosis

Hashimoto’s disease is prevalent in our research into medication adverse reactions for Gardasil and Cervarix and Lupron, with some indications it may develop post Fluoroquinolone injury as well. The symptoms are difficult to distinguish from other neurological and neuromuscular diseases such as chronic fatigue syndrome, fibromyalgia, multiple sclerosis and an array of psychiatric conditions, and so Hashimoto’s often goes undiagnosed or is misdiagnosed and mistreated for some time.

Hashimoto’s, Demyelination and Cerebellar Damage

In some of the more severe adverse reactions to medications and vaccines that would lead to Hashimoto’s, the tell tale cerebellar gait disturbances have been noted and documented, along with a specific type of tremor (discussed below).

Research from other groups shows a strong relationship between thyroid function and myelin/demylenation patterns in nerve fibers in animals. Specifically, insufficient T3 concentrations demyelinates nerve axons, while T3 supplementation elicits myelin regrowth. Myelin is the white sheathing, the insulation that protects nerves and improves the electrical conduction of messages in sensory, motor and other neurons. Like co-axial cable in electrical wiring, when the protective sheathing is lost, electrical conductance is disrupted. The early symptoms of a demyelinating disease neuromuscular pain, weakness, sometimes tremors. These can be misdiagnosed as multiple sclerosis, fibromyalgia, chronic pain, when in reality, the culprit is a diseased thyroid gland.

Back to the Cerebellum

The cerebellum is a focal point of white matter axons – myelinated sensory and motor nerves. The cerebellum is where input becomes coordinated into motor movements or movement patterns. White matter damage in the cerebellum causes cerebellar ataxia, the movement and balance disorders displayed above. Hashimoto’s elicits white matter disintegration. Adverse reactions to medications and vaccines can elicit autoimmune Hashimoto’s disease. See the connection?

The Thiamine – Gut Connection

It gets even more interesting when we add another component of systemic medication adverse reactions – nutritional malabsorption, specifically thiamine deficiency. Almost across the board, patients with medication or vaccine adverse reactions report gut disturbances, from leaky gut, to gastroparesis, constipation, pain and a myriad of other GI issues that make eating and then absorbing nutrients difficult. Gut issues are common in thyroid disease too.

As we learn more, and as individuals are tested, severe nutrient deficiencies are noted, in vitamin D, Vitamin B1, B12, Vitamin A, sometimes magnesium, copper and zine. We’ve recently learned of the connections between Vitamin B1 or thiamine deficiency and a set of conditions affecting the autonomic nervous system called dsyautonomia or Postural Orthostatic Tachycardia Syndrome (POTS) linked to thiamine deficiency in the post Gardasil and Cervarix injury group. It may be linked to other injured groups as well, but we do not know yet.

Thiamine and Cell Survival

Thiamine or vitamin B1, is necessary for cellular energy. It is a required co-factor in several enzymatic processes, including glucose metabolism and interestingly enough, myelin production (the Hashimoto’s – cerebellar connection). We can get thiamine only from diet. When diet suffers as in the case of chronic alcoholism, where most of the research on this topic is focused, or when nutritional uptake is impaired, thiamine deficiency ensues. Thiamine deficiency can elicit cell death by three mechanisms:

  1. Mitochondrial dysfunction (reduced energy access) and cell death by necrosis
  2. Programmed cell death – apoptosis
  3. Oxidative stress – the increase in free radicals or decrease in ability to clear them

Thiamine deficiency in and of itself can elicit a host of serious health symptoms. The cell death and disruption of cellular energy balance can be significant and lead to a totally disrupted autonomic system.

Thiamine and Myelin Growth

Add to those symptoms, the fact that thiamine is involved in the growth myelin sheathing around nerves, and we have a whole host of additional neuromuscular symptoms masking as fibromyalgia, multiple sclerosis, chronic fatigue. Like with MS, limb and body tremors are noted in dysautonomic syndromes such as POTS. (Video of POTS tremors, note the uniqueness of the POTS tremor and the similarity between it and the foot tremor shown above along with cerebellar ataxia).

Let thiamine deficiency continue unchecked for period and we get brain damage, as white matter – the myelin disintegrates in the brainstem, the cerebellum and likely continues elsewhere. One of the most prominent areas of damage in thiamine deficiency, is the cerebellum, and hence, the cerebellar ataxia (movement disorders) noted in chronic alcoholics who are thiamine deficient, but also observed post medication or vaccine adverse reaction.

The Double Whammy on Myelin and Cerebellar Function

In the case medication or vaccine adverse reactions, particularly those that reach the systemic level, we have a double whammy on myelin disintegration: from a diseased thyroid gland and a diseased gut. Hashimoto’s and the reduction of thyroid hormones, particularly T3, impairs nerve conduction by shifting from a constant and healthy remyelinating pattern to one of demyelination, while the lack of thiamine further impairs myelin regrowth, because it is a needed co-factor. Both deficiencies affect peripheral nerves, but both also hit the brainstem, the cerebellum and likely other areas within the brain.

Take Home Points

The science of adverse reactions is new and evolving and much of what I am reporting here remains speculative. However, it has become abundantly clear through our research that to address medication adverse reactions or vaccine adverse reactions in a simplistic fashion, by region, or in an organ specific manner, is to miss the broader implications of the compensatory disease processes that ensue. Moreover, to look for symptoms of adverse reactions simply by the drug’s mechanism of action and/or by the standard outcome variables listed in adverse event reporting systems, again misses the complexity of the human physiological response to what the body is perceiving as a toxin. I believe that the entire framework for understanding the body’s negative response to a medication must be shifted to a much broader, multi-system, and indeed, multidisciplinary approach. In the mean time, we will continue to collect data on adverse reactions and offer our readers points of consideration in their quests for healing. I should note, that finding these connections is entirely contingent on the input our community of patients and health activists, both via the personal health stories that so many of you have been willing to share and the data we collect through our research. You know more about your health and illness than we do.

What we Know So Far – Tests to Consider

If you have had an adverse reaction to a medication or vaccine and neuromuscular difficulties, like pain, numbness, motor coordination problems, tremors etc., consider testing for Hashimoto’s thyroiditis. Also, consider thyroid testing when fatigue, depression, mood lability (switching moods), constipation, attentional and focus difficulties are present. In fact, I would consider thyroid testing, specifically for autoimmune thyroid disease like Hashimoto’s, as one of the first disease processes to rule out.

If you have had an adverse reaction to a medication that includes gut disturbances, consider the possibility that you are deficient in key micronutrients such as Vitamin D, the B’s, Vitamin A, magnesium, copper, zinc. And given the modern diet, consider that you were probably borderline deficient even before experiencing the adverse reaction. These nutrients are critically important to health and healing (and no, I do not have an association with vitamin companies or testing companies). Some tests for these nutrients are more accurate than others, so be sure to do your homework first.

If you have symptoms associated with autonomic systems dysregulation such as those associated with POTS, dysautonomia and its various permutations, consider thiamine testing, especially, transkelotase testing.

Share Your Story

If you have experienced a reaction to a medication or vaccine, please share your story in a blog post. Write for us.

We Need Your Help

If you think what we do is worthwhile, contribute to research and our medical reporting at Hormones Matter. We’re totally unfunded at this point and can use your help to continue operations. Yes, I’d like to support Hormones Matter.

Image Source: Pixabay.

Postscript: This article was published originally on Hormones Matter on October 15, 2013. 

Statistical Shenanigans with Gardasil Research

3962 views

Something’s hinky in the land of Gardasil surveillance and it’s not just the vaccine. It’s the statistics used in one of their widely reported surveillance studies on Gardasil-suspected autoimmune conditions. From the medical marketing and even the abstract of the study, which is all that most will ever read, it looks like there is no connection between the vaccine and the onset of autoimmune conditions. Indeed, all of the major media reported the appropriate PR:

One organization even failed to change the url before directly copying the press release from another agency; (guess which one, I was surprised). It is unlikely that anyone read this study before blasting the PR far and wide. Otherwise, if they had read the dubious and creatively contorted statistical manipulations, the headlines would have been much different. Perhaps, Researchers Choose Statistics Least Likely to Find Results in Gardasil Study, would have been more appropriate.

I have a nasty habit of reading research before I write about it. I’m sure it will get me in trouble at some point, particularly as this blog grows, but I can’t help it. I want to understand the research. So here you go, my opinion and review on the Surveillance of Autoimmune Conditions Following Routine use of Quadrivalent Human Papillomarvirus Vaccine.

Gardasil and Autoimmune Conditions

Anecdotal evidence abounds suggesting that Gardasil is linked to an increased incidence of a wide array of autoimmune responses, but aside from the convoluted VAERs  tabulations, very little in the way of actual data exist.  In Merck’s FDA-mandated post market surveillance of Gardasil (which should have been pre-market testing if you ask me), the initial study conducted at Kaiser Permanente in California, purports no connection between 16 autoimmune conditions and the Gardasil vaccine.  The conditions investigated included:

  • Immune thrombocytopenia
  • Autoimmune hemolytic anemia
  • Systemic lupus erythematosus
  • Rheumatoid arthritis
  • Juvenile rheumatoid arthritis
  • Type 1 diabetes
  • Hashimoto’s disease
  • Graves’ disease
  • Multiple sclerosis
  • Acute disseminated encephalomyelitis
  • Other demyelinating diseases of the central nervous system
  • Guillain-Barré syndrome
  • Optic neuritis
  • Uveitis

Though not a complete list, it’s a start and if that were the only flaw in the research, I wouldn’t be writing about this study, but alas, it is not. There are several hinky statistical maneuvers that make it all but impossible to draw any meaningful conclusions from this research.

Statistical Shenanigans

Hinky maneuver #1. The PR reports and the study abstract indicate that the study followed almost 190,000 women for 180 days after each vaccine dose. This would be a great study if it were true. It is not. Researchers reviewed a possible sample of 190,000 medical records (not actual girls and women, but their records, flawed as they may be) from girls and women who had received at least one dose of the Gardasil vaccine. They subsequently removed all records from patients who had not been Kaiser health plan members for at least a year, leaving 149,000. Still a large number of health records, but not the reported 190,000 girls and women followed post vaccine.

Hinky maneuver #2. From those records, they looked for possible new onset cases of the aforementioned diseases within what they defined as a risk period of up to 180 days post vaccine. Read beyond the abstract and we find that, not each dose received the same time frame. The risk period for the first dose was 60 days. This is problematic because a large percentage of patients chose not to receive all three doses and it often takes multiple months to receive a proper autoimmune disease diagnosis. Those data were not reported here and so, it is not clear how many cases may have been missed by essentially compressing the time of onset to within 60 days post first dose.

Hinky maneuver #3. From the 149,000 health plan members, 1014 potential new onset autoimmune cases were identified, 719 were deemed eligible for review (no definition of eligible was given) and only 347 were sampled for case review: “Because of the large number of potential new-onset cases identified for SLE (systemic lupus erythematosus, RA (rheumatoid arthritis ), JRA (juvenile rheumatoid arthritis), Hashimoto’s and Grave’s disease, a random sample of potential cases for these conditions was included for case review.”  For the other conditions, which apparently didn’t have as high an incidence of new onset cases, all cases were included. Beyond the possibility of the admittedly ‘large number of potential new onset cases’ no reasons for reviewing only the sub-sample of the cases was provided, nor was an explanation of their ‘random’ sampling technique. What is clear though, is that by superficially limiting the number of cases, one skews the statistics and limits the ability to detect differences between the vaccine-related autoimmune and the non-vaccine autoimmune diseases.

Hinky maneuver #4 – the granddaddy of hinky maneuvers. Rather than do a matched case control study or a myriad of other possible, more logical and more powerful study designs to compare the rates or risks for onset of these conditions, this study (mis) used statistical techniques designed to manage missing data points (within a larger data sets), to effectively substitute a control group. There was no control group in this study. It was a statistical manipulation and a poor one at that, unless of course, the goal is to not find statistical differences, then it was a pretty creative choice.

Using a statistical procedure called Rubin’s multiple imputation, the researchers effectively (though not technically, for you stats wonks) estimated the data for the entire control group. According to the study authors,  “by treating the actual status of new onset as missing data for the un-reviewed potential cases,”  they imputed (substituted) 500 cases to come up with median, control group data that was then compared to the vaccine group data of 347 cases (the random sample of potential cases).

If this sounds really hinky, that’s because it is. By imputing the control group, they guaranteed that they would not find differences between the unvaccinated and vaccinated group. Indeed, they changed the question entirely. Their comparisons are no longer about the rates of onset between those vaccinated and those not vaccinated, but rather between those vaccinated verses those “estimated to potentially have a condition based on data imputation” which may or may not be the same as for those in the true unvaccinated population. This is completely different finding than what was reported in the study’s abstract, which is probably the sum total of what most PR and media companies read before regurgitating it endlessly through the news streams. And in that regard, this ‘study’ served the vaccine maker well, but it certainly does not serve the health of the public or scientific process at all.

Post Script. Poking through the statistical shenanigans, if we look only at the raw numbers from the abridged case pool, there appeared to be a high rate of Hashimoto’s, rheumatoid and other autoimmune conditions. However, without a properly designed study, it is difficult to delineate an expected incidence in the given population versus the observed incidence.