How Pesticides Contribute to the Development of Lupus, Rheumatoid Arthritis, Autoimmune Thyroid Disease, Autoimmune Hepatitis, and Other Types of Autoimmune Disease

DISCLAIMER: CONSULT WITH A DOCTOR BEFORE DECIDING ON A TREATMENT PLAN FOR ANY DISEASE OR INJURY.

The link between autoimmune disease and organophosphate exposure exists, and has in fact been studied extensively. Unfortunately, however, the research into this connection is difficult to find, since this is a link that would be devastating to Big Pharma should the public find out about it. Of the research that exists, much of it is fairly convoluted and highly technical. In other words, it’s been designed to be not only difficult to find in the first place, but also difficult to understand for the average person wanting to cure their disease. This makes it so that the average person is more likely to just “pass over”information that applies to their situation, and this person may even assume that this highly technical information doesn’t apply to them at all.This chapter aims to illuminate the connection between organophosphate exposure and autoimmune disease in a way that is easily understandable, yet still backed up by facts. 

 

Scientific research acknowledges that there is indeed a connection between autoimmune dysautonomia and organophosphate exposure. Autoimmune dysautonomia is a condition where the autonomic nervous system, the part of the nervous system that manages involuntary actions in the body, such as hormone release, breathing, heartbeat, blood pressure, body temperature, and more, stops functioning correctly. Patients with this condition may experience difficulty breathing, sexual dysfunction, or problems relating to blood pressure or heart rate, for example. There are many autoimmune diseases where autoimmune dysautonomia may develop, including in Crohn’s disease, sarcoidosis, Sjörgen’s syndrome, ulcerative colitis, Guillain-Barre syndrome, diabetes, and others (note that autoimmune dysautonomia can also occur on its own, separate from any other disease). 

 

(Read more about cures for the autoimmune diseases mentioned above by clicking on the following links: Cures for Crohn’s Disease; Cures for Sarcoidosis; Cures for Sjörgen’s Syndrome; Cures for Ulcerative Colitis; Cures for Guillain-Barre Syndrome; Cures for Diabetes)

 

Exposure to chlorpyrifos, a commonly used organophosphate pesticide, has been shown to increase the presence of autoantibodies against the thyroid gland, smooth muscle, myelin, brush border, autonomic nervous system, and parietal cells (cells that line the stomach and are responsible for the production of stomach acid). Autoantibodies against these areas of the body may lead to conditions such as autoimmune thyroid disease (read more about cures for autoimmune thyroid disease here) and multiple sclerosis (read more about multiple sclerosis cures here).

 

Research has also shown that exposure to this specific organophosphate (chlorpyrifos) can also increase sensitivity to antibiotics and lead to increased atopy (allergic diseases) and production of CD26 cells (which are otherwise known as dipeptidyl-peptidase-4 (DPP4), an enzyme) . 

 

More than one set of research has observed that organophosphate exposure can elevate CD26 cell levels in the body. These cells are a necessary enzyme in the body that plays a role in apoptosis (natural cell death), immune regulation, and the transmission of messages between cells. However, excessively high levels of CD26 can also lead to an autoimmune response or other disease states. For example, liver and kidney fibrosis have been linked to high CD26 levels (read more about cures for pulmonary fibrosis here), and MERS is thought to be able to bind to CD26, thus facilitating the virus’s entry into the cell. While not all autoimmune diseases are connected to elevated CD26 levels, some are, such as systemic lupus erythematosus (follow this link to read more about SLE cures), systemic sclerosis, psoriasis (read more about psoriasis cures here or download our book, The Psoriasis Cure), and Sjörgen’s syndrome.

Organophosphate Exposure and Systemic Lupus Erythematosus

One study observed the effects of malathion, an organophosphate, on an animal model of lupus. In this particular study, exposure to this organophosphate elevated urinary protein levels, increased the size of the lymph nodes in the armpits and backs of the knees, and increased the amount of rheumatoid factor and anti-DNA antibodies in mice with existing lupus-like conditions. Exposure to malathion also caused increased inflammation of the glomeruli (blood vessels leading into the kidneys). Finally, the researchers noted that particularly high doses of malathion increased nitric oxide production and proliferation of splenocytes (white blood cells from the spleen).

Organophosphate Exposure and Rheumatoid Arthritis

Multiple studies have clearly connected organophosphate exposure with rheumatoid arthritis (and other rheumatic conditions). One study looked in-depth at the incidence of rheumatoid arthritis in farmers who had been exposed to various organophosphate insecticides, as well as those who hadn’t ever been exposed to these chemicals. Fonofos, for example, altered the methylation of certain genes involved in the regulation of immune system response, and was one of the chemicals in the study noted to be correlated with an increased incidence of rheumatoid arthritis. According to this study, other organophosphate insecticides associated with a higher risk of development of rheumatoid arthritis included glyphosate, chlorpyrifos, terbufos, and malathion. Other studies have also supported the observations of this study. 

 

In a different study, farmers who had previously been exposed to diazinon, fenitrothion, methidathion, chlorpyrifos, parathion, malathion, and profenofos were shown to have elevated levels of antinuclear antibody (a factor present in many autoimmune disease, including in rheumatoid arthritis, scleroderma, Sjörgen’s syndrome, autoimmune hepatitis, dermatomyositis, systemic lupus erythematosus, mixed connective tissue disease, and others). 

 

Yet another study completed in Greece observed that farmers who had been exposed frequently to chlorpyrifos, phosmet, and/or dimethoate exhibited higher rates of rheumatoid arthritis than the control group, which had not been exposed to these organophosphates. The farmers who had interacted closely with these pesticides also had higher rates of allergic rhinitis. 

 

Read more about cures for rheumatoid arthritis here

Organophosphate Exposure and Autoimmune Hepatitis

Autoimmune hepatitis can be associated with long-term exposure to dichlorvos (note that metrifonate/trichlorfon and Naled, both organophosphates, can break down into dichlorvos both inside of and outside of the body, meaning that exposure to either of these organophosphates can also be considered, ultimately, to be an indirect exposure to dichlorvos). One case study from China reported that dichlorvos exposure had led to liver cirrhosis and the development of autoimmune hepatitis in a 49-year-old woman. Other studies cited in this case report support the finding that chronic dichlorvos exposure can lead to liver injury, including liver cirrhosis and autoimmune hepatitis. 

 

I want to note here that Naled, another organophosphate, not only can break down into dichlorvos, but also contains bromine (a toxic mineral that interferes with iodine absorption, read more about bromine at this link) and is considered “safe” for use in the United States as a method for mosquito control. After Hurricane Katrina in Louisiana, Naled was aerially sprayed over New Orleans in an attempt to control the impending, expected increase in mosquitoes, which in this area, could also result in an increase in certain vector-borne diseases. While this is an example of a time when residents of a particular area were notified that their area was going to be sprayed with an insecticide… I have to wonder (and say, at risk of sounding like a conspiracy theorist) how often this kind of spraying is going on in mosquito-prone areas without the knowledge of residents. 

 

So, Naled not only breaks down into dichlorvos, an organophosphate that can cause severe liver injury and even autoimmune hepatitis when a person is exposed to it long term, but it also contains bromine, a mineral known to inhibit iodine absorption (as well as to cause toxicity symptoms of its own). The addition of bromine in this insecticide makes it especially toxic to humans, since this toxicity of this mineral can cause iodine deficiency; both bromine toxicity and iodine deficiency are implicated in the development of autoimmune diseases as well, with myasthenia gravis being a poignant example of this.

 

Read more about autoimmune hepatitis cures here. 

 

Read more about cures for myasthenia gravis here. 

Autoimmune Thyroid Disease and Organophosphate Poisoning

Autoimmune hypothyroidism and autoimmune hyperthyroidism are becoming increasingly common in the developed world. While I tend to believe that, in many cases, thyroid problems develop as a result of a long-term iodine deficiency (in combination with other unique factors), organophosphate exposure is another important element in the development of these autoimmune conditions. Silent, obscured, and rarely discussed, organophosphate exposure doesn’t get much attention when it comes to autoimmune thyroid disease, but it’s definitely a key part of the puzzle to consider. 

 

One animal study observed that rats who were administered methamidophos at a lethal dose had lower levels of T3 and T4 hormones, and higher-than-normal thyroid stimulating hormone (TSH) levels. The researchers acknowledged that administration of this organophosphate induced hypothyroidism and/or sick euthyroid syndrome in the rats, and that the symptoms of these conditions persisted even after initial treatment.

 

Various studies have noted that school children who have been exposed to organophosphate pesticides tend to have significantly higher levels of TSH than children who do not test positive for the presence of dialkyl phosphates / DAPs in their urine (meaning that they haven’t been exposed to organophosphates. In adults, exposure to organophosphates has also been linked to thyroid cancer, as well as other cancers like breast cancer and ovarian cancer (both of which are linked to low iodine levels and/or thyroid dysfunction) as well as lymphoma. Yet another cohort study in North Carolina and Iowa observed that male and female individuals who had previously used glyphosate (Round Up) were more likely to also have a diagnosis of hypothyroidism. Malathion, diazinon, fonofos, and other organophosphates have also been implicated in the development of autoimmune thyroid problems. 

 

Read more about autoimmune thyroid disease cures at this link. 

 

Learn more about natural cures for breast cancer, ovarian cancer, and lymphoma.

 

I want to add a layer, though, to the problem of autoimmune thyroid disease as caused by organophosphate exposure. The evidence is there to prove that, indeed, organophosphates are toxic to the thyroid and can cause not only autoimmune thyroid disease, but also thyroid cancer, blood/bone cancers, and reproductive organ cancers. Unfortunately, not many scientific resources actually connect the dots on this as to why organophosphates cause these specific problems. Based on our research up to this point, the cause is likely to be an unacknowledged iodine deficiency for many patients who have been exposed to organophosphates. 

 

Organophosphates interfere with the body’s calcium-phosphate balance. They lodge themselves in the bones, creating unhealthy bonds with the calcium that exists there, and provoke a higher-than-normal level of calcium in the blood. Organophosphates also, as acetylcholinesterase inhibitors, cause the overstimulation of nicotinic acetylcholine receptors, which then in turn are made to stop the natural flow of calcium into and out of cells. This leads to a build up of calcium inside of cells throughout the body, eventually resulting in not only calcifications of the mitochondria and other organelles, but the whole cell (meaning cell death). 

 

This excessively high level of calcium is cause for concern for many reasons. For one, calcifications in the cells, tissues/organs, and blood vessels can cause malfunctions on multiple levels of the body, which we talk more about here. But besides the issue of calcifications, high blood calcium levels impede the body’s ability to effectively absorb iodine. In the United States, for people who have been exposed to organophosphates and bromine, and who already don’t consume much iodine in their diets, this is a clear recipe for the development of thyroid conditions, cancer, and reproductive organ problems. 

 

Here’s how this equation works out: 

 

  1. A person is exposed to organophosphates.
  2. This person’s blood calcium levels increase.
  3. As their blood calcium levels increase, their iodine levels decrease.
  4. Their thyroid gland and reproductive organs are slowly, over time, depleted of whatever iodine that they have in their iodine receptors.
    1. NOTE: If bromine is present in the person’s body, it is likely lodged in the iodine receptors and is actively competing for these receptors with whatever iodine the person does have in their body.
  5. As the iodine saturation of the thyroid gland and reproductive organs goes down, these organs struggle to perform their jobs, and may readjust (often in a negative way) in order to be able to maintain as much functionality as possible. General iodine saturation, or lack thereof in this case, will also affect the immune system, which may become confused or malfunctional as iodine levels decrease.
    1. NOTE: Again, bromine in the body in this equation will also act as a kind of poison to the reproductive organs and thyroid gland, making their situation even more dire.

 

There are 2 effective and important medicines to counteract the effects of organophosphates on the thyroid gland, bones/blood, and reproductive organs: vitamin K2 and Lugol’s iodine. Anyone who suspects that they’ve been exposed to organophosphates and are experiencing negative effects from their exposure should start with these two therapies. Read more about how vitamin K2 can cure organophosphate poisoning here. Read more about Lugol’s iodine for organophosphate exposure treatment here

 

 

Root Cause: Common Environmental Toxins and How to Protect Yourself From Them – BUY HERE!

 

Related Posts:

Symptoms of Organophosphate Exposure / Diseases Caused by Organophosphate Exposure

Organophosphate-Induced Delayed Neuropathy (OPIDN) – How Organophosphate Exposure Causes Neuropathy and Polyneuropathy

How RoundUp / Glyphosate Destroys Human Health: Autism, ADHD, Long COVID, Parkinson’s Disease, Autoimmune Disease, and Cancer

Autoimmune Disease as an Infection: The Problem with Consensus-Based Science

Magnesium as an Organophosphate Poisoning Antidote

Introduction to Organophosphates and Organophosphate Poisoning

Kidney Disease due to Organophosphate Exposure: How Common Is It?

Autism, Nutrient Deficiencies, Organophosphate Exposure, and Bromine Toxicity: How to Correct the Deficiencies and Detoxify at the Same Time

Resources: 

 

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Meyer, Armando, et. al. (2017). Pesticide Exposure and Risk of Rheumatoid Arthritis among Licensed Male Pesticide Applicators in the Agricultural Health Study. Retrieved October 21, 2022 from: https://ehp.niehs.nih.gov/doi/full/10.1289/EHP1013 

 

Louisiana Department of Health (2005). 09/13/2005 – Hurricane Katrina #49 – Aerial Mosquito Spraying. Retrieved October 21, 2022 from: https://ldh.la.gov/news/965 

 

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Sater, Salim, et. al. (2005). Effects of Acute Organophosphate Poisoning on Thyroid Hormones in Rats. Retrieved October 26, 2022 from: https://journals.lww.com/americantherapeutics/Abstract/2005/05000/Effects_of_Acute_Organophosphate_Poisoning_on.8.aspx 

 

Leemans, Mitchelle, et. al. (2019). Pesticides with Potential Thyroid Hormone-Disrupting Effects: A Review of Recent Data. Retrieved October 26, 2022 from: https://www.frontiersin.org/articles/10.3389/fendo.2019.00743/full