By Dr. Hilary Booth, ND
Autoimmune disease is a broad term to describe any condition where the body attacks itself. Recently, I wrote about reducing inflammation as part of treating autoimmune disease. In this article, we are going to dig deeper into why the body attacks itself in the first place.
Genetics largely influence our predisposition to autoimmune disease; hence the reason that a thorough family health history is important. However, genetics don’t always set our fate in stone. Environmental factors, including drugs, toxins, and heavy metals have been shown to induce autoimmune disease. In this article we’re going to focus on the role of heavy metal toxicity in triggering autoimmune disease, and learn how to test and treat it to improve autoimmune outcomes.
How does heavy metal exposure trigger autoimmune disease?
Heavy metals, including mercury, silver, gold, lead, aluminum, cadmium, and more, induce autoimmunity by first inducing an immune response to the heavy metal itself. This immune response is like a specific soldier who is designed to fight a specific heavy metal. We’ll call this immune response “Soldier-M”. Soldier-M is produced in response to inhaling vapor, mercury dental amalgams, smoking, pollutant exposure, and eating foods contaminated with heavy metals.
Once Soldier-M is made, he induces a massive T-cell immune response (read: calls a team of search-dogs). When the T-cells arrive, they are shown an example of the heavy metal they’re supposed to attack (read: police dogs sniff an old T-shirt belonging to “perpetrator-M”). Before the body sends the T-cells on the hunt, it checks to make sure each T-cell knows not to attack our own body (read: makes sure each search dog looks for perp-M, and leaves innocent people alone).
In a normal immune response, the body induces cell-death in any T-cells that fail to distinguish between “self” and “not-self”. However, heavy metal exposure prevents these defective T-cells from being killed, and they end up being released and attacking our own body (read: the search dogs attack innocent people, not just the intended perp-M… not so nice, right?). This is how the body’s immune system starts to attack itself in heavy-metal induced autoimmune disease.
Interestingly, research shows that genetics make us either predisposed to this disease process, or resistant to it happening at all. This is why heavy metal exposure does not always lead to autoimmunity in every person.
Research also shows another simple correlation between cadmium and lead exposure, and increased cytokine release (read: inflammation), which contributes to other autoimmune conditions. In addition, heavy metal exposure causes deterioration of the normal gut flora. Since 70% of the immune system is in the gut, this alteration can also trigger autoimmune disease in a similar way as described above.
What puts me at risk for heavy metal exposure?
If you have an autoimmune condition that is worsening over time or poorly controlled, you may want to consider that heavy metal exposure could be part of the cause of your autoimmunity. Heavy metal exposure is also often seen in new or adult-onset autoimmune conditions. If you have been exposed to any of the following risk factors, you should consider heavy metal testing:
- Exposure to exhaust fumes, fossil fuel combustion, or industrial emissions
- Consuming contaminated cereals, fish, or shellfish
- Consuming contaminated drinking water (lead pipes, ground sources)
- Mercury dental amalgams (Note: removal of amalgams can also cause a spike in exposure, so it’s important to weigh the pros and cons of removal)
- Sluggish detoxification pathways (genetically or via an overburdened system)
How are heavy metals tested?
Heavy metals can be tested through hair analysis, which shows heavy metal exposure over approximately the past three months. This testing is simple, accurate, and is the least invasive test for heavy metals.
Blood tests look at current circulating levels of heavy metals, but it is the stored and long-term exposure that is more important in autoimmune disease. For this reason, blood tests provide less information than other tests.
Urine testing can also be done, although it is recommended that a provocation challenge is used. In a provocation challenge, a baseline urine sample is taken, then a heavy metal chelator, such as DMSA, is given to the patient to provoke a release of toxins that are stored in tissues. Urine is then retested at various times to determine the levels of stored toxins as they are excreted via the kidneys. This testing is the most comprehensive, but can be dangerous if high levels of toxins are released. DMSA and other chelating agents also require a prescription from MDs in Ontario.
How is heavy metal toxicity treated?
Depending on the type and severity of heavy metal toxicity, you may be referred to an MD for heavy metal chelation treatment. If your ND decides that natural treatment is safe, the following needs to be addressed:
- Improving liver detoxification pathways using herbs and supplements such as NAC, curcumin, milk thistle, selenium, B vitamins, and IV therapy
- Supporting excretion of toxins through bile production, regular bowel movements, and improving kidney function
- Using nutrients that bind and detoxify heavy metals, such as ALA, NAC, coriander, chlorella, and spirulina
The Bottom Line
Heavy metal exposure is an often overlooked aspect of autoimmune disease treatment. For many people, targeting the detoxification of heavy metals can help to slow or reverse the disease process because it addresses one of the underlying causes of autoimmune disease.
- Aposhian HV. et al. Mobilization of heavy metals by newer, therapeutically useful chelating agents. Toxicology. 1995. 97(1-3):23-8.
- Breton J, et al. Does oral exposure to cadmium and lead mediate susceptibility to colitis? The dark-and-bright sides of heavy metals in gut ecology. Sci Rep. 2016. 6:19200.
- Pollard MK, Hultman P and Kono DH. Toxicology of autoimmune disease. Chem Res Toxicol. 2010. 23(3):455-66.
- Wang MD and Achkar JP. Gene-environment interactions in inflammatory bowel disease pathogenesis. Curr Opin Gastroenterol. 2015. 31(4):277-82.