In chronic Lyme and associated diseases Curcumin is an essential herb that
- decreases pain
- limits and improves Herxheimer die-off reactions,
- boosts the immune system by lowering inflammation cytokines,
- decreases brain injury and damage, and
- may kill Lyme and co-infection germs.
Curcumin is a wonderful herbal medication that I use in most of my treatments. It is a component of turmeric, a seasoning derived from Curcuma longa that is commonly found in Indian food. It is useful for a variety of problems that occur in chronic Lyme and associated diseases.
Curcumin is a potent anti-inflammatory, a strong anti-oxidant, and an effective anti-microbial against bacteria, viruses, yeast, and even parasites. It decreases pain, limits Herxheimer Die-off reactions, decreases brain injury and damage, and may kill Lyme and co-infection germs. It boosts the immune system by lowering excess inflammation cytokines that occur in Lyme disease.
As an anti-oxidant curcumin limits and decreases brain injury. Chronic Lyme infection increases a chemical in the brain called quinolinic acid. Quinolinic acid is elevated in numerous disorders like Alzheimer’s Disease and Parkinson’s. It is an agent that causes brain dysfunction and injury. Curcumin lowers quinolinic acid through its anti-oxidant effect. It also appears that curcumin raises a potent anti-oxidant called glutathione that is found in all of our cells. Glutathione prevents and repairs nerve injury. I recommend curcummin for anyone who has cognition problems with poor memory or difficulty processing information.
Curcumin has anti-bacterial, anti-viral, anti-fungal, and anti-parasite actions. Although there are no studies that show benefit in using curcumin to treat Lyme and the co-infections, it may be useful as an anti-microbial.
Method of Action for Pain and Herxheimer Die-Off Reaction
According to Aggarwal et al.
Numerous lines of evidence suggest that curcumin is a potent anti-inflammatory agent. First, curcumin suppresses the activation of the transcription factor NF–kB, which regulates the expression of pro-inflammatory gene products. Second, curcumin downregulates the expression of COX-2, an enzyme linked with most types of inflammations. Third, curcumin inhibits the expression of another pro-inflammatory enzyme: 5-LOX. Additionally, curcumin has been shown to bind to the active site of 5-LOX and inhibit its activity. Fourth, curcumin downregulates the expression of various cell surface adhesion molecules that have been linked with inflammation. Fifth, curcumin downregulates the expression of various inflammatory cytokines, including TNF, IL-1, IL-6, IL-8, and chemokines. Sixth, curcumin has been shown to inhibit the action of TNF, one of the most pro-inflammatory of the cytokines. Seventh, curcumin is a potent antioxidant, which might contribute to its anti-inflammatory action.<>
I recommend using curcumin encapsulated to increase absorption. Generally curcumin is poorly absorbed into the blood stream. One way to increase the absorption is to microscopically wrap it in fat. This is called liposomal crucumin.
For pain, Herxheimer die-off reactions, and brain injury/cognitive impairment use curcumin 500 mg 1 pills 3 times a day. If this does not help, then try curcumin 500mg 2 pills 3 times a day. As an added benefit curcumin may have anti-microbial action too against bacteria, viruses, parasites and fungae.
Curcumin has been shown to reduce the therapeutic efficacy of cyclophosphamide (Cytoxan) in animal studies. In vitro research revealed that curcumin decreased camptothecin-induced death of cultured breast cancer cells. Curcumin might also interfere with the absorption and efficacy of the chemotherapy drug irinotecan, used to treat colon cancer. The concurrent use of curcumin with these agents should be avoided.
Our patients at The Healing Arts Partnership buy this essential herb here.
1. Aggarwal BB, Sundaram C, Malani N, Ichikawa H. Curcumin: the Indian solid gold. Adv Exp Med Biol. 2007;595:1-75.
2. Halperin JJ, Heyes MP, “Neuroactive kynurenines in Lyme borreliosis” Neurology 1992 Jan;42(1):43-50.
Marty Ross MD