Cinchona officinalis and Quinine to Overcome Cytokine Storms Naturally
The term “cytokine storm” became famous during the COVID pandemic, but other cytokine storm manifestations that are well-known in mainstream media include the hemorrhagic bleeding that occurs as a result of Ebola infection. Cytokine storms tend to develop after the initial part of the infection seems to come under control and stabilize, producing symptoms that indicate worsening right at the moment when patients seem to be getting better. Less familiar is the idea that the “whooping cough” that develops as a result of pertussis infection is a cytokine storm that develops after the initial, acute infection has mostly passed. Cytokine storms are relatively common and knowing about them is important in terms of understanding disease progression and the differences between antioxidants and oxidants (read: reactive oxygen species medicines) in terms of treatment timing.
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Studies have shown that quinine (and thus, Cinchona officinalis at the proper dose), can stop a cytokine storm by inhibiting and modulating cytokine production. Quinine and Cinchona officinalis can reduce and modulate levels of the following inflammation-mediators during infection:- Interleukin-1 / IL-1
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- Stimulates immune cells, but also causes fever, pain, and inflammation.
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- Interleukin-2 / IL-2
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- Stimulates immune cells like T cells, B cells, and NK cells, but also causes flu-like symptoms (fever, chills, fatigue) capillary leak syndrome (low blood pressure, edema), skin rashes, gastrointestinal problems, neurological effects like confusion
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- Interleukin- 6 / IL-6
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- Has diverse effects. Acts as a bridge between adaptive and innate immunity. It drives inflammation and can be detrimental when over-produced, contributing to so-called autoimmune responses, metabolic issues (like anemia), and chronic inflammation.
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- Interleukin-18 / IL-18
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- A pro-inflammatory cytokine that boosts innate immunity, but that also contributes to severe inflammation, cancer development, and autoimmune diseases like lupus, Still’s disease, and rheumatoid arthritis. It also impacts metabolic diseases including obesity, and diabetes.
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- Tumor Necrosis Factor-alpha / TNF-alpha
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- A pro-inflammatory cytokine that regulates inflammation as well as cellular survival and programmed cell death. At moderate levels it can help fight infections and cancer, but when overproduced it can contribute to autoimmune disease symptoms.
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- Interferon-gamma / IFN-gamma
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- A crucial cytokine and signaling protein / chemokine produced by T cells and Natural Killer / NK cells. It is vital for immune defense against viruses, bacteria, and cancerous tumors. It induces inflammation and regulates cell growth, acting as a bridge between innate and adaptive immunity.
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- C-C motif chemokin ligand 2 / CCL2 / MCP-1
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- A signaling protein / chemokine that attracts immune cells to sites of infection.
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- C-X-C motif chemokine ligand 10 / CXCL10 / IP-10
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- A pro-inflammatory protein that acts to guide T cells and NK cells to sites of infection or inflammation. It’s overactivity contributes to severe disease states, however.
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- Inhibition of micro-RNA expression
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- MicroRNAs / miRNAs are non-coding RNA molecules that act to regulate gene expression. However, their misregulation of genes is intimately involved in cancer, heart disease, diabetes, and infection. They can disrupt normal cell function to drive the progression of disease.
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- Decreases TH17-related cytokines
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- Th-17 cytokines are a family of pro-inflammatory molecules like IL-17(A, F), IL-21, IL-22, IL-23, and IL-26. They’re crucial for host defense but also cause autoimmune disease symptoms by causing inflammation and recruiting neutrophils. Dysregulation of TH-17 cytokines lead to conditions like psoriasis, rheumatoid arthritis, and multiple sclerosis.
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- Decreases DNA, RNA, and protein production in thymocytes
NOTE: Quinine can synergistically increase the antibacterial effects of erythromycin or clindamycin, antibiotics that are used in conventional medicine to get rid of diphtheria infection. Combining quinine with erythromycin or related drugs like clindamycin carries risks that must be considered. Erythromycin, for example, inhibits CYP3A4 which can dangerously increase plasma levels of quinine. Clindamycin is safer than erythromycin when used in combination with quinine for diphtheria.
Clindamycin and quinine are also often combined in malaria treatment.
