A review on cannabioids and breast cancer.
Again a focus on Omega 6 cannabinoids.
Again the caveat that the endogenous activators are downstream Omega 3s and 6s, and trying to balance these pathways long term is central.
Plant cannabinoids provide a stick to poke in these pathways that will have more immediate effect - but the reality is we have not yet worked out what they are doing what the long term implications are etc - loosing fat stores of Omega 6 will take a while - but balancing Omega 3s will also impact these pathways, as likely will exercise and part day fasting - see Springer chapter referred to in first post (One of six inter-related chapters in a Springer Publication by me)(with very many thanks to Springer and the Editors) . https://www.researchgate.net/publica..._a_Modern_Diet
If on your radar please discuss use of CBD, diet and exercise with your physician before taking action.
"Future Aspects for Cannabinoids in Breast Cancer Therapy"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6479799/
"Cannabinoids (CBs) from Cannabis sativa provide relief for tumor-associated symptoms (including nausea, anorexia, and neuropathic pain) in the palliative treatment of cancer patients. Additionally, they may decelerate tumor progression in breast cancer patients. Indeed, the psychoactive delta-9-tetrahydrocannabinol (THC), non-psychoactive cannabidiol (CBD) and other CBs inhibited disease progression in breast cancer models. The effects of CBs on signaling pathways in cancer cells are conferred via G-protein coupled CB-receptors (CB-Rs), CB1-R and CB2-R, but also via other receptors, and in a receptor-independent way. THC is a partial agonist for CB1-R and CB2-R; CBD is an inverse agonist for both. In breast cancer, CB1-R expression is moderate, but CB2-R expression is high, which is related to tumor aggressiveness. CBs block cell cycle progression and cell growth and induce cancer cell apoptosis by inhibiting constitutive active pro-oncogenic signaling pathways, such as the extracellular-signal-regulated kinase pathway. They reduce angiogenesis and tumor metastasis in animal breast cancer models. CBs are not only active against estrogen receptor-positive, but also against estrogen-resistant breast cancer cells. In human epidermal growth factor receptor 2-positive and triple-negative breast cancer cells, blocking protein kinase B- and cyclooxygenase-2 signaling via CB2-R prevents tumor progression and metastasis. Furthermore, selective estrogen receptor modulators (SERMs), including tamoxifen, bind to CB-Rs; this process may contribute to the growth inhibitory effect of SERMs in cancer cells lacking the estrogen receptor. In summary, CBs are already administered to breast cancer patients at advanced stages of the disease, but they might also be effective at earlier stages to decelerate tumor progression."
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