It's always difficult to present complex topics on this website, which involve anything more than one drug, treatment, or supplement and there relationship/affect on APC outcomes. It's obvious that it's easier to show a double-blind study of only one treatment/drug etc. and not mix several treatments together, especially when they have not done studies to see how they affect someone with APC.
Nonetheless, for those of you who think it is useful to analyze more complex problems and theories, I'd like to hear your opinions on this video. You might want to focus on the heart health part only, which is important to APC patients, who often have heart disease, or develop heart disease from the ADT drugs. youtu.be/uyAUlHySJdk
Or, one might want to provide their opinion on whether it would be a good or bad idea to take GG, Ubiquinol or tocotrienols, with a statin, which allows the body to lower lipids, while maintaining the body's ability to fully produce ATP, which is "fed" by Ubiquinol and GG.
The biq question, as I see it, is "what causes statins to slow prostate cancer growth/increase CSS mortality?" Is it the direct action of the statin on the cancer, or the effect of the statin lowering cholesterol, which causes the slowing of the cancer? If it's the low cholesterol that is the important factor, then it might be advantageous to take GG and Ubiquinol as well and get the ATP producing energy for a better QoL.
Some people and doctors theorize that reducing ATP production and its process, is what helps slow APC growth. If this is true, then it probably wouldn't be a good idea to promote optimal ATP production in the body. A counter argument would be - "cancer finds a way to grow, regardless of blocking or slowing certain processes in the body". This, if that is true, then it might be best to just take the GG, Ubiquinol and tocotrienols and possibly get more daily energy to get you off the couch and enjoy life more. Plus, more activity and exercise is proven to slow cancer in most people.
Thoughtful comments are welcome. Please watch the video, or else your theories will probably be meaningless.
George
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""what causes statins to slow prostate cancer growth/increase CSS mortality?" Is it the direct action of the statin on the cancer, or the effect of the statin lowering cholesterol, which causes the slowing of the cancer? If it's the low cholesterol that is the important factor, then it might be advantageous to take GG and Ubiquinol as well and get the ATP producing energy for a better"
Annatto tocotrienol has a cholesterol lowering effect in addition to anticancer benefits that may allow statin reduction or elimination. Dr Tan explained the importance of GG for the creation of MK4. K2MK4 has shown anti cancer benefits over a range of cancer and has inhibited anchorage-independent growth and spheroid formation in castrate-resistant prostate cancer cells. I believe pairing annatto tocotrienol and MK4 with boron may offer a synergenic approach to lower contracting prostate cancer as well as an auxiliary to conventional treatment.
Good info. Thanks 82. My ldl tested to low a few weeks ago so I cut back on the statin dose. Going to retreat next week. There is danger in having ldl that’s too low. The rest of your contents are useful info as well. Thanks
Here is a much better study result. I find this paper to be very useful! The only thing that is missing, is that it doesn't analyze prostate cancer. That is the unknown. However, it does address cardiovascular deaths and cancer deaths of any type. Based on what I see, it appears that an LDL-C level around 94, has the lower all-cause mortality for cancer patients. But, as I said before, maybe prostate cancer patients do better with lower LDL than do other types of cancer. All I know, is that I think that my recent LDL of 28 is dangerous. I'm going to raise it. I'm going to find another video for you as well.
Taking Ubiquinol CoQ10 to counter my statin medication, and with no apparent muscle weakness, I understand it is the K2 Mk4 that I miss according to Barry Tan. Would be cheaper adding this rather than the pricey GG supp, or have I missed something?
"Vitamin K2 is the common name for a group of related compounds known as menaquinones. The defining structural characteristic of a menaquinone is a quinone ring, although details such as the length of the carbon tail and number of side chains may vary. The specific name of each menaquinone indicates the number of side chains, or isoprene units, it has. For example, MK-4 is a menaquinone that has four isoprene units. The number of isoprene units primarily affects the transport of the menaquinone to the target tissue"
"The general benefit of vitamin K2 is to help ensure the correct disposition of calcium. This effect primarily consists of placing calcium in bones and blood rather than arteries and muscles. NOTE: If your main objective is for arterial decalcification then best to select a product with the MK-7 version of vitamin K2 for its superior efficacy in this area."
Calcium disposition is an important role MK-4 provides. Dr. Weston Price called it Activator-X and was intrigued with his findings. This link contains some of them:
Dr. Tan is a chemistry professor. With no apparent prostate cancer expertise.
And apparently, Geranylgeraniol is a life-extension supplement.
I am always wary of mixing life extension with prostate cancer. I am always concerned about the supplement contributing to the vitality of the prostate cancer cells.
Bisphosphonate drugs are another category of pharmaceuticals that interfere with endogenous synthesis of GG through the mevalonate pathway. The enzyme target of these drugs is farnesyl pyrophosphate synthase (FPPS) rather than HMG-CoA reductase, so the precise mechanism is different from that of statins. PPS is involved in the steps immediately preceding GG synthesis. A common result of nitrogen-containing bisphosphonate (NBP) use is osteonecrosis of the jaw (ONJ). Effective treatments for this are lacking, and GG has been identified as a potential preventive and therapeutic agent. Most of the research in this area has been done in rodents and cell cultures but results are promising.
GG was shown to reverse the effects of NBPs on reduced angiogenesis, which is speculated to be one of many mechanisms contributing to ONJ. GG has also been shown to reverse the negative effects of NBPs in human fibroblasts, osteogenic cells and HUVEC cells. Endothelial progenitor cells (EPC) co-treated with NBPs and GG showed significantly increased cell viability, migration ability and increased EPC colony density (decreased apoptosis) compared to non-GG-treated controls, effectively reversing the negative effects of NBPs. Researchers concluded that systemic or local GG treatment could be a therapeutic strategy for ONJ. Similar results have been demonstrated for GG reversing the negative effects of NBP on human alveolar osteoblasts, periodontal ligament fibroblasts and oral keratinocytes.
It’s ironic that the influence of NBPs on the mevalonate pathway may result in reduced vitamin K2 synthesis. Vitamin K2 is instrumental in supporting bone mass, so these osteoporosis drugs may actually induce the opposite of their intended effect. Vitamin K2-dependent enzymes play essential roles in calcium trafficking, and a deficit of enzyme activity may contribute to reduced bone mineralization and increased risk for vascular and soft tissue calcification. Although vitamin K1 accounts for over 90% of dietary vitamin K, the K2 form menaquinone-4 makes up over 90% of tissue vitamin K stores.
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🤖 ChatGPT on Cancer-Fighting Exercise💪 vs PCa
Is One Statin Better than Another. 
