My current list of supporting supplements. My being transparent about what I take and how I take it is not an endorsement that you should take these supplements nor take them the same way I do. I’m including links to help you get started on your own research path and from their you can make your own decisions about which, if any, supplements and which doses are right for you.
Tons of research out there for Vitamin D, Vitamin D Receptor (VDR) and pancreatic cancer. Use any search engine with with the words “vitamin D VDR pancreatic cancer cell apoptosis” and it should return a lot of links to data on the topic. I’ve had several genetic sequencing performed, so there is new data coming on-line all the time. I’ve had very good results from including vitamin D at 10k IU per day…I' have my blood serum levels checked every 3-6 months to make sure I’m not too heavily loaded. I did a 23andme test right after I was diagnosed. I did the 23and test for one reason - they provide the raw data. The raw data is really helpful to have as one reads research and investigates new data points. For instance, I located this on NCBI where one of its conclusions is “Patients with both the rs2853564 GG genotype and high 25(OH)D levels had the longest OS (median 11.0 months, 95% CI 7.1–25.5) relative to the other patients (p = 0.0079 for interaction) (Fig 2A).” Well, that’s interesting because via the raw data from my 23andme genetic sequencing it turns out I have the GG variant. However, it looks to my untrained eye as if every category in this data had a longer overall survivability (OS) that the control groups who did not load vitamin D serum levels. You review it and see what you and your physician thinks. On the whole though, I would read a lot of research about vitamin D and VDR related to pancreatic cancer or any solid tumor cancer…lots of info available about vitamin D and VDRs related to colon, breast and other cancers too.
Apigenin is a flavonoid in the same grouping as turmeric and quercetin. Do a search for Fibroblast Growth Factor 23 (FGF23)…interesting stuff . Like turmeric and quercertin, there is a lot of publicly available data speaking to apigenin’s role in, and the mechanics of, mutated cell apoptosis (cell death)…I celebrate the death of mutated cells!. This snippet is from research published in late 2017 “Apigenin has been used as a traditional medicine for centuries because of its physiological functions as an antioxidant and anti-inflammatory [6, 7], its role in lowering blood pressure [8], and its antibacterial and antiviral properties [9]. In addition to those effects, apigenin was proven to have tumor suppression efficacy in the last few decades (Fig. 1). Since Birt et al. first reported that apigenin had anti-cancer activities in 1986 [10], more and more evidence has been presented to demonstrate that apigenin shows antitumor efficacy against various types of cancer with both cell lines in vitro and mouse models in vivo. Apigenin has been demonstrated to show broad anti-cancer effects in various types of cancers, including colorectal cancer, breast cancer, liver cancer, lung cancer, melanoma, prostate cancer and osteosarcoma [11–16]. This flavone inhibits cancer cell proliferation by triggering cell apoptosis, inducing autophagy and modulating the cell cycle. Apigenin also decreases cancer cell motility and inhibits cancer cell migration and invasion. Recently, apigenin was reported to show anti-cancer activities by stimulating an immune response [17]. During those processes, multiple signaling pathways and protein kinases are modulated by apigenin, including PI3K/AKT, MAPK/ERK, JAK/STAT, NF-κB and Wnt/β-catenin.”
I had never heard of Berberine until I read “How to Starve Cancer…” which you can link to via the link on my resources page. The studies seem pretty convincing with respect to Berberin’s ability to induce cell death. There is lot of data publicly available which all seem to confirm the others - but don’t trust me, do a quick search on berberine cancer apoptosis. This came from a published study:
”The G1 phase can allow cells to induce repair mechanisms or apoptotic pathways. Thus, the effects of berberine on apoptosis induction of PANC-1 and MIA-PaCa2 cells were determined, and the results indicated that treatment of pancreatic cancer cells with berberine effectively induced apoptosis, as has been observed for breast cancer, prostate cancer, and colorectal cancer cells (10,19-21). A recent study reported that berberine efficiently suppresses cancer stem cells (22). In particular, the current results indicated that berberine had a greater apoptotic effect in PANC-1 cells than did gemcitabine, which is considered the standard treatment for pancreatic cancer. In some cancers, cells can become resistant to apoptosis and do not respond to chemotherapeutic agents (23). Thus, a variety of agents are useful, as long as they can induce apoptosis via either caspase-dependent or caspase-independent pathways. Upon treatment of PANC-1 and MIA-PaCa2 for 72 h at IC50, the caspase 3/7 activities were almost the same as in control cells. This effect of berberine has also been observed in another pancreatic cancer cell line, PxPC-3 (21). Our caspase 3/7 assay results suggest that the mechanism for apoptosis was caspase 3/7-independent when berberine and gemcitabine are administered at IC50 values. However, at much higher concentrations, the relative caspase 3/7 activities increased several fold, indicating that apoptosis becomes caspase 3/7 dependent. Additionally, when the time courses of caspase 3/7 activities were observed for both compounds, berberine activated caspase 3/7 activity before gemcitabine. Our study results are in agreement with previous findings that ROS production is increased in various cancer cells by treatment with anticancer drugs (10,24,25).”
Theracurmin is an optimized formulation of curcumin which is designed to increase the absorption of curcumin. At least that’s what I’ve read. So, since there is a lot of data on curcumin and its benefits related to cancer (and many other health benefits) I figure more absorption of cur cumin is better than less. So, what about curcumin? There must be hundreds of research into and trials of curcumin for your review, but here is a paragraph from one from way back in 2014. Why didn’t my chemologist tell me about it? Thank God my GP physician knows about it and told me to start taking it as soon as I was diagnosed. I should have been taking it long before and maybe I wouldn’t have found myself being diagnosed. Who knows, but really matters is I now take it every day.
”A growing body of evidence supports the idea that curcumin is a promising anticancer drug. In preclinical models, curcumin has been shown to have anticancer effects, both alone and in combination with other anticancer drugs, through the modulation of a variety of molecular targets. However, the poor bioavailability of curcumin has been the major challenge to its clinical application. This problem has now been solved by the development of highly bioavailable forms of curcumin (THERACURMIN®), which can induce higher plasma curcumin levels without increased toxicity. Further clinical trials will be necessary to test the therapeutic applications of this promising agent in patients with pancreatic cancer.”
Read the full pdf for the fenugreek info below via this link
Objectives Pancreatic cancer is one of the malignant tumors in the digestive system all over the world. It has a very low sur- vival rate. Although there is a great advancement in its therapy either through radiotherapy, chemotherapy, or other therapies, the overall survival is still less than 24 months. Another problem for pancreatic cancer is the resistance to its conventional chemotherapy (e.g., gemcitabine). From this point of view, there is an urgent need to find an effective drug treatment Methods The anticancer activity of the germinated fenugreek seed extract is examined in vitro and in vivo against BXPC-3 pancreatic cancer cell lines. Two groups of albino mice were injected with BXPC-3 cells: the first group remained non-treated and the second group was injected with IC50 of the fenugreek extract. The body weight and the survival rate were observed in the two groups and histological examination of the pancreatic tissue was observed
Results Germinatedfenugreekseedextractcanbeefficientlymaximizedthesurvivalrateinpancreaticcancermiceandprotect the pancreatic tissue from lesions related to cancer.
Conclusion Germinated fenugreek seed extract can be used to fight pancreatic cancer.