utahgal7 wrote:Right now, I am taking 28,000 IU of vitamin d3 weekly. I take a combination supplement with vitamin d3/k2(MK4). I should probably increase my dosage.
That's only 4000 iu/day (the current, *way* too conservative UL that should have been 10,000 or at least 5,000 iu/day).
What's your 25-hydroxy vitamin D blood level(s) vs dose? My wife, like many CRC patients, would have been clearly deficient at that intake level since she was borderline insufficient after months of 11,000-17,000 iu D3 intake per day. Old Joe was less interested in MK4 and was apparently satisfied to stabilize his cancer and diabetes-cardio patients on 50k (to 100k en extremis) megadose D3 with ~5mg/day of MK4 whereas Japanese medicine had already identified 45 mg MK4/day as a target for osteoporosis and some liver cancer patients. Since my wife had liver things and was potentially subject to chemo driven bone loss, the choice seemed clear. Especially after I had blood and lab tissue data that suggested her cancer tissues were ones that responded to MK4 too.
utahgal7 wrote:I feel like there a 2 groups of oncologists. One group is willing to be proactive with a positive Signatera result by initiating chemotherapy. Then, you have the other group who is unwilling to treat based solely on Signatera results but wants confirmation with positive CT scans.
Yep. Std cancer medicine has long treated based on the scans, not a single blood test or even a panel series. In fact, xray series based dose response was mostly all that was possible before CEA, CA199 markers were broadly available. In the early 1970s, ESR, this old inflammation marker was the most common CRC blood "marker" in use for case management, although CEA and CA199 had been recently discovered. However, cancer patients often have 6 - 9 months early warning with blood data, over scans. How to best use that time is a big deal.
However, it appears that some patients may benefit from maintenance like chemo or more aggressive forms, especially if they solve other problems that stymie patient success if left unaddressed (like std). For patients that have well conditioned blood samples and well correlatable blood markers, like my wife, multiple blood panels were faaaar more useful for day to day and month to month cancer/chemo decisions. IMO, there is substantial risk of missed opportunity(s) if you could get a rational multi modal plan with maintenance based strategies, advanced beyond std.
Rock_Robster wrote:[I think the challenge however is that even the most proactive oncologists should be practicing evidence-based medicine, and there is as-yet no body of evidence demonstrating that restarting chemotherapy in the context of stage IV disease and positive Signatera test alone results in a better overall outcome for the patient (PFS/OS). While it could conceivably delay or even prevent a recurrence,
Several concepts of personalization applied correctly can produce results quicker than std EBM approaches that actually have some scientifically unsound practices as well as wasteful habits. Erbitux and PD1 inhibitors could be counted as victorious examples of single variable personalization to cope with EBM requirements that otherwise would have flunked them out.
Also we did not have the chemo damage that is normal for std Maximum Tolerated Dose (MTD to grade ~3), scan response chemo treatment. We could leverage treatment over longer times with less chemo damage and fewer missed treatment opportunities.
Rock_Robster wrote:...it’s equally possible that it only promotes early chemoresistance and results in an overall weakened patient with fewer treatment options available once a recurrence is radiologically proven. Such a conundrum at the moment.
Since the chemo activity of cyclical 5FU alone without -iri or -oxi was typically 3-6-9 months until chemoresistance, this was an issue challenged us in the first year, for several years. Since we had early success with LEF and other alternative adjuncts, including high potency nutrients (before surgery #1), it was not too difficult to merge with Japanese oral chemo (UFT and 5FU itself) literature, which had a much longer experience base than xeloda in 2010. (by ~2020, Xeloda had enough data to do what my wife did with UFT)
One important aspect of chemoresistance/chemosensitivity isn't whether the 3rd huge met ( 22 mm) on a highly metastatic cancerous lymph node chain, is chemoresistant but whether the chemo could destroy or induce somnolence in cancer stem cells, cancer cell clusters floating around, or peripheral, tendril like extensions looking to spread the cancer. Also a less toxic chemo combined with high potency anti-cancer nutrients can often mean a stronger
patient; immunochemo may deliver degree of a self vaccinating cancer phenomenon. This then aggressively combined with surgery seemed to be the crucial step to my wife exiting metastatic cancer that I typically had surgeons and drs instantly giving up on my wife.
Following various literature and examples, we found we could delay chemoresistance and restart chemosensitivity to 5FU multiple times according to well conditioned blood samples.
Salvage surgery with a locally curative cleanout is part of how we busted chemoresistance. Ditto continuous (immuno)chemo on (micro)mets at the nearest point in time after surgery possible, and hereuristic changes to adjuvant formulations to accumulate better and better blood markers.