OK, try again. Had to remove the 2nd of Cashless' links at the end, that got rid of most of the crazy results, except for the inexplicable large/bold type in the last half of that last quote. This is not showing up in the text or in a word processor, only when I preview it here or post it here. Don't know why that is happening:
Thanks, Cashless! All of these do indeed add a bit more info supporting my pet theory of insulin resistance and it's companion higher blood insulin levels stimulates- very significantly- the growth of cancer cells. Even including our favorite
cancer on this forum, PC. Of course, my pet theory is that it is actually the main culprit- possible above all others, in cancers and a large # of the common diseases of modern civilization. That remains to be seen, but I do think there is much evidence, if not yet proof
, that excess insulin is a major player.
From the 1st link:
The improvement of insulin resistance appears to be essential for the prevention of PC growth.....As a meta-analysis has suggested, the relationship between prostate cancer (PC) and T2DM or metabolic syndrome (MetS) is still under discussion.[3-7] However, a recent study has suggested that pre-existing T2DM also is associated with a higher level of mortality in patients with PC, similarly to other cancers... .........
In the algorithm shown fig 3 from that 1st link, notice it shows this straightforward relationship(prediabetes or type 2 diabetes/ T2D could be substituted here for MetS they often go together):
1:Metabolic syndrome(MetS, look out for those spare tires/bowling ball guts as the 1st obvious sign of MetS) followed by:
2:Insulin Resistance(IR) then
3: Hyperinsulinemia(HI, more insulin production needed to over come the resistence to insulin that has developed) then
4: increased PC growth in response to all this extra insulin!
But what about
advanced T2D in the other side of the algorithm? That is where the T2D has advanced so far that the pancreas is becoming worn out, the pancreatic beta cells are damaged and are starting to fall behind on insulin production, and what does that do for PC growth? It is suppressed! But, the new is still not good for this group, because what is the doctor's routine response to these skyrocketing blood sugars due to flagging insulin production which will probably suppress PC? Stop eating any sugar, cut way back on carbs, right? Not likely, it is hard to get a patient to do that. So, simply start the patient on MORE insulin by way of injections. Which bodes ill for all future health areas, including PC. Just inject whatever amount of extra insulin is needed to get a blood acceptable sugar reading, regardless of how many net carbs we consume.
Or, though some of our doctors and health advisors seem loath to emphasize this, we could attack the root cause of the MetS/pre-diabetes/T2D problem: cut sugar and anything that turns into sugar(net carbs which = carb minus fiber) once it is digested and enters our blood stream.
I have seen it advised that PC is different, no need to worry about
sugar because unlike other cancers, PC eats fat rather than sugar, or at least it does not thrive on sugar like other cancers. But there seems to be a lot of increasing evidence that insulin stimulates it's growth just like all other cancers. And if you want more insulin, it has been known for decades how to get more, just eat more net carbs/sugar. That will also help you get more triglycerides, stiffer arteries/higher BP, Alzheimer's, peripheral artery disease leading to amputations, blindness, etc., ad infinitum.
However I got the gist of it, and it surprises me that there is not more discussion between patients and doctors about staying away from sugar. I'm also surprised that drugs like metformin are not more widely used in PC.
From what I've read, in these links and elsewhere, it seems to me, if one were to decide to eliminate one thing from diet, it should be sugar.
Prato, like you, I also find it surprising that our medical and dietary/health advisors don't seem to want to discuss this with us more. I do wonder why. Even with diabetics, often the emphasis seems to be more on prescribing a medication, than in emphasizing the cause of the disease which- if the patient will only do so, a big if I realize- can be readily dealt with. And if dealt with, will lead to abundant overall health benefits, more or less the opposite of the result of prescribing more meds, most especially insulin.
Oh, BTW, exercise is just one more way to deal with an excess insulin problem. Diet and exercise. As long as the diet does not consist of more net carbs. We see the result of that just by glancing at our population(obesity, diabetes, MetS) after the last 40 years of our docs pushing low fat, higher carb diets for our health. Even pushing exercise at the same time was not able to overcome the results of the dietary change.
From Cashless' 2nd link:
However, the initial therapeutic response from ADT eventually progresses to castrate resistant prostate cancer (CRPC) which is currently incurable. ADT rapidly induces hyperinsulinaemia which is associated with more rapid treatment failure. We discuss current observations of cancer in the context of obesity, diabetes, and insulin-lowering medication. We provide an update on current treatments for advanced prostate cancer and discuss whether metabolic dysfunction, developed during ADT, provides a unique therapeutic window for rapid translation of insulin-sensitising medication as combination therapy with antiandrogen targeting agents for the management of advanced prostate cancer.
1. Obesity, Type 2 Diabetes and Prostate Cancer
1.1. Obesity and Cancer Risk
Worldwide rates of obesity have doubled in a generation with a global estimate of ~500 million obese adults (with an additional 1.5 billion overweight) being followed by a generation of 40 million overweight children . In both industrialised and developing countries these staggering numbers pose a soaring economic and health care burden as a result of chronic comorbidities including increased rates of cardiovascular disease, hypertension, stroke, and type 2 diabetes (T2DM) .
Obesity is also a risk factor for a growing number of cancers...........
1.2. Obesity and Cancer Progression
What is indisputable from the epidemiology is the impact of obesity on cancer behaviour. Obesity is consistently identified as a significant risk factor for more aggressive disease and an independent predictor of recurrence and cancer-specific mortality for breast , endometrial, ovarian , and bladder cancer as well as prostate cancer [9, 15]. Men with higher BMI are more likely to be diagnosed with higher-grade cancers and higher Gleason scores and suffer an increased incidence of recurrence [3, 7, 15, 16] and increased cancer-specific mortality than men with a healthy BMI [16–18]. ............
However, it is hyperinsulinaemia, as a result of insulin resistance in classical metabolic tissues, which has been identified as a highly significant risk factor to progression of prostate and other cancers . In prostate cancer, elevated insulin or C-peptide levels (used as a normalised surrogate) have recently been shown to significantly correlate with high-grade prostate cancer and worse patient prognosis [16, 31–36], more significantly than BMI alone, suggesting that at least part of the effect of increased BMI on prostate cancer mortality is related to coincident hyperinsulinaemia........
(excessively sarcastic comment about
our health advisers deleted! I need to censor myself more often! )