How 'bout a little pot-stirring? Article: Why You Should Stop Saying “Sugar Feeds Cancer”

PubMed is my "go-to" site for the science on all things, including nutrition and PCa.

Here's a link to a 2014 Review article on Nutrition and PCa (including sugar, vitamins, supplements, etc.)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4286914/

If you want to do your own reading, enter "nutrition prostate cancer" into the searchbox at PubMed, and find the latest articles (2014+).

For myself, my keto diet was to lose weight ("tight pants" 190lbs down to 175lbs in only three weeks), but if it has some tiny effect on the Warburg effect of the PCa cells, so be it.
My resveratrol/turmeric/Vit C/Noni/Vit D/Modified Citrus Pectin supplements don't seem to be dramatically helping to lower my PSA, since my chemo treatment/Hormone therapy has only lowered my PSA by 57% after five months and five rounds (400-->170). But who knows? My PSA might be 1,000 if I weren't taking them! ;)

Cheers,
Doc

Fact: added sugar (and in fact, all types of refined carbs), raise Triglycerides.
High Triglycerides are a cause of heart disease, independent of high cholesterol.
So why the h@ll mess with sugar.

Don't eat it. It's freakin' bad for you.

Case closed.

Well the Good Lord put animals, plants, and bees on the earth there you go well balanced meal!!!!!

Also, people diagnosed with type 2 diabetes seem to have lower risk of PC cancer. But, type 2 diabetes is often diagnosed in the 40s or 50s(even earlier, these days even 12 year olds are being diagnosed with what used to be called adult onset diabetes). Where as slow growing PC cancer tends to be diagnosed more than a few years later. (or so it seems to me, I don't have the stats in front of me, but as a health care pro I have known a lot more younger people with T2D than I have with PC ).

So, is T2D "protective" for PC because the PC cells don't like sugar and prefer fat? Or is it more because those younger folks diagnosed with T2D almost invariably start treatment, usually starting with both a diet lowering sugar/carbs and Metformin, or maybe other drugs which also improve insulin sensitivity and/or drop blood sugar levels, which lowers blood insulin levels? And this goes on for years covering the normal time when PC is working on becoming detectable?

And thus, just like with most other cancers, lower blood insulin(due to lower blood sugar resulting in lower insulin, plus improved insulin sensitivity) results in lower levels of cancer growth( PC or other cancers), since the insulin which spurs cancer growth is significantly reduced? OK, if so, it is the insulin and not the sugar. But how do you get more insulin? Eat more sugar(carbs). As I am about to do as I allow myself a dessert!
/academic.oup.com/jnci/article/95/1/67/2520195/Insulin-Resistance-and-Prostate-Cancer-Risk

Somebody said...
Because high waist-to-hip ratio (WHR) and high serum insulin levels have been reported to be associated with an increased risk of prostate cancer, we assessed the relationship between insulin resistance and prostate cancer risk in Chinese men....................Relative to men in the lowest tertiles, men in the highest tertile of insulin sensitivity had a reduced risk of prostate cancer (odds ratio [OR] = 0.35, 95% confidence interval [CI] = 0.21 to 0.60), but men in the highest tertile of insulin resistance had an increased risk of prostate cancer (OR = 2.78, 95% CI = 1.63 to 4.72). Considering insulin resistance and WHR together, the effect of insulin resistance was apparent in all tertiles of WHR, with men in the highest tertile of insulin resistance and WHR having the highest risk (OR = 8.21, 95% CI = 2.84 to 23.70). The associations between prostate cancer risk and insulin sensitivity or resistance were independent of total caloric intake and serum levels of insulin-like growth factors, sex hormones, and sex hormone-binding globulin. Because of the retrospective design of this study, the role of insulin resistance in prostate cancer needs to be confirmed in prospective studies.

Post Edited (BillyBob@388) : 10/24/2017 7:38:10 PM (GMT-6)

PeterDisAbelard. said...
Whether the statement "Sugar feeds cancer" is true depends on what you think it means and what you think it implies. In the 1940s a researcher named Otto Heinrich Warburg observed that while there is a large variance in the biochemistry of different types of cancer, one thing that all cancerous tissues have in common is an extremely high rate of glycolysis (using glucose for energy), especially in hypoxic (low oxygen) environments. This is called the "Warburg Effect" and it is generally accepted and appears to be true.

Warburg went further, claiming that this metabolic difference was the cause of cancer. This is called the "Warburg Hypothesis" and it is not widely believed these days, although there are some researchers who support variations of it. As stated by Warburg

The Warburg Hypothesis said...
Cancer, above all other diseases, has countless secondary causes. But, even for cancer, there is only one prime cause. Summarized in a few words, the prime cause of cancer is the replacement of the respiration of oxygen in normal body cells by a fermentation of sugar.

But we don't need the largely-discounted Warburg Hypothesis to answer our question, the Warburg Effect suffices. So, does sugar feed cancer? Yes, in a strictly literal sense it does. Cancerous tissues burn through glucose at a rate 40 times greater than normal tissues, and can continue to do so in the absence of oxygen which other tissues mostly can't.

But does this mean that one can kill cancer cells by eliminating the glucose on which they appear to rely? The answer to this question is technically: "Yes, sorta" but practically: "No." There doesn't seem to be any diet that people will put up with long-term that get the job done. If you reduce the amount of glucose available the cancer cells will simply use up all there is and keep on growing while the rest of the body starves. But... There have been several studies that have shown that a Calorie Reduced Ketogenic Diet -- a diet containing no carbs whatsoever and limited to near-starvation caloric content -- does seem to delay progression of some tumors.

So does cutting out sugar cure cancer? No.

Does it prevent cancer. Mostly no.

Does it have potential as a treatment for cancer? Maybe. We'll see.

Some Wikipedia links for those of you who want to brush up on the high school biology necessary to have an opinion:

The Warburg Effect

Glycolysis

Fatty Acid Metabolism

Good post, interesting. My fav part: "Does it have potential as a treatment for cancer? Maybe. We'll see.".

I've done a bit more reading about the Warburg Effect and prostate cancer and it appears to be another of those things where the more I read the less I know. I am rushing to post this before my last few clues have cancelled out and disappeared.

Normal prostate tissue has an odd metabolism in that it processes glucose to citrate fairly normally but then, rather than oxidizing the citrate for energy it mostly allows it to accumulate. The accumulated citrate is secreted into the semen where it acts as a calcium buffer. This mostly blocks glucose metabolism and prostate tissue relies on lipids for most of its energy.

Early stage prostate cancer cells continue this preference for lipids as an energy source but they do start to use citrate for energy production as well. A reduced citrate concentration in semen has been considered as a potential biomarker for prostate cancer. (1,2) It's not a particularly good biomarker but it does seem to be better than PSA.

Early stage prostate cancer is not generally considered to exhibit the Warburg phenotype. The cells don't ravenously devour glucose but they do use a lot compared to normal prostate tissue. This transition from very little glucose metabolism to some glucose metabolism is an early metabolic dysfunction and it seems to me to be heading in a Warburg-like direction, although it's not there yet. (3,4)

As prostate cancer advances it tends to conform more often to the Warburg phenotype. This seems particularly true for metastases to bone. A glycolytic phenotype is associated with poor prognosis for advanced disease and there is considerable interest in using the associated metabolic changes as a point of attack for treating aggressive, advanced disease, either by blocking the runaway glycolysis (and starving the cancer cells) or by inhibiting the removal of the waste products. (5,6)

So, what does this mean to us here on the forum? Not much. Because early prostate cancer cells aren't that interested in glucose it seem to suggest that glucose metabolism isn't that useful a point of attack for prevention, early detection, or treatment of early-stage disease. It does show some potential for treatment of more advanced disease but it's early days for those approaches -- mostly phase I trials.

But it's interesting... If not, perhaps, worth six footnotes.

(1) Citrate concentrations in human seminal fluid and expressed prostatic fluid determined via 1H nuclear magnetic resonance spectroscopy outperform prostate specific antigen in prostate cancer detection.

(2) Biomarker Discovery in Human Prostate Cancer: an Update in Metabolomics Studies

(3) The Metabolic Phenotype of Prostate Cancer

(4) Glucose Metabolism in the Progression of Prostate Cancer

(5) A glycolytic phenotype is associated with prostate cancer progression and aggressiveness: a role for monocarboxylate transporters as metabolic targets for therapy

(6) TargetingTumor MetabolismWith 2-Deoxyglucose in Patients With Castrate-Resistant Prostate Cancer and Advanced Malignancies

PeterDisAbelard. said...
..........................................

As prostate cancer advances it tends to conform more often to the Warburg phenotype. This seems particularly true for metastases to bone. A glycolytic phenotype is associated with poor prognosis for advanced disease and there is considerable interest in using the associated metabolic changes as a point of attack for treating aggressive, advanced disease, either by blocking the runaway glycolysis (and starving the cancer cells) or by inhibiting the removal of the waste products. (5,6)

So, what does this mean to us here on the forum? Not much. Because early prostate cancer cells aren't that interested in glucose it seem to suggest that glucose metabolism isn't that useful a point of attack for prevention, early detection, or treatment of early-stage disease. It does show some potential for treatment of more advanced disease but it's early days for those approaches -- mostly phase I trials.

But it's interesting... If not, perhaps, worth six footnotes.

(1) Citrate concentrations in human seminal fluid and expressed prostatic fluid determined via 1H nuclear magnetic resonance spectroscopy outperform prostate specific antigen in prostate cancer detection.

(2) Biomarker Discovery in Human Prostate Cancer: an Update in Metabolomics Studies

(3) The Metabolic Phenotype of Prostate Cancer

(4) Glucose Metabolism in the Progression of Prostate Cancer

(5) A glycolytic phenotype is associated with prostate cancer progression and aggressiveness: a role for monocarboxylate transporters as metabolic targets for therapy

(6) TargetingTumor MetabolismWith 2-Deoxyglucose in Patients With Castrate-Resistant Prostate Cancer and Advanced Malignancies

Peter, we have run into this a few other times in relation to non-conventional or nutritional approaches, and maybe we are doing so again? IOW, early stage or non-aggressive or just general prevention, what ever is not not much help. But looking at the more aggressive stages and advanced cases, the ones likely to get you, more impressive results. For example, I have seen that a few times in vitamin D studies. In fact, I even remember from that little poll I ran here in the past, very unscientific though it was, but it confirmed what I have seen in a few studies: Of those who had blood levels checked, only 1(7%) of the low/intermediate risk guys who responded was "sufficient"(above 30ng/ml), and 10(76%) were "insufficient"(21-29), but only 2(15%) were out right deficient (0-19ng/ml). But the high risk guys, once again 1(16%) was sufficient, 2(28%) were insufficient, but a whopping 4(67%) were deficient at 19ng or below.(the lower % showing in the poll thread are based on the higher # of all participants and all risk, but in the % I just posted I am basing it on just the numbers in each category.) Yes, I know, small #s, but I have seen this in real studies also.

So 15% of low intermediate guys were deficient or below 19ng/ml, vs 67% of high risk guys. That is quite a difference, over 4 times. And since there are far more low/intermediate risk guys in the world, if you just look at every one who gets diagnosed regardless of risk, a deiciency may not seem nearly as important. Do you suppose it's possible we are seeing the same thing here when looking at blood sugar? Maybe a little.

When you were doing that above research, did you happen to come on anything about blood insulin levels, especially regarding the higher risk guys or guys who have a failed treatment?

NKinney said...
Comments about "moderation" are spot on!



But with regard to BillyBob questions/comments on Vit D (isn't there, btw, another thread on just Vit D; did you post in the wrong thread?),................

Sorry, even though no I did not post in the wrong thread as far as I'm concerned, I did not intend to hijack or change the subject from sugar to vit D, and yes there are a million Vit D threads. The reason I brought all of that up was to show that IF Peter's post about sugar possibly being more of a player in advanced prostate cancer, but not so much in all PCs, is correct, then this would by no means be the 1st time we have seen such a phenomenon. Said phenom being certain interventions being far more important in the deadlier aspects of this disease than in the lower risk cases, and could Peter's post be showing evidence of this again, but this time in relationship to sugar?