PCa (& other solid cancers) are known to have an increased uptake of cholesterol. In PCa, that is of greater concern, since cholesterol is the starting point for the synthesis of steroid hormones, including androgens.
Resistance to ADT can involve the manufacture of androgen, and PCa cells are also known to sometimes make cholesterol if uptake has been low.
Statins inhibit the production of cholesterol, which reduces the supply available to PCa cells. Statins also inhibit production within cancer cells.
So, it's possible that statins may delay CRPC & improve survival.
The current study reports that:
"During the median follow-up of 6.3 years after the ADT initiation, there were 834 PCa deaths and 1565 PSA relapses in a study cohort. Statin use after ADT was associated with a decreased risk of PSA relapse (HR 0.73 ...) and prostate cancer death (HR 0.82 ...)"
"Statin use after initiation of ADT, but not before, was associated with improved prostate cancer prognosis."
Note that some of the benefit of statin use might be due to reduced inflammation.
. 2021 Mar 31. doi: 10.1038/s41391-021-00351-2. Online ahead of print.
Prostate cancer prognosis after initiation of androgen deprivation therapy among statin users. A population-based cohort study
A I Peltomaa 1 , P Raittinen 2 , K Talala 3 , K Taari 4 , T L J Tammela 5 , A Auvinen # 6 , T J Murtola # 5
Affiliations expand
PMID: 33790420 DOI: 10.1038/s41391-021-00351-2
Abstract
Purpose: Statins' cholesterol-lowering efficacy is well-known. Recent epidemiological studies have found that inhibition of cholesterol synthesis may have beneficial effects on prostate cancer (PCa) patients, especially patients treated with androgen deprivation therapy (ADT). We evaluated statins' effect on prostate cancer prognosis among patients treated with ADT.
Materials and methods: Our study population consisted of 8253 PCa patients detected among the study population of the Finnish randomized study of screening for prostate cancer. These were limited to 4428 men who initiated ADT during the follow-up. Cox proportional regression model adjusted for tumor clinical characteristics and comorbidities was used to estimate hazard ratios for risk of PSA relapse after ADT initiation and prostate cancer death.
Results: During the median follow-up of 6.3 years after the ADT initiation, there were 834 PCa deaths and 1565 PSA relapses in a study cohort. Statin use after ADT was associated with a decreased risk of PSA relapse (HR 0.73, 95% CI 0.65-0.82) and prostate cancer death (HR 0.82; 95% CI 0.69-0.96). In contrast, statin use defined with a one-year lag (HR 0.89, 95% CI 0.76-1.04), statin use before ADT initiation (HR 1.12, 95% CI 0.96-1.31), and use in the first year on ADT (HR 1.02, 95% CI 0.85-1.24) were not associated with prostate cancer death, without dose dependency.
Conclusion: Statin use after initiation of ADT, but not before, was associated with improved prostate cancer prognosis.
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pjoshea13
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"We have shown in a cohort of FinRSPC PCa patients that statin use after initiation of ADT, but not before, is associated with improved prostate cancer survival. The risk decrease remained even after adjusting for co-medications, PCa risk group, FinRSPC randomization group and additional radiation therapy and the risk reduction was dose-dependent. Especially, the finding that survival benefit was limited to statin use occurring after ADT supports synergism with ADT. This study clarifies our previous work observing increased prostate cancer survival, especially in ADT-treated patients using statins [10]."
What does this say about men who use statins prior to ADT and then continue those statins after initiating a ADT? Is the supposed benefit from statins along with ADT somehow lost because they use them prior to ADT??
Sorry to belabor this Patrick. My question is does anything in this report suggest that prior use of statins diminishes their mitigating effect when taken after beginning ADT?
I was on Simcor (a combo of simvastatin+niacin) to lower cholesterol and triglycerides and substituted red yeast rice, which contains a different statin. The rice worked just as well and is probably gentler on my kidneys. Not concerned with ADT interaction since all my numbers are fine. Don't fix what ain't broken.
That was my question too. But hard to believe that there was a special cohort in the study comparing men who used statins prior to ADT and then continued with ADT vs men that stopped statins as soon as they started ADT. To be honest it’s hard to believe there were any men who were using statins that stopped them when they started ADT. This implies to me that unfortunately, the benefit is lost by prior use.
Statins slow the progression to castration resistance and prolong survival...This statements have been confirmed time and again. Top Oncologists like Charles Myers, Mark Sholtz, Laurence Klotz etc have been saying this for over a decade.
I take Atorvastatin and Garlic softgel pills. My total cholesterol is 164. LDH cholesterol is 49. I do not know a good brand of Red Yeast Rice. Nalakrats is a great source when it comes to supplements. You can ask him.
Triglycerides are basically droplets of oil circulating in blood. If fat or Oil is excessive in diet..triglycerides go up. The solution is to cut down fat and Oil significantly and increase physical exercise. If triglycerides still remain high, there are medicines which specifically work to lower triglycerides. Talk about it with your doctor.
"When glucose levels are plentiful, the excess acetyl CoA generated by glycolysis can be converted into fatty acids, triglycerides, cholesterol, steroids, and bile salts. This process, called lipogenesis, creates lipids (fat) from the acetyl CoA and takes place in the cytoplasm of adipocytes (fat cells) and hepatocytes (liver cells). When you eat more glucose or carbohydrates than your body needs, your system uses acetyl CoA to turn the excess into fat. Although there are several metabolic sources of acetyl CoA, it is most commonly derived from glycolysis. Acetyl CoA availability is significant, because it initiates lipogenesis. Lipogenesis begins with acetyl CoA and advances by the subsequent addition of two carbon atoms from another acetyl CoA; this process is repeated until fatty acids are the appropriate length. Because this is a bond-creating anabolic process, ATP is consumed. However, the creation of triglycerides and lipids is an efficient way of storing the energy available in carbohydrates. Triglycerides and lipids, both high-energy molecules, are stored in adipose tissue until they are needed."
The fate of a glucose spike is to be stored as fat. This is something that Americans who follow the government food pyramid don't get - carbs are at the base & fats are at the apex. The food industry responds to demand by creating Lo-Fat & No-Fat products & obesity is now common even in children.
When the above refers to "glucose" it isn't to ingested gluccose. The biological fate of all digestible carbs is glucose.
Agree. Any source of excessive calories can raise triglyceride level. Weight loss ce reduces triglycerides. Mine went from 176 to 81 after losing weight.
I am not aware of any such formula. HDL (good cholesterol) is naturally higher in women particularly in women with larger hips and the heart attack rate is much lower in this group particularly before menopause due to protective effect of estrogens.On the other hand, Men particularly bald men (male pattern baldness) with thick body hairs ..have high rate of heart attack and they generally have low HDL and high testosterone.
Niacin, alcohol and exercise are three common things which increase HDL. Sometimes, omega3 fatty acids also help in increasing HDL.
Many years ago there was an oat bran muffin fad **. Oat bran contains a soluble fiber which binds to bile acids in the gut & prevents their recovery. A major path for cholesterol use involves the production of bile acids.
** because of "The 8-Week Cholesterol Cure" (1987)
Google <statin alternative> & you might find something useful.
-Patrick
Patrick, you might find these of some interest. I usually use red yeast rice instead of a statin (it has the same active ingredient that is in lovastatin but more substances in addition). Dramatically lowered my cholesterol. HPF Cholestene is a good one per 3rd party independent tests.
They tried to ban RYR because it naturally contains a patented drug: Lovastatin. Crazy!
But we are left in ignorance, since the RYR people are forbidden to say how much lovastatin their product contains, if any. So users are mostly flying blind as to dosage.
Additionally, RYR products may contain citrinin, which can damage the kidneys. Presumably, the better brands test for citrinin. The HPF Cholestene label says "citrinin free".
I think I went overboard with my supplements the past few months and was getting unpleasant side effects (dizzy, shaking, GI upset). I stopped them all and am back to basics such as atorvastatin, celecoxib and metformin. Wondering what are your top 3 or top 5 supplements if you had to choose for APC and healthy life?
Coincidentally, when I saw your post, I was in the middle of working on a post (in preparation for a free book - just to get the info out there about what I did, what worked, and what failed)It's not complete. I might add green tea to it. And possibly the Dukoral vaccine. They aren't cures but seem to help and don't have many sides.
I sometimes get a little out of it from overdoing things.
What are your favorites? (statin and metformin and?)
I have a subscription and found ConsummerLab useful at times, especially when selecting phyto chemicals and supplements. I also use Examine.com which I find authoritative. Cheers, Phil
Just check your lipids. Optimally LDL cholesterol is 70 mg/dl though hard to achieve unless also good with diet. less than 100 is considered a “good” level for CV disease risk. Dosing on statins would be maximum tolerated dose until target LDL is reached. I take 80 mg Atorvastatin and LDL runs 50-70.
Those men on statins before starting ADT may have already delayed CR and PC progression (such as from the anti inflammatory effects you pointer out). So they may be already more ahead of it than those who started after ADT. Glass half full.
Here is another study which reports about the same results:
Harshman et al. 2015, Statin Use at the Time of Initiation of Androgen Deprivation Therapy and Time to Progression in Patients With Hormone-Sensitive Prostate Cancer
For my familial hypercholesterolemia I take 20mg atorvastatin and 10mg of ezetimibe. Currently, I am experimenting with super charging the statin combining it with piperine, grapefruit juice and ginger root. I will know if this boosting works after my next blood test.
This interdiction is typical of doctors attitude towards patients or underlying pharma industry interests. The reasoning is that grapefruit will increase the bioavailability of statins. Instead of saying reduce the dosage if taken with grapefruit, they just say DON'T. They either think of their patients as being kids, or just care more for the statins consumption. Take your pick.
Pjoshea13, I think I went overboard with my supplements the past few months and was getting unpleasant side effects (dizzy, shaking, GI upset). I stopped them all and am back to basics such as atorvastatin, celecoxib and metformin. Wondering what are your top 3 or top 5 supplements if you had to choose for APC and healthy life?
I began the year with a lazy attitude. Some mornings, all I could face with my morning coffee was 1,000mg Metformin. & then I never caught up with them all. (I take the 2nd 1,000mg at night.)
I will exclude vitamins that I would take even if healthy (D & K2). & minerals too (magnesium, zinc & boron).
The items that I reached for every day:
-Fisetin - the best bioavailable form you can afford. LOL
-Quercetin - I ignored it for many years, but I'm hot on it lately
-Reveratrol - the micronized form.
-Tocotrinols - delta & gamma
Every other day:
-DIM (BR-DIM)
-5-LOXIN
-Milk Thistle
But I made an April Fool's resolution to take everything every day. The holiday is over.
Thanks Patrick it tells a story! Your core supplements as well as the metformin, and resveratrol and finestin in particular are generally considered ( by me and others) as stabilizers and protectors of the genome via epigenetic modulation (histories deacetylases etc.) via the Sirtuin pathways’ effects on PI3K, AKT, mTOR. And the others are prominent for anti-inflammatory and anti-oxidant (ROS protection of genome mitochondria etc. So these address the two great drivers of the “Hallmarks of Cancer” genome degradation and inflammation. As well as aging and senescence altogether!
But they are more targeted at slowing PC cancer progression rather than fighting already advanced cancer. Curcumin being the exception. And you did not mention Quercetin nor lycopene nor more of “the usual suspects” in our APC community.
Wondering what you think of alpha -lipoic acid combined with l-Carnitine for antioxidant protection of mitochondrial? NMN or other nicotinamide to support the metformin and resveratrol?
I recently switched to pterostylbine for better bioavailability.
Appreciate all your research and knowledge that you share so generously. Paul
On the label it writes: "... 40 times greater (Cmax) and 15 times greater (AUC) ...". IMO, the latter represents the actual amplification factor. Also, Life Extension has a similar product branded "Bio-Quercetin" claiming: "Is up to 50 times more bio-available than standard quercetin". Quantity-wisethe Natural Factors is 167/29=5.76 more when counting the carrier substance.
I did some reading about bergamot orange extract as a replacement for statin to block cholesterol and fatty acids pethway Do anyone here have experience with it?
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