Drugs taken prophetically??? Is that an expression used in the specific field?

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Gotta love auto-correct! prophylactically.

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Is there a short summary of what he proposes?

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Avoid the typical cardiovascular health risks: smoking, get more exercise, be low/moderate weight, etc.

Increased fresh vegetable intake, less red meat.

Inflammation is a risk for prostate cancer - so work to keep inflammation low.
Tomato products (lycopene) seems to be good to help prevent prostate cancer and slow growth (best before tumor starts growing).
Broccoli, soy germ, also good and provide more synergistic benefits (mouse studies).

Soy, high in protein, and very complete for a plant protein. Iso-flavonoids.

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This review includes a laundry list of possible treatments/preventions for prostate cancer. I haven’t read through it yet, hopefully there are good insights.

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The state of the union for prostate cancer treatment. It briefly describes the currently available and under research treatment options.

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The correction factor I have seen for those on Finasteride is double. Doctors typically account for this by doubling the PSA result for men on finasteride when evaluating the risk of prostate cancer. It’s important for anyone undergoing PSA testing to inform their healthcare provider if they are taking finasteride or a similar medication.

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Source: x.com

Related:

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Mysteries of the universe revealed :wink:

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I wonder about this. If people are waking early then although they may then go to pee it may be that they are waking early as the primary issue and then go to pee as a consequence. If they have difficulty getting back to sleep that seems to be the issue.

Since I was a teenager I have woke in the middle of the night to pee, but not had a problem getting back to sleep until later in life. Copious amounts of beer is part of the causality, however. More recently I am generally able to get back to sleep reasonably quickly.

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I have a stainless steel jug on the floor by my bed. When I wake up it’s filled and I don’t remember a thing.

The first thing I’d do is to find out who’s using your jug! :wink:

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Anyone familiar with this test and have any thoughts?

from:

I’m not a urologist, but the ongoing discussions about prostate cancer triggered by the ex-president’s condition prompted me to write this blog post, hoping that it might be helpful to some people.

According to the American Cancer Society, one in eight men will be diagnosed with prostate cancer at some point in their lifetime. It is the second most common cancer among men in the U.S. (after lung cancer).

Prostate cancer often has no early symptoms.

The chance of prostate cancer increases with age (up to 50% by age 50, 60%, by age 60, 70% by age 70, and up to 100% by age 100.)

Many of these are small non-significant cancers that do not require immediate treatment. The risk of over-diagnosis, leading to invasive biopsies is increasing with age. At what age harm exceeds benefits is not established, but studies have demonstrated that the quality-adjusted life-years (QALYs) gained are decreasing, albeit still on the positive side, until the age of 75.

The recommendations to stop screening at that age are based on concerns that screening does not have a large impact on mortality and that it is associated with potential harms, including false-positive results that require invasive prostate biopsies, overdiagnosis and overtreatment with treatment complications, such as incontinence and erectile dysfunction.

The problem is that most PC deaths occur in men after the age 80.

Life span is increasing. The number of centenarians in the USA is projected to quadruple in number in 2054. Prostate cancer will become more frequent and stop testing for it at the age of 75 isn’t a good plan.

The PSA test screening for prostate cancer has successfully reduced prostate cancer mortality in the past, but has led to significant problems with overdiagnosis and overtreatment. As a result, many men are subjected to unnecessary prostate biopsies and overtreatment of indolent cancer in order to save one man from dying of prostate cancer.

In the past 10 years, a new test has become available, which can solve the problem.

A novel blood test known as the 4Kscoretest incorporates a panel of four biomarkers (total PSA, free PSA, intact PSA, and human kallikrein-related peptidase 2) and other clinical information in an algorithm that provides a percent risk for a high-grade (Gleason score ≥ 7) cancer on biopsy and distinguishes men with a low risk for aggressive prostate cancer from those with a high risk who need prompt diagnosis and treatment to prevent spread of the cancer to other organs.

The 4Kscore has reportedly yielded a 99% sensitivity and around 95% negative predictive value for the determination of Gleason grade 7 or greater disease.

Thankfully, today there are very effective treatment options available for prostate cancer including the combination of localized and external radiations which, if done by experts in the field, and if the cancer is caught at an early stage, result in a cure of the disease without any life-altering side effects. The key is to detect the cancer at an early stage so that hormonal suppression therapy (with secondary sexual dysfunction and even possible danger of dementia) is not necessary.

For more information on the 4K blood test check this:

https://www.aruplab.com/4kscore

Related:

Finding the Wolf in Sheep’s Clothing: The 4Kscore Is a Novel Blood Test That Can Accurately Identify the Risk of Aggressive Prostate Cancer

Better biomarkers that can discriminate between aggressive and indolent phenotypes of prostate cancer are urgently needed. In the first 20 years of the prostate-specific antigen (PSA) era, screening for prostate cancer has successfully reduced prostate cancer mortality, but has led to significant problems with overdiagnosis and overtreatment. As a result, many men are subjected to unnecessary prostate biopsies and overtreatment of indolent cancer in order to save one man from dying of prostate cancer. A novel blood test known as the 4Kscore® Test (OPKO Lab, Nashville, TN) incorporates a panel of four kallikrein protein biomarkers (total PSA, free PSA, intact PSA, and human kallikrein-related peptidase 2) and other clinical information in an algorithm that provides a percent risk for a high-grade (Gleason score ≥ 7) cancer on biopsy. In 10 peer-reviewed publications, the four kallikrein biomarkers and algorithm of the 4Kscore Test have been shown to improve the prediction not only of biopsy histopathology, but also surgical pathology and occurrence of aggressive, metastatic disease. Recently, a blinded prospective trial of the 4Kscore Test was conducted across the United States among 1012 men. The 4Kscore Test replicated previous European results showing accuracy in predicting biopsy outcome of Gleason score ≥ 7. In a recent case-control study nested within a population-based cohort from Västerbotten, Sweden, the four kallikrein biomarkers of the 4Kscore Test also predicted the risk for aggressive prostate cancer that metastasized within 20 years after the test was administered. These results indicate that men with an abnormal PSA or digital rectal examination result, and for whom an initial or repeat prostate biopsy is being considered, would benefit from a reflex 4Kscore Test to add important information to the clinical decision-making process. A high-risk 4Kscore Test result may be used to select men with a high probability of aggressive prostate cancer who would benefit from a biopsy of the prostate to prevent an adverse and potentially lethal outcome from prostate cancer. Men with a low 4Kscore Test result may safely defer biopsy.

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I think the situation with the prostate is very clearly linked to aberrant splicing which is on the core aging pathway. Hence unless you resolve the issues with aberrant splicing and you have a prostate it will become cancerous at some point. However, people with prostates often die of things other than prostate cancer even if they have it. (that’s geroscience for you).

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Thank you for mentioning that… Telmisartan is a partial PPARγ agonist (80mg - if you can tolerate it) with potential metabolic and anti-proliferative benefits relevant to prostate cancer, though its effects are milder than those of pioglitazone. However, the safety profile is significantly better.

Absolutely and I agree aberrant splicing is deeply wired into the aging machinery. That said, I’m curious what you think about this nuance: it seems like aberrant splicing in the prostate might actually be downstream of earlier metabolic shifts, especially around zinc and citrate metabolism.

Here’s what I mean:

Healthy prostate epithelial cells are quite unique - they accumulate millimolar levels of citrate and then secrete it into seminal fluid. That’s only possible because they intentionally block their TCA cycle at mitochondrial aconitase, and zinc is the key: it directly inhibits aconitase. But as we age - or in early neoplastic lesions - zinc transporters (like ZIP1) get epigenetically silenced. Without zinc, mitochondrial aconitase is no longer inhibited, so citrate gets burned for energy, shifting the cell’s metabolic identity from citrate-secretory to citrate-oxidative. That’s basically the first step toward transformation.

Now here’s where splicing comes in: loss of citrate means less cytosolic acetyl-CoA, which is needed for histone acetylation and post-translational modification of spliceosome proteins like SRs and hnRNPs. So low citrate → low acetyl-CoA → loss of splicing fidelity. For instance, RBM25 - a splicing factor that controls ACLY splicing - is downregulated in this state, and you get more of the exon-14-skipped ACLY isoform, which fuels a pro-inflammatory, pro-oncogenic metabolic loop.

So maybe the sequence is:

  1. Zinc loss → citrate depletion
  2. Citrate depletion → acetyl-CoA drop → splicing dysregulation
  3. Aberrant splicing → chronic NF-κB activation, AR variants, etc.

That would frame aberrant splicing as a necessary amplifier but not the primary trigger.

What do you think? Could it be that without the initial Zn/citrate shift, splicing would stay largely intact even in aging prostate cells?

Also curious if you’ve seen any data on whether restoring zinc (carefully - avoiding overshooting) reverses early splicing drift, or if the epigenetic silencing of transporters makes that a non-starter.

I agree the aberrant splicing is caused by a shortage of acetyl-CoA.

That means it is not the trigger.

However, I don’t think Zinc ordinarily is part of the issue. I think it is a mixture of damage to mtDNA reducing the mitochondrial membrane potential and citrate efflux from the mitochondria and increases in SASP which reduces the expression of SLC25A1 (known at home as the citrate carrier).

Zinc will be relevant, but I think it is mainly mitochondrial efficency and senescence.

It is interesting to note that mammals have systems to ensure that zygotes are bathed in citrate.

I don’t think the aberrant splicing necessarily causes NF-kappa B activation. It may be the cell sensing a citrate shortage that does that.

NF-kappa B activates SLC25A1.