- The protein NSD2 has been identified as a key factor in prostate cancer development when it binds with the androgen receptor, leading to rapid cell division and growth
- Researchers used a combination of techniques, including CRISPR screening, to study the interaction between NSD2 and the androgen receptor in prostate cancer cells
- Another study debunks the myth linking choline intake to increased prostate cancer risk, highlighting the limitations of the original observational study that suggested this connection
- Poor mitochondrial health, influenced by excess linoleic acid intake, endocrine-disrupting chemicals and electromagnetic field exposure, are the likely root causes of major diseases, including cancer
- Aspirin, particularly immediate-release formulations, has anticancer properties. Low doses taken consistently over long periods show benefits in reducing cancer risk
(Mercola)—According to the American Cancer Society, about 1 in 8 men will be diagnosed with prostate cancer during their lifetime. It’s the second-leading cause of cancer death behind lung cancer.1 But despite its prevalence, a diagnosis is not an automatic death sentence.
Between 1993 and 2013, the death rate of prostate cancer declined by around half, and 3.3 million American men diagnosed with this disease at some point are still alive.2 Furthermore, the National Cancer Institute predicts a 97.5% survival rate after diagnosis.3 But, we’re not out of the woods yet — plenty of research is still being done to learn more about treating this disease, and researchers from the University of Michigan have just pushed the frontier.
NSD2 Protein Implicated as an Activator of Prostate Cancer
In a study4 published in Nature Genetics, researchers discovered a key factor in the development of prostate cancer. Specifically, they noted that when the NSD2 (nuclear receptor binding SET Domain Protein 2) binds with the androgen receptor (AR), it leads to rapid cell division and growth that results in prostate cancer.
Before diving further into this, let’s define some of the basics. Androgens are essentially hormones that trigger the growth and development of the male reproductive system, and the most prominent example is testosterone. They’re responsible for the changes that males go through during puberty, such as thickening of the vocal cords that leads to a deeper voice.5
While androgens are largely associated with males, females produce androgens as well, but in smaller amounts. When androgens are released, they’re converted into estradiol, a type of estrogen. In this converted state, estradiol helps regulate menstruation, as well as conception and pregnancy.6
Now, what is the AR? It’s essentially a protein produced by the AR gene, which then binds to the androgens produced in your body. As noted by MedlinePlus:7
“The receptors are present in many of the body’s tissues, where they attach (bind) to androgens. The resulting androgen-receptor complex then binds to DNA and regulates the activity of certain genes that play a role in male sexual development. By turning the genes on or off as necessary, the androgen receptor complex helps direct the development of male sex characteristics.”
Going back to the Nature Genetics study,8 the researchers were able to crack the code, as it were, between NSD2 and AR using an epigenetics-targeted functional CRISPR (clustered regularly interspaced short palindromic repeats) screening. Interestingly, they noted that NSD2 is also an oncogene in hematologic cancers, and “harbors recurrent activating alterations in over 15% to 20% of multiple myeloma and 10% childhood acute lymphoblastic leukemia.”
Diving Deeper Into the Development of Prostate Cancer
The researchers used different methodologies that comprised human and animal test samples. For human samples, prostate tumor patient tissues were taken from the archives of University of Michigan archives, while mice were provided by the University of Pennsylvania and the University of Michigan, which were kept under humane conditions.9 After completing their assays and analysis, the researchers published these findings:10
“Conventional plasmid-based reporter systems fail to capture intricate epigenetic or chromatin-level regulation of gene expression as they lack the native histone composition or higher-order chromosomal structure. Thus, we engineered an endogenous AR reporter system by using the CRISPR/Cas9 and homologous recombination methodologies.
We edited the KLK3 gene (also known as prostate-specific antigen, PSA) locus in AR-driven LNCaP cells to knock-in the mCherry coding sequence directly downstream of the endogenous promoter and fused in-frame via an endopeptidase sequence to the KLK3 gene …
Using these endogenous AR reporter cell lines, we carried out a functional CRISPR screen, wherein we treated the cells with a custom single guide RNA (sgRNA) library targeting druggable transcriptional cofactors for eight days, stimulated with DHT for 16 h and FACS-sorted into mCherryHIGH and mCherryLOW populations.
Genomic sgRNAs were sequenced and the ratio of normalized counts in mCherryLOW to mCherryHIGH cell populations was used to rank individual sgRNAs. Here, ranked alongside BRD4 and TRIM24, we identified NSD2 as an AR coactivator.”
The study is packed with dense information largely meant for oncology researchers, but the findings above summarize how the researchers were able to sift through large swaths of information and methodologies. Undoubtedly, this new breakthrough will be beneficial for all people receiving prostate cancer treatments.
The researchers concluded that NSD2 plays an important role in the development of prostate cancer. Furthermore, they proposed targeting this protein in further experiments to fully confirm the effectiveness of their findings. In a press release, co-author Dr. Arul M. Chinnaiyan elucidates further:11
“By degrading NSD1 and NSD2, we can more directly target cancer and avoid the normal tissue. Our study suggests if we’re able to develop NSD1/2-targeting agents, they could potentially be combined with FDA-approved androgen receptor antagonists and have a synergist effect in terms of treatment.”
Choline Does NOT Cause Prostate Cancer
Considering the new information published, I’d like to debunk a medical myth about prostate cancer that’s been circulating for a few years now — choline intake and its association with this disease.
The primary study where this notion came from,12 published in 2012, suggested there might be a link between increased choline intake and an increased risk of advanced, lethal prostate cancer. As noted by the authors, “Men in the highest quintile of choline intake had a 70% increased risk of lethal prostate cancer.” However, there are several questionable aspects surrounding this conclusion.
To start, the study was observational only, which means it only suggests associations but cannot prove causation. Since there are many factors, both dietary and environmental, that play a big role in predicting prostate cancer outcomes, pinning the disease to a single nutrient is problematic.
Furthermore, the researchers collected dietary information only six times during 22 years of follow-ups, which raises questions about the accuracy of their collated information. Many people can’t even recall what they ate several days ago, let alone the foods they consumed within a span of 22 years. Other shortcomings of this study include the following:
- It does not account for other components of the diet that could influence prostate cancer risk, such as phytonutrients, fiber and other vitamins and minerals.
- No dose-response relationship across quintiles of choline intake was established. Understanding whether the risk of prostate cancer increases linearly with choline intake or if there’s a threshold effect would be crucial for dietary recommendations.
- The study also looked at post-diagnostic intake of choline and its relationship with lethal prostate cancer among men who were initially diagnosed with nonmetastatic disease and here, no statistically significant link could be found.
In truth, choline is beneficial for your health. Several studies have shown that increasing choline intake has important benefits, such as decreased risk for heart disease,13 cancer14 and nonalcoholic fatty liver disease.15 Based on these findings, you’d be better off increasing your dietary choline intake, and the best sources include grass fed meat and milk, as well as pastured eggs.
Address the Root of Cancer — Poor Mitochondrial Health
I believe that virtually all major diseases like cancer, heart disease and obesity are linked to an inability to produce cellular energy due to impaired mitochondrial function. Without optimal cellular energy, your body cannot properly initiate the repair processes essential to preventing and recovering from disease.
Through the years, I’ve identified three pernicious toxins that damage your mitochondrial function, mainly by affecting intracellular calcium that subsequently impact your cellular health. In essence, exposure to these toxins raise intracellular calcium, which results in increased superoxide and nitric oxide levels. These combine into peroxynitrite, a potent reactive oxygen species that contributes to poor health. These three primary culprits are:
- Excess linoleic acid (LA) intake — An omega-6 polyunsaturated fat (PUFA), LA is abundantly found in seed and vegetable oils as well as ultraprocessed foods, and is one of most harmful ingredients in the Western diet. When consumed in excess, it negatively affects your metabolic rate and gut microbiome, which are the two of the most important factors that impact your health.
- Endocrine-disrupting chemicals (EDC) — Exposure to EDCs from sources like microplastics is over-activating your estrogen receptors. Microplastics are so pervasive that you’re probably eating a credit card’s worth of plastic every week.16 These plastics are loaded with phthalates and bisphenol A (BPA), which activate estrogen receptors. Estrogen increases intracellular calcium levels, which results in the generation of peroxynitrite.
- Excessive electromagnetic field (EMF) exposure — People are bombarded with EMFs, such as from cellphones, every day with hidden consequences to public health. EMFs activate voltage-gated calcium channel (VGCC) receptors within the cell, catalyzing the production of peroxynitrite by triggering an influx of calcium.
Addressing these three factors will help repair and return your mitochondrial function back on track to producing optimal cellular energy. Ultimately, this is the crucial first step to warding off all chronic disease that plague Americans today, such as cancer, and the best way to do it is limiting your exposure to them. To start, I recommend minimizing your LA intake below 5 grams from all dietary sources. If you can get it below 2 grams, that’s even better.
Next, minimize your EMF exposure by turning off the Wi-Fi and using hardwired connections instead. I also recommend using an analog alarm clock instead of relying on your phone’s alarm clock, which most people put beside their bed. The next strategy is reducing your exposure to plastics, which is accomplished by opting for products sold in glass containers and using reusable products over single-use ones.
This is just a preview of the strategies available to restore and repair your mitochondrial function. My newest book, “Your Guide to Cellular Health: Unlocking the Science of Longevity and Joy,” goes into great detail about how these three factors affect your mitochondrial function, as well as practical, healthy strategies to address them.
The eBook is now available, while the print edition will be released on December 10, 2024. I encourage you to pick up a copy, as this contains my latest research that corrects many long-held beliefs I’ve had in the previous years.
Another Anticancer Tip — Aspirin
In addition to addressing the main factors of mitochondrial function, there are other strategies available to help you prevent cancer. One approach is taking aspirin, a drug well-known for its pain-relieving and anti-inflammatory uses.
In my interview with bioenergetic medicine expert Georgi Dinkov, he discusses research using a combination of B vitamins and aspirin against a highly lethal form of human mantle cell lymphoma. He discovered that while the vitamins stopped tumor growth, adding aspirin into the equation regressed the tumor in the animal test subjects. Below, he explains the theoretical basis:
“One of Ray [Peat]’s main theories was that … cancer cells … [are] metabolically dysfunctional, we all know that, and typically a cell like that commits apoptosis. But in order to commit apoptosis, that mechanism is controlled almost entirely by the intracellular pH. And in order for apoptosis to occur, it needs to be in the acidic range.
But the cancer cells are alkaline due to exporting lactate and hydrogen ions. So, if anything can drop the intracellular pH, those cancer cells, because they’re deranged, should actually disappear by themselves.
And one of Peat’s suggestions at the time was, ‘Why don’t you use the drug acetazolamide?’ which as a carbonic anhydrase inhibitor, increases carbon dioxide. Carbon dioxide is acidic, and then that should allow cancer cells to commit apoptosis.
There are some studies in vitro and in vivo showing that acetazolamide may work, but it didn’t really cure the tumors. It was a slower growth, partial regression, but it showed that the idea was on the right track.
So, I said, ‘Let’s find something that’s much more acidic than carbon dioxide.’ And that is this 2,6-dihydroxybenzoic acid, which is just one extra hydroxyl group on top of aspirin. Salicylic acid, really, which is 2-hydroxybenzoic acid. And then this thing is about 10 times more potent than aspirin.”
That said, consider adding aspirin into your health routine. But don’t just select any aspirin available — opt for immediate-release formulations instead of the coated extended-release varieties. Pay attention to the ingredients as well. Ideally, corn starch should be the only additive listed.
After doing my own research, I identified a product meeting these criteria. The appropriate dosage ranges from 82 mg to 325 mg daily, taken with your largest meal, depending on your individual needs.
In the context of cancer prevention, the dosage and duration of aspirin are crucial factors. Low doses (75 to 300 mg/day) have been shown to be as effective as higher doses in reducing colorectal cancer-related mortality,17 which means there’s no need to take large amounts to gain the benefits.
Consistency and long-term use seem to be key, however. Studies indicate that aspirin’s benefits increase with duration, with significant reductions in cancer risk observed after five to 7.5 years of consistent use.18
I personally take 111 mg daily using Health Natura’s USP grade 60 gram aspirin powder, which costs less than $20. This 99% pure USP aspirin powder appeals to me due to its prometabolic, antilipolytic, anti-inflammatory, anticortisol and anti-estrogen effects. Its safety profile is also well-established.
- 1, 2 American Cancer Society, “Key Statistics for Prostate Cancer”
- 3 National Cancer Institute, “Cancer Stat Facts: Prostate Cancer”
- 4 Nat Genet. 2024 Sep 9. doi: 10.1038/s41588-024-01893-6, Abstract
- 5 Britannica, “Androgen”
- 6 Cleveland Clinic, “Androgens”
- 7 MedlinePlus, “AR Gene”
- 8 Nat Genet. 2024 Sep 9. doi: 10.1038/s41588-024-01893-6, Main
- 9 Nat Genet. 2024 Sep 9. doi: 10.1038/s41588-024-01893-6, Ethical Statement
- 10 Nat Genet. 2024 Sep 9. doi: 10.1038/s41588-024-01893-6, Functional CRISPR Screen Reveals NSD2 as an AR Coactivator
- 11 Michigan Medicine, September 9, 2024
- 12 American Journal of Clinical Nutrition 2012 Oct; 96(4): 855–863, Abstract
- 13 Nutrients. 2023 Sep; 15(18): 4036, Abstract
- 14 Scientific Reports, volume 13, Article number: 22144 (2023), Abstract
- 15 European Journal of Clinical Nutrition, volume 77, pages 1160–1166 (2023), Abstract
- 16 World Wildlife Fund, Assessing Plastic Ingestion from Nature to People, page 7
- 17, 18 Cureus. 2024 Feb; 16(2): e54658, Review
Bypass Big Tech Censors
Two Storms, One Harvest
Every food crisis in living memory has been a one-shock event. The 2008 price spike was a commodity bubble. The 2020 shortages were a logistics failure. The 2022 grain scare was a war on one exporter’s ports. Each time, the system bent, adjusted, and recovered, and each time the experts assured us afterward that global markets are simply too big and too diversified to fail.
What nobody in Washington seems eager to discuss is that 2026 is shaping up to be something the modern food system has never actually faced. Two independent shocks, one climatic and one geopolitical, are converging on the same harvest cycle at the same time. Not sequentially. Simultaneously.
Start with the weather. The Pacific Ocean is currently building toward what forecasters now openly call a record event. NOAA’s Climate Prediction Center puts the odds of at least a strong El Niño near 88 percent, with roughly two in three odds it reaches “very strong” status, the tier reserved for perhaps three or four events in the entire satellite era. Every major global model now projects a median peak in Super El Niño territory, and most of them project it exceeding the 2015-16 event, which until now held the modern record. Sea surface anomalies were already brushing the super threshold in mid-July, months before these events normally peak. The atmosphere has already shifted into El Niño mode, and the event is forecast to crest in late fall and early winter.
This is not about “climate change.” It’s about the standard cycles of weather, and the cycle we’re currently in is one that has likely devastated societies in the past. We’re better prepared as a society today, but not all Americans are equally prepared.
Serious households have started doing the quiet math on their own. Grocery bills tell part of the story, and the forecast maps tell the rest, which is why long-term food storage has moved from fringe hobby to mainstream line item in the family budget, with established suppliers like Heaven’s Harvest seeing demand from people who five years ago would have rolled their eyes at the idea. That instinct is not paranoia. It is pattern recognition, and the pattern is worth walking through carefully.
Editor’s Note: Heaven’s Harvest IS a sponsor, but the warnings of this article are real and would be written even if we didn’t have a survival food sponsor. With that said, those who take advantage of what they offer can use promo code “Patriot” for 15% off.
The Fertilizer Clock Is Already Running
While the Pacific warms, the second shock has been unfolding in the Strait of Hormuz. The conflict with Iran turned the world’s most important energy chokepoint into a contested waterway, and the consequences reach far beyond the gas pump. Roughly a third of global fertilizer trade moves through Hormuz, and the disruption sent urea prices up 86 percent year over year by March, with a 53 percent jump in a single month.
The World Bank projects energy prices rising about 24 percent in 2026 and fertilizer about 31 percent. By its own accounting, fertilizer prices ran 35 percent higher in the first five months of this year than the same period last year.
Here is the mechanism the nightly news will not explain. Fertilizer is not a grocery item. It is a time-delayed input. The nitrogen a farmer in Iowa or Punjab could not afford to apply this spring does not show up as a problem this spring. It shows up as a thinner harvest six to twelve months later.
The World Bank’s own food security brief concedes that the effects of reduced applications earlier this season “are likely to become visible only later in harvest outcomes.” Translate that from institutional language into plain English and it means this. The damage is already done, it is already in the ground, and we are simply waiting for it to arrive on the shelf.
Now check the calendar. Six to twelve months from the spring planting season lands us squarely in late 2026 and early 2027. Which is precisely when the strongest El Niño in the instrumental record is forecast to peak, bringing its signature droughts to Southeast Asia, Australia, southern Africa, northern Brazil, and South Asia, the very regions that grow the world’s rice, sugar, and oilseeds.
The World Bank warns openly that a strong El Niño “could disrupt multiple crop belts simultaneously” on top of the conflict-driven input costs. Their baseline projection assumes the Middle East disruptions ease by autumn. What in the last two years of Middle East history suggests that assumption is safe?
The System Has No Slack Left
The comfortable answer is that global markets always adjust. But adjustment requires slack, and the slack is gone. Global cereal production is expected to decline from last year’s records even before El Niño does its work. The UN World Food Programme, hardly a den of right-wing preppers, is calling this the most significant disruption to its supply chains since Covid and the invasion of Ukraine, and its supply chain director put the stakes bluntly.
Today’s supply chain challenges are tomorrow’s hunger crisis.
There is also a political dimension that markets cannot price. When food gets scarce, governments do not behave like economists. They behave like politicians. Export bans, hoarding mandates, and panic buying at the national level turned the modest rice shortfall of 2008 into a global crisis, and analysts are already warning that import-dependent nations are the first dominoes.
The 2015-16 Super El Niño, a far weaker event than what is now forecast, threw tens of millions into food stress across Africa and Asia. This one is projected to be stronger, and it arrives with fertilizer already rationed by price and shipping lanes already contested by missiles.
What Joseph Knew
Scripture does not treat preparation for lean years as faithlessness. It treats it as wisdom delivered in advance to those willing to act on it.
Behold, there come seven years of great plenty throughout all the land of Egypt: And there shall arise after them seven years of famine; and all the plenty shall be forgotten in the land of Egypt.
Joseph did not respond to that warning with a hashtag or a committee. He stored grain during the years of abundance, and when the famine came, Egypt stood while its neighbors begged. The lesson is not that famine is certain. It is that the time to prepare is precisely when preparation still looks optional.
Nobody who filled a pantry in a year of plenty has ever regretted it, and nobody standing in an empty aisle has ever been glad he waited for certainty.
None of this calls for panic, and panic is the enemy of sound judgment anyway. It calls for the same unglamorous prudence our grandparents considered ordinary. Keep some cash margin, know your local growers, and put real food in deep storage while it is cheap and available, because the entire arc of this story is that cheap and available is a closing window.
Families looking for a straightforward place to start can visit Heaven’s Harvest and use promo code Patriot for 15 percent off long-term storable food. The forecasts may yet soften, the strait may yet reopen, and we should pray they do. But hope is a fine thing to hold and a foolish thing to eat.
