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Tag: cancer

The Link Between Breast Cancer and a Virus in Meat and Dairy

Exposure to the bovine leukemia virus from meat and dairy (or a blood transfusion from those who eat meat or dairy) is a risk factor for cancer.

In 2015, researchers in California found bovine leukemia virus (BLV) stitched into the DNA of human breast cancer tumors from mastectomies. The virus was found at much higher rates than in normal breast tissue obtained from breast reduction surgeries. Based on this difference, they calculated that as many as 37% of breast cancer cases may be attributable to exposure to BLV, likely through consuming milk or meat from infected animals.

In response, the milk and meat industries seemed more concerned about consumer confidence than consumer cancer. But scientifically, the research priority turned to the question: Could the California results be replicated? The answer, it turns out, was yes. They were replicated among women in Iran. Replicated in Brazil. In Australia, the link was even stronger. In Texas, they found the same thing. Women diagnosed with breast cancer were found to be so much more likely to have bovine leukemia virus DNA in their breast tissue compared with women without cancer, that the attributable risk was calculated at 51.82%, indicating that this meat and dairy virus may be responsible for at least half of the breast cancer cases among the women in Texas they studied.

All in all, six of the eight studies performed to date found the virus in human breast tissues, which “suggests strongly that BLV does infect humans, and breasts can be targets of infection.” Four of the five studies that compared infection rates in cancerous versus normal breast tissue found that the odds of detecting the virus in tumors were, on average, four times higher. How does that compare to other breast cancer risk factors? If you go on hormone replacement for five years, you can bump up your breast cancer risk by 30%. If you take birth control pills for more than a dozen years, your risk may go up by 40%. If you’re obese when you’re older, your risk can go up by 60%. Having a first-degree relative with breast cancer may double your risk. But having your breast infected with bovine leukemia virus may quadruple your risk, as you can see below and at 2:16 in my video Breast Cancer and the Bovine Leukemia Virus in Meat and Dairy.The only risk factors more potent than BLV infection were having the BRCA gene mutation, like Angelina Jolie has, or a high dose of ionizing radiation, like being in the wrong place at decidedly the wrong time, like Hiroshima and Nagasaki during World War II.

Beyond confirmation, one study suggested that older patients had a greater likelihood of testing positive for bovine leukemia virus. That makes sense if BLV is from exposure to dairy and meat. The older we get, the more meals we’ve had—and the more opportunities to become infected over time. Researchers also discovered that the virus comes first, before the cancer diagnosis; they found it was present in some breast tissues 3 to 10 years before cancer was found. “This argues against the idea of viral invasion of already malignant cells,” quashing the theory that maybe the virus is somehow just attracted to the cancer after the fact. Could this explain the consistent findings that breast cancer tissue is more likely to harbor infection? Again, the data showed no — the virus appeared to come first. While the review doesn’t provide absolute proof that BLV is a cause of breast cancer, based on the best available balance of evidence, BLV infection does indeed appear to be a risk factor for breast cancer.

The latest revelation is that BLV has now been found in human blood, too. This has a number of potential ramifications. Blood banks, for example, don’t screen for it. So, it’s possible you can get it from consuming meat or dairy, as well as from getting blood from someone who consumed meat or dairy. This could also mean that BLV could cause leukemia in people. It does in chimpanzees. Two infant chimps were fed milk from cows naturally infected with BLV, and both died of leukemia. We didn’t even know chimps could get leukemia. This certainly suggests the possibility of transmission or induction of leukemia through the ingestion of milk from BLV-infected cows, or blood-borne spread could carry the virus to other organs. In cattle, the virus causes blood cancers, but this may be just because dairy cattle are slaughtered and turned into hamburger when they are still so young, so maybe they don’t have time for tumors to grow in other organs.

How concerned should we be about bovine leukemia virus? “It is not clear whether this is a good news story or a bad news story.” If future studies show that BLV does cause breast cancer in people, there will be significant repercussions for the dairy and cattle industries. But that means there is something we can do about it. Perhaps action should be taken now to eradicate the infection from cattle, rather than waiting for a final verdict. Twenty-one nations have already eradicated BLV from their dairy cattle. In contrast, the BLV prevalence in the United States just keeps increasing. If industries are not going to step up and try to eliminate the disease, then the least they could do is eliminate some of the practices that spread the disease between animals.

BLV is spread via blood through contaminated needles, saw or gouge dehorners, ear taggers, hoof knives, tattoo pliers, nose tongs, and other tools of the agribusiness trade. Though “in view of the emerging information about BLV in human breast cancer, it is prudent to encourage the elimination of BLV in cattle, particularly in the dairy industry.” The hope is that, either way, it may help reduce the scourge of breast cancer.

Doctor’s Note

If you missed the previous video, see Bovine Leukemia Virus as a Cause of Breast Cancer.

Avoiding infectious risks like BLV is another advantage of making meat without animals. See my video, The Human Health Effects of Cultivated Meat: Food Safety.

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May 8, 2026
Could Bovine Leukemia Virus be a Cause of Breast Cancer?

As many as 37% of breast cancer cases may be attributable to exposure to the bovine leukemia virus.

The incidence of breast cancer continues to increase worldwide. In the United States, this amounted to a 40% increase in the incidence by the turn of the century. Presently, the main approach to preventing mortality is early detection and treatment. That’s important, but why not focus more on primary prevention—protecting people from risk factors so they don’t develop breast cancer at all?

“Overall, it is estimated that 20% of all human cancers have an infectious origin.” Viruses can trigger cancer by turning on cancer genes or turning off cancer-suppressing genes, but they can also contribute to tumor formation just by causing chronic inflammation. Currently, cancer-causing viruses are considered “the major plausible hypothesis for a direct cause of human breast cancer.” How did we get here?

It all started about 40 years ago when a professor of virology at UC Berkeley learned how the mammary tumor virus was discovered in mice. Scientists switched baby mouse pups from mothers with a high incidence of mammary cancer with the babies from mouse strains with a low incidence and found that the cancer incidence in pups matched their foster mothers’—not their biological ones’—showing it wasn’t genetic. “It occurred to me that humans are foster nursed on the cow,” the professor said.

Bovine leukemia virus (BLV) had just been identified as a cancer-causing cow virus. At the time, only about 10% of U.S. dairy cows were infected, but now it’s closer to half. Initially, 66% of herds were affected. Then, it was more like 80%, based on their milk testing positive for the virus, and 100% of the herds in the larger industrial farms. And now, more than 94% of U.S. herds are affected, continuing the historical trend of BLV persistently proliferating within U.S. dairy herds.

We’ve long known that people in countries that consume the most milk have the highest breast cancer incidence. But, as you can see below and at 2:32 in my video, Bovine Leukemia Virus as a Cause of Breast Cancer, the link between dairy consumption and breast cancer incidence isn’t only on the country level.Individual women who are lactose intolerant and consume less dairy also seem to have decreased risk of breast cancer. Milk contains many things that could be contributing to the cancer risk, such as saturated fat and the presence of cancer-promoting growth hormones like IGF-1.

Yes, we know bovine leukemia virus is present in beef and dairy products. About half of the milk and meat samples turn up positive for the virus. In fact, you can sample the virus straight out of the air on dairy farms, on surfaces, and in the milk itself. Most milk is pasteurized, but many dairy products, like raw, aged cheeses, are not. And who hasn’t eaten a pink-in-the-middle hamburger at some point in their life?

Yes, we have evidence that people are exposed to the virus. Yes, we have evidence that people are actively infected with the virus. But it wasn’t until 2015 that we learned infection rates were highest in cancerous breast tissue, as you can see below and at 3:30 in my video.So much so that as many as 37% of breast cancer cases may be attributable to exposure to the bovine leukemia virus.

That was enough for me to make a whole series of videos on the role the virus plays in breast cancer and how the meat and dairy industries responded to the news. What’s the latest update? That’s what I’ll cover next.

Doctor’s Note

You may remember that I’ve previously discussed The Role of Bovine Leukemia in Breast Cancer and the Industry Response to Bovine Leukemia Virus in Breast Cancer.

Stay tuned for the next video: Breast Cancer and the Bovine Leukemia Virus in Meat and Dairy.

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May 6, 2026
Hidden Gut Virus Inside a Common Bacterium May Double Colon Cancer Risk and Could Become a Future Stool-Based Screening Marker

Hidden viruses in the gut are emerging as a new frontier in cancer research, and the virome may be just as important as bacteria when it comes to colorectal cancer risk. A newly described bacteriophage hiding inside common Bacteroides bacteria has been linked to roughly doubled odds of developing colorectal cancer, and it may one day serve as a non‑invasive stool biomarker for earlier detection.

This finding is pushing scientists to look beyond bacteria alone and consider how viral communities in the intestine shape health and disease.

Colorectal Cancer and the Need for Better Screening

Colorectal cancer starts in the colon or rectum, usually from small polyps that can become malignant over many years.

Because early stages often cause no symptoms, detection before spread is crucial for survival and treatment success. When found early, colorectal cancer is usually much more treatable and associated with better long‑term outcomes.

Current screening tools include colonoscopy, sigmoidoscopy, fecal occult blood tests (FOBT/FIT), and stool DNA tests. Colonoscopy is highly effective but invasive, requires bowel preparation, and can be difficult to access for some people.

Stool‑based tests are simpler and non‑invasive, but they can miss early cancers or advanced polyps. These limitations drive interest in new stool biomarkers, including those that come from the gut virome, bacteriophages, and specific Bacteroides strains.

Microbiome, Virome, and Cancer Risk

Most research on colorectal cancer and the gut has focused on the microbiome, the community of bacteria in the intestine. Studies repeatedly show that certain bacteria, such as Fusobacterium and some Bacteroides species, are more common in people with colorectal cancer than in healthy controls.

These microbes may promote inflammation, produce toxins, or form biofilms that help tumors develop and escape immune defenses.

Alongside bacteria, the gut also hosts a rich virome, made up largely of bacteriophages, viruses that infect bacteria, not human cells. Bacteriophages can integrate into bacterial genomes (as prophages) or lyse their hosts. In doing so, they can change which bacteria are present and how they behave.

A bacterium carrying a particular prophage may produce more toxins, adhere more strongly to the gut lining, or interact differently with the immune system.

Because of these effects, the virome is now seen as an important factor in colorectal cancer. Distinct bacteriophage patterns have been observed in stool samples from colorectal cancer patients.

These patterns suggest that certain phages, especially those linked to Bacteroides, could act as both contributors to disease and as stool biomarkers that signal increased risk.

Bacteroides fragilis and a Hidden Bacteriophage

Bacteroides is a major bacterial genus in the human colon and plays key roles in digestion and immune development. Among its species, Bacteroides fragilis is widely present in healthy individuals.

Most strains are harmless or beneficial, but some enterotoxigenic Bacteroides fragilis (ETBF) strains produce toxins that can cause diarrhea and chronic inflammation.

Recent work has revealed a previously unrecognized bacteriophage integrated into Bacteroides fragilis genomes. In its prophage state, this virus sits quietly inside the bacterial DNA and is not visible as an active infection.

Using high‑throughput sequencing of bacterial isolates and stool samples, researchers identified a specific viral sequence that appeared far more often in Bacteroides fragilis from people with colorectal cancer than in those without the disease.

This suggests that the combination of Bacteroides and a particular bacteriophage may matter more than the bacterium alone.

How Strong Is the Association With Colorectal Cancer?

Across large international cohorts, individuals with colorectal cancer were about twice as likely to carry this Bacteroides‑associated bacteriophage compared with cancer‑free controls.

This does not prove that the virus causes cancer, but it signals a strong association worth further study. It raises the possibility that the bacteriophage could affect bacterial virulence, toxin production, or interactions with the gut lining in ways that promote tumor development.

Mechanistically, researchers suspect that prophage integration might alter gene regulation in Bacteroides fragilis, increase production of inflammatory or genotoxic factors, or encourage biofilm formation on the colon mucosa.

Even if the virus itself is not directly oncogenic, it may mark a broader virome and microbiome shift that creates a more cancer‑prone environment. From a screening perspective, this kind of consistent association is valuable, because a reliable marker can help identify people at higher risk.

Virome-Based Stool Biomarkers: A New Screening Frontier

Stool is an ideal medium for non‑invasive testing because it contains DNA and RNA from bacteria, viruses, and the host. Traditional stool tests for colorectal cancer look for blood or human DNA mutations.

Microbiome‑based approaches add information about bacterial composition. Virome‑based testing extends this by targeting bacteriophages and other gut viruses as additional indicators.

Bacteriophages are attractive stool biomarkers because they are abundant and often highly specific to their bacterial hosts. A virome‑focused assay could, in principle, detect the Bacteroides‑associated bacteriophage linked to colorectal cancer.

This could be done with broad metagenomic sequencing or with targeted PCR approaches that look specifically for the viral sequence.

In real‑world use, such a viral marker would likely be combined with bacterial, human DNA, and blood‑based markers in a multi‑parameter stool test, improving sensitivity for early disease while maintaining acceptable false‑positive rates.

Before any virome‑based stool biomarker becomes part of standard care, it must be validated in large prospective studies, tested across diverse populations, and shown to be cost‑effective and practical in routine clinics. Laboratory methods will need standardization, and regulatory approval will be required.

Virome-Driven Advances in Colorectal Cancer Prevention

The emerging link between the gut virome, specific bacteriophages, Bacteroides, and colorectal cancer underscores how complex the intestinal ecosystem is. As research continues, virome‑based stool biomarkers may complement colonoscopy and existing stool tests, offering more personalized and less invasive screening options.

If the Bacteroides‑associated bacteriophage consistently identifies individuals at higher risk, an accessible stool biomarker built around this virome signal could help detect colorectal cancer earlier and guide timely prevention and treatment.

Frequently Asked Questions

1. Can changing my diet modify the gut virome and possibly affect colorectal cancer risk?

A diet rich in fiber, fruits, and vegetables can shift both the microbiome and virome toward more diverse, stable communities, which is generally associated with lower inflammation and may indirectly reduce colorectal cancer risk.

2. Is it possible to remove harmful bacteriophages like the one in Bacteroides with probiotics?

Current probiotics mainly influence bacteria, not specific bacteriophages; while they might alter the overall ecosystem, there is no evidence yet that standard probiotic products selectively remove this Bacteroides‑associated virus.

3. Could antibiotics help by eliminating Bacteroides strains carrying cancer‑linked bacteriophages?

Broad antibiotics can reduce Bacteroides and associated phages, but they also disrupt beneficial microbes and may harm long‑term gut health, so they are not considered a targeted or preventive strategy for colorectal cancer.

4. Are at-home microbiome tests able to detect virome patterns linked to colorectal cancer?

Most consumer microbiome kits focus on bacterial DNA and do not comprehensively profile the virome, so they cannot reliably detect cancer‑associated bacteriophage signatures at this time.

Originally published on Science Times

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April 24, 2026
Understanding Cancer and Why Some Types are More Common Than Others

Cancer affects millions of people each year, and a large share of these cases come from just a few types: breast, prostate, lung, and colon cancer. These cancers are common because they involve large, hormonally active organs that are exposed to everyday lifestyle and environmental factors over many years.

Understanding why they occur so often helps explain the statistics and highlights where prevention and early detection matter most.

What Makes a Type of Cancer “Common”?

When a cancer is called “common,” it usually means it causes many new cases in a population each year or carries a high lifetime risk. Breast, prostate, lung, and colon cancer rank near the top in many countries, especially where people live longer and lifestyles include less movement and more processed foods.

Aging is crucial, because cells that divide over many decades have more chances to accumulate DNA damage that can lead to cancer.

Organs such as the breast, prostate, lung, and colon are biologically active and constantly exposed. Breast and prostate tissues respond strongly to hormones, while lungs and the colon directly contact air, smoke, pollutants, and food contents.

Over time, repeated injury and repair in these tissues increase the odds that abnormal cells will appear. Screening programs that focus on these organs also make them more visible in cancer statistics, as early and mild cases are more likely to be found.

Breast Cancer Basics

Breast cancer begins when cells in the breast grow in an uncontrolled way, often starting in ducts or lobules that carry or produce milk. It is the most frequently diagnosed cancer in women worldwide, and its high numbers reflect both widespread breast tissue and longer life expectancy.

Hormonal exposure is a major factor. Longer lifetime exposure to estrogen and progesterone, through early menstruation, late menopause, or hormone therapy, can raise risk.

Family history and inherited gene changes also matter. Lifestyle factors such as obesity, alcohol use, and lack of physical activity further influence breast cancer risk.

While not all risk can be removed, maintaining a healthy weight, limiting alcohol, exercising, and following recommended mammography schedules support earlier detection and lower overall risk.

Prostate Cancer Basics

Prostate cancer develops in the prostate gland, which sits below the bladder and contributes to seminal fluid in men. It is one of the most common cancers in men, with risk rising sharply with age. Many older men develop small prostate cancers, though not all will progress to serious disease.

Male sex hormones (androgens) strongly affect prostate cells. Over decades, hormonal stimulation and cell turnover increase the chances that harmful mutations will arise. A family history of prostate cancer and inherited gene changes raise risk further. Diet, obesity, and chronic inflammation may also play a role.

Screening with prostate-specific antigen (PSA) tests and examinations can detect prostate cancer earlier, but there is ongoing discussion about balancing early detection with the risk of overdiagnosis and overtreatment, according to the Centers for Disease Control and Prevention.

Lung Cancer Basics

Lung cancer starts in cells of the lungs, usually in the airways or air sacs. It is among the most common cancers globally and a leading cause of cancer-related death. Its frequency is closely tied to tobacco use, although air pollution, occupational exposures, and radon also contribute.

Because lungs are in constant contact with inhaled air, they are directly exposed to harmful substances over long periods.

Smoking remains the dominant cause of lung cancer. The carcinogens in cigarette smoke repeatedly damage lung cells, and the repair process can lock DNA damage into permanent mutations. Secondhand smoke and other pollutants also increase risk.

People who never smoke can still develop lung cancer, but patterns of disease follow smoking rates in most populations. Avoiding tobacco, supporting smoke-free environments, and seeking medical review for persistent cough or breathing changes are key steps for lowering risk and improving early detection.

Colon Cancer Basics

Colon cancer, often grouped with rectal cancer as colorectal cancer, affects the large intestine, where water is absorbed and waste forms. It is one of the most common cancers and a leading cause of cancer death, yet it is also highly preventable through screening.

The cells lining the colon are exposed for hours each day to digested food and its byproducts. Diets high in red and processed meat and low in fiber, combined with obesity, inactivity, alcohol use, and smoking, all raise colon cancer risk.

Age is a major driver, with most cases historically occurring after 50, though rates in younger adults are rising in some regions. Screening tests such as colonoscopy and stool-based checks can identify and remove precancerous polyps, preventing many cases of invasive colon cancer, as per Mayo Clinic.

Why These Four Cancers Are So Common

Breast, prostate, lung, and colon cancer share several risk patterns. Tobacco use, excess body weight, low physical activity, alcohol consumption, and diets rich in processed foods all contribute to multiple cancer types.

These lifestyle factors act on tissues that are hormone-sensitive or constantly exposed to environmental influences, especially as people age.

These cancers are also the focus of many research and screening efforts, which increases detection of early-stage disease.

Only a portion of risk is strictly inherited; in most people, genes, environment, and lifestyle interact. Although no single measure can fully prevent cancer, changes at the individual and population levels can meaningfully reduce the burden of breast, prostate, lung, and colon cancer.

Taking Charge of Cancer Risk: Breast, Prostate, Lung, and Colon Cancer Awareness

Cancer will remain a major health challenge, and breast, prostate, lung, and colon cancer will continue to represent a large share of diagnoses.

Still, understanding why these cancers are so common highlights the importance of avoiding tobacco, staying active, maintaining a healthy weight, choosing more whole foods and fewer processed meats, and limiting alcohol.

Awareness of how cancer develops in the breast, prostate, lung, and colon helps people make more informed choices about screening and everyday habits. Following recommended mammograms, colon tests, and appropriate prostate or lung screening where indicated can lead to earlier detection and better outcomes.

Keeping cancer, including breast, prostate, lung, and colon cancer, in mind as part of long-term health planning opens room for prevention, vigilance, and timely care.

Frequently Asked Questions

1. Can someone have more than one of these cancers in their lifetime?

Yes. A person can develop more than one primary cancer, either at the same time or years apart, especially if they have strong genetic risk factors, significant lifestyle exposures, or are living longer after successful treatment.

2. Do breast, prostate, lung, and colon cancer share any warning signs?

They each have specific symptoms, but shared warning signs can include unexplained weight loss, persistent fatigue, and pain that does not improve. Any ongoing change in the body that is unusual for the person should be checked by a doctor.

3. Is it possible to have cancer without any symptoms?

Yes. Early-stage breast, prostate, lung, or colon cancer may cause little or no noticeable symptoms. This is one reason screening tests are recommended for people in certain age or risk groups.

4. Does regular exercise lower the risk of all four of these cancers?

Regular physical activity is linked to a lower risk of several cancers, including breast and colon cancer, and it helps manage weight and hormone levels. While it cannot remove risk completely, it is a useful, broad protective factor.

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April 17, 2026
Fighting Cancer with Whole Plant Foods
The foundation of cancer prevention is plants, not pills.

“The vast majority of cancer research is devoted to finding cures, rather than finding new ways to prevent disease. The results of these skewed priorities are plain to see.” It’s been nearly 55 years since President Richard Nixon declared war on cancer, yet deaths from the most common cancers in the United States have continued unabated.

“We have been looking at the very nature of cancer in the wrong way. Breast cancer doesn’t begin when a lump is first felt or detected by a mammogram. All the common epithelial cancers (lung, colorectal, breast, prostate, pancreas and ovary), which account for the majority of deaths, have a long latency period—often 20 years or more.” So, it’s not like you were healthy one day, then got cancer the next. You haven’t been healthy—you’ve had cancer growing in you for decades. Indeed, there’s a “bizarre misperception that people are ‘healthy’ until they have actual symptoms of invasive cancer,” but “the barn in which hay is smoldering before it bursts into flames is not a safe place.”

So, what does this professor of pharmacology I’ve been quoting recommend? Drugs, of course. Chemoprevention—putting people on drugs to prevent cancer. The pharmaceutical industry spends tons of money promoting chemoprevention of heart disease and strokes with statins and blood thinners, so why shouldn’t people take drugs every day for the rest of their lives to protect against cancer?

There has to be a better way.

What about using diet and nutrition to prevent and treat cancer? Well, what kind of cancer? There are more than 200 types. But here’s the key: They all share the same hallmarks. In a series of papers cited more than 40,000 times in the biomedical literature, 10 hallmarks of cancer have been identified:
- Increased sensitivity to growth factors
- Evading your body’s tumor suppressors
- Dodging your immune system
- Being able to grow forever
- Tumor-promoting inflammation
- The ability to invade and spread
- The ability to hook up its own blood supply
- The accumulation of DNA mutations
- Disarming the self-destruct mechanisms in place
- Hijacking the cell’s metabolism
And, of course, there are classes of drugs to try to counter each one—chemotherapy agents designed to target each piece of the cancer puzzle. You can see them below and at 2:27 in my video Fighting the Ten Hallmarks of Cancer with Food.

Now, ideally, there would be drugs able to target multiple hallmarks at one time, but that’s not how drugs tend to work. Indeed, “this need to target multiple hallmarks is one of the major reasons why, in the context of cancer research, there are many proponents of investigating plant foods as they can deliver a cocktail of bioactive compounds” that may target most, if not all, of the hallmarks of cancer. Below and at 3:00 in my video, you can see a sampling of compounds found in fruits and vegetables—such as berries, greens, and broccoli—shown to be able to target each of the 10 hallmarks of cancer, at least in a petri dish.

Furthermore, they have the qualities of an ideal chemopreventive agent. If you were to design the perfect candidate, you’d want them to be selective to cancerous or precancerous cells while leaving normal cells alone, be side-effect-free, target most types of cancers, be able to be consumed in a daily diet, be conveniently available almost everywhere, and be relatively inexpensive to boot. Plants meet all these criteria. No wonder people who eat more plant-based foods tend to have lower cancer rates.

To be clear, we aren’t talking about taking supplements containing extracts or puriﬁed phytochemicals, but rather eating whole plant foods themselves—more of a food system–based approach to targeting the hallmarks of cancer. Foods contain thousands of substances that result in vast numbers of possible interactions, yet much of nutritional science “has long been directed towards the impact of single dietary components.” Yes, this kind of reductionist approach can uncover the role of foods or even individual nutrients in disease development, but let’s think about what the optimal research strategy would be to study the effects of bioactive natural plant compounds on disease prevention. Instead of using isolated phytochemicals to manage cancer, why not try whole foods? Sometimes the whole can be greater than the sum of its parts, a concept known as food synergy.

Check out this study involving the simultaneous inhibition of a series of cancer stages in breast cancer cells using a phytochemical supercocktail. Two breast cancer cell lines were treated with six different plant compounds individually, and then all together, at levels typically found in the bloodstream after eating foods like broccoli, grapes, soybeans, and turmeric. And while the compounds were ineffective individually, together they significantly suppressed breast cancer cell proliferation by more than 80%, inhibited cancer cell invasion and migration, stopped the cancer cells in their tracks, and eventually killed them all off. The plant compounds did all this without having any deleterious effects on the normal noncancerous cells used as control.

No wonder the foundation of cancer prevention—based on an update of the most extensive report on diet and cancer ever published—is not pills, but plants, as you can see below and at 5:28 in my video.

In other words, cut down on alcohol, soda, meat, and processed junk, and center your diet around whole grains, vegetables, fruits, and beans.

Doctor’s Note

I have dozens of videos on cancer prevention and treatment. Check the related posts below.
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March 11, 2026
Can It Lower Your Cancer Risk?

Does choosing organic over conventional foods protect against cancer? What are the effects of pesticides on cancer risk?

In a review updating the evidence on human exposure and toxicity of pesticides, the body of evidence linking pesticide exposure and cancer is said to be so massive that pesticides’ role in the development of cancer “cannot be doubted.” However, most of the evidence that shows DNA damage from pesticides is from occupational exposure among farmers and workers in the fields, the pesticide industry itself, or those living in high-spray areas, as you can see at 0:35 in my video Pesticides and Cancer Risk.

There is evidence linking non-occupational pesticide exposure to DNA damage—in this case, single- and double-stranded DNA fragmentation in the sperm of men with higher levels of pesticides flowing through their bodies—but that was in China, where the average pesticide concentrations are as much as four times higher than in some other parts of the world.

Another way pesticides could potentially facilitate tumor growth is through adverse eﬀects on anticancer immunity. Natural killer (NK) cells are our body’s first line of white blood cell defense against cancer cells and virus-infected cells. Pesticides have been shown to induce harmful eﬀects on these defender cells, reducing their ability to kill off tumor cells. For example, if you put a bunch of NK cells in a petri dish along with human leukemia cells without any pesticide, your natural killer cells can clean house and wipe out more than half the cancer. But if you drip a tiny bit of pesticide on them, the NK cells are so disabled that the cancer wins the day, as you can see below and at 1:37 in my video.

But how much pesticide are we talking about? The researchers used the maximum level found in people actively spraying pesticides. But what about looking at just the residual pesticides left on conventional produce? Is choosing organic for cancer prevention worth the investment?

Pesticides are detectable in the blood and urine of more than 90% of the U.S. population, regardless of where they work or live. We know it’s from the food we eat because crossover trials where people are switched between consuming conventionally grown foods and organic foods show you can turn on and off urinary concentrations of pesticide metabolites like a light switch. But that doesn’t necessarily mean the pesticides are harming us.

The health consequences of ingesting pesticide residues from conventionally grown foods remain unknown, but a recent study did find that people who self-reported the highest frequency of organic food consumption had about a 25% lower risk of getting cancer. The study is the first of its kind to evaluate the association between frequency of organic food consumption and cancer risk, controlling for a wide array of other factors. Doesn’t it matter that consumers eating organic are younger? The researchers controlled for that and still found significantly lower cancer risk. But maybe organic consumers get less cancer because they are more affluent or more highly educated or skinnier, or maybe they exercise more or eat less meat or smoke less. No, the researchers controlled for all that and still found significantly lower cancer risk in organic consumers. Maybe their diets were different in other ways, though—more fruits and vegetables overall, or less junk food? No, they still found significantly lower cancer risk. The researchers concluded, “Our results indicate that higher organic food consumption is associated with a reduction in the risk of overall cancer.”

That was the most sophisticated study of its type to date, but there was an earlier study that was even bigger, and little evidence was found for a decrease in the incidence of all cancers except for perhaps one kind of blood cancer—non-Hodgkin lymphoma. You can see the data below and at 3:59 in my video.

The data show no difference in cancer overall between those who never choose organic and those who usually or always do; the only significant findings were a lower risk of non-Hodgkin lymphoma and an increased risk of breast cancer. Is it possible that women who choose organic food are more conscientious about getting screened for breast cancer, and that explains the higher diagnosis rate? We really don’t know.

Of course, what we care about the most is not just cancer but all-cause mortality—the risk of dying prematurely. As it turns out, higher blood levels of a pesticide known as beta-hexachlorocyclohexane are associated with living a significantly shorter life. How do we cut down on our levels? Decades ago, there was a study that found that the breast milk of a vegetarian mother had less beta-hexachlorocyclohexane than the milk of her non-vegetarian sister, who was also breastfeeding at the time. The vegetarian sister apparently had levels of that pesticide that were lower by about a third, compared with her omnivorous sibling, as you can see below and at 4:48 in my video.

That’s no surprise, since this class of chlorinated pesticides is fat-soluble, so they’re found most frequently in foods of animal origin.

A more recent study failed to look at beta-hexachlorocyclohexane, but it examined polychlorinated biphenyls (PCBs) and found that they were linked to increased mortality risk. Again, the toxins were found in the same kinds of foods: eggs, dairy products, and animal fats. So, it’s no surprise that the blood of those eating vegan was found to be “signiﬁcantly less polluted than omnivores” in terms of a whole series of PCBs, including those found in the study to be associated with increased mortality; but the vegans did not have lower levels of beta-hexachlorocyclohexane.

The bottom line: If you’re worried about the adverse health effects of pesticides and pesticide-type compounds, you may want to lower your intake of animal products. But when it comes to fruits and vegetables, the benefits of eating conventionally grown produce likely outweigh any possible risks from pesticide exposure. So, concerns about pesticide risks shouldn’t discourage us from stuffing our faces with as many fruits and vegetables as possible. That would give us a huge health benefit, whereas the potential lifelong damage of any pesticides on those same fruits and veggies has been estimated to cut only a few minutes off a person’s life, on average, which is nothing compared to the nutritional beneﬁts of eating more fruits and vegetables.

Doctor’s Note

For more on organic foods, see related posts below.

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March 6, 2026
The Effects of Fasting on Cancer

Ever since the days of Hippocrates, 2,400 years ago, fasting has been offered as a treatment for acute and chronic diseases, based on the observation that when people get sick they frequently lose their appetite.

Along with fever, decreased food consumption is one of the most common signs of infection. Often regarded as an undesirable manifestation of sickness, it’s actually an active, beneficial defense mechanism. As I discuss in my video Fasting for Cancer: What about Cachexia, chronic under-nutrition can impair our defenses, but data suggest that, in the short-term, immune function can be enhanced by lowering food intake.

Researchers have shown that the blood from starved mice was nearly eight times better at killing off the invading bacteria in a petri dish, dramatically boosting the capacity of their white blood cells to kill off the pathogens. What about people? And what about cancer?

Does Fasting Help Our Natural Killer Cells Fight Cancer Cells?

When study participants fasted for two weeks on an 80-calorie-a-day diet, not only did their white blood cells show the same kind of boost in bacteria-killing ability and antibody production, but their natural killer cell activity increased by an average of 24%. This is especially interesting because our natural killer cells don’t just help clear infections, but they also kill cancer cells. In fact, that’s how the researchers measured natural killer cell activity; they pitted them against K562 cells, which are human leukemia cells.

Fasting is said to improve anticancer immunosurveillance, or, more poetically, by “stimulating the appetite of the immune system for cancer.” So, why isn’t fasting used more to treat cancer? Because so much about cancer care revolves around keeping people’s weight up to try to counteract the cancer-wasting syndrome.

What Causes Cancer Cachexia?

Until recently, fasting therapy was not considered to be a treatment option in cancer, related to the fact that a common therapeutic goal in palliative cancer treatment is to avoid weight loss and counteract the wasting syndrome known as cachexia, which is the ultimate cause of death in many cancer cases.

Tumors are voracious, rapidly expanding and in need of a lot of energy and protein, so cancer metabolically reprograms the body to start breaking down to feed its tumors. It does this by triggering inflammation throughout the body. It’s not just that people lose their appetite. “The fundamental difference between the weight loss observed in CC [cancer cachexia] and that seen in simple starvation is the lack of reversibility with feeding alone.”

Therapeutic nutritional interventions to correct or reverse cachexia frequently fail. The best treatment for cancer cachexia, therefore, is to treat the cause and cure the cancer. In fact, maybe forcing extra nutrition on cancer patients could be playing right into the tumor’s hands. Like in pregnancy when the fetus gets first dibs on nutrients even at the mother’s expense, the tumor may be first in the feeding line. Maybe our loss of appetite when we get cancer is even a protective response.

Is Chemotherapy Enough?

As I discuss in my video Fasting Before and After Chemotherapy and Radiation, for the past 50 years, chemotherapy has been a major medical treatment for a wide range of cancers. Its main strategy has been largely based on targeting cancer cells, by means of DNA damage caused in part by the production of free radicals. Although these drugs were first believed to be very selective for tumor cells, we eventually learned that normal cells also experience severe chemotherapy-dependent damage, which can lead to dose-limiting side effects, including bone marrow and immune system suppression, fatigue, vomiting, diarrhea, and in some cases, even death.

If you do survive chemotherapy, the DNA damage to normal cells can even lead to new cancers down the road. There are cell-protecting drugs that have been tried to reduce the side effects so you can pump in higher chemo doses, but these drugs have not been shown to increase survival––in part because they may also be protecting the cancer cells. What about instead fasting for cellular protection during cancer treatment?

Fasting and Chemotherapy

Many may not recognize the role fasting can play in cancer prevention and treatment. Short-term fasting before and immediately after chemotherapy may minimize side effects, while, at the same time, it may actually make cancer cells more sensitive to treatment. That’s exciting!

During deprivation, healthy cells switch from growth to maintenance and repair, but tumor cells are unable to slow down their unbridled growth, due to growth-promoting mutations that led them to become cancer cells in the first place. This inability to adapt to starvation may represent an important Achilles’ heel for many types of cancer cells.

As a consequence of these differential responses of healthy cells versus cancer cells to short-term fasting, chemotherapy causes more DNA damage and cell suicide in tumor cells, while potentially leaving healthy cells unharmed. Thus, short-term fasting may protect healthy cells against the toxic assault of chemotherapy and cause tumor cells to be more sensitive––or at least that’s the theory.

Researchers found that, in rodents, fasting alone appears to work as well as chemotherapy. What’s more, unbridled tumor growth was also knocked down by radiation therapy—and even more so after the combination of radiation and alternate-day fasting. However, alternate-day fasting alone seemed to do as well as radiation. These data are exciting, but for mice with breast cancer. What about people?

Fasting Put to the Test Against Cancers

As I discuss in my video Fasting Before and After Chemotherapy Put to the Test, several patients diagnosed with a wide variety of cancers elected to undertake fasting prior to chemotherapy and share their experiences. They reported a reduction in fatigue, weakness, and gastrointestinal side effects while fasting and felt better across the board, with zero vomiting. The weight lost during the few days of fasting was quickly recovered by most of the patients and did not lead to any discernable harm. So, overall, fasting under care seems safe and potentially able to ameliorate side effects.

In a randomized clinical study, breast and ovarian cancer patients fasted from 36 hours before chemotherapy until 24 hours after, and fasting did appear to improve quality of life and fatigue. However, another study found no such beneficial effects. There did appear to perhaps be less bone marrow toxicity, given the higher counts of red blood cells and platelet-making cells. But no benefit when it came to saving white blood cells—the immune system cells—so that was a disappointment. Perhaps they didn’t fast long enough?

A systematic review of 22 studies found that, overall, fasting may not only reduce chemotherapy side effects (like organ damage, immune suppression, and chemotherapy-induced death), but it may also suppress tumor progression, including tumor growth and metastasis, resulting in improved survival. But, nearly all the studies were on mice and dogs. The studies on humans were limited to evaluating safety and side effects. The tumor-suppression effects of fasting––for example, its influence on tumor growth, metastasis and prognosis––sadly, were not evaluated.

Does Fasting Make Chemo More Effective?

As I discuss in my video Fasting-Mimicking Diet Before and After Chemotherapy, short-term food withdrawal during chemotherapy may begin to solve the long-standing problem with most cancer treatments: how to kill the tumor without killing the patient. Short-term fasting––for example, for 48 hours before chemo and 24 hours afterwards––may reduce side effects, so-called “chemotherapy-induced toxicity.” However, the potential tumor-suppressing effects of fasting have still not been thoroughly evaluated.

Some argue that reducing chemo’s side effects alone could improve efficacy, since patients could withstand higher doses. For example, the heart and kidney damage associated with the widely prescribed anti-cancer drugs limit their full therapeutic potential. It’s not clear, though, that maximizing the tolerated chemo dose would achieve longer survival or better quality of life. For now, I think we should just be satisfied with the fewer side effects for fewer side effects’ sake.

How Does Fasting Work?

Fasting can reduce the levels of insulin-like growth factor-1 (IGF-1), a cancer-promoting growth hormone. The reduced levels of IGF-1 mediate the differential protection of normal cells and cancer cells in response to fasting and improve chemo’s ability to kill cancer but spare normal cells.

So, reducing IGF-1 signaling may provide dual benefits by protecting normal tissues while reducing tumor progression. It may even help prevent the cancer in the first place. But fasting isn’t the only way to drop IGF-1 levels: A few days of fasting can cut levels in half, but that’s largely because protein intake is being cut. Protein is a key determinant of circulating IGF-1 levels in humans––suggesting that “reduced protein intake may become an important component of anticancer and antiaging dietary interventions,” particularly a reduction in animal protein.

Lowering Protein Intake to Lower IGF-1

If you compare those who eat strictly plant-based diets and get about the recommended daily intake of protein (0.8 grams per kg of body weight) to individuals who are just as slender but consume the higher amount of protein more typical to Americans, going on a calorie-restricted diet may lower IGF-1 a little, but eating a plant-based diet can lower it even more than going low calorie.

So, not only may a diet centered around whole plant foods down-regulate IGF-1 activity, potentially slowing the aging process, but it may be a way of turning anti-aging genes against cancer.

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December 10, 2025
Prostate Cancer and Mushrooms

What can reishi mushrooms, shiitake mushroom extracts, and whole, powdered white mushrooms do for cancer patients?

“A regular intake of mushrooms can make us healthier, fitter, and happier, and help us live longer,” but what is the evidence for all that? “Mushrooms are widely cited for their medicinal qualities, yet very few human intervention studies have been done using contemporary guidelines.”

There is a compound called lentinan, extracted from shiitake mushrooms. To get about an ounce, you have to distill around 400 pounds of shiitakes, about 2,000 cups of mushrooms. Researchers injected the compound into cancer patients to see what happens. The pooled response from a dozen small clinical trials found that the objective response rate was significantly improved when lentinan was added to chemotherapy regimens for lung cancer. “Objective response rate” means, for example, tumor shrinkage, but what we really care about is survival and quality of life. Does it actually make cancer patients live any longer or any better? Well, those in the lentinan group suffered less chemo-related toxicity to their gut and bone marrow, so that alone might be reason enough to use it. But what about improving survival?

I was excited to see that lentinan may significantly improve survival rates for a type of leukemia. Indeed, researchers found that adding lentinan to the standards of care increased average survival, reduced cachexia (cancer-associated muscle wasting), and improved cage-side health. Wait, what? This was improved survival for brown Norwegian rats, so that the so-called clinical beneﬁt only applies if you’re a rat or a veterinarian.

A compilation of 17 actual human clinical studies did find improvements in one-year survival in advanced cancer patients but no significant difference in the likelihood of living out to two years. Even the compilations of studies that purport that lentinan offers a significant advantage in terms of survival are just talking about statistical significance. As you can see below and at 2:15 in my video White Button Mushrooms for Prostate Cancer, it’s hard to even tell these survival curves apart.

Lentinan improved survival by an average of 25 days. Now, 25 days is 25 days, but we “should evaluate assertions made by companies about the miraculous properties of medicinal mushrooms very critically.”

Lentinan has to be injected intravenously. What about mushroom extract supplements you can just take yourself? Researchers have noted that shiitake mushroom extract is available online for the treatment of prostate cancer for approximately $300 a month, so it’s got to be good, right? Men who regularly eat mushrooms do seem to be at lower risk for getting prostate cancer—and apparently not just because they eat less meat or consume more fruits and vegetables in general. So, why not give a shiitake mushroom extract a try? Because it doesn’t work. On its own, it is “ineffective in the treatment of clinical prostate cancer.” Researchers wrote that “the results demonstrate that claims for CAM [complementary and alternative medicine], particularly for herbal and food supplement remedies, can be easily and quickly tested.” Put something to the test? What a concept! Maybe it should be required before individuals spend large amounts of money on unproven treatments, or, in this case, a disproven treatment.

What about God’s mushroom (also known as the mushroom of life) or reishi mushrooms? “Conclusions: No signiﬁcant anticancer effects were observed”—not even a single partial response. Are we overthinking it? Plain white button mushroom extracts can kill off prostate cancer cells, at least in a petri dish, but so could the fancy God’s mushroom, but that didn’t end up working in people. You don’t know if plain white button mushrooms work on real people until you put them to the test.

What I like about this study is that the researchers didn’t use a proprietary extract. They just used regular whole mushrooms, dried and powdered, the equivalent of a half cup to a cup and a half of fresh white button mushrooms a day, in other words, a totally doable amount. The researchers gave them to men with “biochemically recurrent prostate cancer”—the men had already gotten a prostatectomy or radiation in an attempt to cut or burn out all the cancer, but it returned and started growing, as evidenced by a rise in PSA levels, an indicator of prostate cancer progression.

Of the 26 patients who had gotten the button mushroom powder, 4 appeared to respond, meaning they got a drop in PSA levels by more than 50% after starting the mushrooms, as you can see here and at 4:31 in my video.

In the next graphic, below and at 4:22, you can see where the four men who responded started out in the months leading up to starting the mushrooms. Patient 2 (“Pt 2”) was my favorite. He had an exponential increase in PSA levels for a year, then he started some plain white mushrooms, and boom! His PSA level dropped to zero and stayed down. A similar response was seen with Patient 1. Patient 4 had a partial response, before his cancer took off again, and Patient 3 appeared to have a delayed partial response.

Now, in the majority of cases, PSA levels continued to rise, not dipping at all. But even if there is only a 1-in-18 chance you’ll be like Patients 1 and 2, seen below and at 5:12, you may get a prolonged, complete response that continues.

We aren’t talking about weighing the risks of some toxic chemotherapy for the small chance of benefit, but just eating some inexpensive, easy, tasty plain white mushrooms every day. Yes, the study didn’t have a control group, so it may have just been a coincidence, but rising PSAs in post-prostatectomy patients are almost always indicators of cancer progression. And, what’s the downside of adding white button mushrooms to your diet?

In these two patients, their PSA levels became undetectable, suggesting that the cancer disappeared altogether. They had already gone through surgery, had gotten their primary tumor removed, along with their entire prostate, and had already gone through radiation to try to clean up any cancer that remained, and yet the cancer appeared to be surging back—until, that is, they started a little plain mushroom powder.

Doctor’s Note

If you missed the previous blog, check out Medicinal Mushrooms for Cancer Survival.

Also check out Friday Favorites: Mushrooms for Prostate Cancer and Cancer Survival.

For more on mushrooms, see Breast Cancer vs. Mushrooms and Is It Safe to Eat Raw Mushrooms?.

For more videos on prostate cancer, check the related posts below.

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November 29, 2025
Cancer Survival and Medicinal Mushrooms

Did the five randomized controlled trials of reishi mushrooms in cancer patients show benefits in terms of tumor response rate, survival time, or quality of life?

Can mushrooms be medicinal? Mushroom-based products make up a sizable chunk of the $50 billion supplement market. “This proﬁtable trade provides a powerful incentive for companies to test the credulity of their customers and unsupported assertions have come to deﬁne the medical mushroom business.” For example, companies marketing herbal medicines “exploit references to studies on mice in their promotion of mushroom capsules and throat sprays for treating all kinds of ailments”—but we aren’t mice.

It wouldn’t be surprising if mushrooms had some potent properties. After all, fungi are where we’ve gotten a number of drugs, not the least of which is penicillin, as well as the cholesterol-lowering drug lovastatin and the powerful immunosuppressant drug cyclosporin. Still don’t think a little mushroom can have pharmacological effects? Don’t forget they can produce some of our most powerful poisons, too, like the toxic Carolina false morel that looks rather toadstooly, while others, as you can see here and at 1:15 in my video Medicinal Mushrooms for Cancer Survival, have a more angelic look like the destroying angel—that is its actual name—and as little as a single teaspoon can cause a lingering, painful death.

We should have respect for the pharmacological potential of mushrooms, but what can they do that’s good for us? Well, consuming shiitake mushrooms each day improves human immunity. Giving people just one or two dried shiitake mushrooms a day (about the weight-equivalent of five to ten fresh ones) for four weeks resulted in an increase in proliferation of gamma-delta T lymphocytes and doubled the proliferation of natural killer cells. Gamma-delta T cells act as a ﬁrst line of immunological defense, and, even better, natural killer cells kill cancer. Shiitake mushrooms did all this while lowering markers of systemic inflammation.

Oyster mushroom extracts don’t seem to work as well, but what we care about is whether mushrooms can actually affect cancer outcomes. Shiitakes have yet to show a cancer survival benefit, but what about reishi mushrooms, which have been used as a cancer treatment throughout Asia for centuries?

What does the science say about reishi mushrooms for cancer treatment? A meta-analysis of five randomized controlled trials showed that patients who had been given reishi mushroom supplements along with chemotherapy and radiation were more likely to respond favorably, compared to chemotherapy/radiotherapy on its own. Although adding a reishi mushroom extract improved tumor response rates, “the data failed to demonstrate a signiﬁcant effect on tumour shrinkage when it was used alone,” without chemo and radiation. So, they aren’t recommended as a single treatment, but rather an adjunct treatment for patients with advanced cancer.

“Response rate” just means the tumor shrinks. Do reishi mushrooms actually improve survival or quality of life? We don’t have convincing data suggesting reishi mushroom products improve survival, but those randomized to reishi were found to have “a relatively better quality of life after treatment than those in the control group.” That’s a win as far as I’m concerned.

What about other mushrooms? Although whole shiitake mushrooms haven’t been put to the test for cancer yet, researchers have said that lentinan, a compound extracted from shiitakes, “completely inhibits” the growth of a certain kind of sarcoma in mice. But, in actuality, it only worked in one strain of mice and failed in nine others. So, are we more like the 90% of mouse strains in which it didn’t work? We need human trials—and we finally got them. There are data on nearly 10,000 cancer patients who have been treated with the shiitake mushroom extract injected right into their veins. What did the researchers find? We’ll find out next.

Doctor’s Note

Stay tuned for White Button Mushrooms for Prostate Cancer.

Also check out Friday Favorites: Mushrooms for Prostate Cancer and Cancer Survival.

For more on mushrooms, see Breast Cancer vs. Mushrooms and Is It Safe to Eat Raw Mushrooms?.

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November 26, 2025
Elevating pancreatic cancer care | Dietitian Connection
Exocrine pancreatic insufficiency (EPI) affects many patients with pancreatic cancer, yet it is often overlooked in this patient populations, which leads to malnutrition. In this episode, we are joined by Dr. Shelby Yaceczko, DCN, RDN, CNSC. Yacescko is a supporting author on a recently published White Paper on the topic, and she explains what EPI is, how to screen for and treat the condition, and the essential role of dietitians in an interdisciplinary care team managing these patients.

Hosted by Kristin Houts

Biography

Dr. Shelby Yaceczko, DCN, RDN-AP, CNSC is an expert registered dietitian nutritionist, a Doctor of Clinical Nutrition and has research interests in dietitian provider autonomy in advanced-level practice, gastrointestinal cancer, and complex gastrointestinal surgery conditions. She has developed numerous hospital-based nutrition programs and protocols aimed to improve nutrition care in the ICU and ambulatory care settings. Her expertise focuses on managing disorders of the pancreas, stomach, liver, gallbladder, bile ducts, esophagus, and small and large bowel. Yacescko holds leadership roles in national nutrition organizations involved in nutrition support and gastrointestinal diseases and is the founder of a digital health cancer wellness company.
In this episode, we discuss:

How overlapping GI symptoms, lack of standardized screening tools, and limited guidelines contribute to missed EPI diagnoses and delayed treatment

What inspired the development of the White Paper

How to bring EPI management into everyday practice

The ready-to-use checklists, screening forms, and EHR templates within the White Paper designed to standardize treatment
Additional resources:
- A link to the white paper can be found here.
- Canopy Cancer Collective’s resource page can be found here.
- Learn more about diagnosis and management of EPI at EssentialsofEPI.com.
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The content, products and/or services referred to in this podcast are intended for Health Care Professionals only and are not, and are not intended to be, medical advice, which should be tailored to your individual circumstances. The content is for your information only, and we advise that you exercise your own judgement before deciding to use the information provided. Professional medical advice should be obtained before taking action. The reference to particular products and/or services in this episode does not constitute any form of endorsement. Please see  here  for terms and conditions.
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November 21, 2025