Health Journal Online

Tag: cancer

  • Eating to Downregulate a Gene for Metastatic Cancer 

    Eating to Downregulate a Gene for Metastatic Cancer 

    Women with breast cancer should include the “liberal culinary use of cruciferous vegetables.”

    Both the Women’s Intervention Nutrition Study and the Women’s Health Initiative study showed that women randomized to a lower-fat diet enjoyed improved breast cancer survival. However, in the Women’s Healthy Eating and Living Study, women with breast cancer were also randomized to drop their fat intake down to 15 to 20 percent of calories, yet there was no difference in breast cancer relapse or death after seven years.

    Any time there’s an unexpected result, you must question whether the participants actually followed through with study instructions. For instance, if you randomized people to stop smoking and they ended up with the same lung cancer rates as those in the group who weren’t instructed to quit, one likely explanation is that the group told to stop smoking didn’t actually stop. In the Women’s Healthy Eating and Living Study, both the dietary intervention group and the control group started out at about 30 percent of calories from fat. Then, the diet group was told to lower their fat intake to 15 to 20 percent of calories. By the end of the study, they had in fact gone from 28.5 percent fat to 28.9 percent fat, as you can see below and at 1:16 in my video The Food That Can Downregulate a Metastatic Cancer Gene. They didn’t even reduce their fat intake. No wonder they didn’t experience any breast cancer benefit. 

    When you put together all the trials on the effect of lower-fat diets on breast cancer survival, even including that flawed study, you see a reduced risk of breast cancer relapse and a reduced risk of death. In conclusion, going on a low-fat diet after a breast cancer diagnosis “can improve breast cancer survival by reducing the risk of recurrence.” We may now know why: by targeting metastasis-initiating cancer cells through the fat receptor CD36.

    We know that the cancer-spreading receptor is upregulated by saturated fat. Is there anything in our diet that can downregulate it? Broccoli.

    Broccoli appears to decrease CD36 expression by as much as 35 percent (in mice). Of all fruits and vegetables, cruciferous vegetables like broccoli were the only ones associated with significantly less total risk of cancer and not just getting cancer in the first place, as you can see here and at 2:19 in my video.

    Those with bladder cancer who eat broccoli also appear to live longer than those who don’t, and those with lung cancer who eat more cruciferous veggies appear to survive longer, too.

    For example, as you can see below and at 2:45 in my video, one year out, about 75 percent of lung cancer patients eating more than one serving of cruciferous vegetables a day were still alive (the top line in red), whereas, by then, most who had been getting less than half a serving a day had already died from their cancer (the bottom line in green).

    Ovarian cancer, too. Intake of cruciferous vegetables “significantly favored survival,” whereas “a survival disadvantage was shown for meats.” Milk also appeared to double the risk of dying. Below and at 3:21 in my video are the survival graphs. Eight years out, about 40 percent of ovarian cancer patients who averaged meat or milk every day were deceased (the boldest line, on the bottom), compared to only about 20 percent who had meat or milk only a few times a week at most (the faintest line, on the top). 

    Now, it could be that the fat and cholesterol in meat increased circulating estrogen levels, or it could be because of meat’s growth hormones or all its carcinogens. And galactose, the sugar naturally found in milk, may be directly toxic to the ovary. Dairy has all its hormones, too. However, the lowering of risk with broccoli and the increasing of risk with meat and dairy are also consistent with the CD36 mechanism of cancer spread.

    Researchers put it to the test in patients with advanced pancreatic cancer who were given pulverized broccoli sprouts or a placebo. The average death rate was lower in the broccoli sprout group compared to the placebo group. After a month, 18 percent of the placebo group had died, but none in the broccoli group. By three months, another 25 percent of the placebo group had died, but still not a single death in the broccoli group. And by six months, 43 percent of the remaining patients in the placebo group were deceased, along with the first 25 percent of the broccoli group. Unfortunately, even though the capsules for both groups looked the same, “true blinding was not possible,” and the patients knew which group they were in “because the pulverized broccoli sprouts could be easily distinguished from the methylcellulose [placebo] through their characteristic smell and taste.” So, we can’t discount the placebo effect. What’s more, the study participants weren’t properly randomized “because many of the patients refused to participate unless they were placed into the [active] treatment group.” That’s understandable, but it makes for a less rigorous result. A little broccoli can’t hurt, though, and it may help. It’s the lack of downsides of broccoli consumption that leads to “Advising Women Undergoing Treatment for Breast Cancer” to include the “liberal culinary use of cruciferous vegetables,” for example.

    It’s the same for reducing saturated fat. The title of an editorial in a journal of the National Cancer Institute asked: “Is It Time to Give Breast Cancer Patients a Prescription for a Low-Fat Diet?” “Although counseling women to consume a healthy diet after breast cancer diagnosis is certainly warranted for general health, the existing data still fall a bit short of proving this will help reduce the risk of breast cancer recurrence and mortality.” But what do we have to lose? After all, it’s still certainly warranted for general health.



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  • Eating to Help Control Cancer Metastasis 

    Eating to Help Control Cancer Metastasis 

    Randomized controlled trials show that lowering saturated fat intake can lead to improved breast cancer survival.

    The leading cause of cancer-related death is metastasis. Cancer kills because cancer spreads. The five-year survival rate for women with localized breast cancer is nearly 99 percent, for example, but that falls to only 27 percent in women with metastasized cancer. Yet, “our ability to effectively treat metastatic disease has not changed significantly in the past few decades…” The desperation is evident when there are such papers as “Targeting Metastasis with Snake Toxins: Molecular Mechanisms.”

    We have built-in defenses, natural killer cells that roam the body, killing off budding tumors. But, as I’ve discussed, there’s a fat receptor called CD36 that appears to be essential for cancer cells to spread, and these cancer cells respond to dietary fat intake, but not all fat.

    CD36 is upregulated by palmitic acid, as much as a 50-fold increase within 12 hours of consumption, as shown below and at 1:13 in my video How to Help Control Cancer Metastasis with Diet.

    Palmitic acid is a saturated fat made from palm oil that can be found in junk food, but it is most concentrated in meat and dairy. This may explain why, when looking at breast cancer mortality and dietary fat, “there was no difference in risk of breast-cancer-specific death…for women in the highest versus the lowest category of total fat intake,” but there’s about a 50 percent greater likelihood of dying of breast cancer with higher intake of saturated fat. Researchers conclude: “These meta-analyses have shown that saturated fat intake negatively impacts breast cancer survival.”

    This may also explain why “intake of high-fat dairy, but not low-fat dairy, was related to a higher risk of mortality after breast cancer diagnosis.” If a protein in dairy, like casein, was the problem, skim milk might be even worse, but that wasn’t the case. It’s the saturated butterfat, perhaps because it triggered that cancer-spreading mechanism induced by CD36. Women who consumed one or more daily servings of high-fat dairy had about a 50 percent higher risk of dying from breast cancer.

    We see the same with dairy and its relationship to prostate cancer survival. Researchers found that “drinking high-fat milk increased the risk of dying from prostate cancer by as much as 600% in patients with localized prostate cancer. Low-fat milk was not associated with such an increase in risk.” So, it seems to be the animal fat, rather than the animal protein, and these findings are consistent with analyses from the Health Professionals Follow-up Study (HPFS) and the Physicians’ Health Study (PHS), conducted by Harvard researchers.

    There is even more evidence that the fat receptor CD36 is involved. The “risk of colorectal cancer for meat consumption” increased from a doubling to an octupling—that is, the odds of getting cancer multiplied eightfold for those who carry a specific type of CD36 gene. So, “Is It Time to Give Breast Cancer Patients a Prescription for a Low-Fat Diet?” A cancer diagnosis is often referred to as a ‘teachable moment’ when patients are motivated to make changes to their lifestyle, and so provision of evidence-based guidelines is essential.”

    In a randomized, prospective, multicenter clinical trial, researchers set out “to test the effect of a dietary intervention designed to reduce fat intake in women with resected, early-stage breast cancer,” meaning the women had had their breast cancer surgically removed. As shown below and at 4:02 in my video, the study participants in the dietary intervention group dropped their fat intake from about 30 percent of calories down to 20 percent, reduced their saturated fat intake by about 40 percent, and maintained it for five years. “After approximately 5 years of follow-up, women in the dietary intervention group had a 24% lower risk of relapse”—a 24-percent lower risk of the cancer coming back—“than those in the control group.” 

    That was the WINS study, the Women’s Intervention Nutrition Study. Then there was the Women’s Health Initiative study, where, again, women were randomized to lower their fat intake down to 20 percent of calories, and, again, “those randomized to a low-fat dietary pattern had increased breast cancer overall survival. Meaning: A dietary change may be able to influence breast cancer outcome.” What’s more, not only was their breast cancer survival significantly greater, but the women also experienced a reduction in heart disease and a reduction in diabetes.



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  • Dietary Components That May Cause Cancer to Metastasize 

    Dietary Components That May Cause Cancer to Metastasize 

    Palmitic acid, a saturated fat concentrated in meat and dairy, can boost the metastatic potential of cancer cells through the fat receptor CD36.

    The leading cause of death in cancer patients is metastasis formation. That’s how most people die of cancer—not from the primary tumor, but the cancer spreading through the body. “It is estimated that metastasis is responsible for ~90% of cancer deaths,” and little progress has been made in stopping the spread, despite our modern medical armamentarium. In fact, we can sometimes make matters worse. In an editorial entitled “Therapy-Induced Metastasis,” its authors “provide evidence that all the common therapies, including radiotherapy, chemotherapy, fine needle biopsies, surgical procedures and anaesthesia, have the potential to contribute to tumour progression.” You can imagine how cutting around a tumor and severing blood vessels might lead to the “migration of residual tumour cells,” but why chemotherapy? How might chemo exacerbate metastases? “Despite reducing the size of primary tumors, chemotherapy changes the tumor microenvironment”—its surrounding tissues—“resulting in an increased escape of cancer cells into the blood stream.” Sometimes, chemo, surgery, and radiation are entirely justified, but, again, other times, these treatments can make matters worse. If only we had a way to treat the cause of the cancer’s spreading.

    The development of antimetastatic therapies has been hampered by the fact that the cells that initiate metastasis remain unidentified. Then, a landmark study was published: “Targeting Metastasis-Initiating Cells Through the Fatty Acid Receptor CD36.” Researchers found a subpopulation of human cancer cells “unique in their ability to initiate metastasis”; they all express high levels of a fat receptor known as CD36, dubbed “the fat controller.” It turns out that palmitic acid or a high-fat diet specifically boosts the metastatic potential of these cancer cells. Where is palmitic acid found? Although it was originally discovered in palm oil, palmitic acid is most concentrated in meat and dairy. “Emerging evidence shows that palmitic acid (PA), a common fatty acid in the human diet, serves as a signaling molecule regulating the progression and development of many diseases at the molecular level.” It is the saturated fat that is recognized by CD36 receptors on cancer cells, and we know it is to blame, because if the CD36 receptor is blocked, so are metastases.

    The study was of a human cancer, but it was a human cancer implanted into mice. However, clinically (meaning in cancer patients themselves), the presence of these CD36-studded metastasis-initiating cells does indeed correlate with a poor prognosis. CD36 appears to drive the progression of brain tumors, for example. As seen in the survival curves shown below and at 3:21 in my video What Causes Cancer to Metastasize?, those with tumors with less CD36 expression lived significantly longer. It is the same with breast cancer mortality: “In this study, we correlated the mortality of breast cancer patients to tumor CD36 expression levels.” That isn’t a surprise, since “CD36 plays a critical role in proliferation, migration and…growth of…breast cancer cells.” If we inhibit CD36, we can inhibit “the migration and invasion of the breast cancer cells.” 

    Below and at 3:46 in my video, you can see breast cancer cell migration and invasion, before and after CD36 inhibition. (The top lines with circles are before CD36 inhibition, and the bottom lines with squares are after.)

    This isn’t only in “human melanoma- and breast cancer–derived tumours” either. Now we suspect that “CD36 expression drives ovarian cancer progression and metastasis,” too, since we can inhibit ovarian cancer cell invasion and migration, as well as block both lymph node and blood-borne metastasis, by blocking CD36. We also see the same kind of effect with prostate cancer; suppress the uptake of fat by prostate cancer cells and suppress the tumor. This was all studied with receptor-blocking drugs and antibodies in a laboratory setting, though. If these “metastasis-initiating cancer cells particularly rely on dietary lipids [fat] to promote metastasis,” the spread of cancer, why not just block the dietary fat in the first place?

    “Lipid metabolism fuels cancer’s spread.” Cancer cells love fat and cholesterol. The reason is that so much energy is stored in fat. “Hence, CD36+ metastatic cells might take advantage of this feature to obtain the high amount of energy that is likely to be required for them to anchor and survive at sites distant from the primary tumour”—to set up shop throughout the body.

    “The time when glucose [sugar] was considered as the major, if not only, fuel to support cancer cell proliferation is over.” There appears to be “a fatter way to metastasize.” No wonder high-fat diets (HFD) may “play a crucial role in increasing the risk of different cancer types, and a number of clinical studies have linked HFD with several advanced cancers.”

    If dietary fat may be “greasing the wheels of the cancer machine,” might there be “specific dietary regimens” we could use to starve cancers of dietary fat? You don’t know until you put it to the test, which we’ll look at next.



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  • Vietnam Performs World’s First 3D-Printed Femur Transplant on Child with Cancer

    Vietnam Performs World’s First 3D-Printed Femur Transplant on Child with Cancer

    At just eight years old, a Vietnamese boy with bone cancer has received a 3D-printed femur — a medical first that has preserved not only his limb but his childhood.

    In what is now considered a global first, the child underwent a total femur replacement using a fully customized 3D-printed titanium implant. According to the U.S. National Library of Medicine, all previously documented total femur replacements have relied on traditional implant techniques, with no reported cases involving pediatric patients or 3D-printed, growth-adaptive prostheses.

    The breakthrough procedure was carried out at Vinmec Times City International Hospital in collaboration with VinUni’s Biomedical 3D Lab. It marks not only a technical triumph but also a milestone in the advancement of precision medicine in Vietnam.

    Vietnam is fast becoming a key player in Southeast Asia’s healthcare innovation landscape, as hospitals across the region turn to 3D printing to increase self-reliance and deliver more personalized treatment.

    Market projections reflect this momentum. According to Metatech Insights, the Asia Pacific 3D printing healthcare market is set to expand from USD 1.04 billion in 2025 to over USD 6.7 billion by 2035, driven by a CAGR exceeding 20%.

    Within this context, Vinmec’s femoral implant surgery marks more than a clinical breakthrough. As the nation’s only JCI-accredited health system with Centers of Excellence across four key specialties, Vinmec was honored in 2025 as Hospital Group and Technology Innovator of the Year by the Healthcare Asia Awards.

    Custom-Built Bone Implant Marks Breakthrough in Pediatric Cancer Surgery

    Developed through collaboration between Vinmec Times City International Hospital and biomedical engineers at VinUni’s 3D Lab, the modular titanium implant was designed and produced entirely in Vietnam. Its structure accommodates physical development, making it one of the first growth-adaptive implants of its kind used in children.

    Vinmec performs the 3D-printed total femoral replacement on youngest cancer patient, marking a breakthrough for Vietnam in global precision medicine.
    BY VINMEC

    The treatment was carried out in two surgical phases. In January 2024, the tumor was resected and a temporary cement graft was placed to maintain structural integrity. By May 2025, once the patient had stabilized, the graft was replaced with the patient-specific titanium femur.

    “We contacted foreign manufacturers but there was no suitable design. Self-manufacturing the equipment allows us to be proactive in treatment, it also paves the way for a new direction for Vietnamese medicine.” said MSc. Dr. Tran Duc Thanh, doctor directly engaging in the surgery.

    Beyond the innovation lies a deeply emotional story.

    Diagnosed with malignant bone cancer and after undergoing chemotherapy, the child was advised by several hospitals to have his limb amputated as a life-saving measure. But the patient’s mother held firm in her belief that her son deserved more. Her resolve became the catalyst for one of Vietnam’s most advanced surgical efforts.

    Today, the boy walks with a personalized implant that not only restored his mobility but protected his dignity. In a region rapidly embracing technology, Vietnam’s latest success offers a glimpse of what’s possible when innovation meets compassionate care.

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  • Colorectal Cancer Before 50 Linked To Common, Often-Missed Condition Affecting Millions Of Americans

    Colorectal Cancer Before 50 Linked To Common, Often-Missed Condition Affecting Millions Of Americans

    Colorectal cancer cases are spiking, especially among younger adults, leaving scientists racing to uncover the hidden culprits behind this troubling trend. While poor diets, sedentary lifestyles, and environmental factors have long been in the spotlight, a new study reveals a surprising contributor, a condition that is both widespread and frequently missed.

    Researchers have identified a striking link between non-alcoholic fatty liver disease (NAFLD), a silent condition that affects an estimated one in four people globally and millions of Americans, and a significantly increased risk of early-onset colorectal cancer (diagnosed before the age of 50). Despite its prevalence, NAFLD often goes undetected in routine medical care and progresses without obvious symptoms.

    To understand the link between NAFLD and early-onset colorectal cancer, researchers conducted a large-scale, population-based cohort study using data from the Korean National Health Insurance Service involving over 4.6 million adults.

    The participants were between the ages of 20 and 49 who underwent routine health checkups in 2009, with health outcomes tracked through 2019. NAFLD was identified using a validated measure known as the Fatty Liver Index (FLI), with scores of 60 or higher indicating the presence of NAFLD.

    Participants were then grouped based on their FLI scores: those with NAFLD (FLI ≥ 60), borderline NAFLD (FLI between 30 and 59), and no NAFLD (FLI

    Researchers noted that individuals with NAFLD had a 24% higher risk of developing early-onset colorectal cancer compared to those without fatty liver, while those in the borderline NAFLD category had a 12% increased risk.

    Interestingly, the study also found a dose–response relationship between the severity of fatty liver and cancer risk in cancers, in those located in the left colon and rectum. The association was particularly strong among males, younger individuals aged 20–29, and those without diabetes, highlighting the need for targeted early screening and liver health monitoring in these higher-risk populations.

    “These findings highlight the need for multifaceted preventive strategies, including lifestyle interventions and expanded screening for younger populations with NAFLD,” the researchers wrote in the study published in the journal Clinical Gastroenterology and Hepatology.

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  • California Father Battling Lung Cancer Denied Coverage for ‘Last Option’ Treatment, Family Says

    California Father Battling Lung Cancer Denied Coverage for ‘Last Option’ Treatment, Family Says

    A California man battling stage 4 lung cancer was denied insurance coverage for a potentially life-saving double lung transplant just as he was preparing to fly to Chicago for the procedure, his family says.

    Deron Wells, a 59-year-old husband and father of three, had been medically approved for a rare clinical trial lung transplant at Northwestern Medicine in Illinois, according to ABC 7.

    Cigna, his insurer, had initially signed off on the necessary procedures and transport from UCLA Santa Monica Medical Center, where he had been receiving care. But on the day of his scheduled transfer, Cigna reversed course, denying coverage for both the transplant and the out-of-state medical transfer.

    “The last option we have is for us to take him to Northwestern, period. I hope Cigna really understands the seriousness of the situation. We’re not just a number. We are talking about his life,” Janet Savarimuthu, the man’s wife, told the outlet.

    Lung transplants are not typically considered standard treatment for cancer, which Cigna cited in its statement defending the denial, claiming their coverage guidelines are based on national clinical standards.

    Wells’ family and friends launched an appeal and a public campaign in an effort to pressure the insurer to reconsider. A response to the appeal is expected by Thursday.

    The man’s GoFundMe has raised more than $37,000 as of Friday morning.

    Originally published on Latin Times

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  • Popular Dinner Staple May Increase Risk Of Death From Cancer

    Popular Dinner Staple May Increase Risk Of Death From Cancer

    A dinner without chicken feels incomplete for many. Known for its protein-packed benefits, especially for muscle building and energy, chicken has long been a staple for many, particularly those hitting the gym. However, new research cautions that regularly eating chicken may put you at an increased risk of dying from gastrointestinal cancers.

    The findings of the latest study, published in the journal Nutrients, offer a surprising twist since poultry, long considered a “noble food” due to its high protein and low-fat content compared to red meat, may not be as harmless as once thought.

    The Dietary Guidelines for Americans recommend 100 grams as a standard serving of poultry, suggesting it be consumed one to three times a week. However, the latest study raises concerns that exceeding 300 grams weekly could increase the risk of death from gastrointestinal cancers.

    The study, which analyzed the health data and meat consumption habits of 4,869 adults in Italy, revealed that individuals who ate more than 300 grams of poultry per week had a significantly higher incidence of gastrointestinal cancers and a greater risk of early death from these cancers. Those consuming over 300 grams of poultry weekly had a 27% higher likelihood of dying from gastrointestinal cancer compared to those who kept their intake to 100 grams or less each week.

    Another interesting reveal was that men were more at risk of death from gastrointestinal cancers compared to women, even with the same amount of poultry consumption.

    The impact of poultry consumption on the risk of dying from gastrointestinal cancer increased with age. For those around 60, there was no significant difference between eating less than 100 grams or more than 300 grams of poultry a week. However, by 83, the risk of death was twice as high for those eating more poultry. This effect was more noticeable in men, who showed a higher risk even before age 60.

    “We believe it is beneficial to moderate poultry consumption, alternating it with other equally valuable protein sources, such as fish. We also believe it is essential to focus more on cooking methods, avoiding high temperatures and prolonged cooking times,” the researchers conclude.

    However, an important limitation of the study is that it did not consider whether the chicken consumed was processed or how it was cooked. The researchers also did not account for the participants’ levels of physical activity, which could have influenced the results.

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  • This Body Measurement Could Predict Cancer Risk In Men

    This Body Measurement Could Predict Cancer Risk In Men

    Obesity has long been associated with an increased risk of health problems, including cancer. However, researchers have recently discovered that a specific body measurement in men could serve as a strong predictor of their cancer risk.

    Although Body Mass Index (BMI) serves as a strong indicator of health adversities, a recent study published in The Journal of the National Cancer Institute suggests that waist circumference is an even stronger predictor of cancer risk in men.

    The study found that with an additional 4-inch increase in waist size, the risk of cancer rises by 25 percent in men. In comparison, an increase in BMI by 3.7 kg/m² (like going from 24 to 27.7) only raised the risk by 19%. So, even when taking BMI into account, a large waist circumference was still linked to a higher risk of developing obesity-related cancers in men.

    This is because unlike BMI, which only measures body size, waist circumference reflects abdominal fat, a key factor linked to increased health risks like insulin resistance, inflammation, and abnormal blood fat levels. This explains why even with the same BMI, differences in fat distribution can lead to varying cancer risks.

    However, the study showed that for women, both waist circumference and BMI had similar effects on the risk of obesity-related cancers, but the link was weaker than for men. For example, a 12 cm increase in waist size (like going from 80 cm to 91.8 cm) or a 4.3 increase in BMI (like going from 24 to 28.3) both raised the risk by 13%.

    Researchers attribute the difference in cancer risk between men and women to the way fat is distributed in the body. Men tend to accumulate more visceral fat around the abdomen, which is more metabolically active and linked to higher health risks, including cancer. On the other hand, women typically store fat more evenly in peripheral areas like the hips and thighs, where it poses a lower risk.

    “Our study provides evidence that waist circumference is a stronger risk factor than BMI for obesity-related cancers in men, but not in women. Additionally, waist circumference appears to provide additional risk information beyond that conveyed by BMI in men,” the researchers wrote in the news release.

    “Future research incorporating more precise measures of adiposity, along with comprehensive data on potential confounding factors, could further elucidate the relationship between body fat distribution and cancer risk,” they added.

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  • ‘Healthy’ Woman With Terminal Colon Cancer Warns Of Unexpected Symptom

    ‘Healthy’ Woman With Terminal Colon Cancer Warns Of Unexpected Symptom

    A 57-year-old special education teacher from England deemed “fit and healthy” by those around her is now advised to receive end-of-life care after being diagnosed with stage 4 colon cancer. What makes her story even more alarming is that her only warning sign was an unusual symptom most people would not associate with cancer.

    Though the heartbreaking diagnosis came as a sudden blow to Karen Kennerley from Lancashire, England, she is determined to fight the disease and raise awareness among people about little-known signs of colon cancer.

    Colon cancer typically presents with digestive changes like persistent diarrhea, constipation, blood in the stool, rectal bleeding, abdominal pain, or bloating. But Kennerley did not have any of these signs. All that she felt before her devastating diagnosis was a symptom that had nothing to do with her gut.

    “The scary thing is, I had no symptoms apart from a bit of fatigue,” she said. However, the mother of three who worked at a small school for special education kids thought it was just exhaustion from the work.

    “I went to my GP, who ran some blood tests, and referred me for a FIT test and then I was referred for a colonoscopy in January 2023. Everyone was telling me I was fit and healthy, that there was nothing to worry about but they were doing the tests to rule things out,” she recollected.

    During a routine colonoscopy, doctors found a seemingly harmless tumor, but their suspicions grew, and a biopsy soon confirmed the worst: it was cancerous. In June 2023, she underwent surgery to remove the tumor along with part of her large intestine, followed by eight grueling rounds of chemotherapy.

    Though her cancer was initially believed to be in remission, she was hospitalized in March 2024 with suspected appendicitis. However, scans revealed a devastating turn, her cancer had progressed to stage 4 and spread to the ovaries. The medics then advised her to receive palliative cancer treatments offered through the NHS.

    However, Kennerley is now determined to fight as she hopes to receive cancer treatments in Germany that promise her the best chance of survival. She is raising money to fund her treatment.

    “People with stage four cancer feel totally abandoned, I want to change that, not only for me but for everyone else going through this,” she added.

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  • Heme Iron and Cancer 

    Heme Iron and Cancer 

    Laboratory models suggest that extreme doses of heme iron may be detrimental, but what about the effects of nutritional doses in humans?

    In muscle meat, there is a heme protein that contributes to, well, the meaty taste of meat. There’s also a heme protein in the roots of soybean plants that can be churned out to provide a similar flavor and aroma in plant-based meat, which is used to make the Impossible Burger possible. The question is: Are there any downsides?

    When the European Food Safety Authority was considering the safety of adding heme iron to foods, its main concern was a potential increased risk of colon cancer. As you can see below and at 1:00 in my video Does Heme Iron Cause Cancer?, we know meat causes cancer. Processed meat—bacon, ham, hot dogs, sausages, and lunch meat—is considered a Group 1 carcinogen, meaning we know it causes cancer in people with the same level of certainty that something like smoking causes cancer, whereas something like a burger probably causes cancer in people, kind of like DDT. But what’s the role of heme iron? 

    There are all sorts of potential mechanisms to explain the cancer risk. Meat has the pro-inflammatory long-chain omega-6 arachidonic acid and more of the aging- and cancer-associated methionine, trans fat, and endogenous hormones like IGF-1, not to mention the ones that are implanted in animals as “exogenous hormonal growth-promoters.” Then there are all the toxic pollutants that build up the food chain, like pesticides and formaldehyde.

    According to the prestigious IARC, the International Agency for Research on Cancer, “there is strong evidence that HAAs [heterocyclic aromatic amines], by causing DNA damage, contribute to carcinogenic mechanisms associated with the consumption of red meat.” These DNA-damaging compounds are formed when muscle tissue is exposed to high, dry heat like grilling, roasting, baking, and broiling—basically anything above steaming or stewing. There is also “strong evidence” that the formation of so-called N-nitroso compounds contributes to the cancer-causing mechanism. Those are carcinogens that can form inside our gut when we eat meat. However, there is also “strong evidence that haem [heme] iron contributes to the carcinogenic mechanisms associated with red and processed meat.”

    Normally I might leave it there, but other authoritative bodies I respect, like the American Institute for Cancer Research and the World Cancer Research Fund, are more tentative. While they agree there is some evidence that the “consumption of foods containing haem iron might increase the risk of colorectal cancer,” they consider the evidence suggesting such a connection to be limited.

    Much of the available evidence is based on data from lab animals, such as the study titled “Dietary Heme Induces Gut Dysbiosis, Aggravates Colitis, and Potentiates the Development of Adenomas in Mice,” in which dietary heme was found to disrupt the gut flora, aggravate inflammation, and potentiate the development of intestinal tumors in mice. But it’s critical to note that, in all the laboratory animal models that have been used, the rodents ingested meat or heme equivalent to humans eating up to 40,000 pounds (18,000 kilograms) of meat a day. Even the smallest dose would be about a dozen daily Impossible Burgers.

    In another study, ascribing “a central role for heme iron” in the development of colon cancer associated with meat intake, the authors claimed they “aimed at determining, at nutritional doses, which is the main factor involved and proposing a mechanism of cancer promotion by red meat.” So, heme “doses were chosen to mimic red meat consumption,” and, indeed, there was a significant increase in tumor load, as you can see here and at 3:41 in my video. 

    The researchers concluded that their “results strongly suggest that at concentrations that are in line with human red meat consumption, heme iron is associated with the promotion of colon carcinogenesis,” that is, cancer development. However, if you look at the actual diet given to the participants and do the math, it was 500 times the level of heme found in people’s diets, in excess of about 20 pounds of meat a day. Of course, even if they really did use the right doses, they’re still going to end up with data on the wrong species, which brings us to clinical studies that we’ll explore next. 

    This is part of a nine-video series on plant-based meats. If you missed any of the other earlier installments, check out the related posts below.

    The final two videos in the series are coming up next. See Heme-Induced N-Nitroso Compounds and Fat Oxidation and Is Heme the Reason Meat Is Carcinogenic?.



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