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Cancer

Liquid biopsy (cancer screening) featured article

Introduction

Cancer is the second leading cause of death worldwide. Successful treatment hinges on early detection, but conventional screening and diagnostic approaches, often relying on tissue biopsies, come with limitations that hinder their effectiveness.

One promising solution is liquid biopsy, a groundbreaking technique that analyzes bodily fluids, such as blood, urine, lymph, and cerebrospinal fluid, for signs of cancer. When these fluids circulate near a tumor, they can acquire shed tumor cells and their components, such as DNA and RNA.

Liquid biopsies are innovative, non- or minimally-invasive medical procedures that detect and analyze these tumor-derived cells and components for cancer screening, treatment guidance, and follow-up care, potentially revolutionizing early detection and personalized treatment strategies. This article delves into the importance of early cancer detection, the shortcomings of existing screening methods, and the potential of liquid...

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Q&A #70 with Dr. Rhonda Patrick (5/3/25)

Posted on May 15th 2025 (about 2 months)

Dr. Rhonda Patrick discusses cancer prevention, linoleic acid, shingles vaccine and dementia, creatine's kidney effects, and shares her overnight oats recipe.

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Doing THIS Could Cut Your Cancer Risk Significantly

Posted on April 1st 2025 (3 months)

In this clip, Drs. Rhonda Patrick and Kerry Courneya discuss how exercise significantly reduces cancer risk—even in higher-risk individuals.

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How Exercise Enhances Chemotherapy, Radiation, & Immunotherapy Effects

Posted on April 1st 2025 (3 months)

In this clip, Drs. Rhonda Patrick and Kerry Courneya discuss how exercise supports chemotherapy effectiveness and impacts cancer cell behavior.

Topic Pages

  • Alcohol

    Alcohol metabolism produces acetaldehyde and reactive oxygen species, causing DNA adducts and impaired repair that foster cancer initiation.

  • Autophagy

    Autophagy suppresses tumorigenesis by clearing damaged organelles yet facilitates cancer cell survival through recycling essential metabolic substrates.

  • Breast milk and breastfeeding

    Extended lactation diminishes maternal breast cancer risk by suppressing ovulatory estrogen exposure and inducing differentiation-apoptosis of mammary epithelial cells.

  • Liquid biopsy (cancer screening)

    Liquid biopsy enables cancer screening by analyzing circulating tumor DNA, RNA, proteins, or cells shed into blood or other biofluids.

  • Neu5Gc

    Exogenous Neu5Gc integrates into human tumor glycans, provoking anti-Neu5Gc antibody–mediated chronic inflammation that accelerates cancer progression.

  • Nicotinamide mononucleotide

    By replenishing intracellular NAD+, nicotinamide mononucleotide modulates sirtuin- and PARP-dependent signaling pathways implicated in tumorigenesis and chemoresistance.

  • Omega-3 fatty acids

    Omega-3 long-chain polyunsaturated fatty acids modulate eicosanoid signaling, lipid raft composition and NF-κB activity, suppressing tumorigenic proliferation and angiogenesis.

  • Polyphenols

    Polyphenols attenuate cancer initiation and progression by scavenging reactive species and modulating epigenetic, inflammatory, and cell-cycle signaling pathways.

  • Sirtuins

    Sirtuins modulate tumorigenesis by NAD⁺-dependent deacetylation of p53, FOXO and NF-κB, altering DNA repair, metabolism, apoptosis.

  • Sugar-sweetened beverages (SSBs)

    Excessive sugar-sweetened beverage consumption induces hyperglycemia, hyperinsulinemia, adiposity, and oxidative inflammation, stimulating insulin-IGF-1 signaling–mediated tumorigenesis.

  • Sulforaphane

    Sulforaphane induces Nrf2-driven cytoprotective enzymes and inhibits HDAC and NF-κB, promoting apoptosis and growth arrest in cancer cells.

  • Vitamin C

    High-dose ascorbate produces cytotoxic hydrogen peroxide and supports TET/HIF hydroxylases, influencing cancer cell redox balance and epigenetics.

  • Whole-body hyperthermia

    Whole-body hyperthermia potentiates anticancer responses by increasing tumor perfusion, inducing heat-shock protein–mediated apoptosis, and amplifying chemo- and radio-sensitization.

News & Publications

  • Structured, long-term exercise program reduces the risk of colon cancer recurrence or death by 28% and improves physical functioning. www.nejm.org
    Cancer Exercise

    Exercise may be one of the most effective—and underused—tools in cancer care. However, a recent study found that a structured, long-term exercise program reduced the risk of cancer recurrence or death by 28% in people treated for colon cancer.

    The study included 889 people with stage II or III colon cancer who had completed chemotherapy. Researchers assigned half to a three-year supervised exercise program that included moderate-intensity aerobic activity and strength training. The other half received health-education materials but no structured physical activity plan. Throughout the study, participants completed surveys about their activity levels and underwent fitness assessments, treadmill tests, and body measurements. The researchers monitored the patients for nearly eight years to track cancer recurrence and overall survival.

    The benefits of exercise were substantial. Five years after treatment, 80% of the exercise group remained cancer-free, compared to 74% in the education group. After eight years, 90% of those who exercised were still alive, versus 83% of the education group. Patients in the exercise group also reported better physical functioning throughout the study. However, musculoskeletal complaints—like joint or muscle pain—were more common in the exercise group (19%) than in the education group (12%).

    These findings suggest that a structured, long-term exercise program can help colon cancer survivors live longer and stay cancer-free. Participants also reported sustained improvements in physical functioning, further supporting the role of exercise in post-treatment recovery, despite a modest increase in musculoskeletal complaints. Learn more about the science of exercise for cancer in this episode featuring Dr. Kerry Courneya.

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  • High levels of lycopene, a powerful antioxidant found in tomatoes, correlated with an 11% lower risk of cancer development and a 24% lower risk of cancer-associated death. www.frontiersin.org
    Cancer Diet Antioxidant Polyphenol Carotenoids

    Tomatoes are a rich source of lycopene, a powerful antioxidant that may help protect against cancer and cancer-related death. A recent study found that people with the highest blood levels of lycopene were 11% less likely to develop cancer and 24% less likely to die from it than those with the lowest levels.

    Researchers analyzed data from 121 prospective studies involving more than 100,000 people with cancer and more than 10,000 cancer-related deaths. They focused on studies that reported tomato intake, lycopene levels in the blood, or dietary lycopene consumption and how those related to cancer risk and death.

    Compared with people who had the lowest lycopene levels, those with the highest had an 11% lower risk of developing cancer. High tomato and lycopene intake were each linked to a 5% lower cancer risk. When looking at cancer deaths, people who consumed the most tomatoes were 16% less likely to die from cancer, and those who consumed the most lycopene were 24% less likely. Higher blood levels of lycopene also lowered the risk of dying from lung cancer (the leading cause of cancer deaths) by 35%. In addition, a modest increase in blood lycopene—about 10 micrograms per deciliter—was tied to a 5% drop in overall cancer risk.

    These findings suggest that a diet rich in tomatoes and other lycopene-containing foods could offer modest protection against cancer and may even reduce the risk of dying from it. Lycopene is a carotenoid compound found in tomatoes and watermelon. Learn more about lycopene and other carotenoids in our overview article.

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  • Morning-only coffee drinkers demonstrate a 16% lower risk of death from any cause and a 31% lower risk of cardiovascular death—benefits that exceed all-day coffee consumption, regardless of whether it's caffeinated or decaffeinated. academic.oup.com
    Cancer Coffee Caffeine Cardiovascular

    That morning cup of coffee might do more than boost alertness—it might promote longevity. While many studies link moderate coffee drinking to better health, the timing of those effects is less clear. However, a recent study found that morning-only coffee drinkers were more than 30% less likely to die from cardiovascular disease.

    Researchers analyzed data from more than 40,000 adults in the National Health and Nutrition Examination Survey and 1,400 adults in the Women’s and Men’s Lifestyle Validation Study. They searched for patterns in the timing of coffee consumption and tracked participants for an average of nearly 10 years to monitor deaths from all causes, cardiovascular disease, and cancer.

    Two coffee-drinking patterns emerged: a morning-only pattern (4 a.m. to noon) and an all-day pattern. Compared with people who didn’t drink coffee at all, those who drank coffee only in the morning had a 16% lower risk of dying from any cause and a 31% lower risk of dying from cardiovascular disease, indicating that the health benefits of drinking more coffee were strongest among morning-only drinkers. Surprisingly, caffeine didn’t explain the difference. When the researchers adjusted for both caffeinated and decaffeinated coffee intake, the timing of coffee drinking still mattered.

    These findings suggest that drinking coffee earlier in the day offers more health benefits than drinking it over the course of the day. Coffee induces autophagy–a critical process that helps reduce the risk of cancer and other chronic diseases. Learn more in this clip featuring Dr. Guido Kroemer.

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  • Sunburns remain common, with younger adults and higher-income individuals more likely to experience multiple episodes each year, particularly when consuming alcohol. journals.sagepub.com
    Cancer Alcohol Skin

    Sunburns are a major contributor to skin cancer risk, yet many people continue to get sunburned, with some experiencing multiple episodes each year. A recent study found that more than 30% of adults reported between one and five sunburns in the past year, and alcohol consumption was linked to an increased risk, with 21% of people who got sunburned having consumed alcohol at the time.

    Researchers analyzed data from the 2022 Health Information National Trends Survey, which included more than 6,200 participants. They used statistical analysis to identify associations between sociodemographic factors, cancer risk perceptions, sun exposure behaviors, and the number of sunburns reported in the previous 12 months.

    They found that 2.1% of participants reported more than six sunburns, 30.3% had between one and five, and 67.6% experienced none. Alcohol consumption was a contributing factor, with 21.5% of those who reported a sunburn also having consumed alcohol. Younger adults (aged 18 to 39) were more likely to experience sunburns than older adults, and men were at higher risk than women. Additionally, higher-income participants were more likely to get sunburned, with people in the highest income bracket more than four times as likely to report at least one sunburn in the past year.

    These findings suggest that public health interventions should focus on groups most at risk for sunburns, including younger adults, men, and higher-income people. Addressing alcohol consumption during sun exposure could also help reduce sunburn incidence. Sunscreens can protect against sunburns, but some carry health risks. Learn more in this Q&A featuring Dr. Rhonda Patrick.

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  • Regular blood donation promotes beneficial stem cell mutations while minimizing disease risk by inducing genetic changes that preferentially support healthy red blood cell production. ashpublications.org
    Cancer Stem Cells Immune System Genetics

    Donating blood is an act of generosity that saves lives, yet few donors think about how it affects their own health. Each donation triggers a surge in blood cell production, a process that could subtly shape the long-term health of blood-forming stem cells. A recent study found that frequent blood donation promotes the expansion of specific blood stem cell mutations that support healthy red blood cell production.

    Researchers analyzed blood samples from 217 older men who had donated more than 100 times and compared them to 212 men who had donated fewer than 10 times. They looked for clonal hematopoiesis, a condition where blood stem cells acquire genetic changes that allow specific cell populations to expand. They also used gene-editing techniques to study how particular mutations behaved when exposed to erythropoietin, a hormone that increases after blood loss.

    They found that the overall rate of clonal hematopoiesis was similar between frequent and infrequent donors. However, mutations in the DNMT3A gene showed distinct patterns in frequent donors. Some of these mutations responded to erythropoietin by expanding, while others, known to be associated with leukemia, were more likely to grow in response to interferon-gamma, a protein involved in the immune response. Further analysis revealed that the erythropoietin-responsive mutations tended to push blood stem cells toward making more red blood cells rather than leading to abnormal or harmful changes.

    These findings suggest that repeated blood donation encourages the expansion of specific blood stem cell mutations, but the effects support normal blood cell production rather than increase disease risk. Blood donation also lowers levels of iron—a key nutrient that, in excess, harms the brain. Learn more in this episode featuring Dr. Gordon Lithgow.

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  • Melatonin supplementation may heighten DNA repair in night shift workers during daytime sleep, potentially reducing cancer risk. oem.bmj.com
    Cancer Sleep DNA Damage Circadian Rhythm Melatonin Supplements

    Working night shifts may increase the risk of cancer by disrupting the production of melatonin, a hormone essential for DNA repair. This disruption can impair the body’s ability to repair oxidative DNA damage, potentially contributing to cancer development. A recent study found that melatonin supplementation could improve the repair of oxidative DNA damage in night shift workers.

    The researchers conducted a four-week randomized, placebo-controlled trial with 40 night shift workers, providing them a 3-milligram dose of melatonin before their daytime sleep periods. They collected urine samples during daytime sleep and nighttime work periods, measuring 8-hydroxy-2′-deoxyguanosine (8-OH-dG), a marker of DNA repair capacity.

    They found that melatonin supplementation nearly doubled 8-OH-dG excretion during daytime sleep, indicating improved DNA repair. However, they observed no difference in 8-OH-dG excretion during the night shift. Although the melatonin group experienced a slight decrease in wakefulness after falling asleep, the researchers found no differences in total sleep duration or sleepiness levels between the two groups.

    The findings from this small study suggest that melatonin supplementation enhances oxidative DNA repair in night shift workers, offering the potential for reducing cancer risk. More extensive studies may identify optimal dosages and the long-term effects of melatonin supplementation in this population. Learn about the pros and cons of melatonin supplementation in this clip featuring Dr. Satchin Panda.

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  • Higher muscular strength and cardiorespiratory fitness can help reduce the risk of premature death in cancer patients by up to 46%. bjsm.bmj.com
    Exercise Cancer Muscle Mortality Cardiovascular

    Cancer remains one of the leading causes of death globally, with millions of new cases and deaths each year. Despite treatment advancements, cancer patients are at a greater risk of death due to muscle loss, heart complications, and inadequate physical activity. A recent study found that higher muscle strength and cardiorespiratory fitness reduce the risk of death in cancer patients, with a 31% to 46% lower likelihood of premature death.

    Researchers conducted a systematic review and meta-analysis of 42 studies involving more than 47,000 cancer patients across various types and stages to examine how muscle strength and cardiorespiratory fitness influence survival rates. They sought to determine whether higher fitness levels were associated with better outcomes in terms of overall and cancer-specific death.

    Their analysis revealed that patients with higher muscle strength or cardiorespiratory fitness were 31% to 46% less likely to die prematurely from any cause than those with lower fitness levels. Each increase in muscle strength was associated with an 11% lower risk of all-cause mortality. Furthermore, patients with advanced cancer stages, as well as those with lung and digestive cancers, saw significant reductions in death risks—ranging from 8% to 46% lower for all-cause mortality. Increments in cardiorespiratory fitness were particularly important, with each improvement in cardiorespiratory fitness linked to an 18% reduced risk of dying specifically from cancer.

    These findings suggest that boosting muscle strength and cardiorespiratory fitness can improve cancer patients' survival rates. Given the strong connection between physical fitness and mortality risk, health professionals should prioritize fitness assessments for cancer patients as part of their treatment strategies. Learn more about the role of exercise in cancer prevention and recurrence in this episode featuring Dr. Kerry Courneya.

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  • The incidence of advanced-stage prostate cancer in California increased by nearly 7% over ten years, leveling off previous declines in deaths from the disease. jamanetwork.com
    Cancer Mortality Prostate

    Prostate cancer is the most diagnosed cancer among males in the U.S., but its progression varies widely, with some cases remaining harmless and others turning deadly. In recent years, concerns have grown over a rise in advanced prostate cancer, potentially linked to changes in screening recommendations. A recent study found that in California—a racially, ethnically, and geographically diverse state—the incidence of advanced-stage prostate cancer increased by nearly 7% over the past decade, while death rates, which had been declining, leveled off.

    Researchers analyzed data from nearly 388,000 prostate cancer cases diagnosed in California between 2004 and 2021. Using data from state and national cancer registries, they examined trends in incidence and death rates based on cancer stage, age, race, ethnicity, and geographic region. They used statistical models to measure how these rates changed over time, focusing on patterns before and after shifts in screening guidelines.

    They found that between 2011 and 2021, cases of advanced-stage prostate cancer increased by an average of 6.7% per year, with similar trends across racial and ethnic groups and nearly all regions of California. Meanwhile, prostate cancer death rates declined by 2.6% per year from 2004 to 2012 but remained steady through 2021, marking an end to previous declines in deaths from the disease.

    These findings suggest that more men in California are being diagnosed with advanced prostate cancer, and the progress in reducing deaths has stalled. The gold standard for prostate cancer screening is the prostate-specific antigen (PSA) test. The U.S. Preventive Services Task Force recommends PSA screening for prostate cancer in men aged 55 to 69, but only among those at high risk for the disease. This screening can potentially reduce death but also carries risks such as false positives and treatment complications, including incontinence and erectile dysfunction. For men 70 and older, PSA screening is not recommended due to the greater likelihood of harms outweighing benefits.

    Sulforaphane, a bioactive compound derived from broccoli, may reduce the risk for some types of cancer, including prostate cancer. Learn more in this episode featuring Dr. Jed Fahey.

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  • Exposure to synthetic PFAS chemicals in drinking water may increase the risk of certain cancers by up to 33%. www.nature.com
    Cancer Pollution

    Nearly 2 million people in the U.S. were diagnosed with cancer in 2023, and exposure to polyfluoroalkyl substances (PFAS) may be a contributing factor. These synthetic chemicals, found in food packaging, household products, and personal care items, are known endocrine disruptors that persist in the body and increase the risk of cancer, liver damage, and immune system dysfunction. Recent research suggests that PFAS in drinking water may elevate the risk of cancers affecting the mouth and throat as well as the digestive, endocrine, and respiratory systems.

    Researchers collected data on PFAS levels in U.S. public drinking water systems and county-level cancer rates from 2016 to 2021. Then, using statistical analysis, they estimated the number of cancer cases attributable to PFAS exposure.

    They found that PFAS in drinking water was associated with increased cancer rates in the digestive, endocrine, respiratory, and mouth/throat systems, with risk increases of up to 33%. Among men, PFAS exposure was linked to higher rates of leukemia and cancers of the urinary tract, brain, and soft tissues, while among women, it was associated with thyroid, mouth/throat, and soft tissue cancers. Their analysis estimated that PFAS in drinking water contributes to approximately 4,600 to 6,900 new cancer cases annually, depending on the dataset used.

    These findings highlight the potential risks of PFAS exposure. Because PFAS are present in plastics, microplastics are a significant source of exposure. Learn more about PFAS and microplastics in our overview article.

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  • Regular exercise nearly halves the risk of cancer death. bjsm.bmj.com
    Exercise Cancer Mortality

    Cancer is the second leading cause of death worldwide, claiming the lives of nearly 10 million people yearly. A recent study found that people who exercise regularly are nearly half as likely to die of cancer than those who are inactive.

    Researchers assessed the physical activity of more than 28,000 people diagnosed with stage 1 cancer in the year before their diagnosis based on data gathered from fitness devices, gym logs, and organized fitness events. They categorized the participants' activity as none, low (less than 60 minutes weekly), and medium to high (60 minutes or more weekly). Then, they measured their time to cancer progression and death rates.

    They found that participants with low physical activity were 16% less likely to experience cancer progression and 33% less likely to die than those who were inactive. However, those with medium to high activity levels were 27% less likely to experience progression and 47% less likely to die than those who were inactive.

    These findings highlight exercise’s protective role in reducing cancer progression and improving survival. Exercise boosts the body’s immune system, helping it to combat cancer. It also promotes shear—the frictional drag exerted by blood flowing against the inner walls of blood vessels. Shear damages cancer cells, driving their death. Learn more in this clip featuring Dr. Rhonda Patrick.

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  • Food antigens, proteins in meat and milk that trigger allergic reactions, activate immune responses that reduce the risk of small intestinal tumors. www.frontiersin.org
    Cancer Diet Immune System Allergies Protein

    Proteins in milk, meat, and other foods can trigger allergic reactions in some people. However, these proteins—called antigens—can also interact with the immune system to suppress small intestinal tumors. A recent study in mice found that food antigens help activate immune responses in the small intestine, potentially reducing the risk of tumors.

    Researchers fed mice genetically prone to developing intestinal tumors—similar to the genetic predisposition to familial adenomatous polyposis in humans—an antigen-free diet to pinpoint the role of food components in immune activation. They also depleted immune tissues in the animals' small intestines called Peyer’s patches to investigate how food antigens trigger immune cells.

    They found that food antigens activate immune cells in Peyer’s patches, suppressing small intestinal tumor formation. This immune response is crucial for maintaining a tumor-suppressive environment in the gut.

    These findings suggest that food antigens help protect against small intestinal tumors in mice by activating immune cells that promote tumor suppression, highlighting their potential as a protective factor in gut health. The microbiome plays a key role in gut health, too. Learn more in this episode featuring Dr. Eran Elinav.

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  • People with tattoos have a 21% increased risk of malignant lymphoma, with laser tattoo removal further amplifying the risk to 163%. www.thelancet.com
    Cancer Immune System

    Body art is more popular than ever, with roughly one-third of people in the U.S. having at least one tattoo. However, tattoo inks often contain harmful chemicals, including carcinogenic pigments and metals. A recent study found that people with tattoos are 21% more likely to develop malignant lymphoma.

    Researchers conducted a case-control study among roughly 1,400 people diagnosed with malignant lymphoma (“cases”) in people aged 20 to 60 over 10 years. They matched the cases with age- and sex-matched people without cancer (“controls”) from the general population. Then, they gathered information about the participants' tattoo exposure and assessed the relationship between tattoos and lymphoma risk.

    They found that overall, participants with tattoos were 21% more likely to develop malignant lymphoma than those without. The risk of lymphoma among those who had received their first tattoo within the previous two years was 81% higher than those without a tattoo. Risk decreased nearly to baseline between three and 10 years after the first tattoo but increased again to 19% after 11 years, suggesting that long-term exposure to tattoo-related chemicals contributes to a delayed but persistent risk of developing lymphoma.

    Undergoing laser removal of tattoos increased the risk of lymphoma by 163%. Oddly, greater tattoo surface area did not increase risk, with the highest lymphoma risk among people with tattoos smaller than the size of a deck of cards.

    These findings point to potential links between tattoos and an increased risk of lymphoma. The tattooing process involves injecting ink into the skin through repeated punctures, breaching the skin’s protective barrier and triggering an immune response. As the ink enters the body, immune cells called macrophages attempt to engulf and isolate the foreign substance, driving the movement of pigment to nearby lymph nodes. Lasering tattoo ink induces the formation of toxic, carcinogenic substances that can persist in the body.

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  • Flame retardants used in electronics are found in up to 85% of black plastic household items, including kitchen utensils and toys—an unintended consequence of recycling. pubmed.ncbi.nlm.nih.gov
    Cancer Pollution

    Flame retardants commonly used in electronics carry considerable health risks, from carcinogenicity to endocrine disruption. Despite their harmful effects, these chemicals are often recycled into household items, including kitchen utensils, toys, and food packaging. A recent study found that black plastic household products may contain flame retardants, particularly those derived from recycled electronic products.

    Researchers screened 203 black plastic household products for bromine, a compound used in many flame retardants. They further analyzed products with bromine concentrations higher than 50 parts per million (ppm) for specific flame retardants and plastic types, such as acrylonitrile butadiene styrene and high-impact polystyrene, both commonly used in electronics.

    They found that 85% of the analyzed products contained flame retardants, with concentrations as high as 18,600 ppm, or as much as 22,800 milligrams per kilogram. Notably, a banned compound called decaBDE (and its replacement) was found in many household items. Plastics typically used in electronics, such as polypropylene, contained much higher levels of these chemicals than other types.

    These findings suggest that current recycling practices introduce hazardous flame retardants into everyday plastic household products, raising concerns about unintentional exposure to these toxic compounds. As these plastic items degrade, they contribute to the growing problem of microplastics, which can carry harmful chemicals like flame retardants into the environment and the food chain, further amplifying health risks. Learn more about microplastics in this video featuring Dr. Rhonda Patrick.

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  • More than 3,600 food-contact chemicals used in packaging and storage detected in humans, including several toxic substances associated with cancer, fertility issues, and hormone disruption. www.nature.com
    Cancer Bisphenol A Pollution Sauna

    Despite the perceived safety of the U.S. food supply, many chemicals used in food packaging and storage may be hazardous. In fact, food scientists have found that more than 1,800 food-contact chemicals migrate into foods—many of which have never undergone toxicity testing. New research demonstrates that more than 3,600 of these toxic compounds have been detected in humans.

    Researchers compared a list of more than 14,000 known food-contact chemicals to five major biomonitoring programs and several databases that track chemicals in the human body. They then prioritized chemicals frequently found in food packaging and examined evidence for their presence in humans.

    They found that 3,601 of these chemicals have been detected in humans. Of these, 194 were identified in biomonitoring programs, 80 of which carry a high toxicity risk. They also confirmed that 63 of 175 chemicals of concern were present in the human body, and most lacked safety data.

    These findings suggest that human exposure to food-contact chemicals is widespread, highlighting the need for stricter safety regulations. Many food-contact chemicals include bisphenol A, phthalates, and other toxic substances that promote cancer, impair fertility, and disrupt hormone signaling. Although many of these compounds accumulate in the body over time, some are preferentially excreted in sweat. Learn how sauna use promotes sweating, helping the body rid itself of some toxic substances.

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  • Microplastics absorbed in the gut may promote cancer cell migration and metastasis. www.sciencedirect.com
    Cancer Gut Pollution

    Plastic pollution is a growing environmental concern, with tiny plastic particles infiltrating various ecosystems, including the human body. The gut is crucial in this process, serving as the main gateway for microplastics and nanoplastics to enter the body. A recent study found that human colorectal cancer cells can absorb microplastic particles, raising concerns about their potential effects on health.

    Researchers exposed four human colorectal cancer cell lines to polystyrene micro- and nanoplastics of various sizes (0.25, 1, and 10 micrometers) and concentrations. They tracked the particles' uptake into cells and monitored their behavior during cell division.

    They found that all the cancer cells absorbed micro- and nanoplastics, with the highest uptake observed in HCT116 cells—a type of cells commonly used to study various aspects of tumor biology. Notably, the cells didn’t eliminate the absorbed particles. Instead, they passed them on during cell division, sharing them between the original and new cells. Even short-term exposure to the smallest particles (0.25 micrometers) increased the cells' movement, which could facilitate metastasis.

    These findings suggest that micro- and nanoplastics accumulate in cells and pass into progeny cells during cell division. Once inside the cells, they promote cell migration, potentially enhancing the spread of cancer. Some harmful effects of microplastics may be due to compounds commonly used in plastic manufacturing, such as bisphenol A, phthalates, and heavy metals. Learn more about microplastics in our overview article.

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  • Nearly half of all cancer deaths could be prevented with lifestyle changes. acsjournals.onlinelibrary.wiley.com
    Cancer Diet Alcohol Behavior Mortality

    The choices people make in their daily lives—such as whether to smoke, what to eat, and how active they are—can have a profound effect on their cancer risk. These behaviors are not just habits; they are powerful determinants of health. A recent study found that nearly half of cancer deaths among adults in the U.S. are linked to modifiable lifestyle factors.

    The researchers used national data to estimate cancer cases and deaths for 30 types of cancer. They examined the effects of modifiable risk factors such as smoking, obesity, alcohol consumption, diet, physical inactivity, and ultraviolet light exposure on cancer risk.

    They found that 40% of cancer cases and 44% of cancer deaths were linked to modifiable risk factors. Smoking was the leading contributor, accounting for nearly 20% of cases and more than 28% of deaths. Other major risk factors included excess body weight and alcohol use, accounting for more than half of the cases and deaths for 19 out of 30 cancer types.

    These findings suggest that people can reduce their risk of developing cancer by making informed lifestyle choices. Exercise is a powerful lifestyle tool in cancer prevention and survival. During exercise, increased blood flow subjects circulating cancer cells to powerful forces, causing them to self-destruct. Learn more in this clip featuring Dr. Rhonda Patrick.

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  • Vegans show prolonged side effects and slower healing following photodynamic therapy, demonstrating diet's influence on therapeutic outcomes. www.tandfonline.com
    Nutrition Cancer Diet Vegetarian Protein Red Light Therapy

    Photodynamic therapy is a widely used treatment for actinic keratoses—rough, scaly patches on the skin that may develop into cancer if not treated. Typically, complete skin healing after photodynamic therapy takes between five and ten days, but a recent study found that healing rates differ markedly between vegans and omnivores.

    The study involved 60 patients (30 omnivores and 30 vegans) who were treated with photodynamic therapy for actinic keratosis. Researchers compared side effects using a local skin response score at three intervals: three days, seven days, and 30 days post-treatment. They also noted the time required for complete skin healing in both groups.

    They found that vegans experienced higher total local skin response scores at each interval, indicating they had more severe side effects. On day three, vegans had considerably more swelling and blistering than omnivores. By day seven, they had more redness, peeling, swelling, and blistering. At thirty days, redness and peeling were still more noticeable in vegans. The time required for complete skin healing was notably longer for the vegan group.

    These findings suggest that diet influences healing time following photodynamic therapy, with vegans being more prone to prolonged side effects and slower healing.

    Photodynamic therapy involves the use of a photosensitizing agent (a drug that becomes activated by light) and a specific wavelength of light. When the photosensitizer is exposed to this light, it produces reactive oxygen species that can destroy targeted cells. It differs from photobiomodulation—often called red-light therapy—which uses low-intensity light to stimulate cellular processes and promote healing and pain relief. Learn more about photobiomodulation in our overview article.

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  • Consuming olive oil reduces the risk of early death from all causes by 20%. www.nature.com
    Nutrition Cancer Diet Inflammation Mortality Antioxidant Polyphenol Cardiovascular

    Olive oil is rich in bioactive compounds, including polyphenols, carotenoids, and oleic acid. It’s a fundamental component of the Mediterranean diet and is associated with a wide range of health benefits. A recent study found that high olive oil intake—more than 3 tablespoons daily—reduces the risk of early death from all causes by 20%.

    Researchers analyzed data from nearly 23,000 adults enrolled in a long-term cohort study in Italy. Participants completed questionnaires about their olive oil consumption, defined as high (3 tablespoons or more daily) or low (1.5 tablespoons or less daily). The researchers collected information about the participants' lifestyles, assessed their overall diet quality, and measured their biomarkers associated with chronic disease risk.

    They found that compared to low olive oil intake, high intake lowered the risk of early death from all causes by 20%, cancer by 23%, and cardiovascular disease by 25%. However, They found that the effect of high olive oil intake on reducing the risk of dying from all causes and cancer was slightly lower when considering the participants' biomarkers.

    These findings suggest that olive oil reduces the risk of early death from all causes, including cancer and cardiovascular disease. The polyphenols in olive oil exert potent antioxidant, anti-inflammatory, and anti-cancer effects. Learn more about the health benefits of polyphenols in our overview article.

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  • Shorter-chain PFAS alternatives, found in common household products, readily penetrate human skin, potentially increasing the health risks associated with these "forever chemicals." www.sciencedaily.com
    Cancer Immune System Pollution Environment Skin

    Perfluoroalkyl substances, or PFAS, are synthetic compounds found in food packaging, household products, and plastic bottles. These “forever chemicals” persist in the body for indefinite periods, posing significant health risks such as cancer, liver damage, and immune system dysfunction. To address these concerns, chemical companies have introduced shorter-chain PFAS alternatives, which break down more quickly in the environment. However, a recent study found that these alternatives readily penetrate the skin, potentially increasing the health risks associated with PFAS exposure.

    Researchers designed a three-dimensional model that mimicked the qualities of human skin. They applied various PFAS to the model skin, including perfluoroalkyl carboxylic acids (used on/in non-stick cookware, water and stain repellents, and food packaging) and perfluoroalkane sulfonic acids (used on/in carpets, clothing, paper products, and cleaning agents) and assessed whether the compounds were absorbed (consequently taken up into the bloodstream), unabsorbed, or retained within skin tissue.

    The researchers found that the skin absorbed as much as 58.9% of short-chain PFAS, and the absorption rate decreased as the carbon chain length increased. Interestingly, they found that large quantities of longer-chain PFAS (as much as 68.3%) were retained in the skin instead of being absorbed.

    These findings suggest that PFAS, especially shorter-chain forms, readily penetrate human skin and can gain access to the bloodstream. They also underscore the potential health risks of PFAS exposure and the need for further research and regulation.

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  • High levels of "forever chemicals" linked with cancer and reproductive problems found in seafood. www.sciencedaily.com
    Cancer Pollution Environment

    Polyfluoroalkyl substances, or PFAS, are synthetic compounds used in food packaging, household products, and drinking water. PFAS aren’t excreted in bodily fluids like sweat or urine; instead, they persist in the body indefinitely and are often referred to as “forever chemicals.” A recent study found that seafood – including fish and shellfish – contains high PFAS levels.

    Researchers asked more than 1,800 people living in the northeastern U.S. about the amount and types of seafood they ate. Then, they measured PFAS levels in fish, lobster, shrimp, and scallops purchased from a market in that area.

    They found that the participants were regular seafood consumers, with adults consuming approximately 34 grams daily and children consuming 5 grams – slightly higher than national averages. They also found that the fish contained less than 1 nanogram per gram (ng/g) of PFAS; the shrimp contained 1.74 ng/g, and the lobster contained 3.30 ng/g. These levels may pose health concerns among high seafood consumers.

    These findings suggest that seafood is an abundant source of PFAS. Future research may illuminate the benefits and risks of consuming seafood. Exposure to PFAS has been linked to various health issues, including increased cholesterol levels, changes in liver function, and impaired immune function. Some studies suggest a potential association between PFAS exposure and increased risks of certain cancers and reproductive problems

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  • Smoking cessation cuts lung cancer risk by nearly 40 percent just five years after quitting. www.sciencedaily.com
    Cancer Mortality Addiction Tobacco

    Cigarette smoking is the number one risk factor for lung cancer, the second most common form of cancer and a leading cause of death worldwide. A 2017 study found that heavy smokers' lung cancer risk drops by nearly 40 percent just five years after quitting smoking,

    The study involved more than 8,900 people enrolled in two large cohort studies. Researchers tracked the participants' health for an average of 30 years and determined their cancer risk based on whether they were current, former, or never smokers.

    They found that current and former smokers had a higher risk of developing lung cancer than those who never smoked, but that risk increased tenfold if they were heavy smokers (defined as smoking one pack daily for 21 years or longer), with nearly 93 percent of lung cancers occurring in heavy smokers.

    Five years after quitting, former heavy smokers saw a 39 percent reduction in their lung cancer risk compared to current smokers, and this risk continued to decrease over time. However, even 25 years after quitting, heavy smokers' risk of lung cancer was still more than three times higher than that of people who had never smoked.

    These findings suggest that smoking, especially heavy smoking, markedly increases a person’s risk of developing lung cancer. And although quitting smoking reduces lung cancer risk, former smokers' risks remain higher than never smokers'.

    Many harmful behaviors, such as smoking or overeating, are rooted in reward-based processes. Consequently, people often engage in these behaviors in response to triggers, such as emotional or mental stressors, or external prompts, such as advertising and social pressures. Cognitive behavioral approaches like mindfulness can help people who engage in harmful behaviors become more mindful of these triggers. In turn, they can reevaluate their habits and develop strategies that help them avoid engaging in harmful behaviors. Learn more in this clip featuring Dr. Ashley Mason.

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  • Exposure to flame retardants in everyday household items increases the risk of cancer death more than fourfold. www.dailymail.co.uk
    Cancer Mortality Sauna

    Polybrominated diphenyl ethers (PBDEs) are flame retardants – a broad class of compounds commonly applied to fabrics, carpets, furniture, cell phones, and many other household items. New evidence suggests that exposure to flame retardants more than quadruples the risk of dying from cancer.

    Researchers analyzed blood samples from 1,100 adults enrolled in the National Health and Nutrition Examination Survey and tracked their health for about 16 years. They found that PBDE exposure markedly increased the risk of dying from cancer. Participants with the highest serum PBDE levels were more than four times more likely to die of cancer than those with the lowest levels, even after considering age, sex, race, ethnicity, lifestyle, and other factors that influence cancer death risk.

    These findings suggest that PBDE exposure increases the risk of dying from cancer. Although this observational study did not establish a cause-and-effect relationship between PBDEs and cancer risk, PBDEs are known endocrine disruptors. Endocrine disruptors mimic or interfere with normal hormonal processes in the human body and may influence health throughout the lifespan.

    Interestingly, evidence suggests that sweating promotes PBDE elimination. Sweat losses during a typical sauna session may reduce PBDE burden in the body, potentially reducing cancer death risk. Learn more about how sauna use facilitates the elimination of various toxicants in our overview article.

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  • Omega-3s show promise in easing oral mucositis symptoms during head and neck cancer radiation therapy. bmcoralhealth.biomedcentral.com
    Cancer Microbiome Omega-3 Inflammation

    People who undergo radiation therapy for head and neck cancers often experience oral mucositis – inflammation and ulceration of the mouth and throat that makes speaking, chewing, and swallowing difficult. They also demonstrate alterations in the population of the microbes that typically inhabit the mouth – a condition called dysbiosis. However, a recent study found that people who took omega-3 fatty acids before receiving radiation therapy experienced fewer symptoms of oral mucositis than those receiving conventional therapy.

    The study involved 34 patients with head and neck cancer who were about to undergo radiation therapy. Half of the participants received conventional preventive treatment (topical antifungal and anti-inflammatory mouthwash), and the other half received a topical omega-3 gel. Researchers evaluated the patients' symptoms, pain, and quality of life at baseline, three, and six weeks after treatment and assessed changes in their oral microbiomes.

    They found that those who used the topical omega-3 gel exhibited fewer symptoms and had less pain at the six-week point than those who received the conventional treatment. They also had less microbial dysbiosis.

    These findings suggest that omega-3s reduce the symptoms associated with oral mucositis. These effects may be due to omega-3 fatty acids' potent anti-inflammatory, antioxidant, and wound-healing properties. Learn more about omega-3s in our comprehensive overview article.

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  • Exercise reduces inflammation and enhances immune surveillance in people with Lynch syndrome, highlighting its cancer prevention potential. www.medscape.com
    Exercise Cancer Inflammation Immune System

    Lynch syndrome is an inherited condition linked to increased risks of colorectal and endometrial cancers. While exercise is known to curb the risk of many types of cancer, scientists don’t fully understand its effects on Lynch syndrome. A recent study found that regular exercise reduced inflammation and boosted immune surveillance in people with Lynch syndrome.

    The study involved 21 people with Lynch syndrome. About half of the participants engaged in a 12-month cycling program (three sessions per week, 45 minutes per session), while the others received standard care and a single exercise counseling session. Researchers assessed the participants' cardiorespiratory fitness and measured gene expression in colorectal tissue before and after the intervention.

    They found that participants' oxygen consumption increased and colon and blood inflammatory markers decreased in those who exercised but not in those who received standard care. Gene expression analysis revealed heightened levels of natural killer and CD8 T cells in those who exercised.

    Natural killer (NK) cells and CD8 T cells play critical roles in the immune system’s defense against cancer. They are crucial components of the body’s immunosurveillance mechanism, responsible for identifying and eliminating potentially cancerous cells.

    These findings underscore exercise’s potential to intercept cancer in Lynch syndrome and shed light on its immunological effects in high-risk people. Learn about the differential effects of exercise intensity and duration on the body’s immune response in this live Q&A featuring Dr. Rhonda Patrick.

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  • Chronic cold exposure reduces tumor growth by 80 percent and doubles survival rates in mice. www.newscientist.com
    Cancer Cold Stress Brown Fat

    Cancer treatments often target glucose uptake to impede tumor growth, primarily through pharmaceuticals, many of which exert considerable side effects. However, cold exposure is emerging as a potential alternative to these drug-based therapies. A recent study in mice found that cold exposure reduced tumor growth by 80 percent and increased survival rates twofold.

    Researchers conducted a two-part study in mice and humans. First, they exposed mice with cancer to cold (4°C, 39°F) or thermoneutral (30°C, 86°F) temperatures for about three weeks. They found that the cold exposure activated the animals' brown fat, depleting the energy supply available to the tumors. The cold-exposed mice exhibited marked tumor growth inhibition and a nearly twofold increase in survival rates relative to the thermoneutral mice. Interestingly, when they fed the cold-exposed mice a high-glucose diet, the animals did not experience the same extent of tumor growth inhibition, suggesting that glucose scarcity was pivotal in suppressing cancer growth.

    In the second part of the study, they exposed healthy people to cool temperatures (16°C, 61°F) for two to six hours per day for 14 days and found that the participants experienced brown fat activation similar to the mice. Then, they exposed a person with Hodgkin’s lymphoma to cool (22°C, 71°F) temperatures for seven days and found that the participant exhibited activated brown fat and their tumor showed diminished glucose consumption, suggesting the findings in mice translate to humans.

    These findings suggest that cold exposure activates brown fat, reducing blood glucose and impeding tumor growth. Brown fat is a thermogenic (heat-producing) tissue. Studies in animals and humans suggest that brown fat can improve glucose and insulin sensitivity, increase fat oxidation, and protect against diet-induced obesity. Cold exposure increases brown fat volume and metabolism and drives glucose uptake. Learn more about cold exposure and its effects on brown fat in our overview article.

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  • Ovarian cancer tumors, even at advanced stages, may be effectively targeted and eliminated by CAR-T immune therapies, a new study in mice suggests. www.sciencedaily.com
    Cancer Genetic Engineering Immune System

    CAR-T, or chimeric antigen receptor T-cell therapy, is an immunotherapy approach that involves genetically modifying a person’s own T cells so they can recognize and target specific proteins on cancer cell surfaces, enhancing the immune system’s capacity to seek out and destroy malignant cells. CAR-T therapies have been successful against blood cancers, such as leukemia, lymphoma, or myeloma, but have largely failed with solid tumors. Now, a new study in mice demonstrates that CAR-T is effective against ovarian cancer, nearly doubling survival time.

    Researchers identified a unique carbohydrate present only on the surface of solid tumor cells, not healthy ones, and engineered CARs with a strong affinity for the carbohydrate. Then, they delivered the CAR-T therapy via intravenous injection to mice with ovarian cancer. Because ovarian cancer treatments delivered directly into the abdominal area are particularly effective, they also administered the CAR-T therapy into the animals' abdomens.

    They found that the CAR-equipped T cells effectively located and eliminated the cancer cells, promoting tumor shrinkage or elimination with just one dose. The genetically engineered cells maintained their effectiveness for several months, with no evidence of toxicity or adverse effects. Intravenous injection of CAR-T cells increased survival to 145 days, but direct delivery into the animals' abdomens extended survival to 270 days.

    These findings demonstrate that modified CAR-T cells show promise as a potential treatment for ovarian cancer and other solid tumors. Future studies are needed to assess the treatment’s effectiveness in humans. Learn more about genetic engineering in this episode featuring Dr. George Church.

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  • Many cancers are influenced by excess body fat, with overall accumulation playing a larger role than fat distribution, despite sex-specific difference www.eurekalert.org
    Cancer Fat

    Excess body fat increases a person’s risk for many types of cancer. However, body fat distribution patterns tend to be sex-specific, with males carrying more fat in the upper abdomen and females carrying more in the hips, thighs, buttocks, and lower abdomen. A new study has identified differences in obesity-driven cancer rates between males and females.

    Researchers drew on data from more than 440,000 adults enrolled in the UK Biobank study. They used statistical analysis to determine how various measures of body fat, such as body mass index (BMI) and waist circumference, influenced the risk of developing 19 types of cancer over a follow-up period of about 13 years.

    They found that nearly all 19 cancers were associated with excess body fat, except brain, cervical, and testicular cancers. They also found that overall body fat had a greater influence on cancer risk than fat distribution. However, they noted sex-specific effects of body fat on colorectal, esophageal, and liver cancer rates between males and females. For example, excess abdominal fat increased the rates of esophageal cancer in females but not males. Similarly, excess overall fat increased the rates of liver cancer in males but not females.

    These findings suggest body fat plays important but differential roles in cancer risk between males and females. Evidence suggests a ketogenic diet promotes weight loss and reduces cancer risk. Learn more about ketogenic diets and cancer in this episode featuring Dr. Dominic D'Agostino.

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  • Higher omega-3 intake may reduce breast cancer risk by half. www.verywellhealth.com
    Nutrition Cancer Diet Breast Cancer Omega-3

    Higher intake of omega-3 fatty acids may reduce the risk of breast cancer, a 2022 study found. Women with the highest omega-3 intake were as much as 49 percent less likely to develop breast cancer than those with the lowest intake.

    Researchers conducted a study that included more than 3,200 women, roughly half of whom had breast cancer. The women provided information about what they typically ate, including foods rich in omega-3 fatty acids, and whether they were pre- or postmenopausal.

    The researchers found that a higher intake of omega-3 in the form of alpha-linolenic acid reduced breast cancer risk by 49 percent; a higher intake in the form of eicosapentaenoic acid reduced risk by 32 percent. The links between omega-3s and breast cancer risk were strongest among premenopausal women and women with hormone-sensitive tumors. Interestingly, higher omega-3 intake markedly reduced the risk of breast cancer among women who had obesity or overweight but not among those who had healthy weights.

    These findings suggest that omega-3s reduce the risk of breast cancer, the second leading cause of cancer-related death among women. Inflammation plays a key role in the pathogenesis of many cancers, including breast cancer. Learn how omega-3 fatty acids reduce inflammation in this clip featuring Dr. Bill Harris.

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  • Levels of PFAS, a group of synthetic chemicals, were 278 times higher in freshwater fish across the U.S. than in commercially-sold fish. (2023) doi.org
    Cancer Diet Cholesterol Immune System Development Environment

    From the publication:

    Per- and polyfluoroalkyl substances (PFAS), previously referred to as “perfluorinated compounds”, are a class of manufactured chemicals that have been detected in nearly all sampling of geographic locations and environmental matrices worldwide, including sites that had no nearby manufacture or use of PFAS. PFAS are used in hundreds of industrial and consumer products including food packaging and waterproof/stain resistant fabrics. Their strong carbon-fluorine bonds provide both hydrophobic and oleophobic properties, which make these chemicals extremely persistent in the environment. The class of PFAS includes tens of thousands of potential environmental contaminants including over one thousand chemicals previously or currently approved for use in the U.S..

    For PFAS measured at concentrations already found in the general population, exposure may suppress the immune system. Additionally, exposure to PFAS, with most studies on PFOA and PFOS, has been associated with many health harms, including an increased risk of cancer, high cholesterol, thyroid disease, and reproductive and developmental harms.

    The median level of total targeted PFAS in fish fillets from rivers and streams across the United States was 9,500 ng/kg, with a median level of 11,800 ng/kg in the Great Lakes. PFOS was the largest contributor to total PFAS levels, averaging 74% of the total. The median levels of total detected PFAS in freshwater fish across the United States were 278 times higher than levels in commercially relevant fish tested by the U.S. Food and Drug Administration in 2019–2022. Exposure assessment suggests that a single serving of freshwater fish per year with the median level of PFAS as detected by the U.S. EPA monitoring programs translates into a significant increase of PFOS levels in blood serum.

    Additional information:

    In June 2018, the Agency for Toxic Substances and Disease Registry (ATSDR) released a draft Toxicological Profile that derived minimal risk levels (MRLs), which are similar to RfDs, for intermediate duration exposure (15–364 days) of four PFAS routinely measured in NHANES [28]. The MRL [minimal risk levels] values for PFOA (3 ng/kg/day) and PFOS (2 ng/kg/day) are 6.7 and 10 times lower than the RfDs EPA used to develop its 2016 HAs and similar to those developed by New Jersey, though they are based on different studies and endpoints. View full publication

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  • Gene-edited tumor cells used as a "tumor-killing" cancer vaccine in a new approach to treating glioblastoma. medicalxpress.com
    Cancer Immune System Vaccine

    An experimental vaccine killed brain cancer cells and prevented them from returning, a new study in mice has found. The mice lived longer and had improved anti-cancer immunity.

    Using CRISPR-Cas9, a powerful gene editing tool, researchers modified living tumor cells so that they would secrete interferon-beta and granulocyte-macrophage colony-stimulating factor – two potent immunomodulatory and anti-tumor agents. Then they incorporated a “kill switch” in the modified cells that would prevent secondary tumor initiation.

    They found that the modified tumor cells killed glioblastoma tumor cells by inducing apoptosis (cell death) and turning off the activity of cancer growth factors. The modified cells also turned on normal anti-cancer immune cell activities and signaling, improving the animals' survival and promoting their long-term immunity.

    This study in mice provides proof of concept for the use of genetically modified living tumor cells as anti-tumor agents and paves the way for their future use in humans. Learn more about therapeutic uses of gene editing in this episode featuring Dr. George Church.

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  • Vigorous intensity exercise may be even more time-efficient than previously thought. academic.oup.com
    Exercise Cancer Mortality Cardiovascular

    People who regularly engaged in vigorous-intensity exercise were less like to die from cancer, cardiovascular disease, or other causes, according to a new study. Engaging in vigorous-intensity exercise for as little as 54 minutes per week provides optimal mortality reduction – but the catch is that it must be sufficiently vigorous.

    Using wrist-worn accelerometers, nearly 72,000 middle-aged adults enrolled in the UK Biobank study tracked their activity. Researchers monitored the participants' health for approximately six years.

    They found that the participants' risk of dying during the study period varied based on their activity level. The risk of dying among those engaging in no vigorous-intensity activity per week was 4.17 percent; zero to less than 10 minutes, 2.12 percent; 10 to less than 30 minutes, 1.78 percent; 30 to less than 60 minutes, 1.47 percent; and for 60 minutes or more, 1.10 percent. They determined that the “optimal” dose of vigorous-intensity activity was approximately 54 minutes per week, and the “minimal” dose – sufficient to reduce the risk of dying from cancer, cardiovascular disease, or all other causes – was approximately 15 minutes.

    Vigorous-intensity exercise is defined as activity that achieves a heart rate that is 70 to 80 percent of one’s maximum. High-intensity interval training, often referred to as HIIT, is a popular form of vigorous exercise involving short bursts of intense aerobic exercise interspersed with periods of rest or lower-intensity exercise. During a typical HIIT session, exercisers typically achieve 80 to 100 percent of their VO2max (a measure of respiratory function) or maximum heart rate. Most HIIT workouts are brief, lasting just 15 to 30 minutes.

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  • Postmenopausal women with colon cancer lived longer and had a 36% lower risk of dying from the disease if they had taken estrogen supplements. (2006) www.sciencedaily.com
    Cancer Hormones Estrogen Mortality

    From the article:

    The research by Chan and her colleagues drew on data from 834 postmenopausal women enrolled in the Nurses' Health Study – which has tracked the health of more than 100,000 female nurses since 1976 – who had been diagnosed with colon cancer between 1976 and 2000. The researchers found that, compared to women who had never used estrogen, those using the hormone at the time of diagnosis had a 36 percent lower chance of dying of colon cancer and a 26 percent lower chance of dying of any cause. The benefit was most pronounced in women who used estrogen for less than five years. Using it for longer, however, did not seem to provide a similar advantage.

    The authors do not know why using estrogen for more than five years did not improve women’s chances of survival. They theorize that colon tumors that developed in women who had used estrogen for many years may have been less susceptible to estrogen’s growth-slowing effects.

    The precise way by which estrogen foils the growth of colon cancer cells is unclear, as well. The study authors offer three possibilities: the hormone directly suppresses the cells' growth; it decreases the production of bile acids which are known to spur cancer; or it blocks certain genetic changes within colon cells that lead to cancer.

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  • The risk of developing ovarian cancer increased by 220% in postmenopausal women who used estrogen therapy for 20 or more years. (2002) www.sciencedaily.com
    Cancer Hormones Estrogen

    From the article:

    The scientists followed 44,241 women for approximately 20 years. Compared to postmenopausal women not using hormone replacement therapy, users of estrogen-only therapy had a 60 percent greater risk of developing ovarian cancer. The risk increased with length of estrogen use. The women, who were followed from 1979 to 1998, were former participants in the Breast Cancer Detection Demonstration Project, a mammography screening program conducted between 1973 and 1980.

    “The main finding of our study was that postmenopausal women who used estrogen replacement therapy for 10 or more years were at significantly higher risk of developing ovarian cancer than women who never used hormone replacement therapy,” said James V. Lacey, Jr., Ph.D., lead author of the study from NCI’s Division of Cancer Epidemiology and Genetics.

    The relative risk for 10 to 19 years of use was 1.8, which translates to an 80 percent higher risk than non-users, and increased to 3.2 (a 220 percent higher risk than non-users) for women who took estrogen for 20 or more years.

    […]

    Two recent large studies found a link between hormone use and ovarian cancer. A large prospective study published last year (JAMA 2001;285:1460-1465) showed that postmenopausal estrogen use for 10 or more years was associated with increased risk of ovarian cancer mortality, and a recent Swedish study (J. Natl. Cancer Inst. 2002;94:497-504) reported that estrogen use alone and estrogen-progestin used sequentially (progestin used on average 10 days/month) may be associated with an increased risk for ovarian cancer. In contrast, estrogen-progestin used continuously (progestin used on average 28 days/month) seemed to confer no increased ovarian cancer risk.

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  • Coenzyme Q10 reduces fatigue in people with chronic fatigue disorders. www.nutraingredients.com
    Nutrition Cancer Micronutrients

    People with chronic fatigue disorders who took coenzyme Q10 (CoQ10) supplements experienced less fatigue, a recent review and meta-analysis has found. The greatest reduction in fatigue was found with supplements that contained CoQ10 alone, rather than those that contained a mixture of other dietary supplements.

    Researchers analyzed the findings of 13 studies involving more than 1,100 people who had conditions that commonly cause fatigue, such as heart failure, autoimmune disorders, and cancer. The study participants took supplements containing between 60 and 500 milligrams of CoQ10 daily for four to 24 weeks and reported on their fatigue levels. Some of the supplements contained CoQ10 alone, while some also contained NADH (the reduced form of NAD+) or multivitamins.

    The researchers found that participants who took supplements containing CoQ10 alone reported less fatigue than those who didn’t take CoQ10 or took it combined with other compounds. Only one participant reported any adverse effects (gastrointestinal upset).

    CoQ10 is a fat-soluble antioxidant compound produced in the body. It is also widely available as a dietary supplement. CoQ10 is an essential component of the mitochondrial electron transport chain, which is responsible for the production of cellular energy in the form of adenosine triphosphate, or ATP.

    The findings from this review and meta-analysis suggest that CoQ10, especially when taken alone, improves symptoms of fatigue in people with chronic conditions associated with fatigue.

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  • Estrogen metabolites may promote lung cancer - including enhancing the effects of tobacco smoke on the disease, mouse study suggests. (2012) www.sciencedaily.com
    Cancer Hormones Estrogen Tobacco

    From the article:

    To investigate, Peng, Clapper and their colleagues examined the lungs of healthy mice and found that they contained high levels of estrogen metabolites, known as 4‑hydroxy- estrogens (4-OHEs), which are carcinogenic. Specifically, these 4-OHEs help activate processes that promote cell growth, and generate free radicals that damage cells.

    When the researchers exposed the mice to tobacco smoke for 8 weeks, they found that the levels of 4-OHEs increased. “We believe that these metabolites of estrogen can damage cells and contribute to lung cancer,” says Clapper.

    Female mice had twice as much 4-OHE in their lungs compared to male mice after controlling for the level of total estrogen present. Whether this is the same in humans remains to be determined. “While lung cancer is not more common in women, the number of nonsmokers who develop lung cancer is greater for men than for women,” explains Clapper.

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  • Tumor cell-independent estrogen signaling may drive disease progression by mobilizing immune cells associated with tumor treatment resistance. (2016) www.sciencedaily.com
    Cancer Hormones Breast Cancer Immune System Estrogen

    From the article:

    Conejo-Garcia and colleagues found that estrogen signaling is closely linked to both the accumulation and activity of myeloid-derived suppressor cells (MDSCs), a set of immune cells associated with tumors treatment resistance. Estrogen enables immunosuppression in a two-pronged approach involving MDSCs. First, the estrogen drives the mobilization of MSDCs. Then, at the same time, it makes a subset of the MDSCs more immunosuppressive in vivo. Estrogen supplementation accelerated the growth of multiple models estrogen-insensitive tumors in immunocompetent animals, while ablating estrogen production by resecting the ovaries boosted anti-tumor immunity and delayed malignant progression. Importantly, differences in tumor progression disappeared in immunodeficient mice, demonstrating that estrogen-mediated acceleration of tumor growth depends on dampening protective anti-tumor immunity.

    They also demonstrated how ERα is responsible for enhancing the activity of multiple pathways that are already associated with cancer development. This estrogen receptor activated the STAT3 pathway, which has already been linked to cancer cell survival and the expansion of MDSCs in cancer-bearing hosts. It was also able to activate this pathway by enhancing the activity of JAK2 and SRC, two proteins linked to cancer development and immune response.

    These cancer pathways are activated in a variety of inflammatory cancers in non-tumor cells, such as breast cancer, ovarian cancer, and melanoma. Since estrogen is present not just pre-menopausal women but men and post-menopausal women as well, the authors propose that investigating anti-estrogen therapeutic strategies could lead to new treatments for a variety of cancers. This strategy could halt the mobilization of MDSCs and tumor initiation.

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  • Estradiol may induce BDNF/TrkB signaling in non-estrogen-dependent breast cancer to promote brain metastases, mouse study suggests. (2019) www.sciencedaily.com
    Brain Cancer Hormones Breast Cancer Estrogen BDNF

    From the article:

    After all, triple negative breast cancers lack estrogen receptors (along with progesterone receptors and HER2, thus the name triple negative), and so these cancers can’t possibly be influenced by estrogen. Right?

    […]

    Technically, Cittelly and colleagues including postdoctoral researcher, Maria Contreras-Zarate, PhD, found that estrogen induces astrocytes (brain cells) to produce growth factors called brain-derived neurotrophic factor (BDNF) and Epidermal Growth Factor (EGF), and that these factors turns on two genetic migration/invasion switches in cancer cells, namely TRKB and EGFR.

    “This may explain why breast cancers diagnosed in younger women are more likely to metastasize to the brain – pre-menopausal women have more estrogen, and it may be influencing the microenvironment of the brain in ways that aid cancer,” Cittelly says.

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  • Estrogen treatment and overexpression of the estrogen receptor may cause malignant neuroblastoma cells to mature into neuron-like cells. (2018) www.sciencedaily.com
    Cancer Hormones Estrogen

    From the article:

    In a previous study, her group discovered that activation of MYCN [gene that drives tumour cell growth and spread and inhibits the maturation of the cells] results in the formation of specific microRNAs, which are relatively small RNA molecules that regulate proteins. Some of these microRNAs disable the estrogen receptor ERalpha. The present study shows that the inhibition of these microRNA molecules or estrogen therapy in combination with an overexpression of the estrogen receptor can cause aggressive neuroblastoma cells with MYCN activation to mature into neuron-like cells which behave more like normal cells.

    The researchers studied tumour tissue from patients, cultivated human tumour cells and tumours in mouse models for neuroblastoma. In the mice, the neuron-like cells did not grow as quickly as the original cancer cells, and analyses of the tumour tissue from patients show that those with a high level of the estrogen receptor have a better survival rate that those with a low.

    “Our data suggests that estrogen could be a therapeutic method for patients who express high levels of the estrogen receptor,” continues Professor Arsenian-Henriksson. “Another possible therapy could involve deregulating MYCN or upregulating the estrogen receptor and then treating with estrogen. We have previously shown that the deregulation of MYCN leads to a high expression of the estrogen receptor.”

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  • Activating a specific estrogen receptor may stop pancreatic cancer cells from growing and make the tumors more visible to the immune system. (2020) www.sciencedaily.com
    Cancer Hormones Estrogen

    From the article:

    For most cancer types, including pancreas, women generally have better outcomes than men. Although the reasons for this are only now emerging, researchers have known for decades that there is a link between the body’s sex hormones and some types of cancer, especially those arising in reproductive tissues such as breast and prostate. However, the idea that cancers in non-reproductive tissues might also be influenced by sex steroid hormones has only recently been considered.

    […]

    Using new PCRC mouse pancreatic cancer models, the multidisciplinary team was able to show GPER’s [G protein-coupled estrogen receptor] impact on pancreatic cancer growth. In some models, GPER [G protein-coupled estrogen receptor] activation inhibited growth and made tumors more sensitive to anti-PD-1 immunotherapy, pointing to the translational potential of improving the efficacy of existing treatments in a cancer type where PD-1 inhibitors have not historically been very effective.

    The use of GPER activators is a novel idea in cancer therapy, and has a key difference from most anti-cancer agents. Nearly all current cancer drugs act to block the activity of cellular proteins that are needed by not only the cancer cells, but also by normal cells. As a result, most cancer drugs are associated with major toxicity. In contrast, the estrogenic analog used in the Penn study activates GPER. This approach mirrors something that naturally occurs in the body, as GPER is already present and normally activated by estrogen, especially in females during pregnancy.

    “Likely because this is something the human body is already accustomed to, evidence from preclinical animal studies suggested that side effects to this approach would likely be minimal when this moves into the clinic,”

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  • Vitamin D deficiency increases the odds of all-cause mortality by 25%, a mendelian randomization study suggests. (2022) doi.org
    Vitamin D Cancer Mortality Cardiovascular

    From the publication:

    Participants: 307 601 unrelated UK Biobank participants of White European ancestry (aged 37 to 73 years at recruitment) with available measurements of 25-hydroxyvitamin D (25-(OH)D) and genetic data.

    Measurements: Genetically predicted 25-(OH)D was estimated using 35 confirmed variants of 25-(OH)D. All-cause and cause-specific mortality (cardiovascular disease [CVD], cancer, and respiratory) were recorded up to June 2020.

    Results: There were 18 700 deaths during the 14 years of follow-up. The association of genetically predicted 25-(OH)D with all-cause mortality was L-shaped, and risk for death decreased steeply with increasing concentrations until 50 nmol/L. Evidence for an association was also seen in analyses of mortality from cancer, CVD, and respiratory diseases. Odds of all-cause mortality in the genetic analysis were estimated to increase by 25% for participants with a measured 25-(OH)D concentration of 25 nmol/L compared with 50 nmol/L.

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  • Aerobic exercise may reduce the risk of metastatic cancer by 73 percent – and this magnitude of effect may be unique to high-intensity activity. neurosciencenews.com
    Exercise Cancer

    Intense aerobic exercise reduces the risk of metastatic cancer by as much as 73 percent, a recent study has found. It does this by reducing the glucose consumption of the body’s internal organs, effectively diverting energy away from the tumor.

    Researchers quantified the proteins present in the internal organs of mice and the plasma of humans and found that exercise alters multiple aspects of metabolism, including glucose uptake, mitochondrial activity, and carbohydrate utilization.

    Then they analyzed data from a long-term study of more than 2,700 adults living in Israel. They found that high-intensity exercise reduced the risk of developing highly metastatic cancer by 73 percent. They observed similar findings in an animal model of melanoma: animals that exercised before they developed cancer were less likely to experience cancer metastasis.

    Evidence suggests that exercise exerts antitumor effects by increasing the body’s insulin sensitivity, reducing sex-steroid hormone levels, and dampening the immune response (and the accompanying inflammation). It also promotes the release of signaling molecules in skeletal muscle, called myokines, which inhibit tumor growth.

    This study demonstrates that exercise markedly reduces cancer risk in humans. Following a time-restricted eating pattern may reduce cancer risk, too. Learn more in this episode featuring Dr. Ruth Patterson.

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  • A group of international experts takes strong stance on testosterone deficiency treatment. (2016) www.sciencedaily.com
    Cancer Hormones Diabetes Testosterone Prostate Cardiovascular

    From the article:

    After examining the best available scientific evidence, Morgentaler and colleagues – who included experts with specialties in urology, endocrinology, diabetes, internal medicine, and basic science research – agreed on the following:

    – TD [testosterone deficiency] is a well-established, clinically significant medical condition that negatively affects male sexuality, reproduction, general health and quality of life.

    – Symptoms and signs of TD occur as a result of low levels of testosterone and may benefit from treatment regardless of whether there is an identified underlying origin.

    – TD is a global public health concern.

    – Testosterone therapy for men with TD is effective, rational, and evidence-based.

    – There is no testosterone concentration threshold that reliably distinguishes those who will respond to treatment from those who will not.

    – There is no scientific basis for any age-specific recommendations against the use of testosterone therapy in adult males.

    – The evidence does not support increased risks of cardiovascular events with testosterone therapy.

    – The evidence does not support increased risk of prostate cancer with testosterone therapy.

    – The evidence supports a major research initiative to explore possible benefits of testosterone therapy for cardiometabolic disease, including diabetes.

    “It will be surprising to those unfamiliar with the literature to learn how weak the evidence is supporting the alleged risks of cardiovascular disease and prostate cancer,” said Michael Zitzmann, MD, vice-chair of the conference and a Professor in the Centre for Reproductive Medicine and Andrology at the University of Muenster in Germany. “Indeed, there is substantial data suggesting there may actually be cardio-protective benefits of testosterone therapy.”

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  • High levels of free testosterone, but not total testosterone, may increase risk of prostate cancer. (2004) www.sciencedaily.com
    Cancer Hormones Testosterone Prostate

    From the article:

    The researchers measured several forms of testosterone in almost 3,000 blood samples collected over a 40-year period from 759 men in the Baltimore Longitudinal Study on Aging, of whom 111 were diagnosed with prostate cancer. One form of testosterone, called free testosterone, which is biologically active and can actually be used by the prostate, was found to be associated with increased prostate cancer risk, according to J. Kellogg Parsons, M.D., instructor of urology at the Brady Urological Institute at Johns Hopkins and lead researcher of the study.

    “Since testosterone replacement therapy increases the amount of free testosterone in the blood, older men considering or receiving testosterone replacement should be counseled as to the association until data from long-term clinical trials becomes available,” says Parsons.

    The association between free testosterone and prostate cancer risk in older men was not affected by height, weight, percent of body fat, or muscle mass. Total testosterone levels and dehydroepiandrosterone sulfate (DHEAS), another androgenic hormone, were also unrelated to prostate cancer risk, while the protein that binds testosterone in blood, called sex hormone-binding globulin (SHBG), was associated with a slightly decreased risk for prostate cancer.

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  • Long-term testosterone therapy in hypogonadal men does not increase the risk of prostate cancer, study suggests. (2014) www.sciencedaily.com
    Cancer Hormones Testosterone Prostate

    From the article:

    A total of 1,023 patients on T[estosterone] therapy were followed for up to 17 years with a median follow-up of approximately 5 years. Two study cohorts of 261 (cohort 1) and 340 (cohort 2) men were treated by urologists since 2004 and a third cohort of 422 men was treated at an academic andrology center since 1996. Hypogonadism was diagnosed if testosterone was ≤12 nmol/L [345.82 ng/dL] and if other symptoms were present, such as erectile dysfunction, fatigue, depression, or unfavorable changes in body composition (gaining of fat mass and waist circumference despite physical activity). If no contraindications were present, all were started on T therapy.

    There were six (2.3%) diagnoses of PCa [prostate cancer] in cohort 1, there were five (1.5%) diagnoses of PCa in cohort 2, and all biopsies were negative in cohort 3. PCa incidence per 10,000 patient-years in cohorts 1 and 2 was 54.4 and 30.7, respectively, which is lower than 116 reported by the PLCO (Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial) and 96.6 reported by the ERSPC ( European Randomized Study of Screening for Prostate Cancer).

    Investigators stress that if guidelines for T therapy are properly applied, it is safe in hypogonadal men.

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  • Men may have a 2.5-fold increased 10-year risk of death if they have low testosterone, regardless of age. (2008) www.sciencedaily.com
    Cancer Hormones Heart Disease Testosterone Mortality Cardiovascular

    From the publication:

    In the study, Haring and co-workers looked at death from any cause in nearly 2,000 men aged 20 to 79 years who were living in northeast Germany and who participated in the Study of Health in Pomerania (SHIP). Follow-up averaged 7 years. At the beginning of the study, 5 percent of these men had low blood testosterone levels, defined as the lower end of the normal range for young adult men. The men with low testosterone were older, more obese, and had a greater prevalence of diabetes and high blood pressure, compared with men who had higher testosterone levels, Haring said.

    Men with low testosterone levels had more than 2.5 times greater risk of dying during the next 10 years compared to men with higher testosterone, the study found. This difference was not explained by age, smoking, alcohol intake, level of physical activity, or increased waist circumference (a risk factor for diabetes and heart disease), Haring said.

    In cause-specific death analyses, low testosterone predicted increased risk of death due to cardiovascular disease and cancer but not death of any other single cause.

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  • International organizations suggest a cut-off level between 300 -350 ng/dl for testosterone deficiency. (2019)
    Cancer Hormones Heart Disease Testosterone Prostate Stroke Cardiovascular

    From the publication

    The purpose of this paper is to analyze the guidelines for TTh [testosterone therapy] from international organizations and compare their recommendations.

    […]

    All agree that TD [testosterone deficiency] is a clinical syndrome that requires a low testosterone level as well as signs and/or symptoms for a diagnosis to be made. The exact cut -off varies or is not provided, but the organizations suggest a cut -off level between 300 -350 ng/dl. All societies recommend routine laboratory monitoring within the first year and annually after. The guideline committees acknowledge limited data on cardiovascular disease and testosterone. The consensus is to withhold TTh within 3 -6 months of an MI or stroke or in patients with severe heart failure.(2, 4) Prostate cancer is another gray area. Although the consensus is that there is no data to suggest TTh causes prostate cancer.

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  • Patients undergoing testosterone-lowering therapy for prostate cancer had an 88% increased risk of Alzheimer's risk. (2015) www.sciencedaily.com
    Alzheimer's Cancer Hormones Diabetes Testosterone Prostate Cardiovascular

    From the article:

    Using two different methods of statistical analysis, the team showed that the ADT [androgen deprivation therapy] group, compared to the control group, had significantly more Alzheimer’s diagnoses in the years following the initiation of androgen-lowering therapy. By the most sophisticated measure, members of the ADT [androgen deprivation therapy] group were about 88 percent more likely to get Alzheimer’s during the follow-up period.

    The analyses also suggested a “dose-response effect.” The longer individuals underwent ADT the greater their risk of Alzheimer’s disease, they found. The longer-duration ADT patients also had more than double the Alzheimer’s risk of non-ADT controls.

    […]

    How low testosterone would lead to increased Alzheimer’s risk isn’t precisely known, but there is some evidence that testosterone has a general protective effect on brain cells, so that lowering testosterone would leave the brain less able to resist the processes leading to Alzheimer’s dementia. Studies in mice and in humans also have suggested that lower testosterone levels may allow greater production of the Alzheimer’s protein amyloid beta. Moreover, low testosterone may increase Alzheimer’s risk indirectly, by promoting conditions such as diabetes and atherosclerosis that are known to predispose to Alzheimer’s.

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  • Brisk walking reduces cancer cell numbers in colon cancer survivors. pubmed.ncbi.nlm.nih.gov
    Exercise Cancer

    Colon cancer survivors who engaged in moderate-intensity exercise for six months had fewer circulating tumor cells than non-exercising survivors, according to a 2018 study. The researchers attributed these anticancer effects to mechanical stressors that cancer cells experience in the bloodstream during exercise that drive cells to self-destruct.

    Researchers assigned 23 stage I-III colon cancer survivors to engage in either 150 or 300 minutes of moderate-intensity exercise (brisk walking) per week for six months or to continue their normal activities. The researchers measured the participants' circulating tumor cells before and after the intervention.

    They found that after six months, both groups of exercisers experienced reductions in their circulating tumor cells, but non-exercisers did not. Exercisers also lost weight and had lower insulin levels.

    Circulating tumor cells are cancer cells that separate from the primary cancer site and appear in the bloodstream, where they can migrate to and establish themselves in other parts of the body – a process known as metastasis. Exercise increases blood flow and exerts tremendous mechanical forces on circulating tumor cells, sensitizing them to apoptosis, a cellular self-destruct mechanism.

    The findings from this small study suggest that exercise reduces the number of circulating tumor cells in cancer survivors. A larger study showed that stage III colon cancer survivors who exercised were 40 percent less likely to experience a recurrence and 63 percent less likely to die from their cancer compared to non-exercisers. Interestingly, time-restricted eating may help reduce the risk of cancer recurrence, too. Learn more in this episode featuring Dr. Ruth Patterson.

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  • High intensity interval exercise significantly reduced colon cancer cell number in colon cancer survivors. www.medicalnewstoday.com
    Exercise Cancer

    HIIT suppresses colon cancer cell growth.

    Just a single session of HIIT – high-intensity interval training – reduced the number of colon cancer cells in vitro, a 2019 study found. Researchers attributed the cancer-suppressing effect of HIIT to a transient increase in inflammatory cytokines that occurred shortly after the exercise.

    The study involved 20 male colon cancer survivors. Half of the men performed a single, 38-minute bout of HIIT (at 85 to 95 percent of their maximum heart rate), while the other half performed 12 HIIT sessions over a period of four weeks. Researchers treated cultured colon cancer cells with serum taken from the participants at various time points before and up to seven days after their respective HIIT protocols.

    They found that serum collected immediately after engaging in HIIT reduced colon cancer cell numbers in the cultured cells. HIIT also produced increases in pro-inflammatory cytokines interleukin (IL)-6, IL-8, and tumor necrosis factor. Interestingly, the inhibition of cancer growth was transient, lasting less than two hours post-exercise when inflammatory cytokine levels were high. The serum collected at other time points had no effect on the cancer cells' growth.

    The pro-inflammatory response that normally results from exercise peaks roughly an hour post-exercise. It then begins to subside and is followed by a powerful anti-inflammatory response – an essential process for maintaining an appropriate balance of pro- and anti-inflammatory mediators.

    These findings suggest that transient exercise-induced inflammation slows colon cancer growth, potentially influencing cancer survival. Sauna use mimics many of the physiological effects of exercise and may be suitable for cancer survivors with health or mobility issues that make exercising difficult. Learn more about sauna use in our overview article.

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  • The fasting-mimicking diet promotes anticancer immunity in cancer patients. aacrjournals.org
    Cancer Diet Fasting

    The fasting-mimicking diet – a short-term, low-protein, low-carbohydrate diet – improves metabolism and increases immune cell populations that target cancer, according to a 2021 study. Participants who followed the five-day dietary protocol found it easy to adhere to and experienced few ill effects other than fatigue.

    The study involved 101 cancer patients who followed a fasting-mimicking diet that provided up to 600 calories on the first day and up to 300 calories on the remaining days. They repeated the dietary protocol every three to four weeks – up to eight times in all. The patients followed their normal diets between the fasting-mimicking periods but were encouraged to adhere to healthy lifestyles.

    The study’s investigators found that the fasting-mimicking diet reduced the patients' glucose by 18 percent, insulin by 50 percent, and IGF-1 (a growth factor involved in cancer development) by 30 percent. These changes remained stable over the duration of the study. They also found that levels of immunosuppressive cells decreased, but CD8+ T cells – the primary drivers of anti-tumor immunity – increased.

    Research shows that the fasting-mimicking diet creates a hostile microenvironment for cancer cells, sensitizing them to chemotherapy drugs and promoting cell death while preserving healthy cells. This sensitization exploits cancer cells' inability to adapt to extreme environments – a critical aspect of treating certain types of aggressive cancers and preventing their recurrence.

    These findings suggest that the fasting-mimicking diet is a safe and useful adjunct to chemotherapy. Learn about other benefits of the fasting-mimicking diet in this video featuring its creator, Dr. Valter Longo.

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  • High-dose testosterone therapy may help some men with advanced prostate cancer. (2015) www.sciencedaily.com
    Cancer Hormones Testosterone Prostate

    From the article:

    Previous studies, he adds, have shown that taking testosterone at the wrong time – particularly by men with symptoms of active cancer progression who have not yet received testosterone-blocking therapy – can make the disease worse.

    In men whose prostate cancer spreads, doctors typically prescribe drugs that block testosterone production, but cancer cells eventually become resistant to this means of reducing the hormone, says Denmeade, a professor of oncology at the Johns Hopkins University School of Medicine. At that point, physicians switch to other drugs, such as enzalutamide, which block testosterone’s ability to bind to receptors within prostate cancer cells.

    Denmeade says the combination of drugs that block testosterone production and receptors, called androgen deprivation therapy, may make prostate cancer more aggressive over time by enabling prostate cancer cells to subvert attempts to block testosterone receptors. And many men on these drugs experience harsh side effects, including impotence, weight gain, muscle loss and intense fatigue.

    […]

    With this context, the new study tested an approach based on the idea that if prostate cancer cells were flooded with testosterone, the cells might be killed by the hormone shock. The cells also might react by making fewer receptors, which may make the prostate tumor cells vulnerable once more to androgen deprivation therapy.

    […]

    The men were given three 28-day cycles of an intramuscular injection of testosterone and two weeks of a chemotherapy drug called etoposide. Men who showed decreases in PSA levels after three cycles were continued on testosterone injections alone.

    […]

    Of the 14 remaining in the trial, seven experienced a dip in their PSA levels of between 30 and 99 percent, an indication their cancers were stable or lessening in severity. Seven of the men showed no decrease in PSA.

    In addition, four of the seven men stayed on testosterone therapy for 12 to 24 months with continued low PSA levels. Of 10 men whose metastatic cancers could be measured with imaging scans, five experienced tumor shrinkage by more than half, including one man whose cancer completely disappeared.

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  • Testosterone therapy over a five-year period may not be associated with an increased risk of aggressive prostate cancer. (2015) www.sciencedaily.com
    Cancer Hormones Testosterone Prostate

    From the article:

    A new population-based study from The University of Texas Medical Branch at Galveston showed for the first time that exposure to testosterone therapy over a five-year period was not associated with an increased risk of aggressive prostate cancer. Further, risk of high-grade prostate cancer did not increase according to the total number of testosterone injections.

    […]

    Although several longitudinal studies have shown no increased risk of prostate cancer incidence associated with testosterone use, no population-based studies have examined the association of high-grade prostate cancer with testosterone exposure beyond one year.

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  • Testosterone raised the risk of prostate cancer and exacerbated the effects of carcinogenic chemical exposure in rats. (2014) www.sciencedaily.com
    Cancer Hormones Testosterone Prostate

    From the article:

    Two dose-response studies examined the incidence of prostate cancer in rats. The rats were given testosterone through slow-release implant devices. Before the rats were dosed with testosterone, some of the animals were given injections of the carcinogenic chemical N-nitroso-N-methylurea (MNU). These rats were compared to a control group that received MNU but had empty slow-release devices implanted.

    Among the rats that received testosterone without the carcinogenic chemical, 10 to 18 percent developed prostate carcinomas. Testosterone treatment alone did not induce specific tumors at other sites, but compared with control rats, it caused a significant increase in the number of rats with malignant tumors at any site. When rats were exposed to testosterone and the carcinogen, the treatment caused prostate cancer in 50 to 71 percent of the rats. Even when the hormone dose was too low to elevate testosterone levels in the bloodstream, half of the rats developed prostate tumors. Animals that were exposed to the carcinogenic chemical but not testosterone did not develop prostate cancer.

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  • Lactate rejuvenates immune cells that target cancer. www.nature.com
    Exercise Cancer Lactate

    Lactate is a compound that is produced primarily in the muscles via the breakdown of glucose during exercise. It can be “shuttled” from the muscles to various tissues, including the heart, and brain, where it can be used as an energy source. Evidence from a recent study suggests that lactate rejuvenates immune cells that target cancer.

    Specialized immune cells called CD8+ T cells are the primary drivers of anti-tumor immunity. During cancer progression, CD8+ T cells can experience “exhaustion,” a dysfunctional state caused by immune-related tolerance and immunosuppression in the environment surrounding the tumor.

    Researchers injected either lactate or glucose into mice that had cancer. The lactate markedly reduced cancer growth, but the glucose had little effect. They determined that the anti-tumor response was mediated by the CD8+ T cells. Depleting the CD8+ T cells negated lactate’s effect, confirming that lactate promotes anti-tumor immunity through CD8+ T cells.

    They also measured metabolites produced by CD8+ T cells (in culture) that had been treated with lactate. They found that the cells' uptake and subsequent metabolism of lactate increased. In addition, lactate inhibited the activity of histone deacetylases, and in turn, promoted the cells' stemness – the strictly controlled molecular processes that drive stem cell self-renewal and replication.

    These findings suggest that lactate rejuvenates the immune cell populations that target cancer, providing a possible mechanism by which exercise – which increases lactate production – reduces the risk of cancer. Learn more about lactate and the lactate shuttle in this episode featuring Dr. George Brooks.

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  • Many types of leisure time activity may lower risk of death for older adults www.cancer.gov
    Exercise Cancer Aging

    Older adults who engage in leisure time physical activities have lower risk of premature death.

    Leisure time physical activity is a broad term that refers to physical activities performed outside work or typical household responsibilities. Examples include exercise, sports, dancing, gardening, and walking. Findings from a recent study suggest that certain leisure time physical activities are associated with a lower risk of death from all causes of premature death, including cardiovascular disease and cancer, in older adults.

    Most public health organizations recommend that adults of all ages should engage in at least 150 minutes of moderate-intensity aerobic physical exercise or at least 75 minutes of vigorous-intensity aerobic physical exercise each week, or an equivalent combination of both. The bulk of the research focused on the benefits of physical activity has been in younger people, the findings of which might not be translatable to older adults.

    The investigators drew on data from 272,500 older adults (average age, 70 years) enrolled in the National Institutes of Health-AARP Diet and Health Study, an ongoing study of associations between diet and cancer. Participants provided information about their demographics, height, weight, smoking status, mood, educational level, and alcohol consumption. They also answered questions about the average amount of time they spent per week during the previous year engaging in cycling, swimming laps, playing racquet sports, playing golf, walking for exercise, jogging or running, and other aerobic exercises. The investigators calculated the participants' average leisure time activity levels in terms of metabolic equivalents, or METs, a measure of the rate of energy expended per unit of time.

    They found that playing racquet sports was associated with a 16 percent reduction in the risk of death from any cause and running was associated with a 15 percent reduction. The other activities conferred protection as well, but to a lesser extent. Achieving the recommended amount of physical activity through any combination of the seven leisure time activities reduced the risk of death by 13 percent. The protective effects of leisure time physical activity were dose-dependent to a degree, with greater duration conferring greater reduction in risk, but levels beyond those recommended showed diminishing returns.

    These findings suggest that older adults who meet physical activity guidelines through leisure time physical activities, especially aerobic activities such as racquet sports or running, have a reduced risk of premature death from all causes. Learn about the benefits of aerobic exercise in our overview article.

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  • First trial to prove a diet supplement can prevent hereditary cancer www.ncl.ac.uk
    Cancer Diet

    Resistant starch reduces the risk of certain hereditary cancers by roughly half.

    Lynch syndrome increases a person’s risk of having several types of cancer, particularly colorectal cancer. It is an inherited condition, affecting one out of 279 people worldwide and accounting for 2 to 4 percent of all colorectal cancer cases and 2.5 percent of endometrial cancer cases. Findings from a recent study suggest that supplemental resistant starch reduces the risk of cancer among people with Lynch syndrome.

    Resistant starch is a type of carbohydrate that resists digestion in the small intestine. Instead, resistant starch undergoes microbial fermentation in the colon, providing nutrients for the microbes, and producing butyrate, a short-chain fatty acid that supports the health of colonocytes – the cells that line the colon and rectum (the end portion of the colon). Foods that contain resistant starch include breads, pasta, legumes, nuts, seeds, bananas, and starchy vegetables, such as potatoes. A 3-ounce portion of baked potatoes typically provides 3.6 grams of resistant starch. Evidence suggests that resistant starch consumption alters microRNA expression, potentially moderating the cancer risks associated with red meat consumption.

    The study was part of the CAPP2 trial, an ongoing investigation to identify strategies that reduce the risk of certain hereditary cancers. The study involved nearly 1,000 adults (average age at recruitment, 45 years) who had Lynch syndrome. Half of the participants took 30 grams of resistant starch daily for an average of two years, while the other half took a placebo. The investigators tracked the participants for up to 20 years to see if they developed Lynch syndrome-related cancers.

    They found that resistant starch did not reduce the incidence of colorectal cancers, but it did reduce the incidence of other Lynch syndrome-related cancers (especially those of the upper digestive tract) by roughly half. The protective effect of resistant starch on cancer incidence endured for approximately 10 years after discontinuation of the supplement.

    These findings suggest that resistant starch protects against certain forms of hereditary cancers and underscores the role of diet in preventing cancer. For example, some evidence suggests that ketones exert anti-tumor effects. Learn more in this clip featuring Dr. Dominic D'Agostino.

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  • Citrus fruit intake and stomach cancer risk: a quantitative systematic review link.springer.com
    Nutrition Cancer

    Eating citrus fruits reduces the risk of developing stomach cancer.

    Stomach cancer is the fifth most common cancer worldwide. It is among the deadliest cancers, claiming the lives of nearly 800,000 people every year. Lifestyle factors, such as diet, nutrition, and alcohol, are the primary risk factors for the disease. Findings from a 2007 systematic review suggest that eating citrus fruits reduces the risk of developing stomach cancer.

    Citrus fruits include oranges, lemons, limes, grapefruits, pomelos, kumquats, and many others. They are excellent sources of vitamin C, folate, and other vitamins and minerals. Vitamin C is a powerful antioxidant, and folate supports DNA repair. Citrus fruits are also rich in bioactive compounds called flavonoids. Evidence suggests that citrus flavonoids exert anti-atherogenic, anti-inflammatory, anti-cancer, anti-clotting, and antioxidant activities in humans.

    The authors conducted a systematic review, a type of summary of the scientific literature related to a specific topic. Their analysis included 14 epidemiological (population-based) studies that examined links between citrus fruit intake and stomach cancer risk. Citrus fruit intake was categorized as “high” if participants consumed more than three servings per week.

    The reviewers found that high intake of citrus fruits decreased the risk of developing stomach cancer by 28 percent. Their analysis held true even when taking the participants' demographics and other lifestyle factors into account, such as age, sex, education, alcohol intake, and others.

    These findings suggest that eating citrus fruit markedly reduces the risk of developing stomach cancer. The authors of the review posited that the findings indicated that dietary intake alone (rather than supplemental megadoses) may be sufficient to reduce stomach cancer risk.

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  • Removing the visceral fat in female mice reduces intestinal tumors and extends survival (a sex-specific effect) www.sciencedaily.com
    Cancer Obesity Metabolic Syndrome Visceral Fat

    From the article:

    “There has been some skepticism as to whether obesity per se is a bona fide cancer risk factor, rather than the habits that fuel it, including a poor diet and a sedentary lifestyle,” […] “Although those other lifestyle choices play a role, this study unequivocally demonstrates that visceral adiposity is causally linked to intestinal cancer.”

    There was a sex-specific effect:

    The researchers then subdivided the groups by gender. In female mice, the removal of visceral fat was significantly related to a reduction in intestinal tumors, but calorie restriction was not. In male mice, calorie restriction had a significant effect on intestinal tumors, but removal of visceral fat did not.

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  • Longer periods of lactation (breast feeding) may promote lower visceral and pericardial fat, an effect that persists many years through midlife www.sciencedaily.com
    Cancer Pregnancy Development Breast Milk Visceral Fat

    Breastfeeding may reduce fatty deposits around the heart and other organs.

    The benefits of breastfeeding on infant health are widely known, but breastfeeding benefits maternal health, too. For example, evidence suggests that women who breastfeed experience a faster return to pre-pregnancy weight and have a lower risk of developing cardiovascular disease and certain types of cancer Findings from a 2021 study suggest that breastfeeding is associated with having less pericardial and visceral adipose tissue.

    Pericardial adipose tissue is fat that accumulates in and on the pericardium – the membrane that surrounds the heart. Visceral adipose tissue is fat that is stored in the abdominal cavity near the liver, pancreas, and intestines. Evidence suggests that pericardial and visceral fat produce adipokines, cell-signaling molecules that drive metabolic dysfunction.

    The investigators drew on data from the Coronary Artery Risk Development in Young Adults study, an ongoing examination of the risk factors for cardiovascular disease in young adults living in the United States. The participants included 910 women who had given birth at least once during the 25 years of follow-up. They provided information about their reproductive histories, overall health, lifestyles, and how long they breastfed. The investigators used computed tomography to measure the women’s body fat.

    They found that women who breastfed had less pericardial and visceral fat than women who did not, even when considering the women’s age, race, smoking status, body mass index, fasting glucose, family history of diabetes, fat intake, total cholesterol, and physical activity. The protective effects of breastfeeding were duration-dependent, with longer-duration breastfeeding exerting greater effects, and appeared to last through midlife.

    These findings suggest that breastfeeding is associated with having less pericardial and visceral adipose tissue. Learn more about the benefits of breastfeeding in our overview article.

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  • Fibroblast growth factor-2 released by visceral fat tumorigenic: "when the fat secretions had more of FGF2, more of the cells formed cancerous tumors" www.sciencedaily.com
    Cancer Obesity Metabolic Syndrome Visceral Fat

    From the article:

    A new Michigan State University study now offers new details showing that a certain protein released from fat in the body can cause a non-cancerous cell to turn into a cancerous one. The federally funded research also found that a lower layer of abdominal fat, when compared to fat just under the skin, is the more likely culprit, releasing even more of this protein and encouraging tumor growth.

    […]

    “Our study suggests that body mass index, or BMI, may not be the best indicator,” Bernard said. “It’s abdominal obesity, and even more specifically, levels of a protein called fibroblast growth factor-2 that may be a better indicator of the risk of cells becoming cancerous.”

    […]

    She also collected visceral fat tissue from women undergoing hysterectomies and found that when the fat secretions had more of the FGF2 protein, more of the cells formed cancerous tumors when transferred into mice.

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  • Repurposed chemo drug acting on the blood-brain barrier shows dose-dependent increase of dopamine in Parkinson's disease patients www.sciencedaily.com
    Brain Parkinson's Cancer Aging Neurodegeneration Blood-Brain Barrier

    Repurposed chemo drug inactivates protein that destroy’s the blood-brain barrier in Parkinson’s disease:

    The current part of the study just published, examined the cerebrospinal fluid of patients via epigenomics, which is a systematic analysis of the global state of gene expression, in correlation with continuing clinical outcomes. The new analysis helps explain the clinical findings.

    Nilotinib inactivated a protein (DDR1) that was destroying the ability of the blood brain barrier to function properly. When DDR1 was inhibited, normal transport of molecules in and out of the brain filter resumed, and inflammation declined to the point that dopamine, the neurotransmitter depleted by the disease process, was being produced again.

    After 27 months, nilotinib was found to be safe, and patients who received nilotinib showed a dose-dependent increase of dopamine, the chemical lost as a result of neuronal destruction.

    First study to show blood-brain barrier as therapeutic target for Parkinson’s disease:

    “Not only does nilotinib flip on the brain’s garbage disposal system to eliminate bad toxic proteins, but it appears to also repair the blood brain barrier to allow this toxic waste to leave the brain and to allow nutrients in,” Moussa explains. “Parkinson’s disease is generally believed to involve mitochondrial or energy deficits that can be caused by environmental toxins or by toxic protein accumulation; it has never been identified as a vascular disease.”

    “To our knowledge, this is the first study to show that the body’s blood brain barrier potentially offers a target for the treatment for Parkinson’s disease,” Moussa says.

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  • Processes contributing to cancer may reduce risk of Alzheimer's disease, according to post-mortem analysis www.the-scientist.com
    Alzheimer's Cancer Aging Neurodegeneration

    From the article:

    Thanks to those data, which showed participants with cancer had fewer hallmarks of Alzheimer’s disease in their brains as well as a reduced likelihood of neurodegenerative symptoms during their lifetimes, lead study author Erin Abner, a University of Kentucky epidemiologist and aging researcher and her team were able to offer the clearest picture yet of a molecular mechanism that seems to link the two diseases.

    “The connection is becoming more and more apparent,” New York University cancer researcher Eva Hernando-Monge, who didn’t work on the study, tells The Scientist.

    They investigated cancer deaths for traces of Alzheimer’s:

    As cohort members passed away, the team autopsied their brains to look for biomarkers associated with Alzheimer’s disease, including structures such as neurofibrillary tangles and neuritic plaques. They also noted when someone carried the APOE ε4 allele, a known genetic risk factor for the neurodegenerative condition.

    […]

    The analysis revealed “less Alzheimer’s pathology in the people who had cancer, both amyloid and tau,” Abner says. “We also saw evidence [that] another amyloid pathology—cerebral amyloid angiopathy, which is amyloid aggregation in blood vessel walls—was lower.

    Mechanisms of the cancer-Alzheimer’s anti-relationship:

    Processes related to cell growth and survival, as well as the production of specific molecules including the antistress response protein vimentin and the enzyme carbonic anhydrase, are all upregulated in cancer, he finds. Alzheimer’s occurs when these processes and proteins are downregulated.

    Another review, published in Molecular Psychiatry in 2021, identifies the proteins p53 and PIN1 as implicated in both cancer and Alzheimer’s. PIN1 overexpression is associated with myriad cancers, but its absence is linked to the formation of the Alzheimer’s biomarkers tracked in the Brain study. Meanwhile, p53 has a well-established anticancer role, but can also contribute to neurodegenerative disease.

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  • Inhibiting the Mfsd2a transporter that brings omega-3 DHA into the brain promotes leakage of brain barrier www.sciencedaily.com
    Brain Cancer Aging Omega-3 Blood-Brain Barrier

    Impaired transport of DHA disrupts the blood-brain barrier.

    Lipid rafts – cholesterol-filled “bubbles” found in the cell membrane – serve as staging areas for many cellular activities. One type of lipid raft, called caveolae, facilitates the transport of substances across the membrane of endothelial cells. Findings from a 2017 study demonstrate that suppression of caveolae-mediated transport in brain endothelial cells protects the integrity of the blood-brain barrier.

    The blood-brain barrier is a highly selective semi-permeable barrier made up of endothelial cells connected via tight junctions. This barrier separates the circulating blood from the brain’s extracellular fluid and prevents the entry of substances that may be neurotoxic. Disruption of the blood-brain barrier has been implicated in the pathogenesis of neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and multiple sclerosis, among others.

    The investigators' previous research showed that a critical player in blood-brain barrier function is Mfsd2a, a transmembrane protein found exclusively on the endothelial cells that line blood vessels on the barrier. Mfsd2a participates in lipid transport and is the sole means by which lysophospholipid DHA, the brain’s preferred form of DHA (a type of omega-3 fatty acid) is delivered to the brain.

    Using mice that carried a mutation that blocked Mfsd2a’s capacity to transport DHA, the investigators assessed blood-brain barrier function as well as caveolae formation and activity in the animals' brains. Then they compared the lipid composition of brain endothelial cells to lung epithelial cells, which lack Mfsd2a.

    They found that mice that lacked Mfsd2a function had leakier blood-brain barriers and greater caveolae formation and activity than normal mice. They also found that brain endothelial cells had higher lipid concentrations than lung epithelial cells. The most abundant lipid in the brain endothelial cells was DHA, which was found in concentrations that were two to five times higher.

    These findings suggest that Mfsd2a-mediated transport of lipids, particularly DHA, impairs caveolae activity, thereby preserving blood-brain integrity. Learn more about links between Mfsd2a, DHA, and brain health in this open-access peer-reviewed article by Dr. Rhonda Patrick..

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  • Butyrate receptor in colon functions as tumor suppressor. aacrjournals.org
    Cancer Butyrate

    Butyrate, a short-chain fatty acid, may suppress colon cancer growth.

    Colon cancer is one of the leading causes of death in developed nations. Health experts attribute much of the risks associated with colon cancer to dietary patterns, especially those that are high in red meat and low in fruits, vegetables, and fiber. Findings from a 2009 study suggest that butyrate, a short-chain fatty acid, activates a protein called GPR109A in the colon to suppress colon cancer.

    Short-chain fatty acids are produced by the gut microbiota during the fermentation of dietary fiber. In turn, these fatty acids provide energy to cells in the colon and play key roles in maintaining gut health. Butyrate, in particular, functions as a tumor suppressor by inhibiting enzymes called histone deacetylases, which drive tumor growth.

    The investigators assessed the production of GPR109A in the colon tissues of mice and humans (with and without colon cancer) using monoclonal antibodies that targeted the protein. Then they determined whether butyrate bound to GPR109A and how the fatty acid influenced tumor growth. Finally, they gauged the effects of butyrate on cancer cell growth and progression.

    They found that GPR109A was present on the surface of cells in the colons of both mice and humans, where it recognized and bound with butyrate. In the setting of cancer, GPR109A activity was silenced, effectively shutting down its activity. Supplying butyrate switched on the activity of GPR109A, which in turn promoted the death of cancer cells and suppressed the activity of nuclear factor-κB, a transcription factor that drives inflammation and tumor growth.

    These findings suggest that GPR109A mediates the tumor-suppressive effects of butyrate in the colon. Interestingly, evidence indicates that beta-hydroxybutyrate, a type of ketone, also binds with GPR109A, suggesting that the compound exerts anticancer properties in the colon. Learn more about the beneficial health effects of butyrate and beta-hydroxybutyrate in our overview articles.

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  • Childhood cancer survivors have epigenetic alterations that increase biological age www.sciencedaily.com
    Cancer Epigenetics Aging

    Genetic links between childhood cancer and accelerated epigenetic aging identified.

    Childhood cancer is relatively rare, affecting just one in 6,500 children each year. In recent decades, the overall survival rate for children with cancer has increased from 10 percent to 85 percent, due to early diagnosis and marked advancements in treatment. However, findings from a new study suggest that some survivors of childhood cancer are genetically susceptible to experiencing accelerated epigenetic aging.

    Epigenetic age acceleration is a phenomenon that occurs when a person’s epigenetic age exceeds their chronological age. Acceleration may be either intrinsic or extrinsic. Intrinsic aging is largely driven by internal physiological factors such as normal metabolism and genetics, whereas extrinsic aging is associated with lifestyle and environmental exposures, such as diet, tobacco use, ultraviolet radiation, and mental illness.

    The investigators performed a genome-wide association study, a type of observational study that associates specific genetic variations with particular diseases, using multiple epigenetic aging clocks. Their assessment was based on blood-derived DNA from approximately 2,400 childhood cancer survivors and 500 people who had never had cancer.

    They identified single nucleotide polymorphisms, or variants, in two areas of the survivors' DNA – the ¬¬SELP gene and the HLA region – that drive accelerated aging and are associated with age-related disease. The SELP gene encodes for a protein called P-selectin, a cell adhesion molecule that plays roles in atherosclerosis and peripheral artery disease. Its activity is increased in the setting of Alzheimer’s disease. The HLA, or human leukocyte antigen, region is an area on chromosome six that plays important roles in immunity. Mutations in the HLA region, which can occur following exposure to genotoxic drugs (such as chemotherapy) are associated with increased risk for autoimmune disorders, such as type 1 diabetes and celiac disease.

    These findings suggest that genetic variants increase the risk of accelerated epigenetic aging among childhood cancer survivors and underscore the importance of identifying children at risk. Learn about epigenetic aging acceleration in this clip featuring Dr. Steve Horvath.

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  • Restricting dietary fat can slow the growth of tumors in mice www.sciencedaily.com
    Cancer Diet Fat Ketogenic Diet

    Dietary interventions can change metabolite levels in the tumour microenvironment, which might then affect cancer cell metabolism to alter tumour growth. Although caloric restriction (CR) and a ketogenic diet (KD) are often thought to limit tumour progression by lowering blood glucose and insulin levels, we found that only CR inhibits the growth of select tumour allografts in mice, suggesting that other mechanisms contribute to tumour growth inhibition. A change in nutrient availability observed with CR, but not with KD, is lower lipid levels in the plasma and tumours. Upregulation of stearoyl-CoA desaturase (SCD), which synthesises monounsaturated fatty acids, is required for cancer cells to proliferate in a lipid-depleted environment, and CR also impairs tumour SCD activity to cause an imbalance between unsaturated and saturated fatty acids to slow tumour growth. Enforcing cancer cell SCD expression or raising circulating lipid levels through a higher-fat CR diet confers resistance to the effects of CR. By contrast, although KD also impairs tumour SCD activity, KD-driven increases in lipid availability maintain the unsaturated to saturated fatty acid ratios in tumours, and changing the KD fat composition to increase tumour saturated fatty acid levels cooperates with decreased tumour SCD activity to slow tumour growth. These data suggest that diet-induced mismatches between tumour fatty acid desaturation activity and the availability of specific fatty acid species determine whether low glycaemic diets impair tumour growth.

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  • Animal research suggests fragmented sleep promotes cancer through increases in TLR4 which polarize macrophages towards immune suppressive M2 type www.sciencedaily.com
    Cancer Sleep Immune System Toll-Like Receptors

    Poor sleep drives cancer growth by decreasing a type of immune cell that eliminates tumors.

    Scientists have long known that people who don’t get enough sleep are at greater risk of developing cancer. Once a person develops cancer, how long and how well they sleep can influence their disease outcome. A 2014 study implicated tumor-associated macrophages and toll-like receptor (TLR)- 4 as the primary drivers of unfavorable cancer outcomes in the setting of poor sleep.

    Tumor-associated macrophages are white blood cells that play important roles in cancer progression. M1 macrophages, which have a proinflammatory phenotype, can eliminate cancer cells. M2 macrophages, which have an anti-inflammatory phenotype, suppress immune activity and promote blood vessel growth – a critical aspect of tumor survival.

    TLR-4 is a receptor protein found on the surface of immune and other cells. TLR-4 activates transcription factors that promote the expression of pro-inflammatory cytokines. While this inflammatory response is necessary for immunity against bacterial infection, chronic activation of the TLR-4 pathway can accelerate aging and increase the risk for many diseases, including cancer.

    The investigators interrupted the sleep of normal mice and mice that lacked TLR-4, mimicking the effects of several sleep disorders. After the mice developed cancer, the investigators noted characteristics of the animals' tumors, including size, invasiveness, and the type and number of tumor-associated macrophages.

    They found that the mice that experience interrupted sleep had larger, more invasive tumors and larger numbers of tumor-associated macrophages than the mice that had uninterrupted sleep. However, these effects were not observed in the mice that lacked TLR4.

    These findings suggest that poor, fragmented sleep promotes tumor growth and invasiveness via activation of TLR4 pathways and subsequent recruitment of tumor-associated macrophages. Learn more about the varied roles TLR4 plays in human health in our overview article.

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  • Resistant starch may reduce colorectal cancer risk associated with red meat consumption www.sciencedaily.com
    Cancer Diet Microbiome Fiber

    Resistant starch reduces colorectal cancer risks associated with a high-red meat diet.

    Colorectal cancer is the third most common cancer worldwide. Robust evidence suggests that red meat consumption markedly increases a person’s risk of developing colorectal cancer.. Findings from a 2014 study suggest that resistant starch consumption alters microRNA expression, potentially moderating the cancer risks associated with red meat consumption.

    Resistant starch is a type of carbohydrate that resists digestion in the small intestine. Instead, resistant starch undergoes microbial fermentation in the colon, providing nutrients for the microbes and producing butyrate, a short-chain fatty acid that supports the health of colonocytes – the cells that line the colon and rectum (the end portion of the colon). Foods that contain resistant starch include breads, pasta, legumes, nuts, seeds, bananas, and starchy vegetables, such as potatoes. Cooking and preparation techniques alter resistant starch content in foods, however. For example, a study found that a 3-ounce portion of baked potatoes typically provides 3.6 grams of resistant starch, but a similar portion of boiled potatoes provides just 2.4 grams.

    MicroRNAs are single-stranded RNA molecules that play roles in the regulation of gene expression. They calibrate as much as 30 percent of mammalian protein-encoding genes. MicroRNA expression is typically dysregulated in the setting of cancer. However, evidence from an in vitro study suggests that butyrate modulates microRNA expression in colorectal cancer cells.

    The study involved 23 healthy adults between the ages of 50 and 75 years old. Each participant followed two four-week-long dietary interventions (separated by a washout diet): a high-red meat diet (providing 300 grams of red meat daily – about three-fourths of a pound) and a high-red meat diet that also provided 40 grams of butyrylated resistant starch, a chemically modified form of resistant starch that is an effective vehicle for delivering butyrate to the colon. The investigators collected rectal tissue samples via biopsy at the completion of each intervention diet.

    After completing the high-red meat diet, the participants' rectal tissues exhibited a 30 percent increase in a cluster of microRNAs called microRNA 17-92, which participates in the cell cycle, proliferation, apoptosis (cell death), and other processes involved in cancer. But when the participants added resistant starch to their high-red meat diet, their microRNA 17-92 levels returned to baseline levels.

    These findings suggest that butyrylated resistant starch moderates the cancer-promoting effects of a diet high in red meat. Some of this benefit may arise from the delivery of butyrate. Learn more about butyrate in our overview article.

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  • β-Hydroxybutyrate may be a substitute for butyrate in protecting from colon cancer: BHB activates a natural receptor involved in killing cancer cells www.sciencedaily.com
    Nutrition Cancer Diet Ketosis Fiber Butyrate HDAC Inhibitor

    Currently selected for this coming member’s digest by team member Melisa B.

    From the article:

    Researchers report in the April issue of Cancer Research that the GPR109A receptor is activated by butyrate, a metabolite produced by fiber-eating bacteria in the colon. The receptor puts a double-whammy on cancer by sending signals that trigger cell death, or apoptosis, and shutting down a protein that causes inflammation, a precursor to cancer.

    […]

    That got the German research team to search for alternative activators of the receptor, resulting in identification of beta-hydroxybutyrate as a natural receptor activator. The same study showed butyrate also could activate the receptor but with much less potency. That got Dr. Ganapathy thinking about a place where butyrate levels were already high – the colon – which led to his discovery that the receptor was also on colon cells.

    Butyrate plays other protective roles in colon cancer. In 2004, MCG researchers identified a gene, SLC5A8, that transports butyrate inside cells where it inhibits the enzyme HDAC, which gets upregulated in cancer to produce the uncontrolled cell growth that is a disease hallmark.

    “If you block HDAC, you can kill the cancer cell,” Dr. Ganapathy says.

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  • Risk of death from breast cancer was 49 percent lower among women with higher running activity. www.sciencedaily.com
    Exercise Cancer Breast Cancer Mortality Aerobic

    Breast cancer is the most common form of cancer among women, with roughly 237,000 cases diagnosed in the United States each year. Nearly one-fourth of women with breast cancer will die within 15 years of diagnosis. Findings from a 2014 study indicate that running reduces the risk of death from breast cancer.

    Most public health organizations recommend that adults of all ages engage in at least 150 minutes of moderate-intensity exercise or at least 75 minutes of vigorous-intensity exercise each week, or an equivalent combination of both. Most adults fall far short of these recommendations, however.

    Data from epidemiological, clinical, and mechanistic studies suggest that exercise reduces the risk of cancer-related death. However, scientists are unsure about how much or what type of exercise is best. Running and walking are both aerobic forms of exercise, but they differ in intensity, with running categorized as vigorous, and walking categorized as moderate. The authors of the study investigated whether running and walking differed in their effects on breast cancer-related death risk.

    The authors drew on data collected in the National Runners' and Walkers' Health Study, a long-term assessment of the health benefits associated with running and walking. They compared death rates among 272 runners and 714 walkers who had previously been diagnosed with breast cancer, taking age, race, menopause, family history, breastfeeding and oral contraceptive use into account. They quantified the intensity of the women’s activity as metabolic equivalents, or METs, a measure of the rate of energy expended per unit of time.

    Over a nine-year period, the risk of death from breast cancer was 49 percent lower among women who ran or walked 1.8 to 3.6 MET-hours per day and 68 percent lower for 3.6 MET-hours per day, when compared to less active women. Among runners only, the risk of death from breast cancer was 14 percent lower among women who ran 1.07 to 1.8 MET-hours per day, 87 percent lower for 1.8 to 3.6 MET-hours per day had a, and 95 percent lower for 3.6 hours or more per day, when compared to those who ran for less than 1.07 MET-hours per day.

    The findings indicate that running promotes greater survival among women who have had breast cancer. The authors noted that the amount of exercise that provided the greatest protection exceeded current guidelines, suggesting that breast cancer survival could be increased by engaging in greater exercise doses than recommended. Other behaviors that may promote breast cancer survival include dietary modifications, especially time-restricted eating. Learn more about the effects of time-restricted eating on breast cancer survival in this clip featuring Dr. Ruth Patterson.

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  • Aerobic exercise (wheel running) prevents cancer tumor formation, growth, and cachexia (cancer weight loss) in mice www.sciencedaily.com
    Exercise Cancer Immune System Aerobic IL-6

    Effect of aerobic exercise on cancer in mice:

    Training mice regularly on a wheel (the mouse version of a treadmill) decreased the growth of multiple types of tumors, including skin, liver, and lung cancers. Furthermore, mice that exercised regularly had a smaller chance of developing cancer in the first place. The beneficial effects of running went beyond tumor formation and growth, extending to cancer-associated weight loss, a process termed cachexia that is seen in cancer patients. Mice that exercised regularly showed no signs of cancer-associated weight loss in the researchers' lung cancer mouse model.

    Myokine signaling from the muscles:

    The researchers say that, the production of adrenaline results in a mobilization of immune cells, specifically one type of immune cell called a Natural Killer (NK) cell, to patrol the body. These NK cells are recruited to the site of the tumor by the protein IL-6, secreted by active muscles. The NK cells can then infiltrate the tumor, slowing or completely preventing its growth. Importantly, the researchers note that injecting the mice with either adrenaline or IL-6 without the exercise proved insufficient to inhibit cancer development, underlining the importance of the effects derived only from regular exercise in the mice.

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  • High-intensity interval training reduces the growth of colon cancer cells www.sciencedaily.com
    Exercise Cancer Inflammation Aerobic

    From the article:

    Exercise may play a role in reducing the growth of colon cancer cells according to new research. The study found that after a short session of high intensity interval training (HIIT), growth of colon cancer cells was reduced, and this also increased indicators of inflammation.

    […]

    “We have shown that exercise may play a role in inhibiting the growth of colon cancer cells. After an acute bout of HIIT there were specific increases in inflammation immediately after exercise, which are hypothesised to be involved in reducing the number of cancer cells.

    This suggests that a physically active lifestyle may be important in tackling human colorectal tumours. We would now like to look at how these changes in growth occur and understand the mechanisms by which biomarkers in the blood can impact cell growth."

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  • Compounds produced during ketosis may slow prostate cancer growth. www.biorxiv.org
    Cancer Metabolism Ketosis Prostate Carbohydrates Ketogenic Diet

    Prostate cancer is a leading cause of cancer death among men in the United States. While some prostate cancers respond well to local treatment, many cases require systemic treatments, such as chemotherapy or hormone therapies, which can have many side effects. Because having overweight or obesity increases the risk of death from prostate cancer](https://acsjournals.onlinelibrary.wiley.com/doi/full/10.1002/cncr.22443), newer and alternative therapies that slow cancer growth and help patients lose weight are needed. Findings of a new report show that a low carb diet generates ketones and other metabolic compounds associated with slower prostate cancer growth.

    Low carbohydrate and ketogenic diets are popular with adults looking to lose weight, but they also have therapeutic power for a growing list of diseases such as epilepsy, [diabetes](​​https://www.magonlinelibrary.com/doi/full/10.12968/pnur.2020.31.4.176), Parkinson’s disease, and some cancers. In addition to the metabolic benefits of weight loss, many anticancer compounds are produced during ketosis such as beta-hydroxybutyrate, a short-chain fatty acid with documented antioxidant and anti-inflammatory effects. Additional research is needed to characterize the wide range of molecules generated on a low carb diet and explore their relationship to prostate cancer growth.

    The investigators recruited participants who had recurrent prostate cancer and a BMI in the overweight or obese range (greater than 24). They assigned participants to consume a low carbohydrate diet (less than 20 grams of carbohydrates per day) for six months or continue their habitual diet. Participants provided a blood sample to measure metabolic and cancer biomarkers at multiple time points.

    The investigators found increased concentrations of multiple ketone bodies in the blood and increased expression of genes for ketone production, indicating participants succeeded in maintaining ketosis. A low carbohydrate diet altered serum concentrations of multiple amino acids, such as glycine, alanine, and asymmetric dimethylarginine, and increased the expression of genes involved in the synthesis of malate, citrate, and branched-chain amino acids. The researchers found a relationship between increased concentrations of ketosis-related compounds and prostate specific antigen (PSA) double time (a marker of prostate cancer growth rate), indicating that cancer growth was reduced as ketosis intensified.

    These results show that metabolites produced in response to a ketogenic diet may contribute to the beneficial effects of a low carb diet for patients with prostate cancer.

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  • Drinking sugar-sweetened beverages increases risk of death from any cause among women with breast cancer. pubmed.ncbi.nlm.nih.gov
    Cancer Breast Cancer Sugar

    Obesity and metabolic disease are risk factors for developing breast cancer; however, they are highly modifiable with lifestyle changes. Sugar-sweetened beverages are the leading contributor of added sugars in the American diet and consuming them in excess greatly increases the risk of developing obesity and type 2 diabetes. Results of a long-term study show that sugar-sweetened beverage consumption among women with breast cancer increases the risk of death from any cause.

    As adipose tissue accumulates fat, it becomes dysfunctional and can contribute to breast cancer growth by reducing glucose sensitivity and producing hormonal (e.g., estrogen) and inflammatory (e.g., interleukin-6) pro-cancer signals. Sugar-sweetened beverages contribute to the development of obesity and diabetes by providing large quantities of empty calories and spiking blood glucose and insulin levels due to the rapid absorption of sugar. Although previous research has established the mechanisms by which sugar overconsumption encourages cancer growth, few studies have examined the long-term effects of sugar-sweetened beverage consumption on cancer survival.

    The authors examined data from more than 10,000 participants of the Nurses' Health Study (1980-2010) and Nurses' Health Study II (1991-2011), large-scale prospective studies that collected information regarding health and lifestyle from female nurses. Participants completed food frequency questionnaires, which provide a list of specific foods and ask participants to report how often they have consumed that food over the past year, upon entrance to the study and every four years thereafter until 2015. The researchers reviewed only data collected following breast cancer diagnosis.

    Compared to non-consumers, participants who consumed three or more 8-ounce servings of sugar-sweetened beverages per week experienced a 35 percent increased risk of death due to cancer and 28 percent increased risk of death due to any cause. Participants consuming between one and three servings per week experienced a 31 percent increased risk of cancer-related death and 21 percent increased risk of death due to any cause compared to non-consumers. The data revealed no association between breast cancer risk and the consumption of beverages sweetened with non-nutritive (i.e., artificial) sweeteners.

    In this long-term follow-up study, sugar-sweetened beverage consumption increased the risk of death among women with breast cancer, especially in women consuming more than three servings per week.

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  • Alcohol consumption may increase the risk of several types of cancer. www.ncbi.nlm.nih.gov
    Cancer Alcohol

    Alcohol is a group 1 carcinogen, the highest classification of a substance known to cause cancer in humans – and the same classification as asbestos, formaldehyde, and tobacco smoke. Epidemiological data indicate that nearly three-quarters of a million new cancer cases worldwide are directly attributable to alcohol consumption00279-5/fulltext). Findings from a 2015 meta-analysis suggest that alcohol consumption increases the risk of several types of cancer.

    Scientists do not fully understand how alcohol drives cancer, but evidence points to a variety of mechanisms related to how the body metabolizes ethanol, the form of alcohol present in alcoholic beverages. Evidence indicates that the processes and products associated with ethanol metabolism exert genotoxic effects; promote oxidative stress; alter vitamin metabolism (especially folate and vitamin A-related compounds); increase estrogen levels; and drive inflammation.

    The investigators reviewed data from 572 studies involving more than 480,000 cancer cases. They calculated site-specific cancer risk for light, moderate, and heavy drinkers versus non-drinkers.

    They found that cancer risk increased for every category of drinking in a dose-dependent manner. As such, risk was greatest for heavy drinkers (more than four standard drinks per day). For example, compared to non-drinkers, the risk that heavy drinkers would develop cancer oral and pharyngeal cancer was 5.13 times higher; esophageal cancer, 4.95 times higher; laryngeal cancer, 2.65 times higher; breast cancer, 1.61 times higher; and colorectal cancer, 1.44 times higher. Heavy drinkers were also more likely to develop cancers of the stomach, liver, gallbladder, pancreas, and lung.

    These findings suggest that alcohol consumption markedly increases cancer risk in a dose-dependent manner. Alcohol consumption is just one of many lifestyle behaviors that influence cancer risk. Learn how modifying lifestyle behaviors can reduce the risk of breast cancer, for example, as well as other chronic diseases, in this clip featuring Dr. Ruth Patterson.

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  • Long-term weight-loss reduces cancer risk in adults with obesity and type 2 diabetes. www.sciencedaily.com
    Cancer Obesity Diabetes

    Obesity and type 2 diabetes cause perturbations in metabolism and immunity that increase the risk of cancer. Bariatric surgery is the most effective intervention for substantial and enduring weight loss in those with obesity and has been shown to [reverse type 2 diabetes](​​https://pubmed.ncbi.nlm.nih.gov/33485454/) and reduce cancer risk. Findings of a recent report demonstrate a lower risk of cancer in patients with obesity and diabetes up to 31 years following bariatric surgery.

    Weight gain occurs when the body stores excess calories in the form of fat in adipose tissue depots around the body. As the amount of energy stored increases, the body’s tolerance for glucose and other fuels decreases, leading to insulin resistance and type 2 diabetes. The high circulating levels of glucose, insulin, insulin-like growth factors, and inflammatory proteins observed in type 2 diabetes increase cancer cell proliferation and suppress apoptosis (programmed cell death). Reducing energy stores through bariatric surgery or other weight-loss therapies restores insulin sensitivity and reduces cancer risk.

    The authors collected data from an ongoing trial with over 4,000 participants investigating the long-term effects of bariatric surgery in adults with obesity and type 2 diabetes. At their baseline visit, participants underwent a physical exam, gave a blood sample, and completed questionnaires regarding health and lifestyle factors. Participants chose to undergo bariatric surgery or receive conventional obesity treatment during the years of 1987 and 2001. They continue to provide additional questionnaire data and blood samples as the study remains ongoing. The investigators followed participants in the current sample for an average of 21 years.

    Participants who chose to undergo bariatric surgery lost an average of 60 pounds two years after the baseline visit, compared to just 7 pounds in participants who received standard obesity treatment. These levels of weight loss remained stable 10 years after the baseline visit. At two years follow-up, 70 percent of participants who underwent surgery had diabetes remission, compared to 34 percent at 10 years follow-up. Bariatric surgery reduced cancer risk by 48 percent in women and 37 percent in the whole group. Participants who underwent surgery and maintained diabetes remission after 10 years had 55 percent reduction in cancer risk compared to participants with diabetes at 10 years follow-up. Participants who did not undergo surgery but achieved diabetes remission had an even greater risk reduction of 60 percent at 10 years follow-up.

    These findings support long-term weight-loss, including bariatric surgery, as a strategy to reduce type 2 diabetes and cancer risk among adults with obesity.

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  • Muscle produces tumor-suppressing compounds during exercise in men with prostate cancer. www.ecu.edu.au
    Exercise Cancer IL-6

    Exercise oncology is an emerging branch of medicine that studies the application of exercise medicine in the treatment of cancer. Although there is a strong base of epidemiological research that supports a relationship between increased physical activity and decreased cancer severity and death, the molecular mechanisms that underlie this relationship require further research. Findings of a recent report identify myokines that suppress tumor growth in patients with prostate cancer.

    Myokines are molecules released from muscle cells that signal to non-muscle tissues that the body is physically active. Studies in non-human animals have shown that myokines such as oncostatin M, decorin,, and interleukin (IL)-6 suppress cancer growth; however research in humans is lacking.

    The investigators recruited 10 men (average age, 73 years) with prostate cancer who were undertaking androgen deprivation therapy, which includes drugs that block the action of testosterone and other male hormones. Participants completed 12 weeks of exercise training that included three sessions-per-week of supervised resistance training and daily self-directed moderate-to-vigorous physical activity. The investigators measured the participants' muscle strength, body composition, and serum myokine concentration before and after the exercise training intervention. They also grew prostate cancer cells in vitro, exposed them to serum from participants taken before and after exercise training, and observed the effects on cancer cells directly.

    Participants lost about six pounds of fat and eight pounds of total body weight during the intervention period. Participants significantly increased their strength, measured during the leg press (57 pound increase) and chest press (16 pound increase). Serum concentrations of oncostatin M increased by 82 percent while other myokines did not increase or could not be measured. Finally, prostate cancer cells incubated with serum taken post-exercise training reduced cancer growth by 22 percent compared to serum taken prior to exercise training.

    These results show that exercise induced the expression of myokines with tumor-suppressing ability in patients with prostate cancer. Future research is needed to refine the prescription of intensity, frequency, and type of exercise in cancer treatment.

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  • Fat cells relay pro-cancer signals to tumors, especially in people with obesity and type 2 diabetes. www.inverse.com
    Cancer Obesity Breast Cancer Fat

    Obesity and metabolic diseases are strong risk factors for the development and progression of metastatic breast cancers in women who have completed menopause. Breast tumors contain a large number of white blood cells and adipocytes (i.e., fat cells); however, the role of adipocytes in metastatic breast cancer is unknown. Findings of a new report show that adipocytes shed molecular droplets called exosomes that relay cancer-promoting signals.

    Adipocytes play a critical role in the tumor microenvironment, releasing proinflammatory cytokines such as interleukin-6 and tumor necrosis factor-alpha and fats that act as fuel for tumor growth. Tumor metastasis is induced by changes in gene expression that increase cell movement and angiogenesis (i.e., the growth of new blood vessels) and decrease cell death and adhesion (i.e., how tightly cells cling to each other). The mechanisms by which adipocytes deliver these pro-cancer and pro-metastatic signals is understudied.

    The investigators obtained estrogen receptor-positive breast cancer cells and co-cultured them with adipocytes that were collected from female patients with or without type 2 diabetes who underwent bariatric (weight-loss) surgery. The researchers measured changes in gene and protein expression and performed fluorescence imaging to observe physical changes to adipocytes and cancer cells.

    When cultured with adipocytes from patients with obesity, cancer cells increased expression of genes important for a process called epithelial-to-mesenchymal transition, a key stage of tumor metastasis. Compared to exosomes produced by adipocytes from participants without type 2 diabetes, exosomes from participants with diabetes increased the expression of metastasis genes in cancer cells to a greater extent. Microscope imaging revealed that cancer cells from participants with diabetes underwent physical changes associated with metastasis as well as gene expression.

    These results revealed that exosomes shed from adipocytes act as the mechanism for delivery of pro-cancer compounds from adipocytes to breast cancer cells. Also, the strength of this pro-cancer signaling increased as insulin resistance increased. This study provides important insight into the relationship between obesity and cancer.

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  • Physical activity helps prevent cancer. www.sciencedaily.com
    Exercise Cancer

    Cancer is the second leading cause of death among people living in the United States, having claimed the lives of more than 600,000 people in 2020. Lifestyle behaviors, such as poor dietary habits, smoking, and physical inactivity, are key drivers of many cancers. Findings from a recent study suggest that more than 46,000 cancer deaths could be prevented every year if people met current physical activity guidelines.

    Physical activity is a broad term that describes both daily activities, such as gardening, doing household chores, or mowing the lawn, and classical forms of exercise, such as running, swimming, cycling, or boxing. Public health guidelines recommend that adults engage in at least 150 to 300 minutes of moderate-intensity physical activity or 75 to 150 minutes of vigorous-intensity aerobic physical activity (or an equivalent combination of the two) weekly. They also recommend that adults engage in muscle-strengthening activities such as weight lifting at least twice weekly. These recommendations are based on robust evidence that regular physical activity supports a healthy immune system (a critical factor in cancer prevention), reduces chronic inflammation, and helps the body maintain healthy levels of hormones such as insulin and estrogen, which can drive certain types of cancers if unbalanced.

    The authors of the study analyzed self-reported physical activity data for more than 550,000 adults who participated in the National Health and Nutrition Examination Survey. They obtained age-, sex-, and state-specific cancer incidence data from the United States Cancer Statistics database and ranked cancer incidence by site, such as the breast, colon, or other site.

    Their analysis revealed that more than 46,000 new cancer cases each year – roughly 3 percent – were likely attributable to physical inactivity, even after taking age, sex, race, and ethnicity into account. Inactivity-related cancer rates varied considerably by geographical location, with the lowest rates in northern and western states (especially Utah, Montana, Wyoming, Washington, and Wisconsin) and the highest rates in southern states (especially Kentucky, West Virginia, Louisiana, Tennessee, and Mississippi). The most common form of cancer associated with physical inactivity was stomach cancer; the least common was bladder cancer.

    These findings support those of previous studies demonstrating that physical activity plays a key role in reducing the risk of many types of cancer. Narrowing the findings to the state level can help state and community-level public health authorities design appropriate cancer prevention and control programs, potentially reducing the cancer burden nationwide.

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  • High fructose diets promote survival of intestinal cells and improve nutrient absorption – possibly promoting cancer. www.cancer.gov
    Cancer Obesity Sugar

    Since the introduction of high fructose corn syrup in the 1960s, fructose consumption has tripled worldwide. Excess sugar consumption degrades health by contributing to obesity and promoting cancer initiation and progression. Findings of a recent report elucidate the mechanisms by which fructose improves survival of and nutrient absorption by intestinal cells.

    Fructose absorption begins in the epithelium (i.e., skin-like cells) of the small intestine, which measures approximately 320 square feet in surface area (about the size of a small studio apartment). This massive surface area is arranged like shag carpet, with structures called “villi” that protrude from the intestine wall. The longer the villi, the greater the surface area and number of intestinal epithelial cells available to absorb nutrients, such as fat or iron. Previous research has shown that fructose can lead to excessive intestinal epithelial growth (called hyperplasia) and cancer; however, the effects of fructose on non-cancerous intestinal epithelial cells is unknown.

    The investigators gave mice access to normal drinking water or drinking water with 25 percent high-fructose corn syrup (soda contains about 10 percent) for four weeks. Then they fed mice either a normal diet with no fructose, a high-fat diet with no fructose, or a high-fat diet with sucrose, which contains 50 percent fructose and 50 percent glucose. The researchers measured nutrient composition of the feces and examined the intestinal epithelium for changes.

    Mice consuming high-fructose corn syrup in their drinking water showed a 25 to 40 percent increase in intestinal villus length compared to mice consuming normal drinking water. As villus length increased, weight gain and dietary fat absorption also increased. Mice consuming a high-fat diet and fructose gained more weight and had longer intestinal villi than mice consuming a high-fat diet with no fructose, despite consuming and expending the same amount of calories. These mice had less fat in their feces, suggesting an increase in nutrient absorption. The researchers found that intestinal epithelial cells isolated from mice consuming fructose were better able to withstand low-oxygen conditions (called hypoxia), which is a common cause of intestinal cell death.

    The authors concluded that high fructose diets increase intestinal villi length and nutrient absorption capacity. These findings provide greater insight into the pathogenesis of intestinal cancer.

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  • Antibiotics increase risk of some colorectal cancers, but protect against others. www.sciencedaily.com
    Cancer Microbiome Antibiotics

    Colorectal cancer is the third most common cancer and is responsible for approximately 600,000 deaths per year worldwide. Previous evidence has demonstrated an association between antibiotic use and colorectal cancer, which is troubling given rising antibiotic use; however, further research is needed to better understand this association. Authors of a recent report found that antibiotic use increased the risk of proximal colon cancer, but decreased the risk of rectal cancer in females.

    Colorectal cancers occur in three zones - the proximal colon, composed of the first two segments of the large intestine; the distal colon, composed of the second two segments of the large intestine; and the rectum. Most colon cancers occur in the proximal colon with distal colon and rectal cancers more common in males and in adults younger than 50 years. More than half of all colorectal cancer cases are attributable to modifiable risk factors such as smoking, diet, alcohol consumption, physical inactivity, and possibly medication.

    The gut microbiota is composed of the community of bacteria, archaea, fungi, and viruses that live in the human intestine, and its composition is highly sensitive to changes in lifestyle and use of medications. Antibiotics suppress the growth of beneficial gut bacteria in addition to pathogens, causing long term disruption of the gut ecosystem. Use of antibiotics may result in chronic inflammation and tumorigenesis due to overgrowth of pathogens such as Clostridium difficile; however, additional research is needed to understand the difference between classes of antibiotics and the effects of dose and duration.

    The authors collected data regarding colorectal cancer incidence and antibiotic use from the Swedish national population register. They compared data between more than 40,000 participants with colorectal cancer and more than 200,000 participants without colorectal cancer who were matched for age, sex, and home county. The researchers collected additional data about the participants, such as country of origin, socioeconomic status, and healthcare utilization. All data were collected between the years of 2005 and 2016.

    Moderate use of antibiotics (defined as use between 11 and 60 days) was associated with a 15 percent increased risk of colorectal cancer compared to no use. Very high use of antibiotics (defined as use greater than 180 days) was associated with a 17 percent increased risk compared to no use. However, these associations were no longer statistically significant when the investigators removed data regarding antibiotic use in the two years prior to cancer diagnosis. They removed this data to account for reverse causation, meaning use of antibiotics for illnesses caused by cancer. Excluding this data, the investigators found that moderate and very-high antibiotic use was significantly associated with proximal colorectal cancer. Surprisingly, antibiotic use decreased the risk of rectal cancer in females. This decreased risk was not present for proximal or distal colon cancers. Finally, the researchers found that the antibiotic classes quinolones, sulfonamides, and trimethoprims were most associated with proximal colon cancer, while nitrofurantoins, macrolides, and lincosamides were protective against rectal cancer.

    This large study demonstrates a relationship between increased antibiotic use and higher risk of proximal colon cancer. Surprisingly, some antibiotics may be protective against rectal cancer.

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  • Exercise reduces tumor growth via the actions of myokines produced in exercising muscle www.sciencedaily.com
    Exercise Cancer Visceral Fat

    Epidemiological data indicate that regular exercise not only reduces the risk of developing cancer, but it also improves survival among people who have been diagnosed with cancer. Two theories have emerged to explain exercise’s tumor-suppressive effects. Whereas one theory suggests that exercise acts via direct physical effects on tumor cells, the other theory suggests that it acts via indirect effects related to the tumor microenvironment. Findings from a recent study suggest that myokines suppress tumor growth.

    Myokines are cell-signaling proteins produced in muscles during exercise. Evidence indicates that myokines exert direct anti-inflammatory effects on visceral fat and muscles. They also participate in metabolic pathways involving fat oxidation and glucose uptake – critical factors in tumor survival.

    The intervention study involved 10 prostate cancer patients (average age, 73 years) who were undergoing androgen deprivation therapy, a common treatment for prostate cancer that often decreases muscle mass and increases fat mass. The patients engaged in a 12-week exercise program that included resistance and aerobic activities. The patients took a protein supplement that provided 40 grams of protein immediately after each exercise session to promote muscle protein synthesis. The authors of the study assessed the patients' body composition via dual-energy X-ray absorptiometry and measured their muscle strength via the one-repetition maximum method. Before and after the intervention, they measured the patients' fasting blood glucose; serum concentrations of myokines, including oncostatin M (which exibits anti-cancer effects); and prostate cell number and growth rate.

    They found that at the end of the intervention, the patients' fat mass, percent body fat, and body weight had decreased, but their lean mass and strength increased. Concentrations of oncostatin M and prostate cancer cell number and growth rate decreased.

    These findings suggest that exercise exerts anti-tumor effects via the actions of myokines produced in exercising muscles. They also underscore the importance of remaining physically active throughout the lifespan. Learn how exercise, in conjunction with fasting, may work synergistically to benefit health in this episode featuring Dr. Mark Mattson.

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  • Magnesium reduces pancreatic cancer risk. www.sciencedaily.com
    Cancer Magnesium

    Pancreatic cancer is a rare, aggressive cancer, expected to claim the lives of more than 48,000 people this year. The lack of reliable screening tests and the vague, non-specific symptoms associated with pancreatic cancer make diagnosing the disease difficult and often late. Even when diagnosed early, pancreatic cancer has a poor prognosis, with only about 8 percent of people who develop the disease surviving longer than five years. Findings from a 2015 study suggest that magnesium reduces the risk of pancreatic cancer.

    Magnesium is an essential mineral and a cofactor for hundreds of enzymes. It is involved in many physiological processes, including energy production, nucleic acid and protein synthesis, ion transport, and cell signaling. Magnesium deficiency is linked with increased risk of cardiovascular disease, osteoporosis, hypertension, and type 2 diabetes. Current magnesium intakes among people living in the United States are below the recommended dietary allowance (RDA) of 400-420 milligrams per day for males and 310-320 milligrams per day for females.

    The study involved more than 66,000 adults between the ages of 50 and 76 years of age. The authors drew on data from the VITamins and Lifestyle Study, a cohort investigation of the associations of supplement use with cancer risk over an eight-year period.

    Compared to study participants who met the RDA for magnesium, those who obtained 75 to 99 percent of the RDA were 42 percent more likely to develop pancreatic cancer, and those who obtained less than 75 percent of the RDA were 76 percent more likely to develop pancreatic cancer. For every 100-milligram-per-day decrease in magnesium intake, pancreatic cancer occurrence increased 24 percent. This association held true regardless of age, gender, body mass index, or non-steroidal anti-inflammatory drug use.

    These findings suggest that magnesium reduces the risk of pancreatic cancer. They also underscore the importance of obtaining sufficient magnesium from supplemental or dietary sources, such as green leafy vegetables, unrefined grains, legumes, beans, and nuts. To bolster your magnesium intake, try this magnesium-rich smoothie.

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  • A ketogenic diet may be beneficial for people with brain tumors. www.sciencedaily.com
    Cancer Ketosis Ketogenic Diet

    Glioma is a collective term for tumors that arise from the glial cells in the brain. Astrocytoma, the most common form of glioma, arises from star-shaped cells in the brain called astrocytes. The the survival rate for glioma, including astrocytoma, is low. Findings from a recent study suggest that a ketogenic diet is beneficial for people with astrocytoma.

    Ketogenic diets are low in carbohydrates and high in proteins and fats. They cause the body to oxidize fats to produce ketones for energy. For many years, ketogenic diets have been used in the clinical setting to reduce seizures in children. They are currently being investigated for the treatment of cancer because evidence suggests that cancer cells cannot use ketones for energy.

    The eight-week intervention study involved 25 people with astrocytoma whose disease was stable following chemotherapy. Participants followed a weekly dietary protocol consisting of five days of a ketogenic diet (consuming 20 grams or less of carbohydrates per day) and two non-consecutive days of fasting (consuming less than 20 percent of their estimated caloric needs). Participants kept food diaries and provided weekly blood and urine for measuring ketones, insulin, glucose, hemoglobin A1c (a measure of long-term blood glucose control), and IGF-1. They underwent brain scans at the beginning and end of the intervention.

    About half of the participants adhered to the dietary intervention, which was well-tolerated and elicited few adverse events. Despite the relatively low compliance, all the participants had ketones in their urine, with 80 percent achieving moderate levels. Participants' hemoglobin A1c, insulin, and fat body mass decreased, but their lean body mass increased. No changes were noted in glucose or IGF-1 levels. The brain scans showed that ketone concentrations increased in the brain (including the tumor tissue) and correlated with ketone levels in the urine.

    These findings demonstrate that a ketogenic diet is safe for people with astrocytoma and may be beneficial as adjunctive therapy. Learn more about how a ketogenic diet, combined with fasting and the standard of care treatment, may help treat aggressive cancers in this clip featuring Dr. Valter Longo.

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  • Omega-6 and omega-3 fats kill cancer cells. www.eurekalert.org
    Cancer Omega-3 Ketogenic Diet

    Cancer is a leading cause of death in the United States, but new therapies targeting diet and lifestyle may aid in fighting the disease. Emerging research suggests that modulating the kind of nutrients available to cancer cells may encourage or inhibit their growth. Findings of a recent study detail the effects of polyunsaturated fats on cancer growth in mice.

    Polyunsaturated fats are fatty acids that have more than one unsaturated carbon bond in the molecule, such as omega-3 and omega-6 fatty acids. They are present in fish, nuts, and seeds and are more prone to oxidation than other fatty acids. Polyunsaturated fats play critical roles in cardiovascular and neurological health.

    While cancer is often viewed as a genetic disease, metabolic changes occur in cancer cells that contribute to their growth and spread. Cancer cells tend to produce energy by fermenting glucose to produce lactic acid, which acidifies the tumor environment, a phenomenon known as “cancer acidosis.” The acidity of the tumor environment alters the way cancer cells metabolize fats, increasing both the storage and the breakdown of fats.

    Previous research demonstrated that targeting fatty acid metabolism may promote cancer cell death and prevent cancer spread by increasing lipid peroxidation (the breakdown of fats in the presence of iron) resulting in oxidative stress. Peroxidized lipids signal cellular damage, inducing a type of programmed cell death called ferroptosis (apoptosis occurring due to iron). However, it is unclear how different types of dietary fats affect cancer metabolism.

    First, the authors of the present study exposed cervical, colorectal, and pharyngeal (throat) cancer cells to a variety of fats and measured the effects on metabolism. These fats included saturated fats, like those found in butter and palm oil; monounsaturated fats, like those found in olive oil; and polyunsaturated fats, including omega-6 fats, like those found in corn oil, and omega-3 fats, like those found in fish (eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]). Next, they fed mice a diet supplemented with either olive oil or fish oil for four weeks. Two weeks into the diet, the mice developed cancer and the researchers measured the effects of the two diets on cancer progression. Finally, the researchers administered compounds to mice with cancer that induce or inhibit ferroptosis to further explore the mechanisms of cancer cell metabolism.

    In cancer cells, exposure to both omega-6 and omega-3 polyunsaturated fats enhanced fat uptake and storage, which increased lipid peroxidation and induced ferroptosis to a greater extent than saturated or monounsaturated fats. Fats with the least saturation (meaning the most double bonds) were most effective, with the omega-3 fat DHA demonstrating the most cancer-fighting ability. However, this result only occurred in cancer cells with an acidic pH compared to a neutral pH. Mice that received the fish oil supplementation lost harmful white adipose tissue but gained metabolically beneficial brown adipose tissue, improving whole-body metabolism. The fish oil diet delayed cancer growth and increased survival, and this effect was magnified by the addition of a ferroptosis-inducing drug.

    The authors of this important work concluded that polyunsaturated fats may be an effective add-on treatment to complement pharmacological therapies for cancer.

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  • Consuming sugar-sweetened beverages increases the risk of early-onset colorectal cancer among young women. www.sciencedaily.com
    Cancer Sugar Urolithin A

    Colorectal cancer cases and death rates in the United States have been declining since the 1980s, likely due to increased awareness and screening, which typically begins at age 50. However, the number of colorectal cancer cases in young adults – those between the ages of 20 and 49 years – is increasing. Findings from a recent study suggest that consumption of sugar-sweetened beverages increases the risk of early-onset colorectal cancer among young women.

    Dietary factors play critical roles in colorectal cancer risk. Consumption of plant-based foods has been shown to decrease colorectal cancer risk. For example, ellagic acid, a bioactive compound present in walnuts and pomegranates, breaks down in the gut to yield urolithins, a class of compounds that exert anti-inflammatory and anti-cancer effects. Conversely, evidence suggests that consumption of red meat increases colorectal cancer risk by 20 to 30 percent.

    The participants in the present study included approximately 95,000 women who were part of the Nurses Health Study II, a prospective cohort study comprised of female nurses living in the United States during the period spanning 1991 and 2015. The nurses ranged in age between 25 and 42 years and were cancer-free when they enrolled in the study. Every two years, the women provide information about their demographics, lifestyles, and overall health, including whether they have been diagnosed with colorectal cancer. Every four years, they complete food frequency questionnaires that include questions about their dietary patterns. A subset of approximately 41,000 women provided information about their beverage intake during their teen years.

    The authors of study found that 109 of the women in the study group developed early onset colorectal cancer. Women who drank two or more servings of sugar-sweetened beverages per day during adulthood were more than twice as likely to develop early onset colorectal cancer than women who consumed less than one serving per week. This risk was dose-dependent, with a 16 percent higher risk per daily beverage increase. If the women drank sugar-sweetened beverages during their teen years, their risk increased 32 percent for each serving per day increase. Replacing sugar-sweetened beverages with artificially sweetened beverages or milk decreased their risk of early onset colorectal cancer by 17 to 36 percent.

    These findings suggest that consuming sugar-sweetened beverages during adolescence and adulthood markedly increases a woman’s risk of developing colorectal cancer. Dietary modifications that include consumption of artificially sweetened beverages or milk appears to reduce risk.

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  • Mushroom consumption reduces the risk of breast and all cancers. www.sciencedaily.com
    Cancer Mushroom

    Cancer is the second leading cause of death following cardiovascular disease. For many cancers, the risk may be reduced by consumption of a healthy diet rich in plant-based foods because many plants contain anticancer compounds. One team of researchers aimed to determine the role of mushroom consumption in reducing cancer risk.

    Mushrooms are rich in bioactive compounds, including phytochemicals (plant chemicals such as flavonoids and carotenoids), fiber, selenium, vitamins, and antioxidants, such as ergothioneine and glutathione, which may help prevent cancer. While laboratory studies have shown the ability of mushroom compounds to inhibit cancer growth, epidemiological evidence is mixed, with some studies reporting a link between mushroom consumption and decreased cancer risk and others reporting no link.

    The current report is a systematic review and meta-analysis, meaning the authors searched the existing literature on mushroom consumption and cancer risk, selected studies based on a set of criteria meant to select for relevant studies of high quality, and combined the risk data from each trial to calculate a new set of risk estimates. They selected observational studies of mushroom intake and cancer incidence that included at least two doses of mushroom intake and were published between January 1966 and October 2020.

    The authors identified 17 studies that met their selection criteria. Pooled data from these studies showed that higher mushroom consumption was associated with lower risk of total cancer, with participants in the highest consumption group having a 66 percent lower risk of all cancers than participants in the lowest consumption group. Higher mushroom consumption was associated with an 80 percent lower risk for non-breast cancers and a 65 percent lower risk of breast cancer specifically. When the authors calculated risk for specific cancers (lung, breast, prostate, colon, etc.), only breast cancer was significantly associated with mushroom consumption, but they noted this could be due to the small number of studies conducted with non-breast cancers. Finally, the data revealed a significant dose-response association between mushroom consumption and the risk of total cancer with a 45 percent lower risk at high intake (about a quarter cup of sliced mushrooms per day) compared to the lowest intake of zero grams per day.

    The results show a significant benefit of mushroom consumption in preventing breast and non-breast cancers. The authors noted that there are limitations to their study including variation in study design among trials.

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  • Circadian dysregulation of DNA repair drives increased cancer risk among shift workers. www.eurekalert.org
    Cancer Circadian Rhythm

    Large, population-based studies have identified robust links between shift work and increased cancer risk. Much of this risk is associated with disruptions in the body’s circadian rhythms, the 24-hour cycles of biological, hormonal, and behavioral patterns. A recent study suggests that circadian dysregulation of DNA repair mechanisms drives the increased cancer risk associated with shift work.

    Circadian rhythms influence many physiological pathways associated with cancer, such as regulation of the cell cycle, cell proliferation, and inflammation. These rhythms also influence mechanisms that repair DNA damage – which can drive mutations that promote cancer.

    The study involved 14 healthy men and women (22 to 34 years old) who participated in a simulated shift work experiment at a sleep laboratory. Half of the participants completed a simulated night shift schedule for three nights in which they were awake from 6 p.m. to 10 a.m. The other half completed a simulated day shift schedule for three days in which they were awake from 6 a.m. to 10 p.m. The study participants received a snack and provided blood samples every three hours. After completing their three days of respective shift work schedules, they underwent a 24-hour study protocol in which they were kept awake for 24 hours in low light in a semi-recumbent posture and received hourly snacks. Every three hours the study investigators took a blood sample from the participants. They analyzed the white blood cells from the samples and then exposed the cells to radiation in the morning and evening.

    The authors found that the rhythms of many of the cancer-related genes in the white blood cells were different among the night shift workers compared to the day shift workers. Notably, genes related to DNA repair that showed distinct rhythms of expression during the day shift lost their rhythmicity during the night shift. They also found that the night shift workers' cells that were exposed to radiation in the evening showed more DNA damage – an indication that they were more vulnerable to external stressors.

    These findings suggest that night shift work alters circadian DNA repair mechanisms and promotes DNA damage, thereby increasing cancer risk. One strategy for ameliorating the harmful effects of night shift work is time-restricted eating. Learn more in this episode featuring circadian rhythm expert Dr. Satchin Panda..

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  • Vitamin D is a cost-effective means to reduce the number of cancer deaths. febs.onlinelibrary.wiley.com
    Vitamin D Cancer

    Cancer is the second leading cause of death worldwide, claiming the lives of nearly 10 million each year. As the number of cancer drugs has increased in recent years, so too have the costs associated with their use. Findings in a recent report indicate that vitamin D may reduce the number of cancer deaths, saving thousands of dollars.

    The authors of the study drew on data regarding age- and sex-specific cancer deaths in the German Center for Cancer Registry. They estimated the costs of cancer treatment and years of living lost in people over the age of 50 years since most cancer deaths occur in this age group and because most vitamin D trials are conducted in older adults. They also estimated the costs of vitamin D supplementation and summarized the findings from three recent meta-analyses investigating the effects of vitamin D supplementation on cancer deaths.

    The authors estimated that the end-of-life cancer costs in Germany were more than $48,000 USD per patient, but the cost of vitamin D supplementation $30 USD per year. They estimated that 1,000 IU of vitamin D daily would reduce cancer deaths in Germany by 13 percent, or about 30,000 lives, at a savings of more than $308 million USD.

    These findings suggest that vitamin D is a cost-effective means to reduce cancer deaths, especially among older adults. Learn how vitamin D slows epigenetic aging – a driver of cancer – in this episode featuring Dr. Steve Horvath.

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  • Fecal microbiota transplant improves immunotherapy response among melanoma patients. www.eurekalert.org
    Cancer Microbiome

    Fecal microbiota transplant is a therapeutic strategy that involves transfer of feces from a donor to a recipient. The goal of fecal transplant is to restore the microbial balance in the gut of the recipient as a means to improve health. A new study demonstrates that fecal microbiota transplant improves the response to immunotherapy among melanoma patients.

    Immunotherapy exploits the immune system to treat cancer. One type of immunotherapy, anti–programmed cell death protein 1 (PD-1) therapy is beneficial in treating patients with advanced melanoma. However, gut microbial composition influences anti–PD-1 efficacy in preclinical models and cancer patients. About 40 percent of melanoma cancer patients do not respond to immunotherapy.

    The authors of the study performed fecal microbiota transplants and anti-PD-1 immunotherapy (a drug called pembrolizumab) in melanoma patients who had not responded to all other therapies, including anti-PD-1. The fecal microbiota donors were people who demonstrated robust responses to anti-PD-1 immunotherapy.

    More than one-third of the patients who received the transplants responded favorably to the anti-PD-1 immunotherapy despite having not responded before the transplant. The types of gut microbes associated with response to anti–PD-1 increased, as did activation of CD8+ T cells. The number of interleukin-8–expressing myeloid cells (which are involved in immunosuppression) decreased. These findings suggest that fecal microbial transplant is a viable option for improving the response to immunotherapy among melanoma patients and underscore the need for greater understanding of the role the gut microbiota play in immune function.

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  • High sugar intake increases cancer risk. academic.oup.com
    Cancer Sugar

    Current dietary guidelines for people living in the United States recommend limiting calories from sugar intake to less than 10 percent of total daily calories. Despite these recommendations, evidence indicates that some people living in the United States consume as much as 23 percent of their daily calories in the form of added sugars. Findings from a recent study suggest that high dietary sugar intake increases a person’s risk for cancer.

    Cancer is the second leading cause of death in the United States. Unlike normal cells, cancer cells preferentially rely on glycolysis (the breakdown of sugar) to produce energy. This altered metabolism, widely recognized as a hallmark of cancer, promotes cell proliferation and cancer metastasis.

    The authors of the study drew on data from more than 101,000 participants enrolled in NutriNet-Santé, an ongoing observational cohort study based in France. Participants completed online 24-hour dietary records detailing their usual consumption of more than 3,500 food and beverage items. The authors of the study performed statistical analyses to identify associations between sugar intake and cancer risk, taking into account known risk factors, such as socioeconomic status, body size, lifestyle, medical history, and nutritional factors.

    They found that higher dietary sugar intake increased the overall risk of developing cancer 17 percent. The risk of breast cancer increased 50 percent with high sugar intake. These findings suggest that reducing dietary sugar intake decreases a person’s risk of developing cancer and highlight the importance of policies and interventions to reduce intake.

    The effects of sugar extend to longevity, as well. In fact, consumption of sugar-sweetened beverages is associated with dramatically accelerated telomere shortening – equivalent to as much as five years of a person’s life. Watch this clip in which Dr. Elissa Epel discusses the harmful effects of what she calls a “toxic lifestyle,” one that includes the consumption of sugary drinks.

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  • Exercise exploits the immune system to fight cancer. www.sciencedaily.com
    Exercise Cancer Lactate

    Exercise is a critical component of public health recommendations to prevent cancer. A growing body of scientific research demonstrates that engaging in exercise after a cancer diagnosis can improve outcomes, but the mechanisms that mediate these effects are not fully characterized. Findings from a new study demonstrate that exercise alters the metabolism of cytotoxic T cells to improve their ability to attack cancer cells.

    Cytotoxic T cells play key roles in the body’s immune response. They destroy malignant cells by triggering apoptosis – a type of cellular self-destruct mechanism that rids the body of damaged or aged cells.

    The authors of the study placed mice with cancer into one of two groups. Half of the mice exercised on a treadmill, but the other half remained inactive. They transferred cytotoxic T cells from the mice that exercised into the inactive mice. Then they isolated T cells, blood, and tissues from the exercising mice. Finally, the authors injected both groups of mice with antibodies that would destroy the animals' cytotoxic T cells.

    The mice that exercise exhibited slower cancer growth and reduced death rates than those that remained inactive. The inactive mice that received the cytotoxic T cells from exercised mice showed marked improvements in their disease status. The exercising mice had high blood levels of lactate, which altered the T cells' metabolism and increased the cells' activity. Destroying the animals' cytotoxic T cells negated the beneficial effects that the exercise had in terms of cancer growth and survival.

    Taken together, these findings suggest that exercise alters cytotoxic T cells to mediate exercise-induced cancer suppression. Treatment protocols that incorporate exercise might improve outcomes by activating the immune system.

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  • Sulforaphane reduces biochemical recurrence in men who have had prostate cancer. pubmed.ncbi.nlm.nih.gov
    Cancer Prostate Sulforaphane NRF2

    Prostate cancer is the second most common cancer among men, affecting more than 1.3 million men worldwide. Many men undergo radical prostatectomy to treat their cancer. Findings from a 2015 study demonstrated that sulforaphane reduces biochemical recurrence in men who have had prostate cancer.

    Biochemical recurrence is a phenomenon in which serum levels of prostate specific antigen (PSA) levels increase. It is an indicator of localized or metastatic disease. As many as 40 percent of men treated with radical prostatectomy experience biochemical recurrence; 34 percent of these will develop metastatic disease.

    The double-blind, randomized, placebo-controlled study involved 75 men (average age, 69 years) who had undergone radical prostatectomy and were experiencing increased PSA levels. Roughly half of the men took a supplement providing 60 milligrams of sulforaphane for six months; the other half took a placebo. The authors of the study measured the men’s PSA levels before and two months after the treatment ended.

    Increases in the average PSA levels were much lower among the men who took the sulforaphane. The PSA doubling time among men who took sulforaphane was ~29 months; doubling time among the men who took the placebo was ~16 months – an 86 percent difference. The effects of sulforaphane remained up to three months after the intervention.

    These findings suggest that sulforaphane shows promise as a strategy to prevent biochemical recurrence among men who have had radical prostatectomy for prostate cancer. Additional studies are needed to confirm these findings.

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  • Scientists find molecular link between meat and dairy diets and colorectal cancer. pubmed.ncbi.nlm.nih.gov
    Nutrition Cancer

    Currently selected for this coming member’s digest by team member Melisa B.

    The World Health Organizations classifies red meat as a carcinogen based on epidemiological studies showing positive associations between eating red meat and developing colorectal cancer as well as strong mechanistic evidence. Multiple components present in red meat likely contribute to this risk, including saturated fat and heme iron. New research suggests that Neu5Gc, a type of sugar, provides another possible mechanism to explain the cancer-promoting effects of diets high in red meat and dairy products.

    Neu5Gc is a carbohydrate produced by non-human mammals and found in red meat and dairy products. Humans cannot produce Neu5Gc so the body recognizes it as foreign and produces antibodies against it called “anti-Neu5Gc IgG.” Research has demonstrated a link between high anti-Neu5Gc IgG levels and increased colon cancer risk; however, no direct correlation between diet and blood levels of anti-Neu5Gc IgG has been shown.

    The authors of this report collected data from nearly 20,000 participants enrolled in NutriNet-Santé, an ongoing observational cohort study based in France. Participants self-reported their diet using a 24-hour recall method and gave blood for biomarker measurement. After reviewing the diet record data for Neu5Gc content, the authors chose a subset of 120 participants with varying levels of estimated Neu5Gc consumption and measured the anti-Neu5Gc IgG concentration of their banked blood samples.

    The authors reported a distinct dose-dependent positive association between dietary content of Neu5Gc and blood concentrations of anti-Neu5Gc antibodies. Men consumed significantly more Neu5Gc in their diets, especially from red meat, and exhibited corresponding increases in anti-Neu5Gc IgG levels. In addition to the link between diet and antibody concentrations, the authors also report a link between increased meat and dairy consumption and the diversity of anti-Neu5Gc IgG. Antibodies vary slightly in structure so that one antigen may produce many different antibodies. Consuming more Neu5Gc increased the variety of anti-Neu5Gc antibody types in the blood, which may lead to a stronger immune reaction.

    These findings are the first to demonstrate a link between dietary intake of Neu5Gc and anti-Neu5Gc IgG response. This novel observational research may have important implications for colon cancer risk; however, controlled trials are necessary to explore any causative role of Neu5Gc in disease.

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  • A component of cannabis may reduce colon cancer risk. www.forbes.com
    Cancer Cannabinoid

    The chronic inflammation that accompanies ulcerative colitis, a type of inflammatory bowel disease, increases the risk of developing colon cancer. New research in mice suggests a component of cannabis may prevent the development of colitis-associated colon cancer.

    Cannabis, also known as marijuana, contains a family of chemicals called cannabinoids, including the psychoactive compound, tetrahydrocannabinol (THC). THC binds to cannabinoid receptors (CB), present throughout the body, altering appetite, pain, mood, and memory. CB1 receptors are more common in the brain, while CB2 receptors are mainly expressed by the immune system.

    The investigators conducted a two-part study to determine the effects of THC on gut inflammation. In the first part of the experiment, they gave mice that had colitis THC by mouth (10 milligrams per kilogram body weight) or a placebo treatment twice weekly for nine weeks. They then measured inflammation and cancer development in the colonic tissue of the mice. The mice in the treatment group exhibited statistically significant decreases in tumor initiation and colitis severity. The authors of the study attributed this to decreased expression of the pro-inflammatory cytokine interleukin-22.

    In the second part of the experiment, the investigators used a rodent colitis model to study the role of THC in regulating immune cells that express the CB2 receptor. Mice received the same dose of THC daily given to the mice in the first study for seven days or a placebo. Mice in the treatment group had markedly less colonic inflammation. The authors attributed this to decreased activation of the pro-inflammatory dendritic cells and macrophages and increased production of anti-inflammatory T-regulatory cells.

    These findings may be important in the fight against colorectal cancer, but the results have their limitations. The dose of THC used in this study is equivalent to 680 milligrams for a 150-pound person, which is far greater than the 10 to 25-milligram range used in some clinical studies. A Cochrane review on the topic of cannabis use for ulcerative colitis concludes that there is insufficient evidence to make strong recommendations about THC safety and efficacy and that additional investigations of cannabis dosing are warranted.

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  • Low-dose aspirin linked to increased cancer risk in older adults. www.theladders.com
    Cancer

    The National Cancer Institute estimates more than 600,000 Americans will die of cancer in 2020. A number of meta-analyses have demonstrated the ability of prolonged daily aspirin use to reduce the risk of multiple types of cancers (including gastrointestinal cancers, adenocarcinomas, and other solid tumors. A recent study reports aspirin may have adverse effects on the progression of cancer in older adults.

    Many healthcare professionals prescribe aspirin to their older patients to reduce their risk of heart attack and stroke. Aspirin inhibits the enzyme cyclooxygenase (COX)-1 and downstream production of thromboxanes, a group of lipids that causes blood vessel constriction and increases adhesion between platelets and circulating cancer cells. By inhibiting thromboxane production, aspirin decreases inflammation, hypertension, and cancer metastasis.

    This randomized controlled trial included more than 19,000 healthy Australian and US participants over the age of 65 years. The investigators randomly assigned participants to take 100 milligrams of enteric coated aspirin daily or a placebo for an average of nearly five years. They obtained cancer incidence and death rates via clinical records.

    While the rate of new cancer onsetof onset of new cancers was similar between the aspirin and placebo groups, cancer patients in the aspirin group were more likely to be diagnosed with advanced-stage and metastatic cancers. Death rates from solid tumor cancers, but not blood or lymphatic, were higher in the aspirin group.

    Interestingly, the authors suggested this increase in cancer severity and death may be due to aspirin’s anti-inflammatory effects. Inflammation is critical in the body’s fight against cancer, but this defense weakens with age, and aspirin use may further weaken this response.

    The authors note that while their study design was strong, further research is needed to confirm their findings. Several randomized controlled trials further investigating this topic are underway.

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  • Coffee consumption reduces risk of metastasis and death among people with colorectal cancer. www.sciencedaily.com
    Cancer Coffee Polyphenol

    Colorectal cancer, the third most common cancer among men and women living in the United States, will likely claim the lives of more than 50,000 people this year. The cancer often metastasizes, or spreads, to other sites, particularly the lungs, liver, or brain, decreasing a person’s chances of survival from the disease. Findings from a new study suggest that drinking coffee reduces the risk of colorectal cancer metastasis.

    Coffee contains a multitude of polyphenolic compounds that appear to exert beneficial health effects, including quercetin, chlorogenic acid, and others. Drinking coffee is linked with reduced disease burden and increased lifespan, possibly due to coffee’s ability to induce autophagy. Other evidence suggests that coffee’s beneficial effects arise from its antioxidant and anti-inflammatory effects as well as its capacity to maintain healthy blood insulin levels – a critical aspect in colorectal cancer outcomes.

    The prospective observational cohort study involved more than 1,100 people with colorectal cancer who were enrolled in a larger randomized clinical trial investigating the efficacy of chemotherapy drugs. The study participants, who were between the ages of 51 and 67 years, provided information about what they ate and drank using a food frequency questionnaire.

    Over a period of approximately five years, 93 percent of the participants experienced disease progression, or they died. Participants who drank coffee were less likely to die than those who did not, and this association was dose dependent. For example, those who drank two to three cups per day were 18 percent less likely to die, and those who drank four cups per day were 36 percent less likely to die. These associations held true regardless of whether they drank caffeinated or decaffeinated coffee.

    These findings suggest that drinking coffee reduces the risk of disease progression and death in people with advanced or metastatic colorectal cancer. A key player in suppression of tumor growth is autophagy, a biological process that inhibits cancer-cell survival and induces cell death. Learn more about how coffee induces autophagy in this clip featuring autophagy expert, Dr. Guido Kroemer.

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  • Combining aerobic exercise and strength training may be the best strategy for improving healthspan. www.bmj.com
    Exercise Cancer Heart Disease Aerobic Strength

    Current public health guidelines recommend that adults engage in regular physical activity for optimal health. Findings from a new study suggest that a combination of both aerobic and strength activities reduces the risk of death from all causes as well as specific causes.

    According to the guidelines, adults should engage in at least 150 minutes of moderate-intensity aerobic physical activity or at least 75 minutes of vigorous-intensity aerobic physical activity each week, or an equivalent combination of both. They should also engage in muscle-strengthening activities of moderate or greater intensity on two days or more each week.

    The population-based cohort study, which involved nearly 480,000 adults, drew on data from the National Health Interview Survey, an ongoing, cross-sectional survey of people living in the United States. The study participants reported how much leisure time aerobic and strength physical activity they engaged in each week. Then the authors of the study categorized them as having insufficient activity, aerobic activity only, strength activity only, and both aerobic and strengthening activities, based on the guidelines.

    The authors found that the participants who engaged in recommended amounts of aerobic or muscle-strengthening activity had a lower risk of death from all causes, and these benefits were even greater if they engaged in both types of activities. They noted similar reductions in risk of death from cardiovascular disease, cancer, and chronic lower respiratory tract diseases.

    These findings suggest that adherence to public health guidelines for exercise reduce the risk of disease and death and provide support for interventions to improve compliance.

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  • Women with a BDNF genetic variant experience fewer negative cognitive effects during chemotherapy. www.sciencedaily.com
    Brain Cancer Dementia BDNF

    Chemotherapy-associated cognitive impairment is a side-effect of chemotherapy in which people experience difficulties with concentration, decision making, and memory. Findings from a 2015 study suggest that women with a BDNF gene variation experience fewer cognitive problems during chemotherapy compared to those without this variation.

    BDNF is a growth factor that is involved in the growth and repair of neurons. BDNF is expressed in the prefrontal cortex and hippocampus regions of the brain, which are involved in executive function, learning, and memory. A common variation in the BDNF gene called a single nucleotide polymorphism, or SNP, can alter how the BDNF protein functions. The SNP, known as Val66Met, results in the amino acid valine being replaced with methionine in the BDNF protein. Researchers have studied how the Val66Met SNP affects various aspects of cognition.

    Previous research has demonstrated that women with breast cancer who were treated with chemotherapy experienced varying levels of cognitive decline. The current study investigated whether genetics, particularly variations in the BDNF gene, might make a person more susceptible to experiencing these effects.

    The prospective cohort study involved 145 women (average age, 51 years) with early-stage breast cancer who were scheduled to receive chemotherapy. The authors of the study evaluated the participants' cognitive function using neuropsychological tools before, during, and at the end of chemotherapy treatment. Also, the researchers determined which version of the BDNF gene each participant possessed. If a patient’s test score during or at the end of treatment was 15 percent lower than baseline, they were considered to have cognitive impairment.

    The authors observed that 54 women experienced cognitive impairment after treatment; however, those with the Met allele had fewer problems with verbal fluency and multitasking compared to those with the Val allele, particularly in older participants. This information may allow for early interventions in preventing cognitive impairment during chemotherapy.

    These findings suggest that women may differ in their susceptibility to chemotherapy-associated cognitive impairment depending on which version of the BDNF gene they carry. Further research is required to confirm these findings, and brain imaging studies are needed to determine if these findings are the result of changes in brain anatomy.

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  • Cancer cells hijack the body's inflammatory response to protect themselves from viruses. www.crick.ac.uk
    Cancer Virus

    Oncolytic viruses target and kill cancer cells without harming healthy cells by promoting an immune response against a tumor. However, they only work in a minority of patients. Findings from a new study identify potential mechanisms underlying the varied response to oncolytic virus therapies.

    The authors of the cell study investigated the role of cancer-associated fibroblasts, a type of cell involved in the body’s immune and inflammatory responses. They infected cancer cells with herpes simplex virus, the only FDA-approved oncolytic virus, to determine how the fibroblasts mediate the tumor’s response to the virus.

    They found that when fibroblasts come in contact with cancer cells, they activate pathways that mediate the expression of proinflammatory cytokines such as interferon beta-1. Interferons are proteins produced by the body’s cells as a defensive response to viruses. The ensuing inflammation prevents the virus from invading and replicating in the cancer cell, undermining the pathogen’s efficacy.

    These findings identify potential mechanisms that mediate the body’s response to oncolytic viruses and suggest that targeting the pathways that mediate the expression of proinflammatory cytokines might be useful in future cancer therapies.

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  • Some cancers have a reduction in catalase activity, making them more vulnerable than normal cells to hydrogen peroxide from intravenous vitamin C www.sciencedaily.com
    Cancer Vitamin C

    From the article:

    Earlier work by UI redox biology expert Garry Buettner found that at these extremely high levels (in the millimolar range), vitamin C selectively kills cancer cells but not normal cells in the test tube and in mice.

    […]

    “In this paper we demonstrate that cancer cells are much less efficient in removing hydrogen peroxide than normal cells. Thus, cancer cells are much more prone to damage and death from a high amount of hydrogen peroxide,” says Buettner […] “This explains how the very, very high levels of vitamin C used in our clinical trials do not affect normal tissue, but can be damaging to tumor tissue.”

    Some cancers may be more vulnerable than others:

    Buettner says this fundamental information might help determine which cancers and which therapies could be improved by inclusion of high-dose ascorbate in the treatment. “Our results suggest that cancers with low levels of catalase are likely to be the most responsive to high-dose vitamin C therapy, whereas cancers with relatively high levels of catalase may be the least responsive,” he explains.

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  • High-dose injections of vitamin C reduced tumor weight and growth rate by about 50% in mouse models of brain, ovarian, and pancreatic cancer www.sciencedaily.com
    Brain Cancer Vitamin C

    From the article:

    High-dose injections of vitamin C, also known as ascorbate or ascorbic acid, reduced tumor weight and growth rate by about 50 percent in mouse models of brain, ovarian and pancreatic cancers, researchers report in the Proceedings of the National Academy of Sciences. The researchers traced ascorbate’s anti-cancer effect to the formation of hydrogen peroxide in the extracellular fluid surrounding the tumors. Normal cells were unaffected.

    Intravenous administration as a crucial differentiator:

    “Clinical and pharmacokinetic studies conducted in the past 12 years showed that oral ascorbate levels in plasma and tissue are tightly controlled. In the case series, ascorbate was given orally and intravenously, but in the trials ascorbate was just given orally. It was not realized at the time that only injected ascorbate might deliver the concentrations needed to see an anti-tumor effect,” said Levine

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  • Exercise benefits men about to undergo cancer treatment. www.eurekalert.org
    Exercise Cancer Aerobic

    Exercise reduces the risk of developing cancer and improves the quality of life among cancer survivors. A recent study shows that exercise reduces the harmful effects observed among men about to undergo androgen-deprivation therapy (ADT) for prostate cancer.

    Prostate cancer is the most common form of cancer among men living in the United States. The first line of treatment for prostate cancer is commonly ADT, which involves the surgical or pharmaceutical suppression of serum testosterone levels. Side effects of ADT include body fat increases, muscle mass losses, and changes in cardiopulmonary and metabolic fitness.

    The study involved 50 men who were about to start ADT. Half of the men engaged in supervised aerobic and resistance exercise twice a week for an hour for a three-month period, followed by three months of unsupervised exercise. The other half, which served as a control group, maintained their regular activity levels. The authors of the study assessed the men for changes in fat mass, biomarkers, cardiopulmonary fitness, energy levels, and quality of life at the three- and six-month time-points in the study.

    At the three-month point, the men who had engaged in the exercise program did not see reductions in body fat, but they did demonstrate improvements in their respiratory fitness and energy levels. After the exercise program ended, the exercising men had improved quality of life and reduced markers of cardiovascular disease risk, compared to the control group. These findings suggest that low-risk interventions such as exercise can benefit men about to undergo ADT.

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  • Sustained weight loss in women over 50 reduces breast cancer risk www.eurekalert.org
    Nutrition Exercise Cancer Diet Breast Cancer Weight Loss

    Breast cancer is one of the leading causes of death among women living in the United States, claiming the lives of approximately 41,000 women each year. Being overweight or obese increases a woman’s risk of developing breast cancer. Findings from a new study indicate that women who lose weight after the age of 50 years and keep the weight off have reduced risk of developing breast cancer.

    More than two-thirds of women living in the United States are overweight or obese. Excess body fat increases a person’s risk for developing type 2 diabetes, a known risk factor for cancer. Body fat also alters hormone levels, which may increase the risk of developing hormone-sensitive cancers, such as breast cancer. In addition, body fat secretes a wide array of pro-inflammatory substances that damage DNA and inhibit apoptosis.

    The study involved more than 180,000 women who were 50 years of age and older from cohorts of 10 different prospective studies. The women were weighed three times over a period of 10 years. Those who lost weight and kept it off had a lower risk of breast cancer than women who did not lose weight.

    Among women who lost 4 to 10 pounds, 10 to 20 pounds, or 20 or more pounds, risk decreased by 13 percent, 16 percent, and 26 percent, respectively. Among women who lost 20 or more pounds but gained a portion of the weight back, risk was reduced by 23 percent.

    These findings point to the importance of public health interventions that promote weight loss among women as a means to reduce cancer risk.

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  • Prostate cancer was completely eliminated in 80 percent of men treated with MRI-guided ultrasound. newatlas.com
    Cancer Prostate

    Prostate cancer is the second most common cancer among men worldwide. Nearly 165,000 men in the United States will be diagnosed with prostate cancer this year. Findings from a recent study presented at the annual meeting of the Radiological Society of North America indicate that a new ultrasound technique may be a promising treatment for this disease.

    Current prostate cancer treatments often involve surgery to remove malignant tissue. Many men who undergo surgery develop urinary incontinence, and as many as 85 percent experience erectile dysfunction. The new treatment technique, called transurethral ultrasound ablation, or TULSA, is a minimally invasive treatment that uses MRI-guided ultrasound to heat and destroy tumors while sparing normal tissue.

    The multi-center study involved 115 men between the ages of 59 and 69 years old who had been diagnosed with localized prostate cancer. Each of the men received TULSA treatment (average time, 51 minutes) and then were reassessed 12 months later.

    At the 12-month follow-up, 80 percent of the men displayed no evidence of clinically significant cancer; 65 percent of the men had no evidence of cancer in biopsied tissue; and 96 percent of the men had significantly reduced prostate-specific antigen levels, a biomarker for prostate cancer. Only 1 percent of the men were incontinent after the treatment, and 25 percent experienced erectile dysfunction.

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  • Supercentenarians have high level of cytotoxic T cells, which can kill cancer cells. www.sciencedaily.com
    Cancer Aging Immune System

    Supercentenarians – people who live to be 110 years of age or older – have long healthspans, free of disease and the physical and cognitive decline that commonly accompany aging. A critical factor in their long, healthy lives is a robust immune system. Findings from a new study reveal that supercentenarians have high levels of cytotoxic CD4 T-cells, a specialized type of white blood cell.

    CD4 T-cells are key elements in the body’s antigen-specific immune response. They destroy virus-infected and malignant cells by triggering apoptosis – a type of cellular self-destruct mechanism that rids the body of damaged or aged cells. CD4 T-cells are considered “helper” cells in that they assist other cells in the immune response.

    The authors of the study collected circulating immune cells in the blood of seven supercentenarians and five controls, who were between the ages of 50 and 80 years. They found that the supercentenarians had considerably higher levels of CD4 T-cells than the controls, and these CD4 T-cells had unique cytotoxic capabilities. Furthermore, they found that the cytotoxic cells had arisen via clonal expansion, the process by which daughter cells arise from a single parent cell.

    Cytotoxic CD4 T-cells are rare, even among young people, but they play key roles in immunosurveillance and can kill cancer cells. These findings shed light on how supercentenarians maintain good health throughout their lives.

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  • Fecal samples from people with colorectal cancer transplanted into mice caused precancerous lesions. www.pasteur.fr
    Cancer Microbiome

    More than half of all colorectal cancers are sporadic, or nonhereditary. A key driver in the development of sporadic colorectal cancer is dysbiosis – an imbalance in the type and number of microbes that typically reside in the human gut. A recent study found that colorectal dysbiosis induced epigenetic changes and promoted the development of precancerous lesions in the guts of fecal transplant recipient mice.

    The authors of the study transplanted fecal samples from healthy individuals or from individuals with sporadic colorectal cancer into the guts of 136 germ-free mice. Seven and 14 weeks after the transfer, the mice were assessed for dysbiosis, epigenetic changes in their colonic cell DNA, and the presence of aberrant crypt foci (ACF) – precancerous lesions associated with the development of colorectal cancer.

    The mice that received fecal transplants from people with colorectal cancer had dysbiosis and exhibited higher numbers of ACF compared to those that received transplants from healthy people. The mice also exhibited hypermethylation of specific genes. Hypermethylation is a type of epigenetic modification of DNA that drives gene expression and is associated with increased risk for developing ACF.

    Based on these findings, the study authors then analyzed the blood of 1,000 people who were scheduled for routine colonoscopy, looking for the presence of specific colonic bacteria (dysbiosis) and indications of hypermethylation of the same genes identified in the mice. They found that hypermethylation of these genes correlated with sporadic colorectal cancer incidence, which could potentially serve as a diagnostic marker for the disease.

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  • Running associated with lower all-cause, cardiovascular, and cancer mortality. bjsm.bmj.com
    Exercise Cancer Heart Disease Depression Aerobic Cardiovascular

    Public health experts recommend that people get at least 150 minutes of moderate to vigorous physical activity, such as walking, running, or cycling, each week for optimal health. Running, in particular, is associated with improved aerobic fitness and cardiovascular function. A recent meta-analysis found that running, even for short periods, reduced the risk of mortality from all causes, especially cardiovascular- and cancer-related deaths.

    The authors of the study analyzed data from 14 studies of six prospective cohorts involving more than 230,000 people. The cohorts were followed over a span of 5 to 35 years. The data were adjusted for sociodemographic factors, other physical activity besides running, body fatness, health status, and unhealthy lifestyle habits such as smoking, alcohol consumption, and poor diet.

    They found that running was associated with a 27 percent lower all-cause mortality, 30 percent lower cardiovascular mortality, and 23 percent lower cancer mortality. Even the smallest amount of time spent running (less than 50 minutes per week) was linked to a significant reduction in all-cause mortality.

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  • New placebo-controlled trial finds that healthy adults given a broccoli sprout beverage high in sulforaphane had a 63% increase in benzene excretion. academic.oup.com
    Cancer Pollution Sulforaphane NRF2 Glucoraphanin

    A new placebo-controlled trial finds that healthy adults given a broccoli sprout beverage high in sulforaphane had a 63% increase in excretion in the carcinogen benzene which is a compound found in air pollution and tobacco smoke.

    The study also showed that the sulforaphane’s role in benzene excretion was dose-dependant. The high sulforaphane dose increased benzene excretion by 63% and half the sulforaphane dose caused an 11% increase in benzene excretion.

    The high dose broccoli sprout beverage contained 600 μmol of glucoraphanin (sulforaphane precursor) and 40 μmol sulforaphane, whereas the half dose contained 300 μmol of glucoraphanin and 20 μmol of sulforaphane.

    I have referred to other studies showing similar effects of broccoli sprouts on benzene excretion. To learn more about how sulforaphane increases the excretion of carcinogens like benzene check out the in-depth episode we did on sulforaphane. https://www.foundmyfitness.com/episodes/sulforaphane

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  • VITAL study: How vitamin D and fish oil affect risk of heart attack, stroke and cancer www.eurekalert.org
    Vitamin D Cancer Heart Disease Omega-3 Vitamin A

    Finally, the highly anticipated result of the VITAL Study are in - at least for the major endpoints CVD and cancer.

    While at first sight they may seem disappointing and have already prompted the usual, overgeneralizing negative reports from many media outlets, there are some remarkable findings if you look more closely - such as a whopping 77% reduced risk for heart attacks in African Americans taking fish oil (all those media who are now sweepingly reporting that fish oil dies “not reduce CVD”, without mentioning this, such as MdMag*, musk ask themselves whether they are looking at the results through racist glasses, as the investigators certainly didn’t make a secret of this remarkable finding).

    With regard to vitamin D, the results certainly don’t support the strong effect on cancer risk suggested by some observational studies, but there seems to be a modest effect building up over time, and given the fact that 2000 IU is a rather modest dose indeed and not expected to raise the blood level by more than 10 ng/ml, the jury is far from out on vitamin D and cancer.

    Anyway, this is a very high quality trial providing the researchers with a treasure-trove of data that will be subject to many auxillary studies. I’m particularly curious about the upcoming studies regarding autoimmune and mental health endpoints.

    *https://www.mdmag.com/conference-coverage/aha-2018/vital-study-supplements-of-omega3s-or-vitamin-d-do-not-reduce-cvd-or-cancers

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  • Bacteroides fragilis metabolises exopolysaccharides produced by bifidobacteria www.ncbi.nlm.nih.gov
    Cancer Probiotics Antibiotics

    One downside w/ probiotics. “Bacteroides fragilis metabolises exopolysaccharides produced by bifidobacteria” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4946188/

    and fragilis fuels colon cancer https://www.nytimes.com/2018/02/01/health/colon-cancer-bacteria.html?ref=todayspaper

    “Patients with familial adenomatous polyposis harbor colonic biofilms containing tumorigenic bacteria” http://science.sciencemag.org/content/359/6375/592

    the same fragilis is antibiotic resistant Antimicrobial resistance in the Bacteroides fragilis group in faecal samples from patients receiving broad-spectrum antibiotics. https://www.ncbi.nlm.nih.gov/pubmed/28445776

    the same fragilis may or may not cause symptoms Dientamoeba fragilis colonization is not associated with gastrointestinal symptoms in children at primary care level. https://www.ncbi.nlm.nih.gov/pubmed/27784723

    Dientamoeba fragilis: A Family Cluster of Disease Associated With Marked Peripheral Eosinophilia https://academic.oup.com/cid/article/57/6/845/329548

    This is one of the best articles highlighting this microbe ( w/ some contrary evidence from northern Europe). “Dientamoeba fragilis, the Neglected Trichomonad of the Human Bowel” https://cmr.asm.org/content/29/3/553

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  • Cellular stress with changes in microbial profile promotes colorectal cancer development www.sciencedaily.com
    Cancer Microbiome Inflammation Protein Toll-Like Receptors

    Activation of ATF6, a regulator of ER (Endoplasmatic Reticulum) stress, combined with changes in cecal microbial profile, promoted colon adenoma formation.

    [Abstract]

    Methods: We analyzed data from 541 patients with CRC in the TCGA database for genetic variants and aberrant expression levels of unfolded protein response genes. Findings were validated in a cohort of 83 patients with CRC in Germany. We generated mice with intestinal epithelial cell-specific expression of the active form of ATF6 (nATF6IEC) from 2 alleles (homozygous), mice with expression of nATF6IEC from 1 allele (heterozygous), and nATF6IECfl/fl mice (controls). All nATF6IEC mice were housed under either specific-pathogen free or germ-free conditions. Cecal microbiota from homozygous nATF6IEC mice or control mice was transferred into homozygous nATF6IEC mice or control mice. nATF6IEC mice were crossed with mice with disruptions in the myeloid differentiation primary response gene 88 and toll-like receptor adaptor molecule 1 gene (Myd88/TRIF knock-out mice). Intestinal tissues were collected from mice and analyzed by histology, immunohistochemistry, immunoblots, gene expression profiling of unfolded protein response and inflammatory genes, array-based comparative genome hybridization, and 16S rRNA gene sequencing.

    Results: Increased expression of ATF6 was associated with reduced disease-free survival times of patients with CRC. Homozygous nATF6IEC mice developed spontaneous colon adenomas at 12 weeks of age. Compared to controls, homozygous nATF6IEC mice had changes in the profile of their cecal microbiota, increased proliferation of intestinal epithelial cells, and loss of the mucus barrier—all preceding tumor formation. These mice had increased penetration of bacteria into the inner mucus layer and activation of STAT3, yet inflammation was not observed at the pre-tumor or tumor stages. Administration of antibiotics to homozygous nATF6IEC mice greatly reduced tumor incidence, and germ-free housing completely prevented tumorigenesis. Analysis of nATF6IEC MyD88/TRIF knock-out mice showed that tumor initiation and growth required MyD88/TRIF-dependent activation of STAT3. Transplantation of cecal microbiota from nATF6IEC mice and control mice, collected before tumor formation, caused tumor formation in ex–germ-free nATF6IEC mice.

    Conclusions: In patients with CRC, ATF6 was associated with reduced time of disease-free survival. In studies of nATF6IEC mice, we found sustained intestinal activation of ATF6 in the colon to promote dysbiosis and microbiota-dependent tumorigenesis.

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  • Food Additives Causing Harm, Reforms Urgently Needed, AAP Says www.medscape.com
    Brain Cancer Gut Hormones Pregnancy Neurotransmitter Insulin

    The Worst Offenders:

    The statement addresses 2 broad categories of additives: direct and indirect. Indirect additives refers to substances in “food contact materials,” such as “adhesives, dyes, coatings, paper, paperboard, plastic, and other polymers,” the authors of the policy statement explain. Direct food additives include chemicals such as colorings, flavorings, and preservatives added to food during processing. Within those two categories the authors identified six types of additives of most concern, based on accumulating evidence summarized in the report and in an accompanying press release:

    Bisphenols: Used to manufacture plastic containers and food and beverage cans, these compounds have been associated with endocrine and neurodevelopmental disruption and obesogenic activity, with alterations in the timing of puberty, reduced fertility, and impaired neurological and immunological development. One bisphenol, bisphenol A, has already been banned from baby bottles and sippy cups.

Phthalates: As components of plastic wrap and plastic tubing and containers, phthalates similarly have been implicated in endocrine disruption and obesogenic activity. "A robust literature" shows that these chemicals adversely affect male sexual development, may contribute to childhood obesity and insulin resistance, and may also contribute to cardiovascular disease.

Perfluoroalkyl chemicals: These chemicals are used in the manufacture of greaseproof paper and cardboard packaging. They have been associated with immunosuppression, endocrine disruption such as impaired thyroid function, and decreased birth weight.

Perchlorate: Often added to plastic packaging for dry foods to control static electricity, perchlorate has been shown to disrupt production of thyroid hormone, with implications for subsequent cognitive function. Of particular concern is exposure among pregnant women, "given that the developing fetus is entirely reliant on the maternal thyroid hormone during the first trimester of pregnancy," the authors write in the technical report. They suggest that perchlorate "may be contributing to the increase in neonatal hypothyroidism and other thyroid system perturbations that have been documented in the United States."

Nitrates and nitrites: As direct food additives, these compounds are used as preservatives and color enhancers in cured and processed meats, fish, and cheese. There has been "longstanding concern" over their use, the authors write, because of an association with cancers of the nervous and gastrointestinal systems, and methemoglobinemia in infants. They were classified as "probable human carcinogens" in 2006 by the International Agency for Research on Cancer.

Artificial food colors: Often added to products that appeal to children, such as juice drinks, artificial food colors have been associated in some studies with an increased risk for attention-deficit hyperactivity disorder. Although their mechanisms of action are not yet completely understood, and the research "should be interpreted with caution," the authors recommend "a thorough reassessment" of artificial food colors to ensure they are safe.
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  • Suppression of insulin with a ketogenic diet improves the efficacy of cancer drugs known as PI3K inhibitors and shrinks tumors in mice. www.nature.com
    Cancer Ketosis Insulin Ketogenic Diet

    Suppression of insulin with a ketogenic diet improves the efficacy of cancer drugs known as PI3K inhibitors and shrinks tumors in several different animal models of cancer.

    Insulin activates the PI3K pathway is usually which then leads to cell proliferation and tumor growth. Drugs inhibiting the PI3K pathway have not been very effective due to an insulin feedback response. A ketogenic diet lowered the insulin response and made the drugs more effective.

    The researchers point out that this study doesn’t suggest a ketogenic diet alone would treat cancer. Their data showed in a leukemia model, the ketogenic diet seemed to make cancer more aggressive in mice who were not also given a PI3K inhibiting drug. However, the combination of a PI3K inhibitor and ketogenic diet showed efficacy in many different cancer types (in mice).

    Talk of a pilot clinical study in humans is underway.

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  • Acid Suspends the Circadian Clock in Hypoxia through Inhibition of mTOR. - PubMed - NCBI www.ncbi.nlm.nih.gov
    Cancer Metabolism Stress Circadian Rhythm Autophagy

    Citation: Cell. 2018 Jun 28;174(1):72-87.e32. doi: 10.1016/j.cell.2018.05.009. Epub 2018 May 31.

    Abstract Recent reports indicate that hypoxia influences the circadian clock through the transcriptional activities of hypoxia-inducible factors (HIFs) at clock genes. Unexpectedly, we uncover a profound disruption of the circadian clock and diurnal transcriptome when hypoxic cells are permitted to acidify to recapitulate the tumor microenvironment. Buffering against acidification or inhibiting lactic acid production fully rescues circadian oscillation. Acidification of several human and murine cell lines, as well as primary murine T cells, suppresses mechanistic target of rapamycin complex 1 (mTORC1) signaling, a key regulator of translation in response to metabolic status. We find that acid drives peripheral redistribution of normally perinuclear lysosomes away from perinuclear RHEB, thereby inhibiting the activity of lysosome-bound mTOR. Restoring mTORC1 signaling and the translation it governs rescues clock oscillation. Our findings thus reveal a model in which acid produced during the cellular metabolic response to hypoxia suppresses the circadian clock through diminished translation of clock constituents.

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  • A common antimicrobial agent (called Triclosan) was found to increase the severity of colitis symptoms and promote tumor growth. stm.sciencemag.org
    Cancer Gut

    A common antimicrobial agent found in some soaps and toothpaste (called Triclosan) was found to increase the severity of colitis symptoms and promoted colitis-associated colon cancer cell growth (in mice).

    Triclosan has also been linked to hormone disruption and drug-resistant bacteria. It has been found in the urine of about three-fourths of doctors and nurses. It is also among the most common chemicals to be detected in streams.

    In addition to soaps, it has also been found in dust particles in buildings.

    In December 2017, the FDA issued a final rule regarding certain over-the-counter health-care antiseptic products. Companies will not be able to use triclosan or 23 other active ingredients in these products without premarket review due to insufficient data regarding their safety and effectiveness.

    Read more here: https://www.fda.gov/ForConsum%E2%80%A6/ConsumerUpdates/ucm205999.htm

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  • Two types of gut bacteria found to fuel the growth of colon cancer in humans. www.nytimes.com
    Cancer Gut Microbiome

    The bacteria penetrate through the gut barrier and release compounds that damage DNA and inflame colon cells. This can both induce colon cancer and/or allow precancerous cells to grow into cancer.

    The strains of bacteria are Bacteroides fragilis and a strain of E. coli. Not everyone has these two types of bacteria but those that do are thought to have gotten them during childhood.

    This study analyzed 25 tumor samples taken from people with familial adenomatous polyposis and found the two bacterial species present in large quantities.

    Animals were then given a cancer-causing agent to cause mutations in DNA of colon cells. There were few or no tumors until the animals were transplanted with both strains of the gut bacteria…this caused tumor growth.

    It is unclear how people acquire these two strains of bacteria early in life or how to get rid of them. But this is the first step in understanding a complex interaction between certain species of gut bacteria and colon cancer.

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  • Probiotic was engineered to make an enzyme able to produce sulforaphane from the precursor in broccoli extract. It reduced tumor size by over 75%. www.nature.com
    Cancer Sulforaphane NRF2

    Scientists use a probiotic and broccoli extract to target colorectal cancer cells.

    Probiotic was engineered to make an enzyme able to produce sulforaphane from the precursor in broccoli extract. It reduced tumor size by over 75% (in mice).

    This is pretty clever because they modified the e.coli to bind to cancer cells. One issue w/ broccoli extract is that the conversion to sulforaphane in vivo depends on gut bacteria, usually resulting in different bioavailability from person to person.

    For a great discussion on sulforaphane, watch these two podcasts.

    Sulforaphane and Its Effects on Cancer, Mortality, Aging, Brain and Behavior, Heart Disease & More: https://www.foundmyfitness.com/episodes/sulforaphane

    Interview with expert Dr. Jed Fahey: https://www.foundmyfitness.com/episodes/jed-w-fahey

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  • Lifestyle And Diet May Stop Or Reverse Prostate Cancer Progression (Dean Ornish Study) www.sciencedaily.com
    Exercise Cancer Diet Prostate Vitamin A Protein Aerobic

    FTA:

    The research team studied 93 men with biopsy-proven prostate cancer who had elected not to undergo conventional treatment for reasons unrelated to this study. The participants were randomly divided into either a group who were asked to make comprehensive changes in diet and lifestyle or a comparison group who were not asked to do so.

    […] After one year, the researchers found that PSA levels (a protein marker for prostate cancer) decreased in men in the group who made comprehensive lifestyle changes but increased in the comparison group. There was a direct correlation between the degree of lifestyle change and the changes in PSA. Also, they found that serum from the participants inhibited prostate tumor growth in vitro by 70 percent in the lifestyle-change group but only 9 percent in the comparison group. Again, there was a direct correlation between the degree of lifestyle change and the inhibition of prostate tumor growth.

    Participants in the lifestyle-change group were placed on a vegan diet consisting primarily of fruits, vegetables, whole grains, and legumes supplemented with soy, vitamins and minerals. They participated in moderate aerobic exercise, yoga/meditation, and a weekly support group session.

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  • Lower LDL Cholesterol Leads To Lower PSA & Lower Prostate Cancer Risk, Study Suggests www.sciencedaily.com
    Cancer Prostate

    FTA:

    In 2007, a retrospective study showed that men taking statins to lower their cholesterol also experienced a proportional decline in their PSA levels. This new study confirms that evidence and highlights the fact that cholesterol may play a role in prostate cancer development and progression. […] It remains to be seen whether or not lowering your PSA through statin medications could potentially mask the presence of prostate disease.

    It would be nice if it talked about particle size! To understand why particle size matters (in the context of atherogenic dyslipidemia and heart disease), watch this video featuring @rhonda and Dr. Ronald Krauss.

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  • Intravenous vitamin C given to patients with lung cancer nearly doubled the shrinking of their tumors after chemo. time.com
    Cancer Vitamin C Vitamin A

    Around 93% of the people receiving the intravenous vitamin C are responding to chemotherapy and radiation, compared to 40% who usually do. The intravenous vitamin C may also show encouraging results in a small sample of people with glioblastoma. Remember that oral doses of vitamin C (even liposomal) can not achieve the same plasma concentrations that IVC can, which are between 800 to 1,000-fold higher. Other studies have revealed mechanisms by which the IVC works including the production of hydrogen peroxide which selectively kills cancer cells. Normal cells can detoxify the hydrogen peroxide but cancer cells cannot. The IVC also inhibits glucose from being taking up into the cancer cells since it competes for binding to glucose transporters. The multitude of both animal studies and clinical studies on intravenous vitamin C seem like it may be a very promising cancer treatment particularly with the standard of care treatment. I look forward to seeing the results of larger trials.

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  • High-dose intravenous vitamin C selectively kills cancer cells by increasing H2O2 & potently kills cancer stem cells. www.sciencedaily.com
    Cancer Vitamin C Stem Cells Vitamin A

    High-dose intravenous vitamin C has previously been shown to selectively kill cancer cells by increasing hydrogen peroxide and now it has been found to potently kill cancer stem cells. The new study screened a variety of compounds in order to find those that were most potent at killing cancer stem cells, which are the most resistant to any type of cancer treatment. Interestingly, vitamin C was found to be 10 times more potent at killing cancer stem cells (cultured in a dish) than 2-deoxyglucose, a drug that prevents cancer cells from using glucose via glycolysis. While this study was done in a culture dish, other studies have been done in animals and humans. It is important to realize that intravenous vitamin C increases blood levels that are 100-500 times higher than levels that can be achieved with oral ingestion. It is this VERY-high concentration of vitamin C in the blood that results in the generation of hydrogen peroxide that selectively kills cancer cells because normal cells effectively remove it but cancer cells cannot. Also, early phase 1 clinical trials showed that the combination of high-dose, intravenous vitamin C with standard chemotherapy or radiation was well tolerated and improved patient outcome. Larger clinical trials are now underway.

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  • High dose vitamin C selectively kills tumor cells through its oxidized form & starves cancer cells of energy. news.sciencemag.org
    Cancer Vitamin C Vitamin A Antioxidant

    I also want to add that while vitamin C is considered an antioxidant it does not act the same as other antioxidants such as vitamin E and NAC, which have actually been shown to accelerate tumor growth. Vitamin E and NAC can sequester reactive oxygen species (which activates cancer cell death) and prevents cancer cells from dying. Vitamin C does not act the same way. This is why it is VERY important to understand mechanisms and not make generalizations. Vitamin C is in constant homeostasis between oxidized and reduced forms and this depends on many factors including dose. When administered intravenously, the vitamin C dose is so high that it forms the oxidized form and this does a couple of important things that can kill cancer cells. First, it causes oxidative stress in cancer cells (a well known mechanism to activate cell death of a cancer cell). Second, it inhibits the glycolysis pathway, thus starving cancer cells of glucose.

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  • Packing on the muscle via inhibition of cancer-related protein and myostatin increases cancer survival in mice. www.sciencedaily.com
    Cancer Muscle Protein

    FTA:

    There was evidence to suggest that tumors secrete activin, such that circulating levels of the protein rise in those with cancer. Activin is closely related to another protein, called myostatin, which is known to be important in muscle […]

    Animals lacking myostatin or taking treatments that block it grow bigger muscles. There was some evidence to suggest that activin blockers might have a similar effect.

    Based on that hunch, the researchers treated mice with cancer and associated cachexia with a recombinant and soluble version of the ActRIIB receptor (sActRIIB), a kind of molecular “decoy” that potently inhibited both activin and myostatin activity. That treatment reversed the animals' muscle loss and prolonged their survival by several weeks on average.

    “In tumor-bearing mice with profound cachexia, blocking this pathway not only prevents muscle wasting but completely reverses the loss of muscle, strength and anorexia,” Han said. (Anorexia is another symptom of cachexia, but appetite stimulants and nutritional supplements don’t help much.)

    note: cachexia = muscle wasting

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  • "Broccolio-sprout beverage" makes people excrete benzene in their urine, mitigating effects of breathing polluted air www.theatlantic.com
    Cancer Diet Sulforaphane

    A few take-home points from the article:

    Rapid and Sustainable Detoxication of Airborne Pollutants by Broccoli Sprout Beverage: Results of a Randomized Clinical Trial in China. (PubMed Abstract)

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