Cancer
now browsing by category
Cancer is a word most people dread, but it only affects less than half of us. LeanMachine wants to be in the other half, and correct nutrition is the way to get there. Billions of dollars are spent on treatment drugs, but almost nothing is spent on prevention!
Environmental Chemicals Increasingly Linked to Breast Cancer Risk
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/03/26/triclosan-exposure-breast-cancer-risk.aspx
Analysis by Dr. Joseph Mercola March 26, 2025
STORY AT-A-GLANCE
- Women with moderate triclosan exposure face up to 2.33 times greater breast cancer risk
- Triclosan, found in 75% of Americans’ urine, is readily absorbed through skin and commonly appears in antibacterial products, cosmetics and even clothing, making its way into blood, breast milk and the food chain
- Exposure to environmental chemicals like DDT, dioxins and BPA during pregnancy, infancy or puberty significantly increases breast cancer risk decades later by disrupting normal development
- A 2023 study reveals triclosan’s cancer-promoting mechanisms, showing it increases oxidative stress that damages cells and affects telomere length, both of which contribute to breast cancer development
- Simple preventive steps include avoiding antimicrobial products, choosing organic produce, improving indoor air quality and carefully scrutinizing personal care product ingredients to reduce exposure to harmful chemicals
Breast cancer is on the rise worldwide, and research increasingly points toward the often-overlooked role of environmental chemicals like triclosan as key contributors to this escalating health crisis.
Chemicals are pervasive in daily life, from the plastics used to store your food to the ingredients in your personal care products, and the pollutants filling your air and water. Many of these substances, often unseen, mimic or disrupt your body’s delicate hormonal balance and interfere with essential biological processes, laying the groundwork for breast cancer to take hold and progress.
Triclosan Is a Key Culprit in Breast Cancer
A study published in the journal Scientific Reports explored the links between common endocrine-disrupting chemicals (EDCs) — specifically phenols and parabens — and the development of breast cancer in women.1 The study used extensive data from the National Health and Nutrition Examination Survey (NHANES), collected between 2005 and 2014.
The researchers examined urine samples from 4,455 women, quantifying levels of various phenols, including bisphenol A (BPA), triclosan and benzophenone-3, and parabens, such as methyl, ethyl, propyl and butyl paraben.
Among these chemicals, triclosan emerged as a key focus. The researchers found that women in the second quartile of triclosan exposure faced a 2.33 times greater risk and those in the third quartile had a 1.94 times greater risk of developing breast cancer when compared to women in the lowest exposure group.
Interestingly, the study revealed a complex, nonlinear relationship between triclosan exposure and breast cancer risk, specifically an inverted U-shaped curve. This pattern indicates that as triclosan exposure initially increases, the risk of breast cancer also rises, but then, at even higher exposure levels, the risk appears to plateau or slightly recede, though it remains elevated compared to the lowest exposure group.
Overweight women had a stronger association between triclosan exposure and breast cancer risk. Similarly, women under the age of 60, as well as White women, also had a more pronounced connection. While other phenols and parabens were not linked to an overall increased risk of breast cancer in this study, ethyl and butyl paraben exposure were found to increase breast cancer risk specifically among lean women.
Study Reveals Mechanisms Behind Triclosan’s Breast Cancer Link
A 2023 study published in Frontiers in Public Health adds more fuel to the fire regarding triclosan’s dangers, particularly its link to breast cancer.2 Researchers looked at 302 women with breast cancer and compared them to 302 healthy women. They found a clear connection between higher levels of triclosan in the urine and an increased risk of breast cancer. The paper then explains how triclosan is causing this increased risk.
The researchers focused on oxidative stress, which is an imbalance of free radicals and antioxidants in your body. Oxidative stress damages your cells, including your DNA. The researchers measured several markers of oxidative stress and found that women with higher triclosan levels also had higher levels of these markers. This suggests that triclosan contributes to breast cancer by ramping up oxidative stress in the body.
The study also looked at telomeres, which are like protective caps on the ends of your chromosomes. Shorter telomeres have been linked to an increased risk of cancer. Interestingly, this study found a connection between triclosan exposure and longer telomeres, which, surprisingly, has also been linked to breast cancer risk. Triclosan’s influence on telomeres reveals another pathway by which it increases cancer risk.
Save This Article for Later – Get the PDF Now
Triclosan Is Found in Many Everyday Products
Triclosan is an antimicrobial agent incorporated into a vast range of everyday products, from antibacterial soaps and toothpastes to cosmetics and even clothing. Its primary function is to inhibit the growth of bacteria and fungi, extending product shelf life and appealing to consumer desires for cleanliness. However, this additive carries an undesirable trait: it’s readily absorbed into the human body.
Alarmingly, triclosan has been detected in human blood, urine and even breast milk, with widespread exposure across populations. In fact, 75% of the U.S. population has triclosan in their urine.3
This pervasive presence raises concerns, particularly given triclosan’s classification as an endocrine disruptor. Its chemical structure resembles thyroid hormones and several known endocrine disruptors like diethylstilbestrol (DES) and BPA, raising red flags for hormonal interference.
At low concentrations, triclosan appears to increase the growth of estrogen-sensitive breast cancer cells, suggesting it behaves like estrogen. Estrogen plays a complex role in breast cell growth and development. When this signaling is disrupted by chemicals like triclosan, it promotes abnormal cell proliferation, fueling the growth of tumors.
Further, triclosan has been linked to thyroid dysfunction, which itself has been associated with an increased risk of breast cancer. Beyond breast cancer, concerns extend to other developmental and health issues, including smaller head circumference at birth, early breast development in girls and even the promotion of antibiotic resistance and allergies.4
Because triclosan is used in so many personal care products, it often ends up being washed down the drain after use. Triclosan persists through wastewater treatment and accumulates in sewage sludge. This sludge is often used as fertilizer, allowing triclosan to be absorbed by plants, including food crops, introducing this harmful chemical into the food chain.
Early-Life Exposure to Chemicals Increases Breast Cancer Risk Later in Life
In a review published in Environmental Research, numerous epidemiological studies — research that tracks disease patterns in populations — were evaluated against established biological knowledge of how various chemicals interact with the human body at the cellular level.5 By merging these two streams of evidence — population trends and biological understanding — the review achieves a powerful perspective on the environmental chemical-breast cancer link.
The in-depth review found that early life exposures to certain environmental chemicals are particularly concerning for breast cancer risk later in life. Exposure during key windows of development — in utero, during infancy and throughout puberty — has lasting effects and increases vulnerability to breast cancer decades later.
The review specifically pinpoints persistent and pervasive chemicals like DDT and dioxins, along with perfluorooctane-sulfonamide (PFOSA), as posing significant risks when exposure occurs early in life.
Early-life exposure to endocrine disruptors like DDT and dioxins has particularly devastating effects on mammary gland development. Since these chemicals mimic or block natural hormones, it sends confusing signals to developing breast cells, altering their normal growth patterns and ultimately increasing cancer susceptibility. Beyond endocrine disruption, the review details other mechanisms at play.
Polycyclic aromatic hydrocarbons, or PAHs, and air pollution are highlighted as significant risk factors, particularly through the mechanism of DNA damage. PAHs, produced by burning fossil fuels and found in vehicle exhaust and industrial emissions, and components of general air pollution directly damage DNA, the very blueprint of your cells. This DNA damage, if not properly repaired, leads to mutations that drive cancer development.
Other widely used chemicals in consumer products were also named in the review. For instance, BPA, an endocrine disruptor with estrogenic activity, and phthalates and nonylphenols also exhibit endocrine-disrupting properties and have been linked to altered mammary gland development in animal models. Hair dyes and straighteners contain aromatic amines and formaldehyde, respectively, both of which have raised carcinogenicity concerns.
Per- and polyfluoroalkyl substances, commonly known as PFAS, are persistent chemicals with evidence of mammary gland effects and links to cancer. Flame retardants, including PBDEs, also show evidence of endocrine disruption and altered mammary gland development in animal studies.
The review reinforces the conclusion that environmental chemicals are not merely bystanders but active players in the development of breast cancer. It is not just about one or two isolated chemicals; it’s about the complex mixture of exposures you face daily and the cumulative impact these exposures have over your lifetime, especially when exposure occurs during important periods of development.
Proactive Steps to Reduce Your Chemical Exposure
While the risks posed by environmental chemicals is significant, remember that you’re not powerless. You can take meaningful steps to reduce your exposure and lessen your risk of breast cancer and other related health problems. It starts with making informed choices in your daily life and being proactive about your health. Every small change you make to reduce your chemical burden contributes to a healthier you.
1. Scrutinize your personal care products — Personal care products are a common source of triclosan, phthalates and nonylphenols. Start reading labels and opt for products specifically labeled “phthalate-free,” “triclosan-free” and “nonylphenol-free.” In addition, switch to simpler products with fewer ingredients, focusing on natural and organic options whenever possible. Your skin is absorbent, so what you put on your body matters.
2. Avoid antimicrobial products — Avoid “antimicrobial” soaps, toothpastes and other products claiming to be antimicrobial and containing triclosan or 5-chloro-2-(2,4-dichlorophenoxy)phenol — another name for triclosan. Wash your hands with plain soap and water. Antibacterial soaps are no more effective than plain soap for killing germs for everyday activities.
3. Peel your carrots and other root vegetables, or buy organic — Vegetables (especially the outer layer of roots) may be contaminated if sewage sludge is used as a fertilizer.6 Sewage sludge is not allowed in organic farming, so choosing organic produce is wise when possible.
4. Improve your indoor air quality — The air you breathe daily in your home is likely polluted with PAHs, flame retardants and other chemicals. Ensure your home is well-ventilated by opening windows regularly to circulate fresh air and reduce the build-up of indoor pollutants.
Vacuum and dust frequently to minimize dust, which is a significant source of triclosan, flame retardants and other chemicals. An air purifier with a HEPA filter is also a worthwhile investment to further cleanse your indoor air.
5. Consider natural progesterone for estrogen balance — If you’re concerned about the cumulative effects of xenoestrogens — estrogen-mimicking chemicals like triclosan — on your hormonal balance, consider natural progesterone. Natural progesterone works as an estrogen antagonist and helps mitigate some of the negative effects of excessive estrogen in your body.
How to Use Progesterone
Before you consider using progesterone, it is important to understand that it is not a magic bullet, and that you get the most benefit by implementing a Bioenergetic diet approach that allows you to effectively burn glucose as your primary fuel without backing up electrons in your mitochondria that reduces your energy production. My new book, “Your Guide to Cellular Health: Unlocking the Science of Longevity and Joy,” covers this process in great detail.
Once you have dialed in your diet, an effective strategy that can help counteract estrogen excess is to take transmucosal progesterone (i.e., applied to your gums, not oral or transdermal), which is a natural estrogen antagonist. Progesterone is one of only three hormones I believe many adults can benefit from. (The other two are DHEA and pregnenolone.)
I do not recommend transdermal progesterone, as your skin expresses high levels of 5-alpha reductase enzyme, which causes a significant portion of the progesterone you’re taking to be irreversibly converted primarily into allopregnanolone and cannot be converted back into progesterone.
Ideal Way to Administer Progesterone
Please note that when progesterone is used transmucosally on your gums as I advise, the FDA believes that somehow converts it into a drug and prohibits any company from advising that on its label. This is why companies promote their progesterone products as “topical.”
However, please understand that it is perfectly legal for any physician to recommend an off-label indication for a drug to their patient. In this case, progesterone is a natural hormone and not a drug and is very safe even in high doses. This is unlike synthetic progesterone called progestins that are used by drug companies, but frequently, and incorrectly, referred.
Dr. Ray Peat has done the seminal work in progesterone and probably was the world’s greatest expert on progesterone. He wrote his Ph.D. on estrogen in 1982 and spent most of his professional career documenting the need to counteract the dangers of excess estrogen with low LA diets and transmucosal progesterone supplementation.
He determined that most solvents do not dissolve progesterone well and discovered that vitamin E is the best solvent to optimally provide progesterone in your tissue. Vitamin E also protects you against damage from LA. You just need to be very careful about which vitamin E you use as most supplemental vitamin E on the market is worse than worthless and will cause you harm not benefit.
It is imperative to avoid using any synthetic vitamin E (alpha tocopherol acetate — the acetate indicates that it’s synthetic). Natural vitamin E will be labeled “d alpha tocopherol.” This is the pure D isomer, which is what your body can use.
There are also other vitamin E isomers, and you want the complete spectrum of tocopherols and tocotrienols, specifically the beta, gamma, and delta types, in the effective D isomer. As an example of an ideal vitamin E, you can look at the label on our vitamin E in our store. You can use any brand that has a similar label.
You can purchase pharmaceutical grade bioidentical progesterone as Progesterone Powder, Bioidentical Micronized Powder, 10 grams for about $40 on many online stores like Amazon. That is nearly a year’s supply, depending on the dose you choose.
However, you will need to purchase some small stainless steel measuring spoons as you will need a 1/64 tsp, which is 25 mg and a 1/32 tsp, which is 50 mg. A normal dose is typically 25 to 50 mg and is taken 30 minutes before bed, as it has an anti-cortisol function and will increase GABA levels for a good night’s sleep.
If you are a menstruating woman, you should take the progesterone during the luteal phase or the last half of your cycle, which can be determined by starting 10 days after the first day of your period and stopping the progesterone when your period starts.
If you are a male or non-menstruating woman, you can take the progesterone every day for four to six months and then cycle off for one week. The best time of day to take progesterone is 30 minutes before bed as it has an anti-cortisol function and will increase GABA levels for a good night’s sleep.
This is what I have been personally doing for over a year with very good results. I am a physician so do not have any problems doing this. If you aren’t a physician, you should consult one before using this therapy, as transmucosal progesterone therapy requires a doctor’s prescription.
Black cumin seed oil suppresses disease-causing inflammation
Reproduced from original article:
https://www.naturalhealth365.com/black-cumin-seed-oil-suppresses-disease-causing-inflammation.html
by: March 26, 2025
(NaturalHealth365) The research is in – and it demonstrates that black cumin seed oil can wield tremendous power when it comes to preventing and even reversing life-threatening diseases.
Recent studies have shown that black cumin seed oil can help re-establish the delicate balance of an aging immune system, preventing the development of inflammatory conditions such as heart disease, cancer, and arthritis.
Key point: Systemic inflammation triggers chronic disease – including cancer
Although we are conditioned to think of inflammation as harmful, this isn’t always true. Inflammation is the body’s healthy and appropriate defense against threats such as infection, trauma, and malignant cells. However, when inflammation becomes chronic and systemic, it can damage cells, cause mutations that lead to malignant cellular changes, and set the stage for disease. This excessive inflammatory process accounts for close to a quarter of all cancers.
As the body ages, the all-important balance between acute, healthy inflammation and chronic, destructive inflammation can be disturbed – resulting in too much of the “wrong” kind of inflammation and not enough of the “right” kind. Excessive inflammation destroys tissues; simultaneously, a weakened immune response, or immunosenescence, reduces the body’s ability to combat infection – truly the “worst of both worlds,” from a health standpoint.
Black cumin seed oil can reverse this dangerous scenario
Black cumin seed oil contains powerful phytochemicals that inhibit the production and activity of inflammatory factors such as prostaglandins, cytokines, and interleukins. At the same time, black cumin seed oil boosts the infection – and cancer-fighting properties of immune system cells the body needs to utilize to defend against pathogens and cancers.
Black cumin seeds, scientifically known as Nigella sativa and also called black caraway and Roman coriander, contain a phytochemical called thymoquinone. Researchers believe that thymoquinone, a potent antioxidant, is credited for much of the seed oil’s healing powers. Black cumin seeds also contain thymol, a natural antiseptic and antimicrobial.
What does the scientific research say?
In a placebo-controlled study published in Phytotherapy Research, 40 women with rheumatoid arthritis took a placebo containing starch twice a day for a month, then 500 mg of black cumin seed oil twice a day for a month. During the month they took the oil, 42.5 percent of the study participants – a significant amount – reported reduced symptoms, including decreased swelling of joints and a lessening of morning stiffness.
Thymoquinone from black cumin seed oil also shows the potential to dramatically improve osteoarthritis, the most common form of arthritis in the United States. In an animal study published in Experimental Biology and Medicine, thymoquinone reduced levels of MMP-matric metalloproteinase, an enzyme that destroys bone and joint tissue.
In one of the most striking studies published in the Egyptian Journal of Immunology, black cumin seed oil worked as well as the steroid dexamethasone in reducing the number of cytokines and inflammatory cells in lung tissue.
Black cumin seed oil fights cancer through multiple actions
Black cumin seed oil shows potential to aggressively combat cancer – functioning almost like a successful general on the battlefield, rallying and inspiring the troops. Researchers have found that it increases the activity of macrophages, which surround, engulf, and destroy abnormal cells. It also boosts the survival of CD-8 T-cells, which hunt down and kill infected or cancerous cells, while stimulating “helper” T-cells – responsible for marshaling natural killer cells and directing them to their targets.
In one study, participants who took black cumin seed oil experienced a 55 percent increase in the activity of their helper T-cells, along with a 30 percent increase in natural killer cell function.
Black cumin seed oil combats heart disease
This versatile oil could lower the risk of atherosclerosis and, with it, the risk of heart attack and stroke. In studies, black cumin seed oil lowered LDL cholesterol while raising HDL.
Black cumin seed oil may also reduce ischemia-reperfusion injury, which causes the debilitating tissue and organ damage that can occur after a heart attack or stroke.
Added benefit: Allergy and asthma relief
Since allergies and asthma stem from overreactions in the immune system, it’s unsurprising that black cumin seed oil helps alleviate both. Patients with allergic rhinitis reported a significant decrease in nasal congestion, itching, runny nose, and sneezing, while patients with asthma reported relaxation of the trachea and airways.
With its ability to create optimal inflammatory balance safely and naturally, black cumin seed oil may be a game-changer in the ongoing battle against chronic degenerative diseases.
Sources for this article include:
Gut Bacteria’s Hidden Role in Colon Cancer Risk
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/03/17/gut-bacteria-colon-cancer-risk.aspx
Analysis by Dr. Joseph Mercola March 17, 2025
STORY AT-A-GLANCE
- Rising incidence of early-onset colorectal cancer is linked to changes in the gut microbiome, with specific bacterial strains producing mutagenic chemicals that contribute to cancer risk
- Global studies are underway to identify mutational signatures associated with gut bacteria. This highlights the significant role of dysbiosis in colorectal carcinogenesis
- Understanding the influence of gut bacteria on cancer development could lead to innovative therapeutic strategies and offer new avenues for prevention and treatment
- Research has identified a subtype of E. coli producing colibactin, a mutagen associated with cancer. This suggests that early exposure increases the risk of developing cancer at a younger age
- Dysbiosis, characterized by an imbalance in gut microbiota, is linked to colorectal cancer through mechanisms like genotoxicity, inflammation and oxidative stress, with specific bacteria such as Streptococcus bovis and Fusobacterium spp. playing a central role
Early-onset colorectal cancer, defined as colorectal cancer diagnosed before the age of 45, is becoming an increasingly pressing health issue in the U.S. Characterized by symptoms such as unexplained weight loss, persistent abdominal pain and changes in bowel habits, early-onset colorectal cancer poses significant challenges for early detection and treatment.
Younger adults, who are generally considered at lower risk for colorectal cancer, are now facing a higher likelihood of developing this disease. The rise of early-onset colorectal cancer is concerning. Recent studies reveal that the number of early-onset colorectal cancer cases surged by 49% from 1990 to 2021, increasing from 6,256 cases to 9,311 cases annually.1
Additionally, the age-standardized incidence rate per 100,000 population climbed by 34% during the same period. Notably, this upward trend is more pronounced among women and individuals born after 1983, highlighting specific demographic shifts in cancer incidence.
Long-Term Consequences of Early-Onset Colorectal Cancer
The rising incidence of early-onset colorectal cancer marks a significant departure from past trends, where colorectal cancer was predominantly associated with older age groups. Beyond the immediate increase in incidence, early-onset colorectal cancer carries substantial long-term consequences.
• Long-term health challenges — Young adults diagnosed with colorectal cancer face prolonged treatment periods, long-term health complications and a significant impact on their quality of life and productivity.
• Increased strain on health care resources — The rising trend of early-onset colorectal cancer strains health care resources and emphasizes the urgent need for targeted prevention strategies. As early-onset colorectal cancer continues to escalate, it becomes imperative to explore the underlying factors driving this increase.
• Emerging risk factors linked to early-onset colorectal cancer — Changes in diet, lifestyle and gut microbiome composition are emerging as key contributors to the heightened risk of colorectal cancer in younger populations.
• Prevention through research and lifestyle interventions — Addressing these factors through comprehensive research and public health initiatives, as well as individual lifestyle changes, is essential for mitigating the future impact of early-onset colorectal cancer and ensuring better health outcomes for younger generations.
What’s the Role of Gut Bacteria in Colon Cancer?
Conventional treatments for colorectal cancer often involve surgery, chemotherapy and radiation, which have significant side effects such as fatigue, nausea and increased susceptibility to infections. These treatments do not address the root causes of the disease, often leading to recurrence or progression. It’s important to understand that most conventional cancer treatments come with drawbacks that impact the patient’s quality of life.
• Gut microbiome imbalances contribute to colorectal cancer — A significant factor driving early-onset colorectal cancer is alteration in the gut microbiome, where certain bacterial strains like Fusobacterium nucleatum and pks+ E. coli have been implicated. These bacteria produce harmful substances that damage DNA, leading to mutations.
• Diet, lifestyle and environmental factors play a role — Poor diet and sedentary behavior contribute to the disease. Environmental changes, including exposure to pollutants and chemicals, also play a role in altering gut bacteria and increasing cancer risk. These underlying causes contribute to early-onset colorectal cancer by creating an environment conducive to cancer development.
• Harmful gut bacteria contribute to DNA damage — Certain gut bacteria produce toxins that damage DNA in colon cells, leading to mutations that drive cancer progression.
• Processed foods and unhealthy fats elevate cancer risk — A diet high in processed foods, including those high in unhealthy fats like linoleic acid (LA), not only damages your mitochondrial function, reducing cellular energy, but also increases bile acid production, which certain bacteria convert into carcinogenic compounds.
This process, combined with a lack of protective fiber in the diet, leads to inflammation and further DNA damage, setting the stage for cancerous growths. Discover more about the connection between ultraprocessed foods and colon cancer in “Unveiling the Link Between Ultraprocessed Foods and Colon Cancer.”
• Early diagnosis remains a challenge — Diagnosing early-onset colorectal cancer is challenging due to its subtle early symptoms, which often mimic conditions like irritable bowel syndrome. Standard diagnostic methods, such as colonoscopy, have risks and are not guaranteed to reduce your risk of colorectal cancer death.
• Current diagnostic methods fail to detect key bacterial interactions — The complexity of the gut microbiome and its role in cancer development is not fully understood, which means that current diagnostic methods often overlook key bacterial interactions that contribute to the disease.
As research continues, there is hope for more accurate and comprehensive diagnostic approaches that consider the intricate relationship between gut bacteria and colorectal cancer.
Save This Article for Later – Get the PDF Now
New Insights Into Gut Bacteria’s Role in Early-Onset Colorectal Cancer
A commentary by Dr. David Kerr, professor of cancer medicine at the University of Oxford, explored the significant changes in diet and gut microbiome over the past few decades and their connection to the rising cases of early-onset colorectal cancer.2
• Dietary shifts have altered the gut microbiome — Kerr discussed upcoming research comparing the gut bacteria of older and younger colorectal cancer patients from around the world. Researchers hope to uncover whether early exposure to specific gut bacteria-produced mutagens, like colibactin, increases the risk of developing colorectal cancer at a younger age.
“The dominant hypothesis is that, over the past 20 to 25 years or so, there has been a change in diet that has allowed an alteration in the gut microbiome,” Kerr explained, highlighting the shift toward processed foods as a key factor. “We now harbor, in some cases, more bacteria capable of manufacturing, synthesizing, and releasing mutagenic chemicals.”
• Gut bacteria in younger and older colorectal cancer patients — An increase in harmful bacteria leads to an environment where DNA damage is more likely. “There’s a subtype of Escherichia coli, which manufactures one such mutagen called colibactin,” Kerr continued, pointing out one specific bacterial strain implicated in mutating colon cells.
• Bacterial mutagens leave identifiable genetic markers — “They have managed to, using a variety of different techniques — in vitro, observational, and so on — relate exposure to the mutagen colibactin to a particular mutational signature,” Kerr said.
This methodological approach allows scientists to trace the origins of genetic mutations directly back to bacterial activity. “The hypothesis is that, if you’re exposed to this mutagen in childhood, then it increases the tumor mutational burden,” he explains, adding that early exposure has lasting impacts on genetic stability.
• Early exposure to bacterial mutagens accelerates cancer risk — “The earlier these [mutational events] occur, the greater the tumor, the greater the normal single-cellular mutational burden, and the more likely it is to develop cancer sooner rather than later,” Kerr said. This means that mutations accumulate faster, increasing the likelihood of cancer development at a younger age, underscoring the urgency of addressing these microbial changes.
How Gut Microbiota Imbalance Influences Colorectal Cancer
A review published in the World Journal of Gastroenterology further explored how imbalances in gut bacteria, known as dysbiosis, contribute to the development of colorectal cancer. The paper focused on identifying specific bacterial species that are commonly found in individuals with colorectal cancer and exploring the ways these bacteria promote cancer growth.3
• Distinct differences in gut microbiota composition — The study examined gut microbiota from patients diagnosed with colorectal cancer, comparing it to those without the disease. Researchers discovered significant differences in the composition of gut bacteria between these two groups.
Specifically, bacteria such as Streptococcus bovis and Fusobacterium species were found in higher concentrations in cancer patients, suggesting a strong association between these microorganisms and cancer development.
• Streptococcus bovis triggers inflammation and DNA damage — The researchers identified several mechanisms through which these bacteria contribute to colorectal cancer. Streptococcus bovis, for instance, was found to adhere to both healthy and cancerous colon cells.
This attachment triggers inflammation and disrupts normal cell functions, creating an environment conducive to cancer growth. Additionally, these bacteria produce toxins that directly damage DNA, leading to mutations that drive the progression of cancer.
• Fusobacterium nucleatum weakens immune defenses — Fusobacterium nucleatum, another key bacterium identified in the study, interacts with the immune system, dampening your body’s natural defenses against tumor cells and allowing cancer cells to thrive and spread more easily. This bacterium also enhances the ability of cancer cells to move and invade other tissues, making the cancer more aggressive and difficult to treat.
• Escherichia coli strains contribute to genomic instability — Specific E. coli strains belonging to phylogroups B2 and D, are implicated in colorectal carcinogenesis. These strains produce toxins like colibactin, which interfere with the cell cycle and cause DNA damage.
This disruption leads to genomic instability, a hallmark of cancer cells. The presence of these pathogenic E. coli strains in your gut microbiome significantly increases the risk of colorectal cancer by promoting continuous cell proliferation and mutation accumulation.
Learn more about the link between E. coli and cancer development in “E. Coli Toxin Sparks Cancer Concerns Worldwide.”
Gut Dysbiosis Promotes Inflammation and Oxidative Stress
Inflammation emerged as a significant factor linking gut microbiota to cancer. Disruptions in the gut microbiome create an environment where proinflammatory bacteria thrive, triggering immune responses that fuel cancer progression.
• Dysbiosis fuels chronic inflammation — Chronic inflammation caused by an imbalance in gut bacteria allows cancer cells to thrive. The review highlighted that dysbiosis triggers the release of proinflammatory molecules, which not only promote tumor growth but also impair your body’s ability to fight off cancerous cells. This persistent inflammatory state creates a feedback loop that exacerbates cancer development.
• Oxidative stress drives cancer progression — Oxidative stress is another mechanism identified in the review. Certain gut bacteria produce reactive oxygen species (ROS) that cause oxidative damage to cells.
This damage results in mutations and cellular dysfunction, further driving the transformation of normal cells into cancerous ones. The continuous production of ROS by imbalanced gut bacteria undermines your body’s natural defenses and facilitates the progression of colorectal cancer.
• Dysbiosis supports multiple cancer-promoting pathways — The review concluded that dysbiosis plays a major role in colorectal carcinogenesis by supporting multiple pathways that lead to cancer development. By altering the composition of the gut microbiota, these bacteria influence host defenses and promote tumor growth.
• Targeting gut bacteria as a novel cancer prevention strategy — Addressing gut dysbiosis could serve as a therapeutic approach to reduce the risk or slow the progression of colorectal cancer. Understanding the relationship between gut microbiota and colorectal cancer opens new avenues for prevention and treatment.
By maintaining a balanced gut microbiome through diet, probiotics and improved mitochondrial function, you mitigate the risk of developing colorectal cancer.
Intestinal Bacteria’s Influence on Colorectal Cancer Etiology and Treatment
A separate review published in Gut Microbes investigated how specific bacteria residing in the gut elevate the risk of developing colorectal cancer. The research focused on identifying particular bacterial strains that not only contribute to the onset of colorectal cancer but also influence its progression and response to treatment.4
• Certain bacteria are more prevalent in colorectal cancer patients — The review examined individuals diagnosed with colorectal cancer, analyzing their gut bacteria compared to those without the disease.
Researchers discovered that certain bacteria, including Fusobacterium nucleatum and pks+ Escherichia coli, were significantly more prevalent in cancer patients. This suggests a strong link between these microorganisms and the development of colorectal cancer.
• Certain bacteria strains promote cancer growth — Fusobacterium nucleatum, a type of bacteria commonly found in your mouth, was shown to attach to colon cells, promoting cancer growth. Similarly, pks+ Escherichia coli produce colibactin, which damages the DNA of host cells. The review also explored how these bacteria impact cancer treatment.
• Gut bacteria influence chemotherapy effectiveness — The review highlighted that Fusobacterium nucleatum influences the effectiveness of chemotherapy by modulating the immune response. By weakening the immune system’s ability to target cancer cells, this bacterium makes treatments less effective, leading to poorer outcomes for patients.
• Potential for improved cancer risk assessment and treatment — Identifying the presence of harmful bacteria like Fusobacterium nucleatum and pks+ E. coli could allow doctors to better assess an individual’s risk of developing colorectal cancer.
By understanding how organisms influence cancer development and treatment outcomes, researchers and health care professionals can develop more targeted and effective strategies for prevention and therapy.
How to Support Healthy Gut Bacteria and Prevent Colorectal Cancer
Your gut microbiome is pivotal in protecting against the development of colorectal cancer. Maintaining a balanced microbial environment reduces inflammation and supports cellular health. Here are the most effective strategies to optimize your gut health and lower cancer risk.
1. Eliminate processed foods and vegetable oils — The modern diet is rife with processed foods and LA-rich vegetable oils that damage your gut microbiome and promote harmful bacteria. LA is a mitochondrial poison that compromises your cellular energy production, limiting your ability to maintain a healthy gut environment.
In addition to processed foods, avoid nuts and seeds as well to reduce LA intake. It’s also advisable to avoid dining out, since most restaurants use vegetable oils in their cooking, sauces and dressings.
Additionally, limit your consumption of chicken and pork, which are typically high in LA. Replace processed foods with whole, unprocessed foods and healthy fats such as grass fed butter, tallow and ghee. It’s wise to keep your LA intake below 5 grams from all sources. If you can get it below 2 grams, that’s even better. To help track your LA intake, enter all your daily meals into an online nutrition tracker.
2. Optimize carbohydrate intake — The other part of the equation is carefully modulating your carbohydrate intake. Carbohydrates play a role in supporting mitochondrial function since glucose is the preferred fuel for energy production at the cellular level. Tailor your carbohydrate consumption to support a healthy microbiome by aiming for about 250 grams of targeted carbohydrates daily for most adults.
Individuals with higher activity levels may require more. Introduce carbohydrates gradually to allow your gut to adapt, thereby minimizing digestive issues and endotoxin levels. Begin with white rice and whole fruits to nourish beneficial bacteria before considering vegetables, whole grains and starches. Avoiding high-fiber diets initially is important if your gut microbiome is compromised, as excessive fiber will increase endotoxin levels.
If your gut health is severely compromised, focus on easily digestible carbohydrates like dextrose water for the first week or two. Sip it slowly throughout the day to support gradual gut healing.
3. Reduce exposure to environmental toxins — Exposure to synthetic endocrine-disrupting chemicals (EDCs), estrogen and pervasive electromagnetic fields (EMFs) further impair your cells’ ability to generate energy efficiently. This energy deficit makes it challenging to sustain the oxygen-free gut environment necessary for beneficial bacteria like Akkermansia to flourish.
Further, a lack of cellular energy creates an environment in your gut that favors endotoxin-producing bacteria, damaging mitochondria and creating a vicious cycle of worsening health. By tackling excess LA, estrogens (xenoestrogens found in everyday items like plastic), EDCs and EMFs, you restore your cellular energy and start down the path toward optimal health.
4. Minimize antibiotic exposure and consider Akkermansia — Antibiotics devastate beneficial gut bacteria and significantly increase the risk of colon cancer. Use antibiotics only when absolutely necessary and focus on rebuilding gut flora through targeted dietary choices, including fermented foods, afterward.
Additionally, avoid conventionally raised meats that typically contain antibiotic residues by choosing high-quality, responsibly sourced proteins to support a healthy microbiome.
Meanwhile, Akkermansia is essential for a healthy microbiome, but many people have few to none at all. However, it’s important to eliminate all vegetable oils from your diet for at least six months before starting an Akkermansia supplementation program.
This preparatory period allows your body to recover mitochondrial function and create a more hospitable environment in your colon for the beneficial bacteria. By taking these steps, you maximize the benefits of Akkermansia supplementation and support overall gut health.
When selecting Akkermansia supplements, choose those that utilize advanced, timed-release capsules or microencapsulation technology. These methods keep the bacteria dormant and protected until they reach your colon, typically within two to four hours after ingestion, ensuring that a higher number of live bacteria survive the journey through your digestive system.
Frequently Asked Questions (FAQs) About Gut Health and Colon Cancer
Q: Why are more young adults getting colorectal cancer?
A: Poor diet, processed foods, gut microbiome imbalances, and environmental toxins are major factors driving the rise.
Q: What are the early warning signs of colorectal cancer?
A: Unexplained weight loss, persistent abdominal pain and changes in bowel habits are key symptoms to watch for.
Q: How does gut bacteria affect colon cancer risk?
A: Harmful bacteria like Fusobacterium nucleatum and pks+ E. coli produce toxins that damage DNA, increasing cancer risk.
Q: How do processed foods increase cancer risk?
A: They fuel harmful gut bacteria, trigger inflammation, damage mitochondria and create conditions for cancer to grow.
Q: What steps can I take to protect my gut and lower cancer risk?
A: Remove vegetable oils from your diet, reduce toxin exposure, balance your carb intake, limit antibiotic use and introduce Akkermansia after improving diet for six months.
How a mammogram actually causes breast cancer
Reproduced from original article:
https://www.naturalhealth365.com/how-mammogram-actually-causes-breast-cancer.html
by: March 5, 2025
(NaturalHealth365) An X-ray picture of the breast, called a mammogram, is heavily promoted as the ‘primary way to screen’ for breast cancer, according to Western medicine. Conventionally speaking, an annual detection screening is recommended as early as age 40 by both the American Cancer Society and the National Comprehensive Cancer Network, while the United States Preventive Services Task Force recommends screenings every other year starting at age 50.
While mammogram guidelines differ amongst organizations, they all agree there are concerns about the test. Yet, disputes exist amongst experts when it comes to mammography detecting invasive breast cancer. So, the question remains: do the benefits outweigh the risks?
In reality, more and more studies are showing that a mammogram breast screening has some major flaws – which put women at serious health risk and actually increase the risk of cancer.
Strange logic: Zero-stage cancer detected but treated aggressively
Ductal carcinoma in situ (DCIS) refers to the abnormal growth of cells forming a lesion between 1 and 1.5 centimeters in diameter. While this is not cancer, approximately 25 percent (60,000 cases) of all newly diagnosed breast cancer falls within this category each year.
Because evidence indicates that less than half of DCIS cases progress to invasive cancer, some experts declare it should be reclassified as a non-cancerous condition. Additionally, they recommend a “watchful eye” for women who have this condition rather than invasive therapy. After all, why treat someone who doesn’t have cancer with chemotherapy or radiation – which places their immune systems at risk for a lifetime?
However, mammography proponents claim they’re saving lives through early detection and treatment of DCIS. They view it as pre-cancerous or “stage zero cancer” and believe it could eventually cause harm if left untreated. Therefore, they recommend treating it in the same manner as invasive cancer with aggressive treatments. But is this right or fair?
According to Time Magazine, “Cancer has a language problem … A 57-year old woman with low-grade DCIS that will almost certainly never become invasive hears the same word as the 34-year old woman who has metastatic malignancies that will kill her. That’s confusing to patients conditioned to treat every cancer diagnosis as an emergency in a world that still reacts to cancer as though it’s the beginning of the end.”
The latest round of controversy was set off about DCIS treatment after a study was published by JAMA Oncology. After a 20-year analysis of 100,000 women who were diagnosed with DCIS, the mortality rate from breast cancer of these patients was the same as the general population at 3.3 percent.
Radiation from mammogram screening is a breast cancer risk
While several organizations like the Susan G. Komen for the Cure heavily promote mammograms for early screening for breast cancer, it’s ironic that mammogram machines put each woman at risk for the very thing they want to prevent. The ionizing radiation used to detect breast tumors is a risk factor for breast cancer development. Additionally, the crushing compression of this test on the breast tissue may potentially spread cancer if the cancer cells are present.
After several studies, Cornell University determined people who are exposed to ionizing radiation emitted from machines like the mammogram machine place themselves at risk for breast cancer. They also stated, “… female breast tissue is highly susceptible to radiation effects” as it “is one of the most sensitive tissues to the carcinogenic action of ionizing radiation.” They also revealed that it takes a minimum of five to 10 years for radiation-induced breast cancer to develop.
Finally, they concluded that greater levels of radiation exposure lead to a greater risk of breast cancer. Every time a woman is exposed to this form of radiation, she is placing herself at higher risk – especially if the screening is done when there is estrogen stimulation and tissue proliferation that occurs during monthly menstrual cycles.
Prevention of breast cancer is better than detection
While early detection of breast cancer can be done by mammogram screening, it is not the same as “prevention.” Lifestyle choices will help you prevent cancer or any chronic illness. Be sure to eat real whole and organic foods, drink plenty of fresh (clean) water, exercise regularly, get plenty of rest, and manage stress levels.
Sources for this article include:
NIH.gov
CDC.gov
Nccn.org
Time.com
Research links excessive oxalates to breast cancer
Reproduced from original article:
https://www.naturalhealth365.com/research-links-excessive-oxalates-to-breast-cancer.html
by: February 19, 2025
(NaturalHealth365) Information about little-known compounds called oxalates can be confusing and conflicting. They are often equated with the “bad” substances in foods, but, in reality, oxalates are neither good nor bad. They can become problematic, however, when too many of them accumulate in the body.
When there are too many oxalates – they can overwhelm the kidneys and lead to kidney stones and immune deficiency. Furthermore, research indicates that high levels of oxalate in the mammary area have been linked to breast cancer tumor growth as well.
The body itself forms most oxalates
Oxalates (COOH), or oxalic acid, are strongly acidic substances that help plants and animals metabolize. The body’s functions form about 60% to 80% of oxalates. The other 20 to 40% of oxalates come from food.
Most fruits and vegetables contain a small amount of oxalic acid, and they are found in the leaves of plants as opposed to the roots, stalks, and stems. The following foods contain a high amount of oxalates overall:
- Rhubarb
- Chocolate
- Spinach
- Beet greens
- Swiss chard
- Some nuts, especially almonds, cashews, and peanuts
- Some berries, especially gooseberries
- Lemon and lime peel
- Some grains and pasta (except brown rice)
- Some legumes, especially navy beans, black beans, and soybeans
- Okra
- Parsley
How are oxalates linked to breast cancer?
Oxalates are oxidizing substances. As such, they are extremely volatile and can damage tissue in large amounts. Oxalate crystals cause the formation of kidney stones, which can block the flow of urine and lead to kidney infection and bladder cancer.
These crystals are also razor sharp and can cause direct damage and long-lasting inflammation to whatever internal tissues they come into contact with. Oxalate-iron crystals can lead to iron depletion. When calcium-oxalate crystals form, they can lodge in internal organs and bone. As they grow, they crowd out bone marrow, leading to immune deficiency and anemia.
Excess oxalates also can chelate heavy metals. However, oxalates trap metals like mercury and lead in tissues, unlike other chelators. Excess oxalate has been linked to fibromyalgia, vulvodynia (vulvar pain), digestive disorders, and autism.
The most startling new connection between excess oxalates and disease has to do with breast cancer, however. A study conducted by the National University of Cordova in Argentina compared the oxalate levels of breast cancer tumor tissue and regular breast tissue. They found that “all tested breast tumor tissues contain a higher concentration of oxalates than their counterpart non-pathological breast tissue.”
The researchers also discovered that oxalic acid caused tumor proliferation and stimulated the expression of pro-tumor genes. Surprisingly, proliferation did not happen when oxalate was injected into the backs of laboratory mice. This indicates that high oxalate levels do not induce cancer tumor growth in all types of tissue.
Three ways to reduce your oxalate levels
Obtain calcium from natural foods, not calcium supplements.
Calcium has an interesting relationship with oxalates. Approximately 5-15% of the world population will develop some form of kidney stone. Of those, 80% will be calcium-oxalate stones. When calcium is combined with foods that are high in oxalates within the intestines, the two together form an oxalate-calcium crystal that the body cannot absorb.
When this happens, a “stone” is formed that will make its way to the kidneys to eventually be eliminated in the urine. The presence of oxalate-calcium crystals, which can block urine flow and cause kidney infection, can also lead to a higher risk of renal, pelvis, and bladder cancers. These same kinds of crystals can also form in the lungs, nerves, brain, bones, blood vessels, and joints.
Does this mean you should limit calcium intake if you are prone to kidney stones? Not necessarily. Research conducted on vegetarians found that they did not have higher-than-normal rates of calcium deficiency or osteoporosis caused by oxalate interference.
In fact, according to a study published in the European Journal of Epidemiology, vegetarians had a lower rate of kidney stones than meat eaters did. Those who consumed calcium supplements regularly, however, have shown time and again to have higher rates of kidney stones. Calcium supplementation has also been linked to both prostate and breast cancer. Stick to natural and preferably vegetable and fruit-based calcium sources to avoid kidney stones and cancer.
Be aware of your protein intake.
Be cautious about protein, especially if it is derived from meat and dairy. Oxalates are produced from amino acids in the liver.
Amino acids are the building blocks on which proteins are made so some researchers make the connection between total protein amounts and total oxalates formed. For meat-eating women, the general recommendation is around 5 ounces a day. This is equivalent to a small hamburger patty or four eggs. The USDA states that, on average, Americans eat 30% more meat protein than the recommended allowance.
Maintain good intestinal flora.
According to research, some individuals have a physiology prone to higher levels of oxalate uptake in the digestive tract (thus, a higher risk of kidney stones). Although there is evidence to suggest that hereditary disposition plays a role for some people, there is also a strong link between kidney stone formation and disorders of the digestive system, such as inflammatory bowel disease, leaky gut, and Crohn’s.
Could oxalate hyper-absorption have more to do with extreme gut flora imbalance than genetics? The jury is still out on that one. What is known, however, is that it is the job of specific flora, in particular, certain species of Oxalobacter formigenes, Lactobacillus, and Bifidobacteria, to process oxalic acid and prepare it for absorption. Currently, there are several studies underway which focus on the role of oral probiotics in this process.
Let food work for you to keep oxalate levels in balance
Remember that problems only emerge when there is an excess of oxalates in the system. The standard American diet contributes to oxalate overload, but you can also keep it in check by being proactive with prevention. Eating antioxidant-rich food, consuming citrate-rich lemon and lime juice (which experts say can help prevent calcium-oxalate kidney stones), staying hydrated, and watching your salt intake are other ways to keep kidney stones in check.
Also, don’t let the fear of kidney stones prevent you from getting adequate amounts of vitamin C and D. One of the ways that oxalates are formed is through conversion from vitamin C. However, studies thus far have been inclusive as to whether high vitamin C intake actually leads to increased oxalate production.
In regards to vitamin D, deficiency of this vital substance has reached pandemic proportions in the developed world, including among those who have experienced kidney stones. Be sure to get your levels checked the next time you get blood work done. Maintaining a healthy balance of all substances in the body, including oxalates, is the only way to achieve and experience true health naturally.
Sources for this article include:
NIH.gov
NIH.gov
Oxfordjournals.org
MDPI.com
NIH.gov
NIH.gov
NIH.gov
Sciencedaily.com
Scientificamerican.com
Nutrition.org
Natural Molecules With Anti-Cancer Properties Could Help In These Times Of Turbo Cancers
Reproduced from original article:
https://anamihalceamdphd.substack.com/p/natural-molecules-with-anti-cancer
By: Ana Maria Mihalcea, MD, PhD Feb 25, 2025
We live in a time of turbo cancers and a world that is ever increasing its toxicity and danger for human beings. Both prevention and support for cancer patients is important. Many have been discussing the beneficial effects of Ivermectin and Fenbendazole, but there are so many more molecules available that can additionally support cancer patients and all of those who never want to get cancer.
The Magic of Ivermectin in Oncology
A Drug Made for Animals and Taken by Humans to Treat Cancer: Fenbendazole
Mebendazole: A Cancer Fighting Drug We Find at the Supermarket
I wanted to write about some resources that I have been working with for many years. Sometime in 2019, I met Daniel Stanciu, PhD who at that time was writing the internationally known Cancertreatmentsresearch. He was a physicist who’s life changed dramatically when his former wife developed cancer. He researched almost every natural cancer treatment and repurpose drug that was scientifically available in the world. We used to have many conversations as I have been supporting cancer patients in my integrative clinic and we would discuss novel approaches. You can see our interview from 3 years ago here:
Bringing Light To Novel Cancer Treatment Approaches
Here are some of the many possibilities.
Please read here of 10 cases of advanced cancer cases that achieved complete remission:
10 Cases of Complete Remission from Advanced Cancers after using Supplements or Repurposed Drugs
HCA Garcinia Cambodia combined with Alpha Lipoic Acid
The fruit of G. cambogia contains xanthones, which inhibit preneoplastic lesions in Breast and colon cancer, and induced cancer cell death in mouth, leukemia, breast, gastric, and lung cancer cell lines. Garcinol, inhibited cell proliferation and induced cancer cell death in leukemia, breast, colon, prostate, and pancreatic cancer. Combined therapy with Alpha lipoic acid and HCA has been proposed as an antineoplastic regimen that shifts the metabolism of cancer cells from aerobic glycolysis (the Warburg effect) to respiration. Combined lipoic acid and HCA were evaluated in cancer models with lung carcinoma, melanoma, and bladder carcinoma. Several case series and a case report describe the treatment of patients with advanced metastatic cancer with a combination regimen of alpha lipoic acid and oral HCA.
Curcumin
Curcumin (CUR) is a yellow polyphenolic compound derived from the turmeric plant. It is widely used to treat many types of diseases, including cancers such as those of lung, cervices, prostate, breast, bone and liver. High doses of curcumin of 7 grams per day have induced clinical remission in multiple myeloma and reduction of tumor burden in many other cancers.
The Role of Curcumin in Cancer Treatment
Curcumin acts on the regulation of various immune modulators, including cytokines, cyclooxygenase-2 (COX-2), and reactive oxygen species (ROS), which partly explains its anticancer effects. It also takes part in the downregulation of growth factors, protein kinases, oncogenic molecules and various signaling pathways, such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), c-Jun N-terminal kinase (JNK) and signal transducer and activator of transcription 3 (STAT3) signaling.
Quercetin: even more anti-cancer potential than Curcumin?
EGCG
Green tea extracts EGCG a direct anti-tumor effect in several tumor types including chronic lymphocytic leukemia (CLL). Case reports indicate complete remission of CLL with high dose EGCG. EGCG has successfully reduced tumor growth in bladder, colon cancer and been shown to have considerable anti-cancer effects in many other cancer types.
EGCG complete remission Chronic lymphocytic leukemia
Thymoquinone
Thymoquinone which is contained in Black Cumin Seed Oil has been shown to modulate nine out of the ten hallmarks of cancer. Many studies have shown the effects of Nigella sativa on various cancer cells, and the list is long offering up over 57 reviewed papers on the subject finding black cumin to be effective against cancers such as blood, breast, colon, pancreatic, lung, leukemia, skin, fibrosarcoma, renal, prostate, and cervical cancer. It has profound anti-inflammatory effects.
Thymoquinone in the clinical treatment of cancer: Fact or fiction?
Thymoquinone: A Promising Therapeutic Agent for the Treatment of Colorectal Cancer
Citrus Bergamont
Citrus Bergamont (CR) inhibits via the malevolate pathway of cholesterol and fatty acid synthesis that cancers use to grow. The uptake of fatty acids not only by the tumor cells but also the connective tissue cells necessary for building new cancer cells can affect continued tumor progression. CR inhibits this uptake and has been shown to inhibit tumor cell growth in colon cancer. It also inhibits cancer stem cells, and important mechanism that prevents metastatic disease. Statin drugs have been able to inhibit cancer cell growth but have significant side effects. CR exhibits similar benefits of statin drugs without side effects.
Anti Cholesterol Strategy to Fight Cancer
Grape Seed Extract
The key reason Grape Seed Extract is used as a food supplement is its high content of Oligomeric Proanthocyanidins (OPC), powerful substances found in the bark of trees, fruit skins, seeds, and leaves. Natural sources of OPCs include grape seeds and skins, blueberries, cranberries, and coffee. Proanthocyanidins are developed by plants as a defense against biotic and abiotic stressors, protecting them from pathogens and predators. The potential benefits of Proanthocyanidins are extensively studied, covering cardiovascular health, inflammation, skin health, immunity, brain health, gastrointestinal health, metabolic syndrome, microbial infections, and oncology.
These benefits are likely related to their impact on the microbiome, increasing diversity and improving the balance of gut microbes (2).
While there are various areas where OPCs can help, those that stand out the most are:
1. Microbial infections
Pathogen Adhesion: Proanthocyanidins may represent a good support to help the body maintain a healthy response to the adhesion of pathogens to the mucosal surfaces, such as the urinary tract epithelium;
Biofilm Formation: microbes regulate through biofilm formation for survival from host defense, which is often found difficult in its eradication with simple anti-microbial agents. Research indicates Proanthocyanidins may represent a good support for the human body when it comes to adherence, motility and biofilm formation of major microbial infections including Candida albicans
Viruses: Proanthocyanidins maintain a healthy response to external agents (7).
2. Oncology support
Unhealthy Stem Cells: Proanthocyanidins may help reverse EMT through Suppression of TGF- β Signaling Pathway
Angiogenesis: Grape seed proanthocyanidins inhibit MMP-2 and MMP-9 secretion, VEGF and angiopoietin 1 signaling, to inhibit angiogenesis
Hypoxia-Inducible Factors: Proanthocyanidins suppress HIF-1α-dependent pathway
3. Inflammation and pain
Gut Microbiota: Proanthocyanidins may contribute to maintaining healthy gut microbiota, which is essential for a well-functioning immune system.
Neuropathic Pain: Proanthocyanidins have been shown to help suppress matrix metalloproteinase-9/2 (11), inflammasomes in macrophages (12), and inhibiting the activity of pyramidal cells in the insular cortex
C-Reactive Protein (CRP) – marker of inflammation was lowered.
NF-κB Signaling Pathway: Inactivating the NF-κB signaling, and downregulating pro-inflammatory cytokines and mediators such as TNF-α, IL-6, and COX-2
Chrysin
Chrysin is a flavonoid present in various natural sources such as honey, propolis, and certain plant species, exhibiting varying concentrations across different sources. For example, honeydew honey contains approximately 0.10mg/kg of Chrysin, while forest honeys boast a higher concentration of around. Chrysin has gained considerable attention during the recent years due to its outstanding potential to add value to life in multiple key areas of health, including
1. Brain health
Chrysin has been identified as a potential MAO (Monoamine Oxidase) inhibitor and GABA mimetic. MAO is one of the few enzymes involved in the process of dopamine metabolization. As such, Chrysin may offer significant support in a variety of brain related health challenges, such as Alzheimer’s disease, Parkinson’s disease, depression, anxiety, brain tumors, epilepsy, multiple sclerosis, traumatic brain injury, spinal cord injury, and ischemic stroke.
2. Oncology support
Chrysin demonstrates not only modulation of MAO-B but also stronger inhibition of MAO-A, which has implications in oncology (4). Recent research from UCLA suggests that substances blocking MAO-A can enhance the activity of T-cells in the immune system and inhibit tumor-associated macrophages, potentially aiding in immune response against tumors. Multiple scientific studies have suggested that Chrysin has an important potential to suppress the enzyme aromatase (CYP19) relevant when it comes to unhealthy breast cells, since aromatase is the enzyme responsible for the conversion of testosterone into estrogen.
3. Other benefits
Testosterone support: Due to its aromatase inhibition potential, Chrysin is also expected to represent good support for a healthy testosterone level.
Liver and Kidney support: Chrysin, has been also suggested to represent a relevant liver and kidney support in the presence of natural or chemical toxins
Chrysin a promising anticancer agent: recent perspectives
Modified Citrus Pectin
Modified Citrus Pectin is a soluble fiber derived from citrus peels, processed to enhance its absorption and availability to the body’s cells. In its natural form, pectin is a large molecule that is not absorbed by the human digestive tract. Modified citrus pectin is a pectin form that undergoes enzymatic processing to reduce its molecular weight and size. These are smaller particles, called modified citrus pectin, are more easily absorbed through the intestinal lining into the bloodstream. Once it has entered the circulation, Modified Citrus Pectin binds to and blocks galectin-3, a protein that fuels inflammation, hardens tissues and organs—including the arteries—and can give rise to a number of serious health impacts throughout the body.Galectin-3 is also involved with several cellular activities, which include apoptosis, cell migration, proliferation, angiogenesis and epithelial–mesenchymal transition (EMT) and it is therefore known to play a key role in the spread and metastasis process. In unhealthy cells, Galectin-3 over-expressing cells show an increased migration, whereas down-regulation ofgalectin-3 expression results in decreased migratory and invasive characteristics of unhealthy cells. Therefore, Modified Citrus Pectin, as a galectin-3 inhibitor, is expected to support the body in the fight against the spread of unhealthy cells.
Modified Citrus Pectin also possesses chelating properties, enabling it to bind with heavy metals and toxins in the body and facilitate their excretion. This enhances the body’s detoxification abilities.
I have written about the properties of Galectin induced turbo cancers from Lipid nanoparticles and their inhibition by Curcumen, Berberine and Citrus Pectin here:
Glycolysis Inhibitors
Drugs and Supplements that Block Fermentation and Help Fight Cancer
Glucose Absorption Inhibitors to Inhibit Tumor Growth
Glycolysis, the process of breaking down glucose for energy, is essential for cellular function. It is a fundamental metabolic pathway that occurs in the cytoplasm of cells, where glucose (a six-carbon sugar) is broken down into two molecules of pyruvate. This process generates energy in the form of ATP (adenosine triphosphate) and NADH. Glycolysis consists of ten enzymatic steps and is the first stage of both aerobic and anaerobic respiration. Unhealthy cells, have Glycolysis upregulated
(“Warburg effect”) insuring energy production as part of the Fermentation process, in the absence of oxygen (anaerobic process).
Downregulating glycolysis can:
Promote metabolic flexibility, encouraging the body to use other energy pathways, such as fat oxidation. Indeed, it has been suggested that Glycolysis inhibitors can support Ketogenic Diet. Reduce lactate buildup, helping to maintain better cellular function and reduce fatigue as well as supporting the normal function of the immune system. Support overall cellular health, especially in cases of metabolic stress.
Glycolysis Inhibithree
Targeting 3 Key Steps in Glycolysis
PHLORIZIN – derived from the bark of apple trees, natural compound studied for its role in glucose transport.
TANSHINONE IIA – found in the Chinese traditional herb Danshen (Salvia miltiorrhiza), a natural compound studied in relation to HK2 (Hexokinase II).
Shikonin – a natural naphthoquinone compound from the root of Zi Cao (Lithospermum erythrorhizon), a traditional Chinese herb, studied for its role in cellular processes like Pyruvate Kinase M2(PKM2) activity.
AHCC®
Is one of World’s leading immune health supplements.
AHCC® contains an unique Shiitake-Mycelia extract discovered by Japanese scientists in 1989. Today, its potential is supported by over 30 scientific studies, including clinical studies in humans. AHCC® is extracted from Shiitake mushrooms. However, what makes AHCC® different compared to other Shiitake extracts is that it is grown in fermenters. During this process, mushroom enzymes modify the natural polysaccharides to generate active compounds called partially acetylated alpha-glucans. These partially acetylated alpha-glucans are responsible for and contribute to the superior absorption and strong clinical efficacy of AHCC®. Indeed, AHCC® outstanding results have been observed in relation to mechanisms & health challenges such as: Natural Killer and T- cell number and activity, Human Papillomavirus infections. Various Bacterial, Fungal and Viral infections
Genistein
Genistein is a naturally occurring isoflavone found in plants like soy and Sophora japonica, known for its antioxidant and anti-inflammatory properties. It plays a significant role in supporting women’s health, particularly in hormonal balance and bone strength, helping to reduce post menopausal side effects. Additionally, Genistein is being studied for its potential role in oncology, where its influence on cellular pathways and estrogen receptors may offer protective benefits in cancer management. Its dual action makes it valuable for both general well-being and specific therapeutic areas.
Genistein is a potent isoflavone that exerts significant effects on various intracellular mechanisms. It is known to modulate cell signaling pathways, such as the PI3K/Akt and MAPK pathways, which are crucial for cell survival, growth, and differentiation. Genistein also influences apoptosis (programmed cell death) by regulating Bcl-2 proteins and promoting the activation of caspases. Additionally, it affects estrogen receptors and can inhibit the activity of enzymes like tyrosine kinases, as well as topoisomerase II reducing excessive cell proliferation. These mechanisms make Genistein of interest for both hormonal balance and potential anticancer therapies.
Genistein as a Potential Tool to Fight Metastasis & More
Boswellia AKBA
Historically, Boswellia has been valued not only in the context of cultural rituals for its soothing properties and fragrant aroma , but also for its medicinal properties, traditionally used in Ayurvedic medicine for its anti-inflammatory properties. The active compounds, Boswellic acids, are known to help support joint health, reduce inflammation, and have been studied for their potential benefits related to health conditions like arthritis and inflammatory bowel disease. Scientific studies have identified Boswellic Acids, particularly AKBA (Acetyl-11-keto-beta-boswellic acid), as key compounds responsible for its health benefits.
Anti-cancer properties of boswellic acids: mechanism of action as anti-cancerous agent
The mechanisms of activity of BAs comprise a variety of targets, including the enzymes of angiogenesis and others such as topoisomerases, 5-lipoxygenase (5-LO), cytochrome P450, and mitogen-activated protein kinase (MAPK, especially p38) which are either promoted or inhibited by BAs
Apigenin
Apigenin can induce apoptotic cancer cell death via increasing ROS generation in cancer cells, the downregulation of anti-apoptotic factors Bcl-2 and Bcl-xl as well as the up-regulation of apoptotic factors Bax and Bim.
Apigenin can induce cell cycle arrest at the G2/M and S phases.
In suppressing metastasis of cancer cells, apigenin administration interferes with the PI3K/Akt/mTOR signaling pathway as well as suppresses the expression of MMP-9, a factor involved in the progression and invasion of cancer cells.
Most studies indicate activity in Breast Cancer, Lung Cancer, Colon Cancer, Skin Cancer, Pancreatic Cancer, Cervical Cancer, Prostate Cancer. Diminished the incidence of UV light-induced cancers.
Apiginin is a great Nootropic which improves cognitive function and is neuroprotective. It also promotes relaxation with slight sedative effect, supports sleep and ameliorates Post-Stroke Cognitive Deficits.
Glutamine Inhibition
Most Cancer Types are dependent on Glutamine. Glutamine metabolism is upregulated in many forms of cancer as it is required for Nucleotides, Glutathione, ATP and Lipid production. Prostate tumors, Brain tumors, Triple Negative Breast tumors, Leukemia are known to be most dependent on Glutamine Mutations in the genes IDH1 and IDH2, which also change how glutamine products are used in a cell, are common in certain types of brain cancer and leukemia.
Glutamine Inhibition increases the effectiveness of Metformin and 2DG against tumors cells. BRAF inhibition causes a shift of cancer cells to glutamine for resistance & survival. GLS inhibition restores sensitivity to the EGFR inhibitor erlotinib in cells that have developed resistance.
Glutamine Inhibifour
Glutamine Inhibifour is the first food supplement designed with the GLUTAMINOLYISIS pathway in mind.
Targeting glutamine metabolism as a therapeutic strategy for cancer
Omega-3 Fatty Acids, Budwig Diet & their Antitumor Activity
Baicalein
Potential to modulate PI3K/AKT/mTOR, Wnt/β-catenin, MAPK, NF-κB, Notch, ROS, and Shh signaling. Anti-migration and anti-invasion potential. Anti-angiogenesis potential due to inhibition of 12-Lipoxygenase. Outstanding Iron chelator and anti-Fenton property. Inhibits TLR4 and the downstream HIF‐1α and VEGF expressions
Breast Cancer, Lung Cancer, Ovarian Cancer, Colo Rectal Cancer
There are many more possibilities, and you can find out more on the cancertreatmentsresearch.com site.
___________________________________________________________________________
Daniel proceeded to create MCS formulas and design supplements that help cancer patients, while omitting any fillers, toxic nanoparticles. 50% of the proceeds continue to go to research natural cancer solutions. His supplements have been of such tremendous quality that they are used in clinical trials by very esteemed cancer institutions around the world. I have been listed on his site as an integrative Oncology consultant for many years and my book Light Medicine – A New Paradigm – The Science of Light, Spirit and Longevity due to its case reports of using integrative approaches to support cancer patients effectively. I use the MCS formula supplements in my clinic while treating patients with many different natural intravenous molecules in collaboration with their Oncologist. He has branched into antiaging and longevity which is my specialty. Now that we have the good news that Robert F Kennedy Jr has been confirmed, and we have so much needed shake up with our current administration, we are looking into a much more hopeful future in which doctors who use natural cancer treatments supportively may not be hunted by the governmental agencies and specialty boards. There are a lot of possibilities for help. Many pharmaceutical repurpose drugs can be replaced with natural supplements that have equivalent effect. For example instead of Metformin use Berberine, instead of a Statin, which is a mitochondrial toxin, use Citrus Bergamot. In my clinic I use many of these molecules intravenously as well for shedding related chronic illness with remarkable results, like Resveratrol, Quercetin, Curcumin, Artemesinin, EGCG etc. Any cancer patient can use Glycolysis and Glutamate inhibition.
Ozempic Linked to 19 Adverse Health Events
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/02/22/ozempic-linked-to-19-adverse-health-events.aspx
Analysis by Dr. Joseph Mercola February 22, 2025
STORY AT-A-GLANCE
- GLP-1 receptor agonists like Ozempic and Wegovy, originally intended as diabetes medications, have gained popularity for weight loss, leading to global shortages despite having modest benefits
- Research shows these drugs reduce seizures and substance addiction risks, but they increase the likelihood of 19 other health conditions, including fainting, kidney problems and pancreatic issues
- Common side effects include nausea, diarrhea, vomiting and abdominal pain, with potential risks of acute pancreatitis and thyroid cancer, making the trade-off dangerous for users
- Ozempic’s manufacturer Novo Nordisk reported $40.6 billion in revenue, highlighting how the “magic pill” mentality and ultraprocessed food consumption create a profitable cycle for pharmaceutical companies and food manufacturers
- Instead of relying on weight loss drugs, focus on optimizing cellular energy production through dietary changes, avoiding vegetable oils and supporting your gut and mitochondrial health
By now, most people around the world have heard of Ozempic and Wegovy, which are GLP-1 receptor agonists. These drugs, originally made for treating Type 2 diabetes, cause rapid weight loss, thus attracting individuals who have been struggling to lose weight for a long time. In fact, the effectiveness of these drugs has led to a global shortage.1 However, as with many other drugs that promise immediate results, there’s a catch.
Ozempic Hailed as a ‘Miracle Drug,’ but the Downsides Are Sinister
A report from The Epoch Times2 covered a study published in Nature Medicine,3 showing the impact of certain GLP-1 receptor agonists, sold under brand names such as Ozempic and Wegovy. As noted by The Epoch Times, “The media, patients, and even some doctors have dubbed the medications ‘miracle drugs’ because of their profound weight-loss effects.”4
In addition to weight loss, the study also noted that these drugs also lower the risk of “seizures and addiction to substances such as alcohol, cannabis, stimulants and opioids.”5 It’s believed that these drugs affect the brain’s neurological pathways related to reward and impulse control, explaining how these changes in behavior occur.6
Despite these benefits, the researchers caution potential, as there’s a dark side to these drugs that mainstream media and Big Pharma do not want you to see. According to the report, Ozempic increases your risk of developing a slew of other serious health conditions:7
“Researchers warn that these benefits come with an increased risk of 19 health conditions, such as syncope (fainting), arthritic disorders, and kidney and pancreatic problems.”
Similarly, a 2022 study found that commonly reported problems include nausea, diarrhea, vomiting and abdominal pain. An increased risk for acute pancreatitis and thyroid cancer was also noted.8 Meanwhile, Nature Medicine claims the benefits are “modest” at best:9
“While GLP-1RA drugs display effectiveness against a wide array of health problems, the magnitude of associated benefits is modest — about a 10% to 20% reduction for most outcomes.”
A Closer Look at the Research
The Nature Medicine study analyzed 215,970 diabetics using GLP-1 receptor agonists and compared them to multiple control groups: 159,465 taking sulfonylureas, 117,989 using DPP-4 inhibitors, and 258,614 on SGLT2 inhibitors. An additional control group of 536,068 used all three medications, while a separate baseline group of 1,203,097 received only standard care.10
They then produced a master list of health outcomes related to GLP-1 agonist receptor usage. As noted by The Epoch Times, while these drugs produced benefits, there were also significant adverse health outcomes:11
“Compared to usual care, GLP-1RA use was associated with a reduced risk of substance use and psychotic disorders, seizures, neurocognitive disorders (including Alzheimer’s disease and dementia), coagulation disorders, cardiometabolic disorders, infectious illnesses and several respiratory conditions.
There was an increased risk of gastrointestinal disorders, hypotension, syncope, arthritic disorders, nephrolithiasis, interstitial nephritis and drug-induced pancreatitis associated with GLP-1RA use compared to usual care. The results provide insights into the benefits and risks of GLP-1RAs and may be useful for informing clinical care and guiding research agendas.”
In a report by GoodRx, Stacia Woodcock, PharmD., outlines the mechanisms that lead to weight loss and other supposed benefits related to taking these drugs:12
• They signal your pancreas to release more insulin — After a meal, your blood glucose levels go up. Usually, the pancreas releases insulin when this happens to lower blood glucose levels. But in Type 2 diabetics, the body doesn’t always release enough. Incretin mimetics work on the pancreas to help raise insulin levels after you eat, which then lowers your blood glucose level.
• They increase your body’s sensitivity to insulin — Your body may also not respond as well to insulin if you’re diabetic. Incretin mimetics help increase insulin sensitivity, so your body can respond better to insulin when it’s released.
• They tell your liver to stop making glucose — This helps stop the production of new glucose to keep blood levels down.
Save This Article for Later – Get the PDF Now
The Cycle of Ultraprocessed Food and Ozempic Wrecks Public Health
As the weight-loss effects of GLP-1 receptor agonists gained widespread attention, Big Pharma’s profits in this market skyrocketed. According to The New York Times, Novo Nordisk, the maker of Ozempic and Wegovy, reported $40.6 billion in revenue in 2024; this figure is expected to jump by 16% to 24% in 2025.13
In the Tucker Carlson Show interview featured above, Dr. Casey Means, a Stanford-educated surgeon now focusing on functional medicine, expounds on the idea that a “magic pill” that causes weight loss and other supposed benefits appeals to millions of users:14
“I think it’s very dark. It’s a stranglehold on the U.S. population. Almost like solidifying this idea that there is a magic pill — I mean, literally, the book by Johann Ari is called ‘Magic Pill’ — and convincing us that, you know, salvation from our chronic health issues is going to be found in a shot when we are living in a toxic stew that’s destroying our cellular biology.”
Elsewhere in the interview, Means shares how ultraprocessed food contributes to obesity, thus cycling back to taking drugs that cause weight loss. In the end, only Big Pharma and Big Food are the real winners here, as millions of adults struggle with the damage they cause:15
“We are the only species in the world that has an obesity and chronic disease epidemic, the only species in the world that has a chronic disease and obesity epidemic because of ultraprocessed food.
You think about every other animal in the wild — they’re eating real, natural foods except for domesticated animals, which are also getting chronic diseases just like humans because they’re eating our food. But every other animal, they’re able to regulate their satiety. They’re not eating themselves to death like we are. We’re literally eating ourselves to death …
This could be on track to be the most profitable medication ever in human history. It will be if the powers that be let it. And what the unfortunate part is that it doesn’t take our bodies out of the toxic stew that’s crushing our biology. Yes, we may melt some fat and muscle without changing any of the other levers that we just talked about that are crushing our biology. So, this is not the public health solution.”
Practical Ways to Address Underlying Metabolic Challenges
I believe the key to maintaining a healthy weight is optimizing your cellular energy production. This requires a multifaceted approach that takes effort to implement, but it leads to safer, healthier results — something GLP-1 receptor agonists don’t offer. With that in mind, here are my recommendations:
1. Avoid Ozempic and other GLP-1 agonist receptor drugs — The most obvious strategy is avoiding GLP-1 agonist receptors in the first place. If you’re tempted to start, you owe it to yourself to read the study to understand the dangers.
Pills and injections offer short-term relief, but they often mask deeper imbalances in how your cells produce and use energy. Real improvement happens when you remove the factors that strain your metabolism rather than rely on a drug to force quick weight loss.
2. Remove vegetable oils from your diet — If you regularly consume ultraprocessed foods, I recommend stopping right now and replacing them with real, whole foods. Processed foods contain linoleic acid-rich vegetable oils that disrupt your metabolic pathways and alter how your body stores fat. Instead, cook your meals using tallow, grass fed butter or coconut oil.
To protect your health from further damage, limit your intake of linoleic acid to less than 5 grams per day from all sources. I recommend using Cronometer, an online food tracker, so you don’t go over this recommended range.
3. Shift your carbohydrate sources gradually — Avoid making sudden dietary changes that can shock your system. If your gut is compromised, start by introducing easily digestible carbohydrates like whole fruit or white rice before incorporating more complex carbs.
For severe gut issues, sip dextrose water throughout the day as a temporary aid to support healing, but limit its use to about two weeks. The goal is to provide your cells with a steady source of easy-to-digest, healthy carbohydrates for energy.
4. Consider your protein and collagen intake — I suggest aiming for 0.8 grams of protein per pound of lean body mass and balancing that amount so that about one-third comes from collagen. Doing this supports muscle maintenance, tissue repair and hormone balance.
If you exercise frequently, you would probably do well with a higher intake, but take it slow and listen to how your body responds. Stable protein intake is foundational for regulating cravings and stabilizing energy.
5. Support your gut and mitochondrial health with other healthy habits — I recommend getting daily sunlight exposure while being mindful of timing. If your diet previously included vegetable oils, avoid intense midday sun for at least six months to reduce the risk of sunburn and skin damage. Additionally, grounding in low-EMF environments can be beneficial if available — oceans, particularly in North America, tend to be the safest option.
In addition, moderate-intensity movement, such as walking, supports cellular energy production and aids in weight management. Gradual, consistent effort in these areas strengthens your metabolism and leads to lasting health improvements. I believe this approach is far superior to relying on a so-called “magic” drug like Ozempic.
Boost Your GLP-1 Naturally with Akkermansia
The idea of a quick-fix pill may be tempting, but it comes at a long-term cost to your health. A better approach is to naturally boost your GLP-1 levels by supporting Akkermansia, a beneficial gut probiotic that produces a GLP-1-inducing protein. As noted in one study:16
“A. muciniphila increases thermogenesis and glucagon-like peptide-1 (GLP-1) secretion in high-fat-diet (HFD)-induced C57BL/6J mice by induction of uncoupling protein 1 in brown adipose tissue and systemic GLP-1 secretion.”
Many people lack Akkermansia due to various reasons, such as impaired mitochondrial function or an environment that is inhospitable to beneficial gut bacteria. Ideally, Akkermansia should comprise 3% to 5% of your total gut microbiome and it plays many different roles aside from promoting GLP-1.
For example, Akkermansia has the ability to produce mucin, which is a thick, gel-like substance that protects the gut lining from harmful pathogens, irritation from stomach acid and enzymes, as well as mechanical damage. Moreover, mucin helps nourish the gut bacteria already existing in your gut.
To boost Akkermansia naturally, eat plenty of berries and inulin-rich foods such as garlic, asparagus, bananas and leeks. Note, however, that if your gut health is currently out of whack, introducing high amounts of dietary fiber in your system all at once can worsen your gastrointestinal symptoms. So, work on healing your gut first, then gradually increase fiber intake.
- 1, 15 JAMA Netw Open. 2024 Aug 20;7(8):e2423385
- 2, 4, 5, 6, 7 The Epoch Times, January 28, 2025
- 3, 10, 11 Nat Med. 2025 Jan 20
- 8 Front Public Health. 2022 Oct 20;10:996179
- 9 WashU Medicine, January 20, 2025
- 12 GoodRX, October 2, 2023
- 13 The New York Times, February 5, 2025
- 14 YouTube, Tucker Carlson, August 17, 2024
- 16 Nature Microbiology volume 6, pages 563–573 (2021)
Vitamin K 101 — Essential Basics for Bone and Heart Health
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/02/12/vitamin-k-bone-heart-health.aspx
Analysis by Dr. Joseph Mercola February 12, 2025
STORY AT-A-GLANCE
- Vitamin K is a fat-soluble vitamin necessary for blood clotting, bone health and cardiovascular function. It exists in two main forms: K1 (phylloquinone) found in green leafy vegetables, and K2 (menaquinones) found in animal products and fermented foods
- Vitamin K2 is essential for calcium metabolism, significantly impacting bone and cardiovascular health
- Vitamin K2 works synergistically with vitamin D to enhance bone health and reduce the risk of osteoporosis. This combination ensures that calcium is properly utilized and deposited in bones rather than accumulating in arteries
- Vitamin K2 is involved in activating proteins like osteocalcin and matrix Gla protein, which regulate calcium deposition in bones and arteries. This activation helps prevent arterial calcification and promotes bone strength
- The intake of vitamin K2 is often insufficient in Western diets, highlighting the need for increased consumption through dietary adjustments or supplementation to support bone and heart health
Vitamin K is a fat-soluble vitamin known for its essential role in blood clotting. However, its functions extend far beyond coagulation, encompassing processes that maintain bone integrity and cardiovascular health. There are two primary forms of vitamin K: K1 (phylloquinone), predominantly found in green leafy vegetables, and K2 (menaquinones), which is present in animal products and fermented foods.
While both forms are important, vitamin K2 has garnered significant attention for its unique ability to regulate calcium metabolism, directing this mineral to where it’s needed most in your body. As such, it stands out for its pivotal role in enhancing bone density and preventing the calcification of arteries.
Without adequate vitamin K2, calcium accumulates in your arteries, increasing your risk of cardiovascular diseases. Conversely, insufficient calcium in your bones leads to osteoporosis, a condition characterized by weakened bones and an increased risk of fractures.
Despite its benefits, vitamin K2 is often under-consumed in Western diets, primarily due to the limited intake of fermented foods and certain animal products, combined with the overconsumption of processed foods. Certain medical conditions and medications also impair the absorption and metabolism of vitamin K2, increasing deficiency risks.
Optimize Your Health with the Right Forms of Vitamin K
When it comes to maintaining optimal health, vitamin K often doesn’t get the spotlight it deserves. Understanding the different forms of vitamin K and their sources is essential to help you make informed decisions about your diet and supplementation.
Vegetable oils like soybean and canola are rich in vitamin K1, but relying on these oils is a dangerous choice for your overall energy and metabolic health. High intake of vegetable oils, which contain linoleic acid (LA), leads to impairments in mitochondrial energy production, which is essential for cellular function.
While conventional nutrition guidance encourages getting vitamin K1 from these oils, eliminating them from your diet is essential for optimal health. Therefore, diversifying your vitamin K intake from other sources is necessary.
Vitamin K2 offers additional health benefits that K1 does not. MK-7, a form of K2, is especially potent due to its longer half-life in your body, ensuring more consistent levels that support bone density and cardiovascular health. Unlike K1, which is quickly utilized by your liver, K2 travels to your bones and arteries, where it activates proteins that regulate calcium deposition.
This dual action helps prevent osteoporosis and reduces your risk of arterial calcification, a key factor in heart disease.
As for dosage, the European Food Safety Authority recommends an intake of 1 microgram per kilogram of body weight per day of total vitamin K, for both children and adults, including pregnant women.1 However, many experts suggest that higher doses of K2 may be beneficial, especially for those at risk of bone loss or cardiovascular issues.
Common supplementation ranges from 100 to 200 micrograms of MK-7 daily, which has been shown in studies to effectively improve bone mineral density (BMD) and reduce arterial stiffness without adverse effects. It’s important to note that while natural vitamin K supplements are generally safe, synthetic forms like vitamin K3 (menadione) are toxic in high doses and should be avoided.
Incorporating a balanced intake of both K1 and K2 through diet and, if necessary, supplementation supports your body’s needs without the drawbacks associated with excess vegetable oil consumption. Focus on leafy greens for K1 and fermented foods or high-quality supplements for K2 to harness the full spectrum of vitamin K’s health benefits.
Understanding Vitamin K Deficiency
Vitamin K deficiency manifests through symptoms primarily related to impaired blood clotting. You might notice spontaneous cutaneous purpura, which are purple spots on your skin caused by small blood vessels leaking under the surface. Epistaxis, or frequent nosebleeds, is another common indicator.
Additionally, you could experience gastrointestinal bleeding, genitourinary bleeding (i.e., blood in the urine, vaginal bleeding or bleeding from the urethra), gingival bleeding (bleeding gums) or other unexplained bleeding episodes. In addition to poor dietary intake, certain health conditions increase your risk of vitamin K deficiency by impeding your body’s ability to absorb or use vitamin K.
Liver diseases, such as cirrhosis or hepatitis, reduce your liver’s capacity to store and process vitamin K. Cholestasis, a condition where bile flow is reduced or blocked, also hinders vitamin K absorption since it’s a fat-soluble vitamin. Additionally, conditions like cystic fibrosis, alcoholism, and malabsorption disorders (including inflammatory bowel disease) also compromise your vitamin K levels.2
Weight loss surgeries that alter the digestive system also affect nutrient absorption, including vitamin K. So, if you’ve undergone such procedures, monitoring your vitamin K intake becomes essential. Certain drugs also interfere with vitamin K metabolism or absorption.
Coumarin-based anticoagulants, commonly prescribed to prevent blood clots, directly inhibit vitamin K’s role in blood clotting. Antibiotics like rifampicin disrupt gut bacteria that synthesize vitamin K2, further lowering your levels. Further, orlistat, a weight-loss medication, reduces fat absorption, which inadvertently decreases vitamin K absorption since it’s fat-soluble.3
Save This Article for Later – Get the PDF Now
Vitamin K2 for Bone Health, Heart Disease and Cancer
A comprehensive review published in Food Science & Nutrition explored the extensive benefits of vitamin K2, particularly focusing on its impact on bone health, cardiovascular protection and cancer.4 The research looked at how different forms of vitamin K2 contribute to these health outcomes and sought to understand the underlying mechanisms.5
The researchers found that higher intake of vitamin K2 significantly lowers the risk of developing osteoporosis. Additionally, participants who consumed more vitamin K2 had a reduced incidence of heart disease, highlighting the nutrient’s protective role in cardiovascular health.6
One of the standout findings was the relationship between vitamin K2 and cancer. The study highlighted that vitamin K2 has positive effects on the prevention and treatment of malignant tumors, offering a promising avenue for future cancer prevention strategies.7
Furthermore, the research explored the synergistic relationship between vitamin K2 and vitamin D. When these two vitamins are consumed together, their combined effect on bone health is more pronounced than when either is taken alone. This synergy enhances your body’s ability to maintain strong bones by ensuring that calcium is properly used and deposited where it’s needed most.8
If you’re supplementing with vitamin D, it’s especially important to balance it with vitamin K2 and magnesium, as they work together to prevent inappropriate calcification.
Different Forms of Vitamin K2
The featured study also highlighted three different forms of vitamin K2 — MK-4, MK-7 and MK-9. Of these, MK-4 had the highest bioactivity, meaning it’s particularly effective at activating proteins that regulate calcium. MK-7, meanwhile, was noted for its superior bioavailability and longer half-life, allowing it to remain active in your body for extended periods.9 Natto, a traditional Japanese fermented soybean dish, is the richest source of MK-7.10
While the majority of vitamin K1 is stored in your liver, MK-4 is the primary form of vitamin K2 found in human tissues. This distinction indicates that different forms of vitamin K have specific roles and are stored differently within your body.11
Vitamin K2, as mentioned, is particularly involved in the maintenance of calcium homeostasis. Calcium homeostasis refers to the regulation of calcium levels in various biological pathways, ensuring that calcium is available where needed for functions like bone formation while preventing its accumulation in soft tissues and blood vessels.12
By directing calcium to your bones and teeth, vitamin K2 ensures that it’s used effectively, enhancing overall skeletal and cardiovascular health.13 Vitamin K2 achieves this by activating proteins such as osteocalcin and matrix GLA-protein (MGP). Osteocalcin plays a pivotal role in binding calcium to your bone matrix, thereby strengthening bones.
Meanwhile, MGP prevents the deposition of calcium in blood vessel walls, reducing the risk of vascular calcification and subsequent cardiovascular diseases.14 Additionally, vitamin K2 modulates the activity of osteoblasts and osteoclasts, the cells responsible for bone formation and resorption, respectively.
By downregulating the activation of nuclear factor-κB, a protein complex involved in inflammatory responses, vitamin K2 helps maintain a balanced activity of these bone cells, promoting bone health and preventing excessive bone loss.15
The study also touched upon the neuroprotective effects of vitamin K2. Specifically, MK-7 was shown to protect brain cells from apoptosis, or programmed cell death, induced by hypoxic conditions. This finding opens up therapeutic applications for vitamin K2 in treating neurodegenerative diseases and other mitochondrial-associated disorders.16
Vitamin K2’s Role in Mitochondrial Energy Production
Vitamin K2 exhibits a broad spectrum of biological activities, influencing nearly all major body systems, including mitochondrial energy release. Mitochondria are responsible for producing adenosine triphosphate (ATP) through the electron transport chain.
Vitamin K2, which is structurally similar to coenzyme Q10 (CoQ10), plays a role in mitochondrial energy metabolism.17 Studies have shown that vitamin K2 acts as a mitochondrial electron carrier, rescuing mitochondrial dysfunction caused by Pink1 protein deficiency, which is linked to Parkinson’s disease.18 Vitamin K2 facilitates electron transport within mitochondria, thereby enhancing ATP production and improving cellular energy levels.
However, conflicting evidence exists regarding vitamin K2’s role in mammalian mitochondrial function. While some studies suggest beneficial effects on mitochondrial respiration and energy release, others indicate that vitamin K2 does not substitute for CoQ10 in restoring electron flow or ATP synthesis in CoQ10-deficient cells. This discrepancy highlights the need for further research to uncover vitamin K2’s exact role in mitochondrial energy metabolism across different species.
Vitamin K for Optimal Health During Menopause
Menopause induces significant hormonal and physiological changes, contributing to conditions such as osteoporosis, osteopenia and increased vascular calcification. Vitamin K2 has been extensively studied for its beneficial effects in mitigating these menopausal effects.
Clinical trials have demonstrated that vitamin K2 supplementation, particularly in the forms of menaquinone-4 (MK-4) and MK-7, improves bone mineral density (BMD) and bone mineral content (BMC) in postmenopausal women.19
For instance, a meta-analysis of randomized controlled trials revealed that daily intake of MK-4 for three years enhanced hip bone geometry and strength by increasing BMC without significantly altering BMD.20 Additionally, MK-7 supplementation has shown to synergize with calcium and vitamin D3, further supporting bone health by increasing osteocalcin carboxylation and reducing bone resorption markers.21
Vitamin K Has Neuroprotective Properties and Protects Your Liver
Beyond its menopausal benefits, vitamin K2 demonstrates significant hepatoprotective and neuroprotective properties, contributing to liver regeneration and cognitive health. In liver health, vitamin K2 supplementation has been shown to enhance liver regeneration following liver surgery in rat models.22
Additionally, vitamin K2 exhibits cytotoxic effects on liver cancer cells by inducing cell cycle arrest and apoptosis through multiple signaling pathways, including the suppression of NF-κB and MAPK activities.23
Further, vitamin K supports cognitive function and neuronal health. Studies in rodent models have linked adequate vitamin K2 levels with improved cognitive performance and reduced neuroinflammation. Vitamin K2 activates the Gas6/Axl/Akt signaling pathway, which inhibits apoptosis and enhances neuronal survival.24
Moreover, vitamin K2 protects neural cells from oxidative stress and amyloid-beta toxicity, factors implicated in Alzheimer’s disease.25 These neuroprotective mechanisms underscore vitamin K2’s role in preventing and managing neurodegenerative diseases.
Vitamin K for the Treatment of COVID-19
Emerging research also suggests that vitamin K2 may play a role in mitigating the severity of COVID-19. COVID-19 is associated with coagulopathies and excessive inflammation, conditions where vitamin K2’s regulatory functions on coagulation and inflammation are likely beneficial. Observational studies have indicated that vitamin K deficiency is linked to increased disease severity and mortality in COVID-19 patients.26
Vitamin K2 may help in activating vitamin K-dependent proteins like MGP and Protein S, which are key for preventing vascular calcification and thrombosis, common complications in severe COVID-19 cases.27 Furthermore, vitamin K2’s anti-inflammatory properties help in reducing the cytokine storm associated with acute COVID-19, thereby improving patient outcomes.
Vitamin K for Parathyroid Disorders and Cerebral Palsy
A review published in the journal Nutrients also highlighted the impact of vitamin K2 on multiple health conditions. Beyond osteoporosis and cardiovascular disease, studies have shown that adequate vitamin K2 intake positively influences parathyroid disorders, cerebral palsy and sperm motility, suggesting its broad therapeutic potential.28 These findings emphasize the need for optimizing vitamin K2 in the diet to maintain overall health.
Parathyroid disorders, particularly hyperparathyroidism, involve the excessive secretion of parathyroid hormone (PTH), leading to elevated serum calcium levels (hypercalcemia) and subsequent bone resorption. Vitamin K2 plays a role in calcium metabolism, which directly impacts parathyroid function.
Further, researchers demonstrated that vitamin K2 supplementation in hemodialysis patients, who often suffer from secondary hyperparathyroidism, resulted in increased levels of carboxylated osteocalcin without significantly altering PTH, calcium or phosphate levels. This suggests that vitamin K2 mitigates the adverse effects of elevated PTH by enhancing bone mineralization and reducing calcium loss from bones.29
Moreover, vitamin K2’s activation of MGP inhibits vascular calcification, a common complication in hyperparathyroid patients. By preventing the inappropriate deposition of calcium in blood vessels, vitamin K2 indirectly supports parathyroid health by maintaining balanced calcium distribution within the body.
Although vitamin K2 does not directly lower PTH levels, its role in optimizing calcium metabolism offers a complementary approach to managing parathyroid disorders alongside conventional treatments.
Cerebral palsy (CP) is a group of neurological disorders that affect movement, muscle tone and posture, often resulting in decreased BMD and increased fracture risk. Osteoporosis is prevalent among individuals with CP due to reduced mobility and subsequent bone resorption. According to researchers, vitamin K2 supplementation could play a significant role in improving bone health in CP patients.30
Additionally, vitamin K2’s role in regulating bone remodeling also supports overall skeletal integrity in individuals with CP. While direct studies on vitamin K2 and CP are limited, the existing evidence on its impact on bone health provides a compelling rationale for its inclusion in therapeutic regimens aimed at mitigating osteoporosis in CP patients.
Vitamin K Enhances Sperm Motility
Sperm motility is a critical factor in male fertility, governed by the functionality of calcium channels and the integrity of spermatozoa. Vitamin K2 has been implicated in enhancing sperm motility through its involvement in calcium metabolism and the maturation of sperm cells.
Researchers investigated the effects of vitamin K2 on sperm maturation, revealing that K2-dependent proteins are highly expressed in the epididymis, the site of sperm maturation. Warfarin-induced inhibition of vitamin K2 activity resulted in decreased sperm count and motility, underscoring the vitamin’s essential role in maintaining sperm health.31
Vitamin K-Dependent Proteins in Biomineralization
Research published in the International Journal of Molecular Medicine focused on the role of vitamin K in the activation of proteins essential for bone and vascular health, emphasizing its involvement in biomineralization processes.32 The research underscored the importance of vitamin K in the post-translational modification of vitamin K-dependent proteins (VKDPs), which are primarily involved in coagulation and calcification.33
There are 17 identified VKDPs, which include osteocalcin and MGP. Osteocalcin, synthesized by osteoblasts, requires vitamin K for carboxylation, converting glutamic acid residues to gamma-carboxyglutamate (Gla) residues.34 This conversion enhances osteocalcin’s calcium-binding capacity, thereby reinforcing bone structure.35
Without sufficient vitamin K, osteocalcin remains undercarboxylated, reducing its effectiveness in supporting bone health.36 Similarly, MGP gains a higher affinity for calcium upon carboxylation, which prevents its deposition in arterial walls, thereby lowering the risk of cardiovascular diseases like atherosclerosis.37
The study highlights that inadequate vitamin K levels impair MGP’s ability to prevent calcium accumulation, leading to arterial calcification and increased cardiovascular risk.38 Additionally, the study clarified the distinct functions of vitamin K1 and K2, with vitamin K1 playing a major role in coagulation, while vitamin K2 is more prevalent in tissues other than the liver.39
The review also addressed the absorption and transport pathways of vitamin K1 and K2, noting that vitamin K1 is absorbed with triglyceride-rich lipoproteins, while vitamin K2 is primarily transported by low-density lipoproteins (LDL).40 This difference in transport mechanisms influences the distribution and bioavailability of each vitamin K form in your body.41
The Interplay Between Lipids and Vitamin K Metabolism
A review published in Nutrition & Metabolism further explored the intricate relationship between lipids and vitamin K metabolism, specifically focusing on how lipid levels affect the absorption and transportation of vitamin K within the body.42
The paper reviewed data from individuals with varying lipid profiles and those undergoing treatment with cholesterol-lowering medications such as statins. The findings revealed that vitamin K absorption and transportation are significantly influenced by the presence of lipids in the digestive system, underscoring the importance of adequate dietary fat intake for the optimal utilization of vitamin K.43
Vitamin K shares transporters with cholesterol, meaning that both substances compete for the same pathways within your body. This competition impacts the efficiency with which vitamin K is distributed to essential tissues.
The study also explored the role of lipoproteins, which are particles that transport fats, including cholesterol and triglycerides, through the bloodstream. It was found that low-density lipoproteins (LDL), often referred to as “bad cholesterol,” play an important role in transporting vitamin K2 to tissues such as bones and blood vessels.44
Furthermore, statins inhibit the mevalonate pathway, a biochemical pathway that’s involved not only in cholesterol synthesis but also in the production of vitamin K2 isoforms like MK-4. By blocking this pathway, statins reduce the synthesis of vitamin K2, compromising its protective roles in your body.45
For this reason, individuals taking statins benefit from vitamin K2 supplementation to counteract this adverse effect. Moreover, the interplay between lipids and vitamin K metabolism extends to dietary recommendations. Diets that include healthy fats, such as butter and coconut oil, enhance the absorption of vitamin K, improving its bioavailability and efficacy in your body.
Remember, vitamin K is a lipophilic vitamin, meaning it dissolves in fats and is transported through your body via lipid-based carriers. This characteristic necessitates the presence of dietary fats for effective absorption in your small intestine. Once absorbed, vitamin K is packaged into lipoproteins for distribution to various tissues. The efficiency of this process is directly tied to your body’s lipid metabolism, illustrating the interconnectedness of these two important components.46
Vitamin K and Its Impact on Other Nutrients
Understanding how vitamin K interacts with other nutrients is also helpful for optimizing your health and ensuring that you’re getting the most out of your dietary intake and supplements. Insights from pharmacokinetic studies highlight the intricate relationships between vitamin K and other vitamins, particularly those that deplete or compete for its absorption and metabolism.47
One of the most significant interactions involves vitamin K and vitamin E, a powerful antioxidant essential for protecting your cells from oxidative stress. Both are fat-soluble vitamins that share similar metabolic pathways, leading to competition that affects their respective levels in your body. Studies have shown that the presence of vitamin E, as well as other fat-soluble vitamins, significantly reduces the absorption of vitamin K, with absorption rates dropping by 34% to 58%.48
The competition arises because vitamins E and K vie for the same enzymes involved in their metabolism. Specifically, both vitamins compete for cytochrome P450 (CYP450) enzymes, which are responsible for hydroxylating the side chains of these vitamins.49 This competition leads to increased metabolism and excretion of vitamin K when vitamin E levels are high, diminishing vitamin K’s effectiveness in your body.
So, if you’re supplementing with vitamin E, it’s important to monitor your vitamin K intake to prevent deficiencies. For instance, individuals taking high doses of vitamin E supplements might inadvertently reduce their vitamin K levels, increasing the risk of bleeding disorders and bone weakening. To maintain a healthy balance, consider spacing out the intake of these vitamins or consulting with a health care professional to adjust dosages appropriately.
How to Optimize Your Vitamin K2 Levels
Vitamin K2 serves as the body’s master regulator for calcium distribution, ensuring this essential mineral is directed appropriately to support bone strength and prevent arterial calcification. By optimizing your vitamin K2 levels, you enhance bone integrity while safeguarding your cardiovascular health, providing a dual advantage for long-term well-being.
Determining whether you’re getting enough vitamin K is challenging because there’s currently no simple test available to measure vitamin K2 levels directly. Instead, vitamin K2 status is assessed indirectly by evaluating levels of undercarboxylated osteocalcin, a marker that indicates vitamin K2 activity in your body. However, this type of testing is not yet available for commercial use.
Generally, individuals with osteoporosis, heart disease or diabetes are likely to have a vitamin K2 deficiency. If you’re taking statin medications, which are known to reduce vitamin K2 levels, you’re also at risk of deficiency. Moreover, it’s believed that most people do not get enough vitamin K2 and could benefit from increasing their intake. To boost your levels:
1. Prioritize vitamin K2-rich foods — Incorporate natto (fermented soybeans) and other vegetables fermented with vitamin K2-producing bacteria into your daily diet. These options provide the MK-7 form of K2, which remains active in your body for extended periods.
Certain cheeses, including Brie, Munster and Gouda, are also particularly rich in vitamin K2. Grass fed organic animal products, including egg yolks, liver, butter, tallow and dairy products, are also good sources of vitamin K2.
2. Align K2 intake with healthy fats — As vitamin K2 is fat-soluble, it should be consumed alongside healthy fats such as grass fed butter or tallow to enhance absorption. This practice ensures that your body effectively utilizes this nutrient for maintaining both bone density and cardiovascular health.
3. Harmonize K2 with complementary nutrients — Vitamin K2 works synergistically with vitamins D3, calcium and magnesium. When supplementing with vitamin D3, also include K2 to prevent calcium from depositing in your arteries. This balanced nutrient approach promotes bone strength while protecting your cardiovascular system.
4. Opt for premium supplement sources — If you choose to use supplements, select those containing the MK-7 form of K2. The recommended daily intake is 150 to 200 micrograms for most adults. For optimal absorption, take supplements with meals that include healthy fats.
Egg Yolks Are Your Best Source of Vitamin K2 as MK-4
Of the foods highlighted above, egg yolks are among the highest dietary sources of MK-4, a vital form of vitamin K2 that plays a crucial role in bone health, cardiovascular function and calcium regulation. Including egg yolks in your diet can significantly contribute to your MK-4 intake, supporting various aspects of your health.
You just need to be careful about your egg sources as most commercial egg sources — even free-range organic — have high PUFA levels as they are fed grains like soy and corn. Ideally, chickens should be fed rice, barley and split peas. I personally eat six egg yolks a day from chickens who are fed this and have 80% less linoleic acid than regular chickens.
Below is a comprehensive overview of egg yolks as a top source of MK-4, along with additional dietary sources and considerations.
- 1, 2, 3 Nutr Rev. 2021 Sep 2;80(4):677–698
- 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27 Food Science & Nutrition January 6, 2023;11(4):1634–1656
- 28, 29, 30, 31 Nutrients 2021 Feb 21, 13(2), 691
- 32, 33, 34, 35, 36, 37, 38, 39, 40, 41 International Journal of Molecular Medicine November 24, 2023;53(1):6
- 42, 43, 44, 45, 46 Nutrition & Metabolism January 3, 2024; 21:6
- 47, 48, 49 Food Science & Nutrition January 2024, Volume 12, Issue 1, Pages 48-83
Butyrate — A Tiny Molecule with Big Potential for Health and Healing
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/02/10/butyrate.aspx
Analysis by Dr. Joseph Mercola February 10, 2025
STORY AT-A-GLANCE
- Butyrate is a short-chain fatty acid (SCFA) produced when gut bacteria ferment dietary fiber. It provides energy for colon cells and offer health benefits beyond basic nutrition
- Research suggests butyrate helps manage inflammatory bowel disease (IBD) by reducing inflammation, improving symptoms and strengthening gut barrier integrity
- Laboratory studies show butyrate helps inhibit cancer cell growth and trigger cell death in colorectal cancer cells, with clinical trials exploring its use alongside traditional treatments
- Butyrate has been shown to improve insulin sensitivity and glucose metabolism for metabolic disorders, while also influencing appetite-regulating hormones
- Studies show butyrate protects against neurodegenerative diseases by reducing brain inflammation and enhancing neuronal repair and survival
Butyrate is a short-chain fatty acid (SCFA) produced in your gut when beneficial bacteria ferment dietary fiber, which your body cannot digest on its own.
As the primary energy source for colonocytes (the cells lining your colon), butyrate provides up to 70% of their energy needs.1 However, its benefits go far beyond just fueling those cells — it also reduces inflammation, strengthens your gut barrier and supports immune system balance.2 These properties make butyrate a promising molecule for managing a wide variety of conditions and improving overall health.
Your ability to produce butyrate depends on a complex ecosystem of beneficial bacteria in your gut. Both environmental toxins and poor dietary choices can disrupt this microbial balance, reducing your gut’s capacity to ferment fiber and generate butyrate, thereby compromising the protective effects that butyrate provides.
How Butyrate Fights Against Inflammatory Bowel Disease (IBD)
Inflammatory bowel disease (IBD), which encompasses a range of conditions like Crohn’s disease and ulcerative colitis, causes chronic inflammation in your digestive tract. This ongoing inflammation leads to various uncomfortable and sometimes debilitating symptoms, including abdominal pain, persistent diarrhea, weight loss, fatigue and even malnutrition.3
The exact cause of IBD is not fully understood, but it’s believed to involve a combination of genetic factors, immune system dysfunction and environmental triggers.4 Because butyrate is produced directly in the colon, the site of inflammation in IBD, researchers have been investigating its benefits for managing these conditions.
Research5 shows that individuals with IBD often experience a “double hit” — a decline in butyrate-producing microbes and a diminished ability to utilize butyrate effectively. They also have reduced expression of butyrate receptors in the colon, which hampers butyrate uptake. Additionally, inflammatory cytokines like tumor necrosis factor-alpha (TNFα) reduce butyrate oxidation in intestinal epithelial cells, further impairing its utilization.
Decreased butyrate levels linked to IBD also affect aryl hydrocarbon receptor (AHR) activity, a key signaling pathway that promotes gut health by increasing interleukin-22 (IL-22) expression, which plays a protective role in maintaining epithelial integrity and reducing inflammation.
AHR activity is found to be lower in IBD patients, suggesting that reduced butyrate availability impairs this pathway. Experimental models further support this connection, demonstrating that AHR activation protects against colitis in mice,6 highlighting a mechanism by which restoring butyrate levels could improve IBD outcomes.
Clinical research has explored different methods of delivering butyrate directly to the colon, including enemas, which deliver the butyrate directly to the rectum and lower colon.7 Some clinical trials have demonstrated that butyrate enemas helped reduce inflammation, improve bowel movement frequency and enhance mucosal healing in some patients with ulcerative colitis.
These outcomes are attributed to butyrate’s ability to suppress proinflammatory signaling pathways, such as NF-κB, and promote the differentiation of regulatory T cells, which help modulate immune responses.8 Butyrate also strengthens your gut barrier by enhancing the expression of tight junction proteins, reducing intestinal permeability and preventing the translocation of harmful substances that exacerbate inflammation.9
Despite promising results, the effectiveness of butyrate for IBD varies from person to person, and more research is needed to determine the optimal dosage, delivery methods and specific types of IBD that respond best to this treatment.
Butyrate as a Powerful Ally in Colorectal Cancer Therapy
Colorectal cancer is a serious disease affecting the colon or rectum. It often begins as small, noncancerous growths called polyps that form on the inner lining of the colon or rectum. Over time, these polyps become cancerous.
Laboratory studies have demonstrated butyrate’s ability to inhibit the growth of cancer cells and even trigger apoptosis, or programmed cell death, helping stop cancer cells from multiplying uncontrollably and spreading to other parts of your body.10,11
This effect is related to butyrate’s ability to affect gene expression in cancer cells by specifically turning off genes that promote cell growth and turning on genes that promote cell death.12,13 Moreover, by functioning as a histone deacetylase (HDAC) inhibitor, butyrate alters the chromatin structure to switch off oncogenes that drive cancer growth while activating tumor suppressor genes that facilitate apoptosis and repair DNA damage.14
Clinical evidence supports the role of butyrate as a chemopreventive agent. For example, dietary butyrylated high amylose maize starch (HAMSB) has been shown to deliver significant quantities of butyrate to the colon, leading to increased apoptosis in colonic epithelial cells and reduced markers of DNA damage associated with colorectal carcinogenesis.15
A study published in Contemporary Clinical Trials Communications16 investigated the effects of HAMSB in individuals with familial adenomatous polyposis, a condition characterized by a high risk of colorectal cancer. Preliminary findings show that butyrate supplementation reduced polyp growth and helped lower cancer risk.
Beyond prevention, butyrate is an effective complementary agent in cancer therapy. Its ability to enhance the efficacy of chemotherapy and radiation therapy has been demonstrated in preclinical models.17
For instance, butyrate sensitizes cancer cells to 5-fluorouracil and irinotecan, two widely used chemotherapeutic agents, while reducing chemotherapy-induced mucositis. These outcomes are attributed to butyrate’s capacity to regulate immune responses, strengthen gut barrier integrity and suppress inflammatory pathways.18
Save This Article for Later – Get the PDF Now
Butyrate’s Role in Combating Metabolic Disorders
Metabolic disorders, including Type 2 diabetes, obesity and metabolic syndrome, disrupt how your body processes sugar (glucose) and manage energy, leading to serious health issues like heart disease, stroke and kidney disease. At the heart of these conditions is insulin resistance, wherein your cells fail to respond properly to insulin, the hormone that regulates blood sugar levels. This leads to high blood sugar levels, which damage various organs over time.
Research has shown that butyrate improves how your body responds to insulin and regulates blood sugar by activating pathways involved in energy metabolism and mitochondrial function. By enhancing the activity of key regulators like AMPK and PPARs, butyrate boosts your ability to process glucose and improve cellular energy balance. It also supports pancreatic β-cells, which are essential for insulin production.19,20
Moreover, butyrate influences gut-derived hormones that play a significant role in regulating appetite and glucose metabolism, increasing the secretion of hormones like glucagon-like peptide-1 (GLP-1) and peptide YY (PYY). Butyrate also enhances insulin release, suppresses glucagon and promotes feelings of fullness.21,22 This means better control over blood sugar levels and reduced appetite — factors that are important for managing metabolic disorders.
The chronic inflammation associated with metabolic disorders exacerbates insulin resistance and glucose dysfunction. Butyrate combats this by reducing inflammation by inhibiting HDAC and NF-κB, creating a healthier environment for cells to respond to insulin effectively. Additionally, butyrate supports energy expenditure by enhancing fat oxidation and thermogenesis in brown adipose tissue, further contributing to improved metabolic health.23,24
Additional studies using animal models demonstrate the ability of butyrate to improve insulin sensitivity, regulate body weight and reduce inflammation. For example, supplementation with butyrate in mice fed a high-fat diet significantly improved glucose metabolism and prevented weight gain.25
Understanding Butyrate’s Influence on Neurodegenerative Diseases
Neurodegenerative diseases, such as Alzheimer’s and Parkinson’s disease, represent some of the most challenging conditions to manage due to their progressive nature and devastating impact on cognitive and motor functions. These diseases are marked by neuronal loss, chronic inflammation, oxidative stress, mitochondrial dysfunction and disrupted synaptic plasticity.
Research on butyrate’s therapeutic properties offers a compelling avenue for addressing these multifactorial mechanisms. Studies have shown that butyrate modulates proinflammatory cytokines like TNF-α and IL-1β, which are elevated in neurodegenerative diseases. This counteracts chronic neuroinflammation, a driving factor in neuronal damage and synaptic dysfunction.26,27
Animal studies have also demonstrated butyrate’s ability to attenuate inflammation in the cerebral cortex and synaptic regions, contributing to improved neuronal health.28 Its role as an HDAC inhibitor further enhances its neuroprotective potential.
By promoting histone acetylation, butyrate upregulates genes that are vital for neuronal survival, repair and plasticity, including those involved in the production of brain-derived neurotrophic factor (BDNF). BDNF is essential for supporting synaptic health and neurogenesis, both of which are compromised in neurodegenerative conditions.29
In Alzheimer’s test models, butyrate has been shown to alleviate cognitive deficits by reducing amyloid-beta plaque deposition and enhancing synaptic plasticity.30 Similarly, in Parkinson’s test models, butyrate demonstrated neuroprotective effects by mitigating dopaminergic neuron loss and reducing motor deficits.31,32
These effects are likely linked to butyrate’s ability to regulate gut microbiota, as gut dysbiosis is increasingly recognized as a factor in the pathogenesis of neurodegenerative diseases. By promoting the growth of beneficial bacteria and increasing the production of endogenous SCFAs, butyrate reinforces the integrity of your gut-brain axis, which plays a vital role in neuroprotection.33,34
The Integral Role of Butyrate in Gut Health and Immune Function
Beyond the specific diseases discussed above, butyrate plays a vital role in overall gut health and immune function. Your gut, which houses 70% to 80% of the immune system,35 serves as a central hub for immune activity. Maintaining this relationship between your gut and immunity requires a balanced microbiome, an intact intestinal barrier and effective immune communication.
Butyrate is central to this harmony, acting as both a fuel source and a signaling molecule that bridges the gut environment with immune function. Regulatory T cells (Treg) are indispensable for immune tolerance, preventing the overactivation of the immune system and protecting against chronic inflammation.36
Butyrate enhances Treg function by promoting the expression of FOXP3, a transcription factor that stabilizes these cells. This mechanism helps maintain a balanced immune response, reducing the likelihood of autoimmune conditions and inflammatory damage.37
In addition, butyrate strengthens your gut-associated lymphoid tissue (GALT) by enhancing the production of immunoglobulin A (IgA), a mucosal antibody that forms a protective barrier over the gut lining.38 GALT plays a pivotal role in gut immunity by monitoring intestinal contents and triggering appropriate responses to pathogens while tolerating beneficial bacteria.39
As a signaling molecule, butyrate facilitates communication between the gut microbiota and immune cells. It also promotes the growth of beneficial bacteria strains like Faecalibacterium prausnitzii and Roseburia, which further support a healthy microbiome and immune system. This symbiotic relationship reduces the presence of harmful bacteria and minimizes unnecessary immune responses, preventing tissue damage from excessive inflammation.40,41
Your intestinal barrier is another cornerstone of immune health, preventing the translocation of pathogens, antigens and toxins into your bloodstream. Butyrate strengthens this barrier by upregulating tight junction proteins, such as claudin and occludin, which seal gaps between intestinal cells.42
Butyrate’s immunomodulatory effects also extend beyond the gut. By fine-tuning the activity of macrophages and dendritic cells, butyrate promotes a balance between immune activation and tolerance. This regulation is particularly important in preventing overreactions to harmless stimuli, such as dietary proteins or commensal bacteria, which leads to food allergies or autoimmunity.43
How to Approach Fiber Intake to Boost Butyrate Production
Increasing fiber intake is a key step toward promoting butyrate production. However, this approach assumes you already have a balanced and functional gut microbiome. Unfortunately, most people today have compromised gut health due to exposure to metabolic toxins, processed foods and other environmental toxins. In such cases, consuming large amounts of fiber does more harm than good.
This presents a complex challenge, as fiber is generally considered essential for gut health, as its fermentation by beneficial bacteria produces the SCFAs needed for cellular energy in the colon, gut barrier integrity and maintaining a low-oxygen environment.
However, in an imbalanced microbiome, this process is hijacked by harmful bacteria. When these bacteria dominate, they ferment fiber in ways that increase endotoxin production, perpetuating gut damage and metabolic dysfunction. Therefore, the key to leveraging fiber’s benefits while avoiding harm lies in restoring a healthy balance in your gut microbiome.
Healing your gut starts with creating the optimal low-oxygen environment that beneficial, oxygen-intolerant bacteria need to thrive. An essential strategy is elevating carbon dioxide levels in your gut, which is achieved by increasing your carbohydrate intake, particularly easily digestible ones.
If your gut health is severely compromised, I recommend starting with white rice and/or dextrose water — mix pure dextrose with water and sip slowly throughout the day to prevent insulin spikes. After one to two weeks, transition to more complex carbohydrate sources, first from the yellow grouping below, followed by those in the red category.
This approach allows your microbiome to regain balance and ensures that fiber enhances, rather than disrupts, butyrate production. For more guidance on how to repair and optimize your gut health, I recommend exploring the strategies detailed in my new book, “Your Guide to Cellular Health.”
Introducing the Globally Patented Breakthrough — The First 24-Hour, Full-Colon Butyrate Delivery System
You’ve likely heard about the new “Akkermansia” probiotic craze. These high-priced probiotics are prized for producing butyrate, a short-chain fatty acid crucial for soothing gut irritation, repairing leaky gut and supporting immune balance.
Despite the benefits, Akkermansia is costly and challenging to grow, making direct butyrate supplementation a more viable solution. However, most butyrate supplements dissolve too early in the small intestine, limiting their effectiveness.
Good news —We’ve overcome the longstanding challenges of butyrate delivery! Our team is currently developing an advanced liposomal encapsulation that ensures butyrate is released precisely where it’s needed, providing coverage throughout your entire colon over a full 24-hour period.
This globally patented system marks a significant breakthrough in gut-health, eliminating the need for expensive probiotic strains and messy enemas.
With our solution, you can continuously fuel your colon with butyrate, bridging the gap between trying and achieving gut repair. Sign up below to be notified when this product goes live. Don’t miss the chance to experience the difference comprehensive butyrate coverage can make.
- 1, 2, 5, 7, 8, 9, 10 Clinical Nutrition, Volume 42, Issue 2, Pages 61-75
- 3, 4 StatPearls [Internet]. Inflammatory Bowel Disease
- 6 Int J Mol Med. 2018 Feb;41(2):868-876
- 11 Scientific Reports, Volume 13, Article number: 5106 (2023)
- 12 Am J Physiol Gastrointest Liver Physiol. 2021 Jan 6;320(4):G601–G608
- 13 Anticancer Res. 2019 Sep;39(9):4659-4666
- 14, 21 Adv Nutr. 2018 Feb 9;9(1):21–29
- 15, 16 Contemporary Clinical Trials Communications, Volume 32, April 2023, 101092
- 17, 18 Front Cell Infect Microbiol. 2022 Oct 26;12:1023806
- 19, 24 Front Pharmacol. 2022 Feb 2;12:837509
- 20 Obes Rev. 2022 Jul 20;23(10):e13498
- 22 Pharmacological Research, Volume 160, October 2020, 105174
- 23 J. Agric. Food Chem. 2024, 72, 1, 449–460
- 25 JCI Insight. 2023 Feb 22;8(4):e166655
- 26 Neurochemistry International, Volume 99, October 2016, Pages 110-132
- 27, 28 Antioxidants (Basel). 2022 Dec 20;12(1):4
- 29 Journal of Neurochemistry, 110(4), 1226–1240
- 30 J Alzheimers Dis. 2020;74(1):91-99
- 31 Redox Biology, Volume 71, May 2024, 103092
- 32 Front Pharmacol. 2024 Apr 17;15:1388401
- 33 Neurochemistry International, Volume 99, October 2016, Pages 110-132
- 34 Nutrients. 2023 Feb 13;15(4):930
- 35 Nutrients. 2021 Mar 9;13(3):886
- 36, 37 Nature. 2013 Nov 13;504(7480):451-455
- 38 Science Direct, Gut-Associated Lymphoid Tissue
- 39 Mucosal Immunology, Volume 14, Pages 793-802 (2021)
- 40 Biomedicine & Pharmacotherapy, Volume 167, November 2023, 115568
- 41 AMB Expr 11, 33 (2021)
- 42 Biology (Basel). 2021 Mar 9;10(3):205
- 43 J Inflamm Res. 2021 Nov 18;14:6025–6041
Chemotherapy may fuel cancer regrowth: New research reveals disturbing findings
Reproduced from original article:
https://www.naturalhealth365.com/chemotherapy-may-fuel-cancer-regrowth-new-research-reveals-disturbing-findings.html
by: January 29, 2025
(NaturalHealth365) According to current statistics, about one million people a year (in the U.S. alone) undergo chemotherapy in an attempt to beat cancer. Yet this toxic treatment has a poor success rate in treating most kinds of cancer, and its benefits can be short-lived.
Making the picture even grimmer is the fact that cancer recurrence after chemotherapy is frequently deadly. Now, from the front lines of cancer research comes the disturbing news that one particular type of chemotherapy can actually lead to cancer regrowth and recurrence.
One approach to treating cancer creates a breeding ground for cancer stem cells
Chemotherapy-induced senescence, often touted as a new weapon in cancer therapy, involves “putting cancer cells to sleep.” The protocol is intended to place cancer cells in a state of arrested growth, where they are alive but not dividing.
While senescence is supposed to prevent further cancerous growth, new research shows that it can serve as a sort of “nursery” and safe harbor for cancer stem cells – the most dangerous and treatment-resistant type of cancer cells. A pair of recent studies reveal the consequences of therapy-induced senescence.
In an explosive article published in Frontiers in Oncology, Markus Schosserer, Ph.D., wrote that there is ample evidence that senescent cancer cells can produce inflammatory molecules that promote a rich environment for cancer regrowth.
In a breakthrough German study published in Nature, the team presented startling conclusions: senescence not only helps cancer cells avoid death but actually transforms them into cancer stem cells.
This is very bad news, as stem cells – which can break from a tumor and metastasize throughout the body – are also the most resistant to treatment.
Cancer cells can “outmaneuver” induced senescence
In the German study, researchers examined human lymphoma cells treated with drugs to induce senescence and discovered they were developing “stemness.” In other words, the lymphoma cells started to express genes vital for maintaining stem cell function.
When the team “released” the cancer cells from senescence, they discovered an alarming outcome. The cells began to multiply again – and more rapidly than those that had not become senescent.
Although senescence is supposed to be irreversible, the team found evidence that cancer cells can escape it on their own – without the help of the genetic manipulation they used. Testament to this unfortunate possibility is that the scientists found more previously senescent stem cells in tumor patients after lymphoma recurred than had existed in the same individuals when they received their initial treatment.
This demonstrated to the scientists that at least some cells had “figured out” how to outwit senescence. Noted professor of experimental oncology Dr. Jan Paul Medema commented, ‘There is compelling evidence … that … when cancer cells escape from senescence, they have an enhanced ability to drive tumor growth.’
Study leader Dr. Clemens A. Schmitt reported that switching off a specific cell signaling pathway could work to neutralize stemness in the previously senescent cells. However, there is no doubt that the study findings pose a definite setback for a formerly promising protocol.
In addition, other studies have emerged showing that chemotherapy can do more harm than good.
Chemotherapy for breast cancer can spread cancer cells
A common protocol for breast cancer patients is to surgically remove tumors after chemo has been administered. The theory is that the chemo will help shrink the tumor while preventing the spread of cancer throughout the body.
However, the treatment may accomplish the opposite effect.
The toxic chemo drugs may actually switch on a repair mechanism – creating more blood vessel pathways and permitting tumors to grow back even stronger. In a study at the Albert Einstein College of Medicine, researchers found that chemotherapy triggered the circulation of more cancer cells throughout the lungs and the body.
Chemotherapy features toxic side effects
The American Cancer Society acknowledges that chemotherapy damages healthy cells – and reports that chemotherapy side effects include vomiting, diarrhea, anemia, hair loss, fertility problems, chronic fatigue, and infections.
Neutropenia, the most serious side effect, involves the depletion of white blood cells needed to fight diseases and infections. Weight changes and mood changes – with depression, memory loss, and inability to concentrate – may also occur.
Normal cells most likely to be damaged by chemotherapy are cells in hair follicles, blood-forming cells in the bone marrow, cells in the mouth and digestive tract, and cells in the reproductive system.
Experts report that in some situations – for example, the early stages of colorectal cancer – chemotherapy has been shown to provide some benefit, granting extra years of life. But on the whole, chemotherapy yields disappointing results and may even exacerbate cancer cell growth – as shown in this pair of startling studies.
Sources for this article include: