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Compounds That Help Protect Against Melanoma Skin Cancer Adding these antioxidant rich compounds to your diet can improve your skin’s natural defenses: Caffeic Acid: Found in spinach leaves, olive …
Source: Compounds That Help Protect Against Melanoma Skin Cancer
Adding these antioxidant rich compounds to your diet can improve your skin’s natural defenses:
Caffeic Acid: Found in spinach leaves, olive oil, apples, coffee, wine, and cabbage
Tannins: Contained in a variety of fruits and vegetables, nuts, coffee, and tea
Resveratrol: This type of stilbene is found in grapes, berries, and peanuts. Resveratrol helps to inhibit the over-production of melanin
Anthocyanins: Eat blackberries, bilberries, and honeyberries
EGCG: Epigallocatechin-3-gallate (EGCG) has an anti-proliferative effect on cancer cells. Green tea is a rich source of this cancer fighting compound
Quercetin: Protects against genetic alterations leading to irreversible carcinogenesis. Eating whole apples, including their skin, helps protect against harmful UV damage
Ursolic Acid: Holy basil tea contains ursolic acid which shuts down cancer growth and down-regulates the genes associated with cancer growth
Luteolin: A major anticancer flavonoid, luteolin is found in medicinal herbs like chrysanthemum flowers, as well as in fruits and vegetables including celery, parsley, broccoli, carrots, and cabbage
Plants offer an economical and effective way to improve a variety of skin problems such as sunburns, open wounds, and infections. Try the following natural remedies next time you find yourself in need of providing skin pain relief:
Vitamin D exposure is critical to the function of an endless number of life-essential processes. Vitamin D deficiency has been linked to a variety of skin ailments including psoriasis, dermatitis, scleroderma, and vitiligo which is a disease resulting in the loss of patches of skin pigmentation. Vitamin D is essential for healthy skin by promoting DNA repair, hormone responses with anti-carcinogenic abilities, and stimulating enzymes required for melanin production.
Our bodies are constantly burdened by chemicals in our environment. Even the “protective” sunscreens we slather ourselves with contain skin damaging toxins.
Titanium dioxide gives sunscreen its white appearance and is a microscopic metal that binds with impurities. Studies do not definitively conclude that titanium dioxide exposure to skin cells causes immediate cell damage but suggest thattitanium dioxide creates cellular changes and possibly abnormalities from long term exposure. This metal does cause an increase of inflammatory gene expression suggesting it is not as safe as retailers would like you to assume.
Another common toxin which promotes cancer growth is BPA (bisphenol A). BPA is an environmental toxin found in the water you are drinking from plastic bottles and contaminated food microwaved in plastic containers. Both the kidneys and liver aid in removing BPA from the body and are regularly exposed to toxic chemicals. Avoiding all use of plastic materials, especially for food and water storage, can limit your exposure to such carcinogens.
Along with the skin, the liver and kidneys are also major organs involved in converting vitamin D from sunlight and food. Vitamin D deficiency can result when toxic waste accumulates in these organs preventing its absorption and requiring detoxification.
Milk thistle contains a detoxifying agent known as silymarin. Silymarin promotes liver and kidney function and flushes toxins from the gastrointestinal tract. Preventing skin cancer growth is as safe and enjoyable as sipping on milk thistle tea. Also consider taking a supplement containing 200mg of milk thistle daily to cleanse your organs of environmental hazards.
I am a 55 year old female who has had recurrent skin cancer. I have previously had my Scc’s cut out by the Skin Specialist. Recently a lump on the front of my shoulder began growing rapidly a…
Source: Skin cancer stories
http://www.myhomeremedies.com/topic.cgi?topicid=261
I am a 55 year old female who has had recurrent skin cancer. I have previously had my Scc’s cut out by the Skin Specialist. Recently a lump on the front of my shoulder began growing rapidly and looked like my previous Scc’s. Worried about its rapid growth i tried to get an appointment with the Skin Specialist, but because it was near Christmas there were none available. I started researching home treatments, and came across an interesting article on using topical iodine. I started treatment immediately, and to my surprise 6 weeks later my cancer has disappeared completely. I applied the iodine with a small brush to the skin cancer at least 3 to 4 times a day until the cancer was dark brown. Layers of skin over the area will peel, just keep applying the iodine until the area is clear. Occasional stinging is normal and will subside. Do not cover the area unless you have to. The great thing is i have no scar, looks like nothing had ever been there.
I submitted the last post on my success with Lugol’s Solution for the treatment of my squamous cell carcinoma on the front of my shoulder. Once again i have had success removing a scc on my leg and forearm. This time i used a 7% iodine solution which i needed a prescription for from my Dr, and had it filled at my favourite compounding chemist. They post around Australia.
Paint with clear nail polish, repeat as necessary to keep the area covered until it peels off and shows healthy skin {About two weeks}
After 5 weeks of trials I can now confirm that iodine tincture actually works. During this period 3 separate layers of skin actually came off independently before the cancer was completely gone. In the past as stated I simply had them burned off with nitrogen but they always returned, hopefully this time they will stay gone.
Interesting side effect noticed is that after the nitrogen the skin on the back of the hands returned as wrinkled as ever (been in the sun 60+ years) but now, after the iodine, the treated patches which cover about half the hand are as smooth as a baby’s bum. If I hadn’t told everybody for years that wrinkles (and a broken nose) add character to a person I might just consider taking 3 baths a day in the stuff 🙂
As an Aussie I’ve suffered from this type of skin cancer on the back of my hands for years. Up till recently I simply went to the quack and he burned them off with Liquid nitrogen. Now i’m trying something I was told about long ago which is 7% solution iodine tincture 3 or 4 times a day and strangely enough it seems to be working. Hellish slow though compared with the nitrogen. Used to live next to a farmer that used the fruit of the Apple of Sodom (Solanum linnaeanum) on skin cancers around the eyes of his cattle and he swore it always worked but in their wisdom the West Aus Government declared this a noxious Weed and had it virtually eradicated. Strangely enough when it became almost impossible to find in the wild the gov gave a private company permission for ‘trial plots’ to test for medicinal properties. Also known as Afgan thistle, bitter apple, black-spined nightshade, devil’s apple, poison apple. Disclaimer…All remedy’s I have uploaded to this site are for historical purposes only as here under the ‘Therapeutic Goods Act’ I cannot even suggest someone try a bucket of water if their a**e is on fire.
I have been diagnosed and treated for sun-caused skin cancer, or the epidermal variety. This remedy is NOT for melanoma or basal cell cancer.
I was quite ill and weak from a chemical poisoning and all kinds of infection for 5 years. During that time, with my immune system so fragile, I could not tolerate the surgery required even for the simple graft I would need for the removal of the cancer on my nose. My homeopath recommended an ointment of stinging nettle, Urtica Urens, type.
I applied it several times a day, wore a hat and a band-aid and stayed out of the sun. In about 8 weeks, the open sore was healed and the redness gone.
I had other occurances that responded the same.
I have since successfully used the treatment on 8 other people. It worked on seven spots that appeared to be cancers and not on the eighth lesion which turned out to be a basal cell cancer.
The herb Urtica Urens is used to treat burns. I can only guess that the sun caused cancer begins on burn damaged skin. The herb seems to trigger burn healing even though cells have mutated into cancer. It is remarkable that so few people seem to know about this highly effective application.
I was using a common American made homeopathic ointment, but it was petroleum based and I am sensitive to that poison. I now have found a source in New Zealand, the Weleda Company, where you can purchase an ointment with a more inert base oil. It does contain propylene glycol, but is a very high quality potent creme, very effective.
I am so grateful to find a forum to reach people with this affordable and body friendly option.
I still have flare-ups and I avoid exposure always, but skin cancer is not a threat any more.
Glycoalkaloid ointment was developed in Australia (search for Curaderm) and is used there to remove basil cell and squamous cell skin cancers. You can purchase the ointment from http://www.drdavidwilliams.com called Skin Advantage. There is a book called One Answer to Skin Cancer that tells the whole story but it is out of print. Still available on Amazon from used booksellers. I have used this ointment and know others who have used it and it is very effective. It will do the job. It will also remove keretosis. The ointment will not affect healthy tissue.
When it comes to skin cancer, Big Pharma offers only topical chemo creams and surgery. The chemo creams often don’t work but often do cause ugly, painful side effects. Removing skin cancer tu…
When it comes to skin cancer, Big Pharma offers only topical chemo creams and surgery. The chemo creams often don’t work but often do cause ugly, painful side effects. Removing skin cancer tumors surgically usually results with tumors resurfacing sooner or later. Surgeries often leave ugly scars
However, there are inexpensive, effective, safe cures for curing skin cancer that are banned by the mainstream medical monopoly, which are not publicized by the mainstream media.
A relatively new remedy, BEC5, is a spin off from an Australian folk remedy for farm animals. It is available to anyone online. It uses the phyotonutrients extracted from eggplants. Clinical trials and anecdotal testimonies confirmed BEC5’s efficacy and safety on basal cell and squamous cell cancers.
Melanoma is the least common but most dangerous skin cancer with the highest morbidity rate. It can metastasize into internal organs. The maker and distributors for BEC5 make no claims for curing melanoma so far. But at least one person who made a homemade version that anyone can make claimed it cured his melanoma.
The homemade remedy involves a solution of vinegar and eggplant that extracts the same phyotonutrient glycocides and glycoalkaloids contained in BEC5 directly from the eggplant. The glycoalkaloids penetrate cancer cells selectively and destroy them. Normal cells are left alone.
This is an attempt at disclosing what others report cured their skin cancers. It’s purely educational and not meant as medical advice. Some of the anecdotal reports had their skin cancer diagnosed by MDs, with subsequent cures confirmed by MDs (1).
Some have used white vinegar, while others recommend raw organic apple cider vinegar. Get a medium sized eggplant and grind it up. Put that into a glass jar and fill it up with the vinegar. Place the jar into the refrigerator. After around three days with the white vinegar, the liquid should turn to a brownish gold color. That indicates it’s ready to use.
Apple cider vinegar is already a similar color, but three days seasoning in a refrigerator should be enough.
Apply it directly to tumors often with a cotton ball, or secure the soaked cotton onto the tumor with tape. Treatment may take a couple of weeks or more. Both commercial BEC5 cream and the homemade version also work on warts and other unhealthy skin conditions.
One user mentioned that according to his doctor (naturopath?), if the homemade procedure is painful, then it is melanoma that’s under attack. Many of these homemade remedy users were in Australia, where Dr. Bill Cham, MD, PhD, found out about the Devil’s Apple plant used by veterinarians and farmers to cure skin cancers on farm animals.
Dr. Cham claims a high, safe cure rate with non-melanoma skin cancers from his own clinical testing. Detractors claim there are no published reports in medical journals. That could be due to the fact that Dr. Cham had to go it alone testing his cream on skin cancer patients in the UK hospital system. Dr. Cham demonstrates and explains his BEC5 cream in a video (2).
Mainstream medicine always attacks natural non-pharmaceutical cures and their sponsors. However, a well known physician, Dr. Jonathan Wright MD, founder of the holistic Tahoma Clinic in the Seattle Washington area, backs up Dr. Cham. Dr. Wright sells BEC5 creams and explains how it works and how it was tested within the UK system (3 – 4).
Dr. Cham determined that the same curative glycoalkaloids were available in eggplant. From there he went on and pioneered the development of BEC5 in London.
Sources for this article include:
Original source for this article http://www.naturalnews.com/027506_eggplant_skin_cancer.html
The community of beneficial bacteria that live in our intestines, known as the gut microbiome, are important for the development and function of the immune system. There has been growing evidence t…
The community of beneficial bacteria that live in our intestines, known as the gut microbiome, are important for the development and function of the immune system. There has been growing evidence that certain probiotics—therapies that introduce beneficial bacteria into the gut—may help alleviate some of the symptoms of intestinal disorders such as Crohn’s disease. By studying the interplay between genetic risk factors for Crohn’s and the bacteria that populate the gut, researchers at Caltech have discovered a new potential cause for this disorder in some patients—information that may lead to advances in probiotic therapies and personalized medicine.
The results were published online in the May 5 edition of the journalScience.
Previously, scientists had found that patients with Crohn’s disease often exhibit alterations in both their genome and their gut microbiome—the diverse collection of bacteria that reside in the intestine. More than 200 genes have been implicated as having a role in the susceptibility to Crohn’s. For years, researchers in the field have believed that these are genes that normally function by sensing pathogenic bacteria and deploying an immune response to kill the unwanted microbes; when these genes are defective, the pathogenic bacteria survive, multiply in the gut, and lead to disease.
“While we believe that all of that is true, in this study we were curious to see if some of the genes that are important in sensing pathogenic bacteria may also be important in sensing beneficial bacteria to promote immune health,” says the study’s first author, Hiutung Chu, a postdoctoral scholar in biology and biological engineering at Caltech. “Typically, the signals from these beneficial commensal microbes promote anti-inflammatory responses that dampen inflammation in the gut. However, mutations in genes that sense and respond to pathogenic bacteria would also impair the response to the beneficial ones. So it’s kind of a new spin on the existing dogma.”
To figure this out, Chu and her colleagues in the laboratory of Sarkis Mazmanian, the Luis B. and Nelly Soux Professor of Microbiology and a Heritage Principal Investigator, designed several experiments to study how genetic mutations might interrupt the immune-enhancing effects of a known beneficial bacterium,Bacteroides fragilis. The researchers tested their new theory by using B. fragilis to treat mice that had nonfunctional versions of two genes known to play a role in Crohn’s disease risk, called ATG16L1 and NOD2.
The researchers found that if just one of these two genes was absent, the mice were unable to develop disease-protective immune cells called regulatory T cells in response to B. fragilis—and that even after treatment with B. fragilis, symptoms in an ATG16L1-deficient mouse model of intestinal disease remained unchanged.
Chu and Mazmanian then obtained blood samples from both healthy patients and patients with Crohn’s disease at the Cedars-Sinai Medical Center in Los Angeles. “We could see that certain patients’ immune cells responded to Bacteroides fragilis, while immune cells from other patients didn’t respond at all,” Chu says. “Because the cells from Cedars had already been genotyped, we were able to match up our results with the patients’ genotypes: immune cells from individuals with the protective version of ATG16L1 responded to the treatment, but cells from patients who had the mutated version of the gene showed no anti-inflammatory response to B. fragilis.”
Mazmanian says the results suggest that the faulty versions of these genes may cause Crohn’s disease in two different ways: by being unable to assist in destroying pathogenic bacteria and by preventing the beneficial immune signals usually elicited by “good” bacteria. “What Hiutung has shown is that there are specific bacteria in the human microbiome that appear to utilize the pathways that are encoded by these genes—genes normally involved in killing bacteria—to send beneficial signals to the host,” he says.
This work reveals the important relationship between the genome and the microbiome—and it may also one day be used to improve the use of probiotics in clinical trials, Mazmanian says. “For example, our previous work has suggested using B. fragilis as a probiotic treatment for certain disorders. What this new study suggests is that there are certain populations that wouldn’t benefit from this treatment because they have this genetic predisposition,” he notes. “Right now, clinical trials don’t do a good job of identifying which patients might respond best to treatment, but our experiments in mouse models suggest that, conceptually, you could design clinical trials that are more effective.”
The research described in the paper, “Gene-Microbiota Interactions Contribute to the Pathogenesis of Inflammatory Bowel Disease,” was funded by the National Institutes of Health, the Cedars-Sinai F. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, the Lupus Research Institute, the European Union, the Crohn’s and Colitis Foundation of America, the Leona M. and Harry B. Helmsley Charitable Trust, and the Heritage Medical Research Institute.
In addition to Chu and Mazmanian, other Caltech coauthors include former graduate students Arya Khosravi (PhD ’14) and Yue Shen (PhD ’12); research technician assistants Indah Kusumawardhani and Alice Kwon; and Wei-Li Wu, a postdoctoral scholar in biology and biological engineering. Coauthors from other institutions include: Anilton Vasconcelos and Peter Ernst from UC San Diego; Larissa Cunha and Douglas Green from St. Jude Children’s Research Hospital in Memphis; Anne Mayer, Amal Kambal, and Herbert Virgin from the Washington University School of Medicine in St. Louis; Stephan Targan and Dermot McGovern from Cedars-Sinai Medical Center; and Ramnik Xavier from Harvard Medical School.
In the ongoing hustle and bustle of our intestines, where bacteria and food regularly intermingle, there is another substance that, to the surprise of researchers, has been found to rapidly change:…
Source: Dietary Fiber and Microbes Change the Gel That Lines Our Gut
In the ongoing hustle and bustle of our intestines, where bacteria and food regularly intermingle, there is another substance that, to the surprise of researchers, has been found to rapidly change: the gel that lines the gut. A new Caltech study is the first to show how the structure of this gut gel, or mucus, can change in the presence of certain substances, such as bacteria and polymers—a class of long-chained molecules that includes dietary fiber.
The work, to be published online the week of June 13 in theProceedings of the National Academy of Sciences, could lead to the development of new drugs or diets for intestinal conditions such as irritable bowel disease.
Our intestinal tracts are lined with a mucus gel that acts as a protective barrier between the insides of our bodies and the outside world. The gel lets in nutrients and largely blocks out bacteria, preventing infections. It also regulates how some drugs are delivered elsewhere in our bodies.
Researchers had previously studied how the gel can be damaged, for instance when bacteria feed on the gut’s lining. The Caltech study is the first to look at the structure of the gel and how it morphs in the presence of other substances naturally found in the gut.
Performing their experiments in mice, the team tested the effects of polymers, which include dietary fiber as well as therapeutics such as medicines for constipation. The researchers fed some mice a diet rich in polymers and others (the controls) a polymer-free diet. Using a technique called confocal reflectance microscopy they measured the thickness of the gut gel and the degree to which the gel was compressed as a result of the consumed polymers. Mice given a high-polymer diet, they found, had a more compressed gel layer.
“The gel is like a sponge with holes that let material through,” says the paper’s lead author, Sujit Datta, a postdoctoral scholar in the laboratory of Rustem Ismagilov, Ethel Wilson Bowles and Robert Bowles Professor of Chemistry and Chemical Engineering. “We are seeing that polymers, including dietary fiber, can compress the gel, potentially making the holes smaller, and we think that this might offer protective benefits,” Datta adds.
In addition, the researchers applied different kinds of polymers—including dietary fibers like pectin, found in apples—directly to the gel lining to test its response. All of the polymers tested compressed the gel layer.
“It’s too early to draw any conclusions, but it may be that eating an apple a day will affect the shape of the lining in your gut,” says Asher Preska Steinberg, a Caltech graduate student and coauthor of the study.
The researchers also found that dietary fiber and gut bacteria—which are part of a community of microorganisms collectively known as gut microbiota—can work together to influence how the gut gel changes shape. They performed the same polymer/fiber experiments in germ-free mice, which are mice carefully raised to not have any bacteria in their gut. The results showed that the polymers compressed the gut gels of these germ-free mice to a greater degree. This implies that species of bacteria in our gut that are known to break down polymers can weaken the compressing effect.
“We previously thought of the gel as a static structure, so it was unexpected to find an interplay between diet and gut microbiota that rapidly and dynamically changes the biological structures that protect a host,” says Ismagilov.
Both dietary fiber and certain gut microbes have been linked to good health. Fiber has been shown to lower cholesterol and regulate blood sugar levels—factors in heart disease and diabetes, respectively. Meanwhile, some bacteria, including the good “probiotics,” can help treat digestive disorders and may even play a beneficial role in mental health. For instance, a separate Caltech-led study found that probiotics can alleviate autism-like behaviors in mice—a finding that could potentially lead to new therapies for the disorder in humans.
The entire collection of bacteria in our gut can include 1,000 different species or more and weigh a total of three pounds. Exactly how these microscopic organisms influence our health, for good and bad, is an area of active research with many unanswered questions. The White House recently announced the National Microbiome Initiative, with federal funding worth $121 million, to investigate the mysteries of microbes not only living in our bodies but all over the planet. In addition, more than 100 nonfederal agencies have pledged money and support toward researching microbial communities.
“Our study gives biologists and scientists studying diseases of the gut something else to think about,” says Datta. “Now they can take the structure of the gut mucus, and how it responds to its environment, into account.”
This research was funded by the Defense Advanced Research Projects Agency (DARPA) and National Science Foundation.
The study was carried out by researchers from 25 different international institutions, led by Newcastle University in the UK, and was funded by the Alfred Deakin postdoctoral research fellowship and the UK Medical Research Council.
The study was published in the peer-reviewed British Medical Journal (BMJ) on an open-access basis meaning it is free to read online.
While The Guardian gave a good overview of the science behind the study, the Mail Online confused the ability to lose weight with the chances of gaining weight and its headline seemed to take pleasure in pointing a finger at obese people: “It’s not in the genes! You can’t blame your DNA for piling on the pounds”.
Although the Mail’s story later made clear the FTO gene variant does in fact increase the chances of “piling on the pounds”, the tone is set by the headline.
The Telegraph decided the research showed there were “No excuses not to slim” and that carriers of the gene variant will be “bang out of excuses” for their weight.
This was a systematic review and meta-analysis of randomised controlled trials. This type of study is sometimes called the “gold standard” for research, because it pools data from the best quality studies that compare how people respond to different types of treatment. However, it is reliant on the quality of the underlying studies.
Researchers looked for all randomised controlled studies of weight loss treatments carried out in overweight or obese adults, which had information about people’s FTO genotype. They asked the study authors to provide data on the individual patients, not just the summarised published data. They then pooled the data from the studies, and ran a number of tests for potential bias or confounding factors.
They calculated whether there was a difference in the measures of weight of people with and without the FTO variant; whether treatment response varied by FTO variant, and whether this was affected by factors including age, sex, initial weight and ethnic background.
They included studies with measures of body mass index (BMI), waist circumference and body weight. They excluded three studies which they’d wanted to include, but where they could not get individual patient data. They searched only for studies published with an English language abstract, which means some foreign language studies might have been missed.
The researchers found no significant differences between weight loss outcomes in people with and without the FTP variant, regardless of the type of weight loss treatment used. This applied to all measures of weight loss – waist circumference, BMI and body weight – and to all lengths of treatment and study follow up (from eight weeks to three years).
The researchers said their results showed that “people who carry obesity risk FTO genotypes respond equally well to weight loss treatment.”
They say their findings show the genetic predisposition to obesity associated with the FTO variant “can be at least partly counteracted through dietary, exercise, or drug-based weight loss interventions.”
There’s been a lot of interest in how our genes interact with our environment and lifestyle when it comes to body weight.
The discovery that certain gene variants are associated with a higher chance of becoming overweight or obese has been taken by some to mean that people’s weight is genetically determined. That could lead to people fearing there’s no point in them trying to lose weight, but this study shows that isn’t the case.
The results sound like good news for anyone who wants to lose weight for health reasons. Diet and exercise programmes can help, and even if you carry the “obesity gene” variant, these results suggest you have as much chance of success as anyone else.
This is particularly important for the increasing numbers of adults who are overweight or obese. According to the 2014 Health Survey for England, 62% of adults were either overweight or obese and 23% were obese.
There are a few points to bear in mind:
The study was carried out by researchers from the Department of Twin Research and Genetic Epidemiology at King’s College London in the UK, the Department of Microbiology and the Department of…
The study was carried out by researchers from the Department of Twin Research and Genetic Epidemiology at King’s College London in the UK, the Department of Microbiology and the Department of Molecular Biology and Genetics at Cornell University, and the University of Colorado in the US, and the Max Planck Institute for Developmental Biology in Germany.
It was funded by the US National Institutes for Health (NIH), the Cornell Center for Comparative Population Genomics, the Wellcome Trust, the European Community’s Seventh Framework Programme, the European Research Council, and the National Institute for Health Research (NIHR).
The authors declared no conflicts of interest.
The study was published in the peer-reviewed journal, Genome Biology. It is open access, so it’s freely available to read online.
The media reported the story accurately, with the BBC acknowledging that, although there is a link between bacteria in human faeces and levels of obesity, there is no known explanation yet.
This was a cross-sectional observational study carried out on healthy sets of twins.
It aimed to explore the association between the bacteria present in human faeces and obesity.
This type of study can’t prove cause and effect, but is useful for looking at associations between risk factors and outcomes.
So while this study doesn’t prove that bacteria found in human faeces cause visceral fat, it does show there is a relationship between the two.
Researchers studied health volunteers involved in the TwinsUK Adult Twin Registry. Data on body fat was collected from a sample of 3,666 twins.
They looked at the links between bacteria found in faeces and six different measures of body fat.
The sample was mostly of European descent, and the average age was 63.
Faeces samples were collected from 1,313 individuals, and the bacteria in these investigated. Almost all those sampled were female.
The information from study participants on the bacteria present in their faeces was compared with body fat levels.
The six body fat measures included three of visceral fat, two of body fat distribution, and one of body mass index (BMI).
Excess visceral fat in particular is a risk factor for cardiovascular disease and metabolic disease, such as type 2 diabetes.
All but one measure of obesity were significantly associated with a lack of diversity of bacteria in the faeces.
However, the association was strongest for visceral fat, which is found around the internal organs and is a bigger risk factor for cardiovascular and metabolic diseases.
Researchers found the higher the diversity of bacteria in faeces, the lower the level of visceral fat.
The reverse was also shown: the less diverse the bacteria, the more likely participants were to have more visceral fat.
Visceral fat was found to be highly heritable (relative risk [RR] = 0.70, 95% confidence interval [CI] = 0.58 to 0.74). This was true even when adjustments for body mass index (BMI) were made.
Dr Michelle Beaumont, lead author of the study from the Department of Twin Research and Genetic Epidemiology at King’s, said: “This study has shown a clear link between bacterial diversity in faeces and markers of obesity and cardiovascular risk, particularly for visceral fat.
“However, as this was an observational study we cannot say precisely how communities of bacteria in the gut might influence the storage of fat in the body, or whether a different mechanism is involved in weight gain.”
Senior author, Dr Jordana Bell, also from the Department of Twin Research and Genetic Epidemiology, said: “There is a growing body of evidence to suggest that gut bacteria may play a role in obesity, and a number of studies are now exploring this in more detail.
“Further scientific investigation is needed to understand how precisely our gut microbes can influence human health, and if interventions such as faecal transplants can have safe, beneficial, and effective impacts on this process.”
This cross-sectional study found a strong association between visceral fat and bacteria diversity in faeces.
The use of measures other than BMI was one of this study’s strengths, as BMI doesn’t reveal whether weight is from fat tissue or muscle.
The findings suggest that body fat levels may be passed down through families.
However, this is early research and there are a number of things to consider:
It’s important to eat a balanced diet and have an active lifestyle to maintain a healthy weight.
Skin cancers are cancers that arise from the skin. They are due to the development of abnormal cells that have the ability to invade or spread to other parts of the body.[1] There are three main ty…
Source: Melanoma has one of the higher survival rates among cancers
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