Blood test to spot lung cancer relapse hailed as ‘new hope’

Scientists screened their blood for circulating tumour DNA - bits of DNA that had "broken off" from a tumour
Scientists screened their blood for circulating tumour DNA – bits of DNA that had “broken off” from a tumour 

Scientists have developed a blood test which spots the relapse of lung cancer in patients, up to a year before the disease can be detected by CT scans and X-rays.

The groundbreaking TRACERx study, funded by Cancer Research UK, identified the cause of relapse of the disease and how it spreads, in a discovery that could lead to earlier treatment for patients.

By analysing tumours from 100 lung cancer patients, researchers at medical research centre Francis Crick Institute found that those containing a higher proportion of “unstable chromosomes” – those which cause genetic chaos and allow the tumour to evolve – were four times more likely to encounter a relapse or die within two years.

 Genetically diverse tumours are harder to treat as they are more likely to spread and become drug-resistant.

In a study using 96 of those 100 patients, scientists screened their blood for circulating tumour DNA – bits of DNA that had “broken off” from a tumour – in order to uncover defects present in the patient’s cancer.

They used this information to analyse blood samples from 24 patients who had undergone surgery, and were able to identify more than 90% of cancer cases likely to return, up to a year before other clinical methods, such as CT scans or an X-ray, could detect the illness.

Lung cancer is the leading cause of cancer death among men and women in the UK, causing more than 20% of cancer deaths, according to Cancer Research UK.

Scientists also compared levels of tumour DNA in patients’ blood before and after post-surgery chemotherapy in the study, which was published in science journal Nature.

 They found that the cancer returned when levels of tumour DNA in the blood were not reduced after the treatment, showing that the tumour had become partially resistant to the chemotherapy.

The findings could pave the way for the development of new drugs to target resistant parts of lung cancer tumours.

Dr Christopher Abbosh, lead author of the study, said: “In the future patients could be offered personalised treatments that target parts of the cancer responsible for relapse following surgery.

“Using circulating tumour DNA, we can identify patients to treat even if they have no clinical signs of disease, and also monitor how well therapies are working.

“This represents new hope for combating lung cancer relapse following surgery, which occurs in up to half of all patients.”

TRACERx is the first of its kind to trace the evolution of the cancer in real time, from diagnosis to its death.

Professor Karen Vousden, Cancer Research UK’s chief scientist, said: “These findings could also help us to identify how lung cancers respond to therapy, building a bigger picture of the disease and potentially pointing the way to developing new treatments and, crucially, saving more lives.”

What Does Cancer Smell Like?

On a lab bench in Philadelphia sits a tiny box lined with nearly invisible nanotubes and gold. A clear plastic pipe runs through it, and a thicket of pins, each sprouting a red or blue wire, protrudes from its end. As air from the pipe wafts over the nanotubes, electrical signals surge out of the box along the wire threads. The whole apparatus is situated near a vial of blood, “sniffing” the air above it through the pipe.

The box, an electronic nose, is a key part of a theory being explored by George Preti, an organic chemist at the Monell Chemical Senses Center, and an interdisciplinary team that includes physicists and veterinarians at the University of Pennsylvania. Preti is an expert on human odors, having studied them for more than 40 years. He has sniffed — both with machines and with his nose — breath, sweat and other secretions in search of answers about why we smell the way we do. This latest project seeks to answer a question others might have never thought to ask: Does ovarian cancer have a smell?

In modern cancer medicine, doctors tend to rely on advanced imaging techniques and the detection of lumps. The widely acknowledged problem with these methods, though, is that by the time doctors have reason to order a scan or feel something, it’s often too late. Ovarian cancer has usually spread to other organs by the time it’s detected. If it is caught early — which happens only 15 percent of the time, often by accident when doctors are looking for something else — 92 percent of patients live for at least five years. But when it’s caught late, that rate drops to 27 percent. Scent might be a way to get there sooner.

Discovering earlier and better markers for all kinds of cancer, especially in blood, is a priority, said Dr. J. Leonard Lichtenfeld, deputy chief medical officer of the American Cancer Society. Ovarian cancer already has a blood test that has turned out to be not as useful as hoped — giving out both false positives and negatives. A smell-based test would need to perform better.

Diseases can subtly alter people’s fragrance. In the normal course of metabolism, thousands of waste products are swept out in our breath, blood and urine, or simply released into the air above the skin. Metabolic disorders, like diabetes, interfere with the way the body breaks down nutrients and thus make that exhaust especially stinky. People with phenylketonuria (or PKU) tend to smell musty. A faulty or missing digestive enzyme makes people with trimethylaminuria (or TMAU) smell fishy. Untreated diabetics can smell like nail-polish remover: Unable to get energy from sugar, their bodies burn fat for fuel and release acetone as a by-product. (These scents don’t always smell bad; there exists a disorder known as “maple syrup urine disease.”) For Preti, originally from Brooklyn, this makes a subway ride unusually informative. “I often tell people I work with, ‘I bumped into the guy with isovaleric acidemia today.’ ”

Cancer cells, though they don’t alter human metabolism overall, can have altered metabolisms themselves. That means the substances they release could differ from those generated by healthy cells. This idea has been around for decades, but only very recently have biochemical and sensor technology advanced to the point where we can develop portable, hand-held sniffing machines.

Electronic noses have the potential to detect even very small amounts of molecules — but they need to be programmed to look for specific signs wafting up from patient samples. To do that, A.T. Charlie Johnson, a physicist and collaborator of Preti’s at Penn, has the electronic nose sniff blood samples from both sick and healthy patients. As the air passes through the tube, molecules from the samples alight on strands of sticky DNA attached to the carbon nanotubes, changing the electrical signals running out of the box. The team can look for patterns in the signals and use the difference — if there is one — between cancer samples and healthy samples to create an odor-based ovarian cancer test. (Preti is also attempting to identify the specific molecules present in ovarian cancer sufferers’ blood using a much larger machine called a gas chromatograph-mass spectrometer.)

A work in progress, the electronic nose is, for now, an example of how modern medicine can look for answers in unusual places. The impetus that finally pushed Preti and his team to seriously investigate the possibility of cancer detection by smell traces its roots to a dog. In 1989, a letter published in The Lancet reported that a woman had come into the doctor’s office to have a mole looked at. She hadn’t noticed it until her collie-Doberman mix began to sniff the spot intently — even through her pants — and tried to bite it off when she wore shorts. The mole turned out to be an early-stage malignant melanoma, inspiring researchers to test whether dogs, whose smell machinery is at least 10,000 times as sensitive as ours, can tell healthy samples from cancerous ones.

The results from the dog tests have been inconclusive, but to Preti, who has mulled the idea that hidden cancers could be detected from smell molecules since the 1970s, they suggested that there was a real possibility for a new diagnostic. “We think that they’re present very early in the carcinoma process,” Preti said of the scents. “The main question is: Can we be as sensitive as the dogs in picking these things up?”

107 studies published in a cancer journal have just been retracted 

In a massive cleanup, 107 articles have just been retracted from the open-access cancer research journal Tumor Biology.

“After a thorough investigation we have strong reason to believe that the peer review process was compromised,” writes editor-in-chief Torgny Stigbrand in the retraction notice.

Peer review is one of the golden standards that help sort the wheat from pseudoscientific babbling, making the process an integral part of academic publishing.

But there is massive publishing pressure in the scientific community, and with about 2.5 million papers published each year, some of those inevitably end up cutting corners. In this case, the transgression was what’s known as ‘fake peer review’.

Scientists are often asked to provide recommendations for potential reviewers of their work. While that sounds like an obvious invitation to cheat, it actually makes sense when the work is really specific and few others do similar research.

But it’s easy to game the system by providing a fake reviewer email address, impersonating an actual researcher and sending the journal a super-positive review in their name.

“The articles were submitted with reviewer suggestions, which had real researcher names but fabricated email addresses,” Springer representative Peter Butler told Yan Jie at Sixth Tone.

It’s a pretty massive lot of retractions all at once, but a few of the big academic publishers have been sweeping their portfolios for potential breaches, including fake peer review, plagiarism, data fabrication and more.

This time, the 107 papers were published between 2012 and 2016, and most were authored by Chinese researchers, although that doesn’t automatically reflect poorly on their scientific work.

Chinese scientists are known to rely on third-party agencies that provide language editing services, which give the papers a polish, increasing the chance of getting accepted. But it’s possible those companies have also done the authors a massive disservice.

“There is some evidence that so-called third-party language-editing services play a role in manipulating the reviewing process,” an unnamed Springer spokesperson told Cathleen O’Grady at Ars Technica.

While we don’t have details on whether any of the authors had a hand in contributing fake reviews, experts are willing to chalk at least some of the breaches up to those third-party companies, some of which are known to operate unethically.

“If the authors didn’t realise that this is what the editing company was doing, then I feel the authors should have a fair chance,” Elizabeth Wager, editor of the journal Research Integrity & Peer Review, told Ars Technica.

“There’s probably nothing wrong with the research; it just hasn’t been peer reviewed.”

China is one of the biggest scientific contributors in the world, producing more than 300,000 papers every year. With strides in nuclear fusion and revolutionary CRISPR experiments, Chinese researchers are major players in the international research scene.

But any large industry gets its share of scandals. For example, just last year news broke that 80 percent of data in Chinese clinical trials had been fabricated.

As for Tumor Biology, the journal actually moved from Springer to SAGE late last year, and the new publisher was made aware of the investigation into potential peer review fraud. The journal is run by the International Society of Oncology and BioMarkers.

“The society were open about the past instances of peer review fraud, and as part of the relaunch they wanted to address the underlying reasons,” a SAGE spokesperson told Alison McCook at Retraction Watch.

“As part of their transition to a new publisher, the Tumor Biology editorial team have already introduced new robust peer review practices expected from all SAGE journals.”

Every single person who has cancer has a pH that is too acidic. Here is the easiest way to check your pH Balance.

Our body relies on an alkaline environment in order to work efficiently and remain healthy.

When in an alkaline state, the immune system, healthy bacteria, chemical reactions, and cells within the gut work properly. 

If your body becomes too acidic, many body systems will fail to perform normally.

In recent scientific findings, when someone has an acidic gut, or acidosis, they are increasingly susceptible to the diseases below:
▪ Weakened immunity
▪ Premature aging
▪ Osteoporosis, weak or brittle bones, fractures and bone spurs.
▪ Joint pain, aching muscles and lactic acid buildup
▪ Low energy and chronic fatigue
▪ Mood swings
▪ Obesity, slow metabolism and inability to lose weight
▪ Chronic inflammation
▪ High blood pressure
▪ Weight gain, obesity and diabetes
▪ Bladder and kidney conditions, including kidney stones
▪ Slow digestion and elimination
▪ Yeast/fungal overgrowth

Prescription and over the counter drugs, alongside toxic chemicals can lower our pH level. That is what causes all these side effects and explains their inefficiency. When the body’s pH level is below 6.4, it messes up assimilation of minerals, vitamins, food supplements as well as digestion.

It makes the body more vulnerable to harmful bacteria, as acid reduces the ability to detox the body from heavy metals, ability to fix broken cells, reduces the production of energy, making the body vulnerable to illnesses and lethargy.

Scientific research has found that, disease isn’t able to survive in an alkaline environment. However, it was discovered that candida, mold, fungus, yeast, bacteria and cancer cells rely heavily on an acidic and low pH environment.

An acidic environment is primarily caused by an acid-forming diet, toxic overload, emotional stress, nutritional and oxygen deficiencies. Then, our bodies work to make up for the loss by using alkaline stored up in our body, leading to chronic illnesses.

 Having little to no minerals in your diet can lead to build up of acid in cells. When this happens, your body is vulnerable to pain, fibromyalgia, lupus, arthritis, lupus and MS. Interestingly, cancer isn’t able to last in an alkaline environment, meaning the heart will never have cancer due to its high oxygen and pH levels.

When there is no oxygen, glucose goes through a process of fermentation producing lactic acid. As a result, the pH levels in cells drops.

 An example, urine and saliva of patients with terminal cancer can over between 4.0 and 5.5. From Keiichi Morishita, Hidden Truth of Cancer, “In 1964, only 1 person in 214 contracted cancer. Today it is 1 in 3 females and 1 in 2 males.

The determining factor between health and disease is pH. It is not uncommon for the average American to test between 4 pH and 5 pH.”

How To Check Your pH Balance

 You can test your levels at home, as it is simple and quick to do. Your pH levels can be tested during any part of the day. The best time though, is right when you wake up in the morning. Aim for a pH level between 6.5 and 7.5 for your urine.

Saliva pH should be in the same pH level as urine. Best testing time for saliva is two hours after eating.

Before spitting on the strip, fill your mouth up with spit and swallow a couple times to clean your spit. In your dietary routine, be sure to strive for a 70:30 ratio of alkaline-rich foods. Also, manage your stress levels by practicing meditation and deep breathing exercises, even yoga will help. Drink lots of water and eat your vegetables to eliminate acid.

Early Clinical Trial Shows ‘Cancer Vaccines’ Can Protect Humans From Tumours 

Cancer comes in many different forms, and it is not unusual for diagnosed patients to endure multiple kinds of treatments before one that is effective against their particular form of cancer is found.

If it takes too long for doctors to find the right treatment, the consequences can be fatal.


The severity of cancer has fuelled physicians and scientists from all walks of life to explore any possible solution, including those that seem natural to those that may at times seem unconventional.

Well, researchers are now taking vaccines, which typically target viruses and bacteria, and reworking them to zero in on the patient’s specific cancer cells.

Physicians and scientists led by Catherine Wu at the Dana-Farber Cancer Institute in Boston just presented their results of their new cancer therapy to the American Association for Cancer Research (AACR) in Washington, DC.

Their personalised vaccines have prevented early relapse in 12 patients with skin cancer, while also boosting patient immunity when combined with a cancer drug.

While earlier cancer vaccines targeted a singular cancer protein found ubiquitously among patients, these personalised vaccines contain neoantigens, which are mutated proteins specific to an individual patient’s tumour.

 These neoantigens are identified once a patient’s tumour is genomically sequenced, providing physicians with the information they need to pinpoint unique mutations.

Once a patient’s immune system is provided a dose of the tumour neoantigens, it can activate the patient’s T cells to attack cancer cells.

Unlike previous attempts towards cancer vaccines, which did not produce conclusive evidence in halting cancer growth, Wu’s team made their personal vaccine much more specific to each patient’s cancer, targeting about 20 neoantigens per patient.

The vaccines were injected under the patients’ skin for a period of five months and indicated no side effects and a strong T cell response.

All of Wu’s patients who were administered the personal vaccine are still cancer-free more than 2.5 years after the trial.

However, some patients with an advanced forms of cancer also needed an some extra punching power to fend off their diseases.

Two of Wu’s patients who did relapse were administered an immunotherapy drug, PD-1 checkpoint inhibitor, in addition to the personalised vaccine.

Working in conjunction with the enhanced T cell response from the vaccine, the drug makes it difficult for the tumour to evade the immune cells. The fusion of the two therapies eliminated the new tumours from both patients.

But we can’t get too excited yet. While these results are promising, the therapies are relatively new and require much more clinical testing.

Many physicians around the world are working together to test the potency of neoantigens in order to verify if the vaccine works better than current immunotherapy drugs over a sustainable period of time.

Personalised vaccines are costly and take months to create, a limiting factor in providing care to patients with progressing cancers.

Still, this study is an encouraging sign for many oncologists who are interested in using the immune system to fight cancer.

More than a million new patients are diagnosed with cancer each year in the U.S. alone, and even in situations where the cancer is treatable, the available chemotherapy agents themselves can be very toxic.

If proven safe and effective, this personalised cancer vaccine could give patients around the world hope for powerful treatment with fewer side effects.

When Your Doctor Suggests Regular Mammograms, This Is What You Need To Say Back

Dr. Ben Johnson: I wrote a book for women, The Secret of Health Breast Wisdom because we, as a medical society, are giving women breast cancer with our demanding that they get mammograms. Mammograms cause breast cancer. Period. So mammograms are not healthy for women. Women should not be getting routine mammograms. That’s crystal clear, published in the peer review literature.


And yet today, if a woman went to her gynecologist or family doc, she would have this shoved down her throat, extreme coercion to get this mammogram that is causing breast cancer. It’s not saving lives. You have a 4% increased risk of dying if you get mammograms, period.

Ty Bollinger: So the detection technique that we’re using, the primary technique that we use to detect breast cancer, is causing breast cancer.

Dr. Ben Johnson: Absolutely, it’s a terrible test; you know smashing women’s breasts and then irradiating with cancer-causing radiation. And then it’s so insensitive. For women under 50, it’s only like 52% effective, sensitive. That means 52 is pretty close to 50, right?

Ty Bollinger: Yeah.

 Dr. Ben Johnson: So about half. That means that half the women that have breast cancer, it would not detect their cancer. That’s a terrible test. And so there are much better tests. And yet this is what’s still being crammed down women’s throats today. Terrible test causes breast cancer.

Ty Bollinger: And it doesn’t detect, it detects 50% and causes cancer. You said there were better options. What are better options there for detecting breast cancer?

Dr. Ben Johnson: Well there’s two better options. If you’ve got a lump, if you think you’ve got something, ultrasound is great. It’s a test of anatomy. Mammograms are tests of anatomy. Ultrasounds are tests of anatomy. MRIs are tests of anatomy. So if you’ve already got a lump, you want a test of anatomy.

So, that would be like an ultrasound because they can see the lump, they can see its consistency. They can see where there’s calcium in it. And they can look at blood flow because tumors are going to have increased blood flow. So, for instance, a sensitivity of ultrasound is up around 80%. It’s much higher than mammograms. And the sensitivity is higher too.

But if you’re looking for prevention, if you’re talking about screening, there’s really only one device out there, and that is thermography. An infrared thermal camera. Nothing touches the lady. Nothing smashes her breasts. There’s no cancer causing radiation.

 As we sit here, we are omitting heat in the spectrum called infrared. There’s infrared, visual, and ultraviolet. So this is the infrared spectrum of light, which our eyes don’t see, but which is very detectable by the camera. The military developed this so that they could see people sneaking at them at nighttime and so that they could shoot down missiles and things because they’re producing heat.

Ty Bollinger: Sure, like night vision goggles.

Dr. Ben Johnson: There you go. Night vision goggles are infrared goggles. So we use it as a medical application to detect hotspots in the breast.

Well long before there was a tumor there, there were cancer cells. Probably 8 to 10 years before there was a tumor, there were cancer cells starting to grow. Two cells, four cells, 16 cells, 144 cells, etc. It takes about eight years until you get to about a centimeter in size for a mammogram or an ultrasound to detect it. Well, that’s too late. Because of that one-centimeter tumor, about five-sixteenths of an inch, less than half an inch, is about one billion cells.

When you get to one billion cells, cancer has already eroded into the lymphatic system and the venous system, and it’s shedding cancer cells all through the body. So that’s why mammograms—one of the many reasons mammograms don’t save lives,
it is NOT early detection. That’s one of the little lies they’ve propagated along. “Early detection saves lives. Get your mammogram today.”

Ty Bollinger: Right.

Dr. Ben Johnson: Well, that statement’s true. Early detection does save lives. It’s just that mammography is not early detection; it’s too late. And then the cancer-causing radiation. So the long and the short is you’re causing much more breast cancer with mammograms than you are detecting.

The Truth About Cancer

The Truth About Cancer

The Truth About Cancer is committed to ending the cancer pandemic once and for all. Every single day, tens of thousands of people, just like you, are curing cancer (and/or preventing it) from destroying their bodies.

They are dedicated to helping others take matters into their own hands by educating them on real prevention and treatments.


IIT Madras scientists discovers how inexpensive aspirin might be killing cancer cells

For more than three years, word has been going around among scientists that aspirin, the inexpensive painkiller that is also given to heart-disease patients, can kill cancer cells. However, they did not know how, until now.

Recently, a team of scientists from the Indian Institute of Technology – Madras, has discovered how this non-steroidal anti-inflammatory drug terminates cancer cells.

Repretentational Image

More details about the study:

  • The study was published in peer-reviewing journal Scientific Reports
  • It found that aspirin targeted malignant cells which are high in a protein called voltage-dependent anion channel (VDAC)
  • “The drug induces high levels of calcium ions in the mitochondria of the cancer cells. Elevated levels of calcium prevent mitochondria from breaking down food into energy. Aspirin prevents this energy production and releases toxic substances that kill the cell,” said IIT-M Professor of Biotechnology Amal Kanti Bera

Stats on cancer cases in India

  • It is estimated by cancer registries that 14.5 lakh Indians live with the disease
  • Every year, more than seven lakh new cases are registered and 5.5 lakh die of cancer
  • An estimated 71 per cent of all cancer-related deaths occur in the age group 30-69 years
  • On an average, cancer treatment costs Rs 1.75 lakh for a patient. The cost may go up depending on the type and stage of cancer, and the hospital where the treatment is being done

Why is this study important?

This study will help pharmaceutical researchers design more potent anti-cancer drugs, said researcher Debanjan Tewari, who began his PhD work on aspirin three years ago when animal studies showed anti-cancer properties in this protein.

It will be a revolution if low cost molecules and salts like those in aspirin can kill cancer cells. This can pave way for affordable therapy. The scientists are not able to comment on the direct use of aspirin as cancer drugs right now. But with some clinical studies, they are sure they will be able to make good progress in the case.

Artificial thymus can produce cancer-fighting T cells from blood stem cells

Artificial thymus can produce cancer-fighting T cells from blood stem cells
T cells (red) that were produced using artificial thymic organoids developed by UCLA scientists. 

UCLA researchers have created a new system to produce human T cells, the white blood cells that fight against disease-causing intruders in the body. The system could be utilized to engineer T cells to find and attack cancer cells, which means it could be an important step toward generating a readily available supply of T cells for treating many different types of cancer.

 The preclinical study, published in the journal Nature Methods, was led by senior authors Dr. Gay Crooks, a professor of pathology and laboratory medicine and of pediatrics and co-director of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA, and Amelie Montel-Hagen, an associate project scientist in Crooks’ lab.

The thymus sits in the front of the heart and plays a central role in the immune system. It uses to make T cells, which help the body fight infections and have the ability to eliminate cancer cells. However, as people age or become ill, the thymus isn’t as efficient at making T cells.

T cells generated in the thymus acquire specialized molecules, called , on their surface, and those receptors help T cells seek out and destroy virus-infected cells or cancer cells. Leveraging that process has emerged as a promising area of cancer research: Scientists have found that arming large numbers of T cells with specific cancer-finding receptors—a method known as adoptive T cell immunotherapy —has shown remarkable results in clinical trials.

Adoptive T cell immunotherapy typically involves collecting T cells from people who have cancer, engineering them in the lab with a cancer-finding receptor and transfusing the cells back into the patient.

However, adoptive T cell immunotherapy treatments can be time-consuming, and people with cancer might not have enough T cells for the approach to work, according to Dr. Christopher Seet, the study’s first author and a clinical instructor who treats cancer patients in the division of hematology-oncology at UCLA.

Since adoptive T cell immunotherapy was first used clinically in 2006, scientists have recognized that it would be more efficient to create a readily available supply of T cells from donated blood cells or from , which can create any cell type in the body. The challenge with that strategy would be that T cells created using this approach would carry receptors that are not matched to each individual patient, which could ultimately cause the patient’s body to reject the transplanted cells or could cause the T cells to target healthy tissue in addition to .

“We know that the key to creating a consistent and safe supply of cancer-fighting T cells would be to control the process in a way that deactivates all T cell receptors in the transplanted cells, except for the cancer-fighting receptors,” Crooks said.

The UCLA team used a new combination of ingredients to create structures called artificial thymic organoids that, like the thymus, have the ability to produce T cells from blood stem cells. The scientists found that mature T cells created in the artificial thymic organoids carried a diverse range of T cell receptors and worked similarly to the T cells that a normal thymus produces.

Next, the team tested whether artificial thymic organoids could produce the specialized T cells with cancer-fighting T cell receptors. When they inserted a gene that delivers a cancer-fighting receptor to the blood stem cells, they found that the thymic organoids produced large numbers of cancer-specific T cells, and that all other T cell receptors were turned off. The results suggest that the cells could potentially be used to fight cancer without the risk of T cells attacking healthy tissue.

Montel-Hagen said the artificial thymic organoid can easily be reproduced by other scientists who study T cell development. The UCLA researchers now are looking into using the system with pluripotent , which could produce a consistent supply of -fighting T for patients in need of immediate life-saving treatment.

Scientists Have Finally Discovered Why Consuming Red Meat Causes Cancer

Many people grew up being urged to eat pork, beef, and dairy products for their health, but in recent years have received advice to cut back on animal products especially red meat. 

According to a number of studies, the consumption of red meat is linked with increased risk for cancer(s), atherosclerosis (heart disease), stroke, Alzheimer’s, and even Type II Diabetes…  But until now, researchers have not exactly understood why.

As The Telegraph reports, scientists from the University of California in San Diego believe it mainly has to do with sugar. 

While humans, as omnivores, can tolerate eating meat (and have been doing so for many years, but not in the quantity witnessed today) there is unique sugar named Neu5Gc, found in most mammals but not in humans, that triggers an immune responsewhich causes inflammation.

Mice were used for the study which found that all the evidence linking Neu5Gc to cancer was circumstantial or indirectly predicted from experimental setups. According to the scientists, this is the first time they mimicked the exact situation in humans through feeding non-human Neu5Gc and inducing anti-Neu5Gc antibodies. This increased spontaneous cancer in mice.

This sugar can be found in red meats (pork, beef, and other livestock), cow’s milk and certain cheeses. Because the human body is not capable of producing this sugar naturally when the sugar is absorbed into the tissues, it is perceived as a foreign invader and activates the immune system. It is suspected that over time, the chronic inflammation caused by the immune system response plays a role in the development of cancer.

Thus, those who consume red meat on a regular basis are likely to suffer a stronger reaction than those who ingest red meat occasionally.


Evolocumab and Clinical Outcomes in Patients with Cardiovascular Disease.


Evolocumab is a monoclonal antibody that inhibits proprotein convertase subtilisin–kexin type 9 (PCSK9) and lowers low-density lipoprotein (LDL) cholesterol levels by approximately 60%. Whether it prevents cardiovascular events is uncertain.


We conducted a randomized, double-blind, placebo-controlled trial involving 27,564 patients with atherosclerotic cardiovascular disease and LDL cholesterol levels of 70 mg per deciliter (1.8 mmol per liter) or higher who were receiving statin therapy. Patients were randomly assigned to receive evolocumab (either 140 mg every 2 weeks or 420 mg monthly) or matching placebo as subcutaneous injections. The primary efficacy end point was the composite of cardiovascular death, myocardial infarction, stroke, hospitalization for unstable angina, or coronary revascularization. The key secondary efficacy end point was the composite of cardiovascular death, myocardial infarction, or stroke. The median duration of follow-up was 2.2 years.


At 48 weeks, the least-squares mean percentage reduction in LDL cholesterol levels with evolocumab, as compared with placebo, was 59%, from a median baseline value of 92 mg per deciliter (2.4 mmol per liter) to 30 mg per deciliter (0.78 mmol per liter) (P<0.001). Relative to placebo, evolocumab treatment significantly reduced the risk of the primary end point (1344 patients [9.8%] vs. 1563 patients [11.3%]; hazard ratio, 0.85; 95% confidence interval [CI], 0.79 to 0.92; P<0.001) and the key secondary end point (816 [5.9%] vs. 1013 [7.4%]; hazard ratio, 0.80; 95% CI, 0.73 to 0.88; P<0.001). The results were consistent across key subgroups, including the subgroup of patients in the lowest quartile for baseline LDL cholesterol levels (median, 74 mg per deciliter [1.9 mmol per liter]). There was no significant difference between the study groups with regard to adverse events (including new-onset diabetes and neurocognitive events), with the exception of injection-site reactions, which were more common with evolocumab (2.1% vs. 1.6%).


In our trial, inhibition of PCSK9 with evolocumab on a background of statin therapy lowered LDL cholesterol levels to a median of 30 mg per deciliter (0.78 mmol per liter) and reduced the risk of cardiovascular events. These findings show that patients with atherosclerotic cardiovascular disease benefit from lowering of LDL cholesterol levels below current targets.