Walmart CEO Doug McMillon says theft is 'higher than what it has historically been'

Walmart CEO Doug McMillon on Tuesday became the latest retail executive to weigh in on theft, describing it as an "issue" that has worsened. 

During his appearance on CNBC, McMillon said theft is "higher than what it has historically been." He explained Walmart has safety and security measures "that we've put in place by store location" to help combat the issue.

"I think local law enforcement being staffed, and being a good partner is part of that equation, and that’s normally how we approach it," McMillon added.

In mid-September, the National Retail Federation found total losses from shrink, a term retailers use for theft and other types of inventory loss, increased to $94.5 billion in 2021. Organized retail crime incidents soared 26.5% on average in the same year, according to the 2022 National Retail Security Survey.

The Walmart CEO also said during his CNBC appearance that "prices will be higher and/or stores will close" if authorities not being strict about prosecuting theft isn’t "corrected over time."

McMillon, responding to a separate question about what he'd like from policymakers, mentioned "policy consistency and clarity so we can make capital investments with some vision."

Walmart declined to provide specifics to FOX Business about the rising retail crime the company is facing. 

Target and Rite Aid executives are among the other retail leaders who have raised the alarm about retail theft in recent months. 

Michael Fiddelke, Target’s CFO, told investors and analysts in mid-November that, year-to-date, shrink "has already reduced our gross margin by more than $400 million versus last year, and we expect to reduce our gross margin by more than $600 million for the full year.

"This is an industry-wide problem that is often driven by criminal networks, and we are collaborating with multiple stakeholders to find industry-wide solutions," he said. 

At the time, Target CEO Brian Cornell similarly called theft a "growing financial headwind" among retailers, noting the company has "seen an increase in theft and organized retail crime across our business" that has prompted "significant" investments in training and technology to help prevent it.

Rite Aid CEO Heyward Donigan, during the company’s September earnings call, reported the pharmacy chain experienced "unexpected headwinds" from shrink, "particularly in our New York urban stores." The company’s front-end gross profit was "impacted by a $5 million increase in shrink," according to CFO Matt Schroeder.

In January, Home Depot Vice President of Asset Protection Scott Glenn told FOX Business the home improvement company has "been doing more physical security" and "innovating some new tools and technologies to make it a little bit harder for the bad guys and girls to steal products."

https://www.foxbusiness.com/markets/walmart-ceo-doug-mcmillon-says-theft-higher-than-what-has-historically-been

New cancer testing method that makes regular monitoring affordable

 Scientists from the National University of Singapore (NUS) have discovered a novel low-cost method of testing for cancers. Called the Heatrich-BS assay, this new test sequences clinical samples that have been heated in order to isolate cancer-specific signatures found in a patient's blood.

The new method provides a promising non-invasive alternative to tissue biopsies. It costs around S$50 (about US$35) from start to finish, compared to other sequencing methods that can cost up to S$1,000 (about US$740) to conduct. Led by Assistant Professor Cheow Lih Feng, the team comprising researchers from the NUS Department of Biomedical Engineering under the College of Design and Engineering as well as the NUS Institute for Health Innovation & Technology, is now exploring industry partnerships to bring their technology to market.

"When you have a S$50 (about US$35) test, it opens up a lot of avenues because it is affordable, so you can do the test quite regularly," said Asst Prof Cheow, pointing to the potential for their assay to be used in regular cancer monitoring.

Liquid biopsies for cancer

Current methods of testing for cancers can suffer from a lack of sensitivity or from being too expensive to be used for regular screening. The DNA in our blood, the genetic information that tells our cells how to synthesise proteins and other important biological building blocks, is produced by different organs in our body. Cancer cells also release DNA into the bloodstream that can be detected by analysing blood samples, known as liquid biopsies. However, sifting through all the genetic material in a sample -- a method called whole-genome sequencing -- can be expensive and labour intensive.

Some clinicians instead target cancer-specific signatures in cell-free DNA, almost like hunting for specific faces in a large crowd of people instead of inspecting every single individual. Yet, even such methods can be imperfect, Asst Prof Cheow explained. "Some patients may have cancer signatures that look slightly different and allow them to slip through the screening process," he said.

A more sensitive test at a small fraction of the price

Asst Prof Cheow's team has discovered a way to discard the non-informative sections in a patient's DNA to target where most cancer-specific biomarkers are concentrated.

Our DNA is made up of molecules known as nucleotides: adenine (A), thymine (T), guanine (G) and cytosine (C). Cancer-specific signatures tend to be concentrated in areas of the genome that have high repetitions of C and G nucleotides, known as CpG islands, that make up only around 1 per cent of our genome.

"We were performing some unrelated experiments, and one of our researchers heated a sample," Asst Prof Cheow said, recounting the team's accidental discovery that heat destroyed non-informative sections of the genome, but left CpG island largely intact. This allowed them to sequence the remaining genome and detect the presence of cancers for a minute fraction of the average market price.

"We are getting a much more sensitive assay at almost the same costs as compared to simple protein biomarker tests," he said, "Our method really concentrates on sequencing these regions that matter the most."

The NUS team published their findings in the scientific journal Science Advances on 9 September 2022, and a patent has also been filed for their discovery.

Benefitting patients, doctors and scientists

The Heatrich-BS assay has been trialed at the National Cancer Centre in Singapore, monitoring patients with colorectal cancer. By comparing the results of their blood analysis with CT scans that imaged the size of patients' tumours, the team found that there was a high correlation between how much cancer-specific DNA was detected in a patient's blood sample and the size of their tumours over time.

"This way, doctors can monitor patients for their response to treatment and tailor their therapy regimes," Asst Prof Cheow said. He also pointed out that their method has the potential to work universally across all types of cancer since they all demonstrate the property of enriching CpG islands with cancer-specific biomarkers. "It's a one-size fits all," he added.

The assay may also help accelerate future academic research, helping scientists study different subtypes of cancer for a low cost and therefore improving the development of future cancer diagnoses and therapies.

Asst Prof Cheow and his team are now exploring ways to commercialise their assay by partnering with pharmaceutical and biotechnology companies that can help bring the Heatrich-BS assay to market. "We are excited about our results and licensing discussions are underway," he said.

Story Source:

Materials provided by National University of Singapore. Note: Content may be edited for style and length.

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Journal Reference:

1. Elsie Cheruba, Ramya Viswanathan, Pui-Mun Wong, Howard John Womersley, Shuting Han, Brenda Tay, Yiting Lau, Anna Gan, Polly S. Y. Poon, Anders Skanderup, Sarah B. Ng, Aik Yong Chok, Dawn Qingqing Chong, Iain Beehuat Tan, Lih Feng Cheow. Heat selection enables highly scalable methylome profiling in cell-free DNA for noninvasive monitoring of cancer patients. Science Advances, 2022; 8 (36) DOI: 10.1126/sciadv.abn4030

https://www.sciencedaily.com/releases/2022/12/221205104155.htm

Fearlessness can be learned

 The absence of a certain serotonin receptor supports the reduction of previously learned fear responses.

The neurotransmitter serotonin plays a key role in both the onset and in the unlearning of fear and anxiety. A research team from the Department of General Zoology and Neurobiology headed by Dr Katharina Spoida and Dr Sandra Süß in the Collaborative Research Centre "Extinction Learning" at Ruhr University Bochum, Germany, has been investigating the underlying mechanisms. The researchers showed that mice lacking a specific serotonin receptor unlearn fear much faster than the wild type. The results of the study provide a viable explanation how drugs that are typically used for the treatment of post-traumatic stress disorder (PTSD) alter our brain activity. The ability to unlearn fear is often impaired in PTSD patients, making it more difficult to carry out therapies. The study was published in the journal Translational Psychiatry on 19 November 2022.

Fear responses triggered by everyday sensory input

People who have been affected by a traumatic experience sometimes suffer from a long lasting exaggerated fear response. In such cases, the fear response is triggered by certain sensory impressions that occur in our everyday environment and which then can become overwhelming. Experts refer to this condition as post-traumatic stress disorder (PTSD). In this disorder, it is not possible, or only with difficulty, for affected individuals to unlearn the once-learned connection between a neutral environmental stimulus and the learned fear response, which impairs the success of therapies.

Knowing that the neurotransmitter serotonin plays an important role in the development of fear, the research team explored its role in extinction learning, i.e. the unlearning of fear, in greater detail. To this end, they examined so-called knock-out mice that lack a certain serotonin receptor -- the 5-HT2C receptor -- due to genetic modifications. These mice learned in one day to associate a certain sound with a mild but unpleasant electrical stimulus. "As a result of this learning process, on the following day they showed a fear response that was characterized by a motionless pause as soon as the tone was played, which we refer to as 'freezing'," explains Katharina Spoida.

Absence of the receptor is an advantage

In the next step, the researchers repeatedly played the tone to the mice without applying the electrical stimulus. "Interestingly, we noticed that knock-out mice learned much faster that the tone does not predict the fear stimulus than mice who lacked this specific genetic modification," says Katharina Spoida. "Consequently, it looks like the absence of the serotonin receptor provides an advantage for extinction learning."

The researchers investigated this phenomenon in more detail and found that the knock-out mice showed changes in their neuronal activity in two different brain areas. One of these is a specific sub-region of the dorsal raphe nucleus (DRN), which is typically the main site of serotonin production in our brains. In addition, the researchers discovered aberrant neuronal activity in the so-called bed nucleus of the stria terminalis (BNST), which is a part of the so called extended amygdala. "In the knock-out mice, we first found an increased basal activity in certain serotonin-producing cells of the dorsal raphe nucleus. In a subsequent step, we showed that the absence of the receptor also alters neuronal activity in two subnuclei of the BNST, which ultimately supports extinction learning," describes first author Sandra Süß. The research results also indicate a connection between the two brain regions, which leads the scientists to assume that an interplay is significant for improved extinction learning.

Possible effect of medication revealed

The results of the study may reveal how drugs typically used in the treatment of PTSD affect the brain regions analysed in this study. "There are already drugs in clinical use that regulate the amount of available serotonin, so-called selective serotonin reuptake inhibitors, or SSRIs for short," points out Katharina Spoida.

"Taking these drugs over a prolonged period of time causes the relevant receptor to become less responsive to serotonin, similar to our knock-out model. Therefore, we assume that the changes we've described could be essential for the positive effect of SSRIs," adds Sandra Süß. The researchers hope that their findings will help to develop more targeted treatment strategies for PTSD patients in the future.

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Story Source:

Materials provided by Ruhr-University Bochum. Original written by Meike Drießen. Note: Content may be edited for style and length.

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Journal Reference:

1. Sandra T. Süß, Linda M. Olbricht, Stefan Herlitze, Katharina Spoida. Constitutive 5-HT2C receptor knock-out facilitates fear extinction through altered activity of a dorsal raphe-bed nucleus of the stria terminalis pathway. Translational Psychiatry, 2022; 12 (1) DOI: 10.1038/s41398-022-02252-x

https://www.sciencedaily.com/releases/2022/12/221205104218.htm

Could COVID-19 hold a cancer cure? Spike protein reduces lung tumors in lab study

 The notorious spike protein of SARS-CoV-2, the virus that causes COVID-19, caused lung cancer cells to die in laboratory studies conducted by researchers at RUSH University Medical Center, who recently published their findings in the journal Cancers.

The discovery raises the possibility that the pandemic that has afflicted the globe for three years might also yield a treatment for lung cancer, and perhaps other cancers as well.

The coronavirus infects human cells when its spike protein, known as S1, attaches to a molecule on the cell surface called angiotensin-converting enzyme 2. ACE2, as it's called for short, is a beneficial enzyme that plays a key role in the regulation of blood pressure and other cellular processes.

The level of ACE2 also increases in people with cancer, including lung cancer, and studies have found that modifying ACE2 levels may help control lung cancer growth. The involvement of ACE2 in both cancer progression and coronavirus infection prompted the RUSH researchers to investigate the use of the spike protein against the disease.

"It is always important to find mechanisms to stimulate cancer cell death and stop the progression of cancer," said Kalipada Pahan, Ph.D., the Floyd A. Davis professor of neurology at RUSH Medical College and lead investigator of this study. He adds that anecdotal cases of people with lung cancer that improved after they developed and recovered from COVID-19 also suggest the coronavirus' potential as an unlikely ally against cancer.

Cancer is the number two cause of death in U.S., second only to heart disease, according to the U.S. Centers for Disease Control and Prevention. Despite recent advances in treatment, lung cancer is by far the leading cause of cancer deaths throughout the world—more than 130,000 people die of it each year in the U.S. alone. Lung cancer accounts for 25% of cancer deaths in the U.S., more than deaths from colon cancer, breast cancer and prostate cancer combined.

Using a commercially available cloned version of the spike protein, Pahan and his colleagues first tested the protein's effect on the most treatment-resistant and deadliest form of lung cancer, non-small cell lung cancer, or NSCLC. In petri dishes, they combined the spike protein with human NSCLC cell cultures and measured the resulting levels of the proteins and molecules involved in cancer cell growth, compared with untreated NSCLC cells.

They found that in the NSCLC cells combined with S1, the spike protein induced apoptosis—the programmed death of cells that's a routine process in an organism's development. Accordingly, spike treatment decreased the levels of a molecule known as Bcl-2 that is needed for cell survival, and it increased the level of a molecule named BAD that is required for cell death. "Cancer cells do not die from apoptosis due to high level of Bcl-2 and low levels of BAD," Pahan said.

The researchers then examined the results of administering the spike protein to mice with established lung cancer. One group of mice received the spike protein in a mixture with saline solution that was sprayed into their nostrils every other day, while a control group received normal saline solution as a placebo.

After four weeks of spike protein treatment, the mice were euthanized and autopsied. The researchers found the number and size of tumors decreased in the mice that received the spike protein, and higher levels of tumor cell death, compared to the control group.

"If these results are replicated in lung cancer patients, it would uncover an encouraging avenue of treatment of this devastating disease." Pahan said. "Intranasal spike S1 protein could be used for late-stage lung cancer when there's no other therapy to stop the progression."

Pahan and his team currently are seeking partners to study the use of the spike protein in clinical trials of human patients with lung cancer. Since most of the widely available vaccines for COVID-19 target the spike protein, one of the important questions future studies will need to answer is whether vaccination diminishes the protein's efficacy as a cancer intervention.

More information: Monica Sheinin et al, Regression of Lung Cancer in Mice by Intranasal Administration of SARS-CoV-2 Spike S1, Cancers (2022). DOI: 10.3390/cancers14225648

https://medicalxpress.com/news/2022-12-covid-cancer-spike-protein-lung.html

New entryway into cells for virus causing COVID-19

 One of the many pressing research undertakings by the scientific community amid the ongoing COVID-19 pandemic has focused on ways the coronavirus manages to enter host cells.

Now, in a study adding to the pool of knowledge about viral entry, Dr. Marceline Côté's Faculty of Medicine lab and collaborators have published a highly compelling study showing a previously unrecognized entryway for SARS-CoV-2, the virus that causes COVID-19 and the driver of the global health crisis that's transformed the world.

Previous studies have shown that SARS-CoV-2 as well as an earlier coronavirus, SARS-CoV-1, the virus behind the SARS outbreak in 2003, enter cells via two distinct pathways. The new research led by Dr. Côté's lab shows a third entry route.

This viral entryway involves metalloproteinases, enzymes in the body with a catalytic mechanism that requires a metal, such as zinc atoms, to function.

Over a series of experiments starting in 2020, Dr. Côté's research team discovered that SARS-COV-2 can enter cells in a metalloproteinase-dependent manner. The team describes a role for two matrix metalloproteinases—MMP-2 and MMP-9—in the activation of the spike glycoprotein.

What are the ramifications of this kind of viral entry? The study published in a recent issue of iScience, an open access journal from Cell Press, suggests that variants that gravitate toward metalloproteinases may cause more havoc.

The team's experiments showed that some variants clearly prefer the metalloproteinases for activation. For instance, the Delta variant, a more pathogenic variant that surged in 2021, commonly used metalloproteinases for entry. Its less pathogenic successor, Omicron, did not.

"SARS-CoV-2 may be able to use proteins, which are typically secreted by some activated immune cells, to cause more damage and potentially infect a wider range of cells and tissues," says Dr. Côté, a Faculty associate professor who is the holder of the Canada Research Chair in Molecular Virology and Antiviral Therapeutics.

The entry mechanism could also play a role in disease progression.

Dr. Côté says the findings could have implications in the progression to severe illness and some post COVID-19 conditions, such as the complex array of post-infection symptoms known as "long COVID."

More information: Mehdi Benlarbi et al, Identification and differential usage of a host metalloproteinase entry pathway by SARS-CoV-2 Delta and Omicron, iScience (2022). DOI: 10.1016/j.isci.2022.105316

https://medicalxpress.com/news/2022-12-entryway-cells-virus-covid-.html

How antibody therapy affects the breadth of COVID mRNA vaccines

 Nearly three years into the pandemic, many of us now carry antibodies against the virus—due to an infection or two, a few doses of mRNA vaccine, or a round of monoclonal-antibody treatment. But not all immune responses are created equal, and how we first developed our antibodies may influence the character of our body's response to SARS-CoV-2.

Now, a new study describes the unique immune response elicited in individuals who received monoclonal antibodies before taking two doses of an mRNA vaccine. The research, published in Nature, explores a phenomenon known as antibody feedback inhibition, known to alter immune responses to some pathogens while beneficially diversifying the body's antibody repertoire against several others. The findings suggest that feedback inhibition increases the coverage provided by COVID vaccines in people who previously received monoclonal antibodies.

"Depending on the virus, feedback inhibition can either enhance immunity or inhibit it," says Michel C. Nussenzweig, who co-led the study with colleagues Theodora Hatziioannou, Paul Bieniasz, and Marina Caskey. "Our results suggest that pre-existing SARS-CoV-2 antibodies can diversify the antibody response, which may increase the breadth of mRNA vaccines."

Of guinea pigs and antibodies

Antibody feedback inhibition was first discovered at the turn of the century by pioneering epidemiologist Theobald Smith, who demonstrated that excess antibodies could inhibit the immune response to diphtheria in guinea pigs. It seemed like a curious twist—why would the same molecule that supposedly protects the animal from disease occasionally shut the immune system down?

We now know that viruses have multiple epitopes—stand-out bits of antigen that antibodies use to identify the virus and latch on to it. Once the body has produced strong antibodies for one epitope, the immune system moves on and diversifies, instead making antibodies that attach to other parts of the virus. Ideally, this increases the breadth of the immune response—if a virus mutates so that one epitope can no longer be recognized, for example, it might still be vulnerable to antibodies targeting other epitopes.

"Antibody feedback can be a very good thing," Nussenzweig says. "You end up with a collection of neutralizing antibodies to many different parts of the virus, all of which are helpful."

But in other cases, antibody feedback can be more harmful than helpful. HIV and influenza both have a limited number of epitopes—and if one epitope doesn't yield very effective antibodies, a perfect storm may ensue. Upon detecting a surplus of minimally effective antibodies, the body will shut down its production of that line, inadvertently blocking the production of similar antibodies that could potentially have worked better.

"There are only a couple of places on the HIV virus that are worth targeting, and if the initial response blocks those epitopes, we won't get a broadly neutralizing response," Nussenzweig says.

Antibody feedback in COVID

To better understand how antibody feedback impacts COVID immunity, Nussenzweig and colleagues followed volunteers who received a single dose of monoclonal antibody treatment and, later, two doses of an mRNA vaccine. They found that these volunteers had markedly different immune responses than individuals who had received the mRNA vaccines alone.

Two doses of an mRNA COVID vaccine usually gives rise to a preponderance of memory B cells, which express antibodies that target one of three key parts of the receptor-binding domain of the spike protein, without which the coronavirus cannot infect a cell. As expected, Nussenzweig and colleagues found that about half of the antibodies obtained from individuals who received only the vaccines targeted so-called Class 1, 2, or 3 epitopes.

But only 20 percent of antibodies from volunteers who received monoclonal antibodies before the vaccine targeted one of these three epitopes. Instead, nearly 80 percent of their antibodies targeted a fourth part of the receptor-binding domain, or other epitopes altogether. The authors concluded that feedback inhibition was at work—after monoclonal antibody therapy led to the production of antibodies against Class 1, 2, or 3 epitopes, the body stopped producing those, and upon vaccination, shifted to target other epitopes. In this case, the impacts are beneficial.

"Their immune response is different, but certainly not worse," Nussenzweig says. "In fact, individuals who received monoclonal antibodies were extremely well protected."

The findings suggest that monoclonal antibodies received before vaccination may help diversify the immune response to COVID by increasing the breadth of mRNA vaccines. There may also be important lessons for boosting. "Because there are many targets on the receptor-binding domain that can neutralize the virus, antibody feedback is very helpful," Nussenzweig says.

And whether the antibody surplus driving that feedback comes from monoclonal antibodies or additional vaccine booster, he says, "antibody feedback is very good for COVID."

More information: Dennis Schaefer-Babajew et al, Antibody feedback regulates immune memory after SARS-CoV-2 mRNA vaccination, Nature (2022). DOI: 10.1038/s41586-022-05609-w

https://medicalxpress.com/news/2022-12-antibody-therapy-affects-breadth-covid.html

Healthy lifestyle might prevent up to 60% of inflammatory bowel disease cases

 Adopting and maintaining a healthy lifestyle might prevent up to 60% of inflammatory bowel disease cases—Crohn's disease and ulcerative colitis—finds a large international study, published online in the journal Gut.

The findings prompt the study authors to suggest that subject to further research, particularly in those at high risk of developing these conditions, lifestyle changes may be a feasible option for future preventive strategies.

Inflammatory bowel disease, or IBD for short, affects an estimated 3 million adults in the U.S. and another 1.3 million in Europe, and diagnoses have been increasing, particularly in newly industrialized countries.

Previously published research has linked IBD risk with several lifestyle factors, but it's not clear whether adopting and maintaining a healthy lifestyle might lower the risk of developing the condition in the first place. To find out, researchers drew on participant data from the Nurses' Health Study (NHS), NHSII, and the Health Professionals Follow-up Study (HPFS).

The Nurses' Health Study enrolled 121,700 female nurses (aged 30-55) from 11 U.S. states in 1976, while the NHSII study, established in1989, monitored 116,429 female nurses (aged 25-42) from 15 U.S. states. The HPFS included 51,529 male doctors (40-75) from across the U.S. in 1986.

The researchers created modifiable risk scores (MRS) for each participant based on established modifiable risk factors for IBD to estimate the proportion of IBD cases that could have been avoided. The MRS ranged from 0-6, with higher scores denoting more risk factors.

These risk factors included weight (BMI); smoking; use of non-steroidal anti-inflammatory drugs; physical activity; and daily intake of fruit, fiber, vegetables, polyunsaturated fatty acids (PUFAs) and red meat.

The researchers then estimated the proportion of avoidable cases if an overall healthy lifestyle were adopted and maintained. Scores of 0-9 were assigned to each participant, with higher scores indicating a healthier lifestyle.

A healthy lifestyle comprised: BMI between 18.5 and 25; never smoking; at least 7.5 weekly MET hours (METS express the amount of energy [calories] expended per minute of physical activity); at least 8 daily servings of fruit and vegetables; less than half a daily serving of red meat; at least 25 g of fiber/day; at least 2 weekly servings of fish; at least half a daily serving of nuts/seeds; and a maximum of 1 alcoholic drink/day for women or 2 for men.

During the monitoring period (NHS, HPFS: 1986-2016; NHSII: 1991-2017), 346 cases of Crohn's disease and 456 cases of ulcerative colitis were reported.

Based on the MRS scores, the researchers estimated that a low MRS could have prevented 43% and 44.5%, respectively, of Crohn's disease and ulcerative colitis cases.

Similarly, maintaining a healthy lifestyle could have prevented 61% of Crohn's disease cases and 42% of ulcerative colitis cases.

The researchers applied the scoring systems to data from three large European studies to validate their findings: the Swedish Mammography Cohort (37,275 participants); the Cohort of Swedish Men (40,810); and the European Prospective Investigation into Cancer and Nutrition (404,144).

These calculations showed that a low MRS and maintaining a healthy lifestyle could have respectively prevented 44%-51% and 49%-60.5% of Crohn's disease cases, and 21%-28% and 47%-56.5% of ulcerative colitis cases.

This is an observational study, and as such can't establish cause. The researchers acknowledge that the average age at which IBD was diagnosed was older than is typical. Early lifestyle factors that may have been influential were not considered. These included antibiotic prescriptions; breastfeeding; environmental factors such as pollution; stress; and socioeconomic factors.

"A key assumption of our findings is that the relationship between lifestyle factors and IBD development is causal. Though this has yet to be established, several lines of evidence support the critical role of environmental and lifestyle factors in the development of IBD," they write.

"Lifestyle modification may be an attractive target for future prevention strategies in IBD," they add. "This may be of particular relevance to high-risk groups, such as first-degree relatives of IBD patients, who have an estimated 2%-17% risk of developing the disease over their lifetime."

More information: Lifestyle factors for the prevention of inflammatory bowel disease, Gut (2022). DOI: 10.1136/gutjnl-2022-328174

https://medicalxpress.com/news/2022-12-healthy-lifestyle-inflammatory-bowel-disease.html