“The first thing we noticed was that the small intestine increases greatly in size on the high-calorie diet,” says study leader Anika Böttcher. “Together with Fabian Theis’ team of computational biologists at Helmholtz Munich, we then profiled 27,000 intestinal cells from control diet and high fat/high sugar diet-fed mice. Using new machine learning techniques, we thus found that intestinal stem cells divide and differentiate significantly faster in the mice on an unhealthy diet.” The researchers hypothesize that this is due to an upregulation of the relevant signaling pathways, which is associated with an acceleration of tumor growth in many cancers. “This could be an important link: Diet influences metabolic signaling, which leads to excessive growth of intestinal stem cells and ultimately to an increased risk of gastrointestinal cancer,” says Böttcher.
Because the birth-cohort effect in cancer suggests that exposures early in life, during childhood or young adulthood, may be crucial, some have begun looking closely at changes to the microbiome. “We know that diet and lifestyle significantly shape our microbiome. They also significantly shape our immune system, which we need to fight off the development of cancer. And so we are hypothesizing that it’s a complex interplay among the microbiome, diet, lifestyle and your immune system,” Ng says.
I came across this post in my collection of unpublished drafts. I thought I posted this but obviously I didn’t. This article link was intended to be posted before Colorectal Cancer Rates Rising in Ages 50-54. Better late than never, I guess.
More than one quarter of colonoscopies carried out in Americans aged 30 to 49 years reveal some type of neoplasm, and slightly over 6% of these patients have advanced cancer, results of a nationally representative endoscopic registry show.
During the period 1992–2018, there were a total of 101,609 cases of CRC among adults aged 45–59 years. Further analysis showed that the CRC incidence rates rose from 23.4 to 34.0 per 100,000 among people aged 45–49 years and from 46.4 to 63.8 per 100,000 among those aged 50–54 years. Conversely, incidence rates decreased among individuals aged 55–59 years, from 81.7 to 63.7 per 100,000 persons.
Results Some 88 013 patients who were FIT positive complied with colonoscopy (males: 56.1%; aged 50–59 years: 49.1%) while 23 410 did not (males: 54.6%; aged 50–59 years: 44.9%).
The 10-year cumulative incidence of CRC was 44.7 per 1000 (95% CI, 43.1 to 46.3) among colonoscopy compliers and 54.3 per 1000 (95% CI, 49.9 to 58.7) in non-compliers, while the cumulative mortality for CRC was 6.8 per 1000 (95% CI, 5.9 to 7.6) and 16.0 per 1000 (95% CI, 13.1 to 18.9), respectively. The risk of dying of CRC among non-compliers was 103% higher than among compliers (adjusted HR, 2.03; 95% CI, 1.68 to 2.44).
Conclusion The excess risk of CRC death among those not completing colonoscopy after a positive faecal occult blood test should prompt screening programmes to adopt effective interventions to increase compliance in this high-risk population.
Research professor of medicine Martha Shrubsole, Ph.D., and colleagues at Vanderbilt University Medical Center have published the first study to evaluate intakes of meat, cooking methods and meat mutagens and risk of developing sessile serrated polyps (SSPs, also called sessile serrated lesions). Shrubsole previously reported that consuming high levels of red meat increased the risk of developing all types of polyps, but that the likelihood of developing SSPs was two times greater than the risk of developing adenomas and hyperplastic polyps (HP).
Conventional colorectal adenomas are the precursor lesions for most colorectal cancers. SSPs, however, represent an alternative pathway to carcinogenesis that may account for up to 35 percent of colorectal cancers. Because a diagnostic consensus for SSPs was not reached until 2010, few epidemiologic studies have evaluated risk factors.
A finding of any type of polyp in the colon increases the risk for colorectal cancer (CRC), according to new findings from a large Swedish study.
At 10 years, the cumulative colorectal cancer incidence was 1.6% among patients with hyperplastic polyps, 2.5% among those with sessile serrated polyps, 2.7% for tubular adenomas, 5.1% for tubulovillous adenomas, and 8.6% for villous adenomas, as compared with 2.1% for the control group.
However, a higher risk for colorectal-related death was only observed in patients with sessile serrated polyps, tubulovillous adenomas, or villous adenomas.
The study was published online March 16 in Lancet Gastroenterology & Hepatology.
I had my first virtual visit with my physician yesterday. I mentioned that I was postponing my colonoscopy this year for pandemic reasons. She said that’s fine, don’t worry about it. I read this article today. Now I know why I’m on a three year callback.
The research, conducted in a mouse model, suggests how lifestyle and genetics converge. The researchers found that animals with an APC mutation, the most common genetic mutation found in humans with colorectal cancer, developed cancer faster when fed a high-fat diet.
The mice with APC mutations developed benign growths called adenomas. In humans, adenomas are common in the intestine and are routinely removed during colonoscopies. These growths normally take decades to turn into malignant adenocarcinomas. Yet the adenomas in these mice quickly turned cancerous when given high-fat diets.
During the years 2002 to 2013 in national databases, the incidence of colorectal cancer increased in patients younger than age 50 at a rate of 1.5% per year, for an average 15% increase over the study period, according to Hisham Hussan, MD, of the Ohio State University Wexner Medical Center in Columbus.