Last Updated on March 23, 2016 by Patricia Carter
SUMMARY: Learn here that adult young colon cancer diagnoses doubles by 2030.
The number of young adults (aged 20 to 34, and 35 to 49 years) with newly diagnosed colorectal cancer is anticipated to nearly double by 2030.
Worth repeating: By 2030 adult young colon cancer diagnoses doubles
For ages 20 to 34 years, colon cancer increase is 90.0% and rectal cancer increase is 124.2% by the year 2030.
For ages 35 to 49 years, colon cancer increase is 27.7% and rectal cancer increase is 46.0% by the year 2030.
For patients under age 34, the increase is across all stages of disease: localized (confined to the colon or rectum), regional (contiguous and adjacent organ spread, such as to the lymph nodes, kidney and pelvic wall) and distant (referring to remote metastases).
The trends are discussed in this “Science Daily” article and is based on this study, published in the current issue of JAMA Surgery. The study looked at data from the National Cancer Institute’s SEER registry for all patients diagnosed as having colon or rectal cancer from January 1, 1975, through December 31, 2010 and are based on 393,241 patients (that is a lot of patients):
The authors noted obvious risk factors for colon and rectal cancer (CRC) (lack of screening, obesity, and physical inactivity), but then went and encouraged:
reduced consumption of processed and fast food and more vegetables and fruits to reduce risk.
The researchers are warning physicians to be on the lookout for CRC symptoms that might otherwise be dismissed in younger people and only identified as cancer after the disease has progressed.
The UEG – United European Gastroenterology reported In the below video “Is a CRC screening blood test within reach?” that colon cancer represents between 10 to 15% of all cancers across Europe; 214,675 die each year which is equivalent to 1 death every 3 minutes. These figures were published by the International Agency for Research on Cancer (ARC), and they estimate a 12% increase in CRC across Europe by 2020. Additional statistics are available in this WHO “International Agency on Cancer Fact Sheet,“ if interested. In the US, this CDC report, “Vital Signs: Colorectal Cancer Screening Test Use — United States, 2012,” finds CRC to be the second most common cause of US cancer death (15%) among all cancers that affect both men and women. The video updates CRC blood biomarker testing which is important since there is about a ten year window for detection as typically CRC begins as a polyp and then slowly advances to CRC. They report that the sensitivity for blood DNA/miRNA-based biomarkers testing, looking at detection of abnormal DNA methylation patterns and the presence of microRNAs as major factors in the carcinogenic process, is still quite low for early CRC stages.
Time to digress and talk about IBS, not associated with CRC at this time, however CRC is part of the IBS differential diagnosis
Irritable bowel syndrome (IBS) affects up to 15% of the general adult population. Studies to date (here, and here) have not found an association between IBS and CRC. I want to discuss IBS at this point since it is likely that many young aged patients will be handed an IBS diagnosis when it may really be the beginning of CRC. The researchers are warning physicians (see this “Science Daily” article which is based on this study) to be on the lookout for CRC symptoms that might otherwise be dismissed in younger people and only identified as cancer after the disease has progressed since CRC is not on the radar.
Both IBS and CRC have altered gut microbiome: for CRC see this study, “The Gut Microbiome Modulates Colon Tumorigenesis” dated November, 2013, and for IBS see this paper, “Irritable bowel syndrome, inflammatory bowel disease and the microbiome“ dated February 2014 which notes:
“Gene polymorphisms associated with inflammatory bowel disease increasingly suggest that interaction with the microbiota drives pathogenesis. This may be through modulation of the immune response, mucosal permeability or the products of microbial metabolism. Similar findings in irritable bowel syndrome have reinforced the role of gut-specific factors in this ‘functional’ disorder. Metagenomic analysis has identified alterations in pathways and interactions with the ecosystem of the microbiome that may not be recognized by taxonomic description alone, particularly in carbohydrate metabolism. Treatments targeted at the microbial stimulus with antibiotics, probiotics or prebiotics have all progressed in the past year. Studies on the long-term effects of treatment on the microbiome suggest that dietary intervention may be needed for prolonged efficacy.”
This Medical News Today article, “Managing IBS effectively with the right drugs, for the right symptoms” dated November 8, 2014, just listed new IBS prescription guidelines & accompanying technical review published in Gastroenterology, the official journal of the American Gastroenterological Association. The new guidelines do not seemingly recommend FODMAP dietary protocol for IBS despite it’s success for over 74% of IBS patients which is noted in this paper, “Fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAPs) and nonallergic food intolerance: FODMAPs or food chemicals?” dated July 2012. The July 2012 paper summarized the evidence and application of the most common approaches to managing food intolerance in IBS (the low-FODMAP diet, the elimination diet for food chemical sensitivity and others including possible noncoeliac gluten intolerance), noted that FODMAPs is successful for over 74% of IBS patients, and concluded:
“…considerable evidence supporting the low-FODMAP diet for IBS, and the fact that it is relatively easy to implement without significant nutritional concerns, supports the suggestion that this should be the first dietary manipulation trialled in patients presenting with IBS. “
This flies in the face of the new guidelines just published which note:
“Gluten-free and low-FODMAP diets show promise but their precise role(s) in the management of IBS need to be defined… Role of dietary manipulation in IBS: Specialized diets may improve symptoms in individual IBS patients. Recommendation: weak. Quality of evidence: very low. A significant limitation of this study was the lack of blinding regarding the dietary intervention.” There actually is quite a lot of literature supporting the use of FODMAPs, and I plan to post this in the near future. In the meantime, many FODMAP charts are on the Biome Onboard Awareness Facebook Page though you will need to search through the photos.
My main point here is that IBS patients may successfully modify diet using FODMAPs and avoid the need for the new guideline prescription medications which incredibly are: Patients w/IBS-C: linaclotide, lubiprostone, Patients w/IBS-D: rifaximin,alosetron, loperamide. Addtionally, recommendations include for patients w/IBS: tricyclic antidepressants, selective serotonin reuptake inhibitors, and antispasmodics. Totally interesting is how recent science is now publishing many studies linking the gut/brain axis and microbiome link to influencing mood, thought, anxiety, depression, autism… How IBS and CRC tie together, if at all, is yet to be determined but modifying diet (with a specific protocol now known for IBS) are the recommendations for both.
Returning to the CRC study, Dr. George J. Chang, MD, MS, associate professor, Departments of Surgical Oncology and Health Services Research. the principal investigator of the study noted:
“This is an important moment in cancer prevention. We’re observing the potential real impact of CRC among young people if no changes are made in public education and prevention efforts. This is the moment to reverse this alarming trend.”
“While our study observations are limited to CRC, similar concerns are being raised about breast cancer, as we see incidence increasing among younger women,” said Chang. “Identifying these patterns is a crucial first step toward initiating important shifts in cancer prevention.”
The chart and graph below (young adult cancer increases are circled) shows the estimated increases:
- Try to literally count the number of different vegetables eaten at meals and if you have children, make a game out of this. Counting will become a habit and you’ll deliberately choose variety unconsciously.
- Keep your refrigerator stocked with already prepped vegetables so they are easy to grab.
- Use your freezer. It becomes easy to toss frozen vegetables in to bone broth for super quick meals, be it breakfast, lunch, dinner, or snacking. Or, when you fry an egg, first toss into the skillet frozen greens, a few slices of leek or red onion, and coconut oil. Saute them, and as they near final saute, make room along the skillet sides and crack in your eggs. Cover and cook; easy. Vegetables are frozen at the peak of ripeness so they may be even more nutrient packed then that sitting on your grocery shelves. And… no worries of spoilage since they are frozen.
Clearly our bodies are needing the nutrition of Whole Food sources, omission of processed food ingredients that you don’t recognize and can’t pronounce, and this begins at a young age.
The mosaic below shows what Whole Foods looks like this. It is EASY to prepare Whole Foods once you know proper preparation techniques, and I included a couple of recipe conversions just to show you the label decode aspects of cooking Whole Foods:
Proper preparation techniques are so critical. Check out the anti-nutrients and enzyme inhibitors that are neutralized and eliminated during proper preparation of seeds and nuts:
I am working on a post that gives the “How-to’s” and the “Whys” for proper preparation of grains so expect that shortly.
In the meantime, use the Pinterest recipes which already includes proper preparation techniques within the recipe directions:
Last updated: March 23, 2016 at 4:48 am for SEO optimization.
In health through awareness,
[Bullman et al 2017] Analysis of Fusobacterium persistence and antibiotic response in colorectal cancer, https://www.ncbi.nlm.nih.gov/pubmed/29170280
Fusobacterium nucleatum is among the most prevalent bacterial species in colorectal cancer tissues. Here we show that colonization of human colorectal cancers with Fusobacterium and its associated microbiome, including Bacteroides, Selenomonas and Prevotella species, is maintained in distal metastases, demonstrating microbiome stability between paired primary-metastatic tumors. In situ hybridization analysis revealed that Fusobacterium is predominantly associated with cancer cells in the metastatic lesions. Mouse xenografts of human primary colorectal adenocarcinomas were found to retain viable Fusobacterium and its associated microbiome through successive passages. Treatment of mice bearing a colon cancer xenograft with the antibiotic metronidazole reduced Fusobacterium load, cancer cell proliferation and overall tumor growth. These observations argue for further investigation of antimicrobial interventions as a potential treatment for patients with Fusobacterium-associated colorectal cancer.
Microbiome and cancer. More reasons to fix your gut microbiome!
How the Microbiome Can Affect Cancer, http://blog.aacr.org/how-the-microbiome-can-affect-cancer/#.WH-OIoUNRX0.linkedin
Bacteroides fragilis as a particularly bad actor in the gut. This bacterium produces a toxin that damages normal intestinal cells, leading to a chronically inflamed intestinal microbiome prone to generate cancers. When Dr. Sears transferred the bacterium to mice inclined to develop benign intestinal polyps, the mice formed colorectal cancers instead.
The paper, Redundant Innate and Adaptive Sources of IL17 Production Drive Colon Tumorigenesis, http://cancerres.aacrjournals.org/content/76/8/2115, April 2016 found that colorectal cancers associated with B. fragilis could be suppressed, not just by eradicating the microorganism, BUT ALSO BY REDUCING INFLAMMATION. ****This opens up new avenues for preventing colorectal cancers by altering the relationships between the microbiota and immune cells in the gut microbiome. Several other intestinal bacteria are also likely to affect colorectal cancer development. A gut microbiota rich in these pro-cancer bacteria may drive a microbiome toward chronic inflammation and cancer.****
Will altering the microbiota and microbiome be a cornerstone of cancer prevention and treatment? Can so-called probiotics be developed and demonstrated to improve health? What is a healthy microbiome and how can it be maintained? Finding answers to these questions may go a long way toward preventing and treating human cancers.
The influence of the intestinal microbiota on immune responses may even extend to how effectively the body’s immune system can be activated to fight cancers. Two recent reports in Science suggest that the presence of certain bacteria in the intestinal microbiome was accompanied by better anti-cancer responses to immunotherapy. The bacteria enhanced the effects of new immunotherapy drugs like Yervoy (ipilimumab), Opdivo (nivolumab), and Keytruda (pembrolizumab).
Potential of fecal microbiota for early-stage detection of colorectal cancer, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4299606/
Colorectal carcinoma (CRC) is among the three most common cancers with more than 1.2 million new cases and about 600,000 deaths per year worldwide (Jemal et al, 2011). Several bacterial species have been implicated in the development of colorectal carcinoma (CRC), but CRC-associated changes of fecal microbiota and their potential for cancer screening remain to be explored. If CRC is diagnosed early, when it is still localized (American Joint Committee on Cancer (AJCC) stages 0, I, or II), the 5-year survival rate is > 80%, but decreases to < 10% for late diagnosis of metastasized cancer (in AJCC stage IV) (O'Connell et al, 2004). This study investigates the potential of fecal microbiota for noninvasive detection of colorectal cancer in several patient populations from different countries. Included is CRC marker species in inflammatory bowel disease.
Microbiota implicated In CRC: Bacteroides fragilis strains producing genotoxins (BFTs) can induce inflammation, leading to DNA damage in host cells (Wu et al, 2009; Goodwin et al, 2011); similarly, Escherichia coli strains harboring a genomic virulence island (pks) can cause DNA damage and chromosomal instability in the host (Cuevas-Ramos et al, 2010; Arthur et al, 2012), and very recently, Fusobacterium nucleatum strains were reported to promote carcinogenesis upon invasion of host cells (Kostic et al, 2013; Rubinstein et al, 2013). However, it remains unclear how many CRC cases can be attributed to each of these agents, how these exactly interact with the human host or the microbial community in the gut, and whether altered microbial abundances may provide a basis for an accurate CRC screening test.
Cohort 156. Metagenomic sequencing of fecal samples to identify taxonomic markers that distinguished CRC patients from tumor-free controls in a study population.
Findings: CRC-associated changes in the fecal microbiome at least partially reflected microbial community composition at the tumor itself, indicating that observed gene pool differences may reveal tumor-related host-microbe interactions. Indeed, we deduced a metabolic shift from fiber degradation in controls to utilization of host carbohydrates and amino acids in CRC patients, accompanied by an increase of lipopolysaccharide metabolism.
Can 16S be used to screen? Our results indicate functional and taxonomic associations with CRC and conceptually establish the possibility of CRC detection from fecal microbial markers. Their future application in mass screening will depend on the development of cost-effective assays. Toward this goal, we assessed whether 16S sequencing of fecal samples would be a suitable alternative. A 16S-based classifier for CRC detection, cross-validated on the subset of study population F for which we had also generated 16S data (N = 116), achieved almost as good an accuracy (AUC 0.82; Supplementary Fig S10) as the models based on metagenomic community profiles (AUC 0.84–0.87; Supplementary Fig S10). While our work was under review, another study (Zackular et al, 2014) independently arrived at the conclusion that 16S sequencing of fecal samples would allow for accurate CRC screening based on classification models that showed some overlap with our CRC markers at higher taxonomic ranks.
The reference for “about a quarter of us have up to 40% less gut bacteria genes and correspondingly fewer bacteria than average” and thus reduced microbiome diversity is this Danish study: http://news.ku.dk/all_news/2013/2013.8/one_in_four_has_alarmingly_few_intestinal_bacteria/ “This is a representative study sample, and the study results can therefore be generalized to people in the Western world,“ says Oluf Pedersen, Professor and Scientific Director at the Faculty of Health and Medical Sciences, University of Copenhagen. This population had reduced bacterial diversity and harbored more bacteria that caused low-grade inflammation of the body that is representative of obesity, Type 2 Diabetes, and some cardiovascular disorders.
The reference cite for estimated 1/3 population has reduced microbiome is: Dr. Maria Gloria Dominguez-Bello at http://microbirth.com/ video.