Colon and rectal cancer incidence is rising among Gen X and millennials

Earlier this year, researcher Rebecca Siegel of the American Cancer Society published a startling report showing that colon and rectal cancer incidence is rising among Gen X and millennials while falling in older generations.

On Tuesday, after delving further into the data, she and her co-authors identified “a true and perplexing escalation in disease occurrence.” In a paper in JAMA, the Journal of the American Medical Association, they report that deaths from colorectal cancer are increasing for young and middle-aged Americans — though the increase appears, at least so far, to be confined to white men and women.

The U.S. mortality rate for colorectal cancer for ages 20 to 54 fell from 6.3 per 100,000 in 1970 to 3.9 in 2004. It then began to go up by 1 percent annually. By 2014, the rate was 4.3 per 100,000.

Breaking the numbers out by race reveals the  trend, with the outlook becoming better for blacks and people of other races but not for whites.

The mortality rate for whites had been declining for decades, but it began to climb starting in 2004, going from 3.6 per 100,000 to 4.1 per 100,000 in 2014. For blacks, it went down to 6.1 per 100,000 in 2014. While that’s still higher than for whites, the trend is heading in the right direction. For other races, mortality rates declined until 2006 and remained stable through 2014.

Siegel noted that the racial patterns are “inconsistent” with trends in major risk factors for colorectal cancer. These include obesity, which is increasing among all races and would suggest colorectal cancer rates should be going up among all races, too.

 


The mortality rate for white Americans declined for a number of years but began to rise again in 2004. In comparison, the rates for black Americans has declined. (JAMA)

The data, which encompass almost  250,000 people, come from the National Center for Health Statistics and information it collects from death certificates. They raise more questions on whether the country’s screening standards should be revisited. Current guidelines call for regular screening for colorectal cancer to begin at age 50.

The analysis of mortality rates contained another surprise: They are also rising for white men and women in their 50s despite the actual cancer incidence decreasing and screening recommended for this age group for decades. In contrast, the mortality rates for blacks in their 50s has declined since 1993.


Contact Connie or join us at the Health Care Network Alliance to stop cancer with whole foods, exercise, sleep and supplementation that affects the gene expression to effect health, vitality and youth. motherhealth@gmail.com or text 408-854-1883 to tailor fit supplementation based on your health.

card motherhealth

  • Distributorship ID #: USW9578356
  • Distributorship Address: 1708 Hallmark Lane, San Jose, Ca 95124
    • DELLO BUONO, CONNIE
  • Join our team at Health Care Network Alliance as customer or distributor:
  • Get Health Coach training and cert from Connie and join the training in Utah on Sept 14 and 15 to help doctors use a micro nutrient tester and bring unique wellness solutions for each person.

Parkinson’s Disease Linked to Gut Microbiome

Summary: A new study reports a link between the deterioration of motor skills in Parkinson’s disease and alterations in the composition of populations of gut bacteria.

Source: California Institute of Technology.

Caltech scientists have discovered for the first time a functional link between bacteria in the intestines and Parkinson’s disease (PD). The researchers show that changes in the composition of gut bacterial populations–or possibly gut bacteria themselves–are actively contributing to and may even cause the deterioration of motor skills that is the hallmark of this disease.

The work–which has profound implications for the treatment of PD–was performed in the laboratory of Sarkis Mazmanian, the Luis B. and Nelly Soux Professor of Microbiology and Heritage Medical Research Institute Investigator, and appears in the December 1 issue of Cell.

PD affects 1 million people in the US and up to 10 million worldwide, making it the second most common neurodegenerative disease. Characteristic features of PD include symptoms such as tremors and difficulty walking, aggregation of a protein called alpha-synuclein (αSyn) within cells in the brain and gut, and the presence of inflammatory molecules called cytokines within the brain. In addition, 75 percent of people with PD have gastrointestinal (GI) abnormalities, primarily constipation.

“The gut is a permanent home to a diverse community of beneficial and sometimes harmful bacteria, known as the microbiome, that is important for the development and function of the immune and nervous systems,” Mazmanian says. “Remarkably, 70 percent of all neurons in the peripheral nervous system–that is, not the brain or spinal cord–are in the intestines, and the gut’s nervous system is directly connected to the central nervous system through the vagus nerve. Because GI problems often precede the motor symptoms by many years, and because most PD cases are caused by environmental factors, we hypothesized that bacteria in the gut may contribute to PD.”

To test this, the researchers utilized mice that overproduce αSyn and display symptoms of Parkinson’s. One group of mice had a complex consortium of gut bacteria; the others, called germ-free mice, were bred in a completely sterile environment at Caltech and thus lacked gut bacteria. The researchers had both groups of mice perform several tasks to measure their motor skills, such as running on treadmills, crossing a beam, and descending from a pole. The germ-free mice performed significantly better than the mice with a complete microbiome.

“This was the ‘eureka’ moment,” says Timothy Sampson, a postdoctoral scholar in biology and biological engineering and first author on the paper. “The mice were genetically identical; both groups were making too much αSyn. The only difference was the presence or absence of gut microbiota. Once you remove the microbiome, the mice have normal motor skills even with the overproduction of αSyn.”

“All three of the hallmark traits of Parkinson’s were gone in the germ-free models,” Sampson says. “Now we were quite confident that gut bacteria regulate, and are even required for, the symptoms of PD. So, we wanted to know how this happens.”

Image shows the outline of a person and a drawing of bacteria.

When gut bacteria break down dietary fiber, they produce molecules called short-chain fatty acids (SCFAs), such as acetate and butyrate. Previous research has shown that these molecules also can activate immune responses in the brain. Thus, Mazmanian’s group hypothesized that an imbalance in the levels of SCFAs regulates brain inflammation and other symptoms of PD. Indeed, when germ-free mice were fed SCFAs, cells called microglia–which are immune cells residing in the brain–became activated. Such inflammatory processes can cause neurons to malfunction or even die. In fact, germ-free mice fed SCFAs now showed motor disabilities and αSyn aggregation in regions of the brain linked to PD.

In a final set of experiments, Mazmanian and his group collaborated with Ali Keshavarzian, a gastroenterologist at Rush University in Chicago, to obtain fecal samples from patients with PD and from healthy controls. The human microbiome samples were transplanted into germ-free mice, which then remarkably began to exhibit symptoms of PD. These mice also showed higher levels of SCFAs in their feces. Transplanted fecal samples from healthy individuals, in contrast, did not trigger PD symptoms, unlike mice harboring gut bacteria from PD patients.

“This really closed the loop for us,” Mazmanian says. “The data suggest that changes to the gut microbiome are likely more than just a consequence of PD. It’s a provocative finding that needs to be further studied, but the fact that you can transplant the microbiome from humans to mice and transfer symptoms suggests that bacteria are a major contributor to disease.”

The findings have important implications for the treatment of Parkinson’s, the researchers say.

“For many neurological conditions, the conventional treatment approach is to get a drug into the brain. However, if PD is indeed not solely caused by changes in the brain but instead by changes in the microbiome, then you may just have to get drugs into the gut to help patients, which is much easier to do,” Mazmanian says. Such drugs could be designed to modulate SCFA levels, deliver beneficial probiotics, or remove harmful organisms. “This new concept may lead to safer therapies with fewer side effects compared to current treatments.”

ABOUT THIS PARKINSON’S DISEASE RESEARCH ARTICLE

The paper is titled “Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson’s Disease.” Other Caltech coauthors include Taren Thron, Gnotobiotic Facility manager and research technician for the Mazmanian laboratory; undergraduate Gauri G. Shastri; postdoctoral scholar Collin Challis; graduate student Catherine E. Schretter; and Viviana Gradinaru, assistant professor of biology and biological engineering and Heritage Medical Research Institute Investigator.

Funding: The work was funded by the Larry L. Hillblom Foundation, the Knut and Alice Wallenberg Foundation, the Swedish Research Council, Mr. and Mrs. Larry Field, the Heritage Medical Research Institute, and the National Institutes of Health.

Source: Lori Dajose – California Institute of Technology
Image Source: This NeuroscienceNews.com image is adapted from the California Institute of Technology press release.
Video Source: The video is credited to CalTech.
Original Research: Full open access research for “Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson’s Disease” by Timothy R. Sampson, Justine W. Debelius, Taren Thron, Stefan Janssen, Gauri G. Shastri, Zehra Esra Ilhan, Collin Challis, Catherine E. Schretter, Sandra Rocha, Viviana Gradinaru, Marie-Francoise Chesselet, Ali Keshavarzian, Kathleen M. Shannon9, Rosa Krajmalnik-Brown, Pernilla Wittung-Stafshede, Rob Knight, and Sarkis K. Mazmanian in Cell. Published online December 1 2016 doi:10.1016/j.cell.2016.11.018

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
California Institute of Technology. “Parkinson’s Disease Linked to Gut Microbiome.” NeuroscienceNews. NeuroscienceNews, 1 December 2016.
<http://neurosciencenews.com/microbiome-gut-parkinsons-5642/&gt;.

Abstract

Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson’s Disease

Highlights
•Gut microbes promote α-synuclein-mediated motor deficits and brain pathology
•Depletion of gut bacteria reduces microglia activation
•SCFAs modulate microglia and enhance PD pathophysiology
•Human gut microbiota from PD patients induce enhanced motor dysfunction in mice

Summary
The intestinal microbiota influence neurodevelopment, modulate behavior, and contribute to neurological disorders. However, a functional link between gut bacteria and neurodegenerative diseases remains unexplored. Synucleinopathies are characterized by aggregation of the protein α-synuclein (αSyn), often resulting in motor dysfunction as exemplified by Parkinson’s disease (PD). Using mice that overexpress αSyn, we report herein that gut microbiota are required for motor deficits, microglia activation, and αSyn pathology. Antibiotic treatment ameliorates, while microbial re-colonization promotes, pathophysiology in adult animals, suggesting that postnatal signaling between the gut and the brain modulates disease. Indeed, oral administration of specific microbial metabolites to germ-free mice promotes neuroinflammation and motor symptoms. Remarkably, colonization of αSyn-overexpressing mice with microbiota from PD-affected patients enhances physical impairments compared to microbiota transplants from healthy human donors. These findings reveal that gut bacteria regulate movement disorders in mice and suggest that alterations in the human microbiome represent a risk factor for PD.

“Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson’s Disease” by Timothy R. Sampson, Justine W. Debelius, Taren Thron, Stefan Janssen, Gauri G. Shastri, Zehra Esra Ilhan, Collin Challis, Catherine E. Schretter, Sandra Rocha, Viviana Gradinaru, Marie-Francoise Chesselet, Ali Keshavarzian, Kathleen M. Shannon9, Rosa Krajmalnik-Brown, Pernilla Wittung-Stafshede, Rob Knight, and Sarkis K. Mazmanian in Cell. Published online December 1 2016 doi:10.1016/j.cell.2016.11.018