HEALTH ALERT: COFFEE, BEER MAY AFFECT AGING, CANCER

COFFEE, BEER MAY AFFECT AGING, CANCER

Published December 6, 2013 in Food Product Design






Posted in News, International, Science & Research, Coffee, Caffeine, Beer, Alcohol, Beverages, Cancer,Yeast

TEL AVIV, Israel—Coffee and beer, although polar opposites, may be connected to aging and cancer, according to latest research published in PLOS Genetics.

Martin Kupiec, professor at Tel Aviv University's department of molecular biology and biotechnology, and his team, worked with yeast discovering that caffeine shortens and alcohol lengthens telomeres—the end points of chromosomal DNA.

"For the first time we've identified a few environmental factors that alter telomere length, and we've shown how they do it," Kupiec said. "What we learned may one day contribute to the prevention and treatment of human diseases."

Telomeres, made of DNA and proteins, mark the ends of the strands of DNA in the human chromosomes. They are essential to ensuring that the DNA strands are repaired and copied correctly. Every time a cell duplicates, the chromosomes are copied into the new cell with slightly shorter telomeres. Eventually, the telomeres become too short, and the cell dies.

The study was an expansion from a previous 2004 study conducted by Elizabeth Blackburn, who suggested that emotional stress causes the shortening of the telomeres characteristic of aging, presumably by generating free radicals in the cells.

By exposing the yeast cells to 12 environmental stressors, the researchers realized that a low concentration of caffeine, similar to the amount found in a shot of espresso, shortened telomeres, and exposure to a 5% to 7% ethanol solution lengthened telomeres.

To understand these changes researchers scanned 6,000 strains of the yeast, each with a different gene deactivated. They conducted genetic tests on the strains with the longest and shortest telomeres, revealing that two genes, Rap1 and Rif1, are the main players mediating environmental stressors and telomere length. In total, some 400 genes interact to maintain telomere length underscoring the importance of this gene network in maintaining the stability of the genome.

"This is the first time anyone has analyzed a complex system in which all of the genes affecting it are known," Kupiec said. "It turns out that telomere length is something that's very exact, which suggests that precision is critical and should be protected from environmental effects."

More research is needed to prove a causal relationship, not a mere correlation, between telomere length and aging or cancer.

Sources:

• American Friends Tel Aviv University: Coffee or Beer? The Choice Could Affect Your Genome

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HEALTH ALERT: GENE-DIET INTERACTION IDENTIFIED FOR COLORECTAL CANCER

GENE-DIET INTERACTION IDENTIFIED FOR COLORECTAL CANCER

Published October 25, 2013 in Food Product Design

Posted in News, Diet, Nutrition, International, Demographic, Cancer, Digestive Health, Science & Research, Fruits / Vegetables, Fruit, Vegetable, Meat Products, Processed Meats, Beef, Proteins

BOSTON—Researchers have identified a gene-diet interaction that corresponds with the risk of colorectal cancer and the consumption of red or processed meat.

“If replicated, our findings have a relevant public health significance because diet is a modifiable risk factor for colorectal cancer," said Jane Figueiredo, Ph.D., assistant professor of preventive medicine at the University of Southern California Keck School of Medicine.

“It is conceivable that selected individuals at higher risk of colorectal cancer based on genomic profiling could be targeted for screening, diet modification and other prevention strategies," added Dr. Figueiredo, collaborating scientist in the international Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO).

In 10 GECCO observational studies, 9,287 patients with colorectal cancer and a control group of 9,117 individuals without cancer were enrolled. The scientists searched 2.7 million variants to identify those associated with consumption of red and processed meat and fruits and vegetables.

A significant interaction between the genetic variant rs4143094 and processed meat consumption was detected.  This variant is located on the same chromosome 10 region that includes GATA3, a transcription factor gene previously linked to several forms of cancer. The transcription factor encoded by this gene normally plays a role in the immune system.

On chromosome 8, a statistically significant diet-gene interaction was found in another variant, rs1269486. This variant was associated with reduced risk of colorectal cancer.
How specific foods affect the activities of genes has not been established. Drs. Peters and Figueiredo speculate that digestion of processed meat may promote an immunological or inflammatory response that may trigger tumor development.

The group of researchers determined that the lower colorectal cancer risk associated with vegetables, fruit and fiber intake was linked to genetic variants.

The possibility that genetic variants may modify and individual's risk for disease based on diet has not been thoroughly investigated but represents an important new insight into disease development, said Ulrike Peters, Ph.D., M.P.H., the lead author of the study.

This is the first colorectal cancer study with the statistical power to identify gene-dietary interaction across the genome of a large population of individuals, added Li Hsu, Ph.D.

In previous years, the American Meat Institute (AMI) and  the Beef and Pork Checkoff Program,  challenged reports linking meat to cancer.

Sources:

• The American Society of Human Genetics: Novel gene-diet interaction may help explain association between eating red & processed meat and colorectal cancer risk

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HEALTH ALERT: COMPOUND IN MEDITERRANEAN DIET INHIBITS CANCER CELLS

COMPOUND IN MEDITERRANEAN DIET INHIBITS CANCER CELLS

Published May 22, 2013 in Food Product Design

COLUMBUS, Ohio—A compound found in parsley, celery and other plant products, including apples, oranges and nuts that are part of the Mediterranean diet, may stop breast cancer cells from inhibiting their own death, according to a new study published online in the journal Proceedings of the National Academy of Sciences.

The findings suggest by altering a very specific step in gene regulation, the compound—apigenin—essentially re-educates cancer cells into normal cells that die as scheduled.

Much of what is known about the health benefits of nutrients is based on epidemiological studies that show strong positive relationships between eating specific foods and better health outcomes, especially reduced heart disease. But how the actual molecules within these healthful foods work in the body is still a mystery in many cases, and particularly with foods linked to lower risk for cancer.

Ohio State University researchers also showed that apigenin binds with an estimated 160 proteins in the human body, suggesting that other nutraceuticals might have similar far-reaching effects.

“We know we need to eat healthfully, but in most cases we don’t know the actual mechanistic reasons for why we need to do that," said Andrea Doseff, associate professor of internal medicine and molecular genetics at Ohio State and a co-lead author of the study. “We see here that the beneficial effect on health is attributed to this dietary nutrient affecting many proteins. In its relationship with a set of specific proteins, apigenin re-establishes the normal profile in cancer cells. We think this can have great value clinically as a potential cancer-prevention strategy."

Through additional experimentation, the team established that apigenin had relationships with proteins that have three specific functions. Among the most important was a protein called hnRNPA2. This protein influences the activity of messenger RNA, or mRNA, which contains the instructions needed to produce a specific protein. The production of mRNA results from the splicing, or modification, of RNA that occurs as part of gene activation. The nature of the splice ultimately influences which protein instructions the mRNA contains.

The researchers said abnormal splicing is the culprit in an estimated 80% of all cancers. In cancer cells, two types of splicing occur when only one would take place in a normal cell—a trick on the cancer cells’ part to keep them alive and reproducing.

In this study, the researchers observed that apigenin’s connection to the hnRNPA2 protein restored this single-splice characteristic to breast cancer cells, suggesting that when splicing is normal, cells die in a programmed way, or become more sensitive to chemotherapeutic drugs.

“So by applying this nutrient, we can activate that killing machinery. The nutrient eliminated the splicing form that inhibited cell death," Doseff said. “Thus, this suggests that when we eat healthfully, we are actually promoting more normal splice forms inside the cells in our bodies."

Sources:

• Ohio State University: The Compound in the Mediterranean Diet that Makes Cancer Cells ‘Mortal’

Check out my latest e-book entitled: "Social Media Marketing in Agri-Foods: Endless Profit and Painless Gain".  

The book is available on Amazon and Kindle for $4.99 USD. Visit amazon/Kindle to order now:
http://www.amazon.ca/Social-Media-Marketing-Agri-Foods-ebook/dp/B00C42OB3E/ref=sr_1_1?s=digital-text&ie=UTF8&qid=1364756966&sr=1-1

Written by Bruce MacDonald, a 30 year veteran of the Agri-food industry, in "Social Media Marketing in Agri-Foods: Endless Profit and Painless Gain", Bruce applies his background and expertise in Agri-foods and social media to the latest trends, tools and methodologies needed to craft a successful on-line campaign. While the book focuses on the Agri-food market specifically, I believe that many of the points Bruce makes are equally applicable to most other industries.