Dietary fiber, which consists of carbohydrates that our body cannot break down and absorb, passes relatively intact through our stomach and intestines. AICR/WCRF's report, Food, Nutrition, Physical Activity and the Prevention of Cancer: a Global Perspective, concluded that a high-fiber diet can reduce the risk of colorectal cancer. Found in vegetables, fruits, legumes and other plant foods, dietary fiber may have a direct and indirect effect against colon cancer.
Foods high in dietary fiber are relatively low in energy density, contributing to a feeling of fullness that makes over-eating less likely and reducing the risk of overweight and obesity, a cause of seven types of cancer. Fiber may also help the body maintain a healthy bacterial cell turnover in the colon. Emerging research continues to explore the cellular functions and mechanisms that may be responsible for the protective effect of dietary fiber.
"The 2010 Dietary Guidelines for Americans recommend
14 grams of fiber for every 1,000 calories.
In searching for fiber's protective effect, scientists have honed in one of fiber's metabolic by-products: butyrate. AICR grantee Leonard Augenlicht, PhD, Professor of Medicine and Cell Biology at Albert Einstein College of Medicine, hypothesizes that one of the keys to dietary fiber may lie in butyrate – a short-chain fatty acid that is the principal energy source for intestinal cells.
When Augenlicht and colleagues treated cancer cells with butyrate, the cells generally stopped growing, which led to apoptosis. Although butyrate inhibits the growth of cancerous cells, it also serves as an energy source for normal cells and stays at relatively high levels in the intestinal lumen, where digested food passes and nutrients get absorbed. When butyrate is removed from normal cells, cell growth stops.
"Because butyrate seems to affect normal and cancer cells differently, we refer to it as the 'butyrate paradox'," says Augenlicht. "We don't know why butyrate represses tumor cells, but it seems to inhibit the transcription of certain genes that cause cells to proliferate." According to Augenlicht, one of these genes may be cyclin D1, which plays a major role in intestinal tumor growth.
"A lot of questions remain about fiber and butyrate," says Augenlicht. "Dietary fiber appears to be protective, but it hasn't been shown consistently in studies with people because it's difficult to do large intervention studies and tease out all of the competing influences."
Along with fiber, whole grains' high minerals, vitamins and phytochemical content have made whole grains and cancer risk an active area of research. Thus far, the body of evidence on the cancer-protective effects of whole grains connects the benefits of high-fiber with a healthy weight. Yet many studies have suggested other roles for whole grains in cancer protection, such as one recent study of nearly 3,000 middle-aged adults. The study found that adults who consumed several servings of whole grains per day, including dark bread, ready-to-eat cereals, oatmeal, popcorn and brown rice, had lower levels of visceral fat, or fat around the waist, when they limited refined grains. Visceral fat sits deep within the abdomen and is associated with chronic inflammation and high insulin levels, both linked to increased risk of cancer;
The study, published in the American Journal of Clinical Nutrition, found that visceral fat was 10 percent lower in adults who consumed at least three servings of whole grains per day and consumed fewer than one daily serving refined grains, when compared to those who ate no whole grains. Conversely, participants who consumed more refined grains, such as pasta, English muffins, white bread, pizza and rice, had higher levels of visceral fat. "This implies that it is important to make substitutions in the diet, rather than simply adding whole-grain foods," said lead author Nicola M. McKeown, PhD, Assistant Professor at Tufts University.
Excerpted from ScienceNow.
For the first time, the annual report F as in Fat: How Obesity Threatens America's Future 2011, looked at obesity over the past two decades. Twenty years ago, no state had an obesity rate above 15 percent. Today, 38 states have obesity rates over 25 percent, and just one has a rate lower than 20 percent (Colorado).
See how your state ranks and to read more on the report.
A new analysis of the research suggests that it's the population not eating fruits and vegetables who gain the most cancer protection by adding about one serving to their day. The findings mirror other research suggesting that greater benefits are seen among those most deficient.
The study is published in this month's issue of the journal Gastroenterology and was conducted as part of the WCRF/AICR Continuous Update Project.
Study researchers analyzed all relevant research published until May 2010, ending up with 19 studies. The researchers conducted two analysis techniques: linear and non-linear dose response analyses. The linear assumes the dose – or consumption in this case – is proportional to the effect; the non-linear does not. For the linear, high consumption of vegetables alone appeared to provide a small protection against colon cancer compared to those who ate the fewest vegetables.
Yet for the non-linear analysis, both fruits and vegetables lowered risk of colorectal cancer. The greatest change in risk reduction occurred among people who consumed only about one serving daily compared to those who ate none. For fruit, those who ate slightly more than one serving daily – 100 grams, (about half a cup) – compared to those who consumed nothing had the greatest increase in protection. Eating more than that continued to add protection but only relatively slightly. For vegetables, the greatest change in reduced risk was seen among those who ate about two servings per day compared to half that: 200 grams compared to 100 grams.
Source: Dagfinn Aune, et al. "Nonlinear Reduction in Risk for Colorectal Cancer by Fruit and Vegetable Intake Based on Meta-analysis of Prospective Studies." Gastroenterology. Volume 141, Issue 1, Pages 106-118, July 2011.
Being overweight in young adulthood may increase the risk of a premature death from cancer decades later, suggests a new study that adds to the growing body of research on the role of weight throughout life. The study was published in the Annals of Oncology.
The study pulled data from a pool of almost 20,000 male undergraduates at Harvard University. BMI data were first colleted between 1914 and 1952, when the students were 18 years old. It was collected again in the 1960s when the men were middle aged – 45 years old on average.
After tracking the men for another three decades (an average of 56 years after graduation), the study found that men in the study who had the highest BMIs at age 18 were 35 percent more likely to die from cancer than those with lowest BMIs. (This was a relatively slender population overall, with the highest category of men having a BMI over 23 and the lowest a BMI under 20. Today, overweight is categorized as a BMI over 25.)
The associations between higher BMIs and cancer morality were particularly strong for several cancers, including lung and kidney. For every 2.6 unit increase in BMI – such as a BMI from 23 to 25.6 – there was an 11 percent increased risk of cancer mortality overall.
Adjusting for BMI in middle age, smoking, and physical activity did not substantially alter the link between early BMI and later cancer mortality.
Source: L. Gray, M. Lee, HD Sesso, GD Batty. "Association of body mass index in early adulthood and middle age with future site-specific cancer mortality: the Harvard Alumni Health Study." Ann Oncol 2011.
For anyone who has reached out for comfort foods when feeling stressed or depressed, a new laboratory study offers hints that may help explain why. The study points to the role of ghrelin, commonly termed the hunger hormone.
Researchers know that hunger prompts ghrelin levels to increase, sending hunger signals to the brain. Emerging laboratory studies, according to the study authors, also suggests a link between chronic stress and elevated ghrelin levels.
In this study, scientists worked with engineered mice that were unable to sense ghrelin. They subjected mice with and without ghrelin receptors to stress. The animals that could sense ghrelin moved toward a chamber where they knew they would find fatty food – the mouse equivalent of comfort food. Yet the genetically-engineered mice did not show an interest in the fatty food. And when these foods were placed nearby, they did not eat as much as the control animals. This is an early study on the topic, conducted in animals, and as the authors note, future research is needed.
Source: Chuang JC, et al. "Ghrelin mediates stress-induced food-reward behavior in mice." J Clin Invest. 2011 Jun 23. pii: 57660.