How Soy Reduces Diabetes Risk

Science Daily

Wednesday, October 7, 2009

Nutrition scientists led by Young-Cheul Kim at the University of Massachusetts Amherst have identified the molecular pathway that allows foods rich in soy bioactive compounds called isoflavones to lower diabetes and heart disease risk. Eating soy foods has been shown to lower cholesterol, decrease blood glucose levels and improve glucose tolerance in people with diabetes.

According to Kim, the study shows that “what we eat can have tremendous impact on health outcomes by interacting with certain genes. Recent research also suggests that diet can even change the copy number of a certain gene, leading to biological changes.”

Soy is the most common source of isoflavones in food. In experiments with mouse cells, Kim, a molecular nutrition researcher who studies how fat cells develop in the body, and colleagues, focused on daidzein, one of the two main isoflavones found in soy. Many epidemiological observations and human clinical studies have shown that adding soy to one’s diet is associated with lower diabetes risk and improved insulin sensitivity, as well as lower cardiovascular disease risk, Kim notes. However, until now the direct target tissue and molecular pathways by which soy exerts its anti-diabetic effects was not clearly understood.

Kim and colleagues at Southern Illinois University, with others at the universities of Tennessee and Florida, had earlier found that dietary isoflavones reduced the severity of diabetes in an animal model of the disease by increasing the activity of certain transcription regulators in the fat tissue. For the current study, they hypothesized that daidzein and its metabolite, equol, are part of this activation process.

They found that daidzein and equol enhanced adipocyte differentiation, or the formation of fat cells, through activation of a key transcription regulator, the same receptor that mediates the insulin-sensitizing effects of anti-diabetes drugs. Thus, daidzein and equol daidzein and equol seem to work in a similar manner as anti-diabetic drugs currently in the market. Their findings are reported in a September online version of the Journal of Nutritional Biochemistry.

“Our results suggest that soy isoflavones exert anti-diabetic effects by targeting fat cell-specific transcription factors and the downstream signaling molecules that are important for glucose uptake and thus insulin sensitivity,” Kim notes. “The new findings help us to understand the cellular mechanisms.” That is, how these biologically active compounds in soy interact to regulate and initiate metabolic and biological functions.

Results demonstrate that daidzein and equol enhance adipocyte differentiation by activating a specific receptor. The downstream responses include increased expression of three proteins, resulting in enhanced glucose uptake and insulin sensitivity.

“Although some details remain to be worked out, our data provide an additional molecular basis for the mechanism of insulin-sensitizing action by soy isoflavones,” says Kim. “These new findings help fill a critical gap between epidemiological observations and clinical studies on the anti-diabetic benefits of dietary soy.”

Future studies will extend the work to primary cultures of human cells through collaboration with researchers at Pioneer Valley Life Science Institute and Baystate Medical Center in Springfield. If replicated, studies can move on to further work in whole body systems. Full article here…

Black Tea May Fight Diabetes

Science Daily

Wednesday, July 29, 2009

Long known for its antioxidants, immune boosting and, most recently, antihypertensive properties, black tea could have another health benefit. Black tea may be used to control diabetes, according to a study in the Journal of Food Science, published by the Institute of Food Technologists.

Next to water, tea is the second most consumed beverage in the world. Researchers from the Tianjin Key Laboratory in China studied the polysaccharide levels of green, oolong and black teas and whether they could be used to treat diabetes. Polysaccharides, a type of carbohydrate that includes starch and cellulose, may benefit people with diabetes because they help retard absorption of glucose.

The researchers found that of the three teas, the polysaccharides in black tea had the most glucose-inhibiting properties. The black tea polysaccharides also showed the highest scavenging effect on free radicals, which are involved in the onset of diseases such as cancer and rheumatoid arthritis.

“Many efforts have been made to search for effective glucose inhibitors from natural materials,” says lead researcher Haixia Chen. “There is a potential for exploitation of black tea polysaccharide in managing diabetes.”

Do Contaminants Play a Role in Diabetes? Evidence is Growing

Environmental Health News
Andrew McGlashen
Thursday, July 23, 2009

Eat right and exercise, conventional wisdom has it, if you want to avoid joining the diabetes epidemic.

But a new study adds some muscle to a growing body of research suggesting those steps, although beneficial, might not be enough for people exposed to chemicals in the environment.

The scientists linked diabetes and people’s body burdens of DDE, a chemical produced as the body breaks down the pesticide DDT, banned in the United States more than 35 years ago.

“Even though we haven’t used DDT in decades, its metabolites are still detected in almost everyone in the country,” said lead researcher Mary Turyk, an epidemiologist at the University of Illinois-Chicago’s School of Public Health.

Since the early 1990s, researchers have monitored a group of Great Lakes charter boat captains, recreational fishermen and others to learn about the health effects of eating fish tainted with persistent organic pollutants – chemicals that remain in the environment for decades and grow more concentrated as they move up food chains.

For the new study, blood samples from the Great Lakes group showed “consistent, dose-related associations of DDE” with diabetes, the researchers wrote in the July issue of Environmental Health Perspectives.

Among 471 adults, including 36 with diabetes, there was no link to the disease based on the amount of fish consumed or exposure to other pollutants. But the higher the concentration of DDE in the blood, the more likely they were to develop diabetes.

The study is among the strongest voices in a chorus of research supporting the link between environmental chemicals and diabetes, according to David O. Carpenter, director of the Institute for Health and the Environment at the State University of New York, Albany. He was not involved in the study.

“Most people have not thought of diabetes as a disease related to environmental exposure,” he said, “and these studies show that it is. The science has been growing very, very rapidly, and to my mind, it’s one of the most exciting developments in the study of diabetes.”

Diabetics cannot produce or use enough insulin, a hormone that lets glucose – the body’s fuel – enter cells. More than 23 million Americans, or eight percent of the population, are diabetic, and that group swelled by 13.5 percent from 2005 to 2007, according to the American Diabetes Assn.

For the most common type of diabetes, Type 2, obesity and lack of exercise play a key role. The bulk of studies searching for a cause have focused on lifestyle factors, while research on environmental influences hasn’t been prominent in journals devoted to the disease, said Henry Kahn, an epidemiologist with the Centers for Disease Control and Prevention’s Division of Diabetes Translation.

“But maybe it should be. It would be foolish to overlook pollution as a factor,” he said, adding that he and colleagues have lately taken a greater interest in the role of pollutants. “We recognize it’s possibly a very important thing,” he said. “We agree it’s on the list of things worth studying.”

Oliver Jones, a biochemist at the University of Cambridge, wrote in the journal Lancet last year that “if there is indeed a link” between contaminants and diabetes, “the health implications could be tremendous. There has been almost no consideration for the possible influence of environmental factors such as pollution.”

Among the reasons to believe that the environment might be involved in diabetes, according to Carpenter, is that its prevalence varies across geographic areas, and people who move to places where it’s more common become more likely to get sick. Kahn, however, said that effect could be due to people migrating to more developed areas, where a richer diet and more sedentary lifestyle are the norm.

Further evidence came from a sweeping study of more than 2,000 adults, conducted by the U.S. Centers for Disease Control and Prevention, that found people with the highest levels of six pollutants were 38 times more likely to have diabetes than those with the lowest exposure. The chemicals, including PCBs, dioxins and DDE, were chosen because they were present in at least 80 percent of participants.

“That’s just mind-boggling,” Carpenter said.

Also, Vietnam veterans exposed to the dioxin-laced defoliant Agent Orange were significantly more likely than average to become diabetic, prompting the government to offer compensation to diabetic veterans.

The way the new Great Lakes study was conducted makes its findings especially convincing, according to the authors and other experts.

Other research has found similar links between diabetes and pollutants, but they were cross-sectional studies, which means “you measure the level of a chemical and ask people if they have diabetes,” Turyk said.

Those studies could easily be skewed, Turyk said, because they don’t indicate whether diabetes developed before a person was exposed to pollutants. But in the new paper, she and colleagues measured participants’ exposure to DDE from blood samples taken in the mid-1990s, then followed up with them for nearly a decade to see who among them became diabetic, thereby ensuring that diabetics were exposed before they were diagnosed.

The paper further bulwarked the claim by discrediting the hypothesis that the link between the two is a statistical fluke. Critics have suggested that pollutants like DDE only appear to be potential causes of the disease because diabetics more slowly break down the chemicals, and therefore carry more of them.

But Turyk, sharing principal research duties with Henry Anderson of the Wisconsin Division of Public Health and Victoria Persky at the University of Illinois-Chicago, quashed that theory by showing no difference in DDE metabolism rates between diabetics and non-diabetics.

“This paper clearly shows that’s not the case,” said Carpenter. “It’s a very important contribution because of that fact.”

The researchers controlled for obesity, age and other risk factors, and still found a link to DDE exposure. The study didn’t distinguish between Type 2 and Type 1, or early-onset diabetes, but most diabetics in the study suffered from Type 2, which is more common in adults.

The authors said the relatively small number of participants and short duration limit the reliability of the findings. In addition, the link to DDE was relatively weak compared with past research.

Like nearly all human health research, it doesn’t directly show that chemicals in the environment cause diabetes.

“With epidemiology, you gather a body of evidence against something,” she said. “You can never really prove something causes something else.”

Scientists still don’t understand the mechanism by which DDE and other chemicals might contribute to diabetes, according to Carpenter, though he said pollution seems to disrupt the way genes produce proteins and “basically change the biochemistry of the cell.”

“It may be that they’re toxic to the pancreas,” which produces insulin Kahn added. “We don’t know.”

For now, common-sense precautions are everyone’s best bet, Carpenter said.

“Obese people are usually obese because they eat too many animal fats, and animal fats are where these contaminants are commonly found,” he said.

Turyk added that “people should definitely follow sport fish advisories,” which warn about contaminants in waterways.