News Categories
RSS Feed
Latest Updates
Jan
10
Sugar in Western diets increases risk for breast cancer tumors and metastasis
Posted by Customer Support on 10 January 2016 07:27 PM

The high amounts of dietary sugar in the typical Western diet may increase the risk of breast cancer and metastasis to the lungs, according to a study at The University of Texas MD Anderson Cancer Center.

The findings, published in the Jan. 1 online issue of Cancer Research, demonstrated dietary sugar’s effect on an enzymatic signaling pathway known as 12-LOX (12-lipoxygenase).

“We found that sucrose intake in mice comparable to levels of Western diets led to increased tumor growth and metastasis, when compared to a non-sugar starch diet,” said Peiying Yang, Ph.D., assistant professor of Palliative, Rehabilitation, and Integrative Medicine. “This was due, in part, to increased expression of 12-LOX and a related fatty acid called 12-HETE.”

Previous epidemiological studies have shown that dietary sugar intake has an impact on breast cancer development, with inflammation thought to play a role.

“The current study investigated the impact of dietary sugar on mammary gland tumor development in multiple mouse models, along with mechanisms that may be involved,” said co-author Lorenzo Cohen, Ph.D., professor of Palliative, Rehabilitation, and Integrative Medicine. “We determined that it was specifically fructose, in table sugar and high-fructose corn syrup, ubiquitous within our food system, which was responsible for facilitating lung metastasis and 12-HETE production in breast tumors.”

Cohen added that the data suggested that dietary sugar induces 12-LOX signaling to increase risks for breast cancer development and metastasis.

Identifying risk factors for breast cancer is a public health priority, say the authors.  The researchers state that moderate sugar consumption is critical, given that the per capita consumption of sugar in the U.S. has surged to over 100 lbs. per year and an increase in consumption of sugar-sweetened beverages has been identified as a significant contributor to an epidemic of obesity, heart disease and cancer worldwide.

“Prior research has examined the role of sugar, especially glucose, and energy-based metabolic pathways in cancer development,” said Yang. “However, the inflammatory cascade may be an alternative route of studying sugar-driven carcinogenesis that warrants further study.”

No previous studies have investigated the direct effect of sugar consumption on the development of breast cancer using breast cancer animal models or examined specific mechanisms, she added.

The MD Anderson team conducted four different studies in which mice were randomized to different diet groups and fed one of four diets. At six months of age, 30 percent of mice on a starch-control diet had measurable tumors, whereas 50 to 58 percent of the mice on sucrose-enriched diets had developed mammary tumors. The study also showed that numbers of lung metastases were significantly higher in mice on a sucrose- or a fructose-enriched diet, versus mice on a starch-control diet.

“This study suggests that dietary sucrose or fructose induced 12-LOX and 12-HETE production in breast tumor cells in vivo,” said Cohen. “This indicates a possible signaling pathway responsible for sugar-promoted tumor growth in mice. How dietary sucrose and fructose induces 12-HETE and whether it has a direct or indirect effect remains in question.”

The study team believes that the mechanism by which dietary sucrose or fructose affects breast tumor growth and metastasis, especially through the 12-LOX pathways, warrants further investigation.

MD Anderson research team members included Yan Jiang, Yong Pan, Patrea Rhea, and Lin Tan, all of Palliative, Rehabilitation and Integrative Medicine; Mihai Gagea, D.V.M., Ph.D., Veterinary Medicine & Surgery; and Susan Fischer, Epigenetics & Molecular Carcinogenesis.

The study was funded by the National Institutes of Health (P30CA0166672), Mr. and Mrs. H. Leighton Steward and EOG Resources, Inc.


Read more »



Dec
12
Blood Sugar Levels in Response to Foods Are Highly Individual
Posted by Customer Support on 12 December 2015 09:35 PM

The largest study of its kind supports the need for personalized dietary recommendations.

REHOVOT, ISRAEL—November 19, 2015—Which is more likely to raise blood sugar levels: sushi or ice cream? According to a Weizmann Institute of Science study reported in the November 19 issue of the journal Cell, the answer varies from one person to another. The study, which continuously monitored blood sugar levels in 800 people for a week, revealed that the bodily response to all foods was highly individual.

The study, called the Personalized Nutrition Project (www.personalnutrition.org), was conducted by the groups of Prof. Eran Segal of the Department of Computer Science and Applied Mathematics and Dr. Eran Elinav of the Department of Immunology. Prof. Segal said: “We chose to focus on blood sugar because elevated levels are a major risk factor for diabetes, obesity, and metabolic syndrome. The huge differences that we found in the rise of blood sugar levels among different people who consumed identical meals highlights why personalized eating choices are more likely to help people stay healthy than universal dietary advice.” 

Elinav and Segal

Dr. Eran Elinav, left; Prof. Eran Segal, right

Indeed, the scientists found that different people responded very differently to both simple and complex meals. For example, a large number of the participants’ blood sugar levels rose sharply after they consumed a standardized glucose meal, but in many others, blood glucose levels rose sharply after they ate white bread, but not after glucose. “Our aim in this study was to find factors that underlie personalized blood glucose responses to food,” said Dr. Elinav. “We used that information to develop personal dietary recommendations that can help prevent and treat obesity and diabetes, which are among the most severe epidemics in human history.” 

David Zeevi and Tal Korem, PhD students in Prof. Segal’s lab, led the study. They collaborated with Dr. Niv Zmora, a physician conducting PhD studies in Dr. Elinav’s lab, and with PhD student Daphna Rothschild and research associate Dr. Adina Weinberger from Prof. Segal’s lab. The study was unique in its scale and in the inclusion of the analysis of gut microbes, collectively known as the microbiome, which had recently been shown to play an important role in human health and disease. Study participants were outfitted with small monitors that continuously measured their blood sugar levels and were asked to record everything they ate, as well as such lifestyle factors as sleep and physical activity. Overall, the researchers assessed the responses of different people to more than 46,000 meals. 

Segal-Elinav-2

Participants had strikingly different responses to identical foods. In study participant number 445 (top), blood sugar levels rose sharply after eating bananas, but not after cookies with the same amount of calories. The opposite occurred in participant 644 (bottom).

Taking these multiple factors into account, the scientists generated an algorithm for predicting individualized response to food based on the person’s lifestyle, medical background, and the composition and function of his or her microbiome. In a follow-up study of another 100 volunteers, the algorithm successfully predicted the rise in blood sugar in response to different foods, demonstrating that it could be applied to new participants. The scientists were able to show that lifestyle also mattered: The same food affected blood sugar levels differently in the same person, depending, for example, on whether its consumption had been preceded by exercise or sleep.

In the final stage of the study, the scientists designed a dietary intervention based on their algorithm; this was a test of their ability to prescribe personal dietary recommendations for lowering blood-glucose-level responses to food. Volunteers were assigned a personalized “good” diet for one week, and a “bad” diet – also personalized – for another. Both good and bad diets were designed to have the same number of calories, but the diets differed between participants. Thus, certain foods in one person’s “good” diet were part of another’s “bad” diet. The “good” diets indeed helped to keep blood sugar at steadily healthy levels, whereas the “bad” diets often induced spikes in glucose levels – all within just one week of intervention. Moreover, as a result of the “good” diets, the volunteers experienced consistent changes in the composition of their gut microbes, suggesting that the microbiome may be influenced by the personalized diets while also playing a role in participants’ blood sugar responses.

A video animation describing the study is available at the following link: 

REHOVOT, ISRAEL—November 19, 2015—Which is more likely to raise blood sugar levels: sushi or ice cream? According to a Weizmann Institute of Science study reported in the November 19 issue of the journal Cell, the answer varies from one person to another. The study, which continuously monitored blood sugar levels in 800 people for a week, revealed that the bodily response to all foods was highly individual.

The study, called the Personalized Nutrition Project (www.personalnutrition.org), was conducted by the groups of Prof. Eran Segal of the Department of Computer Science and Applied Mathematics and Dr. Eran Elinav of the Department of Immunology. Prof. Segal said: “We chose to focus on blood sugar because elevated levels are a major risk factor for diabetes, obesity, and metabolic syndrome. The huge differences that we found in the rise of blood sugar levels among different people who consumed identical meals highlights why personalized eating choices are more likely to help people stay healthy than universal dietary advice.” 

Elinav and Segal

Dr. Eran Elinav, left; Prof. Eran Segal, right

Indeed, the scientists found that different people responded very differently to both simple and complex meals. For example, a large number of the participants’ blood sugar levels rose sharply after they consumed a standardized glucose meal, but in many others, blood glucose levels rose sharply after they ate white bread, but not after glucose. “Our aim in this study was to find factors that underlie personalized blood glucose responses to food,” said Dr. Elinav. “We used that information to develop personal dietary recommendations that can help prevent and treat obesity and diabetes, which are among the most severe epidemics in human history.” 

David Zeevi and Tal Korem, PhD students in Prof. Segal’s lab, led the study. They collaborated with Dr. Niv Zmora, a physician conducting PhD studies in Dr. Elinav’s lab, and with PhD student Daphna Rothschild and research associate Dr. Adina Weinberger from Prof. Segal’s lab. The study was unique in its scale and in the inclusion of the analysis of gut microbes, collectively known as the microbiome, which had recently been shown to play an important role in human health and disease. Study participants were outfitted with small monitors that continuously measured their blood sugar levels and were asked to record everything they ate, as well as such lifestyle factors as sleep and physical activity. Overall, the researchers assessed the responses of different people to more than 46,000 meals. 

Segal-Elinav-2

Participants had strikingly different responses to identical foods. In study participant number 445 (top), blood sugar levels rose sharply after eating bananas, but not after cookies with the same amount of calories. The opposite occurred in participant 644 (bottom).

Taking these multiple factors into account, the scientists generated an algorithm for predicting individualized response to food based on the person’s lifestyle, medical background, and the composition and function of his or her microbiome. In a follow-up study of another 100 volunteers, the algorithm successfully predicted the rise in blood sugar in response to different foods, demonstrating that it could be applied to new participants. The scientists were able to show that lifestyle also mattered: The same food affected blood sugar levels differently in the same person, depending, for example, on whether its consumption had been preceded by exercise or sleep.

In the final stage of the study, the scientists designed a dietary intervention based on their algorithm; this was a test of their ability to prescribe personal dietary recommendations for lowering blood-glucose-level responses to food. Volunteers were assigned a personalized “good” diet for one week, and a “bad” diet – also personalized – for another. Both good and bad diets were designed to have the same number of calories, but the diets differed between participants. Thus, certain foods in one person’s “good” diet were part of another’s “bad” diet. The “good” diets indeed helped to keep blood sugar at steadily healthy levels, whereas the “bad” diets often induced spikes in glucose levels – all within just one week of intervention. Moreover, as a result of the “good” diets, the volunteers experienced consistent changes in the composition of their gut microbes, suggesting that the microbiome may be influenced by the personalized diets while also playing a role in participants’ blood sugar responses.

A video animation describing the study is available at the following link: 


The scientists are currently enrolling Israeli volunteers for a longer-term follow-up dietary intervention study that will focus on people with consistently high blood sugar levels – and thus are at risk of developing diabetes – with the aim of preventing or delaying this disease. To learn more, please visit www.personalnutrition.org

Also participating in this research were Orly Ben-Yacov, Dar Lador, Dr. Tali Avnit-Sagi, Dr. Maya Lotan-Pompan, Elad Matot, Gal Malka, Noa Kosower, Michal Rein, and Rony Bikovsky in Prof. Segal’s lab; Jotham Suez, Jemal Ali Mahdi, Gili Zilberman-Schapira, Lenka Dohnalova, and Dr. Meirav Pevsner-Fischer in Dr. Elinav’s lab; Dr. David Israeli of the Jerusalem Center for Mental Health; and Prof. Zamir Halpern of the Tel Aviv Sourasky Medical Center.

Prof. Eran Segal’s research is supported by the Crown Human Genome Center, which he heads; the Adelis Foundation; the European Research Council; Mr. and Mrs. Donald L. Schwarz, Sherman Oaks, CA; Leesa Steinberg, Canada; and Jack N. Halpern, New York, NY.

Dr. Eran Elinav’s research is supported by the Abisch Frenkel Foundation for the Promotion of Life Sciences; the Gurwin Family Fund for Scientific Research; the Leona M. and Harry B. Helmsley Charitable Trust; the Crown Endowment Fund for Immunological Research; the Adelis Foundation; the Rising Tide Foundation; the Vera Rosenberg Schwartz Research Fellow Chair; Yael and Rami Ungar, Israel; John L. and Vera Schwartz, Pacific Palisades, CA; Alan Markovitz, Canada; Leesa Steinberg, Canada; Andrew and Cynthia Adelson, Canada; the estate of Jack Gitlitz; the estate of Lydia Hershkovich; Mr. and Mrs. Donald L. Schwarz, Sherman Oaks, CA; Jack N. Halpern, New York, NY; and Aaron Edelheit, Boca Raton, FL. Dr. Elinav is the incumbent of the Rina Gudinski Career Development Chair.

- See more at: http://www.weizmann-usa.org/media/2015/11/19/blood-sugar-levels-in-response-to-foods-are-highly-individual#sthash.zQnhZ1hL.dpuf

The scientists are currently enrolling Israeli volunteers for a longer-term follow-up dietary intervention study that will focus on people with consistently high blood sugar levels – and thus are at risk of developing diabetes – with the aim of preventing or delaying this disease. To learn more, please visit www.personalnutrition.org

Also participating in this research were Orly Ben-Yacov, Dar Lador, Dr. Tali Avnit-Sagi, Dr. Maya Lotan-Pompan, Elad Matot, Gal Malka, Noa Kosower, Michal Rein, and Rony Bikovsky in Prof. Segal’s lab; Jotham Suez, Jemal Ali Mahdi, Gili Zilberman-Schapira, Lenka Dohnalova, and Dr. Meirav Pevsner-Fischer in Dr. Elinav’s lab; Dr. David Israeli of the Jerusalem Center for Mental Health; and Prof. Zamir Halpern of the Tel Aviv Sourasky Medical Center.

Prof. Eran Segal’s research is supported by the Crown Human Genome Center, which he heads; the Adelis Foundation; the European Research Council; Mr. and Mrs. Donald L. Schwarz, Sherman Oaks, CA; Leesa Steinberg, Canada; and Jack N. Halpern, New York, NY.

Dr. Eran Elinav’s research is supported by the Abisch Frenkel Foundation for the Promotion of Life Sciences; the Gurwin Family Fund for Scientific Research; the Leona M. and Harry B. Helmsley Charitable Trust; the Crown Endowment Fund for Immunological Research; the Adelis Foundation; the Rising Tide Foundation; the Vera Rosenberg Schwartz Research Fellow Chair; Yael and Rami Ungar, Israel; John L. and Vera Schwartz, Pacific Palisades, CA; Alan Markovitz, Canada; Leesa Steinberg, Canada; Andrew and Cynthia Adelson, Canada; the estate of Jack Gitlitz; the estate of Lydia Hershkovich; Mr. and Mrs. Donald L. Schwarz, Sherman Oaks, CA; Jack N. Halpern, New York, NY; and Aaron Edelheit, Boca Raton, FL. Dr. Elinav is the incumbent of the Rina Gudinski Career Development Chair.

- See more at: http://www.weizmann-usa.org/media/2015/11/19/blood-sugar-levels-in-response-to-foods-are-highly-individual#sthash.zQnhZ1hL.dpuf

 


Read more »



Dec
1

A new study finds that a component of aspirin binds to an enzyme called GAPDH, which is believed to play a major role in neurodegenerative diseases, including Alzheimer's, Parkinson's and Huntington's diseases.

Researchers at the Boyce Thompson Institute and John Hopkins University discovered that salicylic acid, the primary breakdown product of aspirin, binds to GAPDH, thereby stopping it from moving into a cell's nucleus, where it can trigger the cell's death. The study, which appears in the journal PLOS ONE, also suggests that derivatives of salicylic acid may hold promise for treating multiple .

Senior author Daniel Klessig, a professor at Boyce Thompson Institute and Cornell University, has studied the actions of salicylic acid for many years, but primarily in plants. Salicylic acid is the critical hormone for regulating the plant immune system. Previous studies have identified several targets in plants that are affected by salicylic acid, and many of these targets have equivalents in humans.

In the new study, the researchers performed high-throughput screens to identify proteins in the human body that bind to salicylic acid. GAPDH (Glyceraldehyde 3-Phosphate Dehydrogenase) is a central enzyme in glucose metabolism, but plays additional roles in the cell. Under oxidative stress—an excess of free radicals and other reactive compounds—GAPDH is modified and then enters the nucleus of neurons, where it enhances protein turnover, leading to cell death.

The anti-Parkinson's drug deprenyl blocks GAPDH's entry into the nucleus and the resulting cell death. The researchers discovered that salicylic acid also is effective at stopping GAPDH from moving into the nucleus, thus preventing the cell from dying.

"The enzyme GAPDH, long thought to function solely in , is now known to participate in intracellular signaling," said co-author Solomon Snyder, professor of neuroscience at Johns Hopkins University in Baltimore. "The new study establishes that GAPDH is a target for salicylate drugs related to aspirin, and hence may be relevant to the therapeutic actions of such drugs."

Furthermore, they found that a natural derivative of salicylic acid from the Chinese medical herb licorice and a lab-synthesized derivative bind to GAPDH more tightly than salicylic acid. Both are more effective than salicylic acid at blocking GAPDH's movement into the nucleus and the resulting .

Earlier this year, Klessig's group identified another novel target of salicylic acid called HMGB1 (High Mobility Group Box 1), which causes inflammation and is associated with several diseases, including arthritis, lupus, sepsis, atherosclerosis and certain cancers. Low levels of salicylic acid block these pro-inflammatory activities, and the above mentioned salicylic acid derivatives are 40 to 70 times more potent than salicylic acid at inhibiting these pro-inflammatory activities.

"A better understanding of how salicylic acid and its derivatives regulate the activities of GAPDH and HMGB1, coupled with the discovery of much more potent synthetic and natural derivatives of salicylic acid, provide great promise for the development of new and better -based treatments of a wide variety of prevalent, devastating diseases," said Klessig.


Read more »



Nov
14

In recent months, focus has intensified on Coca-Cola’s financial support for medical researchers and public-health advocacy groups—funding that critics say has watered down and distracted from scientific evidence that soda is a leading culprit in the obesity epidemic. The company revealed in September that it has spent nearly $120 million on such efforts, but this weekend, a small symbolic share of that was returned. The University of Colorado announced that it would give back the $1 million that Coke granted to help start the Global Energy Balance Network, a nonprofit that promotes exercise, not improved diet, as the best way to combat obesity.

Steven N. Blair, the exercise scientist and cofounder of GEBN who became infamous for saying “there’s really virtually no compelling evidence that” diet is the primary cause of obesity, is a professor at Colorado.

“While the network continues to advocate for good health through a balance of healthy eating habits and exercise,” the university said in a statement, “the funding source has distracted attention from its worthwhile goal.”

“The network continues to support a vigorous scientific discussion of the contributions of dietary and physical activity behaviors to the obesity epidemic,” the statement continued. Yet the money is being returned. According to Coca-Cola, it will pass the $1 million along to the Boys & Girls Clubs of America.

In August, The New York Times’ reporting on Coke’s relationship with GEBN sparked media and public interest in the soda company’s dealings with the medical community. While Coca-Cola has long maintained relationships with nutritionist groups and the like that critics lambasted, the recent controversy led Coke to disclose all its spending.

“Our engagement and financial support of these well-respected experts, institutions, and organizations were made with the best of intentions—to inform our business, support our local communities, and support solutions to the public health issues facing people across the United States and around the world,” Sandy Douglas, Coke’s president for North America, said in a statement when the financial disclosures were announced.

Responding to the University of Colorado news, Marion Nestle, a professor of nutrition at New York University and the author of the recent book Soda Politics, told The New York Times, “Let’s hope other groups also decide to do the right thing and end such financial relationships.”


Read more »



Nov
3
Is the snooze button bad for you?
Posted by Sebastian Southam on 03 November 2015 03:22 PM

Relying on your snooze button may be doing you more harm than good, experts say.

Beep, beep, beep. Nothing pushes my buttons quite like that irritating sound coming from my bedside alarm clock in the morning. Luckily, my ticker comes with a snooze feature. Just one tap and I buy myself another nine minutes of slumber.

The rumor: Slapping the snooze button actually makes you more sleepy

I've always assumed that those extra snooze-induced minutes of rest are good for me. But recently I've heard they're not helpful -- in fact, it's said hitting the snooze button can actually make me more tired throughout the day. Is it true?

The verdict: If you hit snooze, you may lose (productivity, that is)

When you doze off after your alarm wakes you in the morning, you're actually setting yourself up to feel less alert and productive later in the day.

"When you hit the snooze button repeatedly, you're doing two negative things to yourself," says Robert S. Rosenberg, medical director of the Sleep Disorders Centers of Prescott Valley and Flagstaff, Arizona.

"First, you're fragmenting what little extra sleep you're getting so it is of poor quality. Second, you're starting to put yourself through a new sleep cycle that you aren't giving yourself enough time to finish. This can result in persistent grogginess throughout the day."

Scientists have identified the culprit behind this stupor that's brought on by a too-brief slumber: sleep inertia. The National Sleep Foundation defines this state as "the feeling of grogginess and disorientation that can come from awakening from a deep sleep."

It slows down your decision-making abilities, impairs your memory and hurts your general performance once you do get out of bed. Even worse, coffee and a cold shower can't combat it: It can take up to an hour and a half to shake off sleep-inertia grogginess.

According to Rosenberg, that's because the snooze button messes with your brain hormones. "You're throwing off your circadian cycle," he says. Disrupting the circadian cycle can impair your ability to feel awake during the day and sleepy at night.

So, is banishing the snooze button enough to make you feel your best during the day? Nope, says Rosenberg. The urge to sleep a bit longer is really a symptom of a larger problem.

"Most people are doing this because they're not getting enough sleep on a daily basis," he says. This chronic sleep deprivation (which is defined as six or fewer hours of sleep a night) is called "social jetlag." Over time, some sufferers have been shown to have a higher body-mass index and anelevated risk of diabetes.

If hitting the snooze button isn't the key to better sleep, what is? Rosenberg has a few suggestions to help you stay alert and refreshed:

Turn in earlier, consistently. Rosenberg suggests going to bed a half-hour earlier than you have been. Over time, he says, this will reduce your overall sleep deprivation. And if it doesn't? Turn in an hour earlier.

Banish computers from the boudoir. Devices like smartphones, digital tablets and laptops emit blue light that hurts your sleep. "The exposure to blue-light-emitting devices results in a delay in melatonin production," says Rosenberg. So give yourself a tech curfew: Turn off those electronics 90 minutes before lights out to help promote sounder sleep.

Make mornings a scavenger hunt. If you're still having trouble getting up, hide the alarm from your groggy early-morning self. "Put that alarm clock where you can't reach it," Rosenberg advises. That search to put an end to the annoying beeping sound is sure to foil your desire to sneak in more Z's. It may seem silly, but it's doctor-approved.

 


Read more »