Tony Pantalleresco – Show of the Month July 9 2012

Final frontier of climate policy – remake humans

IF IT is so hard to change the climate to suit humans, why not alter humans to suit the changing climate, philosophers from Oxford and New York universities are asking.—They suggest humans could be modified to be smaller, dislike eating meat, have fewer children and be more willing to co-operate with social goals.[U1] Behavioural changes might not be enough to prevent climate change even if they were widely adopted, and international agreements for measures such as emissions trading are proving elusive, say Matthew Liao of New York University and Anders Sandberg and Rebecca Roache of Oxford University.—So human engineering deserves serious consideration in the debate about how to solve climate change, they write in a coming paper for the academic journal Ethics, Policy & Environment.–A person’s ecological footprint is directly correlated to size, because larger people eat more than lighter people, their cars need more fuel to carry them and they wear out shoes, carpets and furniture sooner than lighter people, the authors write. They suggest hormone treatments could be used to suppress child growth, or embryos could be selected for smaller size.–Reducing consumption of red meat could have significant environmental benefits, the paper says, citing estimates that as much as 51 per cent of the world’s greenhouse gas emissions come from livestock farming. They say people who lack the motivation or willpower to give up eating meat could be helped by ”meat patches” on their skin to deliver hormones to stimulate their immune system against common bovine proteins.-”Eating ‘eco-unfriendly’ food would induce unpleasant experiences,” the authors say.[U2] –Better educated women have fewer children, so human engineering to improve cognition could reduce fertility as ”a positive side effect from the point of view of tackling climate change”, the paper argues.–Pharmacological treatments such as the ”love drug” oxytocin could encourage people to act as a group and boost their appreciation of other life forms and nature, [U3] the authors say.–The paper has sparked a storm in the blogosphere. The environmentalist Bill McKibben tweeted that the authors had proposed ”the worst climate-change solutions of all time”. They have also been denounced as Nazis and ecofascists.–The authors are bemused but unrepentant. If people were willing to consider ”really dangerous” geoengineering solutions such as using space mirrors to alter the Earth’s solar reflectivity, human engineering should also be on the table, Dr Liao said.—”At least the human engineering solutions we have described rely on tried and tested technology, whose risks, at least at the individual level, are comparatively low and well known.”[U4] —The authors emphasise they are not advocating human engineering be adopted, only that it be considered. They also envisage it as a voluntary activity possibly supported by incentives such as tax breaks or sponsored healthcare, not something coerced or mandatory.—[U5] Dr Sandberg, of the Future of Humanity Institute at Oxford University, said the paper had inadvertently ”managed to press two hot buttons” – climate change and ”messing with human nature”. He predicted the paper would mutate into a story that scientists were working on re-engineering people to be green and it would be adopted as ”yet another piece of evidence of the Big Conspiracy”.—This story was found at: http://www.smh.com.au/world/science/final-frontier-of-climate-policy–remake-humans-20120405-1wfo6.html

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Reverse Engineering Epilepsy’s ‘Miracle’ Diet

ScienceDaily (May 23, 2012) — For decades, neurologists have known that a diet high in fat and extremely low in carbohydrates can reduce epileptic seizures that resist drug therapy. But until now, how the diet worked, and why, was a mystery.—Now, researchers at Dana-Farber Cancer Institute and Harvard Medical School have proposed an answer, linking resistance to seizures to a protein that modifies cellular metabolism in the brain. The research, to be published in the May 24th issue of the journal Neuron, may lead to the development of new treatments for epilepsy.–The research was led jointly by Nika Danial, HMS assistant professor of cell biology at Dana-Farber Cancer Institute, and Gary Yellen,professor of neurobiology at Harvard Medical School. The first author was Alfredo Giménez-Cassina, a research fellow in Danial’s lab.—Epilepsy is a neurological disorder characterized by repeated seizures, an electrical storm in the brain that can manifest as convulsions, loss of motor control, or loss of consciousness. Some cases of epilepsy can be improved by a diet that drastically reduces sugar intake, triggering neurons to switch from their customary fuel of glucose to fat byproducts called ketone bodies. The so-called ketogenic diet, which mimics effects of starvation, was described more than 80 years ago and received renewed interest in the 1990s. Recent studies corroborate that it works, but shed little light on how.–“The connection between metabolism and epilepsy has been such a puzzle,” said Yellen, who was introduced to the ketogenic diet through his wife, Elizabeth Thiele, HMS professor of neurology, who directs the Pediatric Epilepsy Program at MassGeneral Hospital for Children, but was not directly involved in the study. “I’ve met a lot of kids whose lives are completely changed by this diet,” Yellen said. “It’s amazingly effective, and it works for many kids for whom drugs don’t work.“—“We knew we needed to come at this link between metabolism and epilepsy from a new angle,” said Danial, who had previously discovered a surprising double duty for a protein known for its role in apoptosis: The protein, BCL-2-associated Agonist of Cell Death, or BAD, also regulated glucose metabolism.–Giménez-Cassina further discovered that certain modifications in BAD switched metabolism in brain cells from glucose to ketone bodies. “It was then that we realized we had come upon a metabolic switch to do what the ketogenic diet does to the brain without any actual dietary therapy,” said Gimenez-Cassina, who went on to show that these same BAD modifications protect against seizures in experimental models of epilepsy. Still, it wasn’t clear exactly how.—Yellen suspected the solution involved potassium ion channels. While sodium and calcium ion channels tend to excite cells, including neurons, potassium channels tend to suppress cell electrical activity. His lab had previously linked ketone bodies to the activation of ATP-sensitive potassium (KATP) channels in neurons. Yellen had hypothesized that the ketogenic diet workedbecause ketone bodies provide neurons enough fuel for normal function, but when the electrical and energy storm of an epileptic seizure threatens, the activated KATP channels can shut the storm down. But the effects of diets are broad and complex, so it was impossible to say for sure—The effects that Danial’s lab had discovered — BAD’s ability to alter metabolism and seizures — offered a new avenue for studying the therapeutic effects of altered metabolism. Together, the researchers decided to investigate whether Danial’s switch governed Yellen’s pathway, and whether they could reverse engineer the seizure protection of a ketogenic diet.–They could. Working in genetically altered mice, the researchers modified the BAD protein to reduce glucose metabolism and increase ketone body metabolism in the brain. Seizures decreased, but the benefit was erased when they knocked out the KATP channel — strong evidence that a BAD-KATP pathway conferred resistance to epileptic seizures. Further experiments suggested that it was indeed BAD’s role in metabolism, not cell death that mattered. The findings make the BAD protein a promising target for new  epilepsy drugs.—“Diet sounds like this wholesome way to treat seizures, but it’s very hard. I mean, diets in general are hard, and this diet is really hard,” said Yellen, whose wife’s Center for Dietary Therapy in Epilepsy hosts a candy-free Halloween party for its many patients on the ketogenic diet. “So finding a pharmacological substitute for this would make lots of people really happy.”—Story Source-The above story is reprinted from materials provided by Harvard Medical School. The original article was written by R. Alan Leo. —Journal Reference–Alfredo Giménez-Cassina, Juan Ramón Martínez-François, Jill K. Fisher, Benjamin Szlyk, Klaudia Polak, Jessica Wiwczar, Geoffrey R. Tanner, Andrew Lutas, Gary Yellen, Nika N. Danial. BAD-Dependent Regulation of Fuel Metabolism and KATP Channel Activity Confers Resistance to Epileptic Seizures. Neuron, 2012; 74 (4): 719 DOI: 10.1016/j.neuron.2012.03.032

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Glucose Deprivation Activates Feedback Loop That Kills Cancer Cells

In cancer cells, glucose starvation activates a metabolic and signaling feedback loop leading to cell death. Glucose starvation induces generation of reactive oxygen species generation (ROS), thereby inhibiting phosphatases and activating tyrosine kinases, which in turn generate additional ROS. This glucose starvation-induced positive feedback loop amplifies ROS levels until cells undergo ROS-mediated cell death. —ScienceDaily (June 26, 2012) — Compared to normal cells, cancer cells have a prodigious appetite for glucose, the result of a shift in cell metabolism known as aerobic glycolysis or the “Warburg effect.” Researchers focusing on this effect as a possible target for cancer therapies have examined how biochemical signals present in cancer cells regulate the altered metabolic state.—Now, in a unique study, a UCLA research team led by Thomas Graeber, a professor of molecular and medical pharmacology, has investigated the reverse aspect: how the metabolism of glucose affects the biochemical signals present in cancer cells.—In research published June 26 in the journal Molecular Systems Biology, Graeber and his colleagues demonstrate that glucose starvation — that is, depriving cancer cells of glucose activates a metabolic and signaling amplification loop that leads to cancer cell death as a result of the toxic accumulation of reactive oxygen species, the cell-damaging molecules and ions targeted by antioxidants like vitamin C.—The research, which involved UCLA scientists from the Crump Institute for Molecular Imaging, the Institute for Molecular Medicine, the California NanoSystems Institute, the Jonsson Comprehensive Cancer Center, the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, and the Department of Pathology and Laboratory Medicine, demonstrates the power of systems biology in uncovering relationships between metabolism and signaling at the network level.—“Most strikingly, our discovery that glucose withdrawal causes both cell death and increased tyrosine phosphorylation is intriguing because increased tyrosine kinase signaling is normally associated with cell growth,” said Nicholas A. Graham, a senior postdoctoral scholar in Graeber’s lab who helped design the project.—To explain the seemingly contradictory result that glucose deprivation reduced viability and at the same time increased signaling, the authors used an unbiased systems-biology approach that included phospho-tyrosine mass spectrometry and other biochemical profiling techniques.—Assessing the “crosstalk” between metabolism and signaling, they discovered that the glucose deprivation activates a positive feedback loop whereby the withdrawal of glucose induces increased levels of reactive oxygen species, which in turn inhibit negative regulators of tyrosine signaling. The resulting supra-physiological levels of tyrosine phosphorylation then generate additional reactive oxygen species.—“Because cancer cells live on the edge of what is metabolically feasible, this amplifying cycle of oxidative stress ultimately overwhelms and kills the cancer cell,” Graeber explained. “These findings illustrate the delicate balance that exists between metabolism and signaling in the maintenance of cancer cell homeostasis.”—In addition, the authors showed the possibility of exploiting this positive feedback loop for therapeutic intervention. Combining short-term glucose deprivation with an inhibitor of tyrosine phosphatases, they demonstrated synergistic cell death in a cancer cell line.—“Understanding the links between metabolism and signaling will empower new therapeutic approaches toward inducing this metabolic catastrophe,” Graham said. “This study provides a framework for rational design of combinatorial therapeutics targeting both metabolism and signaling in cancer.”—The findings by Graeber and his colleagues add to the emerging concept of systems integration between oncogenic signaling networks and the metabolism of malignant tumors. The work lays a foundation for future studies delineating how signaling and metabolism are linked, with the ultimate goal of refining therapeutic strategies targeting cancer metabolism.—The research team also included collaborators from the department of neurology and the human oncology and pathogenesis program at Memorial Sloan-Kettering Cancer Center and the department of pharmacology at Weill-Cornell Medical College.—The research was funded by the National Institutes of Health, UCLA’s Jonsson Comprehensive Cancer Center, and the California Institute of Technology-University of California, Los Angeles, Joint Center for Translational Medicine.—Story Source-The above story is reprinted from materials provided by University of California – Los Angeles. The original article was written by Jennifer Marcus. —Journal Reference-Nicholas A Graham, Martik Tahmasian, Bitika Kohli, Evangelia Komisopoulou, Maggie Zhu, Igor Vivanco, Michael A Teitell, Hong Wu, Antoni Ribas, Roger S Lo, Ingo K Mellinghoff, Paul S Mischel, Thomas G Graeber. Glucose deprivation activates a metabolic and signaling amplification loop leading to cell death. Molecular Systems Biology, 2012; 8 DOI: 10.1038/msb.2012.20

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Drinking Coffee with Caffeine may Reduce the risk of Basal Cell Carcinoma

Drinking coffee with caffeine may reduce the risk of basal cell carcinoma, the most common form of skin cancer, a new study suggests. —-“Our data indicate that the more caffeinated coffee you consume, the lower your risk of developing basal cell carcinoma,” said Jiali Han, associate professor at Brigham and Women’s Hospital, Harvard Medical School in Boston and Harvard School of Public Health. The findings add to other apparent benefits of coffee, which has been at least suggestively linked to lower risk of depression in women and may counteract cognitive decline. Coffee may even help prevent Alzheimer’s, Parkinson’s disease and type 2 diabetes. [Coffee Habits: Infographic] — “Our results add basal cell carcinoma to a list of conditions for which risk is decreased with increasing coffee consumption,” Han in a statement. “This list includes conditions with serious negative health consequences such as type 2 diabetes and Parkinson’s disease.”— Han and his colleagues studied data from the Nurses’ Health Study, a large and long-running study to aid in the investigation of factors influencing women’s health, and the Health Professionals Follow-up Study, a similar study for men.—Of the 112,897 participants included in the analyses, 22,786 developed basal cell carcinoma during the more than 20 years of follow-up in the two studies, the researchers explained in a statement. Lower risk of developing basal cell carcinoma was linked to consumption of caffeinated coffee as well as caffeine from other sources: tea, cola and chocolate. Decaffeinated coffee did not have the same effect.—These results really suggest that it is the caffeine in coffee that is responsible for the decreased risk of basal cell carcinoma associated with increasing coffee consumption,” Han said. “This would be consistent with published mouse data, which indicate caffeine can block skin tumor formation. However, more studies in different population cohorts and additional mechanistic studies will be needed before we can say this definitively.”—No link was established between caffeine consumption and risk for two other forms of skin cancer, squamous cell carcinoma and melanoma, the most deadly form of the disease.—The findings are detailed in Cancer Research, a journal of the American Association for Cancer Research.

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Moderate Coffee Consumption Offers Protection Against Heart Failure

New research shows a possible benefit from coffee consumption, but like with so many other things we consume, it really depends on how much coffee you drink, the researchers say. —ScienceDaily (June 26, 2012) — While current American Heart Association heart failure prevention guidelines warn against habitual coffee consumption, some studies propose a protective benefit, and still others find no association at all. Amidst this conflicting information, research from Beth Israel Deaconess Medical Center attempts to shift the conversation from a definitive yes or no, to a question of how much.—“Our results did show a possible benefit, but like with so many other things we consume, it really depends on how much coffee you drink,” says lead author Elizabeth Mostofsky, MPH, ScD, a post-doctoral fellow in the cardiovascular epidemiological unit at BIDMC. “And compared with no consumption, the strongest protection we observed was at about four European, or two eight-ounce American, servings of coffee per day.”—The study published June 26 online in the journal Circulation: Heart Failure, found that these moderate coffee drinkers were at 11 percent lower risk of heart failure.—Data was analyzed from five previous studies — four conducted in Sweden, one in Finland — that examined the association between coffee consumption and heart failure. The self-reported data came from 140,220 participants and involved 6,522 heart failure events.—In a summary of the published literature, the authors found a “statistically significant J-shaped relationship” between habitual coffee consumption and heart failure, where protective benefits begin to increase with consumption maxing out at two eight-ounce American servings a day. Protection slowly decreases the more coffee is consumed until at five cups, there is no benefit and at more than five cups a day, there may be potential for harm.—It’s unclear why moderate coffee consumption provides protection from heart failure, but the researchers say part of the answer may lie in the intersection between regular coffee drinking and two of the strongest risk factors for heart failure — diabetes and elevated blood pressure.–“There is a good deal of research showing that drinking coffee lowers the risk for type 2 diabetes, says senior author Murray Mittleman, MD, DrPH, a physician in the Cardiovascular Institute at Beth Israel Deaconess Medical Center, an Associate Professor of Medicine at Harvard Medical School and director of BIDMC’s cardiovascular epidemiological research program. “It stands to reason that if you lower the risk of diabetes, you also lower the risk of heart failure.”—There may also be a blood pressure benefit. Studies have consistently shown that light coffee and caffeine consumption are known to raise blood pressure. “But at that moderate range of consumption, people tend to develop a tolerance where drinking coffee does not pose a risk and may even be protective against elevated blood pressure,” says Mittleman.–This study was not able to assess the strength of the coffee, nor did it look at caffeinated versus non-caffeinated coffee.—“There is clearly more research to be done,” says Mostofsky. “But in the short run, this data may warrant a change to the guidelines to reflect that coffee consumption, in moderation, may provide some protection from heart failure.”–Other study authors are Megan Rice, Sc.D., and Emily Levitan, Sc.D.-The research was supported by grants from the National Institutes of Health.–Story Source-The above story is reprinted from materials provided by Beth Israel Deaconess Medical Center, via Newswise

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