This is your brain on God: Spiritual experiences activate brain reward circuits

"We're just beginning to understand how the brain participates in experiences that believers interpret as spiritual, divine or transcendent," says senior author and neuroradiologist Jeff Anderson. "In the last few years, brain imaging technologies have matured in ways that are letting us approach questions that have been around for millennia." Specifically, the investigators set out to determine which brain networks are involved in representing spiritual feelings in one group, devout Mormons, by creating an environment that triggered participants to "feel the Spirit." Identifying this feeling of peace and closeness with God in oneself and others is a critically important part of Mormons' lives -- they make decisions based on these feelings; treat them as confirmation of doctrinal principles; and view them as a primary means of communication with the divine. During fMRI scans, 19 young-adult church members -- including seven females and 12 males -- performed four tasks in response to content meant to evoke spiritual feelings. The hour-long exam included six minutes of rest; six minutes of audiovisual control (a video detailing their church's membership statistics); eight minutes of quotations by Mormon and world religious leaders; eight minutes of reading familiar passages from the Book of Mormon; 12 minutes of audiovisual stimuli (church-produced video of family and Biblical scenes, and other religiously evocative content); and another eight minutes of quotations. During the initial quotations portion of the exam, participants -- each a former full-time missionary -- were shown a series of quotes, each followed by the question "Are you feeling the spirit?" Participants responded with answers ranging from "not feeling" to "very strongly feeling." Researchers collected detailed assessments of the feelings of participants, who, almost universally, reported experiencing the kinds of feelings typical of an intense worship service. They described feelings of peace and physical sensations of warmth. Many were in tears by the end of the scan. In one experiment, participants pushed a button when they felt a peak spiritual feeling while watching church-produced stimuli. "When our study participants were instructed to think about a savior, about being with their families for eternity, about their heavenly rewards, their brains and bodies physically responded," says lead author Michael Ferguson, who carried out the study as a bioengineering graduate student at the University of Utah. Based on fMRI scans, the researchers found that powerful spiritual feelings were reproducibly associated with activation in the nucleus accumbens, a critical brain region for processing reward. Peak activity occurred about 1-3 seconds before participants pushed the button and was replicated in each of the four tasks. As participants were experiencing peak feelings, their hearts beat faster and their breathing deepened. In addition to the brain's reward circuits, the researchers found that spiritual feelings were associated with the medial prefrontal cortex, which is a complex brain region that is activated by tasks involving valuation, judgment and moral reasoning. Spiritual feelings also activated brain regions associated with focused attention. "Religious experience is perhaps the most influential part of how people make decisions that affect all of us, for good and for ill. Understanding what happens in the brain to contribute to those decisions is really important," says Anderson, noting that we don't yet know if believers of other religions would respond the same way. Work by others suggests that the brain responds quite differently to meditative and contemplative practices characteristic of some eastern religions, but so far little is known about the neuroscience of western spiritual practices. The study is the first initiative of the Religious Brain Project, launched by a group of University of Utah researchers in 2014, which aims to understand.

Type 2 diabetes caused by buildup of toxic fat, study suggests

In type 1 diabetes, patients do not produce enough of the hormone insulin. In type 2 diabetes, although the body produces insulin, it cannot use it properly. Insulin is secreted by the pancreas when it detects sugar intake. Insulin enables cells to accept glucose, which is then processed by the cells and turned into energy. In patients whose insulin is not administered effectively, glucose is not assimilated by the cells but instead builds up in the bloodstream. Diabetes occurs when levels of blood sugar are abnormally high. Although being overweight or obese is a common risk factor for diabetes, researchers have pointed out that diabetes can still occur in people of a healthy weight. Previous research has found that 12 percent of people diagnosed with diabetes between 1990-2011 were at normal weight. The same research indicates that once diagnosed, normal-weight participants were more likely to die from diabetes than their heavier counterparts. Reasons for this were unknown, until now. New research may have shed light on not only why people of a healthy weight are still prone to type 2 diabetes, but also why some people are more susceptible to it than others. It could be that a certain kind of fat is what makes people prone to type 2 diabetes, regardless of their weight. Ceramides triggered insulin resistance, diabetes in mice Senior author Scott Summers, Ph.D., chairman of the University of Utah Department of Nutrition and Integrative Physiology, believes it might be a toxic class of fat metabolites called ceramides that causes type 2 diabetes. The new research from Summer and team shows that a buildup of ceramides prevents the fat tissue from working normally in mice. When we overeat, some of the excess fat gets either stored or burned for energy. But for some people, excess fat just turns into ceramides. "Ceramides impact the way the body handles nutrients. They impair the way the body responds to insulin, and also how it burns calories." Scott Summers, Ph.D. When too many ceramides accumulate in the fat tissue, the body reaches a "tipping point," as Summers puts it. Fat tissue stops working properly, and fat overspills into the blood vessels, heart, or goes on to damage the peripheral tissues. Ceramides have previously been linked to diabetes by at least three different mechanisms: they cause the death of pancreatic beta cells, they increase insulin resistance, and they reduce insulin gene expression. The new study further emphasizes the role of ceramides in creating insulin resistance. Adding extra ceramides to fat cells in mice made them insulin-resistant and unable to burn calories. Conversely, mice that had fewer ceramides did not develop any insulin resistance. Mice with excessive ceramides were also more likely to develop diabetes and fatty liver disease. The results of the study were published in the latest issue of Cell Metabolism. Implications for further research This study suggests that some people are predisposed to turning excess fat into ceramides instead of calories. "[The research] suggests some skinny people will get diabetes or fatty liver disease if something such as genetics triggers ceramide accumulation," said lead author Bhagirath Chaurasia, assistant professor at the University of Utah. Summers points out that some Asian countries have a higher diabetes rate than the U.S., even though the obesity rate is relatively low. Diabetes has already been linked to certain races/ethnicities, with African-Americans, Hispanics, Native Americans, some Asians, and Native Hawaiians or other Pacific Islanders being at a particularly high risk for type 2 diabetes, according to the CDC. "Some people are just not made to deal with dietary fat," says Summers. "It's not just how much you eat, because some people can eat a lot and they just store all the fat effectively and remain healthy." As a consequence, the scientists are now looking at genetic mutations that might make people predisposed to it.

Smoking a pack a day for a year causes 150 mutations in lung cells

Scientists have measured the catastrophic genetic damage caused by smoking in different organs of the body and identified several different mechanisms by which tobacco smoking causes mutations in DNA. Researchers at the Wellcome Trust Sanger Institute, the Los Alamos National Laboratory and their collaborators found smokers accumulated an average of 150 extra mutations in every lung cell for each year of smoking one packet of cigarettes a day. Reported in the Journal Science, the study provides a direct link between the number of cigarettes smoked in a lifetime and the number of mutations in the tumour DNA. The highest mutation rates were seen in the lung cancers but tumours in other parts of the body also contained these smoking-associated mutations, explaining how smoking causes many types of human cancer. Tobacco smoking claims the lives of at least six million people every year and, if current trends continue, the World Health Organization predicts more than 1 billion tobacco-related deaths in this century. Smoking has been epidemiologically associated with at least 17 types of human cancer, but until now no-one has seen the mechanisms by which smoking causes many of these cancer types. Cancer is caused by mutations in the DNA of a cell. In the first comprehensive analysis of the DNA of cancers linked to smoking, researchers studied over 5,000 tumours, comparing cancers from smokers with cancers from people who had never smoked. They found particular molecular fingerprints of DNA damage -- called mutational signatures -- in the smokers' DNA, and counted how many of these particular mutations were found in the different tumours. The authors found that, on average, smoking a pack of cigarettes a day led to 150 mutations in each lung cell every year. These mutations represent individual potential start points for a cascade of genetic damage that can eventually lead to cancer. The numbers of mutations within any cancer cell will vary between individuals, but this study shows the additional mutational load caused by tobacco. Dr Ludmil Alexandrov, first author from Los Alamos National Laboratory, said: "Before now, we had a large body of epidemiological evidence linking smoking with cancer, but now we can actually observe and quantify the molecular changes in the DNA due to cigarette smoking. With this study, we have found that people who smoke a pack a day develop an average of 150 extra mutations in their lungs every year, which explains why smokers have such a higher risk of developing lung cancer." Other organs were also affected, with the study showing that a pack a day led to an estimated average 97 mutations in each cell in the larynx, 39 mutations for the pharynx, 23 mutations for mouth, 18 mutations for bladder, and 6 mutations in every cell of the liver each year. Until now, it has not been fully understood how smoking increases the risk of developing cancer in parts of the body that don't come into direct contact with smoke. However, the study revealed different mechanisms by which tobacco smoking causes these mutations, depending on the area of the body affected. Prof David Phillips, an author on the paper and Professor of Environmental Carcinogenesis at King's College London, said: "The results are a mixture of the expected and unexpected, and reveal a picture of direct and indirect effects. Mutations caused by direct DNA damage from carcinogens in tobacco were seen mainly in organs that come into direct contact with inhaled smoke. In contrast, other cells of the body suffered only indirect damage, as tobacco smoking seems to affect key mechanisms in these cells that in turn mutate DNA." The study revealed at least five distinct processes of DNA damage due to cigarette smoking. The most widespread of these is a mutational signature already found in all cancers. In this case, tobacco smoking seems to accelerate the speed of a cellular clock that mutates DNA prematurely.