"Marvel molecule" could enable new treatments for a range of inflammatory diseases

The newly identified molecule could hold the key to improved treatments for a variety of inflammatory diseases (Shutterstock) A team of researchers at Trinity College Dublin has unearthed what they are calling a "marvel molecule." Said to be capable of suppressing a key activator of various inflammatory diseases, it is hoped the molecule will lead to more effective treatments for conditions ranging from Alzheimer’s disease, to rheumatoid arthritis and motor neuron disease. The massive potential of the molecule lies in its ability to block a key activator of inflammatory diseases known as the NLRP3 inflammasome. Inflammasomes, protein clusters responsible for triggering a range of inflammatory processes, have long been considered potential therapeutic targets for treating a range of conditions. Through the study, the researchers found the molecule, dubbed MCC950, to be very promising in warding off multiple sclerosis. But what really pleased the researchers was the fact that the target, the NLRP3 inflammasome, also plays a strong role in the onset of other inflammatory diseases including Alzheimer’s, atherosclerosis, gout and Parkinson's disease. "MCC950 is blocking what was suspected to be a key process in inflammation," says Dr Rebecca Coll, lead author of the paper. "There is huge interest in NLRP3 both among medical researchers and pharmaceutical companies and we feel our work makes a significant contribution to the efforts to find new medicines to limit it." The findings are said to confirm that while different inflammatory conditions may cause different parts of the body to become inflamed, the diseases all share a common process. This has the potential to spawn new kinds of cheaper, non-invasive treatments for inflammatory diseases. "MCC950 is able to be given orally and will be cheaper to produce than current protein-based treatments, which are given daily, weekly, or monthly by injection," says Professor Matt Cooper from the University of Queensland, a co-senior author of the study. "Importantly, it will also have a shorter duration in the body, allowing clinicians to stop the anti-inflammatory action of the drug if the patient ever needed to switch their immune response back to 100 percent in order to clear an infection.” The researchers say that the molecule may also benefit sufferers of Muckle-Wells disease, a rare genetic disorder that can cause rashes, joint pain and other inflammations. Treating blood samples of patients with Muckle-Wells disease, the molecule was shown to block the rogue gene that triggers these recurring inflammatory processes. "We are really excited about MCC950," says Professor of Biochemistry at Trinity College Dublin and joint senior scientist behind the discovery. "We believe this has real potential to benefit patients suffering from several highly debilitating diseases, where there is currently a dire need for new medicines." The research was published in the journal Nature. Source: Trinity College Dublin

Mars One reduces colonist pool to 100

Artist's concept of the Mars One spacecraft to bring the colonists to the settlement Image Gallery (8 images) The Mars One project aimed at starting the first permanent human settlement on the Red Planet has reduced its pool of prospective colonists to 100 candidates. According to the non-profit company, the selection was winnowed down from the original pool of 202,586 applicants of people from all walks of life from all over the world. However, questions remain about the viability of the project. The third-round selection was from 660 second-round candidates and includes 50 men and 50 women, consisting of 39 from the Americas, 31 from Europe, 16 from Asia, 7 from Africa, and 7 from Oceania. It was based on online interviews with Mars One Chief Medical Officer, Norbert Kraft, that were intended to determine their understanding of the risks of the mission, team spirit, and motivation. Announced in 2012, the Mars One project aims at landing four colonists on Mars in 2025, where they would remain for the rest of their lives with additional colonists sent as Earth and Mars come back into the right launch position every 18 months or so. Living in habitats set up previously by unmanned rovers, the colonists would live off the land for their raw materials while being the focus of a reality television show beamed back to Earth. Despite the progress made by Mars One's candidate selection, the project has attracted a great deal of skeptical comment. The company says that it can start its Martian colony for US$6 billion, of which only about US$760,000 has been raised so far. Such an amount, even if raised, is extremely modest for a manned Mars mission involving multiple rocket launches and the development of a number of technologies, such as Mars-rated spacesuits and highly sophisticated robots to build the outposts. Mars One has said that it plans to raise the money by means of a tie-in reality television show, but recent reports indicate that this has fallen through. US astronaut Chris Hadfield also expressed reservations and suggested that the applicants needed to ask hard questions about the technology and reasoning behind the project. In addition, an MIT study calculated that should a successful landing be made, the outpost's life support system would fail within 10 weeks of the first landing. Another point is that Mars One has shown remarkable optimism about third-party suppliers and off-the-shelf technology to solve problems that even NASA finds daunting, such as building a spacecraft capable of getting to Mars on a very low budget, building a manned spacecraft capable of a powered landings on Mars, and constructing life support systems capable of keeping a permanent settlement alive for an indefinite period of time. Yet despite this, the company not only remains firm after 5 years of work, but boasts in its materials that this is a one-way mission with no hope of the colonists ever seeing Earth again. This raises the question of whether the lack of a return option is a technological limitation or a selling point for a television drama. This question is reinforced by the selection process. The company claims that over 200,000 people have applied, but this was cast into doubt when only 2,782 video applications were counted on the Mars One website. The application process requires an application fee and a video, where they candidate explains why he or she is suitable for the mission. Though a sense of humor is requested, no technical or other qualifications are requested beyond reasonable health. The 100 Mars One candidates are a long way from the Apollo missions, where the astronauts were top-flight, trained to the ninth decimal place test pilots in peak condition – some of whom had PhDs. The current round includes actors, former ballet dancers, liberal arts students, a NASA flight engineer, and a quantum biologist, with ages ranging from 19 to 54. The latter means that if the 2025 launch date holds, the first colonist could be 65-years of age on landing. According to Mars One, the next round of selection will include demonstrations of their suitability and teamwork at an Earthbound copy of the proposed Mars One outpost. Candidates not selected can reapply when new application rounds open this year.   Source: Mars One

Porque devemos beber água morna com limão todas as manhãs

Beber um copo de água morna com limão logo ao acordar, pode trazer-lhe imensos benefícios para a sua saúde e tem sido uma prática ayurvédica desde há muito tempo.   Como preparar ? Amorne um copo de água e junte-lhe o sumo de meio limão. Utilize limões frescos… não vale usar “limão engarrafado”! Beba essa mistura em jejum na primeira hora da manhã.   Os benefícios Ajuda na digestão: A água morna ajuda a estimular o trato gastrointestinal e acredita-se que o limão ajude a estimular e purificar o fígado. Estimula o sistema imunológico: As frutas cítricas como o limão são ricas em vitamina C e ácido ascórbico. A vitamina C pode ajudar a prevenir constipações e o ácido ascórbico ajuda na absorção do ferro. Equilibra o pH do organismo: Quando o corpo está com o pH desequilibrado, torna-se mais susceptível a adoecer. Apesar dos limões serem ácidos, eles são bastante alcalinizantes e muito eficazes a equilibrar os níveis de pH. É diurético: Água com limão é um diurético natural, o que significa que ajuda o seu corpo a eliminar líquidos e toxinas. É energizante: Há quem desista de tomar café de manhã depois de alguns dias a beber água morna com limão. Aparentemente, essa bebida ajuda a oxigenar o sangue, fazendo com que se sinta esplêndido e preparado para enfrentar o dia. Mantém a pele bonita: A vitamina C desempenha um papel crítico na manutenção de uma pele saudável e os antioxidantes podem combater os factores de envelhecimento. Mantém o hálito fresco: E também ajuda a aliviar dores de dentes e gengivite. Mas atenção, como o ácido cítrico pode corroer o esmalte, não escove os dentes logo após beber a água com limão. Prefira aguardar ou então escove os dentes antes de beber. Fonte – www.poupaeganha.pt

Individuals with type 2 diabetes should exercise after dinner

February 18, 2015 University of Missouri-Columbia Individuals with Type 2 diabetes have heightened amounts of sugars and fats in their blood, which increases their risks for cardiovascular diseases such as strokes and heart attacks. Exercise is a popular prescription for individuals suffering from the symptoms of Type 2 diabetes, but little research has explored whether these individuals receive more benefits from working out before or after dinner. Now, researchers at the University of Missouri have found that individuals with Type 2 diabetes can lower their risks of cardiovascular diseases more effectively by exercising after a meal. "This study shows that it is not just the intensity or duration of exercising that is important but also the timing of when it occurs," said Jill Kanaley, professor in the MU Department of Nutrition and Exercise Physiology. "Results from this study show that resistance exercise has its most powerful effect on reducing glucose and fat levels in one's blood when performed after dinner." Kanaley and her colleagues studied a group of obese individuals with Type 2 diabetes. On one occasion, participants performed resistance exercises before eating dinner. During another visit, participants exercised 45 minutes after eating dinner. Participants performed resistance exercises such as leg curls, seated calf raises and abdominal crunches. Compared to levels on a non-exercise day, Kanaley found that the participants who exercised before dinner were able to only reduce the sugar levels in their blood; however, participants who exercised after dinner were able to reduce both sugar and fat levels. Participants consumed a moderate carbohydrate dinner on the evenings of the study. Kanaley said her research is particularly helpful for health care providers who have patients who exercise every day but are not seeing benefits. "Knowing that the best time to exercise is after a meal could provide health care professionals with a better understanding of how to personalize exercise prescriptions to optimize health benefits," Kanaley said. Kanaley also found that improvements in participants' blood sugar and fat levels were short-lived and did not extend to the next day. She suggests individuals practice daily resistance exercise after dinner to maintain improvements. "Individuals who exercise in the morning have usually fasted for 10 hours beforehand," Kanaley said. "Also, it is natural for individuals' hormone levels to be different at different times of day, which is another factor to consider when determining the best time to exercise." In the future, Kanaley said she plans to research how exercising in the morning differs from exercising after dinner and how individuals' hormone levels also affect exercise results. The study, "Post-dinner resistance exercise improves postprandial risk factors more effectively than pre-dinner resistance exercise in patients with type 2 diabetes," was published in the Journal of Applied Physiology. Story Source: The above story is based on materials provided by University of Missouri-Columbia. The original article was written by Diamond Dixon. Note: Materials may be edited for content and length. Journal Reference: T. D. Heden, N. C. Winn, A. Mari, F. W. Booth, R. S. Rector, J. P. Thyfault, J. A. Kanaley. Post-dinner resistance exercise improves postprandial risk factors more effectively than pre-dinner resistance exercise in patients with type 2 diabetes. Journal of Applied Physiology, 2014; DOI: 10.1152/japplphysiol.00917.2014

Epigenomics of Alzheimer's disease progression

Our susceptibility to disease depends both on the genes that we inherit from our parents and on our lifetime experiences. These two components -- nature and nurture -- seem to affect very different processes in the context of Alzheimer's disease, according to a new study published today in the journal Nature. The study was carried out by an interdisciplinary team at MIT and the Broad Institute, and was co-led by Li-Huei Tsai, the Picower Professor at MIT and director of the Picower Institute for Learning and Memory, and Manolis Kellis, a professor in MIT's Computer Science and Artificial Intelligence Laboratory (CSAIL). The researchers analyzed changes that occur in genes and in regions that regulate genes as Alzheimer's disease progresses, using a mouse model of Alzheimer's disease that Tsai's lab originally developed several years ago. The mice were engineered so that the gene for a protein called p25 can be overstimulated in the brain, which prompts the mice to develop symptoms very similar to Alzheimer's disease in humans. "These programmable mice allowed us to study, for the first time, the changes occurring during early stages of the disease, before symptoms even begin to appear," Tsai says. "We could then compare them to changes in later stages of the disease, when neurodegeneration and cognitive impairment are evident." Opposing changes The researchers profiled multiple chemical modifications, known as epigenetic marks, in the hippocampus of mice expressing too much p25 and compared them with control mice. These epigenetic marks reveal the activity of diverse genomic regions -- in particular, the regulatory control regions that control the expression of nearby genes. The researchers also directly profiled the levels of all genes. "We found two opposing signatures associated with disease progression that are consistent with the pathophysiology of Alzheimer's disease," says Elizabeta Gjoneska, joint first author of the paper and a postdoc at the Picower Institute. "Neuronal plasticity processes that are involved in learning and memory were dampened, and immune and inflammatory pathways were activated." The active regions specifically matched regions active in a type of immune cells known as microglia, which are responsible for clearing away infected or damaged cells. They also secrete chemicals that produce inflammation. "Our data suggest that microglia are heavily activated during Alzheimer's disease progression, although it is unknown exactly how they contribute to the disease," Tsai says. "These cells are important for normal brain function and share their key cell-surface markers, CD14, with macrophages that infiltrate the brain from elsewhere in the body during disease progression." Conserved epigenomic signatures The researchers then compared the results in mice with what is known about Alzheimer's disease in humans. They found that differences in gene levels in the Alzheimer's-like mouse brain matched differences previously seen in the brains of Alzheimer's patients, which prompted them to ask if the epigenetic signatures might also be conserved. The researchers found that this was the case -- specifically, the same regulatory regions that were active or repressed in mice showed the same patterns in humans. They also found that the regions with increased activity in the mouse model of Alzheimer's disease had immune functions in humans, and the regions that showed decreased activity had neural functions in humans. "Our results show that functional conservation between human and mouse is not restricted to protein-coding genes," says Andreas Pfenning, joint first author of the study and a postdoc at MIT. "This opens up the use of epigenomics methods in model organisms to study an inaccessible organ like the brain, and how it changes in response to activity or disease." Genetic variants cluster in immune pathways Previous studies of the genomes of Alzheimer's patients had identified common genetic variants associated with the disease, but scientists did not know how these DNA variants could contribute to the disease, since the majority of them are found outside of protein-coding regions. "Our conserved epigenomic maps allowed us to now place these noncoding genetic variants in the context of disease-relevant regulatory regions and interpret their contribution to the disease predisposition," Kellis says. "As inherited common genetic variants always precede disease onset, they are always indicative of causal roles, and thus can shed additional light on the epigenomic alterations." The researchers found that genetic variants associated with Alzheimer's disease were only associated with immune processes, and not with neural processes, indicating that genetic predisposition to Alzheimer's disease primarily affects the circuitry of immune processes, rather than neuronal processes. "Our results suggest that repression of neural pathways does not represent genetic predisposition, even though it is a hallmark of Alzheimer's," Tsai says. "Instead, it may occur as a consequence of environmental factors and aging, and result from interactions with the altered immune pathways." The researchers identified a small number of master regulators that target many of the regulatory regions that overlap Alzheimer's-associated genetic variants in humans. Among these, PU.1 targets a large number of altered regulatory regions, and the genetic region encoding PU.1 is associated with Alzheimer's disease, suggesting PU.1 as a potential therapeutic target. "The new focus on immune-cell types, and the specific regulators uncovered, provide new therapeutic avenues," Kellis says. "Moreover, the conservation of epigenomic signatures between mouse and human provides a platform upon which we can test such therapeutics and their effect on cognition, pathology, and the epigenomic signatures of Alzheimer's."

Keeping atherosclerosis in-check with novel targeted inflammation-resolving nanomedicines

Nanometer-sized "drones" that deliver a special type of healing molecule to fat deposits in arteries could become a new way to prevent heart attacks caused by atherosclerosis, according to a study in pre-clinical models by scientists at Brigham and Women's Hospital (BWH) and Columbia University Medical Center. These findings are published in the February 18th online issue of Science Translational Medicine. Although current treatments have reduced the number of deaths from atherosclerosis-related disease, atherosclerosis remains a dangerous health problem: Atherosclerosis of the coronary arteries is the #1 killer of women and men in the U.S., resulting in one out of every four deaths. In the study, targeted biodegradable nano 'drones' that delivered a special type of drug that promotes healing ('resolution') successfully restructured atherosclerotic plaques in mice to make them more stable. This remodeling of the plaque environment would be predicted in humans to block plaque rupture and thrombosis and thereby prevent heart attacks and strokes. "This is the first example of a targeted nanoparticle technology that reduces atherosclerosis in an animal model," said co-senior author Omid Farokhzad, MD, associate professor and director of the Laboratory of Nanomedicine and Biomaterials at BWH and Harvard Medical School (HMS). "Years of research and collaboration have culminated in our ability to use nanotechnology to resolve inflammation, remodel and stabilize plaques in a model of advanced atherosclerosis." In this study, targeted nanomedicines made from polymeric building blocks that are utilized in numerous FDA approved products to date, were nanoengineered to carry an anti-inflammatory drug payload in the form of a biomimetic peptide. Furthermore, this peptide was derived from one of the body's own natural inflammatory-resolving proteins called Annexin A1. The way the nanomedicines were designed enabled this biological therapeutic to be released at the target site, the atherosclerotic plaque, in a controlled manner. In mouse models with advanced atherosclerosis, researchers administered nanomedicines and relevant controls. Following five weeks of treatment with the nanomedicines, damage to the arteries was significantly repaired and plaque was stabilized. Specifically, researchers observed a reduction of reactive oxygen species; increase in collagen, which strengthens the fibrous cap; and reduction of the plaque necrotic core, and these changes were not observed in comparison with the free peptide or empty nanoparticles. "Many researchers are trying to develop drugs that prevent heart attacks by tamping down inflammation, but that approach has some downsides," said co-senior author Ira Tabas, MD, Richard J. Stock professor of Medicine (Immunology) and professor of Pathology & Cell Biology at Columbia. "One is that atherosclerosis is a chronic disease, so drugs are taken for years, even decades. An anti-inflammatory drug that is distributed throughout the entire body will also impair the immune system's ability to fight infection." That might be acceptable for conditions that severely affect quality of life, like rheumatoid arthritis, but "using this approach to prevent a heart attack that may never happen may not be worth the risk." In addition, it's not enough to deliver an anti-inflammatory drug to the plaques, said Columbia associate research scientist Gabrielle Fredman, PhD, one of the study's lead co-authors. "Atherosclerosis is not only inflammation; there's also damage to the arterial wall. If the damage isn't repaired, you may not prevent heart attacks." The targeted nanomedicines used in this current study were engineered by researchers at BWH. Following preliminary proof-of-principle studies at Columbia University in models of inflammation, they were further tested in a clinically relevant disease model in mice and were shown to be capable of maneuvering through the blood circulation, and traversing leaky regions through to the inside of the plaques, as was demonstrated by fluorescence microscopy imaging of the plaque lesions. Researchers note that in addition to their specific 'sticky' surfaces, their small sub-100 nanometer size is also a key property that facilitates the retention and accumulation of these nanoparticles within the plaques. These nanoparticles are 1000 times smaller than the tip of a single human-hair strand. "These nanomedicines are developed using biodegradable polymers that can break-up over time in the body using the bodies natural mechanisms, and can be nanoengineered using scale-able chemistries and nanotechnologies, which ultimately can facilitate their rapid translation to the clinic," said co-lead author Nazila Kamaly, PhD, instructor in the Laboratory of Nanomedicine and Biomaterials at BWH and HMS. Researchers caution that although plaques in mice look a lot like human plaques, mice do not have heart attacks, so the real test of the nanoparticles will not come until they are tested in humans. "In this study, we've shown, for the first time, that a drug that promotes resolution of inflammation and repair is a viable option, when the drug is delivered directly to plaques via nanoparticles," said Tabas. To be ready for testing in humans, the team plans to fine-tune the nanoparticles to optimize drug delivery and to package them with more potent resolution-inducing drugs. "We think that we can obtain even better delivery to plaques and improve healing more than with the current peptides," , he said. Farokhzad and colleagues have considerable expertise with bench-to-bedside translation of nanotechnologies for medical applications, and foundational work done in part by his team has led to the development and first in human testing of a targeted nanoparticle capable of controlling drug release for treatment of cancers, and the first in human testing of a targeted nanoparticle vaccine capable of orchestrating an immune response to facilitate smoking cessation and relapse prevention. "The inflammation resolving targeted nanoparticles have shown exciting potential not only for the potential treatment of atherosclerosis as described here, but also other therapeutic areas including wound repair, for example, as described in the Feb. 9 online issue of Journal of Clinical Investigation, in addition to other applications currently underway with our collaborators," Farokhzad said. "I'm optimistic that with additional animal validation we will also consider the human testing of the inflammation resolving targeted nanoparticles for a myriad of unmet medical needs--these are exciting times in medicine and the future of nanomedicine is incredibly bright."

New weapon in the fight against cancer could be in your body already

Lithocholic acid, a bile acid produced in the liver, is particularly effective in killing cancer cells. Where can you find the next important weapon in the fight against cancer? Just do a little navel-gazing. New research from Concordia confirms that a tool for keeping the most common forms of cancer at bay could be in your gut. In a report published in the International Journal of Molecular Sciences, Vladimir Titorenko, a professor of biology at Concordia, and his colleagues show that lithocholic acid, a bile acid produced in the liver, is particularly effective in killing cancer cells. For the study, the research team tested thousands of chemicals found in the body with the help of a robot and discovered more than 20 that could delay the aging process, something inevitably linked to cancer. Most effective was lithocholic acid. When entering a cancer cell, the acid goes to "energy factories" called mitochondria and then sends molecular signals that lead to the cells' demise. It not only helped slow the aging process but also had an anti-tumour effect, killing cells of breast, prostate and neuroblastoma cancer -- in a petri dish, that is. Indeed, these results aren't applicable to humans -- yet. Titorenko performed the first round of studies using yeast because the ways aging progresses, and the ways it can be delayed by some diets, are similar in both yeast and humans. "Various cancers are associated with aging -- the older you get, the more instances we see of diseases like breast and prostate cancer -- so studying how diet can slow that aging process is important," says Titorenko, who holds a Concordia Research Chair in genomics, cell biology and aging. In collaboration with Thomas Sanderson from the INRS-Institut Armand-Frappier in Laval, Titorenko is now testing whether the same bile acid can delay the development of prostate cancer in laboratory mice. If those trials confirm the anti-tumour effect of lithocholic acid, the hope is that it will have a similar effect in human patients, along with the possibility of slowing the human aging process in general. The study progresses the fundamental knowledge of how to naturally slow down aging of non-cancerous cells as well as how to kill cancer cells. "We are attempting to understand what kind of molecular processes within our cells are responsible for cell aging and aging-associated death," Titorenko says. "Satisfying our curiosity as scientists pursuing new fundamental knowledge fits with our other objective: to find ways that natural chemical products can delay aging and the diseases associated with it." Story Source: The above story is based on materials provided by Concordia University. Note: Materials may be edited for content and length. Journal Reference: Anthony Arlia-Ciommo, Amanda Piano, Veronika Svistkova, Sadaf Mohtashami, Vladimir Titorenko. Mechanisms Underlying the Anti-Aging and Anti-Tumor Effects of Lithocholic Bile Acid. International Journal of Molecular Sciences, 2014; 15 (9): 16522 DOI: 10.3390/ijms150916522

Unhealthy eating habits outpacing healthy eating patterns in most world regions

Worldwide, consumption of healthy foods such as fruit and vegetables has improved during the past two decades, but has been outpaced by the increased intake of unhealthy foods including processed meat and sweetened drinks in most world regions, according to the first study to assess diet quality in 187 countries covering almost 4.5 billion adults, published in The Lancet Global Health journal. Improvements in diet quality between 1990 and 2010 have been greatest in high-income nations, with modest reductions in the consumption of unhealthy foods and increased intake of healthy products. However, people living in many of the wealthiest regions (eg, the USA and Canada, Western Europe, Australia and New Zealand) still have among the poorest quality diets in the world, because they have some of the highest consumption of unhealthy food worldwide. In contrast, some countries in sub-Saharan Africa and some countries in Asia (eg, China and India) have seen no improvement in their diet quality over the past 20 years. The authors warn that the study presents a worrying picture of increases in unhealthy eating habits outpacing increases in healthy eating patterns across most world regions, and say that concerted action is needed to reverse this trend. Led by Dr Fumiaki Imamura from the Medical Research Council Epidemiology Unit at the University of Cambridge in the UK, a team of international researchers analysed data on the consumption of 17 key food items and nutrients related to obesity and major non-communicable diseases (eg, cardiovascular disease, diabetes, and diet-related cancers) in countries around the world, and changes in diets between 1990 and 2010. This analysis was performed by the Global Burden of Diseases Nutrition and Chronic Diseases Expert Group (NutriCoDE), chaired by Dr Dariush Mozaffarian, senior author on the paper and dean of the Friedman School of Nutrition Science and Policy at Tufts University. NutriCoDE is an ongoing project assessing dietary information from more than 300 dietary surveys across the world and UN Food and Agriculture food-balance sheets, covering almost 90% of the global adult population. The international team examined three different diet patterns: a favourable one based on 10 healthy food items (fruit, vegetables, beans and legumes, nuts and seeds, whole grains, milk, total polyunsaturated fatty acids, fish, omega-3s, and dietary fibre); an unfavourable one defined by seven unhealthy items (unprocessed meats, processed meats, sugar-sweetened drinks, saturated fat, trans fat, dietary cholesterol, and sodium); and an overall diet pattern based on all 17 food groups. The researchers calculated a diet score for each pattern and assessed differences by country, age, sex, and national income, with a higher score indicating a healthier diet (range 0-100). The findings reveal that diet patterns vary widely by national income, with high-income countries generally having better diets based on healthy foods (average score difference +2.5 points), but substantially poorer diets due to a higher intake of unhealthy foods compared with low-income countries (average score difference -33.0 points). On average, older people and women seem to consume better diets. The highest scores for healthy foods were noted in several low-income countries (eg, Chad and Mali) and Mediterranean nations (eg, Turkey and Greece), possibly reflecting favourable aspects of the Mediterranean diet. In contrast, low scores for healthy foods were shown for some central European countries and republics of the former Soviet Union (eg, Uzbekistan, Turkmenistan, and Kyrgyzstan). Of particular interest was that the large national differences in diet quality were not seen, or were far less apparent, when overall diet quality (including both healthy and unhealthy foods) was examined as previous studies have done. "By 2020, projections indicate that non-communicable diseases will account for 75% of all deaths. Improving diet has a crucial role to play in reducing this burden," says Dr Imamura. "Our findings have implications for governments and international bodies worldwide. The distinct dietary trends based on healthy and unhealthy foods, we highlight, indicate the need to understand different, multiple causes of these trends, such as agricultural, food industry, and health policy. Policy actions in multiple domains are essential to help people achieve optimal diets to control the obesity epidemic and reduce non-communicable diseases in all regions of the world." According to Dr Mozaffarian, "There is a particularly urgent need to focus on improving diet quality among poorer populations. If we do nothing, undernutrition will be rapidly eclipsed by obesity and non-communicable diseases, as is already being seen in India, China, and other middle-income countries." Writing in a linked Comment, Carlo La Vecchia from the University of Milan in Italy and Lluis Serra-Majem from the University of Las Palmas de Gran Canaria in Spain say, "The key focus of the paper remains the need to understand the agricultural, trade, and food industry, and health policy determinants to improve dietary patterns and nutrition in various areas, taking into account the traditional characteristics of diets worldwide… Information about the environmental effect of dietary patterns will be needed in the future [particularly from low and middle income countries], because food not only drives human health, but also the health of the planet." Story Source: The above story is based on materials provided by The Lancet. Note: Materials may be edited for content and length. Journal Reference: Fumiaki Imamura, Renata Micha, Shahab Khatibzadeh, Saman Fahimi, Peilin Shi, John Powles, Dariush Mozaffarian. Dietary quality among men and women in 187 countries in 1990 and 2010: a systematic assessment. The Lancet Global Health, 2015; 3 (3): e132 DOI: 10.1016/S2214-109X(14)70381-X