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Friday, 9 January 2015

Playing catch can improve balance, prevent falls in seniors

The simple training exercise of catching a weighted medicine ball can improve balance and may help prevent falls in the elderly, according to research at the University of Illinois at Chicago.
Their results are reported in studies available online to subscribers in advance of print in two journals: Electromyography and Kinesiology, and Experimental Brain Research.
When someone is jostled by a bump or a stumble, the brain uses two strategies to maintain balance and prevent a fall, says Alexander Aruin, professor of physical therapy at UIC and principal investigator on the two studies.
"When the perturbation is predictable, for example, if when walking down the street you see someone about to bump into you, you brace yourself," Aruin said. The brain activates muscles in anticipation of the jolt.
The second strategy is corrective -- the brain engages muscles after the perturbation to prevent us from losing our balance, he said, which might involve taking an extra step, or changing body position.
As we age, we lose our anticipatory postural control, the ability to ready ourselves to maintain balance. As a result, there is no preparatory activation of muscles, Aruin said, leaving us with only compensatory action. In effect, our resources for maintaining balance become more limited, and we become less stable and more prone to falls.
"We know a lot about the elements of postural control," said Aruin, who has studied that mechanism for 20 years. More recently, he and his coworkers began to investigate whether special training or exercises could enhance anticipatory adjustments and help people to utilize them.
In one of the new studies, Aruin and his colleagues asked a group of healthy young adults to stand and catch a medicine ball. In the second study, they asked the same of a group of healthy older adults.
The researchers measured the electrical activity of leg and trunk muscles to look for differences in the two age groups' ability to generate anticipatory postural adjustments both before and after the single short training session.
Training-related improvements were seen in both groups. In older adults, the researchers found that not only can they improve, but they also improve at performing a task that was not part of the training.
"There was a transfer effect," he said. "It tells us that -- potentially -- what people learn in the training might be helpful with other activities.
"Our group is the first to look at whether a specially designed rehabilitation protocol can enhance postural control adjustment and subsequently improve overall balance," Aruin said. He plans now to study the long-term effects of training, which he hopes will show a lasting benefit.
Nearly all the subjects, both young and old, enjoyed the training exercise, Aruin said.
"It seems that most people have very positive memories associated with playing catch," he said.
Source:ournals: Electromyography and Kinesiology, and Experimental Brain Research.

Optimistic people have healthier hearts, study finds

People who have upbeat outlooks on life have significantly better cardiovascular health, suggests a new study that examined associations between optimism and heart health in more than 5,100 adults.
"Individuals with the highest levels of optimism have twice the odds of being in ideal cardiovascular health compared to their more pessimistic counterparts," said lead author Rosalba Hernandez, a professor of social work at the University of Illinois. "This association remains significant, even after adjusting for socio-demographic characteristics and poor mental health."
Participants' cardiovascular health was assessed using seven metrics: blood pressure, body mass index, fasting plasma glucose and serum cholesterol levels, dietary intake, physical activity and tobacco use - the same metrics used by the American Heart Association to define heart health and being targeted by the AHA in its Life's Simple 7 public awareness campaign.
In accordance with AHA's heart-health criteria, the researchers allocated 0, 1 or 2 points - representing poor, intermediate and ideal scores, respectively - to participants on each of the seven health metrics, which were then summed to arrive at a total cardiovascular health score. Participants' total health scores ranged from 0 to 14, with a higher total score indicative of better health.
The participants, who ranged in age from 45-84, also completed surveys that assessed their mental health, levels of optimism, and physical health, based upon self-reported extant medical diagnoses of arthritis, liver and kidney disease.
Individuals' total health scores increased in tandem with their levels of optimism. People who were the most optimistic were 50 and 76 percent more likely to have total health scores in the intermediate or ideal ranges, respectively.
The association between optimism and cardiovascular health was even stronger when socio-demographic characteristics such as age, race and ethnicity, income and education status were factored in. People who were the most optimistic were twice as likely to have ideal cardiovascular health, and 55 percent more likely to have a total health score in the intermediate range, the researchers found.
Optimists had significantly better blood sugar and total cholesterol levels than their counterparts. They also were more physically active, had healthier body mass indexes and were less likely to smoke, according to a paper on the research that appears in the January/February 2015 issue of Health Behavior and Policy Review.
The findings may be of clinical significance, given that a 2013 study indicated that a one-point increase in an individual's total-health score on the LS7 was associated with an 8 percent reduction in their risk of stroke, Hernandez said.
"At the population level, even this moderate difference in cardiovascular health translates into a significant reduction in death rates," Hernandez said. "This evidence, which is hypothesized to occur through a biobehavioral mechanism, suggests that prevention strategies that target modification of psychological well-being - e.g., optimism - may be a potential avenue for AHA to reach its goal of improving Americans' cardiovascular health by 20 percent before 2020."
Believed to be the first study to examine the association of optimism and cardiovascular health in a large, ethnically and racially diverse population, the sample for the current study was 38 percent white, 28 percent African-American, 22 percent Hispanic/Latino and 12 percent Chinese.
Data for the study were derived from the Multi-Ethnic Study of Atherosclerosis, an ongoing examination of subclinical cardiovascular disease that includes 6,000 people from six U.S. regions, including Baltimore, Chicago, Forsyth County in North Carolina, and Los Angeles County.
Begun in July 2000, MESA followed participants for 11 years, collecting data every 18 months to two years. Hernandez, who is an affiliated investigator on MESA, is leading a team in conducting prospective analyses on the associations found between optimism and heart health.
"We now have available data to examine optimism at baseline and cardiovascular health a decade later," said Hernandez, who expects to have an abstract completed in 2015.

Post-traumatic Stress Disorder Doubles Type-2 Diabetes Risk in Women

Women who suffer from post-traumatic stress disorder (PTSD) are almost twice as likely to develop type-2 diabetes, according to public health scientists at Columbia University and Harvard University. 
 Post-traumatic Stress Disorder Doubles Type-2 Diabetes Risk in Women

Researchers analyzed data based on surveys given to nearly 50,000 US women from 1989 to 2011 and found that about half the increased risk for diabetes was attributable to the use of antidepressants (34 percent) and overeating, as measured by elevated body mass index (14 percent). However, the other half of the heightened risk could not be explained, and researchers ruled out potential links to smoking, diet, alcohol intake or exercise. The study also found that the more symptoms of PTSD a woman had, the higher her risk of developing type-2 diabetes. About one in nine women had experienced PTSD at some point. 

Senior author of the study Karestan Koenen said, "Not only is PTSD devastating to mental health, but it affects physical health too, raising risk for cardiovascular disease, diabetes, and obesity." Researchers urged healthcare professionals to lookout for signs of diabetes in women who have endured traumatic events.

Source:The research was published in the journal JAMA Psychiatry.

Exposure to Cold Increases Levels of Zfp516 Protein Which Helps Lose Weight

Exposure to cold temperatures increases levels of a newly discovered protein, called transcription factor Zfp516, which is critical for the formation of brown fat, the type of fat in our bodies that generates heat, according to researchers at the University of California, Berkeley. Researchers also found that with extended exposure to chilly air, Zfp516 protein also helps the more abundant white fat in our bodies, the kind that stores excess energy, become more similar to brown fat in its ability to burn energy.
Brown fat has relatively high levels of mitochondria, the cell's power station. In humans, brown fat was thought to be present only in infants, but stores of it were recently discovered in adults around vital organs like the heart, brain, neck and spinal cord. 

Mice studies revealed that rodents with boosted levels of the Zfp516 protein gained 30 percent less weight than control mice when both groups were fed a high-fat diet. 

Hei Sook Sul, UC Berkeley professor of nutritional science and toxicology, said, "Knowing which proteins regulate brown fat is significant because brown fat is not only important for thermogenesis, but there is evidence that brown fat may also affect metabolism and insulin resistance. If one can somehow increase levels of this protein through drugs, they could have more brown fat, and could possibly lose more weight even if eating the same amount of food." 

Source:The study appears online in the journal Molecular Cell.

Wednesday, 7 January 2015

Harvard Study Unveils What Meditation Literally Does To The Brain

Numerous studies have indicated the many physiological benefits of meditation, and the latest one comes from Harvard University.
An eight week study conducted by Harvard researchers at Massachusetts General Hospital (MGH) determined that meditation literally rebuilds the brains grey matter in just eight weeks. It’s the very first study to document that meditation produces changes over time in the brain’s grey matter. 
“Although the practice of meditation is associated with a sense of peacefulness and physical relaxation, practitioners have long claimed that meditation also provides cognitive and psychological benefits that persist throughout the day. This study demonstrates that changes in brain structure may underlie some of these reported improvements and that people are not just feeling better because they are spending time relaxing.” – (1) Sara Lazar of the MGH Psychiatric Neuroimaging Research Program and a Harvard Medical School Instructor in Psychology
The study involved taking magnetic resonance images (MRI) of the brain’s of 16 study participants two weeks prior to participating in the study. MRI images of the participants were also taken after the study was completed.
“The analysis of MR images, which focused on areas where meditation-associated differences were seen in earlier studies, found increased grey-matter density in the hippocampus, known to be important for learning and memory, and in structures associated with self-awareness, compassion and introspection.” 
For the study, participants engaged in meditation practices every day for approximately 30 minutes. These practices included focusing on audio recordings for guided meditation, non-judgmental awareness of sensations, feelings and state of mind.
“It is fascinating to see the brain’s plasticity and that, by practicing meditation, we can play an active role in changing the brain and can increase our well-being and quality of life. Other studies in different patient populations have shown that meditation can make significant improvements in a variety of symptoms, and we are now investigating the underlying mechanisms in the brain that facilitate this change.” – (1) Britta Holzel, first author of the paper and a research fellow at MGH and Giessen University in Germany

How To Meditate

A common misconception about meditation is that you have to sit a certain way or do something in particular to achieve the various benefits that it can provide. All you have to do is place yourself in a position that is most comfortable to you. It could be sitting cross legged, lying down in a bed, sitting on a couch etc, it’s your choice.
Another common misconception about meditation is that you have to “try” to empty your mind. One important factor I enjoyed reading from the study mentioned above is that participants were engaged in “non-judgmental awareness of sensations, feelings and state of mind.”  When meditating, you shouldn’t try to “empty” your mind. Instead, try to let your thoughts, feelings and whatever emotions you are feeling at the time flow. Don’t judge them, just let them come and go and be at peace with it.
I also believe that meditation is a state of being/mind more than anything else. I feel that one does not have to sit down for half an hour and “meditate” so to speak in order to reap the benefits of it, or to be engaged in the practice itself.  One can be engaged in meditation while they are on a walk, for example, or the time they have right before they sleep. Throughout the day, one can resist judging their thoughts, letting them flow until they are no more, or just be in a constant state of peace and self awareness. Contrary to popular belief, there is more than one way to meditate.
“You will have to understand one of the most fundamental things about meditation: that no technique leads to meditation. The old so-called techniques and the new scientific biofeedback techniques are the same as far as meditation is concerned. Meditation is not a byproduct of any technique. Meditation happens beyond mind. No technique can go beyond mind.” – Osho

Research Shows This One Plant Can Kill Cancer Cells & Treat Diabetes

bitter_melonBitter melon is a fruit that grows abundantly in Asia, Africa and the Caribbean. Traditionally it has been used to treat diabetes and other more mild diseases or illnesses.
More recently, bitter melon juice was shown to kill pancreatic cancer cells in vitro and in mice in a study done by the University of Colorado. Considering the results were seen in both in vitro and in vivo tests, the effectiveness of bitter melon juice in treating pancreatic cancer, and potentially other cancers, at a clinical level are promising.
“IHC analyses of MiaPaCa-2 xenografts showed that BMJ(Bitter Melon Juice) also inhibits proliferation, induces apoptosis and activates AMPK (adenosine monophosphate-activated protein kinase) in vivo. Overall, BMJ exerts strong anticancer efficacy against human pancreatic carcinoma cells, both in vitro and in vivo, suggesting its clinical usefulness.”
Pancreatic cancer is one of the most difficult cancers to treat due to the fact that it is often discovered late, leaving very little time to treat. Since traditional therapies (chemotherapy, radiation, surgery etc) were not showing promising results and littler advancement was being made, researchers have been looking elsewhere to find treatment.
Interestingly, cannabis, specifically cannabinoids, have been shown to induce apoptic (programmed) death of human pancreatic cancer cells in vitro and stop pancreatic tumor growth in vivo.  Cannabis is perhaps one of the most popular treatments being aggressively pursued right now given its promising results both in labs and anecdotally.

Scientific Evidence

Pancreatic Cancer
Many cancerous tumors have insulin receptors which move glucose to cancer cells helping them to grow and divide. Studies have shown that insulin encourages pancreatic cancer cells to grow in a dose dependant manner, since bitter melon has been shown to help regulate insulin levels, this could help prevent pancreatic cancer over the long-term.
The Colorado University study was led by Dr. Rajesh Agarwal. They examined effects of bitter melon on 4 different lines of pancreatic cancer cells (in vitro) and in mice. For the in vivo studies, mice were injected with pancreatic tumor cells and were randomly divided into one of two groups. One group of mice received water, which was the control group, and the other group was given bitter melon juice for six weeks.
Researchers studied the tumors at the end of the study and results showed that bitter melon juice not only inhibited cancer cell proliferation but also induced apoptosis (programmed cell death). Compared to the control, tumor growth was inhibited by 60% in the treatment group and there were no signs of toxicity or negative effects on the body. With toxicity and negative effects being a huge role in traditional mainstream treatments, this was positive to see.
A number of clinical studies have been conducted to evaluate the efficacy of bitter melon for treating diabetes. Since it is believed that diabetes is a precursor for pancreatic cancer, researchers felt bitter melon could treat diabetes as well after seeing pancreatic cancer results.
In 2011, results of a four week long clinical trial were published in the Journal of Ethnopharmacology that showed modest hypoglycemic effects and significant fructosamine management for those taking 2000mg/day of bitter melon.
As published by the study: “Bitter melon had a modest hypoglycemic effect and significantly reduced fructosamine levels from baseline among patients with type 2 diabetes who received 2,000 mg/day. However, the hypoglycemic effect of bitter melon was less than metformin 1,000 mg/day.” 
Another study published in 2008 in the international journal Chemistry and Biology indicated that compounds in bitter melon improved glycemic control, helped cells uptake glucose and improved overall glucose tolerance. This study was done in mice and led to promising advancements in treating diabetes and obesity with bitter melon. 
In contrast, a study published in the Journal of Clinical Epidemiology in 2007 did not show significant benefit of the treatment of diabetes by bitter melon but 2 years later in the British Journal of Nutrition it was stated that “more, better-designed and clinical trials are required to confirm the fruit’s role in diabetes treatment.”
Since that 2007 study, more studies have been done to show beneficial effects which perhaps was a result of better design.


When it comes to bitter melon juice, the current research available is showing strong results for specific types of cancer cell destruction, diabetes treatment and potential prevention of pancreatic cancer. Further research and clinical trials would be helpful to better understand how effective this plant can be and in what specific cases. It remains a very promising option that could be explored under the correct supervision.

Other Uses of Bitter Melon

Bitter melon has been used as a traditional medicine for a long time. It has been used to treat: colic, fever, burns, chronic cough, painful menstruation and skin conditions. 

Science at risk as young researchers increasingly denied research grants

America's youngest scientists, increasingly losing research dollars, are leaving the academic biomedical workforce, a brain drain that poses grave risks for the future of science, according to an article published this week by Johns Hopkins University President Ronald J. Daniels.
The article, which appears in the online Early Edition of the journal Proceedings of the National Academy of Sciences, illustrates how for more than a generation, grants for young scientists have declined.
The proportion of principal investigators with a leading National Institutes of Health grant who are 36 years old or younger dropped from 18 percent in 1983 to 3 percent in 2010. Meanwhile, the average age when a scientist with a medical degree gets her first of these grants has risen from just under 38 years old in 1980 to more than 45 in 2013.
"The implications of these data for our young scientists are arresting," Daniels writes in thePNAS paper. "Without their own funding, young researchers are prevented from starting their own laboratories, pursuing their own research, and advancing their own careers in academic science. It is not surprising that many of our youngest minds are choosing to leave their positions."
If young talent continues to leave academia, Daniels says it could lead to a gradual evaporation of new discoveries, the loss of future leaders and mentors, a less diverse workforce and the loss of scientists at what should be a pivotal point in their career.
Daniels points to three reasons for the decline in research funding for young scientists -- longer training periods, a grant system that may favor incumbents and an increase in the cost of research that is borne by universities, causing some institutions to shy away from unproven researchers in favor of scientists with established funding streams.
"The inability to staunch -- if not reverse -- the above trends stands as an urgent and compelling policy challenge," Daniels says. "The current stewards of the U.S. research enterprise bear a responsibility to sustain and safeguard that enterprise so that it can provide a platform for the scientists and the science of generations to come."
Daniels proposes several policy reforms to better support young scientists including more robust funding for the NIH -- with more of that money dedicated to new talent -- and refining the peer review model to create a more accepting environment for inexperienced scientists and daring proposals. He also suggests creation of a standing body to undertake a continuing review of the issue, assess the effectiveness of any interventions and press stakeholders -- Congress, the NIH, federal agencies, universities and private industry -- into action.

"Other countries are marshaling the will and resources to invest in the next generation of young scientists," Daniels says. "A comparable solution in the United States will require a comparable commitment on the part of all actors in the biomedical science ecosystem. ... Our next generation of scientists, and indeed our next generation of science, demands nothing less."
Source: Proceedings of the National Academy of Sciences

Depression Occurs Due to Inflammation of Body's Immune System

Depression is a result of inflammation caused by the body's immune system, according to psychologists at the University of California in Los Angeles. Researchers found that a family of proteins called cytokines sets off inflammation in the body, and switches the brain into sickness mode.
 Depression Occurs Due to Inflammation of Body's Immune System

During the study it was seen that both cytokines and inflammation flare up during depressive episodes and these levels drop off during the remission period in people with bipolar disorder. Healthy people can also be temporarily put into a depressed and anxious state with a vaccine that causes a spike in inflammation.

Researcher George Slavich said, "Depression does involve psychology, but it also involves equal parts of biology and physical health."

University of California 

Study Uses Organoids to Learn About the Stages of Pancreatic Cancer

Pancreatic cancer, the uncontrollable cell growth in the pancreas, is one of the most lethal malignancies reported in the world. This is due to its late diagnosis and limited response to treatment. The risk of the cancer is manifold as there are no available prognosis methods to start treating pancreatic cancer early, so that the patient's life could be saved.

Hence, tractable methods to identify and interrogate the pathways that are involved in the process of the creation of pancreatic tumor are urgently needed. Scientists have newly developed organoid models, which are miniature organs, grown in vitro, from normal and neoplastic murine and human pancreas tissues in a new study addressing this issue. Pancreatic organoids have the advantage of being generated from rejected tumors and biopsies, survive cryo-preservation and exhibit ductal- and disease-stage-specific characteristics. 

The neoplastic organoids when orthotopically transplanted to the apt place, reiterate the full spectrum of tumor development by forming early-grade neoplasms that progress to locally invasive and metastatic carcinomas. The organoids are a platform to probe genetic cooperation, due to their ability to be genetically manipulated. A Comprehensive transcriptional and proteomic analysis of the murine pancreatic organoids has revealed genes and pathways altered during the progression of the cancer. It was found by the researchers that the confirmation of many of these protein changes in human tissues demonstrates that organoids are a simplistic model system to discover characteristics of the deadly pancreatic cancer malignancy. 


Monday, 5 January 2015

New treatment strategy for epilepsy

IMAGEResearchers found out that the conformational defect in a specific protein causes Autosomal Dominant Lateral Temporal Lobe Epilepsy (ADLTE) which is a form of familial epilepsy. They showed that treatment with chemical corrector called "chemical chaperone" ameliorates increased seizure susceptibility in a mouse model of human epilepsy by correcting the conformational defect. This was published in Nature Medicine (December 8, 2014 electronic edition).
Mutations in the gene LGI1, encoding a secreted protein, cause familial temporal lobe epilepsy. The research group of Professor Masaki Fukata, Associate Professor Yuko Fukata, and Assistant Professor Norihiko Yokoi of the National Institute for Physiological Sciences (NIPS), National Institutes of Natural Sciences (NINS), in collaboration with the group of Professor Masahiko Watanabe of the Hokkaido University Graduate School of Medicine, Professor Dies Meijer of the Erasmus University Medical Center in the Netherlands, and Professor Takao Hamakubo of the Research Center for Advanced Science and Technology, The University of Tokyo, investigated 22 mutations in the LGI1 gene found in patients with human epilepsy. In 19 mutations, LGI1 mutant protein was secretion-defective. One of these mutations was introduced to mice which produced symptoms of epilepsy. In LGI1 mutant mice, there was a decrease in the amount of LGI1 functioning normally outside the cell (i.e., synapse) due to the degradation by an intrinsic quality control system that rapidly degrades and eliminates mutant proteins.
A small molecule called chemical chaperone (4-phenylbutyrate) was administrated to LGI1 mutant mice with a view to correct the misfolding of the LGI1 mutant protein and to cause normal secretion to the synapse. It was found that the mice had decreased seizure susceptibility.
Epilepsy is a common brain disorder that affects 1% of the population. In some cases, current antiepileptic drugs have a limited role in the treatment. According to Professor Masaki Fukata, "Chemical chaperone treatment focused on correcting the misfolding in proteins has been tried in inherited diseases including cystic fibrosis and lysosome disease. This is the first for chemical chaperones to be applied as a therapeutic option for epilepsy. The same therapeutic strategy may also be of benefit to epilepsy caused by genetic mutations other than LGI1 gene. We propose a novel therapeutic strategy for epilepsy."

Diabetes debate: Triglycerides form in liver despite insulin resistance

New Haven, Conn. -- Solving one of the great mysteries of type 2 diabetes, a team of Yale researchers found that triglycerides, a type of fat in the blood and liver, are produced in the liver independent of insulin action in the liver.
In type 2 diabetics, insulin fails to suppress blood sugar production by the liver while paradoxically allowing the production of hepatic triglycerides. This combination results in multiple health risks, including high blood sugar and fatty liver disease. For years, to gain insight into this phenomenon, researchers focused on the role of altered insulin action in the liver in the production of triglycerides. However, Yale researchers tested a theory that triglycerides formed in the liver were more dependent on the delivery of fatty acids to the liver than on insulin action.
In their study, the Yale team -- led by Gerald I. Shulman, the George R. Cowgill professor of medicine and cellular & molecular physiology -- developed a novel method to measure the rate of triglyceride production from fatty acids in three types of animals: normal rats, insulin-resistant rats fed a high-fat diet, and rats with genetically modified insulin receptors. They found that in all of the animals tested increased triglyceride production was primarily dependent on fatty acid delivery and not on insulin action in the liver.
The findings also explain the long-standing paradox of why insulin therapy does not exacerbate, but instead reduces, fatty liver disease in patients with type 2 diabetes. "These results provide new insights into the pathogenesis of non-alcoholic liver disease and provides new approaches to treat fatty liver disease, which is now the most common liver disease in the world," said Shulman.
Shulman and his team plan to apply similar methodology to translate their findings to insulin-resistant patients with type 2 diabetes, hyperlipidemia, and fatty liver disease.

Skin microbes trigger specific immune responses

New research in mice shows that the immune system in the skin develops distinct responses to the various microbes that naturally colonize the skin, referred to as commensals. A team led by scientists at the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, found that each type of microbe triggers unique aspects of the immune system, suggesting that immune cells found in the skin can rapidly sense and respond to changes in microbial communities. These findings help clarify the protective role of skin commensals and may help explain how variation in the microbes at different skin sites contributes to skin disorders.
The skin is home to diverse microbial communities that can change over time. In the current study, investigators found that colonizing mice with different commensals leads to production of commensal-specific immune cells. They describe in detail how the common skin commensal Staphylococcus epidermidis enhances immune responses against pathogens without causing inflammation. Colonizing the skin of mice with S. epidermidis increased the number of CD8+ T immune cells, which produced the chemical messenger IL-17A. Dendritic cells, another type of immune cell, played a key role in generating this specific, non-inflammatory response. Mice colonized with S. epidermidis were protected against infection with a disease-causing fungus. Depleting CD8+ T cells or neutralizing IL-17A removed this protective effect.

The ability of different microbes to trigger distinct aspects of the immune system without causing inflammation opens the possibility of discovering new adjuvants--immune-boosting substances that may be added to vaccines or medications. Future research will focus on identifying specific chemical messengers and understanding how they stimulate the immune system.

Bad Luck is Responsible for Two-Thirds of Cancers Says a New Study

Bad Luck is Responsible for Two-Thirds of Cancers Says a New Study
Have you ever wondered why some people can smoke and drink into their old age while others with healthier lifestyles receive a cancer diagnosis? A landmark study from the Johns Hopkins Kimmel Cancer Center explains that random luck plays a significant role in determining whether or not a person is diagnosed with cancer during their lifetime.

Bad luck is responsible for two-thirds of adult cancer while the remaining cases are due to environmental risk factors and inherited genes, say scientists. 

"All cancers are caused by a combination of bad luck, the environment and heredity, and we've created a model that may help quantify how much of these three factors contribute to cancer development. Cancer-free longevity in people is often attributed to their good genes, but the truth is that most of them simply had good luck," said Bert Vogelstein, a scientist at the Johns Hopkins University School of Medicine. 

The study involved comparing stem cell divisions in 31 cancer types. The research team determined which were driven by the 'bad luck' factor of random DNA mutations and which had a higher incidence due to a combination of bad luck and environmental or hereditary risk factors. 

"It was well known that cancer arises when tissue-specific stem cells make random mistakes, or mutations, when one chemical letter in DNA is incorrectly swapped for another during the replication process in cell division. 

The more these mutations accumulate, the higher the risk that cells will grow unchecked, a hallmark of cancer. The actual contribution of these random mistakes to cancer incidence, in comparison to the contribution of hereditary or environmental factors, was not previously known," notes Mr. Bert. 

However, the study did not include breast cancer, which is the most common cancer in women, or prostate cancer, which is the second most common cancer in men after skin cancer. 

"You can add to your risk of getting cancers by smoking or other poor lifestyle habits. However, many forms of cancer are caused largely due to the bad luck of acquiring a mutation in a cancer driver gene regardless of lifestyle and heredity factors," Vogelstein said. 

Co-researcher Cristian Tomasetti observed that the research made a strong case for early detection.  

"If two-thirds of cancer incidence across tissues is explained by random DNA mutations, then changing our lifestyle habits will be a huge help in preventing certain cancers, but this may not be as effective for a variety of others. We should focus more resources on finding ways to detect such cancers at early, curable stages," he said 

Director of public policy at Cancer Council Australia, Paul Grogan, said putting cancer incidence down to "luck" was an oversimplification, noting that the global cancer burden is expected to nearly double to 21.4 million cases and 13.5 million deaths by 2030.  

"Measures including participation in screening and surveillance programs, being vigilant about your health, getting regular check-ups, avoiding risk factors can help us to prevent or survive cancer, irrespective of our genes," Mr. Paul said. 

Director of programs at Cancer Council NSW Kathy Chapman said research into gene mutations would lead to improved cancer treatment and help us understand at that very microscopic level which treatments will lead to the best outcomes. 

"The findings would help us to understand which genes are really the important ones when somebody is diagnosed with cancer," she said. 
Johns Hopkins University School of Medicine. 


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