Category: Health

{There’s this crave among today’s women to have the best shape and posture and all that.}

New UBC study has found that just one 30-minute bout of exercise makes women feel stronger and thinner. And the positive effect lasts well beyond the activity itself, which may be good news for women concerned about their body image.

“Women, in general, have a tendency to feel negatively about their bodies,” says study senior author Kathleen Martin Ginis, professor in UBC Okanagan’s School of Health and Exercise Sciences. “This is a concern because poor body image can have harmful implications for a woman’s psychological and physical health including increased risk for low self-esteem, depression and for eating disorders. This study indicates exercise can have an immediate positive effect.”

According to the National Institutes of Health, nearly one half of North American women experience some degree of body image dissatisfaction and this has become more prevalent over the last three decades.

“We think that the feelings of strength and empowerment women achieve post exercise, stimulate an improved internal dialogue,” says Martin Ginis. “This in turn should generate positive thoughts and feelings about their bodies which may replace the all too common negative ones.”

Source:Elcrema

{Early life stress encodes lifelong susceptibility to stress through long-lasting transcriptional programming in a brain reward region implicated in mood and depression, according to a study conducted at the Icahn School of Medicine at Mount Sinai and published June 15 in the journal Science.}

The Mount Sinai study focuses on epigenetics, the study of changes in the action of genes caused not by changes in DNA code we inherit from our parents, but instead by molecules that regulate when, where, and to what degree our genetic material is activated. Such regulation derives, in part, from the function of transcription factors — specialized proteins that bind to specific DNA sequences in our genes and either encourage or shut down the expression of a given gene.

Previous studies in humans and animals have suggested that early life stress increases the risk for depression and other psychiatric syndromes, but the neurobiology linking the two has remained elusive until now.

“Our work identifies a molecular basis for stress during a sensitive developmental window that programs a mouse’s response to stress in adulthood,” says Catherine Peña, PhD, lead investigator of the study. “We discovered that disrupting maternal care of mice produces changes in levels of hundreds of genes in the VTA that primes this brain region to be in a depression-like state, even before we detect behavioral changes. Essentially, this brain region encodes a lifelong, latent susceptibility to depression that is revealed only after encountering additional stress.”

Specifically, Mount Sinai investigators identified a role for the developmental transcription factor orthodenticle homeobox 2 (Otx2) as a master regulator of these enduring gene changes. The research team showed that baby mice that were stressed in a sensitive period (from postnatal day 10-20) had suppressed Otx2 in the VTA. While Otx2 levels ultimately recovered by adulthood, the suppression had already set in motion gene alterations that lasted into adulthood, indicating that early life stress disrupts age-specific developmental programming orchestrated by Otx2.

Furthermore, the mice stressed during the early-life sensitive time period were more likely to succumb to depression-like behavior in adulthood, but only after additional adult stress. All mice acted normally before additional adult social stress, but a “second hit” of stress was more likely to trigger depression-like behavior for mice stressed during the sensitive time period.

To test the prediction that Otx2 was actually responsible for the stress sensitivity, the research team developed viral tools that were used to either increase or decrease Otx2 levels. They found that suppression of Otx2 early in life was both necessary and sufficient for increased susceptibility to adult stress.

“We anticipated that we would only be able to ameliorate or mimic the effects of early life stress by changing Otx2 levels during the early sensitive period.” says Dr. Peña. “This was true for long-lasting effects on depression-like behavior, but somewhat to our surprise we could also change stress sensitivity for short amounts of time by manipulating Otx2 in adulthood.”

While early-life critical periods have been understood for processes such as language learning, little is known about whether there are sensitive periods in childhood when stress and adversity most impacts brain development and particularly emotion-regulation systems. This study is the first to use genome-wide tools to understand how early life stress alters development of the VTA, providing new evidence for sensitive windows in emotion development.

“This mouse paradigm will be useful for understanding the molecular correlates of increased risk of depression resulting from early life stress and could pave the way to look for such sensitive windows in human studies,” says Eric J. Nestler, MD, PhD, Nash Family Professor of Neuroscience and Director of the Friedman Brain Institute at Mount Sinai and senior investigator of the study. “The ultimate translational goal of this research is to aid treatment discoveries relevant to individuals who experienced childhood stress and trauma.”

Source:Science Daily

{Mind-body interventions (MBIs) such as meditation, yoga and Tai Chi don’t simply relax us; they can ‘reverse’ the molecular reactions in our DNA which cause ill-health and depression, according to a study by the universities of Coventry and Radboud.}

The research, published in the journal Frontiers in Immunology, reviews over a decade of studies analysing how the behaviour of our genes is affected by different MBIs including mindfulness and yoga.

Experts from the universities conclude that, when examined together, the 18 studies — featuring 846 participants over 11 years — reveal a pattern in the molecular changes which happen to the body as a result of MBIs, and how those changes benefit our mental and physical health.

The researchers focus on how gene expression is affected; in other words the way that genes activate to produce proteins which influence the biological make-up of the body, the brain and the immune system.

When a person is exposed to a stressful event, their sympathetic nervous system (SNS) — the system responsible for the ‘fight-or-flight’ response — is triggered, in turn increasing production of a molecule called nuclear factor kappa B (NF-kB) which regulates how our genes are expressed.

NF-kB translates stress by activating genes to produce proteins called cytokines that cause inflammation at cellular level — a reaction that is useful as a short-lived fight-or-flight reaction, but if persistent leads to a higher risk of cancer, accelerated aging and psychiatric disorders like depression.

According to the study, however, people who practise MBIs exhibit the opposite effect — namely a decrease in production of NF-kB and cytokines, leading to a reversal of the pro-inflammatory gene expression pattern and a reduction in the risk of inflammation-related diseases and conditions.

The study’s authors say the inflammatory effect of the fight-or-flight response — which also serves to temporarily bolster the immune system — would have played an important role in humankind’s hunter-gatherer prehistory, when there was a higher risk of infection from wounds.

In today’s society, however, where stress is increasingly psychological and often longer-term, pro-inflammatory gene expression can be persistent and therefore more likely to cause psychiatric and medical problems.

Lead investigator Ivana Buric from the Brain, Belief and Behaviour Lab in Coventry University’s Centre for Psychology, Behaviour and Achievement said:

“Millions of people around the world already enjoy the health benefits of mind-body interventions like yoga or meditation, but what they perhaps don’t realise is that these benefits begin at a molecular level and can change the way our genetic code goes about its business.

“These activities are leaving what we call a molecular signature in our cells, which reverses the effect that stress or anxiety would have on the body by changing how our genes are expressed. Put simply, MBIs cause the brain to steer our DNA processes along a path which improves our wellbeing.

“More needs to be done to understand these effects in greater depth, for example how they compare with other healthy interventions like exercise or nutrition. But this is an important foundation to build on to help future researchers explore the benefits of increasingly popular mind-body activities.”

Source:Science Daily

{A new research from the University of Nevada has found that being cheated on is linked to depression and anxiety and may also lead to more risky behaviours such as having unprotected sex and binge drinking, according to a report on Medical Daily.}

The study found that being a victim of infidelity can increase the likelihood of psychological distress and may also increase the risk of abusing alcohol and/or drugs and developing an eating or exercise disorder, Medical Daily reported.

“Being cheated on seems to not only have mental health consequences but also increases risky behaviours,” lead author M. Rosie said.

“We also found that people who blamed themselves for their partner cheating, such as feeling like it was their fault or they could have stopped it, were more likely to engage in risky behaviours.

“It is possible that infidelity is such a serious and distressing relationship event that these intense negative reactions occur regardless of whether a person stays in the relationship.

“As we continue this line of research, we hope to better understand the emotional and physical health toll of infidelity.”

The researchers also found that the effects of being cheated on were more or less the same, regardless of whether the individual left or stayed in the relationship after being cheated on.

Source:Elcrema

A collaboration between Saïd M. Sebti, Ph.D., chair of Moffitt Cancer Center’s Drug Discovery Department, and Michele Pagano, M.D., chair of the Department of Biochemistry and Molecular Pharmacology at New York University’s Langone Medical Center, led to the publication of an important study in the latest issue of Nature. The investigation found that the drug, geranylgeranyltransferase inhibitor GGTI-2418 suppresses a new defective PTEN cancer pathway discovered by Pagano’s group.

Fully functional PTEN is well known to suppress tumor growth by antagonizing the PI3K/Akt tumor survival pathway. Pagano’s group discovered a novel mechanism by which PTEN protects cells from cancer by preventing the geranylgeranylated protein FBXL2 from binding and degrading IP3R3. IP3R3 is an important anti-cancer “sensor” recognizing hyper-proliferating cells that use abnormally high levels of energy, and targeting them to self-destruct as an anti-cancer safety mechanism. The PTEN gene binds to IP3R3, protecting its cancer-sensing function. However PTEN is defective in many cancers, and as such, FBXL2 is left unchecked; too much IP3R3 is degraded and fast-multiplying cells are less able to self-destruct.

“FXBL2 may be partially responsible for cancer growth in the many patients with genetic changes that happen to disable PTEN,” said Pagano. The drug GGTI-2418 blocks this cancer-causing activity of FBXL2 by inhibiting its geranylgeranylation which is required for FBXL2 to bind and degrade IP3R3. GGTI-2418 was co-discovered and developed by Sebti and NYU President Andrew Hamilton, Ph.D., while he was at Yale University. .

Another fascinating consequence of this discovery is that cancers with defective PTEN activate two tumor survival circuits to evade cell death, the PI3K/Akt and the FBXL2 pathways. “These findings have important translational implications as patients whose tumors harbor defective PTEN may benefit greatly from a combination of inhibitors of FBXL2 geranylgeranylation, such as GGTI-2418, and inhibitors of Akt, such as TCN-P,” said Sebti. Both GGTI-2418 and TCN-P were co-discovered by Sebti and are now developed by the clinical-stage oncology company Prescient Therapeutics Ltd.

The researchers also found that using GGTI-2418 to block FBXL2 from degrading IP3R3 made the tumors in mice more vulnerable to photodynamic therapy (PDT).”This experimental drug, by itself and with a form of light therapy, countered FBXL2 to let abnormal cells self-destruct,” said Pagano “We will be looking to collaborate with Dr. Sebti on clinical studies combining GGTI-2418 with PDT or TCN-P in patients with low PTEN.”

Source:Science Daily

{Prenatal exposure to maternal fever during the second trimester raised odds of autism spectrum disorder by 40 percent}

Fever during pregnancy may raise the risk for autism spectrum disorder (ASD) in the child, according to a study led by scientists at the Center for Infection and Immunity (CII) at Columbia University’s Mailman School of Public Health. The effect was most pronounced in the second trimester, raising odds for ASD by 40 percent. Risk of an ASD was increased by over 300 percent for the children of women reporting three or more fevers after the twelfth week of pregnancy.

The study is the most robust to date to explore the risk of ASD associated with fevers across the entire span of pregnancy, and of the capacity of two different types of commonly used anti-fever medications — acetaminophen and ibuprofen — to address that risk. Risks were minimally mitigated among the children of women taking acetaminophen for fever in the second trimester. Although there were no cases of ASD among children of mothers who took ibuprofen, a nonsteroidal anti-inflammatory drug, researchers could not ascertain whether risk was mitigated due to the extremely small number of women using this particular drug for fever. Results of the study appear in the journal Molecular Psychiatry.

The researchers followed 95,754 children born between 1999 and 2009, including 583 cases of ASD identified in Norway through the Autism Birth Cohort (ABC) Study. Mothers of 15,701 children (16 percent) reported fever in one or more four-week intervals throughout pregnancy, similar to rates reported in the U.S. ASD risk was increased by 34 percent when mothers reported fever at any time during pregnancy, and by 40 percent in the second trimester. The risk increased in a dose-dependent fashion from 1.3-fold with one or two fever episodes after the twelfth prenatal week to 3.12-fold with three or more episodes.

“Our results suggest a role for gestational maternal infection and innate immune responses to infection in the onset of at least some cases of autism spectrum disorder,” says first author Mady Hornig, associate professor of Epidemiology and director of Translational Research at CII.

Questionnaire analysis did not indicate an association between risk and maternally-reported symptoms of infection in individual organ systems that might implicate specific infectious agents. An ongoing study is testing blood samples collected at mid-pregnancy and at birth to explore the possible role of specific infectious agents and the contribution of distinctive patterns of immune response among mothers and children to understand the mechanisms creating vulnerability.

“Future work should focus on identifying and preventing prenatal infections and inflammatory responses that may contribute to autism spectrum disorder,” says senior author W. Ian Lipkin, John Snow Professor of Epidemiology and director of CII.

Source:Science Daily

{Massive global research project reveals 30 percent of the world’s population affected by weight problems.}

Globally, more than 2 billion children and adults suffer from health problems related to being overweight or obese, and an increasing percentage of people die from these health conditions, according to a new study.

They are dying even though they are not technically considered obese, researchers found. Of the 4.0 million deaths attributed to excess body weight in 2015, nearly 40% occurred among people whose body mass index (BMI) fell below the threshold considered “obese.”

The findings represent “a growing and disturbing global public health crisis,” according to the authors of the paper published today in The New England Journal of Medicine.

“People who shrug off weight gain do so at their own risk — risk of cardiovascular disease, diabetes, cancer, and other life-threatening conditions,” said Dr. Christopher Murray, an author on the study and Director of the Institute for Health Metrics and Evaluation (IHME) at the University of Washington. “Those half-serious New Year’s resolutions to lose weight should become year-round commitments to lose weight and prevent future weight gain.”

The study, which spans 195 countries and territories from 1980 through 2015, was released today at the annual EAT Stockholm Food Forum, which aims to create a healthier, more sustainable food system. It is based on data from the most recent Global Burden of Disease study (GBD), a systematic, scientific effort to quantify the magnitude of health loss from all major diseases, injuries, and risk factors by age, sex, and population. With more than 2,300 collaborators in 133 countries, the GBD study examines 300-plus diseases and injuries.

The paper includes analyses of other studies on the effects of excess weight and potential links between high BMI and cancers of the esophagus, colon and rectum, liver, gallbladder and biliary tract, pancreas, breast, uterus, ovary, kidney, and thyroid, as well as leukemia. IHME is committed to producing more in-depth studies on the implications of obesity and overweight, including through a new partnership with the United Nations, according to Dr. Murray.

He announced at the forum a new agreement between IHME and the UN’s Food and Agriculture Organization (FAO) to exchange data, knowledge, and expertise. The goal is to elevate the world’s collective understanding of what is driving “the current global epidemic of disease” related to high body weight.

The United Nations “Decade of Action on Nutrition” is an initiative covering 2016-2025 to eradicate hunger, end malnutrition in all its forms (undernutrition, micronutrient deficiencies, overweight or obesity), and reduce the burden of diet-related non-communicable diseases in all age groups.

In 2015, excess weight affected 2.2 billion children and adults worldwide, or 30% of all people. This includes nearly 108 million children and more than 600 million adults with BMI exceeding 30, the threshold for obesity, according to the study. The prevalence of obesity has doubled since 1980 in more than 70 countries and has continuously increased in most other nations. Although the prevalence of obesity among children has been lower than among adults, the rate of increase in childhood obesity in many countries was greater than that of adults.

Among the 20 most populous countries, the highest level of obesity among children and young adults was in the United States at nearly 13%; Egypt topped the list for adult obesity at about 35%. Lowest rates were in Bangladesh and Vietnam, respectively, at 1%. China with 15.3 million and India with 14.4 million had the highest numbers of obese children; the United States with 79.4 million and China with 57.3 million had the highest numbers of obese adults in 2015.

“Excess body weight is one of the most challenging public health problems of our time, affecting nearly one in every three people,” said Dr. Ashkan Afshin, the paper’s lead author and an Assistant Professor of Global Health at IHME. “Over the past decade, numerous interventions have been evaluated, but very little evidence exists about their long-term effectiveness. Over the next 10 years, we will closely with the FAO in monitoring and evaluating the progress of countries in controlling overweight and obesity. Moreover, we will share data and findings with scientists, policymakers, and other stakeholders seeking evidence-based strategies to address this problem.”

Source:Science Daily

{Chemists’ novel device quickly detects carcinogenic chemicals, DNA damage from e-cigarette vapor}

A study by chemists at the University of Connecticut offers new evidence that electronic cigarettes or e-cigarettes are potentially as harmful as tobacco cigarettes.

Using a new low-cost, 3-D printed testing device, UConn researchers found that e-cigarettes loaded with a nicotine-based liquid are potentially as harmful as unfiltered cigarettes when it comes to causing DNA damage.

The researchers also found that vapor from non-nicotine e-cigarettes caused as much DNA damage as filtered cigarettes, possibly due to the many chemical additives present in e-cigarette vapors. Cellular mutations caused by DNA damage can lead to cancer.

The findings appear in the journal ACS Sensors.

How much DNA damage e-cigarettes cause depends on the amount of vapor the user inhales, the other additives present, whether nicotine or non-nicotine liquid is used, and other factors, says Karteek Kadimisetty, a postdoctoral researcher in UConn’s chemistry department and the study’s lead author.

But one finding was clear.

“From the results of our study, we can conclude that e-cigarettes have as much potential to cause DNA damage as unfiltered regular cigarettes,” Kadimisetty says.

Electronic cigarettes are battery-powered devices that heat up liquid and turn it into an aerosol vapor that can be inhaled. Using e-cigarettes is also called ‘vaping.’ The contents of e-cigarettes, called e-liquid or e-juice, are usually made up of propylene glycol, glycerine, nicotine, and flavorings such as menthol, cherry, vanilla, or mint. Non-nicotine e-cigarettes are also available.

Frequently viewed as a less toxic alternative for people looking to break their habit of smoking tobacco cigarettes, modern e-cigarettes have steadily risen in popularity since they first appeared on the commercial market in 2004. How much e-cigarettes contribute to serious health problems and whether they serve as a gateway for future tobacco smokers remains the subject of much debate. Growing concerns about the potential health impact of electronic cigarettes however, prompted the U.S. Food and Drug Administration to tighten its regulation of e-cigarettes in 2016.

UConn’s scientists decided to look into whether the chemicals in e-cigarettes could cause damage to human DNA while testing a new electro-optical screening device they developed in their lab. The small 3-D printed device is believed to be the first of its kind capable of quickly detecting DNA damage, or genotoxicity, in environmental samples in the field, the researchers say.

The device uses micropumps to push liquid samples across multiple ‘microwells’ embedded in a small carbon chip. The wells are pre-loaded with reactive human metabolic enzymes and DNA. As the samples drop into the wells, new metabolites that have the potential to cause DNA damage are formed. Reactions between the metabolites and the DNA generate light that is captured by a camera. Within five minutes, users can see how much relative DNA damage a sample produces by the intensity of the light detected in each well.

The device is unique in that it converts chemicals into their metabolites during testing, which replicates what happens in the human body, Kadimisetty says.

Bioassays currently used to determine the genotoxicity of environmental samples may be more comprehensive, but they are often time-consuming and costly. Lab equipment alone can cost tens of thousands of dollars. The array developed at UConn provides an important initial screening tool for genotoxicity in just minutes. The chip central to the device is disposable and costs only a dollar to make, thanks to recent advances in 3-D printing.

“What we developed is very cheap to make, efficient, and can be used by almost anyone,” says UConn chemistry professor James Rusling, the senior researcher on the study.

Affordable and efficient “labs on a chip” is a specialty of Rusling’s lab, which has previously created miniature arrays that can detect antibodies to food allergens and cancer biomarker proteins. Rusling says similar arrays potentially could be used for quick genotoxic screening during drug development, for monitoring or testing fresh water supplies, and for the early detection of aggressive forms of cancer.

In the current study, the researchers extracted samples from e-cigarettes and tobacco cigarettes using an artificial inhalation technique. Cigarettes were connected to a tube that contained a cotton plug. The researchers then used a syringe at the other end of the tube to replicate inhalation. Samples came from the chemicals captured in the cotton.

The team set their test so that 20 puffs of an e-cigarette was roughly equivalent to smoking one tobacco cigarette, a ratio supported by other research. The team gathered samples at 20, 60, and 100 puffs. The potential DNA damage from e-cigarettes increased with the number of puffs, Kadimisetty says.

“Some people use e-cigarettes heavily because they think there is no harm,” he says. “We wanted to see exactly what might be happening to DNA, and we had the resources in our lab to do that.”

There are potentially hundreds of chemicals in e-cigarettes that could be contributing to DNA damage, Kadimisetty says. Rather than test for all of them, the UConn team targeted three known carcinogenic chemicals found in tobacco cigarettes. They then loaded their device’s microwells with specific enzymes that would convert those chemicals into metabolites. If these chemicals were in the sample, the test gave them a reading for genotoxicity. If the chemicals were not present, there would be no reaction.

Source:Science Daily

{A new study from the University of Iowa shows that a pair of common chemicals that manufacturers use to make plastic food containers, water bottles, and other consumer products do not contribute to obesity to the extent of the chemical it’s replacing.}

The chemicals — bisphenol F and bisphenol S (known as BPF and BPS) — are being used increasingly by food packaging manufacturers as substitutes for bisphenol A (BPA), which studies have found disrupts endocrine systems and causes numerous health problems. BPA is used in many kinds of packaging for snacks and drinks, canned foods, and water bottles. The chemical is absorbed into the body mainly through the food or water it contacts in the container.

But concern was raised several years ago when numerous studies found BPA increases the risk of various health issues, in particular obesity, diabetes, and cardiovascular disease. A consumer backlash erupted after the studies received media attention so manufacturers started reducing the use of BPA in some consumer products or even eliminating it in so-called “BPA-free” products by replacing it with such alternatives as BPF and BPS.

However, little is known on the potential impact of BPF and BPS exposure in humans. The new University of Iowa study is the first to determine the health impacts of BPF and BPS exposure on obesity in humans. Using data from a nationwide population-based study conducted by the U.S. Centers for Disease Control (CDC), the researchers confirm that BPA is associated with increased obesity in humans. But the study found no links between obesity and either BPF or BPS at the current exposure levels.

However, the researchers warn that fewer products currently use BPF and BPS — BPA still has more than half the global market share for the chemicals, and the average concentration of BPF and BPS is about one-fourth that of BPA in the US population. Whether BPF and BPS pose an increased risk of obesity at the same population exposure levels as BPA remains unknown. Future studies will be needed to confirm the results, as BPF and BPS are likely to replace BPA in more consumer products.

Source:Science Daily