Category Archives: Research

The steps that can help adults heal from childhood trauma

traumaPrevention is the mantra of modern medicine and public health. Benjamin Franklin said it himself: “An ounce of prevention is worth a pound of cure.”

Unfortunately, childhood adversities such as abuse and neglect cannot be prevented by vaccinations. As we now know, a large proportion of adults go through adverse childhood experiences (ACEs) and can exhibit symptoms such as substance abuse. The symptoms seen in adults can in turn expose the next generation to adverse outcomes – creating a cycle that’s hard to break.

However, we can limit the impact of ACEs on future generations by taking a close look at what we are doing today – not only for our children, but for ourselves, as adults. Therefore, to prevent adversities for children, we must address the healing and recovery of trauma in adults.

Shifting the paradigm

The ACE Study, launched in the 1990s, offered a groundbreaking look at how childhood trauma can impact health decades later.

More than two-thirds of the 17,000-plus adults in our study reported at least one ACE, such as divorce, neglect or domestic violence in the household. These adults were at a greater risk for numerous negative health and behavioral outcomes.

When I present this research, I often get questions about the adult survivors. What has helped these adults survive to tell their childhood histories?

The ACE Study was not conceptualized to examine resilience. But I had always been curious about what helped these trauma survivors thrive. I wanted to understand not only what led to their ill health later in life, but what led some of them to report positive health, despite their backgrounds.

Promoting good health

Modern medicine and public health have traditionally focused on figuring out the origins of disease and how to prevent poor health.

In 1996, medical sociologist and anthropologist Aaron Antonovsky offered a different perspective. He suggested we look at health as a continuum and focus on what can promote good health. This approach, called salutogenesis, suggests that we as humans have the innate capacity to move toward health in the face of hardship.

Today, the World Health Organization defines health as “a state of complete physical, mental and social well-being and not merely the absence of disease or infirmity.” I wondered how this approach might reflect on the adult survivors. What promotes their good health and positive well-being, knowing they are at risk for negative health conditions?

In 2013, my colleagues and I published a study examining approximately 5,000 adults from the original ACE study who reported at least one childhood adversity. We focused on strategies that have been proven to promote good health – such as exercise, abstaining from smoking, access to emotional support and completing education at the high school level or higher.

Indeed, each of the factors listed was associated with reports of excellent, very good or good health among adult survivors. Depending on the factor, there was a 30 to 80 percent increased likelhood that the adult would report positive well-being. Survivors who had a college education were 2.1 times more likely to report positive well-being than those with no high school diploma. These findings were after considering their chronic conditions. We also found that the four factors were associated with a lower likelihood to report depressive feelings.

When I repeated this study with a sample population of adult trauma survivors from four states and the District of Columbia, I found nearly identical results.

What’s more, the greater number of health-promoting activities a person participated in, the better their well-being seemed to be. Adult survivors with at least two factors were 1.5 times more likely to report good to excellent health. Those who reported all four factors were 4.3 times more likely to report good to excellent health, compared to those who engaged in none or one, even after considering their chronic conditions.

On average, trauma survivors who reported at least two of the health promoting factors had also experienced fewer mentally and physically unhealthy days in the past 30 days.

We have also learned that adult trauma survivors use complementary strategies such as yoga, massage, and dance therapy.

With that said, we need more rigorous studies to test these and other approaches that promote health and well-being. The studies presented examined only four factors and cannot be generalized to all adult survivors of ACEs.

How to start healing

From a survival perspective, the body can respond to perceived or actual threats with the “fight or flight” stress response. However, if this threat is constant, the endocrine and neuronal systems stay activated, which can overtax us and prevent the body from establishing homeostasis. Researchhas helped us to understand how disease can result from stress and trauma.

Just as we are biologically equipped with mechanisms to deal with threatening situations, our bodies are also equipped with neurochemicals like dopamine and GABA that provide feelings of security, happiness and motivation. We can ourselves activate these positive feelings through self-care. For example, in one study, massage was found to reduce cortisol and increase dopamine and serotonin.

There is no voodoo here. If we present our body and five senses with positive inputs – like calming music, unprocessed foods and walks through nature – we can stimulate our own system to regulate in a favorable way.

But these interventions may not be sufficient by themselves. Active counseling, the use of cognitive-behavioral therapy and in some cases medications or other health interventions may be needed.

We must recognize the strength and limitations of modern medicine and public health when it comes to addressing and preventing ACEs. Interrupting the cycle of abuse and neglect must first begin with adults. It will require an integrative and multigenerational approach that empowers individuals to heal their bodies, minds and spirits.

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Daunting new research out of the University of Helsinki claims that drinking alcohol, even during the early weeks of pregnancy, can cause irreversible damage to an unborn baby. The researchers claim that in the early stages of pregnancy, even before many women realize that they are pregnant, alcohol exposure can cause symptoms of fetal alcohol syndrome.

Fetal alcohol syndrome is an often brushed-over topic. Reports focus primarily on stunted growth and learning disabilities, but the reality of alcohol’s impact on a baby can be much more encompassing and individualized — affecting behavior, impulse control, learning, and numerous other areas. The research was done on mice, and the scientists say that this research supports earlier theories that drinking even during very early pregnancy can cause permanent damage to children.

The researchers said that maternal alcohol intake in early pregnancy changed the way genes function in the offspring exposed prenatally to alcohol. The changes were lasting and irreversible. The researchers warned that drinking alcohol, even as early as three weeks after conception, can cause symptoms that mirror fetal alcohol syndrome, including structural changes to the face and skull, and lasting, age-inappropriate hyperactivity.

Other symptoms of fetal alcohol exposure include teeth and mouth problems, hearing and ear problems, immune system weakness, defects in organs, muscular problems, hormonal disorders, and many more physical and cognitive issues. Lara Crutchfield, FASD trainer with FASD Today, detailed the specific physical and neurological damage that can be caused when a woman drinks during pregnancy. Some of this damage is unique to fetal alcohol exposure.

The researchers warned that early pregnancy is an especially dangerous time to consume alcohol, because it’s such an active time for cell division and differentiation, according to the Daily Mail. The research into maternal alcohol consumption during early pregnancy focused on the memory and learning center of the brain known as the hippocampus, which is especially sensitive to alcohol exposure. This exposure resulted in typical symptoms of fetal alcohol syndrome, but it also altered the epigenome and the function of many genes in the hippocampi. This damage lasted into the adulthood of the test subjects. The alcohol also changed the gene function of bone marrow. Dr Kaminen-Ahola explained.

“The results support our assumption that alcohol permanently alters gene regulation at a very early stage. This would be significant for the challenging diagnostics of alcohol-induced damage. The mechanisms and biological markers which can aid in diagnosis are studied so that we can offer the developmental support necessitated by the damage as early as possible. Ideally, a swipe sample from inside the mouth of a newborn could reveal the extent of damage caused by early pregnancy alcohol exposure.”

Last fall, research out the the University of North Carolina found that a significantly greater number of children probably suffer from fetal alcohol spectrum disorder than anyone ever suspected. Earlier this year, Professor Peter Hepper from Queen’s University Belfast broke the news that even drinking a half of a glass of wine with dinner could damage a baby’s brain, an earlier Inquisitr article detailed.

Some earlier research indicated that proper maternal intake of folate, choline, and vitamin A might offer some protection to unborn babies against the effects of fetal alcohol exposure.

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Bullied teens more likely to smoke, drink and use drugs

FILE PHOTO - A cigarette burns in an ashtray at a pub in Prague(Reuters Health) – Children who are bullied in fifth grade are more likely to become depressed and experiment with drugs and alcohol during their teen years than their peers who weren’t victimized by other kids, a U.S. study suggests.

Researchers followed almost 4,300 students starting in fifth grade, when they were around 11 years old. By tenth grade, 24 percent of the teens drank alcohol, 15 percent smoked marijuana and 12 percent used tobacco.

More frequent episodes of physical and emotional bullying in fifth grade were associated with higher odds of depression by seventh grade, which was in turn linked to greater likelihood of substance use later in adolescence, the study found.

“We drew on the self-medication hypothesis when trying to understand why peer victimization may lead to substance use over time,” said lead study author Valerie Earnshaw, a human development and family studies researcher at the University of Delaware in Newark.

“This suggests that people use substances to try to relieve painful feelings or control their emotions,” Earnshaw said by email. “So, youth who are bullied feel bad, or experience depressive symptoms, and then may use substances to try to feel better.”

For the study, researchers examined data from three surveys conducted from 2004 to 2011 among students at schools in Houston, Los Angeles and Birmingham, Alabama.

Students were asked if they had used tobacco, alcohol or marijuana in the past 30 days and how often they had been victims of bullying by their peers in the previous year. Questions on peer victimization touched on both physical aggression like shoving and kicking as well as emotional taunts like saying nasty things about them to other kids.

At the start of the study in fifth grade, about 10 percent of participants said they had been victims of bulling. This was more common among kids who had chronic illnesses, sexual minorities and boys.

By seventh grade, almost 2 percent of the students reported symptoms of depression.

And by the end of the study in tenth grade, substance use was more common among the kids who had previously reported bullying and depression.

The study isn’t a controlled experiment designed to prove that bullying directly causes depression or that mental health issues directly cause substance use. Another limitation of the study is its reliance on teens to accurately report any episodes of bullying, symptoms of depression or substance use, the authors note.

It’s also possible that teens who are bullied may later wind up drinking or using drugs because their peer groups include many adolescents who do both of these things, whether on sports teams or among crowds of particularly aggressive kids, said Bonnie Leadbeater, a psychology researcher at the University of Victoria in Canada.

“Being ‘trapped’ in these networks can be particularly problematic in high school, where you see the same people every day,” Leadbeater, who wasn’t involved in the study, said by email.

“Youth with multiple networks beyond school through sports, music, art, religious activities, volunteering and work are more apt to find friends and others who see their talents, strengths and abilities,” Leadbeater added. “These strengths are often established in late elementary school.”

The trouble with bullying that leads to mental health problems is that teens with depression and anxiety are more likely to withdraw from peers and lack interest in most things.

“Young teens need to have ways of dealing with peer conflict before it becomes bullying,” Leadbeater said. “Young teens need to believe that getting help is normative and that bullying is not.”

SOURCE: Pediatrics, online May 9, 2017.

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FASD and epigenetics


This Q&A, is a talk with Western University (Ontario) researcher Ben Laufer about the latest science on FASD and how it influences our genetics.

What is epigenetics?

Traditionally, science has told us that children are the sum of their parents’ genetics. Recently, though, we’ve discovered that it’s actually much more complicated. Just think about identical twins, who can have entirely different personalities and even contract different diseases. Another example is the famous case of Dolly the sheep – she had striking physical and mental differences from the “original” animal from which she was cloned.

Clearly, “nurture” ( life experience) influences “nature” (genetics). But there’s also another factor, one which is responsible for passing on the “memories” of the experiences of previous and current generations. This factor is called epigenetics, which is Latin for “above genetics.”

How does it work?

In a sense, the epigenome can be thought of as the software to our genetic hardware. It’s just like loading Word or Powerpoint on your computer: the software is a set of instructions to tell the hardware what it should do, where it should do it, and when it should happen. Another analogy is that the genetic code is the spelling of a language and the epigenome is the punctuation. A sentence can mean something completely different if you change its punctuation (remember Eats, Shoots, and Leaves?). Like raw computer hardware or a book with no punctuation, every cell in our body has essentially identical DNA. And yet, a liver cell is utterly different from a brain cell – all because of the epigenome.

For scientists, the debate over nature versus nurture has been solved. Rather than being separate forces, the two are intimately connected. In order to form and develop, humans need both genomes and epigenomes.

Epigenetics has resulted in a fundamental paradigm shift in science. It suggests that genetic determinism is an outdated concept. Epigenetic research shows that a child inherits more than the genes of their parents. DNA is not destiny. It’s just one piece of the puzzle.

What does epigenetics have to do with FASD?

Alcohol is part of a class of chemicals called teratogens, which are known for their devastating effect on the developing embryo/fetus. Alcohol is a textbook teratogen that acts by altering epigenetic marks through a complex process known as DNA methylation. Prenatal exposure to alcohol causes the widespread death of cells that the developing brain can’t afford to lose. Alcohol’s impact on the epigenome is what leads to Fetal Alcohol Spectrum Disorders (FASD).

Fetal Alcohol Syndrome (FAS), which is diagnosed in one percent of the general population, is the leading preventable cause of intellectual disability in the Western world. Unfortunately, when it comes to overall fetal alcohol exposure, the numbers are much higher than that. In Canada, 10-15% of pregnant women (depending on province) report they consume some alcohol during pregnancy. We do know that people tend to underreport the amount of alcohol they actually drink, which means the real numbers are probably even higher. Although alcohol-exposed children don’t all go on to develop full-blown FAS, many do fall under the much broader umbrella term of FASD. Even more might display challenges that don’t meet the threshold for an FASD diagnosis, but that may still be connected to the prenatal alcohol exposure. This represents a serious public health issue of unprecedented scale.

What is your research all about?

During my research with Dr. Shiva Singh and his lab at Western University, we’ve conducted numerous molecular and behavioural studies on mice. We found that prenatal alcohol exposure causes massive changes to the epigenome. We’ve also found that differences in the timing and level of alcohol exposure have a huge effect on what kinds of problems occur. Our findings were confirmed by more recent human analyses, which we worked on in collaboration with Dr. Joachim Kaplanga. We even identified a group of epigenetic alterations that can identify prenatal alcohol exposure non-invasively. However, it will be many years before we can develop these findings into a commonly accesible clinical test.

What are the implications of this research?

Despite the slow pace of the research world, the information we’ve discovered should be communicated to the public as soon as possible. One simple statement we can promote is, “No safe time, no safe amount [of alcohol].” Another important observation we can share is that the changes to the brain caused by prenatal alcohol exposure continue to affect brain development throughout childhood and even adulthood.

We’ve also learned two things that are very striking. In the past, we believed that the effects of prenatal alcohol exposure couldn’t be inherited by the affected person’s children. But research has shown that some of the effects of prenatal alcohol exposure can, in fact, be passed on to future generations via the epigenome. We also thought that the mother’s alcohol consumption during pregnancy was the only thing that mattered. What we’ve learned is that the father’s consumption of alcohol can alter his epigenome and cause deficits in his future children. It’s all a lot more complicated than we used to think.

What does this mean for parents, especially adoptive parents? Is there anything we can do with this knowledge?

It’s actually not all bad news! Plasticity is a key part of epigenetic programming and brain development. This means the epigenome is constantly sensing and adapting to its environment. We can’t yet correct the initial damage caused by fetal alcohol exposure, but plasticity means that effects on future development can be corrected, at least to some extent.

Dr. Singh and our lab are now examining how fetal alcohol exposed mice respond to different environments. Intriguingly, and inspiringly, what we see is that good parental care and an enriched environment make all the difference. It doesn’t just help – it actually brings the mouse to a level of mental functioning similar to their unexposed peers that are raised in a standard environment.

The opposite is also true. Fetal alcohol-exposed mice that experience poor levels of care are much more seriously affected. This means that while there may not be an absolute cure, there is a way to greatly help improve the quality of life for alcohol-exposed children: the love, care, and understanding of a family.

Ben Laufer is currently finishing his Ph.D. research in biology with Dr. Shiva Singh at Western University in Ontario. More information about their research and its impact can be found at

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Drinking in pregnancy: Excess transcription factor Heat Shock Factor 1 can delay embryonic neural migration


Summary: Transcription factor Heat Shock Factor 1, which the developing brain releases to shield the vital organ from the ravages of environmental stress, actually can contribute to impairing the embryonic brain when too much Hsf1 is produced, research indicates. While the finding was made in a preclinical model, it raises questions about neural risks for human infants if mothers drink alcohol in the first or second trimester of pregnancy.

When fetuses are chronically exposed to harmful agents in utero, such as alcohol, ethanol or methyl mercury, the experience can negatively affect fetal brain development in unpredictable ways. Some fetal brains show little or no damage, while some fetal brains suffer severe damage. By looking back to the earliest moments of embryonic brain development, an international research team that includes five Children’s National authors sought to explain the molecular and cellular bases for complex congenital brain disorders that can result from exposure to such harmful agents.

“From a public health perspective, there is ongoing debate about whether there is any level of drinking by pregnant women that is ‘safe,’ ” says Kazue Hashimoto-Torii, Ph.D., principal investigator in the Center for Neuroscience Research at Children’s National and senior author of the paper published May 2 in Nature Communications. “We gave ethanol to pregnant preclinical models and found their offspring’s neural cells experienced widely differing responses to this environmental stress. It remains unclear which precise threshold of stress exposure represents the tipping point, transforming what should be a neuroprotective response into a damaging response. Even at lower levels of alcohol exposure, however, the risk for fetal neural cells is not zero,” Hashimoto-Torii adds.

The cerebral cortex — the thin outer layer of the cerebrum and cerebellum that enables the brain to process information — is particularly vulnerable to disturbances in the womb, the study authors write. To fend off insult, neural cells employ a number of self-preservation strategies, including launching the protective Hsf1-Heat shock protein (Hsp) signaling pathway that is used by a wide range of organisms, from single-cell microbes to humans. Developing fetuses activate Hsf1-Hsp signaling upon exposure to environmental stressors, some to no avail.

To help unravel the neurological mystery, the research sleuths used a method that allows a single molecule to fluoresce during stress exposure. They tapped specific environmental stressors, such as ethanol, hydrogen peroxide and methyl mercury — each of which are known to produce oxidative stress at defined concentrations. And, using an experimental model, they examined the Hsf1 activation pattern in the developing cerebral cortex by creating a marker, an encoding gene tagged with a type of fluorescent protein that makes it glow bright red.

“Our results suggest that heterogeneous events of abnormal brain development may occur probabilistically — which explains patterns of cortical malformations that vary with each individual, even when these individuals are exposed to similar levels of environmental stressors,” Hashimoto-Torii adds.

Among the more striking findings, neural cells with excessively high levels of Hsf1-Hsp activation due to ethanol exposure experience disruptions to normal development, with delayed migration by immature cortical neurons. For the fetal brain to develop normally, neurons need to migrate to precise places in the brain at just the right time to enable robust neural connections. When neurons fail to arrive at their destinations or get there too late, there can be gaps in the neural network, compromising efficient and effective communication across the brain’s various regions.

“Even a short period of Hsf1 overactivation during prenatal development causes critical neuronal migration deficiency. The severity of deficiency depends on the duration of Hsf1 overactivation,” she says. “Expression patterns vary, however, across various tissues. Stochastic response within individual cells may be largely responsible for variability seen within tissue and organs.”

The research team found one bright spot: Cortical neurons that stalled due to lack of the microtubule-associated molecule Dcx were able to regain their ability to migrate properly when the gene was replenished after birth. A reduction in Hsf1 activity after birth, however, did not show the same ability to trigger the “reset” button on neural development.

“The finding suggests that genes other than microtubule-associated genes may play pivotal roles in ensuring that migrating neurons reach their assigned destinations in the brain at the right time — despite the added challenge of excessive Hsf1 activation,” according to Hashimoto-Torii.

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Alcohol abuse even before pregnancy may harm offspring


ORLANDO–Mothers who binge drink before they become pregnant may be more likely to have children with high blood sugar and other changes in glucose function that increase their risk of developing diabetes as adults, according to a new study conducted in rats. The results will be presented Sunday at the Endocrine Society’s 99th annual meeting in Orlando, Fla.

“The effects of alcohol use during pregnancy on an unborn child are well known, including possible birth defects and learning and behavior problems. However, it is not known whether a mother’s alcohol use before conception also could have negative effects on her child’s health and disease susceptibility during adulthood,” said principal investigator Dipak Sarkar, Ph.D., DPhil, a distinguished professor at Rutgers University in New Brunswick, N.J., and director of its endocrine research program.

Binge drinking is common in the United States. Among alcohol users 18 to 44 years old, 15 percent of nonpregnant women and 1.4 percent of pregnant women report that they binge drank in the past month, according to a 2012 phone survey from the U.S. Centers for Disease Control and Prevention (CDC). For women, binge drinking is the equivalent of four or more drinks in about two hours.

To assess the effects of preconception alcohol use, Sarkar, with doctoral candidate Ali Al-Yasari, MS, and their colleagues, conducted a study, funded by the National Institutes of Health, in rats, whose basic processes of glucose function are similar to those in humans, Sarkar said. For four weeks, they gave female rats a diet containing 6.7 percent alcohol, which raised their blood alcohol levels to those of binge drinking in humans. Alcohol was then removed from the rats’ diet, and they were bred 3 weeks later, equal to several months in humans. Adult offspring of these rats were compared with control offspring: the offspring of rats that did not receive alcohol before conception. (One control group received regular rat chow and water, and the other received a nonalcoholic liquid diet equal in calories to the alcohol feedings.)

After the rats’ offspring reached adulthood, the researchers used standard laboratory techniques to monitor their levels of blood glucose and insulin and two other important hormones, glucagon and leptin. Glucagon stimulates the liver to convert glycogen (stored glucose) into glucose to move to the blood, making blood glucose levels higher. Although the main function of leptin is inhibiting appetite, it also reduces the glucose-stimulated insulin production by the pancreas.

The research team found that, compared with both groups of control offspring, the offspring of rats exposed to alcohol before conception had several signs of abnormal glucose homeostasis (function). Altered glucose homeostasis reportedly included increased blood glucose levels, decreased insulin levels in the blood and pancreatic tissue, reduced glucagon levels in the blood while being increased in pancreatic tissue, and raised blood levels of leptin.

Additionally, the researchers said they found evidence that preconception alcohol exposure increased the expression of some inflammatory markers in pancreatic tissue. Al-Yasari said this might lower insulin production and action on the liver that increases blood glucose levels. The overexpression of inflammatory markers may be how pre-pregnancy alcohol use altered normal glucose homeostasis in the offspring, he stated.

“These findings suggest that [the effects of] a mother’s alcohol misuse before conception may be passed on to her offspring,” Al-Yasari said. “These changes could have lifelong effects on the offspring’s glucose homeostasis and possibly increase their susceptibility to diabetes.”

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Do Women Really Stop Drinking When They Find Out They’re Pregnant?


Recommendations surrounding women’s health before, during, and after pregnancy haven’t always been straightforward or easy to digest. Prime example: Whether or not it’s safe to drink during pregnancy and how much? To take a closer look at what’s really going on, Katherine Hartmann, M.D., Ph.D., deputy director of the Institute for Medicine and Public Health at Vanderbilt University, went searching for answers—real numbers indicating whether women, specifically newly pregnant women, were actually pouring themselves that glass of red wine.

Hartmann’s research, which was published in the April 2017 issue of Obstetrics & Gynecology, comes after a public firestorm arose when the CDC issued a new recommendation that all women who are planning a pregnancy or not using reliable contraception should abstain from alcohol use entirely. That’s a pretty sweeping call-to-action, considering there are 61 million American women of reproductive age, and about 43 million are considered to be “potentially at risk of becoming pregnant,” according to the study. It’s also a slightly concerning suggestion, given that past research has found conflicting results as to whether it’s actually NBD if a woman has a drink every now and again early on in her pregnancy.

So Hartmann’s team analyzed pregnant women’s alcohol consumption overall, theorizing that “whether or not it was a planned pregnancy or an unintended one, as soon as people had a positive pregnancy test, they [would] quit,” she says. That way, rather than looking at whether or not alcohol is safe in the early conception window, they would find out what habits these pregnant women had in the first place.

Hartmann and her colleagues looked at more than 5,000 female participants enrolled in the Right From the Start program, a study of early pregnancy health conducted in eight different cities around the country. When the women involved found out they were pregnant, the results showed an incredible 90 percent stopped drinking alcohol entirely, while another 8 percent made some sort of reduction of their intake.
Their findings imply that access to inexpensive pregnancy tests—with encouragement to take the test shortly after a missed period—could actually be a stronger preventative strategy to limiting alcohol exposure to the fetus. Just be smart about your contraception methods, and if you’re not looking to get pregnant anytime soon, make sure you’re still practicing safe sex. (Here’s how to find the best birth control for you.)
As for how much women can or should drink during pregnancy, that’s Hartmann’s next area of study. The infographic that lays out Hartmann’s current findings.
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