Birds do it. Bees do it. Even butterflies and chimpanzees do it.

Chimpanzees Self-Medicate With FoodSRxA’s Word on Health was intrigued by a story we read this week in National Geographic.

It seems we could have a lot to learn from the abovementioned animals.  It turns out that they, and many other species self-medicate, using plants and other surprising materials to improve not only their own health but also the health of their offspring.

video of capuchin monkeys at the Edinburgh Zoo shows them rubbing onions and limes on their skin and into their fur as an antiseptic and insect repellent.

Biologists have noticed that parasite-infected female monarch butterflies are more likely to lay their eggs on anti-parasitic milkweed, giving their offspring instant medication, while uninfected females show no preference. And urban birds who incorporate cigarette butts into their nests may be doing so because chemical properties in the smoked cigarettes may repel parasites, according to a 2012 study.

cigarette birds nestsWhile cigarette-butt wallpaper may not appeal to most of us, other ways that animals self-medicate might be worth watching.

Mark Hunter, a University of Michigan ecologist who was involved in the monarch research, says there is plenty to be learned from observing the way animals use the entire outdoors like one big drugstore. It’s something our own species probably once did – and might do well to revisit with modern pharmaceutical engineering and computer modeling techniques.

It’s not the only way, but it seems to me that a sensible way would be to watch what animals do in nature to see how they exploit the natural products, the pharmaceuticals that are available to them in the environment, and try to learn from them,” he says.

Earlier this year, Hunter spent time with people of the Shangaan tribe in South Africa.

shangaan tribeIf you go for a walk with somebody, every plant you pass has a cultural or medicinal significance, and many of those have been learned from watching animals,” Hunter says. The bark of the black monkey thorn tree, for example, is used as a stomach medication, a choice based on watching how elephants behave.

Not long ago primates were thought to be the only animals smart enough to self-medicate. But now we’re learning that ground squirrels chew rattlesnake skins and then lick their fur, a trick likely to deter that particular predator.

Insects have been found to be prolific self-medicators, too. Take the arresting case of the fruit fly Drosophilia melanogasterwhich uses alcohol to protect itself against parasitic wasps. The wasps lay their eggs in the fruit fly larvae; the developing wasp grubs will eventually eat the flies from the inside out and burst forth from their dead bodies. Larvae that consume high doses of alcohol from fermented fruits, however, are less likely to be infected—and if they are, the invading wasp grubs die quite nastily with their internal organs being ejected out of their anus.

Moreover, fruit fly mothers who see female parasite wasps nearby will give their young instant protection by laying their eggs in alcohol-soaked environments – which means they see and remember their nemesis.

Not a bad defense,” says Hunter, adding that this demonstrates the idea that “the cost we’re willing to pay for a medicine depends on the consequences of not using it.” While the alcohol isn’t necessarily good for the flies, they will die if parasitized.

The alcohol has worse effects on the parasites than it does on them. So it’s worth laying your eggs in a high-alcohol environment if it will save your offspring,” he says.

Do animals learn to self-medicate, or is it pure instinct?

monarchWell, plenty of intelligent animals self-medicate, so it’s not always clear. But in the case of the monarch butterfly the mothers don’t hang around to see what happens to their babies, so there’s no learning involved. In this case, the only possibility is that it’s a genetically determined behavior or instinct.

So the next time you’re on your way to the drugstore and pass a monarch hovering around a milkweed, or a bird who seems to have taken up a smoking habit, consider that they might actually be running an errand, just like you!

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Bypassing Genetic Obesity Genes?

obesityFact. Obese mothers tend to have kids who themselves will become obese.

Fact. In 2012, 35.7% of US adults and 16.9% of US children age 2 to 19 were obese, according to the CDC

Fact. Half of all U.S. adults will be obese by 2030 unless they change their ways, according to the Robert Wood Johnson Foundation.

Fact. Obesity raises the risk of numerous diseases, from type 2 diabetes to endometrial cancer, chronic heart disease and stroke.

So we were extremely interested to learn of new research that suggests the unhealthy cycle could be broken by weight-loss surgery.  In a first-of-a-kind study, Canadian researchers tested children born to obese women prior to weight loss surgery and their siblings conceived afterward.

thin_fatThe surprising results?  Kids born after mom lost lots of weight were slimmer than their siblings. They also had fewer risk factors for developing diabetes or heart disease.

Even more intriguing, the researchers discovered that numerous genes linked to obesity-related health problems worked differently in the younger siblings than in their older brothers and sisters.

Although diet and exercise will play a huge role in how fit the younger siblings will continue to be, the findings suggest the children born to mothers who have undergone weight loss surgery might have an advantage.

The impact on the genes, you will see the impact for the rest of your life,” predicts lead researcher Dr. Marie-Claude Vohl of Laval University in Quebec City.

gastric bypassSo why would there be a difference? Clearly weight loss surgery doesn’t change a womans’ genes.  However, it seems as if either the surgery or more likely the subsequent weight loss can change how certain genes operate in her child’s body. The researchers suggest that factors inside the womb seem to affect the chemical  ‘dimmer switches’ that make the fetus’ genes speed up or slow down or switch on and off.

Dr. Susan Murphy of Duke University wasn’t involved in the research says it makes biological sense that the earliest nutritional environment could affect a developing metabolism, although she cautions that healthier family habits after mom’s surgery may play a role, too.

The research has implications far beyond the relatively few women who undergo gastric bypass surgery before having a baby. According to the American College of Obstetricians and Gynecologists, more than half of pregnant women are overweight or obese. Tackling obesity before or during pregnancy can provide a lasting benefit for both mother and baby.

It’s not just a matter of how much moms weigh when they conceive, gaining too much weight during pregnancy increases the child’s risk of eventually developing obesity and diabetes. Overweight mothers have higher levels of sugar and fat in the bloodstream, which in turn makes it to the womb.

How much weight loss is needed to have a healthy baby?

pregnant and obeseIn the study, researchers took blood samples from children born to 20 women before and after the complex gastric bypass surgery, who, on average, lost about 100 pounds. They compared differences in more than 5,600 genes between the younger and older siblings and found significant differences in the activity of certain genes clustered in pathways known to affect blood sugar metabolism and heart disease risk.

Only time will tell if the children born after mom’s surgery really get lasting benefits. Meanwhile, specialists urge women planning a pregnancy to talk with their doctors about their weight ahead of time. Besides having potential long-term consequences, extra pounds can lead to a variety of immediate complications such as an increased risk of premature birth and cesarean sections.

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Does Belly Fat cause tumors to go Belly Up?

belly_fat6People store fat in two ways – one you can see and one you can’t. The fat you can see is just under the skin in the thighs, hips, buttocks, and abdomen. That’s called subcutaneous fat. The fat you can’t see is deeper inside, around the vital organs – heart, lungs, digestive tract, liver as well as in the chest, abdomen, and pelvis. That’s called visceral fat.

Many people are self-conscious about the fat they can see. But actually, it’s the hidden visceral fat that may be a bigger problem, even for thin people.  Having too much of it is linked to a greater chance of developing high blood pressure, type 2 diabetes, heart disease, dementia, and certain cancers.

According to a new study published in the journal Cancer Prevention Research, visceral fat is directly linked to an increased risk for colon cancer.

There has been some skepticism as to whether obesity per se is a bona fide cancer risk factor, rather than the habits that fuel it, including a poor diet and a sedentary lifestyle,” said Derek M. Huffman, Ph.D., postdoctoral fellow at the Institute for Aging Research at the Albert Einstein College of Medicine in Bronx, N.Y. “Although those other lifestyle choices play a role, this study unequivocally demonstrates that visceral adiposity is causally linked to intestinal cancer.

Prior research has shown that obesity markedly increases the likelihood of being diagnosed with, and dying from, many cancers. In this animal study, Huffman and his colleagues wanted to see if removing visceral fat in mice genetically prone to developing colon cancer might prevent or lessen the development of these tumors.

To do this they randomly assigned the mice to one of three groups. Mice in the first group underwent a sham surgery and were allowed to eat an unrestricted “buffet style” diet, which resulted in them becoming obese. Those in the second group were also provided an unrestricted diet and became obese, but they had their visceral fat surgically removed at the outset of the study. Mice in the third group underwent a sham surgery, but were then put on a calorie restricted diet causing them to lose visceral fat.

obese mouseOur sham-operated obese mice had the most visceral fat, developed the greatest number of intestinal tumors, and had the worst overall survival,” Huffman said. “However, mice that had less visceral fat, either by surgical removal or a calorie-restricted diet, had a reduction in the number of intestinal tumors. This was particularly remarkable in the case of our group where visceral fat was surgically removed, because these mice were still obese, they just had very little abdominal fat.”

The researchers then subdivided the groups by gender. In female mice, the removal of visceral fat was significantly related to a reduction in intestinal tumors, but calorie restriction was not. In male mice, calorie restriction had a significant effect on intestinal tumors, but removal of visceral fat did not.

abdominalobesityThese finding suggest what most women have known for years i.e., that there are important gender differences when it comes to weight. But it also provided an explanation for how belly fat, diet and cancer risk are linked.  In addition, the study emphasizes the need to promote strategies that reduce abdominal fat in obese individuals.

So how can you get rid of this dangerous deep belly fat?  According to experts, there are four: exercise, diet, sleep, and stress management.

Exercise: Vigorous exercise trims fat, including visceral fat. It can also slow down the build-up of visceral fat that tends to happen over the years. But forget spot-reducing. There aren’t any moves you can do that specifically target visceral fat. Half an hour of vigorous aerobic exercise, done four times a week is ideal.  Jog, if you’re already fit, or walk briskly at an incline on a treadmill if you’re not yet ready for jogging. Vigorous workouts on stationary bikes and elliptical or rowing machines are also effective.

Diet: There is no magic diet for belly fat. But when you lose weight on any diet, belly fat usually goes first.  A fiber-rich diet may help. Research shows that people who eat 10 grams of soluble fiber per day, without any other diet changes, build up less visceral fat over time than others. That’s as easy as eating two small apples or a cup of green slimpeas.

Sleep: Getting the right amount of shut eye helps. In one study, people who got six to seven hours of sleep per night gained less visceral fat over 5 years compared to those who slept five or fewer hours per night or eight or more hours per night.

Stress: It’s unavoidable, but what you do with your stress matters. When you’re stressed you  tend not to make the best food choices when they’re stressed. Getting social support from friends and family, meditating, and exercising can all help to tame stress.

Short on time? If you could only afford the time to do one of these things, exercise probably has the most immediate benefits, because it tackles both obesity and stress.

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The King Provides Clues to Human Emotion

Last year, while waiting to catch a plane from Washington DC to San Antonio TX, I was joined by a young gentleman, around 24 or 25 years of age and his super-glamorous mom. Initially I was somewhat surprised that they had chosen to sit right next to me, given that the departure area was otherwise empty.

Within seconds he had struck up a conversation, within minutes I was practically his new BFF and before the flight was called he was holding my hand, whispering in my ear and grinning like a teenager.

Before you start thinking “wedding bells” or “cougar time”, what I learned from his mom, was that he had Williams syndrome. What I learned later, after googling the condition, was that people with Williams syndrome have an unusually gregarious personality. They view everyone as their friend, and it’s not unusual for them to rush up to total strangers and strike up conversations as though they are old acquaintances.

Those with the disorder look at the world through a unique lens. Despite their desire to befriend people they have high levels of generalized anxiety poor social judgment, disturbed peer relationships and altered responses to fearful and happy faces.  Their average IQ is 60, they experience severe spatial-visual problems, and suffer from cardiovascular and other health issues. They also have an affinity for music.

This week, I learned that the latter trait is helping scientists shed light on the mystery of emotion and human interaction. Social and emotional responses are so fundamental to human behavior that they are often taken for granted. However, the genetic and neurobiological bases of social behavior are largely unknown, as are the mechanisms for disruptions in social behavior and emotional regulation that appear throughout the lifespan as features of mental illnesses.

In a study led by Julie R. Korenberg, Ph.D., M.D. one of the world’s leading experts in genetics, brain, and behavior of Williams syndrome, people with and without Williams syndrome listened to music while researchers  gauged emotional response by measuring the release of oxytocin and arginine vasopressin – two hormones associated with emotion.

The study, published in PLoS One, signals a paradigm shift both for understanding human emotional and behavioral systems and expediting the treatments of illnesses such as Williams syndrome, post-traumatic stress disorder, anxiety, and possibly even autism.

The study is also the first to reveal new genes that control emotional responses and to show that arginine vasopressin is involved in the response to music.

The trial involved  21 participants – 13 with Williams syndrome and a control group of 8 without the disorder. Before the music was played, participants’ blood was drawn to determine a baseline level for oxytocin. Those with Williams syndrome had three times as much of the hormone as those without the syndrome.

Blood also was drawn at regular intervals while the music played and was analyzed afterward to check for real-time changes.

While other studies have examined how oxytocin affects emotion when artificially introduced into people through nasal sprays, this is the one of the first significant studies to measure naturally occurring changes in oxytocin levels in rapid, real-time as people undergo an emotional response.

Researchers asked the first participant to listen to the 1950’s Elvis Presley classic, “Love Me Tender.” The woman showed no outward response to the song. So, to elicit a greater response from the remaining study participants, the researchers invited them to bring along their favorite music.  Many of them chose heavy metal, but again, there was little outward response to the music.

However, when the blood samples were analyzed, they showed that oxytocin levels, and to a lesser degree arginine vasopressin (AVP), had not only increased but begun to bounce among the William syndrome group. In contrast, both oxytocin and AVP levels remained largely unchanged as those without Williams syndrome listened to music.

Interestingly, the oxytocin level in the woman who’d listened to “Love Me Tender” skyrocketed compared to the levels of participants who listened to different music.

Korenberg believes the blood analyses strongly indicate that oxytocin and AVP are not regulated correctly in people with Williams syndrome, and that the behavioral characteristics unique to people with the condition are related to this problem.

To ensure accuracy of results, study participants were also asked to place their hands in 60° Fahrenheit water to test for negative stress. The same results were produced as when they listened to music. Those with Williams syndrome experienced an increase in oxytocin and AVP, while those without the syndrome did not.

In addition, study participants took three standard social behavior tests that evaluated willingness to approach and speak to strangers, emotional states, and various areas of adaptive and problem behavior. Those test results suggest that increased levels of oxytocin are linked to both increased desire to seek social interaction and decreased ability to process social cues.

The association between abnormal levels of oxytocin and AVP and altered social behaviors found in people with Williams Syndrome points to surprising, entirely unsuspected deleted genes involved in regulation of these hormones and human sociability,” Korenberg said. “It also suggests that the simple characterization of oxytocin as ‘the love hormone’ may be an overreach. The data paint a far more complicated picture.”

However, the results of the study offer great hope. By regulating levels of oxytocin and vasopressin it should be possible to relieve suffering and improve the lives of those with Williams syndrome.

In the meantime, this study certainly brings new meaning to the phrase “mood music.”

T-A T-A to A-T?

SRxA’s Word on Health is delighted to share news that could change the lives of the 500 or so children and families in the US, dealing with a rare and deadly disease.  The breakthrough, announced this week in the online edition of Nature Medicine, suggests that scientists may have found a way to prevent and possibly reverse the most debilitating symptoms of ataxia telangiectasia (A-T) a rare, progressive childhood degenerative disease that leaves children, unable to walk, and in a wheelchair before they reach adolescence.

As regular readers of this blog know, A-T is a cause close to our hearts, and the courage of these children and their families inspire us daily.

Karl Herrup, chair of the Department of Cell Biology and Neuroscience and his colleagues at Rutgers have discovered why this genetic disease attacks certain parts of the brain, including those that control movement coordination, equilibrium, muscle tone and speech.

When the team examined the brain tissue of young adults who died from A-T, they found a protein (HDAC4) in the nucleus of the nerve cell instead of in the cytoplasm where it belongs. When HDAC4 is in the cytoplasm it helps to prevent nerve cell degeneration; however, when it gets into the nucleus it attacks histones – the small proteins that coat and protect the DNA.

What we found is a double-edged sword,” said Herrup. “While the HDAC4 protein protected a neuron’s function when it was in the cytoplasm, it was lethal in the nucleus.”

To prove this point, Rutgers’ scientists analyzed mice, genetically engineered with the defective protein found in children with A-T, as well as wild mice. The animals were tested on a rotating rod to measure their motor coordination. While the normal mice were able to stay on the rod without any problems for five to six minutes, the mutant mice fell off within 15 to 20 seconds.

However, after being treated with trichostation A (TSA), a chemical compound that inhibits the ability of HDAC4 to modify proteins, they found that the mutant mice were able to stay on the rotating rod without falling off – almost as long as the normal mice.

Although the behavioral symptoms and brain cell loss in the engineered mice are not as severe as in humans, all of the biochemical signs of cell stress were reversed and the motor skills improved dramatically in the mice treated with TSA. This outcome proves that brain cell function could be restored.

Neurological degeneration is not the only life-threatening effect associated with A-T. The disease, which occurs in an estimated 1 in 40,000 births, causes the immune system to break down and leaves children extremely susceptible to cancers such as leukemia or lymphoma. There is no known cure and most die in their teens or early 20s.

Herrup says although this discovery does not address all of the related medical conditions associated with the disease, saving existing brain cells and restoring life-altering neurological functions would make a tremendous improvement in the lives of these children.

 “We can never replace cells that are lost,” said Herrup. “But what these mouse studies indicate is that we can take the cells that remain in the brains of these children and make them work better. This could improve the quality of life for these kids by unimaginable amounts.”

A-T families are cautiously excited by the news. The A-T Children’s Project facebook page notes “This is certainly hopeful news, and we look forward to the results from further studies.”

We certainly do. A cure cannot come soon enough.

Be Still My Beating Heart! – Monty Python and the Holy Grail

Look up the term myocardial infarction (MI) in any medical dictionary and the definition will be something along the lines of –  the changes to the myocardium (heart muscle) that occur due to the sudden deprivation of circulating blood. The main change being necrosis, or death of myocardial tissue. Death of myocardial tissue.  As in dead, as in non-viable, as in beyond repair. Kind of reminds me of the infamous Monty Python Dead Parrot sketch… “Passed on! No more! Ceased to be! Expired and gone to meet ‘is maker!”….but I digress.

Fast forward from the British humor of December 1969 to an astonishing paper presented in Britain in April 2012  at the Frontiers in CardioVascular Biology meeting. In a keynote lecture, Dr Deepak Srivastava outlined results that have been described as a “game changer” with the potential to revolutionize the treatment of MI.   Srivastava used viral vectors to deliver genes directly into the hearts of adult mice that had experienced an MI. In his original “proof of principle” study, Srivastava was able to show that all that was needed for the direct  reprogramming of fibroblasts (a major component of scar tissue) into myocytes (the heart muscle cells responsible for  beating)  was the delivery of three genes.  The work , which took place in a Petri dish, was considered groundbreaking since it showed for the first time that unrelated adult cells could be reprogrammed from one cell type to another without having to go all the way back to a stem cell state. “Our ultimate hope is that, during the acute period following MI, patients will be able to receive direct injections of factors that transform the existing fibroblast cells in the “scar” into new myocytes. The resulting increase in muscle mass should help MI survivors to live more normal lives,” explained Srivastava.

Healthy heart tissue is composed of a mixture of several kinds of cells, including cardiomyocytes, which provide beating muscle and cardiac fibroblasts that provide architectural support to the myocytes. “When heart muscle cells become injured and die following an MI, patients have the major problem that these cells have little or no capacity for regeneration,” says Srivastava.  Part of the process of remodelling that occurs following the injury is that fibroblast cells migrate to the site and create the scar. At first, the process can be considered beneficial since without fibroblasts adding structural support damaged hearts would rupture. But later, difficulties arise when the fibrotic scar doesn’t contract like the muscle it has replaced. “Reduced global contractility means the heart has to work much harder, and the extra stress can ultimately lead to heart failure and even death,” said Srivastava.

One of the Holy Grails of cardiovascular research has been to replace these lost myocytes and return functionality to the heart.  Some of the first approaches to be investigated were the introduction of stem or progenitor cells to the sites of injury.  But many hurdles have been encountered including getting cells to integrate with neighboring cells in the heart, and there have been concerns that residual “rogue” cells could persist with the potential to keep dividing and give rise to tumors.

Srivastava, a pediatric cardiologist, explained how he got ahead of the game by “leveraging” knowledge from his work in embryo hearts. Over the past 15 years the focus of Srivastava’s lab has been to identify genetic factors responsible for the formation of embryonic hearts. From this work, his team identified 14 key genes that they felt were the major “on/off” switches for cardiac genetic programming. In this original study they were able to whittle things down to the three factors that were indispensible. The team then injected fibroblasts that had the three genes inserted directly into the scar tissue of mice.  They were able to show the fibroblasts differentiated into cardiomyocyte-like cells. In the latest study  they were able to take the process one step further by injecting a viral vector encoding the  3 genes directly into the scar tissue of mice who had just experienced an MI. “With these studies we’ve obtained even better results showing that the fibroblasts become more like cardiomyocytes and functionally couple with their neighbors. They could beat in synchrony and improve the function of the heart,” said Srivastava.

The next step will be to test the direct injection approach in a larger animal, such as a pig, whose heart is similar in size to a human.  But a big question remains “will the same combination of genes work in human hearts?” SRxA’s Word on Health will be watching and waiting. In the meantime…it’s back to Monty Python!

Finding the Perfect Genes?

Despite a plethora of the “Men Are From Mars…” type of self-help books, many people still think that the differences between men and women are unfathomable. Others think of the differences in terms of broad stereotypes, i.e. women are more nurturing and men are more aggressive.

So it was with great interest that we read some new research that could drastically alter the way we think about what drives us to be who we are.  It turns out that male or female behaviors are regulated by very specific genes that can be turned on and off at will.

The research, which was conducted by scientists at the University of California, San Francisco, aimed to locate those genes that are influenced by the sex hormones- testosterone and estrogen– and that dictate male and female behaviors.

The research team, led by Dr. Nirao Shah, managed to locate 16 genes that were expressed differently in male and female mice and showed that the different expressions were regulated by the sex hormones. They found that they could isolate parts of classic male and female behaviors and pinpoint them as being governed by their own particular genes. They also noticed that each gene regulates a few components of a behavior without affecting other aspects of male and female behavior.

In other words, by flipping the switch, they could turn off a mouse’s sex drive, willingness to spend time with their young, and even their desire to pick fights while leaving every other behavioral element unaffected.

Imagine how crazy it would be if we could do that in humans.

Don’t like that your boyfriend gets into fights or that your girlfriend has “yet another headache?”  Simple…just flip the switch!

Fortunately, there are more serious applications of this research. Understanding the genes that drive male and female behavior could, for example, guide researchers to locate which genes are involved in diseases such as autism, which affects four times as many males as it does females.

As good as all that sounds, there is something a bit unnerving about contemplating your genes as a collection of switches that govern your behaviors. On some level it would be a dream to be able to turn behaviors off and on at will. While it would revolutionize the way we interact, it could also change our conception of what makes us who we are. Fortunately, manipulating them is a complicated process. So it looks like we’ll have to wait a while before we start popping pills to fine tune ourselves.

That’s a relief, because for most of us, managing the hormones we already have is a big enough job!

A Healthy Holiday Dinner Table?

Before you click away, this is NOT one of those stories admonishing you to eat broccoli and brussel sprouts rather than turkey and all the trimmings.  This blog could improve your health without having to forego a single calorie!

Will Grandma be coming up from Florida during Thanksgiving or will Great Uncle Tony be joining you for Christmas?  Do you need something other than the Presidential candidates, Penn State sex scandal, or football scores to talk about over dinner?

Well, according to University of Alabama genetics experts you should use this opportunity to learn more about your family health history from the very people who know.

The holidays are a great time to collect your family history,” says Lynn Holt, M.S., Director of the School of Health Professions Genetic Counseling program. “Most people don’t know much about the family history beyond their first-degree relatives, their own parents and siblings.”

She advises people to talk to their grandparents or great-grandparents about any health problems that they may have had.  Also find out about their immediate family such as  parents, siblings and children. And don’t just talk, jot down names and their year of birth and death. Ask if any siblings died during childhood and if so, why? While many people don’t like to talk about a sibling who died young, knowing if it happened – and why, can produce very valuable information.

We sometimes hear people say they’ve been told their mother’s brother dropped dead at age 20, for example,” says Holt. “Was it because of a genetic heart condition that you might have inherited, or is it simply that brother was guilty of some accident that nobody wants to talk about?

Likewise, if there is cancer in the family, ask about the kind of cancer and at the age at which family members first were diagnosed. Age of diagnosis is more medically valuable than age of death in determining inheritable conditions. Ask similar questions about heart disease, diabetes, mental health conditions and other common conditions. And don’t forget to look into any environmental exposures that may explain family health problems such as occupational exposures, smoking or pollution.

Not only will you learn a great deal, the knowledge you gain can help you protect your own health.  As an added bonus, older family members may welcome the chance to share their story and memories of loved ones who have passed away…and it’s a chance to grow closer as a family.

So rather than bickering over the green beans or sulking into the sweet potatoes, how about serving up a dose of health history these holidays?

After you’ve collect all this information, share it with your physician to help determine if there are any health conditions, based on your family history, that need further evaluation or monitoring.

Happy Holidays!