Risk factor

A Surprising Risk Factor of Coronary Heart Disease

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And no, it’s not smoking or high blood pressure

  • How many times have we heard the “smoking, drinking, and being overweight” warning in relation to heart disease? Yet, one of the longest-running studies contradicts this.
  • A much bigger risk factor is stress—particularly the kind of stress found in a specific personality type that processes anger in a particular way.
  • The Framingham project is the quintessential epidemiological population study, of more than 14,000 people across three generations. And a key piece of lifestyle advice is hidden in the 1980 analysis of the final cohort.
  • Do you feel guilty if you use free time to relax? Ask yourself these “Type A” identifier questions, and check whether you also process stress in these same ways—this stress management protocol is a key driver of coronary heart disease.
  • Physically, anger leads to catecholamine release, which has a host of cardiovascular repercussions. In “fight mode,” the liver synthesizes triglycerides in a boost of energy, which in turn contributes to lipid disorders.
  • If this is you, there’s still no need to be fatalistic. These are behavior patterns that we can train and change, and changes start small. Rome wasn’t built in a day.

According to the National Center for Health Statistics, heart disease is the leading cause of death in the United States. One in five American deaths were due to heart disease in 2020, as reported by the Centers for Disease Control and Prevention (CDC). Worldwide, cardiovascular disease is also the leading cause of death year after year.

Coronary heart disease (CHD) is the most common type of heart disease, killing nearly 383,000 Americans in 2020. Scientists and the medical community are investing much time and money into the study of what keeps the heart healthy and what can stop it from beating.

Many risk factors have been suggested for CHD. Among these, high blood pressure, high blood cholesterol, and smoking have been assumed to be leading causes. Doctors wear themselves out by repeating the same warnings that CHD could be much reduced if people would reduce their bad cholesterol levels by eating healthy food and becoming active. People need to quit dangerous habits that further raise blood pressure such as the three best-known ones: smoking, being overweight, and drinking too much alcohol.

Stress on the heart is terribly bad for you, but it rarely makes the headlines. We all know stress remains unhealthy for both our body and mind, but do we listen? More importantly, do we take action to prevent stress from causing disease in our bodies?

Despite decades of studies, we like to point fingers at the usual subjects. Smoking has the worst reputation of all. How many times have you tried to convince a loved one that smoking may take their life one day? They tell you they do it to calm their nerves, right? You beg them to take a walk instead; you suggest exercise classes and fishing at the lake. You may have printed out studies to show them what those commercially-made cigarettes and nightly booze binges will do to them. Maybe you are helping them avoid the dreaded black lungs we’ve seen in health class photos.

Yet, hold on. We’re talking about heart disease here.

Smoking is bad for your health, and often times fatal in terms of lung disease. But one of the longest running studies on heart disease contradicts what we all assumed about smoking and CHD. In the study, smokers developed fewer cases of CHD than non-smokers.

A much bigger risk factor is not smoking, but stress—the kind of stress found in a particular personality type—and when left unchecked, the manifestation of it can be worse on the heart than smoking.

According to Dr. Yuhong Dong, medical doctor and Ph.D. in infectious diseases, there are many biological and energetic mechanisms occurring concurrently in CHD, but the Type A personality’s unhealthy expression of anger is what makes a larger imprint on our hearts and minds.

A Surprising Risk Factor of Coronary Heart Diseases (CHD)

A counterintuitive twist on smoking’s effect on CHD brings to mind the story of Batuli Lamichhane, one of the oldest women in the world, who told news reporters on her 112th birthday that the secret to a long life is smoking, as she had puffed away on 30 cigarettes a day since she was 17 years old. If her story was just an isolated story that would be one thing, but it’s not. There are stories about many of the oldest people in the world who smoke, drink, and eat to their hearts’ content.

The Framingham project, which began in 1948, is the quintessential epidemiological and largest population study of more than 14,000 people across three generations. The project ultimately found evidence that formed the textbook warning we hear at doctor visits: high blood pressure and high blood cholesterol are major risk factors for CHD. However, we have learned something else from the well-known Framingham Heart Study.

The key lifestyle advice is hidden in the 1980s analysis of the final cohort.

When researchers looked at the long-term patterns in the cardiovascular health of more than 5,000 male and female smokers and non-smokers, consisting of 2,282 men and 2,845 women aged 29 through 62 years (and free from CHD at the initial examination), they found little evidence that smoking is a risk factor for coronary heart disease (CHD).

“In these monumental studies and analysis, smokers and non-smokers showed no differences at all,” said Dr. Dong. “CHD is the product of many risk factors acting synergistically. There is no doubt that smoking is one of many risk factors, but its effects, acting by itself, have been exaggerated.”

Dong said there may be even more to the Framingham Study. Evidence now shows that psychosocial factors, including having a stressed-wired personality, or Type A personality, are more predictive for heart disease than smoking. Even more predictive of CHD is how the Type A personality copes with stress. If Type A’s constantly cope with stress in angry, aggressive, and hostile ways, their odds for getting CHD increase exponentially.

Do You Have Traits of a Type A personality?

Do you feel guilty if you use free time to relax? Do you need to win in order to enjoy games and sports? Do you eat, walk, and move rapidly? Do you try to do more than one thing at a time? Have your loved ones and co-workers told you more than a few times that you need to calm down, mellow out, or take it easy?

You may be a “Type A” personality, or have a Type A behavior pattern (TABP). As much as you get things done and people can count on you to work hard, your health might suffer if you take your high achievement, competitiveness, and impatience too far. Some people can take on multiple projects and carry the weight of the world with grace, but most Type A’s do not.

Whichever questionnaire or survey you take to determine your personality type, your most prominent type is based on a model. Many of us have taken the Myers-Briggs personality test and learned we may be one of 16 personality types composed of four major components. Yet, wait a minute. In most situations, we are a combination of personality archetypes, shifting with age and circumstance. Sometimes we are both Carrie and Miranda. Sometimes we are a little Charlotte.

Since the first years of civilization, philosophers, psychologists, and social scientists have been trying to understand the human psyche and organize people into neat, little piles. The idea is that if we can figure out what makes them act the way they do, we can create a treatment to help them achieve a happy, healthy life.

The first known physicians to make the connection between personalities and illness were the Roman revivalists who warned us of the downside of choleric, sanguine, phlegmatic, and melancholy personality types known at the “Four Temperaments of Personality.”

These four qualities based on Greek theory and elements of earth, air, fire, and water are still used in modern theory to describe disease tendencies. As you may have guessed, the fiery, energetic, and passionate “choleric” personalities are known as today’s Type A’s—with the unfortunate designation: Most likely to develop heart disease.

But descriptions have become more nuanced as the social sciences have developed. A 2018 study from Northwestern University has determined four redefined personality types: “average,” “reserved,” “self-centered,” and “role-model.” From the sound of those names, the Type A could be hiding in any one of the new personality types.

Northwestern’s revamped types are based on five widely-accepted character traits, including neuroticism—a way of being that typically involves negative emotions such as anger. This is the piece of the puzzle cardiologists pay attention to as their predecessors have warned us that how one deals with diversity determines heart health.

What Puts Type A Personalities Further at Risk for Heart Disease?

For more than 100 years, clinical observation of CHD patients has linked this disease with certain personality traits of Type As: impatience, hyper-alertness, aggressiveness, and proneness to anger.

Two American cardiologists, Meyer Friedman and Ray Rosenman, began revisiting the link between behavior patterns and heart disease in the 1950s, pioneering the definition of the Type A personality and its link to heart disease.

The impetus of their work is quite a story. According to a fascinating piece in Scientific American, the cardiologists came upon the heart/stress connection by accident, when their office room upholsterer realized their patients were wearing out the waiting room chairs.

Looking further into the situation, the doctors realized their cardiac patients were impatient with waiting. Because they were Type As, they were unable to sit in their chairs like patient and relaxed Type Bs, and even wore out the arms of the chairs by sitting on the edge of their seats and leaping up too often.

So the two cardiologists began studying their hypothesis that Type A personalities not only wear out chairs, but also wear out their hearts.

In 1976, the cardiologists performed the Western Collaborative Group Study, a longitudinal study of stressed-out behavior and came up with the “Type A” personality definition. They officially characterized the Type A personality as individuals who are highly competitive, ambitious, work-driven, time-conscious, and aggressive. Studies conducted over the next 50 years have found Type A personalities run a higher risk of heart disease and high blood pressure than mellow Type Bs.

Studies carried out on women have not shown such a substantial difference between Type A and Type B and subsequent health, some psychologists say, which may suggest that different stress coping strategies are just as important as personality.

Friedman and Rosenman found evidence  in the early 80s that white, middle-class men with Type A personality are most at risk for CHD.

“It wasn’t till the 1980s that there was enough data for people to say type A is for real,” said Robert Sapolsky, a neurobiologist and primatologist at Stanford University, in an interview with Scientific American. “It is a bigger risk factor for cardiovascular disease than if you smoke, than if you are overweight, than if you have elevated cholesterol levels.”

The Framingham studies supported Friedman and Rosenman’s theories on the key risk group. One study found that specific Type A behaviors such as work overload, suppressed hostility, and frequent job promotions put these men at increased risk of developing CHD, especially in the 55–64 year-old age group.

Among men aged 45–64 years, Type A behavior was associated with a twofold risk of severe chest pain, myocardial infarction, and CHD in general, compared to Type B behavior.

Interestingly, the association was found only among white-collar workers and was also independent of the standard coronary risk factors and other psychosocial scales. This prospective study suggests that Type A behavior and suppressed hostility may be involved in the pathogenesis of CHD in both men and women.

In a multivariate analysis, Type A behavior and suppressing anger were independent predictors of CHD incidence. The Framingham Study found a correlation between Type A women (aged 45–64 years) who developed CHD, and men.

The women were surveyed as having the same coping mechanism of dealing with stressful situations by suppressing hostile emotions. Thousands of Type A respondents said in a survey that they would suppress their feelings of tension and anxiety and would not show or discuss anger.

The study concluded that Type A women developed twice as much CHD and three times as much severe chest pain as Type B women.

What Is Happening in the Body When Hostility and Anger Manifest Illness?

According to the National Institutes of Health, anger can lead to excess catecholamine release and subsequent increased cardiovascular reactivity leading to acute sinus tachycardia, hypertension, decreased coronary perfusion, and cardiac instability.

When a person is in a mental state of anger or hostility or “fighting” mode, their sympathetic nerves are often in a state of excitement which results in a faster heart rate, increased myocardial oxygen consumption, increased cardiac output, higher blood pressure, and higher blood glucose. The liver tends to synthesize triglycerides to supply more energy, which in turn contributes to lipid disorders.

We see how anger and hostility manifest in the body, but now we also have scientific evidence that our cells remember each offense. Studies of the heart have shown it to be the greatest organ for cellular memory.

For instance, cellular memory has been demonstrated in the accounts of heart transplant recipients who retain donor personality traits. Evidence has shown that personality preferences can be transferred to another person with the transplanted organ. Through the work of cell memory study, we learn memory is retained beyond the brain and nerve cells.

Current theories describe six possible mechanisms by which memories can be stored: epigenetic, DNA, RNA, protein, energetic, and what some doctors call the “heart brain.” The heart holds onto emotions, whether negative or positive.

“When we respond to stimuli in a negative way, our personal reactions are stored in our bodies, cells, and organs,” Dong said. “When a similar situation happens again, our cells will respond in a similar way. Repeating such reaction modes over and over will form long-term memories in our cells and body. This means having a negative personality can actually harm our health.”

“The mechanisms of cellular memory are one of the most fascinating fields in science,” she continued, “and there’s so much more to explore. But if we want to eradicate the root cause of diseases like CHD, essentially, we have to treat the ‘illed’ personality, which is really, the materialized spirit.”

How to Treat the Harmful Side of Type A Personality Patterns

A 1991 paper published in the European Journal of Personality by Hans Eysenck, Ph.D., of the University of London examined the Type A personality type risk further.

Eysenck’s analysis of the data indicating anger, aggression, and hostility connecting to CHD physical risk factors made him hopeful for psychological intervention.

He wrote, “No doubt the process is very complex, and may involve many bodily-disease mechanisms. No more is claimed than a beginning to a lengthy, but exciting and worthwhile process of discovery.

In one of Eysenck’s early books, he quotes the sacred texts in the Mahabharata that describe the concept of mind/body illness:

“There are two classes of disease—bodily and mental. Each arises from the other. Neither is perceived to exist without the other. Mental disorders arise from physical ones, and likewise physical disorders arise from mental ones.”

“We now have countless scientific studies in psychology, neurology, and endocrinology that link ‘mind’ and ‘body,’” said Dong. “We are connected with each other, and in fact, interacting with each other on multiple levels.” She added, “One of my previous pharma colleagues, who is a senior microbiologist, shared with me his notion that the human mind and body are one and the same. He told me he recovered from his pain in his leg by using only psychological therapy. In other words, he cured his body by treating his mind. When you treat the mind, you treat the body at the same time.”

Most people know there are proven methods to treat prolonged stress. To find the right method, think about what calms you down. If you don’t like yoga or meditation, there is fishing or reading. There’s something to calm almost any Type A from any cultural background or with any individual interest. The question is, will they see the importance of change to save their lives?

Many Type A people feel they can’t help their hard-wired personalities even though medical and psychological studies show they can develop coping strategies and anger management skills.

“There are pharmaceutical drugs that can help with high blood pressure, and supplements and lifestyle adjustments that can help, but also changing the way you react to situations seems to be essential,” said Dong. “You can go to therapy to learn healthy coping mechanisms to deal with stressful situations, but there are also quite a few things you can do on your own.”

Dong listed three studied ways to help reduce stress for Type A’s who have crossed the line into angry and hostile behaviors.

1) Be more appreciative.

“If we change our views of others, we can be less competitive, but more grateful,” she said.

“Gratitude is good medicine,” said Robert Emmons, Ph.D., a professor of psychology at the University of California Davis and author of The Little Book of Gratitude in an article on heart.org. “Clinical trials indicate that the practice of gratitude can have dramatic and lasting effects on a person’s life. It can lower blood pressure and improve immune function.”

2) Change your environment.

Dong said, “Type As are all about being in control. Try being passive for a day. If you are triggered to anger, move your focus away from the negative emotion by taking a walk in a beautiful place. Listen to traditional music.”

According to a recent Simply Psychology article by Saul McLeod, Ph.D., dealing with stress may not be Type As’ forte because they seem to be in a constant struggle against the clock.

McLeod wrote, “Often, they quickly become impatient with delays and unproductive time, schedule commitments too tightly, and try to do more than one thing at a time, such as reading while eating or watching television.”

Among several techniques the American Psychological Association (APA) suggests in an article titled “How to control anger before it controls you,” one of the key strategies people can teach themselves is to change their environment when they’re angry by giving themselves a break, including scheduling some “personal time” for times of the day that can be particularly stressful. Change your environment. Take breaks.

“Sometimes it’s our immediate surroundings that give us cause for irritation and fury,” the APA wrote. “Problems and responsibilities can weigh on you and make you feel angry at the ‘trap’ you seem to have fallen into and all the people and things that form that trap.”

3) Participate in mindfulness meditation.

In a review published in Springer Science, researchers examined studies on the effects of mindfulness meditation. They found when people participated in meditation and relaxation techniques, they began to react and cope with stress much better and reported increased mindfulness and psychological well-being.

Dong said most people already know that meditation helps with stress and anger, but few people use it to prevent heart disease. “They can learn to handle stressful situations,” she said. “When you distance yourself from your negative emotions, you can return to a balanced emotional state more quickly than letting anger and hostility take control of you. And I truly believe your heart will thank you for it.”

Can people change those parts of themselves that harass them, that may wreak havoc on their hearts? The latest science says, “yes.”

In the words of the Roman philosopher Lucius Seneca: “If you really want to escape the things that harass you, what you’re needing is not to be in a different place, but to be a different person.”

Perhaps your heart is worth it.

How Early Should Obesity Prevention Start?

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Obesity has pervaded the United States and is spreading throughout the world. Following in its wake is type 2 diabetes, which will affect at least half a billion people worldwide by 2030. A majority of U.S. women of childbearing age are overweight or obese (as defined by a body-mass index [BMI, the weight in kilograms divided by the square of the height in meters] >25). These women are likely to gain excessive weight when they’re pregnant, making it harder for them to return to their prepregnancy weight after delivery. Postpartum weight retention not only portends increased lifelong risks for obesity-related complications but also an increased BMI at the inception of future pregnancies. During pregnancy, excessive weight gain, along with other risk factors such as gestational diabetes, can alter fetal growth and metabolism, leading to higher adiposity in the offspring. If the child is female, grows up obese, and becomes pregnant, the cycle begins again. It is time to interrupt this vicious cycle to prevent obesity and chronic diseases in mothers and children.

Once obesity is present, it is challenging to treat because of multiple physiological, behavioral, and cultural feedback loops. The good news is that the prenatal period and the first postnatal year hold critical clues that may lead to interventions to reduce obesity in women and prevent it in children. In a range of animal models (from rodents to nonhuman primates), dietary, hormonal, mechanical, and other perturbations that occur prenatally and during infancy induce lifelong, often irreversible derangements in the offspring’s adiposity and metabolism. These changes involve the environmental alteration of genetic expression, in part through epigenetic mechanisms, rather than changes in the genome itself. Thus, timely intervention during the early, plastic phases of development — unlike corrective efforts made later in life — may lead to improved lifelong health trajectories.

Because of challenges in measuring fetal exposures and the long latency between initial determinants and salient health outcomes, however, it is difficult to translate such proofs of principle in animals to human populations. The first generation of developmental-origins studies in humans linked birth weight to adult obesity-related morbidity and mortality. We now recognize that birth weight and each of its components, gestational duration and fetal growth, are low-resolution, momentary markers for myriad prenatal and perinatal influences. In the past decade, many such influences have been identified and quantified in epidemiologic studies that have involved the period before birth, used modern methods to mitigate confounding, and incorporated biomarkers. These studies have identified prenatal risk factors for obesity ranging from lifestyle factors such as the mother’s smoking status to psychosocial factors including antepartum depression, medical conditions such as gestational diabetes, physiological stress as reflected by fetal exposure to glucocorticoids, and epigenetic markers such as gene-specific DNA methylation levels in umbilical-cord tissue.

After birth, rapid weight gain in the first 3 to 6 months of life is a potent predictor of later obesity and cardiometabolic risk. Lactation cannot be the entire explanation, because breast-fed babies tend to gain more weight than formula-fed babies in the first few months of life. The perinatal hormonal milieu may very well be a contributing factor. In one study, higher leptin levels in umbilical-cord blood, chiefly reflecting placental production, were associated with slower gain in infant weight-for-length and lower adiposity at the ages of 3 years and 7 years. In contrast, higher leptin levels at 3 years of age were associated with faster gains in BMI from 3 to 7 years, suggesting that leptin resistance develops between birth and 3 years of age.1 These findings are consistent with studies in animals showing a critical period of perinatal leptin exposure that allows normal maturation of appetite-regulating neurons in the hypothalamus. Features of infant feeding other than breast versus bottle may also play a role. Among formula-fed infants, the introduction of solids before 4 months was associated with a sixfold increase in the odds of obesity 3 years later.2

Emerging risk factors for obesity include exposure to endocrine disruptors, which appear to do the most damage during times of maximum developmental plasticity, and the gut microbiota. Our bodies contain about 1013 cells but as many as 1014 microorganisms. Certain modifications in the number and type of microorganisms during infancy are associated with excess weight gain, at least in rodents. The infant gut is normally colonized during transit through the birth canal, which could be one reason why children delivered by cesarean section appear to be at elevated risk for obesity.3

Given obesity’s numerous developmental determinants, it is logical that effective prevention would target multiple modifiable factors. In combination, two well-studied prenatal risk factors, excessive gestational weight gain and maternal smoking during pregnancy, and two postnatal factors, fewer months of breast-feeding and a shorter duration of daily sleep during infancy, are associated with wide variation in childhood obesity. In one study, preschool-age children whose mothers did not smoke or gain excessive weight during pregnancy and who were breast-fed for at least 12 months and slept for at least 12 hours per day during infancy had a predicted obesity prevalence of 6%, as compared with 29% among children for whom the opposite was true for all four risk factors4; the rates were similar (4% and 28%, respectively) when the children reached 7 to 10 years of age (see graphPredicted Probability of Obesity at 7 to 10 Years of Age for 16 Combinations of Four Modifiable Prenatal and Postnatal Risk Factors.). These observational data raise the possibility that avoiding some or all of these risk factors could substantially reduce the proportion of childhood obesity.

Preventing racial and ethnic disparities in obesity risk will also require a developmental approach. By school age, rates of obesity among black and Hispanic children in the United States are higher than the rates among white children, even after adjustment for socioeconomic circumstances. Many of the risk factors during pregnancy and early childhood are more prevalent among nonwhite persons, and they explain a substantial proportion of racial and ethnic differences in obesity in mid-childhood.5

Several features of pregnancy and infancy make the prenatal and postnatal periods conducive to behavior change to reduce the risk of obesity and its complications. First, women appear especially willing to modify their behavior during these periods to benefit their children. Second, since pregnant women and infants receive frequent routine medical care, interventions involving improved health care delivery have great potential. Third, these periods are relatively brief, and we know that behavior-change interventions are typically most successful in the short term. Fourth, if effective interventions begun during pregnancy are maintained after birth, they will reduce the risk of maternal obesity for future pregnancies and thus help to interrupt the intergenerational cycle.

Ongoing intervention studies promise to inform medical practice and public health. Many current trials target excessive gestational weight gain, including seven randomized, controlled trials funded by the National Institutes of Health that will together include more than 1000 overweight or obese women and follow infants through at least 1 year of age. It remains to be proven, however, that reducing gestational weight gain reduces the obesity risk in offspring. An alternative approach focuses on dietary quality, independent of calorie content, to ameliorate maternal insulin resistance and excessive placental nutrient transfer. Pilot studies have suggested that a multiple-risk-factor approach during infancy, targeting mothers as conduits for changes in their infants, can improve sleep duration and delay the introduction of solid foods.

But even as we await the results of obesity-prevention trials, some recommendations are warranted because of their beneficial effects on other health outcomes. Pregnant women should not smoke. Treatment of gestational diabetes reduces macrosomia at birth, although such treatment hasn’t been proven to prevent obesity. U.S. rates of elective cesarean sections have apparently leveled off, but reducing these rates, especially of cesarean sections performed before 39 weeks of gestation, is a public health goal. Simple sleep-hygiene measures are worth trying, even in early infancy. The ideal age, in terms of allergy prevention, for introducing solid foods appears to be 4 to 6 months, and further research may show that the same is true in terms of obesity prevention.

 

Source: NEJM

C difficile: Obesity Linked to Community-Onset Infections.

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Obesity may be a risk factor for Clostridium difficile infection (CDI), according to results from a retrospective cohort study of 132 cases seen at a tertiary care medical center.

After potential confounders were taken into account, patients with simple community-onset infections were more than 4 times as likely to be obese as patients who had community-onset infections that came shortly after an exposure to a healthcare facility, according to data reported in an article published in the November issue ofEmerging Infectious Diseases.

“Obesity may be associated with CDI, independent of antibacterial drug or health care exposures,” write the researchers, led by Jason Leung, MD, from the University of Michigan Hospital in Ann Arbor. Such an association could help explain the uptick of community-onset cases in individuals having low levels of traditional risk factors.

The authors propose that obesity may perturb the intestinal microbiome in ways similar to those seen with inflammatory bowel disease and use of antibiotics, both of which are known risk factors for CDI.

“Translational research could help elaborate the dimensions of the interaction of the intestinal microbiota with C. difficile in obese patients,” the researchers maintain. They also suggest that an investigation of a dose–response relationship between body mass index and infection risk might be informative.

“[I]t is critical to establish whether obesity is a risk factor for high rates of C. difficile colonization, as is [inflammatory bowel disease]; if that risk factor is established, prospective observations would improve understanding of whether obesity plays a role in the acquisition of CDI, or alters severity of disease and risk for recurrence,” they write.

As for the patients with community-onset infections after healthcare exposure, the study’s findings highlight “the importance of increased infection control at ancillary health care facilities and surveillance for targeting high-risk patients who were recently hospitalized.”

In the study, the researchers reviewed the microbiology results and medical records of all patients who had laboratory-proven, nonrecurrent CDI at Boston Medical Center in Massachusetts during a 6-month period.

When the patients were classified according to the setting of disease onset, 43% had infections that began in the community without recent exposure to a healthcare facility, 30% had infections that began in a healthcare facility, and 23% had infections that began in the community within 30 days of exposure to a healthcare facility (most often a hospital or long-term care facility).

The prevalence of obesity, defined as a body mass index exceeding 30 kg/m2, was 34% in the group with community-onset infections compared with 23% in the general population (odds ratio, 1.7; 95% confidence interval [CI], 1.02 – 2.99). The value stood at 13% in the group with community-onset healthcare-associated infections and 32% in the group with healthcare-onset infections.

In multivariate analyses, patients with simple community-onset infections were significantly less likely to be older than 65 years (odds ratio, 0.35; 95% CI, 0.13 – 0.92; P < .05) and more likely to be obese (odds ratio, 4.06; 95% CI, 1.15 – 14.36; P < .05) than patients with community-onset healthcare-associated infections.

In addition, patients with simple community-onset infections were significantly less likely to have prior antibiotic exposure (odds ratio, 0.29; 95% CI, 0.11 – 0.76; P < .05) than patients with healthcare-onset infections. There was also a trend whereby they were much more likely to have inflammatory bowel disease (odds ratio, 6.40; 95% CI, 0.73 – 56.17; P < .10).

Finally, patients with community-onset healthcare-associated infections were dramatically less likely to have had prior antibiotic exposure than patients with healthcare-onset infections (odds ratio, 0.08; 95% CI, 0.02 – 0.28; P < .05).

Mid-life stress ‘precedes dementia’

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stressed woman
Mid-life stress may increase a woman’s risk of developing dementia, according to researchers.

In a study of 800 Swedish women, those who had to cope with events such as divorce or bereavement were more likely to get Alzheimer’s decades later.

The more stressful events there were, the higher the dementia risk became, BMJ Open reports.

The study authors say stress hormones may be to blame, triggering harmful alterations in the brain.

Stress hormones can cause a number of changes in the body and affect things such as blood pressure and blood sugar control.

“Start Quote

Current evidence suggest the best ways to reduce the risk of dementia are to eat a balanced diet, take regular exercise, not smoke, and keep blood pressure and cholesterol in check”

Dr Simon Ridley Alzheimer’s Research UK

And they can remain at high levels many years after experiencing a traumatic event, Dr Lena Johansson and colleagues explain.

But they say more work is needed to confirm their findings and ascertain whether the same stress and dementia link might also occur in men.

Stress link

In the study, the women underwent a battery of tests and examinations when they were in either their late 30s, mid-40s or 50s, and then again at regular intervals over the next four decades.

At the start of the study, one in four women said they had experienced at least one stressful event, such as widowhood or unemployment.

A similar proportion had experienced at least two stressful events, while one in five had experienced at least three. The remaining women had either experienced more than this or none.

During follow-up, 425 of the women died and 153 developed dementia.

When the researchers looked back at the women’s history of mid-life stress, they found the link between stress and dementia risk.

Dr Johansson says future studies should look at whether stress management and behavioural therapy might help offset dementia.

Dr Simon Ridley, of Alzheimer’s Research UK, said that from this study, it was hard to know whether stress contributed directly to the development of dementia, whether it was purely an indicator of another underlying risk factor in this population of women, or whether the link was due to an entirely different factor.

“We know that the risk factors for dementia are complex and our age, genetics and environment may all play a role. Current evidence suggests the best ways to reduce the risk of dementia are to eat a balanced diet, take regular exercise, not smoke, and keep blood pressure and cholesterol in check.

“If you are feeling stressed or concerned about your health in general, we would recommend you talk this through with your GP.”

Hydration before contrast cuts CIN in high-risk patients.

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Even patients with advanced kidney disease can steer clear of contrast-induced nephropathy (CIN) if given plenty of hydration, say researchers from the Netherlands. Results from the study of nearly 1,000 patients with stage 3 or 4 kidney disease were published in the June issue of Radiology.

The study found that fewer than 2.5% of the patients examined developed CIN when current guidelines emphasizing hydration were followed, according to the researchers from Radboud University Nijmegen Medical Centre in the Netherlands. The study also found that heart failure, low body mass index, and repeat contrast administration were associated with CIN.

CIN is the third most common cause of acute renal failure in hospitalized patients, and while most cases are limited to mild and transient impairment of renal function, serious morbidity and mortality, as well as longer hospital stays, can occur.

“In current practice, hydration is considered the preventive method of choice; however, evidence supporting its use is limited,” wrote Dr. Corinne Balemans and colleagues. Previous studies have relied on a variety of hydration protocols that were often used inconsistently (Radiology, June 2012, Vol. 263:3 pp. 706-713).

Balemans and colleagues aimed to determine risk factors associated with CIN by evaluating its incidence in patients with an estimated glomerular filtration rate (eGFR) of less than 60 mL/min/1.73 m2 who received iodinated contrast media intravenously and were treated using current guidelines.

Current CIN guidelines developed in Europe and the U.S. emphasize the identification of patients at high risk for CIN and the use of hydration as a preventive measure, either using normal saline or sodium bicarbonate as an alternative option, they wrote.

In the study, patients with renal insufficiency were evaluated at a special outpatient clinic where CIN was assessed and normal saline hydration was prescribed (Centraal Begeleidings Orgaan guidelines, 2007), with renal function assessed after the procedures.

The researchers stratified all patients with eGFR less than 60 mL/min/1.73 m2 for risk of CIN; those at high risk based on absolute GFR and risk factors were hydrated with 1,000 mL of isotonic saline before and after contrast injection. Serum creatinine was measured three to five days later, and CIN was defined as an increase of 25% or more from baseline. Finally, the authors recorded and compared risk factors between patients with CIN and those without using stepwise multiple logistic regression analysis.

The study included 747 patients (43% female; mean age, 71.3 years ± 10) who underwent 944 procedures. Patients were hydrated in 511 (54.1%) procedures. CIN developed after 23 procedures (2.4%).

Independent predictors of CIN were heart failure (odds ratio, 3.0), body mass index (BMI) (odds ratio, 0.9), and repeated contrast material administration (odds ratio, 2.8), Balemans and colleagues wrote. No patients needed dialysis.

The population was carefully prepared before iodinated contrast injection, and only 7.7% of patients at high risk for CIN did not receive hydration.

“Our study provides reliable estimates of CIN and shows that the incidence of CIN is low in a homogeneous population of patients with stage 3 or 4 chronic kidney disease who underwent treatment in accordance with existing guidelines and who received intravenous iodinated contrast material,” the authors wrote.

In the study, money was saved by restricting hydration to about half of the study population; patients at high risk for CIN were hydrated, whereas those at low risk were not. However, it’s possible the incidence could have been reduced further by a less restrictive policy.

Regarding heart failure, a well-known risk factor for CIN, such patients may have more severe atherosclerotic vascular disease and are more prone to hemodynamic changes during and after procedures. For them, hydration may not be helpful, the authors wrote.

The inverse association between BMI and CIN may not have been reported previously, they noted. Patients with low BMI usually have a lower percentage of muscle mass, and as a result the formulas used to calculate eGFR overestimate renal function, Balemans and colleagues wrote.

Another study reported the association between repeat contrast exposure and CIN. In that study (Trivedi and Foley), the increased risk was even notable in patients with preserved renal function.

As for study limitations, the population was large but the number of events was small. Absolute GFR was used to classify risk, and there is debate about whether GFR should be corrected for body surface area.

The incidence of CIN in patients with stage 3 or 4 chronic kidney disease is low when treated in accordance with current guidelines, the authors concluded.

“Our findings support the efficacy of hydration regimens,” they wrote. “The risk of CIN is increased in patients with heart failure, low BMI, and repeated contrast material administration. These risk factors need to be validated in future studies.”

Populations at risk for severe or complicated influenza illness: systematic review and meta-analysis.

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Abstract

Objective To evaluate risk factors for severe outcomes in patients with seasonal and pandemic influenza.

Design Systematic review.

Study selection Observational studies reporting on risk factor-outcome combinations of interest in participants with influenza. Outcomes included death, ventilator support, admission to hospital, admission to an intensive care unit, pneumonia, and composite outcomes.

Data sources Medline, Embase, CINAHL, Global Health, and the Cochrane Central Register of Controlled Trials to March 2011.

Risk of bias assessment Newcastle-Ottawa scale to assess the risk of bias. GRADE framework to evaluate the quality of evidence.

Results 63 537 articles were identified of which 234 with a total of 610 782 participants met the inclusion criteria. The evidence supporting risk factors for severe outcomes of influenza ranged from being limited to absent. This was particularly relevant for the relative lack of data for non-2009 H1N1 pandemics and for seasonal influenza studies. Limitations in the published literature included lack of power and lack of adjustment for confounders was widespread: adjusted risk estimates were provided for only 5% of risk factor-outcome comparisons in 39 of 260 (15%) studies. The level of evidence was low for “any risk factor” (odds ratio for mortality 2.77, 95% confidence interval 1.90 to 4.05 for pandemic influenza and 2.04, 1.74 to 2.39 for seasonal influenza), obesity (2.74, 1.56 to 4.80 and 30.1, 1.74 to 2.39), cardiovascular diseases (2.92, 1.76 to 4.86 and 1.97, 1.06 to 3.67), and neuromuscular disease (2.68, 1.91 to 3.75 and 3.21, 1.84 to 5.58). The level of evidence was very low for all other risk factors. Some well accepted risk factors such as pregnancy and belonging to an ethnic minority group could not be identified as risk factors. In contrast, women who were less than four weeks post partum had a significantly increased risk of death from pandemic influenza (4.43, 1.24 to 15.81).

Conclusion The level of evidence to support risk factors for influenza related complications is low and some well accepted risk factors, including pregnancy and ethnicity, could not be confirmed as risks. Rigorous and adequately powered studies are needed.

What is already known on this topic

  • Certain patient populations are thought to be at higher risk for developing complicated or severe influenza illness
  • These groups are prioritised for vaccination as well as for antiviral treatment
  • The quantity and quality of evidence on risk factors for developing complicated or severe influenza illness is limited
  • While some risk factors could be corroborated, evidence to support other, well established risk factors for severe outcomes could not be found

What this study adds

Source: BMJ

Why Take Follow-Up Biopsies in Celiac Disease?

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Results provide status of mucosal healing, which is associated with risk for lymphoma.
Celiac disease is a risk factor for T-cell lymphomas of the intestine as well as a variety of other malignancies. Some experts believe that adherence to a gluten-free diet mitigates this risk. Guidelines suggest repeating serologic testing after several months on a gluten-free diet, but follow-up biopsy sampling to confirm healing is not routinely performed. Now, researchers consider its value for assessing cancer risk.

To examine the association between mucosal healing in celiac disease and the risk for lymphoproliferative malignancy (LPM), investigators in Sweden conducted a retrospective, population-based cohort study of 7625 patients with celiac disease who had at least one follow-up biopsy taken after diagnosis. Biopsies were taken at least 6 months after initiation of a gluten-free diet and at a median of 1.3 years after diagnosis. LPM occurrence was determined using a nationwide cancer registry.

In multivariate analysis, patients with persistent villous atrophy on follow-up biopsy had a higher risk for LPM compared with the general population (standardized incidence ratio, 3.78; 95% confidence interval, 2.71–5.12) and compared with patients with mucosal healing (hazard ratio, 2.26; 95% CI, 1.18–4.34). The risk estimate was highest for T-cell lymphoma, though not statistically significant. Total or subtotal villous atrophy was more strongly associated with T-cell lymphoma (HR, 9.23) than partial or no villous atrophy (HR, 3.4).

COMMENT

This study confirms the increased risk for lymphoproliferative malignancy in patients with celiac disease. Further, it documents for the first time that the risk for LPM, particularly T-cell lymphoma, is predicted by the degree of mucosal healing on follow-up biopsy. These findings strongly suggest that, as in inflammatory bowel disease, mucosal healing is an important therapeutic goal. Follow-up biopsy at 6 to 12 months after initiation of a gluten-free diet should be considered, with the goal of achieving resolution of villous atrophy.

Source: NEJM

Comparison of global estimates of prevalence and risk factors for peripheral artery disease in 2000 and 2010: a systematic review and analysis.

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Background

Lower extremity peripheral artery disease is the third leading cause of atherosclerotic cardiovascular morbidity, following coronary artery disease and stroke. This study provides the first comparison of the prevalence of peripheral artery disease between high-income countries (HIC) and low-income or middle-income countries (LMIC), establishes the primary risk factors for peripheral artery disease in these settings, and estimates the number of people living with peripheral artery disease regionally and globally.

Methods

We did a systematic review of the literature on the prevalence of peripheral artery disease in which we searched for community-based studies since 1997 that defined peripheral artery disease as an ankle brachial index (ABI) lower than or equal to 0·90. We used epidemiological modelling to define age-specific and sex-specific prevalence rates in HIC and in LMIC and combined them with UN population numbers for 2000 and 2010 to estimate the global prevalence of peripheral artery disease. Within a subset of studies, we did meta-analyses of odds ratios (ORs) associated with 15 putative risk factors for peripheral artery disease to estimate their effect size in HIC and LMIC. We then used the risk factors to predict peripheral artery disease numbers in eight WHO regions (three HIC and five LMIC).

Findings

34 studies satisfied the inclusion criteria, 22 from HIC and 12 from LMIC, including 112 027 participants, of which 9347 had peripheral artery disease. Sex-specific prevalence rates increased with age and were broadly similar in HIC and LMIC and in men and women. The prevalence in HIC at age 45—49 years was 5·28% (95% CI 3·38—8·17%) in women and 5·41% (3·41—8·49%) in men, and at age 85—89 years, it was 18·38% (11·16—28·76%) in women and 18·83% (12·03—28·25%) in men. Prevalence in men was lower in LMIC than in HIC (2·89% [2·04—4·07%] at 45—49 years and 14·94% [9·58—22·56%] at 85—89 years). In LMIC, rates were higher in women than in men, especially at younger ages (6·31% [4·86—8·15%] of women aged 45—49 years). Smoking was an important risk factor in both HIC and LMIC, with meta-OR for current smoking of 2·72 (95% CI 2·39—3·09) in HIC and 1·42 (1·25—1·62) in LMIC, followed by diabetes (1·88 [1·66—2·14] vs 1·47 [1·29—1·68]), hypertension (1·55 [1·42—1·71] vs 1·36 [1·24—1·50]), and hypercholesterolaemia (1·19 [1·07—1·33] vs 1·14 [1·03—1·25]). Globally, 202 million people were living with peripheral artery disease in 2010, 69·7% of them in LMIC, including 54·8 million in southeast Asia and 45·9 million in the western Pacific Region. During the preceding decade the number of individuals with peripheral artery disease increased by 28·7% in LMIC and 13·1% in HIC.

Interpretation

In the 21st century, peripheral artery disease has become a global problem. Governments, non-governmental organisations, and the private sector in LMIC need to address the social and economic consequences, and assess the best strategies for optimum treatment and prevention of this disease.

Source: Lancet.

 

Adult Stature and Risk of Cancer at Different Anatomic Sites in a Cohort of Postmenopausal Women.

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Abstract

Background: Prospective studies in Western and Asian populations suggest that height is a risk factor for various cancers. However, few studies have explored potential confounding or effect modification of the association by other factors.

Methods: We examined the association between height measured at enrollment in 144,701 women participating in the Women’s Health Initiative and risk of all cancers combined and cancer at 19 specific sites. Over a median follow-up of 12.0 years, 20,928 incident cancers were identified. We used Cox proportional hazards models to estimate HR and 95% confidence intervals (CI) per 10 cm increase in height, with adjustment for established risk factors. We also examined potential effect modification of the association with all cancer and specific cancers.

Results: Height was significantly positively associated with risk of all cancers (HR = 1.13; 95% CI, 1.11–1.16), as well as with cancers of the thyroid, rectum, kidney, endometrium, colorectum, colon, ovary, and breast, and with multiple myeloma and melanoma (range of HRs: 1.13 for breast cancer to 1.29 for multiple myeloma and thyroid cancer). These associations were generally insensitive to adjustment for confounders, and there was little evidence of effect modification.

Conclusions: This study confirms the positive association of height with risk of all cancers and a substantial number of cancer sites.

Source: http://cebp.aacrjournals.org

The Taller the Woman, the Greater the Cancer Risk?

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Taller postmenopausal women face higher risks for 10 types of cancer, according to a study in Cancer Epidemiology, Biomarkers and Prevention.

Researchers examined the association between height and cancer risk among some 145,000 Women’s Health Initiative participants. During roughly 12 years of follow-up, 14% received diagnoses of invasive cancer.

After multivariable adjustment, the risk for all cancers increased significantly, by 13%, with each 10-cm (4-inch) increase in height. In particular, risks for the following types of cancer were increased: breast, colon, colorectal, endometrial, melanoma, multiple melanoma, ovarian, rectal, renal, and thyroid. Additional adjustment for cancer screening did not alter the results.

The researchers say height should be considered “a marker for one or more exposures that influence cancer risk rather than a risk factor itself.”

Source:Cancer Epidemiology, Biomarkers & Prevention