Visualization of the dengue fever virus. Courtesy of 3dciencia A fever run amok Its name – dengue fever – vaguely suggests some sort of infectious tropical disease and, until relatively recently, that’s exactly what it was. Until 1970, the ailment characterized by symptoms like fever, headache, muscle and joint pains, and a skin rash resembling the measles was endemic to just nine tropical nations, according to the World Health Organization. Now cases of dengue fever (also colloquially known as breakbone fever) have been reported in more than 110 countries and, according to a new paper in Nature, the annual infection rate may be as many as 400 million cases worldwide, four times higher than the WHO’s prevalence estimate. “Not only are the number of cases increasing, the geographic range is increasing,” study co-author Thomas Scott, an entomologist at UC Davis, told NPR. “So (dengue) is spreading in to areas where it was not previously, but we are also seeing more and more cases.” Climate change is one driving factor, according to some scientists. As more of the planet gets warmer, more of the planet becomes amenable to mosquitoes that carry and transmit the virus. The latest study also blames the spread on the growth of overcrowded slums with poor sanitation. “People living in substandard conditions where they’re storing water and they don’t have proper disposal of waste [are more at risk],” said Scott. “Rainwater accumulates in containers and the mosquito that transmits this virus, Aedes aegypti, then lays its eggs in those places.” Often, dengue produces no or mild symptoms, which may be part of the reason it is under-reported. For a small percentage, however, the infection can develop into life-threatening dengue hemorrhagic fever characterized by bleeding, low levels of blood platelets and blood plasma leakage, or dengue shock syndrome, where dangerously low blood pressure occurs.
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Visualization of the dengue fever virus. Courtesy of 3dciencia

A fever run amok

Its name – dengue fever – vaguely suggests some sort of infectious tropical disease and, until relatively recently, that’s exactly what it was. Until 1970, the ailment characterized by symptoms like fever, headache, muscle and joint pains, and a skin rash resembling the measles was endemic to just nine tropical nations, according to the World Health Organization.

Now cases of dengue fever (also colloquially known as breakbone fever) have been reported in more than 110 countries and, according to a new paper in Nature, the annual infection rate may be as many as 400 million cases worldwide, four times higher than the WHO’s prevalence estimate.

“Not only are the number of cases increasing, the geographic range is increasing,” study co-author Thomas Scott, an entomologist at UC Davis, told NPR. “So (dengue) is spreading in to areas where it was not previously, but we are also seeing more and more cases.”

Climate change is one driving factor, according to some scientists. As more of the planet gets warmer, more of the planet becomes amenable to mosquitoes that carry and transmit the virus.

The latest study also blames the spread on the growth of overcrowded slums with poor sanitation.

“People living in substandard conditions where they’re storing water and they don’t have proper disposal of waste [are more at risk],” said Scott. “Rainwater accumulates in containers and the mosquito that transmits this virus, Aedes aegypti, then lays its eggs in those places.”

Often, dengue produces no or mild symptoms, which may be part of the reason it is under-reported. For a small percentage, however, the infection can develop into life-threatening dengue hemorrhagic fever characterized by bleeding, low levels of blood platelets and blood plasma leakage, or dengue shock syndrome, where dangerously low blood pressure occurs.

Aging tall As a child, the parental mantra was “Eat your vegetables. They’ll make you big and strong,” which seemed reasonably plausible. It was something you could swallow with a grain of salt, and a milkshake. Turns out, though, your eating (and lifestyle) habits in adulthood may influence your height as well. Or more specifically, how long you remain “long.” A massive longitudinal study of 17,708 adults (beginning at age 45) by researchers at the University of Southern California found that healthy habits in later years influence the rate of shrinkage in those later years. For younger study participants who had not yet begun the inevitable shrinking with age, it was easy for scientists to accurately measure height. For older participants, the researchers compared the relationship between current height and length of limbs, which do not shrink with age. They found a strong relationship between height loss and indicators of adult health, not least among them cognitive skills. Participants who had lost more height more rapidly over time were also more likely to perform poorly on standard tests of cognition, such as short-term memory, basic arithmetic and awareness of the date. Urban dwellers lost less height in adulthood than did rural residents. Education was also a key measure. The more schooling, the less height loss. Completing high school, for example, translated into one less centimeter of shrinkage over time. “Height has been recognized as an acceptable proxy for childhood health conditions, but there are complications there,” said economist and co-investigator Geert Ridder. “Some of adult health might be determined by childhood circumstances, but people shrink differentially, and that shrinkage is also a measure of adult health conditions.”
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Aging tall

As a child, the parental mantra was “Eat your vegetables. They’ll make you big and strong,” which seemed reasonably plausible. It was something you could swallow with a grain of salt, and a milkshake.

Turns out, though, your eating (and lifestyle) habits in adulthood may influence your height as well. Or more specifically, how long you remain “long.”

A massive longitudinal study of 17,708 adults (beginning at age 45) by researchers at the University of Southern California found that healthy habits in later years influence the rate of shrinkage in those later years.

For younger study participants who had not yet begun the inevitable shrinking with age, it was easy for scientists to accurately measure height. For older participants, the researchers compared the relationship between current height and length of limbs, which do not shrink with age.

They found a strong relationship between height loss and indicators of adult health, not least among them cognitive skills. Participants who had lost more height more rapidly over time were also more likely to perform poorly on standard tests of cognition, such as short-term memory, basic arithmetic and awareness of the date.

Urban dwellers lost less height in adulthood than did rural residents. Education was also a key measure. The more schooling, the less height loss. Completing high school, for example, translated into one less centimeter of shrinkage over time.

“Height has been recognized as an acceptable proxy for childhood health conditions, but there are complications there,” said economist and co-investigator Geert Ridder. “Some of adult health might be determined by childhood circumstances, but people shrink differentially, and that shrinkage is also a measure of adult health conditions.”

Mitral cells receive information from olfactory receptor neurons and, in turn, help transfer the information to the brain where it’s translated into odors, new and old. Photo courtesy of Charles Greer, Yale University Odor of magnitude Thanks to roughly 5 million olfactory receptors, humans are capable of detecting thousands of odors. On a smell chart, that puts us down among the stinkers. A rabbit, for example, has roughly 20 times more receptors and a bloodhound more than 220 million. Yet even our comparatively diminished sense of smell is nothing to sniff at. Though hypotheses about how we smell date back to the first century B.C. and the Roman philosopher Lucretius, researchers are only now beginning to really tease out the olfactory process. One of the enduring mysteries has been where olfactory neurons – the only neurons capable of regeneration through adult life – come from. In a new study, researchers at the California Institute of Technology have an answer: They derive from neural crest stem cells – multipotent, migratory cells unique to vertebrates that give rise to multiple structures and tissues in the body, such as facial bones and smooth muscle. That’s contrary to previous hypotheses, which have proposed olfactory nerve cells originate from the same embryonic cells that, it’s believed, produce eye and ear sensory neurons. The findings aren’t just fundamental science. They may have therapeutic benefits, such as helping in the development of new treatments for conditions like anosmia, or the inability to smell. “Olfactory neurons are unique in their renewal capacity across species, so by learning how they form, we may gain insights into how neurons in general can be induced to differentiate or regenerate,” said Marianne Bronner, professor of biology and corresponding author on the study. “That knowledge, in turn, may provide new avenues for pursuing treatment of neurological disorders or injury in humans.”
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Mitral cells receive information from olfactory receptor neurons and, in turn, help transfer the information to the brain where it’s translated into odors, new and old. Photo courtesy of Charles Greer, Yale University

Odor of magnitude

Thanks to roughly 5 million olfactory receptors, humans are capable of detecting thousands of odors. On a smell chart, that puts us down among the stinkers. A rabbit, for example, has roughly 20 times more receptors and a bloodhound more than 220 million.

Yet even our comparatively diminished sense of smell is nothing to sniff at. Though hypotheses about how we smell date back to the first century B.C. and the Roman philosopher Lucretius, researchers are only now beginning to really tease out the olfactory process.

One of the enduring mysteries has been where olfactory neurons – the only neurons capable of regeneration through adult life – come from. In a new study, researchers at the California Institute of Technology have an answer: They derive from neural crest stem cells – multipotent, migratory cells unique to vertebrates that give rise to multiple structures and tissues in the body, such as facial bones and smooth muscle.

That’s contrary to previous hypotheses, which have proposed olfactory nerve cells originate from the same embryonic cells that, it’s believed, produce eye and ear sensory neurons.

The findings aren’t just fundamental science. They may have therapeutic benefits, such as helping in the development of new treatments for conditions like anosmia, or the inability to smell.

“Olfactory neurons are unique in their renewal capacity across species, so by learning how they form, we may gain insights into how neurons in general can be induced to differentiate or regenerate,” said Marianne Bronner, professor of biology and corresponding author on the study. “That knowledge, in turn, may provide new avenues for pursuing treatment of neurological disorders or injury in humans.”

A high definition visualization of a million brain fibers. The non-invasive imaging technology can pinpoint where neural fiber breaks have occurred due to traumatic brain injury, something that can’t be seen in CT and MRI scans. Image courtesy of Walt Schneider, University of Pittsburgh Schools of Health Sciences. Head games Any blow to the head can cause brain trauma. It’s a question of degree. For most folks, falling down and banging the noggin on the floor may prove sufficiently concussive, damaging enough to result in lingering headaches or worse. Conversely, for a boxer a full day of sparring with countless jabs and uppercuts to the head could be just another day at work. “They can come to the gym the next day feeling wonderful,” said Dr. Paul Wallace, a member of the California State Athletic Commission and licensed ringside physician for more than 24 years. “In terms of their ability to withstand blows to the head, boxers are clearly a subset of people.” Of course, the real and permanent harm of concussions and associated brain trauma is often not immediately apparent. For that reason and many others, the American Academy of Neurology recently issued new guidelines for when to remove possibly injured athletes from games. The new headline: If you suspect injury, take them out. Period. The AAN guidelines replace 15-year-old rules deemed outdated and inadequate. The Academy noted that old standards for detecting a concussion (symptoms like mental confusion, memory loss or glassy eyes) had become confusing and insufficient. Even the best tests for mild traumatic brain injury can miss up to 20 percent of concussions (later documented through medical imaging), so it’s easy to imagine a coach or doctor at a game making a poor decision. And old, playing field rules like “three concussions and you’re out of the game” didn’t help. They were simply dangerous. The best and safest course of treatment, according to the AAN and the Centers for Disease Control is immediate removal from play, followed by a thorough medical evaluation and time away from the game. Athletes (and everybody else) are at highest risk of further brain injury – a second concussion – in the week or so after the first blow. Multiple concussions can worsen symptoms, slow recovery and increase the likelihood of long-term or permanent brain damage, such as chronic traumatic encephalopathy.
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A high definition visualization of a million brain fibers. The non-invasive imaging technology can pinpoint where neural fiber breaks have occurred due to traumatic brain injury, something that can’t be seen in CT and MRI scans. Image courtesy of Walt Schneider, University of Pittsburgh Schools of Health Sciences.

Head games

Any blow to the head can cause brain trauma. It’s a question of degree.

For most folks, falling down and banging the noggin on the floor may prove sufficiently concussive, damaging enough to result in lingering headaches or worse. Conversely, for a boxer a full day of sparring with countless jabs and uppercuts to the head could be just another day at work.

“They can come to the gym the next day feeling wonderful,” said Dr. Paul Wallace, a member of the California State Athletic Commission and licensed ringside physician for more than 24 years. “In terms of their ability to withstand blows to the head, boxers are clearly a subset of people.”

Of course, the real and permanent harm of concussions and associated brain trauma is often not immediately apparent. For that reason and many others, the American Academy of Neurology recently issued new guidelines for when to remove possibly injured athletes from games.

The new headline: If you suspect injury, take them out. Period.

The AAN guidelines replace 15-year-old rules deemed outdated and inadequate. The Academy noted that old standards for detecting a concussion (symptoms like mental confusion, memory loss or glassy eyes) had become confusing and insufficient. Even the best tests for mild traumatic brain injury can miss up to 20 percent of concussions (later documented through medical imaging), so it’s easy to imagine a coach or doctor at a game making a poor decision. And old, playing field rules like “three concussions and you’re out of the game” didn’t help. They were simply dangerous.

The best and safest course of treatment, according to the AAN and the Centers for Disease Control is immediate removal from play, followed by a thorough medical evaluation and time away from the game.

Athletes (and everybody else) are at highest risk of further brain injury – a second concussion – in the week or so after the first blow. Multiple concussions can worsen symptoms, slow recovery and increase the likelihood of long-term or permanent brain damage, such as chronic traumatic encephalopathy.

Honeybees give their all in defense of the hive. Their barbed stingers cannot be extracted. When a stinging bee pulls away, it leaves behind not just the stinger, but also parts of its digestive system, muscles and nerves.The resulting massive abdominal rupture is fatal. Photo courtesy of Waugsberg. Bee HIV For some people with acute allergies, the sting of the common honeybee can pose a potentially mortal threat. Scientists hope to add human immunodeficiency virus or HIV to that list. Researchers at Washington University in St. Louis are developing a prophylactic vaginal gel containing nanoparticles coated with a toxin found in bee venom. The peptide toxin, called melittin, pokes holes in the protective envelope surrounding HIV, killing the virus. “Our hope is that in places where HIV is running rampant, people could use this gel as a preventive measure to stop the initial infection,” said study author Joshua L. Hood. The melittin does not harm normal cells because researchers added protective bumpers to the nanoparticles’ surfaces. When the nanoparticles come into contact with much larger normal cells, they simply bounce off. HIV, on the other hand, is much smaller than the nanoparticles and slides easily between the bumpers to make contact with the deadly bee toxin. Hood said one advantage of this approach is that the nanoparticles’ attack involves an essential part of the virus’ structure. “We are attacking an inherent physical property of HIV,” he said. “Theoretically, there isn’t any way for the virus to adapt to that. The virus has to have a protective coat, a double-layered membrane that covers the virus.” By contrast, most current anti-HIV drugs focus upon inhibiting viral replication. Some HIV strains have evolved alternative reproductive strategies. Hood thinks the nanoparticle approach could be adapted to treating current HIV infections and tweaked to target other viruses with similar protective envelopes, such as hepatitis B and C.
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Honeybees give their all in defense of the hive. Their barbed stingers cannot be extracted. When a stinging bee pulls away, it leaves behind not just the stinger, but also parts of its digestive system, muscles and nerves.The resulting massive abdominal rupture is fatal. Photo courtesy of Waugsberg.

Bee HIV

For some people with acute allergies, the sting of the common honeybee can pose a potentially mortal threat.

Scientists hope to add human immunodeficiency virus or HIV to that list.

Researchers at Washington University in St. Louis are developing a prophylactic vaginal gel containing nanoparticles coated with a toxin found in bee venom. The peptide toxin, called melittin, pokes holes in the protective envelope surrounding HIV, killing the virus.

“Our hope is that in places where HIV is running rampant, people could use this gel as a preventive measure to stop the initial infection,” said study author Joshua L. Hood.

The melittin does not harm normal cells because researchers added protective bumpers to the nanoparticles’ surfaces. When the nanoparticles come into contact with much larger normal cells, they simply bounce off. HIV, on the other hand, is much smaller than the nanoparticles and slides easily between the bumpers to make contact with the deadly bee toxin.

Hood said one advantage of this approach is that the nanoparticles’ attack involves an essential part of the virus’ structure. “We are attacking an inherent physical property of HIV,” he said. “Theoretically, there isn’t any way for the virus to adapt to that. The virus has to have a protective coat, a double-layered membrane that covers the virus.”

By contrast, most current anti-HIV drugs focus upon inhibiting viral replication. Some HIV strains have evolved alternative reproductive strategies.

Hood thinks the nanoparticle approach could be adapted to treating current HIV infections and tweaked to target other viruses with similar protective envelopes, such as hepatitis B and C.

A false-color scanning electron micrograph of adipose tissue (body fat), showing lobules rich in adipocytes (fat cells). Image courtesy of David Gregory and Debbie Marshal, Wellcome Images. My kid overweight? Fat chance! Everybody knows America has a weight problem. All you have to do is look around. It’s harder, of course, to look in the mirror. And harder still see obesity as a family issue. Consider the latest poll by NPR, the Robert Wood Johnson Foundation and the Harvard School of Public Health. Roughly 69 percent of American adults are overweight or obese; more than 80 percent of Americans think obesity is a major public health problem. But when asked about obesity in their families, only one in five kids had a parent who feared their child would grow up to be overweight as an adult. NPR’s Shankar Vedantam put it this way: “Put another way, assuming current trends persist, parents of 80 percent of American children think all these kids will somehow end up being among the lucky 31 percent of adults who are not overweight.” The math just doesn’t work. This kind of “we’re different, we’ll beat the odds” outlook is not uncommon. “People underestimate their likelihood of experiencing all kinds of negative events, including medical illnesses,” English neuroscientist Tali Sharot told NPR. “And they do that for their family members as well. So not only do we think we are immune more than other people, we think that our kids are also more immune than other kids.” Such optimism is generally a good thing. When we expect to do well, we tend to do better. But in battling public obesity, it can be problematic, say experts. Ominous warnings of future obesity tend to be tuned out quickly. They’re too negative. People may agree with the message, but they don’t think it applies to them. Vedantam says a more effective technique is to exploit everyone’s optimism bias: “Don’t tell parents obesity is a major public health problem. Tell them how family dinners and exercise can turbocharge their kids, and you might get them to think, ‘Yeah, I can totally see my kid being a superstar!’”
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A false-color scanning electron micrograph of adipose tissue (body fat), showing lobules rich in adipocytes (fat cells). Image courtesy of David Gregory and Debbie Marshal, Wellcome Images.

My kid overweight? Fat chance!

Everybody knows America has a weight problem. All you have to do is look around.

It’s harder, of course, to look in the mirror. And harder still see obesity as a family issue.

Consider the latest poll by NPR, the Robert Wood Johnson Foundation and the Harvard School of Public Health. Roughly 69 percent of American adults are overweight or obese; more than 80 percent of Americans think obesity is a major public health problem.

But when asked about obesity in their families, only one in five kids had a parent who feared their child would grow up to be overweight as an adult.

NPR’s Shankar Vedantam put it this way: “Put another way, assuming current trends persist, parents of 80 percent of American children think all these kids will somehow end up being among the lucky 31 percent of adults who are not overweight.”

The math just doesn’t work.

This kind of “we’re different, we’ll beat the odds” outlook is not uncommon. “People underestimate their likelihood of experiencing all kinds of negative events, including medical illnesses,” English neuroscientist Tali Sharot told NPR. “And they do that for their family members as well. So not only do we think we are immune more than other people, we think that our kids are also more immune than other kids.”

Such optimism is generally a good thing. When we expect to do well, we tend to do better. But in battling public obesity, it can be problematic, say experts. Ominous warnings of future obesity tend to be tuned out quickly. They’re too negative. People may agree with the message, but they don’t think it applies to them.

Vedantam says a more effective technique is to exploit everyone’s optimism bias:

“Don’t tell parents obesity is a major public health problem. Tell them how family dinners and exercise can turbocharge their kids, and you might get them to think, ‘Yeah, I can totally see my kid being a superstar!’”

Telomeres (yellow) on human chromosomes. Image courtesy of Michael West. Caught short with a cold Telomeres are the “caps” that sit at the ends of chromosomes in every cell, protecting vital DNA sequences from damage. Think of them as extended bumpers. Over the years, a number of studies have linked shorter telomeres to everything from aging to aging-related conditions like cancer, cardiovascular disease and dementia. Now researchers at Carnegie Mellon University say they’ve found evidence that shorter telomeres affect the well-being of relatively young, healthy people too. These people, the scientists write in JAMA, have a higher risk of catching a cold. The researchers looked at 152 healthy adults, ages 18 to 55, living in and around Pittsburgh. They took blood samples and measured the telomere lengths in leukocytes, white blood cells involved in the immune response. Then they put the participants in quarantine and exposed them to a virus that causes the common cold. More than two-thirds of the volunteers – 105 people, 69 percent – became infected with the virus; 33 actually developed colds. When researchers compared telomere measurements with who got sick, they found that, generally speaking, shorter telomeres in four types of blood cells were associated with a higher risk of infection. Most notably in a type of T-cell (another kind of immune response cell known as a lymphocyte) called CD8CD28. The link between shorter telomeres and catching a cold became stronger with increasing age in the study subjects. The researchers speculate that T-cells with shorter telomeres don’t proliferate as well as T-cells with longer telomeres, making them less effective at removing virus-infected cells. “A provocative possibility is that telomere length is a very stable marker of disease susceptibility, with associations between telomere length and clinical outcomes beginning to emerge in early adulthood,” the authors wrote. It’s too early to know how this basic research will translate clinically. Lots of folks have suggested that maintaining telomere health is akin to maintaining overall well-being. That remains to be proven conclusively, but it does beg the obvious question: How do I keep my telomeres long and healthy? Alas, shortening appears to be part of the aging process (every time a cell divides its DNA for replication, it’s telomeres shorten too), but there is some evidence to suggest that things like reduced stress and a diet rich in omega-3 fatty acids might slow the shortening process or generally boost cellular health.
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Telomeres (yellow) on human chromosomes. Image courtesy of Michael West.

Caught short with a cold

Telomeres are the “caps” that sit at the ends of chromosomes in every cell, protecting vital DNA sequences from damage. Think of them as extended bumpers. Over the years, a number of studies have linked shorter telomeres to everything from aging to aging-related conditions like cancer, cardiovascular disease and dementia.

Now researchers at Carnegie Mellon University say they’ve found evidence that shorter telomeres affect the well-being of relatively young, healthy people too. These people, the scientists write in JAMA, have a higher risk of catching a cold.

The researchers looked at 152 healthy adults, ages 18 to 55, living in and around Pittsburgh. They took blood samples and measured the telomere lengths in leukocytes, white blood cells involved in the immune response. Then they put the participants in quarantine and exposed them to a virus that causes the common cold.

More than two-thirds of the volunteers – 105 people, 69 percent – became infected with the virus; 33 actually developed colds. When researchers compared telomere measurements with who got sick, they found that, generally speaking, shorter telomeres in four types of blood cells were associated with a higher risk of infection. Most notably in a type of T-cell (another kind of immune response cell known as a lymphocyte) called CD8CD28. The link between shorter telomeres and catching a cold became stronger with increasing age in the study subjects.

The researchers speculate that T-cells with shorter telomeres don’t proliferate as well as T-cells with longer telomeres, making them less effective at removing virus-infected cells.

“A provocative possibility is that telomere length is a very stable marker of disease susceptibility, with associations between telomere length and clinical outcomes beginning to emerge in early adulthood,” the authors wrote.

It’s too early to know how this basic research will translate clinically. Lots of folks have suggested that maintaining telomere health is akin to maintaining overall well-being.

That remains to be proven conclusively, but it does beg the obvious question: How do I keep my telomeres long and healthy? Alas, shortening appears to be part of the aging process (every time a cell divides its DNA for replication, it’s telomeres shorten too), but there is some evidence to suggest that things like reduced stress and a diet rich in omega-3 fatty acids might slow the shortening process or generally boost cellular health.

A scanning electron micrograph of ordinary table salt. Courtesy of Smithsonian National Museum of Natural History Salt-ernative thinking It’s pretty much conventional wisdom these days that folks should limit their sodium intake, that too much salt in the diet can lead to high blood pressure, diabetes, heart disease and kidney dysfunction, among other things. On the other hand, it’s pretty hard to avoid. Our modern diet of fast and processed foods is fairly salted with the stuff, so to speak. The average American consumes roughly 3,500 milligrams of salt daily, more than 1,000 mg than generally recommended. The Institute of Medicine puts the maximum healthy intake even lower: 1,500 mg. And the Centers for Disease Control notes the human body, which uses salt for a variety of essential functions, actually requires very little: just 150 to 500 mg per day. Still, less salt is a good thing, right? A new study, published in the journal Hypertension, estimates that gradually but steadily reducing sodium in foods could save 500,000 Americans from premature death over the next decade. A sharper cutback might save 850,000 to 1.2 million lives. These are sweet numbers indeed, but not everybody buys them. In recent years, there has been growing push-back to the notion that consuming lots of salt poses a health risk – and it’s not just the salt industry making the case. For example, a recent seven-year European study, published in JAMA, concluded that sodium intake did not increase hypertension or cardiovascular risk. Quite the contrary: The researchers found that people who consumed the least amount of salt were the most likely to die of any cause during the study period. And a couple of recent Cochrane meta-analyses have come to similar conclusions. The first reported that there was not strong evidence that people without hypertension benefitted by reducing salt consumption. The second study concluded that low-salt diets produced no measurable effects on the hormone and lipid (fat) levels of non-hypertensive people. So what’s the truth? Well, it seems pretty clear that if you belong to an at-risk group, it’s only prudent to be careful about how much salt you consume. Otherwise, it seems the science is far from settled, which means take everything with a grain of salt. Or not.
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A scanning electron micrograph of ordinary table salt. Courtesy of Smithsonian National Museum of Natural History

Salt-ernative thinking

It’s pretty much conventional wisdom these days that folks should limit their sodium intake, that too much salt in the diet can lead to high blood pressure, diabetes, heart disease and kidney dysfunction, among other things.

On the other hand, it’s pretty hard to avoid. Our modern diet of fast and processed foods is fairly salted with the stuff, so to speak. The average American consumes roughly 3,500 milligrams of salt daily, more than 1,000 mg than generally recommended. The Institute of Medicine puts the maximum healthy intake even lower: 1,500 mg. And the Centers for Disease Control notes the human body, which uses salt for a variety of essential functions, actually requires very little: just 150 to 500 mg per day.

Still, less salt is a good thing, right? A new study, published in the journal Hypertension, estimates that gradually but steadily reducing sodium in foods could save 500,000 Americans from premature death over the next decade. A sharper cutback might save 850,000 to 1.2 million lives.

These are sweet numbers indeed, but not everybody buys them. In recent years, there has been growing push-back to the notion that consuming lots of salt poses a health risk – and it’s not just the salt industry making the case.

For example, a recent seven-year European study, published in JAMA, concluded that sodium intake did not increase hypertension or cardiovascular risk. Quite the contrary: The researchers found that people who consumed the least amount of salt were the most likely to die of any cause during the study period.

And a couple of recent Cochrane meta-analyses have come to similar conclusions. The first reported that there was not strong evidence that people without hypertension benefitted by reducing salt consumption. The second study concluded that low-salt diets produced no measurable effects on the hormone and lipid (fat) levels of non-hypertensive people.

So what’s the truth? Well, it seems pretty clear that if you belong to an at-risk group, it’s only prudent to be careful about how much salt you consume.

Otherwise, it seems the science is far from settled, which means take everything with a grain of salt. Or not.

Birth of a notion A new analysis of the U.S. birth rate, published in the journal Pediatrics, reports that the rate at which American women are having babies fell by 1 percent in 2011, continuing a years-long decline. According to the study authors, there were 63.2 births per 1,000 women aged 15 to 44 in 2011. That’s the lowest rate on record, down from 64.1 in 2010 and 66.2 in 2009. The actual number of babies born in the U.S. in 2011: 3,953,593. Some people worry about what this trend portends in terms of national demographics and the future. For example, will there be sufficient numbers of young, working Americans to sustain the safety net for the faster-growing population of elderly. There are, of course, numerous reasons for the birth rate decline: the economy, birth control, a reduction in teen pregnancies, sperm health. That’s right, sperm health. In recent years, some studies have suggested that the sperm count and concentration in modern men has dropped, which naturally lengthens the odds of successful fertilizing a female egg. A new study, though, suggests one potential remedy: More exercise. Published in the British Journal of Sports Medicine, scientists at Harvard School of Public Health surveyed 189 young men (ages 18 to 22) about their exercise and TV-watching habits over a three-month period. They also collected semen samples. The researchers found that men who watched 20 or more hours of TV per week had a sperm concentration 44 percent lower than those who watched virtually no television. Conversely, men who exercised more than 14 hours per week has sperm concentrations 73 percent higher than peers who exercised less than five hours per week. The percentages held true even after factors like body weight and diet were taken into account. So is there a cause-and-effect link between exercise and male fertility? Not necessarily, the Harvard study posits a correlation, but hard data requires a randomized control trial. Plus, some kinds of exercise have been shown to impair semen quality, such as biking and long-distance running. The Harvard researchers say they’ll keep digging. It’s fertile research.
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Birth of a notion

A new analysis of the U.S. birth rate, published in the journal Pediatrics, reports that the rate at which American women are having babies fell by 1 percent in 2011, continuing a years-long decline.

According to the study authors, there were 63.2 births per 1,000 women aged 15 to 44 in 2011. That’s the lowest rate on record, down from 64.1 in 2010 and 66.2 in 2009.

The actual number of babies born in the U.S. in 2011: 3,953,593.

Some people worry about what this trend portends in terms of national demographics and the future. For example, will there be sufficient numbers of young, working Americans to sustain the safety net for the faster-growing population of elderly.

There are, of course, numerous reasons for the birth rate decline: the economy, birth control, a reduction in teen pregnancies, sperm health.

That’s right, sperm health. In recent years, some studies have suggested that the sperm count and concentration in modern men has dropped, which naturally lengthens the odds of successful fertilizing a female egg.

A new study, though, suggests one potential remedy: More exercise.

Published in the British Journal of Sports Medicine, scientists at Harvard School of Public Health surveyed 189 young men (ages 18 to 22) about their exercise and TV-watching habits over a three-month period. They also collected semen samples.

The researchers found that men who watched 20 or more hours of TV per week had a sperm concentration 44 percent lower than those who watched virtually no television. Conversely, men who exercised more than 14 hours per week has sperm concentrations 73 percent higher than peers who exercised less than five hours per week. The percentages held true even after factors like body weight and diet were taken into account.

So is there a cause-and-effect link between exercise and male fertility?

Not necessarily, the Harvard study posits a correlation, but hard data requires a randomized control trial. Plus, some kinds of exercise have been shown to impair semen quality, such as biking and long-distance running.

The Harvard researchers say they’ll keep digging. It’s fertile research.

Gout with tophus formations in the index and little fingers. Image courtesy of the American Society for Surgery of the Hand. Gout on a limb Gout was once called “the disease of kings” or “the rich man’s disease” because it was most commonly associated with excessive consumption of food and alcohol, something that only aristocrats and higher levels of society could afford to indulge. The English King Henry VIII, for example, famously suffered from gout, as did Isaac Newton and Benjamin Franklin. Gout is a kind of acute arthritis that occurs when high levels of uric acid in the blood lead to inflammatory crystalline deposits in joints, which become red, tender, hot, swollen and often quite painful and debilitating. (The image above is a visually extreme example: Monosodium urate crystals have accumulated from repeated attacks of gout in finger joints. Called tophus formations, these accumulations can impair joint function and may break through the skin.) In recent years, gout has made a comeback of sorts, thanks in part to a Western diet that’s overly rich and abundant. Rates of gout approximately doubled between 1990 and 2010. An estimated 1 to 2 percent of Americans will, at some point in their lives, deal with gout. Genetics also plays a significant role. A study earlier this year identified 18 new genetic variations that increase uric acid levels in the blood. While that kind of research presses on, there are plenty of things people can do to avoid gout. Easiest are dietary controls: Gout has a strong association with excessive consumption of alcohol, fructose-sweetened drinks, meat and seafood. Other triggers are physical trauma and surgery. Gout frequently occurs in combination with other medical problems, such as metabolic syndrome, obesity, hypertension and insulin resistance. Treatment of gout typically involves temporary measures to ease symptoms of an acute attack and lifestyle changes and medications for long-term therapy. These include non-steroidal anti-inflammatory drugs and compounds like colchicine, pegloticase and allopurinol.
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Gout with tophus formations in the index and little fingers. Image courtesy of the American Society for Surgery of the Hand.

Gout on a limb

Gout was once called “the disease of kings” or “the rich man’s disease” because it was most commonly associated with excessive consumption of food and alcohol, something that only aristocrats and higher levels of society could afford to indulge.

The English King Henry VIII, for example, famously suffered from gout, as did Isaac Newton and Benjamin Franklin.

Gout is a kind of acute arthritis that occurs when high levels of uric acid in the blood lead to inflammatory crystalline deposits in joints, which become red, tender, hot, swollen and often quite painful and debilitating.

(The image above is a visually extreme example: Monosodium urate crystals have accumulated from repeated attacks of gout in finger joints. Called tophus formations, these accumulations can impair joint function and may break through the skin.)

In recent years, gout has made a comeback of sorts, thanks in part to a Western diet that’s overly rich and abundant. Rates of gout approximately doubled between 1990 and 2010. An estimated 1 to 2 percent of Americans will, at some point in their lives, deal with gout.

Genetics also plays a significant role. A study earlier this year identified 18 new genetic variations that increase uric acid levels in the blood.

While that kind of research presses on, there are plenty of things people can do to avoid gout. Easiest are dietary controls: Gout has a strong association with excessive consumption of alcohol, fructose-sweetened drinks, meat and seafood. Other triggers are physical trauma and surgery.

Gout frequently occurs in combination with other medical problems, such as metabolic syndrome, obesity, hypertension and insulin resistance.

Treatment of gout typically involves temporary measures to ease symptoms of an acute attack and lifestyle changes and medications for long-term therapy. These include non-steroidal anti-inflammatory drugs and compounds like colchicine, pegloticase and allopurinol.