CHICAGO (AP) - American children eat as much salt as adults - about 1,000 milligrams too much, or the same amount as in just one Big Mac. Extra salt is linked with higher blood pressure, even in kids, but government research says those who are overweight and obese may be most vulnerable to its effects.
The new findings from the Centers for Disease Control and Prevention were published online Monday in the journal Pediatrics.
Previous research has shown similar results in adults but studies on salt, weight and blood pressure are scarce in children.
The CDC researchers looked at data on 6,200 kids aged 8 to 18 involved in 2003-08 national health surveys. The children were asked twice over several days to detail all foods they'd eaten the previous day; the researchers calculated salt intake from their answers.
Overall, 15 percent had either high blood pressure or slightly elevated blood pressure called prehypertension.
Those who ate the most salt faced double the risk of having elevated blood pressure, compared with those who ate few salty foods. But among overweight or obese kids, the risk was more than triple.
The recommended daily salt or sodium intake for kids and adults is no more than 1 teaspoon daily, or about 2,300 milligrams. On average, study kids ate 3,300 milligrams daily.
CDC researcher Quanhe (SHWAH'-nuh) Yang says it's unclear why heavier kids would be more sensitive to salt but it could be due to obesity-related hormone changes. The results raise concerns because studies have shown that elevated blood pressure in childhood, even just prehypertension, can lead to full-fledged high blood pressure in adulthood and potentially premature heart disease.
Prehypertension and high blood pressure in children younger than 17 depend on age, height and gender.
In those 18 and up, readings between 120 over 80 and 140 over 90 are prehypertension; 140 over 90 and higher is high blood pressure.
___
Online:
Pediatrics: http://www.pediatrics.org
CDC: http://www.cdc.gov
Blood pressure charts: http://tinyurl.com/8k6egur
___
AP Medical Writer Lindsey Tanner can be reached at http://www.twitter.com/LindseyTanner
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Sunday, September 16, 2012
Thursday, September 13, 2012
Study Links Age to Kids' Weight Gain After Tonsillectomy
A Johns Hopkins study has tied weight gains in children who underwent tonsillectomies to their age at the time of surgery. The results should end speculation in many families that a child's weight gain was caused by the reason for the surgery. Both my daughter and I had tonsillectomies as children and saw a jump on the scale afterward.
The Baltimore researchers studied 115 area children. They discovered that significant weight gains occurred in many under the age of 6, but not in older children, according to Newswise.
In prior generations, doctors used tonsillectomy primarily to treat inflamed or infected tonsils. These days, its most common use is as a treatment for breathing disorders during sleep, such as sleep apnea after other methods fail, says the Mayo Clinic. The procedure also treats recurring or severe tonsillitis, complications associated with enlarged tonsils, and other rare diseases of the tonsils.
Both the tonsils and the adenoids are collections of immune cells located behind the lymph glands. They're positioned in the mouth and behind the patient's nasal passages, according to MedicineNet. It's easiest to picture them as two oval-shaped pads on each side of the back of the throat.
For years, experts believed that weight gain after tonsillectomy was linked to the most common reason to perform the procedure: sleep apnea. The Baltimore study is the first to largely dispel this belief and is also considered the biggest to evaluate weight gain in each age group through age 17.
The researchers hope their results will bring relief to parents concerned that their overweight adolescent children will gain even more weight after the surgery. The results suggest that only children between 2 and 6 who are at normal weight or who are underweight will experience a significant weight gain.
My daughter and I were each 5 when our respective doctors advised tonsillectomies and adenoidectomies. Both of us were close to the limit on charts for normal weight prior to the surgery, but we didn't stand out as overly heavy in a group. My baby book states that within six months after the surgery, this had changed. By the end of kindergarten, my daughter was also overweight.
The Maryland study looked at the records of children between 6 months and 18 years old who had undergone tonsillectomies at the Johns Hopkins Outpatient Center between 2008 and 2011. The average post-surgical weight gain was 2 to 5 pounds and was directly tied to the child's age, not the reason for the surgery.
Parents who remain concerned about the link between age and kids' weight gain after tonsillectomy can use this information to plan for reductions in daily calories if their children fall into the affected age group. The researchers plan to next investigate exactly why age affects a weight gain after this type of surgery.
Vonda J. Sines has published thousands of print and online health and medical articles. She specializes in diseases and other conditions that affect the quality of life.
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Wednesday, September 12, 2012
Helping kids be more sun-safe is a challenge: study
NEW YORK (Reuters Health) - Pediatricians' offices that offer more extensive counseling and information on safer sun practices are no more likely to have parents who follow that advice than offices that offer less intensive counseling, according to a new study.
Another problem: Kids who pursued physical exercise were twice as likely to suffer sunburns. That wasn't surprising, but it concerned the study's authors because the brochures about exercise were separate from those about sun protection and avoiding rays between 10 a.m. and 4 p.m. - meaning some kids might get one message, but not the other.
'Physicians are in the habit of writing prescriptions and advising how to use the medication. It is a huge step for physicians to take the step of engaging the parent/child in the decision to change behavior,' Dr. June Robinson, the senior author of the study, told Reuters Health by email.
It's possible that the way pediatricians offer such counseling - more as a prescription rather than as a way to engage parents and find ways to change their behavior - led to the results, said Robinson, a dermatology professor at Northwestern University Feinberg School of Medicine.
In 2011, the American Academy of Pediatrics recommended that children's doctors should advise their patients about sunburns and tanning.
To get a sense of what advice doctors offer, Robinson and her colleagues surveyed 30 medical staff members at three pediatricians' offices in the Chicago area about their recommendations regarding sun protection.
One office provided the most extensive counseling on sun protection, offering it year-round during regular check-ups, physical exams and when the child came in with a sunburn.
This included advice on wearing and reapplying sun block and protective clothing and seeking shade.
The office that provided the least extensive counseling only advised families about sun protection when they were about to go on a family vacation or to summer camp or when the child had a sunburn.
Staff there also only offered recommendations on wearing sun block.
The other office fell somewhere between the two in how much sun protection counseling it provided.
Robinson's colleagues then surveyed 100 parents who had visited one of the offices with a child between nine and 16 years old.
They asked the parents about their children's behaviors, such as how long they spent in the sun, whether they used indoor tanning, how many sunburns they had had, and whether they used sun block.
The researchers found that the parents who visited the office with the most extensive counseling were no more likely to practice sun-safe habits than the parents who visited the office that offered the least amount of advice.
For instance, children who were seen at the office that gave the most advice scored an average of 10 on a 39-point scale of how well they were sun-protected, compared to a score of 12 among children seen at the office that offered the least advice.
A score of one is considered best protected, while 39 is totally unprotected from the sun.
When Robinson's group took into account factors such as the child's age and skin tone, the differences between the offices were so small that they were likely due to chance.
And those children who exercised outdoors between 10 a.m. and 4 p.m. 'were twice as likely to use inadequate sun protection and sustain sunburns,' according to the study, than those who performed exercise outside of those hours.
COMMUNICATION CHANGES
Robinson said that doctors can be effective at promoting behaviors among families, but that they might need to change their communication style.
'Communication by physicians with parents in a way that incorporates the principles of motivational interviewing, a patient-centered technique that attempts to engage patients in order to find reasons to change behavior that resonate with each individual, may be more effective in promoting behavioral change than admonitions to use sunscreen,' she said.
Lori Crane, a professor of community and behavioral health at the Colorado School of Public Health, has found in an earlier study that doctors who do offer more extensive counseling on sun protection end up with patients more likely to stick to that advice.
'The methodology in (the current) article is not really very strong for coming up with this conclusion that sun protection counseling doesn't have an effect,' said Crane, who did not participate in the latest research.
Crane pointed out that there's no direct measure of how much counseling each family received, leaving room for the possibility that some families at each office received more or less.
Robinson and her colleagues write in their report in The Journal of Pediatrics that because they didn't directly observe the counseling, there could have been potential errors in how much the staff remembered giving.
However, 'since these are stable and well established practices, the pediatricians have a continuing relationship with the families and have counseled prior to the survey,' she said.
Dr. Richard Roetzheim, a professor of family medicine at the University of South Florida, who was not involved in the study, said he 'wasn't really convinced by this study that counseling doesn't work.'
However, he was pleased to see a study like this.
'I think physicians are increasingly being called on to change patients' behaviors,' Roetzheim told Reuters Health, and it's important to see what works.
SOURCE: http://bit.ly/Pble7S The Journal of Pediatrics, online September 5, 2012.
This article is brought to you by RELATIONSHIPS ADVICE.
Another problem: Kids who pursued physical exercise were twice as likely to suffer sunburns. That wasn't surprising, but it concerned the study's authors because the brochures about exercise were separate from those about sun protection and avoiding rays between 10 a.m. and 4 p.m. - meaning some kids might get one message, but not the other.
'Physicians are in the habit of writing prescriptions and advising how to use the medication. It is a huge step for physicians to take the step of engaging the parent/child in the decision to change behavior,' Dr. June Robinson, the senior author of the study, told Reuters Health by email.
It's possible that the way pediatricians offer such counseling - more as a prescription rather than as a way to engage parents and find ways to change their behavior - led to the results, said Robinson, a dermatology professor at Northwestern University Feinberg School of Medicine.
In 2011, the American Academy of Pediatrics recommended that children's doctors should advise their patients about sunburns and tanning.
To get a sense of what advice doctors offer, Robinson and her colleagues surveyed 30 medical staff members at three pediatricians' offices in the Chicago area about their recommendations regarding sun protection.
One office provided the most extensive counseling on sun protection, offering it year-round during regular check-ups, physical exams and when the child came in with a sunburn.
This included advice on wearing and reapplying sun block and protective clothing and seeking shade.
The office that provided the least extensive counseling only advised families about sun protection when they were about to go on a family vacation or to summer camp or when the child had a sunburn.
Staff there also only offered recommendations on wearing sun block.
The other office fell somewhere between the two in how much sun protection counseling it provided.
Robinson's colleagues then surveyed 100 parents who had visited one of the offices with a child between nine and 16 years old.
They asked the parents about their children's behaviors, such as how long they spent in the sun, whether they used indoor tanning, how many sunburns they had had, and whether they used sun block.
The researchers found that the parents who visited the office with the most extensive counseling were no more likely to practice sun-safe habits than the parents who visited the office that offered the least amount of advice.
For instance, children who were seen at the office that gave the most advice scored an average of 10 on a 39-point scale of how well they were sun-protected, compared to a score of 12 among children seen at the office that offered the least advice.
A score of one is considered best protected, while 39 is totally unprotected from the sun.
When Robinson's group took into account factors such as the child's age and skin tone, the differences between the offices were so small that they were likely due to chance.
And those children who exercised outdoors between 10 a.m. and 4 p.m. 'were twice as likely to use inadequate sun protection and sustain sunburns,' according to the study, than those who performed exercise outside of those hours.
COMMUNICATION CHANGES
Robinson said that doctors can be effective at promoting behaviors among families, but that they might need to change their communication style.
'Communication by physicians with parents in a way that incorporates the principles of motivational interviewing, a patient-centered technique that attempts to engage patients in order to find reasons to change behavior that resonate with each individual, may be more effective in promoting behavioral change than admonitions to use sunscreen,' she said.
Lori Crane, a professor of community and behavioral health at the Colorado School of Public Health, has found in an earlier study that doctors who do offer more extensive counseling on sun protection end up with patients more likely to stick to that advice.
'The methodology in (the current) article is not really very strong for coming up with this conclusion that sun protection counseling doesn't have an effect,' said Crane, who did not participate in the latest research.
Crane pointed out that there's no direct measure of how much counseling each family received, leaving room for the possibility that some families at each office received more or less.
Robinson and her colleagues write in their report in The Journal of Pediatrics that because they didn't directly observe the counseling, there could have been potential errors in how much the staff remembered giving.
However, 'since these are stable and well established practices, the pediatricians have a continuing relationship with the families and have counseled prior to the survey,' she said.
Dr. Richard Roetzheim, a professor of family medicine at the University of South Florida, who was not involved in the study, said he 'wasn't really convinced by this study that counseling doesn't work.'
However, he was pleased to see a study like this.
'I think physicians are increasingly being called on to change patients' behaviors,' Roetzheim told Reuters Health, and it's important to see what works.
SOURCE: http://bit.ly/Pble7S The Journal of Pediatrics, online September 5, 2012.
This article is brought to you by RELATIONSHIPS ADVICE.
Tuesday, September 11, 2012
More hospital errors when kids have chronic ills
NEW YORK (Reuters Health) - Medical errors affect about three percent of hospitalized children in the U.S., with the risk being higher if they have a chronic health condition, a new study suggests.
Using a government database, researchers found that of children hospitalized in 38 U.S. states in 2006, 44 percent had at least one chronic health problem, such as asthma, a digestive disorder, diabetes or cancer.
Among hospitalized kids with no chronic health problems, 1.3 percent were affected by a medical error; the figure among children with a chronic condition was just over five percent.
The results, reported in the journal Pediatrics, are not surprising, the researchers say. In fact, they expected to see a higher error rate among kids with chronic disorders.
'They may stay in the hospital longer, and their condition may be more complicated' compared with kids free of chronic ills, explained senior researcher Dr. Huiyun Xiang, of Nationwide Children's Hospital in Columbus, Ohio.
It's not clear from the findings how serious the medical errors were, or how often they caused kids harm. The errors were not even necessarily 'mistakes,' per se, Xiang said.
The researchers used hospital discharge records and counted certain 'codes' as a medical error. That included codes like 'complications peculiar to certain specified procedures.'
Adverse reactions to a medication, an infection following surgery and even bedsores are more general examples of the kinds of potentially preventable events considered medical errors.
The bottom line, according to the researchers, is that everyone needs to be aware of the greater error risk when kids have chronic health problems.
And the risk appears to climb in tandem with the number of conditions a child has. Among kids with one chronic ill, the error rate was around three percent, while for those with two the rate was closer to seven percent.
For parents, Xiang said the risk of medical error should be kept in context. 'Even the overall rate of 5.3 percent among children with chronic conditions is relatively low,' he noted.
This study did not look at potential fixes, Xiang said. But he noted that the federal Agency for Healthcare Research and Quality (AHRQ) has been funding projects to improve hospital patients' safety - like preventing infections, which are the most common complication of hospital stays nationwide.
Those efforts stemmed largely from a 1999 report by the Institute of Medicine (IOM), which found that medical errors cost the U.S. $17 billion to $29 billion a year - and kill nearly 98,000 people.
The IOM said that many errors arise because the healthcare system is 'fragmented,' and stressed that improving safety needs to be a 'team sport.'
AHRQ suggests that hospital patients, or parents of patients, help protect themselves by asking questions. One step is to make sure that someone - like your pediatrician - is coordinating your child's care and making sure everyone is on the same page.
Xiang also said it's important for parents to understand their child's at-home medication regimen, especially if there are multiple health conditions.
'Parents should be very careful in monitoring their child's medication at home,' he said.
Xiang pointed to a recent study in which researchers made home visits to families of children with sickle cell disease or epilepsy. Looking at 280 medication uses, they found 61 errors - like giving the child the wrong dose, or missing a dose altogether.
SOURCE: http://bit.ly/S4kiB8 Pediatrics, online September 10, 2012.
This article is brought to you by RELATIONSHIPS ADVICE.
Using a government database, researchers found that of children hospitalized in 38 U.S. states in 2006, 44 percent had at least one chronic health problem, such as asthma, a digestive disorder, diabetes or cancer.
Among hospitalized kids with no chronic health problems, 1.3 percent were affected by a medical error; the figure among children with a chronic condition was just over five percent.
The results, reported in the journal Pediatrics, are not surprising, the researchers say. In fact, they expected to see a higher error rate among kids with chronic disorders.
'They may stay in the hospital longer, and their condition may be more complicated' compared with kids free of chronic ills, explained senior researcher Dr. Huiyun Xiang, of Nationwide Children's Hospital in Columbus, Ohio.
It's not clear from the findings how serious the medical errors were, or how often they caused kids harm. The errors were not even necessarily 'mistakes,' per se, Xiang said.
The researchers used hospital discharge records and counted certain 'codes' as a medical error. That included codes like 'complications peculiar to certain specified procedures.'
Adverse reactions to a medication, an infection following surgery and even bedsores are more general examples of the kinds of potentially preventable events considered medical errors.
The bottom line, according to the researchers, is that everyone needs to be aware of the greater error risk when kids have chronic health problems.
And the risk appears to climb in tandem with the number of conditions a child has. Among kids with one chronic ill, the error rate was around three percent, while for those with two the rate was closer to seven percent.
For parents, Xiang said the risk of medical error should be kept in context. 'Even the overall rate of 5.3 percent among children with chronic conditions is relatively low,' he noted.
This study did not look at potential fixes, Xiang said. But he noted that the federal Agency for Healthcare Research and Quality (AHRQ) has been funding projects to improve hospital patients' safety - like preventing infections, which are the most common complication of hospital stays nationwide.
Those efforts stemmed largely from a 1999 report by the Institute of Medicine (IOM), which found that medical errors cost the U.S. $17 billion to $29 billion a year - and kill nearly 98,000 people.
The IOM said that many errors arise because the healthcare system is 'fragmented,' and stressed that improving safety needs to be a 'team sport.'
AHRQ suggests that hospital patients, or parents of patients, help protect themselves by asking questions. One step is to make sure that someone - like your pediatrician - is coordinating your child's care and making sure everyone is on the same page.
Xiang also said it's important for parents to understand their child's at-home medication regimen, especially if there are multiple health conditions.
'Parents should be very careful in monitoring their child's medication at home,' he said.
Xiang pointed to a recent study in which researchers made home visits to families of children with sickle cell disease or epilepsy. Looking at 280 medication uses, they found 61 errors - like giving the child the wrong dose, or missing a dose altogether.
SOURCE: http://bit.ly/S4kiB8 Pediatrics, online September 10, 2012.
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Monday, September 10, 2012
More California Private School Parents Opting Out of Vaccines
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Thursday, September 6, 2012
Cranberry juice may beat kids' bladder infections
NEW YORK (Reuters Health) - Cranberry juice rich in certain antibacterial substances may help prevent repeat urinary tract infections in kids, a small study suggests.
Researchers found that cranberry juice made with high concentrations of proanthocyanidins (PACs) cut kids' risk of repeat urinary tract infections by two-thirds, versus a comparison juice.
Since the juice on your supermarket's shelves may not have that PAC level, the researchers say their findings are not an endorsement of any product.
But the results, published in the Journal of Urology, do give support to cranberry as a UTI fighter, according to a pediatric urologist not connected to the study.
PACs are the compounds thought to give cranberries their bacteria-fighting potential. Women have long turned to cranberry juice and supplements to help prevent recurrent urinary tract infections (UTIs) - though studies have been mixed on whether they work.
There has been little research on kids, even though UTIs are relatively common in children. Girls have about an 8 percent chance of contracting the infection at some point in childhood; boys have a 2 percent chance.
Besides being uncomfortable, recurrent UTIs can eventually damage the kidneys in some children. So doctors may prescribe antibiotics to help prevent them.
But antibiotics can have side effects, and using them long-term can breed drug-resistant bacteria. So researchers are looking at whether cranberry products can be a good alternative.
For the new study, doctors at the University of British Columbia in Vancouver, Canada, recruited 40 children who'd had at least two UTIs in the past year. They randomly assigned the kids to drink one of two juices made for the study: a cranberry juice rich in PACs or a juice free of all 'cranberry products.'
Over the next year, kids who drank cranberry juice had UTIs at a rate of 0.4 per child, compared with 1.15 in the comparison group.
The power of cranberries against UTIs 'was initially regarded as an old wives' tale,' said Dr. Hiep Nguyen of Boston Children's Hospital, who was not involved in the study.
But Nguyen said he now often recommends cranberry - either juice or supplements - when kids have recurrent UTIs.
'It can be a great alternative to prophylactic (preventive) antibiotics,' Nguyen said.
That doesn't mean cranberry is the cure-all. If a child has frequent UTIs, Nguyen said, antibiotics may be necessary to 'break the cycle.' On top of that, many children's UTIs are related to less-than-ideal bathroom habits - like 'holding it in,' rather than going when they need to.
Drinking enough fluids, going to the bathroom regularly, and - if needed - tackling constipation problems are all considered important in warding off kids' UTIs.
So Nguyen cautioned parents against simply running to the grocery store for cranberry juice. 'They still should see a doctor, so they can try to address the underlying problem,' Nguyen said.
What's more, there's no guarantee that the cranberry juice you buy would have the PAC content that the juice in this study did.
'The findings of this study should not be construed as an endorsement of any commercially available cranberry products,' write the researchers, led by Dr. Kourosh Afshar. (Afshar could not be reached for comment.)
Nguyen agreed that juice can be tricky. 'Pure cranberry juice often doesn't taste so good,' he noted. So manufacturers often mix it with something more palatable, like apple juice, or add a lot of sugar.
Cranberry juice mixed with other juices would likely have lower PAC levels. If there's added sugar, that means calories; drinking a lot of sugary juice can also cause diarrhea in kids.
'We do worry about the sugar content,' Nguyen said.
So it would be important, he noted, not to overdo cranberry juice. In this study, the daily dose prescribed to each child was based on body weight.
Cranberry tablets are the other option. But no one knows the exact dose needed to prevent any one child's UTIs. Right now, it's basically a matter of following the product's labeling, according to Nguyen.
Six kids in each group of the study dropped out before they had completed it. The top reasons were the parents' belief that the juice wasn't working, and kids just refusing to drink it.
Getting children to drink cranberry juice can be a challenge, Nguyen noted - especially the pure variety without a ton of sugar.
Ocean Spray provided both juices used in the study. The work was funded by the Lions Gate Healthcare Research Foundation.
SOURCE: http://bit.ly/RpIBZm Journal of Urology, online August 20, 2012.
This article is brought to you by RELATIONSHIPS ADVICE.
Researchers found that cranberry juice made with high concentrations of proanthocyanidins (PACs) cut kids' risk of repeat urinary tract infections by two-thirds, versus a comparison juice.
Since the juice on your supermarket's shelves may not have that PAC level, the researchers say their findings are not an endorsement of any product.
But the results, published in the Journal of Urology, do give support to cranberry as a UTI fighter, according to a pediatric urologist not connected to the study.
PACs are the compounds thought to give cranberries their bacteria-fighting potential. Women have long turned to cranberry juice and supplements to help prevent recurrent urinary tract infections (UTIs) - though studies have been mixed on whether they work.
There has been little research on kids, even though UTIs are relatively common in children. Girls have about an 8 percent chance of contracting the infection at some point in childhood; boys have a 2 percent chance.
Besides being uncomfortable, recurrent UTIs can eventually damage the kidneys in some children. So doctors may prescribe antibiotics to help prevent them.
But antibiotics can have side effects, and using them long-term can breed drug-resistant bacteria. So researchers are looking at whether cranberry products can be a good alternative.
For the new study, doctors at the University of British Columbia in Vancouver, Canada, recruited 40 children who'd had at least two UTIs in the past year. They randomly assigned the kids to drink one of two juices made for the study: a cranberry juice rich in PACs or a juice free of all 'cranberry products.'
Over the next year, kids who drank cranberry juice had UTIs at a rate of 0.4 per child, compared with 1.15 in the comparison group.
The power of cranberries against UTIs 'was initially regarded as an old wives' tale,' said Dr. Hiep Nguyen of Boston Children's Hospital, who was not involved in the study.
But Nguyen said he now often recommends cranberry - either juice or supplements - when kids have recurrent UTIs.
'It can be a great alternative to prophylactic (preventive) antibiotics,' Nguyen said.
That doesn't mean cranberry is the cure-all. If a child has frequent UTIs, Nguyen said, antibiotics may be necessary to 'break the cycle.' On top of that, many children's UTIs are related to less-than-ideal bathroom habits - like 'holding it in,' rather than going when they need to.
Drinking enough fluids, going to the bathroom regularly, and - if needed - tackling constipation problems are all considered important in warding off kids' UTIs.
So Nguyen cautioned parents against simply running to the grocery store for cranberry juice. 'They still should see a doctor, so they can try to address the underlying problem,' Nguyen said.
What's more, there's no guarantee that the cranberry juice you buy would have the PAC content that the juice in this study did.
'The findings of this study should not be construed as an endorsement of any commercially available cranberry products,' write the researchers, led by Dr. Kourosh Afshar. (Afshar could not be reached for comment.)
Nguyen agreed that juice can be tricky. 'Pure cranberry juice often doesn't taste so good,' he noted. So manufacturers often mix it with something more palatable, like apple juice, or add a lot of sugar.
Cranberry juice mixed with other juices would likely have lower PAC levels. If there's added sugar, that means calories; drinking a lot of sugary juice can also cause diarrhea in kids.
'We do worry about the sugar content,' Nguyen said.
So it would be important, he noted, not to overdo cranberry juice. In this study, the daily dose prescribed to each child was based on body weight.
Cranberry tablets are the other option. But no one knows the exact dose needed to prevent any one child's UTIs. Right now, it's basically a matter of following the product's labeling, according to Nguyen.
Six kids in each group of the study dropped out before they had completed it. The top reasons were the parents' belief that the juice wasn't working, and kids just refusing to drink it.
Getting children to drink cranberry juice can be a challenge, Nguyen noted - especially the pure variety without a ton of sugar.
Ocean Spray provided both juices used in the study. The work was funded by the Lions Gate Healthcare Research Foundation.
SOURCE: http://bit.ly/RpIBZm Journal of Urology, online August 20, 2012.
This article is brought to you by RELATIONSHIPS ADVICE.
Wednesday, September 5, 2012
How to apply an evolutionary hypothesis about gestation to your pregnancy
First things first. Let s get you up to speed on the gestation research that fed the media that fed the pregnancy questions that sparked this post.
Some impressive colleagues and I just published a paper (1) that pulls the rug out from under a classic anthropological hypothesis that suggests the bipedal-adapted human pelvis constrains human gestation and fetal growth.
The obstetrical dilemma (OD) hypothesis
Simultaneous selection for big-brained (or simply big) babies and bipedal locomotion caused a dilemma because while babies must be large, birth canals must remain small. The consequences of this dilemma, which are often called solutions and tradeoffs, include (a) difficult and dangerous childbirth with universal assistance due to the tight fit, (b) relatively underdeveloped, helpless, often termed secondarily altricial neonates compared to all other primates which are precocial, and (c) compromised or sub-optimal female locomotion, since (d) selection has favored sexual dimorphism in the human pelvis with females having not just relatively wider but absolutely wider dimensions of the birth canal.
Notice how the OD skillfully ties together many unique or fascinating phenomena in human evolution such as human bipedalism, human encephalization, hellish human childbirth, helpless human babies, male-biased human athletic ability, and broad ladies' hips. And we haven't proven this popular story wrong. But our paper throws some serious doubt on it, demonstrating how little of it holds up to current evidence.
For starters, in primate and mammalian comparative contexts, human gestation and fetal growth are not constrained. If anything it looks like we re weirder in the other extreme, having slightly longer gestations than other primates and having relatively big babies. That we're not particularly different in these terms, and definitely not limited, has all been known for decades, as has the understanding that the size of the mammalian mother (a useful proxy for metabolism) predicts the length of gestation and the size of the offspring.
With all this research out there showing how gestation seems to be limited primarily by maternal metabolism, why this notion that we re compromised by our pelves? Why this notion that we could or should keep babies in our wombs longer if it wasn't for bipedalism keeping our birth canals too small for gestating any longer, for growing bigger babies? It s unclear especially given how there is little evidence that wider hips are bad for bipedal walking and running or that slightly wider ones that would make childbirth easier or that would accommodate a more developed neonate would be problematic.
So as an alternative to this weakened hypothesis that the human pelvis constrains gestation length and fetal growth we offered up a new one born of the metabolic observations described above.
The EGG hypothesis
What limits fetal growth during pregnancy? The OD says it's the pelvis implying it's a unique constraint due to bipedalism. But the EGG hypothesis suggests that the primary constraint on fetal growth and gestation length is maternal metabolism (energetics, growth, gestation).
The EGG hypothesizes that mothers give birth when they do because they cannot possibly give any more energy into gestation and fetal growth. And when you look at the data available on pregnancy and lactation metabolism in our species, it suggests that right around 9 months of gestation, mothers reach the metabolic ceiling for most humans.
Here's Herman s Figure 3 from our paper, showing the EGG for humans, plotted with real metabolic data. Circles are the offspring, squares are the mother. Notice how fetal energy demands increase exponentially as the end of a normal human gestation period approaches. To keep it in any longer, mother would have to burst through her normal metabolic ceiling. Instead, she gives birth and remains in a safe and feasible metabolic zone.
The starred dot is a human infant at the developmental equivalency of a newborn chimpanzee. This is the thought experiment that Adolf Portmann (2) and Stephen Jay Gould (3) famously wrote about. That's the age you'd have to birth a human baby to be as advanced as a newborn chimp, since we're born more helpless than chimps. Keeping a fetus in this long that is, adding 7 or more months to our gestation would be physiologically impossible because it would require a mother to exceed and sustain 2.1x the basal metabolic rate (BMR) the ceiling for most humans. Our relative helplessness at birth is indicating how much more neurological growth we have to achieve during our lives, after we re born, than do chimps and other relatives with their smaller brains than ours.
The EGG is a more general incarnation and a broader application of Peter Ellison's "metabolic crossover hypothesis" for the timing of human birth (4). The EGG branches out beyond our species, considering humans to operate within the physiological confines of other primates and mammals. But comparable data for other species, for testing the EGG, are not yet available to our knowledge. This is one of the infrequent times you ll see a human model that s hypothesized to work for other species rather than the other way around!
We named the hypothesis, EGG, for ease of communication, not because we're eggomaniacs. We were tempted to call it HAM (humans are mammals) but felt that EGG better described the idea and was also adorable considering how babies are made.
Part of what has caused many of us to struggle with the OD is that humans do just fine in the face of the tight fit at birth. Just because there's a tight fit, just because childbirth is terrifying, just because it's not an easy or enjoyable experience, that's not necessarily a "bad" thing evolutionarily. Clearly it's the opposite. It's a good thing. We're here to think about it! It can't possibly be "bad" if we keep having babies. The species abides. When you look at childbirth not as a biological failure, or as God's plague on lascivious women invited by Eve, but when you see it instead as a raging success, the obstetrical dilemma hypothesis is much easier to doubt.
The widespread popularity of the OD may be rooted in its adaptationist appeal, where nonoptimality (e.g. human altriciality, or helplessness and relative underdeveloped-ness at birth) is explained as a contribution to the best possible design of the whole (e.g. big brain and efficient bipedalism). Gould and Lewontin (5) famously criticized the adaptationist programme by cautioning that organisms must be analyzed as integrated wholes that are constrained by phyletic heritage, pathways of development, and general architecture and that the constraints themselves become more interesting and more important in delimiting pathways of change than the selective force that may mediate change when it occurs. They faulted the adaptationist approach for failing to consider alternatives to adaptive stories and for its reliance on plausibility alone as a criterion for accepting speculative tales. From this perspective, the EGG is preferred over the OD. Rather than rooting the evolution of human altriciality in a compromise between adaptations for big brains and adaptations for bipedalism, instead it s explained by more basic, conserved, phyletic constraints on pathways of development and general architecture at play (e.g. gestation, pregnancy and fetal growth).
The OD is not killed by the EGG. It's just put in a less omnipotent place. The heaviest burdens should always be on supporting hypotheses for human exceptionalism; we should not default to them. Humans are animals/ mammals/ primates/ hominoids and when we fail at supporting our default view, that's when we can claim human exceptionalism.
***
There have been some very personal reactions to the press that came with our recent paper on the evolution of human gestation length. I don t mean the what do you mean we evolved? kind. I mean the what about my short/ long/ weird pregnancy? kind.
This research has always been wrapped up in questions about human variation and even draws upon observations of human variation in gestation length. So I'm not surprised it's causing people to reflect on their own experiences. And I'm also not totally surprised because I've been on the planet long enough to know that if you claim to know anything about pregnancy, you get all the stories.
But I didn't fully anticipate how strongly our work about humans as a species would be seen as work about "me." I guess we're only human.
The following is for all the people who read media about our paper and are dying to know what it's got to do with their own pregnancy.
Some things first.
1. I see the world through evolution goggles. Take that as close to literal as you can.
2. I have more scholarly experience with skeletonized (dead) and fossilized (extremely dead) humans than living ones.
3. I am not trained in medicine or health sciences.
4. I will not give medical advice.
5. I do not know what doctors are, or should be, telling pregnant women about eating and exercise.
6. It took me five years to write this paper from first notes to publication and I needed the help of brilliant experts (1) to make it as strong as it is. I do not expect to fully appreciate its implications on the week it is published not for human evolution, not for pregnant human mothers, not yet! If you have ideas, go on with your bad self and test them! I'll try to do the same.
Here we go, then.
How to apply an evolutionary hypothesis about gestation to your pregnancy
#1 Thing to think about.
Evolution is everything about you, but it is not all about you.
When reports of our research say "moms" we're not talking about you in particular. We're talking about "moms" in a general comparative evolutionary context, species-wide, primate-wide, mammal-wide.
#2 Thing to think about.
The EGG hypothesis explains species-level phenomena
Many evolutionary papers like ours are about understanding species level phenomena and comparing differences and similarities between species to better understand those phenomena, to explain whether patterns exist and, if they do, how or why.
So using the EGG hypothesis to explain why you gestated 9 days past your due date is a little bit like this: Try using the broad ecological and biological rules and patterns that explain variation in body size across mammals to explain why Fred the elephant is 9 cm taller than Frank the elephant. That's a challenge. That's what you're attempting to do if you read our paper (or reports on it) and think of yourself first rather than your species.
Here's another way to think about it. You might have seen our paper described as finding, "Metabolism, not the hips, limits gestation." Metabolism might get you thinking of yourself but the hips hypothesis (obstetrical dilemma; OD) never did right? I could be so wrong but nobody thinks that there's some way the fetus can sense when its head or shoulders are about to be too big to fit through the birth canal at which point it initiates labor so it can escape. Nobody thinks that the mom's body can detect when the baby is about to get too big to pass through her birth canal at which point she initiates labor so it can escape. Nobody really thinks that these sorts of detectors and mechanisms exist in fetuses or mothers do they? (It's possible but I don't know of any literature suggesting this.) So the hip constraint hypothesis (OD) was never about individuals, it's about our species over evolutionary history, with hips shaping our gestation length to be the right length for babies to escape in time. Generations over deep time that's where your brain needs to be with this EGG idea too.
Sure, we need to consider individual human variation, like yours and mine. To formulate the EGG hypothesis we drew heavily upon Peter Ellison's metabolic crossover (MC) hypothesis for the timing of human birth (1, 4): Babies are born when they begin to starve in utero. This happens when the needs of the fetus surpass the mother s ability to meet them or, in other words, cross over to become larger than what the mother can provide. Labor is then triggered and carried out by a complex biochemical process. Some of the evidence he provides includes:
Gestation length can be truncated according to metabolic parameters.
It's a useful method in evolutionary biology to look at variation within a species and use it to hypothesize why variation exists between species. That is what we have done with EGG. Mother's body sizes differ between species like say, humans and orangutans, and so do their metabolic traits. EGG suggests variation in metabolism between species explains variation in gestation length. It predicts that species do not exceed their species specific metabolic ceiling during pregnancy. It will be exciting to find out whether some species give birth well before they reach their metabolic capacity!
Why do we grow babies that seem too big to fit through our birth canals? It s possible that it s mainly a recent phenomenon and a strong hypothesis is that our diets that have radically changed compared to most of our evolutionary history. Many humans have constant and easy access to high calorie foods while pregnant and they can grow bigger babies over longer pregnancies. There are probably genetic, epigenetic, and environmental affects on our modern metabolisms as well. Very much related to these questions is Herman s recent article in the New York Times: "Debunking the Hunter-Gatherer Workout."
#3 Thing to think about.
Evolution is about common ancestry and change over time. Ideals, optimization, standards, greater value in this form, lesser value in that one these do not exist in nature except in our minds.
You worrying that you gestated too long or too little compared to the species average is a bit like you worrying that you're shorter or taller than average, have a larger or smaller head than average, have more saliva than average, or that you can't intentionally fart. Stop worrying about your normal variation. Variation exists because it works. There's safe wiggle room around most traits and sometimes there's even full-on spasmodic dancing room. We'd be extinct if there wasn't any room for variation in how to survive and reproduce. Celebrate your weirdness, your slightly long healthy gestation, your slightly short healthy gestation, your big healthy baby, your small healthy baby, your freckles, your asymmetrical face, your hairy knuckles, your lack of wisdom teeth, your pterodactyl toes. Who cares! If life's getting on with your weird ass, then you can certainly get on with life.
Further, it helps if you don't require EGG to be all about adaptation. It could be. But it could also be just the way it is. Mothers can only gestate so long. Period. The mechanism that initiates labor based on those metabolic cues (MC)? Totally adaptive. The process the EGG explains? Not really. A limit's a limit! It would be physiologically impossible to exceed it. Adaptive ideas aren't necessary for EGG unless it's somehow adaptive to keep the fetus inside mother right up until that threshold, which is possible. But it could also just be the only way to trigger labor. And so we're back to the EGG being just the way it is.
***
So how should you apply this evolutionary hypothesis to your pregnancy?
It sheds light on why it's difficult for humans to give birth. It sheds light on why babies seem so helpless compared to other primates.
But regarding your specific, individual details about gestation length and neonatal size that differ compared to other human mothers and their babies?
Please talk to your doctor who's your main brain on this. And read read read read read, if you're interested.
References
Follow Scientific American on Twitter @SciAm and @SciamBlogs. Visit ScientificAmerican.com for the latest in science, health and technology news.
© 2012 ScientificAmerican.com. All rights reserved.
This article is brought to you by RELATIONSHIP ADVICE.
Some impressive colleagues and I just published a paper (1) that pulls the rug out from under a classic anthropological hypothesis that suggests the bipedal-adapted human pelvis constrains human gestation and fetal growth.
The obstetrical dilemma (OD) hypothesis
Simultaneous selection for big-brained (or simply big) babies and bipedal locomotion caused a dilemma because while babies must be large, birth canals must remain small. The consequences of this dilemma, which are often called solutions and tradeoffs, include (a) difficult and dangerous childbirth with universal assistance due to the tight fit, (b) relatively underdeveloped, helpless, often termed secondarily altricial neonates compared to all other primates which are precocial, and (c) compromised or sub-optimal female locomotion, since (d) selection has favored sexual dimorphism in the human pelvis with females having not just relatively wider but absolutely wider dimensions of the birth canal.
Notice how the OD skillfully ties together many unique or fascinating phenomena in human evolution such as human bipedalism, human encephalization, hellish human childbirth, helpless human babies, male-biased human athletic ability, and broad ladies' hips. And we haven't proven this popular story wrong. But our paper throws some serious doubt on it, demonstrating how little of it holds up to current evidence.
For starters, in primate and mammalian comparative contexts, human gestation and fetal growth are not constrained. If anything it looks like we re weirder in the other extreme, having slightly longer gestations than other primates and having relatively big babies. That we're not particularly different in these terms, and definitely not limited, has all been known for decades, as has the understanding that the size of the mammalian mother (a useful proxy for metabolism) predicts the length of gestation and the size of the offspring.
With all this research out there showing how gestation seems to be limited primarily by maternal metabolism, why this notion that we re compromised by our pelves? Why this notion that we could or should keep babies in our wombs longer if it wasn't for bipedalism keeping our birth canals too small for gestating any longer, for growing bigger babies? It s unclear especially given how there is little evidence that wider hips are bad for bipedal walking and running or that slightly wider ones that would make childbirth easier or that would accommodate a more developed neonate would be problematic.
So as an alternative to this weakened hypothesis that the human pelvis constrains gestation length and fetal growth we offered up a new one born of the metabolic observations described above.
The EGG hypothesis
What limits fetal growth during pregnancy? The OD says it's the pelvis implying it's a unique constraint due to bipedalism. But the EGG hypothesis suggests that the primary constraint on fetal growth and gestation length is maternal metabolism (energetics, growth, gestation).
The EGG hypothesizes that mothers give birth when they do because they cannot possibly give any more energy into gestation and fetal growth. And when you look at the data available on pregnancy and lactation metabolism in our species, it suggests that right around 9 months of gestation, mothers reach the metabolic ceiling for most humans.
Here's Herman s Figure 3 from our paper, showing the EGG for humans, plotted with real metabolic data. Circles are the offspring, squares are the mother. Notice how fetal energy demands increase exponentially as the end of a normal human gestation period approaches. To keep it in any longer, mother would have to burst through her normal metabolic ceiling. Instead, she gives birth and remains in a safe and feasible metabolic zone.
The starred dot is a human infant at the developmental equivalency of a newborn chimpanzee. This is the thought experiment that Adolf Portmann (2) and Stephen Jay Gould (3) famously wrote about. That's the age you'd have to birth a human baby to be as advanced as a newborn chimp, since we're born more helpless than chimps. Keeping a fetus in this long that is, adding 7 or more months to our gestation would be physiologically impossible because it would require a mother to exceed and sustain 2.1x the basal metabolic rate (BMR) the ceiling for most humans. Our relative helplessness at birth is indicating how much more neurological growth we have to achieve during our lives, after we re born, than do chimps and other relatives with their smaller brains than ours.
The EGG is a more general incarnation and a broader application of Peter Ellison's "metabolic crossover hypothesis" for the timing of human birth (4). The EGG branches out beyond our species, considering humans to operate within the physiological confines of other primates and mammals. But comparable data for other species, for testing the EGG, are not yet available to our knowledge. This is one of the infrequent times you ll see a human model that s hypothesized to work for other species rather than the other way around!
We named the hypothesis, EGG, for ease of communication, not because we're eggomaniacs. We were tempted to call it HAM (humans are mammals) but felt that EGG better described the idea and was also adorable considering how babies are made.
Part of what has caused many of us to struggle with the OD is that humans do just fine in the face of the tight fit at birth. Just because there's a tight fit, just because childbirth is terrifying, just because it's not an easy or enjoyable experience, that's not necessarily a "bad" thing evolutionarily. Clearly it's the opposite. It's a good thing. We're here to think about it! It can't possibly be "bad" if we keep having babies. The species abides. When you look at childbirth not as a biological failure, or as God's plague on lascivious women invited by Eve, but when you see it instead as a raging success, the obstetrical dilemma hypothesis is much easier to doubt.
The widespread popularity of the OD may be rooted in its adaptationist appeal, where nonoptimality (e.g. human altriciality, or helplessness and relative underdeveloped-ness at birth) is explained as a contribution to the best possible design of the whole (e.g. big brain and efficient bipedalism). Gould and Lewontin (5) famously criticized the adaptationist programme by cautioning that organisms must be analyzed as integrated wholes that are constrained by phyletic heritage, pathways of development, and general architecture and that the constraints themselves become more interesting and more important in delimiting pathways of change than the selective force that may mediate change when it occurs. They faulted the adaptationist approach for failing to consider alternatives to adaptive stories and for its reliance on plausibility alone as a criterion for accepting speculative tales. From this perspective, the EGG is preferred over the OD. Rather than rooting the evolution of human altriciality in a compromise between adaptations for big brains and adaptations for bipedalism, instead it s explained by more basic, conserved, phyletic constraints on pathways of development and general architecture at play (e.g. gestation, pregnancy and fetal growth).
The OD is not killed by the EGG. It's just put in a less omnipotent place. The heaviest burdens should always be on supporting hypotheses for human exceptionalism; we should not default to them. Humans are animals/ mammals/ primates/ hominoids and when we fail at supporting our default view, that's when we can claim human exceptionalism.
***
There have been some very personal reactions to the press that came with our recent paper on the evolution of human gestation length. I don t mean the what do you mean we evolved? kind. I mean the what about my short/ long/ weird pregnancy? kind.
This research has always been wrapped up in questions about human variation and even draws upon observations of human variation in gestation length. So I'm not surprised it's causing people to reflect on their own experiences. And I'm also not totally surprised because I've been on the planet long enough to know that if you claim to know anything about pregnancy, you get all the stories.
But I didn't fully anticipate how strongly our work about humans as a species would be seen as work about "me." I guess we're only human.
The following is for all the people who read media about our paper and are dying to know what it's got to do with their own pregnancy.
Some things first.
1. I see the world through evolution goggles. Take that as close to literal as you can.
2. I have more scholarly experience with skeletonized (dead) and fossilized (extremely dead) humans than living ones.
3. I am not trained in medicine or health sciences.
4. I will not give medical advice.
5. I do not know what doctors are, or should be, telling pregnant women about eating and exercise.
6. It took me five years to write this paper from first notes to publication and I needed the help of brilliant experts (1) to make it as strong as it is. I do not expect to fully appreciate its implications on the week it is published not for human evolution, not for pregnant human mothers, not yet! If you have ideas, go on with your bad self and test them! I'll try to do the same.
Here we go, then.
How to apply an evolutionary hypothesis about gestation to your pregnancy
#1 Thing to think about.
Evolution is everything about you, but it is not all about you.
When reports of our research say "moms" we're not talking about you in particular. We're talking about "moms" in a general comparative evolutionary context, species-wide, primate-wide, mammal-wide.
#2 Thing to think about.
The EGG hypothesis explains species-level phenomena
Many evolutionary papers like ours are about understanding species level phenomena and comparing differences and similarities between species to better understand those phenomena, to explain whether patterns exist and, if they do, how or why.
So using the EGG hypothesis to explain why you gestated 9 days past your due date is a little bit like this: Try using the broad ecological and biological rules and patterns that explain variation in body size across mammals to explain why Fred the elephant is 9 cm taller than Frank the elephant. That's a challenge. That's what you're attempting to do if you read our paper (or reports on it) and think of yourself first rather than your species.
Here's another way to think about it. You might have seen our paper described as finding, "Metabolism, not the hips, limits gestation." Metabolism might get you thinking of yourself but the hips hypothesis (obstetrical dilemma; OD) never did right? I could be so wrong but nobody thinks that there's some way the fetus can sense when its head or shoulders are about to be too big to fit through the birth canal at which point it initiates labor so it can escape. Nobody thinks that the mom's body can detect when the baby is about to get too big to pass through her birth canal at which point she initiates labor so it can escape. Nobody really thinks that these sorts of detectors and mechanisms exist in fetuses or mothers do they? (It's possible but I don't know of any literature suggesting this.) So the hip constraint hypothesis (OD) was never about individuals, it's about our species over evolutionary history, with hips shaping our gestation length to be the right length for babies to escape in time. Generations over deep time that's where your brain needs to be with this EGG idea too.
Sure, we need to consider individual human variation, like yours and mine. To formulate the EGG hypothesis we drew heavily upon Peter Ellison's metabolic crossover (MC) hypothesis for the timing of human birth (1, 4): Babies are born when they begin to starve in utero. This happens when the needs of the fetus surpass the mother s ability to meet them or, in other words, cross over to become larger than what the mother can provide. Labor is then triggered and carried out by a complex biochemical process. Some of the evidence he provides includes:
Gestation length can be truncated according to metabolic parameters.
- Gestation is shorter in mothers with lower body fat composition and lower metabolic rates (4,6)
- Mothers living at high altitude can give birth earlier than counterparts at low altitude (7)
- Fetal brain size pathology longer gestation (8)
- Increase maternal caloric intake neonatal increase (9)
- Increase maternal caloric intake preterm births decrease (9)
It's a useful method in evolutionary biology to look at variation within a species and use it to hypothesize why variation exists between species. That is what we have done with EGG. Mother's body sizes differ between species like say, humans and orangutans, and so do their metabolic traits. EGG suggests variation in metabolism between species explains variation in gestation length. It predicts that species do not exceed their species specific metabolic ceiling during pregnancy. It will be exciting to find out whether some species give birth well before they reach their metabolic capacity!
Why do we grow babies that seem too big to fit through our birth canals? It s possible that it s mainly a recent phenomenon and a strong hypothesis is that our diets that have radically changed compared to most of our evolutionary history. Many humans have constant and easy access to high calorie foods while pregnant and they can grow bigger babies over longer pregnancies. There are probably genetic, epigenetic, and environmental affects on our modern metabolisms as well. Very much related to these questions is Herman s recent article in the New York Times: "Debunking the Hunter-Gatherer Workout."
#3 Thing to think about.
Evolution is about common ancestry and change over time. Ideals, optimization, standards, greater value in this form, lesser value in that one these do not exist in nature except in our minds.
You worrying that you gestated too long or too little compared to the species average is a bit like you worrying that you're shorter or taller than average, have a larger or smaller head than average, have more saliva than average, or that you can't intentionally fart. Stop worrying about your normal variation. Variation exists because it works. There's safe wiggle room around most traits and sometimes there's even full-on spasmodic dancing room. We'd be extinct if there wasn't any room for variation in how to survive and reproduce. Celebrate your weirdness, your slightly long healthy gestation, your slightly short healthy gestation, your big healthy baby, your small healthy baby, your freckles, your asymmetrical face, your hairy knuckles, your lack of wisdom teeth, your pterodactyl toes. Who cares! If life's getting on with your weird ass, then you can certainly get on with life.
Further, it helps if you don't require EGG to be all about adaptation. It could be. But it could also be just the way it is. Mothers can only gestate so long. Period. The mechanism that initiates labor based on those metabolic cues (MC)? Totally adaptive. The process the EGG explains? Not really. A limit's a limit! It would be physiologically impossible to exceed it. Adaptive ideas aren't necessary for EGG unless it's somehow adaptive to keep the fetus inside mother right up until that threshold, which is possible. But it could also just be the only way to trigger labor. And so we're back to the EGG being just the way it is.
***
So how should you apply this evolutionary hypothesis to your pregnancy?
It sheds light on why it's difficult for humans to give birth. It sheds light on why babies seem so helpless compared to other primates.
But regarding your specific, individual details about gestation length and neonatal size that differ compared to other human mothers and their babies?
Please talk to your doctor who's your main brain on this. And read read read read read, if you're interested.
References
-
- Dunsworth H., Anna Warrener, Terrence Deacon, Peter Ellison, and Herman Pontzer (2012) Metabolic hypothesis for human altriciality. PNAS on-line early view.
- Portmann A (1969) Biologische Fragmente zu einer Lehre vom Menschen [A Zoologist Looks at Humankind] (Schwabe, Basel, Germany); trans Schaefer J (1990) (Columbia University Press, New York). German.
- Gould SJ (1977) Ontogeny and Phylogeny (Harvard Univ Press, Cambridge, MA).
- Ellison P (2001) On fertile ground: A natural history of human reproduction. Cambridge: Harvard University Press. [link to book]
- Gould, SJ and RC Lewontin (1979) The spandrels of San Marco and the Panglossian paradigm: A critique of the adaptationist programme. Proceedings of the Royal Society of London, Series B 205(1161): 581-598.
- Klein, J, Stein Z, Susser M (1989) Conception to Birth: Epidemiology of Prenatal Development. New York: Oxford University Press.
- Lichty JA, Ting RY, Bruns PD, Dyar E (1957) Studies of babies born at high altitude. Part I. Relation of altitude to birth weight. American Journal of Diseases in Childhood 93: 666-669.
- Higgins LG (1954) Prolonged pregnancy (partus serotinus). Lancet 2: 1154.
- Prentice AM, Whitehead RG, Roberts SB, Paul AA (1981) Long-term energy balance in child-bearing Gambian women. American Journal of Clinical Nutrition 34: 2790-2799.
Follow Scientific American on Twitter @SciAm and @SciamBlogs. Visit ScientificAmerican.com for the latest in science, health and technology news.
© 2012 ScientificAmerican.com. All rights reserved.
This article is brought to you by RELATIONSHIP ADVICE.
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