Cell Phones and The Brain

Wireless telephones, including both cellular phones and cordless home phones, emit electromagnetic radiation in the radiofrequency range. It’s been suggested in recent years that using a wireless phone on a regular basis could expose the brain to large doses of radiofrequency radiation, the risks of which are currently unknown. Particularly because children have rapidly developing brains, could using cell phones or cordless home phones increase the risk of cancer or have other negative health effects?

Radio waves are a type of electromagnetic radiation, which (though the word “radiation” makes them sound scary and dangerous) are very low in energy. As such, they are incapable of doing the kind of damage that, say, x-rays and nuclear radiation can do, as explained in a previous article. However, while radio waves can’t break chemical bonds like certain other types of radiation can, they are nevertheless a type of energy. In fact, cell phone use has been shown to increase the temperature of the skin with which the phone is in contact by more than 2°C over a period of less than 10 minutes (see, for instance, Anderson et al, Straume et al), though very little of this increased temperature is likely due to the radiation itself. It’s also not likely that much of the heat actually makes it through the skull into the brain. Still, because little is known about the potential effects of routine exposure of the brain to radiofrequency radiation, scientists continue to investigate the safety of wireless phones and similar devices.

Radiofrequency energy isn’t very penetrating; it’s absorbed by the head and hand of a cell phone user, but it can’t travel very far into the head. Therefore, if cell phones increase the risk of tumors, the tumors should appear in the regions of the brain nearest the ear. A recently published study with a very large number of participants (more than 350,000) examined the relationship between brain tumors and cell phone use. The authors found no correlation whatsoever, leading them to conclude that cell phone use does not increase the risk of brain tumors (Frei et al).

An even more recent study found, however, that cell phone use does alter the metabolism of glucose in the brain; specifically, using a cell phone increases the extent to which the regions of the brain nearest the phone antenna burn sugar (Volkow et al). Increased glucose metabolism (burning of sugar) is a sign that cells are working harder, so the results of this study suggest that cell phone use alters the operation of brain cells. The authors did not attempt to discern, nor did they propose, a mechanism for this effect. It remains to be determined why radiofrequency radiation would increase brain cell activity, and what ultimate effects that increased activity might have. An animal study, however, suggests that radiofrequency might change certain functional parameters of brain cells (how easily excited they are, for instance), and might alter the release of neurotransmitters, which are brain cell communication molecules (Hyland). The potential involvement of neurotransmitters is a particularly distressing possibility where it comes to a child’s brain, which is still developing and which is quite sensitive to neurotransmitter concentrations (though it’s worth bearing in mind that, as of yet, the involvement of neurotransmitters is purely hypothetical).


Science Bottom Line:* There’s no evidence that cell phones cause cancer, but there is evidence that they affect brain activity, and there’s not much yet known about how they do so, or what the long-term effects might be. A reasonable course of action in situations like this, in which the risks are poorly defined, is to proceed with caution. Using a cell phone for short periods during the day and/or infrequently for longer periods isn’t likely to be a problem, but you may wish to invest in a headset if you (or your child) uses a cell phone frequently or for long periods of time on a regular basis.


Do you worry about the long-term health effects of cell phone use?



Anderson et al. Measurements of skin surface temperature during mobile phone use. Bioelectromagnetics. 2007 Feb;28(2):159-62.

Frei et al. Use of mobile phones and risk of brain tumours: update of Danish cohort study. BMJ. 2011 Oct 19;343:d6387. doi: 10.1136/bmj.d6387.

Hyland, G. Physics and biology of mobile telephony. Lancet. 2000 Nov 25;356(9244):1833-6.

Straume et al. Skin temperature increase caused by a mobile phone: a methodological infrared camera study. Bioelectromagnetics. 2005 Sep;26(6):510-9.

Volkow et al. Effects of cell phone radiofrequency signal exposure on brain glucose metabolism. JAMA. 2011 Feb 23;305(8):808-13.


The Developing Personality

Yesterday evening as I nursed W, she bit me. Pretty commonplace experience, I know. The only thing that made it remarkable is that she’s 10 months old, and it was the first time she’s EVER bitten. I yelped (as one does). What came next surprised me; she started to cry. Not just whimper a little, not cry in anger, but SOB big, broken-hearted, hiccupy sobs. I comforted her and we went back to nursing, and a few minutes later she bit again. I yelped again. She started sobbing again. Comfort, resume nursing…and then a third time (and again with the sobbing). After the third repetition of the entire sequence, she didn’t bite again. I guess she got the message.

It occurred to me afterward, however, that this was the first time she’s ever thought I was upset with her. I wasn’t; my yelp was in pain rather than anger, but she clearly thought I was mad. Apparently she’s a darn sensitive little girl, because she was clingy and needed extra love for hours afterward.

Her personality is starting to shine through more and more every day. Some aspects of who she shows me she is, I’ve known for ages. She’s stubborn, for instance, and very curious. But the sensitivity caught me by surprise; I sort of thought she was a little bruiser, an even-keel kid who didn’t get easily knocked off-kilter emotionally…and apparently, I was dead wrong. Go figure. All of which makes me wonder, what other aspects of her emerging personality will catch me completely off-guard?


What parts of your child’s personality did you see from day one, and which ones surprised you later on?



The Autistic Brain

Despite the efforts of researchers and medical practitioners, autism is still only partially understood. Boys are more susceptible than girls by a factor of about four, which may be due to the way that sex hormones interact with a gene called RORA (Sarachana et al), which is one of the many genes implicated in autism (Nguyen et al). Still, the complete genetic profile of autism isn’t known, and it’s clear that environmental factors also affect whether and to what degree an individual with a genetic predisposition expresses autism.

One of the environmental factors cited anecdotally and by some popular media sources as a contributor to autism is the measles, mumps and rubella (MMR) vaccine. However, over 20 scientific studies of vaccines and their side effects (Poland) have shown that there is no link whatsoever.

Interestingly enough, the environmental factors that help to influence development of autism may be prenatal ones, according to a new study in the Journal of the American Medical Association (Courchesne et al). This study examined the size of the brains of young autistic boys, as compared to the size of the brains of young non-autistic boys. With data adjusted for age, the autistic boys had 67% more neurons (brain cells) in an area of the brain called the prefrontal cortex — this part of the brain deals with things like communication and social interaction — than the non-autistic boys had. The autistic boys’ brains were also about 17% heavier than the brains of same-aged non-autistic boys, despite the fact that normally, brains in same-age children don’t vary significantly in weight. Interestingly enough, however, the researchers found that the increased number of neurons was greater than would be suggested by the increased brain weight. This rules out the possibility that autistic children simply have larger brains than non-autistic children, and instead makes it clear that the autistic brain has too many neurons packed into a given space.

What makes this study important in understanding autism is that the neurons of the prefrontal cortex develop and multiply during the prenatal period. Specifically, these neurons develop between approximately the 10th and 20th week of gestation. Once a baby is born, he has all the prefrontal cortex neurons he will ever have. The brain then begins a process that takes place through babyhood and toddlerhood called apoptosis, or programmed cell death. During apoptosis, the brain kills off those neurons that don’t improve brain function or form meaningful connections. This helps the brain to function more efficiently, and is an important part of neural development. The researchers in the Courchesne study did not attempt to determine whether autistic children had more neurons in the prefrontal cortex because they developed more neurons initially, or because their brains failed to perform apoptosis appropriately. Regardless, the study results help to rule out the notion that a single environmental factor or exposure (such as an MMR vaccine) could cause autism. If the prefrontal cortex of autistic children contains more neurons because they overproliferated during the prenatal period, postnatal environmental factors (such as the MMR vaccine) aren’t causative. If the prefrontal cortex contains more neurons because of a failure of apoptosis, postnatal environmental factors could influence the development of autism, but couldn’t cause it to emerge “all of a sudden” (as some parents have described in response to the MMR vaccine), because apoptosis takes place over a long period of time — many years, to be precise.

This study doesn’t fully explain autism — no single study is likely to do so — but it does help move us toward an increased understanding of the disease. Further, by making it clear that autistic brains are physically different than those of non-autistic children, which rules out vaccines as a possible cause of autism, parents can make more accurate risk-to-benefit decisions regarding health care.


What factors do you think researchers will find are implicated in autism?



Courchesne et al. Neuron number and size in prefrontal cortex of children with autism. JAMA. 2011 Nov 9;306(18):2001-10.

Nguyen et al. Global methylation profiling of lymphoblastoid cell lines reveals epigenetic contributions to autism spectrum disorders and a novel autism candidate gene, RORA, whose protein product is reduced in autistic brain. FASEB J. 2010 Aug;24(8):3036-51. Epub 2010 Apr 7.

Poland. MMR Vaccine and Autism: Vaccine Nihilism and Postmodern Science. Mayo Clin Proc. 2011 Sep;86(9):869-71.

Sarachana et al. Sex Hormones in Autism: Androgens and Estrogens Differentially and Reciprocally Regulate RORA, a Novel Candidate Gene for Autism. PLoS One. 2011 Feb 16;6(2):e17116.

Growing Up Geek — You Can’t Fight Nerd Genes

Today was W’s first Christmas party. It took place in the department where her daddy and I both work at the university. I got her all dressed up in a little skirt and an awesomely geeky shirt that I had made for her, which spells her name using atomic symbols from the periodic table. The shirt was a big hit with my co-workers, but it was, after all, a chemistry department party.

Anyway, all this got me thinking a little bit about my beautiful little girl and the family into which she was born. Her daddy and I are geeks, pure and simple. We were the “other” kids — not the popular kids — in high school. Neither one of us got invited to the parties the cool kids threw, and my prom date was a male friend, while my husband didn’t attend his prom at all. Of course, some of the kids who are weird in high school are the ones who are most interesting afterward (probably because we have to work harder in order to make friends). In the end, while growing up geek kind of sucked at the time, I wouldn’t change a thing about my social experiences in retrospect.

All of which brings me to my daughter. She comes from a family full of scientists, and we all tend to be more analytical than is considered “cool” among the popular kids. Furthermore, we’re readers — my husband and I have walls of books where most people have a TV — and we’re rarely up on pop culture. I certainly won’t prevent my child from watching TV at friends’ houses, but I’m not going to buy one just to ensure that she can get her daily dose of programming. Instead, I will continue to read with her (as I do now), and will hope that as she gets older, she starts sneaking books under the covers with a flashlight after bedtime, just as I did. Am I setting her up to be strange? I’m not going out of my way to try to turn her into a nerd, but the odds aren’t in her favor.

I want my daughter to have a wonderful childhood. I want her to be spared the pain of social ostracization (because if high school was barely tolerable for me, elementary and middle school were torturous, socially-speaking). I want her to enjoy a big circle of friends, as that’s one of the lovely things life has to offer. But I also want to raise a socially conscious thinker. An observer, a philosopher, a constructer of theories and considerer of ideas, regardless of the career path she chooses. I won’t go out of my way to make her not fit in with her childhood peers, but I’m trying to anticipate the possibility that she won’t, and to prepare myself for the heartache of watching her go through what I went through, trying so desperately to fit in, to no avail. As a mother, I want her to have a wonderful childhood, but more than that, I want her to have a beautiful life. Should she end up going down the same social path I did when I was young, I’ll have to remind myself of where that path leads, and how much strength of character it takes to be different when your peers put so much emphasis on being the same.

I’ll just have to wait and see what happens, and I know she’ll be a wonderful person no matter what she does…but a tiny little part of my heart hopes she’ll fly her geek flag proudly, just like mama and daddy.


What do you hope your child does (or doesn’t!) have in common with you?



Challenges Using Positive Discipline With A Toddler

As W approaches 10 months of age, I increasingly find myself needing to set limits. I try to explain these to her, but know that (at least for now), she largely doesn’t understand me when I say things like:

-“Please don’t pinch mama while you nurse; mama likes gentle touches.”
-“Uh oh! Light sockets are dangerous, and mama wants you to be safe!”

-“I know you enjoy dropping your food off your tray, but mama will only pick things up for you one time. After that, they’re gone.”

I love the idea of natural consequences, and some situations lend themselves to such consequences beautifully. Others, however, do not. What’s the natural consequence for crawling away from me while I am changing her diaper? Not getting a diaper? Score! She’d be thrilled. Having to stay in a dirty diaper? She wouldn’t care, but she would get diaper rash. The more she matures, the more she’ll be able to learn from delayed consequences, but she’s too young right now to understand that her bum itches because she refused to let mama change her diaper and she’s been sitting in poop for an hour.

I want to keep things positive, I want to keep things playful, but I want to set limits and allow her to learn from her mistakes as much as possible now, and increasingly as she moves into toddlerhood and the preschool years. With a preverbal child who isn’t capable of understanding delayed consequences, though, I’m sometimes at a loss.


How have you set limits and defined expectations for your almost-toddler or toddler?



Breast Milk and Premature Babies

One of the most fascinating aspects of human breast milk is that the milk literally changes during the course of a nursing relationship. The earliest secretions from the breast — called colostrum — are high in antibodies and protein. Transitional milk comes in a few days post-delivery, and milk changes once again at around two weeks post-delivery. The changes in breast milk occur to meet the changing needs — and changing maturity — of the human infant.

A new study published in the medical journal Pediatrics reports on yet another phase of milk that occurs in the case of a premature delivery (Gabrielli et al). It appears that lactating mothers of premature infants (average age studied was just shy of 28 weeks gestational age) produce milk that is much lower in lactose than the milk produced by mothers of full-term infant.

Lactose is a small sugar molecule made up of two smaller sugar units, called glucose and galactose. To digest lactose, the human intestine uses an enzyme called lactase, which breaks lactose into its separate glucose and galactose components; these are then absorbed into the bloodstream and can be taken up by the cells for energy. While some adults are lactose intolerant, a condition that results from insufficient production of the lactase enzyme, this condition is very, very rare in babies. Premature infants, however, generally don’t digest lactose to the same extent as full-term newborns (see, for instance, MacLean et al, Chiles et al), largely because of reduced lactase activity until the ninth month of gestation (see, for instance, Antonowicz et al, Aurrichio et al, Dahlqvist et al). This reported finding — that breast milk for preemies is especially low in a sugar they find hard to digest — is simply another neat example of human milk conforming to the needs of the human infant, regardless of the circumstances.

Another interesting finding of the study dealt with some pretty technical genetic issues. Stated simply, there are larger sugars than lactose (collectively called oligosaccharides) in human milk, and there are quite a large variety of these larger sugars. While all women produce most of the oligosaccharides, production of some of them requires enzymes that not everyone has. Two different genes (they go by the technical names Le and Se, but we’ll call them Gene 1 and Gene 2 for simplicity’s sake) are involved; women with Gene 1 can make Enzyme 1, and women with Gene 2 can make Enzyme 2. As a result, there are four different types of milk resulting from four different possible gene/enzyme combinations. According to the study, about 70% of women have both genes and produce both enzymes. These women produce the largest number and greatest variety of oligosaccharides. About 20% of the population lacks Gene 1 and therefore lacks Enzyme 1, but has Enzyme 2. About 9% of the population has Gene 1/Enzyme 1, but lacks Gene 2/Enzyme 2. These two groups of women produce fewer total oligosaccharides and a smaller variety of oligosaccharides than women with both genes/enzymes. About 1% of the population lacks both genes, and therefore both enzymes. These women consequently produce the smallest total number and smallest variety of oligosaccharides.

Because oligosaccharides aren’t digested, generally speaking, they don’t contribute to the caloric content or nutritional value of breast milk (Coppa et al). Instead, they pass through the gut and act as soluble fiber, which helps to promote regularity of bowel movements and keep bowel movements soft. They also appear to help prevent pathogenic bacteria from adhering to the gut wall, which helps prevent infection, and they seem to promote the growth of healthy gut bacteria (Bode). Finally, because they pass into the bloodstream to some extent in undigested form (Rudloff et al), it’s hypothesized that they could play a role in immune system function, or act as precursors for a variety of important molecules including some involved in brain function. The milk from mothers of preterm infants appears to be especially high in oligosaccharides, according to the Gabrielli study, which the authors hypothesize is particularly important for these smallest babies. On the basis of their findings, the authors emphasize the importance of human breast milk, ideally from the mother and as opposed to formula, as a source of nutrition for preterm babies.  The authors further note that the differences between women in terms of oligosaccharide production, and the importance of a wide variety of oligosaccharides in milk, justifies the mixing of milk from donors rather than the use of single-donor milk should a baby require breast milk supplementation.


If you’re interested in donating milk, the Human Milk Banking Association of North America needs donations.


Which of human milk’s various properties interests you most?


Antonowicz et al. Development and distribution of lysosomal enzymes and disaccharidases in human fetal intestine. Gastroenterology. 1974 Jul;67(1):51-8.

Aurrichio et al. Intestinal glycosidase activities in the human embryo, fetus, and newborn. Pediatrics. 1965 Jun;35:944-54.

Bode, L. Human milk oligosaccharides: prebiotics and beyond. Nutr Rev. 2009 Nov;67 Suppl 2:S183-91.

Chiles et al. Lactose utilization in the newborn; role of colonic flora. Pediatr Res. 1979; 13:365.

Coppa et al. Characterization of oligo- saccharides in milk and feces of breast-fed infants by high-performance anion- exchange chromatography. Adv Exp Med Biol. 2001;501:307-14.

Dahlqvist et al. Development of the intestinal disaccharidase and alkaline phosphatase activities in the human foetus. Clin Sci. 1966 Jun;30(3):517-28.

Gabrielli et al. Preterm milk oligosaccharides during the first month of lactation. Pediatrics. 2011 Dec;128(6):e1520-31. Epub 2011 Nov 28.

MacLean et al. Lactose malabsorption by premature infants: magnitude and clinical significance. J Pediatr. 1980 Sep;97(3):383-8.

Rudloff et al. Urinary excretion of lactose and oligosaccharides in preterm infants fed human milk or infant formula. Acta Paediatr. 1996 May;85(5):598-603.

The Risks and Benefits of Delayed Cord Clamping

This is the second in a two-part series on umbilical cord-related issues. The first article dealt with cord blood banking.

One of the criticisms that has been leveled against the typical hospital birthing environment is the “assembly line” approach to delivering a baby. In many cases, obstetricians and obstetric nurses have a time frame in which they want to see events take place. It’s been argued that the high Cesarean section rate in the U.S. is among the consequences of this approach. While it’s easy to sit in an armchair and criticize the medical establishment for being too eager to intervene in “normal” deliveries, too quick to augment labor, give medications and episiotomies, and too fast to cut the cord and swoop off with the newborn to measure, bathe, and inoculate, it’s important to remember that there are legitimate medical reasons for many of these interventions (and the speed with which they’re carried out). No, normal birth is not an emergency. However, we live in a very, VERY litigious society, and obstetricians are at exceedingly high risk of being sued. Ever wondered why there aren’t many old obstetricians? It’s not because they burn out or get bored; many truly enjoy their work. It’s because they can be sued by (or on behalf of) each child they deliver until that child turns 18. As such, an obstetrician must continue to carry malpractice insurance for 18 years after the last delivery they attend. Given that malpractice insurance can cost an obstetrician nearly $100,000 a year (a figure impossible to afford when there’s no income to support it), most OBs stop doing deliveries and revert to simple gynecology approximately 20 years before they plan to retire for good. Gives a new perspective on why your OB is quick to intervene, doesn’t it?

In any case, clamping the umbilical cord, which contains the blood vessels that carry oxygen and nutrients from mother to child during pregnancy, is one of the procedures that takes place after delivery. In the case of an emergency — a baby who is born in need of resuscitation, for instance — the cord is clamped immediately so that medical professionals can work freely on the newborn. In the case of a normal, non-emergent delivery, however, there’s been some debate as to when the cord should be cut for the best outcome.

Remember from high school physics that, for each action, there’s an equal and opposite reaction. What this means is that when your baby puts an incredible amount of pressure on your cervix and the tissues of your vagina to stretch them during labor (ouch!), your tissues respond by putting an incredible amount of pressure on your baby in return. Bottom line, your baby gets squeezed — hard — as he or she travels through the birth canal. When a baby who is still connected up to the placenta via an umbilical cord gets squeezed, the result is that blood from the baby literally get squeezed right out the cord and into the placenta.

Imagine, for a moment, a cave-woman giving birth. Once her baby was out, she (or her female attendants) would pick him up and put him to her breast. Cave-mama would cuddle cave-baby and warm him up, and her female attendants would stand around smile and enjoy the beautiful, peaceful scene. Eventually (and this part is speculative, but it’s reasonable and measured speculation), someone would tear the cord (probably using a sharp rock). It’s possible to imagine a similar scenario in, say, pre-Industrial England (but without the cave, and with a scissors instead of a rock). Bottom line, before birthing took place in a hospital, there would have been a natural time gap between the birth of a baby and the returning of the attendants’ attention to the matter at hand (namely, the afterbirth). During this time gap, the baby’s heartbeat would have continued to circulate blood throughout the baby’s body, the umbilical cord, and the placenta. Over the course of several minutes, the quantity of blood in the baby — while low immediately after birth — would have returned to normal. Several minutes later, post-delivery changes in circulation would cause the vessels in the cord to clamp down, naturally sealing the baby off from the placenta and keeping the baby’s blood entirely within its body. At this point, the cord would stop pulsing. A baby allowed to remain attached to the cord until it stops pulsing on its own ends up with a much higher red blood cell count than one who is immediately disconnected; this improves iron status (red blood cells need iron to function), and reduces the need for dietary iron early in life. In fact, breast milk may be low in iron (see an excellent article at Science of Mom on this topic) simply because babies who don’t have their cords cut early don’t need supplemental dietary iron early in life.

Because immediate cord clamping doesn’t allow blood volume in the baby to return to normal, it increases the risk of low neonatal hemoglobin (a marker of too few red blood cells, which can impair oxygen delivery, and leads to increased risk of anemia later in the first year of life). This is associated with a number of potential negative outcomes, including delayed development. Many studies have examined the benefits associated with delaying cord clamping, as opposed to clamping the cord immediately (see, for example, Andersson et al, Ceriani Cernadas et al, Hutton et al, Ultee et al). The studies indicate that the best time to clamp the cord so as to avoid the risk of low neonatal hemoglobin is at approximately three minutes post-delivery.

On the other hand, there’s been speculation (and there’s a small amount of evidence) of risks associated with delayed cord clamping. For instance, Prendiville et al found that delayed clamping can increase the risk of polycythemia (too many red blood cells, proportionally speaking) and hyperbilirubinemia (too much bilirubin, a breakdown product of red blood cells, which leads to jaundice). However, these results haven’t been reproduced in the vast majority of delayed cord clamping studies. Andersson et al, Ceriani Cernades et al, and Ultee et al found no significant increased risk of negative outcome (jaundice or otherwise) with delayed cord clamping (at three minutes post-delivery in each study). Hutton et al found an increased risk of polycythemia in infants whose cords had been clamped at least two minutes post-delivery, but also found that the condition was not associated with any negative outcomes. There is an unpublished study (Mc Donald, PhD thesis) that suggests very delayed cord clamping (5 minutes or longer post-delivery, or when the cord stops pulsing) may increase the risk of jaundice requiring light therapy. While these results have not been replicated elsewhere, it’s probably worth being cautious with extremely delayed cord clamping.

Somewhat delayed cord clamping also appears to benefit premature and low birth-weight babies, though very premature babies are generally born under medically urgent circumstances, and delaying clamping by several minutes is not likely to be feasible. The aforementioned Ultee study focused on slightly premature infants (delivered between 34 and 36 weeks), and showed higher hemoglobin with a three-minute delay. A study of very premature infants (around 28-29 weeks gestational age) found that delaying clamping as much as 30-45 seconds post-delivery as opposed to clamping immediately helped to reduce the otherwise significant risks of late-onset sepsis (infection) and intraventricular hemorrhage (bleeding in the brain) (Mercer et al). The Mercer study didn’t examine the effects of waiting longer than 30-45 seconds, simply because of the emergent nature of extremely preterm births. The authors pointed out that, of course, many very preterm babies would require immediate care, precluding the possibility of waiting even 30 seconds to clamp the cord, but recommend on the basis of their findings that, whenever possible, clamping be delayed a bit. A similar study by Rabe et al found that premature babies in the range of 29-33 weeks gestational age generally had good outcomes when cord clamping was delayed by 45 seconds, despite the delay, and benefited from the delay in terms of reduced need for transfusion.


Science Bottom Line:* If there’s no medical emergency that requires separating baby from mother immediately, the evidence supports waiting three minutes to cut the cord. During this time, the baby should be at the level of the mother (ideally on her chest) to ensure that gravity neither prevents nor inappropriately augments the return of blood into the baby.
Are you in favor of delayed cord clamping?



Andersson et al. Effect of delayed versus early umbilical cord clamping on neonatal outcomes and iron status at 4 months: a randomised controlled trial. BMJ. 2011 Nov 15;343:d7157. doi: 10.1136/bmj.d7157.

Ceriani Cernades et al. The Effect of Timing of Cord Clamping on Neonatal Venous Hematocrit Values and Clinical Outcome at Term: A Randomized, Controlled Trial.  Pediatrics. 2006 Apr;117(4):e779-86. Epub 2006 Mar 27.

Hutton et al. Late vs Early Clamping of the Umbilical Cord in Full-term Neonates. JAMA. 2007 Mar 21;297(11):1241-52.

Mercer et al. Delayed Cord Clamping in Very Preterm Infants Reduces the Incidence of Intraventricular Hemorrhage and Late-Onset Sepsis: A Randomized, Controlled Trial. Pediatrics. 2006 Apr;117(4):1235-42.

Prendiville et al. Care during the third stage of labour. In: Chalmers I, Enkin M, Keirse MJNC editor(s). Effective care in pregnancy and childbirth. Oxford: Oxford University Press; 1989:1145–69.

Rabe et al. A randomised controlled trial of delayed cord clamping in very low birth weight preterm infants. Eur J Pediatr. 2000 Oct;159(10):775-7.

Ultee et al. Delayed cord clamping in preterm infants delivered at 34 36 weeks’ gestation: a randomised controlled trial. Arch Dis Child Fetal Neonatal Ed. 2008 Jan;93(1):F20-3. Epub 2007 Feb 16.