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Investigating foods, drugs, and chemicals.
Melinda Moyer
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by Melinda Moyer in Body Politic
Let’s face it: breast milk is pretty amazing. It contains antibodies that help wee ones establish strong immune systems, and some studies suggest the act of breastfeeding even lowers mom’s breast cancer risk. Now researchers at the Universities of Chicago, Maryland, and Illinois have another potential bonus to add to the mix: according to a study they conducted in pigs, breast milk shapes the expression of bacterial genes in the infant gut, potentially boosting antioxidant activity and protecting against at least one rare debilitating disease.
It’s not crazy to think that breastfeeding might affect the gut flora—diet is known to have a big effect on the microbiome. When scientists assessed the gut flora of babies, they found that breastfed tots had different bacteria present in their intestines than formula-fed ones did. But the significance of these findings has been unclear.
The authors of the recent PLoS ONE study dug one step deeper: instead of just looking at the bacteria, they also used RNA-based techniques to identify all the RNA transcripts, or protein precursors, that the gut bacteria in four three-week-old baby piglets who had been fed by their mothers their whole lives were producing. They compared this to the bacterial RNA found in four three-week-old baby piglets who had been fed formula since birth.
For one thing, the breastfed pigs had more RNA coding for proteins involved in the regulation of oxidative stress, a finding that gives some credence to the idea that breast milk acts as an antioxidant and might protect against some types of tissue damage. But even more interestingly, the researchers found that the breastfed piglets had more RNA coding for enzymes involved in the metabolism of arginine, an amino acid precursor to nitric oxide, which protects the gastroinestinal tract. Arginine has been linked to a deadly form of intestinal inflammation called neonatal necrotizing enterocolitis (NEC): reports have found abnormally low levels of arginine in babies suffering from NEC, and breastfed infants suffer from the disease less frequently than formula-fed babies do.
Perhaps, as the authors of this study suggest, breastfeeding helps the gut bacteria metabolize arginine in such a way that lowers NEC risk. Granted, the study was conducted in pigs and its findings may not be applicable to humans, and no one yet knows whether these particular enzymes are actually protective against the disease, but it’s an idea that warrants further study. If true, breastfeeding may have more benefits than we realize—and that would be good news not just for breastfeeding moms, but for moms who have to rely on formula, too. Once scientists have teased out all of breast milk’s unique benefits, they may one day be able to devise milk formulas that more closely mimic the real (amazing) deal.
Citations:
De Silva M, Senarath U, Gunatilake M, & Lokuhetty D (2010). Prolonged breastfeeding reduces risk of breast cancer in Sri Lankan women: a case-control study. Cancer epidemiology, 34 (3), 267-73 PMID: 20338838
Poroyko V, White JR, Wang M, Donovan S, Alverdy J, Liu DC, & Morowitz MJ (2010). Gut microbial gene expression in mother-fed and formula-fed piglets. PloS one, 5 (8) PMID: 20805981
Turnbaugh, P., Ridaura, V., Faith, J., Rey, F., Knight, R., & Gordon, J. (2009). The Effect of Diet on the Human Gut Microbiome: A Metagenomic Analysis in Humanized Gnotobiotic Mice Science Translational Medicine, 1 (6), 6-6 DOI: 10.1126/scitranslmed.3000322
Penders, J. (2006). Factors Influencing the Composition of the Intestinal Microbiota in Early Infancy PEDIATRICS, 118 (2), 511-521 DOI: 10.1542/peds.2005-2824
AYCICEK, A., EREL, O., KOCYIGIT, A., SELEK, S., & DEMIRKOL, M. (2006). Breast milk provides better antioxidant power than does formula Nutrition, 22 (6), 616-619 DOI: 10.1016/j.nut.2005.12.011
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De Silva M, Senarath U, Gunatilake M, & Lokuhetty D. (2010) Prolonged breastfeeding reduces risk of breast cancer in Sri Lankan women: a case-control study. Cancer epidemiology, 34(3), 267-73. PMID: 20338838
Poroyko V, White JR, Wang M, Donovan S, Alverdy J, Liu DC, & Morowitz MJ. (2010) Gut microbial gene expression in mother-fed and formula-fed piglets. PloS one, 5(8). PMID: 20805981
Turnbaugh, P., Ridaura, V., Faith, J., Rey, F., Knight, R., & Gordon, J. (2009) The Effect of Diet on the Human Gut Microbiome: A Metagenomic Analysis in Humanized Gnotobiotic Mice. Science Translational Medicine, 1(6), 6-6. DOI: 10.1126/scitranslmed.3000322
Penders, J. (2006) Factors Influencing the Composition of the Intestinal Microbiota in Early Infancy. PEDIATRICS, 118(2), 511-521. DOI: 10.1542/peds.2005-2824
AYCICEK, A., EREL, O., KOCYIGIT, A., SELEK, S., & DEMIRKOL, M. (2006) Breast milk provides better antioxidant power than does formula. Nutrition, 22(6), 616-619. DOI: 10.1016/j.nut.2005.12.011
SHAH, V. (2004) Nitric oxide in gastrointestinal health and disease. Gastroenterology, 126(3), 903-913. DOI: 10.1053/j.gastro.2003.11.046
Shah P, & Shah V. (2007) Arginine supplementation for prevention of necrotising enterocolitis in preterm infants. Cochrane database of systematic reviews (Online). PMID: 17636753
LUCAS, A. (1990) Breast milk and neonatal necrotising enterocolitis. The Lancet, 336(8730-8731), 1519-1523. DOI: 10.1016/0140-6736(90)93304-8
by Melinda Moyer in Body Politic
As usual, my readers are raising interesting questions in the comments section (thanks, guys! You’re awesome). In response to my post yesterday highlighting how our food portions have changed (as in, exploded) over the past 20 years, commenter AEK said, “It would be interesting to note how much added sugar was in the foods at both measurement periods.” It’s a point I’ve frequently considered myself, so I decided to do some digging.
As it turns out—and you might guess—our consumption of added sugars has increased over the years. (Note that added sugars are defined as white sugar, brown sugar, raw sugar, corn syrup, corn syrup solids, high fructose corn syrup, malt syrup, maple syrup, pancake syrup, fructose sweetener, liquid fructose, honey, molasses, anhydrous dextrose, crystal dextrose, saccharin, and aspartame—I had no idea there were so many!—that are eaten separately or used as ingredients in processed or prepared foods.) In a study published in August in Nutrients, researchers at the University of Connecticut, Ansan College in Korea, and Michigan State University analyzed data collected from the National Health and Nutrition Examination Surveys (NHANES) I and III, comparing what subjects said they had eaten over the past 24 hours in 1971-1975 with what subjects said they had eaten over the past 24 hours in 1988-1994.
Granted, these data aren’t particularly up-to-date, but nevertheless the findings suggest a trend that is probably continuing today. As the authors note, “compared with NHANES I, the mean dietary intake levels in NHANES III were greater for total energy intake (+144 kcal d−1; +7%), total sugar intake (+10 g d−1; +8%), intake of added sugars, (+9 g d−1; +12%), and total carbohydrate intake (+40 g d−1; +18%).” In other words: we ate more junk food in the 90s. Surprise!
Interestingly, though, the results differed significantly by age. People under 18 actually ate three percent fewer calories in 1988-1994 than they did in 1971-1975, but their consumption of added sugars still jumped by five percent. People over 19, on the other hand, ate 11 percent more calories in 1994, and their added sugar consumption skyrocketed by 18 percent.
Perhaps my favorite part of the study is the researchers’ analysis of exactly what people ate in 1971 versus 1994. The biggest change: people stopped drinking so much milk, replacing the calories in part with grains and carbonated beverages. The paper explains,
The most salient feature of the changes in food items contributing to total energy intake is the rise of “mixtures of mainly grain” from relatively insignificant to the most significant contributor in both age subgroups. This food item includes mixtures having a grain product as a main ingredient, such as burritos, tacos, pizza, egg rolls, quiche, spaghetti with sauce, rice and pasta mixtures; frozen meals in which the main course is a grain mixture; noodle and rice soups; and baby-food macaroni and spaghetti mixtures.
I’m speculating here, but the bye-bye-milk trend may help explain why kids consumed more in the 70s than they did in 90s—after all, a few glasses of milk a day add up to quite a few calories. Today, I’m guessing the anti-milk trend is continuing—how many people under the age of 10 drink milk (and no, McDonald’s milkshakes don’t count)? I’m guessing not a lot, but I’m also guessing that by now, we’ve found some pretty efficient ways to make up the calories. And then some.
Citations:
Ock K. Chun, Chin E. Chung , Ying Wang, Andrea Padgitt, Won O. Song (2010). Changes in Intakes of Total and Added Sugar and their Contribution to Energy Intake in the U.S. Nutrients, 2, 834-854 : 10.3390/nu2080834
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Ock K. Chun, Chin E. Chung , Ying Wang, Andrea Padgitt, Won O. Song. (2010) Changes in Intakes of Total and Added Sugar and their Contribution to Energy Intake in the U.S. Nutrients, 834-854. info:/10.3390/nu2080834
by Melinda Moyer in Body Politic
In response to my earlier post about bisphenol A in soda and beer, reader Skeptic had an insightful comment:
As someone involved in environmental health myself, I have been following the BPA controversy from north of the 49th parallel with some interest. I have often wondered whether the actual data supports regulation of BPA. The first study you cite, for example, hides this line in its discussion: “Thus, median and 95th percentile intake estimates were approximately two to three orders of magnitude below the current health-based guidance value. This result is similar to that given by Ye et al. (2009) for a cohort of Norwegian women, with the estimated average daily intakes of BPA reported to be about three orders of magnitude lower than the RfD and TDI.”
What is your take?
It’s a valid point. Industry and regulatory agencies argue that exposure to BPA is well below recommended limits—so why should we be concerned? I think there are several issues here. First, as we’re discovering more day by day, BPA is everywhere: receipts, reusable water bottles, food storage containers, canned beans and produce, soda, beer. Who knows where else! So yes, a study might conclude that average exposure to BPA through one particular route might be well below recommended daily exposure limits, but that’s not taking into account the myriad other sources we’re being bombarded with on a daily basis.
To be fair, though, studies in the past have assessed BPA levels in human urine, and they have found average levels to be quite low. So let’s assume that we are being exposed to BPA at levels below the recommended exposure limits (which for the US and Europe is .05 mg of BPA per kg of body weight per day). I still don’t think we’re out of the danger zone, because there’s evidence to suggest that we should be questioning the exposure limit itself. For one thing, the EPA doesn’t know what happens to animals (let alone humans) who are exposed to .05 mg/kg of BPA per day. They’ve never tested it. They arrived at this limit by testing what happened to rats exposed to 5 mg/kg per day; then they divided by 100 and assumed that the resulting level would be absolutely safe. As Laura Vandenberg, a BPA expert and biologist at Tufts University explained to me a few months ago, “the way that traditional toxicology is done is by looking at a whopping dose of something and then guessing what would happen at a lower dose. That’s how the safe level of BPA was set.”
And there is evidence to suggest that BPA affects the body at doses below .05 mg/kg per day. In 2007, 38 researchers from institutions including Harvard, Tufts, the University of Texas, and even the EPA published a consensus statement in which they discussed, among other things, the handful of studies suggesting that BPA elicits biological effects at doses much lower than the EPA “safe level.” As Vandenberg explained to me, “the animal literature shows links between BPA and mammary cancer, prostate cancer, infertility, changes in the female reproductive tract, etcetera—we’re talking about studies that show those effects below what the EPA says is safe.” BPA affects hormones, and it could well be that hormone dose-response curves are not linear (i.e., you can’t necessarily assume that if a lot of a substance has a big effect, a little of it will have a small effect). In fact, many compounds have been found to elicit unexpectedly big effects at tiny doses—sometimes they even have opposite effects at low versus high doses—and some researchers argue that regulatory agencies are relying on highly outdated (and more notably, undertested) dose-response models.
Worse, despite the fact that there is evidence to suggest that BPA harms the body at very low doses, agencies all but ignore these findings. In September, for instance, the European Food Safety Authority (EFSA) announced that it saw no reason to include new studies in its BPA exposure limit assessment; to date, the EFSA relies on only two studies that were conducted in rats. (I’m not sure which two studies they are, but if they’re the same two the US relies on, then it’s important to note that they are extremely flawed.) Today there are hundreds of studies published on BPA, but the EFSA says it didn’t consider these other studies because they “had shortcomings.” It’s unclear exactly what the agency means by that, but my guess is that it has something to do with the fact that academic researchers conduct studies differently than regulatory agencies do, a problem (highlighted in this excellent Nature news feature by Brendan Borrell) that is one of the key reasons regulatory and academic scientists cannot seem to agree on the BPA issue.
So, in a nutshell: we shouldn’t ignore BPA because we’re exposed to so little of it (if, indeed, we are exposed to so little of it). The research that exists on the chemical suggests that it affects the body at teeny tiny exposure levels—levels well below what the EPA and EFSA deem to be safe. What we really need is for agencies to acknowledge these studies and consider them in their safety assessments alongside the very few studies they have relied on for years. The science on BPA is moving forward in great leaps and bounds, but regulatory agencies simply aren’t evolving alongside it—and that’s putting everyone’s health at risk.
Citations:
Lakind JS, & Naiman DQ (2010). Daily intake of bisphenol A and potential sources of exposure: 2005-2006 National Health and Nutrition Examination Survey. Journal of exposure science & environmental epidemiology PMID: 20237498
VOMSAAL, F., AKINGBEMI, B., BELCHER, S., BIRNBAUM, L., CRAIN, D., ERIKSEN, M., FARABOLLINI, F., GUILLETTEJR, L., HAUSER, R., & HEINDEL, J. (2007). Chapel Hill bisphenol A expert panel consensus statement: Integration of mechanisms, effects in animals and potential to impact human health at current levels of exposure Reproductive Toxicology, 24 (2), 131-138 DOI: 10.1016/j.reprotox.2007.07.005
Calabrese EJ (2009). Getting the dose-response wrong: why hormesis became marginalized and the threshold model accepted. Archives of toxicology, 83 (3), 227-47 PMID: 19234688... Read more »
Lakind JS, & Naiman DQ. (2010) Daily intake of bisphenol A and potential sources of exposure: 2005-2006 National Health and Nutrition Examination Survey. Journal of exposure science . PMID: 20237498
VOMSAAL, F., AKINGBEMI, B., BELCHER, S., BIRNBAUM, L., CRAIN, D., ERIKSEN, M., FARABOLLINI, F., GUILLETTEJR, L., HAUSER, R., & HEINDEL, J. (2007) Chapel Hill bisphenol A expert panel consensus statement: Integration of mechanisms, effects in animals and potential to impact human health at current levels of exposure. Reproductive Toxicology, 24(2), 131-138. DOI: 10.1016/j.reprotox.2007.07.005
Calabrese EJ. (2009) Getting the dose-response wrong: why hormesis became marginalized and the threshold model accepted. Archives of toxicology, 83(3), 227-47. PMID: 19234688
by Melinda Moyer in Body Politic
A hamburger today is a lot more than it used to be.... Read more »
Herrmann C. (2008) Raising awareness of women and heart disease--women's hearts are different. Critical care nursing clinics of North America, 20(3), 251-63. PMID: 18644507
by Melinda Moyer in Body Politic
The most popular piece in the New York Times today is an Op-Ed published on Monday by Jennifer Ackerman, “How Not to Fight Colds.” It’s an interesting piece and points out something that a lot of people probably don’t know—it’s the immune system, not the virus itself, that causes the cold’s nasty symptoms. But in my opinion, Ackerman takes her assertions a little too far, in the process confusing multiple aspects of the immune response. While it’s probably true that certain immune responses worsen symptoms once a cold infection has been established, Ackerman also implies that a strong immune system does not help the body stave off infections in the first place. And based on the scientific evidence I’ve been able to find, I don’t think that’s a fair conclusion.
The immune system is a machine made of many parts. When a virus attempts to invade the body, the innate immune response, a non-specific system that basically throws darts at the intruder, is the first thing that ramps up. If the virus nevertheless manages to set up shop, the adaptive immune response kicks in, which among other things produces the inflammatory molecules that cause cold symptoms as well as the antibodies that protect you against the same cold in the future. So the immune response that initially fights the invading virus isn’t the same one that kicks in once the infection has established its roots. It stands to reason, then, that while some aspects of immunity (particularly adaptive immunity) may well worsen symptoms, other aspects of immunity may not, and may in fact be very important in protecting against infection. Yet Ackerman writes:
In any case, the supplements, remedies and cereals that claim to strengthen immunity (and thereby protect you from colds) do no such thing. It would be one thing if by some magic they made your body produce antibodies to any particular virus. But they don’t. And though some of these products contain ingredients that have been shown in studies to affect elements of the immune system, there’s scant evidence that they bolster protection against infection by cold viruses. No one knows which immune agents — other than antibodies — accomplish that.
Ackerman argues that antibodies are the body’s only known defense against colds. This would be surprising, given that antibodies are but one tiny part of the immune response to most pathogens; it’s also not backed up by existing evidence. An antiviral protein known as viperin is now thought to play a role in fighting cold infection, for one: a 2008 study published in Respiratory and Critical Care Medicine reported that when viperin activity is stifled during cold infections, the virus replicates more quickly. A 2004 study published in the Journal of Immunology suggests that a protein called human -defensin (HBD)-2 plays a role in host defense against the cold virus, too.
Granted, there is still much left to be learned about how viperin and human -defensin (HBD)-2 affect host protection, and they may not even be the most important players. But the point is, immune proteins other than antibodies do seem to help fight infection—they help to make you better, and perhaps even stave off infection from the getgo. So while Ackerman may be right that ramping up certain aspects of immunity with supplements and vitamins might make you feel more miserable once you have a cold, a robust immune system may not a bad thing when it comes to preventing and fighting the nasty bugs. If it were, then the best defense against a cold would be to stay up all night drinking and then attempt to run a marathon—because that’s a surefire way to pull the body’s resources away from immunity. I don’t know about you, but to me, that really doesn’t seem like a good idea.
Citations:
Proud, D., Turner, R., Winther, B., Wiehler, S., Tiesman, J., Reichling, T., Juhlin, K., Fulmer, A., Ho, B., Walanski, A., Poore, C., Mizoguchi, H., Jump, L., Moore, M., Zukowski, C., & Clymer, J. (2008). Gene Expression Profiles during In Vivo Human Rhinovirus Infection: Insights into the Host Response American Journal of Respiratory and Critical Care Medicine, 178 (9), 962-968 DOI: 10.1164/rccm.200805-670OC
Proud D, Sanders SP, & Wiehler S (2004). Human rhinovirus infection induces airway epithelial cell production of human beta-defensin 2 both in vitro and in vivo. Journal of immunology (Baltimore, Md. : 1950), 172 (7), 4637-45 PMID: 15034083
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Proud, D., Turner, R., Winther, B., Wiehler, S., Tiesman, J., Reichling, T., Juhlin, K., Fulmer, A., Ho, B., Walanski, A.... (2008) Gene Expression Profiles during In Vivo Human Rhinovirus Infection: Insights into the Host Response. American Journal of Respiratory and Critical Care Medicine, 178(9), 962-968. DOI: 10.1164/rccm.200805-670OC
Proud D, Sanders SP, & Wiehler S. (2004) Human rhinovirus infection induces airway epithelial cell production of human beta-defensin 2 both in vitro and in vivo. Journal of immunology (Baltimore, Md. : 1950), 172(7), 4637-45. PMID: 15034083
by Melinda Moyer in Body Politic
Canada deserves a big pat on the back: On Wednesday, our northerly neighbor added bisphenol A (BPA) to its list of known toxic substances. Canada still has to iron out how it will regulate the chemical, but this is definitely a step in the right direction. (Bryan Walsh over at Time just posted a great piece about this, too—among other things he explains why BPA is “a litmus test for environmental health and for risk tolerance.”)
Let me use this news as an excuse to talk some more about my (least) favorite chemical. (You knew it would happen.) We’ve known for a while where BPA hides—canned goods, polycarbonate bottles, and receipts, among other things. But how do these each contribute to our overall body BPA burden?
A study published in March in the Journal of Exposure Science and Environmental Epidemiology strived to answer just this question. Researchers at the University of Maryland and Penn State College of Medicine analyzed data from the 2005-2006 National Health and Nutrition Examination Survey and found that people who had the most BPA in their bodies also happened to consume the most soda, school lunches, and meals prepared outside the home—suggesting that these items might well be big culprits. Bottled water did not make a big difference (which makes sense: purchased bottled waters aren’t made from polycarbonate—it’s the hard re-usable bottles that are.)
School lunches and restaurant food make total sense to me: I’m guessing both rely on canned products to conserve cost. Last time I went to a Middle Eastern restaurant, for instance, I saw huge tins of canned chick peas lining the walls. It made me think twice about eating their hummus (but in the end, I did anyway—who can turn that stuff down?).
As for soda: I feel dumb, but I’ve never really thought of it as a BPA culprit. When I think of the “canned goods” that contain BPA, I tend to think about canned peaches and canned beans, not Coke or Sprite! But of course: BPA lines these cans, too, and Americans drink so damned much of the stuff, it’s bound to be a big contributor. Indeed, a study published by Canadian researchers in August in the Journal of Food Protection found BPA in every single sample of soda they collected from cans (and none in soda collected from bottles). Interestingly, they also found BPA in canned beer: yet another problem I hadn’t even thought about. Budweiser, you’re bad for us for so many reasons.
Citations:
LaKind, J., & Naiman, D. (2010). Daily intake of bisphenol A and potential sources of exposure: 2005–2006 National Health and Nutrition Examination Survey Journal of Exposure Science and Environmental Epidemiology DOI: 10.1038/jes.2010.9
Cao XL, Corriveau J, & Popovic S (2010). Sources of low concentrations of bisphenol A in canned beverage products. Journal of food protection, 73 (8), 1548-51 PMID: 20819371
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LaKind, J., & Naiman, D. (2010) Daily intake of bisphenol A and potential sources of exposure: 2005–2006 National Health and Nutrition Examination Survey. Journal of Exposure Science and Environmental Epidemiology. DOI: 10.1038/jes.2010.9
Cao XL, Corriveau J, & Popovic S. (2010) Sources of low concentrations of bisphenol A in canned beverage products. Journal of food protection, 73(8), 1548-51. PMID: 20819371
by Melinda Moyer in Body Politic
I just stumbled across a thought-provoking study that I have to share. Korean researchers publishing in the International Journal of Obesity have found that weight loss is associated with higher blood levels of persistent organic pollutants (POPs)—chemicals used to make pesticides and solvents that are notorious for accumulating in our bodies and in the environment. The researchers believe that POPs, which typically build up in fat, get released into the bloodstream when fat is burned. There, they could potentially cause health problems, increasing the risk for cancer, nervous system and reproductive damage (in part because many are considered endocrine disruptors).
The scientists conducted the study by interviewing 1099 adults about the weight changes they experienced over the course of the previous 10 years and the previous year. Then they compared these reported changes to the subjects’ current blood POP levels collected as part of the US National Health and Nutrition Examination Survey. (It’s important to note that they did not actually measure the POP levels at the earlier time periods.) They found that blood POP levels were higher in people who had reported long-term weight loss (and, to a lesser degree, short-term weight loss), and that POP levels were lower in people who had gained weight.
The study would have been more compelling if the researchers had measured the “before” and “after” POP concentrations; they were also relying on potentially inaccurate self-reports. But nevertheless, the findings are interesting. Plus, other studies have tracked POP levels and weight over time. For instance, a 2000 study published in the International Journal of Obesity and Related Metabolic Disorders collected blood samples from 39 obese people before and after they dieted for 15 weeks. The authors reported finding statistically significant increases in the blood levels of 15 organochlorine pesticides in the subjects after they dieted. And a 2006 study published in Obesity Surgery reported similar results in morbidly obese people who underwent bariatric surgery—their blood levels of organochlorine pesticidies spiked by more than 50 percent after surgery, and the more weight they lost, the higher their chemical levels rose—a finding that suggests that the chemical increases are not related to dietary changes.
Granted, these studies do not prove that weight loss causes increases in blood chemical levels. (I feel like I’m going to be writing a variant of that sentence in every post.) There could be other factors involved. And of course we all know that there are many health benefits associated with weight loss, so I’m not saying we start living on a diet of bacon and Dunkin’ Donuts, delicious—oh so delicious!—as that might sound. But there is some literature, including studies in PLoS Medicine and the Journal of Internal Medicine, suggesting that weight loss can be accompanied by health problems and even an increased risk of death. Most researchers have attributed these findings to the fact that weight loss can be the result of cigarette smoking or underlying illness, but it’s interesting to wonder whether circulating chemicals could be playing a role, too. Maybe; maybe not. It’s too soon to tell, but it’s certainly an interesting question.
Citations:
Lim JS, Son HK, Park SK, Jacobs DR Jr, & Lee DH (2010). Inverse associations between long-term weight change and serum concentrations of persistent organic pollutants. International journal of obesity (2005) PMID: 20820170
Chevrier, J., Dewailly, �., Ayotte, P., Mauriège, P., Després, J., & Tremblay, A. (2000). Body weight loss increases plasma and adipose tissue concentrations of potentially toxic pollutants in obese individuals International Journal of Obesity, 24 (10), 1272-1278 DOI: 10.1038/sj.ijo.0801380
Hue, O., Marcotte, J., Berrigan, F., Simoneau, M., Doré, J., Marceau, P., Marceau, S., Tremblay, A., & Teasdale, N. (2006). Increased Plasma Levels of Toxic Pollutants Accompanying Weight Loss Induced by Hypocaloric Diet or by Bariatric Surgery Obesity Surgery, 16 (9), 1145-1154 DOI: 10.1381/096089206778392356
Sørensen, T., Rissanen, A., Korkeila, M., & Kaprio, J. (2005). Intention to Lose Weight, Weight Changes, and 18-y Mortality in Overweight Individuals without Co-Morbidities PLoS Medicine, 2 (6) DOI: 10.1371/journal.pmed.0020171
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Lim JS, Son HK, Park SK, Jacobs DR Jr, & Lee DH. (2010) Inverse associations between long-term weight change and serum concentrations of persistent organic pollutants. International journal of obesity (2005). PMID: 20820170
Chevrier, J., Dewailly, �., Ayotte, P., Mauriège, P., Després, J., & Tremblay, A. (2000) Body weight loss increases plasma and adipose tissue concentrations of potentially toxic pollutants in obese individuals. International Journal of Obesity, 24(10), 1272-1278. DOI: 10.1038/sj.ijo.0801380
Hue, O., Marcotte, J., Berrigan, F., Simoneau, M., Doré, J., Marceau, P., Marceau, S., Tremblay, A., & Teasdale, N. (2006) Increased Plasma Levels of Toxic Pollutants Accompanying Weight Loss Induced by Hypocaloric Diet or by Bariatric Surgery. Obesity Surgery, 16(9), 1145-1154. DOI: 10.1381/096089206778392356
Sørensen, T., Rissanen, A., Korkeila, M., & Kaprio, J. (2005) Intention to Lose Weight, Weight Changes, and 18-y Mortality in Overweight Individuals without Co-Morbidities. PLoS Medicine, 2(6). DOI: 10.1371/journal.pmed.0020171
Drøyvold WB, Lund Nilsen TI, Lydersen S, Midthjell K, Nilsson PM, Nilsson JA, Holmen J, & Nord-Trøndelag Health Study. (2005) Weight change and mortality: the Nord-Trøndelag Health Study. Journal of internal medicine, 257(4), 338-45. PMID: 15788003
by Melinda Moyer in Body Politic
Last week, my husband sent me a link to a press release. (He loves sending me press releases that he thinks will incense me.) This one was a doozy: “One Egg Yolk Worse than a KFC Double Down When it Comes to Cholesterol,” the headline read. Um. Wow.
Intrigued (and, I’ll admit, a little incensed), I looked up the study—which actually turned out to be a review article—published in the Canadian Journal of Cardiology. I also looked up what I could find in the scientific literature about the risks associated with eating too many eggs. The general idea is that egg yolks contain upwards of 200mg of cholesterol, and dietary cholesterol is thought to increase blood cholesterol levels and therefore heart disease risk. But dietary cholesterol only contributes a tiny amount to your blood cholesterol—about 70 percent of your cholesterol is actually made by your liver. And I won’t go into this right now, but earlier this year in Slate, I discussed some of the reasons we should question the link between blood cholesterol levels and heart disease risk.
Here’s what I found: according to a handful of epidemiological studies, eggs aren’t so bad (and may even be good) for the heart. A study based on the famous Framingham Heart Study, which investigated the effects of host and environmental factors on the development of coronary heart disease, concluded that there is “no relationship between egg intake and coronary heart disease incidence.” A 1999 study published in the Journal of the American Medical Association drew on data from the Nurses’ Health Study and the Health Professionals Follow-Up Study and reported “no evidence of an overall significant association between egg consumption and risk of CHD or stroke in either men or women,” though the study did find that diabetic subjects had an increased risk of developing heart disease if they ate more than one egg per day. A 2008 study published in the American Journal of Clinical Nutrition analyzed data from 21,327 subjects who participated in the Physicians’ Health Study and concluded that egg consumption was not associated with heart attack or stroke. And finally, an analysis from the National Health and Nutritional Examination Survey (NHANES) III found that people who reported eating more than 4 eggs per week had significantly lower mean serum cholesterol levels that than those who reported eating less than 1 egg per week.
The epidemiological data seem pretty convincing to me, so I wondered how the authors of the review paper were going to address the findings. Interestingly, I found, they chose not to delve immediately into the science—instead, they began by attacking two studies published earlier this year that reported that eating eggs had health benefits, pointing out that the studies were funded by egg marketing agencies. There’s nothing wrong with questioning conflicts of interest in research, of course, but something about the vigor with which they made the point felt funny to me. I glanced to the end of the paper to see whether the authors had any conflicts of interests themselves. Here’s what I found:
None of the authors receives funding from purveyors of margarine or eggs. Dr Spence and Dr Davignon have received honoraria and speaker’s fees from several pharmaceutical companies manufacturing lipid-lowering drugs, and Dr. Davignon has received support from Pfizer Canada for an annual atherosclerosis symposium; his research has been funded in part by Pfizer Canada, AstraZeneca Canada and Merck Frosst Canada Ltd.
Okay, so it seems that Dr. Spence and Dr. Davignon have their own potential biases to contend with. Maybe they’re motivated by more than just concern for the health of their fellow Canadians? But back to the science: what do the authors say? “Concern about dietary cholesterol has been developing over the past 40 years,” they write. “This concern is based on the careful and independent conclusions of Ancel Keys and Mike Hegsted, who formulated our two most commonly used equations relating dietary saturated and polyunsaturated fat and cholesterol to serum cholesterol.” Now, I can’t say that I myself have closely looked at Keys’ and Hegsted’s work, but I know that science writer Gary Taubes has. His famous 2001 piece in Science, for instance, suggests that these “careful conclusions” aren’t actually based on sound data. I’m not going to go into all that here, but suffice it to say, I don’t think an equation that two scientists came up with 40 years ago trumps recent epidemiological data.
Thankfully, towards the end of the article, the authors do address the epidemiological findings. They mention the findings from the Physician’s Health Study suggesting that diabetics may for some reason be adversely affected by high egg consumption. Fine. But what about the risks posed to people without diabetes? “Failure to show harm from eggs in healthy people is likely an issue of statistical power,” they write. “In healthy people, a larger study with longer follow-up would be required.”
In other words, maybe all those studies just aren’t big enough to find evidence that eggs are harmful. Really, guys? The Health Professionals Follow-up Study included 37,851 people. The Nurses’ Health Study had 80,082. NHANES had 27,378. Surely if eggs were deadly, these studies would have found a signal amongst the noise. And as for your implication that people might be better off starting the morning with a KFC Double Down than a single egg yolk, well, that I can’t even dignify with a response.
Citations:
JD Spence, DJ Jenkins, J Davignon (2010). Dietary cholesterol and egg yolks: Not for patients at risk of vascular disease The Canadian Journal of Cardiology, 26 (9)
Dawber TR, Nickerson RJ, Brand FN, & Pool J (1982). Eggs, serum cholesterol, and coronary heart disease. The American journal of clinical nutrition, 36 (4), 617-25 PMID: 7124663
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JD Spence, DJ Jenkins, J Davignon. (2010) Dietary cholesterol and egg yolks: Not for patients at risk of vascular disease. The Canadian Journal of Cardiology, 26(9). info:/
Dawber TR, Nickerson RJ, Brand FN, & Pool J. (1982) Eggs, serum cholesterol, and coronary heart disease. The American journal of clinical nutrition, 36(4), 617-25. PMID: 7124663
Hu, F. (1999) A Prospective Study of Egg Consumption and Risk of Cardiovascular Disease in Men and Women. JAMA: The Journal of the American Medical Association, 281(15), 1387-1394. DOI: 10.1001/jama.281.15.1387
Djoussé L, & Gaziano JM. (2008) Egg consumption in relation to cardiovascular disease and mortality: the Physicians' Health Study. The American journal of clinical nutrition, 87(4), 964-9. PMID: 18400720
Song WO, & Kerver JM. (2000) Nutritional contribution of eggs to American diets. Journal of the American College of Nutrition, 19(5 Suppl). PMID: 11023007
Taubes, G. (2001) NUTRITION: The Soft Science of Dietary Fat. Science, 291(5513), 2536-2545. DOI: 10.1126/science.291.5513.2536
by Melinda Moyer in Body Politic
It’s easy to gloss over health care disparities until they start really affecting you or your loved ones. When I became pregnant this summer, I discovered that there is a dearth of information available about drug safety during pregnancy. (I wrote a little about it in this Slate article published in July.) Women who rely on medication get pregnant—for instance, one in eight pregnant women takes antidepressants—and pregnant women develop complications that require medicine. Yet the only drugs that have been approved by the FDA for use during pregnancy are for gestation- or birth-related problems, not for conditions like depression, hypertension or infection. And if you ask two obstetricians for their opinions about a drug’s safety, they’ll sometimes give you two different answers, as I discovered when I looked into taking Sudafed for a nasty cold I had this fall.
Certainly, it seems unethical to expose a fetus to a potentially dangerous drug in a clinical trial—after all, it cannot consent. But isn’t it worse to expose a fetus to a drug without any safety data at all, and outside the structured trial setting, where there is no patient monitoring? Yes, clinical trials in pregnant women could be dangerous. But not having them is even more so, given that pregnant women have to take drugs anyway—and without any knowledge of how they might affect them or their unborn children. Remember the sedative thalidomide, which caused pregnant women to give birth to babies with missing limbs in the 1950s, and DES, a drug prescribed to prevent miscarriages that increased the risk that female babies would develop rare vaginal cancers? Might we have avoided these disasters, or at least lessened their magnitude, if thalidomide and DES had been tested in controlled clinical trials in pregnant women first?
Thankfully, we haven’t had any major disasters like these in decades, but the FDA still makes drug recommendations based on little data. Take flu shots: The agency has been telling pregnant women to get seasonal flu shots since the 1960s, but the first randomized, prospective trial testing the vaccine on pregnant women and their babies was not completed until 2008—and it was comprised of just 340 subjects in Bangladesh. (Luckily, the trial suggests that flu shots are safe, although it only tracked the health of the babies for 24 weeks after birth.) For decades, then, the FDA’s recommendations and assurances about flu shots were not based on clinical trial evidence, but retrospective data, which is often flawed. “The agency said, ‘there’s so much risk, we won’t put you in a trial—but as soon as it’s approved in a different population, we’ll give it to you,’” explains Francoise Baylis, a bioethicist at the Dalhousie University in Canada. (Not that the FDA is entirely to blame—drug companies certainly have little interest in testing their compounds in pregnant women, a small population that could pose them serious liability risks.)
I struggled over the decision to get a flu shot myself. For one thing, last year in an article in the Atlantic, veteran science journalists Shannon Brownlee and Jeanne Lenzer raised questions over whether the vaccine actually works. And although pregnant women who catch the flu in the first half of their pregnancy are at an increased risk of giving birth to children who develop schizophrenia, given the timing of my pregnancy, I was at low risk for getting the flu then anyway—and I know from conversations with Caltech biologist Paul Patterson that there is a possibility that the vaccine itself confers this same increased risk. (For more about the link between prenatal infections, vaccines and mental illness, check out this feature I wrote in Scientific American MIND in 2008.) On the other hand, I also know that it could be dangerous to get sick in my third trimester, when I will be at an increased risk for serious respiratory problems. In the end, I decided to get the flu shot once I reached the halfway point in my pregnancy, when I felt the potential schizophrenia risk was minimal, and the shot could still (possibly) protect me towards the end of my pregnancy. Still, my decision was a gamble based on a lot of incomplete information.
It’s not just flu shots, though: pregnant women are taking more medicines than ever now, as they’re having babies later in life—when they tend to be on more drugs—and medical breakthroughs have made some pregnancies possible for the very first time. “We have people with cystic fibrosis who never in decades past would survive long enough to consider pregnancy, who are now living well into middle age and beyond,” says Ruth Faden, executive director of the Johns Hopkins Berman Institute of Bioethics. These women typically need to take medications throughout their pregnancy, yet no one knows their effects.
So what’s the solution? There isn’t a perfect one, but Baylis and Faden argue that there should be trials designed to test drugs in pregnant women who are going to be taking them no matter what. That way, structures are at least in place to collect data and look for adverse events. As for new experimental drugs, Baylis recommends incorporating pregnant women into later-stage trials, once the drugs have been shown to be safe and effective for other adults. “Instead of thinking of research as a risky activity,” she says, “we need to think of the continued off-label use of drugs [during pregnancy] as the risky activity.”
Citations:
Zaman, K., Roy, E., Arifeen, S., Rahman, M., Raqib, R., Wilson, E., Omer, S., Shahid, N., Breiman, R., & Steinhoff, M. (2008). Effectiveness of Maternal Influenza Immunization in Mothers and Infants New England Journal of Medicine, 359 (15), 1555-1564 DOI: 10.1056/NEJMoa0708630
Brown, A. (2005). Prenatal Infection as a Risk Factor for Schizophrenia Schizophrenia Bulletin, 32 (2), 200-202 DOI: 10.1093/schbul/sbj052
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Zaman, K., Roy, E., Arifeen, S., Rahman, M., Raqib, R., Wilson, E., Omer, S., Shahid, N., Breiman, R., & Steinhoff, M. (2008) Effectiveness of Maternal Influenza Immunization in Mothers and Infants. New England Journal of Medicine, 359(15), 1555-1564. DOI: 10.1056/NEJMoa0708630
Brown, A. (2005) Prenatal Infection as a Risk Factor for Schizophrenia. Schizophrenia Bulletin, 32(2), 200-202. DOI: 10.1093/schbul/sbj052
by Melinda Moyer in Body Politic
As I approach my third trimester, I’m becoming a bit of an omega-3 fiend. The unsaturated fatty acids have not only been tied to lower heart disease risk in adults, but they have also been shown to boost fetal brain development, especially when consumed in the final few months of pregnancy. Given that I’m not much of a cold water fish fan—the thought of chewing a mouthful of sardines makes me want to gag—I’ve been looking into how else to get them, and what I’ve uncovered has surprised me.
I had always assumed that fish were the best way to go. Don’t get me wrong, they do contain a lot: cooked fresh salmon and canned sardines provide 1.7 and 1.8 grams of omega-3s per four ounce serving, respectively. But as it turns out, some seeds and nuts and their oils pack even more of an omega punch. One ounce of walnuts, for instance, contains 2.6 grams of omega 3s—ounce for ounce, six times more than fresh salmon—and an ounce of flaxseeds provides 1.8 grams. Their oils are fabulous too: a tablespoon of walnut oil contains 1.4 grams, and flaxseed oil has a whopping 6.9 grams (you’d have to eat nearly a whole pound of canned sardines to get that—eww!). Don’t be fooled thinking that olive oil is better, either. It contains just 0.1 grams per tablespoon.
For a breakdown of some common foods and their omega 3 contents, check out this site maintained by Tufts University.
Citations:
PSOTA, T., GEBAUER, S., & KRISETHERTON, P. (2006). Dietary Omega-3 Fatty Acid Intake and Cardiovascular Risk The American Journal of Cardiology, 98 (4), 3-18 DOI: 10.1016/j.amjcard.2005.12.022
JACOBSON, J., JACOBSON, S., MUCKLE, G., KAPLANESTRIN, M., AYOTTE, P., & DEWAILLY, E. (2008). Beneficial Effects of a Polyunsaturated Fatty Acid on Infant Development: Evidence from the Inuit of Arctic Quebec The Journal of Pediatrics, 152 (3), 356-3640 DOI: 10.1016/j.jpeds.2007.07.008
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PSOTA, T., GEBAUER, S., & KRISETHERTON, P. (2006) Dietary Omega-3 Fatty Acid Intake and Cardiovascular Risk. The American Journal of Cardiology, 98(4), 3-18. DOI: 10.1016/j.amjcard.2005.12.022
JACOBSON, J., JACOBSON, S., MUCKLE, G., KAPLANESTRIN, M., AYOTTE, P., & DEWAILLY, E. (2008) Beneficial Effects of a Polyunsaturated Fatty Acid on Infant Development: Evidence from the Inuit of Arctic Quebec. The Journal of Pediatrics, 152(3), 356-3640. DOI: 10.1016/j.jpeds.2007.07.008
by Melinda Moyer in Body Politic
I’ve always been a big fan of Michael Shermer’s Skeptic column in Scientific American, but this month I have to say I’m disappointed. In his piece (which is not yet online), titled “Can You Hear Me Now? Physics shows that cell phones cannot cause cancer,” Shermer argues that it is “virtually impossible” for cell phones to cause cancer because they “do not emit enough energy to break the molecular bonds inside cells.” While this latter statement may be true—the radiation that cell phones emit is not thought to be energetic enough to directly break DNA molecules—it is not fair (or scientific, for that matter) to use this as proof that cell phones do not cause cancer. The issue is far more complex than that.
Biologists once assumed that mutations were responsible for most diseases; now we know that more subtle genetic (and epigenetic) variations play an even bigger role. Many scientists also once thought that “junk DNA” didn’t have a function, but now research is pouring in suggesting that, in fact, non-coding DNA is responsible for many aspects of gene regulation; some RNA molecules once dismissed as garbage might even run the entire show. Genetics isn’t simple, my friends—and neither is cancer, for that matter. Despite decades upon decades of research, scientists still don’t know all of the ways in which cancer can be sparked. So to announce to the world—in an authoritative magazine like Scientific American, no less—that something definitely does not cause cancer simply because it cannot break DNA seems like a really irresponsible thing to do.
You’re probably wondering: how might cell phones cause cancer, then? Cancer develops when the cell cycle goes awry and cells start to multiply when they should not. Considering that thousands of genes are thought to be involved in the cell cycle—and an as yet unknown number of non-protein-coding sequences might regulate them—there are plenty of potential factors to consider. Cell cycle genes can be disrupted because of a mutation or a DNA break, sure, but problems could also arise when, say, something causes a tumor-suppressor gene like p53 (which protects against cancer) to be downregulated, perhaps from a post-translational modification or a change to chromatin structure. Or maybe something in the environment ramps up the expression of a growth-promoting gene, causing a cell to abnormally proliferate. Environmental influences could also disrupt the DNA repair machinery, as this would allow DNA breaks that arose as a result of some other process to go unfixed. If cell phones did any one of these things, they could easily increase cancer risk—but there are all possibilities that Shermer ignores when he concludes at the end of his column that “it is impossible for cell phones to hurt the brain.” For him, it seems, there is only one route to cancer—direct DNA breaks—but that’s simply not true.
So is there any evidence that cell phones can do the things I just mentioned? Actually, yes. A handful of studies, including one published in 2005 in Environmental Health Perspectives and another published in Bioelectromagetics, report that cell phone radiation affects chromatin conformation, which directly impacts gene expression and could, therefore, affect the cell cycle. These studies also found that cells exposed to cell phone radiation produce less of a protein complex called 53BP1 believed to be involved in DNA repair. In addition, research published by University of Washington researchers in the 1990s found that cell phone radiation elicited DNA breaks in rat brain cells (something Shermer doesn’t address in his piece, though it directly contradicts his assertion); the authors speculated that the radiation was probably interrupting the DNA repair process. (As an aside: I interviewed one of these researchers, Henry Lai, for my 2008 article about cell phones in Canada’s The Walrus magazine; after he published this study, a scientific advisory group created by the organization that represents the wireless industry sent a letter to the president of the University of Washington demanding that he and his co-author both be fired. They were not.)
It’s a big step to conclude from these studies that cell phones cause cancer, of course, and I’m not about to do that. I’m also not going to delve into the mess of epidemiological data on the topic, but if you’re curious, you can read more about some of it in my Walrus piece and a related article I wrote for Scientific American in 2008. My point here is not that cell phones are deadly, but rather that in his column, Shermer does a disservice to his readers by unfairly concluding that cell phones must be safe because they do not directly cause DNA breaks. Science—especially biology—is rarely that cut and dried.
Citations:
Belyaev IY, Markovà E, Hillert L, Malmgren LO, & Persson BR (2009). Microwaves from UMTS/GSM mobile phones induce long-lasting inhibition of 53BP1/gamma-H2AX DNA repair foci in human lymphocytes. Bioelectromagnetics, 30 (2), 129-41 PMID: 18839414
Belyaev, I., Hillert, L., Protopopova, M., Tamm, C., Malmgren, L., Persson, B., Selivanova, G., & Harms-Ringdahl, M. (2005). 915 MHz microwaves and 50 Hz magnetic field affect chromatin conformation and 53BP1 foci in human lymphocytes from hypersensitive and healthy persons Bioelectromagnetics, 26 (3), 173-184 DOI: 10.1002/bem.20103
Wang, B. (2002). 53BP1, a Mediator of the DNA Damage Checkpoint Science, 298 (5597), 1435-1438 DOI: 10.1126/science.1076182
... Read more »
Belyaev IY, Markovà E, Hillert L, Malmgren LO, & Persson BR. (2009) Microwaves from UMTS/GSM mobile phones induce long-lasting inhibition of 53BP1/gamma-H2AX DNA repair foci in human lymphocytes. Bioelectromagnetics, 30(2), 129-41. PMID: 18839414
Belyaev, I., Hillert, L., Protopopova, M., Tamm, C., Malmgren, L., Persson, B., Selivanova, G., & Harms-Ringdahl, M. (2005) 915 MHz microwaves and 50 Hz magnetic field affect chromatin conformation and 53BP1 foci in human lymphocytes from hypersensitive and healthy persons. Bioelectromagnetics, 26(3), 173-184. DOI: 10.1002/bem.20103
Wang, B. (2002) 53BP1, a Mediator of the DNA Damage Checkpoint. Science, 298(5597), 1435-1438. DOI: 10.1126/science.1076182
LAI, H. (1996) Single-and double-strand DNA breaks in rat brain cells after acute exposure to radiofrequency electromagnetic radiation. International Journal of Radiation Biology, 69(4), 513-521. DOI: 10.1080/095530096145814
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