Each year, we hear that people are gaining weight and that chronic health problems like obesity, heart problems, and diabetes are on the rise.  It’s commonplace to ascribe these trends to personal lifestyle choices, such as the lack of exercise and diet, as well as the increasingly pervasive nature of fast food and processed, high-sugar foods.

However, there may be additional risk factors that are harder to control, such as genetics, and—as  a provocative new article in PLoS One (open access) suggests—birth order.  Specifically, first-born children might be more prone to these kinds of chronic health issues later in life:

Recent work has suggested that birth order may be a non-modifiable risk factor for obesity. Current evidence suggests that first-born infants grow faster than later-born infants. Dunger et al. suggest that the in-utero growth of first-born babies may be restrained as they have lower birth weight and accelerated post-natal catch-up growth, both of which are risk factors for obesity and cardiovascular and metabolic diseases, in adult life. However, whether first-born individuals have elevated metabolic risk in adulthood remains unknown. A recent study found that first-borns had a 4-fold risk of increased fat mass in early adulthood compared to later-borns. Neither of these studies evaluated the magnitude of metabolic risk induced by such greater weight and adiposity.

…Here we investigate the associations of birth-order with metabolic phenotype in early adulthood using data from a birth cohort of Brazilian young men. We tested two hypotheses. First, we wanted to confirm that first-born status was associated with low birth weight and faster infant growth. Second, we tested the hypothesis that metabolic risk was increased in first-borns compared to later-borns.

What did they find? What implications might their work have for public health given the kinds of global population changes we expect over coming decades?

Some results (excerpts):

• After adjusting for family income, maternal education, household assets score and maternal smoking in pregnancy, first-borns had significantly lower mean birth weight.
• First-borns also showed faster weight gains during infancy and had greater mean height and weight at 43 months.
• This greater weight and height tracked into early adulthood, with first-borns being significantly taller and heavier than later-borns.
• Total cholesterol and low-density lipoproteins were higher among first-borns.
• Our analysis suggests that low birth weight does not itself explain the increased metabolic risk associated with birth order. Rather, rapid post-natal weight gain appears most important, although such rapid growth is itself a response to low birth weight. Broadly similar growth patterns have been linked to the occurrence of type 2 diabetes and coronary events in adults.

So why do these patterns happen?  Here is their hypothesis:

The lower birth weight of first-borns can be attributed to materno-fetal physiological interactions. Following implantation, cells from the outer layer of the blastocyst, known as trophoblast, invade the maternal endometrium and alter the structure of the arteries that transfer blood to the placenta. Such modification decreases maternal resistance and increases placental blood flow. These changes then impact on the placental dynamics of subsequent pregnancies, such that second-born neonates are well known to have higher average birth weight than first-borns. Dunger et al. suggested that first-born children have higher glucose levels compared to later-borns, an effect most likely due to the combined effect of insulin resistance due to the increased adiposity and to the possible in utero programming of the insulin glucose axis. Thus, the increased adult body weight and adiposity of first-borns is likely to be induced at least in part by the maternal constraint of intra-uterine growth. However, other mechanisms may also be important. There is preliminary evidence in animals and in humans, that the novel experience of the first pregnancy could raise the level of apprehension in primigravid women, thereby potentially affecting the growth of the foetus via modulation of the vascular and endocrine functions of the feto-placental unit. Maternal emotional stress is an established risk factor for low birth weight, intrauterine growth retardation, preterm delivery and still-birth. Specifically, circadian cortisol secretion pattern appears to be distinctive in primiparous women and an alteration of the hypothalamus-pituitary axis (HPA) function could modify maternal glucocorticoids levels and affect foetal development. Possible mechanisms for birth-order effects on foetal growth merit further research.

And what potential implications might this have for the health of the global human population as we approach 9 billion people on the planet by 2050 and move through demographic transitions, such as reduced family sizes (emphasis mine)?

Our findings contribute to understanding of the early origins of adult disease. Our data show that a demographic factor relevant to all human populations can generate variability in both early growth and later metabolic risk. These findings also have important implications for understanding the increasing prevalence of the metabolic syndrome worldwide, where many populations are undergoing demographic change in response to economic development. Globally, there is a trend towards lower fertility rate, such that increasing proportion of individuals will be first-borns. In Brazil, for example, the average number of children per women (total fertility rate) dropped from 6.0 in 1960 to 1.8 currently.

They conclude with several important qualifications:

[A] number of questions still merit attention. For example, studies should describe in more detail the growth patterns that appear to lead to elevate metabolic risk, and identify the optimal time periods for intervention. Studies should also clarify the relative contribution of different possible underlying mechanisms (growth patterns, psychological factors) to the effects that we observed in these samples. Third, more research is required to establish the magnitude of the effect, whether it is similar in men and women, and whether it amplifies with age, as adverse metabolic profile consolidates. In these samples of young adults, the magnitude of the effect was relatively small, but degenerative diseases are expressed primarily from middle age and early-life effects tend to become more important through adulthood.

Siervo, M., Horta, B., Stephan, B., Victora, C., & Wells, J. (2010). First-Borns Carry a Higher Metabolic Risk in Early Adulthood: Evidence from a Prospective Cohort Study PLoS ONE, 5 (11) DOI: 10.1371/journal.pone.0013907

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In a forthcoming article in the Proceedings of the National Academy of Sciences, Patric Allard and Monica Colaiácovo use a nemotode (round worm) system to explore how BPA damages genetic processes in animals.

BPA ranks among the highest production volume chemicals with a global annual production scale of ≈4 million metric tons. It is commonly used in the manufacture of several polymers, including polycarbonate and epoxy resins. Thus, BPA is found in a variety of items such as plastic bottles, the lining of both food and beverage cans, and dental sealants. Consistent with its widespread presence, urinary BPA is detected in >90% of the population in the United States. Higher levels of urinary BPA have been correlated with cardiovascular diseases and diabetes and may be associated with an increased risk for miscarriages.

Their results?

Using these conditions, we observed a sixfold reduction in the mean number of eggs laid (increased sterility) and a dramatic increase in embryonic lethality (97.3%; n = 333) in worms exposed to 1 mM BPA compared with vehicle. Furthermore, none of the rare larvae observed either reached adulthood or survived after 3 d in culture (100% larval lethality). Taken together, these phenotypes indicate that BPA impairs C. elegans reproduction and are suggestive of errors in chromosome segregation.

Why was this?  They found that worms exposed to BPA had dysfunctional DNA repair mechanisms that ordinarily fix breaks in genetic material.  It turns out that BPA exerts hormone-like effects and turns off the gene that makes the DNA repair proteins.

Without these repairs, the animals were not able to produce eggs (in an important cell division process called meiosis) with normal genetic material.  This led to incorrect chromosome alignment and separation in the cell division of embryonic worms.

Bottom line:  Exposure to BPA caused these worms to become sterile and exhibit elevated emrbyonic mortality.

There’s always a challenge in using lab animal models to extrapolate to human health.  One of the main criticisms of these kinds of studies is that the exposure concentrations are different than what people are experience on a daily basis.  The authors address this (emphasis mine):

We examined the internal levels of BPA following our exposure protocol and found that worms contained on average 2 μg/g of unconjugated BPA. These levels were within the range or lower than the internal free BPA levels detected in maternal kidneys, liver, and uterus, as well as in fetal liver and total fetal homogenate of pregnant rats perfused with a single dose of BPA at 10 mg/kg. Data on nonblood tissue levels of BPA both in rodent models and in humans are scarce and intraorgan concentrations in the BPA study on mouse meiosis were not measured, making direct exposure comparison difficult. However, it is likely that both our results and those of Susiarjo and colleagues represent the reproductive outcome following elevated BPA exposure. Therefore, our studies bear relevance to occupational exposure studies in humans, and particularly to fetal and neonate exposure levels, as suggested by the up to 10 times higher levels of BPA detected in premature infants in neonatal intensive care units.

Patrick Allard and Monica P. Colaiácovo (2010). Bisphenol A impairs the double-strand break repair machinery in the germline and causes chromosome abnormalities Proceedings of the National Academy of Sciences : 10.1073/pnas.1010386107

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In a fascinating new article in PLOS One (open access), Daniel Nettle asks why we see social gradients in preventative health behaviors:

People of lower socioeconomic position have been found to smoke more, exercise less, have poorer diets, comply less well with therapy, use medical services less, adopt fewer safety measures, ignore health advice more, and be less health-conscious overall, than their more affluent peers. Some of these behaviors can simply be put down to financial constraints, as healthy diets, for example, cost more than unhealthy ones, but socioeconomic gradients are found even where the health behaviors in question would cost nothing, ruling out income differences as the explanation.

As we often assume with environmental or nutritional issues, maybe simply helping to better educate people is all that’s needed? Probably not, as Nettle points out, and with an interesting twist:

Socioeconomic gradients in health behavior are not easily abolished by providing more information. Informational health campaigns tend to lead to greater voluntary behavior change in people of higher socio-economic position, and thus can actually increase socioeconomic inequalities in health, even whilst improving health overall. Thus, we are struck with what we might call the exacerbatory dynamic of poverty: the people in society who face the greatest structural adversity, far from mitigating this by their lifestyles, behave in such ways as to make it worse, even when they are provided with the opportunity to do otherwise.

What are some of the possible explanations for this pattern, and are they sufficient?

Underlying socioeconomic differences in health behavior are differences in attitudinal and psychological variables. People of lower socioeconomic position have been found to be more pessimistic, have stronger beliefs in the influence of chance on health, and give a greater weighting to present over future outcomes, than people of higher socioeconomic position. These explanations seem clear.

However, they immediately raise the deeper question: why should pessimism, belief in chance, and short time perspective be found more in people of low socioeconomic position than those of high socioeconomic position? These deeper questions are at the level which behavioral ecologists call ultimate, as opposed to proximate causation

To develop more of an ultimate explanation, Nettle hypothesized that lower socioeconomic groups are subject to greater hazard or environmental harm or even simply the perception of living a more hazardous life.  This, in turn, discourages healthy behavior.

To test this hypothesis, he developed a mathematical/statistical model predicting the probability of dying in a given year, which is a combination of extrinsic risks that people cannot control as well as intrinsic risks that they can control through modified health behavior.   Thus, people choosing to take the time to engage healthier opportunities reduce their mortality risk.  Now there’s a tradeoff, however, because the more time people choose to undertake healthy behavior, the less time is left over for leisure activities and other life events.

Overall survival is therefore a combination of all of these factors, which can easily be modeled by assuming a range of values for time spent on health vs. other activities to see what kinds of mortality outcomes arise.

Here are the interesting results he found…

If it is the case that lower socioeconomic position is associated with a greater rate of extrinsic hazards (an assumption which needs justifying, see below), then we should expect people to respond to lower socioeconomic position with reduced preventative health behavior, because the benefits of that behavior to them are indeed lessened. This would in turn make their health outcomes worse, and so the gradient in health outcomes should in general be steeper than the underlying gradient in extrinsic risk exposures. Thus, the observed pattern of substantial socioeconomic gradients in health, which are to a  significant extent mediated by differences in health behavior, is exactly what we would predict if people are behaving adaptively given the environment in which they live.

Previous research on social inequalities in health behavior has found that people faced with socioeconomic deprivation endorse a greater belief in the influence of chance on life outcomes, particularly in the domain of health, are more pessimistic, and devalue future outcomes relative to present ones more sharply, than people of higher socioeconomic position. The model presented here is not in any sense an alternative to these accounts. On the contrary, the model here suggests an ultimate reason why these proximal psychological patterns might persist, and the proximal psychological accounts suggest how the adaptive behavior might actually be delivered. Clearly, people do not perform exact actuarial calculations in deciding whether to adopt a particular health behavior. Instead, they presumably employ some simple evolved heuristics. In this case, these might include something like ‘to the extent you see bad and unpredictable health outcomes besetting your peers, worry about today rather than tomorrow’.

And here’s where the environmental link comes in:

Several lines of evidence suggest that the assumption that lower socioeconomic position is associated with a greater degree of extrinsic hazard may not be unreasonable. First, studies of health inequalities generally find that controlling for behavioral factors (smoking, diet, etc.) attenuates socioeconomic gradients in health outcomes, but does not abolish them entirely. Of course, this could simply mean that not enough controls have been included, but it could also suggest that there is a residuum of health hazard which is extrinsic and thus not responsive to individuals’ behavioral decisions. Second, there are some health risk factors whose spatial distribution is socioeconomically patterned, and which people living in more deprived areas can do very little to avoid save for not living there. The clearest examples are noise, lead, and air pollution in the form of fine particles and nitrogen oxides. The levels of these hazards are higher in poor neighbourhoods, and their effects on morbidity and mortality well established. Third, many studies have found effects of living in poor neighbourhoods on health outcomes, above and beyond the effects of individual level socioeconomic characteristics. For example, poorer neighbourhoods are associated with substantially increased chances of accidental death or homicide, and heart disease, even once individual characteristics are adjusted for. This suggests that there are hazards fundamentally associated with living in these areas, which affect whoever it is that lives there.

In general, the model presented here draws the focus of health policy away from merely providing information or exhorting behavioral change, and onto extrinsic mortality. As with other neo-material approaches to health inequalities, it reminds us of the need to address the fundamental economic inequities which mean that some neighbourhoods contain higher risks of pollution, toxicity, and accident than others. More specifically, it suggests that reducing these structural inequities will reap a double dividend. It will have a primary effect on mortality inequality, and also a secondary effect as people respond to the primary effect by increasing their health-promoting behavior. Indeed, the secular trend in health behavior amongst middle-class people could be interpreted in this way. As economic development has eliminated many of the uncontrollable sources of danger, individuals have increased their investment in behaviors that mitigate those risks which do respond to individual choice. We need to create a similar dynamic in the most disadvantaged areas.

However, whilst changing structural conditions is the most important priority, the model also suggests that it is worth paying attention to people’s perceptions of extrinsic mortality. That is, in poor communities, individuals may perceive the local environment to be extrinsically dangerous to a greater extent than is in fact true (for example, because they are affected by social stereotypes or media portrayals). The model suggests that the psychological mechanisms which underlie behavioral decisions should be responsive to perceived levels of extrinsic mortality. If these perceptions are unrealistic, then they may lead to excessive fatalism and consequent disinvestment in health behavior. Thus, researchers and practitioners could usefully examine the genesis and malleability of people’s perceptions of the extrinsic dangers of their environments, and the relationships of these to their health attitudes and health behaviors.

What I love about this article is how it situates problems of sociology, psychology, public health, and justice squarely in the context of the environment—both actual and perceived.  And it encourages those of us interested in public health and well being to borrow a page from people engaged in environmental justice and just sustainability initiatives.

I also like how this result dismantles traditional notions of environmentalism and public health and forces us to consider new ways of studying pervasive problems in our world, where environmental studies scholars collaborate more with sociologists, psychologists, and historians to understand the ultimate causes of linked social-environmental challenges.

Nettle, D. (2010). Why Are There Social Gradients in Preventative Health Behavior? A Perspective from Behavioral Ecology PLoS ONE, 5 (10) DOI: 10.1371/journal.pone.0013371

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Photo credit: postopp1

The apparent bottom line for cell phone safety:

• Use texting instead of voice calling.
• Use an earpiece if you must voice call.
• Keep your cell phone at least an inch away from your body at all times while it’s on.

The full article is worth reading.  Below are a few excerpts of the review and Rogers’ interview with Davis:

In “Disconnect,” Devra Davis, a scientist and National Book Award finalist for “When Smoke Ran Like Water,” looks at the connection between cellphones and health problems, with some disturbing results. Recent studies have tied cellphone use to rises in brain damage, cheek cancer and malfunctioning sperm. She reveals the unsettling fact that many new cellphones now come with the small-print warning that they are to be kept at least one-inch from the ear (presumably for safety reasons) and many insurance companies refuse to insure cellphone companies against health-related claims. Most troubling of all, science has shown that children and teenagers are particularly susceptible to cellphone radiation, raising questions about its effects on coming generations.

What to you is the most compelling evidence that links cellphones to brain cancer?

The brain cancer connection is in fact a very complicated one. Cancer can take a long time to develop. After the Hiroshima bomb fell, there was no increase in brain cancer for 10 years, even 20 years afterward. Forty years later, there was a significant increase in brain cancer in people who survived the bombing. Now, for studies of people who have been heavy cellphone users (defined as someone who has made a half-hour call a day for 10 years), there is a 50 percent increase in brain cancer overall. And among the heaviest users there’s a two- to fourfold increased risk.

We’ve only really been using cellphones for 10 years. Isn’t it a bit early to be drawing these kinds of conclusions?

Well, that’s actually not true. Heavy use of cellphones in the United States is a very recent phenomenon for the general population. In the year 2000, fewer than half of us regularly used cellphones. Now almost all of us do. If there’s a 10-year latency, we still have to wait another five years in the United States to see any general population impacts.

You have to look at all of the evidence and not simply wait for proof of human harm or sick people or dead people. If the debate becomes, “Do we have sufficient proof of human harm?” that means we’re waiting another 20 years. That means we will potentially have an epidemic before we act to prevent harm. Now, some people could be very cynical and say, look, brain cancer is relatively rare so even if it doubles or quadruples it’s still rare. But it’s also, at this point, mostly incurable.

Why are young people so much more at risk?

Their brains are not fully protected with myelin. Myelin is a kind of fatty sheath that goes around neurons [brain cells] and helps to enhance judgment and a whole bunch of other things, like impulse control. Their skulls are also thinner, and a thinner skull admits more radiation. We now know that the young brain doesn’t mature until the mid-20s, later in boys than girls. We need to be much more vigilant about protecting the young brain because it is more vulnerable. We know that from work that’s been done on lead and a number of other agents.

If this research is really as convincing as it seems to be, then why hasn’t it created a widespread uproar?

Well, it has in France. Bills passed both houses of the French national government this spring that ban the marketing and creation of phones uniquely for children. It’s also had an impact in Israel, a country that is very sophisticated in its use of radar and microwaves, and Finland, both of which have issued warnings.

But think about the fine print warning that comes with BlackBerry Torch. It says, If you keep the phone in your pocket, it can exceed the FCC exposure guidelines. What’s that supposed to tell you? It sounds like that phone cannot safely be put in your pocket — well, where do they expect people to keep them?

….The book also describes the aggressive push-back by people affiliated with the cellphone industry against scientists whose findings point to safety concerns — including, in one case, a campaign to discredit someone’s findings by accusing them of manufacturing evidence. It’s pretty explosive stuff.

I think it might have started out as nothing more than companies wanting to make profits, and wanting to keep their products in a positive light. Companies are allowed to make profits; I’m not opposed to that. And I imagine people genuinely thought these kinds of dangers from radiation weren’t possible, because the physics paradigm [at the time] said it wasn’t. But it has since been morphed into something worse. Now even the insurance industry is listening to scientists. Many companies are no longer providing coverage for health damage from cellphones.

We need to be more sophisticated as a society in using experimental data where we have it. We have experimental data on sperm counts. We have experimental data on brain cell damage. We have experimental data on biological markers that we know increase the risk of cancer. These are the same debates that went out over passive smoking, over active smoking, over asbestos, over benzene, over vinyl chloride. They said we don’t have enough sick or dead people. The consequence was to continue exposing people. Is there anybody in the world who believes we should have waited as long as we did?

Read more.

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There’s a new paper in this week’s issue of Science that suggests that growing a landscape mixed with genetically modified (GM) Bt corn and non-GM hybrid varieties of corn can be mutually beneficial to all corn farmers.

Why?  They argue that the populations of GM corn knock down the populations of insect herbivores enough that, on a landscape scale, this effect spills over to nearby farmers growing non-GM corn, which raises yields and profits:

[W]e estimate that cumulative benefits for both Bt and non-Bt maize growers during the past 14 years were almost $6.9 billion in the five-state region (18.7 million ha in
2009)—more than $3.2 billion in Illinois, Minnesota, and Wisconsin, and $3.6 billion in Iowa and Nebraska. Of this $6.9 billion total, cumulative suppression benefits to non-Bt maize growers resulting from O. nubilalis [European corn borer] population suppression in non-Bt maize exceeded $4.3 billion—more than $2.4 billion in Illinois, Minnesota, and Wisconsin, and $1.9 billion in Iowa and Nebraska—or about 63% of the total benefits.

They suggest that the populations of non-GM corn also benefit the Bt corn farmers because the non-GM corn maintains a genetically diverse population of insects, helping prevent the evolution of herbivores resistant to Bt corn.

These results are interesting and —if they hold—could be an example of how GM crops bring environmental and social benefits.  A good outcome for all.

However, there are a couple of important things to consider:

(1) The notion of mixing crop types to minimize herbivory is the one of the fundamental tenets of traditional agroecology and organic agriculture, but instead of relying on GM crops, it could be done with a mix of hybrid crop varieties that doesn’t risk the potential environmental side effects of Bt corn or other unexpected outcomes of GM crops.  This is a major value judgment.   Does having one GM crop and a few dominant corn varieties count as diversity when the Midwest becomes a giant sea of maize?  As I explain in #2 below, probably not.  Could we achieve the same kind of insect pest management using a diversity of non-GM crops?  Yes—it happens all the time in midwestern organic farms.  Multi-crop organic farming is often more labor intensive than industrial agriculture, making the food produced more expensive.  But do we only care about cheap food?

(2) I’ve lived in southern Minnesota, where it’s a giant rotating monoculture of corn and soybeans.  If you look at Figure 1 in this paper, you will see that 50-75% (or more) of the corn grown in many regions of states like Iowa, Nebraska, and Minnesota is Bt corn.  When so much of your landscape is Bt corn, the evolution of resistance to Bt is most likely inevitable, as we saw in a previous post with the use of Roundup-ready crops like soybeans, which are often grown in rotation with Bt corn in these regions.   Acknowledging this fact of life, EPA recommends mixing GM and non-GM corn in an effort to delay the evolution of resistance, not prevent it:

To delay evolution of resistance, the U.S. Environmental Protection Agency (EPA) mandated that a minimum 20 to 50% of total onfarm maize be planted as non-Bt maize within 0.8 km of Bt fields as a structured refuge for susceptible O. nubilalis. Use of non-Bt maize refugia is an important element of long-term insect resistance management.

…Sustained economic and environmental benefits of this technology, however, will depend on continued stewardship by producers to maintain non-Bt maize refugia to minimize the risk of evolution of Bt resistance in crop pest species, and also on the dynamics of Bt resistance evolution at low pest densities and for variable pest phenotypes.

Hutchison, W., Burkness, E., Mitchell, P., Moon, R., Leslie, T., Fleischer, S., Abrahamson, M., Hamilton, K., Steffey, K., Gray, M., Hellmich, R., Kaster, L., Hunt, T., Wright, R., Pecinovsky, K., Rabaey, T., Flood, B., & Raun, E. (2010). Areawide Suppression of European Corn Borer with Bt Maize Reaps Savings to Non-Bt Maize Growers Science, 330 (6001), 222-225 DOI: 10.1126/science.1190242

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Photo credit: Ian Hayhurst

There has been a lot published recently on the source of happiness and what constitutes the good life, with many articles focusing on levels of personal income that mark tipping points, such as the recent claim that we need $75,000 to be happy.

In this week’s Early Edition of the Proceedings of the National Academy of Sciences (open access), Bruce Headey and colleagues describe how happiness is also being explored in terms of fundamental differences between psychological and economic theory:

Research on life satisfaction or happiness used to be a minor branch of psychology, became a major branch, and then in the past decade has attracted huge interest among economists. Some of these economists now use satisfaction measures as proxies for the outcome which economic agents are assumed to maximize—namely, individual utility. But the assumptions and findings of psychologists and economists are contradictory.

In one corner, psychological theory:

The dominant theory in psychology is probably still set-point theory…[which] holds that long-term adult happiness is stable—it has a setpoint—because it depends mainly on genetic factors, including personality traits molded and expressed early in life. It has been shown that major life events can temporarily change happiness levels, but that most people revert to their previous setpoint within a year or two. The theory can be summarized by saying that, “We are all on a hedonic treadmill”.

…An obvious implication is that neither individual choices nor public policy can make a substantial long-term difference to happiness.

In the other corner, economic theory:

Economists who, following the recent advice of the Commission on the Measurement of Economic Performance and Social Progress, now intend to use direct satisfaction-based measures of utility [happiness] must necessarily assume the opposite. There is no point in deploying such measures if individual preferences, behavioral choices, and public policy could not increase long-term satisfaction.

Research on happiness (relabeled as subjective utility) by economists developed rapidly in the 1990s, ironically just as setpoint theory became dominant… Economists have not developed a counter theory, but pursue a strategy of seeking to account for variance in life satisfaction due to individual utility maximizing behavior and policy interventions.

Economists have also developed explanations for why happiness may not appear to change over time that have nothing to do with happiness set points:

…Contrary to what a layperson might suppose, modern economists, starting with Richard Easterlin (the Easterlin paradox), have repeatedly claimed that money does not buy much happiness, especially in wealthy Western countries. The paradox
has been challenged…but critics have never been able to show that long-term income growth produces long-term gains in happiness. This nonoutcome arises mainly because rising incomes are subject to social comparisons with the neighboring Jones’s, whose incomes also keep going up. People adapt to their own and their neighbors’ new levels of income by raising their expectations, with the result that no lasting increase in happiness occurs.

How do you study these ideas?  By using an enormous data set:

…The German Socio-Economic Panel Survey (SOEP) provides by far the longest data series available worldwide. It reports interviews with a very large national representative sample aged 16 and over, who have answered questions about their life satisfaction every year from 1984 to 2008.

What did they find, and who cares?

During this quarter-century, large numbers of respondents recorded substantial and apparently permanent changes in satisfaction…[T]he scale of change indicates that set-point theory is seriously flawed. A key implication is that the economist’s goal of enhancing (subjective) utility via changes in individual behavior and public policy is not condemned to inevitable failure by human psychology. Nonfixed, nongenetic factors, including individual choices and public policy, may influence satisfaction levels, or utility so measured.

The authors go on to talk more about life factors that drive happiness, showing that things people can change about their lifestyle matter as much or more than personality traits or being married—things we might consider to be fixed in our lives.  Some we’ve heard before, but other insights are new and interesting (emphasis mine):

…[W]e have shown that life goals, religion, and personal choices matter for happiness. Key choices relate to one’s partner, the tradeoff between work and leisure, social participation, and healthy lifestyle. Life goals and choices have as much or more impact on life satisfaction than variables routinely described as important in previous research, including extroversion and being married or partnered. If we use these last two variables as benchmarks, it appears that partner’s level of  neuroticism, one’s own commitment to family and altruistic goals, church attendance, participation in social events, and regular exercise are all equally or more important than being extroverted.

…For both men and women, doing fewer paid hours of work than they want apparently has close to the same impact on life satisfaction as not being married/partnered. For women, being obese actually reduces life satisfaction more than not having a partner.

…people who find themselves working much more or less than they want are significantly less satisfied with life than those who come close to making their preferred tradeoff between work and leisure. For both men and women, being underworked is much worse than being overworked, presumably because lost consumption rankles worse than lost leisure.

…people who consistently prioritize non–zero-sum altruistic goals or family goals are more satisfied with life than people who prioritize goals relating to their own careers and material success. Giving priority to altruistic goals is strongly associated with higher life satisfaction, whereas family goals are also satisfaction enhancing. Corroborating some previous research, it appears that prioritizing success and material goals is actually harmful to life satisfaction.

Headey, B., R. Muffels, and G.G. Wagner (2010). Long-running German panel survey shows that personal and economic choices, not just genes, matter for happiness Proceedings of the National Academy of Sciences : 10.1073/pnas.1008612107

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Photo credit: wili_hybrid

Another post this week from the Atlantic (Daniel Fromson covering the Aspen Institute and the Atlantic’s Washington Ideas Forum) that follows up on my earlier posts last week (here and here) about turning nutrition into a bottom-up venture that engages and attracts kids.  This one speaks to the challenges of revolutionizing school cafeterias:

[White House chef Sam Kass, Michelle Obama's food-policy right-hand man and a key player in her effort to combat childhood obesity through the Let's Move Initiative] told the audience that chefs should work directly with schools in order to improve the menus—but acknowledged it won’t be easy. “Chefs need to know more about how our schools operate … Schools are big, autonomous places,” he said. The chefs, he added, need to learn how to work with teachers and administrators: “Improving school lunches starts with the chefs.”

Another excerpt from the Obama administration’s health-policy adviser, Zeke Emanuel:

“A lot of schools don’t have kitchens anymore,” he said. “The other, of course, is money…. How much money you can spend on a meal is one of the biggest challenges.”

Now if more schools had chefs like flame thrower man above, kids would probably love food in the school cafeteria.

UPDATE:  A related video on CNN showcasing an elementary school in D.C..

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Photo credit: liber

Sarah Henry has a nice article in the Atlantic that follows up on my post earlier this week about failure of the American diet and why people just don’t seem to eat enough healthy food.

I argued that it’s no surprise people don’t eat well despite (1) decades worth of top-down, government nutrition campaigns and (2) the increased availability of affordable, healthy food through venues like farmer’s markets.  Rather, nutrition literacy should be complimented by bottom-up approaches, including active engagement of people learning how to grow and cook healthy food, starting with elementary school kids.

Henry’s piece provides evidence supporting these kinds of approaches, building on the successful work of Alice Waters:

Finally, some scientific support for what those of us who have watched kids pick spinach, cook kale, and chew on chard have known all along: Children who grow their own food (and prepare and eat it too) make healthier food choices.

For the past five years I’ve been a volunteer in the kitchen at the Edible Schoolyard, the much-admired organic garden and kitchen program founded by Alice Waters at Martin Luther King Jr. Middle School in Berkeley, California. I’ve also taught afterschool cooking classes to elementary-age kids (and their parents) in Berkeley public schools.

Over the years I’ve witnessed many wonderful things take place in cooking classrooms and out in the field when children are exposed to an edible education. A child discovers kiwi fruit. A student asks for sprouts at the farmers’ market. Leafy greens are dished up and chowed down with gusto.

But until now, school cooking and gardening advocates haven’t had hard data to back up this soft science. A report released today reveals a victory for the vegetables (particularly those of the leafy green variety). “We realized we needed to present numbers and facts to support what is so clear to us from our experience working in the Edible Schoolyard and through the transformation of school lunch in Berkeley,” Waters says. “We knew validation of the work was important in order to reach a wider public. This is one of our first steps in reaching new audiences—particularly the scientific and academic community—and of course we hope it has implications for public policy.”

…Among the key findings of the research, which was commissioned by the Chez Panisse Foundation and is one of the first such studies to evaluate an integrated approach to food education:

• Increased nutritional knowledge among 4th and 7th graders who were fed a steady stream of gardening and cooking curriculum.

• Higher fruit and vegetable consumption among elementary-age students in schools with more SLI [School Lunch Initiative] components than in students at schools with less-developed SLI offerings, including a preference for leafy greens like kale, spinach, and chard.

• Vegetable intake was almost one serving per day greater in the schools with a beefed-up food curriculum, and combined fruit and vegetable consumption increased by 1.5 servings. About 80 percent of this increase came from in-season produce. In comparison, researchers found a nearly quarter-serving drop in produce intake among other students.

• More positive attitudes about the taste and health value of school lunch in students in more highly developed SLI programs than those in lesser-developed SLI schools.

• Small increases in produce consumption occurred among middle-schoolers with higher exposure to nutrition education as opposed to a drop in fruit and vegetable intake by about one serving a day among students in the other group.

Read the rest of Henry’s article here.

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Photo credit:  whirlekid

Erik Eckholm’s  article in today’s NY Times suggests that the movement to limit antibiotics use in healthy farm animals is gaining momentum in the Obama Administration and Congress (links his):

Dispensing antibiotics to healthy animals is routine on the large, concentrated farms that now dominate American agriculture. But the practice is increasingly condemned by medical experts who say it contributes to a growing scourge of modern medicine: the emergence of antibiotic-resistant bacteria, including dangerous E. coli strains that account for millions of bladder infections each year, as well as resistant types of salmonella and other microbes.

Now, after decades of debate, the Food and Drug Administration appears poised to issue its strongest guidelines on animal antibiotics yet, intended to reduce what it calls a clear risk to human health. They would end farm uses of the drugs simply to promote faster animal growth and call for tighter oversight by veterinarians.

The agency’s final version is expected within months, and comes at a time when animal confinement methods, safety monitoring and other aspects of so-called factory farming are also under sharp attack. The federal proposal has struck a nerve among major livestock producers, who argue that a direct link between farms and human illness has not been proved. The producers are vigorously opposing it even as many medical and health experts call it too timid.

Scores of scientific groups, including the American Medical Association and the Infectious Diseases Society of America, are calling for even stronger action that would bar most uses of key antibiotics in healthy animals, including use for disease prevention, as with Mr. Rowles’s piglets. Such a bill is gaining traction in Congress.

“Is producing the cheapest food in the world our only goal?” asked Dr. Gail R. Hansen, a veterinarian and senior officer of the Pew Charitable Trusts, which has campaigned for new limits on farm drugs. “Those who say there is no evidence of risk are discounting 40 years of science. To wait until there’s nothing we can do about it doesn’t seem like the wisest course.”

Read more of the article here.

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Photo credit: crispyking

Two stories in today’s news:

(1) The Washington Post ran an article on the possible pesticide-child behavior link we examined in a previous post.

(2) CNN also picked up the recent report from the Environmental Working Group (video clip and printed story) on pesticide residues in produce:

The Dirty Dozen (may contain 47-67 pesticides per serving—EWG suggests buying or growing these organically)

• Celery
• Peaches
• Strawberries
• Apples
• Domestic blueberries
• Nectarines
• Sweet bell peppers
• Spinach, kale and collard greens
• Cherries
• Potatoes
• Imported grapes
• Lettuce

The Clean 15 (contain fewer or no pesticides—EWG suggests you can buy these conventionally grown)

• Onions
• Avocados
• Sweet corn
• Pineapples
• Mango
• Sweet peas
• Asparagus
• Kiwi fruit
• Cabbage
• Eggplant
• Cantaloupe
• Watermelon
• Grapefruit
• Sweet potatoes
• Sweet onions

The EWG shopper’s guide.

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Photo Credit:  http://www.flickr.com/photos/maheshkhanna/786837829/