Epigenetics and Type 2 Diabetes by Rachael Moeller Gorman
Posted August 15, 2009
The New Heredity
By Rachael Moeller Gorman
For hundreds of years, people in the tiny parish of Överkalix, in northern Sweden, have endured bad times and celebrated good ones with little connection to the outside world. To the north and west are Lapps, and to the east, Finns. Though they technically speak Swedish, residents of Överkalix use a dialect that makes them virtually unintelligible to fellow Swedes.
But since the sixteenth century, the people of Överkalix have kept impeccable records of their lives. Clergy logged births, causes of deaths, and land ownership; other historical records noted harvests and crop prices. When epidemiologist Gunnar Kaati arrived 20 years ago, he found an extensive set of meticulous data for this isolated, homogeneous population—a perfect foundation for the large, multigenerational study he hoped to conduct. Kaati wanted to use the data to probe a new idea in clinical medicine—that exposure to certain environments during crucial points in development might determine whether a child would suffer disease years later.
We’re familiar with the notion that the environment is linked to disease—that a diet high in saturated fat may clog arteries and cause heart disease or that radiation mutates DNA and can lead to cancer. But in the emerging field of the fetal and developmental origins of adult disease, more subtle factors such as the amount of food a mother ate during pregnancy or the type of mothering she provided directly after birth may determine whether her child will develop cardiovascular disease or be left neurologically susceptible to overstress years later.
These effects, some researchers believe, have nothing to do with mutations in the DNA code. Rather, they seem to involve what are known as epigenetic changes: structural alterations to the DNA double helix. The notion is that we experience periods in development when our bodies are programmed to collect information about our environment, then readjust our growth depending on what we find. To make this readjustment, our bodies flick genes on or off, sending us on an irreversible trajectory. For example, if a mother doesn’t eat much during pregnancy, that may signal to her fetus that he is about to emerge into a food-poor environment, and he may be born smaller, with a slower metabolism, than if his mother had eaten heartily. Epigenetic changes can lead to, say, type 2 diabetes years later if the world the adult finds—such as a world full of food—is different from that forecast by the fetus.
Kaati took this idea a step further. He wanted to know not just whether a child’s own early environment caused common diseases later in life but whether the environment a child’s parents or even grandparents encountered had an impact. Animal studies suggest that such effects may persist in DNA for generations, and Kaati’s work, still at an early stage, hints that the same thing may happen in humans. Genes might “remember” what our ancestors ate, felt and experienced, altering our own lives generations later.
For many students of biology and evolution, such ideas immediately bring to mind Jean-Baptiste Lamarck, who theorized that traits acquired by an organism during its life can be passed on to its offspring. The classic example is the giraffe that stretches its neck to reach a tree’s top leaves and then gives birth to longer-necked young. Lamarck died 30 years before the 1859 publication of Charles Darwin’s Origin of Species, which detailed evolution as we now know it—a process by which chance differences (later recognized as mutations) improved an individual’s chance of survival and thus ensured the propagation of those traits. Each man proposed a similar result, but by very different mechanisms; in Lamarck’s view, alterations in a species were more immediately driven by environmental change, whereas Darwin saw a longer process of passive natural selection. The subsequent discovery of genes—the primary unit of natural selection— added credence to Darwin’s theory, and Lamarck’s was shelved, seemingly laughable compared with what had been learned about the body’s sophisticated mode of transferring traits.
Yet advances in epigenetic research suggest that Lamarck may have been onto something. As with the giraffe’s tall tree, environmental factors such as lack of food or inattentive mothering appear to alter our epigenomes and sometimes even those of our offspring. (Some researchers think epigenetic changes have helped speed evolution, causing more rapid alterations than could be explained by mutations alone.)
Though Lamarck’s work may have prefigured modern epigenetics, the term itself wasn’t coined until 1942, by a developmental biologist named Conrad Waddington. In Waddington’s view, epigenetics was what we now call developmental biology—the study of how, during development, our genes give rise to our phenotype, the way we look and behave. By the 1990s a new definition had emerged, and today we consider epigenetics the study of changes in gene expression attributable not to alterations in DNA sequence (mutations that change the protein made by a gene) but in DNA structure (alterations to the scaffolding that carries the code, which can turn entire genes off so they make no protein at all).
Though there are several ways these structural changes can happen, the best known—and the focus of most epigenetic research—is DNA methylation, which occurs when a small chemical compound called a methyl group attaches to a cytosine, one of the four nucleotides in the DNA code. Methylation turns off nearby genes in two ways: by blocking transcription factors from attaching to the gene (and thus keeping those factors from translating the gene’s code into a protein) and by altering the configuration of the DNA itself to make the gene less physically available for transcription. (In addition, some recent studies have suggested that methylation may sometimes alter the configuration to turn genes on.) When a cell divides and copies its DNA, it also copies the methyl group, so the same genes remain shut down in the replicated cells.
As an organism develops from a single cell into its final form, epigenetic mechanisms help cells become distinct tissues. So while every cell contains the same DNA code, each type of tissue—hair, heart, brain—differentiates itself through a unique combination of gene expressions. Epigenetic mechanisms turn off the genes that aren’t needed for a particular tissue type and help determine which proteins are expressed.
In recent years research has hinted that epigenetic mechanisms may be responsible for much more than just normal development. Development is inherently plastic, with organisms able to take a number of different paths depending upon the environment into which a fetus was introduced. But once certain developmental decisions are made, they are irreversible. David Barker, a professor of clinical epidemiology at the University of Southampton in England, has studied this idea in humans since the 1990s. In multiple studies he and others have found that babies with birth weights on the lower end of normal who grow up in affluent societies are much more likely to develop coronary heart disease, type 2 diabetes and hypertension as adults than are heavier babies. Barker has theorized that smaller babies are prepared for a diet low in carbohydrates and fat, and when they encounter just the opposite in the real world, they are predisposed to metabolic illnesses.
To see a mismatch between a baby’s real and predicted environment, consider the Dutch famine of 1944–45 and its legacy. When German forces cut off food supplies to parts of the Netherlands for six months, expectant mothers who starved during the final trimester were more likely to have babies who later developed type 2 diabetes. Programmed to expect hard times, these children grew up in an improving postwar environment. Researchers think epigenetic changes might have occurred in genes that regulate sugar absorption and metabolism. Other studies have linked a baby’s environment to kidney problems, asthma, osteoporosis and mental illness as an adult.
All these studies are merely correlational, with researchers noting that certain populations, having undergone a particular environmental stress early in life, have sometimes fallen ill years later. That raises questions of exactly how this may occur, whether epigenetics is the true mechanism and if there is anything to be done about it. While that has yet to be answered conclusively in humans, animal studies may be pointing the way.
For the purposes of epigenetics research, the agouti mouse is particularly apt. Its fur color is determined by the level of methylation on a piece of DNA found near the agouti gene. As a result, genetically identical offspring may look completely different from one another. One mouse might be yellow (indicating little methylation), another brown (a lot of methylation) and a third mottled (some cells with methylated genes, some not).
Randy Jirtle, an epigenetics researcher at Duke University, was intrigued by those tendencies and wanted to know whether early environmental influences could change the mouse’s levels of methylation. In a 2003 experiment, he fed agouti mothers folic acid, vitamin B12, choline and betaine—all methyl supplementers—during pregnancy. This not only increased the babies’ DNA methylation near the agouti gene but also boosted the likelihood that they would be brown, establishing that changes in DNA methylation are the mechanism that connects a mother’s diet to her offspring’s gene expression.
Then, in a 2006 study, Jirtle fed the mothers genistein, a component of soy, and found that it too increased methylation, making the offspring more likely to be brown. Next, he tracked the offspring’s adult weight and found that they were less likely to be obese. That’s because the agouti gene also governs the part of the brain that affects satiation. “The big question is how something that happens early, as a result of benign environmental influences, is linked to susceptibility to common diseases 20 or 30 years later,” says Jirtle. “At least for the agouti mouse, that link is DNA methylation.”
At about the time Jirtle was doing his mice experiments, Michael Meaney, a neuroendocrinologist at McGill University in Montreal, was working with rats, testing the methylation of a gene important to the stress response—a glucocorticoid receptor gene in the brain. It turns out it’s not just what a mother eats but also how she treats her babies that affects their epigenome—the pattern of epigenetic marks that accumulates throughout development. Some rat mothers are particularly attentive to their pups, excessively licking and nursing during the first week after delivery. Studies have shown that the pups of these mothers are less fearful as adults and less fazed by stressful situations.
Meaney found striking differences in methylation patterns between pups with highly attentive mothers and those with neglectful mothers. Less attentive mothering resulted in more methylation near the glucocorticoid receptor gene, turning it off; better mothering kept it on, producing more receptors and better regulation of the rats’ stress response. To confirm his findings, Meaney transferred pups born to neglectful mothers to highly attentive ones immediately after birth; the methylation patterns of these adoptees were almost indistinguishable from those of the attentive mothers’ natural offspring, and the adopted pups grew up to be as fearless as the natural pups. Although these epigenetic changes happened only during one crucial period—the first week after delivery—their impact persisted into adulthood. Yet when Meaney injected a compound into adult rats that demethylated key genes, neglected animals became less fearful. His work provides the first evidence that the way a mother takes care of offspring might change them forever by altering the epigenome.
These studies demonstrate how a less than ideal environment during a critical developmental period may have long-lasting effects. Now, Michael Skinner, a molecular bioscientist at Washington State University in Pullman, is going further, showing that such exposure may change the lives of the altered animals’ descendants too.
Skinner exposed pregnant rats to the toxin vinclozolin, a hormonelike compound known as an endocrine disrupter, during days eight through 15 of their embryos’ development—when the cells that will become sperm are particularly open to epigenetic changes. He found that almost all males in four subsequent generations descended from the vinclozolin-exposed rats had far fewer and less vigorous sperm than normal and were also more likely to be infertile. Moreover, these effects appeared to relate to patterns of DNA methylation.
“The exposure to vinclozolin apparently reprogrammed the remethylation in the male germ line permanently,” Skinner says. In a later study, he found that vinclozolin exposure during the same period not only caused reproductive defects but also led to a number of adult diseases, including prostate disease, kidney disease and tumor development. It even dampened the rats’ chances of finding a mate.
Skinner was the first to show that epigenetics propagates the effects of the environmental exposure of one generation to multiple subsequent generations. “We have a clearly transgenerational effect for four generations and a very high frequency of disease,” he says.
During his years working with the Överkalix data, Kaati has tried to link environmental developments in the parish with possible epigenetic changes in residents. He has followed the lives of people born in 1890, 1905 and 1920 and consulted crop data compiled during the lives of their parents and grandparents. His goal was to find how much food was available to people during one crucial stage of development: the slow growth period (SGP) before puberty begins (between ages eight and 10 for girls and nine and 12 for boys).
In a series of studies published since 2001, Kaati has shown that when food was scarce during a father’s SGP, his son was far less likely to die of cardiovascular disease. And if a paternal grandfather had plenty to eat during his SGP? His grandchild tended to have a shorter life, and his son had a quadrupled risk of dying of diabetes. (These findings may seem to contradict those of Barker and the Dutch famine researchers, yet the crucial difference may be that a child, during his SGP, requires little food, whereas a fetus requires a great deal.) But while these patterns suggest possible epigenetic links, researchers don’t know yet whether there’s a causal connection or which mechanism might be involved. Still, they have their suspicions. “The slow growth period is a time when sperm cells are maturing and during which information is imprinted on those cells,” says Kaati. “For our study’s next phase, we want to see whether these mechanisms extend beyond the three generations we have discovered.”
And if future studies confirm what Kaati and his fellow researchers suspect? “It might be dangerous to overeat during the slow growth period,” he says. “That’s what is happening now, with kids becoming fatter and fatter.” The resulting harm might conceivably persist for generations to come.
But because these studies are preliminary, researchers are cautious. “There’s almost a wish that epigenetic phenomena affect our lives—that when we change our diet, for example, it might change the way our genes are expressed,” says Adrian Bird, a molecular geneticist at the University of Edinburgh who specializes in methylation. “But we have a way to go before we can be sure.”
Several initiatives may boost this research. The National Institutes of Health names epigenetics one of four “grand challenges in biomedical health/research” that “can be uniquely addressed by NIH as a whole.” Therapies that could turn on important genes, especially for the treatment of cancer, are being developed, and some drugs are believed to modify the epigenome for such diseases as epilepsy and bipolar disorder.
There’s also some concern that industrial chemicals may need to undergo testing to make sure they don’t alter the epigenome in a way that could lead to disease. “In the future, we’ll need to test compounds for their ability not only to mutate our DNA but also to alter the epigenome,” says Duke’s Jirtle.
The field of epigenetics may just be dawning, but it could someday change the way doctors approach medicine. “If you think of the genome as a computer’s hardware, then the epigenome is the software that tells the computer how to work,” says Jirtle. “I think we’ll discover that many diseases aren’t the result of hardware problems—mutations—at all. They’ll turn out to be due to software—epigenetic—problems.”
Dossier
1. “Environmental Epigenomics and Disease Susceptibility,” by Randy L. Jirtle and Michael K. Skinner, Nature Reviews: Genetics, April 2007. A thorough review of the environment’s effects on the epigenome, it uses vivid diagrams and photos to illustrate key points.
2. “Transgenerational Response to Nutrition, Early Life Circumstances and Longevity,” by Gunnar Kaati et al., European Journal of Human Genetics, April 2007. The latest in Kaati’s series of fascinating studies on health in an isolated Swedish village shows that food supply during childhood can alter disease risk generations later.
3. Epigenetics? [http://epigenome.eu] This European site tackles the tough field of epigenetics for the general public with in-depth feature stories, frequent updates from the laboratory and the latest news.
Source: Rachael Moeller Gorman
Be Careful About Your Brain
How To Feed Your Mind
By Rachael Moeller Gorman
EatingWell Magazine
Posted May, 2009
One lazy Friday night last winter, my husband and I watched TV on the couch while our infant son slept upstairs. During a commercial, an image flashed on the screen—a New York City train station. I smiled, because the place was so familiar. I had been there many times, traveling there for conferences or for fun. I could picture the outer façade, the stars on the ceiling, the brass clock. Ah, that station. That old place where the trains parked. That—
“What the heck is the name of that train station?” I asked my husband.
He gave me a funny look. “Grand Central?”
“Yes!” What was wrong with me? Even though I’m just 32 years old, this kind of thing had been happening more and more often and it was getting annoying. The forgetting of words—especially names and places that I obviously knew but couldn’t conjure up—began a few years ago. I’d had a brief return to my old sharper self during my pregnancy, but soon after my son was born, my brain slowly sank back downhill. Why wasn’t it working like it used to? Would it ever come back? Was there something I could do to drag it back to peak performance? What was it about pregnancy that had made it better?
I’m not the only one trying to figure out how to get smarter. Looking for ways to boost our brain power is big business. In addition to ever-popular alertness boosters like coffee and Red Bull, pills like Focus Factor and Brain Advantage are hot items, with customers shelling out $70 per month or more to stay on top of their mental games. Ginkgo biloba, an herbal supplement billed as a memory enhancer, generates nearly $1 billion in annual sales in the U.S. alone. Some folks go even further: as the prestigious journal Nature recently reported, 20 percent of scientists responding to a survey admitted to taking so-called cognition-enhancing drugs like the stimulants Ritalin (to aid focus) and Provigil (to stay alert without caffeine’s jitteriness), without apology. “It is my duty to use my resources to the greatest benefit of humanity,” said one respondent. One-third said they’d even feel pressure to give their own children these drugs if other kids in their circles were also using them.
Though I wasn’t ready to pump myself with drugs in order to remember a name more quickly, I did want to regain control of my mind, and, if I could, head off cognitive decline. The brief lift of brain fog during my pregnancy—a time of heroically conscientious eating—gave me hope. Could improving my diet help? I began scouring the science to find out. I also wondered whether the American diet I’ve been spoon-fed (and am currently spoon-feeding my son) was to blame for my mental malaise. I wanted to figure out whether a smart menu at each stage of life could fend off dullness and make me—and my family—sharper.
The Baby Brain
My intellectual journey began in the far reaches of northern Quebec, in a smattering of small villages on the frigid coast of Hudson Bay. No roads connect the villages to each other or to southern Canada, so when Joseph Jacobson, Ph.D., of Michigan’s Wayne State University and his intrepid crew of researchers first arrived 12 years ago, they flew in on small propeller planes from Montreal. Jacobson studies the Inuit, and he does so for just about the same reason cardiovascular disease researchers have been interested in other northern communities for years: their diet. “The Inuit eat a lot of fish,” says Jacobson from his Detroit office. “Arctic char, a type of salmon, is very big in their diet. And it’s all very rich in DHA.”
DHA, or docosahexaenoic acid, a long-chain polyunsaturated fatty acid in the omega-3 family that’s found in fish and their roe (particularly fattier types like salmon and sardines) is the magic nutrient du jour. I have seen literally hundreds of studies investigating its power to prevent cardiovascular disease. Now the focus has turned to the brain: dozens of studies report that mother animals deprived of DHA have offspring with memory, sensory and visual problems, and that supplementing them with DHA improves their performance on learning, memory and problem-solving tasks. This makes intuitive sense: DHA forms the backbone of much of the brain cells’ membranes.
Jacobson wanted to see whether higher DHA levels, both in the womb and after birth, could have the same positive effect on human infants. So working with midwives in the three largest Hudson Bay villages, his team collected umbilical cord blood from 109 newborns. They analyzed the DHA concentration in their cord blood (a good measure of how much DHA the mother consumed during her last few months of pregnancy), and then tested how well the infants performed on tests throughout their first year. He found that at 6 months and 11 months, infants whose cord blood had the highest concentrations of DHA performed better on a number of different tests—such as recognizing faces—than those with lower levels. “The mother’s intake during the third trimester, when the brain’s neurons and synapses are developing at a very rapid rate, is most important. When we focused on that period, we found the most evidence of beneficial effects,” he says.
My mother certainly didn’t eat salmon while pregnant with me, so that could be my problem, but it’s doubtful: my memory problems only emerged recently. Luckily for my son, my OB/GYN is on top of the literature: when she found out that I couldn’t stomach salmon or other fatty fish, she recommended taking a DHA supplement during my third trimester. (Pregnant mothers are advised to get 300 milligrams per day—the equivalent of about three to four 3-ounce servings of salmon a week.)
Apparently, much of the rest of the country isn’t too fond of fatty fish either. “Most populations, and this is particularly true in the U.S. and southern Canada, are not getting nearly the amount of DHA that humans got prehistorically,” says Jacobson, who like many in his field believes that before the agricultural revolution, fish played a much more prominent role in our diets. “In our original environment, we were getting a lot of DHA,” he comments, “then we switched over to a more grain-based diet.” Compounding the problem, adds Jacobson, is that our diets are rich in another type of fatty acid: arachidonic acid (AA), an omega-6 polyunsaturated fatty acid found in animal fats and formed in the body when we consume linoleic acid from vegetable oils in foods. There’s nothing inherently bad about AA—it’s important for normal growth. But Jacobson and others believe that our prehistoric ancestors evolved to eat a more balanced ratio of omega-6 to omega-3 fatty acids. Today, few people eat enough fish to achieve this balance; the ratio is currently about 10:1 in the U.S. Since AA competes with DHA for space in the membrane and affects other functions in the brain, some experts suggest an abundance of AA is less optimal for cognitive development in babies (and may be associated with early cognitive decline in older adults—more on that later).
Unless they stick to the “eat fish at least twice a week” dietary guideline, it’s hard for most Americans to meet DHA recommendations without supplements. This is why many infant formulas are now fortified with DHA (breast milk can be a great source of DHA, if the mom eats fish or takes supplements herself). Jacobson hints that supplementing formula, however, could be a case of too little too late—in his Inuit study he saw no beneficial effect of breast milk that contained high levels of DHA on the cognitive performance in infancy, although there could still be some beneficial effects on cognitive function in childhood. In the majority of studies that have demonstrated beneficial effects from DHA-enhanced infant formula, he notes, “most of the effects have been limited to preterm babies”—e.g., those who missed getting their full in utero complement of the nutrient. Does this mean that the typically DHA-poor American diet places infants at risk? Jacobson is quick to assure me there is no reason to assume that it does. “You don’t want to oversell the problem, but our data suggest that greater quantities of prenatal DHA intake could be beneficial.”
Milk vs. formula?
DHA is not the only critical substance for developing babies’ brains. Researchers have known for some time that iron is also key, but recently they have been discovering just how long the effects of a deficiency can last. Babies are born with a solid store of iron, but by 5 or 6 months they’ve used much of it up and can’t get enough from breast milk to sustain their ever-growing bodies: they need to take it in from the outside world in food or supplements. Studies show that being deficient at points within the 5- to 12-month age block irrevocably slows academic, social and emotional development. Even if children are fortified with iron soon after the deficiency is detected, they never catch up, and can still show signs of cognitive delay even 10 years later.
Iron is not only needed to transport oxygen to the brain in the bloodstream, but it also helps myelinate, or insulate, nerve fibers so signals travel faster—and helps create the neurotransmitters that relay signals between neurons. Until the early 1970s when manufacturers began adding iron to formula, more than 30 percent of infants were iron-deficient; since fortification, that number has plummeted. (At last count, about 7 percent of toddlers were iron-deficient.) But with the rise in breastfeeding, exclusively breast-fed infants are now at risk, especially as they’re transitioning to solid foods. Breast milk is still the best food (bar none) for infants, but physician groups recommend using rice cereal fortified with iron or supplementing with a vitamin drop during and after that critical transition to solid foods around 5 or 6 months. With irreversible brain delay churning through my gray matter (and after consulting the pediatrician), I drove to the drugstore and bought a multivitamin with iron for my son, who at 7 months was still breastfeeding but beginning to discover the delights of runny rice cereal and mushy peas.
Fuel for School
As children reach school age, DHA and iron continue to be key to brain development, but for kids sitting in class for seven hours a day, it’s even more important to keep their energy-hungry brains satiated. Reams of studies show that fueling the brain with breakfast is important for thinking, acting and learning; that’s the impetus behind the federal School Breakfast Program, which aims to ensure that every child begins the school day with something in his or her stomach.
Children who are undernourished perform poorly on cognitive tasks. Eating breakfast improves performance on attention and memory games, especially in the undernourished, but it also helps children who get enough food. This may be a simple case of refueling after an overnight fast: the brain needs glucose (its exclusive fuel source) and eating just about any food, from a candy bar to five-grain muesli, provides it. But new research is saying there’s more to it than that, and not just any breakfast will do. Margaret Anne Defeyter, Ph.D., a senior lecturer in psychology at Britain’s Northumbria University in Newcastle upon Tyne, studies children and the foods they eat. She has a lot to say about how kids prepare their brains each morning. “I was stunned, absolutely stunned to see what children had for breakfast,” she exclaims. “Children tell me they grab a chocolate biscuit [British for cookie] out of the biscuit barrel on their way to school, or stop at the corner shop and buy a can of cola.”
Defeyter wanted to know if a switch to slower-burning carbohydrates might give kids an advantage on tests of attention and memory. To find out, she gave 64 children either low-glycemic-index All-Bran cereal or high-glycemic-index Coco Pops, and then switched them the next day. Guess which one kept kids’ brains a-chugging most of the morning?
“With the high-GI cereal you get this sudden sugar rush, where you perform very well, but it’s quickly followed by a low,” she says. “Whereas with the low-GI cereal, you get a more sustained level of performance. That’s important for children. You want their concentration and attention maintained throughout the school morning for learning.” Other studies swapping in low-GI oatmeal for a higher-GI cereal have shown a similar effect: the lower the GI of the breakfast, the better kids did on cognitive tasks requiring attention and memory. The few studies looking at the effects of breakfast on adult brains showed similar results: low-glycemic-index meals that released glucose slowly into the bloodstream seemed to be associated with better memory. I thought back to my own childhood, sometimes starting the day with a bowl of Cookie Crisp or, occasionally, Froot Loops. Perhaps it slogged down my timed second-grade multiplication quizzes. But that still didn’t explain why my brain was on the fritz now. Was something else missing?
Iron-Deficient Maidens
Back in early 2007, I came across a study that I still think about all the time. Here’s the gist: 113 young women, aged 18 through 35, came into the lab at Pennsylvania State University. They took eight different tests on a computer that assessed attention, memory and learning, and their blood was drawn to compare their level of iron to their results on the computer tests. The findings were dramatic: women who were even mildly iron deficient—not yet anemic—scored much lower on many of the tasks and took longer to complete the tasks, than the women whose iron levels were normal. About 10 percent of young women are anemic (because of their monthly loss of iron-rich blood), as are 25 percent of pregnant women. In fact, I’d been told early in my pregnancy that I was slightly anemic, but it never occurred to me that it was much of a problem.
“What that study was able to do for the first time is show that even if you are mildly iron-deficient—you don’t have to be anemic—you have changes in cognitive function,” says John Beard, Ph.D., the iron expert who conducted the study. “It’s a scary thing that people don’t like to hear,” he admits, since a good number of us fall into that slightly iron-deficient gray area.
What really gave me hope was the other half of the study, where Beard put half the women on a slow-release iron supplement containing 60 mg of elemental iron for four months. Unlike the results seen in studies with iron-deficient infants, the women receiving the supplements regained normal cognitive functioning. How? Beard says that since the adult brain is already formed, iron’s primary role is to help feed the brain and build neurotransmitters; some of the brain regions most sensitive to iron deficiency are the prefrontal cortex and the hippocampus, centers of higher intellectual functioning and memory.
In Beard’s study, those women whose blood iron levels improved significantly experienced a five- to seven-fold improvement in cognitive performance. So it is a good bet that part of my problem was lack of iron; my temporary brain boost while I was pregnant could have resulted from the iron-rich prenatal vitamins I took every day. I vowed to do a better job of eating fortified cereals, edamame, clams, white beans, spinach, lentils—and of course meat, which contains the most easily absorbed form of iron. And I started taking a supplement on the side. Better safe than stupid.
Of course, if you’re not iron-deficient, taking more iron isn’t going to do anything to make your brain sharper—and too much iron creates problems of its own, including hemochromatosis (high blood iron), which can lead to liver damage, heart failure or diabetes. Since our bodies are unable to get rid of excess iron (except by bleeding), it makes sense to have your blood iron levels checked before you head to the drugstore for a “brain-boosting” iron pill—especially if you’re a woman past menopause or a man.
Heading Off Decline
I’m doing my best to build a first-class brain for my son and I work hard to keep all of our minds lubed. But nothing, even the most tenderly nurtured neurons, lasts forever. With my current fuzz, I fear eventually losing myself (or my husband) to dementia, and I wanted to know how to sandbag my family against it. So I called David Smith, professor emeritus of pharmacology and head of Oxford University’s 20-year-old Oxford Project to Investigate Memory and Aging (OPTIMA), which studies nongenetic risk factors (a.k.a. environmental factors) that cause Alzheimer’s disease. His words made me happy: “It’s my personal belief that we will be able to prevent a large proportion of Alzheimer’s disease in the world.”
Smith sees parallels between Alzheimer’s disease and heart disease—an illness whose prevalence has decreased around 60 percent over the past 40 years, largely because of preventive measures taken at a societal, level such as reducing smoking, increasing exercise, eating well and taking drugs to reduce cholesterol and blood pressure. “If we can find what the risk factors are for Alzheimer’s disease, we can have a similar success.”
Unfortunately, no one yet knows what all these risk factors are, but observational studies are beginning to yield clues: it seems the same things that are good for the heart may also be good for the brain. The connection makes intuitive sense: Alzheimer’s disease likely results in part from the accumulation of so-called senile plaques—abnormal brain proteins called A-beta that many scientists think trigger inflammation and oxidation, damaging neurons. If a person has atherosclerosis, their vessels are gunky and inefficient, resulting in fewer nutrients and less oxygen supplying the brain and fewer waste products leaving it, thus exacerbating Alzheimer’s disease.
Smith was particularly interested in fish because observational studies have shown a strong link between high fish intake and a reduced risk of full-blown Alzheimer’s disease. He wanted to know if eating fish regularly could also help people improve their brain power. So he called up colleague Helga Refsum, a professor of nutrition at the University of Oslo who leads the Hordaland Health Study—one part of a huge national project that gathers extremely detailed information about people’s lives and charts cardiovascular disease all over Norway. The county of Hordaland is on the sea, and people there eat lots of fish. Smith found that, of 2,031 healthy Hordalanders aged 70 to 74, those who ate more than a two-ounce serving per week of any type of fish (not just the fatty, DHA-packed variety) scored much higher on cognitive tests than those who ate less.
I asked Smith how it could be that all types of seafood are linked to improved cognitive function, since every study I’ve ever seen points to omega-3s like DHA as the key brain-boosting component. “Of course, the fatty acids are a strong candidate,” he says, “But it may be something else. Fish is very rich in niacin; there have been reports that niacin intake is related to better cognition in the elderly. Fish is also a good source of vitamin B12.” Because the aging body is less able to absorb B vitamins, particularly B12, he explains, the elderly often have low levels, which has been associated with poorer cognitive function. “So there are several candidates in fish and we want to tease them out.”A Golden Opportunity
Point taken: eat fish for your brain and your heart. But what happens if you’re a vegetarian, have a seafood allergy or can’t afford to eat fish regularly? Or, like me, just don’t like fish? I’ve never quite gotten over my pregnancy-induced aversion to the stuff.
Perhaps I could cover the taste with curry powder and benefit from a seasoning that’s been coming into focus as a potential anti-Alzheimer’s agent, at least in animals: turmeric. Greg Cole at UCLA and his colleagues have reported that curcumin, a phytochemical in turmeric (which gives curry powder its yellow color) not only helps prevent the buildup of toxic A-beta protein in the brain, but it also has antioxidant and anti-inflammatory properties. It has been used for thousands of years in traditional Indian Ayurvedic medicine as a treatment for respiratory conditions (asthma, allergy), liver disorders, anorexia and cough, among other things, and throughout Asia it’s used to treat arthritis pain and other inflammatory conditions. Cole is in the middle of a clinical trial on curcumin, but an interesting observational study came out in 2006 from Singapore that found that healthy people aged 60 to 93 who ate curry “occasionally” (once a month) or “often or very often” scored better on cognitive tests than people who rarely ate it. It’s also quite interesting to note that Indian citizens in their seventies (whose diets are rich in curry) are four times less likely to have Alzheimer’s disease than American septuagenarians.
Ancient Wisdom
To really uncover the secret of a clear mind late in life, though, I turned to the people who walk the walk. Some of the longest-lived people in the U.S. are from Cache County in the far northeast corner of Utah, where a majority of folks are Mormon and their beliefs shape a lifestyle that’s relatively free of vices like caffeine, tobacco and alcohol. Many are open to taking nutritional supplements and have the support of a close-knit community—all factors that may pave the way to a long and healthy life. Scientists have been carefully following 90 percent of the elderly population here—around 5,000 people—for 13 years, to see which part of their lifestyle plays the largest role in their longevity. The researchers have documented foods the residents have eaten, the activities they’ve done, the jobs they’ve had. They drew blood and tested cognition, and revisited the subjects about every three years to see why they live such long, healthy lives.
I asked Peter Zandi, Ph.D., an epidemiologist at the Johns Hopkins Bloomberg School of Public Health and a researcher on the study, what he’s found out about nutritional influences on mind decline, and he put it in a single word: antioxidants. “People who took high-dose supplements of both vitamin E [from 400 to 1,000 IU daily] and vitamin C [500 to 1,000 mg or more] had on the order of 60 to 65 percent reduction of the risk of developing Alzheimer’s disease,” Zandi says. “That’s huge. This led us to the notion that it’s really the synergistic effects of both that may afford protection.” (Currently, the Institute of Medicine’s daily recommendation for vitamin E is 22 IU [15 mg] and 75 to 90 mg for vitamin C.) Zandi thinks this vitamin partnership might work because vitamin E is a potent antioxidant that can slip inside cells and mop up the damaging free radicals, while vitamin C waits patiently outside and replenishes vitamin E when it comes back out so it can continue working. Anytime the body turns glucose into energy, free radicals are produced and oxidation (or damage) to tissue can occur. “The brain uses more energy than any other organ in the body, [thus] the brain is more susceptible to oxidative damage than any other organ in the body,” explains Fernando Gomez-Pinilla, Ph.D., who recently analyzed 160 studies on food’s effect on the brain. A professor of neurosurgery and physiological science at UCLA, Gomez-Pinilla published his meta-analysis this past July in Nature Reviews Neuroscience.
But hold off on buying that mega-antioxidant formula just yet: though some other studies have supported this work, not all are positive, and most experts advise avoiding antioxidant supplements until all the answers are in. Large doses of antioxidants can sometimes have a paradoxical, pro-oxidizing effect and cause cellular damage. However, the research is a strong argument for including more vitamin E-rich foods like walnuts, almonds, sunflower seeds and dark greens in your diet, along with plenty of citrus fruits, tomatoes, cantaloupe and other foods abundant in vitamin C.
Of course, one time-proven, antioxidant-rich way of eating doesn’t involve supplements at all: Mediterranean diets, famously protective against heart disease, may have promise in preventing Alzheimer’s disease as well. Recent studies suggest that people who most closely adhere to the dietary patterns long practiced in the countries surrounding the Mediterranean Sea—plenty of fruits, vegetables and whole grains, little meat, occasional fish and liberal olive oil—have significantly lower risk of developing Alzheimer’s disease later in life. Researchers believe that the antioxidants, omega-3 fatty acids and other micronutrients this way of eating offers may work synergistically to reduce the risk.
Minding our minds
Unfortunately, the typical American diet is far from the brain-boosting ideal. Most Americans don’t eat fish multiple times a week, get nine servings of fruits and vegetables daily or regularly season their food with curry. Babies don’t always get their iron, kids eat candy for breakfast and processed foods fill our grocery-store shopping carts. “Our diet today is really very, very different from primitive man’s diet,” says David Smith. So different that it’s bad for our brain? “I think it might be,” he replies.
In addition to not eating enough of the good things, we tend to eat too much of the bad stuff: a number of recent studies show that eating too much cholesterol, trans fat and saturated fat increases risk of cognitive decline and Alzheimer’s disease. One just-out report found that when rats were fed a diet high in saturated fat and cholesterol for eight weeks, their performance on a battery of memory tests declined significantly. Another study suggests that eating 80 milligrams more cholesterol per day than you normally do (the amount in a four-ounce piece of steak) seems to make your brain work, temporarily, as if it were three years older. Even worse, disease and lifestyle issues that continue to plague us, such as high blood pressure, lack of physical activity and diabetes are all pushing us toward cognitive decline.With the food environment we live in, it’s hard not to eat poorly unless you pay a premium. Rather than subsidizing antioxidant-rich fruits and vegetables, the federal government puts most of its support behind omega-6-rich soybeans as well as corn (thus keeping corn-syrup-laced junk food and sweet cereals cheap). Salmon is typically twice the price of beef. For the school breakfasts that power many kids’ mornings, the federal government’s requirements are broad enough that cheap, sugary cereals or Danish pastries pass muster. (The 2005 Dietary Guidelines declare, “make half your grains whole,” but schools still don’t have to comply. Promisingly, they’re working on the problem, and within two years schools should be more in line with the new guidelines, says Nancy Johner, USDA Under Secretary for Food, Nutrition and Consumer Services.)
Back home in the kitchen, I remember the pink marshmallow Sno Balls and Lucky Charms of my childhood. But my new dietary path already surrounds me on the counter: the baby’s small childproof bottle of multivitamin drops with iron; a cylinder of whole oats for my husband and me; my iron tablets; plenty of vitamin C-rich oranges and vitamin E-packed nuts; salmon (for my husband, and me, if I start liking it again) and lean free-range beef wrapped up in the fridge along with plenty of vegetables and fruits. I have my son’s little mind to think about now, and I’m excited to start. With any luck, I can also head off dementia for my husband and me. Will it work? I’ll tell you in 30 years (if I remember).
Contributing editor Rachael Moeller Gorman won the Bert Greene Food Journalism award for her last EatingWell feature, “Miracle Up North” (June/July 2006).
Source: Rachael Moeller Gorman from “EatingWell” Magazine
Diabetes, Latin Food and Your Health
Eating healthier with Latin faves
By Rachael Moeller Gorman
The Arizona Daily Star
May 9, 2009
On a recent hazy Saturday afternoon in Mexico City, the pungent scent of ripe mango hung thick in the city’s Polanco neighborhood.
Sellers had just sliced their fruit open – orange flesh still dripping with juice and humidity – to lure customers to their stalls. And the customers, typically family members walking hand in hand, haggled and ate. They inspected mounds of papayas, pineapples, guanabana, watermelon, pomegranate and plums at the surrounding tables. Their children chewed peeled oranges on a stick and ran around the tables of red, ripe tomatoes piled on bunches of draped cilantro, huge red beets, an almost infinite variety of peppers, prickly pear pads, avocados and tomatillos.
Not your typical American produce section.
When Mexicans leave their rural homes and move to the cities of the United States, they often leave foods like these behind. They begin eating the American way: a smaller variety of foods; less fresh fruit, rice, and beans; more calories, refined grains, saturated fats, and sugar. Foods they used to eat fresh, they now eat highly processed.
This Americanized diet affects Mexicans the same way it has been affecting the rest of the United States – only worse. According to the national Centers for Disease Control and Prevention, almost three out of four adult Mexican-Americans are overweight. The center also reports that one in four Mexican-Americans over the age of 45 has Type 2 diabetes.
In Mexico City at the end of April, a world-renowned group of scientists, nutritionists and chefs from the United States, Mexico and other Latin American countries came together to figure out how to fix this health crisis.
The issue is a big one in the States. According to the most recent census in 2000, Hispanics now make up 13 percent of the U.S. population.
“The 21st Latin American country is the United States,” said chef and culinary historian Maricel Presilla at the conference. “A new Latin America is being created here.”
The health statistics are scary. According to the National Center for Chronic Disease Prevention and Health Promotion, obesity rates in U.S. Hispanics doubled between 1991 and 2001. Higher weight means a higher risk of diabetes, heart disease, stroke, some cancers and other problems. The CDC has found that the risk of diabetes for Mexican-Americans is twice that of similarly-aged non-Hispanic whites. Diabetes potentially leads to amputation, blindness, kidney failure, heart disease and death.
People still in Mexico are also suffering.
“Twenty to 30 years ago, we had lots of traditional foods that were very healthy,” said Dr. Hector Bourges, director of nutrition at the National Institute of Medical Science and Nutrition in Mexico City. “However, with urbanization we adopted a model we shouldn’t have adopted – the Northern countries’ model.”
Traditional foods were seen as old-fashioned, people began having less time to prepare foods, and fewer people ate at home.
Obesity and its related illnesses are hardly just a problem for the Hispanic community.
“If we continue at this rate, by 2040 everyone in the U.S. will be overweight,” said John Foreyt, professor in the department of medicine at Houston’s Baylor College of Medicine.
But scientists say hope exists: Bringing traditional, healthy and tasty Mexican foods back to the family dinner table – and introducing them in American households – is a huge step in the right direction.
At the conference, Oldways Preservation Trust, a food-issues think tank in Boston and the conference organizer, worked with nutrition experts to revamp its Latin American Diet Pyramid, a food pyramid full of healthy Latin American foods.
The pyramid recommends eating fruits, vegetables and whole grains/tubers/beans/nuts at every meal. In the Mexican diet, this means corn, beans, squash, rice and chiles, among many others.
Poultry, fish, plant oils (like olive, corn, peanut or canola) and dairy foods are recommended daily. Red meat, sweets – typically honey – and eggs are for weekly consumption only.
“Traditionally, sweets were not a thing of everyday,” said Hannia Campos, associate professor of nutrition at the Harvard School of Public Health in Boston.
Many foods are connections to the past, originating during the time before Europeans came to Latin America. Foods are also a connection to flavor. Native American, Spanish and African influences all have their finger in Latin American cuisine, and the fusion is delicious.
“Mexico, in particular, has made food brilliant,” said Dr. Adolfo Chavez, chief of the Salvador Zubiran Medical Sciences and Nutrition Institute in Mexico City.
Daily physical activity forms the base of the pyramid, and alcohol should be consumed in moderation. The pyramid is quite similar to the Mediterranean Diet Pyramid, the gold standard of diets, which has been proven in study after study to reduce heart disease, certain cancers and Type 2 diabetes.
But as we all know, changing how we eat is difficult. Keeping the following themes in mind may help:
● Variety is key. Bring multiple colors, textures and flavors to your diet. Add tropical fruits; they are full of fiber, vitamins and antioxidants, and taste. Choose fresh local produce, if possible.
● Use just a little bit of meat for flavor in stews and other dishes. A small amount can go a long way, and too much is unhealthy (red meat and processed meat have been associated with heart disease). Instead, add beans, which studies have shown lower cholesterol and have lots of vitamins like folate for pregnant women. They also contain fiber, which can prevent heart disease and certain cancers, like colon.
● Make dining an event, not something you do in your car or on the run. Set the table, make it appealing and fun, and eat slowly. “Eating in the company of other people is essential for good nutrition and health,” said Bourges.
● Have a big dinner or party once a week; bring family and friends together. The rest of the week eat simple, flavorful dishes that take less time to prepare.
● Choose smaller plates to trick yourself into eating less.
● Food is emotional, passionate, creative – take advantage.
SIDEBAR
Starting small:
Small changes add up to big health benefits. Losing just 5 percent of your body weight – that’s 10 pounds if you’re 200 pounds – can significantly reduce your risk of Type 2 diabetes, cardiovascular disease and other weight-related illnesses. Here are a few little changes to try at home:
Replace candy bars with a square of at least 70 percent dark chocolate, one of Latin America’s best gifts to the world. When the cocoa content is this high, your body benefits from the same heart-protecting compounds that red wine contains. These squares do have some fat, but not as much as regular candy bars. Eat only one or two squares of a bar a day. The flavor is so strong that’s probably all you’ll want.
Add other traditional Latin American grains to your diet, such as quinoa and amaranth. Also continue to use more familiar ones like corn and brown rice. These grains are great sources of complex carbohydrates, and they give you long-lasting energy. They are also full of nutrients like magnesium and B vitamins.
Eat cooked beans, instead of refried beans. They have far less saturated fat, yet still provide the nutrients, protein and fiber.
Replace potato chips, cheese puffs and the like with a handful of peanuts or almonds. Nuts are an excellent source of healthy unsaturated fat, they make you feel full, they have no cholesterol, and they are full of protein and fiber. The salt on the nut is less than what is found in chips, but go for low-salt varieties anyway to reduce the risk of high blood pressure. Eat a handful for a snack in the afternoon or between breakfast and lunch.
Choose corn tortillas over flour tortillas. Studies show that whole grains, like corn or whole-wheat flour, help protect against heart disease, diabetes, obesity and cancer. And they make you feel full for longer. At the very least, try whole-wheat tortillas, instead of flour. Refined flour has lost most of its beneficial nutrients and also triggers spikes in blood sugars, which is bad for diabetes.
Source: Rachael Moeller Gorman and the Arizona Daily Star
A Whole Country Changed – Rachael Moeller Gorman
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Miracle Up North EatingWell View Web Version June/July 2006 Seppo Holttinen loved to dance. He met his wife on the dance floor. He boogied with his kids. And on September 21, 1976, the forestry engineer danced with friends after a company meeting in the capital city of Joensuu, in Finland’s rugged easternmost province of North Karelia. It would be the last time. The 38-year-old blond-haired, blue-eyed, slim, handsome Finnish father of three collapsed on the floor with his third heart attack and died soon after at the hospital. Just one month earlier, his own father had died of a heart attack. While it might seem shocking, in 1970s North Karelia, Seppo Holttinen’s death was nothing short of ordinary. “Heart disease was so common back then,” said Vesa Korpelainen, executive manager of the North Karelian Center for Public Health. “When people were asked, ‘Do you have coronary disease?’ a very common answer was, ‘Not yet.”’ Finnish men had the world’s highest rate of heart disease mortality, and North Karelia’s rate was 40 percent worse than that-even in a region where most men held physically active jobs like logging and farming. Finns in the 1970s enjoyed butter, whole milk, sausage, salt and cigarettes. Fruits and vegetables were rarely on their menus; for example, by the time Korpelainen did military service at age 20, the only vegetables he had ever eaten – perhaps ten times in his life – were tomatoes and cucumbers. But by the early 2000s, the number of deaths of working-age Finnish men from coronary heart disease had plummeted 75 percent. In North Karelia, the number was even better – 82 percent and life expectancy for every man went up 7 years. Much of this reduction in mortality came from dramatic reductions in risk factors like high blood pressure, high cholesterol and smoking. In less than two generations, the Finnish lifestyle became the envy of the world. What happened? In 1972, a program called the North Karelia Project radically adjusted the habits of a whole community of Finns and, eventually, the entire Finnish population. “It was a question of general lifestyle of the community-not just some people with high risk factors,” said Pekka Puska, M.D., Ph.D., the public health physician who directed the project. “The whole environment had to change-the food industry, restaurants, cafeterias, supermarkets.” In other words, Puska and his team made sure that healthy choices became easy choices for every person in the province. And to do it, they had to fundamentally change society itself. Battling Butter, Salt, and Smokes The price for such celebration, however, was steep: cardiovascular disease for working men skyrocketed to the world’s highest levels. A thousand heart attacks occurred each year in North Karelia, a region of only 180,000 people. Half of those struck men younger than 65, and 40 percent were fatal. One tenth of North Karelian men and women between the ages of 45 and 59 were on disability leave due to heart disease. After years of suffering, the citizens of North Karelia finally petitioned the national government for help in 1971. Something – they didn’t know what – needed to happen to stop their young men from dying. Enter Pekka Puska. Then a 27-year-old doctor with a master’s degree in social science, Puska had been president of the national students’ union and had come of age during a time of unrest in universities all over Europe. He believed entrenched systems could be changed, and quickly became the government’s choice to head up an ambitious program to help North Karelia. Studies had linked certain risk factors to increased heart disease, but it was not yet known whether reducing them would actually stop people from dying. Puska, now the Director General of Finland’s National Public Health Institute, decided that the only way to attack such a systemic problem was a multi-pronged approach, addressing the environment, culture and economy of the entire 180,000 – person province of North Karelia. Homemakers Carry the Torch Especially controversial for people of this dairy-farm-dotted region was the doctors’ advice that they switch from butter to vegetable oils and margarine (this was the pre-trans-fat era, and margarine’s luster as a healthy food had yet to be diminished). “There was quite a lot of discussion that we were fighting against farmers,” said Aulikki Nissinen, a doctor who worked on the project from the beginning. “If you had a few cows of your own, convincing you to switch from something you produce yourself to buying some kind of imported vegetable oil was really difficult,” added Puska. Because of the Nordic climate, fruits and vegetables – which usually had to be imported – faced the same resistance. So the team went in “boots deep in the mud,” as Puska describes it. The North Karelia Project joined forces with the Martha Organization – a national housewives group (similar to 4-H) devoted to educating its members about nutrition, kitchen efficiency and household budgeting (named after the biblical Martha, Lazarus’s sister, who was “busy everywhere,” says Nissinen). Together, the two groups took on traditional, fat-filled recipes and gave them a healthier spin; even the beloved Karelian Stew, a melange of butter-browned meats simmered in heavily salted water, was remade with added rutabagas and reduced sodium. They sponsored over 300 “Parties of Long Life,” where the women gathered on Sundays with their families at schools or community centers to try out the new recipes and listen to medical lectures by Puska and his colleagues. By keeping the pressure on in Finnish homes, the Marthas “were our best allies,” said Puska. At every turn, Puska and his colleagues used positive reinforcement. When worksites lowered the salt in their cafeteria menus, for example, the cooks would pile the unused salt in huge glass jars for all employees to see. There was drama, too: towns were pitted against each other in cholesterol-lowering competitions. “People went to each other’s homes, looked in each other’s refrigerators, to see whether they had vegetables or butter inside,” said Puska. The winning towns received cash prizes, earmarked for programs like bike paths and walkways. And, in what may have been the world’s first reality-TV show, Puska’s group appeared regularly on a program that followed eight to ten high-risk people for weeks as health experts counseled them how to quit smoking and give up other unhealthy habits. Between one-quarter to half of the country watched the show during any given season in its 13 year run. It inspired many: over a quarter of male viewers reduced their fat intake. The Message Spreads Its success, says at least one international observer, was due to the Finnish outlook on life. “The Finns have a very pragmatic nonideological approach to life in general,” said Derek Yach, physician and director of the Rockefeller Foundation’s program on global health and a former World Health Organization colleague of Puska’s. “They see a problem and they don’t have a big long debate about what’s the philosophical reason or individual responsibility. They recognized that these lumberjacks were dropping dead and that it was because their food was not optimal.” Aside from the original, local initiative, Puska and his group were also urging legislative change from the top down. Food labeling laws were changed, first in North Karelia and then nationally, to mandate clearer labeling for low-fat and low-salt foods to make them easier for consumers to find. The national school-lunch program also got a major overhaul: butter on school bread (the biggest source of fat in kids’ diets, since Finns traditionally eat buttered bread at almost every meal) was replaced by margarine. Whole milk was switched to skim milk or water, and cafeteria staff pushed fish, poultry, vegetables and salads. The manufacturers who supplied the food were encouraged to lower salt levels and use salt substitutes. Also targeted were dairy subsidies, which rewarded cream and butter production and taxed margarine so that it cost as much as butter. There was, unsurprisingly, plenty of resistance, since dairy farms were ubiquitous in Finland. But after continuous pressure from Puska’s team-and the subsequent lowering in the consumer demand for butter as a result of their work the subsidies were eventually dropped, opening the door for margarine and vegetable oils to compete. The farmers, however, were offered trade-offs. When scientists developed a type of rapeseed plant that grew well in the northern climate, the project encouraged farmers to replace their lost revenue with the plant, to make their oil – canola – a national product that could viably replace butter. They also reawakened enthusiasm for growing local berries – a longtime Finnish forest tradition that had fallen by the wayside. Today Aulikki Nissinen, one of the project’s founding team members, picks 50 gallons of berries every summer and freezes them to use all year; so do many of her neighbors. Puska’s team also worked with bread companies, urging them to lower the salt and replace butter in their recipes with vegetable oil. They took on sausage makers, too, suggesting substituting mushrooms for some of the pork, for example, and cutting salt. “The sausage industry said in the beginning they couldn’t make the sausage with lower salt,” recalled Nissinen. “Somehow they managed it when people started to demand it.” Now, all the major sausage companies are “working with health,” said Puska. “If you go to a supermarket here, you see lots of low-fat, low cholesterol meat products.” But it was not simply changes in laws and regulations that made the difference, according to Derek Yach. “It was actually that discourse surrounding a proposed law that made the biggest difference, not the law,” he noted. “That’s quite exciting news, because it means that the more you can have an open media debate around changing lifestyles…the more likely you are to achieve sustainable outcomes.” Fitness for all Finns So the project team worked with local governments to make it easier for Finns to be active in any weather. They made sure walking paths were clear and gave out free tractioned shoe clamps to the elderly so they could walk in the winter. They increased the number of miles of bike paths and created well-lit, safe cross country ski parks. “Every municipality, every village has tracks for skiing. Here in Joensuu we have hundreds of kilometers,” said Vesa Korpelainen. In effect, Finnish cities became free, convenient outdoor gyms. As with other Scandinavian cities, “they tend to be smaller, highly walkable and pedestrianized,” said the Rockefeller Foundation’s Yach. In 1980, Finland passed the Sports Act, obligating central and local governments to provide facilities for their citizens to get exercise – tracks, pools, ice rinks and sports halls. Now, the ratio of sports facilities to people is one of the highest in the world. In all, Puska and his team created a system in which every aspect of people’s lives nudged them toward healthy choices and away from unhealthy ones. They did this by removing barriers, making it fun and using social events. They gave people control of their health by helping them monitor their progress and then showing them—and celebrating—positive results. And it worked. Total blood cholesterol declined 18 percent in both North Karelian men and women from 1972 to 1997; for most, a healthier lifestyle is now almost a routine. Almost no one drank low-fat milk in 1972. Now, nearly half of all women and 40 percent of men drink skim or 1 percent milk. While 90 percent of people buttered their bread in 1972, only 10 percent of people do now. More than a third of the country uses vegetable oil rather than butter for cooking, up from just 1 percent back then. On the exercise front, an estimated 65 percent of Finns are regularly active, Puska notes. The latest craze, among all ages, is called Nordic walking—basically, walking with sticks in a summer version of cross-country skiing. Nearly one in five Finns Nordic-walk at least once a week. Kids approve of the healthy, free school lunch. “We have different kinds of salads, we always have bread. People drink skim milk, water or juice. And we have different foods for vegetarians. And yeah. I like our school food,” said Maija Naumanen, a 17-year-old high school student in Joensuu, North Karelia. Most heartening, perhaps, is how cost-effective programs like the North Karelia Project were. During the height of its efforts, from 1971 to 1979, the project spent just $1.75 million total (about $4.8 million in today’s dollars), reported Puska. This figure is low partly because the project used existing infrastructure, working to make health care and university resources more effective. Even so, the reduced numbers of heart attacks and strokes saved the country an estimated $2 million (about $5.5 million today), and the reduction in disability pensions saved another $4 million (now, $10.9 million). That doesn’t count, of course, the incalculable: families spared the loss of loved ones. The Struggle Continues Finland does enjoy a few advantages other countries lack. “It’s a relatively small country with only about 5 million people—Pekka Puska and his colleagues are still grounded in the communities, yet can get on the phone to the prime minister and say, ‘You still aren’t doing enough,’” said Rockefeller’s Derek Yach. But that doesn’t mean its success is limited to similarly small countries. Local governments—cities and states—can have strong impacts, even more powerful if supported by the federal government. Individuals can also make changes, but it’s a tough uphill battle only people with enough money, time and mental health can afford to fight. Or, as Yach has written, “individual responsibility can have its full effect only in a society where governments, private interests and other sectors work together to support individuals making healthy choices.” Puska agrees—and believes the lessons of North Karelia can be used everywhere, as they have in countries as diverse as Iran, Canada and even the United States. “High blood pressure kills everywhere, high cholesterol kills everywhere. Even if the actual situations look very different—a Boston suburb or Africa—human behavior is pretty universal,” said Puska. Healthy choices need to be easy choices, and when they are, people make them. Jukka Holttinen makes good choices, though these choices were unheard of in 1972. “I drink skim milk, eat fruits and vegetables and salads. We don’t use so much salt as back then,” he said. “I do not smoke—my father smoked—and I also exercise every day.” At age 40, he’s two years older than his father was when he collapsed on the dance floor 30 years ago. Jukka has worked to stop the cycle, but he has had help: healthy choices in the supermarket, cheap, ubiquitous exercise facilities and a community of people of a similar mind have all nudged him in the right direction. He is hoping that his kids will have him around to nudge for many more years to come. SIDEBAR “The obesity problem has not been solved anywhere in the world, including Finland,” said Derek Yach, director of the Rockefeller Foundation’s program on global health. “However tough it was to bring down the cardiovascular-disease rates, obesity is going to be much more complex.” First off, the basic structure of our society makes physical activity difficult. Since the post-World War II economic boom, most U.S. communities have been planned around automobiles, so for most of us, any activity—going to school, work, shopping—means getting into a car. And the food that’s cheap and ubiquitous tends to be the most unhealthy. “For a low-to-middle-income person to go to McDonald’s and have an energy-dense bunch of hamburgers and fries is an economically sensible choice in that family,” said Yach. “It’s a tougher choice for them to go and find fruits and vegetables and a balanced diet the way we would prefer them to eat.” And while Finns can expect their national institutions to take on these challenges, we have a different philosophy about government’s role in public health. “I don’t think there will be a reliance on government to help,” said Mark Dessauer, communications director of Active Living by Design (ALbD), a national program that promotes routine physical activity through community design. “The American character is to believe in individual rights.” While certainly not on the scale of Finland, America is starting to fight obesity on myriad levels, public and private. You see proof every time states pass laws to restrict vending machines in schools or when health-insurance companies give discounts for fitness-club attendance. ALbD is itself a force for change: backed by the health-care philanthropy giant Robert Wood Johnson Foundation, it funds 25 partnerships across the country to help make communities more supportive of physical activity, including some highlighted in these pages. Dessauer believes solutions will come not with one big national push, but with many grassroots efforts like the ones ALbD supports. Though federal or state funding for such initiatives is important, the major supports are likely to be private: “It’s going to come from insurance companies, HMOs, corporations that want to be good citizens.” Workplaces will be involved, too, he added, as rising health-care costs compel them to help their workers live better. “General Motors now pays more for health care than for steel.” For his part, Yach sees opportunity: the U.S., facing one of the world’s highest obesity rates, could lead the way in “triggering the societal changes that will start bringing the epidemic down.” He added, “I do think the U.S., when they finally turn their mind to it, will become a world leader in getting it right.” (Sidebar by both Rachael Moeller Gorman and Joyce Hendley) |
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