Wednesday, August 31, 2011

Minum Jus Sayuran, Berat Badan pun Turun

http://www.metrotvnews.com/read/news/2011/08/31/63223/Minum-Jus-Sayuran-Berat-Badan-pun-Turun
Lifestyle + / Rabu, 31 Agustus 2011 13:43 WIB





INGIN berat badan turun tapi tak bisa menahan rasa lapar. Nah, coba saja minum jus sayuran. Selain menurunkan berat badan, jus sayuran pun dapat mencegah penyakit tertentu.

Sebuah studi di Amerika Serikat menemukan orang dewasa yang minum segelas jus sayuran tiap hari akan memenuhi kebutuhan sayuran sebanyak dua kali. Studi itu menunjukkan betapa pentingnya memasukkan sayuran sebagai menu harian.

Peneliti dari University of California-Davis mengatakan makan lebih banyak sayuran merupakan cara sederhana mengelola berat badan. Sebab, sayur merupakan sumber energi yang padat dan mengandung sedikit kalori.

"Studi ini menunjukkan bahwa metode ini tidak hanya akan mendidik masyarakat tentang pentingnya sayuran, tapi juga untuk menunjukkan cara mudah memasukkan mereka ke dalam makanan sehari-hari mereka," kata rekan penulis studi Carl Keen, profesor Gizi dan Kedokteran Internal di University of California-Davis.

Sebuah studi dari Baylor College of Medicine pun menunjukkan bahwa orang gemuk yang minum satu atau dua gelas sayuran setiap hari akan kehilangan bobot badannya lebih banyak ketimbang mereka yang tidak minum jus.

Selain penurunan berat badan, peminum jus sayur mengalami peningkatan signifikan akan asupan sayuran, vitamin C, dan potasium selama penelitian. "Cara mengonsumsi sayuran yang mudah sangat penting karena sayur memiliki begitu banyak manfaat, mulai dari pencegahan penyakit hingga manajemen berat badan," kata John Foreyt, Direktur Riset Perilaku Kedokteran Center di Baylor College of Medicine.

Mungkin rasanya tak akan seenak jus buah. Tapi demi kesehatan, tak ada salahnya mencoba, kan? (MI/RRN)

The 10 most polluted fruit and vegetables

http://uk.lifestyle.yahoo.com/10-polluted-fruit-vegetables-230000006.html
Doctissimo – Thu, Aug 25, 2011 00:00 BST



The 10 most polluted fruit and vegetables
The 10 most polluted fruit and vegetables

© Thinkstock
Between 2000 and 2009, the Environmental Working Group (EWG) tested 53 popular fruits and vegetables, to find those that had high levels of pesticides.
If, in your quest to reduce exposure to pesticides, it’s not possible for you to eat organic food and vegetables (at least for the 10 fruit and vegetables below) all the time, at least try to always eat locally grown produce from reasonable agriculture.


Understanding the impact of pesticides:


  • Why are pesticides toxic? Because they were created to kill living organisms (plants, weeds and insects that attack crops), pesticides present a danger to man as well. Pesticides are accused of provoking nervous system problems, cancer, and hormonal deregulation. Therefore it’s important to avoid pesticides as far as possible, and above all avoid accumulating them in the body.

    • Should we stop eating fruit and vegetables? Of course, not – fruit and vegetables are essential human foods, and guarantee good health while preventing a number of diseases. The benefits of a diet rich in fruit and vegetables remain higher than the known risks involved with pesticide exposure. That being said, by eating organic produce, we can avoid most pesticides.

      • Is washing and peeling my fruit and vegetables effective against pesticides? Not really, as the Environmental Working Group (EWG) study was carried out with washed fruit and vegetables. And while washing all your fruit and vegetables before eating is definitely necessary, systematically peeling them is not the best solution because most of the vitamins and antioxidants are found in the skin. In addition, many fruits and vegetables store the pesticides in the flesh as well.


      The ten most polluted fruit and veg:



      Apples: More than 700 apple samples were tested by the EWG. 98% of them contained traces of pesticides and 92% contained at least 2 different types of pesticide. Along with peaches, apples are one of the most highly pesticide treated fruits, with not less than 56 different chemical substances being employed.

      Blueberries: With their porous and fragile skin, blueberries hold pesticides deep within them. And what about frozen blueberries? While blueberries are often found in the frozen section of your supermarket, it’s best to avoid them as freezing helps preserve the pesticides too. 

      Celery: 
      96% of the celery samples tested positive for pesticides and nearly 90% contained a number of different types of pesticide. The problem with celery is that it takes time to arrive at maturity and is thus exposed to pesticides for a longer period than other vegetables.


      Grapes: On one sample of grapes imported from the US, 14 different pesticides were detected. The presence of these traces is partly explained by the grape’s thin skin, that lets pesticides into the flesh. However, grapes produced locally in France showed that only 17.5% of samples contained traces of pesticides, while a study of European non-organic grapes showed that 99.2% of the samples were contaminated with pesticides.


      Nectarines: 90.8% of the nectarines tested contained traces of at least two types of different pesticides. While the results don’t actually exceed authorised limits for each individual pesticide, these traces can still pose a problem as they become more powerful when combined with each other.


      Peaches: 85.6% of the tested peaches contained traces of at least two different types of pesticide. With their thin skins, peaches are more receptive to absorbing pesticides.


      Strawberries: On a single sample of strawberries, some 13 different types of pesticides were detected. And while you can wash a strawberry, you probably wouldn’t want to try peeling one!


      Peppers: During this study, one sample of peppers contained more than 13 different chemical substances. During the European study, the pepper shone as the vegetable containing the highest number of pesticide traces – 21 in total. Unless they are organic, avoid red and yellow peppers if you can, as they are more mature versions of the green pepper and thus have more exposure time to the pesticides. 

      Potatoes:
       Like all vegetables that grow directly in the earth, potatoes are more exposed to pesticides than other above ground vegetables. And their skin is so thin, that they easily absorb a number of pesticides and fungicides. According to the EWG study, 91.4% of potatoes contained pesticide traces.

      Spinach:
       As spinach also grows close to the earth, they are highly exposed to insects and are thus overly protected with pesticides.

      Jessica Xavier

      Saturday, August 27, 2011

      Lima Pemicu Infertilitas pada Wanita

      http://kesehatan.liputan6.com/read/350732/lima-pemicu-infertilitas-pada-wanita

      Desika Pemita
      27/08/2011 08:40 | Tubuh Wanita

      Liputan6.com, New York: Masalah kesuburan selalu menjadi isu sensitif bagi banyak perempuan. Terutama bagi mereka yang memiliki masalah dalam hal reproduksi. Penting bagi wanita untuk mengetahui pemicu infertilitas.

      Menurut, Doctor Geoffrey Sher, pendiri dari Institut Kedokteran Reproduksi, ada lima hal yang memicu masalah kesuburan pada wanita, yaitu:

      1. Rusak atau tertutupnya saluran tuba
      Penyebab paling umum dari ketidaksuburan pada wanita adalah rusaknya atau tertutupnya saluran tuba fallopi. Hal ini menghambat sel untuk bertemu sel telur dan sperma. Salah satu penyebab adalah penyakit menular seksual seperti klamidia dan gonore.

      2. Endometriosis
      Endometriosis adalah suatu kondisi ketika dinding rahim tumbuh di luar rahim yang menyebabkan jaringan parut, nyeri dan perdarahan berat, juga dapat merusak tuba falopii dan ovarium.

      Munculnya sejumlah endometriosis pada panggul, diyakini memengaruhi kesuburan dengan melepaskan zat beracun yang dapat mengurangi potensi sel telur untuk dibuahi sel sperma.

      3. Kerusakan pada ovarium
      Ovarium yang rusak juga dapat menyebabkan infertilitas. Penyakit seperti penyakit radang panggul atau endometriosis, bisa membuat ovarium berada dalam posisi yang abnormal atau membentuk penghalang, sehingga mengurangi kemampuan "mengambil" telur selama ovulasi.

      4. Abnormal ovulasi
      Ovulasi abnormal juga merupakan penyebab umum dari ketidaksuburan perempuan. Beberapa wanita bahkan tak mengalami ovulasi sama sekali. Sementara orang lain berovulasi terlalu dini atau terlalu terlambat dalam siklus mereka, dan ini sangat memengaruhi kehamilan terjadi dalam kelangsungan hidup.

      Fertilitas biasanya menurun setelah usia 35 tahun. Selain itu, diyakini kualitas telur menurun dengan bertambahnya usia karena kapasitas meiosis sel telur berkurang oleh proses penuaan.

      Kualitas telur wanita adalah salah satu penentu utama dari kehamilan. Seorang wanita juga tidak bisa hamil karena sakit, pembedahan atau infeksi yang merusak lapisan rahimnya. Kerusakan dapat disebabkan oleh jaringan bekas luka atau tumor, seperti fibroid, yang dapat mencegah embrio untuk mengembangkan benar.

      5. Bentuk dan ukuran rahim abnormal
      Kelainan dalam ukuran dan bentuk rahim juga dapat menyebabkan masalah ketidaksuburan. Kadang-kadang wanita dilahirkan dengan rahim berbentuk tidak normal sebagai akibat dari paparan obat tertentu saat ibu mereka sedang hamil. Sebuah contoh klasik dari gangguan ini adalah rahim berbentuk T', yang merupakan ukuran rahim dan rongga rahim yang secara signifikan lebih kecil dari ukuran rahim yang normal.
      (medicmagic/AIS)

      Friday, August 26, 2011

      Cegah Stroke dengan Mengatur Makanan

      http://health.kompas.com/read/2011/08/26/15082143/Cegah.Stroke.dengan.Mengatur.Makanan


      Kompas.com - Lebih baik mencegah daripada mengobati. Demikian kata pepatah. Sekira sebuah penyakit masih bisa dicegah kedatangannya, kita harus mengupayakan banyak cara. Salah satunya dengan mengatur asupan makanan sehari-hari.


      Stroke dapat disebabkan penyumbatan pada arteri yang mengarah ke otak, yang beresiko terganggunya aliran darah. Atau juga disebabkan pecahnya pembuluh darah. Stroke iskemik atau penyumbatan terjadi pada 80 persen kasus stroke. Sementara stroke hemoragik atau pecahnya pembuluh darah di otak adalah penyebab 20 persen stroke.
      Faktor risiko stroke termasuk merokok, hipertensi, penyakit jantung, diabetes, dan kolesterol tinggi. Gaya hidup menjadi faktor kemungkinan Anda terkena stroke atau tidak, termasuk mengonsumsi makanan yang bisa menurunkan risiko.
      Langkah-langkah berikut adalah cara menurunkan risiko terkena stroke melalui pengaturan makanan. Namun, ada baiknya Anda juga berkonsultasi pada dokter.
      Langkah 1
      Mengurangi asupan garam untuk menurunkan tekanan darah. Berhenti menambahkan garam ke dalam makanan ketika Anda memasak atau sedang makan. Jangan lupa untuk membaca label makanan untuk mengetahui kandungan garam di dalam makanan tersebut.
      Langkah 2
      Mengurangi asupan kalori jika Anda termasuk overweight. Obesitas sangat rentan terhadap penyakit jantung dan diabetes. Keduanya adalah faktor risiko stroke. Lebih baik menyantap whole grain, daging tak berlemak, buah, dan sayur serta lemak sehat, misalnya minyak zaitun.
      Langkah 3
      Batasi konsumsi makanan yang mengandung lemak jenuh untuk mengendalikan kolesterol. Hindari daging berlemak, fast food, dan produk susu berlemak tinggi jika kadar kolesterol meningkat.
      Langkah 4
      Mengurangi asupan gula halus untuk menjaga kadar gula darah. Batasi konsumsi minuman bersoda, cake, permen, es krim dan lainnya yang dapat merusak kadar insulin dalam tubuh. (GHS/Dian Savitri)

      Sisi Baik dan Buruk Minum Kopi

      http://health.kompas.com/read/2011/08/26/16102273/Sisi.Baik.dan.Buruk.Minum.Kopi




      KOMPAS.com – Sebagian orang beranggapan, minum kopi adalah kebiasaan buruk. Pada kondisi tertentu, hal ini bisa dianggap benar. Pada ibu hamil misalnya, mereka harus menghindari konsumsi kafein karena dapat menyebabkan komplikasi pada janin.
      Namun di sisi lain, beberapa penelitian mengungkapkan, kopi mempunyai manfaat terapeutik asalkan dikonsumsi dalam jumlah yang tepat. Berikut ini adalah manfaat sekaligus efek buruk yang harus Anda ketahui dari minum kopi :Kebaikan
      * Teh, kopi, dan cokelat merupakan sumber kafein alami. Ketiganya mempunyai manfaat dan memberikan banyak nutrisi dan antioksidan.
      * Penelitian telah menunjukkan bahwa baik biji kakao utuh dan kopi memiliki kemampuan luar biasa untuk melindung otak. Bukti menunjukkan, masyarakat Amerika Latin yang sering minum kopi giling dari biji kopi utuh memiliki risiko kecil terkena Alzheimer dan penyakit Parkinson.
      * Kopi meningkatkan metabolisme hingga 20 persen, menurut penelitian. Bahkan bisa memicu mekanisme peremajaan jaringan otot.
      * Menurut sebuah penelitian, mengonsumsi setara dengan dua cangkir kopi satu jam sebelum olahraga juga dapat membantu mengurangi risiko nyeri otot hingga 48 persen. Sebelum olahraga, kopi akan merangsang produksi energi dan pembakaran lemak.
      * Kafein melakukan pengambilan glutamat yang merupakan penghambatan di otak Anda, sehingga membuat Anda waspada dan siap beraktivitas.
      Keburukan
      * Kafein yang terisolasi tidak memberi manfaat kesehatan dari biji kopi dan dapat menjadi racun.
      * Pengeringan dan pemanggangan biji kopi berdampak negatif pada kesehatan. Anda dapat mendeteksi kualitas kopi dengan mencium aromanya. Kopi yang tidak memiliki aroma baik mungkin sudah basi dan tidak berguna jika dikonsumsi.
      * Minum kopi hitam, harus tanpa gula. Penambah gula tidak akan memberikan manfaat justru akan menyebabkan resistensi insulin.
      * Kopi merupakan zat pembentuk asam dalam tubuh Anda. Pengasaman yang berlebihan dalam tubuh bisa menyebabkan masalaha pada otot dan tulang, dan meningkatkan risiko terhadap penyakit degeneratif. Jadi, jika Anda minum kopi, pastikan asupan buah dan sayuran mentah yang tinggi untuk melawan keasaman kopi.
      * Minum kopi setelah berolahraga adalah tindakan yang salah.
      * Sebagian besar kopi yang dihasilkan telah terkontaminasi dengan pestisida. Untuk keamanan, Anda bisa membeli kopi organik yang bebas pestisida.
      * Kopi adalah zat kuat, dan dapat mempengaruhi kelenjar adrenal. Jika Anda mengalami penurunan fungsi adrenal, sebaiknya hati-hati untuk minum kopi.

      Thursday, August 25, 2011

      What to Eat for Breakfast?

      http://caloriecount.about.com/blog/partners/eat-breakfast-b528038?utm_source=newsletter&utm_medium=email&utm_campaign=newsletter_20110825&utm_term=continue2
      By ismile67 on Aug 25, 2011 10:00 AM in Healthy Eating

      By Brierley Wright, M.S., R.D.

      EatingWell.com 

      Recently, when I went to the USDA in Washington, D.C., to attend the unveiling of the new food icon—MyPlate—to accompany the 2010 Dietary Guidelines, I also met Michelle Obama (!). Full disclosure: I was lucky to be in the right place at the right time and it was brief, but long enough for me to ask the First Lady what she ate for breakfast that morning.

      Michelle Obama's Breakfast

      So, what did she have for her a.m. meal? Scrambled eggsturkey sausage and freshgrapefruit. Delicious, healthy and nearly in line with MyPlate. She was missing her grains and dairy. She fell short on vegetables, too, though if she doubled up on her fruit servings that would have counted as a sufficient substitution for a vegetable serving.

      This made me—and some other editors in the EatingWell office—curious... What do other nutrition and health experts eat—and how do their breakfasts compare to MyPlate?  
      My Breakfast

      In case you’re curious about what I eat for breakfast: My typical weekday meal includes: oatmeal (made with water) with fresh or frozen fruit mixed in (whatever’s on sale that week) and a dash of maple syrup; plus, two cups of coffee with skim milk.

      How my morning meal compares to MyPlate: I ought to step it up in the fruit or vegetable department and consider swapping one of my coffees for a latte to get a little more protein and low-fat dairy.

      Here’s what 4 more nutrition and health experts put on their breakfast plates:

      David Katz, M.D., M.P.H., F.A.C.P.M., F.A.C.P., EatingWell advisor and director of Yale University’s Prevention Research Center. 

      What he eats for breakfast: “My breakfast—most days—is a mix of berries (blueberries, raspberries and blackberries) with whole-grain cereals (usually Nature's Path Multigrainand/or Heritage; and possibly some other, such as Ezekiel's Golden Flax), possibly some other fruit, such as diced banana or apple, and nonfat Greek yogurt.”

      How his morning meal compares to MyPlate: “The meal is more berries than anything else, all of the grain is whole grain and the nonfat Greek yogurt is the dairy and protein shown on MyPlate. I would say my breakfast aligns well with MyPlate, but in many ways surpasses it. It's not half of the grains that are whole but all. The nonfat Greek yogurt is about the most nutrient-dense dairy product there is—and berries are particularly nutrient-dense fruits. A breakfast of champions...or so I hope!”

      Rachel Johnson, Ph.D., R.D., M.P.H., EatingWell advisor, professor of nutrition at the University of Vermont, Vice Chair of the American Heart Association Nutrition Committee and a member of the President's Council on Fitness, Sports and Nutrition Science Board  

      What she eats for breakfast:
      7:30 a.m.: Starbucks grande nonfat (extra-hot) latte
      9:00 a.m.: Whole-wheat 100-calorie sandwich thin with almond butter and maple pumpkin butter
      11:00 a.m.: Heart-to-Heart whole-grain cereal, fresh strawberries and blueberries with skim milk

      How her morning meal compares to MyPlate: “I hit everything on MyPlate—fruits (strawberries, blueberries); vegetables (pumpkin); whole grains (sandwich thin); protein (almond butter); and dairy (skim milk).”

      Karen Ansel, M.S., R.D., spokesperson for the American Dietetic Association and co-author of The Baby & Toddler Cookbook (Weldon Owen, 2011).

      What she eats for breakfast: A cup of coffee with 1% milk, a small glass of calcium-fortified orange juice (sometimes I'll have berries instead), a glass of 1% milk and a bowl of oatmeal with a tablespoon of ground flaxseed.

      How her morning meal compares to MyPlate: “As you can see, noticeably absent are the vegetables... As it turns out, we don't have to [eat vegetables at breakfast]. The sample meal plans [at choosemyplate.gov] contain several breakfasts, which suggest double servings of fruits instead of a fruit and a veggie. Some of the sample breakfast meals also swap in milk for protein, which is great because most of us don't have the calorie allowance at breakfast to eat all of these foods plus a glass of milk to boot. It looks like my weak link is in the produce department. Next time I'll be drinking that juice and eating those berries too.”

      Bonnie Taub-Dix, M.A., R.D., C.D.N., author of Read It Before You Eat It and weight-loss expert in New York.

      What she eats for breakfast: Banana-almond muffin, cottage cheese and yogurt.
      How her morning meal compares to MyPlate: “My muffins are made with 100 percent whole-wheat flour and contain banana and almonds (healthy fat), my cottage cheese and yogurt are non- or low-fat dairy and my cottage cheese is also protein. I fell short in the vegetable department and, honestly, I think that most people will do the same at breakfast. It may just be important to emphasize fruit in the morning and focus on veggies at lunch, dinner and snacks.”



      Your thoughts...

      What did you eat for breakfast this morning and how does it compare?

      Body Volume Index: the New BMI?

      http://caloriecount.about.com/body-volume-index-new-bmi-b528676?utm_source=newsletter&utm_medium=email&utm_campaign=newsletter_20110825&utm_term=continue1

      By carolyn_r on Aug 25, 2011 10:00 AM in Dieting & You
      By Carolyn Richardson


      Numbers are a significant part of trying to lose weight.  Be it pounds, inches, calories, or minutes, we’re all counting our way to a healthier lifestyle.  While many of us have a goal weight, others are focused on a goalBMI.  That is to say, we want to be healthy according to the standard measurement that screens for obesity, called Body Mass Index (BMI).  A comparison of height and weight, BMI is meant to determine a person’s health risks for chronic disease such as heart disease, hypertension, and diabetes.  However, it doesn’t directly measure a person’s body fat, or account for an adults’ age or body composition, leaving many, including pregnant women, athletes, body builders, and the elderly, categorized incorrectly.  Enter Body Volume Index (BVI), a newly proposed measurement that could replace BMI.

      What is BVI?

      Created by Select Research, BVI is an electronic measurement that, along with weight and body fat distribution, accounts for body composition, age, height, gender, and medical history. The process of getting your BVI is much like going through security at the airport.  A 3D scanner takes the image of a person’s body and inputs it into computer software that calculates hundreds of measurements, including waist-to-hip ratio, body fat percentage, and even BMI.  According to its website, the test takes less than 6 seconds and does not use radiation or lasers.   

      The Pros

      Since its launch, BVI has been vetted by the Body Benchmark Project, a research study conducted by the manufacturer itself, and a number of other entities including The Mayo Clinic here in the US.  For medical professionals, this machine may mean better accuracy for tracking patients over time.  Instead of using a tape measure, weight scale, and taking other measurements each visit, using BVI could be more efficient in showing a patient’s progress.  For those who know their BVI who are overweight or obese, it could mean a more personalized approach to treatment and a more clear wake up call for what getting in shape means.

      The Cons

      On the other hand, getting the BVI test may be too much information.  Aside from feeling like you're in an airport in your doctor's office, seeing a 3D scan could send someone with body image issues on the wrong path.  And while doctors do point out the importance of knowing how your weight is distributed, a person with too much abdominal fat for instance could become focused on losing weight in a certain spot, rather than focusing on getting healthier overall. Getting the hundreds of measurements the BVI calculates may be good to know, but practically speaking, many who need to lose weight may be uncomfortable with the possible cost of a doctor's visit and the use of an expensive machine to get the info.  


       
      Your thoughts…

      Would you want to see your BVI scan or is knowing your BMI good enough?

      Wednesday, August 24, 2011

      Why Your DNA Isn't Your Destiny

      http://www.time.com/time/magazine/article/0,9171,1952313,00.html
      By JOHN CLOUD




      Three generations: Dr. Lars Olov Bygren, with son Magnus and grandson Ludvig in Stockholm
      Lars Tunbjork / VU


      The remote, snow-swept expanses of northern Sweden are an unlikely place to begin a story about cutting-edge genetic science. The kingdom's northernmost county, Norrbotten, is nearly free of human life; an average of just six people live in each square mile. And yet this tiny population can reveal a lot about how genes work in our everyday lives.

      Norrbotten is so isolated that in the 19th century, if the harvest was bad, people starved. The starving years were all the crueler for their unpredictability. For instance, 1800, 1812, 1821, 1836 and 1856 were years of total crop failure and extreme suffering. But in 1801, 1822, 1828, 1844 and 1863, the land spilled forth such abundance that the same people who had gone hungry in previous winters were able to gorge themselves for months.

      In the 1980s, Dr. Lars Olov Bygren, a preventive-health specialist who is now at the prestigious Karolinska Institute in Stockholm, began to wonder what long-term effects the feast and famine years might have had on children growing up in Norrbotten in the 19th century — and not just on them but on their kids and grandkids as well. So he drew a random sample of 99 individuals born in the Overkalix parish of Norrbotten in 1905 and used historical records to trace their parents and grandparents back to birth. By analyzing meticulous agricultural records, Bygren and two colleagues determined how much food had been available to the parents and grandparents when they were young.

      Around the time he started collecting the data, Bygren had become fascinated with research showing that conditions in the womb could affect your health not only when you were a fetus but well into adulthood. In 1986, for example, the Lancet published the first of two groundbreaking papers showing that if a pregnant woman ate poorly, her child would be at significantly higher than average risk for cardiovascular disease as an adult. Bygren wondered whether that effect could start even before pregnancy: Could parents' experiences early in their lives somehow change the traits they passed to their offspring?
      It was a heretical idea. After all, we have had a long-standing deal with biology: whatever choices we make during our lives might ruin our short-term memory or make us fat or hasten death, but they won't change our genes — our actual DNA. Which meant that when we had kids of our own, the genetic slate would be wiped clean.

      What's more, any such effects of nurture (environment) on a species' nature (genes) were not supposed to happen so quickly. Charles Darwin, whose On the Origin of Species celebrated its 150th anniversary in November, taught us that evolutionary changes take place over many generations and through millions of years of natural selection. But Bygren and other scientists have now amassed historical evidence suggesting that powerful environmental conditions (near death from starvation, for instance) can somehow leave an imprint on the genetic material in eggs and sperm. These genetic imprints can short-circuit evolution and pass along new traits in a single generation.

      For instance, Bygren's research showed that in Overkalix, boys who enjoyed those rare overabundant winters — kids who went from normal eating to gluttony in a single season — produced sons and grandsons who lived shorter lives. Far shorter: in the first paper Bygren wrote about Norrbotten, which was published in 2001 in the Dutch journal Acta Biotheoretica, he showed that the grandsons of Overkalix boys who had overeaten died an average of six years earlier than the grandsons of those who had endured a poor harvest. 

      Once Bygren and his team controlled for certain socioeconomic variations, the difference in longevity jumped to an astonishing 32 years. Later papers using different Norrbotten cohorts also found significant drops in life span and discovered that they applied along the female line as well, meaning that the daughters and granddaughters of girls who had gone from normal to gluttonous diets also lived shorter lives. To put it simply, the data suggested that a single winter of overeating as a youngster could initiate a biological chain of events that would lead one's grandchildren to die decades earlier than their peers did. How could this be possible?

      Meet the Epigenome
      The answer lies beyond both nature and nurture. Bygren's data — along with those of many other scientists working separately over the past 20 years — have given birth to a new science called epigenetics. At its most basic, epigenetics is the study of changes in gene activity that do not involve alterations to the genetic code but still get passed down to at least one successive generation. These patterns of gene expression are governed by the cellular material — the epigenome — that sits on top of the genome, just outside it (hence the prefix epi-, which means above). It is these epigenetic "marks" that tell your genes to switch on or off, to speak loudly or whisper. It is through epigenetic marks that environmental factors like diet, stress and prenatal nutrition can make an imprint on genes that is passed from one generation to the next.

      Epigenetics brings both good news and bad. Bad news first: there's evidence that lifestyle choices like smoking and eating too much can change the epigenetic marks atop your DNA in ways that cause the genes for obesity to express themselves too strongly and the genes for longevity to express themselves too weakly. We all know that you can truncate your own life if you smoke or overeat, but it's becoming clear that those same bad behaviors can also predispose your kids — before they are even conceived — to disease and early death.

      The good news: scientists are learning to manipulate epigenetic marks in the lab, which means they are developing drugs that treat illness simply by silencing bad genes and jump-starting good ones. In 2004 the Food and Drug Administration (FDA) approved an epigenetic drug for the first time. Azacitidine is used to treat patients with myelodysplastic syndromes (usually abbreviated, a bit oddly, to MDS), a group of rare and deadly blood malignancies. 

      The drug uses epigenetic marks to dial down genes in blood precursor cells that have become overexpressed. According to Celgene Corp. — the Summit, N.J., company that makes azacitidine — people given a diagnosis of serious MDS live a median of two years on azacitidine; those taking conventional blood medications live just 15 months.
      Since 2004, the FDA has approved three other epigenetic drugs that are thought to work at least in part by stimulating tumor-suppressor genes that disease has silenced. The great hope for ongoing epigenetic research is that with the flick of a biochemical switch, we could tell genes that play a role in many diseases — including cancer, schizophrenia, autism, Alzheimer's, diabetes and many others — to lie dormant. We could, at long last, have a trump card to play against Darwin.

      The funny thing is, scientists have known about epigenetic marks since at least the 1970s. But until the late '90s, epigenetic phenomena were regarded as a sideshow to the main event, DNA. To be sure, epigenetic marks were always understood to be important: after all, a cell in your brain and a cell in your kidney contain the exact same DNA, and scientists have long known that nascent cells can differentiate only when crucial epigenetic processes turn on or turn off the right genes in utero.

      More recently, however, researchers have begun to realize that epigenetics could also help explain certain scientific mysteries that traditional genetics never could: for instance, why one member of a pair of identical twins can develop bipolar disorder or asthma even though the other is fine. Or why autism strikes boys four times as often as girls. Or why extreme changes in diet over a short period in Norrbotten could lead to extreme changes in longevity. In these cases, the genes may be the same, but their patterns of expression have clearly been tweaked.
      Biologists offer this analogy as an explanation: if the genome is the hardware, then the epigenome is the software. "I can load Windows, if I want, on my Mac," says Joseph Ecker, a Salk Institute biologist and leading epigenetic scientist. "You're going to have the same chip in there, the same genome, but different software. And the outcome is a different cell type."

      How to Make a Better Mouse
      As momentous as epigenetics sounds, the chemistry of at least one of its mechanisms is fairly simple. Darwin taught us that it takes many generations for a genome to evolve, but researchers have found that it takes only the addition of a methyl group to change an epigenome. A methyl group is a basic unit in organic chemistry: one carbon atom attached to three hydrogen atoms. When a methyl group attaches to a specific spot on a gene — a process called DNA methylation — it can change the gene's expression, turning it off or on, dampening it or making it louder.
      The importance of DNA methylation in altering the physical characteristics of an organism was proposed in the 1970s, yet it wasn't until 2003 that anyone experimented with DNA methylation quite as dramatically as Duke University oncologist Randy Jirtle and one of his postdoctoral students, Robert Waterland, did. That year, they conducted an elegant experiment on mice with a uniquely regulated agouti gene — a gene that gives mice yellow coats and a propensity for obesity and diabetes when expressed continuously. Jirtle's team fed one group of pregnant agouti mice a diet rich in B vitamins (folic acid and vitamin B12). Another group of genetically identical pregnant agouti mice got no such prenatal nutrition.

      The B vitamins acted as methyl donors: they caused methyl groups to attach more frequently to the agouti gene in utero, thereby altering its expression. And so without altering the genomic structure of mouse DNA — simply by furnishing B vitamins — Jirtle and Waterland got agouti mothers to produce healthy brown pups that were of normal weight and not prone to diabetes.

      Other recent studies have also shown the power of environment over gene expression. For instance, fruit flies exposed to a drug called geldanamycin show unusual outgrowths on their eyes that can last through at least 13 generations of offspring even though no change in DNA has occurred (and generations 2 through 13 were not directly exposed to the drug). Similarly, according to a paper published last year in the Quarterly Review of Biology by Eva Jablonka (an epigenetic pioneer) and Gal Raz of Tel Aviv University, roundworms fed with a kind of bacteria can feature a small, dumpy appearance and a switched-off green fluorescent protein; the changes last at least 40 generations. (Jablonka and Raz's paper catalogs some 100 forms of epigenetic inheritance.)

      Can epigenetic changes be permanent? Possibly, but it's important to remember that epigenetics isn't evolution. It doesn't change DNA. Epigenetic changes represent a biological response to an environmental stressor. That response can be inherited through many generations via epigenetic marks, but if you remove the environmental pressure, the epigenetic marks will eventually fade, and the DNA code will — over time — begin to revert to its original programming. That's the current thinking, anyway: that only natural selection causes permanent genetic change.

      And yet even if epigenetic inheritance doesn't last forever, it can be hugely powerful. In February 2009, the Journal of Neuroscience published a paper showing that even memory — a wildly complex biological and psychological process — can be improved from one generation to the next via epigenetics. The paper described an experiment with mice led by Larry Feig, a Tufts University biochemist. Feig's team exposed mice with genetic memory problems to an environment rich with toys, exercise and extra attention. These mice showed significant improvement in long-term potentiation (LTP), a form of neural transmission that is key to memory formation. Surprisingly, their offspring also showed LTP improvement, even when the offspring got no extra attention.

      All this explains why the scientific community is so nervously excited about epigenetics. In his forthcoming book The Genius in All of Us: Why Everything You've Been Told About Genetics, Talent and IQ Is Wrong, science writer David Shenk says epigenetics is helping usher in a "new paradigm" that "reveals how bankrupt the phrase 'nature versus nurture' really is." He calls epigenetics "perhaps the most important discovery in the science of heredity since the gene."

      Geneticists are quietly acknowledging that we may have too easily dismissed an early naturalist who anticipated modern epigenetics — and whom Darwinists have long disparaged. Jean-Baptiste Lamarck (1744-1829) argued that evolution could occur within a generation or two. He posited that animals acquired certain traits during their lifetimes because of their environment and choices. The most famous Lamarckian example: giraffes acquired their long necks because their recent ancestors had stretched to reach high, nutrient-rich leaves.

      In contrast, Darwin argued that evolution works not through the fire of effort but through cold, impartial selection. By Darwinist thinking, giraffes got their long necks over millennia because genes for long necks had, very slowly, gained advantage. Darwin, who was 84 years younger than Lamarck, was the better scientist, and he won the day. Lamarckian evolution came to be seen as a scientific blunder. Yet epigenetics is now forcing scientists to re-evaluate Lamarck's ideas.

      Solving the Overkalix Mystery
      By early 2000, it seemed clear to Bygren that the feast and famine years in 19th century Norrbotten had caused some form of epigenetic change in the population. But he wasn't sure how this worked. Then he ran across an obscure 1996 paper by Dr. Marcus Pembrey, a prominent geneticist at University College London.

      Published in the Italian journal Acta Geneticae Medicae et Gemellologiae, Pembrey's paper, now considered seminal in epigenetic theory, was contentious at the time; major journals had rejected it. Although he is a committed Darwinist, Pembrey used the paper — a review of available epigenetic science — to speculate beyond Darwin: What if the environmental pressures and social changes of the industrial age had become so powerful that evolution had begun to demand that our genes respond faster? What if our DNA now had to react not over many generations and millions of years but, as Pembrey wrote, within "a few, or moderate number, of generations"?

      This shortened timetable would mean that genes themselves wouldn't have had enough years to change. But, Pembrey reasoned, maybe the epigenetic marks atop DNA would have had time to change. Pembrey wasn't sure how you would test such a grand theory, and he put the idea aside after the Acta paper appeared. But in May 2000, out of the blue, he received an e-mail from Bygren — whom he did not know — about the Overkalix life-expectancy data. The two struck up a friendship and began discussing how to construct a new experiment that would clarify the Overkalix mystery.

      Pembrey and Bygren knew they needed to replicate the Overkalix findings, but of course you can't conduct an experiment in which some kids starve and others overeat. (You also wouldn't want to wait 60 years for the results.) By coincidence, Pembrey had access to another incredible trove of genetic information. He had long been on the board of the Avon Longitudinal Study of Parents and Children (ALSPAC), a unique research project based at the University of Bristol, in England. Founded by Pembrey's friend Jean Golding, an epidemiologist at the university, ALSPAC has followed thousands of young people and their parents since before the kids were born, in 1991 and 1992. For the study, Golding and her staff recruited 14,024 pregnant mothers — 70% of all the women in the Bristol area who were pregnant during the 20-month recruitment period.

      The ALSPAC parents and kids have undergone extensive medical and psychological testing every year since. Recently, I met an ALSPAC baby, Tom Gibbs, who is now a sturdy 17-year-old. I accompanied him as clinicians measured his height (178 cm, or 5 ft. 8 in., not including spiked blond hair), the bone density of his left femur (1.3 g/sq cm, which is above average) and a host of other physical traits.

      All this data collection was designed from the outset to show how the individual's genotype combines with environmental pressures to influence health and development. ALSPAC data have offered several important insights: baby lotions containing peanut oil may be partly responsible for the rise in peanut allergies; high maternal anxiety during pregnancy is associated with the child's later development of asthma; little kids who are kept too clean are at higher risk for eczema.

      But Pembrey, Bygren and Golding — now all working together — used the data to produce a more groundbreaking paper, the most compelling epigenetic study yet written. Published in 2006 in the European Journal of Human Genetics, it noted that of the 14,024 fathers in the study, 166 said they had started smoking before age 11 — just as their bodies were preparing to enter puberty. Boys are genetically isolated before puberty because they cannot form sperm. (Girls, by contrast, have their eggs from birth.) That makes the period around puberty fertile ground for epigenetic changes: If the environment is going to imprint epigenetic marks on genes in the Y chromosome, what better time to do it than when sperm is first starting to form?

      When Pembrey, Bygren and Golding looked at the sons of those 166 early smokers, it turned out that the boys had significantly higher body mass indexes than other boys by age 9. That means the sons of men who smoke in prepuberty will be at higher risk for obesity and other health problems well into adulthood. It's very likely these boys will also have shorter life spans, just as the children of the Overkalix overeaters did. "The coherence between the ALSPAC and Overkalix results in terms of the exposure-sensitive periods and sex specificity supports the hypothesis that there is a general mechanism for transmitting information about the ancestral environment down the male line," Pembrey, Bygren, Golding and their colleagues concluded in the European Journal of Human Genetics paper. In other words, you can change your epigenetics even when you make a dumb decision at 10 years old. If you start smoking then, you may have made not only a medical mistake but a catastrophic genetic mistake.

      Exploring Epigenetic Potential
      How can we harness the power of epigenetics for good? In 2008 the National Institutes of Health (NIH) announced it would pour $190 million into a multilab, nationwide initiative to understand "how and when epigenetic processes control genes." Dr. Elias Zerhouni, who directed the NIH when it awarded the grant, said at the time — in a phrase slightly too dry for its import — that epigenetics had become "a central issue in biology."

      This past October, the NIH grant started to pay off. Scientists working jointly at a fledgling, largely Internet-based effort called the San Diego Epigenome Center announced with colleagues from the Salk Institute — the massive La Jolla, Calif., think tank founded by the man who discovered the polio vaccine — that they had produced "the first detailed map of the human epigenome."

      The claim was a bit grandiose. In fact, the scientists had mapped only a certain portion of the epigenomes of two cell types (an embryonic stem cell and another basic cell called a fibroblast). There are at least 210 cell types in the human body — and possibly far more, according to Ecker, the Salk biologist, who worked on the epigenome maps. Each of the 210 cell types is likely to have a different epigenome. That's why Ecker calls the $190 million grant from NIH "peanuts" compared with the probable end cost of figuring out what all the epigenetic marks are and how they work in concert.

      Remember the Human Genome Project? Completed in March 2000, the project found that the human genome contains something like 25,000 genes; it took $3 billion to map them all. The human epigenome contains an as yet unknowable number of patterns of epigenetic marks, a number so big that Ecker won't even speculate on it. The number is certainly in the millions. A full epigenome map will require major advances in computing power. When completed, the Human Epigenome Project (already under way in Europe) will make the Human Genome Project look like homework that 15th century kids did with an abacus.
      But the potential is staggering. For decades, we have stumbled around massive Darwinian roadblocks. DNA, we thought, was an ironclad code that we and our children and their children had to live by. Now we can imagine a world in which we can tinker with DNA, bend it to our will. It will take geneticists and ethicists many years to work out all the implications, but be assured: the age of epigenetics has arrived.