Missing DNA Can Promote Childhood Obesity

By MALCOLM RITTER AP Science Writer
NEW YORK December 6, 2009 (AP)

Some children get severely obese because they lack particular chunks of DNA, which kicks their hunger into overdrive, researchers report.

The British researchers checked the DNA of 300 children who’d become very fat, on the order of 220 pounds by age 10. They looked for deletions or extra copies of DNA segments.

They found evidence that several rare deletions may promote obesity, including one kind they studied further and found in less than 1 percent of about 1,200 severely obese children.

That deletion, on chromosome 16, apparently causes trouble because it removes a gene that the brain needs to respond to the appetite-controlling hormone leptin, said Dr. Sadaf Farooqi of Cambridge University.

In her study, children with a chromosome 16 DNA deletion “have a very strong drive to eat,” said Farooqi, who co-led the research. “They’re very, very hungry, they always want to eat.”

The work, reported online Sunday by the journal Nature, has already produced a real-world payoff. Farooqi said four children with the chromosome 16 deletion had drawn the attention of British child welfare authorities, who blamed the parents for overfeeding them.

“We were able to intervene” and get the parents of two children off the hook, and the other two cases are under discussion, she said.

That’s happened before when the scientists uncovered genetic causes for severe childhood obesity, she said.

“It’s a slightly unusual outcome of our research, but one we think is very important,” she said.

While scientists had previously discovered particular genes that promote obesity when damaged, the new work looked at larger chunks of DNA that can span several genes. The chromosome 16 deletion includes nine genes.

Eric Ravussin, an obesity expert at the Pennington Biomedical Research Center in Baton Rouge, La., who wasn’t involved in the study, said the work provides “a gold mine of information.” That’s because it identifies specific chromosome areas that scientists can explore to discover obesity-related genes, he said.

Nature: http://www.nature.com/nature

DNAWellnessinfo.com Resource:  http://abcnews.go.com/Technology/wirestory?id=9263514&page=1

Blame Your DNA?

Study: Genes may detemine if you’re a fitness fanatic or a couch potato.

Christie Aschwanden Special to Tribune Newspapers

September 29, 2009

For decades, fitness gurus have admonished sofa spuds to adopt a can-do attitude toward exercise, as if the only thing keeping them from the gym or walking path was the right attitude.

Yet a growing body of evidence suggests that it’s not merely motivation but also genetics that separate slouches from fitness fanatics, and at least some of these genes appear to act on the brain’s pleasure and reward center.

Though the science doesn’t imply that people disinclined to exercise can’t get moving, it helps explain why some people find it more difficult than others to “just do it.”

“We all know people who can’t sit still and we all know people who can’t get off the couch,” says J. Timothy Lightfoot, an exercise physiologist at the University of North Carolina in Charlotte.

Studies of twins suggest that some of the differences between these types of people come down to genetics. A 2006 Swedish investigation looked at leisure-time physical activity in 5,334 identical and 8,028 fraternal twins. The findings revealed that the exercise habits of identical twins were twice as closely matched as those of fraternal twins.

Fraternal twins share half their genes on average, whereas identical twins are genetic duplicates, so the finding implies that genes account for much of the variability in physical activity levels between people.

Likewise, a 2006 study that pooled data on exercise participation in more than 37,000 twin pairs from seven European countries calculated the genetic influence on physical activity at somewhere between 48% and 71%.

And these are not isolated findings.

“We now have more than 20 twin studies showing almost unanimously that [identical] twins are more alike in their physical activity than [fraternal] twins,” says geneticist Claude Bouchard, executive director of the Pennington Biomedical Research Center in Baton Rouge, La. The studies make a compelling case that the inclination to exercise runs in families, he says.

Studying mice

In an effort to find the genes involved, physiologist Theodore Garland at UC Riverside turned to rodents. He placed exercise wheels in the cages of ordinary mice and measured how often they scurried around in the wheels.

“This was voluntary exercise,” Garland says. “It’s sort of like how some people jog and others don’t.”

Researchers then selected the mice who ran the most and bred them with other so-called “high-runners” and repeated the experiment for more than 50 generations.

The result was a strain of high-runner mice that run as many as eight hours per night.

Garland’s next step was to find out what caused the mice to want to run. He found clues in the brain.

In a study published in 2003, his group showed that high-runner mice and regular mice respond differently to stimulants such as cocaine and Ritalin. Regular mice would run more when plied with the stimulants. “But we’ve never found a drug that will increase running in high-running mice,” he says. Whatever those drugs do in the brain seemed to be already turned on in the high-runner mice.

Because cocaine and Ritalin alter levels of the brain chemical dopamine, a neurotransmitter involved in pleasure and reward, the drugs’ different effects on the two breeds suggest high-runner and regular mice may process dopamine differently in the brain — and that may dictate how much pleasure they get out of running.

Other studies have also linked physical activity to dopamine.

For instance, a 1998 study showed that mice deficient in a receptor involved in processing dopamine, the D2 receptor, are less active than those with normal D2 receptor levels.

More recently, Lightfoot and his colleague Amy Knab found that two other dopamine-related genes were less active in their high-runner mice.

Says Knab, who is an exercise physiologist at Appalachian State University, “There’s something inherently different in the dopamine systems of the high-runners versus low-runners.”

Human studies have also linked exercise frequency to dopamine. Bouchard’s research team studied physical activity levels in a sample of 721 volunteers from 161 families in Quebec, Canada. They found that variations in the dopamine D2 receptor gene correlated to physical activity levels in women, but not men.

It’s a start

Bouchard says the study is an intriguing start — but he speculates that there are many more genes that influence exercise inclination.

Environment still plays a major role in how much someone exercises, though. “You can’t blame being lazy on your genes,” Knab says.

In fact, a twins study published last year suggests that environment trumps genetics when it comes to the kind of exercise needed for good health.

When University of Washington exercise physiologist Glen Duncan and his colleagues examined data from the university’s twin registry they found that genetics did predict the propensity to exercise up to 60 minutes per week.

But at 150 minutes or more — the amount of exercise that public health officials recommend — “the genetic component went away and the environment was the bigger factor,” Duncan says. For example, if people walk into a building and see a set of stairs first thing, they will probably take them. But if there’s an escalator front and center, they’ll take that instead, he says.

Researchers are now trying to tease out the ways that genes and the environment combine to turn one person into a marathon runner and another into a couch potato. By doing so, they may discover more effective ways to encourage exercise among those not naturally inclined.

“It’s really hard to change people’s physical activity levels,” physiologist Joey Eisenmann at Michigan State University says.

“There are a lot of people working on interventions to increase physical activity, and for the most part they haven’t been shown to be highly effective. As we learn more about genetic factors, that may shed light on why these programs don’t work as well as we’d like.”

Some of this research may eventually lead to more individualized approaches to fitness.

Or — failing that — researchers may even learn to enhance exercise’s gratifying effects with drugs.

“Some day,” Garland says, “we could be giving people pills to make it more pleasurable to run.”

DNAWellnessinfo.com Resource:  http://www.baltimoresun.com/health/sns-health-blame-your-dna,0,3243673.story?page=1

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Bad Eating Habits Can Alter Your DNA

By Margaret Furtado, M.S., R.D. – Posted Fri, Aug 07, 2009, 4:30 am PDT

Role of genes in weight management

weightlossnutrition.com

Science is constantly trying to get behind the main factors for the obesity epidemic. From our hurried, fast food lifestyle to our laziness and penchant for T.V. watching rather than exercise, it seems relatively clear that, in most cases, the obesity epidemic is a result of our lifestyle choices. But for some, their genetics play a role that may be hard to fight against.

Family reunions let everyone in the family come together and see the role that genetics has played in their life; maybe you have Aunt Bertha’s red hair or Cousin Vinny’s brown eyes. Unfortunately, you can also inherit Uncle Roger’s pot belly and Grandpa Joe’s wide tush. This is because genetics plays a role in your fat cells and where they are stored.

Because of your DNA, you have a genetic predisposition to carry fat cells in the same areas as your family. Since families blend the DNA of many different people, you may take after one side of your family more than another. This could mean that you and your brother have the genetic predisposition to having love handles while your older sister doesn’t.

In addition to your propensity to carry fat in certain places, you’ll find that your body’s response to exercise mimics others in your family as well. If you have the right genes, you may find that you build muscle very quickly when weight training or, if you’re on the unfortunate end, you don’t.

But, what is the role of genes in weight management? Can you manipulate your genes to work for you rather than against you? For some with genetically linked health issues like thyroid problems, medications can be a solution. Medications can help your body run as it should and can pick up the slack for any glands that are impaired due to genetic lineage.

For most people, medication is not the answer. Instead, learning how your body responds to food and exercise if key to fighting your genes and managing your weight. If your family is filled with overweight people, and you see the signs in your own body that this is probably your destiny too, follow these steps to head genetics off at the pass.

1. Eat right. Cut out sugars, simple carbohydrates (like white rice and white bread), and stay away from fast food. For some, learned eating habits play a bigger role in weight gain than genetics. Be sure to reevaluate the food lessons you’ve learned from your family and try to make the right decisions regarding what goes in your mouth.
2. Exercise regularly. Ideally, you should exercise for one hour a day, five to six days per week. Unfortunately, real life often gets in the way of this. If you can exercise four times per week for one half hour per work out, you’ll find you can stave off the effects of genetics.
3. Stick with it. Fighting your genes is not easy and you may find that you have to work harder than others to receive fewer results. Just remember the alternative facing you and stick with it.

Before embarking on any new physical fitness routine or new and improved eating plan, you should consult a physician. In addition to letting you know if the routine you want to try is healthy for you, they may have some other helpful tips to give you. Speaking with a nutritionist about your eating plan will also help you get ideas for variety and make sure that you haven’t included any foods that will hurt your weight management goals rather than help them.

DNAWellnessinfo.com Resource:  http://www.weightlossnutrition.org/genes-weight-management/

DNA Guided Nutrition Breakthrough:  http://www.dnaguidedwellnessproducts.com

Melon research sweetened with DNA sequence

Sat, 06/27/2009 – 15:20 – NLN

machineslikeus.com

People smell them, thump them and eyeball their shape. But ultimately, it’s sweetness and a sense of healthy eating that lands a melon in a shopper’s cart.

Plant breeders now have a better chance to pinpoint such traits for new varieties, because the melon genome with hundreds of DNA markers has been mapped by scientists with Texas AgriLife Research. That means tastier and healthier melons are likely for future summer picnics.

Colored melon flesh are full of nutrients. Plant breeders may develop even better varieties now that melon genome with hundreds of DNA markers has been mapped. Credit: Texas AgriLife Photo by Kathleen Phillips.

DNA-Based, Marker-Assisted Selection In Beef Cattle

6/24/2009 2:21:00 PM

cattlenetwork.com

Genetic improvement through selection has been one of the most important contributors to the advancements in animal productivity in the past 50 years. Traditionally, selection in beef cattle has been based on estimating breeding value using expected progeny difference (EPDs). The EPDs are derived from the observable performance (or phenotype) of the animal and its relatives. EPDs statistically predict that animal’s genetic potential for given traits (e.g., weaning weight). The accuracy of the estimate will increase over time as more information from progeny and relatives becomes available.

EPDs are the tools. They are not the plan. In order to effectively use EPDs, it is important to develop a breeding plan with specific goals and objectives (e.g., the most profitable selection criteria) for your herd or production system. Most of the economically relevant traits for cattle production (birth weight, weaning weight, growth, reproduction, milk production, carcass quality, etc.) are complex traits controlled by many genes and influenced by the production environment.

A gene is a segment of deoxyribonucleic acid (DNA) that is made up of pairs of four nucleotides abbreviated as “A”, “C”, “G”, and “T” (see Fig. 1 on the next page). A gene dictates the production of a specific protein. It is possible for the sequence of the DNA that makes up a gene to differ between individuals. These DNA variations in a gene are called alleles, and they often result in differences in the amount or type of protein being produced by that gene among different individual animals.

The protein produced by different alleles may affect the expression of a given trait and influence the observed performance. When an animal has an EPD above the base year average for a certain trait, what that means is that the animal inherited a higher than average proportion of alleles that favorably affect the trait.

It should be noted that traditional selection methods inherently tend to increase the frequency of alleles that have major beneficial effects on selected traits. That is, EPDs as typically used, increase the number of favorable alleles without knowing which specific genes are involved. This contrasts with DNA-based selection where knowledge of which DNA sequences are associated with improvement in a given trait is required, and selection is focused on those known DNA “markers” to make genetic improvement in the trait.

Recently scientists have started to identify regions of DNA that influence production traits. They have used molecular techniques to find differences in the sequence of the nucleotide base pairs in these regions. Tests have been developed to identify these subtle differences in the DNA. This has allowed for the development of genetic markers that scientists can use to identify whether an animal is carrying a segment of DNA that is positively or negatively associated with the trait of interest.

Genetic markers in a given region of DNA may differ from each other by the sequence of only a single nucleotide base pair, such as a single A, C, G, or T (Fig. 1). Such differences are called single nucleotide polymorphisms or SNPs (referred to as “snips”). Genetic tests based on SNPs analyze DNA derived from an individual to determine the DNA sequence that is present at one specific location (nucleotide pair) in among the three billion nucleotide pairs that comprise the genome of the cow!

Genotyping is the term that is used to describe the process of using laboratory methods to determine the equence of nucleotides in the DNA from an individual, usually at one particular gene or specific location in the genome.

Selecting an animal carrying the favorable form of a marker, or one that is associated with a positive impact on the trait of interest, can result in an improvement in the observed phenotype for that trait. Although complex traits are influenced by several genes, the mode of inheritance of each genetic marker is simple. An animal gets one marker allele from both its sire and dam.

Genome Program

Fig. 1. DNA (deoxyribonucleic acid) contains the instructions for making proteins. Differences in the nucleotide sequence of a gene’s DNA can influence the type or amount of protein that is made, and this can have an effect on the observed performance of an animal. Source: Original graphic obtained with permission from the U.S. Department of Energy Human Genome Program (http://www.doegenomes.org).

Marker-Assisted Selection (MAS) is the process of using the results of DNA tests to assist in the selection of individuals to become the parents in the next generation of a genetic improvement program. Genotyping allows for the accurate detection of specific DNA variations that have been associated with measurable effects on complex traits. It is important to remember that markers for complex traits are associated with only one of the many genes that contribute toward that trait.

The presence or absence of the numerous other “unmarked” genes and the production environment will determine whether an animal actually displays the desired phenotype (e.g., large weaning weight, increased marbling). EPDs estimate the breeding value of all the genes (both “marked” and “unmarked”) that contribute toward a given trait and, therefore, should always be considered in selection decisions, even when marker data are available.

Potential benefits from marker-assisted selection are greatest for traits that:

1. Have low heritability (e.g., traits where observed or measured values are poor predictors of breeding value) (Table 1).

2. Are difficult or expensive to measure (e.g., disease resistance).

3. Cannot be measured until after the animal has already contributed to the next generation (e.g., carcass data).

4. Are currently not selected for as they are not routinely measured (e.g., tenderness).

5. Are phenotypically (observed value), but not genetically, correlated with a trait that you do not want to increase (e.g., selection for marbling markers does not genetically increase backfat thickness despite the fact that on the animal these two traits tend to increase in unison).

Table 1

In order of greatest to least degree of benefit, the following categories of traits are likely to benefit the most from marker-assisted selection: (1) disease resistance, (2) carcass quality and palatability attributes, (3) fertility and reproductive efficiency, (4) carcass quantity and yield, and (5) milk production, maternal ability, and growth performance.

This ranking is due to a combination of considerations including: (1) relative difficulty in collecting performance data, (2) relative magnitude of the heritability and phenotypic variation observed in the traits, (3) current amount of performance information available, and (4) when performance data become available in the life cycle.

Recently genetic tests for DNA markers associated with marbling and tenderness have become commercially available. Each of these markers is associated with only one of the genes that contribute toward marbling or tenderness. Other “unmarked” genes, in conjunction with the production setting, will influence whether an animal marbles or has tender meat. Cattle can be genotyped for the desirable form of the marker by analyzing DNA collected from hair, tissue, blood, or semen samples.

It is important to have some idea of how much of the variability for a given trait is accounted for by each DNA marker. Ideally, but not necessarily, the preferred form of a marker would always identify genetically superior animals. Results from studies in commercial herds, comparing the performance of animals with and without the marker, should be an important consideration as they can help to estimate the effect of the marker on the trait under commercial conditions.

In the future it is likely that phenotypic, pedigree, and DNA-marker information will all be included in EPD calculations and that selection on this EPD will be superior to selection based on markers alone. The challenge will be to ensure that the value derived from the genetic progress associated with marker assisted selection for marbling and tenderness, or any other trait, outweighs the expense of collecting the marker information.

Source: Alison Van Eenennaam, University of California, Davis

DNAWellnessInfo.com Resource:  http://www.cattlenetwork.com/Content.asp?ContentID=325457

Genes Play a Role in Glycemic Control in People With Type 1 Diabetes

earthtimes.com – Sat, 06 Jun 2009 13:15:23 GMT

NEW ORLEANS, LA — 06/06/09 — Researchers have proven that glycemic control in type 1 diabetes is not fully dependent on the individual’s behavior, but is in part subject to genetic influence, according to a presentation here today at the American Diabetes Association’s 69th Scientific Sessions. “We identified four genes related to glycemic control in type 1 diabetes,” said Andrew D. Paterson, MBChB, Senior Scientist in the Program for Genetics and Genome Biology, Hospital for Sick Children in Toronto, and lead author of the study. “Two of these genes also affect risk for complications — kidney, eye, and cardiovascular disease — and one gene has a strong effect on the rate of hypoglycemia.”

“This finding does not give people with diabetes the freedom to slack off on their careful nutrition, exercise, and medication regimens because behavior clearly plays the major role in glycemic control,” cautioned Dr. Paterson. “Eventually, the genetic variations we found may be used to identify individuals at risk for poor glycemic control and for diabetic complications, so that steps could be taken to intensify control or implement other measures. But in the interim, this knowledge may influence the design and analysis of genetic studies attempting to identify risk factors for long-term diabetic complications and lead us in new research directions to better understand the mechanisms of glycemic control.”

Nearly 24 million Americans have diabetes, a group of serious diseases characterized by high blood glucose levels that result from defects in the body’s ability to produce and/or use insulin. Diabetes can lead to severely debilitating or fatal complications, such as heart disease, blindness, kidney disease, and amputation. It is a leading cause of death by disease in the United States.

Type 1 is an immune-mediated form of diabetes involving destruction of the insulin-producing beta cells in the pancreas that typically leads to absolute insulin deficiency. Type 1 diabetes accounts for 5% to 10% of all diagnosed cases of diabetes and usually strikes children or young adults, although disease onset can occur at any age.

The first data suggesting that A1C, a measure of average glucose control over the prior two to three months, might be influenced by genetics came in 2001 in a British study looking at identical twins, where one twin had type 1 and the other did not, called discordance. “It was found that when the twin without diabetes had an A1C in the high normal range, the twin with diabetes would have an A1C in the high range for someone with diabetes,” said Dr. Paterson. “Essentially, they were playing to the same drummer but in a different key.”

In the current study, the researchers mined the extensive data available from one of the world’s most well-documented studies of people with type 1 diabetes: the Diabetes Control and Complications Trial (DCCT) — an NIH-sponsored study. It was initiated over 25 years ago and enrolled 1,441 people in a comparison of intensive versus conventional control of blood glucose. Conventional control during the DCCT required only one or two insulin injections and blood checks daily, with the aim of preventing overt diabetes symptoms, and typically yields A1C levels of 9% or more. Intensive control to bring A1C levels as close to normal as possible (6% or less) required at least three insulin injections a day or treatment with an insulin pump, guided by at least four glucose self-monitoring checks a day. The initial results, reported in 1993, demonstrated dramatic reductions in the development of eye, nerve, and kidney damage. Intensive control also lowered the risk of heart disease according to data published in 2005 as part of the follow-up study of DCCT participants, called the Epidemiology of Diabetes Interventions and Complications (EDIC) observation study, which is still continuing.

The researchers in this genetic study had access to every quarterly A1C test performed on people in the original DCCT over the course of an average of 6 1/2 years. To identify important genetic loci (the positions that genes occupy on a chromosome) influencing glycemic control in type 1, they performed high resolution genome-wide studies using the mean A1C values and capillary glucose of people in the conventional treatment group and compared loci of interest to people in the intensive treatment group.

They determined the genotypes of a million SNPs across the genome for over 1,300 participants in the DCCT. (SNPs are single-nucleotide polymorphisms, pronounced “snips” — DNA sequence variations in the genome.) Each of these SNPs was tested for association with the participants’ average A1Cs over the course of the trial.

They identified four major gene loci related to A1C levels. One in both treatment groups reached genome-wide significance — SORCS1 gene 10q25.1. Three achieved close to genome-wide significance: 14q32.13 (GSC) and 9p22 (BNC2) in the combined treatment groups; and 15q21.3 (WDR72) in the intensive group. Further, evidence indicated that SORCS1 was associated with hypoglycemia (low blood glucose), and BNC2 was associated with kidney and eye complications.

“While this information gives us insight into the mechanisms influencing glycemic control in people with type 1, it is important to remember that the overall influence of genes is small and may vary from person to person and, perhaps, in response to behavior,” Dr. Paterson explained. “For example, while the SORCS1 gene accounted for about 5% of the variability in glycemic control in the conventional treatment arm of the DCCT, A1C levels in people with type 1 diabetes have improved since those days as diabetes care teams and patients have learned about the value of more intensive control,” he said. “So we don’t know whether that number would be the same in a contemporary treatment setting.” For example, in the EDIC study, A1C levels of the former conventional control group dropped from 9% to 8.1% after they were taught intensive control at the end of the DCCT.

The American Diabetes Association is leading the fight against the deadly consequences of diabetes and fighting for those affected by diabetes. The Association funds research to prevent, cure and manage diabetes; delivers services to hundreds of communities; provides objective and credible information; and gives voice to those denied their rights because of diabetes. Founded in 1940, our mission is to prevent and cure diabetes and to improve the lives of all people affected by diabetes. For more information please call the American Diabetes Association at 1-800-DIABETES (1-800-342-2383) or visit www.diabetes.org. Information from both these sources is available in English and Spanish.

Abstract 58-OR

Contact:
Diane Tuncer
(703) 299-5510

Colleen Fogarty
(703) 549-1500 ext. 2146

DNAWellnessinfo.com Resource:  http://www.earthtimes.org/articles/show/genes-play-a-role-in,851904.shtml

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10 guilt-free foods you can add to your diet

KGO-TV – San Francisco,CA,USA

Friday, June 05, 2009

Affordably delicious and surprisingly healthful: 10 foods you can add back to your diet without guilt! Amy Albert, senior associate editor of Bon Appetit Magazine, shares her finds.

Every month, Bon Appétit features a column called “Health Wise,” where we offer a guide to eating healthfully while still enjoying your food. It’s designed to help our readers make sense of nutritional information that can sometimes be hard to decipher.

1. BACON

· Jennifer McLagan, author of Fat, tells us that 45% of the fat in bacon is monosaturated – which is a good-for-you-fat that can actually help lower bad cholesterol levels.

· This fat is the same fat found in olive oil (called oleic acid) – so our argument is that bacon is about half as good for you as olive oil and twice as delicious!

· Of course, it’s not a free ride – moderation is key and you should seek out artisanal varieties without preservatives.

· Also remember that when cooking with bacon, a little goes a long way – sometimes you just need one slice to spice up a pot of soup. Or use it as a yummy garnish for fish or sautéed greens.

2. WHOLE MILK

· Whole milk can be good for you – the saturated milk fats you find in whole milk may help us absorb calcium better, and contains big helpings of vitamins A and D. In fact, milk producers are required by the government to fortify low-fat and skim milk with synthetic vitamins that are found naturally in whole milk.

· Other studies have found that low-fat diets can actually be counterproductive to weight loss – so having some fat from whole milk can be good for you. In a Swedish study, researchers found that women who ate one serving of whole milk or cheese a day put on less weight than women who ate these foods less often. · Another study suggested that one or more servings of whole milk a day may even enhance a woman’s fertility

3. PINE NUTS

· You find about 11 grams of protein in about one half cup of pine nuts.

· They are also loaded with cancer-fighting antioxidants and pinolenic acid, a natural appetite suppressant – which will help you eat less.

· And if you are worried about fat in nuts, a 2003 study in the European Journal of Clinical Nutrition found little evidence that eating nuts causes weight gain; some evidence actually pointed to weight maintenance.

· Here’s how you can use them in your cooking: Pine nuts are a terrifically easy way to add a little flavor, richness, and texture to everything from last-minute salads to weeknight pastas

4. DUCK BREAST

· Although duck has a decadent reputation, this doesn’t make it a bad thing to cook at home every once and a while.

· It has a thick layer of fat under the skin – but duck fat is considered to be among the healthiest of animal fast. With 63% unsaturated fat, it beats out beef and is right up there with chicken. And it is absolutely delicious! So you shouldn’t be afraid to splurge on duck breast every now and then.

· A great way to cook it: Score the skin and sauté it skin side down to render out much of the fat, and sprinkle with sea salt.

· We also have a great recipe for Seared Duck Breast in the June issue

5. WATERCRESS

· All greens are good for you, but watercress is especially healthful.

· A 2007 study in the American Journal of Clinical Nutrition found that watercress has a high enough antioxidant count to make a measurable difference in reducing DNA damage to our white blood cells (a precursor to many forms of cancer).

· Eating watercress has also been found to consistently lower elevated blood triglyceride levels, a risk factor for heart disease.

· Watercress tossed with a Dijon vinaigrette is a perfect accompaniment to a grilled grass-fed skirt steak (or even duck breast!).

6. CANNELLINI BEANS

· These are a pantry staple – and are budget-friendly, versatile, and incredible good for you.

· Beans have cholesterol-lowering soluble fiber, potassium and magnesium that can help regulate blood pressure.

· Plus, their complex carbs and protein help keep you feeling full (so you aren’t temped to snack 30 mins after dinner).

· All beans are good for you, but cannellinis are especially great – they are building blocks for delicious soups, salads, sides and appetizers.

· The best place to buy beans is somewhere that moves them in large quantities so you know they haven’t been sitting around.

7. LEEKS

· Did you know that one medium-sized leek can contain more fiber than a bran muffin? Leeks are an incredible source of dietary fiber.

· They also have tons of folic acid, iron, potassium, vitamin C, and cancer-fighting antioxidants.

· They are incredible versatile to cook with as well – use them in potato-leek soup, try them in place of celery in stock and stew recipes, or slow-braise them for a great side dish for roasted meats.

8. ANCHOVIES

· Small, oily fish from cold northern seas – like anchovies – contain a high concentration of omega-3s with a minimum of mercury.

· These omega-3 fatty acids have been recommended by doctors for protection against everything from heart disease to depression.

· Anchovies have just as much omega-3 as salmon and nearly twice as much as halibut.

· Although the serving sizes aren’t the same, anchovies can add incredible depth of flavor to a wide variety of dishes – from pastas to salads to homemade mayonnaise.

· So you can easily get some omega-3′s in surprising and delicious ways.

9. FRESH STRAWBERRIES

· When it comes to healthful eating, scientists have discovered that color is key.

· Brightly colored fruits and vegetables (like strawberries) contain the highest levels of phytonutrients – powerful disease-fighting compounds.

· A study conducted at the University of Illinois found that strawberries may fight inflammation, cancer-causing compounds, and may even be capable of suppressing the progression of tumors

10. BUCKWHEAT

· Most people think that buckwheat is a grain, but it is actually an herb that’s related to rhubarb and sorrel.

· It contains all the essential amino acids, B vitamins, phosphorus, magnesium, iron zinc, copper and manganese, and a fatty acid critical to good health.

· It has 4.5 grams of dietary fiber in every cup – so it’s up there in nutrition with granola.

· You can eat buckwheat in soba noodles, French-style crepes, or use buckwheat flour to make pancakes.

· Because it’s high-protein, you will be getting a low-glycemic index meal that won’t leave you hungry an hour later.

Visit bonappetit.com for tons of recipes that use all of these ingredients.

DNAWellnessinfo.com Resource:  http://abclocal.go.com/kgo/story?section=view_from_the_bay/food_wine&id=6850949

DNA Nutrition Breakthrough:  http://www.dnaguidedwellnessproducts.com

Lab creates an all-it-can-eat mouse

Imagine you’ve bellied up to the all-you-can-eat pasta bar in Berkeley, only to meet one of the mice from Hei Sook Sul’s Nutritional Science and Toxicology Lab.

If you come here often, you know that loading up on carbohydrates is going to make you pretty chubby. But you notice that your fellow diner — the mouse — is pretty slim. How does he do it?

DNA Weight Control

Not only were mice whose DNA-PK gene had been knocked out 40% leaner than normal mice when all were fed a high-carb, low-fat diet; they also had better blood-lipid profiles, suggesting they’d be at lower risk of developing heart disease.

Sul said no one at this point was thinking about gene therapy as a treatment for obesity. Instead, drug developers might look at how the DNA-PK gene calls out other actors to set in motion the conversion of excess calories to fat and find an agent that might disrupt the process.

If they’re successful, you’ll be able to join that mouse at the pasta bar and look just as svelte as he does.

melissa.healy@latimes.com

DNA Wellness Resource:  http://www.latimes.com/news/nationworld/nation/la-sci-carbs21-2009mar21,0,6500843.story

DNA Nutritional Breakthrough:  http://www.dnaguidedwellnessproducts.com

Forever Off-Menu: A Diet All Your Own

By Brandon Keim May 07, 2007 | 3:18:36 PM  WIRED

For a few hundred dollars, you can send away for a genetic test from companies that offer personalized nutrition information — and usually vitamin supplements — based on the results.

Decades from now, we may see these services as we now see miracle cures peddled by traveling salesmen in frontier America. Experts at the cutting edge of nutrigenomics say that current commercial products are based on a sliver of insight into the complex, multi-level system that is metabolism. But soon — perhaps, even, within a decade — personalized diets customized as carefully as a bespoke suit may be an everyday consumer reality.

That was the message of “Nutrigenomics, Nutritional Systems Biology and Personalized Nutrition – Truth or SciFi?,” an afternoon panel discussion at BIO. Genetics alone won’t make this happen, said the speakers; it will require an understanding of our metabolites — the substances made by the human body, with the production influenced by both diet, genetics and the emergent properties of different physiological symptoms. This is the purpose of such research as the Human Metabolome Project, which in January published our metabolome’s first draft.

Once scientists understand how our bodily compounds work, they can associate these with physiology — physical and mental health, energy, longevity, and so on. And then — this is where it gets fun! — people will be able to pose for metabolic portraits. Companies will measure, instead of a handful of genes, the metabolic effect of different foods upon each person. They’ll provide a personal list of nutrients; you’ll be able to plug these into dietary software that tells you what to eat. Send the information to a next-generation grocery store, and the basic components of your ideal diet will be delivered to your door.

Blue-sky? Certainly. Would it take some of the romance out of eating? In the picture painted by the scientists, it sure sounds like it. But while scientists may tell us what to eat, they’re not in the business of selling it to us. If the science ever does progress to that level of culinary customization, I’ve no doubt we’ll see a Julia Child of nutrigenomics, an endless line of chefs showing us how to fold our nutrigenomic recipes like so much origami, and we will eat like (healthy) kings.

DNA News Resource:  http://blog.wired.com/wiredscience/2007/05/forever_offmenu.html

DNA Nutritional Breakthrough:  http://www.dnaguidedwellnessproducts.com