A good friend sent me this recipe its original form was published in the NY Times on 1/27/13. It is very light and packed with lean protein!
TOTAL TIME: 40 minutes
Ingredients
2 tablespoons grapeseed or Grapeola oil (you could olive if you have nothing else with neutral flavor)
4 chicken drumsticks or thighs, skin on, bone in
Salt and black pepper
2 tablespoons chopped garlic
2 tablespoons chopped ginger
24 littleneck clams
1 bunch scallions, white and green parts chopped and separated
1/4 cup cilantro stems, chopped
1/2 cup cilantro leaves, chopped
1. Rinse clams 2-3 times in room temp water. Then place clams in bowl and cover with room temp water. Add 1 tablespoon cornstarch or flour and mix into water. Let clams sit in this water until you are ready for use. You want the clams to open up and start filtering the water so that they release all of the sand in their shell/body.
2. Heat the oil over medium-high heat in a large, deep skillet or broad pot that can later be covered. When the oil is hot, season the chicken pieces with salt and pepper, and add them to the oil. Regulate the heat so that the meat browns evenly, turning as needed. (Drumsticks have 4 sides, really; thighs only 2, so timing is variable.) When the chicken is well browned, it will be almost done.
3. Add the garlic and ginger and cook for a minute, just until they soften a bit. Add the clams and sprinkle them with the scallion whites and the cilantro stems. Cover and cook until all the clams open, about 10 minutes; they will generate a good deal of liquid.
4. Remove the top and cook that liquid down as desired. (Perhaps not at all, perhaps until syrupy — your call.) Discard any clams that have not opened - they could have been dead before you cooked them and can then cause food borne illness. Serve sprinkled with the scallion greens and cilantro leaves.
Remember not to eat the chicken skin - we were just using it to add flavor and keep the chicken moist!
ENJOY!!
Thursday, February 28, 2013
Wednesday, February 27, 2013
Article: Race Linked to childhood food allergies...
Public release date: 23-Feb-2013
Contact: David Olejarz
David.Olejarz@hfhs.org
313-874-4094
Henry Ford Health System
Race linked to childhood food allergies, not environmental allergies
DETROIT – Research conducted at Henry Ford Hospital shows that race and possibly genetics play a role in children's sensitivity to developing allergies. Researchers found:
African-American children were sensitized to at least one food allergen three times more often than Caucasian children.
African-American children with one allergic parent were sensitized to an environmental allergen twice as often as African-American children without an allergic parent.
The study will be presented Saturday at the American Academy of Allergy, Asthma and Immunology annual meeting,
"Our findings suggest that African Americans may have a gene making them more susceptible to food allergen sensitization or the sensitization is just more prevalent in African American children than white children at age 2," says Haejim Kim, M.D., a Henry Ford allergist and the study's lead author. "More research is needed to further look at the development of allergy."
Sensitization means a person's immune system produces a specific antibody to an allergen. It does not mean the person will experience allergy symptoms.
According to an AAAI study from 2009-2010, an estimated 8 percent of children have a food allergy, and 30 percent of children have multiple food allergies. Peanut is the most prevalent allergen, followed by milk and shellfish. 1The Henry Ford study consisted of a longitudinal birth cohort of 543 children who were interviewed with their parents and examined at a clinical visit at age 2. Data included parental self-report of allergies and self-reported race (African American or white/non-Hispanic). The children were skin-tested for three food allergens – egg whites, peanuts and milk – and seven environmental allergens.
Key findings:
20.1 percent of African-American children were sensitized to an food allergen compared to 6.4 percent in Caucasian children.
13.9 percent of African-American children were sensitized to an environmental allergen compared to 11 percent of Caucasian children.
African-American children with an allergic parent were sensitized to an environmental allergen 2.45 times more often than African-American children without an allergic parent.
###
The study was funded by Henry Ford Hospital and National Institute of Allergy and Infectious Diseases.
http://www.eurekalert.org/pub_releases/2013-02/hfhs-rlt022013.php
Contact: David Olejarz
David.Olejarz@hfhs.org
313-874-4094
Henry Ford Health System
Race linked to childhood food allergies, not environmental allergies
DETROIT – Research conducted at Henry Ford Hospital shows that race and possibly genetics play a role in children's sensitivity to developing allergies. Researchers found:
African-American children were sensitized to at least one food allergen three times more often than Caucasian children.
African-American children with one allergic parent were sensitized to an environmental allergen twice as often as African-American children without an allergic parent.
The study will be presented Saturday at the American Academy of Allergy, Asthma and Immunology annual meeting,
"Our findings suggest that African Americans may have a gene making them more susceptible to food allergen sensitization or the sensitization is just more prevalent in African American children than white children at age 2," says Haejim Kim, M.D., a Henry Ford allergist and the study's lead author. "More research is needed to further look at the development of allergy."
Sensitization means a person's immune system produces a specific antibody to an allergen. It does not mean the person will experience allergy symptoms.
According to an AAAI study from 2009-2010, an estimated 8 percent of children have a food allergy, and 30 percent of children have multiple food allergies. Peanut is the most prevalent allergen, followed by milk and shellfish. 1The Henry Ford study consisted of a longitudinal birth cohort of 543 children who were interviewed with their parents and examined at a clinical visit at age 2. Data included parental self-report of allergies and self-reported race (African American or white/non-Hispanic). The children were skin-tested for three food allergens – egg whites, peanuts and milk – and seven environmental allergens.
Key findings:
20.1 percent of African-American children were sensitized to an food allergen compared to 6.4 percent in Caucasian children.
13.9 percent of African-American children were sensitized to an environmental allergen compared to 11 percent of Caucasian children.
African-American children with an allergic parent were sensitized to an environmental allergen 2.45 times more often than African-American children without an allergic parent.
###
The study was funded by Henry Ford Hospital and National Institute of Allergy and Infectious Diseases.
http://www.eurekalert.org/pub_releases/2013-02/hfhs-rlt022013.php
Sunday, February 24, 2013
Article: Who has the guts for gluten?
Who Has the Guts for Gluten?
By MOISES VELASQUEZ-MANOFF
Published: February 23, 2013
WE know that the proteins called gluten, found in wheat and other grains, provoke celiac disease. And we know how to treat the illness: a gluten-free diet. But the rapidly increasing prevalence of celiac disease, which has quadrupled in the United States in just 50 years, is still mystifying.
Scientists are pursuing some intriguing possibilities. One is that breast-feeding may protect against the disease. Another is that we have neglected the teeming ecosystem of microbes in the gut — bacteria that may determine whether the immune system treats gluten as food or as a deadly invader.
Celiac disease is generally considered an autoimmune disorder. The name celiac derives from the Greek word for “hollow,” as in bowels. Gluten proteins in wheat, barley and rye prompt the body to turn on itself and attack the small intestine. Complications range from diarrhea and anemia to osteoporosis and, in extreme cases, lymphoma. Some important exceptions notwithstanding, the prevalence of celiac disease is estimated to range between 0.6 and 1 percent of the world’s population.
Nearly everyone with celiac disease has one of two versions of a cellular receptor called the human leukocyte antigen, or H.L.A. These receptors, the thinking goes, naturally increase carriers’ immune response to gluten.
This detailed understanding makes celiac disease unique among autoimmune disorders. Two factors — one a protein, another genetic — are clearly defined; and in most cases, eliminating gluten from the patient’s diet turns off the disease.
Yet the more scientists study celiac disease, the more some crucial component appears in need of identification. Roughly 30 percent of people with European ancestry carry predisposing genes, for example. Yet more than 95 percent of the carriers tolerate gluten just fine. So while these genes (plus gluten) are necessary to produce the disease, they’re evidently insufficient to cause it.
Animal studies have reinforced that impression. In mice engineered to express those H.L.A.’s, tolerance to gluten must be deliberately “broken.” Without an immunological trigger of some kind, the rodents happily tolerate the protein.
A recent study, which analyzed blood serum from more than 3,500 Americans who were followed since 1974, suggested that such a trigger could strike adults at any time. By 1989, the prevalence of celiac disease in this cohort had doubled.
“You’re talking about an autoimmune disease in which we thought we had all the dots connected,” says Alessio Fasano, head of the Center for Celiac Research and Treatment at the Massachusetts General Hospital for Children in Boston, and the senior author of the study. “Then we start to accumulate evidence that there was something else.”
Identifying that “something else” has gained some urgency. In the United States, improved diagnosis doesn’t seem to explain the rising prevalence. Scientists use the presence of certain self-directed antibodies to predict celiac disease. They have analyzed serum stored since the mid-20th century and compared it to serum from Americans today. Today’s serum is more than four times as likely to carry those antibodies.
BLAME for the increase of celiac disease sometimes falls on gluten-rich, modern wheat varietals; increased consumption of wheat, and the ubiquity of gluten in processed foods.
Yet the epidemiology of celiac disease doesn’t always support this idea. One comparative study involving some 5,500 subjects yielded a prevalence of roughly one in 100 among Finnish children, but using the same diagnostic methods, just one in 500 among their Russian counterparts.
Differing wheat consumption patterns can’t explain this disparity. If anything, Russians consume more wheat than Finns, and of similar varieties.
Neither can genetics. Although now bisected by the Finno-Russian border, Karelia, as the study region is known, was historically a single province. The two study populations are culturally, linguistically and genetically related. The predisposing gene variants are similarly prevalent in both groups.
Maybe more telling, this disparity holds for other autoimmune and allergic diseases. Finland ranks first in the world for Type 1 autoimmune diabetes. But among Russian Karelians, the disease is nearly six times less frequent. Antibodies indicative of autoimmune thyroiditis are also less prevalent, and the risk of developing allergies, as gauged by skin-prick tests, is one-fourth as common.
What’s the Russians’ secret?
“It’s a remote territory of Russia,” says Heikki Hyoty, a scientist at the University of Tampere in Finland. “They live like Finns 50 years ago.”
At the time of this research, roughly a decade ago, Russia’s per-capita income was one-fifteenth of Finland’s. Analysis of house dust and potable water suggests that the Russian Karelians encountered a greater variety and quantity of microbes, including many that were absent in Finland.
Not surprisingly, they also suffered from more fecal-oral infections. For example, three of four Russian Karelian children harbored Helicobacter pylori, a corkscrew-shaped bacterium, while just one in 20 Finnish children did. The bacterium can cause ulcers and stomach cancer, but mounting evidence suggests that it may also protect against asthma.
Professor Hyoty suspects that Russian Karelians’ microbial wealth protects them from autoimmune and allergic diseases by, essentially, strengthening the arm of the immune system that guards against such illnesses.
Meanwhile, Yolanda Sanz, a researcher at the Institute of Agrochemistry and Food Technology in Valencia, Spain, makes a compelling case for the importance of intestinal microbes.
Years ago, Dr. Sanz noted that a group of bacteria native to the intestine known as bifidobacteria were relatively depleted in children with celiac disease compared with healthy controls. Other microbes, including native E. coli strains, were overly abundant and oddly virulent.
How to determine cause or consequence?
In a test tube, she found that those E. coli amplified the inflammatory response of human intestinal cells to gluten. But bifidobacteria switched the response from inflammation to tolerance.
In rats, the E. coli again intensified inflammation to gluten, prompting what’s sometimes called a “leaky gut” — the milieu suspected of contributing to celiac disease. Conversely, bifidobacteria protected the intestinal barrier. Microbes, it seemed, could influence the immune response to gluten.
Bifidobacteria occur naturally in breast milk, which, along with protective antibodies and immune-signaling proteins, conveys hundreds of prebiotic sugars. These sugars selectively feed certain microbes in the infant gut, particularly bifidobacteria. Breast-fed infants tend to harbor more bifidobacteria than formula-fed ones.
All of which may explain a curious historical phenomenon — an “epidemic” of celiac disease that struck Sweden some 30 years ago. Anneli Ivarsson, a pediatrician at Umea University, recalled a sudden wave of “terribly sick” infants.
Sleuthing revealed that, just before the spike, official guidelines on infant feeding had changed. In an effort to prevent celiac disease, paradoxically, parents were instructed to delay the introduction of gluten until their babies were six months old. That also happened to be when many Swedish mothers weaned their children. Coincidentally, companies had increased the amount of gluten in baby food.
This confluence produced an unwitting “experiment with a whole population,” says Dr. Ivarsson — a large quantity of gluten introduced suddenly after weaning. Among Swedes born between 1984 and 1996, the prevalence of celiac disease tripled to 3 percent. The epidemic ebbed only when authorities again revised infant-feeding guidelines: keep breast-feeding, they urged, while simultaneously introducing small amounts of gluten. Food manufacturers also reduced the gluten content of infant foodstuffs. Dr. Ivarsson found that, during the epidemic, the longer children breast-fed after their first exposure to gluten, the more protected they were.
Not all subsequent studies have found nursing protective, but partly as a result of Sweden’s experience, the American Academy of Pediatrics now recommends that infants start consuming gluten while still breast-feeding.
Research by Dr. Sanz of Spain again illuminates how this may work. Some years back, she began following a cohort of 164 newborns with celiac disease in the immediate family. By four months, children with celiac-associated genotypes — 117 of them — had accrued a microbial community with fewer bifidobacteria compared to those without. If bifidobacteria help us tolerate gluten, these children appeared to be edging toward intolerance.
There was one notable exception: Breast-feeding “normalized” the microbes of at-risk children somewhat, boosting bifidobacterial counts.
Dr. Fasano of Boston has made another potentially important find. He followed 47 at-risk newborns, regularly collecting microbes from 16 of them, which he analyzed after two years. Like Dr. Sanz, he found these genetically at-risk children to accumulate a relatively impoverished, unstable microbial community.
But it’s a secondary observation that has Dr. Fasano particularly excited. Two of these children developed autoimmune disease: one celiac disease, another Type 1 diabetes, which shares genetic susceptibility with celiac disease. In both cases, a decline of lactobacilli preceded disease onset.
Assuming that the pattern holds in larger studies, “imagine what would be the unbelievable consequences of this finding,” he says. “Keep the lactobacilli high enough in the guts of these kids, and you prevent autoimmunity.”
The caveats here are numerous: the tiny sample size in Dr. Fasano’s study; Dr. Sanz hasn’t yet revealed who actually developed celiac disease in her cohort; and even if these microbial shifts reliably precede disease onset — as they do in larger studies on allergic disease — they’re still bedeviled by the old “chicken or the egg” question: Which comes first, the aberrant microbial community, or the aberrant immune response?
Bana Jabri, director of research at the University of Chicago Celiac Disease Center, notes that immune disturbances change the microbial ecosystem. But here’s the catch: Even if the chicken comes first, she says, the egg can contribute. Rodent experiments show that intestinal inflammation can select for unfriendly bacteria that further inflame. “You can have a positive feedback loop,” she says.
SO your microbes change you, but your genes also shape your microbes — as do environment, breast milk, diet and antibiotics, among many other factors.
Such complexity both confounds notions of one-way causality and suggests different paths to the same disease. “You have the same endpoint,” Dr. Jabri says, “but how you get there may be variable.”
The intricacies don’t stop there.
Not all breast milk is the same. It varies according to diet and other factors. One study found that milk from overweight mothers had fewer of those bifidobacteria than milk from thinner mothers. Another observed that breast milk from farming mothers, who inhabit a microbially enriched environment, carried more anti-inflammatory proteins compared with urban mothers’ milk. “All these things are going to matter,” Dr. Jabri says. And they’re all potential nudge points in the quest to prevent disease.
The tangled web of possibilities should not, however, distract us from the facts on the ground. In a far-flung corner of Europe, people develop celiac disease and other autoimmune diseases as infrequently as Americans and Finns did a half-century ago. The same genes exposed to the same quantity of gluten do not, in that environment, produce the same frequency of disease.
“We could probably prevent celiac disease if we just give the same environment to the Finnish children as they have in Karelia,” says Dr. Hyoty. “But there’s no way to do it now, except to move the babies there.”
Moises Velasquez-Manoff is the author of “An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Diseases.”
A version of this op-ed appeared in print on February 24, 2013, on page SR1 of the New York edition with the headline: Who Has The Guts For Gluten?.
http://www.nytimes.com/2013/02/24/opinion/sunday/what-really-causes-celiac-disease.html?nl=todaysheadlines&emc=edit_th_20130224&_r=0&pagewanted=all
By MOISES VELASQUEZ-MANOFF
Published: February 23, 2013
WE know that the proteins called gluten, found in wheat and other grains, provoke celiac disease. And we know how to treat the illness: a gluten-free diet. But the rapidly increasing prevalence of celiac disease, which has quadrupled in the United States in just 50 years, is still mystifying.
Scientists are pursuing some intriguing possibilities. One is that breast-feeding may protect against the disease. Another is that we have neglected the teeming ecosystem of microbes in the gut — bacteria that may determine whether the immune system treats gluten as food or as a deadly invader.
Celiac disease is generally considered an autoimmune disorder. The name celiac derives from the Greek word for “hollow,” as in bowels. Gluten proteins in wheat, barley and rye prompt the body to turn on itself and attack the small intestine. Complications range from diarrhea and anemia to osteoporosis and, in extreme cases, lymphoma. Some important exceptions notwithstanding, the prevalence of celiac disease is estimated to range between 0.6 and 1 percent of the world’s population.
Nearly everyone with celiac disease has one of two versions of a cellular receptor called the human leukocyte antigen, or H.L.A. These receptors, the thinking goes, naturally increase carriers’ immune response to gluten.
This detailed understanding makes celiac disease unique among autoimmune disorders. Two factors — one a protein, another genetic — are clearly defined; and in most cases, eliminating gluten from the patient’s diet turns off the disease.
Yet the more scientists study celiac disease, the more some crucial component appears in need of identification. Roughly 30 percent of people with European ancestry carry predisposing genes, for example. Yet more than 95 percent of the carriers tolerate gluten just fine. So while these genes (plus gluten) are necessary to produce the disease, they’re evidently insufficient to cause it.
Animal studies have reinforced that impression. In mice engineered to express those H.L.A.’s, tolerance to gluten must be deliberately “broken.” Without an immunological trigger of some kind, the rodents happily tolerate the protein.
A recent study, which analyzed blood serum from more than 3,500 Americans who were followed since 1974, suggested that such a trigger could strike adults at any time. By 1989, the prevalence of celiac disease in this cohort had doubled.
“You’re talking about an autoimmune disease in which we thought we had all the dots connected,” says Alessio Fasano, head of the Center for Celiac Research and Treatment at the Massachusetts General Hospital for Children in Boston, and the senior author of the study. “Then we start to accumulate evidence that there was something else.”
Identifying that “something else” has gained some urgency. In the United States, improved diagnosis doesn’t seem to explain the rising prevalence. Scientists use the presence of certain self-directed antibodies to predict celiac disease. They have analyzed serum stored since the mid-20th century and compared it to serum from Americans today. Today’s serum is more than four times as likely to carry those antibodies.
BLAME for the increase of celiac disease sometimes falls on gluten-rich, modern wheat varietals; increased consumption of wheat, and the ubiquity of gluten in processed foods.
Yet the epidemiology of celiac disease doesn’t always support this idea. One comparative study involving some 5,500 subjects yielded a prevalence of roughly one in 100 among Finnish children, but using the same diagnostic methods, just one in 500 among their Russian counterparts.
Differing wheat consumption patterns can’t explain this disparity. If anything, Russians consume more wheat than Finns, and of similar varieties.
Neither can genetics. Although now bisected by the Finno-Russian border, Karelia, as the study region is known, was historically a single province. The two study populations are culturally, linguistically and genetically related. The predisposing gene variants are similarly prevalent in both groups.
Maybe more telling, this disparity holds for other autoimmune and allergic diseases. Finland ranks first in the world for Type 1 autoimmune diabetes. But among Russian Karelians, the disease is nearly six times less frequent. Antibodies indicative of autoimmune thyroiditis are also less prevalent, and the risk of developing allergies, as gauged by skin-prick tests, is one-fourth as common.
What’s the Russians’ secret?
“It’s a remote territory of Russia,” says Heikki Hyoty, a scientist at the University of Tampere in Finland. “They live like Finns 50 years ago.”
At the time of this research, roughly a decade ago, Russia’s per-capita income was one-fifteenth of Finland’s. Analysis of house dust and potable water suggests that the Russian Karelians encountered a greater variety and quantity of microbes, including many that were absent in Finland.
Not surprisingly, they also suffered from more fecal-oral infections. For example, three of four Russian Karelian children harbored Helicobacter pylori, a corkscrew-shaped bacterium, while just one in 20 Finnish children did. The bacterium can cause ulcers and stomach cancer, but mounting evidence suggests that it may also protect against asthma.
Professor Hyoty suspects that Russian Karelians’ microbial wealth protects them from autoimmune and allergic diseases by, essentially, strengthening the arm of the immune system that guards against such illnesses.
Meanwhile, Yolanda Sanz, a researcher at the Institute of Agrochemistry and Food Technology in Valencia, Spain, makes a compelling case for the importance of intestinal microbes.
Years ago, Dr. Sanz noted that a group of bacteria native to the intestine known as bifidobacteria were relatively depleted in children with celiac disease compared with healthy controls. Other microbes, including native E. coli strains, were overly abundant and oddly virulent.
How to determine cause or consequence?
In a test tube, she found that those E. coli amplified the inflammatory response of human intestinal cells to gluten. But bifidobacteria switched the response from inflammation to tolerance.
In rats, the E. coli again intensified inflammation to gluten, prompting what’s sometimes called a “leaky gut” — the milieu suspected of contributing to celiac disease. Conversely, bifidobacteria protected the intestinal barrier. Microbes, it seemed, could influence the immune response to gluten.
Bifidobacteria occur naturally in breast milk, which, along with protective antibodies and immune-signaling proteins, conveys hundreds of prebiotic sugars. These sugars selectively feed certain microbes in the infant gut, particularly bifidobacteria. Breast-fed infants tend to harbor more bifidobacteria than formula-fed ones.
All of which may explain a curious historical phenomenon — an “epidemic” of celiac disease that struck Sweden some 30 years ago. Anneli Ivarsson, a pediatrician at Umea University, recalled a sudden wave of “terribly sick” infants.
Sleuthing revealed that, just before the spike, official guidelines on infant feeding had changed. In an effort to prevent celiac disease, paradoxically, parents were instructed to delay the introduction of gluten until their babies were six months old. That also happened to be when many Swedish mothers weaned their children. Coincidentally, companies had increased the amount of gluten in baby food.
This confluence produced an unwitting “experiment with a whole population,” says Dr. Ivarsson — a large quantity of gluten introduced suddenly after weaning. Among Swedes born between 1984 and 1996, the prevalence of celiac disease tripled to 3 percent. The epidemic ebbed only when authorities again revised infant-feeding guidelines: keep breast-feeding, they urged, while simultaneously introducing small amounts of gluten. Food manufacturers also reduced the gluten content of infant foodstuffs. Dr. Ivarsson found that, during the epidemic, the longer children breast-fed after their first exposure to gluten, the more protected they were.
Not all subsequent studies have found nursing protective, but partly as a result of Sweden’s experience, the American Academy of Pediatrics now recommends that infants start consuming gluten while still breast-feeding.
Research by Dr. Sanz of Spain again illuminates how this may work. Some years back, she began following a cohort of 164 newborns with celiac disease in the immediate family. By four months, children with celiac-associated genotypes — 117 of them — had accrued a microbial community with fewer bifidobacteria compared to those without. If bifidobacteria help us tolerate gluten, these children appeared to be edging toward intolerance.
There was one notable exception: Breast-feeding “normalized” the microbes of at-risk children somewhat, boosting bifidobacterial counts.
Dr. Fasano of Boston has made another potentially important find. He followed 47 at-risk newborns, regularly collecting microbes from 16 of them, which he analyzed after two years. Like Dr. Sanz, he found these genetically at-risk children to accumulate a relatively impoverished, unstable microbial community.
But it’s a secondary observation that has Dr. Fasano particularly excited. Two of these children developed autoimmune disease: one celiac disease, another Type 1 diabetes, which shares genetic susceptibility with celiac disease. In both cases, a decline of lactobacilli preceded disease onset.
Assuming that the pattern holds in larger studies, “imagine what would be the unbelievable consequences of this finding,” he says. “Keep the lactobacilli high enough in the guts of these kids, and you prevent autoimmunity.”
The caveats here are numerous: the tiny sample size in Dr. Fasano’s study; Dr. Sanz hasn’t yet revealed who actually developed celiac disease in her cohort; and even if these microbial shifts reliably precede disease onset — as they do in larger studies on allergic disease — they’re still bedeviled by the old “chicken or the egg” question: Which comes first, the aberrant microbial community, or the aberrant immune response?
Bana Jabri, director of research at the University of Chicago Celiac Disease Center, notes that immune disturbances change the microbial ecosystem. But here’s the catch: Even if the chicken comes first, she says, the egg can contribute. Rodent experiments show that intestinal inflammation can select for unfriendly bacteria that further inflame. “You can have a positive feedback loop,” she says.
SO your microbes change you, but your genes also shape your microbes — as do environment, breast milk, diet and antibiotics, among many other factors.
Such complexity both confounds notions of one-way causality and suggests different paths to the same disease. “You have the same endpoint,” Dr. Jabri says, “but how you get there may be variable.”
The intricacies don’t stop there.
Not all breast milk is the same. It varies according to diet and other factors. One study found that milk from overweight mothers had fewer of those bifidobacteria than milk from thinner mothers. Another observed that breast milk from farming mothers, who inhabit a microbially enriched environment, carried more anti-inflammatory proteins compared with urban mothers’ milk. “All these things are going to matter,” Dr. Jabri says. And they’re all potential nudge points in the quest to prevent disease.
The tangled web of possibilities should not, however, distract us from the facts on the ground. In a far-flung corner of Europe, people develop celiac disease and other autoimmune diseases as infrequently as Americans and Finns did a half-century ago. The same genes exposed to the same quantity of gluten do not, in that environment, produce the same frequency of disease.
“We could probably prevent celiac disease if we just give the same environment to the Finnish children as they have in Karelia,” says Dr. Hyoty. “But there’s no way to do it now, except to move the babies there.”
Moises Velasquez-Manoff is the author of “An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Diseases.”
A version of this op-ed appeared in print on February 24, 2013, on page SR1 of the New York edition with the headline: Who Has The Guts For Gluten?.
http://www.nytimes.com/2013/02/24/opinion/sunday/what-really-causes-celiac-disease.html?nl=todaysheadlines&emc=edit_th_20130224&_r=0&pagewanted=all
Tuesday, February 19, 2013
Lamb Stew
Brrrrrr it's cold outside! This lamb stew turned out great last night and it warmed me right up, not to mention got the house smelling tremendous! Be careful it is VERY filling and it made quite a bit so I have plenty in the freezer for another frigid day : )
2 tablespoons olive oil
1 cup leftover lamb roast, cut into 1" cubes
1 cup thin sliced white onions
5 large cloves garlic sliced
3 parsnips, halved lengthwise, then sliced
1 medium yam, peeled, halved lengthwise, sliced
1 medium eggplant, stem removed, cut into 1" dice
1/4 cup pearled barley (not quick cook)
1/4 cup Israeli couscous
1/2 cup brown lentils
1 tablespoon Herbs de Provence
1/8 teaspoon tumeric
1/8 teaspoon curry powder
1/8 teaspoon Saigon cinnamon (has a hint of cayenne pepper)
1/2 tablespoon dried mint
1/2 tablespoon West Indian Blend Spice mix (see recipe below)
salt and pepper
1 quart vegetable stock (I use Pacific Organic because it doesn't have added sugar or oil)
12 oz pale ale beer (I used Sierra Nevada Pale Ale), cold
2 ripe tomatoes, chopped
2 tablespoons chopped fresh rosemary
West Indian Spice Blend
3 tablespoons Curry powder
2 tablespoons Ground cumin
2 tablespoons Ground allspice
3 tablespoons Paprika
2 tablespoons Ground ginger
1 tablespoon Cayenne pepper
2 tablespoons Salt
2 tablespoons Ground black pepper
Makes 1 cup
1. Heat oil in a 2-3 gallon stock pot over medium heat. Cook garlic and onions until soft. Add lamb and let brown slightly about 3 minutes. Season with salt and pepper.
2. Add parsnips, eggplant, yam - let cook 3 minutes.
3. Add cold beer - stir around scraping the bottom of the pan. The alcohol will start to boil off. Let cook about 1 minute, then add all the broth, barley, couscous, lentils and all the seasoning. Stir well to combine.
4. It will take a few minutes to get the ingredients up to temperature since the beer was cold. When it starts to simmer, turn down to low heat, cover (leave a crack) and let simmer about 3 hours, stirring about every 30 minutes so that it doesn't stick to the bottom. When it is ready, you will notice that the starch from the couscous and barley and the breakdown of the yam and lentils has started to thicken the stew.
5. To serve, spoon into bowl and top with some of the fresh rosemary and tomato.
ENJOY!
2 tablespoons olive oil
1 cup leftover lamb roast, cut into 1" cubes
1 cup thin sliced white onions
5 large cloves garlic sliced
3 parsnips, halved lengthwise, then sliced
1 medium yam, peeled, halved lengthwise, sliced
1 medium eggplant, stem removed, cut into 1" dice
1/4 cup pearled barley (not quick cook)
1/4 cup Israeli couscous
1/2 cup brown lentils
1 tablespoon Herbs de Provence
1/8 teaspoon tumeric
1/8 teaspoon curry powder
1/8 teaspoon Saigon cinnamon (has a hint of cayenne pepper)
1/2 tablespoon dried mint
1/2 tablespoon West Indian Blend Spice mix (see recipe below)
salt and pepper
1 quart vegetable stock (I use Pacific Organic because it doesn't have added sugar or oil)
12 oz pale ale beer (I used Sierra Nevada Pale Ale), cold
2 ripe tomatoes, chopped
2 tablespoons chopped fresh rosemary
West Indian Spice Blend
3 tablespoons Curry powder
2 tablespoons Ground cumin
2 tablespoons Ground allspice
3 tablespoons Paprika
2 tablespoons Ground ginger
1 tablespoon Cayenne pepper
2 tablespoons Salt
2 tablespoons Ground black pepper
Makes 1 cup
1. Heat oil in a 2-3 gallon stock pot over medium heat. Cook garlic and onions until soft. Add lamb and let brown slightly about 3 minutes. Season with salt and pepper.
2. Add parsnips, eggplant, yam - let cook 3 minutes.
3. Add cold beer - stir around scraping the bottom of the pan. The alcohol will start to boil off. Let cook about 1 minute, then add all the broth, barley, couscous, lentils and all the seasoning. Stir well to combine.
4. It will take a few minutes to get the ingredients up to temperature since the beer was cold. When it starts to simmer, turn down to low heat, cover (leave a crack) and let simmer about 3 hours, stirring about every 30 minutes so that it doesn't stick to the bottom. When it is ready, you will notice that the starch from the couscous and barley and the breakdown of the yam and lentils has started to thicken the stew.
5. To serve, spoon into bowl and top with some of the fresh rosemary and tomato.
ENJOY!
Thursday, February 7, 2013
More Burgers - Salmon this time!
1 - 6.5oz can salmon
2 tablespoons unseasoned bread crumbs
1 egg
1 tablespoon diced shallots
2 tablespoons diced red bell pepper
1 teaspoon non fat plain Greek yogurt
1 teaspoon dried dill
1/8 teaspoon dried ground ginger (optional)
2 teaspoons olive oil
1. In a bowl break up salmon with fork. Add bread crumbs, shallots, pepper, dill, ginger. Whisk together egg and yogurt in separate dish and then add to salmon. Combine well.
2. Form into 2 patties
3. Heat oil in saute pan over medium-high heat. Cook burgers about 4 minutes on either side covered (to prevent splatter and hold heat in without drying out the fish.
4. Serve topped with mustard or a dill-yogurt sauce or fruit salsa if desired.
ENJOY! approx. 35 grams protein/burger
2 tablespoons unseasoned bread crumbs
1 egg
1 tablespoon diced shallots
2 tablespoons diced red bell pepper
1 teaspoon non fat plain Greek yogurt
1 teaspoon dried dill
1/8 teaspoon dried ground ginger (optional)
2 teaspoons olive oil
1. In a bowl break up salmon with fork. Add bread crumbs, shallots, pepper, dill, ginger. Whisk together egg and yogurt in separate dish and then add to salmon. Combine well.
2. Form into 2 patties
3. Heat oil in saute pan over medium-high heat. Cook burgers about 4 minutes on either side covered (to prevent splatter and hold heat in without drying out the fish.
4. Serve topped with mustard or a dill-yogurt sauce or fruit salsa if desired.
ENJOY! approx. 35 grams protein/burger
Tuesday, February 5, 2013
Better Burgers
It's not quite time for burger season again, but I feel as though this is a point in time when people are taking off to warmer climates for an escape and might be enticed to do some grilling out in the sunshine. While we mostly recognize burgers as greasy/heavy food items, a few simple steps can help to create a less greasy and lighter on the stomach beef (or lamb) burger. While it may seem much easier to buy frozen beef patties, the quality of meat is much lower and thus less flavorful, heavier on the stomach and if that wasn't enough, it often dries out easily. Grilling the meat also helps to melt the fat in it, this provides flavor, and the fat will run out of the meat as it cooks. NEVER press down on the meat with a spatula to get more run off out of the meat, this will compact the burger (makes it harder to cook the center) and also makes it dry out more as it is cooking.
Here are some options for your consideration. These recipes make 4 burgers that raw will weight in at 9oz (ie more then half a pound!) but post-cooking will weight about 6oz - still big! You could easily cut the recipe in half or make 6-8 burgers instead of 4 out of the recipe for more appropriate portion sizes.
Option #1:
Burgers:
1 pound beef chuck
10oz brisket
10oz hanger steak
4 tablespoons extra virgin olive oil
4 teaspoons Kosher salt
Sauce: whisk it all together
1/2 cup fat free mayo
4 teaspoons prepared white horseradish (you can purchase this)
juice from 1 lemon (or 1oz of bottled lemon juice)
1. Trim fat from meat, cut fat into 1" cubes and chill well. Process through a fine grinder (1/8" - Kitchen Aid has an attachment for their mixer that you could use or you can ask the butcher at grocery store to grind it for you)
2. Mix meat with oil, salt - don't over work it - and form into patties (do not tightly pack them)
3. Refrigerate until ready to use but not for more then 1 hour
4. Grill to desired doneness
5. Top with some sauce if desired
Option #2:
1 pound grass fed beef chuck
1 pound grass fed brisket
2 teaspoons Kosher salt
1. Trim fat from meat, cut fat into 1" cubes and chill well. Process through a fine grinder (1/8" - Kitchen Aid has an attachment for their mixer that you could use or you can ask the butcher at grocery store to grind it for you)
2. Mix meat with salt - don't over work it - and form into patties (do not tightly pack them)
3. Refrigerate until ready to use but not for more then 1 hour
4. Grill to desired doneness
Option #3:
Burgers:
2 pounds ground lamb (preferably from leg and shoulder) with about 15% fat - the butcher can grind this mix for you
1 teaspoon Kosher salt
thin slices of semi-firm Feta cheese
Sauce: Cumin 'Mayo'
4oz plain, non fat greek yogurt
1 tablespoon dijon mustard
1 tablespoon ground cumin
1 teaspoon salt
2 tablespoons lemon juice
3/4 cup olive oil or grapeseed oil (which is neutral in flavor)
1 garlic clove
1. Mix meat with salt - don't over work it - and form into patties (do not tightly pack them)
2. Refrigerate until ready to use but not for more then 1 hour
3. Grill to medium rare and top with about 1 tablespoon of sauce if desired.
For the sauce:
1. In a food processor grind up the garlic clove. Then add yogurt, mustard, cumin, salt, lemon juice and combine those item.
2. Stream the oil in while processor is running so that oil will emulsify into the rest of the sauce and not separate.
3. Set aside until ready to use.
(Sauce is also great on grilled chicken or to marinate chicken in before grilling)
ENJOY!
Here are some options for your consideration. These recipes make 4 burgers that raw will weight in at 9oz (ie more then half a pound!) but post-cooking will weight about 6oz - still big! You could easily cut the recipe in half or make 6-8 burgers instead of 4 out of the recipe for more appropriate portion sizes.
Option #1:
Burgers:
1 pound beef chuck
10oz brisket
10oz hanger steak
4 tablespoons extra virgin olive oil
4 teaspoons Kosher salt
Sauce: whisk it all together
1/2 cup fat free mayo
4 teaspoons prepared white horseradish (you can purchase this)
juice from 1 lemon (or 1oz of bottled lemon juice)
1. Trim fat from meat, cut fat into 1" cubes and chill well. Process through a fine grinder (1/8" - Kitchen Aid has an attachment for their mixer that you could use or you can ask the butcher at grocery store to grind it for you)
2. Mix meat with oil, salt - don't over work it - and form into patties (do not tightly pack them)
3. Refrigerate until ready to use but not for more then 1 hour
4. Grill to desired doneness
5. Top with some sauce if desired
Option #2:
1 pound grass fed beef chuck
1 pound grass fed brisket
2 teaspoons Kosher salt
1. Trim fat from meat, cut fat into 1" cubes and chill well. Process through a fine grinder (1/8" - Kitchen Aid has an attachment for their mixer that you could use or you can ask the butcher at grocery store to grind it for you)
2. Mix meat with salt - don't over work it - and form into patties (do not tightly pack them)
3. Refrigerate until ready to use but not for more then 1 hour
4. Grill to desired doneness
Option #3:
Burgers:
2 pounds ground lamb (preferably from leg and shoulder) with about 15% fat - the butcher can grind this mix for you
1 teaspoon Kosher salt
thin slices of semi-firm Feta cheese
Sauce: Cumin 'Mayo'
4oz plain, non fat greek yogurt
1 tablespoon dijon mustard
1 tablespoon ground cumin
1 teaspoon salt
2 tablespoons lemon juice
3/4 cup olive oil or grapeseed oil (which is neutral in flavor)
1 garlic clove
1. Mix meat with salt - don't over work it - and form into patties (do not tightly pack them)
2. Refrigerate until ready to use but not for more then 1 hour
3. Grill to medium rare and top with about 1 tablespoon of sauce if desired.
For the sauce:
1. In a food processor grind up the garlic clove. Then add yogurt, mustard, cumin, salt, lemon juice and combine those item.
2. Stream the oil in while processor is running so that oil will emulsify into the rest of the sauce and not separate.
3. Set aside until ready to use.
(Sauce is also great on grilled chicken or to marinate chicken in before grilling)
ENJOY!
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