Sunday, May 31, 2009
For Those not Scientifically Inclined
Polyunsaturated fats in the diet are mostly omega-6 or omega-3. These get converted into a diverse and influential class of signaling molecules in the body called eicosanoids. On their way to becoming eicosanoids, they get elongated. These elongated versions can be measured in tissue, and the higher the proportion of elongated omega-6 in the total pool, the higher the risk of a heart attack.
Eicosanoids are either omega-6 or omega-3-derived. Omega-6 eicosanoids, in general, are very potent and participate in inflammatory processes and blood clotting. Omega-3 eicosanoids are less potent, less inflammatory, less clot-forming, and participate in long-term repair processes. This is a simplification, as there are exceptions, but in a broad sense seems to be true.
In the modern U.S. and most other affluent nations, we eat so much omega-6 (mostly in the form of liquid industrial vegetable oils), and so little omega-3, that we create a very inflammatory and pro-clotting environment, probably contributing to a number of chronic diseases including cardiovascular disease.
There are two ways to stay in balance: reduce omega-6, and increase omega-3. In my opinion, the former is more important than the latter, but only if you can reduce omega-6 to below 4% of calories. If you're above 4%, the only way to reduce your risk is to outcompete the omega-6 with additional omega-3. Keeping omega-6 below 4% and ensuring a modest but regular intake of omega-3, such as from wild-caught fish, will probably substantially reduce the risk of cardiovascular disease and other chronic illnesses.
Bottom line: ditch industrial vegetable oils such as corn, soybean, safflower and sunflower oil, and everything that contains them. This includes most processed foods, especially mayonnaise, grocery store salad dressings, and fried foods. We aren't meant to eat those foods and they derail our metabolism on a fundamental level. I also believe it's a good idea to have a regular source of omega-3, whether it comes from seafood, small doses of cod liver oil, or small doses of flax.
For Those not Scientifically Inclined
Polyunsaturated fats in the diet are mostly omega-6 or omega-3. These get converted into a diverse and influential class of signaling molecules in the body called eicosanoids. On their way to becoming eicosanoids, they get elongated. These elongated versions can be measured in tissue, and the higher the proportion of elongated omega-6 in the total pool, the higher the risk of a heart attack.
Eicosanoids are either omega-6 or omega-3-derived. Omega-6 eicosanoids, in general, are very potent and participate in inflammatory processes and blood clotting. Omega-3 eicosanoids are less potent, less inflammatory, less clot-forming, and participate in long-term repair processes. This is a simplification, as there are exceptions, but in a broad sense seems to be true.
In the modern U.S. and most other affluent nations, we eat so much omega-6 (mostly in the form of liquid industrial vegetable oils), and so little omega-3, that we create a very inflammatory and pro-clotting environment, probably contributing to a number of chronic diseases including cardiovascular disease.
There are two ways to stay in balance: reduce omega-6, and increase omega-3. In my opinion, the former is more important than the latter, but only if you can reduce omega-6 to below 4% of calories. If you're above 4%, the only way to reduce your risk is to outcompete the omega-6 with additional omega-3. Keeping omega-6 below 4% and ensuring a modest but regular intake of omega-3, such as from wild-caught fish, will probably substantially reduce the risk of cardiovascular disease and other chronic illnesses.
Bottom line: ditch industrial vegetable oils such as corn, soybean, safflower and sunflower oil, and everything that contains them. This includes most processed foods, especially mayonnaise, grocery store salad dressings, and fried foods. We aren't meant to eat those foods and they derail our metabolism on a fundamental level. I also believe it's a good idea to have a regular source of omega-3, whether it comes from seafood, small doses of cod liver oil, or small doses of flax.
For Those not Scientifically Inclined
Polyunsaturated fats in the diet are mostly omega-6 or omega-3. These get converted into a diverse and influential class of signaling molecules in the body called eicosanoids. On their way to becoming eicosanoids, they get elongated. These elongated versions can be measured in tissue, and the higher the proportion of elongated omega-6 in the total pool, the higher the risk of a heart attack.
Eicosanoids are either omega-6 or omega-3-derived. Omega-6 eicosanoids, in general, are very potent and participate in inflammatory processes and blood clotting. Omega-3 eicosanoids are less potent, less inflammatory, less clot-forming, and participate in long-term repair processes. This is a simplification, as there are exceptions, but in a broad sense seems to be true.
In the modern U.S. and most other affluent nations, we eat so much omega-6 (mostly in the form of liquid industrial vegetable oils), and so little omega-3, that we create a very inflammatory and pro-clotting environment, probably contributing to a number of chronic diseases including cardiovascular disease.
There are two ways to stay in balance: reduce omega-6, and increase omega-3. In my opinion, the former is more important than the latter, but only if you can reduce omega-6 to below 4% of calories. If you're above 4%, the only way to reduce your risk is to outcompete the omega-6 with additional omega-3. Keeping omega-6 below 4% and ensuring a modest but regular intake of omega-3, such as from wild-caught fish, will probably substantially reduce the risk of cardiovascular disease and other chronic illnesses.
Bottom line: ditch industrial vegetable oils such as corn, soybean, safflower and sunflower oil, and everything that contains them. This includes most processed foods, especially mayonnaise, grocery store salad dressings, and fried foods. We aren't meant to eat those foods and they derail our metabolism on a fundamental level. I also believe it's a good idea to have a regular source of omega-3, whether it comes from seafood, small doses of cod liver oil, or small doses of flax.
For Those not Scientifically Inclined
Polyunsaturated fats in the diet are mostly omega-6 or omega-3. These get converted into a diverse and influential class of signaling molecules in the body called eicosanoids. On their way to becoming eicosanoids, they get elongated. These elongated versions can be measured in tissue, and the higher the proportion of elongated omega-6 in the total pool, the higher the risk of a heart attack.
Eicosanoids are either omega-6 or omega-3-derived. Omega-6 eicosanoids, in general, are very potent and participate in inflammatory processes and blood clotting. Omega-3 eicosanoids are less potent, less inflammatory, less clot-forming, and participate in long-term repair processes. This is a simplification, as there are exceptions, but in a broad sense seems to be true.
In the modern U.S. and most other affluent nations, we eat so much omega-6 (mostly in the form of liquid industrial vegetable oils), and so little omega-3, that we create a very inflammatory and pro-clotting environment, probably contributing to a number of chronic diseases including cardiovascular disease.
There are two ways to stay in balance: reduce omega-6, and increase omega-3. In my opinion, the former is more important than the latter, but only if you can reduce omega-6 to below 4% of calories. If you're above 4%, the only way to reduce your risk is to outcompete the omega-6 with additional omega-3. Keeping omega-6 below 4% and ensuring a modest but regular intake of omega-3, such as from wild-caught fish, will probably substantially reduce the risk of cardiovascular disease and other chronic illnesses.
Bottom line: ditch industrial vegetable oils such as corn, soybean, safflower and sunflower oil, and everything that contains them. This includes most processed foods, especially mayonnaise, grocery store salad dressings, and fried foods. We aren't meant to eat those foods and they derail our metabolism on a fundamental level. I also believe it's a good idea to have a regular source of omega-3, whether it comes from seafood, small doses of cod liver oil, or small doses of flax.
Lecture with Philip Zimbardo - How good people become evil
Saturday, May 30, 2009
Evidence for...Omega-3 for asthma
The impact of a medical food containing gammalinolenic and eicosapentaenoic acids on asthma management and the quality of life of adult asthma patients.
Surette ME et al.
Curr Med Res Opin. 2008;24:559-67
Asthmatic adult subjects consuming a medical food emulsion containing the essential fatty acids gammalinolenic and epicosapentaenoic acids reported improved quality of life and decreased reliance on rescue medication after 4 weeks' treatment.
Low dietary nutrient intakes and respiratory health in adolescents.
Burns JS et al.
Chest. 2007;132:238-45
Adolescents with low dietary intakes of omega-3 fatty acids had decreased respiratory symptoms (asthma, wheeze, chronic bronchitis symptoms) and increased pulmonary function.
Fat and fish intake and asthma in Japanese women: baseline data from the Osaka Maternal and Child Health Study.
Miyamoto S et al.
Int J Tuberc Lung Dis. 2007;11:103-9.
In this study involving 1002 pregnant Japanese women, fish consumption was independently associated with a decreased prevalence of asthma after age 18 years and current asthma.
Friday, May 29, 2009
Home made Corn Tortillas(without Press).Bean Enchiladas with Roasted Poblano sauce.
Corn Tortillas
Traditionally tortillas are made with a special kind of corn flour called Masa Harina ,nothing but corn flour that has been treated with lime.Mind you rolling the corn tortillas is nothing like rolling the Parathas or roti,using rolling pin doesn't work,the gluten-free corn dough has a different consistency from the stretchable wheat dough. A Tortillas press can make the rolling much easier but with no space to add another appliance in the kitchen,I settle with the unauthentic whatever-works method.Use a thick bottom flat pan or heavy plate to press the dough between sheets of plastic.
Flavor up!
Mix some Spinach or pumpkin puree to add some more flavor and nutrition to the tortillas.
Nutrition
A definite good news for gluten intolerant,the corn is perfect alternative to wheat.A complex carbohydrate low in fat,whole corn is good source of fiber and essential B vitamins.Check the Nutrition facts .
Corn Tortillas
2 cups Corn flour\ masa de harina(I used Quaker)
1 1/3 cup water(little more if needed)
1 teaspoon of olive oil
1/2 teaspoon salt
Method
Prepare the dough by mixing all the ingredient until smooth and well incorporated.
Cover and let sit for at least an hour.
To make tortillas without the Press
Heat a cast iron skillet or thick bottom pan on medium heat.Take a small handful of dough,place between sheets of plastic ,press using a flat thick bottom pan until evenly flattened.At this point you could use your rolling pin over the plastic sheet just to even out the edges.Carefully peel out from the plastic and roast about a minute on each side,should puff up a little.Spread some olive oil if desired before getting it out of the pan.Serve warm.Can be stacked and stored in a plastic bag(ziploc) for a month.Use it to make tortilla chips or Enchiladas ,tacos or Burritos.
Bean Enchiladas with Roasted Pablano Sauce
Beans and mild pablano pepper sauce is one variation of Enchiladas to begin with,can be stuffed with your choicest low fat meat and topped with mildest to hottest pepper sauce.Often enchiladas are baked with the sauce and oodles of cheese,but the following recipe is a simple no-bake low-fat enchiladas made with homemade tortillas.
Roasted Poblano sauce
Ingredients:
2 Poblano peppers
1/2 a medium onion or 1 shallot, chopped
1 big clove garlic,peel and chopped
1 teaspoon cumin(zeera) powder
1 teaspoon salt
1 tablespoon Olive oil
1/2 cup of fresh cilantro
Method
Char the pepper on high heat in a broiler or grill.Turn occasionally with tongs, until skin is blackened, 15 to 20 minutes. Allow to sweat in a brown paper bag for a minute, then peel the skin and remove the seeds.
Blend the roasted pepper with garlic,cilantro,cumin ,oil and salt until smooth.
For Beans Stuffing
Ingredients
2 cup Kidney or pinto beans,cooked
1 plum tomato,chopped
1 medium onion, chopped
1 tablespoon olive oil
1 tablespoon cumin
2 cloves garlic,chopped
1 teaspoon cayenne pepper or chili powder
1/2 teaspoon salt
Method
Saute onion in olive oil until transparent on medium heat.Add garlic and saute for a minute. Add cumin ,tomatoes,when tomatoes are soft in about 5 minutes,add salt and beans.Cook for another 4-5 minutes.
Assemble the Enchiladas
Place some beans mixture in the middle of the tortilla,fold and place on the serving plate.Repeat same with rest of the tortillas,then pour the poblano sauce and serve.Garnish with grilled or roasted corn and fresh chopped tomatoes.
These Enchiladas is my contribution for the Homemade #4 - Tortillas at What's Cooking.
Got Some Spare Time?
Take a lesson in History and Chemistry of Tortillas from Alton Brown, Video 1 and 2.
Governor’s latest budget proposal includes cuts to health care
Ellen Andrews
Thursday, May 28, 2009
Use of ginseng for preventing respiratory tract infections
The Facts:
* A Canadian clinical study involving 179 people investigated whether North American ginseng had any effect in preventing colds.
* People who took ginseng for 4 months had about 30% fewer colds than people who took a dummy drug.
* People who took ginseng also had colds that were less severe than those who took a dummy drug.
Shaun’s comment: Some studies that have tested whether natural products can prevent colds and other respiratory tract infections have been disappointing. This makes the results from this study even more exciting. Ginseng is widely used for a variety of reasons including its antioxidant properties and possible benefits for people with diabetes. These results indicate that it could help prevent those irritating colds, or reduce the severity if you do get one.
Study Reference:
http://dx.doi.org/10.1503/cmaj.1041470
New from Health Affairs –6.9 million more uninsured Americans by 2010, MA reform benefits continue, and cost does not equal quality in health care
A study published today predicts that due to rising health care costs, by the end of 2010 another 6.9 million Americans will be uninsured, bringing the rate to 19.2%. For every 1% increase in health costs relative to income, another 314,000 Americans lose coverage. This model does not include the impact of unemployment, which is rising sharply, so the picture may be much worse. The authors note that previous estimates using this model of increases in the number of uninsured have, unfortunately, been largely accurate.
Study finds MA continues to enjoy benefits of health reform but challenges of costs and workforce remain
Another study published today finds that after health reforms implemented two years ago, MA consumers are getting more access to medical and dental care, preventive services and medications, particularly low income residents. However, emergency room visits have not declined, including those for non-emergencies. Just over 20% of adults reported difficulty getting care because a provider was not taking new patients (or patients with their condition); that rate was about much higher for low-income and patients with public coverage. Problems accessing care were worst in Western Mass. Initial gains in the affordability of coverage from reforms have eroded somewhat. The authors note that these changes occurred before the full impact of penalties in MA’s individual mandate occurred. The authors cite new measures enacted by MA to address cost control and workforce shortages.
Study finds health care quality and cost not linked, even divergent in some cases
A new study by Dartmouth researchers found that spending on health care does not guarantee quality at the level of individual hospitals, and could even be negatively correlated. The study looked at chronically ill Medicare patients’ care in the last two weeks of life across the US. Hospital averages for spending per end-of-life patient varied from $13,840 to $37,010. Earlier studies found that higher spending produces more care but not better care. This study confirmed that higher spending is associated with higher utilization – more hospital visits, longer stays, more specialists, and more tests -- but worse process-of-care performance. Prior research has found a similar lack of connection between spending and quality by region, but this is the first to show that there is no relationship at the hospital level and that there is wide variation within regions. The study has some important limitations – they only studied processes of care (i.e. appropriate antibiotics given for pneumonia), not outcomes (i.e. adult pneumonia death rates). They did not adjust for patient risk (i.e. some hospitals may treat sicker patients), but they chose process measures that should be done for every patient. By focusing on end of life, the study misses hospital successes – very sick patients who are treated and survive. However, the study does provide strong evidence that there are costs that can be wrung out of the health care system without endangering quality, possibly even improving it. The authors argue for better cost and quality reporting.
Ellen Andrews
Wednesday, May 27, 2009
Eicosanoids and Ischemic Heart Disease, Part II
Allow me to explain. These lines are based on values predicted by a formula developed by Dr. Lands that determines the proportion of omega-6 in tissue HUFA (highly unsaturated fatty acids; includes 20- to 22-carbon omega-6 and omega-3 fats), based on dietary intake of omega-6 and omega-3 fats. This formula seems to be quite accurate, and has been validated both in rodents and humans. As a tissue's arachidonic acid content increases, its EPA and DHA content decreases proportionally.
On the Y-axis (vertical), we have the proportion of omega-6 HUFA in tissue. On the X-axis (horizontal), we have the proportion of omega-6 in the diet as a percentage of energy. Each line represents the relationship between dietary omega-6 and tissue HUFA at a given level of dietary omega-3.
Let's start at the top. The first line is the predicted proportion of omega-6 HUFA in the tissue of a person eating virtually no omega-3. You can see that it maxes out around 4% of calories from omega-6, but it can actually be fairly low if omega-6 is kept very low. The next line down is what happens when your omega-3 intake is 0.1% of calories. You can see that the proportion of omega-6 HUFA is lower than the curve above it at all omega-6 intakes, but it still maxes out around 4% omega-6. As omega-3 intake increases, the proportion of omega-6 HUFA decreases at all levels of dietary omega-6 because it has to compete with omega-3 HUFA for space in the membrane.
In the U.S., we get a small proportion of our calories from omega-3. The horizontal line marks our average tissue HUFA composition, which is about 75% omega-6. We get more than 7% of our calories from omega-6. This means our tissue contains nearly the maximum proportion of omega-6 HUFA, creating a potently inflammatory and thrombotic environment! This is a very significant fact, because it explains three major observations:
- The U.S has a very high rate of heart attack mortality.
- Recent diet trials in which saturated fat was replaced with omega-6-rich vegetable oils didn't cause an increase in mortality, although some of the very first trials in the 1960s did.
- Diet trials that increased omega-3 decreased mortality.
But the trend didn't continue into later trials. This makes perfect sense in light of the rising omega-6 intake over the course of the 20th century in the U.S. and other affluent nations. Once our omega-6 intake crossed the 4% threshold, more omega-6 had very little effect on the proportion of omega-6 HUFA in tissue. This may be why some of the very first PUFA diet trials caused increased mortality: there was a proportion of the population that was still getting less than 4% omega-6 in its regular diet at that time. By the 1980s, virtually everyone in the U.S. (and many other affluent nations) was eating more than 4% omega-6, and thus adding more did not significantly affect tissue HUFA or heart attack mortality.
If omega-3 intake is low, whether omega-6 intake is 5% or 10% doesn't matter much for heart disease. At that point, the only way to reduce tissue HUFA without cutting back on omega-6 consumption is to outcompete it with additional omega-3. That's what the Japanese do, and it's also what happened in several clinical trials including the DART trial.
This neatly explains why the French, Japanese and Kitavans have low rates of ischemic heart disease, despite the prevalence of smoking cigarettes in all three cultures. The French diet traditionally focuses on animal fats, eschews industrial vegetable oils, and includes seafood. They eat less omega-6 and more omega-3 than Americans. They have the lowest heart attack mortality rate of any affluent Western nation. The Japanese are known for their high intake of seafood. They also eat less omega-6 than Americans. They have the lowest heart attack death rate of any affluent nation. The traditional Kitavan diet contains very little omega-6 (probably less than 1% of calories), and a significant amount of omega-3 from seafood (about one teaspoon of fish fat per day). They have an undetectable incidence of heart attack and stroke.
In sum, this suggests that the single best way to avoid a heart attack is to reduce omega-6 consumption and ensure an adequate source of omega-3. The lower the omega-6, the less the omega-3 matters. This is a nice theory, but where's the direct evidence? In the next post, I'll discuss the controlled trial that proved this concept once and for all: the Lyon diet-heart trial.
Eicosanoids and Ischemic Heart Disease, Part II
Allow me to explain. These lines are based on values predicted by a formula developed by Dr. Lands that determines the proportion of omega-6 in tissue HUFA (highly unsaturated fatty acids; includes 20- to 22-carbon omega-6 and omega-3 fats), based on dietary intake of omega-6 and omega-3 fats. This formula seems to be quite accurate, and has been validated both in rodents and humans. As a tissue's arachidonic acid content increases, its EPA and DHA content decreases proportionally.
On the Y-axis (vertical), we have the proportion of omega-6 HUFA in tissue. On the X-axis (horizontal), we have the proportion of omega-6 in the diet as a percentage of energy. Each line represents the relationship between dietary omega-6 and tissue HUFA at a given level of dietary omega-3.
Let's start at the top. The first line is the predicted proportion of omega-6 HUFA in the tissue of a person eating virtually no omega-3. You can see that it maxes out around 4% of calories from omega-6, but it can actually be fairly low if omega-6 is kept very low. The next line down is what happens when your omega-3 intake is 0.1% of calories. You can see that the proportion of omega-6 HUFA is lower than the curve above it at all omega-6 intakes, but it still maxes out around 4% omega-6. As omega-3 intake increases, the proportion of omega-6 HUFA decreases at all levels of dietary omega-6 because it has to compete with omega-3 HUFA for space in the membrane.
In the U.S., we get a small proportion of our calories from omega-3. The horizontal line marks our average tissue HUFA composition, which is about 75% omega-6. We get more than 7% of our calories from omega-6. This means our tissue contains nearly the maximum proportion of omega-6 HUFA, creating a potently inflammatory and thrombotic environment! This is a very significant fact, because it explains three major observations:
- The U.S has a very high rate of heart attack mortality.
- Recent diet trials in which saturated fat was replaced with omega-6-rich vegetable oils didn't cause an increase in mortality, although some of the very first trials in the 1960s did.
- Diet trials that increased omega-3 decreased mortality.
But the trend didn't continue into later trials. This makes perfect sense in light of the rising omega-6 intake over the course of the 20th century in the U.S. and other affluent nations. Once our omega-6 intake crossed the 4% threshold, more omega-6 had very little effect on the proportion of omega-6 HUFA in tissue. This may be why some of the very first PUFA diet trials caused increased mortality: there was a proportion of the population that was still getting less than 4% omega-6 in its regular diet at that time. By the 1980s, virtually everyone in the U.S. (and many other affluent nations) was eating more than 4% omega-6, and thus adding more did not significantly affect tissue HUFA or heart attack mortality.
If omega-3 intake is low, whether omega-6 intake is 5% or 10% doesn't matter much for heart disease. At that point, the only way to reduce tissue HUFA without cutting back on omega-6 consumption is to outcompete it with additional omega-3. That's what the Japanese do, and it's also what happened in several clinical trials including the DART trial.
This neatly explains why the French, Japanese and Kitavans have low rates of ischemic heart disease, despite the prevalence of smoking cigarettes in all three cultures. The French diet traditionally focuses on animal fats, eschews industrial vegetable oils, and includes seafood. They eat less omega-6 and more omega-3 than Americans. They have the lowest heart attack mortality rate of any affluent Western nation. The Japanese are known for their high intake of seafood. They also eat less omega-6 than Americans. They have the lowest heart attack death rate of any affluent nation. The traditional Kitavan diet contains very little omega-6 (probably less than 1% of calories), and a significant amount of omega-3 from seafood (about one teaspoon of fish fat per day). They have an undetectable incidence of heart attack and stroke.
In sum, this suggests that the single best way to avoid a heart attack is to reduce omega-6 consumption and ensure an adequate source of omega-3. The lower the omega-6, the less the omega-3 matters. This is a nice theory, but where's the direct evidence? In the next post, I'll discuss the controlled trial that proved this concept once and for all: the Lyon diet-heart trial.
Eicosanoids and Ischemic Heart Disease, Part II
Allow me to explain. These lines are based on values predicted by a formula developed by Dr. Lands that determines the proportion of omega-6 in tissue HUFA (highly unsaturated fatty acids; includes 20- to 22-carbon omega-6 and omega-3 fats), based on dietary intake of omega-6 and omega-3 fats. This formula seems to be quite accurate, and has been validated both in rodents and humans. As a tissue's arachidonic acid content increases, its EPA and DHA content decreases proportionally.
On the Y-axis (vertical), we have the proportion of omega-6 HUFA in tissue. On the X-axis (horizontal), we have the proportion of omega-6 in the diet as a percentage of energy. Each line represents the relationship between dietary omega-6 and tissue HUFA at a given level of dietary omega-3.
Let's start at the top. The first line is the predicted proportion of omega-6 HUFA in the tissue of a person eating virtually no omega-3. You can see that it maxes out around 4% of calories from omega-6, but it can actually be fairly low if omega-6 is kept very low. The next line down is what happens when your omega-3 intake is 0.1% of calories. You can see that the proportion of omega-6 HUFA is lower than the curve above it at all omega-6 intakes, but it still maxes out around 4% omega-6. As omega-3 intake increases, the proportion of omega-6 HUFA decreases at all levels of dietary omega-6 because it has to compete with omega-3 HUFA for space in the membrane.
In the U.S., we get a small proportion of our calories from omega-3. The horizontal line marks our average tissue HUFA composition, which is about 75% omega-6. We get more than 7% of our calories from omega-6. This means our tissue contains nearly the maximum proportion of omega-6 HUFA, creating a potently inflammatory and thrombotic environment! This is a very significant fact, because it explains three major observations:
- The U.S has a very high rate of heart attack mortality.
- Recent diet trials in which saturated fat was replaced with omega-6-rich vegetable oils didn't cause an increase in mortality, although some of the very first trials in the 1960s did.
- Diet trials that increased omega-3 decreased mortality.
But the trend didn't continue into later trials. This makes perfect sense in light of the rising omega-6 intake over the course of the 20th century in the U.S. and other affluent nations. Once our omega-6 intake crossed the 4% threshold, more omega-6 had very little effect on the proportion of omega-6 HUFA in tissue. This may be why some of the very first PUFA diet trials caused increased mortality: there was a proportion of the population that was still getting less than 4% omega-6 in its regular diet at that time. By the 1980s, virtually everyone in the U.S. (and many other affluent nations) was eating more than 4% omega-6, and thus adding more did not significantly affect tissue HUFA or heart attack mortality.
If omega-3 intake is low, whether omega-6 intake is 5% or 10% doesn't matter much for heart disease. At that point, the only way to reduce tissue HUFA without cutting back on omega-6 consumption is to outcompete it with additional omega-3. That's what the Japanese do, and it's also what happened in several clinical trials including the DART trial.
This neatly explains why the French, Japanese and Kitavans have low rates of ischemic heart disease, despite the prevalence of smoking cigarettes in all three cultures. The French diet traditionally focuses on animal fats, eschews industrial vegetable oils, and includes seafood. They eat less omega-6 and more omega-3 than Americans. They have the lowest heart attack mortality rate of any affluent Western nation. The Japanese are known for their high intake of seafood. They also eat less omega-6 than Americans. They have the lowest heart attack death rate of any affluent nation. The traditional Kitavan diet contains very little omega-6 (probably less than 1% of calories), and a significant amount of omega-3 from seafood (about one teaspoon of fish fat per day). They have an undetectable incidence of heart attack and stroke.
In sum, this suggests that the single best way to avoid a heart attack is to reduce omega-6 consumption and ensure an adequate source of omega-3. The lower the omega-6, the less the omega-3 matters. This is a nice theory, but where's the direct evidence? In the next post, I'll discuss the controlled trial that proved this concept once and for all: the Lyon diet-heart trial.
Eicosanoids and Ischemic Heart Disease, Part II
Allow me to explain. These lines are based on values predicted by a formula developed by Dr. Lands that determines the proportion of omega-6 in tissue HUFA (highly unsaturated fatty acids; includes 20- to 22-carbon omega-6 and omega-3 fats), based on dietary intake of omega-6 and omega-3 fats. This formula seems to be quite accurate, and has been validated both in rodents and humans. As a tissue's arachidonic acid content increases, its EPA and DHA content decreases proportionally.
On the Y-axis (vertical), we have the proportion of omega-6 HUFA in tissue. On the X-axis (horizontal), we have the proportion of omega-6 in the diet as a percentage of energy. Each line represents the relationship between dietary omega-6 and tissue HUFA at a given level of dietary omega-3.
Let's start at the top. The first line is the predicted proportion of omega-6 HUFA in the tissue of a person eating virtually no omega-3. You can see that it maxes out around 4% of calories from omega-6, but it can actually be fairly low if omega-6 is kept very low. The next line down is what happens when your omega-3 intake is 0.1% of calories. You can see that the proportion of omega-6 HUFA is lower than the curve above it at all omega-6 intakes, but it still maxes out around 4% omega-6. As omega-3 intake increases, the proportion of omega-6 HUFA decreases at all levels of dietary omega-6 because it has to compete with omega-3 HUFA for space in the membrane.
In the U.S., we get a small proportion of our calories from omega-3. The horizontal line marks our average tissue HUFA composition, which is about 75% omega-6. We get more than 7% of our calories from omega-6. This means our tissue contains nearly the maximum proportion of omega-6 HUFA, creating a potently inflammatory and thrombotic environment! This is a very significant fact, because it explains three major observations:
- The U.S has a very high rate of heart attack mortality.
- Recent diet trials in which saturated fat was replaced with omega-6-rich vegetable oils didn't cause an increase in mortality, although some of the very first trials in the 1960s did.
- Diet trials that increased omega-3 decreased mortality.
But the trend didn't continue into later trials. This makes perfect sense in light of the rising omega-6 intake over the course of the 20th century in the U.S. and other affluent nations. Once our omega-6 intake crossed the 4% threshold, more omega-6 had very little effect on the proportion of omega-6 HUFA in tissue. This may be why some of the very first PUFA diet trials caused increased mortality: there was a proportion of the population that was still getting less than 4% omega-6 in its regular diet at that time. By the 1980s, virtually everyone in the U.S. (and many other affluent nations) was eating more than 4% omega-6, and thus adding more did not significantly affect tissue HUFA or heart attack mortality.
If omega-3 intake is low, whether omega-6 intake is 5% or 10% doesn't matter much for heart disease. At that point, the only way to reduce tissue HUFA without cutting back on omega-6 consumption is to outcompete it with additional omega-3. That's what the Japanese do, and it's also what happened in several clinical trials including the DART trial.
This neatly explains why the French, Japanese and Kitavans have low rates of ischemic heart disease, despite the prevalence of smoking cigarettes in all three cultures. The French diet traditionally focuses on animal fats, eschews industrial vegetable oils, and includes seafood. They eat less omega-6 and more omega-3 than Americans. They have the lowest heart attack mortality rate of any affluent Western nation. The Japanese are known for their high intake of seafood. They also eat less omega-6 than Americans. They have the lowest heart attack death rate of any affluent nation. The traditional Kitavan diet contains very little omega-6 (probably less than 1% of calories), and a significant amount of omega-3 from seafood (about one teaspoon of fish fat per day). They have an undetectable incidence of heart attack and stroke.
In sum, this suggests that the single best way to avoid a heart attack is to reduce omega-6 consumption and ensure an adequate source of omega-3. The lower the omega-6, the less the omega-3 matters. This is a nice theory, but where's the direct evidence? In the next post, I'll discuss the controlled trial that proved this concept once and for all: the Lyon diet-heart trial.
Confusion over the role of fish consumption in a healthy diet
The Facts:
* 1–2 servings of fish each week reduces your risk of dying of heart disease by about a third according to a recent review of the scientific literature.
* Eating fish is also highly beneficial during pregnancy to ensure the healthy development of the baby, although women should find out about pollution levels if they plan to eat fish from freshwater sources.
* More than 5 servings of fish a week could result in health risks due to contaminants although the health benefits are thought to outweigh the risks.
Shaun’s comment: This issue has been very prominent in the media of late. If you have been worried about the bad reports on fish oil supplements then this study is very reassuring. The study involved a comprehensive review of the available data and was published in one of the most important medical journals. The conclusion was that the health benefits outweigh any potential risks and this also applies to women of childbearing age.
Study Reference:
http://jama.ama-assn.org/cgi/content/abstract/296/15/1885
Dare to Bake - Low Fat Apple Strudel from scratch?
The May Daring Bakers’ challenge was hosted by Linda of make life sweeter! and Courtney of Coco Cooks. They chose Apple Strudel from the recipe book Kaffeehaus: Exquisite Desserts from the Classic Cafés of Vienna, Budapest and Prague by Rick Rodgers.
Not as tough as it may seem after the first time,I baked the Strudel 3 times already and each time my friends and family simply loved it.If you can master the subtle rolling and stretching of the dough to a tissue-thin transparency then making this Classic Austrian Pastry can be as easy as baking a pie.Make sure you have ample workspace ,watch professionals roll the pastry here and here . The filling can be varied ,the juicy tart apples ,dried fruits and nuts is the original stuffing of these pastries, make it savory with spicy vegetables.I added Cocoa to the filling for a hint of chocolate flavor.The amount of fat can also be adjusted ,I experimented with brushing both oil or butter.The Olive oil thankfully worked well,one more reason to make this dessert more often.
Use Granny Smith apples for best tasting Apple strudels.
Recipe
Ingredients
For Strudel dough
1 1/3 cups unbleached All Purpose flour
1/8 teaspoon salt
7 tablespoons water, plus more if needed
2 tablespoons vegetable oil, plus additional for coating the dough
1/2 teaspoon cider vinegar
For Green Apple Cocoa Strudel Filling
2 medium Granny Smith Apples,Cored,peeled and sliced
3 tablespoons raisins or dried cranberries or cherries
1/4 teaspoon ground cinnamon
1 teaspoon cocoa powder(optional)
1 tablespoon Brown sugar
1 cup fresh bread crumbs
1 cup Walnuts.coarsely chopped
3 tablespoon Olive oil for brushing over the dough
Method
Prepare the Dough
Combine the flour and salt in a large mixing bowl. Mix the water, oil and vinegar in a measuring cup. Add the water/oil mixture to the flour and make a soft dough and knead for 2 minutes. Make sure it is not too dry, add a little more water if necessary.
Shape the dough into a ball and transfer it to a plate. Oil the top of the dough ball lightly. Cover the ball tightly with plastic wrap. Allow to stand for 30-90 minutes (longer is better).
Prepare the Filling
Mix the raisins,cinnamon ,apple ,walnuts and sugar in a bowl.Heat a tablespoons of oil in a large skillet over medium-high. Add the breadcrumbs and cook whilst stirring until golden and toasted. This will take about 3 minutes. Let it cool completely.
Roll the Dough tissue-thin
Put the rack in the upper third of the oven and preheat the oven to 400°F (200°C).
It would be best if you have a work area that you can walk around on all sides like a 36 inch (90 cm) round table or a work surface of 23 x 38 inches (60 x 100 cm). Cover your working area with table cloth, dust it with flour and rub it into the fabric. Put your dough ball in the middle and roll it out as much as you can.
Pick the dough up by holding it by an edge. This way the weight of the dough and gravity can help stretching it as it hangs. Using the back of your hands to gently stretch and pull the dough. You can use your forearms to support it.
The dough will become too large to hold. Put it on your work surface. Leave the thicker edge of the dough to hang over the edge of the table. Place your hands underneath the dough and stretch and pull the dough thinner using the backs of your hands. Stretch and pull the dough until it's about 2 feet (60 cm) wide and 3 feet (90 cm) long, it will be tissue-thin by this time. Cut away the thick dough around the edges with scissors. The dough is now ready to be filled.
Brush about 2 tablespoons of the oil over the dough using your hands (a bristle brush could tear the dough, you could use a special feather pastry brush instead of your hands). Sprinkle the dough with the bread crumbs. Spread apple mixture about 3 inches (8 cm) from the short edge of the dough in a 6-inch-(15cm)-wide strip.
Fold the short end of the dough onto the filling. Lift the tablecloth at the short end of the dough so that the strudel rolls onto itself. Transfer the strudel to the prepared baking sheet by lifting it. Tuck the ends under the strudel. Brush the top with the remaining oil.
Bake
Bake the strudel for about 30 minutes or until it is deep golden brown. Cool for at least 30 minutes before slicing. Use a serrated knife and serve either warm or at room temperature with any fruit sauce. It is best on the day it is baked.Store in refrigerator for up to a week,if desired warm at 300F oven for about 10 minutes before serving.
To make Raspberry sauce
Cook 1 cup of fresh or frozen berries with 1/2 cup of water until soft,blend to a smooth sauce,I like the crunch from seeds and didn't filter the seeds.Pour over the strudel slice after plating it.
To make Chocolate sauce
Melt 2 ounce of Dark chocolate chopped or chips with 2 tablespoon of whole milk in a double broiler,stir often until smooth and completely melted.Drizzle the warm sauce over the strudel.
WSJ blog highlights uninsured people forming small businesses to get health insurance
Ellen Andrews
Tuesday, May 26, 2009
No evidence to support chiropractic for menstrual pains
Our experience at Non-Profit Healthcare Investor Conference
Our experience at Non-Profit Healthcare Investor Conference
Lemon Brown Rice
Lentils\Legumes,soups,Dip,cake,salad,Pasta to name a few.Be amazed ,not just culinary ,lemons have lot more ingenious uses,including a face cleanser,dandruff fighter and a cleaning agent .
Lemon Brown Rice
The tangy Lemon Rice is a popular South Indian favorite,can be prepared in a snap with fresh lemons and any left over rice.Using Brown rice makes it so much better with all the added fiber and essential vitamins.
Ingredients
2 cups Brown Rice
1 lemon(about 3 tablespoon), squeezed
1 teaspoon Yellow or Chana moong lentil
1/4 cup Peanuts
1/2 inch ginger root peeled and grated
1/2 teaspoon turmeric
1/2 a teaspoon each cumin seeds and mustard seeds
2 dry red chillies
2 green chillies,slit(optional)
1/2 teaspoon lemon zest(optional)
1 table spoon Extra Virgin Olive oil
few curry leaves
Method
Wash and soak the rice in cold water for 20 minutes.Cook in 3 cups of salted water,partially covered until tender about 20-25 minutes.
Roll the lemon to loosen the juices. Mix the lemon juice with rice and keep aside
Heat oil in a deep pan on medium flame. Add all the other ingredients besides turmeric and ginger. when the mustard seeds start to splutter add the turmeric and grated ginger . saute for a minute before adding the lemon rice mixture and the lemon zest;Stir and let the flavors infuse for few minutes before serving.
This is my entry for Weekend Wokking ,in limelight this month are lemons.
New Kaiser website tracks national health reform developments
Ellen Andrews
Monday, May 25, 2009
Transcendental meditation can reduce risks of heart disease
The Facts:
* The metabolic syndrome is thought to contribute to coronary heart disease and this study explored the possibility that meditation could reduce some of the factors thought to contribute to the syndrome.
* A variety of measures including blood pressure and insulin resistance were measured in over 100 people with stable heart disease who either received educational advice or participated in this type of meditation.
* The results showed a clear advantage for the group undertaking transcendental meditation.
Shaun’s comment: Transcendental Meditation or TM is a trademarked form of meditation and the name of a movement led by Maharishi Mahesh Yogi. Advocates of TM claim that scientific research shows its meditation techniques produce a variety of positive effects. In this study, patients using the technique saw an improvement in blood pressure and other factors related to coronary heart disease including insulin resistance. This is consistent with other published studies over the last 35 years and makes TM an interesting option for patients who are worried about their heart disease. Whether the same effects would be seen with other types of relaxation technique or just TM remains to be proven.
Study Reference:
http://archinte.ama-assn.org/cgi/content/abstract/166/11/1218
How to Permanently Clear Acne Almost Overnight? Here is What Will Help You Massively
Acne is a skin condition caused during adolescence and can attack both male and female Reasons for acne are plenty. There are around 20 million people in US alone who suffer from acne. They primarily appear on face, neck and chest areas.
If you want to permanently get rid of acne almost overnight, you can. Determination and positive thinking can go a long way. All you need is proper planning and positive thinking.
• Exercise - Exercise helps in increased blood flow and can help cleanse the toxins.Due to this it will to a great extent stop further breakout of acne.
• Water - Water is something that has the power to permanently clear your acne. Drink as much as you can. They help in flushing away the toxins from our body.
• Chemicals - Stop using chemicals as it is not going to help you in any way. Many treatments have chemicals in them and may be very harmful to the skin. This will only help in spreading the acne and not controlling it
• Use homemade items that will not cause any side effects since there are no chemicals in it
• You can even try baking soda masks or honey masks for an effective solution.
• Completely cut down on the out processed foods. Junk food consumption is not good and we need to go in for processed foods
• Green and leafy vegetables are excellent for removing acne. These vegetables can provide the body what they want and thus help in maintaining the right balance.
• Along with this natural food have some supplement s of zinc and vitamin A that can help reduce breakouts of acne.
There are many programs developed online that promise to cure acne in three days. But it is always better to go in for these preventive measures rather than faster methods as they last longer and may be a permanent cure.
What you don't know yet- I know that what I am about to reveal to you can be almost impossible to believe. But it is 100% truth! Do you know what you can cure any sort of acne within 3 days? Seems impossible right? Well see for yourself follow this link- Click Here
Sunday, May 24, 2009
Eicosanoids and Ischemic Heart Disease
To explain it fully, we have to take a few steps back. Dietary polyunsaturated fatty acids (PUFA) are primarily omega-6 and omega-3. This is a chemical designation that refers to the position of a double bond along the fatty acid's carbon chain. Omega-6 fats are found abundantly in industrial vegetable oils (corn, soybean, sunflower, cottonseed, etc.) and certain nuts, and in lesser amounts in meats, dairy and grains. Omega-3 fats are found abundantly in seafood and a few seeds such as flax and walnuts, and in smaller amounts in meats, green vegetables and dairy.
The body uses a multi-step process to convert omega-3 and omega-6 fats into eicosanoids, which are a diverse and potent class of signaling molecules. The first step is to convert PUFA into highly unsaturated fatty acids, or HUFA. These include arachidonic acid (AA), an omega-6 HUFA, eicosapentaenoic acid (EPA), an omega-3 HUFA, and several others in the 20- to 22-carbon length range.
HUFA are stored in cell membranes and they are the direct precursors of eicosanoids. When the cell needs eicosanoids, it liberates HUFA from the membrane and converts it. The proportion of omega-6 to omega-3 HUFA in the membrane is proportional to the long-term proportion of omega-6 and omega-3 in the diet. Enzymes do not discriminate between omega-6 and omega-3 HUFA when they create eicosanoids. Therefore, the proportion of omega-6- to omega-3-derived eicosanoids is proportional to dietary intake.
Omega-6 eicosanoids are potently inflammatory and thrombotic (promote blood clotting, such as thromboxane A2), while omega-3 eicosanoids are less inflammatory, less thrombotic and participate in long-term repair processes.
Many of the studies that have looked at the relationship between HUFA and heart attacks used blood plasma (serum lipids). Dr. Lands has pointed out that plasma HUFA do not accurately reflect dietary omega-6/3 balance, and they don't correlate well with heart attack risk. What does correlate strikingly well with both dietary intake and heart attack risk is the proportion of omega-6 HUFA in tissue, which reflects the amount contained in cell membranes. That's what we're looking at in the graph above: the proportion of omega-6 HUFA in the total tissue HUFA pool, vs. coronary heart disease death rate.
You can see that the correlation is striking, both between populations and within them. Greenland Inuit have the lowest proportion of omega-6 HUFA, due to a low intake of omega-6 and an exceptionally high intake of seafood. They also have an extraordinarily low risk of heart attack death. The red dots are from the Multiple Risk Factor Intervention Trial (MRFIT), which I'll be covering in a bit more detail in a later post. They're important because they confirm that the trend holds true within a population, and not just between populations.
In the next post, I'll be delving into this concept in more detail, and explaining why it's not just the ratio that matters, but also the total intake of omega-6. I'll also be providing more evidence to support the theory.