I don't want to leave you with those last two posts without giving you some practical ways to improve body composition. Body composition is the ratio of lean tissue to fat. The ideal ratio differs depending on gender and individual differences. In general, 10% and 20% bodyfat are good targets for men and women, respectively. There's no need to measure however, as the eye is a pretty good judge.
The most dangerous fat is visceral fat, or the "beer belly". Fortunately, it's also the most responsive to lifestyle changes.
The strategies I recommend all have one thing in common: they work to restore insulin sensitivity. This will not only improve body composition, it will normalize your metabolism on a fundamental level, reducing the risk of all the common chronic diseases. I may cover these topics again in more detail at another time.
1. Carbohydrate restriction. This is by far the most effective way to improve body composition. It will even benefit people who are already profoundly insulin resistant. Eliminating grains, legumes, potatoes and sugar is the simplest and best way to do this. That includes wheat, corn, rice, beans, oats, honorary grains like buckwheat and quinoa, and especially their derivatives. Carbohydrate is not the devil, but restricting intake to moderate amounts from vegetables and fruit is ideal for someone trying to lose weight. I think starchy root vegetables, soaked or sprouted legumes and soaked, sprouted or fermented non-gluten grains are OK for people who already have a healthy body composition.
2. Exercise. Our hunter-gatherer ancestors had a word for exercise: "life". Exercise helps improve insulin sensitivity by increasing the muscles' demand for fuel. It also builds muscle mass. Any exercise is great, but the best kind is brief and intense (anaerobic). This includes sprinting and brisk weight training. It's more effective than jogging at improving muscle mass, decreasing fat mass, decreasing insulin and improving other markers of metabolic health. Chris at Conditioning Research covers this topic regularly. Traditional sports like soccer and basketball are effective because they have anaerobic and aerobic components. Even walking up stairs or down the street have measurable health benefits, however.
3. Intermittent fasting. This is very effective at improving insulin sensitivity and body composition. IF isn't starvation; it simply postpones calorie intake. Nor is it unhealthy. In fact, it's probably closely in line with the variable energy intake to which we are fundamentally adapted. My method is one 24-hour, water-only fast per week. No juice; that defeats the purpose. If you have elevated insulin like most people, it's best to get into IF gradually. Try skipping breakfast first. If you can skip breakfast and lunch, you've completed a 23-hour fast.
4. Lose the soda! Soda and other sweet foods are the enemy of body composition and general health. Fructose, found abundantly in high-fructose corn syrup, table sugar and agave nectar, seems to have a particular talent for causing insulin resistance. It's rapidly converted to fat in the liver, which is partially stored on the spot, and partially exported into the bloodstream as triglycerides. Diet soda isn't much better. It's been associated with weight gain in humans, and actually causes weight gain in rats. Normalizing insulin through carbohydrate restriction and fasting reduces cravings for sweet foods. A moderate amount of fruit is probably fine.
Monday, March 31, 2008
Body Composition
I don't want to leave you with those last two posts without giving you some practical ways to improve body composition. Body composition is the ratio of lean tissue to fat. The ideal ratio differs depending on gender and individual differences. In general, 10% and 20% bodyfat are good targets for men and women, respectively. There's no need to measure however, as the eye is a pretty good judge.
The most dangerous fat is visceral fat, or the "beer belly". Fortunately, it's also the most responsive to lifestyle changes.
The strategies I recommend all have one thing in common: they work to restore insulin sensitivity. This will not only improve body composition, it will normalize your metabolism on a fundamental level, reducing the risk of all the common chronic diseases. I may cover these topics again in more detail at another time.
1. Carbohydrate restriction. This is by far the most effective way to improve body composition. It will even benefit people who are already profoundly insulin resistant. Eliminating grains, legumes, potatoes and sugar is the simplest and best way to do this. That includes wheat, corn, rice, beans, oats, honorary grains like buckwheat and quinoa, and especially their derivatives. Carbohydrate is not the devil, but restricting intake to moderate amounts from vegetables and fruit is ideal for someone trying to lose weight. I think starchy root vegetables, soaked or sprouted legumes and soaked, sprouted or fermented non-gluten grains are OK for people who already have a healthy body composition.
2. Exercise. Our hunter-gatherer ancestors had a word for exercise: "life". Exercise helps improve insulin sensitivity by increasing the muscles' demand for fuel. It also builds muscle mass. Any exercise is great, but the best kind is brief and intense (anaerobic). This includes sprinting and brisk weight training. It's more effective than jogging at improving muscle mass, decreasing fat mass, decreasing insulin and improving other markers of metabolic health. Chris at Conditioning Research covers this topic regularly. Traditional sports like soccer and basketball are effective because they have anaerobic and aerobic components. Even walking up stairs or down the street have measurable health benefits, however.
3. Intermittent fasting. This is very effective at improving insulin sensitivity and body composition. IF isn't starvation; it simply postpones calorie intake. Nor is it unhealthy. In fact, it's probably closely in line with the variable energy intake to which we are fundamentally adapted. My method is one 24-hour, water-only fast per week. No juice; that defeats the purpose. If you have elevated insulin like most people, it's best to get into IF gradually. Try skipping breakfast first. If you can skip breakfast and lunch, you've completed a 23-hour fast.
4. Lose the soda! Soda and other sweet foods are the enemy of body composition and general health. Fructose, found abundantly in high-fructose corn syrup, table sugar and agave nectar, seems to have a particular talent for causing insulin resistance. It's rapidly converted to fat in the liver, which is partially stored on the spot, and partially exported into the bloodstream as triglycerides. Diet soda isn't much better. It's been associated with weight gain in humans, and actually causes weight gain in rats. Normalizing insulin through carbohydrate restriction and fasting reduces cravings for sweet foods. A moderate amount of fruit is probably fine.
The most dangerous fat is visceral fat, or the "beer belly". Fortunately, it's also the most responsive to lifestyle changes.
The strategies I recommend all have one thing in common: they work to restore insulin sensitivity. This will not only improve body composition, it will normalize your metabolism on a fundamental level, reducing the risk of all the common chronic diseases. I may cover these topics again in more detail at another time.
1. Carbohydrate restriction. This is by far the most effective way to improve body composition. It will even benefit people who are already profoundly insulin resistant. Eliminating grains, legumes, potatoes and sugar is the simplest and best way to do this. That includes wheat, corn, rice, beans, oats, honorary grains like buckwheat and quinoa, and especially their derivatives. Carbohydrate is not the devil, but restricting intake to moderate amounts from vegetables and fruit is ideal for someone trying to lose weight. I think starchy root vegetables, soaked or sprouted legumes and soaked, sprouted or fermented non-gluten grains are OK for people who already have a healthy body composition.
2. Exercise. Our hunter-gatherer ancestors had a word for exercise: "life". Exercise helps improve insulin sensitivity by increasing the muscles' demand for fuel. It also builds muscle mass. Any exercise is great, but the best kind is brief and intense (anaerobic). This includes sprinting and brisk weight training. It's more effective than jogging at improving muscle mass, decreasing fat mass, decreasing insulin and improving other markers of metabolic health. Chris at Conditioning Research covers this topic regularly. Traditional sports like soccer and basketball are effective because they have anaerobic and aerobic components. Even walking up stairs or down the street have measurable health benefits, however.
3. Intermittent fasting. This is very effective at improving insulin sensitivity and body composition. IF isn't starvation; it simply postpones calorie intake. Nor is it unhealthy. In fact, it's probably closely in line with the variable energy intake to which we are fundamentally adapted. My method is one 24-hour, water-only fast per week. No juice; that defeats the purpose. If you have elevated insulin like most people, it's best to get into IF gradually. Try skipping breakfast first. If you can skip breakfast and lunch, you've completed a 23-hour fast.
4. Lose the soda! Soda and other sweet foods are the enemy of body composition and general health. Fructose, found abundantly in high-fructose corn syrup, table sugar and agave nectar, seems to have a particular talent for causing insulin resistance. It's rapidly converted to fat in the liver, which is partially stored on the spot, and partially exported into the bloodstream as triglycerides. Diet soda isn't much better. It's been associated with weight gain in humans, and actually causes weight gain in rats. Normalizing insulin through carbohydrate restriction and fasting reduces cravings for sweet foods. A moderate amount of fruit is probably fine.
Body Composition
I don't want to leave you with those last two posts without giving you some practical ways to improve body composition. Body composition is the ratio of lean tissue to fat. The ideal ratio differs depending on gender and individual differences. In general, 10% and 20% bodyfat are good targets for men and women, respectively. There's no need to measure however, as the eye is a pretty good judge.
The most dangerous fat is visceral fat, or the "beer belly". Fortunately, it's also the most responsive to lifestyle changes.
The strategies I recommend all have one thing in common: they work to restore insulin sensitivity. This will not only improve body composition, it will normalize your metabolism on a fundamental level, reducing the risk of all the common chronic diseases. I may cover these topics again in more detail at another time.
1. Carbohydrate restriction. This is by far the most effective way to improve body composition. It will even benefit people who are already profoundly insulin resistant. Eliminating grains, legumes, potatoes and sugar is the simplest and best way to do this. That includes wheat, corn, rice, beans, oats, honorary grains like buckwheat and quinoa, and especially their derivatives. Carbohydrate is not the devil, but restricting intake to moderate amounts from vegetables and fruit is ideal for someone trying to lose weight. I think starchy root vegetables, soaked or sprouted legumes and soaked, sprouted or fermented non-gluten grains are OK for people who already have a healthy body composition.
2. Exercise. Our hunter-gatherer ancestors had a word for exercise: "life". Exercise helps improve insulin sensitivity by increasing the muscles' demand for fuel. It also builds muscle mass. Any exercise is great, but the best kind is brief and intense (anaerobic). This includes sprinting and brisk weight training. It's more effective than jogging at improving muscle mass, decreasing fat mass, decreasing insulin and improving other markers of metabolic health. Chris at Conditioning Research covers this topic regularly. Traditional sports like soccer and basketball are effective because they have anaerobic and aerobic components. Even walking up stairs or down the street have measurable health benefits, however.
3. Intermittent fasting. This is very effective at improving insulin sensitivity and body composition. IF isn't starvation; it simply postpones calorie intake. Nor is it unhealthy. In fact, it's probably closely in line with the variable energy intake to which we are fundamentally adapted. My method is one 24-hour, water-only fast per week. No juice; that defeats the purpose. If you have elevated insulin like most people, it's best to get into IF gradually. Try skipping breakfast first. If you can skip breakfast and lunch, you've completed a 23-hour fast.
4. Lose the soda! Soda and other sweet foods are the enemy of body composition and general health. Fructose, found abundantly in high-fructose corn syrup, table sugar and agave nectar, seems to have a particular talent for causing insulin resistance. It's rapidly converted to fat in the liver, which is partially stored on the spot, and partially exported into the bloodstream as triglycerides. Diet soda isn't much better. It's been associated with weight gain in humans, and actually causes weight gain in rats. Normalizing insulin through carbohydrate restriction and fasting reduces cravings for sweet foods. A moderate amount of fruit is probably fine.
The most dangerous fat is visceral fat, or the "beer belly". Fortunately, it's also the most responsive to lifestyle changes.
The strategies I recommend all have one thing in common: they work to restore insulin sensitivity. This will not only improve body composition, it will normalize your metabolism on a fundamental level, reducing the risk of all the common chronic diseases. I may cover these topics again in more detail at another time.
1. Carbohydrate restriction. This is by far the most effective way to improve body composition. It will even benefit people who are already profoundly insulin resistant. Eliminating grains, legumes, potatoes and sugar is the simplest and best way to do this. That includes wheat, corn, rice, beans, oats, honorary grains like buckwheat and quinoa, and especially their derivatives. Carbohydrate is not the devil, but restricting intake to moderate amounts from vegetables and fruit is ideal for someone trying to lose weight. I think starchy root vegetables, soaked or sprouted legumes and soaked, sprouted or fermented non-gluten grains are OK for people who already have a healthy body composition.
2. Exercise. Our hunter-gatherer ancestors had a word for exercise: "life". Exercise helps improve insulin sensitivity by increasing the muscles' demand for fuel. It also builds muscle mass. Any exercise is great, but the best kind is brief and intense (anaerobic). This includes sprinting and brisk weight training. It's more effective than jogging at improving muscle mass, decreasing fat mass, decreasing insulin and improving other markers of metabolic health. Chris at Conditioning Research covers this topic regularly. Traditional sports like soccer and basketball are effective because they have anaerobic and aerobic components. Even walking up stairs or down the street have measurable health benefits, however.
3. Intermittent fasting. This is very effective at improving insulin sensitivity and body composition. IF isn't starvation; it simply postpones calorie intake. Nor is it unhealthy. In fact, it's probably closely in line with the variable energy intake to which we are fundamentally adapted. My method is one 24-hour, water-only fast per week. No juice; that defeats the purpose. If you have elevated insulin like most people, it's best to get into IF gradually. Try skipping breakfast first. If you can skip breakfast and lunch, you've completed a 23-hour fast.
4. Lose the soda! Soda and other sweet foods are the enemy of body composition and general health. Fructose, found abundantly in high-fructose corn syrup, table sugar and agave nectar, seems to have a particular talent for causing insulin resistance. It's rapidly converted to fat in the liver, which is partially stored on the spot, and partially exported into the bloodstream as triglycerides. Diet soda isn't much better. It's been associated with weight gain in humans, and actually causes weight gain in rats. Normalizing insulin through carbohydrate restriction and fasting reduces cravings for sweet foods. A moderate amount of fruit is probably fine.
Body Composition
I don't want to leave you with those last two posts without giving you some practical ways to improve body composition. Body composition is the ratio of lean tissue to fat. The ideal ratio differs depending on gender and individual differences. In general, 10% and 20% bodyfat are good targets for men and women, respectively. There's no need to measure however, as the eye is a pretty good judge.
The most dangerous fat is visceral fat, or the "beer belly". Fortunately, it's also the most responsive to lifestyle changes.
The strategies I recommend all have one thing in common: they work to restore insulin sensitivity. This will not only improve body composition, it will normalize your metabolism on a fundamental level, reducing the risk of all the common chronic diseases. I may cover these topics again in more detail at another time.
1. Carbohydrate restriction. This is by far the most effective way to improve body composition. It will even benefit people who are already profoundly insulin resistant. Eliminating grains, legumes, potatoes and sugar is the simplest and best way to do this. That includes wheat, corn, rice, beans, oats, honorary grains like buckwheat and quinoa, and especially their derivatives. Carbohydrate is not the devil, but restricting intake to moderate amounts from vegetables and fruit is ideal for someone trying to lose weight. I think starchy root vegetables, soaked or sprouted legumes and soaked, sprouted or fermented non-gluten grains are OK for people who already have a healthy body composition.
2. Exercise. Our hunter-gatherer ancestors had a word for exercise: "life". Exercise helps improve insulin sensitivity by increasing the muscles' demand for fuel. It also builds muscle mass. Any exercise is great, but the best kind is brief and intense (anaerobic). This includes sprinting and brisk weight training. It's more effective than jogging at improving muscle mass, decreasing fat mass, decreasing insulin and improving other markers of metabolic health. Chris at Conditioning Research covers this topic regularly. Traditional sports like soccer and basketball are effective because they have anaerobic and aerobic components. Even walking up stairs or down the street have measurable health benefits, however.
3. Intermittent fasting. This is very effective at improving insulin sensitivity and body composition. IF isn't starvation; it simply postpones calorie intake. Nor is it unhealthy. In fact, it's probably closely in line with the variable energy intake to which we are fundamentally adapted. My method is one 24-hour, water-only fast per week. No juice; that defeats the purpose. If you have elevated insulin like most people, it's best to get into IF gradually. Try skipping breakfast first. If you can skip breakfast and lunch, you've completed a 23-hour fast.
4. Lose the soda! Soda and other sweet foods are the enemy of body composition and general health. Fructose, found abundantly in high-fructose corn syrup, table sugar and agave nectar, seems to have a particular talent for causing insulin resistance. It's rapidly converted to fat in the liver, which is partially stored on the spot, and partially exported into the bloodstream as triglycerides. Diet soda isn't much better. It's been associated with weight gain in humans, and actually causes weight gain in rats. Normalizing insulin through carbohydrate restriction and fasting reduces cravings for sweet foods. A moderate amount of fruit is probably fine.
The most dangerous fat is visceral fat, or the "beer belly". Fortunately, it's also the most responsive to lifestyle changes.
The strategies I recommend all have one thing in common: they work to restore insulin sensitivity. This will not only improve body composition, it will normalize your metabolism on a fundamental level, reducing the risk of all the common chronic diseases. I may cover these topics again in more detail at another time.
1. Carbohydrate restriction. This is by far the most effective way to improve body composition. It will even benefit people who are already profoundly insulin resistant. Eliminating grains, legumes, potatoes and sugar is the simplest and best way to do this. That includes wheat, corn, rice, beans, oats, honorary grains like buckwheat and quinoa, and especially their derivatives. Carbohydrate is not the devil, but restricting intake to moderate amounts from vegetables and fruit is ideal for someone trying to lose weight. I think starchy root vegetables, soaked or sprouted legumes and soaked, sprouted or fermented non-gluten grains are OK for people who already have a healthy body composition.
2. Exercise. Our hunter-gatherer ancestors had a word for exercise: "life". Exercise helps improve insulin sensitivity by increasing the muscles' demand for fuel. It also builds muscle mass. Any exercise is great, but the best kind is brief and intense (anaerobic). This includes sprinting and brisk weight training. It's more effective than jogging at improving muscle mass, decreasing fat mass, decreasing insulin and improving other markers of metabolic health. Chris at Conditioning Research covers this topic regularly. Traditional sports like soccer and basketball are effective because they have anaerobic and aerobic components. Even walking up stairs or down the street have measurable health benefits, however.
3. Intermittent fasting. This is very effective at improving insulin sensitivity and body composition. IF isn't starvation; it simply postpones calorie intake. Nor is it unhealthy. In fact, it's probably closely in line with the variable energy intake to which we are fundamentally adapted. My method is one 24-hour, water-only fast per week. No juice; that defeats the purpose. If you have elevated insulin like most people, it's best to get into IF gradually. Try skipping breakfast first. If you can skip breakfast and lunch, you've completed a 23-hour fast.
4. Lose the soda! Soda and other sweet foods are the enemy of body composition and general health. Fructose, found abundantly in high-fructose corn syrup, table sugar and agave nectar, seems to have a particular talent for causing insulin resistance. It's rapidly converted to fat in the liver, which is partially stored on the spot, and partially exported into the bloodstream as triglycerides. Diet soda isn't much better. It's been associated with weight gain in humans, and actually causes weight gain in rats. Normalizing insulin through carbohydrate restriction and fasting reduces cravings for sweet foods. A moderate amount of fruit is probably fine.
Stamp Out Acne Once and For All
Most people with acne attempt to treat their irritated skin with external face washes, soaps, lotions and treatments. However, the best way to stamp out acne is by changing your diet and getting rid of acne-causing ingredients such as fried foods.
Healthy Foods Promote Healthy Skin
A healthful diet rich in natural whole foods like vegetables, fruits, whole grains and beans is the first recommendation for treating acne. Foods containing trans-fatty acids, such as milk, milk products, margarine, shortening and other synthetically hydrogenated vegetable oils, as well as fried foods, should be avoided.
It seems the prevalence of acne in the United States is built into the typical American diet. Americans tend to eat fried foods in large quantities, usually cooked in the most harmful of fats and oils. Not all fats are bad, but the fats that typical Americans eat make them more prone to develop acne and skin problems, such as what's in ice cream, cheese, bacon, and milk.
Why Creams and Lotions Do Not Work
Acne cannot really be treated using creams and soaps because the root of the condition lies beneath the skin. Pimples and blemishes are caused by bacteria and other irritants embedded underneath the skin's oil glands and hair follicles, which are generally caused as a result of improper hygiene and poor diet - such as too much processed, fatty, fried and sugary foods.
A skin-healthy diet emphasizes raw and lightly cooked vegetables, especially green leafy vegetables that contain valuable trace minerals and are rich in fiber. Fresh green vegetables are essential. Also include in your diet lean protein sources and complex carbohydrates, such as rice, whole-grain bread, and potatoes. These fiber-rich foods help ensure a clean gastrointestinal tract, which is especially important in the management of acne.
Eat three healthy meals daily to provide important nutrients and to decrease your appetite for sugary or greasy fried foods. Foods rich in vitamin A, like apricots, watermelon, and broccoli, as well as foods like lean beef, nuts, beans and whole grains that are rich in zinc can also be helpful in reducing acne breakouts. It's also imperative to drink lots of water to help flush the toxins out that contribute to breakouts.
Mark Hester runs the http://myeverydaylife.net/stopacne/ where you can read more tips and techniques for treating and even preventing acne. Teenage and adult acne are both covered. Visit http://myeverydaylife.net/stopacne/ today.
Sunday, March 30, 2008
Rheumatoid Arthritis And The Vegan Diet
Here's some interesting research on the benefits of a vegan diet for people with Rheumatoid Arthritis published in the journal Arthritis Research And Therapy:
Introduction
The purpose of this study was to investigate the effects of vegan diet in patients with rheumatoid arthritis (RA) on blood lipids oxidized low-density lipoprotein (oxLDL) and natural atheroprotective antibodies against phosphorylcholine (anti-PCs).
Methods
Sixty-six patients with active RA were randomly assigned to either a vegan diet free of gluten (38 patients) or a well-balanced non-vegan diet (28 patients) for 1 year. Thirty patients in the vegan group completed more than 3 months on the diet regimen. Blood lipids were analyzed by routine methods, and oxLDL and anti-PCs were analyzed by enzyme-linked immunosorbent assay. Data and serum samples were obtained at baseline and after 3 and 12 months.
Results
Mean ages were 50.0 years for the vegan group and 50.8 years for controls. Gluten-free vegan diet induced lower body mass index (BMI) and low-density lipoprotein (LDL) and higher anti-PC IgM than control diet (p <0.005). In the vegan group, BMI, LDL, and cholesterol decreased after both 3 and 12 months (p <0.01) and oxLDL after 3 months (p = 0.021) and trendwise after 12 months (p = 0.090). Triglycerides and high-density lipoprotein did not change. IgA anti-PC levels increased after 3 months (p = 0.027) and IgM anti-PC levels increased trendwise after 12 months (p = 0.057). There was no difference in IgG anti-PC levels. In the control diet group, IgM anti-PC levels decreased both after 3 and 12 months (p <0.01). When separating vegan patients into clinical responders and non-responders at 12 months, the effects on oxLDL and anti-PC IgA were seen only in responders (p <0.05).
Conclusion
A gluten-free vegan diet in RA induces changes that are potentially atheroprotective and anti-inflammatory, including decreased LDL and oxLDL levels and raised anti-PC IgM and IgA levels.
Read the full article.
Introduction
The purpose of this study was to investigate the effects of vegan diet in patients with rheumatoid arthritis (RA) on blood lipids oxidized low-density lipoprotein (oxLDL) and natural atheroprotective antibodies against phosphorylcholine (anti-PCs).
Methods
Sixty-six patients with active RA were randomly assigned to either a vegan diet free of gluten (38 patients) or a well-balanced non-vegan diet (28 patients) for 1 year. Thirty patients in the vegan group completed more than 3 months on the diet regimen. Blood lipids were analyzed by routine methods, and oxLDL and anti-PCs were analyzed by enzyme-linked immunosorbent assay. Data and serum samples were obtained at baseline and after 3 and 12 months.
Results
Mean ages were 50.0 years for the vegan group and 50.8 years for controls. Gluten-free vegan diet induced lower body mass index (BMI) and low-density lipoprotein (LDL) and higher anti-PC IgM than control diet (p <0.005). In the vegan group, BMI, LDL, and cholesterol decreased after both 3 and 12 months (p <0.01) and oxLDL after 3 months (p = 0.021) and trendwise after 12 months (p = 0.090). Triglycerides and high-density lipoprotein did not change. IgA anti-PC levels increased after 3 months (p = 0.027) and IgM anti-PC levels increased trendwise after 12 months (p = 0.057). There was no difference in IgG anti-PC levels. In the control diet group, IgM anti-PC levels decreased both after 3 and 12 months (p <0.01). When separating vegan patients into clinical responders and non-responders at 12 months, the effects on oxLDL and anti-PC IgA were seen only in responders (p <0.05).
Conclusion
A gluten-free vegan diet in RA induces changes that are potentially atheroprotective and anti-inflammatory, including decreased LDL and oxLDL levels and raised anti-PC IgM and IgA levels.
Read the full article.
Thursday, March 27, 2008
nausea/ pregnancy please help all 9 months
I received this email this mroning:
I was wondering if you had any advice or some sort of a consulation available. I was sick all nine months of my first pregnancy and now I am on my second and am sick again, I have been doing EFT and eliminating offending foods, but I am still very sick.
and this was my reply:
sorry to hear about your problem. It's always difficult to advise and, of course, what I am about to write does not replace the advice of properly qualified health and medical professionals, but some people find that vitamin B complex really helps. Also it might be a good idea to consult a homeopath - they seem to do well with this sort of problem.
We have lots of good products to help with other aspects of pregnancy - a self-hynosis pregnancy CD, a TENS machine for childbirth and a homeopathic kit for labour.
I was wondering if you had any advice or some sort of a consulation available. I was sick all nine months of my first pregnancy and now I am on my second and am sick again, I have been doing EFT and eliminating offending foods, but I am still very sick.
and this was my reply:
sorry to hear about your problem. It's always difficult to advise and, of course, what I am about to write does not replace the advice of properly qualified health and medical professionals, but some people find that vitamin B complex really helps. Also it might be a good idea to consult a homeopath - they seem to do well with this sort of problem.
We have lots of good products to help with other aspects of pregnancy - a self-hynosis pregnancy CD, a TENS machine for childbirth and a homeopathic kit for labour.
Visceral Fat and Dementia
This study was released today, demonstrating in 6,583 patients that visceral fat mass in the 40s predicts the risk of dementia in old age. Patients in the highest quintile (20% with the most visceral fat mass) had an almost three-fold higher risk of dementia than patients in the lowest quintile. This is a greater effect than you see from "genetics". Overall fat mass was less strongly correlated with dementia. This study is so timely, they must have heard about my blog post.
They used a measure of visceral fat called the "sagittal abdominal diameter", basically the distance from the back to the belly button. In other words, the beer belly.
What we're looking at is another facet of the pervasive "disease of civilization" that rolls into town on the same truck as sugar and white flour. Weston Price described it in 14 different cultures throughout the world in Nutrition and Physical Degeneration. Diabetes, cardiovascular disease, obesity, cancer and dementia all seem to come hand-in-hand. It's hard to say exactly what the root cause is, but the chain of causality seems to pass through visceral fat and insulin signaling in many people.
They used a measure of visceral fat called the "sagittal abdominal diameter", basically the distance from the back to the belly button. In other words, the beer belly.
What we're looking at is another facet of the pervasive "disease of civilization" that rolls into town on the same truck as sugar and white flour. Weston Price described it in 14 different cultures throughout the world in Nutrition and Physical Degeneration. Diabetes, cardiovascular disease, obesity, cancer and dementia all seem to come hand-in-hand. It's hard to say exactly what the root cause is, but the chain of causality seems to pass through visceral fat and insulin signaling in many people.
Visceral Fat and Dementia
This study was released today, demonstrating in 6,583 patients that visceral fat mass in the 40s predicts the risk of dementia in old age. Patients in the highest quintile (20% with the most visceral fat mass) had an almost three-fold higher risk of dementia than patients in the lowest quintile. This is a greater effect than you see from "genetics". Overall fat mass was less strongly correlated with dementia. This study is so timely, they must have heard about my blog post.
They used a measure of visceral fat called the "sagittal abdominal diameter", basically the distance from the back to the belly button. In other words, the beer belly.
What we're looking at is another facet of the pervasive "disease of civilization" that rolls into town on the same truck as sugar and white flour. Weston Price described it in 14 different cultures throughout the world in Nutrition and Physical Degeneration. Diabetes, cardiovascular disease, obesity, cancer and dementia all seem to come hand-in-hand. It's hard to say exactly what the root cause is, but the chain of causality seems to pass through visceral fat and insulin signaling in many people.
They used a measure of visceral fat called the "sagittal abdominal diameter", basically the distance from the back to the belly button. In other words, the beer belly.
What we're looking at is another facet of the pervasive "disease of civilization" that rolls into town on the same truck as sugar and white flour. Weston Price described it in 14 different cultures throughout the world in Nutrition and Physical Degeneration. Diabetes, cardiovascular disease, obesity, cancer and dementia all seem to come hand-in-hand. It's hard to say exactly what the root cause is, but the chain of causality seems to pass through visceral fat and insulin signaling in many people.
Visceral Fat and Dementia
This study was released today, demonstrating in 6,583 patients that visceral fat mass in the 40s predicts the risk of dementia in old age. Patients in the highest quintile (20% with the most visceral fat mass) had an almost three-fold higher risk of dementia than patients in the lowest quintile. This is a greater effect than you see from "genetics". Overall fat mass was less strongly correlated with dementia. This study is so timely, they must have heard about my blog post.
They used a measure of visceral fat called the "sagittal abdominal diameter", basically the distance from the back to the belly button. In other words, the beer belly.
What we're looking at is another facet of the pervasive "disease of civilization" that rolls into town on the same truck as sugar and white flour. Weston Price described it in 14 different cultures throughout the world in Nutrition and Physical Degeneration. Diabetes, cardiovascular disease, obesity, cancer and dementia all seem to come hand-in-hand. It's hard to say exactly what the root cause is, but the chain of causality seems to pass through visceral fat and insulin signaling in many people.
They used a measure of visceral fat called the "sagittal abdominal diameter", basically the distance from the back to the belly button. In other words, the beer belly.
What we're looking at is another facet of the pervasive "disease of civilization" that rolls into town on the same truck as sugar and white flour. Weston Price described it in 14 different cultures throughout the world in Nutrition and Physical Degeneration. Diabetes, cardiovascular disease, obesity, cancer and dementia all seem to come hand-in-hand. It's hard to say exactly what the root cause is, but the chain of causality seems to pass through visceral fat and insulin signaling in many people.
Visceral Fat and Dementia
This study was released today, demonstrating in 6,583 patients that visceral fat mass in the 40s predicts the risk of dementia in old age. Patients in the highest quintile (20% with the most visceral fat mass) had an almost three-fold higher risk of dementia than patients in the lowest quintile. This is a greater effect than you see from "genetics". Overall fat mass was less strongly correlated with dementia. This study is so timely, they must have heard about my blog post.
They used a measure of visceral fat called the "sagittal abdominal diameter", basically the distance from the back to the belly button. In other words, the beer belly.
What we're looking at is another facet of the pervasive "disease of civilization" that rolls into town on the same truck as sugar and white flour. Weston Price described it in 14 different cultures throughout the world in Nutrition and Physical Degeneration. Diabetes, cardiovascular disease, obesity, cancer and dementia all seem to come hand-in-hand. It's hard to say exactly what the root cause is, but the chain of causality seems to pass through visceral fat and insulin signaling in many people.
They used a measure of visceral fat called the "sagittal abdominal diameter", basically the distance from the back to the belly button. In other words, the beer belly.
What we're looking at is another facet of the pervasive "disease of civilization" that rolls into town on the same truck as sugar and white flour. Weston Price described it in 14 different cultures throughout the world in Nutrition and Physical Degeneration. Diabetes, cardiovascular disease, obesity, cancer and dementia all seem to come hand-in-hand. It's hard to say exactly what the root cause is, but the chain of causality seems to pass through visceral fat and insulin signaling in many people.
The Benefits of Swimming in Eliminating Acne
Everyone knows that swimming is one of the most beneficial activities for anyone's health in general. I have heard of studies showing that the only exercise more beneficial for overall health is running. The difference, however, is that swimming forces slower, deeper breathing and removes the physical strain on joints. In addition, people of all fitness levels can swim at effective paces due to the low impact on the body.
Now how is swimming particularly helpful in eliminating acne? It is a well-known fact that exercise in general promotes healthy skin. In addition to that, the deep breathing allows more oxygen to be processed and circulated by the body assisting in the removal of toxins and dead cells from the body and promoting the regeneration of cells. (see my next post for information on what everyone means when they speak about toxins)
Furthermore, because swimming requires the immersing the whole body (hence the entire skin surface) in water, it allows for the natural moisture absorption of the skin. Since you will most likely either be swimming in chlorinated pools or salt water, the disinfectant properties of the water will also be absorbed by the skin. And as you may or may not remember from a previous post, severe acne is the result of a susceptibility to infection.
In particular, painful pimples are acne blemishes that have become severely infected. Thus, swimming, more so in salt water than chlorinated, is extremely effective in disinfecting the skin and killing bacteria on the skin surface. Salt also dries the skin, limiting the production of sebum.
If you are not yet convinced then simply look at regular or professional swimmers and surfers and notice whether or not they have acne. The results will speak for themselves.
George Cleanthous suffered from acne for over 10 years. He researched and investigated acne and acne treatments for over 2 years and he now writes a blog on acne causes, acne treatments, acne symptoms, acne medicine, and general information on how to deal with acne. For the most effective research on acne, visit Acne
Wednesday, March 26, 2008
Visceral Fat
This week, I stumbled upon a very interesting series of articles from the lab of Dr. Nir Barzilai.
The first article I came across showed that surgical removal of the visceral fat deposit of rats increased their lifespan. Visceral fat (VF) is the "beer belly", and consists of the perinephratic fat around the kidneys and the omental fat in front of the intestines. It doesn't include subcutaneous fat, the fat layer under the skin.
VF is tightly associated with the metabolic syndrome, the quintessential "disease of civilization" that affects 24% of Americans (NHANES III). It's defined by three or more of the following criteria: high blood pressure, large waist circumference, low HDL cholesterol, high triglycerides, and high fasting glucose. The metabolic syndrome is associated with a 3-4-fold increase in the risk of death from cardiovascular disease, and a 6-fold increase in the risk of developing type II diabetes. From a review on the metabolic syndrome (parentheses mine):
This is all well and good, but who cares? What's to say VF plays any role other than as a simple marker for overweight?
The longevity paper led me to Dr. Barzilai's previous papers, which answered this question rather thoroughly. Rats raised on standard rat chow, which is a sad little compressed pellet made of grains and added nutrients, develop elevated insulin and insulin resistance with age, just like humans. Unless they don't have VF. Rats that had their VF surgically removed did not develop insulin resistance or elevated insulin with age, despite rebounding to their original total fat mass rather quickly (VF accounts for ~18% of total fat in these rats). These parameters are unaffected by removing an equal amount of subcutaneous fat, which has been shown in human liposuction patients as well.
Removing VF also improved diabetes-prone Zucker rats, which are profoundly insulin-resistant (leptin receptor loss-of-function). It kept wild-type rats just as insulin-sensitive as calorically restricted controls, which had a small amount of VF. This shows that VF isn't just a passive player; it's essential for the development of insulin resistance. It also shows, along with human studies, that insulin resistance is not an inevitable consequence of aging.
Adipose (fat) tissue is being increasingly recognized as an important endocrine (hormone-secreting) organ. It produces many different hormones that affect insulin sensitivity and appetite regulation, among other things. These hormones are collectively known as fat-derived peptides (FDPs). At least one of these FDPs, TNF-alpha, promotes insulin resistance.
Dr. Barzilai's group went on to explore the mechanism of VF contributing to insulin resistance. They increased the rate of glucose flux into the fat tissue of rats by infusing either glucose or insulin into the bloodstream. These treatments both cause increased glucose uptake by fat cells. What they saw when they dissected the rats was striking. The VF had ramped up its production of FDPs from 2- to 15-fold, while the subcutaneous fat had barely changed. Incidentally, insulin increased glucose uptake by VF twice as much as subcutaneous fat.
I'll say this again, because it's important. They forced glucose into VF cells, and those cells dramatically upregulated FDP production. And again, no visceral fat, no FDPs.
In earlier papers, he also showed that the removal of VF dramatically reduces the expression of TNF-alpha and leptin (two FDPs) in subcutaneous fat on a longer timescale, showing that VF and subcutaneous fat communicate to alter the metabolism. Again, TNF-alpha promotes insulin resistance, making it a possible link between the fat tissue and peripheral effects. VF removal had no effect on triglycerides, suggesting that they're only a marker of insulin dysfunction rather than a cause.
Now to take this research to its logical conclusion. Here's a plausible sequence of events leading up to the metabolic syndrome:
The first article I came across showed that surgical removal of the visceral fat deposit of rats increased their lifespan. Visceral fat (VF) is the "beer belly", and consists of the perinephratic fat around the kidneys and the omental fat in front of the intestines. It doesn't include subcutaneous fat, the fat layer under the skin.
VF is tightly associated with the metabolic syndrome, the quintessential "disease of civilization" that affects 24% of Americans (NHANES III). It's defined by three or more of the following criteria: high blood pressure, large waist circumference, low HDL cholesterol, high triglycerides, and high fasting glucose. The metabolic syndrome is associated with a 3-4-fold increase in the risk of death from cardiovascular disease, and a 6-fold increase in the risk of developing type II diabetes. From a review on the metabolic syndrome (parentheses mine):
The most common alteration related to the impaired glucose metabolism with aging is the progressively increased fasting and postprandial [post-meal] plasma insulin levels, suggesting an insulin-resistant state.
This is all well and good, but who cares? What's to say VF plays any role other than as a simple marker for overweight?
The longevity paper led me to Dr. Barzilai's previous papers, which answered this question rather thoroughly. Rats raised on standard rat chow, which is a sad little compressed pellet made of grains and added nutrients, develop elevated insulin and insulin resistance with age, just like humans. Unless they don't have VF. Rats that had their VF surgically removed did not develop insulin resistance or elevated insulin with age, despite rebounding to their original total fat mass rather quickly (VF accounts for ~18% of total fat in these rats). These parameters are unaffected by removing an equal amount of subcutaneous fat, which has been shown in human liposuction patients as well.
Removing VF also improved diabetes-prone Zucker rats, which are profoundly insulin-resistant (leptin receptor loss-of-function). It kept wild-type rats just as insulin-sensitive as calorically restricted controls, which had a small amount of VF. This shows that VF isn't just a passive player; it's essential for the development of insulin resistance. It also shows, along with human studies, that insulin resistance is not an inevitable consequence of aging.
Adipose (fat) tissue is being increasingly recognized as an important endocrine (hormone-secreting) organ. It produces many different hormones that affect insulin sensitivity and appetite regulation, among other things. These hormones are collectively known as fat-derived peptides (FDPs). At least one of these FDPs, TNF-alpha, promotes insulin resistance.
Dr. Barzilai's group went on to explore the mechanism of VF contributing to insulin resistance. They increased the rate of glucose flux into the fat tissue of rats by infusing either glucose or insulin into the bloodstream. These treatments both cause increased glucose uptake by fat cells. What they saw when they dissected the rats was striking. The VF had ramped up its production of FDPs from 2- to 15-fold, while the subcutaneous fat had barely changed. Incidentally, insulin increased glucose uptake by VF twice as much as subcutaneous fat.
I'll say this again, because it's important. They forced glucose into VF cells, and those cells dramatically upregulated FDP production. And again, no visceral fat, no FDPs.
In earlier papers, he also showed that the removal of VF dramatically reduces the expression of TNF-alpha and leptin (two FDPs) in subcutaneous fat on a longer timescale, showing that VF and subcutaneous fat communicate to alter the metabolism. Again, TNF-alpha promotes insulin resistance, making it a possible link between the fat tissue and peripheral effects. VF removal had no effect on triglycerides, suggesting that they're only a marker of insulin dysfunction rather than a cause.
Now to take this research to its logical conclusion. Here's a plausible sequence of events leading up to the metabolic syndrome:
- A meal high in quickly digested carbohydrate elevates blood glucose. OR, excessive fructose causes insulin resistance in the liver which leads to high fasting glucose.
- Visceral fat responds by increasing production of FDPs.
- FDPs, directly and/or indirectly, cause insulin resistance in the liver, muscle and other tissue. Liver insulin resistance causes alterations in lipoprotein ("cholesterol") profile (more on this in another post). Fat tissue remains insulin-sensitive.
- Fat tissue (including VF) grows in size, because due to its insulin sensitivity it's taking up more than its share of glucose.
- The vicious cycle continues, with increased visceral fat size and glucose uptake increasing FDP production, which makes the liver more insulin resistant, which increases glucose production by the liver, etc.
- In the absence of lifestyle changes, the cycle only stops when the fat tissue becomes insulin-resistant, at which point you lose control over blood sugar and become diabetic.
Visceral Fat
This week, I stumbled upon a very interesting series of articles from the lab of Dr. Nir Barzilai.
The first article I came across showed that surgical removal of the visceral fat deposit of rats increased their lifespan. Visceral fat (VF) is the "beer belly", and consists of the perinephratic fat around the kidneys and the omental fat in front of the intestines. It doesn't include subcutaneous fat, the fat layer under the skin.
VF is tightly associated with the metabolic syndrome, the quintessential "disease of civilization" that affects 24% of Americans (NHANES III). It's defined by three or more of the following criteria: high blood pressure, large waist circumference, low HDL cholesterol, high triglycerides, and high fasting glucose. The metabolic syndrome is associated with a 3-4-fold increase in the risk of death from cardiovascular disease, and a 6-fold increase in the risk of developing type II diabetes. From a review on the metabolic syndrome (parentheses mine):
This is all well and good, but who cares? What's to say VF plays any role other than as a simple marker for overweight?
The longevity paper led me to Dr. Barzilai's previous papers, which answered this question rather thoroughly. Rats raised on standard rat chow, which is a sad little compressed pellet made of grains and added nutrients, develop elevated insulin and insulin resistance with age, just like humans. Unless they don't have VF. Rats that had their VF surgically removed did not develop insulin resistance or elevated insulin with age, despite rebounding to their original total fat mass rather quickly (VF accounts for ~18% of total fat in these rats). These parameters are unaffected by removing an equal amount of subcutaneous fat, which has been shown in human liposuction patients as well.
Removing VF also improved diabetes-prone Zucker rats, which are profoundly insulin-resistant (leptin receptor loss-of-function). It kept wild-type rats just as insulin-sensitive as calorically restricted controls, which had a small amount of VF. This shows that VF isn't just a passive player; it's essential for the development of insulin resistance. It also shows, along with human studies, that insulin resistance is not an inevitable consequence of aging.
Adipose (fat) tissue is being increasingly recognized as an important endocrine (hormone-secreting) organ. It produces many different hormones that affect insulin sensitivity and appetite regulation, among other things. These hormones are collectively known as fat-derived peptides (FDPs). At least one of these FDPs, TNF-alpha, promotes insulin resistance.
Dr. Barzilai's group went on to explore the mechanism of VF contributing to insulin resistance. They increased the rate of glucose flux into the fat tissue of rats by infusing either glucose or insulin into the bloodstream. These treatments both cause increased glucose uptake by fat cells. What they saw when they dissected the rats was striking. The VF had ramped up its production of FDPs from 2- to 15-fold, while the subcutaneous fat had barely changed. Incidentally, insulin increased glucose uptake by VF twice as much as subcutaneous fat.
I'll say this again, because it's important. They forced glucose into VF cells, and those cells dramatically upregulated FDP production. And again, no visceral fat, no FDPs.
In earlier papers, he also showed that the removal of VF dramatically reduces the expression of TNF-alpha and leptin (two FDPs) in subcutaneous fat on a longer timescale, showing that VF and subcutaneous fat communicate to alter the metabolism. Again, TNF-alpha promotes insulin resistance, making it a possible link between the fat tissue and peripheral effects. VF removal had no effect on triglycerides, suggesting that they're only a marker of insulin dysfunction rather than a cause.
Now to take this research to its logical conclusion. Here's a plausible sequence of events leading up to the metabolic syndrome:
The first article I came across showed that surgical removal of the visceral fat deposit of rats increased their lifespan. Visceral fat (VF) is the "beer belly", and consists of the perinephratic fat around the kidneys and the omental fat in front of the intestines. It doesn't include subcutaneous fat, the fat layer under the skin.
VF is tightly associated with the metabolic syndrome, the quintessential "disease of civilization" that affects 24% of Americans (NHANES III). It's defined by three or more of the following criteria: high blood pressure, large waist circumference, low HDL cholesterol, high triglycerides, and high fasting glucose. The metabolic syndrome is associated with a 3-4-fold increase in the risk of death from cardiovascular disease, and a 6-fold increase in the risk of developing type II diabetes. From a review on the metabolic syndrome (parentheses mine):
The most common alteration related to the impaired glucose metabolism with aging is the progressively increased fasting and postprandial [post-meal] plasma insulin levels, suggesting an insulin-resistant state.
This is all well and good, but who cares? What's to say VF plays any role other than as a simple marker for overweight?
The longevity paper led me to Dr. Barzilai's previous papers, which answered this question rather thoroughly. Rats raised on standard rat chow, which is a sad little compressed pellet made of grains and added nutrients, develop elevated insulin and insulin resistance with age, just like humans. Unless they don't have VF. Rats that had their VF surgically removed did not develop insulin resistance or elevated insulin with age, despite rebounding to their original total fat mass rather quickly (VF accounts for ~18% of total fat in these rats). These parameters are unaffected by removing an equal amount of subcutaneous fat, which has been shown in human liposuction patients as well.
Removing VF also improved diabetes-prone Zucker rats, which are profoundly insulin-resistant (leptin receptor loss-of-function). It kept wild-type rats just as insulin-sensitive as calorically restricted controls, which had a small amount of VF. This shows that VF isn't just a passive player; it's essential for the development of insulin resistance. It also shows, along with human studies, that insulin resistance is not an inevitable consequence of aging.
Adipose (fat) tissue is being increasingly recognized as an important endocrine (hormone-secreting) organ. It produces many different hormones that affect insulin sensitivity and appetite regulation, among other things. These hormones are collectively known as fat-derived peptides (FDPs). At least one of these FDPs, TNF-alpha, promotes insulin resistance.
Dr. Barzilai's group went on to explore the mechanism of VF contributing to insulin resistance. They increased the rate of glucose flux into the fat tissue of rats by infusing either glucose or insulin into the bloodstream. These treatments both cause increased glucose uptake by fat cells. What they saw when they dissected the rats was striking. The VF had ramped up its production of FDPs from 2- to 15-fold, while the subcutaneous fat had barely changed. Incidentally, insulin increased glucose uptake by VF twice as much as subcutaneous fat.
I'll say this again, because it's important. They forced glucose into VF cells, and those cells dramatically upregulated FDP production. And again, no visceral fat, no FDPs.
In earlier papers, he also showed that the removal of VF dramatically reduces the expression of TNF-alpha and leptin (two FDPs) in subcutaneous fat on a longer timescale, showing that VF and subcutaneous fat communicate to alter the metabolism. Again, TNF-alpha promotes insulin resistance, making it a possible link between the fat tissue and peripheral effects. VF removal had no effect on triglycerides, suggesting that they're only a marker of insulin dysfunction rather than a cause.
Now to take this research to its logical conclusion. Here's a plausible sequence of events leading up to the metabolic syndrome:
- A meal high in quickly digested carbohydrate elevates blood glucose. OR, excessive fructose causes insulin resistance in the liver which leads to high fasting glucose.
- Visceral fat responds by increasing production of FDPs.
- FDPs, directly and/or indirectly, cause insulin resistance in the liver, muscle and other tissue. Liver insulin resistance causes alterations in lipoprotein ("cholesterol") profile (more on this in another post). Fat tissue remains insulin-sensitive.
- Fat tissue (including VF) grows in size, because due to its insulin sensitivity it's taking up more than its share of glucose.
- The vicious cycle continues, with increased visceral fat size and glucose uptake increasing FDP production, which makes the liver more insulin resistant, which increases glucose production by the liver, etc.
- In the absence of lifestyle changes, the cycle only stops when the fat tissue becomes insulin-resistant, at which point you lose control over blood sugar and become diabetic.
Visceral Fat
This week, I stumbled upon a very interesting series of articles from the lab of Dr. Nir Barzilai.
The first article I came across showed that surgical removal of the visceral fat deposit of rats increased their lifespan. Visceral fat (VF) is the "beer belly", and consists of the perinephratic fat around the kidneys and the omental fat in front of the intestines. It doesn't include subcutaneous fat, the fat layer under the skin.
VF is tightly associated with the metabolic syndrome, the quintessential "disease of civilization" that affects 24% of Americans (NHANES III). It's defined by three or more of the following criteria: high blood pressure, large waist circumference, low HDL cholesterol, high triglycerides, and high fasting glucose. The metabolic syndrome is associated with a 3-4-fold increase in the risk of death from cardiovascular disease, and a 6-fold increase in the risk of developing type II diabetes. From a review on the metabolic syndrome (parentheses mine):
This is all well and good, but who cares? What's to say VF plays any role other than as a simple marker for overweight?
The longevity paper led me to Dr. Barzilai's previous papers, which answered this question rather thoroughly. Rats raised on standard rat chow, which is a sad little compressed pellet made of grains and added nutrients, develop elevated insulin and insulin resistance with age, just like humans. Unless they don't have VF. Rats that had their VF surgically removed did not develop insulin resistance or elevated insulin with age, despite rebounding to their original total fat mass rather quickly (VF accounts for ~18% of total fat in these rats). These parameters are unaffected by removing an equal amount of subcutaneous fat, which has been shown in human liposuction patients as well.
Removing VF also improved diabetes-prone Zucker rats, which are profoundly insulin-resistant (leptin receptor loss-of-function). It kept wild-type rats just as insulin-sensitive as calorically restricted controls, which had a small amount of VF. This shows that VF isn't just a passive player; it's essential for the development of insulin resistance. It also shows, along with human studies, that insulin resistance is not an inevitable consequence of aging.
Adipose (fat) tissue is being increasingly recognized as an important endocrine (hormone-secreting) organ. It produces many different hormones that affect insulin sensitivity and appetite regulation, among other things. These hormones are collectively known as fat-derived peptides (FDPs). At least one of these FDPs, TNF-alpha, promotes insulin resistance.
Dr. Barzilai's group went on to explore the mechanism of VF contributing to insulin resistance. They increased the rate of glucose flux into the fat tissue of rats by infusing either glucose or insulin into the bloodstream. These treatments both cause increased glucose uptake by fat cells. What they saw when they dissected the rats was striking. The VF had ramped up its production of FDPs from 2- to 15-fold, while the subcutaneous fat had barely changed. Incidentally, insulin increased glucose uptake by VF twice as much as subcutaneous fat.
I'll say this again, because it's important. They forced glucose into VF cells, and those cells dramatically upregulated FDP production. And again, no visceral fat, no FDPs.
In earlier papers, he also showed that the removal of VF dramatically reduces the expression of TNF-alpha and leptin (two FDPs) in subcutaneous fat on a longer timescale, showing that VF and subcutaneous fat communicate to alter the metabolism. Again, TNF-alpha promotes insulin resistance, making it a possible link between the fat tissue and peripheral effects. VF removal had no effect on triglycerides, suggesting that they're only a marker of insulin dysfunction rather than a cause.
Now to take this research to its logical conclusion. Here's a plausible sequence of events leading up to the metabolic syndrome:
The first article I came across showed that surgical removal of the visceral fat deposit of rats increased their lifespan. Visceral fat (VF) is the "beer belly", and consists of the perinephratic fat around the kidneys and the omental fat in front of the intestines. It doesn't include subcutaneous fat, the fat layer under the skin.
VF is tightly associated with the metabolic syndrome, the quintessential "disease of civilization" that affects 24% of Americans (NHANES III). It's defined by three or more of the following criteria: high blood pressure, large waist circumference, low HDL cholesterol, high triglycerides, and high fasting glucose. The metabolic syndrome is associated with a 3-4-fold increase in the risk of death from cardiovascular disease, and a 6-fold increase in the risk of developing type II diabetes. From a review on the metabolic syndrome (parentheses mine):
The most common alteration related to the impaired glucose metabolism with aging is the progressively increased fasting and postprandial [post-meal] plasma insulin levels, suggesting an insulin-resistant state.
This is all well and good, but who cares? What's to say VF plays any role other than as a simple marker for overweight?
The longevity paper led me to Dr. Barzilai's previous papers, which answered this question rather thoroughly. Rats raised on standard rat chow, which is a sad little compressed pellet made of grains and added nutrients, develop elevated insulin and insulin resistance with age, just like humans. Unless they don't have VF. Rats that had their VF surgically removed did not develop insulin resistance or elevated insulin with age, despite rebounding to their original total fat mass rather quickly (VF accounts for ~18% of total fat in these rats). These parameters are unaffected by removing an equal amount of subcutaneous fat, which has been shown in human liposuction patients as well.
Removing VF also improved diabetes-prone Zucker rats, which are profoundly insulin-resistant (leptin receptor loss-of-function). It kept wild-type rats just as insulin-sensitive as calorically restricted controls, which had a small amount of VF. This shows that VF isn't just a passive player; it's essential for the development of insulin resistance. It also shows, along with human studies, that insulin resistance is not an inevitable consequence of aging.
Adipose (fat) tissue is being increasingly recognized as an important endocrine (hormone-secreting) organ. It produces many different hormones that affect insulin sensitivity and appetite regulation, among other things. These hormones are collectively known as fat-derived peptides (FDPs). At least one of these FDPs, TNF-alpha, promotes insulin resistance.
Dr. Barzilai's group went on to explore the mechanism of VF contributing to insulin resistance. They increased the rate of glucose flux into the fat tissue of rats by infusing either glucose or insulin into the bloodstream. These treatments both cause increased glucose uptake by fat cells. What they saw when they dissected the rats was striking. The VF had ramped up its production of FDPs from 2- to 15-fold, while the subcutaneous fat had barely changed. Incidentally, insulin increased glucose uptake by VF twice as much as subcutaneous fat.
I'll say this again, because it's important. They forced glucose into VF cells, and those cells dramatically upregulated FDP production. And again, no visceral fat, no FDPs.
In earlier papers, he also showed that the removal of VF dramatically reduces the expression of TNF-alpha and leptin (two FDPs) in subcutaneous fat on a longer timescale, showing that VF and subcutaneous fat communicate to alter the metabolism. Again, TNF-alpha promotes insulin resistance, making it a possible link between the fat tissue and peripheral effects. VF removal had no effect on triglycerides, suggesting that they're only a marker of insulin dysfunction rather than a cause.
Now to take this research to its logical conclusion. Here's a plausible sequence of events leading up to the metabolic syndrome:
- A meal high in quickly digested carbohydrate elevates blood glucose. OR, excessive fructose causes insulin resistance in the liver which leads to high fasting glucose.
- Visceral fat responds by increasing production of FDPs.
- FDPs, directly and/or indirectly, cause insulin resistance in the liver, muscle and other tissue. Liver insulin resistance causes alterations in lipoprotein ("cholesterol") profile (more on this in another post). Fat tissue remains insulin-sensitive.
- Fat tissue (including VF) grows in size, because due to its insulin sensitivity it's taking up more than its share of glucose.
- The vicious cycle continues, with increased visceral fat size and glucose uptake increasing FDP production, which makes the liver more insulin resistant, which increases glucose production by the liver, etc.
- In the absence of lifestyle changes, the cycle only stops when the fat tissue becomes insulin-resistant, at which point you lose control over blood sugar and become diabetic.
Visceral Fat
This week, I stumbled upon a very interesting series of articles from the lab of Dr. Nir Barzilai.
The first article I came across showed that surgical removal of the visceral fat deposit of rats increased their lifespan. Visceral fat (VF) is the "beer belly", and consists of the perinephratic fat around the kidneys and the omental fat in front of the intestines. It doesn't include subcutaneous fat, the fat layer under the skin.
VF is tightly associated with the metabolic syndrome, the quintessential "disease of civilization" that affects 24% of Americans (NHANES III). It's defined by three or more of the following criteria: high blood pressure, large waist circumference, low HDL cholesterol, high triglycerides, and high fasting glucose. The metabolic syndrome is associated with a 3-4-fold increase in the risk of death from cardiovascular disease, and a 6-fold increase in the risk of developing type II diabetes. From a review on the metabolic syndrome (parentheses mine):
This is all well and good, but who cares? What's to say VF plays any role other than as a simple marker for overweight?
The longevity paper led me to Dr. Barzilai's previous papers, which answered this question rather thoroughly. Rats raised on standard rat chow, which is a sad little compressed pellet made of grains and added nutrients, develop elevated insulin and insulin resistance with age, just like humans. Unless they don't have VF. Rats that had their VF surgically removed did not develop insulin resistance or elevated insulin with age, despite rebounding to their original total fat mass rather quickly (VF accounts for ~18% of total fat in these rats). These parameters are unaffected by removing an equal amount of subcutaneous fat, which has been shown in human liposuction patients as well.
Removing VF also improved diabetes-prone Zucker rats, which are profoundly insulin-resistant (leptin receptor loss-of-function). It kept wild-type rats just as insulin-sensitive as calorically restricted controls, which had a small amount of VF. This shows that VF isn't just a passive player; it's essential for the development of insulin resistance. It also shows, along with human studies, that insulin resistance is not an inevitable consequence of aging.
Adipose (fat) tissue is being increasingly recognized as an important endocrine (hormone-secreting) organ. It produces many different hormones that affect insulin sensitivity and appetite regulation, among other things. These hormones are collectively known as fat-derived peptides (FDPs). At least one of these FDPs, TNF-alpha, promotes insulin resistance.
Dr. Barzilai's group went on to explore the mechanism of VF contributing to insulin resistance. They increased the rate of glucose flux into the fat tissue of rats by infusing either glucose or insulin into the bloodstream. These treatments both cause increased glucose uptake by fat cells. What they saw when they dissected the rats was striking. The VF had ramped up its production of FDPs from 2- to 15-fold, while the subcutaneous fat had barely changed. Incidentally, insulin increased glucose uptake by VF twice as much as subcutaneous fat.
I'll say this again, because it's important. They forced glucose into VF cells, and those cells dramatically upregulated FDP production. And again, no visceral fat, no FDPs.
In earlier papers, he also showed that the removal of VF dramatically reduces the expression of TNF-alpha and leptin (two FDPs) in subcutaneous fat on a longer timescale, showing that VF and subcutaneous fat communicate to alter the metabolism. Again, TNF-alpha promotes insulin resistance, making it a possible link between the fat tissue and peripheral effects. VF removal had no effect on triglycerides, suggesting that they're only a marker of insulin dysfunction rather than a cause.
Now to take this research to its logical conclusion. Here's a plausible sequence of events leading up to the metabolic syndrome:
The first article I came across showed that surgical removal of the visceral fat deposit of rats increased their lifespan. Visceral fat (VF) is the "beer belly", and consists of the perinephratic fat around the kidneys and the omental fat in front of the intestines. It doesn't include subcutaneous fat, the fat layer under the skin.
VF is tightly associated with the metabolic syndrome, the quintessential "disease of civilization" that affects 24% of Americans (NHANES III). It's defined by three or more of the following criteria: high blood pressure, large waist circumference, low HDL cholesterol, high triglycerides, and high fasting glucose. The metabolic syndrome is associated with a 3-4-fold increase in the risk of death from cardiovascular disease, and a 6-fold increase in the risk of developing type II diabetes. From a review on the metabolic syndrome (parentheses mine):
The most common alteration related to the impaired glucose metabolism with aging is the progressively increased fasting and postprandial [post-meal] plasma insulin levels, suggesting an insulin-resistant state.
This is all well and good, but who cares? What's to say VF plays any role other than as a simple marker for overweight?
The longevity paper led me to Dr. Barzilai's previous papers, which answered this question rather thoroughly. Rats raised on standard rat chow, which is a sad little compressed pellet made of grains and added nutrients, develop elevated insulin and insulin resistance with age, just like humans. Unless they don't have VF. Rats that had their VF surgically removed did not develop insulin resistance or elevated insulin with age, despite rebounding to their original total fat mass rather quickly (VF accounts for ~18% of total fat in these rats). These parameters are unaffected by removing an equal amount of subcutaneous fat, which has been shown in human liposuction patients as well.
Removing VF also improved diabetes-prone Zucker rats, which are profoundly insulin-resistant (leptin receptor loss-of-function). It kept wild-type rats just as insulin-sensitive as calorically restricted controls, which had a small amount of VF. This shows that VF isn't just a passive player; it's essential for the development of insulin resistance. It also shows, along with human studies, that insulin resistance is not an inevitable consequence of aging.
Adipose (fat) tissue is being increasingly recognized as an important endocrine (hormone-secreting) organ. It produces many different hormones that affect insulin sensitivity and appetite regulation, among other things. These hormones are collectively known as fat-derived peptides (FDPs). At least one of these FDPs, TNF-alpha, promotes insulin resistance.
Dr. Barzilai's group went on to explore the mechanism of VF contributing to insulin resistance. They increased the rate of glucose flux into the fat tissue of rats by infusing either glucose or insulin into the bloodstream. These treatments both cause increased glucose uptake by fat cells. What they saw when they dissected the rats was striking. The VF had ramped up its production of FDPs from 2- to 15-fold, while the subcutaneous fat had barely changed. Incidentally, insulin increased glucose uptake by VF twice as much as subcutaneous fat.
I'll say this again, because it's important. They forced glucose into VF cells, and those cells dramatically upregulated FDP production. And again, no visceral fat, no FDPs.
In earlier papers, he also showed that the removal of VF dramatically reduces the expression of TNF-alpha and leptin (two FDPs) in subcutaneous fat on a longer timescale, showing that VF and subcutaneous fat communicate to alter the metabolism. Again, TNF-alpha promotes insulin resistance, making it a possible link between the fat tissue and peripheral effects. VF removal had no effect on triglycerides, suggesting that they're only a marker of insulin dysfunction rather than a cause.
Now to take this research to its logical conclusion. Here's a plausible sequence of events leading up to the metabolic syndrome:
- A meal high in quickly digested carbohydrate elevates blood glucose. OR, excessive fructose causes insulin resistance in the liver which leads to high fasting glucose.
- Visceral fat responds by increasing production of FDPs.
- FDPs, directly and/or indirectly, cause insulin resistance in the liver, muscle and other tissue. Liver insulin resistance causes alterations in lipoprotein ("cholesterol") profile (more on this in another post). Fat tissue remains insulin-sensitive.
- Fat tissue (including VF) grows in size, because due to its insulin sensitivity it's taking up more than its share of glucose.
- The vicious cycle continues, with increased visceral fat size and glucose uptake increasing FDP production, which makes the liver more insulin resistant, which increases glucose production by the liver, etc.
- In the absence of lifestyle changes, the cycle only stops when the fat tissue becomes insulin-resistant, at which point you lose control over blood sugar and become diabetic.
The Importance of Strong Health Care Governance
As we look at the core competencies of health care leaders in general, and future health care leaders within CHRISTUS Health, one area which is often not developed to the degree necessary, is the knowledge surrounding the governance process. In addition, the importance of governance is often not well articulated by CEOs, and therefore future leaders are often not coached and mentored
The Importance of Strong Health Care Governance
As we look at the core competencies of health care leaders in general, and future health care leaders within CHRISTUS Health, one area which is often not developed to the degree necessary, is the knowledge surrounding the governance process. In addition, the importance of governance is often not well articulated by CEOs, and therefore future leaders are often not coached and mentored
Tuesday, March 25, 2008
Posh Spice's Acne Battle
Victoria Beckham, also known as Posh Spice, has hit the headlines again by appearing naked on a Marc Jacobs t-shirt to raise awareness of skin cancer.
Posh decided to warn others about the dangers of sun-damaged skin since moving to a warmer climate. She said: "Since we moved to California I have realised how important it is to practise safe sun for myself and to keep my three boys' skin well protected as well. Skin cancer is a huge problem and I really wanted to help raise awareness by taking part in Marc's initiative."
However, her decision to participate in this campaign certainly doesn't mean that the former Spice Girl hasn't got skin problems of her own. Like a number of high-profile celebrities such as Cameron Diaz, Victoria suffers from serious adult acne, and even the most expensive make-up artists struggle to mask her spotty skin.
Last October, Victoria was pictured by the paparazzi with an incredibly spotty forehead. Pictures of the former pop star's problem skin made the headlines and were printed in publications throughout the world. More recently, her spotty skin has flared up once again. Victoria blames the problem on stress, particularly due to the Spice Girl's recent reunion tour.
Ever since she was a teenager, Victoria claims to have been plagued by spots and pimples. Although she is older now, dermatologists still believe that her skin is in a bad way. Jane Lewis, a dermatological nurse, believes that Victoria is a serious sufferer of adult acne. After examining a picture of the star's skin, she said: "It's obvious that she suffers from acne. Although she has put makeup on over the top, you can clearly see the little bumps. There are no angry whiteheads or blackheads, so it's not an acute flare-up yet, but this may be the way her acne manifests itself before it comes out fully. (She has) what look like open spots on her forehead and around her eyes, but these are acne scars which inevitably develop over the years - even if you don't pick at them."
Acne scars can cause the sufferer distress, although they can be successfully be reduced with treatment. Laser treatment can also be used to successfully reduce skin inflammation caused by acne.
Source:
The Mirror Daily Mail The Sun
Author: Nikki Rammer
Web: http://www.skinmedical.co.uk
Nikki Rammer is a writer who takes an interest in healthcare, in particular acne treatmentMonday, March 24, 2008
Okinawa and Lard
The inhabitants of Okinawa, an island prefecture of Japan, are one of the longest-lived populations in the world. Their diet and lifestyle have been thoroughly studied for this reason. Papers typically focus on their consumption of vegetables, fish, soy, exercise, and the fact that some of them may have been mildly calorically restricted for part of their lives.
The thing that often gets swept under the rug is that they eat lard. Traditionally, it was their primary cooking fat, and they use it liberally. Of course, they also eat the pork the lard came from.
I'm not saying lard will make you live to 100, but it certainly won't stop you...
The thing that often gets swept under the rug is that they eat lard. Traditionally, it was their primary cooking fat, and they use it liberally. Of course, they also eat the pork the lard came from.
I'm not saying lard will make you live to 100, but it certainly won't stop you...
Okinawa and Lard
The inhabitants of Okinawa, an island prefecture of Japan, are one of the longest-lived populations in the world. Their diet and lifestyle have been thoroughly studied for this reason. Papers typically focus on their consumption of vegetables, fish, soy, exercise, and the fact that some of them may have been mildly calorically restricted for part of their lives.
The thing that often gets swept under the rug is that they eat lard. Traditionally, it was their primary cooking fat, and they use it liberally. Of course, they also eat the pork the lard came from.
I'm not saying lard will make you live to 100, but it certainly won't stop you...
The thing that often gets swept under the rug is that they eat lard. Traditionally, it was their primary cooking fat, and they use it liberally. Of course, they also eat the pork the lard came from.
I'm not saying lard will make you live to 100, but it certainly won't stop you...
Okinawa and Lard
The inhabitants of Okinawa, an island prefecture of Japan, are one of the longest-lived populations in the world. Their diet and lifestyle have been thoroughly studied for this reason. Papers typically focus on their consumption of vegetables, fish, soy, exercise, and the fact that some of them may have been mildly calorically restricted for part of their lives.
The thing that often gets swept under the rug is that they eat lard. Traditionally, it was their primary cooking fat, and they use it liberally. Of course, they also eat the pork the lard came from.
I'm not saying lard will make you live to 100, but it certainly won't stop you...
The thing that often gets swept under the rug is that they eat lard. Traditionally, it was their primary cooking fat, and they use it liberally. Of course, they also eat the pork the lard came from.
I'm not saying lard will make you live to 100, but it certainly won't stop you...
Okinawa and Lard
The inhabitants of Okinawa, an island prefecture of Japan, are one of the longest-lived populations in the world. Their diet and lifestyle have been thoroughly studied for this reason. Papers typically focus on their consumption of vegetables, fish, soy, exercise, and the fact that some of them may have been mildly calorically restricted for part of their lives.
The thing that often gets swept under the rug is that they eat lard. Traditionally, it was their primary cooking fat, and they use it liberally. Of course, they also eat the pork the lard came from.
I'm not saying lard will make you live to 100, but it certainly won't stop you...
The thing that often gets swept under the rug is that they eat lard. Traditionally, it was their primary cooking fat, and they use it liberally. Of course, they also eat the pork the lard came from.
I'm not saying lard will make you live to 100, but it certainly won't stop you...
Recycle Your Mobile Phone
If you're in the UK you can recycle your old mobile phone and help WaterAid raise money for its much needed work. Each phone is worth about £5.00 to them.
Remove the SIM card
Put it in a sturdy enevelope and send to:
WaterAid, Freepost LON16281, London WC1N 3BR
Don't include the charger.
40% of the world's population do not have a safe, clean or private place to go to the toilet.
Remove the SIM card
Put it in a sturdy enevelope and send to:
WaterAid, Freepost LON16281, London WC1N 3BR
Don't include the charger.
40% of the world's population do not have a safe, clean or private place to go to the toilet.
Sunday, March 23, 2008
Real Food IV: Lard
Your great-grandmother would have told you that natural, homemade lard is an excellent cooking fat. It has a mild, savory flavor and a high smoke point. It's well suited for sauteing and frying foods, and it makes the flakiest savory crust. It's also cheap to buy and easy to render. Rendering lard is the process by which fat tissue is turned into pure fat. I buy the best quality lard available for $2/lb at my farmer's market, making it far cheaper than butter and olive oil of equivalent quality.The best place to buy lard is at a local farmer's market. Look for pigs that have been "field-raised" or "pasture-raised", and are preferably organic. This ensures that they receive sunlight and have been treated humanely. The "organic" label by itself simply means they have been fed organic feed; the pigs will often not have had access to the outdoors. I recommend avoiding conventional (non-organic) pork at all costs, because it's profoundly inhumane and highly polluting. This is where I buy my lard.
If you don't have access to good quality local lard, there are a couple of sources on the Local Harvest website. Look for "leaf lard", which is the fat surrounding the kidneys. It's lowest in polyunsaturated oil and thus has the highest smoke point and the lowest omega-6 content. It's also practically pure fat. You will recover 90% of the pre-rendering volume from leaf lard. On to the recipe.
Ingredients and Equipment:
- Lard
- Cheesecloth
- Baking dish
- Jars
2. Cut off any pieces of meat clinging to the fat.
3. Cut fat into small (~1-inch) cubes.
4. Place them into a non-reactive baking dish and then into the oven.
5. Over the next 2-3 hours, periodically mash the fat with a potato ricer or the back of a large spoon. The fat will gradually separate from the residual protein as a clear liquid.
6. When you are satisfied that you've separated out most of the fat, remove the baking dish from the oven and allow it to stand until it's cool enough to be safe, but warm enough to be liquid.
7. Pour through a cheesecloth into jars. Save the "cracklins", these can be eaten.
8. If you plan on using the lard for crusts, cool it as quickly as possible by placing the jars in cold water. If the lard solidifies slowly, it will have a slightly grainy texture that works less well for crusts, but is irrelevant for other purposes.
Finished lard has a long shelf life but I like to keep it in the fridge or freezer to extend it even further.
Real Food IV: Lard
Your great-grandmother would have told you that natural, homemade lard is an excellent cooking fat. It has a mild, savory flavor and a high smoke point. It's well suited for sauteing and frying foods, and it makes the flakiest savory crust. It's also cheap to buy and easy to render. Rendering lard is the process by which fat tissue is turned into pure fat. I buy the best quality lard available for $2/lb at my farmer's market, making it far cheaper than butter and olive oil of equivalent quality.The best place to buy lard is at a local farmer's market. Look for pigs that have been "field-raised" or "pasture-raised", and are preferably organic. This ensures that they receive sunlight and have been treated humanely. The "organic" label by itself simply means they have been fed organic feed; the pigs will often not have had access to the outdoors. I recommend avoiding conventional (non-organic) pork at all costs, because it's profoundly inhumane and highly polluting. This is where I buy my lard.
If you don't have access to good quality local lard, there are a couple of sources on the Local Harvest website. Look for "leaf lard", which is the fat surrounding the kidneys. It's lowest in polyunsaturated oil and thus has the highest smoke point and the lowest omega-6 content. It's also practically pure fat. You will recover 90% of the pre-rendering volume from leaf lard. On to the recipe.
Ingredients and Equipment:
- Lard
- Cheesecloth
- Baking dish
- Jars
2. Cut off any pieces of meat clinging to the fat.
3. Cut fat into small (~1-inch) cubes.
4. Place them into a non-reactive baking dish and then into the oven.
5. Over the next 2-3 hours, periodically mash the fat with a potato ricer or the back of a large spoon. The fat will gradually separate from the residual protein as a clear liquid.
6. When you are satisfied that you've separated out most of the fat, remove the baking dish from the oven and allow it to stand until it's cool enough to be safe, but warm enough to be liquid.
7. Pour through a cheesecloth into jars. Save the "cracklins", these can be eaten.
8. If you plan on using the lard for crusts, cool it as quickly as possible by placing the jars in cold water. If the lard solidifies slowly, it will have a slightly grainy texture that works less well for crusts, but is irrelevant for other purposes.
Finished lard has a long shelf life but I like to keep it in the fridge or freezer to extend it even further.
Real Food IV: Lard
Your great-grandmother would have told you that natural, homemade lard is an excellent cooking fat. It has a mild, savory flavor and a high smoke point. It's well suited for sauteing and frying foods, and it makes the flakiest savory crust. It's also cheap to buy and easy to render. Rendering lard is the process by which fat tissue is turned into pure fat. I buy the best quality lard available for $2/lb at my farmer's market, making it far cheaper than butter and olive oil of equivalent quality.The best place to buy lard is at a local farmer's market. Look for pigs that have been "field-raised" or "pasture-raised", and are preferably organic. This ensures that they receive sunlight and have been treated humanely. The "organic" label by itself simply means they have been fed organic feed; the pigs will often not have had access to the outdoors. I recommend avoiding conventional (non-organic) pork at all costs, because it's profoundly inhumane and highly polluting. This is where I buy my lard.
If you don't have access to good quality local lard, there are a couple of sources on the Local Harvest website. Look for "leaf lard", which is the fat surrounding the kidneys. It's lowest in polyunsaturated oil and thus has the highest smoke point and the lowest omega-6 content. It's also practically pure fat. You will recover 90% of the pre-rendering volume from leaf lard. On to the recipe.
Ingredients and Equipment:
- Lard
- Cheesecloth
- Baking dish
- Jars
2. Cut off any pieces of meat clinging to the fat.
3. Cut fat into small (~1-inch) cubes.
4. Place them into a non-reactive baking dish and then into the oven.
5. Over the next 2-3 hours, periodically mash the fat with a potato ricer or the back of a large spoon. The fat will gradually separate from the residual protein as a clear liquid.
6. When you are satisfied that you've separated out most of the fat, remove the baking dish from the oven and allow it to stand until it's cool enough to be safe, but warm enough to be liquid.
7. Pour through a cheesecloth into jars. Save the "cracklins", these can be eaten.
8. If you plan on using the lard for crusts, cool it as quickly as possible by placing the jars in cold water. If the lard solidifies slowly, it will have a slightly grainy texture that works less well for crusts, but is irrelevant for other purposes.
Finished lard has a long shelf life but I like to keep it in the fridge or freezer to extend it even further.
Real Food IV: Lard
Your great-grandmother would have told you that natural, homemade lard is an excellent cooking fat. It has a mild, savory flavor and a high smoke point. It's well suited for sauteing and frying foods, and it makes the flakiest savory crust. It's also cheap to buy and easy to render. Rendering lard is the process by which fat tissue is turned into pure fat. I buy the best quality lard available for $2/lb at my farmer's market, making it far cheaper than butter and olive oil of equivalent quality.The best place to buy lard is at a local farmer's market. Look for pigs that have been "field-raised" or "pasture-raised", and are preferably organic. This ensures that they receive sunlight and have been treated humanely. The "organic" label by itself simply means they have been fed organic feed; the pigs will often not have had access to the outdoors. I recommend avoiding conventional (non-organic) pork at all costs, because it's profoundly inhumane and highly polluting. This is where I buy my lard.
If you don't have access to good quality local lard, there are a couple of sources on the Local Harvest website. Look for "leaf lard", which is the fat surrounding the kidneys. It's lowest in polyunsaturated oil and thus has the highest smoke point and the lowest omega-6 content. It's also practically pure fat. You will recover 90% of the pre-rendering volume from leaf lard. On to the recipe.
Ingredients and Equipment:
- Lard
- Cheesecloth
- Baking dish
- Jars
2. Cut off any pieces of meat clinging to the fat.
3. Cut fat into small (~1-inch) cubes.
4. Place them into a non-reactive baking dish and then into the oven.
5. Over the next 2-3 hours, periodically mash the fat with a potato ricer or the back of a large spoon. The fat will gradually separate from the residual protein as a clear liquid.
6. When you are satisfied that you've separated out most of the fat, remove the baking dish from the oven and allow it to stand until it's cool enough to be safe, but warm enough to be liquid.
7. Pour through a cheesecloth into jars. Save the "cracklins", these can be eaten.
8. If you plan on using the lard for crusts, cool it as quickly as possible by placing the jars in cold water. If the lard solidifies slowly, it will have a slightly grainy texture that works less well for crusts, but is irrelevant for other purposes.
Finished lard has a long shelf life but I like to keep it in the fridge or freezer to extend it even further.
Flower & Gem Essences
I've added a new section to our online shop for therapists - we've started to sell flower and gem essences and sprays.
So far we've got:
So far we've got:
- Australian Bush Essences
- Alaskan Flower Essences and Sprays
- Bailey Acupuncture Essences
- My own Earth Energies
- Healing Herbs Flower Remedies And Creams - based on the work of Dr Edward Bach
- Indigo Essences
I haven't got much in the way of descriptions yet, but I hope over the next few weeks to add more detailed descriptions and extend the range, but don't let that stop you buying right now!
Saturday, March 22, 2008
The L-word
That's right, ladies and gentlemen: lard. The word alone makes lipophobes cringe like a vampire from garlic. It also makes epicures salivate. But why is lard so unhealthy? Let's take a look.
The fatty acid profile of lard might give us a clue. A major portion of lard is monounsaturated, 40% by weight. This is the same type of fat that predominates in olive oil (73%), and which is widely recommended by mainstream nutrition experts. Another prevalent class of fat in lard is saturated, at 48%. More than one third of this saturated fat is stearic acid, which even the most hardened lipophobe will agree has a "favorable" effect on blood lipids. Then there's the 8% polyunsaturated fat, which has been the darling of mainstream heart disease research for decades due to its ability to lower blood cholesterol (for the record, I believe the polyunsaturate content is lard's least healthy feature). The omega-3:6 ratio depends on how the pig was raised, but is typically skewed more toward omega-6.
So what does that leave us with? 66% fats that we're told are heart-healthy, and 30% non-stearic saturated fats that are supposed to be unhealthy. But if you still believe saturated fats cause heart disease, check out this post, this one and this one.
Lard also contains a small amount of vitamin D. The sun is the best source of vitamin D, since your skin synthesizes it when it's exposed to UVB. But due to the low angle of the sun in winter, and the fact that many people don't spend enough time outdoors even in the summer, extra vitamin D in the diet is helpful.
I think you can see that lard's bad reputation is undeserved. It may be a legacy of the time when hydrogenated vegetable oils were competing with animal fats for the food market.
There is such a thing as unhealthy lard, however. It's the stuff you might find at the grocery store. Store-bought lard is often hydrogenated to make it more shelf-stable. It also comes from confinement-raised pork operations, which aside from being profoundly inhumane, do not allow access to the outdoors. Thus, the fat won't contain vitamin D.
In the next post, I'll talk about how to buy pasture-raised lard and render it yourself.
The fatty acid profile of lard might give us a clue. A major portion of lard is monounsaturated, 40% by weight. This is the same type of fat that predominates in olive oil (73%), and which is widely recommended by mainstream nutrition experts. Another prevalent class of fat in lard is saturated, at 48%. More than one third of this saturated fat is stearic acid, which even the most hardened lipophobe will agree has a "favorable" effect on blood lipids. Then there's the 8% polyunsaturated fat, which has been the darling of mainstream heart disease research for decades due to its ability to lower blood cholesterol (for the record, I believe the polyunsaturate content is lard's least healthy feature). The omega-3:6 ratio depends on how the pig was raised, but is typically skewed more toward omega-6.
So what does that leave us with? 66% fats that we're told are heart-healthy, and 30% non-stearic saturated fats that are supposed to be unhealthy. But if you still believe saturated fats cause heart disease, check out this post, this one and this one.
Lard also contains a small amount of vitamin D. The sun is the best source of vitamin D, since your skin synthesizes it when it's exposed to UVB. But due to the low angle of the sun in winter, and the fact that many people don't spend enough time outdoors even in the summer, extra vitamin D in the diet is helpful.
I think you can see that lard's bad reputation is undeserved. It may be a legacy of the time when hydrogenated vegetable oils were competing with animal fats for the food market.
There is such a thing as unhealthy lard, however. It's the stuff you might find at the grocery store. Store-bought lard is often hydrogenated to make it more shelf-stable. It also comes from confinement-raised pork operations, which aside from being profoundly inhumane, do not allow access to the outdoors. Thus, the fat won't contain vitamin D.
In the next post, I'll talk about how to buy pasture-raised lard and render it yourself.
The L-word
That's right, ladies and gentlemen: lard. The word alone makes lipophobes cringe like a vampire from garlic. It also makes epicures salivate. But why is lard so unhealthy? Let's take a look.
The fatty acid profile of lard might give us a clue. A major portion of lard is monounsaturated, 40% by weight. This is the same type of fat that predominates in olive oil (73%), and which is widely recommended by mainstream nutrition experts. Another prevalent class of fat in lard is saturated, at 48%. More than one third of this saturated fat is stearic acid, which even the most hardened lipophobe will agree has a "favorable" effect on blood lipids. Then there's the 8% polyunsaturated fat, which has been the darling of mainstream heart disease research for decades due to its ability to lower blood cholesterol (for the record, I believe the polyunsaturate content is lard's least healthy feature). The omega-3:6 ratio depends on how the pig was raised, but is typically skewed more toward omega-6.
So what does that leave us with? 66% fats that we're told are heart-healthy, and 30% non-stearic saturated fats that are supposed to be unhealthy. But if you still believe saturated fats cause heart disease, check out this post, this one and this one.
Lard also contains a small amount of vitamin D. The sun is the best source of vitamin D, since your skin synthesizes it when it's exposed to UVB. But due to the low angle of the sun in winter, and the fact that many people don't spend enough time outdoors even in the summer, extra vitamin D in the diet is helpful.
I think you can see that lard's bad reputation is undeserved. It may be a legacy of the time when hydrogenated vegetable oils were competing with animal fats for the food market.
There is such a thing as unhealthy lard, however. It's the stuff you might find at the grocery store. Store-bought lard is often hydrogenated to make it more shelf-stable. It also comes from confinement-raised pork operations, which aside from being profoundly inhumane, do not allow access to the outdoors. Thus, the fat won't contain vitamin D.
In the next post, I'll talk about how to buy pasture-raised lard and render it yourself.
The fatty acid profile of lard might give us a clue. A major portion of lard is monounsaturated, 40% by weight. This is the same type of fat that predominates in olive oil (73%), and which is widely recommended by mainstream nutrition experts. Another prevalent class of fat in lard is saturated, at 48%. More than one third of this saturated fat is stearic acid, which even the most hardened lipophobe will agree has a "favorable" effect on blood lipids. Then there's the 8% polyunsaturated fat, which has been the darling of mainstream heart disease research for decades due to its ability to lower blood cholesterol (for the record, I believe the polyunsaturate content is lard's least healthy feature). The omega-3:6 ratio depends on how the pig was raised, but is typically skewed more toward omega-6.
So what does that leave us with? 66% fats that we're told are heart-healthy, and 30% non-stearic saturated fats that are supposed to be unhealthy. But if you still believe saturated fats cause heart disease, check out this post, this one and this one.
Lard also contains a small amount of vitamin D. The sun is the best source of vitamin D, since your skin synthesizes it when it's exposed to UVB. But due to the low angle of the sun in winter, and the fact that many people don't spend enough time outdoors even in the summer, extra vitamin D in the diet is helpful.
I think you can see that lard's bad reputation is undeserved. It may be a legacy of the time when hydrogenated vegetable oils were competing with animal fats for the food market.
There is such a thing as unhealthy lard, however. It's the stuff you might find at the grocery store. Store-bought lard is often hydrogenated to make it more shelf-stable. It also comes from confinement-raised pork operations, which aside from being profoundly inhumane, do not allow access to the outdoors. Thus, the fat won't contain vitamin D.
In the next post, I'll talk about how to buy pasture-raised lard and render it yourself.
The L-word
That's right, ladies and gentlemen: lard. The word alone makes lipophobes cringe like a vampire from garlic. It also makes epicures salivate. But why is lard so unhealthy? Let's take a look.
The fatty acid profile of lard might give us a clue. A major portion of lard is monounsaturated, 40% by weight. This is the same type of fat that predominates in olive oil (73%), and which is widely recommended by mainstream nutrition experts. Another prevalent class of fat in lard is saturated, at 48%. More than one third of this saturated fat is stearic acid, which even the most hardened lipophobe will agree has a "favorable" effect on blood lipids. Then there's the 8% polyunsaturated fat, which has been the darling of mainstream heart disease research for decades due to its ability to lower blood cholesterol (for the record, I believe the polyunsaturate content is lard's least healthy feature). The omega-3:6 ratio depends on how the pig was raised, but is typically skewed more toward omega-6.
So what does that leave us with? 66% fats that we're told are heart-healthy, and 30% non-stearic saturated fats that are supposed to be unhealthy. But if you still believe saturated fats cause heart disease, check out this post, this one and this one.
Lard also contains a small amount of vitamin D. The sun is the best source of vitamin D, since your skin synthesizes it when it's exposed to UVB. But due to the low angle of the sun in winter, and the fact that many people don't spend enough time outdoors even in the summer, extra vitamin D in the diet is helpful.
I think you can see that lard's bad reputation is undeserved. It may be a legacy of the time when hydrogenated vegetable oils were competing with animal fats for the food market.
There is such a thing as unhealthy lard, however. It's the stuff you might find at the grocery store. Store-bought lard is often hydrogenated to make it more shelf-stable. It also comes from confinement-raised pork operations, which aside from being profoundly inhumane, do not allow access to the outdoors. Thus, the fat won't contain vitamin D.
In the next post, I'll talk about how to buy pasture-raised lard and render it yourself.
The fatty acid profile of lard might give us a clue. A major portion of lard is monounsaturated, 40% by weight. This is the same type of fat that predominates in olive oil (73%), and which is widely recommended by mainstream nutrition experts. Another prevalent class of fat in lard is saturated, at 48%. More than one third of this saturated fat is stearic acid, which even the most hardened lipophobe will agree has a "favorable" effect on blood lipids. Then there's the 8% polyunsaturated fat, which has been the darling of mainstream heart disease research for decades due to its ability to lower blood cholesterol (for the record, I believe the polyunsaturate content is lard's least healthy feature). The omega-3:6 ratio depends on how the pig was raised, but is typically skewed more toward omega-6.
So what does that leave us with? 66% fats that we're told are heart-healthy, and 30% non-stearic saturated fats that are supposed to be unhealthy. But if you still believe saturated fats cause heart disease, check out this post, this one and this one.
Lard also contains a small amount of vitamin D. The sun is the best source of vitamin D, since your skin synthesizes it when it's exposed to UVB. But due to the low angle of the sun in winter, and the fact that many people don't spend enough time outdoors even in the summer, extra vitamin D in the diet is helpful.
I think you can see that lard's bad reputation is undeserved. It may be a legacy of the time when hydrogenated vegetable oils were competing with animal fats for the food market.
There is such a thing as unhealthy lard, however. It's the stuff you might find at the grocery store. Store-bought lard is often hydrogenated to make it more shelf-stable. It also comes from confinement-raised pork operations, which aside from being profoundly inhumane, do not allow access to the outdoors. Thus, the fat won't contain vitamin D.
In the next post, I'll talk about how to buy pasture-raised lard and render it yourself.
The L-word
That's right, ladies and gentlemen: lard. The word alone makes lipophobes cringe like a vampire from garlic. It also makes epicures salivate. But why is lard so unhealthy? Let's take a look.
The fatty acid profile of lard might give us a clue. A major portion of lard is monounsaturated, 40% by weight. This is the same type of fat that predominates in olive oil (73%), and which is widely recommended by mainstream nutrition experts. Another prevalent class of fat in lard is saturated, at 48%. More than one third of this saturated fat is stearic acid, which even the most hardened lipophobe will agree has a "favorable" effect on blood lipids. Then there's the 8% polyunsaturated fat, which has been the darling of mainstream heart disease research for decades due to its ability to lower blood cholesterol (for the record, I believe the polyunsaturate content is lard's least healthy feature). The omega-3:6 ratio depends on how the pig was raised, but is typically skewed more toward omega-6.
So what does that leave us with? 66% fats that we're told are heart-healthy, and 30% non-stearic saturated fats that are supposed to be unhealthy. But if you still believe saturated fats cause heart disease, check out this post, this one and this one.
Lard also contains a small amount of vitamin D. The sun is the best source of vitamin D, since your skin synthesizes it when it's exposed to UVB. But due to the low angle of the sun in winter, and the fact that many people don't spend enough time outdoors even in the summer, extra vitamin D in the diet is helpful.
I think you can see that lard's bad reputation is undeserved. It may be a legacy of the time when hydrogenated vegetable oils were competing with animal fats for the food market.
There is such a thing as unhealthy lard, however. It's the stuff you might find at the grocery store. Store-bought lard is often hydrogenated to make it more shelf-stable. It also comes from confinement-raised pork operations, which aside from being profoundly inhumane, do not allow access to the outdoors. Thus, the fat won't contain vitamin D.
In the next post, I'll talk about how to buy pasture-raised lard and render it yourself.
The fatty acid profile of lard might give us a clue. A major portion of lard is monounsaturated, 40% by weight. This is the same type of fat that predominates in olive oil (73%), and which is widely recommended by mainstream nutrition experts. Another prevalent class of fat in lard is saturated, at 48%. More than one third of this saturated fat is stearic acid, which even the most hardened lipophobe will agree has a "favorable" effect on blood lipids. Then there's the 8% polyunsaturated fat, which has been the darling of mainstream heart disease research for decades due to its ability to lower blood cholesterol (for the record, I believe the polyunsaturate content is lard's least healthy feature). The omega-3:6 ratio depends on how the pig was raised, but is typically skewed more toward omega-6.
So what does that leave us with? 66% fats that we're told are heart-healthy, and 30% non-stearic saturated fats that are supposed to be unhealthy. But if you still believe saturated fats cause heart disease, check out this post, this one and this one.
Lard also contains a small amount of vitamin D. The sun is the best source of vitamin D, since your skin synthesizes it when it's exposed to UVB. But due to the low angle of the sun in winter, and the fact that many people don't spend enough time outdoors even in the summer, extra vitamin D in the diet is helpful.
I think you can see that lard's bad reputation is undeserved. It may be a legacy of the time when hydrogenated vegetable oils were competing with animal fats for the food market.
There is such a thing as unhealthy lard, however. It's the stuff you might find at the grocery store. Store-bought lard is often hydrogenated to make it more shelf-stable. It also comes from confinement-raised pork operations, which aside from being profoundly inhumane, do not allow access to the outdoors. Thus, the fat won't contain vitamin D.
In the next post, I'll talk about how to buy pasture-raised lard and render it yourself.
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