Many athletes have begun to use a strange and alarming array of legal drugs to keep themselves competitive.
Viagra works by relaxing muscles and increasing blood flow through the body, so some athletes take it to help their game, believing that it will improve lung function by increasing oxygenation of the blood to the lungs.
Other athletes take Human Growth Hormone, which can increase metabolism and protein synthesis during exercise, or even ingest baking soda, a practice called “soda doping”, to improve performance.
Sources:
* ABC News June 12, 2008
Showing posts with label Protein. Show all posts
Showing posts with label Protein. Show all posts
3 June 2008
Why You Need to Stretch During Pregnancy
Stretching exercises may be more effective at reducing the risk of preeclampsia than walking for pregnant women who have already experienced the condition and who do not follow a workout routine.
Preeclampsia, or pregnancy-induced hypertension, is among the leading causes of maternal and fetal illness and death worldwide.
Previous studies and literature have suggested that rigorous exercise is the most effective way to reduce the risk of preeclampsia. However, at the end of a recent study, almost 15 percent of women who exercised by walking developed preeclampsia, while less than 5 percent in a group that stretched instead developed the condition.
Stretching my provide protection against preeclampsia by causing the body to produce transferrin, a plasma protein that transports iron through the blood and protects against oxidative stress on the body.
Sources:
* Eurekalert May 28, 2008
Preeclampsia, or pregnancy-induced hypertension, is among the leading causes of maternal and fetal illness and death worldwide.
Previous studies and literature have suggested that rigorous exercise is the most effective way to reduce the risk of preeclampsia. However, at the end of a recent study, almost 15 percent of women who exercised by walking developed preeclampsia, while less than 5 percent in a group that stretched instead developed the condition.
Stretching my provide protection against preeclampsia by causing the body to produce transferrin, a plasma protein that transports iron through the blood and protects against oxidative stress on the body.
Sources:
* Eurekalert May 28, 2008
21 May 2008
Eating Too Much Fat Disrupts Body's Internal Clock, Disrupts Appetite Control
A high-fat diet quickly causes changes to the body's internal clock, which can throw off appetite regulation, according to a new study conducted by researchers at Northwestern University and Evanston Northwestern Healthcare in Illinois. Published in the journal Cell Metabolism, the study was funded by the National Institutes of Health and by grants from Amylin Pharmaceuticals and Eli Lilly and Co.
"The effect can be seen quite rapidly - within a matter of days," lead researcher Joe Bass said.
Researchers conducted the study on two separate groups of mice that were kept in total darkness. Both groups were fed a normal diet for two weeks. Then one group continued with the normal diet, while the other mice were placed on a high-fat diet in which 45 percent of their calories came from fat.
The mice were kept in darkness to prevent light levels and other external cues from being able to act as regulators on their internal clocks.
Known as a circadian clock, the body's internal time regulator is responsible for sending out time-related signals such as hunger, sleepiness and wakefulness. Prior studies have indicated that a poorly regulated circadian clock is associated with an increased risk of obesity and diabetes.
The researchers found that mice on the high-fat diet began to eat and rest at inappropriate times relative to the mice in the control group. These changes took place after only two weeks. These changes appeared to be related to modifications in the expression of the genes that regulate the circadian clock.
"What we found was the expression of the genes that encode the clock is altered under high-fat diets," Bass said. "It is as if the diet erodes away the clock or causes it to rust. It erodes the abundance of the proteins in the cells."
"If you give a mouse a high-fat diet, they will eat excessive amounts," he said. "It is the same thing as human eating at McDonald's or eating too much at a Thanksgiving dinner."
###
"The effect can be seen quite rapidly - within a matter of days," lead researcher Joe Bass said.
Researchers conducted the study on two separate groups of mice that were kept in total darkness. Both groups were fed a normal diet for two weeks. Then one group continued with the normal diet, while the other mice were placed on a high-fat diet in which 45 percent of their calories came from fat.
The mice were kept in darkness to prevent light levels and other external cues from being able to act as regulators on their internal clocks.
Known as a circadian clock, the body's internal time regulator is responsible for sending out time-related signals such as hunger, sleepiness and wakefulness. Prior studies have indicated that a poorly regulated circadian clock is associated with an increased risk of obesity and diabetes.
The researchers found that mice on the high-fat diet began to eat and rest at inappropriate times relative to the mice in the control group. These changes took place after only two weeks. These changes appeared to be related to modifications in the expression of the genes that regulate the circadian clock.
"What we found was the expression of the genes that encode the clock is altered under high-fat diets," Bass said. "It is as if the diet erodes away the clock or causes it to rust. It erodes the abundance of the proteins in the cells."
"If you give a mouse a high-fat diet, they will eat excessive amounts," he said. "It is the same thing as human eating at McDonald's or eating too much at a Thanksgiving dinner."
###
16 May 2008
Do You Have a Lactose-Intolerant Child?
I have many stressed-out mothers in my practice who are convinced that their children are intolerant to cow’s milk-based formulas. I explain that children are rarely born lactose intolerant and most likely their son or daughter has an allergy to processed, pasteurized cow’s milk. I usually try to get the mother to exclusively breast feed and not supplement with a commercial formula, which usually fixes the problem because human breast milk is the perfect food for infants.
However, if breast milk was never started, a soy milk formula is often recommended because it’s not a cow-based milk. There can be a problem with that since 30 percent of the children are also allergic to soymilk, and soymilk presents its own challenges. (Visit www.westonaprice.org to learn about the potential dangers of soy-based formulas.) In these cases, we often have to resort to elemental formulas on the market.
I also tell the parent that when the child is older and weaned off the breast, I recommend trying goat’s milk before they try cow’s milk again. Children manifest an allergy to cow’s milk formula by gastrointestinal symptoms through vomiting and diarrhea, respiratory symptoms like constant sneezing, coughing, and congestion, and even with skin complications, like eczema. Those who are highly allergic need to use goat’s milk or another formula, like Jordan’s homemade formula.
My response is that nearly all infants drink breast milk—their tender stomachs can’t handle any solid foods—but breast milk has lactose. So breast milk, a food that nourishes and sustains newborns and infants while carrying the mother’s antibodies to the baby, is obviously a good thing.
When infants are weaned from breast milk, they are fed formula—a highly processed dried dairy product made from cows that are not fed well or raised properly. Babies sometimes react poorly to commercial formula by screaming to the high heavens, prompting concerned mothers to immediately blame “lactose intolerance” as the cause of their child’s ills.
Many switch to soymilk or a soy-based formula, but as I stated earlier I’m not a total fan of soy products. Here's why: most soy protein comes from genetically modified soybeans. According to Sally Fallon, author of Nourishing Traditions, soybeans are high in phytic acid, which can block the complete intake of essential minerals like calcium, magnesium, copper, iron, and zinc into the intestinal tract. Soy protein must be processed at high temperatures to reduce phytic acid levels, which pretty much destroys the “good proteins” in soy, such as lysine.
Ms. Fallon also points out research showing that soy formulas lack cholesterol (essential for brain development) and lactose and galactose, which play equally important roles in the development of the nervous system.
Most children are not lactose intolerant; otherwise they couldn’t tolerate breast milk. The reason for their stomach distress has more to do with an allergy or sensitivity to the processed protein in the formula, not any abdominal intolerance to lactose.
If your child does not respond well to conventional infant formulas, look for a natural and organic infant formula at your local health food store or try Jordan’s formula recipe found in this issue’s recipe section.
by Dr. Fiona Blair, contributing author for Jordan Rubin’s Children’s Health book
However, if breast milk was never started, a soy milk formula is often recommended because it’s not a cow-based milk. There can be a problem with that since 30 percent of the children are also allergic to soymilk, and soymilk presents its own challenges. (Visit www.westonaprice.org to learn about the potential dangers of soy-based formulas.) In these cases, we often have to resort to elemental formulas on the market.
I also tell the parent that when the child is older and weaned off the breast, I recommend trying goat’s milk before they try cow’s milk again. Children manifest an allergy to cow’s milk formula by gastrointestinal symptoms through vomiting and diarrhea, respiratory symptoms like constant sneezing, coughing, and congestion, and even with skin complications, like eczema. Those who are highly allergic need to use goat’s milk or another formula, like Jordan’s homemade formula.
My response is that nearly all infants drink breast milk—their tender stomachs can’t handle any solid foods—but breast milk has lactose. So breast milk, a food that nourishes and sustains newborns and infants while carrying the mother’s antibodies to the baby, is obviously a good thing.
When infants are weaned from breast milk, they are fed formula—a highly processed dried dairy product made from cows that are not fed well or raised properly. Babies sometimes react poorly to commercial formula by screaming to the high heavens, prompting concerned mothers to immediately blame “lactose intolerance” as the cause of their child’s ills.
Many switch to soymilk or a soy-based formula, but as I stated earlier I’m not a total fan of soy products. Here's why: most soy protein comes from genetically modified soybeans. According to Sally Fallon, author of Nourishing Traditions, soybeans are high in phytic acid, which can block the complete intake of essential minerals like calcium, magnesium, copper, iron, and zinc into the intestinal tract. Soy protein must be processed at high temperatures to reduce phytic acid levels, which pretty much destroys the “good proteins” in soy, such as lysine.
Ms. Fallon also points out research showing that soy formulas lack cholesterol (essential for brain development) and lactose and galactose, which play equally important roles in the development of the nervous system.
Most children are not lactose intolerant; otherwise they couldn’t tolerate breast milk. The reason for their stomach distress has more to do with an allergy or sensitivity to the processed protein in the formula, not any abdominal intolerance to lactose.
If your child does not respond well to conventional infant formulas, look for a natural and organic infant formula at your local health food store or try Jordan’s formula recipe found in this issue’s recipe section.
by Dr. Fiona Blair, contributing author for Jordan Rubin’s Children’s Health book
8 May 2008
New Studies Find Calcium and Vitamin D May Prevent Colon Cancer
Specific vitamins and minerals in the diet appear to prevent the development of colon cancer. However, too much iron may cause malignancies to grow. Emory University scientists recently announced these findings, based on biological markers that influence colon cancer risk, at the American Association for Cancer Research meeting in San Diego.
Earlier studies have suggested that calcium and vitamin D reduce colon cancer risk and the new Emory data may explain why. In a clinical study of 92 patients, the researchers found that diets supplemented with calcium and vitamin D increase the levels of a protein called Bax which "turns on" the programmed death of pre-cancerous cells in the colon, according to Emory researcher Veronika Fedirko.
"We were pleased that the effects of calcium and vitamin D were visible enough in this small study to be significant and reportable. We will have to fully evaluate each marker's strength as we accumulate more data," Fedirko stated.
In other related Emory research, a 200 patient case-control study found high levels of calcium and vitamin D together are associated with increased levels of E-cadherin, the main adhesion molecule of epithelial cells (cells that line internal and external body surfaces, including the inside of blood vessels and small cavities). Loss of E-cadherin mediated adhesion is known to contribute to the change from benign lesions to invasive, metastatic cancer, so an increase of the molecule could protect from colon cancer.
The studies, which used colorectal biopsy samples, are part of a larger effort to identify a host of measurements that together can estimate a person's risk of developing colon cancer. "We want to have the equivalent of measuring cholesterol or high blood pressure, but for colon cancer instead of heart disease," said Roberd Bostick, MD, MPH, professor of epidemiology at Emory's Rollins School of Public Health. "These measurements will describe the climate of risk in the colon rather than spotting individual tumors or cells that may become tumors."
Another Emory study shows that one mineral, iron, in excess might up the risk of colon cancer. High levels of dietary iron were linked to low levels of APC, a protein whose absence in colon cancer cells leads to their runaway growth. Although iron is a necessary nutrient, it is needed only in small amounts. Previous research has shown that when too much iron is absorbed, it is associated with an increased risk for heart disease as well as cancer.
Bostick and his research team are participating in a ten-year multi-center study of the effects of increased vitamin D and calcium and biomarker-guided treatment of colon cancer recurrence. The study involves close to 2,500 people throughout the U.S. who have regular colonoscopies.
Bostick is currently working on the development of non-invasive blood and urine tests for colon cancer risk ((http://whsc.emory.edu/_pubs/hsc/winter0...) .
Most cases of colon cancer begin as small, benign clumps of cells called adenomatous polyps that, over time, transform into colon cancers. About 112,000 people are diagnosed with colon cancer annually according to the American Cancer Society.
About the author
Sherry Baker is a widely published writer whose work has appeared in Newsweek, Health, the Atlanta Journal and Constitution, Yoga Journal, Optometry, Atlanta, Arthritis Today, Natural Healing Newsletter, OMNI, UCLA's "Healthy Years" newsletter, Mount Sinai School of Medicine's "Focus on Health Aging" newsletter, the Cleveland Clinic's "Men's Health Advisor" newsletter and many others.
Earlier studies have suggested that calcium and vitamin D reduce colon cancer risk and the new Emory data may explain why. In a clinical study of 92 patients, the researchers found that diets supplemented with calcium and vitamin D increase the levels of a protein called Bax which "turns on" the programmed death of pre-cancerous cells in the colon, according to Emory researcher Veronika Fedirko.
"We were pleased that the effects of calcium and vitamin D were visible enough in this small study to be significant and reportable. We will have to fully evaluate each marker's strength as we accumulate more data," Fedirko stated.
In other related Emory research, a 200 patient case-control study found high levels of calcium and vitamin D together are associated with increased levels of E-cadherin, the main adhesion molecule of epithelial cells (cells that line internal and external body surfaces, including the inside of blood vessels and small cavities). Loss of E-cadherin mediated adhesion is known to contribute to the change from benign lesions to invasive, metastatic cancer, so an increase of the molecule could protect from colon cancer.
The studies, which used colorectal biopsy samples, are part of a larger effort to identify a host of measurements that together can estimate a person's risk of developing colon cancer. "We want to have the equivalent of measuring cholesterol or high blood pressure, but for colon cancer instead of heart disease," said Roberd Bostick, MD, MPH, professor of epidemiology at Emory's Rollins School of Public Health. "These measurements will describe the climate of risk in the colon rather than spotting individual tumors or cells that may become tumors."
Another Emory study shows that one mineral, iron, in excess might up the risk of colon cancer. High levels of dietary iron were linked to low levels of APC, a protein whose absence in colon cancer cells leads to their runaway growth. Although iron is a necessary nutrient, it is needed only in small amounts. Previous research has shown that when too much iron is absorbed, it is associated with an increased risk for heart disease as well as cancer.
Bostick and his research team are participating in a ten-year multi-center study of the effects of increased vitamin D and calcium and biomarker-guided treatment of colon cancer recurrence. The study involves close to 2,500 people throughout the U.S. who have regular colonoscopies.
Bostick is currently working on the development of non-invasive blood and urine tests for colon cancer risk ((http://whsc.emory.edu/_pubs/hsc/winter0...) .
Most cases of colon cancer begin as small, benign clumps of cells called adenomatous polyps that, over time, transform into colon cancers. About 112,000 people are diagnosed with colon cancer annually according to the American Cancer Society.
About the author
Sherry Baker is a widely published writer whose work has appeared in Newsweek, Health, the Atlanta Journal and Constitution, Yoga Journal, Optometry, Atlanta, Arthritis Today, Natural Healing Newsletter, OMNI, UCLA's "Healthy Years" newsletter, Mount Sinai School of Medicine's "Focus on Health Aging" newsletter, the Cleveland Clinic's "Men's Health Advisor" newsletter and many others.
7 May 2008
Obesity Can Inflame Your Heart
Heart specialists have uncovered what is believed to be the first wide-scale evidence linking severe obesity to prolonged inflammation of heart tissue. The Multiethnic Study of Atherosclerosis (MESA) demonstrates yet one more reason for the estimated 72 million obese American adults to be concerned about their health.
Researchers conducted tests and tracked the development of heart failure in an ethnically diverse group of nearly 7,000 men and women. On average, obese participants were found to have higher blood levels of interleukin 6, C-reactive protein and fibrinogen, which are all immune system proteins involved in inflammation.
A near doubling of average interleukin 6 levels alone accounted for an 84 percent greater risk of developing heart failure in the study population. Similarly, a near tripling of average levels of C-reactive protein in obese study participants increased the chance of heart failure by 36 percent.
Sources:
* Science Daily May 1, 2008
Researchers conducted tests and tracked the development of heart failure in an ethnically diverse group of nearly 7,000 men and women. On average, obese participants were found to have higher blood levels of interleukin 6, C-reactive protein and fibrinogen, which are all immune system proteins involved in inflammation.
A near doubling of average interleukin 6 levels alone accounted for an 84 percent greater risk of developing heart failure in the study population. Similarly, a near tripling of average levels of C-reactive protein in obese study participants increased the chance of heart failure by 36 percent.
Sources:
* Science Daily May 1, 2008
6 May 2008
(NaturalNews) Patients who take the cholesterol drug torcetrapid, intended to increase levels of HDL ("good") cholesterol and lower LDL ("bad") cholesterol levels, have a 58 percent higher risk of death than similar patients who do not take the drug, according to a study led by researchers at the Heart Research Institute in Sydney and published in the New England Journal of Medicine.
Researchers studied 15,067 participants, all considered to be at high risk of cardiovascular disease. All the patients were treated with the cholesterol-lowering drug atorvastatin, while half were also treated with torcetrapid.
Torcetrapid is marketed by Pfizer, as is atorvastatin (under the brand name Lipitor).
Patients receiving both drugs had a 58 percent higher chance of dying and a 25 percent higher chance of experiencing cardiovascular events such as heart attacks than those who were treated only with atorvastatin.
Torcetrapid is one of a new class of drugs called cholesteryl ester transfer protein (CETP) inhibitors. Unlike older cholesterol drugs, which only lower LDL levels, CETP inhibitors are intended to raise HDL levels at the same time. The drugs function by blocking the action of a protein that transfers cholesterol from HDL to LDL, thus forcing the cholesterol to remain in HDL form.
In the recent study, torcetrapid was found to raise HDL levels by an average of 72.1 percent, and lower LDL levels by an average of 24.9 percent.
Scientists are still unclear why torcetrapid appears to increase patient death rates and heart attack risk. While the drug is known to raise blood pressure, many of the patients who died in the recent study actually had blood pressure levels below normal.
Researchers have hypothesized that the drug may increase the levels of a hormone involved in regulating blood pressure, and that this may lead to stress on the cardiovascular system.
Merck and Roche Holding have placed the development of their own CETP inhibitors on hold, pending the results of further trials on torcetrapid.
Researchers studied 15,067 participants, all considered to be at high risk of cardiovascular disease. All the patients were treated with the cholesterol-lowering drug atorvastatin, while half were also treated with torcetrapid.
Torcetrapid is marketed by Pfizer, as is atorvastatin (under the brand name Lipitor).
Patients receiving both drugs had a 58 percent higher chance of dying and a 25 percent higher chance of experiencing cardiovascular events such as heart attacks than those who were treated only with atorvastatin.
Torcetrapid is one of a new class of drugs called cholesteryl ester transfer protein (CETP) inhibitors. Unlike older cholesterol drugs, which only lower LDL levels, CETP inhibitors are intended to raise HDL levels at the same time. The drugs function by blocking the action of a protein that transfers cholesterol from HDL to LDL, thus forcing the cholesterol to remain in HDL form.
In the recent study, torcetrapid was found to raise HDL levels by an average of 72.1 percent, and lower LDL levels by an average of 24.9 percent.
Scientists are still unclear why torcetrapid appears to increase patient death rates and heart attack risk. While the drug is known to raise blood pressure, many of the patients who died in the recent study actually had blood pressure levels below normal.
Researchers have hypothesized that the drug may increase the levels of a hormone involved in regulating blood pressure, and that this may lead to stress on the cardiovascular system.
Merck and Roche Holding have placed the development of their own CETP inhibitors on hold, pending the results of further trials on torcetrapid.
22 April 2008
Managing Arthritis With Diet and Exercise
Positive Lifestyle Changes Can Help You Take Control of Your Arthritis
By STEFAN ASCHAN
"I'll jump out this window before I do any of those exercises today."
Yes, it's a fact that pain can drive you insane, affecting your mood, productivity and even how you express yourself. When you are in pain, the only thing that you are interested in is relief.
Many will automatically reach for pain medication. Yet, is it always necessary to do so? Are there any other solutions that might work just as well, or even better?
To answer this question in relation to arthritis, it might help to take a closer look at what arthritis is and why it is such a painful condition.
A healthy joint consists of strong bones, each with a healthy complement of cartilage, to ease the friction between the ends of the bones when movement occurs. To further this aim, a sac containing synovial fluid also lubricates the joint for smooth function.
It's an elegant system. But overuse and nutritional imbalances can lead to a breakdown of the cartilages, leading to painful friction. This is when arthritis occurs.
A Closer Look at Arthritis
In general, there are two different kinds of joint pain which are classified as arthritis: osteoarthritis and rheumatoid arthritis.
Osteoarthritis also known as degenerative joint disease involves deterioration of the cartilage protecting the ends of the bones. It can be caused by injury, or through an inherited protein defect that causes improper formation of this cartilage. But this kind of arthritis is most commonly blamed on wear-and-tear of the joint through lifestyle, diet and aging.
Rheumatoid arthritis, on the other hand, is an autoimmune disorder. This kind of arthritis develops because the immune system identifies the synovial membrane as foreign. Inflammation results, which damages the cartilage in and around the joint. Fever, fatigue, swelling, weight loss and crippling pain are some of the hallmark signs of rheumatoid arthritis. This type of arthritis also tends to develop all over the body, which makes it particularly difficult.
For either of these conditions, however, a change in lifestyle and diet might help.
Supplements: a Key to Fighting Arthritis?
The potential of supplements to help combat the pain and loss of function that accompanies arthritis is a matter of contention. When it comes to solid, research-proven benefits, the jury is still out. Yet, many swear by certain supplements for this condition. Here are just a few examples:
Bromelain is an enzyme that is thought to help to stimulate the production of prostaglandins, which reduce inflammation. This supplement is often taken between meals.
Essential fatty acids are another nutrient that may help generate prostaglandins, according to some studies. Essential fatty acids such as omega-3 and omega-6 increase production and activity of anti-inflammatory prostaglandins.
Glucosamine and SAMe are thought by some to be important in the formation of the tissues around the joint and fluids. Yet, many have argued against taking these supplements, maintaining that there is no proof that these substances are stored by the body where they are needed.
Yet, the best supplement of all to implement is proper food. Proper, nutritious food has yielded health effects that surpass any kind of supplement that you can take into your body.
Exercising for Pain Relief
You probably thought that you would get away without hearing about exercise when it comes to arthritis relief, right? Well, you're wrong!
Many people with arthritis experience pain not only when they move, but they also experience stiffness soreness in the body after long periods of sitting. One individual with those issues recently told me, "I walk fairly regularly, but I do not do anything else fitness-wise no machines, no weights, floor exercises, exercise balls or classes."
Sorry, but walking is not just enough to improve your condition. Exercises, including activities that engage the full body, are recommended for individuals with arthritis. This is not just to help joint mobility, or to prevent loss of lean muscle tissue through the aging process, or to maintain strength, or to reduce pain and stiffness, or even to mobilize stiff or contracted joints. The most important benefit of this activity is that it helps people with arthritis to stay independent.
Of course, the type of exercise performed needs to be done with due consideration to each individual's stage of arthritis. Yes, it will be sometimes challenging because of fatigue and discomfort following an exercise program. Hence, it is important to find the right balance for your condition. But don't shy away from physical activity; our body's systems are designed to move, and when you stop moving that system starts to fall apart.
Here are a few guidelines for working with pain and stiffness:
Do low-impact activities, which includes walking, speed walking, swimming and lifting weights.
Put all joints through the full range of motion at least once a day, according to your ability. If you need help starting out, hire a personal trainer who can assist you.
Emphasize proper body alignment at all times. As a rule, your toe, ankle, knee, hip and shoulder should be in one line if you look at yourself in front of a mirror.
Modify the intensity on days where you have flare-ups.
Take enough time for warm-up. Prepare your body for your workout activities to come.
It is up to you and your doctor to decide whether you will require supervision of a healthcare practitioner to exercise with arthritis.
But please make an effort to stay mobile, in shape and independent. These days, we are living to 80, 90 and 100. Preparation for your life at that age does not just happen overnight; it is a process. And your progress should start now.
http://www.stefanaschan.com/
By STEFAN ASCHAN
"I'll jump out this window before I do any of those exercises today."
Yes, it's a fact that pain can drive you insane, affecting your mood, productivity and even how you express yourself. When you are in pain, the only thing that you are interested in is relief.
Many will automatically reach for pain medication. Yet, is it always necessary to do so? Are there any other solutions that might work just as well, or even better?
To answer this question in relation to arthritis, it might help to take a closer look at what arthritis is and why it is such a painful condition.
A healthy joint consists of strong bones, each with a healthy complement of cartilage, to ease the friction between the ends of the bones when movement occurs. To further this aim, a sac containing synovial fluid also lubricates the joint for smooth function.
It's an elegant system. But overuse and nutritional imbalances can lead to a breakdown of the cartilages, leading to painful friction. This is when arthritis occurs.
A Closer Look at Arthritis
In general, there are two different kinds of joint pain which are classified as arthritis: osteoarthritis and rheumatoid arthritis.
Osteoarthritis also known as degenerative joint disease involves deterioration of the cartilage protecting the ends of the bones. It can be caused by injury, or through an inherited protein defect that causes improper formation of this cartilage. But this kind of arthritis is most commonly blamed on wear-and-tear of the joint through lifestyle, diet and aging.
Rheumatoid arthritis, on the other hand, is an autoimmune disorder. This kind of arthritis develops because the immune system identifies the synovial membrane as foreign. Inflammation results, which damages the cartilage in and around the joint. Fever, fatigue, swelling, weight loss and crippling pain are some of the hallmark signs of rheumatoid arthritis. This type of arthritis also tends to develop all over the body, which makes it particularly difficult.
For either of these conditions, however, a change in lifestyle and diet might help.
Supplements: a Key to Fighting Arthritis?
The potential of supplements to help combat the pain and loss of function that accompanies arthritis is a matter of contention. When it comes to solid, research-proven benefits, the jury is still out. Yet, many swear by certain supplements for this condition. Here are just a few examples:
Bromelain is an enzyme that is thought to help to stimulate the production of prostaglandins, which reduce inflammation. This supplement is often taken between meals.
Essential fatty acids are another nutrient that may help generate prostaglandins, according to some studies. Essential fatty acids such as omega-3 and omega-6 increase production and activity of anti-inflammatory prostaglandins.
Glucosamine and SAMe are thought by some to be important in the formation of the tissues around the joint and fluids. Yet, many have argued against taking these supplements, maintaining that there is no proof that these substances are stored by the body where they are needed.
Yet, the best supplement of all to implement is proper food. Proper, nutritious food has yielded health effects that surpass any kind of supplement that you can take into your body.
Exercising for Pain Relief
You probably thought that you would get away without hearing about exercise when it comes to arthritis relief, right? Well, you're wrong!
Many people with arthritis experience pain not only when they move, but they also experience stiffness soreness in the body after long periods of sitting. One individual with those issues recently told me, "I walk fairly regularly, but I do not do anything else fitness-wise no machines, no weights, floor exercises, exercise balls or classes."
Sorry, but walking is not just enough to improve your condition. Exercises, including activities that engage the full body, are recommended for individuals with arthritis. This is not just to help joint mobility, or to prevent loss of lean muscle tissue through the aging process, or to maintain strength, or to reduce pain and stiffness, or even to mobilize stiff or contracted joints. The most important benefit of this activity is that it helps people with arthritis to stay independent.
Of course, the type of exercise performed needs to be done with due consideration to each individual's stage of arthritis. Yes, it will be sometimes challenging because of fatigue and discomfort following an exercise program. Hence, it is important to find the right balance for your condition. But don't shy away from physical activity; our body's systems are designed to move, and when you stop moving that system starts to fall apart.
Here are a few guidelines for working with pain and stiffness:
Do low-impact activities, which includes walking, speed walking, swimming and lifting weights.
Put all joints through the full range of motion at least once a day, according to your ability. If you need help starting out, hire a personal trainer who can assist you.
Emphasize proper body alignment at all times. As a rule, your toe, ankle, knee, hip and shoulder should be in one line if you look at yourself in front of a mirror.
Modify the intensity on days where you have flare-ups.
Take enough time for warm-up. Prepare your body for your workout activities to come.
It is up to you and your doctor to decide whether you will require supervision of a healthcare practitioner to exercise with arthritis.
But please make an effort to stay mobile, in shape and independent. These days, we are living to 80, 90 and 100. Preparation for your life at that age does not just happen overnight; it is a process. And your progress should start now.
http://www.stefanaschan.com/
2 April 2008
Message from Dr Lau: My book
Sometime ago, I read somewhere that the birth of a book is no different from the birth of a baby. The author necessarily goes through the same trials, tribulations and birth pangs, as a woman in labor; or perhaps worse, as was experiences with my first book on Curing Scoliosis Naturally.
Since it was my first "pregnancy" the doubts and apprehensions of being able to put my ideas to paper as succinctly as I wanted, weighed heavy on my mind, even as I struggled to brush aside those nagging thoughts and gamely strove to clear all the cobwebs, before rolling up my sleeves to get down to the more serious business of actual writing.
At the outset, since I had no clear agenda or plan in my head, except for my intense desire to help my patients by sharing with them every bit of information that I had painstakingly gathered in my head and through my practical experiences of working with virtually hundreds of scoliosis patients, besides what I randomly picked from medical journals, I decided to begin with an outline, a more formal content plan.
At this point, I decided that I wanted to write not one, but two books, one devoted exclusively to nutritional research --- essentially detailing the good and bad that we derive from food, while dispelling the prevailing myth that there could be a uniform, one-size-fits-all diet for every person on this planet.
In my view, and here I am speak on authority, one of the biggest myth amidst us is that there could be one, “healthy” diet plan for all; a “fix-all” for all health-related problems. On the contrary, as I have explained in my book there is now enough research (I have meticulously marshaled and presented these scientific evidences in my book) to establish that since each one of us is significantly different from the other in terms of genetic make-up and our cultural practices and environmental exposure; our nutritional needs and requirements are also vastly different. Indeed as different as chalk from cheese.
Therefore, if your doctor, dietitian or chiropractor is unable to help you figure out what your exact nutritional requirements are --- in terms of the exact proportion of proteins, fats and carbohydrates that you should be consuming every day --- he/she is doing a disservice to you. Your doctor is in fact also holding back one of the best-kept secrets of the medical world, and that is that diet plans can not be mass marketed and work on everyone.
In my considered vie (and I have strong evidence in support of it) diet plans have to be customized to individual patients in order to be of any use to them. This is as true for patients of scoliosis, as anybody else.
I for all my patients starting a program with me I often struggle to disclose and share all the information I have with these hapless girls and their parents and wish I had some sort of ready literature to thrust into their hands, explaining why bracing or surgery is not effective; and that there could be a much more simpler, easier and a painless way of straightening a curved spine, such as the choice of the right food and a few corrective exercises.
All this marked the first stirrings of an idea in my head.
And that’s how this book, “The Scoliosis Cure” was born. Title needs a bit of work but that will do for now.
Since it was my first "pregnancy" the doubts and apprehensions of being able to put my ideas to paper as succinctly as I wanted, weighed heavy on my mind, even as I struggled to brush aside those nagging thoughts and gamely strove to clear all the cobwebs, before rolling up my sleeves to get down to the more serious business of actual writing.
At the outset, since I had no clear agenda or plan in my head, except for my intense desire to help my patients by sharing with them every bit of information that I had painstakingly gathered in my head and through my practical experiences of working with virtually hundreds of scoliosis patients, besides what I randomly picked from medical journals, I decided to begin with an outline, a more formal content plan.
At this point, I decided that I wanted to write not one, but two books, one devoted exclusively to nutritional research --- essentially detailing the good and bad that we derive from food, while dispelling the prevailing myth that there could be a uniform, one-size-fits-all diet for every person on this planet.
In my view, and here I am speak on authority, one of the biggest myth amidst us is that there could be one, “healthy” diet plan for all; a “fix-all” for all health-related problems. On the contrary, as I have explained in my book there is now enough research (I have meticulously marshaled and presented these scientific evidences in my book) to establish that since each one of us is significantly different from the other in terms of genetic make-up and our cultural practices and environmental exposure; our nutritional needs and requirements are also vastly different. Indeed as different as chalk from cheese.
Therefore, if your doctor, dietitian or chiropractor is unable to help you figure out what your exact nutritional requirements are --- in terms of the exact proportion of proteins, fats and carbohydrates that you should be consuming every day --- he/she is doing a disservice to you. Your doctor is in fact also holding back one of the best-kept secrets of the medical world, and that is that diet plans can not be mass marketed and work on everyone.
In my considered vie (and I have strong evidence in support of it) diet plans have to be customized to individual patients in order to be of any use to them. This is as true for patients of scoliosis, as anybody else.
I for all my patients starting a program with me I often struggle to disclose and share all the information I have with these hapless girls and their parents and wish I had some sort of ready literature to thrust into their hands, explaining why bracing or surgery is not effective; and that there could be a much more simpler, easier and a painless way of straightening a curved spine, such as the choice of the right food and a few corrective exercises.
All this marked the first stirrings of an idea in my head.
And that’s how this book, “The Scoliosis Cure” was born. Title needs a bit of work but that will do for now.
28 March 2008
Re-Growing Organs: the Future is Here
When Lee Spievack sliced off the tip of his finger, his brother Alan, a medical research scientist, sent him a special powder and told him to sprinkle it on the wound. In four weeks, the fingertip grew back completely.
That powder was a substance called extracellular matrix, a mix of protein and connective tissue surgeons use to repair tendons. It signals the body to start the process of tissue regrowth, and holds some of the secrets behind the emerging new science of regenerative medicine.
Many scientists believe that every tissue in the body has cells which are capable of regeneration, and the key is to find enough of those cells and direct them to grow. At least in theory, this process could be used to regrow limbs, organs, and other body parts.
Sources:
* CBS News March 22, 2008
That powder was a substance called extracellular matrix, a mix of protein and connective tissue surgeons use to repair tendons. It signals the body to start the process of tissue regrowth, and holds some of the secrets behind the emerging new science of regenerative medicine.
Many scientists believe that every tissue in the body has cells which are capable of regeneration, and the key is to find enough of those cells and direct them to grow. At least in theory, this process could be used to regrow limbs, organs, and other body parts.
Sources:
* CBS News March 22, 2008
26 March 2008
Message from Dr Lau: Soy
Today Ive posted another article debating the health benefits of soy. From my own personal experiance, soy has never been helpful to my health unless in the fermented state like soya sauce, natto or miso. Due to the high presence of antinutrients that potentially block minerals and the insulin raising effect or this legume, I can confidently say that I feel healthier when i eliminated unfermented soy products like soy milks, tofu etc.
Each person is different and while I am a protein type, those who have a metabolic type closer to a carbo type will be able to handle soy products better. I guess the only one who knows is your own body. So listen to your won body... with some experimentation and guidence with metabolict typing you will be able to find the right foods to eat.
To good health,
Dr Kevin Lau
Each person is different and while I am a protein type, those who have a metabolic type closer to a carbo type will be able to handle soy products better. I guess the only one who knows is your own body. So listen to your won body... with some experimentation and guidence with metabolict typing you will be able to find the right foods to eat.
To good health,
Dr Kevin Lau
Soy Industry Promotes Health Myths to Sell More Soy Products, Says Author
Author Kaayla T. Daniel is challenging what she calls the myth that soy prevents breast cancer. "The truth is that soy protein contains dangerous levels of plant estrogens. Although not identical to human estrogens, these have been proven to increase breast cell proliferation, a widely accepted marker of breast cancer risk." said Daniel, author of "The Whole Soy Story: The Dark Side of America's Favorite Health Food."
"The soy industry consistently plays down the evidence that soy can promote breast cancer," Daniel said. "It is even using Breast Cancer Awareness Month as an excuse to push its products on unsuspecting women."
Daniel disputes the idea that soy is responsible for lower breast cancer rates among those who consume traditional Asian diets. She cites a recent study in the journal "Cancer Causes and Control," which found that Asians who ate more soy did not have lower cancer rates than Asians who ate less.
"The soy industry ... heavily promotes the myth that Asians have lower rates of breast cancer because of soy consumption," Daniel said. "In fact, Asians eat soy in very small quantities, as a condiment in the diet and not as a staple food. What's more, they eat old-fashioned, whole soybean products such as miso, tempeh, natto and tofu, not the new heavily processed products marketed by the soy industry such as soy milk, veggie burgers and 'energy bars.'"
Government officials in Israel and France have concluded that high soy consumption may indeed pose a breast cancer risk. Israeli Health Ministry guidelines recommend that women "exercise caution" in soy consumption, and the French Food Agency has decided to require soy products to contain warning labels.
"The risks are well established," Daniel said. "Soy is clearly not the answer for breast cancer prevention. The evidence is mounting that soy may even be part of the problem."
"The soy industry consistently plays down the evidence that soy can promote breast cancer," Daniel said. "It is even using Breast Cancer Awareness Month as an excuse to push its products on unsuspecting women."
Daniel disputes the idea that soy is responsible for lower breast cancer rates among those who consume traditional Asian diets. She cites a recent study in the journal "Cancer Causes and Control," which found that Asians who ate more soy did not have lower cancer rates than Asians who ate less.
"The soy industry ... heavily promotes the myth that Asians have lower rates of breast cancer because of soy consumption," Daniel said. "In fact, Asians eat soy in very small quantities, as a condiment in the diet and not as a staple food. What's more, they eat old-fashioned, whole soybean products such as miso, tempeh, natto and tofu, not the new heavily processed products marketed by the soy industry such as soy milk, veggie burgers and 'energy bars.'"
Government officials in Israel and France have concluded that high soy consumption may indeed pose a breast cancer risk. Israeli Health Ministry guidelines recommend that women "exercise caution" in soy consumption, and the French Food Agency has decided to require soy products to contain warning labels.
"The risks are well established," Daniel said. "Soy is clearly not the answer for breast cancer prevention. The evidence is mounting that soy may even be part of the problem."
12 February 2008
How Vaccines Can Damage Your Brain
Vaccines, Depression and Neurodegeneration After Age 50: Another Reason to Avoid the Recommended Vaccines.
By Russell L. Blaylock, M.D., CCN
It has been estimated that 14.8 million Americans suffer from major depressive disorder and of this number 6 million are elderly. If we include anxiety disorders, which commonly accompany depression, the number jumps to 40 million adults. At a cost of $44 billon dollars a year just for care of the seniors, this impacts the national budget as well. Depression later in life tends to last longer and be more severe than at younger ages. It is also associated with a high rate of suicide.
Previously, it was thought that major depression was secondary to a deficiency in certain neurotransmitters in the brain, particularly the monoamines, which include serotonin, norepinephrine and dopamine. While alterations in these important mood-related neurotransmitters is found with major depression, growing evidence indicates that the primary culprit is low-grade, chronic brain inflammation. In addition, we now know that inflammatory cytokines can lower serotonin significantly and for long periods by a number of different mechanisms.
Researchers have also discovered that most people with major depressive disease (MDD) have higher levels of the neurotransmitter glutamate in their spinal fluid (CSF) and blood plasma. This is the same glutamate found as a food additive-for example, MSG (monosodium glutamate), hydrolyzed proteins, calcium or sodium casienate, soy protein isolate, vegetable protein concentrate or isolate, etc. Much of the free glutamate in the brain of depressed people comes from within, that is it escapes from special cells within the brain itself (microglia and astrocytes). Free glutamate, that is, existing outside the neurons, is very toxic to brain connections and brain cells themselves -- mainly by a process called excitotoxicity.
This connection between high brain glutamate levels and major depression was discovered quite by accident, when researchers observed that the anesthetic drug ketamine could relieve depression for a prolonged period. Ketamine is a powerful blocking drug for a class of glutamate receptors (NMDA receptors).
For quite some time it was known that depression could cause a loss of neurons in the hippocampus of the brain-the area most important for recent memory (declarative memory or working memory), the form of memory most affected in Alzheimer’s disease. This shrinkage of the brain usually occurred with long-term depression, yet it was shown, using sophisticated testing, that even without brain shrinkage, memory could be adversely affected. Some antidepressants could not only reverse the memory loss but could reverse the shrinkage as well.
The implication was that the elevated brain glutamate, via excitotoxicity, was destroying brain connections and later killing brain cells in the hippocampus and that the antidepressants were lowering brain glutamate levels. Subsequent studies have confirmed that drugs that block excitotoxicity also reduce depression and that some antidepressants reduce brain glutamate levels.
The Link Between Elevated Brain Glutamate and Inflammation
A tremendous amount of research has now demonstrated the link between chronic low-level brain inflammation, elevated brain glutamate levels and major depression. We know that as we age, the level of inflammatory immune cytokines increase (such as interleukin-1ß (IL-1), IL-6 and TNF-a). That is, the level of inflammation in our body increases, with high levels being seen at the extremes of life -- the 80s and 90s.
This progressive elevation in the body’s inflammation increases our risk of a number of inflammation-linked diseases, such as cancer, arthritis, muscle weakness, fatigue, sleep disturbances, memory loss and confusion. People with Alzheimer’s and Parkinson’s disease have even higher levels of these inflammatory cytokines -- much higher.
When inflammatory chemicals are elevated in the brain it makes brain cells more vulnerable to a number of toxins, many of which are in the environment. One study demonstrated, using a series of sophisticated techniques, that if brain cells were exposed to low levels of a pesticide there was little toxicity seen and that if you exposed these same brain cells to an immune stimulant alone, little damage occurred. But if you first exposed the brain cells to the immune stimulant, the same low dose of pesticide could destroy a great number of brain cells.
The importance of this observation was that the vaccine made the brain cells hypersensitive to the toxin so that even in concentrations that normally would do not cause harm, could wiped out most of the neurons. One of the strongest connections between an environmental toxin (pesticides) and a neurological disorder is with Parkinson’s disease. The reason it is more common in the elderly is that they have the highest levels of inflammatory cytokines. This also explains the high incidence of Alzheimer’s disease, which reaches incidences of 50% after age 80.
The link depression was also by accident. Doctors using immune cytokines to treat patients with cancer or hepatitis found that one third of the patients developed major depressive illness within days of the treatment and that it resolved only when the treatment was terminated. Other studies, in which inflammatory cytokine levels were measured in people with major depressive illness, also found most had high levels of these inflammatory chemicals.
To their surprise, they found that many of the antidepressant medications commonly used lowered inflammatory cytokines levels and that patients who failed to respond had the highest level of the cytokines.
So, how is this linked to excitotoxicity? Neuroscientists have known for some time that inflammatory cytokines cause the brain to release higher levels of glutamate -- the more intense the inflammation, the higher the brain glutamate level. The highest levels are found in the prefrontal lobes and limbic system, the areas most related to mood control. MSG also increases brain inflammation.
Vaccination and Brain Inflammation
A great number of studies have shown that when you vaccinate an animal, the body’s inflammatory cytokines not only increase dramatically, but so do the brain’s inflammatory chemicals. The brain has its own immune system that is intimately connected to the body’s immune system. The main immune cell in the brain is called a microglia. Normally, these brain cells are lying throughout the brain in a resting state (called ramified). Once activated, they can move around, traveling between brain cells like amoeba (called amoeboid microglia).
In the resting state, they release chemicals that support the growth and protection of brain cells and their connections (dendrites and synapses). But when activated, they secrete a number of very harmful chemicals, including inflammatory cytokines, chemokines, complement, free radicals, lipid peroxidation products, and two excitotoxins -- glutamate and quinolinic acid.
In essence, these brain immune cells are out to kill invaders, since the body’s immune system sent an emergency message that an invasion had occurred. With most infections, this phase of activation last no more than a few days to two weeks, during which time the immune system successfully kills off the invaders. Once that is accomplished, the immune system shuts down to allow things to cool off and the brain to repair what damage was done by its own immune system.
What researchers knew was that during this period of activation, people generally feel bad and that what they experience closely resembles depression -- a condition called “sickness behavior”. Most of us have experience this when suffering from a viral illness -- such things as restlessness, irritability, a need to get away from people, trouble sleeping, fatigue and difficulty thinking.
Studies have shown that there are two phases to this “sickness behavior”; one in which we have the flu-like symptoms and a later onset of depression-like symptoms that can last awhile. They have also shown that all of these symptoms are due to high levels of inflammatory cytokines in the brain, which come from activated microglia.
A number of studies have also shown that after age 50, people have exaggerated and prolonged “sickness behavior”, much more so than younger people. This is one of the reasons why many elderly hang onto flu symptoms for months after exposure.
There is also another immune phenomenon that plays a major role in vaccine-related brain injury. Researchers discovered that when you vaccinate an animal, the brain microglia immune cells turn on partially (called priming), that is, they are in a state of high readiness. If the immune system is activated again soon after (days, weeks to months), these microglia explode into action secreting levels of their destructive chemicals far higher than normal. This overreaction can be very destructive and make you feel very depressed.
Stimulating the immune system with a vaccine is far different than contracting an infectious illness naturally. Vaccines are made of two components -- the agent you wish to vaccinate against -- for example, the measles virus; and an immune system booster called an immune adjuvant. These adjuvants are composed of such things as aluminum compounds, MSG, lipid compounds and even mercury. Their job is to make the immune system react as intensely as possible and for as long as possible.
Studies have shown that these adjuvants, from a single vaccine, can cause immune overactivation for as long as two years. This means that the brain microglia remain active as well, continuously pouring out destructive chemicals. In fact, one study found that a single injection of an immune activating substance could cause brain immune overactivation for over a year. This is very destructive.
Flu Vaccines and An Expanding Vaccine Schedule for the Elderly
Public health authorities and physician societies are in an all out campaign to have every elderly person vaccinated every year with the flu vaccine as well as a growing number of newer vaccines. When I was practicing neurosurgery, the hospitals had an automatic written order on all older patients’ charts mandating a flu vaccine, unless it was countermanded by the physician, which I always did. Now, they are giving the shots in malls, tents and every available site they can muster. And worse still, using lies and scare tactics to frighten the elderly onto getting the shots (such as the bold lie of 36,000 elderly dying of the flu every year).
As you age your immune system, including that special immune system in your brain, releases significantly more inflammatory immune cytokines than when you were younger. This serves to prime the microglia, as discussed. So, when you get your first flu shot your microglia overreact and does so for a very long period -- perhaps years. Many elderly report that the flu shot gave them the flu. Proponents of vaccines, retort with a condescending laugh, that it is impossible because the flu vaccine contains killed flu viruses. In truth, what these people are reporting is a prolonged, intense “sickness behavior” response to the vaccine. To the body, it is worse than getting the flu. Remember, no one is recording the number of elderly who die after getting the flu shot, especially if they die months later, which can happen with sickness behavior, especially if they have a preexisting chronic illness or are infirm.
Here is the shocking truth. With the elderly already having increased inflammatory cytokine levels both systemically and in their brain, stimulating these primed microglia so that a chronic overstimulation of the brain’s immune system is triggered, will not only increase their risk of developing one of the neurodegenerative diseases, but will also substantially increase their risk of developing major depression. Remember, this also increases their risk of suicide and even homicide dramatically.
Anxiety is a major problem with depression, and vaccinations will greatly worsen the condition. In fact, vaccination, especially multiple vaccinations, will maintain the brain in a state of inflammation that will be self-perpetuating, because the excess release of glutamate in the brain, as well as glutamate in the diet, will further enhance microglial activation and excitotoxicity.
Those who are prone to developing one of the neurodegenerative diseases, such as Alzheimer’s disease or Parkinson’s disease will be at a drastically increased risk as we have seen experimentally when even animals exposed to subtoxic concentrations of environmental toxins and vaccinated develop neurologic worsening.
Most people use pesticides in their home and studies have shown that the concentrations in homes are sufficient to trigger Parkinson’s disease in susceptible people. Vaccinations, as these studies have shown, will greatly increase risk. Most doctors are completely unaware of this important research.
You must keep in mind that “health authorities” urge the elderly to get the flu vaccine each and every year. This will keep the microglia in a primed and even activated state continuously. Recently, neurologists announced that the incidence of neurodegenerative disease had been grossly underestimated and that neurological diseases of aging were increasing at a frightening rate. They have no explanation. Over the last three decades the number of elderly receiving yearly flu vaccines has risen from 20% before 1980 to over 60% today.
If this were not depressing enough, now the public health authorities and medical specialty societies are adding a whole new set of vaccines for those above 50 years of age, including the pneumococcal and meningiococcal vaccines. What is being completely ignored by the promoters of these vaccines is the effect of multiple doses of immune adjuvant that accompany each of these vaccines.
Lets, say you see your doctor and he talks you into getting the flu vaccine, the pneumococcal and meningiococcal vaccine all during the same office visit. That way, he can save you extra office visits. What your doctor ignores is that he is giving you three doses of powerful immune adjuvant all in one sitting, which means that your body and brain are assaulted by a massive dose of powerful immune activators, which have been proven to activate the brain’s immune system to dangerous levels, even when given as a single dose. Proof of this mechanism exists not only in animal studies, but in humans as well.
Mercury and Aluminum
There are other ways that vaccines can cause havoc in the brain. Most vaccines contain aluminum compounds. A multitude of studies have shown that aluminum, especially if combined with fluoride, is a powerful brain toxin and that it accumulates in the brain. With each vaccine injection, a dose of aluminum is given. These yearly aluminum inoculations accumulate not only at the site of the injection, but travel to the brain, where it enters neurons and glial cells (astrocytes and microglia). A number of studies have shown that aluminum can activate microglia and do so for long periods. This means that the aluminum in your vaccination is priming your microglia to overreact. The next vaccine acts to trigger the enhanced inflammatory reaction and release of the excitotoxins, glutamate and quinolinic acid.
You must also appreciate that any infection, stroke, head injury or other toxin exposure will also magnify this inflammatory brain reaction initially triggered by your vaccines. Studies have now indicated that the more one’s immune system is activated the more like he or she will suffer from one of the neurodegenerative diseases.
Mercury is also a powerful activator of brain microglia and can do so in extremely low concentrations-in nanomolar amounts. Because of its numerous reactions with sulfhydral compounds in the body (which are ubiquitous), mercury can poison a number of enzymes both systemically and in the brain. Of special concern is the ability of mercury, especially ethylmercury (the kind found in vaccines called thimerosal) to inhibit the regulation of brain glutamate levels. (It does this by inhibiting the glutamate transfer proteins that control the removal of glutamate from outside the neuron, where it does its harm.)
In essence, mercury, in the concentrations being injected with vaccines, triggers excitotoxicity, increases brain free radicals and lipid peroxidation products, inhibits critical brain enzymes, inhibits antioxidant enzymes and impairs DNA repair ability. The flu vaccine contains enough mercury to do all of these things. You must keep in mind that each flu vaccine adds to the mercury supplied by your last vaccine, that is, it is progressively accumulating in your brain.
In addition, the aluminum in the vaccines also primes microglia and when combined with mercury is infinitively more toxic to the brain. Now, if this is not enough, we also have to consider the contamination of vaccines with foreign viruses and viral components. Studies have shown that this is not a rare occurrence, with up to 60% of vaccines being contaminated in one study of several major manufactured vaccines. When confronted with this fact, vaccine proponents just shrug their shoulders and say -- “We don’t think these things are harmful.”
Yet, the studies say otherwise. It has been found that insertion of viral fragments, not even the whole virus, is sufficient to trigger the brain’s microglial system and subsequent excitotoxicity, leading to progressive brain degeneration. This is accepted to be the mechanism by which the HIV virus causes dementia in a great number of AIDS victims. Fragments of the virus (gp140 and Tat) are engulfed by the microglia and this triggers chronic brain inflammation and excitotoxicity. The herpes virus and measles virus can do the same thing.
Danger of Live Virus Vaccines
A number of studies have shown that live viruses used in vaccines can enter the brain and reside there for a lifetime. One such study, in which autopsied elderly were examined for the presence of the measles virus, found that 20% of the brains had live measles viruses and 45% of other organs were infected. These viruses were highly mutated, meaning that they could be just as potent as other measles viruses, but could be even more virulent. Worse, is that in most cases they cause a smoldering destruction of tissues without the obvious symptoms of infection, which has been shown in a number of studies.
Live virus vaccines are made using a process to attenuate the pathogenic or disease-causing virus by passing it through a series of cultures. The problem is that the reverse can also happen within the body. A number of studies have shown that when we produce free radicals in our body (and we produce tons of such radicals over a lifetime), it mutates the viruses residing in our tissues. This is what was found in the autopsy study I referred to above.
Likewise, these viruses can trigger brain inflammation and degeneration, which has been shown in a number of studies-that is, there exist a chronic degeneration of the brain over years or decades. Because it is so far separated from the time of the original vaccine, physicians just attribute it to old age or heredity, anything but the vaccines.
Virologists are also concerned that such mutated live viruses can also infect other people, leading to outbreaks of disease totally unsuspected by health authorities.
Conclusion
Current recommendations by the CDC for adult vaccinations include a total of 14 separate inoculations with infectious agents and powerful immune adjuvants. To be fair, some of these are for special medical risks and conditions, such as high-risk behaviors, illegal drug use and HIV infected individuals. If we eliminate these, women will be exposed to 10 inoculations and men 7, should they follow CDC guidelines, which doctors follow.
According to CDC recommendations, multiple vaccinations for a single disease are separated by no more than 4 weeks, which is close enough together to produce priming and subsequent hyperactivation of brain microglia. We have seen that this can trigger a smoldering process of brain inflammation and excitotoxicity that can not only result in depression, anxiety and high suicide rates, but can increase one’s risk of developing one of the neurodegenerative diseases as well.
We have also seen that in many cases a person will be injected with several vaccines during a single office visit and that this means their body is exposed to a very large dose of immune adjuvant. Compelling studies, using many animal species as well as humans, have shown that this overactivates brain inflammatory mechanism that can last for years.
In addition, several additives to vaccines, such as mercury and aluminum, are powerful brain toxins that are known to accumulate in the brain over years and can trigger brain inflammatory/excitotoxic mechanisms. Vaccine contaminants, such as bacteria, mycoplasma and viral fragments can also produce prolonged brain inflammation and neurodegeneration.
Because the elderly already have high levels of inflammatory cytokines, they are at a special risk. The very young (babies and small children) are at a high risk because their brains are undergoing the most rapid development at the very time they receive the greatest number of vaccinations -- the first two years of life. In fact, they receive 22 vaccines during the first year of life, one of which contains a full pediatric dose of mercury. Like adults, they receive many inoculations (up to 9 inoculations) in one office visit. This is insane and in my estimation, criminal.
Nasal flu vaccines are even worse, because they introduce a live virus into the nasal passages, which can then travel along the olfactory nerves, which leads to the very part of the brain first and most severely affected by Alzheimer’s disease. A number of studies have shown that viruses and bacteria can pass along this route to the brain. In fact, in one study scientists sprayed a bacterium into the nose of mice and observed a rapid development of Alzheimer’s type plaques in the mouse’s brain.
So, what should older people do? First, studies have shown that the primary cause of immune deficiency in the elderly is purely dietary. The carotenoids, such as beta-carotene, alpha-carotene, canthaxanthin, lutein and lycopene significantly enhance the immunity of the elderly. Zinc, magnesium and selenium are also essential. One should also avoid omega-6 oils (the vegetable oils-corn, safflower, sunflower, canola, soybean and peanut oils), since they greatly enhance inflammation and depress immunity. The EPA component of fish oils (omega-3 oils) is also a powerful immune suppressant. DHA is not. A healthy immune system means that you can fight infections efficiently and rapidly.
Regular exercise, such as brisk walking or weight exercises three to five times a week also boost immunity, while extreme exercise suppresses immunity. Sugar and refined carbohydrates also suppress immunity and inflame the brain. Exercise protects the brain from aging effects and from degeneration.
Adequate sleep is also vital to both brain health and good immune function. Pubic health officials and spokesmen for the major medical societies are lying to the public concerning vaccine safety. We now possess sufficient information from a great number of studies to halt this disastrous vaccine policy. We are facing a medial disaster in this country, which is already well on its way.
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25. Pittenger C, et al. The NMDA receptor as a therapeutic target in major depressive disorder. CNS Neurol Disorders Drug Targets 2007; 6: 101-115.
26. Magaki S et al. Increased production of inflammatory cytokines in mild cognitive impairment. Exp Gerontol 2007; 42: 233-240.
27. Gao H-M et al. Synergistic dopaminergic neurotoxicity if the pesticide rotenone and inflammogen lipopolysacchride: relevance to the etiology of Parkinson’s disease. J Neurosciences 2003; 23: 1228-1236.
28. Holmes C et al. Systemic infection, interleukin 1ß, and cognitive decline. J Neurol Neurosurgery Psychiatry 2003; 74: 788-789.
29. Godbout JP et al. Exaggerated neuroinflammation and sickness behavior in aged mice after activation of the peripheral innate immune system. The FASEB J 2005; 19: 1329-1331.
30. Perry VH et al. The impact of infection on the progression of neurodegenerative disease. Nature Rev Neuroscience 2003;4: 103-112.
31. Feiring B et al. Persisting responses indicating long-term protection after booster dose with meningococcal group B outer membrane vesicle vaccine. Clin Vaccine Immunology 2006; 13: 790-796.
32. Vaccine Excepients and Media Summery Center for Disease Control and Prevention. (also the source for recommended vaccines for adults and children).
By Russell L. Blaylock, M.D., CCN
It has been estimated that 14.8 million Americans suffer from major depressive disorder and of this number 6 million are elderly. If we include anxiety disorders, which commonly accompany depression, the number jumps to 40 million adults. At a cost of $44 billon dollars a year just for care of the seniors, this impacts the national budget as well. Depression later in life tends to last longer and be more severe than at younger ages. It is also associated with a high rate of suicide.
Previously, it was thought that major depression was secondary to a deficiency in certain neurotransmitters in the brain, particularly the monoamines, which include serotonin, norepinephrine and dopamine. While alterations in these important mood-related neurotransmitters is found with major depression, growing evidence indicates that the primary culprit is low-grade, chronic brain inflammation. In addition, we now know that inflammatory cytokines can lower serotonin significantly and for long periods by a number of different mechanisms.
Researchers have also discovered that most people with major depressive disease (MDD) have higher levels of the neurotransmitter glutamate in their spinal fluid (CSF) and blood plasma. This is the same glutamate found as a food additive-for example, MSG (monosodium glutamate), hydrolyzed proteins, calcium or sodium casienate, soy protein isolate, vegetable protein concentrate or isolate, etc. Much of the free glutamate in the brain of depressed people comes from within, that is it escapes from special cells within the brain itself (microglia and astrocytes). Free glutamate, that is, existing outside the neurons, is very toxic to brain connections and brain cells themselves -- mainly by a process called excitotoxicity.
This connection between high brain glutamate levels and major depression was discovered quite by accident, when researchers observed that the anesthetic drug ketamine could relieve depression for a prolonged period. Ketamine is a powerful blocking drug for a class of glutamate receptors (NMDA receptors).
For quite some time it was known that depression could cause a loss of neurons in the hippocampus of the brain-the area most important for recent memory (declarative memory or working memory), the form of memory most affected in Alzheimer’s disease. This shrinkage of the brain usually occurred with long-term depression, yet it was shown, using sophisticated testing, that even without brain shrinkage, memory could be adversely affected. Some antidepressants could not only reverse the memory loss but could reverse the shrinkage as well.
The implication was that the elevated brain glutamate, via excitotoxicity, was destroying brain connections and later killing brain cells in the hippocampus and that the antidepressants were lowering brain glutamate levels. Subsequent studies have confirmed that drugs that block excitotoxicity also reduce depression and that some antidepressants reduce brain glutamate levels.
The Link Between Elevated Brain Glutamate and Inflammation
A tremendous amount of research has now demonstrated the link between chronic low-level brain inflammation, elevated brain glutamate levels and major depression. We know that as we age, the level of inflammatory immune cytokines increase (such as interleukin-1ß (IL-1), IL-6 and TNF-a). That is, the level of inflammation in our body increases, with high levels being seen at the extremes of life -- the 80s and 90s.
This progressive elevation in the body’s inflammation increases our risk of a number of inflammation-linked diseases, such as cancer, arthritis, muscle weakness, fatigue, sleep disturbances, memory loss and confusion. People with Alzheimer’s and Parkinson’s disease have even higher levels of these inflammatory cytokines -- much higher.
When inflammatory chemicals are elevated in the brain it makes brain cells more vulnerable to a number of toxins, many of which are in the environment. One study demonstrated, using a series of sophisticated techniques, that if brain cells were exposed to low levels of a pesticide there was little toxicity seen and that if you exposed these same brain cells to an immune stimulant alone, little damage occurred. But if you first exposed the brain cells to the immune stimulant, the same low dose of pesticide could destroy a great number of brain cells.
The importance of this observation was that the vaccine made the brain cells hypersensitive to the toxin so that even in concentrations that normally would do not cause harm, could wiped out most of the neurons. One of the strongest connections between an environmental toxin (pesticides) and a neurological disorder is with Parkinson’s disease. The reason it is more common in the elderly is that they have the highest levels of inflammatory cytokines. This also explains the high incidence of Alzheimer’s disease, which reaches incidences of 50% after age 80.
The link depression was also by accident. Doctors using immune cytokines to treat patients with cancer or hepatitis found that one third of the patients developed major depressive illness within days of the treatment and that it resolved only when the treatment was terminated. Other studies, in which inflammatory cytokine levels were measured in people with major depressive illness, also found most had high levels of these inflammatory chemicals.
To their surprise, they found that many of the antidepressant medications commonly used lowered inflammatory cytokines levels and that patients who failed to respond had the highest level of the cytokines.
So, how is this linked to excitotoxicity? Neuroscientists have known for some time that inflammatory cytokines cause the brain to release higher levels of glutamate -- the more intense the inflammation, the higher the brain glutamate level. The highest levels are found in the prefrontal lobes and limbic system, the areas most related to mood control. MSG also increases brain inflammation.
Vaccination and Brain Inflammation
A great number of studies have shown that when you vaccinate an animal, the body’s inflammatory cytokines not only increase dramatically, but so do the brain’s inflammatory chemicals. The brain has its own immune system that is intimately connected to the body’s immune system. The main immune cell in the brain is called a microglia. Normally, these brain cells are lying throughout the brain in a resting state (called ramified). Once activated, they can move around, traveling between brain cells like amoeba (called amoeboid microglia).
In the resting state, they release chemicals that support the growth and protection of brain cells and their connections (dendrites and synapses). But when activated, they secrete a number of very harmful chemicals, including inflammatory cytokines, chemokines, complement, free radicals, lipid peroxidation products, and two excitotoxins -- glutamate and quinolinic acid.
In essence, these brain immune cells are out to kill invaders, since the body’s immune system sent an emergency message that an invasion had occurred. With most infections, this phase of activation last no more than a few days to two weeks, during which time the immune system successfully kills off the invaders. Once that is accomplished, the immune system shuts down to allow things to cool off and the brain to repair what damage was done by its own immune system.
What researchers knew was that during this period of activation, people generally feel bad and that what they experience closely resembles depression -- a condition called “sickness behavior”. Most of us have experience this when suffering from a viral illness -- such things as restlessness, irritability, a need to get away from people, trouble sleeping, fatigue and difficulty thinking.
Studies have shown that there are two phases to this “sickness behavior”; one in which we have the flu-like symptoms and a later onset of depression-like symptoms that can last awhile. They have also shown that all of these symptoms are due to high levels of inflammatory cytokines in the brain, which come from activated microglia.
A number of studies have also shown that after age 50, people have exaggerated and prolonged “sickness behavior”, much more so than younger people. This is one of the reasons why many elderly hang onto flu symptoms for months after exposure.
There is also another immune phenomenon that plays a major role in vaccine-related brain injury. Researchers discovered that when you vaccinate an animal, the brain microglia immune cells turn on partially (called priming), that is, they are in a state of high readiness. If the immune system is activated again soon after (days, weeks to months), these microglia explode into action secreting levels of their destructive chemicals far higher than normal. This overreaction can be very destructive and make you feel very depressed.
Stimulating the immune system with a vaccine is far different than contracting an infectious illness naturally. Vaccines are made of two components -- the agent you wish to vaccinate against -- for example, the measles virus; and an immune system booster called an immune adjuvant. These adjuvants are composed of such things as aluminum compounds, MSG, lipid compounds and even mercury. Their job is to make the immune system react as intensely as possible and for as long as possible.
Studies have shown that these adjuvants, from a single vaccine, can cause immune overactivation for as long as two years. This means that the brain microglia remain active as well, continuously pouring out destructive chemicals. In fact, one study found that a single injection of an immune activating substance could cause brain immune overactivation for over a year. This is very destructive.
Flu Vaccines and An Expanding Vaccine Schedule for the Elderly
Public health authorities and physician societies are in an all out campaign to have every elderly person vaccinated every year with the flu vaccine as well as a growing number of newer vaccines. When I was practicing neurosurgery, the hospitals had an automatic written order on all older patients’ charts mandating a flu vaccine, unless it was countermanded by the physician, which I always did. Now, they are giving the shots in malls, tents and every available site they can muster. And worse still, using lies and scare tactics to frighten the elderly onto getting the shots (such as the bold lie of 36,000 elderly dying of the flu every year).
As you age your immune system, including that special immune system in your brain, releases significantly more inflammatory immune cytokines than when you were younger. This serves to prime the microglia, as discussed. So, when you get your first flu shot your microglia overreact and does so for a very long period -- perhaps years. Many elderly report that the flu shot gave them the flu. Proponents of vaccines, retort with a condescending laugh, that it is impossible because the flu vaccine contains killed flu viruses. In truth, what these people are reporting is a prolonged, intense “sickness behavior” response to the vaccine. To the body, it is worse than getting the flu. Remember, no one is recording the number of elderly who die after getting the flu shot, especially if they die months later, which can happen with sickness behavior, especially if they have a preexisting chronic illness or are infirm.
Here is the shocking truth. With the elderly already having increased inflammatory cytokine levels both systemically and in their brain, stimulating these primed microglia so that a chronic overstimulation of the brain’s immune system is triggered, will not only increase their risk of developing one of the neurodegenerative diseases, but will also substantially increase their risk of developing major depression. Remember, this also increases their risk of suicide and even homicide dramatically.
Anxiety is a major problem with depression, and vaccinations will greatly worsen the condition. In fact, vaccination, especially multiple vaccinations, will maintain the brain in a state of inflammation that will be self-perpetuating, because the excess release of glutamate in the brain, as well as glutamate in the diet, will further enhance microglial activation and excitotoxicity.
Those who are prone to developing one of the neurodegenerative diseases, such as Alzheimer’s disease or Parkinson’s disease will be at a drastically increased risk as we have seen experimentally when even animals exposed to subtoxic concentrations of environmental toxins and vaccinated develop neurologic worsening.
Most people use pesticides in their home and studies have shown that the concentrations in homes are sufficient to trigger Parkinson’s disease in susceptible people. Vaccinations, as these studies have shown, will greatly increase risk. Most doctors are completely unaware of this important research.
You must keep in mind that “health authorities” urge the elderly to get the flu vaccine each and every year. This will keep the microglia in a primed and even activated state continuously. Recently, neurologists announced that the incidence of neurodegenerative disease had been grossly underestimated and that neurological diseases of aging were increasing at a frightening rate. They have no explanation. Over the last three decades the number of elderly receiving yearly flu vaccines has risen from 20% before 1980 to over 60% today.
If this were not depressing enough, now the public health authorities and medical specialty societies are adding a whole new set of vaccines for those above 50 years of age, including the pneumococcal and meningiococcal vaccines. What is being completely ignored by the promoters of these vaccines is the effect of multiple doses of immune adjuvant that accompany each of these vaccines.
Lets, say you see your doctor and he talks you into getting the flu vaccine, the pneumococcal and meningiococcal vaccine all during the same office visit. That way, he can save you extra office visits. What your doctor ignores is that he is giving you three doses of powerful immune adjuvant all in one sitting, which means that your body and brain are assaulted by a massive dose of powerful immune activators, which have been proven to activate the brain’s immune system to dangerous levels, even when given as a single dose. Proof of this mechanism exists not only in animal studies, but in humans as well.
Mercury and Aluminum
There are other ways that vaccines can cause havoc in the brain. Most vaccines contain aluminum compounds. A multitude of studies have shown that aluminum, especially if combined with fluoride, is a powerful brain toxin and that it accumulates in the brain. With each vaccine injection, a dose of aluminum is given. These yearly aluminum inoculations accumulate not only at the site of the injection, but travel to the brain, where it enters neurons and glial cells (astrocytes and microglia). A number of studies have shown that aluminum can activate microglia and do so for long periods. This means that the aluminum in your vaccination is priming your microglia to overreact. The next vaccine acts to trigger the enhanced inflammatory reaction and release of the excitotoxins, glutamate and quinolinic acid.
You must also appreciate that any infection, stroke, head injury or other toxin exposure will also magnify this inflammatory brain reaction initially triggered by your vaccines. Studies have now indicated that the more one’s immune system is activated the more like he or she will suffer from one of the neurodegenerative diseases.
Mercury is also a powerful activator of brain microglia and can do so in extremely low concentrations-in nanomolar amounts. Because of its numerous reactions with sulfhydral compounds in the body (which are ubiquitous), mercury can poison a number of enzymes both systemically and in the brain. Of special concern is the ability of mercury, especially ethylmercury (the kind found in vaccines called thimerosal) to inhibit the regulation of brain glutamate levels. (It does this by inhibiting the glutamate transfer proteins that control the removal of glutamate from outside the neuron, where it does its harm.)
In essence, mercury, in the concentrations being injected with vaccines, triggers excitotoxicity, increases brain free radicals and lipid peroxidation products, inhibits critical brain enzymes, inhibits antioxidant enzymes and impairs DNA repair ability. The flu vaccine contains enough mercury to do all of these things. You must keep in mind that each flu vaccine adds to the mercury supplied by your last vaccine, that is, it is progressively accumulating in your brain.
In addition, the aluminum in the vaccines also primes microglia and when combined with mercury is infinitively more toxic to the brain. Now, if this is not enough, we also have to consider the contamination of vaccines with foreign viruses and viral components. Studies have shown that this is not a rare occurrence, with up to 60% of vaccines being contaminated in one study of several major manufactured vaccines. When confronted with this fact, vaccine proponents just shrug their shoulders and say -- “We don’t think these things are harmful.”
Yet, the studies say otherwise. It has been found that insertion of viral fragments, not even the whole virus, is sufficient to trigger the brain’s microglial system and subsequent excitotoxicity, leading to progressive brain degeneration. This is accepted to be the mechanism by which the HIV virus causes dementia in a great number of AIDS victims. Fragments of the virus (gp140 and Tat) are engulfed by the microglia and this triggers chronic brain inflammation and excitotoxicity. The herpes virus and measles virus can do the same thing.
Danger of Live Virus Vaccines
A number of studies have shown that live viruses used in vaccines can enter the brain and reside there for a lifetime. One such study, in which autopsied elderly were examined for the presence of the measles virus, found that 20% of the brains had live measles viruses and 45% of other organs were infected. These viruses were highly mutated, meaning that they could be just as potent as other measles viruses, but could be even more virulent. Worse, is that in most cases they cause a smoldering destruction of tissues without the obvious symptoms of infection, which has been shown in a number of studies.
Live virus vaccines are made using a process to attenuate the pathogenic or disease-causing virus by passing it through a series of cultures. The problem is that the reverse can also happen within the body. A number of studies have shown that when we produce free radicals in our body (and we produce tons of such radicals over a lifetime), it mutates the viruses residing in our tissues. This is what was found in the autopsy study I referred to above.
Likewise, these viruses can trigger brain inflammation and degeneration, which has been shown in a number of studies-that is, there exist a chronic degeneration of the brain over years or decades. Because it is so far separated from the time of the original vaccine, physicians just attribute it to old age or heredity, anything but the vaccines.
Virologists are also concerned that such mutated live viruses can also infect other people, leading to outbreaks of disease totally unsuspected by health authorities.
Conclusion
Current recommendations by the CDC for adult vaccinations include a total of 14 separate inoculations with infectious agents and powerful immune adjuvants. To be fair, some of these are for special medical risks and conditions, such as high-risk behaviors, illegal drug use and HIV infected individuals. If we eliminate these, women will be exposed to 10 inoculations and men 7, should they follow CDC guidelines, which doctors follow.
According to CDC recommendations, multiple vaccinations for a single disease are separated by no more than 4 weeks, which is close enough together to produce priming and subsequent hyperactivation of brain microglia. We have seen that this can trigger a smoldering process of brain inflammation and excitotoxicity that can not only result in depression, anxiety and high suicide rates, but can increase one’s risk of developing one of the neurodegenerative diseases as well.
We have also seen that in many cases a person will be injected with several vaccines during a single office visit and that this means their body is exposed to a very large dose of immune adjuvant. Compelling studies, using many animal species as well as humans, have shown that this overactivates brain inflammatory mechanism that can last for years.
In addition, several additives to vaccines, such as mercury and aluminum, are powerful brain toxins that are known to accumulate in the brain over years and can trigger brain inflammatory/excitotoxic mechanisms. Vaccine contaminants, such as bacteria, mycoplasma and viral fragments can also produce prolonged brain inflammation and neurodegeneration.
Because the elderly already have high levels of inflammatory cytokines, they are at a special risk. The very young (babies and small children) are at a high risk because their brains are undergoing the most rapid development at the very time they receive the greatest number of vaccinations -- the first two years of life. In fact, they receive 22 vaccines during the first year of life, one of which contains a full pediatric dose of mercury. Like adults, they receive many inoculations (up to 9 inoculations) in one office visit. This is insane and in my estimation, criminal.
Nasal flu vaccines are even worse, because they introduce a live virus into the nasal passages, which can then travel along the olfactory nerves, which leads to the very part of the brain first and most severely affected by Alzheimer’s disease. A number of studies have shown that viruses and bacteria can pass along this route to the brain. In fact, in one study scientists sprayed a bacterium into the nose of mice and observed a rapid development of Alzheimer’s type plaques in the mouse’s brain.
So, what should older people do? First, studies have shown that the primary cause of immune deficiency in the elderly is purely dietary. The carotenoids, such as beta-carotene, alpha-carotene, canthaxanthin, lutein and lycopene significantly enhance the immunity of the elderly. Zinc, magnesium and selenium are also essential. One should also avoid omega-6 oils (the vegetable oils-corn, safflower, sunflower, canola, soybean and peanut oils), since they greatly enhance inflammation and depress immunity. The EPA component of fish oils (omega-3 oils) is also a powerful immune suppressant. DHA is not. A healthy immune system means that you can fight infections efficiently and rapidly.
Regular exercise, such as brisk walking or weight exercises three to five times a week also boost immunity, while extreme exercise suppresses immunity. Sugar and refined carbohydrates also suppress immunity and inflame the brain. Exercise protects the brain from aging effects and from degeneration.
Adequate sleep is also vital to both brain health and good immune function. Pubic health officials and spokesmen for the major medical societies are lying to the public concerning vaccine safety. We now possess sufficient information from a great number of studies to halt this disastrous vaccine policy. We are facing a medial disaster in this country, which is already well on its way.
1. McGeer PL and McGeer EG. Local neuroinflammation and progression of Alzheimer’s disease. J Neurovirology 202; 8: 529-538.
2. Tavares RG, et al. Quinolinic acid stimulates synaptosomal glutamate release and inhibits glutamate uptake into astrocytes. Neurochem Int 2002; 40: 621-627.
3. Eastman CL, et al. Increased brain quinolinic acid production in mice infected with a neurotropic measles virus. Exp Neurol 1994; 125; 119-124.
4. Glass JD and Wesselingh SL. Microglia in HIV-associated neurological diseases. Microsc Res Tech 2001; 54: 95-105.
5. Turowski RC and Troozzi PL. Central Nervous System toxicities of cytokine therapy: In: Plotnikoff NP, et al, Eds. Cytokines, Stress and Immunity. Boca Raton, CRC Pres, 1998, pp 93-114.
6. Mrak RE, et al. Glail cytokines and Alzheimer’s disease: Review and pathogenic implications. Human Pathol 1995; 26: 816-823.
7. Klatschmidt C, et al. Stimulation of inotropic glutamate receptors activates transcription factor NFkB in primary neurons. Proc Nat Acad Sci USA 1995; 92: 9618-9622.
8. Gao HM, et al Distinct role for microglia in rotenone-induced degeneration of dopaminergic neurons. J Neurosci 2002; 22: 782-790.
9. Dyatlov VA et al. neonatal lead exposure potentates sickness behavior by Listeria monocytogenes infection in mice. Brain Behav Immun 2002; 16: 477-492.
10. Nakai Y, et al. Apoptosis and microglial activation in influenza encephalopathy. Acta Neuropath (Berl) 2003; 105: 233-239.
11. Anderson T et al. NMDA-receptor antagonist prevents measles virus-induced neurodegeneration. Eur J Neurosci 1991; 3: 66-71.
12. Conner TJ, et al. Depression stress immunological activation: the role of cytokines in depressive disorders. Life Sciences 1998; 62: 583-606.
13. Renault PF, et al. Psychiatric complications of long-term ineterferon-alpha therapy. Arch Internal Medicine 1987; 147: 1577-1580.
14. Adams F et al. Neuropsychiatric manifestations of human leukocyte interferon therapy in patients with cancer. JAMA 1984; 252: 938-941.
15. Broderick PA, et al. Interleukin-1a alters hippocampal and norepinephrine release during open field behavior in Sprague-Dawley animals: differences from the Fawn-Hooded animal model of depression. Prog Neuropsychopharmacol Biology 2002; 26: 1355-1372.
16. Katayama Y, et al. Detection of measles virus nucleoprotein mRNA in autopsied brain tissues. J General Virology 1995; 76: 3201-3204.
17. Nicolson GL et al. High frequency of systemic mycoplasma infections in Gulf War Veterans and civilians with amyotrophic lateral sclerosis. J Clin Sci 2002; 9: 525-529.
18. Blaylock RL. Interaction of cytokines, excitotoxins, and reactive nitrogen and oxygen species in autism spectrum disorders. JANA 2003; 6: 21-35.
19. Blaylock RL. Central role of excitotoxicity in autism. JANA 2003; 6: 7-19.
20. Blaylock RL. Food additive excitotoxins and degenerative brain disorders. Medical Sentinel 1999; 4: 212-215.
21. Blaylock RL. Chronic microglial activation and excitotoxicity secondary to excessive immune stimulation: Possible factors in Gulf War Syndrome and Autism. J Amer Phys Surg 2004; 9: 46-51.
22. Pilc A, et al. Mood disorders: regulation by metabotropic glutamate receptors. Biochem Pharmacol 2007; (Epub ahead of print)
23. Palucha A, Pilc A. The involvement of glutamate in the pathophysiology of depression. 2005; 18: 262-268.
24. Paul IA, Skolnick P. Glutamate and depression: clinical and preclinical studies. Ann NY Acad Sci 2003; 1003: 250-272.
25. Pittenger C, et al. The NMDA receptor as a therapeutic target in major depressive disorder. CNS Neurol Disorders Drug Targets 2007; 6: 101-115.
26. Magaki S et al. Increased production of inflammatory cytokines in mild cognitive impairment. Exp Gerontol 2007; 42: 233-240.
27. Gao H-M et al. Synergistic dopaminergic neurotoxicity if the pesticide rotenone and inflammogen lipopolysacchride: relevance to the etiology of Parkinson’s disease. J Neurosciences 2003; 23: 1228-1236.
28. Holmes C et al. Systemic infection, interleukin 1ß, and cognitive decline. J Neurol Neurosurgery Psychiatry 2003; 74: 788-789.
29. Godbout JP et al. Exaggerated neuroinflammation and sickness behavior in aged mice after activation of the peripheral innate immune system. The FASEB J 2005; 19: 1329-1331.
30. Perry VH et al. The impact of infection on the progression of neurodegenerative disease. Nature Rev Neuroscience 2003;4: 103-112.
31. Feiring B et al. Persisting responses indicating long-term protection after booster dose with meningococcal group B outer membrane vesicle vaccine. Clin Vaccine Immunology 2006; 13: 790-796.
32. Vaccine Excepients and Media Summery Center for Disease Control and Prevention. (also the source for recommended vaccines for adults and children).
1 February 2008
Omega-3 Slows Late-Onset Alzheimer's
Supplements of the omega-3 fat DHA (docosahexaenoic acid) can reduce levels an enzyme linked to Alzheimer's disease.
In both mice and cultured human cells, DHA increased the production of LR11, a protein which clears away enzymes in the brain that make the beta amyloid plaques that are thought to cause Alzheimer's disease.
The research adds to a growing body of science linking omega-3 fats to improved cognitive function and slower cognitive decline.
Sources:
* FoodProductionDaily.com January 25, 2008
In both mice and cultured human cells, DHA increased the production of LR11, a protein which clears away enzymes in the brain that make the beta amyloid plaques that are thought to cause Alzheimer's disease.
The research adds to a growing body of science linking omega-3 fats to improved cognitive function and slower cognitive decline.
Sources:
* FoodProductionDaily.com January 25, 2008
25 January 2008
A Single Meal Can Lead to Good (or Bad) Health
Want to know how many cheeseburgers you'd have to eat before they start doing damage to your body? The answer, according to a review of new dietary research, is just one. Just one high-fat, high-sugar meal can trigger a biochemical cascade, causing inflammation of blood vessels and immediate, detrimental changes to the nervous system, according to the paper, published this week in the Journal of the American College of Cardiology. And just one healthy meal helps return your body to its optimal state. "Your health and vigor, at a very basic level, are as good as your last meal," says lead author James O'Keefe, head of preventive cardiology at the Mid America Heart Institute in Kansas City, Mo.
Here's how it works. When you eat, your body breaks down the food into a stream of nutrients, including glucose (sugar), lipids (fats), and amino acids (the building blocks of protein). If your meal happens to be junk food — say, a processed bun with a cheap beef patty, French fries and a Coke — the rush of sugar causes something called "post-prandial hyperglycemia": a big spike in blood-sugar levels. Poor diet in the long-term leads to hypertension and buildup of gunk in blood vessels that increases heart-attack risk. But there are short-term effects too. "People don't understand this, even most physicians," says O'Keefe. Tissue becomes inflamed, just as it does when infected. Blood vessels constrict. Free radicals, unstable molecules that cause cell damage and are thought to contribute to chronic disease and aging, are generated. The body's stress response has a bigger effect on blood pressure, raising it higher than normal. People may notice they feel crummy a few hours after eating junk food. And the sudden surge and drop in insulin — the hormone that spurs your body to store energy — also leaves them feeling hungry again soon after eating, despite having had plenty of calories.
The good news is that these blood-sugar spikes and crashes are easy to regulate. Blood sugar will rise and fall quickly if, for example, a person eats an easily digested meal of only white bread. Eat some vinegar with the bread, however, and the impact is dampened: The vinegar slows digestion, helping to keep blood-sugar levels more even. The same thing happens if a person takes his bread with nuts or with a glass of wine. (The dampening effect of alcohol reverses after more than a couple units, which may help to explain why moderate drinking, but not heavy drinking, is associated with long life.) The common denominator of all these slow-release foods, says O'Keefe, is a generally high nutritive value with low calories. The healthy foods are exactly the ones you would expect, all that stuff your mom (and your doctor) told you to eat: lots of fresh vegetables and fruits, lean proteins like fish and legumes, and high-fiber whole grains. All of them blunt the post-prandial spike. "To some degree it kind of highlights why some dietary components are healthy for you," says O'Keefe.
Regardless of its benefits, healthy food can leave you feeling unsatisfied if you're used to eating junk. Junk food distorts a person's hormonal profile, says O'Keefe. Note, for example, the previously mentioned drop in insulin that leaves a person hungry not long after eating a heavy meal. Studies suggest that fatty, sugary foods promote excretion of the stress hormone cortisol, which seems to further stimulate appetite for calorie-dense foods. And the big post-meal spikes in blood sugar are more likely in people who don't exercise or those who carry weight around their abdomen. All of it makes it tough for people to stop eating junk food once they're in the habit. "The more you eat it the more you crave it. It becomes a vicious cycle," says O'Keefe. The solution? "I tell people they should get a home glucose monitor," he says. Then you can see immediately what your meals are doing to your body. It may help you stick to your plan to eat well, too. "You can improve your health, basically, from hour to hour," he says.
* Time January 15, 2008
Here's how it works. When you eat, your body breaks down the food into a stream of nutrients, including glucose (sugar), lipids (fats), and amino acids (the building blocks of protein). If your meal happens to be junk food — say, a processed bun with a cheap beef patty, French fries and a Coke — the rush of sugar causes something called "post-prandial hyperglycemia": a big spike in blood-sugar levels. Poor diet in the long-term leads to hypertension and buildup of gunk in blood vessels that increases heart-attack risk. But there are short-term effects too. "People don't understand this, even most physicians," says O'Keefe. Tissue becomes inflamed, just as it does when infected. Blood vessels constrict. Free radicals, unstable molecules that cause cell damage and are thought to contribute to chronic disease and aging, are generated. The body's stress response has a bigger effect on blood pressure, raising it higher than normal. People may notice they feel crummy a few hours after eating junk food. And the sudden surge and drop in insulin — the hormone that spurs your body to store energy — also leaves them feeling hungry again soon after eating, despite having had plenty of calories.
The good news is that these blood-sugar spikes and crashes are easy to regulate. Blood sugar will rise and fall quickly if, for example, a person eats an easily digested meal of only white bread. Eat some vinegar with the bread, however, and the impact is dampened: The vinegar slows digestion, helping to keep blood-sugar levels more even. The same thing happens if a person takes his bread with nuts or with a glass of wine. (The dampening effect of alcohol reverses after more than a couple units, which may help to explain why moderate drinking, but not heavy drinking, is associated with long life.) The common denominator of all these slow-release foods, says O'Keefe, is a generally high nutritive value with low calories. The healthy foods are exactly the ones you would expect, all that stuff your mom (and your doctor) told you to eat: lots of fresh vegetables and fruits, lean proteins like fish and legumes, and high-fiber whole grains. All of them blunt the post-prandial spike. "To some degree it kind of highlights why some dietary components are healthy for you," says O'Keefe.
Regardless of its benefits, healthy food can leave you feeling unsatisfied if you're used to eating junk. Junk food distorts a person's hormonal profile, says O'Keefe. Note, for example, the previously mentioned drop in insulin that leaves a person hungry not long after eating a heavy meal. Studies suggest that fatty, sugary foods promote excretion of the stress hormone cortisol, which seems to further stimulate appetite for calorie-dense foods. And the big post-meal spikes in blood sugar are more likely in people who don't exercise or those who carry weight around their abdomen. All of it makes it tough for people to stop eating junk food once they're in the habit. "The more you eat it the more you crave it. It becomes a vicious cycle," says O'Keefe. The solution? "I tell people they should get a home glucose monitor," he says. Then you can see immediately what your meals are doing to your body. It may help you stick to your plan to eat well, too. "You can improve your health, basically, from hour to hour," he says.
* Time January 15, 2008
19 January 2008
76 Ways Sugar Can Ruin Your Health
Contributed by Nancy Appleton, Ph.D
Author of the book Lick The Sugar Habit
In addition to throwing off the body's homeostasis, excess sugar may result in a number of other significant consequences. The following is a listing of some of sugar's metabolic consequences from a variety of medical journals and other scientific publications.
1.Sugar can suppress your immune system and impair your defenses against infectious disease.1,2
2.Sugar upsets the mineral relationships in your body: causes chromium and copper deficiencies and interferes with absorption of calcium and magnesium. 3,4,5,6
3. Sugar can cause can cause a rapid rise of adrenaline, hyperactivity, anxiety, difficulty concentrating, and crankiness in children.7,8
4. Sugar can produce a significant rise in total cholesterol, triglycerides and bad cholesterol and a decrease in good cholesterol.9,10,11,12
5. Sugar causes a loss of tissue elasticity and function.13
6. Sugar feeds cancer cells and has been connected with the development of cancer of the breast, ovaries, prostate, rectum, pancreas, biliary tract, lung, gallbladder and stomach.14,15,16,17,18,19,20
7. Sugar can increase fasting levels of glucose and can cause reactive hypoglycemia.21,22
8. Sugar can weaken eyesight.23
9. Sugar can cause many problems with the gastrointestinal tract including: an acidic digestive tract, indigestion, malabsorption in patients with functional bowel disease, increased risk of Crohn's disease, and ulcerative colitis.24,25,26,27,28
10. Sugar can cause premature aging.29
11. Sugar can lead to alcoholism.30
12. Sugar can cause your saliva to become acidic, tooth decay, and periodontal disease.31,32,33
13. Sugar contributes to obesity.34
14. Sugar can cause autoimmune diseases such as: arthritis, asthma, multiple sclerosis.35,36,37
15. Sugar greatly assists the uncontrolled growth of Candida Albicans (yeast infections)38
16. Sugar can cause gallstones.39
17. Sugar can cause appendicitis.40
18. Sugar can cause hemorrhoids.41
19. Sugar can cause varicose veins.42
20. Sugar can elevate glucose and insulin responses in oral contraceptive users.43
21. Sugar can contribute to osteoporosis.44
22. Sugar can cause a decrease in your insulin sensitivity thereby causing an abnormally high insulin levels and eventually diabetes.45,46,47
23. Sugar can lower your Vitamin E levels.48
24. Sugar can increase your systolic blood pressure.49
25. Sugar can cause drowsiness and decreased activity in children.50
26. High sugar intake increases advanced glycation end products (AGEs)(Sugar molecules attaching to and thereby damaging proteins in the body).51
27. Sugar can interfere with your absorption of protein.52
28. Sugar causes food allergies.53
29. Sugar can cause toxemia during pregnancy.54
30. Sugar can contribute to eczema in children.55
31. Sugar can cause atherosclerosis and cardiovascular disease.56,57
32. Sugar can impair the structure of your DNA.58
33. Sugar can change the structure of protein and cause a permanent alteration of the way the proteins act in your body.59,60
34. Sugar can make your skin age by changing the structure of collagen.61
35. Sugar can cause cataracts and nearsightedness.62,63
36. Sugar can cause emphysema.64
37. High sugar intake can impair the physiological homeostasis of many systems in your body.65
38. Sugar lowers the ability of enzymes to function.66
39. Sugar intake is higher in people with Parkinson's disease.67
40. Sugar can increase the size of your liver by making your liver cells divide and it can increase the amount of liver fat.68,69
41. Sugar can increase kidney size and produce pathological changes in the kidney such as the formation of kidney stones.70,71
42. Sugar can damage your pancreas.72
43. Sugar can increase your body's fluid retention.73
44. Sugar is enemy #1 of your bowel movement.74
45. Sugar can compromise the lining of your capillaries.75
46. Sugar can make your tendons more brittle.76
47. Sugar can cause headaches, including migraines.77
48. Sugar can reduce the learning capacity, adversely affect school children's grades and cause learning disorders.78,79
49. Sugar can cause an increase in delta, alpha, and theta brain waves which can alter your mind's ability to think clearly.80
50. Sugar can cause depression.81
51. Sugar can increase your risk of gout.82
52. Sugar can increase your risk of Alzheimer's disease.83
53. Sugar can cause hormonal imbalances such as: increasing estrogen in men, exacerbating PMS, and decreasing growth hormone.84,85,86,87
54. Sugar can lead to dizziness.88
55. Diets high in sugar will increase free radicals and oxidative stress.89
56. High sucrose diets of subjects with peripheral vascular disease significantly increases platelet adhesion.90
57. High sugar consumption of pregnant adolescents can lead to substantial decrease in gestation duration and is associated with a twofold increased risk for delivering a small-for-gestational-age (SGA) infant.91,92
58. Sugar is an addictive substance.93
59. Sugar can be intoxicating, similar to alcohol.94
60. Sugar given to premature babies can affect the amount of carbon dioxide they produce.95
61. Decrease in sugar intake can increase emotional stability.96
62. Your body changes sugar into 2 to 5 times more fat in the bloodstream than it does starch.97
63. The rapid absorption of sugar promotes excessive food intake in obese subjects.98
64. Sugar can worsen the symptoms of children with attention deficit hyperactivity disorder (ADHD).99
65. Sugar adversely affects urinary electrolyte composition.100
66. Sugar can slow down the ability of your adrenal glands to function.101
67. Sugar has the potential of inducing abnormal metabolic processes in a normal healthy individual and to promote chronic degenerative diseases.102
68. I.V.s (intravenous feedings) of sugar water can cut off oxygen to your brain.103
69. Sugar increases your risk of polio.104
70. High sugar intake can cause epileptic seizures.105
71. Sugar causes high blood pressure in obese people.106
72. In intensive care units: Limiting sugar saves lives.107
73. Sugar may induce cell death.108
74. In juvenile rehabilitation camps, when children were put on a low sugar diet, there was a 44 percent drop in antisocial behavior.109
75. Sugar dehydrates newborns.110
76. Sugar can cause gum disease.111
Author of the book Lick The Sugar Habit
In addition to throwing off the body's homeostasis, excess sugar may result in a number of other significant consequences. The following is a listing of some of sugar's metabolic consequences from a variety of medical journals and other scientific publications.
1.Sugar can suppress your immune system and impair your defenses against infectious disease.1,2
2.Sugar upsets the mineral relationships in your body: causes chromium and copper deficiencies and interferes with absorption of calcium and magnesium. 3,4,5,6
3. Sugar can cause can cause a rapid rise of adrenaline, hyperactivity, anxiety, difficulty concentrating, and crankiness in children.7,8
4. Sugar can produce a significant rise in total cholesterol, triglycerides and bad cholesterol and a decrease in good cholesterol.9,10,11,12
5. Sugar causes a loss of tissue elasticity and function.13
6. Sugar feeds cancer cells and has been connected with the development of cancer of the breast, ovaries, prostate, rectum, pancreas, biliary tract, lung, gallbladder and stomach.14,15,16,17,18,19,20
7. Sugar can increase fasting levels of glucose and can cause reactive hypoglycemia.21,22
8. Sugar can weaken eyesight.23
9. Sugar can cause many problems with the gastrointestinal tract including: an acidic digestive tract, indigestion, malabsorption in patients with functional bowel disease, increased risk of Crohn's disease, and ulcerative colitis.24,25,26,27,28
10. Sugar can cause premature aging.29
11. Sugar can lead to alcoholism.30
12. Sugar can cause your saliva to become acidic, tooth decay, and periodontal disease.31,32,33
13. Sugar contributes to obesity.34
14. Sugar can cause autoimmune diseases such as: arthritis, asthma, multiple sclerosis.35,36,37
15. Sugar greatly assists the uncontrolled growth of Candida Albicans (yeast infections)38
16. Sugar can cause gallstones.39
17. Sugar can cause appendicitis.40
18. Sugar can cause hemorrhoids.41
19. Sugar can cause varicose veins.42
20. Sugar can elevate glucose and insulin responses in oral contraceptive users.43
21. Sugar can contribute to osteoporosis.44
22. Sugar can cause a decrease in your insulin sensitivity thereby causing an abnormally high insulin levels and eventually diabetes.45,46,47
23. Sugar can lower your Vitamin E levels.48
24. Sugar can increase your systolic blood pressure.49
25. Sugar can cause drowsiness and decreased activity in children.50
26. High sugar intake increases advanced glycation end products (AGEs)(Sugar molecules attaching to and thereby damaging proteins in the body).51
27. Sugar can interfere with your absorption of protein.52
28. Sugar causes food allergies.53
29. Sugar can cause toxemia during pregnancy.54
30. Sugar can contribute to eczema in children.55
31. Sugar can cause atherosclerosis and cardiovascular disease.56,57
32. Sugar can impair the structure of your DNA.58
33. Sugar can change the structure of protein and cause a permanent alteration of the way the proteins act in your body.59,60
34. Sugar can make your skin age by changing the structure of collagen.61
35. Sugar can cause cataracts and nearsightedness.62,63
36. Sugar can cause emphysema.64
37. High sugar intake can impair the physiological homeostasis of many systems in your body.65
38. Sugar lowers the ability of enzymes to function.66
39. Sugar intake is higher in people with Parkinson's disease.67
40. Sugar can increase the size of your liver by making your liver cells divide and it can increase the amount of liver fat.68,69
41. Sugar can increase kidney size and produce pathological changes in the kidney such as the formation of kidney stones.70,71
42. Sugar can damage your pancreas.72
43. Sugar can increase your body's fluid retention.73
44. Sugar is enemy #1 of your bowel movement.74
45. Sugar can compromise the lining of your capillaries.75
46. Sugar can make your tendons more brittle.76
47. Sugar can cause headaches, including migraines.77
48. Sugar can reduce the learning capacity, adversely affect school children's grades and cause learning disorders.78,79
49. Sugar can cause an increase in delta, alpha, and theta brain waves which can alter your mind's ability to think clearly.80
50. Sugar can cause depression.81
51. Sugar can increase your risk of gout.82
52. Sugar can increase your risk of Alzheimer's disease.83
53. Sugar can cause hormonal imbalances such as: increasing estrogen in men, exacerbating PMS, and decreasing growth hormone.84,85,86,87
54. Sugar can lead to dizziness.88
55. Diets high in sugar will increase free radicals and oxidative stress.89
56. High sucrose diets of subjects with peripheral vascular disease significantly increases platelet adhesion.90
57. High sugar consumption of pregnant adolescents can lead to substantial decrease in gestation duration and is associated with a twofold increased risk for delivering a small-for-gestational-age (SGA) infant.91,92
58. Sugar is an addictive substance.93
59. Sugar can be intoxicating, similar to alcohol.94
60. Sugar given to premature babies can affect the amount of carbon dioxide they produce.95
61. Decrease in sugar intake can increase emotional stability.96
62. Your body changes sugar into 2 to 5 times more fat in the bloodstream than it does starch.97
63. The rapid absorption of sugar promotes excessive food intake in obese subjects.98
64. Sugar can worsen the symptoms of children with attention deficit hyperactivity disorder (ADHD).99
65. Sugar adversely affects urinary electrolyte composition.100
66. Sugar can slow down the ability of your adrenal glands to function.101
67. Sugar has the potential of inducing abnormal metabolic processes in a normal healthy individual and to promote chronic degenerative diseases.102
68. I.V.s (intravenous feedings) of sugar water can cut off oxygen to your brain.103
69. Sugar increases your risk of polio.104
70. High sugar intake can cause epileptic seizures.105
71. Sugar causes high blood pressure in obese people.106
72. In intensive care units: Limiting sugar saves lives.107
73. Sugar may induce cell death.108
74. In juvenile rehabilitation camps, when children were put on a low sugar diet, there was a 44 percent drop in antisocial behavior.109
75. Sugar dehydrates newborns.110
76. Sugar can cause gum disease.111
18 January 2008
Lower Your Grains & Lower Your Insulin Levels! A Novel Way To Treat Hypoglycemia.
Hypoglycemia is a common problem. Over the past fifteen years, our dietary establishment has made a virtual industry of extolling the virtues of carbohydrates.
We're constantly told that carbohydrates are the good guys of nutrition, and that, if we eat large amounts of them, the world should be a better place. In such a world, the experts tell us, there will be no heart disease and no obesity.
Under such guidance, Americans are gobbling breads, cereals, and pastas as if there were no tomorrow, trying desperately to reach that 80 to 85 percent of total calories advocated by the high-carb extremists.
This creates a terrible paradox: people are eating less fat and getting fatter! No medical authority will tell you that excess body fat makes you healthier. There is but one alarming conclusion to reach: a high-carbohydrate, low-fat diet may be dangerous to your health.
Overeating carbohydrate foods can prevent a higher percentage of fats from being used for energy, and lead to a decrease in endurance and an increase in fat storage.
Eating fat does not make you fat. It's your body's response to excess carbohydrates in your diet that makes you fat. Your body has a limited capacity to store excess carbohydrates, but it can easily convert those excess carbohydrates into excess body fat.
It's hard to lose weight by simply restricting calories. Eating less and losing excess body fat do not automatically go hand in hand.
Low-calorie, high-carbohydrate diets generate a series of biochemical signals in your body that will take you out of the balance, making it more difficult to access stored body fat for energy. Result: you'll reach a weight-loss plateau, beyond which you simply can't lose any more weight.
Diets based on choice restriction and calorie limits usually fail. People on restrictive diets get tired of feeling hungry and deprived. They go off their diets, put the weight back on (primarily as increased body fat), and then feel bad about themselves for not having enough will power, discipline, or motivation.
Weight loss has little to do with willpower. You need information, not will power. If you change what you eat, you don't have to be overly concerned about how much you eat. Adhering to a diet of low carbohydrate meals, you can eat enough to feel satisfied and still wind up losing fat-without obsessively counting calories or fat grams.
Food Can Be Good or Bad
The ratio of macronutrients protein, carbohydrate, and fat-in the meals you eat is the key to permanent weight loss and optimal health. Unless you understand the rules that control the powerful biochemical responses generated by food, you will never achieve optimal wellness.
Unfortunately, many people don't really know what a carbohydrate is. Most people will say carbohydrates are sweets and pasta. Ask them what a vegetable or fruit is, and they'll probably reply that it's a vegetable or fruit-as if that were a food type all its own, a food type that they can eat in unlimited amounts without gaining weight.
Well, this may come as a surprise, but all of the above-sweets and pasta, vegetables and fruits-are carbohydrates. Carbohydrates are merely different forms of simple sugars linked together in polymers-something like edible plastic.
Of course, we all need a certain amount of carbohydrates in our diet. The body requires a continual intake of carbohydrates to feed the brain, which uses glucose (a form of sugar) as its primary energy source.
In fact, the brain is a virtual glucose hog, gobbling more than two thirds of the circulating carbohydrates in the bloodstream while you are at rest. To feed this glucose hog, the body continually takes carbohydrates and converts them to glucose.
It's actually a bit more complicated than that. Any carbohydrates not immediately used by the body will be stored in the form of glycogen (a long string of glucose molecules linked together).
The body has two storage sites for glycogen: the liver and the muscles. The glycogen stored in the muscles is inaccessible to the brain. Only the glycogen stored in the liver can be broken down and sent back to the bloodstream so as to maintain adequate blood sugar levels for proper brain function.
The liver's capacity to store carbohydrates in the form of glycogen is very limited and can be easily depleted within ten to twelve hours. So the liver's glycogen reserves must be maintained on a continual basis. That's why we eat carbohydrates.
The question no one has bothered to ask until now is this: what happens when you eat too much carbohydrate? Here's the answer: whether it's being stored in the liver or the muscles, the total storage capacity of the body for carbohydrate is really quite limited.
If you're an average person, you can store about three hundred to four hundred grams of carbohydrate in your muscles, but you can't get at that carbohydrate. In the liver, where carbohydrates are accessible for glucose conversion, you can store only about sixty to ninety grams.
This is equivalent to about two cups of cooked pasta or three typical candy bars, and it represents your total reserve capacity to keep the brain working properly.
Once the glycogen levels are filled in both the liver and the muscles, excess carbohydrates have just one fate: to be converted into fat and stored in the adipose, that is, fatty, tissue.
In a nutshell, even though carbohydrates themselves are fat-free, excess carbohydrates ends up as excess fat. That's not the worst of it. Any meal or snack high in carbohydrates will generate a rapid rise in blood glucose. To adjust for this rapid rise, the pancreas secretes the hormone insulin into the bloodstream. Insulin then lowers the levels of blood glucose.
The problem is that insulin is essentially a storage hormone, evolved to put aside excess carbohydrate calories in the form of fat in case of future famine. So the insulin that's stimulated by excess carbohydrates aggressively promotes the accumulation of body fat.
In other words, when we eat too much carbohydrate, we're essentially sending a hormonal message, via insulin, to the body (actually, to the adipose cells). The message: "Store fat."
Hold on; it gets even worse. Not only do increased insulin levels tell the body to store carbohydrates as fat, they also tell it not to release any stored fat. This makes it impossible for you to use your own stored body fat for energy.
So the excess carbohydrates in your diet not only make you fat, they make sure you stay fat. It's a double whammy, and it can be lethal.
Insulin is released by the pancreas after you eat carbohydrates. This causes a rise in blood sugar. Insulin assures your cells receive some blood sugar necessary for life, and increases glycogen storage.
However, it also drives your body to use more carbohydrate, and less fat, as fuel. And, insulin converts almost half of your dietary carbohydrate to fat for storage. If you want to use more fats for energy, the insulin response must be moderated.
Diets high in refined sugars release more insulin thereby allowing less stored fat to be burned. High insulin levels also suppress two important hormones: glucagon and growth hormone. Glucagon promotes the burning of fat and sugar. Growth hormone is used for muscle development and building new muscle mass.
Insulin also causes hunger. As blood sugar increases following a carbohydrate meal, insulin rises with the eventual result of lower blood sugar. This results in hunger, often only a couple of hours (or less) after the meal.
Cravings, usually for sweets, are frequently part of this cycle, leading you to resort to snacking, often on more carbohydrates. Not eating makes you feel ravenous shaky, moody and ready to "crash." If the problem is chronic, you never get rid of that extra stored fat, and your energy is adversely affected.
Does this sound like you? The best suggestion for anyone wanting to utilize more fats is to moderate the insulin response by limiting (ideally, eliminating) the intake of refined sugars, and keeping all other carbohydrate intake to about 40% of the diet. Generally, non-carbohydrate foods-proteins and fats-don't produce much insulin.
Insulin responses can vary greatly from person to person. But generally, more refined foods evoke a stronger and/or more rapid insulin reaction. One reason for this is refined carbohydrates lack the natural fiber which helps minimize the carbohydrate/insulin response.
Consumption of natural fiber with carbohydrates can reduce the extreme blood sugar reactions described above. Low-fat diets cause quicker digestion and absorption of carbohydrates in the form of sugar. By adding some fats to the diet, digestion and absorption is slower, and the insulin reaction is moderated.
Recommendations for them include long-term restriction of carbohydrates and an increase in dietary fats. For some of these people, it means lowering carbohydrate intake to below 40%, sometimes even as low as 20%. By moderating carbohydrate intake you can increase your fat burning as an optimal and efficient source of almost unlimited energy.
Perhaps a third to a half or more of our population is unable to process carbohydrates-sugars and starches efficiently. In many people it's due to genetics, with lifestyle contributing to the condition.
This can be termed insulin resistance or IR. Like many problems, IR is an individual one, affecting different people different ways. You must determine if you are carbohydrate intolerant, and if so, to what degree. Blood tests will only diagnose the problem in the later stages, but the symptoms may have begun years earlier.
As we now know, insulin has many functions. While it can't get glucose into the cells efficiently when they're in a state of insulin resistance, insulin still performs its other tasks, including converting carbohydrates to fat and inhibiting stored fat from being burned.
In a normal person, 40% of the carbohydrates eaten is converted to fat. In the IR person, that number may be much higher. Many people with IR have a family history of diabetes.
Don't think of IR itself as a disease, although left unchecked, it can create problems that lead to disease. It may be quite normal for some humans to be unable to eat large or even moderate amounts of carbohydrates.
As a matter of fact, we evolved for hundreds of thousands of years from the so-called cave man's diet," which consisted solely of meat and vegetables.
With the onset of modern civilization about 5,000 years ago, our physiology suddenly was asked to digest and metabolize larger amounts of sugar and starch especially refined sugars. But if we are unable to utilize the amount of carbohydrates we eat, certain symptoms will develop.
Below is a list of some of the most common complaints of people with IR Many symptoms occur immediately following a meal of carbo-hydrates, and others are constant. Keep in mind that these symptoms may also be related to other problems.
1. Fatigue. Whether you call it fatigue or exhaustion, the most common feature of IR is that it wears people out. Some are tired just in the morning or afternoon; others are exhausted all day.
2. Brain fogginess. Sometimes the fatigue of IR is physical, but often it's mental (as opposed to psychological); the inability to concentrate is the most evident symptom. Loss of creativity, poor memory, failing or poor grades in school often accompany IR, as do various forms of "learning disabilities."
3. Low blood sugar. Brief, mild periods of low blood sugar are normal during the day, especially if meals are not eaten on a regular schedule. But prolonged periods of this "hypoglycemia," accompanied by many of the symptoms listed here, especially mental and physical fatigue, are not normal.
Feeling jittery agitated and moody is common in IR, with an almost immediate relief once food is eaten. Dizziness is also common, as is the craving for sweets, chocolate or caffeine.
These bouts occur more frequently before meals or first thing in the morning. The old hypoglycemic diet, still in use today, recommends frequent snacks, and individuals with IR usually know to eat often. However, the hypoglycemic diet contains too much carbohydrate for most IR people.
4. Intestinal bloating. Most intestinal gas is produced from dietary carbohydrates. IR sufferers who eat carbohydrates suffer from gas, lots of it. Antacids or other remedies for symptomatic relief, are not very successful in dealing with the problem.
Sometimes the intestinal distress becomes quite severe, resulting in a diagnosis of "colitis" or "ileitis," although this is usually not a true disease state. However, IR is often associated with true gastrointestinal disease, which must be differentiated from simple intestinal bloating.
5. Sleepiness. Many people with IR get sleepy immediately after meals containing more than 20% or 30% carbohydrates. This is typically a pasta meal, or even a meat meal which includes bread or potatoes and a sweet dessert.
6. Increased fat storage and weight. For most people, too much weight is too much fat. In males, a large abdomen is the more evident and earliest sign of IR. In females, it's prominent buttocks, frequently accompanied by "chipmunk cheeks."
7. Increased triglycerides. High triglycerides in the blood are often seen in overweight persons. But even those who are not too fat may have stores of fat in their arteries as a result of IR.
These triglycerides are the direct result of carbohydrates from the diet being converted by insulin. In my experience, fasting triglyceride levels over 100 may be an indication of a carbohydrate problem, even though 100 is in the so-called "normal" range.
8. Increased blood pressure. It is well known that most people with hypertension have too much insulin and are IR. It is often possible to show a direct relationship between the level of insulin and the level of blood pressure: as insulin levels elevate, so does blood pressure.
9. Depression. Because carbohydrates are a natural "downer," depressing the brain, it is not uncommon to see many depressed persons also having IR.
Carbohydrates do this by changing the brain chemistry. Carbohydrates increase serotonin, which produces a depressing or sleepy feeling. This is the reason nice hotels place candy on your pillow in the evening; it literally helps you sleep. (Protein, on the other hand, is a brain stimulant, picking you up mentally.
Here's another example of how trends distort the real picture: many people have been taught that sugar is stimulating. This is a significant consideration for those trying to learn, whether at school, home or work.)
10. Insulin Resistance is also prevalent in persons addicted to alcohol, caffeine, cigarettes or other drugs. Often, the drug is the secondary problem, with IR being the primary one. Treating this primary problem should obviously be a major focus of any therapy.
IR sufferers may have other symptoms as well. However, when a person with this problem finally lowers carbohydrate intake to tolerable levels, many if not most of the other symptoms may disappear.
With the stress of IR eliminated, the body is finally able to correct many of its own problems. It is possible, although unlikely, that so many of these symptoms can be found in someone who tolerates carbohydrates quite well.
RULES OF THE ROAD TO REACH BALANCE
1. Protein. Know how much protein your body needs. Never consume more protein than your body requires. And never consume less. For precise measurements our nurse can determine that for you.
You can also perform the calculations reviewed in The Zone. Generally adult protein requirements range from a low of 35 grams per day or a sedentary 250 pound obese individual to as much as 200 grams per day for a lean heavily exercising 100 pound athlete.
You should have protein at EVERY meal and the total per day should equal your daily requirement. For every three grams of protein at a meal you need to have four grams of carbohydrate and 1.5 grams of fat.
You can multiply protein by 1.25 to obtain the amout of carbohdrate and by 0.5 to obtain the amount of fat. This is a rough estimate and you should not become overwhelmed trying to get this absolutely precise. It is important though to be in the general area.
Corrinne Netzer wrote a book The Complete Book of Food Counts that can help you make this calculation. You might also want to make an appointment with our diet counsellor Anne to help you with this process.
Choose your protein based on those recommended for your blood type. This can be found in Dr. D'Adamo's book Eat Right For Your Type. If you are seriously ill you should have your blood subtyped so we can provide an even more accurate recommendation for you.
2. Carbohydrate. You should also choose your carbohydrates from Dr. D'Adamo's book. If you are insulin resistant, (have high blood pressure, high cholesterol, high blood pressure or are overweight) then you need to specifically restrict your carbohydrates based on the Heller's book The Carbohydrate Addict's Lifespan Program.
Combining all three authors is the most powerful method we know to lower your insulin levels and produce optimum health.
If you find yourself hungry and craving sugar or sweets two to three hours after a meal, you probably consumed too many carbohydrates that last meal. Whenever you have a problem with hunger or carbohydrate cravings, look to your last meal for a clue to the reason why.
No matter how consistently you follow this dietary strategy, you are bound to make mistakes. This is especially true at parties or when traveling. Remember, if you're only unbalanced for a short period of time, you're only one meal away from rebalancing. It's like falling off a bike-you just get back up and continue your journey.
3. Fat. Choose your fats based on Dr. D'Adamo's recommendations. Most people can tolerate olive oil and it is the oil of choice. It is best purchased in small glass bottles. Fish is a good source of EPA which is beneficial fat that will help balance out your hormone levels and decrease inflammation.
4. Water. Try to drink at least 64 ounces of pure water per day. If you are a heavy caffeine user, gradually reduce caffeine intake to zero whenever possible as the breakdown products of caffeine will tend to increase insulin levels.
5. Exercise. Try to get 30 to 60 minutes of walking in four to five days a week if the weather permits. If you are seriously debilitated you will have to wait until your health improves. As you are healthier and if you are blood type 0 or B you can shift to more aggressive exercises.
We're constantly told that carbohydrates are the good guys of nutrition, and that, if we eat large amounts of them, the world should be a better place. In such a world, the experts tell us, there will be no heart disease and no obesity.
Under such guidance, Americans are gobbling breads, cereals, and pastas as if there were no tomorrow, trying desperately to reach that 80 to 85 percent of total calories advocated by the high-carb extremists.
This creates a terrible paradox: people are eating less fat and getting fatter! No medical authority will tell you that excess body fat makes you healthier. There is but one alarming conclusion to reach: a high-carbohydrate, low-fat diet may be dangerous to your health.
Overeating carbohydrate foods can prevent a higher percentage of fats from being used for energy, and lead to a decrease in endurance and an increase in fat storage.
Eating fat does not make you fat. It's your body's response to excess carbohydrates in your diet that makes you fat. Your body has a limited capacity to store excess carbohydrates, but it can easily convert those excess carbohydrates into excess body fat.
It's hard to lose weight by simply restricting calories. Eating less and losing excess body fat do not automatically go hand in hand.
Low-calorie, high-carbohydrate diets generate a series of biochemical signals in your body that will take you out of the balance, making it more difficult to access stored body fat for energy. Result: you'll reach a weight-loss plateau, beyond which you simply can't lose any more weight.
Diets based on choice restriction and calorie limits usually fail. People on restrictive diets get tired of feeling hungry and deprived. They go off their diets, put the weight back on (primarily as increased body fat), and then feel bad about themselves for not having enough will power, discipline, or motivation.
Weight loss has little to do with willpower. You need information, not will power. If you change what you eat, you don't have to be overly concerned about how much you eat. Adhering to a diet of low carbohydrate meals, you can eat enough to feel satisfied and still wind up losing fat-without obsessively counting calories or fat grams.
Food Can Be Good or Bad
The ratio of macronutrients protein, carbohydrate, and fat-in the meals you eat is the key to permanent weight loss and optimal health. Unless you understand the rules that control the powerful biochemical responses generated by food, you will never achieve optimal wellness.
Unfortunately, many people don't really know what a carbohydrate is. Most people will say carbohydrates are sweets and pasta. Ask them what a vegetable or fruit is, and they'll probably reply that it's a vegetable or fruit-as if that were a food type all its own, a food type that they can eat in unlimited amounts without gaining weight.
Well, this may come as a surprise, but all of the above-sweets and pasta, vegetables and fruits-are carbohydrates. Carbohydrates are merely different forms of simple sugars linked together in polymers-something like edible plastic.
Of course, we all need a certain amount of carbohydrates in our diet. The body requires a continual intake of carbohydrates to feed the brain, which uses glucose (a form of sugar) as its primary energy source.
In fact, the brain is a virtual glucose hog, gobbling more than two thirds of the circulating carbohydrates in the bloodstream while you are at rest. To feed this glucose hog, the body continually takes carbohydrates and converts them to glucose.
It's actually a bit more complicated than that. Any carbohydrates not immediately used by the body will be stored in the form of glycogen (a long string of glucose molecules linked together).
The body has two storage sites for glycogen: the liver and the muscles. The glycogen stored in the muscles is inaccessible to the brain. Only the glycogen stored in the liver can be broken down and sent back to the bloodstream so as to maintain adequate blood sugar levels for proper brain function.
The liver's capacity to store carbohydrates in the form of glycogen is very limited and can be easily depleted within ten to twelve hours. So the liver's glycogen reserves must be maintained on a continual basis. That's why we eat carbohydrates.
The question no one has bothered to ask until now is this: what happens when you eat too much carbohydrate? Here's the answer: whether it's being stored in the liver or the muscles, the total storage capacity of the body for carbohydrate is really quite limited.
If you're an average person, you can store about three hundred to four hundred grams of carbohydrate in your muscles, but you can't get at that carbohydrate. In the liver, where carbohydrates are accessible for glucose conversion, you can store only about sixty to ninety grams.
This is equivalent to about two cups of cooked pasta or three typical candy bars, and it represents your total reserve capacity to keep the brain working properly.
Once the glycogen levels are filled in both the liver and the muscles, excess carbohydrates have just one fate: to be converted into fat and stored in the adipose, that is, fatty, tissue.
In a nutshell, even though carbohydrates themselves are fat-free, excess carbohydrates ends up as excess fat. That's not the worst of it. Any meal or snack high in carbohydrates will generate a rapid rise in blood glucose. To adjust for this rapid rise, the pancreas secretes the hormone insulin into the bloodstream. Insulin then lowers the levels of blood glucose.
The problem is that insulin is essentially a storage hormone, evolved to put aside excess carbohydrate calories in the form of fat in case of future famine. So the insulin that's stimulated by excess carbohydrates aggressively promotes the accumulation of body fat.
In other words, when we eat too much carbohydrate, we're essentially sending a hormonal message, via insulin, to the body (actually, to the adipose cells). The message: "Store fat."
Hold on; it gets even worse. Not only do increased insulin levels tell the body to store carbohydrates as fat, they also tell it not to release any stored fat. This makes it impossible for you to use your own stored body fat for energy.
So the excess carbohydrates in your diet not only make you fat, they make sure you stay fat. It's a double whammy, and it can be lethal.
Insulin is released by the pancreas after you eat carbohydrates. This causes a rise in blood sugar. Insulin assures your cells receive some blood sugar necessary for life, and increases glycogen storage.
However, it also drives your body to use more carbohydrate, and less fat, as fuel. And, insulin converts almost half of your dietary carbohydrate to fat for storage. If you want to use more fats for energy, the insulin response must be moderated.
Diets high in refined sugars release more insulin thereby allowing less stored fat to be burned. High insulin levels also suppress two important hormones: glucagon and growth hormone. Glucagon promotes the burning of fat and sugar. Growth hormone is used for muscle development and building new muscle mass.
Insulin also causes hunger. As blood sugar increases following a carbohydrate meal, insulin rises with the eventual result of lower blood sugar. This results in hunger, often only a couple of hours (or less) after the meal.
Cravings, usually for sweets, are frequently part of this cycle, leading you to resort to snacking, often on more carbohydrates. Not eating makes you feel ravenous shaky, moody and ready to "crash." If the problem is chronic, you never get rid of that extra stored fat, and your energy is adversely affected.
Does this sound like you? The best suggestion for anyone wanting to utilize more fats is to moderate the insulin response by limiting (ideally, eliminating) the intake of refined sugars, and keeping all other carbohydrate intake to about 40% of the diet. Generally, non-carbohydrate foods-proteins and fats-don't produce much insulin.
Insulin responses can vary greatly from person to person. But generally, more refined foods evoke a stronger and/or more rapid insulin reaction. One reason for this is refined carbohydrates lack the natural fiber which helps minimize the carbohydrate/insulin response.
Consumption of natural fiber with carbohydrates can reduce the extreme blood sugar reactions described above. Low-fat diets cause quicker digestion and absorption of carbohydrates in the form of sugar. By adding some fats to the diet, digestion and absorption is slower, and the insulin reaction is moderated.
Recommendations for them include long-term restriction of carbohydrates and an increase in dietary fats. For some of these people, it means lowering carbohydrate intake to below 40%, sometimes even as low as 20%. By moderating carbohydrate intake you can increase your fat burning as an optimal and efficient source of almost unlimited energy.
Perhaps a third to a half or more of our population is unable to process carbohydrates-sugars and starches efficiently. In many people it's due to genetics, with lifestyle contributing to the condition.
This can be termed insulin resistance or IR. Like many problems, IR is an individual one, affecting different people different ways. You must determine if you are carbohydrate intolerant, and if so, to what degree. Blood tests will only diagnose the problem in the later stages, but the symptoms may have begun years earlier.
As we now know, insulin has many functions. While it can't get glucose into the cells efficiently when they're in a state of insulin resistance, insulin still performs its other tasks, including converting carbohydrates to fat and inhibiting stored fat from being burned.
In a normal person, 40% of the carbohydrates eaten is converted to fat. In the IR person, that number may be much higher. Many people with IR have a family history of diabetes.
Don't think of IR itself as a disease, although left unchecked, it can create problems that lead to disease. It may be quite normal for some humans to be unable to eat large or even moderate amounts of carbohydrates.
As a matter of fact, we evolved for hundreds of thousands of years from the so-called cave man's diet," which consisted solely of meat and vegetables.
With the onset of modern civilization about 5,000 years ago, our physiology suddenly was asked to digest and metabolize larger amounts of sugar and starch especially refined sugars. But if we are unable to utilize the amount of carbohydrates we eat, certain symptoms will develop.
Below is a list of some of the most common complaints of people with IR Many symptoms occur immediately following a meal of carbo-hydrates, and others are constant. Keep in mind that these symptoms may also be related to other problems.
1. Fatigue. Whether you call it fatigue or exhaustion, the most common feature of IR is that it wears people out. Some are tired just in the morning or afternoon; others are exhausted all day.
2. Brain fogginess. Sometimes the fatigue of IR is physical, but often it's mental (as opposed to psychological); the inability to concentrate is the most evident symptom. Loss of creativity, poor memory, failing or poor grades in school often accompany IR, as do various forms of "learning disabilities."
3. Low blood sugar. Brief, mild periods of low blood sugar are normal during the day, especially if meals are not eaten on a regular schedule. But prolonged periods of this "hypoglycemia," accompanied by many of the symptoms listed here, especially mental and physical fatigue, are not normal.
Feeling jittery agitated and moody is common in IR, with an almost immediate relief once food is eaten. Dizziness is also common, as is the craving for sweets, chocolate or caffeine.
These bouts occur more frequently before meals or first thing in the morning. The old hypoglycemic diet, still in use today, recommends frequent snacks, and individuals with IR usually know to eat often. However, the hypoglycemic diet contains too much carbohydrate for most IR people.
4. Intestinal bloating. Most intestinal gas is produced from dietary carbohydrates. IR sufferers who eat carbohydrates suffer from gas, lots of it. Antacids or other remedies for symptomatic relief, are not very successful in dealing with the problem.
Sometimes the intestinal distress becomes quite severe, resulting in a diagnosis of "colitis" or "ileitis," although this is usually not a true disease state. However, IR is often associated with true gastrointestinal disease, which must be differentiated from simple intestinal bloating.
5. Sleepiness. Many people with IR get sleepy immediately after meals containing more than 20% or 30% carbohydrates. This is typically a pasta meal, or even a meat meal which includes bread or potatoes and a sweet dessert.
6. Increased fat storage and weight. For most people, too much weight is too much fat. In males, a large abdomen is the more evident and earliest sign of IR. In females, it's prominent buttocks, frequently accompanied by "chipmunk cheeks."
7. Increased triglycerides. High triglycerides in the blood are often seen in overweight persons. But even those who are not too fat may have stores of fat in their arteries as a result of IR.
These triglycerides are the direct result of carbohydrates from the diet being converted by insulin. In my experience, fasting triglyceride levels over 100 may be an indication of a carbohydrate problem, even though 100 is in the so-called "normal" range.
8. Increased blood pressure. It is well known that most people with hypertension have too much insulin and are IR. It is often possible to show a direct relationship between the level of insulin and the level of blood pressure: as insulin levels elevate, so does blood pressure.
9. Depression. Because carbohydrates are a natural "downer," depressing the brain, it is not uncommon to see many depressed persons also having IR.
Carbohydrates do this by changing the brain chemistry. Carbohydrates increase serotonin, which produces a depressing or sleepy feeling. This is the reason nice hotels place candy on your pillow in the evening; it literally helps you sleep. (Protein, on the other hand, is a brain stimulant, picking you up mentally.
Here's another example of how trends distort the real picture: many people have been taught that sugar is stimulating. This is a significant consideration for those trying to learn, whether at school, home or work.)
10. Insulin Resistance is also prevalent in persons addicted to alcohol, caffeine, cigarettes or other drugs. Often, the drug is the secondary problem, with IR being the primary one. Treating this primary problem should obviously be a major focus of any therapy.
IR sufferers may have other symptoms as well. However, when a person with this problem finally lowers carbohydrate intake to tolerable levels, many if not most of the other symptoms may disappear.
With the stress of IR eliminated, the body is finally able to correct many of its own problems. It is possible, although unlikely, that so many of these symptoms can be found in someone who tolerates carbohydrates quite well.
RULES OF THE ROAD TO REACH BALANCE
1. Protein. Know how much protein your body needs. Never consume more protein than your body requires. And never consume less. For precise measurements our nurse can determine that for you.
You can also perform the calculations reviewed in The Zone. Generally adult protein requirements range from a low of 35 grams per day or a sedentary 250 pound obese individual to as much as 200 grams per day for a lean heavily exercising 100 pound athlete.
You should have protein at EVERY meal and the total per day should equal your daily requirement. For every three grams of protein at a meal you need to have four grams of carbohydrate and 1.5 grams of fat.
You can multiply protein by 1.25 to obtain the amout of carbohdrate and by 0.5 to obtain the amount of fat. This is a rough estimate and you should not become overwhelmed trying to get this absolutely precise. It is important though to be in the general area.
Corrinne Netzer wrote a book The Complete Book of Food Counts that can help you make this calculation. You might also want to make an appointment with our diet counsellor Anne to help you with this process.
Choose your protein based on those recommended for your blood type. This can be found in Dr. D'Adamo's book Eat Right For Your Type. If you are seriously ill you should have your blood subtyped so we can provide an even more accurate recommendation for you.
2. Carbohydrate. You should also choose your carbohydrates from Dr. D'Adamo's book. If you are insulin resistant, (have high blood pressure, high cholesterol, high blood pressure or are overweight) then you need to specifically restrict your carbohydrates based on the Heller's book The Carbohydrate Addict's Lifespan Program.
Combining all three authors is the most powerful method we know to lower your insulin levels and produce optimum health.
If you find yourself hungry and craving sugar or sweets two to three hours after a meal, you probably consumed too many carbohydrates that last meal. Whenever you have a problem with hunger or carbohydrate cravings, look to your last meal for a clue to the reason why.
No matter how consistently you follow this dietary strategy, you are bound to make mistakes. This is especially true at parties or when traveling. Remember, if you're only unbalanced for a short period of time, you're only one meal away from rebalancing. It's like falling off a bike-you just get back up and continue your journey.
3. Fat. Choose your fats based on Dr. D'Adamo's recommendations. Most people can tolerate olive oil and it is the oil of choice. It is best purchased in small glass bottles. Fish is a good source of EPA which is beneficial fat that will help balance out your hormone levels and decrease inflammation.
4. Water. Try to drink at least 64 ounces of pure water per day. If you are a heavy caffeine user, gradually reduce caffeine intake to zero whenever possible as the breakdown products of caffeine will tend to increase insulin levels.
5. Exercise. Try to get 30 to 60 minutes of walking in four to five days a week if the weather permits. If you are seriously debilitated you will have to wait until your health improves. As you are healthier and if you are blood type 0 or B you can shift to more aggressive exercises.
Low Grain and Carbohydrate Diets Treat Hypoglycemia, Heart Disease, Diabetes Cancer and Nearly ALL Chronic Illness
by Joseph Brasco, MD
Unfortunately, the debate over the validity of this concept has primarily been waged in the media and lay publications and not in the scientific journals. Many of the popular books which support this position are gimmicky, and often, lack adequate scientific referencing. Yet, at their core is very important concept -- limiting the intake of carbohydrates, (especially as cereal grains and starches), will improve human health.
Some critics claim that reduced carbohydrate diets are a fashion trend. Well, this so called trend actually dates back some time. Anthropological study of early hominids has concluded that they lived as hunters-gathers. While nuts, seeds, vegetation and fruit made up an important part of the hunter- gather's diet, his mainstay was hunted or scavenged animal prey.
More recent evaluations of early man's nutritional patterns by Dr. Loren Cordain, estimate that as much as 65 percent of his calories were derived from animal products. Granted, early man was not eating corn fed Angus beef from Jewel, but he was eating the meat, the organs and the bones of his prey. Essentially, a high protein/fat diet. It was a mere 10,000 years ago (or less) that man began exploiting an agricultural niche.
This transition was made due to decreasing population of large game prey and an increasing population of humans. While undeniable good has transcended this dietary shift, i.e., growth of the human population, establishment of permanent settlements, the inception of civilization itself - man's health may have suffered in the transition.
Generally, in most parts of the world, whenever cereal-based diets were first adopted as a staple food replacing the primarily animal-based diets of hunter-gatherers, there was a characteristic reduction in stature, a reduction in life span, an increase in infant mortality, an increased incidence of infectious disease, an increase in diseases of nutritional deficiencies (i.e., iron deficiency, pellagra), and an increase in the number of dental caries and enamel defects.
In a review of 51 references examining human populations from around the earth and from differing chronologies, as they transitioned from hunter-gathers to farmers, one investigator concluded that there was an overall decline in both the quality and quantity of life.
There is now substantial empirical and clinical evidence to indicate that many of these deleterious changes are directly related to the predominately cereal-based diets of these early farmers. Since 99.99% of our genes were formed before the development of agriculture, from a biological perspective, we are still hunter-gathers.
Thus, our diet should reflect the sensibilities of this nutritional niche: lean meats; fish; seafood; low glycemic vegetables and fruit, (modern agriculture has significantly increased the sugar and starch content of vegetables and fruits over their Paleolithic counterparts), nuts and seeds - the evolutionary diet.
Glycemic Index
The term glycemic index, (GI) (a qualitative indicator of carbohydrate's ability to raise blood glucose levels), has seen a lot of mileage among the many non-ketogenic low carbohydrate diets. Most of these diets attribute the rise in obesity to the over consumption of high glycemic carbohydrates, and the subsequent over production of insulin.
While this may be an oversimplification, there is growing evidence to support a relationship between GI and non-insulin dependent diabetes (NIDDM), and obesity. In a prospective study of 65,000 US women, researchers were able to demonstrate that the dietary GI was positively associated with the risk of NIDDM.
The authors concluded that diets with a high GI increase insulin demand and thus cause hyperinsulinemia among patients with NIDDM, as well as in normal subjects. If chronic, this hyperinsulinemia can increase the risk for, as well as exacerbate NIDDM.
The issue of carbohydrates and insulin has more recently been addressed in a review article by Grundy. Grundy states that because secretion by pancreatic beta-cells is glucose sensitive, a high intake of carbohydrates has been reported to produce higher post prandial insulin levels. Moreover, it is possible that repeated stimulation of a high insulin output by high-carbohydrate diets could hasten an age-related decline in insulin secretion and lead to an earlier onset of NIDDM.
However, chronic hyperinsulinemia is not only associated with NIDDM, but is also related to a host of other medical conditions jointly known as Syndrome X. The constellation of disorders comprising Syndrome X include hypertriglyceridemia, increased LDL cholesterol, decreased HDL cholesterol, hypertension, hyperuricemia and obesity.
If high GI carbohydrates in fact contribute to chronic hyperinsulinemia as multiple studies suggest, they are likely to be causative of these other conditions as well. In addition to their role in hyperinsulinemia, studies have also linked high GI foods with overeating.
One study found an inverse relationship between satiety and both glycemic and insulin index. In another study,it was found that voluntary energy intake after a high GI meal was 53% greater than after a medium GI meal and was 81% greater than after the low GI meal. The authors concluded that a high GI meal promotes excessive food intake in obese subjects. The literature clearly points to a role of high GI carbohydrates in the development of insulin resistance and its subsequent disorders.
However, GI is obviously not the whole story. One researcher examined the insulin demand generated by isoenergetic portions of common foods. While some of the results were predictable, i.e., the fact that glucose and insulin sources were highly correlated, some were unexpected, i.e., some protein-based foods induced as much insulin secretion as did some carbohydrate rich foods. At first glance, these results seem confounding. However, if one looks at the broader function of insulin, they are consistent.
Insulin is not just responsible for glucose disposal, but for storage and uptake of multiple nutrients. Whether these other nutrients can result in a chronic hyperinsulinemic state, as seen with high GI diets, is not known; it is unlikely due to their compensatory effect on glucagon. The other major difference between the insulin response of other nutrients versus carbohydrate is their effect on blood glucose.
While protein and fat stimulate insulin response, their effect on glucose is minimal. This lack of effect on blood sugar is more than trivial difference. It actually may be the glycosylation of end organs (especially the pancreatic beta-cells) that ultimately leads to NIDDM and its associated conditions. Thus, while a hyperinsulinemic state is not desirable for human health under any circumstance, the combination of hyperinsulinemia with impaired glucose homeostasis is likely to prove even more deliterious.
While the current literature would support limiting the consumption of high GI foods, GI certainly does not provide the final answer. If one was to follow this concept literally (as some popular books suggest) one could argue that potato chips at a GI of 50-59% were more beneficial than carrots at a GIU of 90-99%.
A better way of looking at carbohydrates is to return to the principles of the "evolutionary diet." Robert Crayhon, M.S., author and champion of the "Paleolithic diet", divides carbohydrates into two basic groups, paleocarbs and neocarbs. Paleocarbs include vegetables, fruits and perhaps tubers. Neocarbs (carbohydrates introduced within the last 10,000 years or less), include grains, legumes, and especially flour products, which did not exist for most of human history.
The worst of the neocarbs include sugar and white flour products. If we follow the simple guidelines of restricting ourselves to paleocarbs, we will in general be eating fiber rich, nutrient dense, low glycemic carbohydrates, the best nature has to offer.
Epidemiological Data
Another argument against carbohydrate restriction is based on epidemiological evidence, and the Pima Indians are frequently cited. The Arizona Pima Indians have received the attention of the medical community because of their prodigious rates of obesity, which is nearly 70% among the adult population. Along with the reputation of being one of the most obese people known, the Arizona Pima has a rate of diabetes 8 times the national average with nearly 50% of the adult population over 35 afflicted with this condition.
In spite of innumerable studies, examining the Pima from every imaginable vantage point, there has been no defining discovery explaining the Pima's plight. One hypothesis favored by Eric Ravussn, Ph. D, is that after generations of living in the desert, the only Pima who survived famine and drought were those highly adept at storing fat in times of plenty. These "thrifty" genes which once ensured the Pima's' survival are now at the root of his demise.
Although it is not known for certain what metabolic processes these "thrifty" genes control, insulin resistance and glucose homeostasis are thought to be at the heart of the matter. Since preagricultural, man's diet was primarily derived from animal sources (protein/fat), an insulin resistant genotype would have minimized glucose utilization and thus, proven to be of an evolutionary advantage.
As primitive peoples have become acculturated and have assumed a modern diet, the constant supply of highly refined, high glycemic index carbohydrates has resulted in postprandial hyperinsulinemia and the subsequent diseases associated with this condition i.e. obesity, diabetes, cardiovascular disease, etc.
The Arizona Pima's diet prior to acculturation was essentially that of a hunter-gather with some subsistence farming: (chollacatus buds, honey mesquite, poverty weed, prickly pears, mule deer, white-winged dove, black-tailed jackrabbit, squawfish, and they raised wheat, squash and beans). However, by the end of the second World War, the Pima had almost entirely left their traditional lifestyle and adopted the typical American diet.
There are many problems with the typical American diet, and to blame the Pima's situation on just one element of that diet would be disingenuous. However, given the current scientific and anthropological studies, one could suggest that the high availability of sugar and highly refined, high glycemic carbohydrates (i.e. neocarbs), are at the core of the Pima's health crisis. It could also be extrapolated that, while the Pima's "thrifty" genes may work at a more accelerated pace, it is the same set of genes interacting with the same diet and producing the same results in the average American.
In 1991, the Pima's story became even more interesting. Peter Bennett FRCP, the lead epidemiologist studying the Arizona Pima, discovered in Sierra Madre, Mexico, the remnants of a tribe that once comprised the Southern half of the Pima Nation. However, unlike their Northern brothers, the Mexican Pima remained, in general, unacculterated and living a traditional lifestyle.
Also, unlike their northern counterparts, the Mexican Pimas were not obese, nor did they share in the Arizona Pima's high rate of diabetes and degenerative diseases. This dichotomy has been termed the "Pima Paradox." Since the Mexican Pima consume a diet comprised mostly of beans, potatoes, corn tortillas and the occasional animal product, (i.e. chicken) , this has often been used as the epidemiological case study for the benefit of high carbohydrate diets in obesity management.
However, two issues confound this example. First, on average, the Mexican Pima's have 23 to 26 hours/week of occupational physical activity versus the Arizona Pima's 5 hours or less. Certainly, such high levels of activity could mitigate the hyperinsulinemic effects of the Mexican Pima's diet.
The second issue is the "Enigma" within the "Paradox". Although the Mexican Pima does not have the health issues of the Arizona Pima, they still have a prevalence rate of diabetes at 6.4% (approximately 1.5x greater that the non Pima Mexicans), and a 13% incidence of obesity among the adult population.
While these numbers are impressive compared to the US population, and stellar compared to the Pima population, the question remains why should an essentially unacculturated population performing on average 23-26 hours of physical labor per week have any incidence of diabetes or obesity.
When modern day hunter-gatherers were studied by anthropologists, incidence of these conditions were non existent, even among the eldest members of tribe. The "evolutionary diet" model would thus suggest, in spite of their improved health over the Arizona Pimas, the Mexican Pimas are still consuming a less than optimal diet.
Although conclusions drawn from epidemiological data can sometimes be misleading, the real message that can be taken from the Pimas is that as a species we have proclivity towards obesity, a proclivity that will vary based on our genetic stock.
This genetic predisposition, while multifactorial in nature, probably centers around insulin resistance and glucose homeostasis. Since our preagricultural ancestors did not have ready access to simple carbohydrates, fats were the preferred source of caloric energy, and glucose conservation was evolutionarily advantageous.
In modern times, the detrimental combination of low physical activity, hypercaloric intake, and over consumption of neocarbs is at the root of our obesity crisis. A return to an evolutionary based diet - lean meats, seafood, fish, vegetables, fruits, (raw) nuts and seeds and moderate physical activity, will ultimately be the cure.
Health Risk Associated with reduced Carbohydrate Intake
Another argument against carbohydrate restriction focuses on the purported health risk of this dietary approach. Of the three macronutrients, protein, fat and carbohydrate, it is only carbohydrate that is nonessential to the human diet. Humans can exist for extraordinarily long periods of time without carbohydrate consumption as long as essential protein and fat needs are met. It is thus perplexing why nutritional dogma ascribes so many risks to the restriction of this non-essential nutrient.
Ketosis
Ketosis is a natural physiologic state induced during prolonged states of decreased glucose availability. It is triggered by severe coloric restriction or when carbohydrate intake falls below 20-30 grams, (most of the current low carbohydrate diets are nowhere near this level of restriction).
In ketosis, a set of elaborate metabolic processes occur which have the net result of decreasing insulin secretion, increasing glucagon secretion, switching off glycolysis, turning on lipolysis, switching muscles from glucose to almost entirely fatty acids for fuel, and ultimately providing ketone bodies (produced in the liver), markedly diminishing the need for glucose by the brain in particular and the body in general.
Ketosis was an absolutely vital survival mechanism for early man. It allowed him to survive periods of starvation as well as long periods of carbohydrate deprivation. Despite the role ketosis plays in normal human physiology, its' modern application has often been portrayed with multiple negative health connotations.
However, both scientific and epidemiological data has failed to justify these concerns. The ketogenic diet has been used for nearly 70 years to treat refractory seizures in the pediatric population. Multiple recent studies have described nutritionally balanced, food varied versions of this diet.
One investigator looked at the health profiles of adults who had been treated during childhood with ketogenic diet. He found no evidence of adverse effects on cardiovascular function, including arteriosclerosis, hypertension or cardiac abnormalities. Blood cholesterol determinations were performed on these adults and all were normal. These studies thus fail to reveal any short term complication or long term sequelae associated with ketogenic diets.
In the mid twenties to late thirties, the famed anthropologist V. Stefansson chronicled the life and culture of the Eskimo in a series of books and journal articles. Of the many observations made by Stefansson, he was most intrigued with their diet and health. In spite of a nearly 100% animal based diet, the Eskimo people enjoyed an excellent state of well being and a freedom from many western diseases.
This observation was greeted with a high degree of skepticism in a scientific community that was becoming increasingly hostile toward the role of protein and fat in the American diet. To silence his critics, Steffansson devised a study whereby he would consume an all meat diet for one year.
Under observation at Bellvue Hospital in New York City, Stefansson and a colleague did in fact consume for one year an all meat diet. At years end, to the surprise of the scientific community, both investigators were in excellent health. They demonstrated weight loss with reduction in body fat, normal kidney and liver function, and improvement in blood lipids (within the limits of diagnostic testing of the time).
The "Bellvue ward study" created quite a stir in the scientific community and was detailed in numerous articles appearing both in popular and professional literature. Although long term commentary cannot be made, this remarkable study certainly speaks to the short term safety of a ketogenic diet. Ample scientific, epidemologic and anthropological data exists to support the general safety of a ketogenic diet. However, this data does not exonerate all the modern inceptions of this diet.
Traditional cultures who consumed a largely animal based diet, derived a great deal of their vitamins and nutrients by consuming the organs, eyes, glands and gonads of their prey. Modern ketotic diets are primarily based on common American foods, i.e. meats, eggs and cheeses. They do not qualify the source of animal products (i.e. salmon versus bacon), and are usually overloaded with salt. In general, these diets are only concerned about limiting carbohydrate intake without overall regard to food quality.
In the most popular version of the ketogenic diet, Dr. Atkins New Diet Revolution, Dr. Atkin's writes "at the other end of the spectrum is a convenience food that sounds terrible fatty, but in fact, contains nearly none. Those are the maximizers of crispness - fried pork rinds - the zero carbohydrate consolation prize for corn or potato chip addicts. Virtually all the fat has been rendered off, leaving you with the protein matrix that held the pork fat together. Your pate, sour-cream based dips and guacamole find an exceedingly crisp and comfortable home atop a fried pork rind.
In spite of their potential physiologic benefits, the modern ketogenic diets with their unbalanced, nutrient poor and often absurd dietary suggestion are difficult to support. However, ketogenic diet based on evolutionary appropriate foods would be interesting to pursue in clinical practice.
Lack of fruits, vegetables and grains Aside from the ketogenic diets, most other reduced carbohydrate programs allow for the ample consumption of vegetables and the modest consumption of low glycemic fruit, (the best sources of nutrients and phytonutrients available to man).
Of the major carbohydrate sources mentioned, only grain is heavily restricted. Although present diet dogma portrays grain as the quintessential food source, (it is at the base of the food pyramid after all), many nutritional scientist have called this assertion into question. In a work of prodigious proportions (342 literature citations), Dr. Loren Cordain examines mans double edged relationship with grain.
On one hand man is utterly dependent upon grain as a primary caloric source and yet grain may be at the core of many of our common maladies. As would be predicted by the evolutionary diet model, Dr. Cordain concludes that grain is biologically novel to the diet of mankind as it was introduced as a staple food only 10,000 years (or less) ago. Due to its relatively recent introduction, our species has not fully adapted physiologically to its digestion and metabolism.
In spite of the impressive nutrient profiles of grain, the vitamins and minerals often occur in forms that have low bioavaildality to the human digestive tract. In addition to these poorly utilizable nutrients, grain contains many secondary metabolic components commonly categorized as anti-nutrients.
Anti-nutrients are chemical compounds naturally occurring in grains, which evolved to protect the plants from predators. Processing and cooking does not not fully rid the grain of these elements, thus making them prominent in our diet. Recent scientific study has linked these anti-nutrients to a number of negative biological consequences which include: allergen based disorders; pancreatic hypertrophy and disruption of the gut cell wall tight junctions (thus exposing the systemic circulation to food allergens and gut flora).
One of the most curious of these negative processors associated with grain anti-nutrients is a phenomenon known as molecular mimicry. Molecular mimicry is when a similarity of structure is shared by products of dissimilar genes. When this phenomenon occurs within the human body, the potential for developing an autoimmune reaction is created.
The main body of evidence implicates viral and bacterial pathogens as initiators of cross-reactivity and autoimmunity. However, there is an emerging body of literature supporting the view that dietary antigens including cereal grains may also induce cross-reactivity and hence autoimmunity by virtue of peptide structures homologous to those in the host.
The diseases that may share this common origin are numerous and varied. They may include everything from aphthous ulcers (canker sores), to rheumatoid arthritis to non-insulin dependent diabetes to multiple sclerosis. While many of these assertions may seem preposterous to a society reared on grain, evolutionary pressures would suggest otherwise. The primate gut was initially adapted to both the nutritive and defensive components of dicotyledonous plants rather that the nutritive and defense components of mono- cotyledons cereal grains.
Consequently, humans, like other primates, have had little evolutionary experience in developing a physiology that can both fully utilize and defend against the compounds which naturally occur in cereal grains. So, while the motives for limiting grains may be completely unrelated, many of the popular incarnations of reduced carbohydrate diets may be paying their readers a great - albeit - indirect service.
Increased Saturated Fats
Of all our nutritional mantras, the one most widely and emphatically proclaimed is the relationship between saturated fats and coronary artery disease. One would think a "fact" so ingrained in our social psyche would be supported by mountains of evidence.
However, the reality is the data to support the "diet-heart hypothesis" is flimsy at best - non existent at worst. In an extensive review of existing studies, Ravnskov came to the conclusion that, "Few observations agree with the diet-heart idea, but a large number have falsified most effectively.
Man's diet possibly includes factors of importance to the vessels or the heart, but there is little evidence that saturated fatty acids as a group are harmful or that polyunsaturated fatty acids as a group are beneficial." In a similar review, Dr. Mary Enig was also unable to find a solid relationship between saturated fat consumption and coronary artery disease. She instead came to the conclusion that the inordinate increase in trans fatty acid consumption was more likely the causative factor.
When discussing the "dietary heart hypothesis", the work of Dean Ornish, M.D., is often cited as clinical evidence for the efficacy of dietary fat reduction. However, while Ornish is a major proponent of the "low fat diet", in his studies a number of coronary artery risk factors are addressed, in addition to the dietary changes.
In Ornish's work, study participants underwent vigorous lifestyle changes, which included smoking cessation, stress management, exercise and a low-fat (near vegan) diet (the only animal products allowed were egg whites and one cup of non-fat milk or yogurt per day).
After following these changes for one year, the experimental group did show an overall regression of atherosclerotic plaque, Ornish's study is extraordinarily important because he was able to demonstrate, in quantifiable terms to the medical community, that lifestyle changes could be as powerful as drugs in managing a serious disease. However, to extrapolate that this study proves the value of the low fat diet is fallacious.
Ornish manipulates four separate variables in his study, all of which have purported association with cardiovascular disease. To suggest that any one variable or combination of variables is more important than the other cannot be concluded from Ornish's data.
Even if diet alone is examined, there are multiple variables within the diet, that in and of themselves could have significance. Was it the omission of trans fatty acids (which have been linked to cardiovascular disease)? Was it the increase of antioxidants provided by the intake of fresh fruits and vegetables? Was it the fact that the experimental group experienced an average loss of 22 lbs?
Again, to conclude that it was the "low fat diet" which was primarily responsible for the experimental group's success (as the study is often interpreted), is quite disingenuous. A factor often overlooked in Ornish's work is the effect of low fat/high carbohydrate diets on lipid profiles. While it is true, the experimental group had an overall reduction in cholesterol, there was a concomitant reduction in HDL cholesterol with an increase in triglycerides.
Numerous recent studies have verified this dietary effect. Of these current studies, Berglund specifically looked at the response of the reduction in dietary total and saturated fats and HDL cholesterol subtypes. The study demonstrated a decrease in dietary total and saturated fat resulted in a significant decrease in HDL2 and HDL2b cholesterol concentrations. The authors concluded that the dietary changes suggested to be prudent for a large segment of the population will primarily affect the concentrations of the most prominent antiatherogenic HDL subpopulations.
Although definitive conclusions for the general population may be premature, in individuals demonstrating evidence of hyperinsulinemia and dyslipidemia (i.e. - Syndrome X) carbohydrate restriction is imperative for improved lipid profiles. In nutrition, as well as in life, balance is always the key. Nowhere is balance more crucial than in the discussion of dietary fats.
ANY diet, whether it be high fat - low fat (or anything in-between), if it promotes imbalances in fatty acid profiles, will in the long run have negative health consequences. In the mid '50s, the biochemist, anthropologist, and explorer Hugh Sinclair suggested an alternative explanation for the relationship between dietary fat and cardiovascular disease.
Sinclair noted that several people groups existed that consumed relatively high amounts of fat and yet were free of heart disease. Sinclair detailed the dietary habits of the Eskimos (previously discussed); the Masai people of Kenya who ate large quantities of ruminant milk and meat; and Jamaicans who ate large amounts of saturated fat in the form of coconut oil. All three groups, all consuming high fat diets, were relatively free from heart disease.
Sinclair suggested that the polyunsaturated profiles of these diets were protective, and concluded that the rise in cardiovascular disease was more related to their exclusion from the diet rather than the inclusion of saturated fats or cholesterol. Since Sinclair's day, our biochemical understanding of fat has increased exponentially. We now realize it is not just the polyunsaturated content of the diet, but the ratio of N-6 to N-3 polyunsaturates that may ultimately determine health.
Both dietary extremes discussed fail to introduce balance in this ratio. High carbohydrate diet due to their high grain and plant content will ultimately be low in N-3 fats (especially long chain N-3 fats - i.e. EPA/DHA), thus unbalancing the N-6/N-3 ratio. Low carbohydrate diets, in their popular form, rely heavily on commercially raised grain-fed meats and poultry (the fatty acid profile of the meat from wild game, free range beef and poultry have a significantly higher N-3 to N-6 ratio), eggs (free range hens also make better eggs) and cheeses.
A diet based on these foods will also greatly unbalance the N6/N3 ratio. Although the precise ratio remains controversial, the N6/N3 ratio should probably be in the range of 4-3/1 to optimize human health, western diets rich in vegetable oils, cereal grains and grain fed live stock, drive this ratio to an unprecedented 50-10:1. This imbalance may have implications in a host of diseases, including hyperinsulinemia, artherosclerosis and tumorgenesis.
When the diets of hunter-gatherer populations are studied, authors have concluded that their N6/N3 ratio varied between 4:1 to 1:1. This ratio appears to be biologically optimal. Based on these considerations, investigators, have advocated a return to dietary ratios of ancestral humans. A diet based on lean meats (wild game or free range livestock), fish, raw nuts and seed, vegetables, low glycemic fruit (paleocarbs) - "an evolutionary diet" - not only will be helpful in the management of obesity, but in a host of other common western diseases, including cardiovascular disease.
Dietary Protein and Cardiovascular Disease
Multiple recent studies have demonstrated the benefit of dietary fats (especially N-3 polyunsaturates and monounsaturates) in cardiovascular disease and in the reduction of cardiovascular risk factors. A more recent study trend has examined the possible beneficial role of dietary protein.
Wolfe has published numerous articles demonstrating the positive effects of the isocaloric substitution of protein for carbohydrate on lipid profiles. His studies have demonstrated a decreased LDL-C, an increased HDL-C, and reduction of triglycerides, thus reversing the dietary effects of increased carbohydrates. Wolfe states that substitution of carbohydrate for fat in the diet results in a reduction in HDL apoprotein transport rates along with increased catabolism of apolipoprotein A-1.
The decreases in plasma VLDL and LDL resulting from substitution of protein for carbohydrate in the diet may relate to either increased catabolism or decreased production. Thus, according to Wolfe's work, the simple dietary substitution of protein for carbohydrate could have profound health benefits.
Wolfe's data has recently been validated by Hu. In this study the dietary habits of over 80,000 women were examined. After controlling for variables, high protein intakes were associated with lowered risk of ischemic heart disease. Both animal and vegetable protein sources were protective. This inverse association was noted in women on both low fat or high fat diets. Wolfe's and Hu's work both indicate that dietary protein has cardioprotective properties independent of those of dietary fat.
Given the multiple health benefits ascribed to N-3 polyunsaturates and the evolving data regarding dietary protein - fish may be one of the best foods for human consumption. In a fascinating piece of epidemiological work, Marcovina compared 2 racially homogenous Bantu populations from Tanzania. The only appreciable difference between the groups was their dietary habits.
The Bantu living closer to the shore had a predominantly fish based diet, while the inland Bantu consumed an essentially vegan diet (a diet devoid of animal products ). When plasma lipoprotein (a) (an independent cardiovascular risk factor) levels were compared, those among the fish eating population were 40% lower. This suggests another cardioprotective aspect of fish consumption.
In a recent study by Mori, he demonstrated the inclusion of fish in a weight loss program yielded greater results than either fish consumption or weight loss alone in their obese subjects. The experimental group in their study demonstrated improved glucose, insulin and lipid metabolism, as well as greater reductions in blood pressure, heart rate and weight loss versus controls. This study suggests a novel approach to the dietary management of obesity and NIDDM.
Perhaps the most influential of the studies looking at the benefits of fish, was the Diet and Reinfarction Trial (also known as the DART trial). In this study, the authors demonstrated that the addition of a modest amount of fish (2-3g of EPA per week or the equivalent of 300g of fatty fish per week) reduced post myocardial infarction mortality by about 29% when compared to controls.
One of the more interesting aspects of the study was that the control group was instructed on the standard fat reduction diet and on average had lower cholesterol levels than did the experimental group. The authors theorized that the fish oils had a favorable effect on clotting mechanisms and blood platelets, as well as a potential anti-arrhythmic effect on the ischemic heart. The results of this study are profound, especially given the modest and otherwise innocuous interventions undertaken.
Given the evidence of the benefit of N-3 polyunsaturates, coupled with the potential benefits of dietary protein, fish clearly is a biologically superior food source. The isocaloric substitution of fish for dietary carbohydrates is not only evolutionary appropriate, by may have untoward health benefits from weight control to improved glucose homeostasis to cardiovascular disease prevention.
Risk of Osteoporosis
Of all the potential negative side effects of dietary protein, the issue of osteoporosis is perhaps the most difficult to resolve. The literature is greatly divided on the topic, and clear recommendations are hard to find. In a recent study, Munger found that the intake of dietary protein, specifically from animal sources was associated with a reduced incidence of hip fractures in post menopausal women.
In the articles' discussion, a brief review of protein's controversial role in osteoporosis was undertaken. In the studies showing a potential benefit (as in the author's paper), it has been theorized that dietary protein may strengthen bone by its effect on the structure and function of bone-related proteins.
In studies demonstrating a negative effect, it has been argued that dietary protein (especially in the form of animal based protein) is a primary source of acid ash, which results in the acidification of urine. In order to buffer the urine and maintain acid-base homeostasis, calcium salts are mobilized from the skeleton, resulting in a net calciuria. Over time, this buffering of endogenous acids may contribute to a progressive decline in skeletal mass and, ultimately, lead to osteoporosis.
However, Wachman and Bernstein, the two authors who originally postulated this mechanism for osteoporosis, theorized that by increasing the dietary alkaline ash this process could be halted.
In a study by Sebastian., he was able to reduce calicuria and improve overall calcium/phosphorous balance by the administration of potassium bicarbonate as a buffering agent to postmenopausal women consuming an acid promoting diet. The authors suggest that potassium bicarbonate could be administered long-term as a novel means of preventing and treating postmenopausal osteoporosis.
In a 4-year longitudinal study by Tucker, he was able to demonstrate that a greater bone mineral density was associated with increased dietary potassium and magnesium levels, as well as increased consumption of fruits and vegetables. The authors concluded that this positive association was due to the beneficial effects of potassium and magnesium on calcium balance and bone metabolism, as well as the buffering properties of increased alkaline ash in the form of fruits and vegetables.
Given the divergent nature of the theories, it is highly probable that both have merit. With respect to protein's beneficial effects, protein is certainly necessary for proper bone matrix formation and metabolism. It is likely a chronic suboptimal intake will jeopardize this function. One could conjecture that the studies finding a negative association between protein and osteoporosis have somehow highlighted this aspect of the equation. Those studies finding a positive association between protein and osteoporosis are probably looking at the endogenous acid production issue.
In an article by Remer, he calculated the potential renal acid load (PRAL) of frequently consumed foods in order to help dietitians design diets of varying urinary pH. On their list, animal protein sources (as expected) were calculated to increase PRAL.
However, grain products, legumes and dairy products (especially hard cheeses) also increased PRAL. In fact , according to Remer's data brown rice had a greater PRAL than any of the meat products examined (with the exception of canned corned beef - if you want to call that meat).
Perhaps the most ironic of all, was Remer's finding that cheeses had the highest of the calculated PRALs. Parmesan, cheddar, and processed American cheese had PRALs almost 2 times any meat product. In light of Remer's data, the relationship of protein and osteoporosis cannot fully be determined without addressing the total dietary PRAL. The type of protein being consumed (lean meats vs. Processed meats vs. Cheese) and the other foods in the diet are likely to significantly affect the study's outcome.
The protein osteoporosis controversy was addressed in a review article by Spencer. According to the author, numerous studies have been published on the calcium-losing effect of protein. However, several aspects of the study conditions have to be considered in the interpretation of the results.
Some of these are the type of protein, such as purified proteins (which seem not to promote calciuria): the duration of the study (there may be a transient increase in calciuria followed by a normalization or reduction); whether the phosphorous (which has an independent calcium sparing effect) intake remained the same, was increased, or decreased; whether the diets were under strict control or with outpatient volunteers; whether the protein intake was changed from a low to a high protein intake or was changed from a normal to a high protein intake; and whether excessively high protein intakes were used.
All these factors affect urinary calcium excretion during high protein consumption. After reviewing the available data, based on the aforementioned criteria, the authors concluded, "to our knowledge, no convincing data have been published showing that a high protein diet, using complex proteins for prolonged periods of time under strictly controlled dietary conditions, causes calcium loss."
It is quite obvious that the role of dietary protein in calcium homeostasis is complex and multifactorial in nature. However, given the work of Remer, it may actually be the net PRAL of the diet that is most important in influencing the development of osteoporosis, rather than the diet's absolute protein content. Since most of the current low carbohydrate diets encourage the ample consumption of vegetables, this is likely to offset any potential acidifying effects of increased dietary protein.
In fact, given most individuals do not consume enough vegetables and fruits, these diets are likely to promote better acid-base balance then the average American diet. Unlike the more modified low carbohydrate diets, modern ketogenic diets may pose a risk for calciuria since they rely heavily on animal protein, cheeses, and cured meats, and are usually not salt restricted (the Cl ion- not the Nat ion - can also cause a renal acid load and subsequently calciuria).
However, since most people are in ketosis for only a short period of time (after which they are theoretically supposed to transition into a modified low carbohydrate diet), it is unlikely that these diets will significantly contribute to an individual's overall risk for osteoporosis.
Kidney and Liver Damage
While it is generally accepted that people with pre existing kidney and liver disease will benefit from some level of protein restriction there is no data to support proposition that increased dietary protein will actually cause kidney or liver damage.
In a study by Blum, he examined the kidney function of a group of healthy individuals consuming an ad lib. high-protein diet, as compared to a group of healthy vegetarians (Isn't that an oxymoron?). At the study's end, the authors concluded that protein does not affect kidney function in normal kidneys, and it does not influence the deterioration of kidney function with age.
The relationship of protein and the liver is somewhat more complex. Although there is no evidence that increased dietary protein will cause permanent liver damage, there is an actual dietary "protein ceiling". According to Rudman there is a lever at which dietary protein intake can exceed the liver's ability to metabolize it to the urea, thus leading to a build up of intermediary metabolites. These metabolites can subsequently lead to a toxic state in the affected individual.
The level of protein at which this will occur varies, but it is thought to be possible when protein makes up 30-40% of the calories in an eucaloric diet (the percent calories from protein can be higher in a hypocaloric diet).
"Rabbit Starvation" (a term coined by V. Stefansson to describe the phenomenon of excessive dietary protein) often occurred among explorers who would live for long periods of time on extremely low fat small game animals (i.e. rabbits). The condition was marked by nausea, vomiting, weight loss and fatigue. "Rabbit Starvation" was reversible when the percentage of daily calories from protein began to drop. Although the "Rabbit Starvation" phenomenon could effect an individual consuming a ketogenic diet, it is highly improbable.
In general, if one is consuming commercially available meats (even chicken), the percentage of calories from fat would be too high to induce this condition. In the modified low carbohydrate diets, due to the varied food sources, the risk of protein toxicity, for all practical purposes, is non-existent.
Conclusion
A critical reading of the current literature certainly supports the dietary trends of decreased carbohydrate intake (especially of neocarbs), increased protein intake, and increased fat intake (especially of monounsaturates and N-3 polyunsaturates). The data that supports these contentions comes from a wide spectrum of disciplines, including the basic sciences, medical science, epidemiology, and anthropology.
The one dietary program that addresses these principles in full, is the so called "evolutionary diet." The modern inception of this prehistoric lifestyle would favor the consumption of lean meats (preferably wild game or non-grain fed, free-range domesticated animals), fish, seafood, vegetables, fruits, raw nuts, and seed. Notably absent from this dietary genre are dairy products, cereal grains, beans, legumes and concentrated sweets (except for perhaps the occasional foray into raw honey!).
Adherence to these dietary guidelines will not only address obesity, but may also prove helpful in the management of everything from NIDDM to diseases of autoimmunity to cardiovascular illnesses. The guidelines are broad, but can be made quite specific depending on the goals, lean body mass, activity level, and overall health of the patient.
In the last few years, there has been a literal explosion of data in the nutritional sciences. Sometimes when addressing this data, we are put in the uncomfortable situation of realizing that today's facts are rapidly becoming tomorrow's fiction. However, by keeping an open mind and always questioning what we think we know, we will be able to provide our patients with the best and most innovative care possible.
Unfortunately, the debate over the validity of this concept has primarily been waged in the media and lay publications and not in the scientific journals. Many of the popular books which support this position are gimmicky, and often, lack adequate scientific referencing. Yet, at their core is very important concept -- limiting the intake of carbohydrates, (especially as cereal grains and starches), will improve human health.
Some critics claim that reduced carbohydrate diets are a fashion trend. Well, this so called trend actually dates back some time. Anthropological study of early hominids has concluded that they lived as hunters-gathers. While nuts, seeds, vegetation and fruit made up an important part of the hunter- gather's diet, his mainstay was hunted or scavenged animal prey.
More recent evaluations of early man's nutritional patterns by Dr. Loren Cordain, estimate that as much as 65 percent of his calories were derived from animal products. Granted, early man was not eating corn fed Angus beef from Jewel, but he was eating the meat, the organs and the bones of his prey. Essentially, a high protein/fat diet. It was a mere 10,000 years ago (or less) that man began exploiting an agricultural niche.
This transition was made due to decreasing population of large game prey and an increasing population of humans. While undeniable good has transcended this dietary shift, i.e., growth of the human population, establishment of permanent settlements, the inception of civilization itself - man's health may have suffered in the transition.
Generally, in most parts of the world, whenever cereal-based diets were first adopted as a staple food replacing the primarily animal-based diets of hunter-gatherers, there was a characteristic reduction in stature, a reduction in life span, an increase in infant mortality, an increased incidence of infectious disease, an increase in diseases of nutritional deficiencies (i.e., iron deficiency, pellagra), and an increase in the number of dental caries and enamel defects.
In a review of 51 references examining human populations from around the earth and from differing chronologies, as they transitioned from hunter-gathers to farmers, one investigator concluded that there was an overall decline in both the quality and quantity of life.
There is now substantial empirical and clinical evidence to indicate that many of these deleterious changes are directly related to the predominately cereal-based diets of these early farmers. Since 99.99% of our genes were formed before the development of agriculture, from a biological perspective, we are still hunter-gathers.
Thus, our diet should reflect the sensibilities of this nutritional niche: lean meats; fish; seafood; low glycemic vegetables and fruit, (modern agriculture has significantly increased the sugar and starch content of vegetables and fruits over their Paleolithic counterparts), nuts and seeds - the evolutionary diet.
Glycemic Index
The term glycemic index, (GI) (a qualitative indicator of carbohydrate's ability to raise blood glucose levels), has seen a lot of mileage among the many non-ketogenic low carbohydrate diets. Most of these diets attribute the rise in obesity to the over consumption of high glycemic carbohydrates, and the subsequent over production of insulin.
While this may be an oversimplification, there is growing evidence to support a relationship between GI and non-insulin dependent diabetes (NIDDM), and obesity. In a prospective study of 65,000 US women, researchers were able to demonstrate that the dietary GI was positively associated with the risk of NIDDM.
The authors concluded that diets with a high GI increase insulin demand and thus cause hyperinsulinemia among patients with NIDDM, as well as in normal subjects. If chronic, this hyperinsulinemia can increase the risk for, as well as exacerbate NIDDM.
The issue of carbohydrates and insulin has more recently been addressed in a review article by Grundy. Grundy states that because secretion by pancreatic beta-cells is glucose sensitive, a high intake of carbohydrates has been reported to produce higher post prandial insulin levels. Moreover, it is possible that repeated stimulation of a high insulin output by high-carbohydrate diets could hasten an age-related decline in insulin secretion and lead to an earlier onset of NIDDM.
However, chronic hyperinsulinemia is not only associated with NIDDM, but is also related to a host of other medical conditions jointly known as Syndrome X. The constellation of disorders comprising Syndrome X include hypertriglyceridemia, increased LDL cholesterol, decreased HDL cholesterol, hypertension, hyperuricemia and obesity.
If high GI carbohydrates in fact contribute to chronic hyperinsulinemia as multiple studies suggest, they are likely to be causative of these other conditions as well. In addition to their role in hyperinsulinemia, studies have also linked high GI foods with overeating.
One study found an inverse relationship between satiety and both glycemic and insulin index. In another study,it was found that voluntary energy intake after a high GI meal was 53% greater than after a medium GI meal and was 81% greater than after the low GI meal. The authors concluded that a high GI meal promotes excessive food intake in obese subjects. The literature clearly points to a role of high GI carbohydrates in the development of insulin resistance and its subsequent disorders.
However, GI is obviously not the whole story. One researcher examined the insulin demand generated by isoenergetic portions of common foods. While some of the results were predictable, i.e., the fact that glucose and insulin sources were highly correlated, some were unexpected, i.e., some protein-based foods induced as much insulin secretion as did some carbohydrate rich foods. At first glance, these results seem confounding. However, if one looks at the broader function of insulin, they are consistent.
Insulin is not just responsible for glucose disposal, but for storage and uptake of multiple nutrients. Whether these other nutrients can result in a chronic hyperinsulinemic state, as seen with high GI diets, is not known; it is unlikely due to their compensatory effect on glucagon. The other major difference between the insulin response of other nutrients versus carbohydrate is their effect on blood glucose.
While protein and fat stimulate insulin response, their effect on glucose is minimal. This lack of effect on blood sugar is more than trivial difference. It actually may be the glycosylation of end organs (especially the pancreatic beta-cells) that ultimately leads to NIDDM and its associated conditions. Thus, while a hyperinsulinemic state is not desirable for human health under any circumstance, the combination of hyperinsulinemia with impaired glucose homeostasis is likely to prove even more deliterious.
While the current literature would support limiting the consumption of high GI foods, GI certainly does not provide the final answer. If one was to follow this concept literally (as some popular books suggest) one could argue that potato chips at a GI of 50-59% were more beneficial than carrots at a GIU of 90-99%.
A better way of looking at carbohydrates is to return to the principles of the "evolutionary diet." Robert Crayhon, M.S., author and champion of the "Paleolithic diet", divides carbohydrates into two basic groups, paleocarbs and neocarbs. Paleocarbs include vegetables, fruits and perhaps tubers. Neocarbs (carbohydrates introduced within the last 10,000 years or less), include grains, legumes, and especially flour products, which did not exist for most of human history.
The worst of the neocarbs include sugar and white flour products. If we follow the simple guidelines of restricting ourselves to paleocarbs, we will in general be eating fiber rich, nutrient dense, low glycemic carbohydrates, the best nature has to offer.
Epidemiological Data
Another argument against carbohydrate restriction is based on epidemiological evidence, and the Pima Indians are frequently cited. The Arizona Pima Indians have received the attention of the medical community because of their prodigious rates of obesity, which is nearly 70% among the adult population. Along with the reputation of being one of the most obese people known, the Arizona Pima has a rate of diabetes 8 times the national average with nearly 50% of the adult population over 35 afflicted with this condition.
In spite of innumerable studies, examining the Pima from every imaginable vantage point, there has been no defining discovery explaining the Pima's plight. One hypothesis favored by Eric Ravussn, Ph. D, is that after generations of living in the desert, the only Pima who survived famine and drought were those highly adept at storing fat in times of plenty. These "thrifty" genes which once ensured the Pima's' survival are now at the root of his demise.
Although it is not known for certain what metabolic processes these "thrifty" genes control, insulin resistance and glucose homeostasis are thought to be at the heart of the matter. Since preagricultural, man's diet was primarily derived from animal sources (protein/fat), an insulin resistant genotype would have minimized glucose utilization and thus, proven to be of an evolutionary advantage.
As primitive peoples have become acculturated and have assumed a modern diet, the constant supply of highly refined, high glycemic index carbohydrates has resulted in postprandial hyperinsulinemia and the subsequent diseases associated with this condition i.e. obesity, diabetes, cardiovascular disease, etc.
The Arizona Pima's diet prior to acculturation was essentially that of a hunter-gather with some subsistence farming: (chollacatus buds, honey mesquite, poverty weed, prickly pears, mule deer, white-winged dove, black-tailed jackrabbit, squawfish, and they raised wheat, squash and beans). However, by the end of the second World War, the Pima had almost entirely left their traditional lifestyle and adopted the typical American diet.
There are many problems with the typical American diet, and to blame the Pima's situation on just one element of that diet would be disingenuous. However, given the current scientific and anthropological studies, one could suggest that the high availability of sugar and highly refined, high glycemic carbohydrates (i.e. neocarbs), are at the core of the Pima's health crisis. It could also be extrapolated that, while the Pima's "thrifty" genes may work at a more accelerated pace, it is the same set of genes interacting with the same diet and producing the same results in the average American.
In 1991, the Pima's story became even more interesting. Peter Bennett FRCP, the lead epidemiologist studying the Arizona Pima, discovered in Sierra Madre, Mexico, the remnants of a tribe that once comprised the Southern half of the Pima Nation. However, unlike their Northern brothers, the Mexican Pima remained, in general, unacculterated and living a traditional lifestyle.
Also, unlike their northern counterparts, the Mexican Pimas were not obese, nor did they share in the Arizona Pima's high rate of diabetes and degenerative diseases. This dichotomy has been termed the "Pima Paradox." Since the Mexican Pima consume a diet comprised mostly of beans, potatoes, corn tortillas and the occasional animal product, (i.e. chicken) , this has often been used as the epidemiological case study for the benefit of high carbohydrate diets in obesity management.
However, two issues confound this example. First, on average, the Mexican Pima's have 23 to 26 hours/week of occupational physical activity versus the Arizona Pima's 5 hours or less. Certainly, such high levels of activity could mitigate the hyperinsulinemic effects of the Mexican Pima's diet.
The second issue is the "Enigma" within the "Paradox". Although the Mexican Pima does not have the health issues of the Arizona Pima, they still have a prevalence rate of diabetes at 6.4% (approximately 1.5x greater that the non Pima Mexicans), and a 13% incidence of obesity among the adult population.
While these numbers are impressive compared to the US population, and stellar compared to the Pima population, the question remains why should an essentially unacculturated population performing on average 23-26 hours of physical labor per week have any incidence of diabetes or obesity.
When modern day hunter-gatherers were studied by anthropologists, incidence of these conditions were non existent, even among the eldest members of tribe. The "evolutionary diet" model would thus suggest, in spite of their improved health over the Arizona Pimas, the Mexican Pimas are still consuming a less than optimal diet.
Although conclusions drawn from epidemiological data can sometimes be misleading, the real message that can be taken from the Pimas is that as a species we have proclivity towards obesity, a proclivity that will vary based on our genetic stock.
This genetic predisposition, while multifactorial in nature, probably centers around insulin resistance and glucose homeostasis. Since our preagricultural ancestors did not have ready access to simple carbohydrates, fats were the preferred source of caloric energy, and glucose conservation was evolutionarily advantageous.
In modern times, the detrimental combination of low physical activity, hypercaloric intake, and over consumption of neocarbs is at the root of our obesity crisis. A return to an evolutionary based diet - lean meats, seafood, fish, vegetables, fruits, (raw) nuts and seeds and moderate physical activity, will ultimately be the cure.
Health Risk Associated with reduced Carbohydrate Intake
Another argument against carbohydrate restriction focuses on the purported health risk of this dietary approach. Of the three macronutrients, protein, fat and carbohydrate, it is only carbohydrate that is nonessential to the human diet. Humans can exist for extraordinarily long periods of time without carbohydrate consumption as long as essential protein and fat needs are met. It is thus perplexing why nutritional dogma ascribes so many risks to the restriction of this non-essential nutrient.
Ketosis
Ketosis is a natural physiologic state induced during prolonged states of decreased glucose availability. It is triggered by severe coloric restriction or when carbohydrate intake falls below 20-30 grams, (most of the current low carbohydrate diets are nowhere near this level of restriction).
In ketosis, a set of elaborate metabolic processes occur which have the net result of decreasing insulin secretion, increasing glucagon secretion, switching off glycolysis, turning on lipolysis, switching muscles from glucose to almost entirely fatty acids for fuel, and ultimately providing ketone bodies (produced in the liver), markedly diminishing the need for glucose by the brain in particular and the body in general.
Ketosis was an absolutely vital survival mechanism for early man. It allowed him to survive periods of starvation as well as long periods of carbohydrate deprivation. Despite the role ketosis plays in normal human physiology, its' modern application has often been portrayed with multiple negative health connotations.
However, both scientific and epidemiological data has failed to justify these concerns. The ketogenic diet has been used for nearly 70 years to treat refractory seizures in the pediatric population. Multiple recent studies have described nutritionally balanced, food varied versions of this diet.
One investigator looked at the health profiles of adults who had been treated during childhood with ketogenic diet. He found no evidence of adverse effects on cardiovascular function, including arteriosclerosis, hypertension or cardiac abnormalities. Blood cholesterol determinations were performed on these adults and all were normal. These studies thus fail to reveal any short term complication or long term sequelae associated with ketogenic diets.
In the mid twenties to late thirties, the famed anthropologist V. Stefansson chronicled the life and culture of the Eskimo in a series of books and journal articles. Of the many observations made by Stefansson, he was most intrigued with their diet and health. In spite of a nearly 100% animal based diet, the Eskimo people enjoyed an excellent state of well being and a freedom from many western diseases.
This observation was greeted with a high degree of skepticism in a scientific community that was becoming increasingly hostile toward the role of protein and fat in the American diet. To silence his critics, Steffansson devised a study whereby he would consume an all meat diet for one year.
Under observation at Bellvue Hospital in New York City, Stefansson and a colleague did in fact consume for one year an all meat diet. At years end, to the surprise of the scientific community, both investigators were in excellent health. They demonstrated weight loss with reduction in body fat, normal kidney and liver function, and improvement in blood lipids (within the limits of diagnostic testing of the time).
The "Bellvue ward study" created quite a stir in the scientific community and was detailed in numerous articles appearing both in popular and professional literature. Although long term commentary cannot be made, this remarkable study certainly speaks to the short term safety of a ketogenic diet. Ample scientific, epidemologic and anthropological data exists to support the general safety of a ketogenic diet. However, this data does not exonerate all the modern inceptions of this diet.
Traditional cultures who consumed a largely animal based diet, derived a great deal of their vitamins and nutrients by consuming the organs, eyes, glands and gonads of their prey. Modern ketotic diets are primarily based on common American foods, i.e. meats, eggs and cheeses. They do not qualify the source of animal products (i.e. salmon versus bacon), and are usually overloaded with salt. In general, these diets are only concerned about limiting carbohydrate intake without overall regard to food quality.
In the most popular version of the ketogenic diet, Dr. Atkins New Diet Revolution, Dr. Atkin's writes "at the other end of the spectrum is a convenience food that sounds terrible fatty, but in fact, contains nearly none. Those are the maximizers of crispness - fried pork rinds - the zero carbohydrate consolation prize for corn or potato chip addicts. Virtually all the fat has been rendered off, leaving you with the protein matrix that held the pork fat together. Your pate, sour-cream based dips and guacamole find an exceedingly crisp and comfortable home atop a fried pork rind.
In spite of their potential physiologic benefits, the modern ketogenic diets with their unbalanced, nutrient poor and often absurd dietary suggestion are difficult to support. However, ketogenic diet based on evolutionary appropriate foods would be interesting to pursue in clinical practice.
Lack of fruits, vegetables and grains Aside from the ketogenic diets, most other reduced carbohydrate programs allow for the ample consumption of vegetables and the modest consumption of low glycemic fruit, (the best sources of nutrients and phytonutrients available to man).
Of the major carbohydrate sources mentioned, only grain is heavily restricted. Although present diet dogma portrays grain as the quintessential food source, (it is at the base of the food pyramid after all), many nutritional scientist have called this assertion into question. In a work of prodigious proportions (342 literature citations), Dr. Loren Cordain examines mans double edged relationship with grain.
On one hand man is utterly dependent upon grain as a primary caloric source and yet grain may be at the core of many of our common maladies. As would be predicted by the evolutionary diet model, Dr. Cordain concludes that grain is biologically novel to the diet of mankind as it was introduced as a staple food only 10,000 years (or less) ago. Due to its relatively recent introduction, our species has not fully adapted physiologically to its digestion and metabolism.
In spite of the impressive nutrient profiles of grain, the vitamins and minerals often occur in forms that have low bioavaildality to the human digestive tract. In addition to these poorly utilizable nutrients, grain contains many secondary metabolic components commonly categorized as anti-nutrients.
Anti-nutrients are chemical compounds naturally occurring in grains, which evolved to protect the plants from predators. Processing and cooking does not not fully rid the grain of these elements, thus making them prominent in our diet. Recent scientific study has linked these anti-nutrients to a number of negative biological consequences which include: allergen based disorders; pancreatic hypertrophy and disruption of the gut cell wall tight junctions (thus exposing the systemic circulation to food allergens and gut flora).
One of the most curious of these negative processors associated with grain anti-nutrients is a phenomenon known as molecular mimicry. Molecular mimicry is when a similarity of structure is shared by products of dissimilar genes. When this phenomenon occurs within the human body, the potential for developing an autoimmune reaction is created.
The main body of evidence implicates viral and bacterial pathogens as initiators of cross-reactivity and autoimmunity. However, there is an emerging body of literature supporting the view that dietary antigens including cereal grains may also induce cross-reactivity and hence autoimmunity by virtue of peptide structures homologous to those in the host.
The diseases that may share this common origin are numerous and varied. They may include everything from aphthous ulcers (canker sores), to rheumatoid arthritis to non-insulin dependent diabetes to multiple sclerosis. While many of these assertions may seem preposterous to a society reared on grain, evolutionary pressures would suggest otherwise. The primate gut was initially adapted to both the nutritive and defensive components of dicotyledonous plants rather that the nutritive and defense components of mono- cotyledons cereal grains.
Consequently, humans, like other primates, have had little evolutionary experience in developing a physiology that can both fully utilize and defend against the compounds which naturally occur in cereal grains. So, while the motives for limiting grains may be completely unrelated, many of the popular incarnations of reduced carbohydrate diets may be paying their readers a great - albeit - indirect service.
Increased Saturated Fats
Of all our nutritional mantras, the one most widely and emphatically proclaimed is the relationship between saturated fats and coronary artery disease. One would think a "fact" so ingrained in our social psyche would be supported by mountains of evidence.
However, the reality is the data to support the "diet-heart hypothesis" is flimsy at best - non existent at worst. In an extensive review of existing studies, Ravnskov came to the conclusion that, "Few observations agree with the diet-heart idea, but a large number have falsified most effectively.
Man's diet possibly includes factors of importance to the vessels or the heart, but there is little evidence that saturated fatty acids as a group are harmful or that polyunsaturated fatty acids as a group are beneficial." In a similar review, Dr. Mary Enig was also unable to find a solid relationship between saturated fat consumption and coronary artery disease. She instead came to the conclusion that the inordinate increase in trans fatty acid consumption was more likely the causative factor.
When discussing the "dietary heart hypothesis", the work of Dean Ornish, M.D., is often cited as clinical evidence for the efficacy of dietary fat reduction. However, while Ornish is a major proponent of the "low fat diet", in his studies a number of coronary artery risk factors are addressed, in addition to the dietary changes.
In Ornish's work, study participants underwent vigorous lifestyle changes, which included smoking cessation, stress management, exercise and a low-fat (near vegan) diet (the only animal products allowed were egg whites and one cup of non-fat milk or yogurt per day).
After following these changes for one year, the experimental group did show an overall regression of atherosclerotic plaque, Ornish's study is extraordinarily important because he was able to demonstrate, in quantifiable terms to the medical community, that lifestyle changes could be as powerful as drugs in managing a serious disease. However, to extrapolate that this study proves the value of the low fat diet is fallacious.
Ornish manipulates four separate variables in his study, all of which have purported association with cardiovascular disease. To suggest that any one variable or combination of variables is more important than the other cannot be concluded from Ornish's data.
Even if diet alone is examined, there are multiple variables within the diet, that in and of themselves could have significance. Was it the omission of trans fatty acids (which have been linked to cardiovascular disease)? Was it the increase of antioxidants provided by the intake of fresh fruits and vegetables? Was it the fact that the experimental group experienced an average loss of 22 lbs?
Again, to conclude that it was the "low fat diet" which was primarily responsible for the experimental group's success (as the study is often interpreted), is quite disingenuous. A factor often overlooked in Ornish's work is the effect of low fat/high carbohydrate diets on lipid profiles. While it is true, the experimental group had an overall reduction in cholesterol, there was a concomitant reduction in HDL cholesterol with an increase in triglycerides.
Numerous recent studies have verified this dietary effect. Of these current studies, Berglund specifically looked at the response of the reduction in dietary total and saturated fats and HDL cholesterol subtypes. The study demonstrated a decrease in dietary total and saturated fat resulted in a significant decrease in HDL2 and HDL2b cholesterol concentrations. The authors concluded that the dietary changes suggested to be prudent for a large segment of the population will primarily affect the concentrations of the most prominent antiatherogenic HDL subpopulations.
Although definitive conclusions for the general population may be premature, in individuals demonstrating evidence of hyperinsulinemia and dyslipidemia (i.e. - Syndrome X) carbohydrate restriction is imperative for improved lipid profiles. In nutrition, as well as in life, balance is always the key. Nowhere is balance more crucial than in the discussion of dietary fats.
ANY diet, whether it be high fat - low fat (or anything in-between), if it promotes imbalances in fatty acid profiles, will in the long run have negative health consequences. In the mid '50s, the biochemist, anthropologist, and explorer Hugh Sinclair suggested an alternative explanation for the relationship between dietary fat and cardiovascular disease.
Sinclair noted that several people groups existed that consumed relatively high amounts of fat and yet were free of heart disease. Sinclair detailed the dietary habits of the Eskimos (previously discussed); the Masai people of Kenya who ate large quantities of ruminant milk and meat; and Jamaicans who ate large amounts of saturated fat in the form of coconut oil. All three groups, all consuming high fat diets, were relatively free from heart disease.
Sinclair suggested that the polyunsaturated profiles of these diets were protective, and concluded that the rise in cardiovascular disease was more related to their exclusion from the diet rather than the inclusion of saturated fats or cholesterol. Since Sinclair's day, our biochemical understanding of fat has increased exponentially. We now realize it is not just the polyunsaturated content of the diet, but the ratio of N-6 to N-3 polyunsaturates that may ultimately determine health.
Both dietary extremes discussed fail to introduce balance in this ratio. High carbohydrate diet due to their high grain and plant content will ultimately be low in N-3 fats (especially long chain N-3 fats - i.e. EPA/DHA), thus unbalancing the N-6/N-3 ratio. Low carbohydrate diets, in their popular form, rely heavily on commercially raised grain-fed meats and poultry (the fatty acid profile of the meat from wild game, free range beef and poultry have a significantly higher N-3 to N-6 ratio), eggs (free range hens also make better eggs) and cheeses.
A diet based on these foods will also greatly unbalance the N6/N3 ratio. Although the precise ratio remains controversial, the N6/N3 ratio should probably be in the range of 4-3/1 to optimize human health, western diets rich in vegetable oils, cereal grains and grain fed live stock, drive this ratio to an unprecedented 50-10:1. This imbalance may have implications in a host of diseases, including hyperinsulinemia, artherosclerosis and tumorgenesis.
When the diets of hunter-gatherer populations are studied, authors have concluded that their N6/N3 ratio varied between 4:1 to 1:1. This ratio appears to be biologically optimal. Based on these considerations, investigators, have advocated a return to dietary ratios of ancestral humans. A diet based on lean meats (wild game or free range livestock), fish, raw nuts and seed, vegetables, low glycemic fruit (paleocarbs) - "an evolutionary diet" - not only will be helpful in the management of obesity, but in a host of other common western diseases, including cardiovascular disease.
Dietary Protein and Cardiovascular Disease
Multiple recent studies have demonstrated the benefit of dietary fats (especially N-3 polyunsaturates and monounsaturates) in cardiovascular disease and in the reduction of cardiovascular risk factors. A more recent study trend has examined the possible beneficial role of dietary protein.
Wolfe has published numerous articles demonstrating the positive effects of the isocaloric substitution of protein for carbohydrate on lipid profiles. His studies have demonstrated a decreased LDL-C, an increased HDL-C, and reduction of triglycerides, thus reversing the dietary effects of increased carbohydrates. Wolfe states that substitution of carbohydrate for fat in the diet results in a reduction in HDL apoprotein transport rates along with increased catabolism of apolipoprotein A-1.
The decreases in plasma VLDL and LDL resulting from substitution of protein for carbohydrate in the diet may relate to either increased catabolism or decreased production. Thus, according to Wolfe's work, the simple dietary substitution of protein for carbohydrate could have profound health benefits.
Wolfe's data has recently been validated by Hu. In this study the dietary habits of over 80,000 women were examined. After controlling for variables, high protein intakes were associated with lowered risk of ischemic heart disease. Both animal and vegetable protein sources were protective. This inverse association was noted in women on both low fat or high fat diets. Wolfe's and Hu's work both indicate that dietary protein has cardioprotective properties independent of those of dietary fat.
Given the multiple health benefits ascribed to N-3 polyunsaturates and the evolving data regarding dietary protein - fish may be one of the best foods for human consumption. In a fascinating piece of epidemiological work, Marcovina compared 2 racially homogenous Bantu populations from Tanzania. The only appreciable difference between the groups was their dietary habits.
The Bantu living closer to the shore had a predominantly fish based diet, while the inland Bantu consumed an essentially vegan diet (a diet devoid of animal products ). When plasma lipoprotein (a) (an independent cardiovascular risk factor) levels were compared, those among the fish eating population were 40% lower. This suggests another cardioprotective aspect of fish consumption.
In a recent study by Mori, he demonstrated the inclusion of fish in a weight loss program yielded greater results than either fish consumption or weight loss alone in their obese subjects. The experimental group in their study demonstrated improved glucose, insulin and lipid metabolism, as well as greater reductions in blood pressure, heart rate and weight loss versus controls. This study suggests a novel approach to the dietary management of obesity and NIDDM.
Perhaps the most influential of the studies looking at the benefits of fish, was the Diet and Reinfarction Trial (also known as the DART trial). In this study, the authors demonstrated that the addition of a modest amount of fish (2-3g of EPA per week or the equivalent of 300g of fatty fish per week) reduced post myocardial infarction mortality by about 29% when compared to controls.
One of the more interesting aspects of the study was that the control group was instructed on the standard fat reduction diet and on average had lower cholesterol levels than did the experimental group. The authors theorized that the fish oils had a favorable effect on clotting mechanisms and blood platelets, as well as a potential anti-arrhythmic effect on the ischemic heart. The results of this study are profound, especially given the modest and otherwise innocuous interventions undertaken.
Given the evidence of the benefit of N-3 polyunsaturates, coupled with the potential benefits of dietary protein, fish clearly is a biologically superior food source. The isocaloric substitution of fish for dietary carbohydrates is not only evolutionary appropriate, by may have untoward health benefits from weight control to improved glucose homeostasis to cardiovascular disease prevention.
Risk of Osteoporosis
Of all the potential negative side effects of dietary protein, the issue of osteoporosis is perhaps the most difficult to resolve. The literature is greatly divided on the topic, and clear recommendations are hard to find. In a recent study, Munger found that the intake of dietary protein, specifically from animal sources was associated with a reduced incidence of hip fractures in post menopausal women.
In the articles' discussion, a brief review of protein's controversial role in osteoporosis was undertaken. In the studies showing a potential benefit (as in the author's paper), it has been theorized that dietary protein may strengthen bone by its effect on the structure and function of bone-related proteins.
In studies demonstrating a negative effect, it has been argued that dietary protein (especially in the form of animal based protein) is a primary source of acid ash, which results in the acidification of urine. In order to buffer the urine and maintain acid-base homeostasis, calcium salts are mobilized from the skeleton, resulting in a net calciuria. Over time, this buffering of endogenous acids may contribute to a progressive decline in skeletal mass and, ultimately, lead to osteoporosis.
However, Wachman and Bernstein, the two authors who originally postulated this mechanism for osteoporosis, theorized that by increasing the dietary alkaline ash this process could be halted.
In a study by Sebastian., he was able to reduce calicuria and improve overall calcium/phosphorous balance by the administration of potassium bicarbonate as a buffering agent to postmenopausal women consuming an acid promoting diet. The authors suggest that potassium bicarbonate could be administered long-term as a novel means of preventing and treating postmenopausal osteoporosis.
In a 4-year longitudinal study by Tucker, he was able to demonstrate that a greater bone mineral density was associated with increased dietary potassium and magnesium levels, as well as increased consumption of fruits and vegetables. The authors concluded that this positive association was due to the beneficial effects of potassium and magnesium on calcium balance and bone metabolism, as well as the buffering properties of increased alkaline ash in the form of fruits and vegetables.
Given the divergent nature of the theories, it is highly probable that both have merit. With respect to protein's beneficial effects, protein is certainly necessary for proper bone matrix formation and metabolism. It is likely a chronic suboptimal intake will jeopardize this function. One could conjecture that the studies finding a negative association between protein and osteoporosis have somehow highlighted this aspect of the equation. Those studies finding a positive association between protein and osteoporosis are probably looking at the endogenous acid production issue.
In an article by Remer, he calculated the potential renal acid load (PRAL) of frequently consumed foods in order to help dietitians design diets of varying urinary pH. On their list, animal protein sources (as expected) were calculated to increase PRAL.
However, grain products, legumes and dairy products (especially hard cheeses) also increased PRAL. In fact , according to Remer's data brown rice had a greater PRAL than any of the meat products examined (with the exception of canned corned beef - if you want to call that meat).
Perhaps the most ironic of all, was Remer's finding that cheeses had the highest of the calculated PRALs. Parmesan, cheddar, and processed American cheese had PRALs almost 2 times any meat product. In light of Remer's data, the relationship of protein and osteoporosis cannot fully be determined without addressing the total dietary PRAL. The type of protein being consumed (lean meats vs. Processed meats vs. Cheese) and the other foods in the diet are likely to significantly affect the study's outcome.
The protein osteoporosis controversy was addressed in a review article by Spencer. According to the author, numerous studies have been published on the calcium-losing effect of protein. However, several aspects of the study conditions have to be considered in the interpretation of the results.
Some of these are the type of protein, such as purified proteins (which seem not to promote calciuria): the duration of the study (there may be a transient increase in calciuria followed by a normalization or reduction); whether the phosphorous (which has an independent calcium sparing effect) intake remained the same, was increased, or decreased; whether the diets were under strict control or with outpatient volunteers; whether the protein intake was changed from a low to a high protein intake or was changed from a normal to a high protein intake; and whether excessively high protein intakes were used.
All these factors affect urinary calcium excretion during high protein consumption. After reviewing the available data, based on the aforementioned criteria, the authors concluded, "to our knowledge, no convincing data have been published showing that a high protein diet, using complex proteins for prolonged periods of time under strictly controlled dietary conditions, causes calcium loss."
It is quite obvious that the role of dietary protein in calcium homeostasis is complex and multifactorial in nature. However, given the work of Remer, it may actually be the net PRAL of the diet that is most important in influencing the development of osteoporosis, rather than the diet's absolute protein content. Since most of the current low carbohydrate diets encourage the ample consumption of vegetables, this is likely to offset any potential acidifying effects of increased dietary protein.
In fact, given most individuals do not consume enough vegetables and fruits, these diets are likely to promote better acid-base balance then the average American diet. Unlike the more modified low carbohydrate diets, modern ketogenic diets may pose a risk for calciuria since they rely heavily on animal protein, cheeses, and cured meats, and are usually not salt restricted (the Cl ion- not the Nat ion - can also cause a renal acid load and subsequently calciuria).
However, since most people are in ketosis for only a short period of time (after which they are theoretically supposed to transition into a modified low carbohydrate diet), it is unlikely that these diets will significantly contribute to an individual's overall risk for osteoporosis.
Kidney and Liver Damage
While it is generally accepted that people with pre existing kidney and liver disease will benefit from some level of protein restriction there is no data to support proposition that increased dietary protein will actually cause kidney or liver damage.
In a study by Blum, he examined the kidney function of a group of healthy individuals consuming an ad lib. high-protein diet, as compared to a group of healthy vegetarians (Isn't that an oxymoron?). At the study's end, the authors concluded that protein does not affect kidney function in normal kidneys, and it does not influence the deterioration of kidney function with age.
The relationship of protein and the liver is somewhat more complex. Although there is no evidence that increased dietary protein will cause permanent liver damage, there is an actual dietary "protein ceiling". According to Rudman there is a lever at which dietary protein intake can exceed the liver's ability to metabolize it to the urea, thus leading to a build up of intermediary metabolites. These metabolites can subsequently lead to a toxic state in the affected individual.
The level of protein at which this will occur varies, but it is thought to be possible when protein makes up 30-40% of the calories in an eucaloric diet (the percent calories from protein can be higher in a hypocaloric diet).
"Rabbit Starvation" (a term coined by V. Stefansson to describe the phenomenon of excessive dietary protein) often occurred among explorers who would live for long periods of time on extremely low fat small game animals (i.e. rabbits). The condition was marked by nausea, vomiting, weight loss and fatigue. "Rabbit Starvation" was reversible when the percentage of daily calories from protein began to drop. Although the "Rabbit Starvation" phenomenon could effect an individual consuming a ketogenic diet, it is highly improbable.
In general, if one is consuming commercially available meats (even chicken), the percentage of calories from fat would be too high to induce this condition. In the modified low carbohydrate diets, due to the varied food sources, the risk of protein toxicity, for all practical purposes, is non-existent.
Conclusion
A critical reading of the current literature certainly supports the dietary trends of decreased carbohydrate intake (especially of neocarbs), increased protein intake, and increased fat intake (especially of monounsaturates and N-3 polyunsaturates). The data that supports these contentions comes from a wide spectrum of disciplines, including the basic sciences, medical science, epidemiology, and anthropology.
The one dietary program that addresses these principles in full, is the so called "evolutionary diet." The modern inception of this prehistoric lifestyle would favor the consumption of lean meats (preferably wild game or non-grain fed, free-range domesticated animals), fish, seafood, vegetables, fruits, raw nuts, and seed. Notably absent from this dietary genre are dairy products, cereal grains, beans, legumes and concentrated sweets (except for perhaps the occasional foray into raw honey!).
Adherence to these dietary guidelines will not only address obesity, but may also prove helpful in the management of everything from NIDDM to diseases of autoimmunity to cardiovascular illnesses. The guidelines are broad, but can be made quite specific depending on the goals, lean body mass, activity level, and overall health of the patient.
In the last few years, there has been a literal explosion of data in the nutritional sciences. Sometimes when addressing this data, we are put in the uncomfortable situation of realizing that today's facts are rapidly becoming tomorrow's fiction. However, by keeping an open mind and always questioning what we think we know, we will be able to provide our patients with the best and most innovative care possible.
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