A new study links low consumption of fish early in pregnancy to higher odds of preterm delivery and low birth weight-suggesting that the omega-3 fats in fish and fish oil supplements might help prevent these complications.
Together with past research suggesting fish oil may lower the risk of premature delivery, these findings lay the groundwork for clinical trials on the effects of omega-3 fatty acids during pregnancy.
Their study of nearly 9000 pregnant women in Denmark found that those who said they currently ate no fish were around three times more likely than those who ate the most to have a premature delivery.
Overall, women who ate some fish were less likely than those who did not to deliver prematurely, and their babies tended to weigh more. For instance, the rate of premature birth among women who ate no fish was about 7%, compared with roughly 2% for women who had fish at least once a week.
Indeed, some fish are considered risky during pregnancy.
In the US, the Food and Drug Administration advises pregnant women to avoid eating
* shark,
* swordfish,
* king mackerel and
* tilefish
because they may contain high levels of mercury, which can potentially harm the developing fetal nervous system.
According to the researchers, their results suggest that for women who eat little or no fish, small amounts of omega-3 fatty acids -- through either fish or fish oil supplements -- might help reduce the odds of premature delivery or low birth weight.
British Medical Journal February 23, 2002;324:447-450
19 January 2008
What Happens to Your Body Within an Hour of Drinking a Coke
Do you want to be healthy? Drinking soda is bad for your health in so many ways; science can’t even state all the consequences. Here’s what happens in your body when you assault it with a Coke:
Within the first 10 minutes, 10 teaspoons of sugar hit your system. This is 100 percent of your recommended daily intake, and the only reason you don’t vomit as a result of the overwhelming sweetness is because phosphoric acid cuts the flavor.
Within 20 minutes, your blood sugar spikes, and your liver responds to the resulting insulin burst by turning massive amounts of sugar into fat.
Within 40 minutes, caffeine absorption is complete; your pupils dilate, your blood pressure rises, and your livers dumps more sugar into your bloodstream.
Around 45 minutes, your body increases dopamine production, which stimulates the pleasure centers of your brain – a physically identical response to that of heroin, by the way.
After 60 minutes, you’ll start to have a sugar crash.
Sources:
* Nutrition Research Center October 24, 2007
Can Chinese Food Cause Cancer?
Monosodium glutamate (MSG), a common ingredient in Chinese food, may cause stomach cancer, according to a study by researchers at the Netaji Subhas Chandra Bose Cancer Research Institute.
Their analysis of 134 patients found that nearly half of those with stomach, rectal and colon cancer were regular consumers of Chinese food from middle- or low-end restaurants. Most of them also had ulcers, which were also linked to MSG.
In 2004, the World Health Organization declared MSG unsafe for human consumption, but it is still widely used.
Sources:
* Times of India December 31, 2007
Their analysis of 134 patients found that nearly half of those with stomach, rectal and colon cancer were regular consumers of Chinese food from middle- or low-end restaurants. Most of them also had ulcers, which were also linked to MSG.
In 2004, the World Health Organization declared MSG unsafe for human consumption, but it is still widely used.
Sources:
* Times of India December 31, 2007
U.S. to Study Bizarre Medical Condition
The U.S. Centers for Disease Control and Prevention is paying Kaiser Permanente $338,000 to test and interview patients suffering from Morgellons. This strange ailment causes symptoms such as sores erupting on your skin, with mysterious threads popping out of them, and the feeling tiny bugs are crawling all over you. The one-year effort will attempt to define the condition and determine how common it is.
Some experts believe that Morgellons is a psychiatric phenomenon, a form of delusional parasitosis, the psychosis that causes people to believe they are infected with parasites. But hundreds believe the condition to be a physical illness.
For the study, volunteers will get blood tests and skin exams, as well as psychological evaluations.
Sources:
* Washington Post January 16, 2008
Some experts believe that Morgellons is a psychiatric phenomenon, a form of delusional parasitosis, the psychosis that causes people to believe they are infected with parasites. But hundreds believe the condition to be a physical illness.
For the study, volunteers will get blood tests and skin exams, as well as psychological evaluations.
Sources:
* Washington Post January 16, 2008
Unfavorable Drug Studies Never See Print
A new analysis has found that the makers of antidepressants such as Prozac and Paxil never published the results of about a third of the drug trials that they conducted to win government approval. This has led to a misleading perception of the drugs’ true effectiveness.
When only published trials are considered, about 60 percent of people taking the drugs report significant relief from depression, compared with roughly 40 percent of those on placebo pills. But when the less positive, unpublished trials are included, the drugs only outperform placebos by a very modest margin.
While 94 percent of positive studies found their way into print, only 14 percent of those with disappointing or uncertain results were published.
Sources:
* New York Times January 17, 2008
When only published trials are considered, about 60 percent of people taking the drugs report significant relief from depression, compared with roughly 40 percent of those on placebo pills. But when the less positive, unpublished trials are included, the drugs only outperform placebos by a very modest margin.
While 94 percent of positive studies found their way into print, only 14 percent of those with disappointing or uncertain results were published.
Sources:
* New York Times January 17, 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
Recreational Drugs FAR Less Likely to Kill You than Prescribed Drugs!
By Christopher Kent, D.C., J.D.
Recreational drugs, including cocaine and heroin, are responsible for an estimated 10,000-20,000 American deaths per year [1,2]. While this represents a serious public health problem, it is a "smokescreen" for America's real drug problem. America's "war on drugs" is directed at the wrong enemy. It is obvious that interdiction, stiff mandatory sentences, and more vigorous enforcement of drug laws have failed.
The reason is simple. Cause and effect have been reversed.
The desire to solve problems by taking drugs is a product of our culture. When a child is taught by loving parents that the appropriate response to pain or discomfort is taking a pill, it is obvious that such a child, when faced with the challenges of adolescence, will seek comfort by taking drugs.
Drugs are Dangerous Whether Pushed or Prescribed
While approximately 10,000 per year die from the effects of illegal drugs, an article in the Journal of the American Medical Association (JAMA) reported that an estimated 106,000 hospitalized patients die each year from drugs which, by medical standards, are properly prescribed and properly administered. More than two million suffer serious side effects. [3]
An article in Newsweek [4] put this into perspective. Adverse drug reactions, from "properly" prescribed drugs, are the fourth leading cause of death in the United States. According to this article, only heart disease, cancer, and stroke kill more Americans than drugs prescribed by medical doctors. Reactions to prescription drugs kill more than twice as many Americans as HIV/AIDS or suicide. Fewer die from accidents or diabetes than adverse drug reactions. It is important to point out the limitations of this study. It did not include outpatients, cases of malpractice, or instances where the drugs were not taken as directed.
According to another AMA publication, drug related "problems" kill as many as 198,815 people, put 8.8 million in hospitals, and account for up to 28% of hospital admissions. [5] If these figures are accurate, only cancer and heart disease kill more patients than drugs. Has the situation improved since the publication of this information? Hardly. Null [6] et al have published the most comprehensive and well-documented study I have seen of deaths associated with medical practice. In this report, their research revealed some shocking facts. The findings are summarized in the abstract:
"A definitive review and close reading of medical peer-review journals, and government health statistics shows that American medicine frequently causes more harm than good. The number of people having in-hospital, adverse drug reactions (ADR) to prescribed medicine is 2.2 million. Dr. Richard Besser, of the CDC, in 1995, said the number of unnecessary antibiotics prescribed annually for viral infections was 20 million. Dr. Besser, in 2003, now refers to tens of millions of unnecessary antibiotics.
The number of unnecessary medical and surgical procedures performed annually is 7.5 million. The number of people exposed to unnecessary hospitalization annually is 8.9 million. The total number of iatrogenic deaths shown in the following table is 783,936. It is evident that the American medical system is the leading cause of death and injury in the United States. The 2001 heart disease annual death rate is 699,697; the annual cancer death rate, 553,251."
Drugs Number One Killer
The authors conclude: "When the number one killer in a society is the healthcare system, then, that system has no excuse except to address its own urgent shortcomings. It's a failed system in need of immediate attention. What we have outlined in this paper are insupportable aspects of our contemporary medical system that need to be changed -- beginning at its very foundations."
A recent article in Archives of Internal Medicine [7] stated that in the seven year period from 1998 through 2005, reported serious adverse drug events increased 2.6-fold, and fatal adverse drug events increased 2.7-fold. The authors noted that reported serious events increased 4 times faster than the total number of outpatient prescriptions during the period. Another study concluded that the majority(86%) of the adverse drug reactions for which patients were admitted to a medical intensive care unit were preventable. [8]
One proposed solution to the illegal drug problem was encouraging potential users to ignore peer pressure and "just say no." Interestingly, this strategy is not being recommended for prescription drugs. Bruce Pomeranz, MD , one of the authors of the JAMA paper, said he is not warning people to stay away from drugs. "That would be a terrible message," he said. Lucian Leape, MD, of the Harvard School of Public Health said, "When you realize how many drugs we use, maybe those numbers aren't so bad after all." [4]
Does that mean that the number of deaths due to illegal drugs, suicide, HIV/AIDS, diabetes, accidents, and drunk driving "aren't so bad" either? Does it mean that we shouldn't discourage drunk driving or unsafe sex?
The folly of such double standards should be obvious to all. It is time to address the real drug problem -- the cultural notion that the first solution to seek for relief of life's problems is a drug. That's the drug culture we need to address.
Is Exercise Best With a Little Alcohol?
A little alcohol added to a healthy active lifestyle could be the best combination for a longer life. A new study suggests that both together can cut the risk of heart disease.
Researchers followed nearly 12,000 men and women for almost 20 years, during which 1,242 died from ischemic heart disease (IHD). Researchers found that people who led an active lifestyle were less prone to heart disease, but the risk was cut even further if they drank moderately.
When comparing people who took similar levels of exercise, they found that those who drank moderately were around 30 percent less likely to develop heart disease than non-drinkers. This finding held good both for those people who were completely inactive and those who took vigorous regular exercise, although the overall risk of heart disease also declined as exercise levels increased.
Non-drinkers who were physically active had a 31 to 33 percent reduced risk of IHD compared to inactive non-drinkers. However, physically active people who drank at least one drink a week had a risk level 50 percent lower than that of inactive non-drinkers.
Sources:
* BBC News January 9, 2008
Researchers followed nearly 12,000 men and women for almost 20 years, during which 1,242 died from ischemic heart disease (IHD). Researchers found that people who led an active lifestyle were less prone to heart disease, but the risk was cut even further if they drank moderately.
When comparing people who took similar levels of exercise, they found that those who drank moderately were around 30 percent less likely to develop heart disease than non-drinkers. This finding held good both for those people who were completely inactive and those who took vigorous regular exercise, although the overall risk of heart disease also declined as exercise levels increased.
Non-drinkers who were physically active had a 31 to 33 percent reduced risk of IHD compared to inactive non-drinkers. However, physically active people who drank at least one drink a week had a risk level 50 percent lower than that of inactive non-drinkers.
Sources:
* BBC News January 9, 2008
Type 2 Diabetes Explosion Predicted
Even as health loss caused by most illnesses is predicted to fall, health loss by type 2 diabetes will likely more than double in Australia by 2023. Health loss is measured by the 'disability adjusted life year' (DALY) with one DALY equaling one lost year of healthy life. The DALY represents the gap between current health status and an ideal situation.
New research assesses and predicts the burden of disease and injury in Australia from 1993 to 2023. Currently, 75 percent of health loss is caused by cancer, cardiovascular disease, neurological and sense disorders, chronic respiratory disease and injuries. Cardiovascular disease is the overall biggest cause, and anxiety and depression are the biggest causes for women.
But while many causes of health loss are predicted to fall by 2023, some will rise over that same period. Health loss due to diabetes in particular is likely to rapidly increase.
Sources:
* Science Daily January 14, 2008
New research assesses and predicts the burden of disease and injury in Australia from 1993 to 2023. Currently, 75 percent of health loss is caused by cancer, cardiovascular disease, neurological and sense disorders, chronic respiratory disease and injuries. Cardiovascular disease is the overall biggest cause, and anxiety and depression are the biggest causes for women.
But while many causes of health loss are predicted to fall by 2023, some will rise over that same period. Health loss due to diabetes in particular is likely to rapidly increase.
Sources:
* Science Daily January 14, 2008
Fake "Herbal" Supplements Caused Cancer in Two Men
Two men who sought to boost their sexual performance and grow bigger muscles ended up with advanced prostate cancer instead after taking "herbal" supplements.
Many supplements that are marketed as "safe" and "natural" actually contain unknown and potentially dangerous ingredients.
The product the men took contained the hormones testosterone and estradiol, and laboratory tests proved the supplement fueled the growth of prostate cancer cells more potently than testosterone alone.
The two men have both survived, but have extensive cancer that has spread throughout their bodies.
Sources:
* Reuters January 15, 2008
Many supplements that are marketed as "safe" and "natural" actually contain unknown and potentially dangerous ingredients.
The product the men took contained the hormones testosterone and estradiol, and laboratory tests proved the supplement fueled the growth of prostate cancer cells more potently than testosterone alone.
The two men have both survived, but have extensive cancer that has spread throughout their bodies.
Sources:
* Reuters January 15, 2008
Ron Paul For US President
While I try to keep my news health related as much as possible, on occasions something comes along which I need to rant about. Today I bring a Ron Paul, who is a republican running for the up coming elections in the US.
In this interview with Laura Ingraham, Ron Paul explains why the Constitution should be followed and how unintended consequences are the inevitable effect of current U.S. foreign policy. In the middle of it, he lets Ingraham know that she is actually unintentionally arguing his own points for him. If you want to hear a man speak with passion and principle, this is the interview you should hear.
In this interview with Laura Ingraham, Ron Paul explains why the Constitution should be followed and how unintended consequences are the inevitable effect of current U.S. foreign policy. In the middle of it, he lets Ingraham know that she is actually unintentionally arguing his own points for him. If you want to hear a man speak with passion and principle, this is the interview you should hear.
Sugar and Cancer
Originally printed by The Alternative Research Foundation
It puzzles me why the simple concept "sugar feeds cancer" can be so dramatically overlooked as part of a comprehensive cancer treatment plan.
Of the 4 million cancer patients being treated in America today, hardly any are offered any scientifically guided nutrition therapy beyond being told to "just eat good foods." Most patients I work with arrive with a complete lack of nutritional advice.
I believe many cancer patients would have a major improvement in their outcome if they controlled the supply of cancer's preferred fuel, glucose.
By slowing the cancer's growth, patients allow their immune systems and medical debulking therapies -- chemotherapy, radiation and surgery to reduce the bulk of the tumor mass -- to catch up to the disease.
Controlling one's blood-glucose levels through diet, supplements, exercise, meditation and prescription drugs when necessary can be one of the most crucial components to a cancer recovery program. The sound bite -- sugar feeds cancer -- is simple. The explanation is a little more complex.
The 1931 Nobel laureate in medicine, German Otto Warburg, Ph.D., first discovered that cancer cells have a fundamentally different energy metabolism compared to healthy cells.
The crux of his Nobel thesis was that malignant tumors frequently exhibit an increase in anaerobic glycolysis -- a process whereby glucose is used as a fuel by cancer cells with lactic acid as an anaerobic byproduct -- compared to normal tissues.
The large amount of lactic acid produced by this fermentation of glucose from cancer cells is then transported to the liver. This conversion of glucose to lactate generates a lower, more acidic pH in cancerous tissues as well as overall physical fatigue from lactic acid buildup. Thus, larger tumors tend to exhibit a more acidic pH.
This inefficient pathway for energy metabolism yields only 2 moles of adenosine triphosphate (ATP) energy per mole of glucose, compared to 38 moles of ATP in the complete aerobic oxidation of glucose.
By extracting only about 5 percent (2 vs. 38 moles of ATP) of the available energy in the food supply and the body's calorie stores, the cancer is "wasting" energy, and the patient becomes tired and undernourished. This vicious cycle increases body wasting.
It is one reason why 40 percent of cancer patients die from malnutrition, or cachexia. Hence, cancer therapies should encompass regulating blood-glucose levels via diet, supplements, non-oral solutions for cachectic patients who lose their appetite, medication, exercise, gradual weight loss and stress reduction. Professional guidance and patient self-discipline are crucial at this point in the cancer process. The quest is not to eliminate sugars or carbohydrates from the diet but rather to control blood glucose within a narrow range to help starve the cancer and bolster immune function.
The glycemic index is a measure of how a given food affects blood-glucose levels, with each food assigned a numbered rating. The lower the rating, the slower the digestion and absorption process, which provides a healthier, more gradual infusion of sugars into the bloodstream.
Conversely, a high rating means blood-glucose levels are increased quickly, which stimulates the pancreas to secrete insulin to drop blood-sugar levels. This rapid fluctuation of blood-sugar levels is unhealthy because of the stress it places on the body
Sugar in the Body and Diet
Sugar is a generic term used to identify simple carbohydrates, which includes monosaccharides such as fructose, glucose and galactose; and disaccharides such as maltose and sucrose (white table sugar). Think of these sugars as different-shaped bricks in a wall.
When fructose is the primary monosaccharide brick in the wall, the glycemic index registers as healthier, since this simple sugar is slowly absorbed in the gut, then converted to glucose in the liver. This makes for "time-release foods," which offer a more gradual rise and fall in blood-glucose levels.
If glucose is the primary monosaccharide brick in the wall, the glycemic index will be higher and less healthy for the individual. As the brick wall is torn apart in digestion, the glucose is pumped across the intestinal wall directly into the bloodstream, rapidly raising blood-glucose levels.
In other words, there is a "window of efficacy" for glucose in the blood: levels too low make one feel lethargic and can create clinical hypoglycemia; levels too high start creating the rippling effect of diabetic health problems.
The 1997 American Diabetes Association blood-glucose standards consider 126 mg glucose/dL blood or greater to be diabetic; 111 to 125 mg/dL is impaired glucose tolerance and less than 110 mg/dL is considered normal.
Meanwhile, the Paleolithic diet of our ancestors, which consisted of lean meats, vegetables and small amounts of whole grains, nuts, seeds and fruits, is estimated to have generated blood glucose levels between 60 and 90 mg/dL.
Obviously, today's high-sugar diets are having unhealthy effects as far as blood-sugar is concerned. Excess blood glucose may initiate yeast overgrowth, blood vessel deterioration, heart disease and other health conditions.
Understanding and using the glycemic index is an important aspect of diet modification for cancer patients. However, there is also evidence that sugars may feed cancer more efficiently than starches (comprised of long chains of simple sugars), making the index slightly misleading. A study of rats fed diets with equal calories from sugars and starches, for example, found the animals on the high-sugar diet developed more cases of breast cancer.
The glycemic index is a useful tool in guiding the cancer patient toward a healthier diet, but it is not infallible. By using the glycemic index alone, one could be led to thinking a cup of white sugar is healthier than a baked potato.
This is because the glycemic index rating of a sugary food may be lower than that of a starchy food. To be safe, I recommend less fruit, more vegetables, and little to no refined sugars in the diet of cancer patients.
What the Literature Says
A mouse model of human breast cancer demonstrated that tumors are sensitive to blood-glucose levels. Sixty-eight mice were injected with an aggressive strain of breast cancer, then fed diets to induce either high blood-sugar (hyperglycemia), normoglycemia or low blood-sugar (hypoglycemia).
There was a dose-dependent response in which the lower the blood glucose, the greater the survival rate. After 70 days, 8 of 24 hyperglycemic mice survived compared to 16 of 24 normoglycemic and 19 of 20 hypoglycemic.
This suggests that regulating sugar intake is key to slowing breast tumor growth.
In a human study, 10 healthy people were assessed for fasting blood-glucose levels and the phagocytic index of neutrophils, which measures immune-cell ability to envelop and destroy invaders such as cancer. Eating 100 g carbohydrates from glucose, sucrose, honey and orange juice all significantly decreased the capacity of neutrophils to engulf bacteria. Starch did not have this effect.
A four-year study at the National Institute of Public Health and Environmental Protection in the Netherlands compared 111 biliary tract cancer patients with 480 controls. Cancer risk associated with the intake of sugars, independent of other energy sources, more than doubled for the cancer patients.
Furthermore, an epidemiological study in 21 modern countries that keep track of morbidity and mortality (Europe, North America, Japan and others) revealed that sugar intake is a strong risk factor that contributes to higher breast cancer rates, particularly in older women.
Limiting sugar consumption may not be the only line of defense. In fact, an interesting botanical extract from the avocado plant (Persea americana) is showing promise as a new cancer adjunct.
When a purified avocado extract called mannoheptulose was added to a number of tumor cell lines tested in vitro by researchers in the Department of Biochemistry at Oxford University in Britain, they found it inhibited tumor cell glucose uptake by 25 to 75 percent, and it inhibited the enzyme glucokinase responsible for glycolysis. It also inhibited the growth rate of the cultured tumor cell lines.
The same researchers gave lab animals a 1.7 mg/g body weight dose of mannoheptulose for five days; it reduced tumors by 65 to 79 percent. Based on these studies, there is good reason to believe that avocado extract could help cancer patients by limiting glucose to the tumor cells.
Since cancer cells derive most of their energy from anaerobic glycolysis, Joseph Gold, M.D., director of the Syracuse (N.Y.) Cancer Research Institute and former U.S. Air Force research physician, surmised that a chemical called hydrazine sulfate, used in rocket fuel, could inhibit the excessive gluconeogenesis (making sugar from amino acids) that occurs in cachectic cancer patients.
Gold's work demonstrated hydrazine sulfate's ability to slow and reverse cachexia in advanced cancer patients. A placebo-controlled trial followed 101 cancer patients taking either 6 mg hydrazine sulfate three times/day or placebo. After one month, 83 percent of hydrazine sulfate patients increased their weight, compared to 53 percent on placebo.
A similar study by the same principal researchers, partly funded by the National Cancer Institute in Bethesda, Md., followed 65 patients. Those who took hydrazine sulfate and were in good physical condition before the study began lived an average of 17 weeks longer.
The medical establishment may be missing the connection between sugar and its role in tumorigenesis. Consider the million-dollar positive emission tomography device, or PET scan, regarded as one of the ultimate cancer-detection tools. PET scans use radioactively labeled glucose to detect sugar-hungry tumor cells. PET scans are used to plot the progress of cancer patients and to assess whether present protocols are effective.
In Europe, the "sugar feeds cancer" concept is so well accepted that oncologists, or cancer doctors, use the Systemic Cancer Multistep Therapy (SCMT) protocol. Conceived by Manfred von Ardenne in Germany in 1965, SCMT entails injecting patients with glucose to increase blood-glucose concentrations.
This lowers pH values in cancer tissues via lactic acid formation. In turn, this intensifies the thermal sensitivity of the malignant tumors and also induces rapid growth of the cancer. Patients are then given whole-body hyperthermia (42 C core temperature) to further stress the cancer cells, followed by chemotherapy or radiation.
SCMT was tested on 103 patients with metastasized cancer or recurrent primary tumors in a clinical phase-I study at the Von Ardenne Institute of Applied Medical Research in Dresden, Germany. Five-year survival rates in SCMT-treated patients increased by 25 to 50 percent, and the complete rate of tumor regression increased by 30 to 50 percent.
The protocol induces rapid growth of the cancer, then treats the tumor with toxic therapies for a dramatic improvement in outcome.
The irrefutable role of glucose in the growth and metastasis of cancer cells can enhance many therapies. Some of these include diets designed with the glycemic index in mind to regulate increases in blood glucose, hence selectively starving the cancer cells; low-glucose TPN solutions; avocado extract to inhibit glucose uptake in cancer cells; hydrazine sulfate to inhibit gluconeogenesis in cancer cells; and SCMT.
A female patient in her 50s, with lung cancer, came to our clinic, having been given a death sentence by her Florida oncologist. She was cooperative and understood the connection between nutrition and cancer. She changed her diet considerably, leaving out 90 percent of the sugar she used to eat.
She found that wheat bread and oat cereal now had their own wild sweetness, even without added sugar.
With appropriately restrained medical therapy -- including high-dose radiation targeted to tumor sites and fractionated chemotherapy, a technique that distributes the normal one large weekly chemo dose into a 60-hour infusion lasting days -- a good attitude and an optimal nutrition program which included Sam's formula nine times/day, she beat her terminal lung cancer.
I saw her last month, five years later and still disease-free, probably looking better than the doctor who told her there was no hope.
It puzzles me why the simple concept "sugar feeds cancer" can be so dramatically overlooked as part of a comprehensive cancer treatment plan.
Of the 4 million cancer patients being treated in America today, hardly any are offered any scientifically guided nutrition therapy beyond being told to "just eat good foods." Most patients I work with arrive with a complete lack of nutritional advice.
I believe many cancer patients would have a major improvement in their outcome if they controlled the supply of cancer's preferred fuel, glucose.
By slowing the cancer's growth, patients allow their immune systems and medical debulking therapies -- chemotherapy, radiation and surgery to reduce the bulk of the tumor mass -- to catch up to the disease.
Controlling one's blood-glucose levels through diet, supplements, exercise, meditation and prescription drugs when necessary can be one of the most crucial components to a cancer recovery program. The sound bite -- sugar feeds cancer -- is simple. The explanation is a little more complex.
The 1931 Nobel laureate in medicine, German Otto Warburg, Ph.D., first discovered that cancer cells have a fundamentally different energy metabolism compared to healthy cells.
The crux of his Nobel thesis was that malignant tumors frequently exhibit an increase in anaerobic glycolysis -- a process whereby glucose is used as a fuel by cancer cells with lactic acid as an anaerobic byproduct -- compared to normal tissues.
The large amount of lactic acid produced by this fermentation of glucose from cancer cells is then transported to the liver. This conversion of glucose to lactate generates a lower, more acidic pH in cancerous tissues as well as overall physical fatigue from lactic acid buildup. Thus, larger tumors tend to exhibit a more acidic pH.
This inefficient pathway for energy metabolism yields only 2 moles of adenosine triphosphate (ATP) energy per mole of glucose, compared to 38 moles of ATP in the complete aerobic oxidation of glucose.
By extracting only about 5 percent (2 vs. 38 moles of ATP) of the available energy in the food supply and the body's calorie stores, the cancer is "wasting" energy, and the patient becomes tired and undernourished. This vicious cycle increases body wasting.
It is one reason why 40 percent of cancer patients die from malnutrition, or cachexia. Hence, cancer therapies should encompass regulating blood-glucose levels via diet, supplements, non-oral solutions for cachectic patients who lose their appetite, medication, exercise, gradual weight loss and stress reduction. Professional guidance and patient self-discipline are crucial at this point in the cancer process. The quest is not to eliminate sugars or carbohydrates from the diet but rather to control blood glucose within a narrow range to help starve the cancer and bolster immune function.
The glycemic index is a measure of how a given food affects blood-glucose levels, with each food assigned a numbered rating. The lower the rating, the slower the digestion and absorption process, which provides a healthier, more gradual infusion of sugars into the bloodstream.
Conversely, a high rating means blood-glucose levels are increased quickly, which stimulates the pancreas to secrete insulin to drop blood-sugar levels. This rapid fluctuation of blood-sugar levels is unhealthy because of the stress it places on the body
Sugar in the Body and Diet
Sugar is a generic term used to identify simple carbohydrates, which includes monosaccharides such as fructose, glucose and galactose; and disaccharides such as maltose and sucrose (white table sugar). Think of these sugars as different-shaped bricks in a wall.
When fructose is the primary monosaccharide brick in the wall, the glycemic index registers as healthier, since this simple sugar is slowly absorbed in the gut, then converted to glucose in the liver. This makes for "time-release foods," which offer a more gradual rise and fall in blood-glucose levels.
If glucose is the primary monosaccharide brick in the wall, the glycemic index will be higher and less healthy for the individual. As the brick wall is torn apart in digestion, the glucose is pumped across the intestinal wall directly into the bloodstream, rapidly raising blood-glucose levels.
In other words, there is a "window of efficacy" for glucose in the blood: levels too low make one feel lethargic and can create clinical hypoglycemia; levels too high start creating the rippling effect of diabetic health problems.
The 1997 American Diabetes Association blood-glucose standards consider 126 mg glucose/dL blood or greater to be diabetic; 111 to 125 mg/dL is impaired glucose tolerance and less than 110 mg/dL is considered normal.
Meanwhile, the Paleolithic diet of our ancestors, which consisted of lean meats, vegetables and small amounts of whole grains, nuts, seeds and fruits, is estimated to have generated blood glucose levels between 60 and 90 mg/dL.
Obviously, today's high-sugar diets are having unhealthy effects as far as blood-sugar is concerned. Excess blood glucose may initiate yeast overgrowth, blood vessel deterioration, heart disease and other health conditions.
Understanding and using the glycemic index is an important aspect of diet modification for cancer patients. However, there is also evidence that sugars may feed cancer more efficiently than starches (comprised of long chains of simple sugars), making the index slightly misleading. A study of rats fed diets with equal calories from sugars and starches, for example, found the animals on the high-sugar diet developed more cases of breast cancer.
The glycemic index is a useful tool in guiding the cancer patient toward a healthier diet, but it is not infallible. By using the glycemic index alone, one could be led to thinking a cup of white sugar is healthier than a baked potato.
This is because the glycemic index rating of a sugary food may be lower than that of a starchy food. To be safe, I recommend less fruit, more vegetables, and little to no refined sugars in the diet of cancer patients.
What the Literature Says
A mouse model of human breast cancer demonstrated that tumors are sensitive to blood-glucose levels. Sixty-eight mice were injected with an aggressive strain of breast cancer, then fed diets to induce either high blood-sugar (hyperglycemia), normoglycemia or low blood-sugar (hypoglycemia).
There was a dose-dependent response in which the lower the blood glucose, the greater the survival rate. After 70 days, 8 of 24 hyperglycemic mice survived compared to 16 of 24 normoglycemic and 19 of 20 hypoglycemic.
This suggests that regulating sugar intake is key to slowing breast tumor growth.
In a human study, 10 healthy people were assessed for fasting blood-glucose levels and the phagocytic index of neutrophils, which measures immune-cell ability to envelop and destroy invaders such as cancer. Eating 100 g carbohydrates from glucose, sucrose, honey and orange juice all significantly decreased the capacity of neutrophils to engulf bacteria. Starch did not have this effect.
A four-year study at the National Institute of Public Health and Environmental Protection in the Netherlands compared 111 biliary tract cancer patients with 480 controls. Cancer risk associated with the intake of sugars, independent of other energy sources, more than doubled for the cancer patients.
Furthermore, an epidemiological study in 21 modern countries that keep track of morbidity and mortality (Europe, North America, Japan and others) revealed that sugar intake is a strong risk factor that contributes to higher breast cancer rates, particularly in older women.
Limiting sugar consumption may not be the only line of defense. In fact, an interesting botanical extract from the avocado plant (Persea americana) is showing promise as a new cancer adjunct.
When a purified avocado extract called mannoheptulose was added to a number of tumor cell lines tested in vitro by researchers in the Department of Biochemistry at Oxford University in Britain, they found it inhibited tumor cell glucose uptake by 25 to 75 percent, and it inhibited the enzyme glucokinase responsible for glycolysis. It also inhibited the growth rate of the cultured tumor cell lines.
The same researchers gave lab animals a 1.7 mg/g body weight dose of mannoheptulose for five days; it reduced tumors by 65 to 79 percent. Based on these studies, there is good reason to believe that avocado extract could help cancer patients by limiting glucose to the tumor cells.
Since cancer cells derive most of their energy from anaerobic glycolysis, Joseph Gold, M.D., director of the Syracuse (N.Y.) Cancer Research Institute and former U.S. Air Force research physician, surmised that a chemical called hydrazine sulfate, used in rocket fuel, could inhibit the excessive gluconeogenesis (making sugar from amino acids) that occurs in cachectic cancer patients.
Gold's work demonstrated hydrazine sulfate's ability to slow and reverse cachexia in advanced cancer patients. A placebo-controlled trial followed 101 cancer patients taking either 6 mg hydrazine sulfate three times/day or placebo. After one month, 83 percent of hydrazine sulfate patients increased their weight, compared to 53 percent on placebo.
A similar study by the same principal researchers, partly funded by the National Cancer Institute in Bethesda, Md., followed 65 patients. Those who took hydrazine sulfate and were in good physical condition before the study began lived an average of 17 weeks longer.
The medical establishment may be missing the connection between sugar and its role in tumorigenesis. Consider the million-dollar positive emission tomography device, or PET scan, regarded as one of the ultimate cancer-detection tools. PET scans use radioactively labeled glucose to detect sugar-hungry tumor cells. PET scans are used to plot the progress of cancer patients and to assess whether present protocols are effective.
In Europe, the "sugar feeds cancer" concept is so well accepted that oncologists, or cancer doctors, use the Systemic Cancer Multistep Therapy (SCMT) protocol. Conceived by Manfred von Ardenne in Germany in 1965, SCMT entails injecting patients with glucose to increase blood-glucose concentrations.
This lowers pH values in cancer tissues via lactic acid formation. In turn, this intensifies the thermal sensitivity of the malignant tumors and also induces rapid growth of the cancer. Patients are then given whole-body hyperthermia (42 C core temperature) to further stress the cancer cells, followed by chemotherapy or radiation.
SCMT was tested on 103 patients with metastasized cancer or recurrent primary tumors in a clinical phase-I study at the Von Ardenne Institute of Applied Medical Research in Dresden, Germany. Five-year survival rates in SCMT-treated patients increased by 25 to 50 percent, and the complete rate of tumor regression increased by 30 to 50 percent.
The protocol induces rapid growth of the cancer, then treats the tumor with toxic therapies for a dramatic improvement in outcome.
The irrefutable role of glucose in the growth and metastasis of cancer cells can enhance many therapies. Some of these include diets designed with the glycemic index in mind to regulate increases in blood glucose, hence selectively starving the cancer cells; low-glucose TPN solutions; avocado extract to inhibit glucose uptake in cancer cells; hydrazine sulfate to inhibit gluconeogenesis in cancer cells; and SCMT.
A female patient in her 50s, with lung cancer, came to our clinic, having been given a death sentence by her Florida oncologist. She was cooperative and understood the connection between nutrition and cancer. She changed her diet considerably, leaving out 90 percent of the sugar she used to eat.
She found that wheat bread and oat cereal now had their own wild sweetness, even without added sugar.
With appropriately restrained medical therapy -- including high-dose radiation targeted to tumor sites and fractionated chemotherapy, a technique that distributes the normal one large weekly chemo dose into a 60-hour infusion lasting days -- a good attitude and an optimal nutrition program which included Sam's formula nine times/day, she beat her terminal lung cancer.
I saw her last month, five years later and still disease-free, probably looking better than the doctor who told her there was no hope.
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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