7th June 2004
Rahod,
Here is another interesting article by the medical director of the Atkins Center:
The Atkins Approach to CHD Diet and Treatment
Patrick Fratellone, MD
Half the deaths in the United States since 1900 have been attributed to heart disease. America now leads the world in death rates from heart disease. The conditions included are coronary artery disease, cardiomyopathy, hypertension and arrhythmias.
According to the American Heart Association, every 33 seconds an American dies of cardiovascular disease-which accounts for greater than 950,000 deaths per year. It is also estimated that every 20 seconds an individual has a heart attack. We know that 52.3 percent are women and 47.7 percent are men. We also know that African Americans are more greatly affected than whites. There is enough data to support a prevention and treatment program.
Our experience at the Atkins Center is that diet, nutritional supplements and exercise, in conjunction with medical therapy and enhanced external counterpulsation is a good plan. The common precursor of heart disease is atherosclerosis. The inner arterial walls harden and thicken due to deposits of fatty substances. These substances form plaque which causes narrowing of the arteries. The theory that high levels of cholesterol is the main cause of atherosclerosis is a false idea-a myth you could say. Another theory, the lipid hypothesis as the single cause of atherosclerosis, has not passed scientific tests and is filled with inaccuracies.
The idea that a bad diet leads to high cholesterol which leads to plaque formation thus causing heart disease has been ingrained in our medical education and sold to the public. An atherogenic diet is a diet containing too much cholesterol and saturated fats (which are found in animal products, milk, eggs and even in oils and too little polyunsaturated fats). We believe this is the cause of the initial problem. So blaming the Atkins Diet makes it easier for the public to accept low-cholesterol diets and statin drugs as the treatment of choice. Yet millions of Americans on low cholesterol diet and statin drugs also suffer heart attacks. There is evidence that statin drugs decrease a vital nutrient, Coenzyme Q10, which is needed for every cell, especially the heart muscle. There is evidence that Coenzyme Q10 and an amino acid, L-carnithine, can increase systolic function of the heart. Most published lipid observations on the effects of dietary fat include considerable amounts of carbohydrates in the protocols. Most published observations of high fat, high protein and ultra-low carbohydrates diets (below 20 percent of total calories) show beneficial results. So the culprit may not be cholesterol, but high glycemic foods which increase insulin. Jacobson et al compared conventional low-fat diet therapy with a low carbohydrate ketogenic diet in adolescents. Not only was there an increased weight loss among the latter group but a reduction in triglycerides, total cholesterol and low density lipoproteins and an increase in high-density lipoproteins. Hays et al noted the same lipid profiles in his study. Data extrapolated from Gaziano showed that a high triglycerides/low HDL ratio is more of a risk factor than cholesterol alone and that there is a 16 times likelihood of having a myocardial infarction with this offset ratio.
In the last 10 years there has been an emergence of new risk factors. These cutting-edge risk factors should be part of every cardiology patient's blood profile. These risk factors include homocysteine, fibrinogen, lipoprotein and C-reactive protein. The first of these factors, homocysteine, was first proposed in 1969 by Dr. Kilmer McCully. He proposed that premature vascular damage and disease were a result of high homocysteine levels. Only in the last few years has data confirmed his initially rejected hypothesis from 1969. Now there is data to support the connection between high homocysteine levels and coronary artery disease, peripheral vascular and carotid artery disease. In 1997, the value of high homocysteine levels in 587 patients with heart disease was evaluated. After a follow-up of 4.6 years, only 3.8 percent of patients with homocysteine levels below 9 umol/L had died compared with 24.7 percent mortality for homocysteine levels greater than 15 umol/L.(8) When an individual is deficient in B6 , B12 and folic acid, the body cannot break down methionine effectively, thus leading to high homocysteine levels. The solution is simple-an intake of the B vitamins and folic acid will decrease homocysteine levels.(9) I recommend a dose of folic acid ranging from 2.5 mg to 20 mg with B6 and B12 supplementation. It has been estimated that an increase of folic acid can prevent 20,000 to 40,000 premature cardiovascular deaths.
Working with Patients' Lipoprotien
You always hear about the "bad cholesterol" called LDL, but no one mentions the real killer component of the LDL, called the lipoprotein (a). I describe lipoprotein as a glue-like substance to my patients, and anyone with a family history of heart disease should have this checked. An important but critical reminder is that the statin drugs such as lipitor and mevacor do not lower lipoprotein (a) levels and there has even been suggestions that the statin drugs can increase levels. Lipoprotein (a) inhibits blood thinning and appears to regulate clot formation (thrombosis). Lipoprotein (a) leads to premature myocardial infarctions in patients with normal cholesterol levels. So you can see why cholesterol is not the major problem. The normal levels of lipoprotein (a) range between 20-40. For a patient with a high lipoprotein (a), I prescribe 300 mg Coenzyme Q10 and 2000 mg and above of Vitamin C (titrated to bowel tolerance).
The use of docosahexeonoic acid (DHA) found in many fish oils such as salmon and mackerel, blocks the blood-clotting capabilities and inflammatory properties of lipoprotein (a). The use of vegetables lower lipoprotein (a) by lowering insulin levels; thus a high protein, low carbohydrate diet should be utilized.
C-Reactive Protein
The most controversial topic in cardiology is the possibility that infectious organisms such as herpes, cytomegalovirus, chlamydia and even mycoplasma could trigger a chronic inflammatory response in blood vessels, thus setting off a cascade of events leading to plaque formation. This risk factor is called C- Reactive Protein(CRP). Data in 1997 from Lancet indicated that CRP could predict future vascular events in healthy as well as high-risk patients.
This study revealed a correlation of high fibrinogen and CRP in patients with ongoing inflammatory responses, and those with athersclerotic disease had an elevated CRP. Thus antimicobial agents such as antibiotics could decrease the risk of heart disease. Once a CRP is elevated, investigation by either specific infectious antibody testing and live cell analysis is warranted. More research needs to be undertaken in this controversial area.
As these new millennium risks are embraced and utilized in practice, the concept of cardiovascular prevention will grow. These concepts, in conjunction with ultrafast CT of the heart and conventional testing, will lead to a wider diagnosis of coronary artery disease.
Dr. Fratellone medical director of The Atkins Center for Complementary Medicine, is dedicated to patients who desire to pursue a better well-being. He uses expertise in non-invasive cardiology testing and preventive medicine to help his patients achieve optimal health.
Jeff :jester:
Here is another interesting article by the medical director of the Atkins Center:
The Atkins Approach to CHD Diet and Treatment
Patrick Fratellone, MD
Half the deaths in the United States since 1900 have been attributed to heart disease. America now leads the world in death rates from heart disease. The conditions included are coronary artery disease, cardiomyopathy, hypertension and arrhythmias.
According to the American Heart Association, every 33 seconds an American dies of cardiovascular disease-which accounts for greater than 950,000 deaths per year. It is also estimated that every 20 seconds an individual has a heart attack. We know that 52.3 percent are women and 47.7 percent are men. We also know that African Americans are more greatly affected than whites. There is enough data to support a prevention and treatment program.
Our experience at the Atkins Center is that diet, nutritional supplements and exercise, in conjunction with medical therapy and enhanced external counterpulsation is a good plan. The common precursor of heart disease is atherosclerosis. The inner arterial walls harden and thicken due to deposits of fatty substances. These substances form plaque which causes narrowing of the arteries. The theory that high levels of cholesterol is the main cause of atherosclerosis is a false idea-a myth you could say. Another theory, the lipid hypothesis as the single cause of atherosclerosis, has not passed scientific tests and is filled with inaccuracies.
The idea that a bad diet leads to high cholesterol which leads to plaque formation thus causing heart disease has been ingrained in our medical education and sold to the public. An atherogenic diet is a diet containing too much cholesterol and saturated fats (which are found in animal products, milk, eggs and even in oils and too little polyunsaturated fats). We believe this is the cause of the initial problem. So blaming the Atkins Diet makes it easier for the public to accept low-cholesterol diets and statin drugs as the treatment of choice. Yet millions of Americans on low cholesterol diet and statin drugs also suffer heart attacks. There is evidence that statin drugs decrease a vital nutrient, Coenzyme Q10, which is needed for every cell, especially the heart muscle. There is evidence that Coenzyme Q10 and an amino acid, L-carnithine, can increase systolic function of the heart. Most published lipid observations on the effects of dietary fat include considerable amounts of carbohydrates in the protocols. Most published observations of high fat, high protein and ultra-low carbohydrates diets (below 20 percent of total calories) show beneficial results. So the culprit may not be cholesterol, but high glycemic foods which increase insulin. Jacobson et al compared conventional low-fat diet therapy with a low carbohydrate ketogenic diet in adolescents. Not only was there an increased weight loss among the latter group but a reduction in triglycerides, total cholesterol and low density lipoproteins and an increase in high-density lipoproteins. Hays et al noted the same lipid profiles in his study. Data extrapolated from Gaziano showed that a high triglycerides/low HDL ratio is more of a risk factor than cholesterol alone and that there is a 16 times likelihood of having a myocardial infarction with this offset ratio.
In the last 10 years there has been an emergence of new risk factors. These cutting-edge risk factors should be part of every cardiology patient's blood profile. These risk factors include homocysteine, fibrinogen, lipoprotein and C-reactive protein. The first of these factors, homocysteine, was first proposed in 1969 by Dr. Kilmer McCully. He proposed that premature vascular damage and disease were a result of high homocysteine levels. Only in the last few years has data confirmed his initially rejected hypothesis from 1969. Now there is data to support the connection between high homocysteine levels and coronary artery disease, peripheral vascular and carotid artery disease. In 1997, the value of high homocysteine levels in 587 patients with heart disease was evaluated. After a follow-up of 4.6 years, only 3.8 percent of patients with homocysteine levels below 9 umol/L had died compared with 24.7 percent mortality for homocysteine levels greater than 15 umol/L.(8) When an individual is deficient in B6 , B12 and folic acid, the body cannot break down methionine effectively, thus leading to high homocysteine levels. The solution is simple-an intake of the B vitamins and folic acid will decrease homocysteine levels.(9) I recommend a dose of folic acid ranging from 2.5 mg to 20 mg with B6 and B12 supplementation. It has been estimated that an increase of folic acid can prevent 20,000 to 40,000 premature cardiovascular deaths.
Working with Patients' Lipoprotien
You always hear about the "bad cholesterol" called LDL, but no one mentions the real killer component of the LDL, called the lipoprotein (a). I describe lipoprotein as a glue-like substance to my patients, and anyone with a family history of heart disease should have this checked. An important but critical reminder is that the statin drugs such as lipitor and mevacor do not lower lipoprotein (a) levels and there has even been suggestions that the statin drugs can increase levels. Lipoprotein (a) inhibits blood thinning and appears to regulate clot formation (thrombosis). Lipoprotein (a) leads to premature myocardial infarctions in patients with normal cholesterol levels. So you can see why cholesterol is not the major problem. The normal levels of lipoprotein (a) range between 20-40. For a patient with a high lipoprotein (a), I prescribe 300 mg Coenzyme Q10 and 2000 mg and above of Vitamin C (titrated to bowel tolerance).
The use of docosahexeonoic acid (DHA) found in many fish oils such as salmon and mackerel, blocks the blood-clotting capabilities and inflammatory properties of lipoprotein (a). The use of vegetables lower lipoprotein (a) by lowering insulin levels; thus a high protein, low carbohydrate diet should be utilized.
C-Reactive Protein
The most controversial topic in cardiology is the possibility that infectious organisms such as herpes, cytomegalovirus, chlamydia and even mycoplasma could trigger a chronic inflammatory response in blood vessels, thus setting off a cascade of events leading to plaque formation. This risk factor is called C- Reactive Protein(CRP). Data in 1997 from Lancet indicated that CRP could predict future vascular events in healthy as well as high-risk patients.
This study revealed a correlation of high fibrinogen and CRP in patients with ongoing inflammatory responses, and those with athersclerotic disease had an elevated CRP. Thus antimicobial agents such as antibiotics could decrease the risk of heart disease. Once a CRP is elevated, investigation by either specific infectious antibody testing and live cell analysis is warranted. More research needs to be undertaken in this controversial area.
As these new millennium risks are embraced and utilized in practice, the concept of cardiovascular prevention will grow. These concepts, in conjunction with ultrafast CT of the heart and conventional testing, will lead to a wider diagnosis of coronary artery disease.
Dr. Fratellone medical director of The Atkins Center for Complementary Medicine, is dedicated to patients who desire to pursue a better well-being. He uses expertise in non-invasive cardiology testing and preventive medicine to help his patients achieve optimal health.
Jeff :jester: