Department of Psychiatry, UCLA-Neuropsychiatric Institute, Los Angeles.
OBJECTIVE AND METHOD: A review of the literature on the serotonin syndrome in animals and human beings was conducted, and 12 reports of 38 cases in human patients were then analyzed to determine the most frequently reported clinical features and drug interactions, as well as the incidence, treatment, and outcome of this syndrome. FINDINGS: The serotonin syndrome is most commonly the result of the interaction between serotonergic agents and monoamine oxidase inhibitors. The most frequent clinical features are changes in mental status, restlessness, myoclonus, hyperreflexia, diaphoresis, shivering, and tremor. The presumed pathophysiological mechanism involves brainstem and spinal cord activation of the 1A form of serotonin (5-hydroxytryptamine, or 5-HT) receptor. The incidence of the syndrome is not known. Both sexes have been affected, and patients' ages have ranged from 20 to 68 years. Discontinuation of the suspected serotonergic agent and institution of supportive measures are the primary treatment, although 5-HT receptor antagonists may also play a role. Once treatment is instituted, the syndrome typically resolves within 24 hours, but confusion can last for days, and death has been reported. CONCLUSIONS: The serotonin syndrome is a toxic condition requiring heightened clinical awareness for prevention, recognition, and prompt treatment. Further work is needed to establish the diagnostic criteria, incidence, and predisposing factors, to identify the role of 5-HT antagonists in treatment, and to differentiate the syndrome from neuroleptic malignant syndrome.
PMID: 2035713 [PubMed - indexed for MEDLINE]
Senin, 11 Agustus 2008
International Union of Pharmacology classification of receptors for 5-hydroxytryptamine (Serotonin).
Sandoz Pharma Limited, Basel, Switzerland.
It is evident that in the last decade or so, a vast amount of new information has become available concerning the various 5-HT receptor types and their characteristics. This derives from two main research approaches, operational pharmacology, using selective ligands (both agonists and antagonists), and, more recently, molecular biology. Although the scientific community continues to deliberate about the hierarchy of criteria for neurotransmitter receptor characterisation, there seems good agreement between the two approaches regarding 5-HT receptor classification. In addition, the information regarding transduction mechanisms and second messengers is also entirely consistent. Thus, on the basis of these essential criteria for receptor characterisation and classification, there are at least three main groups or classes of 5-HT receptor: 5-HT1, 5-HT2, and 5-HT3. Each group is not only operationally but also structurally distinct, with each receptor group having its own distinct transducing system. The more recently identified 5-HT4 receptor almost undoubtedly represents a fourth 5-HT receptor class on the basis of operational and transductional data, but this will only be definitively shown when the cDNA for the receptor has been cloned and the amino acid sequence of the protein is known. Although those 5-HT receptors that have been fully characterised and classified to date (and, hence, named with confidence) would seem to mediate the majority of the actions of 5-HT throughout the mammalian body, not all receptors for 5-HT are fully encompassed within our scheme of classification. These apparent anomalies must be recognised and need further study. They may or may not represent new groups of 5-HT receptor or subtypes of already known groups of 5-HT receptor. Even though the cDNAs for the 5-ht1E, 5-ht1F, 5-ht5, 5-ht6, and 5-ht7 receptors have been cloned and their amino acid sequence defined, more data are necessary concerning their operational and transductional characteristics before one can be confident of the suitability of their appellations. Therefore, it is important to rationalise in concert all of the available data from studies involving both operational approaches of the classical pharmacological type and those from molecular and cellular biology.(ABSTRACT TRUNCATED AT 400 WORDS)
PMID: 7938165 [PubMed - indexed for MEDLINE]
It is evident that in the last decade or so, a vast amount of new information has become available concerning the various 5-HT receptor types and their characteristics. This derives from two main research approaches, operational pharmacology, using selective ligands (both agonists and antagonists), and, more recently, molecular biology. Although the scientific community continues to deliberate about the hierarchy of criteria for neurotransmitter receptor characterisation, there seems good agreement between the two approaches regarding 5-HT receptor classification. In addition, the information regarding transduction mechanisms and second messengers is also entirely consistent. Thus, on the basis of these essential criteria for receptor characterisation and classification, there are at least three main groups or classes of 5-HT receptor: 5-HT1, 5-HT2, and 5-HT3. Each group is not only operationally but also structurally distinct, with each receptor group having its own distinct transducing system. The more recently identified 5-HT4 receptor almost undoubtedly represents a fourth 5-HT receptor class on the basis of operational and transductional data, but this will only be definitively shown when the cDNA for the receptor has been cloned and the amino acid sequence of the protein is known. Although those 5-HT receptors that have been fully characterised and classified to date (and, hence, named with confidence) would seem to mediate the majority of the actions of 5-HT throughout the mammalian body, not all receptors for 5-HT are fully encompassed within our scheme of classification. These apparent anomalies must be recognised and need further study. They may or may not represent new groups of 5-HT receptor or subtypes of already known groups of 5-HT receptor. Even though the cDNAs for the 5-ht1E, 5-ht1F, 5-ht5, 5-ht6, and 5-ht7 receptors have been cloned and their amino acid sequence defined, more data are necessary concerning their operational and transductional characteristics before one can be confident of the suitability of their appellations. Therefore, it is important to rationalise in concert all of the available data from studies involving both operational approaches of the classical pharmacological type and those from molecular and cellular biology.(ABSTRACT TRUNCATED AT 400 WORDS)
PMID: 7938165 [PubMed - indexed for MEDLINE]
Jumat, 01 Agustus 2008
:: Angiogenesis in cancer
How angiogenesis complicates cancer
Angiogenesis performs a critical role in the development of cancer. Solid tumors smaller than 1 to 2 cubic millimeters are not vascularized. To spread, they need to be supplied by blood vessels that bring oxygen and nutrients and remove metabolic wastes.
Beyond the critical volume of 2 cubic millimeters, oxygen and nutrients have difficulty diffusing to the cells in the center of the tumor, causing a state of cellular hypoxia that marks the onset of tumoral angiogenesis.
New blood vessel development is an important process in tumor progression. It favors the transition from hyperplasia to neoplasia i.e. the passage from a state of cellular multiplication to a state of uncontrolled proliferation characteristic of tumor cells.
Neovascularization also influences the dissemination of cancer cells throughout the entire body eventually leading to metastasis formation.The vascularization level of a solid tumor is thought to be an excellent indicator of its metastatic potential.
The molecular factors involved in the stimulation of blood vessel growth are described in detail in The process of angiogenesis.
Shortcomings of standard therapies
Standard therapies to combat cancer are usually aimed at interfering with the cellular replication process which is accelerated in tumors. Despite the efforts made since 1971 to fight cancer -- the year the United States declared war on the disease -- new cases of most cancers have increased significantly. Ninety percent of all cancers are solid tumors and thus depend on angiogenesis to support their growth.
Resistance to treatment is a major issue in oncology. In hormone-dependent cancer for instance, after standard anti-hormonal therapy, it is common to see a recurrence of cancer. This occurs when a malignant cell is transformed a second time, thus making its replication independent of hormones. The same phenomenon takes place with cancers treated with chemotherapy. Often a transformed cell exposed to a powerful chemical agent goes through a mutation, giving it a selective advantage for growth, such as the production of a growth factor or resistance to chemotherapeutic agents.
It has also been shown that the resection of a primary tumor is often accompanied by metastases caused by a systemic disturbance of the angiogenic balance of the body. All these standard therapies could profit from a concomitant treatment that would restrict latent tumors in a prevascular phase.
Antiangiogenesis as a strategy against cancer
As early as the 1970s, Dr. Judah Folkman of the Harvard Medical School suggested inhibiting new blood vessel formation as a way to fight cancer.
The malignant tissue would be deprived of its oxygen and nutrient supply, as well as be unable to eliminate metabolic wastes. This in turn would inhibit tumor progression and metastatic progression that accompanies most advanced cancers. These are the main steps of the angiogenic process that can be interrupted:
Inhibiting endogenous angiogenic factors, such as bFGF (basic Fibroblast Growth Factor) and VEGF (Vascular Endothelial Growth Factor)
Inhibiting degradative enzymes (Matrix Metalloproteinases) responsible for the degradation of the basement membrane of blood vessels
Inhibiting endothelial cell proliferation
Inhibiting endothelial cell migration
Inhibiting the activation and differentiation of endothelial cells
However, the challenge is to develop an antiangiogenic factor that does not affect the existing vasculature.
Neovastat is an inhibitor of angiogenesis
A number of studies have shown Neovastat to have antiangiogenic properties. The mechanisms of action include:
Inhibiting degradative Matrix Metalloproteinases,
Blocking receptor sites for the angiogenic growth factor VEGF, which prevents endothelial cells from proliferating, migrating, and organizing to form new blood vessels in vitro.
As well, clinical and pre-clinical studies show Neovastat can be used alone or in combination with other therapies. Clinical experience with 540 patients, some of whom have been administered the drug for almost four years, have confirmed Neovastat’s excellent safety and tolerability profile in monotherapy and in concomitant chemotherapy and radiotherapy.
(Angio World)
Angiogenesis performs a critical role in the development of cancer. Solid tumors smaller than 1 to 2 cubic millimeters are not vascularized. To spread, they need to be supplied by blood vessels that bring oxygen and nutrients and remove metabolic wastes.
Beyond the critical volume of 2 cubic millimeters, oxygen and nutrients have difficulty diffusing to the cells in the center of the tumor, causing a state of cellular hypoxia that marks the onset of tumoral angiogenesis.
New blood vessel development is an important process in tumor progression. It favors the transition from hyperplasia to neoplasia i.e. the passage from a state of cellular multiplication to a state of uncontrolled proliferation characteristic of tumor cells.
Neovascularization also influences the dissemination of cancer cells throughout the entire body eventually leading to metastasis formation.The vascularization level of a solid tumor is thought to be an excellent indicator of its metastatic potential.
The molecular factors involved in the stimulation of blood vessel growth are described in detail in The process of angiogenesis.
Shortcomings of standard therapies
Standard therapies to combat cancer are usually aimed at interfering with the cellular replication process which is accelerated in tumors. Despite the efforts made since 1971 to fight cancer -- the year the United States declared war on the disease -- new cases of most cancers have increased significantly. Ninety percent of all cancers are solid tumors and thus depend on angiogenesis to support their growth.
Resistance to treatment is a major issue in oncology. In hormone-dependent cancer for instance, after standard anti-hormonal therapy, it is common to see a recurrence of cancer. This occurs when a malignant cell is transformed a second time, thus making its replication independent of hormones. The same phenomenon takes place with cancers treated with chemotherapy. Often a transformed cell exposed to a powerful chemical agent goes through a mutation, giving it a selective advantage for growth, such as the production of a growth factor or resistance to chemotherapeutic agents.
It has also been shown that the resection of a primary tumor is often accompanied by metastases caused by a systemic disturbance of the angiogenic balance of the body. All these standard therapies could profit from a concomitant treatment that would restrict latent tumors in a prevascular phase.
Antiangiogenesis as a strategy against cancer
As early as the 1970s, Dr. Judah Folkman of the Harvard Medical School suggested inhibiting new blood vessel formation as a way to fight cancer.
The malignant tissue would be deprived of its oxygen and nutrient supply, as well as be unable to eliminate metabolic wastes. This in turn would inhibit tumor progression and metastatic progression that accompanies most advanced cancers. These are the main steps of the angiogenic process that can be interrupted:
Inhibiting endogenous angiogenic factors, such as bFGF (basic Fibroblast Growth Factor) and VEGF (Vascular Endothelial Growth Factor)
Inhibiting degradative enzymes (Matrix Metalloproteinases) responsible for the degradation of the basement membrane of blood vessels
Inhibiting endothelial cell proliferation
Inhibiting endothelial cell migration
Inhibiting the activation and differentiation of endothelial cells
However, the challenge is to develop an antiangiogenic factor that does not affect the existing vasculature.
Neovastat is an inhibitor of angiogenesis
A number of studies have shown Neovastat to have antiangiogenic properties. The mechanisms of action include:
Inhibiting degradative Matrix Metalloproteinases,
Blocking receptor sites for the angiogenic growth factor VEGF, which prevents endothelial cells from proliferating, migrating, and organizing to form new blood vessels in vitro.
As well, clinical and pre-clinical studies show Neovastat can be used alone or in combination with other therapies. Clinical experience with 540 patients, some of whom have been administered the drug for almost four years, have confirmed Neovastat’s excellent safety and tolerability profile in monotherapy and in concomitant chemotherapy and radiotherapy.
(Angio World)
Process of Angiogenesis
Physiological and pathological angiogenesis
Almost all tissues develop a vascular network that provides cells with nutrients and oxygen and enables them to eliminate metabolic wastes. Once formed, the vascular network is a stable system that regenerates slowly.
In physiological conditions, angiogenesis occurs primarily in embryo development, during wound healing and in response to ovulation.
However, pathological angiogenesis, or the abnormal rapid proliferation of blood vessels, is implicated in over 20 diseases, including cancer, psoriasis and age-related macular degeneration.
The angiogenic sequence
The angiogenic process, as currently understood, can be summarized as follows:
A cell activated by a lack of oxygen releases angiogenic molecules that attract inflammatory and endothelial cells and promote their proliferation.
During their migration, inflammatory cells also secrete molecules that intensify the angiogenic stimuli.
The endothelial cells that form the blood vessels respond to the angiogenic call by differentiating and by secreting matrix metalloproteases (MMP), which digest the blood-vessel walls to enable them to escape and migrate toward the site of the angiogenic stimuli.
Several protein fragments produced by the digestion of the blood-vessel walls intensify the proliferative and migratory activity of endothelial cells, which then form a capillary tube by altering the arrangement of their adherence-membrane proteins.
Finally, through the process of anastomosis, the capillaries emanating from the arterioles and the venules will join, thus resulting in a continuous blood flow.
The normal regulation of angiogenesis is governed by a fine balance between factors that induce the formation of blood vessels and those that halt or inhibit the process. When this balance is destroyed, it usually results in pathological angiogenesis which causes increased blood-vessel formation in diseases that depend on angiogenesis.
More than 20 endogenous positive regulators of angiogenesis have been described, including growth factors, matrix metalloproteinases, cytokines, and integrins. Growth factors, such as vascular endothelial growth factor (VEGF), transforming growth factors (TGF-beta), fibroblast growth factors (FGF), epidermal growth factor (EGF), angiogenin, can induce the division of cultured endothelial cells thus indicating a direct action on these cells.
However, other factors have virtually no effect on the division of cultured endothelial cells or, in the case of TGF-beta and TNF-alpha, paradoxically inhibit their growth indicating that their angiogenic action is indirect.
Almost all tissues develop a vascular network that provides cells with nutrients and oxygen and enables them to eliminate metabolic wastes. Once formed, the vascular network is a stable system that regenerates slowly.
In physiological conditions, angiogenesis occurs primarily in embryo development, during wound healing and in response to ovulation.
However, pathological angiogenesis, or the abnormal rapid proliferation of blood vessels, is implicated in over 20 diseases, including cancer, psoriasis and age-related macular degeneration.
The angiogenic sequence
The angiogenic process, as currently understood, can be summarized as follows:
A cell activated by a lack of oxygen releases angiogenic molecules that attract inflammatory and endothelial cells and promote their proliferation.
During their migration, inflammatory cells also secrete molecules that intensify the angiogenic stimuli.
The endothelial cells that form the blood vessels respond to the angiogenic call by differentiating and by secreting matrix metalloproteases (MMP), which digest the blood-vessel walls to enable them to escape and migrate toward the site of the angiogenic stimuli.
Several protein fragments produced by the digestion of the blood-vessel walls intensify the proliferative and migratory activity of endothelial cells, which then form a capillary tube by altering the arrangement of their adherence-membrane proteins.
Finally, through the process of anastomosis, the capillaries emanating from the arterioles and the venules will join, thus resulting in a continuous blood flow.
The normal regulation of angiogenesis is governed by a fine balance between factors that induce the formation of blood vessels and those that halt or inhibit the process. When this balance is destroyed, it usually results in pathological angiogenesis which causes increased blood-vessel formation in diseases that depend on angiogenesis.
More than 20 endogenous positive regulators of angiogenesis have been described, including growth factors, matrix metalloproteinases, cytokines, and integrins. Growth factors, such as vascular endothelial growth factor (VEGF), transforming growth factors (TGF-beta), fibroblast growth factors (FGF), epidermal growth factor (EGF), angiogenin, can induce the division of cultured endothelial cells thus indicating a direct action on these cells.
However, other factors have virtually no effect on the division of cultured endothelial cells or, in the case of TGF-beta and TNF-alpha, paradoxically inhibit their growth indicating that their angiogenic action is indirect.
Kamis, 31 Juli 2008
What Is Cancer?
Defining Cancer
Cancer is a term used for diseases in which abnormal cells divide without control and are able to invade other tissues. Cancer cells can spread to other parts of the body through the blood and lymph systems.
Cancer is not just one disease but many diseases. There are more than 100 different types of cancer. Most cancers are named for the organ or type of cell in which they start - for example, cancer that begins in the colon is called colon cancer; cancer that begins in basal cells of the skin is called basal cell carcinoma.
Cancer types can be grouped into broader categories. The main categories of cancer include:
Carcinoma - cancer that begins in the skin or in tissues that line or cover internal organs.
Sarcoma - cancer that begins in bone, cartilage, fat, muscle, blood vessels, or other connective or supportive tissue.
Leukemia - cancer that starts in blood-forming tissue such as the bone marrow and causes large numbers of abnormal blood cells to be produced and enter the blood.
Lymphoma and myeloma - cancers that begin in the cells of the immune system.
Central nervous system cancers - cancers that begin in the tissues of the brain and spinal cord.
(For definitions of other cancer-related terms, see NCI's Dictionary of Cancer Terms.)
Origins of Cancer
All cancers begin in cells, the body's basic unit of life. To understand cancer, it's helpful to know what happens when normal cells become cancer cells.
The body is made up of many types of cells. These cells grow and divide in a controlled way to produce more cells as they are needed to keep the body healthy. When cells become old or damaged, they die and are replaced with new cells.
However, sometimes this orderly process goes wrong. The genetic material (DNA) of a cell can become damaged or changed, producing mutations that affect normal cell growth and division. When this happens, cells do not die when they should and new cells form when the body does not need them. The extra cells may form a mass of tissue called a tumor.
(Image from Understanding Cancer Series: Cancer.)
Not all tumors are cancerous; tumors can be benign or malignant.
Benign tumors aren't cancerous. They can often be removed, and, in most cases, they do not come back. Cells in benign tumors do not spread to other parts of the body.
Malignant tumors are cancerous. Cells in these tumors can invade nearby tissues and spread to other parts of the body. The spread of cancer from one part of the body to another is called metastasis.
Some cancers do not form tumors. For example, leukemia is a cancer of the bone marrow and blood.
Cancer Statistics
A new report from the nation's leading cancer organizations shows cancer death rates decreased on average 2.1 percent per year from 2002 through 2004, nearly twice the annual decrease of 1.1 percent per year from 1993 through 2002. (Read more about the Annual Report.)
Estimated new cases and deaths from cancer in the United States in 2008:
New cases: 1,437,180 (does not include nonmelanoma skin cancers)
Deaths: 565,650
NCI's Cancer Stat Fact Sheets provide frequently requested cancer statistics for a number of cancer types.
Additional Information
Find a type of cancer:
A to Z List of Cancers
Cancers by Body Location/System
Cancers that are diagnosed with the greatest frequency in the United States are listed below. (Read more about Common Cancer Types.)
Bladder Cancer Melanoma
Breast Cancer Non-Hodgkin Lymphoma
Colon and Rectal Cancer Pancreatic Cancer
Endometrial Cancer Prostate Cancer
Kidney (Renal Cell) Cancer Skin Cancer (Nonmelanoma)
Leukemia Thyroid Cancer
Lung Cancer
More cancer topics:
Cancer Prevention
Cancer Genetics
Cancer Causes and Risk Factors
Screening and Testing to Detect Cancer
Cancer Treatment
Coping with Cancer
Cancer Statistics
Clinical Trials
Cancer Publications
The risk of developing many types of cancer can be reduced by practicing healthy lifestyle habits, such as eating a healthy diet, getting regular exercise, and not smoking. Also, the sooner a cancer is found and treatment begins, the better the chances are that the treatment will be successful.
Contact Us for Help
NCI cancer information specialists can answer your questions about cancer and help you with quitting smoking. They can also help you with using this Web site and can tell you about NCI's printed and electronic materials. Contact us.
(National Cancer)
Cancer is a term used for diseases in which abnormal cells divide without control and are able to invade other tissues. Cancer cells can spread to other parts of the body through the blood and lymph systems.
Cancer is not just one disease but many diseases. There are more than 100 different types of cancer. Most cancers are named for the organ or type of cell in which they start - for example, cancer that begins in the colon is called colon cancer; cancer that begins in basal cells of the skin is called basal cell carcinoma.
Cancer types can be grouped into broader categories. The main categories of cancer include:
Carcinoma - cancer that begins in the skin or in tissues that line or cover internal organs.
Sarcoma - cancer that begins in bone, cartilage, fat, muscle, blood vessels, or other connective or supportive tissue.
Leukemia - cancer that starts in blood-forming tissue such as the bone marrow and causes large numbers of abnormal blood cells to be produced and enter the blood.
Lymphoma and myeloma - cancers that begin in the cells of the immune system.
Central nervous system cancers - cancers that begin in the tissues of the brain and spinal cord.
(For definitions of other cancer-related terms, see NCI's Dictionary of Cancer Terms.)
Origins of Cancer
All cancers begin in cells, the body's basic unit of life. To understand cancer, it's helpful to know what happens when normal cells become cancer cells.
The body is made up of many types of cells. These cells grow and divide in a controlled way to produce more cells as they are needed to keep the body healthy. When cells become old or damaged, they die and are replaced with new cells.
However, sometimes this orderly process goes wrong. The genetic material (DNA) of a cell can become damaged or changed, producing mutations that affect normal cell growth and division. When this happens, cells do not die when they should and new cells form when the body does not need them. The extra cells may form a mass of tissue called a tumor.
(Image from Understanding Cancer Series: Cancer.)
Not all tumors are cancerous; tumors can be benign or malignant.
Benign tumors aren't cancerous. They can often be removed, and, in most cases, they do not come back. Cells in benign tumors do not spread to other parts of the body.
Malignant tumors are cancerous. Cells in these tumors can invade nearby tissues and spread to other parts of the body. The spread of cancer from one part of the body to another is called metastasis.
Some cancers do not form tumors. For example, leukemia is a cancer of the bone marrow and blood.
Cancer Statistics
A new report from the nation's leading cancer organizations shows cancer death rates decreased on average 2.1 percent per year from 2002 through 2004, nearly twice the annual decrease of 1.1 percent per year from 1993 through 2002. (Read more about the Annual Report.)
Estimated new cases and deaths from cancer in the United States in 2008:
New cases: 1,437,180 (does not include nonmelanoma skin cancers)
Deaths: 565,650
NCI's Cancer Stat Fact Sheets provide frequently requested cancer statistics for a number of cancer types.
Additional Information
Find a type of cancer:
A to Z List of Cancers
Cancers by Body Location/System
Cancers that are diagnosed with the greatest frequency in the United States are listed below. (Read more about Common Cancer Types.)
Bladder Cancer Melanoma
Breast Cancer Non-Hodgkin Lymphoma
Colon and Rectal Cancer Pancreatic Cancer
Endometrial Cancer Prostate Cancer
Kidney (Renal Cell) Cancer Skin Cancer (Nonmelanoma)
Leukemia Thyroid Cancer
Lung Cancer
More cancer topics:
Cancer Prevention
Cancer Genetics
Cancer Causes and Risk Factors
Screening and Testing to Detect Cancer
Cancer Treatment
Coping with Cancer
Cancer Statistics
Clinical Trials
Cancer Publications
The risk of developing many types of cancer can be reduced by practicing healthy lifestyle habits, such as eating a healthy diet, getting regular exercise, and not smoking. Also, the sooner a cancer is found and treatment begins, the better the chances are that the treatment will be successful.
Contact Us for Help
NCI cancer information specialists can answer your questions about cancer and help you with quitting smoking. They can also help you with using this Web site and can tell you about NCI's printed and electronic materials. Contact us.
(National Cancer)
Eat Right for Your Type
What It Is
The Eat Right for Your Type diet encourages people to eat certain foods and avoid others based on their blood type -- A, B, AB, or O.
Peter J. D'Adamo, ND, the author of Eat Right for Your Type: The Individualized Diet Solution to Staying Healthy, Living Longer & Achieving Your Ideal Weight, believes blood types affect the digestive system and that some foods good for people of one type are "dangerous" for another.
The Latest Diets
New diets and weight loss tricks pop up every month. Get the facts on how the new diets work and what's right.
Atkins
Best Life Diet
Biggest Loser
Cabbage Soup
Hallelujah Diet
Jenny Craig
NutriSystem
Ornish
South Beach
3 Day Diet
Weight Watchers
Zone
All Diets A-Z
Related to diet and weight loss Alli, apple cider vinegar, low carb diet, high protien diet, weight loss, metabolism, Mediterranean diet, diet pills, trans fat, BMI calculator, detox diet, diabetes diet, Body for Life
© 2008 WebMD, LLC. All rights reserved.
It goes further than that for D'Adamo, a naturopathic doctor, who believes that your blood type also determines your susceptibility to certain illnesses and how you should exercise.
Critics cite a lack of published evidence backing D'Adamo's blood type-based diet plan. "I know of no plausible rationale behind the diet," says John Foreyt, PhD, a researcher at the Baylor College of Medicine in Houston.
This diet may suit those enthusiastic about a plan that doesn't involve tracking calories or fat grams, while others may find it difficult to stay within the diet's confines, a challenge made greater if more than one person in a household follows the diet -- and has a different blood type.
What You Can Eat
What you can eat -- and how you exercise -- on this plan depends on who you are.
If you're blood type O ("for old," as in humanity's oldest blood line) your digestive tract retains the memory of ancient times, says D'Adamo, so you're metabolism will benefit from lean meats, poultry, and fish. You're advised to restrict grains, breads, legumes, and beans and to enjoy vigorous exercise.
Type A ("for agrarian") flourishes on vegetarian diets, "the inheritance of their more settled and less warlike farmer ancestors," says D'Adamo. The type A diet contains soy proteins, grains, and organic vegetables and encourages gentle exercise.
The nomadic blood type B has a tolerant digestive system and can enjoy low-fat dairy, meat, and produce but, among other things, should avoid wheat, corn, and lentils, D'Adamo says. If you're type B, it's recommended you exercise moderately.
The "modern" blood type AB has a sensitive digestive tract and should avoid chicken, beef, and pork but enjoy seafood, tofu, dairy, and most produce. The fitness regimen for ABs is calming exercises
The Eat Right for Your Type diet encourages people to eat certain foods and avoid others based on their blood type -- A, B, AB, or O.
Peter J. D'Adamo, ND, the author of Eat Right for Your Type: The Individualized Diet Solution to Staying Healthy, Living Longer & Achieving Your Ideal Weight, believes blood types affect the digestive system and that some foods good for people of one type are "dangerous" for another.
The Latest Diets
New diets and weight loss tricks pop up every month. Get the facts on how the new diets work and what's right.
Atkins
Best Life Diet
Biggest Loser
Cabbage Soup
Hallelujah Diet
Jenny Craig
NutriSystem
Ornish
South Beach
3 Day Diet
Weight Watchers
Zone
All Diets A-Z
Related to diet and weight loss Alli, apple cider vinegar, low carb diet, high protien diet, weight loss, metabolism, Mediterranean diet, diet pills, trans fat, BMI calculator, detox diet, diabetes diet, Body for Life
© 2008 WebMD, LLC. All rights reserved.
It goes further than that for D'Adamo, a naturopathic doctor, who believes that your blood type also determines your susceptibility to certain illnesses and how you should exercise.
Critics cite a lack of published evidence backing D'Adamo's blood type-based diet plan. "I know of no plausible rationale behind the diet," says John Foreyt, PhD, a researcher at the Baylor College of Medicine in Houston.
This diet may suit those enthusiastic about a plan that doesn't involve tracking calories or fat grams, while others may find it difficult to stay within the diet's confines, a challenge made greater if more than one person in a household follows the diet -- and has a different blood type.
What You Can Eat
What you can eat -- and how you exercise -- on this plan depends on who you are.
If you're blood type O ("for old," as in humanity's oldest blood line) your digestive tract retains the memory of ancient times, says D'Adamo, so you're metabolism will benefit from lean meats, poultry, and fish. You're advised to restrict grains, breads, legumes, and beans and to enjoy vigorous exercise.
Type A ("for agrarian") flourishes on vegetarian diets, "the inheritance of their more settled and less warlike farmer ancestors," says D'Adamo. The type A diet contains soy proteins, grains, and organic vegetables and encourages gentle exercise.
The nomadic blood type B has a tolerant digestive system and can enjoy low-fat dairy, meat, and produce but, among other things, should avoid wheat, corn, and lentils, D'Adamo says. If you're type B, it's recommended you exercise moderately.
The "modern" blood type AB has a sensitive digestive tract and should avoid chicken, beef, and pork but enjoy seafood, tofu, dairy, and most produce. The fitness regimen for ABs is calming exercises
Dark Chocolate Is Healthy Chocolate
By Daniel J. DeNoon
WebMD Health NewsAug. 27, 2003 -- Got high blood pressure? Try a truffle. Worried about heart disease? Buy a bon-bon.
It's the best medical news in ages. Studies in two prestigious scientific journals say dark chocolate -- but not white chocolate or milk chocolate -- is good for you.
Romance and Chocolate
From the WebMD community
How often do you say, "I love you," to your partner? Everyday... several times a day... my husband likes to hear it and he doesn't let me go to bed until I've said it even if we're fighting. – Katelya
Read more of your thoughts on love
Favorite Screen Romances
Sweet History of Chocolate
Science of Attraction: Feelings or Pheromones?
Today's Love Lingo
Video: Getting the Most Out of Your Relationship
Related to modern love Science of Attraction: Feelings or Pheromones?, Relationship in Distress? Tips to De-stress, When Mars and Venus Collide, Is Modern Life Giving Your Heart a Beating?
© 2008 WebMD, LLC. All rights reserved.
Dark Chocolate Lowers Blood Pressure
Dark chocolate -- not white chocolate -- lowers high blood pressure, say Dirk Taubert, MD, PhD, and colleagues at the University of Cologne, Germany. Their report appears in the Aug. 27 issue of The Journal of the American Medical Association.
But that's no license to go on a chocolate binge. Eating more dark chocolate can help lower blood pressure -- if you've reached a certain age and have mild high blood pressure, say the researchers. But you have to balance the extra calories by eating less of other things.
Antioxidants in Dark Chocolate
Dark chocolate -- but not milk chocolate or dark chocolate eaten with milk -- is a potent antioxidant, report Mauro Serafini, PhD, of Italy's National Institute for Food and Nutrition Research in Rome, and colleagues. Their report appears in the Aug. 28 issue of Nature. Antioxidants gobble up free radicals, destructive molecules that are implicated in heart disease and other ailments.
"Our findings indicate that milk may interfere with the absorption of antioxidants from chocolate ... and may therefore negate the potential health benefits that can be derived from eating moderate amounts of dark chocolate."
Translation: Say "Dark, please," when ordering at the chocolate counter. Don't even think of washing it down with milk. And if health is your excuse for eating chocolate, remember the word "moderate" as you nibble.
The Studies
Taubert's team signed up six men and seven women aged 55-64. All had just been diagnosed with mild high blood pressure -- on average, systolic blood pressure (the top number) of 153 and diastolic blood pressure (the bottom number) of 84.
Every day for two weeks, they ate a 100-gram candy bar and were asked to balance its 480 calories by not eating other foods similar in nutrients and calories. Half the patients got dark chocolate and half got white chocolate.
Those who ate dark chocolate had a significant drop in blood pressure (by an average of 5 points for systolic and an average of 2 points for diastolic blood pressure). Those who ate white chocolate did not.
In the second study, Serafini's team signed up seven healthy women and five healthy men aged 25-35. On different days they each ate 100 grams of dark chocolate by itself, 100 grams of dark chocolate with a small glass of whole milk, or 200 grams of milk chocolate.
An hour later, those who ate dark chocolate alone had the most total antioxidants in their blood. And they had higher levels of epicatechin, a particularly healthy compound found in chocolate. The milk chocolate eaters had the lowest epicatechin levels of all.
( Web MD Health News )
WebMD Health NewsAug. 27, 2003 -- Got high blood pressure? Try a truffle. Worried about heart disease? Buy a bon-bon.
It's the best medical news in ages. Studies in two prestigious scientific journals say dark chocolate -- but not white chocolate or milk chocolate -- is good for you.
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Dark Chocolate Lowers Blood Pressure
Dark chocolate -- not white chocolate -- lowers high blood pressure, say Dirk Taubert, MD, PhD, and colleagues at the University of Cologne, Germany. Their report appears in the Aug. 27 issue of The Journal of the American Medical Association.
But that's no license to go on a chocolate binge. Eating more dark chocolate can help lower blood pressure -- if you've reached a certain age and have mild high blood pressure, say the researchers. But you have to balance the extra calories by eating less of other things.
Antioxidants in Dark Chocolate
Dark chocolate -- but not milk chocolate or dark chocolate eaten with milk -- is a potent antioxidant, report Mauro Serafini, PhD, of Italy's National Institute for Food and Nutrition Research in Rome, and colleagues. Their report appears in the Aug. 28 issue of Nature. Antioxidants gobble up free radicals, destructive molecules that are implicated in heart disease and other ailments.
"Our findings indicate that milk may interfere with the absorption of antioxidants from chocolate ... and may therefore negate the potential health benefits that can be derived from eating moderate amounts of dark chocolate."
Translation: Say "Dark, please," when ordering at the chocolate counter. Don't even think of washing it down with milk. And if health is your excuse for eating chocolate, remember the word "moderate" as you nibble.
The Studies
Taubert's team signed up six men and seven women aged 55-64. All had just been diagnosed with mild high blood pressure -- on average, systolic blood pressure (the top number) of 153 and diastolic blood pressure (the bottom number) of 84.
Every day for two weeks, they ate a 100-gram candy bar and were asked to balance its 480 calories by not eating other foods similar in nutrients and calories. Half the patients got dark chocolate and half got white chocolate.
Those who ate dark chocolate had a significant drop in blood pressure (by an average of 5 points for systolic and an average of 2 points for diastolic blood pressure). Those who ate white chocolate did not.
In the second study, Serafini's team signed up seven healthy women and five healthy men aged 25-35. On different days they each ate 100 grams of dark chocolate by itself, 100 grams of dark chocolate with a small glass of whole milk, or 200 grams of milk chocolate.
An hour later, those who ate dark chocolate alone had the most total antioxidants in their blood. And they had higher levels of epicatechin, a particularly healthy compound found in chocolate. The milk chocolate eaters had the lowest epicatechin levels of all.
( Web MD Health News )
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