Diabetes screening is recommended for many people at various stages of life, and for those with any of several risk factors. The screening test varies according to circumstances and local policy, and may be a random blood glucose test, a fasting blood glucose test, a blood glucose test two hours after 75 g of glucose, or an even more formal glucose tolerance test. Many healthcare providers recommend universal screening for adults at age 40 or 50, and often periodically thereafter. Earlier screening is typically recommended for those with risk factors such as obesity, family history of diabetes, high-risk ethnicity (Hispanic, Native American, Afro-Caribbean, Pacific Islander, or Maori).
Many medical conditions are associated with diabetes and warrant screening. A partial list includes: subclinical Cushing's syndrome, testosterone deficiency, high blood pressure, elevated cholesterol levels[citation needed], coronary artery disease[citation needed], past gestational diabetes, polycystic ovary syndrome, chronic pancreatitis, fatty liver, hemochromatosis[citation needed], cystic fibrosis, several mitochondrial neuropathies and myopathies, myotonic dystrophy, Friedreich's ataxia, some of the inherited forms of neonatal hyperinsulinism. The risk of diabetes is higher with chronic use of several medications, including long term corticosteroids, some chemotherapy agents (especially L-asparaginase), as well as some of the antipsychotics and mood stabilizers (especially phenothiazines and some atypical antipsychotics).
People with a confirmed diagnosis of diabetes are tested routinely for complications. This includes yearly urine testing for microalbuminuria and examination of the retina of the eye for retinopathy.
Tuesday, November 17, 2009
Diabetes : Signs and symptoms
The classical symptoms are polyuria and polydipsia which are, respectively, frequent urination and increased thirst and consequent increased fluid intake. Symptoms may develop quite rapidly (weeks or months) in type 1 diabetes, particularly in children. However, in type 2 diabetes symptoms usually develop much more slowly and may be subtle or completely absent. Type 1 diabetes may also cause a rapid yet significant weight loss (despite normal or even increased eating) and irreducible mental fatigue. All of these symptoms except weight loss can also manifest in type 2 diabetes in patients whose diabetes is poorly controlled, although unexplained weight loss may be experienced at the onset of the disease. Final diagnosis is made by measuring the blood glucose concentration.
When the glucose concentration in the blood is raised beyond its renal threshold (about 10 mmol/L, although this may be altered in certain conditions, such as pregnancy), reabsorption of glucose in the proximal renal tubuli is incomplete, and part of the glucose remains in the urine (glycosuria). This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume will be replaced osmotically from water held in body cells and other body compartments, causing dehydration and increased thirst.
Prolonged high blood glucose causes glucose absorption, which leads to changes in the shape of the lenses of the eyes, resulting in vision changes; sustained sensible glucose control usually returns the lens to its original shape. Blurred vision is a common complaint leading to a diabetes diagnosis; type 1 should always be suspected in cases of rapid vision change, whereas with type 2 change is generally more gradual, but should still be suspected.
Patients (usually with type 1 diabetes) may also initially present with diabetic ketoacidosis (DKA), an extreme state of metabolic dysregulation characterized by the smell of acetone on the patient's breath; a rapid, deep breathing known as Kussmaul breathing; polyuria; nausea; vomiting and abdominal pain; and any of many altered states of consciousness or arousal (such as hostility and mania or, equally, confusion and lethargy). In severe DKA, coma may follow, progressing to death. Diabetic ketoacidosis is a medical emergency and requires immediate hospitalization.
A rarer but equally severe possibility is hyperosmolar nonketotic state, which is more common in type 2 diabetes and is mainly the result of dehydration due to loss of body water. Often, the patient has been drinking extreme amounts of sugar-containing drinks, leading to a vicious circle in regard to the water loss.
Genetics
Both type 1 and type 2 diabetes are at least partly inherited. Type 1 diabetes appears to be triggered by some (mainly viral) infections, with some evidence pointing at Coxsackie B4 virus. There is a genetic element in individual susceptibility to some of these triggers which has been traced to particular HLA genotypes (i.e., the genetic "self" identifiers relied upon by the immune system). However, even in those who have inherited the susceptibility, type 1 diabetes mellitus seems to require an environmental trigger.
There is a stronger inheritance pattern for type 2 diabetes. Those with first-degree relatives with type 2 have a much higher risk of developing type 2, increasing with the number of those relatives. Concordance among monozygotic twins is close to 100%, and about 25% of those with the disease have a family history of diabetes. Genes significantly associated with developing type 2 diabetes, include TCF7L2, PPARG, FTO, KCNJ11, NOTCH2, WFS1, CDKAL1, IGF2BP2, SLC30A8, JAZF1, and HHEX.[22] KCNJ11 (potassium inwardly rectifying channel, subfamily J, member 11), encodes the islet ATP-sensitive potassium channel Kir6.2, and TCF7L2 (transcription factor 7–like 2) regulates proglucagon gene expression and thus the production of glucagon-like peptide-1. Moreover, obesity (which is an independent risk factor for type 2 diabetes) is strongly inherited.
Monogenic forms, e.g., MODY, constitute 1-5 % of all cases.
Various hereditary conditions may feature diabetes, for example myotonic dystrophy and Friedreich's ataxia. Wolfram's syndrome is an autosomal recessive neurodegenerative disorder that first becomes evident in childhood. It consists of diabetes insipidus, diabetes mellitus, optic atrophy, and deafness, hence the acronym DIDMOAD.
Gene expression promoted by a diet of fat and glucose as well as high levels of inflammation related cytokines found in the obese results in cells that "produce fewer and smaller mitochondria than is normal," and are thus prone to insulin resistance.
Pathophysiology
Mechanism of insulin release in normal pancreatic beta cells. Insulin production is more or less constant within the beta cells, irrespective of blood glucose levels. It is stored within vacuoles pending release, via exocytosis, which is primarily triggered by food, chiefly food containing absorbable glucose. The chief trigger is a rise in blood glucose levels after eating
Insulin is the principal hormone that regulates uptake of glucose from the blood into most cells (primarily muscle and fat cells, but not central nervous system cells). Therefore deficiency of insulin or the insensitivity of its receptors plays a central role in all forms of diabetes mellitus.
Most of the carbohydrates in food are converted within a few hours to the monosaccharide glucose, the principal carbohydrate found in blood and used by the body as fuel. The most significant exceptions are fructose, most disaccharides (except sucrose and in some people lactose), and all more complex polysaccharides, with the outstanding exception of starch. Insulin is released into the blood by beta cells (β-cells), found in the Islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage.
Insulin is also the principal control signal for conversion of glucose to glycogen for internal storage in liver and muscle cells. Lowered glucose levels result both in the reduced release of insulin from the beta cells and in the reverse conversion of glycogen to glucose when glucose levels fall. This is mainly controlled by the hormone glucagon which acts in an opposite manner to insulin. Glucose thus recovered by the liver re-enters the bloodstream; muscle cells lack the necessary export mechanism.
Higher insulin levels increase some anabolic ("building up") processes such as cell growth and duplication, protein synthesis, and fat storage. Insulin (or its lack) is the principal signal in converting many of the bidirectional processes of metabolism from a catabolic to an anabolic direction, and vice versa. In particular, a low insulin level is the trigger for entering or leaving ketosis (the fat burning metabolic phase).
If the amount of insulin available is insufficient, if cells respond poorly to the effects of insulin (insulin insensitivity or resistance), or if the insulin itself is defective, then glucose will not be absorbed properly by those body cells that require it nor will it be stored appropriately in the liver and muscles. The net effect is persistent high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as acidosis.
Diagnosis
The diagnosis of type 1 diabetes, and many cases of type 2, is usually prompted by recent-onset symptoms of excessive urination (polyuria) and excessive thirst (polydipsia), often accompanied by weight loss. These symptoms typically worsen over days to weeks; about a quarter of people with new type 1 diabetes have developed some degree of diabetic ketoacidosis (a type of metabolic acidosis which is caused by high concentrations of ketone bodies, formed by the breakdown of fatty acids and the deamination of amino acids) by the time the diabetes is recognized. The diagnosis of other types of diabetes is usually made in other ways. These include ordinary health screening; detection of hyperglycemia during other medical investigations; and secondary symptoms such as vision changes or unexplainable fatigue. Diabetes is often detected when a person suffers a problem that is frequently caused by diabetes, such as a heart attack, stroke, neuropathy, poor wound healing or a foot ulcer, certain eye problems, certain fungal infections, or delivering a baby with macrosomia or hypoglycemia.
Diabetes mellitus is characterized by recurrent or persistent hyperglycemia, and is diagnosed by demonstrating any one of the following:
· Fasting plasma glucose level at or above 126 mg/dL (7.0 mmol/L).
· Plasma glucose at or above 200 mg/dL (11.1 mmol/L) two hours after a 75 g oral glucose load as in a glucose tolerance test.
· Symptoms of hyperglycemia and casual plasma glucose at or above 200 mg/dL (11.1 mmol/L).
A positive result, in the absence of unequivocal hyperglycemia, should be confirmed by a repeat of any of the above-listed methods on a different day. Most physicians prefer to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete and offers no prognostic advantage over the fasting test.[27] According to the current definition, two fasting glucose measurements above 126 mg/dL (7.0 mmol/L) is considered diagnostic for diabetes mellitus.
Patients with fasting glucose levels from 100 to 125 mg/dL (6.1 and 7.0 mmol/L) are considered to have impaired fasting glucose. Patients with plasma glucose at or above 140 mg/dL or 7.8 mmol/L, but not over 200, two hours after a 75 g oral glucose load are considered to have impaired glucose tolerance. Of these two pre-diabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus as well as cardiovascular disease.
While not used for diagnosis, an elevated level of glucose irreversibly bound to hemoglobin (termed glycated hemoglobin or HbA1c) of 6.0% or higher (the 2003 revised U.S. standard) is considered abnormal by most labs; HbA1c is primarily used as a treatment-tracking test reflecting average blood glucose levels over the preceding 90 days (approximately) which is the average lifetime of red blood cells which contain hemoglobin in most patients. However, some physicians may order this test at the time of diagnosis to track changes over time. The current recommended goal for HbA1c in patients with diabetes is 6.5%.
When the glucose concentration in the blood is raised beyond its renal threshold (about 10 mmol/L, although this may be altered in certain conditions, such as pregnancy), reabsorption of glucose in the proximal renal tubuli is incomplete, and part of the glucose remains in the urine (glycosuria). This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume will be replaced osmotically from water held in body cells and other body compartments, causing dehydration and increased thirst.
Prolonged high blood glucose causes glucose absorption, which leads to changes in the shape of the lenses of the eyes, resulting in vision changes; sustained sensible glucose control usually returns the lens to its original shape. Blurred vision is a common complaint leading to a diabetes diagnosis; type 1 should always be suspected in cases of rapid vision change, whereas with type 2 change is generally more gradual, but should still be suspected.
Patients (usually with type 1 diabetes) may also initially present with diabetic ketoacidosis (DKA), an extreme state of metabolic dysregulation characterized by the smell of acetone on the patient's breath; a rapid, deep breathing known as Kussmaul breathing; polyuria; nausea; vomiting and abdominal pain; and any of many altered states of consciousness or arousal (such as hostility and mania or, equally, confusion and lethargy). In severe DKA, coma may follow, progressing to death. Diabetic ketoacidosis is a medical emergency and requires immediate hospitalization.
A rarer but equally severe possibility is hyperosmolar nonketotic state, which is more common in type 2 diabetes and is mainly the result of dehydration due to loss of body water. Often, the patient has been drinking extreme amounts of sugar-containing drinks, leading to a vicious circle in regard to the water loss.
Genetics
Both type 1 and type 2 diabetes are at least partly inherited. Type 1 diabetes appears to be triggered by some (mainly viral) infections, with some evidence pointing at Coxsackie B4 virus. There is a genetic element in individual susceptibility to some of these triggers which has been traced to particular HLA genotypes (i.e., the genetic "self" identifiers relied upon by the immune system). However, even in those who have inherited the susceptibility, type 1 diabetes mellitus seems to require an environmental trigger.
There is a stronger inheritance pattern for type 2 diabetes. Those with first-degree relatives with type 2 have a much higher risk of developing type 2, increasing with the number of those relatives. Concordance among monozygotic twins is close to 100%, and about 25% of those with the disease have a family history of diabetes. Genes significantly associated with developing type 2 diabetes, include TCF7L2, PPARG, FTO, KCNJ11, NOTCH2, WFS1, CDKAL1, IGF2BP2, SLC30A8, JAZF1, and HHEX.[22] KCNJ11 (potassium inwardly rectifying channel, subfamily J, member 11), encodes the islet ATP-sensitive potassium channel Kir6.2, and TCF7L2 (transcription factor 7–like 2) regulates proglucagon gene expression and thus the production of glucagon-like peptide-1. Moreover, obesity (which is an independent risk factor for type 2 diabetes) is strongly inherited.
Monogenic forms, e.g., MODY, constitute 1-5 % of all cases.
Various hereditary conditions may feature diabetes, for example myotonic dystrophy and Friedreich's ataxia. Wolfram's syndrome is an autosomal recessive neurodegenerative disorder that first becomes evident in childhood. It consists of diabetes insipidus, diabetes mellitus, optic atrophy, and deafness, hence the acronym DIDMOAD.
Gene expression promoted by a diet of fat and glucose as well as high levels of inflammation related cytokines found in the obese results in cells that "produce fewer and smaller mitochondria than is normal," and are thus prone to insulin resistance.
Pathophysiology
Mechanism of insulin release in normal pancreatic beta cells. Insulin production is more or less constant within the beta cells, irrespective of blood glucose levels. It is stored within vacuoles pending release, via exocytosis, which is primarily triggered by food, chiefly food containing absorbable glucose. The chief trigger is a rise in blood glucose levels after eating
Insulin is the principal hormone that regulates uptake of glucose from the blood into most cells (primarily muscle and fat cells, but not central nervous system cells). Therefore deficiency of insulin or the insensitivity of its receptors plays a central role in all forms of diabetes mellitus.
Most of the carbohydrates in food are converted within a few hours to the monosaccharide glucose, the principal carbohydrate found in blood and used by the body as fuel. The most significant exceptions are fructose, most disaccharides (except sucrose and in some people lactose), and all more complex polysaccharides, with the outstanding exception of starch. Insulin is released into the blood by beta cells (β-cells), found in the Islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage.
Insulin is also the principal control signal for conversion of glucose to glycogen for internal storage in liver and muscle cells. Lowered glucose levels result both in the reduced release of insulin from the beta cells and in the reverse conversion of glycogen to glucose when glucose levels fall. This is mainly controlled by the hormone glucagon which acts in an opposite manner to insulin. Glucose thus recovered by the liver re-enters the bloodstream; muscle cells lack the necessary export mechanism.
Higher insulin levels increase some anabolic ("building up") processes such as cell growth and duplication, protein synthesis, and fat storage. Insulin (or its lack) is the principal signal in converting many of the bidirectional processes of metabolism from a catabolic to an anabolic direction, and vice versa. In particular, a low insulin level is the trigger for entering or leaving ketosis (the fat burning metabolic phase).
If the amount of insulin available is insufficient, if cells respond poorly to the effects of insulin (insulin insensitivity or resistance), or if the insulin itself is defective, then glucose will not be absorbed properly by those body cells that require it nor will it be stored appropriately in the liver and muscles. The net effect is persistent high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as acidosis.
Diagnosis
The diagnosis of type 1 diabetes, and many cases of type 2, is usually prompted by recent-onset symptoms of excessive urination (polyuria) and excessive thirst (polydipsia), often accompanied by weight loss. These symptoms typically worsen over days to weeks; about a quarter of people with new type 1 diabetes have developed some degree of diabetic ketoacidosis (a type of metabolic acidosis which is caused by high concentrations of ketone bodies, formed by the breakdown of fatty acids and the deamination of amino acids) by the time the diabetes is recognized. The diagnosis of other types of diabetes is usually made in other ways. These include ordinary health screening; detection of hyperglycemia during other medical investigations; and secondary symptoms such as vision changes or unexplainable fatigue. Diabetes is often detected when a person suffers a problem that is frequently caused by diabetes, such as a heart attack, stroke, neuropathy, poor wound healing or a foot ulcer, certain eye problems, certain fungal infections, or delivering a baby with macrosomia or hypoglycemia.
Diabetes mellitus is characterized by recurrent or persistent hyperglycemia, and is diagnosed by demonstrating any one of the following:
· Fasting plasma glucose level at or above 126 mg/dL (7.0 mmol/L).
· Plasma glucose at or above 200 mg/dL (11.1 mmol/L) two hours after a 75 g oral glucose load as in a glucose tolerance test.
· Symptoms of hyperglycemia and casual plasma glucose at or above 200 mg/dL (11.1 mmol/L).
A positive result, in the absence of unequivocal hyperglycemia, should be confirmed by a repeat of any of the above-listed methods on a different day. Most physicians prefer to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete and offers no prognostic advantage over the fasting test.[27] According to the current definition, two fasting glucose measurements above 126 mg/dL (7.0 mmol/L) is considered diagnostic for diabetes mellitus.
Patients with fasting glucose levels from 100 to 125 mg/dL (6.1 and 7.0 mmol/L) are considered to have impaired fasting glucose. Patients with plasma glucose at or above 140 mg/dL or 7.8 mmol/L, but not over 200, two hours after a 75 g oral glucose load are considered to have impaired glucose tolerance. Of these two pre-diabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus as well as cardiovascular disease.
While not used for diagnosis, an elevated level of glucose irreversibly bound to hemoglobin (termed glycated hemoglobin or HbA1c) of 6.0% or higher (the 2003 revised U.S. standard) is considered abnormal by most labs; HbA1c is primarily used as a treatment-tracking test reflecting average blood glucose levels over the preceding 90 days (approximately) which is the average lifetime of red blood cells which contain hemoglobin in most patients. However, some physicians may order this test at the time of diagnosis to track changes over time. The current recommended goal for HbA1c in patients with diabetes is 6.5%.
Friday, November 13, 2009
Diabetes : Other types
Most cases of diabetes mellitus fall into the two broad etiologic categories of type 1 or type 2 diabetes. However, many types of diabetes mellitus have more specific known causes, and thus fall into more specific categories. As more research is done into diabetes, many patients who were previously diagnosed as type 1 or type 2 diabetes will have their condition reclassified.
Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells. The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (MRDM or MMDM, ICD-10 code E12), was deprecated by the World Health Organization when the current taxonomy was introduced in 1999.
Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells. The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (MRDM or MMDM, ICD-10 code E12), was deprecated by the World Health Organization when the current taxonomy was introduced in 1999.
Diabetes : Gestational diabetes
Gestational diabetes mellitus (GDM) resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2%–5% of all pregnancies and may improve or disappear after delivery. Gestational diabetes is fully treatable but requires careful medical supervision throughout the pregnancy. About 20%–50% of affected women develop type 2 diabetes later in life.
Even though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital cardiac and central nervous system anomalies, and skeletal muscle malformations. Increased fetal insulin may inhibit fetal surfactant production and cause respiratory distress syndrome. Hyperbilirubinemia may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Induction may be indicated with decreased placental function. A cesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia.
A 2008 study completed in the U.S. found that more American women are entering pregnancy with preexisting diabetes. In fact the rate of diabetes in expectant mothers has more than doubled in the past 6 years. This is particularly problematic as diabetes raises the risk of complications during pregnancy, as well as increasing the potential that the children of diabetic mothers will also become diabetic in the future.
Even though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital cardiac and central nervous system anomalies, and skeletal muscle malformations. Increased fetal insulin may inhibit fetal surfactant production and cause respiratory distress syndrome. Hyperbilirubinemia may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Induction may be indicated with decreased placental function. A cesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia.
A 2008 study completed in the U.S. found that more American women are entering pregnancy with preexisting diabetes. In fact the rate of diabetes in expectant mothers has more than doubled in the past 6 years. This is particularly problematic as diabetes raises the risk of complications during pregnancy, as well as increasing the potential that the children of diabetic mothers will also become diabetic in the future.
Diabetes : Type 2
Type 2 diabetes mellitus is characterized differently and is due to insulin resistance or reduced insulin sensitivity, combined with relatively reduced insulin secretion which in some cases becomes absolute. The defective responsiveness of body tissues to insulin almost certainly involves the insulin receptor in cell membranes. However, the specific defects are not known. Diabetes mellitus due to a known specific defect are classified separately. Type 2 diabetes is the most common type.
In the early stage of type 2 diabetes, the predominant abnormality is reduced insulin sensitivity, characterized by elevated levels of insulin in the blood. At this stage hyperglycemia can be reversed by a variety of measures and medications that improve insulin sensitivity or reduce glucose production by the liver. As the disease progresses, the impairment of insulin secretion worsens, and therapeutic replacement of insulin often becomes necessary.
There are numerous theories as to the exact cause and mechanism in type 2 diabetes. Central obesity (fat concentrated around the waist in relation to abdominal organs, but not subcutaneous fat) is known to predispose individuals to insulin resistance. Abdominal fat is especially active hormonally, secreting a group of hormones called adipokines that may possibly impair glucose tolerance. Obesity is found in approximately 55% of patients diagnosed with type 2 diabetes. Other factors include aging (about 20% of elderly patients in North America have diabetes) and family history (type 2 is much more common in those with close relatives who have had it). In the last decade, type 2 diabetes has increasingly begun to affect children and adolescents, probably in connection with the increased prevalence of childhood obesity seen in recent decades in some places. Environmental exposures may contribute to recent increases in the rate of type 2 diabetes. A positive correlation has been found between the concentration in the urine of bisphenol A, a constituent of polycarbonate plastic from some producers, and the incidence of type 2 diabetes.
Type 2 diabetes may go unnoticed for years because visible symptoms are typically mild, non-existent or sporadic, and usually there are no ketoacidotic episodes. However, severe long-term complications can result from unnoticed type 2 diabetes, including renal failure due to diabetic nephropathy, vascular disease (including coronary artery disease), vision damage due to diabetic retinopathy, loss of sensation or pain due to diabetic neuropathy, liver damage from non-alcoholic steatohepatitis and heart failure from diabetic cardiomyopathy.
Studies have suggested show that hormones like cortisol and possibly testosterone play a crucial role in the sugar absorption and in the insulin resistance[citation needed]. It has been suggested that subclinical Cushing's syndrome (cortisol excess) is associated with diabetes mellitus type 2. The percentage of sublinical Cushing's syndrome on diabetic population seems to be about 9%, but it also seems that the real percentage is higher than previously believed. Diabetic patients with a pituitary microadenoma can significantly improve insulin sensitivity and glucose tolerance by transsphenoidal surgery, because the remotion of microadenomas can decrease ACTH and cortisol levels.
Hypogonadism is often associated with cortisol excess, and testosterone deficiency is also associated with diabetes mellitus type 2, even if the exact mechanism by which testosterone improve insulin resistance is still not known.
In the early stage of type 2 diabetes, the predominant abnormality is reduced insulin sensitivity, characterized by elevated levels of insulin in the blood. At this stage hyperglycemia can be reversed by a variety of measures and medications that improve insulin sensitivity or reduce glucose production by the liver. As the disease progresses, the impairment of insulin secretion worsens, and therapeutic replacement of insulin often becomes necessary.
There are numerous theories as to the exact cause and mechanism in type 2 diabetes. Central obesity (fat concentrated around the waist in relation to abdominal organs, but not subcutaneous fat) is known to predispose individuals to insulin resistance. Abdominal fat is especially active hormonally, secreting a group of hormones called adipokines that may possibly impair glucose tolerance. Obesity is found in approximately 55% of patients diagnosed with type 2 diabetes. Other factors include aging (about 20% of elderly patients in North America have diabetes) and family history (type 2 is much more common in those with close relatives who have had it). In the last decade, type 2 diabetes has increasingly begun to affect children and adolescents, probably in connection with the increased prevalence of childhood obesity seen in recent decades in some places. Environmental exposures may contribute to recent increases in the rate of type 2 diabetes. A positive correlation has been found between the concentration in the urine of bisphenol A, a constituent of polycarbonate plastic from some producers, and the incidence of type 2 diabetes.
Type 2 diabetes may go unnoticed for years because visible symptoms are typically mild, non-existent or sporadic, and usually there are no ketoacidotic episodes. However, severe long-term complications can result from unnoticed type 2 diabetes, including renal failure due to diabetic nephropathy, vascular disease (including coronary artery disease), vision damage due to diabetic retinopathy, loss of sensation or pain due to diabetic neuropathy, liver damage from non-alcoholic steatohepatitis and heart failure from diabetic cardiomyopathy.
Studies have suggested show that hormones like cortisol and possibly testosterone play a crucial role in the sugar absorption and in the insulin resistance[citation needed]. It has been suggested that subclinical Cushing's syndrome (cortisol excess) is associated with diabetes mellitus type 2. The percentage of sublinical Cushing's syndrome on diabetic population seems to be about 9%, but it also seems that the real percentage is higher than previously believed. Diabetic patients with a pituitary microadenoma can significantly improve insulin sensitivity and glucose tolerance by transsphenoidal surgery, because the remotion of microadenomas can decrease ACTH and cortisol levels.
Hypogonadism is often associated with cortisol excess, and testosterone deficiency is also associated with diabetes mellitus type 2, even if the exact mechanism by which testosterone improve insulin resistance is still not known.
Diabetes : Type 1
Type 1 diabetes mellitus is characterized by loss of the insulin-producing beta cells of the islets of Langerhans in the pancreas leading to a deficiency of insulin. This type of diabetes can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of the immune-mediated nature, where beta cell loss is a T-cell mediated autoimmune attack. There is no known preventive measure which can be taken against type 1 diabetes, which contain approximately 10% of diabetes mellitus cases in North America and Europe (though this varies by geographical location). Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Type 1 diabetes can affect children or adults but was traditionally termed "juvenile diabetes" because it represents a majority of the diabetes cases in children.
The principal treatment of type 1 diabetes, even in its earliest stages, is the delivery of artificial insulin via injection combined with careful monitoring of blood glucose levels using blood testing monitors. Without insulin, diabetic ketoacidosis often develops which may result in coma or death. Treatment emphasis is now also placed on lifestyle adjustments (diet and exercise) though these cannot reverse the progress of the disease. Apart from the common subcutaneous injections, it is also possible to deliver insulin by a pump, which allows continuous infusion of insulin 24 hours a day at preset levels, and the ability to program doses (a bolus) of insulin as needed at meal times. An inhaled form of insulin was approved by the FDA in January 2006, although it was discontinued for business reasons in October 2007. Non-insulin treatments, such as monoclonal antibodies and stem-cell based therapies, are effective in animal models but have not yet completed clinical trials in humans.
The principal treatment of type 1 diabetes, even in its earliest stages, is the delivery of artificial insulin via injection combined with careful monitoring of blood glucose levels using blood testing monitors. Without insulin, diabetic ketoacidosis often develops which may result in coma or death. Treatment emphasis is now also placed on lifestyle adjustments (diet and exercise) though these cannot reverse the progress of the disease. Apart from the common subcutaneous injections, it is also possible to deliver insulin by a pump, which allows continuous infusion of insulin 24 hours a day at preset levels, and the ability to program doses (a bolus) of insulin as needed at meal times. An inhaled form of insulin was approved by the FDA in January 2006, although it was discontinued for business reasons in October 2007. Non-insulin treatments, such as monoclonal antibodies and stem-cell based therapies, are effective in animal models but have not yet completed clinical trials in humans.
Monday, November 9, 2009
Diabetes mellitus
Often referred to simply as diabetes—is a condition in which the body either does not produce enough, or does not properly respond to, insulin, a hormone produced in the pancreas. Insulin enables cells to absorb glucose in order to turn it into energy. In diabetes, the body either fails to properly respond to its own insulin, does not make enough insulin, or both. This causes glucose to accumulate in the blood, often leading to various complications.
Many types of diabetes are recognized: The principal three are:
· Type 1: Results from the body's failure to produce insulin. It is estimated that 5-10% of Americans who are diagnosed with diabetes have type 1 diabetes. Presently almost all persons with type 1 diabetes must take insulin injections.
· Type 2: Results from Insulin resistance, a condition in which cells fail to use insulin properly, sometimes combined with relative insulin deficiency. Most Americans who are diagnosed with diabetes have type 2 diabetes. Many people destined to develop type 2 diabetes spend many years in a state of Pre-diabetes: Termed "America's largest healthcare epidemic,":10-11, pre-diabetes indicates a condition that occurs when a person's blood glucose levels are higher than normal but not high enough for a diagnosis of type 2 diabetes. As of 2009 there are 57 million Americans who have pre-diabetes.
· Gestational diabetes: Pregnant women who have never had diabetes before but who have high blood sugar (glucose) levels during pregnancy are said to have gestational diabetes. Gestational diabetes affects about 4% of all pregnant women. It may precede development of type 2 (or rarely type 1).
Many types of diabetes are recognized: The principal three are:
· Type 1: Results from the body's failure to produce insulin. It is estimated that 5-10% of Americans who are diagnosed with diabetes have type 1 diabetes. Presently almost all persons with type 1 diabetes must take insulin injections.
· Type 2: Results from Insulin resistance, a condition in which cells fail to use insulin properly, sometimes combined with relative insulin deficiency. Most Americans who are diagnosed with diabetes have type 2 diabetes. Many people destined to develop type 2 diabetes spend many years in a state of Pre-diabetes: Termed "America's largest healthcare epidemic,":10-11, pre-diabetes indicates a condition that occurs when a person's blood glucose levels are higher than normal but not high enough for a diagnosis of type 2 diabetes. As of 2009 there are 57 million Americans who have pre-diabetes.
· Gestational diabetes: Pregnant women who have never had diabetes before but who have high blood sugar (glucose) levels during pregnancy are said to have gestational diabetes. Gestational diabetes affects about 4% of all pregnant women. It may precede development of type 2 (or rarely type 1).
Friday, November 6, 2009
Surgical Treatment for Prostate Cancer
According to the Mayo Clinic, prostate cancer is among the most common cancers affecting American men. Nearly one in six men will be affected by the disease in his lifetime. There are a variety of surgical options available, which vary according to the position, size and type of prostate tumor you have.
Surgical Candidates
- Good candidates for surgical treatment should be in good health overall, have no metastasis (spread) of the cancer to bones, have a tumor which is confined to his prostate, be younger than 70 and have at least 10 years to live.
Identification
- Radical prostatectomy removes the prostate gland entirely and can be completed both traditionally and laparascopically. Additional surgical treatments include lymphadenectomy to remove the pelvic lymph nodes, and TURP (transurethral resection of the prostate), which removes specific tissue from the prostate.
Significance
- The prostate gland, seminal vesicles and surrounding tissues are removed during a radical prostatectomy. TURP procedures are performed to alleviate tumor-related symptoms and can be done in men who are not candidates for a radical prostatectomy due to illness or age.
Recovery
- Recovery from a prostate surgery usually involves a three- to seven-day hospital stay and catheterization for two to three weeks.
Side Effects
- Surgical side effects may include urine leakage, impotence or leakage of stool from the rectum. In certain cases doctors may be able to use nerve-sparing techniques which preserve erection-related nerves.
Selon la clinique Mayo, le cancer de la prostate est l'un des cancers les plus courants chez l'homme américain. Près d'un sur six hommes seront touchés par la maladie dans sa vie. Il existe une variété d'options chirurgicales disponibles, qui varient selon la position, la taille et le type de tumeur de la prostate que vous avez.
Surgical candidats
1. Les bons candidats pour le traitement chirurgical doit être en bonne santé en général, n'ont pas de métastases (propagation) du cancer aux os, une tumeur qui se limite à sa prostate, soit moins de 70 ans et avoir au moins 10 ans à vivre.
Identification
2. Prostatectomie radicale enlève la prostate et peut être entièrement achevé à la fois traditionnel et laparascopically. Des traitements chirurgicaux supplémentaires comprennent curage pour enlever les ganglions lymphatiques pelviens et RTUP (résection trans-urétrale de la prostate), ce qui retire le tissu spécifique de la prostate.
Importance
3. La glande de la prostate, les vésicules séminales et les tissus environnants sont retirés au cours d'une prostatectomie radicale. RTUP procédures sont effectuées pour atténuer les symptômes liés à la tumeur et peut être effectué chez les hommes qui ne sont pas candidats à une prostatectomie radicale pour cause de maladie ou d'âge.
Recovery
4. La guérison d'une chirurgie de la prostate implique généralement une durée de trois à sept jours d'hospitalisation et de sondage pour deux à trois semaines.
Effets secondaires
5. Les effets secondaires incluent Surgical mai fuites d'urine, l'impuissance ou la fuite de selles du rectum. Dans certains cas, les médecins mai être en mesure d'utiliser les techniques de conservation des nerfs érecteurs qui permettent de préserver l'érection liés à des nerfs
Thursday, November 5, 2009
Cancer : Colon Cancer
What is Colon Cancer?
(1 Ratings)
What is Colon Cancer?
Colon cancer is cancer of the large intestine (colon). According to the American Cancer Society, colon cancer accounts for about 50,000 deaths in the United States every year. It is ranked after lung and breast cancers as the third most common cancer in the United States, with more than 140,000 new cases every year. Colon cancer is highly preventable. Almost 90% deaths due to colon cancer can be prevented by early screening and lifestyle modification.
Significance
1. The lifetime risk of colon cancer is 5 to 6%. The risk of colon cancer increases rapidly with older ages. The annual rate of colon cancer for people aged 80 and older is 450 per 100,000.
Certain people with genetic syndromes are at high risk for colon cancer. For instance, the probability of getting colon cancer by the age of 70 in people with the HNPCC gene is 70 to 80%. HNPCC stands for Hereditary Nonpolyposis Colorectal Cancer.
The average 5-year survival rate of colon cancer is 60 to 65%. The 5-year survival rate for patients with colon cancers detected at early stages is 80 to 90%. However, for patients with metastatic colon cancer, the 5-year survival rate is merely 25%.
Geography
2. The incidence of colon cancer varies from one countries to another. The incidence of colon cancer in developed countries like United States, and European countries is 10 to 20 times than that in developing countries. Therefore, colon cancer is also known as the disease of rich countries. However, the incidence of colon cancer in countries like China, India is on the rise as people in these countries start to adopt diets similar Western diet.
Identification
3. The major symptoms of colon cancer are rectal bleeding, blood in the stool, or changes in bowel habit, abdominal pain, hematochezia or melena, weakness, anemia and weight loss. In the primary care setting, patients with rectal bleeding and blood in the stool are often ordered a colonoscopy to check whether they have colon cancer.
Ideally, individuals with symptoms of colon cancer should be examined without delay. In reality, there is often a significant delay between symptom and diagnosis. It takes about 4 to 6 months for a patient to be diagnosed with colon cancer after the initial onset of symptoms.
Early detection of colon cancer leads to a much better survival rate. Thus, it is very important to talk to your doctor if you have any of colon cancer symptoms, particularly if you are 50 years old and older.
Theories/Speculation
4. It is believed that 90-95% of colon cancer cases arise from adenomatous polyps (also known as adenoma). This is referred to as the adenoma--carcinoma sequence. Although only a small proportion of adenomas progress to become cancer, it is still not possible to identify which one will become cancer. The adenoma--carcinoma theory is the corner stone of our understanding and management of colon cancer.
Prevention/Solution
5. Colon cancer can be detected early by regular screening. Early detection improves the chance of survival significantly. Studies show that your risk of colon cancer is reduced by 70 to 80%, just by complying to regular screening.
The most effective screening method is colonoscopy. The American Cancer Society recommends colonoscopy screening every 10 year, starting at age 50, for all adults. Any adenoma detected during colonoscopy will be removed by polypectomy. Several clinical trials show that colonoscopy is highly effective in reducing both incidence and mortality of colon cancer.
Other screening tests for colon cancer include stool-based tests such as fecal occult blood test (FOBT), fecal immunochemical test (FIT) and fecal DNA, and full-structural examination such as virtual colonoscopy and sigmoidoscopy.
(1 Ratings)
What is Colon Cancer?
Colon cancer is cancer of the large intestine (colon). According to the American Cancer Society, colon cancer accounts for about 50,000 deaths in the United States every year. It is ranked after lung and breast cancers as the third most common cancer in the United States, with more than 140,000 new cases every year. Colon cancer is highly preventable. Almost 90% deaths due to colon cancer can be prevented by early screening and lifestyle modification.
Significance
1. The lifetime risk of colon cancer is 5 to 6%. The risk of colon cancer increases rapidly with older ages. The annual rate of colon cancer for people aged 80 and older is 450 per 100,000.
Certain people with genetic syndromes are at high risk for colon cancer. For instance, the probability of getting colon cancer by the age of 70 in people with the HNPCC gene is 70 to 80%. HNPCC stands for Hereditary Nonpolyposis Colorectal Cancer.
The average 5-year survival rate of colon cancer is 60 to 65%. The 5-year survival rate for patients with colon cancers detected at early stages is 80 to 90%. However, for patients with metastatic colon cancer, the 5-year survival rate is merely 25%.
Geography
2. The incidence of colon cancer varies from one countries to another. The incidence of colon cancer in developed countries like United States, and European countries is 10 to 20 times than that in developing countries. Therefore, colon cancer is also known as the disease of rich countries. However, the incidence of colon cancer in countries like China, India is on the rise as people in these countries start to adopt diets similar Western diet.
Identification
3. The major symptoms of colon cancer are rectal bleeding, blood in the stool, or changes in bowel habit, abdominal pain, hematochezia or melena, weakness, anemia and weight loss. In the primary care setting, patients with rectal bleeding and blood in the stool are often ordered a colonoscopy to check whether they have colon cancer.
Ideally, individuals with symptoms of colon cancer should be examined without delay. In reality, there is often a significant delay between symptom and diagnosis. It takes about 4 to 6 months for a patient to be diagnosed with colon cancer after the initial onset of symptoms.
Early detection of colon cancer leads to a much better survival rate. Thus, it is very important to talk to your doctor if you have any of colon cancer symptoms, particularly if you are 50 years old and older.
Theories/Speculation
4. It is believed that 90-95% of colon cancer cases arise from adenomatous polyps (also known as adenoma). This is referred to as the adenoma--carcinoma sequence. Although only a small proportion of adenomas progress to become cancer, it is still not possible to identify which one will become cancer. The adenoma--carcinoma theory is the corner stone of our understanding and management of colon cancer.
Prevention/Solution
5. Colon cancer can be detected early by regular screening. Early detection improves the chance of survival significantly. Studies show that your risk of colon cancer is reduced by 70 to 80%, just by complying to regular screening.
The most effective screening method is colonoscopy. The American Cancer Society recommends colonoscopy screening every 10 year, starting at age 50, for all adults. Any adenoma detected during colonoscopy will be removed by polypectomy. Several clinical trials show that colonoscopy is highly effective in reducing both incidence and mortality of colon cancer.
Other screening tests for colon cancer include stool-based tests such as fecal occult blood test (FOBT), fecal immunochemical test (FIT) and fecal DNA, and full-structural examination such as virtual colonoscopy and sigmoidoscopy.
Wednesday, November 4, 2009
Cancer : Beat Skin Cancer
How to Beat Skin Cancer before it Strikes
Skin cancer is a malignant growth on the skin and it develops on the outer part of the skin so that the tumor is visible and more people are affected with it than one thinks, however there are ways to stop it before it strikes, but always make sure to talk to your doctor about it.
· Drink black tea; in fact some different studies according researchers of Arizona University (http://www.cancer.org/docroot/NWS/content/NWS_1_1x_Hot_Tea_May_Lower_Risk_of_Some_Skin_Cancers.asp), state that people that drank good quantities of hot black tea had less of the cell cancer.
· Buy a sun protective laundry treatment and there are some that you can buy at your local grocery store and it works in a way that it washes the equivalent of SPF 30 directly into your clothes.
· Use SPF every time you are out in the sun of at least 15 or higher and it can be either sunscreen or sun block; this seems to be one of the best ways to avoid getting skin cancer. Remember that to use sunscreen not only when you are at the beach or pool but every day that you are going to be out in the sun for an extended period of time.
· Another way is to stop smoking since smokers are more likely to develop skin cancer by at least thirty percent than non smokers, and even if people know that quitting is ultimately best for them it can be hard. To quit ask your doctor or a friend for help and support while you are going through it and know that in the long run this is going to be better for your health.
· Take an aspirin, in fact a dose of aspirin or ibuprofen which contain anti-inflammatory ingredients, may actually fight off the chemical that enables the skin cancer cell. Always talk to your doctor first to see which is best for you and your health before undergoing any medical changes on your own.
Cancer : Cancer Online Information
How to Find Information About Cancer Online
There is so much information about cancer online these days, it can be hard to know where to start. This article will lead you through the guide you should take to find the best, most relevant, and most current information about cancer online :
Start your search for information about cancer online at Google Health or another site that can provide you with a broad overview of symptoms, treatments and prognoses. These overview sites are great for getting a lot of general information in one place and for providing links to more specialized sources of cancer information.
Next, you should search for information about the specific type of cancer that you are researching. Different types of cancer can actually be very different from one another. On sites such as the Mayo Clinic's, you can search for the latest information about particular types of cancer and be confident that your cancer information is coming from the foremost experts in the field.
Look for subjective information about cancer online by searching blogs. Many people write off subjective information as unimportant; however, blogs can give you a sense about the experiences and feelings of people that are actually dealing with cancer. Simply type the name of the cancer you are interested in researching and the word "blog" into any search engine. You'll be surprised to find that there are blogs by people with almost every type of cancer.
So finden Sie Informationen zu Krebs Online
Es gibt so viele Informationen über Krebs online in diesen Tagen, es kann schwer zu sagen, wo ich anfangen soll. Dieser Artikel führt Sie durch die Anleitung Sie sollten sich auf der Suche nach den besten, wichtigsten führen, und die meisten aktuellen Informationen über Krebs online:
Start der Suche nach Informationen über Krebs online bei Google Health oder eine andere Website, die Sie mit einem breiten Überblick über Symptome, Therapien und Prognosen geben kann. Diese Übersicht Seiten sind ausschließlich immer eine Menge allgemeiner Informationen an einem Ort und für die Bereitstellung von Links zu weiteren Quellen von Krebs spezialisiert Informationen groß.
Als nächstes sollten Sie die Suche nach Informationen über die spezifische Art von Krebs, die Sie forschen. Verschiedene Arten von Krebs kann tatsächlich sehr verschieden voneinander. Auf Websites wie der Mayo-Klinik, können Sie die neuesten Informationen über bestimmte Arten von Krebs suchen und darauf vertrauen können, dass Ihr Krebs Information, die von den führenden Experten auf diesem Gebiet.
Anhand der subjektiven Informationen zu Krebs online durch die Suche nach Blogs. Viele Menschen schreiben mir aus subjektiver Informationen als unwichtig, jedoch können Blogs geben Ihnen einen Eindruck über die Erfahrungen und Gefühle der Menschen, die tatsächlich handelt es sich um Krebs. Geben Sie einfach den Namen des Krebses sind Sie bei der Recherche und das Wort "Blog" in eine Suchmaschine interessiert. Sie werden überrascht sein, dass es Blogs, die Menschen mit fast jeder Art von Krebs.
There is so much information about cancer online these days, it can be hard to know where to start. This article will lead you through the guide you should take to find the best, most relevant, and most current information about cancer online :
Start your search for information about cancer online at Google Health or another site that can provide you with a broad overview of symptoms, treatments and prognoses. These overview sites are great for getting a lot of general information in one place and for providing links to more specialized sources of cancer information.
Next, you should search for information about the specific type of cancer that you are researching. Different types of cancer can actually be very different from one another. On sites such as the Mayo Clinic's, you can search for the latest information about particular types of cancer and be confident that your cancer information is coming from the foremost experts in the field.
Look for subjective information about cancer online by searching blogs. Many people write off subjective information as unimportant; however, blogs can give you a sense about the experiences and feelings of people that are actually dealing with cancer. Simply type the name of the cancer you are interested in researching and the word "blog" into any search engine. You'll be surprised to find that there are blogs by people with almost every type of cancer.
So finden Sie Informationen zu Krebs Online
Es gibt so viele Informationen über Krebs online in diesen Tagen, es kann schwer zu sagen, wo ich anfangen soll. Dieser Artikel führt Sie durch die Anleitung Sie sollten sich auf der Suche nach den besten, wichtigsten führen, und die meisten aktuellen Informationen über Krebs online:
Start der Suche nach Informationen über Krebs online bei Google Health oder eine andere Website, die Sie mit einem breiten Überblick über Symptome, Therapien und Prognosen geben kann. Diese Übersicht Seiten sind ausschließlich immer eine Menge allgemeiner Informationen an einem Ort und für die Bereitstellung von Links zu weiteren Quellen von Krebs spezialisiert Informationen groß.
Als nächstes sollten Sie die Suche nach Informationen über die spezifische Art von Krebs, die Sie forschen. Verschiedene Arten von Krebs kann tatsächlich sehr verschieden voneinander. Auf Websites wie der Mayo-Klinik, können Sie die neuesten Informationen über bestimmte Arten von Krebs suchen und darauf vertrauen können, dass Ihr Krebs Information, die von den führenden Experten auf diesem Gebiet.
Anhand der subjektiven Informationen zu Krebs online durch die Suche nach Blogs. Viele Menschen schreiben mir aus subjektiver Informationen als unwichtig, jedoch können Blogs geben Ihnen einen Eindruck über die Erfahrungen und Gefühle der Menschen, die tatsächlich handelt es sich um Krebs. Geben Sie einfach den Namen des Krebses sind Sie bei der Recherche und das Wort "Blog" in eine Suchmaschine interessiert. Sie werden überrascht sein, dass es Blogs, die Menschen mit fast jeder Art von Krebs.
CANCER: Breast Cancer
How to Lower the Risk of Breast Cancer
Lower the risk of breast cancer by following the recommendations of the studies that have been done, and learn from those who have had breast cancer. M.D. Anderson is one of the large cancer centers that does research in the field, and their work is helpful in understanding the risks.
Some risks are uncontrollable, like age and hereditary, but there are risks you can avoid, too.
Some risks are uncontrollable, like age and hereditary, but there are risks you can avoid, too.
(1) Loose the weight. Keep your weight down since weight gain and obesity are risk factors. A diet high in saturated fats also creates a risk.
(2) Get to work. Physical inactivity is one of the risks, so it is important to get exercise regularly.
(3) Eliminate the oral contraceptives. Birth control pills have hormones that create some risk for breast cancer.
(4) Do not consume alcohol. Alcohol consumption in a quantity of more than one drink a day is considered a risk factor.
(5) Cut the tobacco use. Tobacco creates an additional risk for all cancers, including breast cancer. Avoid second-hand smoke, too.
(6) Eat fruits and vegetables, and not much red meat. Diet has a significant bearing on the risk of breast cancer.
(7) Learn your family history to study the genetic risks. We have an article in Resources below to help you learn your family history for genetic risk of disease.
(8) Have routine screenings and do the BSE self-exams as recommended by the studies. Recommendations include a mammogram every one to three years after the age of 20, and every year after the age of 40. You cannot control aging which is one of the key risk factors, but you can be alert and practice early detection recommendations.
(9) Lower the risk of breast cancer by using the information learned from the years of research on the subject. Practice a healthy lifestyle with exercise and proper eating, screening and self-exams, and knowing your genetic risks to lower the risk of breast cancer.
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