ModafinilDog . levitra;cialis viagra online pharmacy

Welcome My Blog

OCCUPATIONAL RHINITIS: ALLERGIC TO YOUR WORK?

March 24th, 2011 by | Posted in Allergies | No Comments »
Most common ways that occupational agents cause rhinitis:
1. Irritant Reactions: Agents that irritate the membrane of our noses are the most common causes of office rhinitis. At the top of the list of such agents is cigarette smoke.
2. Allergic Reactions: This is the most common mechanism of non-office rhinitis. Longshoremen, farmers, veterinarians, and cement workers all can become allergic to agents unique to their workplaces.
When To Suspect Occupational Rhinitis
If you do not know or suspect a specific agent at work as a cause of your symptoms, here are five clues that suggest that something in your office is causing or contributing to your rhinitis, and that you should take a closer look at your workplace:
- Your symptoms worsen at work.
- Your symptoms are least bothersome at home.
- Your symptoms are worse at the end of the work week than at its beginning.
- When you are away from work for extended periods, such as weekends or vacations, you feel much better or clearer.
- More than one-third of your co-workers suffer similar symptoms.
Resolving Occupational Rhinitis
1. Do your best to identify the cause(s).
2. Once the cause is identified, eliminate or correct it. In most cases this is not difficult to do. The most difficult task is to first recognize that a work-related problem exists.
3. Enlist the help of your boss or supervisor if necessary.
4. If you are unable to identify a cause, it would be wise to have the air exchange in your office checked. Frequently, simply improving the exchange of air in your workplace will greatly improve symptoms. The same people who service your air conditioning-heating system either should be able to do this or can advise you of whom to call.
5. At this time, the expense involved in consulting someone skilled in the measurement of particles, smoke, and various chemicals in your environment is futile, since almost none of them are equipped to confirm any suspicions that might be uncovered in such a study.
*24/322/5*

OCCUPATIONAL RHINITIS: ALLERGIC TO YOUR WORK? Most common ways that occupational agents cause rhinitis:1. Irritant Reactions: Agents that irritate the membrane of our noses are the most common causes of office rhinitis. At the top of the list of such agents is cigarette smoke.2. Allergic Reactions: This is the most common mechanism of non-office rhinitis. Longshoremen, farmers, veterinarians, and cement workers all can become allergic to agents unique to their workplaces.
When To Suspect Occupational RhinitisIf you do not know or suspect a specific agent at work as a cause of your symptoms, here are five clues that suggest that something in your office is causing or contributing to your rhinitis, and that you should take a closer look at your workplace:- Your symptoms worsen at work.- Your symptoms are least bothersome at home.- Your symptoms are worse at the end of the work week than at its beginning.- When you are away from work for extended periods, such as weekends or vacations, you feel much better or clearer.- More than one-third of your co-workers suffer similar symptoms.
Resolving Occupational Rhinitis1. Do your best to identify the cause(s).2. Once the cause is identified, eliminate or correct it. In most cases this is not difficult to do. The most difficult task is to first recognize that a work-related problem exists.3. Enlist the help of your boss or supervisor if necessary.4. If you are unable to identify a cause, it would be wise to have the air exchange in your office checked. Frequently, simply improving the exchange of air in your workplace will greatly improve symptoms. The same people who service your air conditioning-heating system either should be able to do this or can advise you of whom to call.5. At this time, the expense involved in consulting someone skilled in the measurement of particles, smoke, and various chemicals in your environment is futile, since almost none of them are equipped to confirm any suspicions that might be uncovered in such a study.*24/322/5*

RELIEVING ARTHRITIS: JUVENILE RHEUMATOID ARTHRITI

March 16th, 2011 by | Posted in Healthy bones Osteoporosis Rheumatic | No Comments »
Juvenile rheumatoid arthritis is a form of chronic arthritis in children that is also referred to as Still’s disease, juvenile chronic polyarthritis, and juvenile chronic arthritis. It rarely begins before the age of one year, but it may start anytime after the first year. There are different types of juvenile rheumatoid arthritis that begin at different ages and more often in one sex or the other. It has been estimated that 5 percent of all cases of rheumatoid arthritis begin before the age of sixteen.
Juvenile rheumatoid arthritis (JRA) is defined as the onset of the disease under age sixteen. It has some features that distinguish it from rheumatoid arthritis (RA) in adults. These clinical differences include high fever, rash, high white blood cell count, eye involvement, growth disturbances, and increased tendency to have the disease localize in a single joint. In about 20 percent of cases the onset is acute and rapidly progressing, with general symptoms of illness such as fever and rash associated with enlargement of the spleen and inflammation of the pericardial sac around the heart, and in some cases these manifestations may be present for several weeks before the joint inflammation is evident.
In one third of these cases the disease begins in a single joint (monoarticular), and in half the cases the onset resembles adult RA and includes more than one joint (polyarticular). Pauciarticular JRA involves only a few joints and may affect the eyes. Skeletal growth in bones adjacent to inflamed joints may be either accelerated or retarded. If the heart is affected, the illness may be confused with acute rheumatic fever, but JRA frequently begins before age five, the joint symptoms do not migrate from joint to joint, the vertebrae in the neck are involved, the white blood cells are markedly increased, and rash frequently occurs.
The synovial tissue lining the joints becomes inflamed and the synovitis may last for weeks, months, or years. If the synovitis persists for a long enough period of time, the cartilage at the ends of the bones within the joint and the bone underlying the cartilage may be damaged. The cartilage may not regenerate at all, although it does have slight regenerative properties. Damage to the ligaments and tendons surrounding joints may also occur. Permanent joint damage occurs because the bones may be dislocated or fused together, tissue may be destroyed, and muscles and other structures surrounding the joint may shorten (contractures), causing deformities in the absence of damage within the joints. These serious complications do not occur often, and most children do not sustain permanent joint damage or deformity.
The diagnosis is based solely on the presence of the characteristic clinical findings and the careful exclusion of other conditions that also are associated with arthritis and joint pains. Destructive joint changes, occurring late in severe cases of the disease will be noted in X-rays, but there are no other specific diagnostic tests that establish the diagnosis.
Complete remission occurs in 50 percent or more of the children with JRA. The major consequences of this illness are permanently restricted joint function, heart disease, and chronic eye inflammation.
At least 75 percent of the children who have JRA will recover from their illness without having any important residual disability if they are given what is generally accepted as proper care during active periods of their illness. Currently approved methods of treatment are symptomatic – directed against the symptoms of the disease – and not curative. This is because the underlying factors responsible for JRA are poorly understood.
Treatment of this chronic illness consists of medication, physical and occupational therapy, psychological reinforcement (to offset the discouraging aspects of JRA), and surgery (to reconstruct joint damage). Education and counseling are important because the affected child’s needs and limitations may have a great impact on family activities and the uncertainty of the diagnosis and prognosis cause severe psychological stress for everyone concerned.
Although cortisone-related (steroid) drugs such as Prednisone can often work magic in this illness, their use must be limited to the severe manifestations that do not respond to aspirin and other non-steroid drugs. The possibility of cardiac damage and loss of vision require careful medical supervision. Another serious problem associated with steroid therapy is that steroids cause growth retardation, and although they may be necessary in the management of this illness, they may augment the growth retardation that is a natural feature of JRA.
It is possible that what we call JRA is more than one disease. If your child is among the estimated 250,000 cases in the United States, the specialist you consult will review this matter with you in depth, since each type of the illness has certain physical and laboratory characteristics, follows a particular course, affects more girls than boys or vice versa, and is associated with different kinds of complications.
*6/295/5*

RELIEVING ARTHRITIS: JUVENILE RHEUMATOID ARTHRITISJuvenile rheumatoid arthritis is a form of chronic arthritis in children that is also referred to as Still’s disease, juvenile chronic polyarthritis, and juvenile chronic arthritis. It rarely begins before the age of one year, but it may start anytime after the first year. There are different types of juvenile rheumatoid arthritis that begin at different ages and more often in one sex or the other. It has been estimated that 5 percent of all cases of rheumatoid arthritis begin before the age of sixteen.Juvenile rheumatoid arthritis (JRA) is defined as the onset of the disease under age sixteen. It has some features that distinguish it from rheumatoid arthritis (RA) in adults. These clinical differences include high fever, rash, high white blood cell count, eye involvement, growth disturbances, and increased tendency to have the disease localize in a single joint. In about 20 percent of cases the onset is acute and rapidly progressing, with general symptoms of illness such as fever and rash associated with enlargement of the spleen and inflammation of the pericardial sac around the heart, and in some cases these manifestations may be present for several weeks before the joint inflammation is evident.In one third of these cases the disease begins in a single joint (monoarticular), and in half the cases the onset resembles adult RA and includes more than one joint (polyarticular). Pauciarticular JRA involves only a few joints and may affect the eyes. Skeletal growth in bones adjacent to inflamed joints may be either accelerated or retarded. If the heart is affected, the illness may be confused with acute rheumatic fever, but JRA frequently begins before age five, the joint symptoms do not migrate from joint to joint, the vertebrae in the neck are involved, the white blood cells are markedly increased, and rash frequently occurs.The synovial tissue lining the joints becomes inflamed and the synovitis may last for weeks, months, or years. If the synovitis persists for a long enough period of time, the cartilage at the ends of the bones within the joint and the bone underlying the cartilage may be damaged. The cartilage may not regenerate at all, although it does have slight regenerative properties. Damage to the ligaments and tendons surrounding joints may also occur. Permanent joint damage occurs because the bones may be dislocated or fused together, tissue may be destroyed, and muscles and other structures surrounding the joint may shorten (contractures), causing deformities in the absence of damage within the joints. These serious complications do not occur often, and most children do not sustain permanent joint damage or deformity.The diagnosis is based solely on the presence of the characteristic clinical findings and the careful exclusion of other conditions that also are associated with arthritis and joint pains. Destructive joint changes, occurring late in severe cases of the disease will be noted in X-rays, but there are no other specific diagnostic tests that establish the diagnosis.Complete remission occurs in 50 percent or more of the children with JRA. The major consequences of this illness are permanently restricted joint function, heart disease, and chronic eye inflammation.At least 75 percent of the children who have JRA will recover from their illness without having any important residual disability if they are given what is generally accepted as proper care during active periods of their illness. Currently approved methods of treatment are symptomatic – directed against the symptoms of the disease – and not curative. This is because the underlying factors responsible for JRA are poorly understood.Treatment of this chronic illness consists of medication, physical and occupational therapy, psychological reinforcement (to offset the discouraging aspects of JRA), and surgery (to reconstruct joint damage). Education and counseling are important because the affected child’s needs and limitations may have a great impact on family activities and the uncertainty of the diagnosis and prognosis cause severe psychological stress for everyone concerned.Although cortisone-related (steroid) drugs such as Prednisone can often work magic in this illness, their use must be limited to the severe manifestations that do not respond to aspirin and other non-steroid drugs. The possibility of cardiac damage and loss of vision require careful medical supervision. Another serious problem associated with steroid therapy is that steroids cause growth retardation, and although they may be necessary in the management of this illness, they may augment the growth retardation that is a natural feature of JRA.It is possible that what we call JRA is more than one disease. If your child is among the estimated 250,000 cases in the United States, the specialist you consult will review this matter with you in depth, since each type of the illness has certain physical and laboratory characteristics, follows a particular course, affects more girls than boys or vice versa, and is associated with different kinds of complications.*6/295/5*

IF YOUR COLON IS INFLAMED: HEALING SUPPLEMENTS – L-GLUTAMINE

March 3rd, 2011 by | Posted in Gastrointestinal | No Comments »
It is only in the last 10 years that we have found that Glutamine is:
1 The primary nutrient for the digestive lining.
2 The primary fuel for the immune system.
3 Vital for the metabolism of muscle.
4 Vital for wound-healing and tissue repair.
5 The body’s most common amino acid.
Dr Douglas Wilmore, MD, Harvard Medical School
L-Glutamine is an amino acid used by nature to build proteins in the body. One of 20, it was formerly thought to be non-essential as it was thought it could be manufactured from other amino acids.
Glutamine in the diet comes from meat, fish and eggs, but cooking easily destroys it. There is barely enough glutamine in the diet if we are healthy. Extra glutamine may be needed during times of stress or after illness, infections or surgery.
Glutamine is the most popular anti-ulcer drug in Asia and its success in treating IBS and inflammatory bowel disease is remarkable. The range of illnesses (including mental illness) where L-Glutamine is proving to be invaluable is too wide to be discussed here. If you would like more information on this send to Higher Nature for Offprint 22, ‘Glutamine Breakthroughs for Immunity, Muscle Strength and Healing the Digestive System’ by Simon Martin (price at the time of writing is 30 pence).
This supplement is available through all nutritional suppliers in powder or capsule form. It is easier to take adequate doses in the powder form. It is white, tasteless and is taken just stirred into water.
*23\326\8*

IF YOUR COLON IS INFLAMED: HEALING SUPPLEMENTS – L-GLUTAMINEIt is only in the last 10 years that we have found that Glutamine is:1 The primary nutrient for the digestive lining.2 The primary fuel for the immune system.3 Vital for the metabolism of muscle.4 Vital for wound-healing and tissue repair.5 The body’s most common amino acid.Dr Douglas Wilmore, MD, Harvard Medical SchoolL-Glutamine is an amino acid used by nature to build proteins in the body. One of 20, it was formerly thought to be non-essential as it was thought it could be manufactured from other amino acids.Glutamine in the diet comes from meat, fish and eggs, but cooking easily destroys it. There is barely enough glutamine in the diet if we are healthy. Extra glutamine may be needed during times of stress or after illness, infections or surgery.Glutamine is the most popular anti-ulcer drug in Asia and its success in treating IBS and inflammatory bowel disease is remarkable. The range of illnesses (including mental illness) where L-Glutamine is proving to be invaluable is too wide to be discussed here. If you would like more information on this send to Higher Nature for Offprint 22, ‘Glutamine Breakthroughs for Immunity, Muscle Strength and Healing the Digestive System’ by Simon Martin (price at the time of writing is 30 pence).This supplement is available through all nutritional suppliers in powder or capsule form. It is easier to take adequate doses in the powder form. It is white, tasteless and is taken just stirred into water.*23\326\8*

HOW WE DIAGNOSE A SEIZURE AND DECIDE WHAT IT WILL MEAN FOR YOUR CHILD: FAINTING CAN PRECEDE AND CAUSE A SEIZURE

February 21st, 2011 by | Posted in Epilepsy | No Comments »
Fainting can precede and cause a seizure, as in Jane’s case, or occur without a seizure, as we have seen in Rebecca’s story. Fainting spells may occur when someone hasn’t eaten, when someone gives blood, or occasionally after insufficient sleep or after extreme tension or anxiety or with overventilation due to anxiety. Fainting spells can occur in individuals who have low blood pressure who stand up too fast.
When we understand the circumstances and the sequence of events, we should be able to distinguish easily between convulsive syncope (seizures with fainting) and other seizures. The preceding paleness and sweatiness described are typical of fainting but not of seizures. Wetting oneself is more common during seizures than after fainting, but can occur in both situations. On the other hand, any person who bites his tongue may be having a seizure since someone who faints does not bite his tongue.
When the sequence of events is unclear, the physician will probably want to wait before making a diagnosis since it is better to be uncertain than to label the event “a seizure.” If the child continues to have these episodes, either the nature of the spells will become clear or further tests are indicated to determine the appropriate diagnosis and treatment. An EEG does not differentiate between fainting and seizures unless an episode occurs when the EEG is running.
Fainting spells are not considered seizures unless they are accompanied by stiffening or jerking. If they are accompanied by stiffening or jerking, they are considered provoked seizures but are not considered serious since they are unlikely to recur except in similar circumstances. They are not considered epilepsy and do not respond to medications used to treat epilepsy. This “convulsive syncope” or convulsive fainting has no more meaning than the fainting episode itself.
*21\208\8*

HOW WE DIAGNOSE A SEIZURE AND DECIDE WHAT IT WILL MEAN FOR YOUR CHILD: FAINTING CAN PRECEDE AND CAUSE A SEIZUREFainting can precede and cause a seizure, as in Jane’s case, or occur without a seizure, as we have seen in Rebecca’s story. Fainting spells may occur when someone hasn’t eaten, when someone gives blood, or occasionally after insufficient sleep or after extreme tension or anxiety or with overventilation due to anxiety. Fainting spells can occur in individuals who have low blood pressure who stand up too fast.When we understand the circumstances and the sequence of events, we should be able to distinguish easily between convulsive syncope (seizures with fainting) and other seizures. The preceding paleness and sweatiness described are typical of fainting but not of seizures. Wetting oneself is more common during seizures than after fainting, but can occur in both situations. On the other hand, any person who bites his tongue may be having a seizure since someone who faints does not bite his tongue.When the sequence of events is unclear, the physician will probably want to wait before making a diagnosis since it is better to be uncertain than to label the event “a seizure.” If the child continues to have these episodes, either the nature of the spells will become clear or further tests are indicated to determine the appropriate diagnosis and treatment. An EEG does not differentiate between fainting and seizures unless an episode occurs when the EEG is running.Fainting spells are not considered seizures unless they are accompanied by stiffening or jerking. If they are accompanied by stiffening or jerking, they are considered provoked seizures but are not considered serious since they are unlikely to recur except in similar circumstances. They are not considered epilepsy and do not respond to medications used to treat epilepsy. This “convulsive syncope” or convulsive fainting has no more meaning than the fainting episode itself.*21\208\8*

DIABETES AND PHYSICAL ACTIVITY: SIGNIFICANCE OF EXERCISE-INDUCED GLUCOSE PATHWAY

February 12th, 2011 by | Posted in Diabetes | No Comments »
What is so important about exercise having its own signaling pathway to remove blood glucose? The insulin mechanism guides glucose from ingested food to tissues for storage. During periods of feasting, insulin repletes glycogen stores (complexed glucose) in skeletal muscle and then in the liver. Once these glycogen stores are filled, insulin directs blood glucose into adipose tissue to be stored as fat. The “thrifty gene” hypothesis states that individuals with more efficient genes are able to store more of a given glucose meal as fat and are thus more likely to survive during famine.
The physical activity mechanism has two parts that likely evolved over 10,000 years ago as a survival advantage during the feast and famine cycles:
1. Physical activity signals the pancreas to markedly lower its release of insulin into the blood, thereby causing blood insulin concentration to fall. In famine, blood insulin concentrations are already low, so if our ancestors undertook physical activity in a hunt, they would not want their blood insulin to go to non-exercising tissues. Exercise (pursuit of food) would then have to stop due to the lack of glucose supply to the muscle. We speculate that alternative mechanisms were selected that allowed the exercising muscle to signal it to take up blood glucose when blood insulin was insufficient, i.e., independent of insulin. These ancient survival mechanisms are still present today, allowing the exercising diabetic muscle to efficiently take up and clear blood glucose.
2. The physical activity mechanism allows only contracting skeletal muscles to remove blood sugar by a localized process, thereby conserving limited blood glucose from non-contracting muscles. It was established in the 1930s that the running distance to exhaustion could be extended if blood glucose were not permitted to fall too low.
The physical activity mechanism in the 21st century does not serve a famine purpose in societies where sedentary individuals have a continuous supply of food. Since our ancient genes require a certain threshold of physical activity for their physiological function, without this stimulus a sort of metabolic chaos results, described as dysfunction or pathophysiology. If all skeletal muscles are inactive, the whole body becomes insulin resistant in a few days, as skeletal muscle is responsible for 75-95% of the body’s glucose clearance. As mentioned above, skeletal muscle is still genetically programmed to conserve blood glucose for a famine by shutting down its ability to take up blood glucose when inactive. Compounding the problem, blood glucose is not as low as during the feast and famine times of our ancestors, and is especially high due to reduced physical activity.
High blood levels of insulin in our ancestors helped store food as fat for the next famine by:
- Increasing the rate of VLDL formation in the liver
- Increasing the rate of cholesterol synthesis in liver
- Enhancing the uptake of triglyceride from the blood into adipose tissue and muscle
- Decreasing the rate of fatty acid oxidation in muscle and liver. The same thrifty genes in our ancestors that efficiently stored food as fat now work continuously to accentuate the above metabolic changes in sedentary individuals predisposed to type 2 diabetes. Thus, physical activity is an absolute necessity to escape whole-body insulin resistance produced by inactive skeletal muscles.
Effects of a single bout of physical activity: The blood glucose and insulin are lowered after an oral glucose tolerance test (which is a surrogate for what happens after eating a meal). The clinical benefit is that post-meal hyperglycemia is less severe, and the magnitude of hyperinsulinemia is reduced. When blood glucose levels are lower, less insulin is signaled to be released from the pancreas.
Effects of repeated bouts of daily physical activity: The post-meal rise in blood glucose and insulin is lowered by slightly more than that seen after a single bout of physical activity of equal work intensity. The clinical significance of a physical activity-induced lowering of post-meal blood glucose and insulin is that they do not reach the post-meal levels seen in pre-diabetic and diabetic patients.
Effects of forced sedentariness: Enforced physical inactivity for 10 days in individuals previously exercising every day reverses the beneficial lowering of the post-meal rises in blood glucose and insulin. Other studies have shown that this effect can occur in only 3 days of physical inactivity!
Restorative effects of even a single bout of physical activity: If physical activity is performed within 24 hours of ending 10 days of being sedentary, the beneficial effect of exercise training is regained. Thus, changes in insulin sensitivity in response to physical activity occur rapidly, i.e., insulin sensitivity increases within 24 hours of an exercise bout and decreases within 2 days of the last exercise bout. The rapidity of this change probably offered survival to our hunter-gatherer ancestors by directing glucose just to the exercised muscles and lasting only long enough to replenish the muscle’s depleted glycogen store, thereby ensuring a glucose supply to allow the next hunt for food.
Many potential mechanisms exist by which physical inactivity initiates skeletal muscle and, subsequently, whole body insulin resistance. Two of these are:
1. Elevation of plasma free fatty acid (FFA) levels, likely from abdominal adipose tissue, which in turn may inhibit insulin action at the peripheral target tissues such as skeletal muscle. This is supported by the fact that thiazolidinedione-mediated improvement in insulin sensitivity
is triggered indirectly via a reduction in FFAs levels.
2. TNF-a and leptin may also cause insulin resistance.
*6/282/5*

DIABETES AND PHYSICAL ACTIVITY: SIGNIFICANCE OF EXERCISE-INDUCED GLUCOSE PATHWAYWhat is so important about exercise having its own signaling pathway to remove blood glucose? The insulin mechanism guides glucose from ingested food to tissues for storage. During periods of feasting, insulin repletes glycogen stores (complexed glucose) in skeletal muscle and then in the liver. Once these glycogen stores are filled, insulin directs blood glucose into adipose tissue to be stored as fat. The “thrifty gene” hypothesis states that individuals with more efficient genes are able to store more of a given glucose meal as fat and are thus more likely to survive during famine.The physical activity mechanism has two parts that likely evolved over 10,000 years ago as a survival advantage during the feast and famine cycles:1. Physical activity signals the pancreas to markedly lower its release of insulin into the blood, thereby causing blood insulin concentration to fall. In famine, blood insulin concentrations are already low, so if our ancestors undertook physical activity in a hunt, they would not want their blood insulin to go to non-exercising tissues. Exercise (pursuit of food) would then have to stop due to the lack of glucose supply to the muscle. We speculate that alternative mechanisms were selected that allowed the exercising muscle to signal it to take up blood glucose when blood insulin was insufficient, i.e., independent of insulin. These ancient survival mechanisms are still present today, allowing the exercising diabetic muscle to efficiently take up and clear blood glucose.2. The physical activity mechanism allows only contracting skeletal muscles to remove blood sugar by a localized process, thereby conserving limited blood glucose from non-contracting muscles. It was established in the 1930s that the running distance to exhaustion could be extended if blood glucose were not permitted to fall too low.The physical activity mechanism in the 21st century does not serve a famine purpose in societies where sedentary individuals have a continuous supply of food. Since our ancient genes require a certain threshold of physical activity for their physiological function, without this stimulus a sort of metabolic chaos results, described as dysfunction or pathophysiology. If all skeletal muscles are inactive, the whole body becomes insulin resistant in a few days, as skeletal muscle is responsible for 75-95% of the body’s glucose clearance. As mentioned above, skeletal muscle is still genetically programmed to conserve blood glucose for a famine by shutting down its ability to take up blood glucose when inactive. Compounding the problem, blood glucose is not as low as during the feast and famine times of our ancestors, and is especially high due to reduced physical activity.High blood levels of insulin in our ancestors helped store food as fat for the next famine by:      - Increasing the rate of VLDL formation in the liver      - Increasing the rate of cholesterol synthesis in liver      - Enhancing the uptake of triglyceride from the blood into adipose tissue and muscle- Decreasing the rate of fatty acid oxidation in muscle and liver. The same thrifty genes in our ancestors that efficiently stored food as fat now work continuously to accentuate the above metabolic changes in sedentary individuals predisposed to type 2 diabetes. Thus, physical activity is an absolute necessity to escape whole-body insulin resistance produced by inactive skeletal muscles.
Effects of a single bout of physical activity: The blood glucose and insulin are lowered after an oral glucose tolerance test (which is a surrogate for what happens after eating a meal). The clinical benefit is that post-meal hyperglycemia is less severe, and the magnitude of hyperinsulinemia is reduced. When blood glucose levels are lower, less insulin is signaled to be released from the pancreas.
Effects of repeated bouts of daily physical activity: The post-meal rise in blood glucose and insulin is lowered by slightly more than that seen after a single bout of physical activity of equal work intensity. The clinical significance of a physical activity-induced lowering of post-meal blood glucose and insulin is that they do not reach the post-meal levels seen in pre-diabetic and diabetic patients.
Effects of forced sedentariness: Enforced physical inactivity for 10 days in individuals previously exercising every day reverses the beneficial lowering of the post-meal rises in blood glucose and insulin. Other studies have shown that this effect can occur in only 3 days of physical inactivity!
Restorative effects of even a single bout of physical activity: If physical activity is performed within 24 hours of ending 10 days of being sedentary, the beneficial effect of exercise training is regained. Thus, changes in insulin sensitivity in response to physical activity occur rapidly, i.e., insulin sensitivity increases within 24 hours of an exercise bout and decreases within 2 days of the last exercise bout. The rapidity of this change probably offered survival to our hunter-gatherer ancestors by directing glucose just to the exercised muscles and lasting only long enough to replenish the muscle’s depleted glycogen store, thereby ensuring a glucose supply to allow the next hunt for food.Many potential mechanisms exist by which physical inactivity initiates skeletal muscle and, subsequently, whole body insulin resistance. Two of these are:1. Elevation of plasma free fatty acid (FFA) levels, likely from abdominal adipose tissue, which in turn may inhibit insulin action at the peripheral target tissues such as skeletal muscle. This is supported by the fact that thiazolidinedione-mediated improvement in insulin sensitivityis triggered indirectly via a reduction in FFAs levels.2. TNF-a and leptin may also cause insulin resistance.*6/282/5*

REDUCING YOUR RISK OF CORONARY ARTERY DISEASE: HOW TO STOP SMOKING – THE RIGHT STRATEGY

February 3rd, 2011 by | Posted in Cardio & Blood-Cholesterol | No Comments »
Once you have decided to quit smoking and have developed an attitude that permits you to approach that effort in a positive manner, the next step is to adopt a method that has the highest possible likelihood of success. There is no single best way to stop smoking. The best way is one that you believe will work for you. No method is easy, and the focal point of every method is maintaining the commitment to quit-permanently.
Several effective techniques for quitting are available. One of the most successful techniques is to stop smoking “cold turkey.” The most effective decision to stop, though, is not made in a cavalier or spontaneous fashion. Rather, the most successful stopping strategy, although sudden, is the result of planning. A specific date or event can be planned as the time for stopping. Some people find that if they tell others they intend to stop on a certain date, their commitment to quit is increased. Others turn the day of quitting into a near ceremonial occasion. Most researchers, doctors, and ex-smokers agree that the more concrete and explicit the decision and act of quitting, the more likely you will succeed. There are many different ways to quit, including nicotine-replacement therapy (gum or skin patches), self-help programs, group programs, and hypnosis.
Despite the numerous behavioral adjustments that will assist you in refraining from tobacco use, the fact that addiction to nicotine is a component of the problem means that you may need additional assistance in overcoming its effect. Nicotine withdrawal begins within hours after your last cigarette. Withdrawal symptoms can include craving, irritability, anxiety, headache,  depression,  restlessness, and difficulty concentrating. Although smoking behavior can and, in most cases, should be stopped abruptly, nicotine withdrawal may be most manageable if it is done more gradually.
*279\252\8*

REDUCING YOUR RISK OF CORONARY ARTERY DISEASE: HOW TO STOP SMOKING – THE RIGHT STRATEGYOnce you have decided to quit smoking and have developed an attitude that permits you to approach that effort in a positive manner, the next step is to adopt a method that has the highest possible likelihood of success. There is no single best way to stop smoking. The best way is one that you believe will work for you. No method is easy, and the focal point of every method is maintaining the commitment to quit-permanently.Several effective techniques for quitting are available. One of the most successful techniques is to stop smoking “cold turkey.” The most effective decision to stop, though, is not made in a cavalier or spontaneous fashion. Rather, the most successful stopping strategy, although sudden, is the result of planning. A specific date or event can be planned as the time for stopping. Some people find that if they tell others they intend to stop on a certain date, their commitment to quit is increased. Others turn the day of quitting into a near ceremonial occasion. Most researchers, doctors, and ex-smokers agree that the more concrete and explicit the decision and act of quitting, the more likely you will succeed. There are many different ways to quit, including nicotine-replacement therapy (gum or skin patches), self-help programs, group programs, and hypnosis.Despite the numerous behavioral adjustments that will assist you in refraining from tobacco use, the fact that addiction to nicotine is a component of the problem means that you may need additional assistance in overcoming its effect. Nicotine withdrawal begins within hours after your last cigarette. Withdrawal symptoms can include craving, irritability, anxiety, headache,  depression,  restlessness, and difficulty concentrating. Although smoking behavior can and, in most cases, should be stopped abruptly, nicotine withdrawal may be most manageable if it is done more gradually.*279\252\8*

BREAST CANCER

January 26th, 2011 by | Posted in Cancer | No Comments »
Breast cancer does not occur in children and the first cases are seen in the late teens and in the early twenties. At that age, the disease is rare but its frequency increases rapidly up to age fifty and then continues to increase, but less rapidly, thereafter. As we noted in the chapter on diet, there is a great deal of variation in breast cancer risk between countries. Social class is also a factor and the breast cancer rate at any age is usually considerably greater in higher socio-economic classes than in lower socio-economic classes. Whether this difference relates to diet or to other factors is still not clear.
The breast is highly sensitive to hormones, particularly oestrogens. Breasts develop with the hormonal changes in puberty in girls. The cyclical changes in hormonen in the menstrual cycle affect breast tissues and their effect can sometimes be the cause of considerable discomfort. Hormones in pregnancy cause the breasts to increase in size and after delivery it is hormones that cause milk production. The most direct link between breast cancer and female hormones is very obvious —breast cancer is very rare in men.
An important relationship between hormones and breast cancer is that the careful use of hormones can be a valuable aid to the treatment of breast cancer. Such therapy used to be carried out with the naturally occurring female hormones, oestrogens and progesterones, and these are still used. However, the best available drug at-present is not a naturally occurring hormone but a synthetic drug called Tamoxifen. This is remarkably well tolerated and is a very useful treatment for established cancers. Although we do not know exactly how Tamoxifen works, we know that it partly blocks naturally occurring hormones which can stimulate the growth of breast cancer.
The features of the reproductive and hormonal cycles in women which are associated with an increased risk of breast cancer are:
• An early onset of menstruation. Women whose periods begin at the age of twelve or before and who rapidly establish regular cycles are several times more likely to develop breast cancer than those whose menstruation does not start until after the age of thirteen.
• A late menopause. Women whose menopause occurs before the age of forty-five have only about half the risk of breast cancer of those whose menopause occurs after the age of fifty-five.
• No pregnancies, or late pregnancies. Women who have lots of babies are less likely to get breast cancer than women who do not This explains why breast cancer is, commoner in single women and in married women who have no children. Most of this effect is determined by the age of the mother when the first baby is born. Women who have their first baby under the age of twenty have only about half the risk of breast cancer of a woman who never has a child. If the first child is born at around about thirty to thirty-five years then there is virtually no protective effect and the risk of getting breast cancer is about the same as that of a woman who has never had a child. If the first child is born when the mother is more than thirty-five years old then the risk of getting breast cancer is probably slightly greater than that of the childless women.
No one can extend these observations into a recommendation that women should all have their children early. There are many other factors that operate in these decisions. Nevertheless, the observations seem to be real and cannot be ignored. They lead us to reinforce the advice that women aged fifty to sixty-four should have careful breast cancer screening. Such advice would be particularly true for those whose age at first motherhood was more than thirty.
*87\194\4*

BREAST CANCERBreast cancer does not occur in children and the first cases are seen in the late teens and in the early twenties. At that age, the disease is rare but its frequency increases rapidly up to age fifty and then continues to increase, but less rapidly, thereafter. As we noted in the chapter on diet, there is a great deal of variation in breast cancer risk between countries. Social class is also a factor and the breast cancer rate at any age is usually considerably greater in higher socio-economic classes than in lower socio-economic classes. Whether this difference relates to diet or to other factors is still not clear.The breast is highly sensitive to hormones, particularly oestrogens. Breasts develop with the hormonal changes in puberty in girls. The cyclical changes in hormonen in the menstrual cycle affect breast tissues and their effect can sometimes be the cause of considerable discomfort. Hormones in pregnancy cause the breasts to increase in size and after delivery it is hormones that cause milk production. The most direct link between breast cancer and female hormones is very obvious —breast cancer is very rare in men.An important relationship between hormones and breast cancer is that the careful use of hormones can be a valuable aid to the treatment of breast cancer. Such therapy used to be carried out with the naturally occurring female hormones, oestrogens and progesterones, and these are still used. However, the best available drug at-present is not a naturally occurring hormone but a synthetic drug called Tamoxifen. This is remarkably well tolerated and is a very useful treatment for established cancers. Although we do not know exactly how Tamoxifen works, we know that it partly blocks naturally occurring hormones which can stimulate the growth of breast cancer.The features of the reproductive and hormonal cycles in women which are associated with an increased risk of breast cancer are:• An early onset of menstruation. Women whose periods begin at the age of twelve or before and who rapidly establish regular cycles are several times more likely to develop breast cancer than those whose menstruation does not start until after the age of thirteen.• A late menopause. Women whose menopause occurs before the age of forty-five have only about half the risk of breast cancer of those whose menopause occurs after the age of fifty-five.• No pregnancies, or late pregnancies. Women who have lots of babies are less likely to get breast cancer than women who do not This explains why breast cancer is, commoner in single women and in married women who have no children. Most of this effect is determined by the age of the mother when the first baby is born. Women who have their first baby under the age of twenty have only about half the risk of breast cancer of a woman who never has a child. If the first child is born at around about thirty to thirty-five years then there is virtually no protective effect and the risk of getting breast cancer is about the same as that of a woman who has never had a child. If the first child is born when the mother is more than thirty-five years old then the risk of getting breast cancer is probably slightly greater than that of the childless women.No one can extend these observations into a recommendation that women should all have their children early. There are many other factors that operate in these decisions. Nevertheless, the observations seem to be real and cannot be ignored. They lead us to reinforce the advice that women aged fifty to sixty-four should have careful breast cancer screening. Such advice would be particularly true for those whose age at first motherhood was more than thirty.*87\194\4*

JUVENILE RHEUMATOID ARTHRITIS: DIAGNOSTIC CRITERIA AND SYSTEMIC JRA

January 16th, 2011 by | Posted in Arthritis | No Comments »
What are the diagnostic criteria for JRA?
Juvenile RA is diagnosed in children 16 years of age and under. The child must have persistent joint pain with inflammation that makes movement very difficult for at least six weeks, and other forms of childhood arthritis first must be excluded.
Is it easy to misdiagnose a child with this disease?
Yes, it is very common to misdiagnose children with this illness. That is why physicians must follow strict guidelines in its diagnosis.
What is systemic JRA?
Systemic juvenile RA causes such symptoms as high fever of about 101°F or greater once or twice a day. These are called fever spikes. A pale pink rash that does not itch is commonly found on the chest. Boys and girls are affected equally, and the peak age of onset is usually between 1 and 6 years of age.
What are some of the clinical problems associated with systemic JRA?
Besides the rash and the fever, there is profound joint pain. The child’s lymph nodes may be enlarged, and there may be inflammation over other areas, such as the lining of the lung or the heart. This can cause pain on breathing or lying down. There can be an increase of the white blood cell count or the platelets and a major rise in the sedimentation rate. To further confuse the doctor, the patient usually has no positive rheumatoid factor. The child’s spleen and liver often enlarge. When the fever goes away, the arthritis resolves and the child can get better. In rare instances, there can be severe complications, but early treatment and diagnosis of this condition are critical.
*19/141/5*

JUVENILE RHEUMATOID ARTHRITIS: DIAGNOSTIC CRITERIA AND SYSTEMIC JRAWhat are the diagnostic criteria for JRA?Juvenile RA is diagnosed in children 16 years of age and under. The child must have persistent joint pain with inflammation that makes movement very difficult for at least six weeks, and other forms of childhood arthritis first must be excluded.
Is it easy to misdiagnose a child with this disease?Yes, it is very common to misdiagnose children with this illness. That is why physicians must follow strict guidelines in its diagnosis.
What is systemic JRA?Systemic juvenile RA causes such symptoms as high fever of about 101°F or greater once or twice a day. These are called fever spikes. A pale pink rash that does not itch is commonly found on the chest. Boys and girls are affected equally, and the peak age of onset is usually between 1 and 6 years of age.
What are some of the clinical problems associated with systemic JRA?Besides the rash and the fever, there is profound joint pain. The child’s lymph nodes may be enlarged, and there may be inflammation over other areas, such as the lining of the lung or the heart. This can cause pain on breathing or lying down. There can be an increase of the white blood cell count or the platelets and a major rise in the sedimentation rate. To further confuse the doctor, the patient usually has no positive rheumatoid factor. The child’s spleen and liver often enlarge. When the fever goes away, the arthritis resolves and the child can get better. In rare instances, there can be severe complications, but early treatment and diagnosis of this condition are critical.*19/141/5*

BACK PAIN: OH! MY ACHING BACK!

January 9th, 2011 by | Posted in Anti-Psychotics | No Comments »
Four out of five adults have back pain severe enough to interrupt their daily routine at least once in their life. A common and frustrating problem to treat, there is no quick, easy cure; recovery is slow; the pain often recurs; and prevention and treatment require life-long commitment.
Self-care is the major factor in preventing and treating back pain.
Understanding the anatomy of the back and the most common injuries may help you decrease your risk of back pain and, if it occurs, quickly begin treatment.
Your backbone consists of 30 small, round, donut-shaped bones called vertebrae. Stacked up in an “S” arrangement, the vertebrae form a protective tunnel for your spinal cord. The spaces between vertebrae are filled by discs, packets of tough cartilage with a jelly-like filling, that cushion and absorb impact. Your spinal cord, a bundle of major nerves, leaves your brain through the vertebral tunnel and sends branches around the discs out to the rest of your body. Large muscles and ligaments support the spine as it twists, bends, stretches, turns and maintains an upright posture.
CAUSES
There are many causes of back pain: muscles can be strained, torn or go into spasm; ligaments and tendons may be overstretched and sprained; discs become worn down, move out of alignment (slipped disc) or rupture (herniated disc); bones wear down or change, such as in arthritis or a fracture; and, occasionally, infection and tumors can be the sources of pain. In addition, back pain may not originate from the back itself but may be referred pain from problems in the prostate in men or reproductive organs in women, or from kidney infections or disorders in the stomach and intestines.
Pain from strains, sprains and minor disc damage is usually sudden, sharp and eases over two to three days with self-care. The sharp pain from a herniated disc or fractured vertebra usually lasts several weeks and requires medical care. A steady ache is often a sign of disease, such as arthritis or referred pain.
Any back problem that causes swelling or a shifting in the alignment of the spine can put pressure on a nerve. Numbness, weakness or tingling are signs of nerve irritation. Nerves in the neck will produce symptoms in the arms and upper body, while spinal nerves in the middle and lower back affect the back, buttocks, legs and feet. Pressure on the sciatic nerve causes sharp, shooting pains down the back of the leg into the foot. Back pain can be constant or come only with movement.
Prevention
Maintain good posture and keep the right amount of curve in your lower back:
Stand tall with your ear, shoulder, hip and ankle in a line. Do not lock your knees. Balance weight evenly on your feet.
Avoid wearing high heels.
Sit tall with your shoulders back and your lower back supported. Keep knees even with or higher than your hips. Avoid sitting in one position for longer than one hour.
Use correct posture when lifting:
Bend your knees and lift with your leg muscles. Keep your back straight.
Never bend forward to lift. Keep the load close to your body.
Avoid turning or twisting while holding a heavy object.
Avoid lifting heavy loads above your waist.
Sleep on a firm surface. Provide support for your lower back and under your knees if it feels more comfortable.
Rise up from a prone position correctly. Rising is actually lifting your body’s weight. Roll to your side and use your arms and legs to lift up.
Maintain correct body weight. Obesity or a large abdomen can pull your lower back out of alignment.
Exercise to maintain good muscle tone in your back and abdomen. Walking, swimming and biking are all good activities.
Learn stress management and muscle-relaxation techniques such as yoga.
What you can do
Restrict activity. One or two days in bed may be needed in severe cases. Resume normal activity very slowly. Avoid any activity that puts stress on your back. Immediately stop any activity that causes or increases pain. Complete recovery may take up to six weeks.
Apply ice or cold packs for 20 minutes every two hours for acute pain; decrease to 20 minutes twice daily once pain has lessened. For protection, place a washcloth between bare skin and ice.
Once pain has lessened, take warm showers with water directed at the painful area.
Take aspirin or ibuprofen to ease pain and inflammation (follow directions on the package). NEVER give aspirin to children/ teenagers. It can cause Reye’s syndrome, a rare but often fatal condition.
Sleep on a firm surface. If possible, place a piece of plywood between the mattress and box springs.
Support your back while sleeping. Place a pillow under your knees or lie on your side, knees bent and with a pillow between them.
If back pain starts with no known cause, look for signs of a problem in another area of your body that may be causing referred pain.
For minor muscle soreness in your back, apply heat for 20 to 30 minutes.
*94\303\2*

BACK PAIN: OH! MY ACHING BACK!Four out of five adults have back pain severe enough to interrupt their daily routine at least once in their life. A common and frustrating problem to treat, there is no quick, easy cure; recovery is slow; the pain often recurs; and prevention and treatment require life-long commitment.Self-care is the major factor in preventing and treating back pain.Understanding the anatomy of the back and the most common injuries may help you decrease your risk of back pain and, if it occurs, quickly begin treatment.Your backbone consists of 30 small, round, donut-shaped bones called vertebrae. Stacked up in an “S” arrangement, the vertebrae form a protective tunnel for your spinal cord. The spaces between vertebrae are filled by discs, packets of tough cartilage with a jelly-like filling, that cushion and absorb impact. Your spinal cord, a bundle of major nerves, leaves your brain through the vertebral tunnel and sends branches around the discs out to the rest of your body. Large muscles and ligaments support the spine as it twists, bends, stretches, turns and maintains an upright posture.CAUSESThere are many causes of back pain: muscles can be strained, torn or go into spasm; ligaments and tendons may be overstretched and sprained; discs become worn down, move out of alignment (slipped disc) or rupture (herniated disc); bones wear down or change, such as in arthritis or a fracture; and, occasionally, infection and tumors can be the sources of pain. In addition, back pain may not originate from the back itself but may be referred pain from problems in the prostate in men or reproductive organs in women, or from kidney infections or disorders in the stomach and intestines.Pain from strains, sprains and minor disc damage is usually sudden, sharp and eases over two to three days with self-care. The sharp pain from a herniated disc or fractured vertebra usually lasts several weeks and requires medical care. A steady ache is often a sign of disease, such as arthritis or referred pain.Any back problem that causes swelling or a shifting in the alignment of the spine can put pressure on a nerve. Numbness, weakness or tingling are signs of nerve irritation. Nerves in the neck will produce symptoms in the arms and upper body, while spinal nerves in the middle and lower back affect the back, buttocks, legs and feet. Pressure on the sciatic nerve causes sharp, shooting pains down the back of the leg into the foot. Back pain can be constant or come only with movement.Prevention Maintain good posture and keep the right amount of curve in your lower back:Stand tall with your ear, shoulder, hip and ankle in a line. Do not lock your knees. Balance weight evenly on your feet.Avoid wearing high heels.Sit tall with your shoulders back and your lower back supported. Keep knees even with or higher than your hips. Avoid sitting in one position for longer than one hour.Use correct posture when lifting:Bend your knees and lift with your leg muscles. Keep your back straight.Never bend forward to lift. Keep the load close to your body.Avoid turning or twisting while holding a heavy object.Avoid lifting heavy loads above your waist.Sleep on a firm surface. Provide support for your lower back and under your knees if it feels more comfortable.Rise up from a prone position correctly. Rising is actually lifting your body’s weight. Roll to your side and use your arms and legs to lift up.Maintain correct body weight. Obesity or a large abdomen can pull your lower back out of alignment.Exercise to maintain good muscle tone in your back and abdomen. Walking, swimming and biking are all good activities.Learn stress management and muscle-relaxation techniques such as yoga.What you can doRestrict activity. One or two days in bed may be needed in severe cases. Resume normal activity very slowly. Avoid any activity that puts stress on your back. Immediately stop any activity that causes or increases pain. Complete recovery may take up to six weeks.Apply ice or cold packs for 20 minutes every two hours for acute pain; decrease to 20 minutes twice daily once pain has lessened. For protection, place a washcloth between bare skin and ice.Once pain has lessened, take warm showers with water directed at the painful area.Take aspirin or ibuprofen to ease pain and inflammation (follow directions on the package). NEVER give aspirin to children/ teenagers. It can cause Reye’s syndrome, a rare but often fatal condition.Sleep on a firm surface. If possible, place a piece of plywood between the mattress and box springs.Support your back while sleeping. Place a pillow under your knees or lie on your side, knees bent and with a pillow between them.If back pain starts with no known cause, look for signs of a problem in another area of your body that may be causing referred pain.For minor muscle soreness in your back, apply heat for 20 to 30 minutes.*94\303\2*

INFECTIVE DISEASES: EPIDEMIC ENCEPHALITIS

December 27th, 2010 by | Posted in Anti-Infectives | No Comments »
Epidemics of brain fever are not an excessively large cause of disability and death in the United States. There have, however, been outbreaks such as the one which occurred in St. Louis in 1933 in which there were more than 1,000 cases. In the St. Louis epidemic there were 100 cases for every 100,000 population and twenty per cent of those who were infected died. In various epidemics the number of cases varies from two cases for every 100,000 people to as many as twenty-two for every 100,000 people. A minor outbreak appeared in Florida in 1962.
Now it is established that the cause of epidemic encephalitis is a virus and that the outbreaks in human beings are closely related to certain similar conditions attacking animals, particularly an epidemic of a similar condition which concerns horses.
In several regions domestic birds such as chickens have been associated with the spread of the condition. In a California outbreak, the
English sparrow and several species of blackbirds were involved. Research has also shown that various mosquitoes and mites as well as ticks may be associated with the spread of this virus.
In the prevention of encephalitis, control of the mosquitoes is of the utmost importance. Vaccines have been developed which may be used in outbreaks among horses. The condition is so serious that its appearance in any community should involve immediate investigation by competent health authorities.
*20/318/5*

INFECTIVE DISEASES: EPIDEMIC ENCEPHALITISEpidemics of brain fever are not an excessively large cause of disability and death in the United States. There have, however, been outbreaks such as the one which occurred in St. Louis in 1933 in which there were more than 1,000 cases. In the St. Louis epidemic there were 100 cases for every 100,000 population and twenty per cent of those who were infected died. In various epidemics the number of cases varies from two cases for every 100,000 people to as many as twenty-two for every 100,000 people. A minor outbreak appeared in Florida in 1962.Now it is established that the cause of epidemic encephalitis is a virus and that the outbreaks in human beings are closely related to certain similar conditions attacking animals, particularly an epidemic of a similar condition which concerns horses.In several regions domestic birds such as chickens have been associated with the spread of the condition. In a California outbreak, theEnglish sparrow and several species of blackbirds were involved. Research has also shown that various mosquitoes and mites as well as ticks may be associated with the spread of this virus.In the prevention of encephalitis, control of the mosquitoes is of the utmost importance. Vaccines have been developed which may be used in outbreaks among horses. The condition is so serious that its appearance in any community should involve immediate investigation by competent health authorities.*20/318/5*

Random Posts