Definition
Diabetes is a life-long disease marked by high levels of sugar in the blood.
Causes, incidence, and risk factors
Diabetes can be caused by too little insulin (a hormone produced by the pancreas to control blood sugar), resistance to insulin, or both.
To understand diabetes, it is important to first understand the normal process of food metabolism. Several things happen when food is digested:
A sugar called glucose enters the bloodstream. Glucose is a source of fuel for the body.
An organ called the pancreas makes insulin. The role of insulin is to move glucose from the bloodstream into muscle, fat, and liver cells, where it can be used as fuel.
People with diabetes have high blood sugar. This is because their pancreas does not make enough insulin or their muscle, fat, and liver cells do not respond to insulin normally, or both.
There are three major types of diabetes:
Type 1 diabetes is usually diagnosed in childhood. The body makes little or no insulin, and daily injections of insulin are needed to sustain life.
Type 2 diabetes is far more common than type 1 and makes up most of all cases of diabetes. It usually occurs in adulthood. The pancreas does not make enough insulin to keep blood glucose levels normal, often because the body does not respond well to the insulin. Many people with type 2 diabetes do not know they have it, although it is a serious condition. Type 2 diabetes is becoming more common due to the growing number of older Americans, increasing obesity, and failure to exercise.
Gestational diabetes is high blood glucose that develops at any time during pregnancy in a woman who does not have diabetes.
Diabetes affects more than 20 million Americans. About 54 million Americans have prediabetes. There are many risk factors for diabetes, including:
A parent, brother, or sister with diabetes
Obesity
Age greater than 45 years
Some ethnic groups (particularly African Americans, Native Americans, Asians, Pacific Islanders, and Hispanic Americans)
Gestational diabetes or delivering a baby weighing more than 9 pounds
High blood pressure
High blood levels of triglycerides (a type of fat molecule)
High blood cholesterol level
Not getting enough exercise
The American Diabetes Association recommends that all adults over age 45 be screened for diabetes at least every 3 years. A person at high risk should be screened more often.
Symptoms
High blood levels of glucose can cause several problems, including frequent urination, excessive thirst, hunger, fatigue, weight loss, and blurry vision. However, because type 2 diabetes develops slowly, some people with high blood sugar experience no symptoms at all.
Symptoms of type 1 diabetes:
Increased thirst
Increased urination
Weight loss in spite of increased appetite
Fatigue
Nausea
Vomiting
Patients with type 1 diabetes usually develop symptoms over a short period of time, and the condition is often diagnosed in an emergency setting.
Symptoms of type 2 diabetes:
Increased thirst
Increased urination
Increased appetite
Fatigue
Blurred vision
Slow-healing infections
Impotence in men
Signs and tests
A urine analysis may be used to look for glucose and ketones from the breakdown of fat. However, a urine test alone does not diagnose diabetes. The following blood glucose tests are used to diagnose diabetes:
Fasting blood glucose level -- diabetes is diagnosed if higher than 126 mg/dL on two occasions. Levels between 100 and 126 mg/dl are referred to as impaired fasting glucose or pre-diabetes. These levels are considered to be risk factors for type 2 diabetes and its complications.
Random (non-fasting) blood glucose level -- diabetes is suspected if higher than 200 mg/dL and accompanied by the classic symptoms of increased thirst, urination, and fatigue. (This test must be confirmed with a fasting blood glucose test.)
Oral glucose tolerance test -- diabetes is diagnosed if glucose level is higher than 200 mg/dL after 2 hours (This test is used more for type 2 diabetes.)
You should also ask your doctor how often to you need your hemoglobin A1c (HbA1c) level checked. The HbA1c is a measure of average blood glucose during the previous 2 to 3 months. It is a very helpful way to determine how well treatment is working.
Ketone testing is another test that is used in type 1 diabetes. Ketones are produced by the breakdown of fat and muscle, and they are harmful at high levels. The ketone test is done using a urine sample. High levels of blood ketones may result in a serious condition called ketoacidosis. Ketone testing is usually done at the following times:
When the blood sugar is higher than 240 mg/dL
During acute illness (for example, pneumonia, heart attack, or stroke)
When nausea or vomiting occur
During pregnancy
Treatment
There is no cure for diabetes. Treatment involves medicines, diet, and exercise to control blood sugar and prevent symptoms and complications.
LEARN THESE SKILLS
Basic diabetes management skills will help prevent the need for emergency care. These skills include:
How to recognize and treat low blood sugar (hypoglycemia) and high blood sugar (hyperglycemia)
What to eat and when
How to take insulin or oral medication
How to test and record blood glucose
How to test urine for ketones (type 1 diabetes only)
How to adjust insulin or food intake when changing exercise and eating habits
How to handle sick days
Where to buy diabetes supplies and how to store them
After you learn the basics of diabetes care, learn how the disease can cause long-term health problems and the best ways to prevent these problems. People with diabetes need to review and update their knowledge, because new research and improved ways to treat diabetes are constantly being developed.
SELF-TESTING
If you have diabetes, your doctor may tell you to regularly check your blood sugar levels at home. There are a number of devices available, and they use only a drop of blood. Self-monitoring tells you how well diet, medication, and exercise are working together to control your diabetes and can help your doctor prevent complications.
The American Diabetes Association recommends that premeal blood sugar levels fall in the range of 80 to 120 mg/dL and bedtime blood levels fall in the range of 100 to 140 mg/dL. Your doctor may adjust this depending on your circumstances.
WHAT TO EAT
You should work closely with your health care provider to learn how much fat, protein, and carbohydrates you need in your diet. A registered dietician can be very helpful in planning dietary needs.
People with type 1 diabetes should eat at about the same times each day and try to be consistent with the types of food they choose. This helps to prevent blood sugars from becoming extremely high or low.
Persons with type 2 diabetes should follow a well-balanced and low-fat diet.
HOW TO TAKE MEDICATION
Medications to treat diabetes include insulin and glucose-lowering pills called oral hypoglycemic drugs.
Persons with type 1 diabetes cannot make their own insulin, so daily insulin injections are needed. Insulin does not come in pill form. Injections that are generally needed one to four times per day. Some people use an insulin pump, which is worn at all times and delivers a steady flow of insulin throughout the day. Other people may use a new type of inhaled insulin.
Insulin preparations differ in how quickly they start to work and how long they remain active. Sometimes different types of insulin are mixed together in a single injection. The types of insulin to use, the doses needed, and the number of daily injections are chosen by a health care professional trained to provide diabetes care.
People who need insulin are taught to give themselves injections by their health care providers or diabetes educators.
Unlike type 1 diabetes, type 2 diabetes may respond to treatment with exercise, diet, and medicines taken by mouth. There are several types of medicines used to lower blood glucose in type 2 diabetes. They fall into one of three groups:
Medications that increase insulin production by the pancreas. They include glimepiride, glipizide, glyburide, repaglinide, nateglinide, and sitaglyptin.
Medications that increase sensitivity to insulin. These include metformin, rosiglitazone, and pioglitazone.
Medications that delay absorption of glucose from the gut. These include acarbose and miglitol.
There are some injectable medicines used to lower blood sugar. They include exenatide and pramlintide.
Most persons with type 2 diabetes will need more than one medication for good blood sugar control within 3 years of starting their first medication. Different groups of medications may be combined or used with insulin.
Some people with type 2 diabetes find they no longer need medication if they lose weight and increase activity, because when their ideal weight is reached, their own insulin and a careful diet can control their blood glucose levels.
It is unknown if hypoglycemic medicines taken by mouth are safe for use in pregnancy. Women who have type 2 diabetes and take these medications may be switched to insulin during pregnancy and while breastfeeding.
Gestational diabetes is treated with insulin and changes in diet.
EXERCISE
Regular exercise is especially important for people with diabetes. It helps with blood sugar control, weight loss, and high blood pressure. People with diabetes who exercise are less likely to experience a heart attack or stroke than diabetics who do not exercise regularly. You should be evaluated by your physician before starting an exercise program.
Here are some exercise considerations:
Choose an enjoyable physical activity that is appropriate for your current fitness level.
Exercise every day, and at the same time of day, if possible.
Monitor blood glucose levels before and after exercise.
Carry food that contains a fast-acting carbohydrate in case you become hypoglycemic during or after exercise.
Carry a diabetes identification card and a mobile phone or change for a payphone in case of emergency.
Drink extra fluids that do not contain sugar before, during, and after exercise.
Changes in exercise intensity or duration may need changes in diet or medication dose to keep blood sugar levels from going too high or low.
FOOT CARE
People with diabetes are prone to foot problems because of the likelihood of damage to blood vessels and nerves and a decreased ability to fight infection. Problems with blood flow and damage to nerves may cause an injury to the foot to go unnoticed until infection develops. Death of skin and other tissue can occur.
If left untreated, the affected foot may need to be amputated. Diabetes is the most common condition leading to amputations.
To prevent injury to the feet, people with diabetes should adopt a daily routine of checking and caring for the feet as follows:
Check your feet every day, and report sores or changes and signs of infection.
Wash your feet every day with lukewarm water and mild soap, and dry them thoroughly.
Soften dry skin with lotion or petroleum jelly.
Protect feet with comfortable, well-fitting shoes.
Exercise daily to promote good circulation.
See a podiatrist for foot problems or to have corns or calluses removed.
Remove shoes and socks during a visit to your health care provider and remind him or her to examine your feet.
Stop smoking, which hinders blood flow to the feet.
Calling your health care provider
Go to the emergency room or call the local emergency number (such as 911) if symptoms of ketoacidosis occur:
Increased thirst and urination
Nausea
Deep and rapid breathing
Abdominal pain
Sweet-smelling breath
Loss of consciousness
Go to the emergency room or call the local emergency number if symptoms of extremely low blood sugar (hypoglycemic coma or severe insulin reaction) occur:
Weakness
Drowsiness
Headache
Confusion
Dizziness
Double vision
Lack of coordination
Convulsions or unconsciousness
Prevention
Maintaining an ideal body weight and an active lifestyle may prevent the onset of type 2 diabetes. Currently there is no way to prevent type 1 diabetes.
May 18, 2007
MEDITATION
Transcendental Meditation - Mind Body Therapy and Alternative Therapy
More and more doctors are prescribing meditation as a way to lower blood pressure, improve exercise performance in people with angina, help people with asthma breathe easier, relieve insomnia and generally relax the everyday stresses of life. Meditation is a safe and simple way to balance a person's physical, emotional, and mental states. It is simple; but can benefit everybody.
Meditation is not just for yoga masters sitting cross-legged on mountaintops in the Himalayas. It's a flexible approach to coping with stress, anxiety, many medical conditions and the day-to-day "static" that robs us of inner peace. Today, the Pittsburgh International Airport boasts a large meditation room featuring a quiet ambiance, comfortable furniture and paintings of clouds. What better place than one of the nation's largest, busiest airports for a refuge from all the hustle and bustle?
The Taoist sage Chuang-tzu referred to meditation, which the Chinese simply call 'sitting still, doing nothing', as 'mental fasting'. Just as physical fasting purifies the essences of the body by withdrawing all external input of food, so the 'mental fasting' of meditation purifies the mind and restores the spirit's primal powers by withdrawing all distracting thoughts and disturbing emotions from the mind. In both physical and mental fasting, the cleansing and purifying processes are natural and automatic, but the precondition for triggering this process of self-rejuvenation is emptying body and mind of all input for a fixed number of minutes or days. Taoists believe that only by 'sitting still, doing nothing' can we muster sufficient mental clarity to focus fully on the difficult task of taming and training the two aspects of temporal mind that govern our lives - the mind of emotion and the mind of intent.
Introduction:
The use of Meditation for healing is not new. Meditative techniques are the product of diverse cultures and peoples around the world. It has been rooted in the traditions of the world's great religions. In fact, practically all religious groups practice meditation in one form or another. The value of Meditation to alleviate suffering and promote healing has been known and practiced for thousands of years.
Of the religions that use meditation, perhaps Buddhism, practiced widely in eastern and central Asia, is the best known. To Buddhists, the practice of meditation is essential for the cultivation of wisdom and compassion and for understanding reality. Buddhists believe that our ordinary consciousness is both limited and limiting. Meditation makes it possible to live life to the full spectrum of our conscious and unconscious possibilities.
In spite of its rich history and traditions, it is only during the past three decades that scientific study has focused on the clinical effects of meditation on health. During the 1960s, reports reached the West of yogis and meditation masters in India who could perform extraordinary feats of bodily control and altered states of consciousness. These reports captured the interest of Western researchers studying self-regulation and the possibility of voluntary control over the autonomic nervous system. At the same time, new refinements in scientific instrumentation made it possible to duplicate and substantiate some of these reports at medical research institutes. Health care professionals who were often dissatisfied with the side effects of drug treatments for stress-related disorders embraced meditation as a valuable tool for stress reduction, and today both patients and physicians enjoy the health benefits of regular meditation practice.
Herbert Benson, M.D., a professor at Harvard Medical School, describes the meditation experience as the "relaxation response." He discovered by studying various yogis and longtime meditators that the meditation process counteracted the effects of the sympathetic nervous system-the one that wants to fight or flee. Whereas the sympathetic system dilates the pupils and gets the heart rate, respiration, and blood pressure up, the parasympathetic system, activated when we meditate, does just the opposite. Muscle tension decreases, blood pressure drops, and for some extraordinary practitioners, even temperature and basal metabolism rates drop during a prolonged meditation. Oxygen needs of the body are reduced when you are in a highly relaxed state, and brain waves change from the busy beta-waves to the blissful alpha waves.
What Is Meditation?
There are various types of meditation - prayer is probably the best known, but there is also TM (Transcendental Meditation), mindfulness meditation, and from the Eastern tradition, Zen meditation, Buddhist meditation, and Taoist meditation.
The meditation encompasses such diverse methods as:
Formal sitting in which the body is held immobile and the attention controlled. e.g., Zazen, Vipassana
Expressive practices , in which the body is let free and anything can happen. e.g., Siddha Yoga, the Latihan, the chaotic meditation of Rajneesh.
The practice of going about one's daily round of activities mindfully. e.g., Mahamudra, Shikan Taza, Gurdjieff's "self-remembering".
All these practices have one thing in common - they all focus on quietening the busy mind. The intention is not to remove stimulation but rather to direct your concentration to one healing element - one sound, one word, one image, or one's breath. When the mind is "filled" with the feeling of calm and peace, it cannot take off on its own and worry, stress out, or get depressed.
According to Joan Borysenko, Ph.D., a pioneer in the field of mind/body medicine, meditation can be broadly defined as any activity that keeps the attention pleasantly anchored in the present moment. When the mind is calm and focused in the present, it is neither reacting to memories from the past nor being preoccupied with plans for the future, two major sources of chronic stress known to impact health. "Meditation," says Dr. Borysenko, "helps to keep us from identifying with the 'movies of the mind."
Types of Meditation - Classification
All the meditation techniques can be grouped into two basic approaches:
Concentrative meditation and
Mindfulness meditation.
Concentrative meditation
Concentrative meditation focuses the attention on the breath, an image, or a sound (mantra), in order to still the mind and allow a greater awareness and clarity to emerge. This is like a zoom lens in a camera; we narrow our focus to a selected field.
The simplest form of concentrative meditation is to sit quietly and focus the attention on the breath. Yoga and meditation practitioners believe that there is a direct correlation between one's breath and one's state of the mind. For example, when a person is anxious, frightened, agitated, or distracted, the breath will tend to be shallow, rapid, and uneven. On the other hand, when the mind is calm, focused, and composed, the breath will tend to be slow, deep, and regular. Focusing the mind on the continuous rhythm of inhalation and exhalation provides a natural object of meditation. As you focus your awareness on the breath, your mind becomes absorbed in the rhythm of inhalation and exhalation. As a result, your breathing will become slower and deeper, and the mind becomes more tranquil and aware.
Mindfulness meditation
Mindfulness meditation , according to Dr. Borysenko, "involves opening the attention to become aware of the continuously passing parade of sensations and feelings, images, thoughts, sounds, smells, and so forth without becoming involved in thinking about them." The person sits quietly and simply witnesses whatever goes through the mind, not reacting or becoming involved with thoughts, memories, worries, or images. This helps to gain a more calm, clear, and non-reactive state of mind. Mindfulness meditation can be likened to a wide-angle lens. Instead of narrowing your sight to a selected field as in concentrative meditation, here you will be aware of the entire field.
How Meditation Works
Studies have shown that meditation (in particular, research on Transcendental Meditation, a popular form of meditation practiced in the West for the past thirty years), can bring about a healthy state of relaxation by causing a generalized reduction in multiple physiological and biochemical markers, such as decreased heart rate, decreased respiration rate, decreased plasma cortisol (a major stress hormone), decreased pulse rate, and increased EEG (electroencephalogram) alpha, a brain wave associated with relaxation. Research conducted by R. Keith Wallace at U.C.L.A. on Transcendental Meditation, revealed that during meditation, the body gains a state of profound rest. At the same time, the brain and mind become more alert, indicating a state of restful alertness. Studies show that after TM, reactions are faster, creativity greater, and comprehension broader.
A laboratory study of practitioners of Maharishi Mahesh Yogi's transcendental meditation (TM), carried out by Benson and Wallace at Harvard Medical School towards the end of the 1960s, provided the first detailed knowledge of the many physiological changes that go with meditation.
Some of the meditators, whose ages ranged from seventeen to forty-one, had been meditating only a few weeks, others for several years. All recorded changes associated with deep relaxation.
The fall in metabolic rate was the most striking discovery. This was indicated by a dramatic drop in oxygen consumption within a few minutes of starting meditation. Consumption fell by up to twenty per cent below the normal level; below that experienced even in deep sleep. Meditators took on average two breaths less and one litre less air per minute. The meditators' heart rate was several beats less per minute.
During meditation, blood pressure stayed at 'low levels', but fell markedly in persons starting meditation with abnormally high levels.
The meditators' skin resistance to an electrical current was measured. A fall in skin resistance is characteristic of anxiety and tension states; a rise indicates increased muscle relaxation. The finding was that though meditation is primarily a mental technique, it soon brings significantly improved muscle relaxation.
Meditation reduces activity in the nervous system. The parasympathetic branch of the autonomic or involuntary nervous system predominates. This is the branch responsible for calming us.
During anxiety and tension states there is a rise in the level of lactate in the blood. Lactate is a substance produced by metabolism in the skeletal muscles. During meditation blood lactate levels decreased at a rate four times faster than the rate of decrease in non-meditators resting lying on their backs or in the meditators themselves in pre-meditation resting.
The likely reason for the dramatic reduction in lactate production by meditators was indicated when further studies of meditators showed an increased blood flow during. Benson and Wallace found that there was a thirty-two per cent increase in forearm blood flow. Lactate production in the body is mainly in skeletal muscle tissue; during meditation the faster circulation brings a faster delivery of oxygen to the muscles and less lactate is produced.
The two investigators summed up the state produced by their meditating subjects as wakeful and hypometabolic. The physiological changes were different in many ways from those found in sleeping people or those in hypnotic trance states. Meditation, they said, produces 'a complex of responses that marks a highly relaxed state'. Moreover, the pattern of changes they observed in meditators suggested an integrated response, mediated by the central nervous system.
"Through meditation we can learn to access the relaxation response (the physiological response elicited by meditation) and to be aware of the mind and the way our attitudes produce stress," says Dr. Borysenko, author of 'Minding the Body, Mending the Mind". "In addition, by quieting the mind, meditation can also put one in touch with the inner physician, allowing the body's own inner wisdom to be heard."
Taoists believe that the mind of emotions is governed by the Fire energy of the heart. When your emotions are not controlled, the fire energy of the heart flares upwards, wastefully burning up energy and clouding the mind. The mind of intent, or willpower, is controlled by the Water energy of the kidneys. When unattended, the water energy flows down and out through the sexual organs, depleting essence and energy and weakening the spirit. Taoists believe that when you are 'sitting still, doing nothing', as in meditation, the flow of Fire and Water are reversed: Water energy from the kidneys and sacrum is drawn up to the head via the Central and Governing channels, while emotional Fire energy from the heart is drawn down into the Lower Elixir Field in the abdomen, where it is refined and transformed and enters general circulation through the energy channels. On the spiritual/mental level, this internal energy alchemy enables the mind of intent (Water) to exert a calming, cooling, controlling influence over the mind of emotion (Fire).
Healing Power of Meditation
Research has shown that Meditation can contribute to an individual's psychological and physiological well-being. This is accomplished as Meditation brings the brainwave pattern into an alpha state, which is a level of consciousness that promotes the healing state.
As discussed in the section "How Meditation Work?", there is scientific evidence that Meditation can reduce blood pressure and relieve pain and stress. When used in combination with biofeedback, Meditation enhances the effectiveness of biofeedback.
Patricia Norris, Ph.D., Director of the Biofeedback and Psychophysiology Clinic at the Menninger Foundation, reports: "In our practice at Menninger we use meditative techniques to enhance immune functioning in cancer, AIDS, and autoimmune patients. We also use meditation in conjunction with neuro-feedback to normalize brain rhythms and chemistry in alcohol and drug addiction, as well as other addictive conditions. Almost all of our patients use meditative techniques in learning self-regulation for disorders such as anxiety and hypertension, and for stress management. We consider meditation a recommended practice for anyone seeking high-level wellness."
In addition to the growing body of research literature on meditation, physicians, psychotherapists, and other professionals are increasingly adding meditative techniques to their practice. Over six thousand physicians have begun the practice of Transcendental Meditation and regularly recommend the TM technique to their patients. Dean Ornish, M.D has demonstrated that heart disease can be reversed with a comprehensive program that includes meditations. Many physicians consider meditation a key element of an integrated health program.
Physical Benefits of Meditation
Psychological Benefits of Meditation
The benefits of an ongoing meditation practice as it impacts our health can be classified further into three categories: physiological, psychological, and spiritual. Most people who practice meditation do so to reduce stress, anxiety, anger and other negative emotions. Increasingly, physicians prescribe meditation as part of the treatment for a large and growing number of medical conditions.
More and more doctors are prescribing meditation as a way to lower blood pressure, improve exercise performance in people with angina, help people with asthma breathe easier, relieve insomnia and generally relax the everyday stresses of life. Meditation is a safe and simple way to balance a person's physical, emotional, and mental states. It is simple; but can benefit everybody.
Meditation is not just for yoga masters sitting cross-legged on mountaintops in the Himalayas. It's a flexible approach to coping with stress, anxiety, many medical conditions and the day-to-day "static" that robs us of inner peace. Today, the Pittsburgh International Airport boasts a large meditation room featuring a quiet ambiance, comfortable furniture and paintings of clouds. What better place than one of the nation's largest, busiest airports for a refuge from all the hustle and bustle?
The Taoist sage Chuang-tzu referred to meditation, which the Chinese simply call 'sitting still, doing nothing', as 'mental fasting'. Just as physical fasting purifies the essences of the body by withdrawing all external input of food, so the 'mental fasting' of meditation purifies the mind and restores the spirit's primal powers by withdrawing all distracting thoughts and disturbing emotions from the mind. In both physical and mental fasting, the cleansing and purifying processes are natural and automatic, but the precondition for triggering this process of self-rejuvenation is emptying body and mind of all input for a fixed number of minutes or days. Taoists believe that only by 'sitting still, doing nothing' can we muster sufficient mental clarity to focus fully on the difficult task of taming and training the two aspects of temporal mind that govern our lives - the mind of emotion and the mind of intent.
Introduction:
The use of Meditation for healing is not new. Meditative techniques are the product of diverse cultures and peoples around the world. It has been rooted in the traditions of the world's great religions. In fact, practically all religious groups practice meditation in one form or another. The value of Meditation to alleviate suffering and promote healing has been known and practiced for thousands of years.
Of the religions that use meditation, perhaps Buddhism, practiced widely in eastern and central Asia, is the best known. To Buddhists, the practice of meditation is essential for the cultivation of wisdom and compassion and for understanding reality. Buddhists believe that our ordinary consciousness is both limited and limiting. Meditation makes it possible to live life to the full spectrum of our conscious and unconscious possibilities.
In spite of its rich history and traditions, it is only during the past three decades that scientific study has focused on the clinical effects of meditation on health. During the 1960s, reports reached the West of yogis and meditation masters in India who could perform extraordinary feats of bodily control and altered states of consciousness. These reports captured the interest of Western researchers studying self-regulation and the possibility of voluntary control over the autonomic nervous system. At the same time, new refinements in scientific instrumentation made it possible to duplicate and substantiate some of these reports at medical research institutes. Health care professionals who were often dissatisfied with the side effects of drug treatments for stress-related disorders embraced meditation as a valuable tool for stress reduction, and today both patients and physicians enjoy the health benefits of regular meditation practice.
Herbert Benson, M.D., a professor at Harvard Medical School, describes the meditation experience as the "relaxation response." He discovered by studying various yogis and longtime meditators that the meditation process counteracted the effects of the sympathetic nervous system-the one that wants to fight or flee. Whereas the sympathetic system dilates the pupils and gets the heart rate, respiration, and blood pressure up, the parasympathetic system, activated when we meditate, does just the opposite. Muscle tension decreases, blood pressure drops, and for some extraordinary practitioners, even temperature and basal metabolism rates drop during a prolonged meditation. Oxygen needs of the body are reduced when you are in a highly relaxed state, and brain waves change from the busy beta-waves to the blissful alpha waves.
What Is Meditation?
There are various types of meditation - prayer is probably the best known, but there is also TM (Transcendental Meditation), mindfulness meditation, and from the Eastern tradition, Zen meditation, Buddhist meditation, and Taoist meditation.
The meditation encompasses such diverse methods as:
Formal sitting in which the body is held immobile and the attention controlled. e.g., Zazen, Vipassana
Expressive practices , in which the body is let free and anything can happen. e.g., Siddha Yoga, the Latihan, the chaotic meditation of Rajneesh.
The practice of going about one's daily round of activities mindfully. e.g., Mahamudra, Shikan Taza, Gurdjieff's "self-remembering".
All these practices have one thing in common - they all focus on quietening the busy mind. The intention is not to remove stimulation but rather to direct your concentration to one healing element - one sound, one word, one image, or one's breath. When the mind is "filled" with the feeling of calm and peace, it cannot take off on its own and worry, stress out, or get depressed.
According to Joan Borysenko, Ph.D., a pioneer in the field of mind/body medicine, meditation can be broadly defined as any activity that keeps the attention pleasantly anchored in the present moment. When the mind is calm and focused in the present, it is neither reacting to memories from the past nor being preoccupied with plans for the future, two major sources of chronic stress known to impact health. "Meditation," says Dr. Borysenko, "helps to keep us from identifying with the 'movies of the mind."
Types of Meditation - Classification
All the meditation techniques can be grouped into two basic approaches:
Concentrative meditation and
Mindfulness meditation.
Concentrative meditation
Concentrative meditation focuses the attention on the breath, an image, or a sound (mantra), in order to still the mind and allow a greater awareness and clarity to emerge. This is like a zoom lens in a camera; we narrow our focus to a selected field.
The simplest form of concentrative meditation is to sit quietly and focus the attention on the breath. Yoga and meditation practitioners believe that there is a direct correlation between one's breath and one's state of the mind. For example, when a person is anxious, frightened, agitated, or distracted, the breath will tend to be shallow, rapid, and uneven. On the other hand, when the mind is calm, focused, and composed, the breath will tend to be slow, deep, and regular. Focusing the mind on the continuous rhythm of inhalation and exhalation provides a natural object of meditation. As you focus your awareness on the breath, your mind becomes absorbed in the rhythm of inhalation and exhalation. As a result, your breathing will become slower and deeper, and the mind becomes more tranquil and aware.
Mindfulness meditation
Mindfulness meditation , according to Dr. Borysenko, "involves opening the attention to become aware of the continuously passing parade of sensations and feelings, images, thoughts, sounds, smells, and so forth without becoming involved in thinking about them." The person sits quietly and simply witnesses whatever goes through the mind, not reacting or becoming involved with thoughts, memories, worries, or images. This helps to gain a more calm, clear, and non-reactive state of mind. Mindfulness meditation can be likened to a wide-angle lens. Instead of narrowing your sight to a selected field as in concentrative meditation, here you will be aware of the entire field.
How Meditation Works
Studies have shown that meditation (in particular, research on Transcendental Meditation, a popular form of meditation practiced in the West for the past thirty years), can bring about a healthy state of relaxation by causing a generalized reduction in multiple physiological and biochemical markers, such as decreased heart rate, decreased respiration rate, decreased plasma cortisol (a major stress hormone), decreased pulse rate, and increased EEG (electroencephalogram) alpha, a brain wave associated with relaxation. Research conducted by R. Keith Wallace at U.C.L.A. on Transcendental Meditation, revealed that during meditation, the body gains a state of profound rest. At the same time, the brain and mind become more alert, indicating a state of restful alertness. Studies show that after TM, reactions are faster, creativity greater, and comprehension broader.
A laboratory study of practitioners of Maharishi Mahesh Yogi's transcendental meditation (TM), carried out by Benson and Wallace at Harvard Medical School towards the end of the 1960s, provided the first detailed knowledge of the many physiological changes that go with meditation.
Some of the meditators, whose ages ranged from seventeen to forty-one, had been meditating only a few weeks, others for several years. All recorded changes associated with deep relaxation.
The fall in metabolic rate was the most striking discovery. This was indicated by a dramatic drop in oxygen consumption within a few minutes of starting meditation. Consumption fell by up to twenty per cent below the normal level; below that experienced even in deep sleep. Meditators took on average two breaths less and one litre less air per minute. The meditators' heart rate was several beats less per minute.
During meditation, blood pressure stayed at 'low levels', but fell markedly in persons starting meditation with abnormally high levels.
The meditators' skin resistance to an electrical current was measured. A fall in skin resistance is characteristic of anxiety and tension states; a rise indicates increased muscle relaxation. The finding was that though meditation is primarily a mental technique, it soon brings significantly improved muscle relaxation.
Meditation reduces activity in the nervous system. The parasympathetic branch of the autonomic or involuntary nervous system predominates. This is the branch responsible for calming us.
During anxiety and tension states there is a rise in the level of lactate in the blood. Lactate is a substance produced by metabolism in the skeletal muscles. During meditation blood lactate levels decreased at a rate four times faster than the rate of decrease in non-meditators resting lying on their backs or in the meditators themselves in pre-meditation resting.
The likely reason for the dramatic reduction in lactate production by meditators was indicated when further studies of meditators showed an increased blood flow during. Benson and Wallace found that there was a thirty-two per cent increase in forearm blood flow. Lactate production in the body is mainly in skeletal muscle tissue; during meditation the faster circulation brings a faster delivery of oxygen to the muscles and less lactate is produced.
The two investigators summed up the state produced by their meditating subjects as wakeful and hypometabolic. The physiological changes were different in many ways from those found in sleeping people or those in hypnotic trance states. Meditation, they said, produces 'a complex of responses that marks a highly relaxed state'. Moreover, the pattern of changes they observed in meditators suggested an integrated response, mediated by the central nervous system.
"Through meditation we can learn to access the relaxation response (the physiological response elicited by meditation) and to be aware of the mind and the way our attitudes produce stress," says Dr. Borysenko, author of 'Minding the Body, Mending the Mind". "In addition, by quieting the mind, meditation can also put one in touch with the inner physician, allowing the body's own inner wisdom to be heard."
Taoists believe that the mind of emotions is governed by the Fire energy of the heart. When your emotions are not controlled, the fire energy of the heart flares upwards, wastefully burning up energy and clouding the mind. The mind of intent, or willpower, is controlled by the Water energy of the kidneys. When unattended, the water energy flows down and out through the sexual organs, depleting essence and energy and weakening the spirit. Taoists believe that when you are 'sitting still, doing nothing', as in meditation, the flow of Fire and Water are reversed: Water energy from the kidneys and sacrum is drawn up to the head via the Central and Governing channels, while emotional Fire energy from the heart is drawn down into the Lower Elixir Field in the abdomen, where it is refined and transformed and enters general circulation through the energy channels. On the spiritual/mental level, this internal energy alchemy enables the mind of intent (Water) to exert a calming, cooling, controlling influence over the mind of emotion (Fire).
Healing Power of Meditation
Research has shown that Meditation can contribute to an individual's psychological and physiological well-being. This is accomplished as Meditation brings the brainwave pattern into an alpha state, which is a level of consciousness that promotes the healing state.
As discussed in the section "How Meditation Work?", there is scientific evidence that Meditation can reduce blood pressure and relieve pain and stress. When used in combination with biofeedback, Meditation enhances the effectiveness of biofeedback.
Patricia Norris, Ph.D., Director of the Biofeedback and Psychophysiology Clinic at the Menninger Foundation, reports: "In our practice at Menninger we use meditative techniques to enhance immune functioning in cancer, AIDS, and autoimmune patients. We also use meditation in conjunction with neuro-feedback to normalize brain rhythms and chemistry in alcohol and drug addiction, as well as other addictive conditions. Almost all of our patients use meditative techniques in learning self-regulation for disorders such as anxiety and hypertension, and for stress management. We consider meditation a recommended practice for anyone seeking high-level wellness."
In addition to the growing body of research literature on meditation, physicians, psychotherapists, and other professionals are increasingly adding meditative techniques to their practice. Over six thousand physicians have begun the practice of Transcendental Meditation and regularly recommend the TM technique to their patients. Dean Ornish, M.D has demonstrated that heart disease can be reversed with a comprehensive program that includes meditations. Many physicians consider meditation a key element of an integrated health program.
Physical Benefits of Meditation
Psychological Benefits of Meditation
The benefits of an ongoing meditation practice as it impacts our health can be classified further into three categories: physiological, psychological, and spiritual. Most people who practice meditation do so to reduce stress, anxiety, anger and other negative emotions. Increasingly, physicians prescribe meditation as part of the treatment for a large and growing number of medical conditions.
May 17, 2007
Prevention is better than cure.....
In sub-Saharan Africa, most HIV infections are heterosexually transmitted, and women are more likely to become infected than men [1]. Most HIV infections in children are acquired through mother-to-child transmission (MTCT) [2, 3]. Rates of perinatal transmission range from 13% to 40% among women not treated for their HIV infection [4]. Early child mortality among HIV-positive and HIV-negative children born to HIV-infected mothers have been reported to be 4 and 1.3–2 times higher, respectively, than that among children born to HIV-negative women [5] (A.M.v.E., personal observation).
There is geographic overlap between HIV and malaria in sub-Saharan Africa. In areas where malaria is endemic, pregnant women have a higher risk of malaria than nonpregnant women, and this risk is further increased among HIV-infected women [6]. Although these malaria infections are usually asymptomatic, parasites sequester in the placenta, and placental malaria is associated with low birth weight (LBW), intrauterine growth retardation, prematurity, and maternal and infant anemia [7–9].
Malaria is a major contributor to infant mortality in sub-Saharan Africa, directly through infant illness and indirectly through placental malaria and its adverse effects. The effect of the combination of maternal HIV infection and malaria during pregnancy on infant survival is not clear [6]. An early study in Malawi suggested that placental malaria was a risk factor for postneonatal infant mortality (PNIM) in children born to HIV-infected women [10]. Malaria, like other coexisting infections, can cause temporary increases in HIV load [11]. It was hypothesized that PNIM could have been increased either because placental malaria increased MTCT of HIV-1 or because placental malaria enhanced the progression of HIV disease in infected infants directly or indirectly (if placental malaria would be a marker for another disease leading to infant death, such as infant malaria). The HIV vertical transmission study in Kisumu was designed to examine these questions. We previously reported that placental malaria was not associated with increased MTCT of HIV but, by contrast, was found to be protective [12]. In the present article, we study the effect of placental malaria, infant malaria, and anemia on PNIM among the infants.
SUBJECTS AND METHODS
Study site and screening procedures. The study was conducted at the Nyanza Provincial General Hospital in Kisumu, western Kenya; enrollment lasted from June 1996 to August 2000, and infant follow-up ended in August 2001. Screening procedures have been described elsewhere [12]. Briefly, healthy pregnant women with an uncomplicated singleton pregnancy of 32 weeks' gestation were invited to participate. After informed consent was obtained and HIV counseling performed, a questionnaire on medical and obstetric history was completed, and blood was obtained for HIV testing. All screened women received routine antenatal care [13] and were encouraged to deliver at the hospital; 50% did, which reflects the low rate of deliveries at health care facilities in this area (37.4%) [14]. For women who gave birth in the hospital, placental smears and blood for maternal hemoglobin and viral load determinations were collected. Within 24 h of birth, infants were weighed, and their gestational age was assessed [15].
Enrollment in the follow-up study. All HIV-seropositive mothers and their normally delivered, live-born infants were eligible for enrollment in the follow-up study. One month postpartum, maternal blood was collected for the determination of CD4+ cell counts. Infants were scheduled to be seen every 4 weeks until the age of 1 year or death. During routine visits, we obtained information on the health of the infant during the preceding month. Capillary blood was collected by finger stick for a blood smear, hemoglobin determination, and polymerase chain reaction (PCR) testing for HIV. CD4+ cell counts were not determined in infants. Infants with malaria parasitemia were treated, regardless of clinical symptoms, with an appropriate antimalarial (sulfadoxine-pyrimethamine [SP] or amodiaquine). Clinical staff treated infants with anemia or complaints in accordance with their findings [9]. If a routine visit was missed, we visited the participant's home to determine whether the caretaker remained interested in participating and to assess the vital status of the infant. For infant deaths, we obtained additional information using verbal autopsy.
Laboratory procedures. Details on standard procedures for blood smears, hemoglobin determination, and maternal HIV testing have been reported elsewhere [12]. Maternal CD4+ cell counts were assessed using commercial, dual-label monoclonal antibodies (Becton-Dickinson Immunocytometry) and standard fluorescence-activated cell sorting analysis after whole-blood lysis [16]. The maternal HIV-1 load was determined in the delivery sample using the Roche Amplicor HIV-1 monitor test (version 1.0; Roche Diagnostics), which has a quantification limit of 400 viral copies/mL. HIV testing of the infants was done by PCR of proviral DNA extracted from peripheral blood mononuclear cells [17].
Definitions.
PNIM was a death occurring between 29 and 364 days of delivery. HIV-positive infants were infants of HIV-seropositive mothers who had 2 consecutive positive PCR tests with the first positive PCR test at age 4 months; HIV-negative infants were infants of HIV-seropositive mothers who had 2 consecutive negative PCR tests and for whom the PCR test at the last visit was negative. Infants for whom we had insufficient PCR data to determine their status were excluded. To obtain a homogenous group of HIV-infected infants, we excluded infants who had their first positive PCR test after the age of 4 months; the different timing of HIV transmission may have resulted in a different immunological status and susceptibility to infectious diseases.
Malaria in infants was defined as the presence of asexual-stage parasites in thick smears, independent of the presence or absence of clinical signs and symptoms and independent of species. Moderate to severe anemia among infants was defined as a hemoglobin level <8 p =" .2),">
Table 2. Postneonatal infant deaths among infants of HIV-seropositive women by infant HIV-status, Kisumu, Kenya, 1996–2001.
Figure 1. Kaplan-Meier survival curve of postneonatal infant mortality by infant HIV status and placental malaria, Kisumu, Kenya, 1996–2001. Log rank tests: A vs. B, P = .7; A vs. C, P = .2; A vs. D, P < .001; B vs. C, P = .4; B vs. D, P < .001; C vs. D, P = .07. Neg, negative; pos, positive. Table 3. Risk factors for postneonatal infant mortality by infant HIV-status among infants of HIV-seropositive women, Kisumu, Kenya, 1996–2001. Placental malaria. HIV-positive infants born to mothers with placental malaria tended to be more likely to survive than those born to mothers without placental malaria (AHR, 0.34 [95% CI, 0.10–1.10]; P = .07, log-rank test) (table 3 and figure 1). Placental malaria was not associated with PNIM in HIV-negative infants (AHR, 1.29 [95% CI, 0.62–2.66]) (table 3). Infant anemia and infant parasitemia. Moderate to severe infant anemia was a risk factor for PNIM among HIV-negative infants but not among HIV-positive infants (table 3). There was no interaction between the infant's HIV status and the effect of infant malaria: malaria parasitemia at a routine visit was a protective factor against PNIM among both HIV-infected and HIV-uninfected infants (table 3). Among HIV-positive infants who died, median survival among 10 infants with at least 1 episode of malaria was 274 days, compared with 134 days among 29 infants without any episodes of malaria (P < .01, Mann-Whitney U test). Among HIV-negative infants, median survival was 263 days (10 infants) and 160 days (26 infants), respectively (P = .08, Mann-Whitney U test). Parasite prevalence among infants generally increases during the first year of life, and it increased in this study population, from 7% at 4 weeks to 22.0% at 44 weeks of age. To assess whether the association between infant malaria parasitemia and PNIM was not merely a proxy for age, we restricted the analysis to infants who completed the first 6 visits; the overall AHR with respect to malaria parasitemia and PNIM remained indicative of protection (0.53 [95% CI, 0.18–1.56]). Infants born to mothers with placental malaria have been reported to have a higher risk of infant malaria [18] and anemia [9]. We therefore determined whether the observed association between infant malaria and PNIM could partially be explained by the effect of placental malaria, which, as shown above, was also associated with PNIM, although the direction of the association differed between HIV-negative and HIV-infected infants. Removal of placental malaria from the models did not substantially change the HR between PNIM and infant parasitemia or anemia (AHR, 0.36 [95% CI, 0.10–1.23] and AHR, 5.06 [95% CI, 1.99–12.90] for parasitemia and anemia, respectively, in HIV-negative infants; AHR, 0.34 [95% CI, 0.08–1.44] and AHR, 1.02 [95% CI, 0.30–3.42] for parasitemia and anemia, respectively, in HIV-positive infants). We examined whether the association between malaria parasitemia was affected by treatment with SP, the antimalarial that was predominantly used in the study (75%) to treat parasitemia. The inclusion of a variable indicating SP use during the month preceding the visit did not change the association between infant malaria and PNIM in any of the models (AHR, 0.72 [95% CI, 0.31–1.67] and AHR, 0.43 [95% CI, 0.13–1.41], for HIV-positive and HIV-negative infants, respectively, adjusted for the factors in the adjusted models in table 3). Because infant parasitemia is associated with anemia, we further examined the effect of these variables in the model among HIV-negative infants. We created a variable indicating whether both, either, or neither of these factors were present at the visit. Compared with the absence of malaria parasitemia or of moderate to severe anemia, the combination of moderate to severe anemia and parasitemia was not significantly associated with PNIM (AHR, 1.13 [95% CI, 0.15–8.53]; P = .9), whereas anemia alone (i.e., without parasitemia at the visit) remained a significant factor (AHR, 5.80 [95% CI, 2.19–15.38]; P < .01), and malaria parasitemia alone continued to be associated with a protective effect (AHR, 0.49 [95% CI, 0.12–2.08]; P = .3). Maternal geometric mean viral load and PNIM. Infant HIV infection and death were associated with a significantly higher maternal viral load (table 4). Placental malaria was not associated with a significantly higher viral load. However, among women who transmitted HIV, maternal viral load was significantly higher when placental malaria was present. Among HIV-positive infants, the geometric mean maternal viral load among the 14 survivors of mothers with placental malaria (16,846 copies/mL) was not significantly different from the viral load among the 31 infants who died and whose mothers did not have placental malaria (8561 copies/mL; P = .4), whereas it was significantly higher than the maternal viral load of the 54 survivors whose mothers did not have placental malaria (3849 copies/mL; P = .02), which indicates that placental malaria may change the association between a high maternal viral load and HIV progression in the infected infant. The mothers with placental malaria of the 2 HIV-infected infants who died had very high maternal viral loads, and this was significant, compared with the HIV-infected survivors of mothers without placental malaria. Table 4. Associations between the geometric mean maternal viral load at the time of delivery, placental malaria, and postneonatal infant mortality, Kisumu, Kenya, 1996–2001. Probable causes of death. For 63 deaths, a probable cause of death was assigned using verbal autopsy. There were no significant differences by infant HIV status, but numbers were small (figure 2). Figure 2. Probable causes of postneonatal infant deaths by infant HIV status among infants of HIV-seropositive women by use of verbal autopsy, Kisumu, Kenya, 1996–2001. Verbal autopsy information was reviewed independently by 3 medical workers (clinical officers or doctors), who each assigned a diagnosis. If 1 diagnosis was given by 2 reviewers, it was assigned as the cause of death. If all 3 causes were different, a fourth reviewer was used to adjudicate. If no verbal autopsy information was available, the cause of death was labeled as undetermined. Malaria and anemia were combined, and HIV-positive infants were compared with HIV-negative infants (P = .06, 2-tailed Fisher's exact test). DISCUSSION Our results underscore that the complex interaction between HIV and malaria is challenging to study. By contrast to the earlier study by Bloland et al. [10], we did not find that placental malaria was a risk factor for PNIM among infants of HIV-seropositive women. Overall, the risk on PNIM was actually lower, although not significantly so, in infants born to HIV-infected mothers with placental malaria (AHR, 0.77 [95% CI, 0.43–1.39]), and this remained so after adjustment for potential confounders, including maternal CD4+ cell counts and LBW. These results are consistent with those of another study [19] that reported a nonsignificant protective effect of placental malaria against PNIM among infants born to HIV-seropositive women (HR, 0.39 [95% CI, 0.11–1.38]). We previously reported that MTCT was significantly lower in infants born to mothers with placental malaria than in those without placental malaria [12]. Several explanations can be considered for the association between placental malaria in HIV-positive women and increased survival time of HIV-infected infants. First, we speculate that prenatal exposure to malaria may modulate the immune system to generate protective immune pathways (involving innate or classical T cell–mediated pathways), which may slow the progression of HIV-1 and contribute to prolonged survival. There is considerable evidence that maternal exposure to malaria modulates immune responses to malaria in utero [20–23]. Second, it has recently become known that HIV-mediated disease progression is correlated with the down-regulation of a regulatory T cell (Treg) subset (Foxp3+CD4+CD25hi T cells), which may be critical for maintaining CD4+ cell counts [24]. It has been shown recently that placental malaria increases the number of Treg cells in cord blood [25], and this may help protect against any rapid decrease in CD4+ cell counts in infants born to HIV-positive mothers with placental malaria. Third, HIV/malarial coinfection can modulate the cytokine environment in the placenta and/or fetus, which may reduce the initial HIV load or slow HIV replication in the fetus. We have shown previously that HIV/malarial coinfection up-regulates (compared with HIV-positive malaria-negative women) some chemokines, including macrophage inflammatory protein (MIP)–1, that can compete with the CCR5 receptor for HIV entry [25, 26]. We were also interested in establishing whether malaria in the HIV-positive infant was associated with enhanced HIV disease progression. Infant malaria parasitemia was not a risk factor for PNIM—indeed, median survival was higher among HIV-infected children with at least 1 documented malaria episode than in children with no malaria, consistent with the results of a previous study in Uganda [27]. Because all infections were treated regardless of the presence of symptoms, frequent treatment with SP may have provided time windows of prophylaxis and reduced subsequent malaria and morbidity in these infants; SP can both treat and protect against malaria because of the long half-life of its components [28]. SP may have an effect on other infections as well (Streptococcus pneumonia, Toxoplasma gondii, and Pneumocystis jiroveci). However, when we included the use of SP in the models, it did not change the direction of the association between infant malaria and PNIM, which indicates that the use of SP is not an explanation for this association. It is possible that low-grade infection with malarial parasites in infants triggers immune responses to malaria that also result in reduced infant HIV-1 loads. Malaria is known to shift the immune system toward Th1-type responses, and progression of HIV-infection has been associated with a shift from a Th1-type to a Th2-type response [29]. In addition, malarial infection can activate chemokines such as MIP-1 and MIP-1, among others [30], that can compete for the HIV entry receptor CCR5 and thereby slow the progression of HIV infection in infants. As explained earlier, malarial infection can also activate the Treg population, which can modulate HIV-associated disease progression [31]. Another possibility is that malaria infection activated innate immune responses, which can help to control HIV-associated opportunistic infections, leading to increased survival time. Among HIV-negative infants of HIV-seropositive women, moderate to severe infant anemia was a significant risk factor for PNIM. Infant anemia may be the culmination of a sequence of events whereby maternal HIV infection, placental malaria, infant malaria, and SES may all contribute. Whatever the contributing factor, moderate to severe anemia in infants can be detected and should be responded to, particularly among infants of HIV-positive women. Our study had several limitations. First, we only enrolled HIV-infected women with no AIDS-defining symptoms; PNIM among women with progressed HIV disease is likely to be higher than our present findings. Our measurement of parasitemia by microscopic examination of smears was inexact compared with other methods, may have misclassified particularly low-density parasitemias, and did not identify intervillous inflammation, but this would have resulted in bias toward the null. The number of HIV-infected infants born to mothers with placental malaria was small; this precludes more-definitive answers and does not rule out a chance finding. An infant needed to make at least 2 follow-up visits for us to be able to make an HIV diagnosis, and loss to follow up was considerable, which may have biased our results. However, the reported PNIM among HIV-infected infants was comparable to results obtained in eastern Africa from a pooled analysis of trials [32], and, consistent with previous reports, a low CD4+ cell count was a significant risk factor for PNIM [32, 33]. Although excluded infants had a lower mean birth weight, the percentage of LBW was similar among both groups, and other characteristics between excluded and included infants were similar as well. Deaths among the excluded infants were not associated with placental malaria. Furthermore, placental malaria was not linked with known factors that have been associated with infant HIV disease progression, such as maternal viral load and maternal CD4+ cell count [12, 33, 34]. Our findings about the effect of placental malaria and infant malaria on PNIM are consistent with reports from other studies [19, 27]. In summary, in this study population of infants of HIV-seropositive women, PNIM was associated with infant HIV infection, moderate to severe infant anemia, LBW, low SES, and low maternal CD4+ cell count. Our results do not confirm the findings of Bloland et al. [10] and do not support our hypothesis that placental malaria may enhance HIV disease progression in the HIV-infected infant. By contrast, we found that infants born to HIV-infected mothers with placental malaria do not have an increased risk of PNIM and that malaria in the HIV-infected infant may further contribute to a protective effect from PNIM, which suggests a complex relationship between maternal and infant immune responses to malaria and HIV. The role of placental malaria in the context of HIV and its effect on PNIM merits further study.
There is geographic overlap between HIV and malaria in sub-Saharan Africa. In areas where malaria is endemic, pregnant women have a higher risk of malaria than nonpregnant women, and this risk is further increased among HIV-infected women [6]. Although these malaria infections are usually asymptomatic, parasites sequester in the placenta, and placental malaria is associated with low birth weight (LBW), intrauterine growth retardation, prematurity, and maternal and infant anemia [7–9].
Malaria is a major contributor to infant mortality in sub-Saharan Africa, directly through infant illness and indirectly through placental malaria and its adverse effects. The effect of the combination of maternal HIV infection and malaria during pregnancy on infant survival is not clear [6]. An early study in Malawi suggested that placental malaria was a risk factor for postneonatal infant mortality (PNIM) in children born to HIV-infected women [10]. Malaria, like other coexisting infections, can cause temporary increases in HIV load [11]. It was hypothesized that PNIM could have been increased either because placental malaria increased MTCT of HIV-1 or because placental malaria enhanced the progression of HIV disease in infected infants directly or indirectly (if placental malaria would be a marker for another disease leading to infant death, such as infant malaria). The HIV vertical transmission study in Kisumu was designed to examine these questions. We previously reported that placental malaria was not associated with increased MTCT of HIV but, by contrast, was found to be protective [12]. In the present article, we study the effect of placental malaria, infant malaria, and anemia on PNIM among the infants.
SUBJECTS AND METHODS
Study site and screening procedures. The study was conducted at the Nyanza Provincial General Hospital in Kisumu, western Kenya; enrollment lasted from June 1996 to August 2000, and infant follow-up ended in August 2001. Screening procedures have been described elsewhere [12]. Briefly, healthy pregnant women with an uncomplicated singleton pregnancy of 32 weeks' gestation were invited to participate. After informed consent was obtained and HIV counseling performed, a questionnaire on medical and obstetric history was completed, and blood was obtained for HIV testing. All screened women received routine antenatal care [13] and were encouraged to deliver at the hospital; 50% did, which reflects the low rate of deliveries at health care facilities in this area (37.4%) [14]. For women who gave birth in the hospital, placental smears and blood for maternal hemoglobin and viral load determinations were collected. Within 24 h of birth, infants were weighed, and their gestational age was assessed [15].
Enrollment in the follow-up study. All HIV-seropositive mothers and their normally delivered, live-born infants were eligible for enrollment in the follow-up study. One month postpartum, maternal blood was collected for the determination of CD4+ cell counts. Infants were scheduled to be seen every 4 weeks until the age of 1 year or death. During routine visits, we obtained information on the health of the infant during the preceding month. Capillary blood was collected by finger stick for a blood smear, hemoglobin determination, and polymerase chain reaction (PCR) testing for HIV. CD4+ cell counts were not determined in infants. Infants with malaria parasitemia were treated, regardless of clinical symptoms, with an appropriate antimalarial (sulfadoxine-pyrimethamine [SP] or amodiaquine). Clinical staff treated infants with anemia or complaints in accordance with their findings [9]. If a routine visit was missed, we visited the participant's home to determine whether the caretaker remained interested in participating and to assess the vital status of the infant. For infant deaths, we obtained additional information using verbal autopsy.
Laboratory procedures. Details on standard procedures for blood smears, hemoglobin determination, and maternal HIV testing have been reported elsewhere [12]. Maternal CD4+ cell counts were assessed using commercial, dual-label monoclonal antibodies (Becton-Dickinson Immunocytometry) and standard fluorescence-activated cell sorting analysis after whole-blood lysis [16]. The maternal HIV-1 load was determined in the delivery sample using the Roche Amplicor HIV-1 monitor test (version 1.0; Roche Diagnostics), which has a quantification limit of 400 viral copies/mL. HIV testing of the infants was done by PCR of proviral DNA extracted from peripheral blood mononuclear cells [17].
Definitions.
PNIM was a death occurring between 29 and 364 days of delivery. HIV-positive infants were infants of HIV-seropositive mothers who had 2 consecutive positive PCR tests with the first positive PCR test at age 4 months; HIV-negative infants were infants of HIV-seropositive mothers who had 2 consecutive negative PCR tests and for whom the PCR test at the last visit was negative. Infants for whom we had insufficient PCR data to determine their status were excluded. To obtain a homogenous group of HIV-infected infants, we excluded infants who had their first positive PCR test after the age of 4 months; the different timing of HIV transmission may have resulted in a different immunological status and susceptibility to infectious diseases.
Malaria in infants was defined as the presence of asexual-stage parasites in thick smears, independent of the presence or absence of clinical signs and symptoms and independent of species. Moderate to severe anemia among infants was defined as a hemoglobin level <8 p =" .2),">
Ethical review.
The study protocol was approved by the review boards of the Kenya Medical Research Institute, Nairobi; the Centers for Disease Control and Prevention, Atlanta, GA; and the Academic Medical Center of the University of Amsterdam, The Netherlands. During the study years, programs for the prevention of MTCT had not yet been introduced in the hospital; this started late 2000, after enrollment of infants had finished [12].
RESULTS :
Description of the study population. Infants from 835 HIV-seropositive women were enrolled. Of these, 265 infant/mother pairs were excluded: 165 infants never made a follow-up visit, 77 infants visited once only, 6 infants had an indeterminate HIV status despite 2 visits, and 17 infants seroconverted after the age of 4 months. The 265 excluded infants had a significantly lower mean birth weight (table 1). Although 27 of the excluded infants were known to have died, none of the 17 infants who seroconverted after the age of 4 months died. The prevalence of placental malaria among excluded infants who died or survived was 29.6% and 23.5%, respectively (P = .5).
Table 1. Characteristics of included and excluded HIV-seropositive mothers and their infants for the analysis of factors associated with postneonatal infant mortality, Kisumu, Kenya, 1996–2001.
The majority of the mothers of included infants had a maternal CD4+ cell count 500 cells/L (table 1). Of the 570 included infants, 67.7% completed the study. Primiparae and mothers with premature or HIV-negative infants were less likely to complete the study (P = .04, P = .01, and P = .04, respectively); women who did not complete the study had a higher median CD4+ cell count and a lower median log10 viral load (P = .05 and P = .01, respectively).
Placental malaria was detected in 141 women (24.7%). All infections were with Plasmodium falciparum, and there were 3 mixed infections with P. malariae. A blood smear and hemoglobin data were not available for 5 and 85 visits, respectively, of the 5083 visits that were made by the infants. Thirteen percent of blood smears were positive; 7 mixed infections with P. malariae and P. falciparum were detected, and all other infections were with P. falciparum. Moderate to severe anemia was diagnosed at 5.2% of the routine visits.
PNIM. Of the 570 infants, 75 (13.2%) died during the postneonatal period. One-third of the deaths occurred at the age of 4–5 months (table 2). As expected, PNIM was significantly more common among HIV-positive infants than among HIV-negative infants (figure 1 and table 2). Factors associated with PNIM in univariate and multivariate Cox regression models are shown in table 3. The adjusted HR (AHR) for placental malaria overall was 0.77 (95% confidence interval [CI], 0.43–1.39). However, effect modifications were observed between placental malaria and infant HIV status (P = .06 for the interaction term) and between infant anemia and infant HIV status (P = .03 for the interaction term).
RESULTS :
Description of the study population. Infants from 835 HIV-seropositive women were enrolled. Of these, 265 infant/mother pairs were excluded: 165 infants never made a follow-up visit, 77 infants visited once only, 6 infants had an indeterminate HIV status despite 2 visits, and 17 infants seroconverted after the age of 4 months. The 265 excluded infants had a significantly lower mean birth weight (table 1). Although 27 of the excluded infants were known to have died, none of the 17 infants who seroconverted after the age of 4 months died. The prevalence of placental malaria among excluded infants who died or survived was 29.6% and 23.5%, respectively (P = .5).
Table 1. Characteristics of included and excluded HIV-seropositive mothers and their infants for the analysis of factors associated with postneonatal infant mortality, Kisumu, Kenya, 1996–2001.
The majority of the mothers of included infants had a maternal CD4+ cell count 500 cells/L (table 1). Of the 570 included infants, 67.7% completed the study. Primiparae and mothers with premature or HIV-negative infants were less likely to complete the study (P = .04, P = .01, and P = .04, respectively); women who did not complete the study had a higher median CD4+ cell count and a lower median log10 viral load (P = .05 and P = .01, respectively).
Placental malaria was detected in 141 women (24.7%). All infections were with Plasmodium falciparum, and there were 3 mixed infections with P. malariae. A blood smear and hemoglobin data were not available for 5 and 85 visits, respectively, of the 5083 visits that were made by the infants. Thirteen percent of blood smears were positive; 7 mixed infections with P. malariae and P. falciparum were detected, and all other infections were with P. falciparum. Moderate to severe anemia was diagnosed at 5.2% of the routine visits.
PNIM. Of the 570 infants, 75 (13.2%) died during the postneonatal period. One-third of the deaths occurred at the age of 4–5 months (table 2). As expected, PNIM was significantly more common among HIV-positive infants than among HIV-negative infants (figure 1 and table 2). Factors associated with PNIM in univariate and multivariate Cox regression models are shown in table 3. The adjusted HR (AHR) for placental malaria overall was 0.77 (95% confidence interval [CI], 0.43–1.39). However, effect modifications were observed between placental malaria and infant HIV status (P = .06 for the interaction term) and between infant anemia and infant HIV status (P = .03 for the interaction term).
Table 2. Postneonatal infant deaths among infants of HIV-seropositive women by infant HIV-status, Kisumu, Kenya, 1996–2001.
Figure 1. Kaplan-Meier survival curve of postneonatal infant mortality by infant HIV status and placental malaria, Kisumu, Kenya, 1996–2001. Log rank tests: A vs. B, P = .7; A vs. C, P = .2; A vs. D, P < .001; B vs. C, P = .4; B vs. D, P < .001; C vs. D, P = .07. Neg, negative; pos, positive. Table 3. Risk factors for postneonatal infant mortality by infant HIV-status among infants of HIV-seropositive women, Kisumu, Kenya, 1996–2001. Placental malaria. HIV-positive infants born to mothers with placental malaria tended to be more likely to survive than those born to mothers without placental malaria (AHR, 0.34 [95% CI, 0.10–1.10]; P = .07, log-rank test) (table 3 and figure 1). Placental malaria was not associated with PNIM in HIV-negative infants (AHR, 1.29 [95% CI, 0.62–2.66]) (table 3). Infant anemia and infant parasitemia. Moderate to severe infant anemia was a risk factor for PNIM among HIV-negative infants but not among HIV-positive infants (table 3). There was no interaction between the infant's HIV status and the effect of infant malaria: malaria parasitemia at a routine visit was a protective factor against PNIM among both HIV-infected and HIV-uninfected infants (table 3). Among HIV-positive infants who died, median survival among 10 infants with at least 1 episode of malaria was 274 days, compared with 134 days among 29 infants without any episodes of malaria (P < .01, Mann-Whitney U test). Among HIV-negative infants, median survival was 263 days (10 infants) and 160 days (26 infants), respectively (P = .08, Mann-Whitney U test). Parasite prevalence among infants generally increases during the first year of life, and it increased in this study population, from 7% at 4 weeks to 22.0% at 44 weeks of age. To assess whether the association between infant malaria parasitemia and PNIM was not merely a proxy for age, we restricted the analysis to infants who completed the first 6 visits; the overall AHR with respect to malaria parasitemia and PNIM remained indicative of protection (0.53 [95% CI, 0.18–1.56]). Infants born to mothers with placental malaria have been reported to have a higher risk of infant malaria [18] and anemia [9]. We therefore determined whether the observed association between infant malaria and PNIM could partially be explained by the effect of placental malaria, which, as shown above, was also associated with PNIM, although the direction of the association differed between HIV-negative and HIV-infected infants. Removal of placental malaria from the models did not substantially change the HR between PNIM and infant parasitemia or anemia (AHR, 0.36 [95% CI, 0.10–1.23] and AHR, 5.06 [95% CI, 1.99–12.90] for parasitemia and anemia, respectively, in HIV-negative infants; AHR, 0.34 [95% CI, 0.08–1.44] and AHR, 1.02 [95% CI, 0.30–3.42] for parasitemia and anemia, respectively, in HIV-positive infants). We examined whether the association between malaria parasitemia was affected by treatment with SP, the antimalarial that was predominantly used in the study (75%) to treat parasitemia. The inclusion of a variable indicating SP use during the month preceding the visit did not change the association between infant malaria and PNIM in any of the models (AHR, 0.72 [95% CI, 0.31–1.67] and AHR, 0.43 [95% CI, 0.13–1.41], for HIV-positive and HIV-negative infants, respectively, adjusted for the factors in the adjusted models in table 3). Because infant parasitemia is associated with anemia, we further examined the effect of these variables in the model among HIV-negative infants. We created a variable indicating whether both, either, or neither of these factors were present at the visit. Compared with the absence of malaria parasitemia or of moderate to severe anemia, the combination of moderate to severe anemia and parasitemia was not significantly associated with PNIM (AHR, 1.13 [95% CI, 0.15–8.53]; P = .9), whereas anemia alone (i.e., without parasitemia at the visit) remained a significant factor (AHR, 5.80 [95% CI, 2.19–15.38]; P < .01), and malaria parasitemia alone continued to be associated with a protective effect (AHR, 0.49 [95% CI, 0.12–2.08]; P = .3). Maternal geometric mean viral load and PNIM. Infant HIV infection and death were associated with a significantly higher maternal viral load (table 4). Placental malaria was not associated with a significantly higher viral load. However, among women who transmitted HIV, maternal viral load was significantly higher when placental malaria was present. Among HIV-positive infants, the geometric mean maternal viral load among the 14 survivors of mothers with placental malaria (16,846 copies/mL) was not significantly different from the viral load among the 31 infants who died and whose mothers did not have placental malaria (8561 copies/mL; P = .4), whereas it was significantly higher than the maternal viral load of the 54 survivors whose mothers did not have placental malaria (3849 copies/mL; P = .02), which indicates that placental malaria may change the association between a high maternal viral load and HIV progression in the infected infant. The mothers with placental malaria of the 2 HIV-infected infants who died had very high maternal viral loads, and this was significant, compared with the HIV-infected survivors of mothers without placental malaria. Table 4. Associations between the geometric mean maternal viral load at the time of delivery, placental malaria, and postneonatal infant mortality, Kisumu, Kenya, 1996–2001. Probable causes of death. For 63 deaths, a probable cause of death was assigned using verbal autopsy. There were no significant differences by infant HIV status, but numbers were small (figure 2). Figure 2. Probable causes of postneonatal infant deaths by infant HIV status among infants of HIV-seropositive women by use of verbal autopsy, Kisumu, Kenya, 1996–2001. Verbal autopsy information was reviewed independently by 3 medical workers (clinical officers or doctors), who each assigned a diagnosis. If 1 diagnosis was given by 2 reviewers, it was assigned as the cause of death. If all 3 causes were different, a fourth reviewer was used to adjudicate. If no verbal autopsy information was available, the cause of death was labeled as undetermined. Malaria and anemia were combined, and HIV-positive infants were compared with HIV-negative infants (P = .06, 2-tailed Fisher's exact test). DISCUSSION Our results underscore that the complex interaction between HIV and malaria is challenging to study. By contrast to the earlier study by Bloland et al. [10], we did not find that placental malaria was a risk factor for PNIM among infants of HIV-seropositive women. Overall, the risk on PNIM was actually lower, although not significantly so, in infants born to HIV-infected mothers with placental malaria (AHR, 0.77 [95% CI, 0.43–1.39]), and this remained so after adjustment for potential confounders, including maternal CD4+ cell counts and LBW. These results are consistent with those of another study [19] that reported a nonsignificant protective effect of placental malaria against PNIM among infants born to HIV-seropositive women (HR, 0.39 [95% CI, 0.11–1.38]). We previously reported that MTCT was significantly lower in infants born to mothers with placental malaria than in those without placental malaria [12]. Several explanations can be considered for the association between placental malaria in HIV-positive women and increased survival time of HIV-infected infants. First, we speculate that prenatal exposure to malaria may modulate the immune system to generate protective immune pathways (involving innate or classical T cell–mediated pathways), which may slow the progression of HIV-1 and contribute to prolonged survival. There is considerable evidence that maternal exposure to malaria modulates immune responses to malaria in utero [20–23]. Second, it has recently become known that HIV-mediated disease progression is correlated with the down-regulation of a regulatory T cell (Treg) subset (Foxp3+CD4+CD25hi T cells), which may be critical for maintaining CD4+ cell counts [24]. It has been shown recently that placental malaria increases the number of Treg cells in cord blood [25], and this may help protect against any rapid decrease in CD4+ cell counts in infants born to HIV-positive mothers with placental malaria. Third, HIV/malarial coinfection can modulate the cytokine environment in the placenta and/or fetus, which may reduce the initial HIV load or slow HIV replication in the fetus. We have shown previously that HIV/malarial coinfection up-regulates (compared with HIV-positive malaria-negative women) some chemokines, including macrophage inflammatory protein (MIP)–1, that can compete with the CCR5 receptor for HIV entry [25, 26]. We were also interested in establishing whether malaria in the HIV-positive infant was associated with enhanced HIV disease progression. Infant malaria parasitemia was not a risk factor for PNIM—indeed, median survival was higher among HIV-infected children with at least 1 documented malaria episode than in children with no malaria, consistent with the results of a previous study in Uganda [27]. Because all infections were treated regardless of the presence of symptoms, frequent treatment with SP may have provided time windows of prophylaxis and reduced subsequent malaria and morbidity in these infants; SP can both treat and protect against malaria because of the long half-life of its components [28]. SP may have an effect on other infections as well (Streptococcus pneumonia, Toxoplasma gondii, and Pneumocystis jiroveci). However, when we included the use of SP in the models, it did not change the direction of the association between infant malaria and PNIM, which indicates that the use of SP is not an explanation for this association. It is possible that low-grade infection with malarial parasites in infants triggers immune responses to malaria that also result in reduced infant HIV-1 loads. Malaria is known to shift the immune system toward Th1-type responses, and progression of HIV-infection has been associated with a shift from a Th1-type to a Th2-type response [29]. In addition, malarial infection can activate chemokines such as MIP-1 and MIP-1, among others [30], that can compete for the HIV entry receptor CCR5 and thereby slow the progression of HIV infection in infants. As explained earlier, malarial infection can also activate the Treg population, which can modulate HIV-associated disease progression [31]. Another possibility is that malaria infection activated innate immune responses, which can help to control HIV-associated opportunistic infections, leading to increased survival time. Among HIV-negative infants of HIV-seropositive women, moderate to severe infant anemia was a significant risk factor for PNIM. Infant anemia may be the culmination of a sequence of events whereby maternal HIV infection, placental malaria, infant malaria, and SES may all contribute. Whatever the contributing factor, moderate to severe anemia in infants can be detected and should be responded to, particularly among infants of HIV-positive women. Our study had several limitations. First, we only enrolled HIV-infected women with no AIDS-defining symptoms; PNIM among women with progressed HIV disease is likely to be higher than our present findings. Our measurement of parasitemia by microscopic examination of smears was inexact compared with other methods, may have misclassified particularly low-density parasitemias, and did not identify intervillous inflammation, but this would have resulted in bias toward the null. The number of HIV-infected infants born to mothers with placental malaria was small; this precludes more-definitive answers and does not rule out a chance finding. An infant needed to make at least 2 follow-up visits for us to be able to make an HIV diagnosis, and loss to follow up was considerable, which may have biased our results. However, the reported PNIM among HIV-infected infants was comparable to results obtained in eastern Africa from a pooled analysis of trials [32], and, consistent with previous reports, a low CD4+ cell count was a significant risk factor for PNIM [32, 33]. Although excluded infants had a lower mean birth weight, the percentage of LBW was similar among both groups, and other characteristics between excluded and included infants were similar as well. Deaths among the excluded infants were not associated with placental malaria. Furthermore, placental malaria was not linked with known factors that have been associated with infant HIV disease progression, such as maternal viral load and maternal CD4+ cell count [12, 33, 34]. Our findings about the effect of placental malaria and infant malaria on PNIM are consistent with reports from other studies [19, 27]. In summary, in this study population of infants of HIV-seropositive women, PNIM was associated with infant HIV infection, moderate to severe infant anemia, LBW, low SES, and low maternal CD4+ cell count. Our results do not confirm the findings of Bloland et al. [10] and do not support our hypothesis that placental malaria may enhance HIV disease progression in the HIV-infected infant. By contrast, we found that infants born to HIV-infected mothers with placental malaria do not have an increased risk of PNIM and that malaria in the HIV-infected infant may further contribute to a protective effect from PNIM, which suggests a complex relationship between maternal and infant immune responses to malaria and HIV. The role of placental malaria in the context of HIV and its effect on PNIM merits further study.
May 16, 2007
Extra ordinary architechts
The tower's façade is to be built from a new generation of vacuum glazing that will only come on the market in 2008. The new top-quality windows are meant to largely shield the interior of the tower from outside heat -- indispensable in a region where outside temperatures can reach 50 degrees Celsius (122 degrees Fahrenheit) in the summer. This is made possible by a new breakthrough in the quality of the materials used: The new vacuum glazing windows transmit as much as two thirds less heat compared to today's products. The architects chose an ancient Persian architectural feature as their model. Hundreds of years ago, wealthy merchants erected wind towers on the roofs of their houses, an idea which was eventually exported to the Arab world. The buildings, which have now become tourist attractions, have a natural air conditioning system. Lateral openings in the towers suck in cool air like a chimney. The heavier cool air sinks down and displaces the lighter hot air, creating a comfortable temperature inside the living space despite the scorching sun. Gerbers's design is designed to function in a similar way: The negative pressure created by winds breaking along the tower will suck the spent air from the rooms out of the building via air slits in the façade. The plan is for fresh air to be pumped into the interior of the building by means of a duct system at the same time. Seawater will be used to pre-cool the air. Three large cooling units in the giant building's cellar will eventually lower the temperature to a comfortable 18 degrees Celsius (64.4 degrees Fahrenheit). Transparent ducts will channel the fresh air into spacious atriums and from there into the corridors and offices. The building's designers want to use high-quality steel ropes to suspend hanging gardens inside the air ducts, transforming a feature which is often regarded as an architectural blemish and hidden behind sheet metal in other buildings. At the same time, the underground cooling center also cools the water in the pipelines running through the underside of each floor's ceiling. The system of tubes is designed to be a modern air-conditioning system which cools gently without unpleasant air currents. The Burj al-Taqa seems like the most recent example of a trend that has been observable for some time. In large cities such as Chicago, New York or Paris, environmentally friendly skyscrapers are being built that win ecological awards and apparently herald a new green wave in the construction of tall buildings.
Burj al-Taqa's cylindrical shape is designed to expose as little surface area to the sun as possible. A protective solar shield reaches from the ground to the roof, covering 60 degrees of the giant circular building. It protects the side most affected from the sun's glaring rays, making sure that none of the rooms are exposed to direct sunlight. The diffuse light on the other sides of the building is tempered by a mineral coating on the windows.
This skyscraper, to be built in Dubai, is called the Burj al-Taqa ('Energy Tower'), and it will produce 100% of its own power. The tower will have a huge (197 foot diameter) wind turbine on its roof, and arrays of solar cells that will total 161,459 square feet in size. Additional energy is provided by an island of solar panels, which drifts in the sea within viewing distance of the tower.
May 15, 2007
Biography of Anna kournikova
Biography
Anna was born in Moscow, Russia, June 7, 1981. Anna is a world class star professional tennis player. Her lean athletic body is truly distracting. Anna's parents who travel with her, are Alla and Sergei, and they refer to her as "Murzik", that means "my little pet" in Russian. She received her first tennis racquet at 5 years old when her parents sold their TV to buy her a present for Christmas. She graduated from a Russian high school in 1997.
At nine years old, Anna was spotted playing in the Kremlin Cup in Moscow, and was offered the opportunity to train at the Nick Bollettieri Tennis Academy in Bradenton, Florida. When Anna was only 13 years old she made it to the final in the Rolex Orange Bowl tournament. There, she unfortunately lost to 18 year old Spaniard Marion Ramon. The revenge for Anna would come as soon as the next year. Then, Anna made it all the way to the final again and there she defeated Sandra Nacuk of Yugoslavia. In 1999, she won her first Grand Slam title with Martina Hingis at doubles in the Australian Open. Though a top ten singles player, Anna's only Grand Slam title to date came in the 1999 Australian open Ladies' Doubles with Hingis. Anna is one of the most glamorous of the new generation of women players.
Anna says she would like to be an actress. She also likes reading, listening to music, watching TV, dancing, going to parties, swimming, giving tennis coaching to children, and she is also quite interested in ice hockey. Anna has collected dolls from every country she has visited.
Though not yet the world's best tennis player, Anna has gained extra popularity due to her good looks and sometimes extravagant behavior and posing as a model. In 2000, she was named the most searched for athlete on the internet and for many years has been the world's best known female athlete.
Presently endorsed by Adidas, Yonex, Berlei the famous sports bra, Omega, and Lycos. Anna has certainly come a long way from the days when her parents could hardly afford to buy her a tennis racket.
Anna's earnings for 1999 stood at $11 million for endorsements alone, and they have surely increased by now, making her the highest paid female tennis player. As a cover girl, Anna was named one of Peoplemagazine's 50 Most Beautiful People in the World in 1998, and graced the cover of Sports Illustrated's June 2000 edition.
Anna has raised the profile of the ladies game to new levels, and she is a major worldwide celebrity, with a lifestyle to match her supermodel looks.
At nine years old, Anna was spotted playing in the Kremlin Cup in Moscow, and was offered the opportunity to train at the Nick Bollettieri Tennis Academy in Bradenton, Florida. When Anna was only 13 years old she made it to the final in the Rolex Orange Bowl tournament. There, she unfortunately lost to 18 year old Spaniard Marion Ramon. The revenge for Anna would come as soon as the next year. Then, Anna made it all the way to the final again and there she defeated Sandra Nacuk of Yugoslavia. In 1999, she won her first Grand Slam title with Martina Hingis at doubles in the Australian Open. Though a top ten singles player, Anna's only Grand Slam title to date came in the 1999 Australian open Ladies' Doubles with Hingis. Anna is one of the most glamorous of the new generation of women players.
Anna says she would like to be an actress. She also likes reading, listening to music, watching TV, dancing, going to parties, swimming, giving tennis coaching to children, and she is also quite interested in ice hockey. Anna has collected dolls from every country she has visited.
Though not yet the world's best tennis player, Anna has gained extra popularity due to her good looks and sometimes extravagant behavior and posing as a model. In 2000, she was named the most searched for athlete on the internet and for many years has been the world's best known female athlete.
Presently endorsed by Adidas, Yonex, Berlei the famous sports bra, Omega, and Lycos. Anna has certainly come a long way from the days when her parents could hardly afford to buy her a tennis racket.
Anna's earnings for 1999 stood at $11 million for endorsements alone, and they have surely increased by now, making her the highest paid female tennis player. As a cover girl, Anna was named one of Peoplemagazine's 50 Most Beautiful People in the World in 1998, and graced the cover of Sports Illustrated's June 2000 edition.
Anna has raised the profile of the ladies game to new levels, and she is a major worldwide celebrity, with a lifestyle to match her supermodel looks.
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