Posted by 2011-07-29T16:52:51+00:00"> – July 29, 2011

Walking may be the best all-around exercise, but as far as bone building goes, strength training is the cream of the crop. The pull of muscle against bone stresses a bone, and that kind of stress is what makes a bone become stronger. Impact also strengthens a bone, but the impact that comes from running or jumping, say, can be otherwise harmful to the body. Muscle working against gravity provides another kind of impact for the bones, stimulating bone formation and slowing loss. Strength training with free weights (including light hand and ankle weights) or weight machines is the most direct way to provide that stress and impact of muscle on bone, which is what makes it ideal for building and preserving bone density.
We know that weight lifters have much denser bones in their back and legs than do runners, for example. Studies do show that walking prevents bone loss in the spine, but strength training has been proved to build bone mass in the spine and hip. One study that (deservedly) got a lot of media attention followed a group of postmenopausal women who were generally healthy—but sedentary. None were taking HRT, or any other bone-related medicines, or taking calcium supplements. Half performed a simple weight-lifting routine twice a week, while the other half stuck with their couch potato ways. After one year, the weight lifters built their bone mass 1 percent on average, at both the hip and spine. That compares favorably to what you’d see with HRT alone. To give you perspective, consider this: the women who did not lift weights lost up to 2.5 percent of their bone mass over the same time period— and also lost muscle mass and gained body fat and weight. The weight lifters became much more active in general (as the researchers calculated it, a 27 percent increase), while the sedentary group became less active. The weight lifters lowered their body fat, gained muscle, and had better balance and more strength. And here’s a wonderful bonus: the researchers had the daughters of the women who lifted weights come in and do the tests their mothers were acing. In every case, the weight-lifting women outperformed their own daughters!
I only wonder how much better they might have done if they also took calcium. Or HRT: another study looked at women taking HRT after surgical menopause, and found that after a year of strength training the average increase in bone density was 4 percent in the wrist and 8 percent in the spine!
Building muscle also increases your metabolic rate—that is, how fast your body burns calories at rest. Think of your metabolism like a fire: a large fire produces more heat and uses more fuel than a small fire. Exercise stokes the flames of your metabolism. That is increasingly important as you age, because your metabolism usually slows as you get older, partly because of muscle loss. Muscle mass begins to decrease in midlife unless you are active. Strength drops, on average, about 15 percent during your sixties, and another 15 percent in your seventies, and 30 percent each successive decade. This is not a result of aging, but of inactivity.
Muscle uses more calories to maintain itself than fat does. The stronger you are (the more muscle you have), the more calories you will burn at all times and the easier it will be to control your weight—and the more you will need to eat to stay at the same weight. Weight-loss diets typically fail because you don’t permanently change the way you eat and work. Restricting the number of calories you take in results in muscle loss, not fat loss. You also end up in double jeopardy because if you just reduce the calories you take in (as opposed to increasing your body’s caloric requirement, with exercise), your metabolism slows to accommodate only the lower number of calories. So when you increase them again (going “off ” the diet), all you will have done is set yourself up for immediate weight gain.
Muscle also helps the body use sugar efficiently, so strength training is an important addition to a diabetes treatment or prevention program. Losing muscle reduces your sugar tolerance. Strength training has been shown to prevent weight gain, fractures, and injury, and to lower the risk of heart attack and colon cancer in ways aerobic exercise alone does not. Loss of muscle impairs your body’s ability to regulate its temperature, too. Just one strength workout a week is enough to prevent the muscle loss that accompanies aging, even in devoted athletes who focus only on cardiovascular exercise. Increasing your strength lowers the risk of injury to joints and muscles. It also improves your balance and so reduces your risk of falling, which in turn reduces the risk of fracture.
As with every other strategy in this book, it is never too late to benefit from strength training. One study of people in their 80s and 90s living in nursing homes who exercised with weight machines three times a week for just eight weeks showed improvements in strength, balance, and walking speed. Even people who are already frail can, with proper exercise using light weights, build up enough leg strength to walk without a cane. I’ve no doubt of the bone benefits that went along with these results, even though they weren’t tracked by the researchers.
Studies show that two 15-minute strength workouts a week is enough to build bone density. As you’ll see in the next chapter, you can target all the major muscle groups with a very compact routine, which should take you no more than about 20 minutes once you’ve got it down. If you prefer machines to hand weights, a thorough workout may take a bit longer just because you need time to adjust each piece of equipment properly before you use it. You should rest at least one day between sessions to allow your muscles to recover, because it is during the recovery period that muscle actually grows. If you want to exercise every day, just alternate which group of muscles you work on which days—that is, do upper body one day and lower body the next. Once you start a regular routine with weights or weight machines, your bones will be denser before a year is up. But if you stop, you’ll start losing bone again immediately. As with dieting, you have to think of embarking on a fitness program that includes strength training as a lifetime plan, not a solution you achieve in a set time period, then don’t have to work on anymore.


Posted by 2011-07-18T16:41:11+00:00"> – July 18, 2011

Coping with anxiety is a crucial step in acceptance of your child and her problem. You may have sensed the teacher’s anxiety when you first told her about your child’s seizures, or perhaps you simply worried how she might react. Maybe her anxiety is a consequence of lack of information. Perhaps she has been exposed to the myths. Perhaps she once had a child in her classroom who fell and hit his head during a seizure. You may be able to reassure the teacher by saying, “I know that you’re worried that Steve will fall and be injured and that I’ll be furious and accuse you of not looking out for him. But I won’t. We’ll both be upset that it happened. But we both have to realize that Steve needs to be in school with his classmates. His seizures are really infrequent, and he usually has a little warning. We need to convince him to let you know that warning has come so that he can be in a safe place. We have to let him take some chances if he’s to have the opportunity to be a normal child.”
This kind of dialogue is critical to an understanding and working relationship between parent, child, and teacher. Teachers often need help in coming to terms with their anxiety, just as you do. Acceptance of the realities and accurate information can do a lot to relieve anxiety for everyone. When you have come to believe what you just said, you have come a long way in accepting your child and his epilepsy.


Posted by 2011-07-05T09:55:35+00:00"> – July 5, 2011

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Posted by 2011-07-03T16:27:09+00:00"> – July 3, 2011

Low HDL cholesterol
HDL cholesterol is the so called ‘good’ cholesterol and can be measured from a fasting blood sample. It has a very high affinity to bind cholesterol and can remove cholesterol from the blockages.
HDL cholesterol level in the blood should be maintained above 40 mg per 100 ml of blood to prevent heart disease.

High blood pressure
The normal blood pressure in adults is between 100/60 to 140/90 mm Hg. If the blood pressure is consistently more than 140/90 on two or more separation occasions, it is called high blood pressure or hypertension. It is a very common disease and about 20% to 30% of adults suffer from hypertension all over the world, but a majority of the people is not even aware that they have this disease because it does not produce any symptoms in a vast number of cases. This is why this disease has been correctly called the ‘silent killer’. High blood pressure puts an extra strain on the heart and the arteries supplying blood to the other organs of the body. Many diseases are caused by high blood pressure such as heart attacks, heart failure, kidney failure, stroke (damage to the brain), and damage to the eyes. Higher the blood pressure, greater are the chances of getting the above diseases, especially heart attack.
High blood pressure can be classified as mild, moderate and severe. It is also one of the major causes of deposition of cholesterol and fat in the coronary arteries. It damages the endothelial lining of the arteries, making them more prone to fat deposition. Besides a high intake of salt, psychological stresses are also implied as important causes of high blood pressure.


Posted by 2011-06-29T16:19:54+00:00"> – June 29, 2011

When allergy-proofing your house, the bedroom is the most important place to start. It is important to air your bed and bed coverings regularly between washes. Bedding should be aired outdoors on sunny days — dust mites are sensitive to ultraviolet radiation and frequent exposure to the sun will reduce their numbers. Mattresses should be vacuumed once a week and blankets dry cleaned or laundered monthly. All bedding should be washed in hot water as mites are not removed in cold water.
Non-toxic, anti-allergenic sprays for mattresses and bedding and special mite-proof mattress covers are commercially available through Allersearch and other outlets. (The efficacy of these products has yet to be demonstrated in the prevention of asthma, but some asthmatics say they are helpful.) Areas around and underneath beds and bedroom furniture should be wiped clean regularly with a damp cloth.
If possible, do not have a carpet in the bedroom. Polished wood, cork or tiles are easier to clean and do not gather dust. Curtains and rugs should be made of synthetic, easy to wash materials. Instead of curtains, consider covering windows with plastic or wooden Venetian blinds; these cannot be penetrated by dust and are easy to wipe down.
Never allow an animal into the bedroom, even if it has the run of the rest of the house. (In most cases, it is best to keep pets outside at all times.) Keep the bedroom free of cigarette smoke and all other chemical odours and fumes. Keep windows and doors shut on windy days, particularly when there is pollen in the air. The house should also be kept completely closed on days of high pollution levels.


Posted by 2011-06-19T16:18:33+00:00"> – June 19, 2011

What causes RA? Researchers, physicians, epidemiologists, and theologians have devoted an enormous amount of time and energy in trying to answer this question. Despite their efforts over the past one hundred years (since the question was first posed, by Sir Archibald Garrod in 1858, when he named rheumatoid arthritis), no single cause of RA has been identified.
Recent studies have given us some clues to the cause of RA, however. There is evidence, for example, that genetics may play a role in its development. Studies have revealed that one specific genetic marker, called HLA-DR4, appears on the white blood cells of approximately 65 percent of people with RA. RA patients with this genetic marker tend to have more severe arthritis than those without it. However, 25 percent of people with HLA-DR4 have no RA at all, so genes are not the whole story. Other genetic markers are also being studied, with similar results. (Although genes may provide a clue to the cause of RA, most people with RA do not know whether they have these genetic markers. Currently, only physicians who are involved in a university-based research project test for the presence of genetic markers.)
Because not everyone who has the genetic markers described above develops RA, we must consider the possibility that a virus, bacteria, or another substance triggers the development of RA in people made susceptible by their genetic makeup. Over the past century, scientists have searched for a link between hundreds of different infections and the development of RA. (Late in the 1920s, for example, tuberculosis was the suspected culprit.) So far, not one of these scientific studies has proven that a virus, bacteria, or other infectious agent can cause RA.
As with other diseases, one concern is whether someone can “catch” RA from another person. In 1950, two investigators tried to “transmit” RA to volunteers by injecting into their joints fluid taken from the joints of people with RA (Levinski and Lansburg 1951). Because none of the volunteers developed RA, scientists were able to conclude that RA is not a persistent infection of the joints. Although the future may show that an infectious agent triggers the onset of RA, we now know that RA is not infectious or contagious.
Recent scientific studies have focused on viruses as potential triggers for the development of KA in the susceptible person. Epstein-Barr virus for example, has been suggested as a triggering agent for RA. (We already know that Epstein-Barr virus causes mononucleosis, or “mono,” an acute illness affecting young adults which causes fever, sore throat, malaise, and swollen lymph glands.) Investigators will continue to search for the cause of RA, and maybe soon we will identify the causative agent. What is important to keep in mind is that even if an infection does trigger the development of RA, it is impossible to catch RA from someone who has it.


Posted by 2011-06-01T16:11:01+00:00"> – June 1, 2011

Some obese people may have excessive numbers of fat cells. This type of obesity, hyperplasia, usually begins to develop in early childhood and perhaps, due to the mother’s dietary habits, even prior to birth. The most critical periods for the development of hyperplasia seem to be the last two to three months of fetal development, the first year of life, and between the ages of 9 and 13. Parents who allow their children to eat without restrictions and to become overweight may be setting their children up for a lifelong excess of fat cells. Central to this theory is the belief that the number of fat cells in a person’s body does not increase appreciably during adulthood. However, the ability of each of these cells to swell and shrink, known as hypertrophy, does carry over into adulthood. Weight gain may be tied to both the number of fat cells in the body and the capacity of each individual cell to enlarge.
An average-weight adult has approximately 25 billion to 30 billion fat cells, a moderately obese adult about 60 billion to 100 billion, and an extremely obese adult as many as 200 billion. People who add large numbers of fat cells to their bodies in childhood may be able to lose weight by decreasing the size of each cell in adulthood, but the large numbers of cells remain, and with the next calorie binge, they fill up and sabotage weight loss efforts. Additional research must be conducted to determine the accuracy of these theories.


Posted by 2011-05-28T16:09:30+00:00"> – May 28, 2011

Insulin resistance can also contribute to weight gain. Insulin resistance is a condition in which receptor sites on the individual cell walls have lost the ability to receive insulin (and the attached sugars) through the cell wall where it can be used properly. The result is increased levels of insulin circulating throughout the blood accompanied by symptoms of low insulin levels. Essentially, insulin is locked out of the cells. Often, the resistance cannot be overcome by replacing the hormone and is a significant issue with many obese people.
One of the most common causes of insulin resistance is obesity itself. As fat in the body accumulates, glucose tolerance diminishes. As the cells become increasingly impervious to the effects of insulin, the whole cycle of pulling glucose into the liver and muscle cells to be burned as energy gets disrupted. In the process, thyroid function is pulled down. As a matter of fact, the whole system of burning food for energy (thus reducing the tendency to store it for future use in BAT cells) shuts down, and the weight just piles on, unimpeded by glucagon or other weight-favoring hormones.
For other people, the overconsumption of processed fats such as margarine, polyunsaturated oil, and other oils has contributed to insulin resistance.13 In a letter to the editor in The Townsend Letter for Doctors, Jeffrey Moss, D.D.S., wrote:
One of the most intriguing and least-known aspects of the insulin model of disease is that it also incorporates ingestion of certain types of fat, specifically, saturated fat, linoleic acid, long chain fatty acids (EPA, EFA, and arachidonic acid), and trans fats. This connection particularly fascinates me because even though we have talked about the dangers and benefits of the above fats, we have never before, as far as I know, been readily able to place these fats into a unified concept of disease that also includes subjects as diverse as ingestion of fruit, physical activity, and stress. . . . [One researcher] presents compelling evidence that not only does saturated fat raise insulin resistance, but linoleic acid and trans fats do the same. Since the Western diet has seen a tremendous increase in the intake of linoleic acid and trans fat due to indiscriminate use of vegetable oils and margarines, this finding is particularly significant.
Did you catch the meaning of what Moss is saying? Those of us who have stripped our cupboards bare of butter in favor of “heart healthy” margarine and corn oil are doing it all wrong! The “trans” fats to which Moss is referring are the artificially saturated fats like margarine and shortening and all foods that contain these fats. Corn and other vegetable oils (except for olive oil and other select vegetable oils) are implicated here as well. These foods are creating a problem with insulin resistance that keeps us heavy and just a little unbalanced in our blood sugar.
Aside from obesity or eating too much of the wrong kinds of fats, there is another cause of insulin resistance. We can be born with enzyme defects that prevent insulin from being taken up and used by the cells. But let’s be honest about it: Most of the time we do it to ourselves! A high-carbohydrate diet wears out the insulin-binding capacity of the cell, as can obesity or muscle inactivity. In other words, sitting around all day eating bonbons and gaining a few extra pounds wears out your body’s ability to use insulin effectively and keep circulating insulin levels down so that you’re not so prone to store those excess carbs as body fat.


Posted by 2011-05-11T16:08:25+00:00"> – May 11, 2011

It certainly is a melting pot for pathogens, just as it is still a melting pot for humans. But is the gathering of foreign pathogens in the melting pot of North America the real problem? Are the most important threats to North America coming from distant places? There certainly is no shortage of pathogens crossing international borders. A new scare surfaces almost every year. In the summer and early fall of 1999 it was the West Nile virus, which killed seven people, some horses, and several thousand crows along the eastern seaboard of the United States. Then the outbreak fizzled. Even when a full-fledged vector-borne pathogen like the dengue virus or the malaria protozoan gets into the United States, it peters out on its own. If these masters of
vector-borne transmission cannot make a go of it in humans, what chance does a West Nile virus have? It is out of its element in humans. It cannot be transmitted from human to mosquito to human even in the best of situations. It attracts attention mainly because it is exotic.
People tend to overestimate the risk of accidents that are rare but sensational—the airplane crashes—relative to the much more dangerous but commonplace accidents—the car crashes. So too we tend to overestimate the danger from the unusual when it is lethal. But statistics can correct our mistakes. People who look at the actual calculations of the probability of dying per mile traveled in an airplane can see that it is vastly less than the probability of dying per mile traveled in a car and adjust their worries accordingly. The same thing can be done with infectious diseases, though people have to spend a bit more effort in educating themselves about the diseases with known microbial causes, the microbes that cause them, and the diseases that may be caused by unknown microbes. If people do not do this extra legwork, the government and its control agencies will continue to go down the path of least resistance. If the public is more frightened about Ebola, hantavirus, Legionnaires’ disease, and West Nile virus than about the probable infectious causes of chronic diseases like cancer, stroke, heart attack, multiple sclerosis, and Alzheimer’s, then the public will get overfunding of low-level infectious threats and underfunding of high-level infectious threats.
Because the AIDS virus originated in sub-Saharan Africa, the AIDS pandemic has fixed worried attention on what might be out there ready to emerge from steamy African jungles or urban Asian swarms, just a plane ride away from the hubs of Euro-American civilization. Many leading experts have called for interventions to block this emergence. Jonathan Mann, the first head of the World Health Organization’s AIDS program, called for a worldwide early warning system “to detect quickly the eruption of new diseases or the unusual spread of old diseases.” It sounds like a good idea on the face of it, but how effective would it be? The history of disease emergence provides some clues.
Even superficial digging unearths many examples of diseases that immigrated into prosperous Western countries from poorer ones: yellow fever, repeated outbreaks of influenza, Asiatic cholera, black plague, malaria, and of course, AIDS. But there is something telling in this list, or any other representative list one might construct. With the exception of AIDS, the diseases first made the trip to Euro-American populations many decades or even centuries ago.
Their global mobility depended on two critical factors: the group size of the traveling humans and the speed of travel. Human travel needed to be sufficiently rapid to allow disease organisms to be maintained within the group of travelers. Meeting this requirement is more tricky than it sounds because the human immune system is so good at subduing pathogens. Within a few weeks pathogens are usually eradicated from the body or so decimated that they have little chance of transmission. Pathogens that had mastered the trick of prolonging infectiousness were probably transported between the Mediterranean and south and central Asia from the earliest days of intercontinental trade. Pathogens that had not mastered the trick would have to wait for improvements in transportation technology to move them throughout the civilized world.
But they would not have to wait for jumbo jets. Caravans and horses were sufficient for diseases such as the black plague to make their way from central Asia to southern Europe nearly two thousand years ago. For other diseases, the movement of big boats permitted travel over expansive tracts of humanless terrain. In the early nineteenth century Asiatic cholera finally made the passage from its south Asian homeland to Europe and then did so repeatedly, causing waves of turbulence in Europe and America until water supplies were protected. Boats filled with dozens of people may have been necessary to permit its passage because the cholera organism can rarely withstand a person’s defenses for more than a couple of weeks. Yellow fever similarly was barred from the Americas until ships could act as microcosms, complete with tiny pools of freshwater in which the mosquito vectors could breed. The African mosquito Aedes aegypti colonized the boats and eventually the urban centers of the New World, thus cycling the virus in people both during and after the transatlantic voyage. Jet travel is overkill, by about five hundred miles per hour.


Posted by 2011-05-02T16:07:39+00:00"> – May 2, 2011

You can wind up with low bone density two different ways. One, you could have an accelerated loss of bone mass, which is what happens to women at menopause. Or you could have slowed bone growth. The latter is currently harder to deal with. We are better at slowing loss than spurring new growth, though new developments in this area are coming fast and furious.
Resorption itself isn’t the enemy. Destroying old or weak bone cells to make way for stronger new bone is crucial for healthy bones. Without remodeling, even dense bone wouldn’t be healthy bone. In fact, many people who suffer fractures as a result of minor trauma have bones with normal density—but poor bone quality. The strategies presented in this book are specifically aimed at creating and maintaining good bone density, but will also give you generally healthy bones (as well as overall good health). The goal is not to stop bone breakdown but to foster the appropriate interrelationship between resorption and formation, making it as close to how it works in healthy young people as possible.
The breakdown of bone takes place relatively quickly, and the better part of each 120-day remodeling cycle is devoted to synthesizing new bone (making the proteins for the matrix as well as assembling the minerals that crystallize on it). Many chemicals in your body signal the starting and stopping of resorption and formation, including thyroid and parathyroid hormones, growth hormone, estrogen and testosterone, and others. The rate at which bone is made and broken down is also affected by calcium intake and your body’s usage of it once it has it (which is in turn regulated by a series of hormones), and the amount of stress placed on the bone (such as from weight-bearing exercise).
When your body gets too many green lights for remodeling, you may get a quickening of the pace at which bone is formed, but it won’t be enough to keep up with the increase in breakdown.
That’s just what happens with the drop in estrogen in menopause, or with any condition that entails an imbalance of hormones (like hyper- or hypothyroidism, for example). Lack of calcium, too, can signal bone remodeling, perhaps prematurely. In addition, rapid turnover of bone cells usually yields bone of low quality, even if the quantity is normal. That’s why, once again, this book is designed not just to build bone but to build and maintain healthy bone.