Minggu, 31 Januari 2010

The Body Fat Setpoint, Part IV: Changing the Setpoint

Prevention is Easier than Cure

Experiments in animals have confirmed what common sense suggests: it's easier to prevent health problems than to reverse them. Still, many health conditions can be improved, and in some cases reversed, through lifestyle interventions. It's important to have realistic expectations and to be kind to oneself. Cultivating a drill sergeant mentality will not improve quality of life, and isn't likely to be sustainable.

Fat Loss: a New Approach

If there's one thing that's consistent in the medical literature, it's that telling people to eat fewer calories does not help them lose weight in the long term. Gary Taubes has written about this at length in his book Good Calories, Bad Calories, and in his upcoming book on body fat. Many people who use this strategy see transient fat loss, followed by fat regain and a feeling of defeat. There's a simple reason for it: the body doesn't want to lose weight. It's extremely difficult to fight the fat mass setpoint, and the body will use every tool it has to maintain its preferred level of fat: hunger, reduced body temperature, higher muscle efficiency (i.e., less energy is expended for the same movement), lethargy, lowered immune function, et cetera.

Therefore, what we need for sustainable fat loss is not starvation; we need a treatment that lowers the fat mass setpoint. There are several criteria that this treatment will have to meet to qualify:
  1. It must cause fat loss
  2. It must not involve deliberate calorie restriction
  3. It must maintain fat loss over a long period of time
  4. It must not be harmful to overall health
I also prefer strategies that make sense from the perspective of human evolution.

Strategies
: Diet Pattern

The most obvious treatment that fits all of my criteria is low-carbohydrate dieting. Overweight people eating low-carbohydrate diets generally lose fat and spontaneously reduce their calorie intake. In fact, in several diet studies, investigators compared an all-you-can-eat low-carbohydrate diet with a calorie-restricted low-fat diet. The low-carbohydrate dieters generally reduced their calorie intake and body fat to a similar or greater degree than the low-fat dieters, despite the fact that they ate all the calories they wanted (1). This suggest that their fat mass setpoint had changed. At this point, I think moderate carbohydrate restriction may be preferable to strict carbohydrate restriction for some people, due to the increasing number of reports I've read of people doing poorly in the long run on extremely low-carbohydrate diets (2).

Another strategy that appears effective is the "paleolithic" diet. In Dr. Staffan Lindeberg's 2007 diet study, overweight volunteers with heart disease lost fat and reduced their calorie intake to a remarkable degree while eating a diet consistent with our hunter-gatherer heritage (3). This result is consistent with another diet trial of the paleolithic diet in diabetics (4). In post hoc analysis, Dr. Lindeberg's group showed that the reduction in weight was apparently independent of changes in carbohydrate intake*. This suggests that the paleolithic diet has health benefits that are independent of carbohydrate intake.

Strategies: Gastrointestinal Health

Since the gastrointestinal (GI) tract is so intimately involved in body fat metabolism and overall health (see the former post), the next strategy is to improve GI health. There are a number of ways to do this, but they all center around four things:
  1. Don't eat food that encourages the growth of harmful bacteria
  2. Eat food that encourages the growth of good bacteria
  3. Don't eat food that impairs gut barrier function
  4. Eat food that promotes gut barrier health
The first one is pretty easy: avoid refined sugar, refined carbohydrate in general, and lactose if you're lactose intolerant. For the second and fourth points, make sure to eat fermentable fiber. In one trial, oligofructose supplements led to sustained fat loss, without any other changes in diet (5). This is consistent with experiments in rodents showing improvements in gut bacteria profile, gut barrier health, glucose tolerance and body fat mass with oligofructose supplementation (6, 7, 8).

Oligofructose is similar to inulin, a fiber that occurs naturally in a wide variety of plants. Good sources are jerusalem artichokes, jicama, artichokes, onions, leeks, burdock and chicory root. Certain non-industrial cultures had a high intake of inulin. There are some caveats to inulin, however: inulin and oligofructose can cause gas, and can also exacerbate gastroesophageal reflux disorder (9). So don't eat a big plate of jerusalem artichokes before that important date.

The colon is packed with symbiotic bacteria, and is the site of most intestinal fermentation. The small intestine contains fewer bacteria, but gut barrier function there is critical as well. The small intestine is where the GI doctor will take a biopsy to look for celiac disease. Celiac disease is a degeneration of the small intestinal lining due to an autoimmune reaction caused by gluten (in wheat, barley and rye). This brings us to one of the most important elements of maintaining gut barrier health: avoiding food sensitivities. Gluten and casein (in dairy protein) are the two most common offenders. Gluten sensitivity is widespread and typically undiagnosed (10).

Eating raw fermented foods such as sauerkraut, kimchi, yogurt and half-sour pickles also helps maintain the integrity of the upper GI tract. I doubt these have any effect on the colon, given the huge number of bacteria already present. Other important factors in gut barrier health are keeping the ratio of omega-6 to omega-3 fats in balance, eating nutrient-dense food, and avoiding the questionable chemical additives in processed food. If triglycerides are important for leptin sensitivity, then avoiding sugar and ensuring a regular source of omega-3 should aid weight loss as well.

Strategies: Micronutrients

As I discussed in the last post, micronutrient deficiency probably plays a role in obesity, both in ways that we understand and ways that we (or I) don't. Eating a diet that has a high nutrient density and ensuring a good vitamin D status will help any sustainable fat loss strategy. The easiest way to do this is to eliminate industrially processed foods such as white flour, sugar and seed oils. These constitute more than 50% of calories for the average Westerner.

After that, you can further increase your diet's nutrient density by learning to properly prepare grains and legumes to maximize their nutritional value and digestibility (11, 12; or by avoiding grains and legumes altogether if you wish), selecting organic and/or pasture-raised foods if possible, and eating seafood including seaweed. One of the problems with extremely low-carbohydrate diets is that they may be low in water-soluble micronutrients, although this isn't necessarily the case.

Strategies: Miscellaneous

In general, exercise isn't necessarily helpful for fat loss. However, there is one type of exercise that clearly is: high-intensity intermittent training (HIIT). It's basically a fancy name for sprints. They can be done on a track, on a stationary bicycle, using weight training circuits, or any other way that allows sufficient intensity. The key is to achieve maximal exertion for several brief periods, separated by rest. This type of exercise is not about burning calories through exertion: it's about increasing hormone sensitivity using an intense, brief stressor (hormesis). Even a ridiculously short period of time spent training HIIT each week can result in significant fat loss, despite no change in diet or calorie intake (13).

Anecdotally, many people have had success using intermittent fasting (IF) for fat loss. There's some evidence in the scientific literature that IF and related approaches may be helpful (14). There are different approaches to IF, but a common and effective method is to do two complete 24-hour fasts per week. It's important to note that IF isn't about restricting calories, it's about resetting the fat mass setpoint. After a fast, allow yourself to eat quality food until you're no longer hungry.

Insufficient sleep has been strongly and repeatedly linked to obesity. Whether it's a cause or consequence of obesity I can't say for sure, but in any case it's important for health to sleep until you feel rested. If your sleep quality is poor due to psychological stress, meditating before bedtime may help. I find that meditation has a remarkable effect on my sleep quality. Due to the poor development of oral and nasal structures in industrial nations, many people do not breathe effectively and may suffer from conditions such as sleep apnea that reduce sleep quality. Overweight also contributes to these problems.

I'm sure there are other useful strategies, but that's all I have for now. If you have something to add, please put it in the comments.


* Since reducing carbohydrate intake wasn't part of the intervention, this result is observational.

Sabtu, 23 Januari 2010

The Body Fat Setpoint, Part III: Dietary Causes of Obesity

What Caused the Setpoint to Change?

We have two criteria to narrow our search for the cause of modern fat gain:
  1. It has to be new to the human environment
  2. It has to cause leptin resistance or otherwise disturb the setpoint
Although I believe that exercise is part of a healthy lifestyle, it probably can't explain the increase in fat mass in modern nations. I've written about that here and here. There are various other possible explanations, such as industrial pollutants, a lack of sleep and psychological stress, which may play a role. But I feel that diet is likely to be the primary cause. When you're drinking 20 oz Cokes, bisphenol-A contamination is the least of your worries.

In the last post, I described two mechanisms that may contribute to elevating the body fat set point by causing leptin resistance: inflammation in the hypothalamus, and impaired leptin transport into the brain due to elevated triglycerides. After more reading and discussing it with my mentor, I've decided that the triglyceride hypothesis is on shaky ground*. Nevertheless,
it is consistent with certain observations:
  • Fibrate drugs that lower triglycerides can lower fat mass in rodents and humans
  • Low-carbohydrate diets are effective for fat loss and lower triglycerides
  • Fructose can cause leptin resistance in rodents and it elevates triglycerides (1)
  • Fish oil reduces triglycerides. Some but not all studies have shown that fish oil aids fat loss (2)
Inflammation in the hypothalamus, with accompanying resistance to leptin signaling, has been reported in a number of animal studies of diet-induced obesity. I feel it's likely to occur in humans as well, although the dietary causes are probably different for humans. The hypothalamus is the primary site where leptin acts to regulate fat mass (3). Importantly, preventing inflammation in the brain prevents leptin resistance and obesity in diet-induced obese mice (3.1). The hypothalamus is likely to be the most important site of action. Research is underway on this.

The Role of Digestive Health

What causes inflammation in the hypothalamus? One of the most interesting hypotheses is that increased intestinal permeability allows inflammatory substances to cross into the circulation from the gut, irritating a number of tissues including the hypothalamus.

Dr. Remy Burcelin and his group have spearheaded this research. They've shown that high-fat diets cause obesity in mice, and that they also increase the level of an inflammatory substance called lipopolysaccharide (LPS) in the blood. LPS is produced by gram-negative bacteria in the gut and is one of the main factors that activates the immune system during an infection. Antibiotics that kill gram-negative bacteria in the gut prevent the negative consequences of high-fat feeding in mice.

Burcelin's group showed that infusing LPS into mice on a low-fat chow diet causes them to become obese and insulin resistant just like high-fat fed mice (4). Furthermore, adding 10% of the soluble fiber oligofructose to the high-fat diet prevented the increase in intestinal permeability and also largely prevented the body fat gain and insulin resistance from high-fat feeding (5). Oligofructose is food for friendly gut bacteria and ends up being converted to butyrate and other short-chain fatty acids in the colon. This results in lower intestinal permeability to toxins such as LPS. This is particularly interesting because oligofructose supplements cause fat loss in humans (6).

A recent study showed that blood LPS levels are correlated with body fat, elevated cholesterol and triglycerides, and insulin resistance in humans (7). However, a separate study didn't come to the same conclusion (8). The discrepancy may be due to the fact that LPS isn't the only inflammatory substance to cross the gut lining-- other substances may also be involved. Anything in the blood that shouldn't be there is potentially inflammatory.

Overall, I think gut dysfunction probably plays a major role in obesity and other modern metabolic problems. Insufficient dietary fiber, micronutrient deficiencies, excessive gut irritating substances such as gluten, abnormal bacterial growth due to refined carbohydrates (particularly sugar), and omega-6:3 imbalance may all contribute to abnormal gut bacteria and increased gut permeability.

The Role of Fatty Acids and Micronutrients

Any time a disease involves inflammation, the first thing that comes to my mind is the balance between omega-6 and omega-3 fats. The modern Western diet is heavily weighted toward omega-6, which are the precursors to some very inflammatory substances (as well as a few that are anti-inflammatory). These substances are essential for health in the correct amounts, but they need to be balanced with omega-3 to prevent excessive and uncontrolled inflammatory responses. Animal models have repeatedly shown that omega-3 deficiency contributes to the fat gain and insulin resistance they develop when fed high-fat diets (9, 10, 11).

As a matter of fact, most of the papers claiming "saturated fat causes this or that in rodents" are actually studying omega-3 deficiency. The "saturated fats" that are typically used in high-fat rodent diets are refined fats from conventionally raised animals, which are very low in omega-3. If you add a bit of omega-3 to these diets, suddenly they don't cause the same metabolic problems, and are generally superior to refined seed oils, even in rodents (12, 13).

I believe that micronutrient deficiency also plays a role. Inadequate vitamin and mineral status can contribute to inflammation and weight gain. Obese people typically show deficiencies in several vitamins and minerals. The problem is that we don't know whether the deficiencies caused the obesity or vice versa. Refined carbohydrates and refined oils are the worst offenders because they're almost completely devoid of micronutrients.

Vitamin D in particular plays an important role in immune responses (including inflammation), and also appears to influence body fat mass. Vitamin D status is associated with body fat and insulin sensitivity in humans (14, 15, 16). More convincingly, genetic differences in the vitamin D receptor gene are also associated with body fat mass (17, 18), and vitamin D intake predicts future fat gain (19).

Exiting the Niche

I believe that we have strayed too far from our species' ecological niche, and our health is suffering. One manifestation of that is body fat gain. Many factors probably contribute, but I believe that diet is the most important. A diet heavy in nutrient-poor refined carbohydrates and industrial omega-6 oils, high in gut irritating substances such as gluten and sugar, and a lack of direct sunlight, have caused us to lose the robust digestion and good micronutrient status that characterized our distant ancestors. I believe that one consequence has been the dysregulation of the system that maintains the fat mass "setpoint". This has resulted in an increase in body fat in 20th century affluent nations, and other cultures eating our industrial food products.

In the next post, I'll discuss my thoughts on how to reset the body fat setpoint.


*
The ratio of leptin in the serum to leptin in the brain is diminished in obesity, but given that serum leptin is very high in the obese, the absolute level of leptin in the brain is typically not lower than a lean person. Leptin is transported into the brain by a transport mechanism that saturates when serum leptin is not that much higher than the normal level for a lean person. Therefore, the fact that the ratio of serum to brain leptin is higher in the obese does not necessarily reflect a defect in transport, but rather the fact that the mechanism that transports leptin is already at full capacity.

Kamis, 21 Januari 2010

Daftar Isi Postingan Akses Informasi Terkini


Rabu, 20 Januari 2010

Krauss's New Article on Saturated Fat Intervention Trials

Dr. Ronald Krauss's group just published another article in the American Journal of Clinical Nutrition, this time on the intervention trials examining the effectiveness of reducing saturated fat and/or replacing it with other nutrients, particularly carbohydrate or polyunsaturated seed oils. I don't agree with everything in this article. For example, they cite the Finnish Mental Hospital trial. They openly acknowledge some contradictory data, although they left out the Sydney diet-heart study and the Rose et al. corn oil study, both of which showed greatly increased mortality from replacing animal fats with polyunsaturated seed oils. Nevertheless, they get it right in the end:
Particularly given the differential effects of dietary saturated fats and carbohydrates on concentrations of larger and smaller LDL particles, respectively, dietary efforts to improve the increasing burden of CVD risk associated with atherogenic dyslipidemia should primarily emphasize the limitation of refined carbohydrate intakes and a reduction in excess adiposity.
This is really cool. Krauss is channeling Weston Price. If this keeps up, I may have no reason to blog anymore!

Sabtu, 16 Januari 2010

The Body Fat Setpoint, Part II: Mechanisms of Fat Gain

The Timeline of Fat Gain

Modern humans are unusual mammals in that fat mass varies greatly between individuals. Some animals carry a large amount of fat for a specific purpose, such as hibernation or migration. But all individuals of the same sex and social position will carry approximately the same amount of fat at any given time of year. Likewise, in hunter-gatherer societies worldwide, there isn't much variation in body weight-- nearly everyone is lean. Not necessarily lean like Usain Bolt, but not overweight.

Although overweight and obesity occurred forty years ago in the U.S. and U.K., they were much less common than today, particularly in children. Here are data from the U.S. Centers for Disease Control NHANES surveys (from this post):

Together, this shows that a) leanness is the most natural condition for the human body, and b) something about our changing environment, not our genes, has caused our body fat to grow.

Fat Mass is Regulated by a Feedback Circuit Between Fat Tissue and the Brain

In the last post, I described how the body regulates fat mass, attempting to keep it within a narrow window or "setpoint". Body fat produces a hormone called leptin, which signals to the brain and other organs to decrease appetite, increase the metabolic rate and increase physical activity. More fat means more leptin, which then causes the extra fat to be burned. The little glitch is that some people become resistant to leptin, so that their brain doesn't hear the fat tissue screaming that it's already full. Leptin resistance nearly always accompanies obesity, because it's a precondition of significant fat gain. If a person weren't leptin resistant, he wouldn't have the ability to gain more than a few pounds of fat without heroic overeating (which is very very unpleasant when your brain is telling you to stop). Animal models of leptin resistance develop something that resembles human metabolic syndrome (abdominal obesity, blood lipid abnormalities, insulin resistance, high blood pressure).

The Role of the Hypothalamus


The hypothalamus is on the underside of the brain connected to the pituitary gland. It's the main site of leptin action in the brain, and it controls the majority of leptin's effects on appetite, energy expenditure and insulin sensitivity. Most of the known gene variations that are associated with overweight in humans influence the function of the hypothalamus in some way (1). Not surprisingly, leptin resistance in the hypothalamus has been proposed as a cause of obesity. It's been shown in rats and mice that hypothalamic leptin resistance occurs in diet-induced obesity, and it's almost certainly the case in humans as well. What's causing leptin resistance in the hypothalamus?

There are three leading explanations at this point that are not mutually exclusive. One is cellular stress in the endoplasmic reticulum, a structure inside the cell that's used for protein synthesis and folding. I've read the most recent paper on this in detail, and I found it unconvincing (2). I'm open to the idea, but it needs more rigorous support.

A second explanation is inflammation in the hypothalamus. Inflammation inhibits leptin and insulin signaling in a variety of cell types. At least two studies have shown that diet-induced obesity in rodents leads to inflammation in the hypothalamus (3, 4)*. If leptin is getting to the hypothalamus, but the hypothalamus is insensitive to it, it will require more leptin to get the same signal, and fat mass will creep up until it reaches a higher setpoint.

The other possibility is that leptin simply isn't reaching the hypothalamus. The brain is a unique organ. It's enclosed by the blood-brain barrier (BBB), which greatly restricts what can enter and leave it. Both insulin and leptin are actively transported across the BBB. It's been known for a decade that obesity in rodents is associated with a lower rate of leptin transport across the BBB (5, 6).

What causes a decrease in leptin transport across the BBB? Triglycerides are a major factor. These are circulating fats going from the liver and the digestive tract to other tissues. They're one of the blood lipid measurements the doctor makes when he draws your blood. Several studies in rodents have shown that high triglycerides cause a reduction in leptin transport across the BBB, and reducing triglycerides allows greater leptin transport and fat loss (7, 8). In support of this theory, the triglyceride-reducing drug gemfibrozil also causes weight loss in humans (9)**. Guess what else reduces triglycerides and causes weight loss? Low-carbohydrate diets, and avoiding sugar and refined carbohydrates in particular.

In the next post, I'll get more specific about what factors could be causing hypothalamic inflammation and/or reduced leptin transport across the BBB. I'll also discuss some ideas on how to reduce leptin resistance sustainably through diet and exercise.


* This is accomplished by feeding them sad little pellets that look like greasy chalk. They're made up mostly of lard, soybean oil, casein, maltodextrin or cornstarch, sugar, vitamins and minerals (this is a link to the the most commonly used diet for inducing obesity in rodents). Food doesn't get any more refined than this stuff, and adding just about anything to it, from fiber to fruit extracts, makes it less damaging.

** Fibrates are PPAR agonists, so the weight loss could also be due to something besides the reduction in triglycerides.

Kamis, 14 Januari 2010

New Saturated Fat Review Article by Dr. Ronald Krauss

I never thought I'd see the day when one of the most prominent lipid researchers in the world did an honest review of the observational studies evaluating the link between saturated fat and cardiovascular disease. Dr. Ronald Krauss's group has published a review article titled "Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease". As anyone with two eyes and access to the medical literature would conclude (including myself), they found no association whatsoever between saturated fat intake and heart disease or stroke:
A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD.
Bravo, Dr. Krauss. That was a brave move.

Thanks to Peter for pointing out this article.

Minggu, 10 Januari 2010

Paleo is Going Mainstream

There was an article on the modern "Paleolithic" lifestyle in the New York Times today. I thought it was a pretty fair treatment of the subject, although it did paint it as more macho and carnivorous than it needs to be. It features three attractive NY cave people. It appeared in the styles section here. Paleo is going mainstream. We can expect media health authorities to start getting defensive about it any minute now.

Sabtu, 09 Januari 2010

How to Prevent Coronary Heart Disease and Heart Attack

Coronary heart disease and heart attack like heart infarction can in great extend be prevented by lifestyle measures.

?
THE DIRECT CAUSES OF HEART DISEASE

The direct causes of coronary heart disease and heart attack are factors like these:

- Narrowing of blood vessels in the heart and the rest of the body by arteriosclerosis.
- High blood cholesterol level.
- High blood pressure.
- Over-weight.
- Diabetes.
- High level of the amino acid homocystein in the blood.
- High content of low density lipoprotein (LDL) and low content of high density lipoprotein (HDL) in the blood. Lipoprotein is a combination of protein and fatty substances bound together.
- Inflammation in the circulatory system.
- High age.
- Inherited tendencies for high cholesterol levels and heart disease.
- Men have somewhat greater chance of getting heart disease than women.

These factors are interrelated in complicated ways, and are causing or amplifying each other. For example, arteriosclerosis will cause higher blood pressure, and high blood pressure will cause even more arteriosclerosis. Many of these factors are ultimately caused or aggravated by these lifestyle factors:

-A too high consume of fat, cholesterol and sugar.
-Consuming the wrong fat types.
-Lack of fibre, vitamins, minerals and other diet deficiencies.
-Stress at work and in the daily life.
-Smoking.
-Lack of exercise.

Lifestyle adjustments will therefore be the main methods of preventing heart failure.


GENERAL DIET ADVICES

A diet with the aim of preventing heart disease is generally the same as a diet to prevent cancer and other diseases. Here are the general diet advices

- Avoid or reduce the amount of food that are industrially processed, artificially made or heavily fried.

- Eat fish at least every second day. Also eat seafood and fouls.

- Do not eat very much red meat.

- Eat 5 fruits or vegetables each day. Each piece should be of the size of an apple or carrot. They should be raw or carefully boiled so that the nutrients are not washed out.

- Eat full corn bread, full corn cereals, peas, beans and potatoes.

- Eat just a moderate amount of fat.

- Consume cholesterol rich foods like egg, spawn or liver in just moderate amounts.

- Ideally most fat you eat, should be of the type mono-unsaturated. You also need some poly-unsaturated fat of the types omega-3, and omega 6, but not too much of omega-6. The consumption of saturated fat should be moderate.

- In order to achieve right fat balance, much of the fat supply should come from a blending of sources like olive, olive oil, canola oil, nuts, nut oil, sunflower, sunflower oil, linseed oil (flax oil), fish and fish oil.

- Use only a moderate amount of soy oil and corn oil in the diet. Only using such oil types will give you too much poly-unsaturated fat of the omega-6-type.

- Use just a very moderate amount of fat sources like butter, coconut oil and palm oil. A high consumption of these fat sources gives you too much saturated fat.

- Avoid altogether fat that has been chemically altered, giving so-called trans-fat. This type of fat is often found in margarine, cookies, snacks, fast food and other pre-made food.

- Consume just a very moderate amount of sugar, refined flour or refined cereals.

- Consume just a moderate amount of tranquilizers and stimulants like alcohol and caffeine.

- Use just a moderate amount of salt in the food. However, in warm weather and by hard physical work, you will need more salt.


DIET SUPPLEMENTS THAT HELP PREVENT HEART DISEASE

Evidence suggests that it will be helpful to take some supplements of natural substances to prevent heart disease and help to ameliorate already manifest heart problems. These supplements are:

- Omega-3-fatty acids derived from fish and other marine sources, especially the fatty acids EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) and alfa-linolaeic acid. 1 gram a day of each of these substances may be taken as a supplement. Higher amounts should only be taken under medical supervision, since higher amount of these substances may cause bleeding tendencies, and may suppress the immune system.

- Supplement of vitamin C has been thought to help prevent heart disease, but newer findings cast doubt upon this.

- Vitamin B6 (Pyridoxine), folic acid / folate, vitamin b12 and riboflavin seem to prevent the building up of the substance homocystein in the blood and thereby help prevent heart disease, according to results from research projects.


GET RID OF OVER-WEIGHT

The lifestyle measures listed in this article will also help you loose weight. If these measures are not enough, you should consider engaging in a more specific weight reduction program. You should choose a program that has a moderate fat content philosophy. Some weight reduction programs have a higher fat and low carbohydrate consume philosophy, and those are probably not the best ones to reduce the chance of getting heart disease.


EXERCISE

You should do some exercise of at least half an hour at least every second day. Condition training as vigorous walking, jogging, cycling or swimming is best for reducing the heart attack probability. Muscular building exercises are also of value, especially exercises building leg muscles


STOP SMOKING

If you smoke, stopping or reducing this habit radically will decrease the chance of getting heart problems.


CONTROL DIABETES

If you suffer from diabetes type 1, a good control of the disease by insulin medication and by diet adjustments will help to prevent heart disease.

Many people over the age of 50, and an increasing number of young people suffer from diabetes type 2 because of bad lifestyle. This disease does not necessarily give dramatic symptoms, but the disease increases the chance of getting serious heart problems, and many have the disease without knowing it. This disease can be prevented by the same lifestyle measures depicted above. If you already have got the disease, a more rigorous control of carbohydrate intake is necessary. And sometimes also medication must be used. People over the age of 50 and younger people that do not feel well should find out if they suffer from this condition.


TAKING ASPIRIN

Low doses of acetyl salicylic acid or aspirin prevent heart disease by persons bearing a high risk for heart disease. However, this medication increases the risk of bleeding and should not be used without constant medical supervision. For persons with a low risk of heart disease, the dangers of aspirin will be greater than the benefits.



About The Author:
Knut Holt is an internet consultant and marketer focusing on health items.----TO FIND natural help against common diseases, for example: Heart problems, over-weight, acne, hypothyroidism, fatigue, depression, anxiety, hemorrhoids, joint pain, allergies, rheumatism, respiratory diseases, and more PLEASE VISIT:--- http://www.abicana.com/shop2.htm

Jumat, 01 Januari 2010

How To Recognize The Symptoms Of Migraine Headaches

You have started to have severe headaches. These headaches last for a few hours and are recurring a couple of times a month. You suspect that it may be migraine headaches but how do you know for sure? This article will give you the signs and symptoms of a migraine. A word or caution. It is not smart to diagnose yourself. If you are having frequent headaches and aren't sure of the cause, see your doctor right away. He may want to do some tests to rule more serious problems
A migraine is a headache that is so severe it can be disabling and it will sometimes be accompanied by an aura. An aura is a warning sign that a migraine is coming. Auras usually appear anywhere from 15 to 30 minutes before a migraine starts. A migraine can last for two hours or it can last for as long as 72 hours if not treated.

Approximately 11 out of 100 people will get migraines, and women get them more than men. Hormonal changes have been thought to be a huge factor in the development of migraines. Other triggers can be certain foods, environmental changes and stress.

The symptoms of migraine headaches are:

Pain. This can range from moderate to severe. Some people will feel pain on either side of the head, while other people may feel it bilaterally. The pain may be described as throbbing or pulsating.

A true migraine will become worse with physical activity. This is why it interrupts your daily activities. Just walking across the room can cause excruciating pain.

The pain can cause nausea and occasionally vomiting. If the vomiting becomes severe you may need to get your doctor to prescribe an anti-emetic, such as Reglan or Compazine.

Hypersensitivity to sounds or lights is another common symptom of migraines. Most people want to lie down in a dark, quiet room until the pain subsides.

Some people that have migraines will experience auras prior to a headache. These auras may continue for the duration of the migraine. An aura can consist of:

- Bright flashes of light
- Bright zigzagging lines that interrupt your vision field.
- Diffuse blind spots in your field of vision.
- A tingling feeling in a leg or an arm.

Migraines themselves pose no real threat to you. But go to the emergency room immediately if you experience a sudden headache that seems to explode inside your head. If you have a headache with fever, mental confusion or a stiff neck. A headache that continues to get worse after coughing or straining or any other sudden movement. These may all be symptoms of a more serious problem and should not be ignored.

Migraines can be manageable with the right treatment. Talk to your doctor about your best options. There is no reason for you to suffer from the symptoms of a migraine headache.

For more help on the prevention, treatment and remedies for migraines please see the Complete Guide To Migraine Headaches.

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