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Misconceptions about the prevalence of heart disease in women has plagued physicians and their patients. A survey by the American Heart Association showed that more than two thirds of women aged 25 to 44 did not realize that heart disease was the major cause of death in women in the US. In the past, women were thought to be at significantly lower risk for heart disease than men. Due to this belief, women were screened less aggressively for risk factors, had less diagnostic testing, and less treatment. Now that we have all but abandoned the notion that hormone replacement therapy reduces the risk of heart disease, at least for the time being, it is time to improve our risk assessment, screening, diagnosis and treatment of heart disease in the postmenopausal woman.

Up until this point, the less aggressive assessment and management of women may have been related to greater frequency of noncoronary chest pain in younger women, the tendency to be 10 years older than men at the initial clinical symptoms and signs of coronary disease, women being 20 years older than men at the time of myocardial infarction, and the 30 year practice of prescribing HRT as an assumed prevention strategy, thinking that not much more was needed.

Lifestyle factors and risk factors are similar in women and men. Dyslipidemia, hypertension and diabetes tend to develop in women at an older age than in men and it is recommended that screening for these conditions begin at about age 45 in women, 10 years later than for men. Lifestyle factors should be assessed at a much earlier age. Screening for smoking, alcohol intake, exercise and nutritional habits, stress, body mass index (BMI) and weight loss/weight gain patterns should be done at a much earlier age as part of regular annual exams.

Overweight women and those with the “apple” fat distribution are at greater risk for developing coronary artery disease than are slim women and those with the pear fat pattern. This abdominal obesity also increases the risk of high blood pressure and diabetes and may lower the HDL-cholesterol level and raise the triglyceride level. A waist-to-hip ratio for middle-aged women <0.8 is considered desirable. A BMI < 25 is associated with a lower risk of cardiovascular disease and a BMI >29 has been associated with triple the risk of coronary heart disease compared with women who were lean and with a BMI of 21. (1) Women with a BMI of 25-28.9 and only moderately overweight had almost double the risk.

Another critical risk factor is family history. Women whose father had a heart attack or stroke before age 50, or a mother before age 65 are at increased risk of premature heart disease.

Diabetes predicts a higher risk of heart disease in women than in men and elevates the risk three to seven times above that of women who do not have diabetes. (2) Women with diabetes also have more adverse lipid profiles, greater obesity and higher blood pressures than diabetic men.

There may be gender differences in risk related to dyslipidemia, although this is not yet clear. Elevated triglycerides may be an independent risk factor for women, but not for men. The combination of high triglycerides and low HDL appears to present substantial risk in women. For older women, the predictive value of total cholesterol and LDL is diminished, yet on the other hand, HDL levels are more predictive in older women than they are in men. (3) For women with no coronary artery disease and fewer than two risk factors, the LDL goal is < 160mg/dL. If no coronary disease and two or more risk factors, then the goal is < 130mg/dL. For women with coronary artery disease, then LDL levels should be < 100 mg/dL.

Several other risk factors should be considered, although are not yet part of the standard risk-factor panel for women or men. Some of these may in fact be more predictive for women than men although it is not yet known whether lowering the levels of these factors will significantly benefit women.

C-reactive protein: C-reactive protein (CRP) is produced in the liver and is a marker of systemic inflammation. It appears to be a risk factor for atherosclerosis and for infarction. In the Women’s Health Study, CRP was the strongest predictor of risk of cardiovascular events. (4) In the Postmenopausal Estrogen/Progestin Interventions (PEPI) trial, all hormonal regimens studied caused a large and sustained increase in CRP, and was hypothesized to be related to the risk of clots and strokes within the first year of initiating HRT in women with pre-existing heart disease. (5)

Homocysteine: Homocysteine is another marker of inflammation and has been shown to be an independent predictor of new coronary events in older men and women. (6) The relative risk of coronary events in women in the Women’s Health Study was 2.0 in those with the lowest levels of homocysteine. (4) It still needs to be determined whether or not reducing homocysteine with folic acid will actually reduce the risk of coronary heart disease (CHD), although most practitioners would consider this to be a simple, safe strategy.

Brown and colleagues conducted a randomized, controlled, double-blind trial comparing placebo treatment with an antioxidant cocktail (vitamin E, 800 IU; vitamin C, 1,000 mg; beta carotene, 25 mg; selenium, 100 mcg), simvastatin, and niacin, or a combination of all three agents in a study population with known coronary heart disease.

The investigators enrolled patients with low-density lipoprotein (LDL) cholesterol levels below 145 mg per dL without medication but depressed high-density lipoprotein (HDL) levels (less than 35 mg per dL). Of the 454 patients who were eligible based on appropriate lipid parameters, 160 were enrolled in the study. Baseline coronary angiography was compared to repeat catheterization after three years of treatment. Lipid levels were followed, and the clinical outcomes were tracked to the occurrence of the first of the following events: nonfatal myocardial infarction, stroke, or revascularization for worsening ischemia.

Patients who received only antioxidants had no significant change in LDL or HDL levels, had angiographic progression of coronary stenoses, and had no significant improvement in clinical outcomes. The group assigned to simvastatin and niacin had LDL reductions averaging 42 percent and HDL increases of 26 percent. Angiographic stenoses regressed slightly in this group, and the incidence of adverse clinical outcomes was significantly reduced (3 percent versus 24 percent for placebo). Patients who had antioxidants added to simvastatin and niacin had less improvement in lipid parameters, progression of coronary stenoses, and loss of the significant reduction in clinical outcomes.

The authors concluded that simvastatin plus niacin improved lipid parameters, angiographic evidence of stenoses, and clinical outcomes in patients with coronary disease and low HDL levels when compared to placebo. The use of antioxidant vitamins had no such effects.

Brown BG, et al. Simvastatin and niacin, antioxidant vitamins, or the combination for the prevention of coronary disease. N Engl J Med November 29, 2001;345:1583-92.

The disparity between African Americans and Caucasians in death rates from coronary heart disease has increased despite a recent overall decline in death rates from the disease, according to a Feb 1, 2002, news release from the American Heart Association. Research findings show that death rates from coronary heart disease declined by 33.3% in African American men from 1979 to 1998 compared to a 46.1% decline of death rates in Caucasian men during the same period. Death rates from the disease decreased 26.6% for African American women, compared to 40.1% for Caucasian women during the same period.

This disparity between African Americans and Caucasians is due in part to heredity and lifestyle habits. African Americans have a high incidence of several risk factors, including high blood pressure, which increases their risk for heart disease and stroke. These findings show that there is a need to develop prevention programs aimed toward education, ethnicity, and other characteristics of populations at increased risk for coronary heart disease.

“Search Your Heart” is a national heart health and stroke prevention initiative of the American Heart Association that is designed to reach African Americans in the church setting. Church programs are led by designated program coordinators who plan and promote events, recruit church volunteers, contact coordinating agencies, and work with a local association representative to present the program to the church. Currently, more than 1,250 churches participate in the program.

More than 100,000 African American deaths annually are attributed to cardiovascular diseases. Cardiovascular diseases accounted for 33.8% of deaths of African American men and 40.8% of deaths of African American women in 1999.

Building and maintaining patient relationships in a large metropolitan area is daunting enough for a healthcare organization. Accomplishing these tasks in a widely dispersed, largely rural region is another challenge altogether. The solution lies in taking a multipronged approach: integrating online and off-line programs to promote service lines and create valuable interaction between the organization and its community.

Early Outreach Efforts

Located in Billings, Mont., Deaconess Billings Clinic (DBC), a multispecialty physician group practice and 272-bed trauma hospital, serves a rural population of more than 500,000 individuals. The nonprofit regional healthcare organization has a service area that spans a 250-mile radius in Montana and northern Wyoming

With such a widely dispersed patient population, we recognize that our organization cannot rely on just face-to-face and phone contact with community members to build and maintain lasting customer relationships. This is due to long driving distances for the public and our clinical staff, the cost of long-distance phone calls, and the need to provide a continuity of quality care, including the availability of DBC physicians.

As an initial participant in VHA’s Women’s HeartAdvantage program in January 2002, we had access to resources such as information packets, media advertisements and Web links, as well as clinical and consumer research and proven process methodologies, that promoted overall awareness of the risk factors and symptoms of heart disease in women. Our plan was to use these resources to improve clinical performance, increase community health and provide our organization with a market advantage.

By all measures, our initial effort worked well. Within 14 days of the Jan. 31 launch, we had more than 1,000 Women’s HeartAdvantage-related calls to DBC Healthline, our call center staffed by nurses. Also, our first two community educational sessions reached capacity by drawing more than 230 women.

As we continued our program, though, we wanted to be sure we could maintain strong relationships with women in our community. We wanted to develop a plan for ongoing contact with the women who participated in the education programs and build lasting customer loyalty among women who had found value in choosing us for their heart health and care.

Adopting New Strategies

DBC engaged Irving, Texas-based HEALTHvision for an answer. In 1998 and 1999, we had relied on the application service provider as a partner in the development of our organization’s Web strategy to improve interactivity with the public, so we knew that HEALTHvision understood our challenge and could work with us to create a solution. In early 2003, for example, we marked a 110 percent annual increase in traffic to our physician referral and nurse triage services in our call center. This was largely a result of our partnership with HEALTHvision, since we chose not to add to our technical infrastructure supporting the delivery of quality content to the public.

In late 2003, HEALTHvision recommended that we enhance our approach to community outreach. In addition to asking community members to attend Women’s HeartAdvantage events, schedule heart health screenings with their physicians or call for more information, HEALTHvision suggested an additional yearlong program for 2004 that focuses on creating continued contact with program participants and promoting organizational objectives.

This comprehensive, interactive customer relationship management (CRM) program for our Women’s HeartAdvantage efforts includes online and off-line marketing elements designed to attract new participants, renew interest in existing participants and create ongoing dialogue between DBC and the women of our community.

The CRM program will be measured against the following goals:

* Acquire 500 new, active participants in the Women’s HeartAdvantage program;

* Retain 75 percent of participants currently active in the program for at least three months;

* Re-engage 25 percent of participants who have not been active in the program for the past six months.

Pushing e-Newsletters

Once our goals were set, the HEALTHvision team began work on developing the program itself. Target audiences were segmented according to heart disease risk levels, with the intent of sending customized communication pieces to each segmented group. The team then developed direct mail pieces, point-of-service signage and HTML e-mails that specifically highlighted the Women’s HeartAdvantage program, our Web site and call center phone number, and–most importantly–encouraged individuals to continue their relationship with DBC.

Capturing this information via phone logs or WebTrends, for example, allows us to send group-specific e-newsletters to program participants. In one month’s e-newsletter, for instance, members of the “high-risk” group received content that emphasized the factors that put people at risk for heart disease. In the same month, members of the “health management” group instead received tips for managing stress.

Objective To examine whether women who develop coronary heart disease have different patterns of fetal and childhood growth from men in the same cohort who develop the disease.

Design Follow up study of women whose body size at birth was recorded and who had an average of 10 measurements of height and weight during childhood.

Setting Helsinki, Finland.

Subjects 3447 women who were born in Helsinki University Central Hospital during 1924-33 and who went to school in Helsinki.

Main outcome measures Hazard ratios for hospital admission for or death from coronary heart disease. Results Coronary heart disease among women was associated with low birth weight (P = 0.08 after adjustment for gestation, P = 0.007 after adjustment for placental weight) and was more strongly associated with short body length at birth (P = 0.001 and P [is less than] 0.0001, respectively). The hazard ratio for women developing coronary heart disease increased by 10.2% (95% confidence interval 4.3 to 15.7) for each cm decrease in length at birth. The effect of short length at birth was greatest in women whose height “caught up” after birth so that as girls they were tall. Such girls tended to have tall mothers. In contrast, men in the same cohort who developed the disease were thin at birth rather than short, showed “catch up” growth in weight rather than height, and their mothers tended to be overweight rather than tall.

Conclusion Coronary heart disease among both women and men reflects poor prenatal nutrition and consequent small body size at birth combined with improved postnatal nutrition and “catch up” growth in childhood. The disease is associated with reductions in those aspects of body proportions at birth that distinguish the two sexes–short body length in women and thinness in men.

Introduction

In both men and women the development of coronary heart disease has been shown to be associated with low birth weight in relation to the length of gestation.[1-3] An interpretation of this is that coronary heart disease originates through adaptations that the fetus makes when it is undernourished.[4] These adaptations include alterations in metabolism, hormonal output, and the distribution of cardiac output, and they may be combined with slowing of growth.[5] Birth weight is a crude marker of fetal growth, as the same birth weight may be the outcome of many different paths of growth.[6] Insights into the fetal adaptations that lead to coronary heart disease have come from studying body proportions at birth. Thinness at birth and shortness at birth–outcomes of different paths of reduced fetal growth–have been found to be associated with different biological risk factors for coronary heart disease.[4] Placental weight has also been found to be an independent predictor of coronary heart disease in some studies.[7 8]

We have previously described death rates from coronary heart disease among a group of men who were born in Helsinki during 1924-33.[8 9] Their body size at birth was recorded in detail. As expected coronary heart disease was associated with low birth weight, after adjustment for gestation, but was more strongly associated with thinness at birth, measured by a low ponderal index (birth weight/length[3]). The growth of these men through childhood and their living conditions were also recorded. This allowed us to examine for the first time the association between childhood growth and death from coronary heart disease, taking into account size at birth. We found that the highest death rates from coronary heart disease occurred in boys who were thin at birth but whose weight caught up so that they had an above average body mass from the age of 7 years.

We report here findings among the corresponding cohort of women born in the same hospital over the same period of time. The tempo of fetal and childhood growth differs in boys and girls.[10 11] Hence the paths of early growth that lead to coronary heart disease may differ in the two sexes.

Methods

We studied a sample of women who were born at the University Central Hospital during 1924-33 and who went to school in the city of Helsinki; 60% of all births in the city occurred in this hospital. Details of the birth records kept there have been previously described? Data on the mothers include age, parity, height, and date of last menstrual period, together with body weight measured on admission in labour. Data on their newborn babies include birth weight, length, head circumference, and placental weight. We studied women who were born at the hospital and who went to school in the city of Helsinki and were still resident in Finland in 1971. School health records for all children attending school in Helsinki are stored in the city archive. Details of these records have been described previously.[9] They include an average of 10 (SD 4) measurements of length and weight between the ages of 6 and 16 years, recorded at periodic medical examinations. They also include the number of other people living in the child’s home–recorded at the time of first examination–and the number of rooms. Since 1971 all residents of Finland have been assigned a unique personal identification number.

Objective To summarise quantitatively the association between moderate alcohol intake and biological markers of risk of coronary heart disease and to predict how these changes would lower the risk.

Design Meta-analysis of all experimental studies that assessed the effects of moderate alcohol intake on concentrations of high density lipoprotein cholesterol, apolipoprotein A I, fibrinogen, triglycerides, and other biological markers previously found to be associated with risk of coronary heart disease.

Participants Men and women free of previous chronic disease and who were not dependent on alcohol. Studies were included in which biomarkers were assessed before and alter participants consumed up to 100 g of alcohol a day.

Interventions Alcohol as ethanol, beer, wine, or spirits.

Main outcome measures Changes in concentrations of high density lipoprotein cholesterol, apolipoprotein A I, Lp(a) lipoprotein, triglycerides, tissue type plasminogen activator activity, tissue type plasminogen activator antigen, insulin, and glucose after consuming an experimental dose of alcohol for 1 to 9 weeks; a shorter period was accepted for studies of change in concentrations of fibrinogen, factor Vii, von Willebrand factor, tissue type plasminogen activator activity, and tissue type plasminogen activator antigen.

Results 61 data records were abstracted from 42 eligible studies with information on change in biological markers of risk of coronary heart disease. An experimental dose of 30 g of ethanol a day increased concentrations of high density lipoprotein cholesterol by 3.99 mg/dl (95% confidence interval 3.25 to 4.73), apolipoprotein A I by 8.82 mg/dl (7.79 to 9.86), and triglyceride by 5.69 mg/dl (2.49 to 8.89). Several haemostatic factors related to a thrombolytic profile were modestly affected by alcohol. On the basis of published associations between these biomarkers and risk of coronary heart disease 30 g of alcohol a day would cause an estimated reduction of 24.7% in risk of coronary heart disease.

Conclusions Alcohol intake is causally related to lower risk of coronary heart disease through changes in lipids and haemostatic factors.

Introduction

The inverse association between moderate alcohol intake and coronary heart disease is documented in over 40 prospective studies in diverse populations.[1-5] Men and women who consume one to three drinks a day have a 10% to 40% lower risk of coronary heart disease than those who abstain. In most large studies risk of coronary heart disease decreases in a downward linear fashion with alcohol intake up to three drinks a day.[6-9] This reduction is generally attributed to the beneficial effects of alcohol on lipids and haemostatic factors.[5 10-13]

Over 75 experimental studies have examined the effects of alcohol intake on lipids, haemostatic factors, vitamins, glucose, insulin, and lipid peroxidation.[10 w1-w55] However, only a few epidemiological studies have simultaneously examined the relation between alcohol intake, biochemical variables, and subsequent risk of coronary heart disease.[w56-w61] From these studies it is estimated that half of the beneficial effect of moderate alcohol intake is due to increased high density lipoprotein cholesterol concentrations. This calculation may, however, be an underestimate because it does not take into account measurement error in the assessment of average alcohol intake or biological variability in high density lipoprotein cholesterol concentrations. In several of these studies potential confounding by other lifestyle factors–for example, diet, obesity, and physical activity–was also not considered. Furthermore, other biochemical variables, such as fibrinogen, triglycerides, von Willebrand factor, and insulin, were not examined in these simultaneous models.

We quantitatively summarised the effects of alcohol on a variety of biomarkers from experimental studies using standard meta-analysis methods, and we projected the impact of those changes on risk of coronary heart disease using data from published studies relating biomarker concentrations to coronary heart disease.

Methods

We searched Medline for all experimental studies of alcohol (ethanol) in humans published in English between 1965 and 1998. We supplemented our search by examining citations in review articles,[1 3 14 15] the proceedings of meetings and symposia, and the Journal of the Alcohol Beverage Medical Research Foundation and Alcohol Research–journals that track alcohol related research. We restricted our search to studies in individuals without diagnosed coronary heart disease, diabetes, or alcohol dependence. We included only those studies that assessed biomarkers consistently modified by alcohol and related to risk of coronary heart disease. For lipid factors we included only studies with an intervention period of at least seven days; shorter intervals seem to have little or no effect. We included all studies of coagulation and thrombolytic factors because effects have been documented within hours after consumption of alcohol. Although we describe studies of lipid peroxidation and platelet aggregation we did not include these in our quantitative analyses because these assays were not comparable across studies owing to major differences in methodology. Furthermore, most were assessed with in vitro assays, which have not consistently been linked to risk of coronary heart disease.

You sure may have heard about ‘blue babies.’ But please don’t get it wrong. The ‘blue’ should not be in any way taken as a reference to their bloodline. Blue babies are not descendants of royal families and noble clans. Well, at least, not necessarily. Blue babies are actually infants inflicted with one of the many possible inborn heart defects. To your surprise, there are even cases of ‘pink babies.’

Congenital heart disease is the abnormal formation of the heart, usually of the large blood vessel. The word congenital means being present at birth. So congenital heart disease means a heart’s defect already present at the onset of birth. Since this kind of defect is already present the moment a human life is born, the condition is most prevalent, if not exclusive, among new born babies. Defects affecting the heart are actually the most ordinary birth defects, causing most of the inborn abnormality-related death cases. Just like most defects affecting the heart, inborn heart disorder is an abnormality to the flow of the blood. It may be in the form of obstruction or incorrect flow pattern.

Of all possible inborn abnormalities, inborn heart defect accounts for eight in every 1,000 cases, close to 1% of newborn babies. A major factor of this disease being congenital is genetic predisposition. Genetic influence accounts for the 5 percent of all babies with inborn heart defects. Genetic diseases such as Apert syndrome, Conradi syndrome, Crouzon syndrome, Carpenter syndrome, Cornelia de Lange syndrome, and cutis laxa are identified by medical research and studies to increase the risk of having inborn heart defects. Mothers having diabetes mellitus, specifically those who have deficient glucose level in the blood during pregnancy, are very likely to give birth to babies with inborn heart defects. Also, pregnant women with phenylketonuria (PKU)and poor diet have high chances of having babies with inborn heart defects. Many pregnant women having retinoic acid treatment for acne increases the risk of their babies having inborn heart disorders. Anticonvulsant drugs (hydantoins or Dilantin) and valproate taken during pregnancy also increases the risk of babies having inborn heart defects.

Disorders in the chromosomes also contribute as high risk factors of inborn heart defects. This factor is known to account for the 3% of infants with inborn heart defects. Down’s Syndrome is a chromosomal disorder leading to inborn heart defects. On rough estimates, almost half of kids having Down’s syndrome also suffer from inborn heart disorders. Patau syndrome and Edwards syndrome are also chromosomal defects known to be high risks factors of inborn heart disorders. Turner syndrome, a disorder in the sex chromosome (having only one x chromosome), places 40 percent risk rate of inborn heart defects. Albeit its lower risk level than the others, environmental components are also contributory to risks of inborn heart defects. German measles and alcoholism of pregnant women can lead to their babies being born with heart defects.

It may be a great wonder for many why pre-birth detection cannot be done to diagnose inborn heart defects. This is so because the fetuses’ blood circulation inside the womb is different from how it is after birth. No need to further elaborate on how do they differ. The point is that the difference leads to bringing to light the inborn heart defects. Usually, inborn heart disorders are only detected once symptoms like shortness of breath, skin discoloration, fainting, dizziness, inferior appetite, and poor growth are observed.

‘Blue babies’ and ‘pink babies’ are the most common but just two of the many types of inborn heart defects. ‘Blue babies’ or cyanotic defect is the bluish discoloration of the skin due to poor oxygen supply in the blood. ‘Pink babies’ or acyanotic defect, on the other hand, is the abnormal shunting (left to right vasculature) or the absence of oxygen. Other types of inborn heart defect are Hypoplastic heart defects (underdeveloped parts), Atrial septal defect, Eisenmenger’s complex, Ventricular septal defect, endocardial cushion defect, Ebstein’s anomaly, and many others.

There exists no single, universal treatment for inborn heart defects. The kind of treatment needed depends on the particulars of each specific case. The type of the inborn heart defect, age, general health condition, and heart size will all matter in determining the necessary treatment. Surgery is the most common option, though.

Eventually almost everyone will experience the problem of having high cholesterol but having high cholesterol as a result of a bad diet is simply inexcusable. For most of us it is nearly impossible to eat a totally healthy diet all of our lives since we don’t have the resolve of Jack LaLanne who at over 90 years old has never eaten anything man made! Still it is vitally important that all of us learn to eat as healthy as possible for the health of our hearts and to have a chance at a longer life.

One thing we know for certain is that if you eat a diet that is high in saturated fats like those found in fatty red meats and cooking oils you are going to see an increase in cholesterol which is proven to be a major factor in heart disease. A recent study that was just released states that just being overweight a few pounds can contribute to heart disease, so you might want to start on that diet and exercise program now!

One simple thing that you can do to prevent heart disease is to eat more fish. Salmon, herring and sardines are all excellent sources of Omega 3 essential fatty acids. Many other fish are good for heart health as well, although Omega 3 may help to get your cholesterol down to a healthier level easier. Even red meat lovers can learn to enjoy seafood and nuts for their main sources of protein.

Use monounsaturated fats such as olive oil to protect your heart, olive oil is an ideal choice for cooking, dressing, or even as a dipping sauce.

It is also well documented that eating a diet high in fiber will help to control cholesterol. Whole grain products are very high in fiber and also help to control sugar absorption which will go a long way to keeping your digestive system healthy.

Choosing the right carbohydrates is also important for heart health. You need to avoid high sugar food like candy, pastries, cakes and cookies and eat healthy carbohydrates like whole grain bread and pasta, brown rice, and plenty of vegetables. As a matter of fact fruits and vegetables should be the core of a healthy diet. A simple rule of thumb to avoid processed foods is to do your shopping on the outside aisles of the grocery store.

As far as cooking methods go, frying is a total no-no. Stir frying in olive oil or canola oil is okay but you should never deep fry foods and that goes for eating out as well. Chicken is healthy and good for you if you remove the skin and bake the chicken instead of frying.

Making these changes will take time before they become habits but just remember that eating healthy is essential for a healthy heart and a long life.

All this time, people or professionals only talk about ways to lower your cholesterol. But, have they really explained to you the significant details about cholesterol that you need to know before trying to lower the level?

If they haven’t, these 5 basic facts about cholesterol are important for you:

1. Cholesterol Levels

There are actually five different ways that you can use in order to get a complete reading on your own cholesterol levels and they are: total cholesterol levels, HDL, LDL, total/HDL ratio, LDL/HDL ratio. Measurement units for checking your cholesterol are conducted as milligrams per deciliter.

Your overall desired level should be below 200 mg/dL, 200 to 240 for a borderline level and total risk above level 240.

2. HDL Level

HDL stands for High Density Lipoproteins. It is actually just a section of your overall cholesterol. The normal range of HDL level for men about 40 to 50 mg/dL, and for women 50 to 60 mg/dL. The higher it is the better. Their role in our body is to carry cholesterol away from the body as soon as LDL has brought it. They’re the ones that help you reduce the risk of heart disease and cardiac problems.

3. LDL Level

LDL stands for Low Density Lipoproteins. When it comes to LDL, you prefer the level to be low. Why? Because they can clog arteries and kill us. That’s why they are called bad cholesterol.

Yet, the balance between HDL and LDL is what gives us general health.

4. How to Lower Your Cholesterol

The alternatives to using drugs are natural cholesterol reducers which could also be found in many whole foods.

One of them is garlic. Garlic is considered a natural reducer because it acts as an inhibitor. The other one is omega 3. Fish oils with their omega-3-fatty acids are also known to reduce heart disease by at least 40%.

5. Risk Factors for High Cholesterol

There are some risk factors that might cause high cholesterol that you’d better avoid.

Fast foods, chips, soft drinks, candy bars, refined sugars, butter cream, fried cheese, fried dough, and cotton candy are foods that we’ve been enjoying since we were kids. But, they are the foods that can contribute to your high cholesterol.

They taste delicious in our mouth but they are harmful for our health. Don’t let a little joy hurt you. Diabetes, kidney disease, liver disease, hyperthyroidism are just some of the dangers that these foods can cause; high cholesterol is just another side effect.

However, this above basic knowledge will be easier to apply if you have decided to lead a healthy lifestyle. Make sure that you won’t suffer from any disease only because of your ignorance of health.

Although it’s more interesting to see both good and bad news about the coffee controversy, the only thing to conclude is that the news keeps getting better for coffee drinkers. In a report published by coffeescience.org. The researchers conclusion was that their was no evidence of an adverse relationship between coffee intake and coronary heart disease.

While you can’t make up your mind by just one study the researchers mention that coffee:

• protects against type 2 diabetes,
• increases stamina,
• decreases leg pain associated with exercise, and
• keeps you alert and active.

Coffee has also be found to be rich in antioxidants, something that is a no-brainer to consider increasing. You should only take advice from your doctor, just be certain that he/she has all the needed information to make a recommendation.

In the study they took into consideration:

• age,
• weight,
• height,
• smoking status,
• parents history,
• plus a few more things.

I’m not trying to convince anybody of anything, we all have our own minds to wrestle. They also mention that coffee is rich in antioxidants and to give them a quote “…men and women who drank six or more cups of coffee a day had a slightly lower risk of fatal coronary heart disease”.