Welcome to Health Disease articles category.

You can find informaion on Health Disease articles and news.

A cluster of cardiovascular disease risk factors, known as the metabolic syndrome, may make arteries look old, according to an April 21, 2004, news release from the American College of Cardiology. Metabolic syndrome is a group of several cardiovascular risk factors, including impaired glucose tolerance, high blood pressure, low high-density lipoprotein cholesterol, and abdominal obesity.

Researchers analyzed data from 471 participants in the Baltimore Longitudinal Study of Aging who were free of pre-existing coronary artery disease. Data collection included ultrasound scans of the right common carotid artery, as well as measurements of blood pressure, body shape and mass, smoking, cholesterol, and blood sugar.

Researchers found that metabolic syndrome increased both the thickness and stiffness of the carotid artery, which are measures of its structure and function. Participants with metabolic syndrome had carotid arteries that were 16% thicker and 32% stiffer than the arteries of participants without those risk factors, and participants with at Least three risk factors had thicker and stiffer arteries than could be explained by simply summing up the effect of each individual risk factor.

Metabolic syndrome appears to accelerate age-related changes in blood vasculature, so that younger participants with metabolic syndrome have carotid artery thickness and stiffness levels similar to those of older people without metabolic syndrome. For example, a 40-year-old person with metabolic syndrome might have arteries that appear to be those of a 55- or 60-year-old individual

FOR years, Shirley Lytle considered herself the picture of health. She was a healthy nonsmoking professional who ran up to 4 miles three days a week, and practiced healthy eating habits.

Then one day, the unthinkable happened. Her doctor told her that she had coronary heart disease and that she could die of a heart attack if she didn’t undergo bypass surgery immediately. She was just 31 years old.

The Phoenix resident, now 43, had a successful operation, but for the rest of her life she will have to contend with coronary heart disease, a condition she inherited from the maternal side of the family.

Shirley Lytle is not alone. Nearly 4 in every 10 non-Hispanic Black adults have cardiovascular disease, according to the American Heart Association. This includes diseases of the heart, stroke, high blood pressure, congestive heart failure, congenital cardiovascular defects, hardening of the arteries and other diseases of the circulatory system, the association says.

Cardiovascular disease is the No. 1 killer of African-Americans, claiming the lives of 37 percent of the nearly 288,000 Blacks who die each year, according to the association. Risk factors include smoking, high blood pressure, diabetes, high cholesterol, obesity, stress and lack of exercise. Doctors say people have no control over some factors, including age, gender and family history.

While the disease strikes African-American men and women alike, it is particularly deadly for Black females, with 5 in every 10 dying each year of cardiovascular diseases, says Dr. Lynne Perry-Bottinger, a New York interventional cardiologist.

The reason is a clustering of risk factors, like diabetes, hypertension and obesity, in African-American women, says Dr. Anne L. Taylor, a professor of medicine at the University of Minnesota and director of the Association of Black Cardiologists’ Women’s Center, who edited and co-authored the recently released book, The African American Woman’s Guide To A Healthy Heart.

The cause of the disease’s deadly effect on African-American women is unclear, but it is believed to be related to genetics, environment and disparity in medical care, doctors say. Studies also show that the risk for cardiovascular disease increases in post-menopausal women. “If you go to the doctor and they make assumptions based on your race or gender, you may be deprived of care,” Dr. Taylor says. “African-Americans, especially women, are less likely to be referred for rehabilitation and diagnostic care. We have to educate the community about who’s at risk and what they can do about it.”

Cardiovascular disease knows no socioeconomic or educational bounds and can touch the lives of everyone, including high-profile performers like Toni Braxton. The singer was recently diagnosed with pericarditis, an inflammation of the pericardium, a thin lining of the heart. Her diagnosis and the experience of seeing several family members suffer or die from the disease led Braxton to become the American Heart Association’s official spokeswoman for the association’s “Go Red for Women” campaign, an initiative designed to help fight heart disease in women.

The staggering number of heart disease deaths in the Black community has set off an alarm throughout the medical community, generating studies like the so-called “African-American Heart Failure Trial.” The study of 1,050 Black patients found that a combination of two rarely used heart drugs, isosorbide dinitrate and hydralazine, cut the annual death rate of African-American heart failure patients by 43 percent and contributed to a 33 percent reduction in first-time hospitalizations.

Some critics described the study as medical profiling since it merely focused on African-Americans. But experts like Dr. Paul Underwood, a Phoenix interventional cardiologist, who is the president of the Association of Black Cardiologists (which co-sponsored the study), called the results significant, saying that Blacks traditionally have been underrepresented in clinical trials.

“The significance of the study is that in the past we had to assume that medicines that were good for the majority were good for African-Americans,” Dr. Underwood says. “By reanalyzing the small number of African-Americans in these trials, we may have different information. The clinical trial has opened up new possibilities in the treatment of cardiovascular diseases in African-Americans.”

The best weapon African-Americans have to help combat cardiovascular disease is education, which leads to preventative care and rapid intervention, as Shirley Lytle of Phoenix learned. Patients need to learn the symptoms so that they can demand better care from medical professionals, doctors say. And many need to change their lifestyles to incorporate exercise in their daily lives, eat healthy diets and train their children to do the same, doctors say.

“After I was diagnosed, I changed my lifestyle and that of my family,” Lytle says. “I exercised at the gym two hours a day. I changed my eating habits and took salt out of the house. There was nothing resembling bacon in my refrigerator. What I thought I was doing was trying to beat heart disease. I wanted it to be like eradicating cancer. Then I realized it was a lifelong effort, one which I am committed to.”

Heart disease is the leading cause of death in the US and is projected to be the leading cause of disability in the world by 2020. Researchers from Johns Hopkins University studied 900 heart disease patients and found that the more infectious agents patients tested positive for, the more likely they were to die of a heart attack. Researchers are not sure how infection causes heart disease, but hypothesize that it may have something to do with direct infection and inflammation of an artery wall. The healing of the infection results in plaque formation.

* Chlamydia Pneumoniae: a common pathogen that is present in respiratory infections such as pneumonia, sinusitis and bronchitis. By age 30, 50% of people have been infected with chlamydia pneumoniae; by age 70, that number rises to 80%. Some researchers suggest that an uneventful chlamydia pneumoniae infection during childhood could start a chronic infection of the coronary arteries that goes unnoticed until a heart attack occurs 50 years after the fact.

* Helicobacter Pylori: In the gastrointestinal tract, H pylori infection has been associated with a chronic lowgrade infection. Researchers are now linking the bacteria to heart disease as well. In one British study, heart attacks were twice as common among people infected with H pylori than people not infected with the bacterium.

* Dental Infections: Gum disease–both gingivitis and periodontal disease–is caused by several types of bacteria. In severe cases, bacteria can escape into the bloodstream and wreak havoc elsewhere in the body. In addition, free radicals generated by the inflammation of periodontal disease may promote the oxidation of LDL cholesterol, enhancing the development of atherosclerosis.

Piercing Your Ears Might Break Your Heart

People with congenital heart disease (which affects more than 1 million Americans) are at greater risk for developing life-threatening endocarditis, an infection of the heart valve, when they have body parts pierced or tattoos done. Performed improperly, piercing and tattooing open up the skin to potentially deadly bacteria. People at risk for this infection should take preventive antibiotics before undergoing any piercing procedures or tattooing.

Though relatively rare, endocarditis can also occur as a result of periodontal infection, urinary tract infection, pneumonia and certain dental procedures. Among high-risk people, endocarditis prevention via antibiotics is recommended for dental procedures including:

* Extractions

* Periodontal procedures including surgery and scaling

* Dental implants

* Root canals

* Placement of orthodontic bands

* Cleaning of teeth when bleeding is expected

The statistics are sobering. Infectious diseases are the third leading cause of death in the US after heart disease and cancer, claiming more than 100,000 Americans’ lives annually and costing more than $30 billion in direct treatment expense alone. Infectious diseases are responsible for a quarter to a third of the 54 million deaths globally each year and are the world’s leading cause of death among children and young adults.

The truth is that we are in the midst of a huge pandemic that is largely ignored by the mainstream medical community. As many as 75% of Americans suffer from some form of bacterial, viral, parasitic or fungal infection, running the gamut from hardly noticeable to devastating. These infections include conditions such as intestinal parasites manifested as ulcers and gastroenteritis, chronic sinus infection, strep throat, yeast (candida) infection, sexually transmitted disease, and urinary tract infection–to name a few. Even more frightening: today’s most virulent killers–heart disease and cancer–can develop from bacterial, viral, fungal, or parasitic infections.

Heart disease is the number one cause of death in this country. Dr. Matthias Rath, an international crusader for disease prevention, and staunch supporter of nutritional supplements, believes heart attacks and strokes are not true diseases, but the result of nutritional deficiencies. The heart may be considered the motor of the cardiovascular system, and as such requires optimum fuel for optimum performance. Superior fuel for the heart includes a variety of nutrients, vitamins, minerals, and more. Modern eating habits combined with an agricultural system dependent on synthetic chemicals accelerate nutritional deficiencies in our country. Dr. Stephen Sinatra, clinical cardiologist at Manchester Memorial Hospital in Connecticut, uses the term nutritionals to refer to vitamins, minerals, and other nutrients he recommends for improving cardiovascular function among his patients.

Vitamin C is essential for preventing cardiovascular disease and maintaining good health on many levels. Vitamin C is a major antioxidant and co-factor for many biochemical reactions. Its most important function is to stimulate the production of collagen, elastin, and other reinforcement molecules in the body. Collagen provides stability for bones, skin, and for the 60,000-mile-long walls of the arteries, veins, and capillaries. Dr. Rath, who worked closely with the great Linus Pauling, emphasizes “(T)he connection between vitamin C deficiency and instability of blood vessels is long established. Unfortunately, the next logical step has not been recognized until now: cardiovascular disease is nothing else than an early form of scurvy.”

Lesions and instability of blood vessel walls are primary causes of cardiovascular disease. Vitamin C is the cement that repairs and stabilizes blood vessel walls. In his book, Why Animals Don’t Get Heart Attacks … But Humans Do, Dr. Rath explains the importance of vitamin C. SAD, the Standard American Diet, provides barely enough vitamin C to prevent frank scurvy, but not enough vitamin C to provide stable, reinforced blood vessel walls. Cracks and lesions appear inside artery walls over time. Vitamin C is necessary for repairing artery walls and other wound healing. Insufficient vitamin C does not allow proper healing. To compensate, the body attempts to repair these lesions and cracks with an alternative method, making cholesterol and fat globules adhere to the inside of vessel walls to repair the damage. Prolonged vitamin C deficiency leads to an overabundance of atherosclerotic deposits in blood vessels. Deposits in arteries leading to the heart cause heart attacks. Deposits in arteries leading to the brain cause stroke. Dr. Rath believes optimum daily intake of vitamin C stabilizes blood vessel walls and helps prevent heart attacks and strokes. The reason animals don’t get heart attacks is because they produce their own vitamin C, whereas humans do not.

Coenzyme Q10

Dr. Stephen Sinatra calls CoQ10 the miracle nutrient of the 21st century, “because it has been proven to both prevent and treat a host of health problems including heart disease, cancer, periodontal disease and neurodegenerative diseases like Alzheimers.” “It can overcome male infertility, improve immune system function, and is an effective anti-aging remedy.

Coenzyme Q10 (ubiquinone) is an important catalyst inside the energy center of each cell, and is in high demand by the heart. “The body requires certain blood levels of CoQ10 to function properly, and when blood levels fall, an increased vulnerability to disease and premature aging occurs.” Dr. Sinatra believes that supplemental CoQ10 improves the quality of life in patients with disease, and saves lives as well. He has had remarkable results using CoQ10 with cardiac patients. CoQ10 has been proven useful in treating a variety of conditions including congestive heart failure, high blood pressure, angina, arrythmia, and other cardiological situations. Dr. Sinatra speaks of the negative bias against CoQ10 in mainstream medicine, where nutritional supplements get very little respect. Since it is not patentable it is not widely promoted among physicians and actually got bad press in a 1996 article in the Harvard Health Letter, which prompted Dr. Sinatra to reply regarding the amazing results he’s witnessed among his own patients.

Coenzyme Q10 protects and strengthens the heart while lowering blood pressure. Statin drugs, prescribed for millions of people to control cholesterol actually depletes CoQ10 levels in the body. Ironically, drugs marketed to reduce the risk of heart disease may, in fact, be increasing the risk of heart disease.
Vitamin E

Vitamin E is the most important fat-soluble antioxidant vitamin and primary ally against heart disease. It protects against free radicals and oxidative damage. Vitamin E is rich in low-density lipoprotein (LDL) and other cholesterol and fat transporting particles useful for preventing oxidation and interior blood vessel wall damage. It reduces the risk of blood clots by making platelets less sticky. A European study showed vitamin E “to be the most important risk factor for heart disease, beyond smoking.” Vitamin E has been shown to dissolve clots, improve heart pump efficiency, widen arteries, and increase the available oxygen in the blood.

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.