BMI may be calculated as follows:

Convert weight in pounds to kilograms by dividing total weight by 2.2.
Determine height and convert to inches.
Convert height in inches to meters. 1 meter equals 39.37 inches. (Height in inches 4 39.37 = height in meters.)
Square the height in meters by multiplying it by itself.
Divide weight in kilograms by height in meters squared.
This calculation can be done by a weight loss physician or over the phone by calling (800) 226-2370.

The Risks of Obesity: The Benefits of Weight Loss
Research has clarified the reasons that fatness increases cardiovascular risks. Obesity forces the heart into intensive labor because useless pounds must be serviced in the same fashion as valuable tissues and organs. The risk of diabetes and hypertension increases almost 3 times in obese individuals. For example, a weight gain of 10% can increase systolic blood pressure by 6.5 mmHg and fasting blood glucose by 2 mg/dL. Blood cholesterol levels typically increase by about 12 mg/dL for each 10% of weight gained and HDL levels decrease (Family Practice Notebook 2000). Even a 5- to 10-pound weight loss can provide significant health benefits such as lowered blood pressure or improved blood glucose control in the diabetic (Chandler 2002). Other factors increasing cardiovascular risk, such as excessive fibrinogen, elevated C-reactive protein, and insulin resistance, often share a common denominator, that is, obesity.

A 10- to 15-pound weight loss can also lessen the risk and progression of Syndrome X. As weight drops, tissues become more insulin sensitive, amending a primary identifiable trait in Syndrome X. Although not all obese individuals develop Syndrome X, the more overweight one is, the greater the risk of developing the syndrome and the clusters of disease factors surrounding it (a discussion of Syndrome X as an antecedent to cardiovascular disease may be found in the section devoted to Newer Cardiovascular Risk Factors).

Overeating in the absence of obesity poses a cardiac risk, as well. Reports from patients indicated that unusually heavy meals were often consumed during a 26-hour period preceding a myocardial infarction (Lopez-Jimenez et al. 2000).

Leptin in Obesity and Heart Disease
Leptin, a hormone produced by fat cells, increases with obesity and appears to play a role in the vascular complications associated with overweight conditions. The discovery of leptin (in the last decade) raised hopes that it could be used as a drug to treat obesity. However, most obese people were later found to have elevated levels of the hormone, making leptin injections inappropriate. However, assessing leptin levels has emerged as a means of screening for heart disease.

The journal Circulation showed that men with established heart disease had blood leptin levels 16% higher than men considered heart healthy. Every 30% increase in leptin increased the risk of a heart attack or a vascular event 25% (Wallace et al. 2001). The association between leptin and heart disease was observed regardless of BMI, suggesting that leptin is a reliable marker for the amount of fat in the body. Body composition (the comparative proportions of protein, fat, water, and mineral components in the body) may thus be a better indicator of risk for heart disease than overall obesity.

The levels of leptin, structurally a cytokine, rise in tandem with C-reactive protein (CRP), a marker of blood vessel inflammation and itself a significant heart risk. These findings imply that body fat influences CRP levels (Mercola 2002a) in addition to a myriad of other health problems.

JAMA recently reported that leptin has a stimulatory effect on platelet aggregation (Nakata et al. 1999; Bodary et al. 2002). The identification of a functional leptin receptor (OB-Rb) on platelets suggests a signaling mechanism between fat cells and platelets. To test the thesis, researchers examined mice deficient in leptin or the leptin receptor after a laboratory-induced vascular injury. Leptin-deficient mice had a prolonged time to occlusion, whereas leptin-deficient mice administered the hormone demonstrated a significant reduction in the time to occlusive thrombosis. Since leptin levels correlate well with adiposity, strategies aimed at weight reduction should remain the first line of defense. Lastly, exercise training in Type II diabetic subjects also reduced serum leptin levels independent of changes in body fat mass, insulin, or glucocorticoids (Ishii et al. 2001).

It is apparent that individuals need to establish a sensible approach to eating, that is, a program that can be comfortably maintained long term, void of either binges or periods of starvation. To lose weight only to regain it poses many health risks. For example, a decrease in HDL cholesterol is often reported in women who chronically cycle their weight from highs to lows (Merz 2000). Weight cyclers typically have 7% lower HDL cholesterol than noncyclers (Olson et al. 2000). To read about dietary supplements that may assist in weight loss, see the subsections relating to L-Carnitine, Chromium, CLA, and nutrients that lower serum insulin levels in the Therapeutic section of this protocol.

DIABETES

The degenerative process that accompanies diabetes significantly affects the heart. Atherosclerosis tends to develop early, progress rapidly, and be more virulent in the diabetic. Data released from the Framingham Study showed a 2.4-fold increase in congestive heart failure in diabetic men and a 5.1-fold increase in diabetic women over the course of the 18-year study (Fein et al. 1994).

Diabetics are particularly susceptible to silent myocardial infarctions, that is, an asymptomatic attack that interrupts the blood flow to coronary arteries. More than 80% of people with diabetes die as a consequence of cardiovascular diseases, especially heart attacks (Whitney et al. 1998). High homocysteine levels also play a significant role in diabetes-induced cardiovascular disease. In fact, hyperhomocysteinemia is considered a reliable predictor of mortality among diabetic patients.

Typically, Type II diabetes develops because of a lack of insulin sensitivity at the cellular level. As a result, the bloodstream becomes overloaded with nonfunctional insulin and a glut of glucose. The reason for this is that as glucose is increasingly unable to be used for energy metabolism and accumulates in the blood, the pancreas secretes more insulin in a futile attempt to restore normal glycemic control. After an extended period of excess insulin secretion, the pancreas may lose its ability to produce insulin, and the Type II diabetic may then become insulin dependent. When insulin loses its sensitivity or receptivity, its metabolic disposition changes, and insulin becomes more of an adversary than an advocate within the host.

Much of the stress of diabetes is due to a constant state of flux, that is, moving from hyperglycemia to hypoglycemia in a relatively short period of time. Nondiabetics are spared glycemic-induced stress. For example, most healthy individuals maintain postabsorptive blood glucose levels of 90-100 mg/dL. Even after fasting or overeating, blood glucose levels seldom fluctuate lower than 60 mg/dL or over 160 mg/dL (Pike et al. 1984). It has been suggested that evolutionary success requires a staunch defense of the range of blood sugar, since exceeding the limits at either end produces dire circumstances. An unstable diabetic lacks the homeostatic mechanisms that provide for intricate glucose balance, and as a result the heart and circulatory system suffer.

Chronic hyperglycemia causes monocytes and adhesion molecules to bind to vessel walls. In turn, cholesterol and other lipids are more easily deposited. Lipids become disorganized, with more of the LDL cholesterol and less of the beneficial HDL cholesterol appearing in the bloodstream (Reaven 2000). As the volume of urine produced increases, life-saving minerals are often excreted with urine. Without adequate mineral representation, the heart can be forced into fatal arrhythmias. Hypertension, abnormal coagulation, and obesity multiply the health concerns that frequently plague diabetic patients.

During hypoglycemia, the ability of the nervous system to function decreases, but the breakdown of fats increases. In this situation, fat assumes the role of a glucose surrogate. Necessary as this mechanism is, it is not without a disadvantage. Substitute pathways are not always well regulated, and excess fats not used as an energy source may accumulate, contributing to the atherogenic process.

The symptoms of hypoglycemia can mimic a heart attack, that is, dizziness, fatigue, sweating, shakiness, lightheadedness, palpitations, and in some cases, unconsciousness. Normal brain function requires 6 grams of glucose an hour, which can be delivered only if arterial blood contains over 50 mg/dL of glucose (Pike et al. 1984). Although hypoglycemia is not a heart attack, the stress imposed upon the heart can be significant.

To learn more about the impact that Obesity, Stress, Gender, and a Sedentary Lifestyle have upon diabetes, consult those subsections in the Traditional Risk Factors section of this protocol; other relative information may be found in the Fibrinolytic Activity and Syndrome X subsections of Newer Risk Factors (also in this protocol). For natural suggestions to benefit a diabetic, read about Alpha-Lipoic Acid, L-Carnitine, Chromium, DHEA, Essential Fatty Acids, Fiber, Garlic, Magnesium, Olive Leaf Extract, Selenium, Vitamin A, Gamma-Tocopherol, Vitamin K, and Zinc in the Therapeutic section of this protocol. The Diabetes protocol in this book should be thoroughly studied by individuals with unstable blood glucose levels.

HYPERCHOLESTEROLEMIA AND DERANGED LIPID PROFILES

Too much cholesterol is not good, but too little may not be good either. The American Heart Association announced in 1999 (at the annual Stroke Conference) that people with cholesterol levels less than 180 mg/dL doubled their risk of hemorrhagic stroke compared to those with cholesterol levels of 230 mg/dL; however, the risk of a stroke escalated as cholesterol levels exceeded 230 mg/dL. It is estimated that high cholesterol levels account for about 10-15% of ischemic strokes; low cholesterol may be a contributing factor in nearly 7% of hemorrhagic strokes. The National Cholesterol Education Program announced that cholesterol levels of approximately 200 mg/dL appear ideal for stroke prevention (CNN 1999; Mercola 1999).

Nonetheless, opinions are still divided as to the magnitude of the hypocholesterolemic risk. Until the quandary has been fully resolved, there are reasons to be cautious about severely reducing dietary fat and serum cholesterol. Recall that in foods, triglycerides carry the fat-soluble vitamins (including vitamin K, an extremely important nutrient in normal blood coagulation) (Whitney et al. 1998). In addition, some researchers believe that hypocholesterolemia weakens cerebral arterial walls, making breakage under pressure more likely (Hama 2001). (About 20% of all strokes result from cerebral hemorrhages.) Various studies indicate that very low levels of cholesterol may also increase the risk of death due to cancer, particularly leukemia and lung cancer (Zyada et al. 1990; Telega et al. 2000).

Cholesterol is so important that the body produces from 800-1500 mg each day to provide for the following metabolic processes:

Cholesterol is present in every cell in the body, strengthening cell walls and assisting in the exchange of nutrients and waste materials across membranes.
The central nervous system, composed of the brain and spinal cord, contains nearly one-fourth of the body's store of cholesterol. As much as 50% of myelin (the insulating sheath on many nerve fibers) is cholesterol. Cholesterol is essential for the conduction of nerve impulses.
Bile acids, formed from cholesterol, are vital for proper fat digestion.
Cholesterol is the precursor of adrenal and reproductive steroid hormones.
Surface cholesterol makes the skin resistant to chemicals and disease organisms, hindering entry through pores. Cholesterol stored in the skin assists in converting sunlight to vitamin D.
Although high concentrations of total serum cholesterol are related to mortality in individuals younger than 65 years, clinical trials have failed (until recently) to look at large numbers of individuals (> 70 years of age) to assess their response to higher cholesterol levels. According to data published in The Lancet, the risk imposed by hypercholesterolemia decreases with age (Weverling-Rijnsburger et al. 1997; Schatz et al. 2001). In fact, hypocholesterolemia (low cholesterol levels) appears associated with higher death rates among elderly people, due to mortality from cancer and infection. Therefore, administering a hypocholesterolemic drug to senior subjects may actually increase their risk of succumbing through other forms of degenerative disease.

Dr. Steven Whiting, dean of the Institute of Nutritional Science, explains how cholesterol can change from an essential sterol to an atheromatous material. Free radicals and hypertension can damage the inside of an artery, causing a small rupture or tear to occur. The body recognizes the problem and attempts to handle it with the materials available. Fibrin, a stringy, insoluble protein, is the first material laid down at a wound sight. Fibrin does what it must: seal or coat the damaged area in the artery. Unfortunately, fibrin can grasp other bloodstream infiltrates in its web-like structure, that is, collagen proteins and minerals that have precipitated out of solution. According to Dr. Whiting, a significant bump in the arterial pathway may have developed and then along comes cholesterol. Cholesterol appears to add the final coat to the plaque, building up in the artery (Whiting 1989).

Optimal Ranges of Blood Lipids
When levels of HDL (high density lipoproteins, also known as good cholesterol) are elevated, cardiovascular disease is reduced. The HDL2 subfraction is even more correlated with cardiac protection and longevity than total HDL cholesterol (Sardesai 1998). Typically, low triglyceride/LDL levels and high HDL levels place an individual in a better position cardiovascularly. HDL levels are considered desirable in a range of 50-70 mg/dL.

Total cholesterol for most individuals appears best managed between 180-200 mg/dL. The "how low can you go" logic is not wise when setting relevant cholesterol goals, considering the many functions assigned to cholesterol and the unsettled questions surrounding the safety of very low cholesterol levels.

The risk factors for heart disease are often calculated by dividing total cholesterol by HDL. Assessment of the HDL-total cholesterol ratio is not standardized, but according to Health and Wellness (Sixth Edition), a value of 4.5 places the individual at an average risk; a ratio above 4.5 indicates an increased risk; and a ratio below 4.5 means a decreased likelihood of developing heart disease (Edlin et al. 1999).

Most laboratories use a reference range of 90-130 mg/dL for LDL cholesterol, but LDL appears optimal at 100 mg/dL or lower. Dr. Henry Ginsberg (Columbia University) estimates that reducing LDL cholesterol 7% may translate into a 15-20% reduction in risk of coronary heart disease (Ginsberg et al. 1998). Note: LDL cholesterol is not measured directly; levels are calculated using the following formula:

LDL = total cholesterol - HDL - (triglycerides 4 5).

Cholesterol tests indicating acceptable levels may convey a false sense of security. Current research indicates that standard cholesterol tests miss 50% of people at risk for heart attacks, due to the inability to detect abnormally small cholesterol particles. Note: Syndrome X is characterized by abnormal lipoprotein metabolism, showing smaller, denser LDL particles. To read more about Syndrome X, please consult the Newer Risk Factors section in this protocol.

LDL pattern B is the smallest and most susceptible to oxidation of all forms of cholesterol. Both LDL pattern B and lipoprotein(a) increase the risk of heart attack threefold; neither can be detected by standard cholesterol tests. Without the detection of the smaller cholesterol subsets and the appropriate treatment, plaque buildup progresses twice as fast. Trapped LDL or lipoprotein(a) over time forms plaque with a fibrous cap. Unstable plaque can rupture, which causes the blood to clot, increasing the risk of sudden heart attacks or strokes. Laboratories providing total screening, that is, testing for normal and abnormal-sized lipoproteins, should be used for evaluations.

Triglyceride levels are usually regarded within a normal range at 30-199 mg/dL, but researchers have found that patients with clinical coronary heart disease were less likely to experience new events if tri-glyceride levels were below 101 mg/dL (Kreisberg et al. 2000). Most clinicians believe that triglycerides are best maintained below 101 mg/dL in all subsets of the population. Perhaps J.M. Gaziano (Harvard Medical School) led the most startling study in regard to the risks imposed by deranged blood lipids. The subjects with the highest ratio of triglycerides to HDL had a 16-fold greater incidence of coronary events compared to those with the lowest ratio (Gazinao et al. 1997).

Triglyceride levels rarely rise unless one has insulin resistance or hyperinsulinemia, conditions often modifiable by controlling carbohydrates in the diet. According to the data reported in Atherosclerosis, elevated triglyceride levels usually modulate when less food is consumed, particularly foods causing a rise in blood sugar levels, that is, bakery products, pastas, and foods with added sugar (Stavenow et al. 1999; Atkins 2002). Note: Other areas in this protocol relating to hyperlipidemia are heredity, sedentary lifestyle, gum disease, hypothyroidism, hemochromatosis, fibrinogen, Lp(a), homocysteine, Syndrome X, and C-reactive protein. Read about natural lipid-reducing agents such as artichoke extract, L-carnitine, chromium, conjugated linoleic acid, curcumin, DHEA, essential fatty acids, fiber, garlic, ginger, grapefruit pectin, gugulipid, hawthorn, niacin, pantethine, policosanol, poly-enylphosphatidylcholine, and tocotrienols in the Therapeutic section of this protocol.

STRESS

More than one-quarter of a million heart episodes occur annually--that is, palpitations, angina, arrhythmias, and heart attack--as a result of a stressful experience. This is particularly evidenced when an ailing heart struggling to keep pace with circulatory demands is forced to deal with an emotional provocation. The journal Circulation reported that an individual who is prone to anger is about 3 times more likely to have a heart attack or sudden cardiac death than someone who is the least prone to anger (Williams et al. 2000).

The journal Life Sciences offers an explanation for stress-related cardiovascular events. Higher levels of homocysteine are associated with feelings of aggression and rage in both men and women (Stoney et al. 2000). Individuals may be spurred into erratic behavior by metabolic processes gone awry. The modulation of homocysteine levels may allow a more docile individual to emerge, less cardiac risk prone from two perspectives (less homocysteine = less violent behavior and less cardiac disease). A comprehensive review of homocysteine appears in the section devoted to Newer Risk Factors. Vitamins and minerals to maintain healthy homocysteine levels are presented in the Therapeutic section.

Type A individuals are also at a greater cardiovascular risk because their lives are dominated by self-imposed stress. Work expectations are driven by an unrelenting desire to achieve. An exaggerated sense of time urgency prompts accelerated locomotion and faster decision-making. Cynicism, hostility, and impatience snuff out many personal relationships and deny the heart a much needed rest from disharmony.

Under stress, the sympathetic nervous system is alerted and the release of adrenaline increases; ultimately, one's breathing, heartbeat, and blood pressure also increase. Cardiac patients are often prescribed beta-adrenergic blocking agents to calm the sympathetic nervous system, a gesture that asks a drug to succeed where attempts at lifestyle changes may have failed.

Type D behavior, another variant having heart disease linkage, was described in The Lancet (Denollet et al. 1996). Withheld and denied emotions, that is, refusing to cry even when weeping is justified and a lack of social connectedness (traits common to a type D personality), appear contributory to heart disease and stroke.

During periods of mental or emotional arousal, a silent ischemic attack (a decreased supply of oxygenated blood) can occur. Although asymptomatic, severe heart damage may result. Unlike an angina attack, which is usually prompted by physical exertion, more than three-fourths of silent ischemic attacks are caused by mental arousal. There is also a definite link between the hardening of the carotid artery and higher levels of stress (Barnett 1997).

A recent study of 2800 men and women over 55 years of age showed that even minor depression can increase cardiac mortality 60%, while major depression may actually triple the rate of cardiac-related deaths (Brenda et al. 2001). There is also convincing evidence that depression significantly increases the risk of mortality following a heart attack or coronary bypass surgery (Baker et al. 2001).

Researchers explain the relationship between mindset and mortality, pointing out that stress response to depression appears to trigger chronically high cortisol levels, a hormone secreted by the adrenal glands (Koenig et al. 1999a). Hormonal imbalances, in turn, can alter insulin resistance and increase blood pressure, magnifying the risks imposed by a heart attack or bypass surgery.

A study conducted at Duke University (Durham, NC) showed that men with established heart disease who underwent 4 months of stress management (1.5 hours weekly) experienced a significant reduction in clinical cardiovascular events. The advantage was observed at the conclusion of counseling and throughout 5 years of assessment, suggesting both economic as well as clinical benefit (Blumenthal et al. 2002).

Stress protracts to so many traditional risk factors that emotions may be the dominant issue in coronary health. Note the following risk factors that share stress as their common bond.

Stress can destroy sound eating habits by the uncaring selection of inappropriate foodstuffs, eating hurriedly, or eating not because of hunger but as a respite from a dismal situation. Stress is a strong contributor to obesity, a factor in cardiovascular disease.
Stress increases blood pressure. In studies involving 3000 Caucasians with depression and anxiety (ages 23-64), these individuals were found to have twice the risk of developing hypertension. The odds worsened for African Americans, with the risk factor for hypertension increasing more than 3 times during periods of unresolved stress. Even the companionship of a pet has been shown to reduce stress and subsequently blood pressure (Alexander et al. 1996; Beck et al. 1996).
Stress makes blood glucose levels more difficult to control (Challem et al. 2000). Diabetes, a long-established risk to heart health, has been termed a disease fueled by emotions.
Alternative Medical News reports that stress increases blood cholesterol levels. Students preparing for exams, Indianapolis 500 drivers (following the race), and accountants after the April 15 deadline show higher cholesterol levels (Alternative Medical News staff 1995).

HEREDITY

Scientific testing has advanced genetic screening far beyond compiling an oral history of ancestral successes and failures. Instead, geneticists are looking for mutated genes that may be expressing themselves as contributors to coronary artery disease. For example, 50% of suppressed HDL cholesterol can be linked to genetic factors. A gene (ABC1), when mutated, appears responsible for increasing the risk of heart disease by lowering levels of HDL cholesterol. Michael Hayden (professor of medical genetics at the University of British Columbia) reports that people with defects in ABC1 have just as much risk for heart disease because of too little HDL as individuals with high levels of LDL cholesterol (Cosgrove 1999).

Assessing Apo-E Status
The apoE4 variant of apoprotein E is the most well-defined genetic trait affecting poor LDL levels. According to Ronald Krauss, M.D., a double allele (referred to as a double E4 genotype) is associated with high blood cholesterol and an increased prevalence of cardiovascular disease (American Heart Association 1998).

The apoE4 allele is very saturated fat sensitive, suggesting dietary manipulation may be an advantage to those with this genetic fault. In 90% or more of the population, modest dietary cholesterol has very little impact upon LDL cholesterol levels (Bland 2001). However, moderate dietary cholesterol intake in apoE4 individuals can lead to significant increases in plasma LDL levels. Jeff Bland, Ph.D., challenges that public health recommendations do not address genotypes that alter dietary guidelines. Recommendations to universally avoid cholesterol-rich foods prevent some who are not cholesterol sensitive from eating a food that is a "pretty good food," such as an egg.

There are three main alleles or variants of the apoE gene: E2, E3, and E4. Every individual inherits two of these alleles: one from each parent. Research has shown that each allele affects cholesterol metabolism differently. Smoking appears to increase the risk of coronary heart disease in men of all genotypes but particularly in men carrying the E4 allele. Researchers hypothesize that the genetic-coronary link may be due to increased oxidation of LDL cholesterol among smokers with this genotype. Compared to individuals who carry two neutral E3 alleles, those who carry at least one E4 allele tend to produce significantly more LDL cholesterol as well as more total cholesterol; those who have at least one E2 allele typically produce less LDL cholesterol (Humphries et al. 2001; Wang et al. 2001).

Establishing an apoE genotype in menopausal women sheds light on the complex issues of estrogen replacement therapy (ERT) as a cardioprotector. For example, women with the apoE-2 genotype (and using ERT) appeared to benefit the most from the lipid-altering effects of hormones compared to other genotypes. Menopausal women with the apoE-2 genotype (and not using ERT) have the lowest levels of protective HDL cholesterol. If on ERT, apoE-2 carriers have the highest HDL levels of all genotypes. This study suggests that the apoE-2 genotype may predispose a woman's body to produce more protective HDL cholesterol in response to ERT than those of other types (Heikkinen et al. 1999).

The study also showed that women with the apoE-3 genotype (and using ERT) had the highest levels of triglycerides. It appears women with the apoE-3 genotype are more sensitive to the triglyceride-raising effects of hormone therapy. A previous placebo-controlled study of over 150 postmenopausal Finnish women found that LDL cholesterol levels in women with the apoE-4 genotype respond less favorably to ERT (Heikkinen et al. 1999).

Studies that fail to consider genotype may explain the wide disparity in results regarding lipid levels and cardiovascular risk in postmenopausal women receiving HRT. With recent advances in genetic testing, another important piece of the puzzle is now available to help physicians predict how hormone replacement therapy will impact each woman's cardiovascular health (Kardia et al. 1999; von Muhlen et al. 2002).

Homocysteine: The Genetic Link
Compiling a family history of cardiovascular health is a common medical assessment, looking particularly at the early onset of disease. Because of an increasing awareness of the risks imposed by newer risk factors, homocysteine is being factored into the genetic equation. With a gene frequency between one in 70 and one in 200, elevated blood levels of homocysteine may be more common than previously thought (Berwanger et al. 1995). Canadian researchers estimate the inherited amino acid disorder (homocysteinemia) is present in approximately 20% of coronary artery disease patients (Superko et al. 1995).

There are multiple mechanisms involved in the pathogenesis of hyperhomocysteinemia, including not only heterozygosity, but dietary factors as well (Kardaras et al. 1995). Note: Heterozygous refers to inheriting a gene for a characteristic from one parent and the alternative gene from the other parent. The offspring of a heterozygous carrier (of a genetic disorder) has a 50% chance of inheriting the gene associated with the trait. In support of the genetic theory of hyperhomocysteinemia, epidemiological evidence has shown homocysteine levels to be 45% lower in Westernized adult black South Africans than in age-matched white adults, revealing racial genetic differences in homocysteine metabolism (Vermaak et al. 1991).

About one-half of individuals with hyperhomocysteinemia respond favorably to higher doses of vitamin B6 due to an inborn cystathionine-B-synthase deficiency; others have a mutation in the methylenetetrahydrofolate reductase gene (MTHFR), which controls the ability to convert folic acid into 5-methyl tetra-hydrofolate, an active contributor in the methyl donation pathway of the folate cycle (James et al. 1999). The disruption of this cycle represents the domino effect, that is, when one system fails to perform, others downstream are affected as well. In this case, homocysteine clearance is disrupted and hyperhomo-cysteinemia, a powerful endangerment to cardiac health, results. The genetic flaw is correctable by administering 5-methyltetrahydrofolate supplements (the active form of folate) to bypass the metabolic block (Bland 2000a).

Additional Inheritable Risks for Degenerative Disease

In 1991, researchers identified the gene responsible for hemochromatosis, a predominantly genetic disease reflecting abnormal iron retention despite eating an ordinary diet. Small numbers of individuals with hemochromatosis acquire the condition through chronic iron supplementation or blood transfusions, but the genetic form is most common. To learn more about hemochromatosis (a significant threat to heart health), consult the Iron Overload section.
The journal Arteriosclerosis, Thrombosis and Vascular Biology reported that carotid plaque was significantly more common in both men and women whose parents died prematurely of coronary heart disease (CHD) than in subjects with no familial history of early cardiac death (Zureik et al. 1999).
Lp(a) is frequently cited in medical literature as an important inheritable cardiac risk factor for individuals without other apparent signs of heart disease. Approximately 50% of children whose parents have elevated Lp(a) will also have similar Lp(a) derangements (Superko 1996). Although Lp(a) levels are influenced by heredity, this marker is often modifiable by targeted nutritional intervention.
Genetic factors can influence obesity and fat distribution. Laval University (Quebec, Canada) determined that pairs of identical twins, overfed by the same amount of calories, showed a similarity with respect to body weight and percentage of fat, with about 3 times more variance among pairs than within pairs. After adjustment for the gains in fat mass, the within-pair similarity was particularly evident with respect to the changes in regional fat distribution and amount of abdominal visceral fat, with about 6 times as much variance among pairs as within pairs. Researchers concluded that the tendency to store energy as either fat or lean tissue is influenced by genetic factors (Bouchard et al. 1990).
A condition known as Dunnigan-type familial partial lipodystrophy (FPLD) bears striking similarities to Syndrome X. The gene mutation responsible for FPLD causes weight gain in the abdomen as well as the face and chest. Affected individuals have high insulin levels, high blood pressure, high triglycerides, and low levels of HDL cholesterol. A recent study confirmed that individuals with FPLD have 6 times the risk of coronary heart disease compared to noncarrier relatives in a control group, that is, 34.8% versus 5.9% at any age and 26.1% versus 0% before the age of 55. The average age of developing heart disease was 46.5 years in individuals with FPLD, with the risk being greater among women than in men. Four of 14 women (about 28%) with FPLD underwent bypass surgery before the age of 55. In contrast, hospitalization data from the general Canadian population in 1996 indicated that one woman in 7350 had been hospitalized between the ages of 35-54 for coronary bypass artery surgery (Canadian Institute for Health Information, http://www.cihi.ca; Hegele 2001; Today's News 2001).

GENDER

At one time, cardiovascular disease was considered to be predominantly a disease affecting men, not women. Statistics do not support this logic. Studies have demonstrated that heart disease is the number one killer for both men and women. Of the 1.1 million heart attacks reported annually, about 500,000 occur among women.

The Framingham Study reported findings involving 5209 participants, 2873 of whom were women (Framingham Heart Study 1998). Results of the study follow:

In both men and women, coronary heart disease has exceeded that of other cardiovascular illnesses, such as stroke or congestive heart failure.
While coronary events occurred twice as often in men, with advancing age the incidence of heart disease in women approaches that seen in men. Menopause appears to be the interval associated with a significant rise in coronary events, as well as a shift to more serious manifestations of the disease.
The New England Journal of Medicine reported that hormone replacement therapy (HRT) in menopausal women with angiographic-determined heart disease did not lower the progression of the disease (Nabulsi 1993; Herrington et al. 2000). New guidelines issued by the American Heart Association agreed that women with cardiovascular disease should not be given HRT for the sole purpose of preventing future heart attacks. In fact, HRT raised the risk of recurrent attack and death during the first year of usage and thereafter lowered it only slightly (Mosca et al. 2001). Although estrogen replacement therapy may be helpful in lowering refractory lipoprotein(a) and high fibrinogen levels, it increases C-reactive protein levels, making its benefit uncertain (please read the previous section on Heredity and Assessing ApoE Status for extremely valuable information regarding HRT in postmenopausal women).
Coronary heart disease manifests itself differently in men and women. In women, angina was the most common initial symptom, whereas in men, myocardial infarction was the most frequent first coronary symptom.
High triglycerides were more predictive of eventual heart disease in women than in men. In fact, high triglycerides threaten the outcome in diabetic women undergoing bypass surgery (Sprecher et al. 2000). Elevations in C-reactive protein (CRP) are the single strongest predictor of future vascular risk, according to the Women's Health Study. Women with the highest levels of CRP in their blood had a fivefold increased risk of future cardiovascular disease and a sevenfold increase in the likelihood of a heart attack compared to those with low levels.
When a heart attack was the first coronary event, nearly half were unrecognized in women, compared to only a third undetected in men.
Only 56% of women experiencing a heart attack can expect to live another year, compared to 73% of male victims. Women under 50 years of age are twice as likely to succumb following the attack compared to similarly afflicted men. Statistics change with age, with men and women between the ages of 60-69 showing similar survival patterns (Mukumal et al. 2001): 27% of men who have a heart attack will likely have a second attack within 6 years compared to 31% of women.
Diabetes is a particularly strong coronary risk factor in women.
The New England Journal of Medicine reported that the risk of myocardial infarction increased among women who used second generation oral contraception, that is, levonorgestrel. Although inconclusive, early trials indicate third generation oral contraceptives, that is, desogestrel or gestodene, may carry a lesser risk (Tanis et al. 2001).
Many studies have demonstrated that men who are physically active tend to live longer, illustrating a clear exercise-response curve, with greater activity more effective than moderate. The New England Journal of Medicine recently reported similar findings for women. Both walking and vigorous exercise are associated with substantial reductions in the incidence of cardiovascular events among postmenopausal women; prolonged sitting is predictive of increased cardiovascular risk (Manson et al. 2002).

Cardiovascular Disease Protocol Pg (1) (2) (3) (4) (5) (6) (7) (8) (9) (10) (11) (12) (13) (14)

These statements have not been evaluated by the FDA. These products are not intended to diagnose, treat, cure, or prevent any disease