~Cardiovascular Disease Comprehensive 3 - Traditional Risk Factors
Traditional Risk Factors, continued
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).
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).
Scientists believe that a properly planned exercise program may be the single greatest preventive measure against cardiovascular disease. However, it is extremely important that the individual and the activity be properly matched. Even among apparently fit persons, intense but sporadic exercise actually increases the risk of a fatal heart attack. A singles tennis match in an unprepared participant increases the risk of a heart attack sixfold.
The exercise level need not be unpleasantly aggressive to be beneficial. In the past, it was thought that an individual using exercise as a cardiovascular protective should select an activity that produced a state of breathlessness and participate in the action several times a week. It has now been determined that cardiovascular strengthening can be obtained from low intensity activity such as walking for 30 minutes a day. In fact, Dr. Shah Ebrahim, a British cardiologist, states that sexually active men, that is, those engaging in sex 3-4 times a week, reduce their risk of either a stroke or a heart attack by half. Some researchers question whether the mild to moderate energy expended during intercourse is the perk favoring a healthier cardiovascular system or if it is the mindset that drives the sexual act.
The New England Journal of Medicine reported findings relating to the impact of exercise upon 180 postmenopausal women (45-64 years) and 197 men (30-64 years) (Stefanick et al. 1998). The participants were divided into four groups: diet plus exercise, diet alone, exercise alone, and controls. LDL cholesterol levels in the diet-plus-exercise group were significantly reduced compared to the three remaining groups. It is also possible that exercise will alter the size of LDL particles. (Recall that abnormally small LDL particles are highly susceptible to oxidation and elude standard testing processes, misrepresenting the end results.)
Exercise reduces blood pressure and heart rate by influencing sympathetic neural and hormonal activity. As epinephrine (adrenaline) and norepinephrine levels are decreased, one's blood pressure and heart rate subsequently decrease (Katona et al. 1982; Duncan et al. 1985; Smith et al. 1989).
The statistics support that a regular exercise program reduces the risk of stroke, not only by lowering blood pressure, but also by increasing peripheral circulation and oxygen delivery. These findings were confirmed in a 10-year study, involving 14,101 Norwegian women (50-101 years of age). The results showed that the risk of dying from stroke declined as physical activity increased; the most active women had approximately 50% lower risk of death from stroke across all age groups (Ellekjaer et al. 2000).
Excessive fibrinogen, a risk factor for cardiovascular disease, is impacted by exercise. A study showed that exercise of moderate intensity increases fibrinolytic activity by increasing tissue plasminogen activators. (Tissue plasminogen activators break down fibrinogen, decreasing the risk of blood clot formation.) The substantiation of this process occurred when 14 sedentary men (average age 35) and 12 physically active men (average age 35) participated in exercise sessions in the morning and evening at 50% maximal oxygen consumption. The results of the study indicated that moderate-intensity exercise increased the activity of tissue plasminogen activators in both physically active and sedentary men, particularly during evening exercise. C-reactive protein, another of the newer risk factors for cardiovascular disease, also appears lowered by exercise (Szymanski et al. 1994; Ford 2002).
A sedentary lifestyle encourages weight gain and worsens Syndrome X, a condition of insulin resistance and compensatory hyperinsulinemia (insulin excess). Conversely, physical fitness increases cellular glucose responsiveness and decreases the amount of insulin secreted after a carbohydrate load (Challem et al. 2000). Exercise makes the vasculature less prone to damage when insulin levels are unstable. The vulnerabilities associated with Syndrome X, that is, diabetes, hypertension, hypertriglyceridemia, and suppressed HDL levels are often modifiable by exercise-induced weight loss.
If cardiovascular disease has manifested, a monitored exercise program can assist in recovery. Exercise helps in building a new network of blood vessels, naturally bypassing those impaired. The conclusion regarding exercise is that it is never too late to reap the benefits from a properly structured program. However, according to the Framingham Heart Study, only recent physical activity makes a significant difference (Sherman et al. 1999). Exercise undertaken earlier in life showed no sustained cardioprotection.
Beneficial as physical activity is, even low-intensity exercise can be a harbinger of free radicals; overexercising can generate enough free radicals to damage the DNA in white blood cells. The remedy is to provide the system with adequate amounts of antioxidants before engaging in physical activity. Also, sweating during exercise can drastically deplete minerals. This phenomenon likely contributes to the numbers of sudden deaths occurring among athletes and joggers. Lost body fluids and minerals should be replaced immediately.
Researchers are examining the role of gum disease in the genesis and progression of heart disease. The inflammatory process, observed in the lining of atherosclerotic blood vessels, appears to be paralleling chronic inflammation observed in periodontal disease. The findings reported in the American Journal of Epidemiology showed that fibrinogen and C-reactive protein (coagulability and inflammatory markers) are increased in individuals with periodontal disease (Wu et al. 2000). Dr. Wu and colleagues at State University of New York reported that gum disease might also be related to hypercholesterolemia, although a weaker link is found between elevated cholesterol and gum disease than for the elevations in CRP and fibrinogen.
Bleeding, red, swollen gums are depictive of gingivitis, a condition of inflammation and bone deterioration promulgated by bacteria. The American Academy of Periodontology recently launched a media story showing that people with periodontal disease are 200-300% more likely to experience a heart attack than those with healthy gums. Allowing for multiple cardiac risk factors, the researchers concluded that gum disease was a greater risk for cardiovascular disease than hypertension (Genco 1997).
A pilot study (involving 38 heart attack patients matched to a comparable group of 38 people without known heart disease) showed a dramatic correlation between periodontal disease, CRP, and cardiac health: 85% of cardiac patients presented with gum disease compared to only 29% in the control group. Not only did the heart attack patients with periodontal disease have higher levels of CRP than those without gum disease, the CRP levels were directly related to the severity of the oral condition (Medscape Wire 2000).
Should the gums be pulling away from the teeth and appear red, swollen, or tender, seek immediate dental care. Other red flags are gums that bleed while brushing, bad breath, or a discharge of pus. Turn to the Calcium, Coenzyme Q10, and Vitamin C subsections in the Therapeutic section to learn about maintaining healthy gum tissue and avoiding periodontal disease.
THYROID DISEASE (HYPO- AND HYPER- THYROIDISM)
Seldom considered but often the source of disease, the thyroid gland (a member of the endocrine system) should be evaluated in all cardiac patients. A healthy thyroid gland benefits the heart by modulating basal metabolic rate, improving one's mindset, lowering cholesterol and homocysteine levels, and regulating one's heartbeat and circulation. As the following dialog will exemplify, disease states are common when either over- or underperformance of an organ occurs.
Researchers became keenly aware of the importance of a healthy thyroid gland after assessing the homocysteine and cholesterol levels in 7000 individuals from the general U.S. population (Morris et al. 2001). After subdividing test participants into two groups (those with hypothyroidism and those with normal thyroid function), researchers realized that about two-thirds of those diagnosed with hypothyroidism had cholesterol levels nearly 4 times higher than normal. Those who tested positive for hypothyroidism were more likely to be white, female, and "slightly older." Interestingly, an increase in plasma thyroxine concentrations (an iodine-containing hormone secreted by the thyroid gland with the chief function of increasing the rate of cell metabolism) typically precedes reductions in plasma cholesterol levels.
Approximately 50% of individuals thyroid-impaired also had high homocysteine levels compared to only 18% with a healthy gland. Researchers determined that about 90% of hypothyroid subjects in the U.S. population are either hyperhomocysteinemic or hypercholesterolemic; in contrast, only 31% of individuals with normal thyroid function have similar physical complaints (Morris et al. 2001).
The age groups affected by poor thyroid performance and cardiovascular disease are widespread. For example, clinicians examining a group of heart attack victims younger than 40 years of age found two common abnormalities: (1) elevations in serum cholesterol levels and (2) reductions in basal metabolic rate.
A 5-year study involving 347 patients (reported in the Journal of the American Geriatric Society) evaluated the effects of thyroid therapy upon atherosclerosis in a subset of the population 54.7-64.5 years old (Wren 1968): 132 of the individuals had experienced heart attacks, strokes, angina pectoris, or disruption in peripheral circulation; the remaining 215 participants were asymptomatic but were considered high risks because of the presence of electrocardiographic abnormalities, hypertension, diabetes, or hypercholesterolemia.
Only 9% of the patients (31 of the total 347) tested positive for hypothyroid conditions. Nonetheless, all were treated with thyroid extract, and substantial clinical improvements occurred in a number of the patients. Of the 132 symptomatic patients, 29 of 41 with angina reported benefits that included increased exercise tolerance, decreased frequency and severity of attacks, and less need for nitroglycerin. Mean cholesterol levels fell by about 22%. During the 5-year study, 11 patients died, less than half of the expected rate based on United States Life Tables (Barnes 1976).
How might poor thyroid function contribute to arteriosclerotic vascular disease, that is, the hardening of the arteries? Researchers speculate that hypothyroidism may slow or decrease the metabolic breakdown of fats such as cholesterol. In addition, a dysfunctional thyroid gland may also impair kidney function and interfere with the activity of a gene (methylenetetrahydrofolate reductase) that the body depends on to process (remethylate) homocysteine.
Also, if the body fails to convert thyroxine (T4) to triiodothyronine (T3), the body's most potent thyroid hormone, T3 becomes less available in the bloodstream, while levels of reverse T3 (rT3), an inactive metabolite of T3, tend to build up (Shanoudy et al. 2001). A low T3-rT3 ratio is associated with a lesser ability of the left ventricle to pump blood and is highly predictive of poorer short-term outcome in patients with severe chronic heart failure.
In 1998, the American College of Physicians established guidelines for maintaining thyroid health, recommending routine assessment of thyroid simulating hormone (TSH) levels in all women over 50 years of age; women ages 35 and older should be evaluated every 5 years.
In addition, a positive test for the thyroid peroxidase antibody (TPOAb) can be an important early warning sign of emerging dysfunction (Stockigt 2002). Having either high TSH or a positive TPOAb raises the risk of progressing to overt hypothyroidism eightfold; having both increases the risk 40-fold. Note: Hypothyroidism affects more women than men, but the risk increases with age for both men and women. In addition, women are about 5-10 times more prone to hyperthyroidism than men.
The attempts to improve cardiovascular performance without factoring in the possibility of a poorly functioning thyroid gland diminish the chances of success. Conversely, remarkable improvements can be expected if hypothyroidism exists and is treated as the primary condition provoking lipid or vascular derangements.
Hyperthyroidism (an overactive thyroid gland) is also an endangerment to cardiac health, forcing blood vessels into a chronic state of prolonged excitability. Italian researchers measured vascular function (before and after treatment for hyperthyroidism) and compared it to a control group with a healthy thyroid gland. Researchers found that excess levels of thyroid hormones had a strong negative impact on the function of the endothelium (the inner lining of blood vessel walls), resulting in upregulation of blood flow through the circulatory route (Napoli et al. 2001).
Compared to individuals with normal thyroid function, hyperthyroid patients produce significantly higher levels of nitric oxide, leading to increased blood flow and dilation of blood vessels in a resting state. Hyperthyroid patients, typically, show an exaggerated vascular reaction to the cardiac effects of acetylcholine (a neurotransmitter) and norepinephrine (a stress hormone synthesized by the adrenal medulla). Patients with overt hyperthyroidism as well as those with subclinical disease who were given echocardiograms showed that a supercharged thyroid gland caused the cardiovascular system to show clear signs of parasympathetic withdrawal (Petretta et al. 2001). Excitory instructions directed to the endothelium explain why even subclinical thyroid dysfunction is an independent risk factor for heart disease. Endo-thelium, stimulated by over-reactive thyroid messages, is implicated in both congestive heart failure as well as heart attacks.
In the early stages of hyperthyroidism (when TSH levels are high, but thyroid hormone levels are still normal), the heart may already be losing its ability to calm itself. Over time, chronic excitability (leading to increased blood circulation and heart rate) overworks the heart and literally wears it out. Interestingly, when following treatment to resolve hyperthyroidism, the vascular mechanics return to normal.
Illustrative of the value of a healthy thyroid gland, the National Health and Nutrition Examination Survey showed that once the thyroid falters in its performance, the heart may not be far behind (Rodriguez 2001). The need for a thyroid evaluation is thus impossible to overstate. Identifying and treating hypo- or hyper- thyroidism can improve both the quality and duration of life.
IRON OVERLOAD (HEMOCHROMATOSIS)
The research to determine the effects of iron excess on cardiovascular health has had mixed findings. The Annals of Epidemiology reported that no association between iron levels and mortality from cardiovascular disease was found in data collected from NHANES II and the National Death Index (Sempos et al. 2000). Reports published in two respected journals (Journal of the American Heart Association and American Journal of Epidemiology) chronicled an opposing view, showing that free iron corresponds to a greater risk of fatal heart attacks and strokes by encouraging free-radical production (Kiechl et al. 1997; Klipstein-Grobusch et al. 1999).
Just as the iron in your car can rust, the iron in your body is susceptible to rust, or oxidation, a process that damages tissues and blood vessel walls. Several studies have found that iron is most damaging to the heart if LDL cholesterol levels are also high. This occurs as free iron oxidizes LDL cholesterol, increasing the damage imposed upon the heart and vascular system.
Hemochromatosis not only increases the oxidation process, but also reduces antioxidants, including glutathione (Young et al. 1994). As glutathione is depleted, free radicals (attacking in the cerebral region) can increase stroke progression. Stroke patients with high blood ferritin (a measurement of the total iron stored in the body) experienced greater poststroke trauma, that is, increased lethargy, aphasia, and unawareness (Davalos et al. 2000).
An iron overload further complicates a cardiovascular outcome by contributing to an irregular heartbeat, heart attacks, and heart failure. Every 1% rise in blood iron increases the risk of heart disease 4% (Whitney et al. 1998). Interestingly, iron-induced cardiac irregularities can affect both young and senior subjects, even anemic patients.
Dr. Hidehiro Matsuoka (Kurume Medical School in Japan) says iron somehow interferes with nitric oxide, a chemical that relaxes blood vessel walls, allowing the blood to flow more freely. As iron levels increase, malondialdehyde (a marker reflecting oxidation and impaired endothelial function) also increases. Individuals with hemochromatosis who were appropriately treated had lower levels of malon-dialdehyde, and their blood vessels performed with greater normalcy (Tzonou et al. 1998; Fox 2002).
Patients with an iron overload are frequently advised to avoid foods rich in vitamin C or vitamin C supplements because of the iron enhancing factors associated with ascorbic acid. Some (with hemochromatosis) can use 500 mg of buffered vitamin C, taken 3 times a day between meals, without difficulty. Cast-iron cookware and iron-fortified foodstuffs should be avoided, and meats and alcohol should be restricted. On the other hand, coffee or tea consumed with meals assists in blocking iron absorption from foods. Fruits (nonascorbic acid varieties) and vegetables are excellent dietary choices for individuals with an iron overload. Simply withdrawing iron-fortified foods from the diet can prompt dramatic changes in iron levels.
Continued . . .
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