Vitamin B-6 May Affect Risk of Heart Disease

HEALTH NEWS

Low levels of vitamin B-6 may increase the risk of inflammation and metabolic conditions—and subsequently, cardiovascular disease risk—according to a new study.

A cross-sectional study with 1,205 people found that higher levels of pyridoxal-5’-phosphate (PLP), the active form of vitamin B-6, were linked to lower levels of C-reactive protein (CRP), a marker of inflammation, as well as lower levels of 8-hydroxy-2’-deoxyguanosine (8-OHdG), a marker for oxidative stress, both of which are related to heart disease risk.

CRP is produced in the liver and is a known indicator of inflammation. Increased levels of CRP are a good predictor for the onset of both type 2 diabetes and cardiovascular disease.

Researchers from the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University reported their findings in the American Journal of Clinical Nutrition.

"Our data suggest that vitamin B-6 may influence cardiovascular disease risk through mechanisms other than [reduction of the amino acid] homocysteine and support the notion that nutritional status may influence the health disparities present in this population," wrote the researchers, led by Jian Shen.

Shen and co-workers measured levels of PLP, CRP and 8-OHdG in 1,205 Puerto Rican adults aged between 45 and 75 living in Massachusetts.

Results showed a strong dose-dependent relationship between PLP levels and CRP levels, with the highest PLP levels associated with CRP levels almost 50% lower than low PLP levels.

Furthermore, the highest average levels of PLP were associated with 8-OHdG concentrations of 108 nanograms per milligram, compared to 124 ng/mg for low PLP levels. The associations were observed even after the researchers took into account homocysteine levels.

Source: American Journal of Clinical Nutrition 91(2):337-342, 2010

It's The Carbs Not The Fats!

Unless you’re living on another planet, you’ve heard this message: reduce your intake of fat and cholesterol to achieve a healthy weight and decrease the likelihood of developing heart disease. In fact, the terms “healthy” and “low fat” seem inextricably linked. But now we know that the rationale for a low-fat diet is based on two overly simplistic ideas that turn out to be wrong.

Wrong Idea #1

 
Fat contains 9 calories per gram; both protein and carbohydrate contain 4 calories per gram. Presumably then, reducing fat intake should allow you to eat a larger total volume of food, feel satisfied, and promote weight loss. Only one problem; it doesn’t work. Just ask all the people who’ve cut their fat intake, but haven’t lost body fat or have actually gained weight.

Why doesn’t it work? The simple reason is that the amount of calories increases when carbs replace fat because fat is inherently more satisfying than carbs and you wind up eating more carbs as you seek satisfaction and a sense of fullness. Where’s the proof that the low-fat approach has backfired? Just look at the skyrocketing rates of obesity (and diabetes) over the past 40 years. That’s the same period in which we’ve been told to cut down on fat—and, as a nation, we have.

Wrong Idea #2

 
The major emphasis on reducing dietary fat (including saturated fat) was based on the assumption that consuming fatty foods increases blood cholesterol levels, which, in turn, which in turn, increases the incidence of heart disease. This assumption is called the “diet-heart hypothesis.” However, despite decades of research funded by the government at a cost of billions of dollars, there’s little evidence to support the premise.

A Look at the Research

The largest and most expensive study on the role of fat in the diet was called the Women’s Health Initiative, which tracked almost 50,000 postmenopausal women for an average of eight years. The women were randomly assigned to one of two diets: one that reduced total fat intake and increased the intake of vegetables, fruits and grains and a control group that was allowed to eat whatever they wanted. Many different researchers published many scientific papers on this study. All came to the same conclusion: there was no significant benefit in terms of weight loss as a result of following a low-fat diet. Nor was there any impact on the incidence of heart disease (or diabetes or cancer).

It turns out that you are not what you eat, so much as what your body does with what you eat. That’s where following the Atkins low-carb approach comes in. Once you eliminate added sugar, white flour and other “junk” carbs and reduce your total intake of carbs, you convert your body to a primarily fat-burning metabolism. The result is that your excess fat stores become a source of energy and your indicators for heart disease improve, as supported in a number of recent studies.

A Sweet Reversal

 
We’re encouraged to see that based upon a recent study published in Circulation: the Journal of the American Heart Association, the association now takes the position that consuming added sugars may cause weight gain and raise triglycerides, both of which contribute to the risk of developing heart disease. It also offers specific guidelines for the upper limits of added sugar intake. In 2006, the American Heart Association (AHA) recommended reducing intake of added sugars, but set no limits. (The study classifies added sugars as any sugar or syrup added at the table or in the processing and preparation of a food, in contrast to naturally occurring sugars in fruit, for example.) The AHA now says that “a prudent upper limit of intake is half of the discretionary calorie allowance, which for most American women is no more than 100 calories per day and for most American men is no more than 150 calories per day from added sugars.” Six teaspoons of sugar pack about 100 calories and a 12-ounce cola contains about 130 calories.

Most eat far in excess of these amounts. A report from the 2001-04 National Health and Nutrition Examination Survey (NHANES) showed the average intake of added sugars by Americans was about 22 teaspoons a day. Lead author of the Circulation study Rachel K. Johnson says that sugar has no nutritional value other than to provide calories. We hope that in its next position statement, the AHA tackles the larger issue of overall carbohydrate intake and its association with heart health.

Source: Reprinted from Atkins Nutritionals  

References:

 
1.    B. V. Howard, J. E. Manson, M. L. Stefanick, S. A. Beresford, G. Frank, B. Jones, et al., “Low-Fat Dietary Pattern and Weight Change over 7 Years: The Women's Health Initiative Dietary Modification Trial,” The Journal of the American Medical Association 295 (2006), 39–49.
2.    L. F. Tinker, D. E. Bonds, K. L. Margolis, J. E. Manson, B. V. Howard, J. Larson, et al., “Low-Fat Dietary Pattern and Risk of Treated Diabetes Mellitus in Postmenopausal Women: The Women's Health Initiative Randomized Controlled Dietary Modification Trial,” Archives of Internal Medicine 168 (2008), 1500–1511.
3.    S. A. Beresford, K. C. Johnson, C. Ritenbaugh, N. L. Lasser, L. G. Snetselaar, H. R. Black, et al., “Low-Fat Dietary Pattern and Risk of Colorectal Cancer: The Women's Health Initiative Randomized Controlled Dietary Modification Trial,” The Journal of the American Medical Association 295 (2006), 643–654.
4.    R. L. Prentice, C. A. Thomson, B. Caan, F. A. Hubbell, G. L. Anderson, S. A. Beresford, et al., “Low-Fat Dietary Pattern and Cancer Incidence in the Women's Health Initiative Dietary Modification Randomized Controlled Trial,” Journal of the National Cancer Institute 99 (2007), 1534–1543.
5.    C. D. Gardner, A. Kiazand, S. Alhassan, S. Kim, R. S. Stafford, R. R. Balise, et al., “Comparison of the Atkins, Zone, Ornish, and LEARN Diets for Change in Weight and Related Risk Factors among Overweight Premenopausal Women: The A TO Z Weight Loss Study: A Randomized Trial,” The Journal of the American Medical Association 297 (2007), 969–977.
6.    I. Shai, D. Schwarzfuchs, Y. Henkin, D. R. Shahar, S. Witkow, I. Greenberg, et al., “Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet,” The New England Journal of Medicine 359 (2008), 229–241.
7.    J. S. Volek, M. L. Fernandez, R. D. Feinman, and S. D. Phinney, “Dietary Carbohydrate Restriction Induces a Unique Metabolic State Positively Affecting Atherogenic Dyslipidemia, Fatty Acid Partitioning, and Metabolic Syndrome,” Progress in Lipid Research 47 (2008), 307–318.
8.    J. Nordmann, A. Nordmann, M. Briel, U. Keller, W. S. Yancy, Jr., B. J. Brehm, et al., “Effects of Low-Carbohydrate vs Low-Fat Diets on Weight Loss and Cardiovascular Risk Factors: A Meta-analysis of Randomized Controlled Trials,” Archives of Internal Medicine 166 (2006), 285–293.
9.    M. Dashti, N. S. Al‑Zaid, T. C. Mathew, M. Al‑Mousawi, H. Talib, S. K. Asfar, et al., “Long Term Effects of Ketogenic Diet in Obese Subjects with High Cholesterol Level,” Molecular and Cellular Biochemistry 286 (2006), 1–9.
10.     G. Boden, K. Sargrad, C. Homko, M. Mozzoli, and T. P. Stein, “Effect of a Low-Carbohydrate Diet on Appetite, Blood Glucose Levels, and Insulin Resistance in Obese Patients with type 2 Diabetes,” Annals of Internal Medicine 142 (2005), 403–411.
11.    E. C. Westman, W. S. Yancy, Jr., J. C. Mavropoulos, M. Marquart, and J. R. McDuffie, “The Effect of a Low-Carbohydrate, Ketogenic Diet Versus a Low-Glycemic Index Diet on Glycemic Control in type 2 Diabetes Mellitus,” Nutrition & Metabolism (London) 5 (2008), 36.
12.    E. H. Kossoff, and J. M. Rho, “Ketogenic Diets: Evidence for Short- and Long-Term Efficacy,” Neurotherapeutics 6 (2009), 406–414.
13.    R. K. Johnson, L. J. Appel,  M. Brands, et al., “Dietary Sugars Intake and Cardiovascular Health,” Circulation 2009;120;1011-1020.

Inflammatory Markers Predict Congestive Heart Failure

HEALTH NEWS

Inflammatory markers are independent predictors of congestive heart failure (CHF) and likely reflect the link between obesity and CHF, a new study suggests.(1) In a new analysis of the Multi-Ethnic Study of Atherosclerosis (MESA), researchers led by Dr Hossein Bahrami (Johns Hopkins, Baltimore, MD) report that serum interleukin-6 (IL-6), C-reactive protein (CRP), and albuminuria all predicted the development of CHF over four years, independent of obesity or other established risk factors.

"Our results suggest that inflammation might be involved, directly or as a marker of other underlying conditions, (emphasis added) in the pathologic pathways that link obesity to left ventricular [LV] dysfunction and ultimately CHF," Bahrami et al write.

The study appears in the May 6, 2008 issue of the Journal of the American College of Cardiology.

Authors of the study calculated the hazard ratios (HRs) linking baseline metabolic syndrome, inflammatory markers, insulin resistance, and albuminuria with incidence CHF in the MESA population, after taking into account standard risk factors, interim myocardial infarction (MI), and left ventricular structure and function. MESA enrolled 6814 participants from multiple ethnic backgrounds; median follow-up for the current analysis was four years.

Baharmi and colleagues report that 79 patients developed CHF during follow-up: while obesity was significantly associated with subsequent CHF, the association lost statistical significance after inflammatory markers were included in the model. Obese patients, however were found to have much higher levels of interleukin 6, CRP, and fibrinogen.

According to Baharmi, the findings suggest a mechanistic link between obesity, inflammation, and CHF.

"The implication may be that greater control of obesity may reduce the risk of heart failure and down the road, maybe targeting inflammatory markers may reduce the risk of heart failure related to obesity."

Inflammation may also help explain the link between the metabolic syndrome and CHF risk: inflammation is a known characteristic of the metabolic syndrome, and metabolic syndrome is associated with a higher risk of developing CHF, the authors note.

Reference 

1. Bahrami H, Bluemke DA, Kronmal R, et al. Novel metabolic risk factors for incident heart failure and their relationship with obesity. The Multi-Ethnic Study of Atherosclerosis Study. J Am Coll Cardiol. 2008;51:1775-1783.

Vitamin D Deficiency Associated with Increased Mortality

HEALTH NEWS

Another study suggesting a link between low levels of vitamin D and cardiac risk has been published, this time showing that vitamin-D deficiency is associated with both cardiovascular mortality and all-cause mortality.(1)

The study, published in the June 23, 2008 issue of the Archives of Internal Medicine, was conducted by a group led by Dr Harald Dobnig (Medical University of Graz, Austria).

They note that it has been estimated that 50% to 60% of people do not have satisfactory vitamin-D status, and this is probably related to factors such as urbanization, demographic shifts, decreased outdoor activity, air pollution and global dimming, and decreases in the cutaneous production of vitamin D with age.

The minimum desirable serum level of 25-hydroxyvitamin D has been suggested to be 20 to 30 ng/mL, and levels lower than this are clearly related to compromised bone-mineral density, falls, and fractures and more recently have also been linked to cancer and immune dysfunction, as well as cardiovascular disease, hypertension, and metabolic syndrome, the authors report.

They point out that recent studies have shown an association of low 25-hydroxyvitamin-D levels with important cardiovascular risk factors, supporting previous findings that demonstrated positive effects of vitamin D and its analogs on fibrinolysis, blood lipids, thrombogenicity, endothelial regeneration, and smooth-muscle-cell growth. "Together, these findings strongly suggest that 25-hydroxyvitamin D has beneficial effects, some involving the cardiovascular system, that are independent of calcium metabolism," they comment.

Low 25-hydroxyvitamin-D levels were also significantly correlated with markers of inflammation (C-reactive protein [CRP] and interleukin 6 [IL-6]), oxidative burden (serum phospholipid and glutathione levels), and cell adhesion (vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 levels).

Dobnig et al say that these results show that a low 25-hydroxyvitamin-D level can be considered a strong risk indicator for all-cause mortality in women and in men.

The authors also report that the increase in risk of all-cause mortality with lower levels of vitamin D was seen regardless of the degree of coronary artery disease seen on angiography, and they comment: "Low 25-hydroxyvitamin-D and 1,25-dihydroxyvitamin-D levels seem to be important mediators of mortality even when there is little or no indication of overt vascular disease."

They say they are unable to tell, based on these results, whether the association between low 25-hydroxyvitamin-D and 1,25-dihydroxyvitamin-D levels and mortality is causal or not. But they believe there are a few indications pointing to a possible link. These include the association with elevated inflammatory markers, which suggests these compounds may have anti-inflammatory properties, and the effects related to oxidative stress and increased cell adhesion suggest that low levels of vitamin D may detrimentally affect vascular biologic function in multiple ways.

They add that other mechanisms whereby low vitamin-D levels may be associated with mortality include effects on matrix metalloproteinases, which have been shown to affect plaque production and stability, increased susceptibility to arterial calcification, or an increase in renin messenger-RNA expression.

They conclude: "This prospective cohort study demonstrates for the first time, to our knowledge, that low 25-hydroxyvitamin-D and 1,25-dihydroxyvitamin-D levels are associated with increased risk in all-cause and cardiovascular mortality compared with patients with higher serum vitamin-D levels. Both vitamins seem to have synergistic biologic action that is largely independent of each other. Based on the findings of this study, a serum 25-hydroxyvitamin-D level of 20 ng/mL or higher may be advised for maintaining general health."

Reference

1. Dobnig H, Pilz S, Scharnagl H, et al. Independent association of low serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D levels with all-cause and cardiovascular mortality. Arch Intern Med 2008; 168:1340-1349.

Hawthorn Extract Seen As Treatment Option for Chonic Heart Failure

HEALTH NEWS

 
A new study published in the Cochrane Database of Systematic Reviews states that there is "a significant benefit in symptom control and physiologic outcomes from hawthorn extract as an adjunctive treatment for chronic heart failure."

In beginning the study, researchers noted: "Hawthorn extract is advocated as an oral treatment option for chronic heart failure. Also, the German Commission E approved the use of extracts of hawthorn leaf with flower in patients suffering from heart failure graded stage II."

Researchers reviewed 14 double-blind, placebo-controlled, randomized clinical trails and concluded that hawthorn berry extract may be used as an oral treatment option for chronic heart failure. In most of the studies, hawthorn was used as an adjunct to conventional treatment. Ten trials including 855 patients with chronic heart failure provided data that were suitable for meta-analysis.

Researchers stated: "For the physiologic outcome of maximal workload, treatment with hawthorn extract was more beneficial than placebo. Exercise tolerances were significantly increased by hawthorn extract. The pressure-heart rate product, an index of cardiac oxygen consumption, also showed a beneficial decrease with hawthorn treatment. Symptoms such as shortness of breath and fatigue improved significantly with hawthorn treatment as compared with placebo."

Source: Cochrane Database of Systematic Reviews Issue 1, 2008.

Health Notes on Congestive Heart Failure (CHF)

CHF and its Symptoms

Congestive heart failure (CHF) is a chronic condition that results when the heart muscle is unable to pump blood as efficiently as is needed. High blood pressure can cause congestive heart failure. Failure of the heart pump can also result from many other causes, such as severe anemia, hyperthyroidism, heart attacks, and arrhythmias of the heart.

Common symptoms of CHF are breathlessness, fatigue, and accumulation of fluid in the lungs or the veins (primarily in the legs) or both.

Helpful Lifestyle Changes

Even with severe disease, appropriate exercise can benefit those with CHF. (1) (2) In a controlled trial, long-term (one year) exercise training led to improvements in quality of life and functional capacity in people with CHF. (3) Nonetheless, too much exercise can be life-threatening for those with CHF. How much is “too much” varies from person to person; therefore, any exercise program undertaken by someone with CHF requires professional supervision.

Non-steroidal anti-inflammatory drugs (NSAIDs) appear to significantly increase the risk of CHF. The use of NSAIDs in one preliminary study was found to double the likelihood of hospital admission with CHF the following week. This likelihood increased by more than 10 times for patients with a history of heart disease. (4) This study did not include people taking low-dose aspirin.

Important Vitamins

People with CHF have insufficient oxygenation of the heart, which can damage the heart muscle. Such damage may be reduced by taking L-carnitine supplements. (5) L-carnitine is a natural substance made from the amino acids, lysine and methionine. Levels of L-carnitine are low in people with CHF;(6) therefore, many doctors recommend that those with CHF take 500 mg of L-carnitine two to three times per day.

Most L-carnitine/CHF research has used a modified form of the supplement called propionyl-L-carnitine (PC). In one double-blind trial, people using 500 mg of PC per day had a 26% increase in exercise capacity after six months.(7) In double-blind research, other indices of heart function have also improved after taking 1 gram of PC twice per day.(8) It remains unclear whether propionyl-L-carnitine has unique advantages over L-carnitine, as limited research in animals and humans has also shown very promising effects of the more common L-carnitine.(9)

Magnesium deficiency frequently occurs in people with CHF, and such a deficiency may lead to heart arrhythmias. Magnesium supplements have reduced the risk of these arrhythmias.(10) People with CHF are often given drugs that deplete both magnesium and potassium; a deficiency of either of these minerals may lead to an arrhythmia.(11) Many doctors suggest magnesium supplements of 300 mg per day.

Whole fruit and fruit and vegetable juice, which are high in potassium, are also recommended by some doctors. One study showed that elderly men who consumed food prepared with potassium-enriched salt (containing about half potassium chloride and half sodium chloride) had a 70% reduction in deaths due to heart failure and a significant reduction in medical costs for cardiovascular disease, when compared with men who continued to use regular salt.(12) While increasing potassium intake can be beneficial for heart patients, this dietary change should be discussed with a healthcare provider, because several drugs given to people with CHF may actually cause retention of potassium, making dietary potassium, even from fruit, dangerous.

Taurine, an amino acid, helps increase the force and effectiveness of heart-muscle contractions. Research (some double-blind) has shown that taurine helps people with CHF.(13)(14)(15)(16) Most doctors suggest taking 2 grams three times per day.

As is true for several other heart conditions, coenzyme Q10 (CoQ10) has been reported to help people with CHF,(17)(18) sometimes dramatically.(19) Positive effects have been confirmed in double-blind research(20) and in an overall analysis of eight controlled trials.(21) However, some double-blind trials have reported modest(22) or no improvement(23)(24)(25) in exercise capacity or overall quality of life. Most CoQ10 research used 90–200 mg per day. The beneficial effects of CoQ10 may not be seen until after several months of treatment. Discontinuation of CoQ10 supplementation in people with CHF has resulted in severe relapses and should only be attempted under the supervision of a doctor.(26)

The body needs arginine, another amino acid, to make nitric oxide, which increases blood flow. This process is impaired in people with CHF. Arginine supplementation (5.6–12.6 grams per day) has been used successfully in double-blind trials to treat CHF.(27) A double-blind trial has also found that arginine supplementation (5 grams three times daily) improves kidney function in people with CHF.(28)

For people with congestive heart failure, intravenous injections of creatine have been found to improve heart function; oral supplementation has not been effective, though it does improve skeletal muscle function.(29)(30)

In a preliminary study, blood levels of DHEA (dehydroepiandrosterone) were found to be lower in people with CHF than in people without the disease. The lowered blood levels of DHEA among these people was proportional to the severity of their disease.(31) However, there is no evidence that DHEA supplementation can prevent or reverse CHF.

In a double-blind study of people with established heart disease or diabetes, participants who took 400 IU of vitamin E per day for an average of 4.5 years developed heart failure significantly more often than did those taking a placebo.(32) Hospitalizations for heart failure occurred in 5.8% of those in the vitamin E group, compared with 4.2% of those in the placebo group, a 38.1% increase. Considering that some other studies have shown a beneficial effect of vitamin E against heart disease, the results of this study are difficult to interpret. Nevertheless, individuals with heart disease or diabetes should consult their doctor before taking vitamin E.

Beneficial Herbs 

Berberine is used in Asia to treat congestive heart failure. In a double-blind trial, supplementation with berberine (300 to 500 mg, four times per day) for eight weeks significantly improved heart function and exercise capacity and reduced the frequency of arrhythmias in people with congestive heart failure.(33)

Clinical trials have shown that standardized extracts made from the leaves and flowers of hawthorn are effective in helping people with early-stage CHF.(34)(35)(36) Hawthorn extracts appear to increase blood flow to the heart, increase the strength of heart contractions, reduce resistance to blood flow in the extremities, and act as an antioxidant.(37)(38)(39) In a large preliminary trial, people with mild to moderate CHF were given 300 mg of hawthorn flower and leaf extract (standardized to contain 2.2% flavonoids) three times a day for two months(40) Symptoms of CHF—including heart palpitations, chest pressure, and swelling in the extremities—decreased throughout the trial during the use of hawthorn. The efficacy of hawthorn for the treatment of CHF has been confirmed in a double-blind trial.(41)

Hawthorn extracts are available in capsules or tablets standardized to either total flavonoid content (usually 2.2%) or oligomeric procyanidins (usually 18.75%). Doctors who work with herbal medicine often suggest 80–300 mg two to three times per day. Hawthorn berry products that are not standardized may be weaker, and the recommended amount is typically 4 to 6 grams per day for the whole herb, or 4–5 ml of the tincture three times per day.

Coleus contains forskolin, a substance that may help dilate blood vessels and improve the forcefulness with which the heart pumps blood.(42) Recent clinical trials indicate that forskolin improves heart function in people with congestive heart failure and cardiomyopathy.(43)(44) A preliminary trial found that forskolin reduced blood pressure and improved heart function in people with cardiomyopathy. These trials have used intravenous infusions of isolated forskolin. It is unknown whether oral coleus extracts would have the same effect. While many doctors expert in herbal medicine would recommend 200–600 mg per day of a coleus extract containing 10% forskolin, these amounts are extrapolations and have yet to be confirmed by direct clinical research.

A small clinical trial found that supplementation with a bark extract of Arjun (Terminalia arjuna) improved heart function as well as lung congestion in patients with severe CHF.(45) Patients in the study took 500 mg of Arjun extract three times per day and began to exhibit significant improvement in heart function within two weeks; improvement continued over the course of approximately two years. The herb extract used in this study was concentrated but not standardized for any particular constituent. Commercial preparations are sometimes standardized to contain 1% arjunolic acid. Larger clinical trials are needed to confirm the results of this small study.

Self-Care Steps

CHF is a serious condition that requires support from health professionals. According to research or other evidence, the following self-care steps may help your heart keep pumping the blood your body needs:

• Get help from hawthorn. Take 300 mg of an herbal extract three times a day to reduce symptoms and improve exercise capacity

• Try taurine. Improve heart muscle contraction by taking 2 grams of this amino acid three times a day

• Add a carnitine to your routine. Take 1,500 to 2,000 mg of an L-carnitine or propionyl-L-carnitine supplement every day to improve heart function and exercise capacity

• Check out coenzyme Q10. To determine how much of this powerful antioxidant supplement you need daily, calculate 0.9 mg for every pound of body weight

• Mix in some magnesium. Take 300 mg a day of this essential mineral to prevent a deficiency that can lead to heart arrhythmias.

• See a specialist. Find a health expert you can trust to help you manage this medical condition

These recommendations are not comprehensive and are not intended to replace the advice of your doctor or pharmacist. Read more in-depth, fully-referenced information on medicines, vitamins, herbs, and dietary and lifestyle changes that may be helpful provided.

Source: Copyright © 2010 Healthnotes, Inc.

References

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3. Belardinelli R, Georgiou D, Cianci G, Purcaro A. Randomized, controlled trial of long-term moderate exercise training in chronic heart failure. Circulation 1999;99:1173–82.

4. Page J, Henry D. Consumption of NSAIDs and the development of congestive heart failure in elderly patients. Arch Intern Med 2000;160:777–84.

5. Bartels GL, Remme WJ, Pillay M, et al. Effects of L-propionylcarnitine on ischemia-induced myocardial dysfunction in men with angina pectoris. Am J Cardiol 1994;74:125–30.

6. Suzuki Y, Masumura Y, Kobayashi A, et al. Myocardial carnitine deficiency in chronic heart failure. Lancet 1982;i:116 (letter).

7. Mancini M, Rengo F, Lingetti M, et al. Controlled study on the therapeutic efficacy of propionyl-L-carnitine in patients with congestive heart failure. Arzneimittelforschung 1992;42:1101–4.

8. Pucciarelli G, Mastursi M, Latte S, et al. The clinical and hemodynamic effects of propionyl-L-carnitine in the treatment of congestive heart failure. Clin Ther 1992;141:379–84.

9. Kobayashi A, Masumura Y, Yamazaki N. L-carnitine treatment for congestive heart failure—experimental and clinical study. Jpn Circ J 1992;56:86–94.

10. Bashir Y, Sneddon JF, Staunton A, et al. Effects of long-term oral magnesium chloride replacement in congestive heart failure secondary to coronary artery disease. Am J Cardiol 1993;72:1156–62.

11. Packer M, Gottlieb SS, Kessler PD. Hormone-electrolyte interactions in the pathogenesis of lethal cardiac arrhythmias in patients with congestive heart failure. Am J Med 1986;80 (Suppl 4A):23–9.

12. Chang HY, Hu YW, Yue CSJ, et al. Effect of potassium-enriched salt on cardiovascular mortality and medical expenses of elderly men. Am J Clin Nutr 2006;83:1289–96.

13. Azuma J, Sawamura A, Awata N, et al. Double-blind randomized crossover trial of taurine in congestive heart failure. Curr Ther Res 1983;34(4):543–57.

14. Azuma J, Hasegawa H, Sawamura N, et al. Taurine for treatment of congestive heart failure. Int J Cardiol 1982;2:303–4.

15. Azuma J, Hasegawa H, Sawamura A, et al. Therapy of congestive heart failure with orally administered taurine. Clin Ther 1983;5(4):398–408.

16. Azuma J, Takihara K, Awata N, et al. Taurine and failing heart: experimental and clinical aspects. Prog Clin Biol Res 1985;179:195–213.

17. Mortensen SA, Vadhanavikit S, Baandrup U, Folkers K. Long-term coenzyme Q10 therapy: a major advance in the management of resistant myocardial failure. Drugs Exp Clin Res 1985;11:581–93.

18. Soongswang J, Sangtawesin C, Durongpisitkul K, et al. The effect of coenzyme Q10 on idiopathic chronic dilated cardiomyopathy in children. Pediatr Cardiol 2005;26:361–6.

19. Folkers K, Langsjoen P, Langsjoen PH. Therapy with coenzyme Q10 of patients in heart failure who are eligible or ineligible for a transplant. Biochem Biophys Res Commun 1992;15:247–53.

20. Morisco C, Trimarco B, Condorelli M. Effect of coenzyme Q10 in patients with congestive heart failure: a long-term multicenter randomized study. Clin Invest 1993;71:S134–6.

21. Soja AM, Mortensen SA. Treatment of chronic cardiac insufficiency with coenzyme Q10, results of meta-analysis in controlled clinical trials. Ugeskr Laeger 1997;159:7302–8.

22. Hofman-Bang C, Rehnqvist N, Swedberg K, et al. Coenzyme Q10 as an adjunctive in the treatment of chronic congestive heart failure. The Q10 Study Group. J Card Fail 1995;1:101–7.

23. Permanetter B, Rossy W, Klein G, et al. Ubiquinone (coenzyme Q10) in the long-term treatment of idiopathic dilated cardiomyopathy. Eur Heart J 1992;13:1528–33.

24. Watson PS, Scalia GM, Galbraith A, et al. Lack of effect of coenzyme Q on left ventricular function in patients with congestive heart failure. J Am Coll Cardiol 1999;33:1549–52.

25. Khatta M, Alexander BS, Krichten CM, et al. The effect of coenzyme Q10 in patients with congestive heart failure. Ann Intern Med 2000;132:636–40.

26. Mortensen SA, Vadhanavikit S, Baandrup U, Folkers K. Long-term coenzyme Q10 therapy: a major advance in the management of resistant myocardial failure. Drug Exptl Clin Res 1985;11:581–93.

27. Rector TS, Bank A, Mullen KA, et al. Randomized, double-blind, placebo controlled study of supplemental oral L-arginine in patients with heart failure. Circulation 1996;93:2135–41.

28. Watanabe G, Tomiyama H, Doba N. Effects of oral administration of L-arginine on renal function in patients with heart failure. J Hypertens 2000;18:229–34.

29. Andrews R, Greenhaff P, Curtis S, et al. The effect of dietary creatine supplementation on skeletal muscle metabolism in congestive heart failure. Eur Heart J 1998;19:617–22.

30. Gordon A, Hultman E, Kaijser L, et al. Creatine supplementation in chronic heart failure increases skeletal muscle creatine phosphate and muscle performance. Cardiovasc Res 1995;30:413–8.

31. Moriyama Y, Yasue H, Yoshimura M, et al. The plasma levels of dehydroepiandrosterone sulfate are decreased in patients with chronic heart failure in proportion to the severity. J Clin Endocrinol Metab 2000;85:1834–40.

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33. Zeng XH, Zeng XJ, Li YY. Efficacy and safety of berberine for congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy. Am J Cardiol 2003;92:173–6.

34. Leuchtgens H. Crataegus special extract (WS 1442) in cardiac insufficiency. Fortschr Med 1993;111:352–4.

35. Schmidt U, Kuhn U, Ploch M, Hübner WD. Efficacy of the hawthorn (Crataegus)Phytomed 1994;1:17–24. preparation LI 132 in 78 patients with chronic congestive heart failure defined as NYHA functional class II.

36. Pittler M, Guo R, Ernst E. Hawthorn extract for treating chronic heart failure. Cochrane Database Syst Rev 2008 Jan 23:CD005312.

37. Maevers VW, Hensel H. Changes in local myocardial blood flow following oral administration of a Crataegus extract to non-anesthetized dogs. Arzneimittelforschung 1974;24:783–5.

38. Weikl A, Noh HS. The influence of Crataegus on global cardiac insufficiency. Herz Gerfässe 1992; 11:516–24.

39. Bahorun T, Trotin F, Pommery J, et al. Antioxidant activities of Crataegus monogynaPlanta Med 1994; 60:323–8. extracts.

40. Schmidt U, Albrecht H, Podzuweit M, et al. High-dose crataegus therapy in patients suffering from congestive heart failure NYHA class I and II. Z Phytotherapie 1998;19:22–30.

41. Rietbrock N, Hamel M, Hempel B, et al. Actions of standardized extract of Crataegus berries on exercise tolerance and quality of life in patients with congestive heart failure [in German]. Arzneimittelforschung 2001;51:793–8.

42. Lindner E, Dohadwalla AN, Bhattacharya BK. Positive inotropic and blood pressure lowering activity of a diterpene derivative isolated from Coleus forskohli: Forskolin. Arzneimittelforschung. 1978;28:284–9.

43. Baumann G, Felix S, Sattelberger U, Klein G. Cardiovascular effects of forskolin (HL 362) in patients with idiopathic congestive cardiomyopathy—a comparative study with dobutamine and sodium nitroprusside. J Cardiovasc Pharmacol 1990;16:93–100.

44. Kramer W, Thormann J, Kindler M, Schlepper M. Effects of forskolin on left ventricular function in dilated cardiomyopathy. Arzneimittelforschung 1987;37:364–7.

45. Bharani A, Ganguly A, Bhargava KD. Salutary effect of Terminalia Arjuna in patients with severe refractory heart failure. Int J Cardiol 1995;49:191–9.

 

Fats for your Heart

In 2002, the American Heart Association released a scientific statement, “Fish Consumption, Fish Oil, Omega-3 Fatty Acids and Cardiovascular Disease,” on the effects of omega-3 fatty acids on heart function (including antiarrhythmic effects), hemodynamics (cardiac mechanics) and arterial endothelial function. The link between omega-3 fatty acids and CVD risk reduction are still being studied, but research has shown that omega-3 fatty acids

• decrease risk of arrhythmias, which can lead to sudden cardiac death
• decrease triglyceride levels
• decrease growth rate of atherosclerotic plaque
• lower blood pressure (slightly)

What do epidemiological and observational studies show?

Epidemiologic and clinical trials have shown that omega-3 fatty acids reduce CVD incidence.  Large-scale epidemiologic studies suggest that people at risk for coronary heart disease benefit from consuming omega-3 fatty acids from plants and marine sources. The ideal amount to take isn’t clear.  Evidence from prospective secondary prevention studies suggests that taking EPA+DHA ranging from 0.5 to 1.8 grams per day (either as fatty fish or supplements) significantly reduces deaths from heart disease and all causes.  For alpha-linolenic acid, a total intake of 1.5–3 grams per day seems beneficial.

Randomized clinical trials have shown that omega-3 fatty acid supplements can reduce cardiovascular events (death, non-fatal heart attacks, non-fatal strokes).  They can also slow the progression of atherosclerosis in coronary patients.  However, more studies are needed to confirm and further define the health benefits of omega-3 fatty acid supplements for preventing a first or subsequent cardiovascular event.  For example, placebo-controlled, double-blind, randomized clinical trials are needed to document the safety and efficacy of omega-3 fatty acid supplements in high-risk patients (those with type 2 diabetes, dyslipidemia, hypertension and smokers) and coronary patients on drug therapy.  Mechanistic studies on their apparent effects on sudden death also are needed.
 

Increasing omega-3 fatty acid intake through foods is preferable.  However, coronary artery disease patients may not be able to get enough omega-3 by diet alone.  These people may want to talk to their doctor about taking a supplement.  Supplements also could help people with high triglycerides, who need even larger doses.  The availability of high-quality omega-3 fatty acid supplements, free of contaminants, is an important prerequisite to their use.

AHA Recommendation
Omega-3 fatty acids benefit the heart of healthy people, and those at high risk of — or who have — cardiovascular disease. 

We recommend eating fish (particularly fatty fish) at least two times a week.  Fish is a good source of protein and doesn’t have the high saturated fat that fatty meat products do.  Fatty fish like mackerel, lake trout, herring, sardines, albacore tuna and salmon are high in two kinds of omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).

We also recommend eating tofu and other forms of soybeans, canola, walnut and flaxseed, and their oils. These contain alpha-linolenic acid (LNA),  which can become omega-3 fatty acid in the body. The extent of this modification is modest and controversial, however. More studies are needed to show a cause-and-effect relationship between alpha-linolenic acid and heart disease.

The table below is a good guide to use for consuming omega-3 fatty acids.
 
Summary of Recommendations for Omega-3 Fatty Acid Intake

Population	Recommendation
Patients without documented coronary heart disease (CHD)	Eat a variety of (preferably fatty) fish at least twice a week. Include oils and foods rich in alpha-linolenic acid (flaxseed, canola and soybean oils; flaxseed and walnuts).
Patients with documented CHD	Consume about 1 g of EPA+DHA per day, preferably from fatty fish.  EPA+DHA in capsule form could be considered in consultation with the physician.
Patients who need to lower triglycerides	2 to 4 grams of EPA+DHA per day provided as capsules under a physician’s care.

Patients taking more than 3 grams of omega-3 fatty acids from capsules should do so only under a physician’s care.  High intakes could cause excessive bleeding in some people. 

Source: American Heart Association, www.americanheart.org

The Role of CoQ10 in Heart Disease

HEALTH NEWS 


The use of CoQ10 as an adjunct therapy in treating serous illness particularly cardiac conditions now gains gradual support from current clinical research and reviews. 

Pharmacology and Therapeutics, an international review journal that presents critical and authoritative reviews of currently important topics in pharmacology and one of the top 10 most cited journals in its field, recently published a study highlighting the role of co-enzyme Q10 in various cardiovascular conditions including congestive heart failure, hypertension, ischemic heart disease, arrythmias, mitral valve prolapse syndrome, Meniere-like syndrome and its protective role during cardiac surgery and against doxorubicin cardiotoxicity. An abstract of the study is made available below.
___________________________________________________________________
 
Pharmacol Ther. 2009 Jul 25.
Role of coenzyme Q10 (CoQ10) in cardiac disease, hypertension and Meniere-like syndrome.

Kumar A, Kaur H, Devi P, Mohan V.

Cardiology Deptt, Govt. Medical College/GND Hospital, Amritsar, Punjab, Amritsar, Punjab, India.


Coenzyme Q10 (ubiquinone) is a mitochondrial coenzyme which is essential for the production of ATP. Being at the core of cellular energy processes it assumes importance in cells with high energy requirements like the cardiac cells which are extremely sensitive to CoQ10 deficiency produced by cardiac diseases. CoQ10 has thus a potential role for prevention and treatment of heart ailments by improving cellular bioenergetics. In addition it has an antioxidant, a free radical scavenging and a vasodilator effect which may be helpful in these conditions. It inhibits LDL oxidation and thus the progression of atherosclerosis. It decreases proinflammatory cytokines and decreases blood viscosity which is helpful in patients of heart failure and coronary artery disease. It also improves ischemia and reperfusion injury of coronary revascularisation. Significant improvement has been observed in clinical and hemodynamic parameters and in exercise tolerance in patients given adjunctive CoQ10 in doses from 60 to 200 mg daily in the various trials conducted in patients of heart failure, hypertension, ischemic heart disease and other cardiac illnesses. Recently it has been found to be an independent predictor of mortality in congestive heart failure. It has also been found to be helpful in vertigo and Meniere-like syndrome by improving the immune system. Further research is going on to establish firmly its role in the therapy of cardiovascular diseases.

___________________________________________________

 

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What Causes Heart Disease? Part 3

Fats And Fast Oxidizers 

Fast oxidizers often develop problems with cholesterol. There are several reasons for this. One cause of elevated cholesterol or high LDL levels in fast oxidizers is a diet high in sugars and carbohydrates. The problem occurs because carbohydrates further unbalance their fast oxidation rate. This places more stress on the body, which in turn can increase the cholesterol level. 

One might think fast oxidizers would have low cholesterol because they burn their fats and other nutrients faster. In theory, this is true. However, many people with a fast oxidizer pattern on their hair analysis are in fact slow oxidizers under stress. The stress is of a type that causes a temporary speed-up of their oxidation rate. We know this is true because on a retest the oxidation rate often slows. Stress of any kind can elevate the cholesterol level as the body seeks to produce more raw material to make stress hormones. 

Fast oxidizers often require some fats or oils in their diet. These often do not further elevate the cholesterol level. Fast oxidizers may become irritable, hungry and nervous if they go on a very low-fat diet. 

If your hair analysis indicates fast oxidation and you wish to restrict your fats, use high-quality vegetable oils which contain no cholesterol. These include avocado, palm oil, coconut oil, olive oil and health store oils like flaxseed and hempseed. Although palm and coconut oils contain saturated fasts, they contain no cholesterol. It is best to avoid processed vegetable oils, like corn, soy, sunflower, safflower, and peanut oils sold in the supermarket. These have had all their vitamin E removed, and can cause more problems. 

Some health authorities recommend restricting all fats and oils when the cholesterol is elevated. However, fast oxidizers often note a reduction in cholesterol when some fats and oils are added to the diet, substituting for high carbohydrates in the diet. 

Fast oxidizers are often deficient in copper, zinc and magnesium. Any of these deficiencies can contribute to cardiovascular disease. Fast oxidizers may also develop excessive constriction of the coronary arteries due to excessive adrenal activity, and low calcium and magnesium levels. This can precipitate sudden and massive heart attacks. 

Slow Oxidation 

Slow oxidizers have more difficulty converting cholesterol into adrenal and sex hormones. The body may compensate by raising cholesterol to help produce more stress hormones. This is one possible cause of elevated cholesterol levels. The solution is to improve glandular activity. Slow oxidizers do not feel as well on fats. Therefore, they do best restricting fats and oils of all types. Slow oxidizers may be under stress for other reasons, which can elevate their cholesterol level. They may also have zinc deficiency and/or high levels of toxic metals such as cadmium, which can lead to arterial disease. 

Low Sodium/Potassium Ratio 

A hair analysis pattern often associated with cardiovascular disease and elevated cholesterol is a ratio of sodium to potassium less than 2.5:1. This is a chronic stress pattern, associated with excessive tissue breakdown, fatigue, diabetes, and heavy metal toxicity, all of which may contribute to cardiovascular disease. 

Other Hair Analysis Patterns 

Other mineral patterns associated with heart disease include low copper, low magnesium, low zinc, elevated cadmium.  

Margarine And Other Plastic Foods

Many people think they are doing themselves a favor by eating margarine. They are not. All margarine is made by heating vegetable oil and bubbling hydrogen through the mixture to produce an artificially saturated fat. (The advertising about polyunsaturated oil used in margarine is misleading. The oil is saturated by the time they finish with it.) The problems with margarine are:

   

• Nutrients in the oil such as vitamin E are destroyed when the product is heated. (Vitamin E deficiency from overeating on refined vegetable oils increases the risk of heart disease).
•  Hydrogenation produces trans-fatty acids. These are non-naturally occurring fatty acids that contribute to inflammation, one of the causes of heart disease. (Some margarines today claim to have the trans-fatty acids removed).
• Nickel is added as a catalyst in making margarine. Nickel is a highly toxic metal - fine for making coins, but not for eating.
•  Artificial color and flavor must be added to margarine to make it palatable. These chemicals have their own toxic effects.
• A recent study showed that margarine elevated the undesirable LDL cholesterol.

The problems with margarine apply equally to commercial peanut butters, vegetable shortening such as Crisco, fake whip cream products such as Cool-Whip, and many fried foods, salad dressings and crackers made with hydrogenated oils. These artificially saturated fats are worse for the body than naturally-occurring fats. 

Reducing Elevated Cholesterol And Triglycerides 

Reducing cholesterol and increasing the HDL/LDL ratio can usually be accomplished with nutritional methods. Here are some guidelines: 

• While some fat restriction may be helpful, other dietary factors are often much more important. A properly performed and interpreted hair analysis will provide much information about diet as well as mineral deficiencies, heavy metal toxicity and supplement recommendations to correct stress patterns.
• Food products containing refined white flour and white sugar - in all its forms - should be totally eliminated from the diet.
• Extra nutrients may be helpful including vitamin C, niacin, chromium, ginger, lecithin, omega-3 oils and extra fiber.
• Conditions such as dental infections and diabetes need to be addressed. 
• Lifestyle considerations are important, including exercise, weight control, adequate rest and sleep, and smoking cessation.

Such a holistic approach is endorsed by Jonathan Wright, MD, a leading holistic physician and former medical columnist for Prevention Magazine. He writes: 

"Only a few patients of the hundreds I've treated for high cholesterol have had to severely limit dietary intake (of fat). Usually, it is a matter of correcting the metabolism rather than the diet".(13)

Cholesterol-Lowering Drugs 

Several classes of drugs are used to lower cholesterol. Unfortunately, many have significant side effects. For example, in one study, patients placed on gemfibrozil did have reduced cardiac events than a placebo group. However, the overall death rate was almost identical. Those taking the drug had a higher incidence of violence, accidents and intercranial hemorrhages.(14) Note that studies show that a low cholesterol level, below 130, is not beneficial either.

New recommendations suggest the use of medication whenever cholesterol is over 200 mg.(15) This ignores the research that total cholesterol is not nearly as important as LDL and its ratio to the total cholesterol.

Drugs do not address the biochemical causes for high cholesterol in most cases. This means that pathology in the body may continue to progress, despite the use of these drugs. Drugs ought be used as a last resort, only after natural methods have been tried.

Natural approaches to cholesterol and heart disease have no side effects, except perhaps improved general health. Also, they address deeper causes to create a more permanent correction. Before stopping any medication, we recommend consulting a physician.

Conclusion 

In summary, high cholesterol can often be a symptom of stress or imbalanced chemistry, but not necessarily the cause. If you are healthy and your cholesterol level is within normal limits, don't be a fat hater and abandon all eggs, butter and meats. Do skip refined foods such as white flour, sugar, margarine and other hydrogenated oil products. Fats and oils are not all the same, by any means. Eating healthful fats and oils often pose no problem, whereas the refined oils can cause significant heart problems.

Some people need to restrict fats, including slow oxidizers and at times those with elevated cholesterol. A mineral analysis will provide more information in this area. By combining a scientific nutrition program with healthful lifestyle and appropriate diet most people can reduce their cholesterol and their risk of heart disease 

without drugs.

References: 

13. Wright, J., M.D., Dr. Wright’s Book of Nutritional Therapy, Rodale Press, Emmaus, Pa. 1979.

14. Frick, M.H. et al, Helsinki Heart Study. Primary Prevention Trial with Gemfibrozil in Middle-aged Men with Dylipidemia, New England Journal of Medicine, 317 (1987), pp. 1237-45. 

15. Journal American Medicine Assn., May 16, 2001;285:2486-2497.

What Causes Heart Disease? Part 2

What Causes Heart Disease? 

If cholesterol is not the cause of heart disease, what are the causes? Many factors may contribute to cardiovascular disease. A properly performed hair mineral analysis can help identify a number of them. Here are some of the major factors suspected in cardiovascular disease. 

•  Klevay showed that copper deficiency is associated with atherosclerosis. Copper is required for connective tissue synthesis.
• Zinc deficiency reduces the flexibility of the arteries and causes hardening. It may also cause inflammation of the arterial walls.
• Magnesium and taurine deficiencies may contribute to high blood pressure and other heart problems. 
• Cadmium toxicity is associated with hardening of the arteries. 
•  Elevated homocysteine levels are a factor in heart disease. Homocysteine is an amino acid. Its level can be reduced by increasing the intake of vitamin B6 and folic acid. 
• According to Rath and Pauling’’s unified theory of heart disease, the causes are deficiencies of vitamin C and lysine. These are required for collagen synthesis. This theory asserts that high levels of lipoprotein-A, part of LDL cholesterol, is responsible for arterial damage.
• Other vitamins and minerals are involved. Chromium supplements, for instance, have been shown to lower cholesterol levels. Chromium, manganese and B-complex vitamins may reduce stress by enhancing carbohydrate metabolism. 
• Low thyroid activity is associated with heart disease. Hypothyroidism may have numerous causes, including nutritional deficiencies and toxic metal poisoning. 
• Inflammation and infections are now known to be important in cardiovascular disease. These can include seemingly unrelated infections such as dental infections. These can spread toxins that affect every organ. 
• High blood pressure from any cause is a factor. 
• Smoking, diabetes, obesity, coffee-drinking and a sedentary lifestyle are risk factors. 
• Oxidant damage from vegetable oils and other oxidant exposure contributes to vascular disease. This factor may explain why populations that consume more animal fats often have less heart disease. 
• Artificially-hydrogenated fats found in margarine, dressings, fried foods and elsewhere may contribute. 
• Chlorinated and fluoridated drinking water, and residues of ionic detergents may be an important factor. 
• Drinking homogenized milk may be harmful for the arteries.   
• Adelle Davis in Let’s Get Well noted that "animals and human volunteers that are fed sugar instead of unrefined carbohydrates develop high cholesterol levels". 
• Familial and genetic tendencies, and emotions such as hostility appear related to heart disease.  

Why Does Cholesterol Rise? 

Modern nutritional science reveals several important facts about cholesterol:

• High cholesterol can be a symptom of an imbalanced body chemistry. One can observe high cholesterol levels in vegetarians who consume no cholesterol at all.
•  Stress can increase cholesterol. Cholesterol is needed to make stress-fighting hormones such as cortisone and cortisol. A body under excessive stress (from internal or external sources) may produce extra cholesterol to increase the anti-stress hormones.
•  Cholesterol plaques may protect weak arteries to prevent breakage. 
• Cholesterol may in fact protect the body against free radical or oxidant damage. This theory was first advanced by Dr. Elmer Cranton in the book, Bypassing Bypass. This may be why high HDL which is non-oxidized cholesterol is positive, while LDL, which is oxidized cholesterol, is more of a risk for heart disease. In coping with oxidant stress, the HDL is oxidized, or converted to LDL. 
• Some people seem to have a familial tendency for elevated cholesterol.
• Excessive consumption of sugar can contribute to high serum lipid levels. 
• Fingerstick cholesterol tests are among the least accurate medical tests. Always have such tests repeated. 
•  HDL and LDL levels are as important or more important than total cholesterol. A simple cholesterol reading is not too revealing.
  

What About Dietary Fat? 

There are many points to be considered. For example, the egg was indicted as a major cause of elevated cholesterol based on studies in the 1940s and 1950s. However, it turned out that in those studies powdered eggs were used.(10) These processed eggs contain oxidized cholesterol, the type known to cause problems. However, when the studies were repeated with fresh eggs, they did not raise cholesterol significantly.(11) However, many physicians and health authorities still quote the old studies. 

Also on the subject of eggs, it has been found that eggs from chickens that are allowed to run free, so-called cage-free eggs, have less cholesterol. This means the way our food is produced influences its nutritional content. 

There are many different types of fats. Studies have shown that a diet high in fish, which contain anti-inflammatory fats, can reduce heart disease.(12) 

In nutritional research, there are different body types. Some handle fats much better than others. Those whom Dr. Paul C. Eck called fast oxidizers require some fats and oils to help normalize body chemistry. Slow oxidizers, by contrast, do poorly on fats. This fact alone means that studies that look at the effects of fats on large groups are flawed unless they take into account different body chemistries. 

This can help account for divergent results of studies, some of which show no ill effect of fats, while others show that saturated fats, for example, are not healthy. Thus, the idea of metabolic types can be most helpful to assess the effects of fats on any particular person. Let us explore this is more detail.

References:

10. Cook, R.P., Cholesterol: Chemistry, Biochemistry, and Pathology, Academic Press, NY, 1958.
11. Passwater, R., Super Nutrition for Healthy Hearts, Deal Press, NY 1977. See also Flynn, M.A. et al, Effects of Dietary Egg on Human Cholesterol and Triglycerides, American Journal of Clinical Nutrition, 32 (May 1979) pp. 1051-1057.

12. Wright, J., M.D., Dr. Wright’s Book of Nutritional Therapy, Rodale Press, Emmaus, Pa. 1979.