Fats, Cholesterol, and your Health Part II

June 9, 2016

Many studies touting the evidence for the lipid hypothesis have recently been shown to be severely flawed. The few studies that do indicate a correlation between fat reduction and a decrease in coronary heart disease mortality also document a concurrent increase in deaths from cancer, brain hemorrhage, suicide and violent death. [12]

 

Says Anthony Colpo in “LDL Cholesterol: Bad Cholesterol, or Bad Science”: “The concept that LDL is ‘bad cholesterol’ is a simplistic and scientifically untenable hypothesis. Independent thinking practitioners must look at the readily available evidence for themselves, instead of relying on the continual stream of anti-cholesterol propaganda emanating from ‘health authorities.’ By doing so, they will quickly realize that the LDL hypothesis is aggressively promoted for reasons other than public health.” [21]

 

Some proponents of the lipid hypothesis argue that the incidence of cardiovascular disease is up because people are living longer than they did in the 1950s. Although it is true that more people reach old age today, the biggest reason for that is a drastic reduction in infant and childhood mortality rates. But the question is, are we really living that much longer?

 

Life Expectancy Statistics [22]

@ Birth     # of years

1920              56.4

1950             68.07

2002              77.3

 

At first glance these statistics seem to back what the proponents of the lipid hypothesis claim, we are in fact living longer. And since CVD is an elderly disease, one could deduce it is the reason the incidence is higher than it was 80 and even 50 years ago. The U. S. seems to be making very positive inroads to life expectancy, until you look at the big picture.

 

We know that 90% of all heart attacks occur over the age of 60. Let’s compare apples to apples and compare the life expectancy of people who reached 60 years of age in the same years as above.

 

@ 60 years of age    # of years

1920                          15.54

1950                          17.04

2002                          22.0

 

If you reached 60 years of age in 1920, you could expect to live an average of 15.54 more years. If you reached 60 years of age in 1950, you were expected to live an average of 17.04 more years. If you reached 60 years of age in 2002 you were expected to live an average of 22 more years. From 1920, when CVD was virtually unheard of, to 1950 when CVD was becoming our number one killer, there was only a 1.5 year difference in life expectancy. And in more than eight decades from 1920 to 2002, with all the advances in medicine and the hundreds of billions spent on health care each year, we’ve only added 6.46 years.

 

I know what you’re thinking: “Mike is out of his mind! I can’t believe he is advocating cutting out polyunsaturated oils and hydrogenated oils while touting the benefits of saturated fats from animals and tropical oils.” The only claim that could be made against saturated fats is that they raise cholesterol levels. And for that claim to be negative, one has to believe higher cholesterol levels are a health risk. Well, as stated earlier, I do not believe this and science is on my side.

 

In a 1988 study to determine whether elevated serum cholesterol levels are associated with all cause mortality, mortality from coronary heart disease, hospitalization for acute myocardial infarction (heart attack), and unstable angina (acute chest pain with no relief from medication or rest, which is a strong predictor of heart attack), 997 subjects, all over the age of 70, were used to determine the ratios of the four-year incidence of all cause mortality. The results showed no support for the Lipid hypothesis. [23]

 

In a workshop held at the National Heart, Lung and Blood Institute, researchers looked at every study that had been published about the risk of having high or low cholesterol and came to the same conclusion: Mortality was higher for woman with low cholesterol than for woman with high cholesterol. [19]

 

Dr. Gilles Dagenais and associates concluded that high cholesterol levels are not associated with CVD in Canadian males. This conclusion was reached after having followed 5,000 healthy middle-aged men for more than 12 years. [19]

 

In Russia, low cholesterol levels were associated with an increased risk of heart disease. [19]

 

In a study published in the Journal of the American Medical Association, Harvard Medical School researchers examined the association between egg consumption and CVD in 37,851 male health professionals and 80,082 female nurses, and found low consumption at one egg per week and high at one or more eggs per day. Researchers also tracked the associated occurrence of heart attacks, stroke, and other types of cardiovascular disease in the male group for eight years and in the female group for 14 years. They found no connection between egg consumption and heart disease. Even after adjusting for factors such as age, weight, high-fat food intake, smoking, high blood pressure, and family history of heart problems, no statistical correlation was identifiable between egg eating and heart disease. Keep in mind eggs contain 200mg of cholesterol each. [24]

 

Why take statin drugs?

 

Thirty years ago you were considered hypercholesterolemia if you were a middle-aged man whose cholesterol was over 240 with other risk factors like smoking or obesity. At the National Institute of Health Consensus Development Conference in December of 1984, the parameters changed to men or women with levels above 200. [25] And a couple months ago I was told that doctors are considering 180 to be high and would like to see everybody around 170. [26] These recommendations are to the point of being unattainable by diet, exercise or any other lifestyle modification.

So-called experts are now recommending that anyone with high cholesterol be given drug therapy, mainly a family of drugs called statins. How convenient for pharmaceutical companies that the levels of cholesterol that are considered high has lowered. Lowering the standards for prescribing statins has literally been worth billions in sales.

 

Is there a conflict of interest? Major consumer groups think so. They found out that eight of the nine "experts" that made the recommendations were on the payroll of pharmaceutical companies that manufacture those drugs. Major scientific organizations have chastised medical journals for allowing the pharmaceutical industry to publish misleading results and half-truths. There is a major push under way to force the pharmaceutical industry (and others) to publish results of all of their studies, and not just the ones that appear positive. The studies that showed negative results would also be forced to be published. [27]

 

Some of the most common drugs to treat people with supposed high cholesterol levels are Lipitor, Zocor and Crestor. Formally referred to as HMG-CoA reductase inhibitors, these drugs (statins) work by inhibiting the enzyme HMG-CoA reductase. Inhibiting this enzyme does reduce cholesterol levels, but it also reduces the production of CoQ10 (Co-enzyme Q 10). CoQ10 is a vital component to all cells in our body and is a very powerful antioxidant (50 times stronger than vitamin E).

 

After age 20, our synthesis of CoQ10 starts to decline, with a fall strikingly after age 50. Combine our decreased ability to synthesize CoQ10 with statins and you have a recipe for disaster. Depletion of this essential enzyme can lead to fatigue, muscle soreness, muscle weakness and heart failure, which happen to be among the most common complaints of statin users. CoQ10 has been shown to be essential for a properly functioning heart as well as preventing heart disease and stroke. [28, 29]

 

Do statins even work in preventing death from CVD? Results from five large statin studies in January 2000 showed that total cholesterol of the more than 30,000 individuals tested was lowered by an average of 20.4%. However, the degree of cholesterol reduction had no association with lower incidence of CVD. If lowering cholesterol levels is so important in combating CVD, why didn’t people who saw the greatest reduction in cholesterol levels get more of a benefit from the drugs? This is a real case for lack of exposure response, which indicates that the factor under investigation is not the true cause, but is secondary to the real cause. [16]

 

An analysis of all the big statin studies reported before 2000 found that long-term use of the cholesterol-lowering drugs for prevention of CVD produced a 1% greater risk of death over 10 years compared to placebo groups. These findings serve as more than enough evidence to negate the use of statins for the purpose of lowering the mortality rate in patients with a CVD risk. [30]

 

Looking past the Lipid Hypothesis

 

At this point, I hope you agree that cholesterol doesn’t cause heart disease; at the very least, I hope I have at least got you thinking that it might not. Cholesterol is essential for life and without it our bodies could not function. It is the building block for many hormones, including testosterone, estrogen, DHEA, human growth hormone, T3 and T4 (thyroid hormones). Our brains are made of mostly cholesterol and saturated fat. Cholesterol is also used by the body for healing. This is the reason cholesterol is found in atheroma blockages: it’s trying to heal an injured area of an artery. So if not cholesterol, what causes heart disease?

 

One of the biggest contributors to disease is free radicals. These chemical marauders wreak havoc on whatever tissue is in their vicinity and are implicated in diseases ranging from CVD to cancer. Although they can be detrimental to our health, free radicals are normally found in conjunction with many functions of the body. For example, when we use fat or glucose for fuel, our mitochondria produce free radicals as byproducts. Our bodies are in a constant battle to keep free radicals under control. With every breath we take, our bodies work to keep a very destructive substance in check -- oxygen.

 

We can also ingest free radicals. One of the biggest sources of dietary free radicals is the refined unnatural oils you buy in the grocery store. Any oil that is not labeled “Cold Pressed,” “Expeller Pressed” or “Extra Virgin” is already rancid and loaded with free radicals. Another major source of dietary free radicals is hydrogenated oils. Read your food labels -- if it has “vegetable oil,” “hydrogenated vegetable oil,” “partially hydrogenated vegetable oil” or “shortening” listed as one of the ingredients, do not buy it. If you already have it, pitch it -- it’s garbage.

 

Free radicals, if not kept in check, can damage the inner lining (intima) of an artery, causing a lesion. Many other substances have also been linked to arterial injury, including tobacco, high blood pressure, diabetes, trans fats, deficiencies in vitamins A and D, bacteria, viruses and more.  Injury causes inflammation and the body responds by producing raised plaques in an effort to heal the vascular lesions. This is known as the Response to Injury Hypothesis presented by Russell Ross and John Glomset in 1976.

 

Cardiovascular disease is recognized as having multiple causes, some known and some unknown. The lipid hypothesis hasn’t a leg to stand on. We know that saturated fat and cholesterol are healthy and essential for life. I hope this article has made you think. The oil and processed food industries are very powerful and are using all their resources to keep their products on the shelves with no regard for our safety or well being. But there are things we can do for ourselves and our families.

 

Below are some guidelines we can follow to be healthier and reduce our risk of cardiovascular disease.

 

Read food labels.

 

Consume whole, unprocessed foods.

Don’t consume any product that contains trans fat.

Don’t be fooled by products that advertise “zero trans fat.” Always read the ingredient list and if “hydrogenated vegetable oil,” “partially hydrogenated vegetable oil” or “shortening” are listed, understand that it has trans fat. By law, companies can claim “zero” if there is .5 grams or less of trans fat per serving. There is no safe level of trans fat.

Don’t consume any product that contains vegetable oil, hydrogenated vegetable oil, partially hydrogenated vegetable oil or shortening listed as one of the ingredients.

Only use oils that are labeled “Cold Pressed,” “Expeller Pressed” or “Extra Virgin.”

Consume eggs laid by true free range chickens. They are a good source of omega-3 fatty acids, biotin, and vitamins A, D and E.

Use peanut oil, sesame oil or olive oil for cooking if you do not want to use animal fats. These oils can also be used for one-time frying.

Use coconut oil for cooking or frying. It’s very stable, and has strong antimicrobial properties.

Use butter, not margarine.

Don’t use trans fat-free spreads. They are still made with highly processed oils that are rancid.

Keep your consumption of polyunsaturated fats to a minimum. They are high in omega-6 fatty acids.

Consume meat.

Don’t eat like a vegetarian. We do not possess multiple stomachs, nor do we chew cud. Our stomachs produce hydrochloric acid, which is not found in herbivores. We are omnivores. There are essential nutrients in animal products that cannot be gotten in sufficient amounts, or in any amount by eating plants.

Don’t feed your children a low-fat diet. If they’re fat, it’s because they sit on their asses too much and eat too much junk. Not coincidentally, these are the same two reasons many adult Americans are overweight.

Supplement your diet with vitamins and other nutrients:  Vitamin D3, CoQ10 (ubiquinol), resveratrol, astaxanthin, omega-3 fatty acids (krill or fish oil), virgin coconut oil,

Don’t smoke.

Exercise at least three days per week.

 

Sources:

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  2. Clifton, P. M., Koegh, J. B., & Noakes, M. (2004). Trans fatty acids in adipose tissue and the food supply are associated with myocardial infarction. The Journal of Nutrition, 134(4), 874-879. Retrieved from http://jn.nutrition.org/content/134/4/874.full

  3. Ascherio, A., Stampfer, M. J., & Willet, W. C. (1999). Trans fatty acids and coronary heart disease . (Background and scientific review, Harvard)Retrieved from http://bit.ly/1V4j4e6

  4. Ban trans fats. (n.d.). Retrieved from http://www.bantransfats.com/transvssat.html

  5. Severson, K. (2004). The trans fat solution: Cooking and shopping to eliminate the deadliest fat from your diet. Berkeley: Ten Speed Press.

  6. Enig, M. (n.d.). Interview by RA Passwater [Personal Interview]. Health risks from processed foods and trans fats. , Retrieved from http://www.healthy.net/scr/interview.aspx?Id=162

  7. Enig, M. (2000). Know Your Fats. Silver Spring: Bethesda Press.

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  9. Severson, K. (2002, January 30) “Hidden Killer, It’s trans fat. It’s dangerous. And it’s in food you eat everyday.” San Francisco Chronicle. Retrieved from http://bit.ly/J4u72n

  10. Watson, R. R. (n.d.). Nutrients and foods in aids. Lauric.org, Retrieved from http://www.lauric.org/watsontextb.hmtl.

  11. Fallon, S., & Enig, M. G. (2000). Nourishing traditions: The cookbook that challenges politically correct nutrition and the diet dictocrats. Warsaw: New Trends Publishing.

  12. (2012). Heart disease and stroke statistics—2012 update a report from the American heart association. Circulation, 125, e2-e220. Retrieved from http://bit.ly/1TQ6GJq

  13. Fallon-Morell, S., & Enig, M. G. (2000). It's the beef. Wise Traditions in food, farming and the healing arts, Retrieved from http://www.westonaprice.org/food-features/its-the-beef  

  14. Guyenet, S. (2012, February 18). [Web log message]. Retrieved from http://bit.ly/1YtP3Dm 

  15. U.S. Department of Agriculture, Economic Research Service. (2011). Caloric sweeteners, percapita availability. Retrieved from website: http://1.usa.gov/1Nv43Az

  16. Ravnskov, U. (2000). The Cholesterol Myths: Exposing the Fallacy that Saturated fat and Cholesterol cause heart disease. Washington, New Trends Publishing.

  17. Malhotra, S. L. (1967) Epidemiology of ischemic heart disease in India with special reference to causation. Br Heart J, 29(6): 895-905. Retrieved from http://1.usa.gov/1Tg4MpC

  18. French Paradox. (n.d.). Nutrition and Well-Being A-Z. Retrieved April 14, 2012, from Answers.com Web site: http://www.answers.com/topic/french-paradox

  19. Guberan, E. (1979). Surprising decline of cardiovascular mortality in Switzerland: 1951-1976. Journal of Epidemiology and community Health, 33(2): 114-120. Retrieved from http://bit.ly/253ldx2

  20. Fallon-Morell, S., & Enig, M. (1999). Inside Japan – Surprising Facts about Japanese Foodways. Wise Traditions in food, farming and the healing arts. Retrieved from http://bit.ly/27pLzb6

  21. Colpo, A. (2005). LDL Cholesterol: Bad Cholesterol, or Bad Science. Journal of American Physicians and Surgeons, 10(3): 83-89. Retrieved from http://bit.ly/1YtQQs9

  22. Arias, E. Center for Disease Control and Prevention, Division of Vital Statistics. (2004). United states life tables, 2002. Retrieved from website: www.cdc.gov/nchs/data/nvsr/nvsr53/nvsr53_06.pdf

  23. Krumholz, H.M., et al. (1994). Lack of association between cholesterol and coronary heart disease mortality and morbidity and all cause mortality in persons older than 70 years. JAMA, 272: 1335-1340. Retrieved from http://bit.ly/1Tg5lQ8 Membership required

  24. Hu, F. B., et al. (1999). A prospective study of egg consumption and risk of cardiovascular disease in men and women. JAMA, 281(15), 1387-1394. Retrieved from http://bit.ly/1TfGybK

  25. U.S. Department of Health and Human Services, NIH. (1984). Lowering blood cholesterol to prevent heart disease: NIH consensus statement. Retrieved from website: http://1.usa.gov/1XtaIgE

  26. Fetterman, T. (2005, December 7). Interview by M.S. Furci [Personal Interview]. Cardiovascular disease, risk factors and prevention.

  27. Rosedale, R. (2005, May 28). Cholesterol is not the cause of heart disease. Mercola.com, Retrieved from http://articles.mercola.com/sites/articles/archive/2005/05/28/cholesterol-heart.aspx

  28. A physicians update on coenzyme q10 in U.S. medicine. A summary of a recent PubMed search and other materials, University of Washington, St. Louis, Missouri. Retrieved from http://bit.ly/1rNKEkm

  29. Langsjoen, P.H. (1994). Introduction to Coenzyme Q10. Retrieved from http://bit.ly/253jrMr

  30. Jackson, P.R., et al. (2001). Statins for primary prevention: at what coronary risk is safety assured? British J of Clinical Pharmacology, 52(4), 439-446. Retrieved from http://1.usa.gov/24TF0LJ

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