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As health-seekers in the know are increasingly consuming butter, lard, tallow and coconut oil, they should expect to see attacks on traditional fats in the media and in the scientific journals—both of which receive substantial financial support from the vegetable oil and fast food industries.

The most recent attack comes from Dr. Mehmet Oz and his co-author Dr. Mike Roizen in a blistering article entitled “Don’t Monkey with Coconut Oil,” widely published in the newspapers in mid November. Dr. Oz is an American cardiothoracic surgeon and prolific author of popular books on diet and health. He became famous for his frequent appearances on the Oprah Winfrey Show and will be launching a daily talk show called Dr. Oz in the fall of 2009. While his views have been described as “alternative” or “holistic,” his recent article on coconut oil places him squarely in the camp of the diet dictocrats.

Roizen, his co-author, seems to have made a career out of attacking saturated fats. In a recent interview, for example, he blames foods full of saturated fats, “like croutons,” for everything from obesity to aging.¹ The only problem is that commerical croutons are made with vegetable shortenings, full of trans fats, not saturated fats. While the writings of Roizen and Oz mention trans fats in passing, their gunsights are focused on the innocent bystander, saturated fats.

Demonizing Saturated Fats

Coconut oil, says Dr. Oz, “is loaded with artery- clogging saturated fat and oozing with calories . . . But the buzz on the street is that it’s a natural miracle food that can melt off unwanted weight, lower your blood pressure, boost your immune system, fight heart disease and fend off cancer—without the artery-clogging effects of other high-sat-fat foods such as beef, cream and cheese.”

WAPF members know that saturated fats do not clog arteries, whether they are the short- and medium-chain type in coconut oil or the longer chain fatty acids in beef, cream and cheese. In these pages we have supplied numerous references to support this statement. One in particular is the 1968 International Atherosclerosis Project, in which over 22,000 corpses in fourteen nations were cut open and examined for plaques in the arteries. Investigators found the same degree of atheroma (artery clogs) in all parts of the world—in populations that consumed large amounts of animal products rich in saturated fats and in those that were largely vegetarian.²

The “buzz on the street” about coconut oil’s benefits is firmly grounded in science. Saturated fats in general enhance the immune system,³ and coconut oil in particular increases body temperature and is preferentially used by the body for energy rather than storage.⁴ The claim about benefits to blood pressure is not one that I have ever made, and as far as I know, there are no human studies that have looked at the effect of coconut oil on blood pressure.

Coconut Oil and Aging

Dr. Oz also claims that all saturated fats cause aging “by turning on a potentially harmful family of genes that we docs call RAS genes. They tell your body to churn out inflammatory proteins that cause heart disease, stroke, wrinkles, impotence and immune system slip-ups.” Actually, what these studies really showed was that fish oil and corn oil activated RAS genes to their carcinogenic form, not saturated fat. (See sidebar, page 51.) In fact, these studies confirm earlier research showing that what causes aging are toxic, rancid modern vegetable oils, full of free radicals, which are known to contribute to heart disease and cancer.⁵ A study by a plastic surgeon found that women who consumed mostly vegetable oils had far more wrinkles than those who used traditional animal fats.⁶

Coconut Oil for the Brain

Oz then mentions a study carried out at Medical University of South Carolina which compared rats fed diets of coconut oil and soybean oil. “[T]he rats who scarfed down the chow laced with coconut oil not only developed more inflammation in their gray matter, but they also made more mistakes in memory tests.” This study was published in the Journal of Alzheimer’s Disease, June 14, 2008.⁷ In the study, rats were fed a diet of 10 percent fully hydrogenated coconut oil and 2 percent purified cholesterol were compared to a control group fed 12 percent soybean oil. Those on the saturated fat diet commited more memory errors and showed signs of inflammation in certain areas of the brain.

It is important to explain why so many animal studies get negative results for coconut oil. The coconut oil used in laboratory studies is usually fully hydrogenated coconut oil. The process of full hydrogenation gets rid of all the unsaturated fatty acids in coconut oil. Researchers began using fully hydrogenated coconut oil to study the effects of essential fatty acid deficiency— they used coconut oil because it is the only fat that can be fully hydrogenated and still be soft enough for rats to eat. The poor results obtained in these studies—such as the mental impairment cited by Oz—are due to essential fatty acid (EFA) deficiency and not the fault of the saturated fats in coconut oil. It is extremely deceitful for commentators to blame coconut oil in studies such as these—as they often do.

In the study quoted by Oz, the rats were also fed 2 percent purified cholesterol. This will speed up the onset of EFA deficiency if the diet is devoid of EFA. (See sidebar, page 51.)

According to Oz, “Sat fat doesn’t do pretty things for your memory, either. It decreases a chemical known as brain-derived neurotrophic factor [BDNF], which is responsible for recall and learning.”

BDNF is a growth stimulus for neurons and some studies indicate that lowered BDNF is associated with depression. However, lowering of BDNF does not always lead to depressive effects. It would appear that BDNF has depressive effects in some parts of the brain and anti-depressive effects in others.⁸

It would indeed be strange if saturated fats depressed brain function since the brain contains more saturated fat than almost any other organ in the body.

The Amazing Story of Mr. Newport

What is not strange is the fact that Dr. Oz’s attack, with its specific emphasis on brain function, follows the amazing story of a case involving coconut oil and recovery from Alzheimer’s disease, widely reported in newspapers and on the Internet.⁹

The story is a report by Dr. Mary Newport, a neonatologist and medical director of the newborn intensive care unit at Spring Hill Regional Hospital in Florida. About six years ago, her husband, an accountant who worked at home, began struggling with daily tasks. His deterioration progressed and he was eventually diagnosed with early onset Alzheimer’s. Dr. Newport searched the Internet for clinical drug trials that would accept her husband and discovered that a drug containing medium-chain triglycerides, the kind of fat in coconut oil, had achieved remarkable results—not just slowing the progression of the disease but providing real improvement.

She decided to give her husband coconut oil, two tablespoons per day, and her husband immediately improved, scoring 18 on a cognitive assessment, four points higher than he had scored the previous day. Within a week he showed tremendous improvement and five months later her husband was leading a relatively normal life, although still unable to resume his work as an accountant, apparently due to permanent brain damage.

One important test for Alzheimer’s progression is to draw the face of a clock from memory. The illustration above shows Mr. Newport’s improvement as he took coconut oil.

Why does coconut oil work so well? Several researchers have been looking into the therapeutic use of high-fat ketonic diets in the treatment of disease. In 2001, Dr. Richard L. Veech of the (National Institutes of Health) NIH, and others, published an article entitled, “Ketone bodies, potential therapeutic uses.”¹⁰ In 2003, George F. Cahill, Jr. and Richard Veech authored, “Ketoacids? Good Medicine?”¹¹ and in 2004, Richard Veech also published a review of the therapeutic implications of ketone bodies.¹² The body produces ketone bodies from coconut oil and these can serve as food for the brain and nervous system when our cells develop insulin resistance, which happens in everyone to a greater or lesser extent as we age. With insulin resistance, ketone bodies derived from coconut oil appear to protect neurons when glucose is not available.¹³

Researchers are now looking into the exciting possibility of using coconut oil as a treatment not only for Alzheimer’s disease but also for Parkinson’s disease, Huntington’s disease, multiple sclerosis and amyotrophic lateral sclerosis (ALS or Lou Gehrig’s disease), drug resistant epilepsy, brittle type I diabetes, and diabetes type II, where there is insulin resistance. Ketone bodies may help the brain recover after a loss of oxygen in newborns through adults. Children with drug resistant epilepsy sometimes respond to an extremely low-carbohydrate ketogenic diet.¹⁴

Industry Damage Control

The attack by Dr. Oz and Mr. Roizen amounts to clever industry damage control. Imagine the loss of income to the pharmaceutical and food industries should the American public learn about the amazing benefits of coconut oil for the brain. Coconut oil holds potential in the treatment of cancer as well, as several studies have indicated coconut oil’s anticarcinogenic effects.¹⁵

Any time an attack like this appears in the media, it is good to remember that coconut and coconut oil are natural foods used by healthy peoples for thousands of years. The attack on coconut oil is not grounded in good science but in the agenda of the food industry.

REFERENCES

1. http://longevity.about.com/od/booksreviews/a/roizen_realage.htm.
2. McGill,HC and others. General Findings of the International Atherosclerosis Project. Laboratory Investigations, 1968, 18:(5):498.
3. http://www.westonaprice.org/knowyourfats/import_sat_fat.html; Lipids, DOI 10.1007/s11745-007- 3132-7.
4. Scalfi L and others. Postprandial thermogenesis in lean and obese subjects after meals supplemented with medium-chain and long-chain triglycerides. Am J Clin Nutr 1991 Mar;53(5):1130-3; Papamandjaris AA and others . Medium chain fatty acid metabolism and energy expenditure: obesity treatment implications. Life Sci 1998;62(14):1203-15; DeLany JP and others. Differential oxidation of individual dietary fatty acids in humans. Am J Clin Nutr 2000 Oct;72(4):905-11.
5. Tappel, AL. Where Old Age Begins. Nutrition Today, December 1967; Harman D. Journal of the American Geriatrics Society 17:721, August 1969 and 20:145, April 1972.
6. E R Pinckney, and C Pinckney, The Cholesterol Controversy, 1973, Sherbourne Press, Los Angeles, pp 44-46
7. Granholm ACand others. Effects of a saturated fat and high cholesterol diet on memory and hippocampal morphology in the middle-aged rat. J Alzheimers Dis. 2008;14(2):133-45.
8. Personal communication, Chris Masterjohn
9. http://forums.hsibaltimore.com/memory/12480-case-study-dr-mary-newport.html
10. Veech RL and others. Ketone bodies, potential therapeutic uses. IUBMB Life, 2001, Vol. 51 No.4, 241-247
11. Cahill GF and others. Ketoacids? Good Medicine? Transactions of the American Clinical and Climatological Association, Vol. 114, 2003.
12. Vech RL. The therapaeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism, Prostaglandins, Leukotrienes and Essential Fatty Acids, 70 (2004) 309-319.
13. Kashiwaya Y and others. D-b-Hydroxybutyrate protects neurons in models of Alzheimer’s and Parkinson’s disease. PNAS, May 9, 2000, Vol. 97 No. 10, 5440-5444.
14. http://forums.hsibaltimore.com/memory/12480-case-study-dr-mary-newport.html
15. Lim-Sylianco CY. Anticarcinogenic effect of coconut oil. The Philippine Journal of Coconut Studies 12:89-102;1987; Reddy BS, Maeura Y. Tumor promotion of dietary fat in azoxymethane-induced colon carcinogenesis in female F 344 rats. Journal of the National Cancer Institute 72:745- 750;1984; Cohen LA and others. Dietary fat and mammary cancer. I. Promoting effects of different dietary fats on N-nitrosomethylurea-induced rat mammary tumorigenesis. Journal of the National Cancer Institute 77:33;1986; Cohen LA and others. Dietary fat and mammary cancer. II. Modulation of serum and tumor lipid composition and tumor prostaglandins by different dietary fats: Association with tumor incidence patterns. Journal of the National Cancer Institute 77:43;1986.

SIDEBAR

How did coconut oil suddenly get so popular?

According to Dr. Oz, “Once trans fats were exposed as the nutritional bad boys they are, food manufacturers started turning to tropical oils like coconut and palm oil to take their place. These plant oils have many of the same qualities that made trans fats so good at preserving the shelf life and flavor of processed foods. So naturally, the food industry (not to mention the diet book industry) would like us to think they’re healthy.”

Oz has it wrong once again. Food manufacturers used tropical oils like coconut oil before the trans fats came on the scene. The vegetable oil industry then embarked on a long campaign of demonizing their competition, namely natural saturated fats like butter, tallow and coconut oil.¹⁰ With the recent revelations about the dangers of trans fats, food manufacturers are simply returning to the fats they used to use.

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Does Saturted Fat Cause Aging and Impair Memory?--What the Studies Really Say

By Chris Masterjohn

According to Dr. Oz, “. . . all sat fat speeds up aging. It does this by turning on a potentially harmful family of genes that we docs call RAS genes. They tell your body to churn out inflammatory proteins that cause heart disease, stroke, wrinkles, impotence and immune system slip-ups.”

There are a number of studies dating back to the 1990s showing that dietary fat can encourage mutations in RAS genes, which appear to activate them to their carcinogenic form, but these studies implicated fish oil and corn oil rather than saturated fat.^a Corn oil dose-dependently increased the activity of RAS genes and the incidence of mammary cancer in mice genetically altered to express the carcinogenic form of a particular RAS gene.^b A case-control study published in the year 2000 found that people who ate more monounsaturated fat were more likely to have mutated RAS genes. Similar associations were noted for saturated fat and carbohydrate but they were not statistically significant.^c The most recent study on the subject followed more than 120,000 people for over seven years and found that intakes of saturated and monounsaturated fat at the beginning of the study had no relationship to colon cancer risk at the end of the study. Those with higher linoleic acid intakes, however, had a higher risk of cancer if mutated RAS genes were their only genetic risk factor.^d These studies clearly implicated polyunsatuturated fats rather than saturated fats.

Regarding claims that saturated fat impairs memory, there are three studies claiming to show that a “saturated-fat diet” decreases levels of brain-derived neurotrophic factor (BDNF).^e,f,g These studies used low-fat control diets providing the majority of calories as starch and compared them to high-fat, high-sugar diets where most of the calories came from lard and sucrose. Lard contains about ten percent of its fat as polyunsaturated fatty acids, which promote oxidative stress,^h,i and the rest as a balance of saturated and monounsaturated fatty acids. Sucrose itself contributes to oxidative stress.^j The most recent study showing that a lard-sucrose diet reduces BDNF levels found that additional vitamin E could normalize these levels (3), suggesting that the diet reduces them by promoting oxidative stress and thus that it is the polyunsaturated fat and sucrose in the diets rather than the saturated fat that are responsible for the problem.

A recent study purportedly showed that “saturated fat and cholesterol” impaired brain structure and memory in mature rats.^k The treatment diet was not only high in saturated fat and cholesterol but completely devoid of essential fatty acids (EFA), which are necessary for brain function. Most of the calories came from casein, sucrose, and corn starch for all the rats. Half of the rats were given 12 percent soybean oil and half were given 10 percent hydrogenated coconut oil and 2 percent cholesterol. It has been known since 1960 that purified cholesterol at half this amount will accelerate the onset of essential fatty acid deficiency and aggravate the resultant dermatitis and testicular degeneration, even though this same amount of cholesterol does not raise the amount of essential fatty acids needed to cure the dermatitis and actually enhances testicular development when essential fatty acids are present.^l The results of this study were most likely due to essential fatty acid deficiency rather than saturated fat. In order to show a destructive effect of saturated fat itself, the researchers should have provided the minimum EFA requirement in both diets.

REFERENCES FOR THIS SIDEBAR

1. Lu J, Jiang C, Fontaine S, Thompson HJ. Ras may mediate mammary cancer promotion by high fat. Nutr Cancer. 1995;23(3):283-90.
2. DeWille JW, Waddell K, Steinmeyer C, Farmer SJ. Dietary fat promotes mammary tumorigenesis in MMTV/v-Ha-ras transgenic mice. Cancer Lett. 1993;69(1):59-66.
3. Slattery ML, Curtin K, Anderson K, Ma KN, Edwards S, Leppert M, Potter J, Schaffer D, Samowitz WS. Associations between dietary intake and Ki-ras mutations in colon tumors: a population-based study. Cancer Res. 2000;60(24):6935-41.
4. Weijenberg MP, Lüchtenborg M, de Goij AF, et al. Dietary fat and risk of colon and rectal cancer with aberrant MLH1 expression, APC, or KRAS genes. Cancer Causes Control. 2007;18(8):865-79.
5. Molteni R, Barnard RJ, Ying Z, Roberts CK, Gómez-Pinilla F. A high-fat, refined sugar diet reduces hippocampal brain-derived neurotrophic factor, neuronal plasticity, and learning. Neuroscience. 2002;112(4):803-14.
6. Wu A, Molteni R, Ying Z, Gomez-Pinilla F. A saturated-fat diet garabatees the outcome of traumatic brain injury on hippocampal plasticity and cognitive function by reducing brain-derived neurotrophic factor. Neuroscience. 2003;119(2):365-75.
7. Wu A, Ying Z, Gomez-Pinilla F. The interplay between oxidative stress and brain-derived neurotrophic factor modulates the outcome of a saturated fat dieto n synaptic plasticity and cognition. Eur J Neurosci. 2004;19(7):1699-707.
8. Saito M, Kubo K. Relationship between tissue lipid peroxidation and peroxidizability index after alpha-linolenic, eicosapentaenoic, or docosahexaenoic acid intake in rats. Br J Nutr. 2003;89(1):19-28.
9. Diniz YS, Cicogna AC, Padovani CR, Santana LS, FAine LA< Novelli EL. Diets rich in saturated and polyunsaturated fatty acids: metabolic shifting in cardiac health. Nutrition. 2004;20(2):230-4.
10. Chaudhary DP, Boparai RK, Bansal DD. Implications of oxidative stress in high sucrose low magnesium diet fed rats. Eur J Nutr. 2007;46:383-90.
11. Granholm AC, Bimonte-Nelson HA, Moore AB, Nelson ME, Freeman LR, Sambamurti K. Effects of a saturated fat and high cholesterol diet on memory and hippocampal morphology in the middle-aged rat. J Alzheimers Dis. 2008;14(2):133-45.
12. Holman RT, Peifer JJ. Acceleration of Essential Fatty Acid Deficiency by Dietary Cholesterol. J Nutr. 1960;70(3):411-17.

This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly journal of the Weston A. Price Foundation, Winter 2008.

About the Authors

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