Heart disease

  • A Natural Approach to Cholesterol Reduction & Heart Health

    Heart and blood vessel (cardiovascular) disease is the number one killer of Americans, and study after study points to elevated cholesterol as a major contributor to the problem. Some authorities have indicated that for every one-percentage point that cholesterol levels are reduced, the risk for cardiovascular disease is reduced by two points. In addition, most people with diabetes have increased risk for heart disease and stroke, due in part to high cholesterol and triglyceride levels, which can result in death. In fact, more than 65 percent of people with diabetes die from heart disease or stroke. By managing diabetes, and blood lipids (cholesterol and triglycerides), however, diabetics can greatly reduce this risk.1

    The current conventional medical treatment is cholesterol- lowering prescription drugs, along with low saturated fat diets. In addition, it makes sense to work with your doctor in trying one or more of the following relatively risk-free dietary supplement approaches as part of your total program for lowering cholesterol and reducing risk of cardiovascular disease.

    Plant Sterols And Stanols
    Plant sterols are natural substances found in small quantities in many fruits, vegetables, nuts, seeds, cereals, legumes, vegetable oils, and other plant sources. Research has demonstrated that taking plant sterols orally significantly reduces total and low-density lipoprotein (LDL) cholesterol levels, but has little or no effect on high-density lipoprotein (HDL) cholesterol levels. LDL is considered to be the “bad cholesterol,” while HDL is considered to be the “good cholesterol.” The way it works is that plant sterols block cholesterol absorption in the intestines, which in turn results in lowered LDL cholesterol in the bloodstream. Plant sterols has been reported to decrease LDL cholesterol levels nine to 20 percent, and usual doses have ranged between 800 mg to six grams per day and given before meals. Plant sterols are typically given in conjunction with a low-fat diet.2,3,4,5,6,7,8,9,10,11 Orally, plant sterols are usually well tolerated. Ezetimibe (Zetia), a medication used to lower cholesterol levels, inhibits intestinal absorption of plant sterols.

    Similar to sterols, plant stanols are natural substances that occur in even smaller quantities in many of the same sources. Like sterols, stanols block the absorption of cholesterol in the intestines. Taking plant stanols orally is effective for reducing total and LDL- cholesterol in about 88 percent of adult patients when used alone or in combination with a low-fat diet or statin drug (drug that inhibits the production of cholesterol in the body).12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27 When used alone it can reduce total and LDL cholesterol levels by 10 to 15 percent. When added to statin drugs, sitostanol reduces total cholesterol and LDL cholesterol by an additional three to 11 percent and seven to 16 percent, respectively. Clinical studies have used from 800 mg to four grams per day.28 Orally, plant stanols seem to be very well tolerated. Plant stanols can reduce absorption and blood levels of beta-carotene, so it should be used at a different time if you are taking beta-carotene supplements.

    Inositol Hexanicotinate High amounts (several grams per day) of niacin lower cholesterol; an effect recognized in the approval of niacin as a prescription medication for high cholesterol.29 At such intakes, however, acute symptoms (flushing, headache, stomachache) may be severe. In an attempt to avoid the side effects of niacin, alternative health practitioners increasingly use inositol hexanicotinate (aka, “no-flush niacin”), recommending 500 to 1,000 mg, taken three times per day, instead of niacin.30,31 This special form of niacin has been reported to lower serum cholesterol but so far has not been found to cause significant toxicity.32

    Omega-3 Fatty Acids From Fish Oil Including fish as a regular part of the diet has been shown to increase HDL cholesterol33 and is linked to a reduced risk of heart disease in the majority of studies.34 One reason that it has this effect is its oils contain the omega-3 fatty acids (O3FA) which appear to protect against heart disease.35 When used supplementally, however, there is contradictory evidence about the effects of fish oil on blood fat levels. Some clinical research shows fish oil supplementation can decrease elevated triglyceride levels, and decrease LDL cholesterol and increase levels of HDL cholesterol.36,37,38 However, other clinical research did not show beneficial effects on cholesterol levels.39 Nevertheless, fish oil from supplements or from dietary sources has been shown to reduce triglyceride levels by 20 to 50 percent. This effect appears to be dose-dependent.40,41,42,43Fish oil preparations providing 465 mg of eicosapentaenoic acid (EPA) and 375 mg of docosahexaenoic acid (DHA) is particularly effective in conjunction with dietary modifications.44

    In addition, research suggests that fish oil supplementation may be superior to the cholesterol-reducing drug rosuvastatin (Crestor®) for patients with heart failure. In a study published in The Lancet,45 researchers gave 1,000 mg of omega-3 fatty acids from fish oil to about 3,500 patients with heart failure, while another 3,500 heart failure patients received a placebo. After four years researchers found that those taking the omega-3 fatty acids had a nine percent relative risk reduction of dying, and an eight percent relative risk reduction for being hospitalized. The researchers concluded their study demonstrated that long-term administration of 1,000 mg daily omega-3 fatty acids effectively reduced all-cause mortality and admissions to hospital for cardiovascular reasons.

    The same researchers conducted a parallel study, giving rosuvastatin to 2,285 heart failure patients, and placebos to 2,289 heart failure patients. After four years researchers found little difference in heart failure rates between those given omega-3 fatty acids and those given rosuvastatin. In comparing the results, the researchers concluded that the omega-3 fatty acids were slightly more effective than rosuvastatin.46

    Dietary Considerations
    I would be remiss if I did not briefly recount the incredibly important role that diet plays in cardiovascular health. Specifically, the Mediterranean diet has extensive patient-oriented outcome data showing a significant risk reduction in mortality rates and in rates of fatal and nonfatal heart attack.47 Strong evidence support Mediterranean dietary patterns, including intake of vegetables and nuts, as protective against coronary heath disease.48


    The Mediterranean Diet

    The Mediterranean diet is based upon the diets of at least 16 countries that border the Mediterranean Sea. Although there are many differences in culture, ethnic background, religion, economy and agricultural production which result in variations in food intake among the population groups, there is still a common Mediterranean dietary pattern which includes:

    • High consumption of fruits, vegetables, bread and other cereals, potatoes, beans, nuts and seeds
    • Olive oil is an important monounsaturated fat source
    • Dairy products, fish and poultry are consumed in low to moderate amounts, and little red meat is eaten
    • Eggs are consumed zero to four times a week
    • Wine is consumed in low to moderate amounts

    In addition, there is strong evidence for the protective effect of monounsaturated fatty acids and prudent dietary patterns.49 Research clearly demonstrates that the people at low risk for CVD eat lots of vegetables, fruits, beans, whole grains and fish: a prudent diet.

    Those at high risk for CVD eat the typical Western pattern diet loaded with red meat, processed meat, refined grains, sweets and desserts, fried foods and high-fat dairy products.50,51 Furthermore, strong evidence has also shown a clear and harmful relationship between CVD and the intake of trans-fatty acids and foods with a high glycemic index or load.52

    In 2006 the American Heart Association released guidelines that integrate recommendations from a variety of diets into a single plan. The emphasis should be on diets that are rich in fruits, vegetables, and healthful fatty acids and that limit saturated fat intake. A stepwise individualized approach may be a practical way to help reduce your cardiovascular disease risk.53 Visit www.americanheart.org for more information.

    Conclusion
    There are many dietary supplements that may be used as part of your total program for lowering cholesterol and/or otherwise help in reducing risk of cardiovascular disease. Good choices include plant sterols/stanols, inositol hexanicotinate, and omega-3 fatty acids from fish oils. In addition, a healthy dietary program such as the Mediterranean diet should be the first line of defense for reducing the risk of cardiovascular disease.

    References:

    1. Diabetes: Heart Disease and Stroke. American Diabetes Association. Retrieved October 4, 2008 from http://www.diabetes.org/diabetes- heart-disease-stroke.jsp.
    2. Becker M, Staab D, Von Bergmann K. Treatment of severe familial hypercholesterolemia in childhood with sitosterol and sitostanol. J Pediatr 1993;122:292–6.
    3. Oster P, Schlierf G, Heuck CC, et al. [Sitosterol in familial hyperlipoproteinemia type II. A randomized, double-blind, cross-over study]. [Article in German]. Dtsch Med Wochenschr 1976;101:1308–11.
    4. Schlierf G, Oster P, Heuck CC, et al. Sitosterol in juvenile type II hyperlipoproteinemia. Atherosclerosis 1978;30:245–8.
    5. Schwartzkopff W, Jantke HJ. [Dose-effect of beta-sitosterin in type IIa and IIb hypercholesterolemias]. [Article in German]. MMW Munch Med Wochenschr 1978;120:1575–8.
    6. Becker M, Staab D, Von Bergman K. Long-term treatment of severe familial hypercholesterolemia in children: effect of sitosterol and bezafibrate. Pediatrics 1992;89:138–42.
    7. Weststrate JA, Meijer GW. Plant sterol-enriched margarines and reduction of plasma total- and LDL-cholesterol concentrations in normocholesterolaemic and mildly hypercholesterolaemic subjects. Eur J Clin Nutr 1998;52:334 –43.
    8. Anon. FDA authorizes new coronary heart disease health claim for plant sterol and plant stanol esters. FDA. 2000. Available at: www. fda.gov/bbs/topics/ANSWERS/ANS01033.html.
    9. Lichtenstein AH, Deckelbaum RJ. Stanol/sterol ester-containing foods and blood cholesterol levels: a statement for healthcare professionals from Nutrition Committee, Council on Nutrition, Physical Activity, Metabolism of American Heart Association. Circulation 2001;103:1177–9.
    10. Matvienko OA, Lewis DS, Swanson M, et al. A single daily dose of soybean phytosterols in ground beef decreases serum total cholesterol and LDL cholesterol in young, mildly hypercholesterolemic men. Am J Clin Nutr 2002;76:57–64.
    11. Neil HA, Meijer GW, Roe LS. Randomised controlled trial of use by hypercholesterolaemic patients of a vegetable oil sterol-enriched fat spread. Atherosclerosis 2001;156:329–37.
    12. Nguyen TT, Dale LC, von Bergmann K, Croghan IT. Cholesterollowering effect of stanol ester in a US population of mildly hypercholesterolemic men and women: a randomized controlled trial. Mayo Clin Proc 1999;74:1198–206.
    13. Vuorio AF, Gylling H, Turtola H, et al. Stanol ester margarine alone and with simvastatin lowers serum cholesterol in families with familial hypercholesterolemia caused by the FH-north karelia mutation. Arterioscler Thromb Vasc Biol 2000;20:500–6.
    14. Weststrate JA, Meijer GW. Plant sterol-enriched margarines and reduction of plasma total- and LDL-cholesterol concentrations in normocholesterolaemic and mildly hypercholesterolaemic subjects. Eur J Clin Nutr 1998;52:334 –43.
    15. Gylling H, Miettinen TA. Cholesterol reduction by different plant stanol mixtures and with variable fat intake. Metabolism 1999;48:575–80.
    16. Gylling H, Puska P, Vartiainen E, et al. Serum sterols during stanol ester feeding in a mildly hypercholesterolemic population. J Lipid Res 1999;40:593–600.
    17. Gylling H, Radhakrishnan R, Miettinen TA. Reduction of serum cholesterol in postmenopausal women with previous myocardial infarction and cholesterol malabsorption induced by dietary sitostanol ester margarine: women and dietary sitostanol. Circulation 1997;96:4226–31.
    18. Gylling H, Miettinen TA. Serum cholesterol and cholesterol and lipoprotein metabolism in hypercholesterolaemic NIDDM patients before and during sitostanol ester-margarine treatment. Diabetologia 1994;37:773–80.
    19. Gylling H, Miettinen TA. Effects of inhibiting cholesterol absorption and synthesis on cholesterol and lipoprotein metabolism in hypercholesterolemic non-insulin-dependent diabetic men. J Lipid Res 1996;37:1776–85.
    20. Gylling H, Puska P, Vartiainen E, et al. Retinol, vitamin D, carotenes and alpha-tocopherol in serum of a moderately hypercholesterolemic population consuming sitostanol ester margarine. Am J Cardiol 1999;145:279–85.
    21. Hallikainen MA, Uusitupa MI. Effects of 2 low-fat stanol estercontaining margarines on serum cholesterol concentrations as part of a low-fat diet in hypercholesterolemic subjects. Am J Clin Nutr 1999;69:403–10.
    22. Jones PJ, Ntanios FY, Raeini-Sarjaz M, et al. Cholesterol-lowering efficacy of a sitostanol-containing phytosterol mixture with a prudent diet in hyperlipidemic men. Am J Clin Nutr 1999;69:1144 –50.
    23. Gylling H, Siimes MA, Miettinen TA. Sitostanol ester margarine in dietary treatment of children with familial hypercholesterolemia. J Lipid Res 1995;36:1807–12.
    24. Miettinen TA, Puska P, Gylling H, et al. Reduction of serum cholesterol with sitostanol-ester margarine in a mildly hypercholesterolemic population. N Engl J Med 1995;333(20):1308-12.
    25. Vanhanen HT, Kajander J, Lehtovirta H. Serum levels, absorption efficiency, faecal elimination and synthesis of cholesterol during increasing doses of dietary sitostanol esters in hypercholesterolaemic subjects. Clin Sci (Colch) 1994;87:61-7.
    26. Plat J, van Onselen EN, van Heugten MM, Mensink RP. Effects on serum lipids, lipoproteins and fat soluble antioxidant concentrations of consumption frequency of margarines and shortenings enriched with plant stanol esters. Eur J Clin Nutr 2000;54:671–7.
    27. Hallikainen MA, Sarkkinen ES, Gylling H, et al. Comparison of the effects of plant sterol ester and plant stanol ester-enriched margarines in lowering serum cholesterol concentrations in hypercholesterolaemic subjects on a low-fat diet. Eur J Clin Nutr 2000;54:715–25.
    28. Law M. Plant sterol and stanol margarines and health. BMJ 2000;320:861–4.
    29. Guyton JR, Blazing MA, Hagar J, et al. Extended-release niacin vs gemfibrozil for the treatment of low levels of high-density lipoprotein cholesterol. Niaspan-Gemfibrozil Study Group. Arch Intern Med 2000;160:1177–84.
    30. Head KA. Inositol hexaniacinate: a safer alternative to niacin. Alt Med Rev 1996; 1:176–84.
    31. Murray M. Lipid-lowering drugs vs. Inositol hexaniacinate. Am J Natural Med 1995; 2:9 –12.
    32. Dorner Von G, Fisher FW. Zur Beinflussung der Serumlipide undlipoproteine durch den Hexanicotinsaureester des m-Inositol. Arzneimittel Forschung 1961; 11:110–3.
    33. Santos MJ, Lopez-Jurado M, Llopis J, et al. Influence of dietary supplementation with fish on plasma total cholesterol and lipoprotein cholesterol fractions in patients with coronary heart disease. J Nutr Med 1992;3:107–15.
    34. Kromhout D, Bosschieter EB, Coulander CdL, The inverse relation between fish consumption and 20-year mortality from coronary heart disease. N Engl J Med 1985;312:1205–9.
    35. Albert CM, Manson JE, O’Donnoell C, et al. Fish consumption and the risk of sudden death in the Physicians’ Health Study. Circulation 1996;94 (suppl 1):I-578 [abstract #3382].
    36. Petersen M, Pedersen H, Major-Pedersen A, et al. Effect of fish oil versus corn oil supplementation on LDL and HDL subclasses in type 2 diabetes. Diabetes Care 2002;25:17048.
    37. Chan DC, Watts GF, Barrett PH, et al. Regulatory effects of HMG CoA reductase inhibitor and fish oils on apolipoprotein B-100 kinetics in insulin-resistant obese male subjects with dyslipidemia. Diabetes 2002;51:2377–86.
    38. Friedberg CE, Janssen MJ, Heine RJ, Grobbee DE. Fish oil and glycemic control in diabetes. A meta-analysis. Diabetes Care 1998;21:494–500.
    39. Balestrieri, G. P., Maffi, V., Sleiman, I., Spandrio, S., Di Stefano, O., Salvi, A., and Scalvini, T. Fish oil supplementation in patients with heterozygous familial hypercholesterolemia. Recenti Prog Med 1996;87(3):102–5.
    40. Roche HM, Gibney MJ. Effect of long-chain n-3 polyunsaturated fatty acids on fasting and postprandial triacylglycerol metabolism. Am J Clin Nutr 2000;71:232S–7S.
    41. Deslypere JP. Influence of supplementation with N-3 fatty acids on different coronary risk factors in men--a placebo controlled study. Verh K Acad Geneeskd Belg 1992;54:189–216.
    42. Simons, L. A., Hickie, J. B., and Balasubramaniam, S. On the effects of dietary n-3 fatty acids (Maxepa) on plasma lipids and lipoproteins in patients with hyperlipidaemia. Atherosclerosis 1985;54(1):75–88.
    43. Nikkila, M. Influence of fish oil on blood lipids in coronary artery disease. Eur J Clin Nutr 1991;45(4):209–13.
    44. Reliant Pharmaceuticals. Omacor package insert. Liberty Corner, NJ; December, 2004.
    45. Effect of n-3 polyunsaturated fatty acids in patients with chronic heart failure (the GISSI-HF trial): a randomised, double-blind, placebocontrolled trial. Lancet; Published online ahead or print, 31 August 2008, doi:10.1016/S0140-6736(08)61239–8.
    46. Effect of rosuvastatin in patients with chronic heart failure (the GISSI-HF trial): a randomised, double-blind, placebo-controlled trial. Lancet; Published online ahead or print, 31 August 2008, doi:10.1016/S0140-6736(08)61240–4.
    47. Walker C, Reamy BV.Diets for cardiovascular disease prevention: what is the evidence? Am Fam Physician 2009;79(7):571–8.
    48. Mente A, de Koning L, Shannon HS, Anand SS. A systematic review of the evidence supporting a causal link between dietary factors and coronary heart disease. Arch Intern Med 2009;169(7):659–69.
    49. Mente A, de Koning L, Shannon HS, Anand SS. A systematic review of the evidence supporting a causal link between dietary factors and coronary heart disease. Arch Intern Med 2009;169(7):659–69.
    50. Hu FB, Rimm EB, Stampfer MJ, Ascherio A, Spiegelman D, Willett WC. Prospective study of major dietary patterns and risk of coronary heart disease in men. Am J Clin Nutr 2000;72(4):912–921.
    51. Liu S, Manson JE, Lee IM, Cole SR, Hennekens CH, Willett WC, Buring JE. Fruit and vegetable intake and risk of cardiovascular disease: the Women’s Health Study. Am J Clin Nutr 2000; 72(4):922–928
    52. Mente A, de Koning L, Shannon HS, Anand SS. A systematic review of the evidence supporting a causal link between dietary factors and coronary heart disease. Arch Intern Med 2009;169(7):659–69.
    53. Walker C, Reamy BV.Diets for cardiovascular disease prevention: what is the evidence? Am Fam Physician 2009;79(7):571–8.
  • Coconut OIL

    In mid-2012, Nestlé Health Science acquired a stake in Accera®, the U.S. maker of Axona®, a medical food targeted at people with mild to moderate Alzheimer’s. Aside from the fact that the purchase shows that Nestlé is placing a strategic bet on the future direction of medical food demand, this acquisition also is interesting for its potential validation of a tropical oil that alternately has been damned and praised for its role in health: coconut oil.

    On the one hand, there are those who still maintain that coconut oil, a source of more saturated fat than butter, lard or beef tallow, is the devil incarnate for brain and heart health. On the other hand, current science is in the process of validating the high regard that the coconut oil enjoys in the Ayurvedic and Chinese traditions of healing.

    Indeed, coconut oil bears a striking overlap in its metabolic implications, in this case for Alzheimer’s disease, with medical foods designed to provide the brain alternate fuel sources. A nice introduction to this topic is Alzheimer’s Disease: What If There Was a Cure? by Mary Newport, MD.

    The scientific backtracking regarding coconut oil recently was put in a nutshell in a New York Times interview of Thomas Brenna, a professor of nutritional sciences at Cornell University.1 Dr. Brenna observed that coconut oil’s bad reputation for cardiovascular health rested mostly on partially hydrogenated coconut oil, oil designed specifically to raise cholesterol levels in the rabbits being used in experiments. Virgin coconut oil differs dramatically in a large number of ways from the trans-fat laden partially hydrogenated item. Even the health dangers of the saturated aspect of coconut oil currently are being debated. As Dr. Brenna remarks in the interview, “I think we in the nutrition field are beginning to say that saturated fats are not so bad, and the evidence that said they were is not so strong.”

    Coconut Oil—A “Good” Saturated Fat
    Coconut oil is saturated (it is solid up to 76° F), consisting of 86.5 percent saturated fatty acids and 5.8 percent monounsaturated fatty acids.2 Lauric acid makes up approximately 46 percent of coconut oil and generally is considered to be the villain in terms of serum cholesterol. However, in clinical trials, the effects of dietary supplementation with coconut oil usually have been found to be either no effect or a small increase in LDL cholesterol and a significant increase in HDL cholesterol, meaning that the ratio—and cardiovascular risk—improves with supplementation.3,4

    Moreover, extra virgin coconut oil consists mostly of medium-chain fatty acids (MCFA), with 50 percent being lauric acid. Medium-chain fatty acids have been used for many years for special health purposes. They have attracted attention as part of a healthful diet because they are absorbed and transported directly into the liver via the portal vein and thereafter metabolized rapidly by beta-oxidation, thus increasing diet-induced thermogenesis.5

    One derivative of coconut MCFA is medium-chain triglyceride (MCT) oil, which is 75 percent caprylic and 25 percent capric acids, fatty acids very similar to lauric acid and present in virgin coconut oil in smaller amounts. MCT oil often is found in the hospital nutrient mixtures for bedridden patients who are dependent upon intravenous nutrition. These fats were developed in part because they do not require the action of bile for digestion, but rather are absorbed directly through the walls of the small intestine and transported to the liver to be used immediately as fuel.

    The special characteristics of coconut MCFA mean that the body prefers to burn it for fuel rather than to store it. You might say that the body treats coconut fatty acids more like it does carbohydrates, but without getting involved with insulin. Scientists know this because of experience with MCT oils. In my book Anti-Fat Nutrients (revised 4th edition, Basic Media), I discuss MCT oil at length. In seriously catabolic patients, MCT oil was found to help prevent the body from depleting lean and muscle tissues. Again, MCT fatty acids are not readily stored as body fat, but rather they are preferentially burned in the mitochondria of the cells to provide energy.6 For some athletes and bodybuilders, this quality has proved useful since excess training depletes the glycogen stores of the muscles, and continued training after that point can only take place partially through the break down of muscle protein for fuel.7 Coconut oil medium-chain fatty acids have properties similar to those of MCT oil, but not as pronounced.

    Does this mean that coconut oil can help dieters? Yes, as long as there are not too many expectations. Indeed, the nutrition author Ray Peat, PhD, has remarked that in the 1940s farmers attempted to use coconut oil for fattening their animals, but they found that it made them lean, active and hungry instead! The fatty acids found in coconut seem to promote the burning of fat for fuel and, as already noted, have a pronounced thermogenic effect. However, the thermogenic and fat-burning qualities of medium-chain fatty acids seem to be more significant for healthy subjects of normal weight and for those moderately overweight than for those who are clinically obese (fortunately, a category that excludes most of us). Moreover, medium-chain fatty acids serve to protect the body’s protein in the lean tissues during the use of low calorie and low carbohydrate diets.8

    Immune and Digestive Benefits
    Coconut oil has many other benefits. Two names are closely associated with the research in this area. These are Jon J. Kabara, PhD, one of the primary researchers into the benefits of lauric acid, and Mary G. Enig, PhD, the great researcher in the area of fats and one of the first (literally decades before the mainstream medical researchers) to point out the health dangers of trans-fatty acids.

    Dr. Enig was the keynote speaker in 2001 at the 36th Annual Conference of the Asian Pacific Coconut Community. There she gave her talk on the benefits of the coconut as a functional food. She noted that approximately 50 percent of the fatty acids in coconut fat are lauric acid, which has the additional beneficial function of being formed into monolaurin in the human body. Monolaurin is a monoglyceride used by the human metabolism to destroy lipid-coated (that is, fat-coated) viruses and a number of other undesirable organisms.

    Approximately 6–7 percent of the fatty acids in coconut fat are capric acid. Dr. Enig points out that capric acid is another medium-chain fatty acid that has a similar beneficial function when it is formed into monocaprin in the human or animal body. Monocaprin has beneficial effects similar to those found with monolaurin.

    The work of Dr. Jon Kabara and others shows that coconut oil components exert their health benefits in a way that is very safe to humans. In general, it is reported that the fatty acids and monoglycerides produce their inactivating effects by destabilizing the membrane that surrounds pathogens, for instance, by causing the disintegration of the virus envelope. Despite such sometimes quite potent actions against unwanted microbes, there is no evidence of any negative effect on probiotic organisms in the gastrointestinal tract.

    In his accessible, yet thoroughly researched book, The Healing Miracles of Coconut Oil (HealthWise), author Bruce Fife, ND, ranges across a number of health topics for which coconut oils has proven to be effective. He notes that coconut oil is so stable that it helps to preserve other oils, thereby reducing antioxidant requirements. Populations that eat large amounts of coconut and coconut products, such as the oil, are characterized by low rates of heart disease. Lauric acid and other medium-chain fatty acids are found in mother’s milk, where among other things, they improve the uptake by the baby of nutrients such as amino acids, calcium and magnesium. Similar effects upon nutrient assimilation have been found in the very ill and in the elderly. Moreover, these health benefits do not even take into account the long accepted uses of coconut oil to nourish the skin and the hair.

    Benefits for Brain Health?
    Let’s return to Nestlé Health Science acquired a stake in Accera, the U.S. maker of Axona, a medical food targeted at people with mild to moderate Alzheimer’s. The basic argument for this medicinal food is that in Alzheimer’s disease, the brain is starved for energy because it has a reduced ability to metabolize glucose. Reduced energy means reduced levels of cognition and memory. Fortunately, there is an alternative to glucose known as ketone bodies. Axona is a proprietary formulation of caprylic triglyceride that is converted by the liver into ketone bodies.

    Recall that coconut oil is a good source of medium-chain triglycerides (MCTs), the fatty acids that are converted in the liver to ketones. Ketones can provide energy to cells without the need for insulin. This is important for several reasons, not the least being that Alzheimer’s is related to insulin resistance and the attempt to get glucose to the brain with a high carbohydrate diet is counterproductive.9 Moreover, access to ketones may more generally promote neurologic health—several neurologic conditions have shown promising results with ketogenic diets. Ketogenic diets may help treat difficult cases of epilepsy and Parkinson’s disease as well as other neurological disorders, indeed perhaps improve cognition and health in general.

    The use of coconut oil with the conditions above at this point is promising, but hardly proven. Moreover, there are not yet much in the way of set rules or recommendations. Dr. Newport was giving her husband as much as 11 tablespoonsful per day, with four to eight tablespoonsful seeming to be a regular recommendation. At 115 calories per tablespoon, a coconut oil supplemented diet should not otherwise continue to be the standard American diet built upon a foundation of refined carbohydrates. Those wanting to add serious amounts of coconut oil to their everyday diets, as opposed to merely switching to it as a cooking oil, might find it useful to explore high protein/low carbohydrate options more generally. The chief warning to those who would try such diets is that Paleolithic-type diets need to include plenty of vegetables and reasonable amounts of whole fruit (avoiding fruit juice).

    Summing Up
    In his book, Bruce Fife asks the rhetorical questions, “If there was [sic] an oil you could use for your daily cooking needs that helped protect you from heart disease...other degenerative conditions, improved your digestion, strengthened your immune system, protected you from infectious diseases, and helped you lose excess weight, would you be interested?” Surely this is a good question. Aside from the record of traditional use, numerous research papers and United States Patents argue for the health-promoting benefits of coconut oil. Now that organic coconut oil/extra virgin coconut oil is readily available in health food stores, perhaps it is time for health-conscious shoppers to give it a try.

    References

    1. Melissa Clark, “Once a Villain, Coconut Oil Charms the Health Food World.” New York Times March 1, 2011.
    2. “Nutrient database, Release 24” (http://ndb.nal.usda.gov/) . United States Department of Agriculture. http://ndb.nal.usda.gov
    3. Assunção ML, Ferreira HS, dos Santos AF, Cabral CR Jr, Florêncio TM. Effects of dietary coconut oil on the biochemical and anthropometric profiles of women presenting abdominal obesity. Lipids. 2009 Jul;44(7):593-601.
    4. Mensink RP, Zock PL, Kester AD, Katan MB. Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials. Am J Clin Nutr. 2003 May;77(5):1146-55.
    5. Aoyama T, Nosaka N, Kasai M. Research on the nutritional characteristics of medium-chain fatty acids. J Med Invest. 2007 Aug;54(3-4):385-8.
    6. Babayan VK. Medium chain triglycerides and structured lipids. Lipids 1987 Jun;22(6):417-20.
    7. Nosaka N, Suzuki Y, Nagatoishi A, Kasai M, Wu J, Taguchi M. Effect of ingestion of medium-chain triacylglycerols on moderate-and high-intensity exercise in recreational athletes. J Nutr Sci Vitaminol (Tokyo). 2009 Apr;55(2):120-5.
    8. Dias VC, et al. Effects of medium-chain triglyceride feeding on energy balance in adult humans. Metabolism 1990;39:887-891.
    9. Seneff S, Wainwright G, Mascitelli L. Nutrition and Alzheimer’s disease: the detrimental role of a high carbohydrate diet. Eur J Intern Med. 2011 Apr;22(2):134-40.
  • L-Theanine: Nature’s Chill Pill

    Virtually everyone has stress. In fact, According to the Stress in America™ survey by the American Psychological Association,1 39 percent of respondents said their stress increased over the past year, and 44 percent said that their stress had increased over the past five years. The question is, how well do you handle your stress, how does it affect your life, and what can you do about it? The same Stress in America survey indicates the following percentage of Americans is only fair or poor at:

    • Preventing themselves from becoming stressed (44 percent)
    • Managing or reducing stress once experienced (39 percent)
    • Recovering fully or recharging after they’ve been stressed (31 percent)

    The ramifications of chronic stress include increases in illness, including headaches, heart disease, immune deficiencies and digestive problems. To a large extent, this appears to be due to an increased production of stress hormones and decreased immune function.2

    So what can be done to help control stress and reduce its ill effects? The answer is really multifaceted and may include a program of diet, exercise, stress-management techniques such as yoga, and even psychological counseling. In addition, when stress rears its ugly head, nature’s chill pill, L-theanine may be able to help.

    L-THEANINE’S MECHANISM OF ACTION
    Asian cultures have often used teas for relaxation effects. The relaxing effect is, at least in part, caused by the presence of a neurologically active amino acid, L-theanine (gamma-ethyl-amino- L-glutamic acid). Tea has the reputation of having less caffeine than coffee but it is the L-theanine in the tea that lessens the stimulant effect of caffeine on the human nervous system. In the brain, L-theanine increases both serotonin and dopamine production3, and possibly GABA as well.4

    Evidence from human electroencephalograph (EEG) studies show that it also significantly increases brain activity in the alpha frequency band which indicates that it relaxes the mind without inducing drowsiness. Alpha activity is also known to play an important role in critical aspects of attention. Research indicates that L-theanine has a significant effect on improving mental alertness while promoting relaxation.5

    L-THEANINE AND RELAXATION
    According to Mason, two small human studies6 showed that within 30–40 minutes of consuming 50 or 200 mg of L-theanine there is an increase of alpha wave activity/electrical signals produced by the brain. The perceived relaxation effect in the subjects coincided with the detection of alpha waves. This shows that L-theanine fosters a state of alert relaxation, which is consistent with the fact that anxious people have fewer or smaller alpha waves.

    The journal Human Psychopharmacology Clinical and Experimental published a double-blind placebo-controlled study7 in which sixteen healthy volunteers received 200 mg L-theanine, a pharmaceutical anxiolytic or placebo. The results showed that L-theanine induced feelings of tranquility in the volunteers.

    L-THEANINE, STRESS AND ANXIETY
    The journal Biological Psychology published a double-blind, placebo-controlled study8 in which twelve participants underwent four separate trials: one in which they took L-theanine at the start of an experimental, stress-inducing procedure, one in which they took L-theanine midway, and two control trials in which they either took a placebo or nothing. The results showed that L-theanine intake resulted in a reduction in some physiological indicators of stress within 15 minutes, compared to the placebo or control condition. Moreover, analyses of heart rate variability indicated that reductions in heart rate were likely attributable to a reduction of sympathetic nervous activation, suggesting that L-theanine had anti-stress effects via the inhibition of cortical neuron excitation.

    Similarly, a placebo-controlled study9 conducted with pharmacy students found that L-theanine (200 mg, twice a day, after breakfast and lunch) was effective at suppressing the initial stress response of students.

    The Journal of Physiological Anthropology published a placebo- controlled study10 in which 14 participants took either L-theanine + placebo, caffeine + placebo, or placebo only (L-theanine 200 mg, caffeine 100 mg) while performing mental tasks and physiological activities under conditions of physical or psychological stress. The results showed that L-theanine significantly reduced anxiety and reduced the blood-pressure increase in high-stress-response adults. Caffeine tended to have a similar but smaller inhibition of the blood-pressure increases caused by the mental tasks.

    The Journal of Functional Foods published a double-blind, placebo-controlled study11 in which 18 normal healthy subjects were divided into two groups referred to as high anxiety propensity group and the minimal anxiety propensity group. Both groups received 200 mg L-theanine and placebo (at different times)(200 mg/100 ml water) and placebo (100 ml water) in a double-blind repeated measurement design protocol. When tested at 15–60 minutes after consumption, results showed significantly enhanced activity of alpha bands, descending heart rate, elevated visual attentional performance, and improved reaction time response among high anxiety propensity subjects compared to a placebo. However, no significant differences were noticed among subjects with a minimal anxiety propensity.

    L-THEANINE AND MENTAL FOCUS
    The journal Neuropharmacology published a double-blind, randomized, cross-over study12 in which 27 participants received 100 mg L-theanine, 50 mg caffeine, a combination of the two, or a placebo. The results were that L-theanine and caffeine each significantly reduced error rates during a sustained attention task. It was noted that the combination of L-theanine and caffeine did not confer any additional benefits over either compound alone.

    Another study13 examined “sensory gating.” Sensory gating describes the processes of filtering out redundant or unnecessary stimuli in the brain from all possible environmental stimuli. Being able to do this is obviously beneficial when you’re trying to focus on a mental task. In the study, L-theanine was given to 14 healthy subjects, and tests were conducted 90 minutes later. The results were that 200 mg and 400 mg significantly improved sensory gating.

    CONCLUSION
    Research shows that L-theanine is effective at helping to promote relaxation while reducing feelings of stress and anxiety. Furthermore, this amino acid is even helpful in promoting mental focus. Truly, L-theanine is nature’s chill pill.

    References
    1. American Psychological Association. Stress in America™: Our Health at Risk. Released January 11, 2012. 78 pgs.
    2. Head KA, Kelly GS. Nutrients and botanicals for treatment of stress: adrenal fatigue, neurotransmitter imbalance, anxiety, and restless sleep. Altern Med Rev. 2009 Jun;14(2):114–40.
    3. L-Theanine monograph. Alternative Medicine Review 2005;10(2):136-8.
    4. Lu K, Gray MA, Oliver C, et al. The acute effects of L-theanine in comparison with alprazolam on anticipatory anxiety in humans. Hum Psychopharmacol Clin Exp 2004;19:457–65.
    5. Nobre AC, Rao A, Owen GN. L-theanine, a natural constituent in tea, and its effect on mental state. Asia Pac J Clin Nutr 2008;17 Suppl 1:167–8.
    6. Mason,R. 200 mg of Zen. Alternative & Complementary Therapies 2001; 7(2):91–95.
    7. Ibid. Lu K, Gray MA, Oliver C, et al.
    8. Kimura K, Ozeki M, Juneja LR, Ohira H. L-Theanine reduces psychological and physiological stress responses. Biol Psychol 2007;74(1):39–45
    9. Unno K, Tanida N, Ishii N, et al. Anti-stress effect of theanine on students during pharmacy practice: positive correlation among salivary á-amylase activity, trait anxiety and subjective stress. Pharmacol Biochem Behav. 2013 Oct;111:128–35.
    10. Yoto A, Motoki M, Murao S, Yokogoshi H. Effects of L-theanine or caffeine intake on changes in blood pressure under physical and psychological stresses. J Physiol Anthropol. 2012 Oct 29;31:28.
    11. Higashyama A, Htay HH, Ozeki M, Juneja LR, Kapoor MP. Effects of l-theanine on attention and reaction time response. Journal of Functional Foods. 2011;3(3):171–8.
    12. Foxe JJ, Morie KP, Laud PJ, Rowson MJ, de Bruin EA, Kelly SP. Assessing the effects of caffeine and theanine on the maintenance of vigilance during a sustained attention task. Neuropharmacology. 2012 Jun;62(7):2320–7.
    13. Ota M, Wakabayashi C, Matsuo J, et al. Effect of L-theanine on sensorimotor gating in healthy human subjects. Psychiatry Clin Neurosci. 2014 May;68(5):337–43.
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