Coconut oil has been consumed in tropical nations for thousands of years and was once quite prevalent in developed nations such as the United States. With a long shelf life and a melting point of 76 degrees, it was a favourite in the baking industry. But a negative campaign facilitated by the vegetable oil industry against saturated fats in general, and the tropical oils in particular, led most food manufacturers to abandon coconut oil in favour of the polyunsaturated oils that come from the main cash crops in the U.S., particularly soy. Many other countries, including traditional tropical oil hotspots such as India, followed the U.S. in this change of direction. Now, instead of consuming natural oil, many consumers are exposed to a partially hydrogenated, oxidized, genetically modified product. So how has this change improved the incidence of chronic disease?
Coconut Oil and Heart Disease
With the help of poor research and lobbying from the seed industry, coconut oil was determined to be a strong contributor to heart disease since according to many health professionals and organizations “the saturated fat in coconut oil will clog arteries and lead to cardiovascular disease.” However, one only needs to look at the research to find that there appears to be no association between tropical oil intake and heart disease. This fact is highlighted by several studies of populations with a high intake of tropical oil (e.g., India, Polynesian and Indonesia) that have consistently found no association between the saturated fat found in tropical oils and cardiovascular disease.
In fact, some India health authorities believe that the replacing of the traditional cooking fats (e.g., coconut/palm oil) condemned to be atherogenic, with refined vegetable oils promoted as "heart-friendly" because of their polyunsaturated fatty acid (PUFA) content has something to do with the rising trend of heart disease and diabetes in this population. The combination of the higher intake of omega-6 fat and oxidized oil is likely a contributing factor.
Some of the early research that showed that the consumption of high amounts of polyunsaturated fat helped lower cholesterol failed to reveal that much of this reduction could be contributed to the fact that the cholesterol (LDL) was being oxidized and deposited elsewhere (e.g., arteries) thus, lowering levels in the blood. Other research condemning coconut oil used hydrogenated coconut oil. This is likely to have negative outcomes. It was this type of research that helped further propel saturated fats such as coconut into a black hole. The producers of trans fatty acids have relied on the anti-saturated fat crusade to protect their markets.
If saturated fat from coconut oil is so bad, why is that when the fatty acid composition of plaques found in arteries are analyzed, the level of saturated fatty acids in the cholesterol esters is only roughly 25 percent saturated with the other 75 percent being unsaturated (with a large amount of trans fat)? Also, none of this fat is reported to be lauric acid, which is the primary fat found in coconut oil. This finding further strengthens the argument that some of the cholesterol lowering effect seen with high intakes of polyunsaturated fat is because of oxidized LDL entering the arteries and is one reason why diets higher in polyunsaturated fats may result in lower LDL levels than diets higher in coconut oil. In addition, results strongly suggest that fat in chylomicrons may be a major source of oxidized lipids in the blood. Medium chain triglycerides that make up most of the fat in coconut oil does not require chylomicrons for transport and would not be a source of these oxidized lipids. Therefore, a meal high in polyunsaturated fat that would increase chylomicron circulation would set up a potential scenario for lipid oxidation.
Coconut oil’s medium chain triglycerides, its anti-viral, anti-microbial capacity and its polyphenol content may help protect the heart. A recent study found that a diet high in coconut oil reduced plasma lipoprotein (a) levels in women. High levels of lipoprotein (a) is a risk factor for heart disease. In addition, virgin coconut oil was found to reduce the amount of LDL that was oxidized. Authors believed one factor for this was the polyphenols (antioxidants) present in the oil. Coconut’s tendency to produce fewer pro-oxidant compounds would also likely be another contributing factor.
Much of the research into the health effects of saturated fat have been conducted on saturated fat from meats and dairy. One cannot forget that the fat from these sources could contain contaminants such as PCBs, dioxins and pesticides since these substances are stored in the fat of the animal, accumulating over the years and then would be transferred to humans with consumption. There is no research to compare the health effects of saturated fat from purely uncontaminated sources and saturated fat derived from conventional agriculture.
In spite of what has been said over the last several decades about the culpability of the saturated fatty acids in heart disease, they are ultimately a lot less to blame than what is assumed. More and more research is showing the problem to be related to oxidized products and of course trans-fat.
One of the great characteristics of coconut oil is that it holds its own against high heat. Since most of the fat in tropical oils such as coconut contain no double bonds and have a high melting point, they do not break down and produce undesirable by-products when heated to high temperatures. In fact, coconut oil can be kept at room temperature for a year or more without turning rancid. Coconut oil's high melting point allows it to be solid at room temperature. However, it’s this hard, white state that makes it easy to understand why this oil is perceived as an artery clogger.
Unfortunately, when vegetable oils are heated to high temperatures in the presence of oxygen, they become oxidized and produce by-products including lipid hydroperoxide that act as pro-oxidants. This is especially true for polyunsaturated fats like linoleic acid that contain more than one double bond as these double bonds are particularly susceptible to breakdown and oxidation. Research in animals indicates that oxidized fat components interfere physically or biochemically with normal cell functions resulting in pathological changes (e.g., decreased fluidity). In addition, cells exposed to pro-oxidants produced from heated oil often responded by cell death. For example, dietary consumption of heated oils may lead to oxidative damage and to cell death in the colon. This may contribute to an enhanced risk of colon cancer due to regenerative cell proliferation.
In addition to the very high intake of fish oil, one of the reasons believed for the reduced heart disease among Eskimos is that they consume the bulk of their food frozen, raw or dried, occasionally boiled, but never deep-fried or after exposure to excessive heat.
Oils that are heated to extreme temperatures and re-used (re-heated) are especially harmful and can form numerous toxic polymer compounds and peroxides. Data shows that these compounds can reach 40% in frying oil. This would be the case with most oil that is used for making French fries. Also, keep in mind that cheap refined oils that are readily available at most supermarkets are already heat treated before hitting the frying pan as heat, along with chemicals, is used to extract as much oil as possible from the seeds.
When these by-products of heated oil are consumed, they are absorbed by the intestine and research shows they can then increase the oxidation of lipoproteins. For example, lipid peroxides would seek out and attack LDL cholesterol molecules in the blood and damage them via their pro-oxidant capabilities. Oxidized LDL cholesterol molecules are scavenged (picked-up) by macrophages and then deposited in arteries which can, over a period of time, lead to blockage (arteriosclerosis) and increased risk of a cardiac event. Those with high LDL levels would be more susceptible to the effects of heated oil since there are more LDL molecules that can become oxidized. Lipoprotein oxidization appears to be even more amplified in those with diabetes with poor sugar control following a meal containing oxidized oils. Just think of the many ways that a Happy Meal can pose a risk to a diabetic.
There is also some indication that LDL levels may rise with increased intake of oxidized fat. Perhaps the body is increasing cholesterol production to help repair damage to cell membranes caused by the pro-oxidants in the heated oil, a theory strengthened by the fact that HDL levels appear to be somewhat reduced with consumption of oxidized oils. Since HDL is involved in the reverse transport of cholesterol out of the blood, it would likely be reduced when the body requires cholesterol (in the form of LDL) to repair damaged membranes. Studies have also found HDL levels to be increased with consumption of coconut oil (one reason why studies show that total cholesterol increases with coconut oil intake), which may indicate that less cholesterol is needed to repair damaged cell membranes that can occur when membranes contain more unsaturated fat that is more susceptible to damage from free radicals.
A study conducted on animals fed thermally heated oil showed retardation of growth, poor efficiencies, rough, greasy mottled coats and shortened life span. That doesn’t sound good! Animal studies have also found that the consumption of oxidized fats can increase the formation of mutagenic compounds and alter enzyme activity and gene expression, especially in the liver. In the liver, this appears to do everything from altering normal liver fat metabolism to decreasing liver glycogen levels. In addition, oxidized fats have shown to alter thyroid function, and the ingestion of a meal rich in fat previously used for deep frying in a commercial fast food restaurant resulted in impaired arterial endothelial function in rats - a finding that suggests that intake of degradation products of heated fat can contribute to endothelial dysfunction. Concerning is that feeding oxidized oil with a high concentration of lipid peroxidation products to female rats during rearing, pregnancy and lactation negatively influenced the development and antioxidant status of fetus and suckling pups. This was demonstrated by higher levels of lipid peroxidation products in the liver of newborn rats, less calories in mothers' milk (lower fat levels) and reduced weight of the litter at birth and diminished weight gain during suckling compared to the animals fed fresh oil.
Unfortunately, much of the research to date on the health impacts of consuming oxidized oils has been conducted on animals, and the same results do not always translate into humans. But the overwhelming evidence found in animal models cannot be ignored and enforces the need for more human studies.
Apparently one does not need to actually consume oxidized oils to experience the negative consequences. It is suspected from epidemiological studies that exposure to fumes from cooking oils could be an important risk factor for lung cancer. Lung cancer was found to be more prevalent in Taiwanese women who waited until oil was heated to high temperatures before beginning to cook. When vegetable oils are heated, they emit carcinogenic polycyclic aromatic hydrocarbons (PAHs) in smoke that then can enter the lungs.
Aging, particularly aging of the brain, is likely to be associated with lipid peroxidation, a process accelerated by regular consumption of oxidized oils and a diet deficient in antioxidants. The brain consists of a high amount of polyunsaturated fat (DHA) and is particularly susceptible to oxidants (free-radicals). There is very good evidence that a large contributor to Alzheimer’s disease is free-radical damage of the brain.
Trans polyunsaturated n-3 fatty acids are formed as a result of high heat treatment of vegetable oils. These trans fatty acids are a different type than that produced by food manufactures (partially hydrogenated oil), and their impact on human health is yet to be fully determined. This transformation is likely not to be benign.
Since the main function of the antioxidant vitamin E is to help prevent lipid peroxidation, supplementation with vitamin E can help reduce the damaging effects of heated oil - an outcome supported by some research. However, constant feeding of oxidized oils may over time deplete the body’s antioxidant levels (e.g., alpha-tocopherol, glutathione), an effect amplified when you consider that individuals who eat a lot of these oils (e.g., fried foods) tend to consume less antioxidants to start off with. Heating vegetable oils also lowers the vitamin E levels present naturally in the oil. Thus, a fast food meal fried in soybean oil (high in polyunsaturated fat) that is not surprisingly low in antioxidants is likely to set up a scenario of increased oxidation and, when repeated over a period of weeks, months and years, can lead to problems. According to health organizations, we should be increasing our intake of ALL polyunsaturated fats – makes you wonder who we should be listening to.
Tip: The fight against lipid oxidation is one reason why vitamin E supplementation (along with vitamin C to regenerate vitamin E) should be considered when supplementing with fish oil (DHA) since this fat is very susceptible to oxidative damage due to its numerous double bonds. Those consuming high amounts of thermally oxidized oils should be encouraged to increase their intake of fruits, vegetables and nuts to help counteract any increased oxidative stress.
Thus, it seems apparent that lipid oxidation products generated in culinary oils during episodes of thermal stressing can give rise to cellular damage and that this effect does not occur with tropical oils. Results show that the oil now most commonly used by street vendors in Egypt (blend of cotton seed and sunflower oil) is the least suitable for frying, while traditional palm oil on the basis of the various chemical parameters studied is the ideal choice. Egypt is a country in which deep-fried vegetable patties ('fallafel') forms the staple food item in the diet. Therefore, the ingestion of decomposition products formed as a result of thermal abuse and oxidation of frying oils may lead to a variety of symptoms and diseases over time. Populations such as this would benefit from returning to traditional tropical oil use and ignore what North American health associations are saying.
Recommendation: Purchase cold-pressed/expeller pressed unrefined oils (e.g., walnut, olive, hempseed) for use in salads and shakes, and use tropical oils for your heating needs. Most people should also be considering a fish oil (EPA/DHA) supplement. And always make sure your diet is sufficient in antioxidants.
The following oils contain a higher percentage of polyunsaturated fat and should be only used in their natural, unheated state:
- Hempseed oil
- Flaxseed oil
- Grapeseed oil
- Soybean oil – many restaurants use this oil and is the oil most likely to be partially hydrogenated
- Sunflower oil – there are some versions that are higher in monounsaturated fat
- Walnut oil
- Corn oil
- Cottenseed oil
- Pumpkin seed oil
Since ultraviolet light can induce oxidation in unsaturated oils, it is important to purchase oils in a dark bottle.
Dietary Sources of Oxidized Oils
The consumer is likely to be exposed to heated and oxidized oils in several ways. Fats and oils are heated at high temperatures during baking, grilling and pan frying. However, deep fat frying is the most common and dangerous method of high temperature treatment and is the way that most consumers would be exposed to the most oxidized oils. Deep fat frying is a popular food preparation method because it produces desirable fried food flavour, golden brown color and crisp texture. Partially hydrogenated oil that has been oxidized is a deadly one-two-punch, making the French fry perhaps one of the worst foods out there. It boggles the mind that the USDA would now define (upon request of the French fry industry) frozen French fries as "fresh vegetables." Apparently the Frozen Potato Products Institute argued that rolling potato slices in a starch coating, frying them and freezing them is the equivalent of waxing a cucumber or sweetening a strawberry.
Less apparent dietary sources of oxidized oils would be vegetable oils used in commercial breads and crackers, supplement energy and cereal bars, margarines and baked goods such as muffins, donuts and cakes. In addition, eating at restaurants and fast-food establishments on a regular basis is likely to involve repeated exposure to these damaged oils. Eating away from the home less often is one solution, as is asking that food be prepared without the use of oil (e.g., poached fish).
Coconut Oil and Weight Management
Medium chain triglycerides (MCTs) have been suggested as efficacious in weight management because they possess greater thermogenic qualities relative to long chain triglycerides. MCTs containing six to 12 carbon fatty acids, differ from long-chain triglycerides (LCTs) - which have fatty acids of > 12 carbons - in that they are absorbed directly into the portal circulation and transported to tissues for rapid oxidation without the need for the lipoprotein and carnitine transport systems. LCTs, however, are transported via chylomicrons into the lymphatic system, allowing for extensive uptake into adipose tissue. It is this characteristic of MCTs that make them a useful dietary source of fat for those who have had portions of their colon removed. Approximately 50% of the fatty acids in coconut fat are the MCT lauric acid, making coconut oil the richest natural source of MCTs.
The few MCTs that are incorporated into fat (adipose) tissue are thought to down-regulate the expression of the major transcription factors involved in adiposity, which leads to reduced expression of genes involved in fatty acid uptake and esterification (fat synthesis), hence reducing fat storage capacity in adipocytes. For example, MCTs have been shown to decrease activity of an enzyme known as lipoprotein lipase which functions to increase adipose fat making. Thus, MCTs can have a direct metabolic impact on adipocytes. This then forces more dietary MCTs and other fats to be delivered to muscle and other non-adipose organs (e.g. liver), in which they are mostly disposed through oxidization, thereby reducing the substrate availability for fat synthesis in fat tissue and increasing the postprandial thermic effects (greater energy expenditure/thermic effect of feeding) of MCTs by up to 50% over LCTs.
Such a difference in post meal routing of dietary fatty acids may lead to lowered energy efficiency in MCT-fed compared with LCT-fed animals, a result demonstrated by research replacing beef tallow (LC) with coconut fat (MCT). Interestingly, it appears that women respond less readily to treatment with MCT than men as shown by reduced rise in energy expenditure after MCT feeding in women than men. Human studies have shown that replacing dietary LCT with MCT increases daily energy expenditure from 100 to 700 kJ per day in men and 138 kJ per day in women. Differences in MCT and LCT consumption on energy expenditure between men and women may be due to hormonal differences or to differences in intakes. Men generally consume more calories than women and, therefore, would have a greater absolute intake of MCT. MCT feeding is also believed to induce greater satiety, an effect attributed to altering the levels of various hormones including cholescytokinin, peptide YY, gastric inhibitory peptide, neurotensin and pancreatic polypeptide. Studies examining the satiating effect of fats of different chain lengths have found that energy intake can be reduced by 100-700 kJ when meals contained MCT than when they contained LCT as the fat source.
It is these mechanisms that are believed to be the reason why several studies in animals and humans have found smaller fat deposits in those consuming a high MCT-diet compared to those consuming the same calories from a high long-chain diet. However, whether effects of MCT on energy expenditure are long lasting and result in actual measurable and sustainable changes in body composition of humans remains to be established. When data examining the increased energy expenditure and reduced appetite associated with MCT intake are combined a negative weight balance of five to 16 kilograms per year maybe produced by substituting MCT for LCT in the diet. However, it is important to remember that this weight change is not likely to occur if MCT is simply added to the diet (e.g., mixed into shakes) in addition to the LCT already consumed (e.g., olive oil in salads, flax oil in protein shakes) and that the intake of MCT may need to be fairly high on a consistent basis. Adding a little coconut oil to the frying pan for scrambled eggs is not likely to induce any significant reduction in pant size due to overall energetics. For these reasons, over rambunctious proponents of coconut oil may indeed be overstating its impact on weight loss as a result of misinterpreting the research on MCTs.
To help solve this controversy, the next step in the evolution of research would be to specifically study coconut oils impact on weight management over a long period of time using identical diets except for the type of fat used.
If you are ready to give coconut oil a try, you should look for virgin organic coconut oil. This will ensure you are buying a high quality product in that no chemicals were used in the extraction process and your coconut oil was produced using ecologically sound practices.
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