The Real Facts About Coconut Oil --
If You HAVE Environmental Illness It May Not Be Good For You
There seems to be some misunderstanding about fats in general and environmental illness, so I thought I would provide some information to you and as a reader, if you have environmental illness of one sort or another the information in the paragraphs below pertain specifically to you. First of all, part of the consequences of injury from environmental illness includes insulin resistance, damage from inflammation and endothelial dysfunction (Helyar) due to bioaccumulation and the chemicals effects on cellular function and signaling. Almost everyone in the US and Canada...in cities or the country that do not grow all their own food on organic farms have some levels of toxins stored in their body and the fat cells are most often, where they are stored. Arsenescu explains how dioxins and PCB both have been shown to increase and expand adipose tissue and therefore, there is significant potential for toxic exposures that lead to obesity, cardiovascular disease, diabetes and cancer (Rutkowski). Yoshanari explains that the effects of toxins are still unclear but there is mounting evidence that toxicants can change the function/secretion of adipokines produced by adipocytes and have important roles in metabolic and endocine function. His research suggests that lipophilic toxicants in adipose tissue "activate the aryl hydrocarbon and the Nrf2 which increase detoxification but also may change the genetic expression of adipokines resulting in unexpected effect on tissue." Interestingly, animals that are AhR-/- do not gain weight in response to dioxin which suggest suppression of expression. (Arsenescu) Abdollahi and Rezg demonstrates subchronic effects of malathion exposure upsets glucose homeostasis and may induce diabetes through mechanisms including increased energy needed for detoxification and a decrease in paraxonase activity. Incidentally, Rezg's findings also show some of the harmful effects of malathion can be aleviated with the addition of the polyphenol caffeic acid which increases acetylcholinesterase.
To some extent the effects of a high-fat diet, atleast in terms of changing gene expression, parallel those of the effects of toxic injury on adipocytes and both exacerbate the impact of each other. A "sedentary lifestyle and overeating are two conditions that are associated with weight gain and obesity that lead to insulin resistance. Insulin resistance is a condition where insulin has less than desired effects of disposal of glucose in the muscle and the improper suppression of glucose production in the liver. Obesity and mitochondrial dysfunction are risk factors for insulin resistance and obese individuals have smaller mitochondria and exhibit compromised mitochondrial bioenergetic capacity. Insulin resistance also occurs with age, and a related defect in fatty acid oxidation has been identified." (Liang) Several conditions can influence the development of insulin resistance and sedentary lifestyles and overeating can be characteristic patterns of behavior of those who are ill. Researchers suspect there are a number of physiological consequences of bioaccumulation including the increase of inflammatory mediators that can lead to insulin resistance, for example, through increases in Tnf-a. Certain fats including those in coconut oil, like Tnf-a, can switch off important genes necessary for cellular metabolism including PGC-1a which may lead to a gradual shut-down of the mitochondria. Environmental influences like these may also explain the development of diabetes in adulthood. (Coghlan) Exercise, sedentary lifestyles and nutritional factors have all been demonstrated to regulate PGC-1a and regulate insulin sensitivity. Inflammation in the "fat" can also leak out and cause inflammation in the muscles surrounding them increasing insulin resistance.
Below is some general information related to fat which is important because insulin resistance is a risk factor for diabetes and diabetes is associated with bioaccumulation and obesity and environmental illness. One needs to understand the concept of triglycerides in addition to fat. Corcoran explains that "intracellular triglycerides are associated with diminished insulin sensitivity in skeletal muscle. This lipid accumulation is likely due to enhanced fatty acid uptake in the muscle coupled with diminished mitochondrial lipid oxidation. Excess fatty acids are esterified and either stored or metabolized to various molecules that may participate or interfere with normal cell signaling, particularly with insulin, mediated signal transduction and subsequently whole body glucose metabolism. Impaired insulin responsiveness if not managed, can lead to diabetes. Chronic over-consumption of calories coupled with deleterious intakes of fats have been shown to increase the risk of insulin resistance." These statements become particularly important to those with chemical injury and environmental illness because inefficient mitochondria and inflammation makes the body more insulin resistant. Most of the studies already published on the health benefits of fats in coconut oil,as far as I can tell, are on healthy people that do not have chemical sensitivities and do not have uncontrolled oxidative stress and do not have diminished mitochondrial function and insulin resistance already present.
Here are some important facts and definitions to understand when it comes to fat: American Diabetes Association
The ADA recommends less than 7% of saturated fat per day for most people. The exact amounts truly depend on a variety of factors including age, physical activity etc. Most Americans get more than that and I would assume so do most Canadians.
Generally, saturated fat raises cholesterol. From what I can see from the research, there is not a lot of evidence of coconut doing so directly, even though the ADA says it might. Saturated fat is in meats, lard, butter etc. Palm, Palm Kernel and Coconut oil are saturated vegetable oils. The have a different molecular formula from traditional longer-chain hydrogenated fats and are made of medium chain fatty acids. Trans fat is what is called hydrogenated oils and we know them as the oils that are more solid and found in snack food that are labelled as such, stick margarine, shortening and fast food.
Monounsaturated fats are those that are the more healthy fats and are sometimes called seed oils and may include canola, avocado, etc.
Polyunsaturated fats include corn oil, sunflower oil, cottonseed oil, etc.
Omega - 3 -- in fish and some plants, ie flax.
Cholesterol -- you body makes it and it comes from your diet.
Note: Coconut oil does not provide a good source of essential fatty acids so it is not a good replacement for sources that do. (Hargrave)
You may have noted some of the recent positive reports that have been published in the media lately not just about coconut oil but also medium chain fatty acids. The first one is they may help prevent diabetes better than long-chained fatty acids. Yes, this may be true if the results of the study are correct. However, this is not the full story. When doing health research or presenting health information to people that are already ill, one needs to dig a little deeper. Lets take a look at the fatty acid profile of coconut oil. By the way, I looked at the label on jars I bought --90% or more of the fat in coconut oil is saturated fat. It does not matter if you buy organic, virgin or extra-virgin coconut oil most of the fat in coconut oil is saturated fat. Also, in case your interested according to most of what I read there is little or no difference in virgin or extra-virgin coconut oil. It is labelled like this to be more marketably friendly so it can more favorably compared to olive oils. Virgin coconut oil is regarded as the highest quality coconut oil and is preferred for food preparation and home medicinal use. 18 members of Asian and Pacific Coconut Community (APCC) make about 85% of the coconut oil produced. (Wipedia)
The Natural Medicine Comprehensive Database has determined there is insufficient evidence that coconut oil can be used effectively to treat the flu, candida, the common cold, HIV/AIDS, preventing maternal HIV transmission, gonorrhea, candida infections, etc. and the safety for use as a medicinal is not known. George Mateljan is an expert on alternative nutrition and started one of the largest organic health food companies in this country. He has written several books about nutrition and his last book, the World's Healthiest Foodsis almost 900 pages and full of well-researched information. It was published in 2007 and even now is considered somewhat outdated because of the advances in research in the study of lipomics. If you want a good resource about nutrition and how to cook good food, it is definitely worth a gander and if you like, a purchase. This is what he writes about coconut oil. "Coconut oil is mostly saturated fat and as it turns out, not all saturated fat is bad for you. Of the saturated fat found in coconut oil, only 9% is made of long-chained fatty acid which are associated with heart disease. (This may be true but there are lots of other health conditions that can be exacerbated by fat!) Most of the fat in coconut oil is lauric acid which has a reputation of being heart-healthy. (Yes, but as you will see, may not be good for MCSers) About 30% of the medium-chain triglycerides can be taken up from the digestive tract and into the blood without metabolic work. Since coconut oil is mostly medium-chain triglycerides it can provide the same benefit. (I would expect if a person has some types of intestinal dysfunction, it could cause diarrhea or a similar malady. It might be beneficial to ask a physician about this!)
I (meaning Mr. Mateljan) have noticed that coconut oil is well promoted on the Internet with many claims for its health benefits. Mostly notably for its antiviral activity. But from the research I have seen, most of the conclusions are preliminary given there is not that much research published on the subject and that is done mostly on the individual components. But it looks pretty good for coconut oil but I (meaning he) will look at the research as it comes in." This is his opinion and again, I have to say that at the time it was published this may have been true. However, there are numerous discoveries on lipid regulation that have been made that he may not have been aware of or are newer than when the book was published and/or written. Also, I am sure he does not research with a perspective of someone with environmental illness because he is a chef, entrepreneur and a nutritionist. The statements in his book are also published on his website and as far as I can tell from what I read, what the website says and what my book says is no different. Again, the name of the book is the World's Healthiest Foods by George Mateljan.
Garvan notes a typical Western diet contains 40% saturated fat, 40% monounsaturated fat, 20% polyunsaturated fat of which most are omega-6 not omega-3. Thus high-saturated fat diets are contributory to diabetes and obesity. In addition, because there are no essential fatty acids in coconut oil, a diet in saturated fat usually is essential fatty acid deficient in linoleic acid an omega-6 fatty acid and alpha-linolenic, an omega-3 fatty acid. (Best)
This is the FA Profile of Coconut Oil: Wipedia
Fatty Acid | Saturation | Carbons | Percent |
|---|---|---|---|
Caproic | Saturated | 6 | 0.5 |
Caprylic | Saturated | 8 | 7.8 |
Capric | Saturated | 10 | 6.7 |
Lauric | Saturated | 12 | 47.5 |
Myristic | Saturated | 14 | 18.1 |
Palmitic | Saturated | 16 | 8.8 |
Stearic | Saturated | 18 | 2.6 |
Arachidic | Saturated | 20 | 0.1 |
Oleic | Monounsaturated | 18 | 6.2 |
Linoleic | Polyunaturated | 18 | 1.6 |
Coconut oil contains approximately 92.1% saturated fatty acids, 6.2% monounsaturated fatty acids, 1.6% polyunsaturated fatty acids. The above numbers are averages based on samples taken. Numbers can vary slightly depending on age of the coconut, growing conditions, and variety. | |||
As you can see from the table above, the most of what is contained in coconut oil is lauric acid, myristic and palmitic saturated fats. First, let me draw your attention to lauric acid. The amount of lauric acid in coconut oil is 47.5% according to the chart above. 3dChem.com describes lauric acid as the main oil in palm oil and coconut oil and that it has antimicrobial properties. It also says that lauric acid is slightly irritating to mucous membranes and is used in soaps and shampoos. Sodium lauryl sulfate is the most common lauric-acid derived compound used for this purpose. Yes, SLS is used in food and several different types of food from regular table food to pharmaceuticals. Lauric acid can react with solvents like water, as well as fats, which is why SLS is used in shampoo. As most people already know many MCSers are very sensitive to SLS. Other studies have shown that it can cause sensitivities in people that take medication made with SLS. In skin, SLS has been demonstrated to inhibit lipid-metabolizing enzymes including PPAR-alpha and PPAR-gamma which if you have read my blog can already be down-regulated by Tnf-a. (Torma) Tnf-a can be produced as a consequence of the stress response and toxic injury and therefore may be quite prevalent in environmental health conditions. One of the functions of PPAR-gamma includes regulating insulin sensitivity (Chatterjee) which is mediated by adiponectin that reduces insulin resistance. Adiponectin also is down-regulated by Tnf-a and has been shown in a study to be down-regulated by the high-fat of coconut oil (Bueno). Another study shows, SLS mediates skin barrier injury after 5-weeks and makes it more sensitivity to external stress. Considering that lauric acid is an irritant and is found in SLS....one can assume that it may be the agent at least in part that causes the irritation from SLS in people who are already sensitive to different "agents". Another study shows ceramides are also increased by SLS and ceramides from mitochondrial dysfunction down-regulate Nrf2 so one may be able to make a connection with further information and research. Nrf2 can be impaired for a number of reasons including age and genetics and makes one more susceptible to oxidative stress and susceptible to aberrant inflammation. It is also down-regulated by hyperglycemia (high blood sugar) and high-fat diets. Now, there is no specific research that says that lauric acid is the only thing in SLS as far as I can tell that may be an irritant, but the fact that it is in there and if a person is sensitive or thinks they may be sensitive to SLS, it might be a good idea to stay away from it. Not all MCSers are sensitive to SLS, but I am one and therefore, no matter how useful it is for cooking, I would never think about using it. I would rather be safe now than sorry later because my reactions can occur quickly or be delayed by hours or even days.
Many studies note that medium-chained fatty acid do not result in the accumulation of fat in muscle and the liver and from all accounts medium-chained fatty acids are better healthwise than long ones. But there are a few things one must consider since the American diet consists of 40% saturated fat which is 33% more than is recommended. In the literature, there seems to be some debate about the effect of long-chained fatty acids on mitochondrial function. Schrauwen says they have little effect and others say they may impair mitochondrial function by example, by opening of the transition pore that increases mitochondrial swelling causing cell death. (Wiekowski, Korge) As noted above, a recent claim was made that short-chain FA can prevent diabetes. (Medical News Today) Well, in actuality the study says it can preserve insulin action in muscle and adipose tissue. Which is great if you have healthy adipose tissue and muscle --and as we have shown people with environmental illness probably do not! In addition, it says that it does increase steatosis (fatty liver) and insulin resistance in the liver and there are alot of mitochondria in liver cells. (Turner) Many people that have been exposed to toxicants have injured livers in addition to impaired functioning of the mitochondria. Personally, I really do not want my liver fatty because it has to last a really long time...well, hopefully anyway! Most people are uneffected by fatty liver but then there are others where the condition results in elevated inflammation and scarring and at its worst, liver failure. (Mayon Clinic) If one reads that coconut oil gives an energy boost the author may be extrapolating from the fact that fats provide energy which I have to argue at least to a point. It may be true but it may not be true in people with mitochondrial disease or dysfunction. Garvan explains a benefit of medium-chain fatty acids is they are small enough to cross the membrane and supply energy to the mitochondria. That is all fine and good if the mitochondria are working well but alot of excess energy is not so good if they aren't. Mitochondrial function naturally generates free radicals and an increase in them may generate an increase in oxidative stress that may impair it further and may induce other aberrant signaling the least of which may include drastic changes in mood. There is evidence the activity of PKC is "defective" in diabetes and obesity and as a result may lead to altered glucose transport. (Corcoran) New research has implicated PKC signaling in fatty-acid induced insulin resistance and others identify PKC involvement in connection with lead poisoning and PTSD although I have yet to follow up on the specifics. Many people including those with environmental illness have stored levels of lead and other metals that are released under physiological stress conditions. Many conditions including exposures may result in a hyperglycemia response, so alterations in PKC signaling is something one must consider. You might recall a recent report showed a higher incidence of metabolic syndrome in those with PTSD. PKC signaling may offer a possible explanation and then again, maybe it doesn't.
Palmitic acid is also known as palmitate which is the salts or esters of palmitic acid. (Wipedia) It is one of the most common fatty acids in plants and animals and is number 3 on the list of fatty acids in coconut oil. It too shows no hypercholesterolemic effects from what I initially saw from the research. But that does not mean it can not in certain people or that it does...it just means I did not find it. Except and this is a big except, in the presence of trans fat which unfortunately, is still a big part of many people's diet even though many try to avoid it. Eli Lilly produced a report that indicates that palmitate causes down-regulation of PGC-1a which is an important requirement for mitochondrial biogenesis which the end result is energy. It is safe to assume that down-regulating PGC-1a can be more detrimental to cells that already have less mitochondria that function abnormally and are insulin resistant. (Otto) eNOS can also be deficient in PGC-1a deficient cells which may increase the risk for endothelial dysfunction that has been implicated as a factor in a number of environmental illnesses. Bonnard's studies suggest that high-fat, high-sugar diets can induce glucose intolerance after 1 month and a longer intervention with the same diet induced diabetes with altered mitochondrial biogenesis, structure and function and concludes that insulin resistance precedes mitochondrial dysfunction in diet-induced diabetes. (Bonnard) Schrauen explains that palmitate, myristate and stearate do activate the NF-kappaB in muscle cells and since if one refers back to the chart above those three acids equals almost 30% of the saturated fat in cocnut oil. NF-kappaB may activate inflammatory processes which some called the "inflammatory cascade" and is implicated as an inflammatory marker in environmental illness. In people with lower Nrf2, NF-kappaB is a concern because Nrf2 normally is responsible for regulating it.
A just released paper indicates that palmitic acid changes brain chemistry in a "relatively short time" and tricks the brain into not realizing when one is full from eating. It does this by making the brain unresponsive to signals from leptin and insulin and therefore may cause one to overeat. (US News) This may contribute to the "expanding adipose tissue" problem and more inflammation we mentioned in the first paragraph. Now, granted palmitic acid makes up only 8% of the total fat content. If your like me, I do not want to be exposed to anything that changes my brain chemistry anymore that it has been already. At least that is, if I can avoid it. I have enough problems with sickness syndrome and brain fog! Palmitic acid has been demonstrated to cause a 75% increase in the expression of Tnf-a and a 75% decrease in Il-10 in adipocytes and Tnf-a is associated with environmental illness and causes insulin resistance and inhibits PGC-1a in vitro cardiac cells. (Palomer) (The increase in Tnf-a may explain some of the weight loss seen in some studies considering that Tnf-a causes cachexia and weight loss. Il-10 is associated with preventing lipid-induced insulin resistance, reducing the severity and length of sickness syndrome and modulating HO-1. All of these factors have been implicated as possible factors in environmental illness. (Bradley) Yamauchi shows that insulin resistance in lipoatrophy can be reversed with expression of both adiponectin and leptin but only partially by either leptin or adiponectin alone. (Yamauchi) In other words, there may be instances that if one or the other of these genes are down-regulated then they may not be able to reverse insulin resistance if already present. Generally, high-fat diets are associated with impaired working memory and hippocampal morphology in animals. (Granholm)
Two important notes about the issues above, one needs to be careful when drawing conclusions about the health aspects of a population in comparison to another. If one population does not eat like another, live like another, work and exercise like another, have the same cultural problems, the same genes, and in this case, share the same disease or health condition it may lead a person to make conclusions that are inaccurate. Most indiginous populations, especially those isolated by geography are not effected by the same environmental influences modern societies are and therefore the aspects of their environmentally-related health conditions are different. I have read what is printed on "more popular" websites and also have read cultural graduate theses and there is some contradiction of the health effects of medium chain high-fat diets in different indiginous population studies. I am not saying comparison studies are not important but the more similar the cultures are the more valuable the data. Here are are few important things one might consider in a population study on fat. Are there other factors such as there are in this case, in the diet or lifestyle that may be offsetting the negative effects of a high-fat diet? Have their bodies adapted to their circumstances over time better than other populations? A recent study has demonstrated that the anti-inflammatory effects of vitamin E may be associated with certain Tnf-a and it has been suggested that the positive benefits of coconut oil are that it is a good source of vitamin E. Could up-regulated or down-regulated genes be altering the expression of proteins or is there a gene polymorphisms in the population being studied that makes them more adaptable to handle a negative influence? Are there comfounding factors that are increasing the health or inhibiting the effects such as more or lack of exercise or the use or no use of trans fat? As you can see from what was written above about the studies from palmitic acid in junk food and coconut oil down-regulating adiponectin, food can change the expression of genes quite quickly and researchers have no idea how long the effects can last. Is it possible these changes can become permanent on a population that has not fully "adapted" to them. Maybe, maybe not. It would be my guess no one will say it can not happen because no one really knows for sure. There is now a whole field of research that explores how changes in gene expression is passed down to the next generation when there is no change in the DNA. Twenty years ago, researchers did not believe epigenetic influences could happen either.
Environmental illness development is largely due to poor (I use this term loosely) diet, lifestyle, and exposures to toxic influences like chemicals and their influence on genetic expression and numerous other factors including bad decisions and choices. In addition, scientists are well aware toxicants can can up-regulate or down-regulate cellular receptors or interact with each differently and may lead to altered cell functions. There are thousands of chemicals now on the market that have the potential to do it. From a political and policy-making standpoint, the problem is how one goes about deciding which ones to to start testing first, who is gonna test them and what standards will be used to test them and also, who is gonna pay for it and how to deal with the economic fall-out afterward! Finally, making health decisions is in the end, a personal one and it is only that person, or mostly so, who has to live or not live with the consequences. Using coconut oil for cooking is still of benefit for one person because it does not produce the levels of aldehydes and does not turn rancid like other oils. But it may not be a wise choice for another who has a sensitivity to it or one of the chemicals in it. On the other hand, detoxification of aldehydes is often limited in environmental illness and therefore, cooking with coconut may be a better option for someone with one environmental illness compared to another person with another environmental illness.On the other hand, in many cases because of the nature of injury and inflammation in environmental illness, limiting fat should be of benefit to most. Unless of course, medical tests show a deficiency. Either way there are good lab tests available that can determine a person's fat and triglyceride status and a physician is more than qualified to discuss the topic.
Sonne, C., Fonfara, S., Dietz, R., Kirkegaard, M., Letcher, R., Shahmiri, S., Andersen, S., and Møller, P. (2007). Multiple cytokine and acute-phase protein gene transcription in west greenland sledge dogs (canis familiaris) dietary exposed to organic environmental pollutants. Archives of Environmental Contamination and Toxicology, 53(1):110-118. http://www.citeulike.org/user/HEIRS/article/1447133
Arsenescu, V., Arsenescu, R. I., King, V., Swanson, H., and Cassis, L. A. (2008). Polychlorinated biphenyl-77 induces adipocyte differentiation and proinflammatory adipokines and promotes obesity and atherosclerosis. 116(6). http://www.citeulike.org/user/HEIRS/article/5792101
Specific Types of Fat. American Diabetes Association. Retrieved on September 16, 2009.
Turner, N., Hariharan, K., TidAng, J., Frangioudakis, G., Beale, S. M., Wright, L. E., Zeng, X. Y., Leslie, S. J., Li, J.-Y., Kraegen, E. W., Cooney, G. J., and Ye, J.-M. (2009). Enhancement of muscle mitochondrial oxidative capacity and alterations in insulin action are lipid species-dependent: Potent tissue-specific effects of medium chain fatty acids. Diabetes. http://www.citeulike.org/user/HEIRS/article/5792208
(2009). How coconut oil could help reduce the symptoms of type 2 diabetes. Medical News Today. http://www.citeulike.org/user/HEIRS/article/5793232
Coconut Oil. Wipedia. Retrieved on September 16, 2009.
Fatty Liver. Wipedia. Retrieved on September 16, 2009.
Keith Ott, O., Jack Dempse, Y., Richar, D., Beckman, N., and Anne Reifel Mille, R. Aicar reverses the effect of palmitate on metabolic gene expression and mitochondrial number in muscle cells and adipocytes. http://www.citeulike.org/user/HEIRS/article/5793413
Bradley, R. L., Fisher, F. F., and Maratos-Flier, E. (2008). Dietary fatty acids differentially regulate production of tnf-alpha and il-10 by murine 3t3-l1 adipocytes. Obesity (Silver Spring, Md.), 16(5):938-944. http://www.citeulike.org/user/HEIRS/article/5791246
Törmä, H., Geijer, S., Gester, T., Alpholm, K., Berne, B., and Lindberg, M. (2006). Variations in the mrna expression of inflammatory mediators, markers of differentiation and lipid-metabolizing enzymes caused by sodium lauryl sulphate in cultured human keratinocytes. Toxicology in vitro : an international journal published in association with BIBRA, 20(4):472-479. http://www.citeulike.org/user/HEIRS/article/5793447
Helyar, S. G., Patel, B., Headington, K., El-Assal, M., Chatterjee, P. K., Pacher, P., and Mabley, J. G. (2009). Pcb-induced endothelial cell dysfunction: role of poly (adp-ribose) polymerase. Biochemical pharmacology. http://www.citeulike.org/user/HEIRS/article/5041282
Chatterjee, V. K. K. (2001). Ppar gamma and human insulin resistance. In Society for Endocrinology Annual Meeting 2001. BioScientifica. http://www.citeulike.org/user/HEIRS/article/5793459
Yamauchi, T., Kamon, J., Waki, H., Terauchi, Y., Kubota, N., Hara, K., Mori, Y., Ide, T., Murakami, K., Tsuboyama-Kasaoka, N., Ezaki, O., Akanuma, Y., Gavrilova, O., Vinson, C., Reitman, M. L., Kagechika, H., Shudo, K., Yoda, M., Nakano, Y., Tobe, K., Nagai, R., Kimura, S., Tomita, M., Froguel, P., and Kadowaki, T. (2001). The fat-derived hormone adiponectin reverses insulin resistance associated with both lipoatrophy and obesity. Nature Medicine, 7(8):941-946. http://www.citeulike.org/user/HEIRS/article/5793464
Keith Ott, O., Jack Dempse, Y., Richar, D., Beckman, N., and Anne Reifel Mille, R. Aicar reverses the effect of palmitate on metabolic gene expression and mitochondrial number in muscle cells and adipocytes. http://www.citeulike.org/user/HEIRS/article/5793413
Corcoran, M. P., Lamon-Fava, S., and Fielding, R. A. (2007). Skeletal muscle lipid deposition and insulin resistance: effect of dietary fatty acids and exercise. Am J Clin Nutr, 85(3):662-677. http://www.citeulike.org/user/HEIRS/article/5791465
Törmä, H. and Berne, B. (2009). Sodium lauryl sulphate alters the mrna expression of lipid-metabolizing enzymes and ppar signalling in normal human skin in vivo. Experimental dermatology. http://www.citeulike.org/user/HEIRS/article/4787882
Harrison, K. (2007). Lauric acid @ 3dchem.com. http://www.citeulike.org/user/HEIRS/article/5793491
Turner, N., Hariharan, K., TidAng, J., Frangioudakis, G., Beale, S. M., Wright, L. E., Zeng, X. Y., Leslie, S. J., Li, J.-Y., Kraegen, E. W., Cooney, G. J., and Ye, J.-M. (2009). Enhancement of muscle mitochondrial oxidative capacity and alterations in insulin action are lipid species-dependent: Potent tissue-specific effects of medium chain fatty acids. Diabetes. http://www.citeulike.org/user/HEIRS/article/5792208
Kim, E., Kim, S., Nam, G. W., Lee, H., Moon, S., and Chang, I. (2009). The alkaline ph-adapted skin barrier is disrupted severely by sls-induced irritation. International journal of cosmetic science, 31(4):263-269. http://www.citeulike.org/user/HEIRS/article/5117257
Mateljan, George.The World's Healthiest Foods. Essential Guide for the Healthiest Way of Eating. George Mateljan Foundation. 2007. pg 55.
Sepp, Dennis, PhD. Sodium Lauryl Sulfate - The Straight Story. Retrieved on September 16, 2009.
Bueno, A. A. A., Oyama, L. M. M., de Oliveira, C., Pisani, L. P. P., Ribeiro, E. B. B., Silveira, V. L. F. L., and Oller do Nascimento, C. M. M. (2008). Effects of different fatty acids and dietary lipids on adiponectin gene expression in 3t3-l1 cells and c57bl/6j mice adipose tissue. Pflügers Archiv : European journal of physiology, 455(4):701-709. http://www.citeulike.org/user/HEIRS/article/5780642
Granholm, A.-C. C., Bimonte-Nelson, H. A., Moore, A. B., Nelson, M. E., Freeman, L. R., and Sambamurti, K. (2008). Effects of a saturated fat and high cholesterol diet on memory and hippocampal morphology in the middle-aged rat. Journal of Alzheimer's disease : JAD, 14(2):133-145. http://www.citeulike.org/user/HEIRS/article/5780645
Palomer, X., Alvarez-Guardia, D., Rodriguez-Calvo, R., Coll, T., Laguna, J. C., Davidson, M. M., Chan, T. O., Feldman, A. M., and Vazquez-Carrera, M. (2009). Tnf-alpha reduces pgc-1alpha expression through nf-kappab and p38 mapk leading to increased glucose oxidation in a human cardiac cell model. Cardiovasc Res, 81(4):703-712. http://www.citeulike.org/user/HEIRS/article/4594676
Bonnard, C., Durand, A., Peyrol, S., Chanseaume, E., Chauvin, M. A., Morio, B., Vidal, H., and Rieusset, J. (2008). Mitochondrial dysfunction results from oxidative stress in the skeletal muscle of diet-induced insulin-resistant mice. The Journal of clinical investigation, 118(2):789-800. http://www.citeulike.org/user/HEIRS/article/3152490
Rutkowski, J. M., Davis, K. E., and Scherer, P. E. (2009). Mechanisms of obesity and related pathologies: The macro- and microcirculation of adipose tissue. FEBS Journal, 9999(9999). http://www.citeulike.org/user/HEIRS/article/5795717
Nonalcoholic fatty liver disease. Mayo Clinic. Retrieved on September 16, 2009.
Wieckowski, M. (2000). Long-chain fatty acids promote opening of the reconstituted mitochondrial permeability transition pore. FEBS Letters, 484(2):61-64. http://www.citeulike.org/user/HEIRS/article/5797786
Korge, P., Honda, H. M., and Weiss, J. N. (2003). Effects of fatty acids in isolated mitochondria: implications for ischemic injury and cardioprotection. Am J Physiol Heart Circ Physiol, 285(1):H259-269. http://www.citeulike.org/user/HEIRS/article/5797780
Belisle, S. E., Leka, L. S., Delgado-Lista, J., Jacques, P. F., Ordovas, J. M., and Meydani, S. N. N. (2009). Polymorphisms at cytokine genes may determine the effect of vitamin e on cytokine production in the elderly. The Journal of nutrition. http://www.citeulike.org/user/HEIRS/article/5800741
Hargrave, K. M., Azain, M. J., and Miner, J. L. (2005). Dietary coconut oil increases conjugated linoleic acid-induced body fat loss in mice independent of essential fatty acid deficiency. Biochimica et biophysica acta, 1737(1):52-60. http://www.citeulike.org/user/HEIRS/article/5800784
Lauric acid. RX List. Retrieved on September 17, 2009.
Yoshinari, K., Okino, N., Sato, T., Sugatani, J., and Miwa, M. (2006). Induction of detoxifying enzymes in rodent white adipose tissue by aryl hydrocarbon receptor agonists and antioxidants. Drug Metab Dispos, 34(7):1081-1089. http://www.citeulike.org/user/HEIRS/article/783432
Liang, H. and Ward, W. F. (2008). Pgc-1: a key regulator of energy metabolism. http://www.citeulike.org/user/HEIRS/article/5805611
Olive Chemistry- The Olive Oil Source. Retrieved on September 17, 2009
Nicholls, S. J., Lundman, P., Harmer, J. A., Cutri, B., Griffiths, K. A., Rye, K.-A. A., Barter, P. J., and Celermajer, D. S. (2006). Consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins and endothelial function. Journal of the American College of Cardiology, 48(4):715-720. http://www.citeulike.org/user/HEIRS/article/5805848
Coghlan, A. (2009). Fat reprograms genes linked to diabetes. NewScientist. http://www.citeulike.org/user/HEIRS/article/5831238
Applied physiology, nutrition, and metabolism = Physiologie appliquée, nutrition et métabolisme, Vol. 33, No. 5. (October 2008), pp. 843-862.
Liang, H. and Ward, W. F. (2008). Pgc-1: a key regulator of energy metabolism. http://www.citeulike.org/user/HEIRS/article/5805611
Olive Chemistry- The Olive Oil Source. Retrieved on September 17, 2009
Nicholls, S. J., Lundman, P., Harmer, J. A., Cutri, B., Griffiths, K. A., Rye, K.-A. A., Barter, P. J., and Celermajer, D. S. (2006). Consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins and endothelial function. Journal of the American College of Cardiology, 48(4):715-720. http://www.citeulike.org/user/HEIRS/article/5805848
Coghlan, A. (2009). Fat reprograms genes linked to diabetes. NewScientist. http://www.citeulike.org/user/HEIRS/article/5831238
Applied physiology, nutrition, and metabolism = Physiologie appliquée, nutrition et métabolisme, Vol. 33, No. 5. (October 2008), pp. 843-862.
Abdollahi, M., Donyavi, M., Pournourmohammadi, S., and Saadat, M. (2004). Hyperglycemia associated with increased hepatic glycogen phosphorylase and phosphoenolpyruvate carboxykinase in rats following subchronic exposure to malathion. Comparative biochemistry and physiology. Toxicology & pharmacology : CBP, 137(4):343-347. http://www.citeulike.org/user/HEIRS/article/2988987
Rezg, R., Mornagui, B., El-Fazaa, S., and Gharbi, N. (2008). Caffeic acid attenuates malathion induced metabolic disruption in rat liver, involvement of acetylcholinesterase activity. Toxicology, 250(1):27-31. http://www.citeulike.org/user/HEIRS/article/5831958
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