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by Brian Shilhavy
Editor, Health Impact News
A new study out of Japan and published in the European Journal of Allergy and Clinical Immunology shows how switching the dietary oil of chow fed to mice from soybean oil to coconut oil reduced skin inflammation.
The skin healing properties of coconut oil, especially virgin coconut oil, applied topically to the skin have been known for a long time.
When we first started importing virgin coconut oil from the Philippines to the U.S. market in 2001, and had started an online discussion group, some of the most powerful testimonies we started receiving from people were how they were using virgin coconut oil for their skin conditions.
Even though coconut oil is sold as a dietary oil, people started applying it topically and seeing tremendous results for their skin conditions such as acne, eczema, keratosis polaris, psoriasis, rosacea, and fungal infections. Read some of these incredible testimonies here:
We have suspected for years that the reason people in tropical climates who eat their traditional diets which are high in the saturated fats of coconut oil had such beautiful skin, even though they are exposed to the sun to a greater degree than westerners, is because of the high amounts of coconut oil in their diet, which does not oxidize and cause free radical damage as polyunsaturated fats do.
Skin cancer, for example, is almost unheard of in tropical climates like the Philippines, but common in western nations, even in colder climates with far less exposure to the sun.
Researchers in Japan apparently wanted to test this theory of dietary coconut oil reducing allergic skin inflammation in the laboratory:
Coconut oil is used as a dietary oil worldwide, and its healthy effects are recognized by the fact that coconut oil is easy to digest, helps in weight management, increases healthy cholesterol and provides instant energy.
Although topical application of coconut oil is known to reduce skin infection and inflammation, whether dietary coconut oil has any role in decreasing skin inflammation is unknown.
In this study, we showed the impact of dietary coconut oil in allergic skin inflammation by using a mouse model of contact hypersensitivity (CHS).
So they replaced the soybean oil commonly used in mice chow with coconut oil.
Soybean oil has been the most common dietary oil in the western diet since World War II, when expeller-pressed seed technology allowed manufactures to extract oil from the soybean, one of the main cash crops in the U.S. and heavily subsidized to dominate the world market in dietary oils.
Soybean oil is high in Omega 6 fatty acids, and it is commonly known that most westerners have an unhealthy balance of Omega 3 to Omega 6 fatty acids leading to various health problems, as most westerners need more Omega 3 fatty acids and far less Omega 6 fatty acids in their diet.
This point was noted by the researchers:
A high n-6/n-3 FA ratio is linked to many chronic inflammatory diseases, including cardiovascular disease, obesity, non-alcoholic fatty liver disease, and inflammatory bowel disease.
Coconut oil does not contain appreciable amounts of either of these classes (Omega 3 or Omega 6) of essential fatty acids.
Previous studies using dietary coconut oil have shown its health benefits toward hepatotoxicity, together with altered lipid profiles in the body.
Another unique feature of coconut oil is the low abundance of both n-3 and n-6 essential FAs.
Omega 3 fatty acids are linked to anti-inflammatory effects, and since coconut oil does not contain any appreciable amount of Omega 3s, they could not be attributed to lower allergic inflammation in the skin with the mice fed the coconut oil diet.
After 2 months of comparing the mice on the standard soybean oil chow and the ones with coconut oil, they found that there was:
Amelioration of skin allergic inflammation in mice maintained on dietary coconut oil.
Numerous studies have suggested the beneficial effects of coconut in the treatment of diabetes, obesity, cardiovascular diseases, and Alzheimer’s disease, through components including dietary fiber, vitamins, minerals, and phenolic compounds.
Here, we show that FAs derived from coconut oil play important roles in the maintenance of health by controlling allergic inflammation in mice; this is consistent with previous reports that topical and dietary coconut oil is beneficial for the prevention and amelioration of dermatitis.
Since there are no essential fatty acids in coconut oil, what did the researchers attribute in the coconut oil as beneficial in reducing allergic skin inflammation?
In terms of FA composition, one of the unique characteristics of coconut oil is the large amount of MCFAs (medium chain fatty acids); these are easy to digest and could potentially contribute to prevention of obesity and diabetes and have demonstrated protective effects against intestinal inflammation and colitis.
Of the medium chain fatty acids found in coconut oil, the most predominate one is lauric acid. Coconut oil is nature’s richest source of lauric acid, making up about 50% of coconut oil, with human breast milk being a distant second.
Apart from the low contents of n-3 and n-6 FAs, coconut oils uniquely are abundantly composed of lauric acid (Figure 2A). Consistently, lauric acid concentration was higher in coconut mice than in soybean mice (Figure 2C), prompting us to examine the probable roles of lauric acid in CHS.
The other component the researchers looked at was mead acid.
Mead acid, a metabolite of oleic acid, has known anti-inflammatory properties. Because mice maintained on coconut oil show EFAD (essential fatty acid deficiency) and body accumulation of mead acid, we compared the abundances of mead acid in the serum of coconut and soybean mice. Mead acid levels were substantially higher in coconut mice.
With the USDA and FDA currently condemning coconut oil as unhealthy due to its high saturated fat content, it is certainly no surprise that allergic skin inflammation diseases are becoming so common in the United States.
If you want healthier skin, cut down on polyunsaturated vegetable oils and switch to coconut oil as a more significant portion of your diet.
“Dietary coconut oil ameliorates skin contact hypersensitivity through mead acid production in mice” – European Journal of Allergy and Clinical Immunology – 06 March 2019 – Prabha Tiwari, Takahiro Nagatake, So‐ichiro Hirata, Kento Sawane, Azusa Saika, Yuki Shibata, Sakiko Morimoto, Tetsuya Honda, Jun Adachi, Yuichi Abe, Junko Isoyama, Takeshi Tomonaga, Hiroshi Kiyono, Kenji Kabashima, Jun Kunisawa. Abstract.
About the author: Unlike many people who write about coconut oil by simply reading about it, Brian Shilhavy actually lived in a coconut producing area of the Philippines for several years with his family, observing firsthand the differences between the diet and health of the younger generation and those of his wife’s parents’ generation still consuming a traditional diet. This led to years of studying Philippine nutrition and dietary patterns first hand while living in a rural farming community in the Philippines. Brian is the author of the best-selling book: Virgin Coconut Oil: How it has changed people’s lives and how it can change yours!
Read the Virgin Coconut Oil eBook on Your Mobile Device!
I’ve posted this recipe before, but it’s worth posting again. This is one of my favorite low carb, gluten free cookie recipes. Imagine, you can snack on something good for you that actually helps you lose weight!
1 1/2 cups unsweetened dried coconut
1/2 cup almond meal (finely ground almonds)
2 t. coconut flour
4 T. warm water
4 T. raw honey
2 eggs, beaten
1 t. vanilla
1/4 t. sea salt
Preheat the oven to 400 degrees. Grease a cookie sheet with coconut oil.
Stir the warm water and honey together. Add the vanilla, eggs, salt, almond meal, coconut flour and coconut. Mix well. If the mixture is runny, let it sit for a few minutes so the coconut can rehydrate. If it is still runny, add another teaspoon of coconut flour. Drop by rounded tablespoons full onto the cookie sheet, about 1 inch apart. Bake for 12 – 15 minutes. The outside of the cookie should be golden brown, while the inside is soft.
Makes about 24 cookies.
If you don’t like the taste of almonds or you want your macaroons whiter, just substitute another 1/2 cup dried coconut for the almond meal.
If you want to get decadent, dip the bottoms of the finished macaroons into melted extra dark chocolate chips mixed with a little coconut oil. Refrigerate.
• • • • •
Learn the secrets thousands are using to lose weight and get healthier with coconut oil diets. Visit our site at http://coconut-oil-diet.com and start losing weight today!
by Paul Fassa
Health Impact News
Independently-sourced research challenges the idea that LDL (low-density lipoprotein) is the “bad cholesterol,” and causes heart disease.
However, the theory that LDL is “bad” persists in the mainstream media and with Big Pharma, mainly because they would lose billions of dollars in drugs and treatments to admit the theory lacks merit.
The hypothesis of saturated fat creating artery-clogging cholesterol as the source of heart disease should be considered dead and incapable of resuscitating, based on the scientific evidence.
But one still sees and hears fearful statements about lowering cholesterol and avoiding heart disease, mostly on mainstream media but even all too often on internet alternative media sources.
Current research is showing LDL is not dangerous and it’s not an accurate marker for pending heart disease.
An Explanation of Cholesterol and How LDL and HDL are Differentiated
Mainstream medicine and pharma-funded research maintains that LDL is the cholesterol that causes coronary congestion.
It’s the “bad cholesterol.”
Perhaps because research has discovered people with high HDL (high-density lipoprotein) live longer than those with low HDL, HDL is now considered the “good cholesterol.”
For the most part, cholesterol is cholesterol and it’s all good for so many hormonal and structural purposes in our bodies.
Cholesterol is a waxy lipid substance. It doesn’t mix with our watery plasma. It needs to be carried in the blood’s plasma by lipoproteins, tiny protein spheres that carry cholesterol to wherever it’s needed in the body.
Our bodies actually need cholesterol for many hormonal and cell building functions.
Cholesterol is categorized by the density of its lipoprotein carriers. The density is a factor of the ratio of protein to cholesterol in the particles. High-density lipoproteins (HDL) are smaller with around 50 percent protein and 20 percent cholesterol.
Low-density lipoproteins (LDL) are larger and contain around 25 percent protein and 50 percent cholesterol.
The mainstream claim is that HDL is the “good cholesterol” because it sweeps up the LDL cholesterol from arteries or other unwanted areas and routes it back to the liver where it came from. (Source)
But if the liver generates LDL cholesterol particles that are carried to various organ tissue areas, including the brain and nervous system as needed, why is it called “bad cholesterol?”
The conventional explanation has been that LDL particles stick to the endothelial cells of inner arterial walls.
Before we explore the veracity of this claim, let’s have a look at how important cholesterol is for our health.
How cholesterol helps keep us at optimum health:
- It helps to produce cell membranes, which are made of fat.
- It is a precursor to the manufacturing of hormones, including sex hormones and cortisone.
- It is the first step in converting the sun’s UVB rays into vitamin D.
- It helps to formulate bile acids for digesting fat.
- It is needed for proper function of serotonin receptors in the brain
- It is involved with supplying the CoQ10 coenzyme, a vital cellular energy source in muscle tissue especially the heart muscle.
- It helps form memories in the brain.
- It is important in maintaining the health of the intestinal wall.
- It builds and maintains the myelin sheath – a protective fatty tissue wrapping nerve fibers, which when damaged causes MS and other neurological diseases.
- It is vital toward building brain cells in the brain, which contains 25 percent of your body’s total cholesterol (Source)
It logically follows that by drastically lowering cholesterol with statin drugs, at least some of the listed functions will be impaired leading to some serious side effects such as muscle or tendon tearing, chronic fatigue, mind fog or impaired memory, and even heart attacks.
Many statin users who had experienced inexplicable side effects recovered completely within a few short weeks after no longer dosing with statins.
The LDL Theory of Heart Disease is Busted – With an Asterisk
Several independent scientists, physicians, and cardiologists have busted the LDL theory of cholesterol arterial clogging.
The title below links to an article covering a review study by several international researchers published in September of 2018. Their peer-reviewed published paper rips the LDL theory of heart disease causation to shreds. See:
Experts Review of 107 Scientific Studies: Cholesterol Does Not Cause Heart Disease – Statin Drugs are Useless
Of course, the research is marginalized and the medical old guard attacked the researchers via mainstream media to keep the war against LDL (the bad cholesterol) going and maintain statin drug profits.
Cholesterol fear is maintained now that LDL remains as the cholesterol culprit for heart disease. The mantra to avoid saturated fat and lower cholesterol continues.
The same network of doctors and scientists, The International Network of Cholesterol Skeptics (THINCS) who put together the review above, supplied suggestions of potential causes of heart disease other than cholesterol. See:
Network of Cholesterol Skeptics Researchers: Abandon the LDL Cholesterol Theory of Heart Disease and Look at More Important Risk Factors
The suggestions in the above article are examples of where heart disease research should go now that the lipid theory of heart disease has been ripped to shreds, not only by THINCS members but others as well.
Dr. Ronald M. Kraus, MD is a co-creator of a device that can sort out VLDL (very low-density lipoprotein), from LDL.
VLDL (very low-density lipoproteins) is the “asterisk” mentioned in the title of this section. It will be covered in the next section after this quote by Dr. Kraus:
Low-fat diets are old news, you say? Try telling that to the makers of, say, Baked Lays. It will take us years to shake off the damage done by broadly implicating fat in the diet. Everybody I know in the field — everybody — recognized that a simple low-fat message was a mistake.
I spend a lot of time talking to reporters and trying to explain that dietary cholesterol is not the same as blood cholesterol. (Source)
In other words, the saturated fat causation of heart disease is wrong, but it still lingers enough for the pharmaceutical and processed food industries to profit from this “cholesterol con.”
Despite this uprising from several in the medical science community, the public perception is still held hostage to the official nutritional and medical dogmatic doctrine of using high LDL as a marker for heart disease.
The mainstream medical monopoly’s use of mainstream media, which thrives from Big Pharma’s advertising revenue, helps keep the cholesterol con afloat. Behind the mainstream public scenes, those who know better are publicly challenged ad hominem while the details of their findings wind up in mainstream media obscurity.
A Little on VLDL – Very Low-Density Lipoproteins
These lipoproteins contain minuscule cholesterol levels but are high in triglyceride lipids. Triglyceride lipids form the fat from unused carbohydrate energy, like sugar.
Triglycerides are intended as storage to be utilized for energy when other dietary energy sources wane or the need for more energy arises.
But that very rarely happens in our culture of accessible cheap foods, especially with processed and junk fast foods.
Add “energy drinks” to the mix, and as the body gets overwhelmed with foods that disrupt metabolic processing, the triglyceride fat just keeps accumulating.
The smaller, heavier VLDL particles can burrow into inner arterial walls and cause inflammation with their oxidation-prone triglycerides.
Guess what tries to patch up that inflammation?
Cholesterol, manufactured and distributed by the liver, aka LDL. Internal tissue repair is one of its functions.
And what’s been discovered and is gradually being accepted everywhere, except for mainstream medicine, government nutritional agencies, and the mainstream media, is that excess sugar, refined carbohydrates, and HFCS (high fructose corn syrup) are the culprits behind obesity, diabetes 2, and coronary artery disease (CAD).
Dr. Robert Lustig, pediatric endocrinologist professor at the University of California, San Francisco, has been on a mission exposing the role sugar and HFCS play with creating heart disease by causing arterial damage with triglyceride fats carried by the VLDL particles.
Dr. Lustig explains:
So we were using the wrong marker [cholesterol] all along. It turned out the triglyceride was way worse. Triglyceride is basically what your liver does to sugar. And again, sugar was the problem, Yudkin* was right, and the food industry killed him. [* added] (Source)
*Around the time Ancel Keys was claiming fat was the source of heart disease, a British Researcher, Professor John Yudkin, was researching sugar as the source. Yudkin’s research was trashed by the sugar industry to avoid financial loss by scapegoating fat as the source of coronary heart disease.
The whole statin drug industry, along with the food industry and its processed low-fat foods that would accommodate the low and no fat diet philosophy are shams based on the totally erroneous assumption that cholesterol from dietary saturated fats is the main source of cardiovascular disease.
Video: Dr. Nadir Ali, MD: The Paradox of Insulin Resistance versus LDL Cholesterol
Comment on this article at HealthImpactNews.com.
- 2-3 lbs. fresh organic spinach
- 2 Tablespoons butter
- 1/2 cup minced onion
- 1/2 cup unsweetened coconut milk
- 1/4 cup crushed blanched almonds, cashews or pine nuts
- 1 teaspoon salt
- 1/2 teaspoon seeded and crushed dried red chili pepper (optional)
- 1 Tablespoon of unsweetened coconut, lightly toasted.
Place spinach in covered pot, with just enough water to cling to leaves. Cook just until spinach is wilted and tender. Set aside.
Saute minced onion in butter. Stir in coconut milk, nuts, salt and chili pepper. Add to spinach. Reheat and serve in heated bowl. Top with toasted coconut.
This recipe is especially good if you are on a coconut oil diet! If you want to learn more about how to lose weight with coconut oil, check out my website at http://coconut-oil-diet.com.