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:

Virgin Coconut Oil for Skin Health

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.

Reference

“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!

Includes 85 recipes – Free shipping available!

Read the Virgin Coconut Oil eBook on Your Mobile Device!

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

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by Paul Fassa
Health Impact News

As has been reported numerous times here at Health Impact News for the past 6 years or so, the pharmaceutical industry has been desperate to find an Alzheimer’s drug to market to an aging baby boomer population with ever increasing numbers of Alzheimer’s Disease cases.

And yet, billions of dollars have been invested in potential drugs only to see these drugs never make it out of the trial phase and come to market, because they do not significantly help Alzheimer’s patients.

Biogen and their partner Eisai are the latest pharmaceutical companies to throw in the towel regarding their Alzheimer’s drug aducanumab, which has failed to make it out of phase 3 trials.

Many drug researchers have now abandoned the theory of amyloid plaque accumulation in the brain as the causative factor of Alzheimer’s. Could aducanumab’s failure be the last nail in the coffin for this theory, as natural approaches to Alzheimer’s such as coconut oil and the ketogenic diet see more positive results?

Biogen Endures the Latest Pharmaceutical Failure with Solving Alzheimer’s Disease

An independent risk assessment during Biogen’s early phase 3 trials signaled the end of their efforts to develop a “blockbuster drug” based on aducanumab for Alzheimer’s.

Aducanumab is a solution of synthetically-derived antibodies based on human cells that have been specifically arranged to attack amyloid beta (AB) antigens. Amyloid beta plaques are considered the stuff of Alzheimer’s disease. Bioengineering antibodies is one aspect of immunotherapy.

Phase 3 trials are near the end of clinical trials involving humans with the largest numbers, 300 to 3,000 humans with the disease the drug is intended for. Before clinical trials begin, there must be satisfactory in vitro and in vivo (lab animal) results that suggest possible medical merits.

Phase 3 trials are considered pivotal towards the final marketing license granted by the FDA upon receiving two apparently positive clinical trial reports from the pharmaceutical company. There’s a phase 4, which is the post-market gathering of adverse side effects. (Source)

Cambridge, Massachusetts-based Biogen and its partner for these trials, Tokyo, Japan-based Eisai wound up sending 3,200 early-phase Alzheimer’s patients to their international homes with a “sorry” and “thanks.“

The independent risk assessment that predicted there would be no successful efficacious outcome on any significant level was convincing enough to drop the risk of losing more money and failing their stockholders. 

The expected outcome was increased memory and mental acuity of most patients with minimal severe side effects for their phase 3 participants with early-stage Alzheimer’s disease. 

If there were no adverse events or safety issues among the participants, as Biogen officially stated, then they were not getting enough restored memories, cognitive improvement, and improved dispositions to continue throwing money at the project.

If the earlier in vitro tests (lab culture experiments) had shown strong evidence of getting rid of amyloid beta plaque, why wasn’t it working to at least marginally improve enough human trial participants to continue the phase 3 trials?

University College of London’s John Hardy’s answer was:

This tells us that removal of amyloid in people with the disease is too late. Amyloid is a disease trigger. Once the neurodegenerative disease process is up and running, it is up and running. (Source)

David Holtzman, Washington University, St. Louis, added:

Even though this trial was in the early symptomatic phase of AD [Alzheimer’s disease], it is still in the phase when Aβ [amyoid beta] is no longer likely to be the driving process but where *tau and inflammation probably are. (Source)

Ron Petersen, Mayo Clinic, Rochester, Minnesota wrote regarding this recent failure to medically solve mainstream medicine’s AD riddle:

I think this solidifies the opinion that amyloid-targeted therapies do not have a clinical effect at the symptomatic stages of the disease process.

We clearly need other targets, and *tau is the leading candidate for now. (Source)

*Tau refers to the protein in brain cells that normally facilitates brain cell communication. It’s hypothesized that damaged or distorted tau proteins in brain cells may be the cause of Alzheimer’s disease that leads to the formation of amyloid beta plaque. (Source) 

These three medical academics seem to be saying it’s possible all the pharmaceutical whizzes so far have been targeting the end result of Alzheimer’s disease instead of the potential source.  

Maybe that’s why, prior to Biogen-Eisai’s failure, Eli Lilly’s AD (Alzheimer’s disease) drug failed during phase 3 trials. Other failures with developing a marketable AD drug include Johnson & Johnson, Pfizer, and Roche.

Thus far, the pharmaceutical industry has struck out each time at bat against AD. (Source)

Natural Options That Have Demonstrated Dramatic Improvements for AD Symptoms

Virgin Coconut Oil

An easier, less expensive, and more accessible alternative natural option for Alzheimer’s and other associated neurological disorders would be coconut oil.

See:

Coconut Oil Offers Hope for Alzheimer’s, Parkinson’s, and ALS

Health experts and medical practitioners not under Big Pharma’s thumb have realized that Alzheimer’s disease and other neurological disorders are symptoms of type 2 diabetes of the brain.

Insulin resistance inhibits glucose from entering into cells for energy. It is the hallmark of diabetes 2.

Because of cellular insulin resistance, glucose is not making it into brain cells to energize them. Insulin is needed to carry glucose into cells for the energy required for proper metabolism. Some are calling this insulin resistance in the brain diabetes type 3.

See:

Research Continues to Show Alzheimer’s is a Type 3 Diabetes

But medium chain fatty acids or triglycerides (MCTs) provide ketones that are energy sources not dependent on insulin to carry them into brain cells. MCTs are not stored as fatty tissue triglycerides for future energy use.

The liver processes MCTs to produce ketones that are available for immediate energy use in brain cells without the need for insulin. That’s why so many have turned to virgin coconut oil to reduce and even reverse symptoms of Alzheimer’s, Parkinson’s disease, and other neurological disorders.

See:

The Failure of the Medical System to Treat Alzheimer’s

Not only are the results without adverse side effects, coconut oil offers other health benefits.

See:

Study: Coconut Oil’s Lauric Acid Reduces High Blood Pressure

Depending on the severity of one’s neurological disorder, two to four tablespoons daily is usually sufficient for improving Alzheimer’s and Parkinson’s conditions as well as performing as a natural antibiotic, anti-fungal, and antiviral agent.

Cannabis

Using cannabis for Alzheimer’s or Parkinson’s disease and other related brain and nervous system disorders usually requires full spectrum cannabis with THC. 

It has even been laboratory tested for what it can do for Alzheimer’s disease by the Salk Institute and the University of California, both in La Jolla, California.

Their findings were published in 2016 as Amyloid proteotoxicity initiates an inflammatory response blocked by cannabinoids with the following conclusion:

Cannabinoids such as tetrahydrocannabinol [THC] stimulate the removal of intraneuronal Aβ, block the inflammatory response, and are protective. Altogether these data show that there is a complex and likely autocatalytic inflammatory response within nerve cells caused by the accumulation of intracellular Aβ, and that this early form of proteotoxicity can be blocked by the activation of cannabinoid receptors. (Study text)

This means that using cannabis with THC for any reason prevents amyloid beta formations and brain cell inflammation significantly, greatly reducing the risk of Alzheimer’s or other neurodegenerative diseases by eliminating the root cause before any symptoms arise, or stated simply, nipping it in the bud.

See:

Study: Cannabis More Effective Than Pharmaceutical Drugs for Age-Related Neurodegenerative Diseases Like Alzheimer’s

Cannabis has opened up dramatically for medical use in over half of America’s states. But not all states have medical cannabis arrangements, and some of those that do may not allow full spectrum cannabis with THC for Alzheimer’s or Parkinson’s disease.

A cannabis doctor or cannabis dispensary consultant can be helpful with advising what condition other than Alzheimer’s or Parkinson’s disease a patient can use that’s allowable under his or her state’s guidelines.

This cannabis medical allowances state by state guide might be helpful.

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