Wednesday, June 28, 2017

How to Get Rid of a Stye in your Eye

How to Get Rid of a Stye in Your Eye

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  • June 28, 2017 • 20,714 views

Story at-a-glance
  • Your eyelids protect your eye from injury, regulate how much light is admitted to your retina and maintain a film of tears by distributing tears over your eye
  • A stye is formed after dirt, dust or skin cells block your Meibomian gland duct and bacterial growth forms a lump, similar to a pimple or a boil, at the edge of your eyelid; this should be differentiated from a chalazion or cellulitis
  • Home treatments for a stye include warm compresses, coriander seed tea wash, tea bag compresses and washing your eyelids with mild soap to eliminate the dirt and dead skin cells that plug your oil gland duct

By Dr. Mercola
Your eyelids protect your eye from injury, help regulate how much light is admitted to your retina and maintain a film of tears by distributing tears over your eye and pumping tears from the conjunctival and lacrimal sacs. You have Meibomian glands at the base of your eyelids, near your eye lashes.
These glands secrete an oil that combines with your watery tears to lubricate and protect your eye from drying.1 Without enough quality tears to lubricate and nourish the eye, the orb can become irritated and you may develop an inflammation of the cornea, leading to blurry vision, redness and a burning and scratchy sensation, if left untreated.2
A stye may develop on your eyelid in the Meibomian gland duct. These irritations present as red lumps along the edge of the eyelid. While they can be annoying or painful, they are rarely serious. Styes can often be successfully treated at home, but before determining your course of treatment, you’ll want to make sure you’re not dealing with chalazion or cellulitis, which may require other or additional medical treatment.
What Is a Stye?
A stye is also known as a hordeolum. It is an infection, often involving the bacteria staphylococcus3 that grows along the edge of your eyelid. The infection creates a small painful bump that may take on the appearance of a small pimple or boil. It’s common for it to be filled with pus. More often than not, styes appear one at a time, as they are not contagious and don’t spread along the lid in the way other infections may.
However, it is possible to have more than one stye at a time. A stye is formed when dead skin, dirt or oil builds up in the oil glands along the edge of your eyelids and bacteria begins to grow inside, causing the stye to develop.4 A stye may also occur under the eyelid, as there are oil gland openings there as well. When this happens it is called an internal hordeolum.5 These styes are treated in the same way as those you find along the edge of your eyelid.
How to Identify a Stye
As a stye grows, your eyelid may become swollen, red and inflamed. The growth period often lasts three days before the stye naturally breaks open and begins to drain.6 Your eyelid may become painful and it may feel like there is something in your eye that doesn’t come out.
A stye may be itchy, but refrain from scratching it. The area may also have crust along the edges of the stye and your eye may water.7 The infected gland triggers these symptoms but, while irritating, they do not threaten your eyesight and are not serious. It is important to differentiate between a stye and another infection of your eyelid that is far more serious and may threaten your eyesight, such as cellulitis.
Cellulitis is also an infection and may occur on the eyelid tissue, but it is an infection that affects a larger area and doesn’t appear similar to a pimple or boil. This infection is often triggered by a trauma to the eyelid, such as an insect bite, or from a sinus infection.8 Although both a stye and cellulitis may cause redness and swelling of the eyelid, cellulitis often causes a greater amount of swelling, including the tissue around your eye.
Complications from cellulitis may include spread of the infection to the eye socket and the eyeball, causing eye pain, vision problems and even blindness. Confusing a stye with cellulitis may lead to serious permanent problems. Take care to fully evaluate your eye swelling and infection before deciding to treat your eye at home.
How to Treat Your Stye at Home
A stye infection typically responds relatively quickly to the treatments you use at home. If you notice the infection getting worse, spreading or becoming more painful, seek medical care for evaluation and treatment. These strategies help reduce the swelling from the stye and help it to mature and heal more quickly.9,10,11
Wash hands frequently
Keep your hands away from your eyes and your face as much as possible. Your hands carry small particles of dust, dirt and grime that may easily clog your oil glands, triggering a stye, or may irritate a stye you already have. Washing your hands frequently helps to reduce the irritation to your eyelid and speed healing.
Warm compress
The most effective means of treating a stye and reducing your discomfort are warm wet compresses over the eyelid. You may make these with a wash cloth and warm water from the sink. Never warm the washcloth in the microwave with the intent of placing it over the delicate skin of your eye as it may burn your skin. Test your warm compress against the skin of your wrist to ensure it’s not too hot.
Keep the compress over your eye for 15 minutes, three to four times each day. When the wet compress becomes cold, run it under warm water again. If it doesn’t cause too much discomfort, you may massage the area while the compress is in place.
Keep your eyelids clean
Styes may be triggered when the glands on your eyelids become clogged, so keeping them clean helps to prevent a new stye and will help to heal the one you already have. Use a mild, chemical-free soap to gently wash your face and eye area.
Refrain from using makeup or contact lenses
The stye is filled with bacteria, so you may infect your makeup and contact lenses with the bacteria and reinfect yourself later.
This includes any makeup that is applied near your eye, such as mascara, eye shadow or concealer. Contact lenses may not only carry the bacteria but may also increase the risk of damage to your eye or your contact lens from the stye. Be sure to throw away any items used near your eye right before the stye developed to avoid reinfection.
Let the stye open naturally
Squeezing the stye can release pus filled with bacteria, and thus spread the infection to other oil glands or to your other eye.
Coriander seed wash
Coriander has antibacterial qualities that may help your stye to heal. Brew a coriander tea from the seeds and then use the fluid to clean your eyes after the fluid has cooled.
Warm tea bags
Typically black or green tea bags work well for warm compresses over your eye. Naturally antibacterial and anti-inflammatory, tea will help reduce the irritating inflammation around your eye and help heal the infection in the stye. Steep a cup of tea and let the bag cool so it doesn’t burn your skin when you apply it. Keep it over your closed eye for 10 minutes and discard the tea bag after one use.
Discomfort relief
Cool moisture helps to bring relief from the discomfort of the stye and reduce the inflammation. Cold cucumber slices are a simple and effective method of reducing the irritation from a stye. Slice a cucumber from the refrigerator and place a slice on your eye for 10 minutes.
Avoid painkillers
A stye is uncomfortable and irritating, but over-the-counter painkillers do nothing to reduce the inflammation or treat the infection. A better option is to frequently use warm compresses and intersperse these with cool moisture to help alleviate the discomfort.
When to Call the Doctor
An infection on your eyelid has the potential for reaching your eye socket or your eye, increasing your risk of vision loss. These are some of the symptoms that may indicate it’s time to seek medical attention:12,13
The stye gets worse quickly
The stye bleeds
Your vision is affected
The stye spreads to your eyeball
The skin around your eye or cheeks becomes red and swollen
Your eye, not just the eyelid, hurts
You can’t open your eye from the swelling
You get recurring styes
Your eyelid turns red
Your stye gets very large
What May Trigger a Stye?
Once you’ve had a stye or eye infection, it’s important to replace your eye makeup, including your mascara and eye shadow, to prevent recurrence of an infection. Eye makeup should also be replaced every six months as it may become a breeding ground for bacterial growth, increasing your risk of infection. Wearing too much eye makeup, eye liner or sharing eye makeup with other women may increase your risk of developing a stye.
Wearing makeup overnight increases the risk of plugging your glands with mascara or eye liner and developing an environment for bacterial growth.14 Men and women who are under a significant amount of stress may also find they experience an increased risk of developing a stye.15 If you touch your eyes frequently, or insert your contact lenses without disinfecting them, you may increase your risk of depositing dust or dirt near the Meibomian gland duct.16
A stye may be triggered when the oil glands are blocked by dirt, grime and dust, so keeping your eyelashes clean helps to prevent styes from developing. A lack of essential fatty acids in your diet may result in flaky skin, which may also block your oil glands. Essential fatty acids are not produced by your body and must be consumed in your diet.
Essential fatty acids help the formation of healthy cell membranes, thyroid and adrenal activity, and support healthy skin and hair and hormone production.17 Linoleic acid is an omega-6 fatty acid and a-linolenic acid is an omega-3 fatty acid, both of which are needed in your diet since you cannot synthesize them in your body. A lack of these fatty acids increases the risk of your skin becoming flaky, and thus increases the risk dead skin may plug your Meibomian glands and develop into a stye.
You might be at higher risk of developing a stye if you suffer from blepharitis, or inflammation of the eyelids when the oil glands are blocked. This may occur more frequently when you suffer from environmental allergies, such as allergies to pollen.18 The condition triggers the formation of dandruff-type scales along the eyelid and eyelashes. In many cases, a regular cleaning routine to your eyelashes will help control the condition.
Stye or Chalazion?
A stye is very similar to a chalazion. In the case of a stye, the inflammation and swelling is the result of a bacterial infection. A chalazion is triggered from some of the same risk factors discussed above, but the swelling does not include a bacterial infection. A stye often resolves within a week with simple home treatments, while a chalazion will present with swelling and redness but not discomfort or pain.
A chalazion is often larger than a stye and will be located under the upper lid and not along the eyelid. The formation of a chalazion occurs when your oil glands are blocked and the oil forms a swelling. The lump is painless, often on the upper lid, and less frequently on the lower lid.19 The fluid in the oil gland thickens and is unable to be excreted. You may experience tearing, mild irritation and blurred vision if the lump is large enough to press against the eyeball.

A chalazion is more common in adults than children, while styes are more commonly found in children. Although many chalazions will disappear without treatment, they often recur if you don’t address the trigger that caused the chalazion in the first place. These triggers are the same as those for styes and also include acne rosacea, seborrhea, viral infections and tuberculosis.20

The Truth About The Armenian Genocide

Can Ginger Beat Out The Acid Blockers?

Can Ginger Beat Out The Multi-Billion Dollar Acid Blockers?

Posted on: Sunday, August 19th 2012 at 5:00 am
Written By: Sayer Ji, Founder
This article is copyrighted by GreenMedInfo LLC, 2012

Did you know that the multi-billion drug category known as "acid blockers," despite being used by millions around the world daily, may not work as well as the humble ginger plant in relieving symptoms of indigestion and heartburn? 
Ginger is a spice, a food, and has been used as a medicine safely for millennia by a wide range of world cultures. Research on the health benefits of ginger is simply staggering in its depth and breadth. In fact, the health benefits of ginger have been studied extensively for over 100 health conditions or symptoms, making it one of the world's most versatile, evidence-based remedies.
The biomedical literature on acid blockers, on the other hand, is rife with examples of the many adverse health effects that come with blocking stomach acid production with xenobiotic, patented drugs, i.e. proton pump inhibitors and H2 antagonists. What started out as "heartburn" – which in its chronic form is now called "acid reflux" or "gastroesophageal reflux disorder" – soon becomes stomach acid barrier dysfunction, when these drugs remove the acid which protects us from infection, helps to break down food, and facilitate the absorption of minerals and nutrients.
The list of 30+ harms is extensive, but here are a few of the most well-established adverse effects you may not be aware of:
  • Clostridium Infections
  • Diarrhea
  • Pneumonia
  • Bone Fractures
  • Gastric Lesions and Cancer
Back to our friend – our "plant ally" – ginger.  What happens when Pharma meets Farm in a biomedical face-off? When acid-blocking drugs are compared in efficacy to our little spicy ginger root? Well, this is what the journal Molecular Research and Food Nutrition found back in 2007 ...
Titled, "Inhibition of gastric H+, K+-ATPase and Helicobacter pylori growth by phenolic antioxidants of Zingiber officinale," the study set out to determine the anti-ulcer and anti-Helicobacter plyori (a bacteria commonly implicated in ulcer formation) capacity of ginger extracts versus conventional acid-blocking agents, such as lansoprazole (trade name Prevacid).[i]  Researchers found that one fraction of ginger exhibited six- to eight-fold better potency over lansoprazole at inhibiting acid production (specifically, gastric cell proton potassium ATPase activity). 
But, this was not all. Ginger was also found to have potent antioxidant properties, protecting both lipids from peroxidation (rancidity) and DNA damage, leading the researchers to conclude that specific fractions within ginger have "potential in-expensive multistep blockers against ulcer."

Also, whereas drugs which interfere and/or remove the stomach acid barrier also deactivate acid-dependent protein-digesting (proteolytic enzymes) such as pancreatic protease, and increases the risk of infection as a result of the loss of the anti-infective effects of the stomach's acid, ginger actually has an exactly opposite set of benefits: it contains a proteolytic enzyme several hundred times more potent than the one found in papaya (papain) and has broad-spectrum antibacterial, antiviral and antiparasitic properties, to name but only a few of its 40+ distinct pharmacological actions.
While this study focused on specific isolates of the whole ginger plant, it must be remembered that whole plants are not drugs, nor should be reduced to "nutraceutical" magic-bullets in order to become new palliative drug alternatives, which is to say, symptom-repressors, leaving the real healing job of changing the underlying nutritional, environmental, emotional context to lead to the problem in the first place, unchanged. 
While taking a ginger pill is usually a better choice than a chemical one, for most folks, ginger should be consumed in whole forms, in moderate and balanced quantities, along with a nourishing, organic, whole-food and traditional foods diet, in order to move beyond the paradigm of popping pills, or proprietary fractions of herbs in order to balance out the pendulum of extremes.
Either way, I think its time with awaken from the sorcery-like spell of pharmacia (Greek word meaning: drug, potion, charm, spell, poison), and realize everything we already need is likely in our backyard, our refrigerators or cupboards – if not altogether within ourselves.
Additional Relevant Research: 

[i] Mugur N Siddaraju, Shylaja M Dharmesh Inhibition of gastric H+, K+-ATPase and Helicobacter pylori growth by phenolic antioxidants of Zingiber officinale. Mol Nutr Food Res. 2007 Mar;51(3):324-32. PMID: 17295419

Sayer Ji is founder of, a reviewer at the International Journal of Human Nutrition and Functional Medicine, Co-founder and CEO of Systome Biomed, Vice Chairman of the Board of the National Health Federation, Steering Committee Member of the Global Non-GMO Foundation.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.
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The Natural Answer to Ulcers

The Hole in the Pharmaceutical Solution to Ulcers & The Natural Answer

Posted on: Tuesday, June 27th 2017 at 12:00 pm

Recently, a disturbing study was published on the leading class of ulcer medication. The study found that proton pump inhibitors erode your mind while suppressing gastric symptoms in your body.
Proton pump inhibitors (PPIs) include popular drugs like Prilosec, Nexium and Prevacid. They are used for ulcers, gastroesophageal reflux syndrome and indigestion because they lower the amount of acid produced in the stomach. But that’s a problem, because stomach acid is crucial for digestion and for protecting you from food-borne and environmental bacteria, viruses and other microbes that can cause infection. In the past, they have been associated with several problems, including increasing your risk of pneumonia (World J Gastrointest Pharmacol Ther 2011;2:17-26; Expert Rev Clin Pharmacol 2012;5:337- 44), interfering with calcium absorption (Am J Med 2005;118:778-81) and causing vitamin B12 deficiency.
But this new study of 73,679 people who did not have dementia when the study started found that the ones who took PPIs had a 44% increased risk of dementia compared to the ones who weren’t taking the drug (JAMA Neurol 2016; doi:10.1001/jamaneurol.2015.4791).
This is not the first time an ulcer medication has been linked to dementia. An earlier study found that continuous use of the histamine-2 receptor antagonists, like Pepcid, Zantac and Tagamet, increases the risk of cognitive impairment by an incredible 242% (Journal of the American Geriatrics Society 2007;551248-53).
As scary as these risks are, this is not the first time the alarm has been sounded about PPIs. It’s just that no one’s listening: they’re still among the most commonly used drugs in the world. A recently published study found that PPIs increase the risk of chronic kidney disease (JAMA Intern Med 2016;176: doi:10.1001/jamainternmed.2015.7193). PPIs are associated, not only with chronic kidney disease, but with progression to end-stage renal disease. Doctors have always thought, though, that they could prescribe these drugs because they could catch the problem before it became chronic: they would see the acute kidney problems that happened on the way. Turns out, that’s not true. When researchers compared 125,596 people who used PPIs to 18,436 people who used over the counter histamine H2 antagonists (H2 blockers) for the same problem over a 5 year period, they found that the ones using PPIs had 26% more chronic kidney disease. But what’s really dangerous is that the assumption about catching chronic kidney disease turned out to be false. Only about half the people who developed chronic kidney disease as a result of taking PPIs had acute kidney disease first. So, not only are PPIs a significant cause of chronic kidney disease and progression to end stage kidney disease, but the researchers warn that the increased risk of chronic kidney disease is often not flagged by prior acute kidney disease. That means that taking a common drug for the symptoms of heartburn could lead to chronic kidney disease without any warning (Kidney International 2017;91(6):1482-94).

Dementia, kidney disease, pneumonia, but that’s not all. A just published study of how diet and drugs affect the intestinal microbiome—the balance of health affecting microorganisms in your intestine—found that, among the many drugs that negatively affect your microbiome, PPIs have an especially strong negative impact (Science 2016;352 (6285):565). Research has linked PPIs to osteoporosis and--get this- -heart attack. Using PPIs for 7 or more years is associated with a 92% increase in the risk of osteoporosis related fractures. After 5 years, there is a 62% increased risk specifically of hip fractures (CMAJ 2008;179:319-26). Women who used PPIs for only 2 years in a study of 79,899 postmenopausal women had a 35% greater risk of hip fracture: the risk was especially great for smokers. When the researchers added this study to 10 others in a meta-analysis, they found a 30% increased risk of hip fracture with PPI use (BMJ 2012;344:e372).
A study published last year concluded that PPIs increase your risk of heart attack by 16% while doubling your risk of dying of a heart attack compared to people not on PPIs (PLoS One 2015;10:e0124653).
Imagine what would happen if a herb or vitamin used for ulcers caused dementia, heart attack, kidney disease, osteoporosis and pneumonia!
The amazing thing is that there is a herb that beats these drugs for ulcers while being perfectly safe. A special form of licorice root called deglycyrrhizinated licorice, or DGL, is the best ulcer healer there is. Unlike the drugs, licorice heals the ulcer by improving the protective lining of the intestines. It protects them from the acid instead of reducing the needed acid.
Licorice has been proven to be as or more effective than ulcer medications in several head-to-head studies. In a study of 100 people with ulcers, 760mg of DGL 3 times a day was as effective as Tagamet (cimetidine) (Gut 1982;23:545- 51).
When 874 people with ulcers were given either DGL, Tagamet or an antacid, 91% of their ulcers healed within 12 weeks, with no significant difference between the treatments. But the DGL came out on top because only 8.2% had relapses compared to 12.9% of the Tagamet group and 16.4% of the antacid group (Irish Med J 1985;78:153-6).
In a third head-to-head study, DGL matched Tagamet at preventing ulcers in 82 people with healed ulcers (Gut 1985;26:599-602).
In a study of 40 people who were referred for surgery because their ulcers were so severe, 3g of DGL for 8 weeks and 4.5g of DGL for 16 weeks improved their ulcers so much that none of them required surgery (Practitioner 1973;210:820-3).

A study of 33 people with ulcers gave either a placebo or 760mg DGL 3 times a day. The 78% reduction in ulcer size in the DGL group was significantly superior to the 34% reduction on the placebo. There was complete healing in 44% of the DGL group but in only 6% of the placebo group (Gut 1969;10:299-303).
Endoscopic examination of a group of 32 people with ulcers revealed that DGL healed the mucosa and, in most cases, returned it to normal.
Several other studies have also confirmed licorice’s powerful ability to heal ulcers (J Assoc Physicians India 1978;26:811-4; Lancet 1982;2:817).
It is now known that one of the leading causes of ulcers is the H. pylori bacteria. H. pylori is causally involved in 80-90% of ulcers. DGL possesses anti-H. pylori activity (J Drug Chem Toxicol 1998;21:355- 70; Arch Pharmacol Res 2000;23:172-77; J Antimicrob Chemother;2004;54:243-6; Planta Med 2007;73:P104). DGL’s activity against H. pylori comes from several flavonoids that have been shown to inhibit H. pylori (Arzneimforsch 1995;45:697-700). Several of those flavonoids have even been shown to inhibit H. pylori that is resistant to antibiotics (Life Sci 2002;71:1449-63).
DGL proved to be significantly better than placebo at eliminating H. pylori in a 60 day study of 100 people with H. pylori (Evid Based Complement Alternat Med 2013;2013:263805).
Herbal authority Rudlf Fritz Weiss, MD says there is no remedy, including drugs, more tailor-made for ulcers. He says that chamomile addresses all the hallmarks of an ulcer: spasm, inflammation and ulceration. Chamomile protects you against ulcers by soothing and healing the protective lining of the gastrointestinal tract. It also contains a flavonoid called apigenin that inhibits H. pylori (Arzneimforsch 1995;45:697-700).
Cabbage Juice
Some of the earliest research on natural treatments for ulcers focussed on cabbage juice. As early as 1949, a study of 13 people with ulcers had shown that fresh cabbage juice healed ulcers remarkably quickly: healing took only 7.3- 10.4 days (Cal Med 1949;70:10). Several other studies have also demonstrated the effectiveness of cabbage juice (Lancet 1954;2:1200; Gaz Med Fr 1965;72:1992- 3; Vopr Pitan 1979;29:29-33; Tidsskr Nor Laegeforen 1986;106:693-4). Cabbage’s ability to heal ulcers may come from its high glutamine content. When a study compared glutamine to conventional therapy, the glutamine won. Glutamine completely healed ulcers in 22 out of 24 people in only 4 weeks (Texas State J Med 1957;53:840-3).
The Newest Herbal Help
The newest herb for ulcers is curcumin, which is no surprise because curcumin seems to be proving to be the newest herbal help for a wide range of complaints. In this new study, 60 people with ulcers who were positive for H. pylori added either a placebo or a low dose of 500mg of curcumin a day. At the end of the 4 week study, although the curcumin did not seem to benefit H. pylori infection more than the placebo, it was significantly better at alleviating the symptoms of the ulcers. The people taking the curcumin had significantly better improvement on total symptoms according to the Hong Kong dyspepsia index (HKDI). They also had significantly greater improvement specifically in upper abdominal dull ache, stomach pain prior to meals and belching. At the end of the study, 27.6% of the curcumin group had no dyspepsia versus only 6.7% of the placebo group: a significant difference. The researchers concluded that adding curcumin to standard therapy for peptic ulcers significantly improves symptoms but not elimination of H. pylori. It would be interesting to see what a more typical larger dose of curcumin would do (Drug Res (Stuttg) 2016;66(8)444-448).
More Help from Supplements
The great wound healing mineral zinc also heals ulcers (Med J Aust 1975;2:793- 6). Aloe vera (J Am Osteopath Assoc 1963;62:731-5) and nettle (Ethopharmacol 2004;90:205-15) have both been shown to help. Peppermint and ginger may also help. Soothing demulcents like slippery elm and marshmallow can also help.
Dos & Don’ts
• Don’t drink alcohol (Gastroenterology 1983;85:1082-7)
• Don’t smoke (Gastroenterology 1983;85:871-4; Gut 1985;26:1333-7; Curr Ther Res 1993;54:313-9)
• Cut back on sugar (BMJ 1980;16:483; Gut 1990;31:993-6)
• Cut back on salt (Gut 1986;27:1138-42)
• Cut back on coffee (N Engl J Med 1975;293:897-9; JAMA 1981;246:248-50)
• Eliminate food allergies (Ann Allergy 1977;38:27-9; Ann Allergy 1983;51:325-8)
• Eliminate milk: contrary to the common recommendation to drink milk to soothe
an ulcer, the more milk you drink, the greater your chance of getting an ulcer (Brit Med J 1986;293:666)
• Don’t take aspirin: aspirin is a serious cause of ulcers (Ailement Pharmacol & Ther 2005;22:795-801; BMJ 2000;321:1183-7; Lancet 2013;382:769-79)
• Do eat a diet rich in fiber and low in refined sugar, because it prevents ulcers (Dig Liver Dis 2000;32:468-72). High fiber diets also reduce the rate of recurrence. 45% of people with recently healed ulcers had a recurrence on a high fiber diet versus 80% on a low fiber diet (Lancet 1982;2:736-9)

Linda Woolven and Ted Snider are the authors of several books on natural health and of the natural health newsletter, The Natural Path.
You can see their books and subscribe to their newsletter on their website.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.
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To comment:

Tuesday, June 27, 2017

President Donald Trump's Travel Ban Reinstated | True News

JUNE 26, 2017

Photo by Mark Taylor | CC BY 2.0
Legendary investigative reporter Seymour Hersh is challenging the Trump administration’s version of events surrounding the April 4 “chemical weapons attack” on the northern Syrian town of Khan Sheikhoun – though Hersh had to find a publisher in Germany to get his information out.
In the Sunday edition of Die Welt, Hersh reports that his national security sources offered a distinctly different account, revealing President Trump rashly deciding to launch 59 Tomahawk missiles against a Syrian airbase on April 6 despite the absence of intelligence supporting his conclusion that the Syrian military was guilty.
Hersh draws on the kind of inside sources from whom he has earned longstanding trust to dispute that there ever was a “chemical weapons attack” and to assert that Trump was told that no evidence existed against the Syrian government but ordered “his generals” to “retaliate” anyway.
Marine General Joseph Dunford, Chairman of the, Joint Chiefs of Staff, and former Marine General, now Defense Secretary James “Mad-Dog” Mattis ordered the attacks apparently knowing that the reason given was what one of Hersh’s sources called a “fairy tale.”
They then left it to Trump’s national security adviser Army General H. R. McMaster to further the deceit with the help of a compliant mainstream media, which broke from its current tradition of distrusting whatever Trump says in favor of its older tradition of favoring “regime change” in Syria and trusting pretty much whatever the “rebels” claim.
According to Hersh’s sources, the normal “deconfliction” process was followed before the April 4 strike. In such procedures, U.S. and Russian officers supply one another with advance details of airstrikes, such as target coordinates, to avoid accidental confrontations among the warplanes crisscrossing Syria.
Russia and Syrian Air Force officers gave details of the flight path to and from Khan Sheikhoun in English, Hersh reported. The target was a two-story cinderblock building in which senior leaders – “high-value targets” – of the two jihadist groups controlling the town were about to hold a meeting. Because of the perceived importance of the mission, the Russians took the unusual step of giving the Syrian air force a GPS-guided bomb to do the job, but the explosives were conventional, not chemical, Hersh reported.
The meeting place was on the floor above the basement of the building, where a source whom Hersh described as “a senior adviser to the U.S. intelligence community,” told Hersh: “The basement was used as storage for rockets, weapons, and ammunition … and also chlorine-based decontaminates for cleansing the bodies of the dead before burial.”
A Bomb Damage Assessment
Hersh describes what happened when the building was struck on the morning of April 4: “A Bomb Damage Assessment by the U.S. military later determined that the heat and force of the 500-pound Syrian bomb triggered a series of secondary explosions that could have generated a huge toxic cloud that began to spread over the town, formed by the release of fertilizers, disinfectants, and other goods stored in the basement, its effect magnified by the dense morning air, which trapped the fumes close to the ground.
“According to intelligence estimates, the strike itself killed up to four jihadist leaders and an unknown number of drivers and security aides. There is no confirmed count of the number of civilians killed by the poisonous gases that were released by the secondary explosions, although opposition activists reported that there were more than 80 dead, and outlets such as CNN have put the figure as high as 92.”
Due to the fog of war, which is made denser by the fact that jihadists associated with Al Qaeda control the area, many of the details of the incident were unclear on that day and remain so still. No independent on-the-ground investigation has taken place.
But there were other reasons to doubt Syrian guilt, including the implausibility of Syrian President Bashar al-Assad choosing that time – while his forces were making dramatic strides in finally defeating the jihadists and immediately after the Trump administration had indicated it had reversed President Obama’s “regime change” policy in Syria – to launch a sarin attack, which was sure to outrage the world and likely draw U.S. retaliation.
However, logic was brushed aside after local “activists,” including some closely tied to the jihadists, quickly uploaded all manner of images onto social media, showing dead and dying children and other victims said to be suffering from sarin nerve gas. Inconsistencies were brushed aside – such as the “eyewitness” who insisted, “We could smell it from 500 meters away” when sarin is odorless.
Potent Images
Still, whether credible or not, these social-media images had a potent propaganda effect. Hersh writes that within hours of watching the gruesome photos on TV – and before he had received any U.S. intelligence corroboration – Trump told his national security aides to plan retaliation against Syria. According to Hersh, it was an evidence-free decision, except for what Trump had seen on the TV shows.
Hersh quotes one U.S. officer who, upon learning of the White House decision to “retaliate” against Syria, remarked: “We KNOW that there was no chemical attack … the Russians are furious – claiming we have the real intel and know the truth…”
A similar event had occurred on Aug. 21, 2013, outside Damascus – and although the available evidence now points to a “false-flag” provocation pulled off by the jihadists to trick the West into mounting a full-fledged assault on Assad’s military, Western media still blames that incident on Assad, too.
In the Aug. 21, 2013 case, social media also proved crucial in creating and pushing the Assad-did-it narrative. On Aug. 30, 2013, then-Secretary of State John Kerry pinned the responsibility on Assad no fewer than 35 times, even though earlier that week National Intelligence Director James Clapper had warned President Obama privately that Assad’s culpability was “not a slam dunk.”
Kerry was fond of describing social media as an “extraordinarily useful tool,” and it sure did come in handy in supporting Kerry’s repeated but unproven charges against Assad, especially since the U.S. government had invested heavily in training and equipping Syrian “activists” to dramatize their cause. (The mainstream media also has ignored evidence that the jihadists staged at least one chlorine gas attack. And, as you may recall, President George W. Bush also spoke glowingly about the value of “catapulting the propaganda.”)
Implications for U.S.-Russia
To the extent Hersh’s account finds its way into Western corporate media, most likely it will be dismissed out of hand simply because it dovetails with Moscow’s version of what happened and thus is, ipso facto, “wrong.”
But the Russians (and the Syrians) know what did happen – and if there really was no sarin bombing – they recognize Trump’s reckless resort to Tomahawks and the subsequent attempts to cover up for the President. All this will have repercussions.
This is as tense a time in U.S-Russian relations as I can remember from my five decades of experience watching Russian defense and foreign policy. It is left to the Russians to figure out which is worse: a President controlled by “his generals” or one who is so out of control that “his generals” are the ones who must restrain him.
With Russia reiterating its threat to target any unannounced aircraft flying in Syrian airspace west of the Euphrates, Russian President Putin could authorize his own generals to shoot first and ask questions later. Then, hold onto your hat.
As of this writing, there is no sign in “mainstream media” of any reporting on Hersh’s groundbreaking piece. It is a commentary on the conformist nature of today’s Western media that an alternative analysis challenging the conventional wisdom – even when produced by a prominent journalist like Sy Hersh – faces such trouble finding a place to publish.
The mainstream hatred of Assad and Putin has reached such extraordinary levels that pretty much anything can be said or written about them with few if any politicians or journalists daring to express doubts regardless of how shaky the evidence is.
Even the London Review of Books, which published Hersh’s earlier debunking of the Aug. 21, 2013 sarin-gas incident, wouldn’t go out onto the limb this time despite having paid for his investigation.
According to Hersh, the LRB did not want to be “vulnerable to criticism for seeming to take the view of the Syrian and Russia governments when it came to the April 4 bombing in Khan Sheikhoun.” So much for diversity of thought in today’s West.
Yet, what was interesting about the Khan Sheikhoun case is that was a test of whom the mainstream media detested more. The MSM has taken the position that pretty much whatever Trump says is untrue or at least deserving of intense fact-checking. But the MSM also believes whatever attacks on Assad that the Syrian “activists” post on social media are true and disbelieves whatever Putin says. So, this was a tug-of-war on which prejudices were stronger – and it turned out that the antipathy toward Syria and Russia is more powerful than the distrust of Trump.
Ignoring Critics
The MSM bought into Trump’s narrative to such a degree that any criticism, no matter how credentialed the critic, gets either ignored or ridiculed.
For instance, the Veteran Intelligence Professionals for Sanity produced a memo on April 11 questioning Trump’s rush to judgment. Former MIT professor Ted Postol, a specialist in applying science to national security incidents, also poked major holes in the narrative of a government sarin attack. But the MSM silence was deafening.
In remarks to Die Welt, Seymour Hersh, who first became famous for exposing the My Lai massacre story during the Vietnam War and disclosed the Abu Ghraib abuse story during the Iraq War, explained that he still gets upset at government lying and at the reluctance of the media to hold governments accountable:
“We have a President in America today who lies repeatedly … but he must learn that he cannot lie about intelligence relied upon before authorizing an act of war. There are those in the Trump administration who understand this, which is why I learned the information I did. If this story creates even a few moments of regret in the White House, it will have served a very high purpose.”
But it may be that the Germans reading Welt am Sonntag may be among the few who will get the benefit of Hersh’s contrarian view of the April 4 incident in Khan Sheikhoun. Perhaps they will begin to wonder why Chancellor Angela Merkel continues with her “me-too” approach to whatever Washington wants to do regarding tensions with Russia and warfare in Syria.
Will Merkel admit that she was likely deceived in parroting Washington’s line making the Syrian government responsible for a “massacre with chemical weapons” on April 4? Mercifully, most Americans will be spared having to choose between believing President Trump and Seymour Hersh. 

More articles by:RAY MCGOVERN

Ray McGovern was an Army officer and CIA analyst for almost 30 year. He now serves on the Steering Group of Veteran Intelligence Professionals for Sanity.  He is a contributor to Hopeless: Barack Obama and the Politics of Illusion (AK Press). He can be reached at: A version of this article first appeared on  

NSAIDs and Heart Attack Risk!!!!!!

Common pain medication increases risk of heart attack after only one week of usage

(NaturalHealth365) In a stunning revelation, a recent study has shown that the common pain medication class called NSAIDs can raise heart attack risk by as much as 100 percent. All five NSAIDs (nonsteroidal anti-inflammatory drugs) studied were found to increase heart attack risk significantly within the first week of use, said researchers.
Risk of myocardial infarction from over the counter drugs like ibuprofen was found to be highest within the first month of taking them, especially if dosage was high. The individual drugs assessed also included diclofenac, naproxen, rofecoxib and celecoxib.
Commonly used pain medication increases the risk of a heart attack by over 100 percent
For the study, researchers assessed 446,763 persons from healthcare databases in Canada, the UK and Finland, 61,460 of whom had had a heart attack. It quickly became clear that heart attack risk associated with NSAID usage was highest during the first month in people who took the highest doses of the drugs.
Potential increase in risk for heart attack in those taking rofecoxib was over 100 percent. Both ibuprofen and naproxen were found to bring an increased heart attack risk of about 75 percent.
The overall odds of suffering a heart attack were up to 50 percent higher when using NSAIDs as compared with not using the drugs, with variances among the individual drugs tested. The study results were published in the BMJ.
Higher doses of NSAID pain medication further increase heart attack risk
Because the risk of heart attack seems to come on so quickly after starting NSAIDs, the researchers recommend that healthcare professionals carefully consider both the benefits and risks of these drugs before recommending them.
This is especially relevant when higher doses are prescribed. While those who experienced heart attack related to NSAID use tended to be at higher risk for heart attack in the first place, the study results should give all users of NSAIDs pause.
NSAIDs have been studied for their possible link to myocardial infarction before; however, the current study is the first to measure dose, timing, treatment duration and comparative risks among different NSAID types.
Seek natural alternatives to NSAID pain medication whenever possible
While the effects of longer-term use were not fully assessed, the conclusion of this study is that NSAIDs should only be used in moderation and for as short a term as possible. Ideally, natural pain relief solutions should be sought.
Some holistic alternatives to NSAIDs include capsaicin (the active element in chili peppers), boswellia (Indian frankincense), South African devil’s claw, South American cat’s claw, curcumin (turmeric), and regular use of omega-3 fatty acids (such as a daily fish oil supplement).
You might also try white willow bark (the predecessor of aspirin) or medical marijuana (if legal in your state). As with any natural cure, we suggest you check with your physician before using any of the supplements mentioned here as alternatives to pain medication.

Sunday, June 25, 2017

List of Good Fats and Oils versus Bad Dr. Cate Shanahan

List of Good Fats and Oils versus Bad
Written by: Dr. Cate on April 9th 2017

This page is YOUR resource list of all things pertaining to edible fats and oils, please bookmark if you are interested in this topic. 
If there’s something YOU want to know about good fats versus bad, please post a question for me in the comments section.
No questions about your personal medical history, please. (Those are not appropriate here and will have to be deleted, sorry!)
Bad Fats: NEVER eat these!
REFINED PUFA-Rich seed OILS a.k.a. “Vegetable oil”
Canola, Corn, Cottonseed, Soy, Sunflower, Safflower, Grapeseed, Rice bran.
ALSO TOXIC: Refined Palm oil. (It’s not very high in PUFAs, but the refining is often more intense).
PLUS: Anything that says hydrogenated because it’s going to start with one of the above and process it further to generate trans fats.
Vegetable oil is an industry term that sometimes includes olive oil, peanut and coconut. However, when you see the word vegetable oil on the ingredients, it’s not going to be olive, peanut or coconut. It will be one of the cheap, refined PUFA-rich, seed oils listed above.
Good Fats: Eat THESE instead!
Avocado oil, Butter, Coconut Oil, Duck Fat, Ghee, Lard, Olive oil, Peanut oil, Tallow, Sesame oil, Flax seed oil, Walnut oil, Almond oil, Macadamia nut oil
Also: Anything that says cold pressed and unrefined. It must say unrefined! If it says cold pressed but is refined, it’s no good. 
Almond oil, Avocado oil, Butter, Coconut, Duck Fat, Ghee, Lard, Macadamia nut oil,  Peanut oil, Tallow
Flax, Sesame, Walnut (Exception: Sesame plus peanut or other more stable oil, see below)
“Limited Use” Defined.
These oils have been refined, but because of their fatty acid profile they can handle the refining process without generating significant levels of mutated fatty acids and are therefore not going to be particularly toxic. However the refining also strips them of significant amounts of minerals and/or antioxidants so they are not as nutritious as their more expensive, higher-quality equivalents. You can think of them as the empty calories of the fat world. If you can afford to, get the better stuff. If you can’t, these are still far better than the high-PUFA oils. You’ll just need to be sure that the rest of your diet supplies plenty of antioxidants (lots of fresh greens and herbs, for example).
Knowledge Base:
Everything you need to know about dietary fats and oils, summarized in one place.
(The short version)
The refining process damages the polyunsaturated fats, mutating the molecules into toxins with long names like 4-hydroxynonanal and 4-hydroxyhexanol, aldehydes, and others. These molecules promote free-radical reactions that damage our cellular machinery including mitochondria, enzymes, hormone receptors, and DNA.
More information on the refining below.
For everything else you need to know about these oils, please read Chapters 7 and 8 of the 2017 edition of Deep Nutrition: Why Your Genes Need Traditional Food)
Our diets do contain too much omega-6, yes. But a common misperception is that vegetable oils are toxic because they contain omega-6, and omega-6 is pro-inflammatory. There are two points about this misperception I want to bring to your attention.
  1. Vegetable oils are toxic because the fats they contain are oxidized. And it’s the double bonds that make PUFAs susceptible to oxidation. But omega-3 fats have more double bonds than omega-6, generally speaking, and so seeds with a high omega-3 content, like canola, actually lead to more toxic degradation products than seeds with a high omega-6, like soy (all else being equal).
  2. Our brains need omega-6. Our brains are made out equal parts omega-6 and omega-3, so we need both in roughly equal amounts.
The fact that we get too much omega-6 now is a result of two major consequences of industrial food making:
  1. Soy is the most commonly used vegetable oil in processed foods and restaurants by a factor of nearly twice over Canola, the second most common.
  2. The animals we eat are fed soy and corn, which contain lots of omega-6, and the feed is often supplemented with other vegetable oils such as cottonseed that are also high in omega-6. The animals do not burn these fats for energy (neither do we), so they are stored in the adipose tissue. This means, for example, bacon from industrially produced pigs contains a lot of omega-6.
How much vegetable oil is too much?
That’s a little like asking how many cigarettes should a 4 year old smoke. More than none is too much. However because these oils are now added to spice mixes that are added to many otherwise healthy foods, it has become almost impossible to avoid entirely. Other than spice mixes, products with vegetable oil are best avoided whenever possible.
Fats are solid at room temperature and oils are liquid. Saturated fats are stiff, so highly saturated fat. (Figure below)

Fats are solid at room temperature because their triglycerides are composed of relatively more straight, saturated fatty acids. Oils are liquid at room temperature because their triglycerides are composed of relatively more flexible unsaturated fatty acids, both mono-unsaturated (one double bond) and poly-unsaturated (two or more double bonds)
Fatty acid refers to a molecule composed of a several carbons linked together, generally anywhere from 4 to 26 carbon atoms, with a special group at the end called a carboxyl. The chain of carbon atoms may be linked together with single bonds, and be saturated, or contain one double bond, and be mono unsaturated, or contain two or more double bonds, and be polyunsaturated. Our bodies cell membranes are composed of all three types of fatty acids. We cannot make certain fatty acids, those have to come from food, these we call essential fatty acids and they come in two types: omega-3 and omega-6.
Fats Most fats and oils we eat are composed of three fatty acids bound to glycerol to form a structure called a triglyceride.  Triglycerides are very large molecules and the general idea is a little like three keys dangling off a keychain. When we eat any fat or oil, our digestive system breaks down the triglyceride into free fatty acids and glycerol so that the molecules can get into our intestinal cells, then the intestinal cell reassembles them back into triglyceride and ships them out in the bloodstream as chylomicrons, a kind of lipoprotein. When we eat too much, we store the extra as fat under our skin, all in the form of triglyceride.
If my oil says expeller pressed does that mean its okay?
No. Here’s why:
Bottles of organic oil often state “expeller pressed” as a selling point, to suggest that it has been gently treated, in an extra-virgin sort of way. But that couldn’t be farther from the truth. Firstly, expeller pressed simply means that the first step of the extraction was mechanical. The second step was probably the standard, solvent extraction using hexane.
But once the expeller-pressed oil has been extracted, it’s generally also refined, bleached and deodorized. These three additional treatments guarantee that the polyunsaturated fatty acid molecules will be oxidized in ways that generate toxins like 4-hydroxyhexanal, 4-hydroxynonanol, aldehydes and more. These compounds aren’t just hard to pronounce, they’re hard for our cells to tolerate and lead to mitochondrial uncoupling, DNA damage, free radical cascades and other cell-damaging events that accelerate the aging process and contribute to disabling disease. Don’t be fooled. (For more information, please read chapters 7 and 8 of the 2017 edition of Deep Nutrition: Why Your Genes Need Traditional Food)
The higher the heat, the more you need to be stirring unless you’re going for a specific effect, like char flavor or crispy skin.
BUTTER+OLIVE: Add a pat of butter to olive oil when cooking at high heat, the saturated fat in the butter protects the olive oil and the antioxidants in the olive oil protect the protein in the butter that might otherwise burn.
SESAME+PEANUT: Add sesame to peanut oil for Asian dishes. The ratio should be roughly 4-8:1 Peanut:Sesame. Sesame is high in PUFA, but it has powerful antioxidants that, when added to low PUFA peanut oil, protect all the PUFAs.
Should I make sure to use a high smoke point oil for pan frying, wok cooking or other high-heat applications?
No. Here’s why:
Smoke point is a sciencey sounding selling point that vegetable oil salesmen use to ooze their way into busy restaurants. If you’ve read about smoke points, you’ve probably read something like this “Refined oils have higher smoke points and typically a more neutral flavor than unrefined oils, which makes them better for sautéing, frying or even deep-frying.” I think the concept of smoke point is bunk. First of all, what chef is going to literally wait for food on the stove to start smoking before stirring it? Have you ever seen that on a cooking show? Secondly, and this is the more important point, the molecular degradation that occurs in these high smoke point oils both during their manufacture and then again when they’re exposed to high heat during cooking invisibly degrades the oil, generating molecules that are dangerous to our health.
If the food you order has black char on it, you’ll probably realize someone in the kitchen wasn’t paying attention to your dish, and send it back. The higher smoke point oils enable chefs to stir less often and in so doing to overheat your food without leaving any evidence.
I’m not saying theres no such thing as smoke point. Of course there is. But the myth is that the product is somehow superior because it has a high smoke point. You can increase the smoke point of any fat by removing proteins, antioxidants, and free fatty acids. For example, ghee has a higher smoke point than butter because the clarification process reduces the protein content.
I recommend using high-quality oils and fats like butter, lard or tallow, and yes, even EVOO, for stovetop frying. But be sure to stir! It should go without saying that overcooking your dishes not a healthy practice. Who needs high smoke points? Just eat properly cooked food.
Manufactures produce a crude oil by extracting it in one of three ways:
  1. Mechanical extraction, either cold pressed (always below 120 degrees) or expeller pressed (the pressure is higher, which increases the temperature). This is the best. But it leaves a lot of oil behind in the seed or fruit, roughly half for expeller pressing, or more for cold pressing, so it’s typically done only by small batch, artisanal producers. Extra virgin olive oil is produced by mechanical extraction, as are other high-quality oils. The highest quality oils do not need to be refined and so the bottles may contain some cloudy-appearing material that’s actually very good for you. (The video below of Figone’s Olive Oil Pressing at Factory is a good example of what today’s mechanical, expeller pressing system looks like on a relatively small scale.)
  2. Double extraction. This is probably how most “expeller pressed” oil is actually produced. The manufacturer will mechanically press it first, obtaining about half of the oil they will ultimately be able to extract from the seed. This produces oil and an oil-rich seed cake. To remove the other half of the oil from the seed cake, they process with hexane, as below, making for a more “cost effective” product. Unfortunately, from a consumer choice standpoint, its not clear that oils produced this way won’t be called cold pressed or expeller pressed, even though that’s only part one of the process. It appears there’s simply no way to distinguish oils that have been only mechanically pressed from these “double extraction” oils, where half has been mechanically extracted and half has been processed by solvent extraction, as below.
  3. Solvent extraction, using hexane (also in your gasoline tank). This is the worst. They do remove as much of the hexane as they can, using bleaches or distillation, and it’s not quite as damaging to the polyunsaturated oil molecules as the refining process.
The highest quality cold pressed oils do not require any further steps and are sold unfiltered and unrefined. These are the most nutritious oils.

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After the double extraction and solvent extraction, a sticky soapy sludge develops on top of the oil as a result of churning the phosphatides (when you work soap into a lather, your churning the phosphatides with water creating the foam). These phosphatides must be removed before refining, and so manufacturers use a “wash” of sodium hydroxide and water to accomplish this.
Cold pressed oils do not generally require degumming
Step one and, if it’s needed, step two produce what’s called a “crude oil.” Other than cold pressed oils,  the crude oils all contain numerous contaminants you would not want to eat. So the manufacturer cleans it up in three more very harsh steps that damage the PUFAs: refining, bleaching and deodorizing.
Refining: This is performed to remove the free fatty acids, which would contribute to a rancid taste. This is accomplished with either an acid or bleaching agent. In the latter case, the since bleaching has been performed the process skips ahead to deodorizing.
Bleaching: This is performed to remove chlorophyll, the chemical in plants that imparts the green color. Chlorophyll must be removed from these high PUFA seed oils because it promotes rapid oxidation of the PUFA fatty acids and would lead to a very sludgy, sticky oil that wouldn’t pour out of the bottle very well.  While bleaching improves its pour-ability, it also generates partially oxidized PUFAs compounds. These are the highly toxic compounds that promote oxidative stress in our bodies and can damage our DNA.
Deodorizing: This is performed to remove flavor components, which would come from chemicals originally present in the seed (such as antioxidant phytonutrients) as well as byproducts of the above steps. This is performed by heating the oil again to 510 F/ 265 c and forcing steam through it to try to capture the volatile materials.
The refined oil can be further treated to raise the melting point to create the desired, more solid texture. One method is hydrogenation, which creates a partially hydrogenated, solid fat. Another is inter-esterification, which rearrange the fatty acid locations on glycerol and also solidifies the fat. Both of these lead to generation of different forms of toxins than the above. Hydrogenation leads to the generation of fatty acids with a single trans bond, which block our body’s enzymes. Interesterification leads to the formation of triglycerides with unusual configurations and has been found to lead to elevated blood glucose levels.
Nature does not make bad fats, factories do. By mass producing oils, we can damage them in two different ways that can lead to rancid taste.
  1. ENZYMES.   When oils and fats are too old, they can break apart into free fatty acids, which taste bad and are one of the major causes of rancidity. Mishandling of the raw material before factory processing also promotes enzyme action. The enzymes that release free fatty acids are called lipases, and this kind of rancidity is called lipolytic rancidity. Rancid dairy is especially gross because it has a high portion of the short chain fatty acids that are powerfully bad tasting and are, in fact, partially responsible for the disgtuisting flavor and smell of vomit.
  2. OXIDATION. Another cause of rancidity occurs due to ultraviolet light or heat or metals and other chemicals contaminating the fat or oil. These cause oxidation reactions, and they affect the PUFA fatty acids first. The off flavor results from the fact that oxidation reactions can release free fatty acids from the triglyceride, just as enzymes can, however the freed fatty acids are also damaged chemically and can be very toxic. Rancidity resulting from oxidative release of fatty acids is called oxidative rancidity. Fish is very high in PUFA fats and both oxidative and lipolytic rancidity play a role in generating the rotten smells of old fish.
Is eating rancid food unhealthy?
Yes, in general.
If it were just enzymatic rancidity at play releasing otherwise normal fatty acids, the answer would be no. In fact, animal like vultures that seek out already killed prey seem to enjoy the released free fatty acids we find disgusting. But these animals are generally eating carcasses that are only a few days old at most and generally the parts they eat at this stage contain mostly oxidation resistant saturated fatty acids.
We don’t eat rotting meat, unless we’re living with a native Greenlander and enjoying Kiviaq (made of auks fermented in a seal skin). So when we are hungry enough to consider downing something rancid its generally going to old nuts or seeds that are high in polyunsaturated fats. Because these PUFA fats oxidize easily, if you’re getting an off flavor from nuts or seeds its unhealthy and best avoided.
Some of the most toxic fats have no flavor at all, and thus we can’t rely on taste to warn us that an oil contains toxic, oxidized fats. In fact, Canola, Soy and the other RBD oils are marketed to restaurants based on their lack of flavor, meaning the chef can use the same oil regardless of the spices and other flavor profiles.
Harvard Gets It Wrong
If you care about your health, ignore Harvard and Yale–at least for now. While many leading MDs are waking up to how wrong we were to insist that saturated fat was unhealthy, these two schools are digging their heels deep in the 1950s-era dogma.  Their recommendations is to avoid saturated fat as much as possible, and get roughly 25% of daily calories from polyunsaturated fat-rich foods like vegetable oils. The only evidence that supports this position is statistical (they do not offer a plausible physiologic mechanism), and their statistical work is seriously flawed by wrong assumptions and confounding variables.
In 2015, scientists at the NIH analyzed autopsy slides that were made as part of a study done in the 1970s. The study compared two diets, one rich in liquid vegetable oils (high polyunsaturated fats) and the other rich in hydrogenated vegetable oil (high in trans and saturated fats). Believe it or not, they found the folks on the hydrogenated vegetable oils had fewer heart attacks and strokes than the people on the liquid vegetable oils.
Walter Willet, the Dean of the School of Public Health, dismissed this finding as “a historical footnote.”
What Made Me Realize Harvard Gets it Wrong
I read a PhD dissertation that explained how polyunsaturated fatty acids (PUFAs) can ignite free radical reactions in our bodies. Free radical reactions are really bad. After reading more about oil processing and PUFA oxidation, I realized everything I’d learned about fats in medical school was wrong, and that it was necessary to reverse my earlier position on good fats and bad. As a practicing doctor, making this shift has not been easy, because it goes against what most of my colleagues still believe.
Technically Speaking:
This section defines some common scientific terms for those interested in more of the chemistry.
BEST METHOD OF DETERMINING OXIDATIVE STABILITY: Activated Oxygen Method or AOM, I think it’s heating to 100C with peroxide, and the longer it takes to get to a certain point, the more it resists oxidation.
RANCIDITY=any off flavor. Two reasons: free fatty acids released from trigylceride, producing an off flavor. And Partial oxidation of the fatty acids.
FREE FATTY ACID FLAVOR (from vegetable oil manual I downloaded):
The liberated free fatty acids have a distinct flavor and odor which are more disagreeable when the fatty acid chain length is shorter than 14 carbons
OXIDIZED FATTY ACID FLAVOR (From veg oil manual)
Hydroperoxides themselves have no flavor or odor but break down rapidly to form aldehydes, many of which have a strong, disagreeable flavor and odor.
“Hydrolytic rancidity, also called hydrolysis or enzymatic oxidation, occurs in the absence of air, but with moisture present. This normally is accomplished through enzymatic peroxidation, where enzymes found naturally in plant oils (i.e., lipoxygenase, cyclooxygenase) and animal fats (i.e., lipase) can catalyze reactions between water and oil.
Another degradation process is microbial rancidity, in which micro-organisms such as bacteria, molds and yeast use their enzymes to break down chemical structures in the oil, producing unwanted odors and flavors. Water needs to be present for microbial growth to occur.”
OXIDATION: Double bonds in the fatty acid reacting with oxygen.
OXIDIZED: Double bonds in the fatty acid that have reacted with oxygen to generate reaction products, usually with toxic e
IODINE VALUE: How many double bonds are present on average in the triglycerides in the oil. Does not distinguish between mono and poly. Higher value represents more double bonds.
PEROXIDE VALUE: Peroxide determination is the most widely accepted method for oil flavor quality determination. Peroxides are the major initial products of lipid oxidation and are measured by techniques based on their ability to liberate iodine from potassium iodide or to oxidize ferrous to ferric iron. Their content usually is expressed as milliequivalents of oxygen per kilogram of fat. Peroxide values of 0.5 meq/kg or less generally are necessary for a high flavor score. Because of the transitory nature or instability of peroxides, the level of peroxides may not serve as a true indicator of the actual state of oxidative rancidity of the fat or oil. During the course of oxidation, peroxide values reach a peak, then decline
Interesterification leads to elevated glucose:

Refining Steps:

Deep Nutrition with Dr. Mercola and Dr. Shanahan

Saturday, June 24, 2017

Children Full of Life - Important Documentary.. Very.

Children Full of Life - Important Documentary.. Very.

Learn the Secrets of the Nakshatras: Krittika The one who Cuts

Ep. 261: Senate Plan Makes ObamaCare Worse

Broccoli in a pill slashes diabetics’ blood sugar

Natural Alternatives to Deadly Prescription Opiates

Natural Alternatives to Deadly Prescription Opiates
Posted on: Friday, June 23rd 2017 at 2:30 pm

Prescription drugs kill nearly fifteen times as many Americans per year than the casualty toll of domestic terrorist attacks from over thirteen years combined, but still natural alternatives are suppressed and maligned despite a growing body of evidence supporting their far greater safety and efficacy. 
Since 1997, when the United States became one of only two developed nations that allows direct-to-consumer pharmaceutical advertising, addiction to prescription drugs and prescription drug overdoses have quadrupled (Real Leaders, 2016). In fact, last year, deaths due to prescription drug overdoses surpassed 50,000 per year, dwarfing the number of deaths due to motor vehicle accidents (37,757) and to gun violence (36,252) (Chicago Tribune, 2016).
Especially culpable are synthetic opioids, a class of central nervous system depressants such as tranquilizers, sedatives, and pain relievers, which claimed a death toll of 9,580 people in 2016, representing a 73% increase (Chicago Tribute, 2016). Although abuse of prescription painkillers such as Vicodin and OxyContin only increased by 4%, they took the largest toll, killing 17,536 (Chicago Tribune, 2016). In fact, the Centers for Disease Control (CDC) reported that for the first time in twenty years, the nation’s life expectancy declined, and cited drug overdoses as a significant contributing factor (Chicago Tribune, 2016).
Although the hyper-politicized war on terror receives far more publicity, prescription drugs kill nearly fifteen times as many Americans per year than the casualty toll of domestic terrorist attacks from over thirteen years combined (Real Leaders, 2016). Rather than stemming from an illicit transaction on a dimly lit street corner with an unscrupulous character, eighty percent of opioid addictions originate from a stethoscope-wearing, prescription-pad wielding physician dispensing legitimate prescriptions for pain medication (Real Leaders, 2016). Furthermore, instead of being distributed via drug trafficking rings commandeered by international drug lords, the opioids are manufactured in pristine labs by Big Pharma, with legal sanction from the Food and Drug Administration (FDA) and Drug Enforcement Administration (DEA) (Tough, 2001).
How Big Pharma Engineered an Epidemic of Opioid Addiction
Much of this is due to a Stamford, Connecticut-based pharmaceutical company, Purdue Pharma, which introduced the opioid analgesic OxyContin, a sustained-release oxycodone preparation, onto the market in 1995. A close cousin of other opium derivatives such as heroin, morphine, fentanyl, methadone, and codeine, OxyContin was developed in a German laboratory in 1916 (Tough, 2001). Its sales ballooned from $48 million dollars in its first year to $3.1 billion a decade later, with over 14 billion prescriptions being dispensed in 2001 and 2002, leading Purdue to corner nearly one-third of the painkiller market (Mariani, 2015; Van Zee, 2009).
One of the three founding brothers of Purdue Pharma, Arthur Sackler, was one of the first pharmaceutical advertisers to cultivate reciprocity relationships with doctors to incentivize physicians to prescribe the drugs they promoted, a model which would later become the modus operandi for the entire pharmaceutical industry (Mariani, 2015). Although OxyContin offered no advantage over its opioid relatives, an aggressive marketing campaign in excess of $200 million pursued by Pharma led to its dominance in the market (Van Zee, 2009).
Purdue employed perfidious tactics such as compiling databases of the highest and least discriminate opioid prescribers and targeting reps to frequent those health care professionals (Van Zee, 2009). According to Van Zee (2009), “A lucrative bonus system encouraged sales representatives to increase sales of OxyContin in their territories, resulting in a large number of visits to physicians with high rates of opioid prescriptions, as well as a multifaceted information campaign aimed at them”. In a single year alone, Purdue paid out over $40 million in sales bonuses to its pharmaceutical reps (General Accounting Office, 2003).
Purdue likewise recruited medical practitioners to attend all-expenses-paid symposia at luxury resorts, a practice which has been demonstrated to influence physician prescribing habits, and initiated a redeemable starter coupon program to supply patients with a free limited-time prescription (General Accounting Office, 2003; Orlowski & Wateska, 1992). Further, according to the DEA, Purdue undertook concerted efforts to distribute branded promotional items to health care providers at an unprecedented rate (General Accounting Office, 2003).
Deliberate Distortion of Statistics Prompts Over-prescribing of Opioids
Purdue similarly encouraged the liberal prescription of opioids by primary care physicians (PCPs), despite expert concerns that PCPs were not qualified to evaluate and manage complex pain management (Tough, 2001). According to Mariani (205), “It would become one of Purdue's preeminent missions to make primary care doctors less judicious when it came to handing out OxyContin prescriptions”.
Despite lack of scientific consensus in the use of opioids for non-cancer related pain, and results of prospective, randomized trials demonstrating “only small to modest improvement in pain relief, with no consistent improvement in physical functioning” in non-terminal pain cases, Purdue forcefully targeted the non-malignant pain market to capture new markets, leading to an approximate tenfold increase in OxyContin prescriptions for chronic pain from 670,000 in 1997 to 6.2 million in 2002 (Van Zee, 2009).
Not only did they mobilize efforts toward physician prescribing, but they also generously donated to patient advocacy organizations such as the American Chronic Pain Association, the American Pain Foundation, and the National Foundation for the Treatment of Pain, in order to transform the negative rhetoric surrounding opiate use. Purdue likewise launched a public education program called Partners Against Pain to expand and secure the opioid market and to enhance their bottom line (Tough, 2001). In fact, “From 1996 through July 2002, Purdue funded more than 20,000 pain-related educational programs through direct sponsorship or financial grants, 19 providing a venue that had enormous influence on physicians’ prescribing throughout the country” (Van Zee, 2009).
Pivotally, according to Van Zee (2009), “A consistent feature in the promotion and marketing of OxyContin was a systematic effort to minimize the risk of addiction in the use of opioids for the treatment of chronic non–cancer-related pain,” citing an extremely small risk of addiction in their brochures and promotional material. Purdue cherry-picked studies and taught their reps to reference a low diversion potential and less than one percent addiction rate; however, literature reviews have elucidated that the prevalence of addiction varies from 0% to 50% according to the criteria employed and cohort studied (Hojsted & Sjogren, 2007).
While addiction prevalence rates vary, Reid and colleagues (2002) found prescription opioid abuse in 24% to 31% of non-cancer chronic pain patients. Katz and colleagues (2003), on the other hand, found drug abuse in 43% of patients maintained on chronic opioid therapy. Another study at the Veterans Administration (VA) Medical Center in Seattle showed that 34% of pain clinic patients using chronic opiates met abuse criteria (Chabal et al., 1997). In addition, a retrospective study of 470 patients in a pain management program highlighted that 45% had abnormal urine screens, indicating opioid abuse (Michna et al., 2007).
Purdue’s deceptive sales tactics led to over 300 lawsuits concerning OxyContin to be filed against their company as of 2003 (General Accounting Office, 2003). The fraudulent misrepresentation of addiction rates led to Purdue Pharma and its affiliate to plead guilty to criminal charges of misbranding and to pay $634 million in fines (Van Zee, 2009).
Recreational OxyContin Use Overtakes Broad Swaths of the Country
Drug abuse escalated with the increasing commercial success and accessibility of OxyContin, as “drug abusers learned how to simply crush the controlled-release tablet and swallow, inhale, or inject the high-potency opioid for an intense morphine-like high” (Van Zee, 2009). As described by one user in Paul Tough’s 2001 New York Times piece, “The Alchemy of OxyContin,” “'When you get that oxy buzz, it's a great feeling. You're happy. Your body don't hurt. Nothing can bring you down. It's a high to where you don't have to think about nothing. All your troubles go away. You just feel like everything is lifted off your shoulders.’'
Prescribing practices differed by geographical area, with patients in Alabama, Maine, West and southwestern Virginia, and Eastern Kentucky being prescribed Oxycontin at five to six times the national average (DEA, 2000). In addition to rural Maine and the rust-belt counties of eastern Ohio and western Pennsylvania, the Appalachian area of Virginia, West Virginia, and Eastern Kentucky were disproportionately hit, so much so that in 2015 Purdue agreed to pay Kentucky $24 million in a civil lawsuit accusing the drugmaker of misleading doctors and patients about their blockbuster drug, leading to an epidemic of addiction, especially among coal miners who were prescribed OxyContin (CBS News, 2015; Tough, 2001). The qualities uniting these areas include dismal economic opportunity, high unemployment rates, histories of prescription drug abuse, possessing large populations of disabled people, having little access to rehabilitation clinics, and being “far from the network of Interstates and metropolises through which heroin and cocaine travel” (Tough, 2001).
Although once labeled “hillbilly heroin” and confined to remote locales, OxyContin abuse began to spread nationally, and by 2004, became the most recreationally used prescription opioid in the United States (Cicero, Inciardi, & Munoz, 2005). The liberalization of prescription opioid use for non-malignant pain led to skyrocketing availability and rates of abuse in other opioids as well. Van Zee (2009) reports that there was a 402%, 226%, and 73% increase in oxycodone, fentanyl, and morphine prescribing between 1997 and 2002, with 641%, 346%, and 113% increases in hospital emergency department mentions of fentanyl, oxycodone, and morphine, respectively, during the same time period (Gilson et al., 2004). By 2002, national deaths from prescription opioid overdoses eclipsed those of heroin and cocaine (Paulozzi, Budnitz, & Yongli, 2006).
Alarmingly, despite only comprising five percent of the global population, America uses 85% of all opioids worldwide (Real Leaders, 2016). With recent increased government regulation, the opioid epidemic has morphed and evolved: “Like a shrewd virus that mutates once it confronts a vaccine, Americans' addiction to opioids has survived the government crackdown on OxyContin and fled to the seedy asylum of heroin. It's a kind of evolution in retrograde, with pill users turning to an old 20th-century scourge that once flourished in urban decay and is uglier, more stigmatized, and more lethal than its pharmaceutical counterpart” (Mariani, 2015).
A Complete Paradigm Shift is Needed
Because the for-profit medical enterprise operates on corporate monopoly and revolves around publicly traded pharmaceutical companies, maximizing shareholder profits, rather than promoting wellness, is their primary objective. Big Pharma counts on a perpetual cycle of future revenue by selling drugs which engender new symptoms and create lifetime users.
Thus, the enemy of our disease management system, which centers around chemical magic-bullet cocktails, is open-source, biocompatible, freely extracted and accessible botanical medicine, since the medical-pharmaceutical industrial complex is based on intellectual property control over synthetic, patentable medications.
As published in the Journal of the American Medical Association, 106,000 hospitalized patients die each year from the properly prescribed used of medications due to adverse drug events, excluding “errors in drug administration, noncompliance, overdose, drug abuse, therapeutic failures, and possible ADRs [adverse drug reactions]” (Lazarou, Pomeranz, & Corey, 1998). Serious ADRs occur in 6.7% of hospitalized patients, and in 1994, ADRs represented between the fourth and sixth leading cause of death (Lazarou et al., 1998).
Likewise, because opioids are inconsistent in efficacy and have well-characterized side effect profiles, including gastrointestinal distress, sedation, respiratory depression, hormonal and immunological toxicity, opioid-induced hyperalgesia, and a high incidence of abuse, addiction, and fatal overdose, a more natural approach is warranted (Ballantyne, 2006).
Evidence-Based Natural Analgesics
As indexed in GreenMedInfo’s extensive databases, there are a wide array of natural, non-toxic, scientifically validated botanical and nutraceutical agents that can be substituted in place of potentially lethal pharmaceutical poisons.
Zingiberaceae family
For instance, members of the Zingiberaceae family, including turmeric (Curcuma longa), ginger (Zingiber officinale), and galangal (Alpinia galanga), have long been analgesic staples in traditional medical systems. A systematic review and meta-analysis from the Journal of Nutrition found that Zingiberaceae extracts were effective in reducing subjective chronic pain, with a dose-response relationship emerging (Lakhan, Ford, & Tepper, 2015). The authors conclude, “Our findings indicated that Zingiberaceae extracts are clinically effective hypoalgesic agents and the available data show a better safety profile than non-steroidal anti-inflammatory drugs” (Lakhan et al., 2015).
Gingerol and zingerone, the primary active anti-inflammatory constituents in ginger, modulate production of inflammatory leukotrienes and prostaglandins and inhibit NF-κB (Lantz et al., 2007; Hsiang et al., 2013; Thomson et al., 2002). For example, a systemic review of randomized controlled trials (RCTs) demonstrated that ginger powder, administered during the first three to four days of the menstrual cycle, is effective for dysmenorrhea (Daily et al., 2015). Other studies have shown that ginger exerts analgesic and anti-inflammatory effects in delayed onset muscle soreness (DOMS) induced by eccentric exercise, or physical exertion to which athletes were unaccustomed (Hoseinzadeh et al., 2015).
Curcuminoids, on the other hand, which are polyphenol derivatives of the spice turmeric, may reduce pain through ATP-sensitive potassium channels and through both opioid and non-opioid mediated mechanisms (De Paz-Campos et al., 2012; Tajik, Tamaddonfard, & Hamzeh-Gooshchi, 2007). In addition, one of the pleiotropic actions of curcumin is to down-regulate nuclear factor (NF)-κB and cyclooxygenase 2 (Cox-2), preventing the expression of inflammatory eicosanoid pain mediators (Sandur et al., 2007; Samad & Abdi, 2001). Another systematic review and meta-analysis of eight RCTs, including 606 patients, elucidated that curcuminoids have been found to significantly reduce pain independent of the dose administered or the duration of treatment (Sahebkar & Henrotin, 2015). For example, pilot human trials have shown efficacy in improving symptoms of both rheumatoid arthritis and inflammatory bowel disease (Chandran & Goel, 2012; Holt, Katz, & Kirschoff, 2005). Curcumin has also been shown to prevent and mitigate diabetic mellitus and its complications, including diabetic neuropathic pain, by reversing abnormalities in voltage-gated sodium channels (VGSCs) in neurons of the injured dorsal root ganglion (DRG) (Meng et al., 2015).
Boswellia serrata
The gum resin extracted from the bark of a traditional Ayurvedic medicine, Boswellia serrata or Indian frankincense, is a potent anti-inflammatory, analgesic, and anti-arthritic agent (Basch et al., 2004). According to Prahavathi et al. (2014), “Its main pharmacologically active ingredients are α and β boswellic acid and other pentacyclic triterpenic acids which have been shown to inhibit pro-inflammatory processes by their effects on 5-lipooxygenase, cyclo-oxygenase and the complement system”. In particular, the boswellic acid acetyl-11-keto-β-boswellic acid (AKBA) inhibits 5-lipoxygenase (5-LOX), a crucial catalyst in the inflammatory cascade (Ernst, 2008). Researchers go so far as to suggest that Boswellia serrata extract (BSE) is a viable alternative to NSAIDs (Abdel-Tawab, Werz, & Schubert-Zsilavecz, 2011).
Boswellia has been shown to significantly increase pain threshold and pain tolerance compared to placebo, and proprietary Boswellia extracts have significantly improved pain scores and functional ability in osteoarthritis subjects after just seven days of supplementation (Sengupta et al., 2010; Prahavathi et al., 2014). Researchers corroborated their human findings with in vitro data showing that Boswellia gum resins inhibit the cartilage degrading enzyme matrix metalloproteinase (MMP)-3 and reduce inflammation via suppression of cell adhesion molecule ICAM-1 (Sengupta et al., 2010).
Medical Marijuana as an Opioid Alternative
Cannabis sativa contains approximately one hundred distinct cannabinoids, which influence the endogenous endocannabinoid system, and thus modulate mood, social behavior, cognition, motor function, and perception of pain (Wei, 2017; Steafano, Liu, & Goligorsky, 1996). CB1 receptors are largely localized in regions of the brain that control higher executive functions, motor functions, and nociception, meaning the response of the sensory nervous system to pain (Pertwee, 1997). In contrast, CB2 cannabinoid receptors are found predominantly in non-neuronal tissue, such as on immune cells, where they govern immunosuppression and inhibit neurotransmission of pain (Pertwee, 1997; Pertwee, 2001).

According to Pertwee (2010), there is potent evidence in animal models that cannabinoids can induce antinociception in acute and tonic pain models by activating CB1 receptors in the amygdala, periaqueductal grey, thalamus, superior colliculus, and both the rostral ventromedial medulla and A5 noradrenergic group of the brainstem. In fact, there is proof that these receptors co-localize with substance P and calcitonin gene-related peptide (CGRP), both of which function in the transmission of pain and neuroinflammation (Pertwee, 2010). Another mechanism by which cannabinoids may inhibit pain is via inhibition of inflammatory eicosanoid release by activation of CB2 receptors on immune cells located in the vicinity of nociceptive neurons. For instance, CB2 may inhibit mast cell degranulation and liberation of inflammatory agents or favorably influence expression of anti-inflammatory agents (Molina-Holgado et al., 1999).
A systemic review of randomized controlled trials examining the use of cannabis in non-cancer chronic pain, including patients with neuropathic pain, rheumatoid arthritis, fibromyalgia, mixed chronic pain, and neuropathic pain, demonstrated a significant improvement in pain and often sleep compared to placebo (Lynch & Campbell, 2009). Another comprehensive meta-analysis of inhaled cannabis supports its efficacy in the short-term treatment of neuropathic pain, and in his survey of randomized controlled trial results, Aggarwal champions its long-term medical use for chronic pain conditions (Andreae et al., 2015; Aggarwal, 2013).
In fact, in 2014, the Italian government authorized use of cannabis for “for all chronic pain conditions, as well as for spasticity, cachexia, and anorexia among AIDS and cancer patients, ocular hypertension in glaucoma, the alleviation of spasms in Tourette syndrome, and some types of epilepsy” and even dedicated its Military Chemical-Pharmaceutical Factory to cultivate lower-cost cannabis (Fanelli et al., 2017). An explorative retrospective analysis of one of the Italian cohorts of 614 chronic intractable pain patients showed that 64.7% reported improvement associated with cannabis therapy, primarily administered as tea, in association with other pain treatments (Fanelli et al., 2017). The study authors conclude that cannabis therapy is safe and effective, given that no severe side effects were observed, and that 76.2% of patients continued cannabinoid therapy at follow-up (Fanelli et al., 2017).
Importantly, studies have demonstrated that implementation of operational medical marijuana laws, as defined by allowances for active dispensaries or home cultivation, was associated with reductions in opioid positivity among 21- to 40-year-old fatally injured drivers, such that legalizing medical marijuana “may reduce opioid use and overdose” (Kim et al., 2016). This is echoed by an average 13 percent drop in opioid overdoses in states where cannabis has been legalized (Williams, 2017).  Further, analysis of the hospital records in 27 states revealed that hospitalization rates due to painkiller abuse and addiction declined 23 percent on average in states offering medical marijuana (Williams, 2017).
An article in the JAMA Internal Medicine likewise found a 25 percent decrease in opioid deaths in states with legal marijuana (Bachuber et al., 2014). In contrast, marijuana has never been linked to a single fatal overdose (Bachhuber et al., 2014). Moreover, a study illuminated that doctors write 1800 fewer opioid prescriptions for patients per year in medical marijuana states (Bradford & Bradford, 2016). The researchers state, “National overall reductions in Medicare program and enrollee spending when states implemented medical marijuana laws were estimated to be $165.2 million per year in 2013” (Bradford & Bradford, 2014).
Because cannabis has analgesic and immunomodulatory effects and directly interacts with our endogenous pain relief system, it has immense therapeutic promise to replace many of the pharmaceutical toxins that are currently being employed as standards of care.
In addition to the aforementioned natural remedies, there are 125 natural substances with analgesic properties catalogued on the GreenMedInfo database, such as lavender, rose, fennel, magnesium, and cinnamon, any of which would help restore balance and ameliorate pain without the devastating effects of opioids.
Lastly, instead of applying the symptom-suppressive lens of conventional biomedicine and putting band-aids on bullet wounds, it would be prudent for us to address the underlying causes of dysfunction, such as toxicant burden, micronutrient depletion, non-restorative sleep, and deviation from the ancestral lifestyle to which we are evolutionary accustomed.
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