Vitamin C and Cancer

Source: iHealthTube.com
August 23, 2017

Find out what new research is showing about the connection between vitamin C and cancer, as well as stress and heart health. And could eating less help you live longer? Find out what scientists are learning when it comes to longevity.

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Treating Advanced Prostate Cancer with Diet: Part 1

Source: NutritionFacts.org
August 23, 2017

Dr. Dean Ornish showed that a plant-based diet and lifestyle program could apparently reverse the progression of prostate cancer; this was for early stage, localized, watch-and-wait cancer. What about for more advanced stage life-threatening disease?

Prostate Cancer BREAKTHROUGH: Three natural substances destroy cancer cells

Source: TheHealthRanger
June 30, 2017

Breakthrough research finds that prostate cancer cells are destroyed by a combination of three natural compounds found in a fruit peel, a berry skin and a root tuber. These three anti-cancer nutrients are safe, affordable and readily available to everyone. So why isn’t the entire medical industry talking about this prostate cancer breakthrough? Because there’s NO MONEY to be made from making people well using low-cost anti-cancer foods and plants. Stay informed at AntiCancer.news.

Natural Alternatives to Deadly Prescription Opiates

Natural Alternatives to Deadly Prescription Opiates
Source: GreenMedInfo.com
GMI Research Group
July 23, 2017

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.

Read More At: GreenMedInfo.com
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In Defense of Coconut Oil: Rebuttal to USA Today

In Defense of Coconut Oil: Rebuttal to USA Today

Source: GreenMedInfo.com
Ali La Vere
June 20, 2017

By now, I’m sure you’ve seen the USA Today article entitled, “Coconut oil isn’t healthy. It’s never been healthy“. Fear-mongering, attention-grabbing headlines certainly sell copy, but do not make for evidence-informed, high quality science reporting.

As I expressed in my recent post on social media,

“The internet is full of erroneous claims. Science writers who forgo the nuances of empirical findings in the interest of sensational headlines.

False extrapolations made by people unequipped to interpret the research. Speculations by bloggers who missed the correlation-does-not-equal-causation lesson in epidemiology.

Over-generalizations from poorly designed, low quality in vitro and animal studies and studies that failed the test of statistical significance. Industry-funded, conflict-of-interest ridden rhetoric.

From eating for your blood type, to saturated fat causing heart disease, to heart-healthy whole wheat, to coffee causing gluten cross reactivity—in the natural and mainstream health communities alike, people take an idea and run with it without once going back to the primary and secondary literature to verify its scientific veracity.

The lack of scientific rigor that abounds in many corners of natural medicine is part of the reason that alternative medicine is marginalized by mainstream medicine. However, conventional medicine is equally culpable when it comes to its standards of care lacking a firm evidence-base.

I hope to fill this void, apply a scientific eye, and impart credence to therapeutic nutrition and holistic medicine by substantiating all my claims with high quality scientific data—instead of pulling statements out of thin air, which sadly is commonplace with headline-grabbing, yet substantive discussion-lacking online articles.”

The USA Today article, written in response to an American Heart Association (AHA) statement advising Americans to replace saturated fat with omega-6 rich polyunsaturated fatty acids from vegetable oils, exemplifies the lack of journalistic integrity, rushing to conclusions, and flagrant misrepresentation of the data to which I was referring.

The Omega-3 to Omega-6 Ratio Determines Inflammatory Potential

Contrary to the implications of this USA Today piece, the evidence has elucidated that omega-6 fatty acids, which occur in the corn, cottonseed, canola, safflower, sunflower, and soybean oil that the AHA was recommending, promote carcinogenesis, whereas omega-3 fatty acids inhibit cancer development (Seaman, 2002). Hence, the Standard American Diet, rich in omega-6 fatty acid consumption, generates the pro-inflammatory state that facilitates tumorigenesis (Rose, 1997).

The detrimental effects of omega-6s are articulated by Fernandes and Venkatraman (1993), with,

“The increased consumption of many vegetable oils particularly of the n-6 series is…viewed as pro-inflammatory and is suspected as one of the possible causes for the rise in certain malignant tumors, rheumatoid arthritis and autoimmune diseases primarily due to the increased production of pro-inflammatory cytokines” (p. S19).

In contrast, long-chain omega-3 fatty acids from wild-caught fatty seafood, such as docosahexaenoic acid (DHA) can modify dynamics of the lipid bilayer, including elastic compressability and membrane permeability, promote membrane fluidity, and favorably modify membrane-bound protein activity (Stillwell & Wassall, 2003).

Thus, DHA is preventive in many inflammatory disorders, including cancer, cardiovascular disease, and neurodegenerative disease (Stillwell & Wassal, 2003). Specifically, DHA mitigates neuro-inflammation as it facilitates more efficient nerve cell communication (Crawford et al., 2013). The brains of patients with Alzheimer’s disease (AD) are deficient in DHA, and loss of structural and functional integrity of the brain correlates with loss of DHA concentrations in cell membranes in these patients (Seaman, 2002).

DHA and its long chain omega-3 precursor, eicosapentaenoic acid (EPA), are likewise involved in modulation of immune responses. In one study, supplementation of these fatty acids prolonged remission of systemic lupus erythematous (SLE) (Das, 1994). In another autoimmune disease, rheumatoid arthritis, omega-3 supplementation was found to suppress the production of inflammatory cytokines and eicosanoids involved in the pathogenesis of the disease (Morin, Blier, & Fortin, 2015). Mechanistically, long chain omega-3 fatty acids suppress proliferation of pathogenic T cells and inhibit synthesis of inflammatory cytokines such as tumor necrosis factor (TNF), interleukin-1 (IL-1), and interleukin-2 (IL-2) (Das, 1994).

The dietary balance of omega-6 to omega-3 fatty acids, which compete for incorporation into the phospholipid bilayer of cellular membranes, is integral for restoration of immune health and for prevention of long-latency, chronic, and degenerative diseases.

In order to generate optimal ratios of omega-6 to omega-3 fatty acids, ditch the toxic industrialized vegetable oils, and moderate consumption of grains and seeds as well, since they contain linoleic acid, the precursor to the omega-6 fatty acid arachidonic acid.

As I illustrated above, arachidonic acid is processed by the enzyme cyclooxygenase (COX) to produce pro-inflammatory signaling molecules called eicosanoids, including leukotrienes, prostaglandins, and thromboxanes. Omega-3 fatty acids, on the other hand, promote the production of less inflammatory mediators. Therefore, USA Today’s recommendation to increase consumption of pro-inflammatory vegetable oils, amidst an epidemic of inflammatory chronic diseases, is negligent and irresponsible.

Applying an Ethnographic and Evolutionary Biology Lens

Of all the diets, an ancestral paleolithic diet reminiscent of ancient foragers has the most optimal omega-6 to omega-3 ratio, of 1:1 (Simopoulos, 1991). Traditional hunter-gatherer cultures whose diets are composed of grass-fed game, pasture-raised poultry and eggs, wild-caught seafood, organic, local fruits and vegetables, roots and tubers, nuts and seeds are virtually free of the long-latency, degenerative diseases that plague Westerners.

Eskimos, for instance, who eat a high fish-based diet replete in omega-3s and very low in omega-6s, do not suffer from any of the diseases of modernity, including cancer, diabetes, heart disease, diverticulitis, appendicitis, gallstones, or autoimmune diseases such as multiple sclerosis, rheumatoid arthritis, psoriasis, or ulcerative colitis (Sinclair, 1981; Nettleton, 1995; Calder, 1998).

In contrast, the Standard American Diet, customary in Western cultures where non-communicable chronic diseases reach epidemic levels, has an omega-6 to omega-3 fatty acid ratio ranging from 10:1 to 25:1 (Simopoulos, 1991). This is largely due to the inclusion of pro-inflammatory, high-heat processed vegetable oils, which are subject to chemically-laden processes such as caustic refining, bleaching, and degumming, and then have to be chemically deodorized to negate rancidity.

In addition to minimizing vegetable oil intake, incorporating plenty of wild-caught, cold-water fatty fish, including mackerel, salmon, herring, caviar, and sardines, can enhance omega-3 levels. Crawford (1968) also demonstrated that wild animals eating their native diets have significantly more omega-3s compared to domesticated livestock. Grass-fed meat, for example, is replete in omega-3 fatty acids and antioxidants such as beta carotene and vitamin E compared to its conventional corn-fed counterparts, so incorporating grass-fed meat into your diet can restore balance in your fatty acid ratio (Daley et al., 2010).

Busting the Cholesterol Myth

Of note, is that the USA Today article vilified coconut oil on the basis that it raises LDL cholesterol. However, the most recent Dietary Guidelines Advisory Committee (DGAC) removed dietary cholesterol as a nutrient of concern, given that there is “no appreciable relationship between dietary cholesterol and serum cholesterol or clinical cardiovascular events in general populations,” so cholesterol content should not deter you from consumption of saturated fat (Mozaffarian & Ludwig, 2015, p. 2421).

Low total cholesterol, formerly believed to be protective against cardiovascular disease, has been demonstrated to have a litany of ill effects. In particular, women with a total cholesterol below 195 mg/dL have a higher risk of mortality compared to women with cholesterol above this cut-off (Petrusson, Sigurdsson, Bengtsson, Nilsen, & Getz, 2012).

Low cholesterol has been correlated with Alzheimer’s disease, dementia, suicide, homicide, accidental deaths, and morbid depression (Boscarino, Erlich, & Hoffman, 2009; Morgan, Palinkas, Barrett-Connor, & Wingard, 1993, Mielke et al., 2005; Seneff, Wainwright, & Mascitelli, 2011).

In a group of men 50 years and older, researchers found depression to be three times more common in the group with low plasma cholesterol (Morgan, Palinkas, Barrett-Connor, & Wingard, 1993). Shockingly, men with total cholesterol below 165 m/dL were also found to be seven times more likely to die prematurely from unnatural causes, including suicide and accidents (Boscarino, Erlich, & Hoffman, 2009).

In fact, Morgan, Palinkas, Barrett-Connor, and Winged (1993) articulate this with, “In several clinical trials of interventions designed to lower plasma cholesterol, reductions in coronary heart disease mortality have been offset by an unexplained rise in suicides and other violent deaths” (p. 75).

In essence, in progressive circles, the cholesterol-demonizing, artery-clogging model of heart disease has been redacted in favor of one where inflammation leads to endothelial and vascular smooth muscle dysfunction as well as oxidative stress. Like firefighters at a fire, cholesterol is present at the scene of the crime, but it is not the perpetrator—rather, it is a protective antioxidant element that repairs damage to arteries.

Moreover, cholesterol is an important precursor to our steroid hormones and bile acids, a membrane constituent that helps maintain structural integrity and fluidity, and an essential component for transmembrane transport, cell signaling, and nerve conduction.

Saturated Fat is Not Bad For You

Further, the recommendations of the AHA are especially surprising in light of the results of the Minnesota Coronary Experiment performed forty years ago, where the saturated fat in the diets of 9000 institutionalized mental patients was replaced with polyunsaturated fats in the form of corn oil. A 2010 re-evaluation of the data from this experiment was published in the British Medical Journal (Ramsden et al., 2016).

According to this re-analysis, these patients experienced a 22% higher risk of death for each 30 mg/dL reduction in serum cholesterol (Ramsden et al., 2016). Thus, although substituting omega-6 fats in place of saturated fat led to reductions in cholesterol, these patients suffered worse health outcomes, highlighting that cholesterol is not the villain it was formerly construed to be.

What’s more, although the USA Today article declares the dangers of saturated fat, a recent meta-analysis in the American Journal of Clinical Nutrition, which compiled data from 21 studies including 347,747 people that were followed for an average of 14 years, concluded that there is no appreciable relationship between saturated fat consumption and incidence of cardiovascular disease or stroke (Siri-Tarino, Sun, Hu, & Krauss, 2010).

Another meta-analysis published in 2015 in the British Journal of Medicine concluded that there is no association between saturated fat and risk of cardiovascular disease, coronary heart disease, ischemic stroke, type 2 diabetes, or all-cause mortality (the risk of death from any cause) (de Souza et al., 2015).

Along similar lines, a trial published in the American Journal of Nutrition in 2016 showed that eating a high fat diet, and deriving a large proportion of calories from saturated fat, improved biomarkers of cardiometabolic risk and insulin resistance, such as insulin, HDL, triglycerides, C-peptide, and glycated hemoglobin (Veum et al., 2016). The researchers conclude, “Our data do not support the idea that dietary fat per se promotes ectopic adiposity and cardiometabolic syndrome in humans” (Veum et al., 2016).

In actuality, saturated fat has been demonstrated to exert beneficial effects on levels of triglycerides and high-density lipoprotein cholesterol (HDL), the latter of which has been characterized as the “good cholesterol” that scavenges or transports cholesterol deposited in the bloodstream back to the liver (Mensink, Zock, Kester, & Katan, 2003). Saturated fat has also been shown to elicit minimal effects on apolipoprotein B, a risk factor for cardiovascular disease, relative to carbohydrates (Mensink, Zock, Kester, & Katan, 2003).

In addition, in a recent article in the Annals of Nutrition and Metabolism, an expert panel held jointly between the Food and Agriculture Organization (FAO) and World Health Organization (WHO) reviewed the relationship between saturated fat and coronary heart disease (CHD) (FAO/WHO, 2009).

From their examination of epidemiological studies, they found that saturated fatty acid intake was not significantly correlated with coronary heart disease events or mortality (FAO/WHO, 2009). Similarly, from their investigation of intervention studies, which are more powerful in that they can prove causality, they found that incidence of fatal coronary heart disease was not reduced by low-fat diets (FAO/WHO, 2009).

According to Mozaffarian and Ludwig (2015), “The 2015 DGAC report tacitly acknowledges the lack of convincing evidence to recommend low-fat–high-carbohydrate diets for the general public in the prevention or treatment of any major health outcome, including heart disease, stroke, cancer, diabetes, or obesity” (p. 2422).

Part of this reversal in guidelines is based on the fact that replacing protein or carbohydrates with healthy fats in excess of the current 35% of the daily caloric fat limit reduces risk of cardiovascular disease (Appel et al., 2005; Estruch et al., 2013).

In a similar vein, “The 2015 DGAC report specifies that, ‘Consumption of ‘low-fat’ or ‘nonfat’ products with high amounts of refined grains and added sugars should be discouraged’” (Mozaffarian & Ludwig, 2015, p.2422). Despite new guidelines, the Nutrition Facts Panel still employs the outdated 30% limit on dietary fat, which Mozaffarian and Ludwig (2015) remark has been “obsolete for more than a decade” (p.2422).

Coconut Oil Doesn’t Negate Health—It Engenders It

Not only do these meta-analyses put the nail in the coffin as far as saturated fat causing heart disease, but a plethora of health benefits have been elucidated in the scientific literature regarding coconut oil consumption. For instance, the following studies, as catalogued in the GreenMedInfo database, have revealed metabolic, immunomodulatory, and cognitive benefits of the dietary inclusion of coconut oil.

For instance, extra virgin coconut oil consumption has been demonstrated to significantly reduce body mass index (BMI) and waist circumference (WC) and produce significant increases in concentrations of HDL cholesterol in patients with coronary artery disease (CAD) (Cardoso et al., 2015). Another study by Liau in colleagues (2011) concluded that virgin coconut oil is efficacious for the reduction of waist circumference, especially in a male cohort. Likewise, a study by Assunção and colleagues (2009) demonstrated that dietary coconut oil reduces visceral adiposity and elevates HDL cholesterol in women, thus improving both anthropometric and biochemical risk factors for metabolic syndrome.

In rodent models, dietary virgin coconut oil improves glycemic control in high fructose fed rats, and is postulated to be “an efficient nutraceutical in preventing the development of diet induced insulin resistance and associated complications possibly through its antioxidant efficacy” (Narayanankutty et al., 2016). Research supports the use of coconut oil for obesity, dyslipidemia, insulin resistance, hypertension, and pathologically elevated LDL, all of which constitute risk factors for diabetes, cardiovascular disease, and Alzheimer’s, the last of which is being re-conceptualized as type 3 diabetes (Fernando et al., 2015).

In addition, in a prospective study of patients with Alzheimer’s, improvements in cognitive function were observed for patients administered extra virgin coconut oil, since “medium chain triglycerides are a direct source of cellular energy and can be a nonpharmacological alternative to the neuronal death for lack of it, that occurs in Alzheimer patients” (Yang et al., 2015). Notably, the hormones, or cytokinins, and phenolic compounds found in coconut may prevent aggregation of amyloid-β peptide into plaques, thus arresting a critical step in pathogenesis of Alzheimer’s (Fernando et al., 2015). Research also suggests that coconut oil may directly stimulate ketogenesis in astrocytes and provide fuel to neighboring neurons as a consequence, thus improving brain health (Nonaka et al., 2016). On a different note, coconut oil mitigates amyloid beta toxicity in cortical neurons by up-regulating signaling of cell survival pathways (Nafar, Clarke, & Mearow, 2017).

Lastly, studies have illuminated anti-inflammatory, analgesic, antibacterial, and anti-pyretic properties of virgin coconut oil (Intahphuak, Khonsung, & Panthong, 2010; Ogbolu et al., 2007). Thus, unless you are part of the minority of the population that carries the APOE4 allele, a polymorphism that confers increased risk with saturated fat consumption, there is no reason to avoid coconut oil or saturated fat (Barberger-Gateau et al., 2011). Thus, instead of trashing your coconut oil, do yourself a favor and eat an extra helping—your body will thank you.

Read more At: GreenMedInfo.com
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References

Appel, L.J., Sacks, F.M., Carey, V.J., Obarzanek, E. Swain, J.F., Miller, E.R. 3rd,…OmniHeart Collaborative Research Group. (2005). Effects of protein, monounsaturated fat, and carbohydrate intake on blood pressure and serum lipids: results of the OmniHeart randomized trial. Journal of the American Medical Association, 294(19):2455-2464.

Assunção, M.L., Ferreira, H.S., dos Santos, A.F., Cabral, C.R., & Florêncio, T.M.M.T. (2009). Effects of dietary coconut oil on the biochemical and anthropometric profiles of women presenting abdominal obesity. Lipids, 44(7), 593-601.

Barberger-Gateua, P., Samieri, C., Feart, C., & Plourde, M. (2012). Dietary omega 3 polyunsaturated fatty acids and Alzheimer’s disease: interaction with apolipoprotein E genotype. Current Alzheimer’s Research, 8(5), 479-491.

Calder, P.C. (1998). Dietary fatty acids and the immune system. Nutritional Reviews, II, S70-S83.

Cardoso et al. (2015). A coconut extra virgin oil-rich diet increases HDL cholesterol and decreases waist circumference and body mass in coronary artery disease patients. Nutrition Hospitals, 32(5), 2144-2152. doi: 10.3305/nh.2015.32.5.9642.

Crawford, M.A., Broadhurst, C.L., Guest, M., Nagar, A., Wang, Y., Ghebremeskel, K., & Schmidt, W. (2013). A quantum theory for the irreplaceable role of docosahexaenoic acid in neural cell signaling throughout evolution. Prostaglandins Leukotrienes and Essential Fatty Acids, 88(1), 5-13.

Daley, C. A., Abbott, A., Doyle, P. S., Nader, G. A., & Larson, S. (2010). A review of fatty acid profiles and antioxidant content in grass-fed and grain-fed beef. Nutrition Journal, 9(1), 10.

Das, U.N. (1994). Beneficial effect of eicosapentaenoic and docosahexaenoic acids in the management of systemic lupus erythematosus and its relationship to the cytokine network. Prostaglandins Leukotrienes and Essential Fatty Acids, 51(3), 207-213.

de Souza et al. (2015). Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: a systematic review and meta-anlaysis of observational studies. British Medical Journal, 351.

Estruch, R., Ros, E., Salas-Salvado, J., Covas, M.I., Corella, D., Aros, F.,…PREDIMED Study Investigators. (2013). Primary prevention of cardiovascular disease with a Mediterranean diet. New England Journal of Medicine, 368(14), 1279-1290. doi: 10.1056/NEJMoa1200303

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Fernando, W.M.A.D.B., Martins, I.J., Goozee, K.G., Brennan, C.S., Jayasena, V., & Martins, R.N. (2015). The role of dietary coconut for the prevention and treatment of Alzheimer’s disease: potential mechanisms of action. British Journal of Nutrition, 1-14.
Intahphuak, S., Khonsung, P., & Panthong, A. (2010). Anti-inflammatory, analgesic, and antipyretic activities of virgin coconut oil. Pharmacological Biology, 48(2), 151-157.

Kalmijn, S., Feskens, E.J.M., & Kromhout, D. (1997). Polyunsaturated fatty acids, antioxidants, and cognitive function in very old men. American journal of Epidemiology, 145, 33-41.

Liau, K.M., Lee, Y.Y., Chen, C.K., & Rasool, A.H.G. (2011). An open-label pilot study to assess the efficacy and safety of virgin coconut oil in reducing visceral adiposity. ISRN Pharmacology. doi: 10.5402/2011/949686
Mensink, R.P., Zock, P.L., Kester, A.D., & Katan, M.B. (2003). Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials. American Journal of Clinical Nutrition, 77(5), 1146-1155.

Mielke, M.M., Zandi, P.P., Sjogren, M., Gustafson, D., Ostling, S., Steen, B., & Skoog, I. (2005). High total cholesterol levels in late life associated with a reduced risk of dementia. Neurology, 64(10), 1689-1695.

Mozaffarian, D., & Ludwig, D.S. (2015). The 2015 US Dietary Guidelines: Lifting the Ban on Total Dietary Fat. Journal of the American Medical Association, 313(24), 2421-2422.

Morin, C., Blier, P.U., & Fortin, S. (2015). Eicosapentaenoic acid and docosapentaenoic acid monoglycerides are more potent than docosahexaenoic acid monoglyceride to resolve inflammation in a rheumatoid arthritis model. Arthritis Research Therapies, 17, 142. doi: 10.1186/s13075-015-0653-y.

Morgan, R.E., Palinkas, L.A., Barrett-Connor, E.L., & Wingard, D.L. (1993). Plasma cholesterol and depressive symptoms in older men. The Lancet, 341(8837), 75-79. doi:10.1016/0140-6736(93)92556-9

Nafar, F., Clarke, J.P., & Mearow, K.M. (2017). Coconut oil protects cortical neurons from amyloid beta toxicity by enhancing signaling of cell survival pathways. Neurochemical International, 105, 64-79. doi: 10.1016/j.neuint.2017.01.008.

Narayanankutty, A., Mukesh, R.K., Ayoob, S.K., Ramavarma, S.K., Suseela, I.M., Manalil, J.J.,…Raghavamenon, A.C. (2016). Virgin coconut oil maintains redox status and improves glycemic conditions in high fructose fed rats. Journal of Food Science and Technology, 53(1), 895-901.

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Ogbolu, D.O., Oni, A.A., Daini, O.A., & Oloko, A.P. (2007). In vitro antimicrobial properties of coconut oil on Candida species in Ibadan, Nigeria. Journal of Medical Foods, 10(2), 384-387.

Petrusson, H., Sigurdsson, J.A., Bengtsson, C., Nilsen, T.I., & Getz, L. (2012). Is the use of cholesterol in mortality risk algorithms in clinical guidelines valid? Ten years prospective data from the Norwegian HUNT 2 study. Journal of the Evaluation of Clinical Practice, 18(1), 159-168.

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Yang, H.Y., de la Rubia Orti, J.E., Sabater, P.S., Castillo, S.S., Rochina, M.J., Ramon, N.M., & Montoya-Castilla, I. (2015). Coconut oil: Non-alternative drug treatment against Alzheimer’s disease. Nutrition in Hospitals, 32(6), 2822-2877.

Ali Le Vere holds dual Bachelor of Science degrees in Human Biology and Psychology, minors in Health Promotion and in Bioethics, Humanities, and Society, and is a Master of Science in Human Nutrition and Functional Medicine candidate. Having contended with chronic illness, her mission is to educate the public about the transformative potential of therapeutic nutrition and to disseminate information on evidence-based, empirically rooted holistic healing modalities. Read more at @empoweredautoimmune on Instagram and at www.EmpoweredAutoimmune.com: Science-based natural remedies for autoimmune disease, dysautonomia, Lyme disease, and other chronic, inflammatory illnesses.

Acupuncture found to be a safe and effective alternative to dangerous painkiller drugs in hospitals

Image: Acupuncture found to be a safe and effective alternative to dangerous painkiller drugs in hospitals
Source: NaturalNews.com
Earl Garcia
June 23, 2017

A recent study published in MJA.com.au revealed that acupuncture may serve as a safe and effective alternative to pain-relieving drugs for patients arriving at a hospital’s emergency room. As part of the study, a team of researchers led by the Royal Melbourne Institute of Technology in Melbourne, Australia that examined 528 patients with acute low back pain, migraine, or ankle sprains who were rushed to emergency rooms of various hospitals between January 2010 and December 2011.

The participants who rated their pain levels at four out of a 10-point scale received three types of treatment, which involved acupuncture alone, pharmacotherapy alone, or a combination of both. The study revealed that less than 40 percent of patients across all treatment groups reported significant reductions in pain after one hour of treatment, while more than 80 percent continued to have a pain rating of four. However, the research team noted that most patients rated their therapies acceptable after a treatment duration of 48 hours. According to the study, nearly 83 percent of patients in the acupuncture only-group said they would repeat the treatment, compared with only 78.2 percent in the pharmacotherapy-only group, and 80.8 percent in the combination treatment group.

“While acupuncture is widely used by practitioners in community settings for treating pain, it is rarely used in hospital emergency departments. Emergency nurses and doctors need a variety of pain-relieving options when treating patients, given the concerns around opioids such as morphine, which carry the risk of addiction when used long-term. Our study has shown acupuncture is a viable alternative, and would be especially beneficial for patients who are unable to take standard pain-relieving drugs because of other medical conditions. But it’s clear we need more research overall to develop better medical approaches to pain management, as the study also showed patients initially remained in some pain, no matter what treatment they received,” lead researcher Professor Marc Cohen quoted in ScienceDaily.com.

“Some Australian emergency departments already offer acupuncture when trained staff are available but further studies are needed on ways to improve pain management overall in emergency departments, and the potential role for acupuncture in this. We need to determine the conditions that are most responsive to acupuncture, the feasibility of including the treatment in emergency settings, and the training needed for doctors or allied health personnel,” Prof. Cohen stated in a separate article in DailyMail.co.uk.

More studies attesting to how acupuncture relieves pain

The recent study was only one of the many research indicating acupuncture’s efficacy in pain management. In fact, a meta-analysis published last year in MayoClinicProceedings.org revealed that acupuncture was among other complementary health practices that showed favorable results in alleviating common pain. To carry out the analysis, a team of researchers from the National Center for Complementary and Integrative Health at the National Institutes of Health reviewed 105 U.S.-based randomized controlled trials and identified treatment that will address one or more of five painful conditions including back pain, osteoarthritis, and neck pain as well as fibromyalgia, severe headaches, and migraine.

The research team found that acupuncture was highly effective in treating back pain. The study also revealed that the alternative treatment can be used in alleviating osteoarthritis of the knee. The results offer both patients and health providers information that is necessary for discussing non-drug approaches in pain management, the research team concluded.

Another study published in Health.USNews.com showed that acupuncture therapy was highly effective in relieving pain and improving the quality of life in patients with fibromyalgia. According to the study, the pain scores of patients who received acupuncture had an average decline of 41 percent at 10 weeks. In contrast, those who received a simulated acupuncture treatment had a 27 percent reduction in pain scores.

Read More At: NaturalNews.com

Sources include:

DailyMail.co.uk

ScienceDaily.com 1

ScienceDaily.com 2

Health.USNews.com

MayoClinic.com

MJA.com.au

Healthy Skin Care Products

Source: DrSaputo
June 17, 2017

The FDA does not regulate the ingredients in skin care products, so it is up to you to take responsibility for your health.

Vicki Saputo, RN has researched safe cosmetics and skin care products for more than 20 years. Her personal list below consists of products she has researched, tested and recommends.

Remember our skin is our body’s largest organ and more than 60% of what we put on our skin is absorbed into our blood stream. We don’t want to absorb hormone disruptors, carcinogens or neurotoxins. Organic, natural products are recommended with the absence of synthetic preservatives, artificial colors (esp. FDC’s), chemical fragrances and chemical additives and nanoparticles. Vicki has done most of the research for you, so go for it and enjoy.

If you want to check your personal care products for safety, you can double check by going to http://www.cosmeticsdatabase.org and go to skin deep.

The FDA does not regulate the ingredients in skin care products, so it is up to you to take responsibility for your health. Vicki saves you lots of time in chosing safe healthy products that nourish your skin.

For more info please visit http://doctorsaputo.com/a/vicki-s-saf…