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.
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?
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.
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).
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).
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).
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).
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).
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.
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).
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).
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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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.
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.
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).
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.
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).
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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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
FAO/WHO. (2009). Fats and fatty acids in human nutrition. Proceedings of the Joint FAO/WHO Expert Consultation. November 10-14, 2008. Geneva, Switzerland. Annals of Nutrition and Metabolism, 55, 1-3.
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.
Nettleton, J. (1995). omega-3 fatty acids and health. New York Chapman & Hall. p. 67-73.
Nonaka, Y., Takagi, T., Inai, M., Nishimura, S., Urashima, S., Honda, K.,…Terada, S. (2016). Lauric acid stimulates ketone body production in the KT-5 astrocyte cell line. Journal of Oleo Science, 65(8), 693-699.
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.
Ramsden et al. (2016). Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-1973). British Medical Journal, 353.Simopoulos, A.P., & Salem Jr., N. (1992). Egg yolk as a source of long-chain polyunsaturated fatty acids in infant feeding. American Journal of Clinical Nutrition, 55, 411-414.
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Seaman, D.R. (2002). The diet-induced pro-inflammatory state: a cause of chronic pain and other degenerative diseases? Journal of Manipulative and Physiological Therapeutics, 25(3), 168-179.
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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.
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.
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.
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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…
Source: GreenMedInfo.com
Margie King, Health Coach
June 11, 2017
Magnesium is the fourth most abundant mineral in your body, and is the reason why vegetables are green. But few people fully appreciate the importance of this miraculous mineral.
The human genome project reveals that 3,751 human proteins have binding sites for magnesium.[i] And so far we know this one essential mineral activates over 350 biochemical processes in the body to keep things flowing.
Plants are green because they contain the light-harvesting molecule chlorophyll which bears a striking resemblance to human hemoglobin (with the difference that the latter contains an oxygen-binding iron atom and not magnesium).
Here are just seven good reasons to get more magnesium-rich foods in your diet today.
1. Prevent Migraines.
According to University of Vermont Professor of Neurology and migraine expert Robert Shapiro, M.D., Ph.D., every year nearly one in five Americans experience some form of migraine attack. One in 25 will have headaches lasting at least 15 days per month. These disabling attacks include severe one-sided, throbbing headaches, and sensitivity to light and sound. They may also involve nasal congestion, cloudy thinking, and nausea.
In one study of 133 migraine patients, supplementing with 500 mg of magnesium oxide for just 12 weeks significantly improved the frequency and severity of migraines.[ii]
And a double blind, placebo controlled study from Kaiser Permanente showed that supplementing with magnesium significantly cut the number of days children suffered with a migraine.[iii]
2. Lower Heart Disease Mortality.
A study in the journal Atherosclerosis found that people with low magnesium levels were more than twice as likely to die of heart disease. They were also more than seven times as likely to die from all causes.[iv]
3. Manage Diabetes.
Magnesium deficiency is common among type 2 diabetics, especially those with neuropathy or coronary disease.[v] A Harvard study found that diabetics taking 320 mg of magnesium for up to 16 weeks significantly improved their fasting blood sugar levels as well as their HDL (good) cholesterol.[vi]
4. Relieve Symptoms of Fibromyalgia.
A double blind, placebo controlled study from the University of Texas showed that magnesium malate improves pain and tenderness in fibromyalgia patients.[vii]
5. Lower Risk of Colon Cancer.
Epidemiologic studies link low magnesium levels with higher rates of colorectal cancer. And a meta-analysis from China confirms that higher magnesium intakes are associated with a lower risk of colorectal cancer and especially colon cancer.
The Chinese researchers analyzed eight prospective studies covering 338,979 participants. Their results, published in the European Journal of Clinical Nutrition, found the highest average intake of magnesium was associated with an 11% reduction in colorectal cancer risk compared to the lowest average intake.
In addition, for every 50 mg per day increase in magnesium, colon cancer was reduced by 7%.
An earlier meta-analysis by Imperial College London and Wageningen University found that for every 100 mg increase in magnesium, colorectal cancer decreased by 13%.
6. Build Strong Bones.
Studies find a significant association between bone density and magnesium levels.[viii] But magnesium content of bones decreases with age.[ix] In addition, sugar and alcohol cause magnesium to be lost through the urine.
Magnesium assists calcium in building bone strength,[x] but it does much more. It stimulates the hormone calcitonin. That helps draw calcium out of the blood and soft tissues and put it back into the bones. Too much calcium in the blood and tissues can increase the risk of arthritis, heart attack, and kidney stones, as well as osteoporosis.[xi]
And getting more magnesium may mean you need less than the government’s recommended 1,200 mg of calcium per day. One study in the American Journal of Clinical Nutrition found that increasing magnesium while lowering calcium to 500 mg per day was enough to increase bone density.[xii]
7. Reduce Signs of Metabolic Syndrome
Mexican researchers looked at the effects of taking oral magnesium supplements on people they categorized as “metabolically obese, normal-weight (MONW) individuals.”
MONW individuals have a body mass index under 25 which is considered normal weight. But they also have hyperinsulinemia and or insulin resistance. And they have high triglycerides and high blood pressure. As a result, these individuals are at higher risk of developing cardiovascular disease and diabetes.
The researchers studied 47 MONW individuals who had low magnesium levels. In a randomized double-blind placebo-controlled trial one group received a daily solution of 30 ml of magnesium (equivalent to 382 mg). The control group received 30 ml of a placebo solution.
Their results were published in the Archives of Medical Research. After only 4 months, markers of metabolic syndrome were significantly lower in the magnesium group. They lowered their systolic pressure by 2.1 points and their diastolic pressure by 3.8 points. Their fasting blood glucose levels dropped 12.3 points and their triglycerides plunged 47.4%.
Magnesium is also known to:
Symptoms of magnesium deficiency include constipation and other digestive problems, low energy, and irregularities in menstrual flow and reproductive health, and migraine headaches.
Magnesium also relaxes the body from tightness, tension, tics, spasms, cramps and stiffness. And it helps prevent the buildup of plaque on your teeth, in your heart and arteries, and even in your brain.
The recommended daily allowance for magnesium is 420 mg for men or 320 mg for women. But it’s estimated that between 80% and 90% of Americans are magnesium deficient. One government study showed that 68% of American women do not consume the recommended daily amount of magnesium. Almost 20% don’t even get half of the recommended amount.[xiii]
In addition, the use of oral contraceptives, diuretics, and laxatives can make magnesium deficiencies worse.
Magnesium deficiency is relatively easy to remedy with food. One of the richest sources of magnesium is high quality chocolate. Dark chocolate has a whopping 176 mg of magnesium in a 3.5 ounce bar. In fact, if you crave chocolate your body may be telling you it’s low in magnesium.
Other high magnesium foods include:
Magnesium supplements are also widely available. They come in many forms including oxide, citrate, carbonate, aspartate, and lactate. Magnesium oxide is the least expensive but also the most difficult for the body to absorb. Magnesium citrate helps with constipation. Magnesium glycinate is a better choice if you don’t want the laxative effect.
Some people have difficulty absorbing magnesium in an oral supplement form. If you eat a high fiber diet, for example, your body doesn’t absorb as much magnesium. Also, taking diuretics, antibiotics or proton pump inhibitors for acid reflux all interfere with magnesium absorption.
For better absorption, try magnesium chloride, or a form known as iMCH, which can be applied topically. It has been called the most effective form of magnesium for cellular detoxification and tissue purification. It comes in the form of oil. You can spray this directly on your skin or even soak your feet in it. The liquid magnesium bypasses the intestines and is absorbed directly into the tissues of the body.
Visit GreenMedInfo’s page on magnesium documenting well over 100 health benefits of magnesium. Also, check out their cutting edge report on how chlorophyll (what makes veggies green!) can help your body to capture the energy of sunlight, with positive consequences to your health and well being.
Read More At: GreenMedInfo.com
________________________________________________________________________
Sources:
https://www.consumerlab.com/reviews/magnesium-supplement-review/magnesium/
http://www.healthcentral.com/medications/r/medications/magnesium-chloride-oral-10702
http://www.ancient-mineral s.com/products/
[i] Damiano Piovesan, Giuseppe Profiti, Pier Luigi Martelli, Rita Casadio. 3,751 magnesium binding sites have been detected on human proteins. BMC Bioinformatics. 2012 ;13 Suppl 14:S10. Epub 2012 Sep 7. PMID: 23095498
[ii] Ali Tarighat Esfanjani, Reza Mahdavi, Mehrangiz Ebrahimi Mameghani, Mahnaz Talebi, Zeinab Nikniaz, Abdolrasool Safaiyan. The effects of magnesium, L-carnitine, and concurrent magnesium-L-carnitine supplementation in migraine prophylaxis. Biol Trace Elem Res. 2012 Dec ;150(1-3):42-8. Epub 2012 Aug 17. PMID: 22895810
[iii] Fong Wang, Stephen K Van Den Eeden, Lynn M Ackerson, Susan E Salk, Robyn H Reince, Ronald J Elin. Oral magnesium oxide prophylaxis of frequent migrainous headache in children: a randomized, double-blind, placebo-controlled trial. Eur J Endocrinol. 2009 Apr;160(4):611-7. Epub 2009 Jan 29. PMID: 12786918
[iv] Thorsten Reffelmann, Till Ittermann, Marcus Dörr, Henry Völzke, Markus Reinthaler, Astrid Petersmann, Stephan B Felix. Low serum magnesium concentrations predict cardiovascular and all-cause mortality. Atherosclerosis. 2011 Jun 12. Epub 2011 Jun 12. PMID: 21703623
[v] M de Lordes Lima, T Cruz, J C Pousada, L E Rodrigues, K Barbosa, V Canguçu. The effect of magnesium supplementation in increasing doses on the control of type 2 diabetes. Diabetes Care. 1998 May;21(5):682-6. PMID: 9589224
[vi] Y Song, K He, E B Levitan, J E Manson, S Liu. Effects of oral magnesium supplementation on glycaemic control in Type 2 diabetes: a meta-analysis of randomized double-blind controlled trials. Cardiovasc Toxicol. 2008;8(3):115-25. Epub 2008 Jul 8. PMID: 16978367
[vii] I J Russell, J E Michalek, J D Flechas, G E Abraham. Treatment of fibromyalgia syndrome with Super Malic: a randomized, double blind, placebo controlled, crossover pilot study. J Rheumatol. 1995 May;22(5):953-8. PMID: 8587088
[viii] Ryder KM et al, Magnesium intake from food and supplements is associated with bone mineral density in healthy older white subjects. J Am Geriatr Soc. 2005 Nov;53(11):1875-80. Pubmed 16274367
[ix] Jahnen-Dechent W., Ketteler M. “Magnesium basics.” Clin. Kidney J. 2012;5:i3–i14. doi: 10.1093/ndtplus/sfr163. [Cross Ref]
[x] Jones, G., M. Riley, and T. Dwyer, Maternal Diet during pregnancy is associated with bone mineral density in children: a longitudinal study. European Journal of Clinical Nutrition, 2000. 54: p. 749-756
[xi] Zofková I, , Kancheva RL. The relationship between magnesium and calciotropic hormones. Magnes Res. 1995 Mar; 8 (1): 77-84. Pubmed 7669510
[xii] Nieves, J.W. 2005. Osteoporosis: The role of micronutrients. American Journal of Clinical Nutrition 81 (5): 1232S-1239S. http://ajcn.nutrition.org/content/81/5/1232S.abstract
[xiii] King DE, Mainous AG 3rd, Geesey ME, Woolson RF. “Dietary magnesium and C-reactive protein levels.” J Am Coll Nutr. 2005 Jun 24(3):166-71.
Source: GreenMedInfo.com
Ali Le Vere, B.S., B.S.
June 13, 2017
Health Begins In the Gut. From a clinical standpoint, insofar as functional medicine is concerned, whether you present with rheumatoid arthritis, multiple sclerosis, ulcerative colitis, or systemic lupus erythematosus—the fundamental objective is the same: heal the gut.
Hippocrates understood the inextricably intertwined relationship between the systemic health of the organism and the nine-meter tube from mouth to anus when he famously uttered, “All disease begins in the gut” over two thousand years ago. The ancient Greek physician also illuminated his understanding of the therapeutic role of nutrition when he championed holistic medicine with his proclamation, “Let food be thy medicine and medicine be thy food”.
After all, covering an average surface area of thirty-two square meters, the size of half a badminton court, the gut represents the second largest interface between the external environment and the internal biochemical milieu of the body (Helander & Fandriks, 2014). Over sixty tons of food will pass through our gastrointestinal tract in our lifetime.
Why is gut health so paramount in prevention and treatment of autoimmune disease? If you are a savvy consumer of holistic health information, you probably already know how important our microbiome—the collection of one hundred trillion commensal bacteria that inhabit our colon, plus their genetic material—is to our health. Although the widely cited 10:1 ratio has been revised, researchers estimate that we have at least as many bacterial cells as human cells, which has led some scientists like Stanford’s Dr. Justin Sonnenberg to hypothesize that humans may merely be elaborate vessels designed for the propagation of bacterial colonies (Sender, Fuchs, & Milo, 2016).
At any single moment, two to six pounds of bacteria resides within us. Even more awe-inspiring is that a single person contains 3.8×10^13 bacteria (38,000,000,000,000 colony forming units)—a number representing more than all the stars in the galaxy (Sender, Fuchs, & Milo, 2016).
Following the advent of germ theory and the discovery of vaccinations, scientists were under the impression that all bacteria were bad bugs, and speculated that specific microbes were the causative agents behind particular disease entities. This led to the reductionist, pill-for-every-ill therapies that predominate in Western medicine, as well as to the maligning of all bacteria as organisms to be feared and eradicated. Thus the age of antibiotics, triclosan-laden anti-bacterial soaps, hand sanitizer, chemical cleaners, and the “there’s a shot for that” mentality was inaugurated.
Ironically, it is rumored that on his deathbed, Louis Pasteur, the father of immunization and pasteurization himself, admitted that it is the terrain—the gut ecology and biochemical milieu—that matters, rather than the infecting pathogen (Tracey, 2017). In other words, our bodies, like plants, are more susceptible to pests, or infection, when our ecosystem is in a state of disharmony—when our microbial soil is depleted and our micronutrient status is compromised.
The magic bullet approach initially introduced by Pasteur, however, was misguided, and has the potential to produce dire consequences for immune health. In fact, the hygiene hypothesis, embraced by many scientists, purports that the reason that autoimmune diseases and atopic disorders (eczema, allergies, asthma) are epidemic in the Western world while virtually absent from developing nations is the hyper-sanitized, antibiotic-ridden society in which we live, which has decimated our gut microflora and thus obliterated their beneficial effects on our immune systems (after all, 70% of our immune system resides within our gut) (Vighi et al., 2008).
According to the hygiene hypothesis, the immune system acquires self-tolerance, or the ability to distinguish self from stranger and safety from danger, and thus prevent overreactions against our own tissue, based on repeated infectious exposures (Eschler, Hasham, & Tomer, 2011). Further, “Some pathogens have the potential to prevent or abrogate rather than induce an autoimmune process,” such that annihilating them with antibiotics results in improper maturation of the immune system and a tendency towards autoimmune reactions (Christen, 2014).
However, antibiotics are not only harmful in that they prevent infections from instructing development of the immune system. They also disrupt the finely tuned symphony of actions orchestrated by our microbiota, or those friendly bugs that inhabit our gut. The microbiota serve innumerable roles, including competing for attachment sites with potentially pathogenic microbes, reducing their virulence, inhibiting the effects of bacterial toxins, and generating anti-microbial substances such as bacteriocidins and hydrogen peroxide that can selectively suppress pathogenic bacteria and fungi (Corr et al., 2009; Castagliuolo et al., 1999).
Our gut microbes also promote the de-conjugation and detoxification of proliferative, carcinogenic estrogen species and other exogenous toxins, reducing their enterohepatic recirculation (Gorbach, 1984). Commensal bacteria likewise aid in nutrient extraction and assimilation, as the secondary bile acids and short-chain fatty acids they produce from fermentation of indigestible carbohydrates lead to liberation of compounds like peptide YY from cells, which decreases intestinal transit, encourages satiety, maximizes nutrient absorption, and increases energy harvested from food (Boulange et al., 2016).
Critically, gut bacteria reinforce the intestinal barrier, preventing metabolic endotoxemia, a process which contributes to metabolic syndrome, non-alcoholic fatty liver disease (NAFLD), coronary heart disease, stroke, and polycystic ovarian syndrome (PCOS) (Neves et al., 2013; Lindheim et al., 2017). The products of microbial fermentation of prebiotic carbohydrates also increase insulin sensitivity and improve glucose balance, which prevents the pathologic insulin resistance, oxidative stress, and endothelial dysfunction that lead to diabetes and cardiovascular disease (Boulange et al., 2016).
The maintenance of the intestinal lining by the microbiota similarly prevents autoimmune disease. For instance, a decrease in bifidobacteria populations leads to intestinal hyperpermeability, or leaky gut, which in turn leads to the translocation of metabolic byproducts, food antigens, bacteria, and lipopolysaccharide (also known as LPS, an immunogenic cell wall component from Gram-negative bacteria) across the gut barrier into systemic circulation (Rapin & Wiernsperger, 2010). This activates the mesenteric lymph nodes and gut-associated lymphoid tissue (GALT) and instigates a downstream inflammatory cascade.
A single course of antibiotics can lead to perturbations in microbiota lasting up to 16 months on average, or 18 to 24 months for Clindamycin and up to four years following triple therapy for Helicobacter pylori (Hawrelak & Myers, 2004; Jernberg et al., 2010; Cotter et al., 2012). Even worse, novel molecular analysis techniques using 16S rRNA have demonstrated that antibiotic-resistant microbes are present up to four years post-antibiotic (Jernberg et al., 2010; Cotter et al., 2012).
Other commonly used medicinal agents, non-steroidal anti-inflammatory drugs (NSAIDs) such as Motrin, Ibuprofen, and Naproxen, increase concentrations of gram-negative bacteria, which produce lipopolysacchide (LPS), the endotoxin that can traverse the gut barrier and generate a milieu favoring insulin resistance, type 2 diabetes, NAFLD, PCOS, coronary heart disease and stroke (Marlicz et al., 2014).
In addition to inducing gastrointestinal ulcers, increasing risk of myocardial infarction by a third, and doubling risk of congestive heart failure, NSAIDs have also been demonstrated to decrease concentrations of bifidobacteria and lactobacilli—beneficial commensal flora populations in our gut (Bhala et al., 2013; Montenegro et al., 2014). Because bifidobacteria are responsible for butyrate production, the short chain fatty acid that heals and seals the gut lining, a decrease in bifidobacteria can perpetuate leaky gut syndrome.
What’s more, acid-blocking drugs, or proton pump inhibitors (PPIs) such as Prilosec and Nexium, used for gastroesophageal reflux disease (GERD), are associated with a decrease in small bowel beneficial bifidobacteria and a significant decline in microbial diversity within seven days of beginning therapy (Seto et al., 2014; Wallace et al., 2011). PPIs have likewise been shown to increase the risk of small intestinal bacterial overgrowth (SIBO) and the potentially fatal infection, Clostridium difficile (Lo & Chan, 2013; Janarthanan et al., 2012).
With antibiotics in particular, however, there is evidence of localized permanent extinction—in other words, some species of microorganisms never recover post-antibiotic, and cannot be “reinoculated” unless you undergo the arduous and expensive process of fecal microbiota transplant (FMT).
Furthermore, even food preparation and processing can influence intestinal permeability. When food is browned or caramelized as part of the Maillard reaction, reducing sugars spontaneously react with lipids, nucleic acids, and aminopeptides, creating advanced glycation end products (AGEs) in a process that generates free radicals, inflammation, and ensuing intestinal permeability (Vlassara & Uribarri, 2004; Bengmark, 2007).
The intestinal barrier is a mucosal surface wherein epithelial cells known as enterocytes are separated by tight junction proteins, desmosomes, and adherens junctions that function as architectural scaffolding and selective gates, opening and closing to allow fluid and nutrients to be absorbed and waste products to be excreted (Groschwitz & Hogan, 2009). According to Turner (2009), epithelial cells “establish a barrier between sometimes hostile external environments and the internal milieu” (p. 799). This barrier is critical because “The mucosa is directly exposed to the external environment and taxed with antigenic loads…at far greater quantities on a daily basis than the systemic immune system sees in a lifetime” (Mayer, 2003).
Tight junctions, regulated by a molecule called zonulin, as well as by conformational changes in the proteins occludin and claudin, are dynamic intercellular structures that modulate the trafficking or passage of macromolecules from the intestinal lumen to the submucosa and into systemic circulation (Fasano, 2012). According to Rapin and Wiernsperger (2010), “Tight junctions play a major role in regulating the paracellular passage of luminal elements” (p. 635).
Under normal circumstances, solutes exceeding a certain size, or molecular radius, are prohibited from absorption across the gut barrier by competent tight junctions (Fasano, 2012). However, when insults such as gluten, dysbiosis, pathogens, toxins, over-exercising, chemotherapy, radiation, and medications such as NSAIDs and steroids disrupt the tight junctions, microbial products and intact food proteins that have not been degraded into their constituent parts translocate across the paracellular space into the body (Fasano, 2012).
Macrophages embedded in the GALT are part of the innate immune system, or the non-specific, first line of defense against infection (Fasano, 2011; Yu & Yang, 2009). These cells, along with dendritic cells, recognize the incoming undigested food particles, toxic agents, and bacterial components as foreign invaders, and present them to cells of the adaptive immune system called T and B lymphocytes, leading to clonal expansion (proliferation or multiplication of specific subsets of T and B cells) and recruitment of more pro-inflammatory immune cells to the gut through a process called leukocyte homing.
The release of inflammatory cytokines, or intercellular signaling molecules such as interleukin-1 (IL-1), interleukin-2 (IL-6), and tumor necrosis factor alpha (TNF-α) at the site of immune activation causes other immune cells migrating throughout the lymphatic vessels of the body to express more cell adhesion molecules (CAMs). CAMS enable white blood cells to stick to and roll along blood vessels and extravasate, or navigate across, the blood vessels made leaky by histamine and other local vasodilators, into the inflamed intestinal tissue. Cytokines contribute to this vicious process of leaky gut syndrome, as they also play a prominent role in compromising tight junction integrity (Watson, Duckworth, Guan, & Montrose, 2009). This culminates in a massive inflammatory response that can become systemic and lead to autoimmunity.
When the amino acid sequence is homologous between the target antigen, such as gluten, against which the immune system is mounting a response, and tissue proteins, such as the thyroid tissue, a case of mistaken identity occurs, and the immune response can become directed against self tissues, manifesting as autoimmune disease (Hashimoto’s thyroiditis in this instance). Summarized by Suzuki (2013), “Disruption of the intestinal tight junction barrier, followed by permeation of luminal noxious molecules, induces a perturbation of the mucosal immune system and inflammation, and can act as a trigger for the development of intestinal and systemic diseases” (p. 631).
A protein called zonulin is responsible for induction of tolerance and orchestration of immune responses by modulating intercellular tight junctions in the gastrointestinal epithelium in a rapid, reversible, and reproducible fashion (Fasano, 2011). Zonulin evolved as an adaptive mechanism to flush out microorganisms as part of the innate immune response against bacterial colonization of the small intestine (Fasano, 2011).
Specific gliadin-permeating peptides can initiate intestinal permeability via MyD88-dependent release of zonulin, which causes conformational changes in tight junction architecture and cytoskeletal assembly that leads to paracellular entry of gliadin (a gluten sub-fraction) into the intestinal submucosa (Thomas, Fasano, & Vogel, 2006). Signaling through the CXCR3-mediated, MyD88-dependent pathway generates a Th1-dominant, pro-inflammatory cytokine milieu that recruits mononuclear cells into the submucosa (Fasano, 2011). After gliadin infiltrates the lamina propria, the barrier function can be further disrupted by the persistence of inflammatory mediators such as TNF-α and interferon-gamma (IFN-γ) (Fasano, 2011).
In those individuals predisposed to celiac disease, gliadin is presented by HLA-DQ and HLA-DR major histocompatibility complex (MHC) molecules, leading to abrogation of oral tolerance and a transition to a Th1/Th17 response (Fasano, 2011). Dendritic cells home to pancreatic and mesenteric lymph nodes and present gliadin, leading to “migration of CD4−CD8−γδ and CD4−CD8+ αβ T cells to the target organ (gut and/or pancreas) where they cause inflammation” (Fasano, 2011). This results in the interaction between T cells and antigen-presenting cells, producing the adaptive immune response that causes profound villous atrophy in celiac disease (Fasano, 2011). Celiac disease patients have higher concentrations of serum zonulin during the acute phase of disease compared with their healthy counterparts, and also have over-expressed CXCR3, the intestinal receptor for gliadin (Fasano, 2011).
However, even in healthy individuals, biopsies reveal a transient zonulin release upon gluten ingestion accompanied by an increase in intestinal permeability that does not reach the level observed in celiac disease (Drago et al., 2006). The authors of the in vitro study state, “Based on our results, we concluded that gliadin activates zonulin signaling irrespective of the genetic expression of autoimmunity, leading to increased intestinal permeability to macromolecules” (Drago et al., 2006, p. 408). Furthermore, when intestinal biopsies were examined from celiac patients with active disease, celiac patients in remission, non-celiac gluten-sensitive patients, and non-celiac controls, intestinal permeability was found to occur after gliadin exposure in all individuals (Hollon et al., 2015).
The same mechanism is implicated in all autoimmune diseases—leaky gut leading to molecular mimicry and/or the bystander effect—biochemical processes that could be characterized as “friendly fire” that are responsible for the resultant tissue damage and symptom expression (Fasano, 2012). Thus, compromised gut integrity, or dysfunctional intestinal permeability, is a precursor and essential trigger for all autoimmune disease, including celiac disease, type 1 diabetes, rheumatoid arthritis, multiple sclerosis, Crohn’s disease, ulcerative colitis, and ankylosing spondylitis, and can also appear in allergic syndromes such as asthma (Fasano, 2012; Drago et al., 2006; Westall, 2007; Edwards, 2008; Yacyshyn & Meddings, 1995; Martinez-Gonzalez et al., 1994; Schmitz et al., 1999; Hijazi et al., 2004).
Moreover, intestinal permeability, as assessed by a lactulose-mannitol test, may predispose a patient to the development of food reactions, as increased intestinal permeability is associated with food allergy (Laudat et al., 1994; Andre, 1986). However, food allergy itself may inflict “mucosal damage caused by local hypersensitivity reactions to food antigens,” creating a pattern in which an individual becomes sensitive to more and more foods (Tatsuno, 1989).
For people resistant to dietary and lifestyle modifications to resolve intestinal permeability, I will share that I am a living testament to the consequences of dysfunctional intestinal permeability, which leads to a domino scenario where autoimmune conditions are developed one after another. This scenario is far from uncommon, as a fourth of patients with autoimmune disease tend to develop additional autoimmune diseases, leading to multiple autoimmune syndrome. It is often cited that an individual is three times as likely to develop another autoimmune disease after acquiring one (Cojocaru, Cojocaru, & Silosi, 2010). Hence, my mission is to save others from the heartache I have endured as a consequence of these devastating chronic illnesses.
The succession of autoimmune diseases I developed due to a confluence of environmental triggers, genetic susceptibilities, and compromised gut barrier speak to the importance of preserving tight junction integrity and acting as a guardian of your gut epithelium. The gravity of leaky gut syndrome is illustrated by Brandtzaeg (2013), who states, “Increased epithelial permeability for antigens is a crucial primary or secondary event in the pathogenesis of several disorders” (p. 67).
In my case, a multitude of factors converged to produce autoimmunity—intestinal hyper-permeability, dysbiosis, food sensitivities, mitochondrial dysfunction, genetic polymorphisms, histamine intolerance, mycotoxins, adrenal dysfunction, heavy metal toxicity, micronutrient deficiencies, hormonal imbalances, and a host of recalcitrant and stealth infections. Reversing an autoimmune disease is magnitudes of order more complex than preventing one, which is why educating the public at large about how intestinal permeability serves as a prelude to autoimmunity is of the utmost importance.
However, if you go to a conventional physician complaining of a leaky gut, your concerns are likely to be dismissed and more often than not, you will leave with a recommendation to spend less time on the internet—or even worse, your symptoms will be branded psychosomatic and your doctor will label you a hypochondriac, as almost half of autoimmune patients experience in the subclinical stages of their disease (AARDA, 2017).
Despite the litany of peer-reviewed studies in the scientific literature on pathologic paracellular intestinal hyper-permeability, the biomedical establishment is by and large ignorant to this condition and its implications. Ironically, although Western medicine relegates leaky gut syndrome to the realm of fanciful fairy tales, the pharmaceutical industry is actively investigating drugs to reverse it (Kato et al., 2017). Only when there is a financial incentive and a pharmaceutical approach developed for a disorder is it anointed with legitimacy in the eyes of the allopathic physician.
If health is your objective, however, restoration of gut barrier integrity should be prioritized, since, “The autoimmune process can be arrested if the interplay between genes and environmental triggers is preventing by re-establishing intestinal barrier function” (Fasano & Shea-Donohue, 2005). Because gluten is pivotally implicated in intestinal hyper-permeability, its exclusion from the diet, along with an oligoantigenic elimination-provocation diet, should be a first line of treatment in any patient on the autoimmune spectrum.
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Source: NaturalNews.com
Isabelle Z.
June 14, 2017
Conventional wisdom says that increasing your vitamin C intake can help ward off colds, but now scientists believe it could be a powerful tool in a much bigger battle: The fight against cancer.
A study that was recently published in Oncotarget found that a combination of antibiotics and Vitamin C could be as much as 100 times more effective than chemotherapy when it comes to killing cancer cells in a mechanism that is essentially a “one-two punch.”
Scientists at the University of Salford subjected cancer cells to increasing doses of the antibiotic in question, doxycycline, over the course of three months and followed this up with Vitamin C, which restricts the cells’ energy source to only glucose. The Vitamin C inhibits most of the cells’ ability to make energy, leaving them alive but weak. When the glucose is then later taken away, the cells essentially starve to death. Unlike normal cells, cancer stem cells have the ability to produce energy using glucose through several pathways, which is one reason they can grow and replicate more efficiently than normal cells. Taking away the glucose prevents these cells from proliferating.
It is believed that this method could prevent cancer cells from developing resistance to treatment, and the results show how combo therapies can be used to help overcome drug resistance. The team also discovered a handful of other drugs with the potential to be used for the “second punch” after the antibiotics, including relatively non-toxic FDA-approved drugs and natural products like berberine, a salt that is found in several plants species.
In March, the same university found that vitamin C on its own is as much as 10 times more effective when it comes to halting the growth of cancer cells than drugs like 2-DG.
Having an effective way to fight cancer is good news under any circumstances, but it’s made even better when the solution entails something nontoxic like Vitamin C.
While Big Pharma would like you to believe that such treatments are dangerous and you have no choice but to buy their poisonous chemotherapy drugs, recent clinical trials concluded that regularly infusing lung and brain cancer patients with as much as 1,000 times the daily recommended intake of Vitamin C is safe as a strategy for improving the outcomes of standard treatments for cancer.
Contrast this with chemotherapy, radiation therapy, and cancer drugs, all of which carry with them their own set of risks. According to the Pharma Death Clock, chemotherapy has killed more than 17 million people in the U.S. since 2000. Moreover, aggressive cancer types do not always respond to these treatments. This means that cancer patients have an uphill battle and must accept a lot of risks when opting for conventional treatments, yet many feel they have little choice. If the efforts of the University of Salford scientists lead to the development of a safer and more effective treatment, it could save countless lives and spare these patients and their families the emotional distress that can accompany cancer.
While the doses of Vitamin C that are used in these treatments are much higher than you could get from your diet, there are still plenty of benefits to upping your intake of this nutrient, even if you don’t have cancer. In fact, it can help reduce the risk of getting certain cancers, like lung cancer, in the first place, and it has also been found to help prevent heart attacks and reduce your risk of stroke. Found naturally in foods like oranges, red peppers, broccoli, brussels sprouts, and kale, Vitamin C is a true powerhouse that could ultimately offer a solution to some of the biggest challenges facing the medical world today.
Read More at: NaturalNews.com
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