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Awareness

Tylenol Damages The Brains of Children, Research Reveals

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In Brief

  • The Facts:

    Tylenol has a wide range of toxic side effects you should be aware of, especially if you are pregnant or use it with your children. Article written by William Parker, Ph.D for Greenmedinfo.com, published here with permission.

  • Reflect On:

    Why do we keep taking Tylenol and other over-the-counter drugs when it's unquestionable that they do more harm than good? Why don't we ever look into healthy ways to alleviate our symptoms?

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A number of non-peer-reviewed articles have been written and published on the web claiming that there is literally nothing to fear from acetaminophen during pregnancy. There are two types of articles that fall into this category. First, reputable watchdog organizations have weighed in on the issue, declaring acetaminophen use during pregnancy and during childhood to be proven safe. In particular, the National Health Service of the UK and the Center for Accountability in Science have both strongly criticized the Spanish study from 2016 showing a link between acetaminophen use during pregnancy and ADHD/autism.

The second type of article is generally written by a science writer working for an organization that runs a website. Often quoting one to three experts who claim that is perfectly safe and that pregnant women and families should not be concerned, many of these articles are published by reputable sources that are generally trustworthy. Typically, an expert is being asked to comment on one particular publication showing a link between acetaminophen use (usually during pregnancy) and some sort of neuropsychiatric problem (autism, lowered IQ, hyperactivity, and/or social/behavioral problems, depending on the study). There are several important things to consider when evaluating these articles:

1.  There are a number of University Professors who have studied the use of acetaminophen on the developing brain and who are keenly aware of the potential dangers. A partial list of these individuals is provided below.

2.  Being an expert in acetaminophen neurotoxicity during development means that considerable time has been invested in studying the issue. Any true expert in this issue will be aware of basic facts regarding acetaminophen neurotoxicity. These facts include the following:

(a) Studies in animal models (both in mice and in rats) demonstrate that acetaminophen use during a sensitive period of brain development causes long-term alterations in the brain and is manifested as problems with social function.

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(b)  Margaret McCarthy, Chair of Pharmacology at the University of Maryland, has worked out the probable mechanism by which acetaminophen-induced brain damage occurs. Her research team has found that the male brain is considerably more sensitive to acetaminophen than the female brain, possibly accounting for the gender bias in autism.

(c) There are (as of January 2017) a total of 8 published studies evaluating the long terms effects on children of acetaminophen use during pregnancy or during childhood. Two of these (one in 2014, one in 2016) were published in JAMA Pediatrics, one of the most highly respected pediatric journals. All studies point toward acetaminophen use being associated with long-term problems with neurological function. Each study design has included some attempt to control for indication. In all studies, acetaminophen use rather than indication has been identified as the key factor associated with cognitive problems. A formal meta-analysis is not currently possible because of the varied outcome measures and study designs, but all 8 studies point in the same direction: Acetaminophen is neurotoxic to the developing brain. The studies are not “cherry picked”, selecting only those which find an effect. All studies point toward a neurotoxic effect of acetaminophen in the developing brain.

(d)   Acetaminophen substantially alters brain chemistry and temporarily impairs awareness of social issues in adult humans.

(e)  Testing of acetaminophen safety in children did not include any evaluation of brain function, and no long-term studies were ever conducted. The primary manufacturer of acetaminophen in the US acknowledges that the drug has never been shown to be safe for brain development when used during pregnancy or in childhood. All safety tests were performed with the assumption that any side effects would be acute in nature (e.g., bleeding or acute organ damage). This assumption was based on observations made with acetaminophen in adults and with aspirin in children. It was not based on any experience with acetaminophen use in children.

3.     Having prescribed tens of thousands of doses of acetaminophen does not make anyone an expert on the neurotoxicity of acetaminophen, any more than eating thousands of pounds of chips makes somebody an expert in the effects of an inflammatory diet. Credentials and certifications that allow physicians to prescribe acetaminophen do not make them experts, and elevated positions in the medical community do not qualify anybody as an expert on the effects of acetaminophen. If somebody does not know those basic facts listed above, then they are not an expert on the neurotoxicity of acetaminophen. Usually, the experts will have published one or more peer-reviewed manuscripts on the topic. Those are the people to ask when an expert is needed.

4.     It is tempting to point accusing fingers at physicians who say that acetaminophen is safe when they literally have no grasp whatsoever of the relevant scientific literature. However, this would be a mistake. I have tracked down a few of these individuals who were quoted in a very public format, and one individual, in particular, didn’t even remember having made a comment on the topic. The most likely explanation is that a reporter asked them if acetaminophen was safe, and their response based on their training (not on the knowledge of the literature) was that it is safe. After all, if they didn’t think it was safe, they would not be administering it dozens of times per day. So, if a reporter asks a physician if something is safe, and they provide their knowledge based on what they have been taught and how they practice, then it is hard to blame them. The reporter didn’t ask them to spend days or even weeks reviewing the literature in detail, but rather assumed that any physician administering something dozens of times per day would know the literature. (This is a false assumption. No physician has the time to study all current literature on every drug they administer.) So, in a nutshell, a tragic propagation of incorrect information is occurring despite the best of intentions of all parties involved.

5.     Unless an organization such as the National Health Service has the time to review a topic thoroughly, they should remain silent on an issue. It took a team of us two years to put together our summary of the evidence, both direct and circumstantial, regarding the potential neurotoxicity of acetaminophen during development. It took the NHS only days to publish their recent criticism of the 2016 Spanish study. Offering questionable criticisms of a single paper without reviewing the literature to see how that publication fits into the big picture is a disservice to the public being served.

6. Reading the published quotes from many “experts” who exonerate acetaminophen, it is apparent that the logic falls into one of two categories.

(a) Everybody is doing it, so it must be OK.

(b) This single study is not perfect, so no change in practice should be made.

Neither of these criticisms is logically sound, of course. These two criticisms are often combined and were, in fact, part of the critical comments directed toward the first paper showing that acetaminophen probably has substantial neurotoxicity during development (published in 2008 by Steve Shultz). Further, the evaluation of study weaknesses is usually skewed and not entirely valid. Since the idea that acetaminophen is safe is being embraced, then any merit in the paper is often undermined to make the case. This is certainly true of the published (peer reviewed) criticisms of the 2008 Shultz paper.

7.     Many on-line sources support the view that acetaminophen can be very dangerous to the developing brain. Probably the most reliable source, the FDA, is remaining silent on the topic until something more definitive is done. The FDA knows that this is extremely urgent, but unfortunately, our FDA is not linked well (in a practical manner) with our NIH, and thus they can’t dictate research priorities.

8.     Here is a list (not comprehensive) of experts regarding the neurotoxicity of acetaminophen during brain development.

a) First, I’ll thank the wonderful team of individuals who helped put together our comprehensive review on this topic. Shu Lin, a professor with me in Duke’s Surgery Department, is a very dear and long-time friend of mine who has supported me through countless projects over the past 22 years. Staci Bilbo, director for research on Autism at Harvard, is a friend and collaborator who has helped me understand what causes inflammation and the role of inflammation in brain dysfunction. Chi Dang Hornik, a pediatric pharmacist at Duke, contributed greatly to our understanding of the frequency of acetaminophen administration and the available formulations of the drug. Many thanks to Martha Herbert. As a Harvard professor and clinician, she has a great appreciation for the clinical data obtained from patients with autism. Cindy Nevison, a professor at the University of Colorado at Boulder, rounds out our team, providing critical information about the epidemiology of autism. (Thanks also to our interns (Rasika Rao and Lauren Gentry) and research analyst (Zoie Holzknecht) who were a tremendous help in compiling information and preparing that information for publication.)

b) Margaret McCarthy, chair of Pharmacology at the University of Maryland, it the most knowledgeable person I know regarding the biochemistry of the human brain and how that is affected by acetaminophen and other drugs in that class.

c) Chittaranjan Andrade, Chair of Psychopharmacology at the National Institute of Mental Health and Neurosciences, Bangalore, India, has written a peer reviewed paper on the topic of acetaminophen induced brain damage. He nicely summarized a number of studies looking at the connection between acetaminophen and neurological damage. His final conclusion is that the drug is probably more associated with ADHD than autism, but the conclusion was limited to exposure during pregnancy and his work was conducted before some critical studies were published in 2016.

d) Henrik Viberg is a professor in the Department of Organismal Biology at Uppsala University in Sweden. He has studied how exposure of mice to acetaminophen during development can cause long term brain damage.

e) In 2015, a group of scientists working with Laurence de Fays at the Federal Agency for Medicines and Health Products in Brussels acknowledged the clinical studies and the studies in animal models which indicated that acetaminophen could be dangerous to the developing fetus, but concluded that paracetamol is “still to be considered safe in pregnancy”. At the same time, they state that “additional carefully designed studies are necessary to confirm or disprove the association (between acetaminophen and brain damage to children)”, and that “care should be taken to avoid raising poorly founded concerns among pregnant females”. We very strongly agree with the conclusion that more studies are needed, but very strongly disagree with the conclusion that women should be kept in the dark about the matter. It is important to point out that several more studies have come out since Laurence de Fays’ report. One of those is a 2016 manuscript in JAMA Pediatrics(see the next expert), a highly reputable peer reviewed journal, which addresses the concerns raised by de Fays, so it is possible that de Fays’ group may now have a different opinion.

f) A team of scientists and doctors working with Evie Stergiakouli at the University of Bristol analyzed data from a prospective birth cohort, and concluded that “children exposed to acetaminophen prenatally are at increased risk of multiple behavioral difficulties”. They found considerable evidence indicating that the association was not due to the confounding factors that concerned de Fays’ group (previous expert).

g) Jordi Julvez at the Centre for Research in Environmental Epidemiology in Barcelona, Spain worked with a team of a dozen clinicians and scientists to publish their 2016 study linking acetaminophen with autism and ADHD.

h) Amany A. Abdin, a professor in the Department of Pharmacology, Tanta University, Egypt, wrote a review of the acetaminophen/autism connection and published it in the journal Biochemistry and Pharmacology: Open Access. Her conclusion in 2013 was that the drug is not safe and that the acetaminophen/autism connection should receive attention.

i) The original paper that identified a connection between neuropsychiatric disorders and acetaminophen was published by Steve Shultz while at the University of California at San Diego. Coauthors on the paper included Hillary Klonoff-Cohen, currently an Endowed Professor and Director of the MPH program at the University of Illinois.

j) Four scientists, including research scientist Ragnhild Eek Brandlistuen and professors Hedvig Nordeng and Eivind Ystrom in the Department of Pharmacy at the University of Oslo, coauthored a study showing a connection between adverse neurodevelopment and acetaminophen use during pregnancy.

k) Jorn Olsen, Professor and Chair of the Department of Epidemiology at UCLA, published one of the more recent papers (2016) showing a connection between autism and acetaminophen use during pregnancy.

l) Five professors (John M. D. Thompson, Karen E. Waldie, Clare R. Wall, Rinky Murphy, and Edwin A. Mitchell) from four different departments at The University of Auckland published their findings in PLOSone in 2014 which “strengthen the contention that acetaminophen exposure in pregnancy increases the risk of ADHD-like behaviours. Our study also supports earlier claims that findings are specific to acetaminophen.”

For evidence-based research on the dangers of acetaminophen, visit the GreenMedInfo.com Research Dashboard.\

Read their related article on Tylenol: 

Tylenol Kills Emotions As Well As Pain, Study Reveals

Sign Up For The Greenmedinfo Newsletter HERE.


William Parker is an Associate Professor at Duke University, where he has worked in the Department of Surgery since 1993.  William is currently investigating a number of issues associated with inflammation and Western society, including vitamin D deficiency, heart disease and alteration of the symbionts of the human body (“biota alteration”). He has been interested in “natural” immune function for some time, which has led him down a path that includes the first studies of immune function in wild rats and the discovery of the function of the human appendix.

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Awareness

Long-Term Consequences of Mumps Vaccination: Many Unanswered Questions

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This is Part II of a two-part series on mumps. Part I discussed how mumps vaccination and the flawed mumps component of Merck’s MMR vaccine are fostering dangerous mumps outbreaks in adolescents and young adults.

It has been about five decades since the U.S. Food and Drug Administration (FDA) approved Merck’s first mumps vaccine. The company began launching combination MMR (measles, mumps and rubella) vaccines in the 1970s. Coincidentally—or not—an infertility crisis has been brewing over roughly the same time period, with dramatic declines in sperm counts and record-lowfertility levels. However, few investigators seem interested in assessing whether mumps outbreaks in highly vaccinated populations of teens and young adults could be having long-termeffects on fertility or other health indicators.

As described in Part I, childhood MMR vaccination has been an unmitigated disaster where mumps is concerned, deferring mumps infection to older ages and leaving adolescents and young adults vulnerable to serious reproductive complications. Public health reports show that the vast majority of mumps cases and outbreaks occur in youth who have been fully vaccinatedwith the prescribed two-dose MMR series, supporting a hypothesis of “waning immunity after the second dose.” FDA and Centers for Disease Control and Prevention (CDC) officials even admitthat mumps outbreaks in the post-vaccination era “typically involve young adults,” and that vaccination is failing to protect those who are college-age and above.

Myopically, many vaccine experts have called for a third MMR dose—or even “booster dosing throughout adulthood”—even though the FDA’s and CDC’s own research shows that MMR boosters in college-age youth barely last one year. As alleged in whistleblower lawsuits wending their way through the courts over the past eight years, Merck presented the FDA with a “falsely inflated efficacy rate” for the MMR’s mumps component, using animal antibodies and other fraudulent tactics to fool FDA—and the public—into believing that the vaccine was effective.

When infection arises after puberty, however, mumps is no laughing matter, presenting an increased risk of complications such as hearing loss, encephalitis and inflammation of the reproductive organs.

Mumps after puberty is no laughing matter

Around the time that the first mumps vaccine came on the market, the 1967 children’s classic The Great Brain humorously depicted mumps infection in childhood as a mere nuisance. The book’s young protagonist goes out of his way to intentionally infect himself with mumps so that he can beat his two brothers to the recovery finish line—and he experiences no adverse consequences other than his siblings’ annoyance.

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When infection arises after puberty, however, mumps is no laughing matter, presenting an increased risk of complications such as hearing loss, encephalitis and inflammation of the reproductive organs. About one in three postpubertal men with mumps develops orchitis(inflammation of the testes), which can damage sperm, affect testosterone production and contribute to subfertility and infertility. During a mumps outbreak in England in the mid-2000s, mumps orchitis accounted for 42% of all hospitalized mumps cases; the researchers attributed this outcome—which was the most common reason for hospitalization—to “the high attack rates in adolescents and young adults” that occurred “despite high coverage with two-dose MMR.” An analysis of a 2006 mumps outbreak in the U.S. reported that male patients were over three times more likely than female patients to experience complications, “due primarily to orchitis.”

An estimated 5% to 10% of postpubertal women will develop oophoritis (swelling of the ovaries) following mumps infection. Oophoritis is associated with premature menopause and infertility, but mumps-related oophoritis has garnered little notice.

Mumps infections are often asymptomatic or produce nonspecific symptoms such as fever, while cases of orchitis may present with no other mumps symptoms. Nonetheless, public health officials advise clinicians that orchitis is an instant cue to test for mumps virus, and testing often reveals elevated mumps antibodies. In a case report of MMR failure, British clinicians isolated a novel genetic strain of mumps virus from the patient’s semen two weeks after the onset of orchitis and found mumps RNA in the semen 40 days later; they also noted “the appearance of anti-sperm antibodies,” with “potential long-term adverse effects on the patient’s fertility.”

In 2017, researchers who reviewed 185 studies conducted in Western nations found that sperm counts had plummeted by 50% to 60% between 1973 and 2011—an average decrease of 1.4% annually. Commenting on this work, one analyst estimated that 20% to 30% of young men in Europe and North America have sperm concentrations associated with a reduced ability to father a child. Given estimates that as much as 40% of reproductive problems have to do with the male partner, there is agreement on the importance of “finding and eliminating [the] hidden culprits in the environment” that most researchers believe are to blame.

An estimated 5% to 10% of postpubertal women will develop oophoritis (swelling of the ovaries) following mumps infection. Oophoritis is associated with premature menopause and infertility, but mumps-related oophoritis has garnered little notice.

MMR’s and MMRV’s potential to impair fertility never studied

Merck has not evaluated either of its two MMR vaccines—the MMR-II and the MMR-plus-varicella (MMRV) vaccine—for their potential to impair fertility. Whether such testing would unearth direct effects on fertility (as appears to be possible with HPV vaccination in women) is thus unknown. However, mumps vaccination undeniably increases reproductive-age individuals’ risk of mumps infection and, in the process, increases the risk of fertility-altering complications. These facts alone should be attracting far more attention.

Unfortunately, because clinicians already tend to underdiagnose mumps infection and underestimate mumps complications, it is likely that they are failing to recognize possible vaccine-induced reproductive health consequences of mumps infection in their adolescent and young adult patients. In one university outbreak, “most physicians…did not suspect mumps,” and even when they became aware of the outbreak, “diagnosing mumps was not always straightforward.” Moreover, although differentiating between vaccine strains of mumps virus and wild types could provide valuable information, few clinicians have the capacity or inclination to perform testing of this type. A Japanese study of cerebrospinal fluid and saliva from patients with mumps complications found vaccine strain in nearly all of the samples and noted the information’s importance in helping determine whether the complications were vaccine-related.

Those who have sought to understand mumps vaccines’ poor performance point to a mixture of explanatory factors. These include waning immunity, the high population density and close quarters encountered in settings such as college campuses, incomplete vaccine-induced immunity to wild virus as well as viral evolution such that “the vaccine triggers a less potent reaction against today’s mumps viruses than those of 50 years ago.” However, some also quietly admit that individuals with “mild vaccine-modified disease” could be perpetuating the chain of transmission. This latter point ought to be raising questions about the logic and wisdom of administering further rounds of MMR boosters during outbreaks while ignoring the problems created by the doses already given.

… some individuals respond poorly to mumps vaccination and vaccine-induced antibody levels correlate poorly with protection from mumps infection, irrespective of the number of additional doses of mumps-containing vaccine they receive.

Most scientists appear to be either resigned to ongoing mumps outbreaks in vaccinated populations or actually accept periodic outbreaks as the cost of doing business. Publications by FDA and CDC researchers reveal these agencies’ awareness that some individuals respond poorly to mumps vaccination and that vaccine-induced antibody levels correlate poorly with protection from mumps infection, “irrespective of the number of additional doses of mumps-containing vaccine they receive.” Considering the effects on fertility, the generally abysmal track record of mumps vaccination and Merck’s fraudulent claims about efficacy, it is hard to fathom medical and public health experts’ complacency about current mumps vaccines and vaccine policies.


Sign up for free news and updates from Robert F. Kennedy, Jr. and the Children’s Health Defense. CHD is planning many strategies, including legal, in an effort to defend the health of our children and obtain justice for those already injured. Your support is essential to CHD’s successful mission.

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Legal Challenge Against Forced Vaccination Filed in New York City

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On April 15, 2019, a legal challenge was filed in the New York State Trial Court by Robert Krakow, Robert F. Kennedy, Jr. and Patricia Finn against the New York City Department of Health and Human Hygiene for their forced Measles-Mumps-Rubella vaccination. The legal team asked for a temporary restraining order against the mandate that the Judge will likely review and provide an ex parte decision. Children’s Health Defense is supporting these efforts.

Last week, Children’s Health Defense reported that the NYC Commissioner of Health declared a public health emergency, ordering all people who live, work or reside in four Brooklyn zip codes to be vaccinated with the Measles-Mumps-Rubella vaccine. Non-compliance with the order is a misdemeanor subject to criminal and civil fines, including imprisonment. Only those with documented immunity, medical contraindications or infants under six months are exempt from the vaccine mandate.

READ THE PETITION
READ THE MEMORANDUM OF LAW
READ THE AFFIRMATION

Sign up for free news and updates from Robert F. Kennedy, Jr. and the Children’s Health Defense. CHD is planning many strategies, including legal, in an effort to defend the health of our children and obtain justice for those already injured. Your support is essential to CHD’s successful mission.

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Awareness

Magnesium Puts Psychiatric Drugs to Shame for Depression

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In Brief

  • The Facts:

    This article was written by Sayer Ji, Founder of Greenmedinfo.com where this article first appeared. Posted here with permission.

  • Reflect On:

    Is the priority of our federal health regulatory agencies and pharmaceutical companies human health, or profit? If there are more effective ways to treat several illnesses, why do they never mention them?

Depression is one of the most widely diagnosed conditions of our time, with over 3 million cases in the U.S. every year, and 350 million believed affected worldwide.1 Conventional medicine considers antidepressant drugs first-line treatments, including the newly approved injected postpartum drug costing $34,000 a treatment, to the tune of a 16 billion dollars in global sales by 2023. Despite their widespread use, these drugs are fraught with a battery of serious side effects, including suicidal ideation and completion — the last two things you would hope to see in a condition that already has suicidality as a co-morbidity. For this reason alone, natural, safe, and effective alternatives are needed more than ever before.

While research into natural alternatives for depression is growing daily — GreenMedInfo.com’s Depression database contains 647 studies on over 100 natural substances that have been studied to prevent or treat depression — it is rare to find quality human clinical research on the topic published in well-respected journals. That’s why a powerful study published in PLOS One titled, “Role of magnesium supplementation in the treatment of depression: A randomized clinical trial,” is so promising. Not only is magnesium safe, affordable, and easily accessible, but according to this recent study, effective in treating mild-to moderate symptoms of depression.

While previous studies have looked at the association between magnesium and depression,2-7 this is the first placebo-controlled clinical study to evaluate whether the use of over-the-counter magnesium chloride (248 mg elemental magnesium a day for 6 weeks) improves symptoms of depression.

The study design was a follows:

“ An open-label, blocked, randomized, cross-over trial was carried out in outpatient primary care clinics on 126 adults (mean age 52; 38% male) diagnosed with and currently experiencing mild-to-moderate symptoms with Patient Health Questionnaire-9 (PHQ-9) scores of 5–19. The intervention was 6 weeks of active treatment (248 mg of elemental magnesium per day) compared to 6 weeks of control (no treatment). Assessments of depression symptoms were completed at bi-weekly phone calls. The primary outcome was the net difference in the change in depression symptoms from baseline to the end of each treatment period. Secondary outcomes included changes in anxiety symptoms as well as adherence to the supplement regimen, appearance of adverse effects, and intention to use magnesium supplements in the future. Between June 2015 and May 2016, 112 participants provided analyzable data.”

The study results were as follows:

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“Consumption of magnesium chloride for 6 weeks resulted in a clinically significant net improvement in PHQ-9 scores of -6.0 points (CI -7.9, -4.2; P<0.001) and net improvement in Generalized Anxiety Disorders-7 scores of -4.5 points (CI -6.6, -2.4; P<0.001). Average adherence was 83% by pill count. The supplements were well tolerated and 61% of participants reported they would use magnesium in the future. Similar effects were observed regardless of age, gender, baseline severity of depression, baseline magnesium level, or use of antidepressant treatments. Effects were observed within two weeks. Magnesium is effective for mild-to-moderate depression in adults. It works quickly and is well tolerated without the need for close monitoring for toxicity.”

 For perspective, conventional antidepressant drugs are considering to generate an “adequate or complete treatment response” with a PHQ-9 score “decrease of 5 points or more from baseline.” At this level of efficacy, their recommended action is: “Do not change treatment; conduct periodic follow-up.” The magnesium’s score of -6.0 therefore represents the height of success within conventional expectations for a complete response, which is sometimes termed “remission.” In contradistinction, conventional antidepressant drugs result in nearly half of patients discontinuing treatment during the first month, usually due to their powerful and sometimes debilitating side effects.8

To summarize the main study outcomes:

  • There was a clinically significant improvement in both Depression and Anxiety scores.
  • 61% of patients reported they would use magnesium in the future.
  • Similar effects occurred across age, gender, severity of depression, baseline magnesium levels, or use of antidepressant treatments.
  • Effects were observed within two weeks.

 The study authors concluded:

“Magnesium is effective for mild-to-moderate depression in adults. It works quickly and is well tolerated without the need for close monitoring for toxicity.”

Beyond Depression: Magnesium’s Many Health Benefits & Where To Source It

Magnesium is a central player in your body’s energy production, as its found within 300 enzymes in the human body, including within the biologically active form of ATP known as MG-ATP. In fact, there have been over 3,751 magnesium binding sites identified within human proteins, indicating that it’s central nutritional importance has been greatly underappreciated.

Research relevant to magnesium has been accumulating for the past 40 years at a steady rate of approximately 2,000 new studies a year. Our database project has indexed well over 100 health benefits of magnesium thus far.  For the sake of brevity, we will address seven key therapeutic applications for magnesium as follows:

  • Fibromyalgia: Not only is magnesium deficiency common in those diagnosed with fibromyalgia, 9,10 but relatively low doses of magnesium (50 mg), combined with malic acid in the form of magnesium malate, has been clinically demonstrated to improve pain and tenderness in those to which it was administered.11
  • Atrial Fibrillation: A number of studies now exist showing that magnesium supplementation reduce atrial fibrillation, either by itself, or in combination with conventional drug agents.12
  • Diabetes, Type 2: Magnesium deficiency is common in type 2 diabetics, at an incidence of 13.5 to 47.7% according to a 2007 study. 13 Research has also shown that type 2 diabetics with peripheral neuropathy and coronary artery disease have lower intracellular magnesium levels. 14 Oral magnesium supplementation has been shown to reduce plasma fasting glucose and raising HDL cholesterol in patients with type 2 diabetes.15 It has also been shown to improve insulin sensitivity and metabolic control in type 2 diabetic subjects.16
  • Premenstrual Syndrome: Magnesium deficiency has been observed in women affected by premenstrual syndrome.17 It is no surprise therefore  that it has been found to alleviate premenstrual symptoms of fluid retention, 18 as well as broadly reducing associated symptoms by approximately 34% in women, aged 18-45, given 250 mg tablets for a 3-month observational period.20 When combined with B6, magnesium supplementation has been found to improve anxiety-related premenstrual symptoms.19
  • Cardiovascular Disease and Mortality: Low serum magnesium concentrations predict cardiovascular and all-cause mortality.21 There are a wide range of ways that magnesium may confer its protective effects. It may act like a calcium channel blocker,22it is hypotensive,23 it is antispasmodic (which may protect against coronary artery spasm),24 and anti-thrombotic.25 Also, the heart muscle cells are exceedingly dense in mitochondria (as high as 100 times more per cell than skeletal muscle), the “powerhouses” of the cell,” which require adequate magnesium to produce ATP via the citric acid cycle.
  • Migraine Disorders: Blood magnesium levels have been found to be significantly lower in those who suffer from migraine attacks.26,27 A recent Journal of Neural Transmission article titled, “Why all migraine patients should be treated with magnesium,” pointed out that routine blood tests do not accurately convey the true body magnesium stores since less than 2% is in the measurable, extracellular space, “67% is in the bone and 31% is located intracellularly.”28The authors argued that since “routine blood tests are not indicative of magnesium status, empiric treatment with at least oral magnesium is warranted in all migraine sufferers.” Indeed, oral magnesium supplementation has been found to reduce the number of headache days in children experiencing frequent migranous headaches,29and when combined with l-carnitine, is effective at reducing migraine frequency in adults, as well.30
  • Aging: While natural aging is a healthy process, accelerated aging has been noted to be a feature of magnesium deficiency,31especially evident in the context of long space-flight missions where low magnesium levels are associated with cardiovascular aging over 10 times faster than occurs on earth.32 Magnesium supplementation has been shown to reverse age-related neuroendocrine and sleep EEG changes in humans.33 One of the possible mechanisms behind magnesium deficiency associated aging is that magnesium is needed to stabilize DNA and promotes DNA replication. It is also involved in healing up of the ends of the chromosomes after they are divided in mitosis.34

 It is quite amazing to consider the afformentioned side benefits of magnesium consumption or supplementation within the context of the well-known side effects of pharmaceutical approaches to symptom

management of disease. On average, conventional drugs have 75 side effects associated with their use, including lethal ones (albeit sometimes rare). When considering magnesium’s many side benefits

and extremely low toxicity, clearly this fundamental mineral intervention (and dietary requirement) puts pharmaceutical approaches to depression to shame.

Best Sources of Magnesium In The Diet

The best source of magnesium is from food, and one way to identify magnesium-containing foods are those which are green, i.e. chlorophyll rich. Chlorophyll, which enable plants to capture solar energy and convert it into metabolic energy, has a magnesium atom at its center. Without magnesium, in fact, plants could not utilize the sun’s light energy.

Magnesium, however, in its elemental form is colorless, and many foods that are not green contain it as well. The point is that when found complexed with food cofactors, it is absorbed and utilized more efficiently than in its elemental form, say, extracted from limestone in the form of magnesium oxide.

 The following foods contain exceptionally high amounts of magnesium. The portions described are 100 grams, or a little over three ounces.

  • Rice bran, crude (781 mg)
  • Seaweed, agar, dried (770 mg)
  • Chives, freeze-dried (640 mg)
  • Spice, coriander leaf, dried (694 mg)
  • Seeds, pumpkin, dried (535 mg)
  • Cocoa, dry powder, unsweetened (499 mg)
  • Spices, basil, dried (422 mg)
  • Seeds, flaxseed (392 mg)
  • Spices, cumin seed (366 mg)
  • Nuts, brazilnuts, dried (376 mg)
  • Parsley, freeze-dried (372 mg)
  • Seeds, sesame meal (346 mg)
  • Nut, almond butter (303 mg)
  • Nuts, cashew nuts, roasted (273 mg)
  • Soy flour, defatted (290 mg)
  • Whey, sweet, dried (176 mg)
  • Bananas, dehydrated (108 mg)
  • Millet, puffed (106 mg)
  • Shallots, freeze-dried (104 mg)
  • Leeks, freeze-dried (156 mg)
  • Fish, salmon, raw (95 mg)
  • Onions, dehydrated flakes (92 mg)
  • Kale, scotch, raw (88 mg)

 Fortunately, for those who need higher doses, or are not inclined to consume magnesium rich foods, there are supplemental forms commonly available on the market. Keep in mind, for those who wish to take advantage of the side benefit of magnesium therapy, namely, its stool softening and laxative properties, magnesium citrate or oxide will provide this additional feature.

For those looking to maximize absorption and bioavailability magnesium glycinate is ideal, as glycine is the smallest amino acid commonly found chelated to magnesium, and therefore highly absorbable.

For more information on natural solutions to resolving depression, download our free e-book on the topic “21st Century Solutions to Depression.” 

References:

1) World Health Organization. Depression fact sheet no. 369 2012 [cited 2016 December 20]. Available from: http://www.who.int/mediacentre/factsheets/fs369/en/.

2) Jacka FN, Overland S, Stewart R, Tell GS, Bjelland I, Mykletun A. Association between magnesium intake and depression and anxiety in community-dwelling adults: the Hordaland Health Study. Aust N Z J Psychiatry. 2009;43(1):45–52. Pmid:19085527.

3) Huang JH, Lu YF, Cheng FC, Lee JN, Tsai LC. Correlation of magnesium intake with metabolic parameters, depression and physical activity in elderly type 2 diabetes patients: a cross-sectional study. Nutrition J. 2012;11(1):41. pmid:22695027; PubMed Central PMCID: PMC3439347.

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7) N Engl J Med. 2000 Dec 28;343(26):1942-50. Managing depression in medical outpatients.

8)  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

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12) GreenMedInfo.com, Atrial Fibrillation and Magnesium (5 studies)

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14)  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

15) 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

16)  Martha Rodríguez-Morán, Fernando Guerrero-Romero. Oral magnesium supplementation improves insulin sensitivity and metabolic control in type 2 diabetic subjects: a randomized double-blind controlled trial. Diabetes Care. 2003 Apr;26(4):1147-52. PMID: 12663588

17)  F Facchinetti, P Borella, G Sances, L Fioroni, R E Nappi, A R Genazzani. Oral magnesium successfully relieves premenstrual mood changes. Obstet Gynecol. 1991 Aug;78(2):177-81. PMID: 2067759

18)  A F Walker, M C De Souza, M F Vickers, S Abeyasekera, M L Collins, L A Trinca. Magnesium supplementation alleviates premenstrual symptoms of fluid retention. J Womens Health. 1998 Nov;7(9):1157-65. PMID: 9861593

19)  S Quaranta, M A Buscaglia, M G Meroni, E Colombo, S Cella. Pilot study of the efficacy and safety of a modified-release magnesium 250 mg tablet (Sincromag) for the treatment of premenstrual syndrome. Am J Gastroenterol. 2008 Dec;103(12):2972-6. PMID: 17177579

20) M C De Souza, A F Walker, P A Robinson, K Bolland. A synergistic effect of a daily supplement for 1 month of 200 mg magnesium plus 50 mg vitamin B6 for the relief of anxiety-related premenstrual symptoms: a randomized, double-blind, crossover study. J Womens Health Gend Based Med. 2000 Mar;9(2):131-9. PMID: 10746516

21) 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

22) Andrea Rosanoff, Mildred S Seelig. Comparison of mechanism and functional effects of magnesium and statin pharmaceuticals. J Am Coll Nutr. 2004 Oct;23(5):501S-505S. PMID: 15466951

23)  GreenMedInfo.com, Magnesium’s Hypotensive Properties.

24) GreenMedInfo.com, Magnesium’s Antispasmodic Properties.

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26) Afshin Samaie, Nabiollah Asghari, Raheb Ghorbani, Jafar Arda. Blood Magnesium levels in migraineurs within and between the headache attacks: a case control study. Pan Afr Med J. 2012 ;11:46. Epub 2012 Mar 15. PMID: 22593782

27) Mahnaz Talebi, Dariush Savadi-Oskouei, Mehdi Farhoudi, Solmaz Mohammadzade, Seyyedjamal Ghaemmaghamihezaveh, Akbar Hasani, Amir Hamdi. Relation between serum magnesium level and migraine attacks. Neurosciences (Riyadh). 2011 Oct ;16(4):320-3. PMID: 21983373

28) Alexander Mauskop, Jasmine Varughese. Why all migraine patients should be treated with magnesium. J Neural Transm. 2012 May ;119(5):575-9. Epub 2012 Mar 18. PMID: 22426836

29)  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

30) 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

31) David W Killilea, Jeanette A M Maier. A connection between magnesium deficiency and aging: new insights from cellular studies. Magnes Res. 2008 Jun;21(2):77-82. PMID: 18705534

32) GreenMedInfo.com, What We Learned From The Accelerated Aging of Astronauts

33) Katja Held, I A Antonijevic, H Künzel, M Uhr, T C Wetter, I C Golly, A Steiger, H Murck. Oral Mg(2+) supplementation reverses age-related neuroendocrine and sleep EEG changes in humans. Pharmacopsychiatry. 2002 Jul;35(4):135-43. PMID: 12163983

34) William J Rowe. Correcting magnesium deficiencies may prolong life. Clin Interv Aging. 2012 ;7:51-4. Epub 2012 Feb 16. PMID: 22379366


Sayer Ji is founder of Greenmedinfo.com, a reviewer at the International Journal of Human Nutrition and Functional Medicine, Co-founder and CEO of Systome Biomed, Vice Chairman of the Board of the National Health Federation, Steering Committee Member of the Global Non-GMO Foundation.


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