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Depression: It’s Not Your Serotonin

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This article was written by Dr. Kelly Brogan, posted here with permission.

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Millions believe depression is caused by ‘serotonin deficiency,’ but where is the science in support of this theory?

“Depression is a serious medical condition that may be due to a chemical imbalance, and Zoloft works to correct this imbalance.”

Herein lies the serotonin myth.

As one of only two countries in the world that permits direct to consumer advertising, you have undoubtedly been subjected to promotion of the “cause of depression.” A cause that is not your fault, but rather; a matter of too few little bubbles passing between the hubs in your brain! Don’t add that to your list of worries, though, because there is a convenient solution awaiting you at your doctor’s office…

What if I told you that, in 6 decades of research, the serotonin (or norepinephrine, or dopamine) theory of depression and anxiety has not achieved scientific credibility?

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You’d want some supporting arguments for this shocking claim.

So, here you go:

The Science of Psychiatry is Myth

Rather than some embarrassingly reductionist, one-deficiency-one-illness-one-pill model of mental illness, contemporary exploration of human behavior has demonstrated that we may know less than we ever thought we did.  And that what we do know about root causes of mental illness seems to have more to do with the concept of evolutionary mismatch than with genes and chemical deficiencies.

In fact, a meta-analysis of over 14,000 patients and Dr. Insel, head of the NIMH, had this to say:

“Despite high expectations, neither genomics nor imaging has yet impacted the diagnosis or treatment of the 45 million Americans with serious or moderate mental illness each year.”

To understand what imbalance is, we must know what balance looks like, and neuroscience, to date, has not characterized the optimal brain state, nor how to even assess for it.

A New England Journal of Medicine review on Major Depression, stated:

” … numerous studies of norepinephrine and serotonin metabolites in plasma, urine, and cerebrospinal fluid as well as postmortem studies of the brains of patients with depression, have yet to identify the purported deficiency reliably.”

The data has poked holes in the theory and even the field of psychiatry itself is putting down its sword. One of my favorite essays by Lacasse and Leo has compiled sentiments from influential thinkers in the field – mind you, these are conventional clinicians and researchers in mainstream practice – who have broken rank, casting doubt on the entirety of what psychiatry has to offer around antidepressants:

Humble Origins of a Powerful Meme

In the 1950s, reserpine, initially introduced to the US market as an anti-seizure medication, was noted to deplete brain serotonin stores in subjects, with resultant lethargy and sedation. These observations colluded with the clinical note that an anti-tuberculosis medication, iproniazid, invoked mood changes after five months of treatment in 70% of a 17 patient cohort. Finally, Dr. Joseph Schildkraut threw fairy dust on these mumbles and grumbles in 1965 with his hypothetical manifesto entitled “The Catecholamine Hypothesis of Affective Disorders” stating:

“At best, drug-induced affective disturbances can only be considered models of the natural disorders, while it remains to be demonstrated that the behavioral changes produced by these drugs have any relation to naturally occurring biochemical abnormalities which might be associated with the illness.”

Contextualized by the ripeness of a field struggling to establish biomedical legitimacy (beyond the therapeutic lobotomy!), psychiatry was ready for a rebranding, and the pharmaceutical industry was all too happy to partner in the effort.

Of course, the risk inherent in “working backwards” in this way (noting effects and presuming mechanisms) is that we tell ourselves that we have learned something about the body, when in fact, all we have learned is that patented synthesized chemicals have effects on our behavior. This is referred to as the drug-based model by Dr. Joanna Moncrieff. In this model, we acknowledge that antidepressants have effects, but that these effects in no way are curative or reparative.

The most applicable analogy is that of the woman with social phobia who finds that drinking two cocktails eases her symptoms. One could imagine how, in a 6 week randomized trial, this “treatment” could be found efficacious and recommended for daily use and even prevention of symptoms. How her withdrawal symptoms after 10 years of daily compliance could lead those around her to believe that she “needed” the alcohol to correct an imbalance. This analogy is all too close to the truth.

Running With Broken Legs

Psychiatrist Dr. Daniel Carlat has said:

“And where there is a scientific vacuum, drug companies are happy to insert a marketing message and call it science. As a result, psychiatry has become a proving ground for outrageous manipulations of science in the service of profit.”

So, what happens when we let drug companies tell doctors what science is? We have an industry and a profession working together to maintain a house of cards theory in the face of contradictory evidence.

We have a global situation in which increases in prescribing are resulting in increases in severity of illness (including numbers and length of episodes) relative to those who have never been treated with medication.

To truly appreciate the breadth of evidence that states antidepressants are ineffective and unsafe, we have to get behind the walls that the pharmaceutical companies erect. We have to unearth unpublished data, data that they were hoping to keep in the dusty catacombs.

A now famous 2008 study in the New England Journal of Medicine by Turner et al sought to expose the extent of this data manipulation. They demonstrated that, from 1987 to 2004, 12 antidepressants were approved based on 74 studies. Thirty-eight were positive, and 37 of these were published.  Thirty-six were negative (showing no benefit), and 3 of these were published as such while 11 were published with a positive spin(always read the data not the author’s conclusion!), and 22 were unpublished.

In 1998 tour de force, Dr. Irving Kirsch, an expert on the placebo effect, published a metaanalysis of 3,000 patients who were treated with antidepressants, psychotherapy, placebo, or no treatment and found that only 27% of the therapeutic response was attributable to the drug’s action.

This was followed up by a 2008 review, which invoked the Freedom of Information Act to obtain access to unpublished studies, finding that, when these were included, antidepressants outperformed placebo in only 20 of 46 trials (less than half!), and that the overall difference between drugs and placebos was 1.7 points on the 52 point Hamilton Scale.  This small increment is clinically insignificant, and likely accounted for by medication side effects strategically employed (sedation or activation).

When active placebos were used, the Cochrane database found that differences between drugs and placebos disappeared, given credence to the assertion that inert placebos inflate perceived drug effects.

The finding of tremendous placebo effect in the treatment groups was also echoed in two different meta-analyses by Khan et al who found a 10% difference between placebo and antidepressant efficacy, and comparable suicide rates. The most recent trial examining the role of “expectancy” or belief in antidepressant effect, found that patients lost their perceived benefit if they believed that they might be getting a sugar pill even if they were continued on their formerly effective treatment dose of Prozac.

The largest, non-industry funded study, costing the public $35 million dollars, followed 4000 patients treated with Celexa (not blinded, so they knew what they were getting), and found that half of them improved at 8 weeks. Those that didn’t were switched to Wellbutrin, Effexor, or Zoloft OR “augmented” with Buspar or Wellbutrin.

Guess what? It didn’t matter what was done, because they remitted at the same unimpressive rate of 18-30% regardless with only 3% of patients in remission at 12 months.

How could it be that medications like Wellbutrin, which purportedly primarily disrupt dopamine signaling, and medications like Stablon which theoretically enhances the reuptake of serotonin, both work to resolve this underlying imbalance? Why would thyroid, benzodiazepines, beta blockers, and opiates also “work”? And what does depression have in common with panic disorder, phobias, OCD, eating disorders, and social anxiety that all of these diagnoses would warrant the same exact chemical fix?

Alternative options

As a holistic clinician, one of my bigger pet peeves is the use of amino acids and other nutraceuticals with  “serotonin-boosting” claims. These integrative practitioners have taken a page from the allopathic playbook and are seeking to copy-cat what they perceive antidepressants to be doing.

The foundational “data” for the modern serotonin theory of mood utilizes tryptophan depletion methods which involve feeding volunteers amino acid mixtures without tryptophan and are rife with complicated interpretations.

Simply put, there has never been a study that demonstrates that this intervention causes mood changes in any patients who have not been treated with antidepressants.

In an important paper entitled Mechanism of acute tryptophan depletion: Is it only serotonin?, van Donkelaar et al caution clinicians and researchers about the interpretation of tryptophan research. They clarify that there are many potential effects of this methodology, stating:

“In general, several findings support the fact that depression may not be caused solely by an abnormality of 5-HT function, but more likely by a dysfunction of other systems or brain regions modulated by 5-HT or interacting with its dietary precursor. Similarly, the ATD method does not seem to challenge the 5-HT system per se, but rather triggers 5HT-mediated adverse events.”

So if we cannot confirm the role of serotonin in mood and we have good reason to believe that antidepressant effect is largely based on belief, then why are we trying to “boost serotonin”?

Causing imbalances

All you have to do is spend a few minutes on http://survivingantidepressants.org/or http://beyondmeds.com/ to appreciate that we have created a monster. Millions of men, women, and children the world over are suffering, without clinical guidance (because this is NOT a part of medical training) to discontinue psychiatric meds. I have been humbled, as a clinician who seeks to help these patients, by what these medications are capable of. Psychotropic withdrawal can make alcohol and heroin detox look like a breeze.

An important analysis by the former director of the NIMH makes claims that antidepressants “create perturbations in neurotransmitter functions” causing the body to compensate through a series of adaptations which occur after “chronic administration” leading to brains that function, after a few weeks, in a way that is “qualitatively as well as quantitatively different from the normal state.”

Changes in beta-adrenergic receptor density, serotonin autoreceptor sensitivity, and serotonin turnover all struggle to compensate for the assault of the medication.

Andrews, et al., calls this “oppositional tolerance,” and demonstrate through a careful meta-analysis of 46 studies demonstrating that patient’s risk of relapse is directly proportionate to how “perturbing” the medication is, and is always higher than placebo (44.6% vs 24.7%). They challenge the notion that findings of decreased relapse on continued medication represent anything other than drug-induced response to discontinuation of a substance to which the body has developed tolerance. They go a step further to add:

“For instance, in naturalistic studies, unmedicated patients have much shorter episodes, and better long-term prospects, than medicated patients. Several of these studies have found that the average duration of an untreated episode of major depression is 12–13 weeks.”

Harvard researchers also concluded that at least fifty percent of drug-withdrawn patients relapsed within 14 months. In fact:

“Long-term antidepressant use may be depressogenic . . . it is possible that antidepressant agents modify the hardwiring of neuronal synapses (which) not only render antidepressants ineffective but also induce a resident, refractory depressive state.”

So, when your doctor says, “You see, look how sick you are, you shouldn’t have stopped that medication,” you should know that the data suggests that your symptoms are withdrawal, not relapse.

Longitudinal studies demonstrate poor functional outcomes for those treated with 60% of patients still meeting diagnostic criteria at one year (despite transient improvement within the first 3 months). When baseline severity is controlled for, two prospective studies support a worse outcome in those prescribed medication:

One in which the never-medicated group experienced a 62% improvement by six months, whereas the drug-treated patients experienced only a 33% reduction in symptoms, and another WHO study of depressed patients in 15 cities which found that, at the end of one year, those who weren’t exposed to psychotropic medications enjoyed much better “general health”; that their depressive symptoms were much milder”; and that they were less likely to still be “mentally ill.” 

I’m not done yet. In a retrospective 10-year study in the Netherlands, 76% of those with unmedicated depression recovered without relapse relative to 50% of those treated.

Unlike the mess of contradictory studies around short-term effects, there are no comparable studies that show a better outcome in those prescribed antidepressants long term.

First Do No Harm

So, we have a half-baked theory in a vacuum of science that that pharmaceutical industry raced to fill. We have the illusion of short-term efficacy and assumptions about long-term safety. But are these medications actually killing people?

The answer is yes.

Unequivocally, antidepressants cause suicidal and homicidal behavior. The Russian Roulette of patients vulnerable to these “side effects” is only beginning to be elucidated and may have something to do with genetic variants around metabolism of these chemicals.  Dr. David Healy has worked tirelessly to expose the data that implicates antidepressants in suicidality and violence, maintaining a database for reporting, writing, and lecturing about cases of medication-induced death that could make your soul wince.

What about our most vulnerable?

I have countless patients in my practice who report new onset of suicidal ideation within weeks of starting an antidepressant. In a population where there are only 2 randomized trials, I have grave concerns about postpartum women who are treated with antidepressants before more benign and effective interventions such as dietary modification and thyroid treatment. Hold your heart as you read through these reportsof women who took their own and their childrens’ lives while treated with medications.

Then there is the use of these medications in children as young as 2 years old. How did we ever get the idea that this was a safe and effective treatment for this demographic? Look no further than data like Study 329, which cost Glaxo Smith Klein 3 billion dollars for their efforts to promote antidepressants to children. These efforts required ghost-written and manipulated data that suppressed a signal of suicidality, falsely represented Paxil as outperforming placebo, and contributes to an irrepressible mountain of harmdone to our children by the field of psychiatry.

RIP Monoamine Theory

As Moncrieff and Cohen so succinctly state:

“Our analysis indicates that there are no specific antidepressant drugs, that most of the short-term effects of antidepressants are shared by many other drugs, and that long-term drug treatment with antidepressants or any other drugs has not been shown to lead to long-term elevation of mood. We suggest that the term “antidepressant” should be abandoned.”

So, where do we turn?

The field of psychoneuroimmunology dominates the research as an iconic example of how medicine must surpass its own simplistic boundaries if we are going to begin to chip away at the some 50% of Americans who will struggle with mood symptoms, 11% of whom will be medicated for it.

There are times in our evolution as a cultural species when we need to unlearn what we think we know. We have to move out of the comfort of certainty and into the freeing light of uncertainty. It is from this space of acknowledged unknowing that we can truly grow. From my vantage point, this growth will encompass a sense of wonder – both a curiosity about what symptoms of mental illness may be telling us about our physiology and spirit, as well as a sense of humbled awe at all that we do not yet have the tools to appreciate. For this reason, honoring our co-evolution with the natural world, and sending the body a signal of safety through movement, diet, meditation, and environmental detoxification represents our most primal and most powerful tool for healing.


Learn more by taking Dr. Kelly Brogan’s E-Course Vital Mind Reset.

GreenMedInfo LLC. . This work is reproduced and distributed with the permission of GreenMedInfo LLC.  Where it first originally appeared. Want to learn more from GreenMedInfo? Sign up for the newsletter here http://www.greenmedinfo.com/greenmed/newsletter.”


Dr. Brogan is boarded in Psychiatry/Psychosomatic Medicine/Reproductive Psychiatry and Integrative Holistic Medicine, and practices Functional Medicine, a root-cause approach to illness as a manifestation of multiple-interrelated systems. After studying Cognitive Neuroscience at M.I.T., and receiving her M.D. from Cornell University, she completed her residency and fellowship at Bellevue/NYU. She is one of the nation’s only physicians with perinatal psychiatric training who takes a holistic evidence-based approach in the care of patients with a focus on environmental medicine and nutrition. She is also a mom of two, and an active supporter of women’s birth experience. She is the Medical Director for Fearless Parent, and an advisory board member for GreenMedInfo.comVisit her website.

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The Mental Health Morass: Good for Pharma, Bad for Youth

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When several hundred Colorado high school students walked out of a post-school-shooting vigil last May to protest the event’s politicization, their departing chant was, “mental health, mental health.” While this response may have unsettled the event’s organizers, it was unsurprising in the context of widespread media accounts of an “epidemic of anguish” among American youth. According to this narrative, not only is “the increase in mental health issues among [U.S.] teens and young adults…nothing short of staggering,” but around the globe, mental illness is set to become the “next major global health challenge” and “pandemic of the 21st century.”

Without making light of the problem or minimizing anyone’s personal suffering, it is clear that one entity that stands to benefit mightily from a deepening mental health crisis is the pharmaceutical industry. Psychiatric medications have long been “growth superstars”—generating billions in sales for companies like Pfizer and Eli Lilly “as the U.S. became Prozac Nation, antipsychotics also became antidepressants, and ADHD [attention-deficit/hyperactivity disorder] a byword.” Already in the mid-2000s, a Harvard economist reported that spending on psychotropic drugs had substantially outpaced overall prescription drug spending—no mean feat given the drug market’s exponential growth.

Outsized drug company profits and clever marketing tactics have prompted many to question the industry’s “oversized role in determining how mental illness is treated.” Even in conventional medical circles, clinicians acknowledge the need for “radical change in the paradigm and practices of mental health care,” including interventions that emphasize prevention and non-pharmacologic treatment modalities. These sorts of recommendations are urgently needed—not least for the young people for whom there is scant evidence of psychotropic medication safety or efficacy.

Overlapping trends

Modern psychiatry situates an alphabet soup of diagnoses under the broad rubric of “mental, emotional and behavioral” (MEB) disorders. It is no longer uncommon for children and adolescents to receive one or more of these diagnoses: anxiety disorder; attention-deficit/hyperactivity disorder; autism spectrum disorder; bipolar disorder; conduct disorder; depression; disruptive behavior disorder; drug abuse or dependence; eating disorders; obsessive-compulsive disorder; oppositional defiant disorder; pervasive developmental disorder; post-traumatic stress disorder; and schizophrenia.

The proliferation of mental health diagnoses in young people overlaps considerably with trends in diagnosed neurodevelopmental disorders. In addition, mental health diagnoses frequently intersect with physical conditions such as asthma, diabetes and epilepsy, which are more often present in children with mental disorders than in children without such disorders. Pediatric hospital admissions for non-behavioral disorders result in higher costs and longer stays when they are comorbid with behavioral disorders.

One of the few large-scale surveys to focus on MEB disorders in children (rather than adults) was the National Comorbidity Survey-Adolescent Supplement (NCS-A), conducted from 2001 to 2004. The NCS-A found that half of U.S. youth (ages 13-18) had been diagnosed with at least one MEB disorder—including one in five with behavior disorders and three in ten with anxiety disorders—with the impairments rated as “severe” in roughly one-fourth of the affected teens. For many of the young people, onset and diagnosis occurred well before adolescence. Reviewing the evidence, the National Research Council and Institute of Medicine reported in 2009 that “early MEB disorders should be considered as commonplace as a fractured limb: not inevitable but not at all unusual.”

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The impact

Recent research has documented some of the impact of these “commonplace” diagnoses in young people. Between 2011 and 2015, for example, visits by U.S. youth to psychiatric emergency departments increased by 28%. By age group, the largest increase—54%—was seen in adolescents (as compared to younger children or youth in their early 20s), in whom the researchers also reported a 2.5-fold increase in suicide-related visits. As of 2010, mood disorders (which include both bipolar and depressive disorders) were the most frequent principal diagnosis given to hospitalized children ages 1-17—up 80% since 1997. The hospitalization rate for bipolar disorders increased fourfold between the two time points (1997–2010), especially in the 10-14 and 15-17 age groups.

Researchers describe comorbid ADHD as “nearly universal” among youth with bipolar disorder, with ADHD and anxiety disorders viewed as common precursors of bipolar disorder. The trend toward increased diagnosis of both ADHD and bipolar disorder has prompted increased use by young people of both inpatient and outpatient mental health services as well as an exponential increase in the prescribing of medication. In office-based settings, where mental health care for young people has increased more rapidly than for adults, psychotropic medication prescriptions for younger patients are often provided by physicians with no psychiatric training.

For both ADHD and bipolar disorder, pharmacologic treatment relies heavily on powerful psychostimulants, antipsychotics and mood stabilizers. Reporting on data collected in 2011–2012, researchers noted that a large proportion (44%) of very young children diagnosed with ADHD (2- to 5-year-olds) were taking medication, most commonly central nervous system stimulants. Nationally, a survey of children with special health care needs conducted in 2009–2010 found that 74% of ADHD-diagnosed children ages 4-17 had received medication in the past week.

Both the scientific community and mainstream media have raised questions about whether widespread administration of mind-altering psychostimulants to young children is safe or “meaningfully beneficial.” In 2016, a Washington Post reporter cited CDC findings when noting that “The long-term effects of those [ADHD] drugs on a young brain and body have not been well studied, and the side effects can be numerous, including poor appetite, sleeplessness, irritability and slowed growth.” Other risks of these freely prescribed drugs include the potential to actually worsen mania, foster addiction or lead to further medication. In the push for increased treatment, clinicians have largely ignored these risks.

In some states, special education funding policies create financial incentives to actively identify and medicate children with ADHD. In those states, children are “about 15 percent more likely to report having ADHD and…about 22 percent more likely to be taking medication for ADHD.” As a medical ethicist has commented, these patterns raise questions about the “muddier” aspects of psychiatric diagnosis and the variability “as regards who and what drive [diagnostic] practices.”

The selective serotonin reuptake inhibitors (SSRIs) commonly prescribed for depression and anxiety disorders have also raised serious concerns—particularly about their potential to promote suicidality, aggression or other unwanted outcomes in children and adolescents. In 2016, the Nordic Cochrane Centre systematically reviewed clinical study reports from 70 trials of SSRIs and similar drugs and described substantial under-reporting of harms. Even with the under-reporting, the reviewed evidence linked the drugs to a doubling in the risk of suicidality and aggression in children and adolescents.

Why is this happening?

Researchers have floated many hypotheses about the underlying causes of the burgeoning youth mental health crisis. But while the mainstream media have been more than willing to give airtime to social explanations such as smartphone use and academic stress, the public has seen far less discussion of other plausible factors such as the gut-brain connection. For example, there is a complex interplay between the gut microbiome, the immune response and vaccination—and experimental evidence links vaccines and vaccine adjuvants to adverse mental health symptoms. There is also ample experimental evidence showing that gut microbiota disruptions caused by subchronic and chronic exposure to glyphosate-based herbicides can increase anxiety and depression-like behaviors at virtually any age. Moreover, research findings are suggestive of potential transgenerational effects of both vaccines and glyphosate. Rather than acquiesce to the perpetuation of hair-splitting mental health diagnoses—and the pharmaceutical “solutions” that always seem to follow close behind—it would seem wise to scrutinize these pervasive environmental threats while keeping in mind the age-old question of cui bono.

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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12,000 Doctors Urge the FDA to Put Cancer Warnings on Cheese

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In Brief

  • The Facts:

    The Physicians Committee for Responsible Medicine (PCRM) recently submitted a citizen petition with the Food and Drug Administration (FDA) to change labeling on cheese to include a cancer warning.

  • Reflect On:

    Why have our federal health regulatory agencies and big food companies marketed dairy products as safe, healthy and necessary when the science clearly suggests otherwise.

What do doctors learn about nutrition in medical school? Shockingly and unfortunately, nothing. Why? Because nutrition does not bring in profit, and treating people with nutrition hasn’t seemed to be an option at all ever since the birth of the mainstream medical industry. The sad reality is that “the medical profession is being bought by the pharmaceutical industry, not only in terms of the practice of medicine, but also in terms of teaching and research. The academic institutions of this country are allowing themselves to be the paid agents of the pharmaceutical industry. I think it’s disgraceful.” – Arnold Seymour Relman (source)

Thankfully, things are changing and changing fast. A lot of people are taking their nutritional education into their own hands, and many doctors are also educating themselves on the power of nutrition through the plethora studies and clinical evidence that’s available out there.

One of the latest examples of doctors educating themselves comes from the Physicians Committee for Responsible Medicine (PCRM), who recently submitted a citizen petition with the Food and Drug Administration (FDA) to change labeling on cheese to include a cancer warning.

Why? Because based on the research, cheese, and dairy from the animal of another is not good, but bad for us. This reality may be hard for many to believe given the fact that it’s been one of the stable food groups for so long. It’s time we start recognizing that “nutritional education” that we grow up with is a product of the big food companies and marketing, it’s not backed by any science and more people are starting to become aware of what the science is actually showing us.

The petition states:

Dairy cheese contains reproductive hormones that may increase breast cancer mortality risk. (This sentence is what they want on dairy cheese products).

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High-fat dairy products, such as cheese, are associated with an increased risk for breast cancer. Components in dairy such as insulin-like growth factor (IGF-1) and other growth hormones may be among the reasons for the increased risk for cancer.

To ensure that Americans understand the potential significant risks, and resulting long-term costs, of consuming dairy cheese products, the FDA should ensure that the notice above is prominently placed on product packaging and labeling for all dairy cheese products.

I find it interesting that they mention IGF-1 growth hormone.

A 2015 study published in Cell Metabolism is one of multiple studies that points out:

Mice and humans with Growth Hormone Receptor/IGF-1 deficiencies display major reductions in age-related diseases. Because protein restriction reduces GHR-IGF-1 activity, we examined links between protein intake and mortality. Respondents (n=6,381) aged 50–65 reporting high protein intake had a 75% increase in overall mortality and a 4-fold increase in cancer and diabetes mortality during an 18 year follow up period. These associations were either abolished or attenuated if the source of proteins was plant-based.

The study above corroborates with a lot of other research showing that animal protein skyrockets IFG-1 growth hormone, thus leading to a wide variety of diseases, in the long term, including cancer. The interesting thing is that protein from plants, as the study points out, “abolished or attenuated” these associations “if the source of proteins was plant-based.”

Fasting has been shown to reduce the risk and even reverse many age related diseases, like Parkinson’s and Alzheimer’s. It’s also been shown to regenerate stem cells and slow down the overall aging process, much of that is due to the fact that fasting drops our IGF-1 growth hormone levels.

A recent study conducted by researchers in California and France found that meat protein is associated with a very sharp increased risk of heart disease, while protein from nuts and seeds is actually beneficial for the human heart.

The study is titled “Patterns of plant and animal protein intake are strongly associated with cardiovascular mortality: The Adventist Health Study-2 cohort,” It was a joint project between researchers from Loma Linda University School of Public Health in California and AgroParisTech and the Institut National de la Recherche Agronomique in Paris, France.

It was published in the International Journal of Epidemiology. The researchers found that people who ate large amounts of meat protein, which is a daily norm for many people, represented a portion of the human population that would experience a 60 percent increase in cardiovascular disease (CVD), while people who consumed large amounts of protein from nuts and seeds actually experienced a 40 percent reduction in CVD.

Dairy “Turning on Cancer.”

Doctor Colin Campbell. author of the “China Study”  discovered that animal protein (casein) can accelerate and “turn on” cancer, while plant based protein has the opposite effect.

“What I did during the early part of my career was nothing more than what traditional science would suggest. I made the observation that diets presumably higher in animal protein were associated with liver cancer in the Philippines. When coupled with the extraordinary report from India showing that casein fed to experimental rats at the usual levels of intake dramatically promoted liver cancer, it prompted my 27-year-long study The China Project, of how this effect worked. We did dozens of experiments to see if this was true and, further, how it worked.” – Dr Colin Campbell, (China Study)

Campbell is an American biochemist who specializes in the effect of nutrition on long term health. He is Professor Emeritus of Nutritional Biochemistry at Cornell University, he has a Ph.D. in nutrition, biochemistry, and microbiology. Scholars like Campbell and their work is so important in a world of medical education and academia that almost completely ignores nutrition.

Casein is the most relevant chemical carcinogen ever identified, make no mistake about it. (source)

Campbell went beyond mere correlation and found using animal studies he conducted that casein actually “turns on” cancer. When animals were fed a diet high in casein, the cancer increased dramatically. What’s even more interesting is when they decided to do a comparison using plant protein.

What we learned along the way is that we could turn on and turn off cancer. Turn it on by increasing casein consumption, turn it off by decreasing it or replacing it with plant protein. That was a really exciting thing that we could take nutrition and turn cancer on and off, I mean that, that was pretty startling. – Campbell (source)

The Takeaway

We are the only species on the planet that consumes the dairy of another animal after weaning.  The reduction of lactase activity after infancy is a genetically programmed event. Approximately 75 % of Earths population is lactose intolerant for a reason, because it’s perfectly natural. We are not meant to drink the milk of another animal and we had to evolve the gene to digest it.  The statistics vary from race to race and country to country but overall they show an abnormal amount of individuals who qualify. In some Asian countries, 90 percent of the population is lactose intolerant.

It seems the big food companies convinced us that it’s a requirement, and that it’s healthy. They used protein and calcium (both of which are present in a number of plant sources, for example) as mass marketing tools to push dairy products on the population in order to turn a very large profit, all at the health expense of human beings.

This is one of multiple examples off mass perception manipulation.

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Awareness

7 Ways to Prevent and Even Reverse Heart Disease with Nutrition

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In Brief

  • The Facts:

    This article was written by Sayer Ji. Founder of Greenmedinfo.com. Posted here with permission.

  • Reflect On:

    Heart disease, while still the #1 cause of mortality in the developed world, can be prevented and even reversed with nutritional interventions, according to a growing body of scientific research.

Considering that heart disease is the #1 cause of death in the developed world, anything that can prevent or reduce cardiac mortality, or slow or even reverse the cardiovascular disease process, should be of great interest to health professionals and the general public alike.

Sadly, millions are still unaware of the extensive body of biomedical literature that exists supporting the use of natural compounds for preventing and even reversing heart disease, which we have indexed on GreenMedInfo.com.

Instead, they spend billions of healthcare dollars annually on highly toxic cholesterol-lowering pharmaceuticals such as statin drugs which have known cardiotoxicity, among 300 other proven side effects, simply because their doctors told them to do so. Bad advice is the rule and not the exception here. For instance, after decades of recommending a so-called ‘low dose’ aspirin to prevent heart disease and stroke, the weight of evidence now points to it being a cause of significantly more harm than good: Doctors Reverse Decades Old Aspirin Recommendation: Deadly Risks Outweigh Benefits for Heart Disease & Stroke

So, with this in mind, let’s look at a small but significant sample of natural, food-based alternatives to these drugs through the lens of the clinical and biomedical literature itself.

Three Natural Substances that Reduce the Risk of Heart-Related Death

  • Omega-3 Fatty Acids: There is a robust body of research indicating that the risk of sudden cardiac death is reduced when consuming higher levels of omega-3 fatty acids. Going all the way back to 2002, the New England Journal of Medicine published a study titled, “Blood levels of long-chain n-3 fatty acids and the risk of sudden death,” which found: “The n-3 fatty acids found in fish are strongly associated with a reduced risk of sudden death among men without evidence of prior cardiovascular disease.” Another 2002 study, published in the journal Circulation, found that Omega-3 fatty acid supplementation reduces total mortality and sudden death in patients who have already had a heart attack.[i] For additional research, view our dataset on the topic of Omega-3 fatty acids and the reduction of cardiac mortality. It should be noted that the best-selling cholesterol drug class known as statins may actually reduce the effectiveness of omega-3 fats at protecting the heart. This has been offered as an explanation as to why newer research seems to show that consuming omega-3 fats does not lower the risk of cardiac mortality.
  • Vitamin D: Levels of this essential compound have been found to be directly associated with the risk of dying from all causes. Being in the lowest 25% percent of vitamin D levels is associated with a 26% increased rate of all-cause mortality.[ii] It has been proposed that doubling global vitamin D levels could significantly reduce mortality.[iii] Research published in the journal Clinical Endocrinology in 2009 confirmed that lower vitamin D levels are associated with increased all-cause mortality but also that the effect is even more pronounced with cardiovascular mortality.[iv] This finding was confirmed the same year in the Journal of the American Geriatric Society, [v] and again in 2010 in the American Journal of Clinical Nutrition.[vi]
  • Magnesium: In a world gone mad over taking inorganic calcium supplementation for manufactured diseases such as T-score defined “osteopenia” or “osteoporosis,”despite their well-known association with increased risk of cardiac mortality, magnesium’s role in protecting against heart disease cannot be overstressed. It is well-known that even the accelerated aging of the heart muscle experienced by those in long space flight is due to magnesium deficiency. In 2010, the Journal of Biomedical Sciences reported that cardiovascular risks are significantly lower in individuals who excrete higher levels of magnesium, indicating its protective role.[vii] Another study published in the journal Atherosclerosis in 2011 found that low serum magnesium concentrations predict cardiovascular and all-cause mortality.[viii] Remember that when you are looking to ‘supplement’ your diet with magnesium go green. Chlorophyll is green because it has a magnesium atom at its center. Kale, for example, is far better a source of complex nutrition than magnesium supplements. But, failing the culinary approach, magnesium supplements can be highly effective at attaining a therapeutic and/or cardioprotective dose.

For an additional list of compounds that may reduce cardiac mortality, including cocoa, tea, wine and yes, even cholesterol itself, view our Reduce Cardiac Mortality page.

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Four Natural Compounds Which May Unclog the Arteries

  • Pomegranate: this remarkable fruit has been found in a human clinical study to reverse the carotid artery thickness (i.e. blockage) by up to 29% within 1 year[ix] There are a broad range of mechanisms that have been identified which may be responsible for this effect, including: 1) lowering blood pressure 2) fighting infection (plaque in arteries often contains bacteria and viruses) 3) preventing cholesterol oxidation 4) reducing inflammation.[x]
  • Arginine: Preclinical and clinical research indicates that this amino acid not only prevents the progression of atherosclerosis but also reverses pathologies associated with the process. (see also: Clogged Arteries and Arginine). One of the mechanisms in which it accomplishes this feat is by increasing the production of nitric oxide which is normally depressed in blood vessels where the inner lining has been damaged (endothelium) resulting in dysfunction.
  • Garlic: Not only has garlic been found to reduce a multitude of risk factors associated with arteriosclerosis, the thickening and hardening of the arteries, but it also significantly reduces the risk of heart attack and stroke.[xi] In vitro research has confirmed that garlic inhibits arteriosclerotic plaque formation.[xii] Aged garlic extract has also been studied to inhibit the progression of coronary artery calcification in patients receiving statin therapy.[xiii] And let us not forget, garlic’s benefits are extremely broad. We have identified over 150 diseases that this remarkable culinary and medicinal herb has been confirmed to be of potential value in treating and preventing and which can be viewed here: Garlic Health Benefits.
  • B-Complex: One of the few vitamin categories that has been confirmed in human studies to not only reduce the progression of plaque buildup in the arteries but actually reverse it is B-complex. A 2009 study published in the journal Stroke found that high dose B-complex vitamin supplementation significantly reduces the progression of early-stage subclinical atherosclerosis in healthy individuals.[xiv] More remarkably, a 2005 study published in the journal Atherosclerosis found a B-vitamin formula decreased the carotid artery thickness in patients at risk for cerebral ischemia.[xv] Another possible explanation for these positive effects is the role B-vitamins have in reducing the production of homocysteine, an artery and otherwise blood vessel scarring amino acid.[xvi]

For additional research on artery unclogging substances visit our page dedicated to the topic Unclogging Arteries.

Additional Heart Unfriendly Things To Avoid

No discussion of preventing cardiac mortality would be complete without discussing things that need to be removed in order to reduce risk, such as:

  • NSAIDs: Drugs like aspirin, ibuprofen, and Tylenol, have well-known association with increased cardiac mortality. Review six studies on the topic here: NSAID Cardiotoxicity.
  • Statin Drugs: It is the height of irony that the very category of drugs promoted to millions globally as the standard of care for primary and secondary prevention of cardiovascular disease and cardiac mortality are actually cardiotoxic agents, linked to no less than 300 adverse health effects. Statin drugs have devastating health effects. Explore the research here: Statin Drug Health Effects.
  • Wheat: while this connection is rarely discussed, even by those who promote grain-free and wheat free diets, wheat has profound cardiotoxic potential, along with over 200 documented adverse health effects: Wheat Toxicity. And why wouldn’t it, when the very countries that eat the most of it have the highest rate of cardiovascular disease and heart-related deaths? For an in-depth explanation read our article: Wheat’s Cardiotoxicity: As Serious As A Heart Attack.

Finally, for additional research on the topic of heart health promoting strategies visit our Health Guide: Heart Health. Interested in healing an injured heart? Read about cardiac tissue regeneration: 6 Bodily Tissues That Can Be Regenerated Through Nutrition.


References

[i] Roberto Marchioli, Federica Barzi, Elena Bomba, Carmine Chieffo, Domenico Di Gregorio, Rocco Di Mascio, Maria Grazia Franzosi, Enrico Geraci, Giacomo Levantesi, Aldo Pietro Maggioni, Loredana Mantini, Rosa Maria Marfisi, G Mastrogiuseppe, Nicola Mininni, Gian Luigi Nicolosi, Massimo Santini, Carlo Schweiger, Luigi Tavazzi, Gianni Tognoni, Corrado Tucci, Franco Valagussa,. Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico (GISSI)-Prevenzione. Circulation. 2002 Apr 23;105(16):1897-903. PMID: 11997274

[ii] Michal L Melamed, Erin D Michos, Wendy Post, Brad Astor. 25-hydroxyvitamin D levels and the risk of mortality in the general population. Arch Intern Med. 2008 Aug 11;168(15):1629-37. PMID: 18695076

[iii] W B Grant. An estimate of the global reduction in mortality rates through doubling vitamin D levels. Eur J Clin Nutr. 2011 Jul 6. Epub 2011 Jul 6. PMID: 21731036

[iv] Stefan Pilz, Harald Dobnig, Giel Nijpels, Robert J Heine, Coen D A Stehouwer, Marieke B Snijder, Rob M van Dam, Jacqueline M Dekker. Vitamin D and mortality in older men and women. Clin Endocrinol (Oxf). 2009 Nov;71(5):666-72. Epub 2009 Feb 18. PMID: 19226272

[v] Adit A Ginde, Robert Scragg, Robert S Schwartz, Carlos A Camargo. Prospective study of serum 25-hydroxyvitamin D level, cardiovascular disease mortality, and all-cause mortality in older U.S. adults. J Am Geriatr Soc. 2009 Sep;57(9):1595-603. Epub 2009 Jun 22. PMID: 19549021

[vi] Karl Michaëlsson, John A Baron, Greta Snellman, Rolf Gedeborg, Liisa Byberg, Johan Sundström, Lars Berglund, Johan Arnlöv, Per Hellman, Rune Blomhoff, Alicja Wolk, Hans Garmo, Lars Holmberg, Håkan Melhus. Plasma vitamin D and mortality in older men: a community-based prospective cohort study. Am J Clin Nutr. 2010 Oct;92(4):841-8. Epub 2010 Aug 18. PMID: 20720256

[vii] Yukio Yamori, Takashi Taguchi, Hideki Mori, Mari Mori. Low cardiovascular risks in the middle aged males and females excreting greater 24-hour urinary taurine and magnesium in 41 WHO-CARDIAC study populations in the world. J Biomed Sci. 2010;17 Suppl 1:S21. Epub 2010 Aug 24. PMID: 20804596

[viii] 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

[ix] Sayer Ji, Research: Pomegranate May Reverse Blocked Arteries

[x] GreenMedInfo.com, Pomegranate’s Health Benefits

[xi] G Siegel, A Walter, S Engel, A Walper, F Michel. [Pleiotropic effects of garlic]. Wien Med Wochenschr. 1999;149(8-10):217-24. PMID: 10483684

[xii] Günter Siegel, Frank Michel, Michael Ploch, Miguel Rodríguez, Martin Malmsten. [Inhibition of arteriosclerotic plaque development by garlic]. Wien Med Wochenschr. 2004 Nov;154(21-22):515-22. PMID: 15638070

[xiii] Matthew J Budoff, Junichiro Takasu, Ferdinand R Flores, Yutaka Niihara, Bin Lu, Benjamin H Lau, Robert T Rosen, Harunobu Amagase. Inhibiting progression of coronary calcification using Aged Garlic Extract in patients receiving statin therapy: a preliminary study. Prev Med. 2004 Nov;39(5):985-91. PMID: 15475033

[xiv] Howard N Hodis, Wendy J Mack, Laurie Dustin, Peter R Mahrer, Stanley P Azen, Robert Detrano, Jacob Selhub, Petar Alaupovic, Chao-ran Liu, Ci-hua Liu, Juliana Hwang, Alison G Wilcox, Robert H Selzer,. High-dose B vitamin supplementation and progression of subclinical atherosclerosis: a randomized controlled trial. Stroke. 2009 Mar;40(3):730-6. Epub 2008 Dec 31. PMID: 19118243

[xv] Uwe Till, Peter Röhl, Almut Jentsch, Heiko Till, Andreas Müller, Klaus Bellstedt, Dietmar Plonné, Horst S Fink, Rüdiger Vollandt, Ulrich Sliwka, Falko H Herrmann, Henning Petermann, Reiner Riezler. Decrease of carotid intima-media thickness in patients at risk to cerebral ischemia after supplementation with folic acid, Vitamins B6 and B12. Atherosclerosis. 2005 Jul;181(1):131-5. Epub 2005 Feb 16. PMID: 15939064

[xvi] Claudio Maldonado, Chirag V Soni, Nathan D Todnem, Sathnur Pushpakumar, Dorothea Rosenberger, Srikanth Givvimani, Juan Villafane, Suresh C Tyagi. Hyperhomocysteinemia and sudden cardiac death: potential arrhythmogenic mechanisms. Curr Vasc Pharmacol. 2010 Jan;8(1):64-74. PMID: 19485933

Originally published: 2018-08-05

Aritcle updated: 2019-07-24


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