SSRI

Concomitant SSRI and Oral Anticoagulant Use Tied to Major Bleeding Risk

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Patients taking both drugs should be closely monitored, researchers advised

A computer rendering of a hemorrhage

Concomitant use of selective serotonin reuptake inhibitors (SSRIs) and oral anticoagulants (OACs) in patients with atrial fibrillation was tied to an increased risk of major bleeding compared with OAC use alone, a case-control study suggested.

The population-based study from the U.K. showed that taking an SSRI and OAC (both direct OACs and vitamin K antagonists [VKAs]) together was associated with a 33% increased risk of major bleeding compared with OACs alone (incidence rate ratio [IRR] 1.33, 95% CI 1.24-1.42), reported Christel Renoux, MD, PhD, of Jewish General Hospital in Montreal, and colleagues.

Compared with use of OACs alone, concomitant use of SSRIs plus OACs was linked to a significantly higher risk for several specific types of major bleeding, they detailed in JAMA Network Openopens in a new tab or window:

  • Gastrointestinal bleeding: adjusted IRR 1.38 (95% CI 1.24-1.53)
  • Intracranial hemorrhage: aIRR 1.56 (95% CI 1.32-1.85)
  • Other major bleeding: aIRR 1.23 (95% CI 1.12-1.36)

This elevated risk peaked during the first few months of concomitant treatment (IRR 1.74, 95% CI 1.37-2.22), and persisted for the first 6 months of treatment and finally stabilized around day 150 of use.

“Given that previous studies have shown that SSRIs reduce serotonin content in platelets by 80% to 90% within a period of 2 to 3 weeks, we anticipated that patients most susceptible to bleeding would experience an event shortly after initiating concomitant use of SSRIs and OACs,” Renoux and co-author Alvi Rahman, MSc, of McGill University in Montreal, jointly told MedPage Today. “Ultimately, our findings were in line with our expectations, with the risk of major bleeding being higher within the first 6 months of concomitant SSRI and OAC use.”

While both direct OACs and VKAs individually were linked with bleeding risk, the magnitude of this risk was slightly less with direct OACs (IRR 1.25, 95% CI 1.12-1.40) than VKAs (IRR 1.36, 95% CI 1.25-1.47). That being said, strong potency SSRIs (IRR 1.34, 95% CI 1.22-1.47) and moderate potency SSRIs (IRR 1.31, 95% CI 1.19-1.43) had similar links to bleeding risk.

In light of these findings, clinicians should take measures to mitigate bleeding risk, the researchers advised. “For example, among OACs, direct OACs may be preferred over VKAs as they have lower potential for pharmacokinetic interactions than VKAs,” Renoux and Rahman suggested. “Moreover, to specifically decrease the risk of gastrointestinal bleeding in patients at high risk, proton pump inhibitors may be considered.”

Furthermore, this doesn’t mean either of these drugs should be withheld, they added. “Both are highly effective treatments for their primary indications.”

Joseph E. Marine, MD, MBA, of Johns Hopkins University School of Medicine in Baltimore, who wasn’t involved with the study, commented that patients on both drugs should “prudently” minimize bleeding risk, but also shouldn’t stop or change therapy without consulting their clinician first.

Matthew Tomey, MD, of the Icahn School of Medicine at Mount Sinai in New York City, added that it has been “long known” that SSRIs may be linked with some bleeding risk, “which may relate to their effects on the interplay between serotonin and platelet function,” though the existing data on this have been inconsistent.

While this is an observational study and should be interpreted with caution, he told MedPage Today that “it is perhaps intuitive” that mixing a medicine with inhibitory effects on platelet function may lend itself to greater bleeding tendency in the context of oral anticoagulant use.

“We encounter this challenge regularly when navigating concurrent indications for anticoagulation and antiplatelet therapy, as in the example of the patient with atrial fibrillation and a coronary stent,” added Tomey, who wasn’t involved with the study. “When good reasons exist for both the anticoagulant and the medicine with antiplatelet effect, we often do need to use both, albeit with an awareness of increased bleeding risk and an imperative to take all reasonable measures to mitigate that bleeding risk.”

Overall, the analysis was “a hypothesis-generating study which should support more research to prove this association,” Marine told MedPage Today. “It would have been interesting for the authors to include a falsification test in the study — for example, was there an association between anticoagulants combined with non-SSRI antidepressants and major bleeding?”

For this study, a total of 42,190 atrial fibrillation patients who were hospitalized with major bleeding were matched with over 1.1 million controls. About 60% of both groups were men, and mean age was 74. Patients with major bleeding tended to have slightly higher rates of hypertension (81.8% vs 79% of controls), coronary artery disease (31.4% vs 28.3%), congestive heart failure (21.7% vs 19%), peripheral arterial disease (6.5% vs 5.7%), venous thromboembolism (6.6% vs 5.7%), stroke or transient ischemic attack (19% vs 17.2%), diabetes (25.7% vs 23.7%), a history of bleeding (14.3% vs 9.2%), and anemia (17.4% vs 13.6%), among others.

Men also had a slightly higher bleeding risk (IRR 1.38, 95% CI 1.26-1.51) than women (IRR 1.27, 95% CI 1.15-1.40). When it came to age, only patients ages 60 and older had an elevated major bleeding risk (ages 60-74: IRR 1.32, 95% CI 1.19-1.46; ages 75 and up: IRR 1.33, 95% CI 1.21-1.46).

Why do antidepressants take so long to kick in?

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SSRIs, or Selective Serotonin Reuptake Inhibitors, are the most commonly prescribed antidepressants for anxiety and depression disorders. They usually take a few weeks before ‘kicking in’ — but why?

A representational image of 'happy pills' being dispensed from a bottle

A representational image of ‘happy pills’ being dispensed from a bottle

  • Globally, nearly one billion people live with a mental health disorder, of which anxiety and depression are the most common.
  • Antidepressants work by regulating the levels of different neurotransmitters in the brain, like serotonin and dopamine.
  • But they take weeks to “kick in” and show effect. A new study may explain this delayed onset.

Mental illness has become endemic worldwide, with the World Health Organization estimating nearly 1 billion people were living with a mental disorder in 2019. Among these, anxiety disorders are the most common, with more than 300 million people affected, closely followed by depression, which affects nearly 280 million people. 

Antidepressants are among the most commonly prescribed medications for the treatment of anxiety and depression. They generally work by affecting levels of neurotransmitters in the brain. 

Antidepressants regulate the levels of chemicals like serotonin, norepinephrine, and dopamine, which play crucial roles in regulating mood and emotion. By influencing the balance of these neurotransmitters, antidepressants aim to alleviate symptoms associated with depressive and anxiety disorders.

SSRIs, or Selective Serotonin Reuptake Inhibitors, belong to a category of antidepressant drugs designed to elevate serotonin levels in the brain. Notable examples of SSRIs include fluoxetine (Prozac), sertraline (Zoloft), and escitalopram (Lexapro).

Why do antidepressants take so long to kick in?
Dopamine and Serotonin pathways in the brain.

These medications generally have few unpleasant side effects and can be highly effective in treating various mood disorders, including depression and certain anxiety disorders. However, one significant drawback of SSRIs is the delayed onset of their therapeutic effects — SSRIs often take several weeks to show noticeable improvements in mood.

This extended period before “kicking in” poses challenges for patients and healthcare providers. Yet, the reason behind this lag in action is not well understood.

Now, a new study by scientists from Copenhagen University has explored the impact of the SSRI escitalopram on synaptic density in healthy individuals, focusing on the time-dependent effects and potential reasons behind the delayed therapeutic response of SSRIs. 

“The mode of action of SSRIs is still debated, and people have been wondering why the therapeutic effects against depression set in so late—sometimes weeks after starting the intake,” Dr. Gitte Knudsen, the lead author of the study, told Interesting Engineering. 

The researchers used SV2A, a protein found in the brain, as a marker for presynaptic density. But before we dive into the research and the findings, let us first understand how SSRIs work.

How do SSRIs work?

Antidepressants, including SSRIs, operate by modulating neurotransmitters in the brain, usually targeting serotonin, norepinephrine, and dopamine. These chemicals play pivotal roles in regulating mood and emotional well-being. By influencing their balance, antidepressants aim to alleviate symptoms associated with anxiety and depression.

SSRIs, such as escitalopram (sold under the brand names Lexapro and Cipralex, among others), belong to a class of drugs that selectively target serotonin. Serotonin, referred to as the “feel-good” neurotransmitter, contributes significantly to mood regulation.

Within the brain, neurons communicate through synapses, small gaps between nerve cells. SSRIs enhance serotonin levels by preventing the reabsorption of serotonin by the sending neuron. This mechanism increases the concentration of serotonin in the synaptic cleft, facilitating improved communication between neurons.

The prolonged presence of serotonin in synapses prompts neuroplasticity, the brain’s ability to reorganize and form new connections. This adaptability is crucial for mood stabilization and emotional regulation. By fostering neuroplastic changes, SSRIs aim to create a more resilient and balanced neural environment.

Tracking the SV2A protein 

“There is scientific support to say that the delayed effects may be due to the drugs taking some time to induce brain changes,” said Dr. Knudsen.

Why do antidepressants take so long to kick in?
How SSRIs work 

To explore these changes, the researchers chose SV2A (synaptic vesicle glycoprotein 2A), a protein found in neurons, as their marker. It is primarily associated with synaptic vesicles, tiny structures within neurons that store and release neurotransmitters. They then measured the impact of escitalopram on synaptic density.

Synaptic density refers to the number and distribution of synapses in the brain. Changes in synaptic density can reflect alterations in the way neurotransmitters such as serotonin are processed in the brain.

In theirdouble-anonymizedd study, the researchers divided 32 healthy participants into two groups: one received 20 milligrams (mg) of escitalopram, and the other received 20 mg of a placebo.

After three to five weeks, researchers used MRI (magnetic resonance imaging) scans to obtain detailed structural images of participants’ brains. PET (positron emission tomography) scans were also performed, employing a radioactive tracer ([11C]UCB-J) to track the presence and distribution of the SV2A protein.

Time-dependent effects of SSRIs

The imaging scans revealed a positive correlation between the radioactive tracer binding and the duration of escitalopram intervention.

“We found that people who took escitalopram (but not those on the placebo) showed a gradual increase in synaptic density over weeks 3-5. The fact that we see a time-dependent increase in SV2A supports the idea that SSRIs take time to work and indeed induce neuroplasticity,” said Dr. Knudsen.

Specifically, the study observed a gradual increase in synaptic density within two crucial brain regions—the neocortex and the hippocampus—among individuals taking SSRIs over time. 

The neocortex, occupying more than half of the brain’s total volume, handles higher cognitive functions, including sensory perception, emotion, and cognition. The hippocampus, located deep within the brain, is integral to memory and learning processes.

The research results imply that synaptic density might play a crucial role in the functioning of antidepressants, presenting a potential target for the development of innovative drugs aimed at treating depression.

Why do antidepressants take so long to kick in?
Neuroplasticity as a mechanism of action for SSRIs has been proven by the study.

This marks the first in vivo evidence supporting the idea that neuroplasticity is a mechanism of action for SSRIs in humans, offering a plausible biological explanation for the delayed treatment response often observed in patients on SSRIs.

However, the exact mechanism of this time dependency is still unclear, with Dr. Knudsen explaining, “We do not know the exact mechanism for how neuroplasticity can help get rid of depressive symptoms. Still, some believe that the drugs change the fixed mode of having ruminating thoughts and behaviors can be changed by neuroplastic effects.”

Effect on patients, doctors & drug development 

Understanding the time-dependence of escitalopram has significant relevance for patients and healthcare providers. However, the study was conducted on healthy individuals, and studying the effects in patients with major depressive disorders could offer more insight, as highlighted by Dr. Knudsen.

For individuals grappling with anxiety and depression, the findings shed light on the prolonged period SSRIs take to manifest therapeutic effects. This awareness can contribute to managing expectations during the initial weeks of treatment, helping patients and their families navigate the often challenging wait for noticeable improvements in mood.

Healthcare providers, especially psychiatrists and general practitioners prescribing SSRIs, can integrate this knowledge into patient consultations.

https://giphy.com/embed/l2YSs8JYxDsHAo5yg

via GIPHY

Armed with the understanding that neuroplastic changes induced by SSRIs take time, doctors can also better guide their patients through the treatment process.

Furthermore, the research underscores the need for ongoing exploration into the mechanisms governing the time-dependent effects of SSRIs. This could pave the way for improved treatment strategies, allowing for more targeted interventions and personalized approaches to mental health treatments.

In essence, the study not only contributes to the scientific understanding of SSRIs but also holds practical implications for those directly involved in giving and receiving mental health treatment.

In terms of drug development, the prospect of identifying substances capable of inducing neuroplasticity at an accelerated pace could be a future focal point. Speaking on this matter, Dr. Knudsen said, “If one could identify drugs that induce neuroplasticity, that could be helpful. Animal studies suggest that psychedelics induce neuroplasticity faster.”

Although the research into using psychedelics for various mental health disorders is still new, the findings may have important implications for antidepressant usage and other areas of drug development.

Study Explains Emotional ‘Blunting’ Caused by Common Antidepressants

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Summary: SSRI antidepressants can make users less sensitive to rewards, resulting in emotional blunting many users experience. The findings provide new evidence for the role serotonin plays in reinforcement learning.

Source: University of Cambridge

Scientists have worked out why common anti-depressants cause around a half of users to feel emotionally ‘blunted’. In a study published today, they show that the drugs affect reinforcement learning, an important behavioral process that allows us to learn from our environment.

According to the NHS, more than 8.3 million patients in England received an antidepressant drug in 2021/22. A widely-used class of antidepressants, particularly for persistent or severe cases, is selective serotonin reuptake inhibitors (SSRIs). These drugs target serotonin, a chemical that carries messages between nerve cells in the brain and has been dubbed the ‘pleasure chemical’.

One of the widely-reported side effects of SSRIs is ‘blunting’, where patients report feeling emotionally dull and no longer finding things as pleasurable as they used to. Between 40-60% of patients taking SSRIs are believed to experience this side effect.

To date, most studies of SSRIs have only examined their short term use, but, for clinical use in depression these drugs are taken chronically, over a longer period of time. A team led by researchers at the University of Cambridge, in collaboration with the University of Copenhagen, sought to address this by recruiting healthy volunteers and administering escitalopram, an SSRI known to be one of the best-tolerated, over several weeks and assessing the impact the drug had on their performance on a suite of cognitive tests.

In total, 66 volunteers took part in the experiment, 32 of whom were given escitalopram while the other 34 were given a placebo. Volunteers took the drug or placebo for at least 21 days and completed a comprehensive set of self-report questionnaires and were given a series of tests to assess cognitive functions including learning, inhibition, executive function, reinforcement behaviour, and decision-making.

The results of the study are published today in Neuropsychopharmacology.

The team found no significant group differences when it came to ‘cold’ cognition – such as attention and memory. There were no differences in most tests of ‘hot’ cognition – cognitive functions that involve our emotions.

However, the key novel finding was that there was reduced reinforcement sensitivity on two tasks for the escitalopram group compared to those on placebo. Reinforcement learning is how we learn from feedback from our actions and environment.

In order to assess reinforcement sensitivity, the researchers used a ‘probabilistic reversal test’. In this task, a participant would typically be shown two stimuli, A and B. If they chose A, then four out of five times, they would receive a reward; if they chose B, they would only receive a reward one time out of five.

This shows a depressed man
Between 40-60% of patients taking SSRIs are believed to experience this side effect.

Volunteers would not be told this rule, but would have to learn it themselves, and at some point in the experiment, the probabilities would switch and participants would need to learn the new rule.

The team found that participants taking escitalopram were less likely to use the positive and negative feedback to guide their learning of the task compared with participants on placebo. This suggests that the drug affected their sensitivity to the rewards and their ability to respond accordingly.

The finding may also explain the one difference the team found in the self-reported questionnaires, that volunteers taking escitalopram had more trouble reaching orgasm when having sex, a side effect often reported by patients.

Professor Barbara Sahakian, senior author, from the Department of Psychiatry at the University of Cambridge and a Fellow at Clare Hall, said: “Emotional blunting is a common side effect of SSRI antidepressants.

“In a way, this may be in part how they work – they take away some of the emotional pain that people who experience depression feel, but, unfortunately, it seems that they also take away some of the enjoyment. From our study, we can now see that this is because they become less sensitive to rewards, which provide important feedback.”

Dr Christelle Langley, joint first author also from the Department of Psychiatry, added: “Our findings provide important evidence for the role of serotonin in reinforcement learning. We are following this work up with a study examining neuroimaging data to understand how escitalopram affects the brain during reward learning.”

How Serotonin Genes and SSRIs Can Contribute to Heart Valve Disease

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Summary: Taking SSRIs and having the “long-long” serotonin SERT genetic variant lowers SERT activity in the mitral valve, leading to degenerative mitral regurgitation, one of the most common heart valve diseases.

Source: CHOP

The neurotransmitter serotonin can adversely affect the heart’s mitral valve, contributing to a heart disease known as degenerative mitral regurgitation, according to a new multicenter study involving researchers from the Pediatric Heart Valve Center at Children’s Hospital of Philadelphia.

The study, which was co-led by CHOP’s Robert J. Levy, MD, and Columbia University’s Giovanni Ferrari, Ph.D., and also involved collaborators at the University of Pennsylvania and Valley Hospital Heart Institute, was recently published in Science Translational Medicine.

Degenerative mitral regurgitation is one of the most common cardiac valve diseases. A healthy mitral valve tightly closes the opening between the left atrium and the left ventricle when the heart contracts. With degenerative mitral valve regurgitation, the mitral valve shape becomes deformed, and the valve cannot close completely when the heart contracts, which allows some blood to leak backwards into the left atrium. This abnormal blood flow is called regurgitation.

Although patients initially are asymptomatic, over time the mitral valve becomes thickened and deformed, and patients progressively feel tired and short of breath. As pumping becomes less efficient due to this leak, the heart needs to work harder. This extra work for the heart eventually causes congestive heart failure.

Certain medications can ease symptoms and prevent complications, but they do not treat the underlying cause of the disease. If the degeneration of the mitral valve becomes severe, surgery to repair or replace the mitral valve is needed.

To better understand factors that contribute to the progression of the disease, CHOP researchers and their collaborators analyzed data from more than 9,000 patients who had undergone surgery for degenerative mitral valve disease and evaluated 100 human mitral valve biopsies, in addition to studying mouse models.

The researchers found that taking selective serotonin reuptake inhibitors (SSRIs)—the most commonly-prescribed antidepressants—was associated with severe mitral regurgitation, which required surgery at a younger age than those not taking SSRIs.

In animal models, they found that normal mice treated with high doses of SSRIs developed thickened mitral valves. They also found that mice lacking the serotonin transporter (SERT) gene, the target of SSRIs,—which transports serotonin into cells, where it cannot bind to receptors and send signals—developed thicker mitral valves.

This shows a heart and a brain
Degenerative mitral regurgitation is one of the most common cardiac valve diseases.

Through genetic analysis, the researchers identified genetic variants in a region of the SERT gene (5HTTLPR) that affect how active SERT is. Patients with two copies of a “long” variation of the gene that make SERT less active—one copy from the mother, and one from the father—had much lower SERT activity and required surgery more often.

Patients with this “long-long” variant were more likely to react to serotonin in a way that could change the shape of the mitral valve. Additionally, “long-long” mitral valve cells were more sensitive to SSRI treatment than cells from other variants.

The researchers noted that they did not find a negative effect with normal doses of SSRIs and that a healthy mitral valve may tolerate low SERT without deforming, as it is unlikely that low SERT can cause degeneration of the mitral valve by itself. They suspect that once the mitral valve has started to degenerate, it may be more susceptible to serotonin and low SERT.

“Our study shows that taking SSRIs and having the ‘long-long’ SERT genetic variant lowers SERT activity in the mitral valve,” said Dr. Levy, attending cardiologist in the Cardiac Center and the William J. Rashkind Endowed Chair in Pediatric Cardiology at Children’s Hospital of Philadelphia.

“We suggest that assessing patients with known degenerative mitral regurgitation for potential low SERT activity by genotyping them for 5HTTLPR may help identify patients that may need mitral valve surgery earlier.”

Even Pregnant Women on SSRIs Suffer Lingering Anxiety, Depression

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Nearly a third of those in a prospective study had clinically relevant depressive symptoms

A gloomy looking pregnant woman hugs a pillow on her couch.

Despite treatment with antidepressant medication, a significant proportion of women still reported symptoms of anxiety and depression during pregnancy, according to a prospective study.

Among a group of 88 women who took selective serotonin reuptake inhibitors (SSRIs), about a third had clinically relevant symptoms of depression during pregnancy and the postpartum period, reported Gabrielle Mesches, MS, of the Northwestern School of Medicine in Chicago, and colleagues.

Only 18% to 29% of pregnant women who took antidepressants maintained remission, the researchers wrote in Psychiatric Research and Clinical Practice.

Around 40% of pregnant women who took SSRIs also had higher levels of anxiety, with a substantial number experiencing increasing symptoms throughout pregnancy, the team found.

“The assumption is that if women are taking antidepressants in pregnancy, they are well. That’s not always the case,” study co-author Katherine Wisner, MD, also of Northwestern, told MedPage Today.

She explained that depressive symptoms during pregnancy are associated with a number of adverse outcomes, including preterm birth, hypertension, cesarean delivery, low birth weight, neonatal intensive care unit admission, and social and emotional impacts on infants.

If women treated with antidepressants throughout pregnancy are not in remission, they should be offered additional treatment, such as therapy, stress management. or mindfulness interventions, Wisner added. “I really believe that, in addition to medication, some kind of additional treatment should be offered in pregnancy.”

The researchers conducted a prospective, longitudinal cohort study to assess monthly patterns of anxiety and depression during pregnancy. Participants were enrolled at one of three urban academic centers or one rural health center. Pregnant women were included if they had at least one prior episode of major depressive disorder, were not in a current episode, and were treated with sertraline, fluoxetine, citalopram, or escitalopram. Women with bipolar disorder or probable antenatal depression were not included.

Participants completed assessments once a month from study entry (less than 18 weeks’ gestation) through delivery, and again at 6 and 14 weeks postpartum. The study investigators used a series of screening tools, including the 10-item Edinburgh Postnatal Depression Scale and the 7-item Generalized Anxiety Disorder Scale, to assess depression and anxiety symptom severity during pregnancy and postpartum, measuring the changes in these outcomes over time. The team adjusted for covariates including body mass index, race, age, and psychiatric comorbidities.

Women were grouped into “trajectories” — or patterns — of depression and anxiety based on the severity of their symptoms. Depressive symptoms were categorized as minimal, mild, or subthreshold (or clinically relevant), and anxiety symptoms were categorized as asymptomatic, minimal, breakthrough (or increasing), or mild.

Overall, 88 women enrolled in the study and 77 provided complete perinatal and postpartum data. All the study participants identified as female, rather than transgender, non-binary, or other. Women were 34 years old on average, and the mean gestational age was approximately 13 weeks. About 90% of participants were white.

A majority of patients were also diagnosed with at least one psychiatric comorbidity. Nearly 80% had a lifetime anxiety disorder, 10% had a substance abuse disorder within the last year, and 16% had a lifetime eating disorder.

Approximately 18% of women who took SSRIs during pregnancy had minimal depressive symptoms, 50% had mild, and 32% had subthreshold, or clinically relevant, depressive symptoms. Regarding anxiety, 7% of women were asymptomatic, 53% had minimal, 18% had increasing, and 23% had mild symptoms.

Symptoms of depression correlated with anxiety, the researchers found. For example, of all women who had clinically relevant symptoms of depression, nearly 70% scored into the two highest levels of anxiety groups.

Study limitations, Mesches and co-authors said, included that the findings are generalizable only to SSRI-treated women like those in the study — i.e., who are predominantly white, married, and have higher levels of education. Additionally, 11 women in the study were lost to follow-up, which prevents a complete picture of postpartum effects, the team noted.

Ask yourself: Why are there no prescription medications without horrific side effects?

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Image: Ask yourself: Why are there no prescription medications without horrific side effects?

The reason there are no prescription medications available today where the side effects aren’t worse than the ailment being treated is because Big Pharma will not treat or heal anything without creating several new issues that keep their “customers for life” coming back for more. Most Americans do not want to stop eating junk food, fast food, corporate franchise restaurant food, microwaveable food, prepared food bar “stuff,” and “diet” food that’s mostly chock full of synthetic sweeteners, GMOs and MSG.

Due almost entirely to these nasty eating habits, about 200 million Americans seek medical doctors to prescribe them chemical-filled pills to kill the pain, quell the hypertension, reduce the inflammation, unclog the clots, numb the anxiety, and nullify the depression.

The FDA and CDC do not allow anything that cures disease or disorders to be labeled “medicine”

Most Americans think the FDA was created to protect us from dangerous chemicals that might wind up in food and medicine, but just the opposite is true. Over the past century, the FDA has tried to destroy all forms of holistic care in America that compete with “slash-and-burn” drug and vaccine treatments that are readily dished out by the allopathic Ponzi sick-care scheme that masquerades as ‘health’ care in this country.

The CDC is a actually a for-profit corporation listed on Dun and Bradstreet. As a health protection agency, the CDC is supposed to save lives and conduct critical science for responding to threats when they arise, but pharma corporations have lobbyists and their vice presidents now in positions of control in the bureaucracy, writing legislation that favors new, untested drug approvals, as they have for decades.

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Both the FDA and the CDC promote toxic chemicals as medicine, including prescription medications, chemotherapy, and vaccines. Meanwhile, any food, herb, tincture, plant, seed, or essential oil that treats, prevents or cures disease is banned as “medicine” while being manipulated in labs, weakened or deadened, patented, and then declared a failure.

Prescription drug deaths skyrocket while the Big Pharma world pretends to search for cures for cancer, dementia, and diabetes

Twenty years ago, only four in every 100,000 people died from taking prescription drugs “as recommended” by their medical doctors. Now, one in every ten Americans struggle with addiction to prescription drugs (think opioids and SSRIs). Right now, over three million Americans are abusing painkillers, two million are misusing tranquilizers, 1.7 million are abusing stimulants, and half a million are misusing sedatives.

More Americans use and abuse “controlled” prescription drugs than heroin, cocaine and methamphetamines combined. How many of them will die this year? About 50 people will die today from overdosing on opioids. And now heroin is the death drug of choice for most people who become addicted to opioid pain relievers. Most teenagers think it’s safer to take a friend’s prescription drugs than to dose some illegal street drugs, just because they were prescribed by a doctor, but that’s not true at all.

The side effects of most prescription drugs that treat depression and anxiety include worsened depression and thoughts of suicide. How ridiculous is that? Every prescription drug advertised on television for all American children and teens to see comes slathered with side effects you wouldn’t wish on your worst enemies. Then they all feature the same tag line, “Ask your doctor if (fill in complex chemical name here) is right for you.”

It would only make sense that natural cures would be banned if they caused side effects like all the prescription medications do, but they don’t. If organic foods caused the health problems conventional foods do, they too would be banned, recalled or stuck with warning labels.

It’s as if we are all living in total idiocy like the movie “Idiocracy.” More than 200 million Americans think it’s okay if their medical doctor prescribes them “medicine” that can cause internal bleeding, loss of vision, coma, feelings of suicide, and thoughts of committing homicide. Wake up America. You’re living inside a real-life nightmare, where the food is toxic, the medicine is more toxic, and the medical doctors have no nutrition education, yet go to school for eight years to learn how to juggle chemical medicines like some Bozo science clowns. Maybe all M.D.s should wear big red wigs with big red noses and big red shoes while scribbling out those toxic prescriptions.

Sources for this article include:

TruthWiki.org

TruthWiki.org

FDA.news

CDC.news

NaturalNews.com

Talbottcampus.com

NaturalNews.com

ADHD and ADD are FAKE disorders stemming from bad schooling practices, HFCS and artificial food coloring

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Image: ADHD and ADD are FAKE disorders stemming from bad schooling practices, HFCS and artificial food coloring

Attention-deficit disorders are defined as brain disorders marked by ongoing patterns of inattention, hyperactivity, and impulsivity, to an extent that it interferes with development and functioning. Symptoms include wandering off task, difficulty sustaining focus, disorganization, defiance, constant movement, fidgeting, tapping, talking, and the inability to delay immediate gratification. Sounds like every adult who’s jacked up on coffee while stuck sitting on a hard chair at some boring work meeting while playing on their smart devices and completely disconnected from the speaker and the content being presented.

Today’s elementary and secondary school curriculum and testing is still based on memorizing rote facts (which are mostly inaccurate), filling in the “blanks,” taking multiple choice quizzes and tests, and raising hands to answer questions posed by the teachers.

Meanwhile, most school breakfasts and lunches (including what most kids bring from home) are chock full of processed foods that contain high fructose corn syrup, artificial coloring, artificial flavoring, concentrated salts, pesticides, and fluoride (think of the water fountains). Children and teens are consuming pop tarts, sugar-laden cereals, soda and energy drinks without knowing the detrimental behavior effects. Plus, kids eat candy throughout the day, some coming from home and the rest from teachers who use genetically modified treats as rewards for “good behavior.” How ironic.

What year did Christopher Columbus arrive in America, and what are the long division steps for dividing 2,437 by 389? Exactly. Who cares.

First off, let’s address what kids are learning in school these days, and how most of the curriculum is cannon fodder, including outdated “skills” and “strategies” that don’t even apply to the real world in any form at all. Unless you’re appearing on the Jeopardy game show, trivia doesn’t matter at all. As for long division, nobody needs to know that dead dinosaur at all. We have computers, smart devices and even watches with calculators now.

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Kids don’t engage learning unless they’re engaged in collaboration, creativity, communication, critical thinking, and citizenship (The 5 C’s of 21st century learning).

Rote memory learning drives any human being crazy. Children are brilliant, and no curriculum in the world that’s based on rote memorization, boring worksheets, and taking multiple choice tests will ever keep them quiet, still, and “paying attention” for more than a couple minutes. Students want to know the answers to their questions like, “What does this have to do with the real world?” and “How does this help us get smarter?”

https://www.real.video/embed/5834171584001

Every single “symptom” of ADHD and ADD is a symptom of poorly planned educational systems, lack of real world connections, and bad diet

In the DSM-IV (The American Psychiatric Association manual and the pages describing diagnostic criteria for Attention Deficit Disorders), any children who can’t pay attention for extended periods of time, who don’t complete their homework, or who are often distracted by “extraneous stimuli” are in need of prescription psyche medications. According to DSM-IV, “symptoms must be present for at least 6 months …” and required to cause “some impairment in at least two settings” for a diagnosis of a brain disorder to be applied. The DSM-V is even worse, and offers no clear guidelines. Well, did the DSM-IV offer any “clear” guidelines? What’s clear is that psychiatrists can now diagnose ANY child or adolescent anytime with ADD or ADHD.

What’s clear is that students need real world education instead of memorizing facts for tests that they completely forget three days later. What’s clear is that science proves that artificial food colorings, soda, and high fructose corn syrup cause severe hypersensitivity reactions, affect behavior, reduce cognition, deplete the retention of information, and cause mental distress. Where’s all that information in the DSM manuals?

15 Million pounds of artificial dyes are put in U.S. foods, drinks, candy, and medicine every year

There has been a 55 percent increase in U.S. toxic food dyes just since the year 2000. There are over 15 million pounds of dyes put in foods, drinks, candy and medicine every year, and the FDA does nothing to protect consumers from the barrage of poison.

Did you know that the industrial-based food dye Yellow #5 affects behavior and induces severe hypersensitivity reactions? Fact: Teenagers who drink more than one large soda (4 glasses) per day experience mental health difficulties, including hyperactivity and mental distress, according to a study recently published in the American Journal of Public Health. Those same soda drinkers also score lower on tests, per the scientific research conducted.

In conclusion, if your child is “suffering” from ADD or ADHD symptoms, before you rush to a medical quack for SSRI drugs that cause severe depression, suicides, and homicidal tendencies, change your child’s diet to organic foods (stop buying school meals all together), and talk to the school’s principals and administrators about engaging the students with some real world curriculum.

Sources for this article include:

HelpforADD.com

NIMH.nih.gov

TotallyADD.com

NaturalNews.com

NaturalNews.com

NCBI.nlm.nih.gov

Food.news

Faster-Acting Antidepressants May Finally Be Within Reach

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Some activity patterns in the brain can be dangerous, producing persistent dark moods that drain people’s motivation, pleasure, and hope. For the past thirty years, pills like Prozac or Zoloft–collectively known as selective serotonin reuptake inhibitors, or SSRIs–have offered millions of Americans a way to shed the heavy cloak of depression and attain more wholesome states of mind.

These medications were designed to increase nerve cells’ access to serotonin, a chemical that helps the brain regulate certain emotions. Yet researchers still don’t know precisely how the drugs work to adjust errant brain chemistry, or how to make them work better.

Now, a team of Rockefeller scientists has for the first time described how SSRIs initiate their action by targeting a particular type of nerve cell. Their findings, published last week in Neuron, may provide a path to new antidepressants that would not only be safer to use than existing ones, but that would also act more quickly.

 Lucian Medrihan, a research associate in the lab of neuroscientist and Nobel laureate Paul Greengard who led the study, explains that while existing SSRIs can produce moderate effects within hours or even minutes, most people don’t really begin to feel better until they’ve been on the drugs for a significant amount of time–a major drawback when it comes to treating clinical depression. The drugs may also cause a wide range of uncomfortable side effects, including nausea, dizziness, weight gain, and sexual dysfunction.

Finding the cells that matter

The basic idea behind SSRIs is relatively simple. When a neuron releases serotonin to signal another cell, it normally reabsorbs excess amounts of the neurotransmitter, preventing it from lingering in the space where the two nerve cells meet. The drugs interfere with this mopping-up step, essentially prolonging the signal.

What happens next has been a hard nut for neuroscientists to crack, however, because of the intrinsic complexity of the brain.

At least 1000 types of neurons could potentially be affected by a surge in serotonin, and they don’t all respond in the same way–some get triggered, for example, while others calm down. “That’s because there are 14 types of serotonin receptors present in various combinations in different neurons,” says Yotam Sagi, a senior research associate in Greengard’s lab. How a cell reacts to the neurotransmitter depends on the particular hodgepodge of receptors it carries.

Sagi and Medrihan set out to identify the earliest molecular steps by which SSRIs curb depression. To narrow their search, they honed in on a region of the brain known as the dentate gyrus, and on a particular group of cells called cholecystokinin (CCK)-expressing neurons, which they suspected were affected by SSRI-induced serotonin changes.

Using a technique called translating ribosome affinity purification, developed at Rockefeller by Nathaniel Heintz and Greengard, Sagi was able to identify the serotonin receptors present on CCK cells. “We were able to show that one type of receptor, called 5-HT2A, is important for SSRIs’ long-term effect,” he says, “while the other, 5-HT1B, mediates the initiation of their effect.”

A potential first step to relieving depression

Next, Medrihan set up a series of intricate experiments to see if he could mimic an SSRI response by manipulating CCK neurons in living mice. He suppressed the activity of these cells with chemogenetics, a technique that makes it possible to switch nerve cells on or off at will, and placed panels of tiny electrodes inside mouse brains. He then monitored the firing of other neurons in the dentate gyrus. “Only five years ago, this research would not have been feasible,” he says of the methods involved.

The results were unmistakable: when a mouse’s CCK neurons were inhibited, the same neural pathways that mediate responses to SSRIs lit up. In targeting these cells, the scientists had seemingly recreated a quickened, Prozac-like response without the drug itself.

They also performed behavioral experiments by placing the mice in a pool and monitoring their swimming patterns. After the CCK neurons had been briefly silenced, the behavior of these animals, which had not received any drugs, was similar to that seen in other mice after Prozac treatment: they swam with prolonged zest.

Greengard, who is Vincent Astor Professor, says the research resolves an important question in the field. “Many different types of synapses throughout the brain use serotonin as their neurotransmitter,” he says. “An issue of major importance has been to identify where in the myriad of neurons the antidepressants initiate their pharmacological action.”

The findings, which identify CCK neurons in the dentate gyrus as the site of interest, will advance scientists’ understanding of how SSRI antidepressants work, and “should also facilitate development of new classes of potent and selective drugs,” Greengard says. Such future therapies would presumably act faster than existing SSRIs, and might also produce fewer side effects.

Source:scienmag.com

Controversial Editorial Claims SSRIs Are Just Industry Hype

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One in 10 Americans are on SSRIs, but one expert claims the drug is no better than a sugar pill at treating depression.

Prozac. Zoloft. Paxil. Selective serotonin reuptake inhibitors, or SSRIs, are some of the most pervasive drugs in modern medicine, with roughly 10 percent of Americans taking them for depression. (Among middle-aged women, that figure is closer to 25 percent.) But according to a new editorial in The British Medical Journal, there is scant scientific evidence that SSRIs—or for that matter, serotonin—play a major role in depression.

“In the 1990s, no academic could sell a message about lowered serotonin. There was no correlation between serotonin reuptake inhibiting potency and antidepressant efficacy. No one knew if SSRIs raised or lowered serotonin levels; they still don’t know,” writes David Healy, a psychiatrist and professor at the University of Bangor in the U.K. and author of the editorial. “There was no evidence that treatment corrected anything.”

Healy goes on to describe a veritable scramble within the ranks of major drug companies to find some use—any use—for serotonin medications. SSRIs easily beat out the competition, tricyclic antidepressants, and gave rise to prominent brand names like Prozac, which have become cultural icons. Meanwhile, Healy writes, the evidence lagged behind the marketing strategy.

“Does a plausible (but mythical) account of biology and treatment let everyone put aside clinical trial data that show no evidence of lives saved or restored function? Do clinical trial data marketed as evidence of effectiveness make it easier to adopt a mythical account of biology?”

This isn’t Healy’s first time writing in opposition to SSRIs. Back in 2005, he published a controversial study that suggested SSRIs doubled a depressed person’s lifetime risk of suicide. Although more recent studies have called some of Healy’s conclusions into question, exactly how much evidence we have that SSRIs help with depression remains unanswered. In any case, many scientists are now pushing for a combined therapeutic approach to depression—one that involves personalized psychotherapy, along with traditional medications.

But experts are quick to point out that we need more research, both in psychotherapy and SSRIs.

“Some patients respond better to psychotherapy than medication—and vice versa—or prefer one type of treatment over another,” writes Richard A. Friedman, a professor of clinical psychiatry at Cornell University, in a recent article in The New York Times. “We need to learn much more about how various types of psychotherapy compare with medications clinically as well as at the level of the brain.”

Selective serotonin reuptake inhibitors (SSRIs) for stroke recovery.

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Abstract

BACKGROUND:

Stroke is the major cause of adult disability. Selective serotonin reuptake inhibitors (SSRIs) have been used for many years to manage depression. Recently, small trials have demonstrated that SSRIs might improve recovery after stroke, even in people who are not depressed. Systematic reviews and meta-analyses are the least biased way to bring together data from several trials. Given the promising effect of SSRIs on stroke recovery seen in small trials, a systematic review and meta-analysis is needed.

OBJECTIVES:

To determine whether SSRIs improve recovery after stroke, and whether treatment with SSRIs was associated with adverse effects.

SEARCH METHODS:

We searched the Cochrane Stroke Group Trials Register (August 2011), Cochrane Depression Anxiety and Neurosis Group Trials Register (November 2011), Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library 2011, Issue 8), MEDLINE (from 1948 to August 2011), EMBASE (from 1980 to August 2011), CINAHL (from 1982 to August 2011), AMED (Allied and Complementary Medicine) (from 1985 to August 2011), PsycINFO (from 1967 to August 2011) and PsycBITE (Pyschological Database for Brain Impairment Treatment Efficacy) (March 2012). To identify further published, unpublished and ongoing trials we searched trials registers, pharmaceutical websites, reference lists, contacted experts and performed citation tracking of included studies.

SELECTION CRITERIA:

We included randomised controlled trials that recruited stroke survivors (ischaemic or haemorrhagic) at any time within the first year. The intervention was any SSRI, given at any dose, for any period. We excluded drugs with mixed pharmacological effects. The comparator was usual care or placebo. In order to be included, trials had to collect data on at least one of our primary (dependence and disability) or secondary (impairments, depression, anxiety, quality of life, fatigue, healthcare cost, death, adverse events and leaving the trial early) outcomes.

DATA COLLECTION AND ANALYSIS:

We extracted data on demographics, type of stroke, time since stroke, our primary and secondary outcomes, and sources of bias. For trials in English, two review authors independently extracted data. For Chinese papers, one review author extracted data. We used standardised mean differences (SMD) to estimate treatment effects for continuous variables, and risk ratios (RR) for dichotomous effects, with their 95% confidence intervals (CIs).

MAIN RESULTS:

We identified 56 completed trials of SSRI versus control, of which 52 trials (4059 participants) provided data for meta-analysis. There were statistically significant benefits of SSRI on both of the primary outcomes: RR for reducing dependency at the end of treatment was 0.81 (95% CI 0.68 to 0.97) based on one trial, and for disability score, the SMD was 0.91 (95% CI 0.60 to 1.22) (22 trials involving 1343 participants) with high heterogeneity between trials (I(2) = 87%; P < 0.0001). For neurological deficit, depression and anxiety, there were statistically significant benefits of SSRIs. For neurological deficit score, the SMD was -1.00 (95% CI -1.26 to -0.75) (29 trials involving 2011 participants) with high heterogeneity between trials (I(2) = 86%; P < 0.00001). For dichotomous depression scores, the RR was 0.43 (95% CI 0.24 to 0.77) (eight trials involving 771 participants) with high heterogeneity between trials (I(2) = 77%; P < 0.0001). For continuous depression scores, the SMD was -1.91 (95% CI -2.34 to -1.48) (39 trials involving 2728 participants) with high heterogeneity between trials (I(2) = 95%; P < 0.00001). For anxiety, the SMD was -0.77 (95% CI -1.52 to -0.02) (eight trials involving 413 participants) with high heterogeneity between trials (I(2) = 92%; P < 0.00001). There was no statistically significant benefit of SSRI on cognition, death, motor deficits and leaving the trial early. For cognition, the SMD was 0.32 (95% CI -0.23 to 0.86), (seven trials involving 425 participants) with high heterogeneity between trials (I(2) = 86%; P < 0.00001). The RR for death was 0.76 (95% CI 0.34 to 1.70) (46 trials involving 3344 participants) with no heterogeneity between trials (I(2) = 0%; P = 0.85). For motor deficits, the SMD was -0.33 (95% CI -1.22 to 0.56) (two trials involving 145 participants). The RR for leaving the trial early was 1.02 (95% CI 0.86 to 1.21) in favour of control, with no heterogeneity between trials. There was a non-significant excess of seizures (RR 2.67; 95% CI 0.61 to 11.63) (seven trials involving 444 participants), a non-significant excess of gastrointestinal side effects (RR 1.90; 95% CI 0.94 to 3.85) (14 trials involving 902 participants) and a non-significant excess of bleeding (RR 1.63; 95% CI 0.20 to 13.05) (two trials involving 249 participants) in those allocated SSRIs. Data were not available on quality of life, fatigue or healthcare costs.There was no clear evidence from subgroup analyses that one SSRI was consistently superior to another, or that time since stroke or depression at baseline had a major influence on effect sizes. Sensitivity analyses suggested that effect sizes were smaller when we excluded trials at high or unclear risk of bias.Only eight trials provided data on outcomes after treatment had been completed; the effect sizes were generally in favour of SSRIs but CIs were wide.

AUTHORS’ CONCLUSIONS:

SSRIs appeared to improve dependence, disability, neurological impairment, anxiety and depression after stroke, but there was heterogeneity between trials and methodological limitations in a substantial proportion of the trials. Large, well-designed trials are now needed to determine whether SSRIs should be given routinely to patients with stroke.

Source: PubMed