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A commonly used anesthetic drug could help people with severe depression. Preliminary research published in the International Journal of Neuropsychopharmacology suggests that propofol may trigger rapid, durable antidepressant effects.

“Severe depression strikes millions of people each year, and up to one-third of these individuals do not respond to currently available treatments (medications, psychotherapy, brain stimulation),” said Brian James Mickey of the University of Utah, the corresponding author of the study.

“Intriguingly, some general anesthetic drugs (ketamine, for example) appear to trigger long-lasting changes in brain function. We hypothesized that brief exposures to the general anesthetic propofol might induce therapeutic neural changes in individuals with treatment-resistant depression.”

In the study, 10 patients with medication-resistant depression received ten rounds of treatment with high-dose propofol.

During the treatments, the patients were kept in deep sedation for 10 to 17.5 minutes. They remained unconscious for another 20 to 47 minutes after propofol was discontinued, but typically met discharge criteria 10 minutes after opening their eyes. No serious adverse events occurred.

“In our open-label (unblinded) trial, we administered propofol to 10 patients with severe treatment-resistant depression who were candidates for electroconvulsive therapy (ECT). Propofol treatment led to clinically significant and lasting improvement in depressive symptoms in 6 of 10 patients, similar to the response to ECT, but without ECT’s side effects,” Mickey explained.

The drug could become a viable treatment for depression, but more research is needed.

“Our initial study suggests, but does not prove, that propofol has robust antidepressant effects,” Mickey told PsyPost. “A blinded trial including an inactive (placebo) intervention is necessary to determine whether the improvement we saw is specific to propofol. It also remains unclear how propofol might work.”
https://www.psypost.org/2019/02/ane...ment-of-medication-resistant-depression-53218
 
Amazing, this is a step in the right direction imo :)

FDA approves new nasal spray medication for treatment-resistant depression; available only at a certified doctor’s office or clinic
The U.S. Food and Drug Administration today approved Spravato (esketamine) nasal spray, in conjunction with an oral antidepressant, for the treatment of depression in adults who have tried other antidepressant medicines but have not benefited from them (treatment-resistant depression). Because of the risk of serious adverse outcomes resulting from sedation and dissociation caused by Spravato administration, and the potential for abuse and misuse of the drug, it is only available through a restricted distribution system, under a Risk Evaluation and Mitigation Strategy (REMS).
"There has been a long-standing need for additional effective treatments for treatment-resistant depression, a serious and life-threatening condition," said Tiffany Farchione, M.D., acting director of the Division of Psychiatry Products in the FDA's Center for Drug Evaluation and Research. "Controlled clinical trials that studied the safety and efficacy of this drug, along with careful review through the FDA’s drug approval process including a robust discussion with our external advisory committees, were important to our decision to approve this treatment. Because of safey concerns, the drug will only be available through a restricted distribution system and it must be administered in a certified medical office where the health care provider can monitor the patient."

Patients with major depressive disorder who, despite trying at least two antidepressant treatments given at adequate doses for an adequate duration in the current episode, have not responded to treatment are considered to have treatment-resistant depression.

The Spravato labeling contains a Boxed Warning that cautions that patients are at risk for sedation and difficulty with attention, judgment and thinking (dissociation), abuse and misuse, and suicidal thoughts and behaviors after administration of the drug. Because of the risk of sedation and dissociation, patients must be monitored by a health care provider for at least two hours after receiving their Spravato dose. The REMS requires the prescriber and the patient to both sign a Patient Enrollment Form that clearly states that the patient understands they should make arrangements to safely leave the health care setting to get home and that the patient should not drive or use heavy machinery for the rest of the day on which they receved the drug. Additionally, Spravato must be dispensed with a patient Medication Guide that outlines the drug’s uses and risks.
The patient self-administers Spravato nasal spray under the supervision of a health care provider in a certified doctor’s office or clinic, and the spray cannot be taken home. The health care provider will instruct the patient on how to operate the nasal spray device. During and after each use of the nasal spray device, the health care provider will check the patient and determine when the patient is ready to leave.

The efficacy of Spravato was evaluated in three short-term (four-week) clinical trials and one longer-term maintenance-of-effect trial. In the three short-term studies, patients were randomized to receive Spravato or a placebo nasal spray. In light of the serious nature of treatment-resistant depresison and the need for patients to receive some form of treatment, all patients in these studies started a new oral antidepressant at the time of randomization and the new antidepressant was continued throughout the trials. The primary efficacy measure was the change from baseline on a scale used to assess the severity of depressive symptoms. In one of the short-term studies, Spravato nasal spray demonstrated statistically significant effect compared to placebo on the severity of depression, and some effect was seen within two days. The two other short-term trials did not meet the pre-specified statistical tests for demonstrating effectiveness. In the longer-term maintenance-of-effect trial, patients in stable remission or with stable response who continued treatment with Spravato plus an oral antidepressant experienced a statistically significantly longer time to relapse of depressive symptoms than patients on placebo nasal spray plus an oral antidepressant.

The most common side effects experienced by patients treated with Spravato in the clinical trials were disassociation, dizziness, nausea, sedation, vertigo, decreased feeling or sensitivity (hypoesthesia), anxiety, lethargy, increased blood pressure, vomiting and feeling drunk.

Patients with unstable or poorly controlled hypertension or pre-existing aneurysmal vascular disorders may be at increased risk for adverse cardiovascular or cerebrovascular effects. Spravato may impair attention, judgment, thinking, reaction speed and motor skills. Patients should not drive or operate machinery until the next day after a restful sleep. Spravato may cause fetal harm and women of reproductive potential should consider pregnancy planning and prevention; women should not breastfeed while being treated.

Esketamine is the s-enantiomer of ketamine. Ketamine is a mixture of two enantiomers (mirror image molecules). This is the first FDA approval of esketamine for any use. The FDA approved ketamine (Ketalar) in 1970.

The FDA granted this application Fast Track and Breakthrough Therapy designations.

The FDA granted the approval of Spravato to Janssen Pharmaceuticals, Inc.
https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm632761.htm
 
Chronic pain involves more than just hurting. People suffering from pain often experience sadness, depression and lethargy. That's one reason opioids can be so addictive—they not only dampen the pain but also make people feel euphoric.

What if it were possible to develop a pain killer that could curb the negative emotions associated with pain without causing euphoria? Researchers at Washington University School of Medicine in St. Louis have taken a step toward that goal. Studying rodents, they have shown they can block receptors in the brain responsible for the emotional components of pain and restore the animal's motivation. Their findings could lay the groundwork for developing new, less addictive approaches to pain treatment.

"We're in the midst of an opioid epidemic, and the euphoria associated with opioids is a major driver of opioid dependence," said senior investigator Jose Moron-Concepcion, Ph.D., an associate professor of anesthesiology, of neuroscience and of psychiatry. "By targeting the emotional aspects of pain, we hope to make pain less debilitating so that patients won't crave the emotional high they get from opioids."

Opioid painkillers, such as morphine, oxycodone and fentanyl, target receptors on brain cells called mu opioid receptors. In contrast, the Washington University researchers studied kappa opioid receptors, which operate very differently. Activating the kappa receptor makes people feel depressed, sad and unmotivated. So Moron-Concepcion and his colleagues at the Washington University Pain Center thought that by blocking those receptors, they also might dampen the negative emotions associated with pain.

Their findings are published March 13 in the journal Neuron.

Some of the rats in the study had been injected in a paw with a substance that causes persistent inflammation. To measure the emotional effects of that pain, the researchers used a rewarding task in which the animals could work for sugar as a way to measure motivation. After being taught to push a lever to get sugar, most rats will keep pushing. In these experiments, the animals had to push the lever progressively more each time they wanted a pellet of sucrose.

"When the animals experienced pain, they were less motivated to work to obtain the reward," said first author Nicolas Massaly, Ph.D., an instructor in anesthesiology. "It's often the same for people in pain who don't get as much pleasure from daily activities they usually enjoy."

But when the rats with inflamed paws were treated with a compound to block kappa opioid receptors in their brains, the animals recovered the motivation to obtain the sugar, and pushed the lever as often as those who did not have inflamed paws.

In addition, the researchers collaborated with Kooresh Shoghi, Ph.D., an associate professor of radiology, using small animal positron emission tomography (PET) imaging to assess the activity of kappa opioid receptors in the animals' brains. They were able to demonstrate that when rats were in pain, their kappa opioid receptors were very active in a part of the brain—the nucleus accumbens—linked to emotion.

The researchers dampened this kappa opioid receptor activity by blocking the release of a natural stimulator of kappa opioid receptors called dynorphin—which is produced in the brain and is kind of like the inverse of the endorphins released by activities such as exercise.

"By blocking dynorphin release, we were able to restore motivation in the animals despite the fact that we did not completely eliminate their pain," Massaly said.

Moron-Concepcion, Massaly and their colleagues acknowledge it's a long journey from rodents to people. But they already have preliminary PET data from people, suggesting it may be possible to influence kappa opioid receptors and potentially prevent the sadness and lack of motivation that can accompany physical pain. They believe that by attacking pain's emotional properties, without affecting the useful element of the pain response that can protect injuries from further damage, it may be possible to improve quality of life for pain patients without having to use any, or as many, habit-forming opioid pain killers.
https://m.medicalxpress.com/news/2019-03-blunting-pain-emotional-component.html
 
While this has been known and studied for quite some time now it's interesting nonetheless. Your hair color can impact your pain threshold and can alter your response to opioids:
Melanocortin-1 receptor gene variants affect pain and μ-opioid analgesia in mice and humans
Background: A recent genetic study in mice and humans revealed the modulatory effect of MC1R (melanocortin-1 receptor) gene variants on κ-opioid receptor mediated analgesia. It is unclear whether this gene affects basal pain sensitivity or the efficacy of analgesics acting at the more clinically relevant μ-opioid receptor.

Objective: To characterise sensitivity to pain and μ-opioid analgesia in mice and humans with non-functional melanocortin-1 receptors.

Methods: Comparisons of spontaneous mutant C57BL/6-Mc1re/e mice to C57BL/6 wildtype mice, followed by a gene dosage study of pain and morphine-6-glucuronide (M6G) analgesia in humans with MC1R variants.

Results: C57BL/6-Mc1re/e mutant mice and human redheads—both with non-functional MC1Rs—display reduced sensitivity to noxious stimuli and increased analgesic responsiveness to the μ-opioid selective morphine metabolite, M6G. In both species the differential analgesia is likely due to pharmacodynamic factors, as plasma levels of M6G are similar across genotype.

Conclusions: Genotype at MC1R similarly affects pain sensitivity and M6G analgesia in mice and humans. These findings confirm the utility of cross species translational strategies in pharmacogenetics.
https://jmg.bmj.com/content/42/7/583

For further reading:
https://www.ucihealth.org/blog/2018/04/redheads-pain
https://www.pbs.org/newshour/science/fact-or-fiction-do-redheads-feel-more-pain
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2938350/
 
Creating opioids with less side effects, i.e. less respiratory depression
Morphine is an alkaloid from the opium poppy used to treat pain. The potentially lethal side effects of morphine and related opioids—which include fatal respiratory depression—are thought to be mediated by μ-opioid-receptor (μOR) signalling through the β-arrestin pathway or by actions at other receptors. Conversely, G-protein μOR signalling is thought to confer analgesia. Here we computationally dock over 3 million molecules against the μOR structure and identify new scaffolds unrelated to known opioids. Structure-based optimization yields PZM21—a potent Gi activator with exceptional selectivity for μOR and minimal β-arrestin-2 recruitment. Unlike morphine, PZM21 is more efficacious for the affective component of analgesia versus the reflexive component and is devoid of both respiratory depression and morphine-like reinforcing activity in mice at equi-analgesic doses. PZM21 thus serves as both a probe to disentangle μOR signalling and a therapeutic lead that is devoid of many of the side effects of current opioids.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5161585/
 
^ sounds like AT-121. Soon these are going to be everywhere.
AT-121 suppressed oxycodone’s reinforcing effects and exerted morphine-like analgesic effects in nonhuman primates. AT-121 treatment did not induce side effects commonly associated with opioids, such as respiratory depression, abuse potential, opioid-induced hyperalgesia, and physical dependence. Our results in nonhuman primates suggest that bifunctional NOP/MOP agonists with the appropriate balance of NOP and MOP agonist activity may provide a dual therapeutic action for safe and effective pain relief and treating prescription opioid abuse.http://stm.sciencemag.org/content/10/456/eaar3483

If that's not enough there's the NOP target to take the fun out of everything..

The nociceptin/orphanin FQ receptor (NOP) as a target for drug abuse medications.

Several studies show that the nociceptin receptor NOP plays a role in the regulation of reward and motivation pathways related to substance abuse.

Administration of the NOP's natural peptide ligand, Nociceptin/Orphanin FQ (N/OFQ) or synthetic agonist Ro 64-6198 has been shown to block rewarding effects of cocaine, morphine, amphetamines and alcohol, in various behavioral models of drug reward and reinforcement, such as conditioned place preference and drug self-administration. Administration of N/OFQ has been shown to reduce drug-stimulated levels of dopamine in mesolimbic pathways.

The NOP-N/OFQ system has been particularly well examined in the development of alcohol abuse in animal models. Furthermore, the efficacy of the mixed-action opioid buprenorphine, in attenuating alcohol consumption in human addicts and in alcohol-preferring animal models, at higher doses, has been attributed to its partial agonist activity at the NOP receptor. These studies suggest that NOP receptor agonists may have potential as drug abuse medications.As with the case of buprenorphine, a mixed-action profile of NOP/opioid activity may provide a more effective drug to treat addiction to various abused substances and/or polydrug addiction.
https://www.ncbi.nlm.nih.gov/pubmed/21050175
 
Johns Hopkins neuroscientists have found that the psychedelic drug MDMA reopens a kind of window, called a "critical period," when the brain is sensitive to learning the reward value of social behaviors. The findings, reported April 3 in Nature, may explain why MDMA may be helpful in treating people with post-traumatic stress disorder (PTSD). Critical periods were first described in the 1930s in snow geese. About 24 hours after a gosling hatches, if mother goose is nowhere to be found, the hatchling will bond with an object, including non-living ones. Yet, if mother goose disappears 48 hours after her gosling hatches, the critical period is over, and the hatchling won't bond to an object. There is evidence for critical periods that smooth the way for development of language, touch and vision. For the current study, neuroscientist Gül Dölen says, "We wanted to know if there was a critical period for learning social reward behaviors, and if so could we reopen it using MDMA, since this drug is well-known to have prosocial effects." Dölen and her team studied groups of mice in enclosures with different bedding. They put several mice together in one enclosure with one type of bedding for 24 hours and, in the next 24 hours, put the same mice by themselves in another enclosure with a different type of bedding. The mice began to associate certain types of bedding with isolation or companionship. Then, they let the mice wander between enclosures with the two types of bedding and tracked how long the mice spent in each enclosure. The more time the mice spent in the bedding linked to their companions indicated more social reward learning. "It's why people gather around the water cooler," says Dölen, assistant professor of neuroscience at the Johns Hopkins University School of Medicine. People are conditioned to know that the water cooler is an optimal place to chitchat with companions. In their experiments, Dölen and her colleagues found that the critical period for social reward learning in mice is around puberty and wanes once they become mature adults. To determine if they could reopen the critical period, the scientists gave MDMA to mature mice, waited 48 hours for the drug to be washed out of their system, and observed how the mice explored their enclosure and behaved with other mice in the enclosure. Following the treatment with MDMA, most of the animals responded to social interactions the same way as juveniles, by forming a positive association between social interactions and the bedding. This effect lasted for at least two weeks after the MDMA treatment, and it was not observed in mice given saline injections. "This suggests that we've reopened a critical period in mice, giving them the ability to learn social reward behaviors at a time when they are less inclined to engage in these behaviors," says Dölen. Dölen and her postdoctoral student and first author of the current study, Romain Nardou, also observed that MDMA works to reopen the critical period only if the drug is given to mice when they are with other mice, not if it is given to mice while they are alone. This suggests that reopening the critical period using MDMA may depend on whether the animals are in a social setting, say the scientists. The mice maintained their ability to learn the rewards of social behavior for up to two weeks from the time they were given MDMA. During this time, Dölen and her colleagues also found that the brains of the mice had corresponding responses to oxytocin, known as the "love hormone," which is made in the hypothalamus and acts in the brain as a signal between neurons that encode information about social rewards. They found these responses by looking more closely at synapses, the spaces between brain cells called neurons. Their experiments showed that, in mature mice given MDMA, oxytocin triggers signaling in the synapses that encodes learning and memory, which does not typically happen in mature mice. Dölen says that opening the critical window for social reward behavior may also have implications for treating psychiatric conditions. A strong bond between a psychotherapist and patient is well-known to be important for successful treatment. If MDMA reopens the critical period for social reward learning in humans in the same way it does for mice, then it could explain why the drug has been successful in treating people with PTSD, perhaps by strengthening the psychotherapist-patient bond. MDMA has been designated by the U.S. Food and Drug Administration as a "breakthrough therapy" for PTSD, meaning that the agency will fast-track the development and review of clinical trials to test it. However, the researchers caution that MDMA may not work for every psychiatric condition linked to social behaviors. "As we develop new therapies or determine when to give these therapies, it's critical to know the biological mechanism on which they act," says Dölen. More information: Romain Nardou et al. Oxytocin-dependent reopening of a social reward learning critical period with MDMA, Nature (2019). DOI: 10.1038/s41586-019-1075-9

 
Really interesting:
Experimental drug shows promise for opioid withdrawal symptoms
While medicines are available to relieve withdrawal symptoms in people recovering from opioid addiction, they cause side effects and can maintain the brain changes that led to addiction in the first place, which can lead to relapse before treatment is completed. New research offers hope that a better solution may be on the horizon. Rapastinel, an experimental drug originally developed as an antidepressant, substantially reversed acute signs of opioid withdrawal in rats in just three days.

The findings suggest rapastinel could be useful to help manage withdrawal during the critical first days after someone has entered treatment and is trying to abstain from opioid use, according to researchers.
"We have found that rapastinel has potential as a new treatment for opioid dependence, as it is effective in reducing withdrawal signs and has not been shown to produce any negative side effects," said Julia Ferrante, an undergraduate at Villanova University who conducted the research with Cynthia M. Kuhn, Ph.D., professor of pharmacology and cancer biology at Duke University. "By reducing withdrawal symptoms, the patient feels less discomfort during treatment, and we hypothesize this would lead to a decreased risk of relapse."
Ferrante will present the research at the American Society for Pharmacology and Experimental Therapeutics annual meeting during the 2019 Experimental Biology meeting, held April 6-9 in Orlando, Fla.
"Our research suggests that new alternatives to standard treatments for opioid dependence have potential to be safer and more effective," Ferrante added. "Rapastinel research for opioid dependency is currently only being done in rodents, but if the drug continues to have successful trials, it may enter clinical trials for use in humans."
Buprenorphine and methadone, the most common drugs used to help people quit opioid abuse, are problematic because they are themselves opioids and can be addictive, have unpleasant and sometimes dangerous side effects and often must be used for months to avoid relapse. Ketamine, which has been proposed as an alternative, non-opioid treatment for opioid withdrawal, also has the potential for abuse and can cause hallucinations and other negative side effects.
Rapastinel, developed as an antidepressant, binds to the same receptor as ketamine but at a different site, where it has a milder effect. While a clinical trial recently concluded rapastinel is not effective against depression, trials have shown it is well tolerated and has no serious side effects.
In the new study, Ferrante and Kuhn modeled opioid dependence in rats and then tracked signs of withdrawal in groups of rats given either rapastinel, ketamine or a saline solution. On the third day, rats given rapastinel showed significantly fewer signs of withdrawal than rats given either ketamine or saline, which showed roughly equal amounts of withdrawal signs.
To move toward clinical trials in humans, researchers will continue to investigate rapastinel's effects on a molecular level and study whether the drug can reduce the likelihood of relapse. If approved for treating opioid dependence, rapastinel would likely be administered intravenously, possibly in an outpatient setting, Ferrante said. It is unknown how long patients would need to use rapastinel to ensure complete recovery from opioid dependence.
https://medicalxpress.com/news/2019-04-experimental-drug-opioid-symptoms.html
 
Ketamine reverses neural changes underlying depression-related behaviors in mice

Researchers have identified ketamine-induced brain-related changes that are responsible for maintaining the remission of behaviors related to depression in mice—findings that may help researchers develop interventions that promote lasting remission of depression in humans. The study, funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health, appears in the journal Science.


Major depression is one of the most common mental disorders in the United States, with approximately 17.3 million adults experienced a major depressive episode in 2017. However, many of the neural changes underlying the transitions between active depression, remission, and depression re-occurrence remain unknown. Ketamine, a fast-acting antidepressant which relieves depressive symptoms in hours instead of weeks or longer, provides an opportunity for researchers to investigate the short- and long-term biological changes underlying these transitions.

"Ketamine is a potentially transformative treatment for depression, but one of the major challenges associated with this drug is sustaining recovery after the initial treatment," said study author Conor Liston, M.D., Ph.D., of Weill Cornell Medicine, New York City.

To understand mechanisms underlying the transition from active depression to remission in humans, the researchers examined behaviors related to depression in mice. Researchers took high-resolution images of dendritic spines in the prefrontal cortex of mice before and after they experienced a stressor. Dendritic spines are protrusions in the part of neurons that receive communication input from other neurons. The researchers found that mice displaying behaviors related to depression had increased elimination of, and decreased formation of, dendritic spines in their prefrontal cortex compared with mice not exposed to a stressor. This finding replicates prior studies linking the emergence of behaviors related to depression in mice with dendritic spine loss.

In addition to the effects on dendritic spines, stress reduced the functional connectivity and simultaneous activity of neurons in the prefrontal cortex of mice. This reduction in connectivity and activity was associated with behaviors related to depression in response to stressors. Liston's group then found that ketamine treatment rapidly restored functional connectivity and ensemble activity of neurons and eliminated behaviors related to depression. Twenty-four hours after receiving a single dose of ketamine, mice exposed to stress showed a reversal of behaviors related to depression and an increase in dendritic spine formation when compared to stressed mice that had not received ketamine. These new dendritic spines were functional, creating working connections with other neurons.

The researchers found that while behavioral changes and changes in neural activity in mice happened quickly (three hours after ketamine treatment), dendritic spine formation happened more slowly (12-24 after hours after ketamine treatment). While further research is needed, the authors suggest these findings might indicate that dendritic spine regrowth may be a consequence of ketamine-induced rescue of prefrontal cortex circuit activity.

Although dendritic spines were not found to underly the fast-acting effects of ketamine on behaviors related to depression in mice, they were found to play an important role in maintaining the remission of those behaviors. Using a new technology developed by Haruo Kasai, Ph.D., and Haruhiko Bito, Ph.D., collaborators at the University of Tokyo, the researchers found that selectively deleting these newly formed dendritic spines led to the re-emergence of behaviors related to depression.

"Our results suggest that interventions aimed at enhancing synapse formation and prolonging their survival could be useful for maintaining the antidepressant effects of ketamine in the days and weeks after treatment," said Dr. Liston.

"Ketamine is the first new anti-depressant medication with a novel mechanism of action since the 1980s. Its ability to rapidly decrease suicidal thoughts is already a fundamental breakthrough," said Janine Simmons, M.D., Ph.D., chief of the NIMH Social and Affective Neuroscience Program. "Additional insights into ketamine's longer-term effects on brain circuits could guide future advances in the management of mood disorders."
https://medicalxpress.com/news/2019-04-ketamine-reverses-neural-underlying-depression-related.html
 
This is very interesting:

Gut microbes eat our medication

Date: June 13, 2019
Source: Harvard University

Summary: Researchers have discovered one of the first concrete examples of how the microbiome can interfere with a drug's intended path through the body. Focusing on levodopa (L-dopa), the primary treatment for Parkinson's disease, they identified which bacteria out of the trillions of species is responsible for degrading the drug and how to stop this microbial interference.

 
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Esketamine approved, and hair color effecting pain threshold.

F’ing amazing . Great thread, btw
 
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So you are prescribed or use benzodiazepines regularly and develop an infection that requires an antibiotic. Something you might want to mention to your doctor, as many are unaware.


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2435654/

And the very BEST thing on Ciprofloxacin ("Ciproxin") is, that it is making muskle tendons torn, mostly the achilles tendon. I already had 6 or 7 patients, only females betweem 50 and 60 and they all did not fall down, there was nothing which could have explained the ruptured achilles tendon.

They all came from my former chef wo is a surgeon - and after a while just also only reading the piece of paper inside i really got sick from my stomach because i could not believe that something like this is STILL on the market. I was lucky, i had to took it once. And when I saw then what could have happened to me I did really don't know what to say


See here:


Please read mostly the side effects because then your done to go to bed..

JJ
 
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Taken from 1984 BBC Horizon Programme 'The Case of the Frozen Addicts'

It really concerns me that in fact, not all of the people who took the tainted MPPP developed symptoms straight away. In short, who knows if an RC will cause serious long-term haem? .
 
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