06/29/15

Overdosing on Energy Drinks

© energy drink by  reticent | stockfresh,com

© energy drink by reticent | stockfresh,com

A healthy 26-year-old Hispanic man with no family history and no apparent risk factors for hear attack went to an ER in Texas complaining of left-sided chest pains. He arrived at the hospital about nine hours after he began having chest pain.  “His left arm felt numb, he was sweating profusely and he reported vomiting prior to his arrival at the hospital.” He reported to the medical personnel that he drank between 8 and 10 energy drinks that day, his typical daily consumption of energy drinks.

In addition, the man also had a pack a day smoking habit for the past two years. He underwent a cardiac catheterization where a 100% occlusion of his left circumflex artery was found. There was no evidence on underlying artery plaque in that region of his heart. And no other evidence of coronary artery disease in his other coronary vessels was noted. A stent was placed in the occluded artery. After two days, he was discharged. “He agreed to stop smoking and consuming energy drinks.” Read a published case report of his medical treatment here.

The authors hypothesized that the large amount of energy drink consumption contributed to the acute thrombus blocking the man’s blood vessel. Excessive levels of caffeine and the possible effects of other substances contained in the energy drinks contributed to the man’s heart problem. They also acknowledged a reasonable alternative hypothesis was that his smoking caused or contributed to his “coronary artery vasospasm.”

Energy drinks have actually been around for a long time, with cocaine-laced Coca Cola being one of the first. Pemberton’s original formula included five ounces of coca leaf per gallon of syrup. Coca-Cola was estimated to contain about nine milligrams of cocaine per glass. It was removed from the syrup formula in 1903 and replaced with caffeine.

The modern introduction of energy drinks can be traced to the initial sale of “Red Bull” in 1997. Today there are a wide variety of additional energy drinks (such as Rock Star and Monster) with multiple energy-producing ingredients. The most common are: caffeine, taurine, glucuronolactone, and ginseng. Guarana is another caffeine-based stimulant commonly used in energy drinks. A typical energy drink contains between 75 milligrams to over 200 milligrams of caffeine per serving. This compares to 34 mg in Coke and 55 mg in Mountain Dew. Eight ounces of brewed coffee contains between 65 and 120 mg of caffeine. Two ounces of espresso contains 60 to 100 mg.

Brown University has a handy page of information on energy drinks where it noted that if a drink advertises no caffeine, the energy probably comes from guarana.  Short-term dangers from energy drinks include: increased heart rate and blood pressure (sometimes to the point of heart palpitations), dehydration, and sleep disturbance. Occasional use of energy drinks was not seen as harmful, but the claims of some for improved performance and concentration was said to be misleading. Thinking of them as highly-caffeinated drinks gives you a more accurate picture of how they affect you.

Mixing energy drinks (a stimulant) with alcohol (a depressant) brings with it a number of potential dangers. The energy drink can give the person the impression they aren’t impaired from the alcohol; or prevent them from realizing how much alcohol they have consumed. “No matter how alert you feel, your blood alcohol concentration (BAC) is the same as it would be without the energy drink.” Once the energy drink wears off, fatigue, respiratory depression and vomiting can occur. Both substances are very dehydrating and can hinder the body’s ability to metabolize alcohol, increasing its toxicity—and therefore the hangover you get the next day.

The FDA has been collecting reports on adverse effects from energy drinks within its Center for Food Safety and Adverse Event Reporting System (CAERS). A report tracking adverse events from Red Bull between January of 2004 and October of 2012 had 22 adverse events. The noted symptoms ranged from dehydration, vomiting, convulsions, anxiety and aggression, to vertigo, blindness, pancreatitis, chest pain, increased heart rate and blood pressure.

Another FDA CAERS report noted adverse events for 5-Hour Energy (92), Monster (40), and Rockstar (13). The symptoms ranged from vomiting, dizziness, increased heart rate, anxiety and diarrhea to convulsions, chest pain, loss of consciousness and even death. There were eleven deaths related to the 5-Hour Energy reports, five for the Monster reports and none for Rockstar.

Health concerns with energy drinks are not just confined to FDA adverse events. A Live Science article last year by Tia Ghose reported that more than 5,000 cases of people getting sick from energy drinks were reported to US poison control centers between 2010 and 2013. Many of the cases involved serious side effects like seizures, irregular heart rhythms, and dangerously high blood pressure. Children under the age of six were frequently consuming the beverages without knowing what they were drinking. Stephen Lipshultz, a pediatrician from Michigan, noticed the association in 2007 and began tracking data from poison control centers from around the world.

In 2011, Lipshultz and his colleagues published their findings in the journal Pediatrics. They discovered that self-report surveys found that energy drinks are used by 30% to 50% of adolescents and young adults. In 2007, 46% of the 5,448 reported caffeine overdoses occurred in those younger than 19 years of age. Energy drinks were found to have no therapeutic benefit. Both the known and unknown pharmacology of the various ingredients in them, combined with reports of toxicity, suggested that energy drinks put some children at risk for serious adverse health effects.

Long-term research objectives should aim to better define maximum safe doses, the effects of chronic use, and effects in at-risk populations (eg, those with preexisting medical conditions, those who consume energy drinks during and after exercise, or those who consume them in combination with alcohol), and better documentation and tracking of adverse health effects. Unless research establishes energy-drink safety in children and adolescents, regulation, as with tobacco, alcohol, and prescription medications, is prudent.

A new study by researchers at the Yale School of Public Health found that middle school children who consume energy drinks are 66% more likely to be at risk for hyperactivity/inattention (ADHD) symptoms. They said that interventions to reduce sweetened beverage consumption should focus on energy drinks and other emerging sweetened beverages such as sports and sweetened coffee drinks. “Boys were more likely to consume energy drinks than girls.”

Over the last few years I’ve seen a regular parade of energy drinks consumed by individuals in early recovery. However I don’t think I ever knew someone drinking 8 to 10 of them daily. Doing the research for this article impressed upon me their potential to contribute to the instability of early recovery. So I think I’ll begin paying more attention to who is drinking them and how many energy drinks they consume.

06/26/15

Christian, What Do You Believe?

© Kuna George | 123RF.com

© Kuna George | 123RF.com

One way or another, the Apostles’ Creed has been part of my worship life since I was a child. Growing up in a liturgical church, we recited it every Sunday. I made a commitment to Christ in another liturgically-minded denomination in my twenties and continued reciting it weekly. For a number of years, I recited it as part of my daily prayer time. The current church I am a member of recites it monthly on our communion Sunday. Parallel to my personal experience, the Apostles’ Creed has been part of the worship life of the church since it was young.

The Apostles’ Creed was used in church history much as the Roman Creed was in the time of the early church: as a baptismal confession; as an outline for teaching; as a summary of faith and belief; as an affirmation in worship; and as a guard against heresy. Ambrose and Augustine suggested the repetition of the Apostles’ Creed in daily devotions. Augustine said in his work, The Enchiridion:

For you have the Creed and the Lord’s Prayer. What can be briefer to hear or to read? What easier to commit to memory?When, as the result of sin, the human race was groaning under a heavy load of misery, and was in urgent need of the divine compassion, one of the prophets, anticipating the time of God’s grace, declared: “And it shall come to pass, that whosoever shall call on the name of the Lord shall be delivered.” Hence the Lord’s Prayer. But the apostle, when, for the purpose of commending this very grace, he had quoted this prophetic testimony, immediately added: “How then shall they call on Him in whom they have not believed?” Hence the Creed.

Martin Luther identified it as one of three binding summaries of belief. John Calvin divided his Institutes into four parts, corresponding to the Apostles’ Creed, which all Christians were familiar with.

For as the Creed consists of four parts, the first relating to God the Father, the second to the Son, the third to the Holy Spirit, and the fourth to the Church, so the author, in fulfilment of his task, divides his Institutes into four parts, corresponding to those of the Creed.

While each of the above noted uses can be identified at various points in church history, it seems to have been its growing use within the devotional and liturgical life of believers that eventually solidified its position as “the mature flower” of Western creedal development. The local variants of the older Roman Creed were increasingly laid aside in the worship and practice of local churches and replaced by the Apostles’ Creed. Thus the journey from the Roman Creed to the Apostles’ Creed is complex, woven together that of the historical documents and additional creeds of the first few centuries of the church.

The earliest evidence for the received text for the Apostles’ Creed or “T” is within the text of a Benedictine missionary manual written sometime between 710 and 724 AD. A comparison of the Roman Creed to the Apostles’ Creed calls for speculation that the additions were largely to address theological problems as the church confronted a series of heresies between the mid–second century and early eighth centuries. Such an understanding of its journey would draw upon the differences in a manner something like the following.

Roman Creed Apostles’ Creed
1. I believe in God the Father Almighty 1. I believe in God the Father Almighty [creator of Heaven and Earth]
2. And in Christ Jesus, his only Son, our Lord; 2. And in Jesus Christ, his only Son, our Lord;
3. Who was born by the Holy Ghost of the Virgin Mary; 3. Who was [conceived] by the Holy Spirit, born of the Virgin Mary;
4. Was crucified under Pontius Pilate and was buried; 4. [Suffered] under Pontius Pilate, was crucified [dead] and buried [ He descended to Hell (Hades)];
5. The third day he rose from the dead; 5. on the third day rose again from the dead;
6. He ascended into heaven; and sitteth on the right hand of the Father; 6. He ascended into heaven; and sits at the right hand of [God] the Father [Almighty];
7. From thence he shall come to judge the quick and the dead. 7. From thence he will come to judge the living and the dead.
8. And the Holy Ghost; 8. [I believe] in the Holy Spirit;
9. The Holy Church; 9. The Holy [Catholic] Church [The communion of saints];
10. The forgiveness of sins; 10. The forgiveness of sins;
11. The resurrection of the body (flesh). 11. The resurrection of the body (flesh);
12. [And eternal life] Amen.

Beginning with the Roman Creed, we see that it contains the Trinitarian formula of Father, Son, and Holy Spirit; and confesses belief in the life, death, and resurrection of Jesus Christ.

The addition of  the phrase “Creator of Heaven and Earth” in the Apostles’ Creed to the first article of the Roman Creed rejects the Gnostic belief that creation was the act of a demiurge Christ; and the Manichean dogma that all matter was intrinsically evil.  The addition to article 3 that Jesus Christ was: “[conceived] by the Holy Ghost, born of the Virgin Mary” explicitly excluded the Ebionite denial in the virgin birth of Christ and the Monarchian denial that Jesus was conceived by the Holy Ghost.

The addition of “I believe” to article 8 adds clarity to the confession of believing in “Father, Son, and Holy Spirit” as God, countering the Modalistic or Monarchian conception of God. It seems the attempt to counter Modalism is within the specification in article 6 that the Father is “God Almighty.” The resurrection of the body in article 11 and the addition of article 12 countered Greek and Gnostic prejudice against the corporal body and specified an existence consistent with the “resurrection life” promised by Christ and distinctly different than the “eternal life” of the mystery cults.  Confessing the real birth, suffering, death (by crucifixion), and burial of Christ in articles 3 through 5 countered the Marcion and Docetic belief that such things were unworthy of the true Christ.

The additions of “Catholic” (meaning universal) and “the communion of saints” in article 9 may suggest an attempt to cope with the problem of unity in diversity within the early church. As distinct subcultures of theology and worship developed within the “catholic” church, there was a desire to acknowledge their legitimacy while attempting to exclude heresies, which also sought acceptance. As the body of Christ grew and diversified, the ears were denying they were a part of the body; the body was questioning the continuing function of the stomach. Despite the diversity within the church, if the “Head” of the creed in articles 1 through 8 was believed and confessed, there was a communion of saints within a universal church that existed beyond physical walls, geographic boundaries, theological particulars, and ultimately time itself. This acknowledgement of unity within diversity became an element of the rule of faith itself.

Unquestionably the Apostle’s Creed is a more detailed and theologically mature creedal statement of belief than the Roman Creed. However, it did not develop solely as a response to the various dogmatic concerns as noted above. There is also strong suggestive evidence that The Apostles’ Creed originated outside of Rome and was eventually accepted as the baptismal rite within the Roman church by the ninth century. Presuming the probability of this line of development, the church beyond the local reach of Rome was merely returning to her an enriched, improved statement of the same rule of faith, which she herself had compiled in the second century.

The Apostles’ Creed continues in modern times as the most widely accepted and used creed among Christians. All the individual articles noted above within it originated before the Nicene Creed was formulated—regardless of whether the final revision appeared as late as the early eighth century. And all the articles are in agreement with the New Testament and the teaching of the apostles. Phillip Schaff observed in his day that an attack on the Apostles’ Creed was also an indirect attack upon the New Testament. But he predicted that the Creed would outlive these assaults and continue in the life of the church, sharing in the victory of the Scriptures over all forms of unbelief.

This description of the Apostles’ Creed (and a previous one on the Roman Creed) was compiled from the New Dictionary of Theology (179-181), by Sinclair Ferguson and J. I. Packer; the Evangelical Dictionary of Theology (72–73), Walter A. Elwell, editor; The Emergence of the Catholic Tradition  (117), by Jaroslav Pelikan; Early Christian Creeds (1–6; 100–166), by  J. N. D. Kelly; and The Creeds of Christendom, Volume 1, The History of the Creeds (14–23; 368–434), by Phillip Schaff.

06/24/15

Debating the Harm from Psychotropics

© iqoncept | 123RF.com

© iqoncept | 123RF.com

In mid-May of 2015, there was a public debate on whether the long-term use of psychiatric medications causes more harm than good. Before saying “Boring” and moving on to something else, realize that prescriptions for antidepressants are on the rise —increasing by 7.5% in Britain since 2013 and over 500% since 1992. Recent research has shown that more people are taking antidepressants for longer periods of time, “often because they become dependent upon them and cannot stop.” Yet there is no good research into the safe long-term use of these drugs.

It seems that the challenge for the debate grew out of several prominent British psychiatrists publically criticizing the launch of the Council for Evidence-Based Psychiatry, an organization aimed at starting a dialogue about the use of psychiatric drugs and treatments. The two sides of the debate jointly published a paper in the British Medical Journal (BMJ).  The original BMJ press release, now removed from the site, inexplicably did not include a declaration of interests for one of the speakers against the motion, Alan H. Young. So what?

Young was initially in print as saying he had no interests to declare, while in fact he had several. This was important information to reveal, not only because it is a BMJ policy, but also because Young was planning to challenge the premise of whether long-term use of psychiatric medication causes more harm than good. In other words, his financial and professional ties to the pharmaceutical industry were initially not reported in a debate where he was defending the use of psychiatric medications. You can view the original press release here; the revised one here. Look at the bottom right column on page 2 for both.

This mistake was caught by one of the speakers for the motion, Peter Gøtzsche, who also reported a series of actions that appeared to be aimed at undercutting  Gøtzsche’s credibility and the information he presented. You can read his description of these “bizarre events” related to the Maudsley debate here. You can review the debate here. Gøtzsche opened his time to speak during the debate by estimating that psychiatric drugs were the 3rd leading cause of death among people aged 65 and over.

I have estimated, based on randomised trials and cohort studies, that psychiatric drugs kill more than half a million people every year among those aged 65 and above in the USA and Europe. This makes psychiatric drugs the third leading cause of death, after heart disease and cancer. The drugs furthermore cripple tens of millions. There are no benefits that can justify so much harm.

Gøtzsche also described how clinical trials include patients already taking other psychiatric medications. These participants are then rapidly withdrawn for their medication. If they are randomly placed in a placebo group, they often experienced withdrawal symptoms. “This design exaggerates the benefits of treatment and increases the harms in the placebo group, and it has driven patients taking placebo to suicide in trials in schizophrenia.”

He called for the establishment of withdrawal clinics to help patients slowly and safely taper off of psychiatric drugs. He estimated that 98% of all psychotropic drugs could be stopped without causing harm. In the revised BMJ press release, it says “we could stop almost all psychotropic drugs without causing harm.” Gøtzsche said this replaced his original statement. This could be accomplished by dropping all antidepressants, ADHD medications, and dementia drugs. Only a small percentage of the antipsychotics and benzodiazepines currently used should be continued.

This would lead to healthier and more long-lived populations.  Because psychotropic drugs are immensely harmful when used long term, they should almost exclusively be used in acute situations and always with a firm plan for tapering off, which can be difficult for many patients.

The Council for Evidence-Based Psychiatry (CEP) began on April 30th of 2014 with an event at the House of Lords and the release of a publication entitled: Unrecognized Facts about Modern Psychiatric Practice. This is linked on the CEP website. You can get a quick introduction to some of the CEP members and what they believe by viewing some short videos linked on their homepage. One of the innovative ways they have attempted to provide a bridge between the public, policy makers and legislators, and the research community that investigates the areas where psychiatry has caused harm, although the intention has been to help.

Unrecognized Facts is a nifty slide show that presents various facts about modern psychiatric practice, with links on each slide to further available information. Here are a few of examples of what you can find there.

Myth of the Chemical Imbalance

Psychiatric drugs have often been prescribed to patients on the basis that they cure a ‘chemical imbalance.’ However, no chemical imbalances have been proven to exist in relation to any mental health disorder. There is also no method available to test for the presence or absence of these chemical imbalances.

Worse Long-Term Outcomes

There has been little research on the long-term outcomes of people taking psychiatric drugs. The available studies suggest that all the major classes of psychiatric drugs add little additional long-term benefit, and for some patients they may lead to significantly worse long-term outcomes.

 Long-Lasting Negative Effects

Psychiatric drugs can have long-lasting negative effects on the brain and central nervous system, particularly when taken long term, which can lead to physical, emotional and cognitive difficulties.

Negative Effects Are Often Misdiagnosed

Psychiatric drugs can have effects that include mental disturbance, including suicide, violence, and withdrawal syndromes. These can be misdiagnosed as new psychiatric presentations, for which additional drugs may be prescribed, sometimes leading to long-term use of multiple different psychiatric drugs in the same person.

06/22/15

The Genetic Connection

© Claudio Ventrella | 123RF.com

© Claudio Ventrella | 123RF.com

Researchers at the University of Texas Austin have announced that they found “convergent evidence” of gene networks related to alcohol consumption in humans. “These networks of coordinately expressed gene sets with common biological functions provide a systems level model of alcohol dependence.” But it would be wrong to conclude, as the Digital Journal did that: “Researchers at the University of Texas Austin successfully identified a genetic network which appears to determine alcohol dependence.” Other news outlets, such as Fox News, said something similar. This is another example of how the media reporting on research runs ahead of the research itself.

But the researchers themselves didn’t make the same mistake. The WCAAR newsletter from the University of Texas Austin, which was cited above, said: “The purpose of this study was to arrive at a comprehensive picture of the gene sets driving the phenotype of alcohol dependence.” They hoped the gene networks they identified could be useful as a reference for future studies, “such as exploration of specific drug targets in the network or identification of new gene isoforms unique to humans.”

The study consisted of doing post mortem biopsies of the prefrontal cortex brain tissues of two groups of individuals—alcoholics and non-alcoholics. They discovered that at a global level, gene connectivity, “representing fully functional biological processes,” was weaker within the alcoholic group. “This dysregulation of normal biological function is a hallmark of alcohol dependence.” Looking at the abstract for the published study in Molecular Psychiatry, the team of researchers said:

Overall, our work demonstrates novel convergent evidence for biological networks related to excessive alcohol consumption, which may prove fundamentally important in the development of pharmacotherapies for alcohol dependence.

The problem seems to have been that the news outlets were attributing causation to what is at this stage of the research only a correlational finding. Here is a short video of Ionica Smeets explaining the difference between correlation and causation; and the dangers of confusing correlation for causation.  In her talk she said: “Jumping to an incorrect conclusion about causality when you see a correlation, is the most often made logical mistake.”

This was a study of the brain tissue of dead alcoholics and non-alcoholics. The post mortem presence of the gene networks was suggestive of a possible predisposing genetic factor for alcoholism, but could not said to be causative.  “This strong interconnectedness of gene networks linked to alcohol dependence was absent in the control tissue.”

The alcohol consumption networks in the alcoholic tissue suggest subtle transcriptome reorganization in response to alcohol dependence. They may also indicate an allostatic mechanism – a physiological process to regain homeostasis – to overcome changes associated with alcohol dependence.

An alostatic mechanism refers to “the wear and tear” or physiological consequences of chronic exposure to heightened neural or neuroendocrine response that is the result of chronic stress—in this case from the lifelong consumption of large amounts of alcohol. So the researchers are suggesting their results indicate the presence of “a physiological process to regain homeostasis”—an attempt by the brains of the alcohol dependent individuals “to overcome changes associated with alcohol dependence.” They see adaptation, but not necessarily causation.

Alcohol dependence runs in families, and is suggestive of genetic causality, but not conclusively so. The Addiction Science Research and Education Center of the University of Texas Austin noted that while alcoholism runs in families and is suggestive of a genetic cause, many things run in families that aren’t genetic, such as speaking Spanish. Although twin and adoption studies indicate susceptibility for alcohol dependence in families, there are some individuals like Jay Joseph who question the scientific validity of twin studies (See “Chasing Ghosts” and “Troubling Twin Studies“). But even Erickson fails to make a causal link between genetics and alcoholism:

Alcohol dependence is not a genetic disease (which suggests destiny); rather, the tendency to become alcoholic is inherited. Thus alcoholism can skip generations, or affect only certain individuals in an alcoholic family. (number 103 of the Alcohol Facts)

An earlier theory of the “cause” of alcoholism was the “THIQ theory.” As Carleton Erickson indicated in his list of “Drug Myths,” the THIQ is an older myth popular in the early 1970s that when alcoholics drink they form opiate-like THIQs in the brain, to which they become “addicted.” There is a short, but helpful description of the THIQ myth on the HAMS Network. I don’t agree with much of what is there about addiction and recovery, as I have a 12 Step, abstinence-based approach to recovery, where they are harm reduction-based. But this seems to be a balanced summary of what is now a discarded theory.

So while there is growing evidence of some kind of genetic connection with alcoholism, that connection is not conclusive at this point in time. Nor can it be said to be causative. And if or when it becomes more conclusive, it seems that a better way of describing it is not as a genetic disease, but an inherited tendency. So the expressed hope of the study’s findings by its researchers can be anticipated, namely that it “may prove fundamentally important in the development of pharmacotherapies for alcohol dependence.”  But it doesn’t provide evidence for a genetic cause of alcohol dependence.

06/19/15

The Old Roman Creed

© Kayco | stockfresh.com Hill at Sunset in Drazovce, Slovakia

© Kayco | stockfresh.com Hill at Sunset in Drazovce, Slovakia

One of the things that fascinated me about the early church is the historical context within which the early creeds developed. We are fast approaching the anniversary of the second millennial since the death and resurrection of Christ. That distance of time has contributed to the vast majority of Christians being largely ignorant of the history shaping their creeds, if not the creeds themselves. For instance, did you know there was a so-called “Roman Creed” that was the model for many of the creedal statements in the West, including the Apostles’ Creed?

A tradition developed in the early church that soon after Pentecost the apostles, when “filled with the Holy Spirit,” gathered together and drafted a short summary of their beliefs. Allegedly this was done so that if they ever were widely scattered from one another, they would not be preaching different messages in their diaspora. In seems that Rufinius wrote of this gathering in his 404 AD exposition of the Apostles’ Creed.

So they met together in one spot and, being filled with the Holy Spirit, compiled this brief token . . . and they decreed that it should be handed out as standard teaching to believers.

As appealing as it may be to believe in such a gathering, it is highly unlikely that it occurred. An early and telling challenge to its historicity was the observation by Marcus Eugenicus in the fifteenth century that the book of Acts never mentioned it, particularly at the first apostolic council at Jerusalem.  Nevertheless, the reality of this event happening some ten days after the Ascension was widely accepted and taught as historical until the fifteenth century.

Although the event itself is fictional, a “rule of faith” believed and taught as early as the second century does seem to have a claim to apostolic origins. There was fluidity evident in the exact wording of orthodox affirmations evident in the various localized confessions of faith. But that variability was not present in the orthodox articles. The ongoing encounter with pagan influences as well as heretical beliefs within the church itself seems to have led to the gradual acceptance of a common creed. But this process was not fully resolved even by the time of the second ecumenical council at Constantinople in 381 AD.

The first early church document to show what appears to be a fixed creed is the Apostolic Tradition written around 200 AD by Hippolytus, a conservative, dissident church leader in Rome. His Tradition seems to have been compiled so “that those who have been rightly instructed may hold fast to the tradition which has continued until now.” The implication here is that an accepted, formal creed or confession of faith existed in the life of the Roman church of that time. It was most likely as a guide to the instruction of catechumens and ultimately for their public confession within the rite of baptism.

While worship, preaching, catechetical instruction, anti–heretical and anti–pagan apologetic efforts all contributed to the need for such expression, the rite of baptism seems to have been the primary circumstance to encourage the development of formal creedal statements. And the available evidence points to the Roman confession or creed as one of the earliest. The original text for the Roman Creed  or “R” as it is conventionally referred to by scholars, seems to have been a three article Trinitarian confession that went something like this:

I believe in God the Father almighty, and in Christ Jesus, his only Son, our Lord,and in the Holy Spirit, the holy Church, the forgiveness of sins, the resurrection of the flesh.

Historical studies have suggested that, in accordance to Jesus’ command in Matthew 28:19, it was formulated as an expression to be declared by converts in the midst of their baptismal rite. Noticeably absent in R is the Christological statement in the current form of the Apostles’ Creed on the birth, death, resurrection, and ascension of Jesus. This declaration was part of the gospel message from the time of Peter’s sermon at Pentecost (Acts 2:14–41). And it had reached a fair degree of consistency in the apostolic times of the church, as an expression of belief in the works of Jesus as Christ, Son, and Lord.

The consistency was in the articles of the statement, namely the birth, death, resurrection, and ascension of Jesus Christ, and not in the exact wording of the articles themselves. Peter’s counsel to those who heard his words and were under conviction in Acts 2:38, “Repent and be baptized every one of you in the name of Jesus Christ for the forgiveness of your sins, and you will receive the gift of the Holy Spirit,” suggests a natural association of such a confession with the rite of baptism.

The work of Christ from his birth to his ascension made the forgiveness of sins possible. Baptism in the name of Jesus Christ declared a catechumen’s belief in the reality of that redemption. A formal declaration of what he or she believed about Christ within the rite of baptism is a logical extension of the original formula. Within the writings of early church fathers such as Irenaeus, Clement of Alexandria, Tertullian and Hippolytus is a ‘rule of faith,’ which was the foundation of teaching provided to catechumens.

A related and important observation is that the inclusion of a Christological statement within a baptismal confession help to exclude those holding to heretical beliefs. Some examples of early heretical groups are the Ebionites, Gnostics, and Docetics (who regarded the sufferings and human aspects of Christ as only apparent, and not part of a real incarnation). All three of these heretical systems were active around 150 AD, and were apologetic and doctrinal concerns within the church, as evidenced by the existing writings of the pre–Nicene church fathers.

Given these observations, the redaction of R in the third decade of the second century to include an elaboration of the belief in “Christ Jesus,” along the traditional doctrinal lines of the rule of faith, seems to be a natural addition to the original three article confession. As J. N. D. Kelly observed after a careful analysis of each phrase of the Christological statement, “Thus in the whole of this section the Old Roman Creed faithfully reflects the feelings of the primitive Church.”

This description of the Roman Creed (and the forthcoming one on the Apostles’ Creed) was compiled from the New Dictionary of Theology (179-181), by Sinclair Ferguson and J. I. Packer; the Evangelical Dictionary of Theology (72–73), Walter A. Elwell, editor; The Emergence of the Catholic Tradition  (117), by Jaroslav Pelikan; Early Christian Creeds (1–6; 100–166), by  J. N. D. Kelly; and The Creeds of Christendom, Volume 1, The History of the Creeds (14–23; 368–434), by Phillip Schaff.

06/17/15

The Coming Depression Apocalypse

© 3quarks | 123RF.com

© 3quarks | 123RF.com

According to the Motley Fool, the pharmaceutical company Alkermes has a potential blockbuster drug for treating major depression in its pipeline. Currently in Phase 3 clinical trials, ALKS-5461 is one step away from Alkermes filing for approval by the FDA. Mental Health Daily reported that ALKS-5461 was given fast track approval by the FDA and is expected to be available in 2016. Its projected use is as a supplementary treatment to current antidepressant drugs. But once approved, the “supplementary” element will likely stop because it’s new and fast acting. The problem is, the drug in ALKS-5461 that is supposed to treat depression is an opioid with addictive potential.

Before going further on this issue, we need to take a short trip into pharmacology and neurotransmitter function in order to understand what’s going on. There are proteins embedded within the membrane of a cell called receptors. These receptors receive chemical signals from outside the cell, and in turn produce a biochemical reaction inside the cell. The chemicals that bind and activate a specific receptor are called agonists. While an agonist causes a reaction, an antagonist blocks that reaction from occurring within the cell. It turns the cell off from the influence of the agonist.

Receptors are activated by either endogenous agonists (hormones or neurotransmitters), or exogenous agonists (drugs). Endogenous agonists are produced by the body. The endogenous opioid agonists include dynorphins, and the more widely known endorphins. If you want more information on biochemistry and neurotransmitter activity, try these Wikipedia pages for starters: opioid receptor, mu-opioid receptor, and agonist.

Opioids are known to have energizing and mood enhancing effects with some users. This effect seems to be associated with dynorphin, which is elevated in depression. Dynorphin is a full agonist for the kappa opioid receptor (KOR). Studies like that done by Knoll and Carlezon, “Dynorphin, Stress and Depression,” suggest that KOR antagonists may have a potential therapeutic potential in treating anxiety and depression. While this biochemical hypothesis makes sense to psychiatrist Daniel Carlat, in The Carlat Psychiatry Report, he was more reserved on the treatment potential of ALKS-5461 than Mental Health Daily and the Motley Fool.

The efficacy of ALKS-5461 for depression remains to be seen. Some trials of ALKS-33 alone have already been performed, particularly in the areas of alcohol dependence and binge-eating disorder. These have been negative.

Now let’s look at my concern with ALKS-5461. First, it is a combination of buprenorphine, and samidorphan, or ALKS-33. Buprenorphine is used in addiction treatment as a detoxification drug and in opioid maintenance therapy, where its brand names are Suboxone (buprenorphine with naloxone) and Subutex (buprenorphine without naloxone). Suboxone and Subutex are classified as Schedule III controlled substances, meaning they have a moderate to low potential for physical and psychological withdrawal. Other Schedule III drugs include ketamine and anabolic steroids.

Buprenorphine is a partial mu opioid agonist, meaning it displaces morphine, methadone, and other full opioid agonists from activating the mu opioid receptor (MOR). But it does not provide the same degree of receptor activation as the full agonists (It doesn’t get you as high), resulting in a net decrease of agonist effect and the onset of withdrawal if it used soon after a full agonist like heroin. Patients planning to begin Suboxone maintenance therapy are told to abstain from opioids for twenty-four hours before their first dose of Suboxone.

At lower doses and with individuals who are not dependent on opioids, both full agonists like heroin and partial agonists like buprenorphine will produce identical euphoric effects. Partial agonists like buprenorphine also have a ceiling effect, meaning that past a certain point, typically 12 to 16 mg, no difference in analgesia, euphoria and respiratory depression will be felt.

Buprenorphine does produce physical dependence. Reportedly, this is to a lesser degree than full opioid agonists; and it is supposed to be easier to discontinue at the end of medication treatment. While this is the received wisdom on websites like NAABT, The National Alliance of Advocates for Buprenorphine Treatment, that has not been the case for what I’ve observed clinically with individuals who have tried buprenorphine. Generally I’ve heard that buprenorphine is harder to kick than heroin. So ALKS-5461 will be treating depression with a drug that may be harder to kick than heroin.

Buprenorphine is also a full antagonist of the kappa opioid receptor (KOR), which underlies its use in ALKS-5461 as an antidepressant. If the production of dynorphine by KOR receptors increases with depression, theoretically then buprenorphine would block these receptors and limit the release of dynorphine—elevating the individual’s mood. Peter Tenore, in “Psychotherapeutic Benefits of Opioid Agonist Therapy,” said that opioids like buprenorphine could be “effective, durable and rapid therapeutic agents for anxiety and depression.”  The problem is with the partial agonist effect that buprenorphine has on mu opioid receptors (MOR) you can still use buprenorphine to get high.

That was the rationale for combining naloxone with buprenorphine in Suboxone. Naloxone is an opioid antagonist that counters the effects of opioids at the mu receptor, but doesn’t trigger a euphoric effect. Marketed under the brand name of Narcan, naloxone is used to counter the effects of opioids in overdose situations. The death of Phillip Seymour Hoffman led to calls for greater availability of naloxone (see “The Opioid-Heroin Cycle”) for individuals to use in overdose situations.

While naloxone is still the standard medication for emergency reversal of opioid overdose, its clinical use in long-term opioid addiction treatment is being superseded by naltrexone. Naltrexone (C20H23NO4) is structurally similar to naloxone (C19H21NO4), and samidorphan (C21H26N2O4). But it has a slightly increased affinity for κ-opioid receptors (KOR) and has a longer duration of action than naloxone. Naltrexone is used as a preventative medication for opioid use disorder in Vivitrol, whose marketing rights are owned by Askemet.

Samidorphan (ALKS-33) is also a full opioid antagonist, acting on the MOR receptor with mixed agonist-antagonist activity at the KOR receptor. Combining samidorphan with buprenorphine is supposed to block the agonist effect of buprenorphine on the MOR receptor, while not inhibiting the buprenorphine antagonist effect on the KOR receptor.  A study by Shram et al. comparing samidorphan to naltrexone was published online ahead of the June 2015 issue of the Journal of Clinical Psychopharmacology. Samidorphin was found to have greater binding affinity than naltrexone to mu receptors and a longer half-life. This was suggestive of prolonged opioid receptor antagonism at lower doses of samidorphin. The study, though, was funded by Askemet.

Suboxone (buprenorphine and naloxone) and ALKS-5461 (buprenorphine and samidorphin) appear to be biochemical twins. And it does not seem to me that the addictive potential of buprenorphine has been entirely neutralized by its combination with samidorphin as claimed. The history of abuse and diversion with Suboxone supports this concern. If my fear is true, then in the name of treating depression, ALKS-5461 will create a huge population of individuals who become dependent upon buprenorphine.

Coming off of buprenorphine is not fun. Here is a personal testimony of someone tapering off of buprenorphine. Oh, and mood swings with bouts of anxiety or depression are common side effects with buprenorphine withdrawal.

Buprenorphine withdrawal symptoms last longer for those who use buprenorphine for longer periods of time or at higher doses. Additionally, those who use buprenorphine other than prescribed (snort, inject, chew) may experience more severe symptoms than someone taking buprenorphine as prescribed. In these cases, physical buprenorphine withdrawal symptoms can last weeks after stopping.However, psychological withdrawal symptoms can last for many months after cessation. It is recommended that you join a support group or see a psychologist who can help see you through the protracted or post acute withdrawal symptoms (PAWS). Many heavy buprenorphine users experience PAWS. With continued use of buprenorphine, there comes a point where the brain produces in an inadequate amount of neurotransmitters in the body. People going through buprenorphine PAWS manifest long lasting changes in the brain as a result of long term use.

The Substance Abuse and Mental Health Services Administration (SAMHSA) estimated that in 2013, 1.8 million people had an opioid use disorder; 517,000 of which had one related to heroin use. SAMHSA also estimated that each year, 9.1% of the adult population experience symptoms consistent with major depression. One 2012 study suggested that 10% to 30% of individuals with major depression suffer from treatment resistant depression. Using a U.S. population estimate of 320.94 million, with a median 20% for individuals with treatment resistant depression, that leaves a target population of over 5.84 million Americans with treatment resistant depression. God help us.

I don’t think it is too strong rhetorically to speak of a pending depression apocalypse. I hope I’m wrong. But widespread use of ALKS-5461 could instigate a huge population of individuals dependent upon buprenorphine. And the problems coming off of ALKS-5461 would eclipse what we now know happens with SSRI withdrawal. Within the biochemical worldview, these symptoms will be reinterpreted as evidence of the underlying depression and proof the individual needs to remain on ALKS-5461. Sound familiar?

06/15/15

Let’s Not Get Ahead of Ourselves

© iqoncept | stockfresh.com

© iqoncept | stockfresh.com

At the 249th annual meeting of the American Chemical Society, Andy LaFrate, the president and director of research of Charas Scientific presented the results his lab found on its analysis of marijuana. Average potencies are around 20% THC. He said that they have seen potency values approaching 30% THC. “As far as potency goes, it’s been surprising how strong a lot of the marijuana is.” But an unexpected consequence of that breeding for higher THC potency has been the lowering of CBD levels in many marijuana strains. CBD is the cannabinoid often touted for its therapeutic value. And unlike THC, CBD does not get people high.

There’s a lot of homogeneity whether you’re talking medical or retail level . . . One plant might have green leaves and another purple, and the absolute amount of cannabinoids might change, which relates to strength. But the ratio of THC to CBD to other cannabinoids isn’t changing a whole lot.

LaFrate said in a video, “Marijuana Testing Yields Fascinating Results,” that a lot of the time the CBD concentration is very low, sometimes too low for their equipment to detect.  The lack of CBD means that many of the hundreds of strains of marijuana actually are very similar, chemically. A lot of the medicinal benefits attributed to THC are actually from CBD, one of the 85 different cannabinoids that can be isolated from cannabis. Some of the most well known ones with known or presumed medicinal properties are reviewed in this crash course, Cannabinoid Profiles , by SC Laboratories and Weedmaps. The video makes the potential for medical marijuana sound exciting and almost limitless. But one thing seemed to be said over and over again—more research needs to be done.

LaFrate also looked for biological and chemical contaminants in the marijuana they tested and the results were surprising. “You’ll see a marijuana bud that looks beautiful. And then we run it through a biological assay, and we see that it’s covered in fungi.” He was startled to find just how dirty a lot of it was. Marijuana is a natural product, so there will be some microbial growth on it, said LaFrate. So the questions become: What’s a safe threshold? And which contaminants do we need to be concerned about?

Contaminant testing is not mandatory yet, but should be soon in Colorado. LaFrate noted that many samples had fungi or bacteria. Some marijuana products tested have butane, used to strip and concentrate THC from the plant. Other samples had heavy metals. He added that when you’re dealing with something like marijuana that’s been under prohibition for the last eighty years, scientific testing gives the consumer confidence that this is something that is safe. It seems that the state-by-state approval strategy of medical marijuana dating back to California has contributed to this issue with contaminants.

Not only can there be purity and contaminant concerns with cannabis, but the majority of the available varieties of cannabis are high in THC, the primary psychoactive ingredient, and low in CBD, the primary medicinal ingredient. Weedmaps provides a graphic of the eight known cannabinoids “that effect you most” with information on the claimed medicinal properties of the eight cannabinoids. A quick look shows that THC, “the most abundant and widely known” cannabinoid in marijuana has limited medicinal properties: it is an analgesic, it reduces vomiting and nausea, it suppresses muscle spasms and it is an appetite stimulant. The only medicinal property unique to THC in the chart is its appetite stimulant properties.

In contrast, cannabidiol (CBD) “may hold the most promise for many serious conditions.” And it’s the second most common in marijuana. In the CBD video found in Cannabinoid Profiles, Josh Wurzer, the Laboratory Director for SC Laboratories said when SC Laboratories began testing marijuana strains a few years ago, most plants were high in THC, typically 10% to 20%, with 1 to 1½ percent CBD. Now they are seeing strains with between 8 and 15 percent CBD and a concurrent 5 or 6 percent of THC. The higher CBD content occurs through the activation of a recessive gene in the cannabis plants. Wurzer said cannabis breeders have to find plants with the high CBD gene locked away and breed them. “The only way you can know if it is high in CBDa is to test it.”

There was an experiment at the Institute of Psychiatry at King College, London, that looked at the relationship of the effects of the two main ingredients in cannabis, THC and CBD. You can see a video of a reporter participating in the experiment here. Her mixture of THC and CBD left her with the giggles: “No matter how hard I tried to take the experiment seriously, it all seems hilarious.” But with pure THC, it was a different story. “It’s horrible. It’s like being at a funeral . . . Worse . . . It’s just so depressing. You want to top [kill] yourself.”

On THC and CBD mixture, she said she seemed flippant; on pure THC, she just didn’t care. With pure THC, she was suspicious, introverted; “weird.” Every question seemed to have a double meaning. She felt morbid. “It’s like a panic attack.” The researchers used the Positive and Negative Syndrome Scale (PNASS), a standard test to measure changes in psychotic symptoms. On the PNASS sub scale used, changes above four was clinically significant; what would be associated with schizophrenic psychosis. She scored fourteen. The effects were temporary.

The suggestion is that high levels of THC “can play havoc with your mind.” Individuals with no history of mental illness and no predisposition to schizophrenia don’t seem to be at long-term risk of THC triggering this reaction. But is seems that CBD has a counteractive effect on the paranoid and psychotic effects of THC. Here is a link to several studies on the positive effects of CBD on schizophrenia found on Project CBD.

There is also an SC Lab/Weedmaps video on the problem with overmedicating with cannabis. The pro medicinal marijuana panel noted that there is a tendency to overmedicate because of the largely nontoxic effects of cannabis. “It’s really safe to take a large dose. And you don’t get a lot of hangovers.” But you do get psychotoxicity (perceived harm).  Bonni Goldstein, MD, the CannaCenters Medical Director said she recommends a process of titrating up—starting with a low dose and waiting to see what the effects are before you add more.

A second panel member, Mike Corral, the co-founder and agricultural Director of W.A.M.M (WO/Men’s Alliance for Medical Marijuana), said that in talking to researchers, medically effective doses are measured in micrograms; a gram should medically last as much as a week. “Invariably, we see people smoking, three, four, five, six, seven grams a day. We come from a stoner culture.” He said that he had no problem with people getting stoned, but that wasn’t medical use. He also thought there should be full legalization to separate the recreational and medicinal users.

Another panel member, Michael Backes, the Founder/Director of Cornerstone Research Collective, said: “Just because something has a drug safety profile that’s favorable, like cannabis does, doesn’t mean there aren’t potentially some issues.”  He noted that one of things they learned from a cannabis pain study is that there was a “sweet spot” of dosage for cannabis, “and you don’t want to go past it.” The graphic within the video read: “Just as a patient who underdoses, one who overdoses will not have their symptoms relieved, therefore exceeding the ‘sweetspot’ is a waste of medicine.”

He said people have to respect their dose more. You could use cannabis in an overdosage for years, with little changes that you don’t notice, because they accumulate over time. Although cannabis is a very nontoxic substance, it is pharmacologically active, “and you’ve got to respect it.” He noted that 10% of individuals will develop a dependency issue, and then he wondered how you counsel people who you know are doing too much. “And how do you convince them “Hey, it’s time to back off?’”

Marijuana legalization continues to move forward on a state-by-state basis, which creates problems in a number of ways. As the above information pointed out, there is not a good system of quality control and contaminant testing available yet, even in Colorado. The majority of marijuana strains available, including those for medical marijuana, appear to be high in THC (the primary psychoactive cannabinoid) and lower in CBD (the primary medicinal cannabinoid). Current dosing practices, according to a panel of pro-medical cannabis individuals, are too high for medicinal purposes and could over time, lead to health problems like “dependency issues.” A cannabis strain high in THC and low in CBD could trigger symptoms associated with schizophrenia.

Before marijuana is legalized in more states, it seems advisable to make some federal changes. First, marijuana should be reclassified as a Schedule II controlled substance. This would make the desperately needed research on the medicinal properties of cannabis easier to do. Second would be to appropriate more funds into medical marijuana research. Third would be to fund the development of marijuana strains that are much higher in CBD and lower in THC. Fourth would be using the established process of clinical trials with the FDA for confirming treatment possibilities for cannabinoids.

Legalization polls  (see this Pew Research Center poll) that distinguish recreational marijuana use from medicinal marijuana use show that more Americans in favor of legalization fall into the medicinal camp. These suggestions would be consistent with the poll’s findings. Legalizing medical marijuana without these steps puts us back to the days of patent medicine. Medical marijuana should be treated like all other substances proposed as medicinal treatments for humans. Let’s not make the mistake of treating marijuana as a special case that doesn’t need to go through the same approval process for all other proposed medical treatments.

06/12/15

Knowing When You Enter Temptation

© Jaroslav Chaplya | 123RF.com

© Jaroslav Chaplya | 123RF.com

When I moved into my current house, there were several yucca plants on the property. For a few weeks they have beautiful flowers, but then they fall off leaving bare, ugly stalks. The remaining plant is a series of spiny, tough, sword-shaped leaves. They have this incredibly hardy tubular root system. And if you don’t dig up and kill off all the pieces of yucca root, the plants will grow back again and again. If you can’t tell yet, I don’t like yucca plants. So I dug up all the plants and their roots and then spent two years making sure the plants didn’t grow back from the small pieces of yucca root I’d missed when digging up the plants. Sin and temptation are like that—like a yucca plant and its roots.

In chapter four of his work, Of Temptation, John Owen describes how someone can recognize when they have entered into temptation. In previous posts we looked at the general nature of temptation (Lead Us Through Temptation), how we fall into temptation (Entering Into Temptation), and how to avoid temptation (Avoiding Temptation).

The first thing Owen wants us to realize is that all sin springs from temptation. As it says in James 1:14: “Each person is tempted when he is lured and enticed by his own desire.” So whenever someone falls into sin, they enter through a temptation. “Sin is a fruit that comes only from that root.” Sometimes, when people disregard this basic fact, they are their own worst enemy.

They repent and address their sin, but not the temptation that triggered the sin. “Hence are they quickly again entangled by it, though they have the greatest detestation of the sin itself that can be expressed.” So if you want victory over any sin, you must uncover the temptations at the root of that sin and get rid of the roots. If you don’t, you will not overcome the sin.

Foolishly, many people hate the bitter fruit, but still cherish the poisonous root. So despite their humiliations from sin, they continue with the companionship, habits and behaviors that come before it. This inevitably results in further sin.

Temptations also have several degrees. Some are so intense and disquieting, that there is little doubt the individual wrestles with a strangely powerful temptation. “When a fever rages, a man knows he is sick.” Lust will infallibly carry a person into eternal ruin, like a stream that empties into the sea. But if a wind of strong temptation blows, they can be driven onto the rocks of innumerable scandalous sins. So when any lust or corruption disquiets your soul and then leads to sin, recognize that some outward temptation has befallen you. Look closer to find out what has triggered the sin in you.

Temptation can also be more discrete. The heart can secretly grow fond of a temptation and be eventually become content to feed and increase it in ways that aren’t necessarily sinful. For example, a person could have a reputation for piety, wisdom, or learning—and be widely seen by others as such. His heart might be tickled to hear this from others, and his pride and ambition affected by it.

If this man now, with all his strength, ply the things from whence his repute, and esteem, and glory amongst men do spring, with a secret eye to have it increased, he is entering into temptation; which, if he take not heed, will quickly render him a slave of lust.

It is true that God will often bring light out of such darkness and turn things to a better outcome. So it may be that a person studies for years—with an eye on his lusts of pride ambition and vain-glory. But then God comes in with his grace and turns the soul to himself, robbing those “Egyptian lusts.” And thus he consecrates for his purposes what was intended for personal idolatry.

This can even be true of the profession of personal piety or of the ministry. Someone might have a reputation for piety and be honored by others for his or her “strict walking.” If the desire for this honor becomes embedded in their heart and influences them into more than ordinary diligence and activity within their faith walk, they have become entangled in temptation. Often it requires nothing more than the whisper in their heart that the avoidance of honor and reputation is itself honorable.

It can attach in this way to preaching the gospel. There are many things that could lead to esteem—their ability, their plainness, their frequency, their success. All of this could be fuel for temptation. “Let, then, a man know that when he likes that which feeds his lust, and keeps it up by ways either good in themselves or not downright sinful, he is entered into temptation.”

When the circumstances of a person’s life brings lust and temptation together with the opportunity of provoking sin, they have certainly entered into temptation—whether they realize it or not. Remember that to enter into temptation is not merely to be tempted, but is to be so under the power of it as to become entangled by it. It is almost impossible for someone to the have both the opportunity and occasion suited for their lust and not become entangled in it. “Some men think to play on the hole of the asp and not be stung, to touch pitch and not be defiled, to take fire in their clothes and not be burnt; but they will be mistaken.”

Sometimes a person becomes negligent or formal in their spiritual duties. As it was with the church at Sardis: “You have the reputation of being alive, but you are dead” (Revelation 3:1). So we can even say there is a rule—if your heart grows cold, if you become negligent or formal in your worship of God, some temptation has got a hold of you.

Men may, upon many sinister accounts, especially for the satisfaction of their consciences, keep up and frequent duties of religion, as to the substance and matter of them, when they have no heart to them, no life in them, as to the spirituality required in their performance.

A digital copy of Owen’s work, Of Temptation, is available here.

06/10/15

Seniors and Antipsychotics

© Laurin Rinder | 123RF.com

© Laurin Rinder | 123RF.com

Healthcare Finance News reported that a long-time Chicago psychiatrist faces over 18 months in prison after he pled guilty to receiving $600,000 in kickbacks from pharmaceutical companies. Dr. Michael Reinstein also agreed to pay $3.79 million in a parallel civil lawsuit settlement for prescribing clozapine in exchange for kickbacks. His medical license has also been suspended.

In 2009, ProPublica and the Chicago Tribune reported that in one year, Reinstein prescribed more clozapine to patients in Medicaid’s Illinois program than all doctors in the Medicaid programs of Texas, Florida and North Carolina combined.

The Chicago Tribune reported that autopsy and court records show that at least three patients under Reinstein’s care died of clozapine intoxication. Medical records for a fifty-year-old man showed that he had more than five times the toxic level of clozapine in his blood when he died. A 27 year-old woman died after her dose of cloazpine was increased twice as fast as recommended. Reinstein served as the psychiatric medical director for 13 different nursing homes.

Up until 2003, the manufacturer of Clozaril (Novartis) paid Reinstein thousands of dollars for speaking engagements to promote the drug, according to Healthcare Finance News. IVAX Pharmaceuticals then began paying him $50,000 per year as a consultant, so he switched his patients to generic clozapine. That arrangement continued when Teva Pharmaceuticals acquired IVAX in 2006. In 2009, as the Tribune began to examine his prescribing habits, Reinstein asked Teva to terminate the consulting agreements. Incidentally, in March of 2014 Teva agreed to pay $27.6 million to settle federal and state claims that the company paid Reinstein to prescribe clozapine.

The actions of Dr. Reinstein were extreme, but not really those of a lone rogue psychiatrist. On March 1, 2015, Robert Pear with The New York Times wrote that federal investigators with the Government Accountability Office (GAO) would announce the next day that they had found evidence of widespread overuse of psychiatric drugs by older adults with Alzheimer’s. Not only was this a concern in nursing homes, but investigators also said officials needed to focus on the overuse of these drugs by individuals with dementia who live at home or in assisted living facilities.

The GAO found that approximately one-third of older adults with dementia who spent more than 100 days in a nursing home in 2012 were prescribed an antipsychotic (neuroleptic). Among older adults with dementia living outside of a nursing home, about 14 percent were prescribed an antipsychotic. While the Department of Health and Human Services (HHS) has taken several steps to address antipsychotic use in nursing homes, nothing has been directed to settings outside of nursing homes. Therefore, the GAO recommended that HHS expand its outreach and educational efforts to include those living outside of nursing homes.

Neuroleptic (antipsychotic) drugs are classified into two sub-groups. The older, “typical” ones were developed in the 1950s. Examples include haloperidol (Haldol) and chlorpromazine (Throazine). The second generation, “atypical” antipsychotics were developed in the 1980s and initially thought to cause fewer side effects than the older, typical antipsychotics. Examples of atypical antipsychotics include aripiprazole (Abilify) and risperidone (Risperdal). Abilify was the number 13 best selling drug for 2014, according to Genetic Engineering & Biotechnology News. Clozapine (Clozaril) is an atypical.

In 2005, the FDA required that atypical antipsychotics carry a boxed warning that they had a higher risk of death related to use among individuals with dementia. In 2008, the FDA required the same warning with typical antipsychotics.

A literature review in Health Policy looked at the extensive off-label use of antipsychotics in nursing homes for residents with dementia and behavioral problems. They were found to have mixed efficacy “with an increased risk of many adverse events, including mortality, hip fractures, thrombotic events, cardiovascular events and hospitalizations.” Non-pharmacological options were recommended as first-line treatment options. The authors also noted when studies were subsidized by the pharmaceutical industry, the studies showed more favorable outcomes with antipsychotics.

Researchers from the University of Michigan Medical School and John Hopkins University reviewed two decades worth of research and concluded: “The evidence for non-pharmaceutical approaches to the behavioral problems often seen in dementia is better than the evidence for antipsychotics.” They noted there still was a place for using antipsychotics when patients have psychosis or aggression that could lead to harming themselves or others. “But these uses should be closely monitored and ended as soon as possible.”

Another study from the University of Michigan (abstract here) examined the records of 91,000 elderly veterans with dementia and found that mortality risks increased in patients taking antipsychotics to reduce symptoms of dementia, when compared to patients not being treated. A MinnPost report of the study said the mortality risks were two to four times higher than previously cited in the medical literature. “The new analysis also revealed that the higher the dose of an antipsychotic medication, the greater the risk of premature death.” Dr. Helen Kales, one of the study’s researchers, said:

Our research indicates that antipsychotics may increase mortality more than previously realized. . . . We hope this creates a dialogue about the advantages and disadvantages of antipsychotic and other psychotropic use as first-line treatment strategies for behavioral symptoms, which are universal and require effective treatments to address serious suffering among patients, families, and caregivers.

I hope it creates a dialogue as well. Thankfully we do not have the older state hospital system where the elderly with dementia and Alzheimer’s were often warehoused. But shackling them mentally with neuroleptics so they can be managed with minimal behavior problems seems to be just about the same thing.

06/8/15

Hype Over Powdered Alcohol

© damedeeso | 123RF.com

© damedeeso | 123RF.com

The Alcohol and Tobacco Tax and Trade Bureau (TTB) approved the sale of a brand of powdered alcohol named “Palcohol” on April 8, 2014 and then rescinded permission on April 21st. An article in Time said the approval for Palcohol was halted because of an error in its labels. The parent company for Palcohol, Lipsmark, said: “there seemed to be a discrepancy on our fill level, how much powder is in the bag.” So when Senator Chuck Schumer called upon the FDA to ban Palcohol, this kid named River Donaghey got the idea to try and make his own powdered alcohol and then document the aftermath for Vice in “Powdered Alcohol Got Me Drunk in the Worst Way.”

Donaghey took a recipe for powdered alcohol off the internet to mix his own, because “I didn’t want to make wimpy powdered booze like Palcohol, which you need half a pouch of to make a single drink. I wanted something strong.” Instead of mixing in 30 grams of alcohol, “which is hardly anything,” he poured in an entire fifth of 192-proof grain alcohol. He knew it was the right mixture when his eyes started to water from the fumes.

He began by ingesting “handfuls of the stuff,” then he got the idea to sprinkle it on pizza. After running into his roommate, Charlie, he gave him a pinch of the powder and they both set off for pizza. Donaghey said the powder drunk crept up on him and he went from mostly sober to buzzed to beyond. He said he thought the powdered booze blended well on pizza. He also kept getting weird looks from people with his Tupperware bowl full of powdered alcohol. They thought he was acting out a scene from the movie Scarface with a bowl full of cocaine.

After leaving the pizza shop, River and Charlie went down to the East River where they decided to set some on fire. “It turns out my homemade powdered alcohol burns like napalm. When he tried to stamp out the fire he ended up spreading it all along the rocky bank of the river. Charlie’s shoe cut on fire. He offered some to a group of high school students, who wisely refused. But there was one more thing he had to try: snorting it. So he went back to the VICE office and “started racking lines.”

The powder turned to glue in his nose and he was immediately plugged up. The fumes burned for a few minutes and then his sinuses became numb. Charlie and he staggered home and went to their respective rooms, hoping that unconsciousness would dull the throbbing inside their heads. Charlie didn’t snort any.

I woke up at 4 AM, with my face caked with blood from my nose. At least I could breathe again. The headache had dulled to a manageable form. I went out into the living room and found Charlie sitting on the couch, sucking on a beer. He handed me one. I slumped down next to him and took a drink.

Given the above, it’s not surprising that as soon as the TBB finally approved the sale of Palcohol on March 10th, 2015, Senator Charles Schumer introduced legislation to ban the sale and distribution of Palcohol and other powdered alcohol products.

We simply can’t sit back and wait for powdered alcohol to hit store shelves across the country, potentially causing more alcohol-related hospitalizations and God forbid, deaths. This legislation will make illegal the production and sale of this Kool-Aid for underage drinking.

Reported in the Time article and on the blog, SB Nation, the original Palcohol website suggested football fans could “Bring Palcohol in and enjoy the game.” And, yes, like River Donaghey tried, they said you could snort Palcohol. “You’ll get drunk almost instantly because the alcohol will be absorbed so quickly in your nose. Good idea? No. It will mess you up. Use Palcohol responsibly.” The current Palcohol website has removed such remarks and hopes to be able to get their production facility up and running to make their product available this summer.

They argued that banning their product would only make people want it more. The ban will create a black market and lose significant tax revenue. They also said it was irresponsible to ban Palcohol, because it probably won’t work. “No one wants the government telling us what we can drink and not drink. We don’t need a nanny. The legislature exists to protect our rights to live how we choose, not to use coercive power to force their values on us.”

Lipsmark sees Palcohol as “a revolutionary new product that can help so many industries.” Airlines can reduce weight and save on fuel costs. Medical personnel want to use it as an antiseptic, especially in remote locations. It would be a “boon to outdoor enthusiasts” wanting to enjoy an adult beverage without having to carry heavy bottles of liquid. They said there has even been interest in using powdered alcohol as a fuel source. “There is talk of multiple military applications from transport fuel to fuel in a soldier’s backpack.”

McCarton Ackerman on The Fix said that the National Conference of State Legislatures reported that 47 bills in 28 states have been introduced to address powdered alcohol. Virginia, Alaska, Louisiana, South Carolina, Massachusetts and Vermont have already banned the distribution of Palcohol, “while others are also considering similar measures.”  Reported by MyFOXdc.com, Maryland announced a ban on the distribution and sale of powdered alcohol on March 25th, 2015. “The likelihood of widespread Palcohol abuse – particularly among underage consumers – carries a real possibility of tragic consequences.”

Of course, Colorado has reversed its initial move to ban it and could be the first to approve its use. It is up to the Colorado Liquor Enforcement Division to write the rules for powdered alcohol sales and distribution. It could be on store shelves in a few months. The video embedded in thedenverchannel.com article illustrates the small size and ease with which the packets could be hidden. “The biggest benefit of powdered alcohol, or Palcohol, is also its biggest danger. It’s convenient, it’s easy and it can be sneaky.”

There have been some limited reports of powdered alcohol being a fake or a hoax. However, it does seem to be a real product. The question seems to be whether or not it is being hyped into becoming a fad. For example, hoaxes.org posted in 2005 that it was possible in theory to create powdered alcohol. However, it also noted that the end product from a formula used would only be 4.8% ethanol by volume, and concluded by saying: “But even if this stuff is real, I can’t imagine powdered rum tastes anything like the real thing.”

In his blog, Tim Vandergrift reported that alcohol (ethanol) is a volatile liquid, meaning that it evaporates very quickly, far faster than water. At room temperature, pure alcohol will evaporate away. It can’t be directly turned into powder, so that is why you have to mix and stabilize it with another substance (like sugar or maltodextrin, as Rive Donaghey did), and then seal it in a vapor-proof package. He then calculated the reported bulk of maltodextrin-alcohol mixture and estimated that you would need 26 packets to make an entire vodka bottle’s worth of cocktails.

Assuming you do make this damp maltodextrin substrate-with-alcohol mix, where does that leave you? With a product that’s only 12% ABV, probably costs more, and bulks much larger than simple beverage alcohol, is tough to dissolve in cold liquid and doesn’t taste like anything without the addition of lots of extra additives. Additionally you’d be consuming some form of unidentified powder in vastly higher quantities than the alcohol you’re seeking. Peachy (Italics).

It’s hard to not see this as a product that is aimed directly at under aged drinkers. Dr. Scott Krakower said the flavored powders would appeal to young people. “Youths are going to be very vulnerable to this.” And even though the company advised against it, “people will snort it”—as we saw with River Donaghey, just to see what it’s like.