Pick Your Poison: Diabetes and Psych Meds

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The American Diabetes Association said 30.3 million Americans, 9.4% of the population, had diabetes in 2015. There are 1.5 million news cases of diabetes diagnosed each year. It is the 7th leading cause of death in the U.S. with 79,535 death certificates in 2015 listing it as the underlying cause of death. A total of 252,806 death certificates listed diabetes as an underlying or contributing cause of death. If the number of deaths from diabetes were equal to 252,806, it would be the third leading cause of death in the US, according to the CDC … and psych meds increase the risk for diabetes.

SSRIs have been associated with an increased risk of diabetes, as Yoon et al. noted in “Antidepressant Use and Diabetes Mellitus.” The researchers ruled out depression itself as a potential confounding variable in the relationship between antidepressants and diabetes. Their findings suggested that antidepressant drug treatment and not the depression increased the risk of diabetes mellitus (DM). “Given the widespread use of antidepressants, the implications of the increased risk are serious.”

The authors noted that while there is disagreement as to the reason for the association between antidepressant use and DM risk, some studies “propose that antidepressants may bio-pharmacologically affect glucose homeostasis and insulin sensitivity.” In “Use of Antidepressants Linked to Diabetes,” Peter Simons of Mad in America noted a study that has supported that hypothesis. A study led by Raymond Noordam and published in The Journal of Clinical Psychiatry, found the use of SSRIs in nondiabetic participants was associated with lower insulin secretion and an increased risk of insulin dependence in type 2 diabetes in older adults.

It is biologically plausible that SSRIs decrease insulin secretion and that this might, therefore, be a mechanism underlying the previously observed association between SSRIs and increased risk of type 2 diabetes. Consequently, type 2 diabetes patients treated with SSRIs might also have a higher risk to develop insulin dependence, a condition associated with an increased risk of mortality.

The researchers also found that participants already diagnosed with diabetes who were taking antidepressants were twice as likely to start insulin treatment than those who did not take antidepressants. They said: “our data might suggest that progression of type 2 diabetes during the use of SSRIs is accelerated.” Simons commented how the higher mortality rate for individuals who require insulin treatments made this “a particularly alarming finding.”

This new study provides additional convincing evidence that although SSRIs are commonly believed to have fewer risks of adverse effects than TCAs, they still carry significant risk. This appears to be particularly relevant when it comes to patients with diabetes. Whenever antidepressant medication is considered, patients and prescribers should carefully weigh the potential risks and benefits.

There was an updated meta-analysis published in PLos One, “The Risk of New-Onset Diabetes in Antidepressant Users.” Their meta-analysis found an increased risk factor of 1.27 between exposure to antidepressants and new-onset diabetes. When they restricted the analyses to higher quality studies, the relative risk was higher. The researchers noted their findings were in line with tow previous meta-analyses that reported “a 1.5-fold increase of diabetes among AD [antidepressant] users.” In an interview with Endocrinology Advisor, the lead investigator of the study extrapolated that given a 13% prevalence rate of antidepressant use in the US, a 1.3-fold increase in diabetes risk would translate to over 1 million cases of diabetes that could be due to concurrent antidepressant use.

Pharmacy Times reported in “Atypical Antipsychotic-Induced Type 2 Diabetes” that patients with schizophrenia were at an increased risk of developing metabolic disorders like type-2 diabetes mellitus (T2DM). Schizophrenic patients had a number of risk factors for T2DM, including family history, increased body mass index (weight gain), a sedentary lifestyle and the use of atypical antipsychotics. There have been several proposed mechanisms for the association of diabetes and atypical antipsychotics, one being the weight gain associated with the medications.

A 2006 study by Alvarez-Jiménez et al. found that 78.8% of patients taking atypical antipsychotics experienced a weight gains greater than 7%, the cut off for clinically meaningful weight gain in the study. In 2004 the FDA required a warning be placed in the medication guides of all atypical antipsychotics warning of the increased risk of hyperglycemia and diabetes.

 Patients with schizophrenia are at increased risk of developing metabolic disorders like type 2 diabetes. This is due to a number of factors, including the treatment of schizophrenia with atypical antipsychotics. There are several potential mechanisms behind antipsychotic-induced diabetes, including the weight gain associated with these medications, the effects on pancreatic receptors and/or glucose transporters, or some other cause not yet discovered. Most likely, it is a combination of these effects. Of the atypical antipsychotics, clozapine [Clozaril] and olanzapine [Zyprexa] are associated with the highest incidence of metabolic dysfunction, whereas ziprasidone [Geodon] and aripiprazole [Abilify] are considered to be the least risky.

In “Antipsychotic-Induced Diabetes Mellitus” published in U.S. Pharmacist, Chhim et al. reported there are several metabolic consequences with antipsychotic use, including weight gain, hyperglycemia (abnormally high blood glucose) and dyslipidemia (an abnormal amount of triglycerides, cholesterol and/or fat phospholipids in the blood). The association of type 2 diabetes mellitus (T2DM) and antipsychotic use is supported by retrospective epidemiologic studies as well as post-marketing assessment. Data indicate the prevalence of diabetes and obesity is 1.5 to 2 times higher in people diagnosed with schizophrenia or affective disorders than the general population.

The authors noted that diabetes was reaching epidemic proportions worldwide, and the contributions of medications to the development of hyperglycemia and other metabolic problems was getting more attention.  “Pharmacists are in a unique position to counsel and encourage appropriate self-monitoring in patients receiving certain drugs, such as antipsychotics, that can contribute to the development of weight gain, hyperglycemia, and dyslipidemia.” They can encourage patients to report adverse events to other health care providers and seek therapeutic substitutions, counseling, and/or treatment for the adverse events.

Another resource addressing these concerns, one that was cited in “Antipsychotic-Induced Diabetes Mellitus,” is the “Consensus Development Conference on Antipsychotic Drugs and Obesity and Diabetes.” This is a joint consensus statement from the American Diabetes Association, the American Psychiatric Association, the American Association of Clinical Endocrinologists, and the North American Association for the Study of Obesity to help reduce the risk of developing diabetes, cardiovascular disease, and other complications of diabetes.

There was a large longitudinal study done in Denmark by Rajkumar et al. that found in addition to the high risk for diabetes conferred by schizophrenia on individuals, “the risk is further increased by both first-generation and second-generation antipsychotics.” Reporting on the study for Mad in America, Bernalyn Ruiz said the authors said the prevalence of diabetes was 4 to 5 times greater in people diagnosed with schizophrenia. “After adjusting for potential confounders, the risk was elevated threefold compared to those without a schizophrenia diagnosis.” No differences were seen between first-generation and atypical antipsychotics.

This large nationwide study confirmed endogenous risk for diabetes among individuals diagnosed with schizophrenia, with risks increasing significantly when antipsychotics are prescribed.

The bottom line is that in addition to their other adverse effects, there is credible scientific evidence that antidepressants and antipsychotics increase the risk of diabetes among individuals taking them. So when you’re advised to use one of these classes of psychiatric medications, it’s a bit like being asked to pick your poison.


“Cash Cows” for the Drug Industry

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The AARP, the American Association for Retired Persons, completed a report looking at the trends in the retail prices of prescription drugs used by older Americans between 2006 and 2015.  And the report’s findings were disturbing. Between 2014 and 2015, the retail prices of 268 widely used brand name prescription drugs increased by 15.5%, the fourth year in a row of double-digit increases. The increase was almost 130 times faster than that of inflation—15.5% to .1% for inflation. The average annual retail cost for one brand name drug was over $5,800 in 2015, almost $1,000 more than the annual cost in 2014. “For the average older American taking 4.5 prescription drugs per month, the annual cost of [drug] therapy would have been more than $26,000 for 2015—more than three times the cost seen 10 years earlier.

This was an industry-wide trend, as the prices of the identified drugs, from all 35 drug manufacturers with at least two brand name drugs assessed within the study, increased faster than the rate of general inflation in 2015. “All but one of the therapeutic categories of brand name drugs had average annual price increases over 5% in 2015. . . . The higher costs are typically passed on to the consumer in the form of higher cost sharing, deductibles, and premiums.”  These increases were far beyond the price increases for other consumer goods and services between 2006 and 2015. The following graph compares the annual price of brand name prescription drugs to rate of general inflation for the corresponding year.

The next figure illustrates how the average annual cost for widely used brand name drugs by older adults grew more than 300% from 2006 to 2015. The Medicare Part D program was first implemented in 2006. Older Americans fill an average of 4.5 prescriptions for medications per month. If they used brand name prescription drugs, their average annual retail cost for medications would be $26,132. “This annual retail cost of brand name prescription drugs exceeds the median annual income for a Medicare beneficiary ($24,150).”

It is no coincidence that these price increases for medications commonly used by older adults occurred after The Medicare Prescription Drug, Improvement, and Modernization Act” was approved in 2003. “It expressly prohibited Medicare from negotiating bulk prescription drug prices.” But the Veterans Health Administration and the Defense Department were allowed to negotiate lower prescription drug prices. Prohibiting Medicare from negotiating bulk drug discounts seems directly related to increases in medications noted above.

The AARP Public Policy Institute found there were six specific brand name drugs with the highest percentage changes in retail price from 2006 to 2015. FIVE of them were from the same pharmaceutical company—Valeant. One mg and two mg tablets of Ativan (for anxiety) increased 2,873% and 2,080% respectively in their retail price. Cara .5% cream (certain skin disorders) increased 2,395%. Wellbutrin (for depression) increased 1,185%. Zovirax 5% cream (certain skin disorders) increased 783%. Eli Lilly’s Humulin R (U-500) 500 units/ml, an insulin drug used to treat diabetes, ONLY increased 530%.

If recent trends in brand name drug prices and related price increases continue unabated, the cost of drugs will prompt increasing numbers of older Americans to stop taking necessary medications due to affordability concerns. Continued excessive brand name drug price increases will also lead to increased cost sharing and premiums, which could ultimately make health care coverage unaffordable and lead to poorer health outcomes and to higher health care costs in the future.Given that health care reform expanded the number of people using prescription drugs, it would have been reasonable to expect smaller brand name drug price increases. Instead, brand name drug prices have accelerated substantially. Clearly, the economics of the pharmaceutical market are not working as expected.

Andy Slavitt, when he was the acting administrator for the Centers for Medicare & Medicaid Services, told the pharmaceutical industry in November of 2016 at a conference that increased medication costs were pervasive. Total prescription drug spending in 2015 was $457 billion, 16.7% of health care spending. Mylan’s Epipen was not even in their top twenty list for high price increases for 2015. Specialty drugs (like hepatitis C drugs) were a big part of the cost increase. They accounted for 31.8% of spending, while representing only 1% of prescriptions. Out of the 20 drugs with the highest per-unity cost increases in Medicaid, seven were generic drugs. Those increases were not to recoup drug development expenditures. See “Pharma’s not Getting the Message” for more on this topic.

The NYT reported there has been a sharp rise in polypharmacy, the use of three or more psychotropic drugs, with older adults. Almost half of these patients DID NOT have a diagnosis for mental health or pain disorder on record. Dr. Maust, a geriatric psychiatrist and lead author of the study, told Psychiatric News: “This begs the question of why physicians are exposing patients to all the risks of these medications, but not for the diagnoses they are intended to treat.” He thought the pattern suggested some inappropriate prescribing. Dr. Dilip Jeste, a geriatric neuropsychiatrist and past president of the American Psychiatric Association, said he was stunned to hear “that despite all the talk about how polypharmacy is bad for older people, this rate has doubled.” Over 90 percent of the office visits examined in the study occurred outside the psychiatric setting.

The AARP Public Policy Institute reported that 65% of adults over the age of 65 reported using 3 or more prescription drugs in the past 30 days. Ninety percent reported using one prescription drug in the past 30 days, while 39% said they used five or more. See the following figure from “Prescription Drug Abuse Among Older Adults.”

Disturbingly, this study looked at polypharmacy with medications noted within the Beers Criteria, named after its originator with the American Geriatrics Society twenty years ago. The Beer Criteria lists dozens of medications and their mutual interactions that are potentially harmful when prescribed to older adults. “Geriatric medical organizations have long warned against overprescribing to older people, who are more susceptible to common side effects of psychotropic drugs, such as dizziness and confusion.” The Psychiatric News article linked above has a chart of the Beer’s list of CNS medications, their potential risks and alternative clinical recommendations. The classes of medications examined in the study include: antipsychotics, benzodiazepines, sedative hypnotics for sleep (like Ambien), antidepressants (tricyclics and SSRIs) and opioids. An article in the Journal of the American Geriatrics Society on the 2015 updated Beers Criteria is available here.

Data reported by the AARP Public Policy Institute in “Prescription Drug Abuse Among Older Adults” also noted that older adults has several unique risk factors making them particularly susceptible to misuse of prescription drugs. Misuse is defined here as “the use of prescription drugs in a way a doctor did not direct.” First, older adults use more prescription drugs than any other age group. They also have higher rates of pain, anxiety, and sleep disorders. There could be memory problems that interfere with taking medications at the right time and in the right doses. The high rates of polypharmacy can also lead to potentially dangerous drug interactions.

Age-related physiological changes can also increase the potential for prescription drug abuse. Changes in metabolism, weight, and body fat can affect how a medication works in the body, increasing the potential for misuse and abuse and potentially dangerous side effects. The combination of alcohol and medications can bring about particularly adverse reactions among older adults, as their bodies detoxify and eliminate medications and alcohol more slowly.

Recommendations to prevent drug misuse with older adults include: regular reevaluation of drug dosages to help compensate for physiological changes and declining drug metabolism. Monitor for any inappropriate prescribing of prescription medications. Use of the Beer Criteria discussed above would be helpful. here Because patients often see multiple healthcare providers and obtain multiple prescriptions, keep an eye on a patient’s entire regimen of prescription and nonprescription drug use.

It seems hard to deny that pharmaceutical companies corralled older adults over the past twenty years and branded them as “cash cows” for the drug industry.


Pharma’s Not Getting the Message

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In response to rapidly increasing prescription drug prices and congressional inability or unwillingness to intervene, individual states are attempting to address the issue. While Californians approved a ballot initiative for recreational marijuana in November of 2016, state voters also turned down one aimed at curbing the high cost of prescription drugs. The California Drug Price Relief Act, or Proposition 61, sought to limit the state’s health programs from paying more than the U.S. Department of Veterans Affairs (VA), which receives the steepest discounts in the country, according to Reuters. Pharma companies lobbying against Proposition 61 spent $100 million to defeat it.

Proposition 61’s opponents, led by global drugmakers such as Pfizer Inc and Amgen Inc, spent around $106 million. They argued that it would benefit only 12 percent of Californians, while putting the other 88 percent, and veterans across the country, at risk of higher drug costs.

The defeat of the measure: “reaffirms the power of the biomedical lobby,” according to Brian Abrahams, a Senior Biotechnology Analyst at CIBC World Markets. Stuart Schweitzer, a professor of health policy and management at the University of California, said the measure would have only had a modest impact on state drug costs. Nevertheless, “They wanted to draw a line in the sand.”  A similar proposition will be on Ohio’s 2017 November ballot.

U.S. New and World Report said New York State approved rules in April of 2017 that will put pressure on pharmaceutical companies if they want to continue doing business in the state. If Pharma companies don’t agree to voluntarily rebate or return money to the state if prescription medication spending is projected to exceed the sum of medical inflation plus 5 percent, New York State could initiate a series of reviews using scientific studies and other information to evaluate whether specific medications are overpriced. “Drug makers generally object to such reviews and often dispute their results.” The NY State Medicaid Director said the law created an incentive for pharmaceutical companies to collaborate and give the state rebates.

New York is not the only state taking action. Vermont lawmakers passed legislation requiring justification for price increases that are driving up spending in state programs like Medicaid. In March of 2017 Maryland lawmakers passed legislation, still not signed by the governor, directing Medicaid to notify the state attorney general when off-patent or generic drugs have “an excessive price increase.” The new law also sets financial penalties if the pharmaceutical company can’t justify the price hike. Louisiana officials are looking into whether a rarely used federal law could be used to “sidestep patents and allow government programs to get lower-cost generic versions of pricey hepatitis C treatments.”

In August of 2017, JAMA gave greater details about the New York legislation in: “Value-Based Pricing and State Reform of Prescription Drug Costs.” Hwang et al. said if the rate of drug spending growth exceeded the 10-year average inflation plus 5% in 2017-2018 or 4% in 2018-2019, the state department of health would be authorized to identify and refer high-cost drugs to a drug utilization review board to determine a target rebate amount. The provisions are likely to trigger a review this year. The board may consider the effectiveness of the drug, its therapeutic alternatives, and the seriousness and prevalence of the disease in formulating its recommendation for a value-based price.

If the state and manufacturer fail to agree on a rebate that is at least 75% of the difference between the drug’s current price and value-based price, the state may waive provisions that currently require managed care plans to cover medically necessary drugs in certain protected classes, including antidepressants, antiretrovirals, and hermatologic drugs. Furthermore, if total drug expenditures continue to increase faster than inflation despite these new rebates, the state may implement more aggressive actions to promote use of clinical alternatives, including directing managed care plans to remove drugs from their formularies that lack new rebate agreements.

The pharmaceutical industry is taking steps to prepare to do battle against these and other steps taken to rein in drug prices. The pharmaceutical lobby, PhRMA (Pharmaceutical Research and Manufacturers of America), is increasing membership dues by 50 percent to raise an additional $100 million PER YEAR to fund its ongoing fight over drug prices.  “PhRMA has consistently ranked among the biggest lobbying spenders in Washington over the past few years.” By August of 2016, it had already spent $11.8 million that year, making it the fourth-largest lobbying group in Washington DC. TV advertising in 2017 was to target how “new drugs could add years to patients’ lives, as well as the years of complex research needed to develop a drug.”

The Intercept reported that newspapers in the Washington D.C. area were getting swamped in April of 2017 with ads warning of the dire consequences of proposals to lower drug prices. The groups placing the ads had no obvious connections to pharmaceutical companies. The ads appeared in the Washington Post, Washington Times, Roll Call, The Hill and Politico just as legislators were taking up proposals to lower drug prices. As it turned out, the organizations had undisclosed financial ties to PhRMA.

A bill proposed by Senator Al Franken would reverse a 2003 law prohibiting Medicare from using its collective bargaining power to negotiate lower drug prices. Legislators who wrote the 2003 bill worked closely with PhRMA lobbyists while drafting the legislation. The bill’s sponsor later became the president of PhRMA.  Franken and others introduced the “Improving Access to Affordable Prescription Drugs Act” on March 29, 2017. Here is a five-page summary of the bill. A companion bill to “Improving Access to Affordable Prescription Drugs Act” was introduced in the House on the same day.

Some of its provisions would include several current problems with prescription drug costs. It would close the coverage gap in Medicare Part D coverage (known as the donut hole) in 2018, two years earlier than under current law. Tax credits given to pharmaceutical companies for their direct-to-consumer (DTC) advertisements would be eliminated. (WE WERE GIVING PHARMA COMPANIES TAX CREDITS WHEN THEY TRY TO GET US TO BUY THEIR DRUGS?) It would allow individuals, wholesalers and licensed U.S. pharmacies to import prescription drugs manufactured at FDA-inspected facilities from licensed Canadian sellers.

Significantly, Section 201 would allow the Secretary of Health and Human Services to negotiate with drug companies to lower prescription drug prices. It directs the Secretary to “prioritize negotiations on specialty and other high-priced drugs.” Under existing law, unlike Medicaid and the VA, Medicare is not allowed to leverage its purchasing power to negotiate lower drug prices.

STAT News reported that the Thursday before the November 2017 election, Andy Slavitt, the acting administrator for Medicare and Medicaid Services, said the rising costs for prescription drugs “will put unsustainable pressure on the Medicare program, and action is going to be necessary to address them.” He was addressing the BioPharma Congress, an industry conference. He said: “Drug costs have become the health policy issue Americans are most anxious to see us act on, and we have a responsibility to them to explore all the options available us to make their medications more affordable.” He told those at the conference that we could have both innovation and affordability. “These two goals shouldn’t be in opposition.”

In every-forward looking industry outside of health care, we see that competition actually fuels innovation, and affordability improves alongside the development of new technologies. . . . There are plenty of policy options and certainly a number of ways innovators like you can choose to respond – from disputing the math and fighting it, to looking for win-wins.

So far, it seems Pharma is ignoring the message. They are still trying to convince the American public and U.S. lawmakers that innovation in drug development will dry up if price caps are enacted.

The debate over the cost of drug development has been going on since the late 1950s, believe it or not. An often-quoted 2003 study, “The Price of Innovation,” which was published in the Journal of Health Economics, estimated it cost $802 million in 2000 dollars to bring a new drug to market. PhRMA’s 2014 profile found that estimate low and said it actually costs $1.2 billion to develop a new drug. However, “Demythologizing the High Costs of Pharmaceutical Research,” in the journal BioSocieties, suggested the true research and development costs were a median of about $43.4 million per new drug. That is about 5.4% of “The Price of Innovation’s” cost projection and 3.6% of the PhRMA estimate. See “Pharma and Its Golden Hoard” for a further discussion of what a new drug costs.


Downward Spiral of Antipsychotics

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Antipsychotic or neuroleptic drugs became big business for pharmaceutical companies about nine years ago, reaching sales of $14.6 billion in 2008. This made them the best selling therapeutic class of medications in the U.S that year. Not only are they used to treat psychosis and bipolar disorder, several have been approved as an add-on medication to treat depression. Additionally they are used off-label with children and the elderly for behavioral control. And they are the primary cause for a serious neurological disorder called tardive dyskinesia.

Tardive dyskinesia (TD) is a group of involuntary movement disorders caused by drug-induced (iatrogenic) neurological damage, primarily from antipsychotic drugs and a few others that block the function of dopamine in the brain. “TD can vary from a disfiguring grimace to a totally disabling array of spasms and often bizarre movements of any part of the body.” If TD is not identified early on and the drugs stopped, “these disorders nearly always become permanent.” Both patients and their doctors often fail to recognize or diagnose its symptoms.

The above short introduction was gleaned from Dr. Peter Breggin’s “Antipsychotic Drugs and Tardive Dyskinesia (TD) Resources Center.” If you can spare a few minutes, watch a ten-minute TD video edited by Dr. Breggin from existing videos available on the Internet. The video contains a series of individuals with the three general types of tardive dyskinesia whose ages range from pre-adolescence to seniors. These types are: tardive dystonia, a series of involuntary movements that include painful muscle contractions or spasms; tardive akathisia, psychomotor agitation; and classic tardive dyskinesia, the rapid, jerky movements or uncontrollable head bobbing or movements of the arms, hands, feet fingers or toes. The following is a reproduction of a table from Psychiatric Drug Withdrawal by Peter Breggin more fully describing the symptoms of tardive dyskinesia.

Symptoms of Tardive Dyskinesia

Tardive Dyskinesia (Classic)

Rapid, irregular (choreiform), or slow and serpentine (athetoid) movements; often bizarre looking; involving any voluntary muscle, including:

Face, eyelids and eye muscles, jaw (chewing movements, tongue biting), mouth lips, or tongue (protruding, trembling curling, cupping)

Head (nodding), neck (twisting, turning), shoulders (shrugging), back, torso (rocking movements), or abdomen

Arms and legs (may move slowly or jerk out of control)

Ankles, feet and toes; wrists, hands, and fingers (sometimes producing flexion, extension or rotation)

Breathing (diaphragm and ribs; grunting), swallowing (choking), and speaking (dysphonis)

Balance, posture, and gait (sometimes worse when slow, often spastic)

Tardive Dystonia

Often painful sustained contractions (spasms) of any voluntary muscle group; potentially causing muscular hypertrophy, arthritis, and fixed joints; frequently involving the following:

Neck (torticolis, retrocollis) and shoulders

Face (sustained grimacing and tongue protrusion)

Mouth and jaw (sustained opening or clamping shut)

Arms and hands; legs and feet (spastic flexion or extension)

Torso (twisting and thrusting movements; flexion of spine)

Eye lids (blepharospasm)

Gait (spastic; mincing)

Tardive Akathisia

Potential agonizing inner agitation or tension, usually (but not always) compelling the patient to move, commonly manifested as the following:

Restless leg movements (when awake)

Foot stamping

Marching in place, pacing


Clasping hands or arms

Inability to sit still

TD can impair any muscle functions that are partially or wholly under voluntary control such as the face, eye muscles, tongue, neck, back, abdomen, extremities, diaphragm and respiration, swallowing, and vocal cords. Coordination and posture can be afflicted. TD can cause tremors, tics, and paresthesias (e.g., burning sensations, numbness). TD can also afflict the autonomic nervous system, especially impairing gastrointestinal functioning.

TD sufferers are often exhausted by these unrelenting body movements; even when they are limited to one area of the body, such as the jaw, neck or feet. They become socially withdrawn and isolated—humiliated by the stigma of their uncontrollable movement disorder. One muscle group, such as the tongue or fingers, or various muscle groups can be afflicted. TD symptoms can also change over time from one muscle group to another. This can occur over a period of minutes, days, weeks or years. “Especially in the dystonic forms, the pain can be very severe, and the physical stress can cause serious orthopedic problems.” Antipsychotic drugs are the primary cause of this neurological disorder.

Antipsychotic drugs are also called neuroleptics. Prescribers often promote them in a misleading fashion as antidepressants, mood stabilizers, bipolar drugs, sleeping pills, and behavior control drugs in children. Recent ones include Risperdal (risperidone), Abilify (aripiprazole), Geodon (ziprasidone), Invega (paliperidone), Latuda (lurasidone), Rexulti (brexpiprazole), Risperdal (risperidone), Saphris (asenapine), Seroquel (quetiapine), and Zyprexa (olanzapine). Older antipsychotics include Haldol (haloperidol) and Thorazine (chlorpromazine). [See a more complete listing of antipsychotics here]

Drug companies have made claims that the newer, so-called atypical antipsychotic drugs are less likely to cause TD, but those claims are false or misleading. A 2008 study by Chouinard found a high prevalence of DIMD (drug-induced movement disorders). Nearly 50% of patients had a definite DIMD. The authors also said that DIMD persisted with atypical antipsychotics. “It is crucial to acknowledge that there is a persistence of DIMD with atypical antipsychotics, which are not recognized and confounded with psychiatric symptoms.” Caroff, Miller and Rosenheck reported in “Extrapyramidal Side Effects” that there were no significant differences in measuring the incident rates of TD and other DIMDs between atypical antipsychotics and an older antipsychotic, perphenazine (Trilafon).

According to Dr. Breggin, TD occurs around a rate of 5 to 8 percent per year in adults up to the age of 40, with an accumulating risk of 20% to 24% after four years. The rates increase rapidly over forty. “For a 40-year-old patient, the risk is 18% at 2 years [9% per year] and 30% at 4 years.” In patients over 45, “the cumulative incident of TD after neuroleptic exposure is 26%, 52%, and 60% after 1, 2, and 3 years, respectively.”

Recently the FDA approved two medications to treat TD. Let this sink in. A serious neurological disease, which is primarily caused by a class of psychiatric medications, is being treated with another medication. Neurology Advisor interviewed two experts medical experts on the current state of treatment for TD. One of the experts interviewed said:

The main issue in the “treatment” of TD is prevention. It is important to use offending agents only when the potential benefit is higher than this risk. Once it appears, the first step is to determine whether symptoms are bothersome or disabling to warrant treatment. If possible, either discontinue the offending agent, although this might not improve symptoms permanently, and they will probably worsen initially, or change to a similar agent less likely to cause TD. In terms of prescription medications for TD, I have observed significant variability in treatment approaches depending on physician choice. Over the last few years, I personally found tetrabenazine to be the most efficient agent.

Tetrabenazine (Xenazine) was approved to treat the movement disorder associated with Huntington’s chorea, but has been used off-label to treat TD. It is now off patent and available as a generic. On patent, it sold for $152,000 per year. The generic version is $96,000 per year. However, there have been two new drugs approved specifically to treat TD: Austedo (deutetrabenazine) and Ingrezza (vabenazine). Both are being priced at around $60,000 per year. All three medications carry “black box” warnings from the FDA because of their risk for depression and suicide. You can read more about these medications here, here, here and here.

In addition to TD, antipsychotics have been linked to adverse cardio vascular events, brain shrinkage, dopamine supersensitivity, weight gain, diabetes, a shortened life span and more. The risk-benefit ratio may see a need for short-term use of antipsychotics, but the long-term benefits of their use are questioned by many credible sources. There have been follow up studies that support that concern. See this blog post by Thomas Insel, the former director of the NIMH, the National Institute of Mental Health.

It seems to be stepping onto a downward spiral to use medications with serious side effects to treat TD, a serious side effect from antipsychotics. As the above quoted expert, suggested, the best treatment for tardive dyskinesia is prevention—avoid antipsychotics if at all possible. For more information on concerns and adverse effects with antipsychotics, see: “Blind Spots with Antipsychotics” Part 1 and Part 2, “Antipsychotic Big Bang”, “Wolves in Sheep’s Clothing” and “Hollow Man Syndrome.”


Tell It Like It Is

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Recently I saw one of the ubiquitous “ask your doctor if … is right for you” commercials for Rexulti. The slick 90-second ad tells you that when Rexulti is added to your antidepressant, it has been shown to reduce symptoms of depression. The smiley faces used by the actors illustrate how: “Even when you’re taking an antidepressant, you may still be struggling with depression.” You learn that 2 out of 3 people taking an antidepressant may experience unresolved symptoms of depression; and that antidepressants can cause unusual changes in behavior, worsening depression and thought of suicide, especially in those 24 and younger. But you never learn that Rexulti is not an antidepressant.

The commercial never claims Rexulti is an antidepressant, but it clearly leads its viewers in that direction. Counter intuitively, in order to make the case for using Rexulti, it not-so-subtly tells you that antidepressants alone aren’t always effective, since 67% of people taking them have “unresolved symptoms” of depression. But then you learn Rexulti has been shown to reduce symptoms of depression when it is added to an antidepressant. The message is that Rexulti is effective relieving symptoms of depression. But let’s deconstruct what the commercial is telling you even further.

In the mix of the marketing rhetoric, you hear a litany of possible adverse medication side effects. The initial side effects are found with antidepressants: there could be unusual changes in behavior, worsening depression, even thoughts of suicide. “Antidepressants can increase these in those 24 and younger.” This information is legitimately about the side effects from antidepressant medications. See “Antidepressant Misuse Disorder” and “Antidepressants: Their Ineffectiveness and Risks” on this website.

Actually, Rexulti is an atypical antipsychotic or neuroleptic; in the same drug class as Abilify, Zyprexa, Seroquel and Risperdal. The other described side effects and warnings in the commercial are commonly found with atypical antipsychotics. See “Adverse Effects of Antipsychotic Medications” by Muench and Hamer for further information.

Looking further, the commercial said: “Elderly dementia patients taking Rexulti have an increased risk of death or stroke.” Antipsychotics were being used to control behavior problems in elderly patients with dementia. Then research demonstrated there was an increased risk of death in the elderly patients given antipsychotics. So the FDA issued a black box warning to that effect. There was also evidence that antidepressants increased the risk of stroke with elderly patients, thus the Rexulti warning. See “Seniors and Antipsychotics” and “Stroke Risk in Elderly Treated with Antipsychotics” for more information on this.

“Uncontrollable muscle movements” in the commercial is likely referring to tardive dyskinesia, a serious and potentially permanent neurological side effect from antipsychotics. The risks for developing metabolic syndrome (high blood pressure, high blood sugar, excess body fat at the waist, and abnormal cholesterol levels) are mentioned as well. Tardive dyskinesia and metabolic syndrome are widely acknowledged as potential adverse effects from antipsychotics, but not antidepressants. Try “Blind Spots with Antipsychotics,” Part 1 and Part 2 for a discussion on metabolic syndrome and other side effects from antipsychotics. Stiff muscles, confusion, and high fever are symptoms of “a possible life threatening condition” known as Neuroleptic Malignant Syndrome (See “Neuroleptic Malignant Syndrome”).

So you wouldn’t know Rexulti was an atypical antipsychotic or neuroleptic drug from listening to the commercial unless you knew the above were typical side effects with that class of drug. And you may not even discover this from reading the required Medication Guide, unless you knew what to look for. The FDA’s highlights of prescribing information for Rexulti, all 38 pages worth, does have a more complete discussion of the warnings and precautions as well as the adverse reactions. And Rexulti is referred to there as an atypical antipsychotic. However, in the shorter, two page medication guide, that is made available to individuals filling a prescription for Rexulti, there is no explicit reference to it being an atypical antipsychotic or neuroleptic.

The Rexulti Medication Guide does describe tardive dyskinesia, “problems with your metabolism” and Neuroleptic Malignant Syndrome as possible side effects, which are all potential side effects from antipsychotic or neuroleptic medications. But the only place in the medication guide that the word “antipsychotics” is used is in the section “What should I tell my healthcare provider before taking Rexulti?” There, the medication guide advised that if you become pregnant while taking Rexulti, you should “talk to your healthcare provider” about registering with the National Pregnancy Registry for Atypical Antipsychotics. The only place in the Rexulti medication guide the word “neuroleptic” in mentioned is when it notes how Neuroleptic Malignant Syndrome is a possible side effect.

This rhetorical sleight-of-hand is also present in the medication guides for three other antipsychotics approved by the FDA as adjunct medications for depression. Aripiprazole (Abilify), Olanzapine (Zyprexa) and Quetispine (Seroquel) all use the same descriptive technique of avoiding reference to the drugs as antipsychotics or neuroleptics in their medication guides. And several have an extended discussion of information on antidepressants. Again, someone not familiar with the medications might think they are taking an antidepressant rather than an antipsychotic medication.

The rational for this would appear to be because the initial market for antipsychotics, treating schizophrenia, is limited. Atypical antipsychotics are now the largest-selling class of drugs in the U.S. with more than $14.6 billion in annual sales for 2014. They also are the class of psychiatric drugs with the most side effects. See “Wolves in Sheep’s Clothing” and “Abilify in Denial” for more on these observations.

Another piece of information about Rexulti in contrast to the other antipsychotics approved as adjunct medications for depression is that it is the only one still on patent. Rexulti patents don’t expire until February of 2027 Abilify, Zyprexa, and Seroquel have all been approved as generics.  So Otsuka Pharmaceutical Company Ltd. has the potential for much greater profits from Resulti over the next ten years than the generic pharmaceutical companies have for the off-patent atypical antipsychotics.

There seems to be a general trend when discussing psychiatric medications to avoid any reference to them as atypical antipsychotics or neuroleptics. You can even see this in the FDA press release for the approval of Rexulti in July of 2015. This means a consumer looking for information on the potential adverse effects from an atypical antipsychotic may have some difficulty finding and then understanding what the risk is for them to take the drug.

For clarity’s sake, I think the FDA should require all consumer medication guides to clearly identify the drug class for approved psychiatric medications. They should also direct a patient to where they can find a more complete discussion of the potential adverse effects of the medication than what is contained within the brief summary of the medication guide. Confusing discussions of depression, its symptoms and the side effects from antidepressants included in antipsychotic medication guides should be clarified or removed entirely by the FDA. Additionally, there should be a truth in advertising requirement that tells it like it is for all psychiatric drug advertisements. An antipsychotic by any other name is still an antipsychotic and the commercials should say so.


Is Ketamine Really Safe & Non-Toxic?

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An article in The Morning Call, a newspaper for Allentown and the Lehigh Valley area of Pennsylvania, announced that a local company, the Lehigh Center for Clinical Research, would be conducting clinical trials for two pharmaceutical companies to gain FDA approval for modified versions of ketamine as a treatment for depression. The psychiatrist running the trials said the drugs could hit the market in the next few years. He said: “It’s exciting and promising but I think we have to wait to see it used in the widespread population to know whether it’ll be safe and non-toxic.” I thought the safety and toxicity of a new drug was supposed to be assessed BEFORE the FDA approved its release into the wider population.

There have been waves of excitement and concern over the past few years about the development and use of ketamine and ketamine-like drugs to treat depression. Ketamine has been an FDA approved medication since 1970, where it was used as an anesthetic in the Vietnam War. It is classified as a Schedule III Controlled Substance by the DEA, meaning it has a potential for moderate to low dependence or high psychological dependence. Ketamine is also a recreational drug known as Special K because of its dissociative properties. “Due to the detached, dreamlike state it creates, where the user finds it difficult to move, ketamine has been used as a ‘date-rape’ drug.” See: “Falling Down the K-Hole” and “Family Likeness in Depression Drugs?”

The excitement over ketamine, as a treatment for depression, centers on its rapid relief of depressive symptoms; sometimes within hours of it being administered. But the effects fade rapidly and require frequent, repeated treatments. Currently ketamine is administered intravenously, similar to its use as an anesthetic. There is an intranasal spray version (Esketamine) in the works. See: “Psychedelic Depression,” Ketamine to the Rescue?,” and Ketamine Desperation.”

The clinical trails being done by the Lehigh Center for Clinical Research would appear to be for Esketamine, by Janssen Research and Development, and Rapastinel, by Allergan. While Esketamine is a nasal spray, Rapastinel is administered by weekly IV injections. Both are currently in Phase 3 clinical trials. This involves randomized, double blind testing in several hundred to several thousand patients. Upon successful completion of their Phase 3 trials, a pharmaceutical company can request FDA approval for marketing their drug. Somewhere around 70 to 80 percent of drugs that make it to Phase 3 are eventually approved.

Although Esketamine and Rapastinel are similar to ketamine in several ways, they are still distinct NMEs (new molecular entities), patented by their respective pharmaceutical companies. Ketamine was first developed in the 1960s and has been off patent for decades, meaning there is no profit in Pharma companies pursuing ketamine-based treatment for depression. But since ketamine is an FDA approved drug, it can be used off label to treat depression. And there are a growing number of ketamine treatment facilities around the U.S. and Canada that do just that.

Earlier in 2017 All Things Considered on NPR featured a story on the off-label use of ketamine to treat depression, “Ketamine for Severe Depression.” Psychiatrist Gerard Sanacora said over 3,000 patients have treated at dozens of clinics with ketamine for depression. He has personally treated hundreds of people with low dose ketamine. Sanacora said when he is asked how he can offer it to people on the limited amount of available information and without knowing the potential long-term risk, he responds “How do you not offer this treatment” to individuals likely to injure or kill themselves, who have unsuccessfully tried the standard treatments?

Sanacora and others authored “A Consensus Statement on the Use of Ketamine in the Treatment of Mood Disorders” that was published in JAMA Psychiatry in April of 2017. They noted how several smaller studies have demonstrated the ability for ketamine “to produce rapid and robust antidepressants effects in patients with mood and anxiety disorders that were previously resistant to treatment.” It also cautioned that while ketamine may be beneficial to some patients, “it is important to consider the limitations of the available data and the potential risk associated with the drug when considering the treatment option.”

Zorumski and Conway published “Use of Ketamine in Clinical Practice” in the May 2017 issue of JAMA Psychiatry. They also noted the increasing evidence from small studies that ketamine has rapid antidepressant effects in patients with treatment-resistant depression. They commented how ketamine is having a major effect on psychiatry. “If clinical studies continue to support the antidepressant efficacy of ketamine, psychiatry could enter an era in which drug infusions and deliveries with more rapid responses become common.” They indicated the cautions of Sanacora et al. were noteworthy and should be emphasized.

Because of the limited data to guide clinical practice, these limitations extend to almost every recommendation in the consensus statement, including, perhaps most importantly, patient selection. The bulk of the literature describes the effects of ketamine in patients with treatment-refractory major depression. The definition of treatment-refractory major depression and where treatments such as ketamine fall in the algorithm for managing treatment-refractory depression remain poorly understood. . . . It is unclear whether patients with depression that is not treatment-refractory or patients with other psychiatric illnesses are appropriate candidates for ketamine treatment, and extreme caution must be exercised in patients with psychotic or substance use disorders.

So then comes the Short et al. study in the journal Lancet Psychiatry in July 2017, “Side Effects Associated with Ketamine Use in Depression.” It was the first systematic review of the safety of ketamine in the treatment of depression. After searching MEDLINE, PubMed, PsycINFO, and Cochrane Databases, they identified 60 out of 288 articles that met their inclusion criteria. “Our findings suggest a selective reporting bias with limited assessment of long-term use and safety and after repeated dosing, despite these being reported in other patient groups exposed to ketamine (eg, those with chronic pain) and in recreational users.”

Science Daily reported that the lead author for the study said there were major gaps in the research literature that should be addressed before ketamine was widely used as a clinical treatment for depression. “Despite growing interest in ketamine as an antidepressant, and some preliminary findings suggesting its rapid-acting efficacy, to date this has not been effectively explored over the long term and after repeated dosing.” Given that ketamine will likely involve multiple, repeated doses over an extended time period, “it is crucial to determine whether the potential side effects outweigh the benefits to ensure it is safe for this purpose.”

Commenting on the Short et el. Study for Mad in America, Peter Simons also noted the expressed concern with the selective reporting bias and a limited assessment of long-tem use and safety after repeated dosing. Researchers are generally careful to report safety and side effect data on studies of ketamine used recreationally or for chronic pain. However, depression research tended to ignore the safety and side effect concerns with ketamine, often not reporting such issues at all.  “Most people receiving ketamine had acute side effects.” Studies that did report adverse events said that after acute dosing, patients in ketamine treatment reported more frequent side effects.

Common side effects led a number of patients to withdraw from the study. Suicidal thoughts were common and there was one suicide attempt reported. Previously reported potential long-term adverse effects from ketamine include: urinary tract problems, liver toxicity, ulcerative cystitis, neurocognitive deficits and memory problems, and dependence or addiction. Some of the many additional side effects that were reported included:


  • Worsening mood
  • Anxiety
  • Emotional blunting
  • Psychosis
  • Thought disorders
  • Dissociation
  • Depersonalization
  • Hallucinations
  • Increased blood pressure
  • Increased heart rate
  • Decreased blood pressure
  • Decreased heart rate
  • Heart palpitations/arrhythmia
  • Chest pain
  • Headaches
  • Dizziness
  • Unsteadiness
  • Confusion
  • Memory loss
  • Cognitive impairment
  • Blurred vision
  • Insomnia
  • Nausea
  • Fatigue
  • Crying/tearfulness

Because of the extensive list of potential adverse effects, as well as the unknown possibility for harm from long-term use, the authors of Short et al. recommended large-scale clinical trials with multiple doses of ketamine. Long-term follow up to assess the safety of long-term regular use was also recommended. “As it stands, the safety of ketamine treatment for depression is unknown—and that is largely due to inadequate and biased reporting of safety issues.”

I hope that these concerns are seriously considered and factored into the FDA’s assessment process for approving Esketamine and Rapastinel. Otherwise, the real safety and toxicity assessment of these drugs will be done on the first wave of depression sufferers prescribed the new drugs for treatment-resistant depression. Given the short length of clinical trials, the long-term effectiveness and impact on a patient’s quality of life, including potential misuse of the drugs, will not be clear  for either Esketamine or Repastinel until Phase 4 Post Marketing Surveillance Trials are completed … after the drugs are on the market. Will they live up to their therapeutic promise or become another example of the Pharma patent medicine show?


Demolishing ADHD Diagnosis

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The Harvard psychologist, Jerome Kagan, sees ADHD as more of an invented condition than a serious illness. Further, he thinks it was invented for “money-making reasons” by the pharmaceutical industry and pro-ADHD researchers. He believes the drastic increase in the number of children diagnosed with ADHD has more to do with “fuzzy diagnostic practices” and relabeling. Fifty years ago, a 7-year-old child who was bored and disruptive in class was seen as “lazy.” Today he is seen as suffering from ADHD.

Every child who’s not doing well in school is sent to see a pediatrician, and the pediatrician says: “It’s ADHD; here’s Ritalin.” In fact, 90 percent of these 5.4 million kids don’t have an abnormal dopamine metabolism. The problem is, if a drug is available to doctors, they’ll make the corresponding diagnosis.

In his interview with Spiegel Online, Kagan went on to say that the inflated diagnosis of ADHD and other so-called childhood mental health disorders means more money for the pharmaceutical industry, psychiatrists and the people doing research. “We’re up against an enormously powerful alliance: pharmaceutical companies that are making billions, and a profession that is self-interested.” As he said, he’s not the only psychologist who is saying this.

Parenting expert and family psychologist, John Rosemond, agrees with Kagan. In 2009 he co-authored The Diseasing of American’s Children where they argued that ADHD and other childhood behavior disorders “were inventions of the psychological-psychiatric-pharmaceutical industry.” They went further than Kagan in saying that ADHD does not exist; that it is a fiction. In his April 9, 2017 article, “ADHD Simply Does Not Exist,” Rosemond referred to Kagan’s declaration on ADHD, noting that he and other psychologists studied Kagan’s books and research papers on children and child development when they were in graduate school. In The Diseasing America’s Children, Rosemond said:

Science depends on verifiable, objective evidence and experimental results that can be replicated by other scientists. Where ADHD is concerned, neither verifiable, objective evidence nor replicable experimental results exist to support the claims of the ADHD establishment.”

Rosemond and his co-author, Bose Ravenel, believe that childhood behavior disorders like ADHD are manifestations of “dysfunctions of discipline and lifestyle” endemic to modern family culture. Once these problems are identified, they can be easily corrected. And once corrected, the errant behavior “usually recovers to a state of normalcy within a relatively short period of time.” They believe children do not need a psychologist when they misbehave, they need discipline—“firm, calm and loving discipline.”

In Debunking ADHD, educational psychologist Michael Corrigan said ADHD is a negative label that does not exist. “Not unlike the many wonderful stories about unicorns, fairies, and leprechauns, the diagnosis of ADHD is a brilliant work of fiction.” He noted that many of the common childhood behaviors (or supposed symptoms) associated with ADHD are also used to identify giftedness in children. When these behaviors are harnessed and focused, they can help children become “incredibly creative, insightful, and successful individuals in adulthood.” If children don’t learn to harness the power of the behaviors ADHD and giftedness have in common, “such behaviors when displayed might seem annoying and immature.” He said:

My biggest reason for writing this book is my desire to show you that the practice of medicating children for acting like children in the name of ADHD is, in two words, wrong and dangerous. Despite the grandiose claims of the mega-pharmaceutical companies selling ADHD drugs to concerned parents, prescribing pills to young children trying to learn how to become young adults is just a quick fix void of any long-term benefits.

Corrigan described eating lunch with a group of children who had just taken their ADHD medication at school. They were now supposedly “good to go” (sufficiently medicated) for an afternoon of learning. It was the longest lunch period he had ever experienced. “Comparing the kids at my table to others in the cafeteria, and slowly watching these playful, creative, energetic, and funny children go from kids being kids to near expressionless robot-like entities, made me sick to my stomach.”

The total number of children on ADHD medication “skyrocketed” from 1.5 million in 1995 to 3.5 million in 2011. “Sales of prescription stimulants quintupled from 2005 to 2015.” The rising rate of ADHD diagnosis has been described as “an unreal epidemic” and a “national disaster of dangerous proportions” by well-known professionals like Allen Frances and Keith Conners. Frances was the chair of the DSM-IV. Conners, now an emeritus professor of medical psychology at Duke University, “spent much of his career in legitimizing the diagnosis of ADHD.”

Allen Frances was one of four authors of an article in the International Journal of Qualitative Studies on Health and Well-Being, “ADHD: A Critical Update for Educational Professionals.” When the DSM-IV was published in 1994, the prevalence of ADHD was estimated to be 3%. Since then, parent-reported ADHD diagnosis increased to 7.8% in 2003; 9.5% in 2007; and to 11% in 2011. Nearly one in five high school boys had been diagnosed with ADHD and around 13.3% of 11-year-old boys were medicated for ADHD.

Teachers and other school personnel are often the first to suggest a child might be “ADHD.” Research suggested teachers felt insecure about dealing with behavioral problems and hesitated to accept responsibility for students with special needs. Frances and his coauthors described six scientifically grounded issues that educational professionals should be aware of when they are confronted with inattention and hyperactivity in the classroom.

First: birth order matters. Several studies have shown “That relative age is a significant determinant of ADHD diagnosis and treatment.” The youngest children in the classroom are twice as likely to be diagnosed with ADHD and receive medication. They suggest teachers take the child’s relative age into account when judging the child’s behavior. “Seeing ADHD as the cause of inattention and hyperactivity is in fact a logical fallacy as it is circular.”

Second, there is no single cause of ADHD. “There are no measurable biological markers or objective tests to establish the presence or absence of ADHD (or any other given DSM syndrome).” ADHD is a description of behavior and is based on “criteria that are sensitive to subjectivity and cognitive biases.” Multiple factors have been associated with ADHD, without necessarily implying causality. Those factors include: divorce, poverty, parenting styles, lone parenthood, sexual abuse, lack of sleep, artificial food additives, mobile phone use and growing up in areas with low solar intensity. “All these factors and more may play a role when a particular child exhibits impairing hyperactive and inattentive behaviours, and there is no conclusive cause of ADHD.”

Third, most children exhibiting “ADHD behavior” have normal-looking brains. Studies that do show small differences in terms of brain anatomy do not apply to all children diagnosed with ADHD. Individual differences refer to slower anatomical development. “They do not reveal any innate defect as is illustrated by the fact that many people with an unusual anatomy or physiology do not experience ADHD related problems.” Also, the test subjects in many brain-related studies are rigorously screened and don’t represent all individuals diagnosed with ADHD.

The samples do not comprise an accurate representation of their respective populations, meaning an average child with a diagnosis of ADHD and an average “normal” child. This problem is particularly urgent since the DSM 5 has lowered the age of onset criterion, as well as the impairment criterion compared to the previous version, the DSM-IV. Alongside the lowered threshold, the potential to generalize earlier research findings has lowered as well.

Fourth, the claims of ADHD being inherited may be overestimated.  The claims vary widely and are subject to debate because of methodological issues used in calculating the heritability coefficient in twin, familial and adoption studies. There is significant difficulty separating genetic influences from environmental ones, such as poverty, parenting styles and divorce, in these studies. “In genetic association studies that really analyse genetic material and that are more powerful when separating the influence of genetics from other etiologic sources, associated genes show only very small effects.” When combined, they explain less than 10% of variance.

This means they occur only slightly more often in diagnosed individuals than in controls, and they do not explain nor predict ADHD behaviours. For educational professionals, this is important to consider as an ADHD label might give a false sense of security with regard to the alleged (genetic) cause of a child’s behaviour and the preferred cure (medication).

Fifth, medication does not benefit most children in the long run. Follow up studies of the long-term effects of the MTA (Multimodal Treatment of Attention Deficit Hyperactivity Disorder) study showed a convergence of outcomes over time between medicated and non-medicated children. Other studies also report either no long-term benefits, or even worse benefits. “While medication may help a small group of children in the long run, most will not benefit from long-term pharmaceutical treatment.”

The sixth and final issue that educational professionals should be aware of when confronted with inattention and hyperactivity in the classroom is the reality that a diagnosis can be harmful to children. A CDC MMWR Report indicated only 13.8% had severe ADHD, with 86.2% having mild (46.7% or moderate (39.5%) ADHD. The authors pointed out a DSM diagnosis opened the door for additional reimbursement to the school for treatment and school services, perhaps promoting a search for pathology in relatively mild cases. “The question is whether in these mild cases the merits of a confirmed diagnosis—such as acknowledgement of problems and access to help—outweigh possible demerits.” Some known disadvantages of a diagnosis are: lower teacher and parent expectations that turn into self-fulfilling prophecies, prejudice and stigmatization of diagnosed children, a more passive role towards problems, difficulties getting life and disability insurances later on in life, and others.

The Allen Frances article linked above was the most accepting of ADHD as a legitimate “neuro-developmental disorder.” Yet it cautioned there was no single cause for ADHD, medications to “treat” ADHD did not have long-term benefits, and there was a problem with its over diagnosis. Jerome Kagan thought 90% children were wrongly diagnosed with ADHD because of “fuzzy diagnostic practices and relabeling.” Michael Corrigan, John Rosemond and questioned the validity of ADHD as a neuro-developmental disorder. Corrigan said it pathologized normal childhood behavior; and medicating these children was wrong and evil. It’s time to demolish the ADHD treatment empire.

Additional articles on ADHD can be found on this website here: “National ADHD Epidemic,” “Misleading Info on ADHD,” “Tip of the ADHD Iceberg,” and “Is ADHD Simply a Case of the Fidgets?” You can also read a longer paper: “ADHD: An Imbalance of Fire Over Water of a Case of the Fidgets?


Dysfunctional fMRIs

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Neuroscientists at Dartmouth placed a subject into an fMRI machine to do an open-ended mentalizing task. The subject was shown a series of photographs depicting human social situations with a specific emotional reaction. The test subject was to determine what emotion the individual in the photo must have been experiencing. When the researchers analyzed their fMRI data, it seemed like the subject was actually thinking about the pictures. What was unusual about this particular fMRI study was that the subject was a dead Atlantic salmon.

Craig Bennett and other researchers wrote up the study to warn about the dangers of false positives in fMRI data. They wanted to call attention to the need to improve statistical methods in the field of fMRI research. But Bennett’s paper was turned down by several publications. However, a poster on their work found an appreciative audience at the Human Brain Mapping conference and neuroscience researchers began forwarding it to each other. The whimsical choice of a test subject seems to have prevented publication of the study, but it effectively illustrated and important point regarding the potential for false positives in fMRI research. The discussion section of their poster said:

Can we conclude from this data that the salmon is engaging in the perspective-taking task? Certainly not. What we can determine is that random noise in the EPI time series may yield spurious results if multiple comparisons are not controlled for. Adaptive methods for controlling the FDR and FWER are excellent options and are widely available in all major fMRI analysis packages.  We argue that relying on standard statistical thresholds (p < 0.001) and low minimum cluster sizes (k > 8) is an ineffective control for multiple comparisons. We further argue that the vast majority of fMRI studies should be utilizing multiple comparisons correction as standard practice in the computation of their statistics.

According to Alexis Madrigal of Wired, Bennett’s point was not to prove that fMRI research is worthless. Rather, researchers should use a set of statistical methods known as multiple comparisons correction “to maintain most of their statistical power while keeping the danger of false positives at bay.” Bennett likened the fMRI data problems to a kind of darts game and said: “In fMRI, you have 160,000 darts, and so just by random chance, by the noise that’s inherent in the fMRI data, you’re going to have some of those darts hit a bull’s-eye by accident.” So what, exactly, does fMRI measure and why is understanding this important?

The fundamental basis for neural communication in the brain is electricity. “At any moment, there are millions of tiny electrical impulses (action potentials) whizzing around your brain.” When most people talk about ‘brain activity,’ they are thinking about the activity maps generated by functional magnetic resonance imaging (fMRI). Mark Stokes, an associate professor in cognitive neuroscience at Oxford University said fMRI does not directly measure brain activity. Rather, fMRI measures the indirect consequences of neural activity, the haemodynamic response, which permits the rapid delivery of blood to active neuronal tissues. This indirect measurement is not necessarily a bad thing, if the two parameters (neural activity and blood flow) are tightly coupled together. The following figure from “What does fMRI Measure?” illustrates the pathway from neural activity to the fMRI.

A standard fMRI experiment generates thousands of measures in one scan (the 160,000 darts in Bennett’s analogy), leading to the possibility of false positives. This wealth of data in an fMRI dataset means that it is crucial to know how to interpret it properly. There are many ways to analyze an fMRI dataset, and the wealth of options may lead a researcher to choose one that seems will give him or her the best result.  The danger here is that then the researcher may then only see what they want to see.

Anders Ecklund, Thomas Nichols and Hans Knutson said that while fMRI was 25 years old in 2016, its most common statistical methods have not been validated using real data. They found that the most commonly used software packages for fMRI analysis (SPM, FSL, AFNI) could result in false positive rates up to 70%, where 5% was expected. The illusion of brain activity in a dead salmon discussed above was a whimsical example of a false positive with fMRI imaging.

A neuroscientist blogging under the pen name of Neuroskeptic pointed out that a root problem uncovered by Ecklund’s research is spatial autocorrelation—“the fact that the fMRI signal tends to be similar (correlated) across nearby regions.” The difficulty is well known and has software tools to deal with it, but “these fixes don’t work properly.”  The issue is the software assumes the spatial autocorrelation function has a Gaussian shape, when it fact, it has long tails, with more long-range correlations than expected. “Ultimately this leads to false positives.” See Neuroskeptic’s article for a graph illustrating this phenomena.

There is an easy fix to this problem. Ecklund and colleagues suggested using non-parametric analysis of fMRI data. “Software to implement this kind of analysis has been available for a while, but to date it has not been widely adopted.” So there is still value in doing fMRI research, but a proper analysis of the dataset is crucial if the results are to be trusted.

Neuroskeptic also discussed an analysis of 537 fMRI studies done by Sprooten et al. that compared task-related brain activation in people with a mental illness and healthy controls. The five diagnoses examined were schizophrenia, bipolar disorder, major depression, anxiety disorders and obsessive-compulsive disorder (OCD). The analysis showed very few differences between the disorders in terms of the distribution of the group differences across the regions of the brain. “In other words, there was little or no diagnostic specificity in the fMRI results. Differences between patients and controls were seen in the same brain regions, regardless of the patients’ diagnosis.”

Sprooten et al. speculated that the disorders examined in their study arose from largely overlapping neural network dysfunction. They cited another recent meat-analysis by Goodkind et al. that also found “shared neural substrates across psychopathology.” Sprooten et al. said: “Our findings suggest that the relationship between abnormalities in task-related networks to symptoms is both complex and unclear.”

Neuroskeptic didn’t think there was a need to assume this transdiagnostic trait was an underlying neurbiological cause of the various disorders. He wondered if something like anxiety or stress during the fMRI scan could have been captured by the scan.

It’s plausible that patients with mental illness would be more anxious, on average, than healthy controls, especially during an MRI scan which can be a claustrophobic, noisy and stressful experience. This anxiety could well manifest as an altered pattern of task-related brain activity, but this wouldn’t mean that anxiety or anxiety-related neural activity was the cause of any of the disorders. Even increased head movement in the patients could be driving some of these results, although I doubt it can account for all of them.

A paper in NeuroImage by Nord et al. commented how numerous researchers have proposed using fMRI biomarkers to predict therapeutic responses in psychiatric treatment. They had 29 volunteers do three tasks using pictures of emotional faces. Each volunteer did the tasks twice one day and twice about two weeks later. While the grouped activations were robust in the scanned brain areas, within-subject reliability was low. Neuroskeptic’s discussion of the study, “Unreliability of fMRI Emotional Biomarkers,” said these results could be a problem for researchers who want “to use these responses as biomarkers to help diagnose and treat disorders such as depression.”

Neuroskeptic asked one of the researchers if it was a “real” biological fact that activity in the brain areas studied actually varied within subject, or was the variability a product of the fMRI measurement? He didn’t know, but thought it wasn’t simply a measurement issue. He also thought it was perfectly possible “that the underlying neuronal responses are quite variable over time.”

Grace Jackson, a board certified psychiatrist, wrote an unpublished paper critiquing how fMRIs and other functional brain scans are being presented to the public as confirming that psychiatric disorders are real brain diseases. She pointed out the failure of media discussions to point out that functional imaging technologies, like fMRI, “are incapable of measuring brain activity.” They assess transient changes in blood flow. She also commented on the existing controversy of using this technology for diagnosis. “Due to theoretical and practical limitations, their application in the field of psychiatry is restricted to research settings at this time.”

She said even if abnormal mental activity could be objectively defined and reliably determined, “it remains unclear how any functional imaging technology could differentiate the brain processes which reflect the cause, rather than the consequence, of an allegedly impairing trait or state. She concluded with a quote from a position paper drafted by the American Psychiatric Association that said imaging research cannot yet be used to diagnose psychiatric illness and may not be useful in clinical practice for a number of years. “We conclude that, at the present time, the available evidence does not support the use of brain imaging for clinical diagnosis or treatment of psychiatric disorders…”

No current brain imaging technology, including fMRI, can be used to diagnose or treat psychiatric disorders. fMRI technology does not directly measure neural activity and has a demonstrated tendency to generate false positives, especially if the statistical analysis of the fMRI dataset is done incorrectly. Given the limitations of functional imaging technology, it is unclear how fMRI—or any other functional imaging technology—will be able to clearly distinguish between brain activity that causes an impaired neural trait or state, and brain activity that is a consequence of an impaired neural trait or state. And yet fMRI scans are presented to the public, by some individuals, as measuring brain activity and proving the existence of some psychiatric disorders. In their hands fMRI technology has become dysfMRI: dysfunctional MRI technology.


Circle the Pfizer Wagons

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The U.S. Preventive Services Task Force (USPSTF) recommended that all adults, including pregnant women and women who have recently given birth, be screened in primary care settings for depression. The screening would be done by: general practitioners, family physicians, nurse practitioners or physician assistants. USPSTF said screening adults for depression in primary care settings was accurate, it was effective in relieving depressive symptoms and the likelihood of harm from screening and treatment was small. The problem is that over 60% of individuals diagnosed with depression in primary care did not meet the DSM criteria for major depressive disorder. This rises to 80% with individuals over 65.

Albert Siu and the USPSTF published “Screening for Depression in Adults” in the January 2016 issue of JAMA. The authors said: “The USPSTF found convincing evidence that treatment of adults and older adults with depression identified through screening in primary care settings with antidepressants, psychotherapy, or both decreases clinical morbidity.” Commonly used screening instruments included the Patient Health Questionnaire (PHQ) in its various forms, as well as several others. But the USPSTF did not believe these instruments were getting as many false positives as noted above. “The accuracy of screening tests in the general adult population was established in the 2002 and 2009 USPSTF reviews and found to be convincing.”

Psychiatrist Vivek Datta pointed out the USPSTF guidelines did recommend that screening occurred when there were “adequate systems in place” for further evaluation and treatment. However, “55% of all US counties do not have a single mental health provider.” He noted that many of the symptoms screened for are nebulous and include “symptoms that are quite common in the general population and do not necessarily indicate a mental disorder requiring treatment.” They could represent the effects of a chronic medical problem. Moods are influenced by a variety of factors, such as our level of physical activity, what we eat, our financial security, alcohol and drug use, to name a few.

Symptoms of depression can occur as a result of lifestyle factors, substance use, medical illness, life events, interpersonal difficulties, and as a consequence of wider social policies. Comprehensive assessment frequently does not occur because of the lack of adequate services for those with mental health problems. The recommendation to screen all adults for depression ignores the social matrix in which depression occurs, will lead to further overdiagnosis and overtreatment of minor morbid mental states, and further overburden mental health services.

A Glut of Antidepressants” was published on August 12, 2013, in The New York Times. It mentioned an April 2013 study published in the journal Psychotherapy and Psychosomatics that found almost 62% of 5,639 individuals “who had been given a diagnosis of depression within the previous 12 months did not meet the criteria for major depressive episode.” Several other studies have reported that: “diagnostic accuracy is low in general practice offices.” The study’s lead author said: “The vast majority of individuals diagnosed with depression, rightly or wrongly, were given medication.” Doctors must resist the temptation “to take out the prescription pad and write down an antidepressant and hand it to the patient.”

The NYT article did indicate that not only are doctors prescribing more medication, their patients are demanding it more. I think this is a likely an outcome of the decision to permit direct-to-the-consumer advertising for pharmaceuticals in 1997. See “Pharma and Advertising” or “Not Everything is As It Appears” for more on this topic. If anything at all was done to “confirm” the patient’s or doctor’s impression that there was a depressed mood state, using a quick screening instrument seems likely given the short time period most patients spend with medical staff in a primary care setting.

James Davies, the co-founder of the Council for Evidence-Based Psychiatry, wrote “The Sedated Society,” where he commented on how a BBC radio program had failed to mention the problem with the PHQ-9 (mentioned above) and the GAD-7, which he said two of the most powerful questionnaires in the NHS (National Health Service). He said they have been used throughout the primary care system in the UK to assess whether or not a person has depression or anxiety. He said: “They set a very low bar for what constitutes having a form of depression or anxiety for which a drug should be prescribed.” He said the tens of millions of people who filled out these screening questionnaires don’t know that Pfizer Pharmaceuticals paid for their development and continues to hold the copyright for them. Their distribution throughout the NHS was paid for by Pfizer, which incidentally makes two of the most prescribed antidepressant and anti-anxiety drugs in the UK.

Although the BBC didn’t get Davies’s message out about the PHQ-9 and GAD-7, several news outlets did. At Vice, Hannah Ewens said “a few of us in the office” took the test, with everyone except one person got at least a score of mild depression. She personally scored within the “moderately severe depression” range, but doesn’t have depression at the moment. “If I have trouble sleeping ‘on several days’ or ‘nearly every day’ that bumps up my score significantly. And herein lies the problem: all of the indicators are symptoms of a modern lifestyle as well as signals of depression.” Ewens added that James Davies believes reliance on these questionnaires is becoming too commonplace because GPs don’t have the time to do proper interviews.

The Telegraph, another UK media outlet, echoed the Davies concern that the threshold for identifying possible depression was too low. Henry Bodkin noted that a PHQ chart was likely present in almost every GP consulting room over the last 20 years. He also said critics like Davies have said the GAD-7, also developed by Pfizer to screen for anxiety, sets the diagnosis bar too low. “These forms have a very low criteria for anxiety and depression. . . . Millions of people have filled them in and got medication, but did they know they were developed by Pfizer?”

Pfizer enlisted two “rock stars” in the field of psychiatric diagnosis to develop the PHQ-9 and GAD-7: Robert Spitzer and Janet Williams. Spitzer was the chairperson for the seminal changes incorporated into the DSM-III. Originally Williams was his text editor; later she became his wife and collaborator. Listen to an All Things Considered broadcast on Spitzer and the DSM, “The Man Behind Psychiatry’s Diagnostic Manual.”

In the September of 2001 issue of the Journal of General Internal Medicine, Kurt Kroenke, Robert Spitzer and Janet Williams published “The PHQ-9.” Their article examined “the validity of a brief, new measure of depression severity” called the PHQ-9. They concluded that data from their two studies provided “strong evidence for the validity of the PHQ-9 as a brief measure of depression severity.” Kroneke et al. also said brief measures were more likely to be used in the busy setting the typical medical practice. The brevity of the PHQ-9 was thought to make it “an attractive, dual-purpose instrument for making diagnoses and assessing severity of depressive disorders.” The Acknowledgements section said the development of the PHQ-9 was underwritten by an educational grant from Pfizer US Pharmaceuticals. Scrolling down further you’ll see:

From the Primary Care Evaluation of Mental Disorders Patient Health Questionnaire (PRIME-MD PHQ). The PHQ was developed by Drs. Robert L. Spitzer, Janet BW Williams, Kurt Kroenke, and colleagues. . . . PRIME-MD is a trademark of Pfizer Inc. Copyright 1999 Pfizer Inc.

Then in the May 2006 issue of JAMA Internal Medicine, the same three authors introduced the GAD-7, a brief self-report scale to identify generalized anxiety disorder (GAD). Not surprisingly, they concluded: “The GAD-7 is a valid and effective tool for screening for GAD and assessing its severity in clinical practice and research.” They expected the GAD-7 to have “considerable utility in busy mental health settings and clinical research.” Once again is an acknowledgement that the development of the GAD-7 was underwritten by an unrestricted educational grant from Pfizer Inc.

If you want to see or use copies of these scales, Pfizer’s lawyers have been clearly involved in dialing back the company’s responsibilities if the scales don’t live up to their creator’s optimistic expectations. On the Pfizer website, on the “Terms of Use” page for the two scales, is the following. Pfizer said since the questionnaires relied on patient self-report, all responses should be verified by the clinician. A definitive diagnosis should be made on clinical grounds, “taking into account how well the patient understood the questionnaire, as well as other relevant information from the patient.” Diagnoses should rule out normal bereavement, Bipolar Disorder, and other potential causes of depressive symptoms. Then there is the following disclaimer. The “all caps” formatting is in the original.


The rhetoric about the GAD-7 and PHQ-9 and its variations related by their creators, Spitzer, Williamson and Kroneke seems to have been negated by Pfizer. Instead of the PHQ-9 being “an attractive, dual-purpose instrument for making diagnoses and assessing severity of depressive disorders” and the GAD-7 being “a valid and efficient tool for screening for GAD and assessing its severity in clinical practice and research,” Pfizer disclaimed all warranties expressed or implied for a particular purpose. Pfizer nor any party involved in creating the PHQ/GAD-7 will be liable for any damages from access or use of these questionnaires. Any users access and use the PHQ and GAD-7 does so “at your own risk.”

It seems that Pfizer circled their wagons to avoid any corporate liability coming from the use of these questionnaires despite the fact they paid for their development and continue to market them aggressively to general practitioners in the US and the UK. But the potential for the over diagnosis and over treatment of depression through the PHQ-9 has now reached a new height. Psychiatry Advisor reported in August of 2017 that Google announced whenever someone searches for ‘clinical depression,’ they have an option to take the PHQ-9. Google partnered with NAMI, the National Alliance on Mental Illness, to make depression screening with the PHQ-9 part of searching for ‘depression’ on the site. NAMI said: “We hope that by making this information available on Google, more people will become aware of depression and seek treatment to recover and improve their quality of life.”

So where did all that effort with the PHQ-9 and GAD-7 get Pfizer? Pfizer currently hold the rights to the brand rights for Xanax (alprazolam), an anti-anxiety drug, and Zoloft (sertraline), an antidepressant. Both have been available as generics for a number of years. And although The Telegraph article didn’t name Pfizer’s top selling antidepressant and anti-anxiety drugs in the UK, they must be the same two. Up-to-date yearly sales data for psychiatric drugs is hard to come by, unless you pay an organization like IMS for access to their sales data. But there is data available from 2013.

IMS Health listed the top 25 dispensed prescriptions in the US in 2013. Xanax and its generic, alprazolam, was the 13th most prescribed medication. Zoloft and its generic, sertraline, was the 18th most prescribed medication. Among the psychotropic medications listed they were number one and number three respectively. PsychCentral reported similar findings, with the added information that Xanax was the number one prescribed psychiatric drug in 2005, 2009, 2011 and 2013. Zoloft sank as low as the 4th most prescribed psychiatric drug in 2009 and the 3rd most in 2011.


It Takes Away Your Soul

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In case you missed it in July, there was an annual day of awareness … for the problems that result from the prescription and use of benzodiazepines. World Benzodiazepine Awareness Day (W-BAD) is on July 11th. The first W-BAD was in 2016, so it’s just getting started. The need for greater awareness of the adverse effects from benzos can be seen in the 2016 W-BAD promotional video, here. It’s over 24 minutes long, so be prepared to spend some time. If that’s too much time for you to take at the moment, here’s one take away quote from Wendy in Melbourne Australia about her experiences while on and then getting off of benzos: “It takes away your soul.”

I was pleasantly surprised to see an extended quote on the dangers of benzodiazepines from Dr. Neil Capretto was used in the 2016 W-BAD video. Dr. Capretto is the Medical Director for Gateway Rehabilitation Center, a drug and alcohol treatment program I’m familiar with in Western Pennsylvania, Dr. Capretto said:

People were innocently put on this medication [benzodiazepines] and in some instances it works out well. [But] there is a significant risk and we see it all of the time. Many people who have lost many years of their lives, who have lost jobs, been on the verge of suicide. I’m aware of cases where people have committed suicide. The drug can be dangerous, it can be fatal. During withdrawal the heart rate can go up, they may have a seizure, sometimes the body temperature can go up and in some cases it’s fatal.

The W-BAD video has individuals from around the world, telling about their experiences while using benzos, when tapering off them, and the ongoing protracted withdrawal experiences they suffered through. For some individuals, those adverse effects lasted months and in some cases were permanent. There were three W-BAD objective listed towards the end if the video, which are listed below.

To encourage the establishment of a mandatory maximum prescribing period of no more than 4 week, including taper period (based on the Committee on Safety of Medicines’ 2-4 week prescribing guidelines).

To encourage the establishment of ‘specialized’ withdrawal facilities for those who so desperately need them.

To encourage the provision of proper training for doctors and medical staff and to help them learn more about proper tapering practices to discontinue the drugs as well as about the serious implications of benzodiazepines.

The Committee on Safety of Medicines is an independent advisory committee that advises the UK Licensing Authority on the quality and safety of medicines. In 2005 it was replaced by the Commission on Human Medicines, combining the functions of the Committee on Safety of Medicines and the Medicines Commission. The Committee issued guidelines for UK physicians and medical professionals on the use of benzodiazepines in January of 1988. Pause for a minute. These concerns were evident almost thirty years ago.

The original document said there had been concerns regarding benzodiazepine dependence for several years, and cited a British Medical Journal article from 1980 to support the claim. It noted that withdrawal symptoms could include anxiety, confusion, insomnia, depression, and perceptual disorders. These symptoms could occur even when following therapeutic doses over SHORT periods of time (emphasis in the original). “These may sometimes be difficult to distinguish from the symptoms of the original illness.”

They discouraged the use of benzodiazepines to treat insomnia, unless it was severe and subjecting the person to extreme distress. If used, they should be used intermittently. “The use of benzodiazepines to treat short-term ‘mild’ anxiety is inappropriate and unsuitable.” When the anxiety is severe, disabling or subjecting the person to unacceptable distress they can be used for short-term relief—“two to four weeks only.”  The Committee then gave the following quote from the above noted article in the March 29, 1980 issue of the British Medical Journal. The point of all this is these concerns and recommendations with benzodiazepines have been know since the 1980s, but have been largely ignored on a global scale, as illustrated in the 2016 W-BAD video linked above.

The committee further noted that there was little convincing evidence that benzodiazepines were efficacious in the treatment of anxiety after four months’ continuous treatment. It considered that an appropriate warning regarding long-term efficacy be included in the recommendations, particularly in view of the high proportion of patients receiving repeated prescriptions for extended periods of time.It further suggested that patients receiving benzodiazepine therapy be carefully selected and monitored and that prescriptions be limited to short-term use.

Finding a “specialized” withdrawal facility can be difficult. Be careful of what the centers promise and their cost. Do your homework when searching for a “specialized benzodiazepine withdrawal facility.” A mere “benzodiazepine withdrawal facility” search will net multiple residential drug and alcohol treatment centers. Not every person who has been using benzodiazepines long enough to need medical inpatient detoxification support has been abusing benzos, and treatment at a drug and alcohol treatment center is often inappropriate. Plus the withdrawal protocol is often too rapid.

The New Beginnings Recovery Center in North Palm Beach Florida is an example of a treatment program that uses a protracted withdrawal method. I have no experience with their treatment program and can’t endorse it. But what I’ve seen of their methods fits with a patient or client-centered method of withdrawal, which I do think is best with benzodiazepines. Here is a link to the New Beginnings page on their Benzodiazepine Withdrawal Treatment Program. Here is a short YouTube video clip discussing the Heather Ashton Method for benzodiazepine withdrawal used at the New Beginnings Recovery Center.

Going slowly, at a pace controlled by the individual withdrawing from benzos, is the method most likely to produce positive results. It will take several weeks, months, and even in some cases, years. I’ve run across two medical professionals who advocate for this protracted withdrawal method, Dr. Peter Breggin and Dr. Heather Ashton.

I am personally familiar with Dr. Breggin’s work and have read many of his resources, including two that would be helpful for benzodiazepine withdrawal: Your Drug May Be Your Problem and Psychiatric Drug Withdrawal. Start with Your Drug May Be Your Problem for personal information on the process and try Psychiatric Drug Withdrawal for more technical discussions, if that’s needed. Both books discuss withdrawal from multiple classes of psychiatric drugs. There is a YouTube channel for Peter Breggin. He also has his own website with more information at: breggin.com.

The Ashton Protocol, or Ashton Method, is new to me, but from what I’ve reviewed it fits with the protracted withdrawal process I’m familiar with in Dr. Breggin’s material. Here is a YouTube clip, “Dr. Heather Ashton- Benzodiazepine Withdrawal.” You can see several other YouTube videos about her method with a “Dr. Heather Ashton” search on YouTube. Dr. Ashton also wrote “Benzodiazepeines: How They Work and How to Withdraw,” which has become known as “The Ashton Manual.”  A digital copy is available here on benzo.org.uk for free. A printed copy can be ordered.

From the brief review I’ve done so far, it seems likely to be a very helpful resource for individuals looking for assistance in getting off of benzodiazepines. Within a documentary by Shane Kenny, “The Benzodiazepine Medical Disaster,” which is linked below, Dr. Asthton said she wrote the manual for patients who weren’t getting help from the doctors. They seemed to know better what to do than the doctors. “It was for them. And the interesting thing is, although patients from all over the world have snapped it up, doctors still don’t read it.”

Protracted withdrawal will extend far beyond any acute medical withdrawal phase, and ongoing medical and therapeutic support on an outpatient basis is advisable. Getting medical support for protracted benzodiazepine withdrawal as an outpatient could be challenging. You may have to educate a willing physician on the necessity of an extended, rather than a shorter-term withdrawal. You can use the material recommended above from Peter Breggin and Heather Ashton to first educate yourself, and then any physician or psychiatrist willing to work with you on a protracted benzodiazepine withdrawal.

There are also many online information and support groups, such as: benzo.org.uk, which as been around since July of 2000. “Benzo.org.uk is dedicated to sufferers of iatrogenic benzodiazepine tranquilliser addiction.” In addition to the link to The Ashton Manual noted above, it has a wealth of information, including a FAQ document and links to online benzodiazepine withdrawal support groups on a support page. They also called out a specific support group called BenzoBuddies.

BenzoBookReview.com is a website with a list of books on benzodiazepine withdrawal. Information there includes memoirs and how-to guide books, with reviews and summaries of each book. The site is for anyone interested in information about benzodiazepine misuse and how to help benzodiazepine sufferers. That includes their families, doctors, psychologists, psychotherapists, drug counselors, and all professionals.

Other helpful resources include: Benzodiazepine Information Coalition, Beyond Meds, and Mad in America. Search the Mad in America site for “benzodiazepines.” Information on their “Withdrawal Resources” page will include a scientific literature review on withdrawal from benzodiazepines, as well as other classes of psychotropic drugs. Mad in America linked a short video by the group Benzodiazepine Recovery, “Benzodiazepine Withdrawal Symptoms” where individuals shared their top three most debilitating benzodiazepine withdrawal symptoms.

There are several helpful YouTube resources, such as Benzo Brains, by Jocelyn Pedersen. W-BAD also has a YouTube channel and a website: w-bad.org. Their YouTube channel has a short informational video (almost 3 minutes) on the risks of taking benzodiazepines. Start there to begin the education process with someone.

Look under Resources on w-bad.org for the Documentaries link. You will find information on “As Prescribed” by Holly Hardman, which is in production. Scrolling further down you will see a link to another documentary, “The Benzodiazepine Medical Disaster” by Shane Kenny. It features an in depth interview with Heather Ashton. Also remember what Melanie said about why this information on benzodiazepines is so important: “It takes away your soul.”