For readers of our newsletter, this post might feel “different” from the others. Usually we like to talk about what you can do to help yourself or your loved one when it comes to addressing substance issues and finding support or treatment that will help changes last. In this post we are going to do something different because we are angry and scared about the misinformation that consumers are faced with everyday as they look for treatment for themselves or someone they care about.
An estimated 2 million Americans are dependent on opioids. The Centers for Disease Control reports that 115 Americans died daily in 2016 from opiate overdoses (42,249 deaths, five times higher in 2016 than 1999), and that 40% of these deaths involved a prescription opiate. Despite this deepening crisis, there is hope that a number of FDA approved, evidence-based Medication Assisted Treatments (e.g., buprenorphine, naltrexone/Vivitrol, methadone) for opioid use disorders can help. Studies have found that these medications support long-term change (including abstinence from opiates) and significantly reduce overdose rates. Yet the traditional drug and alcohol treatment industry has been shockingly slow to support their use. Even more astounding is that many doctors in the treatment industry have not been educated about their effectiveness or trained to use them despite comprehensive efforts such as the Surgeon General’s Report last year reiterating the important role of these treatments.
Why the delay? There continues to be a strong belief in the public and among many treatment providers that if you utilize medication to recover from a drug problem, you are not “really sober”. This bias persists even though mountains of evidence from well-conducted research studies demonstrate that medication-assisted treatments (MATs, like buprenorphine and naltrexone) save lives. Despite their benefits, MATs have been adopted in less than half of private treatment programs. Even in programs that do offer MAT options, only about a third of patients receive them.
In an effort to understand this at the ground level, we decided to do a little experiment. We know that when a family reaches out looking for treatment for a loved one, they are usually vulnerable, scared, and desperate for someone to offer advice and some hope. And often, in their fear, they will take the advice of the first person they speak to, assuming reasonably that that person is educated in substance use and has a clear understanding of current effective treatments. So we did what many people do: an internet search! Just like many desperate families do when they are looking for help. We typed in “top rehabs in the US” and “best rehabs in the country”, created a list of 34 rehabs that came up on these searches, and called them.
We called looking for treatment for “our brother” who was “in trouble with heroin”. In these calls we asked each program the same series of questions about their use of MATs like Vivitrol and Naltrexone (opiate blocking medications), and Suboxone (an opiate maintenance medication), including their treatment policies and stance on these medications. (We asked them a bunch of other questions but that is for another post)! Our mission? To see if the treatment landscape was changing now that multiple studies (over many years!) have found these medications to be life-saving. What we found is disturbing.
Out of the 34 residential programs called, less than 40% (n = 13) of the programs would consider maintaining someone on Suboxone (buprenorphine) or discharging a patient on suboxone. The rest (n = 19) only used Suboxone during detox as a taper medication, while 2 rehabs “never use suboxone”. One of these programs said, “we want to get them off everything, otherwise he would be a hopeless opiate addict for life.”
Hopeless addict for life? Really? Buprenorphine, which is a partial opioid agonist, does activate opioid receptors in the brain but does not produce the maximal effects that full opioid agonists (e.g., heroin) do. It does not produce feelings of euphoria, but it will produce enough effect to quell cravings, provide relief from withdrawal, and satisfy the brain into thinking it is receiving a full agonist. It is protective in lowering overdose risk as it blocks the receptor sites in the brain that opiates would otherwise attach to. It allows many opiate users to build a stable life without fighting off cravings to use everyday and protects them from overdosing if they relapse to opiate use (both “street” opiates like heroin and prescription opiates) while on the medication.
In these 34 contacted programs (“best of the best”!), openness to using Vivitrol was a little higher, with 65% of the rehabs saying that they could consider discharging someone on it. Vivitrol is the intramuscular injection (like a flu shot, for example) of Naltrexone, a medication that blocks opioids from binding with the opioid receptors in the brain, thereby eliminating any sense of a high. It last approximately 4 weeks and multiple studies have found that it contributes to reduced overdose rates among opiate users. It is not an opioid itself (unlike suboxone or methadone), which may account for it’s slightly more positive reception in our surveyed rehabs, by countering some of the (unfounded and stigmatizing) beliefs that an opiate user wanting to be on opioid medication is “just a drug user looking for another drug”.
Unfortunately, of the 12 programs that did not discharge clients on Vivitrol, 4 of them did not even know what it was! One of the programs we called said “We really try and get patients off of everything and we would not want to discharge him on Vivitrol” and another said “I don’t know what that is, but if you spell it for me I can look it up and see if we will use it”. We ask you: does your diabetes doctor not know what insulin is? Does your cancer doctor not believe in chemotherapy?
Many of the inpatient/residential facilities we talked to made comments that showed they do not understand these life-saving medications, that they do not value clients’ experiences or wishes, and that they are using fear and scare tactics to pressure people into treatments that may not be appropriate for them. One intake coordinator said after a 5 minute description of the potential referral, “I don’t want to sound aggressive, but he could die today…” This kind of statement, made after a short phone call and aimed at a scared family, is preying on their fears in an effort to book a client. This is what you’d expect when you’re buying a used car, not what you’re hoping for when you’re looking for help for a life-threatening problem. Several of the programs used other tried and true sales techniques, like transferring callers to many different programs without explanation, or making suggestions that they close the deal and “get on a plane right now.” And others said the fictional brother clearly “needs a lot of treatment, possibly a year,” without offering to speak with him or gathering more information. And “he could die today”? The refusal to consider use of MATs will leave clients treated at these facilities more vulnerable to dying.
In fact, if you seek treatment for an opioid use problem, there is a significant risk that the treatment professional you speak with will either not offer these medications or have ideologically-based opinions about them that negatively influence how you feel about being prescribed them. As many opioid users will attest, there is a sense that you are “just an addict looking for another drug.”
We’ve had countless people come to us at CMC who have been in multiple rehabs and never once were encouraged to be on medicatIon assisted treatments. This is in spite of the data that suggests as many as 90 percent of people detoxed completely off opiates relapse within the first 1-2 months unless treated with these medications.
The takeaway? If you or someone you love is one of the two million Americans estimated to be dependent on opioids, please demand better. Our nation’s opioid struggle is an undeniable tragedy, and is one of the worst public health crises in the nation’s history. It is made all the more tragic by the fact that there are many viable, proven treatments for the problem yet treatment programs continue to refuse to look at the science. This must change if we are to stem the tide of opioid addiction in this nation and prevent more loss of life.
Anyone looking for treatment needs to really investigate the different programs and ask lots of questions. Many people do more research about which car to buy than which treatment program to attend. That needs to be reversed. And clients should enter this process expecting their questions to be answered and answered well! If you’re not sure about something you heard, then it’s probably not right (or the right place for you). Demand better service, and you will have a better experience.
The anesthesia medication ketamine has shown promise in treating depression, but its exact effects on the brain are unclear. Now, researchers have discovered that the drug changes the firing patterns of cells in a pea-size structure hidden away in the center of the brain. This could explain why ketamine is able to relieve symptoms of depression so quickly—and may provide a fresh target for scientists developing new antidepressants.
“It’s a spectacular study,” says Roberto Malinow, a neuroscientist at the University of California, San Diego, who was not involved in the work. “It will make a lot of people think.”
In clinical trials, ketamine appears to act much faster than existing antidepressants, improving symptoms within hours rather than weeks. “People have tried really hard to figure out why it’s working so fast, because understanding this could perhaps lead us to the core mechanism of depression,” says Hailan Hu, a neuroscientist at Zhejiang University School of Medicine in Hangzhou, China, and a senior author on the new study.
Hu suspected the drug might target a tiny region in the middle of the brain called the lateral habenula, the so-called “anti–reward center.” This region inhibits nearby reward areas, which can be useful in learning; for example, if a monkey pulls a lever expecting a treat but never receives it, the lateral habenula will reduce the activity of reward areas, and the monkey will be less likely to pull the lever in the future. But research over the past decade has suggested that the area may be overactive in depression, dampening down those reward centers too much.
In a series of experiments using mouse and rat models of depression reported today in Nature, Hu and her colleagues found that ketamine did affect the lateral habenula—but it was the pattern of firing, rather than the overall amount of activity, that proved crucial. A small proportion of the neurons in the lateral habenula fire several times in quick bursts, rather than firing once at regular intervals; the team found that “depressed” rodents had a lot more of these quick burst cells. In brain slices from normal rats, only about 7% of cells were the bursting type, but in rats bred to display depressionlike behavior, the number was 23%.
Direct recordings from the neurons of live mice showed the same pattern: Animals that had gone through a stressful procedure had more bursting cells in the lateral habenula. And, importantly, this bursting behavior appeared to cause depressionlike states. When researchers used optogenetics—a technique that allows cells to be switched on and off with light—to increase the amount of bursting in the lateral habenula, mice behaved in a more “depressed” way, remaining motionless when forced to swim in a container of water, for example. This kind of despair is thought to be similar to the feelings of hopelessness experienced in depression.
When “depressed” mice and rats were given ketamine, the number of bursting cells was much lower, similar to the number in normal animals, Hu’s team found. And even when the researchers forced the neurons to fire in bursts, animals that had been given ketamine no longer showed depressionlike behaviors.
Hu says that neurons firing several times in quick succession produce a more powerful signal. This means that bursting cells may be sending particularly strong messages to dampen down activity in reward areas, which could lead to depression. “Bursting has a special kind of signaling power,” Malinow says. “You get more bang for your buck.”
The findings could also explain why ketamine acts so quickly. By immediately blocking bursts in the lateral habenula, the drug releases the reward areas from those strong signals. This suggests that other drugs that reduce burst firing could also alleviate depression, whether they act on the same receptors or different ones. “Anything that can block the bursting … should be a potential target based on our model,” Hu says. In an accompanying paper, her team reports that a protein found on astrocytes, another type of brain cell that interacts closely with neurons, could be one of these targets.
Panos Zanos, a neuropharmacologist at the University of Maryland in Baltimore, says the immediate effects of the drug in the lateral habenula were interesting. “I’m very excited … to see whether this [also] applies to the long-lasting antidepressant effects of ketamine,” he says. “This is a great study that adds to the literature on how ketamine might work.”
Reuters Health – Long-term consumption of tiny amounts of lithium may reduce the risk of Alzheimer’s disease and other forms of dementia, but only if the dose isn’t too small, according to a study that looked at levels of the element in drinking water throughout Denmark.
In fact, the wrong amount may actually increase dementia risk, researchers report in JAMA Psychiatry.
Lithium, used for years in drugs to treat depression and bipolar disorder, is a naturally-occurring element in drinking water in Denmark but levels vary by location. The team compared the estimated amount found in the water supplies of 275 municipalities to the rates of dementia, including Alzheimer‘s, in those areas.
Residents who had been diagnosed with dementia from 1995 through 2013 tended to consume lower levels of lithium in their water than residents whose water had higher levels. However, there was a middle level of consumption where dementia risk was elevated or unchanged.
Compared to those whose water contained lithium concentrations of 2 to 5 micrograms of lithium per liter, which served as the baseline, the rate of dementia was 22 percent higher when the drinking water concentration was 5 to 10 micrograms.
Levels of 10.1 to 15 micrograms had no effect on the risk.
But at levels of 15.1 to 27 micrograms per liter, the dementia risk seemed to drop by 17 percent compared to places where the levels were 2 to 5 micrograms.
“It’s a really interesting study but you have to be careful about inferring cause and effect,” said Dr. Brent Forester, head of the geriatric division of McLean Hospital, a psychiatric hospital in Belmont, Massachusetts affiliated with Harvard Medical School, who wasn’t involved in the research.
In a telephone interview with Reuters Health, he called the fact that the effect didn’t strictly increase or decrease based on the lithium dose “a worrisome sign” and said the non-linear trend “could be a warning that there’s another confounding variable. It may not be the lithium itself but something about the mechanism of action might be protecting against developing dementia. The biology of lithium is worth exploring, for sure.”
The chief author of the study, Dr. Lars Vedel Kessing of the University of Copenhagen, did not respond to requests for an interview. But the researchers cautioned in their paper that “it cannot be excluded that other, unobserved environmental or social care factors related to individuals’ municipality of residence might have confounded the association between lithium exposure and dementia rate.”
The idea of a link between lithium and Alzheimer’s has been around for years, Forester said.
“Over a decade ago, a pathology study that looked at the brains of patients who had a lifelong history of bipolar disorder and were treated with lithium versus those with a lifelong history of bipolar disorder who were not on lithium showed that those exposed to lithium had about one sixth the rate of Alzheimer’s pathology,” he said. “It raised a lot of interesting questions and eyebrows about the mechanism.”
Other research has shown that low doses – but doses far higher than found in the drinking water in the Denmark trial – may reduce the odds of Alzheimer‘s. But research has been limited because drug companies don’t stand to make a lot of money from lithium therapy.
Forester said he would not advise people to try using lithium to ward off Alzheimer’s because the drug can harm the kidneys, although the levels seen in the drinking water in Denmark are too low to pose a serious risk.