Addiction Treatment, Science, and Dead Rats

In my last post I teased that I would write about fake science.  I’ll try to make it interesting.

The internet allows everyone to do research about symptoms and treatments for any condition. If not for need for prescriptions, people could act as their own doctors.  But a huge dose of caution is necessary before anyone takes that path.

Realize first that doctors don’t treat themselves or even their family members.  The saying that ‘a person representing himself in court has a fool for a lawyer’ applies double in healthcare.  Treating someone close to one’s self introduces a bias that is hard to explain, but easy to notice.  As an example, I see a doctor annually to monitor a progressive condition that threatens my vision.  I would like to know the answer to a simple question:  how bad is it?  If I have a patient with that condition I can look at images of his/her retina and have an immediate, rough sense about what the person is facing.  But when I look at my own images and test results I sense nothing beyond fear or relief.  The problems with self-assessment are of course greater in the field of psychiatry and addiction.  After my relapse in 2001 I was told I needed treatment, and my assessment called for a brief refresher course on the twelve steps.  Three months later, still in residential treatment, I recognized how wrong I was.

A larger problem is that research on the internet is nothing like the research used by doctors or scientists.  There are a few sites that offer true research, such as Pub Med, where you can search my name and see the articles from my PhD work in the 1980s.   Doctors at academic hospitals or institutions often have access to an electronic database including thousands of peer-reviewed journals.  In grad school I spent time each morning in the library, reading the Science Citation Index for new stories about vasopressin and then searching the stacks for the article (medical libraries have so many journals that they take up 4 or 5 floors or more of a large building, with narrow halls between floor-to-ceiling shelves).  In the stacks I sometimes realized I was standing amidst the results of the hard work of millions of scientists over the past 50 years.

The information on the internet is useful because it helps patients ask the right questions.  But it is a mistake to consider it as research, or even to assume it is correct.  Doctors and scientists (and any good health practitioners) rely only on peer-reviewed literature.  And even then, a good scientist gathers a sense, over time, of the better peer-reviewed journals vs. the ones with less credence.  What is peer review?  When a scientist submits research for publication, the article is sent to 3 or 4 independent reviewers who work in the same field but have no connection to the author of the study.  I am a peer-reviewer for a couple of journals.  When I receive an invitation to review a study I have to disclose any bias or connection to the study or authors.  If I accept the invitation I have several weeks to carefully review the study, noting if the findings are valuable, whether the groups were sufficiently randomized and blinded, whether the statistics are correct or if a statistician should be involved, and whether the findings support the conclusions.  I then tell the journal editor my opinion, including whether the study should be accepted, rejected, or accepted with certain revisions.  Peer reviewers are not paid;  they provide the service because they recognize that the process is necessary and valuable.

The FDA regulates medications based on the results of research studies.  Some of the studies reviewed by the FDA are already published, and some may never end up in a formal publication.  But their process for evaluating medications is similar to the work of a peer-reviewer in that they determine whether the science is ‘good’ – double blinded, properly randomized, good statistics, etc.  Any claims about a medication MUST be deemed accurate by the FDA.

This post was inspired by an ad for Declinol, a supplement marketed to ‘treat’ alcoholism.  Supplements are not medications, and not subject to the same rules. Read the FAQ on the Declinol web site and note the answer about FDA approval.  Declinol is not subject to FDA approval because it is a nutrient, not a medication.  The FDA allows greater latitude for promotional claims about nutrients, but even makers of supplements are not allowed to lie.  The acrobatics of marketers of such products are sometimes funny, at least to us nerds, and Declinol is a classic example.  Note that the web page doesn’t say that it treats alcoholism or cravings;  it is a ‘SUPPORT for physical cravings, calmness, and overall well-being’.  What is a ‘support’?  Your guess is as good as mine.

Instead of making claims that can be found to be false, nutrients often show quotes by ‘satisfied customers’.  If the FDA believes that the quotes are misleading, that’s on ‘Bob from California’, not on the marketer of the nutrient.  Instead of describing how the nutrient works, nutrient marketers provide citations about the nutrient that support whatever the marketers want you to think.  So with Declinol we see ingredients like folic acid, with broad generalizations about the value of that substance.  Yes, Folic acid is valuable.  You can’t live without it.  But that’s a far cry from saying that taking extra folic acid has any value, let alone value in reducing alcohol intake.  We give folate to alcoholics in detox because they sometimes have dietary deficiencies caused by consuming nothing but alcoholic beverages.  If you eat meals a couple of times per day you almost surely have plenty of folic acid in your body, and any extra is metabolized and excreted.

Must nutrient ‘treatments’ or supplements contain a blend of vitamins.  It is very easy to write reassuring and positive statements about vitamins because by definition, vitamins (the term comes from ‘vital amines’) are molecules critical to normal function.  But many studies have shown that a typical diet provides adequate amounts of vitamins, even if that diet includes fast food.

Many nutrient ‘treatments’ also contain a couple special ingredients we’ll call ‘secret sauce’.  One secret sauce in Declinol is Kudzu, and support for Kudzu in reducing alcohol consumption can be found on Pub Med.  Like similar products, Declinol’s marketers take a finding about a substance and grossly generalize the findings to create an impression that was never part of the original finding.  According to the study about Kudzu, 20 people in a ‘natural settings laboratory’ (is that an oxymoron?) were given water, juice, and up to six beers, and told to drink at will.  And (wow) when people were given 2 grams of Kudzu first, they drank beer more slowly, and opened fewer bottles.

A couple of problems, though, in concluding relevance to treating alcoholism.  Were the 20 subjects alcoholics? It doesn’t say, but I would guess not because I don’t know if a study giving beer to alcoholics would pass the ethical review board.  Beyond that, WHY did they drink less alcohol?  If I gave you syrup of ipecac, you would probably drink less alcohol.  If I gave you a tablet of oxycodone, you would probably drink less alcohol.  That doesn’t mean that the substances are useful in treating alcoholism or alcohol cravings.  Why did the Kudzu group drink less alcohol? Did it truly reduce interest in alcohol in a study with very few subjects who may or may not have alcohol problems? Or did it leave a nasty taste in their mouths or destroy their taste buds?  Did it cause nausea or dizziness that made alcohol less enticing? Did it reduce vision so they couldn’t find the beer bottles as easily?

As for the title of this post, when I researched vasopressin one hot idea was that vasopressin enhanced learning and memory.  We measured that improvement in studies using ‘passive avoidance.’  We placed rats in a cage that had dark cubbies in one corner, and when rats invariably went into a certain cubby they received an electric shock.  We repeated the task with or without putting vasopressin into the rats’ brains and some rats ‘learned’ to avoid the electric cubby, supposedly by remembering the shock better than other rats.  There is a major flaw in the study that can often be applied to other ‘experiments’, including the one I cited about Kudzu:  the best performer in a passive avoidance task is a dead rat.

I have no idea whether Declinol reduces cravings or generates ‘well being’, whatever that is.   But nothing on their website pushes me toward that conclusion.  I hope readers will keep some of these comments in mind when the next big cure comes along.