Please help me evaluate this article from a scientific standpoint.

May 16, 2012 6:30 AM

Please help me understand whether the science in this article about SSRIs and inflammation is valid or not.

I know enough about science to understand what this article is saying, but not enough to evaluate its merits. Please help me understand whether the authors are taking undue leaps in logic or whether the foundations of the article are fairly strong.

posted by stoneweaver to science & nature (12 answers total)

Any article that says something like this " It is now common knowledge that low-grade excess inflammation is behind virtually every disease of aging." nonsense. Compare it to any article that would say " It is now common knowledge that toxins are behind virtually every disease of aging." or " It is now common knowledge that engrams are behind virtually every disease of aging."


Inflammation "prevention" is the new "antioxidant" craze. Harmless, probably, but unfounded.
posted by Patbon at 6:38 AM on May 16, 2012

"If you’re keeping up with your health knowledge, you would realize that SSRI antidepressants must be “working” by some type of inflammatory method."

Exactly what health knowledge are they referencing? "SSRIs are believed to increase the extracellular level of the neurotransmitter serotonin by inhibiting its reuptake into the presynaptic cell, increasing the level of serotonin in the synaptic cleft available to bind to the postsynaptic receptor." (Wikipedia) That has nothing to do with "inflammation"; from the first paragraph, the article you link to has its science in a questionable state, if not outright incorrect.

You're also linking to an article by a nutritionist on a site that sells nutritional supplements. SSRI safety and usage -- while still a topic for debate -- is studied and discussed by doctors in proper medical journals. The source itself is suspect.
posted by ellF at 6:47 AM on May 16, 2012 [2 favorites]

They are making a lot of big leaps. They are taking research that is probably perfectly adequate research and drawing sweeping conclusions. It doesn't seem like any of the studies they are citing are large clinical studies.

In evidence-based medicine sometimes we talk about "patient-based outcomes" - i.e. things patients actually care about (will I live longer? will I be able to walk up stairs comfortably? will my migraines become less frequent?) and "disease-oriented outcomes" or "drug-oriented outcomes" (what's my serum cholesterol? how much of drug X crosses the blood-brain barrier? does this substance increase the number of free radicals in a test tube experiment?). The research they cite is mostly looking at disease-oriented outcomes, i.e. not things real people actually care about. And a lot of the papers they cite are sort of "think pieces" with little or no evidence.

In short: I would not change anything about my life based on the research quoted in that article, nor would I encourage anyone else to do so. IANAD, IAAML*.

Also they cite the press release in the first paragraph. That is a BAD SIGN.

* I Am A Medical Librarian
posted by mskyle at 6:47 AM on May 16, 2012 [5 favorites]

Let's unpack that first paragraph.

When you see a headline like this in the news, “Anti-inflammatory Drugs Reduce the Effectiveness of SSRI Antidepressants,” what does it make you think?

Not sure what they're getting at, but it makes me think that NSAIDs might, through either their intended or adverse effects, reduce the uptake of SSRIs.

The impression given is that if you are taking an SSRI then you shouldn’t take any pain pills if you want the antidepressants to work – which is the clear message of the press release that accompanied the study.

Well, no, the clear impression is that they might reduce the effect, so I should discuss taking NSAIDs with my doctor(s) to make sure that if I need to embark on a long term course of NSAIDs, that I might need to adjust SSRI doses *or* change meds.

If you’re keeping up with your health knowledge, you would realize that SSRI antidepressants must be “working” by some type of inflammatory method.

The question is begged!

No. It does not mean that SSRIs work by an inflammatory reaction. It means that NSAIDs, which have many effects beyond anti-inflammatory ones, reduce the effectiveness of SSRIs. Indeed, SSRIs have a limited *anti-inflammatory* effect, mostly against cytokine processes, which is in direct contrast to what the article states.

This article triggered a bunch of my kook signals. I'm ignoring it as a useful source of information on SSRIs. There are some real questions about SSRIs, esp. in regards to effectiveness on mild-to-moderate depression, but this article is just wrong about how they work and why NSAIDs conflict with them. SSRIs, as a class, have repeatedly proved effective against severe depression, and compared to TCAs and MAOIs, they definitely have a better side effect profile.

And, in case anybody's happens to catch this, MAOI + SSRI is *BAD*. Indeed, if you're on an MAOI, you must be very careful about drug and food interactions, and SSRIs are one of the bad ones. Because of side effects, SSRIs and SNRIs have moved to the first tier, TCAs are second, and MAOIs are reserved only for severe cases of depression that do not respond to anything else.
posted by eriko at 6:54 AM on May 16, 2012 [2 favorites]

In brief, one way SSRIs are supposed to work is by enhancing the flow of serotonin – an effect that would be felt immediately upon taking. It is well recognized that an additional mechanism is in play, as for many it takes several weeks or longer before mood seems to improve. This latter effect is due to the SSRI medication progressively accumulating in glial cells, inducing a highly inflammatory toxic response, and triggering the release of BDNF. Now you can understand why taking anti-inflammatory drugs would interfere with SSRI function.

Huh, whut?

I've been reading up on antidepressants and immune suppressors - while I've seen some information that it's not all about the Serotonin, the "article" here doesn't reference the mechanism I've read about, and is implying that the mechanism is only the accumulation of the SSRI in the body. It's not.

Anti-inflammatory statements are redherrings as well, rather (heh) inflammatory to include.

Additionally, not all inflammation is the same, the mechanisms triggering them and controlling them are vastly different in different people. Not all depression is the same, not all 'depression' drugs are the same, and not everyone is affected by their illnesses or the medicines + lifestyle changes to treat them the same.

This dude is trying to sell you magic herbly things.
posted by tilde at 6:58 AM on May 16, 2012

Thank you to mskyle and eriko - those are exactly the kind of answers I'm looking for. When something sets off my "kook signals" I don't want to dismiss it without understanding why it's bad, particularly when it seems to be well cited. I am interested in more unpacking of the science stuff further down in the article if anyone wants to venture there.
posted by stoneweaver at 6:58 AM on May 16, 2012

"Board certified nutritionist" means jack shit. At least in the US, anyone can call themselves a "nutritionist." It's not a protected term like "dietitian." The latter requires training, actual certification, etc.
posted by griphus at 7:00 AM on May 16, 2012

The board by which he is certified, meanwhile, is the "International and American Associations of Clinical Nutritionists" are on Quackwatch's big list of untrustworthy organizations.
posted by griphus at 7:04 AM on May 16, 2012

Comments about the source of the article and the author are much less useful to me. It's easy to dismiss things because of where they come from, but it doesn't help me understand why it's not good science, which is what I'm really interested in.
posted by stoneweaver at 7:05 AM on May 16, 2012

it doesn't help me understand why it's not good science

It's not good science because.........
- Almost no reliable science is presented and what is there is buried in health-scare double-speak.
- This is a marketing website, not a medical resource.
- This guy is not a doctor, but presenting solutions to complex medical issues as if he was one.

This guy is just a New Age Snake Oil Salesman

Way too much info, inflammatory predictions of doom in the title and not enough hard facts. Way, way, way too many Google entries for this person and the customer service 800 number? Please. This person may be qualified in some way, but he seems to be equally, if not more qualified in manipulating SEO. The whole thing just doesn't pass the sniff test. Is it junk science? Probably so. Especially compared to claims of other people like this who turned out to be frauds.

Be safe - consult with a real doctor, not some self styled health expert. If you want real scientific answers, that is a great way to start.

However, if you want to improve your complexion or lose weight or feel that your wallet is just too heavy with all those pesky dollar bills, give him a call. Make sure you have your credit card ready too just for good measure.
posted by lampshade at 7:27 AM on May 16, 2012 [2 favorites]

Nerve cells do not split and divide like other cells in your body. Rather, nerve cells must either fix themselves or have a strategy to develop new nerve growth, and both processes require BDNF. Thus, one way to stimulate BDNF is to injure nerve cells.

It is this latter strategy that SSRI antidepressants utilize – in a manner never intended by Mother Nature. The details of this rather bizarre method of operation are explained in a review article ...

So the article saying that SSRIs damage nerve cells to cause your body to repair itself with BDNF. I am not a scientist but I see nothing of that in the actual study report.

Here's something, though not quite what I was looking for:

The birth of neurons in the mice takes about two or three weeks — about the same time it takes for antidepressants to take effect. Might the psychiatric effects of Prozac and Paxil be related to the slow birth of neurons and not serotonin per se?

...

When Hen measured neuron birth in the hippocampi in depressed monkeys, it was low. When he gave the monkeys antidepressants, the depressed symptoms abated and neuron birth resumed. Blocking the growth of nerve cells made Prozac ineffective.

Hen’s experiments have profound implications for psychiatry and psychology. Antidepressants like Prozac and Zoloft, Hen suggested, may transiently increase serotonin in the brain, but their effect is seen only when new neurons are born. Might depression be precipitated by the death of neurons in certain parts of the brain?
posted by tilde at 7:33 AM on May 16, 2012 [1 favorite]

If you’re keeping up with your health knowledge, you would realize that SSRI antidepressants must be “working” by some type of inflammatory method.

Once I got to this sentence I pretty much stopped because I've walked paths in these woods before. None of them lead to Grandma's house.

Yes. Aspirins are anti-inflammatories and prevent inflammation. But, well, last night I did my first long bike ride of the season and today my legs hurt and are warm to the touch - keeping up with my health knowledge, I know this is IL-6 mediated inflammation. Yet, somehow, I think I'm going to have a hard time finding a market for my article on why Exercise Causes Brain Damage, Breast Cancer, and Early Mortality.

There is definitely a bad side to inflammation, but it's also part of the healing process. You'd miss it if it were gone.
posted by Kid Charlemagne at 8:17 AM on May 16, 2012