NBC News has a good report on a small, new phase 2 clinical study that suggests laughing gas (nitrous oxide) might provide antidepressive benefits for folks who have treatment-resistant depression.

As you might know, ketamine has proven a ground-breaking new treatment for depression by blocking N-methyl-D-asparate receptors in the brain, as opposed to the more traditional serotonin receptors.

Well, researchers suggest laughing gas works via a similar mechanism, and perhaps that’s behind the benefits for treatment-resistant sufferers.

You can read more here, and remember it’s a small study, it’s phase 2 and there’s a lot of work to be done.

Also, this doesn’t, by any means, suggest that traditional SSRIs don’t work.

For some, they work spectacularly well. For others, not. And that’s because we all have different brains and brains are complicated.

The two simple background facts for this interesting, new study.

First, there’s a neurotransmitter in the brain called serotonin. It’s often called the “happy chemical” because it helps stabilize our mood and feelings of well-being and it impacts the whole body.

You’ve heard it before — not enough serotonin (or serotonin imbalance) and you’re set up for depression and anxiety. Thus, we get SSRI antidepressants that seek to increase or rebalance serotonin levels in the brain.

Second, serotonin has a transporter protein, 5-HTT, and it “pumps serotonin away from the cerebral neuron synapases.”

So theoretically, the higher your levels of 5-HTT, the lower your levels of serotonin, because more serotonin is getting pumped away, right?

Now here’s where it gets strange.

Studies have shown that people with depression actually have lower levels of 5-HTT (the transporter) which doesn’t make immediate sense, at all, because that would suggest depressed people have more serotonin in the brain. Or at least, not as much serotonin getting pumped away by 5-HTT.

Well, a brand new study published in Translational Psychiatry suggests, yes, we need to think about rethinking how the serotonin system works in depression.

Researchers treated 17 patients with depression and found that 13 had significant improvement. Great.

Now here’s the interesting thing — after treatment, their levels of 5-HTT averaged about 10% higher than the healthy control group.

In other words, depression treatment raised the levels of the transporter (5-HTT) that pumps serotonin away from the brain!

What does it mean, though?

Researcher Dr. Johan Lundberg explained in the news release:

“One possible interpretation is that the serotonin system doesn’t cause depression but is part of the brain’s defence mechanism for protecting itself against depression.

One might hypothesize, for example, that the level of 5-HTT drops when an individual is subjected to stress, such as during a depressive state, and that the level rises or normalises when this stress goes away.

It’s important to point out, however, that even if these ideas are raised by our study, its design doesn’t allow us to draw any conclusions about why levels of 5-HTT change.”

https://eurekalert.org/pub_releases/2021-05/ki-sti050621.php

This is just another important piece of the depression puzzle, and shows how inscrutable a medical condition it really is. Any brain condition is.

And that’s why it’s so hard to find an antidepressant that brings immediate relief, because everyone is different.

I recently wrote about a wonderful new study, though, that suggests we’re getting closer to finding the right Rx on the very first try.

Researchers at the Indiana University School of Medicine developed a blood test, “composed of RNA biomarkers, that can distinguish how severe a patient’s depression is, their risk of severe depression in the future and their risk of future bipolar disorder, or manic-depressive illness.”

Oh and, crucially, the test then gives doctors the tools to pick the Rx that would work best for you. Without theoretically having to try every singe one on the shelf.

I do think that we’re getting closer to the point where we can go to Quest or LabCorp, get our blood drawn, and then get a great Rx recommendation within a week.

That, of course, would be wonderful and would save so, so many lives.

“This new generation whines, whines, whines,” I can just hear Christians complain.

Well, we dismiss the warning signals at our own peril.

Far worse, at our precious children’s peril.

The New York Times has a terrific read on a rare but real phenomenon — depression among children, ages 3-7.

It’s often a precursor to serious depression later on in life, and I remember my first bout of nihilistic thought around the age of 4-5. And by that I mean, I couldn’t imagine living the rest of my life and just wanted to get it over with. This, despite two loving parents.

Of course, I didn’t share those persistent, nihilistic thoughts with anyone, and of course most children who have them don’t. They barely understand them. But that doesn’t mean they’re not feeling them.

We can already hear the skeptics, right? “You just want to line the pockets of big pharma by giving these kids antidepressants.”

No, child psychiatrists certainly don’t want that for children as young as these.

Instead, there are two things they suggest we do.

First, look out for signs that your child is seriously depressed.

The NY Times:

“When young children are depressed, Dr. Kovacs said, it’s not unusual for “the primary mood to be irritability, not sadness — it comes across as being very cranky.” 

The best way for parents to recognize depression in young children is not so much by what a child says as by what the child does — or stops doing. Look for “significant changes in functioning,” Dr. Kovacs said, “if a child stops playing with favorite things, stops responding to what he used to respond to.”

This might mean a child loses interest in the toys or games or jokes or rituals that used to be reliably fun or entertaining, or doesn’t seem interested in the usual back and forth of family life.

The best way for parents to recognize depression in young children is not so much by what a child says as by what the child does — or stops doing. Look for “significant changes in functioning,” Dr. Kovacs said, “if a child stops playing with favorite things, stops responding to what he used to respond to.”

This might mean a child loses interest in the toys or games or jokes or rituals that used to be reliably fun or entertaining, or doesn’t seem interested in the usual back and forth of family life.”

So what’s a concerned parent to do?

First, talk to your pediatrician. They should know about local resources for helping this kind of thing.

Second, get treatment.

It’s often called PCIT (“Parent-Child Interaction Therapy“) and helps parents learn how to praise their child in ways that bolster their feelings of self-worth, because remember self-loathing is a warning sign of depression in a child.

Third, Christians, we really need to to understand that children are children.

If we tell them they’re accepted by Christ and beloved, what does that really mean to a child who believes they’re not even accepted and loved by anyone?

It’s up to us to model Christ’s love while we tell them about his love. Otherwise, it’s counterproductive.

And remember that a five year old is a five year old!

Their brains aren’t really great yet at even processing Christianity or 99% of the Bible stories most Christian parents tell them. Of if they do, they get the wrong thing from them because these are still kids who think monsters live under the bed. On no evidence, and against our assurances.

I can tell you, without a doubt, that those Bible stories were probably the most disturbing thing swirling around in my four year old brain, and it’s remarkable that in a Christian culture where movies must be “nice, sweet, and gentle” (vomit) even for sixteen year olds, we nevertheless regale kindergartners in Sunday school with stories about God drowning everyone in the world in the flood.

The disconnect is astonishing.

Think about it this way.

When Jesus told the kids to come chat with him, do you think he told them the story of the Flood? Or about Jacob tricking Esau out of his birthright? Or about Adam and Eve? Or about Samson.

I’d guess he told them something very simple and deeply meaningful, reassuring and loving for a five year old — something that proved that he brought nothing but good news to even the smallest among us.

However, remember, that just as in adult depression, childhood depression can be impervious to a message, and if we notice these depressive behaviors in our very young kids, we should talk to our pediatrician, and we should get help and we should also be the help, and run and play with them, and talk with them, and encourage them to name their emotions, and fill their hearts with the fact — the utterly Biblical fact — that they are beyond special, loved without condition, by both us and Jesus.

[Free Photo: Pexels]

At this point, chronic sleep deprivation has been linked to chronic depression, other chronic disease, and pretty much every bad thing in life.

And yet, in our arrogant workaholic culture, we still treat a lack of sleep as some badge of honor. Well, United States of America, enjoy our proinflammatory cytokines, then. Have fun with our increased expression of tnf-alpha.

Well, there’s a great new presentation, delivered at the 2021 Interdisciplinary Autoimmune Summit, showing sleep is “intimately tied” to the proinflammatory markers that make autoimmune disease worse.

Autoimmune dysfunction is tied to unhealthy neuropsychiatric symptoms, and not just because it’s awful living with an autoimmune disease, and “of course you’d feel blue”. The disease itself can attack normal neuronal cell signaling.

Further, a compelling study showed that depression was a massive risk factor in women developing lupus. Even greater than smoking, for example.

Why? Once again, a lack of sleep promotes inflammatory markers that can turn into autoimmune disease.

And then, not surprisingly, those with lupus who didn’t even have depression, pre-lupus, were more likely to develop it once they were diagnosed with lupus.

Healio has a good review on autoimmune disease and sleep, with a presentation of studies and evidence by Aric Prather, an associate professor of psychiatry and behavior sciences.

Basically, sleep disruptions are “rampant” in patients with autoimmune diseases, and the relationship is bidirectional.

Get less sleep, your disease gets worse. Your disease gets worse, you get less sleep.

And the same goes for depression, of course — whether it’s associated with an autoimmune disease or not.

Get less sleep, your depression gets worse. Your depression gets worse, you get less sleep.

You can read about all this in a tremendous review at Harvard Medical School’s readable Health Publishing.

But the money quote is this: ” sleep disruption — which affects levels of neurotransmitters and stress hormones, among other things — wreaks havoc in the brain, impairing thinking and emotional regulation. In this way, insomnia may amplify the effects of psychiatric disorders, and vice versa.”

This is a really tough thing.

How many times have you read something like, “If you struggle with sleep…..” and then an article lists things that are practically impossible for many of us.

“Plan for 8 hours.” Have you ever been a new parent?

“Be less stressed.” Have you ever lived with an anxiety disorder?

“Eat a healthy diet with tons of things that cost a ton and take 10 hours to prepare.”

But the fact is that we’ll probably make precious little improvement in our mental health until we take care of our sleep.

It’s incredibly important for psychiatrists (I’m of course not one) to start talking about sleep. So says a recent article in the American Journal of Psychiatry.

Researchers gave one group of patients with suicidal thoughts and severe insomnia a sleep aid (zolpidem, i.e. Ambien) and the other, a placebo. Both were given antidepressants, as well.

After two months, the patients on Ambien got better sleeps, had fewer suicidal thoughts, better thinking patterns, and more hopeful thoughts about the future.

In other words, in designing a treatment plan for suicidal patients, it’s incredibly important to address insomnia.

Now here comes the concern you were probably already thinking of — what about dependence on sleep aids?

After all, people can get hooked on Ambien and it can lose its efficacy over time.

Well, researchers only gave the patients Ambien for 8 weeks, then stopped, and followed up, two weeks later.

The patients who had taken the Ambien were, after two weeks, still less suicidal and more hopeful about the future.

So if you’re struggling with sleep and severe depression, it might be time to talk with your doctor about this acronym the researchers came up with: REST-IT. “Reducing Suicidal Ideation Through Insomnia Treatment.”

And GET MORE SLEEP! (caps-locking never helps), but still, GET MORE SLEEP!

[Free photo: Pexels]

Some exciting news from the Indiana University School of Medicine.

But first, depressing news.

You know as well as I do how hard it can be to find the right antidepressant. How many Rx’s have you tried before finding the one (it’s almost romantic when it finally works, right?). Maybe you haven’t found the one, and are still playing the SSRI, SNRI, tricyclic, MAOI field. (Okay, enough of that analogy).

Point is — it sucks to have to try tons of different medicines, with side effects, before finding the right one.

Well, Indiana University School of Medicine researchers have developed a blood test, “composed of RNA biomarkers, that can distinguish how severe a patient’s depression is, their risk of severe depression in the future and their risk of future bipolar disorder, or manic-depressive illness.”

And crucially, “the test also informs tailored medication choices for patients.”

If you want to read more about the study, have at it here, but the point is that sometime soon, you might be able to take a simple blood test and find the antidepressant that works best for you.

In the field of psychiatry, that would be a game-changer. In the field of our 24/7, a life-saver.

I’ll leave you with this exciting passage from IU.

According to Niculescu, the work done by his team has opened the door for their findings to be translated into clinical practice, as well as help with new drug development. Focusing on collaboration with pharmaceutical companies and other doctors in a push to start applying some of their tools and discoveries in real-world scenarios, Niculescu said he believes the work being done by his team is vital in improving the quality of life for countless patients.

“Blood biomarkers offer real-world clinical practice advantages. The brain cannot be easily biopsied in live individuals, so we’ve worked hard over the years to identify blood biomarkers for neuropsychiatric disorders,” Niculescu said. “Given the fact that 1 in 4 people will have a clinical mood disorder episode in their lifetime, the need for and importance of efforts such as ours cannot be overstated.”

[Painting: The Birthday, Chagall]