Deplin

[wmro1280]

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I've been reading up on Deplin, the new "medical food" (which is actually L-methylfolate, a derivative of OTC folic acid), but there's something I can't quite figure out.

The FDA defines a "medical food" as "a food which is formulated to be consumed under the supervision of a physician and which is intended for the specific dietary management of a condition for which distinctive nutritional requirements, based on recognized scientific principles, are established by medical evaluation."

My question is, how did Deplin receive FDA approval as a medical food? There are no "distinctive nutritional requirements" for depression, certainly none based on "recognized scientific principles." Sure, it makes sense that vitamin supplementation will help depression, but wouldn't it help virtually every other brain function, too?

Actually, it looks like Pamlab, the manufacturer of Deplin, has already been taken to task for a similar issue related to one of its other products.

Is this just a gimmick?

 

[st2205]

I have no idea but the infectious disease guy I'm currently with is huge on this, as well as cerefolin (same thing -- different dose) as well as metanx.

 

[mgdsh]

I've had good success with Deplin in a few patients. Probably on the rate of 3/5? 4/6?

 

[BobA]

You could also just give normal folic acid which would work for most people.

The Carlat Report has a great article about Deplin: TCPR, June 2009, Vol 7, Issue 6.

 

[st2205]

You could also just give normal folic acid which would work for most people.

The Carlat Report has a great article about Deplin: TCPR, June 2009, Vol 7, Issue 6.

The claim is that something like 10-15% of people lack the enzymes necessary to break folic acid down to L methylfolate (the absorbable form) and that another 30-40% have diminished activity of it. Don't know where the numbers came from and I haven't researched it enough to know if any of those claims have legs.

 

[BobA]

The claim is that something like 10-15% of people lack the enzymes necessary to break folic acid down to L methylfolate (the absorbable form) and that another 30-40% have diminished activity of it. Don't know where the numbers came from and I haven't researched it enough to know if any of those claims have legs.

My understanding is those people have a polymorphism that decreases their efficiency at making L Methylfolate - it's not that they lack it altogether. Why assume that your patient is one of these people and make them pay for that really expensive med they may not need?

Moreover, augmentation with plain folic acid is actually recommended in the APA guidelines for MDD.

 

[davidrpharmboy]

I work with Deplin and can provide some key points on how Deplin may aid patients in treating depression. If you were to visit the Deplin website you would see there are Key Opinion Leaders in Psychiatry, from Harvard, that have conducted PCT with Deplin as an augmentation with SSRIs and SNRIs and have results that indicate, not only strong efficacy, but placebo side effects. What does this mean? There is no such thing here as "snake oil" but an opportunity that may address some non/partial responders that, in theory (Psychiatry in mostly in theory) may have low levels of three essential neurotransmitters. Because the brain requires the L-methylfolate (folic acid is the OTC that does not cross the BBB) as a precursor to BH4, which aids Tyrosine and Tryptophan, thus creating more of the three nuerotransmitters. If a depressed patient has more to work with, in theory, this is how Deplin (7.5mg or 15mg) of L-methylfolate helps SNRIs and SSRIs work faster. Please visit the Deplin website for published studies or for video options. Let me know should you have any questions.

 

[xlithiumx]

I work with Deplin and can provide some key points on how Deplin may aid patients in treating depression. If you were to visit the Deplin website you would see there are Key Opinion Leaders in Psychiatry, from Harvard, that have conducted PCT with Deplin as an augmentation with SSRIs and SNRIs and have results that indicate, not only strong efficacy, but placebo side effects.

This is drug representative language. Key Opinion Leader is a pharmaceutical industry term. We don't need guerrilla marketing on this board.

 

[nitemagi]

this is drug representative language. Key opinion leader is a pharmaceutical industry term. We don't need guerrilla marketing on this board.

+1

 

[OldPsychDoc]

This is drug representative language. Key Opinion Leader is a pharmaceutical industry term. We don't need guerrilla marketing on this board.

But they're from Harvard! 🙄

 

[Doc Samson]

Can I be a Key Opinion Leader?

 

[OldPsychDoc]

Can I be a Key Opinion Leader?

Of course--because...You're from Harvard!

 

[wmro1280]

I work with Deplin and can provide some key points on how Deplin may aid patients in treating depression. If you were to visit the Deplin website you would see there are Key Opinion Leaders in Psychiatry, from Harvard, that have conducted PCT with Deplin as an augmentation with SSRIs and SNRIs and have results that indicate, not only strong efficacy, but placebo side effects. What does this mean? There is no such thing here as "snake oil" but an opportunity that may address some non/partial responders that, in theory (Psychiatry in mostly in theory) may have low levels of three essential neurotransmitters. Because the brain requires the L-methylfolate (folic acid is the OTC that does not cross the BBB) as a precursor to BH4, which aids Tyrosine and Tryptophan, thus creating more of the three nuerotransmitters. If a depressed patient has more to work with, in theory, this is how Deplin (7.5mg or 15mg) of L-methylfolate helps SNRIs and SSRIs work faster. Please visit the Deplin website for published studies or for video options. Let me know should you have any questions.

OK, I have some questions:

(1) How much BH4 is necessary to make the 3 neurotransmitters? Does making more BH4 mean more monoamines, or is the pathway saturated already? Or regulated by some entirely different mechanism?
(2) Can BH4 be made by any other mechanism than L-methylfolate? If so, how significant is the L-methylfolate mechanism?
(3) What is the actual role of the three monoamines in depression? (I'm not trying to be a smart ass, I genuinely would like to know the answer.)

If these questions are too complicated, please direct them to your Key Opinion Leader (maybe even the one from Harvard!), as I am interested in your replies.