![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 16 of 16. This is the beginning of the thread.
Posted by lostforwards on December 13, 2004, at 21:14:18
In reply to St. John's Question (please do not redirect), posted by Dan Perkins on December 13, 2004, at 20:43:34
If you've tried ALL of the other ADs, then it probably won't work. It's mode of action is supposedly weak MAO-A inhibition. I think there are some other theories about how it works.
I'm not sure of this but I think even inhibiting MAO-A would have an impact on dopamine levels. I take it at a very low dose as a cheap way to keep my dopamine levels up while I'm asleep - not as an antidepressants. It keeps me awake, even with one pill. I had the opposite effect with nozinal which I used artificially to induce sleep. Sure it's hard to sleep now, but eventually things will even out again I hope.... that doctor better have had a very good reason for medicating me the way he did.
BTW: It's spelled Wort, not wart.
Posted by Dan Perkins on December 14, 2004, at 3:34:08
I know that this post technically belongs on the Alternative page, but I specifically want to ask this question to this group of people who, I feel, have a lot of knowledge and experience with traditional antidepressant medications.
Have any of you tried St. John's Wart? I have been on the full range of antidepressants and there aren't many traditional meds left for me to try. I am curious if anyone here thinks that St. John's Wart is worth a try.
Posted by Optimist on December 14, 2004, at 3:34:08
In reply to St. John's Question (please do not redirect), posted by Dan Perkins on December 13, 2004, at 20:43:34
> I know that this post technically belongs on the Alternative page, but I specifically want to ask this question to this group of people who, I feel, have a lot of knowledge and experience with traditional antidepressant medications.
>
> Have any of you tried St. John's Wart? I have been on the full range of antidepressants and there aren't many traditional meds left for me to try. I am curious if anyone here thinks that St. John's Wart is worth a try.I've been on St. John's Wort 2700mg a day which is three times the recommended dose. Even at that dose I've found it to be quite mild. The brand I was on was also considered efficatious so I don't think there was a problem with it's potency.
Currently I'm on 450mg Wellbutrin SR, 20mg Prozac, 5mg Adderall XR, 200mg Vitex(herbal dopamine agonist), 3g tryosine, and 200mg-400mg of caffeine per day. I recently switched the SJW to Prozac and feel that the Prozac is more effective.
My dx is dysthymia with atypical features, and social anxiety, with possible SAD features.
I'm thinking of possibly scrapping my current cocktail for a trial of Parnate. We'll see next week after my appt with my pdoc.
IMO, I would say don't bother with the St. John's Wort. If many other AD's haven't helped I highly doubt the STW will.
Posted by Bill LL on December 14, 2004, at 9:05:40
In reply to St. John's Question (please do not redirect), posted by Dan Perkins on December 13, 2004, at 20:43:34
For someone who is treatment resistant to prescription drugs like yourself, St John's Wort will not help because it is not a strong antidepressant.
Failing to respond to antidepressants doesn't really mean very much in and of itself. It's the dose that is important. For example, if 20 mg of Prozac doesn't work, that doesn't mean that it won't work at 40 or 60 mg. Even if a dose does work, it oftentimes needs to be increased after a few months or a year.
You really need to go back on prescription drugs and try higher doses than you did before.
> I know that this post technically belongs on the Alternative page, but I specifically want to ask this question to this group of people who, I feel, have a lot of knowledge and experience with traditional antidepressant medications.
>
> Have any of you tried St. John's Wart? I have been on the full range of antidepressants and there aren't many traditional meds left for me to try. I am curious if anyone here thinks that St. John's Wart is worth a try.
Posted by Larry Hoover on December 14, 2004, at 14:03:29
In reply to St. John's Question (please do not redirect), posted by Dan Perkins on December 13, 2004, at 20:43:34
> I know that this post technically belongs on the Alternative page, but I specifically want to ask this question to this group of people who, I feel, have a lot of knowledge and experience with traditional antidepressant medications.
>
> Have any of you tried St. John's Wart? I have been on the full range of antidepressants and there aren't many traditional meds left for me to try. I am curious if anyone here thinks that St. John's Wart is worth a try.Yes, I think St. John's wort is worth a try. It works by multiple mechanisms, including having a unique ability to inhibit all neurotransmitter reuptake pumps. Its MAOI activity has been exaggerated, but it does have a mild effect on that enzyme.
What's important is: a) that you get a quality product, as herbal products are not regulated in North America; b) that you do not limit yourself to the "standard dose" of 900 mg/day, standardized on hypericin.
If you do a trial as you would with any other antidepressant, i.e. gradually titrate the dose upwards until either a) remission occurs; or, b) side effects become intolerable, you will have appropriately tested the herb's effects.
There is no known overdose of SJW. Most common side effects are stomach problems and headache, but symptomatic treatment of those is fine. They tend to pass after a short time.
No antidepressant has given me better results than SJW did. Your brain may vary.
You will note in the following study that participants had severe depression, and they were dosed at 1800 mg/day of LI 160 (marketed as Kira in the US). Response was similar to imipramine, but the SJW was better tolerated. Another good brand to consider is Perika.
Pharmacopsychiatry. 1997 Sep;30 Suppl 2:81-5.
Efficacy and tolerability of St. John's wort extract LI 160 versus imipramine in patients with severe depressive episodes according to ICD-10.
Vorbach EU, Arnoldt KH, Hubner WD.
Department of Psychiatry and Psychotherapy, Ev. Krankenhaus Elisabethenstift, Darmstadt, Germany.
The special extract of St. John's wort, LI 160, exhibited a superior antidepressant efficacy compared to placebo in several controlled trials. Two further trials demonstrated a similar reduction of depressive symptomatology under LI 160 compared to tricyclics. All these trials were performed in mildly to moderately depressed patients. The present investigation was a randomized, controlled, multicentre, 6-week trial comparing 1800 mg LI 160/die to 150 mg imipramine/die in severely depressed patients according to ICD-10. The main efficacy parameter, a reduction of the total score of the Hamilton Depression Scale, proved both treatment regimens very effective at the end of the 6 week treatment period (mean values 25.3 to 14.5 in the LI 160 group and 26.1 to 13.6 in the imipramine group), but not statistically equivalent within a a-priori defined 25% interval of deviation. The analysis of subgroups with more than a 33% and 50% reduction of the HAMD total score justified the assumption of equivalence within a 25% deviation interval. This view was also supported by the global efficacy ratings from patients and investigators. Regarding adverse events, the nonrejection of the nonequivalence hypothesis denotes a superiority of the herbal antidepressant. These main result indicate that LI 160 might be a treatment alternative to the synthetic tricyclic antidepressant imipramine in the majority of severe forms of depressions. However, more studies of this type must be performed before a stronger recommendation can be made.
Lar
Posted by Tabitha on December 14, 2004, at 14:32:47
In reply to Re: St. John's Question (please do not redirect) » Dan Perkins, posted by Larry Hoover on December 14, 2004, at 14:03:29
Hey Lar, did you take the SJW all at once, or divided doses in the day? The one thing that puts me off the idea of it is having to use it 2x or 3x per day.
Posted by Dan Perkins on December 14, 2004, at 16:20:32
In reply to Re: St. John's Question (please do not redirect) » Larry Hoover, posted by Tabitha on December 14, 2004, at 14:32:47
Hi Larry,
I noticed that you posted some information on Tryptophan above. Between SJW and Tryptophan (and any other non-pharmaceutical treatment), what would you recommend for a very treatment-resistant depression?
Thanks
Posted by pretty_paints on December 14, 2004, at 16:58:58
In reply to Re: St. John's Question - - Larry, posted by Dan Perkins on December 14, 2004, at 16:20:32
My dad takes SJW and it seems to make him feel great! Loads of energy, less uptight, enthusiasm to do things. This has been hard to swallow for me as I have been on a merrygoround of drugs to no avail.
I think SJW works mainly for people who are "normal". Way back before I started to take ADs, I bought some SJW because I was determined to stay off prescription drugs. It did very little for me. A few months ago I gave the rest to my dad, just coz they were there. He was just a little stressed with work, but fine apart from that.
They worked wonders for him but he was fine to begin with! I dont really think they would do that much if you have a true hard-to-budge depression. But that's just my opinion.
Posted by Dan Perkins on December 14, 2004, at 20:08:47
In reply to Re: St. John's Question, posted by pretty_paints on December 14, 2004, at 16:58:58
I think you are probably right. My mother takes Sam-E for her mood and she says it works wonders for her. Only thing is that she is probably the best-adjusted, absolute happiest and least depressed people I have ever come in contact with. It does seem like SJW is too weak to do the trick.
I have been off ADs for several months and have been absolutely miserable (though I wasn't exactly a barrel of laughs when I was on meds anyway). I do need to go back on something but I want to explore some alternative treatments before going back to the pharmaceutical grade stuff.
I have been on so many meds over the past 10 years and as I look back I realize that I am worse off than when I first popped an Antidepressant in the 90s. Not only am I at least as depressed, I think all the meds have done a number on my brain, especially my memory. I have really come to think that antidepressants are some potent drugs and that over time they can really do some damage.
> They worked wonders for him but he was fine to begin with! I dont really think they would do that much if you have a true hard-to-budge depression. But that's just my opinion.
Posted by Larry Hoover on December 15, 2004, at 16:17:22
In reply to Re: St. John's Question - - Larry, posted by Dan Perkins on December 14, 2004, at 16:20:32
> Hi Larry,
>
> I noticed that you posted some information on Tryptophan above. Between SJW and Tryptophan (and any other non-pharmaceutical treatment), what would you recommend for a very treatment-resistant depression?
>
> ThanksI wish things were so easy to predict.
Your lack of response to antidepressants could be because of nutrient deficiencies. Just consider these following abstracts with respect to folate levels and antidepressant response. People are being snowed by the idea that a "balanced diet", whatever that is, can provide all the nutrition one needs. That idea is demonstrably false, but when was the last time your doctor tested your folate level?
http://lpi.oregonstate.edu/infocenter/vitamins/fa/
***This article shows that taking folic acid along with fluoxetine (Prozac) not only increased the level of remission, but it also reduced the side-effects dramatically.***
J Affect Disord. 2000 Nov;60(2):121-30.Comment in:
J Affect Disord. 2002 Dec;72(3):297-8.Enhancement of the antidepressant action of fluoxetine by folic acid: a randomised, placebo controlled trial.
Coppen A, Bailey J.
MRC Neuropsychiatry Laboratory, West Park Hospital, KT19 8PB, Surrey, Epsom, UK.
BACKGROUND: A consistent finding in major depression has been a low plasma and red cell folate which has also been linked to poor response to antidepressants. The present investigation was designed to investigate whether the co-administration of folic acid would enhance the antidepressant action of fluoxetine. METHODS: 127 patients were randomly assigned to receive either 500 microg folic acid or an identical looking placebo in addition to 20 mg fluoxetine daily. All patients met the DSM-III-R criteria for major depression and had a baseline Hamilton Rating Scale (17 item version) score for depression of 20 or more. Baseline and 10-week estimations of plasma folate and homocysteine were carried out. RESULTS: Patients receiving folate showed a significant increase in plasma folate.This was less in men than in women. Plasma homocysteine was significantly decreased in women by 20.6%, but there was no significant change in men. Overall there was a significantly greater improvement in the fluoxetine plus folic acid group. This was confined to women where the mean Hamilton Rating Scale score on completion was 6.8 (S.D. 4. 1) in the fluoxetine plus folate group, as compared to 11.7 (S.D. 6. 7) in the fluoxetine plus placebo group (P<0.001).A percentage of 93. 9 of women, who received the folic acid supplement, showed a good response (>50% reduction in score) as compared to 61.1% of women who received placebo supplement (P<0.005). Eight (12.9%) patients in the fluoxetine plus folic acid group reported symptoms possibly or probably related to medication, whereas in the fluoxetine plus placebo group 19 (29.7%) patients reported such symptoms (P<0.05). LIMITATIONS AND CONCLUSIONS: Folic acid is a simple method of greatly improving the antidepressant action of fluoxetine and probably other antidepressants. Folic acid should be given in doses sufficient to decrease plasma homocysteine. Men require a higher dose of folic acid to achieve this than women, but more work is required to ascertain the optimum dose of folic acid.
***This article shows that in fluoxetine non-responders later given augmentation (either increase in dose, or the addition of another drug along with the fluoxetine), those with normal folate status responded to the augment more than 620% better than those with low folate status.***J Clin Psychiatry. 2004 Aug;65(8):1090-5.
Serum folate, vitamin B12, and homocysteine in major depressive disorder, Part 1: predictors of clinical response in fluoxetine-resistant depression.
Papakostas GI, Petersen T, Mischoulon D, Ryan JL, Nierenberg AA, Bottiglieri T, Rosenbaum JF, Alpert JE, Fava M.
Depression Clinical and Research Program, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. gpapakostas@partners.org
OBJECTIVE: In the present study, we assessed the relationship between serum folate, vitamin B12, and homocysteine levels and clinical response in patients with major depressive disorder (MDD) who had previously failed to respond to open treatment with fluoxetine 20 mg/day and were enrolled in a 4-week, double-blind trial of either (1) fluoxetine dose increase, (2) lithium augmentation of fluoxetine, or (3) desipramine augmentation of fluoxetine. METHOD: Fifty-five outpatients (mean +/- SD age = 41.7 +/- 10.6 years; 50.9% women) with MDD as assessed with the Structured Clinical Interview for DSM-III-R who were enrolled in the double-blind trial had serum folate, vitamin B12, and homocysteine measurements completed at baseline (prior to fluoxetine treatment initiation). Folate levels were classified as either low (< or = 2.5 ng/mL) or normal. Vitamin B12 levels were classified as either low (< or = 200 pg/mL) or normal. Homocysteine levels were classified as either elevated (> or = 13.2 micromol/L) or normal. With the use of a logistic regression, we then assessed the relationship between (1) low or normal folate levels, (2) normal or low B12 levels, and (3) elevated or normal homocysteine levels and clinical response to double-blind treatment. The study was conducted from November 1992 to January 1999. RESULTS: Low serum folate levels (chi2=3.626, p =.04), but not elevated homocysteine (p >.05) or low vitamin B12 levels (p >.05), were associated with poorer response to treatment. The response rates for patients with (N = 14) and without (N = 38) low folate levels were 7.1% versus 44.7%, respectively. CONCLUSION: Low serum folate levels were found to be associated with further treatment resistance among patients with fluoxetine-resistant MDD.
***This article shows that relapse back to depression in fluoxetine monotherapy was over 1340% more likely in those with low folate status.***
J Clin Psychiatry. 2004 Aug;65(8):1096-8.
Serum folate, vitamin B12, and homocysteine in major depressive disorder, Part 2: predictors of relapse during the continuation phase of pharmacotherapy.
Papakostas GI, Petersen T, Mischoulon D, Green CH, Nierenberg AA, Bottiglieri T, Rosenbaum JF, Alpert JE, Fava M.
Depression Clinical and Research Program, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. gpapakostas@partners.org
OBJECTIVE: In the present study, we assessed the relationship between serum folate, vitamin B12, and homocysteine levels on the rate of relapse in outpatients with remitted major depressive disorder (MDD) during a 28-week continuation phase of treatment with fluoxetine. METHOD: Seventy-one outpatients (mean +/- SD age = 40.2 +/- 11.1 years; 56.3% women) with MDD (as assessed with the Structured Clinical Interview for DSM-III-R) who had remitted and who were enrolled in the continuation phase of treatment with fluoxetine had serum folate, vitamin B12, and homocysteine measurements completed at baseline (prior to acute-phase treatment). Patients were followed for 28 weeks of continued treatment with fluoxetine 40 mg/day to monitor
for depressive relapse. Folate levels were classified as either low (< or = 2.5 ng/mL) or normal. Vitamin B12 levels were classified as either low (< or = 200 pg/mL) or normal. Homocysteine levels were classified as either elevated (> or = 13.2 micromol/L) or normal. With the use of separate logistic regressions, we then assessed the relationship between folate, vitamin B12, and homocysteine level status and relapse. The study was conducted from November 1992 to January 1999. RESULTS: The presence of low serum folate levels (p =.004), but not low B12 (p >.05) or elevated homocysteine levels (p >.05), was associated with relapse during continuation treatment with fluoxetine. The relapse rates for patients with (N = 7) and without (N = 64) low folate levels were 42.9% versus 3.2%, respectively. CONCLUSION: Low serum folate levels were found to place patients with remitted MDD at risk for depressive relapse during the continuation phase of treatment with fluoxetine.
The bottom line is, you need to ensure that your nutritional status is optimized, or maybe nothing will work.Lar
Posted by Larry Hoover on December 15, 2004, at 18:08:00
In reply to Re: St. John's Question (please do not redirect) » Larry Hoover, posted by Tabitha on December 14, 2004, at 14:32:47
> Hey Lar, did you take the SJW all at once, or divided doses in the day? The one thing that puts me off the idea of it is having to use it 2x or 3x per day.
I never bother with the multiple dose thing. Once a day, and I never notice any difference. All you risk is a greater peak to trough variability, i.e. a bigger wobble about the average blood concentration. If you go once a day, and you notice too much variability, you might have to split the dose. But like I said, I never noticed anything.
Lar
Posted by jakeman on December 15, 2004, at 22:35:06
In reply to Re: folate and antidepressant response » Dan Perkins, posted by Larry Hoover on December 15, 2004, at 16:17:22
> > Hi Larry,
> >
> > I noticed that you posted some information on Tryptophan above. Between SJW and Tryptophan (and any other non-pharmaceutical treatment), what would you recommend for a very treatment-resistant depression?
> >
> > Thanks
>
> I wish things were so easy to predict.
>
> Your lack of response to antidepressants could be because of nutrient deficiencies. Just consider these following abstracts with respect to folate levels and antidepressant response. People are being snowed by the idea that a "balanced diet", whatever that is, can provide all the nutrition one needs. That idea is demonstrably false, but when was the last time your doctor tested your folate level?
>
> http://lpi.oregonstate.edu/infocenter/vitamins/fa/
>
> ***This article shows that taking folic acid along with fluoxetine (Prozac) not only increased the level of remission, but it also reduced the side-effects dramatically.***
>
>
> J Affect Disord. 2000 Nov;60(2):121-30.
>
> Comment in:
> J Affect Disord. 2002 Dec;72(3):297-8.
>
> Enhancement of the antidepressant action of fluoxetine by folic acid: a randomised, placebo controlled trial.
>
> Coppen A, Bailey J.
>
> MRC Neuropsychiatry Laboratory, West Park Hospital, KT19 8PB, Surrey, Epsom, UK.
>
> BACKGROUND: A consistent finding in major depression has been a low plasma and red cell folate which has also been linked to poor response to antidepressants. The present investigation was designed to investigate whether the co-administration of folic acid would enhance the antidepressant action of fluoxetine. METHODS: 127 patients were randomly assigned to receive either 500 microg folic acid or an identical looking placebo in addition to 20 mg fluoxetine daily. All patients met the DSM-III-R criteria for major depression and had a baseline Hamilton Rating Scale (17 item version) score for depression of 20 or more. Baseline and 10-week estimations of plasma folate and homocysteine were carried out. RESULTS: Patients receiving folate showed a significant increase in plasma folate.This was less in men than in women. Plasma homocysteine was significantly decreased in women by 20.6%, but there was no significant change in men. Overall there was a significantly greater improvement in the fluoxetine plus folic acid group. This was confined to women where the mean Hamilton Rating Scale score on completion was 6.8 (S.D. 4. 1) in the fluoxetine plus folate group, as compared to 11.7 (S.D. 6. 7) in the fluoxetine plus placebo group (P<0.001).A percentage of 93. 9 of women, who received the folic acid supplement, showed a good response (>50% reduction in score) as compared to 61.1% of women who received placebo supplement (P<0.005). Eight (12.9%) patients in the fluoxetine plus folic acid group reported symptoms possibly or probably related to medication, whereas in the fluoxetine plus placebo group 19 (29.7%) patients reported such symptoms (P<0.05). LIMITATIONS AND CONCLUSIONS: Folic acid is a simple method of greatly improving the antidepressant action of fluoxetine and probably other antidepressants. Folic acid should be given in doses sufficient to decrease plasma homocysteine. Men require a higher dose of folic acid to achieve this than women, but more work is required to ascertain the optimum dose of folic acid.
>
>
> ***This article shows that in fluoxetine non-responders later given augmentation (either increase in dose, or the addition of another drug along with the fluoxetine), those with normal folate status responded to the augment more than 620% better than those with low folate status.***
>
> J Clin Psychiatry. 2004 Aug;65(8):1090-5.
>
> Serum folate, vitamin B12, and homocysteine in major depressive disorder, Part 1: predictors of clinical response in fluoxetine-resistant depression.
>
> Papakostas GI, Petersen T, Mischoulon D, Ryan JL, Nierenberg AA, Bottiglieri T, Rosenbaum JF, Alpert JE, Fava M.
>
> Depression Clinical and Research Program, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. gpapakostas@partners.org
>
> OBJECTIVE: In the present study, we assessed the relationship between serum folate, vitamin B12, and homocysteine levels and clinical response in patients with major depressive disorder (MDD) who had previously failed to respond to open treatment with fluoxetine 20 mg/day and were enrolled in a 4-week, double-blind trial of either (1) fluoxetine dose increase, (2) lithium augmentation of fluoxetine, or (3) desipramine augmentation of fluoxetine. METHOD: Fifty-five outpatients (mean +/- SD age = 41.7 +/- 10.6 years; 50.9% women) with MDD as assessed with the Structured Clinical Interview for DSM-III-R who were enrolled in the double-blind trial had serum folate, vitamin B12, and homocysteine measurements completed at baseline (prior to fluoxetine treatment initiation). Folate levels were classified as either low (< or = 2.5 ng/mL) or normal. Vitamin B12 levels were classified as either low (< or = 200 pg/mL) or normal. Homocysteine levels were classified as either elevated (> or = 13.2 micromol/L) or normal. With the use of a logistic regression, we then assessed the relationship between (1) low or normal folate levels, (2) normal or low B12 levels, and (3) elevated or normal homocysteine levels and clinical response to double-blind treatment. The study was conducted from November 1992 to January 1999. RESULTS: Low serum folate levels (chi2=3.626, p =.04), but not elevated homocysteine (p >.05) or low vitamin B12 levels (p >.05), were associated with poorer response to treatment. The response rates for patients with (N = 14) and without (N = 38) low folate levels were 7.1% versus 44.7%, respectively. CONCLUSION: Low serum folate levels were found to be associated with further treatment resistance among patients with fluoxetine-resistant MDD.
>
>
>
> ***This article shows that relapse back to depression in fluoxetine monotherapy was over 1340% more likely in those with low folate status.***
>
> J Clin Psychiatry. 2004 Aug;65(8):1096-8.
>
> Serum folate, vitamin B12, and homocysteine in major depressive disorder, Part 2: predictors of relapse during the continuation phase of pharmacotherapy.
>
> Papakostas GI, Petersen T, Mischoulon D, Green CH, Nierenberg AA, Bottiglieri T, Rosenbaum JF, Alpert JE, Fava M.
>
> Depression Clinical and Research Program, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. gpapakostas@partners.org
>
> OBJECTIVE: In the present study, we assessed the relationship between serum folate, vitamin B12, and homocysteine levels on the rate of relapse in outpatients with remitted major depressive disorder (MDD) during a 28-week continuation phase of treatment with fluoxetine. METHOD: Seventy-one outpatients (mean +/- SD age = 40.2 +/- 11.1 years; 56.3% women) with MDD (as assessed with the Structured Clinical Interview for DSM-III-R) who had remitted and who were enrolled in the continuation phase of treatment with fluoxetine had serum folate, vitamin B12, and homocysteine measurements completed at baseline (prior to acute-phase treatment). Patients were followed for 28 weeks of continued treatment with fluoxetine 40 mg/day to monitor
> for depressive relapse. Folate levels were classified as either low (< or = 2.5 ng/mL) or normal. Vitamin B12 levels were classified as either low (< or = 200 pg/mL) or normal. Homocysteine levels were classified as either elevated (> or = 13.2 micromol/L) or normal. With the use of separate logistic regressions, we then assessed the relationship between folate, vitamin B12, and homocysteine level status and relapse. The study was conducted from November 1992 to January 1999. RESULTS: The presence of low serum folate levels (p =.004), but not low B12 (p >.05) or elevated homocysteine levels (p >.05), was associated with relapse during continuation treatment with fluoxetine. The relapse rates for patients with (N = 7) and without (N = 64) low folate levels were 42.9% versus 3.2%, respectively. CONCLUSION: Low serum folate levels were found to place patients with remitted MDD at risk for depressive relapse during the continuation phase of treatment with fluoxetine.
>
>
> The bottom line is, you need to ensure that your nutritional status is optimized, or maybe nothing will work.
>
> Lar--------------------------------------
Larry,
Very interesting articles, thanks for posting. What becomes a bit problematic for me is obtaining a real determination of my nutritional status. I wonder if a basic blood test measures levels of folate and/or homocysteine. Below is another article on folate and depression.
JakeDepression, Low Folate Levels Linked
Tufts nutrition experts find that the vitamin folate – found in a variety of foods including vegetables and cereals – may help ease depression and prevent memory loss.
Boston [06-23-03] The food you eat may impact more than just your physical health – it could also play a role in your mental health as well. According to recent studies by Tufts nutrition experts, low levels of the vitamin folate – found in a variety of foods – has been linked with depression, low energy levels and even memory loss.
“[Tufts’ Martha Morris and four colleagues] found that those who had experienced major depression had lower concentrations of folate in their bloodstream and red blood cells than those who had never been depressed,” reported the Hartford Courant. “In addition, those with chronic low-level depression - also known as dysthymia - had lower red blood cell levels than the non-depressed.”
The research team, which conducted their research at Tufts’ Jean Mayer USDA Human Nutrition Research Center on Aging, studied data on nearly 3,000 people ages 15 to 39.
“Supplementation possibly helps by reducing fatigue and improving energy levels,” Morris, an epidemiologist who teaches at Tufts’ Gerald J. and Dorothy R. Friedman School of Nutrition Science and Policy, told the newspaper. “People who are diagnosed with depression should then find out whether they are folate deficient to determine if a supplement is warranted.”
Morris’ research opens the door for future research to pinpoint exactly why vitamin deficiencies result in different types of medical conditions.
“Clinical studies show that folate supplementation helps depressed people, although we still don’t have a good idea why depressed people have low folate status,” Morris said.
This isn’t the first time that Tufts researchers have further shown the health benefits of folate. In 2001, Morris and her colleagues found that folate helps significantly modify homocysteine levels in the brain. The presence of homocysteine has been associated with cognitive impairment and has been linked to the onset of Alzheimer disease, dementia and strokes. And, Dr. Irwin Rosenberg, dean of the Friedman School of Nutrition Science and Policy, was among the very first worldwide to explore the relationship between folate, homocysteine and cardiovascular disease resulting in landmark publications.
“Researchers at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University were looking for a relationship between blood homocysteine levels and memory loss,” reported the Agriculture Research Service. “Their research had established that homocysteine levels were higher in elderly people with low intakes of B vitamins, especially folate.”
Despite its benefits, Morris and her colleagues caution that people shouldn’t make a significant increase in their folate intake without consulting a doctor.
“While studies on folate and antidepressant treatment are promising, scientists do not yet know which patients should get folate supplements, in what dose or for how long,” reported the Courant. “Furthermore, the safety of high-dosage supplementation has not been established.”
Good sources for folate include vegetables and fruits such as leafy greens, strawberries, and melons, as well as dried beans and cereals, or any multivitamin.
http://enews.tufts.edu/stories/062303Folate.htm
Posted by Larry Hoover on December 15, 2004, at 23:03:05
In reply to Re: folate and antidepressant response » Larry Hoover, posted by jakeman on December 15, 2004, at 22:35:06
> Very interesting articles, thanks for posting. What becomes a bit problematic for me is obtaining a real determination of my nutritional status. I wonder if a basic blood test measures levels of folate and/or homocysteine. Below is another article on folate and depression.
> JakeNo, neither is part of a basic blood test. They're both "special order" blood tests.
> Despite its benefits, Morris and her colleagues caution that people shouldn’t make a significant increase in their folate intake without consulting a doctor.
>
> “While studies on folate and antidepressant treatment are promising, scientists do not yet know which patients should get folate supplements, in what dose or for how long,” reported the Courant. “Furthermore, the safety of high-dosage supplementation has not been established.”With respect to these two paragraphs, the UL (Upper Limit) of folate intake is set at 1000 micrograms/day, but (and it's a big but), that's 1/5 of the Lowest Observeable Adverse Effects Level, AND, those adverse effects are only found in people who are vitamin B-12 deficient.
So, check out this logic. You aren't supposed to take much folate because you might be B-12 deficient? Because folate intake accelerates the neurological symptoms of another nutrient deficiency?
<Spock eyebrow>
Take some B-12, too. Duh!
Lar
Posted by TeeJay on December 16, 2004, at 20:06:03
In reply to Re: folate and antidepressant response » jakeman, posted by Larry Hoover on December 15, 2004, at 23:03:05
<Spock eyebrow>
Ok, smartypants, lets see you do the <spock ears>
TJ
Posted by barbaracat on December 29, 2004, at 19:39:41
In reply to Re: St. John's Question (please do not redirect) » Dan Perkins, posted by lostforwards on December 13, 2004, at 21:14:18
I've had great success with SJW, but it took me some experimenting to find the magic combo. Brands do differ very much and I was surprised at how I responded to them. Here's a link to my detailed post farther down on this board on what worked and what didn't.
http://www.dr-bob.org/babble/alter/20041212/msgs/435452.html
Posted by barbaracat on December 29, 2004, at 19:44:05
In reply to St. John's answer » lostforwards, posted by barbaracat on December 29, 2004, at 19:39:41
Sorry, this was meant for everyone and I directed it to lostforwords by missssstake.
> I've had great success with SJW, but it took me some experimenting to find the magic combo. Brands do differ very much and I was surprised at how I responded to them. Here's a link to my detailed post farther down on this board on what worked and what didn't.
>
> http://www.dr-bob.org/babble/alter/20041212/msgs/435452.html
This is the end of the thread.
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