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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 14 of 14. This is the beginning of the thread.
Posted by Spriggy on February 23, 2005, at 17:45:46
I just spent 4 days in the psych unit from what the psychiatrist and neurologist called " drug incuded akathasia."
Even as a Christian, I think the term "akathasia" should be changed to "living utter hell on earth" as a diagnosis, but whatever.
So the psych said I needed to stay CLEAR from any SSRI's. He says I have a very sensitive central nervous system ( I had a similar reaction on an anti nausea drug called Compazine).So he now has me on Klonopin (.25 twice a day which is kicking my butt!), and Temazepam for sleep (which is also kicking my butt).
So now I have no anxiety, no longer have akathasia but feel like I'm a zombie. I am SOOOOOOO tired all day ( I slept from 8:30 p.m. last night until 3 p.m. today- so that's what...um... 18 hours of sleep???).
I can't live like this. I have two children to care for, one is autistic and needs any amount of energy I can muster.
I am also noticing that with the lethargy, I am depressed. It could be because I am so tired from these meds.
If I can't have any SSRI's (he says nothing needs to touch my seratonin), can I give Sam-E a try again?
Does Sam-E mess much with seratonin??
I need something for motivation, depression, energy, etc.. and I don't want to go back to the dr. and be put on more pharmaceuticals that will do who knows what to my already wigged out nervous system.
*by the way, I am decreasing my Klonopin after today to only taking .12 twice a day. And trying to go without the Temazepam altogether.
Posted by FredPotter on February 23, 2005, at 18:12:36
In reply to Psych says NO SSRIS for me, posted by Spriggy on February 23, 2005, at 17:45:46
Spriggy I wouldn't have thought Klonopin would do that. I've had fatigue and sleeping like that too. I think it is depression. I take L-tyrosine on an empty stomach 20 minutes before a meal, 3g a day. I find my tiredness has gone, though it may be a coincidence
Fred
Posted by TamaraJ on February 23, 2005, at 19:47:21
In reply to Psych says NO SSRIS for me, posted by Spriggy on February 23, 2005, at 17:45:46
Spriggy,
I have never taken Klonopin, but I have read on the main board that people do experience tiredness/drowsiness when they first start using it. What I seem to recall reading is that this side effect lasts about a week until your body adjusts to the medication.
The suggestion of L-Tyrosine is a good one. Just remember - start low and go slow. You might also want to try NADH Enada. I noticed an increase in energy and motivation when I took it late last year. Although right now I have just started Provigil (a wakefulness med), I may add a small amount of NADH to that.
All the best to you. Take care.
Tamara
Posted by Spriggy on February 23, 2005, at 20:55:27
In reply to Re: Psych says NO SSRIS for me » Spriggy, posted by TamaraJ on February 23, 2005, at 19:47:21
Thank you both for your input.
Could you tell me exactly what those meds will do? What neurotransmitter it will target etc..?
After my experience with Lexapro, I am SOOO drug paranoid.
Posted by FredPotter on February 23, 2005, at 21:55:30
In reply to Re: Psych says NO SSRIS for me, posted by Spriggy on February 23, 2005, at 20:55:27
L-tyrosine is an amino acid available from health stores. It is a precursor of the neurotransmitter norepinephrine, and further downstream, dopamine. My dose may be a bit high though. I have a theory that too much SSRI for too long may deplete these more activating neurotransmitters. I'm only an amateur though
Posted by TamaraJ on February 24, 2005, at 8:27:54
In reply to Re: Psych says NO SSRIS for me, posted by Spriggy on February 23, 2005, at 20:55:27
Hi Spriggy!
Here are a few links to info on NADH. Also, below is an article about the supplement by James South. Also, if you don't mind my asking (and sorry if you have already posted about this), but has your family doctor for thyroid, blood sugar problems and nutritional deficiencies?
http://enada.bizland.com/
http://www.supplementconnection.com/101_txt/2110_03_NADH.html
http://www.nadh.com/site7/SYSact20.htm
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by James South MANADH is the abbreviation used for Nicotinamide Adenine Dinucleotide, one of the most important coenzymes in the human brain and body.
A coenzyme is the active, or working form of a vitamin. NADH is the reduced (electron- energy rich) coenzyme form of vitamin B3, while NAD is the oxidized (burned) coenzyme form of B3.
NAD and NADH are converted into each other in numerous different metabolic activities. In some metabolic reactions it is NAD which is the needed catalyst, with NADH a useful by-product, in other reactions the situation is reversed.
NAD and NADH also serve to activate various enzymes, NAD for example, activates alcohol dehydrogenase and acetaldehyde dehydrogenase that are the two enzymes needed to detoxify the alcohol we drink into carbon dioxide and water.
NADH is the first of five enzyme complexes of the electron transport chain, where much of the ATP bioenergy that runs every biological process of our lives is formed.
NADH its vital chemical role
As already noted, NAD(H) is the coenzyme or active form of vitamin B3. The chemistry of NAD(H) is some of the most complex in the human body. NAD(H) is necessary to oxidize (burn) all foodstuffs (fats, sugars, amino-acids) into ATP bioenergy. There are three interlinked energy production cycles: the glycolytic (sugar burning) and Krebs’ citric acid cycles (amino acids and fats are "burned" through the Krebs’ cycle), and the electron transport side chain.
A glycolytic cycle "waste" end product- pyruvic acid- helps power the Krebs’ cycle, while electron "sparks" released from the step by step slow "burning" that occurs in the Krebs’ cycle provide the fuel used by the electron transport side chain to generate much of the ATP bioenergy that literally powers our life. NAD(H) is involved in all of these different cycles, as well as in the conversion of the pyruvate end product of the glycolytic cycle into the beginning fuel of the Krebs’ citric acid cycle. It is NADH, which captures the electron "sparks" thrown off during Krebs’ cycle oxidation and shuttles them to the electron transport side chain energy production cycle.
Each unit of NADH is capable of generating three units of ATP energy. In a very real sense, NADH is the "energy of life" coenzyme.
NAD(H) is a relatively large and complex molecule, as coenzymes go. It is vitamin B3 (niacinamide) combined with a ribose (5-carbon sugar), a phosphate group and an adenine nucleotide (a DNA component). NAD(H) can be made in the liver and other cells from vitamin B3.
It can also be made from the amino acid L-Tryptophan at the "expensive" ratio of 60mg tryptophan for 1mg B3. Taking in exogenous (from outside the body) B3 or NAD(H) may spare the scarce amino acid tryptophan, which is the least plentiful amino in any normal diet. Tryptophan is the precursor of one of the most important antidepressant neurotransmitters, serotonin.
NADH’s role in Parkinson’s disease
J.D. and W. Birkmayer of the Birkmayer Institute have pioneered the clinical use of NADH only in the last decade for Parkinson Therapy, Vienna, Austria.
The Birkmayers’ are the first to develop a stable and absorbable oral tablet form of NADH. They have also conducted groundbreaking research on the use of NADH in Parkinson’s disease, depression, Alzheimer’s dementia and fatigue.
In a series of scientific papers published between 1989 and 1993 the Birkmayers have related their clinical success with NADH in Parkinson’s, as well as provided supporting biochemical experiments and rationale for their success with NADH.
Parkinson’s disease, one of the most common neurological diseases of aging, involves the gradual and even more severe destruction of the dopamine using neurons, in a brain region called the substantia nigra. Parkinson’s involves movement disorders, speech difficulties, depression and cognitive dysfunction.
The traditional medical therapy for Parkinson’s is L-dopa, the amino acid precursor of dopamine. However, this therapy has serious drawbacks. After a period of use, even higher L-dopa doses are required, and these eventually cause severe side effects. In addition the dopamine formed through L-dopa therapy is prone to auto-oxidation to free radical forms that eventually "burn out" what few dopaminergic neurons are left.
(Parkinson’s disease begins when the substantia nigra neuron population has dropped to 20-30% of normal).
Dopamine is usually made inside the neurons that use it through a two step process. The amino acid tyrosine is first converted to L-dopa through an enzyme called tyrosine hydroxylase (TH). L-dopa is then converted to dopamine. Research has shown that it is the activity of tyrosine hydroxylase, which is the rate-limiting controller of dopamine synthesis, and tyrosine hydroxylase activity is considerably lower in Parkinson’s patients than healthy people.
Research has also shown that giving Parkinson’s disease patients L-dopa diminishes their already weak tyrosine hydroxylase activity, thus further limiting their own L-dopa production and increasing the need for L-dopa supplements in an ever worsening vicious spiral.
The Birkmayers discovered that the coenzyme that activates tyrosine hydroxylase- tetrahydrobiopterin (H4BP) is reduced 50% in the brains of Parkinson’s patients compared to age matched healthy controls. They further discovered that NADH activates the enzyme, which helps produce H4BP.
Cell culture studies showed that NADH could elevate H4BP production, tyrosine hydroxylase activity and dopamine production.
The Birkmayers thus decided to try a therapy that might increase the brain’s own production of dopamine, rather than suppress it as L-dopa therapy eventually does.
The Birkmayers’ treated a group of 885 patients with NADH, 415 with intravenous (IV) NADH and 470 with oral NADH (Acta Neurol Scanda, 1993, PP 32-35).
Both groups showed overall good response to treatment, especially in motor improvements, walking, pushing, posture and speech. They also noted cognitive and emotional improvements in some patients, and surprisingly, the improvement figures for both IV and oral NADH were almost identical, and the maximum total improvement was actually shown by oral NADH users.
The Birkmayers also found increased urinary excretion of dopamine metabolites in the patients, indicating there was an actual NADH induced increase in dopamine production. They also were able to reduce and even eliminate other anti-Parkinson medications in some patients.
NADH and its anti-depressant abilities
Based on their success with NADH treatment of Parkinson’s patients, the Birkmayers decided to try NADH as an antidepressant in 205 depressed patients. There are multiple theoretical rationales for such use.
NADH increases brain dopamine and noradrenaline using brain cells use dopamine to make noradrenaline.
It is generally accepted that dopamine and/ or noradrenaline are frequently diminished in the brains of depressed patients, and drugs that raise brain dopamine/ noradrenaline levels will frequently end depression. In addition, through NADH’s sparing of tryptophan (discussed earlier in this article), more tryptophan would be left to end up as brain serotonin, another neurotransmitter frequently reduced in depressives, and when drugs or tryptophan supplements raise brain serotonin, this frequently halts depression.
Lastly, it should be noted that the human brain must produce and use 20% of the body’s total ATP bioenergy, and PET scans of the brains of depressed and demented people frequently show reduced brain energy production. Thus, through its multiple roles in producing ATP energy, NADH might be expected to literally energize the brain, and depression may be in part the mental/ emotional direct experience of the brain’s lowered energy status.
Not surprisingly therefore, the Birkmayers reported in their 1992 paper in New Trends in Clinical Pharmacology, a beneficial effect in 93% of the NADH treated depressed patients.
As with their Parkinson’s patients, the Birkmayers found that NADH tended to induce serious improvement more in younger (less than 65 years old) than older patients. Their Parkinson’s studies also showed shorter duration illness patients to benefit more than longer duration patients.
NADH and Alzheimer’s disease
Because many Parkinson’s patients exhibit dementia as well as neurotransmitter problems, while many Alzheimer’s patients exhibit neuromotor dysfunction as well as dementia, the Birkmayers next tried oral NADH on 17 Alzheimer’s dementia (AD) patients (unpublished paper). These patients ranged from mildly to severely demented. The results were nothing short of astounding! Not only did NADH halt the progression of Alzheimer’s disease, it significantly reversed the cognitive and behavioral problems, even in the worst cases.
The NADH therapy was even able to restore some patients from being virtual "vegetables" to a semblance of normalcy. The Birkmayers also did before and after urinary analyses of dopamine and noradrenaline metabolites and found evidence indicating significantly improved brain dopamine/ noradrenaline activity. While deficits in the function of acetylcholine neurons is the more well known pathology of Alzheimer’s dementia, studies have also shown seriously diminished dopamine/ noradrenaline nerve activity in Alzheimer’s dementia.
In several patients NADH was halted briefly to determine if the improvements would last without it. After several weeks absence of NADH (after a year’s NADH treatment), deterioration began. Once again, NADH was started, and the previous improvements were regained.
NADH a possible fatigue fighter?
In June 1997 W. Birkmayer was to announce the details of a successful trial using NADH to combat fatigue at a Las Vegas health convention. I was unable to get the details at the time of writing this article.
However, given the multi-dimensional roles of NADH in all aspects of human cellular ATP production, favorable results with NADH in fatigue situations is hardly surprising.
NADH doses and uses
The standard dosage of NADH has been 10mg, taken with water 30 minutes before breakfast.
Animal studies suggest 1000mg per kilogram of body weight (70,000mg for a 154 pound human!) to be a tolerable dosage, so aside from the expense, there is no reason not to experiment with higher doses should 10mg not suffice to bring a hoped for benefit.
Those wishing to use NADH in Parkinson’s cases might do well to accompany it with tyrosine and deprenyl.
Those wishing to try NADH for depression might add DLPA, tyrosine and/ or tryptophan or 5-hydroxy-tryptophan.
Those wishing to try NADH for Alzheimer’s dementia might include acetyl L-carnitine and DMAE or centrophenoxine with NADH.
In serious fatigue situations, B-complex vitamins, alpha lipoic acid, CoQ10 or Idebenone and magnesium would be synergistic with NADH.
In situations involving chronic alcoholism, however the cellular NAD/ NADH ratio is already detrimentally skewed in favor of NADH, so NADH would not be appropriate.
Given the routine interconversions in all cells between niacin, niacinamide (2 forms of vitamin B3), NAD and NADH, as well as B3’s sparing effect on tryptophan, it may be useful to add small (50-100mg) doses of vitamin B3 to any NADH regimen
Tamara
Posted by Spriggy on February 24, 2005, at 12:52:11
In reply to Re: Psych says NO SSRIS for me » Spriggy, posted by TamaraJ on February 24, 2005, at 8:27:54
Thanks for the info, YOu people are so resourceful.
And tamara, yes, the doctor has tested me for every thing known to mankind.
I've had blood sugar checked, thyroid, Cat skan, MRI, x rays, EEG, EKG, echo gram, etc...
ROFL..
I'm generally healthy besides the last few months of my life when I've been introduced to medications that have wigged me out totally.
I have a very sensitive central nervous system ( so I am told). Someone could blow a bubble on me and I'd need to be hospitalized. ROFL
Posted by TamaraJ on February 24, 2005, at 13:16:27
In reply to Re: Psych says NO SSRIS for me, posted by Spriggy on February 24, 2005, at 12:52:11
I'm glad to hear your doctor tested for those things. Some doctors are so quick to diagnose depression and anxiety without looking at other things, including nutritional deficiencies.
And, I'm glad to see that you are still holding on to your sense of humor, in spite of everything you have been going through.
I hope things turn around for the better for you soon. Take good care.
Tamara
> Thanks for the info, YOu people are so resourceful.
>
> And tamara, yes, the doctor has tested me for every thing known to mankind.
>
> I've had blood sugar checked, thyroid, Cat skan, MRI, x rays, EEG, EKG, echo gram, etc...
>
> ROFL..
>
> I'm generally healthy besides the last few months of my life when I've been introduced to medications that have wigged me out totally.
>
> I have a very sensitive central nervous system ( so I am told). Someone could blow a bubble on me and I'd need to be hospitalized. ROFL
Posted by TamaraJ on February 27, 2005, at 10:29:07
In reply to Re: Psych says NO SSRIS for me » Spriggy, posted by FredPotter on February 23, 2005, at 18:12:36
Fred,
Are you taking the L-tyrosine with an AD (I seem to recall reading one of your posts where you said you took it with Celexa, but I may be mixing you up with someone else)? Has the Tyrosine helped with anhedonia, apathy, brain fog, and lack of motivation in addition to increasing energy?
Sorry for all the questions. Thanks in advance.
Thanks.
Posted by FredPotter on February 27, 2005, at 14:02:35
In reply to Re: Question for Fred, posted by TamaraJ on February 27, 2005, at 10:29:07
Hi TamaraJ I was on 40 mg of Celexa (Citalopram or Cipramil) a day. I cut it back to 20mg because of the tiredness and restlessness, anhedonia and lack of motivation. I was on this regime for weeks and when all the Christmas stress was over my mood did improve greatly. I then did the Tyrosine thing and was surprised to notice that I became motivated (even dynamic!). This may have happened anyway of course as I couldn't replicate myself and administer a placebo. I also take Lithium and Xanax (not much now). However about once a week I crash at 8pm and fall into a sweet sleep that lasts 12 hours. I don't understand what that's about.
Good luck
Fred
Posted by TamaraJ on February 27, 2005, at 17:37:23
In reply to Re: Question for Fred » TamaraJ, posted by FredPotter on February 27, 2005, at 14:02:35
Thanks so much Fred. That sounds encouraging! Dynamic sounds wonderful :-) I was always a high energy, enthusiastic person until this second depression hit me almost a year ago, and it has been relentless. I would love to feel dynamic again. I, too, am on Celexa (30 mg). So, I may try the L-Tyrosine if the nausea I am experiencing on Provigil continues to the degree it is now. I don't want to give up yet though. It's just nice to know that someone else on Celexa has had good results by augmenting with L-Tyrosine.
Take good care.
Tamara
> Hi TamaraJ I was on 40 mg of Celexa (Citalopram or Cipramil) a day. I cut it back to 20mg because of the tiredness and restlessness, anhedonia and lack of motivation. I was on this regime for weeks and when all the Christmas stress was over my mood did improve greatly. I then did the Tyrosine thing and was surprised to notice that I became motivated (even dynamic!). This may have happened anyway of course as I couldn't replicate myself and administer a placebo. I also take Lithium and Xanax (not much now). However about once a week I crash at 8pm and fall into a sweet sleep that lasts 12 hours. I don't understand what that's about.
> Good luck
> Fred
Posted by FredPotter on February 27, 2005, at 20:50:54
In reply to Re: Question for Fred » FredPotter, posted by TamaraJ on February 27, 2005, at 17:37:23
Hi Tamara I wish you luck. I must add I don't feel particularly dynamic today. OK but not dynamic. L-Tyrosine is a bit expensive too at that dose. Someone said it stops working after a while (days? weeks?) and you need to give it a break. Then start up again. Perhaps I'm no longer deficient in norepinephrine or dopamine. Tweaking these neurotransmitters must start a cascade of effects. I guess the only thing is try it and see. Please let me know how you get on
best wishes
Fred
Posted by TamaraJ on February 27, 2005, at 20:57:46
In reply to Re: Question for Fred » TamaraJ, posted by FredPotter on February 27, 2005, at 20:50:54
I will and thanks for the feedback. And, here's hoping that tomorrow sees you experiencing a return of feeling dynamic :-)
All the best to you,
Tamara
> Hi Tamara I wish you luck. I must add I don't feel particularly dynamic today. OK but not dynamic. L-Tyrosine is a bit expensive too at that dose. Someone said it stops working after a while (days? weeks?) and you need to give it a break. Then start up again. Perhaps I'm no longer deficient in norepinephrine or dopamine. Tweaking these neurotransmitters must start a cascade of effects. I guess the only thing is try it and see. Please let me know how you get on
> best wishes
> Fred
Posted by FredPotter on February 28, 2005, at 13:51:33
In reply to Re: Question for Fred » FredPotter, posted by TamaraJ on February 27, 2005, at 20:57:46
I'm da maan!
This is the end of the thread.
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