This forum is for questions and support pertaining to mental health issues such as: Anger, Dementia, Depression, Family Problems, Memory Problems, Personality Disorders, Phobias, Schizophrenia, Transitions and Work Problems.
I just ordered "Serenity," an all natural anti-depressant and anti-anxiety supplement. Do these really work? Is there anything in any of them I should be worried about? I have heard of Amoryn as well, I am going to give them a try because I have GAD, and my anxiety is now developing into obsessive thoughts and mild to moderate depression, but I do not want to go on any prescription medication. I would love to hear what anyone has to say about this, thanks.
I had a therapist who suggested taking B12 for depression and anxiety which I did. It really did help. I don't know how severe your issues are so it may not work for you. It took 500 mcg twice a day. I'm not familiar with the other products you mentioned so I cannot give you information there.
Hello I have Gad also, and always think im dying from something. I am now tapering off benzos, and let me tell you that your gad will be unimaginable campared to what it is now once you quit benzos!!! So dont start them please. As far has natural things, there are a number that have worked for me and others. They include, lavender, 5 htp, b complex, fish oils, gaba, a good multi vitamin, drink nothing but good water, and lots of excersise. Dont do to much excersising before bed, or it will be hard to sleep. I hope that helps and dont take the drugs the doc will give they are bad for you.
I have been looking at AMORYN as a natural alternative to anti-depressants. Is anyone familar with this product? I have been on Cymbalta for a year and it's been awful. I've been trying to ween off for over a month now and it's excruciating.
Don't know anything about "Serenity" or "Amoryn", however, Brigham had some good suggestions. I am familiar with GABA and DHA (fish oil). An alternative medical doctor suggested that I take GABA for anxiety as I have "white coat" syndrome. My blood pressure shoots up sky high when I walk into a doctor's office. They get readings like 186/110, whereas, this mornming my blood pressure was 118/82. Normal is considered 120/80.
In order to deal with this anxiety problem, last year I started donating blood. On 09/27/05, I had a reading of 160/87 after taking 1,500 mg of GABA. On 05/24/06, I took a total of 3,750 mg of GABA (2 tabs early AM and 3 just before leaving the house) prior to donating blood. My blood pressure reading by the nurse improved to 131/82! For me, this is proof that GABA does in fact help with my high anxiety when dealing with people in "white coats."
Am I depressed? You can bet your bottom dollar that I am as I have delt with depression and extreme anger for decades. In addition, I have Retinitis Pigmentosis (RP). This is a disease of the eyes that will cause one to have tunnel vision and eventually, the vision will shrink to a pinhole and then you become totally blind (some doctors think that I may never go total). Now if you think you got problems, wait until you have to give up driving. Then you will have something to really be depressed and angry about.
I use DHA (fish oil) to mellow me out so I don't hurt somebody. I use 2,000 mg every day. See my posted response to the question in this forum about "wife dealing with husband anger" for my full blown testimony about DHA.
To become a fully normal person (happy w/o depression), I suspect that I may need to start taking SAMe. The problem is my budget as I already spend more than a hundred dollars a month to treat my various ailments with natural supplements and expensive food-based multi-vitamins/minerals.
You are going in the right direction by pursuing natural cures for your depression/anxiety disorder.
Er, yes, they have, quite exensively -- a least hypericum
and 5-HTP, plus some of the other ingredients.
True. They are not regulated, which is both good and bad.
"so its uncertain how much is in each tablet."
True. Quality control is a problem in this industry. It
should be better. But then, lots of things should be better.
It is not all that bad when you consider the alternative.
If it were "properly" regulated, we would have pills that
are fantastically expensive, instead of affordable.
"Yes some work, to some degree"
Yes, they sure do! However many quality control problem
incidents do occur, usually the quality is pretty good and
the results are gratifying. And best of all, the results
come CHEAPLY. You can manage a wide variety of mood and
related disorders for a buck a day, or less. This is a tiny
fraction of the cost normally encountered. Another advantage
is great relative SAFETY. Nutritional and herbal supplements
seldom or never cause serious side effects; pharmaceutical
products routinely cause serious side effects -- including
upwards of 200,000 deaths per year. (Nutritional supplements
cause ZERO deaths per year.) So, obviously, there are some
very clear advantages, along with the disadvantages.
"you can't rely on them."
True. But then, you can't rely on anything, such as the
"proven" SSRIs and etc. (There exists a spirited debate
in the literature as to whether the SSRIs are truly effective
at all -- and that is apart from the suicide problems, libido
problems, and on and on.) This is all a big **** shoot. You
try a pill, and see if it works or not. Often, it does not,
even if a 10-scazillion-dollar pharmaceutical company is
behind it. Pharmaceutical products have been great for some
few people, but the costs (on all levels) are extremely high.
In an uncertain world, in which nothing is perfectly safe
or perfectly effective or perfectly reliable (or perfectly
anything!), you place your bets and you take your chances.
One of the keys to doing this affordably is to focus first
on the most-affordable stuff. That would be the stuff that is
NOT touted highly in the commerce-oriented health press,
health stores, magazines, etc. I am talking about plain old
megavitamins. This stuff can cost as little as a nickel or
a dime per day, and can have great benefits. FROM THERE, move
up the commercial food chain toward more expensive, more
exotic stuff, as and if necessary. (Then, as a last resort,
go with the pharmaceutical drugs, if absolutely necessary.)
For example, in the case of Brigham's benzo/anxiety problem,
the key nutrient is niacin, or niacinamide. Niacinamide has
been shown to bind to, and stimulate mildly, benzodiazepine
receptors. This reflects at the molecular level the common
clinical experience with high-dose niacin or niacinamide as
a very mild relaxant and anti-anxiety compound (which is
also mentioned in the published literature, occasionally).
Futher, slow-release niacin has been used successfully to
facilitate comfortable benzo withdrawal -- no mean feat!
Here are more details from a paper that I wrote, some years back:
: Tryptophan pyrrolase (TP) can be slightly inhibited in
: humans by large doses of niacinamide (about 1-2 grams per
: day), as evidenced by reductions in plasma and urinary TP
: products . The combination of tryptophan (2-12
: grams/day) with niacinamide (.5-4 grams/day) has been used
: successfully in both depression and mania [110,111];
: co-administration of niacinamide apparently reduced
: tryptophan requirements.
: Large doses of niacinamide have sedative effects in
: animals  and numerous other benzodiazepine- and
: barbiturate-like activities in both animals and humans:
: anticonvulsant, anti-aggressive, muscle relaxant and
: hypnotic (see  and references therein).
: Therapy with slow-release nicotinic acid (1-2 grams/day,
: with glucose) has recently been found effective for
: reducing the frequency and severity of symptoms of drug
: withdrawal in benzodiazepine-dependent humans .
: (Nicotinic acid -- niacin -- is a close chemical relative
: of niacinamide with identical activity as a vitamin and as
: a co-enzyme precursor.) These effects may or may not be
: due to serotonergic enhancement via alterations of TP and
: tryptophan metabolism. In any case, high-dose niacinamide
: has an array of psychopharmacologic activities that render
: it an attractive adjunct to tryptophan in nutritional
: formulations when mild sedative/hypnotic effects are
: 109. Moller SE. Pharmacokinetics of tryptophan, renal
: handling of kynurenine and the effect of nicotinamide on
: its appearance in plasma and urine following L-tryptophan
: loading of healthy subjects. Eur J Clin Pharmacol 21:
: 137-42, 1981.
: 110. Chouinard G, Young SN, Annable L.
: Tryptophan-nicotinamide, imipramine and their combination
: in depression. Acta Psychiatr Scand 59: 395-414, 1979.
: 111. Chouinard G, Young SN, Annable L. A controlled trial
: of L- tryptophan in acute mania. Biol Psychiatry 20:
: 546-57, 1985.
: 112. Beaton JM. The sedative effects of nicotinamide on
: gerbil wheel- running activity. Experientia 32: 1036-7,
: 113. Mohler H, Polc P, Cumin R. Nicotinamide is a brain
: constituent with benzodiazepine-like actions. Nature 278:
: 563-5, 1979.
: 114. Vescovi PP, Gerra G, Ippolito L. Nicotinic acid
: effectiveness in the treatment of benzodiazepine
: withdrawal. Curr Ther Res 41: 1017-21, 1987.
And remember, you can do the high-dose niacin/niacinamide thing
for only a few nickels per day! Go for the most bang for the
buck FIRST, then go on toward more-expensive stuff as and
when necessary. Just remember that you have to ratchet the
dose up to rather high levels, usually. 100mg pills will not
do the job -- though it is good to start at that level just
to test the waters. Typically, a gram or two (or even three)
will be necessary to get serious results; i.e. 1000-3000 mgs.
Another extremely important brain compound is ascorbic acid
(aka "vitamin C").
Check out the fantastic review article below, on ascorbic
acid and the brain. It is comprehensive. The value of a review
like this is that it pulls together and explains hundreds of
individual little papers that would take days or weeks to run
down and digest, oneself.
Ascorbic acid is MUCH more important for the brain than even I
thought 12 years ago. (And I thought it was pretty important
then.) The brain is greedy for ascorbate. The brain accumulates
it and is reluctant to let go of it -- just like cells accumulate
potassium and do not want to let go of it, or like the whole body
accumulates iron and does not let go of it. In these cases, the
element (iron, potassium) is conserved so jealously because it has
proven to be absolutely indispensable to life or to the function
of the given tissue or organ. The mechanisms for this tight grip
are well-developed and are probably very old, in evolutionary
The implication is that ascorbate is to the brain as iron (and
oxidative metabolism) is to higher forms of life! If this is
correct, the clinical implications are profound. This is relevant
to all behavioral/psychiatric problems, as well as for normal
brain function. The brain is an ascorbate-concentrating organ that
uses that ascorbate as a critical neuromodulator (modifier of
neurotransmitter action) and as a protective and repair agent
against the stress of oxidized neurotransmitter derivatives
(hydroxydopamine and etc.). And if the brain does not get an
optimal amount of ascorbate... well... your guess is as good as
mine, but my bet is that this is one (of several) of the keys to
why depression, addiction, character defects, personality
disorders and so forth are so prevalent, and also as to why (by
virtue of cumulative oxidative damage to neurons) these problems
are so darned *persistent*. It might also be one of the causes of
declining intelligence and general competence.
The very high concentration of ascorbate in the brain, its broad
distribution, and its modulation of critical neurotransmission
processes, suggests a fundamental "ground-substance" role for
ascorbate of only slightly less importance than, say, protein or
lipids. What would happen if your brain were even slightly short
of protein or lipids? Well, everything (behaviorally and
cognitively) would start falling apart, and you would soon become
psychotic, or sociopathic, or demented, or something very weird
and undesirable. Ascorbate in the brain reminds me of DHA
(docosahexaenoic acid, omega-3) in the brain: it is present in
great abundance, with roles at one time unknown, but now being
elucidated -- roles with incredible clinical (and social!)
I suspect that most of the population is undersupplied, neurally,
with ascorbate, and especially at-risk and behavior-disordered
segments of the population -- which is unfortunately most of the
population. This is Irwin Stone's "hypoascorbemia", but specific
to the nervous system; hence, perhaps: *neuro-ascorbopenia*. (I'm
taking a page from that book that has described neural
hypoglycemia as "neuro-glycopenia".) Of course this would have
little or nothing to do with classical scurvy.
For the life of me I cannot understand why these
incredibly-significant facts are not front-page news in the
biological psychiatry and addictionology communities.
Once again, ascorbic is supremely economical. You can buy
a pound of the pure crystals at Trader Joe's for 10 bucks;
that's a little over .02 per gram! So even a goodly 5-10
gram-per-day dose is only a dime or two.
Prog Neurobiol 1994 Aug;43(6):537-65
A vitamin as neuromodulator: ascorbate release into the
extracellular fluid of the brain regulates dopaminergic and
Rebec GV, Pierce RC
Department of Psychology, Indiana University, Bloomington 47405.
Ascorbate is an antioxidant vitamin that the brain accumulates
from the blood supply and maintains at a relatively high
concentration under widely varying conditions. Although neurons
are known to use this vitamin in many different chemical and
enzymatic reactions, only recently has sufficient evidence emerged
to suggest a role for ascorbate in interneuronal communication.
Ascorbate is released from glutamatergic neurons as part of the
glutamate reuptake process, in which the high-affinity glutamate
transporter exchanges ascorbate for glutamate. This heteroexchange
process, which also may occur in glial cells, ensures a relatively
high level of extracellular ascorbate in many forebrain regions.
Ascorbate release is regulated, at least in part, by dopaminergic
mechanisms, which appear to involve both the D1 and D2 family of
dopamine receptors. Thus, amphetamine, GBR-12909, apomorphine, and
the combined administration of D1 and D2 agonists all facilitate
ascorbate release from glutamatergic terminals in the neostriatum,
and this effect is blocked by dopamine receptor antagonists. Even
though the neostriatum itself contains a high concentration of
dopamine receptors, the critical site for dopamine-mediated
ascorbate release in the neostriatum is the substantia nigra.
Intranigral dopamine regulates the activity of nigrothalamic
efferents, which in turn regulate thalamocortical fibers and
eventually the glutamatergic corticoneostriatal pathway. In
addition, neostriatonigral fibers project to nigrothalamic
efferents, completing a complex multisynaptic loop that plays a
major role in neostriatal ascorbate release. Although
extracellular ascorbate appears to modulate the synaptic action of
dopamine, the mechanisms underlying this effect are unclear.
Evidence from receptor binding studies suggests that ascorbate
alters dopamine receptors either as an allosteric inhibitor or as
an inducer of iron-dependent lipid peroxidation. The applicability
of these studies to dopamine receptor function, however, remains
to be established in view of reports that ascorbate can protect
against lipid peroxidation in vivo. Nevertheless, ample behavioral
evidence supports an antidopaminergic action of ascorbate.
Systemic, intraventricular, or intraneostriatal ascorbate
administration, for example, attenuates the behavioral effects of
amphetamine and potentiates the behavioral response to
haloperidol. Some of these behavioral effects, however, may be
dose-dependent in that treatment with relatively low doses of
ascorbate has been reported to enhance dopamine-mediated
behaviors. Ascorbate also appears to modulate glutamatergic
transmission in the neostriatum. In fact, by facilitating
glutamate release, ascorbate may indirectly oppose the action of
dopamine, though the nature of the neostriatal
dopaminergic-glutamatergic interaction is far from settled.
Ascorbate also may alter the redox state of the NMDA glutamate
receptor thus block NMDA-gated channel function.(ABSTRACT
TRUNCATED AT 400 WORDS) Publication Types: Review Review,
academic PMID: 7816935, UI: 95116645
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