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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 25 of 30. This is the beginning of the thread.
Posted by linkadge on November 17, 2002, at 7:06:50
I also have added a high dose fish oil regeimen
to my daily routine. I have noticed a definate
curb to my lows of the day, and it has also
improved my sleep quality.Omega 3 has the ability to influence dopamine
transmission which also has an impact on
OCD. Dopamine is so misunderstood that it
is often unstudied in mental disease.Dopamine controlls many things, color preception
movement controll, motivation, jealousy, spatial
function and memory, psychosis, paranoia, mania, anxiety, cortisol production, hunger and eating
disorders, many phobias like calostrophobia and ones involving height space and time, sensation of imagination and mystery, strong role in religious belief.Those who were religious were shown to have higher dopamine levels. And riligous fanatacism and obsession is related to even higher dopamine levels.
Linkadge
Posted by Kari on November 17, 2002, at 13:55:47
In reply to This is true, posted by linkadge on November 17, 2002, at 7:06:50
Do you know what it is that fish oil does to dopamine levels?
TIA.
Posted by Larry Hoover on November 17, 2002, at 14:20:27
In reply to Re: This is true, posted by Kari on November 17, 2002, at 13:55:47
> Do you know what it is that fish oil does to dopamine levels?
> TIA.Darn good question! Thanks for asking, as I hadn't realized this aspect of the effects of DHA. Apparently (according to the last study below), the adverse effects are reversible on supplementation with DHA.
Lipids 2001 Sep;36(9):937-44
Polyunsaturated fatty acids and cerebral function: focus on monoaminergic neurotransmission.
Chalon S, Vancassel S, Zimmer L, Guilloteau D, Durand G.
INSERM U316, Laboratoire Biophysique Medicale et Pharmaceutique, Universite Francois Rabelais, 37200 Tours, France. chalon@univ-tours.fr
More and more reports in recent years have shown that the intake of polyunsaturated fatty acids (PUFA) constitutes an environmental factor able to act on the central nervous system (CNS) function. We recently demonstrated that the effects of PUFA on behavior can be mediated through effects on the monoaminergic neurotransmission processes. Supporting this proposal, we showed that chronic dietary deficiency in alpha-linolenic acid in rats induces abnormalities in several parameters of the mesocortical and mesolimbic dopaminergic systems. In both systems, the pool of dopamine stored in presynaptic vesicles is strongly decreased. This may be due to a decrease in the number of vesicles. In addition, several other factors of dopaminergic neurotransmission are modified according to the system affected. The mesocortical system seems to be hypofunctional overall [e.g., decreased basal release of dopamine (DA) and reduced levels of dopamine D2 (DAD2) receptors]. In contrast, the mesolimbic system seems to be hyperfunctional overall (e.g., increased basal release of DA and increased levels of DAD2 receptors). These neurochemical changes are in agreement with modifications of behavior already described with this deficiency. The precise mechanisms explaining the effects of PUFA on neurotransmission remain to be clarified. For example, modifications of physical properties of the neuronal membrane, effects on proteins (receptors, transporters) enclosed in the membrane, and effects on gene expression and/or transcription might occur. Whatever the mechanism, it is therefore assumed that interactions exist among PUFA, neurotransmission, and behavior. This might be related to clinical findings. Indeed, deficits in the peripheral amounts of PUFA have been described in subjects suffering from neurological and psychiatric disorders. Involvement of the monoaminergic neurotransmission function has been demonstrated or hypothesized in several of these diseases. It can therefore be proposed that functional links exist among PUFA status, neurotransmission processes, and behavioral disorders in humans. Animal models are tools of choice for the understanding of such links. Improved prevention and complementary treatment of neurological and psychiatric diseases can be expected from these studies.
J Lipid Res 2000 Jan;41(1):32-40
Modification of dopamine neurotransmission in the nucleus accumbens of rats deficient in n-3 polyunsaturated fatty acids.Zimmer L, Delion-Vancassel S, Durand G, Guilloteau D, Bodard S, Besnard JC, Chalon S.
INSERM U316, Laboratoire de Biophysique Medicale et Pharmaceutique, Universite Francois Rabelais, Tours, France.
We studied the effects of a diet chronically deficient in alpha-linolenic acid, the precursor of long-chain n-3 polyunsaturated fatty acids, on dopaminergic neurotransmission in the shell region of the nucleus accumbens of rats. In vivo microdialysis experiments showed increased basal levels of dopamine and decreased basal levels of metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), in awake rats from the deficient group compared to controls. The release of dopamine under KCl stimulation was similar in both dietary groups. By contrast, the release of dopamine from the vesicular storage pool under tyramine stimulation was 90% lower in the deficient than in the control rats. Autoradiographic studies in the same cerebral region revealed a 60% reduction in the vesicular monoamine transporter sites in the deficient group. Dopamine D(2) receptors were 35% increased in these rats compared to controls, whereas no change occurred for D(1) receptors and membrane dopamine transporters. These results demonstrated that chronic n-3 polyunsaturated fatty acid deficiency modifies several factors of dopaminergic neurotransmission in the nucleus accumbens. These findings are in agreement with the changes in dopaminergic neurotransmission already observed in the frontal cortex, and with the behavioral disturbances described in these deficient rats.
J Nutr 1998 Dec;128(12):2512-9
Dietary fish oil affects monoaminergic neurotransmission and behavior in rats.Chalon S, Delion-Vancassel S, Belzung C, Guilloteau D, Leguisquet AM, Besnard JC, Durand G.
INSERM U316, Laboratoire de Biophysique Medicale et Pharmaceutique, 37200 Tours, France.
We studied the effects of a fish oil enriched diet on fatty acid composition of cerebral membranes and on several neurochemical and behavioral variables of monoaminergic function in rats. The frontal cortex, striatum, hippocampus and cerebellum were studied in rats fed fish oil (FPO, 50% salmon oil + 50% palm oil), which provided an (n-6)/(n-3) polyunsaturated fatty acid (PUFA) ratio of 0.14 versus 6. 19 in controls fed a diet containing a mixture of African peanut oil and rapeseed oil. In the FPO group compared to the control group, the major modifications in fatty acid composition of cerebral membranes included the following: higher levels in 22:6(n-3), lower levels in 20:4(n-6) and a significantly greater proportion of phosphatidylserine. Dopamine levels were 40% greater in the frontal cortex of rats fed FPO than from those fed the control diet. In this cerebral region there was also a reduction in monoamine oxidase B (MAO-B) activity and greater binding to dopamine D2 receptors. By contrast, a lower binding to dopamine D2 receptors (-7%) was observed in the striatum. Ambulatory activity was also reduced in FPO-fed rats, possibly related to observed changes in striatal dopaminergic receptors. This suggested that the level of (n-6) PUFA, which was considerably lower in the FPO diet than in the control diet, could act on locomotion through an effect on striatal dopaminergic function, whereas the high level of (n-3) PUFA could act on cortical dopaminergic function.
Behav Brain Res 2002 Apr 1;131(1-2):193-203
Influence of a dietary n-3 fatty acid deficiency on the cerebral catecholamine contents, EEG and learning ability in rat.Takeuchi T, Fukumoto Y, Harada E.
Department of Veterinary Physiology, Faculty of Agriculture, Tottori University, 680-0945, Tottori, Japan. takeuchi@muses.tottori-u.ac.jp
Female rats were fed on a diet deficient in (n-3) fatty acid or enriched in docosahexaenoic acid (DHA) diet from mating and throughout pregnancy and lactation. Pups fed on the same diet as their dams were used for experiments. The effects of dietary (n-3) fatty acid deficiency on cerebral catecholamine contents and electroencephalogram (EEG) in rat pups during the postnatal development were investigated. The (n-3) deficient rat pups showed significantly lower levels of noradrenaline (NA) in cerebral cortex, hippocampus and striatum, compared with those in the DHA adequate rats. Dopamine (DA) contents were significantly lower in the (n-3) deficient rats until the 7th day of age. These results were consistent with observations in the EEG analysis, relative powers of fast activities in the EEG recorded from the (n-3) deficient rats were significantly lower than those in the DHA adequate rats. The effect of supplementation with DHA in (n-3) deficient rats on learning ability was also studied in a model of learning, active avoidance test and three-panel run way test, after weaning. Although the percentages of avoidance in the (n-3) deficient rats (saline group) were constantly 20% or less until the 3rd session, the percentage of avoidance in the DHA supplemented rats rapidly increased to 53% following the first administration. While in the three-panel runway test, there were no significant differences between two groups. These results suggest that chronic consumption of a (n-3) fatty acid deficient diet could modify the biosynthesis of catecholamine in the brain, and might induce the behavioral disturbances. Furthermore, the decreased learning ability induced by (n-3) deficiency in the active avoidance test is a reversible following a supplementing DHA after the weaning.
Posted by linkadge on November 17, 2002, at 15:14:28
In reply to Re: This is true, posted by Larry Hoover on November 17, 2002, at 14:20:27
This is another thing, the Omega 3 complex does seem to be very helpful in a broad range of psychatric disorders. I believe that EPA is more involved in Unipolar depression and Bipolar but, DHA seems to be the one that helps most in Schitosfrenia (spelled wrong). It seems that it is very effective at regulating dopamine levels.
The paranoia aspect of Manic and Schisofrenic states is often perpetuated by excess dopamine leves at certain receptors but, Omega 3 improves responces of dopamine at other receptors.
Since the beginning of supplementation I have noticed. Improved color preception, improved memory recall, and and reduced stress.
The reduced stress seems to be the most profound effect. It seems that I can more easily accept who I am and what I can do - I feel much less obligation to conform to others. For instance,
worying about failing a test has been replaced by a sence that I love myself enough take the course again if I need to. I can just stop everything and let time stand still in its tracks.I know this is all very abstract but these are profound changes that have just been growing on me after about two months of high fish oil supplementation. The improvement in color
preception I think is my mind's way of telling
me that this is not just all abstract.
I do recomend it.Linkadge
Posted by Roman on November 17, 2002, at 15:29:14
In reply to Re: This is true, posted by linkadge on November 17, 2002, at 15:14:28
Posted by linkadge on November 17, 2002, at 18:45:53
In reply to How much do you take? -- (nm) » linkadge, posted by Roman on November 17, 2002, at 15:29:14
I take six of the standard 180/120
capsuls a day. I also eat lots of
Tuna and a few omega 3 eggs a week.I am actually quite pleased, as mental
illness has been quite prominant in my
family for a few generations.
You can get Omega 3 from plant sources
as well, (like flax) but it is not EPA or
DHA it is something that the body can
convert to EPA and DHA. It is being proposed
that some individuals my have a hampared
ability to make this conversion, and thats
why taking EPA DHA (in fish oil) - which
goes directly to the brain without conversion -
helps some so much.I figure it will cose around $200 a year
for the fish oil. For the improvment I
am seeing I would be willing to pay much
more.Linkadge
Posted by oracle on November 17, 2002, at 22:26:12
In reply to This is true, posted by linkadge on November 17, 2002, at 7:06:50
Dopamine is so misunderstood that it
> is often unstudied in mental disease.I would suspect this is not true. All thought disorders involve dopamine. The AP's effect
dopamine, and many movement disorders have a
dopamine facet. However, AP's, by effecting dopamine, cause movement disorders, so it is tricky.
Posted by Roman on November 18, 2002, at 0:12:57
In reply to Re: How much do you take? --, posted by linkadge on November 17, 2002, at 18:45:53
I bought some a few months ago but stopped taking them when I started the AD.
I'm going to try it again for awhile and see what happens.
I have Eskimo3 and they're quite expensive. Is there a brand you suggest or one I should not purchase?
Thanks for the info.
-Roman
Posted by linkadge on November 18, 2002, at 13:03:01
In reply to Re: How much do you take? -- » linkadge, posted by Roman on November 18, 2002, at 0:12:57
What I mean to say was unstudied in
Depression. Mentioned was the fact
that amineptine was removed from the market
because it made well people feel better.I think Dopaminergic drugs are generally
considered an evil feel good. Like
a cocaine high. I thihk the government
wants us all very happy and non agressive.Linkadge :)
Posted by Kari on November 18, 2002, at 14:27:17
In reply to Re: This is true, posted by Larry Hoover on November 17, 2002, at 14:20:27
Posted by Kari on November 18, 2002, at 14:33:14
In reply to Re: This is true, posted by linkadge on November 17, 2002, at 15:14:28
Thanks for sharing your experience with fish oil. I am glad to hear this has really helped you.
Kari.
Posted by oracle on November 18, 2002, at 14:57:06
In reply to Re: How much do you take? --, posted by linkadge on November 18, 2002, at 13:03:01
> I think Dopaminergic drugs are generally
> considered an evil feel good.Actually they shut down thoughts and emotions
Posted by Dinah on November 18, 2002, at 16:54:48
In reply to Re: How much do you take? --, posted by oracle on November 18, 2002, at 14:57:06
Could you tell me more about that?
Posted by oracle on November 18, 2002, at 18:57:53
In reply to Re: Do they really? » oracle, posted by Dinah on November 18, 2002, at 16:54:48
> Could you tell me more about that?
Read up an any AP.
Posted by Dinah on November 18, 2002, at 20:46:45
In reply to Re: Do they really?, posted by oracle on November 18, 2002, at 18:57:53
I'm sorry, oracle. I was overtired and my post was brief. I've read and read on risperdal, but your post struck me, in its brevity, by something I was trying to put my finger on in my experience of risperdal.
I didn't find it stopped thought, perhaps because i wasn't on it at a high dose or for very long. But it stopped emotions dead almost immediately. So I asked you to say more in the hopes that it would help me clarify my opinions about the med further.
But yes, of course I'll keep searching.
Dinah
Posted by oracle on November 19, 2002, at 0:24:21
In reply to Re: Antipsychotics » oracle, posted by Dinah on November 18, 2002, at 20:46:45
Dinah,
Give me a little bit and I will be more verbrose.
Many changes at work today, I am tired.
Posted by Dinah on November 19, 2002, at 4:35:43
In reply to Re: Antipsychotics, posted by oracle on November 19, 2002, at 0:24:21
I understand completely, Oracle. Sorry to hear about the changes, they can be stressful. If you get the chance, no pressure.
Take care.
Dinah
Posted by Kari on November 19, 2002, at 13:53:48
In reply to Re: How much do you take? --, posted by oracle on November 18, 2002, at 14:57:06
> I think Dopaminergic drugs are generally
> considered an evil feel good.>Actually they shut down thoughts and emotions
Aren't dopaminergic drugs dopamine agonists? :)
It's true- an excess of this neurotransmitter creates, among other problems, some kind of "high" which feels evil due to its abnormality.
As for APs, the shutting down of thoughts and emotions depends on the problem and the dosage. In cases in which overstimulation causes emotional blunting and a sense of being "out of it", a very low dose of an AP can actually allow the person to regain access to emotions (not that it's so easy:)) and to feel somewhat "real" again. On higher doses it will cause a shutdown of everything, I guess.
Posted by oracle on November 19, 2002, at 14:57:33
In reply to Re: How much do you take? -- » oracle, posted by Kari on November 19, 2002, at 13:53:48
> Aren't dopaminergic drugs dopamine agonists? :)
That is a good question. Many on this board seem to think it is more/less, ie, I need more or less dopamine. It is far more complex than that.
One can show a decrease or increase at some point
but this is just the tip of the iceberg. Also if you effect one NT you effect them all.An NT has many functions, dopamine effects thought and movement. Few seem to be aware
of the serious long term effects of AP's, causing movement disorders. Everyone taking the older AP's will have these problems if they take them long enough.So I think that if your understanding does not take into account the complexity then making treatment choices based on the logic dopamine=good=more is not reasonable. Nor is
it reasonable to see this all as a government plot.Hear this:
We have 50 years experience with the AP's, and they all cause disfiguring movement disorders
long term. Given these drugs work with dopamine I would tread carefully here. You are free to ignore the history for these meds, but remember the meds themselves cover up EPS and TD (movement disorders) and if are some point you are afflected
the damage and movement disorder is permanent.This is not a crit of Essencial Fatty Acids or "Fish Oil". I suspect it is the anti-oxident
effects that are causing many to get better.
No zebras here, just horses.
Posted by Dinah on November 19, 2002, at 15:03:38
In reply to Re: How much do you take? -- » oracle, posted by Kari on November 19, 2002, at 13:53:48
Kari, I can find almost nothing on how antipsychotics work, other than that they don't know. I realize they work on D2 receptors, but that doesn't really explain it in terms of functioning. Is it that excess dopamine causes overstimulation? And what the drug does is to reduce overstimulation?
How does dopamine work in both Parkinsons and Schizophrenia? Do the side effects of antipsychotics mimic Parkinsons? Or is it a different dopamine receptor involved in each. I'm reading Awakenings right now, but haven't found any answers to my befuddlement.
Risperdal worked great on me in a way, but there was almost an on/off switch in terms of emotions. My pdoc said that would wear off, but for me to believe him I have to be able to understand how it works.
I know I'm inundating you with questions, and I certainly don't expect you to know the answers. I can't even find where the scientists know the answers. After having been on SSRI's for a while, I have a pretty good idea of the way they work, at least in me, altho I hear other people have different experiences. Why can't the scientists explain these things better? Or is my lack of Google ability showing again.
Posted by linkadge on November 20, 2002, at 6:47:45
In reply to Re: Antipsychotics » Kari, posted by Dinah on November 19, 2002, at 15:03:38
Antipsychotics block the D2 receptor in the
brain. This is proposed to be the therapudic
action. What this does, is in blocking one
receptor leaves more dopamine for other
receptors.Parkinsons is related to a decrease in the production of dopamine the brain (a part that has nothing to do with emotion) however the drugs used, raise dopamine in the emotion centers as well.
Cocine and other stims can cause psychosis when abused, this is because of enhanced activity of dopamine at the D2 receptor. Stim psychosis is
effectivly relieved with antipsychotics.Dopamine is involved in repeating an action. It brings pleasure from learning and getting better at a previously known action. In excess it creates extreme feelings of power and remarkable self controll. In excess, a person may feel to have special powers and such. It enhances self awareness, movement controll, cognition and spacial skills. This is why someone high on Cocane can generally drive at brakeneck speeds and survive for longer than normal.
As far as depression goes, too little dopamine can result in feelings of weakness, fragility, like not being a real solid and physical being. In some, raising dopamine relieves thoughs of impending heart attack. Have you ever hated the concept of a heart - why did God have to make something that beats all the time and not something stationay (afraid to sleep as if your awareness if it keeps it going?) You may be low on dopamine.
Dopamine is an inhibitoy neurotransmitter at some sites and a excitory at others. It very often closes of 'change' and makes one stubborn, it can make a situation impossible to change -(that is, in the presence of low seritonin)
It has a strong component in Sociability. When too high it provokes feelings of self centeredness and self power - 'what could I possibly learn from them' But when too low, someone may doubt their ability to carry on a conversation - fearing they may say something stupid. An excessivly high dopamine person often becomes disconnected in this way. They feel nobody really understands the powerful insight they get - they feel other's talk is too simplictic that it has no meaning.
You may now see how the symptoms of paranoia can generally be left untreated. The person is very smart insightful and intuitive - they should surely know what is real and what is not. There is a very very fine line between insight and delusions, self confidence and self centerdness which is all controlled by dopamine.
The cocaine high is not all that good. Intead of giving you satisfaction with the world - you all of a sudden SEE all the problems AND you become powerful - your internal dialog speeds up and your ideas don't get stuck at a cetain point anymore - you see them right though - they're attainable. You don't give a darn about others cause it is YOUR power than can get it all.
You can run without the slightest stumble and hop fences with remarkable spacial accuracy. Math skills go nuts as cognition and spacial skills go through the roof - you can see how John Nash - A beautiful mind - might not recognise it as a problem.Psychosis and abject fear go hand in hand. Some peoples anxiety has a psychotic component or a psychotic twinge. Feeling like everything has a devine purpose for example. Feeling like doom and dread, and impending justice will come. This is another reason why antipsychotics help some anxiety disorders and even some panic disorders.
Also note that Dopamine driven, low seritonin depressives very rarely seek help. They feel good about themselves - but that usually itThis is why it is absolutely crutial for the patient to explain the 'thoughts' that accompany the feeling. Saying one is depressed is not enought - fining out what the patient is depressed about - can really help discover what
neurotransmitter is out of whack .In my depression I never had feelings low self worth. I always - throughout the whole thing - thought I was smart - but things just had an unbearable sence of sadness to them. This is why SSRIs worked the best for me. Some others don't feel as sad as they do lousy - feeling worthless as it is called - dopamine has a VERY STRONG component in the feeling of self worth. Ever notice that a psychotic person will almost NEVER feel worthless ?! Low dopamine can also make the world seem dirty and poluteted and dry and stuff like that.
So, people out there, tell us more about your depression, what gets you depressed, what thoughts accompany your depression.
Linkadge
Posted by Kari on November 20, 2002, at 7:59:28
In reply to Re: How much do you take? --, posted by oracle on November 19, 2002, at 14:57:33
Hi oracle,
There seems to have been some misunderstanding regarding my previous message, but you are absolutely right about the need to be cautious with drugs affecting dopamine. That is also the reason I don't take such substances, even though these are the meds which would make a difference in my case. On an old AP I have developed dystonia, TD and parkinsonism and one cannot assume that taking a newer one would guarantee no neurological problems. For people who must take dopamine blockers, however, the new atypicals can be considered a blessing, since the risks are reduced. For others, perhaps it is really better to look for substitutes and hope they work.
As for the "government plot", taking drugs to increase the effect of dopamine simply for pleasure (if I understood correctly) is not a good idea :)
Posted by Kari on November 20, 2002, at 8:55:36
In reply to Re: Antipsychotics » Kari, posted by Dinah on November 19, 2002, at 15:03:38
Hi Dinah,
I guess that as far as meds are concerned, there is a lot more mystery than knowledge. Certain meds can be assumed to affect certain neurotransmitters but that may not be their main mode of action. Side effects, however, seem to be more concrete.
Linkadge wrote a good explanation about the way dopamine works in Parkinson's and schizophrenia. Perhaps the reduction of dopamine in other areas of the brain in which this effect is not needed is responsible for the parkinsonism induced by APs. This lack of specification may also explain the psychotic symptoms induced by drugs which treat Parkinson's.
When you say there was an "on/off" switch of emotions with Risperdal, are you referring to mood swings or to transient symptoms of emotional blunting? Do you still take this med? Have you noticed any positive effects?
I assume that a "dopamine excess" can cause overstimulation resulting in emotional blunting and that dopamine blockers can change this, as I have seen this effect in me and have heard of it in others.
What effect have you noticed with SSRIs? Do you feel blunted on them?
Posted by Kari on November 20, 2002, at 13:59:08
In reply to Re: Antipsychotics, posted by linkadge on November 20, 2002, at 6:47:45
Hi Linkadge,
I found your message about the effects of dopamine very interesting.
Perhaps it gets complicated when a person has symptoms of both high and low dopamine at the same time (different brain areas). It is all so confusing.
Another problem in diagnosis is that high dopamine seems to decrease one's ability to communicate and to volunteer information about unusual feelings or perceptions. It would not be too difficult to identify these in a psychotic person. In the case of personality or other disorders involving a disturbed dopamine balance, the person may feel a need to hide certain thoughts and feelings and succeed in doing so without realizing that his subjective feeling of overwhelming shame is preventing him from receiving appropriate treatment. In other cases he may take these perceptions for granted and fail to realize they are problematic.
Kari.
Posted by Dinah on November 20, 2002, at 18:37:13
In reply to Re: Antipsychotics, posted by linkadge on November 20, 2002, at 6:47:45
Thanks Linkadge.
I'm going to have to take some time to digest all this. Obviously dopamine is a multifaceted neurotransmitter.
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