![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 266 to 290 of 435. Go back in thread:
Posted by Simus on October 11, 2004, at 22:29:59
In reply to Re: Supplements for brain fog? » karaS, posted by raybakes on October 11, 2004, at 8:46:22
> The other article talked about tryptophan excess altering the sensitivity of the dopamine receptors - so maybe something that antagonizes dopamine, may make it's receptors overly sensitive, as a compensation? what do you think?
>
>
> "The greater prolactin response to l-tryptophan infusion in depressed subjects may be the result of an increase in dopamine receptor sensitivity, secondary to reduced dopamine levels."Hmmm... I was thinking of trying tryptophan or 5HTP now that I am on Wellbutrin instead of a SSRI, but it sounds like that still wouldn't be a very good idea. Any insight on this anyone?
Simus
Posted by raybakes on October 12, 2004, at 3:30:59
In reply to Mitochondria, fatty acids, carnitine.....Jlx » raybakes, posted by tealady on October 9, 2004, at 20:20:22
Hi Jan, came across this flow chart for the synthesis of carnitine - it's SAMe that's needed for it's formation, so again it's the whole methylation pathway that needs to work, not just methionine.
http://www.med.unibs.it/~marchesi/carnitine_biosynth.html
came across some articles that say creatine causes depression in some people - I wonder if taking creatine without taking methyl donors can result in a backlog of unactivated creatine, and so have a detrimental effect on brain energy?
Ray
Posted by karaS on October 16, 2004, at 0:50:05
In reply to Re: Supplements for brain fog? » karaS, posted by raybakes on October 11, 2004, at 8:46:22
> > Decreasing estrogen isn't exactly helping my dopamine problems. Boosting dopamine can't help either because my system won't allow for it. Not a hopeful picture...
>
> Hi Kara,> The other article talked about tryptophan excess altering the sensitivity of the dopamine receptors - so maybe something that antagonizes dopamine, may make it's receptors overly sensitive, as a compensation? what do you think?
> "The greater prolactin response to l-tryptophan infusion in depressed subjects may be the result of an increase in dopamine receptor sensitivity, secondary to reduced dopamine levels."
>
> Another abstract made a mention of genetic errors in the dopamine receptor too...
>
> Sorry, don't have any straight answers!
>
> Ray
>Ray,
I keep hearing and reading lately about serotonergics and their antagonistic effect on dopamine via the receptors. I'm not going to take any tryptophan or 5-htp even for sleep. Maybe my idea to start on Cymbalta isn't such a good one either. Even though it's balanced with NE, maybe I shouldn't be taking anything with serotonin activity at all.
Don't apologize for not having the answer. No one does yet. It doesn't exist.
Thanks as always for your imput,
Kara
Posted by karaS on October 16, 2004, at 0:52:42
In reply to Re: Supplements for brain fog, posted by Dave001 on October 11, 2004, at 15:53:48
> >
> > > You really have to see them all to believe the variety. Check out: http://www.cknow.com/ckinfo/emoticons.htm
> >
> > That website on the emoticons is freakin' unbelievable!!! Of course most of them are useless since no one could possibly know them. My favorite is about the eunich but I won't post that here for fear of offending anyone (Dr. Bob really).
> >
>
> Some of the more extravagant examples could almost be mistaken for a regular expression in Perl.
>
> Dave
>
I'll have to take your word on that one - but I bet the meanings of those emoticons are much more interesting!K
Posted by karaS on October 16, 2004, at 0:55:08
In reply to Re: Supplements for brain fog? » raybakes, posted by Simus on October 11, 2004, at 22:29:59
> > The other article talked about tryptophan excess altering the sensitivity of the dopamine receptors - so maybe something that antagonizes dopamine, may make it's receptors overly sensitive, as a compensation? what do you think?
> >
> >
> > "The greater prolactin response to l-tryptophan infusion in depressed subjects may be the result of an increase in dopamine receptor sensitivity, secondary to reduced dopamine levels."
>
> Hmmm... I was thinking of trying tryptophan or 5HTP now that I am on Wellbutrin instead of a SSRI, but it sounds like that still wouldn't be a very good idea. Any insight on this anyone?
>
> Simus
Maybe not a good idea. I know I was pushing it earlier but now I don't think it's worth the potential dopamine antagonism.-K
Posted by tealady on October 16, 2004, at 4:59:25
In reply to Re: Supplements for brain fog?, posted by karaS on October 16, 2004, at 0:50:05
> > The other article talked about tryptophan excess altering the sensitivity of the dopamine receptors - so maybe something that antagonizes dopamine, may make it's receptors overly sensitive, as a compensation? what do you think?
>
> > "The greater prolactin response to l-tryptophan infusion in depressed subjects may be the result of an increase in dopamine receptor sensitivity, secondary to reduced dopamine levels."
> >II'm probably completely off course here, that the problem may be caused by competition for the same enzyme cofactors ...
Dopamine is produced from tyrosine by the action of tyrosine hydroxylase (TH), which uses tetrahydrobiopterin (BH4) as a cofactor. BH4 is also a cofactor for tryptophan and serotonin synthesis, and also for the enzyme nitrous oxide synthetase
or possibly its P5P B6 which I THINK is needed by somehow by tyrosine hydroxylase ?(not sure here) , and low adrenal function meaning it can take up to 21 days(heard that from a doc) to resynthesize enough tyrosine hydroxylase..not sure of this but I think it fits in somewhere with the competiton theory too.
The competiton means making too much of one(say serotonin) will deplete the ability to make the other (say dopamine)..and depletion will eventually cause oversensitivity of the related receptorsI guess.hmm guess I must be low on serotonin looking at this
Jan
http://www.genome.jp/dbget-bin/show_pathway?map00350+1.14.16.2
http://www.genome.jp/dbget-bin/show_pathway?map00380+1.14.16.4
Posted by raybakes on October 17, 2004, at 7:41:55
In reply to Tryptophan/ serotonin, tyrosine/dopamine... RAY, posted by tealady on October 16, 2004, at 4:59:25
Hi Jan, wrote a bit about testosterone in an anxiety thread - did you manage to make any sense of it?
> II'm probably completely off course here, that the problem may be caused by competition for the same enzyme cofactors ...Think that could be a possibility! Have to look out for some research..
>
> Dopamine is produced from tyrosine by the action of tyrosine hydroxylase (TH), which uses tetrahydrobiopterin (BH4) as a cofactor. BH4 is also a cofactor for tryptophan and serotonin synthesis, and also for the enzyme nitrous oxide synthetase
>
> or possibly its P5P B6 which I THINK is needed by somehow by tyrosine hydroxylase ?(not sure here)dopa decarboxylase to dopamine needs p5p...
, and low adrenal function meaning it can take up to 21 days(heard that from a doc) to resynthesize enough tyrosine hydroxylase..not sure of this but I think it fits in somewhere with the competiton theory too.Haven't heard this, but did find an abstract that says vitamin d can stimulate tyrosine hydroxylase gene expression.
Just looked up on pubmed and found this though...
Prevalence and clinical associations of 10 defined autoantibodies in autoimmune polyendocrine syndrome type I.
Department of Medical Sciences, University Hospital, SE-751 85 Uppsala, Sweden.
The prevalence of autoantibodies against nine intracellular enzyme autoantigens, namely 21-hydroxylase, side-chain cleavage enzyme (SCC), 17 alpha-hydroxylase, glutamic acid decarboxylase 65, aromatic L-amino acid decarboxylase, tyrosine phosphatase-like protein IA-2, tryptophan hydroxylase (TPH), tyrosine hydroxylase, cytochrome P450 1A2, and against the extracellular calcium-sensing receptor, was assessed in 90 patients with autoimmune polyendocrine syndrome type I. A multivariate logistic regression analysis was performed for the presence of autoantibodies as independent predictors for different disease manifestations. Reactivities against 21-hydroxylase and SCC were associated with Addison's disease with odds ratios (ORs) of 7.8 and 6.8, respectively. Hypogonadism was exclusively associated with autoantibodies against SCC with an OR of 12.5. Autoantibodies against tyrosine phosphatase-like protein IA-2 were associated with insulin-dependent diabetes mellitus with an OR of 14.9, but with low sensitivity. Reactivities against TPH and, surprisingly, glutamic acid decarboxylase 65, were associated with intestinal dysfunction, with ORs of 3.9 and 6.7, respectively. TPH reactivity was the best predictor for autoimmune hepatitis, with an OR of 27.0. Hypoparathyroidism was not associated with reactivity against any of the autoantigens tested. No reactivity against the calcium-sensing receptor was found. Analysis of autoantibodies in autoimmune polyendocrine syndrome type I patients is a useful tool for establishing autoimmune manifestations of the disease as well as providing diagnosis in patients with suspected disease.
>
> The competiton means making too much of one(say serotonin) will deplete the ability to make the other (say dopamine)..and depletion will eventually cause oversensitivity of the related receptorsI guess.
>
> hmm guess I must be low on serotonin looking at thisI sometimes wonder if balancing the immune system, increasing energy and, blood flow and oxygen, would bring a lot of the body's neurotansmitters into balance? Just seems to be so much juggling and interaction - surely god can't be so mean!!
Thanks for the pathways - bit complicated! Mentioned in a reply to Larry about dopamine and noradrenaline degrading to toxic quinones when monoamine oxidase degrades them - methylation via the enzyme COMT can protect the brain from these quinones (think they are dopachrome, adrenochrome). Another abstract talked about biopterin and it's precursor, protection tyrosine hyroxylase.
The role of adrenochrome in stimulating the oxidation of catecholamines.
Bindoli A, Scutari G, Rigobello MP.
Centro Studio Biomembrane, CNR, Padova, Italy. labbind@civ.bio.unipd.it
Adrenochrome, a stable oxidation product formed after oxidation of adrenaline, strongly stimulates oxygen uptake occurring during the autoxidation of adrenaline, other catecholamines and ascorbate. Oxygen consumed is converted to hydrogen peroxide suggesting the occurrence of a redox cycling process. The reduction of adrenochrome operated by adrenaline is accelerated by the exclusion of oxygen indicating that the oxidation of adrenaline occurs directly and superoxide anion does not necessarily mediate it. Oxygen consumption, observed in the catecholamine/adrenochrome and ascorbate/adrenochrome systems, is due to the autoxidation of leucoadrenochrome that, at variance with adrenaline, easily autoxidizes also at physiological pH. Therefore, in these systems, leucoadrenochrome appears to be the major determinant of the production of superoxide anion.
Ray
Posted by raybakes on October 17, 2004, at 14:06:20
In reply to Re: Supplements for brain fog?, posted by karaS on October 16, 2004, at 0:55:08
Hi Kara, do you know what dopamine receptor is hypersensitive with you? Seen that there are D1, D2, D3, D4, and D5 receptors - the hypersensitivity of D2 seems to be linked with schizophrenia and anxiety - things like coffee tea, chocolate, vitamin A, biopterin, l-dopa, forskolin and biopterin are linked to receptor sensitivity in different dopamine receptors.
Here's one abstract as an example..
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8263772
Ray
Posted by raybakes on October 17, 2004, at 14:11:03
In reply to Re: Supplements for brain fog?, posted by karaS on October 16, 2004, at 0:50:05
and this is interesting too..
Posted by karaS on October 17, 2004, at 17:16:40
In reply to Re: Supplements for brain fog? » karaS, posted by raybakes on October 17, 2004, at 14:06:20
> Hi Kara, do you know what dopamine receptor is hypersensitive with you? Seen that there are D1, D2, D3, D4, and D5 receptors - the hypersensitivity of D2 seems to be linked with schizophrenia and anxiety - things like coffee tea, chocolate, vitamin A, biopterin, l-dopa, forskolin and biopterin are linked to receptor sensitivity in different dopamine receptors.
>
> Here's one abstract as an example..
>
> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8263772
>
> Ray
Unfortunately I don't know which one or ones are involved yet. I have to do more research (if it's even possible for me to figure that out). I certainly hope it's not the Parkinson's (D1?)related receptors. I also recently read (if I'm understanding this correctly) that the problem might instead be with the 1-b adrenergic receptors. They seem to serve as a "trans-synaptic mechanism" which can render the dopamine itself as nonfunctional and would therefore have the same effect as hypersensitive autoreceptors.At any rate, the last sentence of the abstract (copied below) that you provided was very encouraging. It suggests that it is indeed possible to treat this kind of hypersensitivity (at least with respect to the D1 receptor). I'm hopeful that has implications for the other D receptors as well.
"Our data suggests that chronic L-dopa/carbidopa treatment reverses the increased dopaminergic activity and D1 receptor functional supersensitivity seen after 6-hydroxydopamine lesions, and indicates a D1 receptor-mediated action of L-dopa"
Thanks Ray
Posted by karaS on October 17, 2004, at 17:24:08
In reply to Re: Supplements for brain fog? » karaS, posted by raybakes on October 17, 2004, at 14:11:03
> and this is interesting too..
>
> http://www.sliderule.ca/research.htm
So the problem might also be these G-proteins and not necessarily too many presynaptic autoreceptors? It appears that I have lots to investigate!Thanks again.
Kara
Posted by JLx on October 17, 2004, at 18:10:54
In reply to Re: Tryptophan/ serotonin, tyrosine/dopamine... RAY » tealady, posted by raybakes on October 17, 2004, at 7:41:55
> I sometimes wonder if balancing the immune system, increasing energy and, blood flow and oxygen, would bring a lot of the body's neurotansmitters into balance? Just seems to be so much juggling and interaction - surely god can't be so mean!!Don't forget the hormone complications too. For women, we've got the monthly fluctuations when we're young and even worse ones when we get older. I think most of us have extra sensitivity to stress too. We're like the canaries in the mine when it comes to societal issues such as our food supply, changes in our family structures, environmental pollution, etc.
The following article caught my eye recently. Do you think the UK will institute some changes to prevent this? I'm wondering because you have national health insurance, and therefore, some governmental interest in prevention of illness unlike our own system in the US which is dominated by money and political influence by Big Pharma and the medical establishment.
http://millennium-debate.org/indsun27june042.htm
"Change in UK diets 'Could Trigger Mental Health Crisis'
Changes in British diets are going to lead to an explosion in mental health problems, medical experts said yesterday. They warned of a crisis even bigger than the epidemic of obesity afflicting the UK.
They said that most of the increase could probably be blamed on changes in farming and food over the past 20 years, which have led to deficiencies in essential omega-3 fatty acids. ...
pregnant women with lower intakes of omega-3 are more likely to have children who will go on to have behavioural problems, attention disorders and other problems.
The mothers themselves were more likely to suffer from depression if they had lower-than-average intakes of the fatty acid.
Professor Crawford warned: "We are facing a monumental crisis here, and a lot of it is due to the very simple issue of diet."
This follows a study highlighted earlier this year by the Royal College of Psychiatrists, which revealed a world-wide link between a lack of omega-3 in the diet and schizophrenia. This research showed that people who ate high levels of sugar and dairy products, instead of oily fish, were more likely to develop severe mental illness. ...
omega-3 is linked to brain development and mental health and is found in "green" foods such as cabbage due to the photosynthesis process.
Professor Crawford said that at the beginning of the century, people's omega-3 intake was higher because of traditional farming practices where cows and lambs were fed on grass.
However, intensive agriculture practices over the past 50 years have meant that livestock is now fed on grain and vitamins rather than omega-3-rich foods.
Mental health problems are already predicted to become the third most costly burden of disease in the world by 2020."
Btw, I noticed that you said you'd been to a presentation where someone from the Monroe Institute was speaking? What did he say and what did you think of him? I have had some experience with their brainwave technology and there's a thread on it here: http://www.dr-bob.org/babble/alter/20040928/msgs/398366.html
JL
Posted by raybakes on October 18, 2004, at 15:07:43
In reply to Re: Tryptophan/ serotonin, tyrosine/dopamine... RAY » raybakes, posted by JLx on October 17, 2004, at 18:10:54
>
> Don't forget the hormone complications too. For women, we've got the monthly fluctuations when we're young and even worse ones when we get older. I think most of us have extra sensitivity to stress too. We're like the canaries in the mine when it comes to societal issues such as our food supply, changes in our family structures, environmental pollution, etc.Yes, not forgetting the hormones too! Although, pituitary regulation does rely on neurotransmitters, and I read a recent article that found that every single step of hormone production is influenced by the immune system.
I totally agree about omega 3 fatty acids (thanks for the article) and often wonder what the effects will be now and in future generations.
>
> The following article caught my eye recently. Do you think the UK will institute some changes to prevent this? I'm wondering because you have national health insurance, and therefore, some governmental interest in prevention of illness unlike our own system in the US which is dominated by money and political influence by Big Pharma and the medical establishment.Even though we have national health insurance, most doctors get most of their information through the drug companies - the government are also heavily influenced by the drug companies too, as is european government!
>> Btw, I noticed that you said you'd been to a presentation where someone from the Monroe Institute was speaking? What did he say and what did you think of him? I have had some experience with their brainwave technology and there's a thread on it here: > JL
The guy was skip atwater - I've used hemi sync before and found it can reduce the fogginess, and improve alertness, even the ones that are supposed to relax. I've also done a signature sound training course, and like using a large bass speaker to vibrate my whole body with sound!! I did find a frequency once that made a bit difference to my brain (i lost what frequency it was though, doh!) and interestingly,i felt great for two weeks until i had some potato crisps cooked in sunflower oil!
Ray
Posted by raybakes on October 19, 2004, at 9:51:41
In reply to Re: Supplements for brain fog? » raybakes, posted by karaS on October 17, 2004, at 17:24:08
Hi Kara, found these abstracts today...
Grima, G., B. Benz, et al. (2003). "Dopamine-induced oxidative stress in neurons with glutathione deficit: implication for schizophrenia." Schizophr Res 62(3): 213-24.
Glutathione (GSH) is the main non-protein antioxidant and plays a critical role in protecting cells from damage by reactive oxygen species (ROS) generated by dopamine (DA) metabolism. We reported a decrease of GSH levels ([GSH]) in CSF and in prefrontal cortex in vivo in schizophrenics [Eur. J. Neurosci. 12 (2000) 3721]. A GSH deficit may lead to membrane peroxidation and microlesions around dopaminergic terminals, resulting in loss of connectivity. To test this hypothesis, we studied the effect of DA in cultured cortical neurons with low [GSH]. DA alone decreased [GSH] by 40%. This effect appears to result from direct conjugation of DA semiquinone/quinone with GSH. Ethacrynic acid (EA) decreased [GSH] in a concentration-dependent manner. When added to EA, DA further lowers [GSH]. As this additional decrease is blocked by superoxide dismutase (SOD) or D(1)/D(2) receptor antagonists, it likely involves the generation of superoxide via activation of DA receptors. It also reduces the mitochondrial membrane potential. Most interestingly, a significant decrease in number of neuronal processes (spines analogous) was induced by 24-h application of DA only in low [GSH]. These data, compatible with our hypothesis, is consistent with the dendritic spines reduction reported in schizophrenia and could be related to abnormalities in synaptic connectivity.
And this one..
also bought a good book on the thyroid today called "the great thyroid scandal and how to survive it"
Ray
Posted by karaS on October 19, 2004, at 14:14:53
In reply to Re: Supplements for brain fog? » karaS, posted by raybakes on October 19, 2004, at 9:51:41
> Hi Kara, found these abstracts today...
>
> Grima, G., B. Benz, et al. (2003). "Dopamine-induced oxidative stress in neurons with glutathione deficit: implication for schizophrenia." Schizophr Res 62(3): 213-24.
>
> Glutathione (GSH) is the main non-protein antioxidant and plays a critical role in protecting cells from damage by reactive oxygen species (ROS) generated by dopamine (DA) metabolism. We reported a decrease of GSH levels ([GSH]) in CSF and in prefrontal cortex in vivo in schizophrenics [Eur. J. Neurosci. 12 (2000) 3721]. A GSH deficit may lead to membrane peroxidation and microlesions around dopaminergic terminals, resulting in loss of connectivity. To test this hypothesis, we studied the effect of DA in cultured cortical neurons with low [GSH]. DA alone decreased [GSH] by 40%. This effect appears to result from direct conjugation of DA semiquinone/quinone with GSH. Ethacrynic acid (EA) decreased [GSH] in a concentration-dependent manner. When added to EA, DA further lowers [GSH]. As this additional decrease is blocked by superoxide dismutase (SOD) or D(1)/D(2) receptor antagonists, it likely involves the generation of superoxide via activation of DA receptors. It also reduces the mitochondrial membrane potential. Most interestingly, a significant decrease in number of neuronal processes (spines analogous) was induced by 24-h application of DA only in low [GSH]. These data, compatible with our hypothesis, is consistent with the dendritic spines reduction reported in schizophrenia and could be related to abnormalities in synaptic connectivity.
>
> And this one..
>
> http://arjournals.annualreviews.org/doi/abs/10.1146/annurev.neuro.27.070203.144206;jsessionid=j96WSOG9YwX9
>
> also bought a good book on the thyroid today called "the great thyroid scandal and how to survive it"
>
> Ray
Thanks Ray.
I was taking 1200 mg. of NAC for a while but didn't notice any relief. Wouldn't that have provided enough glutathione had that been my problem or is that more the kind of thing where it would take a long time to see any kind of difference? Also, I read another post here a little while back about the perils of taking NAC when you have mercury amalgams (which I have) so I'm a bit worried now about taking it again.
In terms of the second abstract about the G protein-coupled receptor kinases (GRKs), I can't help but think that by the time they have something on the market for that I'll be much too old to care. I really do appreciate your sending me the abstract though. I guess I'm just feeling sorry for myself now. Ok, time for some CBT. Talk to you later.
Kara
Posted by JLx on October 19, 2004, at 20:45:42
In reply to Re: Tryptophan/ serotonin, tyrosine/dopamine... RAY » JLx, posted by raybakes on October 18, 2004, at 15:07:43
>
> >
> > Don't forget the hormone complications too. For women, we've got the monthly fluctuations when we're young and even worse ones when we get older. I think most of us have extra sensitivity to stress too. We're like the canaries in the mine when it comes to societal issues such as our food supply, changes in our family structures, environmental pollution, etc.
>
> Yes, not forgetting the hormones too! Although, pituitary regulation does rely on neurotransmitters, and I read a recent article that found that every single step of hormone production is influenced by the immune system.
>
> I totally agree about omega 3 fatty acids (thanks for the article) and often wonder what the effects will be now and in future generations.
> >
> > The following article caught my eye recently. Do you think the UK will institute some changes to prevent this? I'm wondering because you have national health insurance, and therefore, some governmental interest in prevention of illness unlike our own system in the US which is dominated by money and political influence by Big Pharma and the medical establishment.
>
> Even though we have national health insurance, most doctors get most of their information through the drug companies - the government are also heavily influenced by the drug companies too, as is european government!
> >
>
> > Btw, I noticed that you said you'd been to a presentation where someone from the Monroe Institute was speaking? What did he say and what did you think of him? I have had some experience with their brainwave technology and there's a thread on it here: > JL
>
> The guy was skip atwater - I've used hemi sync before and found it can reduce the fogginess, and improve alertness, even the ones that are supposed to relax. I've also done a signature sound training course, and like using a large bass speaker to vibrate my whole body with sound!! I did find a frequency once that made a bit difference to my brain (i lost what frequency it was though, doh!) and interestingly,i felt great for two weeks until i had some potato crisps cooked in sunflower oil!
>
>
> Ray
Hmm...that IS interesting. I'm getting to where I look forward to my morning CD session. The one I'm listening to now is supposed to be theta and delta but when I listened to it at night once I was awake for hours. I'm surprised more people here don't try these things.JL
Posted by raybakes on October 20, 2004, at 5:50:10
In reply to Re: Supplements for brain fog? » raybakes, posted by karaS on October 19, 2004, at 14:14:53
>
> I was taking 1200 mg. of NAC for a while but didn't notice any relief. Wouldn't that have provided enough glutathione had that been my problem or is that more the kind of thing where it would take a long time to see any kind of difference? Also, I read another post here a little while back about the perils of taking NAC when you have mercury amalgams (which I have) so I'm a bit worried now about taking it again.
Hi Kara,Yes there is always the concern that mercury can be transported into the brain as well as out - in the excellent book "children with starving brains" they have a few protocols listed for heavy metal detoxification - they first use something called 'captomer' which is claimed not to cross the blood brain barrier.
I would be very surprised if glutathione wasn't a problem - there are many ways of raising it, each individual to the person. All the co-factors might be necessary combined with NAC - Thiodox is an excellent supplement. Glutamine is useful in raising glutathione as it can also buffer cellular acidity, as well as supply gluatamate for glutathione. My own practitioner gave me something by jarrow called 'homocysteine pf' yesterday which helped me massively. I talked to her about my concerns about my poor methylation and how it's required for creatine prouction and acidity buffering - so we checked it out and found I was really high in folate (like Jan) but couldn't use it - homocysteine PF got my folate working (checked with kinesiology). As glutamine and methylation improve my fog too, I think part of the 'fogginess' may be because I'm too acid.
Here's a few abstracts....
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8412764&dopt=Abstract
this is interesting about buffering and celluar calcium, sorry it's complex though!
'These results suggest that local ADP buffering by PCr is essential for normal Ca(2+) regulation by the SR.' (SR = sarcoplasmic reticulum)
So when energy is low, and ADP is higher than ATP, the cell becomes more acid - creatine (in my case 'think methylation' ) buffers the acidity and allows a cell to function more efficiently.
Posted by raybakes on October 20, 2004, at 14:11:14
In reply to Re: Supplements for brain fog? » raybakes, posted by karaS on October 19, 2004, at 14:14:53
'PEA also induced a decrease in the density of D1-like dopamine (DA) receptors in the rat striatum'
How do you do on chocolate or salami?!!
Posted by raybakes on October 20, 2004, at 15:18:06
In reply to Re: Supplements for brain fog? » raybakes, posted by karaS on October 19, 2004, at 14:14:53
Sorry, getting a bit carried away!!!
this is interesting, implicating a virus in inhibiting the dopamine transporter (DAT), and so causing damage to dopaminagenic neurons
Posted by Simus on October 20, 2004, at 23:15:28
In reply to Re: Supplements for brain fog? » karaS, posted by raybakes on October 20, 2004, at 14:11:14
> 'PEA also induced a decrease in the density of D1-like dopamine (DA) receptors in the rat striatum'
>
> How do you do on chocolate or salami?!!Sorry to butt in here... I have been following this thread (or trying to anyway) because Kara and I have so many symptoms in common. I have been semi-lost in the later posts, but now you completely lost me. I just have to ask about the chocolate and salami comment... What do they contain (PEA?), and how would you expect Kara (or me) to react after eating them? Thanks in advance.
Simus
Posted by raybakes on October 21, 2004, at 2:36:23
In reply to Re: Supplements for brain fog? » raybakes, posted by Simus on October 20, 2004, at 23:15:28
> Sorry to butt in here... I have been following this thread (or trying to anyway) because Kara and I have so many symptoms in common. I have been semi-lost in the later posts, but now you completely lost me. I just have to ask about the chocolate and salami comment... What do they contain (PEA?), and how would you expect Kara (or me) to react after eating them? Thanks in advance.
Hi Simus, sorry to make things sound so confusing! I'm trying to work my way through it and get some meaning from it too. Kara talked about the supersensitivity of her dopamine receptors and I was looking for things that might downregulate the receptors. I saw references to PEA downregulating the D1 receptor and know PEA is in chocolate but was surprised to find it in salami (and I suppose in other meats and cheeses too?). Personally I know I can feel down and anxious until I eat some plain chocolate - after sex my mood drops, and plain chocolate is sometimes the only thing that raises it! Same with emotion too, can feel difficult to experience emotion, especially after sex, and wonder whether PEA loss is something to do with it?One abstract mentioned that the body can make PEA from phenylalanine, via phenylalanine decarboxylase (magnesium + p5p), but it can also turn phenylalanine, PEA and tyrosine into tyramine, the amine involved in migraines - I used to get headaches when I took DLPA, but don't at the moment - not sure why?
I'm also interested in protecting dopamine and dopamine receptors, and have seen several references to dopamine causing damage to neurons if not metabolised or transported efficiently. Methylation appears to be one way to protect them, glutathione, another, but found the idea of viruses inhibiting dopamine metabolism interesting, as dopamine irregularities are implicted in autism/adhd kids and they respond really well to anti-virals.
Ray
Posted by raybakes on October 21, 2004, at 8:15:03
In reply to Re: Supplements for brain fog? » karaS, posted by raybakes on October 20, 2004, at 15:18:06
found this of interest....
Effect of oestradiol on dopamine receptors and protein kinase C activity in the rat pituitary: binding of oestradiol to pituitary membranes.
Joubert-Bression D, Brandi AM, Birman P, Peillon F.
INSERM U 223, Faculte de Medecine Pitie-Salpetriere, Paris, France.
Oestradiol exerts an important modulatory influence on the release of prolactin which is accomplished partly through disruption of the inhibitory influence of dopamine. We have focused on the status of the anterior pituitary D2 dopamine receptor in female rats treated chronically with oestradiol or progesterone. A direct membrane effect of these steroids on the dopamine system was also investigated in vitro. Both steroids affected the status of the D2 receptor, oestradiol decreasing the number of sites in vitro and progesterone increasing it both in vitro and in vivo. The in vitro studies demonstrated that these steroids exert a direct membrane effect on the D2 receptor. These results correlated with an in vitro short-term physiological effect of oestradiol and progesterone on the dopaminergic inhibition of prolactin release, oestradiol decreasing it while progesterone had the opposite effect. Binding studies with [3H] oestradiol on pituitary membranes revealed a site for oestradiol of high affinity and low capacity, indicating that oestradiol's membrane effects could be mediated by a specific receptor. In vivo treatment with oestradiol also induces proliferation of prolactin-secreting cells (lactotrophs). We focused on the effect of oestradiol on protein kinase C activity, which is involved in both secretion and proliferation. In female rats treated with oestradiol total protein kinase C activity was increased by 74% (particulate 90%, soluble 71%) in comparison with controls. This effect was reversed by concomitant treatment with a dopamine agonist. Thus in the pituitary oestradiol and progesterone affect the characteristics of membrane components that are implicated in the physiological control of the cell. Whether these effects are post-transcriptional only or are also mediated through direct membrane mechanisms needs further investigation.
Posted by raybakes on October 21, 2004, at 9:12:28
In reply to Supplements for brain fog?, posted by KaraS on June 23, 2004, at 23:06:51
sorry to post so much stuff....hope it's still of interest!
Vitamin D(3) attenuates 6-hydroxydopamine-induced neurotoxicity in rats.
Wang JY, Wu JN, Cherng TL, Hoffer BJ, Chen HH, Borlongan CV, Wang Y.
Department of Physiology, National Defense Medical Center, Taipei, Taiwan.
Previous reports have demonstrated that exogeneous administration of glial cell line-derived neurotrophic factor (GDNF) reduces ventral mesencephalic (VM) dopaminergic (DA) neuron damage induced by 6-hydroxydopamine (6-OHDA) lesioning in rats. Recent studies have shown that 1,25-dihydroxyvitamin D(3) (D3) enhances endogenous GDNF expression in vitro and in vivo. The purpose of present study was to investigate if administration of D3 in vivo and in vitro would protect against 6-OHDA-induced DA neuron injury. Adult male Sprague-Dawley rats were injected daily with D3 or with saline for 8 days and then lesioned unilaterally with 6-OHDA into the medial forebrain bundle. Locomotor activity was measured using automated activity chambers. We found that unilateral 6-OHDA lesioning reduced locomotor activity in saline-pretreated animals. Pretreatment with D3 for 8 days significantly restored locomotor activity in the lesioned animals. All animals were sacrificed for neurochemical analysis 6 weeks after lesioning. We found that 6-OHDA administration significantly reduced dopamine (DA), 3,4-dihydroxy-phenylacetic acid (DOPAC) and homovanilic acid (HVA) levels in the substantia nigra (SN) on the lesioned side in the saline-treated rats. D3 pretreatment protected against 6-OHDA-mediated depletion of DA and its metabolites in SN. Using primary cultures obtained from the VM of rat embryos, we found that 6-OHDA or H(2)O(2) alone caused significant cell death. Pretreatment with D3 (10(-10) M) protected VM neurons against 6-OHDA- or H(2)O(2)-induced cell death in vitro. Taken together, our data indicate that D3 pretreatment attenuates the hypokinesia and DA neuronal toxicity induced by 6-OHDA. Since both H(2)O(2) and 6-OHDA may injure cells via free radical and reactive oxygen species, the neuroprotection seen here may operate via a reversal of such a toxic mechanism.
Protective effects of 1 alpha,25-(OH)(2)D(3) against the neurotoxicity of glutamate and reactive oxygen species in mesencephalic culture.Ibi M, Sawada H, Nakanishi M, Kume T, Katsuki H, Kaneko S, Shimohama S, Akaike A.
Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan.
This study was undertaken to determine whether 1 alpha,25-dihydroxyvitamin D3 [1 alpha,25-(OH)(2)D(3)], an active metabolite of vitamin D, protects dopaminergic neurons against the neurotoxic effects of glutamate and dopaminergic toxins using rat mesecephalic culture. Brief glutamate exposure elicited cytotoxicity in both dopaminergic and non-dopaminergic neurons. Pretreatment, but not co-administration, of 1 alpha,25-(OH)(2)D(3) protected both types of neurons against the cytotoxicity of glutamate in a concentration- and time-dependent manner. The neuroprotective effect of 1 alpha,25-(OH)(2)D(3) was inhibited by the protein synthesis inhibitor, cycloheximide. To investigate the mechanisms of these neuroprotective effects, we examined the effects of 1 alpha,25-(OH)(2)D(3) on neurotoxicity induced by calcium ionophore and reactive oxygen species (ROS). Pretreatment with 1 alpha,25-(OH)(2)D(3) protected both types of neurons against the cytotoxicity induced by A23187 in a concentration-dependent manner. Furthermore, 24-h pretreatment with 1 alpha,25-(OH)(2)D(3) concentration-dependently protected both types of neurons from ROS-induced cytotoxicity. A 24-h incubation with 1 alpha,25-(OH)(2)D(3) inhibited the increase in intracellular ROS level following H(2)O(2) exposure. A 24-h exposure to 1-methyl-4-phenylpyridium ion (MPP(+)) or 6-hydroxydopamine (6-OHDA) exerted selective neurotoxicity on dopaminergic neurons, and these neurotoxic effects were ameliorated by 1 alpha,25-(OH)(2)D(3). These results suggest that 1 alpha,25-(OH)(2)D(3) provides protection of dopaminergic neurons against cytotoxicity induced by glutamate and dopaminergic toxins by facilitating cellular functions that reduce oxidative stress.
Posted by Simus on October 21, 2004, at 9:48:36
In reply to Re: Supplements for brain fog? » Simus, posted by raybakes on October 21, 2004, at 2:36:23
Thanks Ray, that is all very fascinating. Your posts aren't confusing. I am just trying to process the vast amount of information I get here with less-than-usual mental faculties...
The reason I perked up at your last post here was the mention of chocolate and salami. I had just a few days ago told Kara about chocolate being my mood "cure-all". And, one thing that I never really understood was my cravings for salami, summer sausage, etc. I just chalked that one up to being drawn to wrong foods.
Something you mentioned in your post to me that I find interesting was "the body can make PEA from phenylalanine, via phenylalanine decarboxylase (magnesium + p5p)". Oddly enough, I was very deficient in both magnesium and B6 and I believe I must still be to some degree (I have symptoms again within a day or two of missing my supplements).
I am going to go out on a limb and ask you a question that may seem really dumb to you. Right now I am digging through my memory archives to place where I have heard "phenylalanine" a lot in the past. Is that in over-the-counter diet pills? (Sorry if I am way off.)
You mentioned viruses also. Whenever I run a low-grade fever I have mental symptoms (depression, anxiety, brain fog...). I am going through that right now in fact. I just associated the mental symptoms with the fever and not so much with the cause of the fever. Now I am rethinking things... The first time I noticed this connection was when I had a severe case of mono 25 years ago (now 43). Do you think that this same virus could remain dormant in my body for this long and pop up every so often causing ugly mental symptoms? Hmmm...
Thanks again,
Simus
Posted by Simus on October 21, 2004, at 10:05:28
In reply to Re: Supplements for brain fog? » KaraS, posted by raybakes on October 21, 2004, at 9:12:28
That is really fascinating. Since I am still processing info and trying to tie everything together...
I am very sensitive to glutamates. Do you think that this could be a vitamin D deficiency? Well, at least it sounds like D would prevent damage caused by glutamates, huh?
Is "1 alpha,25-dihydroxyvitamin D3 [1 alpha,25-(OH)(2)D(3)]" found in the typical vitamin D, or is there a specific form of D or D complex I would need to buy?
Thanks for your patience.
Simus
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