27 replies to this topic

[MrHappy]

http://neuroamer.wor...-and-cognition/

[manic_racetam]

"It is also important to note that hyperactivity in mice refers to increased activity and locomotion, which could result from many things and probably has little or no relationship to the hyperactivity in children with ADHD."

[MrHappy]

Any suggestion on how you'd categorize it instead, though? I'm stumped. Permanently affected, too..

[MrHappy]

(the mice, I meant)

[Ark]

That crap is in everything including canned soup, time to put a warning label on products containing BPA.

[medievil]

Bad garbage this shit, usually im not into a hatehype like with aspartame, but this has bad evidence behind it.

[thedevinroy]

"It is also important to note that hyperactivity in mice refers to increased activity and locomotion, which could result from many things and probably has little or no relationship to the hyperactivity in children with ADHD."

http://www.ncbi.nlm....pubmed/18555207

The effects of environmental neurotoxicants on the dopaminergic system: A possible role in drug addiction.

Humans are routinely exposed to a vast array of environmental neurotoxicants, including pesticides, endocrine disrupters, and heavy metals. The long-term consequences of exposure have become a major human health concern as research has indicated strong associations between neurotoxicants and a variety of dopamine-related neurological disorders. Developmental exposure to pesticides including paraquat, organochlorines, and rotenone produce alterations in the dopaminergic system and has been linked to neurodegenerative disorders, including Parkinson's disease. Endocrine disrupters such as Bisphenol A, mimic estrogenic activity and impact various dopaminergic processes to enhance mesolimbic dopamine activity resulting in hyperactivity, attention deficits, and a heightened sensitivity to drugs of abuse. A second class of endocrine disrupters, the polychlorinated biphenyls, may act directly on dopaminergic processes to disrupt the dopamine system and produce Parkinson-like symptoms. Exposure to the heavy metal lead enhances dopaminergic activity and has been associated with attention deficits, Alzheimer's disease, and increased drug sensitivity. Manganese exposure, in contrast, results in dopamine deficiencies and Parkinson-like symptoms. Therefore, this commentary will discuss the effects and consequences that exposure to these three classes of environmental neurotoxicants have on the dopamine system and related behaviors and disorders. Finally, the recent hypothesis that exposure to environmental compounds which have effects on dopaminergic neurotransmission, including 2,4-dichlorophenoxyacetic acid, Bisphenol A, and multiple heavy metals, may potentiate drug-induced behaviors and increase the brain's vulnerability to drug addiction will be discussed.

[thedevinroy]

How do you detox from it?

How do you prevent BPA from being absorbed?

Are there any herbs known to increase the amount of BPA excreted?

How is it excreted? Attached to glucose? Attached to sulfate? Unscathed?

[Ark]

How do you detox from it?

How do you prevent BPA from being absorbed?

Are there any herbs known to increase the amount of BPA excreted?

How is it excreted? Attached to glucose? Attached to sulfate? Unscathed?

Maybe Bacopa might be able to help remove BPA?

Outside of that, i'd say water but since bpa is in that too these days i dono....

GREAT QUESTION

[thedevinroy]

Damn, no answers, just questions.

[MrHappy]

Appears that because the damage is done during early developmental stages, treatment is going to be a fresh challenge. Removal/chelation I'm still looking, as for correcting the damage, I have some ideas, but need to do some more reading. Looks quite a familiar topic, in fact.

Have a google webcache of a members only article:

http://webcache.goog...u&client=safari

[thedevinroy]

Appears that because the damage is done during early developmental stages, treatment is going to be a fresh challenge. Removal/chelation I'm still looking, as for correcting the damage, I have some ideas, but need to do some more reading. Looks quite a familiar topic, in fact.

Have a google webcache of a members only article:

http://webcache.goog...u&client=safari

I imagine many nootropics will be treatments by definition as a cognitive enhancer.

I encourage everyone to keep researching chelation/removal techniques of BSA's. I'll post any if I find any.

[thedevinroy]

Calcium-D-Glucarate: Inhibits beta-glucuronidase, the enzyme responsible for ripping off the glucuronides from the xenoestrogens marked for urinary removal.

(Article on Chemo Adjunct Therapy: http://findarticles....4/ai_n32175655/ )

Edited by devinthayer, 29 November 2011 - 09:39 PM.

[thedevinroy]

http://cosozo.com/ar...rmone-balancing

Suggests the use of Zinc+Magnesium+Vitamin B's, Diindolylmethane, or Calcium-D-Glucarate.

[thedevinroy]

Sounds like you'd want to take DIM (Diindolylmethane) and Calcium-D-Glucarate at night. It probably will help remove a lot of drugs, including the ones that might be treating cognitive impairments/disorders like ADHD and hyperactivity. For instance, Resveratrol is a phytoestrogen, but also increases dopamine and helps fight breast cancer, among other things like balancing hormone levels (does not make you grow moobies). Taking DIM or Calcium-D-Glucarate during the day would counter the effects, but taking it at night might also reduce tolerance to certain compounds, as well.

Edited by devinthayer, 29 November 2011 - 09:59 PM.

[thedevinroy]

Yay folic acid!

http://www.ncbi.nlm....90/?tool=pubmed

[MrHappy]

Cognitive repair - but it would fall under much the same category.

I'll keep digging on removal.. Has to be something.

[MrHappy]

L-methylfolate would be better? Don't forget B12 with either :p

[medievil]

L methylfolate is coming to me, atleast the cheaper version of solar of 800 microgram, combine with 12 sublinguar or the IM version i use and TMG and your set methylation wise.

[MrHappy]

Yay folic acid!

http://www.ncbi.nlm....90/?tool=pubmed

Folic acid during developmental stages, which hints that BPA breaks something in the methylation during early neural development. I think you're going to need something like uridine+co-factors to trigger this in adults. I've seen the research that showed it to be capable of repairing neural function from foetal-stage dietary impoverished rats, even as adults.

[thedevinroy]

Yay folic acid!

http://www.ncbi.nlm....90/?tool=pubmed

Folic acid during developmental stages, which hints that BPA breaks something in the methylation during early neural development. I think you're going to need something like uridine+co-factors to trigger this in adults. I've seen the research that showed it to be capable of repairing neural function from foetal-stage dietary impoverished rats, even as adults.

Splain please.

[JChief]

Perhaps liquid zeolite would be sufficient to attempt to detox. I remember this study from a while back. The ability to remove toxins from brain, liver and breast seemed interesting. I know Gabriel has a health clinic in AZ. Maybe this could apply to BPA.

http://www.liquidzeo...l-cousens2.html

Full study paper

Edited by JChief, 30 November 2011 - 01:39 PM.

[thedevinroy]

Perhaps liquid zeolite would be sufficient to attempt to detox. I remember this study from a while back. The ability to remove toxins from brain, liver and breast seemed interesting. I know Gabriel has a health clinic in AZ. Maybe this could apply to BPA.

http://www.liquidzeo...l-cousens2.html

Full study paper

Would you recommend the liquid over the tablet/powder form?

[MrHappy]

http://www.ajcn.org/...2/598S.abstract

Despite the isolation of placental folate receptors 25 y ago and progress in defining the mechanism of folate delivery, considerable gaps remain in the literature for each level of the maternal-placental-fetal unit. Although a critical role of placental folate receptors in maternal-to-fetal folate transport was shown by use of the isolated perfused-placental cotyledon model a decade ago, in vivo confirmation is still needed. Knockout of folate receptors in mice, and knock-down of folate receptors by delivery of antisense oligonucleotides at gestation day 8 or antibodies to folate receptor, results in profound developmental abnormalities in the fetus, ranging from neural tube defects to neurocristopathies such as cleft-lip and cleft-palate, cardiac septal defects, and eye defects. These abnormalities can be prevented by ensuring the entry of folate into cells via alternative pathways. Controlled dietary folate restriction studies also identified adverse effects on reproductive performance, implantation, and fetal growth and other subtler (microscopic) defects in murine fetal development. Longitudinal follow-up showed that gestational folate deficiency results in behavioral changes—an anxiety phenotype—during adulthood in these mice, which supports the Barker hypothesis. The extent to which these findings are relevant to humans is unclear, however. Nevertheless, the high incidence of neural tube defects among North Indian women, who chronically subsist on one-third to one-half of the optimum folate needed to prevent birth defects, underscores the magnitude of the public health problem and emphasizes the urgent challenge to define the most efficient way to ensure adequate dietary folate for hundreds of millions of such women at risk in developing countries.

So, if the damage is done during early critical developmental stages, by eg. BPA interfering with folate's role in methylation, you normally are lumped with those problems for life. However, the plasticity of the brain is quite remarkable and it appears that we can possibly trigger some neural growth programs that normally run in utero and possibly to a much lesser degree during adulthood.
http://www.ncbi.nlm....pubmed/17056809

We have previously shown that chronic, but not acute, dietary supplementation with CDP-choline prevents the hippocampal-dependent memory deficits manifested by aged rats and by rats reared under impoverished environmental conditions. In rats, dietary CDP-choline is rapidly metabolized into cytidine and choline; the cytidine is then readily converted to uridine, which enters the brain and, via conversion to UTP and CTP, increases brain levels of membrane phosphatides. Hence, we have assessed whether administering a uridine source (UMP) instead of CDP-choline can also ameliorate the memory deficits in rats reared under impoverished environmental conditions. At weaning, 32 male Sprague-Dawley rats were exposed to either enriched (EC) or impoverished (IC) conditions for 3 mo. Concurrently, IC and EC rats were given access to either a control diet or a diet supplemented with 0.1% UMP. Rats were then assessed for learning and memory skills using 2 versions of the Morris water maze, the hidden platform version that assesses hippocampal-dependent cognitive memory processing, and the visible platform version that assesses striatal-dependent habit memory. As expected, exposure to the impoverished environment impaired hippocampal-dependent, but not striatal-dependent learning and memory. Supplementation with UMP prevented this cognitive dysfunction, as had been observed with supplemental CDP-choline. These results suggest that IC rats do not use and/or remember their spatial strategies for task solving as well as EC rats, and that long-term dietary supplementation with UMP alleviates this dysfunction.

However, it's not just memory that is improved. More importantly for you:
http://www.ncbi.nlm....pubmed/12737935

Rationale. Hypertension is considered a risk factor for the development of cognitive disorders, because of its negative effects on cerebral vasculature and blood flow. Genetically induced hypertension in rats has been associated with a range of cognitive impairments. Therefore, spontaneously hypertensive rats (SHR) can potentially be used as a model for cognitive deficits in human subjects. Consecutively, it can be determined whether certain food components can improve cognition in these rats. Objective. The present study aimed to determine whether SHR display specific deficits in attention, learning, and memory function. Additionally, effects of chronic uridine and choline administration were studied. Methods. 5-7 months old SHR were compared with normotensive Wistar-Kyoto (WKY) and Sprague-Dawley (SD) rats. (a) The operant delayed non-matching-to-position (DNMTP) test was used to study short-term memory function. (b) The five-choice serial reaction time (5-CSRT) task was used to assess selective visual attention processes. © Finally, the Morris water maze (MWM) acquisition was used as a measure for spatial learning and mnemonic capabilities. Results. (1) SHR exhibited significantly impaired performance in the 5-CSRT test in comparison with the two other rat strains. Both the SHR and WKY showed deficits in spatial learning when compared with the SD rats. (2) Uridine and choline supplementation normalized performance of SHR in the 5-CSRT test. (3) In addition, uridine and choline treatment improved MWM acquisition in both WKY and SHR rats. Conclusion. The present results show that the SHR have a deficiency in visual selective attention and spatial learning. Therefore, the SHR may provide an interesting model in the screening of substances with therapeutic potential for treatment of cognitive disorders. A combination of uridine and choline administration improved selective attention and spatial learning in SHR.

So, in adults, I'd suggest that folic acid/folate/l-methylfolate could be useful, but particularly if you are able to increase NGF, BDNF, etc. to make use of that folate during DNA methylation. (uridine + choline + DHA & EPA, etc) Essentially you need to complete the neural growth process you would have partially missed out on due to BPA toxicity. It's not just folate, though. The other B group vitamins, including B6, B12, additionally E and of course, protein. Vitamin E is particularly important for ADD/ADHD. The B group vitamins are there to support the methylation process. However, elevated dopamine receptors promote neurogenesis, so creating a tolerance to dopamine by using MAOIs is counterproductive, also.

[thedevinroy]

http://www.ajcn.org/...2/598S.abstract

Despite the isolation of placental folate receptors 25 y ago and progress in defining the mechanism of folate delivery, considerable gaps remain in the literature for each level of the maternal-placental-fetal unit. Although a critical role of placental folate receptors in maternal-to-fetal folate transport was shown by use of the isolated perfused-placental cotyledon model a decade ago, in vivo confirmation is still needed. Knockout of folate receptors in mice, and knock-down of folate receptors by delivery of antisense oligonucleotides at gestation day 8 or antibodies to folate receptor, results in profound developmental abnormalities in the fetus, ranging from neural tube defects to neurocristopathies such as cleft-lip and cleft-palate, cardiac septal defects, and eye defects. These abnormalities can be prevented by ensuring the entry of folate into cells via alternative pathways. Controlled dietary folate restriction studies also identified adverse effects on reproductive performance, implantation, and fetal growth and other subtler (microscopic) defects in murine fetal development. Longitudinal follow-up showed that gestational folate deficiency results in behavioral changes—an anxiety phenotype—during adulthood in these mice, which supports the Barker hypothesis. The extent to which these findings are relevant to humans is unclear, however. Nevertheless, the high incidence of neural tube defects among North Indian women, who chronically subsist on one-third to one-half of the optimum folate needed to prevent birth defects, underscores the magnitude of the public health problem and emphasizes the urgent challenge to define the most efficient way to ensure adequate dietary folate for hundreds of millions of such women at risk in developing countries.

So, if the damage is done during early critical developmental stages, by eg. BPA interfering with folate's role in methylation, you normally are lumped with those problems for life. However, the plasticity of the brain is quite remarkable and it appears that we can possibly trigger some neural growth programs that normally run in utero and possibly to a much lesser degree during adulthood.
http://www.ncbi.nlm....pubmed/17056809

We have previously shown that chronic, but not acute, dietary supplementation with CDP-choline prevents the hippocampal-dependent memory deficits manifested by aged rats and by rats reared under impoverished environmental conditions. In rats, dietary CDP-choline is rapidly metabolized into cytidine and choline; the cytidine is then readily converted to uridine, which enters the brain and, via conversion to UTP and CTP, increases brain levels of membrane phosphatides. Hence, we have assessed whether administering a uridine source (UMP) instead of CDP-choline can also ameliorate the memory deficits in rats reared under impoverished environmental conditions. At weaning, 32 male Sprague-Dawley rats were exposed to either enriched (EC) or impoverished (IC) conditions for 3 mo. Concurrently, IC and EC rats were given access to either a control diet or a diet supplemented with 0.1% UMP. Rats were then assessed for learning and memory skills using 2 versions of the Morris water maze, the hidden platform version that assesses hippocampal-dependent cognitive memory processing, and the visible platform version that assesses striatal-dependent habit memory. As expected, exposure to the impoverished environment impaired hippocampal-dependent, but not striatal-dependent learning and memory. Supplementation with UMP prevented this cognitive dysfunction, as had been observed with supplemental CDP-choline. These results suggest that IC rats do not use and/or remember their spatial strategies for task solving as well as EC rats, and that long-term dietary supplementation with UMP alleviates this dysfunction.

However, it's not just memory that is improved. More importantly for you:
http://www.ncbi.nlm....pubmed/12737935

Rationale. Hypertension is considered a risk factor for the development of cognitive disorders, because of its negative effects on cerebral vasculature and blood flow. Genetically induced hypertension in rats has been associated with a range of cognitive impairments. Therefore, spontaneously hypertensive rats (SHR) can potentially be used as a model for cognitive deficits in human subjects. Consecutively, it can be determined whether certain food components can improve cognition in these rats. Objective. The present study aimed to determine whether SHR display specific deficits in attention, learning, and memory function. Additionally, effects of chronic uridine and choline administration were studied. Methods. 5-7 months old SHR were compared with normotensive Wistar-Kyoto (WKY) and Sprague-Dawley (SD) rats. (a) The operant delayed non-matching-to-position (DNMTP) test was used to study short-term memory function. (b) The five-choice serial reaction time (5-CSRT) task was used to assess selective visual attention processes. © Finally, the Morris water maze (MWM) acquisition was used as a measure for spatial learning and mnemonic capabilities. Results. (1) SHR exhibited significantly impaired performance in the 5-CSRT test in comparison with the two other rat strains. Both the SHR and WKY showed deficits in spatial learning when compared with the SD rats. (2) Uridine and choline supplementation normalized performance of SHR in the 5-CSRT test. (3) In addition, uridine and choline treatment improved MWM acquisition in both WKY and SHR rats. Conclusion. The present results show that the SHR have a deficiency in visual selective attention and spatial learning. Therefore, the SHR may provide an interesting model in the screening of substances with therapeutic potential for treatment of cognitive disorders. A combination of uridine and choline administration improved selective attention and spatial learning in SHR.

So, in adults, I'd suggest that folic acid/folate/l-methylfolate could be useful, but particularly if you are able to increase NGF, BDNF, etc. to make use of that folate during DNA methylation. (uridine + choline + DHA & EPA, etc) Essentially you need to complete the neural growth process you would have partially missed out on due to BPA toxicity. It's not just folate, though. The other B group vitamins, including B6, B12, additionally E and of course, protein. Vitamin E is particularly important for ADD/ADHD. The B group vitamins are there to support the methylation process. However, elevated dopamine receptors promote neurogenesis, so creating a tolerance to dopamine by using MAOIs is counterproductive, also.

Right, an increase in NGF, BDNF, etc. would be of use in order to correct the function in conjunction with B9 (and other DNA transcription helpers as you've mentioned).

Never heard Vitamin E for attention span, just to protect from Omega-3 radicals. Omega-3's are helpful for ADHD, somewhat. It almost makes me too speedy and fluid, so I can't say it (Fish Oil) is a direct treatment, for me. Never tried just straight Vitamin E. Honestly, there's not a lot that pop's up in Google for it apart from Fish Oil co-supplementation.

As far as using MAOi's, are you under the impression that the net gain in dopamine stimulation is ultimately less than zero (negative)? Or perhaps worsened by presynaptic stimulation, causing an undesireable imbalance? I haven't heard that argument of a net loss of post-synaptic dopamine receptor stimulation. In fact, it seems Selegiline (an MAOi) increases growth factors (http://www.ncbi.nlm....pubmed/11162424 | http://www.ncbi.nlm....pubmed/19777340 | http://onlinelibrary.../jnr.10148/full ) even over time.

[MrHappy]

On my mobile at the moment, but I'll post a few links later showing neurogenesis is increased by increasing the number of dopamine receptors, so tolerance is an issue. I have also read that SSRIs & MAOIs do increase neurogensis, but is that still the case once tolerance is observed? Maybe they cancel each other out?

[MrHappy]

A few articles on my previous comment:
http://www.google.co...lient=firefox-a


Plus more on nucleotide/nucleoside treatment:


http://m.pnas.org/co...4/21/11601.full

Developmental disorder associated with increased cellular nucleotidase activity

Four unrelated patients are described with a syndrome that included developmental delay, seizures, ataxia, recurrent infections, severe language deficit, and an unusual behavioral phenotype characterized by hyperactivity, short attention span, and poor social interaction. These manifestations appeared within the first few years of life. Each patient displayed abnormalities on EEG. No unusual metabolites were found in plasma or urine, and metabolic testing was normal except for persistent hypouricosuria. Investigation of purine and pyrimidine metabolism in cultured fibroblasts derived from these patients showed normal incorporation of purine bases into nucleotides but decreased incorporation of uridine. De novo synthesis of purines and cellular phosphoribosyl pyrophosphate content also were moderately decreased. The distribution of incorporated purines and pyrimidines did not reveal a pattern suggestive of a deficient enzyme activity. Assay of individual enzymes in fibroblast lysates showed no deficiencies. However, the activity of cytosolic 5′-nucleotidase was elevated 6- to 10-fold. Based on the possibility that the observed increased catabolic activity and decreased pyrimidine salvage might be causing a deficiency of pyrimidine nucleotides, the patients were treated with oral pyrimidine nucleoside or nucleotide compounds. All patients showed remarkable improvement in speech and behavior as well as decreased seizure activity and frequency of infections. A double-blind placebo trial was undertaken to ascertain the efficacy of this supplementation regimen. Upon replacement of the supplements with placebo, all patients showed rapid regression to their pretreatment states. These observations suggest that increased nucleotide catabolism is related to the symptoms of these patients, and that the effects of this increased catabolism are reversed by administration of uridine.

* purine-pyrimidine metabolism
* uridine
* brain diseases

Behavioral abnormalities, seizures, developmental delay, and immunodeficiency are known to be associated with several defects of purine and pyrimidine metabolism (1). Seizures and autistic behavior are seen in some patients with dihydropyrimidine dehydrogenase deficiency (2). Individuals with a deficiency of adenylosuccinate lyase activity also display autistic behavior, seizures, and other neurological abnormalities (3). A deficiency of either adenosine deaminase or purine nucleoside phosphorylase causes severe immunodeficiency; neurological symptoms also have been reported with these two enzyme deficiencies (4). Finally, deficiency of hypoxanthine phosphoribosyltransferase causes Lesch–Nyhan syndrome with its characteristic self-injurious behavior, mental retardation, and dystonic posturing (5). Cases of excessive uric acid excretion associated with seizures and autistic behavior are likely to represent defects of purine metabolism, although no specific enzyme abnormality has been identified in these cases (6). In none of these disorders has it been possible to delineate the mechanism through which the enzyme deficiency produces the neurological or behavioral abnormalities. Therapeutic strategies designed to treat the behavioral and neurological abnormalities of these disorders by replacing the supposed deficient metabolites have not been successful in any case.

This report describes four unrelated patients in whom developmental delay, seizures, ataxia, recurrent infections, speech deficit, and an unusual behavioral phenotype were associated with highly elevated activity of cytosolic 5′nucleotidase. Metabolic therapy with pyrimidine compounds appeared to be highly effective in reversing these manifestations.

[JChief]

Perhaps liquid zeolite would be sufficient to attempt to detox. I remember this study from a while back. The ability to remove toxins from brain, liver and breast seemed interesting. I know Gabriel has a health clinic in AZ. Maybe this could apply to BPA.

http://www.liquidzeo...l-cousens2.html

Full study paper

Would you recommend the liquid over the tablet/powder form?

Liquid form and the most studied one which is the NCD (Waiora).