8 replies to this topic

[prunk]

"Improved Working Memory but No Effect on Striatal Vesicular Monoamine Transporter Type 2 after Omega-3 Polyunsaturated Fatty Acid Supplementation.



Abstract


Studies in rodents indicate that diets deficient in omega-3 polyunsaturated fatty acids (n-3 PUFA) lower dopamine neurotransmission as measured by striatal vesicular monoamine transporter type 2 (VMAT2) density and amphetamine-induced dopamine release. This suggests that dietary supplementation with fish oil might increase VMAT2 availability, enhance dopamine storage and release, and improve dopamine-dependent cognitive functions such as working memory. To investigate this mechanism in humans, positron emission tomography (PET) was used to measure VMAT2 availability pre- and post-supplementation of n-3 PUFA in healthy individuals. Healthy young adult subjects were scanned with PET using [(11)C]-(+)-α-dihydrotetrabenzine (DTBZ) before and after six months of n-3 PUFA supplementation (Lovaza, 2 g/day containing docosahexaenonic acid, DHA 750 mg/d and eicosapentaenoic acid, EPA 930 mg/d). In addition, subjects underwent a working memory task (n-back) and red blood cell membrane (RBC) fatty acid composition analysis pre- and post-supplementation. RBC analysis showed a significant increase in both DHA and EPA post-supplementation. In contrast, no significant change in [(11)C]DTBZ binding potential (BP(ND)) in striatum and its subdivisions were observed after supplementation with n-3 PUFA. No correlation was evident between n-3 PUFA induced change in RBC DHA or EPA levels and change in [(11)C]DTBZ BP(ND) in striatal subdivisions. However, pre-supplementation RBC DHA levels was predictive of baseline performance (i.e., adjusted hit rate, AHR on 3-back) on the n-back task (y = 0.19+0.07, r(2) = 0.55, p = 0.009). In addition, subjects AHR performance improved on 3-back post-supplementation (pre 0.65±0.27, post 0.80±0.15, p = 0.04). The correlation between n-back performance, and DHA levels are consistent with reports in which higher DHA levels is related to improved cognitive performance. However, the lack of change in [(11)C]DBTZ BP(ND) indicates that striatal VMAT2 regulation is not the mechanism of action by which n-3 PUFA improves cognitive performance.

http://www.ncbi.nlm....pubmed/23056476

Interesting.

Can someone explain what "the lack of change in [(11)C]DBTZ BP(ND) indicates that striatal VMAT2 regulation is not the mechanism of action" exactly means?

Edited by prunk, 22 February 2013 - 01:06 PM.

[alecnevsky]

This is great. Thanks. Apparently, I am 200mg above tested dose. Hopefully these subjects were not practicing n=backing for 6 months although I can't imagine anyone would.

I can't answer your question though. But I am wondering whether [how] it's possible to increase DHA supplementation without the oxidation risks associated with fish oil.

[Verne]

Oxidation risk? (Seriously, I don't know what that is.. Educate me, please!)

[megatron]

I have been taking Omega-3 for years, and not in hell if it has improved my wm.

[alecnevsky]

Megatrone, is that a yes or a no re: fish oil on working memory? Have you been taking o-3s or eating fish your entire life?

Verne, essentially fish oil in large [mega-dose] quantities leads to lipid peroxides. (note: inuit lifespan is ~65.)

Low doses of eicosapentaenoic acid, docosahexaenoic acid, and hypolipidemic eicosapentaenoic acid derivatives have no effect on lipid peroxidation in plasma.

Vaagenes H, Muna ZA, Madsen L, Berge RK.

Source

Department of Clinical Biochemistry, University of Bergen, Haukeland Hospital, Norway.

Abstract

It was of interest to investigate the influence of both high doses of eicosapentaenoic acid (EPA) and low doses of 2- or 3-methylated EPA on the antioxidant status, as they all cause hypolipidemia, but the dose required is quite different. We fed low doses (250 mg/d/kg body wt) of different EPA derivatives or high doses (1500 mg/d/kg body wt) of EPA and DHA to rats for 5 and 7 d, respectively. The most potent hypolipidemic EPA derivative, 2,2-dimethyl-EPA, did not change the malondialdehyde content in liver or plasma. Plasma vitamin E decreased only after supplementation of those EPA derivatives that caused the greatest increase in the fatty acyl-CoA oxidase activity. Fatty acyl-CoA oxidase activity increased after administration of both EPA and DHA at high doses. High doses of EPA and DHA decreased plasma vitamin E content, whereas only DHA elevated lipid peroxidation. In liver, however, both EPA and DHA increased lipid peroxidation, but the hepatic level of vitamin E was unchanged. The glutathione-requiring enzymes and the glutathione level were unaffected, and no significant changes in the activities of xanthine oxidase and superoxide dismutase were observed in either low- or high-dose experiments. In conclusion, increased peroxisomal beta-oxidation in combination with high amounts of polyunsaturated fatty acids caused elevated lipid peroxidation. At low doses of polyunsaturated fatty acids, lipid peroxidation was unchanged, in spite of increased peroxisomal beta-oxidation, indicating that polyunsaturation is the most important factor for lipid peroxidation.

http://www.ncbi.nlm..../pubmed/9870909

Lipid peroxidation during n-3 fatty acid and vitamin E supplementation in humans.

Allard JP, Kurian R, Aghdassi E, Muggli R, Royall D.

Source

Department of Medicine, University of Toronto, Ontario, Canada.

Abstract


The purpose of this study was to investigate in healthy humans the effect of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) intake, alone or in combination with dL-alpha-tocopherol acetate (vitamin E) supplements on lipid peroxidation. Eighty men were randomly assigned in a double-blind fashion to take daily for 6 wk either menhaden oil (6.26 g, n-3 fatty acids) or olive oil supplements with either vitamin E (900 IU) or its placebo. Antioxidant vitamins, phospholipid composition, malondialdehyde (MDA), and lipid peroxides were measured in the plasma at baseline and week 6. At the same time, breath alkane output was measured. Plasma alpha-tocopherol concentration increased in those receiving vitamin E (P < 0.0001). In those supplemented with n-3 fatty acids, EPA and DHA increased in plasma phospholipids (P < 0.0001) and plasma MDA and lipid peroxides increased (P < 0.001 and P < 0.05, respectively). Breath alkane output did not change significantly and vitamin E intake did not prevent the increase in lipid peroxidation during menhaden oil supplementation. The results demonstrate that supplementing the diet with n-3 fatty acids resulted in an increase in lipid peroxidation, as measured by plasma MDA release and lipid peroxide products, which was not suppressed by vitamin E supplementation."

http://www.ncbi.nlm..../pubmed/9168460



So what I am trying to do is take mega-doses of DHA while minimizing or eliminating the peroxidation via coq10 or c60 or something else. Not sure if it's worth it yet.

Edited by alecnevsky, 23 February 2013 - 09:47 PM.

[megatron]

Megatrone, is that a yes or a no re: fish oil on working memory? Have you been taking o-3s or eating fish your entire life?

I have been taking Omega-3 capsules for years.

[prunk]

Damn.
On the other hand:

Modulating the inflammatory properties of activated microglia with Docosahexaenoic acid and Aspirin.

Abstract

BACKGROUND: Microglia are considered the "resident macrophages" of the brain. When in their resting state, microglia perform routine maintenance and immune surveillance. Once activated, either by injury or an immune stimulus, microglia secrete a variety of pro-inflammatory molecules, such as Nitric Oxide, superoxide, and inflammatory cytokines. Up-regulation of pro-inflammatory molecules is transient, and does not cause neurodegeneration. However, if up-regulation lasts for an extended period of time, neurodegeneration ensues.Many neurodegenerative diseases are characterized by chronic inflammation due to microglial activation. Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) have been proposed as possible preventative treatments for neurodegenerative diseases, due to their anti-inflammatory properties. Docosahexaenoic Acid (DHA) is an omega-3 polyunsaturated fatty acid (PUFA) that has potent anti-inflammatory properties.This research work sought to elucidate whether microglial activation can be modulated by combining Aspirin, a classical NSAID, with Docosahexaenoic Acid, a natural anti-inflammatory agent. The combined ability of Aspirin and DHA to modulate microglial activation was determined in the context of pro-inflammatory cytokines, Nitric Oxide levels, as well as total Glutathione levels.
RESULTS:

Docosahexaenoic Acid increased total Glutathione levels in microglia cells and enhanced their anti-oxidative capacity. It reduced production of the pro-inflammatory cytokines TNF-alpha and IL-6 induced through TLR-3 and TLR-4 activation. Furthermore, it reduced production of Nitric Oxide. Aspirin showed similar anti-inflammatory effects with respect to TNF-alpha during TLR-3 and TLR-7 stimulation. Aspirin did not show any redection in terms of Nitric Oxide production. Combination of Aspirin and Docosahexaenoic Acid showed augmentation in total Glutathione production during TLR-7 stimulation as well as a reduction in IL-6, TNF-alpha and Nitric Oxide.
CONCLUSIONS:

Collectively, these findings highlight the combination of Docosahexaenoic Acid and Aspirin as a possible measure against inflammation of the nervous system, thus leading to protection against neurodegenerative diseases with an inflammatory etiology.

http://www.ncbi.nlm....pubmed/23398903

Contradictive elements..

Speculations?

Edited by prunk, 23 February 2013 - 10:09 PM.

[prunk]

Porn and wm

Pornographic Picture Processing Interferes with Working Memory Performance.


Abstract


Some individuals report problems during and after Internet sex engagement, such as missing sleep and forgetting appointments, which are associated with negative life consequences. One mechanism potentially leading to these kinds of problems is that sexual arousal during Internet sex might interfere with working memory (WM) capacity, resulting in a neglect of relevant environmental information and therefore disadvantageous decision making. In this study, 28 healthy individuals performed 4 experimental manipulations of a pictorial 4-back WM task with neutral, negative, positive, or pornographic stimuli. Participants also rated 100 pornographic pictures with respect to sexual arousal and indicated masturbation urges previous to and following pornographic picture presentation. Results revealed worse WM performance in the pornographic picture condition of the 4-back task compared with the three remaining picture conditions. Furthermore, hierarchical regression analysis indicated an explanation of variance of the sensitivity in the pornographic picture condition by the subjective rating of the pornographic pictures as well as by a moderation effect of masturbation urges. Results contribute to the view that indicators of sexual arousal due to pornographic picture processing interfere with WM performance. Findings are discussed with respect to Internet sex addiction because WM interference by addiction-related cues is well known from substance dependencies.


http://www.ncbi.nlm....pubmed/23167900

Edited by prunk, 08 March 2013 - 12:20 PM.

[NeuroNootropic]

Porn and wm

Pornographic Picture Processing Interferes with Working Memory Performance.


Abstract


Some individuals report problems during and after Internet sex engagement, such as missing sleep and forgetting appointments, which are associated with negative life consequences. One mechanism potentially leading to these kinds of problems is that sexual arousal during Internet sex might interfere with working memory (WM) capacity, resulting in a neglect of relevant environmental information and therefore disadvantageous decision making. In this study, 28 healthy individuals performed 4 experimental manipulations of a pictorial 4-back WM task with neutral, negative, positive, or pornographic stimuli. Participants also rated 100 pornographic pictures with respect to sexual arousal and indicated masturbation urges previous to and following pornographic picture presentation. Results revealed worse WM performance in the pornographic picture condition of the 4-back task compared with the three remaining picture conditions. Furthermore, hierarchical regression analysis indicated an explanation of variance of the sensitivity in the pornographic picture condition by the subjective rating of the pornographic pictures as well as by a moderation effect of masturbation urges. Results contribute to the view that indicators of sexual arousal due to pornographic picture processing interfere with WM performance. Findings are discussed with respect to Internet sex addiction because WM interference by addiction-related cues is well known from substance dependencies.


http://www.ncbi.nlm....pubmed/23167900

How is this of any significance? The findings were that when the participants were watching porn, their working memory suffered. It did not find that porn is detrimental to working memory when not sexually aroused and it probably isn't. In a flight-or-fight situation I bet working memory is also impaired.