99 replies to this topic

[nootropi]

1: Arch Gerontol Geriatr. 1989 May;8(3):247-56.  Related Articles, Links

    Effects of idebenone on the levels of acetylcholine, choline, free fatty acids, and energy metabolites in the brains of rats with cerebral ischemia.

    Kakihana M, Yamazaki N, Nagaoka A.

    Central Research Division, Takeda Chemical Industries, Ltd., Osaka, Japan.

    Cerebral ischemia was induced by a 200-s occlusion of both common carotid arteries in rats in which both vertebral arteries had been permanently cauterized. In the ischemic rats, a significant decrease in acetylcholine (ACh) and a marked increase in choline were observed in the cerebral cortex, hippocampus, striatum, and diencephalon. A slight increase in choline was also observed in the cerebellum and brain stem. Pretreatment with idebenone (10 mg/kg, i.p.) inhibited the decrease in ACh and the increase in choline in the forebrain regions. In addition, the same dose of idebenone inhibited the increments of lactate and free fatty acid contents and tended to inhibit the decrement of the ATP content in the cerebral cortex of the cerebral ischemic rats. These results indicate that idebenone inhibits the alteration of the ACh level and the disruption of membrane phospholipids in the brain of ischemic rats; these effects may be mediated by improved cerebral energy metabolism.

[nootropi]

Arch Gerontol Geriatr. 1989 May;8(3):241-6.  Related Articles, Links

    Protective effect of idebenone against hypoxia in mice.

    Kiyota Y, Miyamoto M, Nagaoka A.

    Central Research Division, Takeda Chemical Industries, Ltd., Osaka, Japan.

    The effects of idebenone on survival time of mice subjected to hypoxia induced by N2 and CO2 inhalation and KCN injection were studied. Idebenone (10, 20, 50 and 100 mg/kg, i.p.) prolonged the survival time of mice exposed to a hypoxic condition (98% N2, 2% O2) in a dose-dependent manner: significant prolongations were observed at doses higher than 20 mg/kg. The drug also exerted a similar elongation effect at the same doses under conditions of 100% CO2 gas inhalation and KCN injection (3 mg/kg, i.v.). The results suggest that idebenone protects against hypoxia by improving cerebral energy metabolism.

[nootropi]

Arch Gerontol Geriatr. 1989 May;8(3):291-7.  Related Articles, Links

    Inhibition of lipid peroxidation by idebenone in brain mitochondria in the presence of succinate.

    Suno M, Nagaoka A.

    Central Research Division, Takeda Chemical Industries, Ltd., Osaka, Japan.

    Lipid peroxidation in brain mitochondria was induced by NADH in the presence of ADP and FeCl3. A novel quinone compound, idebenone, inhibited this peroxidation and the inhibition was markedly enhanced by succinate, a substrate of mitochondrial respiration. The concentration of succinate required to exert the maximal effect was 1.5 mM. The concentration of idebenone giving 50% inhibition (IC50) was 0.5 and 84 microM in the presence and absence of succinate, respectively, indicating that succinate enhances the inhibition by 170-fold. Moreover, the inhibitory effect of idebenone in the presence of succinate was abolished by adding thenoyltrifluoroacetate (TTFA), an inhibitor of complex II in the mitochondrial respiratory chain. These results indicate that idebenone is changed through complex II to its reduced form, which protects mitochondria against lipid peroxidation.

[nootropi]

: Arch Gerontol Geriatr. 1989 May;8(3):225-39.  Related Articles, Links

    Idebenone improves learning and memory impairment induced by cholinergic or serotonergic dysfunction in rats.

    Yamazaki N, Nomura M, Nagaoka A, Nagawa Y.

    Central Research Division, Takeda Chemical Industries, Ltd., Osaka, Japan.

    The effects of idebenone, a cerebral metabolic enhancer, on learning and memory impairment in two rat models with central cholinergic or serotonergic dysfunction were investigated using positively reinforced learning tasks. A delayed alternation task using a T maze was employed to test the effect of idebenone on short-term memory impairment induced by a cholinergic antagonist, scopolamine. A correct response, defined as a turn toward the arm opposite to that in the forced run, was rewarded with food pellets. Scopolamine (0.2 and 0.5 mg/kg, i.p.) significantly decreased the correct responses to the chance level in the 60-s-delayed alternation task. The scopolamine (0.2 mg/kg, i.p.)-induced impairment of short-term memory was improved by idebenone (3-30 mg/kg, i.p.) or an acetylcholinesterase inhibitor, physostigmine (0.1 and 0.2 mg/kg, i.p.), administered simultaneously. The central serotonergic dysfunction model was produced by giving rats a diet deficient in tryptophan, a precursor of serotonin. The rats fed on a tryptophan-deficient diet (TDD) showed a slower learning process in the operant brightness discrimination task (mult V115 EXT) than did rats fed on a normal diet. Idebenone (60 mg/kg/day) admixed with the TDD decreased the number of lever-pressing responses emitted during the extinction periods. The percentage of correct responses was significantly higher in the idebenone-treated group than in the control TDD group. These results suggest that idebenone may improve both the impairment of short-term memory induced by a decreased cholinergic activity and the retardation of discrimination learning induced by central serotonergic dysfunction.

[nootropi]

Arch Gerontol Geriatr. 1989 May;8(3):213-24.  Related Articles, Links

    Effects of idebenone on memory impairment induced in ischemic and embolization models of cerebrovascular disturbance in rats.

    Yamazaki N, Kiyota Y, Take Y, Miyamoto M, Nagawa Y, Nagaoka A.

    Central Research Division, Takeda Chemical Industries, Ltd., Osaka, Japan.

    Two rat models of memory impairment in passive avoidance learning induced by cerebrovascular disturbance, were established to estimate the effects of a cerebral metabolic enhancer, idebenone. Transient and global cerebral ischemia in rats, produced by 4-vessel occlusion for 200 s immediately after the acquisition trial of passive avoidance learning, shortened the latencies in the retention test trial performed 24 h later. This retrograde amnesia was reversed significantly by idebenone administered orally or intraperitoneally at the doses of 10 and 30 mg/kg before the retention test trial. Idebenone at a dose of 10 mg/kg, given intraperitoneally before or immediately after the ischemia, also markedly inhibited the appearance of amnesia. In the second model, permanent and cerebral hemisphere embolization produced by injecting 2,000 microspheres into the internal carotid artery, significantly impaired passive avoidance learning performed 7 days later. The repeated administration of idebenone (30 mg/kg, i.p.). once a day after the embolization, significantly improved the impairment of passive avoidance learning in the embolized rats. Furthermore, physostigmine and arginine-vasopressin as reference compounds improved the impairment of passive avoidance learning in these models. These findings suggest that idebenone ameliorates memory impairment induced by cerebral vascular disturbance in rats.

[nootropi]

Jpn J Pharmacol. 1984 Nov;36(3):357-63.  Related Articles, Links

    Effects of idebenone (CV-2619) on the concentrations of acetylcholine and choline in various brain regions of rats with cerebral ischemia.

    Kakihana M, Yamazaki N, Nagaoka A.

    The concentrations of acetylcholine (Ach) and choline in various brain regions of rats with and without cerebral ischemia and the effects of 6-(10-hydroxy-decyl)-2,3-dimethoxy-5-methyl-1,4-benzoquinone (idebenone, CV-2619) on the levels of these parameters were investigated. Cerebral ischemia was induced by a 200-sec occlusion of both common carotid arteries in animals in which both vertebral arteries had been permanently cauterized. The concentrations of Ach and choline in the brain were determined by means of pyrolysis gas chromatography. In normal rats, CV-2619 (10, 30 and 100 mg/kg, i.p.) did not alter the concentrations of Ach and choline in the brain regions examined. In the ischemic rats, a significant decrease in Ach and a marked increase in choline were observed in the cerebral cortex, hippocampus, striatum, and diencephalon. A slight increase in the concentration of choline was also observed in the cerebellum and brain stem. Pretreatment with CV-2619 (10 mg/kg, i.p.) inhibited the decrease in Ach and the increase in choline in the forebrain regions. Moreover, the same dose of CV-2619 inhibited the increment of lactate content and tended to inhibit the decrement of ATP content in the cerebral cortex. These results indicate that CV-2619 inhibits alterations of the concentrations of Ach and choline in the brain of the ischemic rats; this inhibition may be due to the ameliorating effect of CV-2619 on the disturbance of cerebral energy metabolism under ischemic conditions.

[AORsupport]

Although this may have been posted already, I would like to highlight the fact that there seems to be an inconsistency with the results of this study with the general consensus throughout the medical community that idebenone is a free radical scavenger rather than a creator.

As has been pointed out previously:

http://www.imminst.o...t=0
http://www.imminst.o...t=0

... there is no inconstency between the fact that idebenone is an antioxidant (which no one disputes) and the finding that it increases the generation of ROS in the mitochondrion.

CoQ10 is an antioxidant; it is also, itself, the main source of free radical production in the body in the execution of its normal duties. The two facts are in no way contradictory. All antioxidants can become prooxidants under at least some conditions, which is why it is important to take advantage of the ‘recycling’ action of the networking antioxidants:

http://www.aor.ca/pr...2&exec_sum=summ

What distinguishes CoQ10 and its analogs (such as idebenone) from other antioxidants are their presence in an especially vulnerable spot and their specific role in the electron transport chain. Having accepted electrons to form UQH2 (ubiquinol), CoQ10 is oxidized more or less by ‘bumping into’ the N2 site, generating ubisemiquinone radical which then reacts with oxygen in the matrix and forms superoxide. You can't do anything about this for CoQ10 because of its physiological role (without biotechnology), but you can certainly avoid replacing CoQ10 with an even more ‘fumble’-prone molecule by taking idebenone. Users of idebenone are displacing some CoQ10 with a substance which (in the in vitro studies) is clearly much more "butterfingered" with the electrons in its charge, leading to increased mitochondrial ROS production.

Idebenone is characterized as an antioxidant; as it has proven to be particularly effective in aiding those afflicted with mitochondrial functionality defects.

Again, this is not under dispute. If you have MELAS, Friedrich's ataxia (although the latest studies on this are not promising), or Leber’s hereditary optic neuropathy, it may be a reasonable tradeoff to risk accelerated biological aging for relief of debilitating symptoms. Ironically, the mechanism for the promise and the peril may be one and the same. Indeed, this very paradox is highlighted in the literature on the subject, such as the previously-cited:


Arch Biochem Biophys. 1996 Jun 15;330(2):395-400.
The interaction of Q analogs, particularly hydroxydecyl benzoquinone (idebenone), with the respiratory complexes of heart mitochondria.
Esposti MD, Ngo A, Ghelli A, Benelli B, Carelli V, McLennan H, Linnane AW.

Idebenone promotes a redox bypass of complex I, allowing NADH to be oxidized and enhancing the concentration of quinol substrate for complex III, and at the same time functions as an excellent substrate for succinate oxidation. Both of these effects could result in a potentiation of the bioenergy production of the respiratory chain. ... Nevertheless, our biochemical data suggest that the clinical use of idebenone should be exercised with caution, especially because idebenone could stimulate oxygen radical production in mitochondrial electron transport. Our results also indicate how idebenone may ameliorate mitochondrial defects due to functional impairment of mitochondrial complex I as in the case of LHON [Leber’s hereditary optic neuropathy].

However, if you are instead a fundamentally healthy person hoping to extend your healthy lifespan, it is an unreasonable risk to take a compound which appears to accelerate what most biogerontologists now believe to be the main driving force of aging -- especially since I have yet to see any evidence presented that idebenone is beneficial in normal, healthy humans.

If anyone has any new evidence on the points actually at issue -- ie, the generation (not antioxidative cleanup) of mitochondrial (not cellular or plasma) free radicals, or the benefits of idebenone in normal, healthy humans -- I would be interested to see it. Otherwise, I fail to see the point of continuing to rehash existing evidence and continuing to point out the flaws in the arguments in favor of idebenone's use by life extensionists.

To your health!

AOR

Exp Biol Med (Maywood). 2003 May;228(5):506-13.  Related Articles, Links
   
Mitochondrial production of oxygen radical species and the role of Coenzyme Q as an antioxidant.

[shpongled]

Adam, I don't think you posted enough abstracts. I think we need a little more information.

[nootropi]

It is especially awkward to be so one dimensional on this issue; the majority of the available data contradicts your argument. I listed several citations of research conducted which failed to recognise Idebenone as accelerating aging. In fact, I presented data which supports the converse. In fact, there are SEVERAL instances I cited where idebenone improves the functionality of the human body and brain.

While I recognize that you have some concerns, I am not sure that your theory of aging is necessarily correct.

LOL. What kind of BS sales crap are you trying to pull? Are you getting threatened by your boss, because this message board is not generating any revenues for your illustrous company and its products which have never, (might I add with particular emphasis) been involved in a single scientific study? Here you are on one hand quiblling about the findings of this study, that study, bla bla bla, when there is not one shard of evidence that AOR's products have ever minimized or reverse elements of aging!

AOR support, while I would like to maintain cordial relations with you, it is apparent to me that your role here is not to contribute to discussions, but rather to promote viewers of this board to be entranced enough with your hypnotic banner to be foolish enough to purchase your AOR's overpriced products.

The data which you keep harping on is merely speculation; and let me disabuse you once again of your false perception: your speculation is no better than anybody elses, and we are not fools.

Edited by nootropi, 12 September 2004 - 04:45 AM.

[nootropi]

Adam, I don't think you posted enough abstracts. I think we need a little more information.

LOL! I will add more later...

[nootropi]

If you look through the data that I posted, you will see that clearly several medical professionals strongly believe that idebenone is beneficial to humans; so much so that they publish data which conculdes this. Last time I checked AOR sales support does not conduct any research of its own.

Edited by nootropi, 12 September 2004 - 04:46 AM.

[nootropi]

Arch Gerontol Geriatr. 1989 May;8(3):343-53.  Related Articles, Links

    Effects of idebenone on monoamine metabolites in cerebrospinal fluid of patients with cerebrovascular dementia.

    Kawakami M, Itoh T.

    3rd Department of Internal Medicine, St. Marianna University School of Medicine, Kawasaki, Japan.

    Monoamine metabolites and norepinephrine (NE) in the cerebrospinal fluid of patients with cerebrovascular dementia were measured to study the effects of administration of idebenone. Six patients with cerebral infarction and one with cerebral hemorrhage (mean age 65.4 years) were enrolled as subjects. All the patients had mental and intelligence impairment which was evaluated by the Hasegawa's Dementia Rating (DR) Scale. The patients were medicated with a 90 mg/day dose of idebenone for 1 to 2 months, and homovanillic acid (HVA), 5-hydroxyindole acetic acid (5-HIAA), 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG) and NE in the cerebrospinal fluid were determined by high-performance liquid chromatography before and after the medication of idebenone. Before the medication, the level of HVA was 21.7 +/- 1.4 ng/ml (mean +/- SE), which was significantly lower (p less than 0.01) as compared with that in control subjects of similar age. The level of 5-HIAA was 18.5 +/- 2.7 ng/ml, and that of MHPG 9.5 +/- 0.7 ng/ml, both of which were lower than those of the controls, though statistically not significant. NE was similar to the control value. After administration of idebenone, HVA measured was 27.1 +/- 3.2 ng/ml, showing a tendency to increase. The levels of 5-HIAA and MHPG were 26.7 +/- 2.3 ng/ml and 10.7 +/- 0.6 ng/ml, respectively, which were significantly (p less than 0.05) higher than the premedication values. The percentages of the change were 12.8 +/- 8.0 for HVA, 58.2 +/- 18.5 for 5-HIAA and 14.2 +/- 5.0 for MHPG. The score of the DR scale was improved by 5 or less after the idebenone medication in most subjects. HVA and 5-HIAA increased markedly in the patients who showed a tendency of improvement of mental impairment as evaluated by the DR scale. The results suggested that idebenone would improve abnormalities in neurotransmitters of patients with cerebrovascular dementia, especially promoting serotonin turnover.

[nootropi]

Yes, and I would like to hear more from LifeMirage about his opinion about this interesting substance.

[nootropi]

B...U...M...P

[thumb]

Note: I bumped this thread NOT to rehash the arguments that take up too much space; rather so some of you can take advantage of all the time I took to paste the available abstracts relevant to the discussion on idebenone.

So enjoy the abstracts, and please -- let's try not to get invoved in another argument...

[fletch512]

Here you go again...did you think before you wrote this?

...

What are you saying, you would rather have a communist regime?  Or perhaps you would prefer a dictator?

Unless you are the CEO of a Fortune 500 company, adamp2p, your government does not represent you. The income gap between the rich and the middle-class is the biggest in American history. Adjusted for inflation, the average wage is less than people made in the '50s. Social security will run out of money, but no politician seems to be in any haste to remedy that problem. More and more people go without insurance, and the nonpartisan GAO has recently released a finding that the prescription drug plan will actually decrease benefits for the elderly while enriching drug companies. The increasing deficit, fueled to a large extent by a tax cut for the rich, hampers the government's ability to use our tax dollars for social programs. Environmental protection programs have been curtailed under the current administration, and the EPA's budget has been gutted. I could go on and on about how our "democratic" institutions trade away the needs of the many for the benefit of the few.

And if you think the world is any safer in the aftermath of the Iraq War II, perhaps you need a higher dosage of Idebenone. While we went after Hussein under the guise of a search for WMDs and thinly-veiled allusions to his ties to Al-Qaeda and 9/11, countries like North Korea and Iran have accelerated their nuclear programs, and Al-Qaeda, if you believe the news, is now omnipresent. At the same time, America is feared and hated abroad as I've never witnessed before.

And please don't belittle our intellect by throwing around words like communism and dictatorship. There certainly are worse forms of government than that currently in place in the U.S. However, that does not mean it is not our democratic duty to see the faults of our government and attempt to fix them.

"Naturally the common people don't want war; neither in Russia, nor in England, nor in America, nor in Germany. That is understood. But after all, it is the leaders of the country who determine policy, and it is always a simple matter to drag the people along, whether it is a democracy, or a fascist dictatorship, or a parliament, or a communist dictatorship. Voice or no voice, the people can always be brought to the bidding of the leaders. That is easy. All you have to do is to tell them they are being attacked, and denounce the pacifists for lack of patriotism and exposing the country to danger. It works the same in any country."
--Hermann Goering

[nootropi]

Here you go again...did you think before you wrote this?

...

What are you saying, you would rather have a communist regime?  Or perhaps you would prefer a dictator?

Unless you are the CEO of a Fortune 500 company, adamp2p, your government does not represent you. The income gap between the rich and the middle-class is the biggest in American history. Adjusted for inflation, the average wage is less than people made in the '50s. Social security will run out of money, but no politician seems to be in any haste to remedy that problem. More and more people go without insurance, and the nonpartisan GAO has recently released a finding that the prescription drug plan will actually decrease benefits for the elderly while enriching drug companies. The increasing deficit, fueled to a large extent by a tax cut for the rich, hampers the government's ability to use our tax dollars for social programs. Environmental protection programs have been curtailed under the current administration, and the EPA's budget has been gutted. I could go on and on about how our "democratic" institutions trade away the needs of the many for the benefit of the few.

And if you think the world is any safer in the aftermath of the Iraq War II, perhaps you need a higher dosage of Idebenone. While we went after Hussein under the guise of a search for WMDs and thinly-veiled allusions to his ties to Al-Qaeda and 9/11, countries like North Korea and Iran have accelerated their nuclear programs, and Al-Qaeda, if you believe the news, is now omnipresent. At the same time, America is feared and hated abroad as I've never witnessed before.

And please don't belittle our intellect by throwing around words like communism and dictatorship. There certainly are worse forms of government than that currently in place in the U.S. However, that does not mean it is not our democratic duty to see the faults of our government and attempt to fix them.

"Naturally the common people don't want war; neither in Russia, nor in England, nor in America, nor in Germany. That is understood. But after all, it is the leaders of the country who determine policy, and it is always a simple matter to drag the people along, whether it is a democracy, or a fascist dictatorship, or a parliament, or a communist dictatorship. Voice or no voice, the people can always be brought to the bidding of the leaders. That is easy. All you have to do is to tell them they are being attacked, and denounce the pacifists for lack of patriotism and exposing the country to danger. It works the same in any country."
--Hermann Goering

...wow that was deep. [tung]

[bdnf]

What is LifeMirage's real name? Does he have a doctorate?

[noos]

Why don´t you calm down adamp2p?


Ann N Y Acad Sci. 2002 Apr;959:199-213.
Role of mitochondria in oxidative stress and aging.
Lenaz G, Bovina C, D'Aurelio M, Fato R, Formiggini G, Genova ML, Giuliano G,
Pich MM, Paolucci U, Castelli GP, Ventura B.
Dipartimento di Biochimica G. Moruzzi, Universita di Bologna, Via Irnerio 48,
40126 Bologna, Italy. lenaz@biocfarm.unibo.it

The mitochondrial respiratory chain is a powerful source of reactive oxygen
species (ROS), considered as the pathogenic agent of many diseases and of aging.
We have investigated the role of Complex I in superoxide radical production and found by combined use of specific inhibitors of Complex I that the one-electron donor in the Complex to oxygen is a redox center located prior to the sites where three different types of coenzyme Q (CoQ) competitors bind, to be identified with an Fe-S cluster, most probably N2, or possibly an ubisemiquinone intermediate insensitive to all the above inhibitors. *****Short-chain coenzyme Q analogues enhance superoxide formation, presumably by mediating electron transfer from N2 to oxygen. The clinically used CoQ analogue idebenone is particularly effective, raising doubts about its safety as a drug*****. The mitochondrial theory of aging considers somatic mutations of mitochondrial DNA induced by ROS as the primary cause of energy decline; in rat liver mitochondria, Complex I appears to be most affected by aging and to become strongly rate limiting for electron transfer. Mitochondrial energetics is also deranged in human platelets upon aging, as demonstrated by the decreased Pasteur effect (enhancement of lactate production by respiratory inhibitors). Cells counteract oxidative stress by antioxidants: CoQ is the only lipophilic antioxidant to be biosynthesized. Exogenous CoQ, however, protects cells from oxidative stress by conversion into its reduced antioxidant form by cellular reductases. The plasma membrane oxidoreductase and DT-diaphorase are two such systems: likewise, they are overexpressed under oxidative stress conditions.

Publication Types: Review, Tutorial
PMID: 11976197

FEBS Lett. 2001 Sep 21;505(3):364-8.
The site of production of superoxide radical in mitochondrial Complex I is not a bound ubisemiquinone but presumably iron-sulfur cluster N2.
Genova ML, Ventura B, Giuliano G, Bovina C, Formiggini G, Parenti Castelli G,
Lenaz G.
Dipartimento di Biochimica 'G. Moruzzi', Universita di Bologna, Via Irnerio 48,
40126, Bologna, Italy.

The mitochondrial respiratory chain is a powerful source of reactive oxygen
species, considered as the pathogenic agent of many diseases and of aging. We
have investigated the role of Complex I in superoxide radical production in
bovine heart submitochondrial particles and found, by combined use of specific inhibitors of Complex I and by Coenzyme Q (CoQ) extraction from the particles, that the one-electron donor in the Complex to oxygen is a redox center located prior to the binding sites of three different types of CoQ antagonists, to be identified with a Fe-S cluster, most probably N2 on the basis of several known properties of this cluster. Short chain CoQ analogs enhance superoxide formation, presumably by mediating electron transfer from N2 to oxygen. The clinically used CoQ analog, idebenone, is particularly effective in promoting superoxide formation.
PMID: 11576529

[noos]

All the abstracts you posted are about ischemic/lesioned brains, not "healthy" people/rats


...Cerebral ischemia was induced
...Protective effect of idebenone against hypoxia in mice.
...in the presence of succinate.
...impairment induced by cholinergic or serotonergic dysfunction in rats.
...induced in ischemic and embolization models of cerebrovascular disturbance in rats.
...rats with cerebral ischemia.

[ryan1113]

Adam -- you are completely out of line and abusive. I would hope that the moderators would take note of the abusive/harrassing tone of your postings.

Whoever the people are who write for AOR, they are clearly very talented. It takes a lot of skill and hard work to sift through the full texts of dozens of studies and put the pieces together, and subsequently find a way to effectively explain difficult concepts to non-scientists as effectively as they do. In fact, they seem to do as well or better at this than anyone, including the LEF and IAS.

I'm very impressed with their R-ALA website (http://www.r-lipoic.com), and I see that a number of other companies have shamelessly copied them.

As far as advertising is concerned, it appears to me that AOR tries harder than most to 'NOT' come across as being a shameless spammer. They are, after all, in the business of developing and selling supplements. Advertising is a requisite part of having a successful business. They appear to me to be advertising very responsibly.

And anyone with at least a sciolistic level of knowledge in anti-aging theory would understand why a substance which has been shown by a team of reputable researchers to increase superoxide production by up to 20-fold, would, at the very least, be a cause of concern until more research is published on the matter. The two most popular theories of aging are the free-radical and Mitochondria theories of aging, and superoxide is the main 'root' source of these free radicals, and peroxides as well, as when SOD breaks down superoxide, H2O2 is formed. I have suspended my use of idebenone for the time being. Whether or not the net effect of using idebenone in healthy invidividuals for anti-aging purposes is ultimately harmful or beneficial remains to be conclusively shown.

It may yet turn out to be an effective anti-aging molecule, and I have not yet dismissed it altogether. There is some preliminary evidence that the mitochondria-targeted derivative, for instance, may help to slow aging, at least in tissue culture. But I cannot ignore the warning about the possible increase in superoxide production until more follow-up research is done.
==
Aging Cell. 2003 Apr;2(2):141-3.

MitoQ counteracts telomere shortening and elongates lifespan of
fibroblasts under mild oxidative stress.

Saretzki G, Murphy MP, von Zglinicki T.

Institute of Aging and Health, Newcastle University, Newcastle upon
Tyne NE4 6BE, UK.
==

[nootropi]

Adam -- you are completely out of line and abusive.  I would hope that the moderators would take note of the abusive/harrassing tone of your postings.

I'll take note of your feelings. [:o]

Have a nice day. [lol]

[nootropi]

Why don´t you calm down adamp2p?

Acchem!!! How old is this thread? [glasses] [wis]

Why do you guys want to bring up this topic AGAIN? It's DEAD, Jim!

[bdnf]

Adam was also completely out of line and abusive at the Avant Labs Forum. A member of that forum said:

God damn this crap makes me sick. It should be in the garbage board.
adamp2p if you want to stir up shit take it to the garbage board.

Adam also admitted to being schizophrenic. I personally would not follow any of Adam's suggestions in regards to nootropics.

Avant labs: http://www.avantlabs.com/main.php
Then click 'forum'
Then under chemically correct click 'main'

[nootropi]

I personally would not follow any of Adam's suggestions in regards to nootropics. 

Yeah, your right, bdnf, that Adam guy is crazy! Maybe we should not listen to any of his suggestions regarding nootropics. Do you have any other wise thoughts of similar nature to share with us today? That was really deep, seriously; you are really an intelligent person, I can tell by the way you talk about Adam! LOL. [thumb]


[lol]

[nootropi]

All the abstracts you posted are about ischemic/lesioned brains, not "healthy" people/rats.

Unfortunately, noos, there really are not many such studies at all (nootropics' effect on, as you say "healthy subjects"). Just a handful throughout the world; go ahead, check pubmed.

[bdnf]

Maybe we should not listen to any of his suggestions regarding nootropics

Good idea.

[bdnf]

Adam -- you are completely out of line and abusive. I would hope that the moderators would take note of the abusive/harrassing tone of your postings.

I will send a message to the moderator of this board if he does not stop making out of line and abusive posts.


Cosmos, you were the only person that supported Adam over on the Avant labs board and you seem to be the only person supporting him here. I don't know why, as Adam posts the most absurd things, e.g. his post on DDT (that was just stupid).