8 replies to this topic

[luv2increase]

I've been taking carnosine for a month or so now. I just read in another thread on here that it is possible that carnosine creates more lipofuscin. Do any of you who take carnosine, take centrophenoxine or DMAE to combat the possible extra lipofuscin? What are your thoughts on excess carnosine being found in mentally retarded people? Could carnosine possibly be detrimental to cognitive performance?

Thanks

[edward]

Since I started taking carnosine I started DMAE as well for just this reason. Lipofuscin didn't seem like something I wanted to accumulate.

[edward]

DMAE is a pain though. If I take too much it gives me the "stupid" feeling one gets with too many nootropics.

[luv2increase]

I wonder if ALCAR is strong enough to counteract the excess lipofuscin? I'm a little paranoid now. I think it is time to order the centro.

[niner]

The formation of lipofuscin by carnosine seems to be a speculation on the part of Alan Hipkiss. This is the most recent reference that I found on medline.

Biogerontology. 2000;1(3):217-23.
Carnosine reacts with protein carbonyl groups: another possible role for the anti-ageing peptide?
Hipkiss AR, Brownson C.
Biomolecular Sciences Division, GKT School of Biomedical Sciences, King's College London, Guy's Campus London Bridge, London EC1 1UL, UK. alan.hipkiss@kcl.ac.uk

Carnosine (beta-alanyl-L-histidine) can delay senescence and provoke cellular rejuvenation in cultured human fibroblasts. The mechanisms by which such a simple molecule induces these effects is not known despite carnosine's well documented anti-oxidant and oxygen free-radical scavenging activities. Carbonyl groups are generated on proteins post-synthetically by the action of reactive oxygen species and glycating agents and their accumulation is a major biochemical manifestation of ageing. We suggest that, in addition to the prophylactic actions of carnosine, it may also directly participate in the inactivation/disposal of aged proteins possibly by direct reaction with the carbonyl groups on proteins. The possible fates of these 'carnosinylated' proteins including the formation of inert lipofuscin, proteolysis via the proteasome system and exocytosis following interaction with receptors are also discussed. The proposal may point to a hitherto unrecognised mechanism by which cells/organisms normally defend themselves against protein carbonyls.

PMID: 11707898

Here is a review that Hipkiss wrote in late 99: http://protein.bio.m...l/65070907.html (Full text)

I didn't find any actual evidence of lipofuscin formation via carnosine in my quick search, but I did find an interesting article on Autism. Autistic kids had more lipofuscin than normal (without carnosine), were then given carnosine, and their autism improved. Not evidence one way or the other, but interesting in itself.

Altern Ther Health Med. 2004 Nov-Dec;10(6):22-36; quiz 37, 92.
Oxidative stress in autism.
McGinnis WR.
STATEMENT OF PURPOSE: Indirect markers are consistent with greater oxidative stress in autism. They include greater free-radical production, impaired energetics and cholinergics, and higher excitotoxic markers. Brain and gut, both abnormal in autism, are particularly sensitive to oxidative injury. Higher red-cell lipid peroxides and urinary isoprostanes in autism signify greater oxidative damage to biomolecules. A preliminary study found accelerated lipofuscin deposition--consistent with oxidative injury to autistic brain in cortical areas serving language and communication. Double-blind, placebo-controlled trials of potent antioxidants--vitamin C or carnosine--significantly improved autistic behavior. Benefits from these and other nutritional interventions may be due to reduction of oxidative stress. Understanding the role of oxidative stress may help illuminate the pathophysiology of autism, its environmental and genetic influences, new treatments, and prevention. OBJECTIVES: Upon completion of this article, participants should be able to: 1. Be aware of laboratory and clinical evidence of greater oxidative stress in autism. 2. Understand how gut, brain, nutritional, and toxic status in autism are consistent with greater oxidative stress. 3. Describe how anti-oxidant nutrients are used in the contemporary treatment of autism.

PMID: 15624347

[caston]

Well I think carnosine works so well because its a pH buffer. That is all.

[immortali457]

http://www.jonbarron.../01-01-2005.php

[tintinet]

ISTM the statements in the "Barron Report" regarding carnosine, DMAE, and lipofuscin are highly speculative and don't represent a consensus scientific opinion.

[niner]

Well I think carnosine works so well because its a pH buffer. That is all.

Caston, what makes you think this? No other pH buffer that I know of has the effects of carnosine. Carnosine does act as a buffer in muscle, but it does way more than that outside of muscle.