50 replies to this topic

[triplecrown]

What are the best supplements to prevent lipofuscin buildup or possibly reverse it.
Some of the ones I have heard a few times are dmae, alcar, and piracetam. Are there any others and is there one that does the job better than another as far as effectiveness and safety considerations go.

Thanks

[Logan]

There is not one proven treatment out there. I'm sure I have more of that junk in my brain than I should at my age. I'm hoping for some kind of treatment in 15 or 20 years.

Edited by morganator, 26 January 2011 - 05:52 AM.

[hamishm00]

Apparently centrophenoxine can help, although there is some debate over the meaning of lipofuscin in the study that most rely on when claiming that centrophenoxine reduces lipofuscin build up.

[Johann]

I knew of an older person that had the brown spots on the hands and when taking selenium the spots began to fade. I think the spots the

same lipofuscin as in the brain.

Selenium helps in the production or regeneration of glutathione which is an endogenous antioxidant. I would not take it in pill form but rather get it from Brazil nuts. One to two a day.

Also, avoid polyunsaturated fats as much as possible and eat as much healthy saturated fats. Check out Ray Peat's writings on this.

[curious_sle]

IP6

[triplecrown]

IP6

Doesn't IP6 chelate minerals out of the body (Iron, magnesium, etc). Also by taking IP6 would I have to take into consideration that I supplement with about 1000mg of carnosine per day which is also a good chelater? I guess what I'm asking is would I be over-chelating?

Edited by triplecrown, 26 January 2011 - 08:06 PM.

[Marios Kyriazis]

Lipofuscin is an already formed pigment and chelation won't affect it. It may prevent it from forming. The same with selenium etc. The issue is that there is nothing proven to dissolve existing lipofuscin, but some people have suggested centrophenoxine. I got this from a commercial website just to give you an idea. This was confirmed to me personally by prof Nagy on many occasions:

Professor Imre Zs. Nagy of the University of Debrecen (Hungary) is the author of the ‘membrane’ theory of ageing. Professor Nagy developed and used centrophenoxine to modify the cell structure of elderly animals by removing lipofuscin build-up and by changing the water and lipid/dry mass ratio to that of younger animals. His experiments were so effective that, in addition to a number of behavioural improvements, the longevity of the treated animals increased by up to 40% compared with the controls ! Centrophenoxine has been shown to be effective both at fighting cerebral ageing and reducing excessive levels of lipofuscin. It may also be an essential weapon in the fight against ageing and age-related diseases in general.

[niner]

Lipofuscin is an already formed pigment and chelation won't affect it. It may prevent it from forming. The same with selenium etc. The issue is that there is nothing proven to dissolve existing lipofuscin, but some people have suggested centrophenoxine. I got this from a commercial website just to give you an idea. This was confirmed to me personally by prof Nagy on many occasions:

Professor Imre Zs. Nagy of the University of Debrecen (Hungary) is the author of the ‘membrane’ theory of ageing. Professor Nagy developed and used centrophenoxine to modify the cell structure of elderly animals by removing lipofuscin build-up and by changing the water and lipid/dry mass ratio to that of younger animals. His experiments were so effective that, in addition to a number of behavioural improvements, the longevity of the treated animals increased by up to 40% compared with the controls ! Centrophenoxine has been shown to be effective both at fighting cerebral ageing and reducing excessive levels of lipofuscin. It may also be an essential weapon in the fight against ageing and age-related diseases in general.

You know Nagy, and he claims that centrophenoxine removes lipofuscin? I thought this had been shown not to work, or was based on differing definitions for "lipofuscin", or some such thing. 40% improvement in longevity (however they define that) is pretty impressive, presuming they mean in well-husbanded mammals and not in worms or insects or something. This would be great if true, but something tells me it isn't going to pan out.

[Marios Kyriazis]

Yes, that's what he claims. However, there is nothing new to support this. Below are two links that have some relevance, although somewhat old:

http://www.antiaging...ain-booster.htm

http://www.antiaging...is-of-aging.htm

Also, I remember sometime ago Aubrey (de Grey) was telling me that he was doing some research on certain bacteria that could remove lipofuscin, I don't think anything happened since in this respect.

[niner]

Yes, that's what he claims. However, there is nothing new to support this. Below are two links that have some relevance, although somewhat old:

http://www.antiaging...ain-booster.htm
http://www.antiaging...is-of-aging.htm

Also, I remember sometime ago Aubrey (de Grey) was telling me that he was doing some research on certain bacteria that could remove lipofuscin, I don't think anything happened since in this respect.

Well, here's the newest thing I found with a quick search of medline. The same group had a paper in '96 that mentioned centrophenoxine, but this seems to be the pertinent paper. Otherwise, the centrophenoxine/lipofuscin connection seems to have fallen off a cliff. I think that if this really worked in the general case, Aubrey wouldn't be messing around with bioremediation strategies.

Neurobiol Aging. 1993 Jul-Aug;14(4):319-30.
Age-related decline in multiple unit action potentials of CA3 region of rat hippocampus: correlation with lipid peroxidation and lipofuscin concentration and the effect of centrophenoxine.

Sharma D, Maurya AK, Singh R.

School of Life Sciences, Jawaharlal Nehru University, New Delhi, India.
Abstract

Changes in lipid peroxidation, lipofuscin concentration, and multiple unit activity (MUA recorded in conscious animals) in the CA3 region were studied in the hippocampus of male Wistar rats aged 4, 8, 16, and 24 months. The lipid peroxidation and lipofuscin concentration were increased with age. The MUA, however, declined with age. Correlational analyses were performed for the four age groups to determine the relationship between the age-associated decline in MUA with the age-related alterations in lipid peroxidation and lipofuscin concentrations. The age-related increase in lipid peroxidation correlated positively with the age-associated increase in lipofuscin concentration. The age-related increases in lipid peroxidation and lipofuscin concentration correlated negatively with the changes in MUA. Since lipid peroxidation may affect neuronal electrophysiology, our data suggested that age-related increase in lipid peroxidation may contribute to an age-associated decline in neuronal electrical activity. Centrophenoxine effects were studied on the three above-mentioned age-associated changes in the hippocampus. The drug had no effect on all three parameters in 4- and 8-month-old rats. In 16- and 24-month-old rats, however, the drug significantly increased the MUA but concomitantly decreased lipofuscin concentration and lipid peroxidation. Correlational analyses of the data on MUA, lipid peroxidation and lipofuscin concentration from the centrophenoxine-treated animals showed that the drug-induced diminution in both lipofuscin and lipid peroxidation was significantly correlated with the drug-induced increase in MUA. The differential effect of the drug in younger (4-8 months) and older (16-24 months) animals indicated that the stimulation of MUA was clearly associated with concomitant decrease in lipid peroxidation and lipofuscin concentration.

PMID: 8367013

[DeadMeat]

I have no idea whether their definition of lipofuscin is different from that of Aubrey. But at least curcumin seems to work quite well for some definition of lipofuscin that builds up in the brain.

http://www.ncbi.nlm....pubmed/16802111

Neuroprotective and anti-ageing effects of curcumin in aged rat brain regions.
Bala K, Tripathy BC, Sharma D.
School of Life Sciences, Jawaharlal Nehru University, 110 067, New Delhi, India.

This study investigated the influence of chronically administered curcumin on normal ageing-related parameters: lipid peroxidation, lipofuscin concentration and intraneuronal lipofuscin accumulation, activities of the enzymes superoxide dismutase (SOD), glutathione peroxidase (GPx), and Na(+), K(+), -adenosine triphosphatase (Na(+), K(+), -ATPase) in different brain regions (cerebral cortex, hippocampus, cerebellum and medulla) of 6- and 24-month-old rats. In normal ageing, lipid peroxidation and lipofuscin concentration were found to increase with ageing, the activities of SOD, GPx and Na(+), K(+), -ATPase, however, decreased with ageing. Chronic curcumin treatment of both 6 and 24 months old rats resulted in significant decreases in lipid peroxide and the lipofuscin contents in brain regions, the activities of SOD, GPx and Na(+), K(+), -ATPase however, showed significant increase in various brain regions. The present study, thus, demonstrated the antioxidative, antilipofusinogenesic and anti-ageing effects of curcumin in the brain.

From the full text version:

Curcumin dissolved in corn oil was fed orally to both 6 and 24-month-old animals at a dose of 30 mg ml^-1 kg^-1 body wt daily for one month (Reddy and Lokesh 1996). Equal number of age matched control rats were fed the same amount of corn oil for one month.

[revenant]

Acetyl l carnitine helps flush lipofuscin.

[hamishm00]

ALCAR helps reduce (not sure if it "flushes", but it does reduce) lipofuscin in rats:

Acetyl-L-carnitine enhances Na(+), K(+)-ATPase glutathione-S-transferase and multiple unit activity and reduces lipid peroxidation and lipofuscin concentration in aged rat brain regions.

Kaur J, Sharma D, Singh R.

Neurobiology Laboratory, School of Life Sciences, Jawaharlal Nehru University, 110 067, New Delhi, India.
Abstract

This study investigated the effects of chronically administered acetyl-L-carnitine (ALC) on sodium potassium adenosine triphosphatase (Na(+), K(+)-ATPase), glutathione-S-transferase (GST), glutathione peroxidase (GPx), multiple unit activity (MUA) and lipid peroxidation (LP) and lipofuscin (LF) concentration in brain regions: cerebral cortex, hippocampus, striatum and thalamus, of 24-month-old rats. The activity of Na(+), K(+)-ATPase and GST was enhanced; that of GPx was unaffected. The MUA was increased while the levels of LP and LF were decreased. These novel data provide new additional evidence concerning the antiaging attributes of ALC.

PMID: 11239702 [PubMed - indexed for MEDLINE]

[curious_sle]

IP6

Doesn't IP6 chelate minerals out of the body (Iron, magnesium, etc). Also by taking IP6 would I have to take into consideration that I supplement with about 1000mg of carnosine per day which is also a good chelater? I guess what I'm asking is would I be over-chelating?

Sorry, took a while to look up the reference i had in the back of my mind.
http://www.iovs.org/...34/12/3297.long (IP6 almost as good as CR in preventing accumulation of lipofuscin)

[Michael]

Lipofuscin is an already formed pigment and chelation won't affect it. It may prevent it from forming. The same with selenium etc. The issue is that there is nothing proven to dissolve existing lipofuscin, but some people have suggested centrophenoxine. I got this from a commercial website just to give you an idea. This was confirmed to me personally by prof Nagy on many occasions: Professor Imre Zs. Nagy of the University of Debrecen (Hungary) [...] developed and used centrophenoxine to modify the cell structure of elderly animals by removing lipofuscin build-up and by changing the water and lipid/dry mass ratio to that of younger animals. His experiments were so effective that, in addition to a number of behavioural improvements, the longevity of the treated animals increased by up to 40% compared with the controls ! Centrophenoxine has been shown to be effective both at fighting cerebral ageing and reducing excessive levels of lipofuscin. It may also be an essential weapon in the fight against ageing and age-related diseases in general.

You know Nagy, and he claims that centrophenoxine removes lipofuscin? I thought this had been shown not to work, or was based on differing definitions for "lipofuscin", or some such thing. 40% improvement in longevity (however they define that) is pretty impressive, presuming they mean in well-husbanded mammals and not in worms or insects or something. This would be great if true, but something tells me it isn't going to pan out.

Yeah, bingo on all fronts. Starting with the lifespan claim: well, yes, the "longevity of the treated animals increased by up to 40%" -- but the "animals" in question were fruit flies . (3) I don't know if these were even healthy, normal flies in the first place, but certainly a hell of a lot of useless antioxidant junk increases LS in flies. There have been reports of much smaller increases in LS in mice,(2,4) but the animals were short-lived, due either to strain(2) or husbandry.(4) Another study in a highly cancer-prone group of mice reported no effects on survival or tumor burden.(1)

A fair number of studies have reported slower accumulation of lipofuscin with centrophenoxine treatment or ALCAR, but only a few have claimed actual reversal (ie, less "lipofuscin" after treatment than before) -- and it's not clear in all of these studies that he 'lipofuscin' they're probing is the genuine, aggregated article (see eg (7)). Per contra, seral studies (eg (5,6)) have found no effect at all of centrophenoxine on lipofuscin. And the positive results are confounded by the fact that there is reason to believe in a lot of these studies that the animals were less than well-cared-for, so it could just be a general effect of alleviating oxidative stress that wouldn't apply to humans living typical developed-world lifestyles.

I remember sometime ago Aubrey (de Grey) was telling me that he was doing some research on certain bacteria that could remove lipofuscin, I don't think anything happened since in this respect.

Oh, dear. We really aren't doing a good job of communicating. We've made excellent progress on this front: see, eg,


http://www.sens.org/...themes/lysosens
http://www.sens.org/...radation-of-a2e
http://sens.org/node/1261
http://www.sens.org/node/2275
http://www.sens.org/...35/by_subject/6

... and (8-11).

IP6
http://www.iovs.org/...34/12/3297.long (IP6 almost as good as CR in preventing accumulation of lipofuscin)

I don't think that really proves that IP6 did it -- in fact, I think it's perfectly compatible with IP6 having no effect at all, or even being deleterious! First, there's only about half as much IP6 in oat bran as there is in wheat bran (see eg. here and here); second, as the paper says, "Caloric intake of rats fed the [oat fiber] diet was estimated to be 40% that of animals in the AL group" -- which, taken literally, means that they were more CRed than the CR group (ie, they only ate 40% of the AL group, so that's 60% CR; perhaps they meant, "Caloric intake ... was estimated to be 40% less than that of animals in the AL group"? Either way, any benefit should be entirely attributable to CR -- and if, indeed, the oat fiber group had similar reductions in lipofuscin accumulation despite eating substantially fewer Calories than the CR group, then it either means that there's a floor beyond which further CR cannot decelerate lipofuscin accumulation, or that something about the oat fiber diet impeded the (expected) additional reduction in lipofuscin accumulation.

References
1: Stenbäck F, Weisburger JH, Williams GM. Effect of lifetime administration of dimethylaminoethanol on longevity, aging changes, and cryptogenic neoplasms in C3H mice. Mech Ageing Dev. 1988 Feb;42(2):129-38. PubMed PMID: 3361965.

2: Hochschild R. Effect of dimethylaminoethanol on the life span of senile male A-J mice. Exp Gerontol. 1973 Aug;8(4):185-91. PubMed PMID: 4729429.

3: Hochschild R. Effect of membrane stabilizing drugs on mortality in Drosophila melanogaster. Exp Gerontol. 1971 Apr;6(2):133-51. PubMed PMID: 4397875.

4: Hochschild R. Effect of dimethylaminoethyl p-chlorophenoxyacetate on the life
span of male Swiss Webster Albino mice. Exp Gerontol. 1973 Aug;8(4):177-83.
PubMed PMID: 4147092.

5: Andrews LD, Brizzee KR. Lipofuscin in retinal pigment epithelium of rhesus monkey: lack of diminution with centrophenoxine treatment. Neurobiol Aging. 1986 Mar-Apr;7(2):107-13. PubMed PMID: 3083280.

6: Katz ML, Robison WG Jr. Lipofuscin response to the "aging-reversal" drug centrophenoxine in rat retinal pigment epithelium and frontal cortex. J Gerontol. 1983 Sep;38(5):525-31. PubMed PMID: 6411800.

7: Hasan M, Glees P, Spoerri PE. Dissolution and removal of neuronal lipofuscin following dimethylaminoethyl p-chlorophenoxyacetate administration to guinea pigs. Cell Tissue Res. 1974;150(3):369-75. PubMed PMID: 4367734.

8: Mathieu JM, Wang F, Segatori L, Alvarez PJ. Increased Resistance to oxysterol cytotoxicity in fibroblasts transfected with a lysosomally-targeted Chromobacterium oxidase. Biotechnol Bioeng. 2012 Mar 22. doi: 10.1002/bit.24506. [Epub ahead of print] PubMed PMID: 22447444.

9: Mathieu JM, Schloendorn J, Rittmann BE, Alvarez PJ. Medical bioremediation of age-related diseases. Microb Cell Fact. 2009 Apr 9;8:21. PubMed PMID: 19358742; PubMed Central PMCID: PMC2674406.

10: Schloendorn J, Webb T, Kemmish K, Hamalainen M, Jackemeyer D, Jiang L, Mathieu J, Rebo J, Sankman J, Sherman L, Tontson L, Qureshi A, Alvarez P, Rittmann B. Medical bioremediation: a concept moving toward reality. Rejuvenation Res. 2009 Dec;12(6):411-9. PubMed PMID: 20041735.

11: Rittmann BE, Schloendorn J. Engineering away lysosomal junk: medical bioremediation. Rejuvenation Res. 2007 Sep;10(3):359-65. Review. PubMed PMID: 17708688.

[Musli]

Then, what about http://www.longecity...moval-achieved/ ?

Edited by Musli, 31 March 2012 - 07:23 PM.

[tintinet]

I knew of an older person that had the brown spots on the hands and when taking selenium the spots began to fade. I think the spots the

same lipofuscin as in the brain.

Selenium helps in the production or regeneration of glutathione which is an endogenous antioxidant. I would not take it in pill form but rather get it from Brazil nuts. One to two a day.

Also, avoid polyunsaturated fats as much as possible and eat as much healthy saturated fats. Check out Ray Peat's writings on this.

The brown was probably due to melanin rather than lipofuscin, but what effect selenium would have on either is unclear to me.

[Marios Kyriazis]

.

I remember sometime ago Aubrey (de Grey) was telling me that he was doing some research on certain bacteria that could remove lipofuscin, I don't think anything happened since in this respect.

Oh, dear. We really aren't doing a good job of communicating. We've made excellent progress on this front: see, eg,


http://www.sens.org/...themes/lysosens
http://www.sens.org/...radation-of-a2e
http://sens.org/node/1261
http://www.sens.org/node/2275
http://www.sens.org/...35/by_subject/6
.

I have no doubt that SENS (and many others) are doing excellent research on this topic. However, the fact remains that after over 10 years since the above statement was made, there is still no practical treatment that can be used in this respect.

[Dorian Grey]

Reducing total body iron stores (ferritin) through blood donation might be the easiest way to deal with lipofuscin... It may not eliminate current deposits, but it certainly should reduce new ones.

Get thee to a blood bank!

Also... IP6 is not supposed to cause mineral deficiencies when taken on an empty stomach. It is phytate in food that prevents absorption and creates deficiencies.

Look Here: http://www.pjoes.com...7.2/283-290.pdf

"It has been shown that the antinutritional effect of IP6 could be manifested only when large amounts of IP6 were consumed together with a diet poor in trace elements, but if essential minerals were present in the proper ratio with respect to IP6, there was no modification of mineral balance [7]. Studies in rats fed IP6 showed no significant toxic effects on serum or bone mineral deficiency [8]. Furthermore, the analysis of IP6 effect on mineral status in rats fed for a long time period through a second generation to evaluate possible effects related to a pregnancy and lactation revealed no decrease in mineral bioavailability, with the exception of lower zinc levels in bone [9]. In addition, rats fed an equilibrated purified diet with IP6 showed about 10-fold higher concentrations of zinc in bone compared to the control animal group [6]. It has also been reported that a high IP6-containing diet did not negatively affect rat plasma copper and zinc concentrations [10] and no relation of zinc deficiency with IP6 has been observed in women who ingested vegetarian or meat-based diet with equal IP6 contents [11]."

IP6 helps control iron overload as well as reducing inflammatory cytokines caused by endotoxins/leaky gut... Great Stuff!

Edited by Michael, 12 May 2012 - 06:44 PM.

[Michael]

Then, what about http://www.longecity...moval-achieved/ ?

See here.

I knew of an older person that had the brown spots on the hands and when taking selenium the spots began to fade. I think the spots the same lipofuscin as in the brain.

As Tintinet already noted, it's an entirely different critter, despite Pearson & Shaws' claims of identity.

Selenium helps in the production or regeneration of glutathione which is an endogenous antioxidant.

It does not do this, although this is widely believed. It does, on the other hand, participate in the antioxidant enzyme glutathione peroxidase. However, the effect is saturable at RDAish levels of intake. And, I am not aware of any evidence that supra-RDA intake lowers lipofuscin accumulation.

I would not take it in pill form but rather get it from Brazil nuts. One to two a day.

Brazil nuts are not a safe source of selenium.

Analysis was performed on 72 individual nuts obtained in stores as shelled nuts in bulk and shelled and unshelled nuts in packages. Their average selenium content was 14.66 ppm with a range of 0.2 to 253.0.(1)

This range is WAY too wide to be considered a safe source of Se -- especially granted that all of the nuts in a bag or bin are likely to come from the same crop: if you're unlucky enough to buy a high-Se bag of nuts, you could be taking toxic doses every day for months or a year, since you only eat 1-2/d.

Also, avoid polyunsaturated fats as much as possible and eat as much healthy saturated fats. Check out Ray Peat's writings on this.

Please avoid Ray Peat's writings on this or any other subject.

Reducing total body iron stores (ferritin) through blood donation might be the easiest way to deal with lipofuscin... It may not eliminate current deposits, but it certainly should reduce new ones.

Get thee to a blood bank!

Despite the reasonableness of thinking that it would reduce the risk of a range of age-related diseases, so far "the vast majority of the epidemiological data does not support the hypothesis that body iron stores are directly related to the risk of developing CHD,"(2) and there's no evidence that it's protective against any other age-related disorder.

I remember sometime ago Aubrey (de Grey) was telling me that he was doing some research on certain bacteria that could remove lipofuscin, I don't think anything happened since in this respect.

Oh, dear. We really aren't doing a good job of communicating. We've made excellent progress on this front: see, eg,

I have no doubt that SENS (and many others) are doing excellent research on this topic. However, the fact remains that after over 10 years since the above statement was made, there is still no practical treatment that can be used in this respect.

Well, there's a big difference between saying that "don't think anything happened since in this respect" and that no treatment based on it is yet available. Biomedical research takes time! Dr. de Grey published the proposal of novel hydrolases to degrade age-related intracellular aggregates in 2002 -- but at the time, that's all it was: a proposal. SENS Foundation (as it was then, still a subsection of the Methuselah Foundation) first started funding research on this in 2006. We've made a substantial amount of progress since then, as noted, despite our very low research budget (in fact, since I wrote my original post on this above, we've made another significant step forward), but it would be completely unreasonable to expect that a lysoSENS therapy would even be in animal testing in that time period; to expect it to have undergone human clinical testing and then available would require miracles, not a science program.

Folks have to get this into their heads (and nothing personal here, MrZeta): biomedical research takes time and money. SENS Foundation is making remarkable progress with a teensy-tinesy budget. To get most of the SENS platform in rodents in a decade will require something like $4.4 billion; by numerical coincidence, SENS Foundation's 2012 budget is very closely one onethousandth of this amount. If you want to have any hope of rejuvenation biotechnologies being available in time for you and not just your (grand?) children,initiate or increase your monthly donation, and start writing to your elected representativesdemanding that the NIH, the Medical Research Council, et al start making serious investments in regenerative medicine across the entire sweep of the damage and degeneration of aging.


References
1. Variation In The selenium Content of Individual brazil Nuts
Carol L. Secor, Donald J. Lisk
Journal of Food Safety Volume 9, Issue 4, pages 279–281, January 1989

2. Christopher T. Sempos, Anne C. Looker, Daniel L. McGee and Jürgen Rehm. Iron and Heart Disease: A Review of the Epidemiologic Data. In: Iron Deficiency and Overload. Nutrition and Health, 2010, Part 4, 279-298, DOI: 10.1007/978-1-59745-462-9_16

Edited by Michael, 08 May 2012 - 01:27 PM.

[Dorian Grey]

"Despite the reasonableness of thinking that it would reduce the risk of a range of age-related diseases, so far "the vast majority of the epidemiological data does not support the hypothesis that body iron stores are directly related to the risk of developing CHD,"(2) and there's no evidence that it's protective against any other age-related disorder."


An 88% reduction in heart attack risk ain't too shabby if you ask me!


"Donation of blood is associated with reduced risk of myocardial infarction. The Kuopio Ischaemic Heart Disease Risk Factor Study."

Abstract

Because high body iron stores have been suggested as a risk factor for acute myocardial infarction, donation of blood could theoretically reduce the risk by lowering body iron stores. For this reason, the authors tested the hypothesis that voluntary blood donation is associated with reduced risk of acute myocardial infarction in a prospective epidemiologic follow-up study in men from eastern Finland. The subjects are all participants of the Kuopio Ischaemic Heart Disease Risk Factor Study. A cohort of 2,862 men aged 42-60 years were followed for an average of almost 9 years. One man (0.7%) out of 153 men who had donated blood in 24 months preceding the baseline examination experienced an acute myocardial infarction during 1984 to 1995, whereas 316 men (12.5%) of 2,529 non-blood donors had an acute myocardial infarction (p < 0.0001 for difference between proportions). In a Cox proportional hazards model adjusting for age, examination years and all other predictive coronary disease risk factors, blood donors had a 88% reduced risk (relative hazard = 0.12, 95% confidence interval 0.02-0.86, p = 0.035) of acute myocardial infarction, compared with non-blood donors. These findings suggest that frequent blood loss through voluntary blood donations may be associated with a reduced risk of acute myocardial infarction in middle-aged men.

PMID: 9737556 [PubMed - indexed for MEDLINE]

Edited by synesthesia, 09 May 2012 - 01:59 AM.

[Michael]

Reducing total body iron stores (ferritin) through blood donation might be the easiest way to deal with lipofuscin... It may not eliminate current deposits, but it certainly should reduce new ones.

Get thee to a blood bank!

Despite the reasonableness of thinking that it would reduce the risk of a range of age-related diseases, so far "the vast majority of the epidemiological data does not support the hypothesis that body iron stores are directly related to the risk of developing CHD,"(2) and there's no evidence that it's protective against any other age-related disorder.

An 88% reduction in heart attack risk ain't too shabby if you ask me!


"Donation of blood is associated with reduced risk of myocardial infarction. The Kuopio Ischaemic Heart Disease Risk Factor Study."

PMID: 9737556 [PubMed - indexed for MEDLINE]

Sure. I didn't say -- and the reference I cited (2) doesn't claim -- that no epidemiological data support the hypothesis that body iron stores are directly related to the risk of developing CHD; the report documents that "the vast majority of epidemiological data does not support the hypothesis that body iron stores are directly related to the risk of developing CHD."

References
2. Christopher T. Sempos, Anne C. Looker, Daniel L. McGee and Jürgen Rehm. Iron and Heart Disease: A Review of the Epidemiologic Data. In: Iron Deficiency and Overload. Nutrition and Health, 2010, Part 4, 279-298, DOI: 10.1007/978-1-59745-462-9_16

[Dorian Grey]

The greatest body of "epidemiological data" I can think of is the difference in life expectancy between men who's total body iron loading begins increasing from their mid 20s on, and women who menstruate and lose blood (and iron!) for nearly 40 years of their life...

Half a decade or so of extra longevity spread across all races and cultures ain't too shabby if you ask me.

Now, get thee to a blood bank! Two donations a year is all it takes to dump excess iron and live longer.

Edited by synesthesia, 09 May 2012 - 05:04 PM.

[Michael]

The greatest body of "epidemiological data" I can think of is the difference in life expectancy between men who's total body iron loading begins increasing from their mid 20s on, and women who menstruate and lose blood (and iron!) for nearly 40 years of their life...

... which is a cross-sectional observation, not a prospective finding, and hasn't been linked on an individual person basis to disease outcomes. It is, also, severely confounded by the hormonal milieu which drives it.

Now, get thee to a blood bank! Two donations a year is all it takes to dump excess iron and live longer.

... an assertion, again, with which the epidemiological evidence seems to be at variance.

Edited by Michael, 09 May 2012 - 06:05 PM.

[Dorian Grey]

Heart attacks in females are almost unheard of until menstruation has ceased for 10 years or so and ferritin levels rise to unhealthy levels. If hormones had anything to do with heart disease one would think HRT would show a continuing protection for females, but this simply is not the case.

http://www.ncbi.nlm....pubmed/16595027 ( PMID: 16595027)

"

Although it was believed estrogen conferred cardiac protection and reduced the incidence of myocardial ischemic events and cerebrovascular accidents, the more recent literature indicates that this is not true and that HRT users have a higher risk of cardiac and cerebral events."

It's not estrogen that protects females from heart disease before their senior years... It's menstruation!

[Michael]

Heart attacks in females are almost unheard of until menstruation has ceased for 10 years or so and ferritin levels rise to unhealthy levels. If hormones had anything to do with heart disease one would think HRT would show a continuing protection for females, but this simply is not the case.

http://www.ncbi.nlm....pubmed/16595027 ( PMID: 16595027)

It's not estrogen that protects females from heart disease before their senior years... It's menstruation!

The lack of protection of HRT doesn't disprove that the loss of cardioprotection is due to the shift in the hormonal milieu: HRT is very far removed from restoring the functioning youthful endocrine system, and the "Timing and Duration of Menopausal Hormone Treatment May Affect Cardiovascular Outcomes." IAC, even disproving the hypothesis that the change is due to the hormonal changes wouldn't prove that it is due to rising ferritin levels; and the latter hypothesis is, again based on a broad cross-sectional observation, not a prospective finding, and hasn't been linked on an individual person basis to disease outcomes. If higher ferritin in postmenopausal women as a group drives their higher disease risk, then higher ferritin levels, blood donation, etc in individual men and women should predict disease -- but it doesn't.

[Dorian Grey]

Still a doubting Thomas?

Perhaps we might consider the value of a beating heart once ones brain has turned to mush?

"Getting the Iron Out: Phlebotomy for Alzheimers Disease?"

http://www.ncbi.nlm....les/PMC2732125/

"This communication explores the temporal link between the age-associated increase in body iron stores and the age-related incidence of Alzheimer’s disease (AD), the most prevalent cause of senile dementia. Body iron stores that increase with age could be pivotal to AD pathogenesis and progression. Increased stored iron is associated with common medical conditions such as diabetes and vascular disease that increase risk for development of AD. Increased stored iron could also promote oxidative stress/free radical damage in vulnerable neurons, a critical early change in AD. A ferrocentric model of AD described here forms the basis of a rational, easily testable experimental therapeutic approach for AD, which if successful, would be both widely applicable and inexpensive. Clinical studies have shown that calibrated phlebotomy is an effective way to reduce stored iron safely and predictably without causing anemia. We hypothesize that reducing stored iron by calibrated phlebotomy to avoid iron deficiency will improve cerebrovascular function, slow neurodegenerative change, and improve cognitive and behavioral functions in AD. The hypothesis is eminently testable as iron reduction therapy is useful for chronic diseases associated with iron excess such as nonalcoholic steatohepatitis (NASH), atherosclerosis, hereditary hemochromatosis and thalassemia. Testing this hypothesis could provide valuable insight into the causation of AD and suggest novel preventive and treatment strategies."

[niner]

Still a doubting Thomas?

Perhaps we might consider the value of a beating heart once ones brain has turned to mush?

[hypothesis]

I wouldn't say Michael is a doubting Thomas; more like a rational Thomas. If individual ferritin levels don't predict health outcomes, then the population observations must be due to something else.

[Dorian Grey]

You'll have to pardon my ignorance, but I'm not sure exactly what you're getting at...

Are you saying that because everyone who has high stored iron levels doesn't get heart disease or Alzheimer's, one shouldn't consider accumulating evidence there may be a link between elevated iron storage and disease?

Not all smokers die of heart disease or lung cancer, yet in looking at smoking populations one can clearly see the risk association, even though it has never been scientifically proven in controlled studies with humans.

When one considers the risk/reward potential of lower stored iron, the possibilities seem quite attractive to me.

I was under the impression this site was all about open discussion of cutting edge theory regarding aging and longevity, and I find the iron hypothesis both compelling and intriguing. Like the observations on smoking and health of a half century ago, the evidence is mounting to levels I find hard to ignore.

Perhaps we should move on to cancer...

"Moderate elevation of body iron level and increased risk of cancer occurrence and death"

http://onlinelibrary...560312/abstract

"There is evidence, in this cohort, of elevated cancer risk in those with moderately elevated iron level. This pattern was seen in women as well as in men"

Edited by synesthesia, 11 May 2012 - 12:16 AM.

[Danail Bulgaria]

This topic is becomming very interesting. In the beginning triplecrown wrote about dmae, alcar and piracetam.
What is Your oppinion about the effectiveness of these?