99 replies to this topic

[Logic]

Is it worth constructing a stack from a multi-factoral perspective, for example, supplements to tackle the many different causes of ageing? Or is it best to focus on the most prominent with full force? 

 

Supplementation Choices Based on the 7 SENS Research Foundation Targets:

http://www.longecity...dation-targets/

[Sith]

Here you have been given good recommendations. 
Another good approach for slow aging and for the regeneration of some tissue, included skin regeneration, is Hyperbaric Oxygen Chamber (HBOT), you can buy one Hyperbaric Chamber for home use in United States, on Ebay there are several models.

I hope that in the future I could buy one

Mitochondrial antioxidants are other good approach for slow aging and enhance healthspan, MitoQ, C60 or MB. Personally, I like methylene blue, enhances oxygen consumption, upregulates Nrf2 genes, upregulates complex IV, activates Sirt1, AMPK and produces mitochondrial biogenesis. PQQ is another good ally, sinergizes very well with MB.
My basic stack for now is c60 and MB.

 

http://www.ebay.co.u...ps=true&ff13=80

 

Is that an example of methylene blue or am I highly confused? 

[BieraK]

 

Here you have been given good recommendations. 
Another good approach for slow aging and for the regeneration of some tissue, included skin regeneration, is Hyperbaric Oxygen Chamber (HBOT), you can buy one Hyperbaric Chamber for home use in United States, on Ebay there are several models.

I hope that in the future I could buy one

Mitochondrial antioxidants are other good approach for slow aging and enhance healthspan, MitoQ, C60 or MB. Personally, I like methylene blue, enhances oxygen consumption, upregulates Nrf2 genes, upregulates complex IV, activates Sirt1, AMPK and produces mitochondrial biogenesis. PQQ is another good ally, sinergizes very well with MB.
My basic stack for now is c60 and MB.

 

http://www.ebay.co.u...ps=true&ff13=80

 

Is that an example of methylene blue or am I highly confused? 

 

Yes is Methylene Blue powder... but the recommendation is the use of USP Methylene Blue with a high quality, for avoid metal impurities
Here you can read a review of MB, there are several things about MB that have come to light in recent times not covered in this review, here you can se that they talk about MB http://www.ncbi.nlm....les/PMC3265679/
The secure option is MB from Nyles7, he sells 99,6% MB.

For example here you have some recent studies:
 

Methylene Blue Reduces Acute Cerebral Ischemic Injury via the Induction of Mitophagy.
http://www.ncbi.nlm....pubmed/25998511

Spoiler

Abstract The treatment of stroke is limited by a short therapeutic window and a lack of effective clinical drugs. Methylene blue (MB) has been used in laboratories and clinics since the 1890s. Few studies have reported the neuroprotective role of MB in cerebral ischemia-reperfusion injury. However, whether and how MB protects against acute cerebral ischemia (ACI) injury was unclear. In this study, we investigated the effect of MB on this injury and revealed that MB protected against ACI injury by augmenting mitophagy. Using a rat middle cerebral artery occlusion (MCAO) model, we demonstrated that MB improved neurological function and reduced the infarct volume and necrosis after ACI injury. These improvements depended on the effect of MB on mitochondrial structure and function. ACI caused the disorder and disintegration of mitochondrial structure, while MB ameliorated the destruction of mitochondria. In addition, mitophagy was inhibited at 24 h after stroke and MB augmented mitophagy. In an oxygen-glucose deprivation (OGD) model in vitro, we further revealed that the elevation of mitochondrial membrane potential (MMP) by MB under OGD conditions mediated the augmented mitophagy. In contrast, exacerbating the decline of MMP during OGD abolished the MB-induced activation of mitophagy. Taken together, MB promotes mitophagy by maintaining the MMP at a relatively high level, which contributes to a decrease in necrosis and an improvement in neurological function, thereby protecting against ACI injury.

 

Combined activation of the energy and cellular-defense pathways may explain the potent anti-senescence activity of methylene blue http://www.ncbi.nlm....C4588422/#bib23

Spoiler

Abstract

Methylene blue (MB) delays cellular senescence, induces complex-IV, and activates Keap1/Nrf2; however, the molecular link of these effects to MB is unclear. Since MB is redox-active, we investigated its effect on the NAD/NADH ratio in IMR90 cells. The transient increase in NAD/NADH observed in MB-treated cells triggered an investigation of the energy regulator AMPK. MB induced AMPK phosphorylation in a transient pattern, which was followed by the induction of PGC1α and SURF1: both are inducers of mitochondrial and complex-IV biogenesis. Subsequently MB-treated cells exhibited >100% increase in complex-IV activity and a 28% decline in cellular oxidants. The telomeres erosion rate was also significantly lower in MB-treated cells. A previous research suggested that the pattern of AMPK activation (i.e., chronic or transient) determines the AMPK effect on cell senescence. We identified that the anti-senescence activity of MB (transient activator) was 8-times higher than that of AICAR (chronic activator). Since MB lacked an effect on cell cycle, an MB-dependent change to cell cycle is unlikely to contribute to the anti-senescence activity. The current findings in conjunction with the activation of Keap1/Nrf2 suggest a synchronized activation of the energy and cellular defense pathways as a possible key factor in MB's potent anti-senescence activity.

 

Methylene blue upregulates Nrf2/ARE genes and prevents tau-related neurotoxicity.
http://www.ncbi.nlm....pubmed/24556215

Spoiler

Abstract Methylene blue (MB, methylthioninium chloride) is a phenothiazine that crosses the blood brain barrier and acts as a redox cycler. Among its beneficial properties are its abilities to act as an antioxidant, to reduce tau protein aggregation and to improve energy metabolism. These actions are of particular interest for the treatment of neurodegenerative diseases with tau protein aggregates known as tauopathies. The present study examined the effects of MB in the P301S mouse model of tauopathy. Both 4 mg/kg MB (low dose) and 40 mg/kg MB (high dose) were administered in the diet ad libitum from 1 to 10 months of age. We assessed behavior, tau pathology, oxidative damage, inflammation and numbers of mitochondria. MB improved the behavioral abnormalities and reduced tau pathology, inflammation and oxidative damage in the P301S mice. These beneficial effects were associated with increased expression of genes regulated by NF-E2-related factor 2 (Nrf2)/antioxidant response element (ARE), which play an important role in antioxidant defenses, preventing protein aggregation, and reducing inflammation. The activation of Nrf2/ARE genes is neuroprotective in other transgenic mouse models of neurodegenerative diseases and it appears to be an important mediator of the neuroprotective effects of MB in P301S mice. Moreover, we used Nrf2 knock out fibroblasts to show that the upregulation of Nrf2/ARE genes by MB is Nrf2 dependent and not due to secondary effects of the compound. These findings provide further evidence that MB has important neuroprotective effects that may be beneficial in the treatment of human neurodegenerative diseases with tau pathology.

 

Alternative mitochondrial electron transfer for the treatment of neurodegenerative diseases and cancers:Methylene blue connects the dots.
http://www.ncbi.nlm....pubmed/26603930

Spoiler

Abstract The treatment of stroke is limited by a short therapeutic window and a lack of effective clinical drugs. Methylene blue (MB) has been used in laboratories and clinics since the 1890s. Few studies have reported the neuroprotective role of MB in cerebral ischemia-reperfusion injury. However, whether and how MB protects against acute cerebral ischemia (ACI) injury was unclear. In this study, we investigated the effect of MB on this injury and revealed that MB protected against ACI injury by augmenting mitophagy. Using a rat middle cerebral artery occlusion (MCAO) model, we demonstrated that MB improved neurological function and reduced the infarct volume and necrosis after ACI injury. These improvements depended on the effect of MB on mitochondrial structure and function. ACI caused the disorder and disintegration of mitochondrial structure, while MB ameliorated the destruction of mitochondria. In addition, mitophagy was inhibited at 24 h after stroke and MB augmented mitophagy. In an oxygen-glucose deprivation (OGD) model in vitro, we further revealed that the elevation of mitochondrial membrane potential (MMP) by MB under OGD conditions mediated the augmented mitophagy. In contrast, exacerbating the decline of MMP during OGD abolished the MB-induced activation of mitophagy. Taken together, MB promotes mitophagy by maintaining the MMP at a relatively high level, which contributes to a decrease in necrosis and an improvement in neurological function, thereby protecting against ACI injury.

   

 

Edited by BieraK, 03 January 2016 - 07:36 PM.

[tintinet]

Here you have been given good recommendations. 
Another good approach for slow aging and for the regeneration of some tissue, included skin regeneration, is Hyperbaric Oxygen Chamber (HBOT), you can buy one Hyperbaric Chamber for home use in United States, on Ebay there are several models.

I hope that in the future I could buy one

Mitochondrial antioxidants are other good approach for slow aging and enhance healthspan, MitoQ, C60 or MB. Personally, I like methylene blue, enhances oxygen consumption, upregulates Nrf2 genes, upregulates complex IV, activates Sirt1, AMPK and produces mitochondrial biogenesis. PQQ is another good ally, sinergizes very well with MB.
My basic stack for now is c60 and MB.

 

I'd think hyperbaric oxygen would promote aging via oxidization, no?

 

 

Edited by tintinet, 03 January 2016 - 11:01 PM.

[message]

Is MB > c60oo?

 

 

[niner]

Is MB > c60oo?

 

Not in my experience, but it depends what you want to achieve.  BierraK posted an interesting paper about MB being useful in a stroke model, but note that the effective dose was 5mg/kg in rats.  Even allowing for interspecies scaling, that's still a large dose of MB by the standards of what a lot of people around here use.  It's similar to the dose used in TauRx's early trials for Alzheimers.  MB is a pretty interesting compound, if you take a large enough dose.  Some people champion a microdose strategy which did nothing for me, has no published evidence, and doesn't result in concentrations known to be effective in vitro.  Colored liquids are highly placebogenic, imho.   Given a large enough dose, a combination of MB and c60oo might be synergistic.

Edited by niner, 04 January 2016 - 05:05 AM.

[BieraK]

In the papers of Dr Gonzalez-Lima the low dose of MB is considered between 0.5 - 4 mg/kg. 
Here is a study on humans, with claustrophobic patients that uses 80 mg x 3 a day
http://www.ncbi.nlm....pubmed/25018057

I now use 60-100 mg a day. I'm planning of using it with 98% bottled oxygen, MB upregulates antioxidant genes and improves oxygen consumption of cells, that can produce ROS as good signaling, that combined with other effects of MB like cytochrome c upregulation and biogenesis (SURF1 gene activation), mitochondrial biogenesis (Sirt1, AMPK, PGC-1alpha), looks to me like a good way of improving mitochondria... better if is done in a 3 day fasting. 

Yes I use c60 and MB together, but I ended my bottle, so I will try to make my own DIY c60 oo this week.

The only question that I have between c60 and MB, is the possibility that some c60 effects can block some of the MB effect's, for example the ROS production and the adaptation of the body to that. To me MB+Oxygen looks like a good way of producing mitohormesis and mitophagy, better mitochondria with more resistance to ROS from an improved OXPHOS.

 

Edited by BieraK, 04 January 2016 - 05:53 AM.

[Sith]

 

 

Here you have been given good recommendations. 
Another good approach for slow aging and for the regeneration of some tissue, included skin regeneration, is Hyperbaric Oxygen Chamber (HBOT), you can buy one Hyperbaric Chamber for home use in United States, on Ebay there are several models.

I hope that in the future I could buy one

Mitochondrial antioxidants are other good approach for slow aging and enhance healthspan, MitoQ, C60 or MB. Personally, I like methylene blue, enhances oxygen consumption, upregulates Nrf2 genes, upregulates complex IV, activates Sirt1, AMPK and produces mitochondrial biogenesis. PQQ is another good ally, sinergizes very well with MB.
My basic stack for now is c60 and MB.

 

http://www.ebay.co.u...ps=true&ff13=80

 

Is that an example of methylene blue or am I highly confused? 

 

Yes is Methylene Blue powder... but the recommendation is the use of USP Methylene Blue with a high quality, for avoid metal impurities
Here you can read a review of MB, there are several things about MB that have come to light in recent times not covered in this review, here you can se that they talk about MB http://www.ncbi.nlm....les/PMC3265679/
The secure option is MB from Nyles7, he sells 99,6% MB.

For example here you have some recent studies:
 

Methylene Blue Reduces Acute Cerebral Ischemic Injury via the Induction of Mitophagy.
http://www.ncbi.nlm....pubmed/25998511

Spoiler

Abstract The treatment of stroke is limited by a short therapeutic window and a lack of effective clinical drugs. Methylene blue (MB) has been used in laboratories and clinics since the 1890s. Few studies have reported the neuroprotective role of MB in cerebral ischemia-reperfusion injury. However, whether and how MB protects against acute cerebral ischemia (ACI) injury was unclear. In this study, we investigated the effect of MB on this injury and revealed that MB protected against ACI injury by augmenting mitophagy. Using a rat middle cerebral artery occlusion (MCAO) model, we demonstrated that MB improved neurological function and reduced the infarct volume and necrosis after ACI injury. These improvements depended on the effect of MB on mitochondrial structure and function. ACI caused the disorder and disintegration of mitochondrial structure, while MB ameliorated the destruction of mitochondria. In addition, mitophagy was inhibited at 24 h after stroke and MB augmented mitophagy. In an oxygen-glucose deprivation (OGD) model in vitro, we further revealed that the elevation of mitochondrial membrane potential (MMP) by MB under OGD conditions mediated the augmented mitophagy. In contrast, exacerbating the decline of MMP during OGD abolished the MB-induced activation of mitophagy. Taken together, MB promotes mitophagy by maintaining the MMP at a relatively high level, which contributes to a decrease in necrosis and an improvement in neurological function, thereby protecting against ACI injury.

 

Combined activation of the energy and cellular-defense pathways may explain the potent anti-senescence activity of methylene blue http://www.ncbi.nlm....C4588422/#bib23

Spoiler

Abstract

Methylene blue (MB) delays cellular senescence, induces complex-IV, and activates Keap1/Nrf2; however, the molecular link of these effects to MB is unclear. Since MB is redox-active, we investigated its effect on the NAD/NADH ratio in IMR90 cells. The transient increase in NAD/NADH observed in MB-treated cells triggered an investigation of the energy regulator AMPK. MB induced AMPK phosphorylation in a transient pattern, which was followed by the induction of PGC1α and SURF1: both are inducers of mitochondrial and complex-IV biogenesis. Subsequently MB-treated cells exhibited >100% increase in complex-IV activity and a 28% decline in cellular oxidants. The telomeres erosion rate was also significantly lower in MB-treated cells. A previous research suggested that the pattern of AMPK activation (i.e., chronic or transient) determines the AMPK effect on cell senescence. We identified that the anti-senescence activity of MB (transient activator) was 8-times higher than that of AICAR (chronic activator). Since MB lacked an effect on cell cycle, an MB-dependent change to cell cycle is unlikely to contribute to the anti-senescence activity. The current findings in conjunction with the activation of Keap1/Nrf2 suggest a synchronized activation of the energy and cellular defense pathways as a possible key factor in MB's potent anti-senescence activity.

 

Methylene blue upregulates Nrf2/ARE genes and prevents tau-related neurotoxicity.
http://www.ncbi.nlm....pubmed/24556215

Spoiler

Abstract Methylene blue (MB, methylthioninium chloride) is a phenothiazine that crosses the blood brain barrier and acts as a redox cycler. Among its beneficial properties are its abilities to act as an antioxidant, to reduce tau protein aggregation and to improve energy metabolism. These actions are of particular interest for the treatment of neurodegenerative diseases with tau protein aggregates known as tauopathies. The present study examined the effects of MB in the P301S mouse model of tauopathy. Both 4 mg/kg MB (low dose) and 40 mg/kg MB (high dose) were administered in the diet ad libitum from 1 to 10 months of age. We assessed behavior, tau pathology, oxidative damage, inflammation and numbers of mitochondria. MB improved the behavioral abnormalities and reduced tau pathology, inflammation and oxidative damage in the P301S mice. These beneficial effects were associated with increased expression of genes regulated by NF-E2-related factor 2 (Nrf2)/antioxidant response element (ARE), which play an important role in antioxidant defenses, preventing protein aggregation, and reducing inflammation. The activation of Nrf2/ARE genes is neuroprotective in other transgenic mouse models of neurodegenerative diseases and it appears to be an important mediator of the neuroprotective effects of MB in P301S mice. Moreover, we used Nrf2 knock out fibroblasts to show that the upregulation of Nrf2/ARE genes by MB is Nrf2 dependent and not due to secondary effects of the compound. These findings provide further evidence that MB has important neuroprotective effects that may be beneficial in the treatment of human neurodegenerative diseases with tau pathology.

 

Alternative mitochondrial electron transfer for the treatment of neurodegenerative diseases and cancers:Methylene blue connects the dots.
http://www.ncbi.nlm....pubmed/26603930

Spoiler

Abstract The treatment of stroke is limited by a short therapeutic window and a lack of effective clinical drugs. Methylene blue (MB) has been used in laboratories and clinics since the 1890s. Few studies have reported the neuroprotective role of MB in cerebral ischemia-reperfusion injury. However, whether and how MB protects against acute cerebral ischemia (ACI) injury was unclear. In this study, we investigated the effect of MB on this injury and revealed that MB protected against ACI injury by augmenting mitophagy. Using a rat middle cerebral artery occlusion (MCAO) model, we demonstrated that MB improved neurological function and reduced the infarct volume and necrosis after ACI injury. These improvements depended on the effect of MB on mitochondrial structure and function. ACI caused the disorder and disintegration of mitochondrial structure, while MB ameliorated the destruction of mitochondria. In addition, mitophagy was inhibited at 24 h after stroke and MB augmented mitophagy. In an oxygen-glucose deprivation (OGD) model in vitro, we further revealed that the elevation of mitochondrial membrane potential (MMP) by MB under OGD conditions mediated the augmented mitophagy. In contrast, exacerbating the decline of MMP during OGD abolished the MB-induced activation of mitophagy. Taken together, MB promotes mitophagy by maintaining the MMP at a relatively high level, which contributes to a decrease in necrosis and an improvement in neurological function, thereby protecting against ACI injury.

   

 

 

Thank you! This is fantastic, I do appreciate the help! 

[message]

Are these recommended for all ages or only after certain ages i.e. over 50?

 

I doubt someone who is younger and otherwise healthy will notice any palpable difference.

[YOLF]

Are these recommended for all ages or only after certain ages i.e. over 50?

 

I doubt someone who is younger and otherwise healthy will notice any palpable difference.

Results are better when you start young. An ounce of prevention is worth a pound of cure. Actually, the older you get w/o intervention, the more damage you'll have accelerating your demise I would think. Start taking things at 50 and you might get a little more time or health, but but it won't be as good as the time or health when you're young. I think of it as I think of investing. Earlier investments lead to greater returns.

 

I don't think they are being recommended, just suggested for people to study.

[YOLF]

BTW, if I haven't mentioned it yet, I think MB's action might have something to do with it's abx qualities and enzymes that get released when certain bacteria are killed. Berberine for instance doesn't make it into the blood stream, but it's a potent abx in the GI tract and improves blood sugar, joint problems, skin, and other things.

[Junk Master]

I once read that by the age of 40,"...a man has the face he deserves."  That said, 50 is the new 40, right?

[stefan_001]

I once read that by the age of 40,"...a man has the face he deserves." That said, 50 is the new 40, right?

I thought that 60 is the new 40 :-) ?

[Junk Master]

Well played:)

[message]

 

Are these recommended for all ages or only after certain ages i.e. over 50?

 

I doubt someone who is younger and otherwise healthy will notice any palpable difference.

Results are better when you start young. An ounce of prevention is worth a pound of cure. Actually, the older you get w/o intervention, the more damage you'll have accelerating your demise I would think. Start taking things at 50 and you might get a little more time or health, but but it won't be as good as the time or health when you're young. I think of it as I think of investing. Earlier investments lead to greater returns.

 

I don't think they are being recommended, just suggested for people to study.

 

 

Did the collective crew ever come up with a suggested dosage and retailer? Last I checked dosages ranged from micro to supra

[boxingroo]

If I am out of the target in here with my suggestion, my deep apology please as this supplement is not OTC like in the USA and I don't have much experiences with its use due to the difficulties to obtain it in Australia. I am talking about the DHEA supplement used daily in about 100 mg servings. It is my believe that this product is one of the working substance to extend our lifespan but I would like to see your opinion to my suggestion.

[message]

A safe, not too expensive stack to inhibiting AGE can be:

Green Tea Extract
L-Carnosine
Alpha Lipoic Acid

I currently do not take any of these, but am looking to start. Can anyone comment on the optimal dosing for each?

Alpha-Lipoic Acid:

Is a mild chelator with a short half life that gets past the BBB.
ie: It will get into your brain and chelate some heavy metals like mercury, lead etc, but due to it being weak and having a short half-life; it will 'drop the ball' and the now relocated metal will then be free to do more damage elsewhere all over again...!?
People taking this for chelation purposes take it every 2 hrs, day and night, for extended periods and combine it with other chelators to 'pick up the dropped ball' from ALA.
Do look into this and consider the mild chelator, Garlic, at the very minimum, as something to take with ALA.
Note that D-Limonene kills the Garlic (and DMSO) smell

Another interesting and important consideration is that ALA looks like it locks in the epigenetic changes caused by calorie restriction, or not...
ie: If you are CRing and fasting, ALA will lock in those positive epigenetic changes even if you then go on to a high calorie diet, and visa versa...!?
Do look that up as it is a very important consideration IMHO.

Hmm very interesting.

So do you suggest taking ALA if otherwise healthy and in early 30s?

[evilbaga]

I do something utterly crazy. I buy Ginkgo Biloba leaf powder, mulch it into a warm mush with warm water, rub it all over my face, step into a hot shower. After I get out, my skin feels and looks FREAKING AMAZING. For sure it prevents at least one of the signs of aging.

 

I tried rubbing Turmeric on myself for about an hour before I shower it off about a decade ago. It works.

Unfortunately, the trace residue of turmeric will color your shirts yellow - not worth it.

[evilbaga]

 

A safe, not too expensive stack to inhibiting AGE can be:

Green Tea Extract
L-Carnosine
Alpha Lipoic Acid

 

I currently do not take any of these, but am looking to start.  Can anyone comment on the optimal dosing for each?

 

Alpha-Lipoic Acid:

Is a mild chelator with a short half life that gets past the BBB.
ie:  It will get into your brain and chelate some heavy metals like mercury, lead etc, but due to it being weak and having a short half-life; it will 'drop the ball' and the now relocated metal will then be free to do more damage elsewhere all over again...!?

People taking this for chelation purposes take it every 2 hrs, day and night, for extended periods and combine it with other chelators to 'pick up the dropped ball' from ALA.
Do look into this and consider the mild chelator, Garlic, at the very minimum, as something to take with ALA.
Note that D-Limonene kills the Garlic (and DMSO) smell

Another interesting and important consideration is that ALA looks like it locks in the epigenetic changes caused by calorie restriction, or not...
ie:  If you are CRing and fasting, ALA will lock in those positive epigenetic changes even if you then go on to a high calorie  diet, and visa versa...!?
Do look that up as it is a very important consideration IMHO.

 

 

Andrew Cutler says most food based (like chlorella cilantro etc) chelators are kinda dangerous because they have a single bond, whereas ALA has a double bond so its better and holds on more tightly to the heavy metals.

[YOLF]

If I am out of the target in here with my suggestion, my deep apology please as this supplement is not OTC like in the USA and I don't have much experiences with its use due to the difficulties to obtain it in Australia. I am talking about the DHEA supplement used daily in about 100 mg servings. It is my believe that this product is one of the working substance to extend our lifespan but I would like to see your opinion to my suggestion.

I kinda remember reading something to the effect of SENs targeting a DHEA metabolite as part of their work. It'll help you feel younger, but it may have some other side effects that accelerate aging.

[ceridwen]

@logic the useful bit of garlic is associated with the smell.

[Logic]

@logic the useful bit of garlic is associated with the smell.

 

D-Limonene:

http://www.longecity...ndpost&p=529307

http://www.longecity...ndpost&p=535729

http://www.longecity...ndpost&p=535933

 

http://www.longecity...monene-in-bulk/

[Skyguy2005]

 

I do something utterly crazy. I buy Ginkgo Biloba leaf powder, mulch it into a warm mush with warm water, rub it all over my face, step into a hot shower. After I get out, my skin feels and looks FREAKING AMAZING. For sure it prevents at least one of the signs of aging.

 

I tried rubbing Turmeric on myself for about an hour before I shower it off about a decade ago. It works.

Unfortunately, the trace residue of turmeric will color your shirts yellow - not worth it.

 

 

Yeah, Ginkgo Biloba is my favourite, but Turmeric is an amazing herb.

 

I suppose the solution is wearing yellow shirts, ha!

 

I mostly wear the dark colours, for this exact reason. I'm always spilling stuff on myself and I simply can't be bothered to faff around cleaning things that just have a tiny miniscule stain. Life is a stain on the pristine perfection of nonexistence, for gods' sake.

 

I don't wear white (unless I'm getting married).

Edited by Skyguy2005, 10 January 2016 - 10:59 PM.

[Jim Morrison]

So to get back to the original question: This place here is crowded by extremely knowledgeable people that have a pretty clear picture of the current literature. So, what are your conclusions on the options in terms of drugs/supplements that REALLY make sense for extending life span? What are you actually taking yourself - if anything at all? 

 

Here are my 10 cents: My personal philosophy is that life span extension is not everything, "health span" is as important. My supplement stack is adapted to this idea. 

 

Background: I'm around 40 yo, lean, working out 2-3x a week. Non-smoker, no alcohol. I try to keep my caloric intake low, but it's not real CR. Blood work always looks very good so far (knocking on wood).

 

For >5yrs I'm on the following stack:

 

ED: 4000 IU Vitamin D (cognitive benefits & bone mineralization)

ED: ~1g of Vitamin C (immune function)

ED: 15mg Zinc gluconate (immune function)

ED: 750mg Glucosamine Sulfate (solid evidence for increasing LS & joint protection)

ED: 120mg Ginkgo Biloba (Mainly for cognitive benefits and neuroprotection)

EOD: EPA 465mg / DHA375 mg (cognitive benefits, but I also barely eat fish, this is for balancing my diet, I use Lovaza because I'm scared of heavy metals in fish oil)

5D per week: 500mg ALCAR (cognitive benefits and mito function, I exclusively use biosint branded sup's)

ED: 300-400mg caffeine from Coffee (Energy and neuroprotection)

 

To avoid potential impurities of health food supplements, all of the above, except for the ALCAR, are expensive pharmaceutically pure and standardized products.

 

Currently debating to lower antioxidants in the stack and to remove the EPA/DHA completely because of the Spindler papers.

 

Considering to add:

 

Metformin

Acetylsalicylic acid (anticoagulant effects may be too much with the Ginkgo)

Lipoic acid (played around with this already, but I get stomach troubles, may go for very low dose)

C60 Oil

Weat germ (for its spermidine content, but the potential for food allergy scares me)

 

 

[stefan_001]

Currently debating to lower antioxidants in the stack and to remove the EPA/DHA completely because of the Spindler papers.

 

 

I checked the paper and it says diet was daily Lovaza, Omacor 4.40 g/kg. In my calculation that would convert to approx. 25g of the stuff for a 70kg person. Sounds like an awfull lot....so not sure whether this study tells that much?

[Jim Morrison]

 

Currently debating to lower antioxidants in the stack and to remove the EPA/DHA completely because of the Spindler papers.

 

 

I checked the paper and it says diet was daily Lovaza, Omacor 4.40 g/kg. In my calculation that would convert to approx. 25g of the stuff for a 70kg person. Sounds like an awfull lot....so not sure whether this study tells that much?

 

 

Fully agreed, also there is a lot of really good arguments as to why the mouse studies make little sense, e.g. "mice normally do not eat fish" and "if you ad O3's to mouse chow it will get lots of air exposure and consequently high rates of oxidation" etc.... there is some good discussions on it here in the forum. e.g. here. Personally, all the papers showing negative effects on LS in mice still make me cautious. I get good benefits from EPA/DHA it in terms of cognitive functioning. On top of that I normally don't eat fish. Therefore, I decided to stick to a very low EOD dose. Kind of compensating for occasional meals with fish.

[Never_Ending]

The supplements that target aging are an expanding and developing field.

 

In terms of efficacy it's not a on/off switch it's a dimmer switch

 

Studies will easily deem things as ineffective because their view on testing supplements is similar to that of testing meds however supplements are more mild and the effects might even be drowned out by differences among subjects, so that approach doesn't quite fit. Some studies I'm sure are accurate and important but not all.

 

As an example: If you expose a person to a small amount of radiation... they will look the same of course, and even their blood test will come out basically the same. But does that mean nothing changed? Not necessarily

Edited by Never_Ending, 14 January 2016 - 05:37 PM.

[message]

Jim I like that stack. Rather simple. Did you notice any palpable differences with or without these supps?

[EFTANG]

You can slow down the effects of ageing to a certain extend by keeping your immune system balanced, and  compensate the negative effects of stress (mental, physical, environmental, chemical etc etc).  Stress affects your immune system much more than you might be aware of. On top of that, the immune function already starts declining after 35! 

 

You'll get sick more often, which affects how you feel ( -> causes stress) and which -again- affects your immune system. I recommend a good quality mushroom extract such as Chaga. It can normalize your immune system due to the beta-glucans it contains (make sure these are specified on the label!!) and on top of that Chaga has a high level of anti-oxidants. It also stimulates the production of SOD in the body, which helps to slow down the visible effects of ageing on skin and hair.

 

In short, a good base for lasting health. You can't go wrong with Chaga

[Logic]

AGEs (Advanced Glycation Endproducts) = NF-kb upregulation = Telomerase downregulation = Short telomeres = Epigenetic changes to a more aged phenotype...!

 

AGE blockers/breakers: (from birth!   )

Chebulic Acid

ALT-711

Liposomal Luteolin

other?

Senolytics:

Dasitinib

Quercitan

Navitoclax/ABT-263

 

NF-kB inhibitors:

Astragalus

Purslane

Gingko Biloba (EGB-761)

Other NF-kB inhibitors.  But the root cause is AGEs etc, so NF-kB inhibitors are just a plaster...

 

While Luteolin blocks all 3 stages of AGE formation, it's probably no longer on my list due to NQO1 and NRF2 inhibition...?!

 

The ...?!  is due to 2 of the studies being from the same university and 2 being in cancer cells.
Quite often natural substances do the opposite in healthy cells
NQ01 controls the NAD+/NADPH ratio.

 

http://www.ncbi.nlm....pubmed/24914470

 

http://www.ncbi.nlm....pubmed/24761924

 

http://www.ncbi.nlm....pubmed/24747074
 

Edited by Logic, 04 February 2016 - 11:41 PM.