100 replies to this topic

[Logic]

I suggest reading up on the positive effects of Inositol and IP3 before going on a Lithium binge.

Circadian rhythms (when autophagy takes place)  and the half life of these substances needs to be looked at to get cycling them right. A combined effort on this front would be nice!

 

These recent posts are about finding a combination of supps to upregulate autophagy, not simply popping Lithium!

 

NB the highlighted bits in post # 49 summarised below:

 

Lithium induces autophagy in an mTOR-independent manner.

But it also activates mTOR.

This mTOR activation partially inhibits the autophagy-inducing effects of lithium.

Rapamycin impedes the activation of mTOR that occurs with lithium, eliminating the undesirable mTOR activation. 

Combining rapamycin and lithium enables greater autophagic clearance.

 

Besides Lithium, other mTOR-independent autophagy inducers, are:

• trehalose
• calpastatin
• SMERs (have you considered looking up SMERs...!?)

Combining any/some/one of these with an mTOR inhibitor results in a greater up-regulation of autophagy. (additive effect)

This combined therapy approach should minimize side effects too.

 

Now Rapamycin is an mTOR inhibitor.

but it's also an immunosuppressant increasing the risk of cancer.

It also causes glucose tolerance and insensitivity to insulin etc.

So you want an mTOR inhibitor without those side effects.

Pterostilbene

see post # 49..!

 

Its also nice to use supps with multiple positive effects...  like Pterostilbene and BHT IMHO.

If you want to know how much of what and when to take it; join the club and plz do some research!

 

[normalizing]

so pterostilbene and lithium? because rapamycin and lithium is such a deadly combo. both of them WILL suppress immune function.

[Logic]

so pterostilbene and lithium? because rapamycin and lithium is such a deadly combo. both of them WILL suppress immune function.

 

 

Yep, amongst other things, but a good start.

But when to take what and how much...?

 

Logically Autophagy is upregulated at night, so you want the Lithium maxed then and the Inositol/IP3 lowest.
Pterostilbene is probably good 24/7?

So what's the half life of Lithium and Inositol/IP3?
Do post when you find out! Concentration graphs would be great! 

http://www.ncbi.nlm.nih.gov/pubmed

 

Day/Night cycles:
http://roguehealthan...aging-strategy/

[niner]

Day/Night cycles:
http://roguehealthan...aging-strategy/

 

This is a really great explanation; I recommend it highly.  (the tl;dr:  autophagy mostly happens at night, anabolism mostly during the day.  eating at night will suppress autophagy.  You should fast overnight, eat protein during the day, particularly around workouts.)

[Logic]

Autophagy works in cell nucleus to guard against start of cancer

 

"...The team noted that while autophagy digestion of the nucleus is able to restrain cancer, this machinery is improperly turned on during normal aging. "There is a short term 'tactical' advantage, but a long term 'strategic' defeat," Berger explains. "This mechanism makes a normal cell, even without cancer stress, get old much faster, and in a detrimental way."...

 

...In support of this notion, the team found that in late middle-aged normal cells, blocking the autophagy-driven breakdown of the nuclear lamina can make cells live 60 percent longer. In fact, say the researchers, the age extension is equivalent to a 70-year-old person living to over 110 years old..."

https://www.scienced...51029101144.htm

 

Hmmmm...!??
I think a better strategy is to kill off senescent cells and easily replace them keep the ECM etc 'young'.
http://www.ddw-onlin...-winter-13.html

(Brilliant article!?)

[albedo]

Very interesting thread.

 

• First, my small step after reading it, in particular the important posts by Locic, xEva and Niner is to move my IP6 away from bed time.

• Second, an interesting topic to research is the links between the FOXO3 gene, as it is known to activate autophagy, and its relation to aging (see the article in Cell given by geo12the in this thread, post #34):

Autophagy and Aging

http://www.cell.com/...8674(11)00828-2

“….There are also data in mammals suggesting that FOXO3a can stimulate autophagy in response to starvation or SIRT1 activation. In primary mouse renal cells, SIRT1 is activated by CR and deacetylates FOXO3a, thereby favoring the transactivation of bnip3, which codes for a potent autophagy inducer (Kume et al., 2010). Similarly, FOXO3a inhibition or depletion prevents autophagy induction by starvation in vivo in the mouse muscle (Mammucari et al., 2007), confirming a strong link between transcription factors of the FOXO family and autophagy…”

 

• Third, the Table 2 in the following article gives the autophagy-modulating drugs in clinical trials. It mentions also lithium and trehalose.             I did not study the references given but wonder about (a) the less toxic substances mimicking the effect of those drugs (see also Darryl's post #35) and (b) safety consideration in the trials should address the point xEva made about which stage of the autophagy process the compound affects.

“…Pharmacological approaches to activate or inhibit autophagy are also required because autophagy can play either a protective or destructive role in different diseases, even in different stages of the same diseases. Many drugs and compounds that modulate autophagy are currently receiving considerable attention11,89,108. These include, for example, autophagy inducers such as the mTORC1 inhibitor rapamycin109 and its analogues (e.g., CCI-779109, RAD001110,111, and AP23573112), mTOR kinase inhibitors (e.g., Torin 1113, and PP242114), trehalose115,116, carbamazepine117, and the newly identified autophagy-inducing peptide Tat–beclin 1118; autophagy inhibitors such as chloroquine119,120 and hydroxychloroquine121, Lys05122, 3-methyladenine123 and its derivatives124, PIK3C3 inhibitors125, ATG4B inhibitors126,127, and ATG7 inhibitors128,129..."

 

Autophagy and human diseases

http://www.nature.co...cr2013161a.html

Edited by albedo, 05 March 2016 - 03:48 PM.

[Harkijn]

 

so pterostilbene and lithium? because rapamycin and lithium is such a deadly combo. both of them WILL suppress immune function.

 

 

Yep, amongst other things, but a good start.

But when to take what and how much...?

 

Logically Autophagy is upregulated at night, so you want the Lithium maxed then and the Inositol/IP3 lowest.
Pterostilbene is probably good 24/7?

So what's the half life of Lithium and Inositol/IP3?
Do post when you find out! Concentration graphs would be great! 

http://www.ncbi.nlm.nih.gov/pubmed

 

Day/Night cycles:
http://roguehealthan...aging-strategy/

 

 

 

In this research preterm babies were injected with myo-inositol. Halflife was 5.22hrs but levels were only back to baseline much later:

http://www.ncbi.nlm....pubmed/24067395

 

There is a nice graph to be found there Logic, but I can't seem to copy it in the right size.

[Logic]

 

 

so pterostilbene and lithium? because rapamycin and lithium is such a deadly combo. both of them WILL suppress immune function.

 
 
Yep, amongst other things, but a good start.
But when to take what and how much...?
 
Logically Autophagy is upregulated at night, so you want the Lithium maxed then and the Inositol/IP3 lowest.
Pterostilbene is probably good 24/7?

So what's the half life of Lithium and Inositol/IP3?
Do post when you find out! Concentration graphs would be great! 
http://www.ncbi.nlm.nih.gov/pubmed
 
Day/Night cycles:
http://roguehealthan...aging-strategy/

 

 
 
In this research preterm babies were injected with myo-inositol. Halflife was 5.22hrs but levels were only back to baseline much later:
http://www.ncbi.nlm....pubmed/24067395
 
There is a nice graph to be found there Logic, but I can't seem to copy it in the right size.

 

 
Thx  Harkijn


Samples were collected within scheduled windows, plus additional scavenged samples as available. For this graph, collection times were clustered as follows to obtain mean values: 0 h (baseline) = obtained prior to infusion; 0.3 h (end of infusion) = 0–2 h post-infusion; 4 h = 2–6 h post-infusion; 8 h = 6–10 h post-infusion; 12 h = 10–14 h post-infusion; 24 h= 14–30 h post-infusion; 36 h = 30–42 h post-infusion; 48 h = 43–60 h post-infusion; 72 h = 60–82 h post-infusion; 96 h = >82 h post-infusion. Square = placebo, circle = 60mg/kg, triangle= 120mg/kg, vertical bar = ± 1 SD.
 
If you click the graph to open it in a new window, then right click the pick and choose 'Copy image address'; you can paste it into the popup you get from clicking the 'Image' button.

[Logic]

Curcumin and Cancer Cells: How Many Ways Can Curry Kill Tumor Cells Selectively?

...curcumin was shown to inhibit the Akt/mammalian target of rapamycin/p70 ribosomal protein S6 kinase pathway and activate the extracellular-signal-regulated kinases (ERK) 1/2, thereby inducing autophagy...

 

Less desirable effects on normal cells?:

• Apart from this, human epidermal keratinocytes have been shown to undergo apoptosis when exposed to curcumin through the inhibition of AP-1 (104).
• Low concentrations of curcumin may protect hepatocytes by reducing lipid peroxidation and cytochrome c release. Conversely, higher concentrations provoke glutathione depletion, caspase-3 activation, and hepatocytotoxicity (96). Interestingly, curcumin had no effect on normal rat hepatocytes, which showed no superoxide generation and therefore no cell death (172). 
• Primary cultures of human dermal fibroblasts were less sensitive to lower doses of curcumin (78). Studies have shown that curcumin causes fibroblast apoptosis and that this could be inhibited by co-administration of antioxidants N-acetyl-l-cysteine , biliverdin or bilirubin, suggesting that ROS are involved (221).
• In endothelial cells, curcumin inhibited MAP kinase activity and enhanced TNF-induced apoptosis (218).
• Studies suggests that curcumin induces the apoptosis in human retinal endothelial cells by the regulation of intracellular ROS generation, VEGF expression and release, and VEGF-mediated PKC-beta II translocation (257).
• Curcumin can induce cell death in both quiescent and proliferating normal human lymphocytes, without oligonucleosomal DNA degradation, which is considered a main hallmark of apoptotic cell death (258). Curcumin induces cell death in lymphocytes that can be classified as apoptosis-like cell death (220).

http://www.ncbi.nlm....les/PMC2758121/

 

 

 

[normalizing]

the thing with curcumin is, it has such low bioavailability that a lot of companies out there reformat it in such way to make it much more stronger with much better bioavailability that people will end up mega dosing on it by accident. even the lower quality low bioavailability types are likely to be mega dosed because of their low quality and need for bigger doses and therefore its very difficult to predict how much curcumin is in your system after regular use. that is a concern if high doses of curcumin do cause problems as shown here. kind of sad....

[Logic]

the thing with curcumin is, it has such low bioavailability that a lot of companies out there reformat it in such way to make it much more stronger with much better bioavailability that people will end up mega dosing on it by accident. even the lower quality low bioavailability types are likely to be mega dosed because of their low quality and need for bigger doses and therefore its very difficult to predict how much curcumin is in your system after regular use. that is a concern if high doses of curcumin do cause problems as shown here. kind of sad....

 

 

I'm not so sure about that with Novasol and Longvida.

http://www.longecity...ndpost&p=679135

 

Then there is this:

In spite of the vastly enhanced bioavailability of curcuminoids  from  micelles  which  was  recently  also demonstrated  in  humans  (8),  none  of  the  three curcuminoids was detectable in mouse brain tissue at the end  of  the  administration  period.  This  is  in  agreement with  our  previous  observations  in  mice  administered  50 mg native curcumin per kg bodyweight by gastric intubation,  in  which  no  curcumin  was  detectable  in  the brain 30, 60 or 90 min after administration (11). At present,  it  is  not  known  if  the  enhanced  oral bioavailability of the micellar curcumin [8] may have led transiently  to  sufficiently  high  concentrations  of curcumin to elicit biological activities in the brain.  Thus, very  small  curcumin  concentrations  and/or  curcumin metabolites  may  be  responsible  for  the  beneficial  effects of dietary curcumin on mitochondrial function. Therefore a modulation of transcription factors, enzyme activities or gene expression seems to be more likely as a mechanism of  action  for  curcumin  than  a  direct  antioxidative  effect (5, 16).

http://novasolcurcum...t-Alzheimer.pdf

 

I think the devil is in the dosage and a careful look at the different effects at different dosages is a good idea.

[normalizing]

so they claim they did not detect any of the curcumin metabolites in the brain but curcumin might have indirect effect on the brain, so they shouldnt be looking at any of its metabolites but perhaps something else that has been changed from the indirect antioxidative effect. because, from all those studies i read they continue to claim the same old thing, curcumin is not bioactive enough to be able to cause anything and YET mostly the same studies will report positive effect, including important finding of anti depressive effects which makes no sense if they cannot detect its metabolites in the brain right? it has to be something else that changes with its consumption, but its unknown what or care to explain why the confliction in those studies

[normalizing]

any updates

[playground]

 

Summary from the following site: http://www.anti-agin...fights-aging-2/

 

Not on the list but I think l-lysine helps or assists in the process.

 

AUTOPHAGY - Recap of article

• Fasting activates Autophagy -   caloric restriction affects 5 molecular pathways that activate autophagy
• Sunlight, Vitamin D and Klotho activate Autophagy - there are three ways through which UV light, Vitamin D, and the Klotho pathway activate autophagy via inhibiting the insulin/IGF-1 pathway
• Caffeine activates Autophagy - Caffeine can activate autophagy via an mTOR-dependent mechanism
• Green tea activates Autophagy - ECGC can activate autophagy via an mTOR-dependent mechanism
• Lithium activates Autophagy -  lithium and other compounds can activate autophagy by inhibiting inositol monophosphate and lower IP3 levels – an mTOR-independent mechanism
• Resveratrol activates Autophagy – there are four 4 ways through which resveratrol can activate autophagy – via mTOR-dependent and mTOR-independent mechanism

 

 

forgive my ignorance,  but what's the essential difference between autophagy and macrophagy ?

 

 

 

[Logic]

Very interesting thread.

• First, my small step after reading it, in particular the important posts by Locic, xEva and Niner is to move my IP6 away from bed time.

• Second, an interesting topic to research is the links between the FOXO3 gene, as it is known to activate autophagy, and its relation to aging (see the article in Cell given by geo12the in this thread, post #34):

Autophagy and Aging
http://www.cell.com/...8674(11)00828-2
“….There are also data in mammals suggesting that FOXO3a can stimulate autophagy in response to starvation or SIRT1 activation. In primary mouse renal cells, SIRT1 is activated by CR and deacetylates FOXO3a, thereby favoring the transactivation of bnip3, which codes for a potent autophagy inducer (Kume et al., 2010). Similarly, FOXO3a inhibition or depletion prevents autophagy induction by starvation in vivo in the mouse muscle (Mammucari et al., 2007), confirming a strong link between transcription factors of the FOXO family and autophagy…”

 

I have just remembered that DHA as found in Fish or ,the better option, Krill OIl inhibits FOXA3A.
I have no idea as to the half life of DHA, but moving it to the morning too is probably a good idea.
Better yet would be DHA free EPA (Nordic Naturals) IMHO, unless you are trying to build your brain with NSI-189 etc.
 
http://www.longecity...ndpost&p=601563

 

http://www.longecity...s-on-foxo-gene/

 

• ... the newly identified autophagy-inducing peptide Tat–beclin 1118; autophagy inhibitors such as chloroquine119,120 and hydroxychloroquine121, Lys05122, 3-methyladenine123 and its derivatives124, PIK3C3 inhibitors125, ATG4B inhibitors126,127, and ATG7 inhibitors128,129..."

 
Autophagy and human diseases
http://www.nature.co...cr2013161a.html

 

Interesting.  Thx

Edited by Logic, 16 April 2016 - 05:18 PM.

[Logic]

 

 

Summary from the following site: http://www.anti-agin...fights-aging-2/

 

Not on the list but I think l-lysine helps or assists in the process.

 

AUTOPHAGY - Recap of article

• Fasting activates Autophagy -   caloric restriction affects 5 molecular pathways that activate autophagy
• Sunlight, Vitamin D and Klotho activate Autophagy - there are three ways through which UV light, Vitamin D, and the Klotho pathway activate autophagy via inhibiting the insulin/IGF-1 pathway
• Caffeine activates Autophagy - Caffeine can activate autophagy via an mTOR-dependent mechanism
• Green tea activates Autophagy - ECGC can activate autophagy via an mTOR-dependent mechanism
• Lithium activates Autophagy -  lithium and other compounds can activate autophagy by inhibiting inositol monophosphate and lower IP3 levels – an mTOR-independent mechanism
• Resveratrol activates Autophagy – there are four 4 ways through which resveratrol can activate autophagy – via mTOR-dependent and mTOR-independent mechanism

 

 

forgive my ignorance,  but what's the essential difference between autophagy and macrophagy ?

 

 

https://en.wikipedia.../wiki/Autophagy

 

http://genesdev.cshl...21/22/2861.full

[Logic]

In the interests of completeness I'm reposting a post by Darryl here.

 

Preventative use of nilotinib is unlikely given high cost (its a biologic) and pretty severe side effects (>10% incidence of headache, nausea, rash, itchiness, hair loss, dry skin, muscle aches, fatigue), though I'd be very interested in a trial in early cognitive decline.

Among the numerous compounds that induce autophagy in vitro, I think most attractive at the moment are approved, centrally active, negligible adverse effect small molecules like rilmenidine, which David Rubinsztein has advised at least one Huntington's carrier to take in the hope of delaying that disease's onset. Some other options are presented in 

Chemical inducers of autophagy that enhance the clearance of mutant proteins in neurodegenerative diseases

http://www.jbc.org/c...11061.full.pdf3

 

http://www.longecity...ndpost&p=710115

 

Note that round 2 of a Nilotinib group buy is happening here:

http://www.longecity...roup-buy/page-7

Nilotinib upregulates PARKIN which will lead to the mitophagy of ailing mitochondria only:

http://jcs.biologist...ntent/125/4/795

 

It also upregulates autophagy in general which gets rid of dementia causing misfolded proteins etc-etc.

http://www.ncbi.nlm....les/PMC3975659/
http://www.ncbi.nlm....les/PMC2592826/
http://explore.georg.../news/?ID=70332
https://www.georgeto...sons-study.html
https://gumc.georget...e-in-Parkinsons

 

Is Anti-fibrotic in the liver and kidneys and in general:
http://www.ncbi.nlm....act&holding=npg
http://www.ncbi.nlm....pubmed/21251937
http://www.ncbi.nlm....les/PMC3148703/
http://www.abstracts...hp?nu=ERA10L_36

 

 

[Logic]

Lysosomes in iron metabolism, ageing and apoptosis

http://www.ncbi.nlm....les/PMC2668650/

 

MCOLN1 is a ROS sensor in lysosomes that regulates autophagy

http://www.nature.co...comms12109.html

[Harkijn]

Apigenin was not mentioned in this thread yet, I believe. It stimulates autophagy as described here

https://www.research..._keratinocytes 

and it is a known antigenotoxic.

However, the safety profile is not very clear yet and I certainly wouldn't take this on a daily basis until more gets known . I take 50mgs every now and then for reasons discussed in the NR thread.

[normalizing]

ok here is one that depends heavily on the type of gut bacteria you have; http://www.medicalne...cles/311572.php

 

now, can someone figure out which exact bacteria do you need to break down pomegranates into this compound?

[Logic]

gamesguru posted about galangin here:
http://www.longecity...ndpost&p=777892
A quick goole search brought up some very interesting info!:

...Galangin treatment inhibited cell proliferation and induced autophagy (130 μ mol/l) and apoptosis (370 μ mol/l). In particular, galangin treatment in HepG2 cells caused (1) an accumulation of autophagosomes, (2) elevated levels of microtubule-associated protein light chain 3, and (3) an increased percentage of cells with vacuoles. p53 expression was also increased...
http://www.ncbi.nlm....pubmed/22507894

Galangin: autophagy inducing flavonoid
http://www.sigmaaldr...ng=en&region=ZA

...Galangin is a flavonol, a type of flavonoid. It is found in high concentrations in Alpinia officinarum (lesser galangal)[1] and Helichrysum aureonitens.[2] It is also found in the galangal rhizome (Alpinia galanga)[3] and in propolis.[4] Galangin has been shown to have in vitro antibacterial[5][6] and antiviral activity.[7] The flavonol also inhibits the growth of breast tumor cells in vitro...
https://en.wikipedia.org/wiki/Galangin

[playground]

where on earth do  you buy this plants ?

 - Alpinia officinarum (lesser galangal)[1] and

 - Helichrysum aureonitens.[2]

 

But seriously, is there any compound, anywhere, that does NOT have anti-bacterial activity ?

With a little ingenuity and persistence you could make write a study showing that bananas

are anti-bacterial.

 

 

 

[normalizing]

if there is a plant that is not anti-bacterial, it has dissapeared by now through lack of survival adaptation. people can keep posting exotic expensive plants with anti-bacteria and anti-viral activities all they want on here, but just go outside your home and pick up random plants, just as good

[albedo]

ok here is one that depends heavily on the type of gut bacteria you have; http://www.medicalne...cles/311572.php

 

now, can someone figure out which exact bacteria do you need to break down pomegranates into this compound?

I wish to look better at this but just posted an element of reply here.

[Daniscience]

 

Summary from the following site: http://www.anti-agin...fights-aging-2/

 

Not on the list but I think l-lysine helps or assists in the process.

 

AUTOPHAGY - Recap of article

• Fasting activates Autophagy -   caloric restriction affects 5 molecular pathways that activate autophagy
• Sunlight, Vitamin D and Klotho activate Autophagy - there are three ways through which UV light, Vitamin D, and the Klotho pathway activate autophagy via inhibiting the insulin/IGF-1 pathway
• Caffeine activates Autophagy - Caffeine can activate autophagy via an mTOR-dependent mechanism
• Green tea activates Autophagy - ECGC can activate autophagy via an mTOR-dependent mechanism
• Lithium activates Autophagy -  lithium and other compounds can activate autophagy by inhibiting inositol monophosphate and lower IP3 levels – an mTOR-independent mechanism
• Resveratrol activates Autophagy – there are four 4 ways through which resveratrol can activate autophagy – via mTOR-dependent and mTOR-independent mechanism

 

 

This may explain my succesful fat loss period as I happen to ingest almost every of that LOL

 

- L-Lysine: I take it purely as an amino-acid filler, since I take a lot of hazelnuts and almonds (which lack lysine). Didn't know this aids fat loss.

- Fasting: I am on a keto/IF diet in which I spend 20 hours with no food, and then eat twice a day (4 hours apart) in the midday.

- Sunlight: I live in Spain

- Caffeine and EGCG: I take some fat burners that include these.

 

I don't take Lithium nor Resveratrol, but I am going to try Resveratrol as its so researched at Longecity (its the only supplement that has its own subforum!). Anyway I drink red wine almost everyday (own produced)

 

 

p.s. obviously calorie restriction and exercise are the prime requirements for fat loss, but supplements do contribute.
 

Edited by Daniscience, 03 August 2016 - 06:10 PM.

[normalizing]

i love the p.s. yeh no shit those are the ones to cause fat loss hah and you do it what, 20 hours no food? + you exercise and drink wine wow you need to post pics to see how skinny you really are

[albedo]

I wonder if this study can be useful in this thread (looks like only in vitro results though, see Niner's post):

 

Natural small-molecule enhancers of autophagy induce autophagic cell death in apoptosis-defective cells

http://www.nature.co...icles/srep05510

 

"Resistance of cancer cells to chemotherapy is a significant problem in oncology, and the development of sensitising agents or small-molecules with new mechanisms of action to kill these cells is needed. Autophagy is a cellular process responsible for the turnover of misfolded proteins or damaged organelles, and it also recycles nutrients to maintain energy levels for cell survival. In some apoptosis-resistant cancer cells, autophagy can also enhance the efficacy of anti-cancer drugs through autophagy-mediated mechanisms of cell death. Because the modulation of autophagic processes can be therapeutically useful to circumvent chemoresistance and enhance the effects of cancer treatment, the identification of novel autophagic enhancers for use in oncology is highly desirable. Many novel anti-cancer compounds have been isolated from natural products; therefore, we worked to discover natural, anti-cancer small-molecule enhancers of autophagy. Here, we have identified a group of natural alkaloid small-molecules that function as novel autophagic enhancers. These alkaloids, including liensinine, isoliensinine, dauricine and cepharanthine, stimulated AMPK-mTOR dependent induction of autophagy and autophagic cell death in a panel of apoptosis-resistant cells. Taken together, our work provides novel insights into the biological functions, mechanisms and potential therapeutic values of alkaloids for the induction of autophagy." (bold mine)

 

[Harkijn]

Thank you Albedo, this is quite informative: interesting to see how a number of Longecity topics converge here, such as aspartic acid and spermidine. On a side note: the specific alkaloids discussed in the article are very strong stuff. I know some people on these forums who tend to rashly take some substances as a preventive health measure. Not a good idea in this case!

[albedo]

Reading on the role of autophagy in fighting infectious diseases (and possibly metformin as autophagy inducer) i pop into this study:

 

Autophagy modulation as a potential therapeutic target for diverse diseases

https://www.ncbi.nlm...les/PMC3518431/

 

"... Based on these studies, there is a strong possibility that pharmacological agents that increase autophagy may be effective therapeutic agents for treating certain intracellular bacterial infections, parasitic infections and viral infections. In support of this concept, vitamin D treatment has been shown to inhibit both HIV and M. tuberculosis replication in human macrophages through an autophagy-dependent mechanism^149,150. In addition, the antimycobacterial action of standard antituberculous agents is associated with autophagy induction¹⁵¹, raising the possibility that some drugs that are already in clinical use for the treatment of certain infections may be acting, at least in part, via autophagy...."

 

Interesting also the vitamin D role. See also previous post 13 by Logic in this thread.

 

 

 

 

 

 

 

 

[normalizing]

im glad one of my favorite threads got updated BUT this is not interesting enough for me. vitamin d is this new treatment for all diseases currently and everyone hypes it and makes the ideal supplement to take and be free of worry. ive been using vitamin d to cure my depression for years since i read studies on it, it helped not! but, here is the kicker, it didnt help anything else either. the studies keep saying you might even become "superman"