91 replies to this topic

[stefan_001]

Not a new article but extensive:

Honokiol Potentiates Apoptosis, Suppresses Osteoclastogenesis, and Inhibits Invasion through Modulation of Nuclear Factor-κB Activation Pathway

http://mcr.aacrjourn...nt/4/9/621.full

[stefan_001]

Herein, we have assessed the cytotoxic characteristics of several molecules of natural origin (cerulinin, chrysin, honikiol, limonin, mevinolin, resveratrol, salicin, retinol, ascorbic acid and calciferol) against two different gynecological breast (MCF-7) and Cervix (HeLa) solid tumor cell lines. After exposure to serial concentrations of the test compounds, SRB-u assay was undertaken and viability assessment was performed via fitting to Emax model to identify the cytotoxicity parameters such as, IC50 and resistant fraction (R-value). Tested compounds showed cytotoxic efficacy against both gynecological solid tumor cell lines (MCF-7 and HeLa) with IC50's ranged from 0.61 to 131.1 μg/ml. In MCF-7 breast cancer cell line; cerulinin, honikiol, mevinolin and calciferol showed the highest potency with IC50 less than 5 μg/ml. Chrysin showed moderate potency with IC50 of 7.27 μg/ml. Ascorbic acid and resveratrol showed the weakest cytotoxic activity with IC50 more than 10 μg/ml. In HeLa cervix cancer cell line; cerulinin and mevinolin showed the highest potency with IC50 less than 5 μg/ml. Chrysin, honikiol, resveratrol and calciferol showed moderate potency with IC50 of ranging from 5-10 μg/ml. Ascorbic acid was the weakest cytotoxic molecule with IC50 more than 10 μg/ml. Limonine, salicin and retinol failed to exert any cytotoxic effect against MCF-7 or HeLa cancer cell lines in-vitro. RT-PCR analysis revealed that the cytotoxicity of these products is multi-factorial and not solely dependent on p53 expression. Impressively, molecules of potent and moderate potency (except chrysin) showed low resistant fraction in both gynecological solid tumor cancer cell lines. In conclusion, our data showed wide range of variable efficacy of several molecules of natural origin against two hormone dependent solid tumor cell lines.

http://nodaiweb.univ...F03_107-110.pdf

[Bryan_S]

Nice find 

[Bryan_S]

Hypoglycemic effect and mechanism of honokiol on type 2 diabetic mice

 

https://www.dovepres...xt-article-DDDT

 

 

[stefan_001]

I was trying to find information about dosing. But it only resulted in more questions. I assumed that oral administration would be an effective way but it doesn't see to be the case. Moreover:

- Honokiol, however, has poor aqueous solubility, which adversely affect its intestinal absorption. This limitation has been addressed by developing liposomal formulations. Biologically effective serum concentrations of honokiol can be achieved following intravenous administration; glucuronidation and sulfation are the main metabolic pathways for its clearance.

It's comes from this interesting study:
http://www.ncbi.nlm....39/#!po=56.0606

So when taking a 200mg cap magnolia extract it may only give very little serum level. Any thoughts from anybody?

[Bryan_S]

Admittedly this article is a few years old but the breath of honokiol's influence is covered. He also go's on to suggest some dosage regimens. This guy might be connected with HonoPure. At 400mg per day I'm not on this chart, well I guess I'm at the bottom end in the prevention category. 

 

http://www.faim.org/...army-plant.html

• Active cancer, therapeutic level: 1 gram, 3x/day, with food.
• Long-term maintenance: 500 mg, 2x/day (total of 1 gram/day), with food.
• Prevention: Start with 500 mg 2x/day, and after one month the dosage can be dropped to 500 mg 1x/day, or 250 mg 2x/day.

Edited by Bryan_S, 08 February 2016 - 02:44 AM.

[resveratrol_guy]

Admittedly this article is a few years old but the breath of honokiol's influence is covered. He also go's on to suggest some dosage regimens. This guy might be connected with HonoPure. At 400mg per day I'm not on this chart, well I guess I'm at the bottom end in the prevention category. 

 

http://www.faim.org/...army-plant.html

• Active cancer, therapeutic level: 1 gram, 3x/day, with food.
• Long-term maintenance: 500 mg, 2x/day (total of 1 gram/day), with food.
• Prevention: Start with 500 mg 2x/day, and after one month the dosage can be dropped to 500 mg 1x/day, or 250 mg 2x/day.

For what it's worth, I recently dropped Honopure and reverted to Swanson's 90% because I noticed a strong VOC odor emmanating from the bottle, very unlike the Japanese laquer odor of unrefined magnolia bark extract. But to be fair, maybe that's what pure honokiol smells like, so this is only an advisory. If anyone knows better, please speak up.

Edited by resveratrol_guy, 08 February 2016 - 02:12 PM.

[Bryan_S]

Honokiol inhibits the growth of head and neck squamous cell carcinoma by targeting epidermal growth factor receptor.

 

http://www.ncbi.nlm....pubmed/26020804

 

https://www.scienced...50625145320.htm

 

I posted this before but not in this forum.

 

This article also appeared.

 

Multifunctional effects of honokiol as an anti-inflammatory and anti-cancer drug in human oral squamous cancer cells and xenograft.

http://www.ncbi.nlm....pubmed/25890726

 

Honokiol Inhibits Non-Small Cell Lung Cancer Cell Migration by Targeting PGE2-Mediated Activation of β-Catenin Signaling

http://journals.plos...al.pone.0060749

 

How Does Honokiol Fight Cancer?

http://gaynoroncolog...ancer-activity/

 

It's not just cancers that have sparked great interest.

 

Honokiol blocks and reverses cardiac hypertrophy in mice by activating mitochondrial Sirt3

http://www.nature.co...ncomms7656.html

 

So this compound is something like a swiss army knife and there are other applications.

Edited by Bryan_S, 20 February 2016 - 06:49 PM.

[Bryan_S]

Honokiol inhibits sphere formation and xenograft growth of oral cancer side population cells accompanied with JAK/STAT signaling pathway suppression and apoptosis induction

https://bmccancer.bi...2885-016-2265-6

 

 

 

Preclinical effects of honokiol on treating glioblastoma multiforme via G1 phase arrest and cell apoptosis

http://www.sciencedi...94471131600074X

 

Edited by Bryan_S, 29 March 2016 - 11:12 PM.

[resveratrol_guy]

Bryan, thanks for posting all these articles above on cancer suppression. I have a question, though, which I don't think any existing research addresses. (But maybe it's been addressed informally by the experience of longterm users.) My question is whether low doses of honokiol in the absence of cancer merely force our latent tumor cells to learn to tolerate it. There's a tradeoff between never allowing those tumor cells to evolve or even survive on the one hand, and teaching them how to live with honokiol on the other. On the one hand, if one were diagnosed with cancer, then being honokiol naive would be preferable because one could start with a very punishing dose. But on the other hand, chronic low doses might enable one to remain free of cancer for longer. I realize there's no good answer to this. I would just like to get some idea of current thinking along these lines.

[airplanepeanuts]

I don't think there are latent cancer cells in the body that are adapting to things like bacteria to antibiotics.

[resveratrol_guy]

I don't think there are latent cancer cells in the body that are adapting to things like bacteria to antibiotics.

 

Why not? Chronic low-dose honokiol is an environmental stressor from the perspective of cells which would prefer to grow in an uncontrolled manner. It amounts to selection pressure to escape susceptibility to the supplementation. Either you kill every last aggressive cell, or you create such selection pressure. Having said that, it may well be that it takes much longer for latent cancer cells to evolve around it, and escape every other suppression mechanism like p53, than it would for them to create a malignant neoplasm in the absence thereof. My only point is that the tradeoff is not at all clear, especially in terms of optimal chronic dose in healthy individuals. (BTW I do not think that the optimal dose is zero; if nothing else a bit of hormesis would probably be beneficial.)

Edited by resveratrol_guy, 01 April 2016 - 06:20 PM.

[Bryan_S]

 

I don't think there are latent cancer cells in the body that are adapting to things like bacteria to antibiotics.

 

Why not? Chronic low-dose honokiol is an environmental stressor from the perspective of cells which would prefer to grow in an uncontrolled manner. It amounts to selection pressure to escape susceptibility to the supplementation. Either you kill every last aggressive cell, or you create such selection pressure. Having said that, it may well be that it takes much longer for latent cancer cells to evolve around it, and escape every other suppression mechanism like p53, than it would for them to create a malignant neoplasm in the absence thereof. My only point is that the tradeoff is not at all clear, especially in terms of optimal chronic dose in healthy individuals. (BTW I do not think that the optimal dose is zero; if nothing else a bit of hormesis would probably be beneficial.)

 

 

Apoptosis is the genetically programed goal for cells that naturally reach this stage. In most instances those cells should self destruct but for those that might try and escape, turning up their susceptibility to apoptosis with Honokiol I believe is something we'd all want. However you raise a good question that no study has to-date addressed. Keep in mind that of those cells that "might" reach this state of pushing past the natural cell division hurdles are statistically low to start with, then you'd have to consider an untouched population that "might" evolve an unknown workaround to Honokiol as you suggest?

 

Until a study tests your question I think turning up their susceptibility to apoptosis helps clean out the trash before they can evolve past this point, so to speak. I think the concern might be that we might lose a few more senescent cells to apoptosis before they could activate an unknown cell division workaround. This fits in with the idea of using senolytics, being that these are cells that should die but linger around anyway.

 

If in the end cells push past their natural programed cell death and continue into cell division Honokiol should block the few remaining adaptation pathways, inferring us additional protection, lowering the risk or suspending or slowing mutant cell growth. The small fraction that might get by should be statistically lower. I'd say its a numbers game anyway, wouldn't you?

 

This is not why I take it, I take it as a SIRT3 activator along with (NR) and an unexpected side effect I did not anticipate was it relaxes the smooth muscle tissue of the urethra so my Benign Prostatic Hypertrophy has subsided. I post those cancer study links because these are the on going headlines about this compound for this thread. Are you suggesting I stop taking it for an untested concern?

 

Also as senolytics become available if you follow your line of reasoning won't they become ineffective as well?

 

I will say its cheaper than my previous BPH medication but if there is a valid argument to discontinue taking it I want to hear it.

Edited by Bryan_S, 02 April 2016 - 05:13 AM.

[resveratrol_guy]

Apoptosis is the genetically programed goal for cells that naturally reach this stage. In most instances those cells should self destruct but for those that might try and escape, turning up their susceptibility to apoptosis with Honokiol I believe is something we'd all want. However you raise a good question that no study has to-date addressed. Keep in mind that of those cells that "might" reach this state of pushing past the natural cell division hurdles are statistically low to start with, then you'd have to consider an untouched population that "might" evolve an unknown workaround to Honokiol as you suggest?

 

Until a study tests your question I think turning up their susceptibility to apoptosis helps clean out the trash before they can evolve past this point, so to speak. I think the concern might be that we might lose a few more senescent cells to apoptosis before they could activate an unknown cell division workaround. This fits in with the idea of using senolytics, being that these are cells that should die but linger around anyway.

 

If in the end cells push past their natural programed cell death and continue into cell division Honokiol should block the few remaining adaptation pathways, inferring us additional protection, lowering the risk or suspending or slowing mutant cell growth. The small fraction that might get by should be statistically lower. I'd say its a numbers game anyway, wouldn't you?

 

This is not why I take it, I take it as a SIRT3 activator along with (NR) and an unexpected side effect I did not anticipate was it relaxes the smooth muscle tissue of the urethra so my Benign Prostatic Hypertrophy has subsided. I post those cancer study links because these are the on going headlines about this compound for this thread. Are you suggesting I stop taking it for an untested concern?

 

Also as senolytics become available if you follow your line of reasoning won't they become ineffective as well?

 

I will say its cheaper than my previous BPH medication but if there is a valid argument to discontinue taking it I want to hear it.

 

Good answer. I suppose another important consideration is to take other cancer suppressors, so any cell which finds a way around honokiol will just run into another brick wall. If honokiol activates SIRT3, then at least that's a pretty ancient pathway which in theory should be very difficult to evade. As I said, I don't think the optimal dose is zero. It's "just enough to kill everything that wants to escape honokiol", but no more. I have no idea how to ascertain what that threshold is. Are there any animal lifespan analyses which might provide some clue? Presumably we don't want to be too agressive at killing senescent cells, either, because even they do provide some useful function, particularly the less damaged ones.

 

All the papers you've posted have been relevant and useful. The hard question, though, is what is the right chronic dose?

[Bryan_S]

From a BPH standpoint for me its 200mg twice per day. SIRT3 or cancer protection is a little harder to ascertain but I assume I'm getting some protection. I've tried reducing the dose and the BPH voiding symptoms return so I believe I've arrived at one dose but one thing likely has nothing to do with the other.

Edited by Bryan_S, 03 April 2016 - 06:32 PM.

[resveratrol_guy]

From a BPH standpoint for me its 200mg twice per day. SIRT3 or cancer protection is a little harder to ascertain but I assume I'm getting some protection. I've tried reducing the dose and the BPH voiding symptoms return so I believe I've arrived at one dose but one thing likely has nothing to do with the other.

 

That's a useful data point for BPH sufferers. I still think we need some sort of lifespan data. Even C. elegans would be better than nothing. Presumably, on account of its neurite outgrowth and tumor killing properties, honokiol should extend life. It would almost be a more interesting result if it didn't.

[Bryan_S]

I still think we need some sort of lifespan data. Even C. elegans would be better than nothing. . . honokiol should extend life. It would almost be a more interesting result if it didn't.

 

And you would be right. Ask and you shall receive:

 

Honokiol Mediated Lifespan Extension in Caenorhabditis elegans (C. elegans)

Presenters

• Andrew Ikazaki, Senior, Biology (General)
• Kathlyn Acosta, Senior, Biology (Molecular, Cellular & Developmental)
• Da (Dayae) Kim, Senior, Microbiology

Mentor

• Matt Kaeberlein, Pathology

As we age, the human body becomes increasingly susceptible to damage from internal and external factors. Aging is the greatest risk factor for most of the major causes of death in developed nations, including many neurodegenerative diseases, cardiovascular disease, and most forms of cancer. Identification and disruption of molecular mechanisms critical in the process of aging can inhibit the acquisition and progression of age-related pathologies. The compound honokiol, a component purified from magnolia, is shown to have antioxidant, anti-inflammatory, anti-tumor, and neuroprotective properties in both in vitro and in vivo models. The goal of this research is to examine the effects of honokiol on aging and longevity, and to elucidate the molecular mechanisms associated with its effects, in the invertebrate model Caenorhabditis elegans. C. elegans is a particularly useful model for aging research due to its short lifespan of around twenty three days. In addition, they are non-pathogenic, reproduce rapidly, and share many fundamental genetic pathways with more complex organisms, including humans. In preliminary studies we have observed a significant lifespan extension in C. elegans treated with honokiol. The goal of this project is do further characterize the mechanisms of lifespan extension from honokiol. This will be accomplished initially through genetic epistasis analysis of honokiol in combination with known longevity pathways such as the insulin-IGF signaling (IIS) pathway, the hypoxic response pathway, and the dietary restriction pathway. These studies will generate hypotheses for future experiments in C. elegans and mouse models, and may ultimately contribute to therapies to delay the onset and progression of age-related diseases in people.

 

I would look for more from this group. So let's see if we can get hold of the resulting paper.

 

Also my apologies I thought those points were made early on. Here are some more studies and articles related to aging. I'm sure we can find more but the SIRT3 path looks like the driver of longevity and this is one of the main axis points which helps correct the other cellular deficits.

 

Activator for Important Aging and Cancer Protein Identified

 

David Gius, MD, PhD, professor in Radiation Oncology and Pharmacology, contributed to a paper that identified a compound to reestablish the activity of SIRT3

http://news.feinberg...4/gius-protein/

Original paper

http://www.nature.co...ncomms7656.html

 

“In population studies, increased Sirt3 level due to polymorphism in the gene promoter was linked to extended lifespan of humans, whereas another polymorphism in the Sirt3 gene led to decreased enzymatic activity of Sirt3, and was found to be associated with metabolic syndrome in humans, thus implicating a role of Sirt3 in regulating human ageing”

 

This next article is about skin and cosmetic applications.

https://mibellebioch...gn_Feb_2010.pdf

[Bryan_S]

Funded Grants

•   »  Beneficial effects of Honokiol against liver cancer

https://prevention.c...nts/R21CA185943

 

These results should be in soon.

 

https://projectrepor...cfm?aid=8877813

[normalizing]

yes but this is all based on high pure extracted honokiol, im curious what amount is present in magnolia bark and how bioavailable it is from that source instead?

[resveratrol_guy]

 

I still think we need some sort of lifespan data. Even C. elegans would be better than nothing. . . honokiol should extend life. It would almost be a more interesting result if it didn't.

 

And you would be right. Ask and you shall receive:

 

Honokiol Mediated Lifespan Extension in Caenorhabditis elegans (C. elegans)

Presenters

• Andrew Ikazaki, Senior, Biology (General)
• Kathlyn Acosta, Senior, Biology (Molecular, Cellular & Developmental)
• Da (Dayae) Kim, Senior, Microbiology

Mentor

• Matt Kaeberlein, Pathology

As we age, the human body becomes increasingly susceptible to damage from internal and external factors. Aging is the greatest risk factor for most of the major causes of death in developed nations, including many neurodegenerative diseases, cardiovascular disease, and most forms of cancer. Identification and disruption of molecular mechanisms critical in the process of aging can inhibit the acquisition and progression of age-related pathologies. The compound honokiol, a component purified from magnolia, is shown to have antioxidant, anti-inflammatory, anti-tumor, and neuroprotective properties in both in vitro and in vivo models. The goal of this research is to examine the effects of honokiol on aging and longevity, and to elucidate the molecular mechanisms associated with its effects, in the invertebrate model Caenorhabditis elegans. C. elegans is a particularly useful model for aging research due to its short lifespan of around twenty three days. In addition, they are non-pathogenic, reproduce rapidly, and share many fundamental genetic pathways with more complex organisms, including humans. In preliminary studies we have observed a significant lifespan extension in C. elegans treated with honokiol. The goal of this project is do further characterize the mechanisms of lifespan extension from honokiol. This will be accomplished initially through genetic epistasis analysis of honokiol in combination with known longevity pathways such as the insulin-IGF signaling (IIS) pathway, the hypoxic response pathway, and the dietary restriction pathway. These studies will generate hypotheses for future experiments in C. elegans and mouse models, and may ultimately contribute to therapies to delay the onset and progression of age-related diseases in people.

 

I would look for more from this group. So let's see if we can get hold of the resulting paper.

 

Also my apologies I thought those points were made early on. Here are some more studies and articles related to aging. I'm sure we can find more but the SIRT3 path looks like the driver of longevity and this is one of the main axis points which helps correct the other cellular deficits.

 

Activator for Important Aging and Cancer Protein Identified

 

David Gius, MD, PhD, professor in Radiation Oncology and Pharmacology, contributed to a paper that identified a compound to reestablish the activity of SIRT3

http://news.feinberg...4/gius-protein/

Original paper

http://www.nature.co...ncomms7656.html

 

“In population studies, increased Sirt3 level due to polymorphism in the gene promoter was linked to extended lifespan of humans, whereas another polymorphism in the Sirt3 gene led to decreased enzymatic activity of Sirt3, and was found to be associated with metabolic syndrome in humans, thus implicating a role of Sirt3 in regulating human ageing”

 

This next article is about skin and cosmetic applications.

https://mibellebioch...gn_Feb_2010.pdf

 

 

Very cool! I only just saw this because I've been having notification problems with the website. Anyway, it looks promising. The next obvious step is rodents.

 

@ normalizing, no idea but you can get 90% honokiol from a solid source (Swanson) and 98% from a less well known one (Honopure). I've gone back to Swanson after detecting some VOC odor in the latter.
 

[mrak1979]

is honokiol best orally taken with or without food for best absorption?

[normalizing]

 

 

I still think we need some sort of lifespan data. Even C. elegans would be better than nothing. . . honokiol should extend life. It would almost be a more interesting result if it didn't.

 

And you would be right. Ask and you shall receive:

 

Honokiol Mediated Lifespan Extension in Caenorhabditis elegans (C. elegans)

Presenters

• Andrew Ikazaki, Senior, Biology (General)
• Kathlyn Acosta, Senior, Biology (Molecular, Cellular & Developmental)
• Da (Dayae) Kim, Senior, Microbiology

Mentor

• Matt Kaeberlein, Pathology

As we age, the human body becomes increasingly susceptible to damage from internal and external factors. Aging is the greatest risk factor for most of the major causes of death in developed nations, including many neurodegenerative diseases, cardiovascular disease, and most forms of cancer. Identification and disruption of molecular mechanisms critical in the process of aging can inhibit the acquisition and progression of age-related pathologies. The compound honokiol, a component purified from magnolia, is shown to have antioxidant, anti-inflammatory, anti-tumor, and neuroprotective properties in both in vitro and in vivo models. The goal of this research is to examine the effects of honokiol on aging and longevity, and to elucidate the molecular mechanisms associated with its effects, in the invertebrate model Caenorhabditis elegans. C. elegans is a particularly useful model for aging research due to its short lifespan of around twenty three days. In addition, they are non-pathogenic, reproduce rapidly, and share many fundamental genetic pathways with more complex organisms, including humans. In preliminary studies we have observed a significant lifespan extension in C. elegans treated with honokiol. The goal of this project is do further characterize the mechanisms of lifespan extension from honokiol. This will be accomplished initially through genetic epistasis analysis of honokiol in combination with known longevity pathways such as the insulin-IGF signaling (IIS) pathway, the hypoxic response pathway, and the dietary restriction pathway. These studies will generate hypotheses for future experiments in C. elegans and mouse models, and may ultimately contribute to therapies to delay the onset and progression of age-related diseases in people.

 

I would look for more from this group. So let's see if we can get hold of the resulting paper.

 

Also my apologies I thought those points were made early on. Here are some more studies and articles related to aging. I'm sure we can find more but the SIRT3 path looks like the driver of longevity and this is one of the main axis points which helps correct the other cellular deficits.

 

Activator for Important Aging and Cancer Protein Identified

 

David Gius, MD, PhD, professor in Radiation Oncology and Pharmacology, contributed to a paper that identified a compound to reestablish the activity of SIRT3

http://news.feinberg...4/gius-protein/

Original paper

http://www.nature.co...ncomms7656.html

 

“In population studies, increased Sirt3 level due to polymorphism in the gene promoter was linked to extended lifespan of humans, whereas another polymorphism in the Sirt3 gene led to decreased enzymatic activity of Sirt3, and was found to be associated with metabolic syndrome in humans, thus implicating a role of Sirt3 in regulating human ageing”

 

This next article is about skin and cosmetic applications.

https://mibellebioch...gn_Feb_2010.pdf

 

 

Very cool! I only just saw this because I've been having notification problems with the website. Anyway, it looks promising. The next obvious step is rodents.

 

@ normalizing, no idea but you can get 90% honokiol from a solid source (Swanson) and 98% from a less well known one (Honopure). I've gone back to Swanson after detecting some VOC odor in the latter.
 

 

 

 

i would prefer the bark though, since i used it before it had nice taste and smell when made into tea. im just curious what percent of honokiol is present in it and is it reliable enough to get significant enough dose?
 

[Harkijn]

@normalizing, this 10 year old article, way ahead of it's time

 

http://clltopics.org...to/honokiol.htm

 

also adresses your question and roughly calculates that you would need 8 grams of bark to produce 0.02 grams of honokiol and 0.02 grams of magnolol. For active cancermedication, however, the author estimates that you would need  0.7grams.  So, I think Brian's 200mg is not a bad guess for general prevention.  I have not started taking honokiol as yet, because I recently started with NR and want to monitor it's effects.

[normalizing]

thats not bad then one can just use bark to get combination of the other stuff in there as well. now i wonder if honokiol is actually water soluble tho since the way to consume the bark is basic tea infusion....

[Tom Andre F. (ex shinobi)]

Very exciting :

 

TGF-β1 is well known for its anti-inflammatory and pro-inflammatory properties. However, the presence of TGF-β1 at high levels in the rheumatoid synovium suggests that TGF-β1, alone or in combination with other cytokines, may play an important role in the progression of RA [22]. TGF-β1 increases the mRNA expression levels of several inflammatory cytokines such as IL-1β, TNF-α, IL-8, MIP-1α, and activates NFκB in RASFs [22]. Anti-TNF-α therapy induces a distinct regulatory T-cell population in patients with RA via TGF-β1 [23]. In this study, TNF-α was shown to enhance the expression of TGF-β1 and other cytokines (Table 1). In addition, it may have a synergistic effect on the activation of RASFs through the Akt–IκB-α–NFκB pathway (Figs. 2 and 4), and promote the progression of RA. Honokiol inhibited the expression of TGF-β1, suggesting that the inhibition might be active through degradation of cytosolic IκB [24].

 

They explain all in the full study here: http://abbs.oxfordjo...t/43/5/380.full

 

What I found exciting is that TNF alpha is maybe THE point to attack to control all TGF : and honokiol here help in that sense, its not only very safe, its also mean we should see real benefit for our mitochondria health !

[Steve H]

TGF-β1 is a key player in stem cell decline as shown by the Conboys et all 2015. Reducing it via inhibition of TNF-α is a promising approach and could be a complementary approach with Senolytics. I would certainly give it a try as its cheap and easily available just depends on the dose.

[Jiminy Glick]

I have some Magnolia Bark at my house. The powder taste is awful. I forget if the dosage is a teaspoon or not. However I think I might try several teaspoons, it might work as a sleep aid. I gotta get off of Benadryl which lowers acetycholine while Magnolia Bark highers it. 

Edited by Jiminy Glick, 12 June 2017 - 02:08 AM.

[OP2040]

I'm resurrecting this thread to give my experience.  I've taken a lot of supplements and rarely feel the need to post because there really isn't much to post about.  First a little background.  I've been targeting anxiety my entire life, and the effects of various supplemets I've tried are so subtle as to be pointless as a quality of life intervention.

 

So I was quite surprised when I took 200mg of this (90% Honokiol) and I'm sitting here about as relaxed as can be trying to keep my eyes open.  I didn't even buy this stuff for anxiety, rather for hypertension for which I believe I have a genetic propensity due to the ERAP1 gene.  Though I'm sure it helps with that, it's not why I'm writing. 

 

I noticed a lot of people on this forum focusing on GABA-related issues.  I've always assumed a lot of the talk was by people coming off either alcohol, bezo, etc. addictions.  I know Magnolia affects this pathway as well, but I'd be curious to find out just how it does so.  If I'm not mistaken, one of the problems with tweaking any of the neurotransmitters is that there is a natural set-point, and interventions that don't actually increase the number or health of receptors will not only not help, but probably hurt in medium-long run. 

 

Is that a fair characterization?

[Dstein]

Where do you buy the stuff?

[CarlSagan]

https://www.ncbi.nlm...les/PMC3449263/

 

Honokiol shortened time to & increased amount of NREM sleep without effecting REM sleep in mice. around 0.8mg/kg human dose for the mid range (though this was injected in the study)

 

It went from 63.8 mins NREM onset to 26.8 mins for the upper dose. also significantly shortened sleep onset. 

Honokiol at doses of 10 and 20 mg·kg−1 was found to increase NREM sleep by 2.5 and 3.8 fold and to decrease the total amount of wakefulness by 27% and 43%, respectively, as compared with the baseline values
 

 

They used microparticles for enhanced Honokio oral bioavailability in this rat study:
https://pubs.acs.org...rmaceut.8b01016

"Oral administration of HNK-MP (20 mg/kg) efficiently increased NREM sleep by 60% by enhancing the transition from wakefulness to NREM sleep in rats."

 

Magnolol in magnolia bark increased both

https://www.scienced...028390812002894

Edited by CarlSagan, 18 July 2021 - 02:07 PM.