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C60 experiments @ home

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#3541 sensei

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Posted 18 February 2018 - 06:13 PM

 

about a year ago I read that a mouse trial had shown C60 -oo had stopped metastasis from developing and slowed down the cancer growth to 1/3 what would be expected,
and 70 percent of cancer deaths are caused by metastasis,

 

Yep, metastasis appears to be a kind of controlled apoptosis, when some cancer cells disintegrate in order to spread the remaining cells around. Apoptosis is controlled by mitochondria basically exploding inside cells, and mitochondrial anti-oxidants can block this.

 

 

 

You couldn't be further from the truth.

 

Impaired apoptosis enhances metastasis.

 

"Apoptosis may block metastatic dissemination by killing misplaced cells. Thus, apoptosis serves as an important process for inhibiting metastasis. The success of the metastatic process relies on the ability of malignant cells to escape apoptosis. "

 

 

 

https://www.ncbi.nlm...les/PMC4343053/



#3542 QuestforLife

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Posted 18 February 2018 - 09:15 PM

There's a little more to it than that, Sensei. Apoptosis is used by cells to stop cancer, but once cancer has control of the cell it controls the mitochondria too, and can adjust ROS production to suit its own purposes. Normally cancer just turns mitochondria off, because they grow without the need for oxygen (cancer is like a primitive lifeform or a very early stage embryo). But there is evidence cancer also use mitochondria to metastasize. The following paper has more:

http://www.cell.com/...1247(14)00527-0
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#3543 hav

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Posted 19 February 2018 - 04:15 PM

 

 Best to discuss it with your doctor.

 

 

 

 

Why on earth would you think that best? Do you really imagine his doctor has even heard of it?

 

 

Because a person's cancer doctor would know more about a particular cancer treatment than someone who hasn't made it their life's work.  Comparatively speaking, a doctor finding out about a particular supplement like c60 is easy... almost anyone can do it.  Not a good idea for someone diagnosed with cancer to keep their oncologist in the dark unless they have a death wish. An even worse idea to advise anyone to do that.

 

Howard


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#3544 Turnbuckle

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Posted 19 February 2018 - 04:29 PM

 

 

 Best to discuss it with your doctor.

 

 

 

 

Why on earth would you think that best? Do you really imagine his doctor has even heard of it?

 

 

Because a person's cancer doctor would know more about a particular cancer treatment than someone who hasn't made it their life's work.  Comparatively speaking, a doctor finding out about a particular supplement like c60 is easy... almost anyone can do it.  Not a good idea for someone diagnosed with cancer to keep their oncologist in the dark unless they have a death wish. An even worse idea to advise anyone to do that.

 

Howard

 

 

The cancer doctors I've talked to were only interested in 5 year survival rates. If a particular treatment destroyed your memory they wouldn't care. If you got cancer again at 6 years they would tell you it's a new cancer. So none of them will tell you C60 is a good idea. You don't even need to ask.


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#3545 hav

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Posted 19 February 2018 - 05:10 PM

The cancer doctors I've talked to were only interested in 5 year survival rates. If a particular treatment destroyed your memory they wouldn't care. If you got cancer again at 6 years they would tell you it's a new cancer. So none of them will tell you C60 is a good idea. You don't even need to ask.

 

 

I personally would stop taking c60 myself if undergoing chemo.  Based on Baati observations of the partially protective effect c60 had on rats treated with CCL4.  Baati speculated that such a protective effect might be due to c60 being a powerful anti-oxidant.  Here's the quote:

 

 

Finally, as C60 is known to be a powerfull antioxidant [5,6,21], we checked the effects of C60-olive oil solutions on oxidative stress in a classical model of CCl4 intoxication in rats [28,29]. Although the oxidative stress involved in CCl4 intoxication is unlikely to occur during physiopathological conditions, CCl4 intoxication in rats provides an important model for elucidation of the mechanism of action of hepatotoxic effects such as fatty degeneration (steatosis), fibrosis, hepatocellular death, and carcinogenicity involving oxidative stress [28,29].

My take away from the above is that c60 might be highly protective against carcinogenicity thus preventing cancer but might also be protective in blunting a chemo or other treatment that relies on targeting cancer cells with oxidative stress to destroy them.  Depending on the specific treatment and mechanism of action which I'd expect the prescribing cancer doctor would or should know.
 

Howard



#3546 Turnbuckle

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Posted 19 February 2018 - 06:10 PM

The info on direct action of C60/EVOO on cancer is scant to none, but it certainly could help the side effects such as hepatotoxicity. In that paper C60/EVOO was used, and the researchers found that "fullerene C60 is significantly normalized both blood and liver parameters altered by cyclophosphamide-induced toxicities." It can also have direct effects and as as an adjunct such as with Doxorubicin, where colloidal C60 was used instead of C60/EVOO. However as the studies are with rodents, I doubt that any oncologist is going to approve of it.



#3547 sensei

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Posted 23 February 2018 - 08:32 AM

There's a little more to it than that, Sensei. Apoptosis is used by cells to stop cancer, but once cancer has control of the cell it controls the mitochondria too, and can adjust ROS production to suit its own purposes. Normally cancer just turns mitochondria off, because they grow without the need for oxygen (cancer is like a primitive lifeform or a very early stage embryo). But there is evidence cancer also use mitochondria to metastasize. The following paper has more:

http://www.cell.com/...1247(14)00527-0

 

 

 

Read trhe paper you cited -- it has NOTHING to do with apoptosis, in fact apoptosis is only mentioned once, in that many anti-cancer therapies rely on ROS induced apoptosis.

 

Apoptosis DOES NOT promote metastasis, cellular RESISTANCE TO APOPTOSIS does.



#3548 QuestforLife

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Posted 23 February 2018 - 09:55 AM

Well apoptosis and metastasis both use mitochondria, and mito targeted antioxidants can block both. So I'm not disagreeing with you there. I think overall though that blocking metastasis is likely a fair trade for reduced apoptosis.
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#3549 sensei

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Posted 23 February 2018 - 07:27 PM

Well apoptosis and metastasis both use mitochondria, and mito targeted antioxidants can block both. So I'm not disagreeing with you there. I think overall though that blocking metastasis is likely a fair trade for reduced apoptosis.


Increasing apoptosis decreases metastasis.

Decreasing apoptosis -- increases metastasis.

Edited by sensei, 23 February 2018 - 07:28 PM.

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#3550 Nate-2004

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Posted 23 February 2018 - 11:09 PM

Here's a video I made recently with Tree Czar Comedy, somewhat relevant.

 

 


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#3551 apmark

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Posted 23 February 2018 - 11:27 PM

That is hilarious Nate, more so because I used to love listening to Deborah Harry.once I had a love. Which somehow came up after the olive oil vid on my screen.
That being said I don't like our 2 c60 expert's having any infighting either.

Edited by apmark, 23 February 2018 - 11:30 PM.

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#3552 hav

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Posted 24 February 2018 - 01:05 AM

 


Increasing apoptosis decreases metastasis.

Decreasing apoptosis -- increases metastasis.

 

 

That's probably only meaningful as to existing cancer cells.  Metastasis by definition is the spreading of existing cancer to healthy cells.  Treatment strategies usually involve trying to kill all the cancer before it spreads.  But not healthy cells.  Indeed, destruction of healthy cells reduces treatment survival chances.

 

Howard
 


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#3553 Captain Obvious

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Posted 24 February 2018 - 10:36 AM

 

That's probably only meaningful as to existing cancer cells.  Metastasis by definition is the spreading of existing cancer to healthy cells.

 

 

Isn't metastasis is (by definition) the spreading of cancer cells AMONG healthy cells elsewhere in the body?

 

"Metastases (the plural form of metastasis) most commonly develop when cancer cells break away from the main tumor and enter the bloodstream or lymphatic system. These systems carry fluids around the body. This means that the cancer cells can travel far from the original tumor and form new tumors when they settle and grow in a different part of the body. Metastases can also sometimes develop when cancer cells from the main tumor, typically in the abdominal (belly) cavity, break off and directly “seed” other areas within the abdominal cavity."


Edited by Captain Obvious, 24 February 2018 - 10:38 AM.

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#3554 sensei

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Posted 25 February 2018 - 10:03 PM


Increasing apoptosis decreases metastasis.

Decreasing apoptosis -- increases metastasis.


That's probably only meaningful as to existing cancer cells. Metastasis by definition is the spreading of existing cancer to healthy cells. Treatment strategies usually involve trying to kill all the cancer before it spreads. But not healthy cells. Indeed, destruction of healthy cells reduces treatment survival chances.

Howard

As CA posted, metastasis ONLY RELEVANT TO CANCER.

Therefore, anything that reduces apoptosis, increases the number of viable CANCER cells available to metastasize.

Apoptosis is the programmed call death of ABNORMAL and SENESCENT cells, cancerous or otherwise.

Increased Apoptosis is VIRTUALLY ALWAYS better for survival,of the organism as it allows resources to be used by viable cells.

#3555 hav

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Posted 27 February 2018 - 02:21 AM

 

 

Increasing apoptosis decreases metastasis.

Decreasing apoptosis -- increases metastasis.


That's probably only meaningful as to existing cancer cells. Metastasis by definition is the spreading of existing cancer to healthy cells. Treatment strategies usually involve trying to kill all the cancer before it spreads. But not healthy cells. Indeed, destruction of healthy cells reduces treatment survival chances.

Howard

As CA posted, metastasis ONLY RELEVANT TO CANCER.

Therefore, anything that reduces apoptosis, increases the number of viable CANCER cells available to metastasize.

Apoptosis is the programmed call death of ABNORMAL and SENESCENT cells, cancerous or otherwise.

Increased Apoptosis is VIRTUALLY ALWAYS better for survival,of the organism as it allows resources to be used by viable cells.

 

 

Yes, but apoptosis is a more general concept that also applies to healthy cells.  In fact, increasing apoptosis of healthy cells might not decrease metastasis... unless a quick death results.  Indeed, if treatment excessively targets previously healthy cells short of causing death, while failing to target cancer cells sufficiently, it might increase metastasis. 

 

Howard
 


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#3556 sensei

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Posted 27 February 2018 - 02:49 AM

Apoptosis does not normally happen to healthy cells, even under high ROS load because of catalase and hydroxyperoxidase production

#3557 QuestforLife

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Posted 28 February 2018 - 04:53 PM

I beleive this is relevant to the discussion.

Abstract
Excessive production of mitochondrial reactive oxygen species (mROS) is strongly associated with mitochondrial and cellular oxidative damage, aging, and degenerative diseases. However, mROS also induces pathways of protection of mitochondria that slow aging, inhibit cell death, and increase lifespan. Recent studies show that the activation of the mitochondrial permeability transition pore (mPTP), which is triggered by mROS and mitochondrial calcium overloading, is enhanced in aged animals and humans and in aging-related degenerative diseases. mPTP opening initiates further production and release of mROS that damage both mitochondrial and nuclear DNA, proteins, and phospholipids, and also releases matrix NAD that is hydrolyzed in the intermembrane space, thus contributing to the depletion of cellular NAD that accelerates aging. Oxidative damage to calcium transporters leads to calcium overload and more frequent opening of mPTP. Because aging enhances the opening of the mPTP and mPTP opening accelerates aging, we suggest that mPTP opening drives the progression of aging. Activation of the mPTP is regulated, directly and indirectly, not only by the mitochondrial protection pathways that are induced by mROS, but also by pro-apoptotic signals that are induced by DNA damage. We suggest that the integration of these contrasting signals by the mPTP largely determines the rate of cell aging and the initiation of cell death, and thus animal lifespan. The suggestion that the control of mPTP activation is critical for the progression of aging can explain the conflicting and confusing evidence regarding the beneficial and deleterious effects of mROS on health and lifespan.

From
https://www.ncbi.nlm...les/PMC5595682/

#3558 Rupe

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Posted 28 February 2018 - 06:37 PM

Okay, so hypothetically, if C60 specifically targeted cancerous cells (which it doesn't) while simultaneously up-regulating mitochondrial function and decreasing inflammation, you could potentially suppress metastatic behavior, correct?? Is that what I'm getting or am I way off base with my interpretation of what's being said.



#3559 Zadhu

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Posted 03 March 2018 - 02:40 PM

Hello all, info is great! I was wondering if anyone had tried making C60 oil with hemp seed oil. What are your thoughts?

#3560 hav

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Posted 03 March 2018 - 07:26 PM

Apoptosis does not normally happen to healthy cells, even under high ROS load because of catalase and hydroxyperoxidase production

 

Should happen to every healthy cell... eventually. 

 

https://www.ncbi.nlm...books/NBK26873/

 

The cells of a multicellular organism are members of a highly organized community. The number of cells in this community is tightly regulated—not simply by controlling the rate of cell division, but also by controlling the rate of cell death. If cells are no longer needed, they commit suicide by activating an intracellular death program. This process is therefore called programmed cell death, although it is more commonly called apoptosis (from a Greek word meaning “falling off,” as leaves from a tree).

 

Which lies at the foundation of telomere aging and cancer theories.  See: https://academic.oup.../11/803/2581409

 

It's my personal belief that for cancer prevention, C60 might be extremely synergistic with telomerase activation if keeping telomeres long and healthy delays apoptosis while C60's super antioxidant properties minimize oxidative stress at the cellular level.

 

Howard


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#3561 QuestforLife

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Posted 06 March 2018 - 09:31 AM

From the paper I posted above, we can see that the MPTP opens more and more often as we age, and indeed there is more evidence of mtDNA leakage since then via other mechanisms, see this paper hot off the press:  'BAK/BAX macropores facilitate mitochondrial herniation and mtDNA efflux during apoptosis' (full paper available through Sci-hub).

 

This is very dangerous as free mtDNA in the blood is attacked by the immune system as it recognizes it as bacterial DNA (which it is). This causes a large rise in inflammation, with all the consequent problems that entails (including faster telomere attrition). So absolutely a powerful mitochondrial antioxidant such as C60 in olive oil could block this process. I also suspect C60 is affecting macrophages more directly through accumulation in the spleen (see many posts along these lines by High Desert Wizard).


Edited by QuestforLife, 06 March 2018 - 09:33 AM.

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#3562 ambivalent

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Posted 18 August 2018 - 07:47 PM

Obviously somewhat remiss in risk and conflating c60 with c60oo but this is a big article in a health magazine.

https://www.wddty.co...revolution.html
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#3563 aaCharley

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Posted 01 October 2018 - 03:55 PM

I've never had a problem simply shaking it up.

 

crushing/grinding the C60 into a superfine powder prior to adding the olive oil has always helped prevent sediment deposit

 

sensei,

How do you crush and grind the C60?
 







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