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An effective life extension and a new cancer hypothesis.

telomerase bavituximab cancer

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#1 MrHappy

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Posted 18 September 2011 - 12:14 PM


So it seems that we are faced with a conundrum and it has got me thinking.
I've noticed substances that delay senesence (eg. NOS inhibitors - methylene blue, etc) also turns off the ability for the body to regulate the death of cancer cells via apoptosis (NOS being the usual signaller). The studies I've read for MB indicated that the more pronouced the NOS-I effect. the higher the incidence of lymphatic cancer, etc.
Likewise, the papers on that extremely exciting enzyme, telomerase, showed that repairing the DNA/telomeres in healthy cells also repaired cancerous cells and improved their efficiency.
Studies show Vitamin C helps prevent cancers, yet improves the blood flow to established tumors.

This is also noticeable with the double-edged sword of antioxidants - they clean up the free-radicals in 'healthy' people, but the anti-oxidant effect will stop natural apoptosis in tumors, yet again.


In recent times, we've learnt that 'Bavituximab' is a very impressive engineered drug that has the potential to kill HSV-1,2, EBV, HCV, HIV and even some cancers. It works by binding to a lipid called phosphatidylserine, which is flipped outside the cell wall, only when the cell is infected with an envelope virus. The body's immune system then targets the BTM 'marked' cell and kills it. Normally, the immune system cannot detect or destroy latent viruses hiding inside the cell.


A staggered combination of telomerase and bavituximab would extend life, seemingly indefinitely, as well as taking care of our most feared virii & cancers.

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To me, this says that we may have been looking at cancer all wrong and that tumors are an intended feature of our autoimmune system, not a defect.

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A research paper recently posted on here also showed that tumors also have stem cells and that you can eliminate the rest of the tumor 'colony' by killing those stems cells. This appears to show a strong indication that the tumor is a programmed function, not just random growth. http://www.longecity...cer-stem-cells/


Until the recent studies involving HPV, virii were not considered carcinogenic. We now know that cervical cancer and more recently neck, throat and lung cancers have origins in HPV.

Similarly, the (strangely discredited) Italian doctor, Simoncini, observed a link between the fungus 'candida' and tumors. He may have over-extrapolated, but his research and case studies demonstrated that candida was the source of the white, cheesey appearance of many tumors. Conventional wisdom held that candida was able to invade organs because they were diseased/cancerous. Simoncini was reportedly able to make a malignant tumor disappear after 5 days, simply by injecting it with a highly alkaline solution (bicarb soda + water), killing the fungus. Simoncini was advocating that pharmaceutical companies should be researching anti-fungal drugs for a new chapter of cancer treatment, before his medical license was revoked.

Dr Burzynski has had an impressive success rate, treating cancer patients with a peptide they were deficient in- suggesting that the immune system did not have the raw building materials to deal with the original cause.

The fact that bavituximab is able to selectively kill some cancer cells, because they have exactly the same lipid-flipping qualities of cells infected with envelope virii, suggests heavily that envelope virii may actually be responsible for a large number of cancers.

My hypothesis (and I would welcome medical researchers to either prove or falisfy this), is that tumors are created - just like a cyst - to contain a substance or pathogen that is invading cells and damaging the host DNA. It is a triggered response to shield the DNA from excessive mutation. This could occur after multiple, smaller mutations to the DNA have occured over time to a group of cells, or after a single incidence of high mutation. The cells then switch modes and become a container until the body possesses / learns the ability to deal with it. Normal, 'healthy' people have potentially thousands of 'micro tumors', which are handled by their bodies on a daily basis, without causing alarm. http://www.guardian..../cancer.science

This also may explain why some fauna do not get tumors - their autoimmune system simply doesn't include that function in its programming.

This hypothesis would also explain why some tumors are malignant and others benign:

If the contents of the tumor do not have the ability to replicate (eg. foreign substance / heavy metal), the tumor 'wraps up' the substance, but is unable to immediately kill or process the invader. The tumor doesn't grow and doesn't shrink.

If the contents of the tumor are replicating, the tumor 'wraps up' the invader, as per normal, but is unable to immediately kill or process it. The pathogen keeps replicating and escapes outside the tumor. The body then creates more tumor cells to contain the pathogen and this process repeats as necessary. If the pathogen is able to replicate faster than it can be contained in the tumor and enters the blood-stream, we call it metastasizing and the cycle repeats wherever the pathogen finds a new home.

Radiation derived tumors would be created when the damaged cells become radioactive and then damage the DNA of the cells around them, as well as causing them to become radioactive, thus triggering the tumor response. This is much more difficult to treat, without surgery, as even if the damaged / radioactive cells are contained as a tumor, the radioactivity will still spread to surrounding cells, causing further tumor growth. The immune system will be unlikely to contain and repair the damage by itself.

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So in summary, I am theorising that a tumor may simply be a method of isolating foreign invaders. If the immune system is able to successfully deal with the invader, it then induces normal apoptosis in the cancerous cells via JNK / NOS and begins repairs. The early methods of treating cancers with chemotherapy and radiotherapy probably have been semi-successful, because these extremely harmful substances are sometimes capable of killing the foreign invaders - unfortunately at the same time as the healthy cells. It's a race to see who/what dies first.

Monoclonal treatments, like BTM - if you can isolate the pathogen, or enabling / training the immune system to deal with the pathogen will be far more successful than any previous methods.


I actively welcome all comments or criticism.

#2 AgeVivo

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Posted 18 September 2011 - 09:16 PM

Hi I'll have to read all. Your claim seems to be pure theoretical thinking, based on things that actually are not proven to extend lifespan in mice afaik. Whereas in biology of lifespan, theory often proves wrong. Do you have a way to test telomerase and bavituximab in some system? /have it tested?

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#3 tintinet

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Posted 18 September 2011 - 11:32 PM

Radiation exposure, AFAIK, does not cause cells to become significantly radioactive.

Edited by tintinet, 18 September 2011 - 11:32 PM.


#4 MrHappy

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Posted 19 September 2011 - 12:26 AM

The life extension of NOS inhibitors has been tested in vivo - methylene blue showed some impressive results in mice. The optimal dose appeared to be 100nM.
http://www.fasebj.or...t/22/3/703.long

Telomerase is certainly proven in vivo - crustaceans are a prime example.
http://clincancerres.../7/10/2953.full

The cancer hypothesis is the purely theoretical part..
I'm certainly no expert on radiation, but perhaps the accumulation of radioactive isotopes in the human body from daily life would serve as a viable target for spreading radioactive decay.

#5 MrHappy

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Posted 19 September 2011 - 12:30 AM

Getting access to bavituximab is pretty difficult at the moment, given the phase 2 trial status and expense , so unlikely that any studies on interaction with telomerase have been performed yet.

I don't think the 2 would work at the same time - you'd take a telomerase activator and on a longer alternate cycle, take bavituximab to mop up the cancer cells not killed by normal processes.

#6 niner

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Posted 19 September 2011 - 01:05 AM

The life extension of NOS inhibitors has been tested in vivo - methylene blue showed some impressive results in mice. The optimal dose appeared to be 100nM.
http://www.fasebj.or...t/22/3/703.long

But what dose of MB is required for NOS inhibition? I recall seeing 15mg/kg as a level that was considered optimal, which would be about a thousand times higher than the doses used by people here for mitochondrial effects. I think that NOS inhibition isn't the reason for the observed MB effects in mice; that's a mitochondrial phenomenon.

#7 MrHappy

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Posted 19 September 2011 - 07:14 AM

One study shows 30mM completely inhibits NOS, although complete inhibition is not required to stop apoptosis.

http://www.ncbi.nlm....pubmed/7679577/

#8 niner

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Posted 19 September 2011 - 12:43 PM

One study shows 30mM completely inhibits NOS, although complete inhibition is not required to stop apoptosis.

http://www.ncbi.nlm....pubmed/7679577/

Ok, but 30 uM (mM is milliMolar) is 330 times the dose that we're shooting for.

#9 MrHappy

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Posted 19 September 2011 - 02:07 PM

No doubt... Although, it is the dose they've been trialing on alzheimer's and parkinson's patients. Works out to be 60mg. I think a few people here have tried doses in that range.. Or more, in one well known member's case.


#10 Logan

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Posted 19 September 2011 - 05:42 PM

I might be willing to try 10 to 15 mg, 15 being the dose that was used in the bipolar study. What do you guys think about this? Niner? Maxwatt?

Edited by MorganM, 19 September 2011 - 05:43 PM.


#11 MrHappy

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Posted 20 September 2011 - 12:09 AM

I'd be careful Morgan - the MAO-I effect would be rather pronounced.

The guys previously dosing at 100nM-120nM every 4-5 hours (myself included) noticed the effect. Makes sense, as the half-life is 5 hours, so you'd see spike around 150nM-180nM twice a day. I believe 160nM was the threshold for a noticable effect.

#12 niner

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Posted 20 September 2011 - 02:39 AM

I might be willing to try 10 to 15 mg, 15 being the dose that was used in the bipolar study. What do you guys think about this? Niner? Maxwatt?

I'd be careful Morgan - the MAO-I effect would be rather pronounced.

The guys previously dosing at 100nM-120nM every 4-5 hours (myself included) noticed the effect. Makes sense, as the half-life is 5 hours, so you'd see spike around 150nM-180nM twice a day. I believe 160nM was the threshold for a noticable effect.

I think MrHappy's right that you'd be into the realm of at least partial MAO-A inhibition. I don't know that you would obliterate it, but the IC50 is 164 nM, and my best guess at this point is that you can reach 100 nM with somewhere between .5 and 5 mg. MB has a half life of around 5 hours, and it's a competitive inhibitor rather than a covalent inhibitor like the MAOI's that really cause problems. The cases where serotonin syndrome was observed were substantially higher doses of MB (e.g. half a gram) combined with SSRIs. Since you would be looking for symptoms of serotonin syndrome, I think you'd see it coming from a mile away and could take whatever steps you needed to deal with it, however unlikely. It's not like it would take you by surprise. You could always try a lower dose first, and work up to it. That's probably a better approach than putting 911 on speed-dial...

MrHappy, do you mean micrograms rather than nM? Nanomolar is a blood concentration measurement, and there's no way to know what it is unless you're pulling out some blood and analyzing it. FWIW, I've been up to 2 or 3 milligrams of MB, and I've never seen anything that looked remotely like a MAOI effect. I was hoping I'd see the colors like the other guys... No luck though.

#13 MrHappy

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Posted 20 September 2011 - 03:45 AM

We worked out that given a range of approximately 5-6L of blood per person, a 1mg dose of MB was ballpark 100nM+/-10%

I'd prefer to do a blood sample for accuracy, but this will have to do for now.

At 1mg x3 daily, I definitely noticed the MAO-I effects. Additionally, the withdrawal symptoms while taking a MB holiday. No colours, either! :P

#14 niner

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Posted 20 September 2011 - 04:20 AM

We worked out that given a range of approximately 5-6L of blood per person, a 1mg dose of MB was ballpark 100nM+/-10%

I'd prefer to do a blood sample for accuracy, but this will have to do for now.

At 1mg x3 daily, I definitely noticed the MAO-I effects. Additionally, the withdrawal symptoms while taking a MB holiday. No colours, either! :P

100nm/liter * 6liter *320g/m * 1e-9m/nm = .000192g = 192 mcg.

If you injected 192 mcg into a person with 6 liter blood volume, and the drug didn't partition out of the blood at all, and it wasn't protein bound, and it didn't partition heavily into erythrocytes, and it mixed thoroughly, this would be about right. It's been observed that blood levels from oral dosing are about a factor of ten lower than iv dosing, so if we multiplied this by ten, and all the previous caveats still applied, we'd be looking at 2 mg orally. Of course, we actually want it to partition into the brain and heart and a lot of other places, so this sort of calculation rapidly becomes impossible to do accurately. Rather than being +/-10%, it's probably +/- more like a factor of ten.

At any rate, the MAOI effects seem pretty variable. Some people get a bang out of it, others feel nothing.

#15 Logan

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Posted 20 September 2011 - 05:37 AM

Anyone have any ideas on how an extended release version of MB will be made? Will it simply be the capsule or tablet coating that will make the ER version possible?

So, has anyone just taken it once a day and still felt some effects more than 5 or 6 hours later? Is there any crash? What would MB withdrawal be like?

#16 MrHappy

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Posted 20 September 2011 - 05:55 AM

Yes, the effects are still noticeable.. I found that I could feel them up to 9 hours later. The most obvious test was drinking alcohol towards the end of the cycle and seeing the conflicting effects.

#17 rwac

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Posted 20 September 2011 - 06:26 AM

Anyone have any ideas on how an extended release version of MB will be made? Will it simply be the capsule or tablet coating that will make the ER version possible?

So, has anyone just taken it once a day and still felt some effects more than 5 or 6 hours later? Is there any crash? What would MB withdrawal be like?


The problem with an extended release version is that MB isn't well absorbed in the intestine, and causes problems with gut bacteria, so the tradition ER version likely wont work very well.

I wonder if liposomes or even PEGylated liposomes would work instead to provide a gradual release. Sounds a bit farfetched.

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#18 MrHappy

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Posted 20 September 2011 - 01:35 PM

I recall the rember trials had big problems with extended release. Really though, premixing the lunchtime dose in a water bottle is easy enough. Get a 500ml bottle, mark it every 100ml and pour in 5 doses. There's your working week catered for.


Before this turns into the newest MB thread (chuckle) does anyone else find the concept of cancer as an autoimmune response as meriting further research?




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