Where To Start With Large Brain Tumor?

[managing]

I think the brain initiates autophagy a bit later that most body locations because it has access to so much blood; I would imagine that it'd be exposed to leucine from autophagy elsewhere in the body for longer.

But other things also appear to interact with the mTOR pathway besides leucine and rapamycin, so it would be expected to respond a bit differently due to the different milieu inside of each cell (i.e. cAMP). Each cell in each specific location also has different corepressors in the nucleus, prevent inappropriate DNA from being transcribed. Remember, all cells were at one time identical and have all stemmed from the mitosis of just one cell (1 ⟶ ¹⁄₂ + ¹⁄₂ ⟶ ¹⁄₄ + ¹⁄₄ + ¹⁄₄ + ¹⁄₄)—the ova, which had needed to be differentiated into other cell types and kept that way. You'd think steroid hormones, peptide hormones, oxygen gradients, pH gradients, nitric oxide, calcium, and eventually blood pressure gradients would all contribute to this process. So the simple fact that corepressors exist strongly imply that some cells will respond differently to stimulus which would normally lead to the transcription of the DNA segment onto which said corepressor is attached. Besides have experimental confirmation, there is a philosophical need for such a thing; there needs to be nuclear factors which keep a differentiated cell expressing a unique genome while containing the entire DNA library in its nucleus.

Despite the difference between cell types, I have read of nothing more effective and reliable at inducing autolysis than leucine and rapamycin.

Above you said that leucine inhibits autolysis. I think you meant that here too (you wrote that it induces autolysis)?

Can you elaborate a bit on cAMP's interaction with mTOR pathway?

 

[Travis]

Reads better now: I changed the word 'inducing' to 'influencing.'

Many proteins involved in the mTOR pathways are phosphorylated, and this event is often considered the primary signal. For this to happen a phosphorylated adenosine such as ATP, ADP, AMP, or cAMP is required. I think perhaps proteins are phosphorylated to change their isoelectric point within the cytosol, allowing them to follow the intracellular pH gradient. Little explanation is given to how transcription factors actually get into the nucleus, but using a 'chaperone' protein just leads to an infinite regress because you'd then have to explain what exactly transports that. The only way I can realistically see a transcription factor moving from the cytosol into the nucleus is through diffusion or ionic attraction—being perhaps repelled by the membrane potential. Protein phosphorylations increase the negative charge of a protein.

But mTOR and its satellite proteins are attached to microtubules, a structure which provides a direct link to the nucleus; there is some indication that information can actually transfer down the lumen of the microtubule. All microtubule‐associated proteins are phosphorylated (protein–PO₃⁻), and are often connected to other proteins through phosphodiester bridges (protein–PO₂–protein). So the appearance of certain phosphates (PO₄)²⁻ on certain proteins in certain cellular fractions at certain times could represent the cleavage of that protein from the microtubule wall, either through the phosphodiester bond #1 (yielding the phosphorylated form) or through the tyrosine–phoshate bond #2 (yielding the nonphosphorylated form). So these protein phosphate‐signalling events are hard to decipher, and it's even difficult to imagine how one protein could selectively‐phosphorylate another protein. Moreover: proteins can either be phosphorylated or dephosphorylated nonenzymatically, making protein phosphorylation a relatively low‐fidelity signal.

 

[Obi-wan]

Various natural compounds, including epigallocatechin gallate (EGCG), caffeine, curcumin, and resveratrol, have also been reported to inhibit mTOR when applied to isolated cells in culture;[28][120] however, there is as yet no evidence that these substances inhibit mTOR when taken as dietary supplements. -Wikipedia

EGCG, the most abundant catechin in tea, is a polyphenol under basic research for its potential to affect human health and disease. EGCG is used in many dietary supplements.

It is found in high content in the dried leaves of green tea (7380 mg per 100 g), white tea (4245 mg per 100 g), and in smaller quantities, black tea.[

Plus for caffeine (coffee)! and Tea!

 

[Travis]

Various natural compounds, including epigallocatechin gallate (EGCG), caffeine, curcumin, and resveratrol, have also been reported to inhibit mTOR when applied to isolated cells in culture;[28][120] however, there is as yet no evidence that these substances inhibit mTOR when taken as dietary supplements. -Wikipedia

EGCG, the most abundant catechin in tea, is a polyphenol under basic research for its potential to affect human health and disease. EGCG is used in many dietary supplements.

It is found in high content in the dried leaves of green tea (7380 mg per 100 g), white tea (4245 mg per 100 g), and in smaller quantities, black tea.[

Plus for caffeine (coffee)! and Tea!

The thing about resveratrol, curcumin, and epicatechol gallate inhibiting mTOR is that they've been tested on dozens of enzymes—most molecules would never even get the chance to be a proven in vitro. A drug cannot be said to inhibit an enzyme until its tested on it, and there are thousands of molecules that could perhaps do it better yet we'd never know. This is an interesting thing to ponder: How many phenomena are explained simply because a phytochemical has become exceeding popular? under intense scrutiny: millions of combined of hours of pipette‐filling, centrifugation, chromatography, and spectrometry all devoted to finding out what it can do. The drugs resveratrol, curcumin, and epicatechol gallate are the ones which inhibit the most enzymes—not because they are exceeding unique, but only because these are the most scrutinized phytochemicals in history.

 

[Koveras]

resveratrol

Resveratrol stimulates cortisol synthesis

Niacinamide Lowers Fatty Acid Oxidation By Inhibiting SIRT1

Niacinamide Is Anti-estrogenic

 

[Obi-wan]

Was trying to point out caffeine as a natural mTOR inhibitor. Resveratrol never got good reviews on this forum. Niacinamide has been a shining star but I don't think @Travis ever really commented on it, Same with aspirin, another "wonder drug"

 

[lollipop]

Was trying to point out caffeine as a natural mTOR inhibitor. Resveratrol never got good reviews on this forum. Niacinamide has been a shining star but I don't think @Travis ever really commented on it, Same with aspirin, another "wonder drug"

Thank you @Obi-wan! I think these are great suggestions in addition to the low or no PUFA’s.

 

[BrianF]

[?]

That

He's talking about your "most people who eat meat are chubby". 97% of the population in the US eat meat. It's like saying most people who drink water are chubby. Or most people who use a phone are chubby.

Thanks Aquaman, couldn't have put it better myself.

Travis, if you are looking for a single, isolated causality of the high instance of 'lardassity' amongst yanks, then car usage, in my opinion, would be as likely as meat, to be that culprit. Or even water or phones....

 

[Travis]

That

Thanks Aquaman, couldn't have put it better myself.

Travis, if you are looking for a single, isolated causality of the high instance of 'lardassity' amongst yanks, then car usage, in my opinion, would be as likely as meat, to be that culprit. Or even water or phones....

Do you seriously think that number of titles for automobiles, miles driven, or time driven therein would correlate better with body weight than red meat consumption?—an actual food?

 

[BrianF]

Yes. If people walked more, they wouldn't be such fat bastards.

 

[Glassy]

I think the brain initiates autophagy a bit later that most body locations because it has access to so much blood; I would imagine that it'd be exposed to leucine from autophagy elsewhere in the body for longer.

But other things also appear to interact with the mTOR pathway besides leucine and rapamycin, so it would be expected to respond a bit differently due to the different milieu inside of each cell (i.e. cAMP). Each cell in each specific location also has different corepressors in the nucleus, prevent inappropriate DNA from being transcribed. Remember, all cells were at one time identical and have all stemmed from the mitosis of just one cell (1 ⟶ ¹⁄₂ + ¹⁄₂ ⟶ ¹⁄₄ + ¹⁄₄ + ¹⁄₄ + ¹⁄₄)—the ova, which had needed to be differentiated into other cell types and kept that way. You'd think steroid hormones, peptide hormones, oxygen gradients, pH gradients, nitric oxide, calcium, and eventually blood pressure gradients would all contribute to this process. So the simple fact that corepressors exist strongly imply that some cells will respond differently to stimulus which would normally lead to the transcription of the DNA segment onto which said corepressor is attached. Besides have experimental confirmation, there is a philosophical need for such a thing; there needs to be nuclear factors which keep a differentiated cell expressing a unique genome while containing the entire DNA library in its nucleus.

Despite the difference between cell types, I have read of nothing more effective and reliable at influencing autolysis than leucine and rapamycin.

Doesn’t insulin inhibit autophagy somewhat? I’ve not heard of juice fasting promoting autophagy but it’s logical if leucine is in fact the main inhibitor of it. I thought Dr Valter Longo’s Fasting mimicking diet used prior to chemo was a kind of protein sparing modified fast (ie high protein low cals), but it seems it’s low protein, low cal (high PUFA incidentally).

How did your 60hr fast go? Did you take coffee/caffeine or was it strictly water? Did you feel the adrenaline or get any low blood pressure symptoms? I’d love to hear about your experiences of it but I think it may not be the place for such a discussion.

 

[Travis]

Doesn’t insulin inhibit autophagy somewhat?

Yes: Both insulin and insulin-like growth factor tend towards keeping mTOR in its phosphorlyated and autophagy-inhibited state. However! receptors for insulin and IGF-1 are differentially expressed, and leucine is small enough (11,981 Da vs 131Da) to go nearly anywhere. Moreover, insulin-like growth factor №1 itself is released by the liver largely—if not exclusively—in response to leucine.

But it wouldn't matter much about insulin anyhow since the mTOR complex can sense mitochondrial energy production directly through the ATP/AMP ratio. As mitochondrial respiration decreases—either through either lack of glucose, fatty acids, coenzyme Q₁₀, or damaged mitochondria—the ATP/AMP drops causing reduced mTOR phosphorylation. This is intuitive, as adenosine triphosphate (ATP) has to more phosphates to donate than has adenosine monophosphate (AMP). The mTOR complexes are located near mitochondria and phagosomes are large enough to engulf mitochondria. It has also been speculated that mTOR is inhibited by 'oxidative stress,' or Fenton style free radicals produces by active mitohondria. With these things in mind, it's easy to see the mTOR complex as having been evolved the tendency to induce the recycling (autophagy) of an inefficient mitochondria the moment that it becomes so (through sensing its ATP output, the very best indicator of mitochondrial efficiency).

How did your 60hr fast go? Did you take coffee/caffeine or was it strictly water? Did you feel the adrenaline or get any low blood pressure symptoms? I’d love to hear about your experiences of it but I think it may not be the place for such a discussion.

I have come to the conclusion that its much easier to fast if one has avoided cooked starch for some time prior. Native starch is a double-helix, and unhybridized gelatinized starch can become incorporated directly in the extracellular matrix of the tongue. Besides collagen and elastin, the extracellular matrix is largely polysacchides. Thinking along these lines is reminiscent of Arnold Ehret, who was an early anti-starch proponent and author of books on water fasting written over a century ago. He make the link between cooked starch and 'mucus'—which really is actually a polysaccharide gel (his writings do have chemical plausibility). So I'll be going 100% starch-free (cooked) for another week or two before I fast again. I find the starch detox (elimination) intolerable, and much easier to fast after its been strictly avoided for weeks beforehand.

 

[Obi-wan]

per @Travis -"So perhaps progesterone, being a leucine product, could perhaps inhibit the mTOR pathway by simple negative inhibition? Usually: when a molecular product in increased, the synthesis
of that product slows down. These biochemical negative-feedback mechanisms can range from the simple to the complex: from the product itself (pregnenolone) actually inhibiting the enzyme which produces it through competition with its precursor substrate (cholesterol), to the the genomic effects of vitamin D—preventing its own buildup by powerfully upregulating the very enzyme which destroys it. I'm certainly convinced that tumors can be dissolved in the body—William Koch too had described this—but it would take a bit of patience, discipline, and hard work. Two fatty acids and two amino acids specifically inhibit this process, so aiming to reduce those—linoleic acid, γ-linolenic acid, methionine, and leucine—would certainly seem like a good idea. A considerable amount of Max Gerson's, William Koch's and Herbert Shelton's patients had all done this in the past despite how incredulous the American Medical Association has made it seem (through their propaganda)."

Also "Pregnenolone has the highest affinity for microtubules—the true 'molecular nerves' within the nerves—out of all the steroids, by far, giving the impression that it naturally stabilizes them and initiates myelination. Layer by layer progesterone and pregnenolone stack in shells until the microtubule nerve pathway is stabilized, solidified, and fixed as a long-term memory trace permanent enough to be disrupted only by aluminum."

 

[lollipop]

Update:

My friend had surgery on Tue. The tumor was in the “perfect place” - if there is one in fact - for surgical removal. It did not look malignant but sent off for biopsy. Thank you to everyone who contributed and added in to help.

Hopefully someone in need finds this thread in the future.

 

[jb116]

Yes: Both insulin and insulin-like growth factor tend towards keeping mTOR in its phosphorlyated and autophagy-inhibited state. However! receptors for insulin and IGF-1 are differentially expressed, and leucine is small enough (11,981 Da vs 131Da) to go nearly anywhere. Moreover, insulin-like growth factor №1 itself is released by the liver largely—if not exclusively—in response to leucine.

But it wouldn't matter much about insulin anyhow since the mTOR complex can sense mitochondrial energy production directly through the ATP/AMP ratio. As mitochondrial respiration decreases—either through either lack of glucose, fatty acids, coenzyme Q₁₀, or damaged mitochondria—the ATP/AMP drops causing reduced mTOR phosphorylation. This is intuitive, as adenosine triphosphate (ATP) has to more phosphates to donate than has adenosine monophosphate (AMP). The mTOR complexes are located near mitochondria and phagosomes are large enough to engulf mitochondria. It has also been speculated that mTOR is inhibited by 'oxidative stress,' or Fenton style free radicals produces by active mitohondria. With these things in mind, it's easy to see the mTOR complex as having been evolved the tendency to induce the recycling (autophagy) of an inefficient mitochondria the moment that it becomes so (through sensing its ATP output, the very best indicator of mitochondrial efficiency).

I have come to the conclusion that its much easier to fast if one has avoided cooked starch for some time prior. Native starch is a double-helix, and unhybridized gelatinized starch can become incorporated directly in the extracellular matrix of the tongue. Besides collagen and elastin, the extracellular matrix is largely polysacchides. Thinking along these lines is reminiscent of Arnold Ehret, who was an early anti-starch proponent and author of books on water fasting written over a century ago. He make the link between cooked starch and 'mucus'—which really is actually a polysaccharide gel (his writings do have chemical plausibility). So I'll be going 100% starch-free (cooked) for another week or two before I fast again. I find the starch detox (elimination) intolerable, and much easier to fast after its been strictly avoided for weeks beforehand.

Just curious, do you avoid starch altogether all the time or just to initiate this fasting procedure?

 

[achillea]

Lisa Ferraro :My friend had surgery on Tue. The tumor was in the “perfect place” - if there is one in fact - for surgical removal.

This is not meant snidely but the two favorite phrases of surgeon; I just happen to have an opening next week and/or the tumor is in the perfect place.

Does your friend use wifi and a cell phone? Just would like to know because the 50+ year old lady down the street had a brain tumor removed a year ago and she is an avid cell phone addict.

 

[lollipop]

Lisa Ferraro :My friend had surgery on Tue. The tumor was in the “perfect place” - if there is one in fact - for surgical removal.

This is not meant snidely but the two favorite phrases of surgeon; I just happen to have an opening next week and/or the tumor is in the perfect place.

Does your friend use wifi and a cell phone? Just would like to know because the 50+ year old lady down the street had a brain tumor removed a year ago and she is an avid cell phone addict.

Interesting. Not sure. Will find out.

 

[Syncopated]

Hulda Clark Purifier called the "zapper".
www.zaptheparasites.com

- Get the '"B5" with copper pipes.
Purify your brains immunity with this to dismantle the tumour.
- take a Gram of aspirin every day till all the tumour is dissolved.
- avoid lily family foods, especially garlic and onion.
Eating lots of pineapple, watermelon, tomatoes, coconut oil and cultured milk with intermittent water fasting will dissolve calcium in arteries, arterioles and capillaries if 180 mcg of MK7 K2 is taken daily.

 

[Syncopated]

Hulda Clark Purifier called the "zapper".
www.zaptheparasites.com

- Get the '"B5" with copper pipes.
Purify your brains immunity with this to dismantle the tumour.
- take a Gram of aspirin every day till all the tumour is dissolved.
- avoid lily family foods, especially garlic and onion.
Eating lots of pineapple, watermelon, tomatoes, coconut oil and cultured milk with intermittent water fasting will dissolve calcium in arteries, arterioles and capillaries if 180 mcg of MK7 K2 is taken daily.

Avoid any forms of vinegar, including apple cider vinegar.

 

[Travis]

Just curious, do you avoid starch altogether all the time or just to initiate this fasting procedure?

I think I'll be avoiding it altogether from now on, and have done so in the past. Perhaps the prevailing idea is that our amylases completely transform dietary starch into glucose, which is then absorbed. However, a certain fraction of any starch-containing food is nearly always found to be enzyme-resistant. Since the food industries cannot deny this, they try to turn it into a plus by calling it 'soluble fiber'—but I don't think it's a 'good thing.' Some of this enzyme-resistant starch is bound to be absorbed, as starch is known to do, and could become trapped in the extracellular matrix. You can prove that it's absorbed yourself by checking for 'eye goo,' this being a direct function of dietary starch and will not occur otherwise. Mucus is chemically a polysaccharide gel, and apparently an channel in which exogenous enzyme-resistant starch can be eliminated. I also think there's reason to assume that enzyme-resistant starch could form a substrate for bacteria, this being one dietary item that can metabolized by bacteria yet not by ourselves. But this is not to say that a food cannot be prepared in such a way as to eliminate resistant starch (perhaps potatoes can), but I know that oats are completely out of the question—both on account of experience and from the information contained within the article below:

Muir, Jane. "Measurement of resistant starch: factors affecting the amount of starch escaping digestion in vitro." The American journal of clinical nutrition (1992)​