haidut

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This seems like a very interesting study, but is in French and not available from PubMed. So, I am hoping @burtlancast would be able to obtain it and maybe translate the relevant fractions. The study shows that dietary stearic acid is both incorporated into cell lipids and metabolized further into longer chain fatty acids, which have been shown to have a number of beneficial effects including antiviral, anticancer, antibacterial, antiestrogenic, etc. In fact, one of those metabolites called behenic acid (C22) is licensed as an anti-herpes drug in several countries. It is capable of killing both HSV1 and HSV2 when applied as a 10% cream. The studies with it also showed potent in vivo internal antiherpetic effects from oral HED of 5g - 6g daily.
Finally, the study touches upon the suggestion of @Travis to use stearic acid topically. He thought that this way it would not be metabolized as much into the MUFA oleic acid as through oral administration. This study says it is in fact heavily metabolized but in other saturated acids with longer chain, which is a desirable effect due to their beneficial properties.
Finally, the fact that unmetabolized stearic acid was heavily incorporated into myelin suggests that topical administration of this fat could be beneficial for a number of demyelinating conditions including MS, PML, or even ALS.

https://www.ncbi.nlm.nih.gov/pubmed/821655
"...Subcutaneously injected stearic acid is uptaken by brain and is further incorporated into membrane lipids (especially myelin). The uptake increases regularly up to 20 hrs. in total membranes as in myelin. In total membranes, there is a decrease between 20 and 24 hrs. followed by a recovery of the previous maximal activity. Moreover, the myelin activity increases up to 3 days, so far. Cerebrosides, isolated from both types of preparations, present an activity regularly increasing; but free fatty acids have a stable specific activity and a decreasing relative activity. The injected labelled stearic acid is directly incorporated into membrane lipids or is metabolized inside brain in longer chains (thus providing arachidic behenic and lignoceric acids) or in acetate units (utilized for synthesis of medium chain fatty acids such as palmitic acid)."
 

griesburner

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What would be a practical way to get the most benefit out of it? Once a day lotion the complete body with cocoa butter or shea butter? Would that really have an impact or is this just theoretically important?
 

burtlancast

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Here it is. It's a short article and the summary explains all there is to know.
It's emphasized that during the whole experiment, the blood at any moment contains no other radioactive fatty acid than the one injected, and thus the de-novo synthesis takes place indeed inside the brain.
 

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jandrade1997

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How do we know transdermal stearic acid will indeed be absorbed into the blood without either just being absorbed into the epidermis or being metabolized in the epidermis/dermis for energy or into oleic acid? This study was done with an injection, bypassing these possibilities.
 

Wagner83

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Does this mean topical stearic acid interferes a lot with glucose use if applied throughout the day and more particularly around high-carb meals?
 

Vinero

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I've got a bag of Pure Stearic acid powder, but haven't used it yet. I think Obi-Wan tried to put it on his skin but it didn't absorb and became very sticky.
 

jandrade1997

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Anyone have any ideas on how should we be applying/dissolving stearic acid in hopes of getting comparable absorption to the injection from the study?
 

Travis

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Here it is. It's a short article and the summary explains all there is to know.
It's emphasized that during the whole experiment, the blood at any moment contains no other radioactive fatty acid than the one injected, and thus the de-novo synthesis takes place indeed inside the brain.
I did a copy–paste translation paragraphwise on Google Translate: I also got rid of the interrupting citation numbers, expanded a few acronyms, and only had to re-arranged a few clauses to make the French grammar more English-sounding (the original meaning remains fully intact, I promise):

Abstract: Radioactive stearic acid injected subcutaneously passes into the brain where it is integrated at the level of the membranes (especially myelin). The capture is increasing until 20 hours in the total membranes as in myelin. For the first ones only, there is a decrease between 20 and 24 hours, followed by recovery of the maximum starting activity. On the other hand, myelin for up to 3 days at least shows a regularly increasing activity. Cerebrosides from two types of preparation have an activity that is increasing. On the other hand, the free fatty acids are stable in specific activity (radioactive counts per milligram per lipid extract) but not in relative activity. The injected stearic acid is incorporated directly, as such, into the membranes where it is metabolized in situ before binding to lipids and lengthening to become the longer chained arachidic, behenic and lignoceric acids—or either the shorter chains like palmitic acid from elements of catabolism.

Body: Fatty acids with very long chains occupy a very important place in the building myelin, where they actively participate in its stability. They are synthesized by the brain at the level of microsomes from stearic acid, or mitochondria. Myelinic fatty acids are elaborated in microsomes alone. The brain mouse can synthesize only about 50% of its fatty acids; the rest must therefore have an exogenous origin. Palmitic acid, either injected or given in food, can be picked up by the brain. We therefore propose to determine whether exogenous stearic acid is used by the brain to form its fatty acids membrane (especially myelin). Among the lipids, we we are interested in cerebrosides (they contain very long-lived fatty acids chains).

Materials and Methods: One milli-Curie [a standard unit of radioactive activity] of radioactive ¹⁴C-stearic acid (51 mCi/mM) is neutralized by an equimolecular quantity of soda and solubilized in a solution of albumin. Fifty μl are injected subcutaneously into animals from 15 to 18 days. The animals are sacrificed, the brains taken and washed. The fabric is cut with a razor, washed in an isotonic solution (0.9% NaCl). The fragments are recovered by centrifugation (at 10 minutes at 17,500·g), homogenized with Potter's apparatus and then centrifuged for 60 minutes at 100,000·g. The pellet, which contains all the brain membranes, is washed and centrifuged yet again under the same conditions. This technique eliminates residual elements of blood and any contamination by serum is excluded. Myelin is isolated in a classical way. Lipids are extracted by the chloroform-methanol 2∶1, washed according to Folch, then analyzed by thin layer chromatography. The radioactivity is determined by the scintillation counter (lipids having been localized by iodine). The methyl esters of fatty acids are obtained by methylation of the lipid extract and analyzed by gas chromatography with automatic counting of the eluate. [They nearly always methylate the carboxyl group of fatty acids before gas chromatography, which his makes the lipid less polar. The methyl group shields one of the carboxy-oxygens thereby neutralizing its previous −1 charge. The now-methylated lipid will evaporate at a lower temperature than the respecive native form on account of it having less intermolecular Coulomb forces.]

Results: Figure 1 shows the evolution of the radioactivity found in the lipid extracts. In myelin, this activity rapidly increases the first two hours, the evolution is slower thereafter (at 3 days, the activity continues to grow again). In the membranes, it is remarkable to note that the total radioactivity decreases between 20 and 24 hours, to increase thereafter and reach a stable level equal to that found at 8 pm. Cerebrosides contain a regularly increasing radioactivity in both types of preparation. Table 1 shows the evolution of radioactivity activation in cerebrosides where it is regular and in free fatty acids where it decreases rapidly; this is reported in absolute value (total activity by brain, for example).

table 1.png
table II.png


If the radioactivity of cerebrosides increases, that of free fatty acids remain remarkably constant. The same phenomenon is found at the level of purified myelin (Table II). At zero time, no radioactivity is detected in any case. The analysis of acids shows that the lipids of the membranes contain—in addition to stearic acid—the shorter chained palmitic and the longer chained arachidic, behenic, and lignoceric (Table III). This, already clearly visible in all membranes, is even clearer in myelin (we checked that the fatty acids injected animals were pure; on the other hand, the blood of animals always contains only radioactive stearic acid, no other chain length being detected).

talbe III.png
time course.png ⟵ Click to embiggen

Discussion and Conclusions: A long-chain saturated fatty acid, stearic acid, is thus captured by the brain from the blood stream; this acid then crosses the barrier hematoencephalic. It is integrated into all brain membranes including myelin, which is particularly important. Thus, saturated fatty acids (and presumably their monounsaturated counterparts) from food have a direct effect on myelination (contributed from the environment). We can therefore assume that slight qualitative disturbances in the food will resound on the structure, and on the stability of the myelin membrane. The current pursuit of this work should contribute to verify this hypothesis. On the other hand, in the brain membranes, longer chain fatty acids and shorter are found. Since the rat blood contained only ¹⁴C-stearic acid, it must be deduced that the brain on the one hand degrades stearic acid into acetate units for the resynthesis of other fatty acids . . . and on the other hand lengthens this injected
¹⁴C-stearic acid. Stearic acid thus serves to pre-lengthen the very long chains.
 
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burtlancast

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I did a copy–paste translation paragraphwise on Google Translate: I also got rid of


o_O

Magnificient.

Could you do likewise for this very rare Max Gerson book in German from 1930 ?​
 

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Travis

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o_O

Magnificient.

Could you do likewise for this very rare Max Gerson book in German from 1930 ?​
An entire book? I think we would need help from everybody. If you start a thread—perhaps having an introductory paragraph with a link to Google Translate, detailing how easy this is (and perhaps tell people they get a free puppy for clicking the link)—soliticiting the help of all members, I think it would eventually get done stepwise. I think it would be interesting to read what Max Gerson had to write, and it could help familiarize everyone who participates with the German language.

I went on a 2¹⁄₂ day fast and also had read many newer studies on autophagy—formally called 'autolysis' in earlier works (i.e. Shelton, Tilden), but now defined more specifically. Fasting is certainly interesting to read about and I think it could help many people on this forum.
 

raypeatclips

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An entire book? I think we would need help from everybody. If you start a thread—perhaps having an introductory paragraph with a link to Google Translate, detailing how easy this is (and perhaps tell people they get a free puppy for clicking the link)—soliticiting the help of all members, I think it would eventually get done stepwise. I think it would be interesting to read what Max Gerson had to write, and it could help familiarize everyone who participates with the German language.

I went on a 2¹⁄₂ day fast and also had read many newer studies on autophagy—formally called 'autolysis' in earlier works (i.e. Shelton, Tilden), but now defined more specifically. Fasting is certainly interesting to read about and I think it could help many people on this forum.

How did you feel throughout the fast? Did you feel unwell at any point and did you do anything like keel blood sugar levels monitored? Did you drink water and nothing else?
 

Travis

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How did you feel throughout the fast? Did you feel unwell at any point and did you do anything like keel blood sugar levels monitored? Did you drink water and nothing else?
Pancreatic enzymes monitored by blood glucose for me—kept in range by glycogen derived from the liver, muscle, and extracellular space. I would argue that it's often good to have relatively-low glucose—that is, relative to most Americans eating foods with an unnaturally-high glycemic index. I had read a study where glucose had killed rats having a bacterial infection, yet the rats with their glucose in-check had all survived. I had switched from dates + coffee to figs + coffee, so the food I eat now with highest glycemic index is now either the figs or the pineapples (which are both lower in glycemic index than refined starch or sugar, or dates). I have confidence that my pancreas is working fine, but do think that blood glucose can have upper limits for nearly everybody (yet coffee will help you burn it at an accelerated rate!) When I had fasted, I was thinking about autophaging some spare proteins floating around—extraneous cell debris—and perhaps some lipofuscin, but that was before I had read about amyloid deposits. There's some good indication that actual amylopectin has been found in the brain of some people upon autopsy, yet there is a bit of uncertainly about this on account of polysaccharides being less-reliably characterized than are proteins, lipids, etc. (many polysaccharides consist of glucose units differing only in connectivity). Amylopectin stains with Lugol's yet so does glycogen. However! the polysaccharides found in the brain in two patients having Lafora's disease had stained darker than does glycogen with Lugol's iodine, which of course indicates amylopectin (this is certain: the precise wavelength of the iodine-stained polysaccharides had been accurately determined using absorption spectroscopy); the amyloid deposits had also been hydrolyzed by an enzyme combination specific only to amylopectin, this combination normally failing to completely hydrolyze glycogen. I take all this to mean that the same persorbed starch particles Volkheimer had discovered and recovered inside of multiple organs after dry starch ingestion can also travel to the brain; in fact, this assumption is nearly certain on account of Volkheimer & Crew having detected them in the cerebospinal fluid. So after only a few day's fasting—and still being in the 'glycogen phase'—I would assume that the body would act on any residual starch particles of the intracellular space which had been persorbed at an earlier date—including those from that dry-ish oatmeal that I had consumed a few months ago. Since Lafora's disease is characterized by both dementia and amyloid deposits (likely amylopectin in this case), it follows that fasting could logically be though to reverse this form of dementia by necessitating the hydrolysis of exogenous polysaccharides found in the extracellular space of the brain—the amyloid deposits. Classic fasting literature is full of remarks of fasting improving cognition, and I think this must be true in many cases. Longer fasts which extend past the 'glycogen phase' might logically be expected to induce the total or partial autophagy of intracellular lipofuscin—another inclusion body and presumed cause of dementia—the moment circulating leucine concentrations drops below the point of mTOR activation–deactivation.

I had felt fine during that fast, and nobody should be apprehensive about going for three days. This represents the glycogen phase and is also the same upper time limit recognized as being permissible for 'home use' by numerous fasting authorities including those who preside over thousands of fasting patients per year—the practitioners. Eating clean-burning food and even sometimes restricting it can give a person a good deal of motivation; I think much of this has to do with the autolysis of both intra- and extra-cellular inclusion bodies and perhaps even increased mitochondrial turnover (autophagosomes can engulf whole mitochondria when they found damaged).
 
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Koveras

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Pancreatic enzymes monitored by blood glucose for me—kept in range by glycogen derived from the liver, muscle, and extracellular space. I would argue that it's often good to have relatively-low glucose—that is, relative to most Americans eating foods with an unnaturally-high glycemic index. I had read a study where glucose had killed rats having a bacterial infection, yet the rats with their glucose in-check had all survived. I had switched from dates + coffee to figs + coffee, so the food I eat now with highest glycemic index is now either the figs or the pineapples (which are both lower in glycemic index than refined starch or sugar, or dates). I have confidence that my pancreas is working fine, but do think that blood glucose can have upper limits for nearly everybody (yet coffee will help you burn it at an accelerated rate!) When I had fasted, I was thinking about autophaging some spare proteins floating around—extraneous cell debris—and perhaps some lipofuscin, but that was before I had read about amyloid deposits. There's some good indication that actual amylopectin has been found in the brain of some people upon autopsy, yet there is a bit of uncertainly about this on account of polysaccharides being less-reliably characterized than are proteins, lipids, etc. (many polysaccharides consist of glucose units differing only in connectivity). Amylopectin stains with Lugol's yet so does glycogen. However! the polysaccharides found in the brain in two patients having Lafora's disease had stained darker than does glycogen with Lugol's iodine, which of course indicates amylopectin (this is certain: the precise wavelength of the iodine-stained polysaccharides had been accurately determined using absorption spectroscopy); the amyloid deposits had also been hydrolyzed by an enzyme combination specific only to amylopectin, this combination normally failing to completely hydrolyze glycogen. I take all this to mean that the same persorbed starch particles Volkheimer had discovered and recovered inside of multiple organs after dry starch ingestion can also travel to the brain; in fact, this assumption is nearly certain on account of Volkheimer & Crew having detected them in the cerebospinal fluid. So after only a few day's fasting—and still being in the 'glycogen phase'—I would assume that the body would act on any residual starch particles of the intracellular space which had been persorbed at an earlier date—including those from that dry-ish oatmeal that I had consumed a few months ago. Since Lafora's disease is characterized by both dementia and amyloid deposits (likely amylopectin in this case), it follows that fasting could logically be though to reverse this form of dementia by necessitating the hydrolysis of exogenous polysaccharides found in the extracellular space of the brain—the amyloid deposits. Classic fasting literature is full of remarks of fasting improving cognition, and I think this must be true in many cases. Longer fasts which extend past the 'glycogen phase' might logically be expected to induce the total or partial autophagy of intracellular lipofuscin—another inclusion body and presumed cause of dementia—the moment circulating leucine concentrations drops below the point of mTOR activation–deactivation.

I had felt fine during that fast, and nobody should be apprehensive about going for three days. This represents the glycogen phase and is also the same upper time limit recognized as being permissible for 'home use' by numerous fasting authorities including those who preside over thousands of fasting patients per year—the practitioners. Eating clean-burning food and even sometimes restricting it can give a person a good deal of motivation; I think much of this has to do with the autolysis of both intra- and extra-cellular inclusion bodies and perhaps even increased mitochondrial turnover (autophagosomes can engulf whole mitochondria when they found damaged).

IIRC Ray had said something about higher doses of LSD or mushrooms being stressful through depleting brain glycogen.

Maybe that intensity of energy use has some therapeutic effects - aside from the effects on the neurotransmitter systems.
 

jandrade1997

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Pancreatic enzymes monitored by blood glucose for me—kept in range by glycogen derived from the liver, muscle, and extracellular space. I would argue that it's often good to have relatively-low glucose—that is, relative to most Americans eating foods with an unnaturally-high glycemic index. I had read a study where glucose had killed rats having a bacterial infection, yet the rats with their glucose in-check had all survived. I had switched from dates + coffee to figs + coffee, so the food I eat now with highest glycemic index is now either the figs or the pineapples (which are both lower in glycemic index than refined starch or sugar, or dates). I have confidence that my pancreas is working fine, but do think that blood glucose can have upper limits for nearly everybody (yet coffee will help you burn it at an accelerated rate!) When I had fasted, I was thinking about autophaging some spare proteins floating around—extraneous cell debris—and perhaps some lipofuscin, but that was before I had read about amyloid deposits. There's some good indication that actual amylopectin has been found in the brain of some people upon autopsy, yet there is a bit of uncertainly about this on account of polysaccharides being less-reliably characterized than are proteins, lipids, etc. (many polysaccharides consist of glucose units differing only in connectivity). Amylopectin stains with Lugol's yet so does glycogen. However! the polysaccharides found in the brain in two patients having Lafora's disease had stained darker than does glycogen with Lugol's iodine, which of course indicates amylopectin (this is certain: the precise wavelength of the iodine-stained polysaccharides had been accurately determined using absorption spectroscopy); the amyloid deposits had also been hydrolyzed by an enzyme combination specific only to amylopectin, this combination normally failing to completely hydrolyze glycogen. I take all this to mean that the same persorbed starch particles Volkheimer had discovered and recovered inside of multiple organs after dry starch ingestion can also travel to the brain; in fact, this assumption is nearly certain on account of Volkheimer & Crew having detected them in the cerebospinal fluid. So after only a few day's fasting—and still being in the 'glycogen phase'—I would assume that the body would act on any residual starch particles of the intracellular space which had been persorbed at an earlier date—including those from that dry-ish oatmeal that I had consumed a few months ago. Since Lafora's disease is characterized by both dementia and amyloid deposits (likely amylopectin in this case), it follows that fasting could logically be though to reverse this form of dementia by necessitating the hydrolysis of exogenous polysaccharides found in the extracellular space of the brain—the amyloid deposits. Classic fasting literature is full of remarks of fasting improving cognition, and I think this must be true in many cases. Longer fasts which extend past the 'glycogen phase' might logically be expected to induce the total or partial autophagy of intracellular lipofuscin—another inclusion body and presumed cause of dementia—the moment circulating leucine concentrations drops below the point of mTOR activation–deactivation.

I had felt fine during that fast, and nobody should be apprehensive about going for three days. This represents the glycogen phase and is also the same upper time limit recognized as being permissible for 'home use' by numerous fasting authorities including those who preside over thousands of fasting patients per year—the practitioners. Eating clean-burning food and even sometimes restricting it can give a person a good deal of motivation; I think much of this has to do with the autolysis of both intra- and extra-cellular inclusion bodies and perhaps even increased mitochondrial turnover (autophagosomes can engulf whole mitochondria when they found damaged).

Do you think fasting is the only reliable way to induce autophagy, or do you think there might be more "Peaty" methods? I know thyroid stimulates autophagy, but I suspect that may be from thyroid enhancing energy consumption beyond energy availability, effectively replicating fasting.
 

griesburner

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i find fasting interesting, too and before peat i regularly did a 24h fast in intermittend fasting style. i remember having way less gut problems during this time. But what about elevated free fatty acids during a fast? Would that only be a problem after 3 days when all glycogen is empty?
 

Shai Hulud

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I once looked for stearic acid, but it wasn't available at my location. In the end I bought magnesium stearate. Can anyone tell if effects (at least orally) will be the same or is there a relatively easy way to bring it in acid form?

@burtlancast: Wanna know something specific in that book? I'm German.
 

burtlancast

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@burtlancast: Wanna know something specific in that book? I'm German.

I've caught Gar Hildenbrand from the Gerson Institute claiming based on this book and the one i attach here that Gerson's original tuberculosis diet used principally citrus fruits instead of carrot and green juice for treating degenerative diseases, cancer included (19.00 to 23.00 of the first video).

Would love to have these 2 books translated.
Alas.



 

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Shai Hulud

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I've looked through it and from what I've seen he generally recommends a lot of citrus fruits (mainly lemons), but also apples and vegetable juices. Not knowing his other work I'm unable to say how much his emphasis changed, but it's certainly not one or the other. I'll send you some translated passages, as I don't want to overwhelm this thread with OT.
 
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haidut

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Here it is. It's a short article and the summary explains all there is to know.
It's emphasized that during the whole experiment, the blood at any moment contains no other radioactive fatty acid than the one injected, and thus the de-novo synthesis takes place indeed inside the brain.

Thank you very much!
 

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