41 replies to this topic

[Logic]

It seems that many cases of back pain are caused by bacteria that sneak into damaged disks when the body grows blood vessels to fix the disk.

The biggest culprit is Propionibacterium acnes; better known for causing acne.

This may partly explain why I, and others, found relief from Astragalus; known to boost the immune system.
http://www.longecity...post__p__558918

Also:
http://www.ncbi.nlm....pubmed/19665786

Link:
http://www.guardian....k-pain-patients

[Avatar of Horus]

This seems to support our hypothesis, what we discussed here:
http://www.longecity...ce/page__st__30,
that the pathogens may play a significant role in the aging process, contributing to its degeneraive conditions.
Myself too wanted to do some search for relevant literature about this, so thank you for the links, BTW.

[tydi]

I read about this a while ago and was very intrigued, this is for sure on my list of research materials.

[bgs4669]

from some recent research i have read, and as a person who suffered from a lot of pain since 11 due to perthes of the r hip, is that the lack of protein in diets or free amino acids, and with collagen production declining at around age 25 people generally start suffering. I recently started taking some collagen supplements and totally different person. No pain, and 10 fold increase in mobility...but it is important to make sure what the quality of collagen supplementation is. Antibiotic, pain killers and other drugs have there place but i think with most causing side effects and other inflammation in the body we need to focus on diet and supplementation thereof, focusing on target areas!

[Logic]

from some recent research i have read, and as a person who suffered from a lot of pain since 11 due to perthes of the r hip, is that the lack of protein in diets or free amino acids, and with collagen production declining at around age 25 people generally start suffering. I recently started taking some collagen supplements and totally different person. No pain, and 10 fold increase in mobility...but it is important to make sure what the quality of collagen supplementation is. Antibiotic, pain killers and other drugs have there place but i think with most causing side effects and other inflammation in the body we need to focus on diet and supplementation thereof, focusing on target areas!

One of the things that kills Propionibacterium acnes is good old EVCO (see links in 1st post), which is also good for a large number of other ailments...

[niner]

One of the things that kills Propionibacterium acnes is good old EVCO (see links in 1st post), which is also good for a large number of other ailments...

True, as long as you have 80mg/liter. That's based on lauric acid in liposomal form, in cell culture with p. acnes over some amount of time. When coconut oil is digested, you will in fact get some lauric acid, and most of it will be in the form of something like a liposome, at least for a while. However, lauric acid is treated as food- the body metabolizes it. I worry that EVCO will fail as an antibiotic because of an inability to maintain an active concentration of lauric acid over a sufficient time span, and in the right place (where the target microbes are). I'd feel better about it if there was in vivo evidence of activity. Is there such a thing?

[Logic]

I don't have much time, but found these: (referenced)

http://www.coconutdi...skin_health.htm

http://coconutoil.co...or-skin-health/

[Luminosity]

Don't believe your theory, Logic, either about acne or back problems. If bacteria caused acne, we'd see a lot more of it in places where people had trouble keeping clean, like Africa or the slums of India. Instead their skin is clear. We see more acne in more developed countries.

[Logic]

 

One of the things that kills Propionibacterium acnes is good old EVCO (see links in 1st post), which is also good for a large number of other ailments...

True, as long as you have 80mg/liter. That's based on lauric acid in liposomal form, in cell culture with p. acnes over some amount of time. When coconut oil is digested, you will in fact get some lauric acid, and most of it will be in the form of something like a liposome, at least for a while. However, lauric acid is treated as food- the body metabolizes it. I worry that EVCO will fail as an antibiotic because of an inability to maintain an active concentration of lauric acid over a sufficient time span, and in the right place (where the target microbes are). I'd feel better about it if there was in vivo evidence of activity. Is there such a thing?

 

http://www.ncbi.nlm....Pubmed_RVDocSum

Antimicrobial property of lauric acid against Propionibacterium acnes: its therapeutic potential for inflammatory acne vulgaris.

"...This study evaluated the antimicrobial property of lauric acid against P. acnes both in vitro and in vivo...

...lauric acid yielded minimal inhibitory concentration (MIC) values against the bacterial growth over 15 times lower than those of benzoyl peroxide (BPO)...

...P. acnes is the most sensitive to lauric acid among these bacteria...

...Notably, both intradermal injection and epicutaneous application of lauric acid effectively decreased the number of P. acnes..."


http://www.ncbi.nlm....pubmed/20021093

Effects of Essential Oils and Monolaurin on Staphylococcus aureus: In Vitro and In Vivo Studies.

"...Over 60% of mice survived when receiving a daily combination of Origanum oil and monolaurin..."


http://www.naturalwa...th/coconut-oil/

"...Based on the per capita intake of coconut oil in 1985 as reported by Kaunitz (1992), the per capita daily intake of lauric acid can be approximated. For those major producing countries such as the Philippines, Indonesia, and Sri Lanka, and consuming countries such as Singapore, the daily intakes of lauric acid were approximately 7.3 grams (Philippines), 4.9 grams (Sri Lanka), 4.7 grams (Indonesia), and 2.8 grams (Singapore). In India, intake of lauric acid from coconut oil in the coconut growing areas (e.g., Kerala) range from about 12 to 20 grams per day (Eraly 1995), whereas the average for the rest of the country is less than half a gram. An average high of approximately 68 grams of lauric acid is calculated from the coconut oil intake previously reported by Prior et al (1981) for the Tokelau Islands. Other coconut producing countries may also have intakes of lauric acid in the same range.

It is not known exactly how much food made with lauric oils is needed in order to have a protective level of lauric acid in the diet. Infants probably consume between 0.3 and 1 gram per kilogram of body weight if they are fed human milk or an enriched infant formula that contains coconut oil. This amount appears to have always been protective. Adults could probably benefit from the consumption of 10 to 20 grams of lauric acid per day. Growing children probably need about the same amounts as adults..."


http://www.easihealt.../Monolaurin.pdf

"...Of the saturated fatty acids, Coconut oil is primarily composed of almost 50% Lauric Acid..."


http://www.google.co...3rvTv5eqV9nBHwQ
Over 50% of the fats in coconut are medium chain
triglycerides that are formed from fatty acids of chain length 8:0 to 14:0.

"...When digested in the small intestine, these fats yield saturated medium
chain free fatty acids and monoglycerides such as lauric acid (12:0). Of
these, it is primarily the 14:0 fatty acids that are thought to be atherogenic.
Coconut oil is the highest natural source of lauric acid. Lauric acid and its
derivative monolaurin constitute around 50% of coconut fat derived lipid.
However, unlike long chain fatty acids, these medium chain free fatty
acids and monoglycerides are absorbed intact from the small intestine, and do not undergo degradation and re-esterification processes. They are
directly used in the body to produce energy, and widely used in infant formulas,
nutritional drinks for athletes and intravenous lipid infusions..."

 

 

I hope this better answers the question, but its difficult to find research in a un-patentable, unprofitable substance.

[niner]

 

 

One of the things that kills Propionibacterium acnes is good old EVCO (see links in 1st post), which is also good for a large number of other ailments...

True, as long as you have 80mg/liter. That's based on lauric acid in liposomal form, in cell culture with p. acnes over some amount of time. When coconut oil is digested, you will in fact get some lauric acid, and most of it will be in the form of something like a liposome, at least for a while. However, lauric acid is treated as food- the body metabolizes it. I worry that EVCO will fail as an antibiotic because of an inability to maintain an active concentration of lauric acid over a sufficient time span, and in the right place (where the target microbes are). I'd feel better about it if there was in vivo evidence of activity. Is there such a thing?

 

http://www.ncbi.nlm....Pubmed_RVDocSum

Antimicrobial property of lauric acid against Propionibacterium acnes: its therapeutic potential for inflammatory acne vulgaris.

...Notably, both intradermal injection and epicutaneous application of lauric acid effectively decreased the number of P. acnes..."

http://www.ncbi.nlm....pubmed/20021093

Effects of Essential Oils and Monolaurin on Staphylococcus aureus: In Vitro and In Vivo Studies.

"...Over 60% of mice survived when receiving a daily combination of Origanum oil and monolaurin..."

 

The topical application or intradermal injection of lauric acid working in the case of P. acnes makes sense.  It's pure lauric acid rather than a triglyceride, and it's present at the site of the microbe in high concentration.   In the case of the mice, it was oral dosing, but they were given pure monolaurin.  Monolaurin is a glycerol ester of a single lauric acid molecule.  No doubt some of this is formed from the digestion of coconut oil, but how much?  And what dose was given to the mice?  It was probably quite a lot. 

 

I don't doubt the antimicrobial effects of lauric acid and monolaurin when they can be delivered in high concentration to the site of the microbe, but I'd hate to see someone try to treat an infection by eating a little bit of coconut oil, and ending up septic in the ICU or dead.  I think topical EVCO would be a great thing to try on acne.

[resveratrol_guy]

Of these, it is primarily the 14:0 fatty acids that are thought to be atherogenic.

 

While I doubt whether one could get enough lauric acid via coconut oil to fix a spinal disc problem caused by P. acnes, but eat it anyway on account of its purported benefits, this note concerns me. Coconut oil (extra virgin or not) is supposed to be healthy because it induces the construction of cell membranes that are more resistant to oxidation, on account of the fact that it's loaded with (very stable) saturated fats. Maybe I'm making a mountain out of a molehill, but how significant are these 14:0 FAs? Or is this just a nonissue because it goes back to the days when we concluded that coconut oil was atherogenic due to confusion with dietary consumption of hydrogenated coconut oil (i.e. transfat-laden garbage)?

[Logic]

The topical application or intradermal injection of lauric acid working in the case of P. acnes makes sense.  It's pure lauric acid rather than a triglyceride, and it's present at the site of the microbe in high concentration.   In the case of the mice, it was oral dosing, but they were given pure monolaurin.  Monolaurin is a glycerol ester of a single lauric acid molecule.  No doubt some of this is formed from the digestion of coconut oil, but how much?  And what dose was given to the mice?  It was probably quite a lot. 
 
I don't doubt the antimicrobial effects of lauric acid and monolaurin when they can be delivered in high concentration to the site of the microbe, but I'd hate to see someone try to treat an infection by eating a little bit of coconut oil, and ending up septic in the ICU or dead.  I think topical EVCO would be a great thing to try on acne.

The question is can you get a clinically effective dose of Lauric Acid from eating coconut oil, and will the dose stay high enough long enough to be effective at exposing pathogens to ones immune system.

From the last link it seems that "...these medium chain free fatty
acids and monoglycerides are absorbed intact from the small intestine, and do not undergo degradation and re-esterification processes..."
So it looks like the bioavailability of the Lauric, Carpic etc Acids is excellent and close to the full 1 gram of Lauric acid in every 2 grams of EVCO will be available for this purpose.

This leaves the questions; how much is reqd to disrupt/dissolve the lipd layers on pathogens in vivo and how long does it take for them to do so.
I have not yet found any studies that answer these questions, but did find the educated guess of "... 10 to 20 grams of lauric acid per day..."
So 20 to 40 grams of EVCO per day is the best dosage recommendation I have found so far.

The remaining question is how long does it take this ingested Lauric, Carpic, etc acids are effective at eliminating pathogens.
As the means by which they are effective at eliminating pathogens is by disrupting/dissolving their lipid layers, the question becomes: 'How long does it take these acids to mess with these lipid layers?'

I can not find any info on this but it seems Lauric acid is incorporated into adipose tissue, so perhaps the question is moot due to the acids being around, in one form or another, for a long time?
http://www.ncbi.nlm..../pubmed/2761351

Due to the lack of research (at least that I have been able to find) on the subject and the easy availability of EVCO and in light of the research showing positive effects in other areas of health its probably a good idea to test the effectiveness for oneself.

I once gave about 2 tablespoons to a guy with a bad case of the flu.
About 45 minutes later he was pleasantly shocked to find himself very much improved and I last saw him boarding a plane with a jar of EVCO clutched to his heart.

I have since seen similar results in a number of other people as well as cases where the EVCO did not help. Perhaps in the cases where the EVCO did not help; the virus was not lipid coated?

Edited by Logic, 11 September 2014 - 02:59 PM.

[Logic]

While I doubt whether one could get enough lauric acid via coconut oil to fix a spinal disc problem caused by P. acnes, but eat it anyway on account of its purported benefits, this note concerns me. Coconut oil (extra virgin or not) is supposed to be healthy because it induces the construction of cell membranes that are more resistant to oxidation, on account of the fact that it's loaded with (very stable) saturated fats. Maybe I'm making a mountain out of a molehill, but how significant are these 14:0 FAs? Or is this just a nonissue because it goes back to the days when we concluded that coconut oil was atherogenic due to confusion with dietary consumption of hydrogenated coconut oil (i.e. transfat-laden garbage)?

My understanding is that its all garbage.
http://www.easihealt.../Monolaurin.pdf

[niner]

 

Maybe I'm making a mountain out of a molehill, but how significant are these 14:0 FAs? Or is this just a nonissue because it goes back to the days when we concluded that coconut oil was atherogenic due to confusion with dietary consumption of hydrogenated coconut oil (i.e. transfat-laden garbage)?

My understanding is that its all garbage.
http://www.easihealt.../Monolaurin.pdf

 

That what's all garbage, the atherogenicity? Wow, I wish it was, because I like coconut oil, but try to limit it for that reason. Here's a paper comparing coconut oil to olive oil in an animal model.

That compendium of monolaurin reports gave some dose numbers in their AIDS trial. They used 7.2 and 2.4 grams of monolaurin, and 50 ml coconut oil, in each of three treatment groups. The trial lacked a control group, and the results were pretty lousy for them to use the word "cure" in the title. (No one was cured, although some of them saw viral load drop. Anyway, those monolaurin doses are pretty reasonable. It would be easy to consume that amount, and I wouldn't expect any adverse effects from it. 50 cc coconut oil, on the other hand, is a lot. If nothing else, that's an extra 450 Calories a day.  Monolaurin is available as a supplement.

[resveratrol_guy]

 

 

Maybe I'm making a mountain out of a molehill, but how significant are these 14:0 FAs? Or is this just a nonissue because it goes back to the days when we concluded that coconut oil was atherogenic due to confusion with dietary consumption of hydrogenated coconut oil (i.e. transfat-laden garbage)?

My understanding is that its all garbage.
http://www.easihealt.../Monolaurin.pdf

 

That what's all garbage, the atherogenicity? Wow, I wish it was, because I like coconut oil, but try to limit it for that reason. Here's a paper comparing coconut oil to olive oil in an animal model.

That compendium of monolaurin reports gave some dose numbers in their AIDS trial. They used 7.2 and 2.4 grams of monolaurin, and 50 ml coconut oil, in each of three treatment groups. The trial lacked a control group, and the results were pretty lousy for them to use the word "cure" in the title. (No one was cured, although some of them saw viral load drop. Anyway, those monolaurin doses are pretty reasonable. It would be easy to consume that amount, and I wouldn't expect any adverse effects from it. 50 cc coconut oil, on the other hand, is a lot. If nothing else, that's an extra 450 Calories a day.  Monolaurin is available as a supplement.

 

 

Well I'm not so sure that coconut oil is atherogenic, above and beyond the extent to which lots of added calories could be atherogenic. That study used massive doses: "hamsters fed on coconut oil (150 g/kg diet) and cholesterol (30 g/kg diet)". That's like a human eating 10 kg of coconut oil per day (or getting an intravenous milkshake transfusion at McDonald's)! Even if we adjust for lifespan scaling, it's still beyond the amount that almost anyone could actually stomach. This study should be called "varying effects of hypercaloric diets on hamster atherogenesis". If their point is that under such extreme circumstances, olive oil is better than coconut oil with respect to atherogenesis, then fine, but at that level of intake, it's all moot anyway.

 

But yeah, I do like the idea of monolaurin as a supplement. Thanks for providing that link. Although I wonder if coconut oil's benefits can be reduced to monolaurin. For example, would we still see the Alzheimer's benefits? In any event, supplementation might be the economically optimal way to go.

 

@ Logic, please explain what you meant by "all garbage".

[Logic]

 

 

Maybe I'm making a mountain out of a molehill, but how significant are these 14:0 FAs? Or is this just a nonissue because it goes back to the days when we concluded that coconut oil was atherogenic due to confusion with dietary consumption of hydrogenated coconut oil (i.e. transfat-laden garbage)?

My understanding is that its all garbage.
http://www.easihealt.../Monolaurin.pdf

 

That what's all garbage, the atherogenicity? Wow, I wish it was, because I like coconut oil, but try to limit it for that reason. Here's a paper comparing coconut oil to olive oil in an animal model.

That compendium of monolaurin reports gave some dose numbers in their AIDS trial. They used 7.2 and 2.4 grams of monolaurin, and 50 ml coconut oil, in each of three treatment groups. The trial lacked a control group, and the results were pretty lousy for them to use the word "cure" in the title. (No one was cured, although some of them saw viral load drop. Anyway, those monolaurin doses are pretty reasonable. It would be easy to consume that amount, and I wouldn't expect any adverse effects from it. 50 cc coconut oil, on the other hand, is a lot. If nothing else, that's an extra 450 Calories a day.  Monolaurin is available as a supplement.

 

Thx for that study Niner.
Here is a link to the full study which is worth reading:
http://journals.camb...29e7a33e0a9df0e

Note that this study consisted of 2 studies:


In the first the rats were 1st fed Rat Chow, coconut oil at 150g/kg and cholesterol at 30g/kg for 4 weeks.
8 were then euthanized for autopsy.
The remaining animals were allocated to three
groups.
One continued to be fed on the above diet.
The second got the same chow, coconut oil at 150g/kg and no cholesterol.
The third got the same chow, Extra Virgin Olive Oil at 150g/kg and no cholesterol.
All were then euthanized for autopsy.

Note that the second group getting the same chow and coconut oil, but no cholesterol "...there was a highly significant drop in the cholesterol concentration in the VLDL ... fraction ... Total plasma cholesterol and IDL-cholesterol were also reduced ..."

Aortic plaque "...was prevented by feeding the
coconut-oil-rich diet without added cholesterol..."

Changing the diet to chow with Olive Oil without added cholesterol "...reduced the mean cholesterol content in each of the lipoprotein fractions, except HDL ... The only statistically significant difference ... was a 7-fold difference in the LDL fraction..." and "...reduced the area covered by lesions in the ascending aorta..."

So there was no further damage caused by coconut oil once the cholesterol was stopped, but Extra Virgin (NB!) Olive Oil is good at reversing damage.
Also note the increase in body weight of the hamsters on Olive Oil..!


In the second part of the study hamsters got the same chow and high cholesterol dose as before.
The difference was that Hydrogenated Coconut Oil was use and thy got it for 10 weeks rather than 4.
The diet was then changed to chow and Hydrogenated Coconut Oil or EVCO.
The results show that "...In the ascending aorta the extent of atherosclerosis continued to increase in coconut-oil-fed animals even when
cholesterol was omitted from the diet. By contrast, the
amount of atherosclerosis in the olive-oil-fed animals
remained fairly constant. The pattern of lesion development
in the aortic arch was different, with evidence of regression
in both coconut-oil and olive-oil-fed animals..."
 

These results seem to me to show that coconut oil wont reverse atherosclerosis as well as olive oil does but wont make it worse unless its already advanced?
However I have further issues with this study:

Below is a table I made showing the % of fatty acids in the oils used compared to the % of fatty acids in EVCO gathered from two scources; s1 and s2:
http://www.google.co....75097201,d.bGQ
http://en.wikipedia....iki/Coconut_oil

ACID                 CO used       H'd CO used       OO used      EVCO s1/s2
Caprylic 8:0       4.5                 5.0                        0.?                 8  /  9
capric 10:0        7.9                 7.5                         0.?                7  /  10 ??
lauric 12:0       32.8               32.4                         0.?              48  /  52
myristic 14:0   24.9               24.5                         0.?              16  /  19
palmitic 16:0   13.3               13.6                        11.8               9  /  11
stearic 18:0      4.2                15.0                          3.7               2
oleic 18:1       10.3                  0.8                        73.2               7  /  8
linoleic 18:2      3.1                 0.7                          8.2               2

Vitamin E           ?                    ?                          14.0                0.01
 
From this table you can see that the Olive Oil  used is not Extra Virgin Coconut Oil, while they did use Extra Virgin Olive Oil.

Hydrogenation is also known to make oils more inflammatory and unhealthy.

From this table you can see that the Olive Oil used is not Extra Virgin Coconut Oil, while they did use Extra Virgin Olive Oil.
Hence this study does not tell us much about the effects of EVCO on atherosclerosis.

There is a proven connection between virii and atherosclerosis that may be helped by the Lauric etc. acid content of EVCO.

 

Vitamin E is also known to protect against atherosclerosis.  The amount in EVOO is MUCH higher in that in EVCO and may also have played a large role in the results seen in this study.  As most readers here supplement with Vitamin E they would most likely see different results to those seen in this study.

 

Also humans are known to cook their food in oils.

This generally oxidises the oil making it more unhealthy.

Coconut Oil is known to be the least effected by heating.

 

I would love to see a similar study done, but with the use of EVCO in  stead of whatever was used here, Vitamin E  added and perhaps the heating of the oils to cooking temperatures before use.

[resveratrol_guy]

OK so I located the free full text link and figured this out. They use the measurement of (g oil)/(kg diet), not to be confused with ((g substance)/(kg rat) which was administered via diet as opposed to some more direct method). (They use the notation "(g/kg diet)" in most but not all places, although I assume they always mean the same thing.) So they're quantifying everything in terms of food mass ratio. I guess that's easy to measure, but I have to wonder how much actually got into each rodent.

 

So what does this amount to? It's like saying that when I eat a diet that's 15% coconut oil, I get more atherscelerosis than with a diet that's 15% olive oil (by mass). But maybe that's because the coconut oil adds more calories, if for no other reason than that I eat more of it because I like it more. What I'm not seeing here is a study that says that rodents who ingested (X milligrams of coconut oil) per (kilogram of rodent) developed Y% more atherosclerotic occlusion of the aortic lumen, vs. the same ingestion rate of olive oil.

 

"I would love to see a similar study done, but with the use of EVCO in  stead of whatever was used here" The EVCO-vs-CO distinction is clearly important if your data table is correct, which ultimately only compounds the uncertainty here with regards to the ramifications of health-conscious consumers who consume various amounts of EVCO.

 

Edited by resveratrol_guy, 12 September 2014 - 07:42 PM.

[Logic]

OK so I located the free full text link and figured this out. They use the measurement of (g oil)/(kg diet), not to be confused with ((g substance)/(kg rat) which was administered via diet as opposed to some more direct method). (They use the notation "(g/kg diet)" in most but not all places, although I assume they always mean the same thing.) So they're quantifying everything in terms of food mass ratio. I guess that's easy to measure, but I have to wonder how much actually got into each rodent.

Thx for pointing out.

"I would love to see a similar study done, but with the use of EVCO in  stead of whatever was used here" The EVCO-vs-CO distinction is clearly important if your data table is correct, which ultimately only compounds the uncertainty here with regards to the ramifications of health-conscious consumers who consume various amounts of EVCO.

 

I think the other points about there being a lot of Vit E in OO and that people cook with oil are also important.

If you supplement with E you may be getting the same advantage as the hamsters got from the OO?
BHT and Astaxanthin are worth researching for stopping the oxidation of oils.
C60 may be the best?

If you use OO for cooking the advantages will probably be negated by the oxidation of the oil, while EVCO does not oxidise as much.
This is my understanding from previous reading, but I need to confirm this.

Personally I think using OO raw and CO for cooking as well as some raw ((Oil Pulling etc) may be the best from a practical POV.

[resveratrol_guy]

 

Thx for pointing out.

 

I think the other points about there being a lot of Vit E in OO and that people cook with oil are also important.

If you supplement with E you may be getting the same advantage as the hamsters got from the OO?
BHT and Astaxanthin are worth researching for stopping the oxidation of oils.
C60 may be the best?

If you use OO for cooking the advantages will probably be negated by the oxidation of the oil, while EVCO does not oxidise as much.
This is my understanding from previous reading, but I need to confirm this.

Personally I think using OO raw and CO for cooking as well as some raw ((Oil Pulling etc) may be the best from a practical POV.

 

 

FYI vitamin E supplementation to somewhere above RDI increases mortality rate in senior citizens. Sorry I don't recall the study details offhand, but Google should turn this up. I suspect this may be due to increased hemorragic stroke, but I'm not sure.
 

It's not clear to me why olive oil (especially organic EVOO) seems to be so prolongevity; even the c60oo seminal study demonstrated this (not to mention Jean Calment). Some have suggested beta-sitosterol content, but Wikipedia has some health warnings on it. Maybe it's simply a matter of displacing sugar in the diet as a source of calories.

 

Good point about EVCO for cooking vs. EVOO for unheated food applications. That makes intuitive sense.

 

I'm also glad that you mentioned astaxanthin. It's so easy to get excited about eating the right lipids to make durable cell membranes that we forget to protect them after the fact (which for all its benefits, I doubt that c60oo would do particularly well on account of its proclivity to concentrate in the mitochondria). Astaxanthin inserts itself between the cell's encompassing lipid layers. Dr. Mercola has an article and expert interview video here. (I don't have an hour to view it at the moment, but I trust Dr. Mercola's thoroughness as much as I trust any medical practitioner, even though I don't agree with 100% of his conclusions.) I do know that he recommends it as CT scan prophylaxis, so perhaps adding c60oo would make for a significant reduction in ensuing free radical damage.

 

As to C60 (sic) preventing oil oxidation, I'm not sure we have much data on that, particularly since it appears to be excreted rapidly.

Edited by resveratrol_guy, 14 September 2014 - 08:08 PM.

[Logic]

FYI vitamin E supplementation to somewhere above RDI increases mortality rate in senior citizens. Sorry I don't recall the study details offhand, but Google should turn this up. I suspect this may be due to increased hemorragic stroke, but I'm not sure.

Most supps use synthetic vitamin E derived from petroleum products, so which of the 8+ types are we talking about?
http://en.wikipedia....wiki/Tocopherol
I just try to go for all 8 forms of natural E when I can afford it as I havent yet gone into the subject in detail.
 

It's not clear to me why olive oil (especially organic EVOO) seems to be so prolongevity; even the c60oo seminal study demonstrated this (not to mention Jean Calment). Some have suggested beta-sitosterol content, but Wikipedia has some health warnings on it. Maybe it's simply a matter of displacing sugar in the diet as a source of calories.

I think it one of the reasons may be increased expression of FOXO and SIRT genes:
http://www.longecity...s-on-foxo-gene/
http://www.longecity...ndpost&p=412267
 

Good point about EVCO for cooking vs. EVOO for unheated food applications. That makes intuitive sense.
 
I'm also glad that you mentioned astaxanthin. It's so easy to get excited about eating the right lipids to make durable cell membranes that we forget to protect them after the fact (which for all its benefits, I doubt that c60oo would do particularly well on account of its proclivity to concentrate in the mitochondria). Astaxanthin inserts itself between the cell's encompassing lipid layers. Dr. Mercola has an article and expert interview video here. (I don't have an hour to view it at the moment, but I trust Dr. Mercola's thoroughness as much as I trust any medical practitioner, even though I don't agree with 100% of his conclusions.) I do know that he recommends it as CT scan prophylaxis, so perhaps adding c60oo would make for a significant reduction in ensuing free radical damage.
 
As to C60 (sic) preventing oil oxidation, I'm not sure we have much data on that, particularly since it appears to be excreted rapidly.

Yep Astaxanthin is good stuff and about 100X as potent as Vit E if I remember correctly, but BHT is very interesting to me atm and the most potent lipophilic antioxidant that I know of. Besides maybe C60oo?
The reason I started researching it is the rumour that it may be a telomerase activator or very important to providing the correct environment for telomerase activators to be effective:
http://www.longecity...ndpost&p=377164
http://www.longecity...ndpost&p=376874

The Anti Viral Effect of BHT is also very important to longevity imho:
http://www.longecity...opic/42592-bht/
http://www.longecity...-of-taking-bht/

[niner]

FYI vitamin E supplementation to somewhere above RDI increases mortality rate in senior citizens. Sorry I don't recall the study details offhand, but Google should turn this up. I suspect this may be due to increased hemorragic stroke, but I'm not sure.
 

It's not clear to me why olive oil (especially organic EVOO) seems to be so prolongevity; even the c60oo seminal study demonstrated this (not to mention Jean Calment). Some have suggested beta-sitosterol content, but Wikipedia has some health warnings on it. Maybe it's simply a matter of displacing sugar in the diet as a source of calories.

 

Good point about EVCO for cooking vs. EVOO for unheated food applications. That makes intuitive sense.

 

I'm also glad that you mentioned astaxanthin. It's so easy to get excited about eating the right lipids to make durable cell membranes that we forget to protect them after the fact (which for all its benefits, I doubt that c60oo would do particularly well on account of its proclivity to concentrate in the mitochondria). Astaxanthin inserts itself between the cell's encompassing lipid layers. Dr. Mercola has an article and expert interview video here. (I don't have an hour to view it at the moment, but I trust Dr. Mercola's thoroughness as much as I trust any medical practitioner, even though I don't agree with 100% of his conclusions.) I do know that he recommends it as CT scan prophylaxis, so perhaps adding c60oo would make for a significant reduction in ensuing free radical damage.

 

As to C60 (sic) preventing oil oxidation, I'm not sure we have much data on that, particularly since it appears to be excreted rapidly.

 

I don't know that paper regarding vitamin E supplementation increasing mortality in senior citizens.  Is that a LOT above RDI?  If you find the ref, please post.

 

Olive oil has some very good epidemiology.  It's generally considered to be due to the polyphenols, and it has a pretty good fatty acid profile.  I don't recall hearing it attributed to beta-sitosterol.

 

It's known that a bis-carboxylate c60 analog was seen preferentially in mitochondria, but preferentially doesn't mean entirely, and a long chain fatty acid conjugate of a fullerene, which would be more hydrophobic and membrane-like than the bis-carboxylate, could be expected to like membranes in general.  Based on the biological effects we're seeing from c60oo, it's very likely that it interacts with mitochondria, but it can probably be found in other membranes as well.

 

For what it's worth, there are a lot of well-informed members of the Longecity community who do not hold Dr. Mercola in high regard, although his information on astaxanthin might be ok- I haven't seen it.

 

The c60oo excretion data is based only on serum.   One of the mechanisms for its disappearance from serum is its partitioning into membranes.  While we don't yet have a lot of experimental data that clarifies the mechanism of life extension, a reduction in lipid peroxidation is not unlikely.

[resveratrol_guy]

I don't know that paper regarding vitamin E supplementation increasing mortality in senior citizens.  Is that a LOT above RDI?  If you find the ref, please post.

 

Olive oil has some very good epidemiology.  It's generally considered to be due to the polyphenols, and it has a pretty good fatty acid profile.  I don't recall hearing it attributed to beta-sitosterol.

 

It's known that a bis-carboxylate c60 analog was seen preferentially in mitochondria, but preferentially doesn't mean entirely, and a long chain fatty acid conjugate of a fullerene, which would be more hydrophobic and membrane-like than the bis-carboxylate, could be expected to like membranes in general.  Based on the biological effects we're seeing from c60oo, it's very likely that it interacts with mitochondria, but it can probably be found in other membranes as well.

 

For what it's worth, there are a lot of well-informed members of the Longecity community who do not hold Dr. Mercola in high regard, although his information on astaxanthin might be ok- I haven't seen it.

 

The c60oo excretion data is based only on serum.   One of the mechanisms for its disappearance from serum is its partitioning into membranes.  While we don't yet have a lot of experimental data that clarifies the mechanism of life extension, a reduction in lipid peroxidation is not unlikely.

 

 

The vitamin E supplementation link to increased mortality is more widely studied than I thought: "Another review, published in 2005 in the Annals of Internal Medicine, found that in 19 trials of nearly 136,000 people, supplemental vitamin E increased mortality. Also that year, a study of people with vascular disease or diabetes found that vitamin E increased the risk of heart failure. And in 2011, a study published in the Journal of the American Medical Association tied vitamin E supplements to an increased risk of prostate cancer." See this NY Times article on metastudies, then Google from there. Sorry Logic, no idea which form. Probably alpha, because that's in most drugstore supplements.

 

With particular relevance to lipid peroxidation, the article above seems to posit that insufficient oxidation implies lame hormesis implies premature death (which makes c60oo all the more baffling).

 

To your point about olive oil, I read somewhere that refined olive oil (as opposed to EVOO if not organic EVOO) does not create the elevated HDL benefit, which would support the polyphenol theory (thanks for the tyrosol link, Logic). Unfortunately, I can't find the article at the moment.

 

The BHT theory is intriguing. Hopefully some brave soul here will try it and see if they notice anything. (OTOH if you believe the vitamin E theory, it might be dangerous. IMO there's more to vitamin E's problems than dampening hormesis, e.g. maybe vitamin E is helpful but unhealthy people take a larger quantity of conventional vitamin supplements, thereby increasing hemmoraging of already-atherosclerotic vessels on a systemic level due to its anticoagulative effect).

 

Edited by resveratrol_guy, 15 September 2014 - 11:41 PM.

[AmyHazy]

Last month I received antibiotics for a respiratory infection, and my back pain has not disappeared. I know antibacterial soap helps with my eczema, which is a skin condition that is acne that covers majority of my body. But with skin like mine I do not use oily lotions or scented. I use baby lotion, because it is safer. Haha (: 

[1kgcoffee]

After leaving the jungle recently, I went on a just-in-case course of Nitazoxanide. My body and back do feel more loose. Totally anecdotal. Because Nitozoxanide works by interfering with anaerobic respiration, I wonder if it would be a good agent for pathogens dwelling in low oxygen environments like Propionibacterium. Cheap, only three day course and doesn't seem to have many long-term side effects. Don't take that as medical advice.

Edited by 1kgcoffee, 21 September 2014 - 10:36 PM.

[Logic]

The link speaks about Propionibacterium Acnes being the main but not the only bacteria responsible for lower back pain in 40% of cases AmyHazy. I assume the other bacteria are similar/related, but that just an assumption and it would be nice to know what the other bacteria were as only antibiotics effective against these would work.
http://www.theguardi...k-pain-patients
 
 
Thx for the anecdotal report 1kgcofee. Nitazoxanide sounds very interesting as interfering with anaerobic respiration may also be effective against cancers?
Is Nitazoxanide effective against Propionibacterium Acnes and company?

Edited by Logic, 22 September 2014 - 01:17 PM.

[Logic]

The vitamin E supplementation link to increased mortality is more widely studied than I thought: "Another review, published in 2005 in the Annals of Internal Medicine, found that in 19 trials of nearly 136,000 people, supplemental vitamin E increased mortality. Also that year, a study of people with vascular disease or diabetes found that vitamin E increased the risk of heart failure. And in 2011, a study published in the Journal of the American Medical Association tied vitamin E supplements to an increased risk of prostate cancer." See this NY Times article on metastudies, then Google from there. Sorry Logic, no idea which form. Probably alpha, because that's in most drugstore supplements.

I think it likely that petroleum derived Alpha Tocopherol was used in most of these studies.
I remember reading that taking too much Alpha Tocopherol actually blocks the uptake of the other seven forms of E resulting in an unhealthy imbalance??
This would explain the results and only make them useful as a warning not to take synthetic Alpha Tocopherol.

Here are studies showing that Tocotrienols lengthen telomeres and upregulate telomerase:
http://www.longecity...ate-telomerase/
 

The BHT theory is intriguing. Hopefully some brave soul here will try it and see if they notice anything. (OTOH if you believe the vitamin E theory, it might be dangerous. IMO there's more to vitamin E's problems than dampening hormesis, e.g. maybe vitamin E is helpful but unhealthy people take a larger quantity of conventional vitamin supplements, thereby increasing hemmoraging of already-atherosclerotic vessels on a systemic level due to its anticoagulative effect).

I and others have already been taking BHT:
http://www.longecity...opic/42592-bht/
http://www.longecity...-of-taking-bht/
 
Good Summary:
http://augmentinforc...ALTH EFFECT.htm

This post gets my vote as the most interesting post on BHT here:
http://www.longecity...side-iv/page-23

[AmyHazy]

I just now realized I forgot I have this one red acne spot, right along my back bone. Lol. Perhaps that attributes to the back pain? I've been usiing benzoyl peroxide on it, and it hasn't cleared up a bit. It is tender. Round. I don't know what to do, but to treat it. The weird thing is, I never get back acne. EVER. That is the only blemish spot and noticeable in the middle top half of my back. To be honest, perhaps I'm going crazy, I think it is getting bigger. I look at the size every week, and now its the size of my pinky nail. Normally it was a tiny round zit-lookin' raised dot. Now its repulsive since its noticeable and just there. haha 

 

Please I need suggestions on what to do for this problem! I have no idea what is going on. Answers will be greatly appreciated!

[Logic]

I just now realized I forgot I have this one red acne spot, right along my back bone. Lol. Perhaps that attributes to the back pain? I've been usiing benzoyl peroxide on it, and it hasn't cleared up a bit. It is tender. Round. I don't know what to do, but to treat it. The weird thing is, I never get back acne. EVER. That is the only blemish spot and noticeable in the middle top half of my back. To be honest, perhaps I'm going crazy, I think it is getting bigger. I look at the size every week, and now its the size of my pinky nail. Normally it was a tiny round zit-lookin' raised dot. Now its repulsive since its noticeable and just there. haha 
 
Please I need suggestions on what to do for this problem! I have no idea what is going on. Answers will be greatly appreciated!

I doubt whether the zit has anything to do with your backache apart from the fact that the same bacteria may be causing both. NB that these bacteria bugger up your body's attempt to fix disks and backache is due to other reasons 60% of the time.

Perhaps print out the article; take it to your doc and ask him for antibiotics based on what the article says.
I take probiotics an hour or more after any antibiotics as antibiotics do a number on the good bacteria in your gut and that leads to all sorts of nasty stuff later on. Choose a probiotic that's sold from a fridge and look for lots of bifido's in it. (Bifido's help keep you thin amongst other things) The bottle will say Bifido this - Bifido that.

[niner]

I just now realized I forgot I have this one red acne spot, right along my back bone. Lol. Perhaps that attributes to the back pain? I've been usiing benzoyl peroxide on it, and it hasn't cleared up a bit. It is tender. Round. I don't know what to do, but to treat it. The weird thing is, I never get back acne. EVER. That is the only blemish spot and noticeable in the middle top half of my back. To be honest, perhaps I'm going crazy, I think it is getting bigger. I look at the size every week, and now its the size of my pinky nail. Normally it was a tiny round zit-lookin' raised dot. Now its repulsive since its noticeable and just there. haha 

 

Please I need suggestions on what to do for this problem! I have no idea what is going on. Answers will be greatly appreciated!

 

If I was you, I would show it to a doctor.  What color is it?  Does it have irregular edges, or smooth edges?

[Logic]

If I was you, I would show it to a doctor.  What color is it?  Does it have irregular edges, or smooth edges?

 

 

Are you thinking tick bite?