PUFA Required/essential For Cancer; Stearic Acid Is A PUFA Antagonist & Anti-cancer

[Obi-wan]

Drinking Coffee and Cacao Powder plus Cacao butter and Shea butter transdermal are the best in my opinion for Stearic acid

 

[ddjd]

ive been eating 20g cacao butter, organic, last few days. feel great from it. i feel like its shrinking my belly fat

 

[Travis]

does transdermal stearic acid get into circulation? The abstract for the massaged oil in neonates just says "saturated fats" for the coconut oil. It could be that just myristic acid and smaller get past the skin.

I would imagine that it would. As a relatively nonpolar lipid you'd think that it would have roughly the same kinetics as vitamin D and androgens, which enter circulation. But one of the main differences is that stearic acid is a substrate for β-oxidation and many acyltransferase enzymes; this means that some of it would probably be metabolized for energy before it gets there, and some other incorporated into structural lipids.

 

[raypeatclips]

@Travis I saw you mention broccoli being a big source of selenium. Do you think very well boiled broccoli would be a good addition to the diet? Or would the boiling to prevent the supposed goitrogenic effects reduce the selenium and essentially make it worthless?

 

[Amazoniac]

Travisord, why don't you reduce a broccoli to its ashes in your lab and analyze the selenium content?

 

[Travis]

@Travis I saw you mention broccoli being a big source of selenium. Do you think very well boiled broccoli would be a good addition to the diet? Or would the boiling to prevent the supposed goitrogenic effects reduce the selenium and essentially make it worthless?

You saw that it was a hyperaccumulator, and could concentrate even more selenium that Brazil nuts.

The trees which produce Brazil nuts are all geographically confined to the same region; this, along with their extensive and deep root structure, would be expected to yield nuts having selenium concentrations similar to all other Brazil nuts; broccoli on the other hand is grown everywhere and has a shallow root structure. This of course would mean that broccoli has a highly‐variable selenium content, ranging from the highest concentration found in any food to essentially zero. Believe it or not, the USDA has a map of the selenium content of soils (vide infra). The higher‐selenium broccoli would be expected to have been grown in the bluer regions. The average 'grocery store broccoli' does not list provinance, though it could perhaps be viewed on the large cardboard box in some stores. The more expensive organic broccoli found in smaller packaging would likely have information which would allow one to determine where it had been grown.

https://mrdata.usgs.gov...

There are actually a few studies on this, on selenium‐enriched broccoli and colon cancer. I haven't read one yet, but I will shortly after I leave the room to smoke a cigarette. [...] Okay, looks like there are quite a few titles to choose from—most of which have free full text links:

Finley, J. "Reduction of cancer risk by consumption of selenium-enriched plants: enrichment of broccoli with selenium increases the anticarcinogenic properties of broccoli." Journal of medicinal food (2003)
Davis, C. "Selenium-enriched broccoli decreases intestinal tumorigenesis in multiple intestinal neoplasia mice." The Journal of nutrition (2002)
Finley, J. "Cancer-protective properties of high-selenium broccoli." Journal of agricultural and food chemistry (2001)
Finley, J. "Selenium from high selenium broccoli protects rats from colon cancer." The Journal of nutrition (2000)

It looks like John Finley is spearheading this idea, and has even written a review article on the subject (Finley, 2001). Review articles by experimenters are generally good as they have first‐hand knowledge; David Rose is also an experimenter—who works on lipids and prostaglandins—and is also a very good writer. What I had taken as a 'review article' had actually turned‐out to be an experimental article. He starts out summarizing his previous studies, makes no mention of polyamines, and ostensibly believes that selenium is excerting is carcinostatic effects after dissociating from methionine—acting inorganically:

'Although various forms of Se offer different degrees of protection, those that can be easily converted to methylselenol apparently offer superior protection against carcinogenesis.' ―Finley

'Sulforaphane reduces mammary tumors in rats (18), indole carbinol reduces colonic tumors in rats (19), and chlorophyllin is a potent inhibitor of aflatoxin hepatocarcinogenesis in rainbow trout (20). The antitumorigenic activity of these compounds may serve to further enhance the cancer protective benefits of Se in broccoli.' ―Finley​

I am sure about this, as the cancer incidence of the Japanese and numerous cell culture and DNA replication studies strongly imply that polyamines are the primary causative agent—which selenomethionine limits the formation of. Selenium not connected to the methionine carbon structure does not inhibit polyamines; or at least, not in the same way nor to the same extent. But luckily for us, his experiment is testing selenomethionine (i.e. our polyamine inhibitor) against inorganic selenium (as selenite: (SeO₃)²⁻). Thus, he is testing the idea directly; I would predict that the selenomethionine group would fare better and that Finley will just explain this through 'ancillary phytochemicals in broccoli.'

'The basal diet was a commercially prepared Se-deficient torula yeast‐based diet (Tek-Lad, Madison, WI) to which was added Se in the following amounts and chemical forms:

A: 0.1 µg of Se/g of diet as selenite;
B: 0.1 µg of Se/g of diet as selenite + low-Se broccoli sprouts;
C: 2 µg of Se/g of diet as high-Se broccoli;
D: 2 µg of Se/g of diet as selenite;
E: 2 µg of Se/g of diet as selenite + low-Se broccoli sprouts;
F: 2 µg of Se/g of diet as high-Se broccoli sprouts.' ―Finley​

This is an involved study. Eighteen mice in each group were fed for three weeks, injected with a carcinogen, and then fed an additional eight weeks—after which they were ruthlessly murdered by lethal injection. They had even measured their tissue selenium concentrations.

'Aberrant crypts in the entire colon were counted by a trained microscopist following staining with methylene blue.' ―Finley​

Confiming by expectations, the rats fed selenocysteine had less cancer and aberrsnt crypt foci than those fed selenite:

But what I had not anticipated was that the author does not try to explain this by ancillary compounds in broccoli, apparently because the selenomethionine in garlic had shown like effects. However, he still makes no mention of polyamines.

'Previous research has established a strong association between the dietary form of Se and the cancer-preventive properties of this element (5, 28). This paper extends the evidence that Se in chemical forms known to accumulate in garlic and some Brassica species are especially effective in the prevention of chemically induced carcinogenesis (14, 17).' ―Finley

'Se-enriched broccoli was not more effective than enriched garlic (3) in reducing the number of tumors; this suggests that the combination of sulforaphane, indole carbinol, and chlorophyll with Se did not provide additional protection against mammary tumors.' ―Finley

'Similar to our previous findings concerning the ability of high-Se broccoli to reduce the incidence of colon cancer (17), an equal amount of Se supplied as selenite did not significantly reduce the incidence of ACF. This means that in addition to total Se intake, the form of Se in a particular food or supplement must be taken into consideration.' ―Finley​

So this study is totally in line with with what I'd expect. Inorganic selenium has a slight effect on cancer, but selenomethionine and selenohomocysteine are more effective simply because they compete with and inhibit most of the enzymes involved in polyamine synthesis. It follows from this that high‐selenomethionine broccoli should reduce to 'risk' of gastrointestinal cancer especially coupled with a low‐methionine diet. Although tasty (ask me how I know), soy sauce on steamed broccoli would be counterproductive since this is literally adding polyamines to a polyamine inhibitor—of which broccoli absorbs like a veritable sponge.

 

[Wagner83]

@Travis Ray and others here have often mentioned the anti-thyroid effects of cruciferous veggies, particularly cabbage but I think broccoli would fit the bill. Any thoughts on that?

How do you see the use of a few Brazil nuts to increase selenium intake? Very few are needed.

 

[aquaman]

I have received a few reports from people who have been declared to be in "indefinite remission" (not even sure what that means) with a combination of orlistat (mentioned in a few of the studies I posted), aspirin and niacinamide. I think one had lymphoma, another one had breast cancer, and one had prostate cancer.

Reports from where?

 

[Obi-wan]

Reports from where?

This was a quote from Haidut taken from another post. You would have to ask him

 

[Mito]

stearic acid is a substrate for β-oxidation and many acyltransferase enzymes; this means that some of it would probably be metabolized for energy before it gets there, and some other incorporated into structural lipids.

Transdermal vs dietary stearic acid....which has a better chance of avoiding β-oxidation/acyltransferase enyzmes and then getting incorporated into structural lipids.

 

[chimdp]

It's nearly unavoidable, especially if you eat either dairy or leaves. A person eating mostly grains might have issues with this, but most people get enough. It only takes a few milligrams per day for the liver to create enough DHA for the brain; all excessive DHA gets incorporated into peripheral cell membranes, once the capacity of the brain has been exceeded.

@Travis As a follow up to this question/response... What are other sources of alpha-linolenic acid? Not that I'm looking to load up on the stuff, but wanting to verify I'm getting some. I can't eat dairy/eggs and dont eat many leaves so just curious as to what are other decent/somewhat peat related sources? I eat broccoli, brussel sprouts, and cod filets a few times a week. Thanks for the help!

 

[Travis]

@Travis As a follow up to this question/response... What are other sources of alpha-linolenic acid? Not that I'm looking to load up on the stuff, but wanting to verify I'm getting some. I can't eat dairy/eggs and dont eat many leaves so just curious as to what are other decent/somewhat peat related sources? I eat broccoli, brussel sprouts, and cod filets a few times a week. Thanks for the help!

I think you'd be fine with the crucifers, and consuming fish is consuming DHA directly—eliminating the very need for α-linolenic acid. Fish also has eicosapentaenoic acid, the other product of α-linolenic acid which becomes a membrane lipid; this is the precursor for the 3-series prostaglandins which have less activity than the 2-series. In a cancer cell culture study that I'd read, prostaglandin E₃ had only ~¹⁄₄ the activity as did prostaglandin E₂. I think α-linolenic acid is one of those near unavoidables: as long as a person eats whole foods, they are getting enough. I think the main issue instead would be the ω−6 fatty displacing α-linolenic acid, perhaps leading the arachidonic acid in the brain and other cell membranes. As lacking clothes and fur at birth, I don't think anyone would take issue with the idea that humans had evolved in the tropics. In warm latitudes, plants produce primarily saturated fatty acids (i.e. coconut, shea, macadamia). As humans had spread from the equator over the millennia they naturally had started consuming the ω−6 fatty acids which, if you will allow me to speculate, caused noise in the endogenous eicosanoid system dominated by 3-series prostaglandins. It's not that they necessarily caused noise in the system through sheer numbers, although they often do and are consumed by some people in great amounts, but that their slightly different structure makes for a more powerful eicosanoid. After the mechanical agricultural revolution followed by seed pressing in temperate climates, the human body simply could not adapt in time—the television media anti-saturated fat campaign induced by Ancel Keys' ignorance certainly didn't help. Now we have prostaglandin E₂ feeding cancers left and right, and we also have prostaglandin D₂ causing hair loss.

Fish is fine in this regard. The only objections to fish that I can think of is that it still contains highly unsaturated fatty acids prone to lipid peroxidation, and iron. I haven't looked at the methionine content, but that shouldn't matter as long as you're not feeding a tumour or something similar. We need polyamines for growth, and the anabolic effects of methionine can be seen as a benefit to many. I still need to examine brain–lipid transport kinetics: It's well-known that the brain uses primarily glucose, but it could perhaps import fatty acids in different rates depending on the diet. If so, then the quantity and quality of lipids ingested could theoretically influence the rate of lipofusin formation: a process which has been shown to be accelerated by iron, oxygen, and slowed by vitamin E. Caloric restriction and fasting—or 'food deprivation' as called most modern articles . . . and also sometimes archaically termed 'inanition'—has been shown to initiate autophagy, or autolysis. This has been hypothesized as preventing dementia because Alzheimer's is characterized by protein inclusion bodies, which some biochemists frame as a result of 'autophagy inhibition.' I think it's perhaps the proteolysis-resistant lipofuscin, as elaborated by Brunk Terman, in addition to aluminum-crosslinked phosphorylated proteins which clog the cellular autolysosome giving the impression that 'autophagy is inhibited.' While true, this is only because it's backed-up; lysosomes are filled with crosslinked proteins in which their serine, asparate, and cystein proteases—or caspases—are mostly incapable of degrading. In my opinoin: intermittent fasting, limiting iron, avoiding aluminum, and consuming vitamin E seems to be the most logical approach for avoiding lipofuscin buildup in the neurons; all other cells will divide throughout a lifetime and through mitosis lipofuscin ceases to be an issue. Studies on centenarians reveal that lipofuscin can occupy up to 75% of the interior volume of a neuron.

 

[Travis]

Transdermal vs dietary stearic acid....which has a better chance of avoiding β-oxidation/acyltransferase enyzmes and then getting incorporated into structural lipids.

Transdermal, because stearic acid can be converted into oleic acid by Δ⁹-desaturase in the liver. Certainly this enzyme exists elsewhere, but probably in the concentrations found in the liver. I also think that the tissues have less metabolic activity than the liver. So taken together, I think transdermal would lead to more unmodified stearic acid in the blood despite the slower route.

 

[Obi-wan]

OK @Travis, I am taking your advice on lowering leucine and have stopped taking casein protein since it seems to have a lot in it plus more salads at lunch

 

[ddjd]

Actually better to use transdermal. Stearic acid will stay as stearic acid where if taken orally some will convert to oleic acid

Missing a few letters there yourself. Don't forget the edit button

 

[Obi-wan]

@Joeyd

 

[Glassy]

I have received a few reports from people who have been declared to be in "indefinite remission" (not even sure what that means) with a combination of orlistat (mentioned in a few of the studies I posted), aspirin and niacinamide. I think one had lymphoma, another one had breast cancer, and one had prostate cancer. From what I understand, they do eat fat but just try to limit PUFA intake. With the recent studies on caprylic acid and other SFA completely destroying tumors, I think it is another confirmation that it is just the PUFA that needs to be avoided in cancer patients, not all fat. But regardless of the type of fat, orlistat would block most of the fat absorption anyways. -per Haidut.

I have not tried orlistat, but in my opinion might not be a good idea since I am trying to get Stearic acid into the cell

I got a prescription for it (Xenacal) about 10 years ago before it became available OTC here in Australia. I was literally too scared to fart for fear of ruining another pair of underwear. It’s supposed to teach people to avoid fatty foods but that was back at a time when I thought EFAs were essential and I discontinued its use. It seems to only be active in the digestive tract so it could be taken around food that has questionable PUFA content to minimise absorption. I’m sure you have your PUFA intake dialed in pretty closely and it seems that it would only inhibit your SFA intake which is desirable. If you’re taking your stearic acid topically it shouldn’t be affected.

 

[Glassy]

I mean that pure stearic acid is sold as cosmetic ingredient and it is often made from palm oil.

I don’t know if you can easily get pure stearic acid. It seems USP grade stearic acid is a blend of stearic (C18) acid (min 40%) and palmatic (C16) acid.
Depending on your sources it seems to be about on par with Shae butter and cocoa butter. Stearic acid is about half the price ($4/lb) of cocao butter ($9/lb) on lotion crafter but shipping to Australia is the biggest cost for me and I’d rather put cocao butter on my skin.

 

[Obi-wan]

I use Cocoa butter in the morning and Shea butter at night transdermal. Cocoa powder in my coffee. Tried straight stearic acid but does not work transdermal and still ends up as flakes in my coffee. I agree with @Glassy orlistat is not the way to go

 

[d1d2]

I use Cocoa butter in the morning and Shea butter at night transdermal. Cocoa powder in my coffee. Tried straight stearic acid but does not work transdermal and still ends up as flakes in my coffee. I agree with @Glassy orlistat is not the way to go

Do you find that cocoa butter takes a while to absorb? I tried some last night and found that. I often use some vitamin E mixed with MCT and that absorbs pretty well in comparison. Maybe I used too much. How much surface area of your body are you covering to feel a result?