Obi-wan

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Actually it absorbs quickly and I use it on my whole body
 

managing

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

Just swallowing it? Still seeing benefits?
 

Wagner83

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The few times I used it orally I dif not notice any dramatic effect, except that it doesn't taste near as good as butter.
 

Obi-wan

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Aluminium salts of palmitic acid and naphthenic acid were combined during World War II to produce napalm. The word "napalm" is derived from the words naphthenic acid and palmitic acid-Wikipedia

Palmitic acid is a major component of the oil from the fruit of oil palms (palm oil)

Excess carbohydrates in the body are converted to palmitic acid. Palmitic acid is the first fatty acid produced during fatty acid synthesis and is the precursor to longer fatty acids. As a consequence, palmitic acid is a major body component of animals. In humans, one analysis found it to make up 21–30% (molar) of human depot fat,[12] and it is a major, but highly variable, lipid component of human breast milk.[13] Palmitate negatively feeds back on acetyl-CoA carboxylase (ACC), which is responsible for converting acetyl-CoA to malonyl-CoA, which in turn is used to add to the growing acyl chain, thus preventing further palmitate generation.[1 -Wikipedia

Rats fed a diet of 19% palmitic acid and 56% carbohydrate for extended periods showed alterations in central nervous system control of insulin secretion, and suppression of the body's natural appetite-suppressing signals from leptin and insulin (the key hormones involved in weight regulation).[17] -Wikipedia

Palmitic acid strongly boosts metastasis in mouse models of human oral cancer cells. Among all fatty acids, it has the strongest effect in boosting the metastatic potential of CD36+ metastasis-initiating cells.[18][19] -Wikipedia
 
OP
haidut

haidut

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Palmitic acid strongly boosts metastasis in mouse models of human oral cancer cells. Among all fatty acids, it has the strongest effect in boosting the metastatic potential of CD36+ metastasis-initiating cells.[18][19] -Wikipedia

We discussed that study before. In my opinion, it is fraudulent because nowhere in the study is palmitic acid mentioned as added to the diet, and the authors stopped answering my emails when I pointed out that fact. We exchanged maybe 4-5 emails and as soon as I asked why is palmitic acid not mentioned in the "materials & methods" section they went quiet and stopped answering my emails, even on other topics. See below for more info.
Palmitic Acid (palmitate) Dramatically Inhibits Liver Cancer Progression

I even alerted the Wikipedia author of that paragraph that the claim is "unverifiable" as per Wikipedia's rules and he said "if you think so, then edit it yourself". So, I may edit the Wikipedia page to remove that statement as it has no evidence behind it.
 

Obi-wan

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Thanks Haidut! Still like the napalm info
 

Travis

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We discussed that study before. In my opinion, it is fraudulent because nowhere in the study is palmitic acid mentioned as added to the diet, and the authors stopped answering my emails when I pointed out that fact. We exchanged maybe 4-5 emails and as soon as I asked why is palmitic acid not mentioned in the "materials & methods" section they went quiet and stopped answering my emails, even on other topics. See below for more info.
Palmitic Acid (palmitate) Dramatically Inhibits Liver Cancer Progression

I even alerted the Wikipedia author of that paragraph that the claim is "unverifiable" as per Wikipedia's rules and he said "if you think so, then edit it yourself". So, I may edit the Wikipedia page to remove that statement as it has no evidence behind it.
You should. Those Wikipediatricians are just authoritarian drones who have long traded-in their ability to to be equitable and critical for an easy paycheck and the petty ego strokes they get whenever they revert an edit. They know by now that the more they genuflect to the organizations having the most power—i.e. the AMA, NASA, the USDA—the easier time they'll have with their job, and may even be promoted. Nonetheless, some pages—the nonpolically-charged ones—appear to be democratic enough and Wikipedia is still great for quick reference. We can all work to make it even better.
 

Obi-wan

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Great to have you guys as references! I copy and past all of your profound statements and print them out to read over and over again. Highlight sections as well. I am a good student:happy:
 
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Braveheart

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Great to have you guys as references! I copy and past all of your profound statements and print them out to read over and over again. Highlight sections as well. I am a good student:happy:
:handok:
 

LeeLemonoil

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Stearic acid and carcinogenesis

Decreased membrane rigidity is one of the characteristics of malignant cells, resulting in part from the desaturation of stearic acid into oleic acid. In this study we investigated the influence of stearic acid on tumour cell inhibition in vitro and tumour development in vivo. Stearic acid inhibited the colony-forming ability of 4 out of 5 rat and two human tumour continuous cell lines in vitro. In contrast, the colony-forming ability of rat fibroblasts was not inhibited and that of human foetal lung fibroblasts was inhibited at a higher dose than that required to inhibit human tumour cell lines. Using a model of rat mammary carcinoma induced by nitroso-methyl urea (NMU) the subcutaneous injection of stearic acid at weekly intervals prevented tumour development in 5 to 10 rats. Using iodostearic acid twice weekly, 11 of 19 rats were alive and tumour free at week 22 whilst all of 14 animals injected with NMU alone had died of tumour by the 16th week. The ratio of stearic to oleic acids in erythrocyte membranes was significantly reduced in the tumour-bearing rats, but was normal in tumour-free animals treated with stearic or iodostearic acid. These preliminary data indicate that stearic acid inhibits tumour development in rats.

That's a rather old publication, but given that some of us have discussed the ability of iodine (as part of a discussion that regards iodine more positive than Peat does) to transform oleic acid into iodostearic acid, I do wonder if Iodostearic acid has the same or similar properties as stearic acid. The study above hints at it.

I wonder if the purportd benefits of mediterranean diet stems in part from iodine. It's rather high in oleic acid and fish and seafood which high iodine content might be able to offset the negatives of too much omega-3 and transforms substantial amounts of Oleic acid into Stearic?


@Cirion @tankasnowgod
 
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managing

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Stearic acid and carcinogenesis

Decreased membrane rigidity is one of the characteristics of malignant cells, resulting in part from the desaturation of stearic acid into oleic acid. In this study we investigated the influence of stearic acid on tumour cell inhibition in vitro and tumour development in vivo. Stearic acid inhibited the colony-forming ability of 4 out of 5 rat and two human tumour continuous cell lines in vitro. In contrast, the colony-forming ability of rat fibroblasts was not inhibited and that of human foetal lung fibroblasts was inhibited at a higher dose than that required to inhibit human tumour cell lines. Using a model of rat mammary carcinoma induced by nitroso-methyl urea (NMU) the subcutaneous injection of stearic acid at weekly intervals prevented tumour development in 5 to 10 rats. Using iodostearic acid twice weekly, 11 of 19 rats were alive and tumour free at week 22 whilst all of 14 animals injected with NMU alone had died of tumour by the 16th week. The ratio of stearic to oleic acids in erythrocyte membranes was significantly reduced in the tumour-bearing rats, but was normal in tumour-free animals treated with stearic or iodostearic acid. These preliminary data indicate that stearic acid inhibits tumour development in rats.

That's a rather old publication, but given that some of us have discussed the ability of iodine (as part of a discussion that regards iodine more positive than Peat does) to transform oleic acid into iodostearic acid, I do wonder if Iodostearic acid has the same or similar properties as stearic acid. The study above hints at it.

I wonder if the purportd benefits of mediterranean diet stems in part from iodine. It's rather high in oleic acid and fish and seafood which high iodine content might be able to offset the negatives of too much omega-3 and transforms substantial amounts of Oleic acid into Stearic?


@Cirion @tankasnowgod
This is a fascinating study. But my initial thought is that you are talking about a LOT of olive oil. And while there is also a lot fish, the relative amount of iodine is still quite small, relative to the olive oil. I haven't looked at the stoichiometry of it, but it just doesn't seem like it could shift the ratio all that far. However, if there was something special about iodostearic acid independent of the ratio itself (and this study doesn't consider this either way), then yes, absolutely, this could be a key to why the "Mediterranean Diet" is relatively good despite its high oleic consumption.
 

LeeLemonoil

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Thanks for chiming in @managing
Pls note that it is only a thought that occurred to me, i‘ve not yet searched for anything that corroborated a link between iodolipids/lactones and med-diet effects.


These are the two threads were iodostearic acid was discussed recently (the newer posts):

Mega Dosing Iodine = Bad, Destroys Thyroid Tissue Permanently

No Researcher Knows So Much About Iodine And Human Evolution As The Italian Dr Sebastiano Venturi

And this night adress stoichiometry, a User here who tries out iodine and olive oil

DIY Iodized Oil
 

managing

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Thanks for chiming in @managing
Pls note that it is only a thought that occurred to me, i‘ve not yet searched for anything that corroborated a link between iodolipids/lactones and med-diet effects.


These are the two threads were iodostearic acid was discussed recently (the newer posts):

Mega Dosing Iodine = Bad, Destroys Thyroid Tissue Permanently

No Researcher Knows So Much About Iodine And Human Evolution As The Italian Dr Sebastiano Venturi

And this night adress stoichiometry, a User here who tries out iodine and olive oil

DIY Iodized Oil
Definitely count me as interested and intrigued. I am only saying I think (if it is good) that it is because of the iodostearic itself, and not the ratio you described before. But I too am making wild, mildly informed, guesses.
 

LeeLemonoil

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I wonder if iodine would also saturate phlloquinone/Vit. K1. Would be very cost efficient and might offer some special physiological effects. Can't find anything about it though.
 

dannibo

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Two studies showing that PUFA (linoleic) acid is essential for cancer development. As the studies show, cancer cells accumulate large quantities of oleic acid and the saturation index (SI) - i.e. ratio of stearic/oleic acids in erythrocytes (RBC) is very low in cancer. This SI can also be used as a reliable biomarker not only for cancer but for other serious conditions like AIDS. In addition, both studies show that addition of stearic acid (to the diet or by injection) has significant inhibitory effect on cancer appearance and progression, and it greatly prolongs survival of animals with already established cancers. The second study used a tiny amount of stearic acid - a HED of just 0.4 mg/kg. While the route of administration was subcutaneous in order to prevent first pass metabolism in the liver, just 1 tsp (4g) of oral stearic acid can easily surpass the in vivo concentrations from this experiment. Another interesting observation made by one of the studies is that stearic acid is apparently an inhibitor of the enzyme fatty acid synthase (FAS), which is required for cancer development/progression and is one of the most promising drug candidates in oncology. Peat has mentioned the role of aspirin as a FAS inhibitor and I posted a study on palmitic acid also being a FAS inhibitor. Furthermore, both studies make a case for prostaglandins as the initial immunosuppresive factor that allows cancer cells to evade destruction by the immune system and establish solid tumors. Other have shown that the prostaglandins are also essential for metastases, cachexia, and end-stage cancer organ failure, which solidifies the role of PUFA along the entire path of carcinogenesis. Finally, the second study states that tumor cells release a desaturation producing factor (DPF), which decreases the SI of cells systemically and that SI index varies inversely with tumor size and stage. User @Travis explained in great detail the antagonism between stearic and linoleic acid, and I posted a few other studies corroborating this antagonism. So, I am hoping he can shed some light on what that DPF in tumor cells may be. Also, maybe @Dan Wich can check what labs provide tests for erythrocyte stearic and oleic acids as it seems that this SI biomarker may be relevant not only for cancer but for many other sever chronic conditions (e.g. AIDS, diabetes, Alzheimer, ALS, etc) as well.
The only weak point of both studies is that they simply provided extra stearic acid either as diet or as an injection. While that reduced the percentage of dietary and tissue PUFA, both studies still used enough PUFA to avoid EFA deficiency. If the diet had been completely devoid of PUFA I suspect the beneficial effects of stearic acid against cancer would have been dramatically more pronounced.
The first study is particularly interesting as it shows that the so-called "triple negative" breast cancers, which are highly aggressive and hard to treat, require PUFA's metabolites in order to develop.


Genetic induction and upregulation of cyclooxygenase (COX) and aromatase (CYP19): an extension of the dietary fat hypothesis of breast cancer. - PubMed - NCBI
"...The key feature of the model is elucidation of a common mechanism by which inappropriate induction and upregulation of estrogen biosynthesis occurs with regularity in the ductal epithelium of the mammary gland. Since estrogen is under tight homeostatic regulation, it is hypothesized that the loss of control is facilitated primarily through a second biosynthetic pathway inextricably linked to estrogen biosynthesis. The prostaglandin (PG) cascade is sufficient for this purpose. It is ubiquitous in all cells including mammary epithelium and its controlling genes (especially COX-2) are readily induced and upregulated by a number of intra- and intercellular effector molecules including viral and bacterial antigens, growth regulatory factor and, most importantly, arachidonic acid, which serves as the pathway’s primary substrate (11). In US women, the sustained presence of excess arachidonic acid results from excess consumption of red meat and certain vegetable oils rich in the essential polyunsaturated fatty acid, linoleic acid (12,13). Upon entering adipose and muscle cells, linoleic acid is converted to arachidonic acid which, in turn, activates constitutive transcription and translation of COX genes in the mammary epithelium, thereby leading to autocrine and paracrine effects of mutagenesis (tumor initiation), mitogenesis (tumor promotion), and angiogenesis (tumor metastasis). The model is therefore an extension of the dietary fat hypothesis of breast cancer and, since NSAIDs selectively inhibit cyclooxygenase, it portends an important new area of research in breast cancer chemoprevention (14,15)."


Effects of dietary fatty acids on breast and prostate cancers: evidence from in vitro experiments and animal studies. - PubMed - NCBI
"...Linoleic acid, an n-6 polyunsaturated fatty acid, is essential for normal mammary tissue development, at least in part because it provides the metabolic precursor required for the biosynthesis of key eicosanoids. A similar requirement applies to the growth of estrogen-independent but apparently not to estrogen-dependent rodent mammary and human breast carcinoma cells in vitro. By way of lipoxygenase products, n-6 fattyacids also regulate expression of the invasive phenotype. High-fat, linoleic acid-rich diets promote chemically induced rat mammary carcinogenesis, virally induced mouse mammary tumor development, and the growth and metastasis of estrogen-independent human breast cancer cells in athymic nude mice. In contrast, saturated fatty acids have no discernible effects on mammary carcinogenesis or progression. Most mechanistic studies have focused on the cyclooxygenase and lipoxygenase products of n-6 fatty acid metabolism, and support is accumulating for interactions between these eicosanoids and growth factors and oncogenes. The investigation of dietary fatty acids in prostate cancer is at an early stage and has been handicapped by a lack of satisfactory animal models. However, there are indications that the n-6 fatty acids perform functions in experimental prostate cancer progression similar to those described for breast cancer."


Effect of dietary stearic acid on the genesis of spontaneous mammary adenocarcinomas in strain A/ST mice. - PubMed - NCBI
"...A few studies have attempted to identify the role of individual dietary fatty acids. Hillyard et al. (1980) observed enhanced growth of transplanted tumors in rats when as little as 0.1 % linoleate was added to a fatfree diet. Chan et al. (1983) reported that the major factor influencing the incidence of tumors induced by N-nitrosomethylurea is the total oleate and linoleate content of a high-fat diet. Tinsley et al. (1981), using statistical methods to isolate the effects of individual dietary fatty acids on the incidence of spontaneous mammary tumors in C3H mice, concluded that linoleate, but not oleate, was essential for tumor development. Increased amounts of stearate were associated with lower tumor incidence. In the present study a 15 % fat diet containing over 13% stearic acid was used to determine the effect of this saturated fatty acid on the genesis of spontaneous mammary adenocarcinomas in strain A/St mice. The level of linoleate was sufficient to support normal growth of the animals, allowing the experiments to continue over a 2-year period. Fatty acid distributions of tumors and mammary gland tissues of mice fed the experimental diet were compared to those in tissues excised from mice fed a low-fat (4.5 %) stock diet."

"...Results of this study demonstrate that a high-fat diet per se does not stimulated the development of spontaneous mammary adenocarcinomas in mice. In fact, when stearic acid was used as the major lipid component in a high-fat diet, the development of initial tumors was delayed. The significant increase in the latency period in mice shifted to the SA diet at 11 Yz months of age indicates that the effect of dietary fat on mammary carcinogenesis in mice is not necessarily a long-term effect. This would be consistent with previous observations that dietary fat acts as a promoter in the preneoplastic stage of tumor development. Stearic acid was chosen as the fatty acid to be investigated because it can be acted on by the animal’s desaturaseelongation system, but cannot be converted into linoleic acid and other prostaglandin-active fatty acids. These desaturase systems are related and subject to dietary regulation (Kurata and Privett, 1980). Thus, a large amount of stearic acid might interfere with the synthesis of arachidonic acid from the available linoleic acid. Unlike many of the saturated fat diets used in studying tumorigenic properties of fat, the SA diet contained sufficient linoleic acid to produce normal growth, prevent EFA deficiency symptoms, and sustain mice in a study that would extend over a period of 2 years. Both the stock and the SA diet contained less than then 3 % linoleic acid considered optimal for tumor production (Carroll, 1975); still the production of tumors in mice fed the SA diet was delayed when compared to that in animals fed the low-fat stock diet."

"...If dietary fat, or more specifically linoleic acid, does promote the neoplastic process by limiting the host responsiveness during the early stages of tumor development, the results of fatty acid analysis of mammary gland tissues of mid-pregnant mice are of particular significance. These tissues have a lower percentage of 18:2 available for the synthesis of membranes or arachidonic acid and the prostaglandins. The higher percentage of 18:2 found in the plasma membranes of mammary gland tissues suggests that available 18:2 may be used preferentially for the synthesis of membranes, thus maintaining the fluidity of the membrane. If so, less 18:2 would be available for the tumor-enhancing process. These results are in agreement with those of Tinsley et al. (1981) who found that increasing levels of stearate in high-fat diets were associated with decreased tumor incidence and increased time to tumor development in C3H mice. Other workers have reported that stearic acid differs from other saturated fatty acids in its physiological and biochemical effect. For example, when compared to other saturated fatty acids, stearate has a greater effect on liver lipids, plasma cholesterol and the cholesterol content of the liver (Caster et al., 1975). Stearate is also more effective than palmitate or oleate in inhibiting fatty acid synthesis in Ehrlich cells (McGee and Spector, 1974) hepatocytes (Goodridge, 1973) and fibroblasts (Jacobs and Majerus, 1973). Further, stearate has been reported to inhibit the growth of normal and neoplastic rat mammary epithelial cells (Wicha et at., 1979). Concentrations of other lipid components of tumors and mammary gland tissues of mice fed the SA diet are currently being determined."

Stearic acid and carcinogenesis. - PubMed - NCBI
"...Corvin et al. (1977) have also shown that alteration of membrane lipid structure may change the cancer cell phenotype. The evidence for decreased membrane rigidity in malignant cells is derived from direct physical measurements and lipid analysis. Using fluorescent probes and magnetic resonance studies, decreased microviscosity (decreased membrane rigidity) was found in plasma membranes, as well as in isolated lipid vesicles from leukaemic cells (Petitou et al., 1978; Mountford et al., 1986). Fatty acid analysis of lipids extracted from transformed cells, cell lines, leukaemic cells and solid tumour tissue showed a consistent increase in the oleic acid content relative to stearic acid (Apostolov et al., 1985; Wood et al., 1985)."

"...The normal metabolic flow results in conversion of the saturated stearic acid to the monounsaturated oleic acid by the enzyme complex delta 9 desaturase. The ratio of stearic to oleic acid, the so-called saturation index (SI), reflects the activity of this enzyme (Wood et al., 1985). A significant decrease in the SI of red blood cell membranes was noted in a range of human (Wood et al., 1985) and animal malignancies (Habib et al., 1987b), and it was suggested that this index could be used as a tumour marker. It has also been reported that there is a decrease in the SI of red blood cell membranes in patients suffering from the Acquired Immune Deficiency Syndrome (Apostolov et al., 1987)."

"...These findings prompted the study of the possible use of exogenous stearic acid to prevent or reverse the desaturation of cell membrane stearic acid and thereby inhibit cell division both in vitro and in vivo."

"...Thirty female Sprague-Dawley rats weighing -200g each were divided into 2 groups. The first (n=20) received NMU only, the second (n = 10) received NMU plus stearic acid. NMU in 3% acetic acid (Sigma Chemicals, UK) was dissolved in distilled water (20mgml-1) and was given in three i.v. injections of 5mg 100 g1 body wt, at weeks 1, 4 and 8. Stearic acid (Sigma Chemicals, UK) (0.5 mg) dissolved in liquid paraffin (0.5ml) was injected at weekly intervals s.c. in the flank, starting from the second week. The parenteral route of administration was preferred for our study in order to avoid first call metabolism by the liver of orally-administered lipids."

"...The onset of tumours was monitored by daily inspection and by palpation of the mammary regions twice weekly. At week 22 of the experiment, all surviving animals were sacrificed, autopsies were performed and the tumours were dissected and examined histologically."

"...Nineteen of the 20 rats in the NMU alone group developed mammary tumours by week 16 of the experiment, with a mean latent period of 72 days. These 19 rats had a total of 51 tumours, giving a mean of 2.68 tumours/rat, range 1-5. The range of tumour weight/rat was 5 g to 47.8 g with a mean of 23.6/rat, excluding the tumour free rats. Five of the 10 rats in the NMU plus stearic acid group developed mammary tumours by week 16 of the experiment, with a mean latent period of 74 days. These 5 rats had 7 tumours between them, with a mean of 1.4 tumours/rat (compared to NMU alone group P<0.001). The range of tumour weight/rat was 4.2g to 21.2g, with an average of 16.4g/rat (P<0.01 compared to NMU alone group). By week 22, 19 of the 20 rats in the NMU group were dead with tumours, in contrast with only 2 of 10 rats in the NMU+stearic acid group. Of the remaining 8 that were killed, only 3 had tumours and 5 were tumour-free. All tumours were examined histologically and were adenocarcinomas."

"...This study has shown that stearic acid significantly inhibits the colony-forming ability of some tumour cell lines, in a dose-related manner. Although human cancer cells appear more sensitive to stearic acid than rat cancer cells, the methodology and culture conditions differed. Other workers have shown a similar effect in vitro with a non selective incorporation of fatty acids into cell phospholipids (Doi et al., 1978; Wicha et al., 1979). In those studies the addition of oleic acid had either no effect or stimulated cell division. An important feature of our work has been the demonstration that parenteral administration of stearic acid in vivo can prevent the development of tumours in an experimental animal model. We have also provided indirect evidence that inhibition of mammary carcinogenesis is linked to the maintenance of a normal saturation index within the cell membranes. By preserving the ratio of saturated to unsaturated fatty acid, the membrane rigidity remains normal and cell division is inhibited. Those animals that developed tumours despite treatment with stearic acid had significantly fewer and smaller tumours than the animals given carcinogen alone. Their saturation index in erythrocyte membranes was lower than that of tumour-free animals, but was still significantly higher than that of rats given carcinogen without stearic acid. These observations on the erythrocyte saturation index were the same whether the rats were injected with stearic acid or iodostearic acid (data not included)."

"...We have previously shown (Wood et al., 1985) that a decrease in the saturation index of red blood cell membranes is a characteristic finding in patients with a variety of cancers. That this is a reversible change is shown by the return to normal of the saturation index after surgical excision of the tumour, and a subsequent fall with tumour recurrence. Erythrocytes were chosen because they are endstage non-dividing cells with only one plasma membrane. The extraction procedure used measured the total fatty lipids of the cell membrane rather than the free fatty acids. We have also shown that the drop in saturation index of erythrocytes observed in human cancer can also be seen in rats developing colonic carcinomas following exposure to dimethylhydrazine (Habib et al., 1987b), but does not occur in rats with nutritional cachexia (unpublished observation). Similar changes in cell membrane lipid composition also occur in human leucocytes and platelets in cancer patients (Apostolov et al., 1985), suggesting the presence of a desaturation producing factor (DPF) released by the tumour (Habib et al., 1987a). We therefore postulate that an alteration in the fatty acid composition of cell membranes may play a role in the carcinogenic process (Habib et al., 1987b)."
So here's the bottom line to cut through the tripe.Essential fatty acids are at least 25-33% of the cellular membrane.. ie the construction of the membrane. They if unadulterated allow and facilitate the passage of oxygen along with other nutrients into the mitochondria.They , if unadulterated, which you all are talking about... adulterated, hydrogenated, trans fats. I have to ask myself.. what planet am i on? Real studies have proven the the life essence of L.A. and ALA in our existence, the production of prostaglandins and the benefits of Arachadonic Acid . Pge1 and pgi2 are produced from the EFAs. Ecosinoids and the regulation of platelets. EFAs, L.A. and ALA are the secret to life .. unadulterated.No more studies needed.. professor Crawford.
 
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