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NBE-Research
#11
This IS interesting,

Prostaglandins Leukot Essent Fatty Acids. 1994 Dec;51(6):437-43.

Omega-3 and omega-6 fatty acids and PGE2 stimulate the growth of normal but not tumor mouse mammary epithelial cells: evidence for alterations in the signaling pathways in tumor cells.

McKenzie KE1, Bandyopadhyay GK, Imagawa W, Sun K, Nandi S.
Author information
Abstract
The direct effect of omega-3 and omega-6 fatty acids on the proliferation of mouse mammary tumor cells (MTC) was examined in a serum-free cell culture system. While the EGF-induced proliferation of normal mammary epithelial cells was shown to be enhanced by omega-3 and omega-6 fatty acids and prostaglandins (PGs), a majority (75-80%) of primary mammary tumors were not stimulated by these agents. Compared to normal cells, some MTC cultures showed a higher susceptibility to inhibition by omega-3 fatty acids. The general lack of response of MTC cultures to PGE2 and cyclic adenosine monophosphate (cAMP) suggests some alterations in the cAMP-mediated pathway. However, the PGE2-induced cAMP levels and cAMP-dependent protein kinase (PKA) activities in the tumor cells were comparable to normal cells. We conclude that the proliferation of mammary tumor cells either follow a cAMP-PKA-independent pathway or have some alterations in the serine/threonine kinase mediated signaling pathway.
PMID: 7535935 [PubMed - indexed for MEDLINE]
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#12
Ok, now we're making some progress, "linoleic acid (18:2 omega 6) and prostaglandin E2 or cAMP has synergistic effect on EGF-stimulated growth".

(Linoleic acid is evening primrose oil.)

transducers: amplification of signals from growth factor receptors by fatty acids in mammary epithelial cells.

Abstract
The growth, morphogenesis and differentiation of milk producing epithelial tissues in the developing mammary glands require interaction with extracellular matrices and stimulation by hormones, growth factors and essential fatty acids. In primary culture, the proliferation of mammary epithelial cells (MEC), induced by epidermal growth factor (EGF), is enhanced and sustained by linoleate and its eicosanoid metabolites. Since a combination of linoleic acid (18:2 omega 6) and prostaglandin E2 or cAMP has synergistic effect on EGF-stimulated growth, it is suggested that additional cAMP-dependent protein kinase A (PK-A) independent pathways may also contribute to the linoleate effect on EGF action. Possible involvement of Ca2+/phospholipid-dependent protein kinase C (PK-C) is explored. Both linoleate and arachidonate can activate Type-II and Type-III protein kinase-C in MEC and a PK-C inhibitor can block growth stimulation by EGF and fatty acids. Like 12-O-Tetradecanoly phorbol-13-acetate (TPA), a PK-C activator which also enhances EGF-stimulated growth of MEC, linoleate can phosphorylate a 40-42 KD protein. EGF itself can stimulate transient phosphorylation of the same protein in MEC cultures but when supplemented with linoleate, which does not influence the ligand binding affinity of EGF-receptors, the transient phosphorylation signal in 40-42 KD protein is sustained.(ABSTRACT TRUNCATED AT 250 WORDS)

http://www.ncbi.nlm.nih.gov/pubmed/8424125
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#13
well done Lotus, you found the answer at this question:

"This is a big deal, so anything over
3000 mg of arachidonic acid AA goes to PGE2, but this corse (pathway) up regulate cancer cells (or said to be), what can stop that conversion process?"

Omega 3 fatty acids stop the cancer process.

So a good and healty program should include: omega 3-6 in a proper ratio (1:3, or 1:4), and GLA. Which amounts do you suggest?
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#14
The genius at work helping us understand ourselves through her dedication of helping others find their path . Is a gift and a joy to read about how change is possible if we just start to think outside the box . And with a little bit of imagination and using are minds and belief system we can generate and ignite the power to not only see the change when it happens but also feel it and make it are own. Smile

I just started on one of her programs and i'm very happy that she took the time to help me .

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#15
(17-04-2015, 08:57 AM)-Clelia- Wrote: well done Lotus, you found the answer at this question:

"This is a big deal, so anything over
3000 mg of arachidonic acid AA goes to PGE2, but this course (pathway) up regulate cancer cells (or said to be), what can stop that conversion process?"

Omega 3 fatty acids stop the cancer process.

So a good and healty program should include: omega 3-6 in a proper ratio (1:3, or 1:4), and GLA. Which amounts do you suggest?


Hi Clelia,

Good point about upping omega 3's, and thanks for the input, from what I've read there are certain omega 6's that create inflammation, GLA isn't one of them, e.g. EPO, borage oil, black currant oil. GLA is converted to DGLA which reduces inflammation. PGE2 concerns me, PGE1 reduces inflammation, although I'm not a fan of NSAIDS, (but I consider them to be pro-aromatase). EGF and PGE2 is a serious looking contender for aromatase potential.

IMO EPO is a EFA that should be in an NBE program, it takes consistent use (4-6 months) 2000 to 3000 mg (possibility to increase) before the full benefits are seen. But I see thats par for the course considering NBE is long term. But EFA's are something we should be using long term anyways.

Big Grin
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#16
(18-04-2015, 03:28 AM)karen557 Wrote: The genius at work helping us understand ourselves through her dedication of helping others find their path . Is a gift and a joy to read about how change is possible if we just start to think outside the box . And with a little bit of imagination and using are minds and belief system we can generate and ignite the power to not only see the change when it happens but also feel it and make it are own. Smile

I just started on one of her programs and i'm very happy that she took the time to help me .


Oh stop that lol, Tongue

People might think you're on the payroll, lol j/k Wink seriously though, I'm touched, thank you so much. But I agree "think outside the box",

Btw, I love this....

(18-04-2015, 03:28 AM)karen557 Wrote: And with a little bit of imagination and using are minds and belief system we can generate and ignite the power to not only see the change when it happens but also feel it and make it are own. Smile


That's genius CoolSmile
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#17
Here's an interesting research paper on phytoestrogens and target tissues. The bottome line is that most phytoestrogens increase blood flow in humans (vasodilation). Interactions are important for people to understand, increasing blood flow means NOT to take anything else that increases bleeding (e.g. blood thinning agents like warfarin and others). This finding reinforces that increasing the dosages of phytoestrogens have little to no benefit. Smaller dosages of certain phytoestrogens that target certain tissues (estrogen receptor alpha-aka ER-a mammary and ER-b (beta) Bone) progesterone receptor (e.g. Vitex, FG, Progesterone cream, essential fatty acids EFA's) and NBE super foods continues to out perform PM only intake.

intakes must be above a relatively high threshold level for a lengthy period of time, and little or no extra benefit is observed with intakes above this threshold level.

phyto-oestrogens on tissues.
Anderson JJ1, Anthony M, Messina M, Garne SC.
Author information
Abstract
Recent investigations on the effects of phyto-oestrogens on various tissues have revealed that these diverse molecules may improve human health, particularly by protecting against certain chronic diseases. After a brief examination of the food sources, structures, and general cellular actions of the major phyto-oestrogens, current research findings on cardiovascular disease, skeletal tissues, and reproductive cancers are reviewed. Phyto-oestrogen concentrations in blood may be maintained at high levels in those consuming soyabean (Glycine max)-based food daily at several meals and exert their effects on target cells through either genomic effects via the classical oestrogen receptors or non-genomic effects mediated by membrane-bound oestrogen receptors or other cellular proteins. The expression of oestrogen receptor (OR) subtypes alpha (a) and beta (beta) varies across tissues, and cells that preferentially express OR-beta, which may include bone cells, are more likely to respond to phyto-oestrogens. Conversely, reproductive tissues contain relatively more OR-a and may, thus, be differently affected by phyto-oestrogens. Soyabean phyto-oestrogens appear to prevent the progression of atherosclerosis through multiple interactions, including lowering of plasma lipids and lipoproteins, increased vasodilatation and, possibly, decreased activation of blood platelets and vascular smooth muscle cells. However, a favourable impact on cardiovascular disease morbidity and mortality by a soyabean-enriched western-type diet remains to be shown, and unresolved questions remain regarding dose and form of the phyto-oestrogens in relation to risks and benefits. The isoflavones of soyabean have been shown consistently to have bone-retentive effects in animal studies by several investigators using rodent models, although intakes must be above a relatively high threshold level for a lengthy period of time, and little or no extra benefit is observed with intakes above this threshold level. The reports of modest or no effects on prevention of bone loss in human and non-human primate studies respectively, may be due to the limited doses tested so far. The relationship between soyabean-food intake and cancer risk has been more extensively investigated than for any other disease, but with less certainty about the benefits of long-term consumption of phyto-oestrogen-containing foods on prevention of cancer. The observations that breast and prostate cancer rates are lower in Asian countries, where soyabean foods are consumed at high levels, and the high isoflavone content of soyabeans have led to examination of the potential protective effects of phyto-oestrogens. Establishing diet-cancer relationships has proved difficult, in part because of the conflicting data from various studies of effects of soyabean-diets on cancer. Epidemiological evidence, though not impressive, does suggest that soyabean intake reduces breast cancer risk. The isoflavone genistein has a potent effect on breast cancer cells in vitro, and early exposure of animals to genistein has been effective in reducing later development of mammary cancer. Thus, continuous consumption of soyabean foods in early life and adulthood may help explain the low breast cancer mortality rates in Asian countries. Although the evidence for a protective effect against prostate cancer may be slightly more supportive, more research is needed before any firm conclusions can be made about the phyto-oestrogen-cancer linkages.

http://www.ncbi.nlm.nih.gov/pubmed/19087447
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#18
Hi Clelia,

When you get some time I'd like to talk about Lipoenesis-
De Novo Synthesis in Humans

In humans, fatty acids are formed predominantly in the liver and lactating mammary glands, and, to a lesser extent, the adipose tissue. Most acetyl-CoA is formed from pyruvate by pyruvate dehydrogenase in the mitochondria. Acetyl-CoAproduced in the mitochondria is condensed with oxaloacetate by citrate synthase to form citrate, which is then transported into the cytosol and broken down to yield acetyl-CoA and oxaloacetate by ATP citrate lyase. Oxaloacetate in the cytosol is reduced to malate by cytoplasmic malate dehydrogenase, and malate is transported back into the mitochondria to participate in the Citric acid cycle.
http://en.m.wikipedia.org/wiki/Fatty_acid_biosynthesis

Thus, stimulation of this lactogenic function by prolactin is not the result of its contamination with vasopressin. And vasopressin increases lipogenesis availability of lipogenic substrate (lactate+ pyruvate) and by activating acetyl-CoA carboxylase. Vasopressin (pituitary hormone, up regulates BP and water retention) stimulates fatty acid synthesis by 30-110%, but also up regulates BP and water rentention. Progesterone stimulates alveolar growth, estrogen stimulates ducal growth. Fatty acid synthesis stimulates mammary epithelial growth factor.

Oxytocin and Vasopressin: Genetics and Behavioral Implications
http://refworks.springer.com/mrw/fileadm...480C25.PDF

__________________________________

The pathway for fatty acid synthesis occurs in the cytoplasm, whereas, oxidation occurs in the mitochondria. (Preventing oxidation is the key, it's that ratio again lol, more omega 3's). IMO, a dose of 2000-3000mg of omega 3 to 1000mg of omega 6, 1:3

Metabolism uses various ways to ensure that 2 opposing pathways do not occur at the same time. For the following pair of pathways list 2 ways (different cell location, allosteric effector, covalent modification, different intermediate, different enzyme, or different means of transport).
https://brainmass.com/chemistry/acid-and...her-109814

Fatty acid oxidation and fatty acid synthesis are different from one another in following respects: The pathway for fatty acid synthesis occurs in the cytoplasm, adipose and liver whereas, oxidation occurs in the mitochondrial matrix and muscle.

The other major difference is the use of nucleotide co-factors. Oxidation of fats involves the reduction of FADH+ and NAD+. Synthesis of fats involves the oxidation of NADPH.

Lipoenesis stimulates breast growth, Lipogenesis is the process by which acetyl-CoA is converted to fatty acids. Lipogenesis encompasses both the process of fatty acid synthesis and triglyceride synthesis (where fatty acids are esterifiedwith glycerol to form fats).[1] The products are secreted from the liver in the form of very-low-density lipoproteins (VLDL). VLDL are secreted directly into blood, where they mature and function to deliver the endogenously derived lipids to peripheral tissues.
http://en.m.wikipedia.org/wiki/Fatty_acid_synthesis

Glycerol-3-phosphate dehydrogenase (GAPDH) enzyme which increases Adipocyte volume in the fatty breast tissues.

http://www.nature.com/nrmicro/journal/v5...617-f1.jpg
http://www.nature.com/nrmicro/journal/v5...17_F1.html

http://themedicalbiochemistrypage.org/li...thesis.php

Activation of AMP-activated protein kinase stimulates the nuclear localization of glyceraldehyde 3-phosphate dehydrogenase in human diploid fibroblasts.______________________________________________________________
In addition to its well-known glycolytic activity, GAPDH displays multiple functions, such as nuclear RNA export, DNA replication and repair, and apoptotic cell death. This functional diversity depends on its intracellular localization. In this study, we explored the signal transduction pathways involved in the nuclear translocation of GAPDH using confocal laser scanning microscopy of immunostained human diploid fibroblasts (HDFs). GAPDH was present mainly in the cytoplasm when cultured with 10% FBS. Serum depletion by culturing cells in a serum-free medium (SFM) led to a gradual accumulation of GAPDH in the nucleus, and this nuclear accumulation was reversed by the re-addition of serum or growth factors, such as PDGF and lysophosphatidic acid. The nuclear export induced by the re-addition of serum or growth factors was prevented by LY 294002 and SH-5, inhibitors of phosphoinositide 3-kinase (PI3K) and Akt/protein kinase B, respectively, suggesting an involvement of the PI3K signaling pathway in the nuclear export of GAPDH. In addition, 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR), an activator of AMP-activated protein kinase (AMPK), stimulated the nuclear translocation of GAPDH and prevented serum- and growth factor-induced GAPDH export. AMPK inhibition by compound C or AMPK depletion by siRNA treatment partially prevented SFM- and AICAR-induced nuclear translocation of GAPDH. Our data suggest that the nuclear translocation of GAPDH might be regulated by the PI3K signaling pathway acting mainly as a nuclear export signal and the AMPK signaling pathway acting as a nuclear import signal.
http://www.ncbi.nlm.nih.gov/pubmed/20177150/

Biotin breaks down carbs and fats, the speed of which I don't know yet, ALA, B5, eggs whites cause interactions. What do you think?. Potentiator?

(Biotin is a coenzyme for carboxylase enzymes, involved in the synthesis of fatty acids, isoleucine, and valine, and in gluconeogenesis.)


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#19
Research is like a box of chocolate, Rolleyes you never know what you'll get. Big Grin

SHBG secretes from the liver, and as we know SHBG is a transport protein (plasma) which then carries estrogens and androgens, albumin carries active hormones. The research states (SHBG-sex hormone binding globulin) could control local concentrations of SHBG in the breast and prostate, "thereby regulating RSHBG activation in an autocrine/paracrine manner". In other words quote- the local production of SHBG obtained with transfection could be a useful tool to control cell growth in estrogen-dependent breast cancer. This indicates SHBG can inhibit estradiol. (Now that's pretty cool). Cool
Sex hormone-binding globulin, its membrane receptor, and breast cancer: a new approach to the modulation of estradiol action in neoplastic cells.
http://www.ncbi.nlm.nih.gov/pubmed/10419...t=Abstract

The source of the SHBG that initializes RSHBG signaling in vivo is unclear; it could be taken up from the plasma, where it is relatively abundant, or synthesized in cells in which signaling occurs. In addition to the liver which is well known to be the source of plasma SHBG, and testis (which synthesizes the differentially glycosylated SHBG isoform, androgen binding protein (ABP), SHBG protein and mRNA have been demonstrated in other human tissues, including the prostate and breast [15-19]. The relatively stable concentration of plasma SHBG [20] makes it a less likely source for the initiation of RSHBG signaling, as the physiology of important signaling molecules depends on their variation with time. Other, more variable sources of SHBG would be better candidates. This raises the possibility that the prostate and breast themselves could control local SHBG concentrations, thereby regulating RSHBG activation in an autocrine/paracrine manner.

Human sex hormone-binding globulin gene expression- multiple promoters and complex alternative splicing http://www.ncbi.nlm.nih.gov/pmc/articles...-10-37.pdf











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#20
Ok, I'm gonna give this a shot at defining why essential fatty acids (EFA's) are important for NBE, any car buffs Lol?. Rolleyes

EFA's are like lubricants for car parts (e.g. molecules, steroids, DNA synthesis etc). They help help carry hormones to receptors, in other words, once they arrive at the cell membranes they (EFA's) make them more bioavailable. Soooo.....using these fat solubles supplements keep us squeaky, get it. Big Grin

   

Figure 1: Bioactive lipid synthesis, metabolism and signaling pathways.
http://www.nature.com/nchembio/journal/v...94_F1.html

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