[Lotus]

Thanks POM, DDs, (thanks). For the sake of purpose and anything short insanity (lol), I'm adding info on coconut oil (other fats too) here, in one spot if needed. Yup, it's long.

Coconut Oil- Makes connective tissues stronger, superb antioxidant, neutralizes free radicals and slowing down aging, aids in breast feeding, nature's richest source of MCFAs. 5 ar inhibitor, pro-aromatase. Btw, coconut oil raises body temp, great for thyroid help. (•y•) Denotes boob friendly (or imo an absolute NBE staple). CO oil helps to bind estrogen receptors.

raising body temp activates exactly what?........metabolism (including aromatase).

Some recent research show Aromatase expression in homogenates from scAT was 213% higher. In other words, aromatase in subcutaneous fat is 213% higher.


Br J Nutr. 2014 May 28;111(10):1782-90. doi: 10.1017/S000711451400004X. Epub 2014 Feb 11.
Influence of virgin coconut oil-enriched diet on the transcriptional regulation of fatty acid synthesis and oxidation in rats - a comparative study.
Arunima S1, Rajamohan T1.
Author information

Abstract
The present study was carried out to evaluate the effects of virgin coconut oil (VCO) compared with copra oil, olive oil and sunflower-seed oil on the synthesis and oxidation of fatty acids and the molecular regulation of fatty acid metabolism in normal rats. Male Sprague-Dawley rats were fed the test oils at 8 % for 45 d along with a synthetic diet. Dietary supplementation of VCO decreased tissue lipid levels and reduced the activity of the enzymes involved in lipogenesis, namely acyl CoA carboxylase and fatty acid synthase (FAS) (P< 0·05). Moreover, VCO significantly (P< 0·05) reduced the de novo synthesis of fatty acids by down-regulating the mRNA expression of FAS and its transcription factor, sterol regulatory element-binding protein-1c, compared with the other oils. VCO significantly (P< 0·05) increased the mitochondrial and peroxisomal β-oxidation of fatty acids, which was evident from the increased activities of carnitine palmitoyl transferase I, acyl CoA oxidase and the enzymes involved in mitochondrial β-oxidation; this was accomplished by up-regulating the mRNA expression of PPARα and its target genes involved in fatty acid oxidation. In conclusion, the present results confirmed that supplementation of VCO has beneficial effects on lipid parameters by reducing lipogenesis and enhancing the rate of fatty acid catabolism; this effect was mediated at least in part via PPARα-dependent pathways. Thus, dietary VCO reduces the risk for CHD by beneficially modulating the synthesis and degradation of fatty acids.

Hi Balance321,
Consider coconut oil,


Coconut oil-makes connective tissues stronger for that much desired softness and elasticity. superb antioxidant activities that neutralize free radicals and slowing down aging, aids in breast feeding, Coconut oil is nature's richest source of MCFAs."

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Coconut oil is a 5 alpha reductase-which means it blocks the most potent androgen DHT (dihydrotestosterone) from testosterone

And according to the study below, Lauric Acid, which coconut oil has @ 50%, it's effect is inhibition in the epithelium and stroma as follows: 51% and 42% (lauric acid)

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Why Coconut Oil Is So Good For Pregnant & Nursing Mothers
http://www.modernmom.com/c3443748-3b35-1...4a41e.html

Coconut oil contains large amounts of lauric acid, a powerful anti-microbial fatty acid that protects the immune system of the fetus and newborn. Pregnant and nursing mothers should eat coconut oil to increase the quality of the womb environment and breast milk” - Dr. Claudia Pillow

healthy diet contains mixtures of saturated, monounsaturated and polyunsaturated fats. The unique composition of human breast milk contains about 45 to 50 % saturated fat, about 35% unsaturated and 15-20%polyunsaturated. Lauric acid and capric acid comprise about 20% of total saturated fatty acids found in breast milk. Lauric and capric acid have potent antiviral, antibacterial, and parasiticidal (kills parasites) properties that support the immune system. These fatty acids offer the nursing infant protection from illnesses, viruses such as herpes and HIV, protozoa such as giardia lamblia, and bacteria such as chlamydia and heliocobater.

Coconut oil is high in saturated fat (but not cholesterol since it is from a plant) containing about 50% lauric acid. Other components of coconut oil include capric acid, caprylic acid, tocopherols and tocotrienols. (Vitamin E lipids that act as potent anti-oxidants that can help maintain healthy cell structure and function). A study published in the American Journal of Clinical Nutrition has shown that lactating mothers who eat coconut oil and other coconut products, have significantly increased levels of lauric acid and capric acid in their breast milk, creating milk rich in health promoting nutrients. Coconut oil is easy for an infant’s immature digestive system to absorb and utilize. It also provides energy in the form of medium chain fatty acids to help the baby grow and develop properly.



IDS 89 and its subfractions on 5 alpha-reductase activity in human benign prostatic hyperplasia.

Abstract
Extract from fruit of Sabal serrulata are used in the treatment of human benign prostate hyperplasia (BPH). Therefore, it is of interest whether this phytopharmacon has any influence on the androgen metabolism in the human prostate. It was found that the extract IDS 89 of Sabal serrulata inhibited dose dependently 5 alpha-reductase activity in the epithelium and stroma of human BPH, the mean inhibition being 29% and 45%, respectively. This inhibitory effect is mainly due to the saponifiable subfraction of IDS 89 showing a mean 5 alpha-reductase inhibition of 39% and 38% in epithelium and stroma, respectively. The inhibition was dose dependent and noncompetitive. At a testosterone concentration of 580 nM as substrate for 5 alpha-reductase, the main fatty acids of the extract IDS 89 gave rise to a percentual enzyme inhibition in the epithelium and stroma as follows: 51% and 42% (lauric acid), 5% and 0% (oleic acid), 43% and 34% (myristic acid), 2% and 0% (palmitic acid), respectively. The inhibitory effect of lauric acid was noncompetitive and dose dependent up to a concentration of 0.2 nM, the maximal inhibition in the epithelium and stroma being 52% and 45%, respectively. The nonsaponifiable subfraction, consisting mainly of phytosterols, showed a mean inhibition of 5 alpha-reductase in the epithelium and stroma of 15% and 10%, respectively. Finally, the hydrophilic subfraction, containing carbohydrates, amino acids, and polysaccharides, showed no inhibitory effect. The present in vitro studies suggest that the Sabal serrulata extract IDS 89 has an inhibitory effect on 5 alpha-reductase in the epithelium and stroma of human BPH. This inhibition is mainly due to the fatty acids of the saponifiable subfraction.

** fatty acid synthase (FASN) in (humans)

Gene ID: 2194, updated on 21-Mar-2015

The enzyme encoded by this gene is a multifunctional protein. Its main function is to catalyze the synthesis of palmitate from acetyl-CoA and malonyl-CoA, in the presence of NADPH, into long-chain saturated fatty acids. In some cancer cell lines, this protein has been found to be fused with estrogen receptor-alpha (ER-alpha), in which the N-terminus of FAS is fused in-frame with the C-terminus of ER-alpha. [provided by RefSeq, Jul 2008]
http://www.ncbi.nlm.nih.gov/gene/2194

More scientific proof that fatty acids helps with the binding process of estrogen receptor alpha (ER-a, the growth receptor). Specifically---palmitate (a solid unsaturated fat). I hope this is making sense for everybody. In other words- omega 3's and 6's needs to be in an NBE plan, the health benefits alone are worth looking into, another benefit is its ability to block DHT (e.g. Evening primrose oil, EPO).

Coconut oil
Evening primrose oil
Macadamia nut oil
Krill oil

And organic when possible.

I want to link these posts together, hopefully you'll see the importance of how fatty acids can and does have a huge impact on NBE. And considering how effective FA's are in low concentrations it's particularly appealing.


Inhibition of steroid 5 alpha-reductase by specific aliphatic unsaturated fatty acids.

Human or rat microsomal 5 alpha-reductase activity, as measured by enzymic conversion of testosterone into 5 alpha-dihydrotestosterone or by binding of a competitive inhibitor, [3H]17 beta-NN-diethulcarbamoyl-4-methyl-4-aza-5 alpha-androstan-3-one ([3H]4-MA) to the reductase, is inhibited by low concentrations (less than 10 microM) of certain polyunsaturated fatty acids. The relative inhibitory potencies of unsaturated fatty acids are, in decreasing order: gamma-linolenic acid greater than cis-4,7,10,13,16,19-docosahexaenoic acid = cis-6,9,12,15-octatetraenoic acid = arachidonic acid = alpha-linolenic acid greater than linoleic acid greater than palmitoleic acid greater than oleic acid greater than myristoleic acid. Other unsaturated fatty acids such as undecylenic acid, erucic acid and nervonic acid, are inactive. The methyl esters and alcohol analogues of these compounds, glycerols, phospholipids, saturated fatty acids, retinoids and carotenes were inactive even at 0.2 mM. The results of the binding assay and the enzymic assay correlated well except for elaidic acid and linolelaidic acid, the trans isomers of oleic acid and linoleic acid respectively, which were much less active than their cis isomers in the binding assay but were as potent in the enzymic assay. gamma-Linolenic acid had no effect on the activities of two other rat liver microsomal enzymes: NADH:menadione reductase and glucuronosyl transferase. gamma-Linolenic acid, the most potent inhibitor tested, decreased the Vmax. and increased Km values of substrates, NADPH and testosterone, and promoted dissociation of [3H]4-MA from the microsomal reductase. gamma-Linolenic acid, but not the corresponding saturated fatty acid (stearic acid), inhibited the 5 alpha-reductase activity, but not the 17 beta-dehydrogenase activity, of human prostate cancer cells in culture. These results suggest that unsaturated fatty acids may play an important role in regulating androgen action in target cells.

Inhibition of steroid 5 alpha-reductase by specific aliphatic unsaturated fatty acids.
http://www.ncbi.nlm.nih.gov/pubmed/1637346

GLA- gamma-Linolenic acid (like EPO evening primrose oil),

gamma-Linolenic acid does not inhibit 17 beta HSD dehydrogenase activity, which one has yet to be identified


Btw, 17beta-hydroxysteroid dehydrogenases (17beta-HSDs) play an important role in the regulation of steroid hormones, such as estrogens and androgens.

http://www.ncbi.nlm.nih.gov/pubmed/12570693

It was only a matter of time when this info would be found, enjoy.

Inhibition of steroid 5a-reductase by specific aliphatic unsaturated/fattyacid
http://www.ncbi.nlm.nih.gov/pmc/articles...1-0210.pdf

fatty acids could function as endogenous inhibitors of 5a-reductase


The most potent was y-Linolenic acid, GLA-aka EPO-Evening Primrose Oil.

From the first study,

Type 1 & 5 (17beta HSD) are breast growth potentiators

Thanks Lotus for this info. I really can use it. POM

Thanks Pom, I hope it helps.

PUFA's- polyunsaturated -fats increase estrogen.

Monounsaturated-fats increase testosterone

Polyphenols (specifically Green Tea) promotes aromatase, anti-oxidation, estrogen, modifies signaling transduction pathways, relieves oxidative stress (reduces lipid oxidation), possess potent iron-chelating radical-scavenging and anti-inflammatory activities (polyphenols are powerful free radical destroyers), protects against neurological diseases. Green tea catechins ameliorate adipose insulin resistance.

Sorry for the redundancy, but in case you missed it, this is extremely important:

Considering the potential to block DHT and increase aromatase adding fatty acids makes sense, only don't forget a fitness plan.

Anti-androgenic activity of fatty acids.

In this study, we show that 5alpha-reductase derived from rat fresh liver was inhibited by certain aliphatic free fatty acids. The influences of chain length, unsaturation, oxidation, and esterification on the potency to inhibit 5alpha-reductase activity were studied. Among the fatty acids we tested, inhibitory saturated fatty acids had C12-C16 chains, and the presence of a C==C bond enhanced the inhibitory activity. Esterification and hydroxy compounds were totally inactive. Finally, we tested the prostate cancer cell proliferation effect of free fatty acids. In keeping with the results of the 5alpha-reductase assay, saturated fatty acids with a C12 chain (lauric acid) and unsaturated fatty acids (oleic acid and alpha-linolenic acid) showed a proliferation inhibitory effect on lymph-node carcinoma of the prostate (LNCaP) cells. At the same time, the testosterone-induced prostate-specific antigen (PSA) mRNA expression was down-regulated. These results suggested that fatty acids with 5alpha-reductase inhibitory activity block the conversion of testosterone to 5alpha-dihydrotestosterone (DHT) and then inhibit the proliferation of prostate cancer cells.
http://www.ncbi.nlm.nih.gov/pubmed/19353546

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