This is another guess/question.
In the enormous complexity of the body how does oestrogen react with the desaturase pathway that makes the long chain fats DHA and EPA.
PGE2 produced via cox one and cox two control oestrogen according to trials, which pathway is used in AIs.
But does oestrogen somehow influence or control in part DHA production.
Given the rise in DHA production reported in pregancy, and the need for oestrogen in reprodution it would seem a reasonable question.
This trial would suggest that it may be the case that oestrogen controls production of DAH and EPA at least in part.
The consequence of oestrogen blocking would be blocking DHA and EPA production.
The implication of this for AI takers would be a need to take DHA and EPA.
Fish oil which contain DHA and EPA have been associated with dry eye improvement, dry mouth improvement, impovement in arthritis, and combined with a reduction in omega shix should help with weight loss.
This is the first trial I have seen directly suggesting oestorgen as a controller of the FAS pathways. If I find more I will post.
(Why not a cyclical feed back loop - no DHA EPA = upgrades of oestrogen levels to try and make fats required for reproductive / femininty, upgrades Fattty acid synthesis = impacts on growth factors. The counter of which would be supply DHA EPA - no need to make = downgrade oestrogen downgrade FAS etc. Added to this what happens if no omega three raw material and over supply PGE2 to P450 to E2 to growth factors through excess omega six in diet and membranes etc -?????????)
RB
http://www.ncbi.nlm.nih.gov/entrez/q...ats+desaturase
1: Proc Nutr Soc. 2006 Feb;65(1):42-50. Related Articles, Links
Click here to read
Long-chain n-3 PUFA: plant v. marine sources.
Williams CM, Burdge G.
Hihj Sinclair Unit Human Nutrition, School of Food Biosciences, University of Reading, UK.
c.m.williams@reading.ac.uk
Increasing recognition of the importance of the long-chain n-3 PUFA, EPA and DHA, to cardiovascular health, and in the case of DHA to normal neurological development in the fetus and the newborn, has focused greater attention on the dietary supply of these fatty acids. The reason for low intakes of EPA and DHA in most developed countries (0.1-0.5 g/d) is the low consumption of oily fish, the richest dietary source of these fatty acids. An important question is whether dietary intake of the precursor n-3 fatty acid, alpha-linolenic acid (alphaLNA), can provide sufficient amounts of tissue EPA and DHA by conversion through the n-3 PUFA elongation-desaturation pathway. alphaLNA is present in marked amounts in plant sources, including green leafy vegetables and commonly-consumed oils such as rape-seed and soyabean oils, so that increased intake of this fatty acid would be easier to achieve than via increased fish consumption. However, alphaLNA-feeding studies and stable-isotope studies using alphaLNA, which have addressed the question of bioconversion of alphaLNA to EPA and DHA, have concluded that in adult men conversion to EPA is limited (approximately 8%) and conversion to DHA is extremely low (<0.1%). In women fractional conversion to DHA appears to be greater (9%), which may partly be a result of a lower rate of utilisation of alphaLNA for beta-oxidation in women. However, up-regulation of the conversion of EPA to DHA has also been suggested, as a result of the actions of oestrogen on Delta6-desaturase, and may be of particular importance in maintaining adequate provision of DHA in pregnancy. The effect of oestrogen on DHA concentration in pregnant and lactating women awaits confirmation.
Publication Types:
* Review
PMID: 16441943 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum
1: Hum Reprod. 2006 Jun 23; [Epub ahead of print] Related Articles, Links
Click here to read
Urinary estrogen and progesterone metabolite concentrations in menstrual cycles of fertile women with non-conception, early pregnancy loss or clinical pregnancy.
Venners SA, Liu X, Perry MJ, Korrick SA, Li Z, Yang F, Yang J, Lasley BL, Xu X, Wang X.
Division of Epidemiology and Biostatistics, University of Illinois at Chicago, School of Public Health, Chicago, IL.
BACKGROUND: Knowledge is limited of how estrogen and progesterone variability in fertile women are associated with achieving pregnancy. METHODS: From 1996 to 1998, we enrolled 347 textile workers without hormone treatment in Anhui, China, who provided daily urine and data upon stopping contraception for up to 1 year until clinical pregnancy. Urinary hCG was assayed to detect conception and early pregnancy losses. We compared urinary concentrations of estrone conjugates (E1C) and pregnanediol-3-glucuronide (PdG) in 266 clinical pregnancies, 63 early pregnancy losses and 272 non-conception cycles from 347 women and also in 94 clinical pregnancy and 94 non-conception cycles from the same women. RESULTS: Using generalized estimating equations and relative to 266 clinical pregnancy cycles, log(E1C) was lower in 272 non-conception cycles [beta = -0.3 ng/mg creatinine (Cr); SE = 0.1; P < 0.0001]. On average, daily E1C was 18 ng/mg Cr lower in non-conception cycles than in clinical pregnancy cycles. Relative to 94 clinical pregnancy cycles, log(E1C) was lower in 94 non-conception cycles (beta = -0.4 ng/mg Cr; SE = 0.1; P < 0.0001) from the same women (average difference in daily E1C was 20 ng/mg Cr). The odds of E1C less than the 10th percentile (<30 ng/mg Cr) were higher in early pregnancy loss cycles [odds ratio (OR) = 4.8; P = 0.0027] than in clinical pregnancy cycles in the early luteal phase. Compared with clinical pregnancy cycles, log(PdG) concentrations were lower in non-conception cycles during the follicular phase, but this analysis lacked power for multiple testing. CONCLUSIONS: Estrogen concentrations varied from cycle to cycle, and higher estrogen was associated with achieving clinical pregnancy.
PMID: 16798842 [PubMed - as supplied by publisher]
kat in the delta
Linear Mode
