Dietary sources of estrogen matter

Epidemiology

An estrogen-associated dietary pattern and breast cancer risk in the Swedish Mammography Cohort

1. Holly R. Harris^1,2,*, 
2. Leif Bergkvist³and
3. Alicja Wolk¹

Article first published online: 14 MAY 2015

DOI: 10.1002/ijc.29586

© 2015 UICC

Issue

International Journal of Cancer

Early View (Online Version of Record published before inclusion in an issue)

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How to CiteAuthor InformationPublication HistoryFunding Information

Author Information

1. 1

   Division of Nutritional Epidemiology, National Institute for Environmental Medicine, Karolinska Institutet, Stockholm, Sweden

2. 2

   Obstetrics and Gynecology Epidemiology Center, Brigham and Women's Hospital, Boston, MA

3. 3

   Department of Surgery and Centre for Clinical Research, Central Hospital, Västerås, Sweden

^*Correspondence to: Dr. Holly Harris, Unit of Nutritional Epidemiology, Institute for Environmental Medicine, Karolinska Institutet, P.O. Box 210, SE-171 77 Stockholm, Sweden, Tel.: +46-8-524-86460, Fax: +46-8-304571, E-mail: holly.harris@ki.se

Sat fats and trans fats in humans

http://www.bmj.com/content/351/bmj.h3978?utm_content=buffera50be&utm_medium=social&utm_source=twitter.com&utm_campaign=buffer

But...

http://feinmantheother.com/2015/08/12/meta-analysis-is-to-analysis/

The photon bath

http://www.tandfonline.com/doi/full/10.1080/07315724.2015.1039866#.VcSy6xNVhHw

Do you observe for yourself or relatives that they are right ?

http://m.bjsm.bmj.com/content/early/2015/05/07/bjsports-2015-094911.full.pdf

Cholesterol and the brain: a very complex issue

http://atvb.ahajournals.org/content/24/5/806.abstract

Production and interconversion of HDL particles in CNS and plasma. In brain parenchyma, ABCA1 transporter is expressed in neurons and astrocytes where it promotes the efflux of PL and UC to glia-derived apoE, thus leading to the formation of nascent lipoproteins. Moreover, discoidal apoA-I-containing HDL particles may enter the CNS via SR-BI-mediated uptake and other unknown mechanisms. Discoidal particles can further acquire PL and UC via ABCA1 and ABCG1. Maturation of discoidal particles into spherical lipoproteins likely involves the activity of LCAT, CETP, and PLTP, similar to what happens in plasma. Newly generated particles can be finally uptaken by neurons or astrocytes through the binding of apoE to LDLR family receptors. ABCA1: ATP-binding cassette transporter A1, ABCG1: ATP-binding cassette transporter G1; BBB: blood–brain barrier; CETP: cholesteryl ester transfer protein; CNS: central nervous system; EL: endothelial lipase; HL: hepatic lipase; LDLRs: LDL receptor family receptors; LCAT: lecithin:cholesterol:acyltransferase; PL: phospholipids; PLTP: phospholipid transfer protein; UC: unesterified cholesterol.

http://cardiovascres.oxfordjournals.org/content/103/3/405.full

Major cholesterol and apoE pathways in the CNS. Cholesterol is synthesized de novo in brain cells (neurons, astrocytes, microglial cells). Efflux of CNS cholesterol through the BBB occurs as 24(S)-hydroxycholesterol (24S-OH-C) and 27-hydroxycholesterol (27-OH-C). 24S-OH-C is produced exclusively in the CNS, 27-OH-C is produced in most organs. Unlike cholesterol, 24-S-OH-C and 27-OH-C can cross the BBB because of the hydroxylated side chains. Primarily astrocytes and microglia secrete HDL-like lipoproteins composed of cholesterol and phospholipids and apoE as the major apoprotein. ApoE is the ligand of these lipoproteins to the receptors of the LDL receptor family such as the LDL-receptor and LRP. Exchange of cholesterol and apos between CNS cells occurs via these lipoproteins. In plasma, 24S-OH-C and 27-OH-C are transported on lipoproteins such as LDL and HDL. De novo cholesterol synthesis in CNS cells can be regulated by the apoE-mediated uptake of lipoproteins via the LDL receptor family. ApoE is produced within the CNS and interacts with Aβ. The availability of cholesterol and of apoE are thought to affect amyloidogenesis and apoE (in particular the isoform apoE4) promoting the formation of amyloid fibrils from soluble Aβ in the CNS. The data for the steady state cholesterol pool have been determined from studies in healthy adults. The flux of cholesterol across the whole body is ~700 mg/day (CHOL INPUT/OUTPUT). The flux across the CNS is only 0.9% of whole body (~12 mg/day). The efflux of 24(S)-hydroxycholesterol through the BBB is limited to ~6-7 mg per day [64, 67], the daily influx of 27-hydroxycholesterol into the brain has been estimated to be ~5 mg [1]. Please note that the brain per kg organ contains 10 times more cholesterol than the rest of the body.

http://dmm.biologists.org/content/5/6/746.full

http://jcb.rupress.org/content/138/4/877.full

Coca is funding research on exercise: that is good news because US universities will use this money wisely and efficiently

http://well.blogs.nytimes.com/2015/08/09/coca-cola-funds-scientists-who-shift-blame-for-obesity-away-from-bad-diets/?smid=tw-nytimeswell&seid=auto&_r=1

How liver manage fat of different origins: dietary, de novo synthesis, release from adipose tissue

Overview of hepatic fatty acid metabolism in the postprandial state. Fatty acids enter a pool where they may be partitioned into oxidation (1) or esterification (2) pathways. There are TG storage and secretory pools. Fatty acids liberated from the hydrolysis of TG in the secretory TG pool, or TG particles, may then be partitioned to a storage TG pool (3). TG in the secretory pool is utilised for very low-density lipoprotein (VLDL) production (4) which enters systemic circulation. It remains unclear if fatty acids liberated from the TG pools enter oxidation pathways (dotted line, (5)). Abbreviations: TG, triglyceride; VLDL, very low-density lipoprotein; DNL, de novo lipogenesis; FA, fatty acid; NEFA, non-esterified fatty acids; ApoB, apolipoprotein B; 3OHB, 3-hydroxybutyrate; ER, endoplasmic reticulum.

For instance if you have big fat stores, if you eat lot of sugars and no fat, your liver will synthetize VLDL... Despite your fat intake is very low.
Second example if you are on a low carb diet, if your BMI and W/H ratio are normal your liver has less sources of de novo lipogenesis, less free fatty acids released by fat stores and will only rely on your fat intake to synthesize VLDL.

"Determining the contribution of specific fatty acid sources (Figure 1) can be achieved with the use of stable-isotope tracers. Using a multi-tracer approach Donnelly et al. [48] determined the contribution of specific sources of fatty acid to liver and VLDL-TG in NAFLD patients (n = 8). After five days of labeling, they reported there was no difference in the contribution of fatty acids originating from systemic NEFA, DNL or diet to liver and VLDL-TG [48]. On the basis of this observation, the authors suggested that VLDL-TG may be used as a surrogate marker of the liver TG/fatty acid pool [48]. Dietary fatty acids have been reported to contribute 2%–28% of VLDL-TG [48,49,50,51]. Fatty acids originating from systemic NEFA contribute 45%–75% and from hepatic DNL fatty acids contribute 13%–37% to VLDL-TG [48,49,50,51]. The wide-range in findings may be explained by differences in the length of the postprandial phase, the type of test meal fed and hepatic uptake, and/or alterations in the turnover time of the hepatic TG pool, which may be influenced by size of the pool."

Some insights in the different sources of hepatic synthesis of VLDL.

And this remark:
"These data demonstrate that the most important contributing factor to whether liver fat accumulation occurs is the amount of total energy consumed, rather than the composition of the diet. Notably, liver fat decreases more rapidly when a hypo-caloric diet devoid of carbohydrate is consumed, compared to calorie restriction alone [62,64]."

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4245577/