SFA vs Dietary Cholesterol restriction

[Julie G]

Circ & Stavia- Dr. Dayspring makes the same "MISTAKE" in his posting in this thread: viewtopic.php?f=30&t=1197&start=10

With respect to fat in take - if one wants to choose that for part of a low carb diet or ketogenic diet because they have insulin resistance - one would have to monitor apoB and LDL-P. If they go up, especially if accompanied by increased desmosterol or lathosterol levels (indicating a sat fat induced hyperabsorption of cholesterol) then one could consider reducing saturated fat intake

A double "mistake" makes me think there's more to it. I certainly don't claim to understand. Why doesn't somebody PM Dr. Dayspring for clarification? An error is the obvious answer...but because he repeats it; I'm skeptical of that explanation.

Circ, I agree. Stavia is a treasure

[Stavia]

yah that's the thing I first thought was a typo when I was carefully going thru every word. He may be copying and pasting from the same source, or it may be a repeated typo. He explains everything so very carefully usually, and this is out of left field.
I can't pm him....*cough*.
Volunteers?

[circular]

Haha I'm not sure what the cough means but I guess that leaves moi! Will get back if I hear back ...


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[Julie G]

LOL I forgot...Thanks, Circ.

FWIW, I'm guessing increased desmosterol is typically a sign of hyper-synthesis, BUT if it happens in response to increased fats...it could also be a sign of hyper-absorption- of SFA in particular.

[Stavia]

LOL I forgot...Thanks, Circ.

FWIW, I'm guessing increased desmosterol is typically a sign of hyper-synthesis, BUT if it happens in response to increased fats...it could also be a sign of hyper-absorption- of SFA in particular.

I thought absorption and synthesis were inversely related ie they drive each other in the opposite way?
I'm totally confuzzelled

[circular]

This page is worth a read for a nice overview. Now I will have to call HDLabs and ask why they don't test the L one that synthesizes. Demesterol isn't the main synthesis marker, but not described here as an absorber either. http://www.bostonheartdiagnostics.com/s ... e_test.php


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[circular]

http://www.ncbi.nlm.nih.gov/pubmed/23042211

J Alzheimers Dis. 2013;33(3):881-8. doi: 10.3233/JAD-2012-121453.
Alzheimer's disease: brain desmosterol levels.
Wisniewski T1, Newman K, Javitt NB.
Author information

Abstract
Desmosterol is a C27 sterol intermediate in cholesterol synthesis generated during the metabolic pathway that transforms lanosterol into cholesterol. It has become of particular interest in the pathogenesis of Alzheimer's disease (AD) because of the report that the activity of the gene coding for the enzyme DHCR24, which metabolizes desmosterol to cholesterol, is selectively reduced in the affected areas of the brain. Any change in the pattern of C27 sterol intermediates in cholesterol synthesis merits investigation with respect to the pathogenesis of AD, since neurosteroids such as progesterone can modulate the tissue levels. We therefore analyzed the C27 sterol composition using a metabolomics approach that preserves the proportion of the different sterol intermediates. In AD, the proportion of desmosterol was found to be less than that of age-matched controls. The findings do not directly support the focus on Seladin-1, although they could reflect different stages of a slowly progressive disease.

PMID: 23042211 [PubMed - indexed for MEDLINE] PMCID: PMC3557460 Free PMC Article

It's not likely we'll have a specific test anytime soon for desmosterol levels in key areas of the brain for AD.

Promethease is reporting 3 SNPs at DHCR24. Two are flagged with Alzheimer's Disease. I'm a heterozygote on all three, but it appears that in itself isn't bad on these SNPs … the exact version is more important? The notion in the abstract that "neurosteroids such as progesterone can modulate the tissue levels" of C27 sterol intermediates may be helpful. I wonder what other neurosteroids do this. It's also possible there is enough of one or more other types of sterol intermediates to compensate?????

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Promethease: "[PMID 17510943] men carrying the T allele of rs600491 had an increased risk of Alzheimer's disease (OR 1.7 95% CI 1.2-2.4; P = 0.004, Bonferroni corrected P = 0.048 with 12 tests)."

" Stratification according to gender, however, revealed a statistically significant association between T/T genotype and AD risk in men, in contrast with the results in women. Our findings indicate a gender dependent effect of DHCR24 rs600491 polymorphism on the susceptibility to AD." http://www.ncbi.nlm.nih.gov/pubmed/2291 ... t=Abstract

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Promethease "[PMID 17510943] Alzheimer's disease cases that carry rs718265(G;G) had lower levels of Abeta(42)"

[PMID 17510943] rs638944(T) and rs600491(C) Alzheimer's disease protective haplotype TC with frequency of 0.22 in cases and 0.30 in controls (P < 0.001)
[PMID 17510943] rs638944(G) and rs600491(C) Alzheimer's disease risk haplotype GC with frequency of 0.10 in cases and 0.05 in controls (P < 0.001)
[PMID 15986317OA-icon.png] Identification of risk and age-at-onset genes on chromosome 1p in Parkinson disease.

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More at Promethease … gotta move on ...