Discover and read the best of Twitter Threads about #lcl6
Most recents (17)
1/ "High concentrations of LA (either unoxidized or oxidized) appeared to exhibit cytotoxicity, as evidenced by the observed decrease in cell viability with increasing LA concentration.
2/ "In this case, the unoxidized LA appeared to have a bigger impact than the oxidized LA over most of the concentration range studied."
That's surprising!
#lcl6
That's surprising!
#lcl6
3/ Hmm... "However, the number and morphology of the lipoprotein particles formed depended on the oxidation state of the lipid: the lipoproteins formed in the presence of oxidized LA were smaller, more numerous, and more irregularly shaped...
@realDaveFeldman
@realDaveFeldman
1/ Moving the needle on what causes obesity.
(This is a very dense paper.)
It blows a large hole in the CICO story. "Eat less, move more" is a problem when your body turns down the thermostat.
You can't "move more" (AEE) enough.
(This is a very dense paper.)
It blows a large hole in the CICO story. "Eat less, move more" is a problem when your body turns down the thermostat.
You can't "move more" (AEE) enough.
2/ What they found is that we have seen a decline in human metabolism over the last few decades, despite an INCREASE in activity.
This is paralleled by a decline in body temperature (!).
@fire_bottle
This is paralleled by a decline in body temperature (!).
@fire_bottle
3/ What caused it? It's not carbohydrate, it's not protein...
It's the fat. Specifically, the shift from saturated to unsaturated fat over the last many decades.
It's the fat. Specifically, the shift from saturated to unsaturated fat over the last many decades.
Cardiologists: Lots of cholesterol in atherosclerotic plaques means cholesterol causes heart disease. Don't eat cholesterol!
Also cardiologists: Lots of linoleic acid in plaques means you should eat more linoleic acid! It'll cure those plaques!
#lcl6 1/
Also cardiologists: Lots of linoleic acid in plaques means you should eat more linoleic acid! It'll cure those plaques!
#lcl6 1/
2/
3/
1/2 So much for LDL.
"In our study, apoB48-containing intestinal particles occupied significantly larger area of human carotid atherosclerotic plaques, compared to hepatic apoB100."
@FatEmperor @realDaveFeldman @LDLSkeptic
#LDLBS #lcl6
"In our study, apoB48-containing intestinal particles occupied significantly larger area of human carotid atherosclerotic plaques, compared to hepatic apoB100."
@FatEmperor @realDaveFeldman @LDLSkeptic
#LDLBS #lcl6
2/2 "First Quantification of Intestinal-apoB48 and Hepatic-apoB100 Particles in Human Atherosclerotic Plaque"
doi.org/10.1016/j.cca.…
doi.org/10.1016/j.cca.…
1/ A cardiologist will tell you:
A low-fat diet is healthy.
Lp(a) is a marker for CVD risk.
Lp(a) is genetic.
A low-fat diet is healthy.
Lp(a) is a marker for CVD risk.
Lp(a) is genetic.
2/ "Thirty-seven healthy women were fed two diets. Both diets contained a reduced amount of total and saturated fat. In addition, one diet was low in vegetables and the other was high in vegetables, berries, and fruit. The dietary intake of total fat was...
3/ "...70 g per day at baseline and decreased to 56 g (low-fat, low-vegetable diet) and to 59 g (low-fat, high-vegetable diet). The saturated fat intake decreased from 28 g to 20 g and to 19 g, and the amount of polyunsaturated fat intake increased...
1/ A few thoughts on ApoB.
It's something we're programmed for, genetically.
It's a fundamental component of digestion and energy distribution. (@realDaveFeldman)
So if it causes CVD, then CVD is a genetic disease.
#lcl6 h/t @jimolsen717
It's something we're programmed for, genetically.
It's a fundamental component of digestion and energy distribution. (@realDaveFeldman)
So if it causes CVD, then CVD is a genetic disease.
#lcl6 h/t @jimolsen717
2/ If CVD is genetic, then we should see the current rate of CVD (~50% of deaths) in all human populations.
We don't.
This is demonstrated repeatedly, best here:
Where various genetic populations have near-zero CVD in their natural environment.
We don't.
This is demonstrated repeatedly, best here:
Where various genetic populations have near-zero CVD in their natural environment.
3/ We only see CVD in populations consuming higher amounts of linoleic acid, and, best, low levels of animal fats.
doi.org/10.3389/fnut.2…
doi.org/10.3389/fnut.2…
1/ "Conventional soybean oil (CSO)... predominantly contains linoleic acid (LA; C18:2), a n-6 PUFA. Recently, a modified soybean oil (MSO) enriched in oleic acid (C18:1), a n-9 MUFA, has been developed, because of its improved chemical stability to oxidation."
#lcl6
#lcl6
2/ "The CSO diet decreased plasma lipid levels and the cholesterol content of VLDL and LDL by approximately 18% (p < 0.05), likely from increased hepatic levels of PUFA, which favorably regulated genes involved in cholesterol metabolism...."
@FatEmperor @realDaveFeldman
@FatEmperor @realDaveFeldman
3/ "The MSO diet, but not the CSO diet, suppressed atherosclerotic plaque size compared to the Western control diet (Control Western diet: 6.5 ± 0.9%; CSO diet: 6.4 ± 0.7%; MSO diet: 4.0 ± 0.5%) (p < 0.05), independent of plasma lipid level changes."
@LDLskeptic2
@LDLskeptic2
1/ "Only a few previous studies have examined head-to-head the extent of excess risk explained through high concentrations of remnant cholesterol or triglycerides (substitute markers for high VLDL cholesterol) and high concentrations of LDL cholesterol separately...
2/ "...(18, 19), and none have used directly measured concentrations of both VLDL cholesterol and LDL cholesterol. Consequently, it is presently unknown to what extent directly measured cholesterol in large and small VLDLs, in IDL, and in LDL in head-to-head comparison...
3/ "...each explain excess risk of myocardial infarction in individuals with obesity."
This is from 2021, mind you. 🙄
This is from 2021, mind you. 🙄
Can we trust PhDs?
1/ Claim: "No upper limit (UL) has been set for linoleic acid because of a lack of a defined intake establishing adverse affects (2)."
Reference 2: “An upper boundary for linoleic acid is set at 10 percent of energy for three reasons: ...(3) high intakes
1/ Claim: "No upper limit (UL) has been set for linoleic acid because of a lack of a defined intake establishing adverse affects (2)."
Reference 2: “An upper boundary for linoleic acid is set at 10 percent of energy for three reasons: ...(3) high intakes
2/ "...of linoleic acid create a pro-oxidant state that may predispose to several chronic diseases, such as CHD and cancer."
Read both snapshots.
Hat tip to @MDVilntfluid for getting me to take another look at Whelan.
#lcl6
Read both snapshots.
Hat tip to @MDVilntfluid for getting me to take another look at Whelan.
#lcl6
3/3 Claim in: "Linoleic Acid" doi.org/10.3945/an.113…
Ref 2: "Dietary Reference Intakes for ...Fat, Fatty Acids..." nap.edu/catalog/10490/…
Ref 2: "Dietary Reference Intakes for ...Fat, Fatty Acids..." nap.edu/catalog/10490/…
1/4 Canola (rapeseed) oil is one of the better seed oils, it's ~20% linoleic acid.
But it still goes rancid (toxic), because it contains linoleic acid.
Safest and healthiest fats/oils to eat are low in linoleic acid!
@ZeroAcreFarms #lcl6
But it still goes rancid (toxic), because it contains linoleic acid.
Safest and healthiest fats/oils to eat are low in linoleic acid!
@ZeroAcreFarms #lcl6
2/4 "Triacylglycerol (TG), the main component of edible oil, is oxidized by thermal- or photo- oxidation to form TG hydroperoxide (TGOOH) as the primary oxidation product.
3/4 "Since TGOOH and its subsequent oxidation products cause not only the deterioration of oil quality but also various toxicities, preventing the oxidation of edible oils is essential."
1/ Why do CETP inhibitors fail to improve CVD outcomes?
en.wikipedia.org/wiki/CETP_inhi…
@ethanweiss #lcl6 @FatEmperor @LDLSkeptic
en.wikipedia.org/wiki/CETP_inhi…
@ethanweiss #lcl6 @FatEmperor @LDLSkeptic
2/ (They work by increasing HDL in the blood. HDL is supposed to be the "good" cholesterol.)
3/ But HDL is "good" because it uses CETP to remove the "bad" fats from LDL. These bad fats are overwhelmingly oxidized LA-cholesterol esters.
#lcl6
#lcl6
1/4 So what change is the likely cause of our dietary woes?
"From 1909 to 2010, total availability per capita for animal-based fats (including butter, lard, edible tallow) decreased 58% (21.2–8.8 lbs.) and vegetable-based fats and oils (margarine, shortening, salad, and...
"From 1909 to 2010, total availability per capita for animal-based fats (including butter, lard, edible tallow) decreased 58% (21.2–8.8 lbs.) and vegetable-based fats and oils (margarine, shortening, salad, and...
2/4 "...cooking oils (included only after 1965), and edible fats and oils found in confectionery products and non-dairy creamers) increased 159% (31.7–82.2 lbs.)."
3/4 "As observed... processed and ultra-processed foods dramatically increased over the past two centuries, especially sugar, white flour, white rice, vegetable oils... These changes paralleled the rising incidence of NCDs, while animal fat consumption was inversely correlated."
Dietary PUFA are oxidized preferentially in postprandial period.
"Polyunsaturated:saturated ratio of diet fat influences energy substrate utilization in the human"
pubmed.ncbi.nlm.nih.gov/3123874
#lcl6
1/9
"Polyunsaturated:saturated ratio of diet fat influences energy substrate utilization in the human"
pubmed.ncbi.nlm.nih.gov/3123874
#lcl6
1/9
Diet of 45-40-15%en fat-carbs-protein for 7 days + crossover of two PUFA:SFA ratios (P:S):
- low P:S = 0.24, PUFA 5%en
- high P:S = 1.65, PUFA 17%en
2/9
- low P:S = 0.24, PUFA 5%en
- high P:S = 1.65, PUFA 17%en
2/9
Higher carb vs. fat utilization on higher PUFA diet:
"These differences indicate a shift toward greater carbohydrate and lower fat utilization following an overnight fast in
subjects on the high compared to the low P:S ratio diet."
3/9
"These differences indicate a shift toward greater carbohydrate and lower fat utilization following an overnight fast in
subjects on the high compared to the low P:S ratio diet."
3/9
Susceptibility to sunburns on high n-6 diets:
"UVB and H2O2 induced G2A expression and caused oxidation of linoleate to produce 9-HODE in HaCaT cells. [This] suggests that 9-HODE-G2A signaling plays proinflammatory roles in skin under oxidative conditions."
"UVB and H2O2 induced G2A expression and caused oxidation of linoleate to produce 9-HODE in HaCaT cells. [This] suggests that 9-HODE-G2A signaling plays proinflammatory roles in skin under oxidative conditions."
G2A Plays Proinflammatory Roles in Human Keratinocytes under Oxidative Stress as a Receptor for 9-Hydroxyoctadecadienoic Acid
sciencedirect.com/science/articl…
#lcl6
sciencedirect.com/science/articl…
#lcl6
Why is epidermis rich in LA that is unstable and inflammatory under UVB?
How does diet influence lipid composition of skin?
How does diet influence lipid composition of skin?
1/ Remember the credentialed dopes that sneered at those suggesting a low-sugar diet might be protective for coronavirus?
@DoctorTro @DrAseemMalhotra
#lcl6
@DoctorTro @DrAseemMalhotra
#lcl6
2/ "Oral 100-g portions of carbohydrate from glucose, fructose, sucrose, honey, or orange juice all significantly decreased the capacity of neutrophils to engulf bacteria as measured by the slide technique. Starch ingestion did not have this effect."
3/ "These data suggest that the function and not the number of phagocytes was altered by ingestion of sugars. This implicates glucose and other simple carbohydrates in the control of phagocytosis and shows that the effects last for at least 5 hr...."
"...structural changes in the LDL particle upon its mild oxidation make it also recognizable by immune competent cells and lead to TLR4 activation."
"These data and other results from our group support the hypothesis of convergence of immune responses to oxidation-specific self-antigens and to microbial infection."
"This hypothesis was first substantiated by data from our group showing that a natural autoantibody to mmLDL, EO6, is genetically identical to the classic germline anti-phosphorylcholine antibody T15, which binds avidly to Streptococcus pneumoniae."
"Removal of these CL [cardiolipin] decreases electron-transport activity by ~50% and completely inhibits proton translocation..."
@HyperlipidM
@HyperlipidM
"Peroxidized CL is also much more effective than either H2O2, or tert-BOOH for inactivation, or chemical modification of CcO. [100- to a 1000-fold] less CLOOH are required to modify the CcO subunits than is required for H2O2 or tert-BOOH to modify CcO to a similar extent."
"Because CL is more susceptible to peroxidation than other PLs, CL is expected to be the major source of HNE and MDA within the inner mitochondrial membrane, although this may not be necessarily true for protein bound CL."
