Did we get dietary saturated fats all wrong? The #HADLmodel provides a new understanding and an opportunity to get it right. THREAD👇👇👇
@simondankel @kariannesve

Increased dietary saturated fatty acids lead to increased cholesterol in lipoproteins, but we don’t know why. Enter the #HADLmodel, which explains changes in lipoprotein cholesterol as adaptive homeostatic adjustments that ensure optimal cell membrane fluidity and cell function.
We propose that circulating lipoproteins enable appropriate redistribution of cholesterol molecules between specific cells and tissues, to accomodate changes in dietary fatty acid supply, due to our omnivore nature and variable intake of fatty acids. #HADLmodel
Our #HADLmodel implies that circulating levels of LDL change for protective, not for pathological reasons; an SFA-induced raise in LDL cholesterol in healthy individuals is a normal response, while a lack of this needed response may reflect a deeper pathology in lipid handling.
Circulating lipoproteins may change for pathological reasons, when regulatory mechanisms become disrupted by pathogenic processes related e.g. to inflammatory processes. Diverging lipoprotein responses in healthy versus metabolically unhealthy individuals support this view.
Low grade inflammation can interfere with several fine-tuned signaling pathways necessary for homeostasis, including proper lipid handling. Altered circulating cholesterol levels may here reflect underlying pathogenic processes, unrelated to saturated fat intake. #HADLmodel
Dietary factors causing chronic low-grade inflammation, driven by diet-microbiome interactions, should receive more attention. The role of saturated fats in pathogenesis may be misconceived and greatly exaggerated. #HADLmodel
Is the #HADLmodel impossible? Is there more evidence to support the model? What else do we need to test in high-quality studies? Keep the discussion going - fair and factual. We need to improve the conversation on dietary fats. #publichealth #dietaryguidelines
@zoeharcombe @bigfatsurprise @DrAseemMalhotra @LDLSkeptic @ufferavnskov @malcolmken @LeventalLab @fedonlindberg @drmarkhyman @LorenCordain @chriskresser @ChrisMasterjohn @garytaubes @ProfTimNoakes @PeterAttiaMD @marionnestle @whsource @RobertLustigMD

More from Science

https://t.co/hXlo8qgkD0
Look like that they got a classical case of PCR Cross-Contamination.
They had 2 fabricated samples (SRX9714436 and SRX9714921) on the same PCR run. Alongside with Lung07. They did not perform metagenomic sequencing on the “feces” and they did not get


A positive oral or anal swab from anywhere in their sampling. Feces came from anus and if these were positive the anal swabs must also be positive. Clearly it got there after the NA have been extracted and were from the very low-level degraded RNA which were mutagenized from

The Taq.
https://t.co/yKXCgiT29w to see SRX9714921 and SRX9714436.
Human+Mouse in the positive SRA, human in both of them. Seeing human+mouse in identical proportions across 3 different sequencers (PRJNA573298, A22, SEX9714436) are pretty straight indication that the originals

Were already contaminated with Human and mouse from the very beginning, and that this contamination is due to dishonesty in the sample handling process which prescribe a spiking of samples in ACE2-HEK293T/A549, VERO E6 and Human lung xenograft mouse.

The “lineages” they claimed to have found aren’t mutational lineages at all—all the mutations they see on these sequences were unique to that specific sequence, and are the result of RNA degradation and from the Taq polymerase errors accumulated from the nested PCR process

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