So for people maybe can you first introduce from your perspective what is being put forward by this JDL hypothesis what are the kind of core claims that are being made and then based on that the primary issues that you and your colleagues saw with this that you have illustrated in your rebuttal to that idea?

Sure so basically the hypothesis suggests that there is a bi-directional flux of cholesterol between membranes and lipoprotence and that this is driven by the melting points of the dietary fatty acids. So briefly the lower dietary ratio between Pufas and SFA's would in theory lower the membrane PS ratio and lead to a reduced fluidity of cell membranes. A reduced fluidity of cell membranes would then lead to a shift of surplus cholesterol molecules but in the membranes to the plasma LDLC, a reservoir as they call it and then same in the opposite direction. Higher dietary PS ratio will lead to a higher membrane PS ratio, an increased fluidity of cell membranes and then a retrieval of cholesterol molecules needed to sort of stabilize the membranes from the plasma LDLC reservoir. So that's the main crux of the hypothesis but from the get-go I would say there are some interesting aspects to this hypothesis. I don't fully disregard this as nonsense from from from the beginning I think it's some interesting aspects especially that makes sense to me that cholesterol may be stored in various pools or tissues before excretion that makes sense and membranes may be such a pool, dating, membrane fluidity or viscosity or molecular flow probably impacts cholesterol metabolism just like any other physiochemical property and process impacts any part of cell biology such as temperature pH, pressure, cell volume etc. Lots of things can impact cell biology and also that it's not a new hypothesis it was to the best of my knowledge proposed in the 80s based on some non-human primary studies but they didn't really conclude and sort of the trace stops at some point so I guess it was hard to do this studies that's fair enough and it's also true that like we discussed we don't know exactly how fat the assets at all levels of the molecular pathway we don't know all the steps of how fatty assets affect plasma cholesterol although we know the main players involved so that was my initial response here but the reason why we chose to write the letter to the editor was that Moiret the main author of the paper she actually presented this hypothesis at the research group meeting before the publication at our research group and we then pointed out quite a few of the limitations to the hypothesis which was not considered in the funny version and this should have been no issue at all had she not claimed these ground implications of the hypothesis should it be true and they were at least very active and very vocal in the media here in Norway to try and acquit whole fat dairy products sort of assuming that the hypothesis was correct yeah and so that's why we wrote the LT I can also mention that I discussed this with Kevin Clatt at Berkeley California whom you know I believe and so some of his arguments also shine through in my current standing of this and in our opinion the evidence supporting the hypothesis is very scarce and there is quite a lot of conflicting evidence that was not really highlighted in their original paper and from what we concluded was that the Hadel hypothesis would provide us at least two testable predictions and one is related to those response melting point the melting point or the fatty acids should predict the change in LDLC if this model is correct the melting point of the fatty acid should predict LDLC response but according to the feeding trials that we just discussed this is not the case in fact only a few fatty acids has an effect on plasma LDLC not all up meristic acid mostly than pulmitic acid than loric acid but fatty acids with chain length above 16 carbon atoms has no effect on plasma LDLC and according to Hadel they should drastically increase the Lc also on the other side fatty acids with less than 12 carbon atoms has no effect on plasma LDLC in isolation but should increase LDLC according to Hadel hypothesis same for the proof as both the linoleic acid and alpha linoleonic acid has a similar effect on on lLC but but alpha linoleonic acid should have a more pronounced effect compared to lactic acid and most importantly maybe both EPA and the HA should reduce LDLC drastically if the hypothesis is correct they have no effect so it appears that the melting point isn't really consistently in those in those response related to the effect in plasma LDLC in this and the second prediction that we can make is the temporal sequence which is also necessary in a causal model we should observe one thing before the other we should observe membrane remodeling before the change in the same plasma LDLC but this is again not what we observe in all control trials to date. Past male LDLC responds quite rapidly to dietary change days to weeks but membrane lipid composition occurs much more slow weeks to months and are much more dependent on the plasma or the cell turnover rate so we sort of concluded that this rationale that they presented was it's seen biased in a sense that they don't present information that would contradict their hypothesis only things that corresponds with it and so we concluded that it sort of conflicts with established knowledge and it would likely be correct we cannot say for sure that it's definitely incorrect but it's likely correct and another point to note is of course that as you know in many of these papers there are so many misleading false statements that the sort of the sheer lack of textbook knowledge should falsify or qualify for a desk rejection because I mean there's so many things that it's easy to check the robustness of or the validity of that even if there is some truths to some of the hypothesis the entire thing sort of falls apart based on common knowledge.