Re Catalyst – the ABC program, there was some controversy here in Australia before the second program was aired. I heard the producer on a radio interview saying there were some medical associations calling her and the TV channel asking not to show it, arguing there might be people that would stop taking their cholesterol medication without seeking medical advice and suggestion you should always talk and follow medical advice – thing that didn’t surprise me.

I didn’t have the chance to watch the program – I was at the gym at the time 🙂 but if anyone is interested you can watch them online or download them from:

https://www.abc.net.au/catalyst/stories/3876219.htm
https://www.abc.net.au/catalyst/stories/3881441.htm

That small, dense and dangerous LDL is the one that people should be most concerned about. If your triglycerides are under 70 and your HDL is over 70, you can almost guarantee that most of your LDL is the large, fluffy kind that will not harm you.”

Jimmy Moore Blood work
10/25/12
TC 359
LDL-C 285
HDL-C 65
Trigs 46
LDL-P 3451
Small LDL-P 221
ApoB 238

4/18/13
TC 310
LDL-C 236
HDL-C 66
Trigs 38
LDL-P 2730
Small LDL-P 478

SO – his small LDL-P (the worst kind) has INCREASED on his diet

Quotes from Dr Thomas Dayspring that Jimmy LEFT OUT OF HIS BOOK

If you search on 6 Month Lipid Panel for Jimmy Moore you should find his latest update before this book.

In comments, Thomas Dayspring wrote… “Dr Lipid analysis: Using all the knowledge we possess today, all of the numbers that you are thrilled about have no meaning in the face of a 99th percentile LDL-P. You also should not say an LDL-C of 285 has no meaning. The cholesterol concentrations that often have no meaning are low levels (where an LDL-P is needed to evaluate risk). No one with an LDL-C of 285 with the exception of a Type III dyslipoproteinemia patient have a low apoB or LDL-P. If you have an LDL-C that high, particle testing is not needed. You need to significantly reduce the saturated fat in your diet and see what happens: repeat the NMR in 3 weeks and you will know if your nightmare LDL-P is sat fat related. I’ll bet your LDL-P drops. If it does not, you need serious lipid-modulating medication. We have seen this paradoxical horrific rise in LDL-P in some people who are on ketotic diets.”

Yet here is the quote Jimmy chose for Dayspring in his chapter on LDL particles (Chapter 9):

“The least accurate way of estimating your atherogenic risk on a standard cholesterol panel would be to look at total cholesterol or LDL cholesterol.”

Does this seem like an accurate reflection of Dayspring’s full positions

https://www.lecturepad.org/dayspring/lipidaholics/pdf/LipidaholicsCase291.pdf
“Let’s get rid of the nonsense seen all over the internet that atherosclerosis is an inflammatory disease, not a cholesterol disease. That is baloney-with the reality being that it is both. One cannot have atherosclerosis without sterols, predominantly cholesterol being in the artery wall: No cholesterol in arteries – no atherosclerosis. Plenty of folks have no systemic vascular inflammation and have atherosclerotic plaque. However clinicians have no test that measures cholesterol within the plaque – it is measured in the plasma. It is assumed, that if total or LDL-C or non-HDL-C levels are elevated the odds are good that some of that cholesterol will find its way into the arteries, and for sure there, are many studies correlating those measurements with CHD risk. Yet, we have lots of patients with very low TC and LDL-C who get horrific atherosclerosis. We now recognize that the cholesterol usually gains arterial entry as a passenger inside of an apoB-containing lipoprotein (the vast majority of which are LDLs) and the primary factor driving LDL entry into the artery is particle number (LDL-P), not particle cholesterol content (LDL-C). Because the core lipid content of each and every LDL differs (how many cholesterol molecules it traffics) it takes different numbers of LDLs to traffic a given number of cholesterol molecules: the more depleted an LDL is of cholesterol, the more particles (LDL-P) it will take to carry a given cholesterol mass (LDL-C). The usual causes of cholesterol depleted particles are that the particles are small or they are TG-rich and thus have less room to carry cholesterol molecules. Who has small LDLs or TG-rich LDL’s? – insulin resistant patients! After particle number endothelial integrity is certainly related to atherogenic particle entry: inflamed endothelia have inter-cellular gaps and express receptors that facilitate apoB-particle entry. So the worse scenario is to have both high apoB and an inflamed dysfunctional endothelium. Is it better to have no inflammation in the endothelium – of course! But make no mistake the driving force of atherogenesis is entry of apoB particles and that force is driven primarily by particle number not arterial wall inflammation: please see Ira Tabas, Kevin Jon Williams, Jan Borén. Subendothelial Lipoprotein Retention as the Initiating Process in Atherosclerosis
Update and Therapeutic Implications Circulation. 2007;116:1832-44.