I have answered the @DaveKeto challenge
UPDATE 5-7-2018
Below you will see I found a study that filled all the criteria of Dave's challenge:
Last column below meets @DaveKeto challenge criteria
HDLc greater than 90
Triglycerides 76
LDLc 102 (goal 70, needs statin treatment)
non-HDLc 116 (goal 80, needs statin Rx)
These patients developed coronary artery disease during study.
On 5-4-18 I posted this blog. It is now 5-7-18.
Dave says LDLc of 105 is not high, yet this group developed CAD at this level.
Dave says they smoked and drank alcohol. It was not in the criteria.
Dave says they have to be "healthy". Study states these people were healthy at beginning of trial.
Dave says this is not a "high rate of CAD" yet never defines a high rate of CAD
I maintain that the purpose of this trial is to show that high HDLc and Low TG will not protect against developing CAD. I did this.
George in his twitter makes my point. Nothing is said about insulin resistance in the challenge.
People need to voice their opinion as to why they think I filled the criteria or did not.
Dave needs to define
1- what is a "high rate of CAD" (no CAD becoming CAD is a high rate)
2- what is a high HDLc (over 30 for men and over 40 for women)
3- what is a low LDLc (I say it is between 40-70 on Rx.)
4- what is a high LDLc (I say it is the level that causes CAD as in this study)
On 5-4-18 I posted this blog. It is now 5-7-18.
Dave says LDLc of 105 is not high, yet this group developed CAD at this level.
Dave says they smoked and drank alcohol. It was not in the criteria.
Dave says they have to be "healthy". Study states these people were healthy at beginning of trial.
Dave says this is not a "high rate of CAD" yet never defines a high rate of CAD
I maintain that the purpose of this trial is to show that high HDLc and Low TG will not protect against developing CAD. I did this.
George in his twitter makes my point. Nothing is said about insulin resistance in the challenge.
People need to voice their opinion as to why they think I filled the criteria or did not.
Dave needs to define
1- what is a "high rate of CAD" (no CAD becoming CAD is a high rate)
2- what is a high HDLc (over 30 for men and over 40 for women)
3- what is a low LDLc (I say it is between 40-70 on Rx.)
4- what is a high LDLc (I say it is the level that causes CAD as in this study)
"Participants were excluded from the analysis if they had pre‐existing CHD (previous diagnosis of myocardial infarction, known angina pectoris, a history of hospitalization for unstable angina, or previous coronary revascularization)"
ncbi.nlm.nih.gov/pmc/articles/PMC4187512/ … This study stratifies the TG/HDL in CAD patients. The last 2 columns clearly meet your criteria especially if you use better biomarker of non-HDLc. These people need statins.
If you say that such a level of LDL-c causes heart disease, you are strictly speaking probably not correct. It depends on everything else. It is quite possible to have a considerably higher LDL and NOT get CHD. After all, there is no correlation between LDL per se and individual levels of atheroma. Not on imaging, CAC or post-mortem. Lots of studies.
ReplyDeleteI don't think I said a LDLc of 105 caused atheroma. I said high HDLc and low TG did not protect from atheroma. I said since these patients developed atheroma they need to get there LDLc down to 70. A better biomarker is non-HDLc which was 116 which is surprising considering how high the HDLc was. This number needs to get down below 80 with statin. Remember Tim Russert died with LDLc 68 but non-HDL was 118 despite aggressive treatment. Thus these people who developed CAD with 116, trials have shown that getting their nonHDLc less than 80 will prevent many future events. I am not trying to prove the certainty of the Germ Theory as Koch. I am trying to save lives with what has been proven to work in a convergence of evidence including the best level of evidence: large trials powered to show better mortality in double blinded random control trials.
ReplyDeleteYou write you have evidence that LDLc not correlated with CAC. I ask you to show me those studies. First we know LDLc is a poor biomarker compared to non-HDLc and ApoB. Second, we know calcium score goes up with statins but it has to be adjusted with CAC volume. Using old studies that don't take this new information into account and ignoring the new studies is cherry picking.
The problem with this study, as far as the challenge goes, is that TG is not stratified. The TG associated with HDL >90 is mean 76.0, but the ± SD is 44, meaning the range is wide, and thus this group includes some people with high TGs. So are they the ones at higher risk?
ReplyDeleteIn this paper, healthy people (no CAD) with very high HDL (mean 79 ± 13) have lower TGs, within a narrower range than in the other paper 71 ± 34.
https://www.dropbox.com/s/glpf1xe75coi1jk/Healthy%20HALP.pdf?dl=0
We can imagine HDL being high in someone in whom RCT is impaired, for example CETP being defective, but also it being high in someone whose RCT is optimal. We also have of course ApoA1 Milano where HDL is low but RCT is optimal.
There will be ApoA1 Milano cases in the lowest HDL strata, but these are not the cases driving increased risk there.