Tuesday, May 8, 2018

MY Retraction to my second answer to @DaveKeto challenge

RETRACTION IN UPDATE BELOW


Another trial to answer @DaveKeto lipid challenge

@DaveKeto on challenge on twitter shown below



UPDATE 5-9-18
Mistakenly, I thought baseline statin use before Pitavastatin was 
low.  As seen below it was 91%! 

Thus clearly, it does not fit @DaveKeto challenge criteria

 but, I think it validates my first answer to Dave's challenge. 

 It shows that a "high LDLc" can be as low as 88 
because high dose Pitavastatin with lower LDLc had less mortality than low dose Pitavastatin.

It also shows these 11,000 people developed CAD with normal HDLc and TG. 
Thus the protective effect of HDLc and Triglycerides did not help them.  





Correction:
 these are numbers after 1 month of run-in use of Pitavastatin for everyone before real trial began.

HDLc: 50.7

Triglycerides: 124

LDLc: 88.1

History of acute coronary syndrome 71%

Diabetes 70%

Hypertension 75%

Smoking 15%












5 comments:

  1. The Challenge specifies "non-treated".
    Paper says "The study population represented typical Japanese patients with stable CAD" so not surprising they had that history; almost all were already medicated, so baseline TG/HDL likely reflects that rather than insulin status.

    What we're looking for is a prospective paper showing that high LDL with low TG/LDL is associated with above-average risk of CVD at some future date. That is, does this pattern predict ill-health in a healthy person?
    So far, not in this paper. Not only are these people not treated, so lipids are "native", they weren't even screened for FH genes, likely to be present to a greater extent in higher LDL groups.
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4871717/

    ReplyDelete
  2. Please read http://meandgin.blogspot.com/2018/05/another-trial-to-answer-daveketo-lipid.html to realize your definition of "high LDLc" is out of date. No one has told me what Dave's definition of high level of LDLc is. What is low TG?
    What Is high HDLc. Hard to do the challenge with moving targets. The Japanese study changes definition of high LDLc as does Fournier and Odyssey. Please use studies from this year not cherry pick old articles. The pre-study baseline before giving a statin to everyone had high HDLc and normal TG level less than 150. Surprising how low their LDLc was and yet they already had CAC.
    I am showing a large cohort of Japanese who were not protected by normal HDLc and TG. I am not using the statin trial for the answer to the challenge. I am using the baseline data before the statins were given. Maybe they are not normal now but I believe we can assume they were healthy when they were young. At baseline most were not on statins because the Japanese (Asians) find them difficult to tolerate.

    ReplyDelete
  3. In Table 1, it says "Statins before run-in period 5656 (91.0) 5622 (90.7") - the numbers in brackets are the % on drug in each arm. There are other meds used too.
    They developed CAD we don;t know when, were treated for who knows how long, then were inducted into the trial.
    Even taken at face value, is the mean TG/HDL/LDL value here one associated with high rate of CAD in the Japanese population at large? I doubt that very much - it is the opposite of the lipid triad. Selecting people who already have CAD isn't in the spirit of the challenge. We want to know if attaining high HDL, low TG, but high LDL increases the risk of future CAD compared with - what? Well, for example, how much worse is it than high HDL, low TG, moderate LDL? Is it worse than the lowest-cholesterol pattern of low HDL, low TG, low LDL?
    At this stage I'm prepared to use the Framingham Cohort cut-offs; even though LHMRs can usually do better, we're not likely to find other measures.
    We know that TG/HDL is a good measure of risk, so, once TG/HDL is optimal, how much does variation in LDL alter risk then?

    ReplyDelete
  4. I found this before I read you letter and I posted a retraction above. I understand your "spirit" but it's not in the challenge. I did fail the drug test but I do believe this study puts into question that a HDLc greater than 50 and TG normal at less than 150 did not protect the 11,000 Japanese from CAD, which is the SPIRIT of
    the TRUTH I am trying to show. AIIM-HIGH decrease in TG and increase in HDLc made no difference after 3 years. Genetic studies show LDLc is causal for atherosclerosis. I think this Japanese study does strength my arguments that my first answer to the challenge were valid as it re-defined what a HIGH LDLc is. Lower LDLc was better even when starting from what was thought to be a low LDLc. Please write me the actual numbers for HDLc, TG and LDLc because I don't want to be accused of misrepresenting your position.

    ReplyDelete
  5. AIIM-HIGH decrease in TG and increase in HDLc made no difference after 3 years.

    - yes, if you do this with a DRUG you are going against the metabolic reaction to what and when you eat, it won't necessarily end well. Sometimes drugs just fake the markers.

    Genetic studies show LDLc is causal for atherosclerosis.

    - Genetic studies show that genes that raise LDL-C are associated with an increased risk of athero. They do not show that LDL-C causes athero in people without these genes, or in people who have low TG/HDL (the genes tend to raise TGs as well). Probably what these studies show best is that people with athero need to be able to clear LDL because LDL's role in reverse cholesterol transport is more important in people with athero. Which is why the CETP inhibitor drugs fail - they impair RCT. But the causes of athero - smoking, overweight, hyperinsulinaemia and so on - don't seem to be any different in people with genetically high LDL - they are just much more dangerous, because it is so much harder for LDL to do its job.

    ReplyDelete

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