5 Steps to prevent Heart Disease

Tuesday, October 30, 2018

LDLc calculated is probably the least reliable biomarker.

The Tandem LDLc Drop experiment is very suspect with it's home lipid panel using calculated LDLc when the TG levels are blocked out. Follow nonHDLc instead which Dave does not follow on his podcast from Houston. He also does not calculate remnants for us. I do at my blog. Data from Tandem LDLc Drop by Dave link

From Sniderman
"Indeed, Miller et al have shown that the total errors for
direct HDL-C in abnormal specimens were −19.8% to 36.3% and
for direct LDL-C −26.6% to 31.9%.4

Moreover, there is evidence that directly measured LDL-C is not a more accurate measure of cardiovascular risk than calculated LDL-C.5
What then justifies the additional cost of direct LDL-C?"


"In their commentary, Contois and Delatour make a good point:
the reference standard for apoB falls short of absolute perfection.3
If it can be improved, well and good.
But surely, the same point applies with even greater force to the measurement of
1-triglycerides,
2-high density lipoprotein cholesterol (HDL-C) and
3-low density lipoprotein cholesterol (LDL-C).

None are standardized and the harmonization programs in place are voluntary not mandatory. "

For full letter to editor go to: Sniderman's letter to editior link







Monday, October 29, 2018

White bread and meat fast to lower LDLc?

I am reviewing Dave Feldman's week long fasting experiment at Houston's National Lipid Association meeting.

Bottom line of my review.
Even with week of fasting (weight loss?)
the nonHDLc is still high enough to put Dave at risk as well as the remnants
 (which Dave thinks is the most atherogenic particle?)


THE LDLc TANDEM DROP EXPERIMENT

9-29-2018 Sat AM
Total Cholesterol                               367
HDLc                                                   55
nonHDLc                                          312
TG                                                       78?
LDLc calculated                                296
remnants calculated from panel        16   normal

After "mysterious diet" 9-21-18

Total cholesterol                                317
HDLc                                                   57
nonHDLc                                           260
TG                                                          ?
LDLc                                                  233
remnants                                              27  (greater than 30 high)

9-22-2018
Total cholesterol                                 272
HDLc                                                    51
nonHDLc                                            221
TG                                                            ?
LDLc                                                    198
remnants                                                23

9-23-10
Total cholesterol                                   233
HDLc                                                      50
nonHDLc                                              173
LDLc                                                     160
remnants                                                 13 

9-24-18
Total Cholesterol                                   223
HDLc                                                      43
nonHDLc                                              180  (higher with drop in HDLc) 
LDLc                                                     147
remnants                                                33   (high again) 

9-25-18
Total Cholesterol                                   187
HDLc                                                      42
nonHDLc                                              145 
LDLc                                                     102
remnants                                                 43   (very high again)


9-26-18                             
Total cholesterol                                   165
HDLc                                                      38
nonHDLc                                              127
LDLc                                                       83             
remnants                                                44

Thus I think Dave's experiment should be called

The  nonHDLc & Remnant Tandem Experiment. 

It's leads us to a different conclusion from Dave.
















Sunday, October 28, 2018

My book is about weight loss maintenance

The Chronic Disease of Obesity 2nd edition should come out for sale by December 2018. 

When I was attending obesity conferences in preparation for The American Board of Obesity Medicine in 12-10-2015 I heard two giants in the field of obesity at Columbia University.

Their talks validated My Sponge Syndrome theory that I formulated after hearing a leptin lecture by Rudy Leibel at the Orlando Obesity conference in 2011 and published in The Tubby Traveler from Topeka.  Available for free at

Free book  link

3 min video from Dr. Mike Rosenbaum explaining wt loss maintenance  link

More information about Sponge syndrome here Perfect Storm  link

Saturday, October 27, 2018

New insight into Insulin resistance and lipid fat cells







Adipose tissue dysfunction is associated with low levels of the novel Palmitic Acid Hydroxystearic Acids (PAHSAs)

volume
One
"Is adipose tissue dysfunction associated with reduced PAHSA levels and do they affect adipocyte differentiation."
TWO
GLUT4 and adipocyte hypertrophy

THREE
PAHSAs may improve adipogenesis


I believe this new article adds a part of the puzzle for the

Thursday, October 18, 2018

Insulin is not a hunger hormone, Ghrelin is.


Professor Noakes asks if Insulin is a satiety hormone.
I hope to provide an answer for him in this thread of tweets.

Insulin has to be evaluated in the type of patient:
1-IR (high insulin)
2-DM (low insulin)
3-Obese (high leptin + leptin resistance)
4-Reduced obese (low leptin)
4-Lean

Professor Vassalli 2 min video
















Monday, October 15, 2018

Good charts on genetic studies and drug studies


APOC3, Coronary Disease, and Complexities of Mendelian Randomization link

Below is RED CIRCLE mentioned on twitter
Two new studies report that triglyceride (TG)-lowering mutations in APOC3 reduce coronary heart disease (CHD) 








 The red circle represents the CHD reduction (~46%) that is predicted for a loss-of-function mutation in APOC3 (R19X) (). 

Sunday, October 14, 2018

PEEK 12/ 2nd edition CHRONIC DISEASE OF OBESITY


PEEK 11/ 2nd edition THE CHRONIC DISEASE OF OBESITY


This is my chapter on first office visit to Doctor




Here I reference Eat Rich Live Long by Ivor Cummings and Jeffry Gerber MD


PEEK 10/ 2nd edition THE CHRONIC DISEASE OF OBESITY

Saturday, October 13, 2018

PEEK 9/ 2nd edition CHRONIC DISEASE OF OBESITY

Even with Liposuction the fat cells come back in a different location. 
Bariatric surgery does not reduced the number of fat cells. 





PEEK 8/ 2nd edition CHRONIC DISEASE OF OBESITY


Also read BLOG link


PEEK 7/ 2nd edition THE CHRONIC DISEASE OF OBESITY


You can't break through the plateau with less calories or more exercise.  Low leptin will slow down your resting metabolism even more to prevent starvation.
The KISS diet is designed to make certain you are not under counting calories and to help you lose 3-5 lbs that you recently gained 



PEEK 6/ 2nd Edition of THE CHRONIC DISEASE OF OBESITY


Thursday, October 11, 2018

Tuesday, October 9, 2018

CAC Score vs CAC volume



Do Statins Promote Coronary Calcification? Study Says Yes, and It Might Be a Good Thing

April 02, 2015
"CLEVELAND, OH – The results of a new study suggest that there is a paradoxical relationship between 
1-calcification of the coronary artery and 
2-atheroma volume 
among individuals treated with statin therapy.
 In the analysis, statins, specifically high-intensity statin therapy, actually promoted coronary calcification despite regressing the volume of coronary atheroma[1].
"The question of calcium is very relevant because we have people doing calcium scans as a means to determine the burden of disease," senior investigator Dr Steven Nissen (Cleveland Clinic, OH) told heartwire.
 "What we were struck by in this analysis was that the most aggressively treated patients—the high-intensity statin patient—if anything, developed more calcification. So if we're going to use coronary calcification as a measure of disease burden, you really have to know if the patient has received a lot of statins or not."
The study, led by Dr Rishi Puri (Cleveland Clinic) and published March 30, 2015 in the Journal of the American College of Cardiology, is a
post hoc analysis of eight intravascular ultrasound (IVUS) studies 
that assessed the effect of medical therapies, including statins, on serial changes in coronary atheroma burden. The studies, among them REVERSAL, SATURNILLUSTRATE, and ASTEROID, included 1545 individuals who received high-intensity statin therapy, 1726 who received low-intensity statin therapy, and 224 who didn't receive a statin.
Individuals treated with a high-intensity statin, such as 
1-atorvastatin 80 mg (Lipitor)
 2-rosuvastatin 40 mg (Crestor, AstraZeneca),
 had regression of percent atheroma volume measured by IVUS. 
In these patients, percent atheroma volume declined 0.6% from baseline,
 whereas percent atheroma volume increased 0.8% and 1.0%, respectively, among those who received a low-intensity statin and those not treated with a statin.
Regarding the change in the IVUS-derived 
calcium indexa measure of coronary calcification
all three study arms showed an increase in coronary calcification from baseline. 
In a model that adjusted for the change in percent atheroma volume, 
the increase in coronary calcium was greater among the 
1-low-intensity statin vs no-statin arm (P=0.03) and the  
2-high-intensity statin vs no-statin arm (P=0.007).
 There was no significant difference in the change in coronary calcification among high- and low-intensity statin-treated patients, although there was a numerical difference with more calcification in the high-intensity arm.
The researchers observed no correlation between the change in the calcium index and on-treatment levels of LDL cholesterol or C-reactive protein (CRP).
"It wasn't correlated with the lipid changes," said Nissen. "You can't attribute this just to LDL alterations. It looks like it's related to something that statins do. 
We know the drugs have complex biological effects, and some of those effects have not been worked out scientifically."



OCT 2015 BY Mike 

"In the first study[1], which was led by Dr Khurram Nasir (Baptist Health South Florida, Miami), investigators found that 50% of 4758 MESA participants would be recommended for moderate- or high-intensity statin therapy based on the 2013 American College of Cardiology/American Heart Association (ACC/AHA) clinical guidelines. Moreover, another 12% of patients could be "considered" for statin therapy based on their 10-year 5% to 7.5% risk of atherosclerotic cardiovascular disease (ASCVD)."

"Taken together, 
the researchers say that nearly two-thirds (62%) of the MESA cohort would be recommended or considered for statin therapy.

Yet among those recommended statins—this included   

1-patients w an LDL-cholesterol level greater190 mg/dL,  
 2-DM patients w an LDL-c level 70–189 mg/dL, and   
 3- nonDM patients w an LDLc level 70–189 mg/dL 
 4-and an estimated 10-year ASCVD risk greater than7.5%
more than 40% of these individuals had CAC of zero and an ASCVD event rate of 5.2 per 1000 person-years of follow-up. 
Among those who could B considered 4 statin therapy, 57% of these individuals had a CAC score of zero and an ASCVD event rate of 1.5 per 1000 person-years of follow-up.
Of the entire group eligible for statins, either recommended or considered,
 44% of 2966 pts had  CAC score of zero at baseline 
and a 10-year ASCVD event rate of 4.2 per 1000 person-years."
"Overall, our results showed that nearly 50% of individuals who are statin candidates, if they undergo a test that costs between $75 and $100, would have a calcium score of zero, and their 10-year risk would be below the threshold in which the guidelines recommend statins," Nasir told heartwirefrom Medscape. "This is most important for the patients in the middle, those who have a 10-year risk of 5% to 20%."
"In contrast, 56% of patients considered statin eligible based on the guidelines had coronary calcification identified on the noncontrast computed tomography (CT) scan (CAC>0) and had an ASCVD event rate of 11.2 events per 1000 person-years."

Monday, October 8, 2018

MY REVIEW OF ATTIA'S SUMMATION ON FELDMAN'S THEORY


My comments in purple

From
October 8, 2018

PODCAST

Ultimately Peter found Dave’s model unconvincing
for three reasons, and provided them in the intro of the podcast:
  1. “Dave was unable to explain the mass balance,
  2. meaning how does one account for the greater amount of cholesterol in, and the greater number of, LDL particles.
No one, including Dave,
is disputing that the phenotype of interest
has more LDL-C and more LDL-P.
There are only 3 ways this can happen
(these are [collectively exhaustive,
but not [mutually exclusive]):
make more, clear less, transfer from other pools
that we can’t see (e.g., cell membranes).
Hyperabsorption of cholesterol from Gut?
I think the data make the first of these
by far the most likely driver,
but Dave seemed unable to address this
and could not explain, to me at least,
what could account for this increase in LDL-P/C.
So on first principles,
my doubt of this model has gone up from
the start of this discussion,
as the person who developed the model
could not actually explain the mass balance.
This is one of the most fundamental requirements
of any model.
And to be clear,
even if this fundamental condition were met,
it would not be sufficient to make the case that
[lean mass hyper-responders or LMHRs]
are not at risk.
IMO, Dave's major blind spot is not looking at lifetime risk. He doesn't have CAC's or CIMT's on his LMHRs
(which may be negative before 40 yo), he ignores the risk of residence time of LDLp greater than 1500 for 30 to 40 years.
It’s a [necessary but not sufficient] criteria that, in my mind,
has failed.”
  1. “Dave argues that VLDL production
  2. is driving the LDL concentration, but the fact remains
  3. that in insulin-sensitive people
  4. (which presumably the LMHRs are),
  5. the opposite is true: there are fewer, not more,
  6. TG being exported from the liver
  7. and there is less, not more, apoC-III on the VLDL,
  8. thereby reducing, not increasing, their residence time.
In other words,
LMHR would have less VLDL to LDL conversion
than, say, someone with T2D.
So again, I can see no evidence whatsoever
that his energy model,
which can’t be explained on mass balance,
and can’t be explained on what is known
about the physiology of VLDL and LDL, is plausible.”
  1. “Even if you ignore the points above—
  2. which you can’t—
  3. I am more un-convinced than ever at the notion
  4. that we should exclude the roughly
  5. 2,000 genetic mutations
  6. known to produce a phenotype of
  7. high LDL-C, high HDL-C, and low TG.

We have 2,000 natural experiments.
Surely at least some of these cases (e.g., PCSK9 gain of function) are excellent proxies
for the key features of LMHR.
I am concerned most of these LMHRs have FH or polygenic genetic hypercholesterolemia.
Yet to ignore them for imaginary reasons (e.g., having gain of function PCSK9 is somehow toxic to endothelial cells because it impairs their ability to take up cholesterol despite there being no evidence that endothelial cells require PCSK9 to uptake LDL in a receptor-mediated fashion) is to say, in my opinion, one does not want to know the answer to this question.”
Peter emphasizes that probabilities play a very important role
in diseases like atherosclerosis,
and this nuance is often missing when discussing this disease.
Atherosclerosis is impacted by many things beyond the lipoproteins,
but that doesn’t
diminish their role in the causality of atherosclerosis,
Peter argues.
Note from Peter: Some low carb enthusiasts argue
that as long as they are insulin sensitive,
have high HDL-C and low TG,
their LDL-C (or LDL-P or apoB) is irrelevant.
Their data seems to be based on old low number trials. TG/HDL is supreme marker link
Further, many confuse imaging tests like
calcium scans (CACs) as biomarkers and argue that
as long as CAC = 0, there is no need to treat,
despite the risk predicted by biomarkers.
Fatty streaks don't show up on CAC.
A more sensitive test is CIMT. I had 11 patients with CAC zero but high CIMT. My 200 patient data link
If you are confused by all of the noise on this topic,
consider this example:
A biomarker like LDL-P or apoB is predictive.
It’s like saying you live in a neighborhood with a lot of break-ins.
A CAC is a backward-looking assessment
of damage that has already taken place.
Peter you make a very important point here.
ASHD is present with CAC greater than 1.
If nonHDLc kept less than 80 for rest of life with meds there should be no further build up of plaque (assuming other risk factors under control.)
So it’s more like an investigation
into a break-in
that already happened.
In my opinion,
waiting until there is grossly visible
(i.e., no longer just microscopic)
evidence of disease in the artery
to decide to treat
for risk already predicted by biomarkers
is like saying you won’t get a lock on your door—
even if you live in a high-risk neighborhood—
until you’ve suffered a break-in.
This is bad risk management.
As the saying goes, “When did Noah build the ark?”
Allen Sniderman has pushed for treating LDLc early. Multiplier effect link

Ultimately, it’s up to the individual,
who’s LDL-P and LDL-C
are very high while consuming a low-carb high-fat (LCHF)
or ketogenic diet (KD),
to make a decision:
the hope is that the following discussion
(and related references and material in the show notes)
can help people think through the issues and
make a more informed decision.