My new CIMT data as Black Swan against the ROOT CAUSE of IR

I have written before that I believe Insulin resistance is an important risk factor as part of metabolic syndrome.

However my keeping my LDLp very low over the decades I have had regression of CIMT thickness despite HgbA1c 7.9.

I have had DM 2 since 1999.
I have been obese most of my life.
I have controlled my blood pressure with medicine.

I started Low carbohydrate High fat diet in 2011.
Lab records link
I didn't need LCHF to correct my TG/HDL ratio.
Triglyceride 65
HDLc 51
LDLp 656
On Crestor

I went on LCHF for weight loss or at least to not gain more weight.

Over the decades the one risk factor I have been able to control extremely well was my lipid panel. 

I struggled with weight loss and regain.  I struggled with tight control of my Hgb A1c but not my LDLp.

Readers, please take note.
Do what works for all risk factors.
No matter what stress in your life, no matter where you are in your commitment to your program at the moment you can still take a statin or a nicotinic acid (enduracin) very easily and cheaply.

Atherosclerosis occurs from lifelong exposure to nonHDLc greater than 110 or LDLp greater than 1,000.

Keep those numbers low as I did and you will probably prevent progression of disease regardless of diet or poor control of blood glucose.

I did it and I proved it here

This is long term data.
Very important distinction of people who take CIMT's a few times a year
with short term changes in diet.

Regression Over Nine Years

  DATE                     CCA MEAN              CCA MAX

12-17-09                    0.599                            0.741

11-29-18                    0.567                            0.643
                                                   
Change                      0.32 less                      0.91 less

In the future all Family Docs and Internist will do routine CIMT's on all their patients to monitor and find early atherosclerosis. Then to treat early disease.
 I did this in 2010 with 200 patients in Tubby Theory from Topeka

 My not fasting advanced lipid profile 11-19-18  I was off lipitor for one month

Off Belviq & Victoza yet lose weight with no hunger over Thanksgiving

Off Belviq & Victoza yet lose weight with no hunger over Thanksgiving

Maybe I have been on such a low carb diet with a high ketone level, 
that the ketone level did have a major effect on my satiety?

OFF LIPITOR 10 mg for one month

LDLp 447 off Lipitor for one month but continued Endur-acin (nicotinic acid 1,000 mg a day.) on 60-70 % fat diet. 
Tryglycerides 110 but I was non-fasting.  I like to do a post prandial TG test to see how well I am doing. 

With weight gain and less exercise my Hgb A1c went up a little


Below is a unique slide.  I had another CIMT today. Below is the preliminary result.

       CCA MEAN  .567       CCA MAX .643 

Finding and treating insulin resistance and obesity very important

Before getting into the finer points of the article below that Ivor Cummings sent me to prove there was "massive evidence" that TG/HDLc ratio was much better than LDLc in predicting risk I want to give him and Jeff Gerber MD credit for improving my understanding of the importance of finding insulin resistance early with more aggressive lab work.  Insulin levels should be taken with fasting blood sugars and insulin resistant patients should be treated with low carb high fat diets.
I noted this in the second edition of my book.  The Chronic Disease of Obesity.

No other recent diet book that I admire discuss this.
1-Change Your Biology by Louis J Aronne MD
2-Always Hungry?  by David Ludwig
3-Diet Fix, Why diets fail and how to make yours work by Yoni Freedhoff.

My major critique of Eat Rich and Live Long is an attempt to show that TG/HDLc ratio reigns supreme by Ivor Cummings.  I have critiqued the 3 references he uses to prove his assertion at Only 1250 patients in 3 studies to show ratio reigns supreme

Now Ivor has sent me a retrospective review of cases that claims TG/HDLc is a better predictor.  2015 with 100,000 cases over eight years.

Quick problem with this study: "Being insulin resistant w LDLc less than 142 or nonHDLc less than 173 conferred a higher risk for ischemic events after 8 years than LDLc greater than 160"

These are high LDLc and nonHDLc with IR.

Especially in presence of IR, lipid goals lower

Article showing TG/HDL ratio more predictive than LDLc for CVE link

 The above chart uses 160 LDLc as cut off. 

Being insulin resistant with LDLc less than 142 or nonHDLc  less than 173 conferred a higher risk for ischemic events after 8 years than LDLc greater than 160

My critique of Stephan G's article on ETOH, coffee and chocolate causing obestiy

Go to this link to see full article review

I went over Dr. Guyenet's article on Coffee, chocolate and alcohol in the link above.



On this blog I was curious to see if he had fleshed out his theory of habit forming foods that had drugs in them which made them more habit forming that just extremely good tasting food.

Food Addiction
There is no such thing other than when you are starving to death and then you will eat garbage. 

Photo above is from The Great Starvation Diet by Todd Tucker. On 1550 calories a day.  There would be kicked out of the program if they gained weight from eating garbage.

I went to pain control conferences.

Gambling, shopping, sex may be very habit forming because of dopamine release.

Alcohol, opioids, barbiturates are chemical addictions which when you stop them suddenly you go through severe withdrawal.

Ritalin was said to be addictive,  yet most kids went on drug free weekends.

No one has has to be admitted to the ER for sudden withdrawal of coffee or chocolate.

Disease of Alcoholism is very different from even a daily high intake (5 oz) of alcohol.  Many colleges kids survive it.  They like it but most are not addicted.

Confusing food with addiction is very bad science or at least a tremendous
stretch of logic.

Holiday weight changes on Atkins Nov 2018

My wife and I returned to Kansas for the holidays.  I was surprised I did not gain weight after being in the car for 4 days with little walking

I was not surprised to see my weight go up 10 pounds after 5 days in National Harbor, Washington DC and a short direct plane ride.  I was on Atkins or LCHF as I document on paper.  NK 3.4 

The Big Question here is why did I gain after two weeks of documented nutritional ketosis? 

We celebrated Thanksgiving Thurs, Fri, and Sat with big great meals.  I tried to keep to Atkins or LCHF and was not hungry as I am on Belviq as well and only walked about 6,000 steps a day.  I consciously tried to not overeat the meats and just take a taste of side dishes.  It worked out quite well. 

Thanksgiving 2018 in remembrance of harder times

Last week I stayed at Wyndham resort in National Harbor.
National Harbor is a new 10 year old development most people (like myself) are not aware of.  Nice point of departure to visit D.C.

Some poignant photos.

Critique of NYT article by Gina Kolata Nov 2018

Link to my complete critique of Gina Kolata's article

I love Gina Kolata's work but I believe she underestimates the miracle of the number of diet medications presently available.

Peek 13/ 2nd edition of Chronic Disease of Obesity OCT 2018

I have been on Atkins or LCHF since 2011.
I believe the root cause is not IR but Obesity.
Must not use medications that make Obesity worse such as Insulin & Prednisone.
I helped this patient make her way through a morass of Doctors and medications

My critique of Dr Peter Attia's article on imaging for atherosclerosis

Link to my critique of Attia's tour de force article 

This was a great explanation of atherosclerosis using Dr Tom Dayspring's slides.

However I had a few items to add to Peter's imaging narrative.

1- No mention CIMT
2- No mention of non-HDLc
3- Did not go into treatment,

Here is a sample of how I treated my 200 patients back in 2010

 Go to more data at

Chapter 12 from Tubby Theory from Topeka link

This chart shows how I used Topeka Triple Therapy for early treatment of atherosclerosis. 

At some point get advanced lipid testing for particle count

Thanks to Dr Thomas Dayspring for his great mentoring of me and thousands of others.   Dr. Dayspring posted the article below.  I was lucky to record a great discussion in Cincinnati National Lipid Association meeting between Dayspring and Sniderman.  For most purposes non-LDLc is sufficient to find discordance.  But get at least one advanced lipid testing to be certain as well as Lp(a).

Waist > 40 inches in men is one of five criteria for metabolic syndrome
Thus I coined the term Tubby Factor to tell these people to calculate their non-HDLc to look for discordance as with Tim Russert who had LDLc 68 yet had sudden cardiac death.

The Tubby Factor explained link

100,008 pageviews. A tipping point

I have published 4 books

link to my books

After reading Malcolm's book on the TIPPING POINT I have tried to reach a tipping point.  Tonight I hope I reached the first point?

I have original ideas that I put into my books.
4 original ideas link
I am trying to get the tipping point to get recognition of my ideas.
Sponge Syndrome
Multiplier effect
Topeka triple therapy.

If not an academic or in a big market area it is very difficult to get noticed.

My second edition of The Chronic Disease of Obesity was published on
10-28-18

There is no other book with this title.  There is a obesity epidemic and I try to explain the problems people can't maintain weight loss and the solution.  I use my personal history to illustrate.

May you live as old as Moses. Chapter 21

This chapter 21 from The Tubby Theory from Topeka 2010

Review of anti-statinists article 2018

10-3-2018 Dr. Uffe Ravnskov review link

My comments in purple.

"Conclusion

Our conclusion is that the statements from the supporters of the cholesterol campaign
and the drug companies are invalid, compromised by

1-misleading statistics,

Using relative reduction of risk vs. absolute reduction in risk
is not such an important difference when using RRR for trials of 5,000 people
and then extrapolating to a population of 100,000,000.

2-excluding unsuccessful trials,

This of course is the point.
 The present author is using trials that prove his point,
and he ignores trails that don’t prove his point.  
I doubt I have the time or knowledge to check if
his trails are the same RCT double blind large numbers
with positive primary outcome that the statins academics are using.
 In short I suspect Uffe’s trails are poor trials.
Please use nonHDLc data.

3- minimizing the side effects of cholesterol-lowering, and

Pharma has minimized the amount of muscle related pain.
 I know this from clinical experience.
However if low dose triple therapy can be used instead
there will be a significant drop in nonLDLc with less side effects

4-ignoring contradictory observations from independent investigators."

Again I am dissatisfied that Uffe does not discuss
1-nonHDLc or
2-remnants or
3-LDLp or apoB.

My review in 2015 of Uffe Ravnkov on statins link




In fairness here is a more detailed rebuttal to Statins.

Why statins have failed to reduce mortality

in just about anybody

• Eddie Vos, MEng

• Colin P. Rose, MD, PhD

• Pierre Biron, MD

127 Courser Road, Sutton, QC, Canada J0E 2K0

Department of Medicine, McGill University, Montreal, QC, Canada H3H 1V6

Department of Pharmacology (Retired), Faculty of Medicine

Universite de Montreal, Montreal, QC, Canada H3C 3J7

published online 11 February 2013.

1-"It is unfortunate that in their Counterpoint Sniderman et al

digress from the issue of mortality."

My comment:

This issue of mortality is the first item Sniderman addresses:

“Moreover, the investigators from the Heart Protection Study (HPS)
demonstrated that all-cause mortality was 14% lower
as the result of a 17% reduction in cardiovascular mortality in the
10,269 patients treated with simvastatin compared with the 10,267
who were allocated to the placebo arm.3”

2-"To reiterate, all trials in which investigators used a placebo in women failed,

as stated in the Counterpoint from a reference by Walsh and Pignone1:

“For all trials reporting total mortality,

lipid lowering did not appear to have a beneficial effect for women with or without previous cardiovascular disease

over the 2.8 to 6-year study period in the available trials.”

The relative risks were 1.00 and 0.97, respectively.

Here, too, numerically the most “benefit” was in fewer revascularizations performed,

but this in the secondary prevention group only

[number needed to treat (one year) = ∼140].

That’s it.

Adding another 40,000 on-statin women patient-years to the trial database

cannot change this fact of mortality benefit failure.

Indeed, the article by Brown et al2 referred to in the Counterpoint

showed impressive images of arteries opening

(arguably by delipidation of lesions),

but there was only one death in this study (n = 146)

in which the patient used either

1- lovastatin,

2-30 grams of bile acid sequestrant per day, or

3- a mega-dose of high-density lipoprotein–increasing vitamin B3,

niacin,

arguably the only promoter rather than inhibitor of biochemistry

in cholesterol-affecting studies.

Unfortunately, in this type of study(Brown) one cannot tell

whether an artery has stronger fibrous caps

because cholesterol itself has no known role in the synthesis

of the relevant arterial and cardiac proteins, structural collagen,

and architectural elastin.

If any symptom relief was obtained, as

it well may have,

this could lead to a few less elective revascularizations performed

during such 30-month study length.

However, all this distracts from other potentially life-saving causal avenues

of research.

It also distracts from the

failure of our six-decades-old “war” on cholesterol to have saved lives.

Clinicians should remain mindful that without yearly numbers needed to treat,

nonfatal relative risks and surrogate measures do not represent

life extensions in what is still our most fatal type of disease—

cardiovascular disease—

and that the easiest to count and often-hidden end point

is all-cause mortality in patient groups, witness:

The Cholesterol Treatment Trialists’ Collaboration.

We maintain that statins

have not been demonstrated to be life-extending drugs

except, possibly and for a brief window of time (years),

in younger, high-risk men.

We could say it no better than paraphrasing the cited

mortality is a rather insensitive and unhelpful end point in statin trials

Back to Article Outline

References

1. Walsh JM, Pignone M. Drug treatment of hyperlipidemia in women. J Am Med Assoc. 2004;291:2243–2252

• View In Article

2. Brown BG, Albers JJ, Fisher LD, Schaefer SM, Lin J-T. Regression of coronary artery disease as a result of intensive lipid-lowering therapy in men with high levels apolipoprotein B. N Engl J Med. 1990;323:1289–1298

• View In Article

• MEDLINE

3. Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20 536 high-risk individuals: a randomised placebo-controlled trial. Lancet. 2002;360:7–22

• View In Article

• Abstract

• Full Text

• Full-Text PDF (207 KB)

4. Cholesterol Treatment Trialists' (CTT) Collaboration. Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90 056 participants in 14 randomised trials of statins. Lancet. 2005;366:1267–1278

• View In Article

• Abstract

• Full Text

• Full-Text PDF (162 KB)