The Tubby Factor explained

Non-HDL cholesterol, what is it?

This term is a mouth full. 

In 2010 I suggested we replace non-HDLc with one easier to remember:

The Tubby Factor

Tim Russert died of sudden coronary death on 6-14-2008 with LDLc of 68.

He had metabolic syndrome.

Tim Russert's lab:  

1- Waist greater than 40"  

2- HDLc 37 (it had been in the 20's)

3- Triglycerides 399 (supposedly taking Niacin 2g and Tricor 145)

4- Fasting glucose greater than 99

5- He was on anti-hypertensive medications

Mr. Russert had all five of the criteria for metabolic syndrome.

Mr. Russert was treated to goal of 68 LDLc on statin.

However he was not at non-HDLc goal less than 80.

His non-HDLc was Total cholesterol minus HDLc

TC 155 minus HDLc 37= 118 non-HDLc

After Mr. Russert's surprising episode of SUDDEN DEATH,

the cardiology and CV surgeons on TV said everything was done that could have been done. 

Lipidologists were not interviewed or where afraid to teach the importance of LDLp or apoB particle levels once you find the 

non-HDLc was high after Rx. 

I found Peter's Attia article on internet and posted this excellent chart showing the increased discordance between LDLc and LDLp

This is why I wrote The Tubby Theory from Topeka in 2010.
It was well known among Lipidologists that Mr. Russert was not treated to goal.
Even though he had a normal nuclear stress test,  no one mentioned Glagov remodeling of arteries.
Mr. Russert had coronary plaque that a nuclear stress missed because the plaque did not block off greater than 70% of the coronary artery.  His CAC CT score was 200 ten years earlier.

I believe Doctors did not know about non-HDLc because the term was too cumbersome.  I choose to coin a new term.  The Tubby Factor.   I hope patients would go to their Doctors and ask what their Tubby Factor was.  Dr. Thomas Dayspring did not like the term because 20% of people with metabolic syndrome do not have a large waist.  For the general public I thought it was adequate.  Even in a great book on keto-diets,  Eat Rich and Live Long, Cummings and Gerber fail to mention non-HDLc as a much better biomarker than LDLc in 2018.

I write again about this topic with the help of Dr. Peter Attia's chart to teach the importance of discordance and correcting it with calculating non-HDLc from routine lipid panel or getting advanced lipid testing with LDLp or ApoB particle counts.

Official guidelines for LDLp and apoB seem a little high to me

My comment in purple. 
In my book The Tubby Theory from Topeka written at the end of 2009,  I advised that non-HDL-C be called the Tubby Factor as it is easier to remember to ask your Doctor, what is my Tubby Factor?
Non-HDL-C is more accurate than the LDL-C.  

More accurate than both of those is the particle number 
 (don't get bogged down with particle size, HDLc or Triglycerides). 
 ApoB and LDLp are the best tests. 
 LDLp Ion method done by Quest lab does not use the numbers in this chart.  
The apoB by Quest is the same range as this chart. 

"Dr Sniderman: The first thing I do is measure apoB to determine whether treatment is necessary or not.

If apoB is elevated, then all things being equal, treatment needs to be seriously considered. Treatment is a collaborative process between the patient and the physician and involves diet, exercise, and lifestyle as well as pharmacologic agents if indicated.

For the majority, my target for LDL-lowering therapy is an apoB < 75 mg/dL.

For those at very high risk, my target is an apoB < 65 mg/dL.

These are the equivalent population levels to the LDL-C and non–HDL-C targets chosen by many recent guideline groups. The apoB targets chosen by many of the guideline groups are much too high. It seems that once 1 group selected values, the others just repeated them."

Above quote from Lipid Round table article 

My 6 CIMTs show atheroma regression with low LDLp 

This chart shows LDLc 70 in same row as Non-HDLc  83 and LDLp 720 and apoB 54. 2008

In high risk patients I try to get(in my book from 2009):
 Tubby Factor (Non-HDLc )less than 80.  INEXPENSIVE
LDLc  les than 70 USUALLY CALCULATED AND INACCURATE IN INSULIN RESISTANCE
apo B less than 60 (immunoassay) PARTICLE COUNT
LDLp less than 750 (done by Liposcience NMR) PARTICLE COUNT-  BEST TEST MY OPINION







The 2014 American Diabetic guidelines are still using the old LDLc. 
Diabetics often have discordance between LDLc and Tubby Factor and Particle number.

Post World Cruise Lab Results

I returned home from my 112 day world cruise yesterday.  I weighed in on my home scale at 251.5 pounds.  I attribute the weight loss to taking Victoza injections.  I also attribute the improvement in my Hgb A1c down to 8.1 to Victoza as well.  I tried to walk two hours a day on sea days.   I tried to stay on a low carbohydrate diet.  I drank at least one glass of wine a day.  I was never hungry.

The LDL particle number is the most important lipid metric to prevent heart attacks and strokes.
Berkley Heart Lab does an excellent apo B test.
My apo B before the cruise was 62.  After the cruise on May 2, 2012 my apo B was 47.

The routine lipid panel was also done on 5/2/12:
Total Cholesterol          109
HDL-C                           45
Tubby Factor                  64
LDL-C                            50
Triglycerides                  72

This data is not included in my book, The Tubby Traveler from Topeka as that manuscript is at the printers.


It is very important to focus on the fact that this excellent lipid profile is obtained while eating 60% fat. 

CONFOUNDING COVARIABLES:
I lost 5-7 pounds while on the cruise.
My Hgb A1c improved.

 I switched from Crestor 5 mg to Atorvastatin 20 mg to save money.
 I stopped Endur-acin because I found I had an asymptomatic peptic ulcer.
  I increased my exercise and continued my actos.
  Off the niacin my HDL-C fell, however I don't know what my HDL-P is.   But does it matter?


Dr. Dayspring has always taught that the main goal is the particle number.  We don't treat HDL-C or triglycerides.  The AIM HIGH TRAIL confirmed this.  Particle size is also not important.  I have included as many lipid results in my book because it is a case study.
For the average patient going on a low carbohydrate diet.  Get your CAC, CIMT and Tubby Factor (non-HDL cholesterol).  If you have plaque go on a statin.  If you can afford a baseline LDL-P or apo B, I strongly advise it to make certain you do not have discordance.  As you eat 60% fat in your low carbohydrate diet, please check your Tubby factor or LDL particle number every four months if you are on a statin.

Much of the Low carb promoters push that the LDL-C may go up but the particles are larger.  The HDL-C goes up and the Triglycerides go down.  I try to bridge this point of view to the lipidologist viewpoint that it is the LDL particle number that we have to keep our focus on.

Vegans point out that Ornish had regression of plaque.  Similar to the lipid neutral trials of Gardner and Sachs, the CONFOUNDING COVARIABLE of weight loss obfuscates the interpretation.

In any vegan diet that is low calorie, the total carbohydrates are also reduced.

I hope my case study brings some clarification or at least a reduced fear of going on a high fat diet if you follow your LDL particle number. 

In 2011 I did not gain or lose weight by the end of the year.
My Hgb A1c was worse as I went off actos for a few months.
My exercise was zero to 40 minutes a day.
I tried to minimize the CONFOUNDING COVARIABLES in 2011.
My lipid panel remained quite good during most of  the year and I have no increase in plaque on my serial CIMT.  My CAC increased a little but was done while I was in Atrial fibrillation and was still lower than my highest CAC of 20 before I got my LDL-P below 750.

Update on Tubby Theory from Topeka 2008 to 2016

8 years later

A friend asks me:

"You have been talking about Coronary Calcium Score for a long time. Were you ahead of your colleagues, or in step? Is the Ultra Sound of ..."
07:52 AM - 29 Apr 16



I wrote the book The Tubby Theory from Topeka after I passed the lipid boards and Tim Russert died.
No one in NLA spoke on National media that his non-HDLc was not treated to goal.

I guess they were afraid of being sued.
I thus wrote a book about treating patients in my practice aggressively.
I used the teachings of my mentors at NLA.
I quote them (my mentors) throughout my book.

My only originality was to call non-HDLc the Tubby Factor because patients and physicians could not remember "non-HDL cholesterol" nor how to calculate it. 
I called it the Tubby factor because non-HDLc is usually discordant with LDLc in patients with metabolic syndrome.

Since my book in 2008 I have been gratified to see that CAC and CIMT have proven themselves as significant and independent risk predictors for CVD.
New AHA/ACA guidelines in 2013 by Stone use CAC or CIMT in low risk patients to determine if statins should be started or not.
Niacin is under attack as being a dangerous drug which I believe is just silly.  If low dose wax matrix niacin 1,000 mg/d is used with low dose lipitor 20 mg/d early in the disease of sub-clinical atherosclerosis for long term treatment I believe we can prevent most CVD.

I am very proud of my book and still stand by it. 
Even the low fat diet I suggest might be suitable for some folks who are insulin sensitive and hyper-absorbers of cholesterol.

My contributions to science of Lipids and Obesity

My 4 original ideas as found in my four books. 

ONE: 

"Multiplier effect" is a term I coined for treatment to prevent

 cardiovascular disease in patients

 with at least one risk factor & positive CAC.

I advise treating early with multiple drugs 

(low dose statin, Endur-acin, Zetia).

Hence the term:  Multiplier Effect. 

 Low cost Low side effects.

 Resultant LDLc almost as low as PCSK9's achieve. 

TWO:

Non-HDL cholesterol was not calculated for poor Tim Russert.  

His physician was complacent with target of LDLc less than 70 achieved.  

If my term "The Tubby Factor" was used rather than

 the complex mixture of words non HDL cholesterol, 

more patients and Doctors would know it how to calculate it. 

 (Total cholesterol minus HDLc= Tubby Factor) 

Easy to remember name.  

THREE:

The Sponge Syndrome theory and term I coined to explain 

why the Reduced Obese usually regain weight. 

It's that fat cells never die

 (if they do they are replaced even with liposuction).  

Obese (BMI greater than 30) have billions of extra fats cells (adipocytes).  

When a person loses a large amount of weight

 (even with Bariatric surgery)

 they slowly regain weight 

because the billion of shrunken fats cause LOW LEPTIN LEVELS

 and all the billions of fat cells send out MiRNAs

 to the cells of the body telling the cells

 the body is starving and  to slow down metabolism.  

It's the number of fat cells that count in the Reduced Obese. 

 Not exercise.  

 Reduced Obese will regain weight even with low calorie counts

 because fat cells get priority with the extra calories
to make more fat for long term survival.  

Thus as long as the leptin level is low
 the MiRNA's are sent out

 to tell the body's cells to use the extra calories

 not to make heat but to make fat
the Reduced Obese will regain weight. 

This why it is called the Sponge Syndrome.  

All those billions of shrunken fat cells act like a sponge to make more fat. 

FOUR

Topeka Treatment for high cholesterol, low HDLc and high Triglyceride. 

Use 3 very inexpensive medications in low doses to achieve goal LDLc.

Atorvastatin 10mg
Enduracin (nicotinic acid) 1,000 mg 
Zetia (start with one half tab)

Start with one drug each month and monitor LDLc. 

Irish Medical Nihilism

Ivor Cummins‏ @FatEmperor Sep 13

Replying to @brianedwardsmd @DaveKeto and 

"For how long Brian?

If the single death (Tim Russert's Sudden Cardiac Death) didn't happen on cue,

when did it happen? A few months later, or many years later?

Given that 110/111 not changed, (I have no idea what this ratio means)

it's important to know how much extra time the lucky guy got"

To me Ivor's response about Tim Russert's case (link) is almost incoherent.

I don't think Tim was lucky

I think if a non-HDLc was calculated his Doctor wound have realized Tim was not treated to goal

with his present medication.

Tim had a nuclear stress test one month before his sudden death.

Since it was normal his Doc thought Tim was bulletproof with LDLc 68.

If the Doc calculated:

Total Cholesterol minus HDLc = Non HDLc the Doc would have realized

Tim had discordance due to his metabolic syndrome.

Ivor, this is a month, before Tim had sudden death with no other symptoms.

I suspect in the surgical and intervention atmosphere of then and now:

(President Bush did not need a stent link),

Tim would have had an angio stent or bypass surgery.

He would be alive today.

Thus I have answered Ivor's question above (repeated below):

"For how long Brian?

If the single death (Tim Russert's Sudden Cardiac Death) didn't happen on cue,

when did it happen? A few months later, or many years later?"

And yes non-HDLc discordance and apoB or LDLp further discordance would have alerted Tim's Doctor to do further testing and Tim would be alive today. In my opinion.

Ivor writes:

 @FatEmperor

Replying to @brianedwardsmd @Bill76533323 and 

His diabetes, Trig/HDL, remnant cholesterol etc. showed that he was in for a shaky future - sure. The ApoB doesn't add much to the assessment, if you're riddled with outrageous markers...

I can only think that since Ivor does not treat sick patients he is way out of his wheelhouse.

If Russert's Doc did not calculate, or get a Apo B, or LDLp I doubt he had any idea about remnants.

A simple non-HDLc (The Tubby Factor) would have alerted Doc to discordance and incomplete treatment. Even today many Docs don't know what non-HDLc is.

Total cholesterol minus HDLc = non-HDLc

Much easier than ratios. Simple subtraction.

Numbers obtained from standard lipid panel.

No new cost.

No excuse not to make it the main parameter for CVD risk.

Explanation of The Tubby Factor link

Irish Medical Nihilism Link

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

Update on the Tubby Theory from 2009

In my book Tubby Theory from Topeka, I coined a term the Tubby Factor to represent the term non-HDL-cholesterol.
I also advised a step approach to using 3 low dose lipid lowering medications
I thought it was easier for patients to remember to ask their Doctors for this number and that it was much more predictive than LDLc.
I preferred LDLp or apoB to non-HDLc but I suspected the guidelines would not accept the particle count as the new standard.
Sure enough the guidelines still use LDLc but there is more acceptance of non-HDLc.

This article, High ApoB in Young Adults Predicts Midlife Atherosclerosis 
states:

"Young adults aged 18 to 30 who had higher-than-average apolipoprotein B (apoB) levels showed an increased risk of developing coronary artery calcification (CAC) by middle age, in an analysis from the Coronary Artery Risk Development in Young Adults (CARDIA) study[1]."

"However, although some clinicians favor measuring apoB as well as traditional lipid biomarkers to help predict CVD risk, and apoB is included in some guidelines, it is not part of current ACC/AHA guidelines, and others are not convinced that studies have demonstrated that apoB adds predictive value. ."

"We take the viewpoint that apoB is a more robust biomarker of CVD risk [than LDL cholesterol and non–HDL cholesterol] based on observational studies and clinical trials such as AFCAPS/TexCaps," he told heartwire . "For all patients with metabolic syndrome and type 2 diabetes, I routinely measure either apoB or LDL particle concentration," he said, adding that "it has been shown that apoB or LDL-particle concentration is more strongly associated with CV risk than LDL cholesterol and non–HDL cholesterol in most studies."

'However, Dr Scott Grundy] told heartwire that although there's no question that apoB is a better predictor of atherosclerosis and heart attack than LDL cholesterol, "it's much more difficult to show that apoB is a better predictor than non–HDL cholesterol."

"Furthermore, non–HDL is easily measured in a clinical lab, whereas apoB requires an extra test (an immunoassay) with added cost. "Should we all start going out and measuring apoB? I think the answer is 'No,' " according to Grundy.

It is also not clear if an apoB target treatment goal would be better than a non–HDL goal, he continued. This may be moot, though, since "the latest [ACC/AHA] guidelines [have eliminated treatment targets and] say that you come up with a certain level of risk and treat [the patient] with a statin and don't ever measure cholesterol again."


"For now, "these data suggest a dose-response association between apoB in young adults and the presence of midlife CAC independent of baseline traditional CVD risk factors," the researchers conclude, adding that "further follow-up is warranted to determine if apoB measurement in young adulthood is a marker of later CHD risk as well."


 Page 147 and page 148 of The Tubby Theory from Topeka which I wrote in 2009 and published in 2010.

Back Cover of my book, The Tubby Theory from Topeka.
I am with my son, now a medical student who helped me write the book. 

 

The science of Lipidology and Obesity must be integrated

A letter to my mentors at National Lipid Association and Obesity Medical association.

My path to writing The Chronic Disease of Obesity Feb 2018

My first NLA meeting was in Kansas City at the Intercontinental Hotel on 10-19-06.

I passed the NLA boards on 9-27-08.

I wrote the Tubby Theory from Topeka in Dec 2008 because no one on TV pointed out that Tim Russert was not at goal for nonHDLc.  Suggested we call nonHDLc the Tubby Factor.

  I was honored to be awarded to be a Fellow of the NLA on 5-1-09 in Miami.

 At that Miami meeting Alan Brown promised to let me speak on Obesity at an NLA meeting. 

I heard Dariush Mozaffarian speak about saturated fat at NLA meeting in Washington DC the summer of 2010. It was a sea change for me. 

True to Dr. Brown's  promise, I gave the Hunger Games Lecture in Roosevelt Hotel March 2015 NOLA

I was accepted to put up a poster at the New Orleans meeting in 2016

Published The Tubby Traveler from Topeka April 2012.  Elucidated the idea of the Sponge Syndrome. 

Passed the American Board of Obesity Medicine Exam on 12-10-15

I want to thank you all and especially Dr. Thomas Dayspring for guiding me on a life of scholarship that has been wonderful.  

I was enthralled by Tom when he gave a lecture in Lawrence, KS.

I have tried  to combine both disciplines of Lipidology and Obesity into a coherent approach to maintain weight loss and prevent complex plaque with what I call the multiplier effect of treating early with low dose atoravastatin, endur-acin and ezetimibe for synergy. less side effects and low price. My present book attempts to explain why people regain weight due to low leptin which can be avoided in the long term with multiple lifelong diet medications. 

I hope you will read my short book on line for $4 kindle version and I would love to hear your comments.

Thank you for a wonderful educational experience, I have tried to apply what you taught me in my books.

Flub 5 in Eat Rich Live Long

In Eat Rich Live Long, I like the early diagnosis of insulin resistance with fasting glucose and insulin level and to treat with Low carbohydrate High Fat diet.  

I depart from their advice on lipids except for recognizing the value of CAC CT (calcium scores).  On page 262 in Eat Rich Live Long it is stated that 

"APOB/APO A1 ratio is the Master ratio"

Cummings and Gerber use this 2005 Ridker reference to prove their point with the chart on "Comparison of Risk Predictors"

Unfortunately when I looked up the reference the ApoB/ApoA1 data was misrepresented.  

See big chart from the trial presented below the Comparison of Risk Predictors.  

Eat Rich Live Long chart on P 263 from Ridker data. I don't see this data in trial. Real data below.

 The actually data from Ridker acticle that includes non-HDLc which is not on chart above 

Eat Rich Live Long p262 does not address non-HDLc has same result as LDLc/HDLc ratio with 46 events as the best predictor in Quintile 2 and better than ApoB/ApoA1 with 54 events.

Eat Rich Live Long p262 does not point out that LDLc at the highest quintile #5 shows LDLc has less events at 156 than ApoB/ApoA1 at 200 events.

Total cholesterol/HDLc had 212 events while LDLc had 156 events at the highest quintile.
 Eat Rich Live Long says LDLc is worthless.
P246 "The truth is that when it is high, LDLc is sometimes associated with bad things, but it is a weak and erratic risk factor"
page 255 " If your LDLc value is well above 200 mg/dl, it is more likely to have some meaning"
In this Ridker trial that is sited in Eat Rich Live Long the mean LDLc is 171 (does not have to be greater than 200 to be significant) and the event rate is lower that ApoB/ApoA1 in the 5th quintile.

CONCLUSIONS:

(of the Ridker article that Eat Rich Live Long uses on p 262,263 but contradicts the article.) 

"Non-HDL-C and the ratio of total cholesterol to HDL-C were as good as or better than apolipoprotein fractions in the prediction of future cardiovascular events. 

After adjustment for age, blood pressure, smoking, diabetes, and obesity, high-sensitivity CRP added prognostic information beyond that conveyed by all lipid measures."

Eat Rich Live Long never mentions non-HDLc (The Tubby Factor)

Ridker 2005 sited on p262  Eat Rich Live Long:

COMMENT #1
"ApoB is highly correlated with non-HDLc" 

"The strength of association for non-HDLc is clinically equivalent to that of ApoB"
On page 261 in chapter, My Advanced Lipoprotein Test Has Shifted.  
I agree that apoB or LDLp is better than LDLc.
However, they never mention non-HDLc in the book. 

 COMMENT #2
"ApoB/ApoA-1 ratio not superior to ratio of TC/HDLc
In fairness to Cummings and Gerber on p262 do write "Interestingly, the TC/HDL ratio did even better (than ApoB/ApoA-1)"
However it is strange to me they use a reference that contradicts the titled of the chapter ApoB/ApoA1 THE MASTER RATIO.

COMMENT #3

"support the use of standard lipid measures rather than 

ApoA-1and ApoB in PRIMARY risk prevention"

COMMENT #4
"Non-HDLc ....were as good as or better than apolipoprotein fractions"