Book Cover tease for next Alzheimers Book Year Three 2021

I have four photos I might use for  next book:

The Pursuit of Happiness with Alzheimer's
Joyful Experiential Stimulation of the Brain
YEAR THREE 


ONE


ONE

I liked using a suit and tie in the first cover and now considered a beach shot with my morning beard and rainbow sticking out of my head.  
Very Hemingway. 
Sort of the Old Man of the Sea with Rainbow shooting inspiration and happiness to his brain.


 TWO above:

Early idea that I don't like so much anymore.


THREE
Latest front runner is my life size bust above.
However I was thinking of using a face shot again on the cover. 
I think it tells a story.

Recent selfie I took below:


There are typical face changes in Alzheimers patients.  My future headshots may reflect it. 

Again it's fun to do this creatively.
It's been a very creative productive first quarter of the year. 

I might use this photo below for my back cover author photo
.
  
My other books:

Sixth Book "YEAR ONE" Published Feb 2020



Back cover below with my grandson.


Fifth book "YEAR TWO" published Feb 2019



Fourth Book Published Feb 2017



















Third book after starting Atkins diet 2011


Second Book wrote in Kansas after passing ABOM boards.






My first book that I wrote in Idaho


I am a specialist in Obesity, Lipidology and Internal Medicine 

I have written five books that reflect a sea change or paradigm shift in treating cardiovascular disease and obesity
and Alzheimers. 

First National Lipid Association meeting 10-19-06.

 Passed NLA Boards 9-27-08. 

Wrote The Tubby Theory from Topeka 12-08. 

Became a Fellow of NLA 5-1-09 

Heard Dariush Mozaffarian speak about saturated fats at NLA meeting in Wash DC Summer 2010.

Read Gary Taubes 
Why We Get Fat and What to Do About it, 1-5-11.

Started Atkins diet 1-6-11.
 Published The Tubby Traveler from Topeka April 2012. 
 American Board of Obesity Medicine Exam on 12-10-15.

Travel to Turkey Sumela Monastery

Wait for the punch line

Ginger and I purchased masks for our trip to Japan cruise that was cancelled a week before we disembarked. 

Then  we realized the masks were made in China 

Then I realized Ginger tried on the mask. 

I immediately quarantined her in the bathroom as per CDC Universal Precautions for contagious disease. 

I will let her out when the test is negative after two weeks.

I am a board certified Infectious Disease Specialist

WARNING do not visit till we get results of the tests. 

Update News Flash 2/28/20 5:00 PM

Ginger has been released from quarantine

 from the bathroom!

She looked up on google where the masks she purchased come from as she was allowed to bring a computer in the BR.   (It's not Russia)
She found out the masks were made it USA. 

Announcement: It is safe to visit us again

                               

Examining My Mistake with complicated issue.

I have had trouble loading my edited version of  the article on to my blog.

Go to my google doc here:


Sandesara article on FH and CAC

1- Main article

CAC zero had events in original article not mentioned in review

2- Abstract

3- Review

This is article from Ivor that started this discussion

This is where people thought I made a mistake interpreting the data from CAC and FH article



This was my response:

The Annualized rates of events per 1,000 patients 

 101 events f0r CAC  zero 

62 events for CAC 1-100

43 events for CAC greater than 100.

 Below is original article by Sandesara

Bittencourt review

Confused thinking about not using meds for FH with high LDLc

Marcio Sommer Bittencourt review of Sandesara original article on CAC and FH


2020 article link

My comments in purple

In the current issue of Atherosclerosis, Sandesara shed additional light on
 the understanding of
risk in individuals with very high LDL-C and no previous cardiovascular event 
identified in the Multiethnic Study of Atherosclerosis (MESA)

 Primary prevention strategies to reduce cardiovascular risk
 are mostly based on 
1-non-pharmacologic lifestyle modifications and 
2-pharmacologic management of individual risk factors such as

a-hypertension, 
b-diabetes and,
c- most importantly, hypercholesterolemia. 

However, the objective of those prevention strategies is the
1- reduction of cardiovascular events and 
2-mortality, 
not the sole change in values of biomarkers, such as LDL-C levels.

To include a wider field of evidence has shown that having an LDLc will increase subclinical atherosclerosis in people. 
That why I advise keeping LDLc below 100 in people with CAC greater than zero.

Multiplier Effect link

 Thus, all guidelines on risk stratification recommend
 the estimation of individual cardiovascular risk
 using some validated tool to define the use of lipid lowering medications [2].

Although most international guidelines still recommend a combination of risk estimation and LDL-C levels to define the need and intensity of pharmacologic treatment of inadequate LDL-C levels, 

the American College of Cardiology/American Heart Association (ACC/AHA) guidelines

have not implemented this approach since 2013 [3]. 

The reasons for this decision have been previously detailed but can be summarized as follows: 

1. There is no evidence that the efficacy of statins to reduce cardiovascular risk is variable according to baseline LDL-C 

as the relative risk reduction is fairly constant irrespective of LDL-C levels and

 the absolute risk reduction is dependent only on absolute risk [4]; 

2. Most primary prevention studies used fixed statin doses and the evidence to support a dose adjustment according to LDL-C level is scant; 

3. There is no evidence that reaching exceedingly low LDL-C levels are associated with any increase in risk of adverse cardiovascular or non-cardiovascular events [5,6].

I believe they make these judgements for PRIMARY PREVENTION.

However, there is one clear exception. 

Even according to the latest ACC/AAHA guidelines update,

 those with severe hypercholesteremia, LDL-C levels greater than 190 mg/dL  

are deemed to be at such high risk that pharmacologic treatment should be considered irrespective of the estimated individual risk [3].

 In fact, the recent European Society of Cardiology/European Atherosclerosis Society (ESC/EAS) guidelines have specifically classified them as “high risk”, with an LDL goal of less than 70 [7], which is unlikely to be achieved without additional non-statin agents such as PCSK9 inhibitors. 

The need to be aggressive in this subgroup is based on two considerations. 

First, the concept that a lifetime exposure to very high LDL-C levels leads to an exceedingly high life-time cardiovascular risk that might not be fully captured by traditional risk calculators.

 Second, this cut off can be used as an initial screening to identify individuals with familial hypercholesterolemia (FH), an autosomal dominant disease affecting 1/250 individuals and associated with a substantial increase in cardiovascular risk. 

However, this strategy also assumes that those individuals with very high LDL-C are a homogeneous high-risk population that is more likely to benefit from aggressive treatment irrespective of their calculated risk, despite the lack of evidence to support this.

 In fact, recent studies suggest that coronary atherosclerosis is not a simple function of lipid levels but a multifactorial disease. 

CAD causes are multifactorial but once CAC is positive the best way is to get LDLc below 100. 

Of course treating high blood pressure with medications and preventing Insulin resistance with Low carbohydrate high protein diet is also important.  Ivor makes out that it is all about the "root cause" of insulin resistance. 

Blankstein et al. reported that nearly 1 in 2 individuals with ‘normal’ LDL-C have coronary atherosclerotic disease as measured by coronary artery calcium (CAC) testing [8]

Problem is LDLc is a poor maker.  We need to know LDLp or ApoB was to determine if there was discordance.  Sloppy analysis. 

 and conversely we have shown that even among those with genetically confirmed FH, nearly half show no detectable CAC and appear to have favorable intermediate term prognosis [9].

I pulled up the reference 9 and show it below.

Miname, M.H., Bittencourt, M.S., Moraes, S.R., Alves, R.I.M., Silva, P.R.S., Jannes, C.E. et al. Coronary artery calcium and cardiovascular events in patients with familial hypercholesterolemia receiving standard lipid-lowering therapy. JACC Cardiovas. Imaging. 2019; 12: 1797–1804

"The annualized rates of events per 1,000 patients 

1- for CAC scores of 0 (n = 101 [49%]), 

2- 1 to 100 (n = 62 [30%]) and 

3- greater than100 (n = 43 [21%])"

I don't understand the viewpoint. 

49% FH with CAC score of 0 had cardiovascular events

This is very significant.  High LDLc is very significant. 

Thus, this raises the question if we should treat all subjects with very high LDL-C aggressively, as recommended in the ESC/EAS guidelines update or whether this population could benefit from additional risk stratification with tools such as CAC to guide pharmacological treatment.

I didn't see data of CVE events in FH with CAC greater than 400? Probably they are all on statins or PCSK9 and have less CVE with much lower LDLc.

 Most importantly, can the favorable prognosis of the “power of zero” calcium score observed in our intermediate term follow-up study of relatively young FH patients be extrapolated to severe hypercholesteremic patients (>190mg/dL) in the general population on a longer follow-up? 

Sandesara et al. [1] evaluated the presence of CAC as well its prognostic implication in individuals with severe hypercholesterolemia in MESA. 

The first interesting aspect worth noting is its relatively low prevalence, only 4% of the entire MESA study population was estimated to have a treatment naïve LDL-C greater than190mg/dL. 

Meaning they have FH.

Second, though it may seem surprising, a substantial proportion of individuals (37%) presented with a CAC score of zero at a mean age of 63(±9) years, a prevalence of subclinical atherosclerosis comparable to the overall MESA cohort, despite the very high LDL-C levels. 

However in reference 9 above:

1- for CAC scores of 0 (n = 101 [49%]), in FH patients.

In non FH cases Ivor says they have 1.4% CVE

It is unclear to me why this article thinks people with CAC of zero have preclinical atherosclerosis. What study is that based on? CIMT? Which is what I have used in my practice. 

Moreover, in this rather selected group, (People  with zero CAC)the key predictors of the presence and progression of subclinical atherosclerosis were anything but surprising: older age, male sex, presence of diabetes and smoking. Need reference for this statement. 

 Collectively the prevalence and progression of CAC in this subgroup of individuals was mostly dependent on other well-known risk factors, not on the LDL-C levels. This would be expected considering the homogenously elevated LDL-C of the population.

Ignores the CVE data shown above in their reference nine.

Despite the limited sample size, presence and burden of CAC were clearly associated with both coronary heart disease and cardiovascular disease events during more than 13 years of follow-up. In light of the high prevalence of CAC = 0 in this population, a substantial proportion of individuals with significantly elevated LDL-C could be reclassified as lower risk in a follow-up extending more than 10 years. It is worth noting that in this group the absolute event rate was 3.7%, below the threshold of current ACC/AHA guidelines to recommend any pharmacologic treatment [3]. This is yet another piece of evidence substantiating the favorable prognostic value of CAC zero among those deemed high risk by traditional risk stratification strategies. These findings challenge current dogmatic conventions that risk in this population is so high that risk estimation is unjustified; in fact low risk individuals can be identified.

Although lifelong exposure to high LDL-C level is known to be associated with increased likelihood of subclinical and clinical atherosclerosis [10,11], this recent evidence [1] suggests this effect is heterogeneous, and a considerable subgroup of individuals with very high LDL-C does not develop coronary artery calcifications and has a very low event rate. 

I must ask if the people with very high LDLc were already on statins.

It is important to highlight that in general those were older individuals followed for more than 13 years and population has reach ages above 75 years, though the sample size of the present study was relatively small, and the current evidence cannot be read as definitive

Sample size was "A total of 206 subjects

 (mean age 45 ± 14 years, 36.4% men, baseline and on-treatment low-density lipoprotein cholesterol 269 ± 70 mg/dl and 150 ± 56 mg/dl, respectively)"

Thus LDLc was 269 for those not on treatment

LDLc was 150 for those on treatment.

The big question moving forward is how these findings with all the emerging data on the favorable prognosis on the power of zero inform practice? 

Favorable prognosis? 

"The annualized rates of events per 1,000 patients 

1- for CAC scores of 0 (n = 101 [49%]), 

Apparently they are including those on treatment which may have made it look more favorable?

Both the current study and our previous report support [9] 

I already address this reference 9 above

the consideration of CAC to guide treatment intensity of lipid lowering pharmacologic treatment even among those with significantly elevated LDL-C.

 From a practical standpoint, the unselected treatment of individuals with very high LDL-C (>190mg/dL) irrespective of their clinical risk or the presence of subclinical atherosclerosis might not be the most prudent approach, though current evidence on how to best approach those individuals is still lacking. 

While non-pharmacologic interventions might be recommended to all, potentially statins could be offered with shared decision making to those with elevated LDL-C, though the benefit is less well documented in patients without subclinical atherosclerosis. 

What? 

"The annualized rates of events per 1,000 patients 

1- for CAC scores of 0 (n = 101 [49%]), 

More importantly, more expensive non-statin treatments (PCSK9) should only be considered if there is evidence of extensive atherosclerotic disease based on CAC testing as may be the case in FH [12], though additional studies in those individuals are warranted.

Here is the abstract:

From a more conceptual standpoint, the results of the two recent studies of individuals with very high LDL-C should make us question at least part of our understanding of the pathophysiology of the atherosclerotic process(1, 9). 

What a weak statement with lives on the line.  

Is this what they tell their patients? 

Conceptual but no data?

In particular, the identification of nearly 40% of individuals without atherosclerosis in these groups might be an adequate silo to investigate resilience to this disease despite known risk factors.

 It is unlikely that those individuals’ endothelium survived without a scratch by chance. Is it the case that this population may allow us to better understand atherosclerosis, and maybe novel forms of treatment?

In your cohort there were treatment patient included.

Novel form of treatment was found with PCSK9

Revisiting Ivor's position on LDLc and ratios

Brian Edwards

I am listening to the first podcast by Ivor

No one in USA uses ratios.  I mean no one in the National Lipid Association uses them or talks about them.

Lipidologists don't use "bad" or "good" for LDLc or HDLc.

He ignores the preponderance of multiple trials that confirm the lower the LDLc the better. 

Ivor cherry picks his trials. 

I wrote a blog on Ivor- Irish Nihilism link

The size of particle is another red herring. 

If you have low LDLc or low LDLp if doesn't matter how large they are. 

No good way to measure oxidized LDLp

Health of endothelial wall is huge.  

The best way to keep the wall healthy is to not expose the wall to LDLp greater than 1,000

The healthy HDL vs bad HDL is a real thing but again the best way to deal with this is to lower LDLp and triglycerides.

Ivor says a person with a high LDLp can be healthy if all the endothelial measures are good.
 He has no evidence of any trials with this.
In theory it maybe true but in clinical practice no lipidologist would go alone with it. 

PCSK9 trails get patients LDLc down to 20 with great results. 

I think these podcasts of Ivor might be before the several PCSK9 trials

If Ivor were honest he would not ignore the new data and the old data showing the lower the LDLc the better.

Ivor says treating the high LDLp in a "healthy" patient would be a bad engineering mistake. 

I have shown Ivor my list of 200 patients with ASHD that got their LDLc down.
They did very well. No heart attacks. 

My 200 patient list link

Ivor has never treated any  patient.  

Clinical medicine is very far from engineering.

Totally different discipline.

Ivor came up with the idea of "root cause" being insulin resistance. 

I am a Black Swan to Ivor's theory on "root cause" link

Diabetes is definitely a high risk factor but hypertension is also. 

More importantly  than both DM and HTN,
lowering LDLp or LDLc have been consistently shown by the best scientific trials over decade that
the lower the LDLc the better. 

It is irrefutable!

Ivor's references are refutable.

I dove deep into analysis of Ivor's references in Eat Rich Live Long.
He had no answer to this blog

apoB/apoA ratio is not the best test link

My review of Eat Rich Live Long by Ivor

Review of Eat Rich Live long

March 31,2018

 I would give Eat Rich Live Long five stars based on it's wake up call on insulin resistance. 

If I only considered it's Lipoprotein particle or ApoB and weight maintenance  sections I would give it one star. 

Thus I settled on a 3 star rating.

This is an excellent text.  

A great guide for people interested in LCHF(Low Carbohydrate High Fat) or Atkins type diet.

I have been on LCHF since reading Gary Taubes book, Why We Get Fat: And What To Do About It in Jan 2012.

I decreased my exercise, and eat ad libitum and did not gain weight even while I traveled around the world.

I probably didn’t lose weight because  I ate a lot of protein.

The authors explain this phenomenon on p 309.  

Very high amounts of protein are okay if you are trying build muscle with a weight lifting program.

I was satisfied because I was not hungry and I was not gaining weight with less exercise. 

Subsequently I obtained ketone blood test strips and could closely monitor my nutritional ketosis. 

However I did not lose weight on this diet. 

I had been 280 pounds and lost 80 pounds on traditional 1500 low calorie diet.  

The restrictive discipline after 1.5 years was too much. 

I decided to eat more low glycemic fruit as I increased my exercise to 2.5 hours a day. 

I gained 1.5 lbs. a month till I gained back 50 lbs.  

This is when I learned you cannot outrun your fork and I lost faith in low glycemic fruits.  

I turned to diet medications not just for weight loss but also for weight loss maintenance. 

I believe this book has a wonderful message. 

  This must be incorporated in new guidelines to get Doctors to order it.

The fasting glucose is not enough.

If insulin resistant then LCHF is the essential diet as outlined brilliantly in Eat Rich Live Long. 

The second wonderful message is the importance of a CAC (Coronary Calcium CT) to determine risk for cardiovascular event along with scoring the usual risk factors. 

I am Board Certified in the American Board of Obesity Medicine.  I think any diet can lose weight.  

The challenge is maintaining that weight loss by finding a diet that is ad libitum and can be maintained for life. 

Eat Rich Live Long fails to address the problem of weight loss maintenance in the reduced obese  adequately.

The authors neglect the science that the excess fat cells the obese have never disappear even with Bariatric surgery.  

The large number of shrunken fat cells in the

 Low Leptin tells your brain you are starving. 

Several mechanisms including decreased thermogenesis  and

increased Ghrelin (increased hunger) are 2 ways Leptin causes slow weight regain even on a reduced calorie diet over the long term.  

It is not all about insulin. 

 It is much more complicated than that.

  Dr Gerber sites several of his patients losing weight and maintaining it for 1-2 years.  

All diets can do that.

 LOOK AHEAD showed that over 10 years diet and exercise fail to maintain weight loss. 

As per the National Weight Control Registry(NWCR) only 5% have the willpower to maintain diet of 1500 calories and one hour walk/d to maintain their weight loss. 

Using the science of a calorie is a calorie they(NWCR) should continue to lose weight. 

No, low leptin breaks that rule and this sub-starvation diet (1500 calories) will only maintain weight, not break through the plateau.

Eat Rich Live Long suggests several strategies to maintain weight loss or break through the plateau.

p333:

1- Internalize the books principles. 

2- Follow the 10 action steps on p 72

3-Make these action steps a habit

This is all about WILL POWER which can't be sustained over 5-10 years with terrible hunger caused by a low calorie diet and low leptin. 

Very lame, it is the same message as the lifestyle message of the guidelines. 

The false hope of diet and exercise that failed in the 10 year LOOK AHEAD trial.

p334:

“Love your Ghrelin”.

The author is telling us to use hunger positively. 

This does not work.  You cannot stay on a diet for life if you are always hungry unless you are the 5% in the NWCR (National weight control registry)

Nutritional ketosis and high protein does provided satiety over the short term.  There nothing to show it works more that 5-10 years. 

The number of fat cells has the last word. 

No way to increase the low leptin in the shrunken fat cells other than to regain weight. 

p337

1-Meal spacing.  Eat only 3 meals a day and try to cut it down to two meals a day. 

2-Fasting

3-Decrease the fat in your diet from 160 g/d to 100 g/d. 

This reduces your diet to 1,100 calories. 

The authors write "This is not the cliched "eat less, move more" .

Sorry, cutting out 100g of fat equals 900 calories. 

2200 cal minus 900 cal = 1100 cal a day. 

This is a sub-starvation diet link

For IR patients (insulin resistant) meal spacing will increase hunger unless you are on diet medications. 

For muscle building it is very difficult to get to 130 to 150 grams of protein a day on two meals a day.

  Need high protein snacks in between meals to reach protein goal and for satiety.

Fasting is a draconian measure over the long term. 

Talk about the amount of willpower needed for that. 

Finally,  

The authors fail to recognize the necessity of statins, niacin and Zetia to treat high CAC score or secondary cardiovascular disease or the very high ApoB of Familial Hypercholesterolemia  

On twitter the Authors  told me they are not statin "denialists"  Eat Rich Live Long does not reflect this position. 

p271 "you can't lower your CAC score with the orthodox approach of a low fat diet and medication"

p261 "If there are no insulin resistance or inflammatory issues present, then a high ApoB is very likely not an issue."

P247 William Peter Castelli is a giant in the field of lipidology. 

I have heard him speak. 

He is now 86 yo and his last paper was 1999. 

He is not a current lipid investigator.

Castelli's comments in 1996 are made without benefit of AIM-HIGH 2011, HPS2-THRIVE 2013, ODYSSEY 2018, WESCOPS 2004, IMPROVE-IT 2004, 4S 1994.  Old references have historical valve but must not be used against the preponderance of recent evidence.

The authors cherry pick their data just as Ancel Keyes did. 

I am a Fellow and Board Certified in the National Lipid association.

The preponderance of excellent random controlled trials, double blinded with large number of people in study for significances validates the rule:

the lower the ApoB (lipoprotein particles not cholesterol) the better outcomes in mortality. 

P262" EAT RICH LIVE LONG 

APOB/APO1: The Master Ratio." 

There are many problems with ratios. 

Suffice to say non-HDL cholesterol is much better.

Get it under 80.  

You don’t need to get advanced lipid testing for this. 

Total Cholesterol minus HDLc = nonHDLc.  

The authors never mention this simple calculation that can be done with a standard lipid panel.  

It is much better than LDLc which Ivor uses cherry picking to show how bad LDLc is a bad marker.

Yes it LDLc can have disocordance which is why we use nonHDLc.

LDLp or ApoB particles done on advanced lipid testing should also be done at some point to determine if there is discordance. 

p354 "people with verified FH (familial hypercholesterolemia) should discuss  PREVENTATIVE treatment options with a specialist in the field"

To not mention the PCSK9 treatment option reflects a very biased approach to the medical treatment of high ApoB (lipoprotein particles)

In summary I applaud Eat Rich Live Long program of LCHF as soon as early insulin resistance is detected with 2 hour post prandial glucose and insulin level. 

However their immense blindspot to the benefit of getting LDLc,non-HDLC, LDLp or ApoB as low as possible in people with high CAC by giving statins, niacin or Zetia is a great detriment to Eat Rich Live Long. 

The authors lose credibility for their important message about Insulin Resistance when they cherry pick data to build up the supreme importance of insulin. 

 I think they are reacting to the Ancel Keys disastrous seaqueway to high carbohydrate low fat diets as the only healthy diet.  

Some people are hyper-absorbers of cholesterol.

These people benefit greatly from Zetia.

 Most elevated ApoB or LDLp is genetic rather than diet related. 

 Thus if someone has 5% cardiovascular risk and a positive CAC  (higher than zero) they need to lower their ApoB or LDLp

NonHDLc should be less than 80

 Non-HDL cholesterol and remnants are not discussed in the book. 

These numbers only need the routine lipid panel not advanced testing. 

For my approach which is similar with Eat Rich Live Long buy kindle edition for $3 on Amazon.com by looking up my book The Chronic Disease of Obesity Published Feb 2, 2018 published iUniverse

Boom Ivor!