5 Steps to prevent Heart Disease

Thursday, May 31, 2018

High Protein Diet calculated from Lean Body Weight

I recently read that high protein diet is 1gram of protein per pound. 
In the obese you must calculate your lean body weight. 
I show how I did it with a body compositions scale below. 
This is from my book The Chronic Disease of Obesity



My body impedance composition analysis (BIA) states at 211 pounds right now 5-31-18:

My body fat% is within range for someone with normal activity (not athletic).

My basal metabolic rate is calculated at 1758 calories to maintain my weight without exercise.

If I have a moderate activity level my calorie intake would be 2637 calories to maintain body weight.

Every decade a persons metabolism slows down by 2%.  I believe the BIA takes age into account.

However the BIA does not take into account the reduced metabolism of the Reduced Obese.  It's well known that with 8-10% weight loss, exercise metabolism reduces by 42%. In general when a naturally lean person walks a mile he burns approximately 100 calorie.  The Reduced Obese with Sponge syndrome only burn 58 calories per mile.

Actually it is worse than that as low Leptin causes the resting metabolism to slow down to help regain fat.  70% of resting metabolism is from non-muscles such as Brain, Kidneys, Liver and other organs.  The Reduced Obese often feel cold all the time.  The BIA does not take this into account.

I take Invokana as a type 2 Diabetic.  That means I urinate out about 200 calories a day of glucose.

Nutritional ketosis also urinates calories out in the form of ketones.

In general, the high protein of Atkins, causes satiety and people tend to eat up to 500 less calories a day excluding most carbohydrates but more fat.

In general to maintain weight most people need to stay around 1500 calories.

How people in National Weight Control Registry maintain weight loss link

Lets hypothetically say my exercise would only burn half of what BIA states. So instead of 880 calories from exercise it might be more accurate at 440 calories in the Reduced Obese with low Leptin.

Thus 1758 + 440 =  2198 calories to maintain my weight loss.








Monday, May 28, 2018

MY CHRONIC OBESITY. FIVE TIMES I REGAINED. SPONGE SYNDROME





FIRST WEIGHT LOSS BELOW








SECOND WEIGHT LOSS 


THIRD WEIGHT LOSS









FOURTH WEIGHT LOSS





FIFTH WEIGHT LOSS



Saturday, May 26, 2018

Low Carb High Fat diet trials





Shai trial low carb menu's below. 
Best 2 year trial that I know of.

  Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet link





Friday, May 25, 2018

Discordance documented in Tubby Theory from Topeka patient data

Patients from my Lipid Clinic, Topeka,  Kansas 2009




I culled through the list of  approximately 200 patients from my Lipidology practice in Topeka in 2009.
My list of patients  link.

Look at patients 3 and 4.  I call these the Tim Russert group.
We know they have ASHD from the positive cardiac catheterizations
If advanced NMR Liposcience testing was not done we would have said,
as with Mr. Russert that the goal of less than LDLc of 70 was reached
 or close enough in 2009.
The discordance with LDLc and non-HDLc with LDLp tells us we need to get the LDLp below 750.
 I would add Zetia in patient three who was already on Crestor 5 mg and Enduracin 1,000 mg.
Check LDLp in one month and if not less than 750 I would double Crestor to 10 mg.
Patient four with LDLc 67 is extreme discordance with LDLp 1233. Not even close to goal of LDLp less than 750 with known ASHD on heart catheterization.
Patient already on simvastatin 40 mg (Zocor) and Zetia.  With LDLc 67 no one would add Enduracin 1,000 mg but LDLp 1233 demands it.  In a month if still not at goal I would switch to atorvastatin 40 mg and go up to 80 mg in a month if no side effects and not at goal.

Patient One :

Clearly this patient with a positive coronary cath. needs to start a low dose statin and be checked again.   Perhaps another physician believed a LDLc of 87 did not need to be treated even in a patient with plaque.  The LDLp 1313 shows discordance and should be treated with triple therapy (statin, enduracin and zetia) to LDLp less than 750.

Patient Two:
This patient has a high CAC at 220.  Again he was not started on treatment because the physician thought "why treat an LDLc of 87 in 2010.

Patient Five:

CAC 141.  LDLc 99, why put the patient on lipid lowering agents? Answer: discordance with LDLp 1242.  Patient has atherosclerosis.  We don't know if he has soft inflamed plaque that might break off a clot and cause sudden death  (100,000 deaths a year with death as first sign of disease)  In Patient five we already know he has plaque.  Definitely start low dose atorvastatin 10 mg and check LDLp in one month then consider adding Enduracin 1,000 mg and then Zetia if monthly advanced lipid testing dose not get LDLp down to at least less than 1,000.

Patient Six:

CAC 19.  Many would say not bad.  To me this is the tip of the iceberg of ASHD that has now been documented with positive CAC.  LDLc looks good at 78 on Zocor (simvastatin) 40 mg and Enduracin 1,000 mg. However I would like to get LDLp less than 750 by adding Zetia.

Patient Seven:

CAC Zero.  Perfect right?  The CIMT is at 50% tile for his age and sex which SHAPE task force says "is a positive test for atherosclerosis".  Again with LDLc 87 on Crestor  5mg why would anyone try to get LDLp less than 1,000? This patient had 3 out of 5 criteria for metabolic syndrome.  TG/HDLc was 82/44 after Crestor 5 mg.  I would at least add Enduracin 1,000 mg a day and check advanced lipid profile with Liposcience in one month.

Patient Eight:

CAC zero.  Great but again CIMT was 50% so a positive sign for atherosclerosis. LDLc 111 might lull a general practitioner to not give those "dangerous" statins.
However when I saw big discordance with the LDLp 2007 I knew I wanted to start triple therapy with first step generic atorvastatin (Lipitor).  Very inexpensive and at this dose very few side effects.  Important to check Vitamin D level before giving statin.  Next month add Enduracin 1,000 mg (a over the counter niacin which has a wax matrix pill and does not cause much flush, much cheaper than Zetia.  In a month if still not at goal of less than 1,000 LDLp I would add generic Ezetimibe (Zetia) I might start with just half a pill a day.
This triple therapy very inexpensive  and synergy with low doses very safe.



Patient Nine:

CAC 0.  LDLc 110 on no Lipid lowering drugs.  Okay right?  Until you see the discordance with LDLp at 1439 in a patient with CIMT at 50% tile.  Which SHAPE TASK FORCE say "is a positive sign for atherosclerosis".  Lipitor 10 is very inexpensive and at low dose is very safe.  See Multiplier Effect link.

Patient Ten: 

CAC 12.   LDLc 101 on Lipitor 40 mg (no generic back in 2009) and Zetia.  Again most Doctors in 2009 would have said good enough for government work.  LDLp was 1322,  I would add Enduracin 1,000 mg and try to get LDLp less than 1,000 in a patient with proven atherosclerosis. TG/HDLc ratio 169/52 in female with one criteria for metabolic syndrome(TG 169). Some would say she has positive ratio greater than 3.0 to be diagnosed with metabolic syndrome.  Definitely should add low dose niacin with OTC Enduracin.

Patient Eleven:

CAC Zero.  LDLc 94 on Crestor 5 mg.  All done?  No as there is discordance with LDLp of 1388.  I would like to add Enduracin 1,000 mg.  Her Tg/HDLc is 217/72.  Some would say this might be metabolic syndrome.  If not at LDLp goal in a month I would add Zeta.  Consider Lovaza 4 grams a day to help Niacin lower TG.  In 2018, I would get a 2 hour PP glucose with an Insulin level and start patient on Atkins or Low Carb High Fat diet.












Thursday, May 24, 2018

The Tubby Theory from Topeka 2010 Chapter 12




The Tubby Theory from Topeka 2010. link

Here is a free view of Chapter 12.
 Data of my patients from my Lipidology Clinic. 












Page 86


Page 87




Page 88

After 3 years on prescription meds with no hunger



My quest for normal arteries on high 60% fat diet (Atkins)


Body Composition Data since starting diet meds


4 electrode scale





I have been on Atkins or LCHF (low carb high fat) since Jan 2011.
I have not lost weight with LCHF in nutritional ketosis alone.  
I learned you can't outrun your fork. 
I began losing weight after starting Qsymia 6-25-2018. 
Now about 3 years later, I have stayed on diet medications.
5-24-18 Update: I have been on diet meds for 3 years


I am on Belviq, Victoza, Invokana, Metformin, Caffeine


5-12-16 UPDATE
I went to Obesity clinic yesterday after 5 months of traveling.
On Qsymia, Victoza, Invokana and Metformin with no change in diet or exercise I lost five pounds.
I went on an Oceania Cruise May 11 to June 5, 2015,
I even purchased the beverage package on the cruise for the first 14 days.
 I compensated by walking one hour a day.
I tried to maintain Atkins as best as possible but I did eat less due to the diet medications.


I started Qsymia in June with following body composition and yesterday’s result:


Date          Weight Body Fat%      Muscle Mass Total Body H2O  BMR BMI
6-23-15       244.8             31%  44.9                     51.8               1919 33.9


5-12-16       217.3    27.7      40.8 53.2%            1790 30.1


6-15-16        219.8  26.8%                   41.3   54.1% 1802   30.4   


7-20-16           221.6 27.2                             41.7 53.7% 1807             30.7
5-23-17            199.0 23.8%                            37.4 57.1% 1702            27.5


5-24-18           211.8 28.1%                           39.8 52.8% 1756           29.3

Update on my CIMT scores



       Average CCA Mean               Average CCA Max Region
12-17-09   0.599 mm                           0.741 mm
12-8-11      0.563 mm (.036 less)         0.661 mm (.08 less)
12-20-12    0.566 mm (.003 more)      0.676 mm (.015 more)
12-19-13         0.583 mm (.017 more)    0.709 mm (.033 more)
11-20-14         0.575 mm  (.012 less)            0.679 mm (.030 less)
12-03-15         0.555 mm  (.020 less)           0.675 mm (.004 less)  
12-08-16         0.611 mm   (0.55 more)         0.744 mm  (0.99 more)
12-14-17         0.570 mm (0.41 less)           0.671 mm (0.73 less)             

CAC  reports below over 10 years:
                              Calcium score Calcium volume
2-6-01                           8.93 8.02
1-10-06                        20.5 57.5
12-9-11                        7.9  5.9

7-21-16                        144                            126

Tuesday, May 22, 2018

The Validation of the Sponge Syndrome

I have posted this chapter from my book, 
The Chronic Disease of Obesity

Definition of Sponge Syndrome: I lost 80 lbs on 1500 calorie and exercise.  I gained back 50 lbs despite 2 hours of exercise a day.  I regained weight due to the fact I still had 80 billion fat cells after my 80 lbs. weight loss.  These cells were shrunken and thus secreted little leptin.  This told the brain my body was starving.  

LARGE number of FAT CELLS with LOW LEPTIN levels.  

This is why the Reduced Obese can't maintain their weight loss.



Chapter 12:   Sponge Syndrome Validation   
 I believe my Sponge theory as the main cause of Chronic Obesity
to be verified from multiple scientific discoveries.  
Most important is that we do not know what has caused the epidemic of obesity in the world.
Gaining weight and losing weight is relatively easy.
Maintaining the weight loss is the challenge.
Guidelines advise: Maintain weight loss with more exercise and
watch the calories around 1,000 to 1,500 depending on your height.
This guideline has only worked for about 5% of the chronic obese over the long term. {31}  
The Leptin  hormonal theory of weight regain in the reduced obese has clearly been elucidated.{17}  
The Leptin theory has also been validated by many medications that fool leptin by
telling your brain
it is not starving by several different hormonal pathways downstream from leptin
which are on the market.
Fact: weight loss and bariatric surgery do not reduce the number of fat cells,
they cause shrinkage of the adipocytes with subsequent low levels of Leptin
which acts directly on the brain.{28}  
Fact: small fat cells are more efficient at gaining weight in reduced obese.{22}
There are Leptin receptors throughout the body and the adipocytes also
send out MiRNA to tell the body via episomes to regain weight.{29}
Most diet books ignore all this science.
 As Dr. Aronne reminds us that it takes new science up to 14 years to accept the new data.
Nutrition science might be considered an oxymoron.
Nutrition science has three very good trials.
1- The Predimed trial
2- The Look Ahead trial.
3- DASH diet trial to treat hypertension.
Unfortunately we don’t know if the secret sauce in the Predimed is wine and nutritionists
discount the LOOK AHEAD negative outcomes.


“Consilience of inductions. Call it a “convergence of evidence” {23}
not found for low fat diet despite multiple trials and  
not found for exercise to maintain weight loss(see chapter 10).


I pushed the Sponge Syndrome theory as a common sense answer to
why people regain their weight loss.
What the nutritionists and the guidelines push to maintain weight loss has not worked.  
To give the same advice to maintain weight loss that doesn’t work
for 80-95% of the Reduced Obese might be called insanity.
Resistance to low carbohydrate high fat (LCHF) has been fierce.  
There is finally a paradigm shift.
 Some studies have shown some people do better on low fat diets
but overall the data for LCHF is excellent.
 Is it genetics or is it cultural?
Shifting from high carbohydrate diet to low carbohydrate diet is a difficult change in lifestyle
but it is possible if you stick with the Atkins type (LCHF) long enough
to get over the love of carbohydrates. It takes at least a month.
 I suspect the difficulty is cultural more than genetic. Time will tell.
I want people to lose weight with whatever diet worked before.
 Once they hit the plateau of weight loss, the low fat diet fails in the long run
because it is not ad libitum as the Atkins type diet is.
To be able to stay on a diet for life the diet must satiate hunger
(high protein and nutritional ketosis).
Also fat gives much of food it’s flavor.
You need to follow a reduced calorie diet that you can stay on for the rest of your life
just to maintain your weight loss, not for more weight loss.
Not matter what diet you go on, eventually it will fail because
none of them reduced the number of fat cells.
Only diet medications will overcome the low Leptin levels that tell your brain
the body is starving over the course of a lifetime{35}.
 This is science that is often not mentioned in articles on weight loss maintenance.
I have tried to present some of the science without getting too much into the weeds.
 I have tried to keep the science as simple as possible.
I took the American Board of Obesity Medicine boards.  
Unfortunately the other disciplines don’t know or will not accept this data from the Boards.
Thus  “convergence of evidence” went awry during the decades of low fat dieting.
Possibly the influence of the food production lobbyists  had something to do with it.
Dr. Ludwig writes about guidelines allowing fruit juices might have to do with lobby interests
on the guideline board in his tweets.
“The 2015 to 2020 Dietary Guidelines for Americans (DGAs)
recognize the role of 100% fruit juice
in health and in helping people meet daily fruit recommendations
and state that 100% fruit juice is a nutrient-dense beverage that should be a primary choice,
along with water and low-fat/fat-free milk.”{39}
  For my Sponge syndrome  “to overturn the consensus,
I would need to find flaws with all the lines of supportive evidence and show
a consistent convergence of evidence toward a different theory that explains the data” {23}    
The Hall analysis of the Biggest Loser puts a big question mark next to the advice
of exercise and low calorie intake as that did not work for 13 of 15 people in the trial.{14}
The Look Ahead data showed that after 10 years of the best exercise and diet program
with close personal support to keep behavioral changes
failed in primary outcomes compared to control.  
 This was a random controlled trial with large numbers of participants and a good control over 10 years.
It doesn’t get much better than this in nutrition science.
Yet this data did not change the guidelines.
 Most guidelines still advise 90 minutes or more of exercise to maintain weight. (see chapter 13)
The key to maintaining weight loss is a low calorie diet that you can stay on the rest of your life.
  The answer is an ad libitum diet and diet medications.
No guidelines should be written without a close examination of the many hormonal ways the brain
uses to make you gain weight again.
The Sponge Syndrome is the perfect storm for weight regain in the reduced obese.{34}  
 The number of fat cells has the last word.  
 I asked Dr. Leibel if adipocytes only live 10 years.
 He said there is some discussion of that but there is evidence that
the fat cells that die are rapidly replaced.
Thus the billions of excess fat cells of the obese are present for life in the Reduced Obese
act like a sponge for free fatty acids.
I had the privilege of listening to Dr. Michael Rosenbaum
talk about why weight loss maintenance is so difficult.
 I asked Dr. Rosenbaum if what I call the Sponge Syndrome
might also make it difficult to maintain weight loss.
Small fat cells are efficient at re-gaining fat.
Since the Reduced Obese continued to have a large number of fat cells
despite weight loss all these cells make it easy to gain weight.  
He(Rosenbaum) asked why the skinny people with skinny fat cells don’t also regain weight.
I don’t think he understood that I was referring to the Reduced Obese
who have a much higher Leptin threshold than a lean person
who was never fat and whose small fat cells are not increased in number
and thus don’t have the Sponge Syndrome.


Similar to the Frank Greenway review{19}, I was greatly gratified to find the Ochner review{22}
that also supported much of my Sponge Theory and it’s cause of the Chronic Disease of Obesity.
“Irrespective of starting weight, caloric restriction triggers several biological adaptations
designed to prevent starvation.3
These adaptations might be potent enough to undermine the long-term effectiveness of lifestyle modification
in most individuals with obesity, particularly in an environment that promotes energy overconsumption.”


Ochner adds  preadipocyte proliferation  increases fat storage capacity.  
This goes along with what I hypothesized in my Sponge Theory.


Ochner also says “that these biological adaptations often persist indefinitely,
even when a person re-attains a healthy BMI via behaviourally induced weight loss.3”


In accord with the thesis of my book, The Chronic Disease of Obesity, Ochner goes on to say

“few individuals ever truly recover from obesity;
individuals who formerly had obesity but are able to re-attain a healthy body weight via diet and exercise
still have ‘obesity in remission”

References

14- ‘The Biggest Loser,Their Bodies Fought to Regain”
by Gina Kolata NYT 5-2015


19- Obesity review by Frank Greenway
International Journal of Obesity (2015) 39,
1188–1196; doi:10.1038/ijo.2015.59; published online 26 May 2015


23- Scientific American article on Global Warming