5 Steps to prevent Heart Disease

Saturday, July 30, 2016

Would I add a diet drug to another diet drug that did not meet 5% weight loss goal

Would I add a diet drug to another diet drug that did not meet 5% weight loss goal within required 3 month guidelines?

I was asked this question by a Endocrinology Obesity specialist recently.

When I responded, Yes,

He asked if I had data for that.

I said we do quite a bit of therapy that is not evidence based.  The art of medicine requires we treat patients as individuals.

We presently do not have head to head trials of the four major diet medications.

Does that paralyze us from making judgements as to which diet medication to use first.

The ACA/AHA guidelines on therapy for treating lipids mostly used evidence based medicine and was soundly criticized for that limitation.

The NLA subsequently made additional recommendations to those guidelines and there has been a subsequent consensus statement.

Here I am in a new discipline: The American Board of Obesity Medicine.

The old school of Diet and Exercise is still pushed despite it's dismal 10 year failure in LOOK AHEAD TRIAL.
Yet Diet and Exercise is still in the guidelines in a premiere position.

I am on 5 diet medications
That has to be off label?
Actually, my Endocrinologist and my Obesity Clinic would disagree.
Metformin for DM might be considered a diet medication especially for metabolic syndrome.
Invokana is for DM but I lost 30 lbs. on it when I stopped Insulin. 
Victoza for DM is a Diet medication with a different name Saxenda.
Qsymia has phentermine and topiramate started by my Obesity Clinic while I was already on Meformin, Invokana and Victoza.

Is there data for a patient like me.  I don't think so.
It is advised not to take topiramate with metformin for fear of metabolic acidosis.  This was never advised in the conferences preparing for the Obesity Boards.  Invokana has also been linked to ketoacidosis.  Again I think these are rare occurrences but should be screened for. 

There are just too many permutations of patients to have data for every situation.

We need to approach each patient individually, then follow them closely.

If a patient loses 3% weight on Qsymia after 3 months, I will probably start that patient on Saxenda or Victoza rather than lose that 3% effect.
I suspect adding Victoza will have a great additive effect similar to the ileal brake of Bariatric surgery when bile acids are dumped directly into the ileum by the bypass surgery. The bile acid stimulate secretion of GLP-1 and PYY to cause the ileal brake?
That's the theory.   There is a waterfall response even with Gastric bypass surgery.  Yet this very expensive surgery while thinking it was all due to restriction of food intake?
Thus as an Obesity specialist I believe it is reasonable to use the medication toolbox to the best of my ability to the best interest of the patient rather than refer the patient immediately to Bariatric surgery.

How to choose which diet medication



This is Harold Bays MD slide from Obesity Medicine Certification Review course in Washington DC in Oct 2015.
These are FDA principles in slide above.

Presently PCSK9 has no outcome data yet is being touted strongly as therapy in several areas.

Zetia had no outcome data till recently yet after 8 years the LDLc lowering effect proved effective.

Niacin had it's two trials stopped early after 3 years after falsely significant side effects.
Terry Jacobson's slide from Master's Course in NOLA, 2016

Thus while many guidelines jumped the gun by eliminating Niacin, an inexpensive safe proven drug at 1,000 mg with low dose statin it is still available to the physician to use multiple drugs at low doses for best effect.
A good general principle in the practice of treating chronic diseases such as DM, HTN, HIV and others.

Sunday, July 24, 2016

Once more into the breach of weight loss with muscle gain

The Impossible Dream of
 Weight Loss with Muscle Gain


“All of the men also began a grueling workout routine.
Six days a week they reported to the exercise lab and completed a strenuous full-body weight training circuit, high-intensity intervals, or a series of explosive jumps and other exercises known as plyometric training.”
Forget this for this 64 yo man.  My body won't last two days. 
Important message here is for my LCHF diet.  I usually eat 200 grams protein.  If I calculate 2.4 g protein/kg (of ideal body weight of 84 kg instead of my actual weight of 100 kg),  I should eat 300 grams of protein a day.  That is potential 400 more calories a day, almost one pound of weight more a week.  I guess the extra weight lifting should make up for the difference?   

As I look at the  second Gretchen article of 3 sets of 25 reps four times a week,  I could do that. (until muscles exhausted.) 

The Aronne (Zickerman) method of 2 workouts a week of 10 minutes of absolute muscle failure seem guaranteed to cause me injury despite their advice to go super slow..
It’s the final 10 seconds of going for the burn that worries me.  
 That is the injury zone in my old mind.


Last month I increased my exercised by about 300%. 
I doubled my walks to 40 minutes a day. 
Circuit weight lifting 2-3 days a week. 
Water aerobics 2-3 days a week.

                    Wt.           Fat%       Muscle       H20                BMI
6-15-16        219.8      26.8%       41.3            54.1%            30.4     

7-20-16           221.6          27.2              41.7                53.7%                 30.7

I ate more with more exercise and gained some weight. 
2 pounds weight with half pound of it as muscle. 


Plan:
Lets see what happens with more protein and Gretchen's four sets of 25 reps of light weights four times a week.  
300 grams of protein a day for 85 kg ideal lean body weight. 
I will stop water aerobics. 
          



Friday, July 22, 2016

Despite LDLp less than 300 my CAC increased


“Therefore, in brief:
(I) CAC progression is an independent predictor of events;
(II) statins promote plaque regression; and
(III) statins promote CAC progression.

These paradoxical results are puzzling and warrant the conduction of further studies aimed at the pathophysiological and clinical discrimination between plaque volume progression and CAC progression.

One of the potential explanations might be that conventional reading of CAC studies does not make a distinction between spotty calcifications and dense calcium.
Future discrimination between these two completely different sources of coronary calcium might become a major breakthrough in CAC imaging, since spotty calcifications have been recognized as a marker of high risk plaques (81,82).
Regarding future alternative therapeutic approaches, the combined application of molecular imaging agents with anticalcification drugs such as bisphosphonate might potentially enable targeting at different stages of the disease (18).”


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)    


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

My CIMT scores do not correlate with my CAC increase.

If my increase in CAC (calcium scoring) reflects true increase in risk, why did it happen?

Perhaps the best answer is insulin resistance?

My LDLp has been good.
However perhaps if my LDLp was consistently under 750 I would have had a better CAC number?

I finally have a better handle on the weight and the Hgb A1c.
Weight 220
Hgb A1c 6.8
My systolic BP is usually 120 or less on ramipril.

Recently I went off Niacin (endur-acin) for a short period and it made a difference in my LDLp.  
I will continue the Endur-acin 1,000 mg a day rather than increase the atorvastatin 10 mg. 
While on Atorvastatin 10 mg, Endur-acin 1,000 mg I have had very low LDLp's. 
 Since 12-06-11 I have gone over 800 once while on LCHF. 

I hope to slowly get my weight down to 200 pounds with improved insulin resistance with time with LCHF.

My LCHF is pretty tight as I run nutritional ketosis above 0.5 serum usually.

I drink 2 oz ETOH most days. 

More from the article above: 


Saturday, July 16, 2016

Why are medical premiums so high?

Part one

Original idea:

Use medical insurance premiums to pay for medicine.


My comments in purple:

This is why medical insurance premiums are so high.
Science is not applied to the problem of Obesity.

Lifestyle changes have not been shown to maintain significant weight loss when compared to a control in largest and longest trial that was negative in it’s primary outcome. LOOK AHEAD trial

Kaiser should not spend 50 million dollars from medical premiums to programs that will not help those people that pay the premiums.  The patients that pay the premiums should have coverage for the four new diet medications now available for lifelong treatment.

Instead there is a strategy for bariatric surgery.  Possibly this provides more profit?
After 10 years, 30% of all bariatric surgery patients gain all their weight back.
Unfortunately when the surgery fails rather than start multiple diet drugs, a new more aggressive surgery is advised.

The science of Obesity is available:

Part 2:

Expensive health care plan to Rx. obesity leaves out medicine.

 ConscienHealth article below is about:

Kaiser Permanente’s Approach

The Challenge of Systematic Obesity Care

           
“If you want some insight into the challenges of gearing up to deliver systematic obesity care, a new publication in Current Obesity Reports is well worth reading. For a full understanding, you will have to read carefully between the lines.
Adam Tsai and colleagues give a very thorough description of how Kaiser Permanente invests in delivering obesity care in the most positive terms possible. They describe a “whole systems” approach to obesity at Kaiser that starts at the community level, investing $50 million in healthy eating and active living programs in an effort to reduce the impact of obesity that is straining their systems for delivering healthcare.
As a key learning from these community health initiatives the authors cite the importance of delivering an adequate “dose” of an intervention to achieve an effect. They do not, however, cite evidence that they have found the right dose to deliver a change in health outcomes. The effort is noble, but it might be guided by conviction more than evidence.
In the realm of evidence-based interventions, Tsai describes an impressive investment in high-intensity lifestyle programs and medically supervised diets. The commitment to these interventions is truly systematic.

At the other end of the spectrum, the authors describe system-wide access to bariatric surgery.
But in the middle, one comes away with the impression of a significant gap.
For many patients, lifestyle modification is not adequate and surgery seems undesirable.

Yet coverage for intensive medical management of obesity, using FDA approved pharmacotherapy, is hardly systematic. Only two of seven regions will reimburse patients for obesity medications and only if their physicians certify that it is medically necessary.

Tsai cites
1-misperceptions about the biological basis of obesity,
2- misunderstandings about obesity drugs,
3-and a conviction that obesity “should not require pharmacotherapy”
as reasons for the low utilization of obesity medications.

Kaiser is a unique healthcare delivery system, sometimes described as a model for high-quality healthcare. Yet the problems that interfere with delivering a high standard of obesity care are not so different from the problems seen in other parts of the healthcare system.

Delivering systematic obesity care remains a challenge. A long tradition of systematically excluding obesity from medical care stands in the way. The bias against caring for people with obesity is a luxury that has become unaffordable.
Leaving obesity untreated has created a crushing burden of chronic diseases that result from obesity.”


Sunday, July 10, 2016

National Weight Control Registry 2016 Annual Survey

This is what the disease of Chronic Obesity Looks like link

Today I was asked by NWCR to fill out my annual survey.

The big change in the last year is that I went on Qsymia. 

It has made a major difference without needing to change my ad libitum diet or my 20 minute one mile walk a day.  I also drink alcohol.

Below is a summary of how I maintained weight loss since 2006.



I was 280 pounds when I made this contract with myself:

I lost 80 pounds by 11-06(nine months of diet)
 and maintained that weight till 12-07 (13 months of same diet)
I maintained 80 pound weight loss for 22 months.

(No one told me that nothing gets rid of the billions of shrunken fat cells I had accumulated)

As the slides states, I was able to lose 80 pounds in the first nine months.

I maintained the low plateau weight of 205 to 210 lbs for the next 13 months staying on 1500 calories a day and exercising 2 hours a day.  

This is as good as most bariatric surgery results. 

I gave up on the 1500 calorie diet and concentrated on exercise in
Jan 2008.
 I slowly gained 50 lbs back.
I did not get all the way back up to 280 lbs as I switched to Atkins in Jan 2011.  

By 12-17-09 I was back up to 250 pounds
I maintained a 32 pound weight loss from 2-06 till 1-11.
This still made me a success in the eyes of NWCR.
That is almost 5 years. I have not counted calories since Jan 2008
Remember, 30% of all bariatric surgery patients gain all their weight back


I did not want to continue to gain weight as I knew I would have to back on Insulin.  The high level of exercise was not making a difference for weight loss. ( I later heard the phrase "You can't outrun your fork" from Yoni Freedhof. )

I could not bare the thought of a 1500 calorie diet again.

Then I read Gary Taubes book Why We Get Fat in Jan 2011.
I went on Atkins and I stopped gaining weight.
I probably was not in nutritional ketosis because I ate so much protein.

I did not lose weight but I had cut back on my exercise to 20-40 minutes walking a day.  I ate ad libitum Atkins so I was never hungry.

I maintained the 248 pound weight with the Atkins and 20 min. walk until   

3-3-14 Went off Insulin and started Invokana  weight 262 pounds

6-24-15 Started Qsymia  weight 244 pounds

11-7-15 Tapered off Actos and restarted Victoza 225 pounds

Dr. Louis J Aronne, Chairman of ABOM  has taught me the use of diet medications.  He has taught that several medications may be needed as the body tries to compensate the effects of a single medicine.  This is why drugs are now given in combination for life long treatment of the Chronic Disease of Obesity

7-1-16 No change in ad libitum Atkins and 20 min/mile/walk/d 220 lbs
The only change is I eat less on the 6 diet medications
1-Metformin
2-Invokana 
3-Victoza
4/5- Qsymia (phentermine/topiramate)
6- Caffeine in coffee during day as needed.

(I have increased exercise since 6-20-16 when I started water aerobics and started light weight circuit weights.  I was 216 pounds before the exercise) 


For my case:
1-I was told I could maintain weight loss with 90 minutes exercise a day.
Not true.
I did 2.5 hours of exercise a day with water aerobics, weight lifting with two different trainers during the week, walking and bike riding. (I mixed it up to avoid muscle memory)

2-I was told nutritional ketosis would decrease my appetite and cause weight loss. 
Not true during the period I documented NK with serum strips. 
3-I was told that low glycemic carbs in later phases of the plateau will not cause weight gain especially if burned off by intense exercise.
Not true.
 
To my regret I don't have body composition information during this early period.

Now I do have body composition data since starting Qsymia one year ago:












Friday, July 8, 2016

Overeaters Anonymous  

I went back to an Overeaters Anonymous meeting last night.

My last meeting was more than 20 years ago.  

I never lost weight while in that group but I gained benefit from it.  

Now that I am in a reduced obese state at 220 lbs from my highest weight of 280 lbs in 206 lbs I was very curious to find out if I could get anything out of the program again. 

I was a little concerned that I would be viewed as an interloper as I am now certified in the American Board of Obesity Medicine and I have just opened an Obesity clinic.  I worried as I would be viewed as an opportunist trolling for future patients. 

My hope lay in the fact that the organization is anonymous. 

I only had to share my first name and my personal story. 

How I lost weight and how I tried to maintain weight loss is accepted by the group. 
 Maybe not by individuals. That is for outside the meeting.

There is not supposed to be cross talk and when talking a person is talking to the group not to other individuals.  No one is to interrupt while a person is sharing.  A person notifies they are done talking by stating they pass.  

Last night reminded me what I like about this group.  
Acceptance.  
Tolerance. 
 Listening.  
As a Doctor, I need to go and learn to listen. 

My six medicines have allowed me to get down to 220 pounds while eating ad libitum Atkins and walking 20- 40 minutes a day.  I also drink alcohol. 
 I call it the Bon Vivant diet.  

I only shared two of the medicines I take with the group.  Invokana and Victoza.  
These folks, I suspect are mostly doing the white knuckle method. 

They spoke of one person who has lost 200 pounds and maintained the weight loss for 20 years.  I wanted to interrupt and explain the waterfall effect on results of diet trials.  Some do very well.  

I want to get on my soapbox and teach them about the Sponge theory and how they are doomed because of their low leptin levels.  It's not a food addiction. 

Or is it?

Could this be a group of Binge Eating Disorder (BED)?

In preparation to taking my Obesity Boards in Dec. 2015 I was taught:

BED is most common eating disorder.
20% in bariatric surgery
50% of severely obese

1- Not a food addiction but behavior addiction like gambling or sex.

2- First approach: Cognitive Behavior Therapy

 3-Vyvanase is a CNS stimulant indicated for BED. 

 (Topiramine, Bupropion may help)

4- Criteria:
Lack of control
Eat rapidly
One time a week for 3 months
Not associated with purging.  


Patients are not allowed to undergo Bariatric surgery if they have Binge Eating Disorder. 

They have to undergo Cognitive Behavior Therapy first. 

Here are waterfall results from surgery.




 Bariatric surgery cannot overcome M&M's.




 





 

Tuesday, July 5, 2016

Most important discipline for weight loss patients


Dear Patient,
You write me that you are busy in the morning and don't have time to log in your weight everyday. 

I understand how difficult these changes are,  that is why I ask for very few of them,  because I think they need to be done for the rest of your life.

I write my weight down on a piece of paper.  That way if I don't get to the computer right away, I can get to it later.

1-I avoid asking patients for a food diary because while effective it is unsustainable.

2-I avoid asking patients to walk one hour a day because while shown to work for NWCR it is unsustainable for most.  Injury hinders many.

3-I avoid asking patients to count calories because again not sustainable for life and often inaccurate.  To measure carefully with scales and cups not sustainable. 

4-I avoid asking folks to use prepared meals because while effective it is expensive.

Lifetime rules
Keep it simple, do what works.      (NWCR tend to eat same thing everyday)
Don't let yourself get hungry.                  (High protein snack between meals)
Avoid all carbs.                                        (Especially for insulin resistant)
Walk at least 20 minutes a day.                (For health, not weight loss)
Avoid sitting but keep moving, standing      (for weight loss)

However, it is very important to weigh yourself everyday. 

The NWCR people do this, it prevents sudden large weight gain which the reduced obese are susceptible to. 

It is very important to record it in your internet spreadsheet that only you and I have access to, so that I can monitor your progress and check in with you to encourage you when you are treading up in weight or not recording weights.
 If you are not recording weights I have no idea where you are in the program. 
I am not going to wait a month to see how you are doing.
 Often a patient has an emergency that causes them to miss an appointment and then I don't know a patient's progress for two months.  In the reduced obese patient that is a lifetime.

Monday, July 4, 2016

Explaining NNT over 5 years

Great work by Dr. Underberg & Kristen Monaco
link to whole article above


Stats on Statins

Robinson: In the 2013 ACC/AHA cholesterol guideline we recommended statins for groups of patients where there was a clear margin of benefit [clinical cardiovascular disease, genetic high LDL-C (>190 mg/dl), or diabetes]. When the margin of benefit may be less clear, such as in primary prevention patients with >7.5% 10-year ASCVD risk, we encouraged shared decision-making by the patient and the clinician.
Studies have shown that patients on average think an NNT (number needed to treat) of 30 would be reasonable for a preventive medication, while for physicians a reasonable NNT(number needed to treat) is 50.
Of course the time horizon matters as well. (NNT over 5 yrs. Is much higher over 20 years) My insert.

Underberg: Statins should be used in those who will benefit most from them, with the least likelihood of side effects and even then, a shared decision process between the healthcare practitioner and the patient will allow for an informed decision process that makes the most sense for every individual.
We still take care of patients one at a time, and this means the use of medications needs to be addressed with personalized approach.
What works for one patient may not always be true for others.
When looking at the totality of evidence statins lower LDL-cholesterol and most importantly they reduce cardiovascular events in patients at risk for cardiovascular disease.
Assessing risk prior to use, and a complete discussion of potential side effects is intrinsic to any pharmacologic intervention in the shared decision making paradigm.

Davidson: The statin trials were only 2-5 years in duration and yet there were major clinical benefits demonstrated.
There are very few therapies that can reverse many years of exposure to a causal risk factor such as elevated LDL-C.
Once a lifetime of benefits can be factored in as well, statins have a much more favorable number needed to treat.

Martin: The NNT will tend to decrease over a longer time horizon.
The typical clinical trial duration of 3-5 years for statin therapy is considerably shorter than the anticipated treatment period of decades for many patients.
Therefore,
the often-quoted NNT values are not reflective of the expected NNT in clinical practice.

Erwin: Statins have clearly positively impacted the trajectory of coronary artery disease in both the primary and secondary prevention arenas.
It is important, however, to treat each case separately and use these medications only in the people who are going to obtain the most benefit from them.

Thompson: The criticism that they help relatively few subjects in 5-year studies is misguided. Who wants to live only 5 years?
Five years studies are only proof of concept studies and the proved concept is that statins prevent cardiovascular events.
I know few cardiologists not on these drugs.
Finally, who can say that stopping statins is such a terrible thing?
The West of Scotland follow up demonstrated that only 5 years of statin treatment provided benefit that extended for 20 years after the study, and coronary regression studies show that much of the regression of atherosclerosis occurs in the first two years of statin treatment. Consequently, estimates of the risk of stopping statins are simply estimates because we have not actually studied that risk.

Good reason to determine lifetime risk with:


Calculators for Lifetime risk