2016 Prediction: Diet Medications will be in most Obese' Medicine Cabinets

2016 Prediction: Diet Meds will be in Obese' Medicine Cabinets


Express: If you want to discuss diet meds with your Doc, I have advice on choosing between the specific drugs here

I took the American Board of Obesity Medicine on Dec.10, 2015 when I learned there were 4 new diet medicines indicated for long term treatment of Chronic Obesity. 

I learned in 2011 (My year of maintaining weight loss while cruising) that losing weight is not the problem. 

The challenge is that the reduced obese have reduced leptin which causes their brain to think the body is starving.  
Diet and exercise at that point will maintain weight in very few determined people National Weight Control Registry).

These diet medicines trick the brain into not believing it is starving. 

1n 1998 I entered into an Infectious Disease Fellowship because the triple therapy for AIDS was found to be effective.  This is the same reason I am coming out of retirement to treat weight loss maintenance. 

In my Obesity courses the recidivism of Bariatric surgery after 10 years is that 10% gain their weight back.   I believe the solution is not diet and exercise but multiple diet medications lifelong. 

I lost 80 pounds on traditional 1500 calorie diet with 2 hours exercise a day. 
I hit a plateau so I increased my fruit intake and my exercise. I changed my routine to include water aerobics and hired two trainers. I was probably doing 2.5 hours of exercise a day.  I was probably eating 2500 to 3000 calories a day.  I gained 1.5 pounds a month over four years till I regained 50 pounds. 
 I learned you can't outrun your fork.  

Yet the guidelines presently give that advice of 300 minutes a week of exercise to maintain your weight.  
What the guidelines don't stress is they expect you to stay on your low calorie diet.  
That my friends is staying on a semi-starvation diet for the rest of your life.  Not sustainable.  
(The Great Starvation Diet 1min 33 sec video)  

The Bon Vivant Diet vs. The Great Starvation Diet 


US NEWS HEALTH The New Obesity Drugs: an Rx for Weight Loss? 










  

Worried about eating too much saturated fat this Christmas?

5 Articles discussing if saturated fats are bad (link)

After reading the five articles above, read a balanced article at this link by Maki 


Dr. Maki writes:
"However, caution is warranted because results from studies in nonhuman primates and mice, as reviewed by Dr. Rudel, have suggested that dietary MUFA compared to SFA intake may not protect against the development of coronary artery atherosclerosis, despite favorable changes in serum lipoprotein lipids.40, 42

There is little clinical trial evidence available regarding MUFA intake and CHD outcomes, but in epidemiological studies researchers have examined this relationship."

  
"The net effect of a particular dietary change may also be modified by characteristics of the population being studied. Individuals with

1-insulin resistance,

2-metabolic syndrome,

3-diabetes, or

4-dyslipidemia

may respond differently from those who do not have these conditions."

Good article on MUFA and PUFA by Dr. MAKI

MUFA and PUFA by Dr Maki link


Highlights:

The results from this and other dietary intervention trials suggest that reductions in LDL-C, non-HDL-C, and apo B occured when MUFAs replaced SFAs in the diet.47, 48, 49

When MUFAs replace carbohydrates in the diet, TG, very low-density lipoprotein-C, high-sensitivity C-reactive protein, and blood pressure decrease, while HDL-C and apo A1 increase.48, 49

These changes suggest that increased MUFA intake should reduce the risk of cardiovascular events.

However, caution is warranted because results from studies in nonhuman primates and mice, as reviewed by Dr. Rudel, have suggested that dietary MUFA compared to SFA intake may not protect against the development of coronary artery atherosclerosis, despite favorable changes in serum lipoprotein lipids.40, 42

There is little clinical trial evidence available regarding MUFA intake and CHD outcomes, but in epidemiological studies researchers have examined this relationship.

In the Nurses’ Health Study, modeling an isocaloric replacement of 5% of energy from SFA with carbohydrate was associated with a nonsignificant reduction in CHD risk (Fig. 5).10

When carbohydrates were substituted for MUFAs, CHD risk was increased, whereas when MUFAs were substituted for SFAs there was an apparent reduction in risk.

However, such results are challenging to interpret because MUFA intake is highly correlated with SFA intake (correlation coefficient of 0.81 in the Nurses’ Health Study data) and is moderately correlated with intakes of PUFA (correlation coefficient 0.30) and trans-fatty acids (correlation coefficient 0.55).

Other factors should also be taken into account when considering the relationship between MUFA intake and atherosclerotic CVD risk.

1-For example, MUFAs coexist with SFAs in many foods.

2-In addition, cis- and trans-isomers of MUFAs were sometimes categorized together in epidemiological studies.

3-Studies that specifically assessed trans-fatty acid intake sometimes characterized them poorly, which may have led to residual confounding.

4-Possible effects of the other nutrients in foods being replaced and what is substituted for the displaced foods also have to be considered.

5-Furthermore, the specific food sources of MUFA may influence the results.

For example, relatively unrefined olive oil retains several lipophilic components, whereas highly refined olive oil has a low level of some of these potentially bioactive compounds.

6-The net effect of a particular dietary change may also be modified by characteristics of the population being studied. Individuals with

1-insulin resistance,

2-metabolic syndrome,

3-diabetes, or

4-dyslipidemia

may respond differently from those who do not have these conditions.

Therefore, in light of the uncertainty regarding the relationship between consumption of specific fatty acids and CVD risk, the most prudent recommendation in the author’s view is a dietary pattern that emphasizes whole grains, legumes, nuts and oils, fruits, vegetables, fish, lean meats, and low-fat dairy products, with sparing consumption of refined grains, white rice, potatoes, stick margarines, shortenings, sugar-sweetened sodas, confectionary products, desserts, high-fat meat and high-fat dairy products.52, 53

 

Following Body Composition with 10% weight loss

I started Qsymia on June 23, 2015 at 244 lbs.
I am at 220 lbs now Dec. 13, 2015.

I did this without feeling hungry.

I did this after stopping my weight lifting routine.
I had gained 4 pounds of weight after a month of daily weight lifting.
I had doubled my strength.
I stopped weight lifting because in Kansas if you don't lose 5% of your weight on a diet medication you must stop it or add something to it.

Here is my body composition after weight lifting and before Qsymia on 6-23-15  and 3 days ago at the Clinic after having been on Qsymia since June 23.


                                           6-23-15 after wts lifting             12-11-15          Goals

Weight                                 244.8                                              222.1               220

Total Body Fat                     31%                                               28.1%              less than 30

Fat Free Mass                      68.9%                                             71.8%
                                            167.4 lbs                                       158.2 lbs

Total Body water                49.9%                                                52.8%            more than 50%
                                           121.3 lbs                                          116.4 lbs
     
Muscle Mass                       46.1lbs                                               41.8 lbs


BMI                                     33.9                                       30.8  less than 30 to not be in obese category                                                                                less than 25 to not be in overweight category

BMR                               1919 cal.                                              1818 cal.
(Basal Metabolic Rate)



These measurements taken on same

 Bio-electrical Impedance  G6 Smart Series BodyCompScale.

I took a 28 day cruise on Aug 1, 2015.

I studied for the American Board of Obesity Medicine exam that I finally took on Dec. 10, 2015.
I am retired so I had a lot of time to study and be sedentary and I only walked my dog one mile a day 5 times a week.  I lost 4 lbs of muscle mass despite being on high protein diet with nutritional ketosis.

You can read why I started Qsymia after failing with Atkins and nutritional ketosis and exercise
 at this link


You can read about the different diet medication options at this link

The important question will be, can I maintain this 10% weight loss? 

The answer,  I believe, is yes if continue to treat my condition of Chronic Obesity link with chronic medical drug therapy. 

This is the revolution in medicine.  

Treat obesity first.  
Once it is treated with medicine many of the co-mobidity medicines can be stopped. 
For me, that meant Insulin and Actos was stopped.

However there is a bias against taking Obesity medicine or diet pills.  
Part of it is side effects from past diet medicines now off the market.
Much of that is avoided now with lower doses in combination with other drugs. 
Part of the bias is moral hazard.  There is a feeling the obese need to earn weight loss with hard work. 

Starvation and Exercise. 

 That has only worked for these people in NWCR link.
10,000 people out of millions. 

Obesity is a Chronic disease that must be treated chronically with multiple diet medications.  
Diet and exercise are minor components. 

The Great Starvation diet link is what most diets push and is especially what the present guidelines push to maintain weight loss.

Read this Frank Greenway MD review link to understand the science as to why diet and exercise fail to maintain weight loss.  

I believe Atkins or LCHF diet is the best to maintain weight loss lifelong.   I eat ad libitum and did not gain weight.  However even in nutritional ketosis and extra exercise I did not lose weight till I started Qsymia.  Clearly I ate less calories on Qsymia without trying and lost weight.  Remember I exercised less and was more sedentary as I studied for the boards.  

The important thing is people must realize I gave up Insulin and Actos but now I must stay on Qsymia.  It is lifelong. 

At one point I suddenly realized I was on 5 diet medications link

I first went on LCHF in 2011 and wrote about it here in this free manuscript link

Over the last five years I have documented that being on 60% fat diet has not adversely affected my lipid profile as shown here link

More importantly, I have had serial CIMT's done over the years to show good results here at this link 

I am a Diplomate and Fellow of the National Lipid Association.

I just completed taking the American Board of Obesity Medicine exam. 

I have documented my personal experience with what works.  

I hope the reader has found the information helpful if not entertaining.  

 

 








 

 

Validation of Tubby Theory from Topeka

Dr. Sniderman interviewed Oct 2015 on LDLP and apo B link

My book published in Jan 2010 The Tubby Theory from Topeka
 is validated by Dr. Sniderman who was one of my instructors. 
 He lays out all the evidence that particle number is the important biomarker to follow.
  I documented I did this back in 2009 in my book with my patients in my lipidology practice.  

This interview also discussed the new field of apoC3 which I knew nothing about in 2010.

I suspect this new information explains why I have not had progression of atherosclerosis on 60% fat diet link.

ApoC3 reduced in patients with low triglycerides. 
LCHF diet is well know to reduce triglycerides while low fat diets do not if they contain high carbohydrate levels. 

I write about this transition in
 Free manuscript: The Tubby Traveler from Topeka

Most importantly, I document plaque regression with Serial CIMT's

I believe I am the only person to document that my personal diet is healthy for my arteries by serial CIMT's. 







 

The Message I learned about dieting while studying for the Obesity Boards 2015

It's not about:

THE FALSE HOPE OF DIET AND EXERCISE

It's about

FOUR NEW DIET MEDICATIONS 2015








Questions and Answers about diets

Why did I start diet pill, Qsymia, on June 24, 2015?

I started Qsymia because Atkins and Exercise failed after 6 weeks

I documented my weight, glucose and blood ketones in the above calendar 6 weeks prior to starting Qsymia (phentermine/topiramate).


I clearly was in nutritional ketosis. 
I also was on Invokana which caused me to urinate glucose.

I did the weight machine circuit upper and lower body with walking almost everyday.  My strength just about doubled and I probably gained 4 pounds of muscle. 

However as a diabetic I was keen to get off my Actos and to lose much of my visceral fat to fight my insulin resistance but I did not want to go on a substarvation diet.

Here is what I did instead 

2008 Guidelines for Exercise and Obesity

My exercise prescription:
When starting a diet to lose weight don't start an exercise program.  Just do what you are already doing.   Concentrate on the diet plan you have chosen.  If you must exercise start with walking 5 minutes out and 5 minutes back. 
Then walk 8 minutes after each of the 3 main meals each day. 
Finally minimum walking 20 minutes a day.  40 minutes is great.  Lift light weight 2-3 times a week if able.

To maintain weight loss:  Walk at least 20 minutes a day for health effect. 

 

Guidelines below with evidence

Critique of Exercise Studies presented at OMA meeting in Washington DC 2015
No random control trial for exercise.  
Poor adherence in studies.
  When adherence was good, exercise was good, 
when adherence was poor, exercise results not good.

the higher a person's BMI, the harder their body fights to conserve energy."

 Protein found that prevents weight loss in obese
link to article above 
Written by Catharine Paddock PhD

"In contrast to the more abundant white adipocytes, or white fat cells, that store energy, our bodies contain much smaller amounts of brown adipocytes, or brown fat cells, that burn fat to keep us warm - a process known as thermogenesis.
The new research reveals that a protein known as sLR11 appears to suppress thermogenesis in fat tissue.
The team found that mice unable to produce the protein were more resistant to weight gain when put on a higher-calorie diet. Compared with mice that did not lack the protein, their metabolic rates increased so they burned calories faster.
The researchers also found that in the mice lacking sLR11, genes that are normally active in brown fat tissue were more active in white fat tissue.

The higher the BMI, the harder it is to burn off fat

On further investigation, the team discovered that the protein binds to specific receptors on fat cells so as to block their ability to trigger thermogenesis and convert fat to heat.
Moreover, it appears that sLR11 increases the efficiency of storing energy in fat and stopping any excess being lost to heat generation.
In a final part of the study, the team turned to humans. There, they found higher blood levels of the protein were linked to higher total body fat.
Also, when they looked at obese patients undergoing bariatric surgery, they found the amount of weight loss following surgery was in line with falls in sLR11, suggesting the protein is released by fat cells.
The researchers suggest sLR11 plays an energy conserving role to prevent energy wastage in fat tissue, and this role is exaggerated in overweight and obese people, with the result that the higher a person's BMI, the harder their body fights to conserve energy."

Niacin still a good drug.

Extended Release Niacin in Diabetics link



"Conclusions—In statin-treated men with type 2 diabetes mellitus, Extended Release Niacin decreased plasma Lp(a) concentrations by decreasing the production of apo(a) and Lp(a)-apoB-100. 
Extended Release Niacin also decreased the concentrations of apoB-100–containing lipoproteins by decreasing VLDL production and the transport of these particles down the VLDL to LDL cascade. 
Our study provides further mechanistic insights into the lipid-regulating effects of Extended Release Niacin." 

• Received July 1, 2015.
• Accepted October 20, 2015.

• © 2015 American Heart Association, Inc.

 LDLc treatment and its impact on mortality

 Received: March 2, 2015 Article in press
Journal of Clinical Lipidology

Highlights

• •Hypercholesterolemia is the highest population attributable risk factor for CHD.
•  
• •LDL-C remains the primary treatment target for reduction of ischemic events.
•  
• •Intensive statins and statin/ezetimibe are proven for secondary prevention.
•  
• •Treatment of LDL-C to less tha 50 mg/dL are being tested with novel therapies.

       Public policies are needed to shift-down the whole population LDL-C distribution.

Abstract

Cardiovascular (CV) disease is a leading cause of death worldwide, accounting for approximately 31.4% of deaths globally in 2012.
 It is estimated that, from 1980 to 2000, reduction in total cholesterol accounted for a 33% decrease in coronary heart disease (CHD) deaths in the USA.
In other developed countries, similar decreases in CHD deaths (ranging from 19–46%) have been attributed to reduction in total cholesterol.
 Low-density lipoprotein cholesterol (LDL-C) has now largely replaced total cholesterol as a risk marker and the primary treatment target for hyperlipidemia.
Reduction in LDL-C levels by statin-based therapies has been demonstrated to result in a reduction in the risk of nonfatal CV events and mortality in a continuous and graded manner over a wide range of baseline risk and LDL-C levels.
This article provides a review of: 
1) the relationship between LDL-C and CV risk from a biologic, epidemiologic, and genetic standpoint;
2) evidence-based strategies for LDL-C lowering;
 3) lipid management guidelines;
 4) new strategies to further reduce CV risk through LDL-C lowering; and
 5) population-level and health-system initiatives aimed at identifying, treating, and lowering lifetime LDL-C exposure.



I wrote Tubby Theory from Topeka in 2009, published it in 2010.

At that time I advised people with one risk factor to get a CAC and CIMT.  If they had a plaque, they had subclinical atherosclerosis. 

To get regression of the plaque, I advised low dose combination therapy with statin, niacin and Zetia. 

Slowly add the drugs each month until the one of the following goals is reached:
non-HDLc less than 80
LDLp less than 75 
apo B less than 60.


Low dose combination therapy is the way to avoid side effects especially since we need to treat atherosclerosis early to reduce the residual risk of treating late in the disease process and the patient will be on these drugs for a very long time. 

Update and Validation of Tubby Theory link


 

Serial CIMT to determine if your diet is healthy

I had regression of atheroma in wall of carotid after starting LCHF in 2011.
My data at this link 

           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)