Sunday, November 29, 2015

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


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 


Friday, November 27, 2015

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.




Wednesday, November 25, 2015

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

"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."






Monday, November 23, 2015

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.


 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


 



















Thursday, November 19, 2015

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)


Monday, November 16, 2015

Brown Adipose Tissue also known as BAT


BROWN ADIPOSE TISSUE (BAT) 
AS OPPOSED TO WHITE ADIPOSE TISSUE (WAT)









The above slides are from the OMA Obesity Preparation conference in a lecture given by 
Jeffrey Sicat MD

This is what the disease of Chronic Obesity Looks like









8 years 9 months weight loss maintenance
64 year old next month.
Photo taken 11-15-15
My ideal body wt. at 5’ 11” = 172 lbs IBW

280- 172= 118 lbs EBW (Excess Body Weight)

280- 200= 80 lbs WL  (Wt. Loss)     After 13.5 mos on Cruise 3 Hour Diet

280- 258= 22 lbs WL        1-1-11 or 3 years 6 months after starting diet

280-228= 62 lbs WL          11-13-15 On 5 medicines for weight loss link


My %EBWL:

13.5 months 67%

3 years 6 mos  22%

8 years 9 mos  52% 
                                           Nov, 15, 2015



April 2004 

October 2005

11-28-2006
80 lb weight loss


I maintained my weight loss 
from 11/2006 till Dec 2007
with 1500 calorie diet and 2 hour day exercise

In Dec 2007 I found it impossible to get below 200 pounds with 1500 calorie diet and 2 hours exercise a day.  

I decided I needed to eat more and build up muscle to build up metabolism.  I had not formulated the Sponge Syndrome yet. 

50 lb weight regain
12-1- 2010
Togo, Africa





11-27-10

Gambia 

Charlie the Crocodile 



 
      In 1996 I published the The Fen Fen diet pill program 
       I was 272 pounds with a 49 inch waist Oct. 1995
            I could bench press 340 pounds free weight.
I lost 50 pounds in 3 months on Fastin and Pondimin. 
220 lbs waist 42 inches in 1996.

My first big weight loss was in 1988.  
I went from 245 pounds to 208 pounds. 
I attended Overeaters Anonymous Meetings.
I went to Nautilus weights 3 times a week and jogged daily while on 1,000 calories.  I stayed at this weight for a few months but the deprivation was too much and I quickly went up to 220 pounds. 

6-17-1970  173 lbs waist 35”  5’11” 19yrs 6 mos
 BMI 24    70th %tile

Went on Weight Watchers Diet in High School.  Photo in April 1968, I am at 5'10 and 160 lbs and my BMI is 22 and I'm at 70% tile.

9-19-1965  175 lbs  5'8.5”  BMI 26  13yrs 3mos at 95th % tile                  

I always thought I was a chubby child.  I tried to pull up some photos to document it below. 


above4-1965
 Age 14
Seventh grade
On Andreas Hudde Junior High School Basketball team



above
October 1964      
Age  13 years 10 months
In sixth grade at Public School 89 in Brooklyn, NY


aboveAugust 1960. I was 8 years 8 months.  I was a big kid for my age.  I thought I was overweight.  I ate a tremendous amount and was very active. 
Finished second grade. 


above
1958 
age 7
 I was fitting into the size they called "husky".

My weight record since second grade 


Saturday, November 14, 2015

Which Bariatric Surgery has most weight loss?


Which Bariatric Surgery has most weight loss?

These slides from The Obesity Society's American Board of Obesity Medicine Exam Preparation

Dr. John Morton made these slides.


 my link below

I had 67% EBWL at 13.5 mos with diet. 
and 52% EBWL at 8 yrs with diet medicine 

 Sleeve gastrectomy not on this data.  SG might be the most popular surgery now.  It allows young people to drink alcohol.
It doesn't have as much malnutrition as Roux N-Y Gastric Bypass or the Biliopancreatic Diversion Duodenal Switch. 

GS was the first part of the bigger BPD/DS.  Now that these surgeries are done laproscopically and have much better outcomes, GS and BPD/DS have become their own surgery.  
GS can later be upgraded to BPD/DS if it fails.

 







Friday, November 13, 2015

Slides on Recidivism in Bariatric Surgery 2015 OMA meeting Washington DC Dr. Denis Halmi


Weight regain after Bariatric Surgery from Dr. Denis Halmi slides at OMA meeting in WASH DC 2015


Why does Bariatric surgery fail? Slides from Dr. Denis Halmi OMA meeting in WASH DC 2015


Atkins + 5 diet pills vs. Bariatric surgery




My ideal body wt. at 5’ 11” = 172 lbs IBW

280- 172= 118 lbs EBW

280- 200= 80 lbs WL       After 13.5 months on Jorge Cruise 3 Hour Diet

280- 258= 22 lbs WL        1-1-11 or 3 years 6 months after starting diet

280-228= 62 lbs WL          11-13-15 On 5 medicines for weight loss link


My %EBWL:

13.5 months 67%

3 years 6 mos  22%

8 years 9 mos  52%


At the OMA course in Washington DC 2015
Dr. Denis Halmi on effectiveness of Bariatric Surgery

60 %EBWL in 6 months

75  %EBWL in 12 months

Five years after surgery about 70% of patients maintain 50% of their excess weight loss.

30% of patients regain the lost weight by 10 years.

Thursday, November 12, 2015

Aggressive treatment of hypertension

 Aggressive treatment of hypertension

Links:
NEJM article on getting systolic pressure less than 120

Contrary view 5 min video 
Medical Nihilism

HOPE trial: Ramapril : Jan 2000
Conclusions
"Ramipril significantly reduces the rates of death, myocardial infarction, and stroke in a broad range of high-risk patients who are not known to have a low ejection fraction or heart failure."



My personal story.
I was diagnosed with diabetes type 2 in Jan. 1999 at 242 pounds.  
I hoped to lose weight and exercise to get my glucose down.
A few months later I developed peripheral neuropathy and my denial was shattered. 
Lifestyle changes are always the first step in the guidelines but not productive. 

 As a diabetic, a patient often needs to go on several drugs:
Metformin
ACE inhibitor
Statin 
Aspirin

After my personal experience and studying for the Obesity Boards I would have concentrated on weight loss with Atkins diet or Low Carbohydrate High Fat diet.  I now would offer Invokana and Victoza to help control the glucose and help with weight loss. 

On Invokana with Ramipril my systolic blood pressure in the physicians office varies from 90 to 120. 

On 60% fat diet my LDLp has ranged from less than 300 to 907 since 12-6-11 My data link



On Victoza I lost 6 lbs without changing diet or exercise. 1-12
On Invokana I lost 20 lbs without changing diet or exercise. 3-14
On Qsymia I lost 13 lbs without changing diet of exercise. 6-15


Links:
 My experience with weight loss medicine  

I realized I am on 5 diet medications 







Wednesday, November 11, 2015

Diabetic Drug Trial with 32% RRR in all cause mortality




Empagliflozin (Jardiance) trial link 



"The benefit on survival was seen regardless of the cause of death — empagliflozin prevented one in three cardiovascular deaths, with a significant 38% relative risk reduction in cardiovascular mortality, as well as a significant 32% relative reduction in all-cause mortality."

"CV death was one component of the primary composite outcome, which also included nonfatal myocardial infarction (MI) or nonfatal stroke.
 It was the CV mortality benefit, however, that primarily drove the reduction in this end point."

"Empagliflozin is reducing death, the ultimate outcome," senior author of the study, Silvio Inzucchi, MD, of Yale Diabetes Center, New Haven, Connecticut, told Medscape Medical News. "This is a first in my lifetime — a diabetes drug trial that has shown improved outcomes in high-risk cardiovascular patients."

"He admitted, however, that the investigators "don't understand our findings," because empagliflozin did not seem to have any significant effect on MI or stroke, so "this may not be an atherosclerotic effect. If it were, we would expect to have seen an effect on MI and stroke.

"Most good trials raise more questions than they answer, but it may be that we have had the treatment of diabetes wrong for 50 years," Dr Inzucchi controversially observed. "We can control the glucose, but [we have been doing that] without controlling the calorie excess," he continued. By causing glucose to be excreted in the urine, empagliflozin may be aiding this, "and we may have to rethink our strategy."

Links below:







update trials of Alzheimers

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