Why we eat chocolate when we are not hungry

Cognitive controls of food intake link


“Although humans have the ability to make conscious, voluntary decisions and choices, many of our actions have a subconscious component that escapes voluntary control.  This is why we eat palatable foods such as chocolate in the absence of metabolic need, even if we recognize the negative consequences of such actions."

From p 166 Handbook of Obesity Vol. 1, third edition, 2014 by Bray and Bouchard.

Hit link above for anatomical and CT evidence of this statement. 
 

Set Point Part 2 Dr. Vassellin

Dr. Vasselli on critical question about fat mass regulation link 

one minute 40 second video

I tried to look up "set point" in the Obesity Handbook by Bray and Bouchard.  On pg 168 Vol one:
"Whatever the mechanisms in many obesity-prone individuals, there is a constant upward resetting of the defended body weight in the face of continued excess caloric intake such that whatever level of adiposity an individual reaches when caloric restriction is instituted,  there is a powerful drive to regain that level when caloric restriction is lifted."

Set Point with Fat Part I Dr. Vasselli

Dr. Vasselli explains Set Point in Obesity link to 3 min 55 sec video

Is a Calorie a Calorie? Part 1 based on high protein diet.

Dr Joe Vasselli gives a short answer to a complicated question link

My 3 Books

 

 

The chairman of the American Board of Obesity Medicine tells the reality of weight loss

Dr. Aronne 3 minute 40 second clip


"We are not treating a disorder of willpower.  This is not lifestyle treatment."




This physician has been treating obesity for more than 20 years.  Leptin was discovered 20 years ago.
The usual pablum of lifestyle changes will work if only the patient had enough willpower is still pushed by the false hope of diet and exercise.
 
This lecture was given at NY Presbyterian/Columbia Medical College of Physicians in April 2015 as part of a week long conference on Obesity in preparation of the American Board of Obesity Medicine test to be given in December.

Sponge syndrome has 8 hormones that facilitate regain of weight

6.5 minute video on Sponge Syndrome

Guidelines calls for counting calories while Chairman of Board personally does not agree

Dr Louis Aronne on biggest change in guidelines





Above link is 1 min 45 second video discussing recommendation #4 and #5 in chart below.

Dr. Aronne says he does not personally agree with #4 but he thinks #5 is the biggest and important change in the guidelines. 

Dr. Bove continues to offer the false hope of weight loss with a team approach

Here is Dr. Bove's article with my strong disagreement



Excerpt from above link:

Dr Bove writes:

" For many patients the cost is prohibitive, but with proper motivation, these programs can succeed in initial weight reduction and sustained weight control."

My response:

Again where is the data for this outrageous claim, unless he is saying the 5% weight loss that 1/16? people maintained in LOOK AHEAD is sufficient success?

What to do about Magnesium supplements?

Nice opinion piece about taking Magnesium 2015


Whole article at link above.
Dr George Lundberg

"Foods with high magnesium content include dark leafy greens, especially kale, chard, and spinach; tree nuts and peanuts; seeds; oily fish; beans, lentils, legumes, and whole grains; avocado, yogurt, bananas, and dried fruit; dark chocolate; and molasses. Supplemental magnesium is available over the counter in many forms: citrate, amino acid chelate, chloride, glycinate, malate, taurate, carbonate, and others, which vary in absorption, concentration, and bioavailability.

Because you cannot just draw a blood sample and ask the lab to identify a deficiency,

I advise that if a patient has any of the symptoms I listed, you might best just try that old standby, "trial of therapy," and track what happens."

12 month follow up on LCHF diet in 2014

 

Long term effect of high protein low carb diet link

 

 

 

CONCLUSION:

The short term benefit of higher protein diets appears to persist to a small degree long term.

Benefits are greater with better compliance to the diet.

How does exercise affect appetite- At Columbia Obesity Board review- the jury is still out

Richard Weil answers this question in 3 min 50 seconds video

Dr. Yoni Freedhoff on exercise and obesity

2 minute video clip on exercise and obesity



Dr. Yoni Freedhoff teaches the same as Richard Weil at the Columbia Obesity Review course 4/15:


 2 minute clip on guidelines approach to exercise




As someone who plans to take the American Board Obesity exam in Dec 2015, I wonder what the correct answer will be on the test?  Slides below from Richard Weil.

From Handbook of Obesity Vol 1 Third edition 2014
pg. 282: "Is Exercise associated with reduction in body weight and total adiposity in a dose-response manner?"

"A total of 39 studies met the inclusion criteria...On average, studies with longer duration reported smaller weight loss for a given EE, whereas shorter duration reported greater weight loss."
"Not surprisingly, the exercise-induced changes in fat mass revealed a similar pattern to that observed for weight loss."
"It is also possible that adherence to dietary intake instructions was more readily adhered to in short-term as opposed to long-term trials."
pg. 290: "Clearly, there is a need for additional well-controlled trials that consider the independent effects of exercise on obesity reduction."
"However, although exercise alone is associated with reduction in total and abdominal fat in a dose-responsive manner,  gaps in knowledge persist."
"Nevertheless, the dose-response relationship observed in the short-term studies indicates that to reduce bodyweight by about 0.25kg/week, the required EE (energy expenditure) approximates 2700 kcal/week. 
 Our observations suggest that EE of this magnitude will require exercising for about 50 minutes, five times a week at 70% VO2max (83% of maximum heart rate). 
 It is important to reinforce the observation that these calculations are derived from short-term studies alone. "
 "It is evident that in long term trials, despite the similarity in the EEs prescribed, that the corresponding reduction in both total and abdominal obesities is substantially less."
"demonstration that the adoption of exercise alone as a treatment strategy for obesity reduction can be sustained long term remains a challenge."


From Washington Post 5-15-15:

 Can't outrun a bad diet

Amazing update on a "remarkable" study that seems to have been forgotten

 Go to link below to read about amazing story of two great NYT journalists:


Update from Oct 2015 OMA meeting at Washington DC
I was very happy to see three great experts cite this reference:
Frank Greenway
Ethan Lazarus 
David Ludwig



Link below:
Among overweight and obese young adults compared with pre-weight-loss energy expenditure, isocaloric feeding following 10% to 15% weight loss resulted in decreases in REE and TEE that were greatest with the low-fat diet, intermediate with the low-glycemic index diet, and least with the very low-carbohydrate diet.

My article on Lipid Lecture pad

Diets and Preventing heart disease link

Commentary by Brian Edwards, MD regarding the manuscript: Diets to Prevent Coronary Heart Disease 1957- 2013: What Have We Learned?By James E. Dalen, MD, MPH and Stephen Devries, MD, FACC from the American Journal of Medicine

Why do guidelines and Columbia Obesity Board review persist in teaching the 3500 cal = 1 pound of weight?

 Two slides below are from Alice Lichtenstein's lecture at the Columbia Obesity Board review 4/15

Alice Lichtenstien is asked why guidelines persist in Magical thinking 4 min 30 sec video


Dr. Lichtenstein ended her lecture saying people want to believe in Magical thinking rather than the first law of thermodynamics.  3500 cal = one pound of weight

However I said according this NEJM article, the guidelines have Magical thinking:

Reference #1

Small Sustained Changes in Energy Intake or Expenditure

"Myth number 1: Small sustained changes in energy intake or expenditure will produce large, long-term weight changes.
Predictions suggesting that large changes in weight will accumulate indefinitely in response to small sustained lifestyle modifications rely on the half-century-old 3500-kcal rule, which equates a weight alteration of 1 lb (0.45 kg) to a 3500-kcal cumulative deficit or increment.5,6

 However, applying the 3500-kcal rule to cases in which small modifications are made for long periods violates the assumptions of the original model, which were derived from short-term experiments predominantly performed in men on very-low-energy diets (<800 class="ref" day="" kcal="" per="" span="">5,7

Recent studies have shown that individual variability affects changes in body composition in response to changes in energy intake and expenditure,7 with analyses predicting substantially smaller changes in weight (often by an order of magnitude across extended periods) than the 3500-kcal rule does.5,7

 For example, whereas the 3500-kcal rule predicts that a person who increases daily energy expenditure by 100 kcal by walking 1 mile (1.6 km) per day will lose more than 50 lb (22.7 kg) over a period of 5 years, the true weight loss is only about 10 lb (4.5 kg),6 assuming no compensatory increase in caloric intake, because changes in mass concomitantly alter the energy requirements of the body."


Reference #2

The American Board of Obesity advises that the two volume Handbook of Obesity edited by George A. Bray and Claude Bouchard be used to study for the boards.  I have the 2014 fourth edition.

I have skimmed the book looking for the 3500 cal = 1 pound of body weight rule.  I could not find it.
There was very little about counting calories in this book.  In Volume 2, Fourth edition on page 132 it discussed goal setting.
"The goal in behavioral programs is to achieve a weight loss of 1-2 lb/week. To accomplish this, patients are given goals for total calories (usually 1000- 1500 kcal/day).... and for physical activity (gradually increased from 250 kcal/week to 1,000 kcal/week)."

Reference #3

I can't find anywhere in this obesity text a iron clad first law of thermodynamics statement that 3,500 cal= 1 pound of weight loss or weight gain.

In Volume 1 on page 173 it states "These days, the law of thermodynamics is one of the most fundamental basics of energy metabolism control.
When translated to the regulation of body weight, the law means that the energy (calories) consumed must match the body's energy (caloric) demand to sustain a stable body weight over time.
 Any prolonged deviation from this equilibrium will inevitably result in either weight gain (in case energy intake exceeds energy expenditure) or weight loss (in case energy expenditure exceeds energy intake).
Accordingly, to maintain a stable body weight over time, intake constantly needs to be adjusted for changing energy demands.
 Based on constant changes in this demand, the adjustment of energy intake must be achieved through the (short-term) regulation of caloric intake (e.g. through regulation of the meal size and/or the meal frequency)
 and must take into account (long-term) information about the energy stored as fat in the body.
The complex process of energy metabolism control is tightly regulated by the cross talk of central and peripheral signaling systems and depends on constant signal integration."

Reference #4

Dr Leibel says the reduced obese must decrease net calories 20% more than a person of the same weight who has not dieted to maintain the same weight (1 min 40 second clip).

In the reduced obese the brain thinks from the low leptin levels that the body is starving and will cause the body to be more efficient in using the calories to store fat.  Thus the reduced obese to have energy balance of 20% less just to maintain the weight. This is not a strict 3500 calories = 1 pound rule.  If it was the reduced obese should continue to lose weight. The guidelines totally ignore this science.

Reference #5

Back to Handbook of Obesity Volume 2 pg 174 "Realities.  Calories do count. Calories consumed must equal calories expended even with low density foods."

Reference #6

Back to Handbook of Obesity Volume 1 pg 169:
"However we still do not understand why some individuals are prone to become obese when excess energy is available, while other are obesity-resistant under such circumstances."

Reference #7

Back to Handbook of Obesity Volume 2 pg 147:
"after a period of dieting, resting metabolic rate decreases beyond the level expected from the loss of body mass alone".


Reference #8

Back to Handbook of Obesity Volume 2 pg 209:
"Although the energy balance equation and it's role in weight management appear straightforward, it has proven to be anything but simple.  Intervening on any one component of the energy balance equation has been demonstrated to affect other elements of the equation, and not always for the positive.  For example, exercise interventions with large doses of supervised exercise have been found to produce less weight loss than expected based on the caloric expenditure of the exercise alone, and very-low-calorie meal plans can make increasing levels of activity challenging.  Thus one must keep in mind that exercise-induced increases in caloric expenditure are one part of a complex system with multiple feedback loops, and it is this complexity that likely explains often conflicting findings related to the role of exercise in weight loss."

Reference #9

Handbook of Obesity Volume 2    pg, 210:
"Further, given the many contributing influences to weight, it is somewhat of an oversimplification to address the prevention of weight gain using increased energy expenditure alone.
 The relative contribution of energy intake and energy expenditure in the creation of energy balance to prevent weight gain varies from individual to individual, making it impossible for one recommendation to be appropriate for all individuals."

Reference #10 

Handbook of Obesity Volume  1  pg 577:
"in addition to the direct effects of diet and microbiota on their own, the energy extraction from the diet as well as the byproducts of metabolism, could be influenced by the interactions between them."
"For example it is possible that certain microbial species than others in extracting energy and contributing to weight gain."

Reference #11

"Effects of dietary composition on energy expenditure during weight-loss maintenance."

 Ebbling JAMA 2012 link

Read Gary Taubes 2012 editorial on this important trial link

Read USA Today article about this trial link

Read Gina Koleta Q&A Hirsch 2012 link

Read Response to Hirsch about water loss in trial link

Read Always hungry?  Here's Why May 2014  link

Read JAMA article June 2014 link
Increasing AdiposityConsequence or Cause of Overeating?                                                            David S. Ludwig, MD, PhD^1,2; Mark I. Friedman, PhD³

Reference #12
Effects of energy-restricted high-protein, low-fat compared with standard-protein, low-fat diets: a meta-analysis of randomized controlled trials.Wycherley TP¹

 ^{Wycherley Am J Clin Nutr 2012 link}

Reference #13

Back to Handbook of Obesity Volume 1 pg. 290:

"However, although exercise alone is associated with reductions in total and abdominal fat in a dose-response manner,  gaps in knowledge persist. 

 This is particularly true for short-term studies wherein the weekly EE induced by exercise is either very low or very high. 

 Nevertheless, the dose-response relationship observed in the short-term studies indicate that to reduce body weight by about 0.25 kg/week, the required EE approximates 2700 kcal/week. Our observations suggest that EE of this magnitude will require exercising for about 50 minutes, five times a week at 70% VO2 max   (83% of maximum heart rate). 

 It is important to reinforce the observation that these calculations are derived from short-term studies alone. 

 It is evident from figure 25.1 that in long-term trials, despite the similarity in the EEs prescribed, that the corresponding reduction in both total and abdominal obesities is substantially less."
The 3 graphs below are from pg 287 Handbook of Obesity edited by George A. Bray and Claude Bouchard

Reference #14
Misconception in body weight regulation

Flatt JP¹

Abstract

Energy is a concept of universal importance.
 In applying it to body weight regulation, the focus has been on energy balance and how this balance is affected by intakes and expenditures.
However, energy is an abstract concept without biological equivalent and applying it to explain body weight regulation has led to various misconceptions and created intellectual obstacles in understanding the obesity problem.
When nutrient and substrate interactions are considered, instead, a number of important issues pertaining to body weight regulation and to the obesity epidemic can be much more pertinently addressed.

Reference #15

Central orchestration of peripheral nutrient partitioning and substrate utilization

Denis RG¹, Joly-Amado A¹, Cansell C¹, Castel J², Martinez S², Delbes AS², Luquet S³.

Author information

Abstract

Energy homoeostasis is maintained through a complex interplay of nutrient intake and energy expenditure.
 The central nervous system is an essential component of this regulation, as it integrates circulating signals of hunger and satiety to develop adaptive responses at the behavioural and metabolic levels, while the hypothalamus is regarded as a particularly crucial structure in the brain in terms of energy homoeostasis.
The arcuate nucleus (ARC) of the hypothalamus contains at least two intermingled neuronal populations: the neurons that produce neuropeptide Y (NPY); and the Agouti-related protein (AgRP) produced by AgRP/NPY neurons situated below the third ventricle in close proximity to proopiomelanocortin (POMC)-producing neurons.
POMC neurons exert their catabolic and anorectic actions by releasing α-melanocyte-stimulating hormone (α-MSH), while AgRP neurons oppose this action by exerting tonic GABAergic inhibition of POMC neurons and releasing the melanocortin receptor inverse agonist AgRP.
The release of neurotransmitters and neuropeptides by second-order AgRP neurons appears to take place on a multiple time scale, thereby allowing neuromodulation of preganglionic neuronal activity and subsequent control of nutrient partitioning - in other words, the coordinated regulation of conversion, storage and utilization of carbohydrates vs. lipids.

This suggests that the function of AgRP neurons extends beyond the strict regulation of feeding to the regulation of efferent organ activity, such that AgRP neurons may now be viewed as an important bridge between central detection of nutrient availability and peripheral nutrient partitioning, thus providing a mechanistic link between obesity and obesity-related disorders.

Reference #16

Handbook of Obesity 3rd edition Vol 1 pg 293
Chapter 26: Energy partitioning, Substrate Oxidation Rates and Obesity
"Even if energy partitioning represents a concept that seems to be worthy of consideration in any issue pertaining to metabolic regulation, it is not systematically considered in obesity research."

With the above disclaimer, this chapter had some very provocative sections:
1-"The use of high protein diet was found to accentuate the loss of body weight and fat in obese individuals and to promote weight maintenance in weight reduced obese subjects."
2-"lipogenesis can accommodate excess carbohydrate intake when glycogen stores and glucose oxidation reach their maximal adaptability."
3-"Body fat loss promotes a decrease in fat oxidation."
4-"these variations in fat-lean tissue partitioning seem to be a major determinant of the response to long term over-feeding."
5-"Since insulin can stimulate numerous biological functions such as sympathetic nervous system activity, it is plausible that a muscular insulin resistance to glucose uptake also implies a decreased potential of insulin to activate sympathetically mediated thermogenesis and fat oxidation.
6-"Other biological alterations can contribute to suboptimal muscle functioning in obesity."
7-"It seems that when F-FDGpositive individuals are exposed to a stimulus like cold BAT can play a significant role in body energy partitioning."
8-"leptin, which is secreted at different levels in subcutaneous and visceral fat, increases energy partitioning toward oxidation and also directly alters lipid partitioning in skeletal muscle as well as substrate cycling in adipose tissue."
9-"Adiponectin has the potential to influence energy partitioning through effects on fatty acid oxidation in muscle."
10-"Nesfatin influences food intake and substrate partitioning.
11- "Ghrelin even in the absence of effects on nutrient intake,  affects nutrient partitioning and increases adiposity, with direct effects on adipocytes."
12-"Calcium paradox" significant impact on fat metabolism."
13-"the energy equivalent of a calcium-augmented fecal fat loss ranged from 50 to 75 kcal/d."

The 4 slides below are from Alice Lichtenstein lecture at the NY Presbyterian/Columbia College of Medicine Obesity Board review course in April 2015.   I am surprised that the guidelines 2013 below use the old calories in calories out formula where 500 cal/d deficit leads to weight loss when the Handbook of Obesity text presents many exceptions to this rule especially in the reduced obese.

8 years after writing Rethinking Thin: People still have false hope of diet and exercise

In 2007 I first read about the false hope of dieting in Gina Kolata's book; Rethinking Thin.

Pg. 221:  "I (the author Gina Kolata) wanted Carmen and Graz, and Jerry and Ron and all the others to succeed.  I wanted it so much that I began to suspend belief.  I knew, I knew, the science and the overwhelming convincing evidence that most obese people will not be able to diet, get thin, and stay at a new low weight.  But in those first six months, when everyone was dropping pounds, when Graz lifted her shirt and said to me, "Look I have a waist!" I fell under the dieters spell.  I allowed myself to think that maybe, these people would make it.  Maybe they would fulfill their dreams." 
  

LOOK AHEAD trial graphs has since nailed the coffin on the dream of false hope of dieting, yet at NY Presbyterian/Columbia Obesity Board review in April 2015 I found the false hope perpetuated that somehow St. Luke's program had better results than the largest and longer diet trial ever with millions of dollars poured into it.  Is it explained by scalability as Sharon Akabas suggests below?  



40 sec clip: St Luke's nutritionist avers her program works despite Leptin reset of reduced obese, hence my frustration with even the best weight loss programs: false hope continues.

Brian: Does your calculation for calories needed to lose weight include the extra 20% that Dr. Leibel says the reduced obese need to do just to maintain weight loss Plateau explained?

Betty Kovacs:" Not if their resistance activity is and they replace the muscle loss.  We've got Rich (Weil).
They are supposed to be doing resistance activity. .
If they are not losing (weight) we can adjust it.
They lose (weight) without that factor."

Then Sharon Akabas (the director of the Board Review) doubles down on this false hope.

If people had access to this type of program it would help (link)

Sharon Akabas: "(Betty), your's is an amazing program.  Gary (Taubes) was here last week and he was talking about the issue of scalability.  So to what extent of what you (Betty) are seeing is dependent on you (Betty) and Rich (Weil).."

Betty Kovacs: "The world we live in is not what people... We have a very different environment that we get these people for 75 minutes each week for a year where we get to do all this.  We get to enforce it, hours of exercise and balance of the food.  So I don't believe that everything we see... I said that in the beginning our data does not match what is out there.  Because this is a very different population and a different environment.  Ultimately, if people had access to this kind of intervention it would help."


 I reviewed Richard Weil's lectures at the Obesity Board Review and found him show this graph.  Rich said he has this graph on the wall of his office.  It shows the variability of the results of his program and virtually every other obesity trial.  There is a great variability of results.  Some people do better than others.  This seems to be in conflict about the success of the program that Betty suggested. See link below for his comment on his and Betty's group of patients results. 

Mr. Weil says of his 600 patients 8% don't lose weight link

Back to pg. 221 of Rethinking Thin:

"Some scientists, including Jules Hirsch and Jeff Friedman, suggest an intriguing hypothesis.  The origins of people's recent weight gains may have little to do with their current environment or with their willpower, or lack of it, or with today's social customs to snack and eat on the run or with any other popular belief."

1min 40 sec clip on why we can't maintain weight Loss: Dr Leibel

Jeffrey Friedman, MD, PhD  is a molecular geneticist at New York City's Rockefeller University  His discovery of the hormone leptin and its role in regulating body weight has had a major role in the area of human obesity.

I listened to four great lectures on the science of obesity by Leibel, Rosenbaum and Vasselli.
I was enthralled by these scientist's lecture.
The lectures lead Sharon Arabas to have a different feeling. Introducing a lecture she says in this clip:  "another whole hour of very depressing things to hear" 1 min 40 sec clip

 In summary, the incredible cognitive dissonance displayed but denied at the NY Presbyterian/Columbia College of Medicine where the giants of the science of obesity had just spoken at,  I hear the St. Luke's people (make the same old claim), "but their program is different, it works".

As Dr. Mike Rosenbaum said on April 23, 2015 at this conference: Stop bilking! 3 min video



Revolution in Obesity as far back as 1995 reference:

"Conclusions

Maintenance of a reduced or elevated body weight is associated with compensatory changes in energy expenditure, which oppose the maintenance of a body weight that is different from the usual weight. These compensatory changes may account for the poor long-term efficacy of treatments for obesity."


Leibel RL, Rosenbaum M, and Hirsch J. Changes in energy expenditure resulting from altered body weight. N Engl J Med, 1995, 332: 621-628
http://content.nejm.org/cgi/content/full/332/10/621

Do elderly benefit from weight lifting?

Richard Weil's study on elderly benefiting from lifting weights
 (1 Min)



Richard Weil works at St. Luke's in NYC.  He has 32 years in the field.  This talk was given 4-15.

Why you should lift weights when losing weight on a diet

Fat Free Mass (FFM) loss was only 8% (2 min video)

Richard Weil explained at the Obesity Board review in April 2015 that there is less Fat Free Mass loss if you exercise while losing weight on a diet.  Weight lifting had the best result.

How much exercise to maintain weight loss?

Richard Weil from St. Luke's gives good 2 min advice on exercise

When I took the Lipidology boards the answer was 90  minutes of walking a day to maintain weight loss. 

I am glad to see that Richard Weil points out, it has to be with a low calorie diet, just to maintain weight for the reduced obese.

His program doesn't start exercise till 8 weeks and then may start with resistance training of legs to prevent knee pain.  

Once patient hits plateau he uses individual Rx of exercise for what works for the patient. 

This is how I interpret what he said at the Obesity Board Review 4-15

Calculate Calories needed to maintain weight at diet plateau

"What is true and what is practicable"?? 1 min 52 sec video

These graphs from 8 years of LOOK AHEAD trial do not achieve what Betty says her program below does.

The slides below ignore the fact that the reduced obese must have net 20% less calories than a person of the same weight who never has dieted.

Columbia's Dr. Leibel on the reduced obese 1 min 40 sec clip

At the NY Presbyterian College of Medicine Obesity Board Review these 3 slides were posted when talking about breaking through the plateau.  Need to calculate your calories just to maintain the weight you have lost.  

3391

Three Commonly used Prediction Equations for Resting Metabolic Rate (RMR) from pg 271 Handbook of Obesity edited by Bray and Bouchard.

Reference from Handbook of Obesity pg. 270
"A few equations have proven to be more appropriate for obese individuals, but they remain controversial."
"In overweight and obese subjects, the best approach is to measure the resting component by indirect calorimetry."

At diet plateau how many net calories do you need just to maintain weight?

40 second clip shows nutritionist aver that resistance training breaks plateau

From Ultimate Fitness by Gina Koleta 2003  

"If the man lifts weights and gains 2 kg (4.4 lbs) of muscle,  his metabolic rate would increase by 24 calories a day."

The 5 slides below are from NYC St. Luke's nutritionist lecture. 

She claims the resistance training in her program overcomes the Leptin reset of the reduced obese.

1min 40 sec clip Dr. Leibel discusses 20% diff in Lean and Reduced obese of same weight 

In my opinion and after the science taught at Columbia Board review by Leibel, Rosenbaum and Vasselli,  these slides ignore the science of reduced obese.

Cognitive dissonance

Dr. Rosenbaum says to diet industry: stop bilking

Sponge Syndrome plus perfect storm of reset Leptin threshold and insulin resistance of the reduced obese cause weight regain

Sponge syndrome = millions of skinny fat cells affected by reset Leptin threshold

See My 6 minute video explaining Sponge Syndrome

The Sponge Syndrome is the perfect storm for weight regain in the reduced obese.

I believe I have unified the concept of the Sponge syndrome with the reset Leptin threshold and the insulin resistance of the reduced obese to maintain weight loss maintenance.

I asked Dr. Leibel if adipocytes only life 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 200 million excess fat cells of the obese are still there for life in the reduce obese waiting to be a sponge for free fatty acids.  

I had the privilege today 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 asked why the skinny people with skinny fat cells don’t also regain weight.  I said the they don't have low leptin levels that are reset to be higher if they were never BMI over 30.

 I also heard Dr. R Liebel state that Leptin is the critical hormone in obesity.  

In apparent contrast:

Taubes pg 463 in afterword of Good Calories Bad Calories

From 2001 textbook, Endocrinology:An Integrated Approach to Endocrinology “The overall action of Insulin on the adipocyte is to stimulate fat storage and inhibit mobilization.’

Taubes goes on to say:

“With that physiologic fact as a given, any explanation for obesity or the obesity epidemic that looks beyond the influence of carbohydrates on insulin is one that is willfully trying to complicate an explanation when a simple one might suffice.”

In a more recent Biochemistry text:

Molecules linked to obesity 2014 Biochem text by Ferrier

p307-8 Ferrier text:

“Insulin is the most important hormone coordinating the use of fuels by tissues.  It’s metabolic effects are anabolic, favoring, for example, synthesis of:

1-glycogen

2-triacylglycerols (TAGs) {also known as triglycerides}

3-protein

p 311

“Adipose tissue responds rapidly to a rise in insulin, which causes a significant reduction in the release of fatty acids by inhibiting the the activity of hormone-sensitive lipase, which degrades lipids in adipose tissue.”

“Insulin also increases the transport and metabolism of glucose into adipocytes, providing the glycerol 3-phosphate substrate for TAG (triglyceride) synthesis.”

p 326

“in the fed state, elevated levels of glucose and insulin favor storage of TAG (triglycerides)”

In metabolic syndrome, there is an elevated level of insulin as the beta cells try to keep homeostasis of glucose level in the face of insulin resistance.  

The high levels of insulin make the dyslipidemia of metabolic syndrome.  This is why in the Sponge syndrome insulin and leptin are major players for causing the 300 million starved skinny adipocytes of the reduced obese so easily take on FFA.

In a slide today at the Columbia Obesity Board review in NYC, Dr. Rosenbaum put up this slide:

It’s not clear to me how Liedel and Rosenbaum don’t seem to accept the unifying concept of the  two strongest obesity peptides to prime the excess adipocytes of the reduced obese causing weight gain as I put forward the Sponge syndrome.