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Sunday, May 10, 2015

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, PhD1,2; 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



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

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

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.






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