Google Groups no longer supports new Usenet posts or subscriptions. Historical content remains viewable.
Dismiss
Is Fat Gain a Problem or Solution?
3 views
Skip to first unread message
Ellen K.
Apr 23, 2012, 3:45:23 PM4/23/12
to
http://blogs.plos.org/obesitypanacea/2012/04/12/is-fat-gain-a-problem-or-solution/
Is Fat Gain a Problem or Solution?
By Travis Saunders, MSc, CEP
Posted: April 12, 2012
Earlier this year Dr Jean-Philippe Chaput and I published an editorial in
the journal Bioenergetics: Open Access examining whether weight gain should
be seen as a physiological problem or as merely a logical adaptation to our
current environments.
JP is a prolific researcher and writer, so it was a lot of fun to be able to
work with him on the paper (he gets the vast majority of credit for the
article - I was very much the second author on this one). JP is also a
collaborator on several of my thesis projects, and I'm looking forward to
sharing some of our other work in the near future.
Since the article is open access, I have re-published it in full below. The
original article with citation information can be found here. And for more
on this topic, be sure to check out JP's recent paper in Obesity Reviews
titled Obesity: A Disease or a Biological Adaptation.
Bioenergetics of Obesity: Is Fat Gain a Problem or a Solution?
According to the first law of thermodynamics, fat gain is the result of a
positive energy balance (i.e. energy intake > energy expenditure) [1]. When
an individual experiences a chronic positive energy balance, this can lead
to the accumulation of excess body fat, and ultimately obesity. Obesity
rates have increased so dramatically among industrialized countries in
recent decades that it has been referred to as a "pandemic" [2]. Attenuating
these high rates of obesity is a high priority in many countries not only
from a population health perspective, but from a health care system's
economic perspective [3]. However, reversing this trend is a herculean task
and will likely require a major change in societal norms and the values
underlying those norms [4,5].
A major challenge of today's world is that our so-called "obesogenic"
environment is conducive to the consumption of energy and unfavorable to the
expenditure of energy, therefore predisposing to a chronic positive energy
balance. The modern, money-oriented, computer-dependent, sleep-deprived,
physically-inactive human lives chronically stressed in a society of food
abundance. From a physiological standpoint, the excess fat gain observed in
prone individuals is perceived as a normal consequence (i.e. biological
adaptation) to a changed environment rather than a pathological process [6].
In other words, weight gain is a sign of our contemporary way of living or a
"collateral damage" in the struggle for modernity [7].
Body fat, when kept to an appropriate level (probably defined by an
individual's genetics), is a necessary and healthy energy reserve. Recent
evidence suggests that while fat stays in the fat cells, for which they are
designed, there is little cause for concern [8]. Body fat begins to cause
metabolic problems only when lipid-intolerant nonadipose organs are not
protected against lipid "spillover" during sustained energy surplus [9]. In
fact, it is increasingly recognized that it is visceral fat and the fat
deposited "ectopically" in organs like the liver, pancreas, heart or
skeletal muscles that tends to cause increases in cardio-metabolic risk
[10]. Interestingly, the accumulation of fat under the skin (i.e.
subcutaneous adipose tissue), which is less lipolytically active than other
fat depots and therefore able to safely sequester fat away from ectopic
depots, seems to be associated with reduced cardiometabolic risk [11,12].
1. What are the Benefits of Body Fat Gain?
Obesity, at least when operationally defined as exceeding a specific amount
of body fat and/or body mass index, is associated with certain health
benefits. Examples include the now rarely needed but obvious protection
against starvation in times of food scarcity, protection against
osteoporosis, fractures, frailty, and premature mortality in the elderly, as
well as reduced mortality rates in the face of certain severe illnesses or
injuries [6]. The assumption that adiposity per se increases mortality risk
is also not well supported by the scientific evidence. Many epidemiologic
studies have shown that people who are overweight or moderately obese live
at least as long as normal weight individuals, and often longer [13-15].
Additionally, life expectancy increased dramatically during the same time
period in which body weight rose, and the World Health Organization projects
life expectancy will continue to rise in coming decades [16].
From a physiological standpoint, fat gain is seen as a solution for
maintaining homeostasis and re-establishing energy balance in the current
obesogenic environment. The ability of fat cells to produce molecules
involved in genuine regulatory processes has been known for decades. During
weight gain, many adaptations over time can promote the re-equilibration of
energy balance. These include increases in fat oxidation, sympathetic
nervous system activity, insulinemia at euglycemia, leptinemia, and overall
energy expenditure [6]. The problem related to fat gain as a physiological
compensation to chronic unhealthy lifestyle habits is that it cannot occur
with the same metabolic efficiency as exercise. Specifically, fat gain
relies more on increased concentration of substrates (e.g. free fatty acids)
and hormones (e.g. insulin and leptin) to re-establish energy balance by
increasing total energy expenditure, which likely underlies the occurrence
of the metabolic syndrome which often accompanies obesity. Thus, while
increasing fat reserves may help to restore energy balance, it can also lead
to increased risk of chronic disease. These observations emphasize the
importance of adhering to a healthy lifestyle in order to maintain body
weight stability rather than relying on the overuse of regulatory systems.
2. What are the Adverse Effects of Weight Loss?
Although counter-intuitive, many prospective observational studies suggest
that weight loss increases rather than decreases the risk of premature death
[17-19]. Paradoxically, most short-term weight loss intervention studies do
find improvements in many health indicators. However, given that intentional
weight loss is generally accompanied by a change in dietary and physical
activity behaviors, it is not known whether or to what extent the
improvements can be attributed to the weight loss per se. The case of
liposuction can certainly provide relevant information about the effects of
subcutaneous fat loss in the absence of behavior change. In their study,
Klein et al. [20] evaluated the effects of large-volume abdominal
liposuction on metabolic risk factors in obese women before and 10 to 12
weeks after liposuction. Although the participants lost 10.5 kg of fat,
liposuction did not improve obesityassociated metabolic abnormalities,
suggesting that decreasing adipose tissue mass alone (and especially
reducing subcutaneous fat stores) without behavior change will not achieve
the metabolic benefits of weight loss. In contrast, most health indicators
can be improved through changing health behaviors, regardless of whether
weight is lost or not. For instance, it is well-known that physical activity
participation without weight loss has the capacity to reduce visceral
adiposity and substantially improve the cardio-metabolic risk profile [21].
Similarly bariatric surgery, which dramatically changes the way that food is
consumed and digested, has been shown to result in rapid improvements in
glycemic control just days after surgery, long before any appreciable weight
loss has taken place [22]. These observations agree with the "fat but fit"
[23] and "metabolically healthy but obese" [24] concepts and stress the
importance of regular physical activity and a healthy diet as key components
in any health promotion and disease prevention strategy, regardless of body
weight.
Moreover, attempts to sustain weight loss invoke adaptive responses
involving the coordinated actions of metabolic, neuroendocrine, autonomic
and behavioral changes that oppose the maintenance of a reduced body weight.
The multiple systems regulating energy stores and opposing the maintenance
of a reduced body weight illustrate that body energy stores and fat stores
in particular are actively "defended" by interlocking bioenergetic and
neurobiological systems. The fact that more than over 80% of individuals
return to pre-weight loss levels of body fatness after otherwise successful
weight loss certainly illustrates this "sad" reality [25], whereas studies
of people successful at sustained weight loss indicate that the maintenance
of a reduced degree of body fatness requires a lifetime of meticulous
attention to energy intake and expenditure [26]. Among the adverse effects
of weight loss, it is well-known that body fat loss complicates appetite
control, reduces energy expenditure to a greater extent than predicted,
increases the proneness to hypoglycemia and its related risk towards
depressive symptoms, increases the plasma and tissue levels of persistent
organic pollutants that promote hormone disruption and metabolic
complications, and increases psychological stress, all of which are
adaptations that significantly increase the risk of weight regain [27].
Concluding Remarks
The general perception of obesity today is more pessimistic than optimistic
with words like "global epidemic", "important problem" or "scourge" that are
omnipresent in the popular media as well as in the scientific community. The
corollary of this widespread message is obviously a greater pressure on
obese individuals towards weight loss. However, an accumulating body of
evidence suggests that a focus on weight loss as an indicator of success is
not only ineffective at producing thinner, healthier bodies, but also
damaging, contributing to food and body preoccupation, repeated cycles of
weight loss and regain, reduced self-esteem, eating disorders, and weight
stigmatization and discrimination [28]. It is thus time to shift the focus
away from body weight and center our efforts on the promotion of a healthy
lifestyle if we really want to have an impact on the health of the
population in the long term and reduce the burden on individuals with
obesity.
Our better understanding of obesity, as witnessed by an impressive amount of
publications in the field over the last decades, suggests that body fat can
be both detrimental and protective. Simplistic messaging that body fat is
"bad" and weight loss is "good" for our health can be misleading and ignores
the truth about the biological response and side effects of weight loss, as
well as the importance of fat gain in maintaining body homeostasis in a
"toxic" environment. Fat gain is part of a regulatory strategy that permits
the recovery of energy balance and body weight stability in a world that has
increasingly added obesogenic factors to our lifestyle over time. In this
context, a preventive approach that includes healthy lifestyle habits and
that attempts to reduce the obesogenic nature of our society is the only
long-term viable solution to maximize our health, even if it does not easily
fit within the priorities of an economically globalized world.
Acknowledgements
Dr. Chaput holds a Junior Research Chair in Healthy Active Living and
Obesity Research. Mr. Saunders is supported by Doctoral Research Awards from
the Canadian Diabetes Association and the Canadian Institutes of Health
Research, as well as an Excellence Scholarship from the University of
Ottawa.
References
Jéquier E, Tappy L (1999) Regulation of body weight in humans. Physiol Rev
79: 451-480.
Roth J, Qiang X, Marbán SL, Redelt H, Lowell BC (2004) The obesity pandemic:
where have we been and where are we going? Obes Res 12: 88S-101S.
Anis AH, Zhang W, Bansback N, Guh DP, Amarsi Z, et al. (2009) Obesity and
overweight in Canada: an updated cost-of-illness study. Obes Rev 11: 31-40.
Whitaker RC (2011) The childhood obesity epidemic: lessons for preventing
socially determined health conditions. Arch Pediatr Adolesc Med 165:
973-975.
Novak NL, Brownell KD (2011) Obesity: a public health approach. Psychiatr
Clin North Am 34: 895-909.
Chaput JP, Doucet E, Tremblay A (2012) Obesity: a disease or a biological
adaptation? An update. Obes Rev.
Egger G (2011) Obesity, chronic disease, and economic growth: a case for
"big picture" prevention. Adv Prev Med 2011: 149158.
Lemieux I (2004) Energy partitioning in gluteal-femoral fat: does the
metabolic fate of triglycerides affect coronary heart disease? Arterioscler
Thromb Vasc Biol 24: 795-797.
Unger RH, Scherer PE (2010) Gluttony, sloth and the metabolic syndrome: a
roadmap to lipotoxocity. Trends Endocrinol Metab 21: 345-352.
Arsenault BJ, Beaumont EP, Després JP, Larose E (2011) Mapping body fat
distribution: A key step towards the identification of the vulnerable
patient? Ann Med.
Smith JD, Borel AL, Nazare JA, Haffner SM, Balkau B, et al. (2012) Visceral
adipose tissue indicates the severity of cardiometabolic risk in patients
with and without type 2 diabetes: results from the INSPIRE ME IAA Study. J
Clin Endocrinol Metab.
Snijder MB, Visser M, Dekker JM, Goodpaster BH, Harris TB, et al. (2005) Low
subcutaneous thigh fat is a risk factor for unfavourable glucose and lipid
levels, independently of high abdominal fat. The Health ABC Study.
Diabetologia 48: 301-308.
McAuley PA, Blair SN (2011) Obesity paradoxes. J Sports Sci 29: 773-782.
Flegal KM, Graubard BI, Williamson DF, Gail MH (2005) Excess deaths
associated with underweight, overweight, and obesity. JAMA 293: 1861-1867.
McGee DL (2005) Body mass index and mortality: a meta-analysis based on
person-level data from twenty-six observational studies. Ann Epidemiol 15:
87-97.
Mathers CD, Loncar D (2006) Projections of global mortality and burden of
disease from 2002 to 2030. PLoS Med 3: e442.
Ingram DD, Mussolino ME (2010) Weight loss from maximum body weight and
mortality: the Third National Health and Nutrition Examination Survey Linked
Mortality File. Int J Obes (Lond) 34: 1044-1050.
Sørensen TI, Rissanen A, Korkeila M, Kaprio J (2005) Intention to lose
weight, weight changes, and 18-y mortality in overweight individuals without
co-morbidities. PLoS Med 2: e171.
Williamson DF, Pamuk E, Thun M, Flanders D, Byers T, et al. (1999)
Prospective study of intentional weight loss and mortality in overweight
white men aged 40-64 years. Am J Epidemiol 149: 491-503.
Klein S, Fontana L, Young VL, Coggan AR, Kilo C, et al. (2004) Absence of an
effect of liposuction on insulin action and risk factors for coronary heart
disease. N Engl J Med 350: 2549-2557.
Ross R, Janiszewski PM (2008) Is weight loss the optimal target for
obesity-related cardiovascular disease risk reduction? Can J Cardiol 24:
25D-31D.
Wickremesekera K, Miller G, Naotunne TD, Knowles G, Stubbs RS (2005) Loss of
insulin resistance after Roux-en-Y gastric bypass surgery: a time course
study. Obes Surg 15: 474-481.
Wei M, Kampert JB, Barlow CE, Nichaman MZ, Gibbons LW, et al. (1999)
Relationship between low cardiorespiratory fitness and mortality in
normal-weight, overweight, and obese men. JAMA 282: 1547-1553.
Karelis AD (2008) Metabolically healthy but obese individuals. Lancet 372:
1281-1283.
McGuire MT, Wing RR, Klem ML, Hill JO (1999) Behavioral strategies of
individuals who have maintained long-term weight losses. Obes Res 7:
334-341.
Wing RR, Hill JO (2001) Successful weight loss maintenance. Annu Rev Nutr
21: 323-341.
Tremblay A, Chaput JP (2012) Obesity: The allostatic load of weight loss
dieting. Physiol Behav 106: 16-21.
Bacon L, Aphramor L (2011) Weight science: evaluating the evidence for a
paradigm shift. Nutr J 10: 9.
Travis Saunders is a PhD student researching the relationship between
sedentary time and chronic disease risk in children and youth. He is also a
Certified Exercise Physiologist and competitive distance runner.
Is Fat Gain a Problem or Solution?
By Travis Saunders, MSc, CEP
Posted: April 12, 2012
Earlier this year Dr Jean-Philippe Chaput and I published an editorial in
the journal Bioenergetics: Open Access examining whether weight gain should
be seen as a physiological problem or as merely a logical adaptation to our
current environments.
JP is a prolific researcher and writer, so it was a lot of fun to be able to
work with him on the paper (he gets the vast majority of credit for the
article - I was very much the second author on this one). JP is also a
collaborator on several of my thesis projects, and I'm looking forward to
sharing some of our other work in the near future.
Since the article is open access, I have re-published it in full below. The
original article with citation information can be found here. And for more
on this topic, be sure to check out JP's recent paper in Obesity Reviews
titled Obesity: A Disease or a Biological Adaptation.
Bioenergetics of Obesity: Is Fat Gain a Problem or a Solution?
According to the first law of thermodynamics, fat gain is the result of a
positive energy balance (i.e. energy intake > energy expenditure) [1]. When
an individual experiences a chronic positive energy balance, this can lead
to the accumulation of excess body fat, and ultimately obesity. Obesity
rates have increased so dramatically among industrialized countries in
recent decades that it has been referred to as a "pandemic" [2]. Attenuating
these high rates of obesity is a high priority in many countries not only
from a population health perspective, but from a health care system's
economic perspective [3]. However, reversing this trend is a herculean task
and will likely require a major change in societal norms and the values
underlying those norms [4,5].
A major challenge of today's world is that our so-called "obesogenic"
environment is conducive to the consumption of energy and unfavorable to the
expenditure of energy, therefore predisposing to a chronic positive energy
balance. The modern, money-oriented, computer-dependent, sleep-deprived,
physically-inactive human lives chronically stressed in a society of food
abundance. From a physiological standpoint, the excess fat gain observed in
prone individuals is perceived as a normal consequence (i.e. biological
adaptation) to a changed environment rather than a pathological process [6].
In other words, weight gain is a sign of our contemporary way of living or a
"collateral damage" in the struggle for modernity [7].
Body fat, when kept to an appropriate level (probably defined by an
individual's genetics), is a necessary and healthy energy reserve. Recent
evidence suggests that while fat stays in the fat cells, for which they are
designed, there is little cause for concern [8]. Body fat begins to cause
metabolic problems only when lipid-intolerant nonadipose organs are not
protected against lipid "spillover" during sustained energy surplus [9]. In
fact, it is increasingly recognized that it is visceral fat and the fat
deposited "ectopically" in organs like the liver, pancreas, heart or
skeletal muscles that tends to cause increases in cardio-metabolic risk
[10]. Interestingly, the accumulation of fat under the skin (i.e.
subcutaneous adipose tissue), which is less lipolytically active than other
fat depots and therefore able to safely sequester fat away from ectopic
depots, seems to be associated with reduced cardiometabolic risk [11,12].
1. What are the Benefits of Body Fat Gain?
Obesity, at least when operationally defined as exceeding a specific amount
of body fat and/or body mass index, is associated with certain health
benefits. Examples include the now rarely needed but obvious protection
against starvation in times of food scarcity, protection against
osteoporosis, fractures, frailty, and premature mortality in the elderly, as
well as reduced mortality rates in the face of certain severe illnesses or
injuries [6]. The assumption that adiposity per se increases mortality risk
is also not well supported by the scientific evidence. Many epidemiologic
studies have shown that people who are overweight or moderately obese live
at least as long as normal weight individuals, and often longer [13-15].
Additionally, life expectancy increased dramatically during the same time
period in which body weight rose, and the World Health Organization projects
life expectancy will continue to rise in coming decades [16].
From a physiological standpoint, fat gain is seen as a solution for
maintaining homeostasis and re-establishing energy balance in the current
obesogenic environment. The ability of fat cells to produce molecules
involved in genuine regulatory processes has been known for decades. During
weight gain, many adaptations over time can promote the re-equilibration of
energy balance. These include increases in fat oxidation, sympathetic
nervous system activity, insulinemia at euglycemia, leptinemia, and overall
energy expenditure [6]. The problem related to fat gain as a physiological
compensation to chronic unhealthy lifestyle habits is that it cannot occur
with the same metabolic efficiency as exercise. Specifically, fat gain
relies more on increased concentration of substrates (e.g. free fatty acids)
and hormones (e.g. insulin and leptin) to re-establish energy balance by
increasing total energy expenditure, which likely underlies the occurrence
of the metabolic syndrome which often accompanies obesity. Thus, while
increasing fat reserves may help to restore energy balance, it can also lead
to increased risk of chronic disease. These observations emphasize the
importance of adhering to a healthy lifestyle in order to maintain body
weight stability rather than relying on the overuse of regulatory systems.
2. What are the Adverse Effects of Weight Loss?
Although counter-intuitive, many prospective observational studies suggest
that weight loss increases rather than decreases the risk of premature death
[17-19]. Paradoxically, most short-term weight loss intervention studies do
find improvements in many health indicators. However, given that intentional
weight loss is generally accompanied by a change in dietary and physical
activity behaviors, it is not known whether or to what extent the
improvements can be attributed to the weight loss per se. The case of
liposuction can certainly provide relevant information about the effects of
subcutaneous fat loss in the absence of behavior change. In their study,
Klein et al. [20] evaluated the effects of large-volume abdominal
liposuction on metabolic risk factors in obese women before and 10 to 12
weeks after liposuction. Although the participants lost 10.5 kg of fat,
liposuction did not improve obesityassociated metabolic abnormalities,
suggesting that decreasing adipose tissue mass alone (and especially
reducing subcutaneous fat stores) without behavior change will not achieve
the metabolic benefits of weight loss. In contrast, most health indicators
can be improved through changing health behaviors, regardless of whether
weight is lost or not. For instance, it is well-known that physical activity
participation without weight loss has the capacity to reduce visceral
adiposity and substantially improve the cardio-metabolic risk profile [21].
Similarly bariatric surgery, which dramatically changes the way that food is
consumed and digested, has been shown to result in rapid improvements in
glycemic control just days after surgery, long before any appreciable weight
loss has taken place [22]. These observations agree with the "fat but fit"
[23] and "metabolically healthy but obese" [24] concepts and stress the
importance of regular physical activity and a healthy diet as key components
in any health promotion and disease prevention strategy, regardless of body
weight.
Moreover, attempts to sustain weight loss invoke adaptive responses
involving the coordinated actions of metabolic, neuroendocrine, autonomic
and behavioral changes that oppose the maintenance of a reduced body weight.
The multiple systems regulating energy stores and opposing the maintenance
of a reduced body weight illustrate that body energy stores and fat stores
in particular are actively "defended" by interlocking bioenergetic and
neurobiological systems. The fact that more than over 80% of individuals
return to pre-weight loss levels of body fatness after otherwise successful
weight loss certainly illustrates this "sad" reality [25], whereas studies
of people successful at sustained weight loss indicate that the maintenance
of a reduced degree of body fatness requires a lifetime of meticulous
attention to energy intake and expenditure [26]. Among the adverse effects
of weight loss, it is well-known that body fat loss complicates appetite
control, reduces energy expenditure to a greater extent than predicted,
increases the proneness to hypoglycemia and its related risk towards
depressive symptoms, increases the plasma and tissue levels of persistent
organic pollutants that promote hormone disruption and metabolic
complications, and increases psychological stress, all of which are
adaptations that significantly increase the risk of weight regain [27].
Concluding Remarks
The general perception of obesity today is more pessimistic than optimistic
with words like "global epidemic", "important problem" or "scourge" that are
omnipresent in the popular media as well as in the scientific community. The
corollary of this widespread message is obviously a greater pressure on
obese individuals towards weight loss. However, an accumulating body of
evidence suggests that a focus on weight loss as an indicator of success is
not only ineffective at producing thinner, healthier bodies, but also
damaging, contributing to food and body preoccupation, repeated cycles of
weight loss and regain, reduced self-esteem, eating disorders, and weight
stigmatization and discrimination [28]. It is thus time to shift the focus
away from body weight and center our efforts on the promotion of a healthy
lifestyle if we really want to have an impact on the health of the
population in the long term and reduce the burden on individuals with
obesity.
Our better understanding of obesity, as witnessed by an impressive amount of
publications in the field over the last decades, suggests that body fat can
be both detrimental and protective. Simplistic messaging that body fat is
"bad" and weight loss is "good" for our health can be misleading and ignores
the truth about the biological response and side effects of weight loss, as
well as the importance of fat gain in maintaining body homeostasis in a
"toxic" environment. Fat gain is part of a regulatory strategy that permits
the recovery of energy balance and body weight stability in a world that has
increasingly added obesogenic factors to our lifestyle over time. In this
context, a preventive approach that includes healthy lifestyle habits and
that attempts to reduce the obesogenic nature of our society is the only
long-term viable solution to maximize our health, even if it does not easily
fit within the priorities of an economically globalized world.
Acknowledgements
Dr. Chaput holds a Junior Research Chair in Healthy Active Living and
Obesity Research. Mr. Saunders is supported by Doctoral Research Awards from
the Canadian Diabetes Association and the Canadian Institutes of Health
Research, as well as an Excellence Scholarship from the University of
Ottawa.
References
Jéquier E, Tappy L (1999) Regulation of body weight in humans. Physiol Rev
79: 451-480.
Roth J, Qiang X, Marbán SL, Redelt H, Lowell BC (2004) The obesity pandemic:
where have we been and where are we going? Obes Res 12: 88S-101S.
Anis AH, Zhang W, Bansback N, Guh DP, Amarsi Z, et al. (2009) Obesity and
overweight in Canada: an updated cost-of-illness study. Obes Rev 11: 31-40.
Whitaker RC (2011) The childhood obesity epidemic: lessons for preventing
socially determined health conditions. Arch Pediatr Adolesc Med 165:
973-975.
Novak NL, Brownell KD (2011) Obesity: a public health approach. Psychiatr
Clin North Am 34: 895-909.
Chaput JP, Doucet E, Tremblay A (2012) Obesity: a disease or a biological
adaptation? An update. Obes Rev.
Egger G (2011) Obesity, chronic disease, and economic growth: a case for
"big picture" prevention. Adv Prev Med 2011: 149158.
Lemieux I (2004) Energy partitioning in gluteal-femoral fat: does the
metabolic fate of triglycerides affect coronary heart disease? Arterioscler
Thromb Vasc Biol 24: 795-797.
Unger RH, Scherer PE (2010) Gluttony, sloth and the metabolic syndrome: a
roadmap to lipotoxocity. Trends Endocrinol Metab 21: 345-352.
Arsenault BJ, Beaumont EP, Després JP, Larose E (2011) Mapping body fat
distribution: A key step towards the identification of the vulnerable
patient? Ann Med.
Smith JD, Borel AL, Nazare JA, Haffner SM, Balkau B, et al. (2012) Visceral
adipose tissue indicates the severity of cardiometabolic risk in patients
with and without type 2 diabetes: results from the INSPIRE ME IAA Study. J
Clin Endocrinol Metab.
Snijder MB, Visser M, Dekker JM, Goodpaster BH, Harris TB, et al. (2005) Low
subcutaneous thigh fat is a risk factor for unfavourable glucose and lipid
levels, independently of high abdominal fat. The Health ABC Study.
Diabetologia 48: 301-308.
McAuley PA, Blair SN (2011) Obesity paradoxes. J Sports Sci 29: 773-782.
Flegal KM, Graubard BI, Williamson DF, Gail MH (2005) Excess deaths
associated with underweight, overweight, and obesity. JAMA 293: 1861-1867.
McGee DL (2005) Body mass index and mortality: a meta-analysis based on
person-level data from twenty-six observational studies. Ann Epidemiol 15:
87-97.
Mathers CD, Loncar D (2006) Projections of global mortality and burden of
disease from 2002 to 2030. PLoS Med 3: e442.
Ingram DD, Mussolino ME (2010) Weight loss from maximum body weight and
mortality: the Third National Health and Nutrition Examination Survey Linked
Mortality File. Int J Obes (Lond) 34: 1044-1050.
Sørensen TI, Rissanen A, Korkeila M, Kaprio J (2005) Intention to lose
weight, weight changes, and 18-y mortality in overweight individuals without
co-morbidities. PLoS Med 2: e171.
Williamson DF, Pamuk E, Thun M, Flanders D, Byers T, et al. (1999)
Prospective study of intentional weight loss and mortality in overweight
white men aged 40-64 years. Am J Epidemiol 149: 491-503.
Klein S, Fontana L, Young VL, Coggan AR, Kilo C, et al. (2004) Absence of an
effect of liposuction on insulin action and risk factors for coronary heart
disease. N Engl J Med 350: 2549-2557.
Ross R, Janiszewski PM (2008) Is weight loss the optimal target for
obesity-related cardiovascular disease risk reduction? Can J Cardiol 24:
25D-31D.
Wickremesekera K, Miller G, Naotunne TD, Knowles G, Stubbs RS (2005) Loss of
insulin resistance after Roux-en-Y gastric bypass surgery: a time course
study. Obes Surg 15: 474-481.
Wei M, Kampert JB, Barlow CE, Nichaman MZ, Gibbons LW, et al. (1999)
Relationship between low cardiorespiratory fitness and mortality in
normal-weight, overweight, and obese men. JAMA 282: 1547-1553.
Karelis AD (2008) Metabolically healthy but obese individuals. Lancet 372:
1281-1283.
McGuire MT, Wing RR, Klem ML, Hill JO (1999) Behavioral strategies of
individuals who have maintained long-term weight losses. Obes Res 7:
334-341.
Wing RR, Hill JO (2001) Successful weight loss maintenance. Annu Rev Nutr
21: 323-341.
Tremblay A, Chaput JP (2012) Obesity: The allostatic load of weight loss
dieting. Physiol Behav 106: 16-21.
Bacon L, Aphramor L (2011) Weight science: evaluating the evidence for a
paradigm shift. Nutr J 10: 9.
Travis Saunders is a PhD student researching the relationship between
sedentary time and chronic disease risk in children and youth. He is also a
Certified Exercise Physiologist and competitive distance runner.
Andrew B. Chung, MD/PhD
Apr 23, 2012, 6:45:06 PM4/23/12
to
Ellen K. wrote:
>
> http://blogs.plos.org/obesitypanacea/2012/04/12/is-fat-gain-a-problem-or-solution/
>
> Is Fat Gain a Problem or Solution?
The biggest problem is http://WDJW.net/VAT gain which is a consequence
>
> http://blogs.plos.org/obesitypanacea/2012/04/12/is-fat-gain-a-problem-or-solution/
>
> Is Fat Gain a Problem or Solution?
of overeating, which is the biggest mistake.
The absolutely only **healthy** way to stop overeating without harmful
undernourishment is to http://WDJW.net/Guard (Proverbs 4:23) the heart
by holding to the right amount, which is 32 oz of daily food.
Yes, right amount ( http://WDJW.net/2PD-OMER Approach ) control as
Chris Malcolm, MU, **and** Rod Eastman are doing is much more
sophisticated and smarter:
http://groups.google.com/group/alt.support.diet.low-carb/msg/8d2ef74488074acf?
and
http://groups.google.com/group/sci.med.cardiology/msg/522ce5c058224656?
**and**
http://groups.google.com/group/sci.med.cardiology/msg/da03131060efa3b5?
http://groups.google.com/group/sci.med.cardiology/msg/055f2e7cf3c590ee?
Be hungrier, which really is wonderfully healthier especially for
diabetics and other heart disease patients:
http://groups.google.com/group/sci.med.cardiology/msg/9642aafa0aad16eb?
... because we mindfully choose to openly care with our heart,
Andrew <><
--
Andrew B. Chung, MD/PhD
EmoryIMVC.org Cardiologist
and Author of the 2PD-OMER Approach:
http://groups.google.com/group/sci.med.cardiology/msg/9ad0c19df5ffc2f7?
0 new messages