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Why do we get fat? Why Comparison Can Be the Thief of Happiness
***Disclaimer: this podcast is for informational sharing only. It is not meant and does not give medical advice. Always consult your physicians or healthcare provider for medical advice.***
A quick look into why do we overeat, not just the “we are fat because we overeat” mentality.
Notes:
Set Point:
This is a very complex pathway, but to very much oversimplify it… leptin is a large player.
As fat cells increase in size they will increase leptin release from the fat cell.
Leptin goes to the brain(Hypothalamus) to turn on POM-C —-> Increase energy expenditure and decrease food intake—–>decrease weight back to the set point, bringing your body back to homeostasis essentially.
Or
Fat cells decrease—>decrease leptin—->HRP neuron activated—–>decrease energy expenditure and increase food intake—->weight gain back to homeostasis
The problem is food regulation is also controlled by a subconscious area in the brain (Subcortical, mesolimbic). If this subconscious area is stronger because of a genetic predisposition or if just becomes stronger from using food as a reward for too long this will essentially override your “set-point.”
(Reward food general tends to be hyperpalatable hypercaloric processed foods.)
Then over time we can get things like leptin resistance, decreased functioning of the protective POM-C area, inflammation, reactive gliosis and aging of the hypothalamus so now your body has become metabolically changed allowing your body to have a new set point and to protect the new fat mass. This state or having a component of these changes is termed “metabolic obesity.”
Hedonic Obesity is when a person reward circuitry is now maladaptive and strong.
Different people who are overweight or obese can have one or the other pathways starting to form or formed. And different people can have different severities of these two mechanisms
An example:
A woman who has never been overweight becomes pregnant. Hormonal changes end up upregulating her food intake. She otherwise does not have a genetic predisposition to obesity, she gains 20lbs, has the baby, 6 months later she loses it. People are amazed.
But the same women this time has horrible stress during the pregnancy while increasing food intake from pregnancy-related changes, she also increases food intake to cope with stress. She starts towards “maladaptive” ways of eating to cope with her environment. She has the baby…this time her outcome is very multifactorial. Did the stress go away, did it stay and she continues to rely on food. Maybe still due to some lucky genetics despite prolonged exposure to overeating, she is not pre-dispositioned to leptin resistance etc, etc. She was lucky to not start down the pathway of metabolic obesity, but more is heading to mild hedonic obesity. Hopefully, the stressor goes away, she stops using food as a reward before maladaptive pathways are too strong. She relatively easily loses the weight over the next 6 months. I say relatively because it is still difficult to turn down hyperpalatable hypercaloric food, but at least she is not also having to battle the other metabolic obesity components as discussed above. No to mention other changes that happen in the brain that are not discussed here, but have been found on functional MRI when comparing a brain that has been exposed to high levels of fat mass for years to a brain that has not been exposed to high levels of fat mass.
But if her rewards circuitry became too strong then she will continue to struggle with using food as a reward, continue to struggle with weight gain, feel more and more “out of control” and over time increase risk of then also being metabolically obese.
Some light reading:
Metabolic vs. hedonic obesity: a conceptual distinction and its clinical implications https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5053237/
Y-H Yu. Making sense of metabolic obesity and hedonic obesity. J. Diabetes 2017 Jul;9(7):656-666
Berthoud HR. Metabolic and hedonic drives in the neural control of appetite: who is the boss? Curr Opin Neurobiol 2011; 21: 888–896.
Considine RV, Sinha MK, Heiman ML et al Serum immunoreactive‐leptin concentrations in normal‐weight and obese humans. N Engl J Med 1996; 334: 292–295.
Vasselli JR, Scarpace PJ, Harris RB, Banks WA. Dietary components in the development of leptin resistance. Adv Nutr 2013; 4: 164–175.
Y-H et. al. Metabolic vs. hedonic obesity: a conceptual distinction and its clinical implications. Obes Rev 2015.16(3):234-47
JC Halford & JA Harrold. Satiety-enhancing products for appetite control:science and regulation of functional food for weight management. Proc Nutr Soc. 2012 May;71(2):350-62
K Simpson et. al. 2012 CCK, PYY and PP: The control of Energy Balance, In Appetite Control. Editor H-G Joost p209-230
https://neuroendoimmune.wordpress.com/2013/09/17/its-all-in-your-head-the-neurocircuitry-of-addiction/
Berridge KC, Ho CY, Richard JM, DiFeliceantonio AG. The tempted brain eats: pleasure and desire circuits in obesity and eating disorders. Brain Res 2010; 1350: 43–64.
Schwartz GJ, Zeltser LM. Functional organization of neuronal and humoral signals regulating feeding behavior. Annu Rev Nutr 2013; 33: 1–21. [PubMed]
Y Zhang and RL Leibel. 2017 Leptin and Body Weight. In Eating Disorders and Obesity: A Comprehensive Handbook, 3rd edition(ed KD Brownwell and BT Walsh)
RL Leibel et. al. Changes in energy expenditure resulting from altered body weight. N Engl J Med 1995; 332:621-628
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3380241/
Speakman JR, Levitsky DA, Allison DB et al Set points, settling points and some alternative models: theoretical options to understand how genes and environments combine to regulate body adiposity. Dis Model Mech 2011; 4: 733–745.
Harris RB. Role of set‐point theory in regulation of body weight. FASEB J 1990; 4: 3310–3318.
Pierce RC, Kumaresan V. The mesolimbic dopamine system: the final common pathway for the reinforcing effect of drugs of abuse? Neurosci Biobehav Rev 2006; 30: 215–238.
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By Jennifer K. Hendrix
5
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***Disclaimer: this podcast is for informational sharing only. It is not meant and does not give medical advice. Always consult your physicians or healthcare provider for medical advice.***
A quick look into why do we overeat, not just the “we are fat because we overeat” mentality.
Notes:
Set Point:
This is a very complex pathway, but to very much oversimplify it… leptin is a large player.
As fat cells increase in size they will increase leptin release from the fat cell.
Leptin goes to the brain(Hypothalamus) to turn on POM-C —-> Increase energy expenditure and decrease food intake—–>decrease weight back to the set point, bringing your body back to homeostasis essentially.
Or
Fat cells decrease—>decrease leptin—->HRP neuron activated—–>decrease energy expenditure and increase food intake—->weight gain back to homeostasis
The problem is food regulation is also controlled by a subconscious area in the brain (Subcortical, mesolimbic). If this subconscious area is stronger because of a genetic predisposition or if just becomes stronger from using food as a reward for too long this will essentially override your “set-point.”
(Reward food general tends to be hyperpalatable hypercaloric processed foods.)
Then over time we can get things like leptin resistance, decreased functioning of the protective POM-C area, inflammation, reactive gliosis and aging of the hypothalamus so now your body has become metabolically changed allowing your body to have a new set point and to protect the new fat mass. This state or having a component of these changes is termed “metabolic obesity.”
Hedonic Obesity is when a person reward circuitry is now maladaptive and strong.
Different people who are overweight or obese can have one or the other pathways starting to form or formed. And different people can have different severities of these two mechanisms
An example:
A woman who has never been overweight becomes pregnant. Hormonal changes end up upregulating her food intake. She otherwise does not have a genetic predisposition to obesity, she gains 20lbs, has the baby, 6 months later she loses it. People are amazed.
But the same women this time has horrible stress during the pregnancy while increasing food intake from pregnancy-related changes, she also increases food intake to cope with stress. She starts towards “maladaptive” ways of eating to cope with her environment. She has the baby…this time her outcome is very multifactorial. Did the stress go away, did it stay and she continues to rely on food. Maybe still due to some lucky genetics despite prolonged exposure to overeating, she is not pre-dispositioned to leptin resistance etc, etc. She was lucky to not start down the pathway of metabolic obesity, but more is heading to mild hedonic obesity. Hopefully, the stressor goes away, she stops using food as a reward before maladaptive pathways are too strong. She relatively easily loses the weight over the next 6 months. I say relatively because it is still difficult to turn down hyperpalatable hypercaloric food, but at least she is not also having to battle the other metabolic obesity components as discussed above. No to mention other changes that happen in the brain that are not discussed here, but have been found on functional MRI when comparing a brain that has been exposed to high levels of fat mass for years to a brain that has not been exposed to high levels of fat mass.
But if her rewards circuitry became too strong then she will continue to struggle with using food as a reward, continue to struggle with weight gain, feel more and more “out of control” and over time increase risk of then also being metabolically obese.
Some light reading:
Metabolic vs. hedonic obesity: a conceptual distinction and its clinical implications https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5053237/
Y-H Yu. Making sense of metabolic obesity and hedonic obesity. J. Diabetes 2017 Jul;9(7):656-666
Berthoud HR. Metabolic and hedonic drives in the neural control of appetite: who is the boss? Curr Opin Neurobiol 2011; 21: 888–896.
Considine RV, Sinha MK, Heiman ML et al Serum immunoreactive‐leptin concentrations in normal‐weight and obese humans. N Engl J Med 1996; 334: 292–295.
Vasselli JR, Scarpace PJ, Harris RB, Banks WA. Dietary components in the development of leptin resistance. Adv Nutr 2013; 4: 164–175.
Y-H et. al. Metabolic vs. hedonic obesity: a conceptual distinction and its clinical implications. Obes Rev 2015.16(3):234-47
JC Halford & JA Harrold. Satiety-enhancing products for appetite control:science and regulation of functional food for weight management. Proc Nutr Soc. 2012 May;71(2):350-62
K Simpson et. al. 2012 CCK, PYY and PP: The control of Energy Balance, In Appetite Control. Editor H-G Joost p209-230
https://neuroendoimmune.wordpress.com/2013/09/17/its-all-in-your-head-the-neurocircuitry-of-addiction/
Berridge KC, Ho CY, Richard JM, DiFeliceantonio AG. The tempted brain eats: pleasure and desire circuits in obesity and eating disorders. Brain Res 2010; 1350: 43–64.
Schwartz GJ, Zeltser LM. Functional organization of neuronal and humoral signals regulating feeding behavior. Annu Rev Nutr 2013; 33: 1–21. [PubMed]
Y Zhang and RL Leibel. 2017 Leptin and Body Weight. In Eating Disorders and Obesity: A Comprehensive Handbook, 3rd edition(ed KD Brownwell and BT Walsh)
RL Leibel et. al. Changes in energy expenditure resulting from altered body weight. N Engl J Med 1995; 332:621-628
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3380241/
Speakman JR, Levitsky DA, Allison DB et al Set points, settling points and some alternative models: theoretical options to understand how genes and environments combine to regulate body adiposity. Dis Model Mech 2011; 4: 733–745.
Harris RB. Role of set‐point theory in regulation of body weight. FASEB J 1990; 4: 3310–3318.
Pierce RC, Kumaresan V. The mesolimbic dopamine system: the final common pathway for the reinforcing effect of drugs of abuse? Neurosci Biobehav Rev 2006; 30: 215–238.