Sworder
Member
Hello Meso Members,
Lurkers, Freaks and Geeks,
DEA Officer and AAS manufacturer,
Devils and Angels,
I see you all.
Anyway, I don't mean to drag this out, I will make this quick.
So, I was thinking about a commercial I saw at the gym. If you guys don't already know me, know this, I think in weird ways. What it means in this case, there was a weight loss program that showed those before and after pictures. Then they had some statistics, to which I internalized "What source do they have?"
Those weight loss programs are scams! They don't work. You didn't know that though.
What I mean to say, you thought your HUNGER is based off "random" and that your brain needs to count calories for you. Why? Your body can digest and then metabolize the food, it will make use of each and every gram of those fats, proteins, and carbs. What I mean to say is, think back to when you were 7 years old. Were you fat or skinny? If you were skinny, how does the body maintain it's own weight? Is it REALLY our MINDS that needs to calculate calories? Did our parents count our calories and serve us the exact amount? No, I don't think so. What I think is the likely answer, even thought it goes against EVERYTHING you are currently "think."
The answer is that the body is able to create and maintain stasis on it's own, in fact, our survival depended on this in the past.
The real truth is that mental stress is the cause to almost ALL cases of obesity. Yes, you can quote me on that one!
I will give an example that really made me think about this. I have never had more fat than a "two pack" on my abs, haha. That sounds extraordinary. Anyway, back to the story. Two pack, not 2Pac, I have never had more fat than that, but I was in a coma for 3 weeks in 2018 and it sucked. It sucked really bad! I was in the hospital a couple more times that year and then next. In the hospital I didn't eat anything, IV only. However, I noticed that for the first time in my life had much more fat on my entire stomach. For some reason my body would force my appetite to tempt me to down calories even though I shouldn't have been "hungry" at that time.
A "quicky," when I say I shouldn't be hungry at that time that means that I ate a meal of X amount of calories and then tracked when those kcals were supposed to last until and I was plotting that and the numbers weren't making sense.
So that was odd, why now? Why was I gaining weight for no reason? Well... No reason? I was in the hospital for a long period of time and the bewildering nightmares from the ventilator and being strapped down was pretty vivid in my mind were haunting me. I got two panic attacks for the first time in my life, I didn't "believe" in panic attacks before. I am starting to grasp the mental importance of our physical being and the way it manifests itself.
Another EXTREMELY odd thing happened during those years, two of my cats gained weight too!? I am NOT KIDDING!!!
I am not a firm believer in "random" in fact I have a bunch of Number Theory videos about random. Number Theory
Nothing in this universe is random, we can try to assimilate random things but with [in]finite amounts of ways to replicate things. Nothing is random, nor is anything original. However we will not get into that in this thread. Behave!
So do you want me, Sworder, to believe in the "randomness" of me never having fat on me besides 1/32 years? And then TWO of my CATS?! which is 1/6. So what are the chances? I will tell you what the probability of that is! 1/32x1/6x1/6=0.0008680556. So what's that 0.08%? That's a ZERO point ZERO EIGHT. I believe in no omnipotent being except the beguiling beauty of that of statistics and math.
Back to the topic, I strongly disbelieve that this occurrence was "random." Then I made it a point to pay attention to people when they eat, at parties who is snacking on things, at the book club who is drinking alcohol and who is eating snacks. Is there a relationship maybe between stress and eating? I certainly believe so. Of course I have studies that support this as well, see the bottom. I can produce more studies if requested, also if you guys have any studies that proves any thought you have regarding obesity. Create an account and we can have the debate here.
Lastly, and you guys have been great readers so far! Sworder has been using big words and maths.
How do we control this? How do we lose weight?!
I am aware of how extreme this sounds as I have had the same views as you for 32 of my finest years. The way to lose weight is to relax!
Hakuna Matata.
That is the ticket to a healthy life and body!
Find a way to create inner peace. Do you have inner stress issues? You must have stress or you wouldn't have the eating habits! I am careful about putting out statements that aren't supported by science. I will tell you I feel extremely comfortable stating that! Think about other people's habits too! They can just eat whatever and never gain a pound?
Meditation and learning how to think nothing is a great ability to have in all situations. Too many big bad muscle guys here on Meso, buff up your brains. Get control of your emotions because those are the ones that are literally killing you.
Worth mentioning, eating is one behavior that indicates stress, stress can assume a guise of drugs, alcohol, cigarettes, gum as well to name a few. If you have some issues you want to talk about feel free to PM me or preferably if you can share here in the open it would probably help a lot of members. Last, last thing now, sorry, if you forcefully stop eating for a while it will work for a little but then your body will take your back to square one. Also, this topic is very large, pun intended, if you have any questions about anything regarding this subject. Have at me!
Establish good routines!
Thank you for your time.
----------------------------------------------------------------------------------
Relationship between stress, eating behavior, and obesity
Relationship between stress, eating behavior, and obesity - ScienceDirect
Abstract
Stress is thought to influence human eating behavior and has been examined in animal and human studies. Our understanding of the stress-eating relation is confounded by limitations inherent in the study designs; however, we can make some tentative conclusions that support the notion that stress can influence eating patterns in humans. Stress appears to alter overall food intake in two ways, resulting in under- or overeating, which may be influenced by stressor severity. Chronic life stress seems to be associated with a greater preference for energy- and nutrient-dense foods, namely those that are high in sugar and fat. Evidence from longitudinal studies suggests that chronic life stress may be causally linked to weight gain, with a greater effect seen in men. Stress-induced eating may be one factor contributing to the development of obesity. Future studies that measure biological markers of stress will assist our understanding of the physiologic mechanism underlying the stress-eating relation and how stress might be linked to neurotransmitters and hormones that control appetite.
Inflammation, obesity, stress and coronary heart disease: is interleukin-6 the link?
Inflammation, obesity, stress and coronary heart disease: is interleukin-6 the link? - ScienceDirect
Abstract
Obesity is a chronic disease of multifactorial origin and can be defined as an increase in the accumulation of body fat. Adipose tissue is not only a triglyceride storage organ, but studies have shown the role of white adipose tissue as a producer of certain bioactive substances called adipokines. Among adipokines, we find some inflammatory functions, such as Interleukin-6 (IL-6); other adipokines entail the functions of regulating food intake, therefore exerting a direct effect on weight control. This is the case of leptin, which acts on the limbic system by stimulating dopamine uptake, creating a feeling of fullness. However, these adipokines induce the production of reactive oxygen species (ROS), generating a process known as oxidative stress (OS). Because adipose tissue is the organ that secretes adipokines and these in turn generate ROS, adipose tissue is considered an independent factor for the generation of systemic OS. There are several mechanisms by which obesity produces OS. The first of these is the mitochondrial and peroxisomal oxidation of fatty acids, which can produce ROS in oxidation reactions, while another mechanism is over-consumption of oxygen, which generates free radicals in the mitochondrial respiratory chain that is found coupled with oxidative phosphorylation in mitochondria. Lipid-rich diets are also capable of generating ROS because they can alter oxygen metabolism. Upon the increase of adipose tissue, the activity of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), was found to be significantly diminished. Finally, high ROS production and the decrease in antioxidant capacity leads to various abnormalities, among which we find endothelial dysfunction, which is characterized by a reduction in the bioavailability of vasodilators, particularly nitric oxide (NO), and an increase in endothelium-derived contractile factors, favoring atherosclerotic disease.
Inflammation, Oxidative Stress, and Obesity
Inflammation, Oxidative Stress, and Obesity
Abstract
Obesity is a chronic disease of multifactorial origin and can be defined as an increase in the accumulation of body fat. Adipose tissue is not only a triglyceride storage organ, but studies have shown the role of white adipose tissue as a producer of certain bioactive substances called adipokines. Among adipokines, we find some inflammatory functions, such as Interleukin-6 (IL-6); other adipokines entail the functions of regulating food intake, therefore exerting a direct effect on weight control. This is the case of leptin, which acts on the limbic system by stimulating dopamine uptake, creating a feeling of fullness. However, these adipokines induce the production of reactive oxygen species (ROS), generating a process known as oxidative stress (OS). Because adipose tissue is the organ that secretes adipokines and these in turn generate ROS, adipose tissue is considered an independent factor for the generation of systemic OS. There are several mechanisms by which obesity produces OS. The first of these is the mitochondrial and peroxisomal oxidation of fatty acids, which can produce ROS in oxidation reactions, while another mechanism is over-consumption of oxygen, which generates free radicals in the mitochondrial respiratory chain that is found coupled with oxidative phosphorylation in mitochondria. Lipid-rich diets are also capable of generating ROS because they can alter oxygen metabolism. Upon the increase of adipose tissue, the activity of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), was found to be significantly diminished. Finally, high ROS production and the decrease in antioxidant capacity leads to various abnormalities, among which we find endothelial dysfunction, which is characterized by a reduction in the bioavailability of vasodilators, particularly nitric oxide (NO), and an increase in endothelium-derived contractile factors, favoring atherosclerotic disease.
Do stress reactions cause abdominal obesity and comorbidities?
Error - Cookies Turned Off
Summary
‘Stress’ embraces the reaction to a multitude of poorly defined factors that disturb homeostasis or allostasis. In this overview, the activation of the hypothalamic‐pituitary‐adrenal (HPA) axis and the sympathetic nervous system have been utilized as objective measurements of stress reactions. Although long‐term activation of the sympathetic nervous system is followed by primary hypertension, consequences of similar activation of the HPA axis have not been clearly defined. The focus of this overview is to examine whether or not repeated activation of these two stress centres may be involved in the pathogenesis of abdominal obesity and its comorbidities. In population studies adrenal hormones show strong statistical associations to centralization of body fat as well as to obesity. There is considerable evidence from clinical to cellular and molecular studies that elevated cortisol, particularly when combined with secondary inhibition of sex steroids and growth hormone secretions, is causing accumulation of fat in visceral adipose tissues as well as metabolic abnormalities (The Metabolic Syndrome). Hypertension is probably due to a parallel activation of the central sympathetic nervous system. Depression and ‘the small baby syndrome’ as well as stress exposure in men and non‐human primates are followed with time by similar central and peripheral abnormalities. Glucocorticoid exposure is also followed by increased food intake and ‘leptin resistant’ obesity, perhaps disrupting the balance between leptin and neuropeptide Y to the advantage of the latter. The consequence might be ‘stress‐eating’, which, however, is a poorly defined entity. Factors activating the stress centres in humans include psychosocial and socioeconomic handicaps, depressive and anxiety traits, alcohol and smoking, with some differences in profile between personalities and genders. Polymorphisms have been defined in several genes associated with the cascade of events along the stress axes. Based on this evidence it is suggested that environmental, perinatal and genetic factors induce neuroendocrine perturbations followed by abdominal obesity with its associated comorbidities.
Endoplasmic Reticulum Stress Links Obesity, Insulin Action, and Type 2 Diabetes
Endoplasmic Reticulum Stress Links Obesity, Insulin Action, and Type 2 Diabetes
Abstract
Obesity contributes to the development of type 2 diabetes, but the underlying mechanisms are poorly understood. Using cell culture and mouse models, we show that obesity causes endoplasmic reticulum (ER) stress. This stress in turn leads to suppression of insulin receptor signaling through hyperactivation of c-Jun N-terminal kinase (JNK) and subsequent serine phosphorylation of insulin receptor substrate–1 (IRS-1). Mice deficient in X-box–binding protein–1 (XBP-1), a transcription factor that modulates the ER stress response, develop insulin resistance. These findings demonstrate that ER stress is a central feature of peripheral insulin resistance and type 2 diabetes at the molecular, cellular, and organismal levels. Pharmacologic manipulation of this pathway may offer novel opportunities for treating these common diseases.
Lurkers, Freaks and Geeks,
DEA Officer and AAS manufacturer,
Devils and Angels,
I see you all.
Anyway, I don't mean to drag this out, I will make this quick.
So, I was thinking about a commercial I saw at the gym. If you guys don't already know me, know this, I think in weird ways. What it means in this case, there was a weight loss program that showed those before and after pictures. Then they had some statistics, to which I internalized "What source do they have?"
Those weight loss programs are scams! They don't work. You didn't know that though.
What I mean to say, you thought your HUNGER is based off "random" and that your brain needs to count calories for you. Why? Your body can digest and then metabolize the food, it will make use of each and every gram of those fats, proteins, and carbs. What I mean to say is, think back to when you were 7 years old. Were you fat or skinny? If you were skinny, how does the body maintain it's own weight? Is it REALLY our MINDS that needs to calculate calories? Did our parents count our calories and serve us the exact amount? No, I don't think so. What I think is the likely answer, even thought it goes against EVERYTHING you are currently "think."
The answer is that the body is able to create and maintain stasis on it's own, in fact, our survival depended on this in the past.
The real truth is that mental stress is the cause to almost ALL cases of obesity. Yes, you can quote me on that one!
I will give an example that really made me think about this. I have never had more fat than a "two pack" on my abs, haha. That sounds extraordinary. Anyway, back to the story. Two pack, not 2Pac, I have never had more fat than that, but I was in a coma for 3 weeks in 2018 and it sucked. It sucked really bad! I was in the hospital a couple more times that year and then next. In the hospital I didn't eat anything, IV only. However, I noticed that for the first time in my life had much more fat on my entire stomach. For some reason my body would force my appetite to tempt me to down calories even though I shouldn't have been "hungry" at that time.
A "quicky," when I say I shouldn't be hungry at that time that means that I ate a meal of X amount of calories and then tracked when those kcals were supposed to last until and I was plotting that and the numbers weren't making sense.
So that was odd, why now? Why was I gaining weight for no reason? Well... No reason? I was in the hospital for a long period of time and the bewildering nightmares from the ventilator and being strapped down was pretty vivid in my mind were haunting me. I got two panic attacks for the first time in my life, I didn't "believe" in panic attacks before. I am starting to grasp the mental importance of our physical being and the way it manifests itself.
Another EXTREMELY odd thing happened during those years, two of my cats gained weight too!? I am NOT KIDDING!!!
I am not a firm believer in "random" in fact I have a bunch of Number Theory videos about random. Number Theory
Nothing in this universe is random, we can try to assimilate random things but with [in]finite amounts of ways to replicate things. Nothing is random, nor is anything original. However we will not get into that in this thread. Behave!
So do you want me, Sworder, to believe in the "randomness" of me never having fat on me besides 1/32 years? And then TWO of my CATS?! which is 1/6. So what are the chances? I will tell you what the probability of that is! 1/32x1/6x1/6=0.0008680556. So what's that 0.08%? That's a ZERO point ZERO EIGHT. I believe in no omnipotent being except the beguiling beauty of that of statistics and math.
Back to the topic, I strongly disbelieve that this occurrence was "random." Then I made it a point to pay attention to people when they eat, at parties who is snacking on things, at the book club who is drinking alcohol and who is eating snacks. Is there a relationship maybe between stress and eating? I certainly believe so. Of course I have studies that support this as well, see the bottom. I can produce more studies if requested, also if you guys have any studies that proves any thought you have regarding obesity. Create an account and we can have the debate here.
Lastly, and you guys have been great readers so far! Sworder has been using big words and maths.
How do we control this? How do we lose weight?!
I am aware of how extreme this sounds as I have had the same views as you for 32 of my finest years. The way to lose weight is to relax!
Hakuna Matata.
That is the ticket to a healthy life and body!
Find a way to create inner peace. Do you have inner stress issues? You must have stress or you wouldn't have the eating habits! I am careful about putting out statements that aren't supported by science. I will tell you I feel extremely comfortable stating that! Think about other people's habits too! They can just eat whatever and never gain a pound?
Meditation and learning how to think nothing is a great ability to have in all situations. Too many big bad muscle guys here on Meso, buff up your brains. Get control of your emotions because those are the ones that are literally killing you.
Worth mentioning, eating is one behavior that indicates stress, stress can assume a guise of drugs, alcohol, cigarettes, gum as well to name a few. If you have some issues you want to talk about feel free to PM me or preferably if you can share here in the open it would probably help a lot of members. Last, last thing now, sorry, if you forcefully stop eating for a while it will work for a little but then your body will take your back to square one. Also, this topic is very large, pun intended, if you have any questions about anything regarding this subject. Have at me!
Establish good routines!
Thank you for your time.
----------------------------------------------------------------------------------
Relationship between stress, eating behavior, and obesity
Relationship between stress, eating behavior, and obesity - ScienceDirect
Abstract
Stress is thought to influence human eating behavior and has been examined in animal and human studies. Our understanding of the stress-eating relation is confounded by limitations inherent in the study designs; however, we can make some tentative conclusions that support the notion that stress can influence eating patterns in humans. Stress appears to alter overall food intake in two ways, resulting in under- or overeating, which may be influenced by stressor severity. Chronic life stress seems to be associated with a greater preference for energy- and nutrient-dense foods, namely those that are high in sugar and fat. Evidence from longitudinal studies suggests that chronic life stress may be causally linked to weight gain, with a greater effect seen in men. Stress-induced eating may be one factor contributing to the development of obesity. Future studies that measure biological markers of stress will assist our understanding of the physiologic mechanism underlying the stress-eating relation and how stress might be linked to neurotransmitters and hormones that control appetite.
Inflammation, obesity, stress and coronary heart disease: is interleukin-6 the link?
Inflammation, obesity, stress and coronary heart disease: is interleukin-6 the link? - ScienceDirect
Abstract
Obesity is a chronic disease of multifactorial origin and can be defined as an increase in the accumulation of body fat. Adipose tissue is not only a triglyceride storage organ, but studies have shown the role of white adipose tissue as a producer of certain bioactive substances called adipokines. Among adipokines, we find some inflammatory functions, such as Interleukin-6 (IL-6); other adipokines entail the functions of regulating food intake, therefore exerting a direct effect on weight control. This is the case of leptin, which acts on the limbic system by stimulating dopamine uptake, creating a feeling of fullness. However, these adipokines induce the production of reactive oxygen species (ROS), generating a process known as oxidative stress (OS). Because adipose tissue is the organ that secretes adipokines and these in turn generate ROS, adipose tissue is considered an independent factor for the generation of systemic OS. There are several mechanisms by which obesity produces OS. The first of these is the mitochondrial and peroxisomal oxidation of fatty acids, which can produce ROS in oxidation reactions, while another mechanism is over-consumption of oxygen, which generates free radicals in the mitochondrial respiratory chain that is found coupled with oxidative phosphorylation in mitochondria. Lipid-rich diets are also capable of generating ROS because they can alter oxygen metabolism. Upon the increase of adipose tissue, the activity of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), was found to be significantly diminished. Finally, high ROS production and the decrease in antioxidant capacity leads to various abnormalities, among which we find endothelial dysfunction, which is characterized by a reduction in the bioavailability of vasodilators, particularly nitric oxide (NO), and an increase in endothelium-derived contractile factors, favoring atherosclerotic disease.
Inflammation, Oxidative Stress, and Obesity
Inflammation, Oxidative Stress, and Obesity
Abstract
Obesity is a chronic disease of multifactorial origin and can be defined as an increase in the accumulation of body fat. Adipose tissue is not only a triglyceride storage organ, but studies have shown the role of white adipose tissue as a producer of certain bioactive substances called adipokines. Among adipokines, we find some inflammatory functions, such as Interleukin-6 (IL-6); other adipokines entail the functions of regulating food intake, therefore exerting a direct effect on weight control. This is the case of leptin, which acts on the limbic system by stimulating dopamine uptake, creating a feeling of fullness. However, these adipokines induce the production of reactive oxygen species (ROS), generating a process known as oxidative stress (OS). Because adipose tissue is the organ that secretes adipokines and these in turn generate ROS, adipose tissue is considered an independent factor for the generation of systemic OS. There are several mechanisms by which obesity produces OS. The first of these is the mitochondrial and peroxisomal oxidation of fatty acids, which can produce ROS in oxidation reactions, while another mechanism is over-consumption of oxygen, which generates free radicals in the mitochondrial respiratory chain that is found coupled with oxidative phosphorylation in mitochondria. Lipid-rich diets are also capable of generating ROS because they can alter oxygen metabolism. Upon the increase of adipose tissue, the activity of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), was found to be significantly diminished. Finally, high ROS production and the decrease in antioxidant capacity leads to various abnormalities, among which we find endothelial dysfunction, which is characterized by a reduction in the bioavailability of vasodilators, particularly nitric oxide (NO), and an increase in endothelium-derived contractile factors, favoring atherosclerotic disease.
Do stress reactions cause abdominal obesity and comorbidities?
Error - Cookies Turned Off
Summary
‘Stress’ embraces the reaction to a multitude of poorly defined factors that disturb homeostasis or allostasis. In this overview, the activation of the hypothalamic‐pituitary‐adrenal (HPA) axis and the sympathetic nervous system have been utilized as objective measurements of stress reactions. Although long‐term activation of the sympathetic nervous system is followed by primary hypertension, consequences of similar activation of the HPA axis have not been clearly defined. The focus of this overview is to examine whether or not repeated activation of these two stress centres may be involved in the pathogenesis of abdominal obesity and its comorbidities. In population studies adrenal hormones show strong statistical associations to centralization of body fat as well as to obesity. There is considerable evidence from clinical to cellular and molecular studies that elevated cortisol, particularly when combined with secondary inhibition of sex steroids and growth hormone secretions, is causing accumulation of fat in visceral adipose tissues as well as metabolic abnormalities (The Metabolic Syndrome). Hypertension is probably due to a parallel activation of the central sympathetic nervous system. Depression and ‘the small baby syndrome’ as well as stress exposure in men and non‐human primates are followed with time by similar central and peripheral abnormalities. Glucocorticoid exposure is also followed by increased food intake and ‘leptin resistant’ obesity, perhaps disrupting the balance between leptin and neuropeptide Y to the advantage of the latter. The consequence might be ‘stress‐eating’, which, however, is a poorly defined entity. Factors activating the stress centres in humans include psychosocial and socioeconomic handicaps, depressive and anxiety traits, alcohol and smoking, with some differences in profile between personalities and genders. Polymorphisms have been defined in several genes associated with the cascade of events along the stress axes. Based on this evidence it is suggested that environmental, perinatal and genetic factors induce neuroendocrine perturbations followed by abdominal obesity with its associated comorbidities.
Endoplasmic Reticulum Stress Links Obesity, Insulin Action, and Type 2 Diabetes
Endoplasmic Reticulum Stress Links Obesity, Insulin Action, and Type 2 Diabetes
Abstract
Obesity contributes to the development of type 2 diabetes, but the underlying mechanisms are poorly understood. Using cell culture and mouse models, we show that obesity causes endoplasmic reticulum (ER) stress. This stress in turn leads to suppression of insulin receptor signaling through hyperactivation of c-Jun N-terminal kinase (JNK) and subsequent serine phosphorylation of insulin receptor substrate–1 (IRS-1). Mice deficient in X-box–binding protein–1 (XBP-1), a transcription factor that modulates the ER stress response, develop insulin resistance. These findings demonstrate that ER stress is a central feature of peripheral insulin resistance and type 2 diabetes at the molecular, cellular, and organismal levels. Pharmacologic manipulation of this pathway may offer novel opportunities for treating these common diseases.
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