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On April 01 2014 09:57 Jumperer wrote:Show nested quote +On March 31 2014 22:21 Ghostcom wrote:
As an M.D., I am going to say that you should probably stop posting now. You are digging the hole you are already standing in deeper with every single post you make. Nobody cares about your degree. You win a debate by presenting a stronger argument, not by saying you have a degree and then tell the other person to stop posting.
Do I really have to present an argument as to why genetics or thyroid disease can cause obesity in people with completely healthy eating habits? Let us not go full retard here... I didn't seek to win a debate, I sought to clarify that there was no debate to be had concerning this. I agree I could and probably should have skipped the appeal to authority, however it seemed appropriate to point out that I wasn't a layman.
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i just skipped your post as if it was nothing more then .. well actually it was just nothing. a big fat nothing.
thyroid disease goes both ways: it makes some people fat but it also makes some people skinny. ( makes is a strong word here; better suited would be prone to ). anyway, its a disease; hell, but let's just give them all pensions or something 'cause shit is not fair ...
and about the genetics part - you probably read the same things i do and bought it. i didn't. as such, i saw no point in arguing about beliefs.
i'm here:
Genes contribute to obesity in many ways, by affecting appetite, satiety (the sense of fullness), metabolism, food cravings, body-fat distribution, and the tendency to use eating as a way to cope with stress. and think that those are/should be manageable by ones psyche.
even if you go with
Recently, scientists at Tufts University solved the mystery. They discovered that most of us have inherited a sluggish ADP gene that enables fat to be stored in our tissues very easily and slows down the way that fat it is burnt off or turned into energy you still remain with the fact that the stored fat comes from food and only from food. the gene doesn't produce the fat out of/from nothing.
and the solution to that is: The sluggish gene enabled what little food was available to be readily stored as fat. Fat deposits could then be used as a source of energy and help survival in times of famine. famine
if you know how genes, by themselves, can make people fat, literally, then please do post.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2736391/#S1title
Freely available article here. This is one of the first hits when searching Pubmed using the keywords "obesity" and "genetics" which yields more than 30.000 results. Do me a favour and read the first sentence in the paragraph called "Etiology".
For this article you really only need to read the title:
http://www.nature.com/nature/journal/v392/n6674/abs/392398a0.html
I could keep on linking you articles proving that it is commonly accepted in the medical community that obesity is genetic (though not solely - as with almost everything else there is more than one causative factor and no single one is probably sufficient). It is truly ignorant to think obesity has a single causative factor.
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the ncbi.nlm.nhi.gov article is hogwash. it just tries to explain/make sense of what is happening after it happened without even thinking of what started it or how it came to be like this. its just a long series of remarks like: this like that because it is like that.
a quote from one of the studies based on which that paper was made:
CONCLUSIONS: Genetic influences on BMI and abdominal adiposity are high in children born since the onset of the pediatric obesity epidemic. what caused the onset?. genes started mutating randomly and boom: from now on, thou shalt be fat?.
lets say you inherited your fat genes from your parents, your parents from their parents and so on; but then wait, their grandparents weren't fat. they were skinny ... so then what?, how?, whom?, all of a sudden?.
also, they made the study on 8 to 11 yr olds. some kids as old as 3 can and do eat 3000 calories a day. those are already damaged goods.
the nature article, albeit old, it just says this:
Genes contribute to obesity in many ways, by affecting appetite, satiety (the sense of fullness), metabolism, food cravings, body-fat distribution, and the tendency to use eating as a way to cope with stress. but with different words.
The adipocyte-specific hormone leptin, the product of the obese (ob) gene,regulates adipose-tissue mass through hypothalamic effects on satiety and energy expenditure1, 2, 3, 4
http://www.news-medical.net/health/What-Does-Leptin-Do.aspx
Mechanisms and actions of leptin
Leptin acts as a hormone that modulates the size of the adipose tissues in the body. It regulates food intake and body weight. Leptin also acts on specific receptors in the hypothalamus to inhibit appetite through both counteractive and stimulatory mechanisms:
Leptin counteracts the effects of a feeding stimulant released in the gut called neuropeptide Y as well as the effects of a cannabinoid neurotransmitter called adandamide which stimulates appetite.
Leptin also promotes the synthesis of an appetite suppressant called α-melanocyte-stimulating hormone
even if you read: https://en.wikipedia.org/wiki/Leptin#Discovery
After a meeting where Friedman met Nobel Prize winner, Frenchman Roger Guillemin, he got a letter from him that he recalls saying, “I really liked what you had to say, but I have one quibble: you refer to these as obesity genes, but I think they are lean genes because the normal allele keeps you thin. But calling them lean genes sounds awkward. The nicest sounding root for thin is from Greek, so I propose you call ob and db ‘lepto-genes.’” So Friedman remembered Guillemin’s suggestion, and the hormone was named leptin.[16] Leptin was the first fat cell-derived hormone to be discovered. Subsequent studies confirmed that the db gene encoded the leptin receptor and that it was expressed in the hypothalamus, a region of the brain known to regulate food intake and body weight.
The discovery of leptin has led to the elucidation of a robust physiologic system that maintains fat stores at a relatively constant level, which has been widely validated in several experimental rodent obesity models; nevertheless adequate proof of its equivalent operation in humans remains elusive.
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What are you guys arguing about? It looks like you're both arguing about genetics affecting your weight, but I'm pretty sure that's already well-established.
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Sadly that is exactly what we are arguing as xM)Z seems to hold the conviction that obesity is only caused by an excessive food-intake by those weak of spirit.
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On April 02 2014 22:14 Dark_Chill wrote:
What are you guys arguing about? It looks like you're both arguing about genetics affecting your weight, but I'm pretty sure that's already well-established. nope, we're debating the significance of it (and maybe the 'why') not whether it happens or not.
and nothing is well establish as far as adipocyte biology goes.
Obesity and the obesity-associated metabolic dysfunctions are a major health and economic burden. Adipocytesecreted proteins play an important role in obesity-associated disorders. Therefore it is essential to study the secreted factors of human (pre)adipocytes, not only to understand the underlying mechanisms of obesity-induced metabolic complications, but also to gain more insight in the regulation of weight gain, weight loss, weight re-gain and weight maintenance. This may aid the development of successful treatment strategies for obesity and its related complications.
In vivostudies are usually confined to plasma and other body fluids and as such the results demonstrate the effect of an intervention but not the underlying molecular mechanisms. That is why in vitrostudies of human (pre)adipocytes and adipose tissue are necessary. Technical issues of proteomics technologies, including false positive identification, limited throughput, low sensitivity and quantification still do not allow identifying the complete (pre)adipocyte secretome. However, improved MS approaches developed during the last 10 years have helped to increase the understanding of the adipose tissue/adipocyte proteome and its regulation, including the adipocyte-secreted proteins. Nevertheless, much is still unknown about the molecular mechanisms responsible for the development of obesity and its metabolic complications, as well as strategies to improve the obesity-induced metabolic phenotype.
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On April 02 2014 21:18 xM(Z wrote:the ncbi.nlm.nhi.gov article is hogwash. it just tries to explain/make sense of what is happening after it happened without even thinking of what started it or how it came to be like this. its just a long series of remarks like: this like that because it is like that. a quote from one of the studies based on which that paper was made: Show nested quote +CONCLUSIONS: Genetic influences on BMI and abdominal adiposity are high in children born since the onset of the pediatric obesity epidemic. what caused the onset?. genes started mutating randomly and boom: from now on, thou shalt be fat?. lets say you inherited your fat genes from your parents, your parents from their parents and so on; but then wait, their grandparents weren't fat. they were skinny ... so then what?, how?, whom?, all of a sudden?. also, they made the study on 8 to 11 yr olds. some kids as old as 3 can and do eat 3000 calories a day. those are already damaged goods. the nature article, albeit old, it just says this: Show nested quote +Genes contribute to obesity in many ways, by affecting appetite, satiety (the sense of fullness), metabolism, food cravings, body-fat distribution, and the tendency to use eating as a way to cope with stress. but with different words. Show nested quote +The adipocyte-specific hormone leptin, the product of the obese (ob) gene,regulates adipose-tissue mass through hypothalamic effects on satiety and energy expenditure1, 2, 3, 4 http://www.news-medical.net/health/What-Does-Leptin-Do.aspxShow nested quote +Mechanisms and actions of leptin
Leptin acts as a hormone that modulates the size of the adipose tissues in the body. It regulates food intake and body weight. Leptin also acts on specific receptors in the hypothalamus to inhibit appetite through both counteractive and stimulatory mechanisms:
Leptin counteracts the effects of a feeding stimulant released in the gut called neuropeptide Y as well as the effects of a cannabinoid neurotransmitter called adandamide which stimulates appetite.
Leptin also promotes the synthesis of an appetite suppressant called α-melanocyte-stimulating hormone even if you read: https://en.wikipedia.org/wiki/Leptin#DiscoveryShow nested quote +After a meeting where Friedman met Nobel Prize winner, Frenchman Roger Guillemin, he got a letter from him that he recalls saying, “I really liked what you had to say, but I have one quibble: you refer to these as obesity genes, but I think they are lean genes because the normal allele keeps you thin. But calling them lean genes sounds awkward. The nicest sounding root for thin is from Greek, so I propose you call ob and db ‘lepto-genes.’” So Friedman remembered Guillemin’s suggestion, and the hormone was named leptin.[16] Leptin was the first fat cell-derived hormone to be discovered. Subsequent studies confirmed that the db gene encoded the leptin receptor and that it was expressed in the hypothalamus, a region of the brain known to regulate food intake and body weight. Show nested quote +The discovery of leptin has led to the elucidation of a robust physiologic system that maintains fat stores at a relatively constant level, which has been widely validated in several experimental rodent obesity models; nevertheless adequate proof of its equivalent operation in humans remains elusive.
You didn't actually read the pubmed article did you? You do realise what you just called hogwash was peer-reviewed by medical experts? And that they actually do address your criticism?
More than 300 genetic loci that are potentially involved in human body weight regulation have been identified through analyses in humans, rodents, and C elegans.16,17 Some exceedingly rare gene variants affect gene function and behavior to such an extent that obesity results even without a particularly “obesogenic” environment (Figure 2), but the vast majority of genetic factors are presumed to affect body weight enough to cause obesity only when specific environmental conditions pertain.
You keep trying to make it out as if I or anyone else has claimed genetics to be the single causative factor - which it obviously isn't. That however isn't what we are arguing. Your initial statement was this:
On March 31 2014 18:23 xM(Z wrote:also, being genetically predisposed (even if such a thing would exist), can not make you fat; food does however.
I think I have sufficiently refuted that statement (obviously such a thing as being genetically predisposed does exist and can make you fat).
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On April 02 2014 16:29 Ghostcom wrote:Show nested quote +On April 01 2014 09:57 Jumperer wrote:On March 31 2014 22:21 Ghostcom wrote:
As an M.D., I am going to say that you should probably stop posting now. You are digging the hole you are already standing in deeper with every single post you make. Nobody cares about your degree. You win a debate by presenting a stronger argument, not by saying you have a degree and then tell the other person to stop posting. Do I really have to present an argument as to why genetics or thyroid disease can cause obesity in people with completely healthy eating habits? Let us not go full retard here... I didn't seek to win a debate, I sought to clarify that there was no debate to be had concerning this. I agree I could and probably should have skipped the appeal to authority, however it seemed appropriate to point out that I wasn't a layman.
Thyroid diseases can be easily monitored by taking pills. My mom had hyperthyroid which caused her appetite to boom but then she did surgery TEN years ago so restore to its regular balance.
And genetics wise, well people were LESS fat before (statistically speaking). I've personally talked to people in 80s were saying that back when they were young, instead of playing video games and texting all day, they enjoyed themselves outside exploring the neighborhood. The obesity rate of the world is at an all time high. It isn't a coincidence that the rise of obesity have eclipsed along with the rise of fast food restaurant (and other interactive entertainment).
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I hate to break it to you, Xiphos, but not everyone is like your mother. Thyroid diseases as a general category of disorders are not "easily monitored by taking pills". Similarly, talking to people in their 80s about their activities as youth does not exactly stand as a piece of actionable evidence past supporting the notion that it is indeed nice that you've taken time out of your day to speak to our elderly. Environment and activity patterns most certainly play a role in the prevalence of obesity but the prominence of this role in contrast with other factors is far from established. In other words, when it makes sense to say "it isn't a coincidence", you probably ought to check your conclusion at the door.
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They are easily monitored though. I did some heavy research on this. Why don't you go and check it out by yourself by going to http://chealth.canoe.ca/drug_info_details.asp?brand_name_id=1202 for more information on that particular medicine.
This ENTIRE thread pretty much consists of people giving good argument and people saying "No that's wrong w/ any evidence for rebuttal.". They are either trolls or just butthurt but can't find anything substantial to refute.
And if anyone had any education in science will tell you based upon the law of energy and metabolism will tell you that if you don't utilize the amount of energy you have digested (the calories), they will go into a "reserve" location in your body also known as fat.
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On April 02 2014 23:58 Ghostcom wrote:Show nested quote +On April 02 2014 21:18 xM(Z wrote:the ncbi.nlm.nhi.gov article is hogwash. it just tries to explain/make sense of what is happening after it happened without even thinking of what started it or how it came to be like this. its just a long series of remarks like: this like that because it is like that. a quote from one of the studies based on which that paper was made: CONCLUSIONS: Genetic influences on BMI and abdominal adiposity are high in children born since the onset of the pediatric obesity epidemic. what caused the onset?. genes started mutating randomly and boom: from now on, thou shalt be fat?. lets say you inherited your fat genes from your parents, your parents from their parents and so on; but then wait, their grandparents weren't fat. they were skinny ... so then what?, how?, whom?, all of a sudden?. also, they made the study on 8 to 11 yr olds. some kids as old as 3 can and do eat 3000 calories a day. those are already damaged goods. the nature article, albeit old, it just says this: Genes contribute to obesity in many ways, by affecting appetite, satiety (the sense of fullness), metabolism, food cravings, body-fat distribution, and the tendency to use eating as a way to cope with stress. but with different words. The adipocyte-specific hormone leptin, the product of the obese (ob) gene,regulates adipose-tissue mass through hypothalamic effects on satiety and energy expenditure1, 2, 3, 4 http://www.news-medical.net/health/What-Does-Leptin-Do.aspxMechanisms and actions of leptin
Leptin acts as a hormone that modulates the size of the adipose tissues in the body. It regulates food intake and body weight. Leptin also acts on specific receptors in the hypothalamus to inhibit appetite through both counteractive and stimulatory mechanisms:
Leptin counteracts the effects of a feeding stimulant released in the gut called neuropeptide Y as well as the effects of a cannabinoid neurotransmitter called adandamide which stimulates appetite.
Leptin also promotes the synthesis of an appetite suppressant called α-melanocyte-stimulating hormone even if you read: https://en.wikipedia.org/wiki/Leptin#DiscoveryAfter a meeting where Friedman met Nobel Prize winner, Frenchman Roger Guillemin, he got a letter from him that he recalls saying, “I really liked what you had to say, but I have one quibble: you refer to these as obesity genes, but I think they are lean genes because the normal allele keeps you thin. But calling them lean genes sounds awkward. The nicest sounding root for thin is from Greek, so I propose you call ob and db ‘lepto-genes.’” So Friedman remembered Guillemin’s suggestion, and the hormone was named leptin.[16] Leptin was the first fat cell-derived hormone to be discovered. Subsequent studies confirmed that the db gene encoded the leptin receptor and that it was expressed in the hypothalamus, a region of the brain known to regulate food intake and body weight. The discovery of leptin has led to the elucidation of a robust physiologic system that maintains fat stores at a relatively constant level, which has been widely validated in several experimental rodent obesity models; nevertheless adequate proof of its equivalent operation in humans remains elusive. You didn't actually read the pubmed article did you? You do realise what you just called hogwash was peer-reviewed by medical experts? And that they actually do address your criticism? Show nested quote +More than 300 genetic loci that are potentially involved in human body weight regulation have been identified through analyses in humans, rodents, and C elegans.16,17 Some exceedingly rare gene variants affect gene function and behavior to such an extent that obesity results even without a particularly “obesogenic” environment (Figure 2), but the vast majority of genetic factors are presumed to affect body weight enough to cause obesity only when specific environmental conditions pertain. You keep trying to make it out as if I or anyone else has claimed genetics to be the single causative factor - which it obviously isn't. That however isn't what we are arguing. Your initial statement was this: Show nested quote +On March 31 2014 18:23 xM(Z wrote:also, being genetically predisposed (even if such a thing would exist), can not make you fat; food does however. I think I have sufficiently refuted that statement (obviously such a thing as being genetically predisposed does exist and can make you fat).
from your own quote: genetics control human body weight - agreed from beginning.
the same genes that make one obese can make another one skinny based on gene function, gene behavior, gene expression and so on - very logical but no one knows why. they just point fingers at parents, mcdonalds, sedentarism and whatnot.
exceedingly rare gene variants do exist which results in = obese person without the need of an '“obesogenic” environment' - disease, diabetes and others.
being 'genetically predisposed' can make you fatt-ER then the skinny people while doing what they do - very logical; after all, you are different, it's normal you'd be affected differently by the same things.
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On April 03 2014 00:18 Xiphos wrote:They are easily monitored though. I did some heavy research on this. Why don't you go and check it out by yourself by going to http://chealth.canoe.ca/drug_info_details.asp?brand_name_id=1202 for more information on that particular medicine. This ENTIRE thread pretty much consists of people giving good argument and people saying "No that's wrong w/ any evidence for rebuttal.". They are either trolls or just butthurt but can't find anything substantial to refute. And if anyone had any education in science will tell you based upon the law of energy and metabolism will tell you that if you don't utilize the amount of energy you have digested (the calories), they will go into a "reserve" location in your body also known as fat.
For someone so critical of others arguments, you sure do a poor job of substantiating your own. Linking a drug fact sheet alongside an assurance that you've done some "heavy research" on the topic does not, in fact, establish that thyroid diseases are categorically easy to treat and diagnose. Furthermore, your willingness to ad hoc conflate the law of energy conservation with the incredibly complicated concept of human metabolism speaks to a remarkably incomplete understanding as to how little we truly understand endocrinology. Yes, as a shorthand means of communication, calories in vs. calories out is a good starting place when it comes to diet and body mass but it is by no means the final destination.
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On April 03 2014 00:26 xM(Z wrote:Show nested quote +On April 02 2014 23:58 Ghostcom wrote:On April 02 2014 21:18 xM(Z wrote:the ncbi.nlm.nhi.gov article is hogwash. it just tries to explain/make sense of what is happening after it happened without even thinking of what started it or how it came to be like this. its just a long series of remarks like: this like that because it is like that. a quote from one of the studies based on which that paper was made: CONCLUSIONS: Genetic influences on BMI and abdominal adiposity are high in children born since the onset of the pediatric obesity epidemic. what caused the onset?. genes started mutating randomly and boom: from now on, thou shalt be fat?. lets say you inherited your fat genes from your parents, your parents from their parents and so on; but then wait, their grandparents weren't fat. they were skinny ... so then what?, how?, whom?, all of a sudden?. also, they made the study on 8 to 11 yr olds. some kids as old as 3 can and do eat 3000 calories a day. those are already damaged goods. the nature article, albeit old, it just says this: Genes contribute to obesity in many ways, by affecting appetite, satiety (the sense of fullness), metabolism, food cravings, body-fat distribution, and the tendency to use eating as a way to cope with stress. but with different words. The adipocyte-specific hormone leptin, the product of the obese (ob) gene,regulates adipose-tissue mass through hypothalamic effects on satiety and energy expenditure1, 2, 3, 4 http://www.news-medical.net/health/What-Does-Leptin-Do.aspxMechanisms and actions of leptin
Leptin acts as a hormone that modulates the size of the adipose tissues in the body. It regulates food intake and body weight. Leptin also acts on specific receptors in the hypothalamus to inhibit appetite through both counteractive and stimulatory mechanisms:
Leptin counteracts the effects of a feeding stimulant released in the gut called neuropeptide Y as well as the effects of a cannabinoid neurotransmitter called adandamide which stimulates appetite.
Leptin also promotes the synthesis of an appetite suppressant called α-melanocyte-stimulating hormone even if you read: https://en.wikipedia.org/wiki/Leptin#DiscoveryAfter a meeting where Friedman met Nobel Prize winner, Frenchman Roger Guillemin, he got a letter from him that he recalls saying, “I really liked what you had to say, but I have one quibble: you refer to these as obesity genes, but I think they are lean genes because the normal allele keeps you thin. But calling them lean genes sounds awkward. The nicest sounding root for thin is from Greek, so I propose you call ob and db ‘lepto-genes.’” So Friedman remembered Guillemin’s suggestion, and the hormone was named leptin.[16] Leptin was the first fat cell-derived hormone to be discovered. Subsequent studies confirmed that the db gene encoded the leptin receptor and that it was expressed in the hypothalamus, a region of the brain known to regulate food intake and body weight. The discovery of leptin has led to the elucidation of a robust physiologic system that maintains fat stores at a relatively constant level, which has been widely validated in several experimental rodent obesity models; nevertheless adequate proof of its equivalent operation in humans remains elusive. You didn't actually read the pubmed article did you? You do realise what you just called hogwash was peer-reviewed by medical experts? And that they actually do address your criticism? More than 300 genetic loci that are potentially involved in human body weight regulation have been identified through analyses in humans, rodents, and C elegans.16,17 Some exceedingly rare gene variants affect gene function and behavior to such an extent that obesity results even without a particularly “obesogenic” environment (Figure 2), but the vast majority of genetic factors are presumed to affect body weight enough to cause obesity only when specific environmental conditions pertain. You keep trying to make it out as if I or anyone else has claimed genetics to be the single causative factor - which it obviously isn't. That however isn't what we are arguing. Your initial statement was this: On March 31 2014 18:23 xM(Z wrote:also, being genetically predisposed (even if such a thing would exist), can not make you fat; food does however. I think I have sufficiently refuted that statement (obviously such a thing as being genetically predisposed does exist and can make you fat). from your own quote: genetics control human body weight - agreed from beginning. the same genes that make one obese can make another one skinny based on gene function, gene behavior, gene expression and so on - very logical but no one knows why. they just point fingers at parents, mcdonalds, sedentarism and whatnot. exceedingly rare gene variants do exist which results in = obese person without the need of an '“obesogenic” environment' - disease, diabetes and others. being 'genetically predisposed' can make you fatt- ER then the skinny people while doing what they do - very logical; after all, you are different, it's normal you'd be affected differently by the same things.
This is a position with which I can entirely agree.
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On April 03 2014 00:26 xM(Z wrote:Show nested quote +On April 02 2014 23:58 Ghostcom wrote:On April 02 2014 21:18 xM(Z wrote:the ncbi.nlm.nhi.gov article is hogwash. it just tries to explain/make sense of what is happening after it happened without even thinking of what started it or how it came to be like this. its just a long series of remarks like: this like that because it is like that. a quote from one of the studies based on which that paper was made: CONCLUSIONS: Genetic influences on BMI and abdominal adiposity are high in children born since the onset of the pediatric obesity epidemic. what caused the onset?. genes started mutating randomly and boom: from now on, thou shalt be fat?. lets say you inherited your fat genes from your parents, your parents from their parents and so on; but then wait, their grandparents weren't fat. they were skinny ... so then what?, how?, whom?, all of a sudden?. also, they made the study on 8 to 11 yr olds. some kids as old as 3 can and do eat 3000 calories a day. those are already damaged goods. the nature article, albeit old, it just says this: Genes contribute to obesity in many ways, by affecting appetite, satiety (the sense of fullness), metabolism, food cravings, body-fat distribution, and the tendency to use eating as a way to cope with stress. but with different words. The adipocyte-specific hormone leptin, the product of the obese (ob) gene,regulates adipose-tissue mass through hypothalamic effects on satiety and energy expenditure1, 2, 3, 4 http://www.news-medical.net/health/What-Does-Leptin-Do.aspxMechanisms and actions of leptin
Leptin acts as a hormone that modulates the size of the adipose tissues in the body. It regulates food intake and body weight. Leptin also acts on specific receptors in the hypothalamus to inhibit appetite through both counteractive and stimulatory mechanisms:
Leptin counteracts the effects of a feeding stimulant released in the gut called neuropeptide Y as well as the effects of a cannabinoid neurotransmitter called adandamide which stimulates appetite.
Leptin also promotes the synthesis of an appetite suppressant called α-melanocyte-stimulating hormone even if you read: https://en.wikipedia.org/wiki/Leptin#DiscoveryAfter a meeting where Friedman met Nobel Prize winner, Frenchman Roger Guillemin, he got a letter from him that he recalls saying, “I really liked what you had to say, but I have one quibble: you refer to these as obesity genes, but I think they are lean genes because the normal allele keeps you thin. But calling them lean genes sounds awkward. The nicest sounding root for thin is from Greek, so I propose you call ob and db ‘lepto-genes.’” So Friedman remembered Guillemin’s suggestion, and the hormone was named leptin.[16] Leptin was the first fat cell-derived hormone to be discovered. Subsequent studies confirmed that the db gene encoded the leptin receptor and that it was expressed in the hypothalamus, a region of the brain known to regulate food intake and body weight. The discovery of leptin has led to the elucidation of a robust physiologic system that maintains fat stores at a relatively constant level, which has been widely validated in several experimental rodent obesity models; nevertheless adequate proof of its equivalent operation in humans remains elusive. You didn't actually read the pubmed article did you? You do realise what you just called hogwash was peer-reviewed by medical experts? And that they actually do address your criticism? More than 300 genetic loci that are potentially involved in human body weight regulation have been identified through analyses in humans, rodents, and C elegans.16,17 Some exceedingly rare gene variants affect gene function and behavior to such an extent that obesity results even without a particularly “obesogenic” environment (Figure 2), but the vast majority of genetic factors are presumed to affect body weight enough to cause obesity only when specific environmental conditions pertain. You keep trying to make it out as if I or anyone else has claimed genetics to be the single causative factor - which it obviously isn't. That however isn't what we are arguing. Your initial statement was this: On March 31 2014 18:23 xM(Z wrote:also, being genetically predisposed (even if such a thing would exist), can not make you fat; food does however. I think I have sufficiently refuted that statement (obviously such a thing as being genetically predisposed does exist and can make you fat). from your own quote: genetics control human body weight - agreed from beginning. the same genes that make one obese can make another one skinny based on gene function, gene behavior, gene expression and so on - very logical but no one knows why. they just point fingers at parents, mcdonalds, sedentarism and whatnot. exceedingly rare gene variants do exist which results in = obese person without the need of an '“obesogenic” environment' - disease, diabetes and others. being 'genetically predisposed' can make you fatt- ER then the skinny people while doing what they do - very logical; after all, you are different, it's normal you'd be affected differently by the same things.
I don't propose to argue that genes entirely determine whether you are fat. A fat person exercising will lose a bit more weight than a fat person of the same genetic make up who did nothing. But genetic dispositions exist on a continuum, and I think it is unfair how you seem to paint fat people as generally.lazy and not.helping.thenselves. Some might be so genetically disposed to being fat that in order for them to take prevent measures like exercise requires a huge amount of will power as well as time and money. Fat people who are genetically disposed aren't weak willed - they just need more will power than us to exercise or diet or so on.
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On April 03 2014 00:46 levelping wrote:Show nested quote +On April 03 2014 00:26 xM(Z wrote:On April 02 2014 23:58 Ghostcom wrote:On April 02 2014 21:18 xM(Z wrote:the ncbi.nlm.nhi.gov article is hogwash. it just tries to explain/make sense of what is happening after it happened without even thinking of what started it or how it came to be like this. its just a long series of remarks like: this like that because it is like that. a quote from one of the studies based on which that paper was made: CONCLUSIONS: Genetic influences on BMI and abdominal adiposity are high in children born since the onset of the pediatric obesity epidemic. what caused the onset?. genes started mutating randomly and boom: from now on, thou shalt be fat?. lets say you inherited your fat genes from your parents, your parents from their parents and so on; but then wait, their grandparents weren't fat. they were skinny ... so then what?, how?, whom?, all of a sudden?. also, they made the study on 8 to 11 yr olds. some kids as old as 3 can and do eat 3000 calories a day. those are already damaged goods. the nature article, albeit old, it just says this: Genes contribute to obesity in many ways, by affecting appetite, satiety (the sense of fullness), metabolism, food cravings, body-fat distribution, and the tendency to use eating as a way to cope with stress. but with different words. The adipocyte-specific hormone leptin, the product of the obese (ob) gene,regulates adipose-tissue mass through hypothalamic effects on satiety and energy expenditure1, 2, 3, 4 http://www.news-medical.net/health/What-Does-Leptin-Do.aspxMechanisms and actions of leptin
Leptin acts as a hormone that modulates the size of the adipose tissues in the body. It regulates food intake and body weight. Leptin also acts on specific receptors in the hypothalamus to inhibit appetite through both counteractive and stimulatory mechanisms:
Leptin counteracts the effects of a feeding stimulant released in the gut called neuropeptide Y as well as the effects of a cannabinoid neurotransmitter called adandamide which stimulates appetite.
Leptin also promotes the synthesis of an appetite suppressant called α-melanocyte-stimulating hormone even if you read: https://en.wikipedia.org/wiki/Leptin#DiscoveryAfter a meeting where Friedman met Nobel Prize winner, Frenchman Roger Guillemin, he got a letter from him that he recalls saying, “I really liked what you had to say, but I have one quibble: you refer to these as obesity genes, but I think they are lean genes because the normal allele keeps you thin. But calling them lean genes sounds awkward. The nicest sounding root for thin is from Greek, so I propose you call ob and db ‘lepto-genes.’” So Friedman remembered Guillemin’s suggestion, and the hormone was named leptin.[16] Leptin was the first fat cell-derived hormone to be discovered. Subsequent studies confirmed that the db gene encoded the leptin receptor and that it was expressed in the hypothalamus, a region of the brain known to regulate food intake and body weight. The discovery of leptin has led to the elucidation of a robust physiologic system that maintains fat stores at a relatively constant level, which has been widely validated in several experimental rodent obesity models; nevertheless adequate proof of its equivalent operation in humans remains elusive. You didn't actually read the pubmed article did you? You do realise what you just called hogwash was peer-reviewed by medical experts? And that they actually do address your criticism? More than 300 genetic loci that are potentially involved in human body weight regulation have been identified through analyses in humans, rodents, and C elegans.16,17 Some exceedingly rare gene variants affect gene function and behavior to such an extent that obesity results even without a particularly “obesogenic” environment (Figure 2), but the vast majority of genetic factors are presumed to affect body weight enough to cause obesity only when specific environmental conditions pertain. You keep trying to make it out as if I or anyone else has claimed genetics to be the single causative factor - which it obviously isn't. That however isn't what we are arguing. Your initial statement was this: On March 31 2014 18:23 xM(Z wrote:also, being genetically predisposed (even if such a thing would exist), can not make you fat; food does however. I think I have sufficiently refuted that statement (obviously such a thing as being genetically predisposed does exist and can make you fat). from your own quote: genetics control human body weight - agreed from beginning. the same genes that make one obese can make another one skinny based on gene function, gene behavior, gene expression and so on - very logical but no one knows why. they just point fingers at parents, mcdonalds, sedentarism and whatnot. exceedingly rare gene variants do exist which results in = obese person without the need of an '“obesogenic” environment' - disease, diabetes and others. being 'genetically predisposed' can make you fatt- ER then the skinny people while doing what they do - very logical; after all, you are different, it's normal you'd be affected differently by the same things. I don't propose to argue that genes entirely determine whether you are fat. A fat person exercising will lose a bit more weight than a fat person of the same genetic make up who did nothing. But genetic dispositions exist on a continuum, and I think it is unfair how you seem to paint fat people as generally.lazy and not.helping.thenselves. Some might be so genetically disposed to being fat that in order for them to take prevent measures like exercise requires a huge amount of will power as well as time and money. Fat people who are genetically disposed aren't weak willed - they just need more will power than us to exercise or diet or so on.
No one believes genetics does not play a rol in weight gain/loss. The issue is that rising levels of obesity and overweightness amongst a 300 million people country can be hardly atributed to genetics as the most important factor, and as such, the main contributors COULD be attributed to glutony, lack of self control, sedentarism and lack of understanding in basic nutrition.
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On April 03 2014 10:22 GoTuNk! wrote:Show nested quote +On April 03 2014 00:46 levelping wrote:On April 03 2014 00:26 xM(Z wrote:On April 02 2014 23:58 Ghostcom wrote:On April 02 2014 21:18 xM(Z wrote:the ncbi.nlm.nhi.gov article is hogwash. it just tries to explain/make sense of what is happening after it happened without even thinking of what started it or how it came to be like this. its just a long series of remarks like: this like that because it is like that. a quote from one of the studies based on which that paper was made: CONCLUSIONS: Genetic influences on BMI and abdominal adiposity are high in children born since the onset of the pediatric obesity epidemic. what caused the onset?. genes started mutating randomly and boom: from now on, thou shalt be fat?. lets say you inherited your fat genes from your parents, your parents from their parents and so on; but then wait, their grandparents weren't fat. they were skinny ... so then what?, how?, whom?, all of a sudden?. also, they made the study on 8 to 11 yr olds. some kids as old as 3 can and do eat 3000 calories a day. those are already damaged goods. the nature article, albeit old, it just says this: Genes contribute to obesity in many ways, by affecting appetite, satiety (the sense of fullness), metabolism, food cravings, body-fat distribution, and the tendency to use eating as a way to cope with stress. but with different words. The adipocyte-specific hormone leptin, the product of the obese (ob) gene,regulates adipose-tissue mass through hypothalamic effects on satiety and energy expenditure1, 2, 3, 4 http://www.news-medical.net/health/What-Does-Leptin-Do.aspxMechanisms and actions of leptin
Leptin acts as a hormone that modulates the size of the adipose tissues in the body. It regulates food intake and body weight. Leptin also acts on specific receptors in the hypothalamus to inhibit appetite through both counteractive and stimulatory mechanisms:
Leptin counteracts the effects of a feeding stimulant released in the gut called neuropeptide Y as well as the effects of a cannabinoid neurotransmitter called adandamide which stimulates appetite.
Leptin also promotes the synthesis of an appetite suppressant called α-melanocyte-stimulating hormone even if you read: https://en.wikipedia.org/wiki/Leptin#DiscoveryAfter a meeting where Friedman met Nobel Prize winner, Frenchman Roger Guillemin, he got a letter from him that he recalls saying, “I really liked what you had to say, but I have one quibble: you refer to these as obesity genes, but I think they are lean genes because the normal allele keeps you thin. But calling them lean genes sounds awkward. The nicest sounding root for thin is from Greek, so I propose you call ob and db ‘lepto-genes.’” So Friedman remembered Guillemin’s suggestion, and the hormone was named leptin.[16] Leptin was the first fat cell-derived hormone to be discovered. Subsequent studies confirmed that the db gene encoded the leptin receptor and that it was expressed in the hypothalamus, a region of the brain known to regulate food intake and body weight. The discovery of leptin has led to the elucidation of a robust physiologic system that maintains fat stores at a relatively constant level, which has been widely validated in several experimental rodent obesity models; nevertheless adequate proof of its equivalent operation in humans remains elusive. You didn't actually read the pubmed article did you? You do realise what you just called hogwash was peer-reviewed by medical experts? And that they actually do address your criticism? More than 300 genetic loci that are potentially involved in human body weight regulation have been identified through analyses in humans, rodents, and C elegans.16,17 Some exceedingly rare gene variants affect gene function and behavior to such an extent that obesity results even without a particularly “obesogenic” environment (Figure 2), but the vast majority of genetic factors are presumed to affect body weight enough to cause obesity only when specific environmental conditions pertain. You keep trying to make it out as if I or anyone else has claimed genetics to be the single causative factor - which it obviously isn't. That however isn't what we are arguing. Your initial statement was this: On March 31 2014 18:23 xM(Z wrote:also, being genetically predisposed (even if such a thing would exist), can not make you fat; food does however. I think I have sufficiently refuted that statement (obviously such a thing as being genetically predisposed does exist and can make you fat). from your own quote: genetics control human body weight - agreed from beginning. the same genes that make one obese can make another one skinny based on gene function, gene behavior, gene expression and so on - very logical but no one knows why. they just point fingers at parents, mcdonalds, sedentarism and whatnot. exceedingly rare gene variants do exist which results in = obese person without the need of an '“obesogenic” environment' - disease, diabetes and others. being 'genetically predisposed' can make you fatt- ER then the skinny people while doing what they do - very logical; after all, you are different, it's normal you'd be affected differently by the same things. I don't propose to argue that genes entirely determine whether you are fat. A fat person exercising will lose a bit more weight than a fat person of the same genetic make up who did nothing. But genetic dispositions exist on a continuum, and I think it is unfair how you seem to paint fat people as generally.lazy and not.helping.thenselves. Some might be so genetically disposed to being fat that in order for them to take prevent measures like exercise requires a huge amount of will power as well as time and money. Fat people who are genetically disposed aren't weak willed - they just need more will power than us to exercise or diet or so on. No one believes genetics does not play a rol in weight gain/loss. The issue is that rising levels of obesity and overweightness amongst a 300 million people country can be hardly atributed to genetics as the most important factor, and as such, the main contributors COULD be attributed to glutony, lack of self control, sedentarism and lack of understanding in basic nutrition.
Well that's a check and a mate.
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On April 03 2014 20:03 Jumperer wrote:Show nested quote +On April 02 2014 10:15 kwizach wrote:On April 02 2014 09:35 GoTuNk! wrote:On April 02 2014 08:25 kwizach wrote:Just... no. First of all, the article itself acknowledges that even when you take into account "differences in occupations, positions, education, job tenure, or hours worked per week" between men and women, there is still an unexplained wage gap of 5 cents (actually, it's between 5 and 7 cents, and that's an average - some professions see higher wage gaps even with all of these factors taken into account). But that's not the point. Even if taking these factors into account reduced the wage gap to 0 all other things being equal, the fact is that overall, there is still a 23 cents wage gap between men and women. That women statistically tend to occupy jobs which pay less, are less stable and more part-time is not due to a biological difference between men and women - it's due to cultural factors and the perpetuation of gender roles which get integrated at a very young age. The article casually dismisses those explanations which have been well documented by social sciences, and replies that we should "respect the choices" of women, and that it is "demeaning" to question these choices. Yet nobody is telling individual women that they should not make the choices they're making - the point is that the tendencies we observe at a structural and collective level are not explained by individual choices taken separately: they're largely explained by the cultural factors I just mentioned. So, to sum up, there very much is a wage gap, and it needs to be addressed. So you are saying you can affirm with 100% certainty that the wage up is due to cultural differences and there is no chance that woman and men make different decisions in terms of studies/career choices because there are biological differences? As I wrote earlier in the topic, the decades of scientific research done on the matter do NOT establish the existence of such a biological determinism. If you want a very extensive look at the literature on the topic, I suggest you read Rebecca M. Jordan-Young's book Brain Storm: The Flaws in the Science of Sex Differences (2010), it's extremely exhaustive and well-documented. Her conclusions include that we are not blank slates (predispositions are not completely identical in individuals) but that the binary system of gender does not accurately capture initial differences. Beyond this, biology does not explain the structural differences in career choices between men and women. The first nine chapters of the book do an excellent job of outlining the current research to date. The arguments are on point, and describe the variables, both present and missing (or purposely ommited). Jordan-Young should be commended for the first nine chapters. However, Chapter 10, which I assume to be her thesis argument on the subject matter of sex difference, is flawed and strays completely from the argument outlined in the first nine chapters. Chapter 10 becomes a feminist diatribe that has lost all focus on brain organization as well as sex difference in general. Jordan-Young loses perspective and fails in the overall debate.
Since this is in no way, shape or form an accurate description of the book, and of chapter 10 in particular (in which Jordan-Young explores work done in developmental and evolutionary biology), I decide to google that little paragraph of yours, and sure enough you copy/pasted it entirely from a random Amazon review which happened to say something you thought would serve your argument, discarding the reviews which praise the book. Since that review is simply not true, I'm going to go ahead and ask you for a little intellectual honesty and to put aside the cognitive biases which led you to decide that the book was not accurate simply because it happens to destroy your beliefs with regards to the scope of the biological determinism of genders.
Again, scientific research points to extremely limited biological differences between genders in terms of cognitive features and abilities, differences which, in addition, have virtually no impact compared to the importance of how cognitive development proceeds as one grows up, irrespective of one's gender (hence the importance of fighting gender roles).
I was expecting a reference to such an article from your part, since the study referred to in the article indeed received a lot of publicity in the media when it came out at the end of 2013. Unfortunately for your argument, (1) the scientific results contained in the study do not actually say what was reported by numerous media outlets, including by your article (articles correcting earlier assessments were sometimes published later, such as in the Guardian), (2) the authors of the study themselves make claims which go beyond their actual results (for example, their conclusions presume brain structure to be independent of the environment in which it develops, which has been demonstrated to be false), (3) there are a number of methodological flaws in the study, or at least methodological points which prevent the results from telling us what you think they tell us with regards to gender differences, (4) the extrapolated conclusions from the author are inconsistent with previous research on the matter, in particular a "larger earlier study (from which the participants of the PNAS study were a subset)", as explained here.
You can find a huge article refuting the exact interpretations of the study that you are using as the basis of your argument here, but unfortunately it is in French (perhaps you can use a translator). Luckily, numerous neuroscientists rapidly posted articles online to challenge the erroneous interpretations of the paper that appeared in the media, as well as the flawed claims of the authors of the study themselves. You can find examples of these refutations here, here, here, here, here, here, etc. Some notably touch upon the very misleading image of the blue/yellow connections in female and male brains which appears at the top of the Independent article you linked to.
To sum up, and like I said earlier, the very small biological differences which can on average be observed in terms of cognition between men and women at birth pale in comparison to the flexibility with which the brain develops, in particular in connection to its environment. Biological gender is in this respect not the relevant factor, but the environment (notably culture, including gender roles) is. Biology does not explain the structural differences in career choices between men and women.
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EPT
