Welcome to Debate Club! Please be aware that this is a space for respectful debate, and that your ideas will be challenged here. Please remember to critique the argument, not the author.
Dr Sarah Hallburg: Calories in vs calories out pet peeve
Replies
-
midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »I have an insatiable appetite, and find that satiety isn't just how much volume I eat, but how many calories I eat. There was a time when I was so burdened with hunger and could never achieve calorie goals. Users would tell me to eat light (i.e. not calorie dense) foods because it would keep me full. One day, I ate more than 9 lbs. of salad and was still very hungry.
As for insulin, insulin resistance, and CICO, I believe the truth lies somewhere in the middle of the extremes (one extreme is that CICO is infallible, the other that CICO doesn't matter as long as your macros are the right percentages). I know there have been a lot of points made that weight loss is strictly about CICO and that there is no possible way that how your body moves energy around between glucose, glycogen, and fat will change without a change in CICO. Of course that is a simplistic view because most of us know that net carbs become glucose right away while protein and dietary fat do not. So immediately after eating (actually, while eating because some of that glucose is absorbed through capillaries in the mouth), energy is already affected by which macros you consumed. Continuing on for the next several hours, there are differences with how energy gets into your body, where it goes first, and where it goes next. These differences are not only based on the particular macros consumed, but also what amount and to what degree energy is needed within the proper time frames. And ultimately, timing is an important part of macro consumption and exercise - something that both the CICO method and the LCHF using macro percentages fails to consider.
As a double diabetic (meaning I have both type 1 and type 2 diabetes), I take a lot of insulin. I've also always had serious challenges losing weight, some of which no MFP user can explain. My endocrinologist says the reason I find it so hard to lose weight is because I need so much insulin. If I weighed less, I would be less insulin resistant and would need less insulin. So if I lose some weight, I will find it easier to lose weight. But it is nearly impossible to lose weight to get to where I can find it more possible to lose weight. It's a frustrating situation to encounter, to say the least. It is, on the other hand, really easy to gain weight. When I was first diagnosed with type 1, I was a healthy weight (to some standards, even slightly underweight... that isn't unusual because undiagnosed type 1 causes weight loss). I gained 20 lbs. in the first month after diagnosis and was already a bit overweight at that time. Over the next year, the gains slowed to where I gained 60 lbs. in the year and then another 60 lbs. over the next 1.5-2 years for a total of 120 lbs. of gain in 3 years. I can't lose anywhere near that fast. I really struggle to lose 1 lb. per month. So I agree that insulin does have an impact on weight gain and weight loss because my own experience has been impacted significantly by that exact issue.
CICO isn't a weight loss method, it is a fact of nature. Insulin can't create or destroy energy. Calorie counting is a method. There is no perfect way to track what someone's calories out are, which would include any energy costs of converting glucose into glycogen, or even de novo lipogensis. Your own physiology might be different such that normal calories out predictors are off for you. That doesn't mean there doesn't exist a level of activity that if you consistently stay above and a certain amount of calories that you consistently stay below that will cause weight loss (assuming otherwise proper nutrition).
I think it is more about the actual conversion of calories into energy. For example, those of us who are type 1's can get together and talk about how much 15g of net carbs will affect our blood glucose. We will all take different amounts of insulin, and part of that comes down to insulin resistance, but part of it is due to individual differences. All net carbs should be converted to glucose, and if a calorie is exactly the same for everyone, then 15g of net carbs will increase all of our BG's by the same amount. We will take different amounts of insulin to bring it back down again (and deliver as energy to cells or convert to fat) due to varying levels of insulin resistance, but the rise is exactly the same, right? Well... actually that is wrong. Put 100 type 1 diabetics in a room, give each of them the exact same number of net carbs, give no insulin bolus for the carbs, and measure blood glucose levels before and after full digestion. Chances are good that you will get 100 different numbers (though it is possible a few might be the same, by luck). So then for each individual, the same number of calories in does not result in the same amount of energy. Further complicated is the movement of that glucose to glycogen and/or fat. Now consider that protein and fat are digested differently to begin with, and they don't go directly to glucose either.
I think you mean the conversion of macros into energy.
Also, put 100 type 1s in a room, and probably all 100 have slightly different levels of severity of type 1 diabetes. That would explain the varying results with a more likely scenario than that the conversions are all significantly different (those pathways being very highly conserved). It would not change the effect that you observe, which is that the same amount of insulin for the same amount and type of macros does not produce the same results in different individuals.
Please explain exactly how type 1's can have "a different severity" of type 1.
Hint: It is only possible during the "honeymoon" period when one is in the process of developing type 1. Once all the pancratic beta cells are dead, all type 1's are of the same "severity."
So people with type 1 all lose beta cells at the same age and at the same rate until they are all gone? And this rate is known and documented when not involved in a study (so you can screen those 100 type 1s for those out of the 'honeymoon period' like you didn't say you would do)?
Don't think so, or the new research mentioned in this quote wouldn't have been necessary - it'd have been observed years ago. Plus, you'll notice that the findings were that most beta cells are lost. Which means everyone is not reaching the same nadir:
"In type 1 diabetes, the beta cells do not produce enough insulin. This is generally due to the death of the beta cells. By the time someone is diagnosed with type 1 diabetes, they may have lost 70-80% of their beta cells (it is thought, although more recent studies are testing this number). Beta cell loss occurs gradually over time, beginning before diagnosis, and continuing afterwards, until most beta cells are lost (Cnop et al. 2005). However, new research is also finding that some people with type 1 continue to produce insulin for many years (Davis et al. 2014; Oram et al. 2014), and that beta cell dysfunction (not just death) may also be a significant cause of high blood sugar, at least around the time of diagnosis (Pugliese et al. 2014)."
You'll also note that they are also exploring the possibility that beta cell dysfunction and not death may be an issue. Dollars to donuts that is the case - where there are multiple ways to get a phenotype you can bet all will occur. I would speculate that while the dysfunction may eventually lead to death, it is probably on a similar timescale meaning the person could be producing some level of insulin for years - or maybe not. Mayb
0 -
midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »I have an insatiable appetite, and find that satiety isn't just how much volume I eat, but how many calories I eat. There was a time when I was so burdened with hunger and could never achieve calorie goals. Users would tell me to eat light (i.e. not calorie dense) foods because it would keep me full. One day, I ate more than 9 lbs. of salad and was still very hungry.
As for insulin, insulin resistance, and CICO, I believe the truth lies somewhere in the middle of the extremes (one extreme is that CICO is infallible, the other that CICO doesn't matter as long as your macros are the right percentages). I know there have been a lot of points made that weight loss is strictly about CICO and that there is no possible way that how your body moves energy around between glucose, glycogen, and fat will change without a change in CICO. Of course that is a simplistic view because most of us know that net carbs become glucose right away while protein and dietary fat do not. So immediately after eating (actually, while eating because some of that glucose is absorbed through capillaries in the mouth), energy is already affected by which macros you consumed. Continuing on for the next several hours, there are differences with how energy gets into your body, where it goes first, and where it goes next. These differences are not only based on the particular macros consumed, but also what amount and to what degree energy is needed within the proper time frames. And ultimately, timing is an important part of macro consumption and exercise - something that both the CICO method and the LCHF using macro percentages fails to consider.
As a double diabetic (meaning I have both type 1 and type 2 diabetes), I take a lot of insulin. I've also always had serious challenges losing weight, some of which no MFP user can explain. My endocrinologist says the reason I find it so hard to lose weight is because I need so much insulin. If I weighed less, I would be less insulin resistant and would need less insulin. So if I lose some weight, I will find it easier to lose weight. But it is nearly impossible to lose weight to get to where I can find it more possible to lose weight. It's a frustrating situation to encounter, to say the least. It is, on the other hand, really easy to gain weight. When I was first diagnosed with type 1, I was a healthy weight (to some standards, even slightly underweight... that isn't unusual because undiagnosed type 1 causes weight loss). I gained 20 lbs. in the first month after diagnosis and was already a bit overweight at that time. Over the next year, the gains slowed to where I gained 60 lbs. in the year and then another 60 lbs. over the next 1.5-2 years for a total of 120 lbs. of gain in 3 years. I can't lose anywhere near that fast. I really struggle to lose 1 lb. per month. So I agree that insulin does have an impact on weight gain and weight loss because my own experience has been impacted significantly by that exact issue.
CICO isn't a weight loss method, it is a fact of nature. Insulin can't create or destroy energy. Calorie counting is a method. There is no perfect way to track what someone's calories out are, which would include any energy costs of converting glucose into glycogen, or even de novo lipogensis. Your own physiology might be different such that normal calories out predictors are off for you. That doesn't mean there doesn't exist a level of activity that if you consistently stay above and a certain amount of calories that you consistently stay below that will cause weight loss (assuming otherwise proper nutrition).
I think it is more about the actual conversion of calories into energy. For example, those of us who are type 1's can get together and talk about how much 15g of net carbs will affect our blood glucose. We will all take different amounts of insulin, and part of that comes down to insulin resistance, but part of it is due to individual differences. All net carbs should be converted to glucose, and if a calorie is exactly the same for everyone, then 15g of net carbs will increase all of our BG's by the same amount. We will take different amounts of insulin to bring it back down again (and deliver as energy to cells or convert to fat) due to varying levels of insulin resistance, but the rise is exactly the same, right? Well... actually that is wrong. Put 100 type 1 diabetics in a room, give each of them the exact same number of net carbs, give no insulin bolus for the carbs, and measure blood glucose levels before and after full digestion. Chances are good that you will get 100 different numbers (though it is possible a few might be the same, by luck). So then for each individual, the same number of calories in does not result in the same amount of energy. Further complicated is the movement of that glucose to glycogen and/or fat. Now consider that protein and fat are digested differently to begin with, and they don't go directly to glucose either.
I think you mean the conversion of macros into energy.
Also, put 100 type 1s in a room, and probably all 100 have slightly different levels of severity of type 1 diabetes. That would explain the varying results with a more likely scenario than that the conversions are all significantly different (those pathways being very highly conserved). It would not change the effect that you observe, which is that the same amount of insulin for the same amount and type of macros does not produce the same results in different individuals.
Please explain exactly how type 1's can have "a different severity" of type 1.
Hint: It is only possible during the "honeymoon" period when one is in the process of developing type 1. Once all the pancratic beta cells are dead, all type 1's are of the same "severity."
So people with type 1 all lose beta cells at the same age and at the same rate until they are all gone? And this rate is known and documented when not involved in a study (so you can screen those 100 type 1s for those out of the 'honeymoon period' like you didn't say you would do)?
Don't think so, or the new research mentioned in this quote wouldn't have been necessary - it'd have been observed years ago. Plus, you'll notice that the findings were that most beta cells are lost. Which means everyone is not reaching the same nadir:
"In type 1 diabetes, the beta cells do not produce enough insulin. This is generally due to the death of the beta cells. By the time someone is diagnosed with type 1 diabetes, they may have lost 70-80% of their beta cells (it is thought, although more recent studies are testing this number). Beta cell loss occurs gradually over time, beginning before diagnosis, and continuing afterwards, until most beta cells are lost (Cnop et al. 2005). However, new research is also finding that some people with type 1 continue to produce insulin for many years (Davis et al. 2014; Oram et al. 2014), and that beta cell dysfunction (not just death) may also be a significant cause of high blood sugar, at least around the time of diagnosis (Pugliese et al. 2014)."
You'll also note that they are also exploring the possibility that beta cell dysfunction and not death may be an issue. Dollars to donuts that is the case - where there are multiple ways to get a phenotype you can bet all will occur. I would speculate that while the dysfunction may eventually lead to death, it is probably on a similar timescale meaning the person could be producing some level of insulin for years - or maybe not. Mayb
Age of onset is irrelevant when one compares those who have type 1's. Your argument is that, if we compare all persons at a specific age who at some point get type 1 diabetes regardless of whether they have type 1 or not at the specified age, some have a different "severity" of type 1 because the auto-immune response hasn't yet been triggered (in other words, they don't have type 1 at all at that age).
As I pointed out, the early stages of type 1 (known as the honeymoon stage) is going to be different because the disease is in the process of being created. This starts when the autoimmune response is triggered and ends when all or nearly all beta cells have been depleted. Once that has phase has ended, all type 1's are of the same "severity" in that we all don't make insulin. It's been known for at least decades (I personally have known for decades and learned from those who knew for decades before) that the honeymoon process takes several years. The reason it is news (or at least a reminder) for some is because more and more cases are being identified of adult-onset type 1 (now referred to as LADA or "type 1.5") where the honeymoon phase sometimes takes 10 years or longer. For quite some time (and to a lesser extent, this still happens), type 1's with adult onset (LADA / type 1.5) were misdiagnosed as type 2 because diagnosis was made based on symptoms rather than the underlying cause.
As far as beta cell dysfunction, it is highly unlikely. Type 1 diabetes is an auto-immune disease. My immune system attacked my pancreatic beta cells not to disarm beta cells, but to remove them.0 -
nope, just making a point that it is not necessary to blow out your fat minimum because one thinks carbs are evil..
not sure what is fiction about that statement...
the fictional reference bolded. FUD.
worrying about potential cardiovascular health impacts
that is why I used the qualifier "potential" ....potential means could happen not will happen...
yes, the potential cardiovascular health impacts of the high carbohydrate dietary recommendations are a worry.0 -
I have only skimmed this thread, but basically this woman wants you to think you need her method to lose weight. She hates the term CICO, because it reveals that you don't need anyone's book/product/advice or whatever to lose weight.
Some people love LCHF lifestyles - I wont knock them if they're healthier and happier. I love cake and mashed potatoes.0 -
midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »I have an insatiable appetite, and find that satiety isn't just how much volume I eat, but how many calories I eat. There was a time when I was so burdened with hunger and could never achieve calorie goals. Users would tell me to eat light (i.e. not calorie dense) foods because it would keep me full. One day, I ate more than 9 lbs. of salad and was still very hungry.
As for insulin, insulin resistance, and CICO, I believe the truth lies somewhere in the middle of the extremes (one extreme is that CICO is infallible, the other that CICO doesn't matter as long as your macros are the right percentages). I know there have been a lot of points made that weight loss is strictly about CICO and that there is no possible way that how your body moves energy around between glucose, glycogen, and fat will change without a change in CICO. Of course that is a simplistic view because most of us know that net carbs become glucose right away while protein and dietary fat do not. So immediately after eating (actually, while eating because some of that glucose is absorbed through capillaries in the mouth), energy is already affected by which macros you consumed. Continuing on for the next several hours, there are differences with how energy gets into your body, where it goes first, and where it goes next. These differences are not only based on the particular macros consumed, but also what amount and to what degree energy is needed within the proper time frames. And ultimately, timing is an important part of macro consumption and exercise - something that both the CICO method and the LCHF using macro percentages fails to consider.
As a double diabetic (meaning I have both type 1 and type 2 diabetes), I take a lot of insulin. I've also always had serious challenges losing weight, some of which no MFP user can explain. My endocrinologist says the reason I find it so hard to lose weight is because I need so much insulin. If I weighed less, I would be less insulin resistant and would need less insulin. So if I lose some weight, I will find it easier to lose weight. But it is nearly impossible to lose weight to get to where I can find it more possible to lose weight. It's a frustrating situation to encounter, to say the least. It is, on the other hand, really easy to gain weight. When I was first diagnosed with type 1, I was a healthy weight (to some standards, even slightly underweight... that isn't unusual because undiagnosed type 1 causes weight loss). I gained 20 lbs. in the first month after diagnosis and was already a bit overweight at that time. Over the next year, the gains slowed to where I gained 60 lbs. in the year and then another 60 lbs. over the next 1.5-2 years for a total of 120 lbs. of gain in 3 years. I can't lose anywhere near that fast. I really struggle to lose 1 lb. per month. So I agree that insulin does have an impact on weight gain and weight loss because my own experience has been impacted significantly by that exact issue.
CICO isn't a weight loss method, it is a fact of nature. Insulin can't create or destroy energy. Calorie counting is a method. There is no perfect way to track what someone's calories out are, which would include any energy costs of converting glucose into glycogen, or even de novo lipogensis. Your own physiology might be different such that normal calories out predictors are off for you. That doesn't mean there doesn't exist a level of activity that if you consistently stay above and a certain amount of calories that you consistently stay below that will cause weight loss (assuming otherwise proper nutrition).
I think it is more about the actual conversion of calories into energy. For example, those of us who are type 1's can get together and talk about how much 15g of net carbs will affect our blood glucose. We will all take different amounts of insulin, and part of that comes down to insulin resistance, but part of it is due to individual differences. All net carbs should be converted to glucose, and if a calorie is exactly the same for everyone, then 15g of net carbs will increase all of our BG's by the same amount. We will take different amounts of insulin to bring it back down again (and deliver as energy to cells or convert to fat) due to varying levels of insulin resistance, but the rise is exactly the same, right? Well... actually that is wrong. Put 100 type 1 diabetics in a room, give each of them the exact same number of net carbs, give no insulin bolus for the carbs, and measure blood glucose levels before and after full digestion. Chances are good that you will get 100 different numbers (though it is possible a few might be the same, by luck). So then for each individual, the same number of calories in does not result in the same amount of energy. Further complicated is the movement of that glucose to glycogen and/or fat. Now consider that protein and fat are digested differently to begin with, and they don't go directly to glucose either.
I think you mean the conversion of macros into energy.
Also, put 100 type 1s in a room, and probably all 100 have slightly different levels of severity of type 1 diabetes. That would explain the varying results with a more likely scenario than that the conversions are all significantly different (those pathways being very highly conserved). It would not change the effect that you observe, which is that the same amount of insulin for the same amount and type of macros does not produce the same results in different individuals.
Please explain exactly how type 1's can have "a different severity" of type 1.
Hint: It is only possible during the "honeymoon" period when one is in the process of developing type 1. Once all the pancratic beta cells are dead, all type 1's are of the same "severity."
So people with type 1 all lose beta cells at the same age and at the same rate until they are all gone? And this rate is known and documented when not involved in a study (so you can screen those 100 type 1s for those out of the 'honeymoon period' like you didn't say you would do)?
Don't think so, or the new research mentioned in this quote wouldn't have been necessary - it'd have been observed years ago. Plus, you'll notice that the findings were that most beta cells are lost. Which means everyone is not reaching the same nadir:
"In type 1 diabetes, the beta cells do not produce enough insulin. This is generally due to the death of the beta cells. By the time someone is diagnosed with type 1 diabetes, they may have lost 70-80% of their beta cells (it is thought, although more recent studies are testing this number). Beta cell loss occurs gradually over time, beginning before diagnosis, and continuing afterwards, until most beta cells are lost (Cnop et al. 2005). However, new research is also finding that some people with type 1 continue to produce insulin for many years (Davis et al. 2014; Oram et al. 2014), and that beta cell dysfunction (not just death) may also be a significant cause of high blood sugar, at least around the time of diagnosis (Pugliese et al. 2014)."
You'll also note that they are also exploring the possibility that beta cell dysfunction and not death may be an issue. Dollars to donuts that is the case - where there are multiple ways to get a phenotype you can bet all will occur. I would speculate that while the dysfunction may eventually lead to death, it is probably on a similar timescale meaning the person could be producing some level of insulin for years - or maybe not. Mayb
Age of onset is irrelevant when one compares those who have type 1's. Your argument is that, if we compare all persons at a specific age who at some point get type 1 diabetes regardless of whether they have type 1 or not at the specified age, some have a different "severity" of type 1 because the auto-immune response hasn't yet been triggered (in other words, they don't have type 1 at all at that age).
As I pointed out, the early stages of type 1 (known as the honeymoon stage) is going to be different because the disease is in the process of being created. This starts when the autoimmune response is triggered and ends when all or nearly all beta cells have been depleted. Once that has phase has ended, all type 1's are of the same "severity" in that we all don't make insulin. It's been known for at least decades (I personally have known for decades and learned from those who knew for decades before) that the honeymoon process takes several years. The reason it is news (or at least a reminder) for some is because more and more cases are being identified of adult-onset type 1 (now referred to as LADA or "type 1.5") where the honeymoon phase sometimes takes 10 years or longer. For quite some time (and to a lesser extent, this still happens), type 1's with adult onset (LADA / type 1.5) were misdiagnosed as type 2 because diagnosis was made based on symptoms rather than the underlying cause.
As far as beta cell dysfunction, it is highly unlikely. Type 1 diabetes is an auto-immune disease. My immune system attacked my pancreatic beta cells not to disarm beta cells, but to remove them.
Actually, no, my point is that if you take 100 random type 1s you have no idea if they've all at the same stage or not. Some may have gotten as low as they ever will. Some may not have as of yet.
Even if you assume that all have reached their nadir, you have no idea if all of their 'most are dead' are at the same functional level or not. There is variance.
Just so you know, I've been involved in quite a bit of autoimmune research. I'm not ignorant of the basic mechanisms of that class of diseases. Just because a disease is autoimmune does not necessarily mean the effects are all or nothing. The fact that Type 1 diabetes is an autoimmune disease does not make it any more or less likely that some individuals may have dysfunctional beta cells rather than killed beta cells.0 -
midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »I have an insatiable appetite, and find that satiety isn't just how much volume I eat, but how many calories I eat. There was a time when I was so burdened with hunger and could never achieve calorie goals. Users would tell me to eat light (i.e. not calorie dense) foods because it would keep me full. One day, I ate more than 9 lbs. of salad and was still very hungry.
As for insulin, insulin resistance, and CICO, I believe the truth lies somewhere in the middle of the extremes (one extreme is that CICO is infallible, the other that CICO doesn't matter as long as your macros are the right percentages). I know there have been a lot of points made that weight loss is strictly about CICO and that there is no possible way that how your body moves energy around between glucose, glycogen, and fat will change without a change in CICO. Of course that is a simplistic view because most of us know that net carbs become glucose right away while protein and dietary fat do not. So immediately after eating (actually, while eating because some of that glucose is absorbed through capillaries in the mouth), energy is already affected by which macros you consumed. Continuing on for the next several hours, there are differences with how energy gets into your body, where it goes first, and where it goes next. These differences are not only based on the particular macros consumed, but also what amount and to what degree energy is needed within the proper time frames. And ultimately, timing is an important part of macro consumption and exercise - something that both the CICO method and the LCHF using macro percentages fails to consider.
As a double diabetic (meaning I have both type 1 and type 2 diabetes), I take a lot of insulin. I've also always had serious challenges losing weight, some of which no MFP user can explain. My endocrinologist says the reason I find it so hard to lose weight is because I need so much insulin. If I weighed less, I would be less insulin resistant and would need less insulin. So if I lose some weight, I will find it easier to lose weight. But it is nearly impossible to lose weight to get to where I can find it more possible to lose weight. It's a frustrating situation to encounter, to say the least. It is, on the other hand, really easy to gain weight. When I was first diagnosed with type 1, I was a healthy weight (to some standards, even slightly underweight... that isn't unusual because undiagnosed type 1 causes weight loss). I gained 20 lbs. in the first month after diagnosis and was already a bit overweight at that time. Over the next year, the gains slowed to where I gained 60 lbs. in the year and then another 60 lbs. over the next 1.5-2 years for a total of 120 lbs. of gain in 3 years. I can't lose anywhere near that fast. I really struggle to lose 1 lb. per month. So I agree that insulin does have an impact on weight gain and weight loss because my own experience has been impacted significantly by that exact issue.
CICO isn't a weight loss method, it is a fact of nature. Insulin can't create or destroy energy. Calorie counting is a method. There is no perfect way to track what someone's calories out are, which would include any energy costs of converting glucose into glycogen, or even de novo lipogensis. Your own physiology might be different such that normal calories out predictors are off for you. That doesn't mean there doesn't exist a level of activity that if you consistently stay above and a certain amount of calories that you consistently stay below that will cause weight loss (assuming otherwise proper nutrition).
I think it is more about the actual conversion of calories into energy. For example, those of us who are type 1's can get together and talk about how much 15g of net carbs will affect our blood glucose. We will all take different amounts of insulin, and part of that comes down to insulin resistance, but part of it is due to individual differences. All net carbs should be converted to glucose, and if a calorie is exactly the same for everyone, then 15g of net carbs will increase all of our BG's by the same amount. We will take different amounts of insulin to bring it back down again (and deliver as energy to cells or convert to fat) due to varying levels of insulin resistance, but the rise is exactly the same, right? Well... actually that is wrong. Put 100 type 1 diabetics in a room, give each of them the exact same number of net carbs, give no insulin bolus for the carbs, and measure blood glucose levels before and after full digestion. Chances are good that you will get 100 different numbers (though it is possible a few might be the same, by luck). So then for each individual, the same number of calories in does not result in the same amount of energy. Further complicated is the movement of that glucose to glycogen and/or fat. Now consider that protein and fat are digested differently to begin with, and they don't go directly to glucose either.
I think you mean the conversion of macros into energy.
Also, put 100 type 1s in a room, and probably all 100 have slightly different levels of severity of type 1 diabetes. That would explain the varying results with a more likely scenario than that the conversions are all significantly different (those pathways being very highly conserved). It would not change the effect that you observe, which is that the same amount of insulin for the same amount and type of macros does not produce the same results in different individuals.
Please explain exactly how type 1's can have "a different severity" of type 1.
Hint: It is only possible during the "honeymoon" period when one is in the process of developing type 1. Once all the pancratic beta cells are dead, all type 1's are of the same "severity."
So people with type 1 all lose beta cells at the same age and at the same rate until they are all gone? And this rate is known and documented when not involved in a study (so you can screen those 100 type 1s for those out of the 'honeymoon period' like you didn't say you would do)?
Don't think so, or the new research mentioned in this quote wouldn't have been necessary - it'd have been observed years ago. Plus, you'll notice that the findings were that most beta cells are lost. Which means everyone is not reaching the same nadir:
"In type 1 diabetes, the beta cells do not produce enough insulin. This is generally due to the death of the beta cells. By the time someone is diagnosed with type 1 diabetes, they may have lost 70-80% of their beta cells (it is thought, although more recent studies are testing this number). Beta cell loss occurs gradually over time, beginning before diagnosis, and continuing afterwards, until most beta cells are lost (Cnop et al. 2005). However, new research is also finding that some people with type 1 continue to produce insulin for many years (Davis et al. 2014; Oram et al. 2014), and that beta cell dysfunction (not just death) may also be a significant cause of high blood sugar, at least around the time of diagnosis (Pugliese et al. 2014)."
You'll also note that they are also exploring the possibility that beta cell dysfunction and not death may be an issue. Dollars to donuts that is the case - where there are multiple ways to get a phenotype you can bet all will occur. I would speculate that while the dysfunction may eventually lead to death, it is probably on a similar timescale meaning the person could be producing some level of insulin for years - or maybe not. Mayb
Age of onset is irrelevant when one compares those who have type 1's. Your argument is that, if we compare all persons at a specific age who at some point get type 1 diabetes regardless of whether they have type 1 or not at the specified age, some have a different "severity" of type 1 because the auto-immune response hasn't yet been triggered (in other words, they don't have type 1 at all at that age).
As I pointed out, the early stages of type 1 (known as the honeymoon stage) is going to be different because the disease is in the process of being created. This starts when the autoimmune response is triggered and ends when all or nearly all beta cells have been depleted. Once that has phase has ended, all type 1's are of the same "severity" in that we all don't make insulin. It's been known for at least decades (I personally have known for decades and learned from those who knew for decades before) that the honeymoon process takes several years. The reason it is news (or at least a reminder) for some is because more and more cases are being identified of adult-onset type 1 (now referred to as LADA or "type 1.5") where the honeymoon phase sometimes takes 10 years or longer. For quite some time (and to a lesser extent, this still happens), type 1's with adult onset (LADA / type 1.5) were misdiagnosed as type 2 because diagnosis was made based on symptoms rather than the underlying cause.
As far as beta cell dysfunction, it is highly unlikely. Type 1 diabetes is an auto-immune disease. My immune system attacked my pancreatic beta cells not to disarm beta cells, but to remove them.
Actually, no, my point is that if you take 100 random type 1s you have no idea if they've all at the same stage or not. Some may have gotten as low as they ever will. Some may not have as of yet.
Even if you assume that all have reached their nadir, you have no idea if all of their 'most are dead' are at the same functional level or not. There is variance.
Just so you know, I've been involved in quite a bit of autoimmune research. I'm not ignorant of the basic mechanisms of that class of diseases. Just because a disease is autoimmune does not necessarily mean the effects are all or nothing. The fact that Type 1 diabetes is an autoimmune disease does not make it any more or less likely that some individuals may have dysfunctional beta cells rather than killed beta cells.
Again, correct for all variables and you will find that a gram of carbs does not become the same amount of energy for everyone. I think you have missed my point by focusing on variables and arguing the extent to which they can be controlled for in research. My point still stands, even if you can't figure out how to design a study to prove or disprove it with 100% accuracy.0 -
nope, just making a point that it is not necessary to blow out your fat minimum because one thinks carbs are evil..
not sure what is fiction about that statement...
the fictional reference bolded. FUD.
worrying about potential cardiovascular health impacts
that is why I used the qualifier "potential" ....potential means could happen not will happen...
yes, the potential cardiovascular health impacts of the high carbohydrate fat dietary recommendations are a worry.
*0 -
midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »I have an insatiable appetite, and find that satiety isn't just how much volume I eat, but how many calories I eat. There was a time when I was so burdened with hunger and could never achieve calorie goals. Users would tell me to eat light (i.e. not calorie dense) foods because it would keep me full. One day, I ate more than 9 lbs. of salad and was still very hungry.
As for insulin, insulin resistance, and CICO, I believe the truth lies somewhere in the middle of the extremes (one extreme is that CICO is infallible, the other that CICO doesn't matter as long as your macros are the right percentages). I know there have been a lot of points made that weight loss is strictly about CICO and that there is no possible way that how your body moves energy around between glucose, glycogen, and fat will change without a change in CICO. Of course that is a simplistic view because most of us know that net carbs become glucose right away while protein and dietary fat do not. So immediately after eating (actually, while eating because some of that glucose is absorbed through capillaries in the mouth), energy is already affected by which macros you consumed. Continuing on for the next several hours, there are differences with how energy gets into your body, where it goes first, and where it goes next. These differences are not only based on the particular macros consumed, but also what amount and to what degree energy is needed within the proper time frames. And ultimately, timing is an important part of macro consumption and exercise - something that both the CICO method and the LCHF using macro percentages fails to consider.
As a double diabetic (meaning I have both type 1 and type 2 diabetes), I take a lot of insulin. I've also always had serious challenges losing weight, some of which no MFP user can explain. My endocrinologist says the reason I find it so hard to lose weight is because I need so much insulin. If I weighed less, I would be less insulin resistant and would need less insulin. So if I lose some weight, I will find it easier to lose weight. But it is nearly impossible to lose weight to get to where I can find it more possible to lose weight. It's a frustrating situation to encounter, to say the least. It is, on the other hand, really easy to gain weight. When I was first diagnosed with type 1, I was a healthy weight (to some standards, even slightly underweight... that isn't unusual because undiagnosed type 1 causes weight loss). I gained 20 lbs. in the first month after diagnosis and was already a bit overweight at that time. Over the next year, the gains slowed to where I gained 60 lbs. in the year and then another 60 lbs. over the next 1.5-2 years for a total of 120 lbs. of gain in 3 years. I can't lose anywhere near that fast. I really struggle to lose 1 lb. per month. So I agree that insulin does have an impact on weight gain and weight loss because my own experience has been impacted significantly by that exact issue.
CICO isn't a weight loss method, it is a fact of nature. Insulin can't create or destroy energy. Calorie counting is a method. There is no perfect way to track what someone's calories out are, which would include any energy costs of converting glucose into glycogen, or even de novo lipogensis. Your own physiology might be different such that normal calories out predictors are off for you. That doesn't mean there doesn't exist a level of activity that if you consistently stay above and a certain amount of calories that you consistently stay below that will cause weight loss (assuming otherwise proper nutrition).
I think it is more about the actual conversion of calories into energy. For example, those of us who are type 1's can get together and talk about how much 15g of net carbs will affect our blood glucose. We will all take different amounts of insulin, and part of that comes down to insulin resistance, but part of it is due to individual differences. All net carbs should be converted to glucose, and if a calorie is exactly the same for everyone, then 15g of net carbs will increase all of our BG's by the same amount. We will take different amounts of insulin to bring it back down again (and deliver as energy to cells or convert to fat) due to varying levels of insulin resistance, but the rise is exactly the same, right? Well... actually that is wrong. Put 100 type 1 diabetics in a room, give each of them the exact same number of net carbs, give no insulin bolus for the carbs, and measure blood glucose levels before and after full digestion. Chances are good that you will get 100 different numbers (though it is possible a few might be the same, by luck). So then for each individual, the same number of calories in does not result in the same amount of energy. Further complicated is the movement of that glucose to glycogen and/or fat. Now consider that protein and fat are digested differently to begin with, and they don't go directly to glucose either.
I think you mean the conversion of macros into energy.
Also, put 100 type 1s in a room, and probably all 100 have slightly different levels of severity of type 1 diabetes. That would explain the varying results with a more likely scenario than that the conversions are all significantly different (those pathways being very highly conserved). It would not change the effect that you observe, which is that the same amount of insulin for the same amount and type of macros does not produce the same results in different individuals.
Please explain exactly how type 1's can have "a different severity" of type 1.
Hint: It is only possible during the "honeymoon" period when one is in the process of developing type 1. Once all the pancratic beta cells are dead, all type 1's are of the same "severity."
So people with type 1 all lose beta cells at the same age and at the same rate until they are all gone? And this rate is known and documented when not involved in a study (so you can screen those 100 type 1s for those out of the 'honeymoon period' like you didn't say you would do)?
Don't think so, or the new research mentioned in this quote wouldn't have been necessary - it'd have been observed years ago. Plus, you'll notice that the findings were that most beta cells are lost. Which means everyone is not reaching the same nadir:
"In type 1 diabetes, the beta cells do not produce enough insulin. This is generally due to the death of the beta cells. By the time someone is diagnosed with type 1 diabetes, they may have lost 70-80% of their beta cells (it is thought, although more recent studies are testing this number). Beta cell loss occurs gradually over time, beginning before diagnosis, and continuing afterwards, until most beta cells are lost (Cnop et al. 2005). However, new research is also finding that some people with type 1 continue to produce insulin for many years (Davis et al. 2014; Oram et al. 2014), and that beta cell dysfunction (not just death) may also be a significant cause of high blood sugar, at least around the time of diagnosis (Pugliese et al. 2014)."
You'll also note that they are also exploring the possibility that beta cell dysfunction and not death may be an issue. Dollars to donuts that is the case - where there are multiple ways to get a phenotype you can bet all will occur. I would speculate that while the dysfunction may eventually lead to death, it is probably on a similar timescale meaning the person could be producing some level of insulin for years - or maybe not. Mayb
Age of onset is irrelevant when one compares those who have type 1's. Your argument is that, if we compare all persons at a specific age who at some point get type 1 diabetes regardless of whether they have type 1 or not at the specified age, some have a different "severity" of type 1 because the auto-immune response hasn't yet been triggered (in other words, they don't have type 1 at all at that age).
As I pointed out, the early stages of type 1 (known as the honeymoon stage) is going to be different because the disease is in the process of being created. This starts when the autoimmune response is triggered and ends when all or nearly all beta cells have been depleted. Once that has phase has ended, all type 1's are of the same "severity" in that we all don't make insulin. It's been known for at least decades (I personally have known for decades and learned from those who knew for decades before) that the honeymoon process takes several years. The reason it is news (or at least a reminder) for some is because more and more cases are being identified of adult-onset type 1 (now referred to as LADA or "type 1.5") where the honeymoon phase sometimes takes 10 years or longer. For quite some time (and to a lesser extent, this still happens), type 1's with adult onset (LADA / type 1.5) were misdiagnosed as type 2 because diagnosis was made based on symptoms rather than the underlying cause.
As far as beta cell dysfunction, it is highly unlikely. Type 1 diabetes is an auto-immune disease. My immune system attacked my pancreatic beta cells not to disarm beta cells, but to remove them.
Actually, no, my point is that if you take 100 random type 1s you have no idea if they've all at the same stage or not. Some may have gotten as low as they ever will. Some may not have as of yet.
Even if you assume that all have reached their nadir, you have no idea if all of their 'most are dead' are at the same functional level or not. There is variance.
Just so you know, I've been involved in quite a bit of autoimmune research. I'm not ignorant of the basic mechanisms of that class of diseases. Just because a disease is autoimmune does not necessarily mean the effects are all or nothing. The fact that Type 1 diabetes is an autoimmune disease does not make it any more or less likely that some individuals may have dysfunctional beta cells rather than killed beta cells.
Again, correct for all variables and you will find that a gram of carbs does not become the same amount of energy for everyone. I think you have missed my point by focusing on variables and arguing the extent to which they can be controlled for in research. My point still stands, even if you can't figure out how to design a study to prove or disprove it with 100% accuracy.
This seems like a variant of "well we're not all machines, so calories aren't calories" argument.
Which strikes me as a problem because let's make an analogy about T1D's.
Let's take a standardized measure of calories - the amount available in one gallon of regular 87 octane gasoline
Let's take two 1985 chevy impalas. Now, we'll accept that we've controlled that by being two 1985 chevy impalas with same options, they clearly are more alike than even two identical twin humans. Right down to they have the same size gas tank so the 1 gallon is going to fit similarly.
No one would say a calorie isn't a calorie because two people using the cars can drive them different distances on 1 gallon of gas, even if those two distances are equal work because the terrain is the same. Everyone would say of course things like how fast you burn the gas and accelerate, what the cars actual condition is, etc, are all going to impact how far you can travel on that one gallon of gas. No one would argue the gasoline in the two vehicles was different because of the recorded MPG was different, even though they're the same kind of car. It would be held as a poor argument. Yet people use this argument about humans all the time and human individuality to argue that calories aren't calories because people aren't machines. Well, as far as thermodynamics are concerned, we are machine, we have to obey the known laws of physics, and as far as comparisons go, machines aren't machines - they don't all function the same either, even when they're built to the same standards. This doesn't negate the fact that properly test, 87 octane has, on average, the same amount of calories burnable by properly calibrated equipment per gallon. Within the limits of the food itself we make, it is similar. And yes, just like the MPG sticker on the car, there will be variance on what you get out of them in practical, day to day life. It doesn't mean the gasoline is the issue, or that energy doesn't matter, or that if you take the same car and give it more gasoline, it is probably going to drive further.
Humans will of course be a little more complex. We're kind of like a plug-in hybrid, having different energy sources we can use long and short term, but energy is energy.0 -
2snakeswoman wrote: »I usually ignore advice from people with something to sell.
^^^^^^^THIS0 -
midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »I have an insatiable appetite, and find that satiety isn't just how much volume I eat, but how many calories I eat. There was a time when I was so burdened with hunger and could never achieve calorie goals. Users would tell me to eat light (i.e. not calorie dense) foods because it would keep me full. One day, I ate more than 9 lbs. of salad and was still very hungry.
As for insulin, insulin resistance, and CICO, I believe the truth lies somewhere in the middle of the extremes (one extreme is that CICO is infallible, the other that CICO doesn't matter as long as your macros are the right percentages). I know there have been a lot of points made that weight loss is strictly about CICO and that there is no possible way that how your body moves energy around between glucose, glycogen, and fat will change without a change in CICO. Of course that is a simplistic view because most of us know that net carbs become glucose right away while protein and dietary fat do not. So immediately after eating (actually, while eating because some of that glucose is absorbed through capillaries in the mouth), energy is already affected by which macros you consumed. Continuing on for the next several hours, there are differences with how energy gets into your body, where it goes first, and where it goes next. These differences are not only based on the particular macros consumed, but also what amount and to what degree energy is needed within the proper time frames. And ultimately, timing is an important part of macro consumption and exercise - something that both the CICO method and the LCHF using macro percentages fails to consider.
As a double diabetic (meaning I have both type 1 and type 2 diabetes), I take a lot of insulin. I've also always had serious challenges losing weight, some of which no MFP user can explain. My endocrinologist says the reason I find it so hard to lose weight is because I need so much insulin. If I weighed less, I would be less insulin resistant and would need less insulin. So if I lose some weight, I will find it easier to lose weight. But it is nearly impossible to lose weight to get to where I can find it more possible to lose weight. It's a frustrating situation to encounter, to say the least. It is, on the other hand, really easy to gain weight. When I was first diagnosed with type 1, I was a healthy weight (to some standards, even slightly underweight... that isn't unusual because undiagnosed type 1 causes weight loss). I gained 20 lbs. in the first month after diagnosis and was already a bit overweight at that time. Over the next year, the gains slowed to where I gained 60 lbs. in the year and then another 60 lbs. over the next 1.5-2 years for a total of 120 lbs. of gain in 3 years. I can't lose anywhere near that fast. I really struggle to lose 1 lb. per month. So I agree that insulin does have an impact on weight gain and weight loss because my own experience has been impacted significantly by that exact issue.
CICO isn't a weight loss method, it is a fact of nature. Insulin can't create or destroy energy. Calorie counting is a method. There is no perfect way to track what someone's calories out are, which would include any energy costs of converting glucose into glycogen, or even de novo lipogensis. Your own physiology might be different such that normal calories out predictors are off for you. That doesn't mean there doesn't exist a level of activity that if you consistently stay above and a certain amount of calories that you consistently stay below that will cause weight loss (assuming otherwise proper nutrition).
I think it is more about the actual conversion of calories into energy. For example, those of us who are type 1's can get together and talk about how much 15g of net carbs will affect our blood glucose. We will all take different amounts of insulin, and part of that comes down to insulin resistance, but part of it is due to individual differences. All net carbs should be converted to glucose, and if a calorie is exactly the same for everyone, then 15g of net carbs will increase all of our BG's by the same amount. We will take different amounts of insulin to bring it back down again (and deliver as energy to cells or convert to fat) due to varying levels of insulin resistance, but the rise is exactly the same, right? Well... actually that is wrong. Put 100 type 1 diabetics in a room, give each of them the exact same number of net carbs, give no insulin bolus for the carbs, and measure blood glucose levels before and after full digestion. Chances are good that you will get 100 different numbers (though it is possible a few might be the same, by luck). So then for each individual, the same number of calories in does not result in the same amount of energy. Further complicated is the movement of that glucose to glycogen and/or fat. Now consider that protein and fat are digested differently to begin with, and they don't go directly to glucose either.
I think you mean the conversion of macros into energy.
Also, put 100 type 1s in a room, and probably all 100 have slightly different levels of severity of type 1 diabetes. That would explain the varying results with a more likely scenario than that the conversions are all significantly different (those pathways being very highly conserved). It would not change the effect that you observe, which is that the same amount of insulin for the same amount and type of macros does not produce the same results in different individuals.
Please explain exactly how type 1's can have "a different severity" of type 1.
Hint: It is only possible during the "honeymoon" period when one is in the process of developing type 1. Once all the pancratic beta cells are dead, all type 1's are of the same "severity."
So people with type 1 all lose beta cells at the same age and at the same rate until they are all gone? And this rate is known and documented when not involved in a study (so you can screen those 100 type 1s for those out of the 'honeymoon period' like you didn't say you would do)?
Don't think so, or the new research mentioned in this quote wouldn't have been necessary - it'd have been observed years ago. Plus, you'll notice that the findings were that most beta cells are lost. Which means everyone is not reaching the same nadir:
"In type 1 diabetes, the beta cells do not produce enough insulin. This is generally due to the death of the beta cells. By the time someone is diagnosed with type 1 diabetes, they may have lost 70-80% of their beta cells (it is thought, although more recent studies are testing this number). Beta cell loss occurs gradually over time, beginning before diagnosis, and continuing afterwards, until most beta cells are lost (Cnop et al. 2005). However, new research is also finding that some people with type 1 continue to produce insulin for many years (Davis et al. 2014; Oram et al. 2014), and that beta cell dysfunction (not just death) may also be a significant cause of high blood sugar, at least around the time of diagnosis (Pugliese et al. 2014)."
You'll also note that they are also exploring the possibility that beta cell dysfunction and not death may be an issue. Dollars to donuts that is the case - where there are multiple ways to get a phenotype you can bet all will occur. I would speculate that while the dysfunction may eventually lead to death, it is probably on a similar timescale meaning the person could be producing some level of insulin for years - or maybe not. Mayb
Age of onset is irrelevant when one compares those who have type 1's. Your argument is that, if we compare all persons at a specific age who at some point get type 1 diabetes regardless of whether they have type 1 or not at the specified age, some have a different "severity" of type 1 because the auto-immune response hasn't yet been triggered (in other words, they don't have type 1 at all at that age).
As I pointed out, the early stages of type 1 (known as the honeymoon stage) is going to be different because the disease is in the process of being created. This starts when the autoimmune response is triggered and ends when all or nearly all beta cells have been depleted. Once that has phase has ended, all type 1's are of the same "severity" in that we all don't make insulin. It's been known for at least decades (I personally have known for decades and learned from those who knew for decades before) that the honeymoon process takes several years. The reason it is news (or at least a reminder) for some is because more and more cases are being identified of adult-onset type 1 (now referred to as LADA or "type 1.5") where the honeymoon phase sometimes takes 10 years or longer. For quite some time (and to a lesser extent, this still happens), type 1's with adult onset (LADA / type 1.5) were misdiagnosed as type 2 because diagnosis was made based on symptoms rather than the underlying cause.
As far as beta cell dysfunction, it is highly unlikely. Type 1 diabetes is an auto-immune disease. My immune system attacked my pancreatic beta cells not to disarm beta cells, but to remove them.
Actually, no, my point is that if you take 100 random type 1s you have no idea if they've all at the same stage or not. Some may have gotten as low as they ever will. Some may not have as of yet.
Even if you assume that all have reached their nadir, you have no idea if all of their 'most are dead' are at the same functional level or not. There is variance.
Just so you know, I've been involved in quite a bit of autoimmune research. I'm not ignorant of the basic mechanisms of that class of diseases. Just because a disease is autoimmune does not necessarily mean the effects are all or nothing. The fact that Type 1 diabetes is an autoimmune disease does not make it any more or less likely that some individuals may have dysfunctional beta cells rather than killed beta cells.
Again, correct for all variables and you will find that a gram of carbs does not become the same amount of energy for everyone. I think you have missed my point by focusing on variables and arguing the extent to which they can be controlled for in research. My point still stands, even if you can't figure out how to design a study to prove or disprove it with 100% accuracy.
This seems like a variant of "well we're not all machines, so calories aren't calories" argument.
Which strikes me as a problem because let's make an analogy about T1D's.
Let's take a standardized measure of calories - the amount available in one gallon of regular 87 octane gasoline
Let's take two 1985 chevy impalas. Now, we'll accept that we've controlled that by being two 1985 chevy impalas with same options, they clearly are more alike than even two identical twin humans. Right down to they have the same size gas tank so the 1 gallon is going to fit similarly.
No one would say a calorie isn't a calorie because two people using the cars can drive them different distances on 1 gallon of gas, even if those two distances are equal work because the terrain is the same. Everyone would say of course things like how fast you burn the gas and accelerate, what the cars actual condition is, etc, are all going to impact how far you can travel on that one gallon of gas. No one would argue the gasoline in the two vehicles was different because of the recorded MPG was different, even though they're the same kind of car. It would be held as a poor argument. Yet people use this argument about humans all the time and human individuality to argue that calories aren't calories because people aren't machines. Well, as far as thermodynamics are concerned, we are machine, we have to obey the known laws of physics, and as far as comparisons go, machines aren't machines - they don't all function the same either, even when they're built to the same standards. This doesn't negate the fact that properly test, 87 octane has, on average, the same amount of calories burnable by properly calibrated equipment per gallon. Within the limits of the food itself we make, it is similar. And yes, just like the MPG sticker on the car, there will be variance on what you get out of them in practical, day to day life. It doesn't mean the gasoline is the issue, or that energy doesn't matter, or that if you take the same car and give it more gasoline, it is probably going to drive further.
Humans will of course be a little more complex. We're kind of like a plug-in hybrid, having different energy sources we can use long and short term, but energy is energy.
I'm not saying that the "gasoline" (calories) is different. I'm saying they don't get digested and used quite the same in every person. I wish it were as simple as how many believe CICO works, but it is more complicated than that.0 -
2snakeswoman wrote: »
I usually ignore advice from people with something to sell.
^^^^^^^THIS
Why do people say this??
Just about everyone with a website on the www has something to sell. What about your doctor, he is selling you his service, do you not listen to him either?0 -
midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »I have an insatiable appetite, and find that satiety isn't just how much volume I eat, but how many calories I eat. There was a time when I was so burdened with hunger and could never achieve calorie goals. Users would tell me to eat light (i.e. not calorie dense) foods because it would keep me full. One day, I ate more than 9 lbs. of salad and was still very hungry.
As for insulin, insulin resistance, and CICO, I believe the truth lies somewhere in the middle of the extremes (one extreme is that CICO is infallible, the other that CICO doesn't matter as long as your macros are the right percentages). I know there have been a lot of points made that weight loss is strictly about CICO and that there is no possible way that how your body moves energy around between glucose, glycogen, and fat will change without a change in CICO. Of course that is a simplistic view because most of us know that net carbs become glucose right away while protein and dietary fat do not. So immediately after eating (actually, while eating because some of that glucose is absorbed through capillaries in the mouth), energy is already affected by which macros you consumed. Continuing on for the next several hours, there are differences with how energy gets into your body, where it goes first, and where it goes next. These differences are not only based on the particular macros consumed, but also what amount and to what degree energy is needed within the proper time frames. And ultimately, timing is an important part of macro consumption and exercise - something that both the CICO method and the LCHF using macro percentages fails to consider.
As a double diabetic (meaning I have both type 1 and type 2 diabetes), I take a lot of insulin. I've also always had serious challenges losing weight, some of which no MFP user can explain. My endocrinologist says the reason I find it so hard to lose weight is because I need so much insulin. If I weighed less, I would be less insulin resistant and would need less insulin. So if I lose some weight, I will find it easier to lose weight. But it is nearly impossible to lose weight to get to where I can find it more possible to lose weight. It's a frustrating situation to encounter, to say the least. It is, on the other hand, really easy to gain weight. When I was first diagnosed with type 1, I was a healthy weight (to some standards, even slightly underweight... that isn't unusual because undiagnosed type 1 causes weight loss). I gained 20 lbs. in the first month after diagnosis and was already a bit overweight at that time. Over the next year, the gains slowed to where I gained 60 lbs. in the year and then another 60 lbs. over the next 1.5-2 years for a total of 120 lbs. of gain in 3 years. I can't lose anywhere near that fast. I really struggle to lose 1 lb. per month. So I agree that insulin does have an impact on weight gain and weight loss because my own experience has been impacted significantly by that exact issue.
CICO isn't a weight loss method, it is a fact of nature. Insulin can't create or destroy energy. Calorie counting is a method. There is no perfect way to track what someone's calories out are, which would include any energy costs of converting glucose into glycogen, or even de novo lipogensis. Your own physiology might be different such that normal calories out predictors are off for you. That doesn't mean there doesn't exist a level of activity that if you consistently stay above and a certain amount of calories that you consistently stay below that will cause weight loss (assuming otherwise proper nutrition).
I think it is more about the actual conversion of calories into energy. For example, those of us who are type 1's can get together and talk about how much 15g of net carbs will affect our blood glucose. We will all take different amounts of insulin, and part of that comes down to insulin resistance, but part of it is due to individual differences. All net carbs should be converted to glucose, and if a calorie is exactly the same for everyone, then 15g of net carbs will increase all of our BG's by the same amount. We will take different amounts of insulin to bring it back down again (and deliver as energy to cells or convert to fat) due to varying levels of insulin resistance, but the rise is exactly the same, right? Well... actually that is wrong. Put 100 type 1 diabetics in a room, give each of them the exact same number of net carbs, give no insulin bolus for the carbs, and measure blood glucose levels before and after full digestion. Chances are good that you will get 100 different numbers (though it is possible a few might be the same, by luck). So then for each individual, the same number of calories in does not result in the same amount of energy. Further complicated is the movement of that glucose to glycogen and/or fat. Now consider that protein and fat are digested differently to begin with, and they don't go directly to glucose either.
I think you mean the conversion of macros into energy.
Also, put 100 type 1s in a room, and probably all 100 have slightly different levels of severity of type 1 diabetes. That would explain the varying results with a more likely scenario than that the conversions are all significantly different (those pathways being very highly conserved). It would not change the effect that you observe, which is that the same amount of insulin for the same amount and type of macros does not produce the same results in different individuals.
Please explain exactly how type 1's can have "a different severity" of type 1.
Hint: It is only possible during the "honeymoon" period when one is in the process of developing type 1. Once all the pancratic beta cells are dead, all type 1's are of the same "severity."
So people with type 1 all lose beta cells at the same age and at the same rate until they are all gone? And this rate is known and documented when not involved in a study (so you can screen those 100 type 1s for those out of the 'honeymoon period' like you didn't say you would do)?
Don't think so, or the new research mentioned in this quote wouldn't have been necessary - it'd have been observed years ago. Plus, you'll notice that the findings were that most beta cells are lost. Which means everyone is not reaching the same nadir:
"In type 1 diabetes, the beta cells do not produce enough insulin. This is generally due to the death of the beta cells. By the time someone is diagnosed with type 1 diabetes, they may have lost 70-80% of their beta cells (it is thought, although more recent studies are testing this number). Beta cell loss occurs gradually over time, beginning before diagnosis, and continuing afterwards, until most beta cells are lost (Cnop et al. 2005). However, new research is also finding that some people with type 1 continue to produce insulin for many years (Davis et al. 2014; Oram et al. 2014), and that beta cell dysfunction (not just death) may also be a significant cause of high blood sugar, at least around the time of diagnosis (Pugliese et al. 2014)."
You'll also note that they are also exploring the possibility that beta cell dysfunction and not death may be an issue. Dollars to donuts that is the case - where there are multiple ways to get a phenotype you can bet all will occur. I would speculate that while the dysfunction may eventually lead to death, it is probably on a similar timescale meaning the person could be producing some level of insulin for years - or maybe not. Mayb
Age of onset is irrelevant when one compares those who have type 1's. Your argument is that, if we compare all persons at a specific age who at some point get type 1 diabetes regardless of whether they have type 1 or not at the specified age, some have a different "severity" of type 1 because the auto-immune response hasn't yet been triggered (in other words, they don't have type 1 at all at that age).
As I pointed out, the early stages of type 1 (known as the honeymoon stage) is going to be different because the disease is in the process of being created. This starts when the autoimmune response is triggered and ends when all or nearly all beta cells have been depleted. Once that has phase has ended, all type 1's are of the same "severity" in that we all don't make insulin. It's been known for at least decades (I personally have known for decades and learned from those who knew for decades before) that the honeymoon process takes several years. The reason it is news (or at least a reminder) for some is because more and more cases are being identified of adult-onset type 1 (now referred to as LADA or "type 1.5") where the honeymoon phase sometimes takes 10 years or longer. For quite some time (and to a lesser extent, this still happens), type 1's with adult onset (LADA / type 1.5) were misdiagnosed as type 2 because diagnosis was made based on symptoms rather than the underlying cause.
As far as beta cell dysfunction, it is highly unlikely. Type 1 diabetes is an auto-immune disease. My immune system attacked my pancreatic beta cells not to disarm beta cells, but to remove them.
Actually, no, my point is that if you take 100 random type 1s you have no idea if they've all at the same stage or not. Some may have gotten as low as they ever will. Some may not have as of yet.
Even if you assume that all have reached their nadir, you have no idea if all of their 'most are dead' are at the same functional level or not. There is variance.
Just so you know, I've been involved in quite a bit of autoimmune research. I'm not ignorant of the basic mechanisms of that class of diseases. Just because a disease is autoimmune does not necessarily mean the effects are all or nothing. The fact that Type 1 diabetes is an autoimmune disease does not make it any more or less likely that some individuals may have dysfunctional beta cells rather than killed beta cells.
Again, correct for all variables and you will find that a gram of carbs does not become the same amount of energy for everyone. I think you have missed my point by focusing on variables and arguing the extent to which they can be controlled for in research. My point still stands, even if you can't figure out how to design a study to prove or disprove it with 100% accuracy.
This seems like a variant of "well we're not all machines, so calories aren't calories" argument.
Which strikes me as a problem because let's make an analogy about T1D's.
Let's take a standardized measure of calories - the amount available in one gallon of regular 87 octane gasoline
Let's take two 1985 chevy impalas. Now, we'll accept that we've controlled that by being two 1985 chevy impalas with same options, they clearly are more alike than even two identical twin humans. Right down to they have the same size gas tank so the 1 gallon is going to fit similarly.
No one would say a calorie isn't a calorie because two people using the cars can drive them different distances on 1 gallon of gas, even if those two distances are equal work because the terrain is the same. Everyone would say of course things like how fast you burn the gas and accelerate, what the cars actual condition is, etc, are all going to impact how far you can travel on that one gallon of gas. No one would argue the gasoline in the two vehicles was different because of the recorded MPG was different, even though they're the same kind of car. It would be held as a poor argument. Yet people use this argument about humans all the time and human individuality to argue that calories aren't calories because people aren't machines. Well, as far as thermodynamics are concerned, we are machine, we have to obey the known laws of physics, and as far as comparisons go, machines aren't machines - they don't all function the same either, even when they're built to the same standards. This doesn't negate the fact that properly test, 87 octane has, on average, the same amount of calories burnable by properly calibrated equipment per gallon. Within the limits of the food itself we make, it is similar. And yes, just like the MPG sticker on the car, there will be variance on what you get out of them in practical, day to day life. It doesn't mean the gasoline is the issue, or that energy doesn't matter, or that if you take the same car and give it more gasoline, it is probably going to drive further.
Humans will of course be a little more complex. We're kind of like a plug-in hybrid, having different energy sources we can use long and short term, but energy is energy.
I'm not saying that the "gasoline" (calories) is different. I'm saying they don't get digested and used quite the same in every person. I wish it were as simple as how many believe CICO works, but it is more complicated than that.
They'll get used differently by the same person even. Doesn't really change you can do pretty accurate estimates based on mileage and gas tank emptying to figure out the MPG of your driving style for the vehicle, so long as one is diligent in record keeping.0 -
midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »I have an insatiable appetite, and find that satiety isn't just how much volume I eat, but how many calories I eat. There was a time when I was so burdened with hunger and could never achieve calorie goals. Users would tell me to eat light (i.e. not calorie dense) foods because it would keep me full. One day, I ate more than 9 lbs. of salad and was still very hungry.
As for insulin, insulin resistance, and CICO, I believe the truth lies somewhere in the middle of the extremes (one extreme is that CICO is infallible, the other that CICO doesn't matter as long as your macros are the right percentages). I know there have been a lot of points made that weight loss is strictly about CICO and that there is no possible way that how your body moves energy around between glucose, glycogen, and fat will change without a change in CICO. Of course that is a simplistic view because most of us know that net carbs become glucose right away while protein and dietary fat do not. So immediately after eating (actually, while eating because some of that glucose is absorbed through capillaries in the mouth), energy is already affected by which macros you consumed. Continuing on for the next several hours, there are differences with how energy gets into your body, where it goes first, and where it goes next. These differences are not only based on the particular macros consumed, but also what amount and to what degree energy is needed within the proper time frames. And ultimately, timing is an important part of macro consumption and exercise - something that both the CICO method and the LCHF using macro percentages fails to consider.
As a double diabetic (meaning I have both type 1 and type 2 diabetes), I take a lot of insulin. I've also always had serious challenges losing weight, some of which no MFP user can explain. My endocrinologist says the reason I find it so hard to lose weight is because I need so much insulin. If I weighed less, I would be less insulin resistant and would need less insulin. So if I lose some weight, I will find it easier to lose weight. But it is nearly impossible to lose weight to get to where I can find it more possible to lose weight. It's a frustrating situation to encounter, to say the least. It is, on the other hand, really easy to gain weight. When I was first diagnosed with type 1, I was a healthy weight (to some standards, even slightly underweight... that isn't unusual because undiagnosed type 1 causes weight loss). I gained 20 lbs. in the first month after diagnosis and was already a bit overweight at that time. Over the next year, the gains slowed to where I gained 60 lbs. in the year and then another 60 lbs. over the next 1.5-2 years for a total of 120 lbs. of gain in 3 years. I can't lose anywhere near that fast. I really struggle to lose 1 lb. per month. So I agree that insulin does have an impact on weight gain and weight loss because my own experience has been impacted significantly by that exact issue.
CICO isn't a weight loss method, it is a fact of nature. Insulin can't create or destroy energy. Calorie counting is a method. There is no perfect way to track what someone's calories out are, which would include any energy costs of converting glucose into glycogen, or even de novo lipogensis. Your own physiology might be different such that normal calories out predictors are off for you. That doesn't mean there doesn't exist a level of activity that if you consistently stay above and a certain amount of calories that you consistently stay below that will cause weight loss (assuming otherwise proper nutrition).
I think it is more about the actual conversion of calories into energy. For example, those of us who are type 1's can get together and talk about how much 15g of net carbs will affect our blood glucose. We will all take different amounts of insulin, and part of that comes down to insulin resistance, but part of it is due to individual differences. All net carbs should be converted to glucose, and if a calorie is exactly the same for everyone, then 15g of net carbs will increase all of our BG's by the same amount. We will take different amounts of insulin to bring it back down again (and deliver as energy to cells or convert to fat) due to varying levels of insulin resistance, but the rise is exactly the same, right? Well... actually that is wrong. Put 100 type 1 diabetics in a room, give each of them the exact same number of net carbs, give no insulin bolus for the carbs, and measure blood glucose levels before and after full digestion. Chances are good that you will get 100 different numbers (though it is possible a few might be the same, by luck). So then for each individual, the same number of calories in does not result in the same amount of energy. Further complicated is the movement of that glucose to glycogen and/or fat. Now consider that protein and fat are digested differently to begin with, and they don't go directly to glucose either.
I think you mean the conversion of macros into energy.
Also, put 100 type 1s in a room, and probably all 100 have slightly different levels of severity of type 1 diabetes. That would explain the varying results with a more likely scenario than that the conversions are all significantly different (those pathways being very highly conserved). It would not change the effect that you observe, which is that the same amount of insulin for the same amount and type of macros does not produce the same results in different individuals.
Please explain exactly how type 1's can have "a different severity" of type 1.
Hint: It is only possible during the "honeymoon" period when one is in the process of developing type 1. Once all the pancratic beta cells are dead, all type 1's are of the same "severity."
So people with type 1 all lose beta cells at the same age and at the same rate until they are all gone? And this rate is known and documented when not involved in a study (so you can screen those 100 type 1s for those out of the 'honeymoon period' like you didn't say you would do)?
Don't think so, or the new research mentioned in this quote wouldn't have been necessary - it'd have been observed years ago. Plus, you'll notice that the findings were that most beta cells are lost. Which means everyone is not reaching the same nadir:
"In type 1 diabetes, the beta cells do not produce enough insulin. This is generally due to the death of the beta cells. By the time someone is diagnosed with type 1 diabetes, they may have lost 70-80% of their beta cells (it is thought, although more recent studies are testing this number). Beta cell loss occurs gradually over time, beginning before diagnosis, and continuing afterwards, until most beta cells are lost (Cnop et al. 2005). However, new research is also finding that some people with type 1 continue to produce insulin for many years (Davis et al. 2014; Oram et al. 2014), and that beta cell dysfunction (not just death) may also be a significant cause of high blood sugar, at least around the time of diagnosis (Pugliese et al. 2014)."
You'll also note that they are also exploring the possibility that beta cell dysfunction and not death may be an issue. Dollars to donuts that is the case - where there are multiple ways to get a phenotype you can bet all will occur. I would speculate that while the dysfunction may eventually lead to death, it is probably on a similar timescale meaning the person could be producing some level of insulin for years - or maybe not. Mayb
Age of onset is irrelevant when one compares those who have type 1's. Your argument is that, if we compare all persons at a specific age who at some point get type 1 diabetes regardless of whether they have type 1 or not at the specified age, some have a different "severity" of type 1 because the auto-immune response hasn't yet been triggered (in other words, they don't have type 1 at all at that age).
As I pointed out, the early stages of type 1 (known as the honeymoon stage) is going to be different because the disease is in the process of being created. This starts when the autoimmune response is triggered and ends when all or nearly all beta cells have been depleted. Once that has phase has ended, all type 1's are of the same "severity" in that we all don't make insulin. It's been known for at least decades (I personally have known for decades and learned from those who knew for decades before) that the honeymoon process takes several years. The reason it is news (or at least a reminder) for some is because more and more cases are being identified of adult-onset type 1 (now referred to as LADA or "type 1.5") where the honeymoon phase sometimes takes 10 years or longer. For quite some time (and to a lesser extent, this still happens), type 1's with adult onset (LADA / type 1.5) were misdiagnosed as type 2 because diagnosis was made based on symptoms rather than the underlying cause.
As far as beta cell dysfunction, it is highly unlikely. Type 1 diabetes is an auto-immune disease. My immune system attacked my pancreatic beta cells not to disarm beta cells, but to remove them.
Actually, no, my point is that if you take 100 random type 1s you have no idea if they've all at the same stage or not. Some may have gotten as low as they ever will. Some may not have as of yet.
Even if you assume that all have reached their nadir, you have no idea if all of their 'most are dead' are at the same functional level or not. There is variance.
Just so you know, I've been involved in quite a bit of autoimmune research. I'm not ignorant of the basic mechanisms of that class of diseases. Just because a disease is autoimmune does not necessarily mean the effects are all or nothing. The fact that Type 1 diabetes is an autoimmune disease does not make it any more or less likely that some individuals may have dysfunctional beta cells rather than killed beta cells.
Again, correct for all variables and you will find that a gram of carbs does not become the same amount of energy for everyone. I think you have missed my point by focusing on variables and arguing the extent to which they can be controlled for in research. My point still stands, even if you can't figure out how to design a study to prove or disprove it with 100% accuracy.
This seems like a variant of "well we're not all machines, so calories aren't calories" argument.
Which strikes me as a problem because let's make an analogy about T1D's.
Let's take a standardized measure of calories - the amount available in one gallon of regular 87 octane gasoline
Let's take two 1985 chevy impalas. Now, we'll accept that we've controlled that by being two 1985 chevy impalas with same options, they clearly are more alike than even two identical twin humans. Right down to they have the same size gas tank so the 1 gallon is going to fit similarly.
No one would say a calorie isn't a calorie because two people using the cars can drive them different distances on 1 gallon of gas, even if those two distances are equal work because the terrain is the same. Everyone would say of course things like how fast you burn the gas and accelerate, what the cars actual condition is, etc, are all going to impact how far you can travel on that one gallon of gas. No one would argue the gasoline in the two vehicles was different because of the recorded MPG was different, even though they're the same kind of car. It would be held as a poor argument. Yet people use this argument about humans all the time and human individuality to argue that calories aren't calories because people aren't machines. Well, as far as thermodynamics are concerned, we are machine, we have to obey the known laws of physics, and as far as comparisons go, machines aren't machines - they don't all function the same either, even when they're built to the same standards. This doesn't negate the fact that properly test, 87 octane has, on average, the same amount of calories burnable by properly calibrated equipment per gallon. Within the limits of the food itself we make, it is similar. And yes, just like the MPG sticker on the car, there will be variance on what you get out of them in practical, day to day life. It doesn't mean the gasoline is the issue, or that energy doesn't matter, or that if you take the same car and give it more gasoline, it is probably going to drive further.
Humans will of course be a little more complex. We're kind of like a plug-in hybrid, having different energy sources we can use long and short term, but energy is energy.
I'm not saying that the "gasoline" (calories) is different. I'm saying they don't get digested and used quite the same in every person. I wish it were as simple as how many believe CICO works, but it is more complicated than that.
They'll get used differently by the same person even. Doesn't really change you can do pretty accurate estimates based on mileage and gas tank emptying to figure out the MPG of your driving style for the vehicle, so long as one is diligent in record keeping.
This. Those estimates are way more accurate than many people give them credit for.0 -
I don't think she has anything to sell. I am curious as to what if she does.
lololol.
http://fitteru.us/about/0 -
nope, just making a point that it is not necessary to blow out your fat minimum because one thinks carbs are evil..
not sure what is fiction about that statement...
the fictional reference bolded. FUD.
worrying about potential cardiovascular health impacts
that is why I used the qualifier "potential" ....potential means could happen not will happen...
yes, the potential cardiovascular health impacts of the high carbohydrate dietary recommendations are a worry.
So vegans/vegetarians/blue zones all have high rates of CVD? Obesity has a much causality than carbs. And I am pretty sure, saturated fats are still higher than carbs in terms of correlation.
0 -
midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »I have an insatiable appetite, and find that satiety isn't just how much volume I eat, but how many calories I eat. There was a time when I was so burdened with hunger and could never achieve calorie goals. Users would tell me to eat light (i.e. not calorie dense) foods because it would keep me full. One day, I ate more than 9 lbs. of salad and was still very hungry.
As for insulin, insulin resistance, and CICO, I believe the truth lies somewhere in the middle of the extremes (one extreme is that CICO is infallible, the other that CICO doesn't matter as long as your macros are the right percentages). I know there have been a lot of points made that weight loss is strictly about CICO and that there is no possible way that how your body moves energy around between glucose, glycogen, and fat will change without a change in CICO. Of course that is a simplistic view because most of us know that net carbs become glucose right away while protein and dietary fat do not. So immediately after eating (actually, while eating because some of that glucose is absorbed through capillaries in the mouth), energy is already affected by which macros you consumed. Continuing on for the next several hours, there are differences with how energy gets into your body, where it goes first, and where it goes next. These differences are not only based on the particular macros consumed, but also what amount and to what degree energy is needed within the proper time frames. And ultimately, timing is an important part of macro consumption and exercise - something that both the CICO method and the LCHF using macro percentages fails to consider.
As a double diabetic (meaning I have both type 1 and type 2 diabetes), I take a lot of insulin. I've also always had serious challenges losing weight, some of which no MFP user can explain. My endocrinologist says the reason I find it so hard to lose weight is because I need so much insulin. If I weighed less, I would be less insulin resistant and would need less insulin. So if I lose some weight, I will find it easier to lose weight. But it is nearly impossible to lose weight to get to where I can find it more possible to lose weight. It's a frustrating situation to encounter, to say the least. It is, on the other hand, really easy to gain weight. When I was first diagnosed with type 1, I was a healthy weight (to some standards, even slightly underweight... that isn't unusual because undiagnosed type 1 causes weight loss). I gained 20 lbs. in the first month after diagnosis and was already a bit overweight at that time. Over the next year, the gains slowed to where I gained 60 lbs. in the year and then another 60 lbs. over the next 1.5-2 years for a total of 120 lbs. of gain in 3 years. I can't lose anywhere near that fast. I really struggle to lose 1 lb. per month. So I agree that insulin does have an impact on weight gain and weight loss because my own experience has been impacted significantly by that exact issue.
CICO isn't a weight loss method, it is a fact of nature. Insulin can't create or destroy energy. Calorie counting is a method. There is no perfect way to track what someone's calories out are, which would include any energy costs of converting glucose into glycogen, or even de novo lipogensis. Your own physiology might be different such that normal calories out predictors are off for you. That doesn't mean there doesn't exist a level of activity that if you consistently stay above and a certain amount of calories that you consistently stay below that will cause weight loss (assuming otherwise proper nutrition).
I think it is more about the actual conversion of calories into energy. For example, those of us who are type 1's can get together and talk about how much 15g of net carbs will affect our blood glucose. We will all take different amounts of insulin, and part of that comes down to insulin resistance, but part of it is due to individual differences. All net carbs should be converted to glucose, and if a calorie is exactly the same for everyone, then 15g of net carbs will increase all of our BG's by the same amount. We will take different amounts of insulin to bring it back down again (and deliver as energy to cells or convert to fat) due to varying levels of insulin resistance, but the rise is exactly the same, right? Well... actually that is wrong. Put 100 type 1 diabetics in a room, give each of them the exact same number of net carbs, give no insulin bolus for the carbs, and measure blood glucose levels before and after full digestion. Chances are good that you will get 100 different numbers (though it is possible a few might be the same, by luck). So then for each individual, the same number of calories in does not result in the same amount of energy. Further complicated is the movement of that glucose to glycogen and/or fat. Now consider that protein and fat are digested differently to begin with, and they don't go directly to glucose either.
I think you mean the conversion of macros into energy.
Also, put 100 type 1s in a room, and probably all 100 have slightly different levels of severity of type 1 diabetes. That would explain the varying results with a more likely scenario than that the conversions are all significantly different (those pathways being very highly conserved). It would not change the effect that you observe, which is that the same amount of insulin for the same amount and type of macros does not produce the same results in different individuals.
Please explain exactly how type 1's can have "a different severity" of type 1.
Hint: It is only possible during the "honeymoon" period when one is in the process of developing type 1. Once all the pancratic beta cells are dead, all type 1's are of the same "severity."
So people with type 1 all lose beta cells at the same age and at the same rate until they are all gone? And this rate is known and documented when not involved in a study (so you can screen those 100 type 1s for those out of the 'honeymoon period' like you didn't say you would do)?
Don't think so, or the new research mentioned in this quote wouldn't have been necessary - it'd have been observed years ago. Plus, you'll notice that the findings were that most beta cells are lost. Which means everyone is not reaching the same nadir:
"In type 1 diabetes, the beta cells do not produce enough insulin. This is generally due to the death of the beta cells. By the time someone is diagnosed with type 1 diabetes, they may have lost 70-80% of their beta cells (it is thought, although more recent studies are testing this number). Beta cell loss occurs gradually over time, beginning before diagnosis, and continuing afterwards, until most beta cells are lost (Cnop et al. 2005). However, new research is also finding that some people with type 1 continue to produce insulin for many years (Davis et al. 2014; Oram et al. 2014), and that beta cell dysfunction (not just death) may also be a significant cause of high blood sugar, at least around the time of diagnosis (Pugliese et al. 2014)."
You'll also note that they are also exploring the possibility that beta cell dysfunction and not death may be an issue. Dollars to donuts that is the case - where there are multiple ways to get a phenotype you can bet all will occur. I would speculate that while the dysfunction may eventually lead to death, it is probably on a similar timescale meaning the person could be producing some level of insulin for years - or maybe not. Mayb
Age of onset is irrelevant when one compares those who have type 1's. Your argument is that, if we compare all persons at a specific age who at some point get type 1 diabetes regardless of whether they have type 1 or not at the specified age, some have a different "severity" of type 1 because the auto-immune response hasn't yet been triggered (in other words, they don't have type 1 at all at that age).
As I pointed out, the early stages of type 1 (known as the honeymoon stage) is going to be different because the disease is in the process of being created. This starts when the autoimmune response is triggered and ends when all or nearly all beta cells have been depleted. Once that has phase has ended, all type 1's are of the same "severity" in that we all don't make insulin. It's been known for at least decades (I personally have known for decades and learned from those who knew for decades before) that the honeymoon process takes several years. The reason it is news (or at least a reminder) for some is because more and more cases are being identified of adult-onset type 1 (now referred to as LADA or "type 1.5") where the honeymoon phase sometimes takes 10 years or longer. For quite some time (and to a lesser extent, this still happens), type 1's with adult onset (LADA / type 1.5) were misdiagnosed as type 2 because diagnosis was made based on symptoms rather than the underlying cause.
As far as beta cell dysfunction, it is highly unlikely. Type 1 diabetes is an auto-immune disease. My immune system attacked my pancreatic beta cells not to disarm beta cells, but to remove them.
Actually, no, my point is that if you take 100 random type 1s you have no idea if they've all at the same stage or not. Some may have gotten as low as they ever will. Some may not have as of yet.
Even if you assume that all have reached their nadir, you have no idea if all of their 'most are dead' are at the same functional level or not. There is variance.
Just so you know, I've been involved in quite a bit of autoimmune research. I'm not ignorant of the basic mechanisms of that class of diseases. Just because a disease is autoimmune does not necessarily mean the effects are all or nothing. The fact that Type 1 diabetes is an autoimmune disease does not make it any more or less likely that some individuals may have dysfunctional beta cells rather than killed beta cells.
Again, correct for all variables and you will find that a gram of carbs does not become the same amount of energy for everyone. I think you have missed my point by focusing on variables and arguing the extent to which they can be controlled for in research. My point still stands, even if you can't figure out how to design a study to prove or disprove it with 100% accuracy.
This seems like a variant of "well we're not all machines, so calories aren't calories" argument.
Which strikes me as a problem because let's make an analogy about T1D's.
Let's take a standardized measure of calories - the amount available in one gallon of regular 87 octane gasoline
Let's take two 1985 chevy impalas. Now, we'll accept that we've controlled that by being two 1985 chevy impalas with same options, they clearly are more alike than even two identical twin humans. Right down to they have the same size gas tank so the 1 gallon is going to fit similarly.
No one would say a calorie isn't a calorie because two people using the cars can drive them different distances on 1 gallon of gas, even if those two distances are equal work because the terrain is the same. Everyone would say of course things like how fast you burn the gas and accelerate, what the cars actual condition is, etc, are all going to impact how far you can travel on that one gallon of gas. No one would argue the gasoline in the two vehicles was different because of the recorded MPG was different, even though they're the same kind of car. It would be held as a poor argument. Yet people use this argument about humans all the time and human individuality to argue that calories aren't calories because people aren't machines. Well, as far as thermodynamics are concerned, we are machine, we have to obey the known laws of physics, and as far as comparisons go, machines aren't machines - they don't all function the same either, even when they're built to the same standards. This doesn't negate the fact that properly test, 87 octane has, on average, the same amount of calories burnable by properly calibrated equipment per gallon. Within the limits of the food itself we make, it is similar. And yes, just like the MPG sticker on the car, there will be variance on what you get out of them in practical, day to day life. It doesn't mean the gasoline is the issue, or that energy doesn't matter, or that if you take the same car and give it more gasoline, it is probably going to drive further.
Humans will of course be a little more complex. We're kind of like a plug-in hybrid, having different energy sources we can use long and short term, but energy is energy.
I'm not saying that the "gasoline" (calories) is different. I'm saying they don't get digested and used quite the same in every person. I wish it were as simple as how many believe CICO works, but it is more complicated than that.
They'll get used differently by the same person even. Doesn't really change you can do pretty accurate estimates based on mileage and gas tank emptying to figure out the MPG of your driving style for the vehicle, so long as one is diligent in record keeping.
No, that is my original point. For most, you are correct. However, there are some cars that are very different. Those cars do not operate consistently; they do not operate as most other cars of the same year, make, and model; and they don't even all operate similarly to other vehicles with the same type of problem. Many drivers who have only ever driven cars without such problems would argue that all cars operate the same, but perhaps on a slightly different scale. The argument is made that, even if a car's issues have decreased the mpg by 15%, there are still driving habits that can bring the mpg back to what they get from their car in good condition. They just say that it is more difficult - drivers of those cars must take more extreme measures and try things like shutting off the engine when coasting downhill, not using any temperature management systems, and over-inflating tires. Still, they believe that taking more difficult measures can provide the same results. What those drivers don't know is that those of us with problems on our cars are already taking much more difficult measures and still can't match anywhere close to the same mpg as their car in good condition.0 -
midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »I have an insatiable appetite, and find that satiety isn't just how much volume I eat, but how many calories I eat. There was a time when I was so burdened with hunger and could never achieve calorie goals. Users would tell me to eat light (i.e. not calorie dense) foods because it would keep me full. One day, I ate more than 9 lbs. of salad and was still very hungry.
As for insulin, insulin resistance, and CICO, I believe the truth lies somewhere in the middle of the extremes (one extreme is that CICO is infallible, the other that CICO doesn't matter as long as your macros are the right percentages). I know there have been a lot of points made that weight loss is strictly about CICO and that there is no possible way that how your body moves energy around between glucose, glycogen, and fat will change without a change in CICO. Of course that is a simplistic view because most of us know that net carbs become glucose right away while protein and dietary fat do not. So immediately after eating (actually, while eating because some of that glucose is absorbed through capillaries in the mouth), energy is already affected by which macros you consumed. Continuing on for the next several hours, there are differences with how energy gets into your body, where it goes first, and where it goes next. These differences are not only based on the particular macros consumed, but also what amount and to what degree energy is needed within the proper time frames. And ultimately, timing is an important part of macro consumption and exercise - something that both the CICO method and the LCHF using macro percentages fails to consider.
As a double diabetic (meaning I have both type 1 and type 2 diabetes), I take a lot of insulin. I've also always had serious challenges losing weight, some of which no MFP user can explain. My endocrinologist says the reason I find it so hard to lose weight is because I need so much insulin. If I weighed less, I would be less insulin resistant and would need less insulin. So if I lose some weight, I will find it easier to lose weight. But it is nearly impossible to lose weight to get to where I can find it more possible to lose weight. It's a frustrating situation to encounter, to say the least. It is, on the other hand, really easy to gain weight. When I was first diagnosed with type 1, I was a healthy weight (to some standards, even slightly underweight... that isn't unusual because undiagnosed type 1 causes weight loss). I gained 20 lbs. in the first month after diagnosis and was already a bit overweight at that time. Over the next year, the gains slowed to where I gained 60 lbs. in the year and then another 60 lbs. over the next 1.5-2 years for a total of 120 lbs. of gain in 3 years. I can't lose anywhere near that fast. I really struggle to lose 1 lb. per month. So I agree that insulin does have an impact on weight gain and weight loss because my own experience has been impacted significantly by that exact issue.
CICO isn't a weight loss method, it is a fact of nature. Insulin can't create or destroy energy. Calorie counting is a method. There is no perfect way to track what someone's calories out are, which would include any energy costs of converting glucose into glycogen, or even de novo lipogensis. Your own physiology might be different such that normal calories out predictors are off for you. That doesn't mean there doesn't exist a level of activity that if you consistently stay above and a certain amount of calories that you consistently stay below that will cause weight loss (assuming otherwise proper nutrition).
I think it is more about the actual conversion of calories into energy. For example, those of us who are type 1's can get together and talk about how much 15g of net carbs will affect our blood glucose. We will all take different amounts of insulin, and part of that comes down to insulin resistance, but part of it is due to individual differences. All net carbs should be converted to glucose, and if a calorie is exactly the same for everyone, then 15g of net carbs will increase all of our BG's by the same amount. We will take different amounts of insulin to bring it back down again (and deliver as energy to cells or convert to fat) due to varying levels of insulin resistance, but the rise is exactly the same, right? Well... actually that is wrong. Put 100 type 1 diabetics in a room, give each of them the exact same number of net carbs, give no insulin bolus for the carbs, and measure blood glucose levels before and after full digestion. Chances are good that you will get 100 different numbers (though it is possible a few might be the same, by luck). So then for each individual, the same number of calories in does not result in the same amount of energy. Further complicated is the movement of that glucose to glycogen and/or fat. Now consider that protein and fat are digested differently to begin with, and they don't go directly to glucose either.
I think you mean the conversion of macros into energy.
Also, put 100 type 1s in a room, and probably all 100 have slightly different levels of severity of type 1 diabetes. That would explain the varying results with a more likely scenario than that the conversions are all significantly different (those pathways being very highly conserved). It would not change the effect that you observe, which is that the same amount of insulin for the same amount and type of macros does not produce the same results in different individuals.
Please explain exactly how type 1's can have "a different severity" of type 1.
Hint: It is only possible during the "honeymoon" period when one is in the process of developing type 1. Once all the pancratic beta cells are dead, all type 1's are of the same "severity."
So people with type 1 all lose beta cells at the same age and at the same rate until they are all gone? And this rate is known and documented when not involved in a study (so you can screen those 100 type 1s for those out of the 'honeymoon period' like you didn't say you would do)?
Don't think so, or the new research mentioned in this quote wouldn't have been necessary - it'd have been observed years ago. Plus, you'll notice that the findings were that most beta cells are lost. Which means everyone is not reaching the same nadir:
"In type 1 diabetes, the beta cells do not produce enough insulin. This is generally due to the death of the beta cells. By the time someone is diagnosed with type 1 diabetes, they may have lost 70-80% of their beta cells (it is thought, although more recent studies are testing this number). Beta cell loss occurs gradually over time, beginning before diagnosis, and continuing afterwards, until most beta cells are lost (Cnop et al. 2005). However, new research is also finding that some people with type 1 continue to produce insulin for many years (Davis et al. 2014; Oram et al. 2014), and that beta cell dysfunction (not just death) may also be a significant cause of high blood sugar, at least around the time of diagnosis (Pugliese et al. 2014)."
You'll also note that they are also exploring the possibility that beta cell dysfunction and not death may be an issue. Dollars to donuts that is the case - where there are multiple ways to get a phenotype you can bet all will occur. I would speculate that while the dysfunction may eventually lead to death, it is probably on a similar timescale meaning the person could be producing some level of insulin for years - or maybe not. Mayb
Age of onset is irrelevant when one compares those who have type 1's. Your argument is that, if we compare all persons at a specific age who at some point get type 1 diabetes regardless of whether they have type 1 or not at the specified age, some have a different "severity" of type 1 because the auto-immune response hasn't yet been triggered (in other words, they don't have type 1 at all at that age).
As I pointed out, the early stages of type 1 (known as the honeymoon stage) is going to be different because the disease is in the process of being created. This starts when the autoimmune response is triggered and ends when all or nearly all beta cells have been depleted. Once that has phase has ended, all type 1's are of the same "severity" in that we all don't make insulin. It's been known for at least decades (I personally have known for decades and learned from those who knew for decades before) that the honeymoon process takes several years. The reason it is news (or at least a reminder) for some is because more and more cases are being identified of adult-onset type 1 (now referred to as LADA or "type 1.5") where the honeymoon phase sometimes takes 10 years or longer. For quite some time (and to a lesser extent, this still happens), type 1's with adult onset (LADA / type 1.5) were misdiagnosed as type 2 because diagnosis was made based on symptoms rather than the underlying cause.
As far as beta cell dysfunction, it is highly unlikely. Type 1 diabetes is an auto-immune disease. My immune system attacked my pancreatic beta cells not to disarm beta cells, but to remove them.
Actually, no, my point is that if you take 100 random type 1s you have no idea if they've all at the same stage or not. Some may have gotten as low as they ever will. Some may not have as of yet.
Even if you assume that all have reached their nadir, you have no idea if all of their 'most are dead' are at the same functional level or not. There is variance.
Just so you know, I've been involved in quite a bit of autoimmune research. I'm not ignorant of the basic mechanisms of that class of diseases. Just because a disease is autoimmune does not necessarily mean the effects are all or nothing. The fact that Type 1 diabetes is an autoimmune disease does not make it any more or less likely that some individuals may have dysfunctional beta cells rather than killed beta cells.
Again, correct for all variables and you will find that a gram of carbs does not become the same amount of energy for everyone. I think you have missed my point by focusing on variables and arguing the extent to which they can be controlled for in research. My point still stands, even if you can't figure out how to design a study to prove or disprove it with 100% accuracy.
This seems like a variant of "well we're not all machines, so calories aren't calories" argument.
Which strikes me as a problem because let's make an analogy about T1D's.
Let's take a standardized measure of calories - the amount available in one gallon of regular 87 octane gasoline
Let's take two 1985 chevy impalas. Now, we'll accept that we've controlled that by being two 1985 chevy impalas with same options, they clearly are more alike than even two identical twin humans. Right down to they have the same size gas tank so the 1 gallon is going to fit similarly.
No one would say a calorie isn't a calorie because two people using the cars can drive them different distances on 1 gallon of gas, even if those two distances are equal work because the terrain is the same. Everyone would say of course things like how fast you burn the gas and accelerate, what the cars actual condition is, etc, are all going to impact how far you can travel on that one gallon of gas. No one would argue the gasoline in the two vehicles was different because of the recorded MPG was different, even though they're the same kind of car. It would be held as a poor argument. Yet people use this argument about humans all the time and human individuality to argue that calories aren't calories because people aren't machines. Well, as far as thermodynamics are concerned, we are machine, we have to obey the known laws of physics, and as far as comparisons go, machines aren't machines - they don't all function the same either, even when they're built to the same standards. This doesn't negate the fact that properly test, 87 octane has, on average, the same amount of calories burnable by properly calibrated equipment per gallon. Within the limits of the food itself we make, it is similar. And yes, just like the MPG sticker on the car, there will be variance on what you get out of them in practical, day to day life. It doesn't mean the gasoline is the issue, or that energy doesn't matter, or that if you take the same car and give it more gasoline, it is probably going to drive further.
Humans will of course be a little more complex. We're kind of like a plug-in hybrid, having different energy sources we can use long and short term, but energy is energy.
I'm not saying that the "gasoline" (calories) is different. I'm saying they don't get digested and used quite the same in every person. I wish it were as simple as how many believe CICO works, but it is more complicated than that.
They'll get used differently by the same person even. Doesn't really change you can do pretty accurate estimates based on mileage and gas tank emptying to figure out the MPG of your driving style for the vehicle, so long as one is diligent in record keeping.
No, that is my original point. For most, you are correct. However, there are some cars that are very different. Those cars do not operate consistently; they do not operate as most other cars of the same year, make, and model; and they don't even all operate similarly to other vehicles with the same type of problem. Many drivers who have only ever driven cars without such problems would argue that all cars operate the same, but perhaps on a slightly different scale. The argument is made that, even if a car's issues have decreased the mpg by 15%, there are still driving habits that can bring the mpg back to what they get from their car in good condition. They just say that it is more difficult - drivers of those cars must take more extreme measures and try things like shutting off the engine when coasting downhill, not using any temperature management systems, and over-inflating tires. Still, they believe that taking more difficult measures can provide the same results. What those drivers don't know is that those of us with problems on our cars are already taking much more difficult measures and still can't match anywhere close to the same mpg as their car in good condition.
Here's the problem that everyone ignores about the analogy because they're thinking about it in terms of what they want to happen, instead of the actual tie between the two in terms of thermodynamics. Most people want to lose weight beyond the expected based on calories (that's the good thing to them in that situation), and they want their car to get super high MPG. So people assume an person is more efficient (uses less calories) even though, if you pay attention to how efficiency works, including in the context of evolution fighting to make this happen for billions of years, just like a car, being broken (unhealthy / metabolic abnormality) is most likely to decrease efficiency, meaning you lose weight faster than predicted. Your body is going to do the least amount of work if everything is working as planned - having things not working right means your body has to do extra work, use extra calories, and burn more. Just the same as a car that has issues is going to use more gas and get worse MPG.
Your analogies all about saving gas to get higher MPG show the problem people have with following the analogy based on thinking in terms of desired outcome, instead of in terms of actual mechanics. The nature of the universe is to go towards inefficiency, not spontaneous increases in efficiency.0 -
midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »I have an insatiable appetite, and find that satiety isn't just how much volume I eat, but how many calories I eat. There was a time when I was so burdened with hunger and could never achieve calorie goals. Users would tell me to eat light (i.e. not calorie dense) foods because it would keep me full. One day, I ate more than 9 lbs. of salad and was still very hungry.
As for insulin, insulin resistance, and CICO, I believe the truth lies somewhere in the middle of the extremes (one extreme is that CICO is infallible, the other that CICO doesn't matter as long as your macros are the right percentages). I know there have been a lot of points made that weight loss is strictly about CICO and that there is no possible way that how your body moves energy around between glucose, glycogen, and fat will change without a change in CICO. Of course that is a simplistic view because most of us know that net carbs become glucose right away while protein and dietary fat do not. So immediately after eating (actually, while eating because some of that glucose is absorbed through capillaries in the mouth), energy is already affected by which macros you consumed. Continuing on for the next several hours, there are differences with how energy gets into your body, where it goes first, and where it goes next. These differences are not only based on the particular macros consumed, but also what amount and to what degree energy is needed within the proper time frames. And ultimately, timing is an important part of macro consumption and exercise - something that both the CICO method and the LCHF using macro percentages fails to consider.
As a double diabetic (meaning I have both type 1 and type 2 diabetes), I take a lot of insulin. I've also always had serious challenges losing weight, some of which no MFP user can explain. My endocrinologist says the reason I find it so hard to lose weight is because I need so much insulin. If I weighed less, I would be less insulin resistant and would need less insulin. So if I lose some weight, I will find it easier to lose weight. But it is nearly impossible to lose weight to get to where I can find it more possible to lose weight. It's a frustrating situation to encounter, to say the least. It is, on the other hand, really easy to gain weight. When I was first diagnosed with type 1, I was a healthy weight (to some standards, even slightly underweight... that isn't unusual because undiagnosed type 1 causes weight loss). I gained 20 lbs. in the first month after diagnosis and was already a bit overweight at that time. Over the next year, the gains slowed to where I gained 60 lbs. in the year and then another 60 lbs. over the next 1.5-2 years for a total of 120 lbs. of gain in 3 years. I can't lose anywhere near that fast. I really struggle to lose 1 lb. per month. So I agree that insulin does have an impact on weight gain and weight loss because my own experience has been impacted significantly by that exact issue.
CICO isn't a weight loss method, it is a fact of nature. Insulin can't create or destroy energy. Calorie counting is a method. There is no perfect way to track what someone's calories out are, which would include any energy costs of converting glucose into glycogen, or even de novo lipogensis. Your own physiology might be different such that normal calories out predictors are off for you. That doesn't mean there doesn't exist a level of activity that if you consistently stay above and a certain amount of calories that you consistently stay below that will cause weight loss (assuming otherwise proper nutrition).
I think it is more about the actual conversion of calories into energy. For example, those of us who are type 1's can get together and talk about how much 15g of net carbs will affect our blood glucose. We will all take different amounts of insulin, and part of that comes down to insulin resistance, but part of it is due to individual differences. All net carbs should be converted to glucose, and if a calorie is exactly the same for everyone, then 15g of net carbs will increase all of our BG's by the same amount. We will take different amounts of insulin to bring it back down again (and deliver as energy to cells or convert to fat) due to varying levels of insulin resistance, but the rise is exactly the same, right? Well... actually that is wrong. Put 100 type 1 diabetics in a room, give each of them the exact same number of net carbs, give no insulin bolus for the carbs, and measure blood glucose levels before and after full digestion. Chances are good that you will get 100 different numbers (though it is possible a few might be the same, by luck). So then for each individual, the same number of calories in does not result in the same amount of energy. Further complicated is the movement of that glucose to glycogen and/or fat. Now consider that protein and fat are digested differently to begin with, and they don't go directly to glucose either.
I think you mean the conversion of macros into energy.
Also, put 100 type 1s in a room, and probably all 100 have slightly different levels of severity of type 1 diabetes. That would explain the varying results with a more likely scenario than that the conversions are all significantly different (those pathways being very highly conserved). It would not change the effect that you observe, which is that the same amount of insulin for the same amount and type of macros does not produce the same results in different individuals.
Please explain exactly how type 1's can have "a different severity" of type 1.
Hint: It is only possible during the "honeymoon" period when one is in the process of developing type 1. Once all the pancratic beta cells are dead, all type 1's are of the same "severity."
So people with type 1 all lose beta cells at the same age and at the same rate until they are all gone? And this rate is known and documented when not involved in a study (so you can screen those 100 type 1s for those out of the 'honeymoon period' like you didn't say you would do)?
Don't think so, or the new research mentioned in this quote wouldn't have been necessary - it'd have been observed years ago. Plus, you'll notice that the findings were that most beta cells are lost. Which means everyone is not reaching the same nadir:
"In type 1 diabetes, the beta cells do not produce enough insulin. This is generally due to the death of the beta cells. By the time someone is diagnosed with type 1 diabetes, they may have lost 70-80% of their beta cells (it is thought, although more recent studies are testing this number). Beta cell loss occurs gradually over time, beginning before diagnosis, and continuing afterwards, until most beta cells are lost (Cnop et al. 2005). However, new research is also finding that some people with type 1 continue to produce insulin for many years (Davis et al. 2014; Oram et al. 2014), and that beta cell dysfunction (not just death) may also be a significant cause of high blood sugar, at least around the time of diagnosis (Pugliese et al. 2014)."
You'll also note that they are also exploring the possibility that beta cell dysfunction and not death may be an issue. Dollars to donuts that is the case - where there are multiple ways to get a phenotype you can bet all will occur. I would speculate that while the dysfunction may eventually lead to death, it is probably on a similar timescale meaning the person could be producing some level of insulin for years - or maybe not. Mayb
Age of onset is irrelevant when one compares those who have type 1's. Your argument is that, if we compare all persons at a specific age who at some point get type 1 diabetes regardless of whether they have type 1 or not at the specified age, some have a different "severity" of type 1 because the auto-immune response hasn't yet been triggered (in other words, they don't have type 1 at all at that age).
As I pointed out, the early stages of type 1 (known as the honeymoon stage) is going to be different because the disease is in the process of being created. This starts when the autoimmune response is triggered and ends when all or nearly all beta cells have been depleted. Once that has phase has ended, all type 1's are of the same "severity" in that we all don't make insulin. It's been known for at least decades (I personally have known for decades and learned from those who knew for decades before) that the honeymoon process takes several years. The reason it is news (or at least a reminder) for some is because more and more cases are being identified of adult-onset type 1 (now referred to as LADA or "type 1.5") where the honeymoon phase sometimes takes 10 years or longer. For quite some time (and to a lesser extent, this still happens), type 1's with adult onset (LADA / type 1.5) were misdiagnosed as type 2 because diagnosis was made based on symptoms rather than the underlying cause.
As far as beta cell dysfunction, it is highly unlikely. Type 1 diabetes is an auto-immune disease. My immune system attacked my pancreatic beta cells not to disarm beta cells, but to remove them.
Actually, no, my point is that if you take 100 random type 1s you have no idea if they've all at the same stage or not. Some may have gotten as low as they ever will. Some may not have as of yet.
Even if you assume that all have reached their nadir, you have no idea if all of their 'most are dead' are at the same functional level or not. There is variance.
Just so you know, I've been involved in quite a bit of autoimmune research. I'm not ignorant of the basic mechanisms of that class of diseases. Just because a disease is autoimmune does not necessarily mean the effects are all or nothing. The fact that Type 1 diabetes is an autoimmune disease does not make it any more or less likely that some individuals may have dysfunctional beta cells rather than killed beta cells.
Again, correct for all variables and you will find that a gram of carbs does not become the same amount of energy for everyone. I think you have missed my point by focusing on variables and arguing the extent to which they can be controlled for in research. My point still stands, even if you can't figure out how to design a study to prove or disprove it with 100% accuracy.
This seems like a variant of "well we're not all machines, so calories aren't calories" argument.
Which strikes me as a problem because let's make an analogy about T1D's.
Let's take a standardized measure of calories - the amount available in one gallon of regular 87 octane gasoline
Let's take two 1985 chevy impalas. Now, we'll accept that we've controlled that by being two 1985 chevy impalas with same options, they clearly are more alike than even two identical twin humans. Right down to they have the same size gas tank so the 1 gallon is going to fit similarly.
No one would say a calorie isn't a calorie because two people using the cars can drive them different distances on 1 gallon of gas, even if those two distances are equal work because the terrain is the same. Everyone would say of course things like how fast you burn the gas and accelerate, what the cars actual condition is, etc, are all going to impact how far you can travel on that one gallon of gas. No one would argue the gasoline in the two vehicles was different because of the recorded MPG was different, even though they're the same kind of car. It would be held as a poor argument. Yet people use this argument about humans all the time and human individuality to argue that calories aren't calories because people aren't machines. Well, as far as thermodynamics are concerned, we are machine, we have to obey the known laws of physics, and as far as comparisons go, machines aren't machines - they don't all function the same either, even when they're built to the same standards. This doesn't negate the fact that properly test, 87 octane has, on average, the same amount of calories burnable by properly calibrated equipment per gallon. Within the limits of the food itself we make, it is similar. And yes, just like the MPG sticker on the car, there will be variance on what you get out of them in practical, day to day life. It doesn't mean the gasoline is the issue, or that energy doesn't matter, or that if you take the same car and give it more gasoline, it is probably going to drive further.
Humans will of course be a little more complex. We're kind of like a plug-in hybrid, having different energy sources we can use long and short term, but energy is energy.
I'm not saying that the "gasoline" (calories) is different. I'm saying they don't get digested and used quite the same in every person. I wish it were as simple as how many believe CICO works, but it is more complicated than that.
They'll get used differently by the same person even. Doesn't really change you can do pretty accurate estimates based on mileage and gas tank emptying to figure out the MPG of your driving style for the vehicle, so long as one is diligent in record keeping.
No, that is my original point. For most, you are correct. However, there are some cars that are very different. Those cars do not operate consistently; they do not operate as most other cars of the same year, make, and model; and they don't even all operate similarly to other vehicles with the same type of problem. Many drivers who have only ever driven cars without such problems would argue that all cars operate the same, but perhaps on a slightly different scale. The argument is made that, even if a car's issues have decreased the mpg by 15%, there are still driving habits that can bring the mpg back to what they get from their car in good condition. They just say that it is more difficult - drivers of those cars must take more extreme measures and try things like shutting off the engine when coasting downhill, not using any temperature management systems, and over-inflating tires. Still, they believe that taking more difficult measures can provide the same results. What those drivers don't know is that those of us with problems on our cars are already taking much more difficult measures and still can't match anywhere close to the same mpg as their car in good condition.
Here's the problem that everyone ignores about the analogy because they're thinking about it in terms of what they want to happen, instead of the actual tie between the two in terms of thermodynamics. Most people want to lose weight beyond the expected based on calories (that's the good thing to them in that situation), and they want their car to get super high MPG. So people assume an person is more efficient (uses less calories) even though, if you pay attention to how efficiency works, including in the context of evolution fighting to make this happen for billions of years, just like a car, being broken (unhealthy / metabolic abnormality) is most likely to decrease efficiency, meaning you lose weight faster than predicted. Your body is going to do the least amount of work if everything is working as planned - having things not working right means your body has to do extra work, use extra calories, and burn more. Just the same as a car that has issues is going to use more gas and get worse MPG.
Your analogies all about saving gas to get higher MPG show the problem people have with following the analogy based on thinking in terms of desired outcome, instead of in terms of actual mechanics. The nature of the universe is to go towards inefficiency, not spontaneous increases in efficiency.
That might be true for most people and it might not be... I don't have data to say either way. Personally, I just want to see some (any) improvement in gas mileage when I shut off the engine downhill, over-inflate the tires, and don't use temperature management systems. When I do that for months and see no improvement, despite everyone and even science telling me that those things will work, it is difficult to justify making the extra effort.0 -
midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »I have an insatiable appetite, and find that satiety isn't just how much volume I eat, but how many calories I eat. There was a time when I was so burdened with hunger and could never achieve calorie goals. Users would tell me to eat light (i.e. not calorie dense) foods because it would keep me full. One day, I ate more than 9 lbs. of salad and was still very hungry.
As for insulin, insulin resistance, and CICO, I believe the truth lies somewhere in the middle of the extremes (one extreme is that CICO is infallible, the other that CICO doesn't matter as long as your macros are the right percentages). I know there have been a lot of points made that weight loss is strictly about CICO and that there is no possible way that how your body moves energy around between glucose, glycogen, and fat will change without a change in CICO. Of course that is a simplistic view because most of us know that net carbs become glucose right away while protein and dietary fat do not. So immediately after eating (actually, while eating because some of that glucose is absorbed through capillaries in the mouth), energy is already affected by which macros you consumed. Continuing on for the next several hours, there are differences with how energy gets into your body, where it goes first, and where it goes next. These differences are not only based on the particular macros consumed, but also what amount and to what degree energy is needed within the proper time frames. And ultimately, timing is an important part of macro consumption and exercise - something that both the CICO method and the LCHF using macro percentages fails to consider.
As a double diabetic (meaning I have both type 1 and type 2 diabetes), I take a lot of insulin. I've also always had serious challenges losing weight, some of which no MFP user can explain. My endocrinologist says the reason I find it so hard to lose weight is because I need so much insulin. If I weighed less, I would be less insulin resistant and would need less insulin. So if I lose some weight, I will find it easier to lose weight. But it is nearly impossible to lose weight to get to where I can find it more possible to lose weight. It's a frustrating situation to encounter, to say the least. It is, on the other hand, really easy to gain weight. When I was first diagnosed with type 1, I was a healthy weight (to some standards, even slightly underweight... that isn't unusual because undiagnosed type 1 causes weight loss). I gained 20 lbs. in the first month after diagnosis and was already a bit overweight at that time. Over the next year, the gains slowed to where I gained 60 lbs. in the year and then another 60 lbs. over the next 1.5-2 years for a total of 120 lbs. of gain in 3 years. I can't lose anywhere near that fast. I really struggle to lose 1 lb. per month. So I agree that insulin does have an impact on weight gain and weight loss because my own experience has been impacted significantly by that exact issue.
CICO isn't a weight loss method, it is a fact of nature. Insulin can't create or destroy energy. Calorie counting is a method. There is no perfect way to track what someone's calories out are, which would include any energy costs of converting glucose into glycogen, or even de novo lipogensis. Your own physiology might be different such that normal calories out predictors are off for you. That doesn't mean there doesn't exist a level of activity that if you consistently stay above and a certain amount of calories that you consistently stay below that will cause weight loss (assuming otherwise proper nutrition).
I think it is more about the actual conversion of calories into energy. For example, those of us who are type 1's can get together and talk about how much 15g of net carbs will affect our blood glucose. We will all take different amounts of insulin, and part of that comes down to insulin resistance, but part of it is due to individual differences. All net carbs should be converted to glucose, and if a calorie is exactly the same for everyone, then 15g of net carbs will increase all of our BG's by the same amount. We will take different amounts of insulin to bring it back down again (and deliver as energy to cells or convert to fat) due to varying levels of insulin resistance, but the rise is exactly the same, right? Well... actually that is wrong. Put 100 type 1 diabetics in a room, give each of them the exact same number of net carbs, give no insulin bolus for the carbs, and measure blood glucose levels before and after full digestion. Chances are good that you will get 100 different numbers (though it is possible a few might be the same, by luck). So then for each individual, the same number of calories in does not result in the same amount of energy. Further complicated is the movement of that glucose to glycogen and/or fat. Now consider that protein and fat are digested differently to begin with, and they don't go directly to glucose either.
I think you mean the conversion of macros into energy.
Also, put 100 type 1s in a room, and probably all 100 have slightly different levels of severity of type 1 diabetes. That would explain the varying results with a more likely scenario than that the conversions are all significantly different (those pathways being very highly conserved). It would not change the effect that you observe, which is that the same amount of insulin for the same amount and type of macros does not produce the same results in different individuals.
Please explain exactly how type 1's can have "a different severity" of type 1.
Hint: It is only possible during the "honeymoon" period when one is in the process of developing type 1. Once all the pancratic beta cells are dead, all type 1's are of the same "severity."
So people with type 1 all lose beta cells at the same age and at the same rate until they are all gone? And this rate is known and documented when not involved in a study (so you can screen those 100 type 1s for those out of the 'honeymoon period' like you didn't say you would do)?
Don't think so, or the new research mentioned in this quote wouldn't have been necessary - it'd have been observed years ago. Plus, you'll notice that the findings were that most beta cells are lost. Which means everyone is not reaching the same nadir:
"In type 1 diabetes, the beta cells do not produce enough insulin. This is generally due to the death of the beta cells. By the time someone is diagnosed with type 1 diabetes, they may have lost 70-80% of their beta cells (it is thought, although more recent studies are testing this number). Beta cell loss occurs gradually over time, beginning before diagnosis, and continuing afterwards, until most beta cells are lost (Cnop et al. 2005). However, new research is also finding that some people with type 1 continue to produce insulin for many years (Davis et al. 2014; Oram et al. 2014), and that beta cell dysfunction (not just death) may also be a significant cause of high blood sugar, at least around the time of diagnosis (Pugliese et al. 2014)."
You'll also note that they are also exploring the possibility that beta cell dysfunction and not death may be an issue. Dollars to donuts that is the case - where there are multiple ways to get a phenotype you can bet all will occur. I would speculate that while the dysfunction may eventually lead to death, it is probably on a similar timescale meaning the person could be producing some level of insulin for years - or maybe not. Mayb
Age of onset is irrelevant when one compares those who have type 1's. Your argument is that, if we compare all persons at a specific age who at some point get type 1 diabetes regardless of whether they have type 1 or not at the specified age, some have a different "severity" of type 1 because the auto-immune response hasn't yet been triggered (in other words, they don't have type 1 at all at that age).
As I pointed out, the early stages of type 1 (known as the honeymoon stage) is going to be different because the disease is in the process of being created. This starts when the autoimmune response is triggered and ends when all or nearly all beta cells have been depleted. Once that has phase has ended, all type 1's are of the same "severity" in that we all don't make insulin. It's been known for at least decades (I personally have known for decades and learned from those who knew for decades before) that the honeymoon process takes several years. The reason it is news (or at least a reminder) for some is because more and more cases are being identified of adult-onset type 1 (now referred to as LADA or "type 1.5") where the honeymoon phase sometimes takes 10 years or longer. For quite some time (and to a lesser extent, this still happens), type 1's with adult onset (LADA / type 1.5) were misdiagnosed as type 2 because diagnosis was made based on symptoms rather than the underlying cause.
As far as beta cell dysfunction, it is highly unlikely. Type 1 diabetes is an auto-immune disease. My immune system attacked my pancreatic beta cells not to disarm beta cells, but to remove them.
Actually, no, my point is that if you take 100 random type 1s you have no idea if they've all at the same stage or not. Some may have gotten as low as they ever will. Some may not have as of yet.
Even if you assume that all have reached their nadir, you have no idea if all of their 'most are dead' are at the same functional level or not. There is variance.
Just so you know, I've been involved in quite a bit of autoimmune research. I'm not ignorant of the basic mechanisms of that class of diseases. Just because a disease is autoimmune does not necessarily mean the effects are all or nothing. The fact that Type 1 diabetes is an autoimmune disease does not make it any more or less likely that some individuals may have dysfunctional beta cells rather than killed beta cells.
Again, correct for all variables and you will find that a gram of carbs does not become the same amount of energy for everyone. I think you have missed my point by focusing on variables and arguing the extent to which they can be controlled for in research. My point still stands, even if you can't figure out how to design a study to prove or disprove it with 100% accuracy.
This seems like a variant of "well we're not all machines, so calories aren't calories" argument.
Which strikes me as a problem because let's make an analogy about T1D's.
Let's take a standardized measure of calories - the amount available in one gallon of regular 87 octane gasoline
Let's take two 1985 chevy impalas. Now, we'll accept that we've controlled that by being two 1985 chevy impalas with same options, they clearly are more alike than even two identical twin humans. Right down to they have the same size gas tank so the 1 gallon is going to fit similarly.
No one would say a calorie isn't a calorie because two people using the cars can drive them different distances on 1 gallon of gas, even if those two distances are equal work because the terrain is the same. Everyone would say of course things like how fast you burn the gas and accelerate, what the cars actual condition is, etc, are all going to impact how far you can travel on that one gallon of gas. No one would argue the gasoline in the two vehicles was different because of the recorded MPG was different, even though they're the same kind of car. It would be held as a poor argument. Yet people use this argument about humans all the time and human individuality to argue that calories aren't calories because people aren't machines. Well, as far as thermodynamics are concerned, we are machine, we have to obey the known laws of physics, and as far as comparisons go, machines aren't machines - they don't all function the same either, even when they're built to the same standards. This doesn't negate the fact that properly test, 87 octane has, on average, the same amount of calories burnable by properly calibrated equipment per gallon. Within the limits of the food itself we make, it is similar. And yes, just like the MPG sticker on the car, there will be variance on what you get out of them in practical, day to day life. It doesn't mean the gasoline is the issue, or that energy doesn't matter, or that if you take the same car and give it more gasoline, it is probably going to drive further.
Humans will of course be a little more complex. We're kind of like a plug-in hybrid, having different energy sources we can use long and short term, but energy is energy.
I'm not saying that the "gasoline" (calories) is different. I'm saying they don't get digested and used quite the same in every person. I wish it were as simple as how many believe CICO works, but it is more complicated than that.
They'll get used differently by the same person even. Doesn't really change you can do pretty accurate estimates based on mileage and gas tank emptying to figure out the MPG of your driving style for the vehicle, so long as one is diligent in record keeping.
No, that is my original point. For most, you are correct. However, there are some cars that are very different. Those cars do not operate consistently; they do not operate as most other cars of the same year, make, and model; and they don't even all operate similarly to other vehicles with the same type of problem. Many drivers who have only ever driven cars without such problems would argue that all cars operate the same, but perhaps on a slightly different scale. The argument is made that, even if a car's issues have decreased the mpg by 15%, there are still driving habits that can bring the mpg back to what they get from their car in good condition. They just say that it is more difficult - drivers of those cars must take more extreme measures and try things like shutting off the engine when coasting downhill, not using any temperature management systems, and over-inflating tires. Still, they believe that taking more difficult measures can provide the same results. What those drivers don't know is that those of us with problems on our cars are already taking much more difficult measures and still can't match anywhere close to the same mpg as their car in good condition.
Here's the problem that everyone ignores about the analogy because they're thinking about it in terms of what they want to happen, instead of the actual tie between the two in terms of thermodynamics. Most people want to lose weight beyond the expected based on calories (that's the good thing to them in that situation), and they want their car to get super high MPG. So people assume an person is more efficient (uses less calories) even though, if you pay attention to how efficiency works, including in the context of evolution fighting to make this happen for billions of years, just like a car, being broken (unhealthy / metabolic abnormality) is most likely to decrease efficiency, meaning you lose weight faster than predicted. Your body is going to do the least amount of work if everything is working as planned - having things not working right means your body has to do extra work, use extra calories, and burn more. Just the same as a car that has issues is going to use more gas and get worse MPG.
Your analogies all about saving gas to get higher MPG show the problem people have with following the analogy based on thinking in terms of desired outcome, instead of in terms of actual mechanics. The nature of the universe is to go towards inefficiency, not spontaneous increases in efficiency.
That might be true for most people and it might not be... I don't have data to say either way. Personally, I just want to see some (any) improvement in gas mileage when I shut off the engine downhill, over-inflate the tires, and don't use temperature management systems. When I do that for months and see no improvement, despite everyone and even science telling me that those things will work, it is difficult to justify making the extra effort.
I believe you technically want the MPG to get worse.0 -
midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »midwesterner85 wrote: »I have an insatiable appetite, and find that satiety isn't just how much volume I eat, but how many calories I eat. There was a time when I was so burdened with hunger and could never achieve calorie goals. Users would tell me to eat light (i.e. not calorie dense) foods because it would keep me full. One day, I ate more than 9 lbs. of salad and was still very hungry.
As for insulin, insulin resistance, and CICO, I believe the truth lies somewhere in the middle of the extremes (one extreme is that CICO is infallible, the other that CICO doesn't matter as long as your macros are the right percentages). I know there have been a lot of points made that weight loss is strictly about CICO and that there is no possible way that how your body moves energy around between glucose, glycogen, and fat will change without a change in CICO. Of course that is a simplistic view because most of us know that net carbs become glucose right away while protein and dietary fat do not. So immediately after eating (actually, while eating because some of that glucose is absorbed through capillaries in the mouth), energy is already affected by which macros you consumed. Continuing on for the next several hours, there are differences with how energy gets into your body, where it goes first, and where it goes next. These differences are not only based on the particular macros consumed, but also what amount and to what degree energy is needed within the proper time frames. And ultimately, timing is an important part of macro consumption and exercise - something that both the CICO method and the LCHF using macro percentages fails to consider.
As a double diabetic (meaning I have both type 1 and type 2 diabetes), I take a lot of insulin. I've also always had serious challenges losing weight, some of which no MFP user can explain. My endocrinologist says the reason I find it so hard to lose weight is because I need so much insulin. If I weighed less, I would be less insulin resistant and would need less insulin. So if I lose some weight, I will find it easier to lose weight. But it is nearly impossible to lose weight to get to where I can find it more possible to lose weight. It's a frustrating situation to encounter, to say the least. It is, on the other hand, really easy to gain weight. When I was first diagnosed with type 1, I was a healthy weight (to some standards, even slightly underweight... that isn't unusual because undiagnosed type 1 causes weight loss). I gained 20 lbs. in the first month after diagnosis and was already a bit overweight at that time. Over the next year, the gains slowed to where I gained 60 lbs. in the year and then another 60 lbs. over the next 1.5-2 years for a total of 120 lbs. of gain in 3 years. I can't lose anywhere near that fast. I really struggle to lose 1 lb. per month. So I agree that insulin does have an impact on weight gain and weight loss because my own experience has been impacted significantly by that exact issue.
CICO isn't a weight loss method, it is a fact of nature. Insulin can't create or destroy energy. Calorie counting is a method. There is no perfect way to track what someone's calories out are, which would include any energy costs of converting glucose into glycogen, or even de novo lipogensis. Your own physiology might be different such that normal calories out predictors are off for you. That doesn't mean there doesn't exist a level of activity that if you consistently stay above and a certain amount of calories that you consistently stay below that will cause weight loss (assuming otherwise proper nutrition).
I think it is more about the actual conversion of calories into energy. For example, those of us who are type 1's can get together and talk about how much 15g of net carbs will affect our blood glucose. We will all take different amounts of insulin, and part of that comes down to insulin resistance, but part of it is due to individual differences. All net carbs should be converted to glucose, and if a calorie is exactly the same for everyone, then 15g of net carbs will increase all of our BG's by the same amount. We will take different amounts of insulin to bring it back down again (and deliver as energy to cells or convert to fat) due to varying levels of insulin resistance, but the rise is exactly the same, right? Well... actually that is wrong. Put 100 type 1 diabetics in a room, give each of them the exact same number of net carbs, give no insulin bolus for the carbs, and measure blood glucose levels before and after full digestion. Chances are good that you will get 100 different numbers (though it is possible a few might be the same, by luck). So then for each individual, the same number of calories in does not result in the same amount of energy. Further complicated is the movement of that glucose to glycogen and/or fat. Now consider that protein and fat are digested differently to begin with, and they don't go directly to glucose either.
I think you mean the conversion of macros into energy.
Also, put 100 type 1s in a room, and probably all 100 have slightly different levels of severity of type 1 diabetes. That would explain the varying results with a more likely scenario than that the conversions are all significantly different (those pathways being very highly conserved). It would not change the effect that you observe, which is that the same amount of insulin for the same amount and type of macros does not produce the same results in different individuals.
Please explain exactly how type 1's can have "a different severity" of type 1.
Hint: It is only possible during the "honeymoon" period when one is in the process of developing type 1. Once all the pancratic beta cells are dead, all type 1's are of the same "severity."
So people with type 1 all lose beta cells at the same age and at the same rate until they are all gone? And this rate is known and documented when not involved in a study (so you can screen those 100 type 1s for those out of the 'honeymoon period' like you didn't say you would do)?
Don't think so, or the new research mentioned in this quote wouldn't have been necessary - it'd have been observed years ago. Plus, you'll notice that the findings were that most beta cells are lost. Which means everyone is not reaching the same nadir:
"In type 1 diabetes, the beta cells do not produce enough insulin. This is generally due to the death of the beta cells. By the time someone is diagnosed with type 1 diabetes, they may have lost 70-80% of their beta cells (it is thought, although more recent studies are testing this number). Beta cell loss occurs gradually over time, beginning before diagnosis, and continuing afterwards, until most beta cells are lost (Cnop et al. 2005). However, new research is also finding that some people with type 1 continue to produce insulin for many years (Davis et al. 2014; Oram et al. 2014), and that beta cell dysfunction (not just death) may also be a significant cause of high blood sugar, at least around the time of diagnosis (Pugliese et al. 2014)."
You'll also note that they are also exploring the possibility that beta cell dysfunction and not death may be an issue. Dollars to donuts that is the case - where there are multiple ways to get a phenotype you can bet all will occur. I would speculate that while the dysfunction may eventually lead to death, it is probably on a similar timescale meaning the person could be producing some level of insulin for years - or maybe not. Mayb
Age of onset is irrelevant when one compares those who have type 1's. Your argument is that, if we compare all persons at a specific age who at some point get type 1 diabetes regardless of whether they have type 1 or not at the specified age, some have a different "severity" of type 1 because the auto-immune response hasn't yet been triggered (in other words, they don't have type 1 at all at that age).
As I pointed out, the early stages of type 1 (known as the honeymoon stage) is going to be different because the disease is in the process of being created. This starts when the autoimmune response is triggered and ends when all or nearly all beta cells have been depleted. Once that has phase has ended, all type 1's are of the same "severity" in that we all don't make insulin. It's been known for at least decades (I personally have known for decades and learned from those who knew for decades before) that the honeymoon process takes several years. The reason it is news (or at least a reminder) for some is because more and more cases are being identified of adult-onset type 1 (now referred to as LADA or "type 1.5") where the honeymoon phase sometimes takes 10 years or longer. For quite some time (and to a lesser extent, this still happens), type 1's with adult onset (LADA / type 1.5) were misdiagnosed as type 2 because diagnosis was made based on symptoms rather than the underlying cause.
As far as beta cell dysfunction, it is highly unlikely. Type 1 diabetes is an auto-immune disease. My immune system attacked my pancreatic beta cells not to disarm beta cells, but to remove them.
Actually, no, my point is that if you take 100 random type 1s you have no idea if they've all at the same stage or not. Some may have gotten as low as they ever will. Some may not have as of yet.
Even if you assume that all have reached their nadir, you have no idea if all of their 'most are dead' are at the same functional level or not. There is variance.
Just so you know, I've been involved in quite a bit of autoimmune research. I'm not ignorant of the basic mechanisms of that class of diseases. Just because a disease is autoimmune does not necessarily mean the effects are all or nothing. The fact that Type 1 diabetes is an autoimmune disease does not make it any more or less likely that some individuals may have dysfunctional beta cells rather than killed beta cells.
Again, correct for all variables and you will find that a gram of carbs does not become the same amount of energy for everyone. I think you have missed my point by focusing on variables and arguing the extent to which they can be controlled for in research. My point still stands, even if you can't figure out how to design a study to prove or disprove it with 100% accuracy.
This seems like a variant of "well we're not all machines, so calories aren't calories" argument.
Which strikes me as a problem because let's make an analogy about T1D's.
Let's take a standardized measure of calories - the amount available in one gallon of regular 87 octane gasoline
Let's take two 1985 chevy impalas. Now, we'll accept that we've controlled that by being two 1985 chevy impalas with same options, they clearly are more alike than even two identical twin humans. Right down to they have the same size gas tank so the 1 gallon is going to fit similarly.
No one would say a calorie isn't a calorie because two people using the cars can drive them different distances on 1 gallon of gas, even if those two distances are equal work because the terrain is the same. Everyone would say of course things like how fast you burn the gas and accelerate, what the cars actual condition is, etc, are all going to impact how far you can travel on that one gallon of gas. No one would argue the gasoline in the two vehicles was different because of the recorded MPG was different, even though they're the same kind of car. It would be held as a poor argument. Yet people use this argument about humans all the time and human individuality to argue that calories aren't calories because people aren't machines. Well, as far as thermodynamics are concerned, we are machine, we have to obey the known laws of physics, and as far as comparisons go, machines aren't machines - they don't all function the same either, even when they're built to the same standards. This doesn't negate the fact that properly test, 87 octane has, on average, the same amount of calories burnable by properly calibrated equipment per gallon. Within the limits of the food itself we make, it is similar. And yes, just like the MPG sticker on the car, there will be variance on what you get out of them in practical, day to day life. It doesn't mean the gasoline is the issue, or that energy doesn't matter, or that if you take the same car and give it more gasoline, it is probably going to drive further.
Humans will of course be a little more complex. We're kind of like a plug-in hybrid, having different energy sources we can use long and short term, but energy is energy.
I'm not saying that the "gasoline" (calories) is different. I'm saying they don't get digested and used quite the same in every person. I wish it were as simple as how many believe CICO works, but it is more complicated than that.
They'll get used differently by the same person even. Doesn't really change you can do pretty accurate estimates based on mileage and gas tank emptying to figure out the MPG of your driving style for the vehicle, so long as one is diligent in record keeping.
No, that is my original point. For most, you are correct. However, there are some cars that are very different. Those cars do not operate consistently; they do not operate as most other cars of the same year, make, and model; and they don't even all operate similarly to other vehicles with the same type of problem. Many drivers who have only ever driven cars without such problems would argue that all cars operate the same, but perhaps on a slightly different scale. The argument is made that, even if a car's issues have decreased the mpg by 15%, there are still driving habits that can bring the mpg back to what they get from their car in good condition. They just say that it is more difficult - drivers of those cars must take more extreme measures and try things like shutting off the engine when coasting downhill, not using any temperature management systems, and over-inflating tires. Still, they believe that taking more difficult measures can provide the same results. What those drivers don't know is that those of us with problems on our cars are already taking much more difficult measures and still can't match anywhere close to the same mpg as their car in good condition.
Here's the problem that everyone ignores about the analogy because they're thinking about it in terms of what they want to happen, instead of the actual tie between the two in terms of thermodynamics. Most people want to lose weight beyond the expected based on calories (that's the good thing to them in that situation), and they want their car to get super high MPG. So people assume an person is more efficient (uses less calories) even though, if you pay attention to how efficiency works, including in the context of evolution fighting to make this happen for billions of years, just like a car, being broken (unhealthy / metabolic abnormality) is most likely to decrease efficiency, meaning you lose weight faster than predicted. Your body is going to do the least amount of work if everything is working as planned - having things not working right means your body has to do extra work, use extra calories, and burn more. Just the same as a car that has issues is going to use more gas and get worse MPG.
Your analogies all about saving gas to get higher MPG show the problem people have with following the analogy based on thinking in terms of desired outcome, instead of in terms of actual mechanics. The nature of the universe is to go towards inefficiency, not spontaneous increases in efficiency.
That might be true for most people and it might not be... I don't have data to say either way. Personally, I just want to see some (any) improvement in gas mileage when I shut off the engine downhill, over-inflate the tires, and don't use temperature management systems. When I do that for months and see no improvement, despite everyone and even science telling me that those things will work, it is difficult to justify making the extra effort.
I believe you technically want the MPG to get worse.
Your belief of my desire and my actual desire are not the same.0
This discussion has been closed.
Categories
- All Categories
- 1.4M Health, Wellness and Goals
- 391.2K Introduce Yourself
- 43.4K Getting Started
- 259.7K Health and Weight Loss
- 175.6K Food and Nutrition
- 47.3K Recipes
- 232.3K Fitness and Exercise
- 385 Sleep, Mindfulness and Overall Wellness
- 6.4K Goal: Maintaining Weight
- 8.5K Goal: Gaining Weight and Body Building
- 152.7K Motivation and Support
- 7.8K Challenges
- 1.3K Debate Club
- 96.4K Chit-Chat
- 2.5K Fun and Games
- 3.2K MyFitnessPal Information
- 22 News and Announcements
- 895 Feature Suggestions and Ideas
- 2.2K MyFitnessPal Tech Support Questions