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Intermittent Fasting: help me logic this article
Expatmommy79
Posts: 940 Member
So I am in a discussion about IF with another group. I said with calorie deficit and macros being the same, the Intermittent faster should not lose weight faster than the rest.
Then she presented this:
http://www.ncbi.nlm.nih.gov/m/pubmed/22608008/
Now what?! Was I wrong?
Then she presented this:
http://www.ncbi.nlm.nih.gov/m/pubmed/22608008/
Now what?! Was I wrong?
0
Replies
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So... we let mice eat as much as they want, but some mice we let do this all day, and others we forced them only to do it during 8 hours. We found mice with access to food 24/7 got fatter.we subjected mice to either ad lib or time-restricted feeding (tRF) of a HFD for 8 hr per day.
Okay, past the abstract, the claim is they normalized for body weight and that the energy intake was identical?
Even assuming intake was identical, activity isn't. They mentioned that the ad libium mice are waking during the day to eat, and getting disturbed sleep pattern. I'd say that could explain their metabolic issues just as strongly as anything to do with feeding schedule.2 -
There are mice getting ripped with IF?0
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The time restricted (IF) mice had a higher metabolic rate on both diets according to Fig 1F, hence oxidised more of what they ate.0
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Yep, there's much more to it.0
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It might be worth doing more research on. I've seen human studies that suggest daily eating patterns do influence metabolic rate, including the metabolic rate increasing with extended periods of fasting within the 24 hour period. Overall the change isn't much, and won't matter much long term as far as weight control goes.
I've actually noticed a change in heart rate as the interval between meals increases, and can be somewhat altered by my eating habits.0 -
Just have them look up Jason Fung on YouTube. He is a medical doctor that reverses diabetes on real people with fasting regimens. His videos are amazing and shows proof with studies that fasting is really good for people.0
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One thing that is happening here is the fasted mice are switching primarily to fat metabolism during the fast. When glucose stores get low, the mitochondria begin breaking down triglycerides instead of glucose for fuel, the krebs cycle becomes overwhelmed with ATP (since triglycerides create way more of it per molecule), and the ATP is diverted into the ketogenic pathway, creating ketone bodies. The average human will enter a state of mild ketosis when fasted 10-14 hrs.
There are many many known benefits to ketosis, and I'm sure many more unknown. Fasting has been linked to longer lifespan in animal studies. This might be because there are unique enzymatic pathways activated during ketosis (be it from fasting or carbohydrate restriction), one of them called the sirtuins, which is a family of genes turned on by the mitochondria during fat metabolism and linked to longer lifespan. I think the suggested mechanism is that the mitochondria (which control cellular apoptosis) function more efficiently on fat metabolism (they do not produce the same amount of oxidative stress) and, therefore, do not destroy the cell as quickly. The question here is if fasting increases metabolic rate. I'm not sure of that, but it may benefit by the increased insulin sensitivity or the increased metabolic cost of gluconeogenesis during ketosis, among other metabolic changes.0 -
aqsylvester wrote: »One thing that is happening here is the fasted mice are switching primarily to fat metabolism during the fast. When glucose stores get low, the mitochondria begin breaking down triglycerides instead of glucose for fuel, the krebs cycle becomes overwhelmed with ATP (since triglycerides create way more of it per molecule), and the ATP is diverted into the ketogenic pathway, creating ketone bodies. The average human will enter a state of mild ketosis when fasted 10-14 hrs.
There are many many known benefits to ketosis, and I'm sure many more unknown. Fasting has been linked to longer lifespan in animal studies. This might be because there are unique enzymatic pathways activated during ketosis (be it from fasting or carbohydrate restriction), one of them called the sirtuins, which is family of genes turned on by the mitochondria during fat metabolism and linked to longer lifespan. I think the suggested mechanism is that the mitochondria (which control cellular apoptosis) function more efficiently on fat metabolism (they do not produce the same amount of oxidative stress) and, therefore, do not destroy the cell as quickly. The question here is if fasting increases metabolic rate. I'm not sure of that, but it may benefit by the increased insulin sensitivity or the increased metabolic cost of gluconeogenesis during ketosis, among other metabolic changes.
You're still wrong about how ketosis works.0 -
stevencloser wrote: »aqsylvester wrote: »One thing that is happening here is the fasted mice are switching primarily to fat metabolism during the fast. When glucose stores get low, the mitochondria begin breaking down triglycerides instead of glucose for fuel, the krebs cycle becomes overwhelmed with ATP (since triglycerides create way more of it per molecule), and the ATP is diverted into the ketogenic pathway, creating ketone bodies. The average human will enter a state of mild ketosis when fasted 10-14 hrs.
There are many many known benefits to ketosis, and I'm sure many more unknown. Fasting has been linked to longer lifespan in animal studies. This might be because there are unique enzymatic pathways activated during ketosis (be it from fasting or carbohydrate restriction), one of them called the sirtuins, which is family of genes turned on by the mitochondria during fat metabolism and linked to longer lifespan. I think the suggested mechanism is that the mitochondria (which control cellular apoptosis) function more efficiently on fat metabolism (they do not produce the same amount of oxidative stress) and, therefore, do not destroy the cell as quickly. The question here is if fasting increases metabolic rate. I'm not sure of that, but it may benefit by the increased insulin sensitivity or the increased metabolic cost of gluconeogenesis during ketosis, among other metabolic changes.
You're still wrong about how ketosis works.
Steven, why don't you explain ketosis? And also explain how I'm "wrong about how ketosis works."1 -
http://www.ncbi.nlm.nih.gov/books/NBK21190/
http://sportsscientists.com/2010/01/exercise-and-weight-loss-part-3-fat/
At rest you won't be using much of your glycogen, but instead fat for your energy needs. Glycogen is there for two reasons: keeping your blood sugar normal in between eating is your liver glycogen's job and fuelling intense exercise your muscle glycogen's. Your body doesn't just use it up all willy-nilly.
Overnight is about the most at rest you ever are so the only glycogen you'll be using is going to be for keeping your blood sugar steady. You aren't going to use up all your liver glycogen during that time.
Your glycogen doesn't get low, you're not gonna start producing any more ketones than usually and it's not ATP that's diverted into the ketogenic pathway to begin with anyway. ATP is the end product, usable for getting energy.
Acetyl-CoA gotten from triglycerides gets turned to ketones in the liver because the necessary oxaloacetate for entering the krebs cycle to turn it into ATP is instead being used for gluconeogenesis when your glycogen stores are actually running low to keep you from going hypoglycemic.
So to break down:
You won't use up all your glycogen just overnight while sleeping
You're always breaking down triglycerides for fuel, especially while you're at rest
Your Krebs cycle is neither overwhlemed by ATP nor is it ATP that's creating ketones
P.S. you have about 100-120 g of liver glycogen on average. That's up to 480 kcal or a good quarter of a whole day's worth of calories for a grown man. You don't use 50% of your energy from glucose during the 12-ish hours of mostly rest between your last meal and breakfast next day unless you're running a marathon at night.18 -
aqsylvester wrote: »stevencloser wrote: »aqsylvester wrote: »One thing that is happening here is the fasted mice are switching primarily to fat metabolism during the fast. When glucose stores get low, the mitochondria begin breaking down triglycerides instead of glucose for fuel, the krebs cycle becomes overwhelmed with ATP (since triglycerides create way more of it per molecule), and the ATP is diverted into the ketogenic pathway, creating ketone bodies. The average human will enter a state of mild ketosis when fasted 10-14 hrs.
There are many many known benefits to ketosis, and I'm sure many more unknown. Fasting has been linked to longer lifespan in animal studies. This might be because there are unique enzymatic pathways activated during ketosis (be it from fasting or carbohydrate restriction), one of them called the sirtuins, which is family of genes turned on by the mitochondria during fat metabolism and linked to longer lifespan. I think the suggested mechanism is that the mitochondria (which control cellular apoptosis) function more efficiently on fat metabolism (they do not produce the same amount of oxidative stress) and, therefore, do not destroy the cell as quickly. The question here is if fasting increases metabolic rate. I'm not sure of that, but it may benefit by the increased insulin sensitivity or the increased metabolic cost of gluconeogenesis during ketosis, among other metabolic changes.
You're still wrong about how ketosis works.
Steven, why don't you explain ketosis? And also explain how I'm "wrong about how ketosis works."
Gotta to love the new 'like' buttons
No idea why you are 'wrong', but you may want to Google 'gaslighting'. That's just my guess. (also, 'astroturfing')
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KarlynKeto wrote: »aqsylvester wrote: »stevencloser wrote: »aqsylvester wrote: »One thing that is happening here is the fasted mice are switching primarily to fat metabolism during the fast. When glucose stores get low, the mitochondria begin breaking down triglycerides instead of glucose for fuel, the krebs cycle becomes overwhelmed with ATP (since triglycerides create way more of it per molecule), and the ATP is diverted into the ketogenic pathway, creating ketone bodies. The average human will enter a state of mild ketosis when fasted 10-14 hrs.
There are many many known benefits to ketosis, and I'm sure many more unknown. Fasting has been linked to longer lifespan in animal studies. This might be because there are unique enzymatic pathways activated during ketosis (be it from fasting or carbohydrate restriction), one of them called the sirtuins, which is family of genes turned on by the mitochondria during fat metabolism and linked to longer lifespan. I think the suggested mechanism is that the mitochondria (which control cellular apoptosis) function more efficiently on fat metabolism (they do not produce the same amount of oxidative stress) and, therefore, do not destroy the cell as quickly. The question here is if fasting increases metabolic rate. I'm not sure of that, but it may benefit by the increased insulin sensitivity or the increased metabolic cost of gluconeogenesis during ketosis, among other metabolic changes.
You're still wrong about how ketosis works.
Steven, why don't you explain ketosis? And also explain how I'm "wrong about how ketosis works."
Gotta to love the new 'like' buttons No idea why you are 'wrong', but you may want to Google 'gaslighting'. That's just my guess. (also, 'astroturfing')
Mental abuse? Because someone questions the person who repeatedly posts that no person on the planet loses weight unless they are in ketosis (apparently said ketosis is transient in people who don't actually follow a ketogenic diet)?
Really?5 -
I posted links to a study from a year or more back regarding weight loss in people who ate twice per day versus four times per day but the same calorie count. The people who ate twice per day averaged more weight loss. I can't recall the rationale.0
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stevencloser wrote: »http://www.ncbi.nlm.nih.gov/books/NBK21190/
http://sportsscientists.com/2010/01/exercise-and-weight-loss-part-3-fat/
At rest you won't be using much of your glycogen, but instead fat for your energy needs. Glycogen is there for two reasons: keeping your blood sugar normal in between eating is your liver glycogen's job and fuelling intense exercise your muscle glycogen's. Your body doesn't just use it up all willy-nilly.
Overnight is about the most at rest you ever are so the only glycogen you'll be using is going to be for keeping your blood sugar steady. You aren't going to use up all your liver glycogen during that time.
Your glycogen doesn't get low, you're not gonna start producing any more ketones than usually and it's not ATP that's diverted into the ketogenic pathway to begin with anyway. ATP is the end product, usable for getting energy.
Acetyl-CoA gotten from triglycerides gets turned to ketones in the liver because the necessary oxaloacetate for entering the krebs cycle to turn it into ATP is instead being used for gluconeogenesis when your glycogen stores are actually running low to keep you from going hypoglycemic.
So to break down:
You won't use up all your glycogen just overnight while sleeping
You're always breaking down triglycerides for fuel, especially while you're at rest
Your Krebs cycle is neither overwhlemed by ATP nor is it ATP that's creating ketones
P.S. you have about 100-120 g of liver glycogen on average. That's up to 480 kcal or a good quarter of a whole day's worth of calories for a grown man. You don't use 50% of your energy from glucose during the 12-ish hours of mostly rest between your last meal and breakfast next day unless you're running a marathon at night.
Yes, sorry, I meant Acetyl-CoA instead of ATP. Other than that, don't see anything else incorrect. The Krebs cycle is overwhelmed by Acetyl-CoA during fat metabolism.
And I misunderstood that fasting cycles. I thought it was fasting every other day--confused it with a similar study I read. So maybe they aren't switching to fat metabolism, but at the very least, the study seems to suggest benefits to abstaining from caloric intake. Most who practice intermittent fasting would be doing so for at least 18 hrs, at which point, yes, they would be making ketones.
That being said, I'm not sure what HFD entails. It may have therefore been low in carbohydrates.0 -
The krebs cycle is not overwhelmed by acetyl-coa. The oxaloacetate in the liver is used for something more important than the krebs cycle so the acetyl-coa can't even enter it. the acetyl-coa is instead turned to ketones to be transported elsewhere where it can be used.
I'm doing intermittent fasting and the most common forms of it are 16 hours fasting (which is basically skipping breakfast) which I'm doing or 5:2 which is 5 days of normal maintenance eating with 2 days of low caloric intake with no rules for when to eat as far as I know.
I can assure you I'm not creating any appreciable amount of ketones more than anyone who is eating their breakfast.2 -
stevencloser wrote: »The krebs cycle is not overwhelmed by acetyl-coa. The oxaloacetate in the liver is used for something more important than the krebs cycle so the acetyl-coa can't even enter it. the acetyl-coa is instead turned to ketones to be transported elsewhere where it can be used.
I'm doing intermittent fasting and the most common forms of it are 16 hours fasting (which is basically skipping breakfast) which I'm doing or 5:2 which is 5 days of normal maintenance eating with 2 days of low caloric intake with no rules for when to eat as far as I know.
I can assure you I'm not creating any appreciable amount of ketones more than anyone who is eating their breakfast.
Ok, what is the "something more important"?
And regardless of the details of the steps involved, the end result of fat metabolism is ketones if the average person is in mild ketosis within 10-14 hrs of fasting.0 -
Gluconeogenesis.
Both the Krebs cycle and gluconeogenesis need the oxaloacetate, but in a state of glycogen depletion, gluconeogenesis is pretty much essential for survival to keep your blood sugar from tanking.
And you're still wrong. The end result of fat metabolism is ATP.
Body fat -> triglycerides
triglycerides -> lipolysis -> fatty acids
fatty acids -> beta oxidation -> Acetyl-CoA
Acetyl-CoA -> Krebs Cycle -> ATP
This works entirely without ketones.
I haven't eaten in 11 hours now. And I'm not in mild Ketosis.
Ketosis has a definition.
Ketosis is when the amount of ketones in your urine rises due to increased production.
It can be detected with test strips and the distinct smell, as well as the often experienced keto-flu as the brain which runs on mostly glucose needs to adjust to using ketones in higher amounts. This takes multiple days generally. You'd notice if your glycogen was almost empty.4 -
stevencloser wrote: »http://www.ncbi.nlm.nih.gov/books/NBK21190/
http://sportsscientists.com/2010/01/exercise-and-weight-loss-part-3-fat/
At rest you won't be using much of your glycogen, but instead fat for your energy needs. Glycogen is there for two reasons: keeping your blood sugar normal in between eating is your liver glycogen's job and fuelling intense exercise your muscle glycogen's. Your body doesn't just use it up all willy-nilly.
Overnight is about the most at rest you ever are so the only glycogen you'll be using is going to be for keeping your blood sugar steady. You aren't going to use up all your liver glycogen during that time.
Your glycogen doesn't get low, you're not gonna start producing any more ketones than usually and it's not ATP that's diverted into the ketogenic pathway to begin with anyway. ATP is the end product, usable for getting energy.
Acetyl-CoA gotten from triglycerides gets turned to ketones in the liver because the necessary oxaloacetate for entering the krebs cycle to turn it into ATP is instead being used for gluconeogenesis when your glycogen stores are actually running low to keep you from going hypoglycemic.
So to break down:
You won't use up all your glycogen just overnight while sleeping
You're always breaking down triglycerides for fuel, especially while you're at rest
Your Krebs cycle is neither overwhlemed by ATP nor is it ATP that's creating ketones
P.S. you have about 100-120 g of liver glycogen on average. That's up to 480 kcal or a good quarter of a whole day's worth of calories for a grown man. You don't use 50% of your energy from glucose during the 12-ish hours of mostly rest between your last meal and breakfast next day unless you're running a marathon at night.
I've been reading up on some of the keto adapted endurance people, and they defy this thinking. They stay in ketosis but still replenish glycogen stores by pushing the limits of staying in ketosis but yet "carb loading" in a slow methodical way before races and some training.
I agree with the basics of your post, but have seen some stuff that leads me to think it's a bit more complex than stated. Those in keto retain glycogen stores, but the replenishment part of the picture gets blurry. But then again, replenishment of glycogen even in us carb eaters isn't really quick either, and can somewhat vary.0 -
stevencloser wrote: »Gluconeogenesis.
Both the Krebs cycle and gluconeogenesis need the oxaloacetate, but in a state of glycogen depletion, gluconeogenesis is pretty much essential for survival to keep your blood sugar from tanking.
And you're still wrong. The end result of fat metabolism is ATP.
Body fat -> triglycerides
triglycerides -> lipolysis -> fatty acids
fatty acids -> beta oxidation -> Acetyl-CoA
Acetyl-CoA -> Krebs Cycle -> ATP
This works entirely without ketones.
I haven't eaten in 11 hours now. And I'm not in mild Ketosis.
Ketosis has a definition.
Ketosis is when the amount of ketones in your urine rises due to increased production.
It can be detected with test strips and the distinct smell, as well as the often experienced keto-flu as the brain which runs on mostly glucose needs to adjust to using ketones in higher amounts. This takes multiple days generally. You'd notice if your glycogen was almost empty.
@stevencloser
I understand your definition, but according to UpToDate, which is the evidence-based, peer-reviewed clinical decision resource that I use at my work, the average person will be in mild ketosis after 10-14 hrs of fasting, which equates to a blood ketoacid level of 1 mmol/L. I don't see any mention of the importance of diagnosis with urine ketostrips or any mention that this is the definition of ketosis.
Also my understanding is if the amounts of acetyl-CoA challenge the processing capacity of the Krebs cycle (if activity in Krebs cycle is low due to low amounts of intermediates such as oxaloacetate), the acetyl-CoA is used instead to synthesize ketone bodies.
If we know 1. that ketones have many metabolic and neurological benefits, 2. that they are instigated by fasting (or carbohydrate restriction), then I don't think it's a far leap to say 3. maybe some of these inexplicable benefits of fasting even for less than 24 hrs are related to the effect of ketones, i.e. ketosis, or the process by when they are created (which, for example, creates less oxidative stress, i.e. reactive oxygen species).0 -
I'm by no means an expert in this but recently spent a little time looking for any study which compared IF to "normal" eating protocols in humans.
There were studies which showed that ad libium IF was a useful tool for weight loss (usually in obese subjects) where, presumably, IF simply generated a greater deficit than other protocols.
I could find no studies in which the control and subject groups were fed isocalorifically except where they were specifically studying the effects on exercise performance (which wasn't what I was looking for at the time). Others may have more success?
Going back to Mosley's 5:2 fast diet and re-reading the text and cross refs to studies, it seemed to me that the benefits that he was stating were at the least "on the generous side". I'm not saying I'm anti IF - It is a technique I use often, but rather that for me, it is a tool which helps me to adhere to my allotted calories.0 -
aqsylvester wrote: »stevencloser wrote: »Gluconeogenesis.
Both the Krebs cycle and gluconeogenesis need the oxaloacetate, but in a state of glycogen depletion, gluconeogenesis is pretty much essential for survival to keep your blood sugar from tanking.
And you're still wrong. The end result of fat metabolism is ATP.
Body fat -> triglycerides
triglycerides -> lipolysis -> fatty acids
fatty acids -> beta oxidation -> Acetyl-CoA
Acetyl-CoA -> Krebs Cycle -> ATP
This works entirely without ketones.
I haven't eaten in 11 hours now. And I'm not in mild Ketosis.
Ketosis has a definition.
Ketosis is when the amount of ketones in your urine rises due to increased production.
It can be detected with test strips and the distinct smell, as well as the often experienced keto-flu as the brain which runs on mostly glucose needs to adjust to using ketones in higher amounts. This takes multiple days generally. You'd notice if your glycogen was almost empty.
@stevencloser
I understand your definition, but according to UpToDate, which is the evidence-based, peer-reviewed clinical decision resource that I use at my work, the average person will be in mild ketosis after 10-14 hrs of fasting, which equates to a blood ketoacid level of 1 mmol/L. I don't see any mention of the importance of diagnosis with urine ketostrips or any mention that this is the definition of ketosis.
Also my understanding is if the amounts of acetyl-CoA challenge the processing capacity of the Krebs cycle (if activity in Krebs cycle is low due to low amounts of intermediates such as oxaloacetate), the acetyl-CoA is used instead to synthesize ketone bodies.
If we know 1. that ketones have many metabolic and neurological benefits, 2. that they are instigated by fasting (or carbohydrate restriction), then I don't think it's a far leap to say 3. maybe some of these inexplicable benefits of fasting even for less than 24 hrs are related to the effect of ketones, i.e. ketosis, or the process by when they are created (which, for example, creates less oxidative stress, i.e. reactive oxygen species).
You always have an amount of ketone bodies in your blood, fasting or not. The normal concentration is that 1 mmol/l and is undetectable by Rothera's test, which is the standard test to check if you're in ketosis.2 -
stevencloser wrote: »aqsylvester wrote: »stevencloser wrote: »Gluconeogenesis.
Both the Krebs cycle and gluconeogenesis need the oxaloacetate, but in a state of glycogen depletion, gluconeogenesis is pretty much essential for survival to keep your blood sugar from tanking.
And you're still wrong. The end result of fat metabolism is ATP.
Body fat -> triglycerides
triglycerides -> lipolysis -> fatty acids
fatty acids -> beta oxidation -> Acetyl-CoA
Acetyl-CoA -> Krebs Cycle -> ATP
This works entirely without ketones.
I haven't eaten in 11 hours now. And I'm not in mild Ketosis.
Ketosis has a definition.
Ketosis is when the amount of ketones in your urine rises due to increased production.
It can be detected with test strips and the distinct smell, as well as the often experienced keto-flu as the brain which runs on mostly glucose needs to adjust to using ketones in higher amounts. This takes multiple days generally. You'd notice if your glycogen was almost empty.
@stevencloser
I understand your definition, but according to UpToDate, which is the evidence-based, peer-reviewed clinical decision resource that I use at my work, the average person will be in mild ketosis after 10-14 hrs of fasting, which equates to a blood ketoacid level of 1 mmol/L. I don't see any mention of the importance of diagnosis with urine ketostrips or any mention that this is the definition of ketosis.
Also my understanding is if the amounts of acetyl-CoA challenge the processing capacity of the Krebs cycle (if activity in Krebs cycle is low due to low amounts of intermediates such as oxaloacetate), the acetyl-CoA is used instead to synthesize ketone bodies.
If we know 1. that ketones have many metabolic and neurological benefits, 2. that they are instigated by fasting (or carbohydrate restriction), then I don't think it's a far leap to say 3. maybe some of these inexplicable benefits of fasting even for less than 24 hrs are related to the effect of ketones, i.e. ketosis, or the process by when they are created (which, for example, creates less oxidative stress, i.e. reactive oxygen species).
You always have an amount of ketone bodies in your blood, fasting or not. The normal concentration is that 1 mmol/l and is undetectable by Rothera's test, which is the standard test to check if you're in ketosis.
You are incorrect. 1 mmol/L is not negative/normal baseline. A ketoacid blood level of > 0.6 mmol/L equates to a negative urine test; a blood ketoacid level of 0.6 - 1.5 mmol/L equates to small to moderate urine ketone reading. Blood and urine ketone tests do not always agree because urine could have been sitting in the bladder for many hours, but a blood ketone test is far more accurate.0 -
@StealthHealthStealthHealth wrote: »I'm by no means an expert in this but recently spent a little time looking for any study which compared IF to "normal" eating protocols in humans.
There were studies which showed that ad libium IF was a useful tool for weight loss (usually in obese subjects) where, presumably, IF simply generated a greater deficit than other protocols.
I could find no studies in which the control and subject groups were fed isocalorifically except where they were specifically studying the effects on exercise performance (which wasn't what I was looking for at the time). Others may have more success?
Going back to Mosley's 5:2 fast diet and re-reading the text and cross refs to studies, it seemed to me that the benefits that he was stating were at the least "on the generous side". I'm not saying I'm anti IF - It is a technique I use often, but rather that for me, it is a tool which helps me to adhere to my allotted calories.
I did 5:2 and found it a great adherence tool but do agree that Michael Mosley seems to have done some cherry picking and made some assumptions/conclusions not really backed by, or taken out of context, from the various studies referenced.
If you are interested would suggest looking for the work by Dr Krista Varady who carried out a far more scientific studies/research on ADF.
She actually had a bit of an issue with Mosley and insisted her studies were removed from later print runs of The Fast Diet.
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@StealthHealthStealthHealth wrote: »I'm by no means an expert in this but recently spent a little time looking for any study which compared IF to "normal" eating protocols in humans.
There were studies which showed that ad libium IF was a useful tool for weight loss (usually in obese subjects) where, presumably, IF simply generated a greater deficit than other protocols.
I could find no studies in which the control and subject groups were fed isocalorifically except where they were specifically studying the effects on exercise performance (which wasn't what I was looking for at the time). Others may have more success?
Going back to Mosley's 5:2 fast diet and re-reading the text and cross refs to studies, it seemed to me that the benefits that he was stating were at the least "on the generous side". I'm not saying I'm anti IF - It is a technique I use often, but rather that for me, it is a tool which helps me to adhere to my allotted calories.
I did 5:2 and found it a great adherence tool but do agree that Michael Mosley seems to have done some cherry picking and made some assumptions/conclusions not really backed by, or taken out of context, from the various studies referenced.
If you are interested would suggest looking for the work by Dr Krista Varady who carried out a far more scientific studies/research on ADF.
She actually had a bit of an issue with Mosley and insisted her studies were removed from later print runs of The Fast Diet.
Thanks for that. I'll look into her work (I've heard of her and I think, I may have seen her on TV or a YouTube vid but not sure).0 -
stevencloser wrote: »Ketosis has a definition.
Ketosis is when the amount of ketones in your urine rises due to increased production.
You appear to be defining ketonuria. This may or may not occur when there are ketones in the blood.
Ketosis is more usually defined by elevated levels of ketones in the blood, which needs a test meter or a lab.
I would agree that there aren't many ketones around in overnight fasted people on a normal carbohydrate diet, this can be seen in the baseline fasted characteristics of any study that measures ketones in blood.
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aqsylvester wrote: »[
I understand your definition, but according to UpToDate, which is the evidence-based, peer-reviewed clinical decision resource that I use at my work, the average person will be in mild ketosis after 10-14 hrs of fasting, which equates to a blood ketoacid level of 1 mmol/L. I don't see any mention of the importance of diagnosis with urine ketostrips or any mention that this is the definition of ketosis.
In http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2548350/pdf/JAMMC-23-069.pdf the average in overnight fasted hospitalised children was 0.17 mmol/l B-OHB in serum. Acetoacetate levels were about half that.
http://www.clinsci.org/content/ppclinsci/81/2/189.full.pdf also shows low baseline levels :-
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@stevencloser
According to this talk by Mark Mattson (Chief of the Laboratory of Neurosciences at the National Institute on Aging and professor of Neuroscience at The Johns Hopkins University), if you go to 7:05, he mentions the 8-hr diet, where one restricts energy intake to an 8 hr window, which he says is long enough to shift energy metabolism to fat and get the benefits of ketones.
https://www.youtube.com/watch?v=4UkZAwKoCP8&nohtml5=False
He also mentions that it takes 10-12 hrs before you deplete the glycogen stores in your liver, faster if you exercise, and shift into ketosis... which also aligns well with what I read in UpToDate.
According to Mark Mattson, IF is not just about eating less calories and losing weight. He mentions their research finding an increase in brain derived neurotrophic factors which help increase the number of mitochonidria in nerve cells, thereby increasing learning and memory ability.
So, yeah... I'm not the only one who has thought this. And I'm kinda biased toward peer-reviewed databases and Johns Hopkins professors.
[edited by MFP Moderator]0 -
aqsylvester wrote: »@stevencloser
According to this talk by Mark Mattson (Chief of the Laboratory of Neurosciences at the National Institute on Aging and professor of Neuroscience at The Johns Hopkins University), if you go to 7:05, he mentions the 8-hr diet, where one restricts energy intake to an 8 hr window, which he says is long enough to shift energy metabolism to fat and get the benefits of ketones.https://www.youtube.com/watch?v=4UkZAwKoCP8&nohtml5=False
He also mentions that it takes 10-12 hrs before you deplete the glycogen stores in your liver, faster if you exercise, and shift into ketosis... which also aligns well with what I read in UpToDate.
According to Mark Mattson, IF is not just about eating less calories and losing weight. He mentions their research finding an increase in brain derived neurotrophic factors which help increase the number of mitochonidria in nerve cells, thereby increasing learning and memory ability.
So, yeah... I'm not the only one who has thought this. And I'm kinda biased toward peer-reviewed databases and Johns Hopkins professors.
[edited by MFP Moderator]
It may be 10-12 hours from the moment it starts to utilize it.
That is however not 10-12 hours after you last ate unless your meal didn't contain any carbs itself.0 -
aqsylvester wrote: »[
I understand your definition, but according to UpToDate, which is the evidence-based, peer-reviewed clinical decision resource that I use at my work, the average person will be in mild ketosis after 10-14 hrs of fasting, which equates to a blood ketoacid level of 1 mmol/L. I don't see any mention of the importance of diagnosis with urine ketostrips or any mention that this is the definition of ketosis.
In http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2548350/pdf/JAMMC-23-069.pdf the average in overnight fasted hospitalised children was 0.17 mmol/l B-OHB in serum. Acetoacetate levels were about half that.
http://www.clinsci.org/content/ppclinsci/81/2/189.full.pdf also shows low baseline levels :-
The question is, would you call this state "mild ketosis"?1 -
No I would not call 0.1 mmol mild ketosis, not least because it's the first notch on most measures. 0.5 or above to count in my view, below that the ketone uptake flux is too low to bother about.1
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