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Ketogenic Diets Suppress IGF-1

Not exactly, it takes about that to get there but not to get back into it if you barely took yourself out of it.







Just addressing the entire ketosis conversation above here. This is really not that surprising if you really understand the system, so I want to try to explain it a little.

Just going to bullet point and not go nuts here.

1) Once glycogen has been stored in the muscle, it can not be released back into the blood to be used as blood sugar.
2) Increased Insulin Sensitivity helps the body store more glycogen more efficiently, and CBL increases insulin sensitivity
3) The type of carbs used is also important here. If using easily digested carbohydrate source it takes far less time to for the carbohydrate source to clear the blood. CBL recommends easily digested carbs and avoid harder to digest carbs sources...
4) Eating shy of your maximum carb level post workout will result in storing the glycogen and lowering blood sugar drastically, even to the level of hypoglycemia. Hypoglycemia triggers the need for ketones as there is not enough blood sugar for the brain to be comfy. Hence ketones in the system.

As ValiantThor08 mentions he takes in a hundreds of grams of carbs nightly, and that makes sense if I remember correctly he isn't a small guy and with the amount of muscle I have I am supposed to be able to take in a good 600g a day. So if he is doing 300-400 with everything else in a good balance there is not any reason he couldn't be showing some ketosis on the strips.

Now is he in a depleted state? No not at all, his glycogen stores are far from empty, but his blood sugar stays low enough that ketones are needed for when he is just sitting around chilling. When he gets into working out that energy source shifts to using the glycogen stored in the muscle, but the rest of the day he is probably running off of ketones.

I also forgot to mention that it is quite common for people using CBL to go hypoglycemic in their sleep. Another thing pointing toward low enough blood sugar to require the need for ketones.

I think number 1 in this is the part most people actually do not know about and that makes all the difference in the world.
Thanks for the points Kleen! And I probably dont go beyond 300g carbs for dinner. More like 2 to 300.
 
172.8 5ft 10" in my briefs, before breakfast, after restroom. Lol

Very concise! LMOA! Yeah, I would be you have about 400 or so. Did you ever do the full 10 day primer weighing yourself beforehand and then weighing again once depleted? He uses a formula to figure out how many grams of carbs you need to refill completely based off of how much you lost while depleting.

If you stay below it as you are then your blood sugar is going to go right back too low pretty quickly after the meal, especially if eating the types of carbs he recommends.
 
Very concise! LMOA! Yeah, I would be you have about 400 or so. Did you ever do the full 10 day primer weighing yourself beforehand and then weighing again once depleted? He uses a formula to figure out how many grams of carbs you need to refill completely based off of how much you lost while depleting.

If you stay below it as you are then your blood sugar is going to go right back too low pretty quickly after the meal, especially if eating the types of carbs he recommends.
I only do simple carbs, and before I did CBL I was depleted because I had done keto, and at the time I was around 150, so since then, since July, have gone up to 176 (when holding extra water). Taking Virtus ldopa/green tea extract, so I would predict not holding too much water now. Have been enjoying carbs too much to go an extended time without carbs.
 
It’s too bad that Kiefer is so adamant that CBL won’t work with HIT type training. With my back injury that I train around and my heavy work schedule, HIT is a perfect fit for me.
 
Carb nite or CNS is a 10 day Keto as a primer/reset. Then depending on bf you carb up every 7 days
 
Your right.

I lost 40lbs a few years ago doing something similar. I was just doing a lot of cardio, no weight training(some p90x, but that was only for a bit before my back injury). Strict keto 6 days a week. Never counted a single calorie. Monday nights, anything went. A whole pizza, bottle of wine, and some chocolate covered pretzels or something of the sort. Having that night to look forward to each week kept me sane, and despite how reckless it sounds I dropped weight quick.
 
Not exactly, it takes about that to get there but not to get back into it if you barely took yourself out of it.







Just addressing the entire ketosis conversation above here. This is really not that surprising if you really understand the system, so I want to try to explain it a little.

Just going to bullet point and not go nuts here.

1) Once glycogen has been stored in the muscle, it can not be released back into the blood to be used as blood sugar.
2) Increased Insulin Sensitivity helps the body store more glycogen more efficiently, and CBL increases insulin sensitivity
3) The type of carbs used is also important here. If using easily digested carbohydrate source it takes far less time to for the carbohydrate source to clear the blood. CBL recommends easily digested carbs and avoid harder to digest carbs sources...
4) Eating shy of your maximum carb level post workout will result in storing the glycogen and lowering blood sugar drastically, even to the level of hypoglycemia. Hypoglycemia triggers the need for ketones as there is not enough blood sugar for the brain to be comfy. Hence ketones in the system.

As ValiantThor08 mentions he takes in a hundreds of grams of carbs nightly, and that makes sense if I remember correctly he isn't a small guy and with the amount of muscle I have I am supposed to be able to take in a good 600g a day. So if he is doing 300-400 with everything else in a good balance there is not any reason he couldn't be showing some ketosis on the strips.

Now is he in a depleted state? No not at all, his glycogen stores are far from empty, but his blood sugar stays low enough that ketones are needed for when he is just sitting around chilling. When he gets into working out that energy source shifts to using the glycogen stored in the muscle, but the rest of the day he is probably running off of ketones.

I also forgot to mention that it is quite common for people using CBL to go hypoglycemic in their sleep. Another thing pointing toward low enough blood sugar to require the need for ketones.

I think number 1 in this is the part most people actually do not know about and that makes all the difference in the world.

Great post. Not that I'll ever go full keto probably but still valid info.
 
Really? That is interesting. Does he give any reasoning? I have not read his book, but I should. From what I have read it seems like HIT would work well with CBL.
 
Really? That is interesting. Does he give any reasoning? I have not read his book, but I should. From what I have read it seems like HIT would work well with CBL.

He specifically mentions “mike mentzer heavy duty training” and says it doesnt transpose GLUT4 receptors the way volume training does. In a nutshell, anyway, thats what he said. Give me a bit of rope here.
 
It’s too bad that Kiefer is so adamant that CBL won’t work with HIT type training. With my back injury that I train around and my heavy work schedule, HIT is a perfect fit for me.
You can do HIT with it, but no it is not as ideal, similarly to how slow negatives aren't really considered good for it either.
Carb nite or CNS is a 10 day Keto as a primer/reset. Then depending on bf you carb up every 7 days
Right I think it is 4-7 days depening on leanness and other goals. He said any less than 4 days and you need to move on to CBL. Once at 4 days you are flirting with still having the ability to convert and store carbohydrate as fat. That ability is removed after 4-5 days with minimal carbs as the body stops making the conversion enzyme temporarily.
Sounds more like CKD...
Well that is exactly what it is with some more specific guidelines. Same as The Ultimate Diet and Ultimate Diet 2.0, it is a CKD too but has very specific instructions. The deficit when doing CNS is much lower during the week than your typical Keto diet.
He specifically mentions “mike mentzer heavy duty training” and says it doesnt transpose GLUT4 receptors the way volume training does. In a nutshell, anyway, thats what he said. Give me a bit of rope here.

That really depends on how many warm up sets you are doing as well. However that just means you would probably want to undershoot your max carbs by a little bit to make sure you don't overspill. You are still going to get Glut-4 translocation, just not as much due to the lower volume of work. Also by waiting until the end of the day to have your carbs you burn more fat throughout the day for energy while doing low intensity anything. Your insulin sensitivity will also be high due to not having had any carbs all day and the body wanting them.

Kind of surprised to hear you are using HIT because of a back injury. I would be avoiding HIT on any place I had an injury. The entire idea is to go into the scary and somewhat unsafe zone of intensity where form often breaks down. That just sounds like a bad situation for an injured body part.

How do you incorporate it and how do you feel it helps or is safer over a somewhat higher volume set up?
 
Carb nite or CNS is a 10 day Keto as a primer/reset. Then depending on bf you carb up every 7 days
You might as well drop the fat and do a PSMF at this point.

If for a period of time you don’t have to do any aerobic activity, PSMF will create a greater defecit and a better muscle sparing environment IF you can do it.

Thinking you’d Losing actual LBM in 10 days all while lifting to stimulate and hitting your protein requirements is a preposterous thought.

If your goal was to gain muscle on your cut your probably not anyone on the AM, or you are if you plan on doing it with AAS.

Natural ranges of IGF1 will do **** all for you anyways. It sucks that our hormones won’t do what we desire them to do unless they are at superfluous levels.
 
You might as well drop the fat and do a PSMF at this point.

If for a period of time you don’t have to do any aerobic activity, PSMF will create a greater defecit and a better muscle sparing environment IF you can do it.

Thinking you’d Losing actual LBM in 10 days all while lifting to stimulate and hitting your protein requirements is a preposterous thought.

If your goal was to gain muscle on your cut your probably not anyone on the AM, or you are if you plan on doing it with AAS.

Natural ranges of IGF1 will do **** all for you anyways. It sucks that our hormones won’t do what we desire them to do unless they are at superfluous levels.

He didn't mention what level of fat there would be, or how much of a deficit, so that is a pretty big jump to conclusions. The first week 10 days of CNS is very low calorie too. Not quite 900, but very close. The premise is to create a massive deficit during the week then cut into it just a little with a massive anabolic refeed that increases leptin keeping the metabolism from dropping of like it normally does with a deficit.

If you have more than 10lbs of fat to lose then a PSMF is not going to be ideal because are SUPPOSED to follow the 10-14 days with 2 weeks maintenance to replete leptin levels. At that point CNS blows right by the PMSF in fat loss. With CNS you get very close to the same fat loss and replenish leptin to keep the metabolism from dropping every 4-7 days. Pretty much same premise just takes it one step further to maintain fat loss efficiency, and allows you to be in a big deficit a much higher percent of the time compared to PMSF.

PMSF over a month 10-14 days in deficit and keto style then back to maintenance for 2 weeks = 47% of the month in a steep deficit

CNS over a month - 26 days in deficit and keto style eating, and 4 days in surplus = 87% of the month in a steep deficit

On top of that you can run CNS for a very long time succesfully which you can not do with PMSF, or at least should not do...
 
You can do HIT with it, but no it is not as ideal, similarly to how slow negatives aren't really considered good for it either.

Right I think it is 4-7 days depening on leanness and other goals. He said any less than 4 days and you need to move on to CBL. Once at 4 days you are flirting with still having the ability to convert and store carbohydrate as fat. That ability is removed after 4-5 days with minimal carbs as the body stops making the conversion enzyme temporarily.

Well that is exactly what it is with some more specific guidelines. Same as The Ultimate Diet and Ultimate Diet 2.0, it is a CKD too but has very specific instructions. The deficit when doing CNS is much lower during the week than your typical Keto diet.


That really depends on how many warm up sets you are doing as well. However that just means you would probably want to undershoot your max carbs by a little bit to make sure you don't overspill. You are still going to get Glut-4 translocation, just not as much due to the lower volume of work. Also by waiting until the end of the day to have your carbs you burn more fat throughout the day for energy while doing low intensity anything. Your insulin sensitivity will also be high due to not having had any carbs all day and the body wanting them.

Kind of surprised to hear you are using HIT because of a back injury. I would be avoiding HIT on any place I had an injury. The entire idea is to go into the scary and somewhat unsafe zone of intensity where form often breaks down. That just sounds like a bad situation for an injured body part.

How do you incorporate it and how do you feel it helps or is safer over a somewhat higher volume set up?

Well, in simple terms HIT is machine friendly. Heavy squats, deadlifts and heavy free weights in general are just a no go for me. Also, the slow rep cadence *feels* safer to me than standard lifting.
 
Well, in simple terms HIT is machine friendly. Heavy squats, deadlifts and heavy free weights in general are just a no go for me. Also, the slow rep cadence *feels* safer to me than standard lifting.

Got ya, to be fair any style of training works great on machines. Muscles don't have a clue what the source of the tension is. When it comes to hypertrophy it doesn't matter if it comes from free weight, or a machine. Man it has been so long since I did HIT I forgot he did super slow reps. Hell I still don't remember that part of it. Was, a good 20 years ago probably. I remember going deep into failure with all the drop sets and stuff but the tempo portion escapes my memory. Then again I may have done it wrong back then too. LOL
 
Got ya, to be fair any style of training works great on machines. Muscles don't have a clue what the source of the tension is. When it comes to hypertrophy it doesn't matter if it comes from free weight, or a machine. Man it has been so long since I did HIT I forgot he did super slow reps. Hell I still don't remember that part of it. Was, a good 20 years ago probably. I remember going deep into failure with all the drop sets and stuff but the tempo portion escapes my memory. Then again I may have done it wrong back then too. LOL

Rep cadence is a huge part of it. Strict form is, too. Drop sets and things like that to extend failure are a tool, but generally arent supposed to be used all the time.
 
Rep cadence is a huge part of it. Strict form is, too. Drop sets and things like that to extend failure are a tool, but generally arent supposed to be used all the time.

I have always been very big on form so I wouldn't have noticed that about it, but barely remember the details of HIT now. I actually had pretty good luck going back and forth for a bit between HIT style lifting and German Volume Training. Two ends of the spectrum on volume, but both using sets to failure and that was pretty productive.
 
I have always been very big on form so I wouldn't have noticed that about it, but barely remember the details of HIT now. I actually had pretty good luck going back and forth for a bit between HIT style lifting and German Volume Training. Two ends of the spectrum on volume, but both using sets to failure and that was pretty productive.

Like anything, theres variations. Theres Arthur Jones style(the original), ellington darden style, then mentzer’s evolution of it. More recently, theres Merkola and Drew Baye, but they seem pretry rooted in the Jones/Darden methods.
 
He specifically mentions “mike mentzer heavy duty training” and says it doesnt transpose GLUT4 receptors the way volume training does. In a nutshell, anyway, thats what he said. Give me a bit of rope here.

Lol, I hope you were joking about the give you some rope haha. If not I apologize - it was a serious inquiry and I wasn't trying to crowd ya.

The glut4 thing is understandable - although keep in mind this is one of the big things advocates of interval training say - it increases glut4 translocation. Still, lower volume may reduce this but I am not certain to what extent. And I mean that...I am not sure. It's an interesting angle to think about.

You can do HIT with it, but no it is not as ideal, similarly to how slow negatives aren't really considered good for it either.

Right I think it is 4-7 days depening on leanness and other goals. He said any less than 4 days and you need to move on to CBL. Once at 4 days you are flirting with still having the ability to convert and store carbohydrate as fat. That ability is removed after 4-5 days with minimal carbs as the body stops making the conversion enzyme temporarily.

Well that is exactly what it is with some more specific guidelines. Same as The Ultimate Diet and Ultimate Diet 2.0, it is a CKD too but has very specific instructions. The deficit when doing CNS is much lower during the week than your typical Keto diet.


That really depends on how many warm up sets you are doing as well. However that just means you would probably want to undershoot your max carbs by a little bit to make sure you don't overspill. You are still going to get Glut-4 translocation, just not as much due to the lower volume of work. Also by waiting until the end of the day to have your carbs you burn more fat throughout the day for energy while doing low intensity anything. Your insulin sensitivity will also be high due to not having had any carbs all day and the body wanting them.

Kind of surprised to hear you are using HIT because of a back injury. I would be avoiding HIT on any place I had an injury. The entire idea is to go into the scary and somewhat unsafe zone of intensity where form often breaks down. That just sounds like a bad situation for an injured body part.

How do you incorporate it and how do you feel it helps or is safer over a somewhat higher volume set up?

Again...interesting discussion on CBL and the Glut4/HIT angle. MrKleen73- I think you may have offered to share some info you had on CBL once in a private convo... my interest is high now.

One thing about HIT is that there is a misconception that it involves dangerous practices. Honestly, I feel this is simply untrue. You can be using heavy weights to failure, but you are controlling and moving slowly and getting very little impact on the joints and muscles relative to the weight you are using.

Like everyone I have injuries, but I am one of the few people on here who has no chronic joint issues - in spite of spending years training in this fashion.

And the idea is more geared toward going to failure and only using those increased intensity techniques sparingly. Drop sets, forced reps, negatives do not have to be an every week thing.

Honestly, I feel that using lighter weights with higher volume causes injuries in a lot of people. It becomes highly repetitive on the joints and people tend to have form failure as the reps get higher and sets go on. Beyond that - it dossn't take a lot of weight to injure yourself. I am sure we have all surprised ourselves after injuring ourselves doing something with a light weight - we either twisted just slightly wrong, or we got sloppy and swing a little. Or, speaking of swinging, using a faster tempo often causes people to start swinging and twisting and rushing (not saying it does not have a place, it obviously does).

Still...nothing is injury proof.
 
He didn't mention what level of fat there would be, or how much of a deficit, so that is a pretty big jump to conclusions. The first week 10 days of CNS is very low calorie too. Not quite 900, but very close. The premise is to create a massive deficit during the week then cut into it just a little with a massive anabolic refeed that increases leptin keeping the metabolism from dropping of like it normally does with a deficit.

If you have more than 10lbs of fat to lose then a PSMF is not going to be ideal because are SUPPOSED to follow the 10-14 days with 2 weeks maintenance to replete leptin levels. At that point CNS blows right by the PMSF in fat loss. With CNS you get very close to the same fat loss and replenish leptin to keep the metabolism from dropping every 4-7 days. Pretty much same premise just takes it one step further to maintain fat loss efficiency, and allows you to be in a big deficit a much higher percent of the time compared to PMSF.

PMSF over a month 10-14 days in deficit and keto style then back to maintenance for 2 weeks = 47% of the month in a steep deficit

CNS over a month - 26 days in deficit and keto style eating, and 4 days in surplus = 87% of the month in a steep deficit

On top of that you can run CNS for a very long time succesfully which you can not do with PMSF, or at least should not do...
Sorry but you are bringing in some odd math. When it comes to fat loss it’s CICO. Calories in and calories out. It’s actually 11-12 days with a 2-3 day refeed at the end, after this you can even do another cycle, but he doesn’t recommend, and this is just for cat 1 people. The cat 2 and cat 3 people have it easier and can definitely do it for an extended period of time. CNS makes it seem a 1 day refeed is plenty. That way, a cat 1 can just do cycles of 7 days. 6 days PSMF and 1 day refeed, repeat. Even a cat 2 who gets a refeed day AND a free meal, can stay in a pretty ridiculous defecit.

Not sure what CNS is but it sounds like a week of PSMF, a refeed, moderate dieting, then un-needed Refeeds over again.

I feel your overestimating this metabolic slowdown. Is there an adaptation? Yes, Cause your lighter and need less calories to do things and survive.
 
Lol, I hope you were joking about the give you some rope haha. If not I apologize - it was a serious inquiry and I wasn't trying to crowd ya.

The glut4 thing is understandable - although keep in mind this is one of the big things advocates of interval training say - it increases glut4 translocation. Still, lower volume may reduce this but I am not certain to what extent. And I mean that...I am not sure. It's an interesting angle to think about.



Again...interesting discussion on CBL and the Glut4/HIT angle. MrKleen73- I think you may have offered to share some info you had on CBL once in a private convo... my interest is high now.

One thing about HIT is that there is a misconception that it involves dangerous practices. Honestly, I feel this is simply untrue. You can be using heavy weights to failure, but you are controlling and moving slowly and getting very little impact on the joints and muscles relative to the weight you are using.

Like everyone I have injuries, but I am one of the few people on here who has no chronic joint issues - in spite of spending years training in this fashion.

And the idea is more geared toward going to failure and only using those increased intensity techniques sparingly. Drop sets, forced reps, negatives do not have to be an every week thing.

Honestly, I feel that using lighter weights with higher volume causes injuries in a lot of people. It becomes highly repetitive on the joints and people tend to have form failure as the reps get higher and sets go on. Beyond that - it dossn't take a lot of weight to injure yourself. I am sure we have all surprised ourselves after injuring ourselves doing something with a light weight - we either twisted just slightly wrong, or we got sloppy and swing a little. Or, speaking of swinging, using a faster tempo often causes people to start swinging and twisting and rushing (not saying it does not have a place, it obviously does).

Still...nothing is injury proof.

I will get with you on that CBL stuff on the side.

Actually yes and no on the HIT. What you are saying is true regarding HIT when done correctly. However the same thing can also be said for Cross Fit when done correctly, and both of them are things that are actually hard or to say the least uncommon for people to do correctly. We see injuries all the time, and their are plenty injuries from people who follow this type of training.

HIT is one of those things that is now not only a specific training program, but also the label of an entire type / style of training outside that specific program as well. So when people say HIT it isn't always the specific workout but the type of training of going to failure with low volume and set extension methods.

I will also say the people who are attracted to HIT style training, or for that matter Crossfit are often the type the like to push the envelope a bit. Those people often tend to take risks to reach the next level. Not all, but MANY. So an activity attracting a personality type that is driven and willing to take a few risks are also more likely to have more incidences. That can make the activity as a whole appear more dangerous, but it is more often due to the voracity of the practitioner than the danger level of the activity itself.
I am one of the on the edge guys, I am a form Nazi when it comes to safety but I used to get so close to the edge on intensity that I would often cross the line. Now I am a bit better about it. However sometimes when things have been going really good I push too far while enjoying myself and bam!
 
This HIT conversation could completely derail his thread. Would be a good thread of its own except I don’t know how many participants there would be.
 
Sorry but you are bringing in some odd math. When it comes to fat loss it’s CICO. Calories in and calories out. It’s actually 11-12 days with a 2-3 day refeed at the end, after this you can even do another cycle, but he doesn’t recommend, and this is just for cat 1 people. The cat 2 and cat 3 people have it easier and can definitely do it for an extended period of time. CNS makes it seem a 1 day refeed is plenty. That way, a cat 1 can just do cycles of 7 days. 6 days PSMF and 1 day refeed, repeat. Even a cat 2 who gets a refeed day AND a free meal, can stay in a pretty ridiculous defecit.

Not sure what CNS is but it sounds like a week of PSMF, a refeed, moderate dieting, then un-needed Refeeds over again.

I feel your overestimating this metabolic slowdown. Is there an adaptation? Yes, Cause your lighter and need less calories to do things and survive.

I noticed you brought Cat 2, and Cat 3 people into the conversation. However the person you responded to saying they might as well go to PMSF was definitely a Cat 1, which is what I was addressing. I was not discussing those categories 2 and 3 because they didn't apply to the conversation at hand. That is why I mentioned it not being a good idea for someone with more than 10ish lbs of fat to lose. However I will admit that I should have followed that statement up by qualifying there were other categories that didn't apply to the particular situation. If a cat 1 person runs his PSMF diet like a Cat 2 person it is no longer PSMF, but a bastardization of PSMF that removes some of the intended safety nets needed by a Cat 1 person that doesn't have as much fat stores to borrow from for the fat needed for a multitude of bodily functions.

From your summary in bold here in your quote above explains a lot. You don't have any idea what CNS actually is, but are still staunchly defending your stance that PMSF would be more advantageous and the CICO would be in its favor..

Odd math? Not at all... perhaps creative. I had to be since there wasn't any measurable data listed to use to compare which one would have the bigger deficit over the course of time which is what what really matters here.. Yes I know CICO is the biggest factor in weight loss. However, we had not discussed CICO at any point. You admittedly had no idea how much of a deficit CNS called for or how many more days would be in that deficit. The only measurable thing I could compare with the limited data was the amount of time / days spent in a major deficit over a month on both programs. The amount of actual days in a deficit is about 50 % higher with CNS, and for me the deficit is about 500 calories difference or 30% more than PSMF was for me at 900. So there is about a 20% greater deficit over that period of time in CNS favor when it comes to CICO.

To further illustrate the point I was trying to make since I have actually run them both successfully, I will add in all my actual numbers so you can see the difference. I will use 12 days you listed as the correction for how many days in a deficit for PSMF, but then have to add in the 3 days refeed so the total with the 2 week maintenance period at the end will be at 29 days. This keeps us in the range of days required to complete a Cat 1 PSMF cycle as recommended in the book.
.
PMSF over a 29 day cycle = 12 days @ 900 = 10,800 calories then 3 days (6000 calorie refeeds) = 18000 calories and back to maintenance for at least two weeks mine being 3100 calories x 14 days = 43400 coming out to 72,200 total calories, and 41% of the days spent in deficit burning fat

CNS over a 29 day cycle = 25 days @1400 = 35,000 cals, and 4 days (6000 calorie refeeds) 24,000 cals = 59000 total calories eaten, 86% days of the month in a deficit burning fat.

That is over 13,000 less total calories over the month in my case, while being able to train at a higher intensity than you are supposed to with PSMF, as well being more satiated throughout the month... Benefits galore piling up for CNS here.

You reminded me about the refeed days right after, but you seem to be forgetting the 2 weeks minimum recommendation at maintenance after a cycle of PSMF where you eat higher carbs to allow leptin to recover which increases the metabolism then you can repeat. If I remember correctly the deal was to eat no less than 100 or 120 grams of carbs a day during that period as well. Again to increase leptin levels.

Like you said you can go 2-3 days then go back on it but he does not recommend that. There are a few reasons for that. Fat requirements for health, and Leptin. Leptin stimulates the metabolism and is stored in fat. As you lose fat you lose leptin and the metabolism slows down as a result. It is a negative feedback loop and survival trait to preserve fat and prevent starvation in times of famine. When you eat more carbs it replenishes the leptin in the fat cells which then stimulates the thyroid to increase the metabolism now that it is getting the signal that the danger of starvation has subsided. It is not simply a matter of loss of weight loss. Also you were championing the fact that you will not lose muscle on a PSMF, but then try to say the lower mass caused the slowdown in metabolism. However, only a loss of LBM / muscle would slow down the RMR as fat does not burn energy, it is a store of energy. If not losing any muscle tissue then you are not losing any of the substrate that actually burns the fat, just carrying a little bit less of it around which is not going to have a much of an effect until you have lost a good bit of weight. The bigger slowdown is hormally based in the fact that low leptin levels signal to slow down the metabolism. You shouldn't underestimate the role that leptin plays on managing the metabolism. There is an entire hormonal aspect to this that you should know if you read the book or simply have a thorough understanding of the human metabolism.

Yes CICO is the biggest factor but the metabolism being slowed down due to low leptin levels signalling a risk of starvation also lowers the CO or Caloric Output side of things more significantly than you think. It will even start shutting down what it sees as non-vital systems and bodily functions to do this. It is basically the equivalent of the battery saver on your phone so it doesn't die so fast when getting low on battery. The same way that a phone shuts down or slows down whatever services and applications that are considered non-critical in order to extend the life of the battery as long as possible. The body does the same thing, and only runs the most basic and vital functions needed in the body in order to prevent death or at least extend life as long as possible. Do you really want your body running like a phone in battery saver mode? I don't that is for sure.

As for the Cat 1 with a refeed every week, for a long period of time I wouldn't do it. It also would not be PSMF at that point, but something else similar to PSMF. PSMF has some safety nets built into it for health's sake, and that does not. Although it would answer the leptin situation, the consistently dismal fat content like that is simply not healthy and will result in deficiencies in multiple areas like vitamins, cognition, physical performance, recovery, and if "natural" the damage to your testosterone levels is a serious concern!!! You need cholesterol to make testosterone! You also need fats to carry in fat soluble vitamins and without it some of those vitamins you are taking will not be able to be used by the body so taking a vitamin there does not really resolve the vitamin deficiency issues as you will almost definitely be deficient in fat soluble vitamins. CNS simply has the edge over PSMF healthwise by leaps and bounds, and looking at CICO it destroys Cat 1 PSMF there.

My apologies for not being more clear that I was only referring to the portion of the PSMF diet that would apply to the specific situation. I am normally more detail oriented with my posts but was simply trying to show a quick example based on the situation and left out some qualifying statements. However figured most people would be able to look at the difference in time spent in the deficit and the fact i stated the caloric intake on CNS was not much higher than on a PSMF and see that CNS would end up being lower overall intake over a dietary cycle and didn't want to actually have to do the math to prove my point...
 
This HIT conversation could completely derail his thread. Would be a good thread of its own except I don’t know how many participants there would be.

Lol - Mrkleen73 and I will derail most threads....we may agree on 99% of a topic, but that last 1% involves a lot of long posts.

Plus...you started it :)

I noticed you brought Cat 2, and Cat 3 people into the conversation. However the person you responded to saying they might as well go to PMSF was definitely a Cat 1, which is what I was addressing. I was not discussing those categories 2 and 3 because they didn't apply to the conversation at hand. That is why I mentioned it not being a good idea for someone with more than 10ish lbs of fat to lose. However I will admit that I should have followed that statement up by qualifying there were other categories that didn't apply to the particular situation. If a cat 1 person runs his PSMF diet like a Cat 2 person it is no longer PSMF, but a bastardization of PSMF that removes some of the intended safety nets needed by a Cat 1 person that doesn't have as much fat stores to borrow from for the fat needed for a multitude of bodily functions.

From your summary in bold here in your quote above explains a lot. You don't have any idea what CNS actually is, but are still staunchly defending your stance that PMSF would be more advantageous and the CICO would be in its favor..

Odd math? Not at all... perhaps creative. I had to be since there wasn't any measurable data listed to use to compare which one would have the bigger deficit over the course of time which is what what really matters here.. Yes I know CICO is the biggest factor in weight loss. However, we had not discussed CICO at any point. You admittedly had no idea how much of a deficit CNS called for or how many more days would be in that deficit. The only measurable thing I could compare with the limited data was the amount of time / days spent in a major deficit over a month on both programs. The amount of actual days in a deficit is about 50 % higher with CNS, and for me the deficit is about 500 calories difference or 30% more than PSMF was for me at 900. So there is about a 20% greater deficit over that period of time in CNS favor when it comes to CICO.

To further illustrate the point I was trying to make since I have actually run them both successfully, I will add in all my actual numbers so you can see the difference. I will use 12 days you listed as the correction for how many days in a deficit for PSMF, but then have to add in the 3 days refeed so the total with the 2 week maintenance period at the end will be at 29 days. This keeps us in the range of days required to complete a Cat 1 PSMF cycle as recommended in the book.
.
PMSF over a 29 day cycle = 12 days @ 900 = 10,800 calories then 3 days (6000 calorie refeeds) = 18000 calories and back to maintenance for at least two weeks mine being 3100 calories x 14 days = 43400 coming out to 72,200 total calories, and 41% of the days spent in deficit burning fat

CNS over a 29 day cycle = 25 days @1400 = 35,000 cals, and 4 days (6000 calorie refeeds) 24,000 cals = 59000 total calories eaten, 86% days of the month in a deficit burning fat.

That is over 13,000 less total calories over the month in my case, while being able to train at a higher intensity than you are supposed to with PSMF, as well being more satiated throughout the month... Benefits galore piling up for CNS here.

You reminded me about the refeed days right after, but you seem to be forgetting the 2 weeks minimum recommendation at maintenance after a cycle of PSMF where you eat higher carbs to allow leptin to recover which increases the metabolism then you can repeat. If I remember correctly the deal was to eat no less than 100 or 120 grams of carbs a day during that period as well. Again to increase leptin levels.

Like you said you can go 2-3 days then go back on it but he does not recommend that. There are a few reasons for that. Fat requirements for health, and Leptin. Leptin stimulates the metabolism and is stored in fat. As you lose fat you lose leptin and the metabolism slows down as a result. It is a negative feedback loop and survival trait to preserve fat and prevent starvation in times of famine. When you eat more carbs it replenishes the leptin in the fat cells which then stimulates the thyroid to increase the metabolism now that it is getting the signal that the danger of starvation has subsided. It is not simply a matter of loss of weight loss. Also you were championing the fact that you will not lose muscle on a PSMF, but then try to say the lower mass caused the slowdown in metabolism. However, only a loss of LBM / muscle would slow down the RMR as fat does not burn energy, it is a store of energy. If not losing any muscle tissue then you are not losing any of the substrate that actually burns the fat, just carrying a little bit less of it around which is not going to have a much of an effect until you have lost a good bit of weight. The bigger slowdown is hormally based in the fact that low leptin levels signal to slow down the metabolism. You shouldn't underestimate the role that leptin plays on managing the metabolism. There is an entire hormonal aspect to this that you should know if you read the book or simply have a thorough understanding of the human metabolism.

Yes CICO is the biggest factor but the metabolism being slowed down due to low leptin levels signalling a risk of starvation also lowers the CO or Caloric Output side of things more significantly than you think. It will even start shutting down what it sees as non-vital systems and bodily functions to do this. It is basically the equivalent of the battery saver on your phone so it doesn't die so fast when getting low on battery. The same way that a phone shuts down or slows down whatever services and applications that are considered non-critical in order to extend the life of the battery as long as possible. The body does the same thing, and only runs the most basic and vital functions needed in the body in order to prevent death or at least extend life as long as possible. Do you really want your body running like a phone in battery saver mode? I don't that is for sure.

As for the Cat 1 with a refeed every week, for a long period of time I wouldn't do it. It also would not be PSMF at that point, but something else similar to PSMF. PSMF has some safety nets built into it for health's sake, and that does not. Although it would answer the leptin situation, the consistently dismal fat content like that is simply not healthy and will result in deficiencies in multiple areas like vitamins, cognition, physical performance, recovery, and if "natural" the damage to your testosterone levels is a serious concern!!! You need cholesterol to make testosterone! You also need fats to carry in fat soluble vitamins and without it some of those vitamins you are taking will not be able to be used by the body so taking a vitamin there does not really resolve the vitamin deficiency issues as you will almost definitely be deficient in fat soluble vitamins. CNS simply has the edge over PSMF healthwise by leaps and bounds, and looking at CICO it destroys Cat 1 PSMF there.

My apologies for not being more clear that I was only referring to the portion of the PSMF diet that would apply to the specific situation. I am normally more detail oriented with my posts but was simply trying to show a quick example based on the situation and left out some qualifying statements. However figured most people would be able to look at the difference in time spent in the deficit and the fact i stated the caloric intake on CNS was not much higher than on a PSMF and see that CNS would end up being lower overall intake over a dietary cycle and didn't want to actually have to do the math to prove my point...

Oh man. So much in there. Good post and I agree with a bunch, as usual - but would like to add some differences/angles.

1. You don't replenish leptin in fat cells. Fat cells release leptin as they fill up.

2. Fat weight DOES increase metabolism. This is a view that a lot of people have but it is not really true. For one - just the fact you are carrying the extra weight requires more energy for any movement. Secondly, as you allude to, IF it is true that dieting can speed or slow metabolism through mechanisms, such as leptin, then you have to take a more complex view of the fat cells than as just being "energy storage". Bodyfat is an integral part of the endocrine and immune system - and the signaling involved would be a major component in any "thermostatic" modulation of the metabomism.

3. Just to be challenging - I am not really sure there is actually any convincing science that's shows dieting can slow down your metabolism beyond the reduced caloric expenditure from moving more mass. This is espoused by everyone as fact, and even mentioned in scientific studies as accepted - yet finding studies that demonstrate it and show it actually happens is difficult to say the least. I highly doubt this effect ever reduces your metabolism by more than 10% and I say that with no actual scientific evidence...I have looked for any evidence of a slowdown and never found anything I found satisfactory.

4. It would be interesting to explore and discuss how refeeds effect leptin. Leptin is just one factor, maybe not even the direct benefit of refeeds. Honestly, the perceived metabolic effects of the refeed probably have more to do with the up regulation of glycolysis from filling cells with glycogen than with any kind of mythical metabolic thermostat.

Still...we agree on a lot...just throwing out angles.
 
Something I have learned. When I quote MrKleen73 and debate him even the smallest amount...the longer it takes him to respond, the more epic it becomes. Haha
 
Lol - Mrkleen73 and I will derail most threads....we may agree on 99% of a topic, but that last 1% involves a lot of long posts.

Plus...you started it :)



Oh man. So much in there. Good post and I agree with a bunch, as usual - but would like to add some differences/angles.

1. You don't replenish leptin in fat cells. Fat cells release leptin as they fill up.

, suc2. Fat weight DOES increase metabolism. This is a view that a lot of people have but it is not really true. For one - just the fact you are carrying the extra weight requires more energy for any movement. Secondly, as you allude to, IF it is true that dieting can speed or slow metabolism through mechanismsh as leptin, then you have to take a more complex view of the fat cells than as just being "energy storage". Bodyfat is an integral part of the endocrine and immune system - and the signaling involved would be a major component in any "thermostatic" modulation of the metabomism.

3. Just to be challenging - I am not really sure there is actually any convincing science that's shows dieting can slow down your metabolism beyond the reduced caloric expenditure from moving more mass. This is espoused by everyone as fact, and even mentioned in scientific studies as accepted - yet finding studies that demonstrate it and show it actually happens is difficult to say the least. I highly doubt this effect ever reduces your metabolism by more than 10% and I say that with no actual scientific evidence...I have looked for any evidence of a slowdown and never found anything I found satisfactory.

4. It would be interesting to explore and discuss how refeeds effect leptin. Leptin is just one factor, maybe not even the direct benefit of refeeds. Honestly, the perceived metabolic effects of the refeed probably have more to do with the up regulation of glycolysis from filling cells with glycogen than with any kind of mythical metabolic thermostat.

Still...we agree on a lot...just throwing out angles.

Something I have learned. When I quote MrKleen73 and debate him even the smallest amount...the longer it takes him to respond, the more epic it becomes. Haha

Okay we can play a little but I am just now seeing this.

1. You don't replenish leptin in fat cells. Fat cells release leptin as they fill up.

This entire line is wrong. You absolutely replenish leptin, it is created & stored by the fat cell when calories are ample enough to support it. It is released as fat is lost, not as the cell fill up. When you eat a surplus, and carbs have a much higher effect on it, your fat is signalled to create more leptin. So no it is not replenished as in you load it. However doing a carb load WILL help replenish it quickly. That and the most basic of all to shut this part down. If leptin could not be replenished then none of us would have any by now. However we get low on it then levels rise back up once calories are increased. That means it was replenished.

Take the fact I respected you enough to even go look this up to see if I was mistaken as a compliment to your knowledge, but I am happy to see I am correct.

Quoted from Invalid Link Removed

"How is leptin controlled?
Because leptin is produced by fat cells, the amount of leptin released is directly related to the amount of body fat; so the more fat an individual has, the more leptin they will have circulating in their blood. Leptin levels increase if an individual increases their fat mass over a period of time and, similarly, leptin levels decrease if an individual decreases their fat mass over a period of time."


2. Fat weight DOES increase metabolism. This is a view that a lot of people have but it is not really true. For one - just the fact you are carrying the extra weight requires more energy for any movement. Secondly, as you allude to, IF it is true that dieting can speed or slow metabolism through mechanisms, such as leptin, then you have to take a more complex view of the fat cells than as just being "energy storage". Bodyfat is an integral part of the endocrine and immune system - and the signaling involved would be a major component in any "thermostatic" modulation of the metabomism
.

First I did not say that it did not... I said that the actual effect that had was minimal. Well more to specifically I said "However, only a loss of LBM / muscle would slow down the RMR as fat does not burn energy, it is a store of energy. If not losing any muscle tissue then you are not losing any of the substrate that actually burns the fat, just carrying a little bit less of it around which is not going to have a much of an effect until you have lost a good bit of weight. " I specifically said RMR, or Resting Metabolic Rate, and only energy burning tissue can effect RMR, because RMR is the Resting metabolic rate, and you are not carrying around fat mass while resting, you are resting.

Interesting concept on the fat cells being anything more than storage, I will have to give you this, but then also ask for some specific actions fat does. The mitochondria in a fat cell is not made of fat, it is made of protein, so can we say that because that mitochondria is burning fat in a fat cell that fat is burning fat, or do we have to remind ourselves it is the storage workers, aka mitochondria and not the fat that using that energy? "Trying some of your sideways logic on you... Chicken or egg Sir? WHO THE F KNOWS?!?!?

Now with Brown Fat cells, which is a different thing, and we could bring that into the mix here except for one very important thing... "No one on earth is trying to lose brown fat, and it is used to warm the body not to provide energy to the body... which is why it is a different thing. It has a different purpose altogether." Having more activated brown fat will most definitely increase fat burn if in a colder climate!!!

3. Just to be challenging - I am not really sure there is actually any convincing science that's shows dieting can slow down your metabolism beyond the reduced caloric expenditure from moving more mass. This is espoused by everyone as fact, and even mentioned in scientific studies as accepted - yet finding studies that demonstrate it and show it actually happens is difficult to say the least. I highly doubt this effect ever reduces your metabolism by more than 10% and I say that with no actual scientific evidence...I have looked for any evidence of a slowdown and never found anything I found satisfactory.

I find it odd you can not find details about what happens during starvation where the body starts shutting down systems in order to burn less calories and live longer... Do any of those systems need to be shut down simply because body mass is too low? Obviously not, they could run efficiently right up to the point of death if there were no negative feedback loops to manage this. Then all of those bodily processes would continue at a regular rate regardless of body mass or caloric intake, but that simply is not the case, the body adjusts to survive.

To add to that anecdotally I will refer to what is going on right now with BOSSMAN in the last month or so his calories have increased by double, he weighs the same on the scale, AND IS BURNING FAR LESS CALORIES VIA TRAINING, went from 6 days of cardio to no cardio while almost doubling his calories and hasn't gained a pound... Why? Because his body recognized it is getting more food and has increased his metabolism from the survival mode it was in. We see this over and over. So if the body can increase the metabolism based on how much goes in, would it not be ridiculous to think that it can not also adjust down when needed as well.

We can find a plethora of documentation where the metabolism is slowed by a diseased thyroid, this is a hormone based reaction as well, and demonstrates how much the hormones can slow the metabolism regardless of body mass. Before saying Oh but that is a diseased person, 95% of the information we have about GDA's come from studies on those with blood sugar disorders. It does not change the fact we use them to help figure out what clears blood sugar better in healthy adults.

4. It would be interesting to explore and discuss how refeeds effect leptin. Leptin is just one factor, maybe not even the direct benefit of refeeds. Honestly, the perceived metabolic effects of the refeed probably have more to do with the up regulation of glycolysis from filling cells with glycogen than with any kind of mythical metabolic thermostat.


Mythical metabolic thermostat, nice wording there. - It is funny that you mentioned thermostat, most people metabolism's burn at a rate the keeps their temperature somewhere around 98.6 degrees... those with much lower temperatures often being found to have some form of metabolic slowdown. - I have a relatively slower metabolism than most my weight. Always have, and interestingly enough my normal temp is in between 97.6-97.8 degrees. It isn't uncommon for people who use iodine and other things to also start seeing an increase in body temperature as the thyroid steps up the metabolism.

We definitely know that increasing carbs especially while in a surplus restores leptin levels. We know that outside of a diseased body, or those who have leptin resistance that appropriate levels of leptin results in an unhampered metabolism, while someone low on leptin will be running in an "efficiency mode" to make fat stores last longer. That part is not in question at all. So the real question is... TO WHAT EXTENT... Not sure that is measurable to any global level as we are all a little bit different but anecdotal evidence points to it being pretty substantial.

Your turn... :)
 
I should have branched off from my personal log and made a new log to prove this. To late now, but that could have been a great learning point for the forum.
 
Okay we can play a little but I am just now seeing this.

1. You don't replenish leptin in fat cells. Fat cells release leptin as they fill up.

This entire line is wrong. You absolutely replenish leptin, it is created & stored by the fat cell when calories are ample enough to support it. It is released as fat is lost, not as the cell fill up. When you eat a surplus, and carbs have a much higher effect on it, your fat is signalled to create more leptin. So no it is not replenished as in you load it. However doing a carb load WILL help replenish it quickly. That and the most basic of all to shut this part down. If leptin could not be replenished then none of us would have any by now. However we get low on it then levels rise back up once calories are increased. That means it was replenished.

Take the fact I respected you enough to even go look this up to see if I was mistaken as a compliment to your knowledge, but I am happy to see I am correct.

Quoted from Invalid Link Removed

"How is leptin controlled?
Because leptin is produced by fat cells, the amount of leptin released is directly related to the amount of body fat; so the more fat an individual has, the more leptin they will have circulating in their blood. Leptin levels increase if an individual increases their fat mass over a period of time and, similarly, leptin levels decrease if an individual decreases their fat mass over a period of time."


2. Fat weight DOES increase metabolism. This is a view that a lot of people have but it is not really true. For one - just the fact you are carrying the extra weight requires more energy for any movement. Secondly, as you allude to, IF it is true that dieting can speed or slow metabolism through mechanisms, such as leptin, then you have to take a more complex view of the fat cells than as just being "energy storage". Bodyfat is an integral part of the endocrine and immune system - and the signaling involved would be a major component in any "thermostatic" modulation of the metabomism
.

First I did not say that it did not... I said that the actual effect that had was minimal. Well more to specifically I said "However, only a loss of LBM / muscle would slow down the RMR as fat does not burn energy, it is a store of energy. If not losing any muscle tissue then you are not losing any of the substrate that actually burns the fat, just carrying a little bit less of it around which is not going to have a much of an effect until you have lost a good bit of weight. " I specifically said RMR, or Resting Metabolic Rate, and only energy burning tissue can effect RMR, because RMR is the Resting metabolic rate, and you are not carrying around fat mass while resting, you are resting.

Interesting concept on the fat cells being anything more than storage, I will have to give you this, but then also ask for some specific actions fat does. The mitochondria in a fat cell is not made of fat, it is made of protein, so can we say that because that mitochondria is burning fat in a fat cell that fat is burning fat, or do we have to remind ourselves it is the storage workers, aka mitochondria and not the fat that using that energy? "Trying some of your sideways logic on you... Chicken or egg Sir? WHO THE F KNOWS?!?!?

Now with Brown Fat cells, which is a different thing, and we could bring that into the mix here except for one very important thing... "No one on earth is trying to lose brown fat, and it is used to warm the body not to provide energy to the body... which is why it is a different thing. It has a different purpose altogether." Having more activated brown fat will most definitely increase fat burn if in a colder climate!!!

3. Just to be challenging - I am not really sure there is actually any convincing science that's shows dieting can slow down your metabolism beyond the reduced caloric expenditure from moving more mass. This is espoused by everyone as fact, and even mentioned in scientific studies as accepted - yet finding studies that demonstrate it and show it actually happens is difficult to say the least. I highly doubt this effect ever reduces your metabolism by more than 10% and I say that with no actual scientific evidence...I have looked for any evidence of a slowdown and never found anything I found satisfactory.

I find it odd you can not find details about what happens during starvation where the body starts shutting down systems in order to burn less calories and live longer... Do any of those systems need to be shut down simply because body mass is too low? Obviously not, they could run efficiently right up to the point of death if there were no negative feedback loops to manage this. Then all of those bodily processes would continue at a regular rate regardless of body mass or caloric intake, but that simply is not the case, the body adjusts to survive.

To add to that anecdotally I will refer to what is going on right now with BOSSMAN in the last month or so his calories have increased by double, he weighs the same on the scale, AND IS BURNING FAR LESS CALORIES VIA TRAINING, went from 6 days of cardio to no cardio while almost doubling his calories and hasn't gained a pound... Why? Because his body recognized it is getting more food and has increased his metabolism from the survival mode it was in. We see this over and over. So if the body can increase the metabolism based on how much goes in, would it not be ridiculous to think that it can not also adjust down when needed as well.

We can find a plethora of documentation where the metabolism is slowed by a diseased thyroid, this is a hormone based reaction as well, and demonstrates how much the hormones can slow the metabolism regardless of body mass. Before saying Oh but that is a diseased person, 95% of the information we have about GDA's come from studies on those with blood sugar disorders. It does not change the fact we use them to help figure out what clears blood sugar better in healthy adults.

4. It would be interesting to explore and discuss how refeeds effect leptin. Leptin is just one factor, maybe not even the direct benefit of refeeds. Honestly, the perceived metabolic effects of the refeed probably have more to do with the up regulation of glycolysis from filling cells with glycogen than with any kind of mythical metabolic thermostat.


Mythical metabolic thermostat, nice wording there. - It is funny that you mentioned thermostat, most people metabolism's burn at a rate the keeps their temperature somewhere around 98.6 degrees... those with much lower temperatures often being found to have some form of metabolic slowdown. - I have a relatively slower metabolism than most my weight. Always have, and interestingly enough my normal temp is in between 97.6-97.8 degrees. It isn't uncommon for people who use iodine and other things to also start seeing an increase in body temperature as the thyroid steps up the metabolism.

We definitely know that increasing carbs especially while in a surplus restores leptin levels. We know that outside of a diseased body, or those who have leptin resistance that appropriate levels of leptin results in an unhampered metabolism, while someone low on leptin will be running in an "efficiency mode" to make fat stores last longer. That part is not in question at all. So the real question is... TO WHAT EXTENT... Not sure that is measurable to any global level as we are all a little bit different but anecdotal evidence points to it being pretty substantial.

Your turn... :)

And the dance begins.

1. I definately worded the first point wrong. You got me there. You DO replenish leptin in fat cells - but my point was to clarify that it isn't so much about restoring it in the fat cells. As the cells fill, they create and RELEASE leptin. This extracellular leptin (no longer in the cells) is the signal to the brain that the fat cells are full.

The theory is that when the brain senses the additional leptin and knows the fat cells are full and this says, "speed up metabolism, all systems go. We are full, reduce appetite."

As per the link you provided, the more bodyfat we have, the more leptin we tend to have (because we create it and release it as the cells fill). It also appears that obesity triggers leptin resistance in a similar way to how we become insulin resistant. This makes some sense but I question if the signaling is as direct as we expect.

Of course I question parts of this theory, as we have to keep in mind leptin was originally thought to be a "cure" for obesity.

But, again per your link, as fat cells deplete they STOP producing and releasing leptin, which (in theory) speeds up metabolism and induces hunger. This is why dieting to very low bodyfat levels can cause ravenous hunger - leptin falls dramatically. It is not released as the cells deplete, it is not made. (And this realization in the 90's was the beginning of the idea that bodyfat actually serves an endocrine function).

2. I can give you your point on the RMR and bodyfat having any effect on that. You are likely right with the ONE inconsistency in the overall argument - leptin.

IF leptin increases metabolism, and more fat increases leptin, then more fat increases metabolism. And thus, less fat will slow metabolism.

Again, this is the beginning of the view of fat as being more complex than a simple storage mechanism and actually part of the endocrine and immune systems - and more than just a simple storage mechanism. The fact that we are discussing leptin itself shows it to be more than just storage. And my side ways logic wasn't even necessary at all!! :)

And this is kind of the inconsistency we both somewhat share - likely because we only have pieces of the puzzle at our disposal - but if the metabolism is a thermostat, and leptin has control to any degree over that thermostat, then bodyfat DOES increase metabolism. You say that bodyfat doesn't effect metabolism, but leptin does adjust metabolism. I say fat does have some effect, but I don't necessarily believe metabolism is as adjustable as we think.

3. As far as BOSSMAN and evidence - I missed the bossman log and will have to check it out. I wonder what the macro changes were along with the caloric intake. It would be interesting to discuss more.

But beyond anecdotal evidence, I have not found any scientific studies actually recording and showing such a metabolic adjustment being actually observed and studied. I have looked. I find it strange, as well, that I am unable to find such evidence in a scientific journal, given the strong beliefs out there and the fact that it is claimed to be observed so readily in the wild. What I question about the "in the wild" observations is if something else is going on. Wouldn't it be interesting if we could actually pinpoint what allowed someone to double their intake and not get fat? It obviously isn't just "double your food intake" - because that has failed billions of times.

4. As far as the thyroid point - you are correct. I am not saying the metabolism cannot be adjusted. A good decoupler that I won't mention would easily prove this to be incorrect. And, of course a number of drugs will have varying degrees of effect on metabolism - most well beyond what diet alone would induce (IMO)

What I am saying is that I strongly question that any healthy, functioning body will speed up or slow metabolism to match caloric intake. For one, if that were the case and it happened to any dog if I can't degree - obesity would be a rarity. You would just burn more if you ate more.

Second, it doesn't seem like a good evolutionary tactic to ever INCREASE the number of calories you burn. I mean, you need a certain amount and it would be unwise to waste any.

Maybe I could give in to some minor functions shutting down during starvation - but reproduction and whatever else would have minor consequences - I would be surprised if it was more than 10%. Maybe I am wrong. But I question it strongly.

And I challenge you to find an actual study that shows it happens. Maybe I just missed them?

As far as the body temp angle - yes - I am typically around 96.9-97.3 so I feel the pain.

So, if we use temperature as a proxy for metabolism (which I can agree with) there are two issues.

If the metabolism is so adjustable, why do I run cold? Why doesn't my body just adjust the metabolism upward and heat me up???

Ok, so maybe it is because I am eating too little - but if that is the case, then why am I the same body temperature even when I am gaining significantly more food and gaining weight quickly? Since maintaining body temp is highly critical and one of the biggest determining factors on metabolism, the fact that a significant surplus will not even bump me approx. 2-3% into the normal range and leaves me with a gut hanging over my belt leaves a lot of questions about starvation mode and the adjustable metabolism.

But maybe that is just me. How much food do you need to eat in order to hit 98.6?

I hope I hit everything...thanks for the challenges MrKleen73!!
 
Oh yeah...and I am satisfied with the epicness of MrKleen73's post. Even more impressive that he typed all that without taking the entire weekend!
 
If I had to type that much it would take me the rest of the year!
 
But it’s been shown since the 50s that doing this increases insulin sensitivity, not the other way around. In much later studies it was shown during ketosis, since no insulin is released, it does not compete with local IGF and MGF release, which are increased due to dietetic inflammation. Serum IGF is lower, yes, however that is not the IGF which repairs your muscles. The IGF which does that is a local release. Also this study is partly flawed in that you have to make up for the loss in carbs fully with protein and fat calories. In what I am finding this does not seem to be the case. So they stunted these kids growth with a caloric restriction. Also, we are not children, we do not need as many nutrients to grow properly. So, nutrient deficiency may have played a role as well. Also, add some gear to the mix.

Now I’ll throw you for a loop: many steroids actually inhibit IGF much in the way this claims a keto diet will. And obviously those still help build muscle.

Beta hydroxy butyrate is a key part of the body’s signaling system to build muscle, much in the way HMB is purported to do. A keto is diet has you running very high on BHB, thusly signaling protein synthesis. This why you can deplete fully, go into keto on a keto (ultralean) bulk, and when you finally carb back up you see the results. And get lean simultaneously. But but but that’s impossible. No. With all that inflammation and excess signaling chemical you will be maximizing your MPS and if your protein and fat intake are actually on point you can’t store fat. Your body wants fuel, but has tons of protein, no carbs, and not enough fats. So it mobilizes fat. No calorie restriction required, and I have seen this done many times, did it myself back in the day. Was doing it earlier this year but lost my nerve. My jaw just can’t take chewing tough ass meat all day like that. Because obviously you can’t eat tenderloin six meals a day.

I don’t think it’s the way to live your life if you’re a bodybuilder but it is my preferred way to cut for sure.
 
just take IGF in keto, then, if you want more IGF in keto. You can’t take nearly as much because you’re super sensitive to it. No carbs and take something that works similar to insulin...

Just think about it logically. When you’re in ketosis, if you took 4iu of insulin, you’re dead. Same with IGF. Take 100mcg when you’re in keto and you’ll definitely feel it. That lovely low blood sugar feeling,


Ketosis increases GH release nearly as much as mk677. Personally I think that’s pretty cool.
 
Just to bring some other angles into the ketosis/IGF/Hormonal signaling debate:

Invalid Link Removed

Invalid Link Removed

One thing about these studies that I would think about is - high protein diets often knock people out of ketosis. Maybe some of the perceived benefits of "low carb" actually have something to do with the moderate protein intake that is recommended?

All these studies, to me, point to one specific point. Evolution has created a pretty resilient system that knows what the fugg is up. If you starve in some way - too little calories, too little carbs, too little protein - there is a hormonal cascade that ensues and many of the hormones and chemicals at work pick up various roles. Sure, IGF-1 is reduced, but (as above) BHB is upregulated and picks up some of the slack. IGF-1 may be reduced BECAUSE there is extra BHB around.

If we understand this more, we can modulate things better - eat in ways that improve insulin sensitivity and then capitalize. Eat in ways that improve IGF sensitivity and then capitalize, etc.

In these studies, protein is lacking - so we become more sensitive to insulin. Does this mean we should reduce protein and go on a low-protein diet? No...but it may have some implications in nutrient timing of course. Still, you can see how our body adjusts numerous pathways in any situation to maintain homeostasis as much as possible.
 
To make things a little easier because so much is agreed upon I will just make some notes on your quote for responses.

And the dance begins.

1. I definately worded the first point wrong. You got me there. You DO replenish leptin in fat cells - but my point was to clarify that it isn't so much about restoring it in the fat cells. As the cells fill, they create and RELEASE leptin. This extracellular leptin (no longer in the cells) is the signal to the brain that the fat cells are full.

The theory is that when the brain senses the additional leptin and knows the fat cells are full and this says, "speed up metabolism, all systems go. We are full, reduce appetite."

As per the link you provided, the more bodyfat we have, the more leptin we tend to have (because we create it and release it as the cells fill). It also appears that obesity triggers leptin resistance in a similar way to how we become insulin resistant. This makes some sense but I question if the signaling is as direct as we expect.

Of course I question parts of this theory, as we have to keep in mind leptin was originally thought to be a "cure" for obesity.

But, again per your link, as fat cells deplete they STOP producing and releasing leptin, which (in theory) speeds up metabolism and induces hunger. This is why dieting to very low bodyfat levels can cause ravenous hunger - leptin falls dramatically. It is not released as the cells deplete, it is not made. (And this realization in the 90's was the beginning of the idea that bodyfat actually serves an endocrine function).

Okay, so we both seem to have a slightly different concept of how the leptin is released, and to be honest, I don't really know the answer. What you are saying sounds like it is very possibly correct. I will defer to you there even though I don't know if you are right, but I have a feeling that is correct. I have not actually looked into the exact MOA of the releasing of it. Just the basic understanding of the concept. Regardless of the exact method of how Leptin becomes low, and or is measured low, we know it is due to fat loss, if that means that the fat cells are simply not releasing enough into the blood stream or, it is released as fat burns doesn't change that low levels are a limiting factor to the metabolism.

Also Leptin is made inside of the fat cell is it not? You said it is not made, however that I know of we do not eat leptin. If you can explain to me how we come to have a supply of it without ingesting or producing it I am curious. If we do actually eat it and I am unaware then let me know that. However I think it is made in the fat cell, so you stating it is not made is confusing to me. Especially when just above you said as fat cells deplete they STOP producing and releasing leptin. Please explain.


2. I can give you your point on the RMR and bodyfat having any effect on that. You are likely right with the ONE inconsistency in the overall argument - leptin.

IF leptin increases metabolism, and more fat increases leptin, then more fat increases metabolism. And thus, less fat will slow metabolism.

Leptin manages the metabolism, or more to the point is a safeguard for the body that helps manage the metabolism. Lower leptin levels decrease the metabolism, so instead of looking at it like Leptin increases metabolism, lets look at it more like a regulator than just increasing.

When you are in a good and healthy energy balance leptin levels are going to be optimal, and your metabolism is going to be optimized. If you eat in a way that makes you chronically higher than this you will get fat, and you also risk developing leptin resistance, and when you eat less than ideal you risk slowing the metabolism... The purpose is to regulate, not increase, it is obviously not a more is better case. We know this because we know you can develop leptin resistance which further exacerbates the likelihood of continued obesity.

You have some flawed logic and assumptions in your correlation based "If string" - ,
"If Leptin Increases metabolism" - it regulates, the metabolism adjusts both ways in a response to leptin levels... we can also assume that there is a healthy or optimal range, as things become more disordered the farther away from it you get going in either direction.

"Then more fat increases metabolism" - this is a flawed assumption because someone could be experiencing low levels of leptin while still having plenty of fat mass. I lb of fat in someone in a surplus is going to have far more Leptin in it than 1 lb of fat from someone who has been in a deficit for a while without anything to stimulate new production of leptin. - So fat just for fat's sake does not necessarily mean more leptin. It depends on the the environmental factors effecting the fat. You can actually restore leptin in the fat cells quickly without gaining fat mass by doing a high carbohydrate refeed that puts you in an acute surplus.

In our situation, we are trying to keep the leptin in as close to optimal ranges during a deficit as possible to avoid whatever extent of metabolic slowdown that we can during the dieting process. Often we do this with a refeed. If leptin falls below optimal levels then metabolism begins to slow, replenishing that leptin brings it back up closer to optimal. The increase in the metabolism attributed to leptin we speak of seems more likely to be from when levels of leptin are returning to optimal, and not that leptin continues to drive metabolic rate up.



Again, this is the beginning of the view of fat as being more complex than a simple storage mechanism and actually part of the endocrine and immune systems - and more than just a simple storage mechanism. The fact that we are discussing leptin itself shows it to be more than just storage. And my side ways logic wasn't even necessary at all!! :)

And this is kind of the inconsistency we both somewhat share - likely because we only have pieces of the puzzle at our disposal - but if the metabolism is a thermostat, and leptin has control to any degree over that thermostat, then bodyfat DOES increase metabolism. You say that bodyfat doesn't effect metabolism, but leptin does adjust metabolism. I say fat does have some effect, but I don't necessarily believe metabolism is as adjustable as we think.

You have got to start taking notice of how specific I am... I said Fat Mass specifically, IE the idea that it is the simple weight being carried, and the increase or lowering of the resistance of carrying the additional body fat that increases That is what was stated as the ONLY thing that causes the metabolism to slow... which is simply not true. A factor of course but not the factor.

Just to be clear here, there are two stances, and believe that the body does not have very much ability to down-regulate metabolism in order to try to survive longer in a perceived state of starvation? I have read multiple articles and studies when i was researching IF and starvation that showed how at different stages functions of the body are stopped or slowed to increase the likelihood of survival. I was taught this in High School as well, are you actually saying none of this occurs, or their are no studies that show this, or have you not looked into starvation studies?

I haven't gone back to look for specific studies, but it is hard to find a scientific article on the topic of starvation that does not have this mentioned.



3. As far as BOSSMAN and evidence - I missed the bossman log and will have to check it out. I wonder what the macro changes were along with the caloric intake. It would be interesting to discuss more.

But beyond anecdotal evidence, I have not found any scientific studies actually recording and showing such a metabolic adjustment being actually observed and studied. I have looked. I find it strange, as well, that I am unable to find such evidence in a scientific journal, given the strong beliefs out there and the fact that it is claimed to be observed so readily in the wild. What I question about the "in the wild" observations is if something else is going on. Wouldn't it be interesting if we could actually pinpoint what allowed someone to double their intake and not get fat? It obviously isn't just "double your food intake" - because that has failed billions of times.


Anectdotal evidence is of very high value in the physique world, and there is a plethora of it supporting this.

To the bolded portion, I think the likely answer has become clear to me, have him eat at a 50% deficit for 2 years, and his metabolism slow down as a result, then put him on a reverse diet intended to restore leptin levels and metabolic rate to what is naturally optimal for that person.. and tell his body it is no longer in danger of starvation so it can restore its normal performance levels.

I don't think it is a matter of leptin increasing the metabolism, but regulating it, and correcting the nutritional deficiency restores the metabolism closer to its optimal level.

Calories were 1300-1800 a day on average now hitting about 3000, Macro changes were far more carbohydrate, with reasonable fat and protein levels. He also went from IF to eating throughout the day. This is pretty commonplace to see among coaches.


4. As far as the thyroid point - you are correct. I am not saying the metabolism cannot be adjusted. A good decoupler that I won't mention would easily prove this to be incorrect. And, of course a number of drugs will have varying degrees of effect on metabolism - most well beyond what diet alone would induce (IMO)

What I am saying is that I strongly question that any healthy, functioning body will speed up or slow metabolism to match caloric intake. For one, if that were the case and it happened to any dog if I can't degree - obesity would be a rarity. You would just burn more if you ate more.

The claim that if leptin could increase the RMR, the body would just endlessly burn more and more calories becomes moot if you look at Leptin as a regulator and not just something to increase metabolism. We both know for 100% sure that there are negative reactions associated with chronically elevated leptin levels that make obesity even harder to combat. So lets drop the idea of Leptin only increasing the metabolism and look at it as more of a regulator. Not enough, not good, too much, not good.

Second, it doesn't seem like a good evolutionary tactic to ever INCREASE the number of calories you burn. I mean, you need a certain amount and it would be unwise to waste any.

Again, look at this as a regulator, when all is good metabolism will be running optimally, which is going to be faster than when nutrition is lacking or deficient. Restoring the deficiency improves the performance of the metabolism within it's operable ranges. There is an optimal range, and being optimal would be the ideal goal. Too make it so that the body needs more to be optimal would be a waste. However, I think the real issue is that most in our shoes are not optimal, and what we see as an increase, is actually restoration of what should already be.

Maybe I could give in to some minor functions shutting down during starvation - but reproduction and whatever else would have minor consequences - I would be surprised if it was more than 10%. Maybe I am wrong. But I question it strongly.
"Wait are you minimizing 10%? If you could give me 10% better progress on a diet I would be ecstatic!!!!

And I challenge you to find an actual study that shows it happens. Maybe I just missed them?

Challenge accepted, but will have to be later. I have to find one just because... how could their not be when it is considered almost common knowledge. Hopefully I will have some better luck.

As far as the body temp angle - yes - I am typically around 96.9-97.3 so I feel the pain.

So, if we use temperature as a proxy for metabolism (which I can agree with) there are two issues.

If the metabolism is so adjustable, why do I run cold? Why doesn't my body just adjust the metabolism upward and heat me up???

Ok, so maybe it is because I am eating too little - but if that is the case, then why am I the same body temperature even when I am gaining significantly more food and gaining weight quickly? Since maintaining body temp is highly critical and one of the biggest determining factors on metabolism, the fact that a significant surplus will not even bump me approx. 2-3% into the normal range and leaves me with a gut hanging over my belt leaves a lot of questions about starvation mode and the adjustable metabolism.

But maybe that is just me. How much food do you need to eat in order to hit 98.6?

I hope I hit everything...thanks for the challenges MrKleen73!!

You asked a few things that I can only come up with theories based on what we know, but can't say I will provide any answers.

If the metabolism is so adjustible why do I run cold? Why doesn't my body adjust the metabolism upward to meet me. First, I would say that the metabolism is regulated, moreso than adjustable. They are similar but adjustable lends itself a little more to being in control of the adjustment. Regulated is a bit more accurate, as it is other things that are only somewhat in our control that are doing the adjusting.

I would say from what I know of you that we don't have any clue if your metabolism is not still recovered from the ways that you have dieted in the past. We also do not know that you have ever had a high metabolism. Also, lets recognize that we all have an operable range for things, my highest metabolic rate could be 1000 calories higher or lower than your highest metabolic rate, and that could be a reason my temp is a degree higher, or why yours won't go over a certain point unless you have a fever. Both of our normal temps are a bit below the average, however that doesn't actually mean that we are or are not suffering a deficiency of metabolism. It could just be that is our normal. However there are still fluctuations within my normal range, and this is where you will most likely see the difference from that, the fluctuations within your normal ranges, not so much increasing the range but increasing within that range.

You could also have some sort of issue effecting your thyroid that causes it to be lower than normal, plus you have already mentioned you were heavy when young, and obese into adulthood. We don't know that you have ever had higher metabolism. You could be deficient in iodine levels, and therefor not able to make that adjustment. See the point I am getting to is that there are any number of anomalies that could change how you react to that. There are far too many viable "could be this or could be that" to use this example to prove or disprove anything.
 
But it’s been shown since the 50s that doing this increases insulin sensitivity, not the other way around. In much later studies it was shown during ketosis, since no insulin is released, it does not compete with local IGF and MGF release, which are increased due to dietetic inflammation. Serum IGF is lower, yes, however that is not the IGF which repairs your muscles. The IGF which does that is a local release. Also this study is partly flawed in that you have to make up for the loss in carbs fully with protein and fat calories. In what I am finding this does not seem to be the case. So they stunted these kids growth with a caloric restriction. Also, we are not children, we do not need as many nutrients to grow properly. So, nutrient deficiency may have played a role as well. Also, add some gear to the mix.

Now I’ll throw you for a loop: many steroids actually inhibit IGF much in the way this claims a keto diet will. And obviously those still help build muscle.

Beta hydroxy butyrate is a key part of the body’s signaling system to build muscle, much in the way HMB is purported to do. A keto is diet has you running very high on BHB, thusly signaling protein synthesis. This why you can deplete fully, go into keto on a keto (ultralean) bulk, and when you finally carb back up you see the results. And get lean simultaneously. But but but that’s impossible. No. With all that inflammation and excess signaling chemical you will be maximizing your MPS and if your protein and fat intake are actually on point you can’t store fat. Your body wants fuel, but has tons of protein, no carbs, and not enough fats. So it mobilizes fat. No calorie restriction required, and I have seen this done many times, did it myself back in the day. Was doing it earlier this year but lost my nerve. My jaw just can’t take chewing tough ass meat all day like that. Because obviously you can’t eat tenderloin six meals a day.

I don’t think it’s the way to live your life if you’re a bodybuilder but it is my preferred way to cut for sure.
Interesting on the cutting method. I have always been able to gain muscle and lose weight at the same time. I am quite efficient at it.

On the keto, it definitely increases insulin sensitivity at first, but they are finding now that over the long haul it begins to decrease it.

For you next cut using only beef, get a Sous Vide machine, you can cook chuck steak in it and have it more tender than filet! Plus it makes prepping chicken awesome. No such thing as a dry chicken breast coming from a Sous Vide cooker.



Just to bring some other angles into the ketosis/IGF/Hormonal signaling debate:

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One thing about these studies that I would think about is - high protein diets often knock people out of ketosis. Maybe some of the perceived benefits of "low carb" actually have something to do with the moderate protein intake that is recommended?

All these studies, to me, point to one specific point. Evolution has created a pretty resilient system that knows what the fugg is up. If you starve in some way - too little calories, too little carbs, too little protein - there is a hormonal cascade that ensues and many of the hormones and chemicals at work pick up various roles. Sure, IGF-1 is reduced, but (as above) BHB is upregulated and picks up some of the slack. IGF-1 may be reduced BECAUSE there is extra BHB around.

If we understand this more, we can modulate things better - eat in ways that improve insulin sensitivity and then capitalize. Eat in ways that improve IGF sensitivity and then capitalize, etc.

In these studies, protein is lacking - so we become more sensitive to insulin. Does this mean we should reduce protein and go on a low-protein diet? No...but it may have some implications in nutrient timing of course. Still, you can see how our body adjusts numerous pathways in any situation to maintain homeostasis as much as possible.

I swear you just debate me to have good convo... Look at the bolded above where you champion the body's ability to adjust itself to many different factors in order to try to maintain homeostasis in the exact same thread you just told me that you feel the body is not able to adjust metabolism...

So what is it about metabolism that makes it unable to adapt, or adjust while the rest of the body is so dynamic and adaptive to the environment it is put into. :lame:

:D
 
Im not gonna jump in here to debate but one thing people forget.. Maybe not you two but the average guy doesn't always understand that avoiding carbs doesn't equal fatloss, avoiding fat doesn't equal fatloss.. They've speculated omega 3s can but even if it's nothing to go crazy about. Eating carbs and the body burns carbs, eating more fat the body burns more fat. Carbs fills your muscle up and fat makes them more flat. I prefer high fat but that's because I've built muscle first and I'm quite happy where I'm at. Had I started working out now I think carbs would have been the main fuel source if my goal was to bulk.

I am quite sure both you guys know this it's just confusing for some people to understand you guys when it's so advanced haha..
 
There are a lot of layers here to peel away !!
 
I swear you just debate me to have good convo... Look at the bolded above where you champion the body's ability to adjust itself to many different factors in order to try to maintain homeostasis in the exact same thread you just told me that you feel the body is not able to adjust metabolism...

So what is it about metabolism that makes it unable to adapt, or adjust while the rest of the body is so dynamic and adaptive to the environment it is put into. :lame:

:D

I will answer this one first because it seems more logical to me. To your first point, of course I debate you for the conversation. It's like the intellectual form of wrestling with your buddy. You are a worthy adversary!!! I swear you do the same :)

To the second point - the two posts aren't really in conflict. I understand why you would think that if everything is changing, then metabolism would have to change on the surface. But metabolism is just the sum whole of all the energy expending activities the body undertakes. At the end of the day, the work has to get done and it has an energy cost associated with it. Whether you achieve this through one pathway or another does not really have all that much effect on the end work getting done nor the energy used for that work. There may be some inefficiencies seen in using backup pathways; or even some efficiencies - but ultimately energy is just a measure of the work being done.

But ultimately, metabolism is the sum total, and since we can agree that the body tries to maintain homeostasis, the view that an unchanging metabolism is the correct theory is supported. sses." i.e. - the tendency toward a relatively stable metabolism that is created by a number of pathways. Homeostasis is "the tendency toward a relatively stable equilibrium between interdependent elements, especially as maintained by physiological proce

Another way of looking at it is, the work my body has to do in order to survive is not really increased or decreased by changes in pathways. The multiple pathways are just different ways to achieve the same goal; redundancy. If I have to raise a 20 pound arm (how much does an arm weigh?) - whether I use ketones or carbs will ultimately involve the same work being accomplished with only pretty minor changes in efficiency.


Okay, so we both seem to have a slightly different concept of how the leptin is released, and to be honest, I don't really know the answer. What you are saying sounds like it is very possibly correct. I will defer to you there even though I don't know if you are right, but I have a feeling that is correct. I have not actually looked into the exact MOA of the releasing of it. Just the basic understanding of the concept. Regardless of the exact method of how Leptin becomes low, and or is measured low, we know it is due to fat loss, if that means that the fat cells are simply not releasing enough into the blood stream or, it is released as fat burns doesn't change that low levels are a limiting factor to the metabolism.

Also Leptin is made inside of the fat cell is it not? You said it is not made, however that I know of we do not eat leptin. If you can explain to me how we come to have a supply of it without ingesting or producing it I am curious. If we do actually eat it and I am unaware then let me know that. However I think it is made in the fat cell, so you stating it is not made is confusing to me. Especially when just above you said as fat cells deplete they STOP producing and releasing leptin. Please explain.


Okay, so we both seem to have a slightly different concept of how the leptin is released, and to be honest, I don't really know the answer. What you are saying sounds like it is very possibly correct. I will defer to you there even though I don't know if you are right, but I have a feeling that is correct. I have not actually looked into the exact MOA of the releasing of it. Just the basic understanding of the concept. Regardless of the exact method of how Leptin becomes low, and or is measured low, we know it is due to fat loss, if that means that the fat cells are simply not releasing enough into the blood stream or, it is released as fat burns doesn't change that low levels are a limiting factor to the metabolism.

Also Leptin is made inside of the fat cell is it not? You said it is not made, however that I know of we do not eat leptin. If you can explain to me how we come to have a supply of it without ingesting or producing it I am curious. If we do actually eat it and I am unaware then let me know that. However I think it is made in the fat cell, so you stating it is not made is confusing to me. Especially when just above you said as fat cells deplete they STOP producing and releasing leptin. Please explain.

Yeah - when this started, I was just merely correcting the small detail that it isn't that leptin builds up in fat cells - it is about leptin being released from the fat cells. It was a fairly minor adjustment and I worded the original statement incorrectly/confusingly (see my previous post). Fat cells DO make leptin and it is replenished through this pathway. But the key is the release from the fat cells; it's not stored. It is actually a signalling hormone. It is created by the fat cell, and as it fills more is created. The more lipid we carry, the more leptin is created - except in cases of disease, where you have don't create enough leptin. So, if you have more fat, then you should have more leptin. I'm not saying this is hard and true that if you have X amount of fat you will have Y amount of leptin. What I am saying is that based on your genetics and whatever environmental factors - if you have 10 pounds of fat on your body, you will produce less leptin than if you have 20 pounds.

Even when dieting this is true - this is one of the reasons why someone who is more obese will see almost no benefit from a refeed. They have ample supplies of leptin, even after an extended diet, since they still have ample amounts of fat.

I also worded this wrongly, "But, again per your link, as fat cells deplete they STOP producing and releasing leptin, which (in theory) speeds up metabolism and induces hunger." - when you stop leptin production and levels fall - it SLOWS DOWN metabolism and induces hunger (in theory - if your metabolism adjusts very much is what I am questioning).

One other point, it's not so much dieting itself that causes the drop in leptin - it is the reduction of fat mass as a result of dieting. One thing that is noticed on PSMF diets is that really obese people are REALLY good at fasting. Lean people - not so much. This theory of leptin would explain that.

Leptin manages the metabolism, or more to the point is a safeguard for the body that helps manage the metabolism. Lower leptin levels decrease the metabolism, so instead of looking at it like Leptin increases metabolism, lets look at it more like a regulator than just increasing.

When you are in a good and healthy energy balance leptin levels are going to be optimal, and your metabolism is going to be optimized. If you eat in a way that makes you chronically higher than this you will get fat, and you also risk developing leptin resistance, and when you eat less than ideal you risk slowing the metabolism... The purpose is to regulate, not increase, it is obviously not a more is better case. We know this because we know you can develop leptin resistance which further exacerbates the likelihood of continued obesity.

You have some flawed logic and assumptions in your correlation based "If string" - ,
"If Leptin Increases metabolism" - it regulates, the metabolism adjusts both ways in a response to leptin levels... we can also assume that there is a healthy or optimal range, as things become more disordered the farther away from it you get going in either direction.

"Then more fat increases metabolism" - this is a flawed assumption because someone could be experiencing low levels of leptin while still having plenty of fat mass. I lb of fat in someone in a surplus is going to have far more Leptin in it than 1 lb of fat from someone who has been in a deficit for a while without anything to stimulate new production of leptin. - So fat just for fat's sake does not necessarily mean more leptin. It depends on the the environmental factors effecting the fat. You can actually restore leptin in the fat cells quickly without gaining fat mass by doing a high carbohydrate refeed that puts you in an acute surplus.

In our situation, we are trying to keep the leptin in as close to optimal ranges during a deficit as possible to avoid whatever extent of metabolic slowdown that we can during the dieting process. Often we do this with a refeed. If leptin falls below optimal levels then metabolism begins to slow, replenishing that leptin brings it back up closer to optimal. The increase in the metabolism attributed to leptin we speak of seems more likely to be from when levels of leptin are returning to optimal, and not that leptin continues to drive metabolic rate up.

Well, the theory is that leptin speeds up metabolism. A lack of leptin slows down metabolism. And to your point above; there is likely an optimal level of leptin that you should have in your system. It's a signaling hormone that helps "regulate" but the hormone itself is theorized to increase metabolism.

And, to your point, leptin really doesn't speed up metabolism that much. It has a ceiling and this ceiling seems to be pretty low. This is essentially part of the contradiction we are both facing here. If we want to use leptin to explain that metabolism can be sped up - then how do we get fat in the first place? Because it has a ceiling, we become resistant, it can only work so much - and that effect will not keep us lean.

As for the "low levels of leptin with plenty of fat mass" - see above. This happens in diseased states where people do not produce enough leptin - but if you have plenty of fat and are not specifically diseased, then you will still be producing plenty of leptin. Again, this anecdotal evidence has been observed in the wild and by medical doctors treating patients - obese people have few issues with hunger/fasting. Lean people...it gets really hard.

But overall, the point is, if you TRULY believe that the metabolism is adjustable - leptin is probably one of the best candidates for this function and the more fat you have, the more leptin you create - so the "if/then string" is not flawed unless the underlying assumptions are wrong.

I will quote, from the link you posted, "Because leptin is produced by fat cells, the amount of leptin released is directly related to the amount of body fat; so the more fat an individual has, the more leptin they will have circulating in their blood. Leptin levels increase if an individual increases their fat mass over a period of time and, similarly, leptin levels decrease if an individual decreases their fat mass over a period of time."

So, if the theory of leptin is correct, then fat does impact the signaling to increase metabolism. More fat = higher metabolism. Of course, I can agree this effect is obviously very minor and has a very low ceiling; but that's kind of evidence that the metabolism overall is not all that adjustable I would think....

You have got to start taking notice of how specific I am... I said Fat Mass specifically, IE the idea that it is the simple weight being carried, and the increase or lowering of the resistance of carrying the additional body fat that increases That is what was stated as the ONLY thing that causes the metabolism to slow... which is simply not true. A factor of course but not the factor.

Just to be clear here, there are two stances, and believe that the body does not have very much ability to down-regulate metabolism in order to try to survive longer in a perceived state of starvation? I have read multiple articles and studies when i was researching IF and starvation that showed how at different stages functions of the body are stopped or slowed to increase the likelihood of survival. I was taught this in High School as well, are you actually saying none of this occurs, or their are no studies that show this, or have you not looked into starvation studies?

I haven't gone back to look for specific studies, but it is hard to find a scientific article on the topic of starvation that does not have this mentioned.

But isn't that the point - possibly our best candidate for metabolic increse is leptin, which is directly related to fat mass. On one hand you will argue that metabolism can be adjusted and there is anecdotal evidence of people increasing their metabolism dramatically through reverse dieting (thus indicating dieting slowed metabolism by proxy) - yet you discount the fact that fat itself increases metabolism.

As far as down-regulating the metabolism due to starvation - perhaps it can slightly. Maybe it slows production of reproductive hormones, maybe things tend to break - but on one hand these temporary reductions would be minimal. Things like body heat, brain activity, physical movement are huge energy consumers and these things don't appear to drop by even 2% in most cases (although I will give you that it is difficult to measure a degree of physical fatigue, mental fatigue, etc. - but we demonstrated that body temp barely moves due to diet).

So when I say that metabolism drops by 10% - for most people this is an order of 250 calories a day. So instead of 2500 you burn 2250. And when you go back to "non starvation mode" it should be back to 2500 - not 3,000 or 3,500. Unless something else has changed. Unless something else is happening.

And the idea that we would prepare for starvation by increasing fat storage AND increasing metabolic expenditure; only to drop metabolism when we are starving...well...that's just poor adaptation.

Anectdotal evidence is of very high value in the physique world, and there is a plethora of it supporting this.

To the bolded portion, I think the likely answer has become clear to me, have him eat at a 50% deficit for 2 years, and his metabolism slow down as a result, then put him on a reverse diet intended to restore leptin levels and metabolic rate to what is naturally optimal for that person.. and tell his body it is no longer in danger of starvation so it can restore its normal performance levels.

I don't think it is a matter of leptin increasing the metabolism, but regulating it, and correcting the nutritional deficiency restores the metabolism closer to its optimal level.

Calories were 1300-1800 a day on average now hitting about 3000, Macro changes were far more carbohydrate, with reasonable fat and protein levels. He also went from IF to eating throughout the day. This is pretty commonplace to see among coaches.

Anecdotal evidence. Hundreds of millions of people who have increased caloric intake only to become obese.

Who knows how many Ethiopians who are starving and still have NO fat on their body.

And Bossman (who is a Boss after all).


The claim that if leptin could increase the RMR, the body would just endlessly burn more and more calories becomes moot if you look at Leptin as a regulator and not just something to increase metabolism. We both know for 100% sure that there are negative reactions associated with chronically elevated leptin levels that make obesity even harder to combat. So lets drop the idea of Leptin only increasing the metabolism and look at it as more of a regulator. Not enough, not good, too much, not good.

Yes - too much isn't good. Too little isn't good. I do agree there. I can agree that, in a way, it is a regulator - but again, in reality, (if you believe it can do this) - it increases metabolism. Lack of it decreases metabolism. But this is semantics to some degree I would say....minor.

Again, look at this as a regulator, when all is good metabolism will be running optimally, which is going to be faster than when nutrition is lacking or deficient. Restoring the deficiency improves the performance of the metabolism within it's operable ranges. There is an optimal range, and being optimal would be the ideal goal. Too make it so that the body needs more to be optimal would be a waste. However, I think the real issue is that most in our shoes are not optimal, and what we see as an increase, is actually restoration of what should already be.

Yes - I pretty much would agree with this. IF there is an adjustment, we can likely adjust it back to normal. Where I disagree is that this adjustment is all that impactful.

"Wait are you minimizing 10%? If you could give me 10% better progress on a diet I would be ecstatic!!!!

I can do WAY better than that. Let's assume you have a 3000 calorie BMR. Say you cut out 500 calories a day, and your metabolism adjusts 10%. Now your 3500 calorie deficit yielding 1 pound of fat loss a week just dropped to a 200 calorie deficit - or less than half a pound per week. That 10% reduction reduced the effectiveness of your diet by 60%!!! Still; it's just 300 calories a day. And you won't reverse diet to 3,300 calories being you BMR.

Of course...still no evidence 10% is even realistic.

Although...this is where my carb/fat theory comes in. Ironically, carbs tend to have just under 60% fewer calories/gram than fat. hmmmmm....

Challenge accepted, but will have to be later. I have to find one just because... how could their not be when it is considered almost common knowledge. Hopefully I will have some better luck.

I hope you do to. I may have to look specifically for starvation - that's a good search idea. I've looked though and I found it very interesting to see how TONS of studies referred to a slowing of metabolism, but no one ever seemed to have actually studied it and shown it actually happens. I've seen this in a few situations actually in science. I guess scientists aren't immune to dogma either.


First, I would say that the metabolism is regulated, moreso than adjustable. They are similar but adjustable lends itself a little more to being in control of the adjustment. Regulated is a bit more accurate, as it is other things that are only somewhat in our control that are doing the adjusting.

I would say from what I know of you that we don't have any clue if your metabolism is not still recovered from the ways that you have dieted in the past. We also do not know that you have ever had a high metabolism. Also, lets recognize that we all have an operable range for things, my highest metabolic rate could be 1000 calories higher or lower than your highest metabolic rate, and that could be a reason my temp is a degree higher, or why yours won't go over a certain point unless you have a fever. Both of our normal temps are a bit below the average, however that doesn't actually mean that we are or are not suffering a deficiency of metabolism. It could just be that is our normal. However there are still fluctuations within my normal range, and this is where you will most likely see the difference from that, the fluctuations within your normal ranges, not so much increasing the range but increasing within that range.

You could also have some sort of issue effecting your thyroid that causes it to be lower than normal, plus you have already mentioned you were heavy when young, and obese into adulthood. We don't know that you have ever had higher metabolism. You could be deficient in iodine levels, and therefor not able to make that adjustment. See the point I am getting to is that there are any number of anomalies that could change how you react to that. There are far too many viable "could be this or could be that" to use this example to prove or disprove anything.

Yeah - the way I've dieted in the past is fair to question. One thing I would say is that during my log of my PSMF - after about 3-4 months I got a fitbit. And I used that fitbit, which had no idea of how I was eating, to estimate my metabolic rate each day. Granted, fit bits are supposed to OVER estimate caloric expenditure supposedly. Well, even with that over estimate and given the pretty strict and easily tracked diet I was on - the calories in/out yielded the amount of weight loss that should have been expected if my metabolism was in line with the fitbit. This suggests that my metabolism had not slowed very much - since it was still keeping pace with standardized guides for metabolic rate.

Still - you are pointing out something key - we have a lot of other factors/diseases/etc. that impact this stuff and create false positives. The assumption and blind faith that we can reverse diet to correct this stuff is probably not great - it should be questioned. And deep down you know it is flawed because you aren't saying, "Your body temp is a result of your metabolism. It is low because it is slow. It is slow because you don't eat enough". As a matter of fact - you gave a bunch of other reasons beyond caloric intake.


This is fun....now I gotta get to work...
 
HIT4ME Where you on the Debate Team in School ??
 
Im not gonna jump in here to debate but one thing people forget.. Maybe not you two but the average guy doesn't always understand that avoiding carbs doesn't equal fatloss, avoiding fat doesn't equal fatloss.. They've speculated omega 3s can but even if it's nothing to go crazy about. Eating carbs and the body burns carbs, eating more fat the body burns more fat. Carbs fills your muscle up and fat makes them more flat. I prefer high fat but that's because I've built muscle first and I'm quite happy where I'm at. Had I started working out now I think carbs would have been the main fuel source if my goal was to bulk.

I am quite sure both you guys know this it's just confusing for some people to understand you guys when it's so advanced haha..

Jump in my man!! I'm just making this sh1t up as I go along! Can't you tell?

It's like this. MrKleen73 is holding a beautiful rose. And this rose, he looks at, and he is just happy. It does everything a rose should do.

And then I come along and squeeze his hand as hard as I can ....jabbing the thorns into him. And I say, "See, it isn't perfect".

Now, most people would be like, "Hey, a sshole - stop being a jerk and squeezing my hand. It hurts!"

But MrKleen73, isn't most people ....he thinks, "Wow, this guy really is an a sshat - but you know, I never realized that thorn was there."
 
Shhhhhewwwww we fellas.....almost thought I was gonna be thrown in the category of "starved ethopian " ...
I have been in the "bikini chic" and "baby fetus" category before...
Man oh man you guys are talented....BOSSMAN is soaking it alllllllllllll in...
 
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