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Trying to Gain Weight on LCHF

Nothing meaningful to contribute to you scholars other than to say to Oldvatr , when I saw the premise of your thread, this old fella thought, "well I'm on the LCHF, it's working great and the weights plummeting and so when I achieve my optimal Personal Fat Threshold in about 3 months, I'll just increase the fat and hey presto ....maintenance". Ah hum... I think I'll out this question to the Diet Doctor and see if he has anything to add. Will report back....excellent thread.


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Oldvatr said:
Glucose is not a fat. Glucogen in the blood is also not fat, and it gets stored as glucogen. Both of these are glycerols which are esters. fats get stored as fatty acids (FA) They are packaged for transport in the blood as triglycerides which are packets of FA wrapped up in a bubble of glycerol, which is why carbs are also involved in lipid activity. In extreme circumstances, the process of gluconeogenesis can convert either protein or fat to glucose( just for the brain and neurons). It is is the process of lipogenesis that creates the lipids, but although this can also synthesise fats from glucose, this is very much a last resort, as it takes a lot of energy to do.

It is unusual for gluconeogenesis to be triggered except when bgl levels are low simply because it is a protection system for the brain coz the brain cannot use fat for energy, and relies on there being some glucogen (or ketones) around. This is why we get brain fog when suffering a hypo since the think tank is becoming impaired, and gluconeogenesis is inefficient.
Click to expand...

Once all the easy , store term glucogen stores are full, the body will start laying down fat.
That's why it's the norm to get fat from overeating carbs.
The body is good at converting most things, it's all just variations on carbon, hydrogen and oxygen at the end of the day.

I think the other issue may be there are indeed different variations on metabolisms between posters, and mine may seem to be working a lot better than others seem to be, who claim this bit is missing from their function now.
 
SunnyExpat said:
Once all the easy , store term glucogen stores are full, the body will start laying down fat.
That's why it's the norm to get fat from overeating carbs.
The body is good at converting most things, it's all just variations on carbon, hydrogen and oxygen at the end of the day.

I think the other issue may be there are indeed different variations on metabolisms between posters, and mine may seem to be working a lot better than others seem to be, who claim this bit is missing from their function now.
Click to expand...
We are I believe talking about a situation where someone on an LCHF diet and in prolonged ketosis is not able to gain weight even when the fat intake has been set high. The Sam Fletcher video shows that there is an estimate for weight that was expected given the calorific input level and the exercise regime, but this weight gain did not materialise (literally). Under these conditions, short term glucogen stores should be fully depleted and no longer relevant to this discussion. Short term lipid stores in the cholesterol will be used to provide primary energy and the fat intake should be giving an excess of lipids that are not consumed by the level of body activity. the question I raised was - what happens to this excess, and why is it not being stored as body fat? How come Dr Bernstein reports the same phenomenon, and we now have a mantra that fat intake no longer equates to being fat. So there is supporting evidence for there being another mechanism at play.

As a T2D on orals, I have already reached a proper weight, and would suffer from losing more. My quandary is that if I cannot find a way of controlling my weight upwards, then I must consider giving up LCHF as a viable diet, and hence stop making recommendations to others about it being suitable as a long term solution. It becomes a crash diet like other LC diets.
 
KevinPotts said:
Nothing meaningful to contribute to you scholars other than to say to Oldvatr , when I saw the premise of your thread, this old fella thought, "well I'm on the LCHF, it's working great and the weights plummeting and so when I achieve my optimal Personal Fat Threshold in about 3 months, I'll just increase the fat and hey presto ....maintenance". Ah hum... I think I'll out this question to the Diet Doctor and see if he has anything to add. Will report back....excellent thread.


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Click to expand...
Hi Kevin. Dietdoctor has already reviewed the Sam Fletcher video, and the other one, and made comments. I think that the response given did not really give any answers. There may be more now, but I did not see it.
 
Oldvatr said:
We are I believe talking about a situation where someone on an LCHF diet and in prolonged ketosis is not able to gain weight even when the fat intake has been set high. The Sam Fletcher video shows that there is an estimate for weight that was expected given the calorific input level and the exercise regime, but this weight gain did not materialise (literally). Under these conditions, short term glucogen stores should be fully depleted and no longer relevant to this discussion. Short term lipid stores in the cholesterol will be used to provide primary energy and the fat intake should be giving an excess of lipids that are not consumed by the level of body activity. the question I raised was - what happens to this excess, and why is it not being stored as body fat? How come Dr Bernstein reports the same phenomenon, and we now have a mantra that fat intake no longer equates to being fat. So there is supporting evidence for there being another mechanism at play.

As a T2D on orals, I have already reached a proper weight, and would suffer from losing more. My quandary is that if I cannot find a way of controlling my weight upwards, then I must consider giving up LCHF as a viable diet, and hence stop making recommendations to others about it being suitable as a long term solution. It becomes a crash diet like other LC diets.
Click to expand...

He only did the diet for three weeks didn't he?
 
SunnyExpat said:
He only did the diet for three weeks didn't he?
Click to expand...
Yes. I am taking into account other incidences being reported. It appears Sam Fletcher is not alone, which is why I have not spent time analysing his efforts in any detail. I dare say I could pick holes in it but it would not eliminate the other 'evidence'.

Why has the mantra changed from obesity is caused by overeating fat to fat does not cause obesity - carbs do. Why did Bernstein change his stance on using fat to increase weight on LCHF? Why are some posters here also reporting finding this to be difficult? ( to be fair its only a few, most complain about not being able to lose weight)

If we can find a set of conditions under LCHF that gives this control without losing bgl control, or upping the lipids unecessarily then its a benefit. If however, we find, say, that the excess just increases the cholesterol in a bad way, then it is something that affects all people using LCHF since this means that they have to limit fat intake, and we don't know at what level that would need to be. So this question is more important than simply solving my own personal weight problem
 
Indy51 said:
I'd like to know the answer to that question as well.
Click to expand...
Glucogen is the glucose being transported in the blood, and is what our bgl meters measure. Glycogen is the result of when glucogen enters cell, and is the form that glucose takes when stored. Glycogen is usually used to describe Stored glucose since it is packaged differently from glucogen. It is also the source of glycerols used to make the cholesterol and triglicerides in the lipid system.
 
@Oldvatr

Have you seen the documentary 'The Cereal Killers'?

I believe the guy in that did a programme similar to Sam Fletcher, while under close examination of bloodwork, etc.

Why do you suspect that high fat may negatively affect everyone using LCHF?

That has been clearly demonstrated to not be the case in several studies quoted by Voleck, Phinney and Ken Sikaris (see Sikaris' you tube videos for the refs). I am sorry, I am jsut dipping in to the forum today. No time to track down the links.

Having said that, I am increasingly unconvinced of any argument that claims a high HDL score, on a standard NHS test, is of relevance to my future health. As a society we are fixated on Cholesterol, and it is almost invariably a distraction from far more important issues.
 
I'm not absolutely convinced that if you have a tendency to gain weight that you won't gain weight eating fat, especially if you're consuming excess calories of the stuff. Sam Feltham is what I would term a congenitally slim person. I think it would take a lot to break his metabolism to the point that he would become obese.

There is also the set point theory of weight and that definitely came into play for me. I spontaneously stopped losing weight when I reached a certain level of weight loss despite not increasing my calories and continuing to use intermittent fasting. I've even very slowly regained a few kgs despite eating very similar amounts of food with carbs ranging anywhere from 30gs to 80gs depending on the day.

I don't think anything is simple or easy or predictable when it comes to weight loss/gain, metabolism and Type 2.

Also, it's a lot harder for a weight reduced individual to maintain weight loss than it is for someone who has never been overweight. Even harder for a weight reduced individual who has been a chronic dieter for years.

If you are consuming adequate calories (ie. not starving yourself) then your weight should eventually stabilise at a level your body is comfortable with. I think people who continue to lose weight are in the minority judging by the anecdotal stories I've read on this board over the past few years.
 
Hi, @Brunneria
my post said if lipids were shown to be badly affected by having excess fat intake than gets used up by ketosis and exercise, then I did make an assumption that this would be of interest to all using LCHF since we may need to consider recommending that an upper limit may need to be put in place, whereas at the moment the video shows that there does not appear to be any limit apart from physically gulping it down. It seems according to dietdoctor that lipids were not reviewed during the trial in the video, so we will never know.
 
I have never been over weight but I have been underweight. Some still consider me skinny but my tummy says no. However, I have had to keep within a certain calorie threshold to maintain it.
Times changed when I was progressing to type 1 over a period of time. I didn't know this was what was going on at the time. I had to keep reducing food. Protein and meal size. I started fasting until 2pm and then just had two small salads topped with a few ounces of protein and olive oil. I was doing all this to keep bs control. It kept creeping up so I kept reducing. I would have some nuts as snacks between 2 and 6. However I kept dropping weight slowly but in the end it fell off until I was grossly skinny , weak and very sick. My docs kept telling me I was fine. I told them how little I are or bs would rocket. They did nothing. Finally I was hospitalized, diagnosed T 1 with severe muscle wasting, protein deficiency and malnourishment. Now there was a few month period pre diagnosis that I was eating tons. Setting my alarm to get up and eat an extra meal. BS was crazy high but I was trying to gain weight.
After starting insulin within two months I had gained my 20+ pounds back and now I need to continue to watch portion control. I stayed VLC , moderate protein and higher fat. I will gain weight if I over eat fat now. Or any macro nutrient for that matter. I guess this is a long way of saying that I think how and when we gain or lose weight has much to do with our insulin production, lack of or resistance just or more than it has to do with our basic metabolism.

I could be way off but insulin has made a huge difference with my weight and looking back I can see where it was declining as well. My weight stabilized right where it left off but I need to keep food portions just as I did before I was sick.

Just my thought.
 
Brunneria said:
@Oldvatr

Have you seen the documentary 'The Cereal Killers'?

I believe the guy in that did a programme similar to Sam Fletcher, while under close examination of bloodwork, etc.

Why do you suspect that high fat may negatively affect everyone using LCHF?

That has been clearly demonstrated to not be the case in several studies quoted by Voleck, Phinney and Ken Sikaris (see Sikaris' you tube videos for the refs). I am sorry, I am jsut dipping in to the forum today. No time to track down the links.

Having said that, I am increasingly unconvinced of any argument that claims a high HDL score, on a standard NHS test, is of relevance to my future health. As a society we are fixated on Cholesterol, and it is almost invariably a distraction from far more important issues.
Click to expand...
Prof Sikaris has produced some amazing videos, as have other endocrinologists around the world. I have studied these videos because I am interested in what happen inside me, and that info has recently changed to take LCHF into account. But these seminars seem to only cover part of the process from what I could see.
They all seem to start with the liver packaging fatty acids into triglicerides, and they then describe the transport system of trigs as the fats get used. The seminars omit the process of how lipids and trigs are actually c reated, nor how FA's actually get used in the cells having got through the cell wall.

Eventually LDL gets depleted, and is picked up by HDL and taken back to the liver for recycling. Note, they talk of HDL being recycled, but any remaining fat in it magically disappears. in reality it probably gets pushed out through the bile duct, but this is not mentioned. Where they mention storage, then it is a reference to 'in the liver', but in reality it is in adipose cells that are distributed all over the body, and the liver is not sole storage depot. so this aspect sems to be glossed over in several seminars I watched. It is also not really discussed in dietdoctor either. Bernstein does not mention it when he talks about not gaining weight on LCHF.

So I have a big question mark in my head. Where does excess fat go? Simple question to ask, but no one seems to want to address it. This is like living in a house with no restroom. Where does it all go? If we ingest more FFA than we need, and it does not get stored in adipose cells, and hopefully not in trigs swilling round my system, and my HDL is low so its not there. And if it is excreted unused via the bile duct, is that a safe thing? Am I stressing my gallbladder, or stressing my large intestine? Am I creating excess stem cells in my colon that are being disturbed by this wash of FFA's
Kristin251 said:
I have never been over weight but I have been underweight. Some still consider me skinny but my tummy says no. However, I have had to keep within a certain calorie threshold to maintain it.
Times changed when I was progressing to type 1 over a period of time. I didn't know this was what was going on at the time. I had to keep reducing food. Protein and meal size. I started fasting until 2pm and then just had two small salads topped with a few ounces of protein and olive oil. I was doing all this to keep bs control. It kept creeping up so I kept reducing. I would have some nuts as snacks between 2 and 6. However I kept dropping weight slowly but in the end it fell off until I was grossly skinny , weak and very sick. My docs kept telling me I was fine. I told them how little I are or bs would rocket. They did nothing. Finally I was hospitalized, diagnosed T 1 with severe muscle wasting, protein deficiency and malnourishment. Now there was a few month period pre diagnosis that I was eating tons. Setting my alarm to get up and eat an extra meal. BS was crazy high but I was trying to gain weight.
After starting insulin within two months I had gained my 20+ pounds back and now I need to continue to watch portion control. I stayed VLC , moderate protein and higher fat. I will gain weight if I over eat fat now. Or any macro nutrient for that matter. I guess this is a long way of saying that I think how and when we gain or lose weight has much to do with our insulin production, lack of or resistance just or more than it has to do with our basic metabolism.

I could be way off but insulin has made a huge difference with my weight and looking back I can see where it was declining as well. My weight stabilized right where it left off but I need to keep food portions just as I did before I was sick.

Just my thought.
Click to expand...
Thanks. I note your comments, and it may be Bernstein is correct, that insulin is the only way to go. However, my own situation is improving slightly, and I am almost back to my target, Last night I was only 0.5 kg lower, and this is just with a slight increase in dairy products and a rump steak 2 nights ago. Same carb input at around 30 g,
 
@Oldvatr

In this entry
https://intensivedietarymanagement.com/a-calorie-is-a-calorie-part-ii/
Jason Fung addresses the exact question of by Sam Feltham didn't gain - explaining it as an increase in metabolism. He has links to a series of entries about Total Energy Expenditure and Basal Energy Expenditure that you may find useful.

Will read them myself, when I get the chance, but am beginning to get swamped by my reading lists, so it may take a while.
 
I am also suprised that few I have heard, with possibly the exception of Sarah Halberg MD, fails to connect the importance of the mTor pathways and in particular the nutrient/ hormone (insulin our cases) and (lack t1 or over production t2 ) and the rapamycin molecule's impact in our cell metabolism. From reading around it seeds pretty clear that cell metabolism, growth, proliferation or retardation at a cell physiological level is part of this pathway system, yet I rarely hear this fundamental piece included in presentations.


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If my rough science us correct then, this could be responsive in inability to gain weight (and numerous other anomalies) and what Sabatini declares as the "FDA approved rapamycin component" being used in clinical responses.


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If my rough science is correct then, this could be responsive in the inability to gain weight scenario (and numerous other anomalies) and what Sabatini declares as the "FDA approved rapamycin component" being used in clinical responses


Sent from my iPhone using DCUK Forum mobile app
 
Oldvatr said:
Prof Sikaris has produced some amazing videos, as have other endocrinologists around the world. I have studied these videos because I am interested in what happen inside me, and that info has recently changed to take LCHF into account. But these seminars seem to only cover part of the process from what I could see.
They all seem to start with the liver packaging fatty acids into triglicerides, and they then describe the transport system of trigs as the fats get used. The seminars omit the process of how lipids and trigs are actually c reated, nor how FA's actually get used in the cells having got through the cell wall.

Eventually LDL gets depleted, and is picked up by HDL and taken back to the liver for recycling. Note, they talk of HDL being recycled, but any remaining fat in it magically disappears. in reality it probably gets pushed out through the bile duct, but this is not mentioned. Where they mention storage, then it is a reference to 'in the liver', but in reality it is in adipose cells that are distributed all over the body, and the liver is not sole storage depot. so this aspect sems to be glossed over in several seminars I watched. It is also not really discussed in dietdoctor either. Bernstein does not mention it when he talks about not gaining weight on LCHF.

So I have a big question mark in my head. Where does excess fat go? Simple question to ask, but no one seems to want to address it. This is like living in a house with no restroom. Where does it all go? If we ingest more FFA than we need, and it does not get stored in adipose cells, and hopefully not in trigs swilling round my system, and my HDL is low so its not there. And if it is excreted unused via the bile duct, is that a safe thing? Am I stressing my gallbladder, or stressing my large intestine? Am I creating excess stem cells in my colon that are being disturbed by this wash of FFA's

Thanks. I note your comments, and it may be Bernstein is correct, that insulin is the only way to go. However, my own situation is improving slightly, and I am almost back to my target, Last night I was only 0.5 kg lower, and this is just with a slight increase in dairy products and a rump steak 2 nights ago. Same carb input at around 30 g,
Click to expand...
You certainly have researched this far more than I have but could it be as simple as it just gets excreted? Which would also perhaps answer why some of us need enough fat for proper elimation.
Also looking back in my history, insulin seems to be the definitive key to my weight gains and losses. Pre diabetes I had to keep fat as well as carbs low or I would gain. Of course carbs were the biggest offenders. As I was progressing with diabetes , which I didn't know at the time as my Drs said I was fine, I had to reduce protein but I upped the fat. I did not gain but I wasn't eating gobs. Then a few months before DX I was eating tons of everything. Ounces and ounces of nuts a day, 100 g of protein and still stayed low carb but bs was crazy. Weight was dropping daily. Started insulin and gained my lost weight back but I was eating 20 c per meal. They made me feel awful and couldn't steady bs so dropped the carbs, lowered the insulin and weight gain stopped. Fast forward to 6 months ago I started eating much more fat and gaining a pound a week. That needed to stop so I reduced fat as well as insulin. I have much better bs now too. Well I should say I feel more balanced. So to me this series of events shows the more insulin I have the more weight I gain. I don't think, though I could be wrong, that if I needed to the nutrients I wouldn't be storing them as fat. I was also told at DX that I was starving in the land of plenty. It didn't matter how much I ate that without insulin the nutrients weren't getting into my cells and were starving hence the weight loss. I do think it makes a huge difference in weight gain/ loss how much insulin we are producing and / or how resistant / sensitive we are. So to me I think insulin is the driver and whatever macro we aren't using or needing will be stored as fat and the rest will just be excreted.
For you, if and when the time comes yiu might just consider a very low dose of basal. See how that goes, or a very low dose, such as a half unit with meals. I now take one unit of basal if I'm over 75. If I'm under 75 I have a snack with one unit. Meals are 1/2 unit but small and VLC. I don't fear hypos at these small doses. The basal or small basal bolus could potentially preserve some of your own lancepreatic function and allow you to absorb some more nutrients. You would always have the option of stopping it or just using it for select meals for a little boost. I wish I would have had that option because things really too, a turn for the worst when they put me on amaryl and squeezed my pancreas to death, literally. Now that I know what I know about insulin I would have tried a small basal dose at the very I least in order to support my pancreas and perhaps at least delayed where it m now. Just something to consider.
 
Kristin251 said:
You certainly have researched this far more than I have but could it be as simple as it just gets excreted? Which would also perhaps answer why some of us need enough fat for proper elimation.
Also looking back in my history, insulin seems to be the definitive key to my weight gains and losses. Pre diabetes I had to keep fat as well as carbs low or I would gain. Of course carbs were the biggest offenders. As I was progressing with diabetes , which I didn't know at the time as my Drs said I was fine, I had to reduce protein but I upped the fat. I did not gain but I wasn't eating gobs. Then a few months before DX I was eating tons of everything. Ounces and ounces of nuts a day, 100 g of protein and still stayed low carb but bs was crazy. Weight was dropping daily. Started insulin and gained my lost weight back but I was eating 20 c per meal. They made me feel awful and couldn't steady bs so dropped the carbs, lowered the insulin and weight gain stopped. Fast forward to 6 months ago I started eating much more fat and gaining a pound a week. That needed to stop so I reduced fat as well as insulin. I have much better bs now too. Well I should say I feel more balanced. So to me this series of events shows the more insulin I have the more weight I gain. I don't think, though I could be wrong, that if I needed to the nutrients I wouldn't be storing them as fat. I was also told at DX that I was starving in the land of plenty. It didn't matter how much I ate that without insulin the nutrients weren't getting into my cells and were starving hence the weight loss. I do think it makes a huge difference in weight gain/ loss how much insulin we are producing and / or how resistant / sensitive we are. So to me I think insulin is the driver and whatever macro we aren't using or needing will be stored as fat and the rest will just be excreted.
For you, if and when the time comes yiu might just consider a very low dose of basal. See how that goes, or a very low dose, such as a half unit with meals. I now take one unit of basal if I'm over 75. If I'm under 75 I have a snack with one unit. Meals are 1/2 unit but small and VLC. I don't fear hypos at these small doses. The basal or small basal bolus could potentially preserve some of your own lancepreatic function and allow you to absorb some more nutrients. You would always have the option of stopping it or just using it for select meals for a little boost. I wish I would have had that option because things really too, a turn for the worst when they put me on amaryl and squeezed my pancreas to death, literally. Now that I know what I know about insulin I would have tried a small basal dose at the very I least in order to support my pancreas and perhaps at least delayed where it m now. Just something to consider.
Click to expand...
https://intensivedietarymanagement.com/can-make-fat-insulin-hormonal-obesity-iii/
 
Although I use the HF part of LCHF to control weight, my intake of fat generally is moderate and not much changed from what i was using 10 years ago. I have always used butter instead of marge, avoided the butter spreads, use vegetable and olive oil and avoid canola/rapeseed/ safflower oil if I see it. i generally do not use whole milk, and do not normally use cream. I have always used hard cheeses in preference to soft or lowfat cheeses.

The time I increase my fat intake on this diet is when my weight drops significntly below my target weight. Then i add cream to my coffee, and buy Babybels by the bagfull. I up the butter intake a bit more. I use coconut oil for making sweetpotato chips or wedges. We have more Cauli mash with soft cheese. I use olive oil more as salad dressing.

I think that HF is inherent in LCHF to support the long term use of ketosis. When first going into ketosis, there is significant depletion of local visceral fat, which supplies the fat for fat burning. Then there comes a stage where these stores become depleted, and then we need fat in the lipid system to burn rather than stored fat. This is where the HF is needed, and it stopss the body consuming muscle tissue while in ketosis. A very important aspect of the diet, but only when in prolonged ketosis.

It is perfectly possible to use LCHF as a pure LC diet, without ketosis, and this will control bgl via the glucose pathway. Once visceral fat stores are depleted, then this is probably a sufficient maintenance mode, but ketosis may still be necessary on occasions to keep the visceral fat in trim.

I have recently reduced my girth by a couple of jean sizes, so I have now decided to step back from ketosis by raising my carbs slightly. I have also cut fat, and ,my weight has already dropped 1 kg in a few days. I have not checked my ketones level, so will need to do so to confirm I am not in solid keto mode.
 
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