Hey My Dudes [PUFA, Ketosis, Insulin Resistance]

OP
BigYellowLemon
Joined
Jul 6, 2016
Messages
550
"We found that long-chain unsaturated fatty acids (FAs) promoted aggregate formation of SOD1 mutants in both dose- and time-dependent manners."

The study shows that oleic acid, the most abundant MUFA in food sources, promotes the development of certain neurological disorders.

I'll have to think about this...

I am suspicious of this study, considering they used genetically engineered mice, so as to engineer their study to get the results they wanted.

I remember haidut posted something about oleic acid build-up in Alzheimers patients.

I will have to research this.
 
OP
BigYellowLemon
Joined
Jul 6, 2016
Messages
550
I would say heavily weighted in PUFA, definitely.

I was more leaning to a human preference for larger amounts of fat in the diet. We gravitate toward ice cream and bacon, for example.

Oh okay, I see.

When I went a close to zero-fat diet for a couple of days, with lots of fruit, 2% milk, and sugar, I craved fat so much. I'm on a HFLC diet right now, and I have basically zero craving for any carbs. It's odd.

Something I've noticed, is that those who are on HFLC diets stop craving sugar/carbs, but those on HCLF diets seem to crave fat a TON.

I read your PUFA depletion log, and I remember you mentioning you dreamed of eating a stick of butter :D hahah that was funny to me, I feel like your body was trying to tell you something.

People who eat low-fat tend to report anxiety.

The only problem I have with HFLC is that you smell like acetone, whilst people on fruitarian diets apparently smell great (like fruit), if at all.

I feel like the optimal diet should make you smell good.
 

DaveFoster

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Joined
Jul 23, 2015
Messages
5,027
Location
Portland, Oregon
Oh okay, I see.

When I went a close to zero-fat diet for a couple of days, with lots of fruit, 2% milk, and sugar, I craved fat so much. I'm on a HFLC diet right now, and I have basically zero craving for any carbs. It's odd.

Something I've noticed, is that those who are on HFLC diets stop craving sugar/carbs, but those on HCLF diets seem to crave fat a TON.

I read your PUFA depletion log, and I remember you mentioning you dreamed of eating a stick of butter :D hahah that was funny to me, I feel like your body was trying to tell you something.

People who eat low-fat tend to report anxiety.

The only problem I have with HFLC is that you smell like acetone, whilst people on fruitarian diets apparently smell great (like fruit), if at all.

I feel like the optimal diet should make you smell good.
I appreciate that you checked out my log. I do have high anxiety, and you're right. People who go high-carb also have the problem of feeding gut bacteria too much, and of getting too little salt. (Salt and fat are usually paired.)

I'd agree that I use the health of the individual as a gauge to the usefulness of his or her diet, although this is a fallacy. We generally agree that babies are healthy, and they have a very high pulse and metabolic rate. Smell is definitely worth noting, as is hair quality, nail quality, clear skin (I've noticed vegans tend to have horrendous acne.) Considering the role of gut bacteria in acne, I'll suggest that this is causal.

Peat looks fantastic for his age, as does Mark Sission and most gurus, although Matt Stone not so much. Marcus Rothkranz looks pretty good; he's a vegan.

I think the general's are not too debatable; high calcium, limit iron but don't become anemic, higher protein (we have enzymatic evolutionary adaptation to breakdown larger amounts of protein), salt as much as you like, and obey your sweet tooth.

As for fat, Peat makes the argument that, due to our cooler climate on this planet, living beings require a certain level of membrane permeability, and thus unsaturation in their fat composition. We would do best to minimize the level of unsaturated fats we consume, due to the fact that they accumulate and accelerate the aging process. Again, we need to remember that the goal is not to have a low tissue content of PUFA per say, but to maximize tissue regeneration and repair.

Even if saturated fats (or even monounsaturated fats paired with sugar), yield benefits to mitochondrial respiration in the short-term (which they do not in Peat's view, due to CHO's superior ability to generate CO2 and maintain the cell's molecular structure,) then with the exception of a fully-hydrogenated fat source, these still would lead to the saturation of the tissues with unsaturated fats (pun intended,) which would retard metabolism and maximize localized oxidative stress. This is my understanding of his view.

I'm perfectly willing to entertain the idea that humans require a greater amount of fat; I think our palates are evidence of that. We crave salt, fat, protein, and sugar, so we likely have needs for these. Again, I'm employing a naturalistic fallacy.
 
OP
BigYellowLemon
Joined
Jul 6, 2016
Messages
550
I appreciate that you checked out my log. I do have high anxiety, and you're right. People who go high-carb also have the problem of feeding gut bacteria too much, and of getting too little salt. (Salt and fat are usually paired.)

I'd agree that I use the health of the individual as a gauge to the usefulness of his or her diet, although this is a fallacy. We generally agree that babies are healthy, and they have a very high pulse and metabolic rate. Smell is definitely worth noting, as is hair quality, nail quality, clear skin (I've noticed vegans tend to have horrendous acne.) Considering the role of gut bacteria in acne, I'll suggest that this is causal.

Peat looks fantastic for his age, as does Mark Sission and most gurus, although Matt Stone not so much. Marcus Rothkranz looks pretty good; he's a vegan.

I think the general's are not too debatable; high calcium, limit iron but don't become anemic, higher protein (we have enzymatic evolutionary adaptation to breakdown larger amounts of protein), salt as much as you like, and obey your sweet tooth.

As for fat, Peat makes the argument that, due to our cooler climate on this planet, living beings require a certain level of membrane permeability, and thus unsaturation in their fat composition. We would do best to minimize the level of unsaturated fats we consume, due to the fact that they accumulate and accelerate the aging process. Again, we need to remember that the goal is not to have a low tissue content of PUFA per say, but to maximize tissue regeneration and repair.

Even if saturated fats (or even monounsaturated fats paired with sugar), yield benefits to mitochondrial respiration in the short-term (which they do not in Peat's view, due to CHO's superior ability to generate CO2 and maintain the cell's molecular structure,) then with the exception of a fully-hydrogenated fat source, these still would lead to the saturation of the tissues with unsaturated fats (pun intended,) which would retard metabolism and maximize localized oxidative stress. This is my understanding of his view.

I'm perfectly willing to entertain the idea that humans require a greater amount of fat; I think our palates are evidence of that. We crave salt, fat, protein, and sugar, so we likely have needs for these. Again, I'm employing a naturalistic fallacy.

Ketones are helpful for anxiety, as you may well know. They are similar to GABA/glycine in effect, and are inhibitory. Something to think about.

Babies are apparently in ketosis, but breast-milk is pretty high in carbs, too much for ketosis to occur. Obviously it might be that babies run things a little bit differently, metabolically, than adults do. But perhaps breast-milk is the reason, as in, the fatty acids in it are ketogenic, so they allow the baby to be ketogenic, whilst also consuming lots of carbs.

I've been thinking about running a diet with lots of lactose and ketogenic fatty acids, fatty acids that allow insulin to function. C8 caprylic acid is the main one I'm interested in. Skim milk and MCT's (along with other things of course, maybe some fruit and easily digestible tubers, some leafy greens).

I actually texted my friend about this today! Ray Peat look's amazing for 79, it's absolutely insane! He looks 50, maybe even 40. I think Mark Sisson looks so good because he takes HGH and testosterone. Ray Peat seems to only take the neurosteroids (pregnenolone, progesterone, and some DHEA). I think I'm just gonna follow what Ray Peat says, lol.

I agree about the essentials of what Ray is saying.

I want to move to a warmer climate. It seems like it'd be healthier. I'm still debating whether warm or cold climates would be best though.

I'm really not sure about anything tbh, There's so many very valid viewpoints, but I think they all share a common theme. I'm not sure what that thread linking them all together is though. I guess, increase metabolic rate.

I like Ray's recommendations a lot. They are generally safe, cheap, and effective. Aspirin is great for me. Caffeine is great for me. I think if people followed a very basic "Peat protocol", then a lot of trouble and suffering would be saved.
 

tyw

Member
Joined
Nov 19, 2015
Messages
407
Location
Cairns, Australia
Amazing, thank you for the clarification!

What are the implications of complex 3/4 ROS? For some reason I feel as though that carbohydrates favor this kind of ROS generation.

Thanks.

ROS has exactly the same effect, whether it be produced at Complex 1 or Complex 3.

The question is one of quantity, and the paper I talked about earlier goes into this in good detail -- How mitochondria produce reactive oxygen species

Quote:

Complex III has for a long time been regarded as a source of O2•−within mitochondria [84,100]. When supplied with CoQH2 and when the Qi site is inhibited by antimycin, complex III produces large amounts of O2•− from the reaction of O2 with a ubisemiquinone bound to the Qo site.

However, in the absence of antimycin, the Qo site ubisemiquinone is not stabilized and O2•− production by complex III is low [105].

Inhibition of respiration at points distal to complex III with cyanide or by loss of cytochrome cdoes not increase O2•− production by complex III [100], therefore reduction of the CoQ pool is not sufficient to generate O2•− at complex III.​


Taken independently, Carbs "favour" Complex 3 ROS generation, but that is not comparable in magnitude to the levels of ROS produced by Complex 1 RET. We can say that the highest possible efficiency in mitochondria wrt ATP production, is when there is forward-flow-only state 3 respiration. If anything, properly dosed carbohydrate use favours this state.

In any case, if state 3 (ATP generating) respiration is assumed, both NADH and FADH2 derived electrons have to pass through Complex 3, and have the same effect. As per the quotes above, CoQ couple reduction doesn't affect this site of ROS production.

Comparing Complex 1 to Complex 3 ROS production (note that Δp refers to "protonmotive force", which is driven by delta psi and delta pH):

It may be that high Δp stabilizes the Qo site ubisemiquinone; however, the very high production of O2•−by complex I during RET in the presence of succinate is abolished completely by rotenone [87,95].

Under these conditions, there is a large Δp and a reduced CoQ pool, suggesting that the maximal O2•− production by uninhibited complex III is negligible compared with that by complex I during RET.

However, it is possible that, for mitochondria operating in mode 3, when O2•− production by complex I is low, the contribution of complex III to the overall O2•− flux may then become relatively significant.

Under these conditions, factors that affect the stability of the ubisemiquinone radical in the Qo site, such as loss of cytochrome c or changes in Δp or in the redox state of the CoQ and cytochrome c pools, may modulate O2•−production.​


I think Complex 3 ROS generation comes down to basic queueing mechanics -- you have a queue of incoming electrons, with the need to process them at Complex 4 (typically by accepting them using Oxygen). Those electrons which cannot be terminally accepted get "pushed out of the queue" / leak from the mitochondria, and have the potential to generate ROS, RNS, etc ....

----

Also see the section "Other sites of O2•− production within mitochondria". It goes through more ways by which ROS can be produced, and many of those are related to the inherently more complex processing of fatty acids.

----

On a related topic, I have discussed why "PUFA Depleted Mitochondria" have the ability to deal with large electron flux in these posts:

- PUFAs Role On Skin
- 'Gainz Brah' Bio-energetic Log

.....
 
OP
BigYellowLemon
Joined
Jul 6, 2016
Messages
550
I appreciate that you checked out my log. I do have high anxiety, and you're right. People who go high-carb also have the problem of feeding gut bacteria too much, and of getting too little salt. (Salt and fat are usually paired.)

I'd agree that I use the health of the individual as a gauge to the usefulness of his or her diet, although this is a fallacy. We generally agree that babies are healthy, and they have a very high pulse and metabolic rate. Smell is definitely worth noting, as is hair quality, nail quality, clear skin (I've noticed vegans tend to have horrendous acne.) Considering the role of gut bacteria in acne, I'll suggest that this is causal.

Peat looks fantastic for his age, as does Mark Sission and most gurus, although Matt Stone not so much. Marcus Rothkranz looks pretty good; he's a vegan.

I think the general's are not too debatable; high calcium, limit iron but don't become anemic, higher protein (we have enzymatic evolutionary adaptation to breakdown larger amounts of protein), salt as much as you like, and obey your sweet tooth.

As for fat, Peat makes the argument that, due to our cooler climate on this planet, living beings require a certain level of membrane permeability, and thus unsaturation in their fat composition. We would do best to minimize the level of unsaturated fats we consume, due to the fact that they accumulate and accelerate the aging process. Again, we need to remember that the goal is not to have a low tissue content of PUFA per say, but to maximize tissue regeneration and repair.

Even if saturated fats (or even monounsaturated fats paired with sugar), yield benefits to mitochondrial respiration in the short-term (which they do not in Peat's view, due to CHO's superior ability to generate CO2 and maintain the cell's molecular structure,) then with the exception of a fully-hydrogenated fat source, these still would lead to the saturation of the tissues with unsaturated fats (pun intended,) which would retard metabolism and maximize localized oxidative stress. This is my understanding of his view.

I'm perfectly willing to entertain the idea that humans require a greater amount of fat; I think our palates are evidence of that. We crave salt, fat, protein, and sugar, so we likely have needs for these. Again, I'm employing a naturalistic fallacy.

Also, about vegans and fruitarians having acne...

Some of them look very unhealthy, very sick looking. Others seem to prosper, and look absolutely gorgeous.

I won't link any, as I don't want to talk ***t, but look up some fruitarians if you haven't. Some have vibrant eyes, glowing skin, white teeth. Other's have horrible acne, receding hair, dull eyes, ect.

The fruitarian men generally seem to look worse than the fruitarian women. One thing in common that they all (generally) have, is that they are skinny as ****.
 

ATP

Member
Joined
Oct 15, 2015
Messages
279
ROS has exactly the same effect, whether it be produced at Complex 1 or Complex 3.

The question is one of quantity, and the paper I talked about earlier goes into this in good detail -- How mitochondria produce reactive oxygen species

Quote:

Complex III has for a long time been regarded as a source of O2•−within mitochondria [84,100]. When supplied with CoQH2 and when the Qi site is inhibited by antimycin, complex III produces large amounts of O2•− from the reaction of O2 with a ubisemiquinone bound to the Qo site.

However, in the absence of antimycin, the Qo site ubisemiquinone is not stabilized and O2•− production by complex III is low [105].

Inhibition of respiration at points distal to complex III with cyanide or by loss of cytochrome cdoes not increase O2•− production by complex III [100], therefore reduction of the CoQ pool is not sufficient to generate O2•− at complex III.​


Taken independently, Carbs "favour" Complex 3 ROS generation, but that is not comparable in magnitude to the levels of ROS produced by Complex 1 RET. We can say that the highest possible efficiency in mitochondria wrt ATP production, is when there is forward-flow-only state 3 respiration. If anything, properly dosed carbohydrate use favours this state.

In any case, if state 3 (ATP generating) respiration is assumed, both NADH and FADH2 derived electrons have to pass through Complex 3, and have the same effect. As per the quotes above, CoQ couple reduction doesn't affect this site of ROS production.

Comparing Complex 1 to Complex 3 ROS production (note that Δp refers to "protonmotive force", which is driven by delta psi and delta pH):

It may be that high Δp stabilizes the Qo site ubisemiquinone; however, the very high production of O2•−by complex I during RET in the presence of succinate is abolished completely by rotenone [87,95].

Under these conditions, there is a large Δp and a reduced CoQ pool, suggesting that the maximal O2•− production by uninhibited complex III is negligible compared with that by complex I during RET.

However, it is possible that, for mitochondria operating in mode 3, when O2•− production by complex I is low, the contribution of complex III to the overall O2•− flux may then become relatively significant.

Under these conditions, factors that affect the stability of the ubisemiquinone radical in the Qo site, such as loss of cytochrome c or changes in Δp or in the redox state of the CoQ and cytochrome c pools, may modulate O2•−production.​


I think Complex 3 ROS generation comes down to basic queueing mechanics -- you have a queue of incoming electrons, with the need to process them at Complex 4 (typically by accepting them using Oxygen). Those electrons which cannot be terminally accepted get "pushed out of the queue" / leak from the mitochondria, and have the potential to generate ROS, RNS, etc ....

----

Also see the section "Other sites of O2•− production within mitochondria". It goes through more ways by which ROS can be produced, and many of those are related to the inherently more complex processing of fatty acids.

----

On a related topic, I have discussed why "PUFA Depleted Mitochondria" have the ability to deal with large electron flux in these posts:

- PUFAs Role On Skin
- 'Gainz Brah' Bio-energetic Log

.....
Just for some clarity, other than a PUFA depleted state. What would be the ideal source of energy for the best Metabolic rate and efficiency possible. Fat or sugar?
 
OP
BigYellowLemon
Joined
Jul 6, 2016
Messages
550
Just for some clarity, other than a PUFA depleted state. What would be the ideal source of energy for the best Metabolic rate and efficiency possible. Fat or sugar?

This is what I ask myself all day long.
 
OP
BigYellowLemon
Joined
Jul 6, 2016
Messages
550
ROS has exactly the same effect, whether it be produced at Complex 1 or Complex 3.

The question is one of quantity, and the paper I talked about earlier goes into this in good detail -- How mitochondria produce reactive oxygen species

Quote:

Complex III has for a long time been regarded as a source of O2•−within mitochondria [84,100]. When supplied with CoQH2 and when the Qi site is inhibited by antimycin, complex III produces large amounts of O2•− from the reaction of O2 with a ubisemiquinone bound to the Qo site.

However, in the absence of antimycin, the Qo site ubisemiquinone is not stabilized and O2•− production by complex III is low [105].

Inhibition of respiration at points distal to complex III with cyanide or by loss of cytochrome cdoes not increase O2•− production by complex III [100], therefore reduction of the CoQ pool is not sufficient to generate O2•− at complex III.​


Taken independently, Carbs "favour" Complex 3 ROS generation, but that is not comparable in magnitude to the levels of ROS produced by Complex 1 RET. We can say that the highest possible efficiency in mitochondria wrt ATP production, is when there is forward-flow-only state 3 respiration. If anything, properly dosed carbohydrate use favours this state.

In any case, if state 3 (ATP generating) respiration is assumed, both NADH and FADH2 derived electrons have to pass through Complex 3, and have the same effect. As per the quotes above, CoQ couple reduction doesn't affect this site of ROS production.

Comparing Complex 1 to Complex 3 ROS production (note that Δp refers to "protonmotive force", which is driven by delta psi and delta pH):

It may be that high Δp stabilizes the Qo site ubisemiquinone; however, the very high production of O2•−by complex I during RET in the presence of succinate is abolished completely by rotenone [87,95].

Under these conditions, there is a large Δp and a reduced CoQ pool, suggesting that the maximal O2•− production by uninhibited complex III is negligible compared with that by complex I during RET.

However, it is possible that, for mitochondria operating in mode 3, when O2•− production by complex I is low, the contribution of complex III to the overall O2•− flux may then become relatively significant.

Under these conditions, factors that affect the stability of the ubisemiquinone radical in the Qo site, such as loss of cytochrome c or changes in Δp or in the redox state of the CoQ and cytochrome c pools, may modulate O2•−production.​


I think Complex 3 ROS generation comes down to basic queueing mechanics -- you have a queue of incoming electrons, with the need to process them at Complex 4 (typically by accepting them using Oxygen). Those electrons which cannot be terminally accepted get "pushed out of the queue" / leak from the mitochondria, and have the potential to generate ROS, RNS, etc ....

----

Also see the section "Other sites of O2•− production within mitochondria". It goes through more ways by which ROS can be produced, and many of those are related to the inherently more complex processing of fatty acids.

----

On a related topic, I have discussed why "PUFA Depleted Mitochondria" have the ability to deal with large electron flux in these posts:

- PUFAs Role On Skin
- 'Gainz Brah' Bio-energetic Log

.....

Thank you.

I will read that paper in depth.

What an elegant system, really beautiful.
 

tara

Member
Joined
Mar 29, 2014
Messages
10,368
I understand the CO2 part, but the rest is a mystery to me.
Does it help carbohydrate metabolism?
CO2 is important for many functions.
One of the important things it does is release oxygen to the tissues. Oxygen being essential for efficient glucose oxidation, and hypoxia being a likeley contributor to a number important degenerative processes.
Protective CO2 and aging.
Lactate vs. CO2 in wounds, sickness, and aging; the other approach to cancer

None of these is inherently stressful
Starving is inherently stressful.
 

jyb

Member
Joined
Nov 9, 2012
Messages
2,784
Location
UK
I've tried HFLC at around 50 grams of carbs and I couldn't produce any ketones even with MCT oil. I have a blood ketone meter.

50g is enough to prevent ketosis for some people, at least according to online anecdotes...
 

haidut

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Mar 18, 2013
Messages
19,799
Location
USA / Europe
And an important thing you should be aware of, that I forgot to post clearly, is that excess energetic substrate in the ETC will invariably create superoxide. Not always true and I don't understand it fully, but that's a general mechanic I feel you should be aware of.

Those ETC points are quite valid, but I think the point on PUFA being insulin sensitizing is incorrect. PUFA is a direct insulin receptor antagonist, so it will prevent it from doing its job and make you insulin resistant.
Polyunsaturated fatty acid-mediated suppression of insulin-dependent gene expression of lipogenic enzymes in rat liver. - PubMed - NCBI
"...The effects of dietary polyunsaturated fat on insulin-dependent gene expression of lipogenic enzymes and a possible mechanism for PUFA-mediated suppression of the gene expression have been investigated in rat livers. When diabetic rats were injected with insulin, the insulin dose-dependent induction of lipogenic enzyme mRNAs were markedly reduced with increasing dietary corn oil. On the other hand, the PUFA-mediated suppression of the mRNA concentrations was partially restored by treatment with pioglitazone, a candidate for increasing insulin receptor phosphorylation. Moreover, insulin binding to receptors of liver, receptor autophosphorylation, and kinase activity toward exogenous substrate were lower in the corn oil diet group than in the hydrogenated fat group. The PUFA-mediated suppression of insulin binding was somewhat restored by pioglitazone, and the suppression of insulin receptor phosphorylation was significantly restored. It is suggested that the PUFA-mediated suppression of insulin-dependent gene expression of lipogenic enzymes can be ascribed to a decrease in insulin receptor binding primarily and also to receptor phosphorylation. Thus, PUFA appears to suppress the lipogenic enzyme gene expression stimulated by insulin."

Also, PUFA is the primary inducer of NF-kB and that protein is perhaps THE main player in insulin resistance and diabetes II. There is a reason aspirin, glycine, and progesterone can cure diabetes II and insulin resistance - i.e. they all lower levels of NF-kB, as well as TNFa and such, and none of these are upregulated by saturated fat. So, diabetes is primarily an inflammatory condition, which is supported by the fact that cortisol production is upregulated in diabetes. Saturated fats, especially MCT like coconut oil and butter are insulin sensitizing when eaten without PUFA. The reason superoxide ions are created in the ETC is usually excessive NO production, to which PUFA also contributed. Saturated fat and carbs on their own do not create dangerous levels of superoxides.
So, the TLDR of my rant is this - ANY fat will make you temporarily insulin resistant due to the Randle cycle. However, ONLY the PUFA will give you diabetes and chronic insulin resistance due to its interference with the insulin "receptor" expression and binding profile, induction of inflammation (NF-kB, TNFa, prostaglandins, leukotrienes, etc) and damaging of the beta cells of the pancreas. Saturated fat has none of these effects.
Just my 2c.
 
Last edited:
OP
BigYellowLemon
Joined
Jul 6, 2016
Messages
550
CO2 is important for many functions.
One of the important things it does is release oxygen to the tissues. Oxygen being essential for efficient glucose oxidation, and hypoxia being a likeley contributor to a number important degenerative processes.
Protective CO2 and aging.
Lactate vs. CO2 in wounds, sickness, and aging; the other approach to cancer


Starving is inherently stressful.

My question is, is CO2 good for carbohydrate metabolism, or metabolism in general? I think metabolism in general.

Also, I'm not sure how I feel about fasting. I think it can be good for some people, sometimes, but not for sick people.
 

javacody

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Joined
May 26, 2015
Messages
316
Age
50
After experimenting with a ketogenic diet off and on for years, as well as a PSMF, intermittent fasting, etc. etc.

I think you'll find, just as most of us who've gone that route have found, you'll be much worse off.

I can't tell you the biomechanical/chemical reasons why. But anecdotally, I can tell you that feeling like ***t all the time is aweful.

If you want to risk that, well, no one can stop you. Being high on adrenalin and cortisol is fun at first...
 
OP
BigYellowLemon
Joined
Jul 6, 2016
Messages
550
After experimenting with a ketogenic diet off and on for years, as well as a PSMF, intermittent fasting, etc. etc.

I think you'll find, just as most of us who've gone that route have found, you'll be much worse off.

I can't tell you the biomechanical/chemical reasons why. But anecdotally, I can tell you that feeling like ***t all the time is aweful.

If you want to risk that, well, no one can stop you. Being high on adrenalin and cortisol is fun at first...

Trust me, I am not blind to the stories of failure. I fully realize that many people don't do well with ketosis/HFLC.

Many people however do very well. It's all personal. It makes me sad that people have a hard time finding a diet that works for them.

I am very European, very northern, so I am going to try this out first. Apparently I am extremely neanderthal, according to 23andMe, 99% more neanderthal than everyone on the site (23andMe.com)

I plan on going as low PUFA as possible, 100g carbs, and almost all saturated fat. I think people either go too high in PUFA (avocado, peanut butter, olive oil, ect) or they limit carbs too much (like 30g carbs, where they experience heart pain and they feel super stressed).

I will for sure let you know how it goes. And I am not discarding a carbohydrate driven metabolism. I think that kind of diet also has it's benefits.

I hope it works for me, and I hope you find a diet that works as well.

How long did you do keto/HFLC? There's a lot of variables, and I'm curious why it didn't work for you.

I'v never heard of PSMF until now, that does not sound good at all man.
 

javacody

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Joined
May 26, 2015
Messages
316
Age
50
Trust me, I am not blind to the stories of failure. I fully realize that many people don't do well with ketosis/HFLC.

Many people however do very well. It's all personal. It makes me sad that people have a hard time finding a diet that works for them.

I am very European, very northern, so I am going to try this out first. Apparently I am extremely neanderthal, according to 23andMe, 99% more neanderthal than everyone on the site (23andMe.com)

I plan on going as low PUFA as possible, 100g carbs, and almost all saturated fat. I think people either go too high in PUFA (avocado, peanut butter, olive oil, ect) or they limit carbs too much (like 30g carbs, where they experience heart pain and they feel super stressed).

I will for sure let you know how it goes. And I am not discarding a carbohydrate driven metabolism. I think that kind of diet also has it's benefits.

I hope it works for me, and I hope you find a diet that works as well.

How long did you do keto/HFLC? There's a lot of variables, and I'm curious why it didn't work for you.

I'v never heard of PSMF until now, that does not sound good at all man.

I did a keto diet off and on for 3 to 4 months at a time to lose weight. I never lost a pound unless I also calorie restricted.

I felt great at first each time. But with each successive attempt, that good feeling lasted less and less long. It's a euphoric feeling at first. Especially if you have a big cup of coffee with a healthy dose of heavy whipping cream.

But I was basically zero carb. I kept it under 20 grams. Usually under 10 grams. If you have 100 grams of carbs per day, I think you'll find ketone levels are pretty low, unless you do a lot of physical activity or restrict water.

As another anecdote, I had shrimp cocktail and a liter of Orange Juice last night for dinner and I felt better than I have in years.

I think that a keto diet can be damaging to the gut. And I think that's where many of the problems come from.

Shrimp and OJ are very healing to the gut lining. Both lower lps and inflammation and make me feel better than a keto diet ever did.
 
OP
BigYellowLemon
Joined
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Messages
550
I did a keto diet off and on for 3 to 4 months at a time to lose weight. I never lost a pound unless I also calorie restricted.

I felt great at first each time. But with each successive attempt, that good feeling lasted less and less long. It's a euphoric feeling at first. Especially if you have a big cup of coffee with a healthy dose of heavy whipping cream.

But I was basically zero carb. I kept it under 20 grams. Usually under 10 grams. If you have 100 grams of carbs per day, I think you'll find ketone levels are pretty low, unless you do a lot of physical activity or restrict water.

As another anecdote, I had shrimp cocktail and a liter of Orange Juice last night for dinner and I felt better than I have in years.

I think that a keto diet can be damaging to the gut. And I think that's where many of the problems come from.

Shrimp and OJ are very healing to the gut lining. Both lower lps and inflammation and make me feel better than a keto diet ever did.

I actually am sill adapting I think. Sometimes I feel nauseous, but I am still adapting. If I don't feel better in a month, I am going to reconsider my thoughts and try to either manipulate the keto diet, or scrap the diet and go HCLF. But, it seems to be working.

I think your problem was how low you went on carbs. That's cortisol and adrenaline territory. Ketones are a nice side-effect of HFLC, but they aren't the goal. I see no problem with keeping carbs above 50g and doing a HFLC diet. Hmm, maybe a common mistake on HFLC diet is looking for ketones rather than eating fat and keeping carbs kinda low.

That's good! I am happy for you. The thing about me, is that orange juice can sometimes hurt my gut, and can make me feel strung out. Everything is dependent on it's context. Ray's right.

Saturated fat is quite good at keeping tight junctions healthy and closed. They should block LPS from exiting the gut. But as tyw has posted, saturated fat also exports endotoxin in chylomicrons. I still think this is better than having the endotoxin sit in your gut, or escape via tight-junction in the blood-stream. I rather the body deal with endotoxin than let it float around willy-nilly.
 

javacody

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Joined
May 26, 2015
Messages
316
Age
50
I actually am sill adapting I think. Sometimes I feel nauseous, but I am still adapting. If I don't feel better in a month, I am going to reconsider my thoughts and try to either manipulate the keto diet, or scrap the diet and go HCLF. But, it seems to be working.

I think your problem was how low you went on carbs. That's cortisol and adrenaline territory. Ketones are a nice side-effect of HFLC, but they aren't the goal. I see no problem with keeping carbs above 50g and doing a HFLC diet. Hmm, maybe a common mistake on HFLC diet is looking for ketones rather than eating fat and keeping carbs kinda low.

That's good! I am happy for you. The thing about me, is that orange juice can sometimes hurt my gut, and can make me feel strung out. Everything is dependent on it's context. Ray's right.

Saturated fat is quite good at keeping tight junctions healthy and closed. They should block LPS from exiting the gut. But as tyw has posted, saturated fat also exports endotoxin in chylomicrons. I still think this is better than having the endotoxin sit in your gut, or escape via tight-junction in the blood-stream. I rather the body deal with endotoxin than let it float around willy-nilly.

I wish you nothing but luck. Make sure you document everything. And try to tweak only one parameter at a time (I tend to fail on both counts).

I do know that many people feel like ketones are much more efficient for the heart and the brain. So it's a worthwhile experiment.
 
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