Kasper's thoughts

If you are not sure whether you are doing the diet right, create your own diet diary here, so others can take a look at it.
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dime
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Re: Kasper's thoughts

Post by dime »

Hehe I love that video, I've seen it a million times by now probably :D
Kasper
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Re: Kasper's thoughts

Post by Kasper »

Do bitters help fat digestion ?
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RRM
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Re: Kasper's thoughts

Post by RRM »

Which one?
There are so many bitter tasting compounds.
Bile acids, yes.
Kasper
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Re: Kasper's thoughts

Post by Kasper »

Very intresting video about methanol
http://www.youtube.com/watch?v=MS_gCcevZqY

Eyeopeners for me:
- Alcohol could help detoxify methanol.
- Pectin makes sure methanol from fruit is not toxic.
Kasper
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Re: Kasper's thoughts

Post by Kasper »

That which is measured gets improved.

I'm experiencing the truth of this statement (again).
I'm measuring a couple of things in a simple google spreadsheet.
I get some real motivation if I now the time I have to beat.
I'm not measuring too much, because I now this overwhelmed me.
Just the amount of time I spend at foundation training.
I love to see my statistics improving, gives me kind of the same feeling, as with statistics at the end of a level in a video game.
Kasper
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Re: Kasper's thoughts

Post by Kasper »

The anti-inflammatory effect of glucocorticoids depends, at least in part, on the induction of two regulatory proteins, lipocortin and vasocortin, both preventing the release of inflammatory mediators.
Lipocortin inhibits phospholipase A2 (PLA2) and therefore reduces arachidonic acid metabolites formation.
Vasocortin inhibits histamine release from mast cells. Lipocortin and vasocortin may be regarded as the first two identified members of the (perhaps greater) family of glucocorticoid-induced proteins.
Kasper
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Re: Kasper's thoughts

Post by Kasper »

The last step in the production of AA is the conversion of DGLA to AA by delta5-desaturase.
Therefore, inhibiting this enzyme will lower AA accumulation in cells.
Here is a list of things that may lowers delta5-desaturase activity:
- EPA
- dietary cholesterol
- Conjugated linoleic acid
- sesame seeds/oil
- curcumin

Hormones:
-Glucagon inhibits delta 5 desaturase while insulin stimulates delta 5 desaturase.
overkees
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Re: Kasper's thoughts

Post by overkees »

From what I've read is that the delta5 is poorly studied and that trying to inhibit it is therefore a bad idea. It might be involved in the mead acid metabolism aswell...

My guess is that the body has most of the feedback systems working properly already if there is little to no interference. However eating excess amounts of PUFA (even from olive oil or fatty fish) might already cause troubles. It is better to prevent the source (dietary omega 6) than to inhibit the conversion (when needed by the body).

I tthink it is best oo have the body regulate the PUFAs as good as it can by itself, by at using the mead acid in several cases instead of the omega6s. This would lower the inflammation in reaction to a stress response from the AA release overflow. There are even studies that hint that even AA can be synthesized by the body, but I need to research this further to get a better understanding.
Kasper
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Re: Kasper's thoughts

Post by Kasper »

From what I've read is that the delta5 is poorly studied and that trying to inhibit it is therefore a bad idea. It might be involved in the mead acid metabolism aswell...
What do you mean with poorly studied ? It is involved by mead acid metabolism. If the body is deficient in EFA delta 5 converts oleic acid into mead acid.
It is better to prevent the source (dietary omega 6) than to inhibit the conversion (when needed by the body).
Omega 6 is also a source of DGLA, which don't get converted to AA without delta-5 desaturase activity.
DGLA eicosanoids are known as very beneficial for the body, and are not known to cause chronic inflammation diseases.
My guess is that the body has most of the feedback systems working properly already if there is little to no interference. However eating excess amounts of PUFA (even from olive oil or fatty fish) might already cause troubles.
The body has a negative feedback system.
If EPA is low, delta 5-desaturase activity is increased, which helps converting ALA into EPA.
This is beneficial. The problem is that delta5 also converts DGLA into AA.
I think this is the problem, the body tries to get EPA, but it also gets AA, and therefore lowers DGLA.
If EPA is sufficient, delta 5-desaturase is inhibited, because the job is done.
But if EPA stays low, even if delta 5-destarase is active, the body is only converting DGLA into AA.
This is when the eicosanoids get imbalanced. DGLA low, EPA low and AA high. Chronic inflammation guaranteed.
I tthink it is best to have the body regulate the PUFAs as good as it can by itself, by at using the mead acid in several cases instead of the omega6s. This would lower the inflammation in reaction to a stress response from the AA release overflow.
So far as I've read, DGLA and EPA can do all the anti-inflammatory things that mead acid can do. Why would we need mead acid ?
You need to seriously get deficient in EFA to let the body produce mead acid. This process takes many weeks.
In the mean time, delta5-desaturase is fully induced. This will make sure all of your omega-6 gets converted to AA.
After this, you will indeed get mead acid in your membranes. But this process takes weeks (something like 8 weeks I read).
On the other hand, it takes only a couple of days to get EFA's back to your membranes and mead acid out of it, if you reintroduce EFA back's in your diet.
I think this shows that the body desperately prefers EFA's above mead acid.

Besides that both DGLA and mead acid produce the same serie-1 prostraglandins.
High DGLA in your membranes may have similar effects as mead acid.
overkees
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Re: Kasper's thoughts

Post by overkees »

I think that conclusion is a bit to premature:

http://www.westonaprice.org/know-your-f ... om-fiction
The traditional diets of Pacific islanders free of heart disease, for example, vary widely in their proportions of fat and carbohydrate, but as can be seen in Figure 1, they are all rich in saturated fat and low in PUFA when compared to the standard American dietImage
2% of their diets are PUFAs, I can imagine they would have lots of omega 9 fatty acids. That's about 4-7g/day.
A wai diet, with low use of olive oil (2-3 tablespoons) a few yolks only (3-4 yolks), 200g of salmon and fruits already results in 15g of PUFAs. That is 2-3 times more than the pacific indigineous islanders. I think changing the olive oil with coconut oil and changing the salmon with beef will be a better idea.

The reasons it is soo damn high in breast milk might also be an indiciation of some important functions.

From the experiments on rats and patients I can see that it takes 7-20 days to induce the production of the omega 9 fatty acid. To get all of the AA out of the tissues it might take up to 2-6 years. But it is highly debatable if that is something you want. All I can say is that if you're using coconuts for fats, don't eat any other nuts and seeds and don't eat avocados, then it is very likely that you will get a lot of mead acid in the tissues instead of the AA. But there will still remain a more than essential percentage of AA in there. Whether that is synthesized by the body itself or by the coconut oil and animal fats you eat (egg yolk). And eating a fatty fish every now and then (150-300g a week) will make sure you get everything you need while still staying high on the mead acid production and not impairing the desaturase enzymes.

The whole problem is the super high consumption of omega 6s in the SAD and that makes it, with the (false) assumption that alot of PUFAs (especially omega 3s) are highly beneficial for health, almost impossible to get good researches to show how and when the omega 9s are beginning to form. Now we only have alot of very excluding diets that show the making of omega 9s and it is always associated with a pufa deficiency and therefore seen as a bad thing.
Kasper
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Re: Kasper's thoughts

Post by Kasper »

.
2% of their diets are PUFAs, I can imagine they would have lots of omega 9 fatty acids. That's about 4-7g/day.
You think that there is mead acid production if they have 4-7 gram PUFA's a day ?
Mead acid production only begins if your membranes are deficient in PUFA's.
EPA for example inhibits mead acid production. If those people ate fish, it seems highly unlikely to me that they have mead acid production.
Do you know any study that shows that there is increased mead acid production with 2% PUFAs ?
From the experiments on rats and patients I can see that it takes 7-20 days to induce the production of the omega 9 fatty acid.
Reference ?
To get all of the AA out of the tissues it might take up to 2-6 years. But it is highly debatable if that is something you want.
Do you take those numbers out of the blue ?
All I can say is that if you're using coconuts for fats, don't eat any other nuts and seeds and don't eat avocados, then it is very likely that you will get a lot of mead acid in the tissues instead of the AA.
Please show me one study that there is a lot of mead acid production at 2%PUFA.
In the last study I read, the control group ate 4% calories PUFA.
They use hydrogenated coconut oil, without any omega 6. Normal coconut oil is already too high on omega 6.
But there will still remain a more than essential percentage of AA in there. Whether that is synthesized by the body itself or by the coconut oil and animal fats you eat (egg yolk). And eating a fatty fish every now and then (150-300g a week) will make sure you get everything you need while still staying high on the mead acid production and not impairing the desaturase enzymes.
High mead acid production with 150-300 gram of fish a week ?!?!? Well then my membranes are fully loaded with mead acid for sure...
http://www.sciencedirect.com/science/ar ... 6084902613 Comparably, under a fish oil diet, the n-9 was quickly substituted by n-3 polyunsaturated fatty acids (eicosapentaenoic acid and docosahexaenoic acid). In both cases the n-9 almost disappeared in 6 days
overkees
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Re: Kasper's thoughts

Post by overkees »

Kasper wrote: You think that there is mead acid production if they have 4-7 gram PUFA's a day ?
Mead acid production only begins if your membranes are deficient in PUFA's.
EPA for example inhibits mead acid production. If those people ate fish, it seems highly unlikely to me that they have mead acid production.
Do you know any study that shows that there is increased mead acid production with 2% PUFAs ?
That's what's the problem, you're prejudiced to state that it appears only if you have an EFAD. This is not necessarily true and is something you need to look out for:
http://www.ncbi.nlm.nih.gov/pmc/article ... figure/F4/

As you can see, there is still a small part mead acid if fed olive oil. In the fish oil supplemented group, however, there was little to no mead acid found.
Kasper wrote:
From the experiments on rats and patients I can see that it takes 7-20 days to induce the production of the omega 9 fatty acid.
Reference ?
http://www.jci.org/articles/view/108061/pdf
"EFA deficiency was detected by decreases in linoleic acid and by the appearance of 5, 8, 11-eicosatrienoic acid in lipid fractions of plasma. Linoleic acid decreased significantly during 2 wk of the fat-free diet given intravenously from 48.8 to 9.8% (percent of total fatty acids) in cholesterol esters, from 21.2 to 3.2% in phospholipids, from 9.6 to 2.0% in free fatty acids, and from 14.1 to 2.6% in triglycerides. Eicosatrienoic acid, normally undetectable, appeared 0.6% in cholesterol esters, 2.5% in phospholipids, 0.2% in free fatty acids, and 2.3% in triglycerides."
2 weeks, 5 times decreasing of LA. See what they do here, they automatically assume there is an EFAD if you have the mead acid.

However:
http://www.ncbi.nlm.nih.gov/pubmed/402809
"The linoleic acid (C18:2W6) content of all plasma lipid fractions decreases greatly and plasma eicosatrienoic acid (C20:3W9) increases. We have measured the fatty acid composition of the plasma lipid fractions in six surgical patients receiving parenteral nutritional solutions containing only amino acids, and completely free of glucose, before and after 10 to 14 days of such therapy. Biochemical symptoms of essential fatty acid deficiency did not occur."
10 to 14 days! No signs of EFAD. So please look out with the assumptions you are making.

http://link.springer.com/article/10.100 ... 32?LI=true
"It is proposed that oleic acid competes competitively with linoleic acid as a substrate for the enzymes involved in linoleate transformations when only a very limited supply of linoleic acid is available to the animals and oleic acid is made available in relatively large amounts."

Linoleic acid seems to be the most important factor in limiting the mead acid creation. It inhibits the mead acid production via competition (as shown above) and via its conversion to AA, because AA also inhibits the production of mead acid.
Kasper wrote:
To get all of the AA out of the tissues it might take up to 2-6 years. But it is highly debatable if that is something you want.
Do you take those numbers out of the blue ?
No... of course not:
Ray Peat wrote: The half-life of fats in human adipose tissue is about 600 days, meaning that significant amounts of previously consumed oils will still be present up to four years after they have been removed from the diet. [4]
[4]Beynen, A. C., P. J. J. Hermus, and J. G. A. J. Hautvast, "A mathematical relationship between the fatty acid composition of the diet and that of the adipose tissue in man," Am. J. Clin. Nutr. 33(1), 81-5, 1980.
Kasper wrote: Please show me one study that there is a lot of mead acid production at 2%PUFA.
In the last study I read, the control group ate 4% calories PUFA.
They use hydrogenated coconut oil, without any omega 6. Normal coconut oil is already too high on omega 6.
I think I did with the olive oil research and the other researches above? Anyway, your question is to specific, there is not that kind of research available.. what a shame. And why do you think that normal coconut oil is too high in omega 6? Please motivate your claim.
Kasper wrote: High mead acid production with 150-300 gram of fish a week ?!?!? Well then my membranes are fully loaded with mead acid for sure...
http://www.sciencedirect.com/science/ar ... 6084902613 Comparably, under a fish oil diet, the n-9 was quickly substituted by n-3 polyunsaturated fatty acids (eicosapentaenoic acid and docosahexaenoic acid). In both cases the n-9 almost disappeared in 6 days
Eh... 150g to 300g of salmon is only 642mg PUFAs/day. I think the research you are linking to has nothing to do with these amounts of fish oil.
overkees
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Re: Kasper's thoughts

Post by overkees »

Modulation of adjuvant-induced arthritis by dietary arachidonic acid in essential fatty acid-deficient rats.
http://www.ncbi.nlm.nih.gov/pubmed/9307941

The data showed that 0.5x LA and 10x AA, but not 1x AA, could quickly replete AA, accompanied by the synthesis of AA-derived eicosanoids and restoration of edema. These results suggest that in humans consumption of the average daily amount of AA without concurrent ingestion of LA would not alleviate an EFAD state.

Very interesting, is it not?
Kasper
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Re: Kasper's thoughts

Post by Kasper »

These results suggest that in humans consumption of the average daily amount of AA without concurrent ingestion of LA would not alleviate an EFAD state.
These results show that 0.5x LA quickly replete AA. How much grams is 0.5 times the daily amount of humans ?
We can only conclude that 0.5xLA is already too much (if you want mead acid), right ?
That's what's the problem, you're prejudiced to state that it appears only if you have an EFAD. This is not necessarily true and is something you need to look out for:
http://www.ncbi.nlm.nih.gov/pmc/article ... figure/F4/

As you can see, there is still a small part mead acid if fed olive oil. In the fish oil supplemented group, however, there was little to no mead acid found.
Okay, maybe there is a little bit of mead acid producition if you eat much olive oil, but olive oil also increases AA.

This study shows that not omega6, but omega3 inhibits mead acid production.
Which sounds logical to me. Ray Peat seem to think that omega6 inhibit mead acid production, but in the research I've read they all point out that it is omega3.
Linoleic acid seems to be the most important factor in limiting the mead acid creation. It inhibits the mead acid production via competition (as shown above) and via its conversion to AA, because AA also inhibits the production of mead acid.
Olive oil contains LA and increases AA (in comparison to fish oil), but gives mead acid production.
Fish oil decreases AA, but inhibits mead acid production.

It seems like fish oil is the most important factor to inhibit mead acid production.
Please show me one study that there is a lot of mead acid production at 2%PUFA.
I think I did with the olive oil research and the other researches above? Anyway, your question is to specific, there is not that kind of research available.. what a shame. And why do you think that normal coconut oil is too high in omega 6? Please motivate your claim.
No, you've shown that there is a little bit mead acid production when you eat olive oil.
So maybe the lack of omega 3 and very much MUFA can increase mead acid a little bit, but you said that a diet low in MUFA and containing fish increases mead acid production. Not any of this research indicates that this is true.
Why do you think this is true ?
overkees
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Re: Kasper's thoughts

Post by overkees »

Kasper wrote:So maybe the lack of omega 3 and very much MUFA can increase mead acid a little bit, but you said that a diet low in MUFA and containing fish increases mead acid production.
I never said low MUFA. And I never said increases mead acid production. Please quote me directly. All i said was:
overkees wrote:And eating a fatty fish every now and then (150-300g a week) will make sure you get everything you need while still staying high on the mead acid production and not impairing the desaturase enzymes.
If omega 3 is really essential (and I don't have enough evidence at this moment), I don't want to risk missing out on it. What I do know is that, even if you eat a omega 6 excluding diet, you will still get enough of it. So that is why I incorporated the fatty fish part in my story. My guess is that eating it once a week will make sure you will stay high in de mead acid production by not impairing the desaturase enzymes and such, while also getting very good nurients like B6, B3, zinc, that are all linked to these enzymes operating effectively. The fish oils seem to not nearly as blocking the desaturase enzymes as LA itself does.

Oh and yes, high dietary AA blocks it aswell. You can find studies about that.

Low dietary MUFA you mean by excluding olive oil? But are you aware of the fact that the body can make its own oleic acid and from saturated fats and that it can synthesize the mead acid from oleic acid?

Funny part is, that oleic acid in high amounts also seems to block the desaturases.

And please motivate your claim that 150-300g of salmon on one day of the week is going to get you out of the mead acid production.

Btw, I'm eating only white fish atm (2.5 week and counting) to higher my chances of mead acid production.
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