Kasper's thoughts

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Kasper
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Re: Kasper's thoughts

Post by Kasper »

I never said low MUFA. And I never said increases mead acid production.
Well you did:
Image
2% of their diets are PUFAs, I can imagine they would have lots of omega 9 fatty acids. That's about 4-7g/day.
Well you said that you could imagine that those people on traditional diets (which have low MUFA), would have lots of mead acid.
I interpret omega-9 as mead acid, because otherwise it doesn't make any sense what you're writing.
The fish oils seem to not nearly as blocking the desaturase enzymes as LA itself does.
?!?!? Please I want reference for this claim. It doesn't make any sense.
If LA blocks desaturase enzymes in such extend then LA would have a negative feedback loop for AA production.
That this negative feedback loop doesn't exist (or at least is very weak), is the reason there are so many problems with omega-6.

The truth is exactly the other way around. EPA (fish oil) is a very good inhibitor of D5D. And I can't find anywhere that LA or AA inhibits D5D.
The reason that mead acid production is low when omega 6 is high, is not because it inhibits delta-5 desaturase, but because delta 5-desaturase prefers to convert n-6 above n-9 (in the same way it prefers n-3 above n-6).

At least, this is what I've read. Please show me that LA and AA are better in inhibiting D5D then EPA. I can't find that they even inhibit delta5-desaturase at all.
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.
You've shown 1 study that there is a little bit of mead acid production while PUFA intake was quite normal. But this diet was low on omega 3.
I haven't seen any study that there was high mead acid production on a diet with normal omega 3 levels.
In the Netherlands, they recommend you to eat 300 grams fish per week. In that context, you would your body is EPA sufficient if you eat this amount of fsih.
I haven't seen any evidence that your body will produce mead acid in high amounts if your body is EPA sufficient.
So why would I think that there is any mead acid production?
overkees
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Re: Kasper's thoughts

Post by overkees »

Kasper wrote:
I never said low MUFA. And I never said increases mead acid production.
Well you did:
Image
2% of their diets are PUFAs, I can imagine they would have lots of omega 9 fatty acids. That's about 4-7g/day.
Well you said that you could imagine that those people on traditional diets (which have low MUFA), would have lots of mead acid.
I interpret omega-9 as mead acid, because otherwise it doesn't make any sense what you're writing.
No, you are concluding that from things I posted yourself. I never said it.

How my line of reasoning worked there: My assumption is that low dietary PUFA intake will raise mead acid production, and that 2% is probably low enough for mead acid production.
Kasper wrote:
The fish oils seem to not nearly as blocking the desaturase enzymes as LA itself does.
?!?!? Please I want reference for this claim. It doesn't make any sense.
If LA blocks desaturase enzymes in such extend then LA would have a negative feedback loop for AA production.
That this negative feedback loop doesn't exist (or at least is very weak), is the reason there are so many problems with omega-6.

The truth is exactly the other way around. EPA (fish oil) is a very good inhibitor of D5D. And I can't find anywhere that LA or AA inhibits D5D.
The reason that mead acid production is low when omega 6 is high, is not because it inhibits delta-5 desaturase, but because delta 5-desaturase prefers to convert n-6 above n-9 (in the same way it prefers n-3 above n-6).

At least, this is what I've read. Please show me that LA and AA are better in inhibiting D5D then EPA. I can't find that they even inhibit delta5-desaturase at all.
I get the point with only a single questionmark too. It looks a bit agressive, I just want to optimize a diet and every suggestion is worth my time, I'm not here for debating.. I'm here for establishing thought provoking stuff and what my believes are is not the point (although I like to tell what I think of it ;)). I think we all want to look for what is optimal, right?

I might get back on this, it's very hard to find studies. I must admit that that claim came from a research, but didn't refer to another research so I couldn't check it. I agree it was too hasty.
Kasper wrote:
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.
You've shown 1 study that there is a little bit of mead acid production while PUFA intake was quite normal. But this diet was low on omega 3.
I haven't seen any study that there was high mead acid production on a diet with normal omega 3 levels.

In the Netherlands, they recommend you to eat 300 grams fish per week. In that context, you would your body is EPA sufficient if you eat this amount of fsih.
I haven't seen any evidence that your body will produce mead acid in high amounts if your body is EPA sufficient.
So why would I think that there is any mead acid production?
[/quote]
No, of course not. The consumption of PUFAs is way too high due to seed oils and such on these kind of diets. This is not related to my only coconut oil, a few yolks, red meat low PUFA diet... I can't follow your reasoning here.

But okay, it sounds fair enough. No fatty fish for me until we find out how and when exactly the mead acids begins to form.
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RRM
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Re: Kasper's thoughts

Post by RRM »

overkees wrote:
Kasper wrote:
overkees wrote:The fish oils seem to not nearly as blocking the desaturase enzymes as LA itself does.
?!?!? Please I want reference for this claim. It doesn't make any sense.

I just want to optimize a diet and every suggestion is worth my time, I'm not here for debating.. I'm here for establishing thought provoking stuff and what my believes are is not the point (although I like to tell what I think of it ;)). I think we all want to look for what is optimal, right?
I agree with Kasper.
You need to supply references for 'provoking statements'.
This is not a forum for provocation, but for information.
This is not a playground.
Though provoking stuff is ok, but on this forum that requires scientific back up.
Without backing up your statments, its misinformation / misleading.
Kasper
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Re: Kasper's thoughts

Post by Kasper »

But okay, it sounds fair enough. No fatty fish for me until we find out how and when exactly the mead acids begins to form.
I would go for a diet sufficient high in EPA. But I'm also very interested in what your experiment will lead to.

Here is what I think will happen if you are going to lower EPA drastically (note this is speculation):
After some time, your body is going to signal that your body is low in EPA.
Then you're body is going to increase delta-5 saturase activity (so it can produce EPA).
Delta-5 saturase prefers n-3 above n-6 above n-9. In the beginning the body will try to convert n-3 to EPA.
If you limit n-3 in your diet, D5D will fail to convert n-3 to EPA. Instead it will convert DGLA to AA.
So, an increase in AA and a decrease in DLGA.

As we've seen in one study, if there is much n-9 available, not only n-6 will be converted, but also some n-9.
D5D prefers n-6 above n-9, so this will only be a little bit n-9.
This process will go on, until most of your n-6 are converted to AA.
If you are able to drastically lower your omega-6, after a while there is almost no n-6 left for D5D.
Then, while your body is very low DGLA and EPA, there will be some bright side.
D5D will produce mead acid in very high amounts, and AA will slowly get removed from your membranes.

If you really want to have high mead acid in your membranes, I think you should do close the same thing they did in those experiments.
Really cut down your omega 3 and omega 6 to close to 0% of your calories.

You will get low AA, very low DGLA, very low EPA, and high mead acid in your membranes.
I very much doubt how healthy this is.

I agree that low AA is something desirable. But I think it is better to go for another strategy, inhibit D5D activity (naturally) by eating sufficient EPA (and maybe other stategies).
This will make sure AA will slowly get replaced by DGLA and EPA.

------------------------------------------------------------------------------------------------------------------------------
But I've a little bit AA overdose at this moment. I'm studying how uric acid can cause inflammation at the moment:

"Purine metabolism is an aspect of intrigue in biology. Lower species, such as microbes, process it to the end product of ammonia. Through evolution, its metabolism becomes less and less complete. In mammals, uric acid is processed to become allantoin and uricase expression is confined to peroxisomes in hepatocytes. However, in primates, a silent mutation has eliminated the uricase function, and gout ensues. It has been an interesting discussion as to why such a loss of function was necessary at the expense of a major disease and possibly cardiovascular complications. Two hypotheses have been put forward. One proposal is that loss of uric acid degradation sustains serum salt levels and sufficiently high blood pressure in low salt environments (18). The other, more blithe, idea is that uric acid targets purine receptors in the cerebral cortex in ways similar to caffeine, rendering primates more mentally alert and intellectuals more prone to gouty arthritis (the disease of distinction) (19, 20). In light of the work of Kono et al. (5), we have gained experimental evidence that evolution may have had an additional incentive for eliminating the ability to degrade uric acid. In conjunction with a urate anion exchange regulator in the kidney (21), elevated uric acid levels push to the edge of precipitation. As such, any cell death or tissue insult can immediately raise levels above those required for precipitation (70 μg/ml), thereby bringing into the picture a powerful trigger of inflammation, MSU crystals. By lacking the ability to degrade uric acid, the primate host therefore becomes more efficient at monitoring cellular stress. In large-scale injury and trauma, as well as other situations where inflammation is collectively beneficial to the host, high uric acid could have been a substantial survival advantage (22). If future research supports such reasoning, it is expected that uric acid will be found to participate in sterile inflammation in additional contexts and that it will present the promise of a therapeutic target."

In short, the uric acid balance seems like this:
Low uric acid (MS) << Normal uric acid << High uric acid (Gout)
"One clinical observation that may speak to uric acid’s antioxidative effect is the near absence of multiple sclerosis (MS) in gout patients [5]."

'Another theory, first proposed in the 1950s, suggests that uric acid is structural homolog of caffeine (which in turn is a structural homolog of adenosine), and that high uric acid levels promoted mental alertness for primates and contributed to the development of human intelligence [8]. This hypothesis has been increasingly supported by experimental observations, although its role in evolution remains to be confirmed."
overkees
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Re: Kasper's thoughts

Post by overkees »

Okay, this is what I found in relation to LA:

Cellular MA is lower in rats fed a higher level of LA. Dietary MA can accumulate in leucocytes and suppress inflammatory eicosanoid synthetsis (LTB4). [1]

The data showed that 0.5x LA or 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. [2]

In rats MA in plasma and tissue phospholipids is in proportion to the amount of dietary MA. Addition of LA reduced the amount of MA incorporation.Rats remained apparently healthy with high levels of dietary MA, and a histological survey of major organs revealed no abnormality. [3]

What this to me indicates is that AA doesn't interfere with mead acid incorporation, so also if MA is made in small amounts it will stay there, even if you have high AA. BUT.. LA seems to be the bad guy, if LA is introduced, MA will go away rapidly.

So, I think, if you have chronic inflammatory problems or slow working thyroid, this can be better regulated with the introdoction of mead acid production (that might even be natural) and therefore avoiding LA can be a smart thing to do. Im not into the whole omega 3 story as of now, so I will look into this matter soon. Look in the MA topic, within 2 or 3 days I think I will post a summary of almost all the research I have found.. It can help us in comparing and theorizing what really is natural and better. Or maybe, dependent on context... like if you have chronic inflammation problems (these include.(according to normalbreathing and natasha campbell mcbride) athletes foot, soiling and bad odour, concentration problems).
Kasper
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Uric acid

Post by Kasper »

When I was studying uric acid a bit, I found something really intersting.
In short:
Uric acid is in humans much higher then in other organisms. There must be an evolutionary reason for this.
Uric acid has been linked to intelligence, and it may be that uric acid is a very good neuroprotector.
The sad thing is that uric acid is also something that triggers inflammation (gout), and it is unlikely that elevating uric acid (for better IQ) is a good idea health wise.
BUT, assuming this speculation is true, then CO2 may be even a better idea to boost intelligence. Look at this:

"The link between these different diseases could be the role played by oxidative stress in their aetiology and, in particular, the negative effects of peroxynitrite, a powerful oxidant formed by the reaction of the superoxide with nitric oxide, on the neurons.[51, 56] UA prevents peroxynitrite formation by neutralizing cellular superoxide and preventing its reaction with nitric oxide [56]. UA does not seem to be a direct scavenger of peroxynitrite in vivo, since the peroxynitrite binds to CO2 almost 1000 times faster than to UA.[57] However, UA is a scavenger of free radicals, such as CO3 and NO2, which are formed from the breakdown of peroxynitrite.[25, 26] Thus, a reduced concentration of UA could decrease the body's capacity to prevent the actions of peroxynitrite and other free radicals on the various neuronal components.[26] Besides its antioxidant effects, UA may also have neuroprotective effects through mechanisms mediated by astroglia, preventing the toxicity induced by glutamate.[25, 58] It does not seem likely that protection against these types of disease, with a higher prevalence at advanced ages, was the cause of the loss of uricase. However, it shows us that UA has an important role in neuronal activity, with increasing levels of UA favouring the development of more complex neuronal functions."

I can guarantee that reading this article is worth your time:
http://www.medscape.com/viewarticle/734579
Kasper
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Re: Kasper's thoughts

Post by Kasper »

I never thought about using cheese cloth to strain orange juice, but it works very well:

http://en.wikipedia.org/wiki/Cheesecloth
overkees
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Re: Kasper's thoughts

Post by overkees »

Why don't you use a normal sieve?
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Emeira
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Re: Kasper's thoughts

Post by Emeira »

I always use cheesecloth to juice kiwi fruits, bananas and for making coconut cream
Kasper
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Re: Kasper's thoughts

Post by Kasper »

We have recently shown that a high-fat high-carbohydrate (HFHC) meal induces an increase in plasma concentrations of endotoxin (lipopolysaccharide [LPS]) and the expression of Toll-like receptor-4 (TLR-4) and suppresser of cytokine signaling-3 (SOCS3) in mononuclear cells (MNCs) in addition to oxidative stress and cellular inflammation. Saturated fat and carbohydrates, components of the HFHC meal, known to induce oxidative stress and inflammation, also induce an increase in LPS, TLR-4, and SOCS3. Fasting normal subjects were given 300-calorie drinks of either glucose, saturated fat as cream, orange juice, or only water to ingest. Blood samples were obtained at 0, 1, 3, and 5 h for analysis. Indexes of inflammation including nuclear factor-κB (NF-κB) binding, and the expression of SOCS3, tumor necrosis factor-α (TNF-α), and interleukin (IL)-1β in MNCs, increased significantly after glucose and cream intake, but TLR-4 expression and plasma LPS concentrations increased only after cream intake. The intake of orange juice or water did not induce any change in any of the indexes measured. Although both glucose and cream induce NF-κB binding and an increase in the expression of SOCS3, TNF-α, and IL-1β in MNCs, only cream caused an increase in LPS concentration and TLR-4 expression. Equicaloric amounts of orange juice or water did not induce a change in any of these indexes. These changes are relevant to the pathogenesis of atherosclerosis and insulin resistance.
http://www.citeulike.org/user/booker/article/6551843
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Aytundra
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Re: Kasper's thoughts

Post by Aytundra »

Hey kasper, I was wondering, what are your thoughts on 100% wai?
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Aytundra
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Re: Kasper's thoughts

Post by Aytundra »

Actually what are your thoughts on 100% wai items (not 100% wai items vs. 100% wai items) vs. 100% wai diet (normal vs. warrior)?
Just being curious if you would distinguish them like that.
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