Re: Maximizing ALA conversion to EPA and DHA

[Guest guest]

Sorry but i do not have a degree in biology or chemistry can't really understand

this article. Can anyone break it down to common language?

>

> I ran across an interesting article this evening that I thought may be

> of interest to some:

>

> Quantitation of alpha-linolenic acid elongation to eicosapentaenoic and

> docosahexaenoic acid as affected by the ratio of n6/n3 fatty acids:

>

>

http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed & pubmedid=1922839\

4

>

> The paper's conclusions were as follows:

>

> Our investigations show that exposure of human hepatocytes to different

> mixtures of LA and ALA affected transcript levels of a portfolio of

> genes encoding regulating proteins involved in several stages of fatty

> acid metabolism. This effect strongly depends on the ratio of n6/n3

> fatty acids, indicating the importance of ingesting an appropriate

> amount of fatty acids, but also an appropriate ratio of n6 and n3 fatty

> acids. This is further confirmed by the fact that maximum conversion of

> LA to AA was measured only in the presence of ALA. Omitting ALA seems to

> result in higher oxidation rates as indicated by high transcript levels

> of PPAR. Additionally, the n6/n3 ratio strongly influenced the

> elongation of ALA to EPA and DHA as well as the transcript levels of D5D

> and D6D.

> However, from a nutritional perspective, our findings suggest that a

> diet-induced enhancement of the cell membrane content of highly

> unsaturated fatty acids is only possible up to a certain level.

> Increasing the administered quantity of labeled alpha-linolenic acid

> resulted in a reduced effectiveness of [13C]ALA incorporation.

> Percentage incorporation of [13C]ALA was maximal after exposure of

> [13C]LA/[13C]ALA at a ratio of 4:1 to HepG2 cells.

> With regard to the elongation of ALA to EPA and DHA, our results clearly

> indicate the efficiency of altering the dietary ratio of LA to ALA in

> favor of ALA by increasing the concentration of n3 fatty acids in human

> hepatocytes. At this, administration of LA/ALA at a ratio of 1:1 led to

> the highest formation of LCPUFAs of the n3 series.

>

> Kind regards,

>

> Nick

> ---

[Guest guest]

Hello ohlyvicki,

Let me provide a little background:

Omega-3 and omega-6 fatty acids are known as essential fatty acids

(EFAs) because our bodies cannot manufacture them. They are essential

nutrients, without which good health is not possible, so they need to be

consumed as part of our diets. This is something which medicine has

taken a surprisingly long time to fully appreciate. For example, prior

to 1982, total parenteral nutrition (TPN) was devoid of lipids entirely

- resulting at times in severe complications and sometimes even death.

Tellingly, even after it was recognized that EFA's were a necessary part

of TPN formulations and after the FDA had approved TPN formulas

containing lipid emulsions, the initial formulations utilized safflower

oil which had a high content of omega-6 fat and almost no omega-3 fat

content at all. This caused problems which were finally corrected with

the use of formulations that contained a healthier balance of omega-6

and omega-3 fats.

So, even as late as the early 1980's, clinical practice didn't reflect

what nutrition researchers had known from animal studies by the late

1930's. I personally think that clinical practice in cancer suffers from

this same type of lag.

If you are interested in more background and a historical overview of

how clinical medicine came to appreciate what researchers of nutrition

already new back in the 1930's, have a look at this article:

The Slow Discovery of the Importance of Omega-3 Essential Fatty Acids

in Human Health, R. T. Holman, 1998

jn.nutrition.org/cgi/reprint/128/2/427S.pdf

A little more historical background:

Dr. anna Budwig (1908 - 2003), a German scientist (doctorate degree

in the natural sciences) was working as a senior expert for

pharmaceuticals and fats for Germany's Federal Health Office during the

early 1950's. She became convinced at that time, that one of the

primary causes of the increasing rates of coronary disease, diabetes and

cancer was the growing use of hydrogenated and oxidized oils in food

products (unnatural and damaged fats). She came to this conclusion after

analyzing the blood samples of healthy and unhealthy patients using

paper chromatography techniques that she had to develop expressly for

this purpose. Once convinced that cancer (and other ailments) were

caused in a large part by the ingestion of unhealthy fats, she developed

a nutritional and lifestyle modification program to treat these

ailments. The nutritional portion of her protocol included a large

amount of omega-3 rich flax oil mixed with cottage cheese. She felt

that this flax oil-cottage cheese (FOCC) mixture was a pivotal part of

her protocol in that it corrected nutritional deficits/damage related to

fats and normalized the respiration of tumor cells, resulting in tumor

shrinkage. Dr. Budwig claimed a remarkable success rate (better than

90%) in regressing tumors. Unfortunately, she was dismissed by

mainstream medicine at the time as a crackpot. She did however help a

large number of people and continued to do so right up to her death in

2003.

It should be noted that FOCC was only part of the Budwig Protocol (BP).

The full BP consists of a healthy, well rounded (mostly) vegan diet that

has at its core the FOCC mixture. Lifestyle changes (stress reduction,

mild exercise and moderate exposure to sunlight) are also integral

aspects of the BP.

Fast forward to recent times. In the past few decades, there has been a

growing body of research that confirms Dr. Budwig's views - that fats -

and in particular omega-3 fats can be used to prevent and even regress

tumors. Most of the research however, has been focused on fish oils

that contain high amounts of EPA (eicosapentaenoic fatty acid) and DHA

(docosahexaenoic fatty acid) - which are long chain omega-3 fats. Flax

seed oil, which Dr. Budwig used in her FOCC mixture contains ALA

(alphalinolenic fatty acid) has unfortunately not been studied as

much.

Now we come to the article I posted a link to - which you were inquiring

about. It describes recent experiments which studied some of the factors

which influence the conversion of the shorter chain ALA (as found in

flaxseed oil) into the longer chain EPA and DHA fatty acids. The

article also reported on factors which influence the incorporation of

omega-3 fats into cell membranes. (Studies of these aspects of EFA

metabolism are also mentioned in the Holman article - see above URL.)

Finally, after this long winded answer to your request, I should mention

that I don't think that this article should be used as basis for

specific nutritional recommendations with regard to the best levels of

EFA's for the purpose of preventing or regressing tumors. It is simply

a useful set of experimental results that, taken in context of existing

knowledge, provides another increment towards a more complete picture of

EFA metabolism. It can be used to provide some context, when analyzing

the omega-6:omega-3 balance of he Budwig Protocol, as well as other

nutritional protocols.

Kind regards,

Nick

On Thu, 24 Sep 2009, ohlyvicki wrote:

> Sorry but i do not have a degree in biology or chemistry can't really

> understand this article. Can anyone break it down to common language?

>

> >

> > I ran across an interesting article this evening that I thought may be

> > of interest to some:

> >

> > Quantitation of alpha-linolenic acid elongation to eicosapentaenoic and

> > docosahexaenoic acid as affected by the ratio of n6/n3 fatty acids:

> >

> >

http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed & pubmedid=1922839\

4

> >

> > The paper's conclusions were as follows:

> >

> > Our investigations show that exposure of human hepatocytes to different

> > mixtures of LA and ALA affected transcript levels of a portfolio of

> > genes encoding regulating proteins involved in several stages of fatty

> > acid metabolism. This effect strongly depends on the ratio of n6/n3

> > fatty acids, indicating the importance of ingesting an appropriate

> > amount of fatty acids, but also an appropriate ratio of n6 and n3 fatty

> > acids. This is further confirmed by the fact that maximum conversion of

> > LA to AA was measured only in the presence of ALA. Omitting ALA seems to

> > result in higher oxidation rates as indicated by high transcript levels

> > of PPAR. Additionally, the n6/n3 ratio strongly influenced the

> > elongation of ALA to EPA and DHA as well as the transcript levels of D5D

> > and D6D.

> > However, from a nutritional perspective, our findings suggest that a

> > diet-induced enhancement of the cell membrane content of highly

> > unsaturated fatty acids is only possible up to a certain level.

> > Increasing the administered quantity of labeled alpha-linolenic acid

> > resulted in a reduced effectiveness of [13C]ALA incorporation.

> > Percentage incorporation of [13C]ALA was maximal after exposure of

> > [13C]LA/[13C]ALA at a ratio of 4:1 to HepG2 cells.

> > With regard to the elongation of ALA to EPA and DHA, our results clearly

> > indicate the efficiency of altering the dietary ratio of LA to ALA in

> > favor of ALA by increasing the concentration of n3 fatty acids in human

> > hepatocytes. At this, administration of LA/ALA at a ratio of 1:1 led to

> > the highest formation of LCPUFAs of the n3 series.

> >

> > Kind regards,

> >

> > Nick

> > ---