Re: N-3 versus N-3 PUFA dictate blood fats

[Guest guest]

Hi folks:

I don't know if anyone else had difficulty deciphering the two

abstracts that Al posted (attached below). It took me quite some

time to figure out what they might mean for me. Having spent some

time, reading them over a number of times, here are my conclusions

about what they seem to mean. If anyone has a different view, please

say so. If their data are confirmed by other investigators they may

be important.

First, as Al pointed out, they say that hamsters, apparently, are

probably the closest (one of the closest?) animal analogies for

assessing the behaviour of human blood lipids in response to diet.

This is good to know, as it seems to mean we should pay more

attention to lipid experiments in hamsters than in, say, rats or mice.

Second, the principal experiment looked at ten groups of hamsters.

They were all fed the same except in two respects - type of fat and

amount of cholesterol. Half were fed extra DHA and EPA; the other

half additional omega-6 fat (linoleic I think). Then each of these

two groups were subdivided in to five categories by dietary

cholesterol intake. Five levels of cholesterol intake ranging from

none at all to quite a lot, for each group.

Third, one of the most significant findings seems to have been that

all the omega-3 (DHA and EPA) hamsters had appreciably **lower** HDL

than the corresponding group fed the additional omega-6. This is a

little disconcerting. It may perhaps be, at least part of, the

reason for my historically low HDL, because I eat a little fish

(which contains considerable amounts of DHA and EPA) almost every

day. Of course we would all prefer to have higher HDL, not lower.

So this might be regarded as one possible disadvantage of fish and

fish oil.

Next, their data for the blood plasma levels of LDL and VLDL, for the

two major groups by dietary cholesterol intake are interesting. They

found that, in comparison with the omega-6 hamsters fed little

cholesterol, the omega-3 threes who were fed little dietary

cholesterol had appreciably lower LDL. Not startling. But what was

surprising was that the omega-3s who were fed quite a lot of dietary

cholesterol had appreciably *higher* LDL and VLDL than the omega-6s

that were also fed the higher amounts of dietary cholesterol. So the

relationships are not as simple as one might have suspected.

There were other experiments done, the significance of which is well

beyond my pay scale.

So, from what I can make out, the conclusions appear to be as

follows. If you choose to eat DHA and EPA in one form or another, it

may be important to keep your dietary cholesterol as low as

possible. On the other hand if you do NOT eat fish or fish oil, and

therefore if your diet is tilted more in the direction of omega-6

fats, then the amount of cholesterol you eat does not seem to matter

as much, at least as regards your LDL level, as it does if you DO eat

fish.

This is the second study by the same authors to have found similar

results.

Hope this helps. As I said at the outset if anyone disagrees with my

assessment above, please say so. If anyone can explain any practical

significance to us of their second experiment I would find that very

helpful.

Rodney.

--- In , " old542000 " <apater@m...>

wrote:

>

> Hi All,

>

> The below abstract that is not pdf-available seems

> to report that n-3 fatty acids are reported to induce

> better blood lipid levels than n-6 fatty acids such as

> linoleic acid, which has similar action. Some here

> justifiably use psyllium to improve satiation and

> blood lipids, I believe. Psyllium was shown in the

> Ann Nutr Metabol paper to act better with a diet

> in which n-3 fats were predominant. Cholesterol

> was added to the diet at two levels.

>

> 0.1% cholesterol is about equal to the RDA for

> a 2000 calorie/day CR diet?

>

> The abstract does not describe the dietary fat

> components, but a reference from the same authors

> that is pdf-available from me does describe them.

>

> The details are described at the end of this

> post and appear to represent the article of our

> greatest possible interest.

>

> Experiments were done in the hamster animal model

> system. Rats are the rodents often used to study lipids

> in such systems, but hamsters appear to be better in

> respect to correlating with human lipidology.

>

> Therefore, between the first abstract on

> psyllium and lipids and the paper describing

> the diet components, are two pdf-available

> to all paper citations and excerpts on the

> hamster model system.

>

> Although the Ann Nutr Metab paper is not pdf-available,

> the authors had previously used the same animal

> model system to study the effects of n-3 and n-6 fatty

> acids on cholesterol in the hamster model system

> and therefore may be in our interest, as suggested

> by the pdf excerpts below at the end of this message.

>

> The largest pdf excerpts for the paper that

> may interest us most is at the end of this post.

>

> First, here are the two papers describing the

> hamster model system from the paper at the end of

> the message. For a comparison before this of rats

> and hamster, see:

>

> hamster: A small European rodent (Cricetus frumentarius). It is

> remarkable for having a pouch on each side of the jaw, under the

> skin, and for its migrations.

> A common name used to describe a subfamily of the muridae. Four

of

> the more common genera are cricetus, cricetulus, mesocricetus, and

> phodopus.

> All hamsters are seed and plant feeders, store food, hibernate in

> winter, and breed throughout the year under laboratory conditions.

>

> rat: One of the several species of small rodents of the genus

Mus

> and allied genera, larger than mice, that infest houses, stores,

and

> ships, especially the Norway, or brown, rat (M. andrinus).

These

> were introduced into Anerica from the Old World.

>

> And, now, the relevance to the human system of hamster,

> there are:

>

> 26 Spady DK,Dietschy JM:Interaction of dietary

> cholesterol and triglycerides in the regulation

> of hepatic low density lipoprotein transport in

> the hamster.J Clin Invest 1988;81:300 –309.

> http://www.pubmedcentral.nih.gov/articlerender.fcgi?

> tool=pubmed & pubmedid=2448340

>

> ... The hamster has proved to be a good model in which to

> study these regulatory mechanisms since its concentration of

> plasma LDL-cholesterol responds to changes in dietary lipid

> intake in a manner that is essentially identical to that seen in

> man (15). Furthermore, the kinetics of LDL-cholesterol pro-duction

> and degradation have been worked out in detail in this

> species (13) so that it is possible, in quantitative terms, to

> identify the reason why a particular dietary or pharmacologi-cal

> manipulation results in a change in the steady state plasma

> LDL-cholesterol concentration.

>

> ... 15. Spady, D. K., and J. M. Dietschy. 1985. Dietary saturated

> triacylglycerols suppress hepatic low density lipoprotein receptor

> activ-ity

> in the hamster. Proc. Natl. Acad. Sci. USA. 82:4526-4530.

> http://www.pubmedcentral.nih.gov/picrender.fcgi?

> artid=391135 & action=stream & blobtype=pdf

>

> ... Selection of the male hamster as

> the animal of choice for these studies was dictated by several

> recent observations. Rates of cholesterol synthesis in the

> whole animal in species such as the rat are exceptionally high

> (120 mg/day per kg of body weight), whereas the hamster

> and man have much lower rates (9). Of greater importance,

> the rate of sterol synthesis in the liver of the hamster is

> disproportionately low and in the range found in biopsy

> specimens of human liver (9, 10). Because of this very limited

> synthetic capacity, the liver of man and, particularly, the

> male hamster cannot readily adapt to changes in cholesterol

> flux and so alters rates of LDL transport in response to

> changes in diet or to a pharmacological challenge (4, 7). Thus,

> hamster and man are similar in having significant levels of

> circulating LDL-cholesterol, in their intrinsically low rates of

> hepatic cholesterol synthesis, in their response to different

> diets and drugs, and in the manner in which they handle

> biliary sterol secretion (9, 11, 12). ....

>

> Now, here is the Medline abstract for the psyllium and PUFA

paper.

>

> Ann Nutr Metab. 2004 Nov 22;48(6):374-380 [Epub ahead of print]

> Effects of Psyllium on Plasma Total and Lipoprotein Cholesterol

> and Hepatic

> Cholesterol in Hamsters Fed n-3 PUFA or n-6 PUFA with High

> Cholesterol Levels.

> Liu YC, Liu SY, Lin MH.

> ... n-3 polyunsaturated fatty acids (PUFA) diet ...

> n-3 PUFA plus psyllium (8%, wt/wt) diet

> combined with variable levels of cholesterol (0, 0.05, 0.1%, wt/wt)

> or a

> cholesterol-enriched (0.2%, wt/wt) n-3 PUFA or n-6 PUFA diet that

> contained

> either 8% methyl cellulose or psyllium for 4 weeks. In the n-3 PUFA-

> fed

> hamsters, we have found that psyllium was able to reduce plasma

total

> cholesterol and low density lipoprotein (LDL)-cholesterol

> significantly when

> 0.1% cholesterol was added to the diet. In contrast, the effects of

> psyllium

> were not seen in the n-3 PUFA-fed hamsters without dietary

> cholesterol or with

> 0.05% dietary cholesterol. However, no matter in the presence of

> psyllium or

> not, the increase of plasma total cholesterol, very-low-density

> lipoprotein

> (VLDL)-cholesterol, LDL-cholesterol and high-density lipoprotein

> (HDL)-cholesterol levels was depend on the content of dietary

> cholesterol.

> Although the cholesterol diet increased the liver total cholesterol

> level, 80 g

> psyllium/kg diet resulted in a significantly lower concentration of

> liver total

> cholesterol in the cholesterol-fed hamsters. In the second

> experiment, we have

> also found that psyllium feeding lowered significantly plasma total

> cholesterol

> and VLDL-cholesterol concentrations in hamsters fed n-3 PUFA but

not

> in those

> fed n-6 PUFA. However, the levels of plasma total cholesterol, VLDL-

> cholesterol

> and LDL-cholesterol levels of the (n-6) PUFA-fed hamsters were

> significantly

> lower than those in the (n-3) PUFA-fed hamsters in the absence or

> presence of

> dietary psyllium. Our data also showed that hamsters fed both high-

> cholesterol

> n-3 PUFA and n-6 PUFA diets had a significant decrease in hepatic

> cholesterol

> with intake of psyllium. Liver total cholesterol concentrations were

> significantly lower in n-3 PUFA-fed hamsters compared with the n-6

> PUFA-fed

> groups. ...

> PMID: 15564767 [PubMed - as supplied by publisher]

>

> Now, here is the longer paper detailing the effect of n-3 PUFA

or

> n-6 PUFA with various cholesterol levels in hamsters.

>

> What may be in our interest, is that it appeared that in Fig. 1

> the weights

> of the hamsters were for about 0.04% cholesterol in the diet, not

> significantly

> 38% higher for the n-3 versus n-6 PUFA. In Fig. 2, the plasma

> cholesterol was

> at 0-0.0.25% cholesterol in the diet significantly greater for the

n-

> 3 PUFA and

> for the 0.1 and 0.2% cholesterol diet significantly greater for the

n-

> 6 PUFA.

> for Fig. 3, blood LDL levels were in the same pattern as was total

> cholesterol

> in Fig. 2, but more than the level at 0.2% dietary cholesterol.

HDL

> was about

> 40-100% better in its increased level when using n-6 PUFA in the

diet.

>

> Ann Nutr Metab. 2004 Sep-Oct;48(5):321-8. Epub 2004 Oct 01.

> The amount of dietary cholesterol changes the mode of effects of

> (n-3)

> polyunsaturated fatty acid on lipoprotein cholesterol in hamsters.

> Lin MH, Lu SC, Huang PC, Liu YC, Liu SY.

>

> ... polyunsaturated fatty acids (PUFA) ...

> cholesterol content (0, 0.025, 0.05, 0.1 and 0.2%, w/w) with either

> (n-3) PUFA

> (21 g/100 g fatty acids) or (n-6) PUFA (37.4 g/100 g fatty acids)

fat

> for 6

> weeks. In hamsters fed the nonatherogenic diet (0 or 0.025% dietary

> cholesterol), very low density lipoprotein (VLDL)-cholesterol

levels

> in the

> (n-3) PUFA group were not significantly different from those in the

> (n-6) PUFA

> group, and low density lipoprotein (LDL)-cholesterol levels in the

(n-

> 3) PUFA

> group were significantly lower than those in the (n-6) PUFA group.

In

> contrast,

> in hamsters fed the atherogenic diet (0.1 or 0.2% dietary

> cholesterol), VLDL-

> and LDL-cholesterol levels in the (n-3) PUFA group were

significantly

> higher

> than those in the (n-6) PUFA group, in a dose-dependent manner.

When

> the

> hamsters were fed with 0, 0.025, 0.05, 0.1 or 0.2% (w/w) dietary

> cholesterol,

> high density lipoprotein (HDL) cholesterol concentration was

> significantly lower

> in the (n-3) PUFA group than those in the (n-6) PUFA group. Hepatic

> cholesteryl

> esters were significantly lower, while hepatic microsomal acyl-

> coenzyme

> A:cholesterol acyltransferase activity and VLDL-cholesteryl esters

> were

> significantly higher in hamsters fed (n-3) PUFA with the

atherogenic

> diet (0.1

> or 0.2% dietary cholesterol) than in those fed (n-6) PUFA with the

> atherogenic

> diet. Our results demonstrate that the amount of dietary

cholesterol

> is an

> important factor in determining the mode and extent of effects of

> dietary (n-3)

> PUFA, especially on VLDL- and LDL-cholesterol levels. When dietary

> cholesterol

> intake was above 0.1% (w/w), the plasma cholesterol-lowering effect

> of (n-3)

> PUFA disappeared, and instead, it showed a cholesterol-increasing

> effect.

> However, the effects of dietary (n-3) PUFA on HDL-cholesterol are

> independent of

> dietary cholesterol content.

> PMID: 15467282 [PubMed - in process]

>

> ... the response to dietary (n-3)PUFA

> among different animal species is highly variable.Differ-

> ent animal species also vary greatly in their response to

> dietary cholesterol.Considerable interest has centered on

> the hamster as a model for studying lipoprotein metabo-

> lism.This is because cholesterol metabolism in this spe-

> cies resembles that in human beings in several respects,

> including the response to dietary cholesterol and fat [26 ].

>

> ...The test diets had similar fatty acid compositions

> with the PUFA/SFA ratio set to be 1.0,except that 18 g linoleic

acid/

> 100 g fatty acids in the (n-6)PUFA diet was replaced by (n-3)PUFA,

> mainly EPA and DHA,in the (n-3)PUFA diet.The amounts of

> PUFA,monounsaturated fatty acids (MUFA)and SFA were compa-

> rable in both the (n-6)PUFA and (n-3)PUFA groups.The cholester-

> ol concentration of the fish oil was determined,and the dietary cho-

> lesterol level was adjusted to be the same for both the (n-6)PUFA

> and (n-3)PUFA groups.All diets were supplemented with 0.005 g

> D,L -alpha-tocopherol/kg and stored in the dark at –20 ° C. ...

>

> Table 1. Fatty acid composition of the test diets

> Fatty acid g/100 g fatty acids

> (n-6)PUFA (n-3)PUFA

> 8:0 3.1 2.6

> 10:0 2.4 2.0

> 12:0 12.5 10.5

> 14:0 6.5 8.8

> 16:0 11.7 12.8

> 16:1(n-7)–3.6

> 18:0 4.6 3.5

> 18:1(n-9)17.9 13.4

> 18:2(n-6)37.4 19.2 = linoleic acid

> 18:3(n-3)3.9 2.4

> 18:4(n-3)–1.7

> 20:1(n-9)–1.4

> 20:4(n-6)–0.9

> 20:5(n-3)–10.9 = EPA

> 22:1(n-9)–0.7

> 22:5(n-3)–1.3

> 22:6(n-3)–4.6 = DHA

> SFA 41 40

> PUFA 41 41

> MUFA 18 19

> (n-6)PUFA 37 20

> (n-3)PUFA 4 21

> PUFA/SFA,g/g 1 1

>

> ... Results

> Body Weight Gain and Liver Weight

> The gain in body weight,liver weight and liver-to-body

> weight ratio of hamsters fed diets differing in fat composi-

> tion were similar across all groups (fig.1).There were

> gradual increases of the liver weight and liver-to-body

> weight ratio with increasing intake of dietary cholesterol

> in hamsters fed both (n-6)and (n-3)PUFA diets (fig.1).

>

> Plasma and Lipoprotein Cholesterol

> When no dietary cholesterol was given or dietary cho-

> lesterol was maintained at 0.025%(w/w),plasma choles-

> terol concentration was significantly lower (p !0.05)in

> the (n-3)PUFA group compared to the (n-6)PUFA group

> (fig.2).The lower plasma cholesterol level observed in

> hamsters fed (n-3)PUFA essentially reflected a reduced

> amount of cholesterol carried in both LDL and HDL frac-

> tions (fig.3).However,VLDL-and LDL-cholesterol con-

> centrations in the hamsters ingesting the (n-3)PUFA diet

> were significantly higher than in those ingesting the (n-6)

> PUFA diet when dietary cholesterol intake was above

> 0.1%(fig.3).In the following time course study,our data

> demonstrate that 1 week of feeding high cholesterol

> (0.1%,w/w)diet containing (n-3)PUFA was sufficient to

> produce the maximum increasing of VLDL-and LDL-

> cholesterol concentrations by the diet and to observe max-

> imum differences between the diet groups (fig.4).How-

> ever,the percentage increase of VLDL-and LDL-choles-

> terol concentrations (compared to (n-6)PUFA group)

> gradually decreased toward the end of the 6-week feeding

> period.In the first week,the percentage increase of

> VLDL-cholesterol level was 108%,but in the sixth week,

> it was reduced to 40%.The percentage increase of LDL-

> cholesterol level was 40%in the first week,but in the sixth

> week,it was reduced to 20%(fig.4).HDL-cholesterol lev-

> els were significantly lower in the (n-3)PUFA group than

> those in the (n-6)PUFA group when the hamsters were

> fed with 0,0.025,0.05,0.1 or 0.2%cholesterol (fig.3).In

> hamsters consuming the (n-3)PUFA diets,there were no

> changes in HDL-cholesterol levels with increasing choles-

> terol intake.However,the HDL-cholesterol level in (n-6)

> PUFA group was significantly increased at 0.2%choles-

> terol intake.

>

> Hepatic Cholesteryl Esters

> The hepatic cholesteryl ester content increased pro-

> gressively in a dose-dependent fashion as the dietary cho-

> lesterol intake increased in both (n-6)and (n-3)PUFA

> groups (fig.5).The esterified cholesterol concentration

> was significantly less in the (n-3)PUFA group than in the

> (n-6)PUFA group.

>

> Hepatic Microsomal ACAT Activity

> Hepatic cholesteryl esters were significantly lower,

> while hepatic microsomal ACAT activity and VLDL-cho-

> lesteryl esters were significantly higher in hamsters fed the

> (n-3)PUFA diet with high cholesterol intake (0.1 or 0.2%)

> than in those fed the (n-6)PUFA diet with high cholester-

> ol intake (0.1 or 0.2%)(table 2).

>

> Characteristics of Plasma VLDL

> The molar ratio of the core lipids (cholesteryl esters/

> triglycerides:CE/TG)with cholesterol feeding increased

> more dramatically in the (n-3)PUFA-fed hamsters

> (fig.6).In hamsters fed the atherogenic diet (0.1 or 0.2%

> dietary cholesterol),the molar ratios of the core lipids

> (CE/TG)in the (n-3)PUFA group were significantly high-

> er than those in the (n-6)PUFA group.The molar ratios of

> the total surface to core lipid components (phospholipids

> +free cholesterol/triglycerides +cholesteryl esters:PL +

> FC/TG +CE)were higher in the (n-3)PUFA group than

> those in the (n-6)PUFA group regardless of the concen-

> trations of dietary cholesterol (fig.7).

>

> Discussion

> This most striking finding of this study was the ability

> of the amount of dietary cholesterol to change the mode of

> effects of (n-3)PUFA on lipoprotein cholesterol in ham-

> sters.This study showed that dietary (n-3)PUFA was

> more beneficial than (n-6)PUFA in lowering plasma cho-

> lesterol concentration when hamsters were fed with the

> nonatherogenic diet (0 or 0.025%dietary cholesterol)for

> 6 weeks.The lowering occurred mainly in the LDL and

> HDL fractions.A previous study [25 ]also observed a

> more hypocholesterolemic effect with (n-3)PUFA after 4

> weeks 'feeding of a cholesterol-free diet when compared

> to (n-6)PUFA.However,the hypocholesterolemic effect

> of (n-3)PUFA was only in the HDL fraction.The differ-

> ence in the lipoprotein fractions of the hypocholester-

> olemic effect of (n-3)PUFA may be due to the differences

> in the feeding duration.In contrast,in hamsters fed the

> atherogenic diet (0.1 or 0.2%dietary cholesterol)for 6

> weeks,(n-3)PUFA induces hypercholesterolemia more

> than (n-6)PUFA,the increase being in the VLDL and

> LDL fractions.The results support our earlier observa-

> tions [25 ]made in hamsters fed an (n-3)PUFA-or (n-6)

> PUFA-rich diet supplemented with 5 g/kg cholesterol.

> These studies demonstrated that increases in LDL-choles-

> terol (LDL-C)and VLDL-cholesterol (VLDL-C)with

> (n-3)PUFA consumption when compared to (n-6)PUFA

> are dependent on dietary cholesterol.Surette et al.[23 ]

> also observed 90%greater VLDL-C and LDL-C concen-

> trations in hamsters ingesting a (n-3)PUFA diet contain-

> ing 0.1%cholesterol compared with those consuming an

> oleic acid-rich diet.However,HDL-cholesterol (HDL-C)

> levels were significantly lower in the (n-3)PUFA group

> than those in the (n-6)PUFA group whether the dietary

> cholesterol was added in the diet or not.This parallels sev-

> eral other controlled animal and human feeding trials

> where a decrease in HDL-C has been observed with fish

> oil consumption [34 –37 ].The decrease in cholesterol con-

> centration observed in the HDL fraction with (n-3)PUFA

> consumption was very comparable in the groups of ham-

> sters with increasing consumption of dietary cholesterol.

> Thus,while (n-3)PUFA-induced changes in LDL-C and

> VLDL-C are dependent on dietary cholesterol,changes in

> HDL-C are not.

> Of the two PUFA treatments,(n-3)PUFA was more

> significant in increasing LDL-C levels without a signifi-

> cant change in HDL-C levels,thus increasing the LDL/

> HDL ratio (n-6 PUFA:0.58,0.70,0.76,0.94,0.67;n-3

> PUFA:0.35,0.61,1.04,1.79,2.33).High LDL/HDL

> ratios are associated with an increased risk of vascular dis-

> ease [38 ]and therefore a dietary (n-3)PUFA might be

> disadvantageous in reducing the risk of experiencing this

> disease with increasing intake of dietary cholesterol.

> There are two important implications of this study

> with respect to human nutrition.First,these data suggest

> that the detrimental effect of (n-3)PUFA on LDL-C could

> be minimized if the intake of cholesterol could be reduced

> to 0.05%.The data obtained in the hamsters fed 0.05%

> cholesterol are particularly relevant to the human situa-

> tion since this load of cholesterol corresponds to the

> intake of F 125 mg of cholesterol per 1,000 kcal of dietary

> intake.Second,given the likelihood that Western diets

> will always contain at least several hundred milligrams of

> cholesterol each day,the alternative way in which to

> remain at the reasonably low LDL-C level is to be certain

> that the diet contains (n-6)PUFA that effectively block

> the deleterious effects of the dietary cholesterol.

> Another interesting observation we made in this study

> was that hamsters of the (n-3)PUFA group had signifi-

> cantly lower hepatic cholesteryl ester concentrations than

> hamsters of the (n-6)PUFA group with increasing dietary

> cholesterol.The combination of higher dietary cholesterol

> delivery to the liver and decreased hepatic cholesteryl

> ester formation may reveal the underlying result for the

> decreased LDL-receptor activity in animals consuming

> n-3 PUFA and cholesterol.

> Several human and animal studies [39,40 ]have re-

> cently reported that fish oil feeding induced changes in

> lipoprotein composition and particle size.In our study,

> based on the greater ratio of surface lipids to core lipids of

> VLDL in the (n-3)PUFA group,the particle size of VLDL

> in the (n-3)PUFA group is probably smaller than those in

> the (n-6)PUFA group.Nigon et al.[41 ]demonstrated

> that larger or smaller LDL particles had a lower LDL-

> receptor binding affinity than medium-sized LDL parti-

> cles and might have a slower turnover rate.Therefore,the

> increase in LDL-C observed in hamsters fed the (n-3)

> PUFA with the atherogenic diet (0.1 or 0.2 dietary choles-

> terol)can be at least partially explained by a reduced

> hepatic receptor-mediated uptake of LDL.

> Although cholesteryl esters were significantly lower,

> hepatic microsomal ACAT activity and VLDL-cholester-

> yl esters were significantly higher in hamsters fed (n-3)

> PUFA with the atherogenic diet (0.1 or 0.2%dietary cho-

> lesterol)than in those fed (n-6)PUFA with the atherogen-

> ic diet.It is feasible to postulate that (n-3)PUFA some-

> how stimulated the hepatic cholesteryl esters secretion

> under the challenge of dietary cholesterol.The marked

> decline in hepatic cholesteryl ester can be partly ac-

> counted for by the increased level of secretion of choles-

> teryl ester in the VLDL particles.

>

> Cheers, Al Pater

[Guest guest]

Something that looked somewhat odd to me was the content of myristic

acid in the diet:

> 14:0 6.5 8.8

As we have discussed before, myristic acid is highly cholesteremic.

Cow butterfat has 11% myristic acid, human butterfat has 8%. By

contrast, beef tallow has only 3% myristic acid, and lard has 2%.

I am sure that this factor had a substantial impact on the results of

the experiment.

Tony