39 replies to this topic

[HaloTeK]

Duke, I would still say we need to know more about postprandial effects of a low carb diet. Dr. Davis, who is one of the few bloggers I really respect (along with Stephan), doesn't really have a definitive position on if our blood vessels may be damaged over time by the triglyceride jumps after consuming high fat meals (even if trigs are usually low on a low carbohyrate diet).

And frankly, I still worry about oxidized cholesterol from dietary or internal production (less so). Even if you have sky high HDL -- it can still be damaged (maybe from a postprandial trig jump after huge fat intake?? who knows).

At least in your health program you intermittantly fast -- which could possibly be protecting you from constant postprandial surges in trigs. And remember, your blood vessels have a much larger tolerance when you are younger, what happens when you start reaching your 90s in terms of the postprandial trig surges.

I hope more research comes out in this area.

For those that don't follow the "paleo blogs," check out this new meta analysis in the AJCN finding that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD. Read it here. This should be a big deal for those among us that place great deal of value on the consensus opinion. This review is the consensus moving and, oops, saturated fat is no longer bad.

Really glad to see more and more evidence (and re-evaluation of previous evidence) showing that saturated fat is not associated with heart disease, or any negative conditions.

It just makes zero sense that saturated fat would be a negative health concern. Finally, science is catching up with common sense.

What I'm waiting for now is for the pendulum to swing in the other direction, and for more and more studies that indicate humans are healthier when we consume saturated fat. In other words, saturated fat is not a neutral fat--it's a healthy fat. In fact, low HDL (<40) should be considered as a deficiency in saturated fat intake.

Give nutritional science 20 years, and this will be accepted wisdom.

[s123]

I'm not an proponent of eating a lot of saturated fats just as I'm not an proponent of eating omega-3. Instead, I believe that we don’t have the data yet to conclude this debate and for the mean time we should be careful not to exaggerate too much.

Some studies point out that saturated fats could be linked to a longer lifespan.

Lifespan correlates with the degree of lipid unsaturation and the position of the double bounds.

Barja et al. Free radicals and aging. Trends Neurosci., 2004, 27: 595-600.

Hulbert A. J. On the importance of fatty acid composition of membranes for aging. J. Theor. Biol., 2005, 234: 277-288.

Hulbert et al. Life and death: metabolic rate, membrane composition, and life span of animals. Physiol. Rev., 2007, 87: 1175-1213.

Pamplona et al. Membrane fatty acid unsaturation, protection against oxidative stress, and maximum life span: a homeoviscous-longevity adaptation? Ann. NY Acad. Sci., 2002, 959: 475-490.

Sanz et al. Is the mitochondrial free radical theory of aging intact? Antioxid. Redox Signal., 2006, 8: 582-599.

Shorter-lived laboratory mice have a higher omega-3 content in their membranes than longer-lived wild derived mice.

Hulbert et al. Extended longevity of wild-derived mice is associated with peroxidation-resistant membranes. Mech. Ageing Dev., 2006, 127: 653-657.

Naked mole rats that can live for 30 years have less DHA in their membranes compared to mice, even though they experience a higher level of oxidative damage accumulation.

Mitchell et al. Membrane phospholipid composition may contribute to exceptional longevity of the make mole-rat (Hecephalus glaber): a comparative study using shotgun lipidomics. Exp. Gerontol., 2007, 42: 1053-1062.

Honey bee queens outlive workers by a factor of ten or more and their membranes contain less PUFAs.

Heinze J. and Schrempf A. Aging and Reproduction in Social Insects - A Mini-Review. Gerontology, 2008, 54: 160-167.

The offspring of human nonagenarians have a lower content of PUFAs in their membranes.

Puca et al. Fatty acid profile of erythrocyte membranes as possible biomarker of longevity. Rej. Res., 2008, 11: 63-72.

Zimniak writes: "suggesting a case of "antagonistic pleiotropy" on the metabolic rather than genetic level: the protective role of n-3 PUFAs during most of the life span may be partially offset by accelerated aging due to increased lipid peroxidation."

Piotr Zimniak. Detoxification reactions: relevance to aging. Ageing Research Reviews, 2008, 7: 281-300.

Interesting note, basketball players have a higher amount of saturated fatty acids in their erythrocyte membrane while football players have a lower amount compared to controls.

Tepsic et al. Plasma and erythrocyte phospholipid fatty acid profile in professional basketball and football players. Eur. J. Appl. Physiol., 2009, 107: 359-365.

Edited by s123, 20 January 2010 - 01:35 AM.

[youandme]

My HDL used to be 24 mg/dL before increasing saturated fat and lowering carbs. Last October it was 51 mg/dL. It will be interesting to see what it is since I've been systematically increasing saturated fat of late.

Please do share your blood results

Thanks

[youandme]

Previously been on a low sat fat low any fat diet! for perhaps 3 years...now changing to low carb more sat fat (butter from grass fed cows etc)
Will see how my HDL Trigs etc look in another month...I also have a fatty liver (occured while on the lower fat diet) so will see if this change in diet helps that.
My HDL previously was just below normal range.

[niner]

The offspring of human nonagenarians have a lower content of PUFAs in their membranes.

Puca et al. Fatty acid profile of erythrocyte membranes as possible biomarker of longevity. Rej. Res., 2008, 11: 63-72.

Rejuvenation Res. 2008 Feb;11(1):63-72.
Fatty acid profile of erythrocyte membranes as possible biomarker of longevity.

Puca AA, Andrew P, Novelli V, Anselmi CV, Somalvico F, Cirillo NA, Chatgilialoglu C, Ferreri C.

IRCCS Policlinico Multimedica, Milan, Italy. puca@longevita.org

Offspring of long-lived individuals are a useful model to discover biomarkers of longevity. The lipid composition of erythrocyte membranes from 41 nonagenarian offspring was compared with 30 matched controls. Genetic loci were also tested in 280 centenarians and 280 controls to verify a potential genetic predisposition in determining unique lipid profile. Gas chromatography was employed to determine fatty acid composition, and genotyping was performed using Taqman assays. Outcomes were measured for erythrocyte membrane percentage content of saturated fatty acids, monounsaturated fatty acids, polyunsaturated fatty acids (omega-6 and omega-3), geometrical isomers of arachidonic and oleic acids, and total trans-fatty acids. Also, allele and genotyping frequencies at endothelial-nitric oxide synthase and delta-5/delta-6 and delta-9 desaturase loci were considered. Erythrocyte membranes from nonagenarian offspring had significantly higher content of C16:1 n-7, trans C18:1 n-9, and total trans-fatty acids, and reduced content of C18:2 n-6 and C20:4 n-6. No association was detected at endothelial-nitric oxide synthase and delta-5/delta-6 and delta-9 desaturase loci that could justify genetic predisposition for the increased trans C18:1 n-9, monounsaturated fatty acids and decreased omega-6 synthesis. We concluded that erythrocyte membranes derived from nonagenarian offspring have a different lipid composition (reduced lipid peroxidation and increased membrane integrity) to that of the general population.

PMID: 18160025

More trans-fatty acids? I'd better schedule another trip to McDonalds. This makes me wonder about the difference between dietary vs endogenously produced lipids. Are the children of nonagenarians junk food junkies? Although they didn't find it, there is presumably a genetic component here, unless one posits very long-lasting dietary habits that are passed on from parents to children. Animals do produce trans fats; maybe making more of your own is good, but eating them is bad, or maybe the synthetic trans fats are bad and the animal sourced ones are ok? Erythrocyte membrane lipid composition is significantly different than skeletal muscle membranes, FWIW.

[e Volution]

I'm not an proponent of eating a lot of saturated fats just as I'm not an proponent of eating omega-3. Instead, I believe that we don’t have the data yet to conclude this debate and for the mean time we should be careful not to exaggerate too much.

This is my point exactly, so I think the best idea is to default to this position

Animals do produce trans fats; maybe making more of your own is good, but eating them is bad, or maybe the synthetic trans fats are bad and the animal sourced ones are ok? Erythrocyte membrane lipid composition is significantly different than skeletal muscle membranes, FWIW.

Just read this yesterday on Mark Sisson's blog:

What’s Behind the Natural versus Industrial Trans Fats Comparison?
Perhaps you’ve heard that meat and dairy products contain trans fats as well. Technically, this is true, but the industrially produced trans fats aren’t to be conflated with the natural kind, called vaccenic acid. The digestion process, particularly the stomach bacteria, in ruminant animals naturally adds hydrogen. The result is a small amount of natural trans fat in the animals’ meat and milk that offers a number of benefits, including antiatherogenic effects. Conjugated linoleic acid (CLA), part of the family of naturally occurring trans fats, is a health powerhouse.

Unfortunately, about 80% of Americans’ trans fat intake is the artificial class. As is so often the case, there’s a tendency to throw the baby out with the bath water when it comes to nutritional guidelines.
From his good overview of trans fats Why Are Trans Fats Bad? article. As is usual from Mark however, its a great overview but a little short on hard science.

Edited by icantgoforthat, 20 January 2010 - 04:41 AM.

[Sillewater]

More trans-fatty acids? I'd better schedule another trip to McDonalds. This makes me wonder about the difference between dietary vs endogenously produced lipids. Are the children of nonagenarians junk food junkies? Although they didn't find it, there is presumably a genetic component here, unless one posits very long-lasting dietary habits that are passed on from parents to children. Animals do produce trans fats; maybe making more of your own is good, but eating them is bad, or maybe the synthetic trans fats are bad and the animal sourced ones are ok? Erythrocyte membrane lipid composition is significantly different than skeletal muscle membranes, FWIW.

Maybe because trans fats are more stable?

[oehaut]

maybe making more of your own is good, but eating them is bad, or maybe the synthetic trans fats are bad and the animal sourced ones are ok?

Do trans fatty acids from industrially produced sources and from natural sources have the same effect on cardiovascular disease risk factors in healthy subjects? Results of the trans Fatty Acids Collaboration (TRANSFACT) study.

BACKGROUND: The consumption of monounsaturated trans fatty acids (TFAs) increases the risk of cardiovascular disease (CVD). Putative differences between the effects of TFAs from industrially produced and natural sources on CVD risk markers were not previously investigated in healthy subjects. OBJECTIVE: We aimed to compare the effects of TFAs from industrially produced and natural sources on HDL and LDL cholesterol, lipoprotein particle size and distribution, apolipoproteins, and other lipids in healthy subjects. DESIGN: In a randomized, double-blind, controlled, crossover design, 46 healthy subjects (22 men and 24 women) consumed food items containing TFAs (11-12 g/d, representing approximately 5% of daily energy) from the 2 sources. RESULTS: Forty subjects (19 men and 21 women) completed the study. Compared with TFAs from industrially produced sources, TFAs from natural sources significantly (P = 0.012) increased HDL cholesterol in women but not in men. Significant (P = 0.001) increases in LDL-cholesterol concentrations were observed in women, but not in men, after the consumption of TFAs from natural sources. Apolipoprotein (apo)B and apoA1 concentrations confirmed the changes observed in LDL and HDL cholesterol. Analysis of lipoprotein subclass showed that only large HDL and LDL concentrations were modified by TFAs from natural sources but not by those from industrially produced sources. CONCLUSIONS: This study shows that TFAs from industrially produced and from natural sources have different effects on CVD risk factors in women. The HDL cholesterol-lowering property of TFAs seems to be specific to industrial sources. However, it is difficult in the present study to draw a conclusion about the effect of TFAs from either source on absolute CVD risk in these normolipidemic subjects. The mechanism underlying the observed sex- and isomer-specific effects warrants further investigation.

Looks like they are better... but would still result in an increased in total C (in this study, in women only), albeit small-sized particule (for what it worth)



Study of the effect of trans fatty acids from ruminants on blood lipids and other risk factors for cardiovascular disease.

BACKGROUND: The intake of trans fatty acids (TFA) from industrially hydrogenated vegetable oils (iTFA) is known to have a deleterious effect on cardiovascular health, the effects of TFA from ruminants (rTFA) are virtually unknown. OBJECTIVE: The purpose of the present study was to compare the effects of rTFA and iTFA on plasma LDL concentrations and other cardiovascular disease risk factors in healthy subjects. DESIGN: In a double-blind, randomized crossover controlled study, 38 healthy men were fed each of 4 experimental isoenergetic diets lasting 4 wk each. The 4 diets were high in rTFA (10.2 g/2500 kcal), moderate in rTFA (4.2 g/2500 kcal), high in iTFA (10.2 g/2500 kcal), and low in TFA from any source (2.2 g/2500 kcal) (control diet). RESULTS: Plasma LDL-cholesterol concentrations were significantly higher after the high- rTFA diet than after the control (P = 0.03) or the moderate- rTFA (P = 0.002) diet. Plasma LDL-cholesterol concentrations also were significantly (P = 0.02) higher after the iTFA diet than after the moderate-rTFA diet. Plasma HDL-cholesterol concentrations were significantly (P = 0.02) lower after the high-rTFA diet than after the moderate-rTFA diet. Finally, all risk factors were comparable between the control and the moderate-rTFA diets. CONCLUSIONS: These results suggest that, whereas a high dietary intake of TFA from ruminants may adversely affect cholesterol homeostasis, moderate intakes of rTFA that are well above the upper limit of current human consumption have neutral effects on plasma lipids and other cardiovascular disease risk factors.

Edited by oehaut, 20 January 2010 - 12:58 PM.

[s123]

More trans-fatty acids? I'd better schedule another trip to McDonalds. This makes me wonder about the difference between dietary vs endogenously produced lipids. Are the children of nonagenarians junk food junkies? Although they didn't find it, there is presumably a genetic component here, unless one posits very long-lasting dietary habits that are passed on from parents to children. Animals do produce trans fats; maybe making more of your own is good, but eating them is bad, or maybe the synthetic trans fats are bad and the animal sourced ones are ok? Erythrocyte membrane lipid composition is significantly different than skeletal muscle membranes, FWIW.

Like you said, there could be a difference between natural and synthetic trans fatty acids. The difference would be that artificial made trans fatty acids are a mixture of all kinds of trans fatty acids while nature only creates trans bounds at certain positions in the carbon skeleton (because they are made in an enzymatic way*). So, the issue with trans fats may be more complicated than we tend to think. It may be that some specific trans fats are healthy while others or bad.

You could compare this to the addition of sugar to proteins in a controlled enzymatic way (N- and O-glycolysation) and the random addition of sugars that leads to damage (glycation).

Brie cheese contains 3,8 to 4,7mg of CLA per gram fat (100% cis-9, trans-11).
Cheddar cheese contains 1,4 to 5,9mg of CLA per gram fat (18-100% cis-9, trans-11).
Cottage cheese contains 4,5 to 5,9mg of CLA per gram fat (83-100% cis-9, trans-11).
Edam cheese contains 5,4mg of CLA per gram fat (100% cis-9, trans-11).
Gouda cheese contains 5,9 CLA per gram fat (87% cis-9, trans-11).
Mozarella cheese contains 4,3 to 4,9mg of CLA per gram fat (84-100% cis-9, trans-11).
Parmesan cheese contains 1,9 to 8,6mg of CLA per gram fat (38-100% cis-9, trans-11).
Butter contains 4,7 to 8,1mg of CLA per gram fat (79-90% cis-9, trans-11).
Yoghurt contains 1,7 to 9,0mg of CLA per gram fat (71-100% cis-9, trans-11).
Cow milk contains 0,7 to 10,1mg of CLA per gram fat (59-100% cis-9, trans-11).
Sheep milk contains 10,8 to 29,7mg of CLA per gram fat (99-100% cis-9, trans-11).
Beef contains 1,2 to 8,5mg of CLA per gram fat (21-61% cis-9, trans-11).
Lamb meet contains 5,6mg of CLA per gram fat (92% cis-9, trans-11).
Pork meet contains 0,6mg of CLA per gram fat (82% cis-9, trans-11).
Chicken meet contains 0,9mg of CLA per gram fat (84% cis-9, trans-11).
Turkey meet contains 2,5mg of CLA per gram fat (80% cis-9, trans-11).
Egg yolk contains 0,1 to 0,6mg of CLA per gram fat (62% cis-9, trans-11).

Notice in the above table (in bold) how much of the CLA in natural animal products is made of a single isomer called cis-9, trans-11 CLA (rumenic acid). The variation is caused by the animal feed, season and geographic place. Sea products contains between 0,3 to 0,6mg/g fat (but this is not the cis-9, trans-11) and vegetable oil contains 0,1 to 0,7mg/g fat.

* CLA is made by linolic acid isomerase and CLA-reductase by Butyrivibrio fibrisolvens from linolic acid. When linolic acid is low in the diet of the cows than alpha-linoleic acid will be used as a precursor for the synthesis of CLA. In this case the CLA is made by a desaturase enzyme from vaccenic acid).

Source: Patrick Mullie. Functionele voedingsmiddelen: over noten, soja, pre- en probiotica. Acco, Leuven, 2003.

[stephen_b]

Duke, I would still say we need to know more about postprandial effects of a low carb diet. Dr. Davis, who is one of the few bloggers I really respect (along with Stephan), doesn't really have a definitive position on if our blood vessels may be damaged over time by the triglyceride jumps after consuming high fat meals (even if trigs are usually low on a low carbohyrate diet).

Nice post. I hope we get some answers on whether the increase in postprandial triglycerides following saturated fat intake are a problem.