Source: Rejuvenation Res. 2007 Dec 26 [Epub ahead of print].
Title: Fatty Acid Profile of Erythrocyte Membranes As Possible
Biomarker of Longevity.
Note: Nonagenarians are those between the ages of 90 and 99.
Commentary (by me): This does not mean you should go out and eat food
rich in trans fatty acids, because as the researchers point out, their
findings are consistent with a lipid peroxidation hypothesis for
longevity. However, this is consistent with what I do, and that is to
look for food that is over 50% SFAs, low in cholesterol, and if this
is the case, I don't worry if there are any trans fatty acids at that
point, since it's going to be a stable item and generate little if any
lipid peroxidation (still should not eat it if it has any hint of
rancidity to it). Also, note how they totally contradict the notion
that "trans fat" will cause some sort of structural harm to cells. In
fact, the opposite appears to be the case, and I've pointed out how
ridiculous the anti-"trans fat" claims were for a long time (on
several different levels). Instead, it would make more sense to test
the food item to see how quickly it goes rancid, and there are a few
tests that can be used (Rancimat and ORAC, as examples). However,
will you hear about this study in the "mainstream media?" Or will you
hear yet another report about how "bad" "trans fats" are, with either
no evidence cited or else an "epidemiological" study cited that did
not control for lipid peroxidation (in other words, what most likely
happens when "trans fat" appears to be unhealthy is that those who ate
the most TFAs also ate the most PUFAs and/or had a diet significantly
lower in antioxidant-rich foods).
Taka
Built Differently, Down in the Membranes
You might recall that different fatty acid or lipid composition in
cell membranes was floated as a reason for the ninefold longevity of
naked mole-rats over related rodent species. Plenty of oxidative
stress in the older mole-rats, but little sign of biochemical damage
resulting from it - in comparison to those other rodents long since
aged to death, that is. Better, more damage-resistant building blocks
down at the molecular level might be the cause:
Underlying causes of species differences in maximum life span (MLS)
are unknown, although differential vulnerability of membrane
phospholipids to peroxidation is implicated. ... membranes of longer-
living, larger mammals have less polyunsaturated fatty acid
(PUFA). ... Both species had similar amounts of membrane total
unsaturated fatty acids; however, mice had 9 times more
docosahexaenoic acid (DHA). Because this n-3PUFA is most susceptible
to lipid peroxidation, mole-rat membranes are substantially more
resistant to oxidative stress than are mice membranes ... suggesting
that membrane phospholipid composition is an important determinant of
longevity.
A forthcoming Rejuvenation Research paper discusses the results of a
similar consideration of cell membrane differences and longevity
within the human species:
Fatty Acid Profile of Erythrocyte Membranes As Possible Biomarker of
Longevity:
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.
...
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.
...
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.
Note there again - reduced lipid peroxidation, as for the naked mole-
rats, and therefore more resistant to oxidative stress. This is quite
an interesting line of research, demonstrating some plausible
indications of a structural contribution to longevity at the cellular
level. I'm sure we'll be seeing more of this in the future, as
research and debate continues.
J Lipid Res. 1998 Oct;39(10):1972-80.
Effects of specific fatty acids (8:0, 14:0, cis-18:1, trans-18:1) on
plasma lipoproteins, early atherogenic potential, and LDL oxidative
properties in the hamster.
Nicolosi RJ, Wilson TA, Rogers EJ, Kritchevsky D.
Center for Chronic Disease Control, University of Massachusetts
Lowell, 01854, USA.
Although comparative studies of the cholesterolemic properties of
trans fatty acids relative to cis-unsaturates and saturates have been
conducted in humans and animals, there is no recent information
relating these lipid responses to susceptibility to atherosclerosis.
Therefore, hamsters were fed diets containing equivalent amounts of
cholesterol (0.12% wt/wt) and test fats (20% wt/wt) for 8 weeks. Each
test fat contained between 50-52% of the-total triacylglycerols as a
single fatty acid, i.e., 8:0, 14:0, 18:0, cis-18:1, or trans-18:1
while the balance consisted of 16:0, cis-18:1 and 18:2 that were the
same for all groups. Plasma total cholesterol (TC), low density
lipoprotein cholesterol (LDL-C), and high density lipoprotein
cholesterol (HDL-C) levels were not different for 8:0, cis-18:1, and
trans-18:1, whereas 14:0 caused a significant rise in plasma TC, LDL-
C, and HDL-C. LDL oxidation measurements showed that the lag phase of
conjugated diene formation was longest for the trans-18:1 and cis-18:1
groups while rate of conjugated diene formation was lowest for the
trans-18:1 and cis-18:1 groups. The trans-18:1- and cis-18:1-fed
animals had significantly higher levels of LDL alpha-tocopherol
relative to the 8:0- and 14:0-fed animals. Aortic fatty streak
formation was highest for the 14:0- and 8:0-fed animals and lowest for
the trans-18:1. In conclusion, the plasma lipid and antioxidant
properties of trans-18:1 and cis-18:1 were comparable while the
trans-18:1-fed hamsters had the least amount of early atherosclerosis.
In addition, 8:0-fed animals unexpectedly had early atherosclerosis
formation similar to the 14:0-fed animals.
PMID: 9788243