['pmcglothin' post='399941' date='Apr 16 2010, 01:38 AM']fat(walnuts, olive oil, for example), which helps activate insulin and makes the resulting lipid better.[/quote]
['oehaut' date='Apr 15 2010, 10:05 PM' post='399952']
How does fat helps activate insulin? First time i'm hearing this, but coming from you, it must simply be that i'm ignoring something.
[/quote]
Quote (prophets Apr 15 2010, 10:30 PM )
>That’s what confused me. i thought dietary fat simply slowed the dumping of higher GI >foods into the body (slowing >the digestion rate), reducing the postprandial response.
Thanks to both of you for your kind words and thoughtful comments.
One of insulin's jobs is fat storage, studies show that fat acts as an insulin stimulus, increasing its output. You can also find this in physiology books. Insulin stimulus by fat is part of the glycemic control protocol in
The CR Way.
Regarding the PUFA issue, in my own testing, I have not found fatty acid elongation to be a concern. Here’s a post I wrote about it from The CR Society forum:
*Mitochondrial membrane peroxidizability index is inversely related to
maximum life span in mammals *
Pamplona, et al
*Journal of Lipid Research*. 1998 Oct;39(10):1989-94 PMID:
9788245
The oxidative stress theory of aging predicts a low degree of fatty acid
unsaturation in tissues of longevous animals, because membrane lipids
increase their sensitivity to oxidative damage as a function of their
unsaturation. Accordingly, the fatty acids analyses of liver mitochondria
from eight mammals, ranging in maximum life span from 3.5 to 46 years, show
that the total number of double bonds and the peroxidizability index are
negatively correlated with maximum life span (r = -0. 88, P < 0.003; r -0.87, P < 0.004, respectively). This is not due to a low content of
unsaturated fatty acids in longevous animals, but mainly to a redistribution
between kinds of the polyunsaturated n–3 fatty acids series, shifting from
the highly unsaturated docosahexaenoic acid (r = -0.89, P < 0.003) to the
less unsaturated linolenic acid (r = 0.97, P < 0.0001). This redistribution
pattern strongly suggests the presence of a constitutively low
{Delta}6-desaturase activity in longevous animals (r = -0.96, P < 0.0001).
Studies such as this one, have a lot of relevance to calorie restrictors not
because they prove that taking fish oil dangerously increases membrane
peroxidizability, but because they point out that low delta desaturase
activity redistributes fatty acid content of membranes away from longer
chain fatty acids. I, along with other calorie restrictors in a pilot study
Meredith and I put together and reported at the CR conference in Madison ,
have noticed that in spades in fatty acid testing, observing that despite
high dietary intake of ALA and regular intake of fish oil, very little EPA
or DHA makes it into membranes analyzed in fatty acid testing. This was
observed in the first human CR study, which Meredith and I created with
MetaMetrix Laboratories in 2002.
Consider my fasting glucose of 70mg/dl yesterday morning – on the low side
of typical for serious human calorie restrictors. When glucose gets that low
and stays low for a period of time, fat is burned vociferously. As you
probably have read in Guarente’s work, SIRT1 blocks the PPAR-gamma fat
receptor.
*Nature*. 2004 Jun 17;429(6993):771-6. Epub 2004 Jun 2.
*Sirt1 promotes fat mobilization in white adipocytes by repressing
PPAR-gamma.*
Picard F, Kurtev M, Chung N, Topark-Ngarm A, Senawong T, Machado De Oliveira
R, Leid M, McBurney MW, Guarente L.
Department of Biology, Massachusetts Institute of Technology, Cambridge, MA
02139
…
Here we show that the mammalian SIR2 orthologue, Sirt1 (sirtuin 1),
activates a critical component of calorie restriction in mammals; that is,
fat mobilization in white adipocytes. Upon food withdrawal Sirt1 protein
binds to and represses genes controlled by the fat regulator PPAR-gamma
(peroxisome proliferator-activated receptor-gamma), including genes
mediating fat storage. Sirt1 represses PPAR-gamma by docking with its
cofactors NCoR (nuclear receptor co-repressor) and SMRT (silencing mediator
of retinoid and thyroid hormone receptors). Mobilization of fatty acids from
white adipocytes upon fasting is compromised in Sirt1+/- mice. Repression of
PPAR-gamma by Sirt1 is also evident in 3T3-L1 adipocytes, where
overexpression of Sirt1 attenuates adipogenesis, and RNA interference of
Sirt1 enhances it. In differentiated fat cells, upregulation of Sirt1
triggers lipolysis and loss of fat. As a reduction in fat is sufficient to
extend murine lifespan, our results provide a possible molecular pathway
connecting calorie restriction to life extension in mammals.
PMID: 15175761
Along with the blocking of the PPAR-gamma fat forming complex. desaturase
and elongase enzymes are downregulated, which makes sense since the body
shifts from fat storage and processing mode to fat burning to compensate for
the low energy availability of calorie restriction.
In the unpublished study we created, this was acutely observed when nearly
everyone reported very low levels of long chain fatty acids.
I hope this is helpful. Back to the topic though, psyllium needs a lot of liquid with it to work well and pomegranate juice is just too high to probably be a healthy match up. Another, possibly more effective way to activate peristalsis, control glucose and enjoy some nutrient dense foods to boot is to enjoy some blueberries – say 80 grams with a generous amount of almond milk , a few walnuts if you like possibly some wild rice and then go on a vigorous walk for around 45 minutes. Add some crunches if you feel energetic. You will like your glucose reading at the end of the walk and we now know that keeping glucose low is essential to activating the longevity biochemistry seen in CR’d animals.
Wishing you extraordinary health,
Paul