Prev: Delta6-Desaturase (FADS2) deficiency unveils the role of omega3- and omega6-polyunsaturated fatty acids.
Next: Delta6-Desaturase (FADS2) deficiency unveils the role of omega3-and omega6-polyunsaturated fatty acids.
From: ironjustice on 11 Aug 2008 11:55
Across the industrialized world, women still live 5 to 10 years longer
than men. Among people over 100 years old, 85% are women, according to
Tom Perls, founder of the New England Centenarian Study at Boston
University and creator of the website LivingTo100.com. Time.com asks
him why.

Why Do Women Outlive Men?
Tom Perls, an aging expert at Boston University, explains why women
live five to 10 years longer than men
Q: Why do women live longer than men?

A: One important reason is the big delay — and advantage — women have
over men in terms of cardiovascular disease, like heart attack and
stroke. Women develop these problems usually in their 70s and 80s,
about 10 years later than men, who develop them in their 50s and 60s.
For a long time, doctors thought the difference was due to estrogen.
But studies have shown that this may not be the case, and now we know
that giving estrogen to women post-menopause can actually be bad for
them.

One reason for that delay in onset of cardiovascular disease could be
that women are relatively iron-deficient compared to men — especially
younger women, those in their late teens and early 20s — because of
menstruation. Iron plays a very important part in the reactions in our
cells that produce damaging free radicals, which glom onto cell
membranes and DNA, and may translate into aging the cell. In fact, in
our diets, red meat is the main source of iron, and lack of iron is
probably one major reason that being vegetarian is healthy for you.
There was a very good study looking at the intake of red meat and
heart disease in Leiden in the Netherlands: in regions where people
didn't eat red meat, those populations had half the rate of heart
attack and stroke compared to the populations that did eat red meat.

Another more complicated possibility [for women's longevity] is that
women have two X chromosomes, while men have one. (Men have an X and a
Y.) When cells go through aging and damage, they have a choice in
terms of genes — either on one X chromosome or the other. Consider it
this way: you have a population of cells, all aging together. In some
cells, the genes on one X chromosome are active; in other cells, by
chance, the same set of genes, with different variations, are active
on the other X chromosome. Don't forget, we all have the same genes —
the reason we differ is because we express different variations of
those genes, like different colors of a car. Now, if one set of
variations provides a survival advantage for the cells versus another,
then the cells with the advantage will persist while the other ones
will die off, leaving behind more cells with the genes on the more
advantageous X chromosome. So, in women, cells can perhaps be
protected by a slightly better variation of a gene on the second X
chromosome. Men don't have this luxury and don't get this choice.

It's very unclear [how big an effect that could have]. I've seen men
who have done horrendous damage to themselves over time with smoking
and drinking and who still get to 100 and older — though that's very,
very rare. They might have the right combination of some really
special genetic variations that we call "longevity enabling genes" —
which we're on the mad hunt for. Meanwhile other individuals may do
everything right and only make it into their 80s. That may be because
they have what we call "disease genes," some genetic variations that
are relatively bad for them. Now some of these [disease genes] may be
on the X chromosome, [meaning that women who have the second X
chromosome with which to compensate, would have an advantage]. But
it's really still a very complicated puzzle to tease out.

[There are a few other reasons that men die earlier in life more often
than women.] Men in their late teens and 20s go through something
called "testosterone storm." The levels of the hormone can be quite
high and changeable, and that can induce some pretty dangerous
behavior among young men. They don't wear their seatbelts; they drink
too much alcohol; they can be aggressive with weapons and so on and so
forth. These behaviors lead to a higher death rate.

Another area where we see higher death rates among men is among the
depressed — especially older men. If they attempt suicide, they are
more likely to succeed than women.

Overall, about 70% of the variation around average life expectancy —
[just over 80 for women and just over 75 for men in the U.S.] — is
probably attributable to environmental factors — your behaviors and
your exposures. Probably only 30% is due to genetics. And that's very,
very good news. There's so much we can do. Most of us should be able
to get into our late 80s. What's more, to get to older ages, like the
centenarians, you are necessarily compressing the time you're sick to
the end of your life. It's not a case where the older you get, the
sicker you get. It's very much the case that the older you get, the
healthier you've been.

But, in general, there are maybe three things men do worse than women.
They smoke a lot more. (That gender gap is fortunately shrinking,
since men are smoking less and less.) They eat more food that leads to
high cholesterol. And, perhaps related to that, men tend not to deal
with their stress as well as women. They may be more prone to
internalizing that stress rather than letting go — though that's a
fairly controversial point. Nonetheless, stress plays a very important
role in cardiovascular disease.


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/4rq595


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk




.
From: jay on 11 Aug 2008 14:20
> Why Do Women Outlive Men?
> A: One important reason is the big delay — and advantage — women
> One reason for that delay in onset of cardiovascular disease could be
> that women are relatively iron-deficient compared to men — especially
> younger women, those in their late teens and early 20s — because of
> menstruation. Iron plays a very important part in the reactions in our
> cells that produce damaging free radicals, which glom onto cell
> membranes and DNA, and may translate into aging the cell. In fact, in
> our diets, red meat is the main source of iron, and lack of iron is
> probably one major reason that being vegetarian is healthy for you.

Another factor that affects cellular iron, ROS and DNA damage is
inappropriate activation of Aryl Hydrocarbon Receptor (AhR) Mediated
Pathways. Persistent Organic Pollutants (POPs), combusted carbon-based
matter, etc are strong activators which result in production of iron-
utilizing enzymes. AhR activatord are frequently lipophilic. TCDD, a
dixon, found in the fat of many living things is most potent activator
of AhR-mediated pathways.

1) Human get most of their POPs via dietary animal fat. Men tend to
eat more fat.
2) Women menstruate and breast feed, both of which reduce POP levels.


Factors influencing the induction of DNA single strand breaks in rats
by TCDD.
The ability of TCDD to induce lipid peroxidation and DNA damage in rat
hepatic nuclei was investigated. In addition, the role of iron in
hepatic DNA damage was examined. Female Sprague-Dawley rats were
treated with a single dose of 25--100 micrograms TCDD/kg orally, and
sacrificed 3-14 days after treatment. Liver nuclei were isolated, and
DNA single strand breaks (DNA-SSB) and lipid peroxidation were
determined. Lipid peroxidation was assessed by measuring the content
and production of thiobarbituric acid reactive substances (TBARS)
while DNA-SSB were determined by the alkaline elution technique. The
results demonstrate that TCDD dose and time-dependent increases in
hepatic nuclear TBARS content and production occur in conjunction with
an increase in DNA-SSB. The administration of the dithiolthione
antioxidant oltipraz (30 mg/kg/day for 10 days) resulted in a
significant decrease (47%) in the incidence of TCDD-induced DNA-SSB.
Clofibrate administration (100 mg/kg/day for 12 days) and pair feeding
had no effect on TCDD-induced DNA-SSB. The incubation of hepatic
microsomes and mitochondria from TCDD-treated rats with nuclei from
untreated animals for one hr at 37 degrees C resulted in enhanced DNA
damage which was abolished by the addition of 0.10 mM desferrioxamine
(DFX). Incubation with cytosol had no significant effect. Incubation
of 0.10 mM Fe2+ or Fe3+ with isolated hepatic nuclei from untreated
rats produced significant increases in DNA-SSB, which were abolished
by the addition of 0.10 mM DFX to the incubation medium. TCDD may
produce an increased bioavailability of iron which leads to enhanced
DNA single strand breaks and lipid peroxidation in hepatic nuclei.
PMID: 2554534


Glutathione redox state regulates mitochondrial reactive oxygen
production.
... These results suggest that TCDD produces an AHR-dependent
oxidative stress in mitochondria, with concomitant mitochondrial DNA
damage mediated, at least in part, by an increase in the mitochondrial
thiol reduction state. PMID: 15883162

Comments on the history and importance of aromatic and heterocyclic
amines in public health.
The carcinogenic risk of aromatic amines in humans was first
discovered when a physician related the occurrence of urinary bladder
cancer to the occupation of his patients. They were employed in the
dyestuff industry, chronically exposed to large amounts of
intermediate arylamines. Laboratory investigations disclosed that rats
and mice administered specific azo dyes arylamines or derivatives
developed cancer, primarily in the liver. Also, at that time, a
possible pesticide, 2-aminofluorene, was tested for chronic toxicity,
revealing that it rapidly induced cancers in several organs of
rodents. This led to investigations on the mode of action of this
class of chemicals, including their metabolic conversion. Biochemical
activation to more reactive N-hydroxy compounds was found to occur,
mostly in the liver, through what is now known as the cytochrome p450
enzyme systems, and also through prostaglandin synthetases. There were
species differences. Guinea pigs were resistant to carcinogenesis
because of the low titer of the necessary activating enzymes. In
target tissues, a second essential reaction was necessary, namely
acylation or sulfate ester formation. The reactive compounds produced
display attributes of genotoxicity in appropriate test systems.
Interest in this class of compounds increased when of Sugimura and
colleagues discovered the formation of mutagens at the surface of
cooked meat or fish, that were identified as heterocyclic amines
(HCAs). These compounds undergo the same type of activation reactions,
as do other arylamines. Epidemiological data suggest that meat eaters
may have a higher risk of breast and colon cancer. HCAs induced cancer
in rats in these organs and also in the prostate and the pancreas. In
addition, there is some evidence that they affect the vascular system.
The formation of HCAs during cooking can be decreased by natural and
synthetic antioxidants, by tryptophan or proline, or by removing the
essential creatine through brief microwave cooking prior to frying or
broiling. The amounts of HCAs in cooked foods are small, but other
components in diet such as omega-6-polyunsaturated oils have powerful
promoting effects in target organs of HCAs. On the other hand, the
action of HCAs may be decreased by foods containing antioxidants, such
as vegetables, soy, and tea. Some constituents in foods also induce
phase II enzymes that detoxify reactive HCA metabolites. Additional
mechanisms involved decreased growth of neoplasms by intake of
protective foods. Possibly, the carcinogenic effect of HCAs is
accompanied by the presence of reactive oxygen species (ROS), which
are also inhibited by antioxidants. World-wide, there have been many
contributors to knowledge in this field. Adequate information may
permit now to adjust lifestyle and lower the risk of human disease
stemming from this entire class of aryl and HCA. PMID: 12351140
From: ironjustice on 11 Aug 2008 18:06
On Aug 11, 11:20 am, jay <jaym1...(a)hotmail.com> wrote: snip <<

Well Tom Perls, founder of the New England Centenarian Study at
Boston
University didn't think your . hypothesis was .. or .. held enough
water to mention .. you should write to him .. and tell him about the
iron and HOW .. **you** believe it gets there .. ?

Have you done that .. ?
I see you had enough time to post to a .. loons' .. thread .. eh ..
jay ..

Did you write to .. Tom Perls, founder of the New England Centenarian
Study at Boston University .. ?

I'm beginning to think you are that .. follower .. I've been warned
about ..

That .. follower ..

Heh .. heh ..


Who loves ya.
Tom


Jesus Was A Vegetarian!
http://tinyurl.com/2r2nkh


Man Is A Herbivore!
http://tinyurl.com/4rq595


DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk





> > Why Do Women Outlive Men?
> > A: One important reason is the big delay — and advantage — women
> > One reason for that delay in onset of cardiovascular disease could be
> > that women are relativelyiron-deficient compared to men — especially
> > younger women, those in their late teens and early 20s — because of
> > menstruation.Ironplays a very important part in the reactions in our
> > cells that produce damaging free radicals, which glom onto cell
> > membranes and DNA, and may translate into aging the cell. In fact, in
> > our diets, red meat is the main source ofiron, and lack ofironis
> > probably one major reason that beingvegetarianis healthy for you.
>
> Another factor that affects cellulariron, ROS and DNA damage is
> inappropriate activation of Aryl Hydrocarbon Receptor (AhR) Mediated
> Pathways. Persistent Organic Pollutants (POPs), combusted carbon-based
> matter, etc are strong activators which result in production ofiron-
> utilizing enzymes. AhR activatord are frequently lipophilic. TCDD, a
> dixon, found in the fat of many living things is most potent activator
> of AhR-mediated pathways.
>
> 1) Human get most of their POPs via dietary animal fat. Men tend to
> eat more fat.
> 2) Women menstruate and breast feed, both of which reduce POP levels.
>
> Factors influencing the induction of DNA single strand breaks in rats
> by TCDD.
> The ability of TCDD to induce lipid peroxidation and DNA damage in rat
> hepatic nuclei was investigated. In addition, the role ofironin
> hepatic DNA damage was examined. Female Sprague-Dawley rats were
> treated with a single dose of 25--100 micrograms TCDD/kg orally, and
> sacrificed 3-14 days after treatment. Liver nuclei were isolated, and
> DNA single strand breaks (DNA-SSB) and lipid peroxidation were
> determined. Lipid peroxidation was assessed by measuring the content
> and production of thiobarbituric acid reactive substances (TBARS)
> while DNA-SSB were determined by the alkaline elution technique. The
> results demonstrate that TCDD dose and time-dependent increases in
> hepatic nuclear TBARS content and production occur in conjunction with
> an increase in DNA-SSB. The administration of the dithiolthione
> antioxidant oltipraz (30 mg/kg/day for 10 days) resulted in a
> significant decrease (47%) in the incidence of TCDD-induced DNA-SSB.
> Clofibrate administration (100 mg/kg/day for 12 days) and pair feeding
> had no effect on TCDD-induced DNA-SSB. The incubation of hepatic
> microsomes and mitochondria from TCDD-treated rats with nuclei from
> untreated animals for one hr at 37 degrees C resulted in enhanced DNA
> damage which was abolished by the addition of 0.10 mM desferrioxamine
> (DFX). Incubation with cytosol had no significant effect. Incubation
> of 0.10 mM Fe2+ or Fe3+ with isolated hepatic nuclei from untreated
> rats produced significant increases in DNA-SSB, which were abolished
> by the addition of 0.10 mM DFX to the incubation medium. TCDD may
> produce an increased bioavailability ofironwhich leads to enhanced
> DNA single strand breaks and lipid peroxidation in hepatic nuclei.
> PMID: 2554534
>
> Glutathione redox state regulates mitochondrial reactive oxygen
> production.
> ... These results suggest that TCDD produces an AHR-dependent
> oxidative stress in mitochondria, with concomitant mitochondrial DNA
> damage mediated, at least in part, by an increase in the mitochondrial
> thiol reduction state. PMID: 15883162
>
> Comments on the history and importance of aromatic and heterocyclic
> amines in public health.
> The carcinogenic risk of aromatic amines in humans was first
> discovered when a physician related the occurrence of urinary bladder
> cancer to the occupation of his patients. They were employed in the
> dyestuff industry, chronically exposed to large amounts of
> intermediate arylamines. Laboratory investigations disclosed that rats
> and mice administered specific azo dyes arylamines or derivatives
> developed cancer, primarily in the liver. Also, at that time, a
> possible pesticide, 2-aminofluorene, was tested for chronic toxicity,
> revealing that it rapidly induced cancers in several organs of
> rodents. This led to investigations on the mode of action of this
> class of chemicals, including their metabolic conversion. Biochemical
> activation to more reactive N-hydroxy compounds was found to occur,
> mostly in the liver, through what is now known as the cytochrome p450
> enzyme systems, and also through prostaglandin synthetases. There were
> species differences. Guinea pigs were resistant to carcinogenesis
> because of the low titer of the necessary activating enzymes. In
> target tissues, a second essential reaction was necessary, namely
> acylation or sulfate ester formation. The reactive compounds produced
> display attributes of genotoxicity in appropriate test systems.
> Interest in this class of compounds increased when of Sugimura and
> colleagues discovered the formation of mutagens at the surface of
> cooked meat or fish, that were identified as heterocyclic amines
> (HCAs). These compounds undergo the same type of activation reactions,
> as do other arylamines. Epidemiological data suggest that meat eaters
> may have a higher risk of breast and colon cancer. HCAs induced cancer
> in rats in these organs and also in the prostate and the pancreas. In
> addition, there is some evidence that they affect the vascular system.
> The formation of HCAs during cooking can be decreased by natural and
> synthetic antioxidants, by tryptophan or proline, or by removing the
> essential creatine through brief microwave cooking prior to frying or
> broiling. The amounts of HCAs in cooked foods are small, but other
> components in diet such as omega-6-polyunsaturated oils have powerful
> promoting effects in target organs of HCAs. On the other hand, the
> action of HCAs may be decreased by foods containing antioxidants, such
> as vegetables, soy, and tea. Some constituents in foods also induce
> phase II enzymes that detoxify reactive HCA metabolites. Additional
> mechanisms involved decreased growth of neoplasms by intake of
> protective foods. Possibly, the carcinogenic effect of HCAs is
> accompanied by the presence of reactive oxygen species (ROS), which
> are also inhibited by antioxidants. World-wide, there have been many
> contributors to knowledge in this field. Adequate information may
> permit now to adjust lifestyle and lower the risk of human disease
> stemming from this entire class of aryl and HCA. PMID: 12351140

From: Laurie on 14 Aug 2008 14:11
ironjustice wrote:
> that women are relatively iron-deficient compared to men �
> especially younger women, those in their late teens and early 20s �
> because of menstruation.
Nonsense!
Try a little arithmetic and actually calculate the amount of Fe
"lost" during men-stru-ation.
http://ecologos.org/menses.htm

> Jesus Was A Vegetarian! http://tinyurl.com/2r2nkh
Nonsense!
Jesus was, and still IS, our Sun and its trajectory.
http://www.youtube.com/watch?v=sEMxx8S8s_U
http://www.youtube.com/watch?v=WwzDFvqfcdc
http://www.youtube.com/watch?v=gAuR8T6HNC4&amp;feature=related

> Man Is A Herbivore! http://tinyurl.com/4rq595
More nonsense!
http://ecologos.org/anatomy.htm

We are frugivorous apes
http://www.gate.net/%7Erwms/primegendist.html
http://ecologos.org/pix/Health/chimpdiet.xls

Laurie

--
Scientifically-credible info on plant-based human diets:
http://ecologos.org/ttdd.html
news:alt.food.vegan.science




From: AndyS on 15 Aug 2008 09:19
Please stop your crossposting....

The newsgroup that I am on does not bother with whackos.........

If you have something useful to contribute about issues,
then I'm sure everyone here would be interested.

Andy in Eureka, Texas
 |  Next  |  Last
Pages: 1 2
Prev: Delta6-Desaturase (FADS2) deficiency unveils the role of omega3- and omega6-polyunsaturated fatty acids.
Next: Delta6-Desaturase (FADS2) deficiency unveils the role of omega3-and omega6-polyunsaturated fatty acids.