B1 derivative protects against diabetes complications
JXStern
In study, drug blocks diabetes complications
By Anita Manning, USA TODAY
WASHINGTON — A prescription medicine used in Germany to treat sciatica
and other nerve problems may be a key to preventing blindness, limb
loss and other devastating complications of diabetes, researchers
report Monday in Nature Medicine.
The drug, benfotiamine, is a synthetic derivative of thiamine, or
vitamin B1, says lead researcher Michael Brownlee of the Albert
Einstein College of Medicine. In studies involving diabetic rats, it
was found to enhance activity of an enzyme that stops high glucose
from damaging blood vessels.
Thiamine has been known to give a 20% boost to the enzyme, but
benfotiamine is more easily absorbed and therefore is "much more
efficient," Brownlee says. Enzyme action increased 300% to 400% and
was "completely unexpected," he says.
...
J.
None
We should be able to import this...
"JXStern" <JXSternC...@gte.net> wrote in message
news:ace05vsilpifhc6uu...@4ax.com...
> http://www.usatoday.com/news/health/2003-02-16-diabetes_x.htm
>
> In study, drug blocks diabetes complications
> By Anita Manning, USA TODAY
>
> WASHINGTON - A prescription medicine used in Germany to treat sciatica
JXStern
>So how will this help P?
Dunno. Hope someone thinks to find out.
Thought evetsm might want to see it.
J.
Randall
> So how will this help P?
Hi,
It may be a help to diabetic psoriatics. After some of
them use it for awhile i would like to hear their feedback.
Julie Bove and others have been a great help in this
regard.
And since its anti ROS more then a few of the rest
of us would benefit if there are no other side effects.
And what if some marginal dose of this stuff
slows down loss of eyesight?
We still want to see if we have P as we get older
don't we?
BENFOTIAMIN PREVENTS THE CONSEQUENCES OF HYPERGLYCEMIA-INDUCED MITOCHONDRIAL
OVERPRODUCTION OF REACTIVE OXYGEN SPECIES, AND EXPERIMENTAL DIABETIC
RETINOPATHY
http://www.easd.org/37th/Abs01/148.html
Furthermore, if i ever do bumP into evetsm i want to
check out his seb derm in great detail. Unless his
NAC regime has cleared him beyond all recognition these
days.
BTW, where is he? With the semi vindication of Atkins
you'd think he would be living the vida loca and not
licking his wounds.
randall
evetsm
> "None" <nos...@hell.com> wrote in message news:<Jnd4a.15295$Yv2....@nwrddc02.gnilink.net>...
> > So how will this help P?
>
> Hi,
>
> It may be a help to diabetic psoriatics. After some of
> them use it for awhile i would like to hear their feedback.
>
> Julie Bove and others have been a great help in this
> regard.
>
> And since its anti ROS more then a few of the rest
> of us would benefit if there are no other side effects.
I am still around. I have had my seb derm head inside some free
radical reading lately. This could be of the subversive type, and
would not be the first time I have been accused of being a free
radical. Man, the more I read about oxidative damage the more I am
seeing a common thread to many of these so-called "modern" diseases.
Diabetes and glycation or oxidation of glucose, psoriasis and seb derm
characterised by lipid peroxidation and low levels of antioxidants,
heart disease ditto, cystic fibrosis, parkinson's, possibly
alzheimers, Chronic fatigue, AIDS, cancer. They all have marked free
radical involvement. The connundrum, as always, is cause and effect.
But more and more studies are showing amelioration or reversal of many
of these diseases with heavy antioxidant supplementation and
importantly with BOTH water and fat soluble antioxidants based
primarily on Ascorbic acid (accept no substitutes) d-alpha tocopherol
(natural vit E). AND of course, very important IMO, low carb to
prevent those glycation oxidizing glucose spikes.
My seb derm is very much under control. Still using NACysteine, Alpha
Lipoic acid (both are thiols that seem crucial), added split dose of
6g ascorbic acid per day, 2000 IU E (heavy man , heavy), and I found a
herb(berry) called shizendra that has powerful antioxidant and liver
regenerating properties. Also take some tumeric now and then
(carotinoids (sp?)). If I drop dead right now, I'd at least be
embalmed :)
Absolutely got to reduce that oxidation load.
Is the essential difference between a paleolithic and a modern
lifestyle the difference in the oxidative stress ? I am starting to
believe it.
Randall
> ranh...@aol.com (Randall) wrote in message news:<df7e2c67.03021...@posting.google.com>...
> > "None" <nos...@hell.com> wrote in message news:<Jnd4a.15295$Yv2....@nwrddc02.gnilink.net>...
> >
> > And since its anti ROS more then a few of the rest
> > of us would benefit if there are no other side effects.
>
>
> I am still around. I have had my seb derm head inside some free
> radical reading lately.
Free rads aren't. They come at an expense somewhere down the line.
If we can limit it to the mitochondrial germs and O we'd be
looking pretty good.
> This could be of the subversive type, and
> would not be the first time I have been accused of being a free
> radical. Man, the more I read about oxidative damage the more I am
> seeing a common thread to many of these so-called "modern" diseases.
From one free rad to the next, stick this one in your noodle,
Another IMID condition with to MUCH SOD and GPx.
This runs counterintuitive to my whey of thinking, concerning
the IMIDs in general.
Hows that sherlock? To much of anything can cause things to
go awry. Even H2O begs for some diuretics at times.
>
> Diabetes and glycation or oxidation of glucose, psoriasis and seb derm
> characterised by lipid peroxidation and low levels of antioxidants,
> heart disease ditto, cystic fibrosis, parkinson's, possibly
> alzheimers, Chronic fatigue, AIDS, cancer. They all have marked free
> radical involvement. The connundrum, as always, is cause and effect.
Which pathway is skewing what is more like it.
I came into this group believing that Delta 6 desaturase was
downregulated and Delta 5 D. upregulated by sugar and
that led to PGE 2's doing their funky business of making
arachidonic acids (AA)and eicosanoids et al, that led to inflammation
being
the supreme factor in psoriasis. So all i had to
do was some version of atkins and i'd clear like
crazy provided i took out the bad oils/fats and increased
the good ones.
Was that the key?
Here is a link to what your doing and what i was
ruminating on,
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12068073&dopt=Abstract
Untill i read the xoma.pdf link that Jstern posted
i would have rated the above factors a little higher then
i do now.
I fooled around with increasing my good flora for
years that led me to believe that most ND's, chiro's
and alts were full of beans as to the leaky gut
syndrome and bad bacteria and that rigmarole.
Consequently, i took huge amounts of antioxidants,
to attempt to overcome the free rads doing their
nasty business and making my psoriasis worse.
Nice to know we shared that common delusion.
NOt that it isn't easily arrived at.
NONE of these treatments panned out and led me
back to optimizing the organs that may lead to p.
How does one make the liver work better?
If its fouled by gut permeability then the
large intestine is the culprit, providing that
there are no other discernible culprits.
How much crud gets into us? Is it due to some
thing else? Is the gut leaking or just permeable?
Are all IMIDs affected by it, to the extent
that most are due to the downregulation of
the GPx and the SOD?
I did take a ton of selenium for SOD that led
nowhere. Didn't clear a thing on my hide.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12571418&dopt=Abstract
(click on the "related articles" for a bunch more if
you don't believe this abstract")
Here's another using caco with gut permeability in the
pubmed search. And use the related articles click on
to view many more on this topic. Its in the upper
right hand corner of the abstract. The link out
click on is another good tool for researchers like
you. If you find one good russian abstract you
can compare it to the rest of the scientific world
with one little click!
I posted many times to our p newsgroup on the
Caco 2 gut link! Is it one more chink in our armor?
> But more and more studies are showing amelioration or reversal of many
> of these diseases with heavy antioxidant supplementation and
> importantly with BOTH water and fat soluble antioxidants based
> primarily on Ascorbic acid (accept no substitutes) d-alpha tocopherol
> (natural vit E). AND of course, very important IMO, low carb to
> prevent those glycation oxidizing glucose spikes.
Wait a minute. Taking out the white sugar and flour helps
but isn't the be all end all any more then swallowing a ton
of antioxidants to upregulate SOD and GPx. Recall the
down syndrome folks in the first abstract above.
They have to much of that GOOD stuff.
Unskewing the immune system due to the translocation
of endogenous bacteria (LPS) is the only whey to
achieve homeostasis in my psoriasis paradigm.
Sure i can cheat/eat my forbidden foods that
previously flared me uncontrollably.
Those delicious foods lead back to psoriatic flares
eventually, albeit a lot slower. Without the good flora
blocking the "translocation of endogenous bacteria (LPS)"
the flares haPPen in less then a few days in my case.
>
>
> My seb derm is very much under control.
Wait a minute. I need better demographics then this.
How much better percent wise and from what level of
coverages?
> Still using NACysteine, Alpha
> Lipoic acid (both are thiols that seem crucial), added split dose of
> 6g ascorbic acid per day, 2000 IU E (heavy man , heavy), and I found a
> herb(berry) called shizendra that has powerful antioxidant and liver
> regenerating properties. Also take some tumeric now and then
> (carotinoids (sp?)). If I drop dead right now, I'd at least be
> embalmed :)
Schizandra lowers the anger fire in the kidneys! Mucho good
for your liver and immune system. Now if we could only figure
out what the heck the Ch'i (Qi, chi) really really is.
If it isn't the free electrons from hydrogen ions fame in
the meridians then it MUST be the memory of hydrogen ions
in those human rivers of life. ;) lol
Certainly to refined for my mind to say the least.
I do have a theory or two! Yep, you stePPed in it!
Curcumin, ginger, greentea, NAC, Flax seed oil, sesame
seeds and many many more can be used to block those
PPAR's quite successfully in my usage of them.
There is something almost magical in the use of whole
foods as a defense in the war against inflammation.
Even elegant when those same foods taste good and
are easily incorporated into your lifestyle without to
much trouble.
Time to grab some thyme and sage outa my garden
to add to the greentea with sliced ginger. yummmmO!
Or how about rosemary?
As to vitamin C, be carefull to not upregulate
iron. It feeds the colon denizens and i feel that
with whatever levels of bad bacteria that leads
to seb derm and p any levels of iron above
normal accelerates the conditions.
Driving down the road with your foot on the
gas and brakes again.
Swill down the C water between meals and at
least two hours of leeway on both sides.
And if it where me, i'd drop down to
3 grams and then 2 in a week or so and
then 1. That should be enough.
And what about to much protein? That is an
akins problem, right? And not corrected with vitamins
either.
And don't forget to add in the tremendous effects
of PRAL in YOUR equations. Its a biggy for psoriasis,
If calcium ways in to your situation as much as ours,
then you can't not have to figure out
those pathways and the whys. Especially in regards
to NO and the skewed immune factors.
>
> Absolutely got to reduce that oxidation load.
Yes, and thru the manipulation of all the inflammatory
pathways makes the most sense. Hint- you were on to something
with the PPAR's. I just couldn't get you to focus on
them. I tried untill i tired out on that vein.
Shall we revisit them?
>
> Is the essential difference between a paleolithic and a modern
> lifestyle the difference in the oxidative stress ? I am starting to
> believe it.
Yes. Funky comfort foods designed to prevent spoilage
and increase shelf life aren't really all that convenient
if your interests are for less inflammation and a longer
life filled with quality and quantity.
In your case i would avoid all extraneous thinking as that
has a tendency to require huge amounts of brain sugars
where most of it ends uP pondering the cure of our
conundrums. Cravings can be the fires that drive
the desires that leads to inflammatory pyres.
Well sort of.
HoPe does sPring infernal at times.
randall
evetsm
The key seems to be a cocktail of different fat and water soluble
antioxidants for optimal oxidation protection and enough of them to
put a blanket over the fire. To little and you probably only get
antioxdants donating electrons to free rads and themselves(the
antioxidants) becoming unquenchd free rads(pro-oxidants). Enough and
variety(since different antioxidants regenerate each other eg E and C)
is a good starting point. Of course the body uses oxidation as one of
the first line antimicrobial defenses(MPO enzymes in the neutrophils),
so we have mechanisms destructive to the body used to protect the
body. Talk about dying to live ! The assumption (so far) is that
antioxidants protect the body without disabling the oxidation defense
mechanism. Or at least I hope so !
Antioxidative effects of turmeric, rosemary and capsicum extracts on
membrane phospholipid peroxidation and liver lipid metabolism in mice.
Asai A, Nakagawa K, Miyazawa T.
Laboratory of Biodynamic Chemistry, Tohoku University Graduate School
of Agriculture, Sendai, Japan. as...@biochem.tohoku.ac.jp
Phospholipid hydroperoxides (PLOOH) in the plasma, red blood cells
(RBC) and liver of mice were measured after dietary supplementation
for one week (1% w/w of diet) with a turmeric extract (curcuminoid),
hexane extract of rosemary, and supercritical CO2-extracted capsicum
pigment (supplemented with alpha-tocopherol to prevent fading). A
lower PLOOH level was found in RBC of the spice extract-fed mice
(65-74% of the non-supplemented control mice). The liver lipid
peroxidizability induced with Fe2+/ascorbic acid was effectively
suppressed by dietary supplementation with the turmeric and capsicum
extracts to mice. While no difference in the plasma lipids was
observed, the liver triacylglycerol concentration of the turmeric
extract-fed mice was markedly reduced to one-half of the level in the
control mice. These findings suggest that these spice extracts could
act antioxidatively in vivo by food supplementation, and that the
turmeric extract has the ability to prevent the deposition of
triacylglycerols in the liver.
evetsm
by some phytochemicals
---------------------------------------------------------------------------
Effects of three dietary phytochemicals from tea, rosemary and
turmeric on inflammation-induced nitrite production.
Chan MM, Ho CT, Huang HI.
Department of Biological Sciences, Rutgers, State University of New
Jersey, Piscataway 08855-1059, USA.
In chronic inflammation, cytokines induce the production of nitric
oxide (NO.) that is converted to DNA damaging and carcinogenic
peroxynitrite and nitrite. The compounds epigallocatechin gallate
(EGCG), carnosol, and curcumin are non-vitamin phytochemicals
contained in commonly consumed dietary plants. They are known to be
anti-inflammatory and cancer preventive. Therefore, we studied their
effect on the generation of peroxynitrite radicals and nitrite. They
inhibited lipopolysaccharide (LPS) and interferon-gamma (IFN gamma)
induced nitrite production by mouse peritoneal cells by more than 50%
at 2.5-10 microM. Cell viability assays verified that the inhibition
was not due to general cellular toxicity.
PMID: 7553604 [PubMed - indexed for MEDLINE]
Randall
Hi,
Hi,
So if your taking some vitamins, do you think/feel they will help
when your 92?
Antioxidant Vitamin Intake and Risk of Alzheimer Disease
Jose A. Luchsinger, MD; Ming-Xin Tang, PhD; Steven Shea, MD; Richard
Mayeux, MD
Background The generation of oxygen free radicals is involved in the
pathogenesis of Alzheimer disease (AD).
Objective To determine whether the intake of antioxidant vitamins
decreases the risk of AD.
Methods We investigated the relationship between AD and the intake of
carotenes, vitamin C, and vitamin E in 980 elderly subjects in the
Washington Heights-Inwood Columbia Aging Project who were free of
dementia at baseline and were followed for a mean time of 4 years.
Semiquantitative food frequency questionnaires were administered
between baseline and the first follow-up visit. Cox proportional
hazards regression models were conducted with quartiles of each
vitamin intake as the exposure of interest and incident AD as the
outcome, adjusted for age, level of education, sex, APOE 4 status,
ethnicity, and smoking.
Results There were 242 incident cases of AD in 4023 person-years of
follow-up (6 per 100 person-years). Intake of carotenes and vitamin C,
or vitamin E in supplemental or dietary (nonsupplemental) form or in
both forms, was not related to a decreased risk of AD. Trend tests for
the association between quartiles of total intake of vitamins C and E
also were not significant.
Conclusion Neither dietary, supplemental, nor total intake of
carotenes and vitamins C and E was associated with a decreased risk of
AD in this study.
Arch Neurol. 2003;60:203-208
^^^^^^^^^^^
Those vitamins didn't help much, now did they?
How about if you drink/eat fresh grapefruit every day?
They should be healthy huh?
Then again maybe not. They sure can start a fire on my hide.
So, lets drop the vitamins and foods that sound groovy and
look at the NO pathway and what happens with LPS
being absorded from your large intestine.
You can take loads of things for all the free radicals from LPS,
but wouldn't it be better to stop it from getting thru the natural
barriers to begin with?
Of course. Without stopping the LPS, the curse of P never stops
and thats a fact.
Can the NO keep us young forever with the LPS sneaking in?
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9951625&dopt=Abstract
The nitric oxide hypothesis of aging.
(and randalls P theory of it's only craP/LPS)
McCann SM, Licinio J, Wong ML, Yu WH, Karanth S, Rettorri V.
Pennington Biomedical Research Center (LSU), Baton Rouge 70808-4124,
USA. mcca...@mhs.pbrc.edu
Nitric oxide (NO), generated by endothelial (e) NO synthase (NOS) and
neuronal (n) NOS, plays a ubiquitous role in the body in controlling
the function of almost every, if not every, organ system. Bacterial
and viral products, such as bacterial lipopolysaccharide (LPS), induce
inducible (i) NOS synthesis that produces massive amounts of NO toxic
to the invading viruses and bacteria, but also host cells by
inactivation of enzymes leading to cell death. The actions of all
forms of NOS are mediated not only by the free radical oxidant
properties of this soluble gas, but also by its activation of
guanylate cyclase (GC), leading to the production of cyclic guanosine
monophosphate (cGMP) that mediates many of its physiological actions.
In addition, NO activates cyclooxygenase and lipoxygenase, leading to
the production of physiologically relevant quantities of prostaglandin
E2 (PGE2) and leukotrienes. In the case of iNOS, the massive release
of NO, PGE2, and leukotrienes produces toxic effects. Systemic
injection of LPS causes induction of interleukin (IL)-1 beta mRNA
followed by IL-beta synthesis that induces iNOS mRNA with a latency of
two and four hours, respectively, in the anterior pituitary and pineal
glands, meninges, and choroid plexus, regions outside the blood-brain
barrier, and shortly thereafter, in hypothalamic regions, such as the
temperature-regulating centers, paraventricular nucleus containing
releasing and inhibiting hormone neurons, and the arcuate nucleus, a
region containing these neurons and axons bound for the median
eminence. We are currently determining if LPS similarly activates
cytokine and iNOS production in the cardiovascular system and the
gonads. Our hypothesis is that recurrent infections over the life span
play a significant role in producing aging changes in all systems
outside the blood-brain barrier via release of toxic quantities of NO.
NO may be a major factor in the development of coronary heart disease
(CHD). Considerable evidence has accrued indicating a role for
infections in the induction of CHD and, indeed, patients treated with
a tetracycline derivative had 10 times less complications of CHD than
their controls. Stress, inflammation, and infection have all been
shown to cause induction of iNOS in rats, and it is likely that this
triad of events is very important in progression of coronary
arteriosclerosis leading to coronary occlusion. Aging of the anterior
pituitary and pineal with resultant decreased secretion of pituitary
hormones and the pineal hormone, melatonin, respectively, may be
caused by NO. The induction of iNOS in the temperature-regulating
centers by infections may cause the decreased febrile response in the
aged by loss of thermosensitive neurons. iNOS induction in the
paraventricular nucleus may cause the decreased nocturnal secretion of
growth hormone (GH) and prolactin that occurs with age, and its
induction in the arcuate nucleus may destroy luteinizing
hormone-releasing hormone (LHRH) neurons, thereby leading to decreased
release of gonadotropins. Recurrent infections may play a role in
aging of other parts of the brain, because there are increased numbers
of astrocytes expressing IL-1 beta throughout the brain in aged
patients. IL-1 and products of NO activity accumulate around the
plaques of Alzheimer's, and may play a role in the progression of the
disease. Early onset Parkinsonism following flu encephalitis during
World War I was possibly due to induction of iNOS in cells adjacent to
substantia nigra dopaminergic neurons leading to death of these cells,
which, coupled with ordinary aging fall out, led to Parkinsonism. The
central nervous system (CNS) pathology in AIDS patients bears striking
resemblance to aging changes, and may also be largely caused by the
action of iNOS. Antioxidants, such as melatonin, vitamin C, and
vitamin E, probably play an important acute and chronic role in
reducing or eliminating the oxidant damage produced by NO.
WOw, i don't know about you but i'm having a gonad/seminal moment.
Ok, its passed. :)
If NO is so ubiquitous whats it have to do with P?
This abstract ties LPS from the gut to your brains and nads!
All that NO, generated to fry the viri and bacteria, uPregulates
il1 and tnf and the rest is P history. And if you don't take heed
yours is shorten too.
Could those horny goat weed eaters be onto something?
NOw, how are we poised to eradicate the lps pests?
The current biologics deal with the effects by hooking uP with
TNF and interleukins etc. Wouldn't stoPPing the crap
in the guts (LPS) be the First Priority? The Prime objective?
What is "The Immune System's Dark Side"?
If we pig out on to much pig/meat do we end up needing
statins, aspirin and AGE's to repair the damage?
Just taking out the refined sugars and white flours helps
to square that equation for longer healthier life. But it
all tastes so good and the refined sugars help upload tryptophan/
amino acids into the brain for conversion to serotonin
and other brain opiates for feel good times. Are we being
snookered by our own comfort foods?
And why is it that we can't metabolize the fatty acids
properly? Who's at fault there? The diet and some
combo of nutrients that leads to pathways that cause
inflammation? Even if you subsist on a vegetarian/macrobiotic
diet that excludes most AA (arachidonic acid), that will not stop
the body from converting it outa some phosphatidyl choline
by way of the phospholipase A(2) enzyme.
BTW, phospholipase can be made from triglycerides
that come from carbohydrates. So whats so smart about
eating that way?
How do we get into a zone that benefits us the
2% of the population that doesn't want to be thought
of as whatever it is you think they think about us.
Whoops, almost forgot. You have seborrhea dermatitis huh?
Oh well it all pertains to both of us uP to a Point.
randall...
evetsm
get rid of the LPS ? Are they part of the system , even in healthy
people, but as long as your antioxidant defenses are intact they never
bother you, or have they set up residence in the system because the
immune system became compromised and why was that ? Bad diet ,
malabsorption or one leading to the other ? If bad diet is at the
root, then what is a good diet ? Surely we are back to the caveman ?
Any way, loading up on antioxidants cannot be a bad thing, if you are
already overloaded with oxidative stress. Next step is trying to get
at the root of this interminal loop.
Pre-existing oxidative stress looks like it comes before iron
oxidation, and we know where oxidised iron leads us. Eventually the
ATP disappears and you literally run out of energy. Chronic Fatigue
anyone ?
"Oxidative stress depletes adenosine triphosphate (ATP) and adenine
nucleotides"
"In the absence of efficient protection by antioxidant factors and
other molecules such as flavonoids, oxidative stress is responsible
for the release of iron in reactive form, predisposing red cells to
hemolysis through the formation of senescence antigen. Other
well-known sources of oxidative stress in red cells are free radical
production outside the red cell by activated phagocytes, endothelial
metabolism, hyperoxia, ischemia-reperfusion and the arachidonic acid
cascade."
------------------------------------------------------------------------
Oxidant injury in neonatal erythrocytes during the perinatal period.
Bracci R, Perrone S, Buonocore G.
Department of Pediatrics, Obstetrics and Reproductive Medicine,
University of Siena, Siena, Italy.
It has been known for many decades that oxidative stress leads to
oxidation of hemoglobin and damage to the erythrocyte membrane. More
recently, the factors involved in denaturating of membrane proteins
and lipid peroxidation have been investigated in detail, as well as
the mechanism of reactive oxygen species formation in red cells.
Oxidative stress depletes adenosine triphosphate (ATP) and adenine
nucleotides, whereas adenosine monophosphate (AMP) deaminase seems to
depress energy metabolism by blocking the salvage pathway of purine
nucleotides. Depletion of ATP and activation of AMP deaminase are
related to calcium ion concentrations. Denaturating of membrane
proteins generally precedes lipid peroxidation and consequent
phagocytosis due to caspase activation. Extensive investigations
demonstrated the key role of oxidative stress and iron release in a
reactive form causing membrane protein damage via the Fenton reaction
and hydroxyl radical production. In the absence of efficient
protection by antioxidant factors and other molecules such as
flavonoids, oxidative stress is responsible for the release of iron in
reactive form, predisposing red cells to hemolysis through the
formation of senescence antigen. Other well-known sources of oxidative
stress in red cells are free radical production outside the red cell
by activated phagocytes, endothelial metabolism, hyperoxia,
ischemia-reperfusion and the arachidonic acid cascade. CONCLUSION: The
recent insight into the mechanism of oxidative injury of red cells and
evidence of relationships between erythrocyte oxidative stress and
hypoxia suggest that increased hemolysis is induced by severe hypoxia
and acidosis in the fetus as well as the newborn.
--------------------------------------------------------------------
evetsm
and iron overload and oxidative disease.
PS : I do think that Atkins has either been misrepresented or may be
wrong on the amount of protein his diet is perceived to contain, and
the perceived lack of antioxidants or overload oxidative foods. I
don't agree that protein intake is limitless, fat intake should be
increased rather, also I don't believe that a meat only diet is
optimal for antioxidant intake and low carb greens, berries and nuts
serve ample antioxidants and I don't believe that Atkins oxidant laden
fried eggs, bacon, etc are any good at all. Adjust Atkins for these
factors and you pretty much have a caveman diet.
The paradoxical nature of hunter-gatherer diets: meat-based, yet
non-atherogenic.
Cordain L, Eaton SB, Miller JB, Mann N, Hill K.
Department of Health and Exercise Science, Colorado State University,
Fort Collins, Colorado, USA. cor...@cahs.colostate.edu
OBJECTIVE: Field studies of twentieth century hunter-gathers (HG)
showed them to be generally free of the signs and symptoms of
cardiovascular disease (CVD). Consequently, the characterization of HG
diets may have important implications in designing therapeutic diets
that reduce the risk for CVD in Westernized societies. Based upon
limited ethnographic data (n=58 HG societies) and a single
quantitative dietary study, it has been commonly inferred that
gathered plant foods provided the dominant energy source in HG diets.
METHOD AND RESULTS: In this review we have analyzed the 13 known
quantitative dietary studies of HG and demonstrate that animal food
actually provided the dominant (65%) energy source, while gathered
plant foods comprised the remainder (35%). This data is consistent
with a more recent, comprehensive review of the entire ethnographic
data (n=229 HG societies) that showed the mean subsistence dependence
upon gathered plant foods was 32%, whereas it was 68% for animal
foods. Other evidence, including isotopic analyses of Paleolithic
hominid collagen tissue, reductions in hominid gut size, low activity
levels of certain enzymes, and optimal foraging data all point toward
a long history of meat-based diets in our species. Because increasing
meat consumption in Western diets is frequently associated with
increased risk for CVD mortality, it is seemingly paradoxical that HG
societies, who consume the majority of their energy from animal food,
have been shown to be relatively free of the signs and symptoms of
CVD. CONCLUSION: The high reliance upon animal-based foods would not
have necessarily elicited unfavorable blood lipid profiles because of
the hypolipidemic effects of high dietary protein (19-35% energy) and
the relatively low level of dietary carbohydrate (22-40% energy).
Although fat intake (28-58% energy) would have been similar to or
higher than that found in Western diets, it is likely that important
qualitative differences in fat intake, including relatively high
levels of MUFA and PUFA and a lower omega-6/omega-3 fatty acid ratio,
would have served to inhibit the development of CVD. Other dietary
characteristics including high intakes of antioxidants, fiber,
vitamins and phytochemicals along with a low salt intake may have
operated synergistically with lifestyle characteristics (more
exercise, less stress and no smoking) to further deter the development
of CVD.
evetsm
http://pinch.com/skinny?medline=disease+hunter+gatherer
--------------------------------------------------------------------------
Cordain L, et al.
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Bockarie MJ, et al.
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Mann N.
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Cuthbertson WF.
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Randall
>
> http://pinch.com/skinny?medline=disease+hunter+gatherer
>
>
> --------------------------------------------------------------------------
> Cordain L, et al.
>
> The paradoxical nature of hunter-gatherer diets: meat-based, yet
> non-atherogenic.
> Eur J Clin Nutr. 2002 Mar;56 Suppl 1:S42-52. Review.
> [PubMed - indexed for MEDLINE]
> PMID: 11965522; UI: 21961980.
>
I get your point. Cordains star is ascendant post
current atkins mania.
Clicking on the related articles to this one gives
159 hits. And cordain L returns 16 with 8 showing no
abstract info. :( i hate that.
The one that caught my eye, takes my back to
that chloride co-transporter swedish study, that
we haven't heard a darn thing about since then.
Wasn't the scientist looking to farm the info
to genentech or someone? We need some psoriasis spys.
Call the NPF.
I suppose i could live on a 65/35 protein to carb ratio.
But for how long without my salt shaker?
And don't forget that pepper post and the peperine
effect on cyp3a enzymes. Gosh, you must read all the posts
in the psoriasis newsgroup, evetsm. Or at least mine! lol
And did the paleo gourmand eat his meat raw or charred rare?
Were the quests for fire for warmth and grilling sorta
happened?
Cooking makes a huge difference in the lipase equations
on potential renal acid load (PRAL).
And would negate the arguments of the atkin critics,
that its highly acid and renal damaging.
A food question to ask in PRAL, regards, why
the counterintuitive effects due to calcium ions
in the paleo diet and why the reverse occurs. NO stones!
Is it due to vitamin D dependency on lattitude
or a faulty homeostatic mechanism in the time
of season, length of day and dietary restrictions
due to those factors? Or the mixing of genes
of folks from varying latitudes that causes some SNP's.
My guess is the lack of carbs in the winter and
two genes vying for brain sugar and some HPA renal
conversions of D3 hampered by STRESS.
The refined sugars furthermore being the death of the conversion
of the D3. Hence the D3 gooP in the creams that are
available now.
I wouldn't be surprised if meat tartare realizations gain momentum
even in the face of E. coli 151. Recall the AAjonus thread!
Most important to all of this, is paleo-man's wife and
children. The paleo prodigy were breast fed by a mom
whose diet was meat from grass grazed game. That being, low omega 6
high omega 3's and a much different ratio from grain fed
stock today. Toss in vegetalble oils and french fries
and all the hydrogenated flour products and the
paleo 4:1 one ratio climbs to 50:1 or higher
and causes excessive growth hormones and a host of
downstream problems to note.
These easy sleasy comfort foods are insidious as
far as cancer and heart disease are concerned.
Most people don't want the downstream effects to
catch them when they are retiring.
I would suspect that commensal gut bacteria have
also been evolving and even more so due to the antiobiotics
revolution. A battle we may find hard to fight some day.
How does the thinking past and present fit to-gether?
Try this,
ME want meat now. Fish not as fierce as bear. To
get them i need a net or hook with mono filament line.
But to many bears in the neighbor hood will take
my hard earned fish. So, i need bob and tombo to
help me drive bears away. One day we will make
a colt 45 and get those bears. Toss another gallbladder
on the fire we must thank X?X? that bear not eat us.
OH, and we are great hunters. ;)
Yes and i heard tombo say to bob-O that eating
bear gallbladder makes him plenty concupiscent!
So lets try some of that grass that the horny
goats eat, they are randy creatures too.
Yes, we will eat the wild oats even if they
have lectins and glutins and not worry about
our GreatGGGGGGGGGG...grand children with psoriasis.
But whats the connections? Just DNA? Boring!
randall... i'm really feeling my oats now!