2011-01-17

you want to subsidize corn and healthcare?!

1.17: web.health/glycemic index of various corn products:
65 Sweet corn, (has fiber and germ)
70 corn flour (same as sucrose)
85 corn starch (same as white bread)
-- the de-germed flour of the corn kernel
115 corn syrup --[ higher than 100 indicates a toxin .
   . it's measuring the rise in blood glucose
with pure glucose assigned an index of 100;
if the rise is faster than glucose,
it means something in it
is preventing cells from using it,
thereby keeping it dammed in the blood stream .]
70 high-fructose corn syrup drinks, hfcs sodas
--[ should be 115:
this is corn syrup with fructose added;
while the glycemic index appears low
it's because they testing a dilution .
. fructose doesn't become glucose
so it has a zero glycemic index;
but it does turn into triglycerides
that are making glucose less easy to use .
. by diluting the corn syrup
there's less of it test;
whereas the usefulness of the test
is not in showing how much a given calorie load
will turn into a given blood sugar load,
but rather,
in giving an idea of how fast
the blood sugar is increasing
-- important because the body can
put out insulin only so fast,
and if it can't keep up with that soda,
then there are short bursts of
brain-damaging high blood sugar;
in its rush to catch up, the insulin overcompensates:
bringing the blood sugar too low,
then the system protects itself from low brain sugar
by using cortisol to make the body insulin resistant
so there will be more for the brain;
at the next can of soda,
this insulin resistance will make the problem worse .]

what's cooking, doc?

1.17: news.health/stroke belt is frying poly'fats:
HSI - Jenny Thompson hsiresearch@healthiernews.com
HSI e-Alert - Southern fried Jan 17, 2011 at 5:07 AM

. within the states between the stroke belt
the risk of stroke seems higher for southeastern states
between Arkansas and the Carolinas;
this was curious because they eat plenty of fish
known for reducing strokes;
but an Emory University analysis of 21,000 usa diets
found that their fish is mostly fried,
at high heat, in oil rich in polyunsaturates,
or trans fats .
. another study showed fried fish is
increasing risk of heart attack and earlier death .

Problem #1: AGE's from high-heated poly'fats;
Mount Sinai School of Medicine 2009
compared normal food with an "AGE-less" diet
where foods were slow-cooked with plenty of moisture,
such as steaming or poaching.
. inflammatory markers (such as C-reactive protein)
were reduced while vascular function improved.

Problem #2: Trans fatty acids:
. people still use partially hydrogenated oils
or other sources of trans fatty acids;
even small daily amounts raise cardiovascular risks .

Problem #3: acrylamide from hot battered meat:
. most dietary acrylamide is formed by the
Maillard reaction:
when aspargine and reducing sugars
are heated above 100C° (212F).
brown-frying is temp > 170 °C (338 °F);
golden-frying reduces acrylamide formation:
145 to 170 °C (293 to 338 °F)
. typical sources of acrylamide are
coffee (54% of intake),
fried potatoes (12% of intake),
and toast (9% of intake).

food-browning can happen at low temperatures:
. fruit is dried at around 70C°(158F);
dark dried whole pears and prunes
contain surprising amounts of acrylamide .

. acrylamide (acrylic amide) is a potent neurotoxin,
and can also cause nausea, sweating,
urinary incontinence, myalgia[muscle pain],
speech disorders, numbness, paresthesia[tingling],
and weakened legs and hands.

. the body can break down acrylamide for fuel
via the citric acid cycle or
gluconeogenesis [liver-produced glucose];
but, along the way
this process can result in high levels of
the excitotoxic neurotransmitter aspartate .

. this is done with L-asparaginase
which removes an ammonium to form
the excitotoxic neurotransmitter aspartate;
A transaminase then converts the aspartate
to oxaloacetate .

. acrylamide is produced by any browning reaction
between a very common protein
(asparagine = aspartate + ammonia)
and a reducing sugar (glucose or fructose)
or a reactive carbonyl (aldehydes, ketones, carboxylic acid and esters).
. nearly any whole food with sugars
will also contain asparagine
unless L-asparaginase is added to break it down
into excitotoxic aspartate.

. the modern diet is rich in reducing sugars:
most popular sweeteners include them,
and should not be used in cooking .
# Honey is 38.2% Fructose, 31.3% Glucose;
# inverted sugar syrup is 50% glucose 50% fructose .

. table sugar (sucrose = glucose + fructose)
doesn't form acrylamide until there is
sufficient processing to break sucrose's binding
into separate molecules of glucose and fructose .
. in the usa, subsidized HFCS has replaced sucrose .

. High-fructose corn syrup (HFCS)
starts out as corn starch (glucose chains)
enzymatically degraded to glucose,
and converted to varying fractions of fructose .
HFCS 42 (for foods) is 42% fructose and 53% glucose.
HFCS 55 (for soft drinks) is 55% fructose, 42% glucose;
-- usually HFCS 42 + HFCS-90, 90% fructose, 10% glucose .

L-asparaginase can be used in cooking
to reduce levels acrylamide;
but, 10% of dietary acrylamide is not caused by asparagine;
so, breaking that down with L-asparaginase wouldn't always;
conversely,
avoid baking powder (ammonium hydrogencarbonate, NH4HCO3, E 503)
as it promotes much more acrylamide formation
than Baking soda (sodium hydrogencarbonate, NaHCO3, E501).

glycidamide formation:
links to cancer:
. acrylamide is metabolised in the liver
into the reactive epoxide, glycidamide .
. this epoxide forms DNA adducts,
ie, causing mutagenicity by adding things to DNA .

. glycidamide can also be directly formed in food
from high-temperature reactions between
acrylamide and poly'fats
but, most of the diet's glycidamide load
is from metabolizing acrylamide .

Advanced Glycation End-products (AGEs):
Foods with significant browning, caramelization,
cooking done at temperatures above 120°C (248°F),
the use cooking oils high in polyunsaturates
as opposed to monounsaturates (olive oil, almond oil, ...)
will result in Advanced Glycation Endproducts (AGEs).

Food manufacturers for the last 50 years
have added many AGEs to foods,
as flavor enhancers and colorants .
. foods with very high AGEs include:
donuts, cake, barbecued meats,
and dark colored soda pop.
. AGEs are also made naturally by the body
when excessive sugar is consumed
or when insulin resistance has developed .

Glycation:
Glycation is unintended chemistry between
saccaride derivatives (glucose, alpha-oxoaldehydes, ...)
and biochemistry (protein, phospholipids, guanyl nucleotides);
-- Glycation is also called non-enzymatic glycosylation;
ie, the intended chemistry is called glycosylation
and that depends on control by enzymes .

3-Deoxyglucosone (3DG)
3DG rapidly reacts with protein amino groups
to form AGEs such as imidazolone, pyrraline,
N6-(carboxymethyl)lysine and pentosidine.

. 3DG as well as AGEs play a role in the
modification and cross-linking of long-lived proteins
such as crystallin and collagen,
contributing to inflammation and aging diseases,
and the vascular complications of diabetes:
atherosclerosis, hypertension, Alzheimer’s disease,
and retinal circulation issues leading to blindness .





2010-12-31

se-methylselenocysteine preventing cancer

Se-methylselenocysteine -- at iherb and amazon--
is a uniquely non-toxic form of selenium,
the essential mineral;
I've routinely taken 20doses a day
-- that's 4mg*... (that would be too toxic in other forms).
. here are more references to articles about
how it prevents cancer, and maybe old-age blindness
(this will be added to my selenium knol).

12.12: web.health/se/se-methylselenocysteine:
TRAIL (TNF-Related Apoptosis-Inducing Ligand)
International Journal of Oncology May 2009 Volume 34 Number 5
. Se-MSC rapidly and specifically down-regulates
expression of the Bcl-2 at transcriptional level.
The forced expression of Bcl-2
attenuated Se-MSC plus TRAIL-mediated apoptosis,
suggesting that Se-MSC's reduction of Bcl-2 expression
is critical to the increased sensitivity
to TRAIL in renal cancer cells.
In addition, we demonstrate that the synergistic effects
of Se-MSC and TRAIL
result from the activation of the
caspase-dependent pathways.
Co-administration of HA14-1,
a small molecule Bcl-2 inhibitor
and TRAIL increased apoptosis in Caki cells.
Taken together, Se-MSC-mediated down-regulation of Bcl-2
is able to sensitize Caki cells for
TRAIL-induced apoptosis.
Programmed Cell Death
Programmed cell death (PCD), or apoptosis,
can be triggered by a wide range of stimuli,
including cell surface receptors like Fas
or tumor necrosis factor receptor 1 (TNFR1).
It constitutes a system for the removal of
unnecessary, aged, or damaged cells
. the relative abundance of
proapoptotic and antiapoptotic proteins
determines the susceptibility of the cell
to programmed death.

The proapoptotic proteins Bax, Bad, Bid, Bik, and Bim
contain an a-helical BH3 death domain
that fits the hydrophobic BH3 binding pocket
on the antiapoptotic proteins Bcl-2 and Bcl-xL,
forming heterodimers that block
the survival-promoting activity of Bcl-2 and Bcl-xL.

. things that result in more pro-apopt's
include: growth factor withdrawal
, genotoxic insult
, uv irradiation,
-- this reminds that chronically high
insulin (a growth factor)
can reduce one of your own sources of pro-apopt's .

The proapoptotic proteins act at
the surface of the mitochondrial membrane
to decrease the mitochondrial transmembrane potential
and promote leakage of cytochrome c.
In the presence of dATP,
cytochrome c complexes with and activates Apaf-1.
Activated Apaf-1 binds to downstream caspases,
such as pro-caspase-9,
and processes them into
proteolytically active forms.
This begins a caspase cascade
resulting in apoptosis.

Smac/Diablo is released from the mitochondria
and blocks IAP proteins that normally interact with
caspase-9 to inhibit its conversion to
the apoptosis-effecting caspases-{3, 6, 7}

The graphic shows the conserved apoptotic pathway
in the organism C. elegans .
CED-3 encodes a caspase whose function is facilitated by CED-4,
which is highly similar to Apaf-1.
CED-4 function is blocked by CED-9,
which protects cells against apoptosis
and is similar to the human antiapoptotic protein Bcl-2.
CED-9 activity is inhibited by EGL-1,
which is similar to the proapoptotic Bcl-2 family members.
Se-methylselenocysteine inhibits
phosphatidylinositol 3-kinase activity
Breast Cancer Res (2005) 7: R699-707
Se-methylselenocysteine (MSC),
a naturally occurring selenium compound,
is a promising chemopreventive agent
against in vivo and in vitro models of
carcinogen-induced mouse and rat mammary tumorigenesis.
We have demonstrated previously that MSC
induces apoptosis after a cell growth arrest in S phase
in a mouse mammary epithelial tumor cell model (TM6 cells) in vitro.
The present study was designed to examine the involvement of
the phosphatidylinositol 3-kinase (PI3-K) pathway
in TM6 tumor model in vitro after treatment with MSC.
RESULTS: PI3-K activity was inhibited by MSC
followed by dephosphorylation of Akt.
The phosphorylation of p38 MAPK was also downregulated
after these cells were treated with MSC.
In parallel experiments MSC inhibited the
Raf-MEK-ERK signaling pathway.
CONCLUSION:
These studies suggest that MSC blocks
multiple signaling pathways
in mouse mammary tumor cells.
MSC inhibits cell growth by inhibiting the activity of PI3-K
and its downstream effector molecules
in mouse mammary tumor cells in vitro.
Se-methylselenocysteine (MSC) chemically synthesized:
. [these 2 ref's were given]:
# SYNTHESIS OF [TRIMETHYLSELENONIUM-SE-75 IODIDE
FROM [SELENOCYSTINE-SE-75]
Source: ANALYTICAL BIOCHEMISTRY Volume: 137 Issue: 1 Pages: 205-209
Published: 1984 Reprint Address: FOSTER, SJ (reprint author),
UNIV WISCONSIN, DEPT NUTR SCI, MADISON, WI 53706 USA
ISSN: 0003-2697
# Chemical Form of Se,
Critical Metabolites, and Cancer Prevention:
Methylated selenides are prominent metabolitesat the dietary levels
used for obtaining anticarcinogenic effects with selenium.
The present study reports the chemopreventive activities
of 2 novel selenium compounds,
Se-methylselenocysteine and
dimethyl selenoxide,
Other treatment groups were supplemented with either
selenite or selenocystine for comparative purposes.
Results of the carcinogenesis experiments showed that
the relative efficacy with the four compounds was
Se-methylselenocysteine > selenite
> selenocystine > dimethyl selenoxide.
In correlating the chemical form
and metabolism of these selenium compounds
with their anticarcinogenic activity,
it is concluded that:
(a) selenium compounds that are able to generate
a steady stream of methylated metabolites,
particularly the monomethylated species,
are likely to have good chemopreventive potential;
(b) anticarcinogenic activity is lower for selenoamino acids,
such as selenocysteine following conversion from selenocystine,
which have an escape mechanism via
random, nonstoichiometric incorporation into proteins;
(c) forms of selenium, as exemplified by
dimethyl selenoxide,
which are metabolized rapidly and quantitatively
to dimethyl selenide and trimethylselenonium
and excreted,
are likely to be poor choices.
We also undertook a separate bioavailability study
using
Se-methylselenocysteine
, dimethyl selenoxide
, and trimethylselenonium
as the starting compounds for delivering selenium with
one, two, or three methyl groups,
and measured the ability of these compounds to restore
glutathione peroxidase activity in selenium-depleted animals.
All three compounds were able to
fully replete this enzyme,
although with a wide range of efficiency
(Se-methylselenocysteine >
dimethyl selenoxide > trimethylselenonium),
suggesting that complete demethylation
to inorganic selenium
is a normal process of selenium metabolism.
However, the degree to which this occurs
under chemoprevention conditions
would argue against the involvement of selenoproteins
in the anticarcinogenic action of these selenium compounds.
-- Sodium selenite was obtained from
Sigma Chemical Co. (St Louis, MO, USA).
--. wholesaler only:
but they do have Se-methylselenocysteine:
M6680 Sigma Se-(Methyl)selenocysteine hydrochloride 95% (TLC)
CAS Number: 863394-07-4
Empirical Formula (Hill Notation): C4H9NO2Se · HCl
Molecular Weight: 218.54
MDL number: MFCD03412450
PubChem Substance ID: 24278564
Description: Se-(Methyl)selenocysteine
. a chemopreventive agent that blocks
cell cycle progression and proliferation of
premalignant mammary lesions;
and, induces apoptosis of cancer cell lines in culture.
M6680-100MG /$ 164.50
Sigma-Aldrich Corp
St. Louis, MO, USA
Phone: 314-771-5765, Fax: 314-771-5757
E-mail: OC_DOM_HC@sial.com
Ordering & Customer Service
Phone: 800-325-3010

# Opening a Sigma-Aldrich Account
Accounts are generally established for a company or institution
rather than for individuals.
# Your business or institution must have an established
Customer Account with Sigma-Aldrich
to establish an account, and be approved for on-line ordering;
you will need to contact Support by phone.
You cannot establish an account on-line.
12.12: news.health/se/se-methylselenocysteine/Protease inhibitors:
Protease inhibitors suppress apoptotic features induced by MSC
These results confirm previous observations
that caspase-3 is crucial for inducing apoptosis by MSC treatment,
and further suggest the possibility that
an unknown member of the serine protease family
is involved in MSC-mediated apoptosis.
Our results strengthen the possibility that
MSC can be used to prevent or cure cancer
as either a chemopreventive or a chemotherapeutic agent.
Further studies are required to differentiate between
the chemopreventive effects on normal cells
and cancer cells in vitro.
12.26: health/se/age-related macular degeneration:

I lamented how mom's eyes still got cataracts
even with supplemental selenium
-- not because selenium is quack
but because of
stress-induced melatonin disfunction
not allowing the selenium to be useful;
and now hearing about macular degeneration
I found only one article saying it helps that
when I know it helps so much more
(anti-cancer, anti-heart disease)
because of the way it enables selenium!

. in answering the question:
Does melatonin have any bad side effects
in someone mom's age?

here's something that starts as a warning
"(replacement of melatonin just for being elderly
is not recommended)
but actually becomes a great encouragement:
Although elderly people often have difficulty sleeping
it's not from being elderly
but from being either emotionally ill
(making too many stress hormones
that suppress melatonin secretion)
or using drugs that suppress melatonin secretion
(e.g., aspirin, ibuprofen, beta-blockers).
Adults with insomnia, heart disease, or schizophrenia
routinely have lower melatonin levels.

I found this study ok'ing elderly women 64 to 80 years
(it measures cortisol and dhea!)

Effects of six months melatonin treatment
on sleep quality and "serum concentrations of
estradiol, cortisol, dehydroepinadrosteron sulfate,"
and somatomedin C in elderly women
M. Pawlikowski, M. Kolomecka, A. Wojtczak & M. Karasek:
October 9 , 2002 NEUROENDOCRINOLOGY LETTERS
CONCLUSIONS:
On the basis of this preliminary open study
it seems that melatonin administration
may be beneficial for elderly subjects.
A significant decrease of estradiol concentrations
was observed after 6 months of the melatonin treatment
in comparison to initial levels.
IGF-I was found to be slightly but significantly
increased after the 6 months melatonin therapy.
Cortisol levels did not change significantly,
during the melatonin treatment.
DHEAS concentrations increased
after melatonin therapy.
-- a higher DHEAS/cortisol ratio .
Melatonin treatment did not influence significantly
either the parameters of total blood count
or glucose and serum lipids levels.
OBJECTIVES:
The role of melatonin in aging
is still under debate.
Therefore, an open pilot study on the effects of melatonin
was performed in elderly women.
SUBJECTS AND METHODS:
The study was performed on 14 women (volunteers),
aged from 64 to 80 years (mean age 71±4.6 years).
Melatonin (2 mg daily at 19:00 h) was administered during 6 months.
Before and after melatonin treatment
the peripheral venous blood samples
were taken in the morning (approx. at 08:00 h)
after the overnight fast.
The total blood count, glucose, total cholesterol,
LDL, HDL, and triglycerides were estimated by
routine laboratory methods.
The serum concentrations of the following hormones
were determined: 17-beta-estradiol,
dehydroepiandrosterone sulfate (DHEAS),
cortisol, and somatomedin C (IGF-I).
12.26: web.health/se/macular degeneration/se's role:
links from i-care:
# Glutathione and its related enzyme precursor amino acids
(N-Acetyl-Cysteine, L-glycine and glutamine,
as well as selenium)
are protective against damage to
human retinal pigment epithelium cells,
and may help prevent retinal damage in AMD.
Invest Ophthalmol Vis Sci 1993 Dec;34(13):3661-8
# Consumption of fruits and vegetables is protective against
progression of macular degeneration.
Cho, Seddon, et al Arch Ophthalmol. 2004 Jun;122(6):883-92
# In a clinical trial 60% of subjects with ARMD
or diabetic macular edema [...] So Med J, 1987.
[. interesting term: diabetic macular edema
had me convinced that metabolic disorder
-- caused from the use of carb's
by carb'intolerant elders --
was the primary reason elders were getting armd .
so another source of damage besides
not getting the se to the gluthione peroxidase
is not having the circulation for
getting the glutathione to the retina .]

ironwood tree planting in tucson

12.1: proj.apt`yard/tree#n.ironwood replanting:
. being soaked made it heavy
and more likely to traumatize the roots;
but, I was hoping things would stay in place
if dirt was around before the sleeve was removed .
. the instructions are very different from last year,
saying to pull the sleeve without dirt surrounding it,
and then use your finger to pull some roots loose!
I stayed with last year's advice .
. I cut across the bottom,
and then around the bottom,
then checked that the sleeve would pull up
before packing dirt around it;
but I packed it too tight,
and the whole plant would lift
as I was trying to pull the sleeve out;
so I wondered if I ripped away a layer of roots
as they fell with the soil .
. the instructions reminded me not to add
any supplements like peat moss,
and I notice this was very dark soil
like what was brought in for the privets;
I also added several cups of vitamixed garbage
a few weeks ago,
but that was a small percentage of
what the roots will be exposed to ...
. in short,
I wasn't sure how desert-like the soil was,
so, I arranged the tree to be higher than ground,
with a deep moat around it,
so it's easy to both soak and drain .
. it got a shower to help pack the dirt
around the new root ball,
along with filling the moat .
. it smelled like the root ball's bottom
was overly watered a lot,
but the tree looks good .

preventing frame damage in tadpole trikes

12.13: gear/trike`frame/potholes need suspension:
. the trice front-suspension add-on is expensive,
but it's quite likely the frame will be ruined
unless speeds are low or potholes are avoided .

gear/trike`frame/potholes need rider pivot:
12.13:
. the trice already has rear suspension
which helps deflect rider weight from bending frame;
but that doesn't help z-axis rolling
where one front wheel is potholed but the other isn't
and the whole frame falls into a rolling motion
to one side or another .
. if the rider's chair is frozen to the frame
then the rider's weight is resisting that z-roll,
which could increase stress at the cruciform joint .
12.14:
. how rigidly can riders' weight
prevent rolling about z-axis for potholes?
# if rider's seat were not bolted to main tube,
but instead pivoted sideways,
then there'd be less stress on frame during potholes;
# if seat was closer to main tube,
with thick cusion under rider;
then z-axis rotation could happen stress-free
even without pivot .

12.15: gear/trike/replacing front suspension:
. the cheap sure-tech way to stop
frame bends from potholes
is to unbolt the seat from the z-tube,
make a platform that is anchored to
both the z- & x-tube;
and, bolt the seat to that platform .
. if steering doesn't fit with platform,
it can be moved from sides to center .

2010-12-29

existence proof

12.29: relig/god/existence proof:
. you can't disprove this universe isn't a
conspiracy involving a centralized emotion maker
(emotions aren't personal, they happen against our will
and are a sort of natural disaster:
they alone support overpopulation,
religous wars, and mental illness);
likewise,
you'd hardly deny the existence of terrorists
just because there's no current proof of existence;
therefore,
it would be taking more risk than necessary
to assume there's no conspiracy
unless it causes a dangerous aversion to risk
(if mob's, plagues, or politics
could upset your plans,
then you might want to put god out of mind).
. the corollary of conspiracy theory
is that Shush Happens Inside There!
and, in the long term, a belief in conspiracy
can be a healthy driver of preparation for
several worst-case scenerios converging .

2010-12-25

moving qubes`way on the mac

11.07: vm (virtual machine)-based security:
. an intro to security with virtualization
and a getting started manual for mac os x .
 .  this shows how some security experts have agreed,
vmware`Fusion can make the mac more secure .
[2013 update: my mac was destroyed while using
either vmware`Fusion/linux/pdf reader, or a usb stick.]

2010-12-22

the higher power

12.20: relig/god/the higher power:

. recalling my blog of speeder cameras;
. along with my usual view that
human policing can apply the law unequally;
there's also a god-related issue
(significant since such issues are
splitting the country in half
so you'd expect little reminders of such):

. the god fearing young driver would be saved by
thinking a god is catching every cheating moment;
while the godless would be saved only by
the sure justice of knowing there are robocops
everywhere all the time;
therefore,
robocops could be a symbol of the godless,
and a hate of robocops could be a swipe at
free-thinking anti-dogmatic humanists,
or Democrats .

. can you actually teach kids to fear god?
in the political debate
it's always presented as an option!
(school prayer leads to kids praying;
and packing kids in school leads to
gang violence ... or lots of prayer!)

. I myself thought kids could be saved
either by
stressing the bible as proof of the supernatural
or by diligently watching kids until
their youthful minds became future aware;
but to nix both the supernatural training
and the constant guidance
is tantamount to saying
a kid should remain seeable because nobody sees
-- that is a likely future killer .

. then again,
if you think kids are better off god-aware
imagine how many adults are not god-aware
and yet still caught cheating?
I suppose they figure god is only the devil;
"( so what if God sees all? he loves everything! ).

. the real significance of god
is knowing who has your ears:
is it your selfish impulses?
or a higher power?
but when you call "(god) your higher power
(rather than, say, the Chinese Premiere)
what is your higher power saying?
my clerics say, my books say,
my big fat trust me really told you;
so, it's just my line in the sand,
having fun -- like I always do!

. the Buddha had it right:
the real plain truth is understood by
self agreeing with elders:
without elder checks there is foolishness,
without self checks there is corruption .