2019.8.26: health/diet/selenium/mercury-binding losses:
2020.1.7: summary:
. selenium (se) is an essential mineral
but it binds to mercury,
and there is a lot of mercury in some foods
especially since the industrial age,
(and some fillings release mercury;
and some flu vaccines may contain mercury).
so some may need more se than others,
ie, you may need more than is recommended.
. some lakes are low in se,
but the ocean has plenty of it,
so most ocean fish have more se than mercury,
however, even if ocean fish are not a
mercury hazard, they still have carcinogenic
endocrine disruptors such as PCB, and dioxins.
. in addition to using sardines for se,
(also omega-3 oils, and plenty of minerals)
I get se from Se-Methyl L-Selenocysteine
since it may have additional benefits
before being degraded into elemental selenium
that can bind mercury and be used in proteins.
Showing posts with label selenium. Show all posts
Showing posts with label selenium. Show all posts
2015-07-13
some flu #vaccines don't contain mercury
7.12: news.med/flu vaccine/beware thimerosal:
. some flu vaccines still contain thimerosal
delivering about 25 micrograms of ethylmercury.
It is known that as little a 0.5 micromole
[114.825 micrograms]* of ethylmercury
[ 5 years of thimerosal-flu vaccines ]
can produce a 50% inhibition of the
brain's most important protective system
against excitotoxicity.
. some flu vaccines still contain thimerosal
delivering about 25 micrograms of ethylmercury.
It is known that as little a 0.5 micromole
[114.825 micrograms]* of ethylmercury
[ 5 years of thimerosal-flu vaccines ]
can produce a 50% inhibition of the
brain's most important protective system
against excitotoxicity.
2014-06-13
#selenium helps preserve #vitaminC
1.20: news.health/counterexample to elder's vit'c use:
nutrition.org 1989:
nutrition.org 1989:
. in the elderly, supplementing with vit'cnews.health/se/#selenium helps preserve #vitaminC:
resulted in raising the ratio of
dehydro-ascorbate (oxidized C) to ascorbate;
this may be due to their lesser glutathione function
which is needed to reduce dehyrdo-C to vit'C .
how to raise #glutathione #health
1.19: news.health/diet/how to raise glutathione:
Mark Hyman, M.D. practicing physician
and founder of The UltraWellness Center,
a pioneer in functional medicine.
Mark Hyman, M.D. practicing physician
and founder of The UltraWellness Center,
a pioneer in functional medicine.
. free radicals are handled by a cascade:
from vitamin C to vitamin E to lipoic acid
and then finally to glutathione .
. the production or functioning of glutathione
is depleted by poor diet, toxic medications,
stress, trauma, infections and pollution
(80,000 toxic industrial chemicals,
electromagnetic radiation, mercury and lead).
[see all Glutathione-lowering pollutants .]
. supplements taken consistently:
multivitamin[with good minerals],
fish oil, [long-chain omega-3]
and the following glutathione boosters:
2014-01-31
acetylcysteine can inhibit anti-cancer p53 protein
30: news.health/acetylcysteine can inhibit anti-cancer p53 protein:
31: summary:
. N-acetylcysteine or NAC is a source of cysteine,
but is too powerful an antioxidant .
. a better source of cysteine is egg yolk:
it too is great at raising glutathione,
a safe antioxidant made by the body .
31: summary:
. N-acetylcysteine or NAC is a source of cysteine,
but is too powerful an antioxidant .
. a better source of cysteine is egg yolk:
it too is great at raising glutathione,
a safe antioxidant made by the body .
2014-01-27
methylated B vitamins #glutathione
25: health/glutathione/methylated B vitamins:
. I was hearing the best form of vit'B for glutathione
(the magic associated with selenium)
is the pro-methylation forms .
. Now Foods thought that the pro-methyl form of b6
needed to be enteric,
so being sublingual might be very important
(either way avoids the stomach acid).
. anyway, here's more about methylation
if you were looking to variety for security .
. I am going to try using Methyl-Guard Plus
sublingually (see below).
I may also try enteric B6 (pyridoxal 5-phosphate) .
. I was hearing the best form of vit'B for glutathione
(the magic associated with selenium)
is the pro-methylation forms .
. Now Foods thought that the pro-methyl form of b6
needed to be enteric,
so being sublingual might be very important
(either way avoids the stomach acid).
. anyway, here's more about methylation
if you were looking to variety for security .
. I am going to try using Methyl-Guard Plus
sublingually (see below).
I may also try enteric B6 (pyridoxal 5-phosphate) .
2013-12-31
variety best for sourcing selenium?
10.2: co.amazon/cook/
Frontier Bulk Garlic Granules, CERTIFIED ORGANIC:
where is it sourced from?!
Frontier Bulk Garlic Granules, CERTIFIED ORGANIC:
where is it sourced from?!
. this is the perfect granule size,
just large enough for me to feel confident that
all the substance is actually garlic ...
. it tastes great but I'm interested in garlic because
it is a selenium accumulator,
with a very healthy form of selenium:
se-methy-seleno-cysteine .
. however, if it comes from China,
then there are many places there that have
very low levels of selenium in the soil .
. so my new strategy is to just get variety,
and not depend on any one brand .
. I'm also going for quantity too,
and not worrying as much about organic
when it comes to garlic .
2013-12-27
supplements for radiation #fukushima
12.5: web.health/supplements for radiation:
Dr. Melissa Patterson, NDtalks about supp's you may need for
dealing with the increased radiation levels
coming from the fukushima nuclear accident .
If large doses of C,E, and B (especially B5),
are taken before exposure,
the radiation sickness can be reduced to a large degree.
Vitamin A can be toxic to a pregnancy .
2013-12-24
onion #superfood #prebiotics #selenium
11.4: todo.health/probiotics/is onion a health food?:
. onion is a glycemic food
but has se-msc, the favored form of selenium;
and unlike garlic, it doesn't make you smell bad .
. npr radio was talking about microbiome profiles,
and they said good food for the probiotics (the beneficial bacteria)
includes garlic, onion, and leeks .
. onion is a glycemic food
but has se-msc, the favored form of selenium;
and unlike garlic, it doesn't make you smell bad .
. npr radio was talking about microbiome profiles,
and they said good food for the probiotics (the beneficial bacteria)
includes garlic, onion, and leeks .
2013-12-19
Se-methylselenocysteine resources update #selenium #cancer #prevention
12.18: update knol.health/se
/{new source of selenate, vrp.com se-msc}:
19: intro:
. this is a summary of updates to my knol:
health/anti-cancer selenium-cysteine compounds .
. following that is an amazon review for
the new selenate source .
/{new source of selenate, vrp.com se-msc}:
19: intro:
. this is a summary of updates to my knol:
health/anti-cancer selenium-cysteine compounds .
. following that is an amazon review for
the new selenate source .
2013-12-17
#quackwatch mineral supps deemed useless
12.17: web.health/selenium
/#quackwatch mineral supps deemed useless:
editorial by a medical journal:
cancer could be considered to be
"morbidity due to major chronic diseases";
so, the editor of this journal
seems to be asserting that
mineral supplementation would prevent no cancers .
/#quackwatch mineral supps deemed useless:
editorial by a medical journal:
"Fortmann et al reviewed trial evidence to update. since most cancers happen to the elderly,
the usa's Preeventive Services Task Force recommendation
on the efficacy of vitamin supplements
for primary prevention in community-dwelling adults
with no nutritional deficiencies .
[ and no mineral deficiencies -- notice that .]
. after reviewing 3 trials of multivitamin supplements
and 24 trials of single or paired vitamins
that randomly assigned more than 400,000 participants,
the authors concluded that there was no
clear evidence of a beneficial effect
of supplements on all-cause mortality,
cardiovascular disease, or cancer ."
". the only supplements not gaining in popularity
are beta-carotene (some uses increased lung cancer)
and vitamin E (some uses increased all-causes mortality)."
"... mineral supplements are ineffective for
preventing mortality or morbidity
due to major chronic diseases."
cancer could be considered to be
"morbidity due to major chronic diseases";
so, the editor of this journal
seems to be asserting that
mineral supplementation would prevent no cancers .
2012-07-10
the spirits and molecules of autism
6.22:
. this file started out as a political issue
-- 5.20/pol/energy/Autism related to Coal's mercury --
but mercury policy has improved
while autism rates have increased,
so, it's been reassigned as a health issue .
7.10:
. however, it may also be a socioeconomic issue
as worsening underemployment
increases reliance on children's disability payments .
. nevertheless,
even if parents were encouraging the diagnosis
for collecting child disability payments,
there is still evidence of increased autism risk
from environmental pollutants
(pcb's, pesticides, estrogenics, mercury)
and a degraded food supply quality
(increased use of gmo's, pesticides,
and herbicides -- thanks to gmo's;
non-organic farming creates a lack of
selenium in food
which is needed to counteract mercury).
7.9:
. another theory explaining increased autism
is what I call two-headed dominance syndrome
where one of the heads tends to submit
in order to let the other head take control .
. likewise, in sociology,
when a population starts to feel
a loss of economic opportunities
there may tend to be more silent tension,
and an increase in dependent personalities .
. at the same time, unique to our times
is a tendency to demand much more of students;
whereas, in the past,
the developmentally challenged may have been
understood to be simply a rowdy or lonely laborer .
6.22: web: autism is on the rise:
. this file started out as a political issue
-- 5.20/pol/energy/Autism related to Coal's mercury --
but mercury policy has improved
while autism rates have increased,
so, it's been reassigned as a health issue .
7.10:
. however, it may also be a socioeconomic issue
as worsening underemployment
increases reliance on children's disability payments .
. nevertheless,
even if parents were encouraging the diagnosis
for collecting child disability payments,
there is still evidence of increased autism risk
from environmental pollutants
(pcb's, pesticides, estrogenics, mercury)
and a degraded food supply quality
(increased use of gmo's, pesticides,
and herbicides -- thanks to gmo's;
non-organic farming creates a lack of
selenium in food
which is needed to counteract mercury).
7.9:
. another theory explaining increased autism
is what I call two-headed dominance syndrome
where one of the heads tends to submit
in order to let the other head take control .
. likewise, in sociology,
when a population starts to feel
a loss of economic opportunities
there may tend to be more silent tension,
and an increase in dependent personalities .
. at the same time, unique to our times
is a tendency to demand much more of students;
whereas, in the past,
the developmentally challenged may have been
understood to be simply a rowdy or lonely laborer .
6.22: web: autism is on the rise:
2011-11-04
#thyroid optimization may save bone,vision #health
11.2 ..11.4: health/thyroid/
lifestyle choices that improve function:
summary:
low thyroid is very common:
. age-related hypo-thyroid
-- ie "(normal) TSH levels --
is as common as the many modern diseases,
and that may be more than a coincidence .
. there are ties to bone loss,
atrial fibrillation,
and blindness due to glaucoma
(you may be at increased risk if you are
nearsighted or hypo-thyroid).
. I will first explain how common low thyroid is,
and how it can be mistaken for hyper-thyroid
-- that's important to realize because
some are avoiding the iodine they need
under the assumption that they are hyper-thyroid
when, in fact,
both the low and high thyroid extremes
can have the same symptoms
of a rapid or erratic heart .
. the unprecedented rate of obesity starting in the 1980's
may be due to the combination of
not only replacing sugar with high-fructose corn syrup,
but also replacing the iodine in bakery goods
with bromides that actually inactivate
what little iodine you might already be getting !
lifestyle choices that improve function:
summary:
low thyroid is very common:
. age-related hypo-thyroid
-- ie "(normal) TSH levels --
is as common as the many modern diseases,
and that may be more than a coincidence .
. there are ties to bone loss,
atrial fibrillation,
and blindness due to glaucoma
(you may be at increased risk if you are
nearsighted or hypo-thyroid).
. I will first explain how common low thyroid is,
and how it can be mistaken for hyper-thyroid
-- that's important to realize because
some are avoiding the iodine they need
under the assumption that they are hyper-thyroid
when, in fact,
both the low and high thyroid extremes
can have the same symptoms
of a rapid or erratic heart .
. the unprecedented rate of obesity starting in the 1980's
may be due to the combination of
not only replacing sugar with high-fructose corn syrup,
but also replacing the iodine in bakery goods
with bromides that actually inactivate
what little iodine you might already be getting !
2011-06-29
lifestyle choices for blindness prevention
intro
6.21: intro:. 48% of world blindness is attributed to
Age-related cataract;
. the term "(aging) actually refers to
an increasing amount of metabolic disorder
including diabetes, hypertension, and hypothyroidism .
extent of cataract formation by age range:
42% affected by ages of 52 to 64,
60% affected by ages 65 and 74,
91% affected by ages 75 and 85 .
[. macular degeneration is the leading cause of
age-related blindness .
. there are some dietary factors that may prevent this;
but the most important contributary causes
are the same as for cataracts:
one's lifestyle or medication choices
can affect the rate of aging .
. for example,
at the same time there were cataracts [6.29:
within my circle of friends ]
there was also use of Dalmane,
a benzodiazepine sleeping medication
that is known to increase the likelihood of cataract .
. children and other behaviors are increasingly being
medicated with tranquilizers and other psychotropics
that contribute to the big 3 metabolic disorders:
diabetes, hypertension, and hypothyroidism .
. risk factors are [6.29:
proportional to one's lifetime dose,
and dose variations for ]
sunlight, smoking, alcohol, other medications .
. dietary protective factors
include:
# high-fiber vs high-carb':
[6.29: ie, high-carb diets are good only whenmuch of the carb is fiber,
and none of it has a high glycemic index .]
# good fat vs bad fat:
[6.29: mono'fats are good fats for energy;other fats are essential for body maintenance;
use only low doses of fish-related poly'fats,
and even lower doses of non-fish poly'fats;
sat'fats cause carb'intolerance,
so they don't mix with a glycemic diet .]
# moderate fat vs high or low fat:
[6.29: mono'fats (olive oil, almonds, hazels)are a safe source of energy;
but fats are a special source of
carcinogenic pollutants and mold toxins;
moreover,
low calorie is safer than high calorie .]
# peak resistance training
[6.29: short bursts of moving heavy thingscan increase insulin sensitivity,
and reduce carb'intolerance .]
Ann Epidemiol. 1996 Jan; 6(1):41-6.
. this study indicates that diet
plays a considerable role in
the risk of [needing and being eligible for]
cataract extraction
in at least a certain Italian population,
with a protective action played by
some vegetables, fruit, calcium, folic acid,and vitamin E,
and an increased risk
associated with elevated salt and fat intake [6.29:
-- this could have been a measure of
where these Italians were getting their
extra doses of salt and fat:
the usual culprit is luncheon meat
-- known to promote diabetes by
mixing sugar with the meat .]
. a significant inverse trend in risk,
were found for intake of
meat (OR 0.6, 95% CI 0.4 to 0.9),
cheese (OR 0.7, 95% CI 0.5 to 1.0),
[implied a more low-carb' diet?
the atkins effect .
6.19: ie,
not necessarily an endorsement
of cheese ! ]
cruciferae (OR 0.5, 95% CI 0.3 to 0.8),
spinach (OR 0.6, 95% CI 0.4 to 0.9),
tomatoes (OR 0.5, 95% CI 0.4 to 0.8),
peppers (OR 0.7, 95% CI 0.4 to 1.1),
citrus fruit (OR 0.5, 95% CI 0.2 to 1.3),
and melon (OR 0.5, 95% CI 0.4 to 0.8).
. a significant increase in risk
was found for
the highest intake of
(compared to the lowest intake)
butter (OR 2.8, 95% CI 1.2 to 6.4),
[6.29: apparently Italian cheese is
not a significant source of butter ? ]
total fat(OR 1.8, 95% CI 1.2 to 2.8),
[ie, sat'fats vs oils]
salt (OR 2.4, 95% CI 1.4 to 4.0)
[luncheon meats vs fresh meats]
. a significant increase in risk
was found for consumption of
oil other than olive oil
[mono'fats vs poly'fats]
(OR 1.6, 95% CI 1.1 to 2.2).
Among micronutrients,
lower ORs for cataract extraction
(highest quintile of intake compared to the lowest)
were found for intake of
calcium (OR 0.5, 95% CI 0.3 to 0.8),
folic acid (OR 0.4, 95% CI 0.2 to 0.7),
and vitamin E (OR 0.5, 95% CI 0.3 to 1.0),
[this may have more to do with
the foods that provided these micronutrients]
. intakes of
methionine, retinol, beta-carotene,
and vitamins A, C, and D
were not associated with cataract risk .
foods that prevent macular degeneration:
6.20:. being low on zeaxanthin or lutein
is associated with risk of amd
(age-related macular degeneration);
it's easy to get lutein
-- dark green leafy vegetables --
but zeaxanthin is a bit less common;
so this section has a list of
zeaxanthin-specific foods
sorted by density .
. some other carotenoids were included
for their anti-cancer importance .
. this research confirms previous reports
that the primary eyecare superfoods
are egg yolks for zeaxanthin
and dark green leafies for lutein .
. corn and sweet citrus are high in zeaxanthin
but not so relative to either
corn's glycemic and inflammation indices,
or citrus's fructose levels
(a source of liver-produced triglycerides).
--
. I noticed huge variations among 2 databases:
eg, the lab that gave percentages of zeaxanthins
differed wildly from percentages implied by
usda's nutrient density data;
so, consider this to be a very rough estimate
for where your eyecare diet should be .
sources of zeaxanthin:
. many texts give levels of carotenoids in foods;here is a source that tells
what percentage of the carotenoids there are
for these famous varieties:
{zeaxanthins, lutein, lycopenes, beta-carotenes}
(as a percentage when counting by molecules,
not a percentage by weight):
Fruits and vegetables that are sources for lutein and zeaxanthin:
the macular pigment in human eyes
O. Sommerburg, J. Keunen, A. Bird, and F. J G M van Kuijk
Br J Ophthalmol. 1998 August; 82(8): 907–910.
todo:see the articles that cited that one:
# elders respond postively to egg consumption
# controversial role of lutein and zeaxanthin
in protecting against age-related macular degeneration:
. most of the dark green leafy vegetables,[6.20:
have 15-47% of their carotenoids as lutein,
but very little zeaxanthin (0-3%)
... not many were tested, however ...
. the reason dark green leafies may still
help to avoid macular degeneration
despite being short zeaxanthin,
is that this disease depends a lot on
metabolic disorder and clogged arteries
whereas dark green foods have a lot of
the magnesium from chlorophyll
that can support the insulin sensitivity
that prevents metabolic disorder;
and, they are also high in the
vitamin K that can hold calcium in bones
to prevent calcium-clogged arteries
(a major cause of irreversable circulation loss).
. this list is sorted by a food's
zeaxanthin density, which is a product of
both the ratio of zeaxanthin to other carotenoids,
and the total carotenoid density .
. even though corn appears to have
great values for zeaxanthins,
high-glycemic foods like corn
can bring down HDL; and ]
while most of the absorbed carotenoid[6.21:
is carried in LDL,
53% of the (lutein, zeaxanthins) group
is carried by HDL .
. another source that conflicted with my first was:
Lutein and Zeaxanthin Scientific Review:
for instance, they claimed cooked spinach had
0.2 mg Zeaxanthin rather than 0.0000 .
. they gave a list of zeaxanthins per 100g servings,
which I have appearing like this:
[corn 0.5mg Z per 100g] -- with a Z added;
if the Z is not there, then it refers to
combined {zeaxanthins, lutein} amounts .]
== high-density zeaxanthin sources ==
ratio's ofzeaxanthins,
lutein,
beta-carotene,
and lycopenes(omitted if zero):
[plus amounts of (zeaxanthins, lutein) per serving]
35,54,0 Egg yolk [0.5 mg per 2 eggs (100g)][6.29:
^-- that number(35) mean 35% of the 0.5mg
is the rare zeaxanthins form ]
-- selenium 17.2 mcg (varies widely)
[Persimmons, Japanese, raw 0.49 Z per 100g]
[Spinach, raw 0.33 Z per 100g]
37,8,21 orange pepper [1.6mg Z per 100g]
2,27,11 brussel sprouts, [2.389mg per 155g]
3,36,12 green pepper [0.586 mg per 136 g]
5,47,5 zucchini squash [1.15mg per 100g of
... Squash, summer, zucchini, includes skin, boiled,]
3,27,0 scallions, [1.137mg per 100g of
. . . Onions, spring or scallions (tops and bulb).]
3,22,5 green beans, [0.64mg per 100g of
. . Beans, snap, green, raw, 0.44mg canned]
2,32,0,1 celery [0.494 mg per 150 g]
[Turnip greens, cooked 0.27 Z per 100g]
[Collard greens, cooked 0.27 Z per 100g]
[Lettuce. cos or romaine, raw 0.19 Z per 100g]
[Spinach, cooked 0.18 Z per 100g]
[Kale, cooked 0.17 Z per 100g]
== moderate-density zeaxanthin sources ==
ratio's of zeaxanthins, lutein, beta-carotene,and lycopenes(omitted if zero):
[plus amounts of (zeaxanthins, lutein) per serving]
25,60,0 corn [0.19 mg per 28g --
. . a safe 100-colorie dose for this inflammatory grain]
http://nutritiondata.self.com/facts/cereal-grains-and-pasta/5687/2
[Tangerine, mandarin 0.14 Z per 100g]
20,15,8 orange juice [0.10mg per orange(86g)]
. 15,7,11,11 orange [0.17mg per peeled(131 g)]
. 6,6,48 nectarine [0.185mg per peeled(142g)]
18,17,48 honeydew melon [0.027 mg per 100g]
16,2,20,6 mango [0.023 mg per 100g]
10,43,16,5 red seedless grapes [0.072 mg per 100g of
. . . red or green seedless has ]
. 7,25,7 green grapes
. 4,33,6 red grapes [0.064mg per 100g of
. . Grapes, muscadine(has seeds).]
8,5,50 peach [0.089 mg per 98g]
4,38,4 cucumber [0.07mg per veg(301g)]
2,11,16,57 tomato juice (needs heat & oil)
0,6,12,82 tomato whole [0.08mg per 100g
. . but the lycopene is 9.66mg ]
1,19,17,13 apple(red delicious) [0.029mg per 100g of
. . . Apples, raw, with skin ]
== low-zeaxanthins relative to lutein ==
ratio's of lutein, beta-carotene,and lycopenes(omitted if zero):
-- these are among the many examples of
high-lutein foods that have no zeaxanthins .
49,21 pumpkin
47,16,4 spinach
44,9 yellow squash
41,5 pea
37,0 butternut squash
22,27 brocolli
16,0 lettuce
12,0 yellow pepper
7,3 red pepper [0.05 mg per 100g]
2,55 carrots
1,87,3 cantaloupe
### top lutein+zeaxanthin foods at usda database: ###
. nutrients per food .. foods rich in a given nutrient .
### Lutein + zeaxanthin ###
[. this data(pdf) was merged with the
zeaxanthin table (above) ]
### Lutein content of best sources ##
(extracted from a pdf)Spinach, frozen, boiled, 130g 25.606 mg
Spinach, canned, 214 g 22.631 mg
-- Magnesium 87 mg per mg
-- Vitamin K (phylloquinone) mcg 493 per 100g
Kale, frozen, boiled, 130g 25.606 mg
Kale, boiled, 130 g 23.720 mg
-- Vitamin K (phylloquinone) mcg 817 per 100g
-- Magnesium 18 mg per mg
Turnip greens, frozen, boiled, 164 g 19.541 mg
Collards, frozen, boiled, 170 g 18.527 mg
Collards, boiled, 190 g 14.619 mg
-- Vitamin K (phylloquinone) mcg 440 per 100g
-- Magnesium 20 mg per mg
Turnip greens, boiled, 144 g 12.154 mg
Dandelion greens, boiled, 105g 9.616 mg
Mustard greens, boiled, 140g 8.347 mg
Squash, summer, boiled, 180 g 4.048mg
Peas, green, frozen, boiled, 360 g 3.840 mg
Peas, edible-podded, frozen, boiled, 160g 1.429 mg
Peas, edible-podded, boiled, 160 g 1.123 mg
Squash, winter, baked, 205g 2.901 mg
Beet greens, boiled, 144g 2.619mg
Pumpkin, boiled, 245 g 2.484 mg
Squash, summer, raw 113g 2.401 mg
Broccoli, frozen, boiled, 184g 2.015 mg
Broccoli, boiled, 156 g 1.685 mg
Broccoli, raw 88 g 1.235 mg
Lettuce, raw 1 head 163 g 1.993 mg
-- butterhead (includes boston and bibb types),
Lettuce, raw 1 head 539 g 1.493 mg
Lettuce, cos or romaine, 56 g 1.295 mg
-- iceberg (includes crisphead types),
Lettuce, green leaf, raw 56 g 0.969 mg
Asparagus, frozen, boiled, 180 g 1.112 mg
Carrots, boiled, 156 g 1.072 mg
Leeks, (bulb and lower leaf-portion), boiled, 104 g 0.962 mg
Asparagus, boiled, 60 g 0.463 mg
Asparagus, canned, 72 g 0.454 mg
Pepper, sweet, red, raw 119 g 0.061 mg
#### lycopene content of best sources ####
Watermelon, raw 6.889 mg per 152 gTomatoes, red, ripe, canned, 6.641 mg per 240 g
Tomatoes, red, ripe, raw, 4.631 mg per 180 g
Papayas, raw 2.559 mg per 140 g
grapefruit 1.745 mg per 123 g
supp's that may reduce blindness risk
(from macular degeneration and cataracts)5 mg zeaxanthin,
10 mg lutein:
800 mg magnesium,
400 mg potassium
Lutein and zeaxanthin offer protect from both
age-related macular degeneration and cataracts .
. Carotenoids are fat-soluble,
and are therefore absorbed with oil;
eg, after steam-sterilizing the greens,
puree them with olive oil .
. leafy greens are a good source of
lutein, magnesium, and potassium;
esp'ly spinach . green = magnesium .
. supp's are economical .
0.5 ... 3.0 mg Melatonin at bedtime
400 mcg selenium
600 mg N-Acetyl-Cysteine or eggs
210 .. 420 mg R-ala (alpha lipoic acid)
. melatonin stimulates glutathione production;[6.21:
it is a potent inhibitor of cataracts;
proven in animal models .
Melatonin production slows after age 40,
but by age 60 virtually no melatonin is produced
at a time when most cataracts develop.
. 3 mg of mel at bedtime in elders with AMD
prevented further vision loss (Yi 2005).
. melatonin needs selenium and cysteine to work;
egg yolk has 250mg of cysteine;
but it's not as stable as N-acetyl-cysteine;
so, it's recommended it be taken with vit'C,
and other anti-oxidants found in a normal diet,
along with the r-ala .]
. ala prevents cataract by[. the Vitamin Book said vit'E's job was
protecting glutathione synthesis.
. in animal models it reduced cataract by 40%
and protected the lens from losing
vitamins C, E, and glutathione.
. vitamin C is a first-line neutralizer of radical;
it is then recycled by glutathione .
. Selenium works with alpha-lipoic acid
to increase cellular concentrations of glutathione,
. Low plasma levels of vitamin E
increase the risk of lens opacities.
facilitating the transport of selenium;
there have been contradictory results from
trying to megadose vit'E as an anti-oxidant .]
. cysteine is a component of glutathione;50 .. 150 mg riboflavin:
A combination of diallyl disulfide
(a major organosulfide in garlic oil)
and N-acetyl-cysteine (NAC)
completely prevented cataract development in animals.
Riboflavin reduces oxidized glutathione;250 mg Inositol nicotinate:
it is a precursor FADH
(reduced flavin adenine dinucleotide)
which is used by glutathione reductase,
to reduce and activate glutathione;
it makes glutathione available for the enzyme
glutathione-selenium peroxidase,
which neutralizes peroxide free radicals .
. occurs in high concentrations in the lens.2.5 mg folic acid
Inositol quenches reactive oxygen .
50 mg B6 [6.29: that's a high dose; addicting?]
1 mg B12
. B-6 prevents free-radicals by100-200 mg CoQ10;
properly metabolizing homocysteine
and is required for absorption of vitamin B12,
and proper synthesis of nucleic acids.
. . low levels of the B vitamins that are
critical to the metabolism of homocysteine),
will result in elevated levels of homocysteine,
which is a risk factor for both AMD and
other cardiovascular diseases .
. supplementing with folic acid, B6, and B12
can significantly reduce the risk of AMD
in adults with high homocysteine (Christen 2009).
500mg acetyl-L-carnitine
+ 500mg arginine base
[= acetyl-L-carnitine arginate? 6.29:
-- perhaps a patents issue]:
. Mitochondrial dysfunction can result inDHEA
reactive oxygen species
linked to both cataracts
and macular degeneration;
a combination of CoQ10, acetyl-L-carnitine,
and proper diet,
improved mitochondrial function .
Acetyl-L-carnitine can reduce cataract risk
by acetylating potential glycation sites
that would otherwise cloud lens crystallins .
. abnormally low in patients with AMD (Bucolo 2005).[6.21:
DHEA also has been shown to protect the eyes against
oxidative damage (Tamer 2007).
. do not take this hormone orally;
it can be very effective nasally
in micronized form 5..10mg;
or blenderize dhea into a progesterone cream .
. exercise can raise dhea,
as can lowering cortisol .
[6.29: my cortisol-lowering diet module is this:]
a low carb diet; and,
arginine+lysine several times:
1 tsp 3 times per day;
and 6tsp at night .]
120 mg Gingko biloba
100 mg bilberry
Gingko biloba has anti-cataract potential;500-1000 mg carnosine
Bilberry, a proanthocyanidin,
Gingko biloba and bilberry may restore
microcapillary circulation.
. bilberry contains Anthocyanidins
and Cyanidin-3-Glucoside (C3G);
. anthocyanidins may prevent leakage from capillaries,
prevalent in neovascular AMD.
Studies also show that bilberry increases
oxidative stress defense mechanisms in the eyes (Milbury 2007).
C3G fights inflammation by
inhibiting inducible nitric oxide synthase (iNOS),
C3G increases cytokine adiponectin
[. helps burn energy instead of letting it
raise sugar levels and increase fat .]
C3G may be protect against Alzheimer’s
[. that wouldn't be surprising,
if it does reduce sugar spiking .]
C3G helps to induce apoptosis
in a number of human cancer lines .
Bioflavonoids are powerful inhibitors of
the enzyme aldose reductase.
If aldose reductase activity falls,
sorbitol is not synthesized.
This reduces the accumulation of
water in the lens.
The bioflavonoids quercetin, myrcetin,
and kaempferol (from limes)
specifically inhibit diabetic cataracts.
Gingko is a widely used flavonoid that
maintains microcirculation to the eye
and inhibits free radicals.
inhibits formation of AGEsEye drops containing N-acetyl-L-carnosine
(advanced glycation end products)
can delay vision senescence in humans:Phil Micans PharmB, Vice President, IAS Group:
effective in 100% of primary senile cataract cases
and 80% of mature senile cataract cases.
N-acetyl-L-carnosine eye drops are approved for
human use in Russia for the treatment of many eye diseases.
Brite Eyes II contains
1% N-acetyl-L-carnosine
L-Carnosine is an anti-glycation agent;
Topically applied N-acetyl-carnosine
prevented light-induced DNA strand breaks
and repaired damaged DNA strands (Specht 2000),
and has improved visual acuity,
glare and lens opacification
in animals and humans with advanced cataracts
(Williams 2006, Babizhayez 2009).
Dr. Mark Babizhayev:
. the application of L-carnosine for the treatment ofupdate understanding of cataract:
human cataracts is misleading.
This is because L-carnosine readily becomes a substrate for
the activity of natural peptidases (i.e. carnosinase)
in the aqueous humor.
So much so, that there is
no sign of L-carnosine in the aqueous humor
within 15 minutes after instillation.
Furthermore,
I consider that L-carnosine eye-drops
may even be harmful for eyes because
it gradually releases histamine,
which, located as it would be
in the presence of the eye-lens
is a very toxic agent.
However, NAC eye-drops are resistant to
hydrolysis with natural carnosinase.
Therefore, NAC is the only currently known agent
which reverses and prevents human cataracts.
NewsRx.com 01-29-10/Study data from M.A. Babizhayev and colleagues
"The antioxidant activity of L-carnosine (beta-alanyl-L-histidine,wrote M.A. Babizhayev and colleagues.
bioactivated in ocular tissues)
versus N-acetylcarnosine (N-acetyl-beta-alanyl-L-histidine,
ocular-targeted small dipeptide molecules)
was studied in aqueous solution
and in a lipid environment,
employing liposomes as a model of lipid membranes.
Reactive oxygen species (ROS) were generated by an
iron/ascorbate promoter system for induction of lipid peroxidation (LPO),"
investigators in Russia report .
"L-carnosine, which is stabilized from enzymatic hydrolysis,
operates as a universal aldehyde and ROS scavenger
in both aqueous and lipid environments
and is effective at preventing ROS-induced damage
to biomolecules.
Second-generation carnosine analogs bearing the
histidyl-hydrazide moiety
were synthesized and tested versus L-camosine
for their ability to reverse the glycation process,
also known as the Maillard reaction,
and reverse the stable intermolecular cross-links,
monitored in the glucose-ethylamine Schiff base model,
ultimately resulting in the formation of
the advanced glycation end products (AGES)
from nonenzymatic glycation,
accumulating in numerous body tissues and fluids.
The obtained data demonstrate the transglycation properties
of the ophthalmically stabilized L-camosine
and L-carnosine histidyl-hydrazide derivatives tested
and can be used to decrease or predict the occurrence of
long-term complications of AGE formation
and improve therapeutically the quality of vision
and length of life for diabetes mellitus patients
and survivors with early aging.
Scientists at Innovative Vision Products, Inc. (IVP),
developed lubricant eyedrops designed as a
sustained-release 1% N-acetylcarnosine prodrug of L-camosine.
The eyedrops contain a mucoadhesive cellulose-based compound
combined with corneal absorption promoters
and glycerine in a drug-delivery system.
Anti-aging therapeutics with the
eyedrop formula including N-acetylcarnosine
showed efficacy in the nonsurgical treatment of
age-related cataracts for enrolled participants
in the prospective, randomized, double-masked,
placebo-controlled crossover clinical trial
after controlling for age, gender, and daily activities.
In a cohort in excess of 50,500 various patients
seeking cutting-edge medical care,
the N-acetylcamosine topical eyedrops target therapy
was demonstrated to have significant efficacy, safety,
and good tolerability for the prevention and treatment of
visual impairment in this older population
with relatively stable patterns of causes
for blindness and visual impairment.
Overall, accumulated study data demonstrate that
the IVP-designed new vision-saving drugs,
including N-acetylcarnosine eyedrops,
promote health vision and prevent vision disability from
senile cataracts, primary open-angle glaucoma,
age-related macular degeneration, diabetic retinopathy,
and aging.
N-acetylcarnosine eyedrop therapy is the crown jewel of the
anti-aging medical movement
and revolutionizes early detection, treatment,
and rejuvenation of aging-related eye-disabling disorders,"
Babizhayev and colleagues published their study in
American Journal of Therapeutics
(
N-Acetylcarnosine Lubricant Eyedrops
Possess All-In-One Universal Antioxidant Protective Effects
of L-Carnosine in Aqueous and Lipid Membrane Environments,
Aldehyde Scavenging, and Transglycation Activities
Inherent to Cataracts:
A Clinical Study of. American Journal of Therapeutics,
UNKNOWN DATE;16(6):517-533
).
For additional information, contact
M.A. Babizhayev, Innovat Vis Prod Inc.,
Moscow Division, Ivanovskaya 20, Suite 74, Moscow 127434, Russia.
The publisher of the American Journal of Therapeutics
can be contacted at: Lippincott Williams & Wilkins,
530 Walnut St., Philadelphia, PA 19106-3621, USA.
medications that increase blindness risk
6.22:pills vs eyes 2008:
Open-angle glaucoma((a bunch of corticosteroids))
Angle-closure glaucoma:
--[ what do these drugs have in common with eph? ][any anticholinergic may precipitate narrow-angle glaucoma]
cimetidine TAGAMET
ephedrine PRIMATENE, eph
epinephrine ADRENALINE, PRIMATENE MIST
fluoxetine PROZAC, SERAFEM
fluvoxamine LUVOX
ipratropium ATROVENT
paroxetine PAXIL, PEXEVA
ranitidine ZANTAC
sulfamethoxazole (with trimethoprim) BACTRIM, COTRIM, SEPTRA
sulfisoxazole GANTRISIN
topiramate TOPAMAX
venlafaxine EFFEXOR, EFFEXOR XR
Cataracts
betamethasone ALPHATREX, DIPROLENE, DIPROSONEbusulfan BUSULFEX, MYLERAN
chlorpromazine THORAZINE
desoximetasone TOPICORT
dexamethasone DECADRON, HEXADROL, MYMETHASONE
fluocinolone SYNALAR
fluocinonide LIDEX-E, LIDEX
hydrocortisone (oral) CORTEF, HYDROCORTONE
hydrocortisone (topical) ALA-CORT, HI-COR, HYTONE, NEACLEAR LIQUID OXYGEN SCAR, PENECORT, SYNACORT
methylprednisolone MEDROL
prednisolone PRELONE
prednisone DELTASONE
thioridazine MELLARIL
triamcinolone (injectable)
triamcinolone (topical) ARISTOCORT, KENALOG, TRIACET, TRIDERM
Retinal Abnormalities
acitretin SORITANEchloroquine ARALEN
chlorpromazine THORAZINE
etretinate TEGISON
hydroxychloroquine PLAQUENIL
isotretinoin ACCUTANE
tamoxifen NOLVADEX
thioridazine MELLARIL
tretinoin RENOVA, RETIN-A
vitamin A (retinol) AQUASOL A
Optic Nerve Diseases
amiodarone CORDARONE, PACERONEethambutol
linezolid ZYVOX
sildenafil VIAGRA
tadalafil CIALIS
vardenafil LEVITRA
sleeping aids
dalmane is a benzodiazepinedalmane cataracts heavily affect females:
. of the few people developing Cataracts while on Dalmane
most were women, and 21% were
age 20..30 -- very early for cataracts .
[6.29:
. keep in mind that nothing here is proven;
because, it's epidemiology,
not data from randomized studies .
-- this reminds that the pharm'industry
was once notorious for allowing women to be users,
but not including women in their pre-market trials;
dalmane could be one of these?
had they taken women's chemistry into account,
there may have been a different presentation of it ? ]
anti-aggressives
benzodiazepines are related to anti-aggressives:Epidemiological reviews have suggestedref# Exposure to phenothiazine drugs and risk of cataract.
a possible link between cataract occurrence
and other psychotropic medications,
including benzodiazepines .
. long-term use of corticosteroids, phenothiazines,
certain other antipsychotic drugs,
some antineoplastic agents, and amiodarone
may increase cataract incidence.
. in the mid-1960s,
a decade after the marketing of phenothiazines,
drug-related ocular changes were reported in
patients who had been receiving years of
high-dose antipsychotic medication;
chlorpromazine was the primary offender.
Research also associated cataract occurrence with
other phenothiazines;
thioridazine, thiothixene,
trifluoperazine, levomepromazine,
and perphenazine are frequently cited examples.
A 1999 study of cataract occurrence
compared schizophrenic patients (26%)
with the general population (<1%).
. in addition to pharmaceutical exposures
schiz'ics often have additional risk factors:
smoking and poor dietary habits,
along with emotion-based metabolic disorders
(high cortisol, high insulin,
and blood sugar instabilities) .
[6.21:
. some of the new atypicals are clearly
increasing carb' intolerance,
and thus any cataracts blamed on sugar instabilities
must again point the blame at these meds .]
Epidemiological reviews have suggested
a possible link between cataract occurrence
and other psychotropic medications,
including benzodiazepines
and certain antidepressants
of the tricyclic and mao inhibitor classes .
Arch Ophthalmol. 1991;109(2):256-260.
Clinical reports have indicated an increased risk ofref# Sunlight and other risk factors for cataracts:
ocular opacities in users of phenothiazine drugs,
and some recent epidemiologic studies have found
an association between cataract and a
history of tranquilizer use.
To examine the effects of major tranquilizers
(phenothiazines and haloperidol)
on the risk of cataract extraction,
while controlling for suspected risk factors
such as diabetes and steroid use,
a matched cohort study was performed .
The use of either antipsychotic
or other phenothiazine drugs
increased the risk of cataract extraction
by roughly 3.5 times
in those who were both current users
and were exposed some time in the
2 to 5 years prior to their extraction.
Risk was also increased in individuals with
prior use of
antidiabetic agents,
systemic steroids,
and benzodiazepines.
an epidemiologic study.
American Journal of Public Health, Vol. 78, Issue 11 1459-1462
. relation between individual exposure to sunlightrenewed interest in issue with anti-aggressives
and the risk of cataracts.
Sunlight exposure was very slightly related to
all types of opacities combined.
Although the numbers of cases with
each type of opacity was small,
the risk of cataracts was slightly increased
in medium and high exposure categories
for persons having cortical or
posterior subcapsular opacities only,
but not nuclear sclerotic changes.
Persons with dark brown or hazel eyes
are at increased risk.
An unexpected finding was that
persons who reported using tranquilizers
for six months were at increased risk.
. recent questions about quetiapine (seroquel)-- agingeye.net's summary:
as a possible cataract inducer
have increased the current interest in this issue
across the antipsychotic pharmacotherapy spectrum.
. photosensitizing agents
like chlorpromazine and its metabolites
denature proteins,
which become opacified when exposed to sunlight
and are deposited in the lens, cornea, and skin.
Melanin is also considered a probable cause
of lens discoloration
because it traps free radicals produced by
chlorpromazine.
Melanin and chlorpromazine
have a strong bonding affinity.
When chlorpromazine interacts with
ultraviolet-B light,
it produces purple or bluish colored
free-radical metabolites.
This phototoxic reaction creates the
cataract cellular changes.
Thorazine has been shown to be associated with
pigmented corneal deposits
and anterior capsular cataracts.
Pigmentary retinopathy is usually associated with
a much higher dose (>2400 mg/d).
Pigment deposition on the cornea and lens
appears to be dose related and is usually irreversible.
Chlorpromazine-induced anterior cataracts
do not normally extend to the rest of the lens
even when patients continue taking chlorpromazine.
They usually enjoy good vision for a long period
despite a dense cataract at the pupillary region.
Thioridazine (Mellaril)
has also been reported to induce[6.29:
lenticular changes unrelated to pigmentary retinopathy.
[Siddall J:
Ocular complications related to phenothiazines.
Dis Nerv Syst 1968; 29:10-13]
However, contrary reports have indicated
no evidence of lens opacity
in patients taking this drug.
[Barnes G, Cameron M:
Skin and eye changes with chlorpromazine therapy.
Med J Aust 1966; 1:478-481]
the risk of cataract occurrence remains unclear.
it's mainly known for retinopathy:
(Thioridazine can remain bound to melanin
in the retinal pigment epithelial cells
for many years with progressive visual loss
despite discontinuation of their use.)]
Ziprasidone (Geodon)
Cataract occurrence was observed as an infrequent finding6.22:
during screening for adverse events
before ziprasidone was approved for clinical use.
[Geodon, in Physicians' Desk Reference, 56th ed.
Montvale, NJ, Medical Economics Co, 2002, pp 2688-2692]
However, there is no known causal connection
between this drug and lenticular opacities.
Claudio Cepeda`Psychotic symptoms in children and adolescents
. cataracts from chlorpromazine, thioridazine, and perphenazineHandbook of Psychiatric Drug Therapy
seem to be more frequent in young schiz'ic's
with rates in 22 ... 26%;
the young schiz'ics have an 82%
overall ocular pathology rate .
. these numbers seemed consistent with
smoking and diabetic effects
and there are multiple sources of diabetes
in most schiz'ics:
chronic stress, poor sleep, and bad diet .
. thioridazine > 800 mg results in
irreversible retinal pigmentation
which can result in blindness .
By Lawrence A. Labbate,
[. among the antipersonell drugs
-- anti-psychotics, anti-aggressives --
all the highly sedating ones
{ thioridazine
, chlorpromazine
, quetiapine
} are suspected of causing cataracts;
is this true also for any of the
moderately sedating: ?
{ fluphenazine
, trifluoperazine
, loxapine
, molindone
} ]
. any anticholinergic may precipitate[trazodone is weakly anticholinergic
narrow-angle glaucoma;
this happens less with the higher-potency 1st gen's,
and by avoiding co.use of antiparkinson drugs,
most of which are anticholinergics
(another class of antiparkinson drugs
is the dopamine releaser, eg: amantadine).
. thioridazine has potent anticholinergic effects .
. the antipsychotics best known for
not causing weight gain (abilify, geodon)
also may cause insomnia that leads to
co.use of benzodiazepines or trazodone;
benzodiazepines are anticholinergic .
but used cautiously on elders who have
glaucoma, especially angle-closure .]
. non-sedating antipsychotics are also[6.29:
the most likely among
later generation antipsychotics to cause
akathisia (6.29:
that is the feeling of
getting sick from having to sit still;
but moving around doesn't really help
because the lack of stimulation
has to do with the way certain meds
can affect your neuro-hormones .
people with natural akathisia
are said to have attention deficit disorder,
and the cure is amphetamines;
generally the opposite of anti-dopaminergics)
. akathisia is more likely in
the higher-powered 1st-gen's
(they have less anticholinergic properties);
so they may be co.used with
sedatives:
# beta-adrenergic blockers
(propranolol or nadolol);
# or rarely a benzodiazepine or clonidine .
. quetiapine induces cataracts in animals
so the product label susggests slit-lamp exam's;
ophthalmologic studies find no evidence
supporting regular eye exam's;
however, since schiz'ics have
other risk factors for cataracts,
a referral to an ophthalmologist
for an eye exam
can be part of routine medical care
. but that shouldn't be expected;
not in tightly managed hmo's, right? ]
[. in the section on endocrine side effects
there's no mention of effects on thyroid;
of course,
there's no mention of insulin either,
but there's a whole section reserved for
"(weight gain),
and that's all with a chapter titled:
"(metabolic monitoring for 2nd-gen antipsychotics) !
...
. plus, what do you say about something like dhea,
after your profession has publically said
dhea seems to have no function ? ]
. diabetic ketoacidosis remains a rare possiblity[ziprasidone is not a sedative;
for all these antipsychotics .
. among the new anti-aggressives,
ziprasidone and aripiprazole cause
the least weight gain,
if you're used to sedatives,
it can cause eno' anxiety to inhibit appetite .]
. all schiz'ics on 2nd-generation antipsychotics[is ziprasidone 2nd generation?
should be monitored at least twice yearly
for glucose abnormalities
and lipid profile .
it specifically prefaced the call for
diabetes monitoring
with the assertion that ziprasidone
was causing no glucose abnormalities .
6.29:
. yea, but geodon's anx might increase
carb intolerance?
or they could be saying that
one may as well operate as if
geodon is not being used,
because they don't think highly of it
(they mention the profession was finding out
the dose needed to suppress aggression
is considerably higher than documented
and the new dose and rate of attack
could precipitate a cardiac event .]
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
phosphatidylinositol 3-kinase activity
Breast Cancer Res (2005) 7: R699-707
. [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:
Sigma Chemical Co. (St Louis, MO, USA).
--. wholesaler only:
but they do have Se-methylselenocysteine:
M6680 Sigma Se-(Methyl)selenocysteine hydrochloride 95% (TLC)
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
Protease inhibitors suppress apoptotic features induced by MSC
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
links from i-care:
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 .]
-- 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-regulatesProgrammed Cell Death
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 (PCD), or apoptosis,Se-methylselenocysteine inhibits
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.
phosphatidylinositol 3-kinase activity
Breast Cancer Res (2005) 7: R699-707
Se-methylselenocysteine (MSC),Se-methylselenocysteine (MSC) chemically synthesized:
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.
. [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-- Sodium selenite was obtained from
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.
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: 863394-07-4Sigma-Aldrich Corp
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
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 Account12.12: news.health/se/se-methylselenocysteine/Protease inhibitors:
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.
Protease inhibitors suppress apoptotic features induced by MSC
These results confirm previous observations12.26: health/se/age-related macular degeneration:
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.
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:12.26: web.health/se/macular degeneration/se's role:
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).
links from i-care:
# Glutathione and its related enzyme precursor amino acids[. interesting term: diabetic macular edema
(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.
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 .]
2009-12-31
inflammation syndrome and colon cancer
11.16: health/colon cancer
summary:
. inflammation syndrome seems to be a key;
foods tend affect risk in proportion to their inflammation index:
grain-fed meats, high-glycemic fruits
are inflammatory,
while wild fish and low-glycemic veg's
are anti-inflammatory
. aspirin too reduces both risk and inflammation,
though the dose that might be useful
might also be kidney problems .
inflammation syndrome
risk-factors-colorectal-cancer
summary:
. inflammation syndrome seems to be a key;
foods tend affect risk in proportion to their inflammation index:
grain-fed meats, high-glycemic fruits
are inflammatory,
while wild fish and low-glycemic veg's
are anti-inflammatory
. aspirin too reduces both risk and inflammation,
though the dose that might be useful
might also be kidney problems .
inflammation syndrome
. conditions that contributes to inflammation of the colon can lead to cancer.
Diabetes Can Lead to Colon Cancer
According to WebMD, people with diabetes have a 30-40%
increased risk of colon cancer.
So it's important to maintain a normal weight
and to lose weight if an individual is obese.
risk-factors-colorectal-cancer
. a person who already has had colorectal cancer
may develop the disease a second time.
. those who have chronic inflammatory conditions of the colon,
such as ulcerative colitis or Crohn's disease,
also are at higher risk of developing colorectal cancer.
# Diet. A diet high in fat and calories and low in fibermay be linked to a greater risk of developing colorectal cancer.
# Lifestyle factors.You may be at increased risk for developing colorectal cancer if youdrink alcohol, smoke, don't get enough exercise,and if you are overweight.
# Diabetes.People with diabetes have a 30-40% increased riskof developing colon cancer.
2006, vol. 15, no12, pp. 2391-2397
More Evidence Stress and Cancer are Linked Posted by: Dr. Mercola
Cancer Research November 1, 2006; 66(21): 10357-10364
Science Daily November 3, 2006
Obesity and diabetes are established risk factorsSmoking:
for colorectal cancer but have mainly been assessed independently.
There are few data about whether the metabolic syndrome,
which refers to a clustering of cardiovascular disease risk factors
thought to be related to insulin resistance,
including obesity, type 2 diabetes, hyperlipidemia, and hypertension,
is associated with colorectal cancer risk.
Out of the markers of the metabolic syndrome assessed,
overweight and diabetes are risk factors for colorectal cancer,
whereas, in contrast to their role in cardiovascular disease,
elevated blood pressure and hypercholesterolemia are not.
It has been shown that smokers have a 30-40% greater chancehttp://www.aicr.org.uk/ColonCancerFAQs.stm
of acquiring colon cancer than non- smokers.
Obesity can increase the risk of cancer of the colon by up to one third.obesity from eating for stress may be another link
High alcohol intake is also known to increase the risk of colon cancer.
However, some common drugs, such as aspirin-like painkillers
and hormone replacement therapy,
are known to reduce the risk of bowel cancer.
Low fat, high fibre diets appear to carry a lower risk.
Greater consumption of vegetables and fruit has also been shown to reduce the risk.
Increased consumption of red meat and processed meat
has been linked to a higher risk.
By comparison, eating fish does not appear to be a risk factor.
Some evidence suggests that certain dietary supplements,
such as calcium, selenium and, possibly, folic acid
can reduce the risk.
More Evidence Stress and Cancer are Linked Posted by: Dr. Mercola
Cancer Research November 1, 2006; 66(21): 10357-10364
Science Daily November 3, 2006
Stress
Norepinephrine, a hormone produced during periods of stress, may increase the growth rate of cancer.
The norepinephrine can stimulate tumor cells to produce two compounds (matrix metalloproteinases called MMP-2 and MMP-9) that break down the tissue around the tumor cells and allow the cells to more easily move into the bloodstream.
Once there, they can travel to other organs and tissues and form additional tumors, a process called metastasis.
Norepinephrine may also stimulate the tumor cells to release a chemical (vascular endothelial growth factor, or VEGF) that can aid in the growth of the blood vessels that feed cancer cells. This can increase the growth and spread of the cancer.
Researchers traced the harmful effect of norepinephrine after applying it to cancer cell lines used to study nasopharyngeal carcinoma (NPC), an incurable head and neck cancer associated most frequently with those of Chinese descent.
2009-12-28
evangelizing non-toxic selenium
Se-methylselenocysteine is the most valuable form of selenium
[11.3: . garlic grown in a selenium-rich medium can produce Se-methylselenocysteine;
which has been demonstrated in animal carcinogenesis bioassays
to be a potent cancer chemopreventive agent . ]
[2012.2.18: updated table of contents:]
- supporting se-msc as cancer preventive
- medical resources
notes
for further work
//knol.google.com/k/philip-torrance/anti-cancer-selenium-cysteine-compounds/
but first, do the revisions and see if the link changes .
11.5: todo.health/se:
. put in summary first lesson of anti cancer
any form of se can prevent many cases of cancer if local soil has deficient in se .
. 2nd point is unproven but worth exploring:
use of non-toxic forms to prevent more cases with mega-dosing .
Ghose A, Fleming J, El-Bayoumy K, Harrison PR.
Enhanced sensitivity of human oral carcinomas
Enhanced sensitivity of human oral carcinomas
to induction of apoptosis by selenium compounds:
involvement of mitogen-activated protein kinase and Fas pathways.
Comparison of Selenium Levels and Sources
involvement of mitogen-activated protein kinase and Fas pathways.
Cancer Res. 2001 Oct 15;61(20):7479-87.
Whanger PD. Selenium and its relationship to cancer: an update.
it was shown by Hoffman J L (1975) selenium toxicity and methyl group metabolism
that se-methionine was not metabolized to selenocysteine as readily as methionine
Whanger PD. Selenium and its relationship to cancer: an update.
Br
J Nutr. 2004;91(1):11-28. (PubMed)
phil.whanger@orst.edu
Se-broccoli similar to se-garlic
J Med Food. 2003 Spring;6(1):19-26.
Reduction of cancer risk by consumption of selenium-enriched plants:
enrichment of broccoli with selenium increases the anticarcinogenic properties of broccoli.
jfinley@gfhnrc.ars.usda.gov
Med Hypotheses. 2006;67(2):318-22. Epub 2006 Mar 30.
Cancer chemoprevention: selenium as a prooxidant, not an antioxidant.
Rocky Mountain Selenium, Inc.,
endrake@airbits.com
Lessons from Basic Research in Selenium and Cancer Prevention
Journal of Nutrition Vol. 128 No. 11 November 1998, pp. 1845-1854
[. similar effects have been shown in humans,
with significant reductions in occurrences of the major cancers in the U.S. population:
(
lung: 54 % (P = 0.04),
colon: 37 % (P = 0.002)
prostate: 42 % (P = 0.03)
)
. the study was documented by Clark et al. (1996):
Effects of selenium supplementation for cancer prevention
in patients with carcinoma of the skin.
J. Am. Med. Assoc. 1996; 276:1957-1985
. the Clark et al. (1996) trial used a [a non-methionine form]
( Selenomax¨ from Nutrition 21 La Jolla, Calif.)
--
. according to Life Extension: A Practical Scientific Approach (p#671)
Selenomax¨ is not your typical selenized yeast:
. most selenized yeasts are primarily selenomethionine
which is less effective than non-organics (eg selenite)
at elevating deficient levels of glutathione peroxidase;
an exception is selenized yeast from Nutrition 21
which exhibits good results in this test .
. while being organic, Selenomax¨ is most likely a seleno-trisulfide
and not primarily selenomethionine .
[or a di-methyl-di-selenide
. according to Dr.Whanger's ref's
yeast's se forms may vary like so:
0...4 % selenate
0...25 % selenite
6...20 % Se-methylselenocysteine
23...63 % (Nutrition 21: 16 %) se-methionine
13...21 % (Nutrition 21: 11 %) se-cysteine
13...51 % (Nutrition 21: 81 %) other:
seleno-lanthionine,
seleno-cystathionine,
{gamma}-glutamyl-seleno-ethionine,
Se-adenosyl seleno-homocysteine,
Se-ally selenocysteine,
Se-propenyl selenocysteine,
and unknown.
#46 Speciation of selenoamino acids and organoselenium compounds in selenium-enriched yeast
using high-performance liquid chromatography-inductively coupled plasma mass spectrometry.
J Anal Atomic Spect12 :785 Ð788,1997 .
#47 Analytical selenoamino acid studies
by chromatography with interfaced atomic mass spectrometry and atomic emission spectral detection.
Fresenius J Anal Chem362 :447 Ð456,1998 .
#50 Identification of the principal selenium compounds in selenium-enriched natural sample extracts
by ion-pair liquid chromatography with inductively coupled plasma- and electrospray ionization-mass spectrometric detection.
Anal Commun36 :249 Ð252,1999 .
#54 Characterization of selenium species in biological extracts
by enhanced ion-pair liquid chromatography with inductively coupled plasma-mass spectrometry and by reference electrospray ionization-mass spectrometry.
Spectrochimica Acta54 :1573 Ð1591,1999 .
what are selenotrisulfides?
Selenocompounds in Plants and Animals and their Biological Significance
Journal of the American College of Nutrition, Vol. 21, No. 3, 223-232 (2002)
. when selenite was given to animals,
it represented only 14% of the overall quantity of selenium [found in tissues]
and the seleno-trisulfide metabolites,
as a percentage of total selenium absorbed, were:
( seleno-di-cysteine: 10 %;
, mixed seleno-tri-sulfide of cysteine and reduced glutathione: 14 %;
, seleno-di-glutathione: 8 %
). [seleno-tri-sulfides are apparently 1 part se, and 2 parts
sulfer-based organic ]
. selenized yeast often contains mostly Selenomethionine
but the amount can vary markedly depending upon the growth conditions.
[ eg, incorporation of selenite with cysteine, cystine and glutathione
into Seleno-di-cysteine and seleno-di-glutathione
is greatly affected by pH. {Czauderna, Samochocka}
] [and may vary on storage conditions:
All the yeast-based supplements and one yeast-free supplement
formed S-(methylseleno)cysteine on heating
(from a reaction between di-methyl-di-selenide and cysteine or cystine)
-- there were similar speciation patterns observed between
yeast-based supplements subject to extended storage
and those heated briefly at elevated temperatures . ]
. plants and animals may contain some inorganic se;
when inorganics are found, they are usually selenate .
. most plants contain se-methionine,
which animals can uses as either se or methionine
[hence the reason animals short on protein (esp'ly methionine)
will still be deficient in se after getting se-methionine]
. animals contain mostly variants of se-cysteine;
any se-methionine used as se rather than protein
will soon be reduced and reconstructed as some se-cysteine .
. the few plants that contain mostly se-cysteine (esp'ly Se-methylselenocysteine)
-- when they contain any se at all --
include garlic, onions, wild leeks, and broccoli florets or sprouts .
]
the scientific conclusion:
[11.4:
. what was proven here was not that increasing se decreases cancer risk,
but that being se deficient does increase cancer risk .
. it's an essential mineral, and plants don't need it,
so the only sure source is seafood and or supplements .
]
Chemical transformations of selenium in living organisms.
Improved forms of selenium for cancer prevention.
phil.whanger@orst.edu
Selenomethionine (Semet) is the major seleno-compound in cereal grains and enriched yeastProc Nutr Soc. 2005 Nov;64(4):527-42.
whereas Se-methylselenocysteine (SeMCYS) is the major seleno-compound in Se-accumulator plants
and some plants of economic importance such as garlic and broccoli exposed to excess Se.
Animals can metabolize both Semet and SeMCYS.
Epidemiological studies have indicated an inverse relationship
between Se intake and the incidence of certain cancers.
Blood or plasma levels of Se are usually lower in patients with cancer
than those without this disorder,
but inconsistent results have been found with toenail-Se values
and the incidence of cancer.
There have been eight trials with human subjects conducted
on the influence of Se on cancer incidence or biomarkers,
and except for one,
all have shown a positive benefit of Se on cancer reduction
or biomarkers of this disorder.
This is consistent with about 100 small-animal studies
where Se has been shown to reduce the incidence of tumours in most of these trials.
Se-enriched yeast is the major form of Se used in trials with human subjects.
In the mammary-tumour model,
SeMCYS has been shown to be the most effective seleno-compound
identified so far in reduction of tumours.
Several mechanisms have been proposed on the mechanism whereby Se reduces tumours.
Even though SeMCYS was shown to be the most effective seleno-compound
in the reduction of mammary tumours,
it may not be the most effective seleno-compound for reduction of colon tumours.
Selenium in cancer prevention: a review of the evidence and mechanism of action.
Se is an unusual trace element in having its own codon in mRNA
that specifies its insertion into selenoproteins as selenocysteine (SeCys),
by means of a mechanism requiring a large SeCys-insertion complex.
This exacting insertion machinery for selenoprotein production
has implications for the Se requirements for cancer prevention.
If Se may protect against cancer, an adequate intake of Se is desirable.
However, the level of intake in Europe and some parts of the world
is not adequate for full expression of protective selenoproteins.
The evidence for Se as a cancer preventive agent
includes that from geographic, animal, prospective and intervention studies.
Newly-published prospective studies on oesophageal, gastric-cardia and lung cancer
have reinforced previous evidence,
which is particularly strong for prostate cancer.
Interventions with Se have shown benefit in reducing the risk of
cancer incidence and mortality in all cancers combined,
and specifically in liver, prostate, colo-rectal and lung cancers.
The effect seems to be strongest in those individuals with the lowest Se status.
As the level of Se that appears to be required for optimal effect
is higher than that previously understood to be required to maximise
the activity of selenoenzymes,
the question has been raised as to whether
selenoproteins are involved in the anti-cancer process.
However, recent evidence showing an association between Se,
reduction of DNA damage and oxidative stress
together with data showing an effect of selenoprotein genotype on cancer risk
implies that selenoproteins are indeed implicated.
The likelihood of simultaneous and consecutive effects at different cancer stages
still allows an important role for
anti-cancer Se metabolites such as methyl selenol
formed from gamma-glutamyl-selenomethyl-SeCys and selenomethyl-SeCys,
components identified in certain plants and Se-enriched yeast
that have anti-cancer effects.
There is some evidence that Se may affect
not only cancer risk but also progression and metastasis.
Se-broccoli similar to se-garlic
J Med Food. 2003 Spring;6(1):19-26.
Reduction of cancer risk by consumption of selenium-enriched plants:
enrichment of broccoli with selenium increases the anticarcinogenic properties of broccoli.
jfinley@gfhnrc.ars.usda.gov
Plant-based diets and phytochemicals present in plants
are associated with decreased risk of cancer.
Brassica species, and broccoli in particular,
are associated with reduced risk of several important cancers.
Broccoli accumulates Se many-fold beyond the concentration of Se in the soil,
and the chemical form of Se in broccoli
is similar to the chemical form in high-Se garlic,
a food with unique chemoprotective properties.
Se from broccoli grown to accumulate more than 500 micro g Se/g
did not accumulate in rat tissues
or increase glutathione peroxidase enzyme activity
to the same extent as Se salts or seleno-amino acids.
Se from high-Se broccoli decreased the incidence of aberrant crypts in rats
with chemically induced colon cancer by more than 50%, compared with controls.
Se from high-Se broccoli also decreased the incidence of mammary tumors in rats
treated with 7,12-dimethylbenz(a)anthracene (DMBA)
and tumor number and volume in APC(min) mice.
These results suggest that development of methods to increase
the natural accumulation of Se in broccoli
may greatly enhance its health-promoting properties.
Med Hypotheses. 2006;67(2):318-22. Epub 2006 Mar 30.
Cancer chemoprevention: selenium as a prooxidant, not an antioxidant.
Rocky Mountain Selenium, Inc.,
endrake@airbits.com
Although the average daily dietary selenium (Se) intake in the United States11.4:
is consistently above the adult RDA of 55 microg Se/day,
supranutritional supplements of 200 microg Se/day have been shown to provide
chemopreventive benefits against several cancers, particularly prostate cancer.
The hypothesis herein contends
that selenium compounds with the greatest anticarcinogenic potency
are likely to be sodium selenite with Se in the +4 oxidation state
and methylseleninic acid.
These compounds exert their cancer chemopreventive effects
by directly oxidizing critical thiol-containing cellular substrates,
and are more effective
than the more frequently preferred (used) supplements of
selenomethionine and
Se-methylselenocysteine
that lack oxidation capability.
Selenate (+6 Se) the immediate precursor of selenite (+4 Se)
can be metabolically reduced,
and although less potent than the +4 Se compounds cited above,
appears to be a more effective anticarcinogen than organic forms of dietary selenium.
Apoptosis, an important, Se-induced anticarcinogenic mechanism,
is accomplished by the direct oxidation of
vicinal sulfhydryl groups in cysteine clusters within the catalytic domains of
cellular enzymes (e.g., protein kinase C),
and by the production of CH3Se-,
which reacts with O2 to generate superoxide
and other reactive oxygen species (ROS).
Activated oncogenes "prime" cells for Se-induced prooxidative apoptosis
thereby providing the needed margin for "killing" cancer cells
while leaving normal, healthy cells unharmed.
Selenoethers, such as selenomethionine and Se-methylselenocysteine
are not oxidizing agents,
and first, must be converted to methylselenol (CH3Se-)
that can be directly oxidized to methylseleninic acid.
The addition of methioninase, to selenomethionine,
or beta-lyase to Se-methylselenocysteine,
rapidly produces significant amounts of methylselenol,
which may be oxidized to methylseleninic acid
or may react with O2 to produce superoxide and ROS,
resulting in anticarcinogenic activities comparable to selenite
or methylseleninic acid.
The relatively large amounts of selenomethionine or Se-methylselenocysteine needed
to produce apoptosis in cancer cells
compared with selenite or methylseleninic acid
are a probable consequence of low tissue levels of the required enzymes.
Even though many studies have consistently shown that
selenomethionine is an ineffective anticarcinogen
at doses corresponding to those currently allowed by the FDA,
it has been chosen as the Se intervention agent in the
32,500-man (phase III), NCI-funded SELECT trial,
which tests the effectiveness of dietary supplements of dietary supplements of Se and tocopherol,
individually or in combination, in the prevention of prostate cancer.
In 2013, when the data are in,
the value of using Se supplements for cancer chemoprevention
is likely to be underestimated.
Lessons from Basic Research in Selenium and Cancer Prevention
Journal of Nutrition Vol. 128 No. 11 November 1998, pp. 1845-1854
Selenium, in the form of selenite or selenomethionine,
functions as an essential micronutrient at levels of
[approx] 0.1 ppm (mg/kg) in the animal diet,
but it becomes a toxin at levels of 8-10 ppm (Jacobs and Frost 1981).
At the other extreme,
selenium deficiency is customarily induced in laboratory animals by
[a dose of less than ] 0.01 ppm Se.
the effect of selenium deficiency on carcinogenesis.
The information in this particular topic is not only sketchy
but also inconsistent.
[anti-cancer effects unrelated to resolving deficiency issues
involve dosing at levels ] above dietary requirement,
usually in the range of 1-5 ppm Se.
More than 90% of the selenium cancer chemoprevention experiments
have used either sodium selenite or selenomethionine
as the test reagent because they are commercially available.
Both of these compounds are known to suppress carcinogenesis in many animal models
(Combs 1997, El-Bayoumy 1991, Ip 1986, Medina and Morrison 1988).
The effect is not organ specific,
because tumor inhibition has been reported in
mammary gland, liver, skin, pancreas, esophagus, colon and a few other sites.
[. similar effects have been shown in humans,
with significant reductions in occurrences of the major cancers in the U.S. population:
(
lung: 54 % (P = 0.04),
colon: 37 % (P = 0.002)
prostate: 42 % (P = 0.03)
)
. the study was documented by Clark et al. (1996):
Effects of selenium supplementation for cancer prevention
in patients with carcinoma of the skin.
J. Am. Med. Assoc. 1996; 276:1957-1985
. the Clark et al. (1996) trial used a [a non-methionine form]
( Selenomax¨ from Nutrition 21 La Jolla, Calif.)
--
. according to Life Extension: A Practical Scientific Approach (p#671)
Selenomax¨ is not your typical selenized yeast:
. most selenized yeasts are primarily selenomethionine
which is less effective than non-organics (eg selenite)
at elevating deficient levels of glutathione peroxidase;
an exception is selenized yeast from Nutrition 21
which exhibits good results in this test .
. while being organic, Selenomax¨ is most likely a seleno-trisulfide
and not primarily selenomethionine .
[or a di-methyl-di-selenide
. according to Dr.Whanger's ref's
yeast's se forms may vary like so:
0...4 % selenate
0...25 % selenite
6...20 % Se-methylselenocysteine
23...63 % (Nutrition 21: 16 %) se-methionine
13...21 % (Nutrition 21: 11 %) se-cysteine
13...51 % (Nutrition 21: 81 %) other:
seleno-lanthionine,
seleno-cystathionine,
{gamma}-glutamyl-seleno-ethionine,
Se-adenosyl seleno-homocysteine,
Se-ally selenocysteine,
Se-propenyl selenocysteine,
and unknown.
#46 Speciation of selenoamino acids and organoselenium compounds in selenium-enriched yeast
using high-performance liquid chromatography-inductively coupled plasma mass spectrometry.
J Anal Atomic Spect12 :785 Ð788,1997 .
#47 Analytical selenoamino acid studies
by chromatography with interfaced atomic mass spectrometry and atomic emission spectral detection.
Fresenius J Anal Chem362 :447 Ð456,1998 .
#50 Identification of the principal selenium compounds in selenium-enriched natural sample extracts
by ion-pair liquid chromatography with inductively coupled plasma- and electrospray ionization-mass spectrometric detection.
Anal Commun36 :249 Ð252,1999 .
#54 Characterization of selenium species in biological extracts
by enhanced ion-pair liquid chromatography with inductively coupled plasma-mass spectrometry and by reference electrospray ionization-mass spectrometry.
Spectrochimica Acta54 :1573 Ð1591,1999 .
what are selenotrisulfides?
Selenocompounds in Plants and Animals and their Biological Significance
Journal of the American College of Nutrition, Vol. 21, No. 3, 223-232 (2002)
. when selenite was given to animals,
it represented only 14% of the overall quantity of selenium [found in tissues]
and the seleno-trisulfide metabolites,
as a percentage of total selenium absorbed, were:
( seleno-di-cysteine: 10 %;
, mixed seleno-tri-sulfide of cysteine and reduced glutathione: 14 %;
, seleno-di-glutathione: 8 %
). [seleno-tri-sulfides are apparently 1 part se, and 2 parts
sulfer-based organic ]
. selenized yeast often contains mostly Selenomethionine
but the amount can vary markedly depending upon the growth conditions.
[ eg, incorporation of selenite with cysteine, cystine and glutathione
into Seleno-di-cysteine and seleno-di-glutathione
is greatly affected by pH. {Czauderna, Samochocka}
] [and may vary on storage conditions:
All the yeast-based supplements and one yeast-free supplement
formed S-(methylseleno)cysteine on heating
(from a reaction between di-methyl-di-selenide and cysteine or cystine)
-- there were similar speciation patterns observed between
yeast-based supplements subject to extended storage
and those heated briefly at elevated temperatures . ]
. plants and animals may contain some inorganic se;
when inorganics are found, they are usually selenate .
. most plants contain se-methionine,
which animals can uses as either se or methionine
[hence the reason animals short on protein (esp'ly methionine)
will still be deficient in se after getting se-methionine]
. animals contain mostly variants of se-cysteine;
any se-methionine used as se rather than protein
will soon be reduced and reconstructed as some se-cysteine .
. the few plants that contain mostly se-cysteine (esp'ly Se-methylselenocysteine)
-- when they contain any se at all --
include garlic, onions, wild leeks, and broccoli florets or sprouts .
]
. the Nutrition 21 Selenomax¨ trial was
double-blind, randomized, placebo-controlled, and involving
1312 basal cell or squamous cell carcinoma of the skin patients (mostly men)
from a selenium-deficient area (eastern coastal plains of USA).
. the blinded phase of the trial was stopped early
primarily because of the apparent reductions in total cancer mortality
and total cancer incidence in the selenium group .
. it was originally set up to determine whether
selenium would decrease the incidence of skin cancer;
and while it failed to show any effect there,
it did show that giving se to se-deficient people (200 µg of selenium per day)
was capable of significant harm reduction:
reductions in total cancer incidence:
(77 cancers in the selenium group
vs 119 in controls [RR, 0.63; 95% CI, 0.47-0.85])
reductions in total cancer deaths:
(29 deaths in the selenium treatment group
vs 57 deaths in controls [RR, 0.50; 95% CI, 0.31-0.80]) .
the scientific conclusion:
[11.4:
. what was proven here was not that increasing se decreases cancer risk,
but that being se deficient does increase cancer risk .
. it's an essential mineral, and plants don't need it,
so the only sure source is seafood and or supplements .
]
. one reason for the variation of success could beGanther H. E., Lawrence J. R.
the degree to which apoptosis is involved or prevented;
eg, calcium channel blockers can inhibit apoptosis
and increasing doses of them are known to
increase the risk of cancer in the elderly . [48]
Chemical transformations of selenium in living organisms.
Improved forms of selenium for cancer prevention.
Tetrahedron 1997; 53:12299-12310
11.12:
web.health/se/yolk and whey not a sure source of se:
. no it does depend on the animal's diet .
J APPL POULT RES 2009. 18:151-157. doi:10.3382/japr.2008-00069
Poultry Science Association
Selenium contents of eggs from broiler breeders supplemented with
11.12:
web.health/se/yolk and whey not a sure source of se:
. no it does depend on the animal's diet .
J APPL POULT RES 2009. 18:151-157. doi:10.3382/japr.2008-00069
Poultry Science Association
Selenium contents of eggs from broiler breeders supplemented with
sodium selenite or zinc-L-selenium-methionine
This study evaluated the effects of sources and levels of Seon egg production and Se concentration in eggs.A comparison between treatments with single Se sourcesdemonstrated that the concentration of Se in eggsfollowed the increased levels in the feeds when ZnSeMet was used.However, the supplementation of a combination of sources
(Na2SeO3 and ZnSeMet) produced similar egg Se concentrations.
Laying hens were fed a diet that contained either 0.10 mg/kg natural selenium,0.10 mg/kg natural selenium plus0.32 mg/kg selenite selenium,or 0.42 mg/kg natural selenium.After the hens had been fed these diets for 180 days,tissues and eggs from hens fed 0.42 mg/kg natural seleniumcontained significantly more selenium thantissues and eggs from hens fed the selenite selenium.. when hens were fed 0.1 mg/kg of selenite selenium,significantly more selenium was present in the yolkthan in the white of the egg.Selenium in the white resulting from the selenite feedingcould be removed by dialysis but not that in the yolk.
Comparison of Selenium Levels and Sources
and Dietary Fat Quality
in Diets for Broiler Breeders and Layer HensPoult Sci
2008. 87:2605-2612. doi:10.3382/ps.2008-00174
. to study the effects of Se sources,
in interaction with dietary level of Se or dietary fats
on performance, Se incorporation into
tissues (blood, liver, breast muscle, and egg) and eggs,
hatchability, and glutathione peroxidase (GPX) activitiesin tissues and blood.
Both experiments involved a 3 x 2 factorial arrangement of 3 Se sources
(selenite, Se yeast, or B-Traxim Se)
and either 2 levels of each source (0.1 or 0.3 mg/kg)
or 2 fats (fresh or oxidized).
Egg production was not affected by Se source or dietary fat in both experiments.
Egg production was greater in breast muscle of layers.
It is concluded that broiler breeders require supplementation of 0.3 mg/kg of Se,
and that there are numerous measurable advantages
in using organic rather than inorganic sources for both breeders and layers.
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