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Science Forum Index » Life Extension Forum » Selenium deficiency (Keshan disease)...
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| Taka... |
 Posted: Tue May 27, 2008 7:50 pm |
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Guest
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The heart muscle has high content and metabolism of PUFAs like AA
especially in the reproductive age and growing people.
http://en.wikipedia.org/wiki/Keshan_disease
Definition of Keshan disease
Keshan disease: Condition caused by deficiency of the essential
mineral selenium. Keshan disease is a potentially fatal form of
cardiomyopathy (disease of the heart muscle). It was first observed in
Keshan province in China and since has been found elsewhere (including
New Zealand and Finland) in areas where the selenium level in the soil
is low. Treatment is selenium supplementation. The recommended dietary
allowance (RDA) is currently 55 micrograms of selenium per day for
adult men and women, 60 micrograms per day for women during pregnancy
and 70 micrograms per day for women during lactation.
Common Misspellings: keshan diease, keshan desease
Nippon Eiseigaku Zasshi. 2002 Jan;56(4):641-8.
Keshan disease--a review from the aspect of history and etiology
Liu Y, Chiba M, Inaba Y, Kondo M.
Department of Epidemiology and Environmental Health, Juntendo
University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421,
Japan.
OBJECTIVE: Keshan disease is an endemic cardiomyopathy found in
Keshan, north-east China. The first patient was identified in 1935.
This disease is characterized by a blood circulation disorder,
endocardium abnormality and myocardium necrosis. Selenium (Se)
deficiency is thought to be a major factor by Chinese scientists.
However, the exact etiology has not been clarified up to now. The
government decided to apply sodium selenite to growing crops, and the
incidence of the disease decreased dramatically. However, a few cases
still occur as chronic or latent types. This paper reviews Keshan
disease from a historical aspect and also the present situation.
METHODS: We made a reference survey and summarised the etiology,
pathological changes, clinical manifestation, and other views of
Keshan disease. RESULT: So far, epidemiological surveys have shown
that Keshan disease occurs in large areas in 14 provinces in China,
mainly in the countryside. It has been confirmed by clinical and
pathological studies that Keshan disease is an independent endemic
myocardial disease caused by biological and geological factors. The
largest prevalence age rates are boys under 15 years old and women of
childbearing age. There are several hypotheses; acute carbon monoxide
poisoning, virus infection, malnutrition, or selenium deficiency. The
first is not currently believed to be the cause. The following was
pointed out; studies on the relationship between diet and the endemic
areas of Keshan disease in 1961, where the food custom of the local
residents was relatively simple and a so-called "one-sided
diet" (eating a limited variety of food) might be related to the
incidence of Keshan disease. In 1973, large-scale investigations on
the natural environments were performed in the endemic areas of Keshan
disease in the whole country. As a result, it was reported that there
was a relationship between the incidence of Keshan disease and the
special natural environment in the endemic areas and the cause of
Keshan disease was strongly supported by nutritional, biological,
geological and chemical (selenium deficiency) factors. In 1981, on the
other hand, it was found that the levels of antibodies against
Coxsackie virus were higher in the serum of Keshan disease patients
than of normal subjects. This fact supposed that the cause of Keshan
disease was related to a virus infection. However, it is difficult to
explain why the clinical and pathological manifestations of Keshan
disease are similar to those of other diseases, e.g. idiopathic
dilatational myocardial disease. Further research should be performed
on Keshan disease to clarify the etiology.
PMID: 11868394
Notice how the "experts" are still wondering - is it the virus or the
Se deficiency? If you read Monty's site you can understand that the
causality is clear here:
Se deficiency = no lipid peroxide detoxification = lipid peroxide
accumulation (if iron present - for Tom) = viruses get stressed and
clingy = tissue destruction
This is nicely discussed in another paper worth reading on prostate
cancer and fats:
QUOTE: The combination of prevention of lipid oxidation by tocopherols
and repair of oxidized phospholipids by seleniumcontaining
peroxidases may explain the interrelationship between
polyunsaturated fatty acid intake, vitamin E status,
selenium intake, and disease incidence (148). A particularly
intriguing
example of this interaction is provided by the pathogenesis
of Keshan disease, in which the oxidative stress associated
with viral infection and polyunsaturated fatty acids,
together with deficiencies of vitamin E and selenium, causes
myocardial injury and viral mutations that lead to increased
virulence (149). Although observational epidemiologic studies
provided limited support of a protective effect for vitamin E
(a-tocopherol) (150,151) and selenium (152) against prostate
cancer, two recent intervention trials (153,154) suggested that
these agents might have chemopreventive effects. The lipophilic
carotenoid lycopene, a potent quencher of singlet oxygen damage
(155), concentrates in prostate tissue and has also been inversely
associated with prostate cancer incidence in some reports
(156–158). Dietary vitamin E and lignan consumption can
also affect fatty acid composition in tissues and cells (159,160).
Clearly, if dietary polyunsaturated fat is involved in the development
of prostate cancer through a mechanism involving oxidative
stress, future studies need to assess multiple parameters
associated with such a mechanism. Variations
in dietary and/or tissue levels of specific fatty
acids, vitamin E, selenium, and other lipophilic
antioxidants, as well as a history of
prostate infection, could mask or enhance the
effects of fat intake on prostate cancer development. UNQUOTE.
SOURCE: http://jnci.oxfordjournals.org/cgi/content/abstract/91/5/414
(they also show how PUFAs like linoleic acid inhibit gap junctions and
thus act as strong cancer promoters)
Taka |
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| Taka... |
| Posted: Tue May 27, 2008 10:02 pm |
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Guest
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The above was about the selenium dependent glutathione peroxidase
(GPX) which detoxify e.g. malondialdehyde (MDA).
Glutathione (GSH) detoxify lipid peroxides also with the contribution
of GST. Butyrate raises GST and thus helps getting rid of the
genotoxin 4-HNE (which you don't get in the first place if you go
EFAD):
Toxicological Sciences 2005 86(1):27-35; doi:10.1093/toxsci/kfi171
Genotoxicity of 4-Hydroxy-2-Nonenal in Human Colon Tumor Cells Is
Associated with Cellular Levels of Glutathione and the Modulation of
Glutathione S-Transferase A4 Expression by Butyrate
Nadine Knoll*, Carola Ruhe*, Selvaraju Veeriah*, Julia Sauer*, Michael
Glei*, Evan P. Gallagher and Beatrice L. Pool-Zobel*,1
* Department of Nutritional Toxicology, Institute for Nutritional
Sciences, Friedrich Schiller University, Dornburger Straße 25, D-07743
Jena, Germany, and Department of Environmental and Occupational
Health Sciences, University of Washington, 4225 Roosevelt Way NE,
Suite 100, Seattle, Washington 98105
Received November 8, 2004; accepted April 4, 2005
The cellular production of 4-hydroxy-2-nonenal (HNE), a product of
endogenous lipid peroxidation, constitutes a genotoxic risk factor for
carcinogenesis. Our previous studies have shown that human HT29 colon
cells developed resistance toward HNE injury after treatment with
butyrate, a diet-associated gut fermentation product. This resistance
was attributed to the induction of certain glutathione S-transferases
(hGSTP1-1, hGSTM2-2, and hGSTA1-1) and also for the tripeptide
glutathione (GSH) synthesizing enzymes. In the present study, we have
investigated in HT29 cells whether hGSTA4-4, which has a high
substrate specificity for HNE, was also inducible by butyrate and,
thus, could contribute to the previously observed chemoresistance. In
addition, we investigated if cellular depletion of GSH by L-buthionine-
S,R-sulfoximine (BSO) enhances chemosensitivity to HNE injury in HT29
cells. Incubation of HT29 cells with butyrate (2–4 mM) significantly
elicited a 1.8 to 3-fold upregulation of steady state hGSTA4 mRNA over
8–24 h after treatment. Moreover, 4 mM butyrate tended to increase
hGSTA4-4 protein concentrations. Incubation with 100 µM BSO decreased
cellular GSH levels by 77% without significant changes in cell
viability. Associated with this was a 2-fold higher level of HNE-
induced DNA damage as measured by the comet assay. Collectively, the
results of this study and our previous work indicate that the
genotoxicity of HNE is highly dependent on cellular GSH status and
those GSTs that contribute toward HNE conjugation, including hGSTA4-4.
Since HNE contributes to colon carcinogenesis, the favorable
modulation of the GSH/GST system by butyrate may contribute to
chemoprevention and reduction of the risks.
Key Words: L-buthionine-(S,R)-sulfoximine (BSO); butyrate; DNA damage;
glutathione (GSH); 4-hydroxy-2-nonenal (HNE); glutathione S-
transferases; hGSTA4. |
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| Marshall Price... |
| Posted: Mon Jun 02, 2008 11:07 pm |
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Taka wrote:
Quote: The heart muscle has high content and metabolism of PUFAs like AA
especially in the reproductive age and growing people.
snip
Nippon Eiseigaku Zasshi. 2002 Jan;56(4):641-8.
snip
Notice how the "experts" are still wondering - is it the virus or the
Se deficiency?
Notice how the date is January, 2002? Robbins Pathology 7, copyright
2005, isn't so ambiguous:
-----
*Selenium deficiency.* Selenium, like vitamin E, protects against
oxidative damage of membrane lipids. The deficiency of this element is
well known in China as /Keshan disease,/ which presents as a congestive
cardiomyopathy, mainly in children and young women. It results from a
markedly low level of the mineral in soil, water, and food.
-----
BTW, selenium is a component of glutathione peroxidase.
Quote: If you read Monty's site you can understand that the
causality is clear here:
Se deficiency = no lipid peroxide detoxification = lipid peroxide
accumulation (if iron present - for Tom) = viruses get stressed and
clingy = tissue destruction
Stressed and clingy viruses? Sounds like a bit of a stretch, if you
ask me.
I'll check it out.
--
Marshall Price of Miami
Known to Yahoo as d021317c |
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| Taka... |
| Posted: Tue Jun 03, 2008 3:23 pm |
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On Jun 4, 2:26 am, Marshall Price <d0213... at (no spam) yahoo.com> wrote:
Quote: I don't understand why you say "they also show how PUFAs like
linoleic acid inhibit gap junctions and thus act as strong cancer
promoters". Not only do they fail to say *how* it is so, they don't
even say *that* it is so, only that the poor communication between
cancer cells and normal cells is worthy of further investigation,
apparently considering reference 167, a cell culture study.
It has been already investigated further ... Look at the work of
Trosko who pushes the gap-junction cancer connection and I believe he
is damn right:
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=%22Trosko+JE%22%5BAuthor%5D
Taka |
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| Taka... |
| Posted: Sun Jun 08, 2008 4:32 am |
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On Jun 8, 9:17 pm, Marshall Price <d0213... at (no spam) yahoo.com> wrote:
Quote: Taka wrote:
On Jun 4, 2:26 am, Marshall Price <d0213... at (no spam) yahoo.com> wrote:
I don't understand why you say "they also show how PUFAs like
linoleic acid inhibit gap junctions and thus act as strong cancer
promoters". Not only do they fail to say *how* it is so, they don't
even say *that* it is so, only that the poor communication between
cancer cells and normal cells is worthy of further investigation,
apparently considering reference 167, a cell culture study.
It has been already investigated further ... Look at the work of
Trosko who pushes the gap-junction cancer connection and I believe he
is damn right:
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&...
Taka
I got the impression that the reason cancer cells don't die by
apoptosis is that apoptosis begins with a process within the
mitochondrion which cannot proceed because the cancer pathology disrupts
it somehow. True, more or less?
Very true. If the mitochondria are just downregulated due to hypoxia
(HIF) or too much sugar it is "easily" curable with the Taubes type of
diet. But some have mutated mtDNA which lead to overproduction of ROS
and drives uncontrolled cell division (esp. in late stage metastatic
cancers) and it may be harder to cope with this. In such a case EFAD
may help because all the cell division mediators, immunity suppressors
and protease inducers are basically derived from arachidonic acid but
if your fat stores are loaded with linoleic acid (as in most "normal"
people) it is impossible to achieve before the cancer kills you. Then
you are left with an Omega-3 + intravenous high dose VitC
chemotherapy ... You can also use antioxidants/NSAIDs to slow down
the spreading process. BTW I have seen a bunch of recent papers
showing how highy aggresive cancer cells revert to normal phenotype
when you exchange their mitochondria for those from normal cells
(which are not mutated).
Taka |
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| Marshall Price... |
| Posted: Sun Jun 08, 2008 7:17 am |
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Guest
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Taka wrote:
Quote: On Jun 4, 2:26 am, Marshall Price <d0213... at (no spam) yahoo.com> wrote:
I don't understand why you say "they also show how PUFAs like
linoleic acid inhibit gap junctions and thus act as strong cancer
promoters". Not only do they fail to say *how* it is so, they don't
even say *that* it is so, only that the poor communication between
cancer cells and normal cells is worthy of further investigation,
apparently considering reference 167, a cell culture study.
It has been already investigated further ... Look at the work of
Trosko who pushes the gap-junction cancer connection and I believe he
is damn right:
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=%22Trosko+JE%22%5BAuthor%5D
Taka
I got the impression that the reason cancer cells don't die by
apoptosis is that apoptosis begins with a process within the
mitochondrion which cannot proceed because the cancer pathology disrupts
it somehow. True, more or less?
--
Marshall Price of Miami
Known to Yahoo as d021317c |
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| John Hasenkam... |
| Posted: Sun Jun 08, 2008 11:13 am |
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Guest
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"Taka" <taka0038 at (no spam) gmail.com> wrote in message
news:7ebff4f3-80ec-465e-b6a5-b57e6eb09d0e at (no spam) 56g2000hsm.googlegroups.com...
Quote: On Jun 8, 9:17 pm, Marshall Price <d0213... at (no spam) yahoo.com> wrote:
Taka wrote:
On Jun 4, 2:26 am, Marshall Price <d0213... at (no spam) yahoo.com> wrote:
I don't understand why you say "they also show how PUFAs like
linoleic acid inhibit gap junctions and thus act as strong cancer
promoters". Not only do they fail to say *how* it is so, they don't
even say *that* it is so, only that the poor communication between
cancer cells and normal cells is worthy of further investigation,
apparently considering reference 167, a cell culture study.
It has been already investigated further ... Look at the work of
Trosko who pushes the gap-junction cancer connection and I believe he
is damn right:
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&...
Taka
I got the impression that the reason cancer cells don't die by
apoptosis is that apoptosis begins with a process within the
mitochondrion which cannot proceed because the cancer pathology disrupts
it somehow. True, more or less?
Very true. If the mitochondria are just downregulated due to hypoxia
(HIF) or too much sugar it is "easily" curable with the Taubes type of
diet. But some have mutated mtDNA which lead to overproduction of ROS
and drives uncontrolled cell division (esp. in late stage metastatic
cancers) and it may be harder to cope with this. In such a case EFAD
may help because all the cell division mediators, immunity suppressors
and protease inducers are basically derived from arachidonic acid but
if your fat stores are loaded with linoleic acid (as in most "normal"
people) it is impossible to achieve before the cancer kills you. Then
you are left with an Omega-3 + intravenous high dose VitC
chemotherapy ... You can also use antioxidants/NSAIDs to slow down
the spreading process. BTW I have seen a bunch of recent papers
showing how highy aggresive cancer cells revert to normal phenotype
when you exchange their mitochondria for those from normal cells
(which are not mutated).
Taka
Thanks Taka, good stuff. There might emerge a renewed interest in targeting
mts in cancer. Mts are "control organelles" is initiating death signals, so
finding a way to make them spark up again might be useful in some cancers.
Look up DCA. |
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