60 replies to this topic

[sensei]

Of note is that ascorbate and copper are necessary for synthesis of superoxide dismutase in humans.

 

Deficiency in either (and I don't mean the RDA levels) will lead to a deficiency in SOD synthesis.

 

This is probably one reason that ascorbate and copper compounds are constituents of effective anti-wrinkle facial cremes

Edited by sensei, 27 December 2014 - 07:44 PM.

[pone11]

Of note is that ascorbate and copper are necessary for synthesis of superoxide dismutase in humans.

 

Deficiency in either (and I don't mean the RDA levels) will lead to a deficiency in SOD synthesis.

 

This is probably one reason that ascorbate and copper compounds are constituents of effective anti-wrinkle facial cremes

 

Superoxide dismutase (SOD) in cytoplasm contains copper & zinc atoms.   SOD in mitochondria contains manganese.   Correct me if I am wrong, but I think what we should care about most is mitochondrial SOD not cytoplasmic.   The reason is that these free radicals are produced as a side effect of the electron transport chain (ETC) and aerobic metabolism.  And the ETC lives on the surface of the mitochondria.   If you put the SOD in cytoplasm, but leave it out of mitochondrial matrix, the free radicals destroy reactive lipids in the mitochondrial membrane and only get neutralized in cytoplasm by the SOD after the damage is already done.    Am I thinking about this incorrectly?

 

This is such an important topic that I decided to start a new thread, because SOD is really not a C60 topic:

 

http://www.longecity...ation/?p=704673

[sensei]

 

Of note is that ascorbate and copper are necessary for synthesis of superoxide dismutase in humans.

 

Deficiency in either (and I don't mean the RDA levels) will lead to a deficiency in SOD synthesis.

 

This is probably one reason that ascorbate and copper compounds are constituents of effective anti-wrinkle facial cremes

 

Superoxide dismutase (SOD) in cytoplasm contains copper & zinc atoms.   SOD in mitochondria contains manganese.   Correct me if I am wrong, but I think what we should care about most is mitochondrial SOD not cytoplasmic.   The reason is that these free radicals are produced as a side effect of the electron transport chain (ETC) and aerobic metabolism.  And the ETC lives on the surface of the mitochondria.   If you put the SOD in cytoplasm, but leave it out of mitochondrial matrix, the free radicals destroy reactive lipids in the mitochondrial membrane and only get neutralized in cytoplasm by the SOD after the damage is already done.    Am I thinking about this incorrectly?

 

This is such an important topic that I decided to start a new thread, because SOD is really not a C60 topic:

 

http://www.longecity...ation/?p=704673

 

 

SOD1 handles ROS within the cytoplasm-- ones that can attack the nucleus and cause damage to nuclear DNA. Said damage can cause early senescence, apoptosis, cross-linkage, or mutation.

SOD3 handles extracellular ROS and also contributes an anti-inflammatory action. Inflammation is known to be part of the etiology of atherosclerotic plaques, among other disease states.

 

SO, no I don't believe that SOD2 (mitochondrial) is the only SOD we need to worry about.

[pone11]

 

 

Of note is that ascorbate and copper are necessary for synthesis of superoxide dismutase in humans.

 

Deficiency in either (and I don't mean the RDA levels) will lead to a deficiency in SOD synthesis.

 

This is probably one reason that ascorbate and copper compounds are constituents of effective anti-wrinkle facial cremes

 

Superoxide dismutase (SOD) in cytoplasm contains copper & zinc atoms.   SOD in mitochondria contains manganese.   Correct me if I am wrong, but I think what we should care about most is mitochondrial SOD not cytoplasmic.   The reason is that these free radicals are produced as a side effect of the electron transport chain (ETC) and aerobic metabolism.  And the ETC lives on the surface of the mitochondria.   If you put the SOD in cytoplasm, but leave it out of mitochondrial matrix, the free radicals destroy reactive lipids in the mitochondrial membrane and only get neutralized in cytoplasm by the SOD after the damage is already done.    Am I thinking about this incorrectly?

 

This is such an important topic that I decided to start a new thread, because SOD is really not a C60 topic:

 

http://www.longecity...ation/?p=704673

 

 

SOD1 handles ROS within the cytoplasm-- ones that can attack the nucleus and cause damage to nuclear DNA. Said damage can cause early senescence, apoptosis, cross-linkage, or mutation.

SOD3 handles extracellular ROS and also contributes an anti-inflammatory action. Inflammation is known to be part of the etiology of atherosclerotic plaques, among other disease states.

 

SO, no I don't believe that SOD2 (mitochondrial) is the only SOD we need to worry about.

 

 

I am okay with boosting all three types of SOD, assuming that is even possible.

 

If I could only choose one, I would choose the mitochondrial type.   The reason is that aerobic metabolism happens on the inner mitochondrial membrane, and that is where most of the free radicals are formed.   Get them at the source.

[sensei]

 

 

 

Of note is that ascorbate and copper are necessary for synthesis of superoxide dismutase in humans.

 

Deficiency in either (and I don't mean the RDA levels) will lead to a deficiency in SOD synthesis.

 

This is probably one reason that ascorbate and copper compounds are constituents of effective anti-wrinkle facial cremes

 

Superoxide dismutase (SOD) in cytoplasm contains copper & zinc atoms.   SOD in mitochondria contains manganese.   Correct me if I am wrong, but I think what we should care about most is mitochondrial SOD not cytoplasmic.   The reason is that these free radicals are produced as a side effect of the electron transport chain (ETC) and aerobic metabolism.  And the ETC lives on the surface of the mitochondria.   If you put the SOD in cytoplasm, but leave it out of mitochondrial matrix, the free radicals destroy reactive lipids in the mitochondrial membrane and only get neutralized in cytoplasm by the SOD after the damage is already done.    Am I thinking about this incorrectly?

 

This is such an important topic that I decided to start a new thread, because SOD is really not a C60 topic:

 

http://www.longecity...ation/?p=704673

 

 

SOD1 handles ROS within the cytoplasm-- ones that can attack the nucleus and cause damage to nuclear DNA. Said damage can cause early senescence, apoptosis, cross-linkage, or mutation.

SOD3 handles extracellular ROS and also contributes an anti-inflammatory action. Inflammation is known to be part of the etiology of atherosclerotic plaques, among other disease states.

 

SO, no I don't believe that SOD2 (mitochondrial) is the only SOD we need to worry about.

 

 

I am okay with boosting all three types of SOD, assuming that is even possible.

 

If I could only choose one, I would choose the mitochondrial type.   The reason is that aerobic metabolism happens on the inner mitochondrial membrane, and that is where most of the free radicals are formed.   Get them at the source.

 

NADPH produces intracellular and extracellular superoxides (some is used in phagocytosis of microbes by the immune system -- but the leftovers are hydrogen peroxide and bleach) (yes really)

 

And hydrogen peroxides leak from the mitochondria to the cytoplasm as well 

 

I say increase all 3 -- make sure you are not deficient in Cu, Zn, or Mn and take at least 3000mg ascorbate a day (1000mg x3)

Edited by sensei, 28 December 2014 - 05:25 AM.

[pone11]

NADPH produces intracellular and extracellular superoxides (some is used in phagocytosis of microbes by the immune system -- but the leftovers are hydrogen peroxide and bleach) (yes really)

 

And hydrogen peroxides leak from the mitochondria to the cytoplasm as well 

 

I say increase all 3 -- make sure you are not deficient in Cu, Zn, or Mn and take at least 3000mg ascorbate a day (1000mg x3)

 

 

I don't find an NADPH supplement.  How do you suggest we get that?

 

Is there any test for measuring NADPH?

[sensei]

NADPH oxidase is not a supplement -- it creates ROS  -- we don't want to take any of that

Edited by sensei, 28 December 2014 - 05:37 AM.

[niner]

Of note is that ascorbate and copper are necessary for synthesis of superoxide dismutase in humans.

 

Deficiency in either (and I don't mean the RDA levels) will lead to a deficiency in SOD synthesis.

 

This is probably one reason that ascorbate and copper compounds are constituents of effective anti-wrinkle facial cremes

 

The only form of copper that I know of being used as a facial creme is complexed to a specific tripeptide (GHK, I think) which serves as a growth stimulator.  Copper by itself is pretty ugly stuff.  Like iron, it engages in Fenton chemistry that results in the production of highly reactive hydroxyl radicals.   RDA amounts of copper are plenty.  Copper supplementation has a pretty bad history.

[sensei]

 

Of note is that ascorbate and copper are necessary for synthesis of superoxide dismutase in humans.

 

Deficiency in either (and I don't mean the RDA levels) will lead to a deficiency in SOD synthesis.

 

This is probably one reason that ascorbate and copper compounds are constituents of effective anti-wrinkle facial cremes

 

The only form of copper that I know of being used as a facial creme is complexed to a specific tripeptide (GHK, I think) which serves as a growth stimulator.  Copper by itself is pretty ugly stuff.  Like iron, it engages in Fenton chemistry that results in the production of highly reactive hydroxyl radicals.   RDA amounts of copper are plenty.  Copper supplementation has a pretty bad history.

 

 

RDA amounts for copper are not plenty

 

The RDA for copper is 900mcg, about 60% of what is really minimally needed: see below

 

http://www.ncbi.nlm..../pubmed/7355779

"On consideration of a calculated surface loss of 0.25 mg/day, the requirement is 1.55 mg/day. The requirement was unaffected by the type of fiber source. A review of published data revealed that this requirement substantially exceeds the amount of copper found in many conventional diets."

 

But the RDA upper limit is actually 10mg/day -- lots of sway in there.

 

And we know that the RDA for vitamin C (90mg) is a joke as is the upper limit of 2000mg -- I've personally taken 12,000 mg/day in 1000-1500mg doses during flu/fever.

 

The issue is that under oxidative stress more superoxide dismutase is needed -- this is likely why Klenner noticed an increased need (based on the empirical evidence of increased bowel tolerance) for Ascorbate as oxidative stress increases -- the same is true for Zinc.

 

 

Edited by sensei, 28 December 2014 - 09:58 PM.

[niner]

Upon what do they base the UL of 10mg/d?  Probably not based on what it would do to your odds of getting Alzheimers or various other conditions you'd rather not have.  There's also a difference between the form of dietary copper and the form of most supplemental copper.  It's possible that someone with a really crappy diet could benefit from a small amount of supplemental copper, but I prefer to eat a good diet and skip the supplemental form.  It's not very hard to find multivitamins with more copper than even a person with a bad diet might need.  A lot of people get various amounts of copper from their water supply, due to the large installed base of copper plumbing.

[sensei]

Upon what do they base the UL of 10mg/d?  Probably not based on what it would do to your odds of getting Alzheimers or various other conditions you'd rather not have.  There's also a difference between the form of dietary copper and the form of most supplemental copper.  It's possible that someone with a really crappy diet could benefit from a small amount of supplemental copper, but I prefer to eat a good diet and skip the supplemental form.  It's not very hard to find multivitamins with more copper than even a person with a bad diet might need.  A lot of people get various amounts of copper from their water supply, due to the large installed base of copper plumbing.

"Researchers at The Birchall Centre at Keele University in the UK released research in February that provided “unequivocal” evidence that copper protects the human brain against damage from beta amyloid. They also said it’s “highly unlikely” that copper is responsible for the formation of brain plaques."

 

http://www.healthlin...zheimers-081913

 

A better way to test than shooting copper into mice is to find areas with high copper content in the groundwater and epidemiologically evaluate the % of alzheimers in that population vs population as a whole.

 

Then there is Menke's Disease -- where copper cannot cross the blood brain barrier into the brain -- death by age 3.

 

Edited by sensei, 28 December 2014 - 10:31 PM.

[pone11]

Upon what do they base the UL of 10mg/d?  Probably not based on what it would do to your odds of getting Alzheimers or various other conditions you'd rather not have.  There's also a difference between the form of dietary copper and the form of most supplemental copper.  It's possible that someone with a really crappy diet could benefit from a small amount of supplemental copper, but I prefer to eat a good diet and skip the supplemental form.  It's not very hard to find multivitamins with more copper than even a person with a bad diet might need.  A lot of people get various amounts of copper from their water supply, due to the large installed base of copper plumbing.

 

Buy this mineral test kit and your body will tell you whether you need copper or not:

 

http://www.bodybio.c...uidMinerals.pdf

 

You will probably be surprised.

 

Remember that zinc and copper have a co-relationship, and people who supplement high doses of zinc are at particular risk of falling short of copper.   If you don't supplement either it is highly unlikely that you have optimal levels from diet alone.

 

And "multivitamins" are not associated with improved health in research literature.   Much better to take individual supplements and test for dosing using a strategy like the one I quote above.  You can continuously redose zinc and copper using a strategy like the above.

 

Drinking tap water is a terrible idea.   If they used lead solder on your pipes you are getting a significant amount of lead that won't come off your bones for 20 or more years.   Drink spring water.

Edited by pone11, 28 December 2014 - 10:31 PM.

[sensei]

 

Upon what do they base the UL of 10mg/d?  Probably not based on what it would do to your odds of getting Alzheimers or various other conditions you'd rather not have.  There's also a difference between the form of dietary copper and the form of most supplemental copper.  It's possible that someone with a really crappy diet could benefit from a small amount of supplemental copper, but I prefer to eat a good diet and skip the supplemental form.  It's not very hard to find multivitamins with more copper than even a person with a bad diet might need.  A lot of people get various amounts of copper from their water supply, due to the large installed base of copper plumbing.

 

Buy this mineral test kit and your body will tell you whether you need copper or not:

 

http://www.bodybio.c...uidMinerals.pdf

 

You will probably be surprised.

 

Remember that zinc and copper have a co-relationship, and people who supplement high doses of zinc are at particular risk of falling short of copper.   If you don't supplement either it is highly unlikely that you have optimal levels from diet alone.

 

And "multivitamins" are not associated with improved health in research literature.   Much better to take individual supplements and test for dosing using a strategy like the one I quote above.  You can continuously redose zinc and copper using a strategy like the above.

 

Drinking tap water is a terrible idea.   If they used lead solder on your pipes you are getting a significant amount of lead that won't come off your bones for 20 or more years.   Drink spring water.

 

Yup -- Just like Calcium Magnesium and Phosphorus need to be balanced

[pone11]

 

Upon what do they base the UL of 10mg/d?  Probably not based on what it would do to your odds of getting Alzheimers or various other conditions you'd rather not have.  There's also a difference between the form of dietary copper and the form of most supplemental copper.  It's possible that someone with a really crappy diet could benefit from a small amount of supplemental copper, but I prefer to eat a good diet and skip the supplemental form.  It's not very hard to find multivitamins with more copper than even a person with a bad diet might need.  A lot of people get various amounts of copper from their water supply, due to the large installed base of copper plumbing.

"Researchers at The Birchall Centre at Keele University in the UK released research in February that provided “unequivocal” evidence that copper protects the human brain against damage from beta amyloid. They also said it’s “highly unlikely” that copper is responsible for the formation of brain plaques."

 

http://www.healthlin...zheimers-081913

 

A better way to test than shooting copper into mice is to find areas with high copper content in the groundwater and epidemiologically evaluate the % of alzheimers in that population vs population as a whole.

 

Then there is Menke's Disease -- where copper cannot cross the blood brain barrier into the brain -- death by age 3.

 

 

Copper and zinc dysregulation (both too much and too little) is associated with a number of neurotransmitter disorders including some forms of depression and schizophrenia.   You can't make blanket statement that a given individual needs more or less, but just need to test.

 

The only metal that unambiguously creates the neuronal degeneration and tangles of the type seen in alzheimers is mercury.  This video is impressive:

[pone11]

Yup -- Just like Calcium Magnesium and Phosphorus need to be balanced

 

 

I didn't know about Phosphorous needing to be balanced against those.  What is the story there?

 

Is there a straightforward way to test phosphorous balance?

 

I don't eat most of the foods that contain phosphorous.  Is there a straightforward way to supplement it?

[sensei]

 

Yup -- Just like Calcium Magnesium and Phosphorus need to be balanced

 

 

I didn't know about Phosphorous needing to be balanced against those.  What is the story there?

 

Is there a straightforward way to test phosphorous balance?

 

I don't eat most of the foods that contain phosphorous.  Is there a straightforward way to supplement it?

 

Basically your bones need calcium and phosphorus. As part of natural remodeling of bone, calcium and phosphorus are lost, so both need to be replaced.

 

Also the ratio of Ca to P directly regulates intestinal absorption and bone mineralization.

 

Calcium/Magnesium imbalance (too little magnesium) leads to impaired vitamin D activation (requires magnesium), and impaired calcium absorption (requires magnesium)

[niner]

 

Upon what do they base the UL of 10mg/d?  Probably not based on what it would do to your odds of getting Alzheimers or various other conditions you'd rather not have.  There's also a difference between the form of dietary copper and the form of most supplemental copper.  It's possible that someone with a really crappy diet could benefit from a small amount of supplemental copper, but I prefer to eat a good diet and skip the supplemental form.  It's not very hard to find multivitamins with more copper than even a person with a bad diet might need.  A lot of people get various amounts of copper from their water supply, due to the large installed base of copper plumbing.

"Researchers at The Birchall Centre at Keele University in the UK released research in February that provided “unequivocal” evidence that copper protects the human brain against damage from beta amyloid. They also said it’s “highly unlikely” that copper is responsible for the formation of brain plaques."

 

http://www.healthlin...zheimers-081913

 

A better way to test than shooting copper into mice is to find areas with high copper content in the groundwater and epidemiologically evaluate the % of alzheimers in that population vs population as a whole.

 

Then there is Menke's Disease -- where copper cannot cross the blood brain barrier into the brain -- death by age 3.

 

"Unequivocal" is pretty strong language as the takehome from an in vitro experiment.  In vitro work is frequently if not usually irrelevant to the human case; It's not something that you would want to base clinical decisions on.   That is particularly true in this case, where there is so much countervailing evidence that excess copper is harmful.  (As is pointed out in that very link)

 

Menke's Disease lets us know that the U-shaped curve is alive and well.   (For any essential nutrient, a plot of "bad outcome" vs. consumption or biological concentration will be shaped like the letter 'U'.)

You may want to look at this and this, and references therein.

[sensei]

 

 

Upon what do they base the UL of 10mg/d?  Probably not based on what it would do to your odds of getting Alzheimers or various other conditions you'd rather not have.  There's also a difference between the form of dietary copper and the form of most supplemental copper.  It's possible that someone with a really crappy diet could benefit from a small amount of supplemental copper, but I prefer to eat a good diet and skip the supplemental form.  It's not very hard to find multivitamins with more copper than even a person with a bad diet might need.  A lot of people get various amounts of copper from their water supply, due to the large installed base of copper plumbing.

"Researchers at The Birchall Centre at Keele University in the UK released research in February that provided “unequivocal” evidence that copper protects the human brain against damage from beta amyloid. They also said it’s “highly unlikely” that copper is responsible for the formation of brain plaques."

 

http://www.healthlin...zheimers-081913

 

A better way to test than shooting copper into mice is to find areas with high copper content in the groundwater and epidemiologically evaluate the % of alzheimers in that population vs population as a whole.

 

Then there is Menke's Disease -- where copper cannot cross the blood brain barrier into the brain -- death by age 3.

 

"Unequivocal" is pretty strong language as the takehome from an in vitro experiment.  In vitro work is frequently if not usually irrelevant to the human case; It's not something that you would want to base clinical decisions on.   That is particularly true in this case, where there is so much countervailing evidence that excess copper is harmful.  (As is pointed out in that very link)

 

Menke's Disease lets us know that the U-shaped curve is alive and well.   (For any essential nutrient, a plot of "bad outcome" vs. consumption or biological concentration will be shaped like the letter 'U'.)

You may want to look at this and this, and references therein.

 

"Four classes of etiologic agents can produce toxic, hereditary, infectious and deficiency diseases. Recent research on Alzheimer's disease generally addresses pathogenesis related to the first three classes of agents with little emphasis on cause. Low copper and cytochrome oxidase in Alzheimer brain can be attributed to low copper intakes or higher than average nutritional requirements. Experiments with animals deficient in copper involving amyloid, ceruloplasmin, copper transport, cytochrome oxidase, myelination, organ analysis and oxidative defense are consonant. Decreased cognition and increased tau in cerebrospinal fluid in Alzheimer's disease also are associated with low copper status. A high requirement for copper may explain early onset of Alzheimer's disease in Down's syndrome. Copper deficiency is a plausible cause of Alzheimer's disease. This hypothesis should be tested with a lengthy trial of copper supplementation."

 

http://www.ncbi.nlm....pubmed/17928161

 

As seen  by evidence showing low copper states are associated with worse cognition in Alzheimers, and also zinc deficiency; a likely contributing factor in AL-D is faulty enzymatic production and/or out of balance Zn-Cu.  This results in low levels of SOD, leaving the brain unable to handle oxidative stress.

 

Couple that with low ascorbate, and you have multiple deficiencies that lead to issues with Zn-Cu complex synthesis as well as clearance of neurofibbrilary tangles and exess metals (of all kinds).

 

Ascorbate dissolves amyloid plaques

 

http://www.scienceda...10818101645.htm

 

"When we treated brain tissue from mice suffering from Alzheimer's disease with vitamin C, we could see that the toxic protein aggregates were dissolved. Our results show a previously unknown model for how vitamin C affects the amyloid plaques,"

 

Furthermore Ascorbic acid chelates metals -- and increases clearance from the body.

Edited by sensei, 29 December 2014 - 06:16 PM.

[david ellis]

 

Yup -- Just like Calcium Magnesium and Phosphorus need to be balanced

 

 

I didn't know about Phosphorous needing to be balanced against those.  What is the story there?

 

Is there a straightforward way to test phosphorous balance?

 

I don't eat most of the foods that contain phosphorous.  Is there a straightforward way to supplement it?

 

 

 

There is a product, extracted from cattle bones, that is in many bone supplements.   This product contains both calcium and phosphorous, probably in a satisfactory proportion needed for human bones.

[niner]

"Unequivocal" is pretty strong language as the takehome from an in vitro experiment.  In vitro work is frequently if not usually irrelevant to the human case; It's not something that you would want to base clinical decisions on.   That is particularly true in this case, where there is so much countervailing evidence that excess copper is harmful.  (As is pointed out in that very link)
 
Menke's Disease lets us know that the U-shaped curve is alive and well.   (For any essential nutrient, a plot of "bad outcome" vs. consumption or biological concentration will be shaped like the letter 'U'.)
You may want to look at this and this, and references therein.

Four classes of etiologic agents can produce toxic, hereditary, infectious and deficiency diseases. Recent research on Alzheimer's disease generally addresses pathogenesis related to the first three classes of agents with little emphasis on cause. Low copper and cytochrome oxidase in Alzheimer brain can be attributed to low copper intakes or higher than average nutritional requirements. Experiments with animals deficient in copper involving amyloid, ceruloplasmin, copper transport, cytochrome oxidase, myelination, organ analysis and oxidative defense are consonant.  [/font][/color]Decreased cognition and increased tau in cerebrospinal fluid in Alzheimer's disease also are associated with low copper status. A high requirement for copper may explain early onset of Alzheimer's disease in Down's syndrome. Copper deficiency is a plausible cause of Alzheimer's disease.[/size][/size] This hypothesis should be tested with a lengthy trial of copper supplementation."
 
http://www.ncbi.nlm....pubmed/17928161

This reference is to a journal called "Medical Hypotheses". They publish speculation and guesses, if the author can make a reasonable case for them, but this isn't data, and there is a ton of evidence that copper and other metals are more likely to cause than to prevent Alzheimer's. Did you look at the two threads I linked? They lay out some of the wealth of evidence that copper supplementation at doses commonly found on the market is not a great idea for most people.

[pone11]

 

 

"Unequivocal" is pretty strong language as the takehome from an in vitro experiment.  In vitro work is frequently if not usually irrelevant to the human case; It's not something that you would want to base clinical decisions on.   That is particularly true in this case, where there is so much countervailing evidence that excess copper is harmful.  (As is pointed out in that very link)
 
Menke's Disease lets us know that the U-shaped curve is alive and well.   (For any essential nutrient, a plot of "bad outcome" vs. consumption or biological concentration will be shaped like the letter 'U'.)
You may want to look at this and this, and references therein.

Four classes of etiologic agents can produce toxic, hereditary, infectious and deficiency diseases. Recent research on Alzheimer's disease generally addresses pathogenesis related to the first three classes of agents with little emphasis on cause. Low copper and cytochrome oxidase in Alzheimer brain can be attributed to low copper intakes or higher than average nutritional requirements. Experiments with animals deficient in copper involving amyloid, ceruloplasmin, copper transport, cytochrome oxidase, myelination, organ analysis and oxidative defense are consonant.  [/font][/color]Decreased cognition and increased tau in cerebrospinal fluid in Alzheimer's disease also are associated with low copper status. A high requirement for copper may explain early onset of Alzheimer's disease in Down's syndrome. Copper deficiency is a plausible cause of Alzheimer's disease.[/size][/size] This hypothesis should be tested with a lengthy trial of copper supplementation."
 
http://www.ncbi.nlm....pubmed/17928161

 

This reference is to a journal called "Medical Hypotheses". They publish speculation and guesses, if the author can make a reasonable case for them, but this isn't data, and there is a ton of evidence that copper and other metals are more likely to cause than to prevent Alzheimer's. Did you look at the two threads I linked? They lay out some of the wealth of evidence that copper supplementation at doses commonly found on the market is not a great idea for most people.

 

 

The only metal that in experiments causes the same tangles seen in Alzheimers is Mercury.  See the video I posted earlier in this thread.  The same research group tried to inject other metals including aluminum and copper into solution with neurons, and neither of those causes the same type of neurodegeneration of tubulin that is classic in alzheimers.  That isn't to say that copper or aluminum might not be co pathologies in alzheimers, but to implicate them as primary causes - or potential cures - don't we want physical evidence about the actual cause for the physical damage to neurons seen in alzheimer's?

 

Dentistry started using amalgam mercury fillings around 1860, and alzheimers first showed up about 1903.    This timing is extremely suspicious, particularly given compelling physical evidence of how mercury interacts with neurons, and given our knowledge that ethyl mercury from amalgams continuously leaks gas that is easily absorbed into brain tissue.

 

Copper and zinc are in a careful balance, and you obviously need to be careful when supplementing them.   Better to monitor your RBC levels of each nutrient over time and adjust dose accordingly.   Use something like a BodyBio mineral taste test kit to help determine if you are over supplementing in between tests.  You cannot use the fact that some people over supplement copper as a reason to not provide supplementation to those who fall short of their requirements for copper.

Edited by pone11, 01 January 2015 - 01:05 AM.

[pone11]

 

 

"Unequivocal" is pretty strong language as the takehome from an in vitro experiment.  In vitro work is frequently if not usually irrelevant to the human case; It's not something that you would want to base clinical decisions on.   That is particularly true in this case, where there is so much countervailing evidence that excess copper is harmful.  (As is pointed out in that very link)
 
Menke's Disease lets us know that the U-shaped curve is alive and well.   (For any essential nutrient, a plot of "bad outcome" vs. consumption or biological concentration will be shaped like the letter 'U'.)
You may want to look at this and this, and references therein.

Four classes of etiologic agents can produce toxic, hereditary, infectious and deficiency diseases. Recent research on Alzheimer's disease generally addresses pathogenesis related to the first three classes of agents with little emphasis on cause. Low copper and cytochrome oxidase in Alzheimer brain can be attributed to low copper intakes or higher than average nutritional requirements. Experiments with animals deficient in copper involving amyloid, ceruloplasmin, copper transport, cytochrome oxidase, myelination, organ analysis and oxidative defense are consonant.  [/font][/color]Decreased cognition and increased tau in cerebrospinal fluid in Alzheimer's disease also are associated with low copper status. A high requirement for copper may explain early onset of Alzheimer's disease in Down's syndrome. Copper deficiency is a plausible cause of Alzheimer's disease.[/size][/size] This hypothesis should be tested with a lengthy trial of copper supplementation."
 
http://www.ncbi.nlm....pubmed/17928161

 

This reference is to a journal called "Medical Hypotheses". They publish speculation and guesses, if the author can make a reasonable case for them, but this isn't data, and there is a ton of evidence that copper and other metals are more likely to cause than to prevent Alzheimer's. Did you look at the two threads I linked? They lay out some of the wealth of evidence that copper supplementation at doses commonly found on the market is not a great idea for most people.

 

 

Does anyone with access to the full text of that study know if they determined copper deficiency by biopsy of brain tissue, or was their assessment in RBC only?

[sensei]

 

 

The only metal that in experiments causes the same tangles seen in Alzheimers is Mercury.  See the video I posted earlier in this thread.  

Dentistry started using amalgam mercury fillings around 1860, and alzheimers first showed up about 1903.    This timing is extremely suspicious, particularly given compelling physical evidence of how mercury interacts with neurons, and given our knowledge that ethyl mercury from amalgams continuously leaks gas that is easily absorbed into brain tissue.

 

 

 

The only issue I have with this is that Japan, a country that has one of the highest seafood/fish consumption (and by extension mercury) in the world, has one of the lowest AL rates in the world.

[niner]

 

The only metal that in experiments causes the same tangles seen in Alzheimers is Mercury.  See the video I posted earlier in this thread.  

Dentistry started using amalgam mercury fillings around 1860, and alzheimers first showed up about 1903.    This timing is extremely suspicious, particularly given compelling physical evidence of how mercury interacts with neurons, and given our knowledge that ethyl mercury from amalgams continuously leaks gas that is easily absorbed into brain tissue.

 

The only issue I have with this is that Japan, a country that has one of the highest seafood/fish consumption (and by extension mercury) in the world, has one of the lowest AL rates in the world.

 

In addition, they don't like copper plumbing in Japan, considering it to be a source of toxicity.  Pretty clueful, IMHO.  When Japanese people migrate to Hawaii, where copper plumbing is common, their AD rates resemble those of the Hawaiian population.  30% of North American households have copper levels in their tap water that are at or above levels that were shown to produce AD pathology in animals.  Pone11, did you find that mercury thing on one of the internet mercury fear-mongering sites?   There is no single thing that is "THE" cause of AD, but copper is a significant problem, as is aluminum.  Overexposure to copper is widespread, and again, there is a wealth of evidence that copper is problematic.  Here is yet another entree into the literature on it.

[Jembe]

niner, do you think zinc supplementation helps counteract overexposure to copper?

[Xerxes]

Jembe, I'm clearly not niner but I know that high daily doses of zinc will cause ones copper levels to decrease, and continued use can lead to copper deficiency (unless you take zinc with the right ratio to copper). So in theory, zinc could protect you from 'overexposure' to copper as it would keep the levels low. I remember reading somewhere that zinc and copper compete for receptor sites, which is why there is a ratio one should keep to when supplementing. Don't forget though that chronically high doses of zinc can be harmful and cause zinc toxicity. However, I have no idea if zinc would reverse the EFFECTS of overexposure to copper, if that was what you meant. 

[APBT]

 

Does anyone with access to the full text of that study know if they determined copper deficiency by biopsy of brain tissue, or was their assessment in RBC only?

 

 

FULL TEXT:  Alzheimer’s disease as copper deficiency

Attached Files

•  Alzheimer’s disease as copper deficiency.pdf   108.22KB   16 downloads

[niner]

Copper orotate was tested as a therapy for AD.  It didn't work:
 

J Neural Transm. 2008 Aug;115(8):1181-7. doi: 10.1007/s00702-008-0080-1. Epub 2008 Jun 28.
Intake of copper has no effect on cognition in patients with mild Alzheimer's disease: a pilot phase 2 clinical trial.
Kessler H, Bayer TA, Bach D, Schneider-Axmann T, Supprian T, Herrmann W, Haber M, Multhaup G, Falkai P, Pajonk FG.

Disturbed copper (Cu) homeostasis may be associated with the pathological processes in Alzheimer's disease (AD). In the present report, we evaluated the efficacy of oral Cu supplementation in the treatment of AD in a prospective, randomized, double-blind, placebo-controlled phase 2 clinical trial in patients with mild AD for 12 months. Sixty-eight subjects were randomized. The treatment was well-tolerated. There were however no significant differences in primary outcome measures (Alzheimer's Disease Assessment Scale, Cognitive subscale, Mini Mental Status Examination) between the verum [Cu-(II)-orotate-dihydrate; 8 mg Cu daily] and the placebo group. Despite a number of findings supporting the hypothesis of environmental Cu modulating AD, our results demonstrate that oral Cu intake has neither a detrimental nor a promoting effect on the progression of AD.

PMID: 18587525 PMCID: PMC2516533  Free PMC Article

Also of interest:
 

Front Aging Neurosci. 2014 May 16;6:92. doi: 10.3389/fnagi.2014.00092. eCollection 2014.
Alzheimer's disease causation by copper toxicity and treatment with zinc.
Brewer GJ.

Evidence will be presented that the Alzheimer's disease (AD) epidemic is new, the disease being very rare in the 1900s. The incidence is increasing rapidly, but only in developed countries. We postulate that the new emerging environmental factor partially causal of the AD epidemic is ingestion of inorganic copper from drinking water and taking supplement pills, along with a high fat diet. Inorganic copper can be partially directly absorbed and elevate the serum free copper pool. The Squitti group has shown that serum free copper is elevated in AD, correlates with cognition, and predicts cognition loss. Thus, our inorganic copper hypothesis fits well with the Squitti group data. We have also shown that AD patients are zinc deficient compared to age-matched controls. Because zinc is a neuronal protective factor, we postulate that zinc deficiency may also be partially causative of AD. We carried out a small 6 month double blind study of a new zinc formulation and found that in patients age 70 and over, it protected against cognition loss. Zinc therapy also significantly reduced serum free copper in AD patients, so efficacy may come from restoring normal zinc levels, or from lowering serum free copper, or from both.

PMID: 24860501 PMCID: PMC4030141 Free PMC Article

[pone11]

 

 

 

The only metal that in experiments causes the same tangles seen in Alzheimers is Mercury.  See the video I posted earlier in this thread.  

Dentistry started using amalgam mercury fillings around 1860, and alzheimers first showed up about 1903.    This timing is extremely suspicious, particularly given compelling physical evidence of how mercury interacts with neurons, and given our knowledge that ethyl mercury from amalgams continuously leaks gas that is easily absorbed into brain tissue.

 

 

 

The only issue I have with this is that Japan, a country that has one of the highest seafood/fish consumption (and by extension mercury) in the world, has one of the lowest AL rates in the world.

 

 

Remember, it is not about how much mercury goes into you, but rather how much you retain once you account for disposal through liver and kidneys.  One of the problems with liver disposal through bile is that much of it then gets reabsorbed, and maybe as little as 5% gets out on each trip through intestines.   There could be genetic issues or diet issues that improve the disposal rate through bile, preventing long term accumulation.   I don't think anyone has really done population studies to look at that.

 

Consider genetic issues around APO-E gene.   The source below says "The brain has a house-cleaning protein that removes dangerous waste products, which comes in three varieties: APO-E2, APO-E3, and APO-E4. The APO-E2 protein can carry 2 atoms of mercury out of the brain; APO-3, one; and APO-E4, none. The genes we acquire from each parent determine which two we have. People with two APO-E4 proteins (and thus no APO-E2 or -E3) have an 80 percent chance of acquiring Alzheimer's disease. And according to one study, autistic children have a huge preponderance of APO-E4 protein in their brains."

http://archive.lewro...r/miller14.html

 

Now look at the distribution by country of APO-E genes.  Japan has one of the lowest APO-E4 concentrations in the world!   See Table 1 here:

http://onlinelibrary...9.6340301.x/pdf

 

Scandinavian countries have one of the highest E4 concentrations, and they lead the world in Alzheimer's disease:

http://www.worldlife...tia/by-country/

 

You can go back and forth like this and never prove anything, but to me the physical evidence in vitro with mercury making neurons form tangles is reason enough that scientists should start looking at mercury very very intensely as a possible primary cause for alzheimers.

Edited by pone11, 02 January 2015 - 08:00 AM.

[Dorian Grey]

Acu-Cell (hair mineral analysis) has an interesting page on copper: http://www.acu-cell.com/crcu.html

 

Their historical records seem to indicate copper deficiency is almost unheard of, and excess is the norm in most populations as they age.  

I like their opinion that most trace mineral issues are not related to deficiencies, but rather to isolated and individual mineral excesses that result in imbalances.  

 

My own research seems to indicate it's very hard to be truly deficient in most any trace mineral, even if you live on junk food and beer.  It is excesses and imbalances that create problems.  The over-mineralization theory of aging and disease is one of my favorite topics of discussion and I feel chelation to more youthful mineral profiles has been the fountain of youth for me.  

 

I donate blood to lower iron and take IP6 to chelate excess trace minerals.  My hair was going gray at my temples 15 years ago, but since I've been lowering iron, it's gone back to brown.  My God, I'm getting younger!   

 

Don't supplement minerals (if you're over 30)...  Chelate them!  My only exceptions to this rule are magnesium (the most common mineral deficiency) and zinc, which is too important to ever run short on.  As I take IP6 which chelates these, I do supplement them in low doses, well away from my IP6 fountain of youth pill.  

Edited by synesthesia, 02 January 2015 - 08:59 AM.