Dad's got atherosclerosis - what to do?

[Guest guest]

Vitamin K2 will prevent and reverse soft tissue calcification; Vit. D,

magnesium (400-800mg. as tolerated); palm tocotrienols, r lipoic acid,

2-3 grams of vit. C and lysine, n- acetyl cysteine

[Guest guest]

forgot to mention trans resveratrol and POM juice.

[Guest guest]

--- <jeremytfox@...> wrote:

> It's not even clear free radicals are themselves bad.

, yes, the immune system generates free radical as part of it's

defensive system. A quick google turned this up:

Free Radical Introduction

http://www.exrx.net/Nutrition/Antioxidants/Introduction.html

============================================================

.... free radicals are naturally produced by some systems within the

body and have beneficial effects that cannot be overlooked. The immune

system is the main body system that utilizes free radicals. Foreign

invaders or damaged tissue is marked with free radicals by the immune

system. This allows for determination of which tissue need to be

removed from the body. Because of this some question the need for

antioxidant supplementation, as they believe supplementation can

actually decrease the effectiveness of the immune system.

============================================================

Also, here's an interesting and detailed discussion of selenium from

the same web site:

http://www.exrx.net/Nutrition/Antioxidants/Selenium.html#anchor3688468

I haven't finished looking at the web site, but it looks interesting

from what I've seen so far.

[Guest guest]

>

> Also, here's an interesting and detailed discussion of selenium from

> the same web site:

> http://www.exrx.net/Nutrition/Antioxidants/Selenium.html#anchor3688468

>

> I haven't finished looking at the web site, but it looks interesting

> from what I've seen so far.

>

, I didn't read the full article, but check this out from the

conclusion: " Furthermore, selenium soil content is adequate in North

America and most of the world. Those places with low selenium add the

mineral to livestock feed. The adequacy of selenium warrants no need for

supplementation with the mineral. Athletes will gain no competitive

advantage by utilizing selenium as an ergogenic aid or exercise recovery

aid. The toxic effects of the mineral are devastating and can be

detrimental. Therefore, supplementation with the mineral is not

recommended. "

[Guest guest]

--- <chriskresser@...> wrote:

> I didn't read the full article, but check this out from the

> conclusion: " Furthermore, selenium soil content is adequate in

> North America and most of the world. Those places with low selenium

> add the mineral to livestock feed. The adequacy of selenium warrants

> no need for supplementation with the mineral. Athletes will gain no

> competitive advantage by utilizing selenium as an ergogenic aid or

> exercise recovery aid. The toxic effects of the mineral are

> devastating and can be detrimental. Therefore, supplementation with

> the mineral is not recommended. "

K, my feeling is that we should be able to get the nutrition

that we need from food, provided we are careful in our food choices.

I was reading a little more about selenium and it looks like the

animal form of selenium, selenocysteine is part of glutathione

peroxidase which is in turn involved in the body's handling of free

radicals. So, I'm wondering if the animal form may be more

beneficial, since it is already selenocyteine, whereas the plant form

is selenomethionine, which I'm guessing must be converted into

selenocysteine to form glutathione peroxidase. I don't know if

selenocysteine is absorbed directly in digestion, but I'm guessing

that it is. That would make it more readily available for

construction of glutathione peroxidase than the plant form.

Of course, this is pure speculation on my part

But it seems that very often, animal forms of nutrients are more

bio-available than plant forms.

[Guest guest]

> K, my feeling is that we should be able to get the nutrition

> that we need from food, provided we are careful in our food choices.

Thanks for the link to the exercise site. This site was very informative about

the limited

state of knowledge about antioxidants in health, as of 2000 when the site was

written.

It seems one of two criteria should be sufficient for supplementation of some

micronutrient:

1. Information that modern diets have far less of this micronutrient than

healthy, primitive

settled diets or hunter-gatherer diets. There is little question these groups

suffered less

degeneration and chronic disease than modern, Western populations. This theory,

plus a

recent test showing I have limited circulating vitamin D compared to say

lifeguards, is why

I supplement vitamin D above the amount in cod liver oil. The supposed

allegations by

Weston Price (I lack the exact reference in his book) that modern diets contain

1/10th of

the levels of say vitamin A that native diets do, plus the work by M, is

why I take cod

liver oil.

2. Evidence from a randomized clinical trial that supplementing the

micronutrient reduces

total mortality. I don't know of any supplement that meets this criteria for the

general

population. Perhaps niacin and omega 3 PUFAs meet this criteria for those with

cardiovascular disease. For a pro-niacin website (kind of shady...), look at

http://www.cholesterolscore.com/

Backing up criteria #1 would be suggestive but not conclusive clinical evidence.

The cancer

study for vitamin D (AJCN, 2007) hyped up by the vitamin D council falls into

this

category.

[Guest guest]

> K, my feeling is that we should be able to get the nutrition

> that we need from food, provided we are careful in our food choices.

- I completely agree and that's what I shoot for in my own life. My dad

is trying in

this regard but certain aspects of his work and lifestyle make the transition

challenging.

So I'm trying to help him through and make the best of the situation as it is.

>

> I was reading a little more about selenium and it looks like the

> animal form of selenium, selenocysteine is part of glutathione

> peroxidase which is in turn involved in the body's handling of free

> radicals. So, I'm wondering if the animal form may be more

> beneficial, since it is already selenocyteine, whereas the plant form

> is selenomethionine, which I'm guessing must be converted into

> selenocysteine to form glutathione peroxidase. I don't know if

> selenocysteine is absorbed directly in digestion, but I'm guessing

> that it is. That would make it more readily available for

> construction of glutathione peroxidase than the plant form.

I may have misunderstood the antioxidant article, but I thought their point was

that

because free radicals are used by the immune system to mark foreign invaders or

damaged tissue for removal, overuse of antioxidants could actually decrease the

effectiveness of the immune system.

In this sense, wouldn't selenocysteine be just as potentially harmful as

selenomethionine?

BTW, is methyl-selenocysteine the same as selenocysteine in terms of

supplementation?

[Guest guest]

, &

Thanks again for your contributions. I'm concerned about my dad and want to

make sure I

help him in the best way possible.

I've also seen many studies and reports of the effectiveness of omega-3 fatty

acids and

niacin for CVD. I asked this in a previous post in this thread, but I'll

mention it again.

PUFA increases the risk of oxidative damage, and n-3 FAs are PUFA of course.

And Chris

M's recent report suggests that EFAs aren't essential after all. From this I

would expect n-

3s to make CVD worse. However, n-3s counter the inflammatory effects of n-6s -

so

perhaps this explains their beneficial effect in CVD? I've been trying to get

my head

around this for a while.

The JELIS trial showed that omega-3 intake (EPA + DHA) is associated with

carotid

intimal-medial thickness, an index of body-wide atherosclerosis. This may be of

particular interest to someone like my dad who already has atherosclerosis.

What do you think?

Regarding vitamin D, what total amount are you shooting for daily. I've seen a

huge range

of recommendations, anywhere from 1000 - 3000 IU daily. How much do you get

from

CLO, and how much from a supplement? Do you use D3?

Chris

>

> > K, my feeling is that we should be able to get the nutrition

> > that we need from food, provided we are careful in our food choices.

>

> Thanks for the link to the exercise site. This site was very informative about

the limited

> state of knowledge about antioxidants in health, as of 2000 when the site was

written.

>

> It seems one of two criteria should be sufficient for supplementation of some

> micronutrient:

>

> 1. Information that modern diets have far less of this micronutrient than

healthy,

primitive

> settled diets or hunter-gatherer diets. There is little question these groups

suffered less

> degeneration and chronic disease than modern, Western populations. This

theory, plus a

> recent test showing I have limited circulating vitamin D compared to say

lifeguards, is

why

> I supplement vitamin D above the amount in cod liver oil. The supposed

allegations by

> Weston Price (I lack the exact reference in his book) that modern diets

contain 1/10th of

> the levels of say vitamin A that native diets do, plus the work by M, is

why I take

cod

> liver oil.

>

> 2. Evidence from a randomized clinical trial that supplementing the

micronutrient

reduces

> total mortality. I don't know of any supplement that meets this criteria for

the general

> population. Perhaps niacin and omega 3 PUFAs meet this criteria for those with

> cardiovascular disease. For a pro-niacin website (kind of shady...), look at

>

> http://www.cholesterolscore.com/

>

> Backing up criteria #1 would be suggestive but not conclusive clinical

evidence. The

cancer

> study for vitamin D (AJCN, 2007) hyped up by the vitamin D council falls into

this

> category.

>

>

>

[Guest guest]

On Sat, Jul 26, 2008 at 3:40 PM, cbrown2008 <cbrown2008@...> wrote:

> Alan, did you read the bit in Taubes' " Good Calories, Bad Calories " on

> deficiency diseases, where he talks about the hypothesis that vitamin C

> is only needed in large amounts to counteract the effect of excess

> amounts of starch and sugar, because glucose uptake competes with vit C

> uptake? Just curious to see if you had an opinion.

>

Interesting, I hadn't seen that, sounds like something worth learning more

about. Do you recall if he provided support for that?

--

Alan (alanmjones@...)

[Guest guest]

> Interesting, I hadn't seen that, sounds like something worth learning

more

> about. Do you recall if he provided support for that?

Support for which part? The one about vit C and glucose is well-known,

I would suggest a physiology text for that one. The hypothesis itself

comes from the studies he mentions in the books - it is one way to

explain the data, and all the researchers he mentioned, and their

publications, are in the biblio.

It's in the section on the " golden age " of deficiency diseases like

beri beri, pellagra, scurvy. All the deficiency diseases were found in

populations who ate a disproportionate amount of starch/sugar at the

expense of protein and fat. This could explain why Stephansson did not

get scurvy in his year-long experiment (low vit C) or, if you've

read " Two Years Before the Mast, " by Dana (really good), how they ate

beef three times a day on shipboard and did not get scurvy. Contrasted

with the British Navy who did get it eating hardtack, molasses, rum,

and I guess salt pork until it ran out.

Then when you add vitamin C sources from plants, scurvy goes away. So

nutritionists ever since have said we need X vitamin C, while ignoring

the other explanation of, perhaps we need less starch and sugar

(proportionally).

Connie

[Guest guest]

I just finished reading the antioxidant study in JAMA. One interesting note in

the comment

section just before the conclusion:

" Because we examined only the influence of synthetic antioxidants, our findings

should not

be translated to potential effects of fruits and vegetables. "

And, one would assume, animal products like CLO.

Chris

[Guest guest]

> I've also seen many studies and reports of the effectiveness of omega-3 fatty

acids and

> niacin for CVD. I asked this in a previous post in this thread, but I'll

mention it again.

> PUFA increases the risk of oxidative damage, and n-3 FAs are PUFA of course.

And

Chris

> M's recent report suggests that EFAs aren't essential after all. From this I

would expect

n-

> 3s to make CVD worse. However, n-3s counter the inflammatory effects of n-6s

- so

> perhaps this explains their beneficial effect in CVD? I've been trying to get

my head

> around this for a while.

I wish I could help, but it seems like the relationship between omega 3s and

disease reoccurrence in cardiac patients is poorly understood. Some nutritional

interventions have

shown success. This could just be from displacing omega 6's in the diet, from

creating a

more balanced ratio of omega 3's to omega 6's, from some benefit of omega 3's

independent of omega 6's, or who knows what.

You might also look at the GISSI-Prevention trial.

> Regarding vitamin D, what total amount are you shooting for daily. I've seen

a huge

range

> of recommendations, anywhere from 1000 - 3000 IU daily. How much do you get

from

> CLO, and how much from a supplement? Do you use D3?

I had been taking around 1500 IU of vitamin D a day, from 0.5 teaspoons of

fermented

cod liver oil. I also get about 20-30 minutes of midday sun exposure three times

a week

during the summer. I got a test result a week or two ago saying I had around a

serum

vitamin D level of 33 ng/mL. Someone who spends a lot of time in the sun but

does not

supplement should be 50 ng/mL. This test result scared me because if these are

my levels

in the summer, what are my levels in the winter?

I have switched to adding two capsules with 2000 IU of vitamin D3 each, for a

total daily

intake of 5500 IU, plus tiny amounts in egg yolks and seafood. I take the butter

oil with

the cod liver oil, but I am worried about the PUFAs in cod liver oil.

I will retest in a few months to see what my circulating levels of vitamin D

are. 5000 IU is

what vitamin D enthusiast Cannell takes in the winter.

[Guest guest]

>

> You might also look at the GISSI-Prevention trial.

I've seen the GISSI Prevention trail and that seemed to me like fairly

convincing evidence

that fish oil can benefit people with cardiovascular disease (14-20% relative

reduction in

total deaths). Interestingly, vitamin E was also studied in the same trial and

did not reach

statistical significance. They did determine that adding vitamin E did not

increase the

benefit of n-3 PUFA.

>

> > Regarding vitamin D, what total amount are you shooting for daily. I've

seen a huge

> range

> > of recommendations, anywhere from 1000 - 3000 IU daily. How much do you get

from

> > CLO, and how much from a supplement? Do you use D3?

>

> I had been taking around 1500 IU of vitamin D a day, from 0.5 teaspoons of

fermented

> cod liver oil. I also get about 20-30 minutes of midday sun exposure three

times a week

> during the summer. I got a test result a week or two ago saying I had around a

serum

> vitamin D level of 33 ng/mL. Someone who spends a lot of time in the sun but

does not

> supplement should be 50 ng/mL. This test result scared me because if these are

my

levels

> in the summer, what are my levels in the winter?

>

> I have switched to adding two capsules with 2000 IU of vitamin D3 each, for a

total daily

> intake of 5500 IU, plus tiny amounts in egg yolks and seafood. I take the

butter oil with

> the cod liver oil, but I am worried about the PUFAs in cod liver oil.

>

> I will retest in a few months to see what my circulating levels of vitamin D

are. 5000 IU

is

> what vitamin D enthusiast Cannell takes in the winter.

This sounds like a good strategy and is similar to what I've read in terms of

beneficial

amounts.

Thanks,

Chris

[Guest guest]

Would he be open to any type of , say....Yoga?' If he is a high stress kinda

guy, changing diet in whatever way will be kinda mute if he is still pumping all

that adrenalin into his blood stream.

[Guest guest]

and others taking the fermented clo,

how does it taste? I've heard that it can burn the back of your throat. what has

your

experience with it been?

>

> > I've also seen many studies and reports of the effectiveness of omega-3

fatty acids

and

> > niacin for CVD. I asked this in a previous post in this thread, but I'll

mention it again.

> > PUFA increases the risk of oxidative damage, and n-3 FAs are PUFA of course.

And

> Chris

> > M's recent report suggests that EFAs aren't essential after all. From this

I would

expect

> n-

> > 3s to make CVD worse. However, n-3s counter the inflammatory effects of

n-6s - so

> > perhaps this explains their beneficial effect in CVD? I've been trying to

get my head

> > around this for a while.

>

> I wish I could help, but it seems like the relationship between omega 3s and

disease

reoccurrence in cardiac patients is poorly understood. Some nutritional

interventions have

> shown success. This could just be from displacing omega 6's in the diet, from

creating

a

> more balanced ratio of omega 3's to omega 6's, from some benefit of omega 3's

> independent of omega 6's, or who knows what.

>

> You might also look at the GISSI-Prevention trial.

>

> > Regarding vitamin D, what total amount are you shooting for daily. I've

seen a huge

> range

> > of recommendations, anywhere from 1000 - 3000 IU daily. How much do you get

from

> > CLO, and how much from a supplement? Do you use D3?

>

> I had been taking around 1500 IU of vitamin D a day, from 0.5 teaspoons of

fermented

> cod liver oil. I also get about 20-30 minutes of midday sun exposure three

times a week

> during the summer. I got a test result a week or two ago saying I had around a

serum

> vitamin D level of 33 ng/mL. Someone who spends a lot of time in the sun but

does not

> supplement should be 50 ng/mL. This test result scared me because if these are

my

levels

> in the summer, what are my levels in the winter?

>

> I have switched to adding two capsules with 2000 IU of vitamin D3 each, for a

total daily

> intake of 5500 IU, plus tiny amounts in egg yolks and seafood. I take the

butter oil with

> the cod liver oil, but I am worried about the PUFAs in cod liver oil.

>

> I will retest in a few months to see what my circulating levels of vitamin D

are. 5000 IU

is

> what vitamin D enthusiast Cannell takes in the winter.

>

>

>

[Guest guest]

> how does it taste? I've heard that it can burn the back of your throat. what

has your

> experience with it been?

It is unpleasant. I take it only because it may be less processed than other

types.

[Guest guest]

After reading the full text of the study in JAMA on the increase in

mortality with antioxidant supplements, I am wondering about its

implications.

The authors of the study speculate - like the authors of the article

that linked to - that by eliminating free radicals from our

organism, we interfere with some essential defensive mechanisms like

apoptosis, phagocytosis and detoxification.

If this is true, a few questions arise:

1. Has the role of oxidative damage in the pathogenicity of disease been

overstated? The JAMA study authors suggest that this could be another

case of confusing causation with correlation. In other words, OD is the

result of underlying disease processes rather than the cause.

2. Are the antioxidants present in fruit, vegetables and animal products

likely to increase mortality in the same way as synthetic antioxidants?

It seems to me that if the authors are correct in their speculation of

the mechanism by which antioxidants increase mortality, then ANY

antioxidant that reduces free radicals beyond a certain threshold -

regardless of the source - could be detrimental to health.

3. There is so much research suggesting that OD is a primary cause of

heart disease? Do the results of this study cast doubt on this theory?

In any event, if the authors are correct it seems that the best strategy

from a dietary perspective is to strictly avoid PUFA and limit

carbohydrate intake (to avoid AGEs) rather than taking large amounts of

antioxidants.  

Of course this is what we should have been doing anyways, but what is

different (for me, at least) is the understanding that even in people

who are likely to have high PUFA intake (like all of the people in the

studies reviewed) it is not a good idea to take antioxidants.

Previously I was under the impression that if someone has a high n-6

PUFA intake, then they should be taking antioxidants to offset the

damage.

I'd love to hear your thoughts.

>

> > K, my feeling is that we should be able to get the nutrition

> > that we need from food, provided we are careful in our food choices.

>

> Thanks for the link to the exercise site. This site was very

informative about the limited

> state of knowledge about antioxidants in health, as of 2000 when the

site was written.

>

> It seems one of two criteria should be sufficient for supplementation

of some

> micronutrient:

>

> 1. Information that modern diets have far less of this micronutrient

than healthy, primitive

> settled diets or hunter-gatherer diets. There is little question these

groups suffered less

> degeneration and chronic disease than modern, Western populations.

This theory, plus a

> recent test showing I have limited circulating vitamin D compared to

say lifeguards, is why

> I supplement vitamin D above the amount in cod liver oil. The supposed

allegations by

> Weston Price (I lack the exact reference in his book) that modern

diets contain 1/10th of

> the levels of say vitamin A that native diets do, plus the work by

M, is why I take cod

> liver oil.

>

> 2. Evidence from a randomized clinical trial that supplementing the

micronutrient reduces

> total mortality. I don't know of any supplement that meets this

criteria for the general

> population. Perhaps niacin and omega 3 PUFAs meet this criteria for

those with

> cardiovascular disease. For a pro-niacin website (kind of shady...),

look at

>

> http://www.cholesterolscore.com/

>

> Backing up criteria #1 would be suggestive but not conclusive clinical

evidence. The cancer

> study for vitamin D (AJCN, 2007) hyped up by the vitamin D council

falls into this

> category.

>

>

>

[Guest guest]

L carnitine fummarate is the preferred cardiovascular carnitine; acetyl

l carnitine will cross the blood brain barrier, but is also good for

the heart. Both will cross the mitochondrial membrane. Carnitine is

also made from the aminos methionine and lysine, and requires activated

B6 for conjugation.

[Guest guest]

The JAMA study is convincing (to me) that there cannot possibly be any large

mortality

benefit of taking synthetic antioxidant supplements other than selenium. The

chance of an

increase in mortality is large. If the underlying reason is that free radicals

have beneficial

roles in the body as well as harmful roles, then I believe this conclusion would

extend to antioxidants in foods.

Still, I had some blueberries last night and was more worried about the fructose

content

than the antioxidant content!

The Wikipedia article on oxidative stress says

" Oxidative stress (as formulated in Harman's free radical theory of aging) is

also thought

to contribute to the aging process. While there is good evidence to support this

idea in

model organisms such as Drosophila melanogaster and Caenorhabditis elegans,

recent

evidence from Ristow's laboratory suggests that oxidative stress may

also

promote life expectancy of Caenorhabditis elegans by inducing a secondary

response to

initially increased levels of reactive oxygen species. This process was

previously named

mitohormesis or mitochondrial hormesis on a purely hypothetical basis. The

situation in

mammals is even less clear. Recent epidemiological findings support the process

of

mitohormesis, and even suggest that antioxidants may increase disease prevalence

in

humans (although the results were influenced by studies on smokers). "

The last sentence is in reference to the JAMA article. There was a letters to

the editor and

reply section in JAMA and I don't think removing the smoking studies changes the

results.

As for theories of heart disease being overturned by the JAMA meta analysis, I

wouldn't go

that far, although all heart disease theories are by their nature speculative.

However, at

middle age I would take advantage of a test than can directly measure plaque,

like the

" Track Your Plaque " program mentioned by another poster.

I don't know of any studies that look at the differential effects of antioxidant

use by

omega 6 dietary intake.

> >

> > > K, my feeling is that we should be able to get the nutrition

> > > that we need from food, provided we are careful in our food choices.

> >

> > Thanks for the link to the exercise site. This site was very

> informative about the limited

> > state of knowledge about antioxidants in health, as of 2000 when the

> site was written.

> >

> > It seems one of two criteria should be sufficient for supplementation

> of some

> > micronutrient:

> >

> > 1. Information that modern diets have far less of this micronutrient

> than healthy, primitive

> > settled diets or hunter-gatherer diets. There is little question these

> groups suffered less

> > degeneration and chronic disease than modern, Western populations.

> This theory, plus a

> > recent test showing I have limited circulating vitamin D compared to

> say lifeguards, is why

> > I supplement vitamin D above the amount in cod liver oil. The supposed

> allegations by

> > Weston Price (I lack the exact reference in his book) that modern

> diets contain 1/10th of

> > the levels of say vitamin A that native diets do, plus the work by

> M, is why I take cod

> > liver oil.

> >

> > 2. Evidence from a randomized clinical trial that supplementing the

> micronutrient reduces

> > total mortality. I don't know of any supplement that meets this

> criteria for the general

> > population. Perhaps niacin and omega 3 PUFAs meet this criteria for

> those with

> > cardiovascular disease. For a pro-niacin website (kind of shady...),

> look at

> >

> > http://www.cholesterolscore.com/

> >

> > Backing up criteria #1 would be suggestive but not conclusive clinical

> evidence. The cancer

> > study for vitamin D (AJCN, 2007) hyped up by the vitamin D council

> falls into this

> > category.

> >

> >

> >

>

>

>

>

[Guest guest]

,

Very interesting. I agree about the usefulness of the Heart Scan. I'm going to

recommend

that my dad get one; in fact, his doctor had already ordered the test but he

hasn't done it

yet.

The question, though, is what to do if there is significant plaque? Previous to

reading the

JAMA article I would have said reducing oxidative stress by eating antioxidant

foods or

taking antioxidant supplements would be one part of the solution. I couldn't

say that with

any confidence now, however.

One might question the need to limit PUFA so dramatically if oxidative stress is

not the

dangerous beast it has been thought to be. But of course there are many other

reasons to

limit n-6 PUFA, though. In the context of heart disease, studies have shown

that 75% of

plaques are made up of unsaturated fat (approx 25% MUFA and 50% PUFA, I

believe), and

that higher concentration of n-6 PUFA in plaques make them more likely to

rupture. The

correlation is continuous and monotonic.

I also wonder about antioxidants such as CoQ10 which exert more " specific "

effects on the

heart and vessels. I've seen a lot of (what seems to be) good data correlating

CoQ10 with

reduced cardiac events and reduced mortality.

And what about tocotrienols and mixed tocopherols? There is also data

indicating a

protective role for these in heart disease.

Since these were not included in the JAMA review, it's hard to know whether they

are

advisable for people with pre-existing CVD. Going by what I've seen of the

available data,

I would say yes. But the JAMA analysis casts some doubt on that for me.

> The JAMA study is convincing (to me) that there cannot possibly be any large

mortality

> benefit of taking synthetic antioxidant supplements other than selenium. The

chance of

an

> increase in mortality is large. If the underlying reason is that free radicals

have

beneficial

> roles in the body as well as harmful roles, then I believe this conclusion

would extend to

antioxidants in foods.

>

> Still, I had some blueberries last night and was more worried about the

fructose content

> than the antioxidant content!

>

> The Wikipedia article on oxidative stress says

>

> " Oxidative stress (as formulated in Harman's free radical theory of aging) is

also thought

> to contribute to the aging process. While there is good evidence to support

this idea in

> model organisms such as Drosophila melanogaster and Caenorhabditis elegans,

recent

> evidence from Ristow's laboratory suggests that oxidative stress may

also

> promote life expectancy of Caenorhabditis elegans by inducing a secondary

response to

> initially increased levels of reactive oxygen species. This process was

previously named

> mitohormesis or mitochondrial hormesis on a purely hypothetical basis. The

situation in

> mammals is even less clear. Recent epidemiological findings support the

process of

> mitohormesis, and even suggest that antioxidants may increase disease

prevalence in

> humans (although the results were influenced by studies on smokers). "

>

> The last sentence is in reference to the JAMA article. There was a letters to

the editor

and

> reply section in JAMA and I don't think removing the smoking studies changes

the

results.

>

> As for theories of heart disease being overturned by the JAMA meta analysis, I

wouldn't

go

> that far, although all heart disease theories are by their nature speculative.

However, at

> middle age I would take advantage of a test than can directly measure plaque,

like the

> " Track Your Plaque " program mentioned by another poster.

>

> I don't know of any studies that look at the differential effects of

antioxidant use by

> omega 6 dietary intake.

>

>

[Guest guest]

Isn't Vitamin E usually given as alpha tocopherol? The JAMA article covered

that: no effects

either way. I would suspect there have not been many clinical trials of the less

common

forms of tocopherols.

Here is the Mayo Clinic page on coenzyme Q10. The entry for heart disease

basically says

there is little work in this area. Maybe M. should give his theoretical

reasoning. Why

also haven't gotten the full story of why recommends ceasing vegetable

intake.

Chris?

http://www.mayoclinic.com/health/coenzyme-q10/NS_patient-coenzymeq10

>

> > The JAMA study is convincing (to me) that there cannot possibly be any large

mortality

> > benefit of taking synthetic antioxidant supplements other than selenium. The

chance

of

> an

> > increase in mortality is large. If the underlying reason is that free

radicals have

> beneficial

> > roles in the body as well as harmful roles, then I believe this conclusion

would extend

to

> antioxidants in foods.

> >

> > Still, I had some blueberries last night and was more worried about the

fructose

content

> > than the antioxidant content!

> >

> > The Wikipedia article on oxidative stress says

> >

> > " Oxidative stress (as formulated in Harman's free radical theory of aging)

is also

thought

> > to contribute to the aging process. While there is good evidence to support

this idea

in

> > model organisms such as Drosophila melanogaster and Caenorhabditis elegans,

recent

> > evidence from Ristow's laboratory suggests that oxidative stress may

also

> > promote life expectancy of Caenorhabditis elegans by inducing a secondary

response

to

> > initially increased levels of reactive oxygen species. This process was

previously

named

> > mitohormesis or mitochondrial hormesis on a purely hypothetical basis. The

situation

in

> > mammals is even less clear. Recent epidemiological findings support the

process of

> > mitohormesis, and even suggest that antioxidants may increase disease

prevalence in

> > humans (although the results were influenced by studies on smokers). "

> >

> > The last sentence is in reference to the JAMA article. There was a letters

to the editor

> and

> > reply section in JAMA and I don't think removing the smoking studies changes

the

> results.

> >

> > As for theories of heart disease being overturned by the JAMA meta analysis,

I

wouldn't

> go

> > that far, although all heart disease theories are by their nature

speculative. However,

at

> > middle age I would take advantage of a test than can directly measure

plaque, like the

> > " Track Your Plaque " program mentioned by another poster.

> >

> > I don't know of any studies that look at the differential effects of

antioxidant use by

> > omega 6 dietary intake.

> >

> >

>

[Guest guest]

> Isn't Vitamin E usually given as alpha tocopherol? The JAMA article covered

that: no

effects

> either way. I would suspect there have not been many clinical trials of the

less common

> forms of tocopherols.

I can't remember if I heard this from M. or somewhere else, but I recall

that " mixed

tocopherols " are more effective than alpha-tocopherol itself. Gamma-tocopherol

seemed

particularly important. But this might all be negated by the JAMA review.

>

> Here is the Mayo Clinic page on coenzyme Q10. The entry for heart disease

basically

says

> there is little work in this area. Maybe M. should give his theoretical

reasoning.

Why

> also haven't gotten the full story of why recommends ceasing vegetable

intake.

> Chris?

>

> http://www.mayoclinic.com/health/coenzyme-q10/NS_patient-coenzymeq10

Here's a site which describes what the studies that have been performed so far

on CoQ10

and heart disease have revealed.

http://www.oralchelation.com/technical/coq101.htm

Yes, I'd be interested in hearing M.'s opinion on this and also his

reasoning on

limiting or eliminating vegetable intake.

>

>

>

[Guest guest]

--- <chriskresser@...> wrote:

> I may have misunderstood the antioxidant article, but I thought

> their point was that because free radicals are used by the immune

> system to mark foreign invaders or damaged tissue for removal,

> overuse of antioxidants could actually decrease the effectiveness of

> the immune system.

K, that was my understanding also.

> In this sense, wouldn't selenocysteine be just as potentially

> harmful as selenomethionine?

I just read what wiki has to say about selenomethionone,

selenocysteine, and glutathione peroxidase:

http://en.wikipedia.org/wiki/Selenocysteine

http://en.wikipedia.org/wiki/Selenomethionine

http://en.wikipedia.org/wiki/Glutathione_peroxidase

If wiki is correct, it appears that selenomethianone is an antioxidant

and has little other function, whereas selenocysteine is used by the

body in several enzymes, including " glutathione peroxidases,

tetraiodothyronine 5' deiodinases, thioredoxin reductases, formate

dehydrogenases, glycine reductases and some hydrogenases " .

Also:

" Glutathione peroxidase is the general name of an enzyme family with

peroxidase activity whose main biological role is to protect the

organism from oxidative damage. The biochemical function of

glutathione peroxidase is to reduce lipid hydroperoxides to their

corresponding alcohols and to reduce free hydrogen peroxide to water. "

I'm not sure if the anitoxidant potential of selenomethionone is as

specific as for glutathione peroxidase. Since selenocyteine is part

of several other enzymes, I would guess that overall it should be more

beneficial than selenomethionone and I'm not even sure if

selenomethionone has any real benefit.

> BTW, is methyl-selenocysteine the same as selenocysteine in terms of

> supplementation?

I'm not sure. But I wouldn't take a supplement for any kind of

selenium. I'm content to get selenium from animal foods

[Guest guest]

> I'm not sure. But I wouldn't take a supplement for any kind of

> selenium. I'm content to get selenium from animal foods

>

,

It does seem like selenocysteine may have benefits that selenomethionine doesn't

have.

What foods aside from fish and shellfish are high in selenium? I minimize my

intake of fish

for economic and environmental reasons.

Chris

[Guest guest]

--- <chriskresser@...> wrote:

> 1. Has the role of oxidative damage in the pathogenicity of disease

> been overstated? The JAMA study authors suggest that this could be

> another case of confusing causation with correlation. In other

> words, OD is the result of underlying disease processes rather than

> the cause.

my suspicion is that this is true.

> 2. Are the antioxidants present in fruit, vegetables and animal

> products likely to increase mortality in the same way as synthetic

> antioxidants? It seems to me that if the authors are correct in

> their speculation of the mechanism by which antioxidants increase

> mortality, then ANY antioxidant that reduces free radicals beyond a

> certain threshold - regardless of the source - could be detrimental

> to health.

I suspect that there is no simple answer on this one. There are so

many kinds of natural antioxidants, I can see how a few of them might

actually be beneficial for most people. But many plant antioxidants

serve as pesticides and may have detrimental effects in our body as

well, and even more so for sensitive people.

> 3. There is so much research suggesting that OD is a primary cause

> of heart disease? Do the results of this study cast doubt on this

> theory? In any event, if the authors are correct it seems that the

> best strategy from a dietary perspective is to strictly avoid PUFA

> and limit carbohydrate intake (to avoid AGEs) rather than taking

> large amounts of antioxidants. Of course this is what we should

> have been doing anyways, but what is different (for me, at least) is

> the understanding that even in people who are likely to have high

> PUFA intake (like all of the people in the studies reviewed) it is

> not a good idea to take antioxidants. Previously I was under the

> impression that if someone has a high n-6 PUFA intake, then they

> should be taking antioxidants to offset the damage.

Yes, I agree on the goal to minimize PUFA and eat low-carb. This is

the first that I have read that antioxidants may be detrimental for

those on a high-PUFA diet. Interesting! Again, though, there are so

many antioxidants, I'm not sure how meaningful this is for ALL

antioxidants.