Dad's got atherosclerosis - what to do?

[Guest guest]

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

> What foods aside from fish and shellfish are high in selenium?

K, here's what I have in my Excel dietary nutrition calculator,

based on USDA nutrient data for conventional food sources:

mcg/100g

154.0 Mollusks, oyster, Pacific, cooked, moist heat

111.4 Lamb, variety meats and by-products, liver, cooked, braised

82.5 Turkey, liver, all classes, cooked, simmered

82.4 Chicken, liver, all classes, cooked, simmered

80.4 Fish, tuna, light, canned in water, drained solids

65.7 Fish, tuna, white, canned in water, drained solids

65.5 Fish, caviar, black and red, granular

65.0 Pork, cured, bacon, cooked, pan-fried

64.0 Mollusks, clam, mixed species, cooked, moist heat

58.0 Braunschweiger (a liver sausage), pork

58.0 Pork, liver sausage, liverwurst

56.0 Egg, yolk, raw, fresh

52.7 Fish, sardine, Atlantic, canned in oil, drained solids with bone

51.8 Mollusks, squid, mixed species, cooked, fried

51.7 Fish, roe, mixed species, cooked, dry heat

51.6 Fish, mackerel, Atlantic, cooked, dry heat

48.6 Mollusks, clam, mixed species, canned, drained solids

46.8 Fish, pollock, Atlantic, cooked, dry heat

44.8 Mollusks, squid, mixed species, raw

41.4 Fish, salmon, Atlantic, farmed, cooked, dry heat

40.3 Fish, roe, mixed species, raw

39.6 Crustaceans, shrimp, mixed species, cooked, moist heat

39.0 Turkey, fryer-roasters, dark meat, meat and skin, cooked, roasted

38.0 Fish, salmon, coho, wild, cooked, dry heat

38.0 Mutton, cooked, roasted (Navajo)

37.6 Fish, cod, Atlantic, cooked, dry heat

37.1 Pork, loin, country-style ribs, separable lean and fat, roasted

36.1 Beef, variety meats and by-products, liver, cooked, braised

35.8 Mollusks, oyster, eastern, canned

31.7 Egg, whole, raw, fresh

30.8 Lamb, domestic, leg, sirloin half, separable lean only, trimmed

to 1/4 " fat, choice, cooked, roasted

30.8 Egg, whole, cooked, hard-boiled

30.0 Game meat, bison, ground, cooked, pan-broiled

29.9 Turkey, fryer-roasters, light meat, meat and skin, roasted

29.2 Beef, top sirloin, trimmed to 1/8 " fat, all grades, broiled

28.3 Beef, chuck, arm pot roast, trimmed to 1/8 " fat, braised

27.9 Mollusks, scallop, (bay and sea), cooked, steamed

27.8 furter, pork

27.7 Lamb, ground, cooked, broiled

25.4 Salami, Italian, pork

24.1 Chicken, broilers or fryers, light meat, meat and skin, roasted

22.5 Egg, whole, cooked, scrambled

22.2 Mollusks, scallop, mixed species, raw

21.1 Beef, ground, 95% lean meat / 5% fat, patty, cooked, pan-broiled

20.7 Beef, ground, 90% lean meat / 10% fat, patty, cooked, pan-broiled

20.3 Beef, ground, 85% lean meat / 15% fat, patty, cooked, pan-broiled

20.2 Chicken, broilers or fryers, dark meat, meat and skin, roasted

19.8 Pork, cured, ham, boneless, regular (~11% fat), roasted

18.2 Cheese, swiss

17.7 Cheese, parmesan, grated

16.1 Cheese, mozzarella, whole milk, low moisture

14.6 Beef, cured, sausage, cooked, smoked

14.5 Cheese, colby

14.5 Cheese, monterey

14.5 Cheese, provolone

13.9 Cheese, cheddar

12.7 Bologna, pork

12.5 furter, meat

10.7 Beef jerky, chopped and formed

10.3 Game meat, deer, ground, cooked, pan-broiled

9.0 Cheese, cottage, creamed, large or small curd

8.2 furter, beef

3.7 Milk, whole, 3.25% milkfat

2.4 Cheese, cream

2.2 Cream, sour, cultured

2.2 Yogurt, plain, whole milk, 8 grams protein per 8 ounce

1.8 Cream, fluid, half and half

1.0 Butter, without salt

0.6 Cream, fluid, light (coffee cream or table cream)

0.5 Cream, fluid, heavy whipping

0.2 Fat, beef tallow

0.2 Fat, mutton tallow

0.2 Lard

It looks like liver and egg yolks are the best bet besides seafood.

Bacon is up there too. I just had some last night

[Guest guest]

Information here:

http://ods.od.nih.gov/factsheets/selenium.asp

I've heard that one must make sure that the Brazil nuts come from

Brazil, as nuts grown in other places (like California) will have been

grown in selenium depleted soil and not contain optimal amounts of this

mineral.

-Patty

>>

> What foods aside from fish and shellfish are high in selenium?

[Guest guest]

Thanks, .

OT: tell me about the Excel nutrition data calculator. Is that available

publicly, or did you

make it up yourself?

Thanks,

Chris

[Guest guest]

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

> OT: tell me about the Excel nutrition data calculator. Is that

> available publicly, or did you make it up yourself?

K, I made the Excel nutrition calculator for my own use, but I

am sharing it to the public here:

http://stay-healthy-enjoy-life.blogspot.com/2007/08/dietary-nutrition-calculator\

..html

You do have to have Excel to use it.

[Guest guest]

> > OT: tell me about the Excel nutrition data calculator. Is that

> > available publicly, or did you make it up yourself?

>

> K, I made the Excel nutrition calculator for my own use, but I

> am sharing it to the public here:

>

http://stay-healthy-enjoy-life.blogspot.com/2007/08/dietary-nutrition-calculator\

..html

>

> You do have to have Excel to use it.

>

Thanks . Amazingly useful!

[Guest guest]

,

> Keep in mind, the idea behind this meta analysis is that in individual

> studies, there

> typically is not a long enough duration or number of participants to detect

> a statistically

> significant effect on total mortality, because mortality risk of an

> individual in any given

> short time period is very small. The meta analysis combined many studies you

> might have

> never heard of because the original studies had other endpoints than

> mortality. The meta

> analysis authors then get the mortality data from the original authors and

> pool all the

> studies.

That's the strength of a meta-analysis, while the drawbacks are that

they treat all studies as the same rather than differentiating between

the strengths and weaknesses or in some cases simply important

differences.

> To answer your question, Table 5 of the meta analysis lists 24 studies for

> vitamin E given

> singly. There were a total of 47,000 participants, and the relative risk for

> vitamin E was

> 1.02 with a confidence interval of 0.98-1.05. So we can statistically reject

> that vitamin E is

> very beneficial or very hurtful for total mortality.

Not really, because we'd have to look at the studies in more detail.

For example, do the drug-metabolizing enzymes whose expression vitamin

E alters interact with specific drugs that the people were on in the

study? If we analyzed the results separately for those on

pharmaceuticals or relevant pharmaceuticals and those not, do we get

different results? Are results different for alpha-tocopherol,

gamma-tocopherol, and mixed tocopherols? Is vitamin E effective in

certain combinations, but not singly, or not in certain other

combinations? For example, is it effective with CoQ10, but not

singly, or not in combination with beta-carotene?

> There were some studies

> with " high risk

> of bias " included in the list of 24. However, the story with vitamin E given

> in combination

> but with low risk only studies is about the same: a relative risk of around

> 1.

Were the combinations the same in the studies?

[snip]

> The conclusion that vitamin A is bad rests on five studies (including the

> two A only

> studies) satisfying " vitamin A given singly or in combination with other

> antioxidant

> supplements after exclusion of high-bias risk and selenium trials. " The

> relative risk is

> 1.16 (bad) with a confidence interval of 1.10-1.24.

I would want to see the results if they excluded the CARET trial

(which I assume they included), since the results were, based on

further animal experimentation, clearly due to the beta-carotene.

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.

>

He used to meditate, and he's going to start up again. He also exercises daily,

which can

help with stress reduction.

[Guest guest]

K,

>> Getting him totally off all vegetables and supplementing with a combo

>> of CoQ10 and mixed tocopherols.

>

> Why off all vegetables? Or did you mean off all vegetable oil?

Yes, vegetable oils, sorry.

> I read the meta-analysis linked to. The jury still isn't out on

> Vitamin A, but it did

> raise some cause for concern. The authors admit that " vitamin C and

> selenium need more

> study " . It's really hard to know what to do with so much uncertainty and

> contradictory

> information in the literature.

I really don't think a meta-analysis is the way to try to make sense of it.

> It seems like a moderate dosage of C along with methyl-selenocysteine would

> likely not be

> harmful and may be helpful. Would you agree?

That seems probable. I'm not sure what methyl-selenocysteine is,

however, versus selenocysteine, off the top of my head. Methylated

version sounds like it would be a detox product. I'd use

selenocysteine if it's available.

> It seems that the research is fairly clear on the benefits of D in

> cardiovascular disease.

Is it?

> But

> is it advisable to supplement with D without adequate intake of K2 and A?

Absolutely not. I think that's probably a recipe for kidney stones.

Chris

[Guest guest]

K,

> The main question for me now is whether to suggest that my father take CLO

> (is the A

> beneficial or dangerous?) or just supplement with D alone. If he does do D

> alone, should

> it be D3?

It should be D3. There is a study in NEJM a while back showing

protection against atherosclerosis in pigs using CLO. One scientist

wrote in a letter suggesting the vitamin A might have been responsible

and noting a possible mechanism. Vitamin A, by the way, prevents

kidney calcification, and there is a relationship between kidney

stones and heart disease -- it might prevent arterial calcification

too, perhaps.

Chris

[Guest guest]

,

> It's not even clear free radicals are themselves bad. Quoting from the meta

> analysis:

Free radicals are definitely not bad if they are produced under

controlled conditions and contained, but they are bad when they exceed

containment, and, for example, leak into the cell membrane or

mitochondrial membrane.

> " There are several possible explanations

> for the negative effect of antioxidant

> supplements on mortality .

> Although oxidative stress has a

> hypothesized role in the pathogenesis

> of many chronic diseases, it may be

> the consequence of pathological conditions.

> By eliminating free radicals

> from our organism, we interfere with

> some essential defensive mechanisms

> like apoptosis , phagocytosis , and

> detoxification. Antioxidant

> supplements are synthetic and not

> subjected to the same rigorous toxicity

> studies as other pharmaceutical

> agents. Be t t e r unde r s t a ndi ng of

> mechanisms and actions of antioxi-

> dants in relation to a potential disease

> is needed.

A more plausible explanation that actually has scientific support is

that some antioxidants act as pro-oxidants at high concentrations.

The idea that oxidative stress does not cause pathology but that

pathology causes oxidative stress almost reaches a certain point of

silliness, in that, although it's totally reasonable that pathology

could cause oxidative stress, it is totally unreasonable to deny all

the literature substantiating causal mechanisms whereby oxidation

products damage proteins, DNA, and other cellular constituents.

Chris

[Guest guest]

K,

> 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?

It would, but did they cite a study showing that antioxidants do, in

fact, reduce the activity of phagocytic cells? A more plausible

explanation for the toxicity of selenium, IMO, would be that selenium

is a toxic pro-oxidant at high concentrations.

Chris

[Guest guest]

K,

> 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.

Aren't you leaving out the fact that this was exclusively in people

who just had a heart attack recently, and when they broke the people

up by risk of arrhythmia, they found that the benefit was ONLY in

people who had left ventricular dysfunction or were prescribed

beta-blockers?

I have not looked at all the evidence but my preliminary findings

suggest that n-3 fatty acids are beneficial for those at risk for

cardiac arrhythmia but are either fairly ineffective or harmful for

others. There was only one study cited in a meta-analysis I looked at

that was primary prevention, and it found n-3 fatty acids increased

the risk 8-fold. They noted that it was a poorer quality study

compared to others, but it was the only one treating people who didn't

already have heart disease.

M

[Guest guest]

That's interesting. It certainly goes to show we are a meat-eating

species. Until we genetically modify ourselves to be able to

survive on nothing but fruits and veggies.

mike

>

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

known,

> I would suggest a physiology text for that one.

[Guest guest]

,

> 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

Vegetable was a typo, meant vegetable oil. My reasoning is that coQ10

is the primary antioxidant in LDL, not vit E, not carotenoids, not

anything else. However, it is possible that the CoQ10 recycles

vitamin E, so there might be a synergistic effect. I haven't seen a

human study on CoQ10 in this respect yet, but there is a study in Apo

E-/- mice, who develop atherosclerosis, and CoQ10 is clearly

beneficial and there might be a positive interaction with E.

Chris

[Guest guest]

> I have not looked at all the evidence but my preliminary findings

> suggest that n-3 fatty acids are beneficial for those at risk for

> cardiac arrhythmia but are either fairly ineffective or harmful for

> others. There was only one study cited in a meta-analysis I looked at

> that was primary prevention, and it found n-3 fatty acids increased

> the risk 8-fold. They noted that it was a poorer quality study

> compared to others, but it was the only one treating people who didn't

> already have heart disease.

You don't happen to remember the citation (or even journal and year) for the

8-fold risk

study? That is scary!

[Guest guest]

> It should be D3. There is a study in NEJM a while back showing

> protection against atherosclerosis in pigs using CLO. One scientist

> wrote in a letter suggesting the vitamin A might have been responsible

> and noting a possible mechanism. Vitamin A, by the way, prevents

> kidney calcification, and there is a relationship between kidney

> stones and heart disease -- it might prevent arterial calcification

> too, perhaps.

M,

So, do you recommend people consume vitamin A through cod liver oil or through a

separate

pill?

[Guest guest]

> Vegetable was a typo, meant vegetable oil. My reasoning is that coQ10

> is the primary antioxidant in LDL, not vit E, not carotenoids, not

> anything else. However, it is possible that the CoQ10 recycles

> vitamin E, so there might be a synergistic effect. I haven't seen a

> human study on CoQ10 in this respect yet, but there is a study in Apo

> E-/- mice, who develop atherosclerosis, and CoQ10 is clearly

> beneficial and there might be a positive interaction with E.

>

> Chris

>

& ,

Here's something I found on the relationship between E & CoQ10, FWIW:

" Partnership with vitamin E

Vitamin E, on the other hand, is a double-edged sword. A series of

groundbreaking

studies by Roland Stocker and his colleagues at The Heart Research Institute in

Sydney,

Australia demonstrates that vitamin E (alpha-tocopherol) systematically promotes

LDL

oxidation. Stocker calls this pro-oxidant action of vitamin E

" tocopherol-mediated

peroxidation, " or TMP. Through TMP, vitamin E amplifies mild oxidative stresses

so that

they do much more damage to LDL. There has been a spate of papers and much

lively

debate in recent years on pro-oxidant side effects of vitamin E, but as we shall

see below

vitamin E works better in cooperation with CoQ10 than it does in isolation.

Why didn't decades of vitamin E research detect this problem sooner? One reason

is that

scientists apply heavy oxidative stress to LDL in the laboratory to achieve

rapid results,

while TMP (tocopherol-mediated peroxidation) happens under the more realistic

conditions of chronic mild oxidative stress. Another reason is that, as

Stocker's group

discovered, the CoQ10 naturally present in the body protects against TMP. They

showed

that one molecule of CoQ10 can prevent two TMP chain reactions involving as many

as

40-80 free radicals. In pilot studies they tested LDL from the blood of human

subjects

given vitamin E and/or CoQ10 supplements. CoQ10 supplements reduced TMP, while

vitamin E supplements increased it. When given together, the CoQ10 supplement

significantly counteracted the TMP side-effect of the vitamin E supplement.

The work of Stocker and his colleagues agrees with other lines of recent

research

suggesting that CoQ10 cooperates with vitamin E in a complex partnership that we

are

only beginning to understand. Indeed these " co-antioxidants " are always found

together

in cell membranes and LDL. CoQ10 regenerates vitamin E, which would otherwise be

quickly exhausted fighting oxidative stress. Vitamin E breaks off the chain

reaction of lipid

peroxidation, while CoQ10 helps to prevent it from starting.

The many studies of vitamin E supplementation published over the years did not

take into

account the CoQ10 naturally present in the body, but we can now see that this

was a

crucial factor. In these studies of vitamin E, CoQ10 served as the " silent

partner, "

amplifying the effect of vitamin E, regenerating vitamin E as it was exhausted,

and

preventing TMP.

Natural (endogenous) antioxidants form a balanced complete system that, like the

partnership between vitamin E and CoQ10, we are only beginning to understand. As

we

gain a more subtle understanding of the way antioxidants work in the body, we

can use

this knowledge to support the body's antioxidant defense system more

intelligently. "

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

[Guest guest]

K,

If you would track down some of these CoQ10 trials mentioned in the link and

describe

your conclusions to the list, that would be great.

>

>

> > Vegetable was a typo, meant vegetable oil. My reasoning is that coQ10

> > is the primary antioxidant in LDL, not vit E, not carotenoids, not

> > anything else. However, it is possible that the CoQ10 recycles

> > vitamin E, so there might be a synergistic effect. I haven't seen a

> > human study on CoQ10 in this respect yet, but there is a study in Apo

> > E-/- mice, who develop atherosclerosis, and CoQ10 is clearly

> > beneficial and there might be a positive interaction with E.

> >

> > Chris

> >

>

> & ,

>

> Here's something I found on the relationship between E & CoQ10, FWIW:

>

> " Partnership with vitamin E

>

> Vitamin E, on the other hand, is a double-edged sword. A series of

groundbreaking

> studies by Roland Stocker and his colleagues at The Heart Research Institute

in Sydney,

> Australia demonstrates that vitamin E (alpha-tocopherol) systematically

promotes LDL

> oxidation. Stocker calls this pro-oxidant action of vitamin E

" tocopherol-mediated

> peroxidation, " or TMP. Through TMP, vitamin E amplifies mild oxidative

stresses so that

> they do much more damage to LDL. There has been a spate of papers and much

lively

> debate in recent years on pro-oxidant side effects of vitamin E, but as we

shall see

below

> vitamin E works better in cooperation with CoQ10 than it does in isolation.

>

> Why didn't decades of vitamin E research detect this problem sooner? One

reason is that

> scientists apply heavy oxidative stress to LDL in the laboratory to achieve

rapid results,

> while TMP (tocopherol-mediated peroxidation) happens under the more realistic

> conditions of chronic mild oxidative stress. Another reason is that, as

Stocker's group

> discovered, the CoQ10 naturally present in the body protects against TMP. They

showed

> that one molecule of CoQ10 can prevent two TMP chain reactions involving as

many as

> 40-80 free radicals. In pilot studies they tested LDL from the blood of human

subjects

> given vitamin E and/or CoQ10 supplements. CoQ10 supplements reduced TMP, while

> vitamin E supplements increased it. When given together, the CoQ10 supplement

> significantly counteracted the TMP side-effect of the vitamin E supplement.

>

> The work of Stocker and his colleagues agrees with other lines of recent

research

> suggesting that CoQ10 cooperates with vitamin E in a complex partnership that

we are

> only beginning to understand. Indeed these " co-antioxidants " are always found

together

> in cell membranes and LDL. CoQ10 regenerates vitamin E, which would otherwise

be

> quickly exhausted fighting oxidative stress. Vitamin E breaks off the chain

reaction of

lipid

> peroxidation, while CoQ10 helps to prevent it from starting.

>

> The many studies of vitamin E supplementation published over the years did not

take

into

> account the CoQ10 naturally present in the body, but we can now see that this

was a

> crucial factor. In these studies of vitamin E, CoQ10 served as the " silent

partner, "

> amplifying the effect of vitamin E, regenerating vitamin E as it was

exhausted, and

> preventing TMP.

>

> Natural (endogenous) antioxidants form a balanced complete system that, like

the

> partnership between vitamin E and CoQ10, we are only beginning to understand.

As we

> gain a more subtle understanding of the way antioxidants work in the body, we

can use

> this knowledge to support the body's antioxidant defense system more

intelligently. "

>

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

>

[Guest guest]

,

> You don't happen to remember the citation (or even journal and year) for the

> 8-fold risk

> study? That is scary!

I haven't read it yet, but it was included in this meta-analysis,

which has results given separately in tables:

http://www.ncbi.nlm.nih.gov/pubmed/15824290?dopt=Abstract

Interestingly, I think " Burr " here is the wife of Burr, the

second Burr in " Burr and Burr " who discovered the essential fatty

acids!

Chris

[Guest guest]

,

> So, do you recommend people consume vitamin A through cod liver oil or

> through a separate

> pill?

I would use high-vitamin cod liver oil and/or liver ideally.

Chris

[Guest guest]

A few observations on this JAMA meta-analysis:

===

1.

===

They state that in 79% of the trials, the antioxidant supplements were

provided free of charge by pharmaceutical companies. Although I think

this should always be performed, I think this makes it imperative for

the laboratory to independently test the contents of the antioxidants.

It is in the interest of the pharmaceutical companies to show that

antioxidant supplements do not work!

For example, Pfizer is financing review articles by sycophants who

argue that 1) oxidation is now realized to be as important or more

important to heart disease than lipid levels per se; 2) antioxidant

trials have shown that supplements do not work or are harmful; 3)

statins have antioxidant properties and have shown to be beneficial.

Therefore, the antioxidant theory of heart disease is now an

acceptable theory to Big Pharma because it shows that the appropriate

treatment is statins.

Umm... if you were testing CoQ10 against heart disease, would you take

it free from Pfizer after reading that? Without testing the CoQ10

level or testing it for additives, toxins, etc? I wouldn't.

I believe independent verification of supplement dose is now often

performed, but I don't know how universal or common it is.

===

2.

===

Of the two trials of vitamin A singly, one administered 200,000 IU on

a single day and followed it up for three months in elderly patients

to see if it reduced infections (it didn't.) The other was 3.8 years

at 25,000 IU a day.

I wouldn't advocate either of these doses without a very substantial

amount of D and K2. I'm not surprised that this had no effect or

possibly increased mortality.

===

3.

===

I don't have time to follow up all the references, but of the three

references they cite on antioxidants interfering with important

oxidant functions, one of them in the title sounded like it contained

experimental evidence rather than just speculation (granted I didn't

read the other two so they might also contain good info). That one

was on apoptosis, and the one in vivo study it cited in this respect

that I could see from scanning it used a diet totally devoid of

vitamins A and E to increase apoptosis and decrease tumor weight in

mice who were genetically engineered to express an SV40 virus promoter

that led to spontaneous tumor development.

So the study concluded that a diet with no vitamin A or E is

beneficial. Is it in non-genetically engineered people? Probably

not.

Chris

[Guest guest]

>

>

> K,

>

> If you would track down some of these CoQ10 trials mentioned in the link and

describe

> your conclusions to the list, that would be great.

>

>

I've definitely got that on my list. Hopefully I'll get to it tomorrow.

Chris

[Guest guest]

Very good points, Chris. I'm particularly wary of the agendas of Big Pharma in

these

studies as well. What's more, as you have pointed out, the relationship between

A, D & K2

is never considered and that may be a hugely significant factor. I also wonder

about the

quality, dosage and chemical form of the supplements chosen. For example, in

the study

you mentioned earlier they used beta-carotene instead of vitamin A, which we

would

expect to cause increases in mortality.

This is where the importance of looking at the diets of traditional peoples who

did not

suffer from high rates of heart disease, cancer and autoimmune disease comes in.

Surely

we've made great strides in our scientific understanding of the body, nutrition

and health;

but as this recent discussion confirms, we seem to know just enough to be

dangerous. I

have grown increasingly wary of reductionist methods of inquiry because they are

often

insufficient when it comes to studying a complex system like the human body.

K.

--- In , " Masterjohn "

<chrismasterjohn@...>

wrote:

>

> A few observations on this JAMA meta-analysis:

>

> ===

> 1.

> ===

>

> They state that in 79% of the trials, the antioxidant supplements were

> provided free of charge by pharmaceutical companies. Although I think

> this should always be performed, I think this makes it imperative for

> the laboratory to independently test the contents of the antioxidants.

> It is in the interest of the pharmaceutical companies to show that

> antioxidant supplements do not work!

>

> For example, Pfizer is financing review articles by sycophants who

> argue that 1) oxidation is now realized to be as important or more

> important to heart disease than lipid levels per se; 2) antioxidant

> trials have shown that supplements do not work or are harmful; 3)

> statins have antioxidant properties and have shown to be beneficial.

> Therefore, the antioxidant theory of heart disease is now an

> acceptable theory to Big Pharma because it shows that the appropriate

> treatment is statins.

>

> Umm... if you were testing CoQ10 against heart disease, would you take

> it free from Pfizer after reading that? Without testing the CoQ10

> level or testing it for additives, toxins, etc? I wouldn't.

>

> I believe independent verification of supplement dose is now often

> performed, but I don't know how universal or common it is.

>

> ===

> 2.

> ===

>

> Of the two trials of vitamin A singly, one administered 200,000 IU on

> a single day and followed it up for three months in elderly patients

> to see if it reduced infections (it didn't.) The other was 3.8 years

> at 25,000 IU a day.

>

> I wouldn't advocate either of these doses without a very substantial

> amount of D and K2. I'm not surprised that this had no effect or

> possibly increased mortality.

>

> ===

> 3.

> ===

>

> I don't have time to follow up all the references, but of the three

> references they cite on antioxidants interfering with important

> oxidant functions, one of them in the title sounded like it contained

> experimental evidence rather than just speculation (granted I didn't

> read the other two so they might also contain good info). That one

> was on apoptosis, and the one in vivo study it cited in this respect

> that I could see from scanning it used a diet totally devoid of

> vitamins A and E to increase apoptosis and decrease tumor weight in

> mice who were genetically engineered to express an SV40 virus promoter

> that led to spontaneous tumor development.

>

> So the study concluded that a diet with no vitamin A or E is

> beneficial. Is it in non-genetically engineered people? Probably

> not.

>

> Chris

>

[Guest guest]

> Aren't you leaving out the fact that this was exclusively in people

> who just had a heart attack recently, and when they broke the people

> up by risk of arrhythmia, they found that the benefit was ONLY in

> people who had left ventricular dysfunction or were prescribed

> beta-blockers?

>

> I have not looked at all the evidence but my preliminary findings

> suggest that n-3 fatty acids are beneficial for those at risk for

> cardiac arrhythmia but are either fairly ineffective or harmful for

> others. There was only one study cited in a meta-analysis I looked at

> that was primary prevention, and it found n-3 fatty acids increased

> the risk 8-fold. They noted that it was a poorer quality study

> compared to others, but it was the only one treating people who didn't

> already have heart disease.

>

> M

>

I confess I wasn't aware of the distinction you pointed out, so thanks for

setting me

straight. Just to clarify: are you saying the only patients that benefited are

those that had

left ventricular dysfunction, those who were taking beta-blockers and those at

risk for

cardiac arrhythmia?

What about people with atherosclerotic carotid arteries? I just found out that

this is what's

going on with my Dad. It seems he's more at risk for a stroke than a heart

attack. He's

going to go in and get a heart scan to see what the condition of his coronary

arteries is.

If the study indicating that n-3 fats increase the risk 8-fold is true, we have

yet another

major crisis on our hands. Nearly EVERYONE with heart disease is being told to

consume

n-3 fats in abundance, even by relatively " sane " authorities like Dr. in

the Track Your

Plaque program. At least he gets that cholesterol isn't the problem and statins

aren't the

answer. But fish oil is a huge part of his program, and he claims to have

success reducing

the Heart Scan scores. Whether that has translated into a reduction of

mortality or CVD

events, I don't know.

Chris

[Guest guest]

K,

> I confess I wasn't aware of the distinction you pointed out, so thanks for

> setting me

> straight. Just to clarify: are you saying the only patients that benefited

> are those that had

> left ventricular dysfunction, those who were taking beta-blockers and those

> at risk for

> cardiac arrhythmia?

The study was done in patients who had just had a heart attack. Then,

once they got their results, they stratified them according to left

ventricular dysfunction and not, and found the benefit appeared in the

former and not in the latter. Then, they stratified according to

beta-blockers and not, and found the benefit appeared only in the

former. I think they took both to be an indicator of arrhythmia risk,

although I think the ventricular dysfunction is more direct because,

if I remember right, beta-blockers are used for arrhythmia and other

issues.

> What about people with atherosclerotic carotid arteries? I just found out

> that this is what's

> going on with my Dad. It seems he's more at risk for a stroke than a heart

> attack. He's

> going to go in and get a heart scan to see what the condition of his

> coronary arteries is.

There is some limited evidence that fish is inversely related to the

risk of stroke. Total PUFA and carbohydrate, however, have the

opposite relationship. Animal fat and animal protein have inverse

relationships with stroke.

> If the study indicating that n-3 fats increase the risk 8-fold is true, we

> have yet another

> major crisis on our hands. Nearly EVERYONE with heart disease is being told

> to consume

> n-3 fats in abundance, even by relatively " sane " authorities like Dr.

> in the Track Your

> Plaque program. At least he gets that cholesterol isn't the problem and

> statins aren't the

> answer. But fish oil is a huge part of his program, and he claims to have

> success reducing

> the Heart Scan scores. Whether that has translated into a reduction of

> mortality or CVD

> events, I don't know.

The fish oil, statistically, is associated with a benefit in secondary

prevention trials, i.e. those with established heart disease. But

there's no evidence for prevention in the general population, from the

preliminary look I've done. It's possible I'll change my mind as I

read more so don't take this as the final word.

Chris