Fwd: Doctor Murray's Newsletter | Natural Facts For November 12, 2004

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Doctor Murray's Newsletter | Natural Facts For November 12, 2004

Fri, 12 Nov 2004 14:43:17 -0800

 

 

2:14:2004

Vitamin E, Heart Disease, and Mortality

 

Introduction

 

In 2003 during a keynote address to the dietary supplement industry titled

" Challenges, Solutions, & Inspirations " I spoke on how the results from clinical

studies will be used to adversely effect the public's appreciation for natural

products. The two primary examples that I gave were studies with echinacea

utilizing less than ideal preparations and studies on the effect of vitamin E in

cardiovascular disease. The recent proclamation by a set of researchers that

vitamin E may actually increase the risk of mortality and the resulting media

fervor reporting this story is not surprising to me at all. In fact, I predicted

it and based upon the research it is easy to understand how this conclusion

could be made.

 

Although many experts and organization will be focusing on the shortcoming in

the methodology in the recent meta-analysis, my feeling is that time is better

spent trying to understand the results instead of trying to discredit them. The

results simply reflect some inherent defects in the manner in which research is

conducted with antioxidant nutrients. Nonetheless, it is important to point out

that the interpretation of the data is based upon an analysis of 19 earlier

published vitamin E studies with a built-in bias toward the risk of harm rather

than potential benefit. Focusing on the impact on the all-cause mortality

outcome seems inappropriate given that none of the 19 studies analyzed were

designed with this as the primary endpoint; the studies chosen represented quite

a diversity of subjects, disease conditions, treatments and durations of

intervention; and the follow-up time was relatively short ranging from 1.4 years

to 8.2 years. It is also important to point out that while

these studies were not designed to evaluate all-cause mortality statistics as

the primary outcome, many of the studies used in the meta-analysis showed

positive results on the primary outcomes they were designed to measure such as

reduced progression of advanced age-related macular degeneration and cataracts;

reduced incidence of heart attacks, and slowed progression of atherosclerosis

and Alzheimer's Disease.

 

The Beta-carotene Analogy

 

The results from this analysis of vitamin E research are quite similar to those

of synthetic beta-carotene in cancer prevention. In case you missed this line of

research with beta-carotene, studies indicated that synthetic beta-carotene

supplementation contributed to earlier death in high-risk groups for cancer and

cardiovascular disease. These studies did not invalidate the hundreds of studies

showing the preventive effect of a diet rich in carotenes and nutritional

antioxidants against cancer and cardiovascular disease. These results seem to

indicate the need for a diet high in carotenes and, if carotene supplementation

is desired, people should not smoke, natural forms should be used, and the

beta-carotene needs to be protected against the formation of toxic derivatives

by taking extra vitamin C and E, and selenium.

 

It is important to realize that not all antioxidants are created equal. When it

comes to quenching free radicals, antioxidant compounds exert different (and

usually very narrow) range of activity. For example, beta-carotene is an

effective quencher of a free radical known as singlet oxygen, but is virtually

powerless against the dozens of other types of free radicals. As a result, it

has a very narrow range of benefit and is very susceptible to being damaged

itself and forming a free radical without additional antioxidant support. Most

antioxidants require some sort of " partner " antioxidant that allows it to work

more efficiently. And scientists have discovered that beta-carotene itself can

become damaged if it's used alone (that is, without its partner antioxidants

vitamin C, vitamin E, and selenium). For example, while studies showed that

synthetic beta-carotene supplements given alone actually increased the risk of

cancer in smokers, when beta-carotene was given along with vitamin

E and selenium it reduced cancer deaths by a significant 13 percent. Damaged

beta-carotene is extremely toxic to the liver, the lining of the arteries, and

the lungs. This fact alone may explain some of the disappointing results from

the recent beta-carotene studies.

 

Undoubtedly there will be similar discoveries about the importance of other

antioxidant nutrients in the support of vitamin E's antioxidant benefit.

 

The Importance of Synergy

 

While the scientific research is quite clear that diets high in antioxidants are

protective against many diseases, the data is not as solid with antioxidant

supplements. There are three main points to keep in mind when looking at

research with antioxidant supplements:

 

The antioxidant system of the body relies on a complex interplay of many

different dietary antioxidants.

Taking any single antioxidant nutrient is not enough. Total protection

requires a strategic, comprehensive dietary and supplement program.

Although dietary supplements are important, they cannot replace the

importance of consuming a diet rich in antioxidants.

 

A shortcoming of many of the intervention studies with antioxidant nutrients is

that researchers often focus on the effects of just one factor. In a way, this

is like judging an entire symphony by listening to a single trombone. Such

research has its value, but it's not complete and often raises more questions

than it answers.

 

Antioxidants and Heart Disease

 

The research is quite clear that dietary antioxidant nutrients like vitamin E,

lycopene, lutein, selenium, and vitamin C offer significant protection against

the development of cardiovascular disease. Fats and cholesterol are particularly

susceptible to free radical damage. When damaged, fats and cholesterol form

lipid peroxides and oxidized cholesterol which can then damage the artery walls

as well as accelerate the progression of atherosclerosis (hardening of the

arteries). Antioxidants block the formation of these damaging compounds.

 

While diets rich in antioxidant nutrients have consistently shown tremendous

protection against cardiovascular disease, clinical trials utilizing antioxidant

vitamins and minerals have produced inconsistent results.1,2 This failure may be

due to several factors, most importantly the fact that the human antioxidant

system represents a complex scenario of interacting components. It is unlikely

that any single antioxidant would be proven to be effective especially in the

absence of a supporting cast. Most antioxidants require some sort of " partner "

antioxidant that allows it to work more efficiently. The most salient example of

this point is the partnership between the two primary antioxidants in the human

body - vitamin C and vitamin E. Vitamin C is an " aqueous phase " antioxidant

while vitamin E is a " lipid phase " antioxidant. Although some studies have shown

that supplementation with these nutrients reduces atherosclerotic lesions more

protection is likely required to insure optimal

effect.3 In addition to vitamin C, vitamin E also requires selenium and

coenzyme Q10 to work efficiently (discussed in more detail below). Further

adding to the shortcoming of many of the studies on antioxidant nutrients is the

lack of consideration on the importance of phytochemicals and plant derived

antioxidants that in addition to exerting benefit on their own are well-known to

potentiate the activities of vitamin and mineral antioxidants.

 

The support of non-antioxidant vitamins and minerals may also be important in

assisting the effectiveness of antioxidants. Taking a multiple vitamin and

mineral supplement seems appropriate.

 

The Research on Vitamin E

 

Although clinical studies have shown inconsistent effects, it is clear that

vitamin E does play a role in the protection against the oxidation of LDL

cholesterol because of its ability to be easily incorporated into the LDL

molecule. Vitamin E may offer additional benefit in protecting against heart

disease and strokes by its ability to:

 

reduce LDL cholesterol peroxidation and increase plasma LDL breakdown

inhibit excessive platelet aggregation

increase HDL cholesterol levels

increase fibrinolytic activity

reduce C-reactive protein levels

improve endothelial cell function

improve insulin sensitivity

 

Two early large-scale studies with relatively low dosages of vitamin E

supplements demonstrated a significant reduction in the risk of dying of a heart

attack or a stroke. The Nurses Health Study of 87,245 nurses concluded that

those who took 100IU of vitamin E daily for more than 2 years had a 41% lower

risk of heart disease compared with non-users of vitamin E supplements.81 In the

Physicians Health Study of 39,910 male health care professionals found similar

results: a 37% lower risk of heart disease with the intake of more than 30 IU of

supplemental vitamin E daily.4 Subsequent studies have been equivocable.5

 

Large-scale studies examining the impact of vitamin E supplementation in

patients with existing heart disease have also shown somewhat conflicting

results.6 Some the disappointing results may have been the choice of synthetic

vitamin E (D,L-alpha tocopherol) versus the more active natural form (D-alpha

tocopherol). There is also the problem with interference by statin drugs of

vitamin E and coenzyme Q10 metabolism - thereby increasing the needs for both

compounds. In fact, one of the reasons why more recent studies with vitamin E

have not shown the same benefit as earlier studies may turn out to be that

higher dosages of vitamin E alone and in combination with CoQ10 are required to

compensate for the detrimental effects of the now extremely popular statin drugs

have on their metabolism.

Table 1. Examples of intervention trials with vitamin E for secondary

preventionStudy# SubjectsDosageDurationOutcomeHOPE (2000)9,541400 IU

(d-alpha)4.5 yNo EffectSPACE (2000)196800IU

(d-alpha)1.4 y-70%GISSI (1999)11,324300 IU

(synthetic)3.5 y-35% (vs. placebo)CHAOS (1996)9,541400-800 IU

(d-alpha)1.4 y-47%

HOPE = Heart Outcomes Protestion Evaluation Trial; CHAOS = Cambridge Heart

Antioxidant Study; GISSI = Gruppo Italiano per lo Studio della Sopravvivenza

nell'Infarto miocardico

 

Vitamin E and CoQ10 work synergistically and each is required for the

regeneration of the other. For example, CoQ10 is present in the blood in both

oxidized (inactive) and reduced (active) form. During times of increased

oxidative stress or low vitamin E levels, more CoQ10 will be converted to its

oxidized (inactive form). Thus, by providing higher levels of vitamin E and the

biological activity and function of CoQ10 is enhanced and vice versa. Several

studies in humans and animals have shown that the combination of vitamin E and

CoQ10 work better than either alone. For example, in a study in baboons, while

supplementation with vitamin E alone reduced C-reactive protein (CRP) levels,

co-supplementation with CoQ, however, significantly enhanced this effect of

vitamin E. Similar results have been seen in other animal studies on other

aspects associated with atherosclerosis including LDL oxidation and lipid

peroxide content within the aorta.7-9 It appears that taking 50 mg of CoQ10 for

every 400 IU of vitamin E offers a rational approach to supporting the

antioxidant activities of both nutrients.

 

In addition to CoQ10, vitamin E also requires adequate selenium status for

optimal antioxidant effects. Selenium functions primarily as a component of the

antioxidant enzyme glutathione peroxidase. This enzyme works closely with

vitamin E to prevent free radical damage to cell membranes. Studies looking only

at vitamin E's ability to reduce cancer and heart disease are often faulty

because they failed to factor in the critical partnership between selenium and

vitamin E not to mention the interrelationship between vitamin E and coenzyme

Q10. Several studies have clearly demonstrated that low selenium status is

significantly associated with CAD.10,11 Failure to cosupplement with selenium as

well as vitamin C and CoQ10, may be a major reason for the inconsistent results

in intervention trials with vitamin E supplementation alone. A dosage of 100 to

200 mcg of selenium per day is all that is usually required.

 

The " Take Home " Message

 

In regards to supplementation with vitamin E at higher dosages (e.g., >400 IU

daily), I will continue to make this recommendation to people with heart

disease, diabetes, etc., and will do so in the same manner that I have

consistently done over the past 20 years. I have repeatedly written and stated

that the use of any single antioxidant nutrient at higher dosages must be made

within the context of a truly comprehensive approach that focuses on a diet rich

in antioxidant nutrients (i.e., vegetables, fruits, nuts, seeds, and legumes)

and a strong foundation of nutritional supplementation. The three key dietary

supplements that I recommend to provide a strong foundation for a proper

nutritional supplement plan are:

 

A high-potency multiple vitamin and mineral formula (MultiStart).

A " greens " drink product (Enriching Greens).

A pharmaceutical grade fish oil supplement (RxOmega-3 Factors).

 

The dietary recommendations and foundational supplements work synergistically

and in harmony with each other because of the key roles they each play in

promoting vibrant health.

 

 

 

Key References:

 

Clarke R, Armitage J. Antioxidant vitamins and risk of cardiovascular

disease. Review of large-scale randomised trials. Cardiovasc Drugs Ther

2002;16:411-5

Vivekananthan DP, Penn MS, Sapp SK, et al. Use of antioxidant vitamins for

the prevention of cardiovascular disease: meta-analysis of randomised trials.

Lancet 2003;361:2017-23

Salonen RM, Nyyssonen K, Kaikkonen J, et al. Six-year effect of combined

vitamin C and E supplementation on atherosclerotic progression: the Antioxidant

Supplementation in Atherosclerosis Prevention (ASAP) Study. Circulation

2003;107:947-53

Stampfer MJ, Hennekens CH, Manson JE. Vitamin E consumption and the risk of

coronary disease in women. N Engl J Med 1993;328:1444-9

Rimm EB, Stampfer MJ, Ascherio A. Vitamin E consumption and the risk of

coronary heart disease in men. New Engl J Med 1993;328:1450-6

Eidelman RS, Hollar D, Hebert PR, Lamas GA, Hennekens CH. Randomized trials

of vitamin E in the treatment and prevention of cardiovascular disease. Arch

Intern Med. 2004;164(14):1552-6.

Kaikkonen J, Nyyssonen K, Tomasi A, et al. Antioxidative efficacy of parallel

and combined supplementation with coenzyme Q10 and d-alpha-tocopherol in mildly

hypercholesterolemic subjects: a randomized placebo-controlled clinical study.

Free Radic Res 2000;33:329-40

Wang XL, Rainwater DL, Mahaney MC, et al. Cosupplementation with vitamin E

and coenzyme Q10 reduces circulating markers of inflammation in baboons. Am J

Clin Nutr 2004;80:649-55

Thomas SR, Leichtweis SB, Pettersson K, et al. Dietary cosupplementation with

vitamin E and coenzyme Q(10) inhibits atherosclerosis in apolipoprotein E gene

knockout mice. Arterioscler Thromb Vasc Biol 2001;21:585-93

Yegin A, Yegin H, Aliciguzel Y, et al. Erythrocyte selenium-glutathione

peroxidase activity is lower in patients with coronary atherosclerosis. Jpn

Heart J 1997;38:793-8

Bor MV, Cevik C, Uslu I, et al. Selenium levels and glutathione peroxidase

activities in patients with acute myocardial infarction. Acta Cardiol

1999;54:271-6

 

 

 

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