Am J Clin Nutr mostly papers

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Hi All,

Regarding the all-PDFs-available American Journal of Clinical Nutrition

(plus a little more):

It seemed to me that the first paper

Effects of vitamin C and vitamin E on in vivo lipid peroxidation: results of

a randomized controlled trial

Han-Yao Huang, Lawrence J Appel, D Croft, Edgar R , III,

Trevor A Mori, and Ian B Puddey

Am J Clin Nutr 2002;76 549-555

was interesting in that it said either vitamin C or E will reduce oxidized

fats in the blood and using both is a waste in this regard. They seem to

use alpha form of vitamin E, which struck my attention. Using both seemed

to give a not significant, but lower effect, actually. The fact that the

oxygen-radical absorbance capacity assay gave different results suggests it

is not so reliable maybe.

“…..a placebo-controlled, 2 x 2 factorial trial of vitamin C (500 mg

ascorbate/d) and vitamin

E (400 IU RRR--tocopheryl acetate/d) supplementation in 184 nonsmokers. The

mean duration of supplementation was 2 mo. The outcome measures were changes

from baseline in urinary 8-iso-prostaglandin F2, urinary malondialdehyde +

4-hydroxyalkenals, and serum oxygen-radical absorbance capacity.

Results: The within-group mean changes (and 95% CIs) in urinary

8-iso-prostaglandin F2 (pg/mg creatinine) were 9.0 (–125.1, 143.1), –150.0

(–275.4, –24.6), –141.3 (–230.5, –52.1), and –112.5 (–234.8, 9.8) in the

placebo, vitamin C alone, vitamin E alone, and vitamins C + E groups,

respectively. No synergistic effect of these 2 vitamins on urinary

8-iso-prostaglandin F2 was observed (P = 0.12). Neither vitamin had an

effect on urinary malondialdehyde + 4-hydroxyalkenals. Vitamin C, but not

vitamin E, increased serum oxygen-radical absorbance capacity (P = 0.01).

Conclusions: Supplementation with vitamin C or vitamin E alone reduced lipid

peroxidation to a similar extent. Supplementation with a combination of

vitamins C and E conferred no benefit beyond that of either vitamin alone.”

The next paper seemed to paint whole-grains much better than the CR list on

average does. It seems that the ingredients that help reduce the bad

effects of glucose and insulin are fiber, magnesium, low glycemic index and

weight reducing effect the whole grains have.

Am J Clin Nutr 2002;76, 535-540

Whole-grain intake and the risk of type 2 diabetes: a prospective study in

men1,2,3

…. and Walter C Willett

“Design: Men from the Health Professionals Follow-up Study without a history

of diabetes or cardiovascular disease in 1986 (n = 42898) were followed for

12 y. Intakes of whole and refined grains, measured every 4 y by use of

food-frequency questionnaires, were used to predict subsequent type 2

diabetes risk through multivariate analysis.

Results: We ascertained 1197 cases of incident type 2 diabetes. After

adjustment for age; physical activity; cigarette smoking; alcohol

consumption; family history of diabetes; and fruit, vegetable, and energy

intakes, the relative risk of type 2 diabetes was 0.58 (95% CI: 0.47, 0.70;

P for trend < 0.0001) comparing the highest with the lowest quintile of

whole-grain intake. The association was moderately attenuated when

additionally adjusted for body mass index (relative risk: 0.70; 95% CI:

0.57, 0.85; P for trend = 0.0006). Intake of refined grains was not

significantly associated with risk of type 2 diabetes. After further

adjustment for magnesium intake, cereal fiber intake, and glycemic load, the

association between whole grains and type 2 diabetes was attenuated and the

trend no longer significant.

Conclusions: In men, a diet high in whole grains is associated with a

reduced risk of type 2 diabetes in men that may be mediated by cereal fiber.

Efforts should be made to replace refined-grain with whole-grain foods.”

The next paper seemed to say that eating when not hungry goes to pot when

the snack is rich in carbohydrate but not protein.

Snacks consumed in a nonhungry state have poor satiating efficiency:

influence of snack composition on substrate utilization and hunger

Corinne Marmonier, Didier Chapelot, Marc Fantino, and Jeanine

Louis-Sylvestre

Am J Clin Nutr 2002;76 518-528

This next paper is from a different journal for which the PDF is also

available. It is mainly on the failure of bone mineral density to perform

as well in older people. In it, though, it seemed to say that weight and

height are not important for figuring out the relation between the

reliability of the method. There has been a lot of pooh-poohing of the

ability of the bone mineral density assays to predict risk correctly in the

“underweight”. This may address this?

Journal of Clinical Epidemiology, 55, July 2002, 642-646

“………bone mineral density (BMD) …….. Discriminant analysis derived

multivariate equations that assessed fracture risk. Age was not in the best

models at the spine and forearm sites. Weight and height contributed to the

relationship for the forearm sites only. At the proximal femur, the BMD

level that separates fracture cases from nonfracture cases, increases with

age. These separation levels of BMD were higher than the WHO's level of

osteoporosis (T-score < -2.5 SD) at ages older than 62 years. This

increasing BMD threshold with age suggests that other age-related risk

factors assume increasing importance among the elderly”

The next paper says corn (maize) is a poor diet for getting zinc normally, I

think. Just counting zinc from vegetarian sources may grossly overestimate

your actual intake. 17% is low.

Zinc absorption from a low-phytic acid maize

L , Hambidge, Victor Raboy, A Dorsch, Lei

Sian, L Westcott, and F Krebs

Am J Clin Nutr 2002;76 556-559

“The corresponding fractional absorptions of zinc were 0.30 ± 0.13 and 0.17

± 0.11, respectively (P < 0.005). Conclusion: Substitution of a low–phytic

acid grain in a maize-based diet is associated with a substantial increase

in zinc absorption”.

This next paper looked at a lot of different diseases and the flavonoids

that seem to prevent them. There were many studied, but they were followed

only one year, which seemed to be too short a time. Diseases examined were

cerebrovascular disease, lung cancer, prostate cancer, asthma and type 2

diabetes. It seems to give recipes for preventing the diseases. Since the

particular compounds were unique, it sounds pretty specific, so if you have

a particular concern, selecting the best may be something to think about

doing. Let me see, I want to take kaempferol, naringenin, and hesperetin to

prevent stroke, which my father had plenty of and my uncle died from at 48

years. I have never heard of them, to my immediate recollection. Okay:

hesperetin, a citrus flavonoid.

The title is:

Flavonoid intake and risk of chronic diseases

Knekt, Jorma Kumpulainen, Ritva Jarvinen, Harri Rissanen, Markku

Heliovaara, Antti Reunanen, Timo Hakulinen, and Arpo Aromaa

Am J Clin Nutr 2002;76 560-568

A good PDF-available review is:

Ross JA, Kasum CM.

DIETARY FLAVONOIDS: Bioavailability, Metabolic Effects, and Safety.

Annu Rev Nutr. 2002;22:19-34.

PMID: 12055336 [PubMed - in process]

The next paper simply correlated questionnaire data with plasma

concentrations of vitamin E, vitamin A, and carotenoids. However, it was

pretty good because none of the women took supplements. The fact that

vitamin E but not other vitamins was associated with heart plaque was

confidence building. The results were:

“Results: The occurrence of atherosclerotic plaques at the carotid

bifurcation was inversely associated with tertiles of vitamin E intake; the

test for a linear trend across tertiles was significant (P < 0.05).

Similarly, the ratio of plasma vitamin E to plasma cholesterol was inversely

related to the presence of plaques at the carotid bifurcation; the test for

a linear trend across tertiles was significant (P < 0.02). No association

was found between the intake of other antioxidant vitamins (vitamins A and C

and carotenoids) or their plasma concentrations and the presence of carotid

plaques.”

The article is:

Dietary and circulating antioxidant vitamins in relation to carotid plaques

in middle-aged women

Arcangelo Iannuzzi, Egidio Celentano, Salvatore Panico, Rocco Galasso,

Giuseppe Covetti, Lucia Sacchetti, Federica Zarrilli, De Michele, and

Paolo Rubba

Am J Clin Nutr 2002;76 582-587

http://www.ajcn.org/cgi/content/abstract/76/3/582

The next paper seems to address the effectiveness of satietrol in different

diets. It concluded:

“In women, the feeling of satiety caused by cholecystokinin release is

enhanced by increasing either the fiber or fat content of a low-fat,

low-fiber meal.”

The paper is:

Plasma cholecystokinin is associated with subjective measures of satiety in

women

Britt Burton-Freeman, A , and Barbara O Schneeman

Am J Clin Nutr 2002;76 659-667.

The next paper is attached to this email and is a letter, actually. It says

it is copper in chocolate that gives its great effects in LDL oxidation

reduction. Its title is:

Extra dietary copper inhibits LDL oxidation

M Klevay

Am J Clin Nutr 2002;76 687-688.

In their reply to this letter, the authors say it could very well be so, but

the diets had basically the RDAs of copper. RDAs are always question marks,

though. The reply is:

Reply to LM Klevay

Ying Wan, Fishell, Dee Maddox, and Penny M Kris-Etherton

Am J Clin Nutr 2002;76 688

Pass me the chocolate guar gum pudding, would you please?

And finally, from this web site:

http://www3.who.int/whosis/hale/hale.cfm?path=whosis,burden_statistics,hale &

language=english

I transcribed from their table with all the countries:

Healthy life expectancy at birth

Country All Men Women

Canada 70.0 68.3 71.7

USA 67.2 65.7 68.8

Long healthy CRON life expectancy wishes.

Cheers, Al.

Alan Pater, Ph.D.; Faculty of Medicine; Memorial University; St. 's, NF

A1B 3V6 Canada; Tel. No.: (709) 777-6488; Fax No.: (709) 777-7010; email:

apater@...

[AJCN] [Nutrition Week 2003]

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American Journal of Clinical

Nutrition, Vol. 76, No. 3,

687-688, September 2002

© 2002 American Society for

Clinical Nutrition

--------------------

Letter to the Editor

Extra dietary copper inhibits

LDL oxidation

M Klevay

US Department of Agriculture, Agricultural Research Service Grand Forks

Human Nutrition Research Center PO Box 9034 Grand Forks, ND 58202-9034

E-mail: lklevay@...

Wan et al (1) fed cocoa powder and dark chocolate to subjects for 4 wk and

found that LDL oxidation was inhibited in vitro. This favorable effect on

cardiovascular risk status was attributed to flavonoids, a group of

polyphenolic compounds with antioxidant characteristics. An increase in

dietary copper during this experiment may have contributed to their

results.

The Western diet often is low in copper: approximately one-third of 849

diets that were analyzed provided 1 mg/d (2). The interquartile range was

0.91–1.86 mg/d. Milk chocolate and cocoa powder are in the upper quartile

of 235 foods evaluated by Lurie et al (3), ranking 186 and 232,

respectively, in copper concentration. Calculations using Lurie et al’s

values for chocolate and cocoa powder of 2.86 and 50.0 µg/g, respectively,

show that these supplements would have added nearly 1.15 mg Cu to the basal

diet each day. Dark chocolate contains more copper than does light

chocolate and would have increased this estimated amount even more. It

seems likely that the total daily intake of copper might have been 3 times

the daily estimated average requirement (0.7 mg) or twice the recommended

dietary allowance (0.9 mg) for adults (4).

Although copper salts (at 10 µmol/L) and LDL are highly reactive in vitro,

this phenomenon is probably irrelevant to human physiology because copper

ions are virtually nonexistent (1 amol/L) in vivo (5–7). Indeed, after

providing copper supplementation to middle-aged subjects, Rock et al (8)

found that the subjects’ erythrocytes were more resistant to oxidation in

vitro. Although this improvement occurred without an increase in the

activity of superoxide dismutase (EC 1.15.1.1), an enzyme that provides

defense against oxidative damage, the results may indicate that the

subjects ordinarily ate too little copper and had other means of defense.

Perhaps the usual copper intakes of the subjects studied by Wan et al were

too low also. Their basal diet probably was low in copper because it

excluded beans and soybeans, 2 foods in the top quartile (see above).

Control of the diets for copper intake as well as for intakes of caffeine,

cholesterol, fat, and fiber would have been informative because the

increased copper intake from chocolate seems smaller than some beneficial

amounts given by Rock et al (8). Perhaps chocolate enhances the

absorbability of copper.

Copper is an antioxidant nutrient for cardiovascular health (7) and has no

prooxidant activity at a considerably higher intake (8) than that given by

Wan et al. Diets low in copper are suggested as an explanation for much of

the epidemiology and pathophysiology of ischemic heart disease (9).

Chocolate is a pleasant dietary supplement.

REFERENCES

1. Wan Y, Vinson JA, Etherton TD, Proch J, Lazarus SA, Kris-Etherton PM.

Effects of cocoa powder and dark chocolate on LDL oxidative

susceptibility and prostaglandin concentrations in humans. Am J Clin

Nutr 2001;74:596–602.[Abstract/Full Text]

2. Klevay LM. Lack of a recommended dietary allowance for copper may be

hazardous to your health. J Am Coll Nutr 1998;17:322–6.[Abstract/Full

Text]

3. Lurie DG, Holden JM, Schubert A, Wolf WR, -Ihli NJ. The copper

content of foods based on a critical evaluation of published

analytical data. J Food Comp Anal 1989;2:298–316.

4. Food and Nutrition Board, Institute of Medicine. Dietary reference

intakes for vitamin A, vitamin K, arsenic, boron, chromium, copper,

iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and

zinc. Washington, DC: National Academy Press, 2001:7.1–27.

5. May PM, Linder PW, DR. Ambivalent effect of protein binding

on computed distributions of metal ions complexed by ligands in blood

plasma. Experientia 1976;32:1492–4.[Medline]

6. May PM, Linder PW, DR. Computer simulation of metal-ion

equilibria in biofluids: models for the low-molecular-weight complex

distribution of calcium(II), magnesium(II), manganese(II), iron(III),

copper(II), zinc(II), and lead(II) ions in blood plasma. J Chem Soc

Dalton Trans 1977;588–95.

7. KG, Klevay LM. Copper: an antioxidant nutrient for

cardiovascular health. Curr Opin Lipidol 1994;5:22–8.

8. Rock E, Mazur A, O’Connor JM, Bonham MP, Rayssiguier Y, Strain JJ. The

effect of copper supplementation on red blood cell oxidizability and

plasma antioxidants in middle-aged healthy volunteers. Free Radic Biol

Med 2000;28:324–9.[Medline]

9. Klevay LM. Trace element and mineral nutrition in disease: ischemic

heart disease. In: Bogden JD, Klevay LM, eds. Clinical nutrition of

the essential trace elements and minerals: the guide for health

professionals. Totowa, NJ: Humana Press Inc, 2000:251–71.

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