New not Medlined Am J Clin Nutr papers available as PDFs

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Hi All, New not Medlined Am J Clin Nutr papers available as PDFs at email:

apater@... . They same to be on such diverse topics that to begin is not

to end it would seem to me. I put in abstracts and titles and two letters.

Cheers, Al.

Genetic variation and the lipid response to dietary intervention: a

systematic review

Lindsey F Masson, Geraldine McNeill, and Alison Avenell

Am J Clin Nutr 2003;77 1098-1111

There is wide interindividual variation in the lipid and lipoprotein responses

to dietary change, and the existence of consistent

hypo- and hyperresponders supports the hypothesis that responsiveness is related

to genetic variation. Many studies have

investigated the possibility that the heterogeneity in responsiveness to changes

in dietary fat, cholesterol, and fiber intake is

explained by variation in genes whose products affect lipoprotein metabolism,

eg, apolipoproteins, enzymes, and receptors. A

systematic review of the literature was carried out to investigate the effect of

genetic variation on the lipid response to dietary

intervention. A search strategy for the MEDLINE database retrieved 2540 articles

from 1966 to February 2002. This strategy

was adapted and performed on the EMBASE database, which retrieved 2473 articles

from 1980 to week 9, 2002. Reference

lists from relevant journal articles were also checked. This is the first

systematic review of the literature, and it summarizes

results available from 74 relevant articles. There is evidence to suggest that

variation in the genes for apolipoprotein (apo) A-I,

apo A-IV, apo B, and apo E contributes to the heterogeneity in the lipid

response to dietary intervention. However, the effects

of genetic variation are not consistently seen and are sometimes conflicting.

Future studies need to have much larger sample

sizes based on power calculations and carefully controlled dietary interventions

and should investigate the effects of

polymorphisms in multiple genes instead of the effects of polymorphisms in

single genes.

Key Words: Polymorphism • genotype • diet • lipids • lipoproteins •

cardiovascular disease

Postprandial effects of dietary trans fatty acids on apolipoprotein(a) and

cholesteryl ester transfer

Lissa M Gatto, R Sullivan, and Samir Samman

Am J Clin Nutr 2003;77 1119-1124

Background: The consumption of trans fatty acids adversely affects fasting

plasma lipoprotein concentrations.

Objective: This study aimed to investigate whether postprandial lipoprotein

metabolism is affected by the consumption of trans

fatty acids.

Design: In a randomized crossover study, 19 healthy men consumed fatty meals

that were identical except that 10% of energy

was provided as trans 18:1 acids in the trans meal and as oleic acid in the cis

meal.

Results: The meals induced similar responses in plasma lipids. Cholesteryl ester

transfer (CET) was activated after

consumption of both meals (P < 0.0001); however, it was 28% higher after the

trans meal than after the cis meal (280 ± 129

compared with 219 ± 116 nmol cholesteryl ester/mL plasma • 6 h; time x diet

interaction: P < 0.0001). Plasma

apolipoprotein(a) [apo(a)] concentrations remained constant; however,

triacylglycerol-rich lipoproteins formed 4 h after

ingestion of the trans meal contained a higher concentration of apo(a) than did

those formed after ingestion of the cis meal

(48.9 ± 6.6 compared with 39.6 ± 5.4 U/L; P < 0.02). The change in CET and in

the proportion of plasma apo(a) in the

triacylglycerol-rich lipoprotein fractions correlated with indexes of alimentary

lipemia.

Conclusions: Consumption of meals high in trans fatty acids results in higher

CET and postprandial lipoprotein concentrations

enriched in apo(a) than does consumption of meals free of trans fatty acids.

This study highlights the importance of

double-bond configuration in determining postprandial lipoprotein composition.

Key Words: Postprandial lipemia • trans fatty acids • apolipoprotein(a) •

cholesteryl ester transfer • men

Effect of individual dietary fatty acids on postprandial activation of

blood coagulation factor VII and fibrinolysis in healthy young men

Tine Tholstrup, J , Anette Bysted, and Brittmarie

Sandstrom

Am J Clin Nutr 2003;77 1125-1132

Background: Hypertriglyceridemia may represent a procoagulant state involving

disturbances to the hemostatic system.

Plasminogen activator inhibitor type 1 (PAI-1) is increased in the presence of

hypertriglyceridemia. Free fatty acids (FFAs) in

plasma may promote factor VII (FVII) activation.

Objective: We tested the hypothesis that FVII activation would be less after

consumption of saturated fatty acids than after

other fatty acids.

Design: The effects of 6 matching dietary test fats, rich in stearic (S),

palmitic (P), palmitic + myristic (M), oleic (O), trans

18:1 (T), and linoleic (L) acid, respectively, on the postprandial lipid and

hemostatic profile (after 2, 4, 6, and 8 h) were

investigated in 16 young men. High-fat meals (1 g fat/kg body wt; 43% from the

test fatty acid) were served in the morning on 6

separate days.

Results: All fats increased FVII activation. The S fat resulted in a lower

increase in activated FVII (FVIIa) than did the T fat

and in a lower FVII coagulant activity (FVII:c) than did the O fat (P < 0.02,

diet x time interaction). When the data were

pooled, the saturated (S, P, and M) test fats resulted in a smaller postprandial

increase in FVIIa (P = 0.036, diet effect), a

smaller increase in FVII:c (P < 0.001, diet x time interaction), a greater rise

in tissue plasminogen activator concentrations (P =

0.028, diet effect), and a tendency to a greater postprandial decline in PAI-1

(P = 0.06, diet effect) compared with the

unsaturated test fats (O, T, and L). The increase in FVIIa was not significantly

associated with the level of lipemia, plasma

FFAs, or plasma lipoprotein lipase activity.

Conclusion: Our results indicate a lesser increase in FVIIa after the

consumption of saturated fats, especially the S fat, than

after unsaturated test fats.

Key Words: Factor VII • plasminogen activator inhibitor type 1 • PAI-1 • tissue

plasminogen activator • stearic acid •

saturated fatty acids • unsaturated fatty acids • postprandial lipemia • men

Diacylglycerols affect substrate oxidation and appetite in humans

Marleen MJW Kamphuis, J Mela, and Margriet S

Westerterp-Plantenga

Am J Clin Nutr 2003;77 1133-1139

Background: Meals rich in diacylglycerols (DGs) instead of triacylglycerols

(TGs) show beneficial effects on lipid metabolism

and energy balance. These effects are probably attributable to differences in DG

and TG metabolism, especially postprandial fat

oxidation.

Objective: We assessed the effects of partial replacement of TGs with DGs on

substrate oxidation, energy expenditure (EE),

relevant blood variables, and appetite.

Design: Twelve healthy, dietarily unrestrained women participated in a

single-blind, placebo-controlled, randomized trial with

crossover design. For 3 d before and throughout a 36-h stay in a respiration

chamber, subjects were fed energy-maintenance

amounts of a diet consisting of 55% of energy from carbohydrate, 15% from

protein, and 30% from fat. In the respiration

chamber, 40% of the fat was consumed as DG-rich (80% DGs) oil or as TG-based

control oil with a similar fatty acid profile.

Results: Fat oxidation was significantly higher with DG treatment than with TG

treatment. Appetite profiles during day 1 (24 h)

did not differ significantly between the DG and TG treatments; however, feelings

of hunger, appetite, estimated prospective

food intake, and desire to eat were all significantly lower on day 2 (12 h) with

DG treatment. Mean plasma ß-hydroxybutyrate

tended to be higher with DG treatment, and the difference between the 2

treatments was significant at 1130 on day 2. Plasma

lipid concentrations and resting and 24-h EE did not differ significantly

between the 2 treatments.

Conclusion: Consumption of DGs in place of TGs does not alter EE but produces

metabolic effects, particularly increases in

fat oxidation, which may be associated with improved appetite control and energy

balance.

Key Words: Substrate oxidation • thermogenesis • energy expenditure • appetite •

diacylglycerols • respiration chamber •

women

Metabolism of stearidonic acid in human subjects: comparison with the

metabolism of other n-3 fatty acids

J , Virginia M Ursin, and G Cleland

Am J Clin Nutr 2003;77 1140-1145

Metabolism of stearidonic acid in human subjects: comparison with the

metabolism of other n-3 fatty acids

J , Virginia M Ursin, and G Cleland

Am J Clin Nutr 2003;77 1140-1145

Effects of dietary fatty acids and carbohydrates on the ratio of serum

total to HDL cholesterol and on serum lipids and apolipoproteins: a

meta-analysis of 60 controlled trials

P Mensink, L Zock, Arnold DM Kester, and Martijn B Katan

Am J Clin Nutr 2003;77 1146-1155

Background: The effects of dietary fats on the risk of coronary artery disease

(CAD) have traditionally been estimated from

their effects on LDL cholesterol. Fats, however, also affect HDL cholesterol,

and the ratio of total to HDL cholesterol is a more

specific marker of CAD than is LDL cholesterol.

Objective: The objective was to evaluate the effects of individual fatty acids

on the ratis of total to HDL cholesterol and on

serum lipoproteins.

Design: We performed a meta-analysis of 60 selected trials and calculated the

effects of the amount and type of fat on

total:HDL cholesterol and on other lipids.

Results: The ratio did not change if carbohydrates replaced saturated fatty

acids, but it decreased if cis unsaturated fatty acids

replaced saturated fatty acids. The effect on total:HDL cholesterol of replacing

trans fatty acids with a mix of carbohydrates

and cis unsaturated fatty acids was almost twice as large as that of replacing

saturated fatty acids. Lauric acid greatly increased

total cholesterol, but much of its effect was on HDL cholesterol. Consequently,

oils rich in lauric acid decreased the ratio of

total to HDL cholesterol. Myristic and palmitic acids had little effect on the

ratio, and stearic acid reduced the ratio slightly.

Replacing fats with carbohydrates increased fasting triacylglycerol

concentrations.

Conclusions: The effects of dietary fats on total:HDL cholesterol may differ

markedly from their effects on LDL. The effects of

fats on these risk markers should not in themselves be considered to reflect

changes in risk but should be confirmed by

prospective observational studies or clinical trials. By that standard, risk is

reduced most effectively when trans fatty acids and

saturated fatty acids are replaced with cis unsaturated fatty acids. The effects

of carbohydrates and of lauric acid–rich fats on

CAD risk remain uncertain.

Key Words: Diet • fatty acids • carbohydrates • serum lipoproteins • coronary

artery disease risk

Patterns of food consumption and risk factors for cardiovascular disease in

the general Dutch population

Rob M van Dam, Grievink, Marga C Ocke, and Edith JM Feskens

Am J Clin Nutr 2003;77 1156-1163

Background: The effects of dietary fats on the risk of coronary artery disease

(CAD) have traditionally been estimated from

their effects on LDL cholesterol. Fats, however, also affect HDL cholesterol,

and the ratio of total to HDL cholesterol is a more

specific marker of CAD than is LDL cholesterol.

Objective: The objective was to evaluate the effects of individual fatty acids

on the ratis of total to HDL cholesterol and on

serum lipoproteins.

Design: We performed a meta-analysis of 60 selected trials and calculated the

effects of the amount and type of fat on

total:HDL cholesterol and on other lipids.

Results: The ratio did not change if carbohydrates replaced saturated fatty

acids, but it decreased if cis unsaturated fatty acids

replaced saturated fatty acids. The effect on total:HDL cholesterol of replacing

trans fatty acids with a mix of carbohydrates

and cis unsaturated fatty acids was almost twice as large as that of replacing

saturated fatty acids. Lauric acid greatly increased

total cholesterol, but much of its effect was on HDL cholesterol. Consequently,

oils rich in lauric acid decreased the ratio of

total to HDL cholesterol. Myristic and palmitic acids had little effect on the

ratio, and stearic acid reduced the ratio slightly.

Replacing fats with carbohydrates increased fasting triacylglycerol

concentrations.

Conclusions: The effects of dietary fats on total:HDL cholesterol may differ

markedly from their effects on LDL. The effects of

fats on these risk markers should not in themselves be considered to reflect

changes in risk but should be confirmed by

prospective observational studies or clinical trials. By that standard, risk is

reduced most effectively when trans fatty acids and

saturated fatty acids are replaced with cis unsaturated fatty acids. The effects

of carbohydrates and of lauric acid–rich fats on

CAD risk remain uncertain.

Key Words: Diet • fatty acids • carbohydrates • serum lipoproteins • coronary

artery disease risk

Folic acid and reduction of plasma homocysteine concentrations in older

adults: a dose-response study

Floor VA van Oort, Alida Melse-Boonstra, Ingeborg A Brouwer,

e, Clive E West, Martijn B Katan, and Petra Verhoef

Am J Clin Nutr 2003;77 1318-1323

Background: Elevated homocysteine concentrations, a likely risk factor for

cardiovascular disease, can be lowered effectively

with folic acid. The minimum dose of folic acid required for maximal reduction

of homocysteine concentrations is not yet known

reliably.

Objective: We aimed to determine the lowest folic acid dose that decreases

plasma homocysteine concentrations adequately in

healthy older adults.

Design: A dose-response trial with a randomized, double-blind, parallel-group,

placebo-controlled design was carried out

among 316 Dutch men and women aged 50–75 y. Subjects received daily for 12 wk

either a placebo or 1 of the 6 following

folic acid doses: 50, 100, 200, 400, 600, or 800 µg. The relative changes in

plasma homocysteine concentration in response to

increasing doses of folic acid were used to calculate the dose-response curve.

An adequate dose of folic acid was defined as

the dose that induced 90% of the maximal reduction in homocysteine

concentration.

Results: The relative decrease in plasma homocysteine concentration was

associated exponentially with increasing doses of

folic acid. From the dose-response curve, the adequate daily dose of folic acid

was estimated to be 392 µg, which decreased

plasma homocysteine concentrations 22%.

Conclusion: In older adults, daily supplementation with folic acid effectively

lowers plasma homocysteine concentrations, and a

daily dose of 400 µg [RDA is ~ 250] is the minimum dose required for adequate

homocysteine reduction.

Key Words: Folic acid • homocysteine • dose response • food fortification •

dose-response curve • adult population

Vitamin D supplementation and bone mineral density in early postmenopausal

women

Lucy , B Clifton-Bligh, M Liza Nery, Gemma Figtree,

Twigg, Hibbert, and Bruce G

Am J Clin Nutr 2003;77 1324-1329

Background: Elevated homocysteine concentrations, a likely risk factor for

cardiovascular disease, can be lowered effectively

with folic acid. The minimum dose of folic acid required for maximal reduction

of homocysteine concentrations is not yet known

reliably.

Objective: We aimed to determine the lowest folic acid dose that decreases

plasma homocysteine concentrations adequately in

healthy older adults.

Design: A dose-response trial with a randomized, double-blind, parallel-group,

placebo-controlled design was carried out

among 316 Dutch men and women aged 50–75 y. Subjects received daily for 12 wk

either a placebo or 1 of the 6 following

folic acid doses: 50, 100, 200, 400, 600, or 800 µg. The relative changes in

plasma homocysteine concentration in response to

increasing doses of folic acid were used to calculate the dose-response curve.

An adequate dose of folic acid was defined as

the dose that induced 90% of the maximal reduction in homocysteine

concentration.

Results: The relative decrease in plasma homocysteine concentration was

associated exponentially with increasing doses of

folic acid. From the dose-response curve, the adequate daily dose of folic acid

was estimated to be 392 µg, which decreased

plasma homocysteine concentrations 22%.

Conclusion: In older adults, daily supplementation with folic acid effectively

lowers plasma homocysteine concentrations, and a

daily dose of 400 µg is the minimum dose required for adequate homocysteine

reduction.

Key Words: Folic acid • homocysteine • dose response • food fortification •

dose-response curve • adult population

Calcium, protein, and fruit and vegetables as dietary determinants of bone

health

A New and D Joe Millward

Am J Clin Nutr 2003;77 1340-1341

The recent paper by Dawson- and (1) suggests that an increase in

dietary protein is beneficial to the skeleton,

provided that dietary intakes of calcium and vitamin D meet recommended amounts

(2). Because the calcium supplement used

provided an alkali source (citrate and malate), a point noted by the authors, it

might be prudent to examine further the relation

between total potassium and alkali intakes and rates of bone loss in this data

set. Frassetto et al (3) showed that the ratio of

protein to potassium predicts net acid excretion and, in turn, net renal acid

excretion predicts calcium excretion. They propose a

simple algorithm for determining the net rate of endogenous noncarbonic acid

production by calculating both the acidifying effect

of protein (mainly through sulfate excretion) and the alkalizing effect of

potassium (resulting from the dietary intake of potassium

as salts of weak organic acids). The baseline results of the Aberdeen

Prospective Osteoporosis Screening Study were

reanalyzed (4, 5); those women with a high intake of endogenous noncarbonic acid

(ie, a higher protein intake but a lower

potassium intake) had a lower peripheral and axial bone mineral density and a

higher level of bone resorption than did women

who had a low intake of endogenous noncarbonic acid (ie, a lower protein intake

but a higher potassium intake) (6). These

findings have also been confirmed in the longitudinal Aberdeen Prospective

Osteoporosis Screening Study (7).

Furthermore, the article by Hannan et al (8) is cited by Dawson- and

as providing evidence that dietary protein is

beneficial to bone mass; subjects with higher total and animal protein intakes

had lower rates of bone loss than did subjects

consuming less protein. However, in previous analyses of this cohort, high

intakes of potassium (and fruit and vegetables) were

associated with lower rates of bone loss in men and of greater bone mass in

women (9). This suggests, therefore, that in the

Framingham cohort, dietary protein intake was beneficial to bone, at least in

part because its potential acidifying influence was

balanced by the alkalizing effect of the dietary potassium intake.

As argued by Heaney (10) in the editorial accompanying the article by

Dawson- and , the magnitude and

importance of the bone protein pool is such that, considered in isolation, a

positive effect of protein on bone is not surprising.

Indeed there is considerable evidence for a limitation on the synthesis of

glycine (11), which accounts for 25% of collagen, so

that competition for glycine between collagen and its other important metabolic

demands might prevent its reutilization during

bone collagen turnover. However, it is now becoming clear that in maintaining

the bone matrix, the amino acid supply is as

important as is the sufficient stimulation of appropriate concentrations of

insulin-like growth factor I and other important growth

factors through the regulatory influence or anabolic drive of dietary protein

(12). In the past, this was mainly discussed in the

context of bone length growth stimulation (13). What is not yet clear is the

relation between these insulin-like growth factor

I–mediated anabolic influences acting on the matrix and the parathyroid

hormone–mediated responses to any protein-derived,

acid-stimulated increased urinary calcium loss. We suggest that, in the absence

of sufficient dietary alkali to neutralize the

protein-derived acid, net calcium loss ensues and the anabolic drive of dietary

protein on the bone matrix is ineffective in

maintaining bone mineral density. However, provision of dietary alkali (either

in the type of calcium supplement used in the

current study by Dawson- and or as fruit and vegetables) prevents

urinary calcium loss and enables the full

expression of the dietary protein–mediated anabolic drive on bone. This is

supported by previous work by this group, which

showed that calcium supplementation in the form of calcium citrate malate was

more effective in reducing bone loss than was

supplementation in the form of calcium carbonate (14).

Thus, the exciting findings of Dawson- and (1) further support the

arguments that maintenance of acid-base

homeostasis is crucial to preserving skeletal health (15). Hence, calcium

supplements may be favorable to bone health, not just

through the additional mineral that they supply but also (and possibly more so)

through their provision of additional alkali salts.

Indeed, the challenge remains to establish the extent of any need for additional

calcium in the presence of adequate dietary

protein and fruit and vegetable intakes.

REFERENCES

1.Dawson- B, SS. Calcium intake influences the association of

protein intake with rates of bone loss in

elderly men and women. Am J Clin Nutr 2002;75:773–9.[Abstract/Free Full

Text]

2.Food and Nutrition Board, Institute of Medicine. Dietary reference intakes:

calcium, phosphorus, magnesium, vitamin D

and fluoride. Washington, DC: National Academy Press, 1997.

3.Frassetto L, Todd K, RC Jr, Sebastian A. Estimation of net

endogenous noncarbonic acid production in humans

from dietary protein and potassium contents. Am J Clin Nutr

1998;68:576–83.[Abstract]

4.New SA, Bolton- C, Grubb DA, Reid DM. Nutritional influences on bone

mineral density: a cross-sectional study

in premenopausal women. Am J Clin Nutr 1997;65:1831–9.[Abstract]

5.New SA, Robins SP, MK, et al. Dietary influences on bone mass and

bone metabolism: further evidence of a

positive link between fruit and vegetable consumption and bone health? Am J

Clin Nutr

2000;71:142–51.[Abstract/Free Full Text]

6.New SA, Macdonald HM, Grubb DA, Reid DM. Positive association between net

endogenous non-carbonic acid

production (NEAP) and bone health: further support for the importance of

the skeleton to acidbase balance. Bone

2001;28(suppl):S94 (letter).

7.Macdonald HM, New SA, Fraser WD, Reid DM. Estimates of NEAP are associated

with increased bone turnover in

early postmenopausal women: findings from APOSS longitudinal. J Bone Miner

Res 2001;17:1131 (abstr).

8.Hannan MT, Tucker KL, Dawson- B, Cupples LA, Felson DT, Kiel DP.

Effect of dietary protein on bone loss

in elderly men and women: the Framingham osteoporosis study. J Bone Miner

Res 2000;15:2404–512.

9.Tucker KL, Hannan MT, Chen H, Cupples A, PWF, Kiel DP. Potassium and

fruit and vegetables are

associated with greater bone mineral density in elderly men and women. Am J

Clin Nutr

1999;69:727–36.[Abstract/Free Full Text]

10.Heaney RP. Protein and calcium: antagonists or synergists? Am J Clin Nutr

2002;75:609–10.[Free Full Text]

11. AA. The glycine story. Eur J Clin Nutr 199;45:59–65.

12.Schürch MA, Rizzoli R, Slosman D, Vadas L, Vergnaud P, Bonjour JP. Protein

supplements increase serum insulin-like

growth factor-I levels and attenuate proximal femur bone loss in patients

with recent hip fracture. Ann Intern Med

1998;128:801–9.[Medline]

13.Millward DJ, Rivers JPW. The need for indispensable amino acids: the

concept of the anabolic drive. Diabetes Metab

Rev 1989;5:191–212.[Medline]

14.Dawson- B, Dallal GE, Krall EA, Sadowski L, Sahyoun N, Tannenbaum S.

Acontrolled trial of the effect of

calcium supplementation on bone density in postmenopausal women. N Engl J

Med 1990;323:878–83.[Abstract]

15.New SA. The role of the skeleton in acid-base homeostasis. The 2001

Nutrition Society Medal Lecture. Proc Nutr Soc

2002;61:1–15.

Reply to SA New and DJ Millward

Bess Dawson-

Am J Clin Nutr 2003;77 1341

Many components of the diet influence bone health. We recently addressed the

association of protein intake with rates of bone

loss in elderly men and women taking either supplemental calcium citrate malate

and vitamin D or placebo. We found a positive

association between dietary protein intake and change in bone mineral density in

the supplemented group but not in the placebo

group (1).

New and Millward suggest that it would have been prudent to examine the relation

between total potassium and alkali

intakesand bone loss in our data set. Such an examination was not a goal of our

study; however, we may undertake such an

examination in the future.

New and Millward’s letter does draw into focus the possibility that the

different potassium and alkali intakes across the protein

tertiles that we used could have influenced our results. In both the

supplemented and placebo groups, the potassium intake was

similar across the protein tertiles. In addition, the ratios of urinary

potassium to creatinine were similar across the tertiles in both

groups. These observations support our conclusion that protein intake may have a

favorable effect on change in bone mineral

density in elderly men and women supplemented with calcium citrate malate and

vitamin D.

REFERENCE

1.Dawson- B, SS. Calcium intake influences the association of

protein intake with rates of bone loss in

elderly men and women. Am J Clin Nutr 2002;75:773–9.[Abstract/Free Full

Text]