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Hi All, Nuts, peanuts and diabetes is the subject of the PDF available

article below. I liked it.

Things like body mass index and magnesium did have quite an effect on

lowering the significance.

Cheers, Al.

JAMA. 2002;288:2554-2560

Nut and Peanut Butter Consumption and Risk

of Type 2 Diabetes in Women

Rui Jiang, MD; JoAnn E. Manson, MD; Meir J.

Stampfer, MD;

Simin Liu, MD; Walter C. Willett, MD, DrPH; B.

Hu, MD, PhD

Context Nuts are high in unsaturated

(polyunsaturated and

monounsaturated) fat and other nutrients that may

improve glucose

and insulin homeostasis.

Objective To examine prospectively the relationship

between nut

consumption and risk of type 2 diabetes.

Design, Setting, and Participants Prospective

cohort study of

83 818 women from 11 states in the Nurses' Health

Study. The

women were aged 34 to 59 years, had no history of

diabetes,

cardiovascular disease, or cancer, completed a

validated dietary

questionnaire at baseline in 1980, and were followed

up for 16 years.

Main Outcome Measure Incident cases of type 2

diabetes.

Results We documented 3206 new cases of type 2

diabetes. Nut

consumption was inversely associated with risk of

type 2 diabetes

after adjustment for age, body mass index (BMI),

family history of

diabetes, physical activity, smoking, alcohol use,

and total energy

intake. The multivariate relative risks (RRs) across

categories of nut

consumption (never/almost never, <once/week, 1-4

times/week, and

5 times/week) for a 28-g (1 oz) serving size were

1.0, 0.92 (95%

confidence interval [CI], 0.85-1.00), 0.84 (0.95%

CI, 0.76-0.93), and

0.73 (95% CI, 0.60-0.89) (P for trend <.001).

Further adjustment for

intakes of dietary fats, cereal fiber, and other

dietary factors did not

appreciably change the results. The inverse

association persisted

within strata defined by levels of BMI, smoking,

alcohol use, and other

diabetes risk factors. Consumption of peanut butter

was also

inversely associated with type 2 diabetes. The

multivariate RR was

0.79 (95% CI, 0.68-0.91; P for trend <.001) in women

consuming

peanut butter 5 times or more a week (equivalent to

140 g [5 oz] of

peanuts/week) compared with those who never/almost

never ate

peanut butter.

Conclusions Our findings suggest potential benefits

of higher nut

and peanut butter consumption in lowering risk of

type 2 diabetes in

women. To avoid increasing caloric intake, regular

nut consumption

can be recommended as a replacement for consumption

of refined

grain products or red or processed meats.

Type 2 diabetes affects approximately 16 million

people in the United

States1 and 135 million people worldwide2; the

number of people with

diabetes will reach an estimated 300 million

worldwide by 2025.2

Because management of diabetes and its complications

such as

cardiovascular disease, amputation, blindness, and

renal failure

imposes enormous medical and economic burdens,

primary

prevention has become a public health imperative.

Recent studies have shown that diet and lifestyle

modifications are

important means of preventing type 2 diabetes.3-5

Evidence indicates

that specific types of dietary fat rather than total

fat (as percentage of

energy) intake predict risk of type 2 diabetes.6

Nuts contain 70% to

80% fat, and most fatty acids in nuts are

unsaturated

(polyunsaturated and monounsaturated), which may be

beneficial for

glucose and insulin homeostasis. Several studies

have shown that a

higher intake of monounsaturated and polyunsaturated

fat improves

insulin sensitivity.7-10 A higher intake of

polyunsaturated fat is

associated with a lower risk of type 2 diabetes,11

whereas a higher

intake of saturated fat and trans-fat adversely

affects glucose

metabolism and insulin resistance8, 12-14 and

thereby may increase

the risk of type 2 diabetes.11 Other components of

nuts such as fiber

and magnesium decrease insulin demand and

resistance15-22 and

have been inversely associated with risk of type 2

diabetes.23, 24 Nuts

are also a rich source of many vitamins, minerals,

and antioxidants

and of plant protein, which could also be

beneficial.

Although several components of nuts have been

inversely associated

with risk of type 2 diabetes, the overall

association of nut

consumption with diabetes risk has not been studied.

We therefore

examined prospectively the association between nut

consumption

and risk of type 2 diabetes in a large cohort of

women from the

Nurses' Health Study.

METHODS

Study Population

The Nurses' Health Study was established in 1976

when 121 700

female registered nurses, aged 30 to 55 years and

from 11 states,

completed a mailed questionnaire designed to study

etiologies of

heart disease, cancer, and other major illnesses.25

Information on

lifestyle, health behaviors, and disease status has

been collected on

biennially mailed questionnaires since 1976, and

information about

vitamin supplement use has been collected the same

way since

1980. Diet was assessed in 1980, 1984, 1986, 1990,

and 1994 by

using semiquantitative food-frequency

questionnaires. For this

analysis, at baseline in 1980, we excluded women

with 10 or more

food items left blank or with implausibly high

(>3500 kcal/d) or low

(<500 kcal/d) total energy intake. We also excluded

women with a

history of diabetes, cardiovascular disease (angina,

coronary bypass

or angioplasty, myocardial infarction, or stroke),

and cancer (except

for nonmelanoma skin cancer). After these

exclusions, 83 818

participants remained in the analysis.

Dietary Assessment

The semiquantitative food-frequency questionnaire at

baseline (1980)

included 61 foods and was revised and expanded to

about twice the

number of foods in subsequent cycles.26, 27

Participants were asked

to report their average frequency of consumption of

selected foods

and beverages with a specified commonly used unit or

portion size

during the previous year. The reproducibility and

validity of the dietary

questionnaires are described in detail elsewhere.27

In the 1980 and 1984 dietary questionnaires, we

asked the

participants how often, on average, they had

consumed nuts (serving

size, 28 g [1 oz]) during the previous year:

never/almost never, 1 to 3

times a month, once a week, 2 to 4 times a week, 5

to 6 times a

week, once a day, 2 to 3 times a day, 4 to 6 times a

day, or more

than 6 times a day. In the 1986, 1990, and 1994

dietary

questionnaires, the question for nuts was split into

2 categories:

peanuts and other nuts. Total nut consumption was

the sum of the

intakes for peanuts and other nuts. Consumption of

peanut butter was

assessed in 1980, 1984, 1986, 1990, and 1994, with

the same 9

responses as those for nut consumption (serving

size, 15 mL [1

tablespoon]). Although peanuts are botanically

classified as legumes,

the fatty acid and nutrient profiles of peanuts are

very similar to other

nuts.28 A validation study of the food-frequency

questionnaires in the

Nurses' Health Study indicated that nuts and peanut

butter were

reported reasonably accurately; the correlation

coefficient was 0.75

between intakes assessed by the 1980 questionnaire

and by 4

one-week diet records for nuts and peanut butter.29

Nutrient intakes,

such as for fats and fiber, were computed by

multiplying the

consumption frequency of each food by the nutrient

content of the

specified portion and then summing these products

across all the

food items. The food composition values were

obtained from the

Harvard University Food Composition Database derived

from US

Department of Agriculture sources30 and supplemented

with

manufacturer information.

Measurement of Nondietary Factors

In 1982, 1988, and 1992, the participants provided

information on

family history of diabetes in first-degree

relatives. The participants

also provided information on their body weight and

cigarette smoking

every 2 years during the follow-up. The correlation

coefficient between

self-reported weight and measured weight was 0.96.31

Physical

activity was assessed by a shorter questionnaire in

1980 and 1982.32

More detailed information on physical activity was

first collected in

1986 and was updated in 1986, 1988, and 1992. We

used the

cumulative average number of hours a week spent in

moderate or

vigorous recreational activities, including brisk

walking, vigorous

sports, jogging, bicycling, heavy gardening, and

heavy housework.

Outcome Ascertainment

The outcome was incident type 2 diabetes. To all

women who

reported a diagnosis of diabetes on any biennial

follow-up

questionnaire, we mailed a supplementary

questionnaire regarding

symptoms, diagnostic tests, and treatments. The

diagnosis of

diabetes was established when at least 1 of the

following criteria was

reported on the supplementary questionnaire: (1) 1

or more classic

symptoms (excessive thirst, polyuria, weight loss,

hunger, or coma)

plus a fasting plasma glucose concentration of 140

mg/dL (7.8

mmol/L) or higher or a random plasma glucose

concentration of 200

mg/dL (11.1 mmol/L) or higher; or (2) at least 2

elevated plasma

glucose concentrations on different occasions

(fasting, 140 mg/dL

[7.8 mmol/L]; random, 200 mg/dL [11.1 mmol/L]; or

random, 200

mg/dL [11.1 mmol/L] after at least 2 hours of oral

glucose tolerance

testing) in the absence of symptoms; or (3)

treatment with

hypoglycemic medication (insulin or oral

hypoglycemic agents). The

diagnostic criteria for type 2 diabetes were changed

in 1997.33

However, we used the criteria proposed by the

National Diabetes Data

Group34 because all our cases were diagnosed before

June 1996. We

excluded women with type 1 diabetes and women

classified as having

gestational diabetes only. A validation study in a

subsample of this

cohort demonstrated that our supplementary

questionnaire is highly

reliable in confirming diabetes diagnoses.35 Among a

random sample

of 84 women classified by our criteria as having

type 2 diabetes

according to the information reported on the

supplementary

questionnaire, medical records were available for

62. An

endocrinologist blinded to the information reported

on the

questionnaire reviewed the records. The diagnosis of

type 2 diabetes

was confirmed in 61 (98%) of the 62 women.

Statistical Analysis

Each participant contributed follow-up time from the

date of returning

the 1980 questionnaire to the date of first

diagnosis of type 2

diabetes, death, or June 1, 1996. Women were

excluded from

subsequent follow-up if they developed diabetes. In

the primary

analyses, incidence of type 2 diabetes was related

to nut

consumption at baseline. In further analyses,

incidence of type 2

diabetes was related to the cumulative average of

nut consumption

from dietary questionnaires administered in 1980,

1984, 1986, 1990,

and 1994.36 We separated women into 4 categories

according to their

frequency of nut consumption: never/almost never,

less than once a

week (1-3 times/month), 1 to 4 times a week, and at

least 5 times a

week. Relative risks (RRs) of diabetes were

estimated from

proportional hazards models.37 Potential confounding

variables

including body mass index (BMI), family history of

diabetes, physical

activity, smoking, alcohol consumption, and

multivitamin supplements

were updated during follow-up. In multivariate

models, we adjusted for

age, BMI, family history of diabetes, physical

activity, smoking,

alcohol use, and total energy intake. We also

adjusted for several

dietary confounding variables such as glycemic load,

multivitamin

use, and intakes of polyunsaturated fat, saturated

fat, trans-fat, cereal

fiber, magnesium, whole grains, vegetables, fruits,

and fish.

In a secondary analysis, we performed a propensity

analysis38 in

which we used a logistic regression model to predict

nut consumption

(5 times/week vs never/almost never) from a

multitude of dietary and

lifestyle factors. We then examined the association

between nut

consumption and diabetes risk from a

proportional hazards

model adjusting for the predicted propensity scores.

We also calculated mean weight change from 1980 to

1996 for

women according to frequency of nut consumption at

baseline (4

categories) by using general linear models (least

square means).39 In

this analysis, we adjusted for age, family history

of diabetes, physical

activity, smoking, alcohol use, and baseline weight

and excluded

women who developed cancer, heart disease, or

diabetes during the

follow-up.

All P values were 2-sided. Tests for trend were

conducted using the

median value for each category of nut consumption

analyzed as a

continuous variable in the regression models. All

analyses were

performed with SAS version 6.12 software (SAS

Institute, Cary, NC).

RESULTS

At baseline in 1980, about 35% of women in this

cohort reported

consuming nuts almost never; 36%, consuming them

less than once

a week; 24%, 1 to 4 times a week; and 5%, at least 5

times a week.

Women who consumed more nuts generally weighed less

(Table 1).

Women with frequent nut consumption were less likely

to smoke and

more likely to exercise. Nut consumption was

positively associated

with intakes of polyunsaturated fat, dietary fiber,

magnesium, alcohol,

and multivitamin supplements and inversely

associated with glycemic

load and intake of trans-fat. Consumption of

vegetables and fruits was

similar for women with frequent nut consumption and

those who rarely

ate nuts, but women who consumed more nuts generally

ate less

meat and refined grain products.

We documented 3206 incident cases of type 2 diabetes

during

1 282 892 person-years of follow-up from 1980 to

1996. The nut

consumption at baseline was used to classify women

into 4

categories (never/almost never, <once/week, 1-4

times/week, and 5

times/week) so that the age-adjusted RR of diabetes

was 0.55 (95%

confidence interval [CI], 0.45-0.66), comparing

women who ate nuts at

least 5 times a week with those who never/almost

never ate nuts (P

for trend <.001) (Table 2). In multivariate models,

BMI was the

strongest confounder. The RR was attenuated to 0.74

(95% CI,

0.61-0.89; P for trend <.001) after BMI was added to

the model by

using it as a categorical variable (8 categories)

and was 0.72 (95% CI,

0.59-0.87; P for trend <.001) when BMI was used as a

continuous

variable. The RR was virtually unchanged after

further control for family

history of diabetes, physical activity, smoking,

alcohol consumption,

and total energy intake. After controlling for other

dietary variables

such as glycemic load, multivitamin use, and intakes

of

polyunsaturated fat, saturated fat, trans-fat,

cereal fiber, magnesium,

whole grains, vegetables, fruits, and fish, the RR

did not appreciably

change (0.71; 95% CI, 0.57-0.87). Updated analyses

using the

cumulative average of nut consumption yielded

similar results

(multivariate RR, 0.76; 95% CI, 0.59-0.97; P for

trend = .001).

In the secondary analysis controlling for propensity

scores, those who

ate nuts at least 5 times a week still had a lower

diabetes risk

compared with those who never/almost never ate nuts

(RR, 0.73; 95%

CI, 0.56-0.96).

To examine further whether the relationship between

nut consumption

and type 2 diabetes risk was independent of other

potential risk

factors for type 2 diabetes, we conducted

multivariate analyses within

strata defined by levels of these factors. We found

no apparent

modification of the relationship by these factors,

and the inverse

association persisted in all subgroups (Table 3).

We also examined the relationship between

consumption of peanut

butter and risk of type 2 diabetes. Frequent

consumption of peanut

butter was associated with a significantly reduced

risk of type 2

diabetes (Table 4). The multivariate RR was 0.79

(95% CI, 0.68-0.91),

comparing women who ate peanut butter at least 5

times a week with

those who never/almost never ate peanut butter.

To address the concern that higher nut consumption

may lead to

more weight gain, we calculated average weight

change during 16

years of follow-up according to frequency of nut

consumption at

baseline. After adjustment for age, family history

of diabetes, physical

activity, smoking, alcohol use, and baseline weight,

the average

weight gain across categories of nut consumption

(never/almost

never, <once/week, 1-4 times/week, 5 times/week) was

not

significantly different (6.5, 6.4, 6.4, and 6.3 kg,

respectively).

COMMENT

In this large prospective cohort study of women, we

found that

consumption of nuts and peanut butter was inversely

associated with

risk of type 2 diabetes, independent of known risk

factors for type 2

diabetes, including age, obesity, family history of

diabetes, physical

activity, smoking, and dietary factors. The inverse

association with

nuts persisted in all subgroup analyses.

The major concern of our analysis is residual

confounding by body

weight because obesity is the most important

determinant of type 2

diabetes. In our analyses, we adjusted for BMI by

using detailed

categories and continuous variables, and the results

did not change

appreciably. Although we cannot rule out the

possibility of residual

confounding by other potential risk factors, it is

unlikely that they can

explain the observed inverse association. The

likelihood of bias is

minimized because of the prospective study design,

high follow-up

rate, and repeated measures of diet with validated

food-frequency

questionnaires. Another issue deserving attention is

that the

diagnostic criteria for type 2 diabetes used in this

study were

changed in 1997 so that lower fasting glucose levels

(126 mg/dL [7.0

mmol/L]) would now be considered the diagnostic cut

point.33 If the

new criteria were used, some women classified as

being without

diabetes would have been reclassified as having

diabetes. However,

this change would not explain our results, because

inclusion of those

with diabetes in the group without diabetes would

tend to weaken the

association.

Although the relationship between nut consumption

and risk of type 2

diabetes has not been evaluated previously, several

studies have

examined the relationship between the major

constituents of nuts (eg,

specific types of fat) and insulin resistance and

type 2 diabetes.6-14,

24, 40-52 Most clinical and epidemiological studies

have observed no

effect of total fat intake on insulin sensitivity

and risk of type 2

diabetes.11, 24, 42, 43, 47-49 The findings on types

of dietary fat have

been inconsistent.8, 11, 12, 24, 40, 42-44, 50-52

Some of the

inconsistency could be due to methodological

limitations in many

studies, such as small sample size, short duration,

crude dietary

assessment methods without documented validity, and

absence of

control for confounding (eg, other types of fats,

fiber intake, obesity,

and physical activity). More recent clinical and

epidemiological

studies with better design suggest that specific

types of fat rather

than total fat as percentage of energy play an

important role in the

development of type 2 diabetes.6, 8, 11 A

multicenter study involving a

3-month intervention among 162 healthy men and women

showed that

a diet high in saturated fat (18% of energy)

decreased insulin

sensitivity compared with a diet high in

monounsaturated fat (21% of

energy) with the same total fat content.8 An

analysis11 from the

Nurses' Health Study with 14 years of follow-up

showed that women

in the highest quintile of vegetable fat intake had

a 40% lower risk of

type 2 diabetes than those in the lowest quintile.

The RR comparing

extreme quintiles of polyunsaturated fat intake was

0.75 (95% CI,

0.65-0.88). An Italian study showed that a higher

consumption of oils

consisting mostly of polyunsaturated fat was

associated with lower

fasting plasma concentrations of glucose.40

The mechanisms by which specific types of dietary

fat affect insulin

sensitivity are not well understood. It has been

shown that the fatty

acid composition of the phospholipids in the

skeletal muscle cell

membranes is directly related to insulin sensitivity

in humans.53 A

specific fatty acid in cell membranes could

influence insulin action

through altering insulin receptor binding or

affinity and influencing ion

permeability and cell signaling. Changes in dietary

fatty acid

composition alter fatty acid composition of the

phospholipids in cell

membranes, perhaps modulating insulin action and

sensitivity.

Nuts are also rich in fiber and magnesium and have a

relatively low

glycemic index. In several clinical studies,

high-fiber diets decreased

insulin demand among patients with type 2

diabetes.15-17 Also,

metabolic studies suggest an inverse association

between

intracellular magnesium and insulin resistance,18,

22 and magnesium

supplementation increased insulin sensitivity among

patients with

type 2 diabetes19, 20 and among healthy subjects.21

Higher intakes of

fiber and magnesium and foods with a low glycemic

index have been

associated with reduced risk of type 2 diabetes in

several prospective

studies.23, 24, 54, 55

Nuts may protect against type 2 diabetes through

additional

mechanisms. The persistence of an association when

intakes of

types of fats, fiber, and magnesium were in the

model indicates that

the apparent benefit of nuts was not explained

entirely by content of

fats, fiber, and magnesium. Thus, other constituents

of nuts such as

vitamins, minerals, antioxidants, and plant protein

or interactions

among these factors may also play important roles in

reducing risk of

type 2 diabetes.

There have been concerns that frequent nut

consumption may result

in weight gain and increased risk of coronary heart

disease because

of the high fat content. However, in our cohort, we

did not find an

appreciable association between nut consumption and

weight

change. Also, several large prospective studies56-59

have consistently

found an inverse association between nut consumption

and the risk of

coronary heart disease. The epidemiological findings

are supported by

several clinical studies28, 60-63 in which diets

high in nuts had

beneficial effects on blood lipids. These results

contradict the

conventional wisdom that intake of high-fat foods

leads to obesity and

heart disease. Given the observed inverse

association between nuts

and risk of coronary heart disease as well as type 2

diabetes, it is

advisable to recommend regular nut consumption as a

replacement

for refined grain products64 or red or processed

meats,65 which would

avoid increasing caloric intake.

In conclusion, higher consumption of nuts and peanut

butter was

associated with a lower risk of type 2 diabetes in

this large cohort

study of women. Our data, combined with other

clinical and

epidemiological data, support potential benefits of

increasing nut

consumption in reducing type 2 diabetes risk.

REFERENCES

1.

American Diabetes Association.

Diabetes facts and figures, 2000.

Available at: http://www.diabetes.org/.

Accessibility verified October

2, 2002.

2.

King H, Aubert RE, Herman WH.

Global burden of diabetes, 1995-2025: prevalence,

numerical

estimates, and projections.

Diabetes Care.

1998;21:1414-1431.

MEDLINE

3.

Knowler WC, Barrett-Connor E, Fowler SE, et al.

Reduction in the incidence of type 2 diabetes with

lifestyle

intervention or metformin.

N Engl J Med.

2002;346:393-403.

MEDLINE

4.

Tuomilehto J, Lindstrom J, sson JG, et al.

Prevention of type 2 diabetes mellitus by changes in

lifestyle among

subjects with impaired glucose tolerance.

N Engl J Med.

2001;344:1343-1350.

MEDLINE

5.

Hu FB, Manson JE, Stampfer MJ, et al.

Diet, lifestyle, and the risk of type 2 diabetes

mellitus in women.

N Engl J Med.

2001;345:790-797.

MEDLINE

6.

Hu FB, van Dam RM, Liu S.

Diet and risk of type II diabetes: the role of types

of fat and

carbohydrate.

Diabetologia.

2001;44:805-817.

MEDLINE

7.

Parillo M, Rivellese AA, Ciardullo AV, et al.

A high-monounsaturated-fat/low-carbohydrate diet

improves peripheral

insulin sensitivity in non-insulin-dependent

diabetic patients.

Metabolism.

1992;41:1373-1378.

MEDLINE

8.

Vessby B, Unsitupa M, Hermansen K, et al.

Substituting dietary saturated for monounsaturated

fat impairs insulin

sensitivity in healthy men and women: the KANWU

Study.

Diabetologia.

2001;44:312-319.

MEDLINE

9.

Houtsmuller AJ, van Hal-Ferwerda J, Zahn KJ, Henkes

HE.

Favourable influences of linoleic acid on the

progression of diabetic

micro- and macroangiopathy.

Nutr Metab.

1980;24:105-118.

MEDLINE

10.

Heine RJ, Mulder C, Popp-Snijders C, van der Meer J,

van der Veen

EA.

Linoleic-acid-enriched diet: long-term effects on

serum lipoprotein and

apolipoprotein concentrations and insulin

sensitivity in

noninsulin-dependent diabetic patients.

Am J Clin Nutr.

1989;49:448-456.

MEDLINE

11.

Salmeron J, Hu FB, Manson JE, et al.

Dietary fat intake and risk of type 2 diabetes in

women.

Am J Clin Nutr.

2001;73:1019-1026.

MEDLINE

12.

Feskens EJ, Kromhout D.

Habitual dietary intake and glucose tolerance in

euglycaemic men:

the Zutphen Study.

Int J Epidemiol.

1990;19:953-959.

MEDLINE

13.

Marshall JA, Hamman RF, Baxter J.

High-fat, low-carbohydrate diet and the etiology of

non-insulin-dependent diabetes mellitus: the San

Valley

Diabetes Study.

Am J Epidemiol.

1991;134:590-603.

MEDLINE

14.

Christiansen E, Schnider S, Palmvig B, Tauber-Lassen

E, Pedersen

O.

Intake of a diet high in trans monounsaturated fatty

acids or saturated

fatty acids: effects on postprandial insulinemia and

glycemia in obese

patients with NIDDM.

Diabetes Care.

1997;20:881-887.

MEDLINE

15.

Rivellese A, Riccardi G, Giacco A, et al.

Effect of dietary fibre on glucose control and serum

lipoproteins in

diabetic patients.

Lancet.

1980;2:447-450.

MEDLINE

16.

Simpson HC, Simpson RW, Lousley S, et al.

A high carbohydrate leguminous fibre diet improves

all aspects of

diabetic control.

Lancet.

1981;1:1-5.

MEDLINE

17.

JW, Gustafson NJ, CA, Tietyen-

J.

Dietary fiber and diabetes: a comprehensive review

and practical

application.

J Am Diet Assoc.

1987;87:1189-1197.

MEDLINE

18.

Paolisso G, Scheen A, D'Onofrio F, Lefebvre P.

Magnesium and glucose homeostasis.

Diabetologia.

1990;33:511-514.

MEDLINE

19.

Sjogren A, Floren CH, Nilsson A.

Oral administration of magnesium hydroxide to

subjects with

insulin-dependent diabetes mellitus: effects on

magnesium and

potassium levels and on insulin requirements.

Magnesium.

1988;7:117-122.

MEDLINE

20.

Paolisso G, Sgambato S, Pizza G, Passariello N,

Varricchio M,

D'Onofrio F.

Improved insulin response and action by chronic

magnesium

administration in aged NIDDM subjects.

Diabetes Care.

1989;12:265-269.

MEDLINE

21.

Paolisso G, Sgambato S, Gambardella A, et al.

Daily magnesium supplements improve glucose handling

in elderly

subjects.

Am J Clin Nutr.

1992;55:1161-1167.

MEDLINE

22.

Resnick LM.

Ionic basis of hypertension, insulin resistance,

vascular disease, and

related disorders: the mechanism of " syndrome X. "

Am J Hypertens.

1993;6:123S-134S.

MEDLINE

23.

Salmeron J, Manson JE, Stampfer MJ, Colditz GA, Wing

AL, Willett

WC.

Dietary fiber, glycemic load, and risk of

non-insulin-dependent

diabetes mellitus in women.

JAMA.

1997;277:472-477.

MEDLINE

24.

Salmeron J, Ascherio A, Rimm EB, et al.

Dietary fiber, glycemic load, and risk of NIDDM in

men.

Diabetes Care.

1997;20:545-550.

MEDLINE

25.

Colditz GA, Manson JE, Hankinson SE.

The Nurses' Health Study: 20-year contribution to

the understanding

of health among women.

J Womens Health.

1997;6:49-62.

MEDLINE

26.

Willett WC, Sampson L, Stampfer MJ, et al.

Reproducibility and validity of a semiquantitative

food frequency

questionnaire.

Am J Epidemiol.

1985;122:51-65.

MEDLINE

27.

Willett WC.

Nutritional epidemiology.

In: Rothman KJ, Greenland S, eds. Modern

Epidemiology. 2nd ed.

Philadelphia, Pa: Lippincott-Raven Publishers;

1998:623-642.

28.

O'Byrne DJ, Knauft DA, Shireman RB.

Low fat-monounsaturated rich diets containing

high-oleic peanuts

improve serum lipoprotein profiles.

Lipids.

1997;32:687-695.

MEDLINE

29.

Salvini S, Hunter DJ, Sampson L, et al.

Food-based validation of a dietary questionnaire:

the effects of

week-to-week variation in food consumption.

Int J Epidemiol.

1989;18:858-867.

MEDLINE

30.

Composition of FoodsRaw, Processed, and Prepared,

1963-1992.

Washington, DC: US Dept of Agriculture; 1993.

31.

Rimm EB, Stampfer MJ, Colditz GA, Chute CG, Litin

LB, Willett WC.

Validity of self-reported waist and hip

circumferences in men and

women.

Epidemiology.

1990;1:466-473.

MEDLINE

32.

Manson JE, Hu FB, Rich- JW, et al.

A prospective study of walking as compared with

vigorous exercise in

the prevention of coronary heart disease in women.

N Engl J Med.

1999;341:650-658.

MEDLINE

33.

Report of the Expert Committee on the Diagnosis and

Classification

of Diabetes Mellitus.

Diabetes Care.

1997;20:1183-1197.

MEDLINE

34.

National Diabetes Data Group.

Classification and diagnosis of diabetes mellitus

and other categories

of glucose intolerance.

Diabetes.

1979;28:1039-1057.

MEDLINE

35.

Manson JE, Rimm EB, Stampfer MJ, et al.

Physical activity and incidence of

non-insulin-dependent diabetes

mellitus in women.

Lancet.

1991;338:774-778.

MEDLINE

36.

Hu FB, Stampfer MJ, Manson JE, et al.

Dietary fat intake and the risk of coronary heart

disease in women.

N Engl J Med.

1997;337:1491-1499.

MEDLINE

37.

DR, Oakes D.

Analysis of Survival Data.

London, England: Chapman & Hall; 1984.

38.

D'Agostino RB Jr.

Propensity score methods for bias reduction in the

comparison of a

treatment to a non-randomized control group.

Stat Med.

1998;17:2265-2281.

MEDLINE

39.

Kleinbaum DG, Kupper LL, Muller KE.

Applied Regression Analysis and Other Multivariable

Methods.

Boston, Mass: PWS-KENT Publishing; 1988.

40.

Trevisan M, Krogh V, Freudenheim J, et al.

Consumption of olive oil, butter, and vegetable oils

and coronary heart

disease risk factors: the Research Group ATS-RF2 of

the Italian

National Research Council.

JAMA.

1990;263:688-692.

MEDLINE

41.

Feskens EJ, Loeber JG, Kromhout D.

Diet and physical activity as determinants of

hyperinsulinemia: the

Zutphen Elderly Study.

Am J Epidemiol.

1994;140:350-360.

MEDLINE

42.

Lundgren H, Bengtsson C, Blohme G, et al.

Dietary habits and incidence of noninsulin-dependent

diabetes

mellitus in a population study of women in

Gothenburg, Sweden.

Am J Clin Nutr.

1989;49:708-712.

MEDLINE

43.

Feskens EJ, Kromhout D.

Cardiovascular risk factors and the 25-year

incidence of diabetes

mellitus in middle-aged men: the Zutphen Study.

Am J Epidemiol.

1989;130:1101-1108.

MEDLINE

44.

Feskens EJ, Virtanen SM, Rasanen L, et al.

Dietary factors determining diabetes and impaired

glucose tolerance:

a 20-year follow-up of the Finnish and Dutch cohorts

of the Seven

Countries Study.

Diabetes Care.

1995;18:1104-1112.

MEDLINE

45.

Storlien LH, Baur LA, Kriketos AD, et al.

Dietary fats and insulin action.

Diabetologia.

1996;39:621-631.

MEDLINE

46.

Mayer- EJ, Monaco JH, Hoen HM, et al.

Dietary fat and insulin sensitivity in a triethnic

population: the role of

obesity: the Insulin Resistance Atherosclerosis

Study (IRAS).

Am J Clin Nutr.

1997;65:79-87.

MEDLINE

47.

BV, Abbott WG, Swinburn BA.

Evaluation of metabolic effects of substitution of

complex

carbohydrates for saturated fat in individuals with

obesity and NIDDM.

Diabetes Care.

1991;14:786-795.

MEDLINE

48.

Borkman M, LV, Chisholm DJ, Storlien LH.

Comparison of the effects on insulin sensitivity of

high carbohydrate

and high fat diets in normal subjects.

J Clin Endocrinol Metab.

1991;72:432-437.

MEDLINE

49.

Swinburn BA, Boyce VL, Bergman RN, BV,

Bogardus C.

Deterioration in carbohydrate metabolism and

lipoprotein changes

induced by modern, high fat diet in Pima Indians and

Caucasians.

J Clin Endocrinol Metab.

1991;73:156-165.

MEDLINE

50.

Uusitupa M, Schwab U, Makimattila S, et al.

Effects of two high-fat diets with different fatty

acid compositions on

glucose and lipid metabolism in healthy young women.

Am J Clin Nutr.

1994;59:1310-1316.

MEDLINE

51.

Schwab US, Niskanen LK, Maliranta HM, Savolainen MJ,

Kesaniemi

YA, Uusitupa MI.

Lauric and palmitic acid-enriched diets have minimal

impact on serum

lipid and lipoprotein concentrations and glucose

metabolism in

healthy young women.

J Nutr.

1995;125:466-473.

MEDLINE

52.

Louheranta AM, Turpeinen AK, Schwab US, Vidgren HM,

Parviainen

MT, Uusitupa MI.

A high-stearic acid diet does not impair glucose

tolerance and insulin

sensitivity in healthy women.

Metabolism.

1998;47:529-534.

MEDLINE

53.

Borkman M, Storlien LH, Pan DA, AB, Chisholm

DJ,

LV.

The relation between insulin sensitivity and the

fatty-acid composition

of skeletal-muscle phospholipids.

N Engl J Med.

1993;328:238-244.

MEDLINE

54.

Meyer KA, Kushi LH, s DR Jr, Slavin J, Sellers

TA, Folsom AR.

Carbohydrates, dietary fiber, and incident type 2

diabetes in older

women.

Am J Clin Nutr.

2000;71:921-930.

MEDLINE

55.

Liu S, Manson JE, Stampfer MJ, et al.

A prospective study of whole-grain and risk of type

2 diabetes mellitus

in US women.

Am J Public Health.

2000;90:1409-1415.

MEDLINE

56.

Fraser GE, Sabate J, Beeson WL, Strahan TM.

A possible protective effect of nut consumption on

risk of coronary

heart disease: the Adventist Health Study.

Arch Intern Med.

1992;152:1416-1424.

MEDLINE

57.

Fraser GE, Sumbureru D, Pribis P, Neil RL, son

MA.

Association among health habits, risk factors, and

all-cause mortality

in a black California population.

Epidemiology.

1997;8:168-174.

MEDLINE

58.

Prineas RJ, Kushi LH, Folsom AR, Bostick RM, Wu Y.

Walnuts and serum lipids.

N Engl J Med.

1993;329:359.

MEDLINE

59.

Hu FB, Stampfer MJ, Manson JE, et al.

Frequent nut consumption and risk of coronary heart

disease in

women: prospective cohort study.

BMJ.

1998;317:1341-1345.

MEDLINE

60.

Grundy SM, Denke MA.

Dietary influences on serum lipids and lipoproteins.

J Lipid Res.

1990;31:1149-1172.

MEDLINE

61.

Sabate J, Fraser GE, Burke K, Knutsen SF, H,

Lindsted KD.

Effects of walnuts on serum lipid levels and blood

pressure in normal

men.

N Engl J Med.

1993;328:603-607.

MEDLINE

62.

Spiller GA, DJ, Cragen LN, et al.

Effect of a diet high in monounsaturated fat from

almonds on plasma

cholesterol and lipoproteins.

J Am Coll Nutr.

1992;11:126-130.

MEDLINE

63.

Abbey M, Noakes M, Belling GB, Nestel PJ.

Partial replacement of saturated fatty acids with

almonds or walnuts

lowers total plasma cholesterol and

low-density-lipoprotein

cholesterol.

Am J Clin Nutr.

1994;59:995-999.

MEDLINE

64.

Willett W, Manson J, Liu S.

Glycemic index, glycemic load, and risk of type 2

diabetes.

Am J Clin Nutr.

2002;76:274S-280S.

MEDLINE

65.

van Dam RM, Willett WC, Rimm EB, Stampfer MJ, Hu FB.

Dietary fat and meat intake in relation to risk of

type 2 diabetes in

men.

Diabetes Care.

2002;25:417-424.

MEDLINE

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