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for categorical variables. *P value calculated for race distribution; for ethnicity (Hispanic vs. non-His-
panic), P 0.39.
Barnard and Associates
DIABETES CARE, VOLUME 29, NUMBER 8, AUGUST 2006 1779
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6
1
Low-fat vegan diet and type 2 diabetes
1780 DIABETES CARE, VOLUME 29, NUMBER 8, AUGUST 2006
the Pearsons correlation of weight change
with A1C change was r 0.51, P
0.0001 (within the vegan group [n 24],
r 0.39, P 0.05; within the ADAgroup
[n 33], r 0.49, P 0.004).
Body weight fell 5.8 kg in the vegan
group (P 0.0001) and 4.3 kg in the
ADAgroup (P 0.0001) (between-group
P 0.082; baseline-adjusted P 0.066).
Among medication-stable participants,
vegan participants lost 6.5 kg compared
with 3.1 kg for ADA participants (P
0.001; baseline-adjusted P 0.001).
The reduction in urinary albumin was
signicant in the vegan group (P 0.002)
but not in the ADA group (P 0.14). The
unadjusted between-group difference
was not signicant. However, after adjust-
ment for baseline values, the effect of diet
was signicant (P 0.013).
For the entire sample, there were no
between-group differences in lipid val-
ues. Among those whose lipid-controlling
medications remained constant (80% [39
of 49] of vegan group, 82% [41 of 50] of
ADA group), reductions in total choles-
terol were 0.866 mmol/l (33.5 mg/dl,
17.6%) for the vegan group and
0.491 mmol/l (19.0 mg/dl, 9.7%)
for the ADAgroup (P 0.0125). Changes
in LDL cholesterol were 0.58 mmol/l
(22.6 mg/dl, 21.2%) for the vegan
group and 0.277 mmol/l (10.7 mg/dl,
9.3%) for the ADA group (P 0.023).
Changes in HDL cholesterol were 0.16
mmol/l (6.0 mg/dl, 11.0%) for the
vegan group and 0.07 mmol/l (2.8
mg/dl, 5.7%) for the ADA group (P
0.14). The total-to-HDL cholesterol ratio
fell for both groups, as did triglyceride
concentrations.
There were no treatment-related seri-
ous adverse events.
CONCLUSIONS Both diets were
associated with signicant clinical im-
provements, as indicated by reductions in
A1C, body weight, plasma lipid concen-
trations, and urinary albumin excretion.
Among medication-stable participants,
changes in A1C, weight, BMI, waist cir-
cumference, total cholesterol, and LDL
cholesterol were signicantly greater in
the vegan group. The magnitude of A1C
reduction in medication-stable vegan
group participants, 1.23 percentage
points, compares favorably with that ob-
served in single-agent therapy with oral
diabetes drugs (15).
A low-fat plant-based diet inuences
nutrient intake and body composition in
several ways that may, in turn, affect in- P
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Barnard and Associates
DIABETES CARE, VOLUME 29, NUMBER 8, AUGUST 2006 1781
sulin sensitivity. First, because such diets
are low in fat and high in ber, they typ-
ically cause associated reductions in di-
etary energy density and energy intake,
which are not fully compensated for by
increased food intake (16,17). Our data
suggest that the weight-reducing effect of
the vegan diet (4) is responsible for a sub-
stantial portion of its effect on A1C.
Independent of their effect on body
weight, reductions in total fat intake and
in the proportion of dietary saturated to
unsaturated fat increase insulin sensitivity
(18), as do increased intake of low
glycemic index and high-ber foods (1).
Finally, limited evidence suggests
that reductions in iron stores increase in-
sulin sensitivity (19). A vegan diet pro-
vides iron in its nonheme form, which is
somewhat less absorbable than heme
iron. A study comparing 30 ovolactoveg-
etarians and 30 meat eaters, all of whom
were healthy and had BMIs 23 kg/m
2
,
showed that vegetarians had adequate,
but lower, body iron stores, compared
with meat eaters (serum ferritin concen-
tration 35 g/l [95% CI 2149] vs. 72
g/l [45100]). The vegetarians also
demonstrated less insulin resistance
(steady-state plasma glucose concentra-
tion 4.1 mmol/l [3.55.0] vs. 6.9 mmol/l
[5.27.5], respectively) (19).
Insulin resistance is related to lipid
accumulation within muscle cells (in-
tramyocellular lipid), apparently due to a
genetically based reduction in mitochon-
drial activity identiable many years be-
fore diabetes manifests (20). This lipid
accumulation may be responsive to diet.
High-fat diets appear to downregulate the
genes required for mitochondrial oxida-
tive phosphorylation in skeletal muscle
(21). In contrast, a case-control study
found that soleus muscle intramyocellu-
lar lipid concentrations were signicantly
lower in a group of 21 vegans compared
with 25 omnivores (9.7 [95%CI 16.2
to 3.3], P 0.01) (22).
The lipid-lowering effect of vegan di-
ets, attributable to their absence of dietary
cholesterol, lowsaturated fat content, and
a specic cholesterol-reducing effect of
soluble ber and other plant constituents
(23), is particularly important given that
cardiovascular complications are the pri-
mary cause of morbidity and mortality in
diabetes. While diets high in rened car-
bohydrate may increase triglyceride con-
centrations, high-ber and lowglycemic
index foods appear to have the opposite
result (24).
The limited compliance of the ADA
group merits comment. Researchers have
long lamented the difculties in adhering
to diets for diabetes (25). The A1C reduc-
tion observed in the ADA group was sim-
ilar to that found in previous studies (26).
A potential weakness of the ADA guide-
lines is that they require portion size lim-
its for overweight individuals, and
limitations on saturated-fat intake are
based on these limited energy intakes. In-
dividuals who exceed their prescribed en-
ergy intake limits with overly large
portions can, as a result, easily exceed rec-
ommended limits on saturated fat. In con-
trast, the vegan diet includes no animal
fat, so variations in food quantity are less
likely to result in substantial increases in
saturated fat intake. Because the vegan
diet is based on the elimination of certain
foods, it may be easier to understand than
regimens that limit quantities of certain
foods without proscribing any. The ac-
ceptability of low-fat vegan diets in clini-
cal studies is similar to that of seemingly
more moderate diets (27).
This studys strengths include its
analysis of dependent measures without
regard to variations in dietary adherence
and applicability outside the research set-
ting. A study limitation was that both di-
ets made participants vulnerable to the
hypoglycemic effect of their diabetes
medications, resulting in medication re-
ductions that confound the interpretation
of A1C changes and necessitating a sub-
group analysis of medication-stable par-
ti ci pants. Because these epi sodes
occurred early in the trial, there was no
opportunity to bring interim laboratory
values forward. Also, most study partici-
pants were taking antihypertensive med-
ications, which may have blunted the
effect of diet on blood pressure.
In conclusion, in individuals with
type 2 diabetes participating in a 22-week
clinical trial, both a low-fat vegan diet and
a diet following ADAguidelines improved
glycemic control; however, the changes
were greater in the vegan group. Further
research is necessary to establish longer-
term diet effects and sustainability.
Acknowledgments The study was sup-
ported by grant R01 DK059362-01A2 from
the National Institute of Diabetes and Diges-
tive and Kidney Diseases and by the Diabetes
Action Research and Education Foundation.
The authors express appreciation to Paul
Poppen, PhD, for statistical analyses.
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DIABETES CARE, VOLUME 29, NUMBER 8, AUGUST 2006 1783