"Sonos" <[email hidden]> wrote in message news:<[email hidden]>...
Quoted message said:Sonos said:On 13-May-2004, [email hidden]
(fresh~horses) said:Soy: tastes horrid and the texture is worse. And: it
is a *very* highly processed food, when I choose to
eat as unprocessed as possible. However, I do
sometimes eat edamame, and soy beans in recipes like
any other bean.
Zee
I have also found that in the US, obtaining a reliable,
nutrient dense and low processed source of soy is
difficult and expensive. It is ironic because the US is
a world leader in soybean production!
I should say unless you purchase the dried soybean from
the farmer. In my state, 60 lbs of certified organic
soybeans costs only $18.00 when purchased from the field.
Ok while I'm dragging my sack in read this. Sorry no url
for this pdf. And the tables, graphs and charts didn't
copy properly.
Original Research
Address correspondence to: Jeff S. Volek, Ph.D., R.D.,
Assistant Professor, Department of Kinesiology, 2095
Hillside Road, Unit 1110, University of Connecticut, Storrs,
CT 06269-1110.
E-mail: [email hidden] This study was supported by
a grant from The Robert C. Atkins Foundation, New York, NY.
Presented in part at Federation of American Societies for
Experimental Biology, San Diego, CA, April, 2003. Journal of
the American College of Nutrition, Vol. 23, No. 2, 177–184
(2004) Published by the American College of Nutrition 177
Comparison of a Very Low-Carbohydrate and Low-Fat Diet on
Fasting Lipids, LDL Subclasses, Insulin Resistance, and
Postprandial Lipemic Responses in Overweight Women
Jeff S. Volek, PhD, RD, FACN, Matthew J. Sharman, MA, Ana L.
Go´mez, MS, Chris DiPasquale, MS, Melissa Roti, PhD, Amy
Pumerantz, BS, and William J. Kraemer, PhD
Human Performance Laboratory, Department of Kinesiology,
University of Connecticut, Storrs, Connecticut
Key words: triglycerides, weight loss, postprandial lipemia,
lipoprotein subclasses, Atkins diet
Objective: Very low-carbohydrate diets are widely used for
weight loss yet few controlled studies have determined how
these diets impact cardiovascular risk factors compared to
more traditional low-fat weight loss diets. The primary
purpose of this study was to compare a very low-carbohydrate
and a low-fat diet on fasting blood lipids, LDL subclasses,
postprandial lipemia, and insulin resistance in overweight
and obese women.
Methods: Thirteen normolipidemic, moderately overweight
(body fat 30%) women were prescribed two hypocaloric (500
kcal/day) diets for 4 week periods, a very low-carbohydrate
(10% carbohydrate) and a low-fat (30% fat) diet. The diets
were consumed in a balanced and randomized fashion. Two
fasting blood draws were performed on separate days and an
oral fat tolerance test was performed at baseline, after the
very low-carbohydrate diet, and after the low-fat diet.
Results: Compared to corresponding values after the very low-
carbohydrate diet, fasting total cholesterol, LDL-C, and HDL-
C were significantly (p 0.05) lower, whereas fasting
glucose, insulin, and insulin resistance (calculated using
the homeostatic model assessment) were significantly higher
after the low-fat diet.
Both diets significantly decreased postprandial lipemia and
resulted in similar nonsignificant changes in the total
cholesterol/ HDL-C ratio, fasting triacylglycerols, oxidized
LDL, and LDL subclass distribution.
Conclusions: Compared to a low-fat weight loss diet, a short-
term very low-carbohydrate diet did not lower LDL-C but did
prevent the decline in HDL-C and resulted in improved
insulin sensitivity in overweight and obese, but otherwise
healthy women. Small decreases in body mass improved
postprandial lipemia, and therefore cardiovascular risk,
independent of diet composition.
INTRODUCTION
Very low-carbohydrate diets have been promoted for several
decades as a superior alternative weight loss approach, best
exemplified by the best-selling Atkins diet having sold
several million copies [1]. Very low-carbohydrate diets have
recently been examined in several clinical trials that
primarily focused on weight loss. Results generally indicate
that very low-carbohydrate diets result in greater weight
loss compared to traditional low-fat diets [2–5]. However,
few studies have rigorously examined the effects of very low-
carbohydrate diets on risk factors for cardiovascular
disease including postprandial lipemia, a significant and
independent risk factor for coronary artery disease [6,7].
Although carbohydrate restriction could favorably impact
certain aspects of lipid metabolism compared to low-fat
diets, such as decreasing hepatic production of
triacylglycerols [8], they are inherently high in saturated
fat and cholesterol, and therefore could be potentially
atherogenic.
In addition to studies aimed at determining the effects of
carbohydrate restriction on weight loss and body
composition, an understanding of the effects on accepted
risk factors for cardiovascular disease should be known in
different populations before this diet is widely
recommended. To address this concern, our laboratory has
assessed the effects of very low carbohydrate diets in normal-
weight men and women under conditions of weight maintenance
to isolate the effects of the diet independent of weight
loss. Collectively these studies have shown that short-term
carbohydrate restriction (10% of total energy) for 4 to 8
weeks reduces fasting triacylglycerols, postprandial lipemic
responses to a fat-rich meal, and insulin levels, and
increases HDL-C, LDL-C, and LDL particle size [9–12].
Whether similar responses occur in overweight women
consuming a hypocaloric very low-carbohydrate weight loss
diet is unknown.
Thus, the primary purpose of this study was to shed light on
the short-term cardiovascular risk responses to consumption
of a hypocaloric very low-carbohydrate diet in overweight
women. Since weight loss alone tends to improve risk status,
the responses were compared to those achieved after
consumption of a traditional low-fat diet. We tested the
hypothesis that a very low-carbohydrate diet would not have
a detrimental effect on cardiovascular risk status compared
to a low-fat diet. Because blood lipid responses to diet are
quite variable, we utilized a within subjects design in
order enhance statistical power and the chances of detecting
significant differences between diets.
MATERIALS AND METHODS
Subjects Thirteen moderately overweight and obese
(percentage body fat 30%) but otherwise healthy women
volunteered to participate in this investigation. Their
physical characteristics were (mean SD) age 34.0 8.6
years, body mass 76.2
12.9 kg, body fat 42.0 5.1% (determined by dual-energy
X-ray absorptiometry) and body mass index 29.6 4.0
kg/m2. The subjects had been weight stable for the past
month (2 kg), were not adhering to special diets or
regular consumers of nutritional supplements (except a
daily multi-vitamin/mineral) and habitually consumed
between 27% and 41% of energy as fat (assessed via a seven-
day food diary at baseline). All subjects were
nonsmokers, not prescribed any medication known to
affect serum lipoproteins, and premenopausal. All blood
samples were obtained during days 2–4 of the follicular
phase to control for possible effects of menstrual phase
on lipoproteins, even though the variation is small
[13]. Subjects were either sedentary or moderately
active and maintained the same level of physical
activity throughout the study documented by analysis of
log sheets on which all exercise sessions were recorded.
The study was conducted in accordance with the
guidelines of the Institutional Review Board at the
University of Connecticut.
Experimental Design Subjects consumed two experimental
weight loss diets for 4 week periods, a low-fat and a very
low-carbohydrate diet. The diets were consumed in a balanced
and randomized fashion. Two fasting blood draws were
performed at the same time of day on separate days (to
account for diurnal and day-to-day variation in lipids), and
an oral fat tolerance test was performed at baseline, after
the very low-carbohydrate diet and after the low-fat diet.
Diet Interventions Both experimental diets were designed to
be hypoenergetic (500 kcal/day). Energy levels were
assigned to the nearest 200 kcal increment based on resting
energy expenditure obtained using indirect calorimetry
(MedGraphics CPX/D, Medical Graphics Corporation, St. Paul,
MN) at the start of the study and appropriate activity
factors. Standard diabetic exchange lists were used to
ensure a constant energy and macronutrient balance of
protein (20% energy), fat (25% energy), and carbohydrate
(55% of energy) during the low-fat diet. The low-fat diet
was also designed to contain 10% saturated fat and 300 mg
cholesterol (i.e., a Step I diet). Foods encouraged during
the low-fat diet included whole grains (breads, cereals and
pastas), fruit/fruit juices, vegetables, vegetable oils, and
low-fat dairy and meat products. We developed customized
diabetic exchange lists for the very low-carbohydrate diet
period in order to ensure a constant energy and balance of
protein (30% energy), fat (60% energy) and carbohydrate
(10% of energy) throughout the day. There were no
restrictions on the type of fat from saturated and
unsaturated sources or cholesterol levels. Foods commonly
consumed on the very lowcarbohydrate diet were beef (e.g.,
hamburger, steak), poultry
(e.g., chicken, turkey), fish, oils, various nuts/seeds and
peanut butter, moderate amounts of vegetables, salads
with low-carbohydrate dressing, moderate amounts of
cheese, eggs, protein powder, and water or low-
carbohydrate diet drinks. Low-carbohydrate bars and
shakes (Atkins Nutritionals, Inc., Hauppauge, NY) were
provided to subjects during the very lowcarbohydrate
diet. A daily multi-vitamin/mineral complex that
provided micronutrients at levels 100% of the RDA was
given to subjects during both experimental diets. All
subjects received extensive initial instruction and follow-
up by registered dietitians on how to translate
foods/meals into diabetic exchanges. Subjects were also
provided with a packet outlining specific lists of
appropriate foods, recipes and sample meal plans that
were compatible with their individual preferences for
both experimental diets. Subjects received follow- up
counseling on a weekly basis during which time body
mass was measured, compliance was assessed and further
dietetic education provided.
Subjects received thorough instructions for completing
detailed weighed food records during weeks 1, 3, and 4 of
each experimental diet (21 days total). Food measuring
utensils and scales were provided to subjects to ensure
accurate reporting of food/beverage amounts consumed. Food
diaries were analyzed for energy and macro/micronutrient
content (Nutritionist Pro™, Version 1.3, First Databank Inc,
The Hearst Corporation, San Bruno, CA).
The program had no missing values for the nutrients
reported. The database was extensively modified by our group
to include new foods and recipes. To ensure that
carbohydrates were restricted throughout the very low-
carbohydrate diet, subjects tested their urine daily using
reagent strips (Bayer Corporation, Elkhart, IN). The test is
specific for acetoacetic acid, which produces a relative
color change when it reacts with nitroprusside. We have
found this to be a very sensitive indicator of carbohydrate
restriction and compliance to a very low-carbohydrate diet
in our prior studies [9–11].
Fasting Blood Collection Blood samples were obtained on two
separate days before and after each 4 week experimental
diet. Samples were obtained following an overnight fast and
abstinence from alcohol and strenuous exercise for 24
hours. Subjects reported to the laboratory between 0700 and
0900 hours, rested quietly for 10 minutes in the supine
position, and a blood sample was obtained from an
antecubital vein and collected into a tube coated with a
silicone-gel. Blood was separated by centrifugation at 1500
g for 15 minutes at 4°C.
Oral Fat Tolerance Test An oral fat tolerance test was
performed after each experimental diet using standard
procedures in our laboratory [9–11]. Subjects arrived at the
laboratory after a 12 hour overnight fast and abstinence
from alcohol and strenuous exercise for 24 hours. A flexible
catheter was inserted into a forearm vein and blood samples
were obtained from a 3-way stopcock connected to the end of
the catheter. Blood was collected with a syringe and
transferred to a silicone-gel-coated tube for processing as
above for determination of triacylglycerol. The catheter was
kept patent with a constant saline drip. Subjects rested in
a seated position for 10 minutes and two baseline blood
samples were obtained separated by 10 minutes. The test meal
(150 mL heavy whipping cream, sugar-free pudding, 5 mL
canola oil,
28.5 g macadamia nuts) was then consumed. This meal
provided 867 kcal, 13% carbohydrate, 3% protein, 84%
fat, 38 g saturated fat, 33 g monounsaturated fat, 4 g
polyunsaturated fat, and 207 mg cholesterol.
Postprandial blood samples were obtained immediately
after the meal and hourly for a total of eight hours.
Subjects rested quietly in a seated position and
consumed exactly one liter of water only during the 8
hour postprandial period.
Determination of Serum Lipids, Oxidized LDL, Glucose, and
Insulin After processing, serum collected for the
determination of insulin, LDL particle size and oxidized LDL
(oxLDL) were immediately stored at 80°C. The remaining
serum (3 mL) was sent to a certified medical laboratory
(Quest Diagnostics, Wallingford, CT) for determination of
glucose, total cholesterol, HDL-C, and triacylglycerol
concentrations using automated enzymatic procedures (Olympus
America Inc., Melville, NY). The Friedewald formula [14] was
used to calculate LDL-C: [LDL-C total cholesterol (HDL-C
triacylglycerols/
29)]. Fasting oxidized LDL-C was determined in duplicate
using an enzyme-linked immuno sorbent assay (American
Laboratory Products Company, Windham, NH) that is based
on the direct sandwich technique in which two monoclonal
antibodies are directed against separate antigenic
determinants on the oxidized apolipoprotein B molecule
[15]. Intra-assay coefficient of variance was 7.9%.
Fasting serum insulin concentrations were determined in
duplicate using an ELISA kit with a sensitivity of 1.81
pmol/L (#10-1600, Diagnostic Systems Laboratory, Webster,
TX). Intra-assay coefficient of variance was
30.5%. Absorbances were read on a multilabel counter (Versa-
Max, Molecular Devices, Sunnyvale, CA). The homeostasis
model assessment (HOMA) was used to estimate insulin
resistance using the formula: glucose (mmol/L)
[insulin (mU/L)/
30.1] [1]. Normal-weight subjects aged 35 years have an
insulin resistance of 1 [16].
Determination of Lipoprotein Particle Size Lipoprotein
particle size was determined using non-gradient
polyacrylamide gel electrophoresis (Lipoprint LDL System,
Quantimetrix Co., Redondo Beach, CA). The method has been
described in detail in a recent publication by our
laboratory [10] and others [17] and validated against non-
denaturing gradient gel electrophoresis and nuclear magnetic
resonance spectroscopy
[31]. Seven bands of LDL, 3 bands of IDL, and VLDL were
quantitatively evaluated using computer software (NIH
imaging software, utilizing the Lipoprint LDL macro).
The scanned gel image is divided at designated Rf
values identified by their relative mobility, which is
based on particle size (smaller particles migrate
further). The area under the curve is calculated for
each fraction. The percentage of LDL, IDL, and VLDL in
each band and mean and peak LDL particle diameter are
reported. Based on the distribution of LDL subclasses,
subjects were classified as either Pattern A
(predominance of large LDL particles) or Pattern B
(predominance of small LDL particles).
Statistical Analysis All statistical analyses were done with
Statistica software, Version 5.5 (StatSoft Inc, Tulsa, OK).
Means for fasting serum total cholesterol, HDL-C, LDL-C, and
triacylglycerols were calculated from both fasting samples
obtained at each time point and used for statistical
analysis. Paired comparison t tests (two-tailed) were used
to evaluate values after each diet intervention.
Triacylglycerol total area under curve (AUC) was calculated
from individual values obtained during the oral fat
tolerance test using the trapezoidal method. The alpha level
for significance was set at 0.05.
RESULTS Dietary Intakes All dietary macronutrients were
significantly different when women were on the very low-
carbohydrate diet compared to the low-fat diet with the
exception of total dietary energy and alcohol (Table 1). We
achieved our goals for each diet with 21% of total energy
coming from fat on the low-fat diet and 9% of total energy
coming from carbohydrate on the very lowcarbohydrate diet.
All subjects were in ketosis throughout the very low-
carbohydrate diet as indicated by color changes on the
urinary reagent strips (data not shown), indicating
compliance in terms of carbohydrate restriction. Subjects
lost significantly more weight on the very low-carbohydrate
diet (2.96 1.45 kg) compared with the low-fat diet (1.06
2.07 kg). Fasting Lipids, Glucose, and Insulin Fasting
total cholesterol, LDL-C, and HDL-C were significantly lower
after the low-fat diet but there was no significant
difference between diets for the total cholesterol/HDL-C
ratio. Fasting triacylglycerol responses were not different
between diets but the triacylglycerol/HDL-C ratio was
significantly lower after the very low-carbohydrate diet.
Fasting oxidized LDL was unchanged by either diet. Fasting
glucose, insulin, and insulin resistance HOMA were
significantly lower after the very low-carbohydrate diet
Lipoprotein Particle Size All but one subject was classified
as Pattern A at the start of the study, which is reflected
by the low percentage of smaller LDL-3 particles (1%).
There were no differences in the relative percent of
lipoprotein fractions or LDL size responses between diets
with the exception of VLDL, which was significantly lower
after the very low-carbohydrate diet.
Analysis performed on 7 days of diet records during baseline
and 21 days during the very low-carbohydrate and low-fat
diets. There was a significant relation between peak LDL
size at the start of the study and the change in LDL peak
size after the very lowcarbohydrate (r 0.59) but not the
low-fat (r 0.49) diet (Table 3), (Fig. 1).
Oral Fat Tolerance Test Postprandial triacylglycerol values
generally peaked about 3 hours after the meal and gradually
returned to baseline after 7 to 8 hours (Fig. 2). Compared
to the baseline triacylglycerol AUC (1304 555 mg/dL 8
hours), postprandial lipemic responses were reduced to a
similar extent after the very low-carbohydrate (927 452
mg/dL 8 hours) compared to the low-fat (984 444 mg/dL
8 hours) diet.
DISCUSSION Interest in very low-carbohydrate diets for the
purpose of weight loss has increased in recent years. These
diets have been criticized because they differ from
traditional recommendations for healthy weight loss [19–21].
We studied overweight, but otherwise healthy women with
normal lipid profiles. In this population, the results of
this study demonstrate both a shortterm hypocaloric very low-
carbohydrate and low-fat diet had a similar effect on
cardiovascular risk as shown by similar changes in the total
cholesterol/HDL-C ratio and fasting and postprandial
triacylglycerols. However, a very low-carbohydrate diet was
more effective than a low-fat diet at improving insulin
sensitivity as measured by the homeostatic model assessment
using fasting glucose and insulin, but the significance of
this small decrease is probably not physiological relevant
in terms of glucose clearance or insulin effectiveness. Fig.
2. Values are means SEM, n 13. Serum triacylglycerol
responses after ingestion of a high-fat meal at baseline and
after a 4 week very low-carbohydrate diet and a 4 week low-
fat diet in overweight women.
Our prior work in men indicated that a very low-carbohydrate
diet improved the lipid abnormalities characteristic of the
metabolic syndrome (i.e., the diet decreased fasting and
postprandial triacylglycerols, increased HDL-C, and
increased LDL size distribution) [9,10]. The magnitude of
these improvements was related to the severity of the
dyslipidemia. That is men who started with higher
triacylglycerols, lower HDL-C, and/or smaller LDL particles,
demonstrated the greatest improvements in response to the
very low-carbohydrate diet. In the present study, there were
no significant differences between the very low-carbohydrate
and low-fat diets on fasting and postprandial
triacylglycerols and LDL particle distribution. Different
from the men in our prior studies, the overweight women in
this study showed little evidence of any dyslipidemia. In
fact only one woman was characterized as Pattern B at
baseline. This is consistent with other research showing
that women have larger less atherogenic LDL particles than
men [22–25]. Similar to our prior work [9–11], we did
observe an inverse correlation between baseline peak LDL
size and the change in LDL size to the very low-carbohydrate
indicating that women who have smaller more atherogenic LDL
particles do increase LDL size in response to a very low-
carbohydrate diet. As expected the low-fat diet decreased
both LDL-C and HDL-C resulting in no change in the total cholesterol/HDL-
C ratio. The very low-carbohydrate diet did not lower LDL-C,
but it prevented the decline in HDL-C also resulting in no
change in the total cholesterol/HDL-C ratio. The lack of a
decrease in LDL-C on a very low-carbohydrate diet could be
of concern because several clinical trials clearly show that
LDL-lowering therapy reduces risk of coronary heart disease
and is therefore a primary target of therapy [26]. The goal
of this study was not to isolate a particular nutrient but
rather to examine how a diet pattern characterized by a very
low-carbohydrate intake affects cardiovascular risk factors.
However, the lower fiber intake on the very low-carbohydrate
diet could be an important factor that contributed to the
lack of a decrease in LDL-C because fiber alters metabolic
pathways of hepatic cholesterol and lipoprotein metabolism,
resulting in lowering of plasma LDL-C [27].
Caution should be taken when interpreting these short-term
changes in lipids, because whether subjects are weight
stabilized or actively losing weight will affect the
magnitude of the LDL-C and the direction of the HDL-C
responses [28,29]. Regardless of whether weight is
stabilized or at a plateau, HDL-C responses are better
maintained or increased and LDL-C does not decrease as much
on a very low-carbohydrate diet compared to a low-fat diet
[9–11] and a recent study showed that this pattern of LDL-C
and HDL-C response is sustained for one year [2]. Elevated
postprandial lipemia is a significant and independent risk
factor for cardiovascular disease [6,7]. Fasting and
postprandial triacylglycerols are higher in obesity,
especially abdominal obesity [30]; however, few studies have
examined the effect of moderate weight loss on postprandial
lipemia. Women in this study demonstrated a "normal"
postprandial lipemic response to the fat-rich meal,
consistent with their relatively low fasting
triacylglycerols. However, the small weight loss resulted in
rather dramatic improvements in the total area under the
triacylglycerol curve. We hypothesized the magnitude of the
reduction would be greater after the very low-carbohydrate
diet based on our prior work in normalweight men [9,10], normal-
weight women [11], and overweight men [31]. However, the
decrease on the very low-carbohydrate diet (29%) was
similar to the low-fat diet (25%). The reason for this
difference is unclear. Women have been shown to have lower
postprandial lipemic responses compared to men
[32], an anti-atherogenic trait shown to be due to a greater
contribution of skeletal muscle to lipid clearance [33].
One important feature of the design used in this study
was that the fat tolerance test was similar in
composition to the very lowcarbohydrate diet and
therefore may have gave an advantage to this diet
because individuals tend to metabolize a meal that
reflects the composition of their background diet more
effectively
[33]. From this perspective, a hypocaloric low-fat diet
could be viewed as having an advantage because it
resulted in a similar reduction in postprandial
lipemia despite being quite different in composition
to the test meal.
Women lost more weight on the very low-carbohydrate diet
(2.96 kg) than the low-fat diet (1.06 kg). Based on the
expected changes in lipids with weight loss [35], the
change in body weight alone should have decreased TC, LDL-
C, HDL-C, and triacylglycerols by 5.7, 2.3, 0.8, and 3.9
mg/dL, respectively, on the very low-carbohydrate diet and
by 2.1, 0.8, 0.3, and 1.4 mg/dL, respectively, on the low-
fat diet. This is much different than the actual changes
observed (Table 2), suggesting that the composition of the
diet, not weight loss per se, is the major stimulus for
changes in lipids.
There is concern that very low carbohydrate diets,
especially diets high in saturated fat, might lead to
insulin resistance; however we observed a significant
reduction in insulin resistance after the very low-
carbohydrate diet as measured by the homeostatic model
assessment technique [16], which uses fasting levels of
glucose and insulin. Adaptation to a threeweek very low
carbohydrate diet (8% carbohydrate, 75% fat) in healthy
subjects resulted in no change in resting or
insulinstimulated total glucose disposal [36]. There was
however a significant decrease in insulin-stimulated glucose
oxidation and a proportional increase in nonoxidative
glucose metabolism, presumably glycogen formation [36]. This
study also showed that insulin-stimulated suppression of
lipid oxidation was nearly prevented (i.e., insulin was
ineffective at inhibiting oxidation of fat) after a low
carbohydrate diet compared to an 80% reduction after a
standard diet [36]. Similar results were obtained in healthy
men who consumed 3 isoenergetic liquid diets equal in
protein (15% of energy) but different in carbohydrate (2%,
44% and 85% of energy) [37]. Glucose disposal was similar
between all three diets but the low carbohydrate diet
resulted in lower rates of insulin-stimulated glucose
oxidation and increased nonoxidative glucose disposal. The
low carbohydrate diet also prevented insulin-stimulated
inhibition of lipid oxidation. Collectively, these findings
do not support the notion that very low carbohydrate diets
exacerbate risk of type II diabetes mellitus and insulin
resistance. The results of this study indicate that,
although short-term hypocaloric low-fat and very low-
carbohydrate diets have different effects on HDL-C and LDL-C
metabolism, they have a similar effect on the total cholesterol/HDL-
C ratio. This study shows that even small reductions in body
mass resulting from either type of diet can result in
significant improvements in the postprandial lipemic
response to a fat-rich meal. The overall clinical
significance of these changes in lipids and insulin
sensitivity are unknown, and it remains to be determined if
these short-term responses can be sustained or are
reflective of long term benefits that are associated with
reduced morbidity and mortality. Limitations of this study
include a short duration, small sample size, and the fact
that we did not measure all cardiovascular biomarkers such
as those related to inflammation, endothelial function and
thrombosis, nor did we assess other important clinical
endpoints such as renal function or bone health. These data
should be viewed as pilot data that warrant further in-depth
studies to determine the robustness and ability to
generalize these data. The findings do support the concept
that overweight individuals have some flexibility and can
choose different dietary strategies depending on a number of
factors such as food preference, baseline lipid profile,
degree of obesity and the like.
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