PROTEIN INTAKE AND BLOOD
PRESSURE
The AHA Nutrition Committee suggests that
high-protein intake may increase blood pressure.
However, there is no scientific evidence
supporting this contention. In fact, a negative
correlation has been shown between protein
intake and systolic and diastolic blood pressures
in several epidemiological surveys analyzed by
Obarzanek et al.13 For example,
• Honolulu Heart Study. In this study of 6,406
Japanese-American men, a negative
relationship was observed between systolic
and diastolic blood pressures and the amount
protein consumed.14
• Chinese Study. In this investigation of 2,672
adults men and women, a negative
relationship was found between systolic
pressure and the amount of animal protein
consumed.15
• MRFIT Study. Based on 11,342 adult men,
investigators observed a negative relationship
between systolic blood pressure and the
amount of total protein consumed.16
In both normotensive and hypertensive rats,
increasing the dietary protein level enhances
both urine and the amount of sodium excreted,
although the mechanism behind these effects is
unknown and still speculative.17 Interestingly,
one study in human volunteers with a family
history of hypertension has shown that a highprotein
diet may counteract the adverse effects of
excessive salt intake.18 For more information on
protein intake and blood pressure, see the recent
review by Debry.17
PROTEIN INTAKE AND HEART DISEASE
Recent findings by Hu et al. suggests that
replacing carbohydrates with protein may be
associated with a lower risk of ischemic heart
disease.25 This result is consistent with evidence
from metabolic studies that replacement of
dietary carbohydrate with protein has favorable
effect on plasma lipoprotein and lipid
concentrations. However, because an increase
in protein intake from animal products such as
meats, dairy products, and eggs is often
accompanied by increases in intakes of
saturated fat and cholesterol, dietary advice to
improve public health based on these findings
should be made with caution.25
Recent novel approaches have shown that
glucose and lipid intake may induce an
increase in the generation of reactive oxygen
species (ROS) and oxidative stress. For
example, Mohanty et al. produced evidence
that all three major macronutrients induce an
increase in ROS generation.26 However, their
data also show that different nutrients produce
distinct patterns of stimulation of ROS
generation after their intake. Of the three
nutrients, glucose induced the greatest ROS
generation, followed in decreasing order by
fat (cream) and by protein (casein). The
detriment of oxidative stress is that it may
damage proteins and lipids, the latter through
lipid peroxidation. Lipid peroxidation of
LDL-C particles is an essential step in the
development of atherosclerosis.27
PROTEIN INTAKE AND LIVER
FUNCTION
AHA Nutrition Committee suggests that highprotein
intake may have detrimental effects
on liver function. However, there is no
scientific evidence whatsoever supporting this
contention. Protein is needed not only to
promote liver tissue repair, but also to provide
lipotropic agents such as methionine and
choline for the conversion of fats to
lipoprotein for removal from the liver, thus
preventing fatty infiltration.20
Rodents fed very high protein intakes have
been found to exhibit morphological changes
in the liver mitochondria, which could be
pathological. However, Jorda et al. reported
that the liver responds to the high-protein diet
by a proliferation of normally functioning
mitochondria.24 Further, the branched-chain
amino acids to aromatic amino acids ratio was
also increased, indicating the absence of hepatic
failure in these animals. The authors concluded
that “the increased protein content of diet
induced rapid increases in several
characteristics of hepatocytes… The results
presented here constitute a good example of how
the hepatocyte adapts to a continuing metabolic
stress.”
Further, protein catabolism is increased in liver
disease and may be exacerbated by inadequate
protein in the diet.19 Unless there is
encephalopathy (vide infra), the diet should
provide high-quality protein in the amount of 1.5
to 2 g/kg.19 In alcoholic liver disease, a highcalorie,
high-protein diet has been shown to
improve hepatic function and reduce mortality.
In one study, this was achieved by providing a
regular diet plus supplements of 60 g/day of
protein and 1600 kcal/day for the first 30 days
and followed by supplements of 45 g/day of
protein and 1200 kcal/day for the next 60 days.21
Finally, the role of protein restriction in patients
with chronic hepatic encephalopathy (HE) has
been questioned recently as the efficacy of
protein withdrawal in patients with HE has never
been subjected to a controlled trial.29 According
to Srivastava et al., “the emphasis in the
nutritional management of patients with HE
[hepatic encephalopathy] should not be on the
reduction of protein intake. Instead, the goal
should be to promote synthesis by making
available ample amounts of amino acids, while
instituting other measures to reverse the ongoing
catabolism.”29
EFFECTS OF VERY-LOWCARBOHYDRATE
DIET ON LEAN BODY
MASS
According to the AHA Nutrition Committee,
“Some popular high-protein/low-carbohydrate
diets limit carbohydrates to 10 to 20 g/d, which
is one fifth of the minimum 100 g/day that is
necessary to prevent loss of lean muscle tissue.”
Clearly, this is an incorrect statement since
catabolism of lean body mass is reduced by
ketones, which probably explains the
preservation of lean tissue observed during
very-low-carbohydrate diets.
For example, Volek et al. examined the
effects of 6-week carbohydrate-restricted diet
on total and regional body composition and
the relationships with fasting hormones.22
Twelve healthy normal-weight men switched
from their habitual diet (48% carbohydrate) to
a carbohydrate-restricted diet (8%
carbohydrate) for 6 weeks and 8 men served
as controls, consuming their normal diet.
Subjects were encouraged to consume
adequate dietary energy to maintain body
mass during intervention.
Fat mass was significantly decreased (-3.4 kg)
and lean body mass significantly increased
(+1.1 kg) at week 6. However, there were no
significant changes in composition in the
control group. The Authors concluded that a
carbohydrate-restricted diet resulted in a
significant reduction in fat mass and a
concomitant increase in lean body mass in
normal-weight men. They hypothesized that
elevated β-hydroxybutyrate concentrations
may have played a minor role in preventing
catabolism of lean tissue but other anabolic
hormones were likely involved (e.g., growth
hormone).
Oddly, the AHA Nutrition Committee ignores
the fact that energy restriction increases protein
requirements. It has been know for about a half
century that inadequate energy intake leads to
increased protein needs, presumably because
some of the protein normally used to synthesize
both functional (enzymatic) and structural
(tissue) protein is utilized for energy under these
conditions.1 For example, Butterfield has shown
that feeding as much as 2 g protein/kg/day to
men running 5 or 10 miles per day at 65% to
75% of their VO2max is insufficient to maintain
nitrogen balance when energy intake is
inadequate by as little as 100 kcal/day.30 Thus,
when trying to lose weight, it is important to
keep protein levels moderately high. The
reduction in calories needed to lose weight
should be at the expense of saturated fats and
carbohydrates, not protein.
CONCLUSION
It is clear that the American Heart Association
Nutrition Committee´s statement on dietary
protein and weight reduction contains misleading
and incorrect information. Certainly, such public
warnings should be based on a thorough analysis
of the scientific literature, not unsubstantiated
fears and misrepresentations. For individuals
with normal renal function, the risks are minimal
and must be balanced against the real and
established risk of continued obesity.23
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